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"Murray, Joseph"
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Coronary artery disease is associated with an altered gut microbiome composition
Alteration of gut microbiome composition has been linked to cardiovascular diseases. To identify specific bacterial communities associated with coronary artery diseases (CAD), we conducted a case-control study with 53 advanced CAD patients and 53 age-, sex-, race-, and BMI-matched controls. V3-V5 regions of the 16S rDNA from the fecal gut material were analyzed to compare the gut microbiome composition between CAD patients and controls. The alpha diversity, including Chao-1, Shannon-index, and the number of observed taxonomy units were significantly decreased in CAD patients indicating, decreased richness and evenness of gut microbiome. Among 23 different abundant taxa at the genus level, 12 taxa belonged to Lachnospiraceae family, which are known to produce butyrate. Further, we identified five taxa which showed more than two log-fold changes with maximum proportion >0.002, including Ruminococcus gnavus, Lachnospiraceae anaerosporobacter, Lachnospiraceae NK4B4 group, Lachnospiraceae UCG-004, and Ruminococcus gauvreauii. After adjustment for coronary risk factors (diabetes mellitus and dyslipidemia), decreased relative abundance of Lachnospiraceae NK4B4 group and Ruminococcus Gauvreauii and increased relative abundance of Ruminococcus gnavus were associated with the presence of advanced CAD. The observed differences in taxa between CAD patients and controls in this study may provide insight into the link between the gut microbiome and CAD.
Journal Article
Several faces of refractory coeliac disease type 2
Correspondence to Dr Joseph A Murray, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA; murray.joseph@mayo.edu Enteropathy-associated t-cell lymphoma (EATL) is a rightly feared complication of coeliac disease (CeD) often presenting as the first manifestation of CeD or a complication of preexisting refractory coeliac disease type 2 (RCD2).1 Cording et al in Gut have provided in exquisite detail the molecular landscape of RCD2 and the resultant EATL.2 It provides not so much of a road map to guide us, but rather a sketch of what has gone wrong in this severe complication of CeD. The face of RCD2 for the gastroenterologist: gastroenterologists looking after these patients are often faced with an ill patient who has very advanced malnutrition as well as a propensity to infection.5 This face of CeD requires the clinician to confirm preexisting CeD, then detect and treat concurrent conditions such as small intestinal bacterial overgrowth, exocrine pancreatic insufficiency, microscopic colitis, motility changes, lactose or other maldigestive problems. In the author’s experience, the early and aggressive use of topical budesonide formulated to be delivered to proximal small bowel often improves symptoms, corrects malnutrition, and in many cases suppresses inflammation.6 In addition to this clinical management, it is also critical to verify that the patients are gluten-free by expert dietary review and perhaps allied with testing stool or urine for gluten immunogenic peptides. A recently published tool based on low albumin, haemoglobin, patient age and molecular characteristics seems to help predict mortality of patients and may allow the ability to stratify patients for therapeutic interventions.12 Identifying more specific interventions such as targeting Interleukin-15 or pathways such as the JAK1-STAT3 and NFKB pathways provide hope that this disease may be interrupted in its progression.
Journal Article
Frequency multiplexed coherent φ-OTDR
We present a comprehensive analysis of a frequency multiplexed phase-measuring φ-OTDR sensor platform. The system uses a train of frequency-shifted pulses to increase the average power injected into the fiber and provide a diversity of uncorrelated Rayleigh backscattering measurements. Through a combination of simulations, numerical analysis, and experimental measurements, we show that this approach not only enables lower noise and mitigates interference fading, but also improves the sensor linearity. We investigate the sensor dependence on the length of the pulse train and characterize the sensor performance as a function of range, demonstrating operation from 1 to 50 km. Despite its relative simplicity, this platform enables state-of-the-art performance, including low crosstalk, high linearity, and a minimum detectable strain of only 0.6
p
ε
/
Hz
in a 10 km fiber with 10 m spatial resolution and a bandwidth of 5 kHz.
Journal Article
Deaf gain : raising the stakes for human diversity
\" Deaf people are usually regarded by the hearing world as having a lack, as missing a sense. Yet a definition of deaf people based on hearing loss obscures a wealth of ways in which societies have benefited from the significant contributions of deaf people. In this bold intervention into ongoing debates about disability and what it means to be human, experts from a variety of disciplines--neuroscience, linguistics, bioethics, history, cultural studies, education, public policy, art, and architecture--advance the concept of Deaf Gain and challenge assumptions about what is normal.Through their in-depth articulation of Deaf Gain, the editors and authors of this pathbreaking volume approach deafness as a distinct way of being in the world, one which opens up perceptions, perspectives, and insights that are less common to the majority of hearing persons. For example, deaf individuals tend to have unique capabilities in spatial and facial recognition, peripheral processing, and the detection of images. And users of sign language, which neuroscientists have shown to be biologically equivalent to speech, contribute toward a robust range of creative expression and understanding. By framing deafness in terms of its intellectual, creative, and cultural benefits, Deaf Gain recognizes physical and cognitive difference as a vital aspect of human diversity.Contributors: David Armstrong; Benjamin Bahan, Gallaudet U; Hansel Bauman, Gallaudet U; John D. Bonvillian, U of Virginia; Alison Bryan; Teresa Blankmeyer Burke, Gallaudet U; Cindee Calton; Debra Cole; Matthew Dye, U of Illinois at Urbana-Champaign; Steve Emery; Ofelia García, CUNY; Peter C. Hauser, Rochester Institute of Technology; Geo Kartheiser; Caroline Kobek Pezzarossi; Christopher Krentz, U of Virginia; Annelies Kusters; Irene W. Leigh, Gallaudet U; Elizabeth M. Lockwood, U of Arizona; Summer Loeffler; Mara Lúcia Massuti, Instituto Federal de Santa Catarina, Brazil; Donna A. Morere, Gallaudet U; Kati Morton; Ronice Muller de Quadros, U Federal de Santa Catarina, Brazil; Donna Jo Napoli, Swarthmore College; Jennifer Nelson, Gallaudet U; Laura-Ann Petitto, Gallaudet U; Suvi Pylvanen, Kymenlaakso U of Applied Sciences; Antti Raike, Aalto U; Paivi Rainò, U of Applied Sciences Humak; Katherine D. Rogers; Clara Sherley-Appel; Kristin Snoddon, U of Alberta; Karin Strobel, U Federal de Santa Catarina, Brazil; Hilary Sutherland; Rachel Sutton-Spence, U of Bristol, England; James Tabery, U of Utah; Jennifer Grinder Witteborg; Mark Zaurov. \"-- Provided by publisher.
Book
ACG clinical guidelines: diagnosis and management of celiac disease
This guideline presents recommendations for the diagnosis and management of patients with celiac disease. Celiac disease is an immune-based reaction to dietary gluten (storage protein for wheat, barley, and rye) that primarily affects the small intestine in those with a genetic predisposition and resolves with exclusion of gluten from the diet. There has been a substantial increase in the prevalence of celiac disease over the last 50 years and an increase in the rate of diagnosis in the last 10 years. Celiac disease can present with many symptoms, including typical gastrointestinal symptoms (e.g., diarrhea, steatorrhea, weight loss, bloating, flatulence, abdominal pain) and also non-gastrointestinal abnormalities (e.g., abnormal liver function tests, iron deficiency anemia, bone disease, skin disorders, and many other protean manifestations). Indeed, many individuals with celiac disease may have no symptoms at all. Celiac disease is usually detected by serologic testing of celiac-specific antibodies. The diagnosis is confirmed by duodenal mucosal biopsies. Both serology and biopsy should be performed on a gluten-containing diet. The treatment for celiac disease is primarily a gluten-free diet (GFD), which requires significant patient education, motivation, and follow-up. Non-responsive celiac disease occurs frequently, particularly in those diagnosed in adulthood. Persistent or recurring symptoms should lead to a review of the patient's original diagnosis to exclude alternative diagnoses, a review of the GFD to ensure there is no obvious gluten contamination, and serologic testing to confirm adherence with the GFD. In addition, evaluation for disorders associated with celiac disease that could cause persistent symptoms, such as microscopic colitis, pancreatic exocrine dysfunction, and complications of celiac disease, such as enteropathy-associated lymphoma or refractory celiac disease, should be entertained. Newer therapeutic modalities are being studied in clinical trials, but are not yet approved for use in practice. Given the incomplete response of many patients to a GFD-free diet as well as the difficulty of adherence to the GFD over the long term, development of new effective therapies for symptom control and reversal of inflammation and organ damage are needed. The prevalence of celiac disease is increasing worldwide and many patients with celiac disease remain undiagnosed, highlighting the need for improved strategies in the future for the optimal detection of patients.
Journal Article