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News Article | May 3, 2017
Site: co.newswire.com

bioMONTR Labs is proud to announce that its Laboratory Director, Dr. Susan Fiscus, has been named as the 2017 recipient of the Ed Nowakowski Senior Memorial Clinical Virology Award presented by the Pan American Society for Clinical Virology. This accolade is awarded to individuals who have made a major impact on the epidemiology, treatment or understanding of the pathogenesis of viral diseases. Prior to joining bioMONTR Labs, Dr. Fiscus served as the director of UNC’s Retrovirology Core Laboratory. Preceding her 25-year career at UNC, Dr. Fiscus earned her bachelor’s degree from Bates College, her master’s degree in botany from Duke University and her doctoral degree in microbiology from Colorado State University. During her time at UNC, Fiscus worked on studies for the AIDS Clinical Trials Group (ACTG), the Pediatric ACTG, the HIV Prevention Trials Network, and the Centers for Disease Control (CDC) among other organizations. Each year, PASCV’s awards program provides an array of awards that recognize the contributions made by individuals to the field of clinical virology. These awards will be presented next week during the 2017 Clinical Virology Symposium in Savannah, Georgia. bioMONTR Labs is a privately owned CLIA Certified lab located in Research Triangle Park, NC. The company offers a comprehensive menu of high-complexity molecular assays as well as other proprietary and esoteric molecular testing. Please visit http://www.biomontr.com for more information on the company, its management, test menu, and capabilities.


Pan N.,Core Laboratory | Frome W.L.,Core Laboratory | Dart R.A.,Center for Human Genetics | Tewksbury D.,Marshfield Clinic Research Foundation
Clinical Medicine and Research | Year: 2013

Background: The renin-angiotensin system (RAS) is present in human placental tissue and participates in regulation of maternal-fetal blood flow during pregnancy. RAS expression in placental tissue is regulated by various hormones and is altered in various disease conditions. An in vitro system is needed to further investigate regulation of the placental RAS. To this end, we studied RAS expression in the human placenta-derived cell line, CRL-7548. Methods: CRL-7548 cells were cultured in plastic plates. Total RNA was extracted, reverse transcribed, and amplified by polymerase chain reaction (PCR) with specific primers. Angiotensin II peptide in the culture media was measured by radioimmunoassay. Renin activity was detected by radioimmunoassay measuring angiotensin I generated. Angiotensin receptor type I was detected by Western blot. Results: Specific mRNA for angiotensin, renin, angiotensin converting enzyme, and angiotensin receptor type I was detected by real-time PCR. Renin activity was detected in the placental cell lysate, and angiotensin II peptide, the final product of the RAS system, was detected in cell culture media by radioimmunoassay. Angiotensin receptor type I was identified as a 41 kDa protein in cell lysates by Western blot. Conclusions: These results demonstrate that all necessary components of the classic RAS are expressed in the human placental cell line CRL-7548. This cell line may prove useful as an in vitro system for studying RAS regulation in the placenta. ©2013 Marshfield Clinic.


News Article | December 9, 2016
Site: www.technologyreview.com

Last April, Omar and Natasha Rajani rented a hall, invited 130 guests, and hired a magician to entertain the little ones. In Natasha’s family, first birthday parties are major celebrations. And the Rajanis, who live in Toronto, felt particularly enthusiastic because for a long time they weren’t sure they’d ever be able to throw one. Natasha, 35, struggled for four years to get pregnant. She and Omar, 40, tried naturally at first; then they used hormones, which led to an ectopic pregnancy, in which the fertilized egg implants outside the uterus—usually in the narrow fallopian tube—and must be removed. Then more hormones. Then in vitro fertilization (IVF). Nothing worked. Natasha’s obstetrician next offered an unusual option: the couple could try a new method meant to improve the odds of IVF, offered by a Boston-area company called OvaScience. The approach, called Augment (for Autologous Germline Mitochondrial Energy Transfer), is so far available only in Canada and Japan ­(OvaScience hasn’t yet sought approval from U.S. regulators). It required the doctor to gather cells from one of Natasha’s ovaries and harvest their mitochondria—the tiny power plants that fuel our cells. These extracted mitochondria would then be injected into one of her eggs along with her husband’s sperm, and the embryo would be transferred to her uterus during a standard IVF procedure. According to OvaScience, the extra energy from the ovarian mitochondria would give her egg a boost, promoting fertilization. “What Natasha and I liked about it was it was kind of like self-treatment,” says Omar. “We thought that it was something that was safe, and it was almost like the body treating and healing itself. We were very, very excited about the opportunity to try it.” In the round of IVF that Natasha had after trying the new procedure, she got pregnant with a boy, Zain, now almost two. It doesn’t really matter, the ­Rajanis say, whether Augment was the reason for the successful pregnancy. All they know is that it felt like a miracle. They have a toddler with an always-sunny disposition—“He’s just an absolute joy of a child,” Natasha says—and two more frozen embryos that might one day become his siblings. Whether Augment actually made the difference in Zain’s conception could have far-reaching implications for how we think about both infertility and aging. Infertility affects more than 10 percent of American women—a number that is rising as many women wait longer before considering parenthood. Female fertility starts to decline after age 35. Among women who turn to assisted reproduction techniques such as IVF, only 40 percent of attempts by those under 35 result in a live birth, while 2 percent of those among women over 44 do—largely because of a dwindling number of eggs and a decline in their quality. Not only could OvaScience’s procedure help many women whose fertility has declined with age, but it would be one of the first successful efforts to slow the body’s relentlessly ticking clock, providing tantalizing clues for ways to halt aging more generally. Company cofounder and Harvard University genetics professor David Sinclair says conquering the overall aging process is a matter of when, not if. “We are at a point where we know how to extend life span in mammals, and now there’s a race to see who can prove that we can do this in humans,” Sinclair says. Female fertility, he says, is one of the first bodily systems to break down with age, and he sees reversing infertility as a gateway to reversing aging itself. The goal, Sinclair proclaims, is “to have revolutionary technologies like OvaScience available to everybody—and not to just treat fertility, but another 2,000 age-related diseases, from diabetes through Alzheimer’s.” Despite Sinclair’s enthusiasm, it’s possible—even likely, some scientists say—that OvaScience’s procedure did nothing at all. For one thing, IVF is notoriously unpredictable. The Rajanis might have just gotten lucky the second time, just as they were unlucky the first. More than a dozen interviews with experts in fertility and early development reveal little scientific justification for what was done to Natasha Rajani’s eggs and those of the 300 other women who have gone through the procedure, which costs an IVF clinic from $6,000 to $7,000. (The fee that clinics charge patients will vary.) The company harvests the mitochondria from what it believes are immature egg cells found in the ovarian lining; the idea is that these so-called egg-precursor cells have fresher mitochondria than the aging mature eggs. But there is little convincing evidence that they are what ­OvaScience says they are: cells with the power to turn into eggs. And even if such egg-­precursor cells exist and their mitochondria are more youthful than those in a woman’s eggs, does it prove that such an energy boost can improve fertility? “There is very little data supporting the benefit of these procedures, and often the biological rationale is incoherent,” says Jacob Hanna, an expert in embryonic stem cells at the Weizmann Institute of Science in Israel, who reviewed ­OvaScience’s information at the request of MIT Technology Review. “I hope the company can provide solid data and experimentation on these approaches… It sounds more at the moment like voodoo, or alchemy.” So is OvaScience leading a breakthrough in battling one of the most basic processes of aging, or selling false hopes with little scientific justification? Youthful Marriage The founding of OvaScience came about as a marriage of two of medicine’s most audacious and often controversial areas: anti-aging research and infertility research. The company specifically traces its scientific origins to the work of the reproductive biologist Jonathan Tilly, now at Northeastern University in Boston. Beginning with a 2004 paper, Tilly has been challenging decades of scientific dogma that girls are born with their whole life’s supply of “primordial” egg cells, which will eventually mature into eggs. After puberty, this stock of eggs matures at the rate of about one a month, and it never renews. The decline in female fertility around 35 occurs as this supply dries up, and menopause strikes when the eggs run out. But Tilly’s research suggested—first in mice and then in people—that the lining of the ovary contains the makings of a new supply. If Tilly is right about his conclusions, solving infertility might be just a matter of finding these egg-precursor cells and triggering them to mature (see 10 Breakthrough Technologies 2012: Egg Stem Cells). Sinclair says it was natural for him to collaborate with Tilly, who was then at Harvard. Tilly’s work touched on subjects that fascinated Sinclair: how the body ages and what might be done to slow that process. “I’d been trying to figure out what are the major reasons we grow old and why don’t cells function the older we get,” Sinclair says. Sinclair introduced Tilly to two biotech entrepreneurs, Rich Aldrich and Michelle Dipp, with whom Sinclair had previously run an anti-aging company called Sirtris Pharmaceuticals. That company was based on Sinclair’s research into sirtuins, proteins that may slow the aging process and can be activated by resveratrol, a compound most found in red wine. Sirtris was sold to GlaxoSmithKline in 2008 for $720 million (GSK closed down its Sirtris facility in 2013, absorbing the sirtuin work into its own research efforts), and the biotech investors were looking for their next big play. When the potential partners asked Tilly how he might commercialize his research, ­Sinclair says, Tilly came up with the idea of Augment, using the precursor cells to rejuvenate aging eggs. (Tilly declined to comment for this story.) That was enough for the group to create ­OvaScience, where Dipp served as CEO until last summer. Sinclair hypothesizes that mitochondria are crucial to aging. The idea is simple. Aging cells have old, slow mitochondria; young mitochondria equal young cells. Hence the Augment program to rejuvenate eggs with mitochondria from cells that are younger and more energetic. Sinclair has also cofounded two other companies, MetroBiotech of Boston and CohBar of Menlo Park, California, to develop drugs related to mitochondrial functions. CohBar hopes peptides made by mitochondria could be useful against diabetes, obesity, and Alzheimer’s, among other diseases, while MetroBiotech is pursuing a therapy to treat diseases associated with malfunctioning mitochondria. It is testing a drug that boosts levels of nicotinamide adenine dinucleotide, NAD, a compound involved in energy metabolism in the mitochondria. “The same molecules [in the drug] we think will treat aging itself,” Sinclair says, citing a 2013 paper his team published in Cell. Sinclair’s interest in aging has become personal. Now 47 and working in a high-stress job at Harvard, he has time to exercise “barely more than once a week.” In addition to his academic and commercial duties, he also sits on the advisory board of InsideTracker, a company based in Cambridge, Massachusetts, that uses levels of glucose, vitamin D, and other blood factors to determine a client’s “inner age,” as opposed to the chronological one. In 2011, Sinclair says, he clocked in at 57, a decade and a half beyond his actual age. In July 2015, convinced he was going to die young, he upped his daily doses of resveratrol. He also added MetroBiotech’s NAD precursor, which has yet to be tested in people and is too expensive for anyone who’s not making it to use. Sinclair says InsideTracker’s aging markers now put him at 31. He’s lost the weight he’d been carrying since college and has been allowing himself to eat dessert again, because his body can handle it. (Weight loss isn’t his goal, he says, but mitochondria are also responsible for burning fat, so weight loss “might be a side effect” of the treatment.) “The results in mice and my single-person experiment indicate that aging is more reversible than we thought,” he says. Too Early In a pristine lab overlooking a busy highway in the Boston suburbs, OvaScience researchers identify and count what they believe are egg-precursor cells. These constitute, OvaScience says, about 6 percent of the cells on the surface of the ovarian cortex. In the Augment procedure, an IVF surgeon laparoscopically removes a section of this layer about half the size of a dime. The tissue is shipped to an OvaScience lab, where the mitochondria are extracted and shipped back to the fertility clinic. Just before fertilization, the mitochondria are inserted into the egg alongside the sperm. Then IVF proceeds as usual. Preliminary data suggests that the procedure improves fertility. In its latest study, released at a conference in November, OvaScience reported a 31 percent success rate among 75 patients who had undergone at least one previous round of IVF before trying Augment. It’s notoriously difficult to get good data on fertility clinic results, but in a 2015 study in the Journal of the American Medical Association, British researchers found that about 30 percent of women are successful in their first round of IVF and 16 to 25 percent are successful in each subsequent round (without Augment). So if the results for Augment prove to be real, it increases success rates from about 20 percent to 30 percent per round—a significant, if modest, improvement. However, those results simply record the experience of Augment patients. As is the case in many early research studies, they were not compared with controls, so there’s no convincing evidence that the procedure made the difference. OvaScience expects to get data from two more trials, including about 300 patients, in the second half of 2017. However, ­OvaScience’s patents on the cells and procedures protect the company’s business interests and prevent outsiders from testing its protocol. So there have been no independent tests. I asked one scientist to examine and comment on OvaScience’s Augment research. After looking at the material the company had presented to me, he declined to say anything. There wasn’t any science to review, he said—just anecdotes. OvaScience plans two other projects for these egg-precursor cells. In a program it’s calling OvaPrime, the cells are extracted from the outer rind of the ovary, isolated, and then reimplanted into the main part of the ovary, where they are projected to mature into healthy, viable eggs. The procedure is designed to help women who don’t make enough eggs—about 30 percent of infertile women, according to the Centers for Disease Control and Prevention. The company is doing safety and feasibility trials now and expects to soon decide whether to pursue this approach commercially. In another program, called ­OvaTure, OvaScience hopes eventually to perform IVF without hormones. Hormones are now needed to stimulate a woman’s body to release as many eggs as possible. But for many women, hormone injections are the worst part of IVF, with the potential to cause mood swings, nausea, vomiting, abdominal pain, and a very small risk of death. With OvaTure, the woman would have some precursor cells removed, and they would be coaxed in a lab dish to mature into fully functional eggs, all without hormones. The company, however, is still studying whether this technique will work. These projects will largely determine just how important OvaScience’s contribution to fertility and anti-aging science will be. Augment might have a limited effect even if the precursor egg cells are not truly capable of turning into eggs, as many scientists believe. And Stock says at around $7,000 per treatment, Augment is a good deal if it saves families from another round of IVF, which can easily run $10,000 to $15,000 per cycle. But the two more ambitious efforts, OvaPrime and OvaTure, will never work unless ­Tilly’s conclusions are right. His research was roundly criticized by colleagues in 2004, and his later publications did not erase the skepticism. Mice may very well have these egg-precursor cells, several scientists say. But large, long-lived animals are quite different from mice in terms of reproduction—and Tilly hasn’t yet convinced other researchers that women carry around cells capable of extending their fertility. Still, more scientists are coming around to the possibility that egg-precursor cells exist, says Evelyn Telfer, a reproductive biologist at the University of Edinburgh. Initially quite dubious of Tilly’s findings, she changed her mind after touring his lab, welcoming him into her own, and working with the egg-­precursor cells herself. “As with all things that are new, it takes time to get into the consciousness of people,” says Telfer, who now collaborates with ­OvaScience. A small study she has recently finished suggests that egg-precursor cells may help women regenerate their egg supply after experiencing a catastrophe, like chemotherapy for cancer. “It’s an observation we’ve made, and we have to do a lot more work to find out what these cells are doing to the ovary and why we’re seeing an increased number of eggs,” she says. Regardless of what these cells are, the dozen scientists interviewed—most of whom didn’t want their names associated with the company—questioned the idea of using them to “rejuvenate” older eggs. It’s not scientifically obvious that adding extra energy to egg cells would make them more fertile. Carol Hanna, a staff scientist for the Assisted Reproductive Technology Core Laboratory at the Oregon Health & Science University in Portland, says she and others in the field truly hope that Tilly’s science is accurate, but they feel it shouldn’t have moved so quickly to commercialization. “I think a lot of people fall in that middle—they want to believe it but haven’t seen that one piece of information that convinces them,” she says. Renee Reijo Pera, a reproductive and stem-cell biologist at Montana State University, is even more blunt: “Almost everybody thinks that the commercial side of the whole enterprise got way out ahead of the science.” In most areas of medicine other than fertility, it’s standard practice to prove that something works before offering it to patients. Regulations in many countries, however, allow fertility clinics to try a procedure first and test it years later. As a result, dozens of so-called add-on procedures to IVF are available to women with very little scientific justification. Industry leaders defend this approach; the first test-tube baby would never have been born if there had been more regulations. But this lack of rigorous oversight also makes patients vulnerable to abuse, says Carl Heneghan, director of the University of Oxford’s Centre for Evidence-Based Medicine. “The sheer number of treatments that are available tells you they all can’t work,” suggests Heneghan. “People will try anything. That’s where the problem starts.” But there actually aren’t many alternatives available to infertile couples, says Jake Anderson-Bialis, a venture capitalist turned fertility advocate who cofounded the patient community FertilityIQ. International adoptions have become much more difficult; IVF is costly and puts women on a hormonal roller coaster; and buying another woman’s eggs if their own are too old can add $30,000 or more to that cost. Anderson-Bialis says he doesn’t blame OvaScience for taking its products to market before the science is firmly established. The infertility business has always been that way. And in his view, the problem of infertility is so big that it justifies some risk-taking. Improving the odds This has been a busy few months for ­OvaScience. In 2016, the company signed on seven new clinics in Canada and Japan, bringing its total to nine worldwide. Harald Stock, who jumped from the board into the CEO’s chair in July, says company officials have begun speaking with the U.S. Food and Drug Administration to explore what it would take to bring Augment to the market in the United States. He will soon decide whether to proceed with the OvaPrime and OvaTure programs. And the company, which had more than $130 million in cash as of September 30, decided to move away from its initial business plan of installing small labs in each of the clinics that use its products, instead relying on a centralized lab, which is cheaper and easier for quality control. Launching a product and a company takes time and personnel, so Stock says he’s committed to moving slowly and deliberately. “We need to stay disciplined to not get overwhelmed,” he says. “We’re still a 100-some-person company and can’t be everywhere.” The company has chosen to build its business in Canada first, because it can cover most of the country from just a few cities, Stock says, meaning there’s no need for a massive sales force. He’s waiting to start marketing until enough clinics have been trained, so that anyone who wants Augment can get it. IVF is a growing business. It’s projected to expand from about $10 billion today to $22 billion globally by 2020. Augment, he says, could help women who fail to get pregnant in a first round of IVF. A bigger prize for the company could be in its other projects. OvaPrime could make it possible for women who lack viable eggs to have biological children, he says. And anyone undergoing IVF would prefer to skip the hormones. In the end, though, OvaScience’s market may not turn out to be very big. IVF has been getting markedly better over the last few years. And freezing embryos and even eggs, which costs about the same as IVF plus an annual storage fee of $500 to $1,000, has recently made it much easier for women to preserve high-­quality eggs into their late 30s and 40s. It’s the age of the egg—not the woman—that seems to matter: women in their 40s fare just as well as younger women if the quality of their frozen eggs is high, says Hal ­Danzer, cofounder of the Southern California Reproductive Center, a fertility clinic in Beverly Hills, California. Freezing embryos, meanwhile, allows labs to select those that are most likely to succeed, and transfer them after the hormones needed to stimulate egg production have left the body. Improved IVF success rates leave less room for Augment to shine. Still, boosting the odds even somewhat will entice some prospective parents. Danzer says his patients, many of whom put off parenthood for their careers, are desperate to get pregnant. He has referred several patients to clinics in Canada so they can try Augment, though when asked whether he’d use it in his own clinic, he says: “I think it’s a little too early to say.” Karen Weintraub is a freelance health and science writer in Cambridge, Massachusetts. This story was updated to include additional detail about ongoing studies of Augment.


Wilk M.A.,Medical College of Wisconsin | McAllister J.T.,Medical College of Wisconsin | Cooper R.F.,Marquette University | Dubis A.M.,Moorfields Eye Hospital | And 16 more authors.
Investigative Ophthalmology and Visual Science | Year: 2014

Purpose. Albinism is associated with disrupted foveal development, though intersubject variability is becoming appreciated. We sought to quantify this variability, and examine the relationship between foveal cone specialization and pit morphology in patients with a clinical diagnosis of albinism. Methods. We recruited 32 subjects with a clinical diagnosis of albinism. DNA was obtained from 25 subjects, and known albinism genes were analyzed for mutations. Relative inner and outer segment (IS and OS) lengthening (fovea-to-perifovea ratio) was determined from manually segmented spectral domain-optical coherence tomography (SD-OCT) B-scans. Foveal pit morphology was quantified for eight subjects from macular SD-OCT volumes. Ten subjects underwent imaging with adaptive optics scanning light ophthalmoscopy (AOSLO), and cone density was measured. Results. We found mutations in 22 of 25 subjects, including five novel mutations. All subjects lacked complete excavation of inner retinal layers at the fovea, though four subjects had foveal pits with normal diameter and/or volume. Peak cone density and OS lengthening were variable and overlapped with that observed in normal controls. A fifth hyper-reflective band was observed in the outer retina on SD-OCT in the majority of the subjects with albinism. Conclusions. Foveal cone specialization and pit morphology vary greatly in albinism. Normal cone packing was observed in the absence of a foveal pit, suggesting a pit is not required for packing to occur. The degree to which retinal anatomy correlates with genotype or visual function remains unclear, and future examination of larger patient groups will provide important insight on this issue. © 2014 The Association for Research in Vision and Ophthalmology, Inc.


News Article | December 23, 2016
Site: www.eurekalert.org

In findings they call counterintuitive, a team of UCLA-led researchers suggests that blocking a protein, which is crucial to initiating the immune response against viral infections, may actually help combat HIV. Findings from a study in animals appear to demonstrate that temporarily blocking a type of protein, called type I interferon, can restore immune function and speed up viral suppression during treatment with anti-viral drugs for people with chronic infection of the virus that causes AIDS. This is the first study to show the role that type I interferon plays in driving the body's immune destruction during HIV infection, said Scott Kitchen, associate professor of medicine in the division of hematology/oncology at the David Geffen School of Medicine at UCLA and senior author of the study published in the peer-reviewed Journal of Clinical Investigation. "This finding is completely counterintuitive, because many believe that the more interferon at work, the better," said Kitchen, a member of the UCLA AIDS Institute. "We show that the type of interferon being produced during chronic stages of HIV infection has detrimental effects on the body's ability to fight off HIV and other types of infection or cancer and could actually be contributing to accelerated HIV disease." HIV cripples the immune system by destroying immune cells called CD4 T cells, which are activated during early HIV infection by type I interferon. CD4 T cells are also known as "helper" cells because they signal another type of T cell, the CD8, to destroy HIV-infected cells. Also, HIV evades the body's CD8 cells by constantly mutating, escaping recognition by CD8 cells and making them ineffective. The chronically heightened state of inflammation and activation eventually leads to what is known as immune exhaustion when the immune cells can no longer function properly to clear infected cells. This, along with the loss of CD4 T cells ultimately leads to the destruction of the immune system. The researchers' idea is to block type I interferon to reduce chronic activation of the immune cells, which could give the exhausted CD8 T cells the opportunity to restore their abilities to fighting strength. Combine that with antiretroviral therapy and it may be possible to both restore immune function and eradicate HIV throughout the body. The researchers used "humanized mice," which have had their immune systems replaced with human immune system cells, thymus tissue and bone marrow. They treated HIV-infected mice with antibodies that blocked type I interferons, which allowed the mice's immune systems to revert from the state of exhaustion. This made it possible for their immune systems to produce sufficient amounts of CD8 T cells that were primed to attack and kill HIV-infected cells. When combined with antiretroviral therapy, the treatment accelerated the effect of antiretroviral therapy in suppressing HIV. "We found -- counterintuitively -- that blocking this immune response against the virus had beneficial effects in lowering the amounts of virus and increasing the ability of the immune response to clear out the virus," said Kitchen, who is also director of the UCLA Humanized Mouse Core Laboratory. Kitchen noted that these findings offer a proof of principle in a humanized mouse system and are not definitive. More experiments are needed in non-human primates before moving on to human clinical trials to determine whether the researchers' theory holds up and this treatment is safe in humans. But the findings offer a new perspective into the function of type I interferon during untreated and treated HIV chronic infection, said Anjie Zhen, a postdoctoral scholar and member of the UCLA AIDS Institute who led the study. "This could have profound implications for the development of therapies that include such approaches as interferon alpha therapy," Zhen said. "This shows that a proper balance is required when administering this type of therapy, where too much can have detrimental effects in suppressing important immune responses." Study co-authors are Valerie Rezek, Cindy Youn, Brianna Lam, Nelson Chang, Jonathan Rick, Mayra Carrillo, Heather Martin, Saro Kasparian, Philip Syed, and Nicholas Rice of UCLA, and David Brooks of the Princess Margaret Cancer Center in Toronto, Canada and of the University of Toronto. Grants from the National Institutes of Health (AI078806, AI110306-01, AI085043, T32AI060567), the UCLA AIDS Institute (P30AI28697), the California Center for Regenerative Medicine (TR4-06845), the UC Multicampus Research Program and Initiatives, the California Center for Antiviral Drug Discovery, the California HIV/AIDS Research Program (F12-LA-215) and the UCLA Center for AIDS Research (AI28697) funded this study.


INDIANAPOLIS, Oct. 31, 2016 (GLOBE NEWSWIRE) -- The Indiana Biosciences Research Institute (IBRI) today announced Michael Pugia, Ph.D., as a Research Fellow and Director of the new Bioanalytics Core Laboratory.  Pugia comes to the IBRI following a successful 30-year career in the biomedical in-vitro diagnostic industry. There he contributed to more than 20 new product launches for Bayer and Siemens and spent 15 years as a director of research and development working on next generation analytical and diagnostic technologies in collaboration with leading institutions and companies.  His primary research interest is the development of single-cell bioanalytical technology for proteomic biomarkers discovery in the fields of endocrinology and oncology. “Creating new capabilities that enable IBRI researchers and others to do unique research is a key focus for us,” said David Broecker, President and CEO of the IBRI.  “Establishing the new single-cell, bioanalytics core laboratory will provide researchers with tools to isolate individual cells for evaluation under a variety of different biological conditions to identify new targets for the development of novel diagnostics and therapeutics.” “The technology goal for the new core laboratory is to combine pioneering microfluidics methods and systems for single cell isolation alongside next generation mass spectrometry and immune and molecular assays,” said Pugia.  “Joining the IBRI will enable me to create something that is extremely novel, building off my experiences and research interests. In my early discussions with other IBRI researchers and corporate stakeholders, I have found tremendous support for my plans and ideas in establishing these capabilities.” In 2009 Pugia was awarded the Siemens Inventor of the Year for his work on a miniaturized “lab-on-a-chip” diagnostic tool. He also was recognized with 9 Bayer Science and Technology Awards including the Outstanding Bayer Technology Award, the Bayer Corp Quality Excellence Award, and the Near Patient Testing Segment, General Manager Award for Exceptional Leadership. The American Association of Chemistry honored him as the Samuel Natelson Senior Investigator in recognition of outstanding service for the advancement of clinical chemistry, and as the winner of the 1st Annual AI Free Memorial Lectureship. Pugia holds 367 U.S. and foreign patents and has 72 pending patents, and has 55 manuscripts, 13 book chapters and hundreds of conference papers and lectures in a wide variety of chemistry disciplines to his name. He earned his Ph.D. in chemistry from Texas Tech University and his bachelor’s degree in chemistry from Clarkson University. While working in industry, he has held adjunct positions as a Visiting Scholar at the University of Notre Dame and as a Clinical Research Professor at the University of Louisville Medical School. Zane Baird will join Pugia’s lab as Staff Scientist. He graduated from Purdue University in 2016 with a Ph.D. in analytical chemistry and holds a bachelor’s degree in chemistry from Southern Utah University. The Indiana Biosciences Research Institute (IBRI) is an independent, nonprofit discovery science and applied research institute focused on innovation targeting cardio-metabolic diseases, diabetes and poor nutrition. Inspired by the state and Indiana’s leading life sciences companies, research universities and philanthropic community, the IBRI is building a world-class organization of researchers, innovators, and entrepreneurs that will catalyze scientific discovery and its application, resulting in improved health outcomes for patients. For more information about IBRI and donation or collaboration opportunities, please visit www.indianabiosciences.org.


Summers C.G.,University of Minnesota | Connett J.E.,University of Minnesota | Holleschau A.M.,University of Minnesota | Anderson J.L.,Core Laboratory | And 3 more authors.
Clinical and Experimental Ophthalmology | Year: 2014

Background: Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that supplying a precursor to dopamine, levodopa, may improve visual acuity in albinism by enhancing neural networks. This study examines the safety and effectiveness of levodopa on best-corrected visual acuity in human subjects with albinism. Design: Prospective, randomized, placebo-controlled, double-masked clinical trial conducted at the University of Minnesota. Participants: Forty-five subjects with albinism. Methods: Subjects with albinism were randomly assigned to one of three treatment arms: levodopa 0.76mg/kg with 25% carbidopa, levodopa 0.51mg/kg with 25% carbidopa, or placebo and followed for 20 weeks, with best-corrected visual acuity measured at enrollment, and at weeks 5, 10, 15, and 20 after enrollment. Side-effects were recorded with a symptom survey. Blood was drawn for genotyping. Main Outcome Measures: Side-effects and best-corrected visual acuity 20 weeks after enrolment. Results: All subjects had at least one mutation found in a gene known to cause albinism. Mean age was 14.5 years (range: 3.5 to 57.8 years). Follow up was 100% and compliance was good. Minor side-effects were reported; there were no serious adverse events. There was no statistically significant improvement in best-corrected visual acuity after 20 weeks with either dose of levodopa. Conclusions: Levodopa, in the doses used in this trial and for the time course of administration, did not improve visual acuity in subjects with albinism. © 2014 Royal Australian and New Zealand College of Ophthalmologists.


Sharma R.,Core Laboratory | Ahlawat S.,Core Laboratory | Tantia M.S.,Core Laboratory
Iranian Journal of Veterinary Research | Year: 2015

This is the first description of the polymorphisms of arylalkylamine-N-acetyltransferase (AA-NAT) gene in Indian goats with different reproductive traits (twinning percentage and age of sexual maturity). Based on the important role of AA-NAT in reproduction, it is considered as a possible candidate gene for this trait. Two novel synonymous SNPs, C825T (exon2) and C1249T (exon3) were identified. All three possible genotypes (CC,CT and TT) were identified for C825T mutation whereas two genotypes were observed (CC and CT) for C1249T mutation. SNPs C825T and C1249T changed recognition site of restriction enzyme BtsCI (GGATG) and AciI (CCGC) and thus can be genotyped by the relatively simple and cost effective technique of PCR-RFLP for establishing further association with reproductive traits. Present results add to the meager existing knowledge and extend the spectrum of genetic variation of caprine candidate genes of reproductive traits, which is another step towards improvement of goat genetic resources and breeding.


Darabi A.,Core Laboratory | Hocquet D.,University Hospital | Dowzicky M.J.,Pfizer
Diagnostic Microbiology and Infectious Disease | Year: 2010

We report here on the in vitro activity of tigecycline and comparators against a global collection of Streptococcus pneumoniae and Haemophilus influenzae collected between 2004 and 2008 as part of the Tigecycline Evaluation and Surveillance Trial. A total of 6785 S. pneumoniae and 6642 H. influenzae isolates were collected, most from North America. The percentages of penicillin-intermediate resistance and penicillin resistance among S. pneumoniae in North America were 27.8% and 14.3%, respectively. Penicillin resistance ranged from 9.3% in Europe to 25.1% in the Asia-Pacific Rim. The rate of β-lactamase-producing H. influenzae was 25.8% in North America, and among the other regions, it ranged from 8.7% in South Africa to 26.8% in the Asia-Pacific Rim. Tigecycline MIC90's were 0.03 to 0.12 mg/L and 0.5 to 2 mg/L, depending on the region considered, against S. pneumoniae and H. influenzae, respectively. Tigecycline had low MIC90's against S. pneumoniae and H. influenzae, irrespective of resistance to β-lactams. © 2010 Elsevier Inc.


PubMed | Core Laboratory
Type: Journal Article | Journal: Iranian journal of veterinary research | Year: 2016

This is the first description of the polymorphisms of arylalkylamine-N-acetyltransferase (AA-NAT) gene in Indian goats with different reproductive traits (twinning percentage and age of sexual maturity). Based on the important role of AA-NAT in reproduction, it is considered as a possible candidate gene for this trait. Two novel synonymous SNPs, C825T (exon2) and C1249T (exon3) were identified. All three possible genotypes (CC, CT and TT) were identified for C825T mutation whereas two genotypes were observed (CC and CT) for C1249T mutation. SNPs C825T and C1249T changed recognition site of restriction enzyme BtsCI (GGA T G) and AciI (C C GC) and thus can be genotyped by the relatively simple and cost effective technique of PCR-RFLP for establishing further association with reproductive traits. Present results add to the meager existing knowledge and extend the spectrum of genetic variation of caprine candidate genes of reproductive traits, which is another step towards improvement of goat genetic resources and breeding.

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