Monthly Archives: June 2012

Pthalate exposure linked to obesity and eczema in children in new studies


Presented at the Endocrine society’s annual meeting in Houston. A research study suggests plastics may alter fat metabolism.  Phthalates are manufactured, endocrine-disrupting chemicals that can mimic the body’s natural hormones. Phthalates are primarily used to soften polyvinyl chloride (PVC) in products.
Click here to read the 2012 obesity study by pediatrist Dr Mi-Jung Par which reports that children with the highest levels of a common pthalate (DEHP) in their blood were five times likely to be obese as children with the lowest levels of this pthalate.
Click here to read the 2012 eczema study by Dr Alan Just and colleagues at Columbia Center of Children’s Environmental Health, NY: Prenatal exposure to a pthalate (BBzP) commonly found in household dust and vinyl flooring may increase a child’s risk of developing eczema. Click here to read more.

DEHP may do two different things that increase fat development, Park said. It may reduce the effect of androgen — a male sex hormone — which lowers body-mass index (BMI). It may also disrupt thyroid function, which plays a role in weight gain. Interfering with androgen or thyroid hormones can affect appetite or a person’s rate of metabolizing food..Click here to read more.

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Why the same drug acts differently in two people: how your NAT2 genes dictate the drug’s action in your body


Two people are in pain. Both of you take the same drug; one of you feels in less pain faster than the other. How? Why? The answer, that your genes may be different is making the drug manufacturers wonder if they can take better care of your health by first requesting a genetic test. Could it be, that a drug might be personalized to work just for your genes? Sure, say most drug manufacturers. The advantage would be that there would be fewer bad reactions from two people taking the same drug with exactly similar prescriptions, but with one person showing side reactions, while the other is simply fine.

Personalized Medicine
Many factors control why you respond differently to the same drug from another person. One is the gene factor. Allow me to enlarge upon a single gene called NAT2. I choose this gene because it is my favorite gene. It explains so much so simply. When a drug company develops a drug through clinical trials it tries to judge dosage by weight and height and more complex formulae. None, however, take into account that the genes may have subtle differences, although the drug companies may have researched and stored this data. Today, a drug company sells one drug to all people. Soon the day is coming when the drug company will ask you, “How do you want your drug?” Well, not exactly that phrase. They will test your genes, figure out what your body can tolerate and then calculate a dose close to what you should be able to tolerate.

Here’s how one gene controls your body’s drug reaction
Genetic variability in the NAT2 gene has long been recognized to be the cause of differential ability to metabolize a variety of medicinal drugs. The NAT2 gene produces an enzyme mainly in the intestine and liver. It detoxifies through arylhydrazine compounds. NAT2 gene produces important enzymes that breakdown drugs for major diseases like tuberculosis. Some people have a variation of the NAT2 gene that may make them more susceptible to bladder cancer. Which means that if you have a different variation of the gene you may rest assured you may never get bladder cancer, no matter what you eat or which water you wade into.

International anthropologists have gathered vast amounts of genetic data from various world populations (click hereto read). It shows that if your ancestors were hunter – gatherers then, your NAT2 gene was different than if your ancestors were agricultural – pastoral.

The NAT2 gene will control your destiny.  Soon, perhaps, NAT2 gene will be a household word, discussed just like your high blood pressure or baldness in the family. Either you have the NAT2 gene that is a drug manufacturer’s dream, or can never have bladder cancer, or have to have a personalized drug manufactured for your ability to breakdown the drug for your disease. You will care to know more about this gene. NAT2 is already working inside you. Are you working for your own NAT2 or your neighbor’s NAT2 is the question?

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The Gut Microbiota: your good germ friends to nurture to strengthen your immune system against “Allergy”


Your gut has both good microbes and sometimes, dangerous microbes. The trick is to know how to encourage the good microbes to grow inside your gut while creating a very difficult environment for the bad microbes inside your body. The good microbes codevelop inside your body since birth say a wonderful international group of physician and microbial scientists from five countries including Singapore, Sweden, USA, England and France. What germs your body can harbor depends firstly on your genes, and that means not everybody can tolerate all good microbes. Following your personal genes through your personal nutrition choices tailored to your specific lifestyle decides your microbiota. Believe it or not, your gut microbes control your brain, muscles, and your liver through your gut cells. Gives a whole new meaning to the term, “You are what you eat”. I would not add, “Your brain is what you eat”. These scientists strongly suggest that it is imperative to understand the individual gut microbiota, which means your good microbes, to get a better understanding of how to keep your brain and your muscles in peak performance by assisting your immune regulatory system. Apparently, your immune system is assisted by your good microbes. David Artis and his team at University of Pennsylvannia have become the leading scientists calling for an overhaul of the study of what is allergy and the immune system, based on gut microbiota research.

Have you ever wondered how that poor kid playing in the filth is healthier than your kid brought up in a sterilized home and school environment and playground? Well, the answer may lie in the good microbes that co-develop in the gut since birth. The articles below may be of interest to you. Your gut is “infested” fortunately by trillions of beneficial microbes that occupy their own favorite niches inside the intestine, as it folds its way inside your body. You might want to reconsider next time you have that antibiotic – it may indiscriminate and kill the bacteria that help you along with that single one that is harming you, currently. Have you ever wondered how some people are better able to “fight” off infection? They may actually have a stronger gut.  The term “my gut reaction” may not be that funny after all!

1)  Host-Gut Microbiota Metabolic Interactions
2) Crossover Immune Cells Blur the Boundaries
3) Innate Lymphoid Cells Promote Anatomical Containment of Lymphoid-Resident Commensal Bacteria
4) Immunology: Allergy challenged

1)  Host-Gut Microbiota Metabolic Interactions

Published Online June 6 2012
Science 8 June 2012:
Vol. 336 no. 6086 pp. 1262-1267
DOI: 10.1126/science.1223813
  • REVIEW

Host-Gut Microbiota Metabolic Interactions

  1. Jeremy K. Nicholson1,*,
  2. Elaine Holmes1,
  3. James Kinross1,
  4. Remy Burcelin2,
  5. Glenn Gibson3,
  6. Wei Jia4,
  7. Sven Pettersson5,*

+Author Affiliations


  1. 1Biomolecular Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Exhibition Road, South Kensington, London SW7 2AZ, UK.

  2. 2Institut National de la Santé et de la Recherche Médicale, U1048, and Institut des Maladies Métaboliques et Cardiovasculaire I2MC, Rangueil Hospital, BP84225, 31432 Toulouse, France.

  3. 3Department of Food and Nutritional Sciences, The University of Reading, Whiteknights, Reading, UK.

  4. 4Department of Nutrition, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA.

  5. 5Department of Microbiology, Tumor, and Cell Biology (MTC), Karolinska Institutet, Stockholm 117 77, Sweden, and School of Biological Sciences and National Cancer Centre, 11 Hospital Drive, Singapore 169610.
  1. *To whom correspondence should be addressed. E-mail: j.nicholson@imperial.ac.uk (J.K.N.);sven.pettersson@ki.se (S.P.)

ABSTRACT

The composition and activity of the gut microbiota codevelop with the host from birth and is subject to a complex interplay that depends on the host genome, nutrition, and life-style. The gut microbiota is involved in the regulation of multiple host metabolic pathways, giving rise to interactive host-microbiota metabolic, signaling, and immune-inflammatory axes that physiologically connect the gut, liver, muscle, and brain. A deeper understanding of these axes is a prerequisite for optimizing therapeutic strategies to manipulate the gut microbiota to combat disease and improve health.

 2) Crossover Immune Cells Blur the Boundaries

NEWS FOCUSIMMUNOLOGYCrossover Immune Cells Blur the Boundaries

  • Mitch Leslie

Science 8 June 2012: 1228-1229.

3)

Published Online June 6 2012
Science 8 June 2012:
Vol. 336 no. 6086 pp. 1321-1325
DOI: 10.1126/science.1222551
  • REPORT

Innate Lymphoid Cells Promote Anatomical Containment of Lymphoid-Resident Commensal Bacteria

  1. Gregory F. Sonnenberg1,
  2. Laurel A. Monticelli1,
  3. Theresa Alenghat1,
  4. Thomas C. Fung1,
  5. Natalie A. Hutnick2,
  6. Jun Kunisawa3,4,
  7. Naoko Shibata3,4,
  8. Stephanie Grunberg1,
  9. Rohini Sinha1,
  10. Adam M. Zahm5,
  11. Mélanie R. Tardif6,
  12. Taheri Sathaliyawala7,
  13. Masaru Kubota7,
  14. Donna L. Farber7,
  15. Ronald G. Collman8,
  16. Abraham Shaked9,
  17. Lynette A. Fouser10,
  18. David B. Weiner2,
  19. Philippe A. Tessier6,
  20. Joshua R. Friedman5,
  21. Hiroshi Kiyono3,4,11,
  22. Frederic D. Bushman1,
  23. Kyong-Mi Chang8,12,
  24. David Artis1,13,*

+Author Affiliations


  1. 1Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

  2. 2Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

  3. 3Division of Mucosal Immunology, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.

  4. 4Department of Medical Genome Science, Graduate School of Frontier Science, The University of Tokyo, Chiba 277-8562, Japan.

  5. 5Department of Pediatrics, Division of Gastroenterology, Hepatology, and Nutrition, Perelman School of Medicine, University of Pennsylvania, Children’s Hospital of Philadelphia, Philadelphia, PA 19104, USA.

  6. 6Centre de Recherche en Infectiologie, Centre Hospitalier de l’Université Laval, Faculty of Medicine, Laval University, Quebec, Canada.

  7. 7Department of Surgery and the Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY 10032, USA.

  8. 8Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

  9. 9Department of Surgery, University of Pennsylvania, Philadelphia, PA 19104, USA.

  10. 10Inflammation and Immunology Research Unit, Biotherapeutics Research and Development, Pfizer Worldwide R&D, Cambridge, MA 02140, USA.

  11. 11Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Tokyo 102-0075, Japan.

  12. 12Philadelphia VA Medical Center, Philadelphia, PA 19104, USA.

  13. 13Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  1. *To whom correspondence should be addressed. E-mail: dartis@mail.med.upenn.edu

ABSTRACT

The mammalian intestinal tract is colonized by trillions of beneficial commensal bacteria that are anatomically restricted to specific niches. However, the mechanisms that regulate anatomical containment remain unclear. Here, we show that interleukin-22 (IL-22)–producing innate lymphoid cells (ILCs) are present in intestinal tissues of healthy mammals. Depletion of ILCs resulted in peripheral dissemination of commensal bacteria and systemic inflammation, which was prevented by administration of IL-22. Disseminating bacteria were identified as Alcaligenes species originating from host lymphoid tissues. Alcaligenes was sufficient to promote systemic inflammation after ILC depletion in mice, and Alcaligenes-specific systemic immune responses were associated with Crohn’s disease and progressive hepatitis C virus infection in patients. Collectively, these data indicate that ILCs regulate selective containment of lymphoid-resident bacteria to prevent systemic inflammation associated with chronic diseases.

  • Received for publication 28 March 2012.
  • Accepted for publication 24 April 2012.

Immunology: Allergy challenged

Nature

 484,

458–459

(26 April 2012)

doi:10.1038/484458a

Published online

 25 April 2012

An article suggesting that allergic responses may not be an accident of an off-target immune system, but rather a deliberate defence against potential harm, provokes the question of whether our understanding of allergy needs an overhaul. Immunologists provide their opinions. See Perspective p.465

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Author information

Affiliations

  1. David Artis is in the Department of Microbiology and the Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

  2. Rick M. Maizels is at the Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh EH9 3JT, UK.

  3. Fred D. Finkelman is in the Department of Medicine, Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio 45220, USA, and in the Department of Internal Medicine, University of Cincinnati College of Medicine, and the Division of Cellular and Molecular Immunology, Cincinnati Children’s Hospital Medical Center.

Corresponding authors

Correspondence to:

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The world’s top influenza (Flu) research laboratories decided to institute a self-imposed moratorium


Should research work that attempts to make the H5N1 virus more potent, virulent, dangerous and transmissible under laboratory conditions be allowed? A meeting will be held in New York in July that will discuss whether the voluntary ban should be lifted.

The controversy over influenza risky levels of research ban and non-publication issues began over research by Netherlands researchers. They took an influenza (flu) virus that previously could only infect birds. They selected mutations from Influenza (Flu) viruses that had caused human pandemics with millions of deaths in 1918, and other years. They combined these mutations with the bird (avian) flu virus and passed it through ferrets. The reason they passed it through ferrets was that these animals most closely resemble how a person behaves when they are sick with the flu – the ferrets sneeze. The flu virus changed a little bit with each passage helped by the scientist to pass it from one sick ferret to a healthy ferret. In the first passage the scientist had to help or assist the mutant bird virus to infect the ferret by actually introducing it into the ferret. It could not “fly” through the air when the infected ferret sneezed to infect a healthy ferret in the vicinity. However, by the fifth passage onwards, this bird flu virus had mutated or picked up the ability to infect a healthy ferret by “flying” through the air in a sneeze pellet released by a sick ferret. The Dutch scientists could show how a new dangerous flu virus could emerge to cause a pandemic in people by existing previously in birds only, but by picking up mutations in flu virus infecting other animals or people and becoming able to “fly” in the air and infect a population. The scientists feel that knowing this ability will help them arm in advance and better equip governments to prepare in advance for the next pandemic. None of the ferrets died from this infection, a result of genetic engineering and multiple ferret transmission.

This research, by Ron Fouchier, PhD, of Erasmus Medical Center in the Netherlands and colleagues, was announced in a meeting of scientists and along with other researchers announcing their research on similar topics. Click here to read the reaction of the other researchers and policy makers present. Derek Smith, of the University of Cambridge, coauthored the second science paper, on June 21, 2012 gave a press release saying that such a pandemic event was in the realm of reality. Yoshihiro Kawaoka at the University of Wisconsin–Madison, published online by Nature discovered how the flu virus recognizes and stabilizes on a host cell through a protein during an influenza attack process. (Every human being is made up of several cells, as are all living things like birds, ferrets and plants; just in case you did not have a biology class in school. Also, a virus is not a bacterium. Only bacterial diseases can be cured by antibiotics. Viral diseases cannot be fought or cured by antibiotics).

The Dutch people were pondering on not allowing publication of research that might be dangerous in the hands of the wrong scientist, who might want to hurt all people. This view was contested by other scientists, including Nobel prize winner and head of the National Institute of Health, USA, who believe that the Dutch scientists research and similar research by University of Wisconsin scientists should be published in full. Click here to read what proposals made the Dutch Government reconsider their decision on banning this pubication of a bird flu study.

So, the question here is:
Is it better to be knowleadgeable and thus prearmed and prepared for the pandemic war that could possibly arise in the near future given the three deadly pandemics since the first one in 1918 last century?
Or,
is it better to just wait and see what hits the public with a severe health blow to millions of people (about 50 million are estimated to have died in 1918) and then figure out what flu combination is causing the pandemic and look for scientists available to find a vaccine to prevent further spread?
You may contact via email: r.fouchier@erasmusmc.nl This group did show that …”The transmissible viruses were sensitive to the antiviral drug oseltamivir”….

Related Articles about the controversial flu virus current research
Bird flu study published after terrorism debate ….could start a deadly pandemic among humans. These initial findings were presented last September in Malta at the European Scientific Working group on Influenza meeting to an auditorium packed with fellow scientists and policy makers…
Fouchier anticipates resuming H5N1 studies soon….said the voluntary 60-day moratorium on lab-modified H5N1 viruses expired Mar 20 and added that researchers are waiting for national governments to release their lab biosecurity assessments. These assessments were a component of a plan stemming from a World Health Organization (WHO) meeting of technical experts in February.

Fouchier made his comments during a live episode of virologist Vincent Racaniello’s “This Week in Virology” (TWiV), which was broadcast via webcast from the Society for General Microbiology conference in Dublin, Ireland. Racaniello, a virologist at Columbia University, authors Virology Blog and hosts the weekly virology podcast series.

Fouchier’s group at Erasmus and a University of Wisconsin team led by Yoshihiro Kawaoka, DVM, PhD, conducted experiments that involved engineering an H5N1 virus and an H1N1-H5N1 hybrid, respectively, that were transmissible in ferrets via airborne droplets.

The studies have been accepted for publication in Science and Nature, but advisors to the US government in December recommended against publishing the full details of the studies, due to bioterrorism concerns….
Debate Persists Over Publishing Bird Flu Studies – you may click to hear a NPR discussion on this subject by biosecurity expert D.A. Henderson on the risks of publishing the research.
N.Y. Times: H5N1 ferret research should not have been done – by virology blog shows the New York Times editorial on 8 January 2012, entitled ‘An Engineered Doomsday’.
Mutant-flu paper published: Controversial study shows how dangerous forms of avian influenza could evolve in the wild. By Ed Yong on 02 May 2012 in Nature.com …Kawaoka found that the hybrid virus could spread between ferrets in separate cages after acquiring just four mutations. Three of these allow the HA protein to stick to receptor molecules on mammalian cells, and the fourth stabilizes the protein. “Before we initiated this experiment, we knew that receptor specificity is important,” says Kawaoka. “We didn’t know what else was needed.”…

Related Articles: The Controversial Flu virus papers being discussed above
1. Airborne Transmission of Influenza A/H5N1 Virus Between Ferrets in Science 22 June 2012: Vol. 336 no. 6088 pp. 1534-1541
by Sander Herfst and colleagues – A report. (…..The genetically modified A/H5N1 virus acquired mutations during passage in ferrets, ultimately becoming airborne transmissible in ferrets. None of the recipient ferrets died after airborne infection with the mutant A/H5N1 viruses. Four amino acid substitutions in the host receptor-binding protein hemagglutinin, and one in the polymerase complex protein basic polymerase 2, were consistently present in airborne-transmitted viruses. ……)
2. Pathogenesis and Transmission of Swine-Origin 2009 A(H1N1) Influenza Virus in Ferrets / http://www.sciencexpress.org / 2 July 2009 / Page 1 / 10.1126/science.1177127
3. Severity of Pneumonia Due to New H1N1 Influenza Virus in Ferrets Is Intermediate between That Due to Seasonal H1N1 Virus and Highly Pathogenic Avian Influenza H5N1 Virus. J Infect Dis. (2010) 201 (7): 993-999. doi: 10.1086/651132

Related Articles about the history of the Flu virus and vaccine development
History of the 1918 pandemic and the search for a vaccine
Should I get a flu vaccine this year?
Why am I feeling fatigued after getting the flu vaccine?

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Expression of novel genes in response to various stimuli in the human dermatophyte Trichophyton rubrum

Abstract

Background

Cutaneous mycoses are common human infections among healthy and immunocompromised hosts, and the anthropophilic fungus Trichophyton rubrum is the most prevalent microorganism isolated from such clinical cases worldwide. The aim of this study was to determine the transcriptional profile of T. rubrum exposed to various stimuli in order to obtain insights into the responses of this pathogen to different environmental challenges. Therefore, we generated an expressed sequence tag (EST) collection by constructing one cDNA library and nine suppression subtractive hybridization libraries.

Results

The 1388 unigenes identified in this study were functionally classified based on the Munich Information Center for Protein Sequences (MIPS) categories. The identified proteins were involved in transcriptional regulation, cellular defense and stress, protein degradation, signaling, transport, and secretion, among other functions. Analysis of these unigenes revealed 575 T. rubrum sequences that had not been previously deposited in public databases.

Conclusion

In this study, we identified novel T. rubrum genes that will be useful for ORF prediction in genome sequencing and facilitating functional genome analysis. Annotation of these expressed genes revealed metabolic adaptations of T. rubrum to carbon sources, ambient pH shifts, and various antifungal drugs used in medical practice. Furthermore, challenging T. rubrum with cytotoxic drugs and ambient pH shifts extended our understanding of the molecular events possibly involved in the infectious process and resistance to antifungal drugs.

Background

Trichophyton rubrum is a cosmopolitan dermatophyte that colonizes human skin and nails and is the most prevalent cause of human dermatophytoses [1,2]. During the initial stages of the infection, dermatophytes induce the expression of adhesins and unspecific proteases and keratinases that have optimum activity at acidic pH values [3], which is probably because the human skin has an acidic pH value [4]. The secretion of these proteases, which have been identified as an important step in fungal pathogenicity and virulence [5,6], act on keratinous and nonkeratinous substrates to release peptides that are further hydrolyzed to amino acids by putative peptidases. The metabolism of some amino acids shifts the extracellular pH from acidic to alkaline values at which most known keratinolytic proteases have optimal enzymatic activity[79]. T. rubrum also responds to the environmental pH by altering its gene expression profile[9,10].

Molecular studies have been performed with human pathogens such as Candida albicans,Histoplasma capsulatum, and Paracoccidioides brasiliensis, and the results thus obtained have helped to determine the fungal transcriptional profile and characterize the genes involved in host-pathogen interactions and environmental stress responses [1113]. Previously, a collection of T. rubrum expressed sequence tags (ESTs) was obtained from distinct developmental phases[14,15]. However, determining the transcriptional profiles in response to different cell stimuli is necessary for extending our understanding of diverse cellular events, and the results from such studies may reveal new signal transduction networks and the activation of specific metabolic pathways. Functional analysis of the genes involved in these molecular events will help in evaluating their roles as putative cellular targets in the development of new antifungal agents.

Our study aimed to extend the T. rubrum genomic database by adding expressed gene resources that cover different aspects of cellular metabolism. Moreover, the data can help to generate useful information to screen valuable genes for functional and postgenomic analyses. The EST collection described here revealed the metabolic adaptations of the human pathogen T. rubrum to changes in the ambient pH and carbon sources and also provided information on the adaptive responses to several cytotoxic drugs. 

__________________________________________________________________________________

Transcriptional profiling reveals the expression of novel genes in response to various stimuli in the human dermatophyte Trichophyton rubrum

Nalu TA Peres1Pablo R Sanches1Juliana P Falcão1,3Henrique CS Silveira1Fernanda G Paião1Fernanda CA Maranhão1Diana E Gras1Fernando Segato1Rodrigo A Cazzaniga1,Mendelson Mazucato1Jeny R Cursino-Santos1Roseli Aquino-Ferreira1Antonio Rossi2and Nilce M Martinez-Rossi1*

Author Affiliations

1Departamento de Genética, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto 14049-900, SP, Brazil

2Departamento de Bioquímica e Imunologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto 14049-900, SP, Brazil

3Current address: Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, 14040-903, Ribeirão Preto, SP, Brazil

For all author emails, please log on.

 
 
 
 

BMC Microbiology 2010, 10:39 doi:10.1186/1471-2180-10-39

 

The electronic version of this article is the complete one and can be found online at:http://www.biomedcentral.com/1471-2180/10/39

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June 20, 2012 · 11:48 pm

Proteins neuroligins and neurexins are important in Autism and Schizophrenia


Although heredity has been implicated in over 80% of Autism and Schizophrenia and Bipolar disorder cases, no single gene or cluster of genes has stood out to be the culprit or cause for these disorders. Genes are normally present as a single entity on a chromosome strand. Sometimes, more than one copy of a gene on a strand may be present. The copy number of genes that encode for proteins neurexins and neuroligin are variable and likely to be present in some individuals who have autism or schizophrenia. However, they may not be the cause of autism or schizophrenia in every  individual carrying a copy number variation of these genes. This complicates research.  Another external factor has to be the “triger” which when present (could it be an environmental toxin or perhaps a bout of gastroenteritis during a MMR vaccine shot or an unknown factor/s) along with a variable copy number of neurexin or neuroligin gene may result in an autistic child or a schizophrenic individual.

Abstract

There is strong evidence that genetic factors make substantial contributions to the etiology of autism, schizophrenia and bipolar disorders, with heritability estimates being at least 80% for each. These illnesses have complex inheritance, with multiple genetic and environmental factors influencing disease risk; however, in psychiatry, complex genetics is further compounded by phenotypic complexity. Autism, schizophrenia and bipolar disorder are effectively syndromic constellations of symptoms that define groups of patients with broadly similar outcomes and responses to treatment. As such the diagnostic categories are likely to be heterogeneous and the boundaries between them somewhat arbitrary. Recent applications of whole-genome technologies have discovered rare copy number variants and common single-nucleotide polymorphisms that are associated with risk of developing these disorders. Furthermore, these studies have shown an overlap between the genetic loci and even alleles that predispose to the different phenotypes. The findings have several implications. First, they show that copy number variations are likely to be important risk factors for autism and schizophrenia, whereas common single-nucleotide polymorphism alleles have a role in all disorders. Second, they imply that there are specific genetic loci and alleles that increase an individual’s risk of developing any of these disorders. Finally, the findings suggest that some of the specific genetic loci implicated so far encode proteins, such as neurexins and neuroligins, that function in synaptic development and plasticity, and therefore may represent a common biological pathway for these disorders.

One cannot help wondering naturally, if Autism and Schizophrenia can be prevented. With more research on genetics and environment or trigger, with a lot of public help. What kind of help? If the research community joined the public community to form a scientific table of exposures and gene copy variation and family occupations and bouts of gastroenteritis a few months before or after vaccination and toxic spill near home community or home built on previously heavily fertilized agricultural land or father working in a pesticide or herbicide exposed occupation or home lawn heavily sprayed with a pesticide or herbicide or community water exposed to run-off from pesticide and herbicide or a toxic dump site and so much more. Science research is not funded enough to recruit large scale public help or to inspire large community assistance. Together we can tackle this scourge and prevent future cases of Autism, and perhaps Schizophrenia. Inspire your community to encourage scientists to join in a larger than ever world-wide community to volunteer information in a legitimate manner that can be scientifically analyzed. Together we can do it!

A journal article published in Genome Medicine 2009, 1:102  by Liam S Carroll and Michael J Owen, which you may click here to read, researchers the genetics in detail described above. An excerpt is quoted below.

Background

It has long been recognized that psychiatric disorders and symptoms aggregate in families and the evidence for a substantial role for genetic factors is incontrovertible [1]. Genetic epidemiological studies of autism, bipolar disorder and schizophrenia show that the risk of developing one of these specific psychiatric illnesses is proportional to the amount of genetic material shared with an affected individual [1]. Heritability has been estimated as being at least 80% for all these disorders [24], which, to put it in context, is equivalent to that for type I diabetes (about 80%) [5] but greater than that for breast cancer [6] or Parkinson’s disease [7].

 Do encourage this researcher with requests for further research on this topic if you appreciated this research group’s work. Do write to the research lab, do invite them for talks if they are near you, and do encourage them in your own unique style. Mention that you enjoyed their 2009 journal article on the variable gene copy number of the brain proteins.
Email:   Michael J Owen OwenMJ@cf.ac.uk
Address:
Liam S Carroll and Michael J Owen
MRC Centre for Neuropsychiatric Genetics and Genomics,
Department of Psychological Medicine and Neurology, Cardiff University,
Henry Wellcome Building, Heath Park,
Cardiff CF14 4XN, UK

http://genomemedicine.com/content/1/10/102

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Destroying the Holy river Ganges by building a dam before we have understood the healing properties of the river


The Indian Government is planning to build a dam on the sacred river Ganges to help provide electricity to the people of India. The problem is that the river Ganges is considered Holy because it has been claimed to have miracle healing powers through the centuries. There is a gallon of water bottled by the University of Calcutta, West Bengal, India which several decades later has still no bacterial contamination. How is that?

The Fisherman on the River Ganga (Ganges) by Sumit Sen

The Fisherman on the River Ganga (Ganges) by Sumit Sen

A microbiological answer?
The interests of a record 120 million devotee bathers this year attending the Kumbh Mela this year could not be ignored by the Government of India. They requested that the tanneries and other small industries along the river defer the release of toxic pollutants, such as chromium, into the river during this festival. Prevention of toxic chemical release should be enforced all year round, and is excellent public policy. Perhaps, such a policy deserves more vigorous support than building a dam over a river providing millions with healing relief; something modern medicine cannot fathom, simply because modern medicine has yet to master the intricacies of the human brain and immune system. Read “India Stems Tide of Pollution Into Ganges River“, by National Geographic.

Why do people claim to feel healthier after bathing or tasting this water? Why do people say their sick babies are miraculously cured after being dipped in the “Holy river Ganga”? Why do environmental scientists show that this river decomposes organic matter 20-30 times faster than any other river? They do not have an answer and neither do any microbiologists to date.  None of us truly understand the power of nature.  True the holy river has been declared polluted beyond what is safe for human consumption and also unsafe to be used as irrigation water. Yet, millions of people continue to bathe and drink the Holy water straight from the river and live to talk about it. How does this Holy water continue to safely allow people to “taste” and bathe in it? What are it’s “magical” properties? Is there a microbiological answer or is it an answer that we are unequipped to answer with the current technology available but may have the tools to answer some day in the future?  Perhaps for the same reasons people claim it is healthier to swim in the ocean rather than the swimming pool because of the oceans “magical curing properties”.

Dam this Holy river
It appears we may not have much of an opportunity though. The Indian government has decided to dam this Holy river, despite widespread protests and polite requests to leave this Holy river alone.  Building dams to provide electricity is old technology.  Today, there are alternative energy options to be pursued for providing electricity such as solar panels and wind turbines.  Northern India has plenty of sunny, hot and windy days.  Alternative energy options must be actively explored for long-term solutions – finite resources being shared by exploding population growth.  People of India are patient and can tolerate great personal inconveniences to preserve their nature. The Holy Ganges is more precious to them than their electricity needs.

The Holy place where the Kumbh Mela is held every 12 years
When the nature of the miracle of the Holy river Ganges is not understood, how can it be lost to society by being damed? The Triveni Sangam are holy places in India where two actual rivers and a third “mythical” or “under-terrestrial” river meet.  Yes, there are a few such holy places where “three rivers” meet in India.  The river Ganges (Ganga) runs through the ancient city of Prayag, which is modern Allahabad, and meets the river Yamuna (Jamuna), and the river Ganga also meets the ocean, at the Bay of Bengal Delta.  The meeting of these two Yamuna and Ganga rivers is easily observed. The Yamuna is quite deep and of a different color while the Ganga is only a few feet deep. Yet, a third river, Saraswati, is said to be meeting these two rivers. The devotees cannot “see” this third river but “know” it exists. The Triveni Sangam in Prayag (Allahabad) is where the three rivers, Jamuna, Ganga and Saraswati meet; and every 12 years, this is the site of the Kumbh Mela; a month long holy festival attended by several million devotees.

To question this devotion is to try to understand if ancient Indians knew the geology and geography of rivers, their origins, and destinations, using a method modern scientists have not understood. After all, what is an undercurrent? Why is a tsunami so unexpected? Why do rivers originate? Do modern scientists know where all rivers originate? Why do all rivers meet other rivers? Do all rivers meet other rivers? Why do most rivers end in the ocean, or do they? Do all rivers run “above ground”? After all, we do understand the concept of “ground water” which we tap for building our wells. Where does this “ground water” originate, does it meet other rivers at “Triveni Sangams” in an “under-terrestrial method” and then end in the ocean or does ground water never meet other “above ground” rivers and oceans? Do all countries have “Triveni Sangams” or is India the only country with more than one Triveni Sangams? Perhaps, the gurus of ancient India had knowlege of water ways which other countries had not begun to explore.

It is certainly a matter of contemplation before contempt. Only the ignorant choose to belittle the depth of unwritten knowledge of ancient India, passed down through generations of “mythological” stories. India (Bharat) is over 10,000 years old and assuming ancestral humans were just curious as modern humans, geological explorations must have delivered cumulative results over the years and the concept of “Triveni Sangam” was chosen to be preserved. Why?

Why was Mahatma Gandhi cremated at this Triveni Sangam in 1948?  It is believed that Ram from the Indian mythology of “Ramayana” visited here during his fourteen year exile.  Ancient Indian mythology narrates that Lord Brahma performed “Prakista Yajna” here, and that is why Prayag (Allahabad) is called the Tirtha Raj,  or king of all holy places.

How can you help?

You can add your voice to those concerned about daming a Holy river by visiting the websites listed below and by calling the phone numbers listed below for MOWR (Ministry of Water Resources). We have not found email addresses.

You may click here to read an excellent article with several photos covering the importance, source, uses and controversies and history of the Holy river Ganges.  Are there any other wonders of nature that we will be losing by humankind’s lesser minds?
Is this not your world? Do we not have just one planet Earth? Your knowledge or wisdom may answer an unknown question – What lies behind the miracles and wonders of the river Ganges claimed for millennia by the Gurus of Ancient India.

You may visit the Ministry of Environment & Forests, India by clicking here.

You may visit the Ministry of Water Resorces, India by clicking here to read details of the water resources advice session attended in 2011 by leading executives from various industries in India. The ministry heads names, designations and phone numbers are listed below:

 Name  Designation  Phone

1.

Shri Dhruv Vijai Singh

Secretary, MoWR

011‐23715919

2.

Shri G. Mohan Kumar

Additional Secretary, MoWR

011‐23710619

3.

Shri Sudhir Garg

Joint Secretary, MoWR

011‐23710343

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Norovirus, reactive arthritis and should a child with diarrhea be vaccinated?


Below is a wonderful, detailed, thorough excerpt from the Centers of Disease Control about the Norovirus. When infected, the symptoms include diarrhea, vomiting and cramping.  In some individuals, perhaps with a genetic predisposition, a reactive arthritis appears following a norovirus attack. As a result of the infection by the norovirus the body’s immune system continues to attack “self” cells believing they are enemy “norovirus” cells. Read the detailed original description of the Norovirus here. Cruise ships, nursing homes, college dorms are places were a norovirus infection spreads quickly where people live in enclosed conditions.

A cruise ship with a reported norovirus infection during a year when there were several diarrhea epidemics on cruise ships. Photo inlay of Norovirus. Photo ABC news

My question was that should a child with diarrhea or gastroenteritis be allowed to be vaccinated say perhaps with MMR vaccine or should this child wait until the child is fully recovered? How long should this gap be? The MMR vaccine contains components of three viruses to prevent three diseases. The vaccine aims to train the child’s immune system to recognize the foreign material and train in advance to prepare against an infection. Is the child with gasteroenteritis or diarrhea compromised in any way prior to being vaccinated? I could not find any scientific study published to answer this question. Is there any study on how many children had an infection upto one month prior to any immunization? How did they fare after that?

The second question which follows is which is more dangerous – losing a child to measles given a 1 in 1000 chance or having a child live a dependent life forever with Autism Spectrum Disorder with a 1 in 100 chance? I wonder which is more of a public burden. Should it be safer to ask a family with a norovirus infection to give a far lengthier gap prior to vaccinating a child? Except for an Italian court ruling a connection between a child with autism and a MMR vaccine (following a gastroenteritis infection), all official scientific studies have ruled out a connection between the MMR vaccine and autism. Yet, most parents continue to insist that their child was a normal baby who was able to communicate prior to the MMR vaccine. Could the norovirus provide one more clue to this puzzle?

Quote:

Biology and Epidemiology

The Virus

Noroviruses are a group of nonenveloped, single-stranded RNA viruses classified into the genus Norovirus (previously referred to as Norwalk-like viruses [NLVs] or small round-structured viruses [SRSVs]) of the family Caliciviridae. Other genera within the Caliciviridae family include Sapovirus (previously referred to as Sapporo-like viruses [SLVs]), which also cause acute gastroenteritis (AGE) in persons, as well as Lagovirus, Vesivirus, and Nebovirus, which are not pathogenic for humans (11). Noroviruses can be divided into at least five genogroups, designated GI–GV, based on amino acid identity in the major structural protein (VP1) (12). The strains that infect humans (referred to collectively as “human noroviruses”) are found in GI, GII, and GIV, whereas the strains infecting cows and mice are found in GIII and GV, respectively (Figure 1). Although interspecies transmission of noroviruses has not been documented, strains that infect pigs are found in GII (13), and a GIV norovirus was discovered recently as a cause of diarrhea in dogs (14), suggesting the potential for zoonotic transmission. On the basis of >85% sequence similarity in the complete VP1 genome, noroviruses can be classified further into genotypes, with at least eight genotypes belonging to GI and 21 genotypes belonging to GII (12,13; CDC, unpublished data, 2011). Since 2001, GII.4 viruses have been associated with the majority of viral gastroenteritis outbreaks worldwide (15). Recent studies have demonstrated that these viruses evolve over time through serial changes in the VP1 sequence, which allow evasion of immunity in the human population (15,16).

Clinical Features

Noroviruses cause acute gastroenteritis in persons of all ages. The illness typically begins after an incubation period of 12–48 hours and is characterized by acute onset, nonbloody diarrhea, vomiting, nausea, and abdominal cramps. Some persons might experience only vomiting or diarrhea. Low-grade fever and body aches also might be associated with infection, and thus the term “stomach flu” often is used to describe the illness, although there is no biologic association with influenza. Although symptoms might be severe, they typically resolve without treatment after 1–3 days in otherwise healthy persons. However, more prolonged courses of illness lasting 4–6 days can occur, particularly among young children, elderly persons, and hospitalized patients (17,18). Approximately 10% of persons with norovirus gastroenteritis seek medical attention, which might include hospitalization and treatment for dehydration with oral or intravenous fluid therapy (7,19,20). Norovirus-associated deaths have been reported among elderly persons and in the context of outbreaks in long-term–care facilities (21,22). Necrotizing enterocolitis in neonates, chronic diarrhea in immunosuppressed patients, and postinfectious irritable bowel syndrome also have been reported in association with norovirus infection (23–25); however, more data from analytic studies are needed to confirm a causal link with these conditions.

Norovirus is shed primarily in the stool but also can be found in the vomitus of infected persons, although it is unclear if detection of virus alone indicates a risk for transmission. The virus can be detected in stool for an average of 4 weeks following infection, although peak viral shedding occurs 2–5 days after infection, with a viral load of approximately 100 billion viral copies per gram of feces (26). However, given the lack of a cell culture system or small animal model for human norovirus, whether these viruses represent infectious virus is unknown, and therefore the time after illness at which an infected person is no longer contagious also is unknown. Furthermore, up to 30% of norovirus infections are asymptomatic, and asymptomatic persons can shed virus, albeit at lower titers than symptomatic persons (26–28). The role of asymptomatic infection in transmission and outbreaks of norovirus remains unclear.

Immunity

Protective immunity to norovirus is complex and incompletely understood. In human challenge studies, infected volunteers were susceptible to reinfection with the same strain as well as to infection with heterologous strains (29–32). In addition, those with preexisting antibodies were not protected from infection unless repeated exposure to the same strain occurred within a short period. Two of these studies demonstrated that homologous antibody protection might last anywhere from 8 weeks to 6 months (30,31). However, the infectious dose of virus given to volunteers in these challenge studies was several-fold greater than the dose of virus capable of causing human illness, and thus immunity to a lower natural challenge dose might be greater and more cross-protective.

Because preexisting antibodies among challenged volunteers did not necessarily convey immunity, and some persons seemed to remain uninfected despite significant exposure, both innate host factors and acquired immunity have been hypothesized to contribute to the susceptibility to infection (31). Histo-blood group antigens (HBGAs), including H type, ABO blood group, and Lewis antigens have been proposed as candidate receptors for norovirus. Expression of HBGAs is associated with strain-specific susceptibility to norovirus infection (17,33–38). Resistance to norovirus infections has been associated with mutations in the 1,2-fucosyltransferase (FUT2) gene leading to a lack of expression of HBGAs on the surface of intestinal cells (33–35,39). Thus, persons who have the normal FUT2 gene and who express these antigens are termed “secretors” whereas mutations in the FUT2 gene leading to the absence of HBGA expression result in “nonsecretor” persons who are less susceptible to infection. However, secretor status does not completely explain the differences seen among infected and uninfected persons for all strains of norovirus. Thus, additional mechanisms of immunity are likely involved, and this remains an ongoing field of research. In addition, evidence suggests that new GII.4 variants evolve to escape the build-up of acquired immunity and innate resistance in the human population (16,40).

Transmission

Norovirus is extremely contagious, with an estimated infectious dose as low as 18 viral particles (41), suggesting that approximately 5 billion infectious doses might be contained in each gram of feces during peak shedding. Humans are the only known reservoir for human norovirus infections, and transmission occurs by three general routes: person-to-person, foodborne, and waterborne. Person-to-person transmission might occur directly through the fecal-oral route, by ingestion of aerosolized vomitus, or by indirect exposure via fomites or contaminated environmental surfaces. Foodborne transmission typically occurs by contamination from infected food handlers during preparation and service but might also occur further upstream in the food distribution system through contamination with human waste, which has been demonstrated most notably by outbreaks involving raspberries and oysters as vehicles (42–46). A recent outbreak involving consumption of delicatessen meat also demonstrated the potential for norovirus contamination during processing (47). Finally, recreational and drinking water can serve as vehicles of norovirus transmission and result in large community outbreaks (48,49). These outbreaks often involve well water that becomes contaminated from septic tank leakage or sewage (50) or from breakdowns in chlorination of municipal systems (51).

Sporadic Disease

As diagnostic methods have improved and become more widely available, the role of noroviruses as the leading cause of sporadic gastroenteritis in all age groups has become clear. Approximately 21 million illnesses caused by norovirus are estimated to occur each year in the United States, approximately one quarter of which can be attributed to foodborne transmission (52). A recent systematic review of 31 community, outpatient, and hospital-based studies in both developed and developing countries estimated that noroviruses accounted for 10%–15% of severe gastroenteritis cases in children aged <5 years and for 9%–15% of mild and moderate diarrhea cases among persons of all ages (53). Although laboratory-based data on endemic norovirus disease in the United States are sparse, recent studies suggest that norovirus is the leading cause of acute gastroenteritis in the community and among persons seeking care in outpatient clinics or emergency departments across all age groups (54,55; CDC, unpublished data, 2011).

Serosurveys have demonstrated that norovirus infections are prevalent throughout the world, with initial exposure typically occurring early in life (5). In population-based studies from Australia, England, Hong Kong, and the Netherlands, norovirus infection has accounted for 9%–24% of gastroenteritis cases (19,20,56–58). In these studies, infection was more frequent in certain age groups (e.g., children aged <5 years and adults aged >65 years). In studies that have used sensitive molecular assays, a relatively high prevalence of norovirus-positive samples in asymptomatic persons has been detected, ranging from 5% in the Netherlands to 16% in England (20,56). This background rate of asymptomatic infection, coupled with innate resistance attributable to secretor status and acquired immunity, helps explain why attack rates rarely exceed 50% in outbreaks.

Outbreaks

Noroviruses are the predominant cause of gastroenteritis outbreaks worldwide. Data from the United States and European countries have demonstrated that norovirus is responsible for approximately 50% of all reported gastroenteritis outbreaks (range: 36%–59%) (5). Outbreaks occur throughout the year although there is a seasonal pattern of increased activity during the winter months. In addition, periodic increases in norovirus outbreaks tend to occur in association with the emergence of new GII.4 strains that evade population immunity (Table) (40,59). These emergent GII.4 strains rapidly replace existing strains predominating in circulation and can sometimes cause seasons with unusually high norovirus activity, as in 2002–2003 and 2006–2007. Because the virus can be transmitted by food, water, and contaminated environmental surfaces as well as directly from person to person, and because there is no long lasting immunity to norovirus, outbreaks can occur in a variety of institutional settings (e.g., nursing homes, hospitals, and schools) and affect people of all ages. Whereas prior national estimates of outbreak attribution by mode of transmission were likely biased toward foodborne disease (60,61), more recent data from individual states indicate that the majority of norovirus outbreaks primarily involve person-to-person transmission (62,63). Multiple routes of transmission can occur within an outbreak; for example, point-source outbreaks from a food exposure often result in secondary person-to-person spread within an institution or community. Of the 660 norovirus outbreaks laboratory confirmed by CDC during 1994–2006 that indicated the setting, 234 (35.4%) were from long-term–care facilities (e.g., nursing homes); 205 (31.1%) were from restaurants, parties, and events; 135 (20.5%) were from vacation settings (including cruise ships); and 86 (13.0%) were from schools and communities (59). Although GII.4 variants predominate overall, the role of GI and other GII genotypes appears to be greater in settings that involve foodborne or waterborne transmission (Figure 2).

Long-Term Care and Other Health-Care Facilities

Health-care facilities including nursing homes and hospitals are the most commonly reported settings of norovirus outbreaks in the United States and other industrialized countries (59,60,63–65). Virus can be introduced from the community into health-care facilities by staff, visitors, and patients who might either be incubating or infected with norovirus upon admission or by contaminated food products. Outbreaks in these settings can be prolonged, sometimes lasting months (66). Illness can be more severe in hospitalized patients than for otherwise healthy persons (18), and associated deaths have been reported (21,22). Strict control measures (including isolation or cohorting of symptomatic patients, exclusion of affected staff, and restricting new admissions into affected units) are disruptive and costly but might be required to curtail outbreaks (9,67,68).

Restaurants and Catered Events

Norovirus is now recognized as the leading cause of foodborne disease outbreaks in the United States. Norovirus accounted for 822 (35%) of the 2,367 foodborne disease outbreaks reported to CDC during 2006–2007 (Figure 3) and half of the 1,641 foodborne disease outbreaks with a confirmed or suspected etiology (69,70). Food can become contaminated with norovirus at any point during production, processing, distribution, and preparation. Thus, a variety of products have been implicated in outbreak investigations; foods eaten raw (e.g., leafy vegetables, fruits, and shellfish) are identified most commonly (69,70). Handling of ready-to-eat foods by infected food employees is commonly identified as a contributing factor in outbreaks of foodborne norovirus associated with food-service establishments (71,72). Norovirus outbreaks also have resulted from fecal contamination of certain food products at the source. For example, oysters harvested from fecally contaminated growing waters and raspberries irrigated with sewage-contaminated water have been implicated in outbreaks (44,73). Because gross sewage contamination will contain a collection of viruses circulating in the community, multiple norovirus genotypes often are detected in such outbreaks. Contamination with norovirus also can occur during processing, as demonstrated by a recent outbreak involving delicatessen meat (47). Only a small dose of virus is needed to cause infection, and thus infected food handlers can contaminate large quantities of product. For example, approximately 500 cases of gastroenteritis were reported during a 2006 outbreak caused by a foodhandler who vomited at work (74). Drinking water or ice also might become contaminated with norovirus and result in outbreaks in food-service settings. Secondary person-to-person transmission is common following point-source food or water exposures.

Schools and Other Institutional Settings

Norovirus outbreaks occur in a range of other institutional settings including schools, child care centers, colleges, prisons, and military encampments. Outbreaks of gastroenteritis in child care centers also are caused by other pathogens, including rotavirus, sapovirus, and astrovirus, as a result of a lack of immunity to these viruses in young populations (75). Outbreaks have been reported recently from multiple universities in different states and have led to campus closures (76). An intervention study in elementary schools demonstrated that improved hand hygiene and surface disinfection can lead to lower rates of absenteeism caused by nonspecific gastroenteritis and reduced surface contamination with norovirus (77). Norovirus was also the most common cause of gastroenteritis in U.S. marines during Operation Iraqi Freedom (78) and a common cause of outbreaks among deployed British troops (79).

Cruise Ships and Other Transportation Settings

Passengers and crew aboard cruise ships are affected frequently by norovirus outbreaks (80). Virus generally is introduced on board by passengers or crew infected before embarkation but might also result from food items contaminated before loading or persistently contaminated environmental surfaces from previous cruises. Virus also might be acquired when ships dock in countries where sanitation might be inadequate, either through contaminated food or water or passengers becoming infected while docked. Repeated outbreaks can occur in subsequent sailings as a result of environmental persistence or infected crew, particularly if control measures have not been implemented consistently and thoroughly. Genotyping of outbreak strains from repeated outbreaks has demonstrated that this can occur through the introduction of new virus or recrudescence of virus from one sailing to the next (81,82). CDC’s Vessel Sanitation Program assists the cruise ship industry in preventing and controling the introduction and transmission of gastrointestinal illness by inspecting cruise ships, monitoring gastrointestinal illnesses, and responding to outbreaks (http://www.cdc.gov/nceh/vsp). Outbreaks also have been reported in association with bus tours and air travel, in which environmental contamination and proximity to ill passengers facilitated norovirus transmission (83,84).

Unquote
Read the entire original article here by Centers of Disease Control of the United States.

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World’s largest collection of frozen Autism brains ruined in freezer malfunction


Harvard University’s brain bank at McLean Hospital in Belmont,Massachusetts, had frozen 147 brains for research purposes. They were damaged in late May 2012 for three to four days, in a freezer malfunction. The distressing fact is that 53 or one-third of those brains had been derived from rare, diseased autistic persons. This will certainly slow Autism research in particular, since the rise in Autism cases has been observed only in recent decades and the reason for this spike is not understood. About 1 in 100 children born today in the developed world may be diagnosed with Autism spectrum disorder with the percentage observed to be higher in boys than girls. These frozen autistic brains may have held a clue. They may have provided a direction for future autism research direction. They may have helped autism researchers suggest current, preventive measures faster, and sooner so that as a society we can help prevent any child in the future to be burdened with this “mind fogging, communication disabling” brain condition.

The loss of these brains to the researchers is a major step back for the public health of a developed country like USA or Sweden. Somali immigrants from Somalia, Africa to USA and Sweden have noticed that autism has been diagnosed only in the Somali children born in USA or Sweden but not in Somalia. They insist it has never been observed in the Somali children born in Somalia (Read here). Recently, researchers have begun to look at what environmental or exogenous conditions, in addition to perhaps a genetic predisposition could cause a child to develop the Autism Spectrum Disorder. Such research teams are being led by CDC Director Dr. Thomas Frieden and the University of Rochester Medical Center’s Dr. Susan Hyman, the chair of the Autism Subcommittee of the American Academy of Pediatrics. To better understand what they do not know, to identify the risk factors, to pinpoint why boys are five times more likely than girls and to better prevent Autism are some of the goals of the researchers (Read here May 29, 2012 interview by pbs.org).

The NICHD Brain and Tissue Bank for Developmental Disorders at the University of Maryland and the Harvard center at McLean are the only repositories in the US that distribute autism brain tissue to researchers around the world. Autism brain donors are in short supply.

Walk Now For Autism Research say Thomas, who has an amazing lightening-fast brain; and his mom, Dagny Power, a member of “Libertyville district 70” team

To read the scientific explanation and implication of the loss of the frozen brains click on this link for the premier blog by nature.com on June 11, 2012. What is perplexing is that both the main alarm and the back up alarm to monitor the temperature of the freezer failed. This article discusses in detail the human and technological errors that may have caused such a major loss. Apparently, all the frozen brains had been transferred to a single freezer instead of the normal 24 freezers because of a special visit by the Autism tissue program in preparation for distribution to brain sample requests by autism researchers.

Fortunately, the DNA in these brains will probably be intact into the infinite future. However, the RNA and protein matter by nature is very fragile and was destroyed, and lost to researchers. It is a public loss.

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New York scientists Invent a novel way to remotely switch on an engineered gene to produce insulin.


Jeffrey Friedman, a molecular geneticist at the Rockefeller University in New York and colleagues came up with a novel way to switch on an engineered calcium-sensitive gene that produces insulin. Their method would allow scientists to manipulate cells remotely. Although they demonstrated it in mice, in the future this will have applications to develop medicines that can be controlled from far away. Some scientists predict this process may be a major breakthrough in health management. Click here to read original article in the journal science published on May 2012.

Importance of this discovery
Scientists now have the ability to remotely activate and deactivate genes. What does that mean? An example: Obesity and diabetes are the twin problems facing modern society, as a rising epidemic in 2012. Scientists all over the world are working on curing and preventing this double scourge. Diabetes patients require a regulated method of producing insulin. One team has invented a way to remotely order cells to produce insulin. You can imagine the implications of this remote-cell-control method with multiple uses. While the scientists used the process to demonstrate controlling insulin levels inside cells, they say that it could be used for other health issues. The importance of this discovery lies in the fact that radio waves could be used to remotely control a cell activity through a gene producing a desired product. Click here to read original article and find scientist affiliations.

How does this discovery work?
The process which Friedman and his colleagues used involved coated iron oxide nanoparticles with antibodies which then would bind to a modified version of an ion channel on the surface of cells. Let’s break this down step by step.

The target was a modified version of the temperature-sensitive ion channel known as TRPV1 and the researchers injected the particles into tumors growing under the skin of the mice being studied.

The researchers then utilized a magnetic field to heat the nanoparticles.

Low-frequency radio waves targeted the nanoparticles and heated them to 42 degrees Celsius;

the ion channel was activated;

allowing calcium to flow into the cells and trigger secondary signals;(Calcium is a super important element in the body. Read articles on “how and why to regulate calcium in Autism” below in related articles and also “how too much calcium can break bones and nails”)

a signal cascade pathway activated an engineered calcium-sensitive gene which produced insulin.

How long did the total process take? 30 seconds. That’s it! In a total of 30 seconds after exposure to radio waves, insulin levels in the mice increased and blood sugar levels dropped. A clever invention.

Goal of the inventors
The scientists did not aim to cure insulin levels remotely. Current methods may be far more convenient to the patient. However, this discovery has a potential to activate genes to produce other proteins to control various diseases.

The important milestones reached here:
Low frequency radio waves penetrating a body to reach nanoparticles to activate an engineered gene.
TRPV1 can focus those radio waves locally.
The research is still in very early stages and has many more milestones to reach.

Great steps achieved here:
coated iron oxide nanoparticles with antibodies;
that bind to a modified version of the temperature-sensitive ion channel TRPV1, which sits on the surface of cells;
injection of these particles into tumours grown under the skins of mice; (imagine the team work here)
using the magnetic field generated by a device similar to a miniature magnetic-resonance-imaging machine to heat the nanoparticles with low-frequency radio waves;
the nanoparticles heating the ion channel to its activation temperature of 42 °C;(knowledge of ion channel);
Opening the channel allowed calcium to flow into cells, (knowledge of calcium flow levels in cells);
triggering secondary signals that switched on an engineered calcium-sensitive gene that produces insulin (knowledge of a signal cascade or a pathway, distant from the original gene or protein targetted).

This research is just in its fledgling stages at the moment and this study is more of a proof of concept than anything else.

How to contact and encourage the scientists
Here we always urge our readers to contact the scientists to let them know how much you appreciate their efforts to improve society and health. Do invite them for talks. Do shower them with appreciation. Please, contact the scientists directly via email or snail mail at:

Jeffrey M. Friedman, Sarah A. Stanley1, Shadi Damanpour
Laboratory of Molecular Genetics, Rockefeller University, New York, NY 10065, USA.
E-mail: friedj@mail.rockefeller.edu

Jennifer E. Gagner
Department of Materials Science and Engineering, Rensselaer Nanotechnology Center, Rensselaer Polytechnic Institute, Troy, NY 12180, USA.

Mitsukuni Yoshida
Elizabeth and Vincent Meyer Laboratory of Systems Cancer Biology, Rockefeller University, New York, NY 10065, USA.

Jonathan S. Dordick
Department of Chemical and Biological Engineering, Department of Biology, Center for Biotechnology and Interdisciplinary Studies, Rensselaer Polytechnic Institute, Troy, NY 12180, USA.

Click here to read original article.

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