Medical research and innovation : Innovation + Job News

A neuroscientist at Johns Hopkins has unlocked the mystery of how mammals control their brain circuitry by combining a truly old school research technique with modern molecular genetics. The technique dates back 136 years and when applied to modern molecular genetics technology Dr. David Ginty has been able to see how a mammal's brain shrewdly revisits and reuses the same molecular cues to control the complex design of its circuits.

Details of the observation in lab mice, published Dec. 24 in Nature, reveal that semaphorin, a protein found in the developing nervous system that guides filament-like processes, called axons, from nerve cells to their appropriate targets during embryonic life, apparently assumes an entirely different role later on, once axons reach their targets. In postnatal development and adulthood, semaphorins appear to be regulating the creation of synapses, those connections that chemically link nerve cells.

"With this discovery we're able to understand how semaphorins regulate the number of synapses and their distribution in the part of the brain involved in conscious thought," says Dr. Ginty, a professor in the Neuroscience Department at the Johns Hopkins University School of Medicine and a Howard Hughes Medical Institute investigator. "It's a major step forward, we believe, in our understanding of the assembly of neural circuits that underlie behavior."

Because the brain's activity is determined by how and where these connections form, Ginty says that semaphorin's newly defined role could have an impact on how scientists think about the early origins of autism, schizophrenia, epilepsy and other neurological disorders.

The discovery came as a surprise finding in studies by the Johns Hopkins team to figure out how nerve cells develop axons, which project information from the cells, as well as dendrites, which essentially bring information in. Because earlier work from the Johns Hopkins labs of Ginty and Alex Kolodkin, Ph.D., showed that semaphorins affect axon trajectory and growth, they suspected that perhaps these guidance molecules might have some involvement with dendrites.

Kolodkin, a professor in the Neuroscience Department at Johns Hopkins and a Howard Hughes Medical Institute investigator, discovered and cloned the first semaphorin gene in the grasshopper when he was a postdoctoral fellow. Over the past 15 years, numerous animal models, including strains of genetically engineered mice, have been created to study this family of molecules.

Using two lines of mice -- one missing semaphorin and another missing neuropilin, its receptor -- postdoctoral fellow Tracy Tran used a classic staining method called the Golgi technique to look at the anatomy of nerve cells from mouse brains. (The Golgi technique involves soaking nerve tissue in silver chromate to make cells' inner structures visible under the light microscope; it allowed neuroanatomists in 1891 to determine that the nervous system is interconnected by discrete cells called neurons.)

Tran saw unusually pronounced "spines" sprouting willy-nilly in peculiar places and in greater numbers on the dendrites in the neurons of semaphorin-lacking and neuropilin-lacking mice compared to the normal wild-type animals. It's at the tips of these specialized spines that a lot of synapses occur and neuron-to-neuron communication happens, so Tran suspected there might be more synapses and more electrical activity in the neurons of the mutant mice.

The researchers tested this hypothesis by examining even thinner brain slices under an electron microscope.

The spines of both semaphorin-lacking and neuropilin-lacking mice were dramatically enlarged, compared to those of the smaller, spherical-looking spines in the wild-type mice. In wild types, Tran generally noted a single site of connection per spine. In the mutants, the site of connection between two neurons was often split.

Source: Johns Hopkins University
Writer: Walaika Haskins

The results of a preliminary study by scientists at the National Institutes of Health and Johns Hopkins show that "mini" stem cell transplantation may safely reverse severe sickle cell disease in adults.

The phase I/II study to establish safety of the procedure, published Dec. 10 in the New England Journal of Medicine, describes 10 patients with severe sickle cell disease who received intravenous transplants of blood-forming stem cells. The transplanted stem cells came from the peripheral blood of healthy related donors matched to the patients' tissue types.

Using this procedure, nine of 10 patients treated have normal red blood cells and reversal of organ damage caused by the disease.

Jonathan Powell, M.D., Ph.D., associate professor at the Johns Hopkins Kimmel Cancer Center, says the intravenous transplant approach for sickle cell disease, caused by a single mutation in the hemoglobin gene, does not replace the defective gene, but transplants blood stem cells that carry the normal gene.

Sickle cell disease, named for the "deflated" sickle-shaped appearance of red blood cells in those with the disease, hinders the cells' ability to carry oxygen throughout the body. In severe cases, it causes stroke, severe pain, and damage to multiple organs, including the lungs, kidneys and liver.

All patients in the study, ranging in age from 16 to 45, were treated at the NIH with what researchers call a non-myeloablative or "mini" transplant, along with an immune-suppressing drug called rapamycin.

Conventional transplant methods use high doses of chemotherapy to wipe out the immune system before the transplanted cells are injected, a process that has many side effects, including serious bacterial and fungal infections, which may kill some patients. In mini-transplants, lower doses of medication and radiation are used to make room for the donor's cells, the new source for healthy red blood cells in the patient.

According to Powell, side effects, including low white blood cell counts, were few and very mild compared with conventional bone marrow transplantation. But in nine of the 10, donor cells now coexist with the patients' own cells. One patient was not able to maintain the transplanted cells long term.

Mini-transplants for sickle cell disease were tested in patients almost a decade ago, but were unsuccessful because the patients' immune systems rejected the transplanted cells, says Powell.

By employing the drug rapamcyin, he says, this new approach promotes the coexistence of the host and donor cells.

Powell's earlier research in mice showed that rapamycin inhibits an enzymatic pathway that suppresses the immune system and makes the host and donor cells tolerant to each other.

The NIH/Johns Hopkins team is conducting further studies on immune cells gathered from patients in their study, and looking at a combination of rapamycin with a well-known cancer drug called cyclophosphamide.

Other teams at Johns Hopkins are studying the use of half-matched donors for transplants in sickle cell patients, helping to widen the pool of potential donors for stem cell transplantation.

Funding for the study was provided by the National Institute of Diabetes, Digestive, and Kidney Diseases and the National Heart, Lung and Blood Institute at the NIH.

Study authors at the NIH include principal investigator John Tisdale, as well as Matthew Hsieh, Elizabeth Kang, Courtney Fitzhugh, M. Beth Link, Roger Kurlander, Richard Childs, and Griffin Rodgers.

Source: Johns Hopkins University
Writer: Walaika Haskins

Working with mice, scientists at Johns Hopkins have shown that a protein made by a gene called "Twist" may be the warning sign that can accurately distinguish stem cells that drive aggressive, metastatic breast cancer from other breast cancer cells.

Building on recent work suggesting that it is a relatively rare subgroup of stem cells in breast tumors that drives breast cancer, scientists have surmised that this subgroup of cells must have some very distinctive qualities and characteristics.

In experiments designed to identify those special qualities, the Hopkins team focused on the gene "Twist" (or TWIST1) � named for its winding shape � because of its known role as the producer of a so-called transcription factor, or protein that switches on or off other genes. Twist is an oncogene, one of many genes we are born with that have the potential to turn normal cells into malignant ones.

"Our experiments show that Twist is a driving force among a lot of other players in causing some forms of breast cancer," says Venu Raman, Ph.D., associate professor of radiology and oncology, Johns Hopkins University School of Medicine. "The protein it makes is one of a growing collection of markers that, when present, flag a tumor cell as a breast cancer stem cell."

Previous stem cell research identified a Twist-promoted process known as epithelial-to-mesenchymal transition, or EMT, as an important marker denoting the special subgroup of breast cancer stem cells. EMT essentially gets cells to detach from a primary tumor and metastasize. The new Hopkins research shows that the presence of Twist, along with changes in two other biomarkers � CD 24 and CD44 � even without EMT, announces the presence of this critical sub-group of stem cells.

"The conventional thinking is that the EMT is crucial for recognizing the breast cancer cell as stem cells, and the potential for metastasis, but our studies show that when Twist shows up in excess or even at all, it can work independently of EMT," says Farhad Vesuna, Ph.D., an instructor of radiology in the Johns Hopkins University School of Medicine. "EMT is not mandatory for identifying a breast cancer stem cell."

Working with human breast cancer cells transplanted into mice, all of which had the oncogene Twist, the scientists tagged cell surface markers CD24 and CD44 with fluorescent chemicals. Following isolation of the subpopulation containing high CD44 and low CD24 by flow cytometry, they counted 20 of these putative breast cancer stem cells. They then injected these cells into the breast tissue of 12 mice. All developed cancerous tumors.

"Normally, it takes approximately a million cells to grow a xenograft, or transplanted tumor," Vesuna says. "And here we're talking just 20 cells. There is something about these cells � something different compared to the whole bulk of the tumor cell � that makes them potent. That's the acid test � if you can take a very small number of purified "stem cells" and grow a cancerous tumor, this means you have a pure population."

Previously, the team showed that 65 percent of aggressive breast cancers have more Twist compared to lower-grade breast cancers, and that Twist-expressing cells are more resistant to radiation.

Twist is what scientists refer to as an oncogene, one that if expressed when and where it's not supposed to be expressed, causes oncogenesis or cancer because the molecules and pathways that once regulated it and kept it in check are gone.

This finding � that Twist is integral to the breast cancer stem cell phenotype � has fundamental implications for early detection, treatment and prevention, Raman says. Some cancer treatments may kill ordinary tumor cells while sparing the rare cancer stem cell population, sabotaging treatment efforts. More effective cancer therapies likely require drugs that kill this important stem cell population.

This study was supported by the Maryland Stem Cell Research Foundation. In addition to Vesuna and Raman, authors of the paper include Ala Lisok and Brian Kimble, also of Johns Hopkins.

Source: Johns Hopkins University
Writer: Walaika Haskins

The completion of the human genome may have answered some of medical researches fundamental questions, however, the discovery has led to more complex questions for scientists. One in particular has left researchers studying gene control perplexed, "How is it that humans, being far more complex than the lowly yeast, do not proportionally contain in our genome significantly more gene-control proteins?"

A collaboration among scientists at the Johns Hopkins School of Medicine that examined protein-DNA interactions across the whole genome may have an answer. Researchers have uncovered more than 300 proteins that appear to control genes, a heretofore undiscovered function for these proteins that were previously known to play other roles in cells. The results, which appear in the Oct. 30 issue of Cell, provide a partial explanation for human complexity over yeast but also throw a curve ball in what we previously understood about protein functions.

"Everyone knows that transcription factors bind to DNA and everyone knows that they bind in a sequence-specific manner," says Heng Zhu, Ph.D., an assistant professor in pharmacology and molecular sciences and a member of the High Throughput Biology Center. "But you only find what you look for, so we looked beyond and discovered proteins that essentially moonlight as transcription factors."

The team suspects that many more proteins encoded by the human genome might also be moonlighting to control genes, which brings researchers to the paradox that less complex organisms, such as plants, appear to have more transcription factors than humans. "Maybe most of our genes are doing double, triple or quadruple the work," says Zhu. "This may be a widespread phenomenon in humans and the key to how we can be so complex without significantly more genes than organisms like plants."

Source: Heng Zhu, Ph.D., Johns Hopkins
Writer: Walaika Haskins

Saint Agnes Hospital has received the American College of Cardiology Foundation's NCDR ACTION Registry�GWTG Gold Performance Achievement Award for 2009. The South Baltimore hospital is 1 of only 121 hospitals nationwide to do so. The award recognizes Saint Agnes' commitment and success in implementing a higher standard of care for heart attack patients, and signifies that the hospital has set an aggressive goal of treating coronary artery disease patients with 85% compliance to core standard levels of care outlined by the American College of Cardiology/American Heart Association clinical guidelines and recommendations. 

In order to receive the ACTION Registry�GWTG Gold Performance Achievement Award, Saint Agnes consistently followed the treatment guidelines in ACTION Registry�GWTG for 24 consecutive months. These include aggressive use of medications like cholesterol-lowering drugs, beta-blockers, ACE inhibitors, aspirin, and anticoagulants in the hospital.

"The American College of Cardiology Foundation and the American Heart Association commend Saint Agnes Hospital for its success in implementing standards of care and protocols," says Christopher Cannon, MD, ACTION Registry�GWTG Steering Committee Chairperson and Associate Professor of Medicine at Harvard Medical School and Associate Physician in the Cardiovascular Division at Brigham and Women's Hospital in Boston.

"The full implementation of acute and secondary prevention guideline-recommended therapy is a critical step in saving the lives and improving outcomes of heart attack patients," adds Gregg C. Fonarow, MD, ACTION Registry- GWTG Steering Committee Vice- Chairperson and Director of Ahmanson-UCLA Cardiomyopathy Center.

"The time is right for Saint Agnes to be focused on improving the quality of cardiovascular care by implementing ACTION Registry�GWTG. The number of acute myocardial infarction patients eligible for treatment is expected to grow over the next decade due to increasing incidence of heart disease and a large aging population," says Dr. Stephen Plantholt, Chief of Cardiology at Saint Agnes.

Created by the merger of the American College of Cardiology Foundation's NCDR ACTION Registry® and the American Heart Association's Get With The Guidelines-CAD program, ACTION Registry�GWTG combines the best of both programs into a single, unified national registry. The new registry joins the robust data collection and quality reporting features of the ACTION Registry with the collaborative models, unique tools, and quality improvement techniques of the GWTG-CAD program. With the collective strengths of these two programs, ACTION Registry�GWTG empowers health care provider teams to consistently treat heart attack patient according to the most current, science-based guidelines; and establishes a national standard for understanding and improving the quality, safety, and outcomes of care provided for patients with coronary artery disease, specifically high-risk STEMI and NSTEMI patients.

Saint Agnes Hospital is a 307-bed hospital founded by the Daughters of Charity in 1862.

Source: Dr. Stephen Plantholt, Saint Agnes
Writer: Walaika Haskins

University of Maryland School of Medicine researchers have teamed with Sisters Network, Inc., a national African-American breast cancer survivorship organization, to create a patient education video to help African-American women not only survive but thrive following their breast cancer diagnosis.

The 30-minute educational video was produced to address the special challenges African-American breast cancer survivors face. It presents evidence-based guidelines developed by the Institute of Medicine in 2006 to help cancer survivors make a plan of follow-up care that promotes a healthy lifestyle and help prevent the recurrence of their cancer.

The video was produced as part of a research study led by Renee Royak-Schaler, Ph.D., funded by Susan G. Komen for the Cure.

"Developing feasible plans for self-care after breast cancer can be a daunting task, and this is particularly true for African-Americans, whose risk of recurrence and poor health outcomes is greater than for Caucasian patients. Many women don't have a clear plan for follow-up care after their initial treatment, which can seriously affect their overall health and well-being," says Dr. Royak-Schaler, an associate professor of epidemiology and preventive medicine.

Breast cancer deaths are 38 percent higher in African-American women than in white women. This disparity has been linked to lack of access to primary health care and being diagnosed at a later stage when the disease is less treatable. Many African-American women also have what is known as "triple-negative" breast cancer, which doesn't respond as well to therapy.

"Sisters Network is pleased to collaborate with University of Maryland School of Medicine to increase breast cancer survivorship awareness," says Karen Jackson, founder and chief executive officer of Sisters Network, Inc. "Women need to know that survivorship is not only about defeating cancer, but adopting a healthy, active lifestyle that hopefully will prevent the cancer from returning."

The video features African-American breast cancer survivors talking about their experiences Stacy D. Garrett-Ray, M.D., a family medicine physician and clinical assistant professor of family and community medicine, and Cynthia L. Drogula, M.D., a breast surgeon and assistant professor of surgery.

"It's imperative that breast cancer survivors communicate with their doctors and understand what they need to do to take good care of themselves. Eating a healthy diet and exercising are very important. Taking part in a support group can also be very helpful in dealing with all the unique challenges of life after cancer," Dr. Garrett-Ray says. She is also medical director of the Baltimore City Cancer Program at the University of Maryland Marlene and Stewart Greenebaum Cancer Center, which provides free cervical and breast cancer screening for uninsured women in Baltimore.

"We hope that this video will prove to be a useful educational tool not only for African-American breast cancer survivors but also the doctors who care for them," Dr. Garrett-Ray says.

Source: Dr. Renee Royak-Schaler, University of Maryland School of Medicine
Writer: Walaika Haskins

Researchers have known for some time that 95 percent of the cells that shuttle sound to the brain are large, lively neurons found deep within the ear. These big boys have accounted for most of what scientists know about how hearing works. That said, however, scientist have also speculated that there could be a second set of rare, tiny cells that carry signals from the from the inner ear to the brain and play a part in how sound is processed.

A team of Johns Hopkins researchers report in the Oct. 22 issue of Nature that rat experiments have measured and recorded electrical activity of the type II neurons in the cochlea, snail-shell-like structure within the ear, for possibly the first time. Their research seems to confirm what had previously been posited that the cells do carry signals from the ear to the brain, and the sounds they likely respond to would need to be loud, such as sirens or alarms that might be even be described as painful or traumatic.

According to the researchers, they've also discovered that these cells perform by responding to glutamate, a neurotransmitter found throughout the nervous system that stimulate the cochlear to transmit acoustic information to the brain, released from sensory hair cells of the inner ear.

"No one thought recording them was even possible," says Paul A. Fuchs, Ph.D., the John E. Bordley Professor of Otolaryngology-Head and Neck Surgery and co-director of the Center for Sensory Biology in the Johns Hopkins University School of Medicine, and a co-author of the report. "We knew the type II neurons were there and now at last we know something about what they do and how they do it."

Working with week-old rats, neuroscience graduate student Catherine Weisz removed live, soft tissue from the fragile cochlea and, guided by a powerful microscope, touched electrodes to the tiny type II nerve endings beneath the sensory hair cells. Different types of stimuli were used to activate sensory hair cells, allowing Weisz to record and analyze the resulting signals in type II fibers.

Results showed that, unlike type I neurons which are electrically activated by the quietest sounds we hear, and which saturate as sounds get louder, each type II neuron would need to be hit hard by a very loud sound to produce excitation, Fuchs says.

Fuchs and his team postulate that the two systems may serve different functional roles. "There's a distinct difference between analyzing sound to extract meaning - Is that a cat meowing, a baby crying or a man singing? - versus the startle reflex triggered by a thunderclap or other sudden loud sound." Type II afferents may play a role in such reflexive withdrawals from potential trauma."

Source: Paul Fuchs, Ph.D., Johns Hopkins University School of Medicine
Writer: Walaika Haskins

Jhpiego, an international non-profit health care organization affiliated with Johns Hopkins University, has been selected as The Daily Record's 2009 Innovator of the Year Awards.

"We are honored to be named a 2009 Innovator of the Year by The Daily Record," says Dr. Leslie Mancuso, president and CEO of Jhpiego. "At Jhpiego, we are dedicated to saving the lives of women and their families. We do that by taking the science and creativity of Johns Hopkins University and use that knowledge to create low-cost health solutions that can be utilized in remote locations with few resources, like running water or electricity around the world.."

The Daily Record began the Innovator of the Year Awards in 2002 as a way to recognize Marylanders and Maryland-based companies for their innovative spirit � for creating new products, new programs, new services, or new processes that have helped their companies, industries, or communities.

There were more than 80 nominations for the 2009 awards nominated by readers, economic development agencies, chambers of commerce, and the business community at large. Nominees are then asked to complete an application, which explains their innovation, and the impact it has made on Maryland.

A renowned panel of judges reviewed the applications and whittled the list down to 25 winners for 2009, including the top Innovator of the Year. The winners were honored on October 14 at a cocktail reception, held at Baltimore's American Visionary Art Museum. Winners also were profiled in a special magazine that was included in the October 16 issue of The Daily Record.

Source: Leslie Mancuso, Jhpiego
Writer: Walaika Haskins

Baltimore-based BioMarker Strategies, LLC has been awarded a Fast-Track Small Business Innovation Research (SBIR) contract from the National Cancer Institute to develop the SnapPath live-tumor-cell testing system. BioMarker Strategies is developing the SnapPath system to enable oncologists to determine the most effective drug treatment for their cancer patients.

Under this contract, the company will receive an initial award of $254,000 and be eligible to receive an additional $2 million when the first phase of work is completed�for a total potential contract amount of $2.3 million.

"We are gratified by this award from the NCI to support the development of our SnapPath technology and plan to use these funds to expedite production of a prototype of our live-tumor-cell testing system," says Karen Olson, CEO of BioMarker Strategies.

BioMarker Strategies was awarded this funding under NCI contract opportunity #257, Biopsy Instruments and Devices that Preserve the Molecular Profiles in Tumors, designed to identify "innovative approaches for tumor biopsy that preserve the molecular profile (that) will create an entirely new diagnostic area and market in molecular therapeutics, which will not only facilitate pharmacodynamic assessment of targeted therapeutics but also enable individualized molecular therapy of solid tumors based on accurate information about signal transduction pathways, molecular drug targets and biomarkers."

Source: Karen Olson, BioMarker Strategies
Writer: Walaika Haskins

FASgen, Inc., a Baltimore-based developer of small molecule therapeutics and diagnostics fatty acid biosynthesis targets, was awarded a $1.4 million Small Business Innovation and Research (SBIR) Phase II NIH grant for continued research for obesity. FASgen has conducted extensive research into the effects of inhibition of the fatty acid biosynthesis pathway on the regulation of appetite and weight loss for some time.

The company has developed numerous families of compounds that act on the well identified targets in the pathway, including fatty acid synthase (FAS), carnitine palmitoyl transferase-1 (CPT-1) and mitochondrial glyceraol-3aclytransferase (GPAT). The current research effort will optimize FASgen's compounds for use in future clinical trials. The research is in part conducted in cooperation with labs at Johns Hopkins University under a research agreement between the FASgen and Johns Hopkins.

"This grant supplements the Company's extensive product development efforts in the metabolic disease field. The weight loss effects seen to date in preclinical in vivo experiments have applications in various indications, including obesity, diabetes, and fatty liver disease, including specifically non-alcoholic steatohepatitis," says Susan Medghalchi, Ph.D., FASgen's principal investigator under the grant.
 
FASgen's Chairman, Eric F. Stoer, also says that the metabolic program runs in parallel with the company's successful efforts to develop a different set of FAS inhibitor compounds for use in the treatment of cancer. The company's oncology program was partnered with J&J last year and that collaboration continues to demonstrate the validity of the principle that FASi can and does safely kill cancer cells.


Source: Susan Medghalchi, PH.D., FASgen
Writer: Walaika Haskins

Johns Hopkins University researcher Carol Greider, Ph.D., received the 2009 Nobel Prize in Physiology or Medicine from the Royal Swedish Academy of Sciences. One of the world's pioneering researchers on the structure of chromosome ends known as telomeres,  The Academy recognized Greider for her 1984 discovery of telomerase, an enzyme that maintains the length and integrity of chromosome ends and is critical for the health and survival of all living cells and organisms.

Greider is the Daniel Nathans Professor and Director of Molecular Biology and Genetics in the Johns Hopkins Institute for Basic Biomedical Sciences. She shares the award with Elizabeth Blackburn, a professor of biochemistry and biophysics at the University of California, San Francisco, and Jack Szostack, Ph.D., of Harvard Medical School, who discovered that telomeres are made up of simple, repeating blocks of DNA building blocks and are found in all organisms. The trio also shared the 2006 Albert Lasker Award for Basic Medical Research for this work. Each of the three will receive a medal, a diploma and will split a cash prize of $1.4 million that will be handed out at a ceremony held in Stockholm on Dec. 10.

"What intrigues basic scientists like me is that any time we do a series of experiments, there are going to be three or four new questions that come up when you think you've answered one. Our approach shows that while you can do research that tries to answer specific questions about a disease, you can also just follow your nose," says Greider.


Source: Carol Greider, Ph.D., Johns Hopkins University
Writer: Walaika Haskins

The National Institutes of Health (NIH) has awarded some $5 billion in grants to support research seeking to develop cures for cancer and other diseases, and to create jobs.

President Barack Obama made the announcement Wednesday at the NIH campus in Bethesda, Md., with Health and Human Services Secretary Kathleen Sebelius.

The money is part of the feds $787 billion economic stimulus program designed to help create jobs and stop the U.S. economy's downward spiral. It is part of an overall $100 billion, $10 billion for the NIHan investment in science and technology to lay the foundation for the innovation economy of the future.

More than $1 billion of the grant funding is dedicated to research applying the technology produced by the Human Genome Project between 1990 and 2003. This new funding will allow researchers to make quantum leaps forward in studying the genomic changes linked to cancer, heart, lung, and blood disease and autism- potentially leading to new treatments and cures. The investment includes $175 million for The Cancer Genome Atlas (TCGA) to collect more than 20,000 tissue samples from more than 20 cancers, and determine in detail all of the genetic changes in thousands of these tumor samples. TCGA involves more than 150 scientists at dozens of institutions around the country. All data will be rapidly deposited in databases accessible to the worldwide research community.

The $5 billion will help fund more than 12,000 existing projects and create tens of thousands of jobs in research and education over the next two years, as well as medical equipment makers and suppliers.


"We are about to see a quantum leap in our understanding of cancer," says Francis S. Collins, M.D., Ph.D., director, NIH. "Cancer is a disease of DNA--it occurs when glitches in the DNA cause a good cell to go bad. This ambitious effort promises to open new windows into the biology of all cancers, transform approaches to cancer research and raise the curtain on a more personalized era of cancer care. This is an excellent example of how the Recovery Act is fueling discoveries that will fundamentally change the way we fight disease and improve our lives."

Source: Francis S. Collins, NIH
Writer: Walaika Haskins

Johns Hopkins' Center for the Epigenetics of Common Human Disease has been selected as one of four recipients of a $45 million National Institutes of Health (NIH) grant for Centers of Excellence to advance genomics research. The Hopkins Center will receive $16.8 million over five years.

"We're grateful for such generous support to continue our work in understanding how epigenetic control affects disease," says the center's director, Andrew Feinberg, M.D., M.P.H.

For five years, Feinberg, professor of molecular medicine at the Johns Hopkins University School of Medicine, has led a team of researchers at the center to study the epigenetic basis of common health problems, including cancer, autism and psychiatric illnesses.

Epigenetics, or "above the genome," refers to changes in genes outside of the DNA sequence itself. The changes affect which genes are turned on or off, and therefore which proteins are produced in cells. According to Feinberg that's because epigenetic variation may be at least as great between individuals as variations in the DNA sequences themselves, understanding the epigenome may help explain how errors occur in normal development and how environmental factors lead to cancer, autism and other disorders.

The center has already developed novel statistical and analytical tools to identify epigenetic modifications across the human genome. With the new funds, awarded by two NIH institutes � the National Human Genome Research Institute (NHGRI) and the National Institute of Mental Health � Feinberg and his colleagues plan to refine these tools so they can be used efficiently and cost effectively in large studies. The team will focus their efforts on studying the epigenetics of bipolar disorder, aging and autism. They will also explore how other factors, such as a person's genetic makeup, lifestyle choices and environmental exposures, interact with epigenetic factors to cause disease.

Source: Andrew Feinberg, Johns Hopkins University School of Medicine
Writer: Walaika Haskins

Arginetix, a Baltimore-based biopharmaceuticals firm, closed a Series A financing round after raising $10.75 million. The company is developing small molecule inhibitors of the enzyme arginase for the treatment of endothelial dysfunction, including pulmonary arterial hypertension, atherosclerosis and asthma.

Both Quaker BioVentures and MedImmune Ventures, a wholly owned venture capital fund of the AstraZeneca Group, led the financing.. Maryland Health Care Product Development Corp., Osage University Partners, Red Abbey Venture Partners, and company co-founder Acidophil LLC also participated in the round.

The financing will be used for continued research and development of Arginetix's first-in-class arginase inhibitors for cardiovascular and pulmonary indications. The company's scientific foundation is based on licensed intellectual property of its scientific co-founders, David Christianson, Ph.D. at the University of Pennsylvania and Dan Berkowitz, M.D. at The Johns Hopkins University.

"This financing is an important endorsement for the potential for Arginetix' discovery and development programs," said Gary Lessing, CEO and co-founder. "The company is fortunate to be working with a talented and experienced group of investors, including both traditional and corporate-based life sciences firms. Their expertise in the discovery and development of drugs and their track record at building world-class companies will be invaluable to Arginetix' continued success."

"Arginetix is pursuing major clinical opportunities using their technology for patients with cardiovascular and pulmonary diseases. The company's recent research has added further validation for this important innovation," says Dr. Geeta Vemuri, partner at Quaker BioVentures.

"Arginase appears to be an attractive target with therapeutic potential in a wide range of cardiovascular and pulmonary indications. We are pleased to support their development efforts through this investment and look forward to working with the management team," says Eva M. Jack, Managing Director at MedImmune Ventures.

Source: Gary Lessing, Arginetix
Writer: Walaika Haskins

The Johns Hopkins University has received 250 research grants, for a total of $114 million, as a result of the federal stimulus package designed to advance scientific and medical knowledge while jump-starting the U.S. economy.

The grants will underwrite scientific investigations ranging from the best strategies to motivate drug addicts released from in-patient rehabilitation to agree to enroll in continuing sobriety support programs to the role certain proteins play in the development of muscle-wasting diseases, such as muscular dystrophy.

In addition to advancing the medical communities knowledge and understanding, the grants also serve to generate jobs at Johns Hopkins, boosting the region's economy, as employees spend their paychecks and Hopkins' laboratories hire personnel and buy supplies.

"This milestone is a testament to the outstanding research that our world-class faculty is conducting across the university," says Lloyd Minor, provost and senior vice president for academic affairs. "They have responded to the opportunities created by the stimulus package with the drive, commitment and entrepreneurial spirit that continues to distinguish Johns Hopkins."

Source: Lloyd Minor, Johns Hopkins University
Writer: Walaika Haskins