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28.11.2010: Collecting feathers from live geese [1]
The European Food Safety Agency assessed the welfare implications of collecting feathers from live geese. The Agency writes that this practice can be carried out without causing pain, suffering or injury to the birds if done at a time when the birds are moulting and if brushing and combing techniques are used. However, under current commercial conditions, plucking feathers causes pain.
In the opinion, the Panel points out that brushing or combing live geese to collect moulting feathers causes no tissue damage, whereas plucking feathers (that is pulling them out) will result in pain and other forms of suffering, such as bleeding and skin damage. However, not all the birds in a flock moult at the same time, and different parts of the body moult at different times, some feathers may be unavoidably plucked when brushing and combing techniques are used.
The Agency recommends that a control system should be put in place to ensure that only moulting feathers are gathered from live geese. Operators should be familiar with the difference between feathers that are ripe for collection and those that are not. Suffering should be avoided or minimised when catching and handling the geese and that operators should be aware of good animal handling methods. The presence of bloody feathers, skin injuries, posture changes (e.g. hanging wings), and broken or dislocated bones can be used to assess the welfare of geese submitted for feather collection. The Agency also suggested that further animal-based indicators should be developed and that future research in the field should be carried out to establish methods to evaluate the maturity of feathers.
Ducks hatched in the spring are usually ready to pick in hot weathr. Ducks are usually ready to pick when they are two months old. After that they can be picked every six weeks until cold weather. [2]
Small scale operations remove the molting feathers from under the wings. Most waterfowl molt their feathers every six weeks and can be harvested then. However, pulling the feathers out until the birds are bald and often bleeding is inhuman and leave the birds without the protection of their feathers and down. [3]
[1] EFSA looks at welfare implications of collecting feathers from live geese. 25.11.2010.
http://www.efsa.europa.eu/en/press/news/ahaw101125.htm
[2] Plucking Ducks. Gina Hilton. Bittersweet, Volume I, No. 3, Spring 1974
http://www.appropedia.org/Plucking_Ducks
[3] Goose Down Feather Pillow - Hungarian White Goose Down Pillows
http://www.wise4living.com/bbpillow/goose.htm
27.11.2010: Cholera epidemic 2010 in Haiti [1]
Cholera is transmitted through fecal contamination of water or food and causes an acute, severe, watery diarrhoea that can result in hypovolemic shock and death if not treated with fluid replacement promptly.
The cholera epidemic in Haiti killed 1400 people. 25000 went sick and are being medicated.
According to Dr. Scott Dowell of CDC it is not possible to find out how the cholera came to Haiti.
Cholera can be treated with antibiotics but the usual best course is giving intravenous fluids, salts and sugars to restore what is lost through diarrhoea and vomiting. It seems hard to get the bacterium out of Haiti and the country will have to deal with the disease for a long time.
Genetic tests show the Vibrio cholerae bacteria isolated in Haiti is almost identical to one another, which supports the theory of a single source. It is the same strain previously found in countries in South Asia and elsewhere, and can be trace . Back to a pandemic in Indonesia 49 years.in Sulawesi, Indonesia. The outbreak of cholera in Haiti was first seen affecting workers in rice paddies in the Artibonite Department. They were drinking untreated water and practiced open defecation. Haiti lacks piped, treated water and adequate sanitation.
The Haitian population has no pre-existing immunity to cholera. The toxigenic strain Vibrio cholerae O1, serotype Ogawa, biotype El Tor was identified. The strain is susceptible to tetracycline, ciprofloxacin, and kanamycin; and resistant to trimethoprim-sulfamethoxazole, furazolidone, nalidixic acid, sulfisoxazole, and streptomycin. The CDC stresses the importance of preventing infection by promoting water treatment, adequate sanitation and hygiene, and safe food preparation. [2]
Prevention and control measures [3]
The CDC reports that prevention and control measures are focused on 1) providing better access to treated drinking water; 2) providing education on improvement of sanitation, hygiene, and food preparation practices; 3) advising ill persons to begin using oral rehydration solution immediately and seek health care at the onset of watery diarrhoea; 4) enhancing cholera treatment capacity at existing health-care institutions; and 5) establishing cholera treatment centres.
Individual protection from Cholera [4]
The CDC recommends individual measures to protect from the disease:
- Drink and use safe water. Boil it for at least 1 minute, or treat it with chlorine.
- Wash your hands often with soap and safe water.
- Use latrines or bury your faeces; do not defecate in any body of water. If there are no latrines installed defecate at least 30 meters away from any body of water and then bury your faeces.
- Cook food well, especially seafood, keep it covered, eat it hot, and peel fruits and vegetables. Boil it, Cook it, Peel it, or Leave it.
- Clean up safely - in the kitchen and in places where the family bathes and washes clothes. Read more
[1] Cholera in Haiti - update 4 WHO Cholera Tahiti 24.11.2010
http://www.who.int/csr/don/2010_11_24/en/index.html
[2] Centers for Disease Control and Prevention (CDC): Cholera outbreak --- Haiti, October 2010. MMWR Morb Mortal Wkly Rep. 2010 Nov 5;59(43):1411
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5943a4.htm
[3] Centers for Disease Control and Prevention (CDC): Update
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5945a1.htm
[4] Protect Yourself from Cholera. CDC Prevention Message.
http://www.cdc.gov/haiticholera/pdf/cholera_preventionmessages.pdf
25.11.2010: Antibiotic resistance of bacteria [1]
Spízek and colleagues 2010 write that resistance to antibiotics and other antimicrobial compounds continues to increase and suggest protection strategies against pathogenic microorganisms. Such strategies should focus on new vaccines, use of specific bacteriophages, search for new antibiotics, sequencing microbial genomes to identify related genes and analysing DNA from the environment (metagenomics).
Study explains antibiotic resistance mechanism of bacteria [2]
Desai and Miller 2010 assessed the mechanisms used by bacteria to fight antibiotics. The authors used bromoacetate as an environmental threat to simulate antibiotics. In this study Escherichia coli produced protective proteins allowing its survival even at lethal concentration of bromoacetate.
The authors identified nine genes from Escherichia coli whose overexpression affords survival in the presence of a normally lethal concentration of bromoacetate. Eight genes encode putative transporters or transmembrane proteins, while one encodes the enzyme UDP-N-acetylglucosamine enolpyruvoyl transferase (MurA), which is irreversibly inactivated by bromoacetate via alkylation of a critical active-site cysteine. Also 63 strains were found by the authors to be susceptible to bromoacetate. One hypersensitive bacterium lacks yliJ, a gene encoding a glutathione transferase.
The techniques described allows to predict the resistance to specific antibiotics, identify the resistance mechanisms and may enable researchers to reverse the resistance to antibiotics.
Assessing the hygromycyn bacterial resistance [3]
Stogios and colleagues 2010 write that the aminoglycoside phosphotransferase APH(4)-Ia is one of two enzymes responsible for bacterial resistance to hygromycin B (hygB). The authors studied the crystal structure of APH(4)-Ia enzyme. The enzyme was found to form an hydrogen bond network with hygB primarily through polar and acidic side chain groups, and binding affinity is spread across a distributed network. The APH(4)-Ia enzyme contains a cluster of hydrophobic residues which interact with hygromycin, and similar to APH(2″) utilize either ATP or GTP for phosphoryl transfer, this pathway may be used to tailor new aminoglycoside antibiotics or inhibitors of this enzyme suggest the authors.
CmeG gene is linked to resistance to antimicrobials and oxidative defence [4]
Campylobacter jejuni presets rising resistance to antimicrobials. Jeon and colleagues studied the cmeG (Cj1375) gene in Campylobacter jejuni which encodes a putative efflux transporter. The authors report that overexpression of the cmeGH operon in Campylobacter jejuni significantly increased its resistance to fluoroquinolones. The authors concluded that CmeG gene is a multidrug efflux transporter involved in antibiotic resistance and oxidative defence of Campylobacter.
Peptide antibiotic bacterial resistance of Bacillus subtilis [5]
Staron, Finkeisen Mascher 2010 describe three peptide antibiotic sensing and detoxification modules in Bacillus subtilis consist of two-component system which induces the expression of an ABC transporter which removes the antibiotic from the bacterial cell wall resulting in resistance of the cell:
BceRS-AB responds to bacitracin, plectasin, mersacidin and actagardine. YxdJK-LM is induced by a cationic antimicrobial peptide, LL-37. The PsdRS-AB system primarily responds to lipid II-binding lantibiotics, such as nisin and gallidermin.
The authors suggest the PbceA and PpsdA promoters as novel whole cell biosensors for high-throughput screening.
Pan-resistant NDM1 bacteria [6]
NDM1 is an enzyme that confers resistance to one of the most potent classes of antibiotics, known as carbapenems. It is found in many different types of bacteria and one in 10 of these strains is resistant to all known antibiotics. For the moment there is no new antimicrobial being developed.
The NDM enzyme genes that The NDM1 gene set has been found in Escherichia coli and can move easily from other bacteria.
The WHO in its 2000 report Overcoming antimicrobial resistance called the rise of antimicrobial resistance a global crisis. In 2001 the organization released a global strategy and campaign which should be updated and rejuvenated. Of concern is selling for human use antibiotics over the counter in Asia,Africa Central and South America. Also of high concern is the use of antibiotics as growth promoters in animal feed and bee-hives.
WHO calls on the responsibility of governments to regulate these isues, such as happened in the European Union where the use of antimicrobial growth promotion in livestock was banned.
Postgenomic strategies profit from foregoing activities of antibacterial drug development [7]
Brötz-Oesterhelt and Sasss 2010 stress that any use of antibiotics triggers bacterial resistance to the drug due to their short reproduction time leading to mutations and the exchange of genetic material with other strains. The authors call, therefore, for proper hygiene, skilful and restricted use of antibiotic treatment.
The classical strategy discovered all currently used antibiotic classes by screening natural product extracts or synthetic compounds for their antibacterial activity.
New genetic discoveries initiated a ”genomic” strategy replaced the classical strategy. However, research focused on synthetic quinolones class and synthetic low molecular weight compounds and bacterial genomic information faced a fruitless time. The High-Throughput Screening (HTS) strategy failed to produce significant results.
The postgenomic strategy now uses knowledge and libraries of foregoing researches and focuses on screening for new or underexploited natural products and structure-based drug design. Efforts to avoid bacterial resistance to antimicrobials should be further supported by alternative treatment options together with anti-virulence strategies and immunotherapeutic approaches
Alternatives to the emergence of carbapenemases in Enterobacter [8]
Looking for alternatives to the emergence of carbapenemases in Enterobacteriaceae Livermore and colleagues 2010 found that ACHN-490, a sisomicin derivative evades all plasmid-mediated aminoglycoside-modifying enzymes. Carbapenem-resistant isolates are sensitive to ACHN-490, except those strains containing 16S rRNA methylases. Apramacin evades 16S rRNA methylases and is being suggested by the authors as a starting point for future aminoglycoside development.
Cervimycin C resistance in Bacillus subtilis described [9]
Krügel and colleagues 2010 report two mutations in the intergenic region preceding the ABC transporter gene bmrA in cervimycin C-resistant clones of Bacillus subtilis, The authors stress that the cumulative of these two mutations are responsible for ABC transporter confers antibiotic resistance by the cumulative effects of two mutations in the promoter region.
Mathematical model of drug resistance predicts variation in population of pathogen bacteria [10]
Variation in the population of antibiotic non-resistant/ resistant organisms such as methicillin-resistant staphylococcus aureus can be predicted by a mathematical model developed by Friedman and colleagues 2010. The model predicts that antibacterial drugs initially decrease the load of the non-resistant bacteria, reaching a low level after 6 weeks. The load of drug-resistant bacteria will also decrease at first but rise again to a high level later on. This level can be reduced with increasing drug dosis or decreased contact between health care workers and patients says the authors.
[1] Spízek J, Novotná J, Rezanka T, Demain AL: Do we need new antibiotics? The search for new targets and new compounds. J Ind Microbiol Biotechnol. 2010 Dec;37(12):1241-1248.
http://www.ncbi.nlm.nih.gov/pubmed/21086099
[2] K. K. Desai, B. G. Miller. Recruitment of genes and enzymes conferring resistance to the nonnatural toxin bromoacetate. Proceedings of the National Academy of Sciences, 2010; DOI: 10.1073/pnas.1007559107
http://www.pnas.org/content/early/2010/09/29/1007559107
[3] Stogios PJ, Shakya T, Evdokimova E, Savchenko A, Wright GD.Structure and function of APH(4)-IA, a hygromycin B resistance enzyme. J Biol Chem. 2010 Nov 17.
http://www.jbc.org/content/early/2010/11/17/jbc.M110.194266.long
[4] Jeon B, Wang Y, Hao H, Barton YW, Zhang Q: Contribution of CmeG to antibiotic and oxidative stress resistance in Campylobacter jejuni. J Antimicrob Chemother. 2010 Nov 17.
http://www.ncbi.nlm.nih.gov/pubmed/21081547
[5] Staron A, Finkeisen DE, Mascher T: Peptide antibiotic sensing and detoxification modules of Bacillus subtilis. Antimicrob Agents Chemother. 2010 Nov 15.
http://www.ncbi.nlm.nih.gov/pubmed/21078927
[6] Conly J: Antimicrobial resistance: revisiting the “tragedy of the commons”. Bull World Health Organ. 2010 November 1; 88(11): 805–806. Doi: 10.2471/BLT.10.031110.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2971513/?tool=pubmed
[7] Brötz-Oesterhelt H, Sasss P: Postgenomic strategies in antibacterial drug discovery. Future Microbiology, October 2010, Vol. 5, No. 10, Pages 1553-1579 , DOI 10.2217/fmb.10.119
http://www.futuremedicine.com/doi/full/10.2217/fmb.10.119
[8] Livermore DM, Mushtaq S, Warner M, Zhang JC, Maharjan S, Doumith M, Woodford N: Activity of aminoglycosides, including ACHN-490, against carbapenem-resistant Enterobacteriaceae isolates. J Antimicrob Chemother. 2010 Nov 14..
http://www.ncbi.nlm.nih.gov/pubmed/21078604
[9] Krügel H, Licht A, Biedermann G, Petzold A, Lassak J, Hupfer Y, Schlott B, Hertweck C, Platzer M, Brantl S, Saluz HP: Cervimycin C resistance in Bacillus subtilis is due to a promoter up-mutation and increased mRNA stability of the constitutive ABC-transporter gene bmrA. FEMS Microbiol Lett. 2010 Dec;313(2):155-163. doi: 10.1111/j.1574-6968.2010.02143.x.
http://www.ncbi.nlm.nih.gov/pubmed/21077936
[10] Friedman A, Ziyadi N, Boushaba K: A model of drug resistance with infection by health care workers. Math Biosci Eng. 2010 Oct;7(4):779-92. doi: 10.3934/mbe.2010.7.779.
http://www.ncbi.nlm.nih.gov/pubmed/21077707
21.11.2010: Mathematical approach to test how hot chilli peppers are [1]
Capsaicinoids are the spicy compounds of chilli peppers. These compounds act on pain receptors in the mouth and throat, producing a burning sensation in the tissue and triggers increases in heart rate and perspiration, as well as the release of endorphins . They can be analysed using liquid chromatography. To reduce costs of such chemical analysis Kennet Bush and colleagues 2010 developed a multivariate regression analysis which is a mathematical approach comparing unknown pepper with spectral data of known plant types and predicts the hot taste of the unknown pepper. Such test will be valuable for food quality monitoring.
Clinical properties of capsinoids of CH-19 sweet pepper are comparable to hot chilli pepper [2]
Luo, Peng and Li 2010 write that capsaicinoids of hot chilli peppers consist of capsaicin, dihydrocapsaicin, nordihydrocapsaicin, homodihydrocapsaicin, and homocapsaicin, and others. Capsaicinoids are looked at for pain relief, cancer prevention, weight loss, display benefits on cardiovascular and gastrointestinal system, and act as agonists of capsaicin receptor or transient receptor potential vanilloid subfamily member 1 (TRPV1).
TRPV1 is a nonselective cation channel that may be activated by a wide variety of exogenous and endogenous physical and chemical stimuli. The best-known activators of TRPV1 are heat greater than 43°C and capsaicin, the pungent compound in hot chilli peppers. The activation of TRPV1 leads to painful, burning sensation. Its endogenous activators include: low pH (acidic conditions), the endocannabinoid anandamide, N-arachidonoyl-dopamine. TRPV1 receptors are found mainly in the nociceptive neurons of the peripheral nervous system, but they have also been described in many other tissues, including the central nervous system. TRPV1 is involved in the transmission and modulation of pain (nociception), as well as the integration of diverse painful stimuli. [3]
Capsinoids: Luo and colleagues stress that capsinoids from CH-19 sweet peppers present similar structure with capsaicinoids and consist of capsiate, dihydrocapsiate, and nordihydrocapsiate and others. They are less pungent and less toxic than capsaicinoids and present the same cancer prevention and weight loss properties of capsicinoids.
Naga chilli, the hottest chilli in the world [4]
Naga chilli or Bhoot Jolokia (Capsicum chinense Jacq.) of the northeast region of India is the hottest chilli in the world. Meghvansi and colleagues in a review stresses the potential of capsaicinoids in various ethnopharmacological applications such as pain therapy, body temperature regulation, anti-obesity treatments, anticancer therapy and as antioxidant and antimicrobial agent, where scientific researchis needed to close the gap between traditional medicinal knowledge and modern medicine.
Liu and Nair 2010 found capsaicin (C) and dihydrocapsaicin (DHC) in Bhut Jolokia (Capsicum chinense Jacq.) to be 5.36% and was about 338 and 18 times greater than hot peppers Jalapeno (Capsicum annuum) and Scotch Bonnet (Capsicum chinense). The authors also determined lipid peroxidation and cyclooxygenase (COX-1 and -2) enzymes inhibitory concentrations. [5]
Analysis of capsaicin and dihydrocapsaicin [6]
Peña-Alvarez, Ramírez-Maya,, Alvarado-Suárez describe the analysis of capsaicin and dihydrocapsaicin in peppers and pepper sauces by solid phase microextraction-gas chromatography-mass spectrometry.
Pungency of chilli pepper is a response to microbes [7]
Tewksbury and colleagues 2008 suggest that the pungency in chillies may be an adaptive response to a microbial pathogen. The authors report that geographic variation in the production of capsaicinoids of chilli pepper Capsicum chacoense was directly linked to the damage caused by a Fusarium fungus to the seeds of the chilli pepper. The authors concluded that capsaicinoids protect chilli seeds from the fungus and insects which feed on the seeds and facilitates the entry of Fusarium mould in the seeds, the primary cause of predispersal chilli seed mortality.
[1] Testing Chilli Peppers: Chemists Heat Things Up with New Model to Determine Heat of a Pepper. 01.01.2010.
http://www.aip.org/dbis/stories/2010/20006.html
[2] Luo XJ, Peng J, Li YJ: Recent advances in the study on capsaicinoids and capsinoids. Eur J Pharmacol. 2010 Oct 12. J Ethnopharmacol. 2010 Oct 28;132(1):1-14. Epub 2010 Aug 20.
http://www.ncbi.nlm.nih.gov/pubmed/20946891
[3] Wikipedia: TRPV1
http://en.wikipedia.org/wiki/Capsaicin_receptor
[4] Meghvansi MK, Siddiqui S, Khan MH, Gupta VK, Vairale MG, Gogoi HK, Singh L: Naga chilli: a potential source of capsaicinoids with broad-spectrum ethnopharmacological applications. J Ethnopharmacol. 2010 Oct 28;132(1):1-14
http://www.ncbi.nlm.nih.gov/pubmed/20728519
[5] Liu Y, Nair MG: Capsaicinoids in the hottest pepper Bhut Jolokia and its antioxidant and antiinflammatory activities. Nat Prod Commun. 2010 Jan;5(1):91-4.
http://www.ncbi.nlm.nih.gov/pubmed/20184029
[6] Peña-Alvarez A, Ramírez-Maya E, Alvarado-Suárez LA. Analysis of capsaicin and dihydrocapsaicin in peppers and pepper sauces by solid phase microextraction-gas chromatography-mass spectrometry. J Chromatogr A. 2009 Apr 3;1216(14):2843-7. Epub 2008 Oct 18.
http://www.ncbi.nlm.nih.gov/pubmed/19100557
[7] Tewksbury JJ, Reagan KM, Machnicki NJ, Carlo TA, Haak DC, Peñaloza AL, Levey DJ: Evolutionary ecology of pungency in wild chillies. Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):11808-11. Epub 2008 Aug 11.
http://www.ncbi.nlm.nih.gov/pubmed/18695236
17.11.2010: Increased Pacific oyster mortality reported in France, United Kingdom and Republic of Ireland [1]
The European Food Safety Authority EFSA studied the causes of the increased Pacific oyster (Crassostrea gigas) mortality reported in France, United Kingdom and Republic of Ireland 2008-2009, with special focus on Ostreid Herpesvirus-1(OsHV-1) µvar), as well as environmental factors.
The Animal Health and Welfare (AHAW) panel found that OSHV-1 infection is a necessary cause but may not be sufficient by itself as other factors appear to be important. The role of other pathogenic agents such as Vibrio spp. has not yet been resolved.
Climatic and seasonal factors alone are not likely to be a sufficient cause for the increased Pacific oyster mortality although these events are seasonal in their occurrence. An increase or a sudden change in the temperature of the water around oysters has been shown to be an important risk factor predisposing for the disease. Up to now no outbreaks have been reported when the water temperature is below 16ºC. Husbandry practices such as introduction of non certified possibly infected spat, movements and mixing of populations and age groups are probably important risk factors.
Events of increased mortality have been only observed in Pacific oyster. In addition to C. gigas, there is evidence of susceptibility to OsHV-1 in Ostrea edulis, Pecten maximus and Ruditapes philippinarum. There was no investigation on susceptibility to OsHV-1 µvar made on other mollusc species other than C. gigas.
OsHV-1 (reference strain and µvar) was detected by PCR in Pacific oyster older than 18 months associated with increased mortality. Therefore it is concluded that oysters older than 18 months can be a source of virus and it is not safe to transfer oysters older than 18 months from affected areas to areas not affected by increased mortality events.
The Panel calls for a description of the Pacific oyster aquaculture industry in Europe namely regarding number of farms, production figures, and traceability on movements/transfers both on hatchery and grow out sites should be achieved in accordance to the requirements by Council Directive 2006/88/EC. [2]
There is also a need to establish the health status of oyster spat at source. An assessment of the health status should include results of regular batch laboratory testing (at least in regards to OsHV-1, ref strain and µvar, Vibrio species, and histopathological examination) and epidemiological assessment. Improved diagnostic methods should be developed to check for the presence of OsHV-1 µvar and other strains.
[1] Scientific Opinion on the increased mortality events in Pacific oysters, Crassostrea gigas. EFSA European Food Safety Authority. Question number: EFSA-Q-2010-00011 . 27 October 2010.
http://www.efsa.europa.eu/en/scdocs/scdoc/1894.htm?WT.mc_id=EFSAHL01&emt=1
[2] Council Directive 2006/88/EC of 24 October 2006 on animal health requirements for aquaculture animals and products thereof, and on the prevention and control of certain diseases in aquatic animals.
http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2006:328:0014:0056:EN:PDF
16.11.2010: EFSA guidance on environmental impact of GM plants [1]
The European Food Safety Authority (EFSA) has published updated guidance for the environmental risk assessment (ERA) of Genetically Modified (GM) plants focused in particular on data generation, collection and analysis and the evaluation of possible long-term effects of GM plants and potential effects on non-target organisms, such as those insects which are not meant to be the target of the toxin produced by some GM plants.
The Guidance covers persistence and invasiveness of the GM plant, possible gene transfer from the plant to micro-organisms, how the GM plant could affect cultivation, management and harvesting techniques, and effects on human and animal health.
In order to assess the safety of a GM plant EFSA requires all applicants to follow its guidance documents which specify the type of data and information that should be submitted. Seven specific areas were reviewed which include the persistence and invasiveness of the GM plant, considering the possible plant-to-plant gene transfer; the likelihood and consequences of gene transfer from the plant to micro-organisms; the potential evolution of resistance in target organisms; the potential effects on non-target organisms; the biogeochemical processes, such as changes in soil composition, and the potential impact of the cultivation, management and harvesting techniques of the GM plant.
The guidance document includes detailed requirements for: the choice of appropriate non-GM comparators with which the GM plant is compared during the safety evaluation. Also types of receiving environments have to be considered; long-term effects and the experimental design of laboratory and field studies; and their statistical analysis are defined in guidance.
Amendment of Directive 2001/18/EC liberalising GMO cultivation in Europe [2]
In July 2010, the Commission adopted a proposal which amends Directive 2001/18/EC, giving members states the freedom to allow, restrict or ban cultivation of GMO on their territory. The proposal, has to go through a co-decision process, however the plan is being disapproved by anti-GMO states and also pro-GMO states alleging fragmentation within the single market, and being incompatible with rules set by the WTO.
[1] Scientific Opinion: Guidance on the environmental risk assessment of genetically modified plants EFSA Panel on Genetically Modified Organisms (GMO) European Food Safety Authority (EFSA), Parma, Italy
http://www.efsa.europa.eu/en/scdocs/doc/1879.pdf
[2] GMOs: Member States to be given full responsibility on cultivation in their territories.
http://europa.eu/rapid/pressReleasesAction.do?reference=IP/10/921
14.11.2010: Rising temperatures will decrease Asian rice production [1][1]
Rice is a staple food for three billion people, many are undernourished. A study predicts that the net impact of rising global temperatures will cause a net reduction of the production of rice in Asia. Yield growth rate already sunk by 10-20 percent in several locations during the last 25 years, according to a study of Welch and colleagues. In this study, published in 2010, a multiple regression model was used to monitor temperature and radiation during both the vegetative and ripening phases.
The authors report that if the minimum temperature rises and nights get hotter, yield will fall, whereas higher maximum temperature will raise it, however, yield also falls if maximum temperatures rises further. Overall, a net negative impact on yield from moderate warming in coming decades is to be expected. This scenario will worsen as temperatures rise further towards the middle of the century.
Energy strategies based on carbon fuels should be avoided. Biofuels produced by plantations of palm oil, soy, canola, sugar cane should not be developed any further as they compete with food plantations. Safety of food supply is being questioned. Alternative energies, such as solar energy, wind turbines and the production of hydrogen as energy storage and as clean fuel should become a global strategy to avoid further increase of temperatures, and to secure arable fields for the production of food.
Rice is a staple food for three billion people, many are undernourished. A study predicts that the net impact of rising global temperatures will cause a net reduction of the production of rice in Asia. Yield growth rate already sunk by 10-20 percent in several locations during the last 25 years, according to a study of Welch and colleagues. In this study, published in 2010, a multiple regression model was used to monitor temperature and radiation during both the vegetative and ripening phases.
The authors report that if the minimum temperature rises and nights get hotter, yield will fall, whereas higher maximum temperature will raise it, however, yield also falls if maximum temperatures rises further. Overall, a net negative impact on yield from moderate warming in coming decades is to be expected. This scenario will worsen as temperatures rise further towards the middle of the century.
Energy strategies based on carbon fuels should be avoided. Biofuels produced by plantations of palm oil, soy, canola, sugar cane should not be developed any further as they compete with food plantations. Safety of food supply is being questioned. Alternative energies, such as solar energy, wind turbines and the production of hydrogen as energy storage and as clean fuel should become a global strategy to avoid further increase of temperatures, and to secure arable fields for the production of food.
[1] Welch JR, Vincent JR, Auffhammer M, Moya PF, Dobermann A, Dawe D: Rice yields in tropical/subtropical Asia exhibit large but opposing sensitivities to minimum and maximum temperatures. Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14562-7. Epub 2010 Aug 9
http://www.ncbi.nlm.nih.gov/pubmed/20696908
14.11.2010: Sulforaphane, the powerful cancer-fighting agent in broccoli [1]
Sulforaphane is a chemopreventive phytochemical. It is found in broccoli and to a lesser extent in other cruciferous vegetables.
Sulforaphane can be released from its parent compound glucoraphanin by bacteria in the lower gut and absorbed into the body. This increases broccoli's cancer-preventive power according to a study of Jeffery, Miller and Lai 2010. Overcooking broccoli destroys the plant enzyme which turn sulforaphane free. In this study the authors demonstrated that microbiota in our digestive tract can turn glucoraphanin into sulforaphane. Three to five servings a week is enough to have an anti-cancer effect.
Sulforaphane also has anti-inflammatory properties, responsible to chronic diseases associated with obesity and ageing.
To boost heath effects of broccoli the authors suggest to feed the desirable bacteria with prebiotics like fiber, or combine broccoli with a yogurt sauce that contains the hydrolyzing bacteria.
Inflamatory pathway NF- kappaB [2]
Prasad and colleagues 20101 stress that lifestyle risk factors such as tobacco, alcohol, high-fat diet, radiation, and infections increase risk of cancer. Lifestyle risk factors have been found to activate NF- kappaB and NF- kappaB-regulated genes, mediating inflammation and tumor cells.
Diet consisting of fruits and vegetables spices and nuts, rich in flavones, flavanones, flavonols, isoflavones, anthocyanins, and chalcones can prevent cancer can suppress the proinflammatory cell signaling pathways of cancer.
Neuroprotective activity of antioxidant nutraceuticals [3]
Natural neuroprotective antioxidant compounds directly scavenge free radicals or increase endogenous cellular antioxidant defenses, such as the nuclear factor erythroid-derived 2-related factor 2 (Nrf2) transcription factor pathway, modulation of signal transduction cascades or effects on gene expression. Kelsey and colleagues 2010 cites such neuroprotective antioxidants.
According to Greco and Fiskum 2010 oxidative stress promotes Ca(2+)-dependent opening of the mitochondrial inner membrane permeability transition pore (PTP). This causes bioenergetic failure and subsequent cell death. To avoid such oxidative stress the activation of the Nrf2/ARE pathway of antioxidant gene expression by sulforaphane was found to confers resistance of brain mitochondria to redox-regulated PTP opening. [4]
Sharma and colleagues 2010 stresses the downregulation of Bcl-2, COX-2 and IL-1β upon treatment with sulforaphane, explaining the anti-proliferative, anti-inflammatory, anti-oxidant and anti-cancer activities od sulforaphane. [5]
Kalpana and colleagues 2010 found sulforaphane to be very successful in combating the oxidative stress mediated mitochondrial dysfunction in experimental lung carcinogenesis induced by benzo(a)pyrene.[6]
Bladder cancer induced by tobacco smoke [7]
A human bladder carcinogen present on tobacco smoke is 4-aminobiphenyl (ABP). Ding and colleagues 2010 demonstrated that sulforaphane inhibits ABP-induced DNA damage in bladder cells. Dings and colleagues 2010 write that sulforaphane activates NF-E2 related factor-2 (Nrf2), which is kown as a chemopreventive target and activates the Nrf2-regulated cytoprotective signaling pathway.
The authors also report that sulforaphane-enriched broccoli sprout extracts strongly inhibits N-butyl-N-(4-hydroxybutyl)nitrosamine-induced bladder cancer development, supporting epidemiologic observation that consumption of broccoli is inversely associated with bladder cancer risk and mortality.
Chronic inflammation, a major mediator of tumor [8]
Gupta and colleagues 2010 write that as 35% of all cancers can be prevented by dietary changes. The study focuses on nutraceuticals, such as allicin, apigenin, berberine, butein, caffeic acid, capsaicin, catechin gallate, celastrol, curcumin, epigallocatechin gallate, fisetin, flavopiridol, gambogic acid, genistein, plumbagin, quercetin, resveratrol, sanguinarine, silibinin, sulforaphane, taxol, gamma-tocotrienol, and zerumbone, derived from spices, legumes, fruits, nuts, and vegetables. They reduce the risk of cancer modulating inflammatory pathways and thus affect the survival, proliferation, invasion, angiogenesis, and metastasis of the tumor.
The chemopreventive activity of broccoli may be higher than found by animal studies [9]
Abdull Razis and colleagues 2010 studied the ability of the stereoisomers R- and S-sulforaphane to modulate the cell enzyme systems. They found that R-sulforaphane elevated glutathione S-transferase (GSTα, GSTμ) and quinone reductase in liver and in lung, in comparision S-sulforaphane presented lower effect or even no effect at all. The authors concluded that R-sulforaphane was the more active isomer of both. Animal studies using S-sulforaphane present results which are too low for human diet which provides mainly the high active R- racemic form.
[1] Lai R-H, Miller MJ, Jeffery E: Glucoraphanin hydrolysis by microbiota in the rat cecum results in sulforaphane absorption. Food & Function, 2010; 1, 161-166. Doi: 10.1039/C0FO00110D
http://pubs.rsc.org/en/Content/ArticleLanding/2010/FO/c0fo00110d
[2] Prasad S, Phromnoi K, Yadav VR, Chaturvedi MM, Aggarwal BB: Targeting inflammatory pathways by flavonoids for prevention and treatment of cancer. Planta Med. 2010 Aug;76(11):1044-63. Epub 2010 Jul 15.
http://www.ncbi.nlm.nih.gov/pubmed/20635307
[3] Kelsey NA, Wilkins HM, Linseman DA: Nutraceutical antioxidants as novel neuroprotective agents. Molecules. 2010 Nov 3;15(11):7792-814.
http://www.ncbi.nlm.nih.gov/pubmed/21060289
[4] Greco T, Fiskum G: Brain mitochondria from rats treated with sulforaphane are resistant to redox-regulated permeability transition. J Bioenerg Biomembr. 2010 Nov 9.
http://www.ncbi.nlm.nih.gov/pubmed/21061051
[5] Sharma C, Sadrieh L, Priyani A, Ahmed M, Hassan AH, Hussain A: Anti-carcinogenic effects of sulforaphane in association with its apoptosis-inducing and anti-inflammatory properties in human cervical cancer cells. Cancer Epidemiol. 2010 Oct 16.
http://www.ncbi.nlm.nih.gov/pubmed/20956097
[6] Kalpana Deepa Priya D, Gayathri R, Gunassekaran GR, Sakthisekaran D: Protective role of sulforaphane against oxidative stress mediated mitochondrial dysfunction induced by benzo(a)pyrene in female Swiss albino mice. Pulm Pharmacol Ther. 2010 Sep 15.
http://www.ncbi.nlm.nih.gov/pubmed/20833254
[7] Ding Y, Paonessa JD, Randall KL, Argoti D, Chen L, Vouros P, Zhang Y: Sulforaphane inhibits 4-aminobiphenyl-induced DNA damage in bladder cells and tissues. Carcinogenesis. 2010 Nov;31(11):1999-2003.
http://www.ncbi.nlm.nih.gov/pubmed/20810543
[8] Gupta SC, Kim JH, Prasad S, Aggarwal BB: Regulation of survival, proliferation, invasion, angiogenesis, and metastasis of tumor cells through modulation of inflammatory pathways by nutraceuticals. Cancer Metastasis Rev. 2010 Sep;29(3):405-34.
http://www.ncbi.nlm.nih.gov/pubmed/20737283
[9] Abdull Razis AF, Iori R, Ioannides C: The natural chemopreventive phytochemical R-sulforaphane is a far more potent inducer of the carcinogen-detoxifying enzyme systems in rat liver and lung than the S-isomer. Int J Cancer. 2010 Aug 19.
http://www.ncbi.nlm.nih.gov/pubmed/20726001
12.11.2010: Ocean fertilisation with iron may stimulate toxic algae [1]
Mary Silver and colleagues warn that the addition of iron to sea waters can stimulate rapid growth of diatoms in the genus Pseudo-nitschia. This alga produces domoic acid, a neurotoxin which can enter the food chain leading to closure of fisheries. domoic acid poisons marine mammals and birds that feed on contaminated fish.
Iron fertilization of the oceans has been suggested as way to reduce atmospheric concentrations of carbon dioxide and thereby combat global warming. The authors stress that the findings urge to redouble the efforts to reduce carbon emissions instead of changing the biology of the sea.
Other scientists involved in foregoing studies were Ken Bruland and Coale. They analysed old samples collected during iron-enrichment experiments conducted in 1995 and 2002, noting that domoic acid was not broken down in samples stored for years.
Natural iron input due to dust brought in by sandstorms, or melting glacier ice bearing trapped iron are short timed events limited to restricted areas. Now the idea of ocean fertilisation is being locked by a UN moratorium on the practice stating that the potential dangers outweigh the benefits.
In 1958, domoic acid was originally isolated from the red alga called "doumoi" (Chondria armata) in Japan. "Doumoi" is used as an anthelmintic in Tokunoshima, Kagoshima.[citation needed] Domoic acid is also produced by diatoms of the genus Pseudo-nitzschia and the species Nitzschia navis-varingica. [2]
Iron fertilization studies: [2]
Ironex II, 1995
SOIREE (Southern Ocean Iron Release Experiment), 1999
EisenEx (Iron Experiment), 2000
SEEDS (Subarctic Pacific Iron Experiment for Ecosystem Dynamics Study), 2001
SOFeX (Southern Ocean Iron Experiments - North & South), 2002
SERIES (Subarctic Ecosystem Response to Iron Enrichment Study), 2002
SEEDS-II, 2004
EIFEX (European Iron Fertilization Experiment), 2004
CROZEX (CROZet natural iron bloom and Export experiment), 2005
LOHAFEX (Indian and German Iron Fertilization Experiment), 2009
A number of scientists published a statement in Science in 2008 maintaining that it would be "premature to sell carbon offsets from the first generation of commercial-scale OIF experiments unless there is better demonstration that OIF effectively removes CO2, retains that carbon in the ocean for a quantifiable amount of time, and has acceptable and predictable environmental impacts."[3]
Street and Paytan 2007 were concerned about the efficacy and advisability of iron fertilization of the sea. They write that foregoing experiments resulted in only small carbon export fluxes to the depths necessary for long-term sequestration. Engineering the complex ocean system may also result in unpredictable response, the authors warn [4].
Commercial interests behind ocean fertilisation [5]
US companies, such as Climos and Planktos were hoping to profit by selling the carbon credits they would earn by triggering algal blooms but are having hard times to collect funds for their activities.[6]
A full-scale international plankton restoration program could regenerate approximately 3–5 billion tons of carbon sequestration capacity worth 75 billion Euro or more in carbon offset value.
The domoic acid of Pseudo-nitzschia is a "chelator", binding to iron to make more of it available to the algae. Easy access to this nutrient would allow algae to out-compete other species, says Silver.
The findings raise serious concern over the net benefit and sustainability of large-scale iron fertilizations concerning the coastal food webs. [7]
LOHAFEX southern ocean fertilisation fails to capture significant CO2 amounts [8]
Artificially fertilized with several million tons of iron oxide, the ocean could remove three and a half gigatons of carbon dioxide from the atmosphere. This amounts to an eighth of the yearly emissions created by burning oil, gas and coal. This strategy is controversial since environmentalists fear such geo-engineering could knock the ecosystem out of balance. For this reason, the UN Convention on Biological Diversity in May 2008 called for a moratorium on such plans, at least until further scientific results are available.
The researchers of India’s National Institute of Oceanography and the Alfred Wegener Institute for Polar and Marine Research in Germany on the Polarstern ship tried to stimulate a giant bloom of phytoplankton fertilising the Antarctic sea with10 tons of iron sulphate spread over 300 square kilometres. Tiny algae were to absorb carbon dioxide when they grow and sink to the bottom of the sea when dead.
The research, led by Wajih Naqvi and Victor Smetacek in 2009, created a bloom of phytoplankton but crustaceans called copepods gobbled the phytoplankton up so quickly that only a small amount of CO2 was dispatched to the ocean floor. The researchers say their experiment failed because foregoing natural blooms had depleted the area of silicic acid which is needed for shellmaking of diatoms protecting them from copepodes which feed on microalgae. Diatoms may, therefore, created great algal blooms and trap much CO2 from the atmosphere. During the experiment, however, the low of silicic acid and high of iron environment Phaeocystis, algae without an silica shell, developed. Copepodes could feed on this group of algae and thze bloom was timely limited. As a result iron fertilisation removed less CO2 from the atmosphere than initially calculated by the expedition.
Alternatives to carbon-based fuels avoid the emission of CO2
Solar energy, wind turbines geothermal power stations, tidal and wave energy, together with hydrogen technology can provide 100% of energy and fuel which is almost free of CO2 emission. It is the responsibility of governments and of the scientists which work as advisor, to work toward a global strategy for a sustainable carbon-free energies.
Read more
[1] Iron stimulates blooms of toxin-producing algae in open ocean, study finds
http://www.eurekalert.org/pub_releases/2010-11/uoc--isb110810.php
[2] Wikipedia: Iron fertilization
http://en.wikipedia.org/wiki/Iron_fertilization
[3] Buesseler, KO; Doney, SC; Karl, DM; Boyd, PW; Caldeira, K; Chai, F; Coale, KH; de Baar, HJ; Falkowski, PG; Johnson, KS; Lampitt, RS; Michaels, AF; Naqvi, SW; Smetacek, V; Takeda, S; and Watson, AJ (11 January, 2008) "Ocean Iron Fertilization--Moving Forward in a Sea of Uncertainty." Science, 319(5860):162. DOI:10.1126/science.1154305
http://www.sciencemag.org/cgi/content/summary/319/5860/162
[4] Street JH, Paytan A: Iron, phytoplankton growth, and the carbon cycle. Met Ions Biol Syst. 2005;43:153-93.
http://www.ncbi.nlm.nih.gov/pubmed/16370118
[5] Ocean seeding fails the acid test. NewScientist.12 June 2008
http://www.science.org.au/nova/newscientist/106ns_009.htm
[6] Venture to Use Sea to Fight Warming Runs Out of Cash. New York Times Febraury 14, 2008.
http://www.nytimes.com/2008/02/14/technology/14planktos.html?_r=1
[7] Trick CG, Bill BD, Cochlan WP, Wells ML, Trainer VL, Pickell LD: Iron enrichment stimulates toxic diatom production in high-nitrate, low-chlorophyll areas. Proc Natl Acad Sci U S A. 2010 Mar 30;107(13):5887-92.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851856/?tool=pubmed
[8] Who ate all the algae? Using phytoplankton to trap carbon dioxide faces a snag. The Economist. 26 March 2009.
http://www.economist.com/node/13361464?story_id=13361464
12.11.2010: Pesticides and agricultural chemicals, manganese copper and lead may increase risk of Parkinson Disease [1]
Exposure to pesticides and agricultural chemicals in rural areas was reported to trigger Parkinson Disease. Willis and colleagues 2010 in a new study, analysed the environmental risk factors in urban areas. They found that manganese and copper emissions may be some of the triggers of the disease in susceptible individuals. Data from 1988 to 1998 of the Toxic Release Inventory of the Environmental Protection Agency were used. No strong correlation between industrial lead output and the incidence of Parkinson Disease was found. This, however, may be due to other sources, such as lead paint, lead in the water, or other sources.
The authors suggest that all these environmental contaminants may have a neurotoxic effect in the same area of the brain affected in Parkinson Disease, interfering with the ability to eliminate toxic radicals. The metals may also induce or accelerate the formation of protein clumps during neurodegeneration.
The authors concluded that urban Parkinson Disease incidence is greater in counties with high reported industrial release of copper or manganese. Environmental exposure to metals may increase risk of Parkinson Disease in urban areas. However, research should concentrate on overall metal pollution levels rather than focusing on any particular industry.
[1] Willis AW, Evanoff BA, Lian M, Galarza A, Wegrzyn A, Schootman M, Racette BA: Metal Emissions and Urban Incident Parkinson Disease: A Community Health Study of Medicare Beneficiaries by Using Geographic Information Systems. Am J Epidemiol. 2010 Oct 19.
http://www.ncbi.nlm.nih.gov/pubmed/20959505
09.11.2010: Greaseproofing chemicals used in wrapping materials and popcorn bags are source of contaminants in food [1]
D'eon and Mabury 2010 write that polyfluoroalkyl phosphate esters (PAPs) are chemicals used in food wrappers and microwave popcorn bags. These chemicals migrate to the food and digestion breaks them down forming perfluorinated carboxylic acids (PFCAs), such as perfluorooctanoic acid (PFOA). PAPs are found in kitchen pans, clothing and food packagings like pop-corn bags, used as greaseproofing agents. In this study the authors demonstrated that PAPs are the major source of human PFCA exposure, resulting from food contact applications. Findings of PFOS in the environment should not divert the attention from packaging material as an important source of these contaminants, say the authors.
In this study data of PAP concentrations in human blood, together with the PAP and PFCA data from experiments with rats were used to calculate human PFOA exposure from PAP metabolism.
As a reaction to the results of latest studies, the government of Canada, the United States and Europe begin monitoring programs for these chemicals and their use in packaging materials.
Perfluorinated compounds in environment, biota and humans [2]
Perfluorinated compounds such as perfluorooctane sulfonate (PFOS) and perfluorooctane acid (PFOA) are environmental pollutants of global importance. Suja, Pramanik and Zain 2009 describe distribution, bioaccumulation and toxic effects of PFOS and PFOA in the tap and surface water. PFOS and PFOA were detected globally in the tissues of fish, bird and marine mammals and humans, demonstrating a global bioaccumulation in the ecosystem. The authors write that atmospheric transport of these compounds might explain the worldwide distribution of these compounds.
[1] D'eon JC, Mabury SA: Exploring Indirect Sources of Human Exposure to Perfluoroalkyl Carboxylates (PFCAs): Evaluating Uptake, Elimination and Biotransformation of Polyfluoroalkyl Phosphate Esters (PAPs) in the Rat. Environmental Health Perspectives, 2010; DOI: 10.1289/ehp.1002409
http://ehp03.niehs.nih.gov/article/info%3Adoi%2F10.1289%2Fehp.1002409
[2] Suja F, Pramanik BK, Zain SM: Contamination, bioaccumulation and toxic effects of perfluorinated chemicals (PFCs) in the water environment: a review paper. Water Sci Technol. 2009;60(6):1533-44.
http://www.ncbi.nlm.nih.gov/pubmed/19759456
09.11.2010: Docosahexaenoic acid (DHA) improves cognition in age-related cognitive decline (ARCD) and reduces the risk of Alzheimer disease [1]
The "Memory Improvement with Docosahexaenoic Acid Study" (MIDAS) by Yurko-Mauro and colleagues 2010 says that 6 month supplementation with 900 mg/d docosahexaenoic acid (DHA) may improve memory and learning in older adults with mild cognitive impairments.
The authors say that low DHA levels are associated with cognitive decline in healthy elderly and Alzheimer's patients, high DHA levels help reduce the risk of Alzheimer's disease. The MIDAS study focused on a population of healthy adults with age-associated memory impairment.
No benefit of DHA, however, in patients previously diagnosed with Alzheimer's disease [2]
Quinn and colleagues found in a study published in 2010 that DHA did not caused significant benefit on cognitive function in patients previously diagnosed with Alzheimer's disease. The authors stress that their results should not be applied to groups where DHA is administered before the disease apparent.
DHA supplements, and other dietary supplements should be taken over time and before a disease becomes notorius. Heathy nutritional habits should include a well-balanced diet, regular physical activity and dietary supplements may slow down ageing impairments, such as age-associated memory impairment.
[1] Karin Yurko-Mauro, Deanna McCarthy, Dror Rom, Edward B. Nelson, Alan S. Ryan, Andrew Blackwell, Norman Salem Jr., Mary Stedman. Beneficial effects of docosahexaenoic acid on cognition in age-related cognitive decline. Alzheimer's and Dementia, 2010; 6 (6): 456 DOI: 10.1016/j.jalz.2010.01.013
http://www.alzheimersanddementia.com/article/S1552-5260%2810%2900040-3/abstract
[2] J. F. Quinn, R. Raman, R. G. Thomas, K. Yurko-Mauro, E. B. Nelson, C. Van Dyck, J. E. Galvin, J. Emond, C. R. Jack, M. Weiner, L. Shinto, P. S. Aisen. Docosahexaenoic Acid Supplementation and Cognitive Decline in Alzheimer Disease: A Randomized Trial. JAMA: The Journal of the American Medical Association, 2010; 304 (17): 1903 DOI: 10.1001/jama.2010.1510
http://jama.ama-assn.org/cgi/content/abstract/304/17/1903
08.11.2010: Mechanism of atherosclerosis caused by trans fats [1]
Chen and colleagues 2010 report that a diet rich in trans fats cause atherosclerosis by reducing the responsiveness of a protein, the transforming growth factor (TGF)-beta.
The authors found that the suppression of the responsiveness of TGF-beta in aortic endothelium and other tissues was caused by dietary trans fats, mediated by deposition of cholesterol into the cellular membranes in vascular tissue. This may also be the cause of other trans fat-related diseases and disorders, such as cancer and immunity.
In this study high trans fat diet increased the expression of VCAM-1, a marker of early lesions of atherosclerosis, reduced the expression of TGF-β type I and II receptors and decreased the levels of phosphorylated Smad2, important TGF-β response indicator. These markers returned to normal levels when diet was shifted to low trans fats.
The authors concluded that transforming growth factor (TGF)-beta protects against atherosclerosis.
[1] Chen CL, Tetri LH, Neuschwander-Tetri BA, Huang SS, Huang JS: A mechanism by which dietary trans fats cause atherosclerosis. J Nutr Biochem. 2010 Oct 30.
http://www.ncbi.nlm.nih.gov/pubmed/21036587
08.11.2010: Macrophage cells in fat tissue may explain the link between obesity and diabetes[1]
Wentworth and colleagues 2010 found that the presence of macrophage cells in fat tissue are closely related to insulin resistance in human obesity. Macrophage cells are special white blood cells which are produced by the bone marrow as a response to an infection.
In obese people, macrophages move into the fat tissue where they cause inflammation and release cytokines, Certain cytokines cause cells to become resistant to the effects of the hormone insulin, leading to diabetes and heart disease. The authors write that complications of obesity such as insulin resistance and diabetes, cardiovascular disease associated with hardening of the arteries, and liver problems are the result of the inflammation. Developing drugs which control the macrohage release of cytokines may reduce the risk of these diseases, say the authors.
The authors also report that weight reduction caused the macrophages in the fat tissue to disappear reducing the risk of developing insulin resistance and diabetes.
[1] Wentworth JM, Naselli G, Brown WA, Doyle L, Phipson B, Smyth GK, Wabitsch M, O'Brien PE, Harrison LC: Pro-Inflammatory CD11c+CD206+ Adipose Tissue Macrophages Are Associated With Insulin Resistance in Human Obesity. Diabetes, 2010; 59 (7): 1648 DOI: 10.2337/db09-0287
http://diabetes.diabetesjournals.org/content/59/7/1648
07.11.2010: Conjugated linoleic acid CLA, the cause of insulin resistance and fatty liver [1]
Conjugated linoleic acid (CLA), known as “trans-10, cis-12 CLA”, is found in partially hydrogenated vegetable oils and some dietary supplements. CLA is found to be related to non-alcoholic fatty liver disease causing diabetes and obesity.
Darshan S. Kelley and colleagues found that DHA (docosahexaenoic acid), and EPA (eicosapentaenoic acid) from fish oils may reduce the effects of CLA. Fish-oil, together with CLA supplements, prevented harmful side effects of CLA in animals.
DHA (docosahexaenoic acid), and EPA (eicosapentaenoic acid) occur in different amounts and ratios in fatty or oily fish and other sea food. The authors determined which one of these fatty acids is the active part of fish oils. They found that DHA protects against both CLA-induced insulin resistance and CLA-induced non-alcoholic fatty-liver disease. EPA offered only partial protection against CLA-induced fatty liver disease and no protection against insulin resistance.
Adinopectine hormone is associated with diabetes
Adinopectine is an hormone produced by fat cells. Low levels of this hormone is associated with insulin resistance, leading to diabetes. CLA depletes the adipose tissue where adiponectin is made. DHA can restore adipose tissue, and adiponectin levels may return to normal levels. This mechanism explains how DHA protects against insulin resistance, say the authors.
[1] Eat Fish! Nutrition Studies Zero In on Health Benefits. ARS October 5, 2010.
http://www.ars.usda.gov/is/AR/archive/oct10/nutrition1010.htm
07.11.2010: New Fish Feeds Made from Fish Byproducts [1]
Dong-Fang Deng and Peter Bechtel developed new fish feeds made of discarded fish portions, such as head, tail, bone, skin and internal organs. The researchers report that many of the Alaska fish parts, added to plant-protein-based feed, act on shrimps as feeding stimulants. The researchers are currently examining how to best use fish byproducts to develop practical feeds that are nutritionally balanced, cost effective and safe for the environment.
Many of the Alaska fish parts act as feeding stimulants that, as their name implies, stimulate fish to eat their rations. That occurred in studies with Pacific white shrimp that were fed plant-protein-based feeds to which fish-processing leftovers had been added.
The scientists say that from 2 million tons of wild-caught fish 1 million tons are undervalued leftovers which are ground, dried, and then sold as ingredients for products such as aquaculture feeds or pet foods
Valuable fish gelatin
Gelatin from the discarded skins of Alaskan pollock maybe used in medicine. Bor-Sen Chiou 2010 develops films made from fish gelatine and the bioplastic polylactic acid (PLA) which comes from fermented corn sugar.
The fish- and corn-derived films may be used to produce semi-synthetic tissue to speed repair of injured bone or cartilage and nanofibres of this material may act as matrix on which cultured human cells may replicate. This may be used as allergen-free transplants.
Alternative Fish Feeds for Aquaculture [2]
Aquaculture now supplies half of the seafood produced for human consumption, but are running short of fishmeal from small, bony fish species like menhaden, herring and capelin.
To satisfy these demands, Barrows and his colleagues at the ARS Small Grains and Potato Germplasm Research Unit in Hagerman, Idaho, are developing alternative fish feeds for trout, salmon, white sea bass and yellow tailmade from concentrated plant proteins. Protein levels in most grain and oilseed sources are low and need to be concentrated to reach the high protein requirements of fish. Combinations of alternative proteins, plus a fishmeal diet are being tested. Ingredients such as corn, gluten meal, and soy proteins are used to develop feeds that contain less fishmeal.
Various plant- and animal-based alternatives are now used or available for industrial aquafeeds, depending on relative prices and consumer acceptance, and the outlook for single-cell organisms to replace fish oil is promising. [3]
Smoking and fermenting fish leftovers provides spoilage protection [4]
Alaska salmon oils are rich in n-3 polyunsaturated fatty acids used in food and pharmaceutical industries. Bower and Hietala 2010 preserved pink salmon leftovers of the oil extraction using a combination of smoke-processing and acidification with lactic acid bacteria, fermented below pH 4.7, and lactic acid concentrations over 15 g/L. The salmon tissue discarded after oil extraction may be used in the production of high-protein crackers and other fish-based food products with smoke-flavouring and antioxidant factors extending the shelf life of the final product.
[1] Fish Leftovers: New Life Ahead for Today’s Discards?
http://www.ars.usda.gov/is/AR/archive/oct10/leftovers1010.htm
[2] ARS USDA: Finding Alternative Fish Feeds for Aquaculture
http://www.ars.usda.gov/is/AR/archive/oct10/feeds1010.htm
[3] Naylor RL, Hardy RW, Bureau DP, Chiu A, Elliott M, Farrell AP, Forster I, Gatlin DM, Goldburg RJ, Hua K, Nichols PD: Feeding aquaculture in an era of finite resources. Proc Natl Acad Sci U S A. 2009 Sep 8;106(36):15103-10.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2741212/?tool=pubmed
[4] Bower C, Hietala K: Stabilizing smoked salmon (Oncorhynchus gorbuscha) tissue after extraction of oil. J Food Sci. 2010 Apr;75(3):C241-5
http://www.ncbi.nlm.nih.gov/pubmed/20492273
03.11.2010: Mould in Dubai buildings [1]
Rushed construction and poorly designed air-conditioning systems in almost nine out of 10 buildings of Dubai present serious problems with air conditioning system. The equipment is unable to dry the air properly. Mould develops and spores of Aspergillus and Alternaria intensify allergies and asthma. Another health threat is Legionella pneumophila, a bacterium which breeds in air-conditioning systems and in water tanks and fittings.
Air conditioners must, therefore, be capable to dehumidify incoming air, and regular maintenance is necessary. Faulty placed airconditioning vents and insufficient airing of rooms are common reason of mould in housings. Maintaining the room temperature at 24°C instead of 20°C will rise the dew point, but soon or later humidity will settle at less aerated places. Air humidity of the air should be kept below 52% and rooms should be aerated properly. Hygrometers which measure the air humidity are cheap and give information on the quality of indoor air quality.
Prediction of increase of spores in air using an artificial neural network (ANN) [2]
Grinn-Gofroń and colleagues 2010 examined the incidence of the airborne fungi Alternaria and Cladosporium related to meteorological parameters and air pollutant concentrations. The authors also created an artificial neural network (ANN) forecasting model to predict the rise of spore concentration and environmental parameters as well as pollutants. Results could be confirmed by the Spearman's correlation rank analysis. Alternaria and Cladosporium spores may thus be predicted from meteorological conditions and air pollution recorded three days in advance.
Meteorological factors influencing transportation of air particulates [3]
According to Jones 2004 pollen, fungal spores, bacteria, viruses, or fragments of plant and animal matter make up a quarter of the total airborne particulate. Meteorological variables, such as temperature, humidity and wind speed will affect the release and the transportation of pollen, fungal spores, bacteria and viruses. The authors stress, however, that the concentration of bacteria declines less rapidly than that of fungal spores and can therefore be transported at longer distances as noted with spores.
Fungi harmful to humans, animals and plants [4]
De Lucca 2007 points out that most fungi are saprophytic and not pathogenic to plants, animals and humans. However, few fungal species such as members of the Aspergillus, Fusarium Alternaria, Mucor genera may produce diseases in humans, animals and plants. Death due to aflatoxins has been reported in humans, animals and birds.
Saprophytic fungi can be opportunistic pathogens that enter via wounds or due to a weakened state of the host and true pathogens may depend on living plant or human tissues for nutrients but can also survive outside of the hosts.
Suggested guidelines for acceptable levels of fungi in indoor ambient air [5]
Gots, Layton and Pirages 2003 report noncomplaint for commercial buildings with 233 colony forming units (CFU) per cubic meter, with outdoor ambient air levels averaged 983 CFU/m(3). However, some commercial building presented total indoor spore counts ranging from 610 to 1040 spores/m(3), associated with outdoor spore counts of 400 to 80,000 spores/m(3).
In residential building noncomplaint count was 1252 CFU/m(3) with an average outdoor level of 1524 CFU/m(3). Total spore counts detected indoors ranged between 68 and 2307 spores/m(3), with associated outdoor spore levels between 400 to 80,000 spores/m(3).
The authors stress that many buildings have a noncomplaint indoor ambient air fungal concentrations above 500 CFU/m(3), which however, requires remediation when nonspecific adverse health symptoms occur.
Data to set quality standards for animal dwellings air [6]
Matković, Vucemilo and Vinković 2009 found that fungi sore count in the stable housing dairy cows ranged from 3.98 x 103 CFU m-3 to 5.11 x 104 CFU m-3 and in the coop for laying hens from 6.89 x 104 CFU m-3 to 1.13 x 105 CFU m-3. The most common were the fungi Aspergillus sp., Penicillium sp., and yeasts, followed by Cladosporium sp., Fusarium sp., Mucor sp., Scopulariopsis sp., Alternaria sp., and Rhizopus sp. The authors call for more studies to sett air quality standards for animal dwellings.
Sick building syndrome [7]
Symptoms of sick building syndrome (SBS) was found to be associated with mould, mites, and volatile organic compounds, renovation, air freshener, carpet, use of benzine, use of thinner, use of coating materials, smell of house, and feeling of having insufficient sleeping hours. Important moulds were Auerbasidum genus, Alternaria alternata, Aspergillus sp., Aureobasidium pullulans, Cladosporium cladosporioides, Fusarium sp., Penicillium sp., Rhodotorula minuta, and Wallemia sebi, and volatile organic compounds of concern were limonene, o,m-tolualdehyde, 2-pentanone, tetrachloroethylene, n-decane, and n-heptane. The authors recommend modification of lifestyle and ways of living factors..
One technique to reduce energy consumption while maintaining adequate air quality, is “demand controlled ventilation”. Instead of setting throughput at a fixed air replacement rate, carbon dioxide sensors are used to control the rate dynamically, based on the emissions of actual building occupants. [8]
In the UK classrooms are required to have 2.5 outdoor air changes per hour. In halls, gym, dining, and physiotherapy spaces, the ventilation should be sufficient to limit carbon dioxide to 1,500 ppm. In the USA, and according to ASHRAE Standards, ventilation in classrooms is based on the amount of outdoor air per occupant plus the amount of outdoor air per unit of floor area, not air changes per hour. In classrooms, the requirements in the ASHRAE standard 62.1, Ventilation for Acceptable Indoor Air Quality, would typically result in about 3 air changes per hour, depending on the occupant density. [9]
Mould grows at cold spots of the room [10]
The ability of air to hold water vapour decreases as the air temperature is lowered. If a unit of air contains half of the water vapour it can hold, it is said to be at 50% relative humidity (RH). As the air cools, the relative humidity increases.
Relative humidity and temperature often vary within a room, while the absolute humidity in the room air can usually be assumed to be uniform. Therefore, if one side of the room is warm and
the other side cool, the cool side of the room has a higher RH than the warm side. The highest relative humidity in a room is always next to the coldest surface, mould will grow there.
Keep humidity under 45-50%
Mould and mites need a relative humidity in excess of 45–50%. The relative humidity during the heating season should be below this value. Even under such conditions, however, relative humidity can be higher on colder internal surfaces. Heat and moisture transfer analyses should search for defective thermal isolation and avoid thermal bridges.
Visual Inspection [11]
Currently there are no United States Federal, New York State, or New York City regulations for the assessment or remediation of mould growth.
A visual inspection is the most important initial step in identifying a possible mold problem and in determining remedial strategies. The extent of any water damage and mold growth should be visually assessed and the affected building materials identified. A visual inspection should also include observations of hidden areas where damages may be present, such as crawl spaces, attics, and behind wallboard. Carpet backing and padding, wallpaper, moldings (e.g. baseboards), insulation and other materials that are suspected of hiding mold growth should also be assessed.
Ventilation systems should be visually checked for damp conditions and/or mould growth on system components such as filters, insulation, and coils/fins, as well as for overall cleanliness.
Equipment such as a moisture meter or infrared camera (to detect moisture in building materials) or a borescope (to view spaces in ductwork or behind walls) may be helpful in identifying hidden sources of mould growth, the extent of water damage, and in determining if the water source is active.
Measuring concentrations of microorganisms (particularly fungi) in indoor air [12]
Culture-based methods: To date, no standard methods are available for detecting
and enumerating fungi in indoor environments. Traditional culture methods have proven to be of limited use for quantitative assessment of exposure. Culture-based techniques thus usually provide qualitative rather than quantitative data.
[1] Complaints of mould in homes 'on increase'. The National 31.10.2010.
http://www.thenational.ae/news/uae-news/environment/complaints-of-mould-in-homes-on-increase
[2] Grinn-Gofroń A, Strzelczak A, Wolski T: The relationships between air pollutants, meteorological parameters and concentration of airborne fungal spores. Environ Pollut. 2010 Oct 26.
http://www.ncbi.nlm.nih.gov/pubmed/21030122
[3] Jones AM, Harrison RM: The effects of meteorological factors on atmospheric bioaerosol concentrations--a review. Sci Total Environ. 2004 Jun 29;326(1-3):151-80.
http://www.ncbi.nlm.nih.gov/pubmed/15142773
[4] De Lucca AJ: Harmful fungi in both agriculture and medicine. Rev Iberoam Micol. 2007 Mar;24(1):3-13.
http://www.reviberoammicol.com/2007-24/003013.pdf
[5] Gots RE, Layton NJ, Pirages SW: Indoor health: background levels of fungi. AIHA J (Fairfax, Va). 2003 Jul-Aug;64(4):427-38.
http://www.ncbi.nlm.nih.gov/pubmed/12908856
[6] Matković K, Vucemilo M, Vinković B: Airborne fungi in dwellings for dairy cows and laying hens. Arh Hig Rada Toksikol. 2009 Dec;60(4):395-9.
http://www.ncbi.nlm.nih.gov/pubmed/20061239
[7] Nakayama K, Morimoto K: Risk factor for lifestyle and way of living for symptoms of sick building syndrome: epidemiological survey in Japan. Nippon Eiseigaku Zasshi. 2009 May;64(3):689-98.
http://www.ncbi.nlm.nih.gov/pubmed/19502765
[8] Wikipedia: Indoor air quality
http://en.wikipedia.org/wiki/Indoor_air_quality
[9] American Society of Heating and Air-Conditioning Engineers, Inc: ASHRAE Standard 62.1-2010. Vetilation for Acceptable Indoor Air Quality.
http://openpub.realread.com/rrserver/browser?title=/ASHRAE_1/ashrae_62_1_2010_1024
[10] CDC: Moisture, Mold and Mildew
http://www.cdc.gov/niosh/pdfs/appenc.pdf
[11] New York City Department of Health and Mental Hygiene (DOHMH): Guidelines on Assessment and Remediation of Fungi in Indoor Environments. 2008.
http://home2.nyc.gov/html/doh/html/epi/moldrpt1.shtml
[12] WHO guidelines for indoor air quality: dampness and mould
http://www.euro.who.int/__data/assets/pdf_file/0017/43325/E92645.pdf
01.11.2010: Nanocapsules for food preservation and storage [1]
Zambrano-Zaragoza and colleagues 2010 described the production of polymeric nanocapsules by the emulsification-diffusion method. These nano-capsules may become useful in food formulation. Using the Response Surface Methodology the authors found that these nanocapsules were produced at a shear rate of 10,917 s−1, with a polymer-wall concentration of 256 mg poly-epsilon-caprolactone and a stabilizer concentration of 0.5 g/L of polyvinyl alcohol. These nano-capsules have an oil core whith superior functionalities over other nano-particulate systems. The oil core may be used as a protective barrier to transport food additives and dietary supplements requiring encapsulation, preserving their functionality and bioavailability, or prevent incompatibilities.
Response surface methodology (RSM) [2]
In statistics, response surface methodology (RSM) explores the relationships between several explanatory variables and one or more response variables. The main idea of RSM is to use a sequence of designed experiments to obtain an optimal response. This model is only an approximation, but it is used because it is easy to estimate and apply, even when little is known about the process. Nonetheless, response surface methodology has an effective track-record of helping researchers improve products and services.
Ebrahimpour and colleagues 2008 report that artificial neural network (ANN) was superior over RSM for both data fitting and estimation capabilities, when used for their study. ANN, however, requires large amounts of training data in comparison with RSM. This disadvantage may be avoided using statistical experimental design to reduce the number of experiments. [3]
Artificial neural network (ANN) [4]
An artificial neural network (ANN), usually called "neural network" (NN), is a mathematical model or computational model that is inspired by the structure and/or functional aspects of biological neural networks. A neural network consists of an interconnected group of artificial neurons, and it processes information using a connectionist approach to computation. In most cases an ANN is an adaptive system that changes its structure based on external or internal information that flows through the network during the learning phase.
Basri and colleagues 2007 write that the classical method of optimization of processes involves varying one parameter at a time that ignores the combined interactions between physicochemical parameters. RSM and ANNs are better suited for modelling biochemical and chemical processes, compared with the classical method. [5]
Takayama and colleagues 2003 say that response surface method (RSM) based on the second-order polynomial equation used for optimization of drug formulations provide poor results. The authors describe the basic concept of the multi-objective simultaneous optimization technique, in which an artificial neural network (ANN) is incorporated. [6]
[1] Zambrano-Zaragoza ML, Mercado-Silva E, Gutiérrez-Cortez E, Castaño-Tostado E, Quintanar-Guerrero D: Optimization of Nanocapsules Preparation by the Emulsion-Diffusion Method for Food Applications. LWT - Food Science and Technology. 2010. Doi: 10.1016/j.lwt.2010.10.004
http://dx.doi.org/10.1016/j.lwt.2010.10.004
[2] Wikipedia: Response Surface Methodology.
http://en.wikipedia.org/wiki/Response_surface_methodology
[3] Ebrahimpour A, Abd Rahman RN, Ean Ch'ng DH, Basri M, Salleh AB: A modeling study by response surface methodology and artificial neural network on culture parameters optimization for thermostable lipase production from a newly isolated thermophilic Geobacillus sp. strain ARM
BMC Biotechnol. 2008 Dec 23;8:96.
http://www.ncbi.nlm.nih.gov/pubmed/19105837
[4] Wikipedia: Artificial neural network
http://en.wikipedia.org/wiki/Artificial_neural_network
[5] Basri M, Rahman RN, Ebrahimpour A, Salleh AB, Gunawan ER, Rahman MB: Comparison of estimation capabilities of response surface methodology (RSM) with artificial neural network (ANN) in lipase-catalyzed synthesis of palm-based wax ester. BMC Biotechnol. 2007 Aug 30;7:53.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2211475/?tool=pubmed
[6] Takayama K, Fujikawa M, Obata Y, Morishita M: Neural network based optimization of drug formulations. Adv Drug Deliv Rev. 2003 Sep 12;55(9):1217-31.
http://www.ncbi.nlm.nih.gov/pubmed/12954200