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News Article | May 12, 2017
Site: www.chromatographytechniques.com

Science funding is intended to support the production of new knowledge and ideas that develop new technologies, improve medical treatments and strengthen the economy. The idea goes back to influential engineer Vannevar Bush, who headed the U.S. Office of Scientific Research and Development during World War II. And the evidence is that science funding does have these effects. But, at a practical level, science funding from all sources supports research projects, the people who work on them and the businesses that provide the equipment, materials and services used to carry them out. Given current proposed cuts to federal science funding—the Trump administration has, for instance, proposed a 20 percent reduction for the National Institutes of Health—it’s important to know what types of people and businesses are touched by sponsored research projects. Most existing research into the effects of science funding tries to quantify research artifacts, such as publications and patents, rather than tracking people. I’ve helped start an emerging project called the UMETRICS initiative, which takes a novel approach to thinking about innovation and science. UMETRICS identifies people employed on scientific projects at universities and the purchases made to carry out those projects. It then tracks people to the businesses and universities that hire them, and purchases to the vendors from which they come. Since UMETRICS relies entirely on administrative data provided by member universities (now around 50), the U.S. Census Bureau and other naturally occurring data, there are no reporting errors, sample coverage concerns or burden for people. It covers essentially all federal research funding, as well as some funding from private foundations. Our administrative data allow us to identify everyone employed on research projects, not just those who appear as authors on research articles. This is valuable because we’re able to identify students and staff, who may be less likely to author papers than faculty and postdocs but who turn out to be an important part of the workforce on funded research projects. We compared the distribution of people supported on research projects at some of the largest National Science Foundation (NSF) Divisions and National Institutes of Health (NIH) Institutes and Centers. Together, the NSF and NIH support close to 70 percent of federally funded academic R&D. The striking thing is that the majority of people employed on research projects are somewhere in the training pipeline, whether undergraduates; graduate students, who are particularly prevalent at NSF; or postdocs, who are more prevalent at NIH. Staff frequently constitute 40 percent of the NIH-supported workforce, but faculty are a relatively small portion of the workforce at all NIH Institutes and NSF Divisions. Based on these results, it seems likely that changes in federal research funding will have substantial effects on trainees, which would naturally have implications for the future STEM workforce. Given the importance of trainees in the research workforce, we have focused much of our research on graduate students. We mapped the universities in our sample and the share of graduate students in each state one year after graduation. Our data show many grad students contribute to local economies—12.7 percent are within 50 miles of the universities where they trained. For six of our eight universities, more people stayed in state than went to any other single state. At the same time, graduate students fan out nationally, with both coasts, Illinois and Texas common destinations. The doctoral recipients in our sample are also more likely to take jobs at establishments that are engines of the knowledge economy. They are heavily overrepresented in industries such as electronics, semiconductors, computers and pharmaceuticals, and underrepresented in industries such as restaurants, grocery stores and hotels. Doctoral degree recipients are almost four times as likely as the average U.S. worker to be employed by an R&D-performing firm (44 percent versus 12.6 percent). And, the establishments where the doctoral degree recipients work have a median payroll of more tha $90,000 per worker compared to $33,000 for all U.S. establishments and $61,000 for establishments owned by R&D performing firms. Taken as a whole, our research indicates that the workers trained on research projects play a critical role in the industries and at companies critical for our new, knowledge economy. Another way in which sponsored research projects affect the economy in the short run is through purchases of equipment, supplies and services. Still-unpublished work studying the vendors who sell to sponsored research projects at universities shows that many of the firms are frequently high-tech and often local. Moreover, firms that are vendors to university research projects are more likely to open new establishments near their campus customers. Thus, there is some evidence that research projects directly stimulate local economies. So while the goal of sponsored research projects is to develop new knowledge, they also support the training of highly skilled STEM workers and support activity at businesses.


News Article | May 11, 2017
Site: www.cemag.us

McAlpine, who gained international acclaim in 2013 for integrating electronics and novel 3D-printed nanomaterials to create a “bionic ear,” says this new discovery could also be used to print electronics on real human skin. This ultimate wearable technology could eventually be used for health monitoring or by soldiers in the field to detect dangerous chemicals or explosives. “While we haven’t printed on human skin yet, we were able to print on the curved surface of a model hand using our technique,” McAlpine says. “We also interfaced a printed device with the skin and were surprised that the device was so sensitive that it could detect your pulse in real time.” McAlpine and his team made the unique sensing fabric with a one-of-a kind 3D printer they built in the lab. The multifunctional printer has four nozzles to print the various specialized “inks” that make up the layers of the device — a base layer of silicone, top and bottom electrodes made of a conducting ink, a coil-shaped pressure sensor, and a sacrificial layer that holds the top layer in place while it sets. The supporting sacrificial layer is later washed away in the final manufacturing process. Surprisingly, all of the layers of “inks” used in the flexible sensors can set at room temperature. Conventional 3D printing using liquid plastic is too hot and too rigid to use on the skin. These flexible 3D-printed sensors can stretch up to three times their original size. “This is a completely new way to approach 3D printing of electronics,” McAlpine says. “We have a multifunctional printer that can print several layers to make these flexible sensory devices. This could take us into so many directions from health monitoring to energy harvesting to chemical sensing.” Researchers say the best part of the discovery is that the manufacturing is built into the process. “With most research, you discover something and then it needs to be scaled up. Sometimes it could be years before it ready for use,” McAlpine says. “This time, the manufacturing is built right into the process so it is ready to go now.” The researchers say the next step is to move toward semiconductor inks and printing on a real body. “The possibilities for the future are endless,” McAlpine says. In addition to McAlpine, the research team includes University of Minnesota Department of Mechanical Engineering graduate students Shuang-Zhuang Guo, Kaiyan Qiu, Fanben Meng, and Sung Hyun Park. The research was funded by the National Institute of Biomedical Imaging and Bioengineering of the National Institutes of Health (Award No. 1DP2EB020537). The researchers used facilities at the University of Minnesota Characterization Facility and Polymer Characterization Facility for testing.


News Article | May 10, 2017
Site: www.eurekalert.org

Six biological pigments called rhodopsins play well-established roles in light-sensing in the fruit fly eye. Three of them also have light-independent roles in temperature sensation. New research shows that a seventh rhodopsin, Rh7, is expressed in the brain of fruit flies where it regulates the fly's day-night activity cycles. The study appears in Nature and was funded by the National Eye Institute, part of the National Institutes of Health. "Rh7 is the first example of a rhodopsin that is important in setting circadian rhythms by being expressed in the central brain, rather than the eye," said Craig Montell, Ph.D., Duggan Professor of Molecular, Cellular and Developmental Biology at the University of California Santa Barbara and senior author of the study. This newly discovered role for Rh7 could have clinical implications down the road. "Identifying new roles for light-sensitive opsins is essential for understanding degenerative retinal disorders and developing potential new treatments," said Lisa Neuhold, Ph.D., program director at the National Eye Institute. Rhodopsins, discovered in the 1870s, are well-known for their important role in light-sensing and image formation. The six previously known fly rhodopsins account for the full function of photoreceptor cells in the fly's eyes, so although the fruit fly genome contained the sequence of a seventh rhodopsin, the role of Rh7 was unclear. To investigate the role of Rh7, Montell and collaborators at the University of California, Irvine, first confirmed that Rh7 sensed light by doing genetic experiments that replaced Rh1, the primary light-sensor in photoreceptor cells of the fly eye, with Rh7. The researchers found that Rh7 could functionally substitute for Rh1 in flies missing Rh1, as measured by electroretinogram, which is an extracellular recording of a neural signal in the fly eye in response to light. Next, the researchers used antibodies recognizing Rh7 to determine its expression pattern. They found that it was expressed in the brain's central pacemaker neurons, which play a role in regulating circadian rhythms. Montell and his team reared fruit flies under a 12-hour light/12-hour dark cycle, then extended one light cycle to 20 hours and measured how quickly the flies adjusted their daily activity to match the new light/dark cycle. By measuring how often the flies crossed an infrared beam positioned in the center of the vial, the researchers could track daily patterns of activity. They showed that the flies missing Rh7 took significantly longer to adjust than the normal, wild type flies. The researchers also examined the effect of light pulses in the middle of the night, which disrupt the normal circadian cycle, and again found that the readjustment took longer in flies missing Rh7. The central pacemaker neurons were already known to have a light sensor called cryptochrome, but the ability of flies who were genetically engineered to lack cryptochrome to regulate light/dark cycles is only partially impaired. So, the researchers suspected that another molecule might be involved -- and that turns out to be Rh7, which is more light-sensitive than cryptochrome. "It appears Rh7 provides a more sensitive way of detecting light and setting circadian rhythms," explained Montell. However, more research is still needed. A light sensor in the brain makes sense in the fruit fly, because light can pass through the cuticle covering the head. But what could opsins be doing in the mammalian brain, where light may not effectively penetrate the skull? Montell suggested that the fly's central pacemaker neurons may correspond to a type of cell in the mammalian eye, rather than cells in the mammalian brain. In the eye, retinal ganglion cells (RGCs) relay signals from light-sensing rods and cones and to the brain via the optic nerve. But about 1 percent of RGCs are intrinsically photosensitive (ipRGCs). These ipRGCs, which contain melanopsin (another type of light-sensitive pigment), do not have roles in image formation but are important for the regulation of circadian rhythms. Due to their similar function and similar molecular features, Montell believes that the fly's central pacemaker neurons expressing Rh7 are the equivalent of mammalian ipRGCs. However, a mystery remains as to why opsins are also expressed in the mammalian brain and spinal cord, where they may not receive sufficient light to be light activated. The work was supported by grants from the National Eye Institute (EY008117), the National Institute on Deafness and Other Communication Disorders (DC007864), and the National Institute of General Medical Sciences (GM102965 and GM107405). Ni JD, Baik LS, Holmes TC, Montell C. 2017. A rhodopsin in the brain functions in circadian photoentrainment in Drosophila. Nature XXX NEI leads the federal government's research on the visual system and eye diseases. NEI supports basic and clinical science programs to develop sight-saving treatments and address special needs of people with vision loss. For more information, visit https:/ . About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.


News Article | May 9, 2017
Site: www.prweb.com

Tech Coast Angels (TCA) congratulates Savara Inc. (NASDAQ: SVRA) on its recent listing on the Nasdaq Capital Market. The clinical-stage specialty pharmaceutical company’s Series B round in 2012-13 was the largest single raise by TCA ($3.2 M). Overall, TCA members together with a few family and friends have invested over $6M in various financing rounds of Savara, the most for any portfolio company since TCA’s inception in 1997. In total, Savara received almost $50M in non-institutional capital, and has been supported by a $4M grant from the National Institutes of Health as well as a $1.7M research award from the Cystic Fibrosis Foundation. Nearly every funding round was oversubscribed and extended. Sergio Gurrieri, TCA deal lead, current president of the San Diego chapter of TCA, and observer on the Savara Board since 2012, explained three key elements that made Savara such a winning formula for angel investors: “First of all, Rob Neville, Savara’s CEO and chairman, is truly exceptional. He adheres to a well-balanced and extremely effective decision-making process whereby every single stakeholder’s opinion is considered. Also, Rob's execution skills are outstanding, his integrity is impeccable, his communication skills powerful, and his management style highly professional.” “Secondly, the entire Savara team is phenomenal,” Gurrieri continued. “The team’s ability to execute is second to none. In particular, Dr. Taneli Jouhikainen, COO, has been indispensable, co-leading Savara, its programs, and corporate development activities. Taneli is one of the most talented, and knowledgeable COO's I have ever had the pleasure of knowing.” “And finally, the board of directors is truly outstanding. The level of expertise, the collective wisdom and experience, the constructive conversations, resulted in an extraordinary board for an extraordinary company,” Gurrieri concluded. “We truly appreciate the support from Tech Coast Angels’ members and we thank each investor for believing in Savara’s purpose to find new therapies and treatment for rare and debilitating lung diseases,” said Mr. Neville. “Through our excellent team and proven ability to execute, Savara presents an attractive business opportunity with our pipeline of unique products with considerable market potential. We will continue to diligently work to make their investment a success.” About Tech Coast Angels: Tech Coast Angels (TCA) is one of the largest and most active angel investor networks in the nation, and a leading source of funding for seed-stage and early-stage companies across all industries in Southern California. TCA members are accredited investors who individually invest in startup companies, and as a group, have invested up to $6M in a single company. The companies TCA invest in go through well-structured, transparent, and time efficient screening and due diligence. TCA members are themselves founders and executive level business leaders who have extensive knowledge in the investment process and world-class business practices. TCA members thus provide companies with more than just capital; they also contribute counsel, mentoring and access to an extensive network of investors, customers, strategic partners and management. TCA is a catalyst in the growth of the thriving Southern California entrepreneurial ecosystem of innovation, funding mostly emerging technologies and life science companies. The most recent Halo Report rated TCA as #2 nationally in a number of funded deals. A recent analysis by CB Insights ranked TCA #1 out of 370 angel groups on “Network Centrality” and #5 overall in “Investor Mosaic.” Since its founding in 1997, TCA has invested over $190 million in more than 335 companies and has helped attract more than $1.5 billion in additional capital/follow-on rounds, mostly from venture capital firms. For more information, please visit http://www.techcoastangels.com.


News Article | May 9, 2017
Site: www.eurekalert.org

Many contributors to patient satisfaction, such as sociodemographics and psychological factors, are beyond the physician's control BUFFALO, N.Y. -- Patient satisfaction is playing an increasingly important role in evaluating the quality of health care and reimbursing physicians for it. Exactly what drives that satisfaction has been difficult to determine. A new University at Buffalo study of 483 patients with irritable bowel syndrome (IBS) revealed that many factors that contribute to patient satisfaction are beyond the doctor's control. The results of the study were presented in Chicago today (May 9) at Digestive Disease Week during the Clinical Practice Distinguished Abstract Plenary. The study's title is "(Can't Get No) Patient Satisfaction: The Predictive Power of Demographic, GI and Psychological Factors in IBS Patients." "Ideally, patient satisfaction should be strictly based on how care is delivered," said Jeffrey Lackner, PsyD, professor in the Department of Medicine in the Jacobs School of Medicine and Biomedical Sciences at UB and senior author on the study. "But patient satisfaction is a subjective construct that is influenced by factors beyond quality of care." Lackner directs UB's Behavioral Medicine Clinic where he and his colleagues treat patients with a variety of painful disorders, including IBS. He also is a researcher with the Clinical and Translational Science Institute at UB, funded by a National Institutes of Health Clinical and Translational Science Award. In the UB study, 16 percent of participants said they were "very satisfied" with prior care for their digestive problems, while those who rated their experience as either below average or average to good was the same, at 42 percent each. Participants were asked to rate their experience on a scale of 0 to 10 with 0 being the worst health care possible and 10 the best health care possible. Surprisingly, the researchers found that patient satisfaction for these IBS patients was unrelated to either the severity or duration of their IBS symptoms or the impact that IBS had on their lives. Lackner noted that while patient satisfaction has proven difficult to characterize, it has far-reaching implications for many aspects of the doctor-patient relationship including patient loyalty, adherence to treatment, readmission rates and the potential for malpractice. In addition, it is becoming an increasingly important criterion for determining how care will be reimbursed. "Patient satisfaction is a significant metric that impacts reimbursement as health care emphasizes the value of care not the volume of care," Lackner explained. The goals of the study were to assess how patient factors, gastrointestinal symptoms and conditions and other physical and psychological factors impact patient satisfaction among IBS patients. Because IBS is a difficult and complex disorder that is associated with high rates of coexisting illnesses, Lackner said that gastroenterologists may be at a disadvantage in reimbursement schemes that focus on patient satisfaction ratings that can be influenced by nondigestive health factors. "We began this study because we don't really know what drives patient satisfaction for functional gastrointestinal disorders like IBS," he said. In the first part of their study, the UB researchers found that the more diagnostic tests (such as colonoscopies) that patients underwent, the more satisfied they were, but that finding seemed to be driven by whether or not a patient saw a gastroenterologist. "When we introduced into the model whether or not the patient had seen a gastroenterologist, the power of tests to predict patient satisfaction went away," Lackner explained. "This leads us to believe that for this population, the gastroenterologist provides reassurance that the patient doesn't have a life-threatening disease. So the reassurance they get from gastroenterologists is what predicts patient satisfaction, not the number of tests they undergo." Eighty percent of participants were female and the average age was 41. Participants were being evaluated for a large, multicenter National Institutes of Health-funded trial Lackner is leading that will evaluate the efficacy of non-drug treatments for IBS patients. "The bottom line is, there are a lot of factors that influence patient satisfaction and it turns out that many of them are not part of the delivery of care," said Lackner. UB co-authors on the study are Chris Sova; Rebecca Firth; Anne Marie Carosella, PhD; Gregory Gudleski, PhD; Leonard Katz, MD; Susan Krasner, PhD; Brian Quigley, PhD; Michael Sitrin, MD; Chris Radziwon, PhD. Darren Brenner, MD, of Northwestern University, Laurie Keefer, PhD, of Mt. Sinai and Jim Jaccard, PhD, of New York University, were also co-authors. The research was funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the NIH. Founded in 1846, the Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo is beginning a new chapter in its history with the largest medical education building under construction in the nation. The eight-story, 628,000-square-foot facility is scheduled to open in 2017. The new location puts superior medical education, clinical care and pioneering research in close proximity, anchoring Buffalo's evolving comprehensive academic health center in a vibrant downtown setting. These new facilities will better enable the school to advance health and wellness across the life span for the people of New York and the world through research, clinical care and the education of tomorrow's leaders in health care and biomedical sciences. The school's faculty and residents provide care for the community's diverse populations through strong clinical partnerships and the school's practice plan, UBMD Physicians' Group.


News Article | May 9, 2017
Site: www.chromatographytechniques.com

Certain blood vessels in the brainstem constrict when blood vessels elsewhere in the body would dilate. And that contrary behavior is what keeps us breathing, according to a new paper by UConn researchers published May 8 in eLife. If the body were a marching band, the brainstem would be the drum major. It keeps our heart beating and our lungs breathing in the essential rhythms of life. And just like a drum major, the job is more complex than it looks. If cellular waste products build up in the body, the brainstem has to jolt the lungs into action without disrupting other bodily functions, as surely as a drum major reins in a wayward woodwind section without losing the low brass. Neuroscientists studying the brainstem have focused on neurons, which are brain cells that send signals to one another and all over the body. But focusing just on the neurons in the brainstem is like staring only at the drum major's hands. Recently, neuroscientists have come to understand that astrocytes, cells once thought to simply provide structure to the brain, also release signaling molecules that regulate neurons' function. But until now, no one even considered the possibility that blood vessels may be similarly specialized. For more than a century, doctors and scientists have known that blood vessels dilate when cellular waste products like carbon dioxide build up. Widening the vessels allows fresh blood to flush through, carrying in oxygen and washing away the acidic carbon dioxide. This has been shown to be true throughout the body, and is standard dogma in undergraduate physiology classes. UConn physiologist Dan Mulkey was teaching exactly that to undergraduates one day when he realized that it couldn't possibly be true in a certain part of the brainstem. "I thought, wow. If that happened in the region of the brain I study, it would be counterproductive," Mulkey says. He studies the retrotrapezoid nucleus (RTN), a small region in the brainstem that controls breathing. He's shown in the past that RTN neurons respond to rising levels of carbon dioxide in the bloodstream by stimulating the lungs to breathe. But if the blood vessels in the RTN dilated in response to rising carbon dioxide the same way blood vessels do everywhere else, it would wash out that all-important signal, preventing cells in the RTN from doing their job driving us to breathe. It would be as if the drum major didn't notice the percussion section wandering off to left field. When Mulkey returned to the lab, he asked his team, including NIH postdoctoral fellow Virginia Hawkins, to see how blood vessels in thin slices of brainstem respond to carbon dioxide. And they saw it was indeed true - RTN blood vessels constricted when carbon dioxide levels rose. But blood vessels from slices of cortex (the wrinkled top part of the brain) dilated in response to high carbon dioxide, just like the rest of the body. But how did the blood vessels know to act differently in the RTN? Mulkey guessed that RTN astrocytes had something to do with it. He suspected that the astrocytes were releasing adenosine triphosphate (ATP), a small molecule cells can use to signal one another. And that was causing the RTN blood vessels to constrict. When they tested it, they found the hypothesis was correct. The astrocytes in the RTN were behaving differently than astrocytes anywhere else in the body. When these brainstem astrocytes detected high levels of carbon dioxide, they released ATP signaling to the neurons and blood vessels. When the researchers induced the astrocytes artificially to release ATP, they got the same results. Bathing the RTN blood vessels directly in ATP also caused them to constrict. Blocking ATP receptors blocked the ability of blood vessels to respond to carbon dioxide. When the team did the same experiments in live animals, they got the same results. Perhaps most importantly, manipulating blood vessels in the RTN actually influenced how animals breathe, thus linking regulation of blood vessel diameter to behavior. The majority of this research was done by UConn undergraduates, including Ashley Trinh, Colin Cleary, and Todd Dubreuil, as well as Elliot Rodriguez, a summer student in the National Science Foundation (NSF) Research Experience for Undergraduates in Physiology and Neurobiology program at UConn, who studies at Gettysburg College in Pennsylvania the rest of the year. The students' work uncovered a major discovery in neurophysiology. The work was funded in part by grants from the National Institutes of Health (HL104101 HL126381) and the Connecticut Department of Public Health (150263). "This is a big change in how we think about breathing," Mulkey says. And about blood vessels. Even in a single organ like the brain, the purpose of blood flow is not the same everywhere. Tailored responses in the RTN keep the body's drum major conducting, and let the band play on.


News Article | May 11, 2017
Site: www.eurekalert.org

LA JOLLA, CA - May 11, 2017 - In their quest to replicate themselves, viruses have gotten awfully good at tricking human cells into pumping out viral proteins. That's why scientists have been working to use viruses as forces for good: to deliver useful genes to human cells and help patients who lack important proteins or enzymes. A team of researchers led by Associate Professor Vijay Reddy at The Scripps Research Institute (TSRI) has now uncovered the structural details that make one virus a better tool for future therapies than its closely related "cousin." As Reddy and his colleagues reported this week in the journal Science Advances, the structure of a less prevalent species D adenovirus may work well as a gene-delivery vector because its structure doesn't let it get spirited away to the liver, minimizing liver toxicity. The Reddy Lab's study is the first to show the structural details on species D's surface that set it apart from another common subtype of adenovirus, called species C, which does travel to the liver. "Greater understanding of the structures of adenoviruses from different species will help generate better gene therapies and/or vaccine vectors," said Reddy. Using an imaging technique called cryo-electron microscopy, the researchers discovered that while these two species of adenoviruses share the same shell-like core, they have different surface structures, which Reddy called "decorations" or "loops." These loops are key to a virus's behavior. They determine which receptors on human cells the virus can bind to. For species C adenoviruses, specific loops help the virus attach to blood coagulation factors (adaptor proteins) and get targeted to the human liver. Species D adenoviruses display distinctly different loop decorations. For use in gene and vaccine therapies, the virus would deliver helpful genes instead. Plus, species D has one more important advantage over species C: Humans are constantly exposed to species C adenoviruses, so most people have developed antibodies to fight them off. These same antibodies would fight off the species C viruses even if they were designed for beneficial therapies. On the flip side, many of the species D adenoviruses are rare, and it's unlikely that a patient would have antibodies to fight them off. That makes species D viruses better for delivering therapies. In fact, Reddy said scientists are already testing ways to use it to generate malaria and Ebola virus vaccines. The researchers next plan to look at members of the other five species of adenoviruses to see if they would have useful traits as viral therapy vectors. In addition to Reddy, the first authors of the study, "Cryo-EM structure of human adenovirus D26 reveals the conservation of structural organization among human adenoviruses," were Xiaodi Yu and David Veesler, formerly at TSRI, now at Pfizer Worldwide R&D, and the University of Washington, Seattle, respectively. Additional authors were Melody Campbell, formerly at TSRI, now at the University of California, San Francisco; Mary E. Barry and Michael A. Barry of the Mayo Clinic; and Francisco Asturias of TSRI. Reddy also thanked Bridget Carragher and Clint Potter, directors of the National Resource for Automated Molecular Microscopy (NRAMM) facility for their support and collaboration. The study was supported by the National Institutes of Health (grants R01AI070771, R21AI103692 and GM103310). The Scripps Research Institute (TSRI) is one of the world's largest independent, not-for-profit organizations focusing on research in the biomedical sciences. TSRI is internationally recognized for its contributions to science and health, including its role in laying the foundation for new treatments for cancer, rheumatoid arthritis, hemophilia, and other diseases. An institution that evolved from the Scripps Metabolic Clinic founded by philanthropist Ellen Browning Scripps in 1924, the institute now employs more than 2,500 people on its campuses in La Jolla, CA, and Jupiter, FL, where its renowned scientists--including two Nobel laureates and 20 members of the National Academies of Science, Engineering or Medicine--work toward their next discoveries. The institute's graduate program, which awards PhD degrees in biology and chemistry, ranks among the top ten of its kind in the nation. In October 2016, TSRI announced a strategic affiliation with the California Institute for Biomedical Research (Calibr), representing a renewed commitment to the discovery and development of new medicines to address unmet medical needs. For more information, see http://www. .


LAWRENCEVILLE, N.J., May 12, 2017 (GLOBE NEWSWIRE) -- Celsion Corporation (NASDAQ:CLSN), an oncology drug development company, today announced financial results for the quarter ended March 31, 2017 and provided an update on its development programs for ThermoDox®, its proprietary heat-activated liposomal encapsulation of doxorubicin and GEN-1, an IL-12 DNA plasmid vector encased in a nanoparticle delivery system, which enables cell transfection followed by persistent, local secretion of the IL-12 protein.  The Company's lead program is ThermoDox® which is currently in Phase III development for the treatment of primary liver cancer and in Phase II development for the treatment of recurrent chest wall breast cancer.  The Company's immunotherapy program consists of GEN-1 and is currently in Phase I development for the localized treatment of ovarian cancer. "Celsion continues to make major progress with respect to our ongoing global, pivotal Phase III OPTIMA Study in primary liver cancer.  This ground-breaking study continues to attract interest and support from the medical community, international regulatory agencies, and research organizations like the National Institutes of Health," said Michael H. Tardugno, Celsion's chairman, president and CEO.  "Our product development efforts in immuno-oncology are equally important. We have demonstrated the potential of our GEN-1 IL-12 immunotherapy program to be an effective adjuvant, in both first and second-line ovarian cancer. Recruiting the immune system to work in combination with the standard of care in this patient population has been the goal of medical researchers worldwide.  With GEN-1, we believe there is the potential for a break-through and we look forward to reporting comprehensive clinical results and translational research data from our Phase 1B OVATION Study at the ASCO Annual Meeting in June 2017." Announced the Publication of Preclinical Results of ThermoDox® for the Treatment of Bladder Cancer in the International Journal of Hyperthermia.  The Company reported results from porcine in vivo studies to evaluate ThermoDox® in combination with loco-regional mild hyperthermia for targeted drug delivery to the bladder wall as a potential treatment for bladder cancer.  Doxorubicin accumulation and distribution within the bladder wall with ThermoDox® plus mild bladder hyperthermia was achieved at concentrations nearly ten times higher than with free intravenous doxorubicin combined with mild bladder hyperthermia. The study was conducted under a Cooperative Research and Development Agreement (CRADA) with the National Institutes of Health (NIH) to evaluate whether ThermoDox® combined with mild heating of the bladder can target drug delivery in the bladder. Announced Support for the OPTIMA Study from the China FDA and Vietnam Ministry of Health.  The Company discussed ThermoDox® and the OPTIMA Study with regulatory agencies in two key markets, China and Vietnam.  The Company met with the China Food and Drug Administration (CFDA) to review the ongoing Phase III OPTIMA Study and regulatory pathway for ThermoDox® in China. CFDA was presented with the final overall survival data from the Chinese patient cohort of the HEAT study, which demonstrated a survival benefit in patients treated with ThermoDox® plus optimized RFA versus optimized RFA alone. The CFDA informed the Company that if the ongoing Phase III OPTIMA Study is successful, the trial could serve as the basis for a direct regulatory filing in China without the need to file for prior approval in the U.S. or European Union which is currently required for foreign company application. This would allow the Company to accelerate its plans for a regulatory filing in China and, if approved, provide for a significantly earlier launch date in China than originally expected. The Company's management team also met with the Ministry of Health in Vietnam and based on that meeting, it will move forward with launching additional trial sites for the OPTIMA Study in that country. The Company plans to activate 5 additional clinical trial sites in Vietnam by the second quarter of 2017. Vietnam represents a significant market for ThermoDox® where HCC incidence rates are among the highest in the world. Announced the Issuance of Two New Patents for ThermoDox.  In January 2017, the Company announced the issuance of two patents which are directly applicable to the method of treating cancer using our current ThermoDox® formulation.  These new patents further strengthen the Company’s global patent portfolio around novel heat-sensitive liposome engineered to address a broad range of difficult-to-treat cancers. Announced Continuing Positive Data from the OVATION Study in Newly Diagnosed Advanced Ovarian Cancer Patients.  In January 2017, the Company announced data from the first four cohorts of patients in its Phase Ib dose escalating clinical trial (the OVATION Study) combining GEN-1 with the standard of care for the treatment of newly-diagnosed patients with advanced ovarian cancer who will undergo neoadjuvant chemotherapy followed by interval debulking surgery.  In the first twelve patients dosed in the OVATION Study, GEN-1 plus standard chemotherapy produced impressive results, with no dose limiting toxicities and highly promising efficacy signals in this difficult to treat cancer. The efficacy data included highly encouraging tumor response rates - 100% disease control rate (DCR) and 75% objective response rate (ORR), successful surgical resections of the eligible patients’ tumors, impressive pathological responses and dramatic, clinically meaningful drops in CA-125 protein levels.  In February 2017, the Company presented two posters at the American Society of Clinical Oncology (ASCO) - Society for Immunotherapy of Cancer (SITC) Clinical Immuno-Oncology Symposium held from February 23 - 25, 2017 in Orlando, FL.  The ASCO-SITC Clinical Immuno-Oncology Symposium focused on the latest clinical and translational research in immuno-oncology and the implications for clinical care. Raised $6.8 Million Through Two Equity Offerings in December 2016 and February 2017.  The Company completed two equity offerings of shares of common stock, or pre-funded warrants in lieu thereof, to purchase common stock with institutional healthcare and retail investors totaling $6.8 million in gross proceeds. For the quarter ended March 31, 2017, Celsion reported a net loss of $5.2 million, or $0.12 per share, compared to a net loss of $5.7 million, or $0.24 per share, in the same period of 2016. Operating expenses were $4.9 million in the first quarter of 2017 compared to $5.3 million in the same period of 2016.  This decrease was primarily due to lower general and administrative expenses. Research and development (R&D) costs were relatively constant at $3.5 million and $3.4 million in the first quarters of 2017 and 2016, respectively.  Clinical development costs for the Phase III OPTIMA Study were $1.6 million in the first quarter of 2017 compared to $1.0 million in the same period of 2016 due to higher patient enrollment and investigator grant expenses in the trial.  R&D costs for other development programs were lower as a result of the Company’s tighter clinical development focus around the pivotal Phase III OPTIMA Study for the treatment of primary liver cancer and the clinical development program for GEN-1 IL-12 immunotherapy for the localized treatment of ovarian cancer coupled with lower costs in the first quarter of 2017 associated with the production of ThermoDox® clinical supplies to support the OPTIMA Study.  General and administrative expenses decreased $0.4 million, from $1.9 million in the first quarter of 2016 to $1.5 million in the first quarter of 2017.  This 21% decrease in general and administrative expenses in 2017 is primarily the result of reduction in personnel costs and lower professional fees. Net cash used in operations was $3.1 million in the first quarter of 2017 compared to $4.7 million in the same period of 2016.  The Company ended the first quarter of 2017 with $4.5 million of total cash and cash equivalents.  In February 2017, the Company raised $5 million in gross proceeds under a secondary public offering with various institutional and retail investors. The Company is hosting a conference call to provide a business update and discuss year-end 2016 financial results at 11:00 a.m. ET on Friday, May 12, 2017. To participate in the call, interested parties may dial 1-888-282-4591 (Toll-Free/North America) or 1–719-457-2605 (International/Toll) and ask for the Celsion Corporation First Quarter 2017 Earnings Call (Conference Code: 4060768) to register ten minutes before the call is scheduled to begin. The call will also be broadcast live on the internet at www.celsion.com. The call will be archived for replay on Friday, May 12, 2017 and will remain available until May 26, 2017.  The replay can be accessed at 1-888-203-1112 (Toll-Free/North America) or 1-719-457-0820 (International/Toll) using Conference ID: 4060768.  An audio replay of the call will also be available on the Company's website, www.celsion.com, for 90 days after 2:00 p.m. ET Friday, May 12, 2017. Celsion is a fully-integrated oncology company focused on developing a portfolio of innovative cancer treatments, including directed chemotherapies, immunotherapies and RNA- or DNA-based therapies. The Company's lead program is ThermoDox®, a proprietary heat-activated liposomal encapsulation of doxorubicin, currently in Phase III development for the treatment of primary liver cancer and in Phase II development for the treatment of recurrent chest wall breast cancer.  The pipeline also includes GEN-1, a DNA-based immunotherapy for the localized treatment of ovarian and brain cancers.  Celsion has two platform technologies for the development of novel nucleic acid-based immunotherapies and other anti-cancer DNA or RNA therapies.  For more information on Celsion, visit our website: http://www.celsion.com (CLSN-FIN). Celsion wishes to inform readers that forward-looking statements in this release are made pursuant to the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995.  Readers are cautioned that such forward-looking statements involve risks and uncertainties including, without limitation, unforeseen changes in the course of research and development activities and in clinical trials; the uncertainties of and difficulties in analyzing interim clinical data, particularly in small subgroups that are not statistically significant; FDA and regulatory uncertainties and risks; the significant expense, time, and risk of failure of conducting clinical trials; the need for Celsion to evaluate its future development plans; possible acquisitions or licenses of other technologies, assets or businesses; possible actions by customers, suppliers, competitors, regulatory authorities; and other risks detailed from time to time in the Celsion's periodic reports and prospectuses filed with the Securities and Exchange Commission.  Celsion assumes no obligation to update or supplement forward-looking statements that become untrue because of subsequent events, new information or otherwise.


News Article | May 9, 2017
Site: www.chromatographytechniques.com

Chronic sleep loss increases pain sensitivity, according to a new mouse study from Harvard Medical School researchers at Boston Children’s Hospital and Beth Israel Deaconess Medical Center. The study suggests that chronic pain sufferers can get relief by getting more sleep, or, short of that, by taking medications to promote wakefulness, such as caffeine. Both approaches performed better than standard painkillers in a rigorous study in mice, described in Nature Medicine on May 8. Pain physiologist Alban Latremoliere, HMS research fellow in neurology at Boston Children’s, and sleep physiologist Chloe Alexandre, HMS instructor in neurology at Beth Israel Deaconess, who were co-first authors of the study, precisely measured the effects of acute or chronic sleep loss on sleepiness and sensitivity to both painful and nonpainful stimuli. They then tested standard pain medications such as ibuprofen and morphine, as well as wakefulness-promoting agents like caffeine and modafinil. Their findings reveal an unexpected role for alertness in setting pain sensitivity. The research was supported by a National Institutes of Health program that required a pain scientist to join a nonpain scientist to tackle a completely new area of research, said Thomas Scammell, HMS professor of neurology at Beth Israel Deaconess and co-senior author of the study. “This cross-disciplinary collaboration enabled our labs to discover unsuspected links between sleep and pain, with actionable clinical implications for improving pain management,” Scammell said. The team started by measuring normal sleep cycles, using tiny headsets that took electroencephalography (EEG) and electromyography (EMG) readings. “For each mouse, we have exact baseline data on how much they sleep and what their sensory sensitivity is,” said Latremoliere, who works in the lab of Clifford Woolf, professor of neurology at HMS and Boston Children’s and co-senior author of the study. Next, unlike other sleep studies that force mice to stay awake by walking treadmills or falling from platforms, Alexandre, Latremoliere and colleagues deprived mice of sleep in a way that mimics what happens with people: They entertained them. “We developed a protocol to chronically sleep-deprive mice in a nonstressful manner by providing them with toys and activities at the time they were supposed to go to sleep, thereby extending the wake period,” said Alexandre, who works in the Scammell lab. “This is similar to what most of us do when we stay awake a little bit too much watching late-night TV each weekday,” Alexandre said. To keep the mice awake, researchers kept vigil too, providing the mice with custom-made toys as interest flagged, while being careful not to overstimulate them. “Mice love nesting, so when they started to get sleepy, as seen by their EEG/EMG pattern, we would give them nesting materials like a wipe or cotton ball,” said Latremoliere. “Rodents also like chewing, so we introduced a lot of activities based around chewing; for example, having to chew through something to get to a cotton ball.” In this way, they kept groups of six to 12 mice awake for as long as 12 hours in one session, or six hours for five consecutive days, monitoring sleepiness and stress hormones (to make sure they weren’t stressed) and testing for pain along the way. Pain sensitivity was measured in a blinded fashion by exposing mice to controlled amounts of heat, cold, pressure or capsaicin—the agent in hot chili peppers—and then measuring how long it took the animal to move away or lick away the discomfort caused by capsaicin. The researchers also tested responses to nonpainful stimuli, such as jumping when startled by a sudden loud sound. “We found that five consecutive days of moderate sleep deprivation can significantly exacerbate pain sensitivity over time in otherwise healthy mice,” said Alexandre. “The response was specific to pain, and was not due to a state of general hyperexcitability to any stimuli.” Common painkillers such as ibuprofen did not block the pain hypersensitivity induced by sleep loss. Even morphine lost most of its efficacy in sleep-deprived mice. If similar results are observed in people, it would suggest that patients using these drugs for pain relief have to increase their dose to compensate for sleep loss, thereby increasing their risk for side effects. In contrast, caffeine and modafinil, drugs used to promote wakefulness, successfully blocked the pain hypersensitivity caused by both acute and chronic sleep loss. In non sleep-deprived mice, caffeine and modafinil had no painkilling properties. “This represents a new kind of analgesic that hadn’t been considered before, one that depends on the biological state of the animal,” said Woolf, director of the F.M. Kirby Neurobiology Center at Boston Children’s. “Such drugs could help disrupt the chronic pain cycle, in which pain disrupts sleep, which then promotes pain, which further disrupts sleep.” Based on their findings in mice, the researchers hypothesize that rather than just taking painkillers, patients with chronic pain might benefit from better sleep habits or taking sleep-promoting medications at night, coupled with daytime alertness-promoting agents to try to break the pain cycle. Some painkillers already include caffeine as an ingredient, although its mechanism of action isn’t yet known. Both caffeine and modafinil boost dopamine circuits in the brain, which may provide a clue. “Many patients with chronic pain suffer from poor sleep and daytime fatigue, and some pain medications themselves can contribute to these co-morbidities,” said Kiran Maski, a specialist in sleep disorders at Boston Children’s. “This study suggests a novel approach to pain management that would be relatively easy to implement in clinical care.” “Clinical research is needed to understand what sleep duration is required and to test the efficacy of wake-promoting medications in chronic pain patients,” Maski added.


News Article | May 9, 2017
Site: www.biosciencetechnology.com

Chronic sleep loss increases pain sensitivity, according to a new mouse study from Harvard Medical School researchers at Boston Children’s Hospital and Beth Israel Deaconess Medical Center. The study suggests that chronic pain sufferers can get relief by getting more sleep, or, short of that, by taking medications to promote wakefulness, such as caffeine. Both approaches performed better than standard painkillers in a rigorous study in mice, described in Nature Medicine on May 8. Pain physiologist Alban Latremoliere, HMS research fellow in neurology at Boston Children’s, and sleep physiologist Chloe Alexandre, HMS instructor in neurology at Beth Israel Deaconess, who were co-first authors of the study, precisely measured the effects of acute or chronic sleep loss on sleepiness and sensitivity to both painful and nonpainful stimuli. They then tested standard pain medications such as ibuprofen and morphine, as well as wakefulness-promoting agents like caffeine and modafinil. Their findings reveal an unexpected role for alertness in setting pain sensitivity. The research was supported by a National Institutes of Health program that required a pain scientist to join a nonpain scientist to tackle a completely new area of research, said Thomas Scammell, HMS professor of neurology at Beth Israel Deaconess and co-senior author of the study. “This cross-disciplinary collaboration enabled our labs to discover unsuspected links between sleep and pain, with actionable clinical implications for improving pain management,” Scammell said. The team started by measuring normal sleep cycles, using tiny headsets that took electroencephalography (EEG) and electromyography (EMG) readings. “For each mouse, we have exact baseline data on how much they sleep and what their sensory sensitivity is,” said Latremoliere, who works in the lab of Clifford Woolf, professor of neurology at HMS and Boston Children’s and co-senior author of the study. Next, unlike other sleep studies that force mice to stay awake by walking treadmills or falling from platforms, Alexandre, Latremoliere and colleagues deprived mice of sleep in a way that mimics what happens with people: They entertained them. “We developed a protocol to chronically sleep-deprive mice in a nonstressful manner by providing them with toys and activities at the time they were supposed to go to sleep, thereby extending the wake period,” said Alexandre, who works in the Scammell lab. “This is similar to what most of us do when we stay awake a little bit too much watching late-night TV each weekday,” Alexandre said. To keep the mice awake, researchers kept vigil too, providing the mice with custom-made toys as interest flagged, while being careful not to overstimulate them. “Mice love nesting, so when they started to get sleepy, as seen by their EEG/EMG pattern, we would give them nesting materials like a wipe or cotton ball,” said Latremoliere. “Rodents also like chewing, so we introduced a lot of activities based around chewing; for example, having to chew through something to get to a cotton ball.” In this way, they kept groups of six to 12 mice awake for as long as 12 hours in one session, or six hours for five consecutive days, monitoring sleepiness and stress hormones (to make sure they weren’t stressed) and testing for pain along the way. Pain sensitivity was measured in a blinded fashion by exposing mice to controlled amounts of heat, cold, pressure or capsaicin—the agent in hot chili peppers—and then measuring how long it took the animal to move away or lick away the discomfort caused by capsaicin. The researchers also tested responses to nonpainful stimuli, such as jumping when startled by a sudden loud sound. “We found that five consecutive days of moderate sleep deprivation can significantly exacerbate pain sensitivity over time in otherwise healthy mice,” said Alexandre. “The response was specific to pain, and was not due to a state of general hyperexcitability to any stimuli.” Common painkillers such as ibuprofen did not block the pain hypersensitivity induced by sleep loss. Even morphine lost most of its efficacy in sleep-deprived mice. If similar results are observed in people, it would suggest that patients using these drugs for pain relief have to increase their dose to compensate for sleep loss, thereby increasing their risk for side effects. In contrast, caffeine and modafinil, drugs used to promote wakefulness, successfully blocked the pain hypersensitivity caused by both acute and chronic sleep loss. In non sleep-deprived mice, caffeine and modafinil had no painkilling properties. “This represents a new kind of analgesic that hadn’t been considered before, one that depends on the biological state of the animal,” said Woolf, director of the F.M. Kirby Neurobiology Center at Boston Children’s. “Such drugs could help disrupt the chronic pain cycle, in which pain disrupts sleep, which then promotes pain, which further disrupts sleep.” Based on their findings in mice, the researchers hypothesize that rather than just taking painkillers, patients with chronic pain might benefit from better sleep habits or taking sleep-promoting medications at night, coupled with daytime alertness-promoting agents to try to break the pain cycle. Some painkillers already include caffeine as an ingredient, although its mechanism of action isn’t yet known. Both caffeine and modafinil boost dopamine circuits in the brain, which may provide a clue. “Many patients with chronic pain suffer from poor sleep and daytime fatigue, and some pain medications themselves can contribute to these co-morbidities,” said Kiran Maski, a specialist in sleep disorders at Boston Children’s. “This study suggests a novel approach to pain management that would be relatively easy to implement in clinical care.” “Clinical research is needed to understand what sleep duration is required and to test the efficacy of wake-promoting medications in chronic pain patients,” Maski added.

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