June 2010 - OurFood-news

30.06.2010: Genetic of plant disease-causing bacteria
Virulence gene complement olive knot disease causing Pseudomonas savastanoi pv. Savastanoi NCPPB 3335 [1]

Pseudomonas savastanoi pv. savastanoi is a tumour-inducing pathogen of Olea europaea L. causing olive knot disease. Rodríguez-Palenzuela and colleagues 2010 analysed the genome sequence of Pseudomonas savastanoin revealing similarities with Pseudomonas syringae pv. phaseolicola 1448A and Pseudomonas syringae pv. Tabaci 11528.



The authors report that twelve variable genomic regions of NCPPB 3335 contains twelve variable genomic regions which are not present in Pseudomonas syringae. These genes make the strain capable to survive in a plant host, and 73 predicted coding genes that are NCPPB 3335-specific were found in Pseudomonas savastanoi pathovar indicating specific adatations of P savastanoi.



Prevail of Pseudomonas savastanoi pv. savastanoi type III mutant in olive plants [2]

Pérez-Martínez and colleagues 2010 describe the sequencing of the hrpS-to-hrpZ region of NCPPB 3335, elucidating its phylogenetic position relative to Pseudomonas syringae hrp clusters.



The authors report the construction of a mutant of NCPPB 3335, termed T3, with deletion of the 3' end of the hrpS gene to the 5' end of the hrpZ operon. T3 mutant does not induce tumor formation in woody olive plants, however, it can induce knot formation on young micropropagated olive plants, but without necrosis and formation of internal open cavities, seen with wild-type strain and differed in distribution within the host tissue.



Virulence determining genes in Pseudomonas syringae [3]

Lindeberg and colleagues 2008 describe the virulence-associated genes for three Pseudomonas syringae strains. These genes, described in the DC3,000 genome annotation are associated with the ability to grow on plant surface, to segregate plant- and insect-active toxins, and virulence regulators.



The authors highlight a strong segregation of the HrpL regulon with variable genome regions (VR), whose distribution, together with other sequenced bacterial genomes were discussed by the authors as a virulence sources.



Pseudomonas syringae equipped with an Atypical Type III Secretion System [4]

Christopher and colleagues 2010 stress that Pseudomonas syringae causes a plant disease by translocating immune-suppressing effector proteins into plant cells through a type III secretion system (T3SS).

The authors describe a new Phrp/hrc cluster which differs from the typical Pseudomonas syringae hrp/hrc cluster coding for a T3SS. This new hrp/hrc cluster misses the genes hrpK and hrpS, of the classical P. syringae hrp/hrc cluster. The group 2c strain also revealed distant similarities with the Pseudomonas syringae effector genes avrE1 and hopM1 and the P. aeruginosa effector genes exoU and exoY.



Two virulence domains of AvrPto are conserved in different Pseudomonas syringae [5]

Hanh and colleragues 2010 write that the Pseudomonas syringae pv. tomato type III effector protein AvrPto encode virulence in susceptible tomato plants and also defence responses in resistant tomato and tobacco genotypes. The authors stress that two virulence domains of AvrPto are conserved in diverse pathovars and may be active during infection of diverse plant species.



Pseudomonas syringae pv. tomato DC3000 Type III Effector HopAA1-1 redundant with chlorosis-promoting factor PSPTO4723 to produce bacterial speck lesions in tomato [6]

Cathy and colleagues 2009 report that Pseudomonas syringae pv. tomato DC3000 kill yeast and promote bacterial speck disease in tomato by injection of 28 Avr/Hop effector proteins HopAA1-1, using the type III secretion system.

Deleting hopAA1-1 from DC3000 reduces the formation of necrotic speck lesions in tomato leaves if effector-gene cluster IX or just PSPTO4723 within this region has been deleted. PSPTO4723 does not encode an effector and is associated with chlorosis.



Studying host specificity of Pseudomonas syringae [7]

According to Lindeberg and colleagues 2009 Pseudomonas syringae, using the type III secretion system, injects effector proteins that suppress basal innate immunity of the host cytoplasm. This, however, may be recognized by cognate resistance (R) proteins in a second level of the host defence. Following latest data the nature and evolution of P. syringae host specificity and nonhost resistance may now be further elucidated. [8]



Common toxin fold explains interaction between microbial attack and plant [9]

Ottmann and colleagues 2009 describe the necrosis and ethylene-inducing peptide 1 (Nep1)-like proteins (NLPs) which trigger leaf necrosis and immunity-associated responses in various plants.

The authors found that NLP-mediated phytotoxicity and plant defence gene expression share identical fold requirements, indicating that toxins trigger plant immunologic responses.

These NLPs proteins present fold similarities to toxins produced by marine organisms like actinoporins. Structure of NLPs from Phytophthora parasitica and Pectobacterium carotovorum, revealed a high extent of this fold conservation.

The authors also stress that plant defences activated by these toxins are reminiscent of microbial toxin-induced inflammasome activation in vertebrates suggesting a link between animal and plant innate immunity.



[1] Rodríguez-Palenzuela P, Matas IM, Murillo J, López-Solanilla E, Bardaji L, Pérez-Martínez I, Rodríguez-Moskera ME, Penyalver R, López MM, Quesada JM, Biehl BS, Perna NT, Glasner JD, Cabot EL, Neeno-Eckwall E, Ramos C: Annotation and overview of the Pseudomonas savastanoi pv. savastanoi NCPPB 3335 draft genome reveals the virulence gene complement of a tumour-inducing pathogen of woody hosts. Environ Microbiol. 2010 Apr 1. p 1604-1620. Doi: 10.1111/j.1462-2920.2010.02207.x

http://www.ncbi.nlm.nih.gov/pubmed/20370821



[2] Pérez-Martínez I, Rodríguez-Moreno L, Lambertsen L, Matas IM, Murillo J, Tegli S, Jiménez AJ, Ramos C: Fate of a Pseudomonas savastanoi pv. savastanoi type III secretion system mutant in olive plants (Olea europaea L.). Appl Environ Microbiol. 2010 Jun;76(11):3611-9. Epub 2010 Apr 2.

http://www.ncbi.nlm.nih.gov/pubmed/20363790



[3] Lindeberg M, Myers CR, Collmer A, Schneider DJ: Roadmap to new virulence determinants in Pseudomonas syringae: insights from comparative genomics and genome organization. Mol Plant Microbe Interact. 2008 Jun;21(6):685-700.

http://apsjournals.apsnet.org/doi/abs/10.1094/MPMI-21-6-0685



[4] Christopher R. Clarke, Rongman Cai, David J. Studholme, David S. Guttman, and Boris A. Vinatzer: Pseudomonas syringae Strains Naturally Lacking the Classical P. syringae hrp/hrc Locus Are Common Leaf Colonizers Equipped with an Atypical Type III Secretion System. Mol Plant Microbe Interact. .February 2010, Volume 23, Number 2. Pages 198-210

Doi: 10.1094/MPMI-23-2-0198

http://apsjournals.apsnet.org/doi/abs/10.1094/MPMI-23-2-0198



[5] Hanh P. Nguyen, Inhwa Yeam, Aurelie Angot and Gregory B. Martin: Two virulence determinants of type III effector AvrPto are functionally conserved in diverse Pseudomonas syringae pathovars. New Phytologist. Doi: 10.1111/j.1469-8137.2009.03175.x Published Online: 28 Jan 2010

http://www3.interscience.wiley.com/journal/123266047/abstract



[6] Kathy R. Munkvold, Alistair B. Russell, Brian H. Kvitko, and Alan Collmer: Pseudomonas syringae pv. tomato DC3000 Type III Effector HopAA1-1 Functions Redundantly with Chlorosis-Promoting Factor PSPTO4723 to Produce Bacterial Speck Lesions in Host Tomato. Molecular Plant-Microbe Interactions Nov 2009, Volume 22, Number 11: 1341-1355. Doi: 10.1094/MPMI-22-11-1341

http://apsjournals.apsnet.org/doi/abs/10.1094/MPMI-22-11-1341



[7] Magdalen Lindeberg, Sébastien Cunnac, Alan Collmer: The evolution of Pseudomonas syringae host specificity and type III effector repertoires. Molecular Plant Pathology Nov 2009, Volume 10, Number 6: 767-775. Doi: 10.1111/j.1364-3703.2009.00587.x

http://www3.interscience.wiley.com/journal/122612876/abstract



[8] Nalvo F. Almeida, Shuangchun Yan, Magdalen Lindeberg, David J. Studholme, David J. Schneider, Bradford Condon, Haijie Liu, Carlos J. Viana, Andrew Warren, Clive Evans, Eric Kemen, Dan MacLean, Aurelie Angot, Gregory B. Martin, Jonathan D. Jones, Alan Collmer, Joao C. Setubal, and Boris A. Vinatzer: A Draft Genome Sequence of Pseudomonas syringae pv. tomato T1 Reveals a Type III Effector Repertoire Significantly Divergent from That of Pseudomonas syringae pv. tomato DC3000. Molecular Plant-Microbe Interactions Jan 2009, Volume 22, Number 1: 52-62. Doi: 10.1094/MPMI-22-1-0052

http://www3.interscience.wiley.com/journal/122612876/abstract



[9] C. Ottmann, B. Luberacki, I. Kufner, W. Koch, F. Brunner, M. Weyand, L. Mattinen, M. Pirhonen, G. Anderluh, H. U. Seitz, T. Nurnberger, and C. Oecking: A common toxin fold mediates microbial attack and plant defense. Proceedings of the National Academy of Sciences Jun 2009, Volume 106, Number 25: 10359-10364

http://www.pnas.org/content/106/25/10359


29.06.2010: Health risk of the BP oil spill on April 20, 2010[1]

Crude oil contains a mixture of volatile hydrocarbon compounds - polycyclic aromatic hydrocarbons that typically include the carcinogens benzene, toluene, and xylene. According to the CDC, symptoms of exposure to these compounds include drowsiness, dizziness, rapid or irregular heartbeat, headaches, tremors, confusion, and unconsciousness.



Total petroleum hydrocarbons (TPH) is a term used to describe a large family of several hundred chemical compounds that originally come from crude oil. It is not practical to measure each one separately, therefore the total amount of TPH are measured and referred to.



Some of the TPH compounds can affect your central nervous system. One compound can cause headaches and dizziness at high levels in the air. Another compound can cause a nerve disorder called "peripheral neuropathy," consisting of numbness in the feet and legs. Other TPH compounds can cause effects on the blood, immune system, lungs, skin, and eyes.



Animal studies have shown effects on the lungs, central nervous system, liver, and kidney from exposure to TPH compounds. Some TPH compounds have also been shown to affect reproduction and the developing fetus in animals.

TPH and cancer: The International Agency for Research on Cancer (IARC) has determined that one TPH compound (benzene) is carcinogenic to humans. IARC has determined that other TPH compounds (benzo[a]pyrene and gasoline) are probably and possibly carcinogenic to humans. Most of the other TPH compounds are considered not to be classifiable by IARC.



Regulations and limits: There are no regulations or advisories specific to TPH. The following are recommendations for some of the TPH fractions and compounds:

The EPA requires that spills or accidental releases into the environment of 10 pounds or more of benzene be reported to the EPA.



The Occupational Safety and Health Administration has set an exposure limit of 500 parts of petroleum distillates per million parts of air.

The Occupational Safety and Health Administration (OSHA) and the Air Force Office of Safety and Health (AFOSH) have set a permissible exposure level (PEL) of 400 parts of petroleum distillates per million parts of air (400 ppm) for an 8-hour workday, 40-hour workweek.



The National Institute for Occupational Safety and Health (NIOSH) recommends that average workplace air levels not exceed 350 milligrams of petroleum distillates per cubic meter of air (350 mg/m³) for a 40-hour workweek.



The Department of Transportation (DOT) lists fuel oils as hazardous materials and, therefore, regulates their transportation.



Worshop of the IOM on health risks related to the BP oil spill [2]

The IOM workshop on June 22 and 23, 2010 in New Orleans, discussed the health concerns related to the BP oil spill.



Scott Barnhart stressed that crude oil contains a complex mixture of heavy metals and volatile and nonvolatile polyaromatic hydrocarbons, Exposure by skin contact, inhalational and ingesting oil-contaminated foods may lead to cancer, neurologic, renal, hepatic, dermatologic, and hematologic effects.



Gina Solomon reported that BP data showed levels of benzene and 2-butoxyethanol (the dispersant chemical) above the Recommended Exposure Limit set by the National Institute for Occupational Safety and Health. Dr. Solomon recommends residents not to fish in any areas that have been declared off-limits or where they see evidence of oil contamination, and fish or shellfish that has an oily odour should be discarded and not eaten. Noting a strong odour of oil or chemicals, and are concerned about health effects, residents should seek refuge in an air conditioned environment, preferably with the air conditioner on recirculation mode to avoid intake of polluted air.



Maureen Lichtveld pointed out that the psychosocial aspect needs to have a much higher priority as it is being focused on. She referred to Exxon Valdez oil spill which caused a significant increases in depression, posttraumatic stress disorder, and other anxiety disorders, as well as generally poorer scores on mental health assessments. There are not enough data to predict whether there could be future elevations in cancer risks, reproductive issues, or neurological sequelae from this oil spill this must stay under observation.





[1] CDC: Gulf Oil Spill 2010: Information for Health Professionals

http://emergency.cdc.gov/gulfoilspill2010/health_professionals.asp



[2] Medscape Medical News: CDC and IOM Warn of Adverse Psychosocial, Cancer Effects From Gulf Oil Spill. Emma Hitt, PhD. June 28, 2010.

http://www.medscape.com/viewarticle/724299





25.06.2010: Vibrio vulnificus a pathogen in Gulf Coast oysters
Limiting the Sale of Raw Oysters Harvested from the Gulf of Mexico [1]

The Center for Science in the Public Interest warns the consumers from Vibrio vulnificus, a deadly bacteria found in almost all Gulf Coast oysters harvested in warmer months.

The Californian plan to reduce the risk of Vibrio vulnificus has proved to be effective, but it was binding only in this state.[2] The plan banned the sale of untreated Gulf Coast oysters reducing number of deaths from about five a year to zero. This approach will now be adopted nationwide by a new FDA policy. The shellfish industry were opposed to the oyster treatment to kill the pathogen.



The Department of Health Services (DHS) has amended California Code of Regulations (CCR), Title 17, Section 13675, [1ab]to prevent V. vulnificus illnesses and deaths associated with the consumption of raw Gulf oyster, restricting the sale of raw oysters harvested from the Gulf of Mexico during April 1 through October 31, unless the oysters are treated with a scientifically validated process to reduce V. vulnificus to non-detectable levels. Raw Gulf oysters received during April through October that have not been processed to reduce V. vulnificus to non-detectable levels are considered adulterated.[3] Treatments to kill Vibrio vulnificus without affecting taste are cold pasteurization, hydrostatic pressure, cost of the processes are low and increase food safety. [4]



Post-Harvest Processed Oysters [5]

Freezing, heat-cool pasteurization, and high hydrostatic pressure are used commercially on oysters as post-harvest processes to kill spoilage bacteria and reducing Vibrio spp. bacteria to non-detectable levels.The treamtment increases the shelf life of the product. The organisation SafeOyster.org, however, stresses that not all bacteria and viruses may be killed. The organisation recommends high-risk patients not to eat oysters, even when they were post-harvest processed. As a safety measure, these patients should eat cooked oysters.



The Center for Science in the Public Interest (CSPI) says Gulf Cost oysters are not safe [4]

According to David W. Plunkett, a CSPI staff attorney, some Gulf oysters may be ‘safe’ from oil contamination, but are not ‘safe’ to eat. Plunkett contradicts several reassuring statements that seafood from the Gulf on the market is safe. Vibrio vulnificus contaminates Gulf oysters in the spring and summer. While it may cause mild illnesses in healthy individuals, it can kill people who have diabetes, liver disease, hemochromatosis or compromised immune systems, causing the death of 10 people last year.



The Food and Drug Administration FDA affirms on its website that shellfish harvested from areas unaffected by the spill are safe to eat [6]

Plunkett remids that last year Mike Taylor, a Deputy of the FDA called Vibrio vulnificus a significant hazard, and now FDA ignores the risk of the pathogen bacteria.

The CSPI says that the FDA eventually backed down from its plans under pressure from Members of Congress who responded to industry posturing over potential job losses, and only California has implemented an effective control plan to protect its consumers.



Vibrio vulnificus infection [7]

Vibrio vulnificus is a bacteria which is present in marine environments such as estuaries, brackish ponds, or coastal areas, It causes an infection eating seafood, especially raw or undercooked oysters; the bacteria can also enter the body through open wounds when swimming or wading in infected waters, or via puncture wounds from the spines of fish such as tilapia. Symptoms include vomiting, diarrhea, abdominal pain, and a blistering dermatitis that is sometimes mistaken for pemphigus or pemphigoid. In people with compromised immune systems such as in chronic liver disease, a cut infected with Vibrio bacteria can quickly become worse and spread into the bloodstream. Severe symptoms and even death can then occur.



Vibrio illness in Florida [8]

Weis and colleagues 2010 report 834 vibrio infections in 825 individuals in Florida from 1998 to 2007. The incidence was Vibrio vulnificus 33%, V. parahaemolyticus 29%, and V. alginolyticus 16%, causing 45% ofwound infections and 42% gastroenteritis. Prevention is focused on oyster consumption. The authors call for educational messages focusing wound infections of high-risk populations.



Foodborne pathogens in oysters of South China food markets [9]

Chen and colleagues 2010 looking at the pathogens in shellstock Pacific oysters in the food markets in South China say that Vibrio vulnificus and Vibrio parahaemolyticus (89.3%) but no Listeria monototogenes could be detected in the samples. The authors concluded that Vibrio vulnificus and pathogenic Vibrio parahaemolyticus in oysters are a risk to public health in south China.



Vibrio bacteria in Brazilian oysters [10]

Vieira and colleagues 2010 analysed oyster samples from a coastal aquaculture in Euzebio, Ceará, Brazil, The authors identified Vibrio parahaemolyticus. Vibrio carchariae and Vibrio. Vulnificus, stressing that oysters should never be eaten raw or undercooked becaause of the risk presented by Vibrio bacteria.



Temperature effects on the depuration of Vibrio parahaemolyticus and Vibrio vulnificus from oysters [11]

Chae, Cheney and Su 2009 investigated temperature effects on depuration for reducing Vibrio parahaemolyticus and Vibrio vulnificus in American oyster. Depuration of oysters at 22 degrees C had limited effects. Best reults were obtained with water temperature of 15 degrees C after 96 h of depuration at 15 degrees C. Depurations at 10 and 5 degrees C were less effective than at 15 degrees C.



Elektrolyzed water as sanitizer in food industry [12]

Hricova, Stephan and Zweifel 2008 report that electrolyzed water is obtained by electrolysing a dilute sodium chloride solution dissociating into acidic electrolyzed water (AEW) with a pH of 2 to 3, an oxidation-reduction potential of >1,100 mV, and an active chlorine content of 10 to 90 ppm, and basic electrolyzed water (BEW), which has a pH of 10 to 13 and an oxidation-reduction potential of -800 to -900 mV.



AEW reduced bacteria in suspension > 6.0 log CFU/ml. However, surface type and the presence of organic matter reduce the efficiency of AEW Applying BEW followed by AEW may lead to higher reductions than AEW only. The authors say electrolyzed water technology should be further discussed as industrial sanitization of equipment and decontamination of food products, but must be accompanied by good manufacturing and hygiene practices.





Electrolyzed oxidizing (EO) water treatment on reducing V. parahaemolyticus and V. vulnificus [13]

Holding vibrio contaminated oysters in electrolyzed oxidizing water containing 1% NaCl reduced the number of Vibrio parahaemolyticus and Vibrio vulnificus significantly in 4 to 6 h, but extended exposure (> 12 h) of oysters in electrolyzed oxidizing water and chlorine levels over 30 ppm caused death of oysters. Ren and Su 2006, authors of the study, suggested to use electrolyzed oxidizing water treatment for 4 to 6 h as post-harvest treatment of oysters to reduce Vibrio contamination limited to 4 to 6 h to avoid death of oysters.



Weak acidic electrolyzed oxidizing water post-harvest treatment of oysters [14]

Quan and colleagues 2010 report that Vibrio vulnificus and Vibrio parahaemolyticus were killed with a treatment of 15 s and more of weak acidic electrolyzed oxidizing water (WAEW) containing an available chlorine concentration (ACC) higher than 20mg/L. The effect of the treatment was reduced, when the ACC of WAEW was less than 15mg/L. The authors stress that the bactericidal activity of WAEW was primarily affected by ACC rather than treatment time, and WAEW is more effective than sodium hypochlorite (NaClO).



Vibrio vulnificus resistance to bile and other stresses [15]

Chen, Oliver and Wong 2010 describe the adaptation of Vibrio vulnificus and an rpoS isogenic mutant to bile and other stresses. An in vitro tolerance of the bacterium to 10% bile was attained by the authors, The bile-tolerant strain was more resistant to high pH, heat, high salinity and detergents than the rpoS mutant which had a lower bile-adaption rate.

The authors report further that production of GroEL was not markedly influenced but DnaK was inhibited in the bile-adapted cells, and RpoS plays a significant role in the response of Vibrio vulnificus to bile.



The interaction between low salinity and other common stresses in V. vulnificus [16]

Wong and Liu 2006 studied the cross-protective response of sublethal heat-, acid-, or bile-adapted Vibrio vulnificus against lethal low-salinity stress.



The authors found that Vibrio vulnificus adapted to an acidity of pH 4.4 and 41 degrees C heat-adapted V. vulnificus died in 0.04% NaCl low-salinity environment. The bile-adapted bacteria were resistant to low salinity, however 0.12% NaCl low-salinity adaption made them sensible to 12% bile stress.



Identification and subtyping of Vibrio parahaemolyticus and V. vulnificus targeting 16S-23S rRNA intergenic spacer regions [17]

Hoffmann and colleagues 2010 developed rapid polymerase chain reaction (PCR)-based intergenic spacer (IGS)-typing system for vibrios based on the IGS regions located between the 16S and 23S rRNA genes of vibrios.

The IGS-typing method demonstrated distinct IGS-typing patterns indicative of subspecies divergence in both populations making this technique equally useful for intraspecies differentiation, as well. The authors concluded that the new method is useful to identify vibrios down to sub-species level, and may be applied in time saving epidemiological investigations.



González-Escalona, Jaykus and DePaola reported in 2006 that amplification of the 16S-23S rDNA spacer region (ISR1) is a simple and rapid procedure for subtyping bacteria, especially those with several ribosomal operons including Vibrio vulnificus. V. vulnificus contains nine ribosomal operons with four or five ISR1 classes that differ in size and sequence. Clinical isolates formed a single cluster containing ISR1 patterns I, V, XI, and XII all carrying the type B 16S rDNA (rrs) sequence associated with human illness. Shellfish isolates presented high variability in the ISR1 patterns. The different classes differed in their tRNA gene composition, allowing subtyping of Vibrio vulnificus. The authors suggest that ISR1 patterns are linked with the virulence of the bacteria. [18]



Two fish-pathogenic serovars of Vibrio vulnificus biotype 2 [19]

According to Fouz and colleagues 2010 Vibrio vulnificus biotype 2 is subdivided into serovar E, infecting fish and humans, and serovar A, infecting only fish, such as eel in brackish water. Serovar A caused infections of freshwater-cultured eels vaccinated against serovar E resulting in haemorrhagic intestine. Both serovars infect healthy eels, tilapia, sea bass and rainbow trout, but not sea bream, serovar A entering mainly by the anus and serovar E by the gills.

The authors stress that serovar A form a new antigenic form of Vibrio vulnificus biotype 2 better adapted to fresh water than serovar E.



Vibrio vulnificus found in food and environmental samples of the Mediterranean area [20]

Cañigral and colleagues 2010 found that samples of seawater, oyster and wastewater from a coastal area in Spain near the Mediterranean.were positive by real time PCR, and Vibrio vulnificus could be isolated from these samples. The authors stress that Vibrio vulnificus presents a risk to humans in the Mediterranean area.



Rapid detection of Vibrio vulnificus in shellfish and Gulf of Mexico [21]

Panicker and colleagues 2004 described the optimization of SYBR Green I-based real-time PCR parameters to detect the presence of vibrios in seafood or environmental samples, using vvh-specific oligonucleotide primers. The method is completed in 8 hours.



[1] FDA Acts to Protect Consumers from Vibrio in Oysters. CSPI October 19, 2009.

http://www.cspinet.org/new/200910191.html



[2] Article 10.5. Raw Oysters. §13675. Raw Gulf Oysters: Labeling, Written Warnings and Additional Requirements. State of California.

http://www.cdph.ca.gov/services/Documents/fdb%20Raw%20Gulf%20Oyst%20Regs.pdf



[3] Environmental Health: Oysters:Limiting the Sale of Raw Oysters Harvested from the Gulf of Mexico. (Information from the California Department of Health Services)

http://www.co.el-dorado.ca.us/emd/envhealth/oyster.html



[4] Gulf Coast Oysters Unsafe (But Not For the Reason You Think). Deadly Vibrio Vulnificus Bacteria, Not Oil, Contaminate Gulf Oysters Every Summer. CSPI Newsroom. June 24, 2010.

http://www.cspinet.org/new/201006241.html



[5] SafeOysters.org - Health Care Providers. Vibrio vulnificus. Infection from Consumption of Raw. Shellfish or Marine-Related Wounds.

http://safeoysters.org/medical/prevention.html



[6] FDA: Multi-government agency response to the Gulf of Mexico oil spill. Gulf of Mexico Oil Spill Update - June 14, 2010

http://www.fda.gov/Food/ucm210970.htm



[7] Wikipedia: Vibrio vulnificus

http://en.wikipedia.org/wiki/Vibrio_vulnificus



[8] Weis KE, Hammond RM, Hutchinson R, Blackmore CG: Vibrio illness in Florida, 1998-2007. Epidemiol Infect. 2010 Jun 14:1-8.

http://www.ncbi.nlm.nih.gov/pubmed/20546636



[9] Chen Y, Liu XM, Yan JW, Li XG, Mei LL, Mao QF, Ma : .Foodborne pathogens in retail oysters in south China. Biomed Environ Sci. 2010 Feb;23(1):32-6.

http://www.ncbi.nlm.nih.gov/pubmed/20486433



[10] Vieira RH, de Sousa OV, Costa RA, Theophilo GN, Macrae A, Fonteles Filho AA, Rodrigues Ddos P: Raw oysters can be a risk for infections. Braz J Infect Dis. 2010 Feb;14(1):66-70.

http://www.ncbi.nlm.nih.gov/pubmed/20428657



[11] Chae MJ, Cheney D, Su YC: Temperature effects on the depuration of Vibrio parahaemolyticus and Vibrio vulnificus from the American oyster (Crassostrea virginica). J Food Sci. 2009 Mar;74(2):M62-6.

http://www.ncbi.nlm.nih.gov/pubmed/19323759



[12] Hricova D, Stephan R, Zweifel C: Electrolyzed water and its application in the food industry. J Food Prot. 2008 Sep;71(9):1934-47.

http://www.ncbi.nlm.nih.gov/pubmed/18810883



[13] Ren T, Su YC: Effects of electrolyzed oxidizing water treatment on reducing Vibrio parahaemolyticus and Vibrio vulnificus in raw oysters. J Food Prot. 2006 Aug;69(8):1829-34.

http://www.ncbi.nlm.nih.gov/pubmed/16924906



[14] Quan Y, Choi KD, Chung D, Shin IS: Evaluation of bactericidal activity of weakly acidic electrolyzed water (WAEW) against Vibrio vulnificus and Vibrio parahaemolyticus. Int J Food Microbiol. 2010 Jan 1;136(3):255-60. Epub 2009 Dec 7.

http://www.ncbi.nlm.nih.gov/pubmed/20004034



[15] Chen WL, Oliver JD, Wong HC: Adaptation of Vibrio vulnificus and an rpoS mutant to bile salts. Int J Food Microbiol. 2010 Jun 15;140(2-3):232-8.

http://www.ncbi.nlm.nih.gov/pubmed/20406715



[16] Wong HC, Liu SH: Susceptibility of the heat-, acid-, and bile-adapted Vibrio vulnificus to lethal low-salinity stress. J Food Prot. 2006 Dec;69(12):2924-8.

http://www.ncbi.nlm.nih.gov/pubmed/17186660



[17] Hoffmann M, Brown EW, Feng PC, Keys CE, Fischer M, Monday SR: PCR-based method for targeting 16S-23S rRNA intergenic spacer regions among Vibrio species. BMC Microbiol. 2010 Mar 23;10:90.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856557/?tool=pubmed



[18] González-Escalona N, Jaykus LA, DePaola A: Typing of Vibrio vulnificus strains by variability in their 16S-23S rRNA intergenic spacer regions. Foodborne Pathog Dis. 2007 Fall;4(3):327-37.

http://www.ncbi.nlm.nih.gov/pubmed/17883316



[19] Fouz B, Llorens A, Valiente E, Amaro C: A comparative epizootiologic study of the two fish-pathogenic serovars of Vibrio vulnificus biotype 2. J Fish Dis. 2010 May;33(5):383-90.

http://www.ncbi.nlm.nih.gov/pubmed/20158583



[20] Cañigral I, Moreno Y, Alonso JL, González A, Ferrús MA: Detection of Vibrio vulnificus in seafood, seawater and wastewater samples from a Mediterranean coastal area. Microbiol Res. 2010 Jan 25.

http://www.ncbi.nlm.nih.gov/pubmed/20106642



[21] Panicker G, Myers ML, Bej AK: Rapid detection of Vibrio vulnificus in shellfish and Gulf of Mexico water by real-time PCR: Appl Environ Microbiol. 2004 Jan;70(1):498-507.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC342803/?tool=pubmed





15.06.2010: Monosodium Glutamate not related to the Chinese Restaurant Syndrome [1]

Jinab and Hajeb 2010 of the University Putra Malaysia reviewed application, benefits of monosodium glutamate as flavor enhancer. The authors say that glutamate adds a fifth basic taste to the four basic ones, whicch are saltiness, sourness, sweetness and bitterness. It is also an energy source, acts as a substrate for glutathione synthesis and enhances food intake in older individuals. Glutamate may partially replace salt in food preparation. The Joint Expert Committee on Food Additives of the United Nations Food and Agriculture Organization and World Health Organization classified glutamate as safe. The authors stress that there are no consistent clinical data to support believes that glutamate causes asthma, migraine headache, Chinese Restaurant Syndrome, and there are no evidences indicating that individuals may be uniquely sensitive to glutamate.



The position of the Food Standards Australia New Zealand [2]

The Food Standards Australia New Zealand in a technical report of 2003 found that some studies reported a complex of symptoms which came to be known as the Chinese restaurant syndrome (CRS) because they typically followed ingestion of a Chinese meal. Two outstanding studies were Kwok, R. (1968) [3] and Schaumburg HH(1969) [4] suggesting monosodium glutamate as the causative agent in CRS embracing symptoms such as headache, numbness/tingling, flushing, muscle tightness, and generalised weakness. MSG symptom complex is now being used instead of CRS. A possible association between MSG and bronchospasm in asthmatic individuals were also suggested.



Conclusions: The FSA study found no convincing evidence that MSG is a significant factor in causing systemic reactions resulting in severe illness or mortality, and studies have failed to demonstrate a causal association with MSG. Some reactions were noted by administrating large doses (≥3g) of MSG without food were not serious and are likely to be attenuated when MSG is consumed with food. Bronchospasm in asthmatic individuals is, according to actual data, not significantly triggered by MSG



Patricia Tagliaferro in an article of 1995 [5], stressed inconsistent data of studies on the possible effect ofMSG. The study of Jinab and Hajeb 2010 confirms that glutamate is not related to asthma, migraine headache and Chinese Restaurant Syndrome.



[1] Jinap S and Hajeb B: Glutamate: Its applications in food and contribution to health. Appetite.

Published online ahead of print, doi: 10.1016/j.appet.2010.05.002

http://www.ncbi.nlm.nih.gov/pubmed/20470841



[2] Monosodium Glutamate, A safety Assessment. Food Standards Australia New Zealand 2003

http://www.foodstandards.gov.au/_srcfiles/MSG%20Technical%20Report.pdf



[3] Kwok, R. (1968), Chinese Restaurant Syndrome (letter). N Engl J Med, 278:796.



[4] Schaumburg HH, Byck R, Gerstl R, Mashman JH: Monosodium L-glutamate: its pharmacology and role in the Chinese restaurant syndrome. Science. 1969 Feb 21;163(869):826-8

http://www.ncbi.nlm.nih.gov/pubmed/5764480



[5] Taliaferro, Patricia J.: Monosodium glutamate and the Chinese Restaurant Syndrome: a review of food additive safety. Journal of Environmental Health, Vol. 57, 1995
http://www.thefreelibrary.com/Monosodium+glutamate+and+the+Chinese+Restaurant+Syndrome:+a+review+of+...-a017087836





14.06.2010: Harvest Plus and Maize biofortification [1]

While many micronutrients are available from fruits, vegetables, and animal products, most of the poor are unable to grow or buy these micronutrient-rich foods. Their diets are characterized by high intakes of staple food crops (such as maize, wheat, and rice) but low consumption of micronutrient-rich foods such as fruits, vegetables, and animal and fish products. By providing a regular daily dose of vitamins and minerals, biofortified staple crops do not need to provide the entire recommended daily allowance (RDA) of micronutrients, but they can be effective in reducing hidden hunger as part of a strategy that includes dietary diversification, supplementation, and commercial fortification, among others.



HarvestPlus focuses on three critical micronutrients that are recognized by the World Health Organization (WHO) as most limiting in diets: iron, zinc, and vitamin A. HarvestPlus envisions that in fifteen years, millions of people suffering from micronutrient malnutrition will be eating new biofortified crop varieties, such as orange sweet potato rich in vitamin A, orange maize and rice with increased zinc.



Biofortification [2]

Biofortification is a method of breeding crops to increase their nutritional value of staple crops. This can be done either through conventional selective breeding, or through genetic engineering. Biofortification differs from ordinary fortification because it focuses on making plant foods more nutritious as the plants are growing, rather than having nutrients added to the foods when they are being processed

Selective breeding:Using this method, plant breeders search seed or germplasm banks for existing varieties of crops which are naturally high in nutrients. They then crossbreed these high-nutrient varieties with high-yielding varieties of crops, to provide a seed with high yields and increased nutritional value. This method is quicker, cheaper, and less controversial than genetically engineering crops. For example, HarvestPlus primarily use conventional breeding techniques to develop biofortified crops.

Genetic modification: Golden rice is an example of a GM crop developed for its nutritional value. Golden rice contains genes from the soil bacterium Erwinia and either maize or daffodil plants, and contains increased levels of beta-carotene which can be converted by the body into vitamin A. This can help alleviate symptoms of vitamin A deficiency.



Here are some studies concerning improvement of micronutrients in staple foods.



Provitamin A biofortification of maize using crtRB1 alleles [3]

New breedings are focused on biofortification to improve the dietary vitamin A status in developing world. Yan and colleagues 2010, studying the genetic code of maize (Zea mays L.), report that the gene encoding beta-carotene hydroxylase 1 (crtRB1) associated with beta-carotene which may increase the concentration of provitamin A in maize kernel 18 times compared with standard maize. Alleles of crtRB1 are being introgressed via inexpensive PCR marker-assisted selection into tropical maize. The researchers avoided to introduce alien genes in maize. They use the natural variation of the crtRB1 gerne within the same plant increasing the production of provitamin A and reducing its transformation to other, not biologic active chemical structures. Davis and colleagues 2008 studying the biologic activity of other carotenoids report that twice the molar amount of beta-cryptoxanthin was as efficacious as beta-carotene. [4]



Biofortification of staple food crops [5]

Nestel and collegues 2010 highlights the progress which has been made to control micronutrient deficiencies through supplementation and food fortification. The authors stress that biofortification is being supported by predictive cost-benefit analyses, however additional public work is needed to induce producers and consumers to accept biofortified crops. Activities, such as the good seed systems, the development of markets and products, and demand creation may be helpful to achieve this goal.



Good seeds is supported by Bill & Melinda Gates Foundation and the Rockefeller Foundation. It helps to create new varieties of seeds and make improved seeds much more accessible in Africa, especially to rural farmers. [6]



Genes related to carotenogenesis and heat resistance in maize [7]

Li and colleagues 2008 studied the carotenoid expression in maize. The authors report that maize endosperm carotenoid accumulation requires PSY1 expression, but this was not related to PSY2 or PSY3.

Better understanding of the timing of PSY1 transcript critical information allowed to choose breeding alleles. The authors also found that PSY1 is required for carotenogenesis in the dark and for heat stress tolerance. Leaf carotenogenesis was shown to require photoregulation of PSY2 plus nonphotoregulatiing PSY1 expression.



Natural genetic variations used for biofortification of maize [8]

Harjes and colleagues 2008 describe the variation at the lycopene epsilon cyclase (lcyE) locus which alters the two branches of the pathway of the alpha-carotene versus beta-carotene. Four natural lcyE polymorphisms could lead to a threefold difference in provitamin A compounds. The best suited lcyE alleles may now be selected using inexpensive molecular markers developing maize with higher provitamin A levels.



[1] HarvestPlus: Nutrients. What is hidden hunger?

http://www.harvestplus.org/content/about-harvestplus



[2] Wikipedia: Biofortification

http://en.wikipedia.org/wiki/Biofortification



[3] Yan J, Kandianis CB, Harjes CE, Bai L, Kim EH, Yang X, Skinner DJ, Fu Z, Mitchell S, Li Q, Fernandez MG, Zaharieva M, Babu R, Fu Y, Palacios N, Li J, Dellapenna D, Brutnell T, Buckler ES, Warburton ML, Rocheford T: Rare genetic variation at Zea mays crtRB1 increases beta-carotene in maize grain. Nat Genet. 2010 Apr;42(4):322-7.

http://www.ncbi.nlm.nih.gov/pubmed/20305664



[4] Davis CR, Howe JA, Rocheford TR, Tanumihardjo SA: The xanthophyll composition of biofortified maize (Zea mays Sp.) does not influence the bioefficacy of provitamin a carotenoids in Mongolian gerbils (Meriones unguiculatus). J Agric Food Chem. 2008 Aug 13;56(15):6745-50. Epub 2008 Jul 11.

http://www.ncbi.nlm.nih.gov/pubmed/18616269



[5] Nestel P, Bouis HE, Meenakshi JV, Pfeiffer W: Biofortification of staple food crops. J Nutr. 2006 Apr;136(4):1064-7.

http://www.ncbi.nlm.nih.gov/pubmed/16549478



[6] Bill & Melinda Gates Foundation: Good Seeds, Better Lives for Poor Farmers.

http://www.gatesfoundation.org/agriculturaldevelopment/pages/connecting-poor-farmers-to-good-seeds-feature.aspx



[7] Li F, Vallabhaneni R, Yu J, Rocheford T, Wurtzel ET: The maize phytoene synthase gene family: overlapping roles for carotenogenesis in endosperm, photomorphogenesis, and thermal stress tolerance. Plant Physiol. 2008 Jul;147(3):1334-46.

http://www.plantphysiol.org/cgi/content/full/147/3/1334



[8] Harjes CE, Rocheford TR, Bai L, Brutnell TP, Kandianis CB, Sowinski SG, Stapleton AE, Vallabhaneni R, Williams M, Wurtzel ET, Yan J, Buckler ES: Natural genetic variation in lycopene epsilon cyclase tapped for maize biofortification. Science. 2008 Jan 18;319(5861):330-3.

http://www.ncbi.nlm.nih.gov/pubmed/18202289





12.06.2010: Monitoring the stability of nanoparticles under pH conditions found in living cells [1]

According to Murphy and colleagues 2010 the stability of nanoparticles may be affected by changes of the pH of the cell environment altering their potential for uptake into organisms. The pH in cells varies within the different compartments such as the cytosol or intracellular fluid which is slightly basic with a pH of 7.2. The interior of lysosomes is acidic at a pH is about 4.5. The efficacy of the anti-clumping coating often depends on the pH of such environment.



The technology developed by the authors can study the behaviour and aggregation of nanoparticles in the variable environment found in biological systems. The authors used dynamic light scattering to measure the aggregation of nanoparticles after pH jumps in aqueous solutions of photoacid generator and ultraviolet light. This avoids the delays from mixing or stirring of the solution.



The authors stress that such studies may improve the design of nanoparticles for tumour treatment where acidity conditions different from normal cells. Also a better understand the environmental, health and safety implications of nanoparticles are expected as outcome of the studies.



[1] Murphy RJ, Pristinski D, Migler K, Douglas JF, Prabhu VM: Dynamic light scattering investigations of nanoparticle aggregation following a light-induced pH jump. The Journal of Chemical Physics, 2010; 132 (19): 194903 DOI: 10.1063/1.3425883

http://jcp.aip.org/jcpsa6/v132/i19/p194903_s1?bypassSSO=1





11.06.2010: Replacing saturated fats [1]

Reviewing studies related to the effects of saturated fats on heart health, Micha and Mozzafarian 2010 found that replacing saturated fatty acids (SFA) with polyunsaturated fat modestly lowers coronary heart disease risk. Replacing SFA with carbohydrate has no benefit and replacing SFA with monounsaturated fat has uncertain effects. Results of studies found mixed and unclear effects of SFA on vascular function, insulin resistance, diabetes, and stroke.

The authors highlight the need of more studies, and warns from public health programs on reducing SFA consumption without considering the replacement nutrient or other food-based risk factors for heart diseases.



Poly unsaturated fats should replace saturated fats and not be reduced in human nutrition [2]

Mozaffarian, Micha and Wallace 2010 report that studies recommend to reduced saturated fat (SFA) consumption to reduce the risk of coronary heart disease (CHD), and some even recommend to lower or limit polyunsaturated fat (PUFA) consumption.



The authors reviewing studies found that PUFAS consumption of 14.9% energy presented a CHD risk reduction of 10%, compared with groups consuming 5.0% PUFAS. The overall pooled risk reduction was 19%, corresponding to 10% reduced CHD risk for each 5% energy of increased PUFAS.

The authors concluded that polyunsaturated fatty acids should therefore be used as replacement of saturated fats and PUFAS should not be reduced as they proved to reduce coronary heart disease.



Trans-fatty acids and their isomers in different food sources [3]

Micha and colleagues 2010 looked at food sources of individual plasma phospholipid trans fatty acid isomers which are known to increases the risk of coronary artery disease.



TFAS were associated with foods made with partially hydrogenated vegetable oils. The authors found including biscuits, chips and/or popcorn, fried foods. Bakery foods were associated with t-18:2 isomers,animal foods, including red measts and butter and high-fat dairy with t-16:1n-7, Margarine was associated with t-16:1n-9 isomers.



The authors stress the importance to consider the isomer forms of trans fatty acids in studies and their different food sources. Isomers of trans fatty acids differ in their health effects.



[1] Micha R, Mozaffarian D: Saturated Fat and Cardiometabolic Risk Factors, Coronary Heart Disease, Stroke, and Diabetes: a Fresh Look at the Evidence. Lipids. 2010 Mar 31.

http://www.ncbi.nlm.nih.gov/pubmed/20354806



[2] Mozaffarian D, Micha R, Wallace S: Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010 Mar 23;7(3):e1000252. Review.

http://www.ncbi.nlm.nih.gov/pubmed/20351774



[3] Micha R, King IB, Lemaitre RN, Rimm EB, Sacks F, Song X, Siscovick DS, Mozaffarian D: Food sources of individual plasma phospholipid trans fatty acid isomers: the Cardiovascular Health Study. Am J Clin Nutr. 2010 Apr;91(4):883-93.

http://www.ncbi.nlm.nih.gov/pubmed/20219966




11.06.2010: Processed meat like bacon and sausages increase risk of heart disease and diabetes, says a meta-analysis [1]

Micha, Wallace and Mozaffarian 2010 found that Consumption of processed meats, but not red meats, is associated with higher incidence of CHD and diabetes mellitus. It takes only 50 g (one hot Dog) of processed meat per day to increase heart disease by 42% and type 2 diabetes by 19%. No link between eating unprocessed red meat like beef or pork and risk of heart disease and diabetes was found by the authors. High levels of salt and nitrate preservatives in sausages, bacon and deli meats, rather than saturated fats, might explain the higher risk of heart disease and diabetes seen with processed meats, but not with unprocessed red meats.



The authors call for studies looking at processed and unprocessed meats separately and focus on salt and nitrate preservatives.



[1] Micha R, Wallace SK, Mozaffarian D: Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis.

Circulation. 2010 Jun 1;121(21):2271-83

http://www.ncbi.nlm.nih.gov/pubmed/20479151




10.06.2010: EPA Moves to Terminate All Uses of Insecticide Endosulfan to Protect Health of Farmworkers and Wildlife. [1]

Endosulfan, a highly controversial organochlorine insecticide and acaricide. It is registered since the 1950s. It is used also is used on vegetables, fruits, cotton, ornamental shrubs, trees, and herbaceous plants. The U.S. Environmental Protection Agency (EPA) is taking action to end all uses of the insecticide in the United States, causing an unacceptable neurological and reproductive risks to farmworkers and wildlife and can persist in the environment.

According to the EPA new data show that the risks are greater than previously known for farmworkers, aquatic and terrestrial wildlife, as well as to birds and mammals that consume aquatic prey which have ingested endosulfan. Endosulfan is used on a very small percentage of the U.S. food supply and does not present a risk to human health from dietary exposure.



Makhteshim Agan of North America, the manufacturer of endosulfan, is in discussions with EPA to voluntarily terminate all endosulfan uses.

The WHO estimates that the worldwide production of endosulfan is 12,800 tons per year.

Due to its acute toxicity, potential for bioaccumulation, and role as an endocrine disruptor it was banned in more than 62 countries, including the European Union and several Asian and West African nations. It is still used extensively in many other countries including India, Brazil, and Australia. It is produced by Bayer CropScience, Makhteshim Agan, and Government-of-India–owned Hindustan Insecticides Limited among others. Because of its threats to the environment, a global ban on the use and manufacture of endosulfan is being considered under the Stockholm Convention. 10.06.2010: EPA Moves to Terminate All Uses of Insecticide Endosulfan to Protect Health of Farmworkers and Wildlife. %5B1%5D Endosulfan, a highly controversial organochlorine insecticide and acaricide. It is registered since the 1950s. It is used also is used on vegetables, fruits, cotton, ornamental shrubs, trees, and herbaceous plants. The U.S. Environmental Protection Agency %28EPA%29 is taking action to end all uses of the insecticide in the United States, causing an unacceptable neurological and reproductive risks to farmworkers and wildlife and can persist in the environment. According to the EPA new data show that the risks are greater than previously known for farmworkers, aquatic and terrestrial wildlife, as well as to birds and mammals that consume aquatic prey which have ingested endosulfan. Endosulfan is used on a very small percentage of the U.S. food supply and does not present a risk to human health from dietary exposure. Makhteshim Agan of North America, the manufacturer of endosulfan, is in discussions with EPA to voluntarily terminate all endosulfan uses. The WHO estimates that the worldwide production of endosulfan is 12,800 tons per year. Due to its acute toxicity, potential for bioaccumulation, and role as an endocrine disruptor it was banned in more than 62 countries, including the European Union and several Asian and West African nations. It is still used extensively in many other countries including India, Brazil, and Australia. It is produced by Bayer CropScience, Makhteshim Agan, and Government-of-India%E2%80%93owned Hindustan Insecticides Limited among others. Because of its threats to the environment, a global ban on the use and manufacture of endosulfan is being considered under the Stockholm Convention.%5B2%5D %5B1%5D EPA to Terminate All Uses of Insecticide Endosulfan To Protect Health of Farmworkers and Wildlife. June 08, 2010. http://www.epa.gov/pesticides/reregistration/endosulfan/endosulfan-cancl-fs.html %5B2%5D Wikipedia: Endosulfan http://en.wikipedia.org/wiki/Endosulfan
[2]



[1] EPA to Terminate All Uses of Insecticide Endosulfan To Protect Health of Farmworkers and Wildlife. June 08, 2010.

http://www.epa.gov/pesticides/reregistration/endosulfan/endosulfan-cancl-fs.html



[2] Wikipedia: Endosulfan

10.06.2010: EPA Moves to Terminate All Uses of Insecticide Endosulfan to Protect Health of Farmworkers and Wildlife. %5B1%5D Endosulfan, a highly controversial organochlorine insecticide and acaricide. It is registered since the 1950s. It is used also is used on vegetables, fruits, cotton, ornamental shrubs, trees, and herbaceous plants. The U.S. Environmental Protection Agency %28EPA%29 is taking action to end all uses of the insecticide in the United States, causing an unacceptable neurological and reproductive risks to farmworkers and wildlife and can persist in the environment. According to the EPA new data show that the risks are greater than previously known for farmworkers, aquatic and terrestrial wildlife, as well as to birds and mammals that consume aquatic prey which have ingested endosulfan. Endosulfan is used on a very small percentage of the U.S. food supply and does not present a risk to human health from dietary exposure. Makhteshim Agan of North America, the manufacturer of endosulfan, is in discussions with EPA to voluntarily terminate all endosulfan uses. The WHO estimates that the worldwide production of endosulfan is 12,800 tons per year. Due to its acute toxicity, potential for bioaccumulation, and role as an endocrine disruptor it was banned in more than 62 countries, including the European Union and several Asian and West African nations. It is still used extensively in many other countries including India, Brazil, and Australia. It is produced by Bayer CropScience, Makhteshim Agan, and Government-of-India%E2%80%93owned Hindustan Insecticides Limited among others. Because of its threats to the environment, a global ban on the use and manufacture of endosulfan is being considered under the Stockholm Convention.%5B2%5D %5B1%5D EPA to Terminate All Uses of Insecticide Endosulfan To Protect Health of Farmworkers and Wildlife. June 08, 2010. http://www.epa.gov/pesticides/reregistration/endosulfan/endosulfan-cancl-fs.html %5B2%5D Wikipedia: Endosulfan http://en.wikipedia.org/wiki/Endosulfan
http://en.wikipedia.org/wiki/Endosulfan




09.06.2010: The hazardous work, working conditions, and environment in India using the example of the Union Carbide plant of Bhopal [1]

Asish Kumar Mandal 2009 reports that hazardous work, working conditions, and environment in India threatens health of workers culminating in the Bhopal Gas Tragedy, in 1984. This accident forced the Indian government to review their legislative measures to improve the occupational health situation. A new National Health Policy was announced in 2002, however, inadequate strategies, policies, and the lack of a proper monitoring mechanism hinder results. The authors presents suggestions how to improve the health conditions of the workers.



Safety of industrial plants and heath issues must attain top priority in occupational health policies, and tight controls of engineering of industrial facilities are necessary, primarily in developing countries, where cost reduction may lead to accidents comparable with the disaster of Bhopal.



Genetic alteration resulting from exposure to methyl isocianate of the Union Carbide plant [2]

Bhargava and colleagues 2010 assessed the immunotoxic effects of methyl isocyanate gas from the Bhopal pesticide plant. The authors found  a significant increase in the levels of all circulating inflammatory biomarkers ((IL-8, IL-1beta, IL-6, TNF, IL-10, IL-12p70 cytokines and C-reactive protein) in the methyl isocianate exposed group, compared to a non-exposed group. The authors suggest that the rise of the inflammatory biomarkers are a result a toxin induced genetic and/or epigenetic alteration, and call for more studies to confirm their results.



Exposure of parents to poisons of the Bhopal accident affected offsprings [3]

Sarangi and colleagues 20101 report that the exposure of parents to toxic gases in the Bhopal incident caused an very high increase of initial 5-year mortality of their offspring. Male offspring of these parents were stunted in growth until puberty, and post-puberty effect on head circumference was found in females exposed to gases in utero.



Clinical findings and genetic implications of the Bhopal accident [4]

More than 500 000 victims survived the tragedy of Bhopal, presenting chronic illnesses such as pulmonary fibrosis, bronchial asthma, chronic obstructive pulmonary disease, emphysema, recurrent chest infections, keratopathy and corneal opacities. Mishra and colleagues 2009 reviewed the clinical findings and trials of the disaster, pointing out that in-utero exposure to methyl isocyanate in the first trimester of pregnancy caused a persistent immune system hyper-responsiveness. The immunotoxic implications and genomic effect of Bhopal gases have been studied in cultured mammalian cells. The authors recommend long-term monitoring of the Bhopal area to analyse the accident to determine the possible elements of the Bhopal cloud and their long-termed effect on humans



The Bhopal disaster [5]

The Bhopal disaster was an industrial disaster that took place at a Union Carbide pesticide plant in the Indian city of Bhopal, Madhya Pradesh. On 3 December 1984, 40 Tons of methyl isocyanate gas were accidentally released from the plant, exposing more than 500,000 people to the poisonous chemicals.. The first official immediate death toll was 2,259. The government of Madhya Pradesh has confirmed a total of 3,787 deaths related to the gas release.Others estimate 8,000-10,000 died within 72 hours and 25,000 have since died from gas-related diseases. 40,000 more were permanently disabled, maimed, or rendered subject to numerous grave illnesses; 521,000 exposed in all.



Some 390 tons of toxic chemicals abandoned at the UCIL plant continue to leak and pollute the groundwater in the region and affect surroundings. In June 2010, seven Indian ex-employees were convicted in Bhopal of causing death by negligence and sentenced to two years imprisonment each.



Warren Anderson, the head of Union Carbide Corp, the company itself and two subsidiary companies were also on trial, but have never appeared in court proceedings.The court in Bhopal asked for the extradition of Anderson.

Union Carbide was found liable for the disaster, but has denied responsibility. Dow says the legal case was resolved in 1989 claiming that Union Carbide paid $470 million as settlement. The responsibility relies now on the government of Madhya Pradesh, which now owns the site.



Causes of the disaster [6]

Water entered a sealed tank containing the highly reactive gas causing pressure in the tank to rise too high. Union Carbide Corp said the accident was an act of sabotage, but could never prove it. Lax safety standards or faulty plant design are most likely to be the real cause. The Central Bureau of Investigation alleges that proper safety procedures had not been followed . The hazardous design of the plant and the additional hazards due to design modifications were known by the leading experts of the company and Warren Anderson.



Cost reductions are the main cause of global hazards

Governments must exert strong supervision of industrial activities of the chemical and petroleum industries. Safety measures are played down to reduce production costs to improve the global competitiveness. This advice is strongly directed to the US government and emerging industrial countries like the Asian region.



[1] Mandal AK: Strategies and policies deteriorate occupational health situation in India: A review based on social determinant framework.Indian J Occup Environ Med. 2009 Dec;13(3):113-20. Doi: 10.4103/0019-5278.58913.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862442/?tool=pubmed



[2] Bhargava A, Punde RP, Pathak N, Dabadghao S, Desikan P, Jain A, Maudar KK, Mishra PK: Status of inflammatory biomarkers in the population that survived the Bhopal gas tragedy: a study after two decades. Ind Health. 2010;48(2):204-8.

http://www.ncbi.nlm.nih.gov/pubmed/20424351



[3] Sarangi S, Zaidi T, Pal RK, Katgara D, Gadag VG, Mulay S, Varma DR: Effects of exposure of parents to toxic gases in Bhopal on the offspring. Am J Ind Med. 2010 Mar 8.

http://www.ncbi.nlm.nih.gov/pubmed/20213748



[4] Mishra PK, Samarth RM, Pathak N, Jain SK, Banerjee S, Maudar KK: Bhopal Gas Tragedy: review of clinical and experimental findings after 25 years. Int J Occup Med Environ Health. 2009;22(3):193-202.

http://www.ncbi.nlm.nih.gov/pubmed/19819837



[5] Indian court convicts 7 in Bhopal gas tragedy. Arab News.com. June 7, 2010.

http://arabnews.com/world/article62200.ece



[6] How the Bhopal gas tragedy trial unraveled: Rediff News June 08, 2010.

http://news.rediff.com/report/2010/jun/08/how-the-bhopal-gas-tragedy-trial-unraveled.htm





06.06.2010: The Nicotera Diet as reference Italian Mediterranean diet [1]

Nicotera, a small town in the Calabria Region in Southern Italy was selected as reference of Mediterranean diet studies. The population of Nicotera has a high consumption of virgin olive olive oil, legumes, vegetables, cereals and fish. Little meat, eggs, Cheese and milk are consumed and men drink red wine moderately.



A very low myocardial infarction of 4 cases out of 598 examined in 1957 in men was reported, together with only few cases of hypertension, overweight and obesity. Similar findings were observed in another study of 1960 at Corfu.



The Nicotera Diet is rich in: Bread, Cereals, legumes, potatoes, vegetables, fresh fruit, nuts, fish, vegetable oils-especially virgin olive oil and moderate red wine consume by men.



Milk, cheese, meat, eggs, animal fat and margarines, sweet beverages, cakes/pies/cookies, sugar are sparingly consumed in the Mediterranean diet.



Italian Mediterranean Diet reduces cardiovascular diseases risk factor and the progression of renal diseases  [2] 

De Lorenzo and colleagues 20101 compared the effects of the Italian Mediterranean Diet, consisting of organic versus conventional foods in a healthy individuals and in Chronic Kidney Disease (CKD) patients in order to decrease cardiovascular diseases risk factor and the progression of renal diseases. The body composition and biochemical parameters after 14 days of Italian Mediterranean Organic Diet, according to the "Nicotera diet" were measured.



The authors report improvements in the levels tHcy, phosphorus, microalbuminuria levels and cardiovascular diseases risk in healthy individuals and in CDK patients.



[1] Flaminio Fidanza, Adalberta Alberti, Daniela Fruttini Simopoulos AP (ed): The Nicotera Diet: The Reference Italian Mediterranean Diet. Nutrition and Fitness: Mental Health, Aging, and the Implementation of a Healthy Diet and Physical Activity Lifestyle. World Rev Nutr Diet. Basel, Karger, 2005, vol 95, pp 115-121

http://www.ncbi.nlm.nih.gov/pubmed/16151276



[2] De Lorenzo A, Noce A, Bigioni M, Calabrese V, Della Rocca DG, Di Daniele N, Tozzo C, Di Renzo L: The effects of Italian Mediterranean organic diet (IMOD) on health status. Curr Pharm Des. 2010;16(7):814-24.

http://www.ncbi.nlm.nih.gov/pubmed/20388092





04.06.2010: Brown algae genetic code may explain origin of higher living beings [1]

Unicellular organisms originated animals, plants, fungi, red algae and brown algae. Researchers decoded the genetic code of the brown alga Ectocarpus siliculosus. This alga performs photosynthesis and is extreme versatile which are central requirements for higher life on earth.



Klaus Valentin, biologist of the Alfred-Wegener-Institute explains that scientist will choose one species of each of these five groups, and decode their genome to search for comparable genetic informations. Ectocarpus siliculosus was chosen as target in the brown algae group. The finding demonstrate that brown algae resulted from the fusion of a green alga with a red alga.



The scientists will perform further studies to see how the alga reacts to drought, UV light and rising temperatures.



The Ectocarpus genome and the evolution of brown algae [2]

Brown algae are photosynthetic organisms differ from plants in their evolution. Their genome contains 214 Millionen DNA base pairs (In molecular biology, two nucleotides on opposite complementary DNA or RNA strands that are connected via hydrogen bonds are called a base pair). Further 16.000 genes were found. Light-harvesting and pigment biosynthesis genes and new metabolic processes such as halide metabolism shows how the alga cope with the variable tidal environment. The evolution of multicellularity in this lineage is correlated with the presence of a rich array of signal transduction genes. A family of receptor kinases was found to be been linked with the emergence of multicellularity in both the animal and green plant lineages.



The Ectocarpus Genome Consortium: The Ectocarpus Genome Project started in June 2004 by an international consortium of 34 laboratories, coordinated in Roscoff, submitted a whole genome sequencing project to the French sequencing centre Genoscope. Automated annotations were obtained using the EuGene system adapted to the specificities of the Ectocarpus genome. [3]



Development and physiology of the brown alga Ectocarpus siliculosus [4]

Charrier and colleagues 2008 stress that brown algae are able to perform photosynthesis and have a cellulosic cell, but are only distantly related to plants considering the evolutionary origin of both groups. Therefore the brown algae present own features and experienced an evolution which was independent from other groups. The authors reviewed the work of the consortium of laboratories, including the Station Biologique in Roscoff and Genoscope, and two centuries of research work on Ectocarpus siliculosus.



A genetic map for the brown alga Ectocarpus siliculosus [5]

Heesch and colleagues 2010 presented A sequence-tagged genetic map for the brown alga Ectocarpus siliculosus which was proposed as a genetic and genomic model for the brown algae a genetic map using microsatellite markers that were designed based on the sequence supercontigs. The genetic map was constructed using 406 markers, resulting in 34 linkage groups. The Ectocarpus genetic map provides a large-scale assembly of the genome sequence and may be useful for further studies of the genetic of Ectocarpus siliculosus. .



[1] Erbgut entziffert. Braunalge verrät, wie höheres Leben entsteht. Spiegel Online 03.06.2010.

http://www.spiegel.de/wissenschaft/natur/0,1518,698444,00.html



[2] Cock JM, Sterck L, Rouzé P, Scornet D, Allen AE, Amoutzias G, Anthouard V, Artiguenave F, Aury JM, Badger JH, Beszteri B, Billiau K, Bonnet E, Bothwell JH, Bowler C, Boyen C, Brownlee C, Carrano CJ, Charrier B, Cho GY, Coelho SM, Collén J, Corre E, Da Silva C, Delage L, Delaroque N, Dittami SM, Doulbeau S, Elias M, Farnham G, Gachon CM, Gschloessl B, Heesch S, Jabbari K, Jubin C, Kawai H, Kimura K, Kloareg B, Küpper FC, Lang D, Le Bail A, Leblanc C, Lerouge P, Lohr M, Lopez PJ, Martens C, Maumus F, Michel G, Miranda-Saavedra D, Morales J, Moreau H, Motomura T, Nagasato C, Napoli CA, Nelson DR, Nyvall-Collén P, Peters AF, Pommier C, Potin P, Poulain J, Quesneville H, Read B, Rensing SA, Ritter A, Rousvoal S, Samanta M, Samson G, Schroeder DC, Ségurens B, Strittmatter M, Tonon T, Tregear JW, Valentin K, von Dassow P, Yamagishi T, Van de Peer Y, Wincker P: The Ectocarpus genome and the independent evolution of multicellularity in brown algae. Nature. 2010 Jun 3;465(7298):617-21.

http://www.ncbi.nlm.nih.gov/pubmed/20520714



[3] Ectocarpus Genome Project: Bioinformatics University of Gent Belgium

http://bioinformatics.psb.ugent.be/genomes/view/Ectocarpus-siliculosus



[4] Charrier B, Coelho SM, Le Bail A, Tonon T, Michel G, Potin P, Kloareg B, Boyen C, Peters AF, Cock JM: Development and physiology of the brown alga Ectocarpus siliculosus: two centuries of research. New Phytol. 2008;177(2):319-32.

http://www.ncbi.nlm.nih.gov/pubmed/18181960



[5] Heesch S, Cho GY, Peters AF, Le Corguillé G, Falentin C, Boutet G, Coëdel S, Jubin C, Samson G, Corre E, Coelho SM, Mark Cock J: A sequence-tagged genetic map for the brown alga Ectocarpus siliculosus provides large-scale assembly of the genome sequence. New Phytol. 2010 Apr 28.

http://www.ncbi.nlm.nih.gov/pubmed/20456050





04.06.2010: Phycodnaviruses may alter geochemical cycling and weather patterns [1]

Dunigan and colleagues 2006 point out that the family Phycodnaviridae consists of six genera. Their genomes range from 160 to 560kb. The phycodnaviruses have evolutionary roots that connect with several other families of large DNA viruses, referred to as the nucleocytoplasmic large DNA viruses (NCLDV).



The genome analyses have revealed more than 1000 unique genes, but only 14 homologous genes held in common among the three genera of the phycodnavirses which stands for a high gene diversity.



The authors stress the importance of phycodnaviruses infections of the phytoplankton because their effect may alter geochemical cycling and weather patterns.



Wilson, Van Etten and Allen 2009 reinforce the importance of the phycodnaviruses on infections of phytoplankton and their global global affects, on water biology. [2]



Large dsDNA viruses is integrated in the DNA of Ectocarpus siliculosus [3]

The Ectocarpus siliculosus virus-1 (EsV-1) is a lysogenic dsDNA virus belonging to the super family of nucleocytoplasmic large DNA viruses (NCLDV). It infects the brown alga Ectocarpus siliculosus. Delaroque and Bolan 2008 reports that the viral genome is integrated into the DNA of the alga.

In this study labelled EsV-1 DNA was used to identify the integration sites of the viral genome.



The authors found that some of the gene products are not encoded by EsV-1 but are present in the genome of other members of the NCLDV family, suggesting that the Ectocarpus algal genome contains traces of the integration of a large dsDNA viral genome and may be the ancestor of the extant NCLDV genomes. These viral DNA pieces might have originated EsV-1 genome through a complex integration and recombination system, using an enzyme similar to a new class of tyrosine recombinases. The authors concluded that some dsDNA viruses evolved principally through genome reduction.



Phycodnaviridae are large DNA algal viruses [4]

Van Etten and colleagues 2002 describes the genome of the Ectocarpus siliculosus virus (EsV-1) and the Paramecium bursaria chlorella virus (PBCV-1). Both are members of the family Phycodnaviridae . They infect eukaryotic algae. The 336 kb genome of EsV-1 has approximately 231 protein-encoding genes. The 331 kb genome of PBCV-1 genome has 11 tRNA genes and approximately 375 protein-encoding genes.



The two viruses have only 33 genes in common because of their different habitat. EsV-1 infects a marine brown alga, and PBCV-1 infects freshwater green algae.



[1] Dunigan DD, Fitzgerald LA, Van Etten JL: Phycodnaviruses: a peek at genetic diversity. Virus Res. 2006 Apr;117(1):119-32. Epub 2006 Mar 6.

http://www.ncbi.nlm.nih.gov/pubmed/16516998



[2] Wilson WH, Van Etten JL, Allen MJ: The Phycodnaviridae: the story of how tiny giants rule the world. Curr Top Microbiol Immunol. 2009;328:1-42.

http://www.ncbi.nlm.nih.gov/pubmed/19216434



[3] Delaroque N, Boland W: The genome of the brown alga Ectocarpus siliculosus contains a series of viral DNA pieces, suggesting an ancient association with large dsDNA viruses. BMC Evol Biol. 2008 Apr 12;8:110.

http://www.ncbi.nlm.nih.gov/pubmed/18405387



[4] Van Etten JL, Graves MV, Müller DG, Boland W, Delaroque N: Phycodnaviridae--large DNA algal viruses. Arch Virol. 2002 Aug;147(8):1479-516.

http://www.ncbi.nlm.nih.gov/pubmed/12181671