Genetics questions for Annalise
Genetics questions for Annalise.

By: BCatWork

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Genetics questions for Annalise - Video

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Genetics 003
Pre mendelian hybridization experiments,mendels laws of inheritence,reason for the success,trait of pea studied by mendel grade x.

By: Sandeep Changlani

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Genetics 003 - Video

Recommendation and review posted by Bethany Smith

NEW YORK (AP) -- Shares of Myriad Genetics Inc. rose Wednesday after the test maker reported a stronger profit and higher sales in the first quarter and raised its estimates for the full year.

THE SPARK: The Salt Lake City company said Tuesday its net income rose 28 percent to $37.9 million, or 46 cents per share. Revenue grew 21 percent to $156.5 million.

Analysts were expecting adjusted earnings of 39 cents per share on $148.1 million in revenue, according to FactSet.

For the quarter ended March 31, Myriad said total diagnostic testing revenue grew 20 percent to $148.4 million. Revenue from its BRACAnalysis breast and ovarian cancer test rose 9 percent to $115.4 million. The company also reported greater revenue from its Prolaris prostate cancer test, which was approved in 2012.

BRACAnalysis looks for mutations on the breast cancer predisposition gene, or BRCA. Women with mutations on that gene have a three- to seven-times greater risk of developing breast cancer and also a higher risk of ovarian cancer.

THE BIG PICTURE: Myriad now expects to earn $1.65 to $1.67 per share this fiscal year on $595 million to $600 million in revenue. Previously it expected earnings of $1.55 to $1.58 per share on revenue of $575 million to $585 million.

Analysts expected $1.58 per share on $583.6 million in revenue.

The company said revenue should grow in the low double digits in fiscal 2014, which starts July 1. That implies revenue of at least $660 million.

Analysts expect Myriad to report $635.9 million in revenue for that fiscal year, 9 percent above their estimates for fiscal 2013.

In mid-April the Supreme Court heard a case related to the patenting of human genes: the case challenges two patents Myriad holds on genes related to the BRACAnalysis test. The American Civil Liberties Union and other groups have argued that the government shouldn't award patents on genes. The Patent & Trademark office has been awarding such patents for decades.

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Myriad Genetics rises on 3Q and stronger outlook

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LOS ANGELES, May 8, 2013 (GLOBE NEWSWIRE) -- Response Genetics, Inc. (RGDX), a company focused on the development and sale of molecular diagnostic tests that help determine a patient's response to cancer therapy, announced today that Thomas A. Bologna, Chairman and CEO, will present at the 2013 UBS Global Healthcare Conference in New York, NY.

Mr. Bologna's presentation is scheduled to begin at 8:00 a.m. EDT on May 22, 2013. Interested investors can access a live webcast of the presentation by going to the Investor Relations tab on the Response Genetics website: http://www.responsegenetics.com.

About Response Genetics, Inc.

Response Genetics, Inc. (the "Company") is a CLIA-certified clinical laboratory focused on the development and sale of molecular diagnostic testing services for cancer. The Company's technologies enable extraction and analysis of genetic information derived from tumor cells stored as formalin-fixed and paraffin-embedded specimens. The Company's principal customers include oncologists and pathologists. In addition to diagnostic testing services, the Company generates revenue from the sale of its proprietary analytical pharmacogenomic testing services of clinical trial specimens to the pharmaceutical industry. The Company's headquarters is located in Los Angeles, California. For more information, please visit http://www.responsegenetics.com.

Forward-Looking Statement Notice

Except for the historical information contained herein, this press release and the statements of representatives of the Company related thereto contain or may contain, among other things, certain forward-looking statements, within the meaning of the Private Securities Litigation Reform Act of 1995.

Such forward-looking statements involve significant risks and uncertainties. Such statements may include, without limitation, statements with respect to the Company's plans, objectives, projections, expectations and intentions, such as the ability of the Company, to provide clinical testing services to the medical community, to continue to strengthen and expand its sales force, to continue to build its digital pathology initiative, to attract and retain qualified management, to continue to strengthen marketing capabilities, to expand the suite of ResponseDX(R) products, to continue to provide clinical trial support to pharmaceutical clients, to enter into new collaborations with pharmaceutical clients, to enter into areas of companion diagnostics, to continue to execute on its business strategy and operations, to continue to analyze cancer samples and the potential for using the results of this research to develop diagnostic tests for cancer, the usefulness of genetic information to tailor treatment to patients, and other statements identified by words such as "project," "may," "could," "would," "should," "believe," "expect," "anticipate," "estimate," "intend," "plan" or similar expressions.

These statements are based upon the current beliefs and expectations of the Company's management and are subject to significant risks and uncertainties, including those detailed in the Company's filings with the Securities Exchange Commission. Actual results, including, without limitation, actual sales results, if any, or the application of funds, may differ from those set forth in the forward-looking statements. These forward-looking statements involve certain risks and uncertainties that are subject to change based on various factors (many of which are beyond the Company's control). The Company undertakes no obligation to publicly update forward-looking statements, whether because of new information, future events or otherwise, except as required by law.

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Response Genetics to Present at the 2013 UBS Global Healthcare Conference

Recommendation and review posted by Bethany Smith

RUTHERFORD, N.J.--(BUSINESS WIRE)--

Cancer Genetics, Inc.s (CGIX) (CGI or the Company) wholly-owned subsidiary, Cancer Genetics Italia, S.r.l. (CGI Italia), has entered into an agreement with Nikon Instruments S.p.A. (Nikon) for the distribution of oncology-focused DNA Probes intended for fluorescence in situ hybridization (FISH) in the Italian market. This new partnership extends CGIs global distribution network and provides more evidence that its best-in-class cancer diagnostic technologies are becoming widely accepted in the global oncology healthcare community.

FISH allows for the detection of targeted DNA rearrangements commonly found in cancers, and is therefore widely used for the diagnosis, outcome prediction and clinical management of cancer patients. Characterized by a fast turnaround time, high sensitivity, and the ability to study the cell cycle at different stages, this methodology represents the leading technology in the molecular cytogenetics market. With approximately 70,000 tests performed annually in Italy, this new partnership is expected to rapidly gain market share in Italy through the offering of a complete solution, including microscopy and reagents, to cytogenetics and cancer laboratories.

Nikon is ranked among the top microscope manufacturers worldwide, and offers a wide line of products intended to help laboratories to deliver quality research and clinical results. Nikons microscopes and imaging software systems, both automated and user-friendly, provide cytogenetics laboratories with solutions that improve workflow efficiency and reduce subjectivity. Combined with the CGI Italia DNA-FISH Probes, which allow for more efficient pinpointing of genetic aberrations, this full solution will allow laboratories to perform simultaneous multicolor FISH testing with complex image analysis in academic and clinical settings.

Through research, CGI has designed and developed a set of outstanding DNA-FISH Probes for diagnosis of genomic aberrations currently recognized as essential in clinical practice, says Raju Chaganti, professor at the Memorial Sloan-Kettering Cancer Center and founder of the Company. Joining hands with Nikon is a great opportunity for both companies, and it advances the cause of personalized cancer management.

Nikon appreciates the great opportunity to distribute CGI Italia DNA-FISH Probes in the Italian market. This partnership allows us to complete our instrumentation and consumables line for FISH applications, says Cristiana Ricci of Nikon. Nikon has developed, especially for the Oncology/Hematology field, a microspots system to investigate FISH on a microchannel, and CGI Italias probes are very important to complete our full solution offer for our customers.

This partnership further enables the Companys mission to provide clinical laboratory professionals with robustly designed products for FISH and cancer diagnostics. While focused initially on the Italian market, this partnership is expected to expand to other Western European countries. CGI estimates that over 350,000 FISH-based diagnostic tests are done annually in Western Europe.

About Nikon Instruments S.p.A

Nikon Instruments S.p.A., the Italian subsidiary of Nikon Corporation, Japan, was founded in 1995. The companys principal activity is to distribute diagnostic, research and measurement instruments. The Nikon Instruments division provides products used for leading-edge research purposes in clinical, educational usage and training applications. For more information about Nikon Instruments SPA, please visithttp://www.nikoninstruments.com.

About Cancer Genetics Italia S.r.l.

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Cancer Genetics Announces Distribution Partnership with Nikon Instruments

Recommendation and review posted by Bethany Smith

WALTHAM, Mass.--(BUSINESS WIRE)--

Interleukin Genetics, Inc. (ILIU) announced today the online publication in Osteoarthritis and Cartilage of a study with investigators at the Thurston Arthritis Research Center of the University of North Carolina entitled, IL-1 receptor antagonist gene as a predictive biomarker of progression of knee osteoarthritis in a population cohort.

The newly published paper reports that individuals with radiographic knee osteoarthritis (OA) with a specific pattern of gene variations in the interleukin-1 receptor antagonist gene (IL1RN), which is involved in controlling inflammation, were more likely to progress to severe disease than those without the gene variations. In addition, the effect of these gene variations was particularly important in those with high body mass index, while not having a strong effect in those with lower body mass index.

The study was performed under the direction of Dr. Joanne Jordan, Director of the Thurston Arthritis Research Center at the University of North Carolina. Progression of knee osteoarthritis often leads to severe disability and total knee replacement in many patients. The factors determining progression are poorly understood, said Dr. Jordan, and the genetic markers we reported appear to substantially improve our ability to identify which knee OA patients are more likely to progress. Our goal of course is to use such information to improve drug development and medical management for our OA patients.

The study evaluated radiographic progression of knee OA using the Johnston County Osteoarthritis Project, a well characterized population in North Carolina. Of 1,153 subjects, 154 had radiographic signs of knee OA initially. If they had the specific pattern of IL1RN gene variations that is found in approximately 40% of Caucasians they were more than twice as likely to have radiographic progression of the disease during the 4 to 11 years monitoring period than all other individuals with knee OA.

This study was a critical validation of the importance of IL-1 receptor antagonist genetic variations in knee osteoarthritis that we and others have seen in other cohorts, said Dr. Kenneth Kornman, Chief Executive Officer of Interleukin Genetics. We hope to start using this genetic information in partnerships to help guide therapeutic development to improve the management of knee OA.

About Osteoarthritis

Osteoarthritis affects an estimated 27 million people in the United States and is the most common type of arthritis, which is the leading cause of disability. OA was responsible for 686,000 total knee replacements in 2009, and no drugs are currently available to slow the progression of OA. Current medical management involves pain management and efforts such as weight loss to reduce stress on the knee.

About Interleukin Genetics, Inc.

Interleukin Genetics, Inc. (ILIU) develops and markets a line of genetic tests under the Inherent Health and PST brands.The products empower individuals to prevent certain chronic conditions and manage their existing health and wellness through genetic-based insights with actionable guidance. Interleukin Genetics leverages its research, intellectual property and genetic panel development expertise in metabolism and inflammation to facilitate the emerging personalized healthcare market. The Company markets its tests through partnerships with health and wellness companies, healthcare professionals and other distribution channels. Interleukin Genetics flagship products include its proprietary PST genetic risk panel for periodontal disease and tooth loss susceptibility sold through dentists and the Inherent Health Weight Management Genetic Test that identifies the most effective diet and exercise program for an individual based on genetics. Interleukin Genetics is headquartered in Waltham, Mass. and operates an on-site, state-of-the-art DNA testing laboratory certified under the Clinical Laboratory Improvement Amendments (CLIA). For more information, please visit http://www.ilgenetics.com.

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Interleukin Genetics and University of North Carolina Publish Genetic Factors Predictive of Progression of Knee ...

Recommendation and review posted by Bethany Smith

CAMBRIDGE, Mass.--(BUSINESS WIRE)--

Good Start Genetics, Inc.,an innovative molecular diagnostics company that has developed the new gold standard in carrier screening, today announced that it has closed a non-dilutive loan facility for up to $28 million of capital from Capital Royalty L.P. Good Start Genetics will use the proceeds to support its long-term corporate growth initiatives for the companys next-generation sequencing (NGS) based carrier screening platform.

Our investment in Good Start Genetics is consistent with our focus on providing flexible financing solutions for innovative companies with commercial technologies, said Charles Tate, chairman and founder of Capital Royalty L.P. We are excited about the significant long-term growth potential of Good Start given the combination of its unique next-generation sequencing based technology, applicability of GoodStart Select in large and growing markets, and very capable management team.

Good Start Genetics is a leading provider of carrier screening for the in vitro fertilization (IVF) market. Since its April 2012 commercial launch targeting the 460 IVF centers in the United States, Good Start Genetics high-complexity, CLIA- and CAP-accredited laboratory has processed tens of thousands of test orders. The GoodStart Select carrier screening service provides testing for all 23 diseases recommended by major medical societies and detects both common disease-causing mutations, as well as rare pathogenic mutations that would go undetected by laboratories using older, traditional genotyping-based technologies.

Were proud to have the support of Capital Royalty through this investment and under very attractive, non-dilutive terms, said Don Hardison, president and chief executive officer of Good Start Genetics. These funds further position us to continue growing our NGS-based GoodStart Select carrier screening presence within the IVF community, while evaluating potential opportunities to expand our reach into other areas, including global carrier screening markets. We are now in a strong financial position with sufficient capital to take us far beyond our projected 2013 profitability and cash flow operating goals.

About Good Start Genetics, Inc.

Good Start Genetics has developed the new gold standard in carrier screening by making testing for the most comprehensive set of known and novel disease-causing mutations accessible for routine clinical practice. After years of development and rigorous validation, Good Start Genetics has harnessed the power of next-generation sequencing and other best-in-class technologies to provide highly accurate, actionable and affordable tests for all disorders recommended for genetic testing by ACOG and ACMG. For these reasons, fertility specialists and their patients can have a high degree of confidence in their carrier screening results, and no longer have to compromise accuracy for price. For more information, visit http://www.goodstartgenetics.com.

About Capital Royalty L.P.

Capital Royalty L.P. is a market pioneer and innovator in healthcare investing focused on intellectual property investments in approved products through structures including royalty bonds, secured debt, revenue interests and traditional royalty monetizations. Capital Royalty works directly with leading healthcare companies, research institutions and inventors to provide customized solutions to meet their unique financing needs. The value of each investment is based on the future revenue of commercialized biopharmaceutical products and medical technologies. Capital Royalty is actively making investments through its managed investment funds.

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Good Start Genetics Announces $28 Million Financing from Capital Royalty

Recommendation and review posted by Bethany Smith

Seattle Genetics, Inc. (SGEN) reported first quarter 2013 net loss per share of 14 cents, narrower than the Zacks Consensus Estimate of a loss of 19 cents, but wider than the year-ago loss of 11 cents per share.

First quarter revenues were $57.3 million, compared with $48.2 million in the year-ago quarter. Revenues surpassed the Zacks Consensus Estimate of $54 million.

Net revenues for the first quarter included Adcetris revenues (down 1.7% to $33.9 million), collaboration and license agreement revenues (up 52.8% to $21 million) and royalty revenues. With Adcetris generating $33.9 million of revenues in this quarter, Seattle Genetics is on track to achieve its guidance of $130 million to $140 million by the end of 2013.

Research and development expenses increased 24% year over year to $47.7 million. Selling, general and administrative expenses fell 1.3% year over year to $21.9 million.

Pipeline Update

Seattle Genetics is making efforts to expand Adcetris label. In Jan 2013, a global phase III study (ECHELON-2) was initiated on Adcetris. In this study, Adcetris plus chemotherapy will be evaluated for the front-line treatment of CD30-positive mature T-cell lymphomas (:MTCL) including patients with systemic anaplastic large cell lymphoma (sALCL) and other types of peripheral T-cell lymphomas.

Seattle Genetics intends to submit a supplemental biologics license application (sBLA) in the first half of 2013 for the use of Adcetris in the retreatment of patients and for extended duration of use beyond 16 cycles of therapy. Adcetris is approved for the treatment of relapsed or refractory Hodgkin lymphoma (HL) and sALCL.

By mid-2013, Seattle Genetics will initiate a phase I/II study of Adcetris in combination with bendamustine for second-line HL patients.

In the second half of 2013, Seattle Genetics will initiate a phase II frontline study of Adcetris in combination with Roche Holding / Biogen Idecs (RHHBY / BIIB) Rituxan and standard chemotherapy (R-CHOP) for patients with diffuse large B-cell lymphoma.

Seattle Genetics has collaborations with various companies for the development of antibody-drug conjugates (ADCs). ADC collaborators are progressing on various programs.

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Narrower-than-Expected Loss at Seattle Genetics

Recommendation and review posted by Bethany Smith

May 8, 2013 A gene associated with both protection against bacterial infection and excessive blood clotting could offer new insights into treatment strategies for deep-vein thrombosis -- the formation of a harmful clot in a deep vein. The gene produces an enzyme that, if inhibited via a specific drug therapy, could offer hope to patients prone to deep-vein clots, such as those that sometimes form in the legs during lengthy airplane flights or during recuperation after major surgery.

The research, which was led by Yanming Wang, a Penn State University associate professor of biochemistry and molecular biology, and Denisa Wagner, senior author with decades of research on thrombosis at the Boston Children's Hospital and the Harvard University Medical School, will be published in in the Online Early Edition of the journal Proceedings of the National Academy of Sciences during the week ending 10 May 2013.

The team's new findings are an extension of previous research by Wang and other scientists. In earlier studies, Wang and his colleagues had revealed that a gene in mice called Pad4 (peptidylarginine deiminase 4) produces an enzyme that plays an important role in protecting the body from infection. The researchers discovered that cells with a functioning PAD4 enzyme are able to build around themselves a protective, bacteria-killing web that is dubbed a NET (neutrophil extracellular trap).

Now, in their new research, team members have studied the PAD4 enzyme's role in clotting. Wang explained that, as a part of its NET-producing duties, PAD4 regulates the formation of chromatin -- the condensed form of DNA that the cell remodels to form chromosomes. "PAD4 decondenses chromatin by loosening up the interaction between DNA and special proteins called histones. The resulting chromatin threads then combine with protein fibers, blood platelets, and other materials to become, not only the bacteria-killing NET, but also the fluffy, scattered ball that comprises a blood clot." Wang added that, in some individuals, blood clots tend to form within deep veins. These clots can then travel to the heart, causing cardiac arrest, or to the lungs, causing breathing problems.

In one of their experiments, team members compared mice with a normally functioning Pad4 gene to mice with a defective gene. They found that, when veins were constricted, genetically normal mice -- those able to produce the PAD4 enzyme -- formed clots as expected. However, genetically mutated mice -- those unable to produce the enzyme -- did not form clots normally. In fact, the scientists noted a two-fold difference in clot formation between genetically normal and genetically abnormal mice at six hours after the procedure. After 48 hours, the difference had reached 10-fold. "We noted some clotting activity in these genetically abnormal mice, but the clots were not as bulky and were not maintained over time," Wang said. "Clearly, the PAD4 enzyme plays a critical role in the formation of a blood clot, as well as in the formation of a bacteria-fighting NET."

In another experiment, the research team transferred infection-combatting white blood cells -- called neutrophils -- from normal mice to genetically mutated mice. First author Kim Martinod, a graduate student in the Immunology Graduate Program at the Harvard University Medical School, found that, in response to vein constriction, these "rescued" mice now could function normally, forming clots as efficiently as mice with a functioning Pad4 gene, demonstrating that the Pad4 gene did produce a functioning PAD4 enzyme in these white blood cells to regulate blood clotting.

"PAD4, which is also called PADI4 in humans, is a necessary enzyme involved in multiple disorders," Wang explained. "On the one hand, it plays an integral part in the body's defense system, as we showed in earlier work: It is necessary in the production of the protective, bacteria-killing NET. On the other hand, our earlier work also showed that this enzyme acts to silence tumor-suppressor genes. Now, in our new research, we are starting to see that its overactivity also may be part of the reason that some individuals suffer from deep-vein clotting." Wang added that patients prone to deep-vein thrombosis might benefit from drugs that target the PAD4 enzyme. "In future research, specific drug therapies could be developed and tested with the goal of targeting this enzyme," Wang said. "If we could find a way to dial back the enzyme's clot-forming effects, we might be able to offer new hope to patients suffering from clotting disorders and deep-vein thrombosis."

In addition to Wang, Wagner, and Martinod, other scientists who contributed to this research include Jing Hu from Penn State; Melanie Demers, Tobias A. Fuchs, Siu Ling Wong, and Alexander Brill from the Harvard University Medical School and Boston Children's Hospital; and Maureen Gallant from Boston Children's Hospital.

The research was funded by the National Heart, Lung, and Blood Institute of the National Institutes of Health and the National Cancer Institute.

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Gene offers clues to new treatments for a harmful blood clotting disorder

Recommendation and review posted by Bethany Smith

Spinal Cord Injury: Kevin Oldt Walks in KAFO Leg Braces
Spinal cord injury patient Kevin Oldt walks in KAFO leg braces at Good Shepherd Rehabilitation Network. http://www.GoodShepherdRehab.org.

By: GoodShepherdRehab

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Spinal Cord Injury: Kevin Oldt Walks in KAFO Leg Braces - Video

Recommendation and review posted by sam

Bonita Springs, Florida (PRWEB) May 07, 2013

The Alliance for the Advancement of Stem Cell Therapy and Research monetarily supports some of the treatments provided by Intercellular Sciences. The Alliance is a non-profit organization dedicated to promoting research and treatment of life altering diseases with adult stem cells.

Howie Linderman, founding board member of The Alliance, says, The Alliance is very proud to be a part of helping people obtain this breakthrough treatment. When I had my stem cell treatment in 2008, the process was much more complex. This new protocol will change the way the world views cardiac problems and we are excited to participate.

To become a supporting member, please visit http://www.thestemcellalliance.org

John C. and Eddie W. have had Dilated Cardiomyopathy for many years and as time has gone on their heart muscle has continued to weaken. The deterioration of their hearts function deteriorated to the point that walking across the room was impossible without shortness of breath. Eddie had become so bad that he was restricted to a wheelchair. Modern science has not been able to stop the progression of this devastating disease. All the medications and defibrillators can do is treat the symptoms. Both men were facing a very grim prognosis. In March they each underwent a treatment using their own stem cells to regenerate the heart muscle. Within several weeks they were both feeling better and able to do much more activity than before. Eddie was out of his wheel chair. John went back to bowling.

John C. (age 62, Dickson, TN), has had Cardiomyopathy since he was a young man. First diagnosed while in college he has had to adjust his life style to adapt to his weak heart function. His doctors recommended a defibrillator a few years ago and he has been dependent on it since. His symptoms became rapidly progressive in the last couple of months. He had to stop many of his activities including cardiac rehab. It had become just too difficult for him. Johns ejection fraction (the percent of pumping of the heart) had dropped to under 10%. His doctors were not optimistic. He and his wife Karen refused to accept such a grim fate and searched for alternative treatment. They soon found an option: adult stem cell therapy. I have much more energy now, said John after his treatment. Im back to walking the perimeter of my 6 acre property and Im back at cardiac rehab. I have even started bowling again which I had stopped. Karen says that the change has been Amazing! An echocardiogram done 3 weeks after his treatment showed an increase in his ejection fraction of 50%. It is expected that his heart function will continue to improve for up to 6 months.

Eddie W. (age 41, Americus, GA) has battled heart disease for the last 14 years. He went through several years with just mild symptoms but, the last year has been devastating. His heart function deteriorated to such a degree that he has been hospitalized twice recently for severe swelling and shortness of breath. The doctors told his wife Leslie to get his affairs in order. While he was in the hospital this last time his family searched for other options. Coming across adult stem cell treatment for heart disease they took a leap of faith and made arrangements for treatment that has to be done outside the United States. Eddie was so weak that he could only get around being pushed in a wheelchair. He also had a pump attached that delivered a medication called Primacor to help his heart. Leslie had to fill the pump once a day with this life sustaining medicine. Eddie was treated in March. The treatment was a success. Within one week the pump was discontinued. Within two weeks he was getting around without the wheelchair. We hosted a church function and Eddie was able to keep up the whole time. Leslie says He could barely get out of his wheelchair before and now to be hosting a party, I cant believe it. Im so grateful. My boys have their father back. Eddies treatment was in part supported by The Alliance for The Advancement of Stem Cell Therapy and Research.

Zannos G. Grekos, MD, MAAC, FACC, chief science officer of Intercellular Sciences and a Florida-based pioneer in the field of adult stem cell therapy explains how, in this groundbreaking treatment, cardiologists insert a catheter into the patients heart similar to a heart cath. In 20 minutes, about 30 separate injections of Regenocytes (activated stem cells) are introduced into the damaged part of the heart. The process of tissue repair begins almost immediately.

The activation provides a key step in the process, Dr. Zannos Grekos explains. The lab extracts the stem cells, concentrates and activates them into over a billion of regenerative adult stem cells while educating them to assist the specific organ that needs regeneration. These cells we call Regenocytes.

Patients remain in the hospital overnight for observation, and are typically discharged the next day. Patients are scheduled for regular subsequent visits after the stem cell treatment to monitor their progress and measure their results.

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The Alliance for the Advancement of Adult Stem Cell Therapy and Research Recently Has Proven Stem Cells To Be ...

Recommendation and review posted by simmons

A new drug treatment that can switch off a key gene involved in skin cancer has been developed and tested in a world-first trial on Sydney patients.

The first-ever human trials of the drug, called Dz13, have shown it not only shrank the basal-cell carcinoma (BCC) skin cancers, but seemed to encourage the body's own immune system to fight them as well.

In a study published in the Lancet medical journal on Tuesday, Levon Khachigian from the University of NSW showed that for the first time Dz13 appears to be both safe and effective in humans, and could potentially be used in a number of cancers and other conditions.

[Turning off the gene] sends the tumour into a death spiral, which then triggers the body's own natural inflammatory and immune system to go into battle and shrink the tumour, he said.

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An international research team that included scientists from institutions across NSW were involved with developing and trialling the drug, funded by the Cancer Institute NSW, the Cancer Council, and the National Health and Medical Research Council.

Professor Khachigian said Dz13 was enormously promising because it targeted the "c-jun" gene we all have, which is overactive in skin cancers, as well as other conditions including macular degeneration and diabetic retinopathy.

It's a pivotal growth gene, or survival gene, he said.

Usually it stays relatively inactive, but when it is switched on it triggers the production of a protein that supports unhealthy cell growth.

We think it is a bit of a lynchpin protein, he said. We don't really know why it gets switched on, except in BCCs, where we know sunlight turns it on."

Link:
Skin cancer drug switches off gene

Recommendation and review posted by Bethany Smith

May 6, 2013 UCLA life scientists have identified a gene previously implicated in Parkinson's disease that can delay the onset of aging and extend the healthy life span of fruit flies. The research, they say, could have important implications for aging and disease in humans.

The gene, called parkin, serves at least two vital functions: It marks damaged proteins so that cells can discard them before they become toxic, and it is believed to play a key role in the removal of damaged mitochondria from cells.

"Aging is a major risk factor for the development and progression of many neurodegenerative diseases," said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research. "We think that our findings shed light on the molecular mechanisms that connect these processes."

In the research, published today in the early online edition of the journal Proceedings of the National Academy of Sciences, Walker and his colleagues show that parkin can modulate the aging process in fruit flies, which typically live less than two months. The researchers increased parkin levels in the cells of the flies and found that this extended their life span by more than 25 percent, compared with a control group that did not receive additional parkin.

"In the control group, the flies are all dead by Day 50," Walker said. "In the group with parkin overexpressed, almost half of the population is still alive after 50 days. We have manipulated only one of their roughly 15,000 genes, and yet the consequences for the organism are profound."

"Just by increasing the levels of parkin, they live substantially longer while remaining healthy, active and fertile," said Anil Rana, a postdoctoral scholar in Walker's laboratory and lead author of the research. "That is what we want to achieve in aging research -- not only to increase their life span but to increase their health span as well."

Treatments to increase parkin expression may delay the onset and progression of Parkinson's disease and other age-related diseases, the biologists believe. (If parkin sounds related to Parkinson's, it is. While the vast majority of people with the disease get it in older age, some who are born with a mutation in the parkin gene develop early-onset, Parkinson's-like symptoms.)

"Our research may be telling us that parkin could be an important therapeutic target for neurodegenerative diseases and perhaps other diseases of aging," Walker said. "Instead of studying the diseases of aging one by one -- Parkinson's disease, Alzheimer's disease, cancer, stroke, cardiovascular disease, diabetes -- we believe it may be possible to intervene in the aging process and delay the onset of many of these diseases. We are not there yet, and it can, of course, take many years, but that is our goal."

'The garbage men in our cells go on strike'

To function properly, proteins must fold correctly, and they fold in complex ways. As we age, our cells accumulate damaged or misfolded proteins. When proteins fold incorrectly, the cellular machinery can sometimes repair them. When it cannot, parkin enables cells to discard the damaged proteins, said Walker, a member of UCLA's Molecular Biology Institute.

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Boosting 'cellular garbage disposal' can delay the aging process

Recommendation and review posted by Bethany Smith

American researchers found that the gene, which has previously been implicated in Parkinsons Disease, extended the healthy lifespan of fruit flies by more than 25 per cent.

They said that the research could have important implications for ageing and disease in humans.

The gene, called parkin, serves at least two functions: marking damaged proteins so that cells can discard them before they become toxic and removing damaged mitochondria from cells.

David Walker, an associate professor of integrative biology and physiology at University of California, Los Angeles, said: Ageing is a major risk factor for the development and progression of many neurodegenerative diseases. We think that our findings shed light on the molecular mechanisms that connect these processes.

In the research, published in the journal Proceedings of the National Academy of Sciences, Dr Walker and his colleagues demonstrated how parkin modulated the ageing process in fruit flies, which typically live less than two months. The researchers increased parkin levels in the cells of the flies and found that this extended their lifespan by more than 25 per cent, compared with a control group.

Dr Walker added: In the control group, the flies are all dead by Day 50. In the group with parkin overexpressed, almost half of the population is still alive after 50 days. We have manipulated only one of their roughly 15,000 genes, and yet the consequences for the organism are profound.

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Dorian Gray gene could add decades to life

Recommendation and review posted by Bethany Smith

Previous studies have suggested that protein build up within cells may play an important role in aging.

The fountain of youth might be more like a trash shredder of youth.

Scientists at UCLA have found a single gene that, when stimulated to be overexpressed, extends the healthy life span of fruit flies by more than 25 percent.

[ALSO:Gene Mutation Linked to Migraines, Researchers Say]

The gene, called parkin, plays an important role in disposing of damaged proteins within a cell. Previous studies have suggested that protein build up within cells may play an important role in aging. In fruit flies, and potentially in humans, parkin "marks" damaged proteins and instructs the cell to dispose of them.

By stimulating parkin expression, thereby boosting the power of the "cellular garbage disposal," David Walker, lead author of the study, was able to keep a group of fruit flies alive much longer than normal.

"In the control group, the flies are all dead by day 50," Walker said in a statement. "In the group with parkin overexpressed, almost half of the population is still alive after 50 days. We have manipulated only one of their roughly 15,000 genes, and yet the consequences for the organism are profound."

[READ:Girls With Autism May Need Different Treatments Than Boys]

According to the study, published Monday in Proceedings of the National Academy of Sciences, overexpression of parkin led to "a significant increase in longevity without any physiological tradeoffs. Fruit flies altered to overexpress parkin remained "healthy, active and fertile" much longer than a control group.

Walker said that parkin has previously been linked to Parkinson's Disease in humans, but his finding suggests that parkin might play a role in other age-related diseases as well. Previous fruit fly studies have found that removing parkin leads to earlier death.

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Single Gene May Extend Lifespan by 25 Percent

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Public release date: 6-May-2013 [ | E-mail | Share ]

Contact: Michael C. Purdy purdym@wustl.edu 314-286-0122 Washington University School of Medicine

Scientists' picture of how a gene strongly linked to Alzheimer's disease harms the brain may have to be revised, researchers at Washington University School of Medicine in St. Louis have found.

People with harmful forms of the APOE gene have up to 12 times the risk of developing Alzheimer's disease compared with those who have other variations of the gene.

Many researchers believe that the memory loss and cognitive problems of Alzheimer's result from the buildup over many years of brain amyloid plaques. The plaques are made mostly of a sticky substance called amyloid beta.

For years, researchers have thought that the APOE gene increases Alzheimer's risk by producing a protein that binds to amyloid beta. Scientists thought that this bond could make it easier for plaques to form.

But in a new study now available online in the Proceedings of the National Academy of Sciences, Washington University researchers show that APOE and amyloid beta don't bind together in cerebrospinal fluid and in fluids present outside cells grown in dishes. This means they are unlikely to bind together in the fluids circulating in the brain. The cerebrospinal fluid was taken from people who were cognitively normal but have forms of APOE that increase the risk of Alzheimer's.

"This is the first time we've looked at naturally produced APOE and amyloid beta to see if and how much they bind together, and we found that they have very little interaction in the fluids bathing the brain," said David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of neurology. "This suggests that we may need to rethink any therapeutic strategies that target APOE to slow amyloid plaque accumulation and Alzheimer's."

According to Holtzman, leading Alzheimer's researchers recently agreed that targeting APOE is a promising approach both for improving treatments for Alzheimer's. But to do that, scientists must first fully understand how the harmful forms of APOE increase risk of the disease.

"APOE is a major player in Alzheimer's, there's no question about that," said Philip Verghese, PhD, a postdoctoral research associate. "We did some additional studies in mice and cell cultures that suggested the APOE protein may be blocking a pathway that normally helps degrade amyloid beta."

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New perspective needed for role of major Alzheimer's gene

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Los Angeles, May 7 (IANS) Scientists have zero-ed in on a gene linked to Parkinson's disease that plays a role in delaying ageing in fruit flies, says a US study.

The University of California, Los Angeles (UCLA) life scientists have identified a gene previously implicated in Parkinson's disease that can delay the onset of ageing and extend the healthy life span of fruit flies.

The research, they say, could have important implications for ageing and disease in humans.

The gene, called parkin, serves at least two vital functions: It marks damaged proteins so that cells can discard them before they become toxic, and it is believed to play a key role in the removal of damaged mitochondria from cells.

"Ageing is a major risk factor for the development and progression of many neurodegenerative diseases," said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research. "We think that our findings shed light on the molecular mechanisms that connect these processes."

In the research, published Tuesday in the early online edition of the journal Proceedings of the National Academy of Sciences, Walker and his colleagues show that parkin can modulate the ageing process in fruit flies, which typically live less than two months.

The researchers increased parkin levels in the cells of the flies and found that this extended their life span by more than 25 percent, compared with a control group that did not receive additional parkin.

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'Parkinson's gene could extend lifespan'

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Posted with photos, video at: http://www.washington.edu/news/2013/05/06/new-device-can-extract-human-dna-with-full-genetic-data-in-minutes/

Newswise Take a swab of saliva from your mouth and within minutes your DNA could be ready for analysis and genome sequencing with the help of a new device.

University of Washington engineers and NanoFacture, a Bellevue, Wash., company, have created a device that can extract human DNA from fluid samples in a simpler, more efficient and environmentally friendly way than conventional methods.

The device will give hospitals and research labs a much easier way to separate DNA from human fluid samples, which will help with genome sequencing, disease diagnosis and forensic investigations.

"It's very complex to extract DNA," said Jae-Hyun Chung, a UW associate professor of mechanical engineering who led the research. "When you think of the current procedure, the equivalent is like collecting human hairs using a construction crane."

This technology aims to clear those hurdles. The small, box-shaped kit now is ready for manufacturing, then eventual distribution to hospitals and clinics. NanoFacture, a UW spinout company, signed a contract with Korean manufacturer KNR Systems last month at a ceremony in Olympia, Wash.

The UW, led by Chung, spearheaded the research and invention of the technology, and still manages the intellectual property.

Separating DNA from bodily fluids is a cumbersome process that's become a bottleneck as scientists make advances in genome sequencing, particularly for disease prevention and treatment. The market for DNA preparation alone is about $3 billion each year.

Conventional methods use a centrifuge to spin and separate DNA molecules or strain them from a fluid sample with a micro-filter, but these processes take 20 to 30 minutes to complete and can require excessive toxic chemicals.

UW engineers designed microscopic probes that dip into a fluid sample saliva, sputum or blood and apply an electric field within the liquid. That draws particles to concentrate around the surface of the tiny probe. Larger particles hit the tip and swerve away, but DNA-sized molecules stick to the probe and are trapped on the surface. It takes two or three minutes to separate and purify DNA using this technology.

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New Device Can Extract Human DNA with Full Genetic Data in Minutes

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Senator Durbin Defends Rallying with Communists and Anarchists
Senator Durbin Defends Rallying with Communists and Anarchists.

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Senator Durbin Defends Rallying with Communists and Anarchists - Video

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May 7, 2013 UCLA researchers led by Drs. Peiyee Lee and Richard Gatti at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research have used induced pluripotent stem cells (iPSC) to advance disease-in-a-dish modeling of a rare genetic disorder, Ataxia Telangiectasia (A-T). Their discovery shows the positive effects of drugs that may lead to effective new treatments for the neurodegenerative disease. iPSC are made from patient skin cells rather than from embryos and can become any type of cells, including brain cells, in the laboratory.

The study appears online ahead of print today in the journal Nature Communications.

Patients with A-T begin life with neurological deficits that become devastating through progressive loss of function in a part of the brain called the cerebellum, which leads to severe difficulty with movement and coordination. A-T patients also suffer frequent infections due to their weakened immune systems and have increased cancer risk. A-T is caused by lost function in a gene, ATM, which normally repairs damaged DNA in the cells and preserves normal function.

Laboratory mouse models are commonly used to study A-T; however, mice with A-T do not experience the more debilitating effects that humans do. In mice with A-T, the cerebellum appears normal and they do not exhibit the obvious degeneration seen in the human brain. Therefore, it was critical to develop a human neural cell model to understand the neurodegenerative process of A-T and create a platform for testing new treatments.

Lee and colleagues used iPSC-derived neural cells developed from skin cells of A-T patients with a specific type of genetic mutation to create a disease-in-a-dish model. The researchers were able to model the characteristics of A-T in the laboratory, such as the cell's lack of ATM protein and inability to repair DNA damage. The model also allowed the researchers to identify potential new therapeutic drugs, called small molecule read-through (SMRT) compounds that increase ATM protein activity and improve the model cells' ability to repair damaged DNA.

"A-T patients with no ATM activity have severe disease but patients with some ATM activity do much better. This makes our discovery promising, because even a small increase in the ATM activity induced by the SMRT drug can potentially translate to positive effects for patients, slowing disease progression and hopefully improving their quality of life." Lee said.

These studies suggest that SMRT compounds may have positive effects on all other cell types in the body, potentially improving A-T patients' immune function and decreasing their cancer susceptibility. Additionally, the patient-specific iPSC-derived neural cells in this study combined with the SMRT compounds can be an invaluable tool for understanding the development and progression of A-T. This iPSC-neural cell A-T disease model also can be a platform to identify more potent SMRT drugs. The SMRT drugs identified using this model can potentially be applied to most other genetic diseases with the same types of mutation. This research was supported by training and research grants from the California Institute of Regenerative Medicine (CIRM), the National Institutes of Health, APRAT, A-T Ease and Scott Richards Foundation.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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Stem cell researchers move toward treatments for rare genetic nerve disease

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Newswise UCLA researchers led by Drs. Peiyee Lee and Richard Gatti at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research have used induced pluripotent stem cells (iPSC) to advance disease-in-a-dish modeling of a rare genetic disorder, Ataxia Telangiectasia (A-T). Their discovery shows the positive effects of drugs that may lead to effective new treatments for the neurodegenerative disease. iPSC are made from patient skin cells rather than from embryos and can become any type of cells, including brain cells, in the laboratory. The study appears online ahead of print today in the journal Nature Communications.

Patients with A-T begin life with neurological deficits that become devastating through progressive loss of function in a part of the brain called the cerebellum, which leads to severe difficulty with movement and coordination. A-T patients also suffer frequent infections due to their weakened immune systems and have increased cancer risk. A-T is caused by lost function in a gene, ATM, which normally repairs damaged DNA in the cells and preserves normal function.

Laboratory mouse models are commonly used to study A-T; however, mice with A-T do not experience the more debilitating effects that humans do. In mice with A-T, the cerebellum appears normal and they do not exhibit the obvious degeneration seen in the human brain. Therefore, it was critical to develop a human neural cell model to understand the neurodegenerative process of A-T and create a platform for testing new treatments.

Lee and colleagues used iPSC-derived neural cells developed from skin cells of A-T patients with a specific type of genetic mutation to create a disease-in-a-dish model. The researchers were able to model the characteristics of A-T in the laboratory, such as the cells lack of ATM protein and inability to repair DNA damage. The model also allowed the researchers to identify potential new therapeutic drugs, called small molecule read-through (SMRT) compounds that increase ATM protein activity and improve the model cells ability to repair damaged DNA.

A-T patients with no ATM activity have severe disease but patients with some ATM activity do much better. This makes our discovery promising, because even a small increase in the ATM activity induced by the SMRT drug can potentially translate to positive effects for patients, slowing disease progression and hopefully improving their quality of life. Lee said.

These studies suggest that SMRT compounds may have positive effects on all other cell types in the body, potentially improving A-T patients immune function and decreasing their cancer susceptibility. Additionally, the patient-specific iPSC-derived neural cells in this study combined with the SMRT compounds can be an invaluable tool for understanding the development and progression of A-T. This iPSC-neural cell A-T disease model also can be a platform to identify more potent SMRT drugs. The SMRT drugs identified using this model can potentially be applied to most other genetic diseases with the same types of mutation. This research was supported by training and research grants from the California Institute of Regenerative Medicine (CIRM), the National Institutes of Health, APRAT, A-T Ease and Scott Richards Foundation.

The stem cell center was launched in 2005 with a UCLA commitment of $20 million over five years. A $20 million gift from the Eli and Edythe Broad Foundation in 2007 resulted in the renaming of the center. With more than 200 members, the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research is committed to a multi-disciplinary, integrated collaboration of scientific, academic and medical disciplines for the purpose of understanding adult and human embryonic stem cells. The center supports innovation, excellence and the highest ethical standards focused on stem cell research with the intent of facilitating basic scientific inquiry directed towards future clinical applications to treat disease. The center is a collaboration of the David Geffen School of Medicine, UCLAs Jonsson Cancer Center, the Henry Samueli School of Engineering and Applied Science and the UCLA College of Letters and Science. To learn more about the center, visit our web site at http://www.stemcell.ucla.edu.

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UCLA Stem Cell Researchers Move Toward Treatments for Rare Genetic Nerve Disease

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The University of Arizona Genetics Core (UAGC), located in the Thomas W. Keating Bioresearch Building on the UA campus, is home to rows of rectangular machines that hum busily at all hours of the day and night. These machines, with names like Illumina HISEQ 2000 and Ion Torrent, are the inanimate workhorses of the UAGC, producing hundreds of thousands of pieces of data in a single run. They sequence DNA and RNA, the genetic code and the genetic messages that program the building blocks forming a plant, animal or human. This is Ryan Sprissler's workplace and his intellectual playground.Sprissler, staff scientist and manager at the UAGC, and a Ph.D. candidate in the UA genetics program, enjoys spreading the word about genetics and the mission of the UAGC. He and his colleagues use genetic tools to explore topics including the story of human migration, and the mysteries of human disease. Sprissler describes a particularly interesting project to which the UAGC contributed--the Genographic Project.The purpose of the Genographic Project, a collaboration involving the UAGC, National Geographic, IBM and researchers from around the world, was to study patterns of migration based on the genetics of human populations. If a population stays in one place long enough and experiences little or no exchange of genes with other groups, gene sequences common to the group will become fixed. Once fixed, they serve as genetic identifiers or markers for that group.Geneticists can test for these markers, associate them with locations on the globe and track human migration patterns--sometimes over tens of thousands of years.During the course of the project, more than 500,000 genetic samples were analyzed in laboratories like the UAGC. The UAGC provided kits for the collection of cheek cells for people who wanted to make personal DNA contributions. The UA completed its obligation to the Genographic Project and Sprissler has a new mission."My favorite projects are those that are the most applied," says Sprissler. "They are [the projects] using genetic research to directly affect individuals diagnostically." He seems most fond of an undertaking that may help discover the genetic causes of human neurological disorders.He tells the story of a young girl with a devastating disease of the nervous system. Doctors could not find a cause, and for years the disorder was misdiagnosed. The girl's physicians thought she might have Rett syndrome or a seizure disorder. Relying on trial and error, they prescribed medication that made little improvement in her condition.Eventually the girl and her family were connected with UAGC scientists. The UAGC sequenced the girl's individual exome--her genome minus uninformative repetitive sequences. They found the mutation that caused her disorder. Unfortunately there was still no cure for the disease, and the girl eventually died. Understanding the genetic underpinnings of the girl's disorder, however, brought some comfort to her family.Helping to solve genetic mysteries relating to human disease pushes Sprissler to work in overdrive. His goal is making personalized medicine a reality. Someday, he hopes, people will be able to sequence their genomes quickly and inexpensively in order to find disease susceptibility genes.Sprissler is an outgoing, but modest man who doesn't like to be the center of attention. His colleagues notice that quality and speak up on his behalf. "Ryan is a good leader, not just because of his skills in molecular biology, but also because he always has a positive attitude, making it fun to work with him," says Taylor Edwards, Assistant Staff Scientist at the UAGC and recent winner of the10th Jarchow Conservation award for his work on desert tortoise conservation genetics."This is like watching my mom talk about me," says Sprissler in response to Edwards' comments.Susan Miller, manager of scientific data analysis with the UA Biocomputing Service, also works with Sprissler. She says, "I love working with Ryan because, for whatever reason, we always end up laughing." She points to doodles Sprissler left on her whiteboard. "There's a part of him that's still a kid."It's probably that very quality that makes Sprissler a favorite of students who visit the UAGC. On a tour last fall, Sprissler bounded down the hall with a dozen molecular biology students in tow. He explained his favorite projects, and ended the tour by passing out his business cards. "Call me if you're interested in working here," said Sprissler to the students, as they got ready to leave. "Awesome," said a couple of them as they took his card. 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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Solving the Mysteries of the Human Condition Using Genetic Tools

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Public release date: 7-May-2013 [ | E-mail | Share ]

Contact: Markus M. Lerch lerch@uni-greifswald.de The JAMA Network Journals

Two genome-wide association studies and a subsequent meta-analysis have found that certain genetic variations are associated with susceptibility to Helicobacter pylori, a bacteria that is a major cause of gastritis and stomach ulcers and is linked to stomach cancer, findings that may help explain some of the observed variation in individual risk for H pylori infection, according to a study in the May 8 issue of JAMA.

"[H pylori] is the major cause of gastritis (80 percent) and gastroduodenal ulcer disease (15 percent-20 percent) and the only bacterial pathogen believed to cause cancer," according to background information in the article. "H pylori prevalence is as high as 90 percent in some developing countries but 10 percent of a given population is never colonized, regardless of exposure. Genetic factors are hypothesized to confer H pylori susceptibility."

Julia Mayerle, M.D., of University Medicine Greifswald, Greifswald, Germany, and colleagues conducted a study to identify genetic loci associated with H pylori seroprevalence. Two independent genome-wide association studies (GWASs) and a subsequent meta-analysis were conducted for anti-H pylori immunoglobulin G (IgG) serology in the Study of Health in Pomerania (SHIP) (recruitment, 1997-2001 [n =3,830]) as well as the Rotterdam Study (RS-I) (recruitment, 1990-1993) and RS-II (recruitment, 2000-2001 [n=7,108]) populations. Whole-blood RNA gene expression profiles were analyzed in RS-III (recruitment, 2006-2008 [n = 762]) and SHIP-TREND (recruitment, 2008-2012 [n=991]), and fecal H pylori antigen in SHIP-TREND (n=961).

Of 10,938 participants, 6,160 (56.3 percent) were seropositive for H pylori. GWAS meta-analysis identified an association between the gene TLR1 and H pylori seroprevalence, "a finding that requires replication in non-white populations," the authors write.

"At this time, the clinical implications of the current findings are unknown. Based on these data, genetic testing to evaluate H pylori susceptibility outside of research projects would be premature."

"If confirmed, genetic variations in TLR1 may help explain some of the observed variation in individual risk for H pylori infection," the researchers conclude.

(JAMA. 2013;309(18):1912-1920; Available pre-embargo to the media at http://media.JAMAnetwork.com)

Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

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Genetic variations associated with susceptibility to bacteria linked to stomach disorders

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Let #39;s Play The Sims 3 - Perfect Genetics Challenge - Episode 1
This is a POSSIBLE LP that I am starting - I have recorded 3 episodes and will look at the responses (comments and likes) to determine if I will add this cha...

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Myriad Genetics Inc. (MYGN: Quote) Tuesday reported third-quarter profit of $37.9 million or $0.46 per share, up from $29.6 million or $0.34 per share in same period last year.

On average, 17 analysts polled by Thomson Reuters expected the company to earn $0.40 per share for the quarter. Analysts' estimates typically exclude special items.

Revenues improved to $156.47 million from $129.78 million last year. Analysts expected revenues of $148.25 million.

Looking ahead, the company has raised its full-year 2013 earnings outlook to a range of $1.65 to $1.67 per share from the previous guidance of $1.55 to $1.58 per share.

Revenues are currently projected in a range of $595 million to $600 million, up from $575 million to $585 million, issued previously. Analysts currently expect the company to report full-year earnings of $1.58 per share on revenues of $583.50 million.

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