Contact Information

Available for logged-in reporters only

Newswise Stony Brook, NY, October 15, 2014 The proteins that drive DNA replicationthe force behind cellular growth and reproductionare some of the most complex machines on Earth. The multistep replication process involves hundreds of atomic-scale moving parts that rapidly interact and transform. Mapping that dense molecular machinery is one of the most promising and challenging frontiers in medicine and biology.

Now, a team of scientists from Stony Brook University, the U.S. Department of Energys Brookhaven National Laboratory (BNL), Cold Spring Harbor Laboratory, and the Imperial College in London have pinpointed crucial steps in the beginning of the replication process, including surprising structural details about the enzyme that unzips and splits the DNA double helix so the two halves can serve as templates for DNA duplication. Their findings are published today online in the journal Genes and Development.

The genesis of the DNA-unwinding machinery is wonderfully complex and surprising, said study coauthor Huilin Li, a Professor of Biochemistry and Cell Biology at Stony Brook University and a biologist at BNL. Seeing this helicase enzyme prepare to surround and unwind the DNA at the molecular level helps us understand the most fundamental process of life, and how the process might go wrong. Errors in copying DNA are found in certain cancers, and this work could one day help develop new treatment methods that stall or break dangerous runaway machinery.

The research combined electron microscopy, perfectly distilled proteins, and a method of chemical freezing to isolate specific moments at the start of replication. It picks up where two previous studies by Li and colleagues left off. They first determined the structure of the "Origin Recognition Complex" (ORC), a protein that identifies and attaches to specific DNA sites to initiate the entire replication process. The second study revealed how the ORC recruits, cracks open, and installs a crucial ring-shaped protein structure (Mcm2-7) that lies at the core of the helicase enzyme.

But DNA replication is a bi-directional process with two helicases moving in opposite directions. The key question, then, was how does a second helicase core get recruited and loaded onto the DNA in the opposite orientation of the first?

To our surprise, we found an intermediate structure with one ORC binding two rings, said Brookhaven Lab biologist and lead author Jingchuan Sun. This discovery suggests that a single ORC, rather than the commonly believed two-ORC system, loads both helicase rings.

One step further along, the researchers also determined the molecular architecture of the final double-ring structure left behind after the ORC leaves the system, offering a number of key biological insights.

We now have clues to how that double-ring structure stably lingers until the cell enters the DNA-synthesis phase much later on in replication, said study coauthor Christian Speck of Imperial College, London. This study revealed key regulatory principles that explain how the helicase activity is initially suppressed and then becomes reactivated to begin its work splitting the DNA.

Follow this link:

Scientists Map Key Moment in Assembly of DNA-Splitting Molecular Machine

The proteins that drive DNA replication -- the force behind cellular growth and reproduction -- are some of the most complex machines on Earth. The multistep replication process involves hundreds of atomic-scale moving parts that rapidly interact and transform. Mapping that dense molecular machinery is one of the most promising and challenging frontiers in medicine and biology.

Now, scientists have pinpointed crucial steps in the beginning of the replication process, including surprising structural details about the enzyme that "unzips" and splits the DNA double helix so the two halves can serve as templates for DNA duplication.

The research combined electron microscopy, perfectly distilled proteins, and a method of chemical freezing to isolate specific moments at the start of replication. The study -- authored by scientists from the U.S. Department of Energy's Brookhaven National Laboratory, Stony Brook University, Cold Spring Harbor Laboratory, and Imperial College, London -- published on Oct. 15, 2014, in the journal Genes and Development.

"The genesis of the DNA-unwinding machinery is wonderfully complex and surprising," said study coauthor Huilin Li, a biologist at Brookhaven Lab and Stony Brook University. "Seeing this helicase enzyme prepare to surround and unwind the DNA at the molecular level helps us understand the most fundamental process of life and how that process might go wrong. Errors in copying DNA are found in certain cancers, and this work could one day help develop new treatment methods that stall or break dangerous runaway machinery."

The research picks up where two previous studies by Li and colleagues left off. They first determined the structure of the "Origin Recognition Complex" (ORC), a protein that identifies and attaches to specific DNA sites to initiate the entire replication process. The second study revealed how the ORC recruits, cracks open, and installs a crucial ring-shaped protein structure (Mcm2-7) that lies at the core of the helicase enzyme.

But DNA replication is a bi-directional process with two helicases moving in opposite directions. The key question, then, was how does a second helicase core get recruited and loaded onto the DNA in the opposite orientation of the first?

"To our surprise, we found an intermediate structure with one ORC binding two rings," said Brookhaven Lab biologist and lead author Jingchuan Sun. "This discovery suggests that a single ORC, rather than the commonly believed two-ORC system, loads both helicase rings."

One step further along, the researchers also determined the molecular architecture of the final double-ring structure left behind after the ORC leaves the system, offering a number of key biological insights.

"We now have clues to how that double-ring structure stably lingers until the cell enters the DNA-synthesis phase much later on in replication," said study coauthor Christian Speck of Imperial College, London. "This study revealed key regulatory principles that explain how the helicase activity is initially suppressed and then becomes reactivated to begin its work splitting the DNA."

Precision methods, close collaboration

Read the original:

Key moment mapped in assembly of DNA-splitting molecular machine

Select a researcher... Aboody, Karen S., M.D. Al-Abdullah, Ismail, Ph.D. Ann, David K., Ph.D. Research Awasthi, Sanjay, M.D. Research Bailis, Adam, Ph.D. Research Barish, Michael, Ph.D. Research Berlin, Jacob, Ph.D. Research Bhatia, Ravi, M.D. Bhatia, Smita, M.D., M.P.H. Research Boldin, Mark, M.D., Ph.D. Research Borneman, Tami, R.N., M.S.N., C.N.S., F.P.C.N. Cantin, Edouard, Ph.D. Research Chatterjee, Saswati, Ph.D. Research Chen, Ching-Cheng, Ph.D. Research Chen, Shiuan, Ph.D. Laboratory Chen, WenYong, Ph.D. Chen, Yuan , Ph.D. Chow, Warren A., M.D., F.A.C.P. Laboratory Chu, Fong Fong, Ph.D. Laboratory Crocitto, Laura E., M.D. Research Diamond, Don, Ph.D. Ferrell, Betty, Ph.D., M.A.,F.A.A.N., F.P.C.N. Research Ferreri, Kevin, Ph.D. Research Forman, Stephen J., M.D., F.A.C.P. Laboratory Glackin, Carlotta, Ph.D. Laboratory Grant, Marcia, R.N., D.N.S.c., F.A.A.N. Research Hanson, Jo, R.N., M.S.N., C.N.S., O.C.N. Research Horne, David, Ph.D. Huang, Wendong, Ph.D. Huss, Janice, Ph.D. Research Ikeda, Kazuo, Ph.D. Research Itakura, Keiichi, Ph.D. Research Jandial, Rahul M.D., Ph.D. Jones, Jeremy, Ph.D. Laboratory Jovanovic-Talisman, Tijana Ph.D. Kalkum, Markus, Ph.D. Laboratory Kane, Susan, Ph.D. Laboratory Kong, Mei, Ph.D. Kortylewski, Marcin, Ph.D. Laboratory Krontiris, Theodore G., M.D., Ph.D. Research Ku, Hsun Teresa, Ph.D. Research Kuo, Ya-Huei, Ph.D. Research La Rosa, Corinna, Ph.D. Research Lee, Terry, Ph.D. Research Lin, Ren-Jang, Ph.D. Research Liu, Chih-Pin, Ph.D. Research Yilun Liu Qiang Lu, Ph.D. Research Malkas, Linda H., Ph.D. Miller, Marcia M., Ph.D. Research Mullen, Yoko, M.D. Ph.D. Research Natarajan, Rama, Ph.D, F.A.H.A, F.A.S.N. Research Neuhausen, Susan L., Ph.D. Research Newman, Edward, Ph.D. Research Ngo, Vu, Ph.D. OConnor, Timothy, Ph.D. Laboratory Otis-Green, Shirley, M.S.W., A.C.S.W., L.C.S.W, O.S.W-C Pfeifer, Gerd, Ph.D. Riggs, Arthur D., Ph.D. Research Rossi, John J., Ph.D. Research Salvaterra, Paul, Ph.D. Research Schones, Dustin E., Ph.D. Laboratory Shen, Binghui, Ph.D. Shi, Yanhong, Ph.D. Shively, John, Ph.D. Research Singer-Sam, Judith, Ph.D. Laboratory Smith, Steven, Ph.D. Laboratory Stark, Jeremy, Ph.D. Research Sun, Zuoming, Ph.D. Szabo, Piroska E., Ph.D. Termini, John, Ph.D. Research Todorov, Ivan Ph.D. Research Tomoda, Toshifumi, M.D., Ph.D. Vaidehi, Nagarajan, Ph.D. Wang, Emily, Ph.D. Wong, K.K., M.D. Yee, Jiing-Kuan, Ph.D. Yen, Yun, M.D., Ph.D. Yu, Hua, Ph.D. Laboratory Yuan, Yuan, M.D., Ph.D. Zaia, John A., M.D. Laboratory Zeng, Defu, M.D. Research

Develop new therapies, diagnostics and preventions in the fight against cancer and other life-threatening diseases.

Read more here:

Molecular Medicine | Beckman Institute of City of Hope ...

Researchers at Yale School of Medicine have uncovered a molecular process in the brain known to control eating that transforms white fat into brown fat. This process impacts how much energy we burn and how much weight we can lose. The results are published in the Oct. 9 issue of the journal Cell.

Obesity is a rising global epidemic. Excess fatty tissue is a major risk factor for type 2 diabetes, cardiovascular disease, hypertension, neurological disorders, and cancer. People become overweight and obese when energy intake exceeds energy expenditure, and excess calories are stored in the adipose tissues. The adipose organ is made up of both white and brown fat. While white fat primarily stores energy as triglycerides, brown fat dissipates chemical energy as heat. The more brown fat you have, the more weight you can lose.

It has previously been shown that energy-storing white fat has the capacity to transform into energy-burning brown-like fat. In this new study, researchers from the Yale Program in Integrative Cell Signaling and Neurobiology of Metabolism, demonstrate that neurons controlling hunger and appetite in the brain control the browning of white fat.

Lead author Xiaoyong Yang, associate professor of comparative medicine and physiology at Yale School of Medicine, conducted the study with Tamas Horvath, professor and chair of comparative medicine, and professor of neurobiology and Obstetrics/gynecology at Yale School of Medicine, and their co-authors.

The team stimulated this browning process from the brain in mice and found that it protected the animals from becoming obese on a high-fat diet. The team then studied the molecular changes in hunger-promoting neurons in the hypothalamus and found that the attachment of a unique sugar called O-GlcNAc to potassium ion channels acts as a switch to control brain activity to burn fat.

Our studies reveal white fat browning as a highly dynamic physiological process that the brain controls, said Yang. This work indicates that behavioral modifications promoted by the brain could influence how the amount of food we eat and store in fat is burned.

Yang said hunger and cold exposure are two life-history variables during the development and evolution of mammals. We observed that food deprivation dominates over cold exposure in neural control of white fat browning. This regulatory system may be evolutionarily important as it can reduce heat production to maintain energy balance when we are hungry. Modulating this brain-to-fat connection represents a potential novel strategy to combat obesity and associated illnesses.

Other authors on the study include Hai-Bin Ruan, Marcelo O. Dietrich, Zhong-Wu Liu, Marcelo R. Zimmer, Min-Dian Li, Jay Prakash Singh, Kaisi Zhang, Ruonan Yin, and Jing Wu.

The study was funded by the National Institutes of Health, American Diabetes Association, Ellison Medical Foundation, American Heart Association, and CNPq/Brazil.

Here is the original post:

Hunger Games: How the brain 'browns' fat to aid weight loss

Contact Information

Available for logged-in reporters only

Newswise LOS ANGELES (Oct. 8, 2014) Cedars-Sinai Health System announced today that it has finalized an agreement with two of the nations most prominent orthopedic and sports medicine physician groups -- Kerlan-Jobe Orthopaedic Clinic and Santa Monica Orthopaedic and Sports Medicine Group -- to become formally affiliated with Cedars-Sinai.

The agreement is the final step in a process that was announced in late 2013 when the entities entered into a letter of intent to jointly pursue strategies for leadership in orthopedics and sports medicine regionally, nationally and internationally.

The collaboration between the two prominent orthopedic groups, which have an unequaled role in the care of professional sports teams and individual elite athletes, and the nationally renowned orthopedic physicians and staff at Cedars-Sinai, creates the framework for a new model of patient-centered, high-quality care, integrating the latest research and treatment options.

The affiliation also expands the geographic footprint of each of the partners, enhancing the communitys access to high-quality orthopedics and sports medicine. Kerlan-Jobe and Santa Monica Orthopaedic and Sports Medicine Group facilities include medical offices and other clinical services in Santa Monica, Pasadena, Anaheim and West Los Angeles.

The affiliation with Cedars-Sinai will enhance patient care by facilitating a wide variety of collaborations among the three entities, including expanded clinical trials and research, access for patients to Cedars-Sinai when needed, and collaborative consultations on complex cases.

Although now affiliated with Cedars-Sinai under the Institute for Sports Sciences, Kerlan-Jobe and Santa Monica Orthopaedic and Sports Medicine Group will each continue to see patients under each of their respective brands.

Kerlan-Jobe, Santa Monica Orthopaedic and Sports Medicine, and Cedars-Sinai Orthopaedic Center also plan to collaborate on a wide variety of research and clinical trials, including the advanced use of orthobiologics (including stem cells and other molecular and cellular-based experimental treatments for sports injuries) and new approaches to orthopedic treatments that minimize surgery whenever possible. Other areas of focus include pediatric sports medicine, sports neurology and concussion, a movement performance center and a return-to-work program coordinated with employers.

While each of the three groups offers sought-after advanced training programs for physicians, they will also be looking for opportunities to collaborate and expand their education and training programs.

Go here to see the original:

Kerlan-Jobe Orthopaedic Clinic and Santa Monica Orthopaedic and Sports Medicine Group Officially Join Cedars-Sinai

Contact Information

Available for logged-in reporters only

Newswise PHILADELPHIA Penn Medicine will receive $3.5 million over the next five years to establish a National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) consortium to study new ways to treat diabetes. The program will be led by Klaus H. Kaestner, PhD, the Thomas and Evelyn Suor Butterworth Professor in Genetics and an investigator with the Institute for Diabetes, Obesity and Metabolism, at the Perelman School of Medicine, University of Pennsylvania. The consortium is a joint effort between the Kaestner lab and that of Benjamin Glaser, MD, head of the Endocrinology and Metabolism Service, Department of Internal Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.

This award will enable us to continue a fruitful collaboration begun four years ago during a sabbatical stay in Jerusalem, says Kaestner. By leveraging Dr. Glasers clinical expertise with the technology development ongoing in my lab we hope to make rapid progress towards new treatments for diabetes.

The prevalence of diabetes has reached epidemic proportions worldwide and is predicted to increase rapidly in the future, putting a tremendous strain on health care budgets in both developed and developing countries. There are two major forms of diabetes and both are associated with decreased beta cell number or function, explains Kaestner. No treatments have been devised that increase beta cells in humans, and transplantation of beta cells is extremely limited due to lack of appropriate donors. For these reasons, increasing functional beta cells before or after transplantation has become a primary objective of diabetes research.

The teams previous studies have shown that adult human beta cells can be induced to replicate, and importantly, that these cells can maintain a normal response to glucose levels. However, the replication rate achieved is still too low for clinical applications.

The team aims to develop better ways to increase functional beta cells by inducing replication of adult beta cells, and by restoring juvenile properties to aged beta cells. To accomplish these aims, they will use cutting-edge and emerging technologies that are already established or are being developed. They will combine clinical experience with expertise in molecular biology and extensive experience in genomic modification aimed at enhancing beta-cell replication. By basing interventions on changes found in human disease and normal aging, this approach will increase the chances that discoveries made can be translated more rapidly into clinically relevant protocols.

The NIDDK grant is 1UC4DK104119-01.

###

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.

Read the original:

Penn Medicine Receives $3.5 Million NIH Grant to Study New Ways to Combat Diabetes

by Chloe Nordquist

azfamily.com

Posted on October 3, 2014 at 3:03 PM

Updated today at 3:03 PM

PHOENIX -- Phoenix Children's Hospital has announced its partnership with the Chan Soon-Shiong Institute of Molecular Medicine that will help children with cancer with more precision.

The new Chan Soon-Shiong Children's Precision Medicine Institute will combine genomics research and new genomic technology to identify treatments and cures for young patients facing cancer or other serious illnesses.

Dr. Patrick Soon-Shiong's vision is to apply genomics to fight cancer and other disorders.

"When you get cancer, one of the problems is that cancer has thousands and thousands of mutations," Soon-Shiong said. "So what we need to do, we take the DNA and through our supercomputer find the mutation that is the one driving this cancer so we can know what drug to give you."

The trial and repeat diagnosis method of treating cancer will be more accurate with the new database.

The treatment will be chosen based on proteins within the cancer cells and not the DNA itself.

More:

Phoenix Children's Hospital announces genomics institute

PUBLIC RELEASE DATE:

1-Oct-2014

Contact: Kimberly Brown kbrown@snmmi.org 703-652-6773 Society of Nuclear Medicine @SNM_MI

Reston, Va. (October 1, 2014) Researchers at Memorial Sloan Kettering found that PET/CT imaging of patients younger than 40 who were initially diagnosed with stage IIII breast cancer resulted in change of diagnosis. As reported in the October issue of The Journal of Nuclear Medicine, while guidelines recommend FDG-PET/CT imaging only for women with stage III breast cancer, it can also help physicians more accurately diagnose young breast cancer patients initially diagnosed with earlier stages of the disease.

Assessing if and how far breast cancer has spread throughout the body is what doctor's refer to as staging. Most women nowadays are diagnosed at earlier stages, meaning stage 1 or 2 of possible 4 stages (stated Christopher Riedl, MD). Current National Comprehensive Cancer Network (NCCN) guidelines consider systemic FDG-PET/CT staging for only stage III breast cancer patients. More recently it has been debated whether factors other than stage should be considered in this decision. One such factor is patient age, as young breast cancer patients often have more aggressive tumors. In this study, a team of researchers from Memorial Sloan Kettering Cancer Center in New York evaluated for the first time the impact of FDG PET/CT staging specifically in a young patient cohort. The study suggests that breast cancer patients under the age of 40 may benefit from systemic staging with FDG PET/CT at earlier stages than NCCN guidelines suggest.

"Proper staging right after the breast cancer has first been diagnosed will help doctors make the right treatment decisions. And figuring out which breast cancer patients will benefit most from this 'advanced staging' with FDG PET/CT helps us to improve patient care while avoiding unnecessary tests," stated Christopher Riedl, MD, one of the team's lead researchers. "Our data suggest that women younger than 40 may benefit from PET/CT staging at earlier stages than doctors previously believed."

The study included 134 patients with initial diagnoses of stage I to IIIC breast cancer; those with signs of distant metastases or with prior malignancy were excluded. PET/CT findings lead to upstaging to stage III or IV in 28 patients (21%). Unsuspected extra-axillary regional nodes were found in 15/134 (11%) and distant metastases in 20/134 (15%), with 7/134 (5%) demonstrating both. PET/CT revealed stage IV disease in 1/20 (5%) patients with initial clinical stage I, 2/44 (5 %) stage IIA, 8 /47 (17 %) stage IIB, 4/13 (31%) stage IIIA, 4/8 (50%) of IIIB, and 1/2 (50%) of stage IIIC patients. All 20 patients upstaged to stage IV were histologically confirmed. Four synchronous thyroid and 1 rectal malignancies were identified.

"Future NCCN guidelines for initial staging of breast cancer patients may need to consider other factors in addition to clinical stage. This study provides further evidence that molecular imaging and nuclear medicine can help us make better cancer staging and treatment decisions," said Gary Ulaner, MD, PhD, assistant professor at Memorial Sloan Kettering. "Of course, our findings should still be confirmed in a prospective trial," he added. "Our next step will be to look at factors other than patient age to understand which breast cancer patients benefit most from FDG-PET/CT."

###

Authors of the article "Retrospective analysis of FDG PET/CT for staging asymptomatic breast cancer patients below 40 years of age" include Christopher C Riedl, Elina Slobod, Maxine Jochelson, Monica Morrow, Debra A. Goldman, Mithat Gonen, Wolfgang Andreas Weber, and Gary A Ulaner, Memorial Sloan Kettering Cancer Center, New York.

View post:

FDG-PET/CT shows promise for breast cancer patients younger than 40

San Francisco, California (PRWEB) September 30, 2014

The global market for molecular diagnostics is expected to reach USD 8,020.1 million by 2020, according to a new study by Grand View Research, Inc. Growing demand for personalized medicine and theranostics, and the subsequent introduction of advanced cancer diagnostic technologies are expected to be key factors driving market growth over the next six years. Moreover, the growing global base of geriatric population and chronic diseases such as cancer, coupled with disease triggering lifestyle habits such as smoking and excessive alcohol consumption will positively impact market growth.

View full reports with TOC at http://www.grandviewresearch.com/industry-analysis/molecular-diagnostics-market

Molecular diagnostic reagent products dominated the overall market, accounting for over 50% of global revenue in 2013. Reagent market revenue is expected to reach USD 4,739.9 million by 2020, growing at a CAGR of 9.9% from 2014 to 2020. High consumption rates of molecular diagnostic reagents and the growing number of research and development initiatives pertaining to the field of molecular diagnostics are two key drivers of this product segment. The point of care end-use market for molecular diagnostics is expected to be the fastest growing product segment, at an estimated CAGR of 13.3% from 2014 to 2020, on account of factors such as the growing demand for point of care diagnostic procedures as an effective diagnostic tool rendering rapid and accurate results and the introduction of government initiatives such as CLIA (Clinical Laboratory Improvement Amendments) waived tests.

Request free sample of this report at http://www.grandviewresearch.com/industry-analysis/molecular-diagnostics-market/request

Further key findings from the study suggest:

Browse all reports of this category at http://www.grandviewresearch.com/industry/biotechnology

For the purpose of this study, Grand View Research has segmented the global molecular diagnostics market on the basis of product and region:

Browse all upcoming reports by Grand View Research at http://www.grandviewresearch.com/ongoing-reports

About Grand View Research

See the rest here:

Global Molecular Diagnostics Market Is Expected To Be Worth $8,020.1 million by 2020: Grand View Research, Inc.

BETHESDA, MD (PRWEB) September 29, 2014

The very first sensitive and specific molecular imaging technique to detect bone metastases was recently developed by NFCR-funded scientist Paul B. Fisher, M.Ph., Ph.D., at the Virginia Commonwealth University Massey Cancer Center and VCU Institute of Molecular Medicine in collaboration with Martin G. Pomper, M.D., Ph.D., at the Johns Hopkins Medical Institutions.

This new genetic-based imaging technique is able to detect cancerous cells through expression of a gene called AEG-1, which was originally discovered by Dr. Fisher. AEG-1 is expressed at high levels in all cancer types investigated so far, with limited expression in normal tissue.

Importantly, laboratory work with metastatic tumor models demonstrated that this technique was even able to detect prostate cancer lesions that have metastasized (spread) to the bone. Bone metastasis is the number one cause of death for patients with prostate cancer.

Bone metastases are notoriously difficult to detect with molecular imaging, said Dr. Fisher. There is currently no sensitive and specific imaging technique clinically available to detect cancer in the bones. The results indicate that this new technique represents a great improvement over current clinical imaging techniques.

We expect this to have applications well beyond bone metastasis in prostate cancer, said Dr. Fisher. Because AEG-1 is expressed in the majority of cancers, this research could potentially lead to earlier detection and treatment of metastases originating from a variety of cancer types.

The imaging system may even have applications beyond diagnostic imaging; it has been suggested that it could be combined with therapeutic agents, allowing physicians to image drug delivery in real time. Dr. Fisher and colleagues are working to overcome the remaining obstacles and move this technology into the clinic as soon as possible.

Dr. Fishers work represents a true breakthrough in the fight against cancer, said Franklin Salisbury, Jr., president of the National Foundation for Cancer Research At NFCR we firmly believe that basic research can and should be translated from the bench to the bedside. This is what we mean by Research for a Cure.

This work was funded in part by the National Foundation for Cancer Research. The results were published in the September 18, 2014 Online First edition of the journal Cancer Research.

About the National Foundation for Cancer Research

Follow this link:

New Non-invasive Technique Developed by NFCR-supported Scientist May Significantly Improve Detection and Treatment of ...

Foster City, CA (PRWEB) September 26, 2014

Molecular Biology deals with the basic molecular mechanisms occurring in the cell for the regulation of cellular activity and its behaviour. It emphasise on physical, chemical and biochemical interactions between genes and with its environment within the genome. Knowledge on molecular biology helps us in innovation of new and novel therapeutic methodologies for the diagnosis, prognosis and the treatment of the various lethal syndromes.

On this occasion, Dr. Srinubabu Gedela, MD of OMICS Publishing Group acknowledging the recent developments in the field of genomics, cellular & molecular biology and gene technology has enhanced our understanding of gene structure and function, thus taking us towards advanced therapeutic approach at the molecular level.

OMICS Group International has been in Open Access publishing with more than 400 front-line peer-reviewed, Open Access Journals. A strong network of 30,000 scientists, researchers and authors form the editorial board of OMICS Group Journals that cater to the requirements of 3 million readers worldwide. OMICS Group also organizes over 300 International Conferences annually all over the world with the support of nearly 1000 International Societies related to the fields of Molecular biology, Neurology, Medical, Clinical, Pharmaceutical, Chemical, OMICS, Engineering, Technology, Management, and Life sciences.

The below mentioned OMICS Group Genetics & Molecular Biology Journals offer 25% discount on all the articles submitted for publication during Open Access Week

Journal of Molecular and Genetic Medicine Cell Science & Therapy Hereditary Genetics Cloning & Transgenesis Gene Technology Current Synthetic & Systems Biology International Journal of Genomic Medicine Advancements in Genetic Engineering Single Cell Biology Fungal Genomics & Biology Journal of Biotechnology & Biomaterials Fertilization: In Vitro Journal of Biochemistry & Physiology Journal of Microbial & Biochemical Technology Biological Systems Advanced Techniques in Biology & Medicine Molecular Biology Journal of Cell & Developmental Biology

Researchers can submit their valuable manuscripts at the following link. Authors are encouraged to submit their articles using the below mentioned web link only to be considered for special offer.

http://omicsonline.org/open-access-week/submission.php

For any further inquiries please contact:

Alex Stewart Editorial Assistant Genetics & Molecular Biology Group - Journals 731 Gull Ave, Foster City CA 94404, USA Tel: +1-650-268-9744 Fax: +1-650-618-1414 E-mail: submission(at)omicsonline(dot)org

Original post:

Understanding Genetics and Molecular Biology to Avert Dreadful Medical Challenges during Open Access Week

Administrators behind the revamping of Molecular and Cellular Biology did not have to wait long to gauge the popularity of their new programs, courses, and requirement changes, said Alexander F. Schier, department chair of MCB.

MCB 60: Cellular Biology and Molecular Medicine, our new gateway course, has enrolled more than 100 students, twice as many as expected, Schier said.

After bringing on more teaching fellows to accommodate high enrollment, Schier, along with his MCB 60 teaching partners Vladimir Denic and Briana Burton, was eager to begin the new class, which implements curricular changes that relate lessons from the classroom to the science seen in news stories.

The changes we made became possible because molecular and cellular biology has become highly relevant for understanding human physiology and disease, said Schier. It is now possible to directly connect most of the biological mechanisms we teach to human disease, ranging from cancer to Ebola.

The teaching team has worked to leverage the increasing relevance of science at the molecular level to stories of outbreaks and popularly reported science. Highlighting these connections will help make the material more accessible to a broad range of students, Schier said.

When you spend all your time in the classroom, youre not paying as much attention to where it will lead you, said Chris D. M. Mukasa 17, a prospective MCB concentrator. Its really helpful to see how people who have graduated with similar degrees make use of their education in productive ways.

The new gateway course is part of MCBs concerted effort to engage concentrators by highlighting the application of MCB to real-world science in addition to fostering a concentration community. Besides MCB 60 and MCB 63: Biochemistry and Molecular Medicine, concentration administrators have launched associated programming, like MCBs inaugural movie night.

The administrators organized a showing of the film Contagion for concentrators and pre-concentrators of MCB and Chemical and Physical Biology. Halfway through the movie, a panel of public health experts led a discussion on the epidemiology and biology featured in the movie. The students and the panelincluding Barry R. Bloom, professor at the Harvard School of Public Health, and members of Pardis C. Sabetis lab, who have worked on sequencing the Ebola genome this fallarrived at a consensus on the films science.

We MCB concentrators thought they could have done a better job making it seem like an actual pathogen, said Bianca Mulaney 16, an MCB concentrator who attended the event, of the fictional disease in Contagion.

Despite disputes with the technical accuracy of the film, Mulaney said that she thought the movie screening was an effective way to open discussion of MCB topics to a broader undergraduate audience.

Continued here:

MCB Concentration Updates Receive Good Reviews

BOULDER, Colo.--(BUSINESS WIRE)--miRagen Therapeutics, Inc., a biopharmaceutical company developing innovative microRNA-based therapeutics, announced today that findings from a research collaboration between the Company and Yale University have demonstrated that promiR-29 reversed fibrosis in a mouse model of pulmonary fibrosis. These findings were published in the journal EMBO Molecular Medicine http://onlinelibrary.wiley.com/doi/10.15252/emmm.201303604/full on September 19, 2014.

The mimic, when injected into the blood, goes to the lung and it has a sustained effect. We are very impressed that it can reverse fibrosis, not only prevent it, said Naftali Kaminski, M.D., a professor at Yale School of Medicine and section chief of pulmonary, critical care and sleep medicine and a corresponding author of the study.

Results from the collaborative research conducted by miRagen and Yale have led to the award of a Centers for Advanced Diagnostics and Experimental Therapeutics in Lung Diseases Stage II grant from the National Institutes of Health to further evaluate this potential therapeutic approach.

miRagen is committed to translating these pre-clinical findings into transformative therapies for patients with Idiopathic Pulmonary Fibrosis, said Dr. David Rodman, Executive Vice President of Research and Development at miRagen Therapeutics, Inc. We are excited about the collaboration with Dr. Kaminski and by the potential for accelerated progression to human clinical trials afforded by the CADET II grant award.

About microRNAs

MicroRNAs have emerged as an important class of small RNAs encoded in the genome, acting as master regulators of gene expression. Recent studies have indicated that microRNAs appear to be associated with many disease processes. Because they are thought to be single molecular entities that dictate the expression of fundamental regulatory pathways, microRNAs represent potential drug targets for controlling many biologic and disease processes.1

About microRNA-29

The microRNA-29 family is a well-established regulator of extracellular matrix genes. The expression of the three family members is consistently down-regulated in a number of pathological fibrotic conditions, including cardiac, renal, hepatic, and pulmonary fibrosis, as well as systemic sclerosis2,3,4,5. Numerous studies in cell-culture and genetic replacement in rodents have also demonstrated the potential of miR-29 normalization to correct many drivers of pathological fibrosis.

About miRagen Therapeutics, Inc.

miRagen Therapeutics, Inc., is a biopharmaceutical company focused on the discovery and development of innovative microRNA (miRNA)-targeting therapies in disease areas of high unmet medical need. The Company seeks to leverage in-house expertise in miRNA biology, oligonucleotide chemistry, and drug development to evaluate and advance promising technologies and high-potential product candidates for its own pipeline and in conjunction with strategic collaborators. For certain cardiovascular disease programs, miRagen has a collaboration and license agreement with Servier, an independent French research-based pharmaceutical company. miRagen retains all rights for the Servier-partnered programs in the U.S. and Japan. For more information, please visit http://www.miragenrx.com.

See the original post here:

Research Findings Demonstrate miRagen Therapeutics Synthetic microRNA-29 Mimic (promiR-29) Reverses Pulmonary Fibrosis

Contact Information

Available for logged-in reporters only

Newswise Bioluminescence, nanoparticles, gene manipulation these sound like the ideas of a science fiction writer, but, in fact, they are components of an exciting new approach to imaging local and metastatic tumors. In preclinical animal models of metastatic prostate cancer, scientists at Virginia Commonwealth University Massey Cancer Center, VCU Institute of Molecular Medicine and Johns Hopkins Medical Institutions have provided proof-of-principle of a new molecular imaging approach that could revolutionize doctors ability to see tumors that have metastasized to other sites in the body, including the bones.

Recently published in the OnlineFirst edition of the journal Cancer Research, a journal of the American Association for Cancer Research, this multiple institution study is the first to develop in vivo (in animal models) a systemically administered, non-invasive, molecular-genetic technique to image bone metastases resulting from prostate cancer. The new method relies on the detection of a gene known as AEG-1, which was originally discovered by the study's co-lead investigator Paul B. Fisher, M.Ph., Ph.D., and has been shown to be expressed in the majority of cancers but not in normal, healthy cells. In preclinical studies, the researchers were able to image bone metastases with greater accuracy than any clinically approved imaging method.

Currently, we do not have a sensitive and specific non-invasive technique to detect bone metastases, so we are very encouraged by the results of this study says Fisher, Thelma Newmeyer Corman Endowed Chair in Cancer Research and co-leader of the Cancer Molecular Genetics research program at VCU Massey Cancer Center, chairman of the Department of Human and Molecular Genetics at the VCU School of Medicine and director of the VCU Institute of Molecular Medicine. Additionally, because AEG-1 is expressed in the majority of cancers, this research could potentially lead to earlier detection and treatment of metastases originating from a variety of cancer types.

Imaging the expression of a gene in real time is not an easy task. To do it, the scientists used a promoter called AEG-Prom. A promoter is a set of chemical instructions coded in DNA that initiates activity in a gene. The team combined AEG-Prom with imaging agents consisting of a gene that produces firefly luciferase, the bioluminescent substance that makes fireflies glow, and a gene called HSV1tk, which initiates a chemical reaction when specific radioactive compounds are administered. The team then inserted the combination into tiny nanoparticles that are injected intravenously. When exposed to specific proteins that activate the AEG-Prom, including the c-MYC protein that is elevated in many cancer cells, the AEG-Prom initiates activity in the imaging agent, and the location of cancer cells expressing the imaging agent are made visible using sensitive imaging devices.

"The imaging agents and nanoparticle used in this study have already been tested in unrelated clinical trials. Moving this concept into the clinic to image metastasis in patients is the next logical step in the evolution of this research," says co-lead author Martin G. Pomper, M.D., Ph.D., William R. Brody Professor of Radiology at Johns Hopkins Medical Institutions. "My colleagues and I are working toward this goal, and we look forward to opening a study to deploy this technology as soon as possible."

Fisher and Pomper are pioneering the use of cancer-specific and cancer-selective gene promoters to image cancer. Previous studies in melanoma and breast cancer leveraged another gene originally discovered by Fisher called progression elevated gene-3 (PEG-3) using a promoter known as PEG-Prom. In addition to imaging, this approach could also be used to deliver therapeutic agents, such as targeted therapies, directly to local and distant tumors sites and allow physicians to monitor drug delivery in real time. Separate studies are currently under way to examine the therapeutic potential of this strategy.

Fisher and Pomper collaborated on this research with Siddik Sarkar, Ph.D., postdoctoral research scientist in the Department of Human and Molecular Genetics at the VCU School of Medicine, as well as Akrita Bhatnagar, Ph.D., Yuchuan Wang, Ph.D., Ronnie C. Mease, Ph.D., Matthew Gabrielson, M.D., Polina Sysa, M.D., lL Minn, Ph.D., Gilbert Green, Brian Simmons, Ph.D., and Kathleen Gabrielson, D.V.M., Ph.D., all from Johns Hopkins Medical Institutions.

This study was supported by National Cancer Institute grant CA151838, the Prostate Cancer Foundation, the Patrick C. Walsh Foundation, the National Foundation for Cancer Research and, in part, by VCU Massey Cancer Centers NIH-NCI Cancer Center Support Grant P30 CA016059.

Read this article:

New Non-Invasive Technique Could Revolutionize the Imaging of Metastatic Cancer

PUBLIC RELEASE DATE:

15-Sep-2014

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research

Molecular mechanisms of the Kruppel-like family of transcription factors (KLFs) have been studied more in proliferating cells than in post-mitotic cells such as neurons. Prof. Jeffrey L. Goldberg who comes from University of California San Diego, USA and his team recently found that KLFs regulate intrinsic axon growth ability in central nervous system (CNS) neurons including retinal ganglion cells, and hippocampal and cortical neurons. With at least 15 of 17 KLF family members expressed in neurons and at least 5 structurally unique subfamilies, it is important to determine how this complex family functions in neurons to regulate the intricate genetic programs of axon growth and regeneration. By characterizing the molecular mechanisms of the KLF family in the nervous system, including binding partners and gene targets, and comparing them to defined mechanisms defined outside the nervous system, we may better understand how KLFs regulate neurite growth and axon regeneration. The relevant study has been published in the Neural Regeneration Research (Vol. 9, No. 15, 2014).

###

Article

"Molecular mechanisms of the suppression of axon regeneration by KLF transcription factors" by Akintomide Apara1, Jeffrey L. Goldberg2 (1 University of Miami Miller School of Medicine, Miami, FL, USA; 2 Shiley Eye Center, University of California San Diego, La Jolla, CA, USA)

Apara A, Goldberg JL. Molecular mechanisms of the suppression of axon regeneration by KLF transcription factors. Neural Regen Res. 2014;9(15):1418-1421.

Neural Regeneration Research

Excerpt from:

Molecular mechanisms of the suppression of axon regeneration by KLF transcription factors

PUBLIC RELEASE DATE:

15-Sep-2014

Contact: Scott LaFee slafee@ucsd.edu 619-543-6163 University of California - San Diego @UCSanDiego

During cancer development, tumor cells decorate their surfaces with sugar compounds called glycans that are different from those found on normal, healthy cells. In the Sept. 15 online Early Edition of the Proceedings of the National Academy of Sciences (PNAS), researchers at the University of California, San Diego School of Medicine report that sialic acids at the tips of these cancer cell glycans are capable of engaging with immune system cells and changing the latter's response to the tumor for good and bad.

"These cell surface glycans can promote or inhibit cancer progression, depending upon the stage of the disease," said principal investigator Ajit Varki, MD, Distinguished Professor of Medicine and Cellular and Molecular Medicine. "Our findings underscore the complexity of cancer and the consequent challenges in conquering it. The immune system may be a double-edged sword in cancer, tumor-promoting or tumor-inhibiting, depending upon circumstances."

Specifically, the researchers found that receptors called siglecs on subsets of neutrophils and macrophages (two types of immune cell) can bind to sialic acids on the surface of tumor cells. Depending upon the stage of cancer and the tumor model used, the scientists reported that interaction between immune cell siglecs and tumor cell sialic acids produced opposite outcomes.

"During initial stages of growth, cancer cells appear to protect themselves from extermination by neutrophils by engaging siglecs via sialic acid-capped glycans," said Varki, who is also a faculty member of the UC San Diego Moores Cancer Center. "But once the tumor was established, further growth was inhibited by engagement of siglecs on macrophages."

The findings follow upon research by Varki and colleagues published earlier this year in PNAS that showed anti-tumor antibodies also behave contrarily. Low concentrations of antibodies can support cancer growth, but higher concentrations may inhibit it.

"The fact that the immune system can exert a promoting or inhibiting effect on cancer progression, depending on the situation and stage of disease, has importance for designing clinical trials with drugs that target the immune system," said first author Heinz Lubli, MD, PhD.

For example, siglecs might prove viable drug targets for preventing early cancer progression. Study co-author Ann Schwartz, PhD, MPH, of the Karmanos Cancer Institute at Wayne State University School of Medicine in Detroit investigated 332 patients with lung cancer to assess whether they had a natural siglec variant that reduced binding to tumor cell surface sialic acids. Such patients have a greater chance for survival after two years, but the effect diminishes and disappears later.

The rest is here:

Cancer and the immune system: A double-edged sword

LB5222 - Oculus Rift and molecular medicine

By: diana bobeico

The rest is here:

LB5222 - Oculus Rift and molecular medicine - Video

PUBLIC RELEASE DATE:

12-Sep-2014

Contact: Barry Whyte barry.whyte@embo.org EMBO @EMBOcomm

Different types of dendritic cells in human skin have assorted functions in the early and more advanced stages of psoriasis report researchers in the journal EMBO Molecular Medicine. The scientists suggest that new strategies to regulate the composition of dendritic cells in psoriatic skin lesions might represent an approach for the future treatment of the disease.

"We urgently need new ways to treat psoriasis, treatments that will deliver improved benefits to patients and reduce the incidence of known side effects for existing drugs," says EMBO Member Maria Sibilia, a Professor at the Medical University of Vienna in Austria, and one of the lead authors of the study. "Our experiments have revealed that increases in the number of plasmacytoid dendritic cells are important early triggers of the disease while other types of dendritic cells, the Langerhans cells, help to protect the balance of the immune response that is established during inflammation of the skin."

Psoriasis is an autoimmune disease that affects around 125 million people worldwide. Symptoms, which include the formation of red inflamed lesions that appear on the skin, vary from mild to severe. The disease is often associated with other serious health conditions such as diabetes, heart disease and depression.

The researchers observed an increase in the accumulation of plasmacytoid dendritic cells in the psoriatic lesions of patients as well as in mice that are model organisms for the study of the disease. Plasmacytoid dendritic cells are a specific type of immune cell that can infiltrate damaged tissue during the early phase of psoriasis. In contrast, the levels of another type of dendritic cells known as Langerhans cells, were significantly decreased in the lesions compared to healthy skin in humans and mice. If the levels of plasmacytoid dendritic cells in mice were decreased during the early stages of the disease then the symptoms of psoriasis were quelled. A similar decrease in Langerhans cells at an early stage of the disease had no effect. If the levels of Langerhans cells were reduced at advanced stages of the disease, the symptoms of psoriasis were exacerbated.

"The changes in the severity of symptoms we have observed related to changes in the composition of dendritic cells most likely impact the balance of inflammatory mediators at the site of disease. It may well be that by inducing favourable compositions of dendritic cells at the early stages of psoriasis we may be able to help reduce the effects of psoriasis by achieving a better balance of these mediators at the site of the disease. Further work is needed before we can say with any certainty if such an approach will lead to a viable clinical treatment for psoriasis."

###

Specific roles for dendritic cell subsets during initiation and progression of psoriasis

See the rest here:

Dendritic cells affect onset and progress of psoriasis

THURSDAY, Sept. 11, 2014 (HealthDay News) -- A novel study of mice has shed new light on the molecular basis for glaucoma, which is a leading cause of blindness in the United States.

Based on their findings, researchers from Northwestern University Feinberg School of Medicine in Chicago said they are working to develop eye drops that might one day cure the disease in people.

"This is a big step forward in understanding the cause of the disease that steals the eyesight from 60 million people worldwide," study senior author Dr. Susan Quaggin, a Northwestern nephrologist, said in a university news release. "This gives us a foothold to develop new treatments."

Glaucoma, which has no cure, blocks the drainage of fluid from the eye, which then builds up pressure that can damage the retina and the optic nerve.

The vessel that is essential for proper drainage in the eye is known as Schlemm's canal. Using a mouse model of glaucoma, the researchers identified a chemical signaling pathway that is essential for growth, development and proper functioning of the canal. The pathway requires a substance called Tie2 and a growth factor called angiopoietin. If either was missing, the mice were not able to make Schlemm's canals and developed glaucoma, reports the study, published Sept. 9 in The Journal of Clinical Investigation.

"We really nailed that pathway as being critical," Quaggin noted. "Now we know these two substances are key factors in the development of glaucoma, which wasn't known before."

Although the study involved mice, and animal studies often fail to produce similar results in humans, the researchers said their findings are expected to be relevant for glaucoma in people. Both Tie2 and angiopoietin are likely involved in human glaucoma, they suggested.

"The mouse model is so similar to what we see in patients with glaucoma," said Quaggin. "Now we can understand how raised pressure leads to the damage of the neurons in the optic nerve."

Quaggin, who is director of the Feinberg Cardiovascular Research Institute and chief of nephrology and hypertension at Feinberg and Northwestern Memorial Hospital, is working with a team of scientists to develop an eye drop that triggers regrowth of the clogged vessel, or Schlemm's canal.

"Our goal now is to grow new 'pipes' or vessels to cure the glaucoma," concluded Quaggin, who is also the Charles Mayo Chair of Medicine at Feinberg. "Just imagine if we could grow a bigger Schlemm's canal in anybody with glaucoma to lower the pressure in the eye. That's what we're hoping for with this new eye drop."

Go here to read the rest:

Researchers Probe Molecular Cause for Glaucoma

09/08/2014 | 09:57am US/Eastern

The Cerami award, which includes a $20,000 prize, is conferred semi annually by the peer-reviewed, open-access journal Molecular Medicine published by the Feinstein Institute. A monograph authored by Dr. Hansson, entitled "A Journey in Science: Medical Scientist in Translation," will be published online September 5 in Molecular Medicine.

"The Anthony Cerami Award in Translational Medicine was created to recognize investigators who provided the crucial, early insight and ideas that are the essence of discovery, creating new fields and research trajectories followed by the persistent clinical investigation that ultimately changes how disease is prevented, diagnosed and treated," said Kevin J. Tracey, MD, president of the Feinstein Institute, editor emeritus of Molecular Medicine and Cerami Award committee member. "Professor Hansson's monograph is an inspiring story of genius and persistence that illuminates the discovery of how inflammation causes atherosclerosis, a major killer in the modern world."

"I am obviously very honored to be recognized in this way," said Dr. Hansson. "Being a scientist and having the opportunity to make discoveries is very rewarding in itself. To be selected for the Anthony Cerami Award in Translational Medicine is a wonderful recognition by my peers that the work my colleagues and I are doing contributes to the translation of science into medicine. I am particularly honored to follow in the footsteps of two of my role models in science - Anthony Cerami, after whom the award is named, and Carl Nathan, who received the first Cerami Award."

In the monograph, Dr. Hansson describes his journey in deciding whether to be a clinician or scientist, and notes a patient he met as a resident in internal medicine helped him solve this question. The patient had suffered a major stroke, and at the time there was no treatment available to help him. Hansson writes "The best they could hope for was that the man would die soon. Meeting this patient made me realize the limitations of clinical medicine. As a physician, you can do a lot for your patient -- but not more than the tools of medicine available at the time allow. As a clinician, your hands are tied by the limitations of medicine. As a physician-scientist, you can help stretch those limitations."

The Feinstein Institute is committed to celebrating the stewardship of the scientific process and imparting that perspective to young scientists. The Feinstein Institute also recognizes that the story behind making a discovery in medicine and healthcare is cherished and should be documented. The goal of the Cerami Award and its associated monographs, is to document such innovations and discoveries, so that they endure and inspire future generations of investigators.

In addition to his role at the Karolinska Institutet, Dr. Hansson is secretary of the Nobel Committee for Physiology or Medicine, director of the Medical Nobel Institute and member of the Royal Swedish Academy of Sciences. His research deals with immune and inflammatory mechanisms in atherosclerosis. Atherosclerosis is the buildup of fats, cholesterol and other substances in and on artery walls (plaques), which can restrict blood flow. Dr. Hansson discovered that the atherosclerotic plaque is the site of an inflammatory/immune response involving activated T-cells and their cytokines. His work has shown that low-density lipoprotein (LDL) elicits a cellular immune response and that humoral immunity contains atheroprotective activity.

The Anthony Cerami Award in Translational Medicine was made possible made possible by the generosity of the Anthony Cerami, PhD, and Ann Dunne Foundation for World Health. Dr. Cerami's breakthrough translational work includes the identification of anti-TNF's potential to treat a number of inflammatory diseases including rheumatoid arthritis, and the development of the HbA1c Diagnosic Test, currently the gold standard for the diagnosis and control of diabetes. He is currently working on a potential treatment of diabetes as CEO of Araim Pharmaceuticals.

(c) 2014 GlobalData Provided by SyndiGate Media Inc. (Syndigate.info).

See more here:

Molecular Medicine : Feinstein Institute Presents Cerami ...