tbuckley/cabot-search huggingface dataset:
Acne vulgaris: an investigation into the number of anaerobic diphtheroids and members of Micrococcaceae the in normal and acne skin
Authors: K.T. HOLLAND, W.J. CUNLIFFE, C.D. ROBERTS
Journal: British Journal of Dermatology (1977)

A quantitative study was made of the microflora of 174 acne and 68 non-acne subjects. Two groups of organisms were investigated, the anaerobic diphtheroids and members of the Micrococcaceae. The results showed high numbers of both groups of bacteria in skin bearing blackheads, papules or pustules and in non-acne adolescent skin. There were significantly lower numbers of bacteria in the pilosebaceous ducts of normal looking skin in acne areas and in pre-adolescent skin when compared with non-acne adolescent skin. It is suggested that increased numbers of bacteria alone do not predispose to acne, but that their interaction with the skin, which is a function of the localized skin environment, may be important.
Cross-talk between hypoxia and insulin signaling through Phd3 regulates hepatic glucose and lipid metabolism and ameliorates diabetes
Authors: Cullen M Taniguchi, Elizabeth C Finger, Adam J Krieg, Colleen Wu, Anh N Diep, Edward L LaGory, Kevin Wei, Lisa M McGinnis, Jenny Yuan, Calvin J Kuo, Amato J Giaccia
Journal: Nature Medicine (2013)
The Superficial Femoral Vein
Authors: Warner P. Bundens
Journal: JAMA (1995)

<h3>Objective.</h3> —To assess the potential for error in interpretation of venous duplex reports that use the term "superficial femoral vein." <h3>Design.</h3> —Three surveys conducted by mail. <h3>Setting.</h3> —Three multispecialty medical groups, anatomy departments of all US medical schools, and vascular laboratories. <h3>Participants.</h3> —A total of 46 family practitioners and general internists, 95 chairpersons of departments of anatomy, and 85 laboratory directors. <h3>Main Outcome Measures.</h3> —Proposed treatment of a patient with leg pain and an acute thrombosis of the superficial femoral vein; what nomenclature(s) for the deep thigh veins is (are) felt to be correct, what are acceptable alternatives, what is taught to students and which is preferred; and what terminology is being used in lower limb venous duplex reports. <h3>Results.</h3> —Only 24% (11/46) of the respondents would have administered anticoagulants to the patient as described. Only 3% (3/95) of anatomists felt the term "superficial femoral vein" was correct, 22% (21/95) felt it was an acceptable alternative (though only 9% [9/95] taught it to medical students), and only 7% (7/95) of anatomists felt the term was preferred for everyday use. The term "superficial femoral vein" is used by 93% (79/85) of vascular laboratories in lower limb venous duplex reports. <h3>Conclusion.</h3> —although the overwhelming majority of vascular laboratories use the term "superficial femoral vein" in venous duplex reports, the use of this term is potentially hazardous to patients. Most primary care physicians have not been taught and are not aware that the superficial femoral vein is a deep vein and that acute thrombosis of this vessel is potentially life threatening. (<i>JAMA</i>. 1995;274:1296-1298)
Development and Present Status of an Electrocatalytic Glucose Sensor
Authors: G J Richter, G Luft, U Gebhardt
Journal: Diabetes Care (1982)

For the determination of glucose in body fluids the electrocatalytic sensor seems to be quite favorable, particularly for long-term intracorporeal operation. The measuring response is disturbed by the fluctuating concentrations of interfering substances that are present in body fluids. However, the disturbance can be for the most part controlled, as shown in the case of amino acids. Their marked influence on glucose oxidation is suppressed at a membrane-covered sensor electrode by using a potential step method.
Prospective Evaluation of Dietary and Other Predictors of Fatal Stroke in Shanghai, China
Authors: Ronald K. Ross, Jian-Min Yuan, Brian E. Henderson, Jinha Park, Yu-Tang Gao, Mimi C. Yu
Journal: Circulation (1997)

Background Although a number of risk factors for fatal stroke are well established in Western populations, this is less true for Asian countries, many of which have stroke mortality rates that are historically high. In a prospective study in Shanghai, China, we determined whether the same factors predict risk for fatal stroke as in the West. We also studied a number of potential dietary associations, particularly those with dietary antioxidants because these have been suggested to reduce atherogenesis. Methods and Results Between 1986 and 1989, 18 244 men aged 45 to 64 years living in four geographically defined areas of Shanghai, China were recruited to participate in a prospective study of diet and cancer. All participants completed an in-person, structured interview and provided blood and urine samples. As of March 1994, fatal stroke accounted for 245 of the 980 observed deaths. The most important risk factor for stroke mortality was a history of hypertension (multivariate relative risk, 4.5; 95% confidence interval, 3.3, 6.2). Cigarette smoking was not strongly associated with risk, and alcohol consumption increased risk only in the extreme categories of lifetime consumption. Educational level was strongly, inversely associated with fatal stroke, and this could not be explained by adjustment for any other risk factors. No macronutrient was associated with risk, including total energy, fat consumption, or any component of fat. There also were no significant inverse associations for stroke mortality with several micronutrients of interest, including vitamin C, carotene, vitamin E, riboflavin, or calcium. Conclusions Our data demonstrate that hypertension is by far the most important contributor to stroke mortality in Shanghai and that among dietary factors, only alcohol consumption shows any evidence whatsoever of being a risk factor.
Randomised controlled trial of long term portographic follow up versus variceal band ligation following transjugular intrahepatic portosystemic stent shunt for preventing oesophageal variceal rebleeding
Authors: D Tripathi
Journal: Gut (2004)

<b>Background/aims:</b> Transjugular intrahepatic portosystemic stent shunt (TIPSS) is effective in the prevention of variceal rebleeding but requires invasive portographic follow up. This randomised controlled trial aims to test the hypothesis that combining variceal band ligation (VBL) with TIPSS can obviate the need for long term TIPSS surveillance without compromising clinical efficacy, and can reduce the incidence of hepatic encephalopathy. <b>Patients/methods:</b> Patients who required TIPSS for the prevention of oesophageal variceal rebleeding were randomised to either TIPSS alone (n = 39, group 1) or TIPSS plus VBL (n = 40, group 2). In group 1, patients underwent long term TIPSS angiographic surveillance. In group 2, patients entered a banding programme with TIPSS surveillance only continued for up to one year. <b>Results:</b> There was a tendency to higher variceal rebleeding in group 2 although this did not reach statistical significance (8% <i>v</i> 15%; relative hazard 0.58; 95% confidence interval (CI) 0.15–2.33; p = 0.440). Mortality (47% <i>v</i> 40%; relative hazard 1.31; 95% CI 0.66–2.61; p = 0.434) was similar in the two groups. Hepatic encephalopathy was significantly less in group 2 (20% <i>v</i> 39%; relative hazard 2.63; 95% CI 1.11–6.25; p = 0.023). Hepatic encephalopathy was not statistically different after correcting for sex and portal pressure gradient (p = 0.136). <b>Conclusions:</b> TIPSS plus VBL without long term surveillance is effective in preventing oesophageal variceal rebleeding, and has the potential for low rates of encephalopathy. Therefore, VBL with short term TIPSS surveillance is a suitable alternative to long term TIPSS surveillance in the prevention of oesophageal variceal rebleeding.
Angiotensin-II-induced increase in transcoronary protein clearance: role of hypertension vs. nitric oxide or cyclo-oxygenase products
Authors: H. H. Sigusch, R. Ou, L. C. Katwa, S. E. Campbell, V. K. Ganjam, H. K. Reddy, K. T. Weber
Journal: Cardiovascular Research (1995)

Elevations in plasma angiotensin II (AngII) are associated with an efflux of plasma macromolecules into the perivascular and contiguous interstitial space. Whether this exudative response is related to associated hypertension or another effect of AngII is uncertain. We therefore monitored plasma and cardiac lymph total protein, albumin and fibronectin and calculated transvascular clearances for total protein (TVPC) and albumin (TVAC) and lymph fibronectin transport (LFT) every 30 min in open-chested, instrumented dogs. After baseline observations were obtained over 30 min, pressor (250 ng.kg.min-1) or nonpressor (11 ng.kg.min-1) doses of AngII were given intravenously for 90 min. Saline-treated, instrumented dogs served as controls. To address a potential secondary effect of AngII on vascular protein clearance, we monitored lymph prostaglandin E2 and cGMP (a marker of released nitric oxide, NO). At > or = 30 min, each dose of AngII was associated with a significant (P < or = 0.05) and comparable increase in TVPC, TVAC and LFT over baseline, indicating that increase in protein clearance was not related to elevated arterial pressure. Lymph cGMP rose significantly (P < or = 0.05) at 30 min for each dose of AngII and remained elevated thereafter. Lymph PGE2 was increased at > or = 60 min (P < or = 0.05) but only with the pressor dose. To determine the contribution of NO and PGE2 on AngII-induced transcoronary protein clearance, each dose of AngII was accompanied by co-administration of either the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the cyclo-oxygenase inhibitor, indomethacin. L-NAME completely inhibited the release of cGMP and the increase in protein clearance was not seen. Indomethacin suppressed the release of PGE2, but did not prevent the increase in protein clearance. Thus, AngII-induced increase in transcoronary protein clearance is not related to arterial hypertension or the release of PGE2, but instead appears to be mediated by NO release.
Calmodulin kinase II–mediated sarcoplasmic reticulum Ca2+ leak promotes atrial fibrillation in mice
Authors: Mihail G. Chelu, Satyam Sarma, Subeena Sood, Sufen Wang, Ralph J. van Oort, Darlene G. Skapura, Na Li, Marco Santonastasi, Frank Ulrich Müller, Wilhelm Schmitz, Ulrich Schotten, Mark E. Anderson, Miguel Valderrábano, Dobromir Dobrev, Xander H.T. Wehrens
Journal: Journal of Clinical Investigation (2009)

A trial fibrillation (AF), the most common human cardiac arrhythmia, is associated with abnormal intracellular Ca2+ handling. Diastolic Ca2+ release from the sarcoplasmic reticulum via "leaky" ryanodine receptors (RyR2s) is hypothesized to contribute to arrhythmogenesis in AF, but the molecular mechanisms are incompletely understood. Here, we have shown that mice with a genetic gain-of-function defect in Ryr2 (which we termed Ryr2R176Q/+ mice) did not exhibit spontaneous AF but that rapid atrial pacing unmasked an increased vulnerability to AF in these mice compared with wild-type mice. Rapid atrial pacing resulted in increased Ca2+/calmodulin-dependent protein kinase II (CaMKII) phosphorylation of RyR2, while both pharmacologic and genetic inhibition of CaMKII prevented AF inducibility in Ryr2R176Q/+ mice. This result suggests that AF requires both an arrhythmogenic substrate (e.g., RyR2 mutation) and enhanced CaMKII activity. Increased CaMKII phosphorylation of RyR2 was observed in atrial biopsies from mice with atrial enlargement and spontaneous AF, goats with lone AF, and patients with chronic AF. Genetic inhibition of CaMKII phosphorylation of RyR2 in Ryr2S2814A knockin mice reduced AF inducibility in a vagotonic AF model. Together, these findings suggest that increased RyR2-dependent Ca2+ leakage due to enhanced CaMKII activity is an important downstream effect of CaMKII in individuals susceptible to AF induction.
Natural selection of PAH-degrading bacterial guilds at coal-tar disposal sites.
Authors: W C Ghiorse, J B Herrick, R L Sandoli, E L Madsen
Journal: Environmental Health Perspectives (1995)

Microbial activity patterns at buried coal-tar disposal sites have been under investigation for several years to determine the response of naturally occurring microflora to polycyclic aromatic hydrocarbons (PAHs) at the sites. At one site in upstate New York, data have shown enrichment of PAH-degrading bacteria in subsurface contaminated zones but not in uncontaminated zones. Similar work at a midwestern site showed that the same trends existed in a heterogeneous disposal site except that a borehole outside the plume showed some PAH-mineralization activity. Polymerase chain reaction amplification of DNA extracted from sediment samples from the New York site indicated the presence of naphthalene metabolism genes nahAc and nahR, similar to those found on the NAH7 plasmid of Pseudomonas putida G7. Significant sequence polymorphism was observed in amplified nahAc products, indicating that divergent homologs of nahAc were present in the native community. Protozoan numbers were elevated in sediment samples displaying relatively high PAH-degrading activity, suggesting that a food chain was established based on PAH-degrading bacteria. Removal of the coal-tar source at the site occurred in 1991. In 1992, sampling of three key borehole stations revealed that mixing and backfilling operations had introduced soil microorganisms into the source area and introduced 14C-PAH-mineralization activity into the previously inactive pristine area. Thus removal of the source of the contaminants and restoration at the site have altered the microbial activity patterns outside the contaminant plume as well as in the source area.
Prisoners' Access to Medications
Authors: Harold L. Appel
Journal: JAMA (1993)

<h3>To the Editor.</h3> —As someone who has devoted a good part of the past 19 years to the health care needs of New York City prisoners, I was intrigued by your excellent and provocative article<sup>1</sup>and Editorial<sup>2</sup>concerning the medical problems of newly arrested diabetic patients with no access to medication. It is my impression (at least with regard to epilepsy, the illness that I deal with) that the main cause for the sudden interruption of medical treatment in this setting is the police confiscating the patients' medication at the time of arrest. I doubt, in fact, whether the people taking medication for diabetes, epilepsy, asthma, and the like keep this information to themselves as the article suggests. What my patients tell me is that they complain vociferously but to no avail. In other words, I question the statement: "In order to receive any medication, recently arrested prisoners
Glyceraldehyde-3-Phosphate Dehydrogenase Binds to the AU-Rich 3′ Untranslated Region of Colony-Stimulating Factor–1 (CSF-1) Messenger RNA in Human Ovarian Cancer Cells: Possible Role in CSF-1 Posttranscriptional Regulation and Tumor Phenotype
Authors: Nathalie Bonafé, Maureen Gilmore-Hebert, Nancy L. Folk, Masoud Azodi, Yi Zhou, Setsuko K. Chambers
Journal: Cancer Research (2005)

Abstract The overexpression of the colony-stimulating factor–1(CSF-1) by epithelial ovarian cancer cells enhances invasiveness and metastatic properties, contributing to the poor prognosis of the patients. It has been suggested that CSF-1 3′ untranslated region containing AU-rich elements (ARE) could regulate CSF-1 posttranscriptional expression and be responsible for its aberrant abundance in such cancer cells. In this study, normal (NOSE.1) and malignant (Hey) ovarian epithelial cells were used to examine CSF-1 expression and regulation. CSF-1 overexpression in Hey cells was found to associate with increased invasiveness, motility, urokinase activity, and virulence of tumorigenicity, compared with NOSE.1 cells, which expressed little CSF-1. CSF-1 ARE was further found to serve as an mRNA decay element that correlates with down-regulation of protein translation. Moreover, such down-regulation was found more prominent in NOSE.1 than in Hey cells, suggesting differences in posttranscriptional regulation. As a variety of trans-acting factors [AU-binding protein (AUBP)] are known to modulate messenger stability through binding to such elements, we examined the protein content of both cell lines for their ability to bind the CSF-1 ARE. Our results strongly suggested the abundance of such AUBP activity in Hey cells. We isolated a 37-kDa AUBP, which was identified as glyceraldehyde-3-phosphate dehydrogenase (GAPDH). To summarize, our study identified GAPDH as an AUBP abundant in Hey cells, where it binds to CSF-1 ARE that imparts mRNA decay. These data suggest that GAPDH binding to CSF-1 ARE sequence prevents CSF-1 mRNA decay and subsequent down-regulation of CSF-1 protein translation, leading to CSF-1 overexpression and increased metastatic properties seen in ovarian cancer.
Mechanisms of chloroform and carbon tetrachloride toxicity in primary cultured mouse hepatocytes.
Authors: R J Ruch, J E Klaunig, N E Schultz, A B Askari, D A Lacher, M A Pereira, P J Goldblatt
Journal: Environmental Health Perspectives (1986)

Mechanisms of chloroform (CHCl3) and carbon tetrachloride (CCl4) toxicity to primary cultured male B6C3F1 mouse hepatocytes were investigated. The cytotoxicity of both CHCl3 and CCl4 was dose- and duration-dependent. Maximal hepatocyte toxicity, as determined by lactate dehydrogenase leakage into the culture medium, occurred with the highest concentrations of CHCl3 (5 mM) and CCl4 (2.5 mM) used and with the longest duration of treatment (20 hr). CCl4 was approximately 16 times more toxic than CHCl3 to the hepatocytes. The toxicity of these compounds was decreased by adding the mixed function oxidase system (MFOS) inhibitor, SKF-525A (25 microM) to the cultures. The addition of diethyl maleate (0.25 mM), which depletes intracellular glutathione (GSH)-potentiated CHCl3 and CCl4 toxicity. The toxicity of CHCl3 and CCl4 could also be decreased by adding the antioxidants N,N'-diphenyl-p-phenylenediamine (DPPD) (25 microM), alpha-tocopherol acetate (Vitamin E) (0.1 mM), or superoxide dismutase (SOD) (100 U/mL) to the cultures. These results suggest that: in mouse hepatocytes, both CHCl3 and CCl4 are metabolized to toxic components by the MFOS; GSH plays a role in detoxifying those metabolites; free radicals are produced during the metabolism of CHCl3 and CCl4; and free radicals may be important mediators of the toxicity of these two halomethanes.
Outcome and assessment after the modified Fontan procedure for hypoplastic left heart syndrome.
Authors: P E Farrell, A C Chang, K A Murdison, J M Baffa, W I Norwood, J D Murphy
Journal: Circulation (1992)

We reviewed the outcome of 76 consecutive patients (age range, 5 months to 6 years; median age, 19 months) who underwent a modified Fontan procedure after initial palliative surgery for hypoplastic left heart syndrome (HLHS) between January 1984 and December 1989.Modifications of the Fontan procedure included transatrial baffle of pulmonary venous return to the tricuspid valve (n = 10) or inferior vena cava baffle within the right atrium to the superior vena caval-pulmonary artery anastomosis, with pulmonary artery augmentation (n = 66). Actuarial survival rates were 74% (1 month), 58% (12 months), 56% (2 years), and 52% (4 years). Of the 43 survivors, 25 patients have returned for postoperative cardiac catheterization at a medium of 13 months after the Fontan procedure. Mean +/- SD hemodynamic values were cardiac index, 2.8 +/- 0.6 l/min/m2; right arterial pressure, 11 +/- 2 mm Hg; pulmonary artery wedge pressure, 6 +/- 3 mm Hg; and arterial oxygen saturation, 94 +/- 3%. No patient had significant tricuspid or native pulmonary valve insufficiency.Survival after the Fontan procedure in patients with HLHS is comparable to survival after a Fontan procedure in patients with other complex congenital heart lesions. In the subgroup of patients with HLHS who survived both reconstructive surgery and a Fontan procedure and have been evaluated by cardiac catheterization after a Fontan procedure, the use of the right ventricle as the systemic ventricle yielded excellent intermediate results for Fontan physiology.
Abstract 1658: Fenretinide induces lethal autophagy in pancreatic cancer cells
Authors: Maria C. Messner, Myles C. Cabot
Journal: Cancer Research (2010)

Abstract Background: Recent studies show that the synthetic vitamin A analog fenretinide (4-HPR) is cytotoxic in a number of human tumor cell lines and is a chemopreventative agent that is well-tolerated clinically. 4-HPR has been shown to augment intracellular levels of reactive oxygen species (ROS) and ceramides, and to activate the MAPK family of kinases. Pancreatic cancer cells are sensitive to increased levels of ROS, ceramides, and MAPK phosphorylation, suggesting 4-HPR will be an effective agent against this disease. Results: 4-HPR exposure markedly decreased viability of MIA PaCa-2 and PANC-1 cells, as shown by a dose-dependent decrease in absorbance from an MTS assay and a 3-fold increase in propidium iodide staining. A 50% reduction in [3H]thymidine incorporation showed that cell proliferation was halted as well. 4-HPR treatment caused a 3-fold increase in de novo ceramide production at 24 h and a time- and dose-dependent generation of ROS. 4-HPR led to a minor increase in caspase 3/7 activity and in FITC-Annexin V-positive cells. However, other measures of apoptosis were lacking, suggesting apoptosis was not the major death pathway elicited by 4-HPR. Further investigation of the mechanism of cell death suggests that the dominant pathway triggered by 4-HPR is lethal autophagy. After 4-HPR treatment, microscopic analysis of cells exposed to acridine orange showed bright red autophagic vesicles, and Western blot showed a robust increase in LC3 II protein expression. Pretreatment with the autophagy inhibitor 3-methyladenine (3-MA) or the ROS scavenger vitamin E (VE) abrogated the increase in LC3 II expression caused by 4-HPR exposure, and both 3-MA and VE partially preserved viability. A sustained, dose-dependent increase in phosphorylation of the stress kinases JNK and p38 was observed following incubation with 4-HPR, whereas phosphorylation of the mitogenic kinase ERK 1/2 decreased. Pretreatment with myriocin (an inhibitor of de novo ceramide production), 3-MA, or VE attenuated the increase in JNK and p38 phosphorylation caused by 4-HPR. Additionally, VE pretreatment blocked the decrease in ERK 1/2 phosphorylation elicited by 4-HPR. Conclusions: These data suggest that 4-HPR induces lethal autophagy in human pancreatic cancer cells by a mechanism that involves generation of ROS and engagement of the MAPK and sphingolipid signaling pathways. 4-HPR used alone or in combination with current therapies or signaling pathway modulators may be a promising avenue for future pancreatic cancer therapies. [Support: NIH/NIGMS grant no. GM077391] Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1658.