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Hebert, Stanbrook and MacDonald 2010 point to the health risk of energy drinks due to inadequate labelling requirements, a lack of awareness of caffeine’s harmful effects and clever marketing aimed at children. Energy drinks contain 80 to 140 mg of caffeine per 250 mL, the equivalent caffeine in one cup of coffee. New formulations with caffeine concentrations as high as 500 mg per can are now being marketed.
The authors stress that many countries are working on strict regulations. Red Bull is being sold only in pharmacies in Norway. It is prohibited in Denmark. Herbert and colleagues recommend all products with caffeine levels exceeding 100 mg to have label and advertising with warnings comparable to those required for caffeine tablets. There should be no advertising targeting children, and public education should focuse on the health consequences of caffeine in children.
Energy shots : Similar to energy drinks, energy shots contain caffeine, vitamins, and herbs such as guarana, ginseng or ginkgo biloba, taurine, maltodextrin, inositol, carnitine, creatine or glucuronolactone. The central ingredient in most energy shots is caffeine, the same stimulant found in coffee or tea.
The average 50 ml energy shot has about 80 mg of caffeine ranging up to 200 mg per shot, and 200-1000 mg Taurin. This is approximately equivalent to a cup of coffee.
Micro shots: These are shots with 1-5 teaspoons of liquid, such as Dynapep and FIXX Extreme with 400 mg caffeine. [2]
Excessive energy shot intake [3]
According to the German Federal Institute for Risk Assessment (BfR) energy shots are a new kind of energy drinks that contain caffeine and taurine. In advertisements, these are claimed to increase concentration and capacity or physical performance. They are marketed in smaller portions (25-75 ml) than the more common energy drinks yet contain a higher concentration of caffeine and in some cases taurine per litre than energy drinks. The compositions of energy shots known to BfR vary significantly and contain between 50-200 mg caffeine and 200-1000 mg taurine per portion. In contrast to energy drinks, these energy shots are labelled with the manufacturer’s suggested intake levels recommending one portion per day.
Health risks: BfR writes that health risks can result if the suggested intake level is exceeded considerably. The extent of potential health risks depends on the intake amounts (caffeine and taurine) and the manner of intake (e.g. once, rapid intake over a short period of time, high amounts distributed over several single doses), on individual consumer sensitivity to the effects of caffeine, the usual amount of caffeine consumed daily, the amount of caffeine consumed through other sources of caffeine as well as potential parallel factors such as alcohol intake or strenuous physical/sports activity.
According to BfR, there is a risk that energy shots are not used in accordance with the manufacturer’s advice for intended use. The Institute assumes that energy shots are sometimes consumed in place of energy drinks without quantitative limit. It should also be noted that consumers in night clubs may choose to increase their energy shot intake in an attempt to counteract fatigue or to reach a state of arousal.
According to BfR, the desire to improve performance produces a risk of excessive energy shot intake. As consumers can be expected to disregard the advice for intended use, thus taking in high doses of caffeine which could result in adverse effects, the Institute deems energy shots unsafe.
The compositions of energy shots assessed here vary significantly (caffeine concentrations 1.3-6 g/L, taurine concentrations 4-20 g/L). With respect to the manufacturer’s advice for intended use (1 portion/day), caffeine intake ranges from 50-200 mg and taurine intake ranges from 200-1000 mg/day. The interaction of caffeine with other constituents in energy drinks (e.g. taurine) or with ethanol in the alcoholic beverages consumed together with energy shots or with physical exertion (e.g. extended, physically strenuous dancing) or sports activities could amplify the adverse effects of caffeine.
The use of caffeine as pharmaceutical product [3]:
- For the indication “to temporarily counteract symptoms of fatigue”, single doses of 100 to 200 mg caffeine are used, which can be repeated if necessary, but not more than twice within 24 hours (BGA, 1988; pharmaceutical product information of a caffeine monopreparation, 2008).
- With regard to “side effects”, the information states that the appearance of side ef-fects depends on the above named factors and that even low doses (this probably refers to 100 mg) can cause tachycardia, insomnia, apprehension and gastrointestinal disturbances, while doses over 200 mg can cause irritability, headaches and intensified physiological muscle tremors even in individuals with low sensitiv-ity (pharmaceutical product information of a caffeine monopreparation, 2008).
- In section “special warnings and special precautions for use” patients with hyperthyroidism (may increase) and patients with cirrhosis of the liver (caffeine may accumulate) are advised to take caffeine at a low dosage (about 100 mg) and only under medical supervision (pharmaceutical product information of a caffeine monopreparation, 2008).
- “Overdosing” contains the information that symptoms of poisoning can occur at 1g caffeine and more if the amount is taken in a short time span. It also states that fa-tal doses of caffeine range from 3 g and 10 g (pharmaceutical product information of a caffeine monopreparation, 2008).
Warning labels about excessive consumption of caffeine and taurine rejected by the EU Commission [4]
In July 2010 the European Commission rejected the German motion to require energy drinks to carry warning labels because of concerns about excessive consumption of caffeine and taurine.
The Commission found no evidence of a specific risk associated with these substances that would require additional labelling. This disregards several international warnings.
Energy drink consumption and alcohol intoxication [5]
Thombs and colleagues 2010 assessed the consumption of energy drink, alcohol intoxication and intention to drive a motor vehicle. The authors found that consuming alcohol mixed with energy drinks increased the risk 3-fold of leaving a bar highly intoxicated, as well as a 4-fold increased risk of intending to drive, compared to other drinkers who did not consume alcoholic beverages mixed with energy drinks. The authors concluded that energy drink consumption by young adults at bars is a marker for elevated involvement in nighttime risk-taking behaviour. The authors call for further research to develop sound regulatory policy on alcohol/energy drink sales practices of on-premise establishments.
[1] Hebert P, Stanbrook M, MacDonald N:"Caffeinating" children and youth
CMAJ 2010. July 26. DOI:10.1503/cmaj.100953
http://www.cmaj.ca/cgi/rapidpdf/cmaj.100953v1.pdf
[2] Fixxtreme: Micro shots
http://www.getyourfixx.com/
[3] Health risks of excessive energy shot intake. BfR Opinion No. 001/2010, 2 December 2009
http://www.bfr.bund.de/cm/245/health_risks_of_excessive_energy_shot_intake.pdf
[4] Nutraingredients: EC: Energy drinks don’t need warning labels. 20.07.2010.
http://www.nutraingredients.com/Regulation/EC-Energy-drinks-don-t-need-warning-labels
[5] Thombs DL, O'Mara RJ, Tsukamoto M, Rossheim ME, Weiler RM, Merves ML, Goldberger: BA: Event-level analyses of energy drink consumption and alcohol intoxication in bar patrons. Addict Behav. 2010 Apr;35(4):325-30. Epub 2009 Nov 24.
http://www.ncbi.nlm.nih.gov/pubmed/19954894
26.07.2010: Ultraviolet damage repair mechanism in plant and animals by photolyase enzyme [1]
Zhong and colleagues 2010 found that ultraviolet radiation damages the DNA by forming a 6-4 photoproduct (6-4PP) bond between two adjacent pyrimidine rings. This lesion interferes with replication and transcription, and may result in mutation and cell death. In many plants and animals a flavoenzyme called photolyase uses blue light energy to repair the 6–4PP by means of a cyclic proton and electron transfer between the enzyme and the damaged DNA. Human UV repair enzymes are less effective than those found in plants, microbes and animals. Chronic sun burns may therefore lead to skin cancer.
The researchers explain that a direct electron transfer takes place from the excited enzyme to the 6–4PP bond and a catalytic proton transfer between a histidine residue in the active site and the 6–4PP bond. After the DNA healing process, the electron and proton are returned to the photolyase enzyme which can start another reverse of the sun damage.
[1] Jiang Li, Zheyun Liu, Chuang Tan, Xunmin Guo, Lijuan Wang, Aziz Sancar & Dongping Zhong. Dynamics and mechanism of repair of ultraviolet-induced (6%u20134) photoproduct by photolyase. Nature, July 25, 2010 DOI: 10.1038/nature09192 .
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature09192.html
26.07.2010: New fish species of the Gulf of Mexico endangered by BP oil spill [1]
Researchers published in the Journal of Fish Biology the description of the Halieutichthys aculeatus species complex (pancake batfishes). Three species are recognized. Halieutichthys aculeatus was already known and two new species Halieutichthys intermedius and Halieutichthys bispinosus are now described by the authors. Arm-like fins are used to move along the bottom of the sea.
All species live in immediate proximity of the BP oil spill which threatens all marine life of the Gulf and part of the Atlantic ocean. The researchers are also concerned with the microscopic fauna of the region. Phase out of oil economy should be the most urgent aim of US government. Hydrogen economy present a feasible alternative to fossil energy.
[1] Ho HC, Chakrabarty P, Sparks JS: Review of the Halieutichthys aculeatus species complex (Lophiiformes: Ogcocephalidae), with descriptions of two new species. Journal of Fish Biology. Published Online 15 July 2010.
http://www3.interscience.wiley.com/journal/123584238/abstract
24.07.2010: Fungal invasion pathway of plant and animal cells [1]
Kale and colleagues 2010 relate that special proteins from fungi and oomycetes, known as effectors are transferred to the interior of host cells suppressing its natural defences. This pathway may explain the Irish potato famine in the nineteenth century, actual soybean diseases and fatal infectious diseases in humans.
The effector proteins bind a specific lipid molecule found on the cell surface, the lipid phosphatidylinositol 3-phosphate (PI3P), and can enter the cell using the lipid raft, a region of the cell's outer membrane. The PI3P lipid acts as a bridge between the effector protein and the lipid raft.
Bacteria puncture the host cell's membrane and then inject their effectors into the host cell's membrane with a needle-like structure. Fungi and oomycetes lack such an injection structure. They slip their effectors into plant cells by means of the PI3P found at the surface of plant cells, animal cells, and some human cells. The effector proteins N-terminal RXLR and dEER motifs enable oomycetes to bind with the PI3P to enter into host cells via the lipid raft of the cells wall. Fungi, contain functional variants of the RXLR motif which may also enter human cells and may be targeted by new therapeutic measures, which act on the RXLR terminal or on the PI3P lipid of the cell, say the authors.
The lipid raft of cell walls [2]
The plasma membrane of cells is made of a combination of glycosphingolipids and protein receptors organized in glycolipoprotein microdomains termed lipid rafts. These specialized membrane microdomains compartmentalize cellular processes by serving as organizing centers for the assembly of signaling molecules, influencing membrane fluidity and membrane protein trafficking, and regulating neurotransmission and receptor trafficking. Lipid rafts are more ordered and tightly packed than the surrounding bilayer, but float freely in the membrane bilayer.
[1] Kale S, Gu B, Capelluto DGS, Dou D, Feldman E, Rumore A, Arredondo FD, Hanlon R, Fudal I, Rouxel T, Lawrence CB, Shan W, Tyler BM. External lipid phophatidylinositol 3-phosphate mediates entry of eukaryotic pathogen effectors into plant and animal host cells. Cell, 2010; DOI: 10.1016/j.cell.2010.06.008
http://www.cell.com/retrieve/pii/S0092867410006628
[2] Wikipedia: Lipid raft
http://en.wikipedia.org/wiki/Lipid_raft#T-cell_antigen_receptor_signaling
20.07.2010: Sulforaphane from broccoli in the prevention of different cancers [1]
Phosphatase and tensin homolog (PTEN) is a protein that, in humans, is encoded by the PTEN gene.Mutations of this gene are a step in the development of many cancers.
PTEN acts as a tumor suppressor gene through the action of its phosphatase protein product. This phosphatase is involved in the regulation of the cell cycle, preventing cells from growing and dividing too rapidly. [2]
PTEN is one of the most commonly lost tumor suppressors in human cancer. During tumor development, mutations and deletions of PTEN occur that inactivate its enzymatic activity leading to increased cell proliferation and reduced cell death. Frequent genetic inactivation of PTEN occurs in glioblastoma, endometrial cancer, prostate cancer, and reduced expression is found in many other tumor types such as lung and breast cancer.
Traka and colleagues 2010 assessed the diet and its relation to counteract the loss of PTEN expression to contribute to the prevention of prostate cancer or reduce the rate of cancer progression. The authors focused on the interaction between sulforaphane, PTEN expression and gene expression in pre malignant prostate tissue.
Sulforaphane is an organosulfur compound that exhibits anticancer, antidiabetic, and antimicrobial properties. It is obtained from cruciferous vegetables such as broccoli. The enzyme myrosinase transforms glucoraphanin, a glucosinolate, into sulforaphane upon damage to the plant (such as from chewing). [3]
Traka and colleagues suggest that sulforaphane suppresses transcriptional changes induced by PTEN deletion and induces additional changes in gene expression associated with cell cycle arrest and programmed cell death Such changes can be induced in humans with a broccoli-rich diet. The authors point to the complex interaction between diet, genotype and gene expression, and the importance of small bioactive components of a varied diet.
Sulforaphane and iberin of broccoli are associated with a reduced risk of prostate cancer [4]
Chambers and colleagues 2009 report that isothiocyanates derived from glucosinolates that accumulate in broccoli are dietary compounds that have health effects. Sulforaphane derives from heading broccoli (calabrese) and iberin from sprouting broccoli, and both increase the expression of tumor suppressor gene PLAGL1 and suppressed expression of the tumor promoting genes IFITM1, CSPG2, and VIM in epithelial cells. The authors stress that sulforaphane and iberin interfere with cancer prevention genes, and recommend further studies on iberin.
Broccoli consumption interferes in its signalling pathway of inflammation and cancer of prostate [5]
Traka and colleagues 2008 stress that eating more than one portion of cruciferous vegetables per week reduces the risk of prostate cancer. The authors report that a six month broccoli-rich diet induced a significant increase of the gene expression of glutathione S-transferase mu 1 (GSTM1) associated with transforming growth factor beta 1 (TGFbeta1) and epidermal growth factor (EGF) signalling pathways. No such changes were found in a pea-rich diet
The authors explain further that sulforaphane from broccoli interacts with TGFbeta1, EGF and insulin peptides to form thioureas, and enhances TGFbeta1/Smad-mediated transcription reducing inflammation and cancer risk of prostate.
Sulforaphane derived from broccoli, may exhibit chemopreventive properties by inducing cell cycle arrest via induction of cyclin-dependent kinase inhibitor 1A (p21(waf1/cip1)). In 2009, Traka and colleagues explained the role of the transcription factor Kruppel-like factor 4 (KLF4) in mediating the induction of p21(waf1/cip1) and cellular differentiation by sulforaphane and iberin from broccoli. These results suggest that induction of p21(waf1/cip1) by SF or IB may be partly mediated by KLF4 in some colon cancer cells and tissues. [6]
[1] Traka MH, Spinks CA, Doleman JF, Melchini A, Ball RY, Mills RD, Mithen RF.The dietary isothiocyanate sulforaphane modulates gene expression and alternative gene splicing in a PTEN null preclinical murine model of prostate cancer. Mol Cancer. 2010 Jul 13;9(1):189.
http://www.ncbi.nlm.nih.gov/pubmed/20626841
[2] Wikipedia: PTEN (gene)
http://en.wikipedia.org/wiki/PTEN_%28gene%29
[3] Wikipedia: Sulforaphane
http://en.wikipedia.org/wiki/Sulphoraphane
[4] Chambers KF, Bacon JR, Kemsley EK, Mills RD, Ball RY, Mithen RF, Traka MH: Gene expression profile of primary prostate epithelial and stromal cells in response to sulforaphane or iberin exposure. Prostate. 2009 Sep 15;69(13):1411-21.
http://www.ncbi.nlm.nih.gov/pubmed/19489030
[5] Traka M, Gasper AV, Melchini A, Bacon JR, Needs PW, Frost V, Chantry A, Jones AM, Ortori CA, Barrett DA, Ball RY, Mills RD, Mithen RF.Broccoli consumption interacts with GSTM1 to perturb oncogenic signalling pathways in the prostate. PLoS One. 2008 Jul 2;3(7):e2568.
http://www.ncbi.nlm.nih.gov/pubmed/18596959
[6] Traka MH, Chambers KF, Lund EK, Goodlad RA, Johnson IT, Mithen RF: Involvement of KLF4 in sulforaphane- and iberin-mediated induction of p21(waf1/cip1). Nutr Cancer. 2009;61(1):137-45.
http://www.ncbi.nlm.nih.gov/pubmed/19116884
16.07.2010: Antitumor effect of low levels of arsenic in treatment of brain cancer and leukemia [1]
Arsenic is a known carcinogen, however, used as drug it has therapeutic effect in the treatment of leukemia and interferes in the cellular signaling cascade, the Hedgehog pathway. Aberrant Hedgehog pathway activation is linked to cancers of diverse tissues and organs, and the tumor growth-inhibiting effects of pathway antagonists.
Beachy and colleagues 2010 found that low levels of arsenic trioxide, use in treating patients with acute promyelocytic leukemia, block one of the last steps of the Hedgehog pathway, unlike cyclopamine, which acts near the beginning of the signaling cascade. Because only the tail end of the pathway is affected, a cancer cell has fewer opportunities to acquire resistance to arsenic.
Cyclopamine binds to a protein on the surface of the cell called Smoothened, blocking its ability to transmit the Hedgehog signal. Arsenic trioxide acts at the end of the Hedgehog pathway blocking the ability of the Gli2 protein to induce gene transcription in the nucleus. It stops Gli2 from moving into the cell's primary cilium, a communication hub, where many of the events of Hedgehog signaling take place. Without Gli2 in the cilium, the Hedgehog message is interrupted.
Certain type of brain tumor, medulloblastoma which depends on Hedgehog signaling, responded to the treatment with arsenic trioxide combined with cyclopamine in cultured cells. The authors conclude that arsenic might be useful to treat some types of cancers in combination with other drugs that act at different levels of the Hedgehog pathway, in resistant diseases or when cyclopamine resistance take place.
High levels of arsenic interferes in Hedgehog pathway increasing the risk of cancer of lung, skin and bladder [2]
Karagas and colleagues 2010 point out that arsenic act as co-carcinogen activating the Hedgehog pathway, alterating its signaling and targets a transcription factor. High levels of arsenic exposure are associated with high levels of Hedgehog activity. Hedgehog protein is a signaling pathway of cancer. Exposure to arsenic increases the risk of cancer of lung, skin and bladder. Karagas and colleagues explain that arsenic activates the Hedgehog signaling by decreasing the stability of the repressor form of GLI3, which is one of the transcription factors that regulate Hedgehog activity.
These findings are important to understand the aetiology of arsenic-induced disease. Millions of people worldwide who are exposed to environmentally relevant arsenic levels, such as found in Taiwan, Bangladesh, Argentina and United States where arsenic concentrations are above the current maximum contaminant level of 10 μg/L often found in private, unregulated drinking water systems.
Vitamines protect from bladder cancer [3]
Brinkman and colleagues 2010 report that higher total intakes of carotenoids, vitamin D, thiamin, niacin, and vitamin E were inversely related to bladder cancer risk among older individuals. Future studies should focus on high risk groups such as heavy smokers and older individuals. This study supports the importance of diet rich in fruits, vegetables and vitamin E rich oils.
Increase of lung cancer at lower levels of arsenic exposure [4]
Heck and colleagues 2010 report a higher risk of small-cell and squamous-cell lung cancer induced by low levels of arsenic exposure for toenail arsenic concentration > or = 0.114 microg/g, versus < 0.05 microg/g. Other lung diseases, such as bronchitis, chronic obstructive pulmonary disease, or fibrosi were found associated with increased lung cancer with toenail arsenic > or = 0.05 microg/g , compared with persons with low toenail arsenic and no history of lung disease. The authors concluded that there are indications that low to moderate levels of concentrations of arsenic (< 100 microg/L) in drinking water. increase lung cancer risk, and recommend further large scale studies.
High-level environmental arsenic exposure reduce risk of bladder death, says the New Hampshire study [5]
Bladder cancer patients who have been exposed to high levels of environmental arsenic may have a lower risk of death compared with those exposed to low levels, according to Andrew and colleagues 2009. High toenail arsenic levels was associated with longer overall survival, the association with drinking water levels and the trend observed for bladder cancer-specific deaths were not statistically significant. The authors also found that the protective effect of high levels of arsenic exposure applied to smokers but not to non-smokers. Arsenic exposure may be related to the survival of patients with bladder cancer.
Bajorin, Halabi and Small 2009, however, reported that the use of arsenic trioxide at a dosage of 0.3 mg/kg for five days every 28 days in patients with recurrent urothelial cancer did not reduce mortality and was associated with substantial toxicity. The authors suggest that arsenic treatment post-diagnosis is not effective. The longer survival observed in the New Hampshire study may be explained by chronic arsenic exposure inducing development of less aggressive tumor type. [6]
[1] Kim J, Lee JJ, Kim J, Gardner D, Beachy PA: Arsenic antagonizes the Hedgehog pathway by preventing ciliary accumulation and reducing stability of the Gli2 transcriptional effector. Proc Natl Acad Sci U S A. 2010 Jul 12.
http://www.pnas.org/content/early/2010/07/08/1006822107
[2] American Association for Cancer Research: Arsenic Exposure Activates an Oncogenic Signaling Pathway; Leads to Increased Cancer Risk
http://www.aacr.org/home/public--media/aacr-press-releases.aspx?d=1768
[3] Brinkman MT, Karagas MR, Zens MS, Schned A, Reulen RC, Zeegers MP: Minerals and vitamins and the risk of bladder cancer: results from the New Hampshire Study. Cancer Causes Control. 2010 Apr;21(4):609-19. Epub 2009 Dec 31.
http://www.ncbi.nlm.nih.gov/pubmed/20043202
[4] Heck JE, Andrew AS, Onega T, Rigas JR, Jackson BP, Karagas MR, Duell EJ: Lung cancer in a U.S. population with low to moderate arsenic exposure. Environ Health Perspect. 2009 Nov;117(11):1718-23.
http://www.ncbi.nlm.nih.gov/pubmed/20049123
[5] Kwong RC, Karagas MR, Kelsey KT, Mason RA, Tanyos SA, Schned AR, Marsit CJ, Andrew AS: Arsenic exposure predicts bladder cancer survival in a US population. World J Urol. 2009 Oct 16.
http://www.ncbi.nlm.nih.gov/pubmed/19834714
[6] Bajorin DF, Halabi S, Small E: Arsenic trioxide in recurrent urothelial cancer: a cancer and leukemia group B phase II trial (CALGB 99903). Clin Genitourin Cancer. 2009 Oct;7(3):E66-70.
http://www.ncbi.nlm.nih.gov/pubmed/19815484
15.07.2010: Genetics of Alzheimer disease [1]
The genes CLU, PICALM, and CR1 were identified as responsible for late-onset Alzheimer disease by the Genome-wide association studies (GWAS) analysing the genetics of 35,000 persons. [2] Seshadri and colleagues 2010 report recent identification of the two novel loci rs744373 near BIN1 and rs597668 near EXOC3L2/BLOC1S3/MARK4 which, together with loci CLU and PICALM are associated with Alzheimer disease. The authors point out that both new genes are important for future research, but they are not clinically useful, because they do not improve Alzheimer disease risk prediction.
Sleegers and colleagues 2010 comment the findings of CLU, CR1 and PICALM genes which support existing hypotheses about the amyloid, lipid, chaperone and chronic inflammatory pathways in Alzheimer pathogenesis. The authors present suggestions on how these findings may improve patient care and future drug development.[3]
In another study Bettens and colleagues 2010 point out that no single functional risk variant was identified besides the three causal genes-amyloid precursor protein and presenilin 1 and 2 genes-and one risk gene apolipoprotein E (APOE), suggesting a possible involvement of rare alleles and other types of genetic variants involved in the aetiology of Alzheimer disease. [4]
Genome-wide association study [2]
A genome-wide association study is an approach that involves rapidly scanning markers across the complete sets of DNA, or genomes, of many people to find genetic variations associated with a particular disease. such as asthma, cancer, diabetes, heart disease and mental illnesses.
With the completion of the Human Genome Project in 2003 and the International HapMap Project in 2005, researchers now have a set of research tools, include computerized databases. Researchers already have reported considerable success in undestanding diseases such as age-related macular degeneration. type 2 diabetes, Parkinson's disease, heart disorders, obesity, Crohn's disease and prostate cancer, as well as genetic variations that influence response to anti-depressant medications.
[1] Seshadri S, Fitzpatrick AL, Ikram MA, DeStefano AL, Gudnason V, Boada M, Bis JC, Smith AV, Carassquillo MM, Lambert JC, Harold D, Schrijvers EM, Ramirez-Lorca R, Debette S, Longstreth WT Jr, Janssens AC, Pankratz VS, Dartigues JF, Hollingworth P, Aspelund T, Hernandez I, Beiser A, Kuller LH, Koudstaal PJ, Dickson DW, Tzourio C, Abraham R, Antunez C, Du Y, Rotter JI, Aulchenko YS, Harris TB, Petersen RC, Berr C, Owen MJ, Lopez-Arrieta J, Varadarajan BN, Becker JT, Rivadeneira F, Nalls MA, Graff-Radford NR, Campion D, Auerbach S, Rice K, Hofman A, Jonsson PV, Schmidt H, Lathrop M, Mosley TH, Au R, Psaty BM, Uitterlinden AG, Farrer LA, Lumley T, Ruiz A, Williams J, Amouyel P, Younkin SG, Wolf PA, Launer LJ, Lopez OL, van Duijn CM, Breteler MM; CHARGE Consortium; GERAD1 Consortium; EADI1 Consortium: Genome-wide analysis of genetic loci associated with Alzheimer disease. JAMA. 2010 May 12;303(18):1832-40.
http://www.ncbi.nlm.nih.gov/pubmed/20460622
[2] National Human Genome Research Institute: Genome-Wide Association Studies
http://www.genome.gov/20019523
[3] Sleegers K, Lambert JC, Bertram L, Cruts M, Amouyel P, Van Broeckhoven C: The pursuit of susceptibility genes for Alzheimer's disease: progress and prospects. Trends Genet. 2010 Feb;26(2):84-93. Epub 2010 Jan 18. Trends Genet. 2010 Feb;26(2):84-93. Epub 2010 Jan 18.
http://www.ncbi.nlm.nih.gov/pubmed/20080314
[4] Bettens K, Sleegers K, Van Broeckhoven C: Current status on Alzheimer disease molecular genetics: from past, to present, to future. Hum Mol Genet. 2010 Apr 15;19(R1):R4-R11. Epub 2010 Apr 13.
http://www.ncbi.nlm.nih.gov/pubmed/20388643
14.07.2010: Vitamin E reduces the risk of dementia and Alzheimer Disease [1]
Devore and colleagues 2010 studied the intake of vitamin E, vitamin C, beta carotene, and flavonoids relative to long-term risk of dementia and Alzheimer disease. The authors, using data of the Rotterdam Study [2], found that persons with highest intake of vitamin E (18.5 mg per day, just over the recommended daily intake of 15 mg.) were 25% less likely to develop dementia and Alzheimer disease. Dietary intake levels of vitamin C, beta carotene, and flavonoids were not associated with dementia risk or Alzheimer disease. The authors concluded that high intake of foods rich in vitamin E may reduce the risk of dementia and Alzheimer disease.
This underlines the importance of a nutrition rich in fruit, vegetables and vitamin E of wheat germ, nuts such as almonds and hazelnuts, vegetable oils such as sunflower and safflower oils, and some green vegetables, such as spinach and broccoli. High doses of vitamin E from supplements increase risk of bleeding, adults should consume no more than 1,000 mg of vitamin E per day. Foods, however, cannot provide such high levels of vitamin E.
[1] Devore EE, Grodstein F, van Rooij FJ, Hofman A, Stampfer MJ, Witteman JC, Breteler MM: Dietary Antioxidants and Long-term Risk of Dementia. Arch Neurol. 2010 Jul;67(7):819-25.
http://www.ncbi.nlm.nih.gov/pubmed/20625087
[2] Wikipedia: The Rotterdam Study
http://en.wikipedia.org/wiki/Rotterdam_Study
14.07.2010: Vitamin D and cognitive decline or dementia [1]
Llewellyn and colleagues 2010 studied the connection between cognitive decline and low levels of serum 25-hydroxyvitamin D (25[OH]D) using data of the InCHIANTI study [2] conducted in Italy between 1998 and 2006. The Mini-Mental State Examination (MMSE) [3] was used to evaluate cognitive decline. Severe serum 25(OH)D deficiency were found with levels <25 nmol/L), levels ≥25 to <50 nmol/L were considered as insufficient, whereas levels of 25(OH)D >/=75 nmol/L were considered as sufficient.
Evaluating their data, the authors state that low levels of vitamin D are associated with substantial cognitive decline in the elderly population, and status of vitamin D should be considered en treatment and prevention.
Data from the Third National Health and Nutrition Survey (NHANES III) [4] also show that vitamin D deficiency is associated with an increased risk for cognitive impairment in older persons. According to Dr. Llewellyn vitamin D seems to play a role in processes that may be important for dementia risk, including vascular health and amyloid clearance from the brain.
Controversies
McGrath and colleagues 2007 also using data from NHANES III did not find an association between vitamin D levels and cognitive performance. Llewelly says that results of McGrath study may be related to methodology which used only delayed verbal memory from the Mini-Mental State Examination (MMSE) and the East Boston Memory Test. [5]
Andrew Grey, MD, and Mark Bolland, in an editorial comment the study of Llewellyn and colleagues, pointing out that it is unlikely that a single vitamine could play such a substantial role in preventing diseases. The authors say that it is more likely that low vitamin D is not the cause, but only a marker of overall poor health, low sunlight exposure, low physical activity, high adiposity. [6]
[1] Llewellyn DJ, Lang IA, Langa KM, Muniz-Terrera G, Phillips CL, Cherubini A, Ferrucci L, Melzer D: Vitamin d and risk of cognitive decline in elderly persons. Arch Intern Med. 2010 Jul 12;170(13):1135-41.
http://www.ncbi.nlm.nih.gov/pubmed/20625021
[2] The InCHIANTI Study
http://www.inchiantistudy.net/obtain_data.html
[3] Wikipedia: Mini-mental state examination
http://en.wikipedia.org/wiki/Mini-mental_state_examination
[4] Third National Health and Nutrition Examination Survey (NHANES III)
http://www.cdc.gov/nchs/products/elec_prods/subject/nhanes3.htm
[5] McGrath J, Scragg R, Chant D, Eyles D, Burne T, Obradovic D: No association between serum 25-hydroxyvitamin D3 level and performance on psychometric tests in NHANES III.
Neuroepidemiology. 2007;29(1-2):49-54.
http://www.ncbi.nlm.nih.gov/pubmed/17898524
[6] Grey A, Bolland M: Vitamin d: a place in the sun? Arch Intern Med. 2010 Jul 12;170(13):1099-100
http://www.ncbi.nlm.nih.gov/pubmed/20625012
13.07.2010: Estradiol may switch on eating disorder genes [1]
According to Klump and colleagues 2010, estradiol is an estrogen which regulates gene transcription important for eating-related genes in puberty. The authors report that afternoon saliva samples which were low for estradiol levels monozygotic (MZ) and dizygotic (DZ) twin correlated with all body dissatisfaction and binge eating/compensatory behavior subscales of the Minnesota Eating Behavior Survey (MEBS scales) suggesting little genetic influence. Whereas high estradiol levels presented MZ twin correlation more than double of the DZ twin correlation, indicating genetic effects of estradiol.
The authors suggest that estradiol may switch on the genes for eating disorders. Better understanding of estradiol physiology may lead to new treatments of eating disorders, say the authors.
The Minnesota Eating Behavior Survey: [2] The Minnesota Eating Behavior Survey is a brief measure of disordered eating attitudes and behaviours. It is a 30-item questionnaire developed for use with children as young as 10 years as well as adults to be used in cross-sectional and longitudinal research involving individuals of a wide range of ages.
[1] Klump KL, Keel PK, Sisk C, Burt SA: Preliminary evidence that estradiol moderates genetic influences on disordered eating attitudes and behaviors during puberty. Psychol Med. 2010 Jan 11:1-9.
http://www.ncbi.nlm.nih.gov/pubmed/20059800
[2] von Ranson KM, Klump KL, Iacono WG, McGue M: The Minnesota Eating Behavior Survey: a brief measure of disordered eating attitudes and behaviors. Eat Behav. 2005 Dec;6(4):373-92. Epub 2005 Jan 13.
http://psych.ucalgary.ca/eatinglab/sites/psych.ucalgary.ca.eatinglab/files/MEBS_psychometrics_-_EB.pdf
13.07.2010: Wound healing properties of honey [1]
Salomon and colleagues 2010 describe the wound healing properties of honey. The high concentration of sugar constitute a hyperosmotic medium with antimicrobial properties. The authors also stress that different enzymes, including glucose-oxidase that generates hydrogen peroxide and gluconic acid in the presence of glucose and water. In addition, honey presents favourable viscosity and the hygroscopic qualities allowing spread on the wound bed. The authors concluded that honey is an efficient treatment of chronic wounds of the lower leg and also of abdominal wounds.
Bacteriostatic effects of honey [2]
Kwakman and colleagues 2010 described all bactericidal factors in a medical-grade honey. Bacillus subtilis, methicillin-resistant Staphylococcus aureus, extended-spectrum β-lactamase producing Escherichia coli, ciprofloxacin-resistant Pseudomonas aeruginosa, and vancomycin-resistant Enterococcus faecium, were killed by 10–20% (v/v) honey, whereas more than 40% (v/v) of a honey-equivalent sugar solution was required for similar activity.
Activity against all other bacteria tested depended on sugar, H2O2, methylglyoxal, and bee defensin-1, contributing to the effects of honey in medicine, whereas bee defensin-1 was the most active compound.
According to Boukraâ and Sulaiman 2009, honey, propolis, royal jelly and bee venom have a strong antibacterial activity, but considerably variability is found within the same product and its botanical origin. Propolis presents the strongest antibacterial activity based on its richness in flavonoids. The authors stress that food quality of honey and royal jelly contain pollen and other particles which might cause allergies when used in wound care. Fine filters must therefore be used in the production of medical products. A safety issue of honey and their products for medical use is the presence of viable spores which includes clostridia. The growing number of licensed medical bee products will increase understanding of its use, which, however, should be limited to those which are safe and with certified antibacterial activities, say the authors. [3]
Chernev and colleagues 2010 report benefits of combined, noncontact, low-frequency ultrasound and topical application of medical honey in treatment of chronic and delayed healing wounds.[4]
No manuka honey resistant mutants found so far [5]
Cooper and colleagues 2010 report that honey-resistant bacteria have not been isolated from wounds treated with honey. However, bacteria isolated from wounds, exposed to sub-lethal concentrations of manuka honey presented a stepwise resistance training, but changes were not permanent and honey-resistant mutants were not detected. The authors concluded that high concentrations of honey will keep the risk of development of honey resistant mutants low.
Antibacterial properties of tualang honey [6]
Mohd Nasir compared the properties of tualang honey with that of manuka honey in treatment of burn wounds. The authors found that tualang honey has a bactericidal as well as bacteriostatic effect, it is less sticky compared to Manuka honey. Tualang honey was less effective for Gram positive bacteria as silver-based dressing or medical grade honey dressing.
Classic treatment of burn wounds recommended instead of honey products [7]
Topical antimicrobials are employed for prophylaxis and treatment of burn wound infections. Glasser and colleagues 2010 point out that no defined susceptibility breakpoints exist and standards need to be established for topical antimicrobial. The authors recommend continuing to use silver products for prophylaxis against gram-negatives and mafenide acetate for treatment, and mupirocin for methicillin-resistant Staphylococcus aureus.
Susceptibility beakingpoints: Susceptibility beakingpoints are used to define susceptibility and resistance to antibacterials. Depending on the testing method, they are expressed as either a concentration (in mg/liter or g/ml) or a zone diameter (in mm). Susceptibility breakpoints allow communication from the clinical laboratory to the prescriber regarding the likelihood that a particular antibacterial regimen will be clinically useful in the treatment of patients with infections. [8]
[1] Salomon D, Barouti N, Rosset C, Whyndham-White C: Honey: from Noe to wound care. Rev Med Suisse. 2010 Apr 28;6(246):871-4.
http://www.ncbi.nlm.nih.gov/pubmed/20455385
[2] Kwakman PH, te Velde AA, de Boer L, Speijer D, Vandenbroucke-Grauls CM, Zaat SA. How honey kills bacteria. FASEB J. 2010 Jul;24(7):2576-82. Epub 2010 Mar 12. DOI: 10.1096/fj.09-150789
http://www.ncbi.nlm.nih.gov/pubmed/20228250
[3] Boukraâ L, Sulaiman SA: Rediscovering the antibiotics of the hive. Recent Pat Antiinfect Drug Discov. 2009 Nov;4(3):206-13.
http://www.ncbi.nlm.nih.gov/pubmed/19673699
[4] Chernev I, Liguori PA, Senno SL, Peters KL, Bowers JM. Combined Noncontact, Low-Frequency Ultrasound and Medical Honey for the Treatment of Chronic Wounds: A Case Series. J Wound Ostomy Continence Nurs. 2010 Jun 20.
http://www.ncbi.nlm.nih.gov/pubmed/19683834
[5] Cooper RA, Jenkins L, Henriques AF, Duggan RS, Burton NF: Absence of bacterial resistance to medical-grade manuka honey. Eur J Clin Microbiol Infect Dis. 2010 Jun 13.
http://www.ncbi.nlm.nih.gov/pubmed/20549529
[6] Mohd Nasir NA, Halim AS, Banga Singh KK, Dorai AA, Muhammad Haneef MN: Antibacterial properties of tualang honey and its effect in burn wound management: a comparative study. BMC Complement Altern Med. 2010 Jun 24;10(1):31.
http://www.ncbi.nlm.nih.gov/pubmed/20576085
[7] Glasser JS, Guymon CH, Mende K, Wolf SE, Hospenthal DR, Murray CK: Activity of topical antimicrobial agents against multidrug-resistant bacteria recovered from burn patients. Burns. 2010 Jun 7.
http://www.ncbi.nlm.nih.gov/pubmed/20542641
[8] Turnidge J, Paterson DL: Setting and revising antibacterial susceptibility breakpoints.
Clin Microbiol Rev. 2007 Jul;20(3):391-408
http://cmr.asm.org/cgi/reprint/20/3/391.pdf
11.07.2010: Passerines are more important avian flue transmitter than aquatic birds [1]
Waterfowl are linked with avian influenza, however, Fuller and colleagues 2010 emphasizes that 22 species of song birds and perching birds are also reservoirs of influenza.
The authors point out that the influenza prevalence in passerines is high. These birds share the same habitat as poultry and are more effective transmitters of the disease to humans than aquatic birds. Cloacal samples indicate that the prevalence of influenza in passerines is greater than the prevalence in eight other avian orders.
Data of this study identifies the Great Plains and the Pacific Northwest as high-risk areas for Avian influenza virus. The authors also stress that the amount of harvested cropland are highly significant predictors of Avian influenza virus, because of the reduction of natural habitat available to avian migrants, This is also valid for the first day of the year when a county is snow free and birds may move in.
[1] Trevon L Fuller, Sassan S Saatchi, Emily E Curd, Erin Toffelmier, Henri A Thomassen, Wolfgang Buermann, David F DeSante, Mark P Nott, James F Saracco, C J Ralph, John D Alexander, John P Pollinger, Thomas B Smith. Mapping the risk of avian influenza in wild birds in the US. BMC Infectious Diseases, 2010; 10 (1): 187 DOI: 10.1186/1471-2334-10-187
http://www.biomedcentral.com/1471-2334/10/187
09.07.20101: Meat 'blown pack' spoilage
Gaseous spoilage of vacuum-packaged chilled meats were reported in Germany in July 2010. Clostridium estertheticum was found to generate the gas with nauseating odour. Health officials declared the phenomena as not heath threatening,. The affected meat had be destroyed. Clostridium estertheticum represents, therefore a financial threat for chilled meat producers.
Clostridium estertheticum gaseous spoilage of chilled meats [1]
Collins and colleagues 1992 performed a taxonomic study of an unknown anaerobic Gram-positive, spore-forming, psychrophilic bacterium isolated from spoiled vacuum-packed refrigerated beef and proposed it to be classified as a new species of the genus Clostridium, as Clostridium estertheticum sp. nov. The type strain is NCIMB 12511.
Contamination of vacuum-packed chilled meats with Clostridium estertheticum [2]
Clemens, Adam and Brightwell 2010 studied the contamination levels of Cl. estertheticum spores causing gaseous spoilage of vacuum-packaged chilled meats, beef and lamb, stored at two different temperatures, -1.5 and 2 degrees C.
The authors stress that onset of blown pack spoilage is delayed storing meat at -1.5 degrees C, compared with storage at 2 degrees C. To avoid the risk of “blown pack”spoilage, contamination with spores of Clostridium estertheticum must be reduced to a minimum by strict observance of hygienic handling of meat.
PCR amplification procedure to detect clostridia causing spoilage of vacuum-packed chilled meats [3]
Broda DM, Boerema JA, Brightwell 2009 determine preslaughter and processing sources of psychrophilic and psychrotolerant clostridia causing spoilage of vacuum-packed chilled meats using the polymerase chain reaction (PCR) amplification of specific 16S rDNA fragments.
Clostridium gasigenes, C. estertheticum and C. algidicarnis/C. putrefaciens were commonly detected in farm, faeces, fleece and processing environmental samples collected at the slaughter floor operations, but only 4 out of 26 cooling floor and chiller environmental samples were positive for all of them. Frequency of C gasigenes and C. estertheticum was low, and high frequency of C. algidicarnis/C. Putrefaciens was detected in boning room. Detection frequence of C. gasigenes and C. estertheticum was high, but low for C. algidicarnis and/or C. putrefaciens in samples of faecis.
The authors concluded that control of meat spoilage by clostridia is best approached individually for each group.
Describing the bacteria isolated from blown packs of vacuum-packaged beef [4]
Yang, Gill and Balamurugan 2009 describe the bacteria recovered from the microflora of blown packs of vacuum-packaged beef identified as Leuconostoc mesenteroides, Lactococcus lactis, Carnobacterium maltaromaticum, and Clostridium estertheticum, with Leuconostoc mesenteroides predominant.
The authors stress that Clostridium estertheticum may predominate during the early stages of development of the spoilage microflora of vacuum-packaged beef but will likely be inhibited by a falling pH later on.
Inhibition by Lactobacillus sakei of spoilage bacteria on vacuum-packed meat [5]
Jones 2009 and colleagues describe the abilities of five Lactobacillus sakei strains and one Lactococcus lactis strain to retain inhibitory activity against target organisms on vacuum-packaged lamb and beef.
Among others findings, the authors report that in beef packs inoculated with Clostridium estertheticum spores and L. sakei strain 27, 44 or 63, the development of blown-pack spoilage was delayed by up to one week. The authors suggest a set of Lactobacillus sakei strains which may extended shelf life of minimally processed fresh beef and lamb.
Temperature and contamination level influences onset of vacuum-packed meat spoilage [6]
Moschonas and colleagues 2010 examined the effect of storage temperature and inoculum level on the time of onset of 'blown pack' spoilage caused by psychrotolerant bacteria in vacuum-packed meats. Clostridium estertheticum ssp. estertheticum presented at all inoculum levels/storage temperature combinations examined the earliest 'blown pack' spoilage of all other bacteria in test. They stress the importance contamination level control and low storage temperature to delay the onset of 'blown-pack' spoilage of meat.
Isolation and source of 'blown pack' spoilage bacteria identification [7]
Moschonas and colleagues 2009 report that DNA-based techniques were the most efficient methods to determine the presence and distribution of blown pack spoilage at beef abattoirs of Clostridium estertheticum and Clostridium gasigenes, compared with culture-methods which presented poor results. The authors point out that hides and faeces were found to be the main reservoirs of 'blown pack' spoilage clostridia in the abattoirs.
Glucose and lactose utilisation by Clostridium estertheticum [8]
According to Yang X, Balamurugan S, Gill 2009 blown pack spoilage of vacuum packaged beef is caused by the psychrophile Clostridium estertheticum, which grow exponentially on glucose with simultaneous hydrolysis of glycogen. Growth ceased when glucose in the media was depleted; but hydrolysis of glycogen continued at a reduced rate, and lactate was consumed rapidly.
The authors suggest that reducing the availiability of glucose may limit the growth of Clostridium estertheticum and other gas generating bacteria on vacuum packaged beef . Lactate fermentation, however, will continue, even after growth ceases.
PCR detection of psychrophilic Clostridium spp. [9]
Broda, Boerema and Bell 2003 developed a practical molecular procedure that directly, without isolation, and specifically detects the presence of clostridia which cause 'blown pack' spoilage of vacuum-packed meat containing as few as 100 clostridial cells per gram.
Clostridium gasigenes was confirmed as the causative agent of 'blown pack' spoilage insome packages, and Clostridium estertheticum in others.
The described procedure may also be used in in epidemiological trace back of 'blown pack' spoilage incidents in meat processing plants.
Controlling 'blown pack' spoilage in meat processing plants [10]
Broda and colleagues 2002 identified abattoir sources of psychrophilic clostridia causing 'blown pack' spoilage of vacuum-packed chilled meats. Restriction fragment length polymorphism analysis of the 16S rDNA gene (PCR-RFLP) and 16S-23S rDNA internal transcribed spacer (ITS) analysis were used by the authors.
The authors found that soil particles attached to hide or present in faeces are the primary reservoir of 'blown pack' clostridia contaminating meat end products. The authors recommend strong dressing procedure hygiene to control the spread of psychrophilic Clostridium spp. in a meat plant.
[1] Collins MD, Rodrigues UM, Dainty RH, Edwards RA, Roberts TA: Taxonomic studies on a psychrophilic Clostridium from vacuum-packed beef: description of Clostridium estertheticum sp. Nov. FEMS Microbiol Lett. 1992 Sep 15;75(2-3):235-40.
http://www.ncbi.nlm.nih.gov/pubmed/1383083
[2] Clemens RM, Adam KH, Brightwell G: Contamination levels of Clostridium estertheticum spores that result in gaseous spoilage of vacuum-packaged chilled beef and lamb meat.
Lett Appl Microbiol. 2010 Jun 1;50(6):591-6.
http://www.ncbi.nlm.nih.gov/pubmed/20406381
[3] Broda DM, Boerema JA, Brightwell G: Sources of psychrophilic and psychrotolerant clostridia causing spoilage of vacuum-packed chilled meats, as determined by PCR amplification procedure. J Appl Microbiol. 2009 Jul;107(1):178-86. Epub 2009 Mar 3.
http://www.ncbi.nlm.nih.gov/pubmed/19302329
[4] Yang X, Gill CO, Balamurugan S: Effects of temperature and pH on the growth of bacteria isolated from blown packs of vacuum-packaged beef. J Food Prot. 2009 Nov;72(11):2380-5.
http://www.ncbi.nlm.nih.gov/pubmed/19903404
[5] Jones RJ, Zagorec M, Brightwell G, Tagg JR: Inhibition by Lactobacillus sakei of other species in the flora of vacuum packaged raw meats during prolonged storage. Food Microbiol. 2009 Dec;26(8):876-81. Epub 2009 Jun 12.
http://www.ncbi.nlm.nih.gov/pubmed/19835775
[6] Moschonas G, Bolton DJ, Sheridan JJ, McDowell DA: The effect of storage temperature and inoculum level on the time of onset of 'blown pack' spoilage. J Appl Microbiol. 2010 Feb;108(2):532-9.
http://www.ncbi.nlm.nih.gov/pubmed/19659695
[7] Moschonas G, Bolton DJ, Sheridan JJ, McDowell DA: Isolation and sources of 'blown pack' spoilage clostridia in beef abattoirs. J Appl Microbiol. 2009 Aug;107(2):616-24.
http://www.ncbi.nlm.nih.gov/pubmed/19302293
[8] Yang X, Balamurugan S, Gill CO: Substrate utilization by Clostridium estertheticum cultivated in meat juice medium. Int J Food Microbiol. 2009 Jan 15;128(3):501-5. Epub 2008 Oct 31.
http://www.ncbi.nlm.nih.gov/pubmed/19027974
[9] Broda DM, Boerema JA, Bell RG: PCR detection of psychrophilic Clostridium spp. causing 'blown pack' spoilage of vacuum-packed chilled meats. J Appl Microbiol. 2003;94(3):515-22.
http://www.ncbi.nlm.nih.gov/pubmed/12588561
[10] Broda DM, Bell RG, Boerema JA, Musgrave DR: The abattoir source of culturable psychrophilic Clostridium spp. causing 'blown pack' spoilage of vacuum-packed chilled venison. J Appl Microbiol. 2002;93(5):817-24.
http://www.ncbi.nlm.nih.gov/pubmed/12392528
09.07.2010: Sewage water treatment plants in Kuwait [1]
Drinking water is becoming scarce. Technology of ultra-filtration and reverse osmosis are playing key roles in desert countries to recycle water.
According to Kuwait's Ministry of Public Works, Kuwait is a desert and suffers from severe heat and harsh weather conditions, and water resources are scarce, given the low levels of rainfall and the lack of fresh water, the paper explained. The consumption of water per individual in Kuwait was very high compared to the rest of the world, leading to large volumes of sewage water.
Treated water has become one of the main resources for the irrigation of crops, including the farms in Abdali, as well as green areas in the city. It is also used in concrete mixes, and private enterprises are being encouraged to use it in their daily operations such as cleaning and cooling.
The Sulabiya Treatment Plant has an output capacity of 425,000 cubic meters per day, and is the largest sewage water treatment plant in the world that used reverse osmosis.
The Rigga Treatment Plant, has an output capacity of 180,000 cubic meters per day, and there are plans to close it down and to build an alternative plant by 2020 that covers the whole southern area of the country. The Jahra Treatment Plant is working at a capacity of 65,000 cubic meters and will be closed down in 2011 after the completion of a new plant in Chabd. The smallest plant is that of Umm Al-Haiman, designed to generate an output of 27,000 cubic meters per day.
A new plant in the southern area of Kuwait with an overall output capacity of 400,000 cubic meters, to replace the plants in Rigga and Umm Al-Haiman by 2020. In 1984 chlorine was included in the treatment process and reverse osmosis was included in 2004.
The waste water treatment plant of Ardiya is being used as pre-treatment stage and is connected to the Salaibiya treatment plant where it is treated to potable water standards.
Ardiy pre-treatment plant: Wastewater from Kuwait City is forwarded to the Ardiya plant an aerated grit chamber excludes sand and grit down to a particle size of 0.2mm. Two 20,000m³ circular buffer tanks balance the influent variation. Agitators within the buffer tanks maintain a flow velocity greater than 0.3m/s to avoid sedimentation problems.
Sulaibiya treatment plant: [2] The Sulaibiya waste water treatment plant removes organics, minimises nitrate release, reduces phosphate outflow. There are nine aeration tanks with a total volume of 208,900m³, offering anaerobic, anoxic and aerobic treatment zones.
The Sulaibiya plant comprises three elements - biological nutrient removal, reverse osmosis / ultra-filtration membranes and sludge treatment.The finished effluent is delivered to the nearby brackish water gathering centre prior to use, while the membrane system brine overflow is returned to the sea.
Part of the activated sludge from the anaerobic zone is transferred to the (RAS) denitrification chamber to serve as a carbon source. With no available oxygen present, phosphate re-dissolves to be later re-incorporated at an enhanced rate into biomass in the aerobic zones. Although this means that high phosphate concentrations occur when the mixed liquor enters the anoxic zone, it subsequently leads to the requisite phosphate reduction necessary to protect the reverse osmosis membranes. In addition, nitrified activated sludge is returned into the anoxic zone to keep the nitrate concentration in the aerobic zone low, leading to the lowered levels required in the secondary effluent.
Sludge is treated to provide a material suitable for unrestricted agricultural use, requiring it to be dry, with a low organic content and free of pathogens. The resulting product is subsequently stored for more than six months before consignment for use. The UF / RO removes residual pollutants, dissolved solids and pathogens from secondary effluent, to yield potable quality water.
The ultra-filtration systerm comprises 60µm disc filters. The cross-flow, dead-end membranes will be cleaned by chemical enhanced backwash using a primary acid wash, followed up with chlorine rinse if required.
The reverse osmosis facility comprises 24 first array skids, 20cm x 1m membrane modules per vessel. The facility is fitted with an in situ cleaning system. Air stripping tower de-gassifiers remove CO2 from the permeate and a chlorine dosing facility also forms part of the plant.
[1] Kuwait presents paper on sewage water treatment. Kuwait Times. July 01, 2010.
http://www.kuwaittimes.net/read_news.php?newsid=NjE4MzMyMDky
[2] Water Technology: Sulaibiya Wastewater Treatment and Reclamation Plant, Kuwait
http://www.water-technology.net/projects/sulaibiya/
08.07.2010: Findings on the biochemistry of sleep
Adenosine triphosphate (ATP) and Phosphorylated AMP-activated protein kinase (P-AMPK) participate in the biochemistry of sleep [1]
Dworak aand colleagues 2010, experimenting with rats, reported that ATP levels increase in the initial hours of spontaneous sleep in wake-active but not in sleep-active brain regions. The surge is dependent on sleep when neuronal activity is reduced, but is not related to time of day. Phosphorylated AMP-activated protein kinase (P-AMPK), which has a cellular energy sensing and regulation, reacts inversely to ATP.
The authors concluded that ATP level in brain and P-AMPK levels give insights to the biochemistry of sleep.
Adenosine key factor of sleep control [2]
Elmenhorst and colleagues 2009 report that adenosine acts via the A(1) adenosine receptor (A(1)AR). It is a key factor in the control of sleep. The authors suggest that cerebral A(1)ARs are involved in effects of sleep deprivation and the regulation of sleep maintaining the responsiveness to increased adenosine levels, and the effect of sleep deprivation and is in line with a sleep-induced homoeostatic reorganization at the synaptic level.
Sleep deprivation and its effect on neurotransmitter receptor [3]
Longordo and colleagues 2009 describe alterations in neurotransmitter receptor function in diverse neuronal cell types caused by sleep deprivation, focusing on sleep deprivation procedures that control for side-effects such as stress. The authors call for more studies on the effect of sleep deprivation on neurotransmitter receptor to increase knowledge of the detrimental effects of sleep loss.
Shift work effect on IL-6 and TNF-alpha immune system [4]
van Mark and colleagues 2010 write that short-term sleep deprivation lead to overstimulation of proinflammatory immune mechanisms and moderates metabolic changes, such as lymphocyte count or level of IL-6 or TNF-alpha serum concentration. This increase cardiovascular disease risk.. The authors report, however, that chronic sleep did not always lead to an activation of these indicators of immune system activation, between shift workers and day workers.
The authors concluded that the effect of chronic sleep restriction may be compensated by a long-term immune regulation which protects against an overstimulation of proinflammatory immune mechanisms and moderates metabolic changes.
[1] Dworak M, McCarley RW, Kim T, Kalinchuk AV, Basheer R: Sleep and brain energy levels: ATP changes during sleep. J Neurosci. 2010 Jun 30;30(26):9007-16.
http://www.ncbi.nlm.nih.gov/pubmed/20592221
[2] Elmenhorst D, Basheer R, McCarley RW, Bauer A: Sleep deprivation increases A(1) adenosine receptor density in the rat brain. Brain Res. 2009 Mar 3;1258:53-8.
http://www.ncbi.nlm.nih.gov/pubmed/19146833
[3] Longordo F, Kopp C, Lüthi A: Consequences of sleep deprivation on neurotransmitter receptor expression and function. Eur J Neurosci. 2009 May;29(9):1810-9.
http://www.ncbi.nlm.nih.gov/pubmed/19492440
[4] van Mark A, Weiler SW, Schroder M, Otto A, Jauch-Chara K, Groneberg DA, Spallek M, Kessel R, Kalsdorf B: The impact of shift work induced chronic circadian disruption on IL-6 and TNF-alpha immune responses. J Occup Med Toxicol. 2010 Jul 5;5(1):18.
http://www.ncbi.nlm.nih.gov/pubmed/20602750
07.07.2010: CSPI finds food frauds at cafeteria of FDA headquarters [1]
CSPI found fraudulent claims on drinks sold by the cafeteria of Food and Drug Administration headquarters in the White Oak area of Silver Spring, Md.
These claims were:
Purity Organic Functional Drinks Pomegranate Blueberry
Crystal Light Immunity Berry Pomegranate
SoBe Lifewater B-Energy Black Cherry Dragonfruit see picture
These drinks contain plenty of sugar but only traces of fruit juice.
Consumer should mistrust any labelling claim containing “Organic”, “Functional” “Immunity”, “Lifewater”, “B-Energy” “fitness”and pictures of fruits, Logos of organic organisations or logos of fitness. The FDA seems to be incapable to stop the flood of such fraudulent claims. The consumer should protect himself and avoid such products.
The CSPI says: “Consumers who want to ensure that they’re getting enough vitamins and minerals should focus on eating a wide variety of fruits and vegetables first. No one should believe that the added vitamins, herbs or other ingredients in these flavoured waters are going to ward off disease, improve memory, or make one more energetic.”
[1] CSPI Says Federal Labelling Cops Should Raid Their Own Cafeteria. July 7, 2010
http://www.cspinet.org/new/201007071.html
06.07.2010: L-arginine supplementation improves arterial responses in disease with endothelial dysfunction [1]
According to Guttman and colleagues 2010 longterm supplementation of L-arginine improves large artery elasticity index (LAEI) in patients with multiple cardiovascular risk factors, and decreased systolic blood pressure, peripheral vascular resistance as well as a decrease in aldosterone levels. The authors stress that long term L-arginine supplementation may improve artery compromised by disease with endothelial dysfunction.
[1] Guttman H, Zimlichman R, Boaz M, Matas Z, Shargorodsky M: Effect of Long-Term L-Arginine Supplementation on Arterial Compliance and Metabolic Parameters in Patients with Multiple Cardiovascular risk Factors: Randomized, Placebo-Controlled Study. J Cardiovasc Pharmacol. 2010 Jun 7.
http://www.ncbi.nlm.nih.gov/pubmed/20531213
06.07.2010: Long-term treatment with antioxidants (vitamin C, vitamin E, coenzyme Q10 and selenium) improves artery health, humoral factors and inflamatory markers in case of multiple cardiovascular risk. [2]
Shargorodsky and colleagues 2010 report that daily oral supplementation with vitamin C (1000 mg/day), vitamin E (400 i.u/day), coenzyme Q10 (120 mg/day) and selenium (200 mcg/day) during six month improved the large arterial elasticity index (LAEI) as well as small arterial elasticity index (SAEI). HbA1C was reduced and HDL-cholesterol was increased.
The authors concluded that antioxidant supplementation significantly improved vascular health, glucose and lipid metabolism as well as decrease in blood pressure.
[1] Shargorodsky M, Debbi O, Matas Z, Zimlichman R: Effect of long-term treatment with antioxidants (vitamin C, vitamin E, coenzyme Q10 and selenium) on arterial compliance, humoral factors and inflammatory markers in patients with multiple cardiovascular risk factors. Nutrition & Metabolism, 2010.
http://www.nutritionandmetabolism.com/content/7/1/55/abstract
04.07.2010: Understanding coral leaching and susceptibility to disease [1]
Low immunity response may increase the risk of coral leaching and its susceptibility to disease.
Palmer, Bythell and Willis 2010 found an inverse correlation of the content of melanin, size of melanin-containing granular cells, and phenoloxidase activity, as well as concentrations of fluorescent proteins to thermal bleaching and disease susceptibility, in hard (Scleractinia) and soft (Alcyonacea) corals. These indicators are known to be related to immunity in invertebrates.
The authors stress that pheniloxidase activity, melanin-containing granular cell size, and fluorescent proteins concentration are predictors of susceptibility and are important in coral immunity. The authors call for a holistic approach to study coral reef bleaching and disease susceptibility.
[1] Palmer CV, Bythell JC, Willis BL: Levels of immunity parameters underpin bleaching and disease susceptibility of reef corals. FASEB J. 2010 Mar 10.
http://www.ncbi.nlm.nih.gov/pubmed/20124432
30.06.2010: Genetic of plant disease-causing bacteria
Virulence gene complement olive knot disease causing Pseudomonas savastanoi pv. Savastanoi NCPPB 3335 [1]
Pseudomonas savastanoi pv. savastanoi is a tumour-inducing pathogen of Olea europaea L. causing olive knot disease. Rodríguez-Palenzuela and colleagues 2010 analysed the genome sequence of Pseudomonas savastanoin revealing similarities with Pseudomonas syringae pv. phaseolicola 1448A and Pseudomonas syringae pv. Tabaci 11528.
The authors report that twelve variable genomic regions of NCPPB 3335 contains twelve variable genomic regions which are not present in Pseudomonas syringae. These genes make the strain capable to survive in a plant host, and 73 predicted coding genes that are NCPPB 3335-specific were found in Pseudomonas savastanoi pathovar indicating specific adatations of P savastanoi.
Prevail of Pseudomonas savastanoi pv. savastanoi type III mutant in olive plants [2]
Pérez-Martínez and colleagues 2010 describe the sequencing of the hrpS-to-hrpZ region of NCPPB 3335, elucidating its phylogenetic position relative to Pseudomonas syringae hrp clusters.
The authors report the construction of a mutant of NCPPB 3335, termed T3, with deletion of the 3' end of the hrpS gene to the 5' end of the hrpZ operon. T3 mutant does not induce tumor formation in woody olive plants, however, it can induce knot formation on young micropropagated olive plants, but without necrosis and formation of internal open cavities, seen with wild-type strain and differed in distribution within the host tissue.
Virulence determining genes in Pseudomonas syringae [3]
Lindeberg and colleagues 2008 describe the virulence-associated genes for three Pseudomonas syringae strains. These genes, described in the DC3,000 genome annotation are associated with the ability to grow on plant surface, to segregate plant- and insect-active toxins, and virulence regulators.
The authors highlight a strong segregation of the HrpL regulon with variable genome regions (VR), whose distribution, together with other sequenced bacterial genomes were discussed by the authors as a virulence sources.
Pseudomonas syringae equipped with an Atypical Type III Secretion System [4]
Christopher and colleagues 2010 stress that Pseudomonas syringae causes a plant disease by translocating immune-suppressing effector proteins into plant cells through a type III secretion system (T3SS).
The authors describe a new Phrp/hrc cluster which differs from the typical Pseudomonas syringae hrp/hrc cluster coding for a T3SS. This new hrp/hrc cluster misses the genes hrpK and hrpS, of the classical P. syringae hrp/hrc cluster. The group 2c strain also revealed distant similarities with the Pseudomonas syringae effector genes avrE1 and hopM1 and the P. aeruginosa effector genes exoU and exoY.
Two virulence domains of AvrPto are conserved in different Pseudomonas syringae [5]
Hanh and colleragues 2010 write that the Pseudomonas syringae pv. tomato type III effector protein AvrPto encode virulence in susceptible tomato plants and also defence responses in resistant tomato and tobacco genotypes. The authors stress that two virulence domains of AvrPto are conserved in diverse pathovars and may be active during infection of diverse plant species.
Pseudomonas syringae pv. tomato DC3000 Type III Effector HopAA1-1 redundant with chlorosis-promoting factor PSPTO4723 to produce bacterial speck lesions in tomato [6]
Cathy and colleagues 2009 report that Pseudomonas syringae pv. tomato DC3000 kill yeast and promote bacterial speck disease in tomato by injection of 28 Avr/Hop effector proteins HopAA1-1, using the type III secretion system.
Deleting hopAA1-1 from DC3000 reduces the formation of necrotic speck lesions in tomato leaves if effector-gene cluster IX or just PSPTO4723 within this region has been deleted. PSPTO4723 does not encode an effector and is associated with chlorosis.
Studying host specificity of Pseudomonas syringae [7]
According to Lindeberg and colleagues 2009 Pseudomonas syringae, using the type III secretion system, injects effector proteins that suppress basal innate immunity of the host cytoplasm. This, however, may be recognized by cognate resistance (R) proteins in a second level of the host defence. Following latest data the nature and evolution of P. syringae host specificity and nonhost resistance may now be further elucidated. [8]
Common toxin fold explains interaction between microbial attack and plant [9]
Ottmann and colleagues 2009 describe the necrosis and ethylene-inducing peptide 1 (Nep1)-like proteins (NLPs) which trigger leaf necrosis and immunity-associated responses in various plants.
The authors found that NLP-mediated phytotoxicity and plant defence gene expression share identical fold requirements, indicating that toxins trigger plant immunologic responses.
These NLPs proteins present fold similarities to toxins produced by marine organisms like actinoporins. Structure of NLPs from Phytophthora parasitica and Pectobacterium carotovorum, revealed a high extent of this fold conservation.
The authors also stress that plant defences activated by these toxins are reminiscent of microbial toxin-induced inflammasome activation in vertebrates suggesting a link between animal and plant innate immunity.
[1] Rodríguez-Palenzuela P, Matas IM, Murillo J, López-Solanilla E, Bardaji L, Pérez-Martínez I, Rodríguez-Moskera ME, Penyalver R, López MM, Quesada JM, Biehl BS, Perna NT, Glasner JD, Cabot EL, Neeno-Eckwall E, Ramos C: Annotation and overview of the Pseudomonas savastanoi pv. savastanoi NCPPB 3335 draft genome reveals the virulence gene complement of a tumour-inducing pathogen of woody hosts. Environ Microbiol. 2010 Apr 1. p 1604-1620. Doi: 10.1111/j.1462-2920.2010.02207.x
http://www.ncbi.nlm.nih.gov/pubmed/20370821
[2] Pérez-Martínez I, Rodríguez-Moreno L, Lambertsen L, Matas IM, Murillo J, Tegli S, Jiménez AJ, Ramos C: Fate of a Pseudomonas savastanoi pv. savastanoi type III secretion system mutant in olive plants (Olea europaea L.). Appl Environ Microbiol. 2010 Jun;76(11):3611-9. Epub 2010 Apr 2.
http://www.ncbi.nlm.nih.gov/pubmed/20363790
[3] Lindeberg M, Myers CR, Collmer A, Schneider DJ: Roadmap to new virulence determinants in Pseudomonas syringae: insights from comparative genomics and genome organization. Mol Plant Microbe Interact. 2008 Jun;21(6):685-700.
http://apsjournals.apsnet.org/doi/abs/10.1094/MPMI-21-6-0685
[4] Christopher R. Clarke, Rongman Cai, David J. Studholme, David S. Guttman, and Boris A. Vinatzer: Pseudomonas syringae Strains Naturally Lacking the Classical P. syringae hrp/hrc Locus Are Common Leaf Colonizers Equipped with an Atypical Type III Secretion System. Mol Plant Microbe Interact. .February 2010, Volume 23, Number 2. Pages 198-210
Doi: 10.1094/MPMI-23-2-0198
http://apsjournals.apsnet.org/doi/abs/10.1094/MPMI-23-2-0198
[5] Hanh P. Nguyen, Inhwa Yeam, Aurelie Angot and Gregory B. Martin: Two virulence determinants of type III effector AvrPto are functionally conserved in diverse Pseudomonas syringae pathovars. New Phytologist. Doi: 10.1111/j.1469-8137.2009.03175.x Published Online: 28 Jan 2010
http://www3.interscience.wiley.com/journal/123266047/abstract
[6] Kathy R. Munkvold, Alistair B. Russell, Brian H. Kvitko, and Alan Collmer: Pseudomonas syringae pv. tomato DC3000 Type III Effector HopAA1-1 Functions Redundantly with Chlorosis-Promoting Factor PSPTO4723 to Produce Bacterial Speck Lesions in Host Tomato. Molecular Plant-Microbe Interactions Nov 2009, Volume 22, Number 11: 1341-1355. Doi: 10.1094/MPMI-22-11-1341
http://apsjournals.apsnet.org/doi/abs/10.1094/MPMI-22-11-1341
[7] Magdalen Lindeberg, Sébastien Cunnac, Alan Collmer: The evolution of Pseudomonas syringae host specificity and type III effector repertoires. Molecular Plant Pathology Nov 2009, Volume 10, Number 6: 767-775. Doi: 10.1111/j.1364-3703.2009.00587.x
http://www3.interscience.wiley.com/journal/122612876/abstract
[8] Nalvo F. Almeida, Shuangchun Yan, Magdalen Lindeberg, David J. Studholme, David J. Schneider, Bradford Condon, Haijie Liu, Carlos J. Viana, Andrew Warren, Clive Evans, Eric Kemen, Dan MacLean, Aurelie Angot, Gregory B. Martin, Jonathan D. Jones, Alan Collmer, Joao C. Setubal, and Boris A. Vinatzer: A Draft Genome Sequence of Pseudomonas syringae pv. tomato T1 Reveals a Type III Effector Repertoire Significantly Divergent from That of Pseudomonas syringae pv. tomato DC3000. Molecular Plant-Microbe Interactions Jan 2009, Volume 22, Number 1: 52-62. Doi: 10.1094/MPMI-22-1-0052
http://www3.interscience.wiley.com/journal/122612876/abstract
[9] C. Ottmann, B. Luberacki, I. Kufner, W. Koch, F. Brunner, M. Weyand, L. Mattinen, M. Pirhonen, G. Anderluh, H. U. Seitz, T. Nurnberger, and C. Oecking: A common toxin fold mediates microbial attack and plant defense. Proceedings of the National Academy of Sciences Jun 2009, Volume 106, Number 25: 10359-10364
http://www.pnas.org/content/106/25/10359
29.06.2010: Health risk of the BP oil spill on April 20, 2010[1]
Crude oil contains a mixture of volatile hydrocarbon compounds - polycyclic aromatic hydrocarbons that typically include the carcinogens benzene, toluene, and xylene. According to the CDC, symptoms of exposure to these compounds include drowsiness, dizziness, rapid or irregular heartbeat, headaches, tremors, confusion, and unconsciousness.
Total petroleum hydrocarbons (TPH) is a term used to describe a large family of several hundred chemical compounds that originally come from crude oil. It is not practical to measure each one separately, therefore the total amount of TPH are measured and referred to.
Some of the TPH compounds can affect your central nervous system. One compound can cause headaches and dizziness at high levels in the air. Another compound can cause a nerve disorder called "peripheral neuropathy," consisting of numbness in the feet and legs. Other TPH compounds can cause effects on the blood, immune system, lungs, skin, and eyes.
Animal studies have shown effects on the lungs, central nervous system, liver, and kidney from exposure to TPH compounds. Some TPH compounds have also been shown to affect reproduction and the developing fetus in animals.
TPH and cancer: The International Agency for Research on Cancer (IARC) has determined that one TPH compound (benzene) is carcinogenic to humans. IARC has determined that other TPH compounds (benzo[a]pyrene and gasoline) are probably and possibly carcinogenic to humans. Most of the other TPH compounds are considered not to be classifiable by IARC.
Regulations and limits: There are no regulations or advisories specific to TPH. The following are recommendations for some of the TPH fractions and compounds:
The EPA requires that spills or accidental releases into the environment of 10 pounds or more of benzene be reported to the EPA.
The Occupational Safety and Health Administration has set an exposure limit of 500 parts of petroleum distillates per million parts of air.
The Occupational Safety and Health Administration (OSHA) and the Air Force Office of Safety and Health (AFOSH) have set a permissible exposure level (PEL) of 400 parts of petroleum distillates per million parts of air (400 ppm) for an 8-hour workday, 40-hour workweek.
The National Institute for Occupational Safety and Health (NIOSH) recommends that average workplace air levels not exceed 350 milligrams of petroleum distillates per cubic meter of air (350 mg/m³) for a 40-hour workweek.
The Department of Transportation (DOT) lists fuel oils as hazardous materials and, therefore, regulates their transportation.
Worshop of the IOM on health risks related to the BP oil spill [2]
The IOM workshop on June 22 and 23, 2010 in New Orleans, discussed the health concerns related to the BP oil spill.
Scott Barnhart stressed that crude oil contains a complex mixture of heavy metals and volatile and nonvolatile polyaromatic hydrocarbons, Exposure by skin contact, inhalational and ingesting oil-contaminated foods may lead to cancer, neurologic, renal, hepatic, dermatologic, and hematologic effects.
Gina Solomon reported that BP data showed levels of benzene and 2-butoxyethanol (the dispersant chemical) above the Recommended Exposure Limit set by the National Institute for Occupational Safety and Health. Dr. Solomon recommends residents not to fish in any areas that have been declared off-limits or where they see evidence of oil contamination, and fish or shellfish that has an oily odour should be discarded and not eaten. Noting a strong odour of oil or chemicals, and are concerned about health effects, residents should seek refuge in an air conditioned environment, preferably with the air conditioner on recirculation mode to avoid intake of polluted air.
Maureen Lichtveld pointed out that the psychosocial aspect needs to have a much higher priority as it is being focused on. She referred to Exxon Valdez oil spill which caused a significant increases in depression, posttraumatic stress disorder, and other anxiety disorders, as well as generally poorer scores on mental health assessments. There are not enough data to predict whether there could be future elevations in cancer risks, reproductive issues, or neurological sequelae from this oil spill this must stay under observation.
[1] CDC: Gulf Oil Spill 2010: Information for Health Professionals
http://emergency.cdc.gov/gulfoilspill2010/health_professionals.asp
[2] Medscape Medical News: CDC and IOM Warn of Adverse Psychosocial, Cancer Effects From Gulf Oil Spill. Emma Hitt, PhD. June 28, 2010.
http://www.medscape.com/viewarticle/724299
25.06.2010: Vibrio vulnificus a pathogen in Gulf Coast oysters
Limiting the Sale of Raw Oysters Harvested from the Gulf of Mexico [1]
The Center for Science in the Public Interest warns the consumers from Vibrio vulnificus, a deadly bacteria found in almost all Gulf Coast oysters harvested in warmer months.
The Californian plan to reduce the risk of Vibrio vulnificus has proved to be effective, but it was binding only in this state.[2] The plan banned the sale of untreated Gulf Coast oysters reducing number of deaths from about five a year to zero. This approach will now be adopted nationwide by a new FDA policy. The shellfish industry were opposed to the oyster treatment to kill the pathogen.
The Department of Health Services (DHS) has amended California Code of Regulations (CCR), Title 17, Section 13675, [1ab]to prevent V. vulnificus illnesses and deaths associated with the consumption of raw Gulf oyster, restricting the sale of raw oysters harvested from the Gulf of Mexico during April 1 through October 31, unless the oysters are treated with a scientifically validated process to reduce V. vulnificus to non-detectable levels. Raw Gulf oysters received during April through October that have not been processed to reduce V. vulnificus to non-detectable levels are considered adulterated.[3] Treatments to kill Vibrio vulnificus without affecting taste are cold pasteurization, hydrostatic pressure, cost of the processes are low and increase food safety. [4]
Post-Harvest Processed Oysters [5]
Freezing, heat-cool pasteurization, and high hydrostatic pressure are used commercially on oysters as post-harvest processes to kill spoilage bacteria and reducing Vibrio spp. bacteria to non-detectable levels.The treamtment increases the shelf life of the product. The organisation SafeOyster.org, however, stresses that not all bacteria and viruses may be killed. The organisation recommends high-risk patients not to eat oysters, even when they were post-harvest processed. As a safety measure, these patients should eat cooked oysters.
The Center for Science in the Public Interest (CSPI) says Gulf Cost oysters are not safe [4]
According to David W. Plunkett, a CSPI staff attorney, some Gulf oysters may be ‘safe’ from oil contamination, but are not ‘safe’ to eat. Plunkett contradicts several reassuring statements that seafood from the Gulf on the market is safe. Vibrio vulnificus contaminates Gulf oysters in the spring and summer. While it may cause mild illnesses in healthy individuals, it can kill people who have diabetes, liver disease, hemochromatosis or compromised immune systems, causing the death of 10 people last year.
The Food and Drug Administration FDA affirms on its website that shellfish harvested from areas unaffected by the spill are safe to eat [6]
Plunkett remids that last year Mike Taylor, a Deputy of the FDA called Vibrio vulnificus a significant hazard, and now FDA ignores the risk of the pathogen bacteria.
The CSPI says that the FDA eventually backed down from its plans under pressure from Members of Congress who responded to industry posturing over potential job losses, and only California has implemented an effective control plan to protect its consumers.
Vibrio vulnificus infection [7]
Vibrio vulnificus is a bacteria which is present in marine environments such as estuaries, brackish ponds, or coastal areas, It causes an infection eating seafood, especially raw or undercooked oysters; the bacteria can also enter the body through open wounds when swimming or wading in infected waters, or via puncture wounds from the spines of fish such as tilapia. Symptoms include vomiting, diarrhea, abdominal pain, and a blistering dermatitis that is sometimes mistaken for pemphigus or pemphigoid. In people with compromised immune systems such as in chronic liver disease, a cut infected with Vibrio bacteria can quickly become worse and spread into the bloodstream. Severe symptoms and even death can then occur.
Vibrio illness in Florida [8]
Weis and colleagues 2010 report 834 vibrio infections in 825 individuals in Florida from 1998 to 2007. The incidence was Vibrio vulnificus 33%, V. parahaemolyticus 29%, and V. alginolyticus 16%, causing 45% ofwound infections and 42% gastroenteritis. Prevention is focused on oyster consumption. The authors call for educational messages focusing wound infections of high-risk populations.
Foodborne pathogens in oysters of South China food markets [9]
Chen and colleagues 2010 looking at the pathogens in shellstock Pacific oysters in the food markets in South China say that Vibrio vulnificus and Vibrio parahaemolyticus (89.3%) but no Listeria monototogenes could be detected in the samples. The authors concluded that Vibrio vulnificus and pathogenic Vibrio parahaemolyticus in oysters are a risk to public health in south China.
Vibrio bacteria in Brazilian oysters [10]
Vieira and colleagues 2010 analysed oyster samples from a coastal aquaculture in Euzebio, Ceará, Brazil, The authors identified Vibrio parahaemolyticus. Vibrio carchariae and Vibrio. Vulnificus, stressing that oysters should never be eaten raw or undercooked becaause of the risk presented by Vibrio bacteria.
Temperature effects on the depuration of Vibrio parahaemolyticus and Vibrio vulnificus from oysters [11]
Chae, Cheney and Su 2009 investigated temperature effects on depuration for reducing Vibrio parahaemolyticus and Vibrio vulnificus in American oyster. Depuration of oysters at 22 degrees C had limited effects. Best reults were obtained with water temperature of 15 degrees C after 96 h of depuration at 15 degrees C. Depurations at 10 and 5 degrees C were less effective than at 15 degrees C.
Elektrolyzed water as sanitizer in food industry [12]
Hricova, Stephan and Zweifel 2008 report that electrolyzed water is obtained by electrolysing a dilute sodium chloride solution dissociating into acidic electrolyzed water (AEW) with a pH of 2 to 3, an oxidation-reduction potential of >1,100 mV, and an active chlorine content of 10 to 90 ppm, and basic electrolyzed water (BEW), which has a pH of 10 to 13 and an oxidation-reduction potential of -800 to -900 mV.
AEW reduced bacteria in suspension > 6.0 log CFU/ml. However, surface type and the presence of organic matter reduce the efficiency of AEW Applying BEW followed by AEW may lead to higher reductions than AEW only. The authors say electrolyzed water technology should be further discussed as industrial sanitization of equipment and decontamination of food products, but must be accompanied by good manufacturing and hygiene practices.
Electrolyzed oxidizing (EO) water treatment on reducing V. parahaemolyticus and V. vulnificus [13]
Holding vibrio contaminated oysters in electrolyzed oxidizing water containing 1% NaCl reduced the number of Vibrio parahaemolyticus and Vibrio vulnificus significantly in 4 to 6 h, but extended exposure (> 12 h) of oysters in electrolyzed oxidizing water and chlorine levels over 30 ppm caused death of oysters. Ren and Su 2006, authors of the study, suggested to use electrolyzed oxidizing water treatment for 4 to 6 h as post-harvest treatment of oysters to reduce Vibrio contamination limited to 4 to 6 h to avoid death of oysters.
Weak acidic electrolyzed oxidizing water post-harvest treatment of oysters [14]
Quan and colleagues 2010 report that Vibrio vulnificus and Vibrio parahaemolyticus were killed with a treatment of 15 s and more of weak acidic electrolyzed oxidizing water (WAEW) containing an available chlorine concentration (ACC) higher than 20mg/L. The effect of the treatment was reduced, when the ACC of WAEW was less than 15mg/L. The authors stress that the bactericidal activity of WAEW was primarily affected by ACC rather than treatment time, and WAEW is more effective than sodium hypochlorite (NaClO).
Vibrio vulnificus resistance to bile and other stresses [15]
Chen, Oliver and Wong 2010 describe the adaptation of Vibrio vulnificus and an rpoS isogenic mutant to bile and other stresses. An in vitro tolerance of the bacterium to 10% bile was attained by the authors, The bile-tolerant strain was more resistant to high pH, heat, high salinity and detergents than the rpoS mutant which had a lower bile-adaption rate.
The authors report further that production of GroEL was not markedly influenced but DnaK was inhibited in the bile-adapted cells, and RpoS plays a significant role in the response of Vibrio vulnificus to bile.
The interaction between low salinity and other common stresses in V. vulnificus [16]
Wong and Liu 2006 studied the cross-protective response of sublethal heat-, acid-, or bile-adapted Vibrio vulnificus against lethal low-salinity stress.
The authors found that Vibrio vulnificus adapted to an acidity of pH 4.4 and 41 degrees C heat-adapted V. vulnificus died in 0.04% NaCl low-salinity environment. The bile-adapted bacteria were resistant to low salinity, however 0.12% NaCl low-salinity adaption made them sensible to 12% bile stress.
Identification and subtyping of Vibrio parahaemolyticus and V. vulnificus targeting 16S-23S rRNA intergenic spacer regions [17]
Hoffmann and colleagues 2010 developed rapid polymerase chain reaction (PCR)-based intergenic spacer (IGS)-typing system for vibrios based on the IGS regions located between the 16S and 23S rRNA genes of vibrios.
The IGS-typing method demonstrated distinct IGS-typing patterns indicative of subspecies divergence in both populations making this technique equally useful for intraspecies differentiation, as well. The authors concluded that the new method is useful to identify vibrios down to sub-species level, and may be applied in time saving epidemiological investigations.
González-Escalona, Jaykus and DePaola reported in 2006 that amplification of the 16S-23S rDNA spacer region (ISR1) is a simple and rapid procedure for subtyping bacteria, especially those with several ribosomal operons including Vibrio vulnificus. V. vulnificus contains nine ribosomal operons with four or five ISR1 classes that differ in size and sequence. Clinical isolates formed a single cluster containing ISR1 patterns I, V, XI, and XII all carrying the type B 16S rDNA (rrs) sequence associated with human illness. Shellfish isolates presented high variability in the ISR1 patterns. The different classes differed in their tRNA gene composition, allowing subtyping of Vibrio vulnificus. The authors suggest that ISR1 patterns are linked with the virulence of the bacteria. [18]
Two fish-pathogenic serovars of Vibrio vulnificus biotype 2 [19]
According to Fouz and colleagues 2010 Vibrio vulnificus biotype 2 is subdivided into serovar E, infecting fish and humans, and serovar A, infecting only fish, such as eel in brackish water. Serovar A caused infections of freshwater-cultured eels vaccinated against serovar E resulting in haemorrhagic intestine. Both serovars infect healthy eels, tilapia, sea bass and rainbow trout, but not sea bream, serovar A entering mainly by the anus and serovar E by the gills.
The authors stress that serovar A form a new antigenic form of Vibrio vulnificus biotype 2 better adapted to fresh water than serovar E.
Vibrio vulnificus found in food and environmental samples of the Mediterranean area [20]
Cañigral and colleagues 2010 found that samples of seawater, oyster and wastewater from a coastal area in Spain near the Mediterranean.were positive by real time PCR, and Vibrio vulnificus could be isolated from these samples. The authors stress that Vibrio vulnificus presents a risk to humans in the Mediterranean area.
Rapid detection of Vibrio vulnificus in shellfish and Gulf of Mexico [21]
Panicker and colleagues 2004 described the optimization of SYBR Green I-based real-time PCR parameters to detect the presence of vibrios in seafood or environmental samples, using vvh-specific oligonucleotide primers. The method is completed in 8 hours.
[1] FDA Acts to Protect Consumers from Vibrio in Oysters. CSPI October 19, 2009.
http://www.cspinet.org/new/200910191.html
[2] Article 10.5. Raw Oysters. §13675. Raw Gulf Oysters: Labeling, Written Warnings and Additional Requirements. State of California.
http://www.cdph.ca.gov/services/Documents/fdb%20Raw%20Gulf%20Oyst%20Regs.pdf
[3] Environmental Health: Oysters:Limiting the Sale of Raw Oysters Harvested from the Gulf of Mexico. (Information from the California Department of Health Services)
http://www.co.el-dorado.ca.us/emd/envhealth/oyster.html
[4] Gulf Coast Oysters Unsafe (But Not For the Reason You Think). Deadly Vibrio Vulnificus Bacteria, Not Oil, Contaminate Gulf Oysters Every Summer. CSPI Newsroom. June 24, 2010.
http://www.cspinet.org/new/201006241.html
[5] SafeOysters.org - Health Care Providers. Vibrio vulnificus. Infection from Consumption of Raw. Shellfish or Marine-Related Wounds.
http://safeoysters.org/medical/prevention.html
[6] FDA: Multi-government agency response to the Gulf of Mexico oil spill. Gulf of Mexico Oil Spill Update - June 14, 2010
http://www.fda.gov/Food/ucm210970.htm
[7] Wikipedia: Vibrio vulnificus
http://en.wikipedia.org/wiki/Vibrio_vulnificus
[8] Weis KE, Hammond RM, Hutchinson R, Blackmore CG: Vibrio illness in Florida, 1998-2007. Epidemiol Infect. 2010 Jun 14:1-8.
http://www.ncbi.nlm.nih.gov/pubmed/20546636
[9] Chen Y, Liu XM, Yan JW, Li XG, Mei LL, Mao QF, Ma : .Foodborne pathogens in retail oysters in south China. Biomed Environ Sci. 2010 Feb;23(1):32-6.
http://www.ncbi.nlm.nih.gov/pubmed/20486433
[10] Vieira RH, de Sousa OV, Costa RA, Theophilo GN, Macrae A, Fonteles Filho AA, Rodrigues Ddos P: Raw oysters can be a risk for infections. Braz J Infect Dis. 2010 Feb;14(1):66-70.
http://www.ncbi.nlm.nih.gov/pubmed/20428657
[11] Chae MJ, Cheney D, Su YC: Temperature effects on the depuration of Vibrio parahaemolyticus and Vibrio vulnificus from the American oyster (Crassostrea virginica). J Food Sci. 2009 Mar;74(2):M62-6.
http://www.ncbi.nlm.nih.gov/pubmed/19323759
[12] Hricova D, Stephan R, Zweifel C: Electrolyzed water and its application in the food industry. J Food Prot. 2008 Sep;71(9):1934-47.
http://www.ncbi.nlm.nih.gov/pubmed/18810883
[13] Ren T, Su YC: Effects of electrolyzed oxidizing water treatment on reducing Vibrio parahaemolyticus and Vibrio vulnificus in raw oysters. J Food Prot. 2006 Aug;69(8):1829-34.
http://www.ncbi.nlm.nih.gov/pubmed/16924906
[14] Quan Y, Choi KD, Chung D, Shin IS: Evaluation of bactericidal activity of weakly acidic electrolyzed water (WAEW) against Vibrio vulnificus and Vibrio parahaemolyticus. Int J Food Microbiol. 2010 Jan 1;136(3):255-60. Epub 2009 Dec 7.
http://www.ncbi.nlm.nih.gov/pubmed/20004034
[15] Chen WL, Oliver JD, Wong HC: Adaptation of Vibrio vulnificus and an rpoS mutant to bile salts. Int J Food Microbiol. 2010 Jun 15;140(2-3):232-8.
http://www.ncbi.nlm.nih.gov/pubmed/20406715
[16] Wong HC, Liu SH: Susceptibility of the heat-, acid-, and bile-adapted Vibrio vulnificus to lethal low-salinity stress. J Food Prot. 2006 Dec;69(12):2924-8.
http://www.ncbi.nlm.nih.gov/pubmed/17186660
[17] Hoffmann M, Brown EW, Feng PC, Keys CE, Fischer M, Monday SR: PCR-based method for targeting 16S-23S rRNA intergenic spacer regions among Vibrio species. BMC Microbiol. 2010 Mar 23;10:90.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856557/?tool=pubmed
[18] González-Escalona N, Jaykus LA, DePaola A: Typing of Vibrio vulnificus strains by variability in their 16S-23S rRNA intergenic spacer regions. Foodborne Pathog Dis. 2007 Fall;4(3):327-37.
http://www.ncbi.nlm.nih.gov/pubmed/17883316
[19] Fouz B, Llorens A, Valiente E, Amaro C: A comparative epizootiologic study of the two fish-pathogenic serovars of Vibrio vulnificus biotype 2. J Fish Dis. 2010 May;33(5):383-90.
http://www.ncbi.nlm.nih.gov/pubmed/20158583
[20] Cañigral I, Moreno Y, Alonso JL, González A, Ferrús MA: Detection of Vibrio vulnificus in seafood, seawater and wastewater samples from a Mediterranean coastal area. Microbiol Res. 2010 Jan 25.
http://www.ncbi.nlm.nih.gov/pubmed/20106642
[21] Panicker G, Myers ML, Bej AK: Rapid detection of Vibrio vulnificus in shellfish and Gulf of Mexico water by real-time PCR: Appl Environ Microbiol. 2004 Jan;70(1):498-507.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC342803/?tool=pubmed
15.06.2010: Monosodium Glutamate not related to the Chinese Restaurant Syndrome [1]
Jinab and Hajeb 2010 of the University Putra Malaysia reviewed application, benefits of monosodium glutamate as flavor enhancer. The authors say that glutamate adds a fifth basic taste to the four basic ones, whicch are saltiness, sourness, sweetness and bitterness. It is also an energy source, acts as a substrate for glutathione synthesis and enhances food intake in older individuals. Glutamate may partially replace salt in food preparation. The Joint Expert Committee on Food Additives of the United Nations Food and Agriculture Organization and World Health Organization classified glutamate as safe. The authors stress that there are no consistent clinical data to support believes that glutamate causes asthma, migraine headache, Chinese Restaurant Syndrome, and there are no evidences indicating that individuals may be uniquely sensitive to glutamate.
The position of the Food Standards Australia New Zealand [2]
The Food Standards Australia New Zealand in a technical report of 2003 found that some studies reported a complex of symptoms which came to be known as the Chinese restaurant syndrome (CRS) because they typically followed ingestion of a Chinese meal. Two outstanding studies were Kwok, R. (1968) [3] and Schaumburg HH(1969) [4] suggesting monosodium glutamate as the causative agent in CRS embracing symptoms such as headache, numbness/tingling, flushing, muscle tightness, and generalised weakness. MSG symptom complex is now being used instead of CRS. A possible association between MSG and bronchospasm in asthmatic individuals were also suggested.
Conclusions: The FSA study found no convincing evidence that MSG is a significant factor in causing systemic reactions resulting in severe illness or mortality, and studies have failed to demonstrate a causal association with MSG. Some reactions were noted by administrating large doses (≥3g) of MSG without food were not serious and are likely to be attenuated when MSG is consumed with food. Bronchospasm in asthmatic individuals is, according to actual data, not significantly triggered by MSG
Patricia Tagliaferro in an article of 1995 [5], stressed inconsistent data of studies on the possible effect ofMSG. The study of Jinab and Hajeb 2010 confirms that glutamate is not related to asthma, migraine headache and Chinese Restaurant Syndrome.
[1] Jinap S and Hajeb B: Glutamate: Its applications in food and contribution to health. Appetite.
Published online ahead of print, doi: 10.1016/j.appet.2010.05.002
http://www.ncbi.nlm.nih.gov/pubmed/20470841
[2] Monosodium Glutamate, A safety Assessment. Food Standards Australia New Zealand 2003
http://www.foodstandards.gov.au/_srcfiles/MSG%20Technical%20Report.pdf
[3] Kwok, R. (1968), Chinese Restaurant Syndrome (letter). N Engl J Med, 278:796.
[4] Schaumburg HH, Byck R, Gerstl R, Mashman JH: Monosodium L-glutamate: its pharmacology and role in the Chinese restaurant syndrome. Science. 1969 Feb 21;163(869):826-8
http://www.ncbi.nlm.nih.gov/pubmed/5764480
[5] Taliaferro, Patricia J.: Monosodium glutamate and the Chinese Restaurant Syndrome: a review of food additive safety. Journal of Environmental Health, Vol. 57, 1995
http://www.thefreelibrary.com/Monosodium+glutamate+and+the+Chinese+Restaurant+Syndrome:+a+review+of+...-a017087836
14.06.2010: Harvest Plus and Maize biofortification [1]
While many micronutrients are available from fruits, vegetables, and animal products, most of the poor are unable to grow or buy these micronutrient-rich foods. Their diets are characterized by high intakes of staple food crops (such as maize, wheat, and rice) but low consumption of micronutrient-rich foods such as fruits, vegetables, and animal and fish products. By providing a regular daily dose of vitamins and minerals, biofortified staple crops do not need to provide the entire recommended daily allowance (RDA) of micronutrients, but they can be effective in reducing hidden hunger as part of a strategy that includes dietary diversification, supplementation, and commercial fortification, among others.
HarvestPlus focuses on three critical micronutrients that are recognized by the World Health Organization (WHO) as most limiting in diets: iron, zinc, and vitamin A. HarvestPlus envisions that in fifteen years, millions of people suffering from micronutrient malnutrition will be eating new biofortified crop varieties, such as orange sweet potato rich in vitamin A, orange maize and rice with increased zinc.
Biofortification [2]
Biofortification is a method of breeding crops to increase their nutritional value of staple crops. This can be done either through conventional selective breeding, or through genetic engineering. Biofortification differs from ordinary fortification because it focuses on making plant foods more nutritious as the plants are growing, rather than having nutrients added to the foods when they are being processed
Selective breeding:Using this method, plant breeders search seed or germplasm banks for existing varieties of crops which are naturally high in nutrients. They then crossbreed these high-nutrient varieties with high-yielding varieties of crops, to provide a seed with high yields and increased nutritional value. This method is quicker, cheaper, and less controversial than genetically engineering crops. For example, HarvestPlus primarily use conventional breeding techniques to develop biofortified crops.
Genetic modification: Golden rice is an example of a GM crop developed for its nutritional value. Golden rice contains genes from the soil bacterium Erwinia and either maize or daffodil plants, and contains increased levels of beta-carotene which can be converted by the body into vitamin A. This can help alleviate symptoms of vitamin A deficiency.
Here are some studies concerning improvement of micronutrients in staple foods.
Provitamin A biofortification of maize using crtRB1 alleles [3]
New breedings are focused on biofortification to improve the dietary vitamin A status in developing world. Yan and colleagues 2010, studying the genetic code of maize (Zea mays L.), report that the gene encoding beta-carotene hydroxylase 1 (crtRB1) associated with beta-carotene which may increase the concentration of provitamin A in maize kernel 18 times compared with standard maize. Alleles of crtRB1 are being introgressed via inexpensive PCR marker-assisted selection into tropical maize. The researchers avoided to introduce alien genes in maize. They use the natural variation of the crtRB1 gerne within the same plant increasing the production of provitamin A and reducing its transformation to other, not biologic active chemical structures. Davis and colleagues 2008 studying the biologic activity of other carotenoids report that twice the molar amount of beta-cryptoxanthin was as efficacious as beta-carotene. [4]
Biofortification of staple food crops [5]
Nestel and collegues 2010 highlights the progress which has been made to control micronutrient deficiencies through supplementation and food fortification. The authors stress that biofortification is being supported by predictive cost-benefit analyses, however additional public work is needed to induce producers and consumers to accept biofortified crops. Activities, such as the good seed systems, the development of markets and products, and demand creation may be helpful to achieve this goal.
Good seeds is supported by Bill & Melinda Gates Foundation and the Rockefeller Foundation. It helps to create new varieties of seeds and make improved seeds much more accessible in Africa, especially to rural farmers. [6]
Genes related to carotenogenesis and heat resistance in maize [7]
Li and colleagues 2008 studied the carotenoid expression in maize. The authors report that maize endosperm carotenoid accumulation requires PSY1 expression, but this was not related to PSY2 or PSY3.
Better understanding of the timing of PSY1 transcript critical information allowed to choose breeding alleles. The authors also found that PSY1 is required for carotenogenesis in the dark and for heat stress tolerance. Leaf carotenogenesis was shown to require photoregulation of PSY2 plus nonphotoregulatiing PSY1 expression.
Natural genetic variations used for biofortification of maize [8]
Harjes and colleagues 2008 describe the variation at the lycopene epsilon cyclase (lcyE) locus which alters the two branches of the pathway of the alpha-carotene versus beta-carotene. Four natural lcyE polymorphisms could lead to a threefold difference in provitamin A compounds. The best suited lcyE alleles may now be selected using inexpensive molecular markers developing maize with higher provitamin A levels.
[1] HarvestPlus: Nutrients. What is hidden hunger?
http://www.harvestplus.org/content/about-harvestplus
[2] Wikipedia: Biofortification
http://en.wikipedia.org/wiki/Biofortification
[3] Yan J, Kandianis CB, Harjes CE, Bai L, Kim EH, Yang X, Skinner DJ, Fu Z, Mitchell S, Li Q, Fernandez MG, Zaharieva M, Babu R, Fu Y, Palacios N, Li J, Dellapenna D, Brutnell T, Buckler ES, Warburton ML, Rocheford T: Rare genetic variation at Zea mays crtRB1 increases beta-carotene in maize grain. Nat Genet. 2010 Apr;42(4):322-7.
http://www.ncbi.nlm.nih.gov/pubmed/20305664
[4] Davis CR, Howe JA, Rocheford TR, Tanumihardjo SA: The xanthophyll composition of biofortified maize (Zea mays Sp.) does not influence the bioefficacy of provitamin a carotenoids in Mongolian gerbils (Meriones unguiculatus). J Agric Food Chem. 2008 Aug 13;56(15):6745-50. Epub 2008 Jul 11.
http://www.ncbi.nlm.nih.gov/pubmed/18616269
[5] Nestel P, Bouis HE, Meenakshi JV, Pfeiffer W: Biofortification of staple food crops. J Nutr. 2006 Apr;136(4):1064-7.
http://www.ncbi.nlm.nih.gov/pubmed/16549478
[6] Bill & Melinda Gates Foundation: Good Seeds, Better Lives for Poor Farmers.
http://www.gatesfoundation.org/agriculturaldevelopment/pages/connecting-poor-farmers-to-good-seeds-feature.aspx
[7] Li F, Vallabhaneni R, Yu J, Rocheford T, Wurtzel ET: The maize phytoene synthase gene family: overlapping roles for carotenogenesis in endosperm, photomorphogenesis, and thermal stress tolerance. Plant Physiol. 2008 Jul;147(3):1334-46.
http://www.plantphysiol.org/cgi/content/full/147/3/1334
[8] Harjes CE, Rocheford TR, Bai L, Brutnell TP, Kandianis CB, Sowinski SG, Stapleton AE, Vallabhaneni R, Williams M, Wurtzel ET, Yan J, Buckler ES: Natural genetic variation in lycopene epsilon cyclase tapped for maize biofortification. Science. 2008 Jan 18;319(5861):330-3.
http://www.ncbi.nlm.nih.gov/pubmed/18202289
12.06.2010: Monitoring the stability of nanoparticles under pH conditions found in living cells [1]
According to Murphy and colleagues 2010 the stability of nanoparticles may be affected by changes of the pH of the cell environment altering their potential for uptake into organisms. The pH in cells varies within the different compartments such as the cytosol or intracellular fluid which is slightly basic with a pH of 7.2. The interior of lysosomes is acidic at a pH is about 4.5. The efficacy of the anti-clumping coating often depends on the pH of such environment.
The technology developed by the authors can study the behaviour and aggregation of nanoparticles in the variable environment found in biological systems. The authors used dynamic light scattering to measure the aggregation of nanoparticles after pH jumps in aqueous solutions of photoacid generator and ultraviolet light. This avoids the delays from mixing or stirring of the solution.
The authors stress that such studies may improve the design of nanoparticles for tumour treatment where acidity conditions different from normal cells. Also a better understand the environmental, health and safety implications of nanoparticles are expected as outcome of the studies.
[1] Murphy RJ, Pristinski D, Migler K, Douglas JF, Prabhu VM: Dynamic light scattering investigations of nanoparticle aggregation following a light-induced pH jump. The Journal of Chemical Physics, 2010; 132 (19): 194903 DOI: 10.1063/1.3425883
http://jcp.aip.org/jcpsa6/v132/i19/p194903_s1?bypassSSO=1
11.06.2010: Replacing saturated fats [1]
Reviewing studies related to the effects of saturated fats on heart health, Micha and Mozzafarian 2010 found that replacing saturated fatty acids (SFA) with polyunsaturated fat modestly lowers coronary heart disease risk. Replacing SFA with carbohydrate has no benefit and replacing SFA with monounsaturated fat has uncertain effects. Results of studies found mixed and unclear effects of SFA on vascular function, insulin resistance, diabetes, and stroke.
The authors highlight the need of more studies, and warns from public health programs on reducing SFA consumption without considering the replacement nutrient or other food-based risk factors for heart diseases.
Poly unsaturated fats should replace saturated fats and not be reduced in human nutrition [2]
Mozaffarian, Micha and Wallace 2010 report that studies recommend to reduced saturated fat (SFA) consumption to reduce the risk of coronary heart disease (CHD), and some even recommend to lower or limit polyunsaturated fat (PUFA) consumption.
The authors reviewing studies found that PUFAS consumption of 14.9% energy presented a CHD risk reduction of 10%, compared with groups consuming 5.0% PUFAS. The overall pooled risk reduction was 19%, corresponding to 10% reduced CHD risk for each 5% energy of increased PUFAS.
The authors concluded that polyunsaturated fatty acids should therefore be used as replacement of saturated fats and PUFAS should not be reduced as they proved to reduce coronary heart disease.
Trans-fatty acids and their isomers in different food sources [3]
Micha and colleagues 2010 looked at food sources of individual plasma phospholipid trans fatty acid isomers which are known to increases the risk of coronary artery disease.
TFAS were associated with foods made with partially hydrogenated vegetable oils. The authors found including biscuits, chips and/or popcorn, fried foods. Bakery foods were associated with t-18:2 isomers,animal foods, including red measts and butter and high-fat dairy with t-16:1n-7, Margarine was associated with t-16:1n-9 isomers.
The authors stress the importance to consider the isomer forms of trans fatty acids in studies and their different food sources. Isomers of trans fatty acids differ in their health effects.
[1] Micha R, Mozaffarian D: Saturated Fat and Cardiometabolic Risk Factors, Coronary Heart Disease, Stroke, and Diabetes: a Fresh Look at the Evidence. Lipids. 2010 Mar 31.
http://www.ncbi.nlm.nih.gov/pubmed/20354806
[2] Mozaffarian D, Micha R, Wallace S: Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010 Mar 23;7(3):e1000252. Review.
http://www.ncbi.nlm.nih.gov/pubmed/20351774
[3] Micha R, King IB, Lemaitre RN, Rimm EB, Sacks F, Song X, Siscovick DS, Mozaffarian D: Food sources of individual plasma phospholipid trans fatty acid isomers: the Cardiovascular Health Study. Am J Clin Nutr. 2010 Apr;91(4):883-93.
http://www.ncbi.nlm.nih.gov/pubmed/20219966
11.06.2010: Processed meat like bacon and sausages increase risk of heart disease and diabetes, says a meta-analysis [1]
Micha, Wallace and Mozaffarian 2010 found that Consumption of processed meats, but not red meats, is associated with higher incidence of CHD and diabetes mellitus. It takes only 50 g (one hot Dog) of processed meat per day to increase heart disease by 42% and type 2 diabetes by 19%. No link between eating unprocessed red meat like beef or pork and risk of heart disease and diabetes was found by the authors. High levels of salt and nitrate preservatives in sausages, bacon and deli meats, rather than saturated fats, might explain the higher risk of heart disease and diabetes seen with processed meats, but not with unprocessed red meats.
The authors call for studies looking at processed and unprocessed meats separately and focus on salt and nitrate preservatives.
[1] Micha R, Wallace SK, Mozaffarian D: Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis.
Circulation. 2010 Jun 1;121(21):2271-83
http://www.ncbi.nlm.nih.gov/pubmed/20479151
10.06.2010: EPA Moves to Terminate All Uses of Insecticide Endosulfan to Protect Health of Farmworkers and Wildlife. [1]
Endosulfan, a highly controversial organochlorine insecticide and acaricide. It is registered since the 1950s. It is used also is used on vegetables, fruits, cotton, ornamental shrubs, trees, and herbaceous plants. The U.S. Environmental Protection Agency (EPA) is taking action to end all uses of the insecticide in the United States, causing an unacceptable neurological and reproductive risks to farmworkers and wildlife and can persist in the environment.
According to the EPA new data show that the risks are greater than previously known for farmworkers, aquatic and terrestrial wildlife, as well as to birds and mammals that consume aquatic prey which have ingested endosulfan. Endosulfan is used on a very small percentage of the U.S. food supply and does not present a risk to human health from dietary exposure.
Makhteshim Agan of North America, the manufacturer of endosulfan, is in discussions with EPA to voluntarily terminate all endosulfan uses.
The WHO estimates that the worldwide production of endosulfan is 12,800 tons per year.
Due to its acute toxicity, potential for bioaccumulation, and role as an endocrine disruptor it was banned in more than 62 countries, including the European Union and several Asian and West African nations. It is still used extensively in many other countries including India, Brazil, and Australia. It is produced by Bayer CropScience, Makhteshim Agan, and Government-of-India–owned Hindustan Insecticides Limited among others. Because of its threats to the environment, a global ban on the use and manufacture of endosulfan is being considered under the Stockholm Convention. [2]
[1] EPA to Terminate All Uses of Insecticide Endosulfan To Protect Health of Farmworkers and Wildlife. June 08, 2010.
http://www.epa.gov/pesticides/reregistration/endosulfan/endosulfan-cancl-fs.html
[2] Wikipedia: Endosulfan
http://en.wikipedia.org/wiki/Endosulfan
09.06.2010: The hazardous work, working conditions, and environment in India using the example of the Union Carbide plant of Bhopal [1]
Asish Kumar Mandal 2009 reports that hazardous work, working conditions, and environment in India threatens health of workers culminating in the Bhopal Gas Tragedy, in 1984. This accident forced the Indian government to review their legislative measures to improve the occupational health situation. A new National Health Policy was announced in 2002, however, inadequate strategies, policies, and the lack of a proper monitoring mechanism hinder results. The authors presents suggestions how to improve the health conditions of the workers.
Safety of industrial plants and heath issues must attain top priority in occupational health policies, and tight controls of engineering of industrial facilities are necessary, primarily in developing countries, where cost reduction may lead to accidents comparable with the disaster of Bhopal.
Genetic alteration resulting from exposure to methyl isocianate of the Union Carbide plant [2]
Bhargava and colleagues 2010 assessed the immunotoxic effects of methyl isocyanate gas from the Bhopal pesticide plant. The authors found a significant increase in the levels of all circulating inflammatory biomarkers ((IL-8, IL-1beta, IL-6, TNF, IL-10, IL-12p70 cytokines and C-reactive protein) in the methyl isocianate exposed group, compared to a non-exposed group. The authors suggest that the rise of the inflammatory biomarkers are a result a toxin induced genetic and/or epigenetic alteration, and call for more studies to confirm their results.
Exposure of parents to poisons of the Bhopal accident affected offsprings [3]
Sarangi and colleagues 20101 report that the exposure of parents to toxic gases in the Bhopal incident caused an very high increase of initial 5-year mortality of their offspring. Male offspring of these parents were stunted in growth until puberty, and post-puberty effect on head circumference was found in females exposed to gases in utero.
Clinical findings and genetic implications of the Bhopal accident [4]
More than 500 000 victims survived the tragedy of Bhopal, presenting chronic illnesses such as pulmonary fibrosis, bronchial asthma, chronic obstructive pulmonary disease, emphysema, recurrent chest infections, keratopathy and corneal opacities. Mishra and colleagues 2009 reviewed the clinical findings and trials of the disaster, pointing out that in-utero exposure to methyl isocyanate in the first trimester of pregnancy caused a persistent immune system hyper-responsiveness. The immunotoxic implications and genomic effect of Bhopal gases have been studied in cultured mammalian cells. The authors recommend long-term monitoring of the Bhopal area to analyse the accident to determine the possible elements of the Bhopal cloud and their long-termed effect on humans
The Bhopal disaster [5]
The Bhopal disaster was an industrial disaster that took place at a Union Carbide pesticide plant in the Indian city of Bhopal, Madhya Pradesh. On 3 December 1984, 40 Tons of methyl isocyanate gas were accidentally released from the plant, exposing more than 500,000 people to the poisonous chemicals.. The first official immediate death toll was 2,259. The government of Madhya Pradesh has confirmed a total of 3,787 deaths related to the gas release.Others estimate 8,000-10,000 died within 72 hours and 25,000 have since died from gas-related diseases. 40,000 more were permanently disabled, maimed, or rendered subject to numerous grave illnesses; 521,000 exposed in all.
Some 390 tons of toxic chemicals abandoned at the UCIL plant continue to leak and pollute the groundwater in the region and affect surroundings. In June 2010, seven Indian ex-employees were convicted in Bhopal of causing death by negligence and sentenced to two years imprisonment each.
Warren Anderson, the head of Union Carbide Corp, the company itself and two subsidiary companies were also on trial, but have never appeared in court proceedings.The court in Bhopal asked for the extradition of Anderson.
Union Carbide was found liable for the disaster, but has denied responsibility. Dow says the legal case was resolved in 1989 claiming that Union Carbide paid $470 million as settlement. The responsibility relies now on the government of Madhya Pradesh, which now owns the site.
Causes of the disaster [6]
Water entered a sealed tank containing the highly reactive gas causing pressure in the tank to rise too high. Union Carbide Corp said the accident was an act of sabotage, but could never prove it. Lax safety standards or faulty plant design are most likely to be the real cause. The Central Bureau of Investigation alleges that proper safety procedures had not been followed . The hazardous design of the plant and the additional hazards due to design modifications were known by the leading experts of the company and Warren Anderson.
Cost reductions are the main cause of global hazards
Governments must exert strong supervision of industrial activities of the chemical and petroleum industries. Safety measures are played down to reduce production costs to improve the global competitiveness. This advice is strongly directed to the US government and emerging industrial countries like the Asian region.
[1] Mandal AK: Strategies and policies deteriorate occupational health situation in India: A review based on social determinant framework.Indian J Occup Environ Med. 2009 Dec;13(3):113-20. Doi: 10.4103/0019-5278.58913.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862442/?tool=pubmed
[2] Bhargava A, Punde RP, Pathak N, Dabadghao S, Desikan P, Jain A, Maudar KK, Mishra PK: Status of inflammatory biomarkers in the population that survived the Bhopal gas tragedy: a study after two decades. Ind Health. 2010;48(2):204-8.
http://www.ncbi.nlm.nih.gov/pubmed/20424351
[3] Sarangi S, Zaidi T, Pal RK, Katgara D, Gadag VG, Mulay S, Varma DR: Effects of exposure of parents to toxic gases in Bhopal on the offspring. Am J Ind Med. 2010 Mar 8.
http://www.ncbi.nlm.nih.gov/pubmed/20213748
[4] Mishra PK, Samarth RM, Pathak N, Jain SK, Banerjee S, Maudar KK: Bhopal Gas Tragedy: review of clinical and experimental findings after 25 years. Int J Occup Med Environ Health. 2009;22(3):193-202.
http://www.ncbi.nlm.nih.gov/pubmed/19819837
[5] Indian court convicts 7 in Bhopal gas tragedy. Arab News.com. June 7, 2010.
http://arabnews.com/world/article62200.ece
[6] How the Bhopal gas tragedy trial unraveled: Rediff News June 08, 2010.
http://news.rediff.com/report/2010/jun/08/how-the-bhopal-gas-tragedy-trial-unraveled.htm
06.06.2010: The Nicotera Diet as reference Italian Mediterranean diet [1]
Nicotera, a small town in the Calabria Region in Southern Italy was selected as reference of Mediterranean diet studies. The population of Nicotera has a high consumption of virgin olive olive oil, legumes, vegetables, cereals and fish. Little meat, eggs, Cheese and milk are consumed and men drink red wine moderately.
A very low myocardial infarction of 4 cases out of 598 examined in 1957 in men was reported, together with only few cases of hypertension, overweight and obesity. Similar findings were observed in another study of 1960 at Corfu.
The Nicotera Diet is rich in: Bread, Cereals, legumes, potatoes, vegetables, fresh fruit, nuts, fish, vegetable oils-especially virgin olive oil and moderate red wine consume by men.
Milk, cheese, meat, eggs, animal fat and margarines, sweet beverages, cakes/pies/cookies, sugar are sparingly consumed in the Mediterranean diet.
Italian Mediterranean Diet reduces cardiovascular diseases risk factor and the progression of renal diseases [2]
De Lorenzo and colleagues 20101 compared the effects of the Italian Mediterranean Diet, consisting of organic versus conventional foods in a healthy individuals and in Chronic Kidney Disease (CKD) patients in order to decrease cardiovascular diseases risk factor and the progression of renal diseases. The body composition and biochemical parameters after 14 days of Italian Mediterranean Organic Diet, according to the "Nicotera diet" were measured.
The authors report improvements in the levels tHcy, phosphorus, microalbuminuria levels and cardiovascular diseases risk in healthy individuals and in CDK patients.
[1] Flaminio Fidanza, Adalberta Alberti, Daniela Fruttini Simopoulos AP (ed): The Nicotera Diet: The Reference Italian Mediterranean Diet. Nutrition and Fitness: Mental Health, Aging, and the Implementation of a Healthy Diet and Physical Activity Lifestyle. World Rev Nutr Diet. Basel, Karger, 2005, vol 95, pp 115-121
http://www.ncbi.nlm.nih.gov/pubmed/16151276
[2] De Lorenzo A, Noce A, Bigioni M, Calabrese V, Della Rocca DG, Di Daniele N, Tozzo C, Di Renzo L: The effects of Italian Mediterranean organic diet (IMOD) on health status. Curr Pharm Des. 2010;16(7):814-24.
http://www.ncbi.nlm.nih.gov/pubmed/20388092
04.06.2010: Brown algae genetic code may explain origin of higher living beings [1]
Unicellular organisms originated animals, plants, fungi, red algae and brown algae. Researchers decoded the genetic code of the brown alga Ectocarpus siliculosus. This alga performs photosynthesis and is extreme versatile which are central requirements for higher life on earth.
Klaus Valentin, biologist of the Alfred-Wegener-Institute explains that scientist will choose one species of each of these five groups, and decode their genome to search for comparable genetic informations. Ectocarpus siliculosus was chosen as target in the brown algae group. The finding demonstrate that brown algae resulted from the fusion of a green alga with a red alga.
The scientists will perform further studies to see how the alga reacts to drought, UV light and rising temperatures.
The Ectocarpus genome and the evolution of brown algae [2]
Brown algae are photosynthetic organisms differ from plants in their evolution. Their genome contains 214 Millionen DNA base pairs (In molecular biology, two nucleotides on opposite complementary DNA or RNA strands that are connected via hydrogen bonds are called a base pair). Further 16.000 genes were found. Light-harvesting and pigment biosynthesis genes and new metabolic processes such as halide metabolism shows how the alga cope with the variable tidal environment. The evolution of multicellularity in this lineage is correlated with the presence of a rich array of signal transduction genes. A family of receptor kinases was found to be been linked with the emergence of multicellularity in both the animal and green plant lineages.
The Ectocarpus Genome Consortium: The Ectocarpus Genome Project started in June 2004 by an international consortium of 34 laboratories, coordinated in Roscoff, submitted a whole genome sequencing project to the French sequencing centre Genoscope. Automated annotations were obtained using the EuGene system adapted to the specificities of the Ectocarpus genome. [3]
Development and physiology of the brown alga Ectocarpus siliculosus [4]
Charrier and colleagues 2008 stress that brown algae are able to perform photosynthesis and have a cellulosic cell, but are only distantly related to plants considering the evolutionary origin of both groups. Therefore the brown algae present own features and experienced an evolution which was independent from other groups. The authors reviewed the work of the consortium of laboratories, including the Station Biologique in Roscoff and Genoscope, and two centuries of research work on Ectocarpus siliculosus.
A genetic map for the brown alga Ectocarpus siliculosus [5]
Heesch and colleagues 2010 presented A sequence-tagged genetic map for the brown alga Ectocarpus siliculosus which was proposed as a genetic and genomic model for the brown algae a genetic map using microsatellite markers that were designed based on the sequence supercontigs. The genetic map was constructed using 406 markers, resulting in 34 linkage groups. The Ectocarpus genetic map provides a large-scale assembly of the genome sequence and may be useful for further studies of the genetic of Ectocarpus siliculosus. .
[1] Erbgut entziffert. Braunalge verrät, wie höheres Leben entsteht. Spiegel Online 03.06.2010.
http://www.spiegel.de/wissenschaft/natur/0,1518,698444,00.html
[2] Cock JM, Sterck L, Rouzé P, Scornet D, Allen AE, Amoutzias G, Anthouard V, Artiguenave F, Aury JM, Badger JH, Beszteri B, Billiau K, Bonnet E, Bothwell JH, Bowler C, Boyen C, Brownlee C, Carrano CJ, Charrier B, Cho GY, Coelho SM, Collén J, Corre E, Da Silva C, Delage L, Delaroque N, Dittami SM, Doulbeau S, Elias M, Farnham G, Gachon CM, Gschloessl B, Heesch S, Jabbari K, Jubin C, Kawai H, Kimura K, Kloareg B, Küpper FC, Lang D, Le Bail A, Leblanc C, Lerouge P, Lohr M, Lopez PJ, Martens C, Maumus F, Michel G, Miranda-Saavedra D, Morales J, Moreau H, Motomura T, Nagasato C, Napoli CA, Nelson DR, Nyvall-Collén P, Peters AF, Pommier C, Potin P, Poulain J, Quesneville H, Read B, Rensing SA, Ritter A, Rousvoal S, Samanta M, Samson G, Schroeder DC, Ségurens B, Strittmatter M, Tonon T, Tregear JW, Valentin K, von Dassow P, Yamagishi T, Van de Peer Y, Wincker P: The Ectocarpus genome and the independent evolution of multicellularity in brown algae. Nature. 2010 Jun 3;465(7298):617-21.
http://www.ncbi.nlm.nih.gov/pubmed/20520714
[3] Ectocarpus Genome Project: Bioinformatics University of Gent Belgium
http://bioinformatics.psb.ugent.be/genomes/view/Ectocarpus-siliculosus
[4] Charrier B, Coelho SM, Le Bail A, Tonon T, Michel G, Potin P, Kloareg B, Boyen C, Peters AF, Cock JM: Development and physiology of the brown alga Ectocarpus siliculosus: two centuries of research. New Phytol. 2008;177(2):319-32.
http://www.ncbi.nlm.nih.gov/pubmed/18181960
[5] Heesch S, Cho GY, Peters AF, Le Corguillé G, Falentin C, Boutet G, Coëdel S, Jubin C, Samson G, Corre E, Coelho SM, Mark Cock J: A sequence-tagged genetic map for the brown alga Ectocarpus siliculosus provides large-scale assembly of the genome sequence. New Phytol. 2010 Apr 28.
http://www.ncbi.nlm.nih.gov/pubmed/20456050
04.06.2010: Phycodnaviruses may alter geochemical cycling and weather patterns [1]
Dunigan and colleagues 2006 point out that the family Phycodnaviridae consists of six genera. Their genomes range from 160 to 560kb. The phycodnaviruses have evolutionary roots that connect with several other families of large DNA viruses, referred to as the nucleocytoplasmic large DNA viruses (NCLDV).
The genome analyses have revealed more than 1000 unique genes, but only 14 homologous genes held in common among the three genera of the phycodnavirses which stands for a high gene diversity.
The authors stress the importance of phycodnaviruses infections of the phytoplankton because their effect may alter geochemical cycling and weather patterns.
Wilson, Van Etten and Allen 2009 reinforce the importance of the phycodnaviruses on infections of phytoplankton and their global global affects, on water biology. [2]
Large dsDNA viruses is integrated in the DNA of Ectocarpus siliculosus [3]
The Ectocarpus siliculosus virus-1 (EsV-1) is a lysogenic dsDNA virus belonging to the super family of nucleocytoplasmic large DNA viruses (NCLDV). It infects the brown alga Ectocarpus siliculosus. Delaroque and Bolan 2008 reports that the viral genome is integrated into the DNA of the alga.
In this study labelled EsV-1 DNA was used to identify the integration sites of the viral genome.
The authors found that some of the gene products are not encoded by EsV-1 but are present in the genome of other members of the NCLDV family, suggesting that the Ectocarpus algal genome contains traces of the integration of a large dsDNA viral genome and may be the ancestor of the extant NCLDV genomes. These viral DNA pieces might have originated EsV-1 genome through a complex integration and recombination system, using an enzyme similar to a new class of tyrosine recombinases. The authors concluded that some dsDNA viruses evolved principally through genome reduction.
Phycodnaviridae are large DNA algal viruses [4]
Van Etten and colleagues 2002 describes the genome of the Ectocarpus siliculosus virus (EsV-1) and the Paramecium bursaria chlorella virus (PBCV-1). Both are members of the family Phycodnaviridae . They infect eukaryotic algae. The 336 kb genome of EsV-1 has approximately 231 protein-encoding genes. The 331 kb genome of PBCV-1 genome has 11 tRNA genes and approximately 375 protein-encoding genes.
The two viruses have only 33 genes in common because of their different habitat. EsV-1 infects a marine brown alga, and PBCV-1 infects freshwater green algae.
[1] Dunigan DD, Fitzgerald LA, Van Etten JL: Phycodnaviruses: a peek at genetic diversity. Virus Res. 2006 Apr;117(1):119-32. Epub 2006 Mar 6.
http://www.ncbi.nlm.nih.gov/pubmed/16516998
[2] Wilson WH, Van Etten JL, Allen MJ: The Phycodnaviridae: the story of how tiny giants rule the world. Curr Top Microbiol Immunol. 2009;328:1-42.
http://www.ncbi.nlm.nih.gov/pubmed/19216434
[3] Delaroque N, Boland W: The genome of the brown alga Ectocarpus siliculosus contains a series of viral DNA pieces, suggesting an ancient association with large dsDNA viruses. BMC Evol Biol. 2008 Apr 12;8:110.
http://www.ncbi.nlm.nih.gov/pubmed/18405387
[4] Van Etten JL, Graves MV, Müller DG, Boland W, Delaroque N: Phycodnaviridae--large DNA algal viruses. Arch Virol. 2002 Aug;147(8):1479-516.
http://www.ncbi.nlm.nih.gov/pubmed/12181671
29.05.2010; Genetics of Celiac disease [1]
According to Fasano celiac disease is associated with specific HLA class II genes known as HLA-DQ2 and HLA-DQ8 located on chromosome 6p21. Approximately 95% of CD patients express HLA-DQ2, and the remaining patients are usually HLA-DQ8 positive. Either one of these genes is necessary for disease development but additional non-HLA genes are also involved. These additional genes were found by the genome-wide association studies.
It is being suggested that the genetic predisposition to CD is primarily linked to the effect of HLA-DQ2/DQ8 on the immune response to gluten peptides, together with other genes influencing the adaptive immune reactions, intestinal permeability, and a general predisposition to autoimmunity.
The author stresses that the HLA-DQ genes are the only genes for which testing is currently recommended. Presence of symptoms alone does not necessarily predict which individuals might have CD. Individuals with potential CD in high risk groups should be submitted to an accurate, two-step strategy for screening consisting of HLA-DQ typing and longitudinal serologic CD-screening only in subjects positive for HLA DQ2 and/or DQ8.
The presence of DQ2 or DQ8 does not confirm the diagnosis. Conversely, the absence of both HLA types has a negative predictive value of over 99% and virtually excludes the diagnosis of CD. [2]
The genome-wide association study [3]
A genome-wide association study is an approach that involves rapidly scanning markers across the complete sets of DNA, or genomes, of many people to find genetic variations associated with a particular disease. Once new genetic associations are identified, researchers can use the information to develop better strategies to detect, treat and prevent the disease. Such studies are particularly useful in finding genetic variations that contribute to common, complex diseases, such as asthma, cancer, diabetes, heart disease and mental illnesses.
[1] Fasano A: Celiac Disease and HLA-DQ2/DQ8. Emedicine, 29.12.2010.
http://emedicine.medscape.com/article/1790189-overview
[2] Fasano A.Should we screen for coeliac disease? Yes. BMJ. 2009 Sep 17;339:b3592. doi: 10.1136/bmj.b3592.
http://www.ncbi.nlm.nih.gov/pubmed/19762413
[3] The genome-wide association studies
http://www.genome.gov/20019523
29.05.2010: Wheat stem rust fungus Ug99 [1]
The stem rusts are caused by the fungus Puccinia graminis. It affects cereal crops such as wheat. The fungus enters the stems of a wheat plant and destroys the vascular tissue. Ug99 is the most serious pathogen of three cereal rusts. The Ug99 fungus is reddish-brown, and is wind-borne and destroys from 80 percent to 100 per cent of the crops. It is was found in Uganda in 1999 and spread to Kenya, Ethiopia, Sudan, Yemen and Iran.
Four new mutations of Ug99 present a new danger to wheat crops. These new mutations are worrying the Borlaug Global Rust Initiative. The Global Cereal Rust Monitoring System of the FAO say that the new mutations of Ug99 are moving from Africa to Asia, South America, Australia and North America. The new mutations of UG99 evade two stem rust-resistant genes of wheat. Dr. Ravi Singh, says that all new wheat varieties are resistant to both Ug99 and the new races.
Zak Pretorius reports that 47 percent of 129 South African commercial cultivars and advanced breeding lines are susceptible one or both of the new stem rust races.
New breeding lines with high defenses against Ug99 and varieties of stem rust strains are being multiplied and distributed with the financial assistance of USAID in the most threatened areas. The researchers say that the best strategy against the Ug99 race is to replace the susceptible varieties with the new high-yielding, resistant varieties.
Ug99 spreads through East Africa, Yemen, Sudan and Iran and is predicted to proceed to North Africa, Middle East and Asia. [2]
Markers for wheat stem rust resistant genes Sr25 and Sr26 [3]
A new mutation of stem rust agent named TTKSK (syn. Ug99)can evade stem rust resistance genes. The Genes Sr25 and Sr26 transferred into wheat from Thinopyrum ponticum are now used to control this new race and its. DNA markers for Sr25 and Sr26 are needed. The dominant markers Gb for Sr25 and Sr26#43 for Sr26 are known to be valid for eight wheat lines.
Liu and colleagues 2010 tested STS (sequence tagged site) markers amplifying diagnostic bands of Th. ponticum. Marker BF145935 was found to be useful as a co-dominant marker for Sr25, and Multiplex PCR with marker Sr26#43 and 6A-specific marker BE518379 can be used as a co-dominant marker for Sr26.
[1] University of Minnesota scientists battle global wheat scourge. Startribune.com. May 20, 2010.
http://www.startribune.com/business/94357064.html?page=1&c=y
[2] Ug99 wheat rust could threaten world wheat production. Startribune.com 27.05.2010.
http://www.startribune.com/newsgraphics/92531084.html?elr=KArks:DCiU1OiP:DiiUiacyKUU
[3] Liu S, Yu LX, Singh RP, Jin Y, Sorrells ME, Anderson JA: Diagnostic and co-dominant PCR markers for wheat stem rust resistance genes Sr25 and Sr26. Theor Appl Genet. 2010 Feb;120(4):691-7. Epub 2009 Oct 31.
http://www.ncbi.nlm.nih.gov/pubmed/19882111
28.05.2010: Indoor tanning definitively linked to skin cancer [1]
According to DeAnn Lazovic and colleagues 2010 the use of indoor tanning devices increases the risk of melanoma by 74 percent if tanning beds are used for any amount of time. Frequent uses of tanning beds increases melanoma risk 2.5 to 3 times compared with persons who never use it.
Frequent users of indoor tanning beds (50 plus hours, more than 100 sessions, or for 10-plus years.) are 2.5 to 3 times more likely to develop melanoma than those who never use tanning devices. The risk was directly related to the time spent tanning. These findings were independent of the type of tanning device, gender or age, contradicting previous studies of Cokkinides and the position of the American Cancer Society which say that indoor tanning before the age of 35 years increases the risk of melanoma.
The Cokkinides study: The study of Cokkinides and colleagues 2010 refers to the meta analysis which says that indoor tanning use before the age of 35 years increases the risk of melanoma. These believes leaded to state legislation restricting minors' access to indoor tanning [2]
The American Cancer Society position: The American Cancer Society says that using a tanning bed before age 35 increases a person's risk of developing melanoma by 75 percent. Physicians hope that recent actions by the FTC, along with TMA-supported state legislation placing age restrictions on minors' use of tanning beds, will spur the tanning industry to operate more responsibly and stop spreading false information to the public. [3]
Public health implication of tanning beds [4]
Tanning bed proponents claim that vitamin D supplementation supports indoor tanning health effect. They support the theory that reduced vitamin D levels or certain vitamin D receptor polymorphisms may increase melanoma risk.
Woo and Eide 2010 clarify that ultraviolet A is used by most tanning devices. This light is relatively ineffective in stimulating vitamin D synthesis. Health benefits from this association is therefore significant. The authors stress, therefore, the importance of education of the general public and a stricter indoor tanning legislation to reduce public health risks.
The Tanning Bed Cancer Control Act [5]
The proposed Tanning Bed Cancer Control Act intends to regulate the use of tanning beds. It proposes a limit on the amount of UV rays emitted by a tanning bed and how long someone can be exposed to them, along with an age limit of over 18. Download the Bill
Occupational solar exposure and skin cancer [6]
Incidence rates of skin cancer are rising in Great Britain. Some occupations are exposed to sunlight, such as farmers, construction workers and some public service workers. Young 2009 found a clear association between solar radiation and skin cancer and calls for protective measures to reduce the burden of occupational skin cancer in Great Britain.
[1] U of M study definitively links indoor tanning to melanoma. University of Minesota. May 27, 2010.
http://www.ahc.umn.edu/media/releases/indoortanning/index.htm
[2] Cokkinides V, Weinstock M, Lazovich D, Ward E, Thun M: Indoor tanning use among adolescents in the US, 1998 to 2004. Cancer. 2009 Jan 1;115(1):190-8.
http://www.ncbi.nlm.nih.gov/pubmed/19085965
[3] Conde C: Killer tans: state, feds crack down on indoor tanning. Tex Med. 2010 May 1;106(5):47-51.
http://www.ncbi.nlm.nih.gov/pubmed/20437310
[4] Woo DK, Eide MJ: Tanning beds, skin cancer, and vitamin D: An examination of the scientific evidence and public health implications. Dermatol Ther. 2010 Jan;23(1):61-71.
http://www.ncbi.nlm.nih.gov/pubmed/20136909
[5] New Bill to Help Prevent Tanning Bed Cancers -U.S. Reps. Maloney & Dent, Kate White, Doctors, Cancer Survivors Gather at Cosmo HQ to Discuss New Tanning Bed Cancer Control Act-
http://maloney.house.gov/index.php?option=content&task=view&id=2010&Itemid=61
[6] Young C: Solar ultraviolet radiation and skin cancer. Occup Med (Lond). 2009 Mar;59(2):82-8.
http://www.ncbi.nlm.nih.gov/pubmed/19233827
27.05.2010: Ammonium nitrate is an environmental stress to frog larval [1]
Ortiz-Santaliestra and colleagues 2010 found that sublethal effects of toxicants, such as ammonium nitrate impairs behavioural responses to predators. Detection of predators and mobility may be reduced following the effect of pollution. Tadpoles may be hampered to escape from predators. The authors noted that tadpoles exposed to ammonium nitrate were consumed by crayfishes faster than controls. According to the study nitrogenous fertilizers can impair larval defensive behaviours. Tadpoles may be hampered to escape from predators. The authors write that environmental stresses should not be neglected while performing toxicological studies on amphibians.
The effects of pollution on amphibians are increased when combined with stress by other environmental factors such as water salinity.
In another study in 2010, the same authors report that embryos of frogs exposed to ammonium nitrate and water salinity were up to 17% smaller than controls. Mortality rate due to predators was increased facing a single stress and further increased under the effect of two stressors. Embryos could develop a natural adaptation to salinity and mortality was then not increased. The authors concluded that multiple stressors should be considered when testing environmental pollution effect on amphibians. [2]
[1] Ortiz-Santaliestra ME, Fernández-Benéitez MJ, Marco A, Lizana M: Influence of ammonium nitrate on larval anti-predatory responses of two amphibian species. Aquat Toxicol. 2010 May 19.
http://www.ncbi.nlm.nih.gov/pubmed/20493565
[2] Ortiz-Santaliestra ME, Fernández-Benéitez MJ, Lizana M, Marco A: Adaptation to osmotic stress provides protection against ammonium nitrate in Pelophylax perezi embryos. Environ Pollut. 2010 Mar;158(3):934-40. Epub 2009 Oct 3.
http://www.ncbi.nlm.nih.gov/pubmed/19800720
27.05.2010: Effect of herbicide Atrazine on fish reproduction [1]
Atrazine is the most frequent pesticide detected in streams in agricultural areas like the Corn Belt states, and is known for its effects on the hypothalamus-pituitary-gonad axis in certain vertebrate species, Tillitt and colleagues 2010 looked at the effects on fish reproduction at concentrations of 0, 0.5, 5.0, and 50mug/L of atrazine.
The authors found that total egg production, due to reduced numbers of spawning events, was lower under Atrazine exposure compared to Antrazine free breeding. Gonad abnormalities and alteration of final maturation of oocytes were also observed. The authors call for more studies to evaluate the atrazine risk on fishes.
[1] Tillitt DE, Papoulias DM, Whyte JJ, Richter CA: Atrazine reduces reproduction in fathead minnow (Pimephales promelas). Aquat Toxicol. 2010 Apr 22.
http://www.ncbi.nlm.nih.gov/pubmed/20471700
22.05.2010: Reliability of real-time reverse-transcription PCR in clinical diagnostics [1]
Real-time PCR has played a decisive role in the sequencing of the human genome, comprehensive genomic, mRNA and miRNA expression profiling of many diseases, detection of human pathogens, diagnosis and prognosis, treatment monitoring and transplant biology. Murphy and Bustin 2009 cite, however, some technical deficiencies such as the demonstrated through its association with the measles, mumps and rubella vaccine/autism controversy. The authors call for careful experimental design, validation and analysis.
The need of gidelines for qPCR data publications [2]
According to Bustin 2009 real-time quantitative PCR (qPCR) due to ill-assorted pre-assay conditions, poor assay design and inappropriate data analysis methodologies resulted in inconsistent or misleading publication. Materials and methods informations are often insufficient for an evaluation of presented data. A set of guidelines of minimum standard for the provision of information for qPCR experiments ("MIQE"). These guidelines may improve the reliability of qPCR nucleic acid quantification technology.
Data normalization and reference genes for RT-qPCR [3]
Galiveti and colleagues 2010 report that numerous non-protein-coding RNA (npcRNA) molecules form a class of untranslated RNAs with significant biochemical activities. Reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) lack appropriate internal controls in the analysis of npcRNA. The expression of protein-coding reference genes, also termed "housekeeping" genes (HKGs) vary among tissues and different experimental conditions and are, therefore, questionable as reference in npcRNA expression analyses.
The authors determined the most suitable internal control with least expression variance. They found that five npcRNAs presented better expression levels in different tissues than common HKGs. The authors termed these genes as housekeeping RNAs (HKRs) These genes may be used for RT-qPCR data normalization in human transcriptome analysis, and might also be used as reference genes.
The Minimum Information for Publication of Quantitative Real-Time PCR Experiments (MIQE) guidelines [4]
Bustin and colleagues 2009 stress the lack of consensus on how to perform and interpret quantitative real-time PCR (qPCR) experiments. To improve the reliablility and the interpretation of qPCR results the authors developed the Minimum Information for Publication of Quantitative Real-Time PCR Experiments (MIQE) guidelines. These guidelines describe the minimum information together with a checklist which should be included in the manuscript submitted to publishers. Data such as disclosure of all reagents, sequences, and analysis methods are essential for the work of reviewers which assess the validity of the protocols. These guidelines aim to improve the reliablility and the interpretation of qPCR results.
Quantification of mRNA using real-time RT-PCR [5]
Nolan, Hands and Bustin 2005 describe a series of RT-qPCR protocols that illustrate the essential technical steps required to generate quantitative data that are reliable and reproducible.
[1] Murphy J, Bustin SA: Reliability of real-time reverse-transcription PCR in clinical diagnostics: gold standard or substandard? Expert Rev Mol Diagn. 2009 Mar;9(2):187-97. Review.
http://www.ncbi.nlm.nih.gov/pubmed/19298142
[2] Bustin SA: Why the need for qPCR publication guidelines?--The case for MIQE. Methods. 2010 Apr;50(4):217-26. Epub 2009 Dec 16.
http://www.ncbi.nlm.nih.gov/pubmed/20025972
[3] Galiveti CR, Rozhdestvensky TS, Brosius J, Lehrach H, Konthur Z: Application of housekeeping npcRNAs for quantitative expression analysis of human transcriptome by real-time PCR.RNA. 2010 Feb;16(2):450-61. Epub 2009 Dec 29.
http://www.ncbi.nlm.nih.gov/pubmed/20040593
[4] Bustin SA, Benes V, Garson JA, Hellemans J, Huggett J, Kubista M, Mueller R, Nolan T, Pfaffl MW, Shipley GL, Vandesompele J, Wittwer CT: The MIQE guidelines: minimum information for publication of quantitative real-time PCR experiments. Clin Chem. 2009 Apr;55(4):611-22. Epub 2009 Feb 26.
http://www.clinchem.org/cgi/content/full/55/4/611
[5] Nolan T, Hands RE, Bustin SA: Quantification of mRNA using real-time RT-PCR. Nature Protocols 1, - (2006). Published online: 9 November 2005. Doi:10.1038/nprot.2006.236.
http://www.nature.com/nprot/journal/v1/n3/abs/nprot.2006.236.html
22.05.2010: Synthetic chromosome take over the control of bacteria [1]
Venter and colleagues report in 2010 that they exchanged the chromosome of a bacterial cell with a chromosome synthesized in their laboratory. Only available chemicals were used for the synthesis of the artificial chromosome. The bacteria with the new chromosome could replicate and produce a new set of proteins. In this experiment Mycoplasma genitalium was used. This bacterium is very small. It lives in cattle and goats. The researchers sequenced the code of its DNA and succeeded in their synthesis.
The new bacteria was called “Synthia” and will be used to create carbon-capturing algae and other useful bacteria.
[1] Pennisi E: Genomics: Synthetic Genome Brings New Life to Bacterium. Science 21 May 2010: Vol. 328. no. 5981, pp. 958 – 959. Doi: 10.1126/science.328.5981.958
http://www.sciencemag.org/cgi/content/summary/328/5981/958
21.05.2010: Increasing sustainable palm oil market [1]
New Britain Palm Oil (NBPOL), together with Loders Croklaan and Lipidos Santiga dominate the sustainable oil market. NBPOL produces palmoil and palm kernel oil which has been kept apart from not certified oil during the whole supply chain. Refining takes place at the plant in Liverpool, UK. The company increases its plantation area by more than 50 per cent, and has already 25,000 hectares of plantations in Papua New Guinea.
Certificates on sustainable palm oil [2]
The Roundtable on Sustainable Palm Oil (RSPO) promotes the growth and use of sustainable oil palm products through credible global standards and engagement of stakeholders. It has 328 members including all global players such as Aarhus Karlshamn, Cargill, Danisco, Unilever and Vandemoortele, All take profit out of the sustainable image.
The New Britain Palm Oil is an executive member of the Roundtable on Sustainable Palm Oil, bearing the vice presidency of RSPO. Green Palm Sustainability issues the certificates on the sustainability of RSPO and sells these certificates. [3]
[1] New Britain Palm Oil: Sustainability, Environmental Policy.
http://www.nbpol.com.pg/environment/index.html
[2] Roundtable on Sustainable Palm Oil (RSPO): Members.
http://www.rspo.org/?q=membersearch
[3] Roundtable on Sustainable Palm Oil
http://www.nbpol.com.pg/environment/rspo.html