tbuckley/cabot-search huggingface dataset:
Type I interferon signalling in the intestinal epithelium affects Paneth cells, microbial ecology and epithelial regeneration
Authors: Markus Tschurtschenthaler, Jun Wang, Cornelia Fricke, Teresa M J Fritz, Lukas Niederreiter, Timon E Adolph, Edina Sarcevic, Sven Künzel, Felix A Offner, Ulrich Kalinke, John F Baines, Herbert Tilg, Arthur Kaser
Journal: Gut (2014)

<h3>Objective</h3> Intestinal epithelial cells (IECs) at the internal/external interface orchestrate the mucosal immune response. Paneth cells secrete antimicrobial peptides and inflammatory mediators, protect from pathogens and shape the commensal microbiota. Prompted by the genetic association of the locus harbouring the type I interferon (IFN) receptor (<i>IFNAR1</i>) with Crohn9s disease, and a transcriptional signature for type I IFN signalling in Paneth cells, we studied the function of IFNAR1 in IECs. <h3>Design</h3> Type I IFN signalling was studied in mice with conditional deletion of <i>Ifnar1</i> in IECs. Phenotype was characterised at baseline, and gut microbiota composition was assessed by 16S rDNA ribotyping. The role of IFNAR1 was also investigated in experimental colitis induced by dextran sodium sulfate (DSS) and colitis-associated cancer induced by DSS in conjunction with azoxymethane (AOM). <h3>Results</h3> <i>Ifnar1<sup>−/−(IEC)</sup></i> mice displayed expansion of Paneth cell numbers and epithelial hyperproliferation compared with <i>Ifnar1</i>-sufficient littermates. While <i>Ifnar1<sup>−/−(IEC)</sup></i> mice did not exhibit spontaneous inflammation or increased severity in DSS colitis compared with <i>Ifnar1<sup>+/+(IEC)</sup></i> mice, they exhibited an increased tumour burden in the AOM/DSS model. Both hyperproliferation and tumour promotion were dependent on the microbial flora, as the differences between genotypes were marked upon separately housing mice, but disappeared when <i>Ifnar1<sup>−/−(IEC)</sup></i> and <i>Ifnar1<sup>+/+(IEC)</sup></i> mice were co-housed. Accordingly, ribotyping revealed marked differences between <i>Ifnar1<sup>−/−(IEC)</sup></i> and <i>Ifnar1<sup>+/+(IEC)</sup></i> mice that where diminished upon co-housing. <h3>Conclusions</h3> IFNAR1 in IECs, and Paneth cells in particular, contributes to the regulation of the host–microbiota relationship, with consequences for intestinal regeneration and colitis-associated tumour formation.
PTH/PTHrP and Vitamin D Control Antimicrobial Peptide Expression and Susceptibility to Bacterial Skin Infection
Authors: Beda Muehleisen, Daniel D. Bikle, Carlos Aguilera, Douglas W. Burton, George L. Sen, Leonard J. Deftos, Richard L. Gallo
Journal: Science Translational Medicine (2012)

Vitamin D and parathyroid hormone work together to maximize innate immune resistance to skin infections.
Angina pectoris and oesophageal angina
Authors: M BORTOLOTTI
Journal: Gut (1999)

Editor,—I enjoyed the prospective study by Cooke et al ( Gut 1998; 42 :323–329) on the relation between oesophageal abnormalities and chest pain in patients with normal coronary angiograms and with angina pectoris. This study confirms the findings of previous studies1 2 that the oesophagus is responsible for chest pain in a high percentage of patients with coronary artery disease, and that an episode of gastro-oesophageal reflux nearly always triggers this pain.

However, no explanation for this unexpected finding has been given. The tentative proposition that it is the result of a decreased angina threshold3 and a reflex coronary ischaemia, both induced …
Transient Painless Thyroiditis with Hyperthyroidism: A Variant of Lymphocytic Thyroiditis?*
Authors: PAUL D. WOOLF
Journal: Endocrine Reviews (1980)

WITHIN the past decade and particularly within the past 5 years, an unusual form of hyperthyroidism has received increasing attention (1–22). The hyperthyroid manifestations are generally self limiting, although some cases relapse, are accompanied by chronic inflammatory changes within the thyroid parenchyma, and are marked by a very low 131I uptake. Despite the usually abrupt onset of symptoms and the diffuse lymphocytic infiltration, thyroidal pain and/or tenderness is completely absent. Because this syndrome overlaps many of the features of both lymphocytic thyroiditis and subacute thyroiditis, there has been much debate about how to categorize it or whether to consider it a new disease entity. Nomenclature used by the several groups describing it includes: painless thyroiditis (7, 11, 17, 20), silent thyroiditis (3, 9, 19, 22), occult subacute thyroiditis (1), painless subacute thyroiditis (10, 14), subacute nonsuppurative thyroiditis (2), atypical ("silent") subacute thyroiditis (16), lymphocytic thyroiditis with spontaneously resolving hyperthyroidism (22), hyperthyroiditis (6), lymphocytic thyroiditis (4, 18) and autoimmune disease and thyroiditis (12). The current review was undertaken, therefore, because of this confusion and because of the newly emerging clinical importance of this syndrome. It will focus on the manifestations of this self-limited form of hyperthyroidism and will try to place it into perspective with the more conventional forms of thyrotoxicosis. Although far from clear cut, the data supporting a possible immunological basis will be discussed.
Metformin for Treatment of Antipsychotic-Induced Amenorrhea and Weight Gain in Women With First-Episode Schizophrenia: A Double-Blind, Randomized, Placebo-Controlled Study
Authors: Ren-Rong Wu, Hua Jin, Keming Gao, Elizabeth W. Twamley, Jian-Jun Ou, Ping Shao, Juan Wang, Xiao-Feng Guo, John M. Davis, Philip K. Chan, Jing-Ping Zhao
Journal: American Journal of Psychiatry (2012)

Data on the treatment of antipsychotic-induced amenorrhea, particularly when occurring with weight gain, are limited. The authors investigated the efficacy and safety of metformin in the treatment of antipsychotic-induced amenorrhea and weight gain in women with first-episode schizophrenia. Eighty-four women (ages 18-40 years) with first-episode schizophrenia who suffered from amenorrhea during antipsychotic treatment were randomly assigned, in a double-blind study design, to receive 1000 mg/day of metformin or placebo in addition to their antipsychotic treatment for 6 months. The primary outcome measures were restoration of menstruation and change in body weight and body mass index (BMI). Secondary outcome measures were changes in levels of prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol, and testosterone; in fasting levels of insulin and glucose; in LH/FSH ratio; and in insulin resistance index. Repeated mixed models with repeated-measures regression analyses and binary logistic regression were used in the analysis. A total of 76 patients completed the 6-month trial. Significantly more patients in the metformin group (N=28, 66.7%) than in placebo group (N=2, 4.8%) resumed their menstruation. Among patients treated with metformin, BMI decreased by a mean of 0.93 and the insulin resistance index by 2.04. In contrast, patients who received placebo had a mean increase in BMI of 0.85. The prolactin, LH, and testosterone levels and LH/FSH ratio decreased significantly in the metformin group at months 2, 4, and 6, but these levels did not change in the placebo group. Metformin was effective in reversing antipsychotic-induced adverse events, including restoration of menstruation, promotion of weight loss, and improvement in insulin resistance in female patients with schizophrenia.
TRICHOPHYTIN TESTING BY THE MULTIPLE-PUNCTURE METHOD.
Authors: S. R. WOOD
Journal: British Journal of Dermatology (1962)

Journal Article TRICHOPHYTIN TESTING BY THE MULTIPLE‐PUNCTURE METHOD. Get access S. R. WOOD, M.B., M.R.C.P. S. R. WOOD, M.B., M.R.C.P. Medical Research Council Unit for Research on the Experimental Pathology of the Skin, University of Birmingham, and United Birmingham Hospitals Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 74, Issue 2, 1 February 1962, Pages 57–61, https://doi.org/10.1111/j.1365-2133.1962.tb13453.x Published: 01 February 1962
Aromatase Inhibitors in Human Lung Cancer Therapy
Authors: Olga K. Weinberg, Diana C. Marquez-Garban, Michael C. Fishbein, Lee Goodglick, Hermes J. Garban, Steven M. Dubinett, Richard J. Pietras
Journal: Cancer Research (2005)

Abstract Lung cancer is the most common cancer in the world. It is a highly lethal disease in women and men, and new treatments are urgently needed. Previous studies implicated a role of estrogens and estrogen receptors in lung cancer progression, and this steroidal growth-stimulatory pathway may be promoted by tumor expression and activity of aromatase, an estrogen synthase. We found expression of aromatase transcripts and protein in human non–small cell lung cancer (NSCLC) cells using reverse transcription-PCR and Western immunoblots, respectively. Aromatase staining by immunohistochemistry was detected in 86% of archival NSCLC tumor specimens from the clinic. Further, biological activity of aromatase was determined in NSCLC tumors using radiolabeled substrate assays as well as measure of estradiol product using ELISA. Significant activity of aromatase occurred in human NSCLC tumors, with enhanced levels in tumor cells compared with that in nearby normal cells. Lung tumor aromatase activity was inhibited by anastrozole, an aromatase inhibitor, and treatment of tumor cells in vitro with anastrozole led to significant suppression of tumor cell growth. Similarly, among ovariectomized nude mice with A549 lung tumor xenografts, administration of anastrozole by p.o. gavage for 21 days elicited pronounced inhibition of tumor growth in vivo. These findings show that aromatase is present and biologically active in human NSCLCs and that tumor growth can be down-regulated by specific inhibition of aromatase. This work may lead to development of new treatment options for patients afflicted with NSCLC. (Cancer Res 2005; 65(24): 11287-91)
In vivo IgA coating of anaerobic bacteria in human faeces.
Authors: L A van der Waaij, P C Limburg, G Mesander, D van der Waaij
Journal: Gut (1996)

<h3>Objective</h3> To determine that children with arterial ischemic stroke (AIS) due to an identifiable arteriopathy are distinct from those without arteriopathy and that each arteriopathy subtype has unique and recognizable clinical features. <h3>Methods</h3> We report a large, observational, multicenter cohort of children with AIS, age 1 month to 18 years, enrolled in the International Pediatric Stroke Study from 2003 to 2014. Clinical and demographic differences were compared by use of the Fisher exact test, with linear step-up permutation min-<i>p</i> adjustment for multiple comparisons. Exploratory analyses were conducted to evaluate differences between cases of AIS with and without arteriopathy and between arteriopathy subtypes. <h3>Results</h3> Of 2,127 children with AIS, 725 (34%) had arteriopathy (median age 7.45 years). Arteriopathy subtypes included dissection (27%), moyamoya (24.5%), focal cerebral arteriopathy–inflammatory subtype (FCA-i; 15%), diffuse cerebral vasculitis (15%), and nonspecific arteriopathy (18.5%). Children with arteriopathic AIS were more likely to present between 6 and 9 years of age (odds ratio [OR] 1.93, <i>p</i> = 0.029) with headache (OR 1.55, <i>p</i> = 0.023), multiple infarctions (OR 2.05, <i>p</i> &lt; 0.001), sickle cell anemia (OR 2.9, <i>p</i> = 0.007), and head/neck trauma (OR 1.93, <i>p</i> = 0.018). Antithrombotic use and stroke recurrence were higher in children with arteriopathy. Among arteriopathy subtypes, dissection was associated with male sex, older age, headache, and anticoagulant use; FCA-i was associated with hemiparesis and single infarcts; moyamoya was associated with seizures and recurrent strokes; and vasculitis was associated with bilateral infarctions. <h3>Conclusion</h3> Specific clinical profiles are associated with cerebral arteriopathies in children with AIS. These observations may be helpful indicators in guiding early diagnosis and defining subgroups who may benefit most from future therapeutic trials.
Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up
Authors: Joshua P. Thaler, Michael W. Schwartz
Journal: Endocrine Reviews (2010)

Abstract Obesity induced by high-fat (HF) feeding is associated with low-grade inflammation in peripheral tissues that predisposes to insulin resistance. Recent evidence suggests the occurrence of a similar process in the hypothalamus, which favors weight gain through impairment of leptin and insulin signaling. In addition to its implications for obesity pathogenesis, this hypothesis suggests that centrally targeted antiinflammatory therapies may prove effective in prevention and treatment of this disorder. This article highlights molecular and cellular mechanisms by which hypothalamic inflammation predisposes to diet-induced obesity.
The Impact of Targeted Molecular Therapies on the Level of Renal Cell Carcinoma Vena Caval Tumor Thrombus
Authors: Nicholas G. Cost, Scott E. Delacroix, Joshua P. Sleeper, Paul J. Smith, Ramy F. Youssef, Brian F. Chapin, Jose A. Karam, Stephen Culp, E. Jason Abel, James Brugarolas, Ganesh V. Raj, Arthur I. Sagalowsky, Christopher G. Wood, Vitaly Margulis
Journal: European Urology (2011)
Mouse Myeloma: Differentiation of Neoplastic Cells Accompanied by an Increase in Intracellular Virus&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: L. E. Volkman, E. A. Smuckler, R. G. Krueger
Journal: JNCI Journal of the National Cancer Institute (1971)

A primary myeloma tumor was induced by insertion of a 0.45-μ Millipore filter cemented to a Lucite ring into the peritoneal cavity of a BALB/c mouse. After 9 months, ascites tumor cells were periodically removed and injected into other BALB/c mice. A secondary tumor arising in one of these mice was composed of cells morphologically resembling small lymphocytes or reticulum cells. These cells characteristically contained very few, if any, A-type virus particles. Analysis of the serum of tumor-bearing animals by Disc gel electrophoresis revealed that the tumor was producing a γG globulin. In the fourth and succeeding tumor generations, cells derived from this tumor line resembled neoplastic plasma cells. They produced the same electrophoretic species of immunoglobulin but had a greatly increased content of intracisternal A-type virus particles.
Autosomal dominant polycystic kidney disease.
Authors: J C Lieske, F G Toback
Journal: Journal of the American Society of Nephrology (1993)

Autosomal dominant polycystic kidney disease (ADPKD) is an important cause of medical morbidity in the United States that affects one-half million persons and accounts for ESRD in about 10% of the chronic dialysis population. In addition to its effects on the kidney, the disease has important manifestations in the cardiovascular system (aneurysms, hypertension) and the gastrointestinal tract (hepatic cysts). Clinically important renal complications can develop as the disease progresses that require specialized attention, such as urinary tract infection, pain, and nephrolithiasis. The underlying cellular defect that causes ADPKD has eluded investigators thus far, but abnormalities in cellular proliferation, the tubular basement membrane, and cell fluid secretion appear important in pathogenesis. Factors that mediate progressive interstitial fibrosis and failure of renal function are undefined, although rigorous control of blood pressure appears to be an important therapeutic measure. Recent advances in molecular biology have localized the abnormal gene to chromosome 16 in 90% of families, making early genetic screening of asymptomatic family members possible in many cases. A positive diagnosis may have important effects on employment status, as well as health insurance, so that family members sometimes refuse to be assessed for the presence of the disease. Because of such complex social factors, counseling of an asymptomatic individual by his or her physician is required when considering the use of screening tests for ADPKD. Inadequate patient education may still represent an impediment to early detection, genetic counseling, and timely treatment of disease complications.
A Portrait of Osler by His Contemporaries
Authors: S. Gordon Ross
Journal: JAMA (1969)

I never met Osler, but I feel I know him well. My aim is to bring an impression of Osler to you by describing my friendship and association with many of his contemporaries. Each recollection of these men helps to paint the larger portrait which is Osler as I know him. These contemporaries were life-long friends and remained in close touch with each other. I was George Dock's associate in Pasadena, Calif, for 25 years until his death in 1952. Many of his old associates made prolonged winter visits, and some of them retired in California. This gave me the opportunity of knowing them. I began my study of medicine at Toronto about the time of Osler's death. Many of my professors were close to Osler, and I had the opportunity of learning about Osler's moves from Toronto, to Montreal, to Philadelphia, to Baltimore, and to Oxford. Now, after half
Inherent limits on the identification of a neural basis for general intelligence
Authors: Clancy Blair
Journal: Behavioral and Brain Sciences (2007)

Abstract The target article provides a thoughtful review and synthesis of studies examining the neural basis of cognitive abilities associated with intelligence test performance. In its attempt to present a new or generative theory of the neural basis for intelligence, however, the review faces specific limits to its theoretical model that relate to processes of development and the role of automaticity in cognition.
The possibility of subisomorphic experiential differences
Authors: Christopher D. Viger
Journal: Behavioral and Brain Sciences (1999)

Palmer's main intuition pump, the “color machine,” greatly underestimates the complexity of a system isomorphic in color experience to humans. The neuroscientific picture of this complexity makes it clear that the brain actively produces our experiences by processes that science can investigate, thereby supporting functionalism and leaving no (color) room for a passive observer to witness subisomorphic experiential differences.
One-Hour Glucose During an Oral Glucose Challenge Prospectively Predicts β-Cell Deterioration and Prediabetes in Obese Hispanic Youth
Authors: Joon Young Kim, Michael I. Goran, Claudia M. Toledo-Corral, Marc J. Weigensberg, Myunghan Choi, Gabriel Q. Shaibi
Journal: Diabetes Care (2013)

In adults, 1-h glucose during an oral glucose tolerance test (OGTT) predicts the development of type 2 diabetes independent of fasting and 2-h glucose concentrations. The purpose of the current investigation was to examine the utility of elevated 1-h glucose levels to prospectively predict deterioration in β-cell function and the development of prediabetes in high-risk youth.Obese Latino youth with a family history of type 2 diabetes (133 male and 100 female; age 11.1 ± 1.7 years) completed a baseline OGTT and were divided into two groups based upon a 1-h glucose threshold of 155 mg/dL (<155 mg/dL, n = 151, or ≥ 155 mg/dL, n = 82). Youth were followed annually for up to 8 years for assessment of glucose tolerance, body composition by dual-energy X-ray absorptiometry, and insulin sensitivity, insulin secretion, and the disposition index by the frequently sampled intravenous glucose tolerance test.Over time, the ≥ 155 mg/dL group exhibited a significantly greater decline in β-cell function compared with youth with a 1-h glucose <155 mg/dL (β = -327.8 ± 126.2, P = 0.01). Moreover, this decline was independent of fasting or 2-h glucose and body composition. When the data were restricted to only participants with normal glucose tolerance at baseline, a 1-h glucose ≥ 155 mg/dL was independently associated with a 2.5 times greater likelihood of developing prediabetes during follow-up (95% CI 1.6-4.1, P = 0.0001).These data suggest that a 1-h glucose ≥ 155 mg/dL during an OGTT is an independent predictor of β-cell deterioration and progression to prediabetes among obese Latino youth.
INTRAVENOUS IMMUNOGLOBULIN VERSUS ORAL CORTICOSTEROIDS IN ACUTE IMMUNE THROMBOCYTOPENIC PURPURA IN CHILDHOOD
Authors: P Imbach, W Berchtold, A Hirt, C Mueller-Eckhardt, E Rossi, H.P Wagner, G Gaedicke, P Joller, B Müller, S Barandun
Journal: The Lancet (1985)
Effects of prolonged alcohol administration and a high carbohydrate-low protein diet on the activities of the jejunal brush border enzymes in the rat.
Authors: F Raul, M Doffoel, J Marescaux, R Bockel, J F Grenier
Journal: Gut (1982)

The effects of prolonged alcohol administration were studied on the brush border enzyme activities of the jejunum in rats receiving either a normal laboratory diet or a high carbohydrate-low protein for several weeks. Alcohol (15%) given in association with the normal diet provoked a stimulation of sucrase, maltase, and lactase activities after four weeks, but no significant modification in aminopeptidase activity. These results obtained for the disaccharidases were very similar to those observed with the high carbohydrate-low protein diet given without alcohol, although major differences were obvious in the timing of enzyme stimulation. In contrast, this dietary condition initiated a drop in aminopeptidase activity. When alcohol was given in association with the high carbohydrate-low protein diet, no modification in aminopeptidase activity was detected and the stimulation for the disaccharidase activities was similar to that observed with the high carbohydrate-low protein diet given alone. The present results suggest that the mechanisms involved in the stimulation of brush border disaccharidase activities were different for alcohol and for the high carbohydrate-low protein diet.