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News Article | May 15, 2017
Site: www.prnewswire.com

"The development of a child inside the mother affects that child its entire life, and low birth weight has lifelong health implications for a child," says Mark Steinhoff, MD, corresponding author on the study and director of the Global Health Center at Cincinnati Children's Hospital Medical Center. "The overall positive effect of performing these vaccinations – which is not expensive – is quite significant." Funded by the Bill and Melinda Gates Foundation (grant 50274), the research team focused its study on the subtropical terai plains of southern Nepal in south Asia. This underdeveloped, agrarian region is known for a subsistence lifestyle, high rates of malnutrition and limited access to healthcare, and is representative of many tropical regions where 40 percent of the world's births occur. Researchers traveled to villages in southern Nepal during normal routine health visits by Nepalese members of the team. Participating households were then followed up and surveilled on a weekly basis during home visits. Collaborating on the study were researchers from the Nepal Nutrition Intervention Project and the Tribhuvan University Institute of Medicine, both based in the Nepalese capital of Kathmandu. In households where women between the ages of 15 and 40 were pregnant, volunteer participants were administered either influenza vaccine or placebo as part of a randomized, placebo-controlled Phase 4 clinical trial.  The trial was registered with ClinicalTrials.gov and the protocol was reviewed and approved by the institutional review boards of participating institutions. From April 2011 through September 2013, 3,693 mothers were recruited and randomized into two different annual research groups (or cohorts). In the first cohort of 2,090, 1,040 mothers were given placebo, and 1,049 were administered seasonally recommended trivalent inactivated vaccine (which contains three inactivated flu viruses). In the second cohort of 1,603 mothers, 805 were given placebo and 798 received vaccine. There were a total of 3,646 live births in both groups. The researchers assessed three primary outcomes: the incidence of laboratory confirmed infant influenza from 0-180 days post birth; the incidence of low birth weight; and the incidence of influenza-like illness in mothers 0-180 days following delivery. In cohort 1, compared to the placebo group influenza-like illness was reduced by 9 percent in pre- and post-partum mothers who received vaccine. In cohort 2, flu-like illness was reduced by 36 percent. This placed the average flu reduction rate for both groups of vaccinated mothers at 19 percent. For infants, lab-confirmed flu infections in cohort 1 decreased 16 percent in babies with vaccinated mothers. In cohort 2 they decreased by 60 percent – putting the average rate of reduction for both cohorts at 30 percent. As for birth weight, flu immunizations in pregnant mothers reduced the rate of low birth weight (less than 2,500 grams/5.5 pounds) by 15 percent in cohort 1 and by 15 percent in cohort 2 (average 15 percent for both groups). There were 111 infant deaths during the study – 50 in the placebo group and 51 in the vaccine group; and seven maternal deaths – five in the placebo group and two in the vaccine group. Researchers are following up their current study by gathering additional data to support the expansion of year-round flu vaccination to other regions where it is needed. Steinhoff said this is especially important for developing countries like Nepal and where influenza has a more significant impact on birth weights than in developed nations. An estimated 40 percent of the world's population lives in subtropical/tropical zones, although flu vaccine is not widely used in these areas, according to the authors. The benefits of vaccinating pregnant women is well documented in developed countries. Its use has not been prevalent in underdeveloped subtropical/tropical regions, where many local officials have believed until recently that influenza virus does not even exist. Study authors note that the timing, circulation and type of flu virus are highly variable in subtropical and tropical regions. During the current study in Nepal, the circulation of flu increased during the South Asian Southwest monsoon season in July-October. Active symptomatic flu virus was present among study participants for 24 (or 66 percent) of the study months, with two more strains of virus circulating during 18 of these months. Researchers also pointed out that most of positive effect from flu vaccination was observed in the second study group of mothers and infants. This second group received two different formulations of flu vaccine with a broader range of antigens to account for virus variability in the region. This high variability of influenza virus in the study region (and other subtropical/tropical climates) will require improved vaccines with broader antigenic coverage, the authors report. Other collaborating institutions include: the Johns Hopkins Bloomberg School of Public Health; the University of Washington, School of Medicine; the Milken Institute of Public Health at George Washington University. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/year-round-flu-vaccinations-promote-healthier-infants-in-subtropics-300457594.html


News Article | May 22, 2017
Site: www.prnewswire.com

"We found that when T cells activate and go through extraordinarily rapid cell division during initial immune responses, it leads to an unusual level of genomic stress in the cells," explains Michael B. Jordan, MD, lead author and physician/scientist in the divisions of Bone Marrow Transplantation and Immune Deficiency and Immunobiology. "Because T cells are always in a race with different viruses and bacteria, they have learned how to adapt and divide rapidly to respond, but this stress on their DNA means they also are living right on the edge of death," Jordan says. "In our experiments we selectively interrupted DNA damage repair in rapidly expanding T cells, and we threw them off balance and into a chasm of death." PPCA is a newly minted acronym for "p53 potentiation with checkpoint abrogation." The therapeutic approach was developed by Jordan and his colleagues, including Jonathan Katz, PhD, and David Hildeman, PhD, (Division of Immunobiology). It was conceived during experiments on mouse and donated human immune cells called lymphocytes, which include the aggressively effective germ killers, T cells and B cells. Researchers hypothesized that along with the highly adaptable and proliferative abilities of T cells came an abundance of genomic stress. They observed as T cells used DNA damage response pathways to survive while adapting and gearing up to attack lymphocytic choriomeningitis virus (LCMV) as it tried to infect cells and animal models. A gene and its protein called p53 (also called the "guardian of the genome") helps initiate DNA damage repair – the primary reason researchers decided to target it in T cells. They also leveraged a concept developed for the treatment of cancer called cell cycle checkpoint inhibition or abrogation – in which cells are forced to lose normal control over the mitotic cell division cycle. In selective instances of rapid T cell expansion in mouse models of HLH and experimental autoimmune encephalomyelitis (experimental mouse MS), the researchers used a small molecule called Nutlin to alter the activities of p53. They also inhibited cell cycle checkpoint proteins known as CHK1/2 or WEE1.  This prevented the T cells from pausing and repairing their DNA damage, which prompted them to die off. In mouse models of HLH – mainly a childhood disease where the immune system overheats, attacks healthy tissues, damages organs and causes early death – PPCA reduced disease in the animals and allowed them to survive long-term. The researchers also tested PPCA treatment in mice with experimental autoimmune encephalomyelitis (EAE) used to model multiple sclerosis. In MS, autoimmune-driven inflammation damages a protective insulating sheath on nerves called myelin. This causes disruptions in the central nervous system that disrupt signals between the brain and extremities, which can lead to paralysis and other symptoms. In EAE mouse models of MS, PPCA treatment killed off aggressively expanding T cells, tempered autoimmune processes and either reversed or prevented paralysis in the animals, authors report in their study. Jordan and his research colleagues – including first author Jonathan P. McNally (a recently graduated PhD student in the Immunology graduate program) – caution that their experimental results are early. Years of additional research are needed before knowing whether the current findings will eventually apply to clinical treatment in humans. The authors now plan to test PPCA in laboratory models of other autoimmune disorders to see how widely applicable it might be. Jordan is listed as an inventor of PPCA in a U.S. patent filing through the Center for Technology Commercialization at Cincinnati Children's. Funding support for the research came in part from the National Institutes of Health (RO1DK081175, RO1AI109810, RO1AI057753 and a Research Innovation Grant from Cincinnati Children's. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/experimental-therapy-for-immune-diseases-hits-achilles-heel-of-activated-t-cells-300461369.html


News Article | May 22, 2017
Site: www.eurekalert.org

CINCINNATI - Immune diseases like multiple sclerosis and hemophagocytic lymphohistiocytosis unleash destructive waves of inflammation on the body, causing death or a lifetime of illness and physical impairment. With safe and effective treatments in short supply, scientists report in PNAS Early Edition (Proceeding of the National Academy of Sciences) discovery of an experimental treatment that targets an Achilles heel of activated immune cells - killing them off and stopping autoimmune damage. Researchers at Cincinnati Children's Hospital Medical Center report in a study published the week of May 22 that a treatment modality they call PPCA takes advantage of DNA damage in rapidly expanding T cells, which they show was therapeutically beneficial in mouse models of hemophagocytic lymphohistiocytosis (HLH) and multiple sclerosis (MS). And for the most part it appears to be so without harming other immune system components needed to protect the body from infection. "We found that when T cells activate and go through extraordinarily rapid cell division during initial immune responses, it leads to an unusual level of genomic stress in the cells," explains Michael B. Jordan, MD, lead author and physician/scientist in the divisions of Bone Marrow Transplantation and Immune Deficiency and Immunobiology. "Because T cells are always in a race with different viruses and bacteria, they have learned how to adapt and divide rapidly to respond, but this stress on their DNA means they also are living right on the edge of death," Jordan says. "In our experiments we selectively interrupted DNA damage repair in rapidly expanding T cells, and we threw them off balance and into a chasm of death." PPCA is a newly minted acronym for "p53 potentiation with checkpoint abrogation." The therapeutic approach was developed by Jordan and his colleagues, including Jonathan Katz, PhD, and David Hildeman, PhD, (Division of Immunobiology). It was conceived during experiments on mouse and donated human immune cells called lymphocytes, which include the aggressively effective germ killers, T cells and B cells. Researchers hypothesized that along with the highly adaptable and proliferative abilities of T cells came an abundance of genomic stress. They observed as T cells used DNA damage response pathways to survive while adapting and gearing up to attack lymphocytic choriomeningitis virus (LCMV) as it tried to infect cells and animal models. A gene and its protein called p53 (also called the "guardian of the genome") helps initiate DNA damage repair - the primary reason researchers decided to target it in T cells. They also leveraged a concept developed for the treatment of cancer called cell cycle checkpoint inhibition or abrogation - in which cells are forced to lose normal control over the mitotic cell division cycle. In selective instances of rapid T cell expansion in mouse models of HLH and experimental autoimmune encephalomyelitis (experimental mouse MS), the researchers used a small molecule called Nutlin to alter the activities of p53. They also inhibited cell cycle checkpoint proteins known as CHK1/2 or WEE1. This prevented the T cells from pausing and repairing their DNA damage, which prompted them to die off. In mouse models of HLH - mainly a childhood disease where the immune system overheats, attacks healthy tissues, damages organs and causes early death - PPCA reduced disease in the animals and allowed them to survive long-term. The researchers also tested PPCA treatment in mice with experimental autoimmune encephalomyelitis (EAE) used to model multiple sclerosis. In MS, autoimmune-driven inflammation damages a protective insulating sheath on nerves called myelin. This causes disruptions in the central nervous system that disrupt signals between the brain and extremities, which can lead to paralysis and other symptoms. In EAE mouse models of MS, PPCA treatment killed off aggressively expanding T cells, tempered autoimmune processes and either reversed or prevented paralysis in the animals, authors report in their study. Jordan and his research colleagues - including first author Jonathan P. McNally (a recently graduated PhD student in the Immunology graduate program) - caution that their experimental results are early. Years of additional research are needed before knowing whether the current findings will eventually apply to clinical treatment in humans. The authors now plan to test PPCA in laboratory models of other autoimmune disorders to see how widely applicable it might be. Jordan is listed as an inventor of PPCA in a U.S. patent filing through the Center for Technology Commercialization at Cincinnati Children's. Funding support for the research came in part from the National Institutes of Health (RO1DK081175, RO1AI109810, RO1AI057753 and a Research Innovation Grant from Cincinnati Children's.


News Article | May 31, 2017
Site: www.prnewswire.com

Functional magnetic resonance imaging (fMRI) found significantly greater brain activation in 4-year-old children who were more highly engaged during story listening, suggesting a novel improvement mechanism of engagement and understanding. The study reinforces the value of "dialogic reading," where the child is encouraged to actively participate. "The takeaway for parents in this study is that they should engage more when reading with their child, ask questions, have them turn the page, and interact with each other," said John Hutton, MD, a pediatrician at Cincinnati Children's and lead author of the study. "In turn, this could fuel brain activation--or "turbocharge" the development of literacy skills, particularly comprehension, in preschool aged children." The study involved functional MRI scans of 22 girls, age 4, to explore the relationship between engagement and verbal interactivity during a mother-child reading observation and neural activation and connectivity during a story listening task. Children exhibiting greater interest in the narrative showed increased activation in right-sided cerebellar areas of the brain, thought to support cognitive skill acquisition and refinement via connection to language, association and executive function areas. "Our findings underscore the importance of interventions explicitly addressing both parent and child reading engagement, including awareness and reduction of distractions such as cellphones, which were the most common preventable barrier that we observed," said Hutton. Hutton says long-term studies are needed beginning in infancy to better understand mother-child factors contributing to healthy brain development and literacy skills, as this current study does not establish causation. Dr. Hutton is a clinical researcher in the Division of General and Community Pediatrics and the Reading and Literacy Discovery Center at Cincinnati Children's. Support for this study was provided by a grant (1R01HD066115-01A1) from the Eunice Kennedy Shriver National Institute for Child Health and Human Development. Support for neuroimaging, reading observations and related analyses were provided via a Ruth L Kirschstein National Research Service Award and an Academic Pediatric Association Young Investigator Award for Primary Care Strategies for the Promotion of Early Literacy and School Readiness Supported by Reach Out and Read. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/storytime-a-turbocharger-for-a-childs-brain-300466388.html


News Article | June 1, 2017
Site: www.eurekalert.org

CINCINNATI - A detour on the road to regenerative medicine for people with muscular disorders is figuring out how to coax muscle stem cells to fuse together and form functioning skeletal muscle tissues. A study published June 1 by Nature Communications reports scientists identify a new gene essential to this process, shedding new light on possible new therapeutic strategies. Led by researchers at the Cincinnati Children's Hospital Medical Center Heart Institute, the study demonstrates the gene Gm7325 and its protein - which the scientists named "myomerger" - prompt muscle stem cells to fuse and develop skeletal muscles the body needs to move and survive. They also show that myomerger works with another gene, Tmem8c, and its associated protein "myomaker" to fuse cells that normally would not. In laboratory tests on embryonic mice engineered to not express myomerger in skeletal muscle, the animals did not develop enough muscle fiber to live. "These findings stimulate new avenues for cell therapy approaches for regenerative medicine," said Douglas Millay, PhD, study senior investigator and a scientist in the Division of Molecular Cardiovascular Biology at Cincinnati Children's. "This includes the potential for cells expressing myomaker and myomerger to be loaded with therapeutic material and then fused to diseased tissue. An example would be muscular dystrophy, which is a devastating genetic muscle disease. The fusion technology possibly could be harnessed to provide muscle cells with a normal copy of the missing gene." One of the molecular mysteries hindering development of regenerative therapy for muscles is uncovering the precise genetic and molecular processes that cause skeletal muscle stem cells (called myoblasts) to fuse and form the striated muscle fibers that allow movement. Millay and his colleagues are identifying, deconstructing and analyzing these processes to search for new therapeutic clues. Genetic degenerative disorders of the muscle number in the dozens, but are rare in the overall population, according to the National Institutes of Health. The major categories of these devastating wasting diseases include: muscular dystrophy, congenital myopathy and metabolic myopathy. Muscular dystrophies are a group of more than 30 genetic diseases characterized by progressive weakness and degeneration of the skeletal muscles that control movement. The most common form is Duchenne MD. A previous study authored by Millay in 2014 identified myomaker and its gene through bioinformatic analysis. Myomaker is also required for myoblast stem cells to fuse. However, it was clear from that work that myomaker did not work alone and needed a partner to drive the fusion process. The current study indicates that myomerger is the missing link for fusion, and that both genes are absolutely required for fusion to occur, according to the researchers. To find additional genes that regulate fusion, Millay's team screened for those activated by expression of a protein called MyoD, which is the primary initiator of the all the genes that make muscle. The team focused on the top 100 genes induced by MyoD (including GM7325/myomerger) and designed a screen to test the factors that could function within and across cell membranes. They also looked for genes not previously studied for having a role in fusing muscle stem cells. These analyses eventually pointed to a previously uncharacterized gene listed in the database - Gm7325. Researchers then tested cell cultures and mouse models by using a gene editing process called CRISPR-Cas9 to demonstrate how the presence or absence of myomaker and myomerger - both individually and in unison - affect cell fusion and muscle formation. These tests indicate that myomerger-deficient muscle cells called myocytes differentiate and form the contractile unit of muscle (sarcomeres), but they do not join together to form fully functioning muscle tissue. The researchers are building on their current findings, which they say establishes a system for reconstituting cell fusion in mammalian cells, a feat not yet achieved by biomedical science. For example, beyond the cell fusion effects of myomaker and myomerger, it isn't known how myomaker or myomerger induce cell membrane fusion. Knowing these details would be crucial to developing potential therapeutic strategies in the future, according to Millay. This study identifies myomerger as a fundmentally required protein for muscle development using cell culture and laboratory mouse models. The authors emphasize that extensive additional research will be required to determine if these results can be translated to a clinical setting. Multiple authors with the Cincinnati Children's Heart Institute contributed to this study, including the listed first author Malgorzata Quinn, PhD. A complete list is included in the study abstract. Funding support came from the Cincinnati Children's Hospital Research Foundation, the National Institutes of Health (R01AR068286), and the Pew Charitable Trusts.


News Article | February 22, 2017
Site: www.eurekalert.org

CINCINNATI - Scientists propose in Nature blocking a molecule that drives inflammation and organ damage in Gaucher and maybe other lysosomal storage diseases as a possible treatment with fewer risks and lower costs than current therapies. An international research team led by Cincinnati Children's Hospital Medical Center, which also included investigators from the University of Lübeck in Germany, report their data Feb. 22. The study was conducted in mouse models of lysosomal storage disease and in cells from blood samples donated by people with Gaucher disease. Current treatments for Gaucher and other lysosomal storage diseases (LSDs) include enzyme replacement therapy or substrate reduction therapy. These break down or prevent the accumulation of certain fatty molecules and other waste particles that clog cells to cause inflammation, cell and organ damage and, in some cases, death. People with LSDs lack enzymes that break down used-up proteins and other spent particles, preventing their cells from shedding these waste materials and functioning normally. Individually, the 50 genetic diseases characterized as LSDs are considered rare. But collectively they have a frequency of one in 8,000 births, making LSDs a major challenge for the health care system, according to information from the National Institutes of Health. Study authors stress there is a need for new therapies. "Current enzyme replacement and substrate reduction therapies are expensive and still associated with inflammation, increased risk of malignancies and Parkinson's disease," says Manoj Pandey, PhD, study first author and a scientist in the Division of Human Genetics at Cincinnati Children's. "We suggest that targeting a molecule called C5aR1 may serve as a viable treatment option for patients with Gaucher disease and possibly other LSDs." Pandey is co-corresponding author on the paper along with Jörg Köhl, MD, director of the Institute for Systemic Inflammation Research at the University of Lübeck, and adjunct professor in the Division of Immunobiology at Cincinnati Children's. In laboratory mouse models and human cells, researchers show that C5aR1 is a critical part of a molecular pathway that drives pro-inflammatory processes in Gaucher disease, which is initiated by mutations of a gene known as GBA1. GBA1 encodes the lysosomal enzyme glucocerebrosidase (GCase), which degrades the fatty molecule glucosylceramide (GC). C5aR1 is a receptor for a small peptide (a protein component) that is derived from the complement system (part of the immune system) called C5a, which drives inflammation in several different types of immune cells. The disease process starts by GBA1 mutation driving extensive accumulation of glucosylceramide in immune cells. Before the current study, the molecular process that connects glucosylceramide accumulation to inflammation was unknown, as was the role of inflammation in disease development. Pandey and colleagues show inflammatory glucosylceramide accumulation in spleen, liver, lung and bone marrow immune cells in Gaucher mouse models drives the induction of auto-antibodies against glucosylceramide, which form immune complexes. These immune complexes promote the production of C5a and activation of its receptor C5aR1. In organ tissues from disease mouse models, the researchers found evidence of abundant and active C5aR1, which fuels glucosylceramide accumulation through its control of an enzyme that produces the fatty molecule. According to the authors, C5aR1 activation is what tips the balance between glucosylceramide formation and its degradation. The researchers also found similar evidence of C5aR1 and related pro-inflammatory molecules in cells from the donated blood samples of Gaucher patients. Based on evidence of C5aR1's involvement in the Gaucher disease process, the researchers decided to test targeting the molecule pharmacologically in laboratory mouse models. Taking advantage of a C5aR antagonist (C5aRA) developed by Köhl (patent owned by Cincinnati Children's), the scientists injected C5aRA into the peritoneal cavities of mice. The infiltration of pro-inflammatory immune cells (macrophages) was substantially reduced in the lungs, livers and spleens of mice, and glucosylceramide accumulation was almost completely abolished, as was overall disease burden, the authors report. Because the current project was conducted in mouse models and human blood cells, Pandey and his colleagues stress that additional study is needed before determining whether targeting C5aR1 would be effective and safe enough to test in human patients. Pandey said researchers will continue testing the C5aRA molecule used in the mouse study (which is effective in targeting human and mouse C5aR). They also will test a commercially available anti-C5 monoclonal antibody called eculizumab, which is produced by Alexion Pharmaceuticals (which helped fund the current study). This will allow the researchers to test these compounds as a novel adjunctive therapeutic approach for human patients with Gaucher, and as a possible therapy for other lysosomal storage diseases. Funding support for the study came from Division of Human Genetics at Cincinnati Children's, the German Research Foundation (EXC 306/2, CL XII, IRTG 1911) and the Alexion Rare Disease Innovation Fund (31-91910-584000).


News Article | February 16, 2017
Site: www.eurekalert.org

CINCINNATI - Genomic testing of biopsies from patients with deadly, treatment-resistant cancerous blood syndromes called histiocytoses allowed doctors to identify genes fueling the ailments and use targeted molecular drugs to successfully treat them. Researchers from the Cincinnati Children's Cancer and Blood Diseases Institute report their data in Journal of Clinical Investigation Insight (JCI Insight). They recommend the regular use of comprehensive genomic profiling at diagnosis to positively impact clinical care, as well as rigorous clinical trials to verify and extend the diagnostic and treatment conclusions in their study. Histiocytoses are a group of disorders in which abnormal accumulations of white blood cells form tumors on vital organs, leading to systemic organ damage or death. About half of the patients can be treated successfully with chemotherapy, but others are treatment resistant. Study authors conducted genomic profiling of biopsies from 72 child and adult patients with a variety of treatment-resistant histiocytoses, including the most common one in children, Langerhans cell histiocytosis (LCH), according to the lead investigator, Ashish Kumar, MD, PhD. Twenty-six patients with treatment-resistant disease had gene mutations involving either BRAF or MAP2K1 that directly activate the MAP-kinase cancer pathway. Researchers determined such patients would benefit from the targeted molecular therapies dabrafenib or trametinib, which block the MAP kinase pathway. The approved cancer drugs were prescribed off label to the histiocytosis patients. "In the last year, three patients we treated were infants with disease that was resistant to several rounds of intense chemotherapy. In the past, these children either would have suffered serious complications including death or would have had to endure more intensive treatments and the ensuing toxicities, including the risk of death," Kumar said. "All three are thriving now on one oral medication that put their disease into remission." In their JCI Insight paper, the researchers also offer detailed case summaries involving four histiocytosis patients between the ages of 9 months and 36 years. In one case a 22-month-old child was referred to Cincinnati Children's for treatment-resistant LCH that was complicated by a secondary diagnosis of HLH (hemophagocytic lymphohistiocytosis). HLH is a difficult-to-treat and often-fatal autoimmune disorder in which an overheated immune system causes uncontrolled inflammation and organ damage. The little girl, whose condition was worsening with organ failure, had a mutation in the BRAF gene. Two days after starting targeted treatment with oral dabrafenib (which blocks the MAP-kinase pathway) the little girl's fever disappeared and a week later her organ function returned to normal, according to study authors. For their JCI Insight research project, in addition to their own laboratory tests, study authors drew from data in previous research papers by a number of institutions, which examined genetic and molecular processes affecting white blood cell expansion in different types of histiocytosis. As Kumar and his colleagues continue their research, they plan to test methodologies that could expand the use of genomic profiling of patient biopsies and targeted molecular therapies in more patients with recurrent, treatment-resistant disease. "It's important for physicians and patients to know that LCH and other forms of histiocytosis are not that mysterious anymore," Kumar said. "We now have new treatments that dramatically improve outcomes for these patients." The JCI Insight study is a collaborative effort of investigators in several divisions at Cincinnati Children's, including first author and oncologist Lynn H. Lee, MD. Kumar is a member of the Division of Bone Marrow Transplant and Immune Deficiency and director of the Langerhans Cell Histiocytosis Center at Cincinnati Children's. Funding support for the research came from the National Heart, Lung, and Blood Institute (R01-HL111192) and the Leukemia and Lymphoma Society (TRP-6076-14).


News Article | February 16, 2017
Site: globenewswire.com

CINCINNATI, Feb. 16, 2017 (GLOBE NEWSWIRE) -- The Hyatt Regency Cincinnati announced that Phase Two of its multi-million dollar renovation has commenced, making it the newest full-service, renovated hotel in Cincinnati. Perched in the heart of downtown, The Hyatt Regency Cincinnati sits across the street from the Duke Energy Convention Center, close to many of Cincinnati's largest employers, and a short walk to Over-the-Rhine (OTR), The Banks and the Riverfront Sports Complex, home of the Cincinnati Bengals and Cincinnati Reds stadiums. The hotel includes over 40,000 square feet of versatile meeting space, including the largest hotel ballroom in the city, the Red Roost Tavern, The Market (proudly serving Starbucks® Coffee), a 24-hour full service fitness facility, and an indoor heated saline pool – the first in downtown Cincinnati. www.cincinnati.hyatt.com completed Phase One of their renovation in the summer of 2013 that included all public and meeting spaces (now equipped with electronic reader boards), the restaurant, market, guest room carpet, vinyl, and curtains. New artwork was added throughout the hotel, many of which are Cincinnati inspired themes. Hyatt's complimentary 24-hour StayFit™ gym features the latest high-tech cardio and strength-training equipment, complete with flat-screen televisions from industry leader, Life Fitness®. Every one of the hotel's 491 guest rooms are being refurbished and updated to include crisp white stone finish vanities and desk tops with contemporary gray earth tone furniture, spacious desks, blue tooth docking iHome® clock radios, bedside lighting and will feature the new Hyatt Grand Bed II. The renovation also includes all guest room baths, which are being revitalized with new tile, fixtures, counters, and lights. Recharge after a long day with multiple electrical outlets conveniently located for today's discerning traveler. Included are wall mounted swivel HD televisions. Complimentary phone chargers are available upon request. In addition, the hotel will be converting twelve hospitality suites to studio suites to better meet the needs of guests who need a more functional space during their stay. Many rooms boast stunning river or city views. Meeting planners will enjoy the new features offered with this update, including the new bandwidth control and monitoring platform in the 40,000 square feet of meeting space that is housed in redundant data centers featuring: For more information about The Hyatt Regency Cincinnati, visit www.cincinnati.hyatt.com. Photos accompanying this release are available at:


News Article | February 16, 2017
Site: www.prnewswire.com

CINCINNATI, Feb. 16, 2017 /PRNewswire-USNewswire/ -- Genomic testing of biopsies from patients with deadly, treatment-resistant cancerous blood syndromes called histiocytoses allowed doctors to identify genes fueling the ailments and use targeted molecular drugs to successfully treat...


CINCINNATI, Feb. 16, 2017 /PRNewswire/ -- Home Care Assistance of Cincinnati, the leading provider of in-home care for seniors, announced today that the company received the distinguished Best of Home Care Leader in Excellence Award from Home Care Pulse, the leading firm in quality...

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