tbuckley/cabot-search huggingface dataset:
Is there a connection between carbon monoxide exposure and hypertension?
Authors: D G Penney, J W Howley
Journal: Environmental Health Perspectives (1991)

Exposure to carbon monoxide in our society is a frequent occurrence, from auto exhaust, industrial effluents, and cigarette smoke, and takes place over a wide range of concentrations. It has been suggested that chronic CO inhalation may alter blood pressure, even possibly provoking hypertension by acting alone or in combination with other environmental stressors. Some studies examining the response to CO exposure have reported decreases in blood pressure, whereas others have found increases or no change. Blood pressure in long-term cigarette smokers is generally decreased relative to nonsmokers, albeit a slight decrease. The strength of this finding is somewhat clouded by the effect of the lower body weight in smokers. The increases in blood pressure observed acutely with smoking are mainly due to nicotine. Chronically, the hypertensive action of nicotine is largely offset by the hypotensive action of CO. Several studies support the notion that environmental CO exposure or smoking accelerates or exacerbates hypertension in some people. It has been asserted that chronic CO exposure increases the development of atherosclerotic disease; however, convincing evidence from animal experiments is lacking. Nevertheless, CO may elevate plasma cholesterol and does appear to enhance atherosclerosis when serum cholesterol is greatly elevated by diet. Using the borderline hypertensive rat, an animal model reputed to have increased sensitivity to environmental stimuli, we found no evidence to suggest a provocatory role for CO in the development of hypertension; instead, CO exposure produced hypotension. On the whole, the human and animal literature, as well as our studies, fail to support the hypothesis that long-term CO exposure is capable of provoking an increase in blood pressure, even in borderline hypertensive or sensitive individuals.
A Randomized Trial Comparing Stenting With Balloon Angioplasty in Small Vessels in Patients With Symptomatic Coronary Artery Disease
Authors: Adnan Kastrati, Albert Schömig, Josef Dirschinger, Julinda Mehilli, Franz Dotzer, Nicola von Welser, Franz-Josef Neumann
Journal: Circulation (2000)

Background —More than 30% of the lesions currently treated with interventional approaches are situated in vessels smaller in size than those representing an established indication for stenting. The objective of this randomized trial was to assess whether compared with PTCA, stenting of small coronary vessels is associated with a reduction of restenosis. Methods and Results —Patients with symptomatic coronary artery disease with lesions situated in native coronary vessels between 2 and 2.8 mm in size were randomly assigned to be treated with either stenting (n=204) or PTCA (n=200). Adjunct therapy consisted of abciximab, ticlopidine, and aspirin. Repeat angiography at 6-month follow-up was performed in 83% of the patients. The primary end point of the study was the incidence of angiographic restenosis (≥50% diameter stenosis) at follow-up; adverse clinical events, such as death, myocardial infarction, stroke, or target vessel revascularization, were assessed as secondary end points. After 7 months, there were no significant differences in the infarct-free survival rates between the 2 study groups: 96.6% for stent patients, and 97.0% for PTCA patients ( P =0.80). Target vessel revascularization was needed in 20.1% of the stent patients and 16.5% of the PTCA patients ( P =0.35). The primary end point of angiographic restenosis was found in 35.7% of the stent patients and 37.4% of the PTCA patients ( P =0.74). The net lumen gain observed at follow-up was identical (0.76±0.78 in the stent group versus 0.76±0.63 mm in the PTCA group, P =0.93). Conclusions —Stenting and PTCA are associated with equally favorable results when used for treating lesions in small coronary vessels.
Hemophagocytic syndrome associated with aggressive natural killer cell leukemia
Authors: Tsukasa Okuda, Shinichi Sakamoto, Takeshi Deguchi, Shinichi Misawa, Kei Kashima, Takao Yoshihara, Satoshi Ikushima, Shigeyoshi Hibi, Shinsaku Imashuku
Journal: American Journal of Hematology (1991)

Abstract We describe a patient who had aggressive natural killer cell leukemia with profound hemophagocytosis. This combination must be underscored as one of several hemophagocytic syndromes. Activated phagocytes in the bone marrow appeared morphologically normal and could possibly be proliferating in response to some cytokine(s) such as interferon‐gamma produced by leukemic cells, whose serum level was found to be extremely elevated in this case.
PROBLEMS IN ESTABLISHING AND MAINTAINING PSYCHIATRIC UNITS IN GENERAL HOSPITALS
Authors: A. E. BENNETT
Journal: American Journal of Psychiatry (1959)

Any hospital interested in planning a psychiatric unit could obtain from the administration of any one of these hospitals or the chief of psychiatry, complete information which could be used to reassure the hospital medical staff and lay board. The establishment of a psychiatric unit is completely feasible and it can be operated successfully with a minimal difficulty to the hospital. It is our responsibility to educate all concerned with the management of general hospitals that these units increase the institution's usefulness and value to the community, enrich its training program for interns, nurses and staff doctors, and open up new research vistas. Besides all this, the hospital becomes truly a general hospital, a term misnomer as long as it excludes one of the commonest of all disorders. The facetious remark that what America needs is a good five dollar psychiatrist should be interpreted as a challenge. All general hospitals from now on must prepare to take over complete treatment of acute mental illness. All psychiatrists should become crusaders and move into general hospitals to take their proper role in this new era of medicine.
Efficacy and safety of different doses and retreatment of rituximab: a randomised, placebo-controlled trial in patients who are biological naive with active rheumatoid arthritis and an inadequate response to methotrexate (Study Evaluating Rituximab's Efficacy in MTX iNadequate rEsponders (SERENE))
Authors: P. Emery, A. Deodhar, W. F. Rigby, J. D. Isaacs, B. Combe, A. J. Racewicz, K. Latinis, C. Abud-Mendoza, L. J. Szczepanski, R. A. Roschmann, A. Chen, G. K. Armstrong, W. Douglass, H. Tyrrell
Journal: Annals of the Rheumatic Diseases (2010)

<h3>Objectives</h3> This phase III study evaluated the efficacy and safety of rituximab plus methotrexate (MTX) in patients with active rheumatoid arthritis (RA) who had an inadequate response to MTX and who were naïve to prior biological treatment. <h3>Methods</h3> Patients with active disease on stable MTX (10–25 mg/week) were randomised to rituximab 2×500 mg (n=168), rituximab 2×1000 mg (n=172), or placebo (n=172). From week 24, patients not in remission (Disease Activity Score (28 joints) ≥2.6) received a second course of rituximab; patients initially assigned to placebo switched to rituximab 2×500 mg. The primary end point was American College of Rheumatology 20 (ACR20) response at week 24. All patients were followed until week 48. <h3>Results</h3> At week 24, both doses of rituximab showed statistically superior efficacy (p&lt;0.0001) to placebo (ACR20: 54%, 51% and 23%; rituximab (2×500 mg) + MTX, rituximab (2×1000 mg) + MTX and placebo + MTX, respectively). Secondary end points were also significantly improved for both rituximab groups compared with placebo. Further improvements in both rituximab arms were observed from week 24 to week 48. Rituximab + MTX was well tolerated, demonstrating comparable safety to placebo + MTX through to week 24, and between rituximab doses through to week 48. <h3>Conclusions</h3> Rituximab (at 2×500 mg and 2×1000 mg) plus MTX significantly improved clinical outcomes at week 24, which were further improved by week 48. No significant differences in either clinical or safety outcomes were apparent between the rituximab doses.
High Risk of Brain Metastases in Surgically Staged IIIA Non–Small-Cell Lung Cancer Patients Treated With Surgery, Chemotherapy, and Radiation
Authors: Harvey J. Mamon, Beow Yong Yeap, Pasi A. Jänne, Jason Reblando, Sarah Shrager, Michael T. Jaklitsch, Steven Mentzer, Jeanne M. Lukanich, David J. Sugarbaker, Elizabeth H. Baldini, Stuart Berman, Arthur Skarin, Raphael Bueno
Journal: Journal of Clinical Oncology (2005)

Lung cancer is the leading cause of cancer mortality in the United States. We sought to review our experience with surgically staged IIIA (N2) non-small-cell lung cancer (NSCLC), focusing on the patterns of failure in consecutively treated patients from 1988 to 2000.The records of 177 patients were reviewed. Collected data included stage, histology, use of chemotherapy and radiation, initial and subsequent sites of failure, and survival. One hundred twenty-four patients have died; follow-up time is 35 months among the remaining patients.The median survival from the time of surgery was 21.0 months, with a 3-year overall survival (OS) of 34%. Nodal downstaging to N0 disease correlated with OS and progression-free survival (PFS; P < .001). The most common site of recurrence was the brain. Thirty-four percent of patients recurred in the brain as their first site of failure, and 40% of patients developed brain metastases at some point in their course. In patients with nonsquamous histology and residual nodal involvement after neoadjuvant therapy, the risk of brain metastases was 53% at 3 years.Patients treated with neoadjuvant therapy for N2-positive stage IIIA NSCLC enjoy an advantage in both OS and PFS if their lymph node status is downstaged to N(0). Because brain metastases constitute the most common site of failure in these patients, future studies focusing on prophylaxis of brain metastases may improve the outcome in patients with stage IIIA NSCLC.
MiR-21 Indicates Poor Prognosis in Tongue Squamous Cell Carcinomas as an Apoptosis Inhibitor
Authors: Jinsong Li, Hongzhang Huang, Lijuan Sun, Mei Yang, Chaobin Pan, Weiliang Chen, Donghui Wu, Zhaoyu Lin, Chunxian Zeng, Yandan Yao, Peter Zhang, Erwei Song
Journal: Clinical Cancer Research (2009)

Abstract Purpose: We aim to examine miR-21 expression in tongue squamous cell carcinomas (TSCC) and correlate it with patient clinical status, and to investigate its contribution to TSCC cell growth, apoptosis, and tumorigenesis. Experimental Design: MicroRNA profiling was done in 10 cases of TSCC with microarray. MiR-21 overexpression was quantitated with quantitative reverse transcription-PCR in 103 patients, and correlated to the pathoclinical status of the patients. Immunohistochemistry was used to examine the expression of TPM1 and PTEN, and terminal deoxynucleotidyl transferase–mediated dUTP labeling to evaluate apoptosis. Moreover, miR-21 antisense oligonucleotide (ASO) was transfected in SCC-15 and CAL27 cell lines, and tumor cell growth was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, adherent colony formation, and soft agar assay, whereas apoptosis was determined by Annexin V assay, cytochrome c release, and caspase 3 assay. Tumorigenesis was evaluated by xenografting SCC-15 cells in nude mice. Results: MiR-21 is overexpressed in TSCC relative to adjacent normal tissues. The level of miR-21 is reversely correlated with TPM1 and PTEN expression and apoptosis of cancer cells. Multivariate analysis showed that miR-21 expression is an independent prognostic factor indicating poor survival. Inhibiting miR-21 with ASO in TSCC cell lines reduces survival and anchorage-independent growth, and induces apoptosis in TSCC cell lines. Simultaneous silencing of TPM1 with siRNA only partially recapitulates the effect of miR-21 ASO. Furthermore, repeated injection of miR-21 ASO suppresses tumor formation in nude mice by reducing cell proliferation and inducing apoptosis. Conclusions: miR-21 is an independent prognostic indicator for TSCC, and may play a role in TSCC development by inhibiting cancer cell apoptosis partly via TPM1 silencing.
Clinical Outcome and Tolerability of a 2-Year Sublingual Allergen Immunotherapy (AIT) with a 5-Grass Pollen Tablet in Polyallergic Patients – Real-Life Medical Practice Data
Authors: Meike Hadler, Efstrathios Karagiannis, Kija Shah-Hosseini, Ralph Mosges
Journal: Journal of Allergy and Clinical Immunology (2015)
Direct Epstein-Barr virus (EBV) typing on peripheral blood mononuclear cells: no association between EBV type 2 infection or superinfection and the development of acquired immunodeficiency syndrome-related non-Hodgkin's lymphoma
Authors: D. Van Baarle, E. Hovenkamp, M. J. Kersten, M. R. Klein, F. Miedema, M. H. J. Van Oers
Journal: Blood (1999)
Smoking cessation practice in male versus female family physicians in Turkey
Authors: Leyla Yilmaz Aydin, Davut Baltaci, Fatih Alasan, Mehmet Halis Tanriverdi, Harun Deler
Journal: European Respiratory Journal (2013)

BACKGROUND: To examine the effect of sex of family physicians in smoking cessation practice

METHODS: The sub-group analysis of a multi-center, cross-sectional, self-administered questionnaire study among 1185 family physicians (FP) on effect of gender of doctors in smoking cessation practice was performed.

RESULTS: 42.8% of FP participating were female. Percentages of current smokers in males and females were 31.6% and 37.3%; respectively. Cessation rates were higher for male (17.2% and 11.6%). (P=0,000). Years of smoking was higher among female (16.53 and13.43) (p=0.000). Females (58.6%) received training on smoking cessation practice higher than men (p=0.02). There was no relationship between gender of doctor and felt ready for smoking cessation process (p=0.539). Former smoker female doctors felt themselves more ready than never and current smokers females (p= 0.005). There is no relationship between gender and asking smoking status but never smoker male doctors were asking smoking status more (p=0.001). Doctors smoking status and incidence of asking smoking in both sexes were analyzed separately. In both sexes never and former smokers were more asking than the others however, only males accounted for a statistically significant difference (p=0.016). Postgraduate training was the main effecting factor for “ask” (p<0,0001) 

CONCLUSIONS: Among the participants current smokers were high in both sexes. Female physicians are more resistant to smoking cessation; more participated in postgraduate training programs; about smoking cessation. Female physicians who gave up smoking feel themselves ready for smoking cessation intervention. Main factor to ask and advise is postgraduate training.
Insulin-like growth factor receptor 1 (IGFR-1) is significantly associated with longer survival in non-small-cell lung cancer patients treated with gefitinib
Authors: F. Cappuzzo, L. Toschi, G. Tallini, G.L. Ceresoli, I. Domenichini, S. Bartolini, G. Finocchiaro, E. Magrini, G. Metro, A. Cancellieri, R. Trisolini, L. Crino, P.A. Bunn, A. Santoro, W.A. Franklin, M. Varella-Garcia, F.R. Hirsch
Journal: Annals of Oncology (2006)
Open Trial of Psychodynamic Psychotherapy for Panic Disorder: A Pilot Study
Authors: B Milrod, F Busch, A C Leon, T Shapiro, A Aronson, J Roiphe, M Rudden, M Singer, H Goldman, D Richter, M K Shear
Journal: American Journal of Psychiatry (2000)

OBJECTIVE: This report contains preliminary data from an open trial of brief psychodynamic psychotherapy for panic disorder. METHOD: Fourteen patients with primary DSM-IV panic disorder completed a 24-session, twice-weekly course of psychodynamic psychotherapy. Other psychiatric treatment was not permitted throughout the 12-week treatment period and the 6-month follow-up. Symptoms were assessed at baseline, treatment termination, and 6-month posttermination follow-up (40 weeks). RESULTS: Statistically significant, clinically meaningful improvements appeared in panic, depression, anxiety, and functional impairment both at treatment termination and at 6-month follow-up. CONCLUSIONS: Psychodynamic monotherapy can be used successfully to retain and treat patients with panic disorder. Psychodynamic interventions warrant further study for patients with panic disorder.
Initiation and perpetuation of rat adjuvant arthritis is inhibited by the anti-CD2 monoclonal antibody (mAb) OX34
Authors: J. C Hoffmann, C. Herklotz, H. Zeidler, B. Bayer, H. Rosenthal, J. Westermann
Journal: Annals of the Rheumatic Diseases (1997)

The purpose of this study was to investigate the therapeutic potential of the anti-CD2 mAb OX34 first with regard to bone protection in established rat adjuvant arthritis (AA) and secondly with regard to prevention of AA induction.Established AA was treated with dexamethasone (1 mg/kg body weight) for two days plus OX34 mAb or control mAb over three days (2 mg and then 1 mg) starting at different time points of the disease. For prevention studies animals were injected as above with mAb before induction of AA. Arthritis score (AS), hindpaw thickness, and body weight were blindly measured three times per week. Flow cytometry and hindpaw radiography were performed at the end of the study (day 29).Treatment of early AA with OX34 mAb combined with dexamethasone but not dexamethasone plus control mAb dramatically suppressed established AA as assessed by AS and hind paw thickness (> 65% and > 80% reduction, respectively; p < 0.05). Most importantly, early treatment in the course of AA almost completely prevented bone destruction in established AA. When given before AA induction OX34 alone prevented the initiation of arthritis compared with controls (AS reduction 83-95%, p < 0.05). In addition, OX34 plus dexamethasone treatment resulted in depletion of CD4+ T cells but not CD8+ T cells. IL2R+ and CD45RC- ('memory') T cells were significantly reduced.Anti-CD2 mAb treatment prevents AA induction confirming the role of CD4+ T cells in the induction phase of AA. In addition, early OX34 plus dexamethasone treatment resulted in pronounced clinical improvement and joint protection. OX34 treatment therefore inhibits the initiation and the perpetuation of rat AA.
Epigenetics in Diabetic Kidney Disease
Authors: Marpadga A. Reddy, Rama Natarajan
Journal: Journal of the American Society of Nephrology (2011)

Regulated gene expression by transcription factor networks is critical for normal kidney function. Disruption of these complex networks leads to biochemical aberrations associated with many renal diseases. Epigenetic mechanisms not involving changes in DNA sequence, such as DNA methylation and post-translational modifications of nucleosomal histones, also play a critical role in gene regulation by modulating chromatin access to the cellular machinery for transcription. These epigenetic modifications can be affected by intrinsic and extrinsic environmental factors and play a central role in dictating biologic phenotypes including pathologic disease. Emerging evidence also suggests, apart from traditional genetic predisposition, that epigenetic processes can persist across generations to play a modulating role in the development of renal diseases such as diabetic nephropathy. Recent advances in epigenome research has increased our understanding of epigenetic mechanisms involved in renal dysfunction that in turn may lead to identification of novel new therapeutic targets.
Ezrin interacts with cortactin to form podosomal rosettes in pancreatic cancer cells
Authors: H M Kocher, J Sandle, T A Mirza, N F Li, I R Hart
Journal: Gut (2008)

<h3>Objective</h3> We aimed to identify pathogenic variants in a girl with epilepsy, developmental delay, cerebellar ataxia, oral motor difficulty, and structural brain abnormalities with the use of whole-exome sequencing. <h3>Methods</h3> Whole-exome trio analysis and molecular functional studies were performed in addition to the clinical findings and neuroimaging studies. <h3>Results</h3> Brain MRI showed mild pachygyria, hypoplasia of the cerebellar vermis, and abnormal foliation of the cerebellar vermis, suspected for a variant in one of the genes of the Reelin pathway. Trio whole-exome sequencing and additional functional studies were performed to identify the pathogenic variants. Trio whole-exome sequencing revealed compound heterozygous splice variants in <i>DAB1</i>, both affecting the highly conserved functional phosphotyrosine-binding domain. Expression studies in patient-derived cells showed loss of normal transcripts, confirming pathogenicity. <h3>Conclusions</h3> We conclude that these variants are very likely causally related to the cerebral phenotype and propose to consider loss-of-function <i>DAB1</i> variants in patients with RELN-like cortical malformations.
Evaluation of the FDA Warning Against Prescribing Citalopram at Doses Exceeding 40 mg
Authors: Kara Zivin, Paul N. Pfeiffer, Amy S.B. Bohnert, Dara Ganoczy, Frederic C. Blow, Brahmajee K. Nallamothu, Helen C. Kales
Journal: American Journal of Psychiatry (2013)

Patients benefitting from high-dosage citalopram must decide between adhering to an FDA warning and possible worsening depression from too low a dosage. This well-controlled large study found no elevated risks of ventricular arrhythmia or all-cause mortality associated with citalopram dosages >40 mg/day.
Rho GTPases and Leukocyte Adhesion Receptor Expression and Function in Endothelial Cells
Authors: Eva Cernuda-Morollón, Anne J. Ridley
Journal: Circulation Research (2006)

Rho family GTPases are key signal transducers that regulate cell adhesion and migration and a variety of other cellular responses, including changes in gene expression. In this review, we discuss how Rho GTPases regulate signaling by endothelial cell receptors involved in leukocyte extravasation. First, Rho GTPases affect the expression of some leukocyte adhesion molecules on endothelial cells, such as intracellular adhesion molecule-1 and E-selectin, that can be induced by proinflammatory mediators, hypoxia, or shear stress. Second, Rho GTPases are activated by engagement of several leukocyte adhesion receptors and contribute to both early morphological changes and subsequent alterations in gene expression. Rho GTPases are therefore candidate targets for inhibiting leukocyte transendothelial migration in heart disease and chronic inflammatory disorders.
Utilization of sialic acid as a coreceptor is required for reovirus-induced biliary disease
Authors: Erik S. Barton, Bryan E. Youree, Daniel H. Ebert, J. Craig Forrest, Jodi L. Connolly, Tibor Valyi-Nagy, Kay Washington, J. Denise Wetzel, Terence S. Dermody
Journal: Journal of Clinical Investigation (2003)

Infection of neonatal mice with some reovirus strains produces a disease similar to infantile biliary atresia, but previous attempts to correlate reovirus infection with this disease have yielded conflicting results. We used isogenic reovirus strains T3SA– and T3SA+, which differ solely in the capacity to bind sialic acid as a coreceptor, to define the role of sialic acid in reovirus encephalitis and biliary tract infection in mice. Growth in the intestine was equivalent for both strains following peroral inoculation. However, T3SA+ spread more rapidly from the intestine to distant sites and replicated to higher titers in spleen, liver, and brain. Strikingly, mice infected with T3SA+ but not T3SA– developed steatorrhea and bilirubinemia. Liver tissue from mice infected with T3SA+ demonstrated intense inflammation focused at intrahepatic bile ducts, pathology analogous to that found in biliary atresia in humans, and high levels of T3SA+ antigen in bile duct epithelial cells. T3SA+ bound 100-fold more efficiently than T3SA– to human cholangiocarcinoma cells. These observations suggest that the carbohydrate-binding specificity of a virus can dramatically alter disease in the host and highlight the need for epidemiologic studies focusing on infection by sialic acid–binding reovirus strains as a possible contributor to the pathogenesis of neonatal biliary atresia.