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State College, PA, United States

Penn State Milton S. Hershey Medical Center, located in Hershey, Pennsylvania, 10 miles east of Harrisburg, is Penn State’s medical school and academic medical center. Wikipedia.


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News Article | May 12, 2017
Site: www.eurekalert.org

Immune cells, called macrophages, may rely on a compound to signal an attack to beat back attacks from parasitic worms, according to an international team of researchers, including Zissis C. Chroneos, associate professor of pediatrics, and microbiology and immunology at Penn State College of Medicine. The findings could lead to better drugs to fight common infections. It is estimated that parasitic worms infect hundreds of millions of people, mainly in the developing world. These roundworms and flatworms -- collectively known as helminths -- often infect the intestinal system, causing anemia and malnutrition. But worms can also infect other organs and systems, such as the lungs, urinary tract or bloodstream, causing a range of health problems. For example, the common worm infection schistosomiasis can lead to high blood pressure in lung arteries. Chroneos and his co-investigators studied a roundworm, called Nippostrongylus brasiliensis, that infects the lungs of rodents. A compound called interleukin 4, or IL-4, was used to activate large white blood cells -- macrophages -- to kill the parasite and promote healing in the lung tissue. The study, published in Science, helps to explain how this process works. The researchers discovered that IL-4 helps the outer layer of lung cells to boost production of the defense protein SP-A. This protein binds macrophages and enhances their ability to multiply and activate against the parasite. Chroneos discovered that the SP-A protein binds at a receptor called myosin 18A. IL-4 triggers the appearance, or expression, of the receptor on macrophages. "You cannot kill the worm if you don't have myosin 18A," Chroneos said. To test this, researchers in his lab developed antibodies to block the myosin 18A receptor. When it was blocked in mice, rats and human lung cells, the growth of macrophages against parasites was reduced. The findings have implications beyond the lungs, Chroneos said. The researchers found that the receptor myosin 18 also allows macrophages to bind to a different defense protein called C1q in the abdomen of mice. Macrophages from mouse liver, spleen and fat tissue expressed myosin 18A when exposed to the immune compound IL-4, which suggests that the receptor is important for fighting infections throughout the body. In the future, the new knowledge could be used to develop drugs against infections that trigger the IL-4 immune response. "Now that we know how this works, we can potentially use molecules that activate the myosin 18A pathway or the IL-4 pathway to kill the disease," Chroneos said. Other researchers on this project were Carlos M. Minutti, from the Complutense University of Madrid, the Instituto de Salud Carlos III, and the University of Edinburgh; Lucy H. Jackson-Jones, Johanna A. Knipper, Nicola Logan, Emma Rinqvist, David A. Ferenbach and Dietmar M. Zaiss, from the University of Edinburgh; Belén García-Fojeda and Cristina Casals from the Complutense University of Madrid and the Instituto de Salud Carlos III; Tara E. Sutherland from the University of Edinburgh and the University of Manchester; Raquel Guillamat-Prats and Antonio Artigas from the Instituto de Salud Carlos III and the Universitat Autònoma de Barcelona; Cordula Stamme from the University of Lu?beck; and Judith E. Allen from the University of Edinburgh and the University of Manchester. Minutti was recipient of fellowships from the Spanish Ministry of Science and Institute of Health Carlos III. This work was supported by the Spanish Ministry of Economy and Competitiveness, Institute of Health Carlos III, Medical Research Council UK, Wellcome Centre for Cell-Matrix Research, Medical Research Council, European Union, and National Institute of Health.


News Article | April 24, 2017
Site: www.eurekalert.org

How happy a mother is in her relationship and the social support she receives may affect the risk of infant colic, according to Penn State College of Medicine researchers. The study sheds new light on the factors that may contribute to infant fussiness, a common complaint, especially among first-time mothers. Social conditions related to mental health during pregnancy, such as maternal anxiety and low social support, have previously been associated with infant colic. Researchers have also linked postpartum maternal depression with an increased risk of colic. The study measured first-time mothers' relationship happiness and general social support, as well as support in taking care of the baby by their partners. The researchers, who reported their findings in a recent issue of Child: Care, Health and Development, looked at these factors during pregnancy and one month after birth in more than 3,000 women, 18 to 35 years old, who gave birth at 78 hospitals in Pennsylvania between January 2009 and April 2011. Overall, 11.6 percent of mothers in the study self-reported that their infants had colic, defined as crying or fussiness three or more hours a day. Relationship happiness, general social support and partner-baby support all protected against colic in the study. The happier a woman reported being in her partner relationship during and after pregnancy, the lower the risk of colic in her infant. This was the strongest association and held even in women experiencing postpartum depression and in those whose partners were not their babies' biological fathers. The researchers said it is unknown why this association exists, but offered a few suggestions. "Maybe the baby cries less if the mom and dad are happier," said Kristen Kjerulff, professor of public health sciences and senior study author. Another possibility is that mothers in happier relationships may not perceive their baby's crying as negatively, and may not report it as colic, she said. Women who rated their partners as supportive also had babies with a lower risk of colic. In particular, the more helpful their partners were with the baby, and the warmer, more loving, and more affectionate they were toward the baby, the less colic was reported. General social support from friends and family was also associated with a lower risk of colic. Women were less likely to report having a colicky baby if they had someone to turn to for suggestions about how to handle a personal problem and someone to confide in about their problems. Interestingly, babies of single women had the lowest rate of colic. Although this association was not statistically significant, the finding further suggests that social support is important for reducing colic. Women in the study who did not have a partner reported having higher levels of general social support, according to Kjerulff. "If you don't have a partner you can still have lots of social support, lots of love and lots of happy relationships, and all of that's going to be better for the baby," she said. "Love makes a difference." The first author of the study, Chandran Alexander, assistant professor of pediatrics at Penn State College of Medicine, said, "Mothers' significant others have a role to play in reducing the burden of colic. Society should avoid pinning the blame for colic on mothers' competence, self-esteem or depression." Alexander, a pediatric gastroenterologist, said he was inspired to study factors that influence colic after observing first-time mothers with colicky babies making frequent visits to their pediatricians and pediatric gastroenterologists. Some of the therapies for infant colic that are currently offered are expensive and unproven, he said. "We need to impress upon society the importance of supporting families in their care of newborns," Alexander said. Next, Alexander and Kjerulff plan to study whether relationship and social-support factors influence child health outcomes associated with colic, such as gastrointestinal problems or food allergies, as children age. Other researchers on the study were Junjia Zhu, assistant professor of public health sciences, and Ian Paul, professor of pediatrics and public health sciences, both at Penn State College of Medicine. This research was funded by the National Institutes of Health.


News Article | May 3, 2017
Site: www.futurity.org

Speech or language impairments may not be the cause of more frequent tantrums in children with autism, a new study suggests. Children with autism experience more tantrums than children without, and speech and language problems often take the blame for the frequent outbursts. Some children with autism spectrum disorder aren’t able to speak or have speech that is not clear or well-understood by others. For a new study, published in the Journal of Development and Physical Disabilities, researchers looked at the relationship between language and tantrum frequency in 240 children with autism between the ages of 15 and 71 months of age. The children’s IQ, their ability to understand language, and their ability to use words and speak clearly, explained less than 3 percent of their tantrums. “We had children in our sample with clear speech and enough intelligence to be able to communicate, and their tantrums were just as high in that group,” says Cheryl D. Tierney, associate professor of pediatrics at Penn State College of Medicine, and section chief, behavior and developmental pediatrics at Penn State Children’s Hospital. Further, children who spoke at the level of a two-year-old with normal development had more tantrums than children with lower speech skills. “There is a common pervasive misbelief that children with autism have more tantrum behaviors because they have difficulty communicating their wants and their needs to caregivers and other adults,” Tierney says. “The belief is that their inability to express themselves with speech and language is the driving force for these behaviors, and that if we can improve their speech and their language the behaviors will get better on their own. “But we found that only a very tiny percentage of temper tantrums are caused by having the inability to communicate well with others or an inability to be understood by others.” Tierney and co-investigator Susan D. Mayes, professor of psychiatry, addressed the limitations in previous research by including a larger sample of children and capturing more measurements. The new study measures IQ and separates speech and language as different variables that might affect tantrum behavior in children with autism. “IQ is extremely important because a child that has the mental capacity to understand and use language may display different behaviors compared to a child who doesn’t have the mental capacity and comprehension to use language,” Tierney says. Understanding the difference between language and speech is an important consideration, she says. “Language is a child’s ability to understand the purpose of words and to understand what is said. Speech is their ability to use their mouth, tongue, lips, and jaw to form the sounds of words and make those sounds intelligible to other people.” The study doesn’t answer the question of what causes tantrums in children with autism, but mood dysregulation and a low tolerance for frustration—two common traits—are likely factors that should be studied further. Enough evidence has accumulated to shift the emphasis from improving speech to improving behavior, Tierney says. “We should stop telling parents of children with autism that their child’s behavior will get better once they start talking or their language improves, because we now have enough studies to show that that is unlikely to happen without additional help.” Help should come in the form of applied behavior analysis, and having a well-trained and certified behavior analyst on a child’s treatment team, Tierney says. “This form of therapy can help children with autism become more flexible and can show them how to get their needs met when they use behaviors that are more socially acceptable than having a tantrum.”


News Article | May 3, 2017
Site: www.eurekalert.org

Speech or language impairments may not be the cause of more frequent tantrums in children with autism, according to Penn State College of Medicine researchers. The findings could help parents of children with autism seek out the best treatment for behavior problems. Children with autism experience more tantrums than children without, according to the researchers, and speech therapists, preschool teachers, parents and others often blame these frequent outbursts on speech and language problems. Some children with autism spectrum disorder are not able to speak or have speech that is not clear or well-understood by others. To investigate this correlation, the researchers studied the relationship between language and tantrum frequency in 240 children with autism between the ages of 15 and 71 months of age. The researchers, who published their results in a recent issue of the Journal of Development and Physical Disabilities, said that the children's IQ, their ability to understand language and their ability to use words and speak clearly, explained less than 3 percent of their tantrums. "We had children in our sample with clear speech and enough intelligence to be able to communicate, and their tantrums were just as high in that group," said Cheryl D. Tierney, associate professor of pediatrics, College of Medicine, and section chief, behavior and developmental pediatrics, Penn State Children's Hospital. The researchers also found that children who spoke at the level of a 2-year-old with normal development had more tantrums than children with lower speech skills. "There is a common pervasive misbelief that children with autism have more tantrum behaviors because they have difficulty communicating their wants and their needs to caregivers and other adults," Tierney explained. "The belief is that their inability to express themselves with speech and language is the driving force for these behaviors, and that if we can improve their speech and their language the behaviors will get better on their own. But we found that only a very tiny percentage of temper tantrums are caused by having the inability to communicate well with others or an inability to be understood by others." In the study, Tierney and co-investigator Susan D. Mayes, professor of psychiatry, addressed the limitations in previous research by including a larger sample of children and capturing more measurements. They add that their study is unique because it measures IQ and it separates speech and language as different variables that might affect tantrum behavior in children with autism. "IQ is extremely important because a child that has the mental capacity to understand and use language may display different behaviors compared to a child who doesn't have the mental capacity and comprehension to use language," Tierney said. She also explained the difference between language and speech in the study of children with autism. "Language is a child's ability to understand the purpose of words and to understand what is said," she said. "Speech is their ability to use their mouth, tongue, lips and jaw to form the sounds of words and make those sounds intelligible to other people." The study doesn't answer the question of what causes tantrums in children with autism, but mood dysregulation and a low tolerance for frustration -- two common traits -- are likely factors that should be studied further, Tierney said. Tierney suggests enough evidence has accumulated to shift the emphasis from improving speech to improving behavior. "We should stop telling parents of children with autism that their child's behavior will get better once they start talking or their language improves, because we now have enough studies to show that that is unlikely to happen without additional help," she said. That help should come in the form of applied behavior analysis, and having a well-trained and certified behavior analyst on a child's treatment team is key to improved outcomes, Tierney added. "This form of therapy can help children with autism become more flexible and can show them how to get their needs met when they use behaviors that are more socially acceptable than having a tantrum," Tierney said. Robin Lockridge, of the department of psychiatry, also worked on this research.


News Article | April 26, 2017
Site: www.eurekalert.org

A diet supplemented with soy protein may be an effective adjunct therapy for inflammatory bowel diseases, Penn State researchers reported after completing a study that included mice and cultured human colon cells. The findings are significant because inflammatory bowel diseases -- including ulcerative colitis and Crohn's disease -- are characterized by either continuous or periodic inflammation of the colon and represent a significant risk factor for colon cancer. Also known as IBD, inflammatory bowel diseases affect nearly 4 million people worldwide and have an economic impact of more than $19 billion annually in the United States alone. The development of dietary strategies to mitigate IBD is of considerable public health importance, said Joshua Lambert, associate professor of food science in the College of Agricultural Sciences. He said his team found that soy-protein concentrate can exert antioxidant and cytoprotective effects in cultured human bowel cells and can moderate the severity of inflammation in mice that have an induced condition similar to ulcerative colitis. Zachary Bitzer and Amy Wopperer, former graduate students in the Department of Food Science and the lead researchers, substituted soy-protein concentrate into the diet of the mice and removed corresponding amounts of the other protein sources, equaling about 12 percent. They kept human equivalents in mind as they determined the amount. "We didn't want to get carried away with using doses that were really high and would crowd out all the other protein that was there," Bitzer said. "Instead, we wanted to find a scenario that was going to fit into a more human-relevant situation." The dietary soy-protein concentrate at the 12-percent dose level ameliorated body-weight loss and swelling of the spleen in the mice with induced inflammatory bowel disease. "Soy-protein concentrate mitigates markers of colonic inflammation and loss of gut barrier function in the mice with induced IBD," Wopperer said. Follow-on studies will focus on whether the results of this research with mice, published in The Journal of Nutritional Biochemistry, are readily translatable to people. Because soy protein is a widely used food ingredient -- often used as a meat substitute and commonly referred to as "texturized vegetable proteins" in ingredient lists -- Lambert believes human studies could be arranged in the near future. "Since it is already out there commercially, that makes it more straightforward," he said. "But practically speaking, the actual clinical studies are a little bit out of our area of expertise. I think the most likely thing to happen will be for us to try to identify a collaborator either through the Clinical Translational Science Institute on campus or with someone at the Penn State College of Medicine Inflammatory Bowel Disease Center." However, Lambert's laboratory soon will start a related investigation of whether the inflammation-moderating effects triggered in the mouse colons are due solely to the soy protein or also may be caused by soy fiber. Soy-protein concentrate is 70 percent protein by weight, but it also has quite a bit of soybean fiber in it, he explained. Also participating in the study were Benjamin Chrisfield, a master's degree student in food science; Ling Tao, a former doctoral student in food science; Timothy Cooper, associate professor of comparative medicine at the Penn State College of Medicine; and Jairam Vanamala, Ryan Elias and John Hayes, all associate professors of food science, Penn State. Technical assistance and primer synthesis services were provided by the Penn State Genomics Core Facility. The Pennsylvania Soybean Board, the American Institute for Cancer Research and the U.S. Department of Agriculture's Hatch Program supported this research. Both Wopperer and Bitzer were supported in part by the Roger and Barbara Claypoole Distinguished Graduate Fellowship in the College of Agricultural Sciences.


News Article | April 24, 2017
Site: www.chromatographytechniques.com

Like air-traffic controllers scrambling to reconnect flights when a major hub goes down, the brain has a remarkable ability to rewire itself after suffering an injury. However, maintaining these new connections between brain regions can strain the brain's resources, which can lead to serious problems later, including Alzheimer's Disease, according to researchers. After a head injury, the brain can show enhanced connectivity by using alternative routes between two previously connected regions of the brain that need to communicate, as well as make stronger connections, said Frank G. Hillary, associate professor of psychology, Penn State. These new connections between damaged areas are often referred to as hyperconnections, he added. "Hyperconnectivity has been called a compensatory reaction to brain injury and it's a little counterintuitive because it implies that the brain can increase its functional response when you take away physical resources," said Hillary. "If the axon — the physical connection — between brain areas is removed, the brain can retain that connection functionally by using alternative routes. So what we're seeing is there are all sorts of ways in which the brain can adapt and one way is to heighten the response, but the question is what does that do for you in the short term and what are the potential secondary consequences in the long term." Because neural networks are typically designed to communicate as efficiently as possible, disruptions may mean that new networks are less efficient and use more energy, said Hillary, who worked with Jordan H. Grafman, director, brain injury research at Shirley Ryan Abilitylab and professor of physical medicine and rehabilitation, neurology and psychiatry and behavioral sciences at the Northwestern University in Chicago. "It's costly metabolically and it's costly with respect to how quickly you think," said Hillary. "One of the primary cognitive deficits in all neurological disorders — multiple sclerosis, traumatic brain injury, schizophrenia — is impairments in how quickly you can think, called processing speed. In neurological disorders, processing speed diminishes and it can be related to a decrease in brain efficiency." Over time, these chronic inefficiencies may cascade into serious brain disorders, according to the researchers, who report their findings in the current issue of Trends in Cognitive Science. "If we know which patients would be susceptible to pathological hyperconnectivity following a traumatic brain injury, we might be able to develop new interventions to alter the course of that process," said Grafman. Prior research has suggested a connection between brain injury and Alzheimer's Disease, according to the researchers. "We know that brain injury is a risk factor for Alzheimer's Disease later in life and the long-term effect of hyperconnections may be a link to how it happens," said Hillary, who also is a faculty member at Penn State College of Medicine. Just as inefficient motors tend to pollute more, inefficient neural connections may build up harmful deposits that can further impair the brain. Although other factors, such as genetics, are likely involved, the researchers noted that higher deposits of amyloid beta — a marker of Alzheimer's Disease — are often located at sites where there is the highest connectivity. "Where there's a lot of activity going on, it increases metabolic byproducts and if you don't clear them, they collect," said Hillary. "Heavy activation, heavy connectivity can put pressure on network hubs and that's why those hubs are some of the first to go in Alzheimer's." While more research is needed and possible treatment targets for Alzheimer's or other neurological conditions remain uncertain, Hillary said the findings underscore the need to take precautions against brain injury. "What I always tell my students is be good to your brain," said Hillary. "You only get one brain and while it can adapt to some injuries over your life, there is probably a cost for those adjustments."


News Article | April 24, 2017
Site: www.eurekalert.org

Like air-traffic controllers scrambling to reconnect flights when a major hub goes down, the brain has a remarkable ability to rewire itself after suffering an injury. However, maintaining these new connections between brain regions can strain the brain's resources, which can lead to serious problems later, including Alzheimer's Disease, according to researchers. After a head injury, the brain can show enhanced connectivity by using alternative routes between two previously connected regions of the brain that need to communicate, as well as make stronger connections, said Frank G. Hillary, associate professor of psychology, Penn State. These new connections between damaged areas are often referred to as hyperconnections, he added. "Hyperconnectivity has been called a compensatory reaction to brain injury and it's a little counterintuitive because it implies that the brain can increase its functional response when you take away physical resources," said Hillary. "If the axon -- the physical connection -- between brain areas is removed, the brain can retain that connection functionally by using alternative routes. So what we're seeing is there are all sorts of ways in which the brain can adapt and one way is to heighten the response, but the question is what does that do for you in the short term and what are the potential secondary consequences in the long term." Because neural networks are typically designed to communicate as efficiently as possible, disruptions may mean that new networks are less efficient and use more energy, said Hillary, who worked with Jordan H. Grafman, director, brain injury research at Shirley Ryan Abilitylab and professor of physical medicine and rehabilitation, neurology and psychiatry and behavioral sciences at the Northwestern University in Chicago. "It's costly metabolically and it's costly with respect to how quickly you think," said Hillary. "One of the primary cognitive deficits in all neurological disorders -- multiple sclerosis, traumatic brain injury, schizophrenia -- is impairments in how quickly you can think, called processing speed. In neurological disorders, processing speed diminishes and it can be related to a decrease in brain efficiency." Over time, these chronic inefficiencies may cascade into serious brain disorders, according to the researchers, who report their findings in the current issue of Trends in Cognitive Science. "If we know which patients would be susceptible to pathological hyperconnectivity following a traumatic brain injury, we might be able to develop new interventions to alter the course of that process," said Grafman. Prior research has suggested a connection between brain injury and Alzheimer's Disease, according to the researchers. "We know that brain injury is a risk factor for Alzheimer's Disease later in life and the long-term effect of hyperconnections may be a link to how it happens," said Hillary, who also is a faculty member at Penn State College of Medicine. Just as inefficient motors tend to pollute more, inefficient neural connections may build up harmful deposits that can further impair the brain. Although other factors, such as genetics, are likely involved, the researchers noted that higher deposits of amyloid beta -- a marker of Alzheimer's Disease -- are often located at sites where there is the highest connectivity. "Where there's a lot of activity going on, it increases metabolic byproducts and if you don't clear them, they collect," said Hillary. "Heavy activation, heavy connectivity can put pressure on network hubs and that's why those hubs are some of the first to go in Alzheimer's." While more research is needed and possible treatment targets for Alzheimer's or other neurological conditions remain uncertain, Hillary said the findings underscore the need to take precautions against brain injury. "What I always tell my students is be good to your brain," said Hillary. "You only get one brain and while it can adapt to some injuries over your life, there is probably a cost for those adjustments." The National Center for Advancing Translational Sciences supported this work.


News Article | April 17, 2017
Site: phys.org

"Most cells generate and secrete extracellular vesicles," says Siyang Zheng, associate professor of biomedical engineering and electrical engineering. "But they are difficult for us to study. They are sub-micrometer particles, so we really need an electron microscope to see them. There are many technical challenges in the isolation of nanoscale EVs that we are trying to overcome for point-of-care cancer diagnostics." At one time, researchers believed that EVs were little more than garbage bags that were tossed out by cells. More recently, they have come to understand that these tiny fat-enclosed sacks—lipids—contain double-stranded DNA, RNA and proteins that are responsible for communicating between cells and can carry markers for their origin cells, including tumor cells. In the case of cancer, at least one function for EVs is to prepare distant tissue for metastasis. The team's initial challenge was to develop a method to isolate and purify EVs in blood samples that contain multiple other components. The use of liquid biopsy, or blood testing, for cancer diagnosis is a recent development that offers benefits over traditional biopsy, which requires removing a tumor or sticking a needle into a tumor to extract cancer cells. For lung cancer or brain cancers, such invasive techniques are difficult, expensive and can be painful. "Noninvasive techniques such as liquid biopsy are preferable for not only detection and discovery, but also for monitoring treatment," says Chandra Belani, professor of medicine and deputy director of the Cancer Institute, Penn State College of Medicine, and clinical collaborator on the study. "We invented a system of two micro/nano materials," Zheng says. "One is a labeling probe with two lipid tails that spontaneously insert into the lipid surface of the extracellular vesicle. At the other end of the probe we have a biotin molecule that will be recognized by an avidin molecule we have attached to a magnetic bead." The surface-modified magnetic beads are 400 to 500 nanometers in diameter and the labeling probes is on the order of 10 nanometers. When the system is optimized, the researchers can isolate the EVs from blood plasma samples in about 15 minutes. The EVs and their contents can then be analyzed in a lab setting or sent to a commercial diagnostic lab to characterize the DNA, RNA and proteins. In a paper published online today, April 10, and as the cover article for April in Nature Biomedical Engineering, lead author Yuan Wan, a postdoctoral researcher in Zheng's lab, describes using the nanoprobes to capture EVs from the blood plasma of 19 patients with non-small-cell lung cancer. "Aided with this new approach, we successfully isolated EVs from 19 patients with advanced lung cancer and identified DNA mutations that can guide precision therapy instead of routine chemotherapy," Wan says. "From collecting blood to obtaining EV-derived DNA, the whole procedure can be completed within one hour. It only requires a magnet and a common benchtop centrifuge. Compared to prevalent methods, the nanoprobe system would greatly facilitate clinical laboratory examination." Because the technology requires only materials and an external magnet, it is relatively inexpensive and fast compared to the current gold standard of separation, called ultracentrifugation, which requires expensive equipment and takes hours to complete. Once validated in a larger study, Zheng and Belani believe that this technique can be applied not only to lung cancer but also to most if not all solid tumors, which are responsible for 80-90 percent of cancer deaths. "Sequencing the DNA isolated from the EVs will serve as a promising tool to track cancer evolution and monitor tumor dynamics with the ultimate goal of improving cancer survival," Belani concludes. Explore further: Studies find promise for innovations in liquid biopsies More information: Rapid isolation of extracellular vesicles via lipid nanoprobes, Nature Biomedical Engineering (2017). nature.com/articles/doi:10.1038/s41551-017-0058


Anson J.A.,Penn State College of Medicine
Anesthesiology | Year: 2014

Intraosseous vascular access is a time-tested procedure which has been incorporated into the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation. Intravenous access is often difficult to achieve in shock patients, and central line placement can be time consuming. Intraosseous vascular access, however, can be achieved quickly with minimal disruption of chest compressions. Newer insertion devices are easy to use, making the intraosseous route an attractive alternative for venous access during a resuscitation event. It is critical that anesthesiologists, who are often at the forefront of patient resuscitation, understand how to properly use this potentially life-saving procedure. Copyright © 2014, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins.


Fitzpatrick L.R.,Penn State College of Medicine
International Reviews of Immunology | Year: 2013

Several experimental approaches have been utilized, in order to critically examine the roles of IL-17 family members in intestinal inflammation. These approaches have included: (1) the use of IL-17A and IL-17F-deficient mice, (2) specific antibodies directed against IL-17, (3) an IL-17 vaccine, (4) methods to block the IL-17 receptor and (5) small-molecule inhibitors of IL-17. Previous studies found somewhat conflicting results in preclinical models of Inflammatory Bowel Disease (IBD), using specific strains of IL-17-deficient mice. This paper will review the preclinical results using various pharmacological approaches specific IL-17 antibodies, an IL-17 receptor fusion protein, IL-12/IL-23 p40 subunit and IL-17 vaccine approaches, as well as a small molecule inhibitor (Vidofludimus) to inhibit IL-17 in animal models of IBD. Recent clinical results in patients with IBD will also be discussed for Secukinumab (an IL-17A antibody), Brodalumab (an IL-17 receptor antibody) and two small-molecule drugs (Vidofludimus and Tofacitinib), which inhibit IL-17 as part of their overall pharmacological profiles. This review paper will also discuss some pharmacological lessons learned from the preclinical and clinical studies with anti-IL-17 drugs, as related to drug pharmacodynamics, IL-17 receptor subtypes and other pertinent factors. Finally, future pharmacological approaches of interest will be discussed, such as: (1) Retinoic acid receptor-related orphan nuclear receptor gamma t (Rorγt) antagonists, (2) Retinoic acid receptor alpha (RARα) antagonists, (3) Pim-1 kinase inhibitors and (4) Dual small-molecule inhibitors of NF-κB and STAT3, like synthetic triterpenoids. © 2013 Informa Healthcare USA, Inc.

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