tbuckley/cabot-search huggingface dataset:
Irritable Bowel Syndrome
Authors: William D. Chey, Jacob Kurlander, Shanti Eswaran
Journal: JAMA (2015)

Irritable bowel syndrome (IBS) affects 7% to 21% of the general population. It is a chronic condition that can substantially reduce quality of life and work productivity.To summarize the existing evidence on epidemiology, pathophysiology, and diagnosis of IBS and to provide practical treatment recommendations for generalists and specialists according to the best available evidence.A search of Ovid (MEDLINE) and Cochrane Database of Systematic Reviews was performed for literature from 2000 to December 2014 for the terms pathophysiology, etiology, pathogenesis, diagnosis, irritable bowel syndrome, and IBS. The range was expanded from 1946 to December 2014 for IBS, irritable bowel syndrome, diet, treatment, and therapy.The database search yielded 1303 articles, of which 139 were selected for inclusion. IBS is not a single disease but rather a symptom cluster resulting from diverse pathologies. Factors important to the development of IBS include alterations in the gut microbiome, intestinal permeability, gut immune function, motility, visceral sensation, brain-gut interactions, and psychosocial status. The diagnosis of IBS relies on symptom-based criteria, exclusion of concerning features (symptom onset after age 50 years, unexplained weight loss, family history of selected organic gastrointestinal diseases, evidence of gastrointestinal blood loss, and unexplained iron-deficiency anemia), and the performance of selected tests (complete blood cell count, C-reactive protein or fecal calprotectin, serologic testing for celiac disease, and age-appropriate colorectal cancer screening) to exclude organic diseases that can mimic IBS. Determining the predominant symptom (IBS with diarrhea, IBS with constipation, or mixed IBS) plays an important role in selection of diagnostic tests and treatments. Various dietary, lifestyle, medical, and behavioral interventions have proven effective in randomized clinical trials.The diagnosis of IBS relies on the identification of characteristic symptoms and the exclusion of other organic diseases. Management of patients with IBS is optimized by an individualized, holistic approach that embraces dietary, lifestyle, medical, and behavioral interventions.
Relation Between Growth Hormone and Somatomedin
Authors: J J Van Wyk, L E Underwood
Journal: Annual Review of Medicine (1975)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Evidence from comparative genomics for a complete sexual cycle in the 'asexual' pathogenic yeast Candida glabrata
Authors: Simon Wong, Mario A Fares, Wolfgang Zimmermann, Geraldine Butler, Kenneth H Wolfe
Journal: Genome biology (2003)

Candida glabrata is a pathogenic yeast of increasing medical concern. It has been regarded as asexual since it was first described in 1917, yet phylogenetic analyses have revealed that it is more closely related to sexual yeasts than other Candida species. We show here that the C. glabrata genome contains many genes apparently involved in sexual reproduction. By genome survey sequencing, we find that genes involved in mating and meiosis are as numerous in C. glabrata as in the sexual species Kluyveromyces delphensis, which is its closest known relative. C. glabrata has a putative mating-type (MAT) locus and a pheromone gene (MFALPHA2), as well as orthologs of at least 31 other Saccharomyces cerevisiae genes that have no known roles apart from mating or meiosis, including FUS3, IME1 and SMK1. We infer that C. glabrata is likely to have an undiscovered sexual stage in its life cycle, similar to that recently proposed for C. albicans. The two Candida species represent two distantly related yeast lineages that have independently become both pathogenic and 'asexual'. Parallel evolution in the two lineages as they adopted mammalian hosts resulted in separate but analogous switches from overtly sexual to cryptically sexual life cycles, possibly in response to defense by the host immune system.
Assertive community treatment and medication compliance in the homeless mentally ill
Authors: L Dixon, P Weiden, M Torres, A Lehman
Journal: American Journal of Psychiatry (1997)

This study describes medication compliance rates among a group of homeless mentally ill subjects who received assertive community treatment.The medication compliance of 77 homeless persons who had been referred to an assertive community treatment program was prospectively evaluated at baseline and quarterly for 1 year.A minority of the cohort (29%) was compliant at entry into the assertive community treatment program. Compliance significantly increased after 3 months (57%) and remained high through the year. Medication compliance was associated with fewer psychiatric symptoms but not with better housing placements or fewer days in the hospital.Medication compliance rates among a cohort of homeless persons with severe mental illness were markedly higher after they entered a program of assertive community treatment.
Differences defined by bone marrow transplantation suggest that lpr and gld are mutations of genes encoding an interacting pair of molecules.
Authors: R D Allen, J D Marshall, J B Roths, C L Sidman
Journal: The Journal of Experimental Medicine (1990)

Homozygosity for either of the lymphoproliferation (lpr) or generalized lymphoproliferative disease (gld) mutations of mice causes the development of systemic lupus erythematosus-like autoimmune syndromes that are characterized by severe lymphadenopathy and highly elevated serum immunoglobulin levels. Although the mutations are nonallelic, analysis of homozygous lpr/lpr and gld/gld mice on the same strain background has indicated that the pathology and severity of the autoimmune syndromes induced by these mutations are indistinguishable. To explain this, it has previously been suggested that lpr and gld may represent mutations in molecules involved in sequential steps of an intracellular metabolic pathway of T cells. We have now investigated the behavior of both lpr and gld in a variety of bone marrow chimeras and have found that functional differences between lpr and gld become apparent after bone marrow transfer. Transfer of lpr/lpr bone marrow to irradiated congenic +/+ recipients caused the development of a graft-vs.-host-like lymphoid wasting syndrome, whereas transfer of gld/gld bone marrow to +/+ recipients resulted in development of a gld-like autoimmune syndrome. Additionally, gld/gld hosts behaved like +/+ hosts irrespective of the genotype of the donor bone marrow, whereas lpr/lpr hosts behaved unlike +/+ hosts when reconstituted with either lpr/lpr, gld/gld, or +/+ bone marrow. These are the first clear differences between these two mutations yet described. Our studies indicate that the molecule altered by the gld mutation is expressed only by bone marrow-derived cells, whereas the molecule altered by the lpr mutation is expressed by both bone marrow-derived cells and by one or more peripheral radioresistant cell populations. To reconcile these differences with the fact that homozygous lpr/lpr and gld/gld mice are indistinguishable, we suggest an alternative model for the relationship between the lpr and gld mutations in which the two molecules affected represent an interacting ligand-receptor pair expressed by different cells.
How to monitor SLE in routine clinical practice
Authors: M M A Fernando
Journal: Annals of the Rheumatic Diseases (2005)

<h3>Background</h3> Post-stroke inflammation contributes to poor outcomes, but its impact on patients with stroke receiving endovascular thrombectomy (EVT) remains unknown. <h3>Methods</h3> We enrolled adult patients with stroke who received EVT, with blood sampling immediately before (T1) and after EVT (T2), and at 24 hours after EVT (T3). Non-stroke controls and patients with non-EVT stroke were also enrolled. The medical information, image findings and levels of serum amyloid A (SAA) and C-reactive protein (CRP) were analyzed to clarify the association with poor functional outcome (modified Rankin Scale 4–6) at 3 months after stroke. <h3>Results</h3> A total of 93 patients with stroke receiving EVT, 51 non-stroke controls, and 64 with non-EVT stroke were enrolled in this study. The SAA and CRP levels at T1 to T3 in patients with stroke receiving EVT were higher compared with those in controls (all p&lt;0.001), and their levels at T3 were significantly higher than those at T1 (both p&lt;0.0001) while similar to those in patients with non-EVT stroke. The SAA levels at the three time points were significantly associated with poor functional outcome (p=0.003 to 0.009). Furthermore, adding SAA level at T3 significantly improved the basic prediction model for 3-month poor functional outcome by receiver operating characteristic (ROC) analysis (areas under ROC curves from 0.803 to 0.878, p=0.03). <h3>Conclusions</h3> Our findings demonstrate that plasma levels of SAA at an early stage are significant predictors for poor functional outcomes at 3 months in patients with stroke receiving EVT, indicating the substantial role of systemic inflammation in shaping stroke outcomes following EVT.
Temsirolimus combined with sorafenib in hepatocellular carcinoma: a phase I dose-finding trial with pharmacokinetic and biomarker correlates
Authors: R.K. Kelley, H.S. Nimeiri, P.N. Munster, M.T. Vergo, Y. Huang, C.-M. Li, J. Hwang, M.F. Mulcahy, B.M. Yeh, P. Kuhn, M.S. Luttgen, J.A. Grabowsky, L. Stucky-Marshall, W.M. Korn, A.H. Ko, E.K. Bergsland, A.B. Benson, A.P. Venook
Journal: Annals of Oncology (2013)
Paul Stuart Barclay
Authors: Alison Menzies, Ian T Miller
Journal: BMJ (2006)

of medicine at Oxford, Emory, Yale, and Washington, who discovered the pathology of fever in infections and advocated death with dignity At the height of the brain drain, when Britain was haemorrhaging researchers to the United States, Paul Beeson left a chair of medicine at Yale to become Nuffield professor of medicine at Oxford.He reformed the curriculum, edited two textbooks and the Oxford Companion to Medicine, and laid the foundations for Oxford's pre-eminence in infectious diseases.He was awarded an honorary KBE.Beeson inspired generations of students with his concern for patients.He showed that hepatitis could be transmitted by blood transfusion, and brought new insights into the causes of high persistent fevers.He also discovered the cytokine interleukin-1.During the second world war he was one of the volunteer US doctors who staffed Harvard Hospital in Salisbury.He was professor of medicine at three US universities: Emory, Yale, and Washington.Although he started as a conservative who intended to follow a career in private practice, he ended as a liberal concerned with the uninsured and old, medical ethics, and the medical consequences of nuclear warfare.Professor John Stein of Oxford University told the BMJ, "Paul Beeson was a wonderful clinician, and incredibly kind to young people like me."Paul Beeson was born in rural Montana, United States, and brought up in Anchorage, Alaska, where
The global burden of musculoskeletal conditions for 2010: an overview of methods
Authors: Damian G Hoy, Emma Smith, Marita Cross, Lidia Sanchez-Riera, Rachelle Buchbinder, Fiona M Blyth, Peter Brooks, Anthony D Woolf, Richard H Osborne, Marlene Fransen, Tim Driscoll, Theo Vos, Jed D Blore, Chris Murray, Nicole Johns, Mohsen Naghavi, Emily Carnahan, Lyn M March
Journal: Annals of the Rheumatic Diseases (2014)

The objective of this paper is to provide an overview of methods used for estimating the burden from musculoskeletal (MSK) conditions in the Global Burden of Diseases 2010 study. It should be read in conjunction with the disease-specific MSK papers published in Annals of Rheumatic Diseases. Burden estimates (disability-adjusted life years (DALYs)) were made for five specific MSK conditions: hip and/or knee osteoarthritis (OA), low back pain (LBP), rheumatoid arthritis (RA), gout and neck pain, and an 'other MSK conditions' category. For each condition, the main disabling sequelae were identified and disability weights (DW) were derived based on short lay descriptions. Mortality (years of life lost (YLLs)) was estimated for RA and the rest category of 'other MSK', which includes a wide range of conditions such as systemic lupus erythematosus, other autoimmune diseases and osteomyelitis. A series of systematic reviews were conducted to determine the prevalence, incidence, remission, duration and mortality risk of each condition. A Bayesian meta-regression method was used to pool available data and to predict prevalence values for regions with no or scarce data. The DWs were applied to prevalence values for 1990, 2005 and 2010 to derive years lived with disability. These were added to YLLs to quantify overall burden (DALYs) for each condition. To estimate the burden of MSK disease arising from risk factors, population attributable fractions were determined for bone mineral density as a risk factor for fractures, the occupational risk of LBP and elevated body mass index as a risk factor for LBP and OA. Burden of Disease studies provide pivotal guidance for governments when determining health priority areas and allocating resources. Rigorous methods were used to derive the increasing global burden of MSK conditions.
Hormone-Induced Chromosomal Instability in p53-Null Mammary Epithelium
Authors: Debananda Pati, Bassem R. Haddad, Albert Haegele, Henry Thompson, Frances S. Kittrell, Anne Shepard, Cristina Montagna, Nenggang Zhang, Gouqing Ge, Subhendu Kumar Otta, Maureen McCarthy, Robert L. Ullrich, Daniel Medina
Journal: Cancer Research (2004)

The absence of p53 function increases risk for spontaneous tumorigenesis in the mammary gland. Hormonal stimulation enhances tumor risk in p53-null mammary epithelial cells as well as the incidence of aneuploidy. Aneuploidy appears in normal p53-null mammary epithelial cells within 5 weeks of hormone stimulation. Experiments reported herein assessed a possible mechanism of hormone-induced aneuploidy. Hormones increased DNA synthesis equally between wild-type (WT) and p53-null mammary epithelial cells. There were two distinct responses in p53-null cells to hormone exposure. First, Western blot analysis demonstrated that the levels of two proteins involved in regulating sister chromatid separation and the spindle checkpoint, Mad2 and separase (ESPL1) were increased in null compared with WT cells. In contrast, the levels of securin and Rad21 proteins were not increased in hormone-stimulated p53-null compared with WT cells. ESPL1 RNA was also increased in p53-null mouse mammary cells in vivo by 18 h of hormone stimulation and in human breast MCF7 cells in monolayer culture by 8 h of hormone stimulation. Furthermore, both promoters contained p53 and steroid hormone response elements. Mad2 protein was increased as a consequence of the absence of p53 function. The increase in Mad2 protein was observed also at the cellular level by immunohistochemistry. Second, hormones increased gene amplication in the distal arm of chromosome 2, as shown by comparative genomic hybridization. These results support the hypothesis that hormone stimulation acts to increase aneuploidy by several mechanisms. First, by increasing mitogenesis in the absence of the p53 checkpoint in G2, hormones allow the accumulation of cells that have experienced chromosome missegregation. Second, the absolute rate of chromosome missegregation may be increased by alterations in the levels of two proteins, separase and Mad2, which are important for maintaining chromosomal segregation and the normal spindle checkpoint during mitosis.
Septic encephalopathy: when cytokines interact with acetylcholine in the brain
Authors: Qing-Hong Zhang, Zhi-Yong Sheng, Yong-Ming Yao
Journal: Military Medical Research (2014)

Sepsis-associated encephalopathy (SAE) is a brain dysfunction that occurs secondary to infection in the body, characterized by alteration of consciousness, ranging from delirium to coma, seizure or focal neurological signs. SAE involves a number of mechanisms, including neuroinflammation, in which the interaction between cytokines and acetylcholine results in neuronal loss and alterations in cholinergic signaling. Moreover, the interaction also occurs in the periphery, accelerating a type of immunosuppressive state. Although its diagnosis is not specific in biochemistry and imaging tests, it could potentiate severe outcomes, including increased mortality, cognitive decline, progressive immunosuppression, cholinergic anti-inflammatory deficiency, and even metabolic and hydroelectrolyte imbalance. Therefore, the bilateral communication between SAE and the multiple peripheral organs and especially the immune system should be emphasized in sepsis management.
Approach to therapy of diffuse large B-cell lymphoma in the elderly: the International Society of Geriatric Oncology (SIOG) expert position commentary
Authors: V.A. Morrison, P. Hamlin, P. Soubeyran, R. Stauder, P. Wadhwa, M. Aapro, S.M. Lichtman
Journal: Annals of Oncology (2015)
Chronic Health Conditions and Obesity Among Children and Youth—Reply
Authors: Jeanne Van Cleave
Journal: JAMA (2010)

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Next-Generation Histopathologic Diagnosis: A Lesson From a Hepatic Carcinosarcoma
Authors: Claudio Luchini, Paola Capelli, Matteo Fassan, Michele Simbolo, Andrea Mafficini, Federica Pedica, Andrea Ruzzenente, Alfredo Guglielmi, Vincenzo Corbo, Aldo Scarpa
Journal: Journal of Clinical Oncology (2014)
ER stress induces epithelial differentiation in the mouse oesophagus
Authors: Sanne L Rosekrans, Jarom Heijmans, Nikè V J A Büller, Jessica Westerlund, Amy S Lee, Vanesa Muncan, Gijs R van den Brink
Journal: Gut (2014)

Objective Stress in the endoplasmic reticulum (ER) leads to activation of the unfolded protein response (UPR). Xbp1, a key component of the UPR has recently been linked to the risk of developing oesophageal squamous cell carcinoma, suggesting an important role for the UPR in the oesophageal epithelium. Here we examined the role of ER stress and the UPR in oesophageal epithelial homoeostasis. Design We examined the expression of components of the UPR in the oesophageal epithelium. We used a pharmacological approach and a genetic approach to examine the effects of ER stress in vivo in the mouse oesophagus. The oesophagus of these mice was examined using immunohistochemistry and real-time reverse transcription (RT)-PCR. Results Components of the UPR were heterogeneously expressed in the basal layer of the epithelium. Induction of ER stress by 24-h treatment with thapsigargin resulted in depletion of proliferating cells in the basal layer of the oesophagus and induced differentiation. We next activated the UPR by inducible deletion of the major ER chaperone Grp78 in Ah1Cre-Rosa26-LacZ-Grp78−/− mice in which mutant cells could be traced by expression of LacZ. In these mice LacZ-positive mutant cells in the basal layer lost their proliferative capacity, migrated towards the oesophageal lumen and were replaced by LacZ-negative non-mutant cells. We observed no apoptosis in mutant cells. Conclusions These results show that ER stress induces epithelial differentiation in precursor cells in the oesophageal epithelium. This UPR induced differentiation may serve as a quality control mechanism that protects against oesophageal cancer development.
Reliable change assessment in sport concussion research: a comment on the proposal and reviews of Collie<i>et al</i>
Authors: G H Maassen
Journal: British Journal of Sports Medicine (2005)

The proposal of Collie et al for determining reliable change in sports medicine and their review of other current procedures did not address mathematical or theoretical aspects. This article attempts to fill this lacuna, in order to examine the validity of their proposal and the suitability of their review. The conclusions drawn are that Collie et al presented their method too carelessly and their review of other methods leaves serious drawbacks and mistakes unnoticed. A scheme is here provided showing which of the current methods can be used in which situation.
Differential gene expression and regulation of angiotensin II receptor subtypes in rat cardiac fibroblasts and cardiomyocytes in culture.
Authors: H Matsubara, M Kanasaki, S Murasawa, Y Tsukaguchi, Y Nio, M Inada
Journal: Journal of Clinical Investigation (1994)

Although both rat cardiac nonmyocytes (mostly fibroblasts) and cardiomyocytes have a functional angiotensin II (AngII) receptor, the regulation mechanism of its subtype expression in the rat heart remains unknown. In this study, by using a binding assay and a competitive reverse-transcriptase polymerase chain reaction, we examined the regulation of AngII types 1a and 1b (AT1a-R and AT1b-R) and type 2 receptor (AT2-R) expression in embryonal day 19 (E19) and neonatal (1-d) rat cardiac fibroblasts and cardiomyocytes. The number of AT2-R in E19 fibroblasts was dramatically decreased (from 305 to 41 fmol/mg protein) in 1-d fibroblasts, whereas that of AT1-R and the mRNA levels remained unchanged. The ratio of AT1a-R to AT1b-R mRNA in both E19 and 1-d fibroblasts was 9:1. The number of AT2-R in E19 cardiomyocytes was also significantly decreased (from 178 to 87 fmol/mg protein) in 1-d cardiomyocytes, whereas the magnitude was less prominent compared with that in fibroblasts. AT1-R expression remained unaltered in E19 and 1-d cardiomyocytes. In E19 and 1-d cardiomyocytes, the AT1b-R mRNA level was 1.5-fold higher than that of AT1a-R mRNA. Dexamethasone induced significant increases in AT1a-R mRNA (2.1-fold) and numbers (1.8-fold) without changing the affinity, whereas neither AT1b-R mRNA nor the number of AT2-R was affected by dexamethasone. The AT1a-R gene transcription rate, determined by means of a nuclear run-off assay, was increased (2-fold) by dexamethasone. The half-life of AT1a-R mRNA (18 h) was unchanged by dexamethasone. These data indicate that AngII receptor subtype expression in the rat heart is regulated in a cell- and subtype-specific manner.