SATURDAY, Feb. 23 (HealthDay News) -- Race and possibly genetics play a role in childhood allergies, according to a new study.

Researchers at the Henry Ford Hospital in Detroit skin-tested more than 500 children, all of whom were 2 years old, for three food allergens -- egg whites, peanuts and milk -- and seven environmental allergens.

The tests showed that about 20 percent of black children and 6.5 percent of white children were sensitized to a food allergen, while nearly 14 percent of black children and 11 percent of white children were sensitized to an environmental allergen.

Black children with an allergic parent were sensitized to an environmental allergen about two and a half times more often than black children without an allergic parent, according to the study, scheduled for Saturday presentation at the annual meeting of the American Academy of Allergy, Asthma and Immunology, in San Antonio, Texas.

Sensitization means that a person's immune system produces a specific antibody to an allergy -- not that a person will experience allergy symptoms, the researchers pointed out.

"Our findings suggest that African-Americans may have a gene making them more susceptible to food allergen sensitization or the sensitization is just more prevalent in African-American children than white children at age 2," allergist and study lead author Dr. Haejim Kim said in a Henry Ford Health System news release.

"More research is needed to further look at the development of allergy," Kim added.

Studies presented at medical meetings should be viewed as preliminary until published in a peer-reviewed journal.

-- Robert Preidt

Copyright 2013 HealthDay. All rights reserved.

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Childhood Allergies May Be Affected by Race, Genetics

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AMES, Iowa, Feb. 25, 2013 /PRNewswire/ --NewLink Genetics Corporation (NLNK) today announced that its Fourth Quarter and fiscal year ended December 31, 2012 financial results will be released before the market opens on Thursday, February 28, 2013. The NewLink management team will host a conference call discussing the company's financial results and recent corporate developments on Thursday, February 28, 2013, at 10:00am EST. The call can be accessed by dialing 1-(877) 363-5052 (domestic) or 1-(914) 495-8600 (international) five minutes prior to the start of the call and providing the passcode 16064630. A replay of the call will be available approximately two hours after the completion of the call and can be accessed by dialing 1-(855) 859-2056 (domestic) or 1-(404) 537-3406 (international), providing the passcode 16064630. The replay will be available for two weeks from the date of the live call.

The live, listen-only webcast of the conference call can be accessed by visiting the investors section of the NewLink website at http://investors.linkp.com/. A replay of the webcast will be archived on the company's website for two weeks following the call.

About NewLink Genetics Corporation

NewLink Genetics Corporation is a biopharmaceutical company focused on discovering, developing and commercializing novel immunotherapeutic products to improve cancer treatment options for patients and physicians. NewLink's portfolio includes biologic and small-molecule immunotherapy product candidates intended to treat a wide range of oncology indications.

Contacts: Gordon Link Chief Financial Officer NewLink Genetics 1.515.598.2925 glink@linkp.com

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NewLink Genetics Announces Timing of Fourth Quarter and Year-End 2012 Financial Results Conference Call

Recommendation and review posted by Bethany Smith

SEATTLE--(BUSINESS WIRE)--

Atossa Genetics, Inc. (ATOS) (Atossa or the Company) received a Warning Letter (Letter) from the FDA on February 21, 2013, regarding its Mammary Aspirate Specimen Cytology Test (MASCT) System and MASCT System Collection Test (together, the System). The Letter arises from certain FDA findings during a July 2012 inspection, to which the Company responded in August 2012, explaining why the Company believed it was in compliance with applicable regulations and/or was implementing changes responsive to the findings of the FDA inspection. The FDA alleges in the Letter that following 510(k) clearance the Company changed the System in a manner that requires submission of an additional 510(k) notification to the FDA. Specifically, the FDA observes that the Instructions For Use (IFU) in the original 510(k) submission stated that the user must Wash the collection membrane with fixative solution into the collection vial and the current IFU states apply one spray of Saccomannos Fixative to the collection membrane and that this change fixes the NAF specimen to the filter paper rather than washing it into a collection vial. At the time that the changes were made the Company determined that a new 510(k) was not required in accordance with the FDAs guidance document entitled Deciding When to Submit a 510(k) for a Change to an Existing Device.

The Letter also raises certain issues with respect to the Companys marketing of the System and the Companys compliance with FDA Good Manufacturing Practices (cGMP) regulations, among other matters.

The Company is committed to working with the FDA to resolve these issues in the best interests of patients and their doctors. If the FDA does not agree with the Companys position concerning clearance of the System, Atossa may be required to submit and receive clearance of a new 510(k) notice for the current form of the System or revert to marketing the System using the prior NAF processing method.

The Company has until March 14, 2013 to respond to the Letter and is currently working to prepare that response. Among other things, the Company currently expects that the response will explain why the Company believes that the System in its current form has been and continues to be appropriately marketed under a cleared 510(k) premarket notification, and why it is in substantial compliance with applicable regulations, including cGMP.

Management notes that the FDA could direct other compliance-verification activities or take other actions in connection with matters raised in the Letter and in connection with other matters that the FDA could identify in the future. Until these issues are resolved Atossa may be subject to additional regulatory action by the FDA, and any such actions could disrupt the Companys ongoing business and operations.

About Atossa Genetics, Inc.

Atossa Genetics, Inc. (ATOS), The Breast Health Company, is based in Seattle, WA, and is focused on preventing breast cancer through the commercialization of patented, FDA-cleared diagnostic medical devices and patented, laboratory developed tests (LDT) that can detect precursors to breast cancer up to eight years before mammography, and through research and development that will permit it to commercialize treatments for pre-cancerous lesions.

Forward-Looking Statements

Except for the historical information contained herein, the matters set forth in this press release, including statements regarding Atossas plans, regulatory actions, Atossas responses to regulatory actions, expectations, projections, potential opportunities, goals and objectives are forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially from the anticipated or estimated future results, including the risks and uncertainties associated with actions by the FDA, regulatory clearances, responses to regulatory matters, Atossas ability to continue to manufacture and sell its products, the efficacy of Atossas products and services, the market demand for and acceptance of Atossas products and services and other risks detailed from time to time in the Atossas, filings including its registration statement form S-1 filed January 28, 2013, as amended and supplemented from time to time. All forward-looking statements are qualified in their entirety by this cautionary statement, and Atossa undertakes no obligation to revise or update any forward-looking statement to reflect events or circumstances after the issuance of this press release.

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Atossa Genetics Receives Warning Letter From the Food and Drug Administration

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BREATHING EASIER - 25/02/2013
Cystic Fibrosis sufferers are welcoming a gene therapy breakthrough in mice.

By: 9NewsAdel

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BREATHING EASIER - 25/02/2013 - Video

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Research at Michigan Tech: Polymeric Nanocarriers for Suicide Gene
2013 Graduate Research Students at Michigan Tech Talk about their research projects: Topic: Guanosine Prodrug Incorporated Polymeric Nanocarriers for Suicide Gene Therapy; Alicia J. Sawdon, Ching-An Peng; Department of Chemical Engineering, Michigan Technological University

By: michigantechengineer

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Group 62AM Alzheimer #39;s Stem Cell Therapy
Group 62AM #39;s video for Biology 1103 at UGA

By: Brooke Dillard

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Advocacy In Action: How Breast Cancer Advocates Talk About Personalized Medicine To Patients
Vital Options International presents Advocacy in Action bringing together influential leaders of the cancer advocacy community to address: Personalized Medicine: What it means, its relevance for patients, collection of tissue specimens, and a discussion on metastatic breast cancer in young women. This is Part 1 of 4. Joining Vital Options Founder and CEO, Selma Schimmel, as co-hosts of the 3rd Annual Advocacy in Action Forum -- Elyse Spatz Caplan (Director, Programs Partnerships, Living Beyond Breast Cancer), Ginny Mason (Executive Director, Inflammatory Breast Cancer Research Foundation), Shirley Mertz (Board Member - Metastatic Breast Cancer Network MBCN), CJ "Dian" Corneliussen-James (Executive Director, METAvivor). Dr. Larry Norton is Deputy Physician-In-Chief For Breast Cancer Programs and the Medical Director of the Evelyn H. Lauder Breast Center at Memorial Sloan-Kettering Cancer Center (MSKCC). He is the first incumbent of the Norna S. Sarofim Chair in Clinical Oncology at MSKCC and recipient of the American Society of Clinical Oncology #39;s 2004 David A. Karnofsky Memorial Award.

By: vitaloptions

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Advocacy In Action: How Breast Cancer Advocates Talk About Personalized Medicine To Patients - Video

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Spinal Cord Injury Quadriplegia (C5-C6 level) Treatment and Rehabilitation in Mumbai, India
Spinal Cord Injury Treatment and Rehabilitation in Mumbai, India Patient is a C5-C6 quadriplegia since last 4 years with the history of backward jumping in to swimming pool and sustained a fracture of C5 with cord compression. He got operated for decompression with corpectomy followed by fusion anteriorly. Over a period of time he recovered with sensations and motor power of shoulder and elbow muscles. Neurologically, he is hypertonic and hyperreflexic. He has grade 1+ spasticity according to modified Ashworth Scale. He has reduced sensation in left leg by 40% as compared to other area of body. He is on indwelling catheter and has no bladder and bowel motor control. Functionally, he is wheelchair bound and is dependent for almost all his ADL. On ASIA Impairment Scale he scores "C". On FIM he scores 49. After Stem Cell Therapy 1. Overall stamina improved. 2. Lower limb spasticity reduced. 3. Now, he can do arm flexion and extension faster than before. 4. He can do thumb movements, which were not possible before. 5. His sitting balance has improved. Now, he has initiated to sit without support for 2-3 minutes. Earlier, not possible. 6. He can now do supine to right sidelying with minimal support for leg adjustment, which was not possible before. 7. Earlier, he could do supine to sit in with initial 10-15 minutes in semi sleep position. Now, he can directly come to sitting without discomfort (ie dizziness) 8. He can tolerate standing with backrest for 10 minutes which was ...

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Public release date: 24-Feb-2013 [ | E-mail | Share ]

Contact: The Press Office pressinfo@ki.se 46-852-486-077 Karolinska Institutet

Researchers at Karolinska Institutet in Sweden have identified a new so-called pseudogene that regulates the tumour-suppressing PTEN gene. They hope that this pseudogene will be able to control PTEN to reverse the tumour process, make the cancer tumour more sensitive to chemotherapy and to prevent the development of resistance. The findings, which are published in the scientific journal Nature Structural and Molecular Biology, can be of significance in the future development of cancer drugs.

The development of tumours coincides with the activation of several cancer genes as well as the inactivation of other tumour-suppressing genes owing to damage to the DNA and to the fact that the cancer cells manage to switch off the transcription of tumour-suppressor genes. To identify what might be regulating this silencing, the researchers studied PTEN, one of the most commonly inactivated tumour-suppressor genes. It has long been believed that the switching-off process is irreversible, but the team has now shown that silenced PTEN genes in tumour cells can be 'rescued' and re-activated by a 'pseudogene', a type of gene that, unlike normal genes, does not encode an entire protein.

"We identified a new non-protein encoding pseudogene, which determines whether the expression of PTEN is to be switched on or off," says research team member Per Johnsson, doctoral student at Karolinska Institutet's Department of Oncology-Pathology. "What makes this case spectacular is that the gene only produces RNA, the protein's template. It is this RNA that, through a sequence of mechanisms, regulates PTEN. Pseudogenes have been known about for many years, but it was thought that they were only junk material."

No less than 98 per cent of human DNA consists of non-protein encoding genes (i.e. pseudogenes), and by studying these formerly neglected genes the researchers have begun to understand that they are very important and can have an effect without encoding proteins. Using model systems, the team has shown that the new pseudogene can control the expression of PTEN and make tumours more responsive to conventional chemotherapy.

"This means that we might one day be able to re-programme cancer cells to proliferate less, become more normal, and that resistance to chemotherapy can hopefully be avoided," says Per Johnsson. "We also believe that our findings can be very important for the future development of cancer drugs. What we're seeing here is just the tip of the iceberg. The human genome conceals no less than 15,000 or so pseudogenes, and it's not unreasonable to think that many of them are relevant to diseases such as cancer."

###

The study was conducted in collaboration with scientists at The Scripps Research Institute, USA, and the University of New South Wales, Australia, and was made possible with grants from the Swedish Childhood Cancer Foundation, the Swedish Cancer Society, the Cancer Research Funds of Radiumhemmet, Karolinska Institutet's KID programme for doctoral studies, the Swedish Research Council, the Erik and Edith Fernstrm Foundation for Medical Research, the National Institute of Allergy and Infectious Diseases, the National Cancer Institute and the National Institutes of Health.

Publication: 'A pseudogene long noncoding RNA network regulates PTEN transcription and translation in human cells', Per Johnsson, Amanda Ackley, Linda Vidarsdottir, Weng-Onn Lui, Martin Corcoran, Dan Grandr och Kevin V. Morris, Nature Structural and Molecular Biology, AOP 24 February 2013, doi: 10.1038/nsmb.2516. Embargoed until 24 February 2013 at 1800 London time / 1900 CET / 1300 US Eastern time.

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New type of gene that regulates tumor suppressor PTEN identified

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Feb. 24, 2013 Researchers at Karolinska Institutet in Sweden have identified a new so-called pseudogene that regulates the tumour-suppressing PTEN gene. They hope that this pseudogene will be able to control PTEN to reverse the tumour process, make the cancer tumour more sensitive to chemotherapy and to prevent the development of resistance.

The findings, which are published in the scientific journal Nature Structural and Molecular Biology, can be of significance in the future development of cancer drugs.

The development of tumours coincides with the activation of several cancer genes as well as the inactivation of other tumour-suppressing genes owing to damage to the DNA and to the fact that the cancer cells manage to switch off the transcription of tumour-suppressor genes. To identify what might be regulating this silencing, the researchers studied PTEN, one of the most commonly inactivated tumour-suppressor genes. It has long been believed that the switching-off process is irreversible, but the team has now shown that silenced PTEN genes in tumour cells can be 'rescued' and re-activated by a 'pseudogene', a type of gene that, unlike normal genes, does not encode an entire protein.

"We identified a new non-protein encoding pseudogene, which determines whether the expression of PTEN is to be switched on or off," says research team member Per Johnsson, doctoral student at Karolinska Institutet's Department of Oncology-Pathology. "What makes this case spectacular is that the gene only produces RNA, the protein's template. It is this RNA that, through a sequence of mechanisms, regulates PTEN. Pseudogenes have been known about for many years, but it was thought that they were only junk material."

No less than 98 per cent of human DNA consists of non-protein encoding genes (i.e. pseudogenes), and by studying these formerly neglected genes the researchers have begun to understand that they are very important and can have an effect without encoding proteins. Using model systems, the team has shown that the new pseudogene can control the expression of PTEN and make tumours more responsive to conventional chemotherapy.

"This means that we might one day be able to re-programme cancer cells to proliferate less, become more normal, and that resistance to chemotherapy can hopefully be avoided," says Per Johnsson. "We also believe that our findings can be very important for the future development of cancer drugs. What we're seeing here is just the tip of the iceberg. The human genome conceals no less than 15,000 or so pseudogenes, and it's not unreasonable to think that many of them are relevant to diseases such as cancer."

The study was conducted in collaboration with scientists at The Scripps Research Institute, USA, and the University of New South Wales, Australia, and was made possible with grants from the Swedish Childhood Cancer Foundation, the Swedish Cancer Society, the Cancer Research Funds of Radiumhemmet, Karolinska Institutet's KID programme for doctoral studies, the Swedish Research Council, the Erik and Edith Fernstrm Foundation for Medical Research, the National Institute of Allergy and Infectious Diseases, the National Cancer Institute and the National Institutes of Health.

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New type of gene that regulates tumour suppressor PTEN identified

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Aka, How to Twist Science to Reinforce Gender StereotypesGenes are subject to multiple layers of regulation. An early regulatory point is transcription. During this process, regulatory proteins bind to DNA regions (promoters and enhancers) that direct gene expression. These DNA/protein complexes attract the transcription apparatus, which docks next to the complex and proceeds linearly downstream, producing the heteronuclear (hn) RNA that is encoded by the gene linked to the promoter. The hnRNA is then spliced and either becomes structural/regulatory RNA or is translated into protein.Transcription factors are members of large clans that arose from ancestral genes that went through successive duplications and then diverged to fit specific niches. One such family of about fifty members is called FOX. Their DNA binding portion is shaped like a butterfly, which has given this particular motif the monikers of forkhead box or winged helix. The activities of the FOX proteins extend widely in time and region. One of the FOX family members is FOXP2, as notorious as Fox News - except for different reasons: FOXP2 has become entrenched in popular consciousness as "the language gene". As is the case with all such folklore, there is some truth in this; but as is the case with everything in biology, reality is far more complex.FOXP2, the first gene found to "affect language" (more on this anon), was discovered in 2001 by several converging observations and techniques. The clincher was a large family (code name KE), some of whose members had severe articulation and grammatical deficits with no accompanying sensory or cognitive impairment. The inheritance is autosomal dominant: one copy of the mutated gene is sufficient to confer the trait. When the researchers definitively identified the FOXP2 gene, they found that the version of FOXP2 carried by the KE affected members has a single point mutation that alters an invariant residue in its forkhead domain, thereby influencing the protein's binding to its DNA targets.Like all transcription factors, FOXP2 regulates many promoters. The primary domains of FOXP2 influence are brain and lung development. Some of its downstream targets are themselves regulators of brain function (most prominently neurexin CNTNAP2). Not surprisingly, deleting or mutating both FOXP2 copies in mice results in early death, whereas doing so to one copy leads to decreased vocalization and slightly impaired motor learning. FOXP2 is broadly conserved across vertebrates, but its critical functional regions have tiny but telling differences even between humans and their closest ape relatives. Like other genes that influence human-specific attributes, human FOXP2 seems to have undergone positive selection during the broad intervals of crucial speciation events. Along related lines, Neanderthals and Denisovans apparently had the same FOXP2 allele as contemporary humans, and by this criterion were fully capable of the articulation that makes language possible.Which brings us to the nub of the issue. What does FOXP2 do in brain? Genes don't encode higher-order functions, let alone behavior. Also recall that the KE family members have a very circumscribed defect, despite its dramatic manifestation. Finally, keep firmly in mind that language in humans includes a complex genetic component that involves many loci and just as many environmental interactions. FOXP2 does not encode inherent language ability. Instead, the time and place of its expression as well as studies in cell systems and other organisms (zebra finches, rodents) indicate that FOXP2 may be involved in neuronal plasticity, which in turn modulates capacity for learning by forming new synaptic connections. FOXP2 may also be involved in regulation of motor neuron control in certain brain regions (cortical motor areas, cerebellum, striatum) that affect the ability to vocalize, sing and, in humans, form the complex sounds of language.Given its connection, however over-interpreted, to "what makes a human" as well as its chromosomal location (in 7q31, which also harbors candidates for autism and dementia), it's not surprising that FOXP2 has acquired quasi-mythic dimensions in the lay imagination. However, careful studies have shown that the genes on 7q31 responsible for autism and dementia are distinct from FOXP2. Also, as I said earlier, FOXP2 does not code for language ability - and even less for its culturally determined manifestations (many of which are a minefield of confirmation biases, unquestioned assumptions and simply sloppy work).The latest round in the misrepresentation of FOXP2 is the gone-viral variation of "there's more of this 'language protein' in the left hemisphere of 4-year girls and that's why women are three times as talkative as men". This came from the PR pitch of a research team who did a study primarily on rats (which confirmed the link between FOXP2 levels and vocalization) and then, perhaps attempting to latch onto a catchy soundbite, extended the gender link to humans based on... a single PCR amplification of ten Broca's area cortices (from postmortem brains of 4-year olds, five from each sex; Broca's area is involved in language processing).To begin with, all studies conducted so far definitively show that women and men utter the same number of words by any metric chosen - and that in fact men talk more than women in mixed-gender conversations (to say nothing of the gender-linked ratio of interruptions). And whereas it's true that girls develop vocal competence slightly earlier than boys and show higher linguistic skills during the early acquisition window, this difference is transient. Furthermore, the FOXP1 control that the authors of the study argue does not show a gender-correlated change (unlike FOXP2) in fact is on the verge of doing so, and the relative statistical significances might well change if a larger number of samples were tested. Finally, whereas decrease of FOXP2 reduces vocalization and increases pitch in male rat pups, it has the opposite effect in female rat pups. In other words, the correlation between FOXP2 levels and vocalization/pitch is not straightforward even in rats.In the larger context of expression and reception of vocalizations, the difference is not how much women talk, but how welcome and/or valued their input is. Even trivial zomboid blathering is given higher value if it's culturally coded as masculine (examples: sport newscasters; most congressmen). In fairness to the researchers of the study that caused all this rehashing of kneejerk stereotypes and evopsycho Tarzanism, here is the concluding paragraph of their paper. It states something both measured and, frankly, obvious: "Gender is a purely human construct consisting of both self and others' perception of one's sex and is arguably the first and most salient of all phenotypic variables. Sex differences in how language is received and processed and how speech is produced has the potential to influence gender both within and external to an individual. Whether human sex differences in FOXP2, and possibly FOXP1 as well, contribute to gender variation in language is a question for future research." Relevant publications and links:Lai CS, Fisher SE, Hurst JA, Vargha-Khadem F, Monaco AP (2001). A forkhead-domain gene is mutated in a severe speech and language disorder. Nature 413(6855):519-23.White SA, Fisher SE, Geschwind DH, Scharff C, Holy TE (2006). Singing mice, songbirds, and more: models for FOXP2 function and dysfunction in human speech and language. J. Neurosci. 26(41):10376-9.Bowers JM, Perez-Pouchoulen M, Edwards NS, McCarthy MM (2013). FOXP2 mediates sex differences in ultrasonic vocalization by rat pups and directs order of maternal retrieval. J. Neurosci. 33(8):3276-83.Mark Liberman. Gabby Guys: The Effect size (Language Log, Sept. 23, 2006)Mark Liberman. An Invented Statistic Returns (Language Log, Feb. 22, 2013)Athena Andreadis. Eldorado Desperadoes: Of Mice and Men (Starship Reckless, July 18, 2009)Athena Andreadis. Miranda Wrongs: Reading Too Much into the Genome (Starship Reckless, June 10, 2011) Follow Scientific American on Twitter @SciAm and @SciamBlogs.Visit ScientificAmerican.com for the latest in science, health and technology news. 2013 ScientificAmerican.com. All rights reserved.

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The "Language" Gene and Women's Wagging Tongues

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Biotechnology and Genetic Engineering
Video Notes on Biotechnology and Genetic Engineering

By: dovebiology

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Biotechnology and Genetic Engineering - Video

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New Delhi, Feb. 24: Novel genetic mutations in malaria parasites and an infected population without symptoms observed for the first time in Bengal may hamper efforts to control a lethal form of malaria, researchers have said.

The genetic mutations appear linked to drug resistance in malaria parasites and highlight the need to revise the existing primary treatment strategy, said scientists at Vidyasagar University, Midnapore, who spotted the mutations have.

In an independent study, researchers at the Calcutta School of Tropical Medicine have detected a tribal population in Purulia district infected with the malaria parasite, Plasmodium falciparum, but without any symptoms whatsoever of the disease.

While doctors have sporadically reported cases of such asymptomatic infections earlier from states with high malaria prevalence, such as Chhattisgarh, Jharkhand and Orissa, scientists say this is the first report from Bengal.

"Asymptomatic infected persons remain a hidden reservoir of the parasite," said Swagata Ganguly, a medical researcher and a member of the CSTM team. "They don't seek treatment and facilitate transmission of the parasite."

The CSTM team led by Ardhendu Maji examined about 1,040 members of a tribal population in a forested area of Purulia in June 2012 and found that about eight per cent of the population had Plasmodium falciparum without symptoms. The findings are published this week in the Journal of Clinical Microbiology. Maji said the CSTM hopes to conduct similar studies in other parts of Bengal.

The findings come at a time when Vidyasagar University microbiologists have reported what they say are novel mutations in the parasite that seem associated with resistance to sulfadoxine and pyrimethamine, a drug combination used to treat malaria.

Their study suggests that a mutation in a gene called dhfr is associated with the parasite's resistance to pyrimethamine, and a set of quadruple mutations ' at four points on the parasite's genome ' in another gene called dhps seem strongly linked to resistance to sulfadoxine. Their study is also published this week in the International Journal of Antimicrobial Agents.

"The parasite is changing ' it is quickly adapting to our medicines," said Amiya Kumar Hati, a medical entomologist and former director of the CSTM who has collaborated with the Midnapore team.

India's malaria control programme had recommended in 2009 the use of a combination of drugs ' artemisinin with sulfadoxine and pyrimethamine ' to treat malaria caused by Plasmodium falciparum, the most dangerous of malaria parasites.

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Twin tests for malaria control

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BJ Angus Genetics - 41
BJ Angus Genetics 12th Annual Spring Production Sale Friday, March 15, 2013 at 12:30 pm at the ranch in Manhattan, KS John Bonnie Slocombe 785-539-4726 or 785-532-9777 bjangus.com

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BJ Angus Genetics - 40
BJ Angus Genetics 12th Annual Spring Production Sale Friday, March 15, 2013 at 12:30 pm at the ranch in Manhattan, KS John Bonnie Slocombe 785-539-4726 or 785-532-9777 bjangus.com

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Daily V-log #2 [P-1]
Hello, long times, no see. [NOTE]: I do NOT own this music, I #39;m advertising it because it #39;s good. Music: ---------- Zedd - The Legend Of Zelda (Original Mix) Savage Genetics - Silent Hill (Dubstep Remix) FREE DL ---------- Have a good one!

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BJ Angus Genetics - 43
BJ Angus Genetics 12th Annual Spring Production Sale Friday, March 15, 2013 at 12:30 pm at the ranch in Manhattan, KS John Bonnie Slocombe 785-539-4726 or 785-532-9777 bjangus.com

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BJ Angus Genetics - 42
BJ Angus Genetics 12th Annual Spring Production Sale Friday, March 15, 2013 at 12:30 pm at the ranch in Manhattan, KS John Bonnie Slocombe 785-539-4726 or 785-532-9777 bjangus.com

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BJ Angus Genetics - 44
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BJ Angus Genetics - 46
BJ Angus Genetics 12th Annual Spring Production Sale Friday, March 15, 2013 at 12:30 pm at the ranch in Manhattan, KS John Bonnie Slocombe 785-539-4726 or 785-532-9777 bjangus.com

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BJ Angus Genetics - 45
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BJ Angus Genetics - 47
BJ Angus Genetics 12th Annual Spring Production Sale Friday, March 15, 2013 at 12:30 pm at the ranch in Manhattan, KS John Bonnie Slocombe 785-539-4726 or 785-532-9777 bjangus.com

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BJ Angus Genetics - 47A
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BJ Angus Genetics - 48
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BJ Angus Genetics - 1218
BJ Angus Genetics 12th Annual Spring Production Sale Friday, March 15, 2013 at 12:30 pm at the ranch in Manhattan, KS John Bonnie Slocombe 785-539-4726 or 785-532-9777 bjangus.com

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