Wednesday, February 19, 2014 3:00 p.m. - 4:00 p.m. BSEB 272 Guest Speaker - Dr. Joseph Miano University of Rochester School of Medicine & Dentistry "Regulatory Control of Smooth Muscle Cell Phenotypes" Wednesday, January 15, 2014 12:00 - 1:00 p.m. BSEB East Lecture Hall Research Grand Rounds - Dr. Cam Patterson University of North Carolina at Chapel Hill

Wednesday, November 20, 2013 4:00 p.m. BRC 109 Guest speaker, Dr. Depei Liu, will present "Protective Roles of SIRT1 in vascular diseases" Friday, November 15, 2013 12:00 p.m. BSEB 276 Guest speaker, Dr. Ingrid Fleming, will present "The AMPK: homeostasis angiogenesis and mircroRNA"

Friday, October 18, 2013 4:00 - 5:00 p.m. BSEB 306D Dr. Yue Wu - Research Data Presentation Zhaoyu Liu - Journal Club Friday, October 11, 2013 4:00 - 5:00 p.m BSEB 306D Dr. Kate Coughlan - Research Data Presentation

Wednesday, October 9, 2013 12:15 - 1:00 p.m. BSEB East Lecture Hall Guest speaker, Dr. Joseph Loscalzo, will present "Pulmonary Arterial Hypertension: Newer Concepts in Pathobiology and Treatment" Friday, September 20, 2013 4:00 - 5:00 p.m. BSEB 306D Dr. Ouyang Changhan - Research Data Presentation Dr. Kate Coughlan - Journal Club

Friday, September 13, 2013 4:00 - 5:00 p.m. BSEB 306D Dr. Wencheng Zhang - Research Data Presentation Friday, September 6, 2013 4:00 - 5:00 p.m. BSEB 306D Dr. Xiaoyan Dai - Research Data Presentation Dr. Hairong Xu - Journal Club

Friday, August 30, 2013 4:00 - 5:00 p.m. BSEB 306D Dr. Qilong Wang - Research Data Presentation Dr. Changhan Ouyang - Journal Club Friday, August 9, 2013 4:00 - 5:00 p.m. BSEB 306D Dr. Huaiping Zhu- Research Data Presentation Dr. Ping Song- Journal Club Friday, June 28, 2013 12:00 - 1:00 p.m. BSEB 306D Zhaoyu Liu- Research Data Presentation Friday, June 23, 2013 12:00 - 1:00 p.m. BSEB 276 Dr. Ramani Ramchandran from the University of Wisconsin will present "EV2 Transcriptional Regulation During Cardiac Progenitor Cell Development" Friday, June 21, 2013 12:00 - 1:00 p.m. BSEB 306D Dr. Qiongxin Wang- Research Data Presentation Monday, June 17, 2013 9:00 - 10:15 a.m. BSEB 276 Dr. David Weber from the University of South Alabama will present "Reactive Oxygen Species Regulation of Vascular Remodeling During Stenosis" Friday, June 7, 2013 12:00 - 1:00 p.m. BSEB 306D Dr. Cate Moriasi- Research Data Presentation Friday, May 7, 2013 12:00 - 1:00 p.m. BSEB 306D Dr. Kate Coughlan- Research Data Presentation

Friday, May 3, 2013 12:00 - 1:00 p.m. BSEB 306D Dr. Hairong Xu- Research Data Presentation

Wednesday, May 1, 2013 9:00 a.m. BSEB 272 Dr. Patrice Delafontaine of Tulane University will present "Angiotensin II: Novel Effects on Skeletal Muscle"

Friday, April 26, 2013 12:00 - 1:00 p.m. BSEB 306D Braxton Nottingham- Research Data Presentation

Friday, April 19, 2013 12:00 - 1:00 p.m. BSEB 306D Dr. Changhan Ouyang- Research Data Presentation

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Newswise Researchers at the University of California, San Diego School of Medicine have found that too little or too much of an enzyme called SRPK1 promotes cancer by disrupting a regulatory event critical for many fundamental cellular processes, including proliferation.

The findings are published in the current online issue of Molecular Cell.

The family of SRPK kinases was first discovered by Xiang-Dong Fu, PhD, professor in the Department of Cellular and Molecular Medicine at UC San Diego in 1994. In 2012, Fu and colleagues uncovered that SPRK1 was a key signal transducer devoted to regulating alternative pre-mRNA splicing, a process that allows a single gene to produce multiple mRNA isoforms, which in many cases encode functionally distinct proteins. In this pathway, SRPK1 was a downstream target of Akt, also known as protein kinase B. Akt- activated SRPK1 moves to the nucleus to induce its targeted splicing factors.

In their latest paper, Fu and colleagues report that SRPK1 was found to act as a tumor suppressor because when ablated or removed from mouse embryonic fibroblasts, unwanted cell transformation occurred. Unexpectedly, when SRPK1 was overexpressed in mouse cells, tumor development also happened.

To my knowledge, this is the first time it has been shown that a signal kinase behaves as a tumor suppressor or a promoter, depending upon its abundance in the same cell said Fu. The point is that too much or too little are both bad.

Such contrary phenomena are due to a surprising role of SRPK1 in regulating the activity of Akt via a specific Akt phosphatase discovered earlier by Alexandra C. Newton, PhD, professor of pharmacology at UC San Diego. The Akt phosphatase cannot find Akt when there is too little SRPK1 to assist, and the phosphatase is tied up when there is too much SRPK1. In both cases, the result is a dampening of Akt inactivation.

As Akt plays a key role in many cellular processes, such as glucose metabolism, apoptosis, proliferation and all key aspects of tumor development, the elucidated mechanism provides a critical insight into tumorigenesis in humans. Indeed, compared to normal cells, many tumors show SRPK1 overexpression while others display reduced expression.

The findings may have future therapeutic implications, but Fu said the challenges remain daunting. Most tumors show SRPK1 overexpression, so it may be possible to treat certain cancers with a specific SRPK1 inhibitor. This has been already demonstrated by others. But suppressing a cancer not related to SRPK1 overexpression could actually stimulate that cancer.

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Cancer and the Goldilocks Effect

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Newswise PHILADELPHIA A new study in a mutant fruitfly called sleepless (sss) confirmed that the enzyme GABA transaminase, which is the target of some epilepsy drugs, contributes to sleep loss. The findings, published online in Molecular Psychiatry, were led by Amita Sehgal, PhD, head of the Chronobiology Program at the University of Pennsylvanias Perelman School of Medicine. The findings shed light on mechanisms that may be shared between sleep disruption and some neurological disorders. A better understanding of this connection could enable treatments that target both types of symptoms and perhaps provide better therapeutic efficacy.

Epilepsy is essentially an increase-in-firing disorder of the brain and maybe a decrease in activity of the neurotransmitter GABA, too, says Sehgal, who is also a professor of Neuroscience and an investigator with the Howard Hughes Medical Institute (HHMI). This connects our work to drugs that inhibit GABA transaminase. Changes in GABA transaminase activity are implicated in epilepsy and some other psychiatric disorders, which may account for some of the associated sleep problems.

The team looked at the proteomics of the sss mutant brain a large-scale study of the structure and function of related proteins -- and found that GABA transaminase is increased in the sss brain compared to controls. This enzyme breaks down GABA, so GABA is decreased in the sss brain. Because GABA promotes sleep, there is a decrease in sleep in the sss mutant fly, as the name implies.

The relationship between the SSS protein and GABA is not fully understood. The SSS protein controls neural activity, and its absence results in increased neural firing, which likely uses up a lot of energy, says Sehgal. GABA transaminase works in the mitochondria, the energy-production organelle in the glial cells of the brain, which provide fuel for neurons. The large energy demand created by the increased neural firing in sss brains probably alters mitochondrial metabolism, including GABA transaminase function in glia.

In the sss mutant fly, there is a stream of connections that leads to its signature loss of sleep: The sss mutant has increased neuron firing caused by downregulation of a potassium channel protein called Shaker. Recently, the Sehgal lab showed that SSS also affects activity of acetylcholine receptors. Both of these actions may directly cause an inability to sleep. In addition, increased energy demands on glia, which increase GABA transaminase and decrease GABA, may further contribute to sleep loss. On the other hand, if GABA is increased, then sleep is increased, as in flies that lack GABA transaminase.

Coauthors are Wen-Feng Chen, Sarah Maguire, Mallory Sowcik, Wenyu Luo, all from Penn and Kyunghee Koh from Thomas Jefferson University. The study was funded by HHMI.

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Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.

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Fruitfly Study: Epilepsy Drug Target Implications for Sleep Disruption in Brain Disorders

PUBLIC RELEASE DATE:

1-Apr-2014

Contact: Sarah Avery sarah.avery@duke.edu 919-660-1306 Duke University Medical Center

DURHAM, N.C. Duke Medicine researchers studying tiny, antennae-like structures called cilia have found a potential way to ease some of the physical damage of numerous genetic disorders that result when these essential cellular components are defective.

Different genetic defects cause dysfunction of the cilia, which often act as sensory organs that receive signals from other cells. Individually, disorders involving cilia are rare, but collectively the more than 100 diseases in the category known as ciliopathies affect as many as one in 1,000 people. Ciliopathies are characterized by cognitive impairment, blindness, deafness, kidney and heart disease, infertility, obesity and diabetes.

Recent research has added key insights into the overall role and function of cilia in cells and what occurs when the organelle is defective.

"Cilia are required for regulation of a whole host of signaling pathways for cellular development," said Nicholas Katsanis, PhD, professor of cell biology and director of the Center for Human Disease Modeling at Duke. "They are not the only signaling regulators, but they are critical. It's been important for us to understand how they do this."

In the current study, published April 1, 2014, in the Journal of Clinical Investigation, Katsanis and colleagues describe a common mechanism that appears to account for how dysfunctional cilia cause so many different problems in cellular signaling pathways.

Using both cells and animal models, they focused on the ubiquitin-proteasome system, the cell's machinery tasked with regulating the cellular environment by breaking down proteins that are either damaged or in need of removal.

"Imagine regular housekeeping" Katsanis said. "Taking out waste is part and parcel to the process, but not if you end up throwing away your valuables."

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Common molecular defect offers treatment hope for group of rare disorders

MERRILLVILLE | Brian Hansen, a two-time Olympian in long track speedskating who lives in the northern suburbs of Chicago, will appear at an upcoming health and wellness expo.

Hosted by the Foundation for Molecular Medicine of Crown Point, the event will take place from 10 a.m.-6 p.m. April 18 and from 8 a.m.-4 p.m. April 19 at Radisson Hotel at Star Plaza, 800 E. 81st Ave.

The annual event will include exhibitors, demonstrations, health screenings and presentations.

The expo is a fundraising event to support the work of the Foundation for Molecular Medicine, which is a nonprofit organization that focuses on cancer research, early detection and education on health and wellness programs that prevent cancer and other degenerative diseases.

The fee is $4, and it can be discounted in half with a coupon obtained from the website http://www.ffmm.org. For more information, to become an exhibitor or a sponsor, contact the foundation at (219) 644-3237.

Diabetes, eye health in focus

MUNSTER | Dr. Rand Diab, a board certified ophthalmologist, will give a presentation about the link between diabetes and eye damage.

The talk will last from 6-7 p.m. April 3 at Franciscan Hammond Clinic Specialty Center, 7905 Calumet Ave.

Attendees will learn how diabetes affects the eyes, what eye conditions diabetics are most at risk for, specific eye tests, treatment options and how to maintain good eye health.

Call (800) 931-3322 to register.

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HEALTH BRIEFS: Expo to feature Olympian

MERRILLVILLE | Brian Hansen, a two-time Olympian in long track speedskating who lives in the northern suburbs of Chicago, will appear at an upcoming health and wellness expo.

Hosted by the Foundation for Molecular Medicine of Crown Point, the event will take place from 10 a.m.-6 p.m. April 18 and from 8 a.m.-4 p.m. April 19 at Radisson Hotel at Star Plaza, 800 E. 81st Ave.

The annual event will include exhibitors, demonstrations, health screenings and presentations.

The expo is a fundraising event to support the work of the Foundation for Molecular Medicine, which is a nonprofit organization that focuses on cancer research, early detection and education on health and wellness programs that prevent cancer and other degenerative diseases.

The fee is $4, and it can be discounted in half with a coupon obtained from the website http://www.ffmm.org. For more information, to become an exhibitor or a sponsor, contact the foundation at (219) 644-3237.

Diabetes, eye health in focus

MUNSTER | Dr. Rand Diab, a board certified ophthalmologist, will give a presentation about the link between diabetes and eye damage.

The talk will last from 6-7 p.m. April 3 at Franciscan Hammond Clinic Specialty Center, 7905 Calumet Ave.

Attendees will learn how diabetes affects the eyes, what eye conditions diabetics are most at risk for, specific eye tests, treatment options and how to maintain good eye health.

Call (800) 931-3322 to register.

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HEALTH BRIEFS: Wellness expo to feature Olympian

Cellular Molecular Basis of Cardiac Disease of Aging
Presented By: Mark Entman, M.D. Professor, Department of Medicine, Pathology and Immunology Chief, Cardiovascular Sciences Section Baylor College of Medicine...

By: UTHSCSA Barshop

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Cellular & Molecular Basis of Cardiac Disease of Aging - Video

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Newswise Physicians have long suspected that chemotherapy can accelerate the aging process in patients treated for cancer. Using a test developed at UNC Lineberger Comprehensive Cancer Center to determine molecular aging, UNC oncologists have directly measured the impact of anti-cancer chemotherapy drugs on biological aging.

Researchers measured the level of p16, a protein that causes cellular aging, in the blood of 33 women over the age of 50 who had undergone chemotherapy for curable breast cancer. Samples were taken for analysis of molecular age from patients before chemotherapy, immediately following chemotherapy and a year after therapy finished. The analysis showed that curative chemotherapy also caused an increase in a patients molecular age that on average was equivalent to 15 years of normal aging. The same was true in a separate group of 176 breast cancer survivors who had received chemotherapy on average three and a half years prior.

The study, headed by Hanna Sanoff, MD, MPH, assistant professor with the UNC School of Medicine and member of UNC Lineberger, is published in this weeks Journal of the National Cancer Institute. Dr. Sanoff said that the results indicate that the p16 test holds promise as a means of evaluating how chemotherapy will affect a patients long-term health and survival and as a predictive biomarker for the long-term toxicity of chemotherapy.

Our theory is that if you have an advanced molecular age to begin with, it will be harder for you to tolerate chemotherapy, said Dr. Sanoff. We believe a high level of p16 before treatment could mean that a patient will have a harder time making new blood cells after each chemotherapy treatment, and therefore be at greater risk for anemia and infection during chemotherapy.

The key role of p16 in human aging has been established over the last decade in the lab of UNC Lineberger Director Dr. Norman Sharpless. Research conducted in Sharpless lab showed in 2004 that the levels of p16 increase exponentially with aging, and developed the p16 blood test for human use in 2009.

The next direction for this research, ongoing under the leadership of Dr. Hyman Muss, director of UNC Linebergers Geriatric Oncology Program, involves determining if markers of molecular age predict patients physical function and outcome in a number of clinical settings.

While these findings are highly provocative, we have much more to study and will have to verify in future trials how these changes in molecular aging affect long term survival, said Dr. Muss. Adjuvant chemotherapy has dramatically improved breast cancer survival and pending further data, the results of our study should not effect adjuvant chemotherapy decisions.

The p16 test seems particularly well-suited as an aging marker for this purpose as it plays a causal role in biological aging, is strongly correlated with chronological aging, and increases exponentially in response to pro-aging stimuli. Dr. Sanoff said she believes the test has promise as the basis of a clinical tool allowing physicians to evaluate the degree to which a given treatment accelerates biological and physical aging.

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Cancer Chemotherapy Accelerates 'Molecular Aging'

Dr David Agus at 2nd Annual Rebels with a Cause Gala #USC #CAMM @DavidAgus
http://www.redcarpetreporttv.com Mingle Media TV and Red Carpet Report host Paige Sullivan were invited to come back and cover the 2nd Annual Rebels with a C...

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Molecular Medicine Video with Katie

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Molecular Medicine Video with Katie - Video

Accelerating Precision Medicine with Efficient Drug Sensitivity Screening
Recently identified associations between variants of cancer genes and drug resistance have increased the value for comprehensive drug sensitivity screening i...

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Accelerating Precision Medicine with Efficient Drug Sensitivity Screening - Video

(PRWEB) March 25, 2014

The Latin American Bioinformatics Market by Sector (Agriculture, Molecular Medicine, Research & Animal), Segment (Sequencing Platforms, Knowledge Management Tools & Data Analysis Services) & Application (Genomics, Proteomics & Drug Design) - Forecasts to 2017 analyzes and studies the major market drivers, restraints, opportunities, and challenges in Brazil, Mexico, Chile, Argentina, Peru, and Rest of Latin America.

Browse more than 133 market data tables with 23 figures spread through 257 pages and in-depth TOC on "Latin American Bioinformatics Market" http://www.marketsandmarkets.com/Market-Reports/latin-american-bioinformatics-market-2908323.html

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Latin American bioinformatics market was valued at $232 million in 2012 and is poised to grow at a CAGR of 22% from 2012 to 2017, to reach $627 million by 2017.

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Based on the use of bioinformatics, the various sectors covered in this report are medicine, agriculture, environment, animal, forensic, academics, and others (homeland security and defense, law-enforcement groups, bioweapon creation, antibiotic resistance, and evolutionary biotechnology).

The segments in the bioinformatics application market are genomics, proteomics, chemoinformatics, molecular phylogenetics, metabolomics, transcriptomics, and others (glycomics, cytomics, physiomics, and interactomics). Genomics contributed the highest share to the bioinformatics market in 2012.

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The Latin American bioinformatics market displays lucrative growth potential. It is propelled by the rising number of training and development programs on usage of bioinformatics tools, which leads to an increase in the use of bioinformatics tools by industrial and academic bioinformaticians in life sciences research. In addition, the market is further driven by the high concentration of bioinformatics research institutes in Latin America that aim to facilitate the use of bioinformatics in life sciences research. Increasing pharmaceutical innovations as well as increasing R&D spending are factors that unfold new opportunities for the application of bioinformatics in the drug discovery process in Latin America.

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Latin American Bioinformatics Market (Genomics, Proteomics & Drug Design) Worth $627 Million by 2017 - New Report by ...

Brad Grey, CEO of Paramount Studios, at 2nd Annual Rebels with a Cause Gala #USC #CAMM
http://www.redcarpetreporttv.com Mingle Media TV and Red Carpet Report host Paige Sullivan were invited to come back and cover the 2nd Annual Rebels with a C...

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Brad Grey, CEO of Paramount Studios, at 2nd Annual Rebels with a Cause Gala #USC #CAMM - Video

Jennifer Missoni at 2nd Annual Rebels with a Cause Gala #USC #CAMM @JenniferMissoni
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Jennifer Missoni at 2nd Annual Rebels with a Cause Gala #USC #CAMM @JenniferMissoni - Video

BJ Novak at 2nd Annual Rebels with a Cause Gala #USC #CAMM @bjnovak
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BJ Novak at 2nd Annual Rebels with a Cause Gala #USC #CAMM @bjnovak - Video

David Foster at 2nd Annual Rebels with a Cause Gala #USC #CAMM @officialdfoster
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David Foster at 2nd Annual Rebels with a Cause Gala #USC #CAMM @officialdfoster - Video

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Dr. Tsongalis is the director of the Molecular Pathology laboratory and co-director of the translational research program in the Geisel School of Medicine at Dartmouth, the Dartmouth Hitchcock Medical Center, and the Norris Cotton Cancer Center in Lebanon, N.H. In 1994, he completed his post-doctoral training in clinical chemistry at the University of North Carolina, Chapel Hill, where he was first exposed to molecular diagnostics. Throughout his career, Dr. Tsongalis has been striving to apply molecular techniques to diagnostic questions that are not adequately addressed by traditional laboratory methods and has challenged the boundaries between clinical pathology and anatomic pathology. His early work described methods for localized in situ amplification of DNA and RNA targets in tissue sections as well as the identification of mutation carriers in the BRCA1 and BRCA2 breast cancer risk genes. He described some of the first applications of molecular methods in identity testing of clinical specimens when mislabeling or a mix-up was suspected. His laboratory was an early adopter of automation for high-volume molecular infectious disease testing and active in the development of molecular techniques for use with unconventional specimen types. His laboratory is currently applying state-of-the-art molecular techniques to improve patient management through precision medicine. His laboratory continually pushes the application of molecular technologies beyond their traditional uses and is now focusing on nanotechnologies for routine use in the clinical setting. His work has led to 140 publications and eight textbooks in the field of molecular pathology. Dr. Tsongalis has served on many professional society committees, including the AACC board of directors, and the editorial boards of several medical journals, including Clinical Chemistry.

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Dartmouth Cancer Researcher on Genetic-Based Testing and Treatment for Breast Cancer

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Paramount Studio chief Brad Grey

In a town that understands how stars are made, Dr. David B. Agus is a medical supernova, which is why a glittering constellation of Hollywood notables turned out Thursday night to raise a stunning $9 million to support his pioneering cancer research.

The Paramount Pictures fundraiser -- labeled "Rebels with a Cause" -- was put together by the studios chief, Brad Grey, who amassed $4.5 million in contributions from the entertainment industry. When high-tech multi-billionaire and Oracle founder Larry Ellison, who was being honored for his longtime support of Agus cutting-edge research into cancers genetic roots, was informed of that total, he promptly offered to match it with a personal donation. That brought the nights total to $9 million.

STORY: 17 of Hollywood's Biggest Philanthropists

ThoughAgusis perhaps best known for treatingSteve Jobsin the final years of his advanced illness, it was the physicians treatment of Viacom chairmanSumner Redstonethat prompted entertainment industry philanthropists to take notice of his work. Redstone credits Agus with saving his life after he was diagnosed with an aggressive form of prostate cancer. The USC medical researcher's patient roster also includesNeil Young, Ted Kennedy, Lance ArmstrongandRobin Quivers. (Agus recently appeared on theHoward Sternshow where the radio host credited him with saving Quivers' life.)

"I met David through Sumner Redstone three years ago," Grey toldThe Hollywood Reporter. "He said to me, 'DavidAgusis a genius.' We became very good friends and I got to know quite a lot about what he's up to. And it's simply inspiring.

"I'm just a show business guy -- these are the real heroes," Grey said ofAgus. "But I think we have some role in this, which is to do anything and everything we can to raise money and fund research so that it's not just this community that is getting this treatment, it's the world. That's why we're here."

Apart from a star-studded patient roster, Agus also has a personal connection to the entertainment industry, since hes married to actress Amy Joyce Povich, daughter of syndicated talk show host MauryPovich, which makes Connie Chung his mother-in-law.

Thursdays turnout, which included an unusually wide mix of stars and moguls, underscored Agus rising celebrity and high-level Hollywood belief in the personal medicine he has pioneered. That approach tailors cancer treatment to a patients unique genetic and molecular makeup, while emphasizing treatments that keep a persons entire system healthy, thereby mobilizing the bodys own cellular defenses and arresting cancers possible spread. The physicians two companies develop the technologies to analyze an individual patients genomes and proteomes so as to identify their unique on-off switches to cancer.

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Paramount's Star-Studded Gala Raises $9 Million for USC Cancer Researcher

PUBLIC RELEASE DATE:

20-Mar-2014

Contact: Tan Yun Yun tan_yun_yun@a-star.edu.sg 656-826-6273 Biomedical Sciences Institutes (BMSI)

1. Scientists at A*STAR's Institute of Molecular and Cell Biology (IMCB) have developed a method to generate human induced pluripotent stem cells (hiPSCs) from a single drop of finger-pricked blood. The method also enables donors to collect their own blood samples, which they can then send to a laboratory for further processing. The easy access to blood samples using the new technique could potentially boost the recruitment of greater numbers and diversities of donors, and could lead to the establishment of large-scale hiPSC banks.

2. By genetic reprogramming, matured human cells, usually blood cells, can be transformed into hiPSCs. As hiPSCs exhibit properties remarkably similar to human embryonic stem cells, they are invaluable resources for basic research, drug discovery and cell therapy. In countries like Japan, USA and UK , a number of hiPSC bank initiatives have sprung up to make hiPSCs available for stem cell research and medical studies.

3. Current sample collection for reprogramming into hiPSCs include invasive measures such as collecting cells from the bone marrow or skin, which may put off many potential donors. Although hiPSCs may also be generated from blood cells, large quantities of blood are usually required. In the paper published online on the Stem Cell Translational Medicine journal, scientists at IMCB showed for the first time that single-drop volumes of blood are sufficient for reprogramming into hiPSCs. The finger-prick technique is the world's first to use only a drop of finger-pricked blood to yield hiPSCs with high efficiency. A patent has been filed for the innovation.

4. The accessibility of the new technique is further enhanced with a DIY sample collection approach. Donors may collect their own finger-pricked blood, which they can then store and send it to a laboratory for reprogramming. The blood sample remains stable for 48 hours and can be expanded for 12 days in culture, which therefore extends the finger-prick technique to a wide range of geographical regions for recruitment of donors with varied ethnicities, genotypes and diseases.

5. By integrating it with the hiPSC bank initiatives, the finger-prick technique paves the way for establishing diverse and fully characterised hiPSC banking for stem cell research. The potential access to a wide range of hiPSCs could also replace the use of embryonic stem cells, which are less accessible. It could also facilitate the set-up of a small hiPSC bank in Singapore to study targeted local diseases.

6. Dr Loh Yuin Han Jonathan, Principal Investigator at IMCB and lead scientist for the finger-prick hiPSC technique, said, "It all began when we wondered if we could reduce the volume of blood used for reprogramming. We then tested if donors could collect their own blood sample in a normal room environment and store it. Our finger-prick technique, in fact, utilised less than a drop of finger-pricked blood. The remaining blood could even be used for DNA sequencing and other blood tests."

7. Dr Stuart Alexander Cook, Senior Consultant at the National Heart Centre Singapore and co-author of the paper, said "We were able to differentiate the hiPSCs reprogrammed from Jonathan's finger-prick technique, into functional heart cells. This is a well-designed, applicable technique that can unlock unrealized potential of biobanks around the world for hiPSC studies at a scale that was previously not possible."

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A*STAR scientists create stem cells from a drop of blood

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Newswise PHILADELPHIA Michael S. Parmacek, MD, Herbert C. Rorer Professor of Medical Sciences, has been named Chair of the Department of Medicine at the Perelman School of Medicine at the University of Pennsylvania. Dr. Parmacek has been with Penn for over 15 years, most recently serving as the interim chair of the department and the chief of the Division of Cardiovascular Medicine. The Department of Medicine at Penn is the oldest in the country and includes 12 divisions, with origins dating back to 1765 when John Morgan, MD, assumed leadership as the first department chair in the first medical school in the United States.

As Chair of the Department of Medicine, Dr. Parmacek will lead the largest department in the Perelman School of Medicine and the University of Pennsylvania Health System, said J. Larry Jameson, MD, PhD, Executive Vice President for the Health System and Dean of the Perelman School of Medicine. His exceptional leadership and strategic vision will be invaluable to the talented clinicians and researchers in the department who work each day to provide exceptional patient care and push medical technology and innovation at Penn to new levels.

Dr. Parmacek is currently the Herbert C. Rorer Professor of Medicine, Chief of the Division of Cardiovascular Medicine, and Director of the Penn Cardiovascular Institute. He came to Penn as Chief of Cardiovascular Medicine in 1998, following successful roles at the University of Michigan and the University of Chicago. A nationally recognized expert in cardiovascular biology and medicine, he has distinguished himself at Penn with significant research advances and at the same time has built one of the nations leading cardiovascular medicine divisions. Dr. Parmacek has been named to multiple important local, regional and national leadership positions, including the Advisory Council of the National Institutes of Health/National Heart, Lung, and Blood Institute, the Commonwealth of Pennsylvania Health Research Advisory Council and the Founding Director of Penns nationally renowned Cardiovascular Institute.

Over the course of his career, he has made multiple seminal discoveries which have impacted the understanding the molecular and genetic basis of congenital heart disease, atherosclerosis, aortic aneurysm and dissection and heart failure. He has published a substantial body of scholarly work in high-impact journals, including Science, the Proceedings of the National Academy of Science, Genes and Development and the New England Journal of Medicine. Dr. Parmacek was elected an Established Investigator by the American Heart Association (AHA), President of the Association of Professors of Cardiology, Fellow of the AHA and American College of Cardiology, and member of the American Society of Clinical Investigation and the Association of American Physicians.

Dr. Parmacek earned his medical degree from Northwestern University. He completed residency training in Internal Medicine at the University of Michigan and Cardiovascular Disease fellowship training at Northwestern University. Following his clinical training, Dr. Parmacek performed a postdoctoral research fellowship in molecular cardiology at the Howard Hughes Medical Institute at the University of Michigan.

In the almost 250 years since it was established, the Department of Medicine at Penn has been served by 23 Chairs. Today, the department includes 500 full-time faculty members, over 200 associated faculty, and over 300 academic support staff. The most recent NIH Report ranks the department #3 in funding among all departments of Medicine in U.S. medical schools, with just over $110,000,000 in grant support.

The Department of Medicine also has a long history of training the future leaders in American medicine, and Dr. Parmacek will be at the forefront of these highly competitive training programs, which currently include 166 residents and 157 subspecialty fellows. In addition to these rigorous training programs, the department is responsible for more than 430,000 outpatient encounters and more than 25,000 inpatient admissions each year.

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Michael S. Parmacek, MD, Named Chair of the Department of Medicine at Penn