Newswise — Women need to maintain good health years before they become pregnant. After all, healthy women are most likely to give birth to healthy babies. A web-based app, www.healthymomshra.com, can now help women gauge the level of their health and learn what changes they can make to enhance not only their own wellbeing, but also the health of any babies born to them in the future. “Our goal with the app is to encourage good health practices in women so they will be healthy for pregnancies, planned or unplanned,” said Adam T. Perzynski, PhD (Twitter: @ATPerzynski), director of the Patient Centered Medical Lab, and a sociologist with the Case Western Reserve University School of Medicine and MetroHealth Center for Health Care Research and Policy team, that developed the Healthy Moms Health Risk Assessment prototype at www.healthymomshra.com. Much infant mortality can be traced to low birth weight or early gestational birth age of newborns, which is often related to the poor health of the mother. The developers of the web-based app sought to help women reverse the major risk factors that negatively affect them in the categories of health habits, social support, driving safety, substance use, tobacco use, mental health, physical health, environmental risks, ethnicity, age and neighborhood of residence. The online Healthy Moms Health Risk Assessment features a user-friendly test where each question, regardless of a yes or no answer, is greeted with encouraging, helpful tips across the categories of health risks. All answers are based on Centers for Disease Control and Prevention (CDC) guidelines firmly grounded in scientific evidence. The test concludes with a report of the woman’s individual health risk in the categories. The report is color coded from green to red, so the more green the report, the better the test-taker’s health. “The main difference with this app is that it focuses on the preconception phase rather than exclusively on pregnant women,” Perzynski said. “Up to 50 percent of pregnancies are unplanned, so it’s important that a woman engage in healthy behaviors to prepare for the fact that she might become pregnant at some point.” Armed with latest wellness information from CDC for women, the Case Western Reserve team used flexible and scalable cloud-based computing environment to develop an app that would provide immediate, useful answers and offer a summary scorecard. The Healthy Moms Health Risk Assessment app was so impressive that it won an honorable mention at the recent Cleveland Medical Hackathon competition where the Case Western Reserve team vied with other teams to develop the best innovation to address an unmet health care need. “In many cases, mothers have health issues before they become pregnant, and those health issues can be challenging to resolve once they are pregnant,” Perzynski said. “We tailored our app to help women consider how health behaviors, activities and social circumstances might affect the health of a baby should a pregnancy happen, with the goal of empowering women to make healthy choices.”
Newswise — A new study in mice by researchers at Fred Hutchinson Cancer Research Center has found that a specialized type of immunotherapy — even when used without chemotherapy or radiation — can boost survival from pancreatic cancer, a nearly almost-lethal disease, by more than 75 percent. The findings are so promising, human clinical trials are planned within the next year. The study, led by Drs. Sunil Hingorani and Phil Greenberg, both members of the Clinical Research Division at Fred Hutch, tested the immunotherapy on mice genetically engineered to grow pancreatic tumors very similar to those of human pancreatic cancer. The mouse model, developed by Hingorani, already has led to a first-in-humans clinical trial that is showing early promise in some patients with advanced pancreatic cancer. Pancreatic cancer is notoriously difficult to treat, said Hingorani, because it recruits the body’s natural systems to construct both a tough physical barrier around tumors as well as an immune-cloaking device that keeps other, disease-fighting immune cells from recognizing the cancer. Unlike any other cancer, pancreatic tumors are able to survive with a significantly decreased blood supply. As a consequence, chemotherapy, commonly administered via the bloodstream, has a difficult time getting inside. The tumors not only commonly grow quite large before patients will ever notice something is wrong, but they are very prone to metastasize, or spread to other sites in the body. The investigators’ new study, published Thursday in Cancer Cell, breaches pancreatic cancer’s physical and immunological walls by using immunotherapy, a type of treatment that harnesses or refines the body’s own immune system, to recognize and destroy cancer cells. The researchers devised a therapy using T cells, disease-fighting immune cells, that they engineered in the lab to recognize and attack pancreatic cancer. T-cell therapy is showing promise as a treatment for several types of blood cancers, based on early results from Fred Hutch and other research centers, but aiming these cells at solid tumors like pancreatic cancer has historically proven more difficult, Hingorani said. Part of the challenge comes from the access to tumor cells — or lack thereof. T-cell therapy is administered through the bloodstream, like chemo. It’s easy enough to see why solid tumors may present more of a challenge to treat with this kind of immunotherapy than blood cancers such as leukemia and lymphoma. The researchers didn’t think the engineered T cells would stand a chance against pancreatic cancer on their own. But they needed somewhere to start, Greenberg said. But to their surprise, the T cells — engineered to recognize and kill cells bearing a protein called mesothelin, which is overproduced by virtually all pancreatic tumors — got into the mice’s tumors and started attacking them. In the mouse model of the disease — which is actually slightly more aggressive than the human version, Hingorani said — animals that received T cells engineered to recognize a non-cancerous protein survived on average 54 days after their cancer became detectable. Those that received the mesothelin-directed cells lived an average of 96 days, a 78 percent bump. Although the researchers weren’t expecting to take this first version of the T-cell therapy to clinic, that’s now their plan. Their team has already built the human version of the special T-cell protein that recognizes mesothelin. They’re planning to launch a phase 1 clinical trial to test the therapy’s safety in patients with advanced pancreatic cancer within the next year. “As best we can tell, this would be a better therapy than anything that exists for pancreatic cancer right now,” Greenberg said. “It’s hard to be this optimistic without ever having treated a pancreatic cancer patient with this [therapy], but the biology of what we’re doing looks so remarkably true and good.” The study was funded in part by the National Institutes of Health, the Giles W. and Elise G. Mead Foundation and Juno Therapeutics.
Newswise — A federally funded analysis of MRI scans of the aging hearts of nearly 3,000 adults shows significant differences in the way male and female hearts change over time. Results of the research, led by investigators at Johns Hopkins, do not explain exactly what causes the sex-based differences but they may shed light on different forms of heart failure seen in men and women that may require the development of gender-specific treatments, the scientists say. “Our results are a striking demonstration of the concept that heart disease may have different pathophysiology in men and women and of the need for tailored treatments that address such important biologic differences,” says senior study author João Lima, M.D., M.B.A., a professor of medicine and radiological science at the Johns Hopkins University School of Medicine and director of cardiovascular imaging at its Heart and Vascular Institute. The research, published online Oct. 20 in the journal Radiology, is believed to be the first long-term follow-up using MRI showing how hearts change as they age. Previous studies have assessed heart changes over time using ultrasound, but, the researchers say, MRI scans tend to provide more detailed images — and more reliable information — about the structure and function of the heart muscle. In both sexes, the main heart chamber, the left ventricle — which fills with and then forces out blood — gets smaller with time. As a result, less blood enters the heart and less gets pumped out to the rest of the body. But in men, the study reveals, the heart muscle that encircles the chamber grows bigger and thicker with age, while in women, it get retains its size or gets somewhat smaller. “Thicker heart muscle and smaller heart chamber volume both portend heightened risk of age-related heart failure but the gender variations we observed mean men and women may develop the disease for different reasons,” says lead investigator John Eng, M.D., associate professor of radiological science at the Johns Hopkins University School of Medicine. A condition that affects more than five million Americans, heart failure is marked by the gradual “floppiness” and weakening of the heart muscle and eventual loss of pumping ability. To lower the risk, cardiologists often prescribe medications designed to reduce the thickness of the heart muscle over time and boost cardiovascular performance. But the finding that in women, the heart muscle tends to shrink or remain the same size means they may not derive the same benefit from such treatments, researchers say. The research team cautions that its study was not designed to find what exactly fuels the differences in cardiac physiology between the sexes but says this “fascinating discrepancy” demands further investigation to figure it out. For the study, researchers analyzed MRI scans performed on nearly 3,000 older adults, ages 54 to 94, without preexisting heart disease. Participants were followed between 2002 and 2012, at six hospitals across the United States where each one of them underwent MRI testing at the beginning of the study and once more after a decade. The MRI scans provided researchers with 3-D images of the heart’s interior and exterior, allowing them to determine the size and volume of the heart muscle. Adding these to the already known density of the muscle, they were able to calculate its weight. Over a period of 10 years, the weight of the heart’s main pumping chamber — the left ventricle — increased by an average of 8 grams in men and decreased by 1.6 grams in women. The heart’s filling capacity — marked by the amount of blood the left ventricle can holds between heartbeats — declined in both sexes but more precipitously so in women, by about 13 milliliters, compared with just under 10 milliliters in men. The differences in size, volume and pumping ability occurred independently of other risk factors known to affect heart muscle size and performance, including body weight, blood pressure, cholesterol levels, exercise levels and smoking. The study is part of an ongoing, long-term project called the Multi-Ethnic Study of Atherosclerosis (MESA), which is following nearly 7,000 men and women of different ethnic backgrounds across the country. The study was designed to enroll adults with no symptoms of heart disease to determine who develops heart disease or heart failure, what factors precipitate the disease and who is more likely to die from it. Other institutions involved in the study include the University of Washington; the University of California, Los Angeles; Wake Forest Baptist Medical Center; Brigham and Women’s Hospital; the National Heart, Lung, and Blood Institute; Vanderbilt University; and Columbia University. The research was funded by the National Heart, Lung, and Blood Institute under grants N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168 and N01-HC-95169, and by the National Center for Research Resources under grants UL1-TR-000040 and UL1-RR-025005. Fast facts: --Men’s and women’s hearts don’t grow old the same way. --Aging hearts: Gender matters. --Gender differences in heart aging may underlie sex differences observed in heart failure. --Research points to need for gender-tailored treatments for age-related heart failure.
Newswise — ST. LOUIS -- Note to Mimi, Didi, Gigi, G-Ma and the rest of the gang who have swapped out your own pet names for Grandma: Being a grandparent is good for your health. So says Angela Sanford, M.D., assistant professor of geriatrics at Saint Louis University. “You can’t be unhappy around little kids. They’re mood lifters,” says the SLUCare geriatrician and mother of three children, ages 1, 2 and 3. “Little ones typically adore and look up to their grandparents, which is great for your sense of self-worth and self-esteem. By spending time with them, you know you’re helping them to become better people, which in turn helps you feel like you’re making a huge contribution to the world.” As boomers become grandparents, they’re redefining the role the same way they’ve redefined their roles since they were young. They’re embracing their change in family status with the type of enthusiasm they demonstrate when the next generation of the iPhone comes out, except amplified exponentially to the levels of a Led Zeppelin concert. And the good news is beyond the feel-good Hallmark moments that abound in simply being a grandparent, specific activities most grandparents enjoy with their grandchildren are actually good for them. Physical play: When you are active with your grandchild – playing tag, pushing a swing, walking around the zoo or wrestling on the living room floor – you are exercising, which is a key contributor to good health, Sanford says. “Exercise reduces your risk of falling, which is a really big deal. About 20 percent of the time falls cause serious injuries like broken bones that can undermine your ability to function independently,” she says. “You also tend not to focus on your aches and pains if you are active. But beyond the physical strength, agility and balance that you gain by being active, exercise improves your mood and is important for brain health. It gets the blood pumping to your brain and can prevent or slow the progression of dementia.” Cooking: Generally you eat healthier when you cook because you may be more likely to prepare whole foods (those located around the perimeter of a supermarket) instead of turning to quick, ready-to-eat processed foods. Measuring ingredients, stirring, chopping and pouring strengthen a variety of fine motor skills, which helps with arthritis or tremors, Sanford says. Sharing your own grandmother’s recipes with your grandchildren passes along a family legacy, and frequently the stories and family lore that go with it. This reminiscence strengthens cognition and is good for memory. But perhaps the most important part of cooking is what follows –- eating, Sanford says, because malnutrition in older adults is a huge problem. “A lot of older people simply don’t eat because they don’t have anyone to eat with,” Sanford says. “Enjoying a meal is a social activity, and sharing food and conversation makes eating a pleasant experience that we anticipate rather than something we have to do simply to survive.” Playing games and putting together puzzles: Games – cards, chess, matching, “I Spy,” trivia and video games – not only are fun, they’re also good for your memory, may stimulate visual-spatial skills and make you think in other ways – all great exercises for brain health. “Depending on what is involved with the game or if you add conversation to the mix, you improve your ability to multi-task, which can decline with aging,” Sanford says. Being generally busy: Let’s face it, kids get bored easily, so most grandparents mix it up when they’re spending time with a grandchild. They might read a book, listen to music, prepare a snack together, go on a walk, build a fort, play tag, watch a TV show and put together a puzzle. Tiring? Maybe, but it beats the alternative. “Activity triggers a whole cycle of well-being,” Sanford says. “It helps you eat, sleep and even digest food better -– which are problems many older adults have. And when you’re busy, you’re not sitting in a chair, thinking about the arthritis in your knees. You’re up and moving and sometimes you forget about the pain. Your whole body feels like it is working better.” Taking a nap: OK, you’ve got legitimate permission not to feel lazy when you join the young and restless by catching a few Z’s at naptime. “A short power nap of about 20 minutes can make you feel more alert and give you the extra energy to enjoy your day,” Sanford says. “Many executives close their doors for a little snooze to regenerate. The key is to not let yourself sleep for so long that you are too rested to go to bed at night.” Staying flexible: You had planned to go to the library, but your granddaughter would rather dig for worms in the backyard. You had all of the ingredients to bake chocolate chip cookies, but your grandsonhad his heart set on walking to the ice cream store instead. Sometimes you scuttle your plans, shift gears and move onto something else, which prepares you to be more flexible and resilient. That practice can serve you well whether you are dealing with a significant change, such as the loss of a loved one, or something much smaller, like your favorite waitress not working when you show up at a restaurant for dinner. “With kids, you have to go with the flow and be adaptable. It’s never about you and is always about them,” Sanford says. “But it’s great to have that variety of experiences, and being flexible is good for you. It helps you handle life’s highs and lows much better, so when things go wrong, you’re better able to adapt.” Saying prayers: When we pray, we stop and reflect on our blessings, which shifts our perspective from what we don’t have to what we do. Prayer and meditation helps us cope better with adversity. In addition, the act of slowing down to contemplate something bigger than ourselves is relaxing – slowing the heart rate, dropping blood pressure and making our breathing more constant – which can bring a feeling of peaceful tranquility. “When my children’s great grandfather, who is 90, visits every week, he prays with the kids,” Sanford says. “In addition to doing something that is meaningful for him and good for his health, he’s passing on to that generation the comfort that a religious belief can bring, a source of strength in times of trouble. When he talks to them about prayer, he feels as though he is doing his job in passing along important values.” For many grandparents, caring for their grandchildren offers the pleasures of being a parent without the pain. It reminds them of what they loved about a wonderful time of their life, when they were raising children, without having to be a disciplinarian or do other difficult jobs that come with parenting. For others, being a grandparent gives them a chance to be more involved than they were with their own kids, especially if they were the breadwinner. And, of course, there is an endpoint. Typically, grandchildren go home. “Being a grandparent turns your focus outward. If you’re taking care of a little one, there’s no time for a pity party,” Sanford says. “But perhaps most important, being a grandparent lets you leave a legacy. Most of us aren’t going to be famous. But if you can make an imprint on those closest to us, when you’ve touched those around you in a profound way, that is what counts.” Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: infectious disease, liver disease, cancer, heart/lung disease, and aging and brain disorders.
Newswise — In their quest for healthy eating, many Americans are turning to restrictive diets – from vegan to Paleo to low-carb – that they believe are the most “pure” or beneficial. But when people decide to go beyond these and severely limit the types of foods they consume, they could be putting themselves at risk for nutritional deficiencies. People who obsessively refine and restrict their diet to conform to their ideal of what is healthy could be suffering from orthorexia nervosa – which translates from Greek as “correct appetite.” Although not an officially recognized disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), orthorexia can be likened to clinically defined eating disorders, such as anorexia nervosa, says Charlotte Markey, a Rutgers University–Camden psychologist who teaches a course titled “The Psychology of Eating” and studies eating behaviors, body image and weight management. She is the author of Smart People Don’t Diet: How the Latest Science Can Help You Lose Weight Permanently. Rutgers Today spoke with Markey about this condition, how to identify it and how it is best treated. Rutgers Today: What is orthorexia? Markey: Orthorexia is a form of maladaptive eating that can begin with good intentions: People start eliminating foods they consider “impure” or “bad” – sweets, sugars, carbohydrates – and before they know it, they are eating a highly limited diet. They think there is room for improvement and that they can always eat “healthier.” They cut out sugar, then salt, then wheat, then dairy, and so on. They become obsessed with what they should not be eating and keep whittling down the foods they will allow – which often impacts them socially since food is such a part of our social experiences. Since they think they are doing the “right” thing, they don’t question that there might be a negative impact to their health. Rutgers Today: What are the dangers of orthorexia? Markey: What people don’t realize is that many of those foods they are restricting, like carbohydrates, which are an important source of energy, really do serve a function. When diets become so restrictive, more than nutritional deficiencies can result: Orthorexics also can experience low energy and are at risk for depression. In severe cases, orthorexia eventually leads to malnourishment when critical nutrients are eliminated from the diet. Rutgers Today: Can orthorexia be linked to other disorders clinically defined by the DSM-5? Markey: In the past edition of the DSM, there was a category called “Eating Disorders Not Otherwise Specified.” This classification would likely include people, like orthorexics, who are obsessed with food and how they eat. Anorexia nervosa can be similar psychologically to orthorexia in the respect that they are both a restrictive obsession when it comes to food – it’s just that orthorexics are more concerned with the quality of food rather than quantity. Anorexics eat far fewer calories than orthorexics, who oftentimes look “normal” in terms of weight. Rutgers Today: How can people tell if they or someone they love is orthorexic? Markey: The nutritional effects of this extreme dieting are not often obvious, but behavioral changes can be a red flag. What differentiates orthorexics from people who, say, avoid GMOs, are vegan or consume only organic foods, is that the quest for a healthy diet takes over their lives. They spend an inordinate amount of time thinking about food or they avoid social situations so as not to be tempted to eat the foods they are restricting. It’s time to be concerned when someone’s life is being negatively affected or there is evidence of the person being distraught. Rutgers Today: How is orthorexia treated? Markey: I advise a two-pronged approach to treatment. A registered dietitian can assess whether a person is being deprived of key nutrients and, if so, help him or her structure a diet that is more rounded. The person should also find a counselor who specializes in eating disorders. Often, when people engage in negative eating patterns there is an underlying mental health issue. Maladaptive eating behaviors can be linked with depression, addictions and even anxiety disorders such as obsessive compulsive disorder, which can be treated successfully with both medication and cognitive-behavioral therapy. While we want people to eat healthily, we don’t want any eating pattern to become such an obsession that it detracts from their psychological, and even physical, health. For more information or to interview Charlotte Markey, contact Patti Verbanas at 848-932-0551 email@example.com
Newswise — There are two common approaches to protecting humans from infectious disease: Targeting pathogens and parasites with medicines like antibiotics, or dealing with the conditions that allow transmission. A paper published today in the journal Nature Scientific Reports demonstrates the effectiveness of a third strategy: Adjusting the landscape of the human body to remove the mechanism that allows pathogens to cause disease. The discovery is the result of serendipity and collaboration between high-level scientists in different fields. "It was pure luck that I ended up on this paper," says Dan Theodorescu, MD, PhD, director of the University of Colorado Cancer Center. "Bill Petri and I had been social friends for years – Christmas parties, that kind of thing. When I was at Virginia it happened that we were on a recruitment committee together and the candidate was late, so we started talking." His conversation with William A. Petri, Jr., MD, PhD, chief of the Division of Infectious Diseases & International Health at the University of Virginia led to the idea of applying an innovative cancer science technique to the study of infectious disease. With first author Chelsea Marie, PhD, postdoctoral researcher in the Petri Laboratory at Virginia, the group decided to silence genes in human cells to discover if the loss of any single gene would confer immunity to the parasite E. histolytica, which infects 50 million people and causes 40,000-110,000 deaths via severe diarrhea worldwide. "Chelsea is a fearless experimenter. She took a library of cells that Dan had developed in his work with bladder cancer and then sequentially killed them with E. histolytica parasites," Petri says. Specifically, the group used the technique called RNAi to create a library of bladder cancer cells with thousands of independent, silenced genes. Then they challenged these cultures with the parasite E. histolytica. "We do this all the time in cancer research," Theodorescu says. "Commonly, we're looking for genes that, when silenced, will make cells more susceptible to chemotherapy." In this case the analogue of chemotherapy was the infectious, dangerous pathogen. "This amoeba is a cluster bomb – a voracious killer. In the back of my mind I was thinking the parasite was going to decimate the host cells no matter what we did with their genetics," Marie says. For the vast majority of cells in this genome-wide screen, Chelsea Marie was correct; E. histolytica decimated many thousands of these independent cell cultures. However, a small number of cells seemed to resist the parasite. Was this the random chance of lucky survival or had silenced genes somehow offered immunity to these cells? To find out, Marie discarded the killed cells and retested the cells that had survived; again she infected these survivor cells with E. histolytica. "It wasn't a fluke," says Marie. "We did this over nine generations of cells, each time selecting the cells that survived and then re-applying the parasite. Over these generations of selection, we saw the cultures becoming more and more enriched for cells lacking specific genes." Using next generation sequencing, Marie identified the genes that conferred resistance and found that many were involved in managing the flow of potassium into and out of human cells. Specifically, the identified genes KCNA3, KCNB2, KCNIP4, KCNJ3, and SLC24A3 are involved in what is called potassium transport. A follow-up experiment showed that new intestinal cells treated with E. histolytica showed potassium efflux – the flow of potassium from inside a cell out through the cell wall – directly before cell death. "We started to see a pretty clear line of reasoning," says Theodorescu. "The parasite was causing potassium efflux right before cell death and cells that happened to be unable to transport potassium didn't die." To ensure that lack of potassium transport was, in fact, causing resistance to the parasite, the group reversed the direction of their experiments. Marie started with new cells and used drugs to block their ability to transport potassium. Blocking potassium efflux created cells that were resistant to E. histolytica. "There is a clear need for new drugs targeting E. histolytica," Petri says. "Right now there is a single antibiotic that works against this parasite. We know that eventually the parasite will develop resistance to the antibiotic and at that point there's no plan B. This could be the plan B – targeting the human genes that enable the parasite to cause disease." Marie is pushing forward. She recently learned from a mentor at John's Hopkins how to isolate stem cells from human tissue to grow what she calls "mini guts" to test therapeutics that may be useful in human patients. And technological advances make this study's general technique more efficient, allowing the use of what are called CRISPR libraries instead of RNAi screens. "This is a major finding with translational implications for this infection that causes so many deaths worldwide, but also proof that this cancer-science approach can be used to explore genetic mechanisms of resistance in the field of infectious disease," Theodorescu says. The field of infectious disease has been focused on the infection, targeting pathogens and their transmission. This study shows that in addition to characteristics of the parasite, mortality due to disease can be prevented by manipulating characteristics of the host.
RUTGERS CANCER INSTITUTE ONE OF FEW CENTERS ON EAST COAST TO OFFER IMMUNOTHERAPY CLINICAL TRIAL TARGETING LEUKEMIA/LYMPHOMA
Newswise — New Brunswick, N.J., September 8, 2015– Rutgers Cancer Institute of New Jersey is one of a few East Coast sites to offer a clinical trial investigating an experimental drug known as REGN1979 in the treatment of non-Hodgkin’s lymphoma (NHL) and chronic lymphocytic leukemia (CLL). The drug – designed to use the body’s own defenses to fight illness – targets a specific protein (called CD20) found in these particular types of cancer and targets another protein (called CD3) found on T-cells, a type of cell in the immune system. REGN1979 is designed to help T cells find and destroy B cells, including those cancerous B cells found in NHL and CLL. The goal is to determine how much of the drug can be given safely to patients who have the CD20 protein on their lymphoma or CLL cells. “By harnessing the body’s own natural defenses, there is an opportunity to provide alternate therapies for patients with NHL and CLL whose disease has stopped responding to standard treatments,” notes Rajat Bannerji, MD, PhD, medical oncologist and principal investigator of the trial at Rutgers Cancer Institute of New Jersey and associate professor of medicine at Rutgers Robert Wood Johnson Medical School. Participants are expected to be involved in the study for at least one year. Patients enrolled into the study will receive an infusion of the study drug through a vein. Participants also will be asked permission for scientists to study tissue samples taken from tumors or bone marrow collected during certain clinic visits. Adults aged 18 and older who are diagnosed with NHL or CLL and have had prior treatment with a particular antibody therapy (anti-CD20) are eligible to take part in the trial, provided they meet additional entry criteria. Prior to being enrolled into the study, participants would be required to undergo a number of tests including blood work and a physical exam. For more information on how to take part in this trial, sponsored by Regeneron Pharmaceuticals, Inc., individuals should call the Cancer Institute’s Office of Human Research Services at 732-235-8675 or e-mail firstname.lastname@example.org. Clinical trials, often called cancer research studies, test new treatments and new ways of using existing treatments for cancer. At the Cancer Institute, researchers use these studies to answer questions about how a treatment affects the human body and to make sure it is safe and effective. There are several types of clinical trials that are currently underway at the Cancer Institute, including those that diagnose, treat, prevent, and manage symptoms of cancer. Many treatments used today, whether they are drugs or vaccines, ways to do surgery or give radiation therapy, or combinations of treatments, are the results of past clinical trials. As New Jersey’s only National Cancer Institute-designated Comprehensive Cancer Center, the Cancer Institute offers patients access to treatment options not available at other institutions within the state. The Cancer Institute currently enrolls more than 1,200 patients in clinical trials annually, including approximately 17 percent of all new adult cancer patients and approximately 70 percent of all pediatric cancer patients. Enrollment in these studies nationwide is fewer than five percent of all adult cancer patients. About Rutgers Cancer Institute of New JerseyRutgers Cancer Institute of New Jersey (www.cinj.org) is the state’s first and only National Cancer Institute-designated Comprehensive Cancer Center. As part of Rutgers, The State University of New Jersey, the Cancer Institute of New Jersey is dedicated to improving the detection, treatment and care of patients with cancer, and to serving as an education resource for cancer prevention. Physician-scientists at the Cancer Institute engage in translational research, transforming their laboratory discoveries into clinical practice, quite literally bringing research to life. To make a tax-deductible gift to support the Cancer Institute of New Jersey, call 848-932-3637 or visit www.cinj.org/giving. Follow us on Facebook at www.facebook.com/TheCINJ. The Cancer Institute of New Jersey Network is comprised of hospitals throughout the state and provides the highest quality cancer care and rapid dissemination of important discoveries into the community. Flagship Hospital: Robert Wood Johnson University Hospital. System Partner: Meridian Health (Jersey Shore University Medical Center, Ocean Medical Center, Riverview Medical Center, Southern Ocean Medical Center, and Bayshore Community Hospital). Major Clinical Research Affiliate Hospitals: Carol G. Simon Cancer Center at Morristown Medical Center and Carol G. Simon Cancer Center at Overlook Medical Center. Affiliate Hospitals: JFK Medical Center, Robert Wood Johnson University Hospital Hamilton (CINJ Hamilton), and Robert Wood Johnson University Hospital Somerset.
3D Printing is reaching new heights according to sources from the FDA as well as WebMD, and the clinical trials of a new medication being tested for epilepsy. In a recent report from Aprecia Pharmaceuticals, the agency has developed a 3D printed tablet for epilepsy that rapidly disintegrates with a sip of liquid. The tablet is called Spritam and is the first 3D printed drug to be approved for sale in the U.S. and it is expected to be available early next year, in 2016. “For the last 50 years we have manufactured tablets in factories and shipped them to hospitals and for the first time this process means we can produce tablets much close to the patient,” Dr. Mohamed Albed Alhnan, a lecturer in pharmaceutics at the University of Central Lancashire in the United Kingdom, explained in an interview with BBC News. Nearly 3 million Americans have been diagnosed with epilepsy, including 460,000 children according to WebMD.com and the numbers continue to rise. The financial expense and physical care some patients need can be overwhelming to the family and/or the caregiver, 3D printing can make the frustration of being able to obtain prescriptions easier and possibly even approach new, more effective medication technology. 3D printing is already a leading technology in the development of medical devices. There is still a long road ahead for 3D printing pharmaceuticals. From developing printers that can print a higher quantity pharmaceuticals at a time all the way down to the specific benefits of 3D printing like drugs that can be personalized using different layers to create a more effective release of the medication into the body, a more person specific medication experience. “The uniformity of dosage control with this type of manufacturing method is at least as good, if not far better, than conventional manufacturing” said Michael J. Cima, PhD., Massachusetts Institute of Technology.
Dental Tips from Texas A & M can help you encourage healthy dental habits away from home. 1. Eat healthy foods at home A healthy diet won’t just improve your child’s growth and physical health; it will also improve their dental health. Most natural foods contain lower amounts of sugars and aren’t as damaging to the teeth. One of the easiest things you can do to ensure your child will make healthy, tooth-conscious decisions at school is to eat healthy foods at home. Aim to serve your child a balanced diet, including fruits, vegetables, whole grains, dairy products and protein. “Parents need to serve these foods at home so their children will imitate those eating habits when they are elsewhere,” Pace said. 2. Pack fruits and dairy Natural is usually better when it comes to foods in general, and the same goes for snacks. Instead of popular snacks that may lead to unhealthy teeth or dental habits, try going the au naturel route. Packing fruit will satisfy your child’s sweet cravings and help them gain all the proper nutrients they need to grow healthy. Milk doesn’t just help their bones grow stronger, it can also help their teeth stay healthier as well. One of the best snacks you can pack in your child’s lunch is a dairy product. Try throwing in a string cheese or a carton of milk to their lunchbox. “Cheese or other dairies are a great way to end meals,” Pace remarked. “They can help protect tooth enamel, which is key to preventing decay.” 3. Avoid sticky and sugary foods “In general, any food that is sticky, crunchy or has sugar can promote cavities,” Pace warned. Sticky foods like candy or gummies are not only loaded with sugar, but they can also be difficult to dislodge later. Anything that sticks to the teeth can potentially damage them or cause decay. “Frequent sugar consumption is one of the worst things for your teeth that can cause tooth decay. Unfortunately, sugar is in almost everything,” Pace said. Avoid packing food with extra sugar like cookies, sugary beverages or candy in children’s daily lunches. Sugary, prepackaged snacks may be convenient short term, but they may also help a cavity thrive later on. Check all the sugar content on any prepackaged foods or snacks, and opt for more natural or low-sugar foods instead. Switch out your kid’s sugar-bomb applesauce for the no sugar added variety. If you’re having trouble thinking of appropriate snacks, fruits with peels can satisfy your little one’s sweet tooth without promoting cavities. 4. Be active in their dental care Participate in your child’s morning and nightly teeth cleaning rituals, and teach them the tools to keep those pearly whites healthy and happy. You can also take it a step further by acting as a dental advocate yourself to promote healthy habits in your children. “Children love to imitate, so let them watch you brush your teeth and floss. Or even better, do it with them,” Pace suggested. “Really try to have your kids brush their teeth after breakfast.” Healthy habits start at home, so try to make your child’s formative years fun and memorable. While brushing teeth, sing a favorite song or play a catchy tune on your phone to make it enjoyable, and always serve them healthy foods at home. These are habits they’ll take with them throughout their lifetime. Report by Texas A & M
Newswise — ST. LOUIS — In research published inCancer Cell, Thomas Burris, Ph.D., chair of pharmacology and physiology at Saint Louis University, has, for the first time, found a way to stop cancer cell growth by targeting the Warburg Effect, a trait of cancer cell metabolism that scientists have been eager to exploit. Unlike recent advances in personalized medicine that focus on specific genetic mutations associated with different types of cancer, this research targets a broad principle that applies to almost every kind of cancer: its energy source. The Saint Louis University study, which was conducted in animal models and in human tumor cells in the lab, showed that a drug developed by Burris and colleagues at Scripps Research Institute can stop cancer cells without causing damage to healthy cells or leading to other severe side effects. The Warburg EffectMetabolism – the ability to use energy – is a feature of all living things. Cancer cells aggressively ramp up this process, allowing mutated cells to grow unchecked at the expense of surrounding tissue. “Targeting cancer metabolism has become a hot area over the past few years, though the idea is not new,” Burris said. Since the early 1900s, scientists have known that cancer cells prefer to use glucose as fuel even if they have plenty of other resources available. In fact, this is how doctors use PET (positron emission tomography) scan images to spot tumors. PET scans highlight the glucose that cancer cells have accumulated. This preference for using glucose as fuel is called the Warburg effect, or glycolysis. In his paper, Burris reports that the Warburg effect is the metabolic foundation of oncogenic (cancer gene) growth, tumor progression and metastasis as well as tumor resistance to treatment. Cancer’s Goal: To Grow and DivideCancer cells have one goal: to grow and divide as quickly as possible. And, while there are a number of possible molecular pathways a cell could use to find food, cancer cells have a set of preferred pathways. “In fact, they are addicted to certain pathways,” Burris said. “They need tools to grow fast and that means they need to have all of the parts for new cells and they need new energy.” “Cancer cells look for metabolic pathways to find the parts to grow and divide. If they don’t have the parts, they just die,” said Burris. “The Warburg effect ramps up energy use in the form of glucose to make chemicals required for rapid growth and cancer cells also ramp up another process, lipogenesis, that lets them make their own fats that they need to rapidly grow.” If the Warburg effect and lipogenesis are key metabolic pathways that drive cancer progression, growth, survival, immune evasion, resistance to treatment and disease recurrence, then, Burris hypothesizes, targeting glycolysis and lipogenesis could offer a way to stop a broad range of cancers. Cutting off the Energy SupplyBurris and his colleagues created a class of compounds that affect a receptor that regulates fat synthesis. The new compound, SR9243, which started as an anti-cholesterol drug candidate, turns down fat synthesis so that cells can’t produce their own fat. This also impacts the Warburg pathway, turning cancer cells into more normal cells. SR9243 suppresses abnormal glucose consumption and cuts off cancer cells’ energy supply. When cancer cells don’t get the parts they need to reproduce through glucose or fat, they simply die. Because the Warburg effect is not a feature of normal cells and because most normal cells can acquire fat from outside, SR9243 only kills cancer cells and remains non-toxic to healthy cells. The drug also has a good safety profile; it is effective without causing weight loss, liver toxicity, or inflammation. Promising ResultsSo far, SR9243 has been tested in cultured cancer cells and in human tumor cells grown in animal models. Because the Warburg pathway is a feature of almost every kind of cancer, researchers are testing it on a number of different cancer models. “It works in a wide range of cancers both in culture and in human tumors developing in animal models,” Burris said. “Some are more sensitive to it than others. In several of these pathways, cells had been reprogramed by cancer to support cancer cell growth. This returns the metabolism to that of more normal cells.” In human tumors grown in animal models, Burris said, “It worked very well on lung, prostate, and colorectal cancers, and it worked to a lesser degree in ovarian and pancreatic cancers.” It also seems to work on glioblastoma, an extremely difficult to treat form of brain cancer, though it isn’t able to cross the brain/blood barrier very effectively. The challenge for researchers in this scenario will be to find a way to allow the drug to cross this barrier, the body’s natural protection for the brain, which can make it difficult for drug treatments to reach their target. And, in even more promising news, it appears that when SR9243 is used in combination with existing chemotherapy drugs, it increases their effectiveness, in a mechanism apart from SR9243’s own cancer fighting ability. Other researchers on the study include Colin A. Flaveny, Kristine Griffett, Bahaa El-Dien M. El-Gendy, Melissa Kazantzis, Monideepa Sengupta, Antonio L. Amelio, Arindam Chatterjee, John Walker, Laura A. Solt and Theodore M. Kamenecka. Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: cancer, liver disease, heart/lung disease, aging and brain disease, and infectious diseases.