tbuckley/cabot-search huggingface dataset:
Mechanism of retarded liver regeneration in plasminogen activator-deficient mice: Impaired activation of hepatocyte growth factor after Fas-mediated massive hepatic apoptosis
Authors: Masahito Shimizu, Akira Hara, Masataka Okuno, Hiroyuki Matsuno, Kiyotaka Okada, Shigeru Ueshima, Osamu Matsuo, Masayuki Niwa, Kuniharu Akita, Yasuhiro Yamada, Naoki Yoshimi, Toshihiko Uematsu, Soichi Kojima, Scott L. Friedman, Hisataka Moriwaki, Hideki Mori
Journal: Hepatology (2001)

Urokinase-type plasminogen activator (uPA) is implicated in the regulation of hepatic regeneration by activating hepatocyte growth factor (HGF). Here, we investigated its role in the hepatic regeneration after Fas-mediated massive hepatocyte death employing mice deficient in either uPA or its inhibitor, plasminogen activator inhibitor-1 (PAI-1). We measured kinetics of hepatic levels of proliferating cell nuclear antigen (PCNA)-labeling index, plasmin activity, mature HGF, and its phosphorylated receptor, c-Met. In the genetically targeted and wild-type mice, hepatocytes fell into the same extent of apoptosis 6 to 12 hours after an intraperitoneal injection with anti-Fas antibody, as judged from histologic analysis and a histon-DNA enzyme-linked immunosorbent assay (ELISA). In the wild-type mice, mature HGF emerged in the liver 6 hours following anti-Fas injection, and hepatic PCNA-labeling index started to increase following 24 hours and peaked at 48 hours. In the uPA(-/-) mice, emergence of mature HGF was delayed 12 hours and hepatic regeneration peaked at 96 hours. Supplementation with the uPA gene to the uPA(-/-) mice by in vivo lipofection restored hepatic plasmin levels, and improved a delay in the expression of both mature HGF and phosphorylated c-Met, accompanying a normal rate of liver regeneration. In contrast, PAI-1(-/-) mice showed accelerated liver regeneration; mature HGF emerged as early as 3 hours, and PCNA-labeling index increased at 24 hours. This accelerated regeneration was abolished by administration with anti-HGF antibody. These results strongly suggest a physiologic role of uPA in the proteolytic maturation of HGF, and thereby in hepatic regeneration after Fas-mediated massive hepatocyte death.
Interleukin 2 inhibits in vitro growth of human T cell lines carrying retrovirus.
Authors: K Sugamura, S Nakai, M Fujii, Y Hinuma
Journal: The Journal of Experimental Medicine (1985)

Four human T cell lines, TL-Mor, TL-Su, TL-TerI, and TL-OmI, carrying human T cell leukemia virus (HTLV), were established previously. TL-Mor, TL-Su, and TL-TerI were derived from interleukin 2 (IL-2)-dependent parental cell lines cloned from peripheral blood leukocytes (PBL) of three healthy HTLV carriers, while TL-OmI was directly established from PBL of a patient with adult T cell leukemia. These four TL cell lines grow autonomously without IL-2. When they were cultured in the presence of IL-2, their growth was inhibited after a few days. This growth inhibition depended on the dose of IL-2, and the effective dose significantly promoted growth of their parental IL-2-dependent cell lines. The growth inhibition is demonstrated to be due to specific binding of IL-2 to receptors on the TL cells.
The Breathprints in Patients With Liver Disease Identify Novel Breath Biomarkers in Alcoholic Hepatitis
Authors: Ibrahim A Hanouneh, Nizar N Zein, Frank Cikach, Luma Dababneh, David Grove, Naim Alkhouri, Rocio Lopez, Raed A Dweik
Journal: Clinical Gastroenterology and Hepatology (2013)
Emergence of Community-Acquired Methicillin-Resistant <i>Staphylococcus aureus</i> USA 300 Clone as the Predominant Cause of Skin and Soft-Tissue Infections
Authors: Mark D. King, Bianca J. Humphrey, Yun F. Wang, Ekaterina V. Kourbatova, Susan M. Ray, Henry M. Blumberg
Journal: Annals of Internal Medicine (2006)

Background: Studies have shown that community-acquired methicillin-resistant Staphylococcus aureus (MRSA) causes S. aureus skin and soft-tissue infection in selected populations. Objective: To determine the proportion of infections caused by community-acquired MRSA, the clinical characteristics associated with community-acquired MRSA, and the molecular epidemiology of community-acquired MRSA among persons with community-onset S. aureus skin and soft-tissue infection. Design: Active, prospective laboratory surveillance to identify S. aureus recovered from skin and soft-tissue sources. Setting: 1000-bed urban hospital and its affiliated outpatient clinics in Atlanta, Georgia. Patients: 384 persons with microbiologically confirmed community-onset S. aureus skin and soft-tissue infection. Measurements: Proportion of infections caused by and clinical factors associated with community-acquired MRSA among persons with community-onset S. aureus skin and soft-tissue infection. Pulsed-field gel electrophoresis and antimicrobial susceptibility patterns were used to epidemiologically classify community-onset S. aureus infections. Community-acquired MRSA was defined by MRSA isolates that either demonstrated a USA 300 or USA 400 pulsed-field type or had a susceptibility pattern showing resistance only to β-lactams and erythromycin (for isolates not available for pulsed-field gel electrophoresis). Results: Community-onset skin and soft-tissue infection due to S. aureus was identified in 389 episodes, with MRSA accounting for 72% (279 of 389 episodes). Among all S. aureus isolates, 63% (244 of 389 isolates) were community-acquired MRSA. Among MRSA isolates, 87% (244 of 279 isolates) were community-acquired MRSA. When analysis was restricted only to MRSA isolates that were available for pulsed-field gel electrophoresis, 91% (159 of 175 isolates) had a pulsed-field type consistent with community-acquired MRSA; of these, 99% (157 of 159 isolates) were the MRSA USA 300 clone. Factors independently associated with community-acquired MRSA infection were black race (prevalence ratio, 1.53 [95% CI, 1.16 to 2.02]), female sex (prevalence ratio, 1.16 [CI, 1.02 to 1.32]), and hospitalization within the previous 12 months (prevalence ratio, 0.80 [CI, 0.66 to 0.97]). Inadequate initial antibiotic therapy was statistically significantly more common among those with community-acquired MRSA (65%) than among those with methicillin-susceptible S. aureus skin and soft-tissue infection (1%). Limitations: Some MRSA isolates were not available for molecular typing. Conclusions: The community-acquired MRSA USA 300 clone was the predominant cause of community-onset S. aureus skin and soft-tissue infection. Empirical use of agents active against community-acquired MRSA is warranted for patients presenting with serious skin and soft-tissue infections.
Immunohistochemichal expression of biomarkers: a comparative study between diagnostic bronchial biopsies and surgical specimens of non-small-cell lung cancer
Authors: L. Taillade, F. Penault-Llorca, T. Boulet, P. Fouret, S. Michiels, E. Taranchon, G. Mountzios, P. Validire, J. Domont, P. Girard, D. Grunenwald, T. Le Chevalier, J-C Soria
Journal: Annals of Oncology (2007)
Effect of osteoclast activating factor from human leukocytes on bone metabolism.
Authors: L G Raisz, R A Luben, G R Mundy, J W Dietrich, J E Horton, C L Trummel
Journal: Journal of Clinical Investigation (1975)

The effects of osteoclast activating factor (OAF) released by normal human peripheral blood leukocytes cultured with phytohemagglutinin have been examined in organ culture. Like parathyroid hormone (PTH), OAF causes a rapid increased in the release of previously incorporated 45Ca from fetal rat bone after brief or continuous exposure; the bones also lose stable calcium and collagen content. The resorption response to OAF also resembles that of PTH in having a steep dose response curve and being only transiently inhibited by calcitonin and partially inhibited by increasing medium phosphate concentration. OAF-stimulated resorption was inhibited more effectively by cortisol than was PTH stimulation. The response to maximally effective doses of OAF was not enhanced by PTH or prostaglandin E2, but submaximal doses gave additive effects. Both OAF and PTH inhibit collagen synthesis in fetal rat calvaria at the concentrations that stimulate bone resorption.
Pten signaling in gliomas
Authors: C. B. Knobbe, A. Merlo, G. Reifenberger
Journal: Neuro-Oncology (2002)

In 1997, the PTEN gene (phosphatase and tensin homolog deleted on chromosome 10) was identified as a tumor suppressor gene on the long arm of chromosome 10. Since then, important progress has been made with respect to the understanding of the role of the Pten protein in the normal development of the brain as well as in the molecular pathogenesis of human gliomas. This review summarizes the current state of the art concerning the involvement of aberrant Pten function in the development of different biologic features of malignant gliomas, such as loss of cell-cycle control and uncontrolled cell proliferation, escape from apoptosis, brain invasion, and aberrant neoangiogenesis. Most of the tumor-suppressive properties of Pten are dependent on its lipid phosphatase activity, which inhibits the phosphatidylinositol-3′-kinase (PI3K)/Akt signaling pathway through dephosphorylation of phosphatidylinositol-(3,4,5)-tri phosphate. The additional function of Pten as a dual-specificity protein phosphatase may also play a role in glioma pathogenesis. Besides the wealth of data elucidating the functional roles of Pten, recent studies suggest a diagnostic significance of PTEN gene alterations as a molecular marker for poor prognosis in anaplastic astrocytomas and anaplastic oligodendrogliomas. Furthermore, the possibility of selective targeting of PTEN mutant tumor cells by specific pharmacologic inhibitors of members of the Pten/PI3K/Akt pathway opens up new perspectives for a targeted molecular therapy of malignant gliomas.
Pulmonary radiofrequency ablation in a single lung patient
Authors: M C Ambrogi, O Fanucchi, R Lencioni, R Cioni, A Mussi
Journal: Thorax (2006)

Recurrence in the contralateral lung of patients who have undergone pneumonectomy for lung cancer is often not surgically treatable. Percutaneous radiofrequency ablation (RFA) of tumours is an emerging minimally invasive technique which has recently been used in the treatment of lung cancer. The case history is presented of a patient who had previously undergone pneumonectomy in whom recurrence of lung cancer was treated by RFA. The procedure was performed under CT guidance and was uneventful. At follow up 9 months later the tumour appeared to have ablated. To our knowledge, no similar case has previously been reported in the literature.
Is tai chi beneficial for improving aerobic capacity? A systematic review
Authors: M S Lee, E-N Lee, E Ernst
Journal: British Journal of Sports Medicine (2008)

Tai chi has been claimed to generate beneficial effects with respect to a wide range of diseases. The purpose of this systematic review was to evaluate evidence from randomised clinical trials (RCTs) testing the effectiveness of tai chi for increasing aerobic capacity. Systematic searches were conducted on 14 electronic databases without restrictions on population characteristics or the language of publication. The outcome measures considered for inclusion were changes in maximal oxygen consumption as a test for aerobic capacity. Five RCTs met all inclusion criteria. Three RCTs compared the effects of tai chi with no treatment. The meta-analysis failed to show an effect of tai chi on aerobic capacity compared with sedentary controls (n = 151, weight mean difference, ml/kg/min, 0.50, 95% CI -1.14 to 2.15, p = 0.55). Two RCTs compared tai chi with conventional physical exercise including brisk, low intensity and moderate intensity walking, and aerobic exercise. The results show that tai chi was not statistically significantly superior to physical exercise. In conclusion, the existing evidence does not suggest that regular tai chi is an effective way of increasing aerobic capacity.
Threshold Haemoglobin Levels and the Prognosis of Stable Coronary Disease: Two New Cohorts and a Systematic Review and Meta-Analysis
Authors: Anoop D. Shah, Owen Nicholas, Adam D. Timmis, Gene Feder, Keith R. Abrams, Ruoling Chen, Aroon D. Hingorani, Harry Hemingway
Journal: PLoS Medicine (2011)

Low haemoglobin concentration has been associated with adverse prognosis in patients with angina and myocardial infarction (MI), but the strength and shape of the association and the presence of any threshold has not been precisely evaluated.A retrospective cohort study was carried out using the UK General Practice Research Database. 20,131 people with a new diagnosis of stable angina and no previous acute coronary syndrome, and 14,171 people with first MI who survived for at least 7 days were followed up for a mean of 3.2 years. Using semi-parametric Cox regression and multiple adjustment, there was evidence of threshold haemoglobin values below which mortality increased in a graded continuous fashion. For men with MI, the threshold value was 13.5 g/dl (95% confidence interval [CI] 13.2-13.9); the 29.5% of patients with haemoglobin below this threshold had an associated hazard ratio for mortality of 2.00 (95% CI 1.76-2.29) compared to those with haemoglobin values in the lowest risk range. Women tended to have lower threshold haemoglobin values (e.g, for MI 12.8 g/dl; 95% CI 12.1-13.5) but the shape and strength of association did not differ between the genders, nor between patients with angina and MI. We did a systematic review and meta-analysis that identified ten previously published studies, reporting a total of only 1,127 endpoints, but none evaluated thresholds of risk.There is an association between low haemoglobin concentration and increased mortality. A large proportion of patients with coronary disease have haemoglobin concentrations below the thresholds of risk defined here. Intervention trials would clarify whether increasing the haemoglobin concentration reduces mortality.
Dose dependent effects of protracted ingestion of small amounts of gliadin in coeliac disease children: a clinical and jejunal morphometric study.
Authors: C Catassi, M Rossini, I M Ratsch, I Bearzi, A Santinelli, R Castagnani, E Pisani, G V Coppa, P L Giorgi
Journal: Gut (1993)

This study aimed to investigate the effects of chronic ingestion of small amounts of gliadin on children with coeliac disease. A four week challenge was performed on 20 children who had been on a gluten free diet for mean (SD) 14 (3) months. They were given a daily dose of either 100 mg (group A, n = 10, mean age 4 (2) years) or 500 mg of gliadin (group B, mean age 5 (3) years). The effects of the gliadin were monitored by morphometric study of the jejunal mucosa, intestinal permeability test with cellobiose/mannitol, and serum antigliadin antibody test. After the challenge, group A patients showed a significant increase in the mean intraepithelial lymphocyte count (before challenge 11 (3), afterwards 19 (6)) and a decrease in the villous height/crypt depth ratio (beforehand 1.5 (0.1), afterwards 1.3 (0.2)), while the intestinal permeability test remained normal and the IgA-antigliadin antibody increased in four of 10 children. After the challenge group B showed more pronounced histological changes, an increase in the mean urinary cellobiose/mannitol % (beforehand 0.028 (0.020), afterwards 0.058 (0.028)), and IgA-antigliadin antibody positivity in six of eight subjects. The discriminant analysis function showed that the pretreatment group, group A after challenge, and group B after challenge were correctly classified in 90% of cases by functions based on the individual intraepithelial lymphocyte count and the villous height/crypt depth ratio. This study shows that chronic ingestion of small amounts of gluten causes dose-dependent damage to the small intestinal mucosa in children with coeliac disease. The predictive value of laboratory tests, such as the antigliadin antibody test and the intestinal permeability test seems to be lower in treated patients than in those with active coeliac disease.
Serological changes in the course of traditional and biological disease modifying therapy of rheumatoid arthritis
Authors: Christoph Böhler, Helga Radner, Josef S Smolen, Daniel Aletaha
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Objective</h3> To investigate changes of rheumatoid factor (RF) and antibodies against citrullinated peptides (ACPA) during therapy with disease modifying antirheumatic drugs. <h3>Methods</h3> We obtained clinical and serological data of patients from the treatment start and after 6 months of therapy. With non-parametric tests, we analysed changes of ACPA and RF levels between the two visits and the influence of treatment response. Furthermore, we analysed potential influential factors as disease chronicity, different therapeutics and the trend over 18 months. <h3>Results</h3> 143 ACPA and RF positive patients were included. The median (25th/75th percentile) relative changes after 6 months were −35.6% (−63.3; −8.3) for RF and −15.2% (−40.0; 10.0) for ACPA (p&lt;0.001 for both). Changes of RF levels were significantly greater than those seen for ACPA (p&lt;0.001). The decrease of ACPA and RF was significantly higher in treatment responders (p=0.034 and p=0.01, respectively). Aside from changes in disease activity, only a short disease duration showed an independent effect on changes of RF levels (p=0.087). <h3>Conclusions</h3> ACPA and RF levels decreased significantly after 6 months of therapy. Reductions of both autoantibodies were closely linked to a reduction of disease activity. RF declined faster, to a larger extent and in greater numbers of patients than ACPA.
Regulation of alveolar epithelial function by hypoxia
Authors: G. Zhou, L. A. Dada, J. I. Sznajder
Journal: European Respiratory Journal (2008)

Patients with acute respiratory distress syndrome and high-altitude pulmonary oedema build up excess lung fluid, which leads to alveolar hypoxia. In patients with acute respiratory distress syndrome and hypoxia, there is a decrease in oedema fluid clearance, due in part to the downregulation of plasma membrane sodium–potassium adenosine triphosphatase (Na,K-ATPase). In alveolar epithelial cells, acute hypoxia promotes Na,K-ATPase endocytosis from the plasma membrane to intracellular compartments, resulting in inhibition of Na,K-ATPase activity. Exposure to prolonged hypoxia leads to degradation of plasma membrane Na,K-ATPase. The downregulation of plasma membrane Na,K-ATPase reduces adenosine triphosphate demand, as part of a survival mechanism of cellular adaptation to hypoxia. Hypoxia has also been shown to disassemble and degrade the keratin intermediate filament network, a fundamental component of the cell cytoskeleton, affecting epithelial barrier function. Accordingly, better understanding of the mechanisms regulating cellular adaptation to hypoxia may lead to the development of novel therapeutic strategies for acute respiratory distress syndrome and high-altitude pulmonary oedema patients.
MULTIMARKER RISK MODEL CONTAINING TROPONIN, INTERLEUKIN-10, MYELOPEROXIDASE AND PLACENTAL GROWTH FACTOR PREDICTS LONG-TERM CARDIOVASCULAR RISK AFTER NON-ST-SEGMENT ELEVATION ACUTE CORONARY SYNDROME
Authors: Rohit M. Oemrawsingh, Timo Lenderink, K. Martijn Akkerhuis, Christopher Heeschen, Stephan Baldus, Stephan Fichtlscherer, Christian W. Hamm, Maarten L. Simoons, Eric Boersma
Journal: Journal of the American College of Cardiology (2010)
Genotype Score in Addition to Common Risk Factors for Prediction of Type 2 Diabetes
Authors: James B. Meigs, Peter Shrader, Lisa M. Sullivan, Jarred B. McAteer, Caroline S. Fox, Josée Dupuis, Alisa K. Manning, Jose C. Florez, Peter W.F. Wilson, Ralph B. D'Agostino, L. Adrienne Cupples
Journal: New England Journal of Medicine (2008)

Multiple genetic loci have been convincingly associated with the risk of type 2 diabetes mellitus. We tested the hypothesis that knowledge of these loci allows better prediction of risk than knowledge of common phenotypic risk factors alone.
Adult Attention Deficit Disorder
Authors: P Krener
Journal: JAMA (1988)

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Systematic Assessment of Etiology in Adults With a Clinical Diagnosis of Young-Onset Type 2 Diabetes Is a Successful Strategy for Identifying Maturity-Onset Diabetes of the Young
Authors: Gaya Thanabalasingham, Aparna Pal, Mary P. Selwood, Christina Dudley, Karen Fisher, Polly J. Bingley, Sian Ellard, Andrew J. Farmer, Mark I. McCarthy, Katharine R. Owen
Journal: Diabetes Care (2012)

Misdiagnosis of maturity-onset diabetes of the young (MODY) remains widespread, despite the benefits of optimized management. This cross-sectional study examined diagnostic misclassification of MODY in subjects with clinically labeled young adult-onset type 1 and type 2 diabetes by extending genetic testing beyond current guidelines.
Gastric lesion in dermatitis herpetiformis.
Authors: D P O'Donoghue, M Lancaster-Smith, G D Johnson, P J Kumar
Journal: Gut (1976)

Five of 33 patients with dermatitis herpetiformis (DH) were found to have gastric parietal cell antibody in their sera, whereas it was not found in 30 healthy controls of comparable age distribution. Fifteen of the patients with DH underwent further studies to investigate the histological and functional state of their gastric mucosa. Atrophic gastritis was found in all five patients whose sera contained gastric parietal cell antibody and in three of 11 patients with no antibody in their sera. In addition, there was marked impairment of acid secretion in the DH group as a whole, but, apart from one patient with overt pernicious anaemia (PA), there was no evidence of malabsorption of B12.