July 2010 - OurFood-news

29.07.2010: Health risks of energy drinks and energy shots [1]

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] Clin Microbiol Rev. 2007 Jul;20-3:391-408



[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