tbuckley/cabot-search huggingface dataset:
Metabolic Syndrome and Risk of Cancer
Authors: Katherine Esposito, Paolo Chiodini, Annamaria Colao, Andrea Lenzi, Dario Giugliano
Journal: Diabetes Care (2012)

OBJECTIVE Available evidence supports the emerging hypothesis that metabolic syndrome may be associated with the risk of some common cancers. We did a systematic review and meta-analysis to assess the association between metabolic syndrome and risk of cancer at different sites. RESEARCH DESIGN AND METHODS We conducted an electronic search for articles published through October 2011 without restrictions and by reviewing reference lists from retrieved articles. Every included study was to report risk estimates with 95% CIs for the association between metabolic syndrome and cancer. RESULTS We analyzed 116 datasets from 43 articles, including 38,940 cases of cancer. In cohort studies in men, the presence of metabolic syndrome was associated with liver (relative risk 1.43, P &amp;lt; 0.0001), colorectal (1.25, P &amp;lt; 0.001), and bladder cancer (1.10, P = 0.013). In cohort studies in women, the presence of metabolic syndrome was associated with endometrial (1.61, P = 0.001), pancreatic (1.58, P &amp;lt; 0.0001), breast postmenopausal (1.56, P = 0.017), rectal (1.52, P = 0.005), and colorectal (1.34, P = 0.006) cancers. Associations with metabolic syndrome were stronger in women than in men for pancreatic (P = 0.01) and rectal (P = 0.01) cancers. Associations were different between ethnic groups: we recorded stronger associations in Asia populations for liver cancer (P = 0.002), in European populations for colorectal cancer in women (P = 0.004), and in U.S. populations (whites) for prostate cancer (P = 0.001). CONCLUSIONS Metabolic syndrome is associated with increased risk of common cancers; for some cancers, the risk differs betweens sexes, populations, and definitions of metabolic syndrome.
Feasibility and Effectiveness in Clinical Practice of a Multifactorial Intervention for the Reduction of Cardiovascular Risk in Patients With Type 2 Diabetes
Authors: Olga Vaccaro, Laura Franzini, Roberto Miccoli, Franco Cavalot, Diego Ardigò, Massimo Boemi, Pierpaolo De Feo, Gianpaolo Reboldi, Angela Albarosa Rivellese, Mariella Trovati, Ivana Zavaroni
Journal: Diabetes Care (2013)

To evaluate the feasibility and effectiveness of an intensive, multifactorial cardiovascular risk reduction intervention in a clinic-based setting.The study was a pragmatic, cluster randomized trial, with the diabetes clinic as the unit of randomization. Clinics were randomly assigned to either continue their usual care (n = 5) or to apply an intensive intervention aimed at the optimal control of cardiovascular disease (CVD) risk factors and hyperglycemia (n = 4). To account for clustering, mixed model regression techniques were used to compare differences in CVD risk factors and HbA1c. Analyses were performed both by intent to treat and as treated per protocol.Nine clinics completed the study; 1,461 patients with type 2 diabetes and no previous cardiovascular events were enrolled. After 2 years, participants in the interventional group had significantly lower BMI, HbA1c, LDL cholesterol, and triglyceride levels and significantly higher HDL cholesterol level than did the usual care group. The proportion of patients reaching the treatment goals was systematically higher in the interventional clinics (35% vs. 24% for LDL cholesterol, P = 0.1299; 93% vs. 82% for HDL cholesterol, P = 0.0005; 80% vs. 64% for triglycerides, P = 0.0002; 39% vs. 22% for HbA1c, P = 0.0259; 13% vs. 5% for blood pressure, P = 0.1638). The analysis as treated per protocol confirmed these findings, showing larger and always significant differences between the study arms for all targets.A multifactorial intensive intervention in type 2 diabetes is feasible and effective in clinical practice and it is associated with significant and durable improvement in HbA1c and CVD risk profile.
Aerosolized Steroids for Croup
Authors: Louis I. Landau, Gary C. Geelhoed
Journal: New England Journal of Medicine (1994)

In this issue of the Journal, Klassen et al. report that the nebulized glucocorticoid budesonide produces prompt and substantial clinical improvement in children who present to the emergency room with mild-to-moderate croup1. These authors report faster discharge from the emergency room and a reduced rate of subsequent admission to the hospital. However, there was subsequent use of dexamethasone in both the budesonide group and the placebo group, an indication that the attending physicians continued to be concerned about their patients.Although viral croup is the most common upper airway disease in children in the first four years of life, . . .
SURGERY IN CANCER OF THE PROSTATE
Authors: Frank Hinman
Journal: JAMA (1942)

<h3>To the Editor:—</h3> An opinion expressed inThe Journal, March 7, page 855, in answer to a query from a doctor in California is entirely false and is not held, I am sure, by a majority of urologists. Carcinoma of the prostate differs from carcinoma elsewhere in the body in no particular respect so far as treatment is concerned except for the newer procedures of diethylstilbestrol and castration. An early diagnosis of carcinoma of the prostate can and has been repeatedly made, and when made by the urologist trained to do radical prostatectomy, it can and has been repeatedly cured. The problem is one of early diagnosis, and this has been made and confirmed when the lesion is not larger than 1 cm. in diameter. In these cases, confirmation has usually been made by frozen section after perineal exposure, and if after such biopsy the presumptive clinical diagnosis has been
Treatment of deep vein thrombosis with streptokinase.
Authors: F Duckert, G Muller, D Nyman, A Benz, S Prisender, G Madar, M A Da Silva, L K Widmer, H E Schmitt
Journal: BMJ (1975)

From September 1962 to May 1972 145 patients with acute or subacute deep vein thrombosis confirmed by phlebography were treated with streptokinase. During the same period 42 patients considered unfit for thrombolytic therapy were treated with herapin and oral anticoagulants. The results, assessed by repeat phlebography, in 93 of the patients treated with streptokinase were compared with those in 42 patients treated with heparin. The age, sex, and severity of occlusion were roughly similar in both groups. Streptokinase treatment was successful in 42 per cent, partially successful in 25 per cent, and unsuccessful in 32 per cent of the 93 patients compared with none, 10 per cent, and 88 percent respectively in the 42 patients treated with heparin. Streptokinase was more effective when the thrombus was in proximal rather than calf veins. Thrombi of more than six days old were readily lysed. Plasma fibrinogen levels were below 0-8 g/1 (80 mg/100 ml) in nearly all patients successfully treated. The incidence of pulmonary embolism was no greater with streptokinase than with heparin treatment. Only prolonged follow-up would show whether thrombolytic treatment would be effective in preventing late complications of deep vein thrombosis such as chronic venous insufficiency.
A Randomized Controlled Trial of the Tumor Necrosis Factor Antagonist Infliximab for Treatment-Resistant Depression
Authors: Charles L. Raison, Robin E. Rutherford, Bobbi J. Woolwine, Chen Shuo, Pamela Schettler, Daniel F. Drake, Ebrahim Haroon, Andrew H. Miller
Journal: JAMA Psychiatry (2012)

<h3>Context</h3>Increased concentrations of inflammatory biomarkers predict antidepressant nonresponse, and inflammatory cytokines can sabotage and circumvent the mechanisms of action of conventional antidepressants.<h3>Objectives</h3>To determine whether inhibition of the inflammatory cytokine tumor necrosis factor (TNF) reduces depressive symptoms in patients with treatment-resistant depression and whether an increase in baseline plasma inflammatory biomarkers, including high-sensitivity C-reactive protein (hs-CRP), TNF, and its soluble receptors, predicts treatment response.<h3>Design</h3>Double-blind, placebo-controlled, randomized clinical trial.<h3>Setting</h3>Outpatient infusion center at Emory University in Atlanta, Georgia.<h3>Participants</h3>A total of 60 medically stable outpatients with major depression who were either on a consistent antidepressant regimen (n = 37) or medication-free (n = 23) for 4 weeks or more and who were moderately resistant to treatment as determined by the Massachusetts General Hospital Staging method.<h3>Interventions</h3>Three infusions of the TNF antagonist infliximab (5 mg/kg) (n = 30) or placebo (n = 30) at baseline and weeks 2 and 6 of a 12-week trial.<h3>Main Outcome Measures</h3>The 17-item Hamilton Scale for Depression (HAM-D) scores.<h3>Results</h3>No overall difference in change of HAM-D scores between treatment groups across time was found. However, there was a significant interaction between treatment, time, and log baseline hs-CRP concentration (P = .01), with change in HAM-D scores (baseline to week 12) favoring infliximab-treated patients at a baseline hs-CRP concentration greater than 5 mg/L and favoring placebo-treated patients at a baseline hs-CRP concentration of 5 mg/L or less. Exploratory analyses focusing on patients with a baseline hs-CRP concentration greater than 5 mg/L revealed a treatment response (≥50% reduction in HAM-D score at any point during treatment) of 62% (8 of 13 patients) in infliximab-treated patients vs 33% (3 of 9 patients) in placebo-treated patients (P = .19). Baseline concentrations of TNF and its soluble receptors were significantly higher in infliximab-treated responders vs nonresponders (P &lt; .05), and infliximab-treated responders exhibited significantly greater decreases in hs-CRP from baseline to week 12 compared with placebo-treated responders (P &lt; .01). Dropouts and adverse events were limited and did not differ between groups.<h3>Conclusions</h3>This proof-of-concept study suggests that TNF antagonism does not have generalized efficacy in treatment-resistant depression but may improve depressive symptoms in patients with high baseline inflammatory biomarkers.<h3>Trial Registration</h3>clinicaltrials.gov Identifier: NCT00463580.
Ramadan Fasting: A Study of Changes in Glucose Profiles Among Patients With Diabetes Using Continuous Glucose Monitoring
Authors: Nader Lessan, Haydar Hasan, Maha T. Barakat
Journal: Diabetes Care (2012)

Fasting during the Muslim holy month of Ramadan entails abstinence from eating, drinking, and smoking from dawn to sunset. Although the sick are exempted (Holy Koran, Al-Bakarah, 183–185), many patients, including those with diabetes, choose to go ahead with fasting, often for social and cultural as well as religious reasons (1).

We have explored changes in glucose profiles of patients with type 2 diabetes in a prospective observational study using continuous glucose monitoring (CGM; Medtronic MiniMed CGMS Gold). This was performed for at least 3 consecutive days during Ramadan (2). Nonfasting CGM for the same length of time was obtained on each patient either before or after Ramadan. A mean CGM curve for all patients was obtained during and outside the Ramadan fasting period …
Induction of pyloric hypertrophy by pentagastrin. An animal model for infantile hypertrophic pyloric stenosis.
Authors: J A Dodge, A A Karim
Journal: Gut (1976)

Administration of pentagastrin in depot form to 20 pregnant bitches produced pyloric hypertrophy in about 28% and gastroduodenal ulceration in about 16% of their pups. The two lesions were not necessarily found in the same individuals. Histological appearances of the pylorus in affected pups closely resembled those of human infantile pyloric stenosis.
THE STUDY OF MEDICINE IN THE FUTURE
Authors: R. R. Newell
Journal: JAMA (1960)

To the Editor:—  I am deeply concerned about medical education's consuming so many years before the physician begins to deliver some dividends on the investment made in him. I read Dr. Visscher's essay inThe Journal, July 30, page 1425, with hopeful interest. I like his careful distinction between graduate and postgraduate study. The confusion between science and art is a common failing (Newell, R. R.: Stanford M. Bull.  8 :181-183 [Nov.] 1950). He quotes John Russell: Medicine is an art, a science and a business. I would like to expand this and say that the practice of medicine is an art. It has a scientific foundation. It is quite usually a way of earning a living and sometimes a way of life.  It would be wholesome if we could get overt acceptance of the fact, which Visscher sees clearly, that medical colleges are parallel to schools of engineering rather
A novel locus for primary focal hyperhidrosis mapped on chromosome 2q31.1
Authors: J. Chen, M. Lin, X. Chen, Z. Cao, Z. Tan, W. Xiong, Y. Tu, J. Yang
Journal: British Journal of Dermatology (2014)

Funding sources: The work was supported by the Key Program of Scientific Research of Fujian Medical University (09ZD016), Natural Science Foundation of Fujian Province (2010J06010, 2013J01303), Program for New Century Excellent Talents in Fujian Province University (JA10127), Professor Academic Development Fund of Fujian Medical University (JS12003) and National Natural Science Foundation of China (8107096). Conflicts of interest: none declared. J.C. and M.L. contributed equally to this work. Dear Editor, Primary focal hyperhidrosis (PFH) is a disorder characterized by excessive sweating in specific body areas such as the palm, sole and axillae beyond physiological need, leading to severe psychological, social and occupational dysfunction.1 2 The cause of primary hyperhidrosis still remains unclear. It seems to be associated with neurohumoral or secretory cell metabolic abnormalities, but without structural defects in the sweat glands.3 Much evidence implies that PFH could be a genetic disorder with an autosomal dominant mode of transmission, incomplete penetrance and variable phenotype.4 5 Only one PFH locus has been mapped to chromosome 14q11.2–q13, but no disease‐causing gene has been identified.6
Increased Oxidative Stress Is Associated With Serum Levels of Triglyceride, Insulin Resistance, and Hyperinsulinemia in Japanese Metabolically Obese, Normal-Weight Men
Authors: Akira Katsuki, Yasuhiro Sumida, Hideki Urakawa, Esteban C. Gabazza, Shuichi Murashima, Kaname Nakatani, Yutaka Yano, Yukihiko Adachi
Journal: Diabetes Care (2004)

Metabolically obese, normal-weight (MONW) subjects (BMI <25 kg/m2) are characterized by an excess (≥100 cm2 by abdominal computed tomography scanning) visceral fat area (VFA), insulin resistance, and hyperinsulinemia (1,2). The criteria for MONW subjects and the insulin resistance syndrome are very similar, and the pathophysiological events occurring in MONW subjects have recently been the focus of many investigators (1–4).

Several studies have reported the association of oxidative stress with insulin resistance and hyperinsulinemia in obese subjects (5,6). However, the degree of oxidative stress and its correlation with insulin resistance and insulin secretion have not yet been evaluated in MONW subjects.

The present study comprised 18 Japanese MONW (aged 34.7 ± 1.7 …
ROCK-phosphorylated vimentin modifies mutant huntingtin aggregation via sequestration of IRBIT
Authors: Peter O Bauer, Roman Hudec, Anand Goswami, Masaru Kurosawa, Gen Matsumoto, Katsuhiko Mikoshiba, Nobuyuki Nukina
Journal: Molecular Neurodegeneration (2012)

Abstract Background Huntington's Disease (HD) is a fatal hereditary neurodegenerative disease caused by the accumulation of mutant huntingtin protein (Htt) containing an expanded polyglutamine (polyQ) tract. Activation of the channel responsible for the inositol-induced Ca 2+ release from ensoplasmic reticulum (ER), was found to contribute substantially to neurodegeneration in HD. Importantly, chemical and genetic inhibition of inositol 1,4,5-trisphosphate (IP3) receptor type 1 (IP3R1) has been shown to reduce mutant Htt aggregation. Results In this study, we propose a novel regulatory mechanism of IP3R1 activity by type III intermediate filament vimentin which sequesters the negative regulator of IP3R1, IRBIT, into perinuclear inclusions, and reduces its interaction with IP3R1 resulting in promotion of mutant Htt aggregation. Proteasome inhibitor MG132, which causes polyQ proteins accumulation and aggregation, enhanced the sequestration of IRBIT. Furthermore we found that IRBIT sequestration can be prevented by a rho kinase inhibitor, Y-27632. Conclusions Our results suggest that vimentin represents a novel and additional target for the therapy of polyQ diseases.
Primary effusion lymphoma with B-cell phenotype
Authors: Masahito Iwahashi, Syuji Iida, Shigeki Sako, Souichi Inoue, Hiroshi Kikuchi, Eiichi Otsuka, Masaru Nasu
Journal: American Journal of Hematology (2000)

We describe here a case of primary effusion lymphoma that occurred in a 78-year-old woman. She was successively treated with prednisolone but died 15 months after the diagnosis of primary effusion lymphoma. The immunohistochemistry revealed the neoplastic cells to be CD19+, CD20+, CD21+, Sm-Ig+, and HLA-DR+. This patient exhibited clonal IgH and clonal κ light chain gene rearrangement, indicating a B-cell origin. The present case was distinguished from the majority cases of HHV-8-positive primary effusion lymphoma. Here we present clinical details of response to therapy in this case. Am. J. Hematol. 64:317–318, 2000. © 2000 Wiley-Liss, Inc.
Points: Evaluation of portable haemoglobinometer in general practice
Authors: R. Quinn
Journal: BMJ (1987)

sensitivity to halothane in children with a, anti- trypsin deficiency,3 but they refer to an article in the New England 3rournal of Medicine.4Again, there is no mention of this sensitivity.This is an example ofan error compounded through misread- ing and referencing.The authors present seven cases of suspected halothane hepatitis.In case 7, however, they found no halothane antibody, but they still classified this child as having halothane hepatitis, explaining that it is possible that the antibody was produced but was undetectable.In the case report they state that a 3½/2 year old boy weighed 1800 g.This is an extremely small child.Though halothane hepatitis may occur in children, it is extremely rare, and Dr Kenna and coworkers cannot give the incidence that might be expected in children.In a review article on halothane hepatitis Stock et al concluded that there is no diagnostic test that is specific for halothane induced liver damage and that therefore the diagnosis can be made only by excluding all other causes of postoperative liver dysfunction.5Walton states that non-A, non-B hepatitis may be responsible for halothane hepatitis after a single exposure.6Thus we still cannot define specifically the diagnostic criteria for halothane hepatitis.If it exists it remains extremely rare in children and has an incidence less than that of non-A, non-B hepatitis in the general population.An extensive clinical study of preoperative liver function in asymptomatic children who received halothane and were then followed up for a long period would be needed to provide clearer conclusions.
Effects of Neutrophil Elastase Inhibitor on Bleomycin-Induced Pulmonary Fibrosis in Mice
Authors: YASUYUKI TAOOKA, AKIHIRO MAEDA, KEIKO HIYAMA, SHINICHI ISHIOKA, MICHIO YAMAKIDO
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

Neutrophils play an important role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). To elucidate the possible involvement of neutrophil elastase (NE) in pulmonary fibrosis, we investigated the efficacy of a new specific NE inhibitor (ONO-5046 Na) in a murine model of human IPF, bleomycin-induced pulmonary fibrosis. Bronchoalveolar lavage (BAL) and histopathological analysis were performed on bleomycin-treated mice (group A), bleomycin and ONO-5046 Na-treated mice (group B), and saline control groups at 1, 15, and 29 d after the end of bleomycin treatment. At 29 d, multifocal fibrosis was observed in group A, whereas no fibrotic regions were observed in group B. Interleukin-1 beta and macrophage inflammatory protein-2 mRNA levels in BAL cells on day 1, and platelet-derived growth factor-A and insulin-like growth factor-1 mRNA levels on days 1 and 15, were significantly lower in group B than in group A. Thus, we demonstrated an inhibitory effect of ONO-5046. Na on pulmonary fibrosis in mice, indicating the involvement of NE in the pathogenesis of pulmonary fibrosis. We propose that this effect might be related to suppressed expression of particular cytokines in alveolar macrophages and that this specific NE inhibitor could be a novel therapeutic agent for IPF.
Binding of Dipyridamole to Human Platelets and to α1 Acid Glycoprotein and its Significance for the Inhibition of Adenosine Uptake
Authors: Kuchibhotla Subbarao, Boguslaw Rucinski, Michael A. Rausch, Karl Schmid, Stefan Niewiarowski
Journal: Journal of Clinical Investigation (1977)

The interactions of dipyridamole with alpha(1) acid glycoprotein of plasma and with human platelets are related to inhibition of adenosine uptake by platelets. Binding studies by equilibrium gel filtration suggested that 1 mol of dipyridamole binds per mol of alpha(1) acid glycoprotein with a dissociation constant of 1.6 muM. Platelets contain two populations of binding sites, one with high and another with lower affinity for the drug. The binding of dipyridamole to the high-affinity sites follows a Michaelis-Menten binding pattern with a dissociation constant of 0.04 muM. Approximately 2 x 10(4) dipyridamole molecules are bound at the high-affinity sites of each platelet. The lower affinity sites bind the drug with a dissociation constant of 4 muM. In the presence of alpha(1) acid glycoprotein of plasma, the binding of dipyridamole to human platelets is inhibited. Correspondingly, the dipyridamole inhibition of adenosine uptake by platelets is reduced 1,000-fold by purified alpha(1) acid glycoprotein. The binding of dipyridamole to human platelets was found to be essential for its inhibition of adenosine uptake by platelets. Dipyridamole decreases the incorporation of [(14)C]adenosine radioactivity in platelet nucleotides and reduces the [(14)C]-ATP to [(14)C]ADP ratio. Purified alpha(1) acid glycoprotein reverses these effects of dipyridamole on adenosine metabolism of platelets in a concentration-dependent manner. An equilibrium of dipyridamole binding to alpha(1) acid glycoprotein and to platelets is proposed.
Tissue-specific phosphorylation of complement receptors CR1 and CR2.
Authors: P S Changelian, D T Fearon
Journal: The Journal of Experimental Medicine (1986)

CR1 of neutrophils and monocytes may exist in a resting state, in which it only binds ligand-coated particles, or an activated state, in which it mediates phagocytosis. Because the activated state of CR1 can be induced by the stimulation of protein kinase C with PMA, CR1 was assessed for phosphorylation. Purified human neutrophils, monocytes, eosinophils, tonsilar lymphocytes, SB cells, and erythrocytes were labeled with 32PO4 and incubated with buffer or 100 ng/ml PMA. Membrane proteins were immunoprecipitated and analyzed by SDS-PAGE and autoradiography. CR1, unlike HLA class I heavy chain, was not constitutively phosphorylated by any cell type. PMA induced phosphorylation of CR1 in three phagocytic cell types, but did not induce the phosphorylation of CR3 or FcR. FMLP also induced the phosphorylation of CR1 in neutrophils. In contrast, PMA did not induce phosphorylation of CR1 in tonsilar B lymphocytes, SB cells, or erythrocytes, indicating restriction of this reaction to phagocytic cell types. This may be due to differences in the structure or presentation of the cytoplasmic domain of CR1 in phagocytic vs. nonphagocytic cells. Phosphorylation of CR2, however, did occur in PMA-treated B lymphocytes and SB cells, suggesting that this receptor, rather than CR1, may be involved in regulation of B lymphocyte function.