Category Archives: Cell Biology

Simon Atkinson appointed IUPUI vice chancellor for research – IU Newsroom

INDIANAPOLIS -- Indiana University-Purdue University Indianapolis Chancellor Nasser H. Paydar has announced the appointment of Simon Atkinson as vice chancellor for research, effective July 1.

Atkinson, Chancellor's Professor and professor of biology in the School of Science at IUPUI since 2010, has served as IUPUI's interim vice chancellor for research since August 2015. He also holds adjunct appointments in the Indiana University School of Medicine Division of Nephrology and Department of Biochemistry and Molecular Biology.

Atkinson is a cell biologist specializing in research on kidney diseases. His background spans science, medicine and business. His interactions extend beyond his core research on the kidney, including numerous scientific collaborations with investigators across campus, especially in the Herman B Wells Center for Pediatric Research at the IU School of Medicine.

"I am delighted that Simon will continue to guide IUPUI's research office," Paydar said. "His expertise, extensive leadership experience, and outstanding accomplishments in research and education greatly benefit the campus community and beyond. He will keep us on track to implement IUPUI's strategic priorities that expand research and creative activity."

Atkinson first joined Indiana University in 1994 as an assistant professor in the Division of Nephrology at the School of Medicine. He served as graduate advisor and director of the Ph.D. program in biomolecular imaging and biophysics from 2004 to 2010. He served as chair of the Department of Biology in the School of Science at IUPUI from 2010 to 2015.

In recent years, Atkinson's research team has focused on efforts to understand and treat acute kidney injury, a common and life-threatening complication in seriously ill patients, using state-of-the-art methods including multiphoton microscopy, RNA interference and gene therapy.

Atkinson is also a biomedical entrepreneur. He co-founded INphoton -- a customized, proprietary company that provided microscopy services and consulting for pharmaceutical and biotech companies in the preclinical phase of drug discovery and development. He and other IU investigators also developed the technology used by Rene Medical Inc., a startup medical device company that targets the treatment and prevention of acute kidney injury.

Atkinson's research has been funded by the National Institutes of Health and has garnered foundation and industry support. He has also held leadership roles with the American Society for Cell Biology.

"Chancellor Paydar has set ambitious goals for our researchers, and I'm committed to seeing the campus recognized as one of the leading research institutions in the nation," Atkinson said. "My colleagues in the Office of the Vice Chancellor for Research are doing exceptional work to help realize the tremendous research potential at IUPUI. I look forward to continuing my association with them."

Atkinson earned his B.Sc. in cell and molecular biology from King's College London and his Ph.D. in molecular biology from the University of Cambridge in England. He also served a postdoctoral fellowship at Johns Hopkins University School of Medicine.

Atkinson will serve as vice chancellor for up to four years.

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Simon Atkinson appointed IUPUI vice chancellor for research - IU Newsroom

The Q&A: Xiang Zhang – Texas Tribune

With each issue, Trib+Health brings you an interview with experts on issues related to health care. Here is this weeks subject:

Dr. Xiang Zhang is associate professor of molecular and cellular biology at the Lester and Sue Smith Breast Center at Baylor College of Medicine. He recently led research on a study that developed a new lab technique to test the effectiveness of treatments for breast cancer metastases in bones.

Editors note: This interview has been edited for length and clarity.

Trib+Health: Can you expand on the study you led that developed a new lab technique to rapidly test the effectiveness of treatments for breast cancer metastases in bones?

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Xiang Zhang: Most preliminary clinical studies these days use primary tumors as models. In the clinic, what were already trying to cure are metastases, which kill around 90 percent of breast cancer patients. There hasnt been a great model, though.We are trying to put the cancer cells into the bone environment, and we actually invented a platform to have many specimens at once so we can perform multiple parallels to pass the efficacy of different drugs. We are hoping to accelerate the pre-clinical studies looking for effective drugs to treat cancer-related bone metastases.

So what we recently published is basically the methodology of how to perform such experiments using mice as a model. We found that the approach is actually pretty effective, because it allows us to very quickly check over 100 drugs most of which are already FDA-approved to treat other diseases.

We tested over 100 drugs and found a couple that exhibited extraordinary efficacies when they are in the bone microenvironment specifically, but they are not as effective or they have different efficacies with the cancer cell by themselves. But these drugs become more effective in the bone microenvironment. That raised the possibility that we could try these drugs in a clinic to treat patients with high risk of bone metastases or are already diagnosed with bone metastases.

Trib+Health: What were some of the more unexpected aspects of the study?

Zhang: There is also some surprise because some of the newly developed drugs that are currently in clinical trials and are supposed to act against cancer actually promote cancer in our model. That was very unexpected, and we are looking into the mechanisms, but that really alarmed us to use caution when we try new drugs because they can sometimes have unexpected or adverse effects. And that really raised the question to us that were going to need to test these drugs with the right model before we go to clinical trials.

Trib+Health:What are the next steps in your research following this study?

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Zhang: We are looking into the molecular reasons behind this unexpected efficacy. Our surprise finding doesnt necessarily mean those drugs cannot or should not be used, it just means we dont understand the entire system and need to go deeper. We already have some clues why that is the case, but this involves very complicated molecular mechanisms. That actually leads us to other discoveries, which are in process.

For the drugs that work extraordinarily well, we are also looking into the possibility to use them in the clinic as quickly as possible to make some clinical impact.

Trib+Health: Do you have a projected timeline for when those drugs may be used in a clinic for trials?

Zhang: I cant give you an exact timeline because I need to collaborate with the clinicians first. But Im very active in the discussion with my clinical colleagues here. Some of them are very excited about this, and were hoping we can move this forward as quickly as we can.The bright side is, as I said, some of these drugs are already FDA approved, or theyre in an advanced stage of the clinical pipeline for other diseases.

Trib+Health:Is there anything youd like to add to todays conversation?

Zhang: I would like to emphasize the importance of combining basic research with clinical studies. Right now, theres a significant gap between them. Clinicians and scientists need to work together. Scientists need to understand the real clinical need from patients, but clinicians also need to collaborate more closely to understand the basic mechanisms and design clinical trials in a more informed manner.I hope our study will further the collaboration between the two sides.

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The Q&A: Xiang Zhang - Texas Tribune

The remarkable promise of cell-free biology – The Economist

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The remarkable promise of cell-free biology - The Economist

USCA students earn research awards at Discover USC – Aiken Standard

Several USC Aiken students shared their research recently in Columbia as part of Discover USC, and many brought home honors.

More than 1,000 presenters shared their scholarly efforts as part of the event. Pacers made a total of 44 presentations and received 16 awards: four first place, eight second place and four honorable mentions.

USC Aiken students represented our campus very well, said Dr. Bill Pirkle, who leads USCAs sponsored research program.

Discover USC showcases research, scholarship, leadership and creative projects by undergraduate and graduate students, postdoctoral scholars and medical scholars representing the entire USC System, from the Upstate to the Lowcountry.

Rebecca Beaudry, biology. Mentor, Dr. William Jackson, biology/geology. Development of a bicistronic vector system to test anti-HIV 1 siRNAs that target the accessory protein VIF. Biology and Biomedical Sciences Poster Session F.

Christian Fay, biology. Mentor, Dr. William Jackson, biology/geology. siRNA mediated downregulation of HIV-Tat in anti-Tat siRNA protected Lymphocyte populations. Biology and Biomedical Sciences Poster Session G.

as-050617-ne-training-track-2, psychology, Magellan Scholar. Mentor, Dr. Keri Weed, psychology. The Influence of Perceived Control over Task Difficulty on Coping with Math Anxiety. Psychology and Neurosciences Poster Session E.

Davont Jenkins, communication. Mentor, Dr. William Harpine, communication. The Effects of Speaker Credibility in Race Relations: A Study of Two Speeches. Social Sciences Oral Session H.

Erin McLaughlin, biology, Magellan Scholar, Honors Program graduate. Mentor, Dr. William Jackson, biology/geology. Expression of Vif-resistant ApoBEC3G from a HIV-1-dependent lentiviral vector. Biology and Biomedical Sciences Poster Session H.

Natalie Arthur, biology. Mentor, Dr. William Jackson, biology/geology. Generating a HIV-1-dependent chimeric vector to deliver a pro-apoptotic gene. Biology and Biomedical Sciences Poster Session H.

Jazmine Benjamin, biology. Mentor, Dr. Nathan Hancock, biology/geology. Determining the Sequences Involved in mPing Transposition. STEM Oral Session C.

Tiana Chandler, biology, Honors Program graduate. Mentor, Dr. Nathan Hancock, biology/geology. Development of an mPing-based Activation Tag for Zebrafish Mutagenesis. STEM Oral Session E.

Harli Eggenberger, exercise and sports science, Magellan Scholar, and Brooke Clark, communication, Magellan Scholar, Honors Program graduate. Mentor, Dr. Brian Parr, exercise and sports science. Candy and Soda for Breakfast: Developing visual communication tools to promote healthy eating. Public Health Poster Session D.

Lianna Epstein, exercise and sports science. Mentor, Dr. Andrew Hatchett, exercise and sports science. A comparison of energy expenditure between motorized and non-motorized treadmills. Public Health Poster Session H.

Kenneth Glenn, biology, Magellan Scholar. Mentor, Dr. April DeLaurier, biology/geology. Generating mef2ca and mef2cb transgenic zebrafish lines using BAC-mediated recombination. STEM Oral Session Session A.

Meredith Hawcroft, English, Magellan Scholar, Honors Program graduate. Mentor, Dr. Todd Hagstette, English. The Battle of Bachelorhood and Domesticity in William Gilmore Simms Castle Dismal. Social Sciences and Humanities Poster Session.

Lisete Payero, biology, Magellan Scholar. Mentor, Dr. Nathan Hancock, biology/geology. Determining the role of homologous recombination in replicative transposition of mPing. Biology and Biomedical Sciences Poster Session E.

Johnny Carroll, biology. Mentor, Dr. William Jackson, biology/geology. T-Bid expression in ptBidTNG(INS2)R to induce Apoptosis in a HIV infected Cell. Biology and Biomedical Sciences Poster Session F.

Emma Nettles, psychology, Magellan Scholar. Mentor, Dr. Adam Pazda, psychology. Perspective Taking and Self-Other Overlap: How Self-Compassion Mitigates the Negative Effect of Blame on Helping Behavior. Psychology and Neuroscience Poster Session E.

Sara Puckett, psychology, and Matthew Haslinger, psychology. Mentors, Drs. Elaine Clanton Harpine, education; Adam Pazda, psychology; and William Harpine, Communication. Teaching Phonemic Awareness Improved Reading, Spelling, and Comprehension. Social Sciences Poster Session I.

Lauren Spires, biology. Mentor, Dr. William Jackson, biology/geology. Developing a HIV-1 Dependent Lentiviral Vector that Expresses an Innate Human Anti-Retroviral Gene. Biology and Biomedical Sciences Poster Session F.

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USCA students earn research awards at Discover USC - Aiken Standard

Advanced prostate cancer treatment failure due to cell reprogramming – Science Daily

Columbia University Medical Center (CUMC) researchers have discovered a molecular mechanism that reprograms tumor cells in patients with advanced prostate cancer, reducing their response to anti-androgen therapy. The findings, based on a study in mice, could help to determine which patients should avoid anti-androgen therapy and identify new treatments for people with advanced prostate cancer.

The study was published online April14th in the journal Cancer Discovery.

Since androgens (male hormones) are known to drive prostate cancer, patients with recurrent or advanced disease are typically treated with anti-androgen medications. However, most patients fail treatment and develop an aggressive form of prostate cancer known as castration-resistant prostate cancer, or CRPC.

"It's been a mystery why some patients do not respond to anti-androgens, and why a subset of these patients actually get worse after treatment," said study co-leader Cory Abate-Shen, PhD, the Michael and Stella Chernow Professor of Urological Oncology and professor of urology, medicine, systems biology, and pathology and cell biology at CUMC. "Our findings show that in many of these patients, the tumor cells are reprogrammed so that they are no longer dependent on androgens."

To learn about the molecular mechanisms that drive resistance to anti-androgens, Drs. Abate-Shen and Michael Shen co-led a team to develop a strain of mice that lack two tumor-suppressor genes, Trp53 and Pten. These genes are both mutated in about 25 percent of patients with advanced prostate cancer. Mice that were treated with the anti-androgen drug abiraterone failed to respond and had accelerated tumor growth -- similar to some humans with advanced prostate cancer who do not respond to anti-androgen therapy.

"We found a number of genes that were overexpressed in mice with CRPC and also conserved in patients with the disease. Among the most interesting of these was SOX11, which regulates the development of the nervous system," said study co-leader Michael M. Shen, PhD, professor of medical sciences at CUMC.

Most localized, slow-growing prostate cancers are largely composed of epithelial cells, which are rich in androgen receptors that increase their susceptibility to anti-androgen therapy. In contrast, aggressive prostate cancers, particularly those that fail treatment, often contain many neuroendocrine-like cells, which lack androgen receptors and are therefore less responsive to anti-androgen therapy.

"This raised the question, where are the neuroendocrine-like cells in prostate tumors coming from?" said Dr. Abate-Shen. "While previous research hinted that epithelial tumor cells may be reprogrammed to become neuroendocrine-like cells, our study provides the first direct evidence that this reprogramming is actually occurring and that it is mediated, at least in part, by SOX11."

The researchers also demonstrated that SOX11 acts in a similar fashion in human prostate cancer cells.

"By giving anti-androgens to patients with CRPC, we are eliminating the cancer cells that need androgen to survive and enriching the tumor with the remaining neuroendocrine-like cells. The net effect is to create an even more aggressive tumor," said Dr. Shen.

The researchers also identified several "master regulators" -- genes that control SOX11 and other genes involved in prostate cancer reprogramming -- that might be targeted for new prostate cancer treatments.

"Based on our findings, genetic testing to identify SOX11 and the master regulators may be considered before embarking on anti-androgen therapy for patients with advanced prostate cancer," said Dr. Shen.

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Advanced prostate cancer treatment failure due to cell reprogramming - Science Daily

Platelets suppress T cell immunity against cancer – Medical Xpress – Medical Xpress

May 5, 2017 Stylized illustration of a platelet and T cell. Plus and negative signs are used to symbolically indicate the positive (clotting) and negative (downregulating T cell immunity) effects of platelets. Credit: Emma Vought of the Medical University of South Carolina.

Blood platelets help disguise cancer from the immune system by suppressing T cells, report scientists at the Medical University of South Carolina (MUSC) in the May 5, 2017 issue of Science Immunology. In extensive preclinical tests, a promising T cell therapy more successfully boosted immunity against melanoma when common antiplatelet drugs such as aspirin were added.

Zihai Li, M.D., Ph.D., senior author on the article, is chair of the MUSC Department of Microbiology and Immunology, the program leader for the Cancer Immunology Research Program at MUSC Hollings Cancer Center, and the SmartState Sally Abney Rose Chair in Stem Cell Biology & Therapy. Li studies how tumors hide themselves from the immune system.

Li's team found that platelets release a molecule that suppresses the activity of cancer-fighting T cells. That molecule, unsurprisingly, was TGF-beta, which has been recognized for decades for its role in cancer growth.

Yet this study is the first of its kind. Most TGF-beta is inactive. Li and his group found that the surface of platelets has a protein called GARP, a molecular hook that is uniquely able to trap and activate TGF-beta. Platelets, which are small cell fragments that circulate throughout the blood and are normally involved in clotting, become the major source of activated TGF-beta that invading tumor cells use to suppress T cells. In other words, platelets help give tumors their invisibility cloak from the immune system.

Scientists have known for several years that certain cancers suppress T cells to avoid the immune system. That is why adoptive T cell therapy is one of the most promising advances in modern cancer treatment. It is a type of immunotherapy that awakens the immune system by retraining a patient's T cells to recognize their cancer. T cells are isolated from a patient's blood and retrained, or "primed," to recognize tumor cells. They are then injected back into the patient's bloodstream where they can now hunt and fight cancer.

There was some evidence that platelets might make cancer worse. For example, patients who have excessive clotting related to their cancer almost always have a worse prognosis, according to Li.

"Over the years, it has become appreciated that platelets are doing more than just clotting," says Li.

The first clue that cancer-fighting T cells might be suppressed by the body's own clotting system came when the researchers gave melanoma to mice with genetically defective platelets. Melanoma tumors grew much more slowly and primed T cells were much more active than in mice with normal platelets.

Next, the team isolated platelets and T cells from blood drawn from humans and mice. In both cases, platelets with activated clotting activity suppressed T cell response. It then used mass spectrometry to thoroughly identify the molecules released by activated platelets that most suppressed T cell activity. The molecule with the most T cell suppression was TGF-beta.

Li and his team then studied how platelets activate TGF-beta. In genetically modified mice without GARP, the molecular hook on the surface of platelets, adoptive T cell therapy was more successful at controlling melanoma. This meant that platelets without the ability to grab and activate TGF-beta were not able to suppress cancer-fighting T cells. Similar experiments confirmed this result in mice with colon carcinoma.

Finally, mice with normal platelets that were given melanoma and then adoptive T cell therapy survived longer and relapsed less when aspirin and clopidogrel, two antiplatelet drugs, were added. The researchers noted that antiplatelet drugs by themselves were not successful in combating melanoma in their experiments.

This study could inform future treatment of melanoma and other cancers and offers a sound reason to test antiplatelet drugs in clinical trials of adoptive T cell therapy. In patients with melanoma or other cancers, adoptive T cell therapy may be successful if highly available platelet-blocking drugs such as aspirin are added to the treatment. However, the current standard of care for melanoma is not adoptive T cell therapy, but so-called checkpoint inhibitors.

Li and his group want to know if combination therapy with antiplatelet drugs could improve existing cancer treatment. They are waiting for approval to begin a clinical trial that will test certain checkpoint inhibitors in combination with aspirin and clopidogrel for the treatment of patients with advanced cancers. Li's trial will complement clinical trials that are already testing adoptive T cell therapy as a single treatment for cancer.

"I'm very excited about this," says Li. "We can test simple, over-the-counter antiplatelet agents to really improve immunity and make a difference in how to treat people with cancer."

Explore further: Aspirin slows growth of colon, pancreatic tumor cells

More information: "Platelets subvert T cell immunity against cancer via GARP-TGF axis," Science Immunology (2017). immunology.sciencemag.org/lookup/doi/10.1126/sciimmunol.aai7911

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If you scanned the body for relatively higher TGF concentrations, could you use that information to find active cancers?

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Platelets suppress T cell immunity against cancer - Medical Xpress - Medical Xpress

Advanced prostate cancer treatment failure due to cell reprogramming – Medical Xpress

May 4, 2017 Micrograph showing prostatic acinar adenocarcinoma (the most common form of prostate cancer) Credit: Wikipedia

Columbia University Medical Center (CUMC) researchers have discovered a molecular mechanism that reprograms tumor cells in patients with advanced prostate cancer, reducing their response to anti-androgen therapy. The findings, based on a study in mice, could help to determine which patients should avoid anti-androgen therapy and identify new treatments for people with advanced prostate cancer.

The study was published online April14th in the journal Cancer Discovery.

Since androgens (male hormones) are known to drive prostate cancer, patients with recurrent or advanced disease are typically treated with anti-androgen medications. However, most patients fail treatment and develop an aggressive form of prostate cancer known as castration-resistant prostate cancer, or CRPC.

"It's been a mystery why some patients do not respond to anti-androgens, and why a subset of these patients actually get worse after treatment," said study co-leader Cory Abate-Shen, PhD, the Michael and Stella Chernow Professor of Urological Oncology and professor of urology, medicine, systems biology, and pathology and cell biology at CUMC. "Our findings show that in many of these patients, the tumor cells are reprogrammed so that they are no longer dependent on androgens."

To learn about the molecular mechanisms that drive resistance to anti-androgens, Drs. Abate-Shen and Michael Shen co-led a team to develop a strain of mice that lack two tumor-suppressor genes, Trp53 and Pten. These genes are both mutated in about 25 percent of patients with advanced prostate cancer. Mice that were treated with the anti-androgen drug abiraterone failed to respond and had accelerated tumor growthsimilar to some humans with advanced prostate cancer who do not respond to anti-androgen therapy.

"We found a number of genes that were overexpressed in mice with CRPC and also conserved in patients with the disease. Among the most interesting of these was SOX11, which regulates the development of the nervous system," said study co-leader Michael M. Shen, PhD, professor of medical sciences at CUMC.

Most localized, slow-growing prostate cancers are largely composed of epithelial cells, which are rich in androgen receptors that increase their susceptibility to anti-androgen therapy. In contrast, aggressive prostate cancers, particularly those that fail treatment, often contain many neuroendocrine-like cells, which lack androgen receptors and are therefore less responsive to anti-androgen therapy.

"This raised the question, where are the neuroendocrine-like cells in prostate tumors coming from?" said Dr. Abate-Shen. "While previous research hinted that epithelial tumor cells may be reprogrammed to become neuroendocrine-like cells, our study provides the first direct evidence that this reprogramming is actually occurring and that it is mediated, at least in part, by SOX11."

The researchers also demonstrated that SOX11 acts in a similar fashion in human prostate cancer cells.

"By giving anti-androgens to patients with CRPC, we are eliminating the cancer cells that need androgen to survive and enriching the tumor with the remaining neuroendocrine-like cells. The net effect is to create an even more aggressive tumor," said Dr. Shen.

The researchers also identified several "master regulators"genes that control SOX11 and other genes involved in prostate cancer reprogrammingthat might be targeted for new prostate cancer treatments.

"Based on our findings, genetic testing to identify SOX11 and the master regulators may be considered before embarking on anti-androgen therapy for patients with advanced prostate cancer," said Dr. Shen.

Explore further: Study uncovers an additional strategy for targeting treatment-resistant prostate cancer

More information: Min Zou et al, Transdifferentiation as a Mechanism of Treatment Resistance in a Mouse Model of Castration-resistant Prostate Cancer, Cancer Discovery (2017). DOI: 10.1158/2159-8290.CD-16-1174

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Advanced prostate cancer treatment failure due to cell reprogramming - Medical Xpress

Researchers catch up on each other’s work at forum – Yale News

From neutrinos to fly vision to follicle regeneration, university researchers talked about a wide array of research at the Yale Science and Engineering Forum on May 3.

The Yale Quantum Institute hosted the event, which has taken place annually since 1995. Professor A. Douglas Stone, who has been one of the principal organizers of the event since it began, said the intent is to give Yale faculty members a chance to see what their colleagues have been working on.

Over the years, many people who have spoken at this have gone on to become leaders in their field, and various collaborations have come out of it, said Stone, the Carl A. Morse Professor of Applied Physics and professor of physics, who serves as director of Yales Division of Physical Sciences.

Although the presentations are aimed at scientists, theyre also designed to be accessible to researchers from all disciplines. That means Stone will occasionally break into a presenters talk to ask that a particularly jargon-laden sentence be rephrased. Others in the audience are also encouraged to speak up if they lose the thread of the discussion.

The event was broken into three sessions quantitative biology and biophysics, physics of the visible and invisible, and regenerative biology and featured a diverse roster of speakers:

Damon Clark, assistant professor of molecular, cellular, and developmental biology, discussed how flies sense motion a process that involves putting the insects on tiny spherical treadmills and how they ably elude the swatter despite having relatively low-resolution vision.

Jonathon Howard, the Eugene Higgins Professor of Molecular Biophysics and Biochemistry and professor of physics, discussed a family of motor proteins known as kinesin and how they travel along microtubules.

Peter Rakich, assistant professor of applied physics, discussed how the power of sound can be used to amplify light waves on a silicon microchip and the new applications this could lead to (navigational sensors, and low-noise lasers, for instance).

Karsten Heeger, professor of physics and director of the Wright Laboratory, presented his research on neutrinos, dark matter, and other mysteries of the universe.

Josien van Wolfswinkel, assistant professor of molecular cellular and developmental biology, discussed a group of flatworms known as planaria that have the capability to regenerate any missing body region.

Valerie Horsley, the Maxine F. Singer '57 Associate Professor of Molecular, Cellular, and Developmental Biology and associate professor of dermatology, discussed adipocytes cells that store energy as fat and their role in the regrowth of hair follicles and the healing of skin wounds.

We try to get to a good mix that would appeal to a wide range of scientists, said one of the events organizers, Thomas Pollard, Sterling Professor of Molecular, Cellular, and Developmental Biology, and professor of cell biology and of molecular biophysics and biochemistry. Its just a chance for the science community at Yale to enjoy the excitement of their colleagues work. Were all so busy during the rest of the year that we dont get much of a chance to hear our colleagues speak.

The event does more than just satisfy scientific curiosity; its been known to kick start cross-disciplinary collaborations. Audience member Richard Prum, the William Robertson Coe Professor of Ornithology of Ecology and Evolutionary Biology, recalled his talk at the event in 2005 on his research into the optics of bird feathers.

We had made some very important general progress, but we were still far from an analytical solution, he said. Attendee Eric Dufresne, then a professor in Yales chemical engineering department, suggested that one of Prums images looked like a spinodal decomposition and was perhaps part of a phase separation process.

I said, Ive got no idea what youre talking about, but lets have lunch. They did, and it turned out Dufresnes intuition was correct. More than 12 years later, the collaboration continues, and has brought in more faculty members from engineering and physics. Its an example of why events such as Wednesdays forum are so important, Prum said.

Its hard to get scientists out of their own labs, he said, so this is absolutely necessary to bring people out of their silos.

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Researchers catch up on each other's work at forum - Yale News

Starvation leads to ‘cell death’ which isn’t good for the body – Hindustan Times

Cell death, caused due to lack of glucose in which cells die in an unexpected manner, follows a process similar to what we would expect from an immune response, a new study found.

Are you one of those who starve yourselves for losing weight? You might want to think that again. According to a new study, researchers have characterized the cell death process due to starvation, in which the endoplasmic reticulum plays a leading role.

The study got published in journal Molecular and Cellular Biology.

Usually, programmed cell death -- also called apoptosis -- follows a biochemical pathway related to the permeabilization of mitochondria; However, we observed that in cases of cell death due to lack of glucose, cells die in an unexpected way, following a process similar to what we would expect from an immune response, stated Dr. Cristina Muoz-Pinedo, studys lead author.

The study finds that in cell-death-related treatments such as chemotherapy, the mitochondrial pathway is activated. Instead, when starved, cells activate the so-called death receptors on their membrane, which are normally used by the lymphocytes of the immune system to attack and destroy infected cells.

Starving yourself to losing weight may not be the bet options, the study found.

The researchers have been able to relate the activation of these membrane receptors to the endoplasmic reticulum, a cellular organelle involved in protein synthesis and lipid metabolism, as well as intracellular transport.

Feeling the stress produced by the lack of nutrients, the reticulum send an alarm signal that triggers the appearance of death receptors in the membrane, said Dr Muoz-Pinedo.

According to our in vitro results, we assume that this is how the tumour cells located in the centre of a tumour -- the so-called necrotic core -- die, because there are never enough nutrients in those areas. On the other hand, in ischemia, besides the lack of oxygen there is also cell death due to lack of glucose, so this process could also be related to the activity of the endoplasmic reticulum at a biochemical level, added the IDIBELL researcher.

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Starvation leads to 'cell death' which isn't good for the body - Hindustan Times

UCD’s Jodi Nunnari elected to National Academy of Sciences – Davis Enterprise

Professor Jodi Nunnari, chair of the department of molecular and cellular biology in the College of Biological Sciences at UC Davis, has been elected as a member of the National Academy of Sciences.

Nunnari studies mitochondria, tiny structures that provide energy to living cells and that are implicated in a wide range of diseases, including heart disease, stroke and inherited conditions.

Jodi Nunnari. Courtesy photo

Beginning as a postdoctoral researcher, Jodi has made discoveries that have transformed her field and helped demystify the genesis of a broad range of diseases, said Ralph Hexter, interim chancellor of UCD.

Her pioneering work is a prime example of our universitys commitment to fundamental research to improve the human condition. I could not be happier to see her receive this much-deserved recognition.

Nunnaris lab studies the behavior of mitochondria which have their own DNA, separate from the cell nucleus inside cells. Her work looks at the mechanisms through which mitochondria divide and fuse together, and at how mitochondrial DNA is organized and transmitted.

Nunnari is among 84 new members and 21 foreign associates elected to the academy this year. She is one of 27 current or retired UCD faculty who are members or foreign associates of the academy.

Election to the National Academies of Sciences is among the highest honors a scientist can receive in recognition of their distinguished scholarly contributions, said Mark Winey, dean of the College of Biological Sciences.

Jodis election is very well deserved for her groundbreaking work on mitochondria. As powerhouses of the cell, mitochondrial failure is linked to a variety of inherited diseases, as well as neurological disorders and aging.

Nunnari earned her bachelors degree from the College of Wooster in Ohio and her doctorate, in pharmacology, from Vanderbilt University. She carried out her postdoctoral research in the laboratory of Peter Walter at UC San Francisco, where she discovered that mitochondria form a dynamic network with the cell. This concept has led her to fundamental insights into how mitochondria grow, divide and function.

The National Academy of Sciences is a private, nonprofit institution that was established under a congressional charter signed by President Abraham Lincoln in 1863. Together with the National Academy of Engineering and the National Academy of Medicine, it provides advice on science, engineering, and health policy to the federal government and other organizations.

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UCD's Jodi Nunnari elected to National Academy of Sciences - Davis Enterprise