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News Article | February 28, 2017
Site: www.eurekalert.org

COLUMBIA, Mo. (Feb. 28, 2017) -- Hepatocellular carcinoma is the most common form of liver cancer, but treatment options are limited and many patients are diagnosed in late stages when the disease can't be treated. Now, University of Missouri School of Medicine researchers have developed a new treatment that combines chemotherapy and immunotherapy to significantly slow tumor growth in mice. The researchers believe that with more research, the strategy could be translated to benefit patients with the disease. "The current drug approved by the U.S. Food and Drug Administration to treat hepatocellular carcinoma only increases the average survival of patients by about three months," said Kevin Staveley-O'Carroll, M.D., Ph.D., chair of the MU School of Medicine's Hugh E. Stephenson Jr., M.D., Department of Surgery and director of Ellis Fischel Cancer Center. "While any extension of life is valuable, our research team is developing a new therapeutic strategy that might extend and improve the quality of life for these patients." Immunotherapy boosts the body's natural defenses to fight off cancer. The therapy has been used to help treat several cancers, such as melanoma and lung cancer. However, little research exists on combining immunotherapy with chemotherapy. During the study, one group of mice was treated with the chemotherapy agent sunitinib and another group was treated with an immunotherapy antibody known as anti-PD-1. Over a period of four weeks, tumors in mice treated with sunitinib grew 25 times larger. Tumors in mice treated with immunotherapy grew at a slower rate and were 15 times larger. However, a third group of mice treated with a combination of chemotherapy and immunotherapy experienced even slower tumor growth at a size that was only 11 times larger. "Our results show that a combined chemo-immunotherapeutic approach can slow tumor growth in mice more effectively than either individual treatment," said Guangfu Li, Ph.D., D.V.M., assistant professor in the MU Department of Surgery. "This innovative combination promotes an anti-tumor immune response and better suppresses growth of the cancer. Our findings support the need for a clinical trial to test whether this could become a cost-effective treatment that could help improve the lives of patients with liver cancer." The study, "Successful Chemo-immunotherapy against Hepatocellular Cancer in a Novel Murine Model," was published in the January issue of the Journal of Hepatology. Research reported in this publication was supported by the National Cancer Institute of the National Institutes of Health (1 R01 CA164335-01A1 and R01-CA-025000) and the National Institute of Diabetes and Digestive Kidney Diseases of the National Institutes of Health (R01DK 057830). The researchers have no conflicts of interest to declare related to this study. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funding agencies.


News Article | February 15, 2017
Site: www.eurekalert.org

A $6.1 million, five-year grant from the National Institute of Diabetes, Digestive and Kidney Diseases at the National Institutes of Health may help researchers leverage massive amounts of genomic data to develop medical treatments and pharmaceuticals, according to an international team of researchers. The project -- called VISION or Validated Systematic Integration of Hematopoietic Epigenomes -- will integrate and functionally validate large amounts of emerging genomic and epigenetic data, according to Ross Hardison, T. Ming Chu Professor of Biochemistry and Molecular Biology, Penn State and a member of the Genome Sciences Institute of the Huck Institutes of the Life Sciences. Hardison, who will lead the international multidisciplinary team, added that the group will try to develop new tools for using data to facilitate advances both in basic research as well as medical applications, such as precision medicine. The project will focus on blood cell development as a model system for gene regulation in mammals. Blood cell development is vitally important to health because humans must continually replace old and damaged cells, and because many diseases, like leukemias and anemias, result from mis-regulation of gene expression during blood formation. "We are excited about this project because the methods we are developing can be applied not only to diseases that affect blood, but others as well," Hardison said. "A person's genetic profile can have a significant impact on disease susceptibility and response to specific treatments. However, the critical genetic variants that make up that genetic profile most often do not code for protein, but rather they are located in the much larger noncoding genome. We are studying these noncoding regions and finding new ways to extract valuable information about functional elements within them, which in turn informs us about how genetic variants play a role in disease." The results of the VISION project are being provided to the research community in readily accessible, web-based platforms and online tools that will allow researchers to extract meaningful, experimentally validated interpretations from the data and produce a guide for investigators to translate insights from mouse models to human clinical studies. Hardison is working with Cheryl Keller, project manager, Yu Zhang, associate professor of statistics, and Feng Yue, assistant professor of biochemistry and molecular biology, College of Medicine, all at Penn State; Mitchell Weiss, chair of the department of hematology, St. Jude Children's Research Hospital; Gerd Blobel, Professor of Pediactrics, University of Pennsylvania abd Children's Hospital of Philadelphia; James Taylor, associate professor of biology and associate professor of computer science, Johns Hopkins University; David Bodine, chief and senior investigator, National Human Genome Research Institute, NIH; Berthold Göttgens, principal investigator and professor of haematology, Cambridge Stem Cell Institute, University of Cambridge; Douglas Higgs, group head and principal investigator, and Jim Hughes, associate professor of genome biology, both of the Weatherall Institute of Molecular Medicine, Oxford University.


DUBLIN--(BUSINESS WIRE)--Research and Markets has announced the addition of the "Global Endoscopy Devices Market (2016-2022)" report to their offering. Endoscopy is the close examination of internal organs and vessels of the human body, which is used to inspect a person's digestive tract. It helps to suspect if an organ or precise area of the body is damaged, infected or cancerous. There are many types of endoscopic devices for detecting different types of diseases. One such device is Gastrointestinal Endoscopic Devices, used to inspect any infection or abnormalities in the function of the gastrointestinal tract. Other devices include endoscopes, visualization systems and operative devices. Factors affecting the growth of the market are the rise in the digestive and gastric diseases, affordable endoscopy device, and advancement in endoscopy technology. According to National Institute of Diabetes & Digestive and Kidney Diseases, 60 to 70 million people are affected by different digestive diseases. Based on region, Endoscopy Devices market is segmented into North America (US, Canada, Mexico and Rest of North America), Europe (Germany, UK, France, Russia, Spain, Italy and Rest of Europe), Asia-Pacific (China, Japan, India, South Korea, Singapore, Malaysia and Rest of Asia-Pacific) and Latin America, and Middle East & Africa. North America remained the dominant region in the global Endoscopy Devices market in 2015. Asia-Pacific would witness promising CAGR during the forecast period (2016-2022). For more information about this report visit http://www.researchandmarkets.com/research/vkg7xz/global_endoscopy.


News Article | December 2, 2016
Site: www.eurekalert.org

ANN ARBOR, Mich. - According to an annual data report from the United States Renal Data System (USRDS), hospitalization and mortality rates for patients with chronic kidney disease continue to decline in the U.S. Along with those rates, the report highlights several current trends in kidney disease in the U.S., including Medicare spending in the patient population and number of kidney transplants. This year's report provides data from 2014 and is released by the USRDS coordinating center based at the University of Michigan Kidney Epidemiology and Cost Center, in partnership with Arbor Research Collaborative for Health. The report states that hospitalization rates among end-stage kidney disease patients decreased to 1.7 admissions per patient per year, as compared to 2.1 in 2005, or a reduction of 19 percent. End-stage kidney disease is the last stage of chronic kidney disease when the kidneys can no longer remove waste and excess water from the body, and dialysis or kidney transplantation is necessary for survival. In addition, mortality rates continue to decrease for dialysis and transplant patients, falling by 32 percent and 44 percent, respectively, since 1996. "Most recent estimates indicate 14.8 percent of U.S. adults have chronic kidney disease," says Rajiv Saran, M.D., professor of internal medicine at the University of Michigan and director of the USRDS coordinating center. "Fortunately, we've seen steeper declines in mortality rates in more recent years in this patient population, which is promising." "An interesting note on kidney transplants is a relatively recent initiative called kidney paired donation," Saran says. "The initiative is aimed at increasing the availability of living donor transplants, and in its simplest form is essentially when two living donors do not match with the respective recipients and decide to perform an exchange whereby the donation goes to each other's compatible recipient. Kidney paired donation transplants have risen sharply in recent years with 552 performed in 2014, representing 10 percent of living donor transplants that year." According to Saran, earlier diagnosis and treatment of chronic kidney disease can improve patient outcomes. "As newly reported cases of end-stage kidney disease continue to happen each year, physicians and patients need to have continued dialogue about the disease and how best to manage it," Saran says. "We hope this report provides fellow clinicians and researchers with valuable information they can use when discussing the disease with their patients and colleagues." Authors: In addition to Saran, the report's U-M authors include Bruce Robinson, M.D., Vahakn Shahinian, M.D., John Ayanian, M.D., Jennifer Bragg-Gresham, Ph.D., Debbie Gipson, M.D., Yun Han, M.S., Kevin He, Ph.D., William Herman, M.D., Michael Heung, M.D., Richard A. Hirth, Ph.D., David Hutton, Ph.D., Yi Li, Ph.D., Yee Lu, M.D., Hal Morgenstern, Ph.D., Brahmajee Nallamothu, M.D., Brett Plattner, M.D., Ronald Pisoni, Ph.D., Panduranga Rao, M.D., Douglas E. Schaubel, Ph.D., David T. Selewski, M.D., Peter Song, Ph.D., and Kenneth J. Woodside, M.D. Funding: Funding for the project came from the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, and the U.S. Department of Health and Human Services, under contract HHSN276201400001C, and the USRDS Coordinating Center Team, which consists of investigators and staff from the University of Michigan Health System, the Kidney Epidemiology and Cost Center, in partnership with Arbor Research Collaborative for Health. Disclosures: Dr. Hal Morgenstern is a consultant at Arbor Research Collaborative for Health. Dr. Jennifer Bragg-Gresham is a consultant with IMPAQ, and with Medical Education Institute (MEI) involving quality of life performance measures. Reference: United States Renal Data System. 2016 USRDS annual data report: Epidemiology of kidney disease in the United States. National Institutes of Health. National Institute of Diabetes and Digestive and Kidney Disease, Bethesda, MD, 2016. http://www. .


Strachinariu R.T.,National Institute of Diabetes
Romanian Journal of Diabetes, Nutrition and Metabolic Diseases | Year: 2013

There is a worldwide epidemic increase in the number of type 2 diabetes (T2DM) patients who frequently associate with cardiovascular disease (CVD). There are data suggesting that glycemic control does not substantially reduce CVD risk but hyperglycemia increases the risk of CVD. This apparent paradox could be explained by the role of post-prandial hyperglycemia in the pathogenesis of cardiovascular complications in T2DM. There is numerous evidences, both experimental and clinical, for this association but controversies on this topic persist. The aim of this paper was to review the current literature regarding the role of postprandial glucose in the genesis of CVD in T2DM. © 2013 ILEX PUBLISHING HOUSE, Bucharest, Roumania.


Gagniuc P.,University of Bucharest | Ionescu-Tirgoviste C.,National Institute of Diabetes
BMC Genomics | Year: 2013

Background: Gene promoters have guided evolution processes for millions of years. It seems that they were the main engine responsible for the integration of different mutations favorable for the environmental conditions. In cooperation with different transcription factors and other biochemical components, these regulatory regions dictate the synthesis frequency of RNA molecules. Predominantly in the last decade, it has become clear that nuclear organization impacts upon gene regulation. To fully understand the connections between Homo sapiens chromosomes and their gene promoters, we analyzed 1200 promoter sequences using our Kappa Index of Coincidence method.Results: In order to measure the structural similarity of gene promoters, we used two-dimensional image-based patterns obtained through Kappa Index of Coincidence (Kappa IC) and (C+G)% values. The center of weight of each promoter pattern indicated a structure similarity between promoters of each chromosome. Furthermore, the proximity of chromosomes seems to be in accordance to the structural similarity of their gene promoters. The arrangement of chromosomes according to Kappa IC values of promoters, shows a striking symmetry between the chromosome length and the structure of promoters located on them. High Kappa IC and (C+G)% values of gene promoters were also directly associated with the most frequent genetic diseases. Taking into consideration these observations, a general hypothesis for the evolutionary dynamics of the genome has been proposed. In this hypothesis, heterochromatin and euchromatin domains exchange DNA sequences according to a difference in the rate of Slipped Strand Mispairing and point mutations.Conclusions: In this paper we showed that gene promoters appear to be specific to each chromosome. Furthermore, the proximity between chromosomes seems to be in accordance to the structural similarity of their gene promoters. Our findings are based on comprehensive data from Transcriptional Regulatory Element Database and a new computer model whose core is using Kappa index of coincidence. © 2013 Gagniuc and Ionescu-Tirgoviste; licensee BioMed Central Ltd.


Perciun R.,National Institute of Diabetes
Medical ultrasonography | Year: 2010

The aim of the study was to evaluate by ultrasonography the local dystrophies caused by insulin subcutaneous injections. The insulin treated diabetic patients must inject their long life insulin into normal tissue. The objective was to add ultrasonographic arguments to the clinic examination in order to periodically reconsider the available area to be used. Forty insulin treated patients (14 male, 26 female) were clinically diagnosed with hypertrophic, atrophic, nodular, or inflammatory-like tissue dystrophies as a consequence of injections. These local dystrophies are not always conspicuous, barely suggesting a subdermal pathology. US evaluation, mainly subcutis, was used for assessing them. Besides the clinical signs, ultrasonography offers some distinct appearances: a simple subcutis hypertrophy, a variety of nodular-shaped or diffuse hyperechogenity, subcutis atrophy, complex multilayer changes or possible inflammatory reactions. These abnormal entities have led to erratic insulin absorption and glucose control deterioration, if the patients have continued to inject into the same areas. Ultrasound interrogation should be used as a non-invasive measure for diagnosing insulin injections local dystrophies. Once diagnosed, their future evolution should be observed. By making a real ultrasonographic map of the injected areas a functional insulin treatment could be obtained and preserved.


Gagniuc P.,University of Bucharest | Ionescu-Tirgoviste C.,National Institute of Diabetes
BMC Genomics | Year: 2012

Background: The main function of gene promoters appears to be the integration of different gene products in their biological pathways in order to maintain homeostasis. Generally, promoters have been classified in two major classes, namely TATA and CpG. Nevertheless, many genes using the same combinatorial formation of transcription factors have different gene expression patterns. Accordingly, we tried to ask ourselves some fundamental questions: Why certain genes have an overall predisposition for higher gene expression levels than others? What causes such a predisposition? Is there a structural relationship of these sequences in different tissues? Is there a strong phylogenetic relationship between promoters of closely related species?Results: In order to gain valuable insights into different promoter regions, we obtained a series of image-based patterns which allowed us to identify 10 generic classes of promoters. A comprehensive analysis was undertaken for promoter sequences from Arabidopsis thaliana, Drosophila melanogaster, Homo sapiens and Oryza sativa, and a more extensive analysis of tissue-specific promoters in humans. We observed a clear preference for these species to use certain classes of promoters for specific biological processes. Moreover, in humans, we found that different tissues use distinct classes of promoters, reflecting an emerging promoter network. Depending on the tissue type, comparisons made between these classes of promoters reveal a complementarity between their patterns whereas some other classes of promoters have been observed to occur in competition. Furthermore, we also noticed the existence of some transitional states between these classes of promoters that may explain certain evolutionary mechanisms, which suggest a possible predisposition for specific levels of gene expression and perhaps for a different number of factors responsible for triggering gene expression. Our conclusions are based on comprehensive data from three different databases and a new computer model whose core is using Kappa index of coincidence.Conclusions: To fully understand the connections between gene promoters and gene expression, we analyzed thousands of promoter sequences using our Kappa Index of Coincidence method and a specialized Optical Character Recognition (OCR) neural network. Under our criteria, 10 classes of promoters were detected. In addition, the existence of " transitional" promoters suggests that there is an evolutionary weighted continuum between classes, depending perhaps upon changes in their gene products. © 2012 Gagniuc and Ionescu-Tirgoviste; licensee BioMed Central Ltd.


Manea S.-A.,Institute Of Cellular Biology And Pathology N Simionescu | Robciuc A.,Institute Of Cellular Biology And Pathology N Simionescu | Guja C.,National Institute of Diabetes | Heltianu C.,Institute Of Cellular Biology And Pathology N Simionescu
Biochemical and Biophysical Research Communications | Year: 2011

The study aim was to investigate NOS3 VNTR, NOS3 G894T, EDN1 C8002T, ACE I/D, AGT M235T and AGTR1 A1166C in nonobese and obese T2DM patients, and their interaction with the incidence of microangiopathy. T2DM subjects (n= 250; 166 nonobese, and 84 obese) were genotyped for the gene variants by PCR/RFLP. The interaction of these polymorphisms with obesity and their contribution to microangiopathy were analyzed by multivariate regression analysis. A higher frequency of NOS3 4a allele was found in obese (P= 0.027) vs. nonobese subjects. ACE D (P= 0.009) and AGT 235T (P= 0.026) alleles were associated with the reduced risk of diabetic nephropathy in nonobese and obese patients, respectively. In obese subjects, NOS3 4a (P= 0.011) had a converse effect to NOS3 894T (P= 0.043), and EDN1 8002T (P= 0.035) on the prevalence of combined microangiopathy (neuropathy/retinopathy/nephropathy) vs. microangiopathy-negative subjects. The study indicates association of RAS variants with obesity and nephropathy, and an opposite effect of NOS3 VNTR and NOS3 G894T on the occurrence of combined microangiopathy. © 2011 Elsevier Inc.


News Article | November 2, 2016
Site: www.eurekalert.org

Baltimore, MD-- New work led by Carnegie's Steven Farber sheds light on how form follows function for intestinal cells responding to high-fat foods that are rich in cholesterol and triglycerides. Their findings are published in the Journal of Biological Chemistry. Enterocytes are specialized cells that line the insides of our intestines. The intestinal surface is like a toothbrush, with lots of grooves and protrusions that allow the cells there to grab and absorb nutrients from food as it is digested, including the lipid molecules from fatty foods. The cells absorb, process, and package these lipids for distribution throughout our bodies. Clearly they are very important for sustaining good health and keeping us alive, since lipids are necessary for many of the body's functions, including nutrient absorption and hormone production. "When we eat fatty foods, our body's response is coordinated between our digestive organs, our nervous system, and the microbes living in our gut," explained Farber. "Our research used zebrafish to focus on one aspect of this system--how the enterocyte cells inside our intestines respond to a high-fat meal." It turns out that fatty foods cause enterocyte cells to do some interior remodeling. Cells are like tiny factories, where different functions are carried out by highly specialized structures called organelles. In enterocytes, several of these organelles undergo changes in their shape in response to an influx of fats from rich foods. One such shape shift occurs in the nucleus, where the cell's DNA is stored. Farber's team demonstrated that the nucleus takes on a rapid and reversible ruffled appearance after fatty foods are consumed. This is of interest because a cell's genetic material is housed in the nucleus, and this is the location where different genes get turned on and off in response to external stimuli, such as the presence of lipids from fatty foods. So the team examined this issue further and found that the shape shifting in the nucleus coincides with the activation of certain genes that regulate the intestinal cell's ability to package and distribute the lipids to other parts of the body. The team was able to determine that this activation process occurs within an hour of eating high-fat foods. "Our working hypothesis is that the whole response to fat in the enterocyte--the remodeling and gene activation--may be coordinated by an organelle called the endoplasmic reticulum," said lead author Erin Zeituni. If the cell is a factory, then the endoplasmic reticulum it is the assembly line, where various cellular products are synthesized, stored, and packaged for distribution outside of the cell. It is constructed of a series of interconnected tube-like shapes. When the research team used pharmaceuticals to inhibit one function of the endoplasmic reticulum (the building of so-called lipoprotein particles that will export fats out of the cell), the gene activation process was inhibited for many key genes and nuclear ruffling was also altered. This demonstrated that the flux of fat in the endoplasmic reticulum is crucial for initiating the intestinal response to a fatty meal. "So much of the process by which enterocytes prepare and package fats for distribution to the circulatory and lymphatic system is poorly understood," Farber said. "These findings should help increase our understanding of the basic molecular and cellular biology of intestinal cells." This work was supported by the National Institute of Diabetes and Digestive and Kidney, National Institute of General Medicine, and the Zebrafish Functional Genomics Consortium. The Carnegie Institution for Science is a private, nonprofit organization headquartered in Washington, D.C., with six research departments throughout the U.S. Since its founding in 1902, the Carnegie Institution has been a pioneering force in basic scientific research. Carnegie scientists are leaders in plant biology, developmental biology, astronomy, materials science, global ecology, and Earth and planetary science.

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