tbuckley/cabot-search huggingface dataset:
PROCESSES OF "SPONTANEOUS" RECOVERY FROM THE PSYCHONEUROSES
Authors: IAN STEVENSON
Journal: American Journal of Psychiatry (1961)

1. Several independent studies of untreated psychoneurotic patients have shown that between 40 and 60% of such patients recover within a few years of the first observations of their conditions. Treated and untreated patients probably recover through the same processes which include and require the learning of new behavioral responses. We have some evidence that treatment which emphasizes the practice by the patient of new behavioral responses in periods between his therapeutic sessions will shorten the number of interviews required and possibly the total duration of the illness. 2. Examples are given from some 20 cases of spontaneous improvements or recoveries derived from observations or reports of patients, experiences of other persons, or published accounts of such recoveries. 3. The following circumstances or processes seem to facilitate recovery from psychoneuroses: (a) desensitization through recall, verbalization and assimilation of past painful experiences; (b) desensitization through association of painful experiences with new pleasurable experiences; (c) increased supplies of respect, reassurance, and affection; (d) entry into the patient's life of new models of behavior; (e) occurrence in the patient's life of new situations requiring different behavioral responses; (f) shifts in motivation brought about by fear, shame, or desperation. 4. Further study of so-called spontaneous recoveries from mental illnesses may teach us much more about experiences which prove valuable to patients. From this we may learn more about what we need to do to assist patients to recover more rapidly than they would without psychotherapy.
TCTAP A-049 Retrograde Approach Is as Effective and Safe as Antegrade Approach in Contemporary Percutaneous Coronary Intervention for Chronic Total Occlusion: A Single-center Registry Study
Authors: Chih-kuo Lee, Ching-Chang Huang, Ying-Hsien Chen, Mao-Shin Lin, Hsien-Li Kao
Journal: Journal of the American College of Cardiology (2014)
Neutrophil degranulation and cell lysis is associated with clinical severity in virus-induced asthma
Authors: P.A.B. Wark, S.L. Johnston, I. Moric, J.L. Simpson, M.J. Hensley, P.G. Gibson
Journal: European Respiratory Journal (2001)

Acute exacerbations of asthma are frequently caused by viral infections, but the inflammatory mechanisms in virus-induced asthma are poorly understood. The aim of the present study was to determine whether viral infection in acute asthma was associated with increased sputum neutrophil degranulation and increased cellular lysis and whether these changes are related to clinical severity. Adults (n=49) presenting to the emergency department with acute asthma were examined for infection by means of sputum direct-fluorescence antigen detection, sputum culture, and sputum polymerase chain reaction for Mycoplasma, Chlamydia and Legionella pneumophila , and all common respiratory viruses. Subjects infected with one of these agents were classed as having an infective exacerbation. Spirometry and sputum induction were performed on presentation and 4–5 weeks later. Thirty-seven subjects (76%) had virus infection and acute asthma. Those with virus infection had increased sputum neutrophils (p&lt;0.05) and increased neutrophil elastase (p&lt;0.05), this was related to increased elevated sputum lactate dehydrogenase (LDH). Subjects with noninfective asthma had an increase in the proportion of sputum eosinophils. Both groups had elevated sputum eosinophil cationic protein (ECP) concentrations. Higher levels of sputum LDH and ECP were associated with a longer hospital stay. Virus infection and acute asthma is associated with neutrophilic inflammation, cell lysis and more severe clinical disease.
Protein Kinase G Inhibits Flow-Induced Ca2+ Entry into Collecting Duct Cells
Authors: Juan Du, Wei-Yan Wong, Lei Sun, Yu Huang, Xiaoqiang Yao
Journal: Journal of the American Society of Nephrology (2012)

The renal cortical collecting duct (CCD) contributes to the maintenance of K(+) homeostasis by modulating renal K(+) secretion. Cytosolic Ca(2+) ([Ca(2+)](i)) mediates flow-induced K(+) secretion in the CCD, but the mechanisms regulating flow-induced Ca(2+) entry into renal epithelial cells are not well understood. Here, we found that atrial natriuretic peptide, nitric oxide, and cyclic guanosine monophosphate (cGMP) act through protein kinase G (PKG) to inhibit flow-induced increases in [Ca(2+)](i) in M1-CCD cells. Coimmunoprecipitation, double immunostaining, and functional studies identified heteromeric TRPV4-P2 channels as the mediators of flow-induced Ca(2+) entry into M1-CCD cells and HEK293 cells that were coexpressed with both TRPV4 and TRPP2. In these HEK293 cells, introducing point mutations at two putative PKG phosphorylation sites on TRPP2 abolished the ability of cGMP to inhibit flow-induced Ca(2+) entry. In addition, treating M1-CCD cells with fusion peptides that compete with the endogenous PKG phosphorylation sites on TRPP2 also abolished the cGMP-mediated inhibition of the flow-induced Ca(2+) entry. Taken together, these data suggest that heteromeric TRPV4-P2 channels mediate the flow-induced entry of Ca(2+) into collecting duct cells. Furthermore, substances such as atrial natriuretic peptide and nitric oxide, which increase cGMP, abrogate flow-induced Ca(2+) entry through PKG-mediated inhibition of these channels.
The gastric mucosa in radiologically negative acute gastrointestinal bleeding
Authors: M. J. S. Langman, J. H. Hansky, R. A. B. Drury, F. A. Jones
Journal: Gut (1964)

EDITORIAL SYNOPSIS This is a studv of acid secretion and gastric mucosal histology in patients who had gastrointestinal bleeding.Patients with normal biopsies had high acid secretion and were believed to have acute or chronic duodenal ulcer; those with chronic gastritis and lower acid secre- tion suggested that the bleeding was due to acute gastric ulceration.The gastric mucosae of 22 additional patients with bleeding acute gastric ulcers removed surgically all showed chronic gastritis.In the main group of 30 patients studied there was no clear-cut histological difference between those patients taking aspirin and those who had not.
Disinfection of the flexible fibreoptic bronchoscope against Mycobacterium tuberculosis and M gordonae.
Authors: D Davis, H W Bonekat, D Andrews, J W Shigeoka
Journal: Thorax (1984)

In view of recent reports of contamination of the fibreoptic bronchoscope by tuberculous and non-tuberculous mycobacteria, we evaluated the disinfecting properties of aqueous glutaraldehyde (Cidex) and an iodophor (Prepodyne) against Mycobacterium tuberculosis and M gordonae. We found that a 15 minute disinfection procedure with either agent, coupled with initial vigorous mechanical cleaning of the bronchoscope and its accessories, is a quick and reliable method for preventing the contamination of the bronchoscope with mycobacteria.
Estrogen Receptor Gene Analysis in Estrogen Receptor-Positive and Receptor-Negative Primary Breast Cancer
Authors: N Roodi, L R Bailey, W Y Kao, C S Verrier, C J Yee, W D Dupont, F F Parl
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Estrogen Receptor Gene Analysis in Estrogen Receptor-Positive and Receptor-Negative Primary Breast Cancer Get access Nady Roodi, Nady Roodi Search for other works by this author on: Oxford Academic PubMed Google Scholar L. Renee Bailey, L. Renee Bailey Search for other works by this author on: Oxford Academic PubMed Google Scholar Woei-Yau Kao, Woei-Yau Kao Search for other works by this author on: Oxford Academic PubMed Google Scholar Carmel S. Verrier, Carmel S. Verrier Search for other works by this author on: Oxford Academic PubMed Google Scholar Cindy J. Yee, Cindy J. Yee Search for other works by this author on: Oxford Academic PubMed Google Scholar William D. Dupont, William D. Dupont Search for other works by this author on: Oxford Academic PubMed Google Scholar Fritz F. Parl Fritz F. Parl Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 6, 15 March 1995, Pages 446–451, https://doi.org/10.1093/jnci/87.6.446 Published: 15 March 1995 Article history Received: 03 August 1994 Revision received: 01 December 1994 Accepted: 30 December 1994 Published: 15 March 1995
Cytolytic lymphocytic cells with complement receptor in human blood. Induction of cytolysis by IgG antibody but not by target cell-bound C3.
Authors: P Perlmann, H Perlmann, H J Müller-Eberhard
Journal: The Journal of Experimental Medicine (1975)

Human blood lymphocytes were fractionated on glass bead columns charged with sheep erythrocyte (Es) membranes-bearing human C3b (7,000-10,000 molecules/Es). In the passaged cells the proportion of C receptor lymphocytes was strongly reduced, in parallel with the capacity to lyse chicken erythrocytes (Ec) in the presence of IgG-rabbit anti-Ec antibody. In other experiments, lymphocytes forming rosettes with Es bearing activated rabbit complement [C(ra)] from C6-deficient rabbits were removed by centrifugation through human serum albumin-gelatine mixtures. This procedure also depleted the lymphocyte preparations of antibody-dependent cytolytic effector cells. The results suggest that rations of antibody-dependent cytolytic effector cells. The result suggest that such effector cells have receptors for human C as well as for C(ra). Lymphocytes were not able to lyse erythrocytes bearing either human C3b (similar to 30,000 molecules/Ec) or activated C(ra) in the absence if IgG antierythrocyte antibodies. Under the same experimental conditions these target cells were efficiently lysed in the presence of small amounts of IgG antitarget cell antibodies. This suggests that the interaction between the cellular Fcreceptors and the Fc part of the inducing antibodies is of special significance for the triggering of the cell-mediated lytic reaction. However, although target cell-bound C did not trigger cytolysis, it seemed to potentiate antibody-dependent cytolysis, probably by enhancing effector cell-target cell contacts.
Deficiency of the reduced nicotinamide adenine dinucleotide dehydrogenase component of complex I of mitochondrial electron transport. Fatal infantile lactic acidosis and hypermetabolism with skeletal-cardiac myopathy and encephalopathy.
Authors: C L Hoppel, D S Kerr, B Dahms, U Roessmann
Journal: Journal of Clinical Investigation (1987)

A mitochondrial defect was investigated in an infant with fatal congenital lactic acidosis (3-14 mM), high lactate-to-pyruvate ratio, hypotonia, and cardiomyopathy. His sister had died with a similar disorder. Resting oxygen consumption was 150% of controls. Pathological findings included increased numbers of skeletal muscle mitochondria (many with proliferated, concentric cristae), cardiomegaly, fatty infiltration of the viscera, and spongy encephalopathy. Mitochondria from liver and muscle biopsies oxidized NADH-linked substrates at rates 20-50% of controls, whereas succinate oxidation by muscle mitochondria was increased. Mitochondrial NADH dehydrogenase activity (complex I, assayed as rotenone-sensitive NADH oxidase, NADH-duroquinone reductase, and NADH-cytochrome c reductase) was 0-10% of controls, and NADH-ferricyanide reductase activity was 25-50% of controls in the mitochondria and in skin fibroblasts. Activities of other electron transport complexes and related enzymes were normal. Familial deficiency of a component of mitochondrial NADH dehydrogenase (complex I) proximal to the rotenone-sensitive site thus accounts for this disorder.
Immunosuppression through HNF-1β signaling in human ovarian clear cell cancer
Authors: Hiroshi Nishio, Juri Sugiyama, Tomonori Yaguchi, Daisuke Aoki, Yutaka Kawakami
Journal: Journal for ImmunoTherapy of Cancer (2013)

Meeting abstracts Cancer-induced immunosuppression is one of the major problems for development of cancer immunotherapies. A transcriptional factor HNF-1β preferentially activated in human ovarian clear cell cancer (OCCC) was reported to contribute to various malignant features including
Sleep-disordered breathing in deep vein thrombosis and acute pulmonary embolism
Authors: Michael Arzt, Ruth Luigart, Carola Schum, Lars Lüthje, Annika Stein, Iris Koper, Cornelia Hecker, Rio Dumitrascu, Richard Schulz
Journal: European Respiratory Journal (2012)

Sleep-disordered breathing (SDB) may trigger thromboembolic events by enhancing intravascular clot formation. The primary objective of the present nested case–control study was to investigate whether the prevalence of SDB is increased in patients with deep vein thrombosis (DVT) and/or acute pulmonary embolism (PE). 82 consecutive patients with DVT and/or PE (cases) were prospectively enrolled irrespective of SDB-related symptoms and formed matched pairs with patients without DVT and/or PE (controls) according to sex and pre-defined categories of age and body mass index. The prevalence of SDB (respiratory disturbance index assessed by polygraphy ≥15 events·h −1 ) was significantly greater in the cases with DVT and/or PE than in controls (40 versus 26%, p=0.046) and was predominantly obstructive in nature. Multiple regression analysis revealed that SDB was significantly associated with DVT and/or PE (OR 2.28, 95% CI 1.08–4.85; p=0.032) independent of established risk factors for thrombosis. In the sex-specific analyses this association was significant in females (OR 4.14, 95% CI 1.05–16.36; p=0.042), but not in males (OR 1.55, 95% CI 0.57–4.21; p=0.391). SDB occurs more frequently in females with DVT and/or PE than in controls matched for anthropometric variables, and is independently associated with the occurrence of these thromboembolic events.
Criteria for clinical stability in hospitalised patients with community-acquired pneumonia
Authors: Stefano Aliberti, Anna Maria Zanaboni, Tim Wiemken, Ahmed Nahas, Srinivas Uppatla, Letizia Corinna Morlacchi, Paula Peyrani, Francesco Blasi, Julio Ramirez
Journal: European Respiratory Journal (2012)

The American Thoracic Society (ATS) and Infectious Diseases Society of America (IDSA) suggested two sets of criteria in 2001 and 2007 to define clinical stability in community-acquired pneumonia (CAP). The present study aimed to evaluate the level of agreement between these two sets of criteria and how well they can predict clinical outcomes. A retrospective cohort study was carried out of 487 consecutive patients hospitalised with CAP. Level of agreement was tested using a survival curve analysis, while prediction of outcomes at 30-day follow-up was evaluated through receiver operating characteristic (ROC) analysis. A discrepancy between ATS 2001 and ATS/IDSA 2007 criteria in identifying clinical stability was detected in 62% of the patients. The median (interquartile range) time to clinical stability was 2 (1–4) days based on ATS 2001 and 3 (2–5) days based on ATS/IDSA 2007 criteria (p = 0.012). The daily distribution of patients who reached clinical stability evaluated with both sets was different (p = 0.002). The ROC analysis showed an area under the curve of 0.705 for the ATS 2001 criteria and 0.714 for ATS/IDSA 2007 criteria (p = 0.645). ATS 2001 and ATS/IDSA 2007 criteria for clinical stability in hospitalised patients with CAP are clinically equivalent and both can be used in clinical practice as well as in clinical research.
Impact of MACC1 on human malignant glioma progression and patients' unfavorable prognosis
Authors: C. Hagemann, S. Fuchs, C. M. Monoranu, P. Herrmann, J. Smith, T. Hohmann, U. Grabiec, A. F. Kessler, F. Dehghani, M. Lohr, R.-I. Ernestus, G. H. Vince, U. Stein
Journal: Neuro-Oncology (2013)

Metastasis-associated in colon cancer 1 (MACC1) has been established as an independent prognostic indicator of metastasis formation and metastasis-free survival for patients with colon cancer and other solid tumors. However, no data are available concerning MACC1 expression in human astrocytic tumors. Glioblastoma multiforme (GBM) is the most prevalent primary brain tumor of adulthood, and due to its invasive and rapid growth, patients have unfavorable prognoses. Although these tumors rarely metastasize, their invasive and migratory behavior is similar to those of metastatic cells of tumors of different origin. Thus, we hypothesized that MACC1 may be involved in progression of human gliomas.We performed real-time measurements of proliferation and migration in MACC1-transfected GBM cell lines (U138, U251) and evaluated tumor formation in organotypic hippocampal slice cultures of mice. Semiquantitative and quantitative real-time reverse transcription PCR analyses were performed for MACC1 and for its transcriptional target c-Met in human astrocytoma of World Health Organization grade II (low-grade astrocytoma) and GBM biopsies. Data were validated by MACC1 immunohistochemistry in independent matched samples of low-grade astrocytoma and GBM.MACC1 increases the proliferative, migratory, and tumor-formation abilities of GBM cells. The c-Met inhibitor crizotinib reduced MACC1-induced migration and tumor formation in organotypic hippocampal slice cultures of mice. Analyzing patients' biopsies, MACC1 expression increased concomitantly with increasing World Health Organization grade. Moreover, MACC1 expression levels allowed discrimination of dormant and recurrent low-grade astrocytomas and of primary and secondary GBM. Strong MACC1 expression correlated with reduced patient survival.MACC1 may represent a promising biomarker for prognostication and a new target for treatment of human gliomas.
Comparison of Omapatrilat and Enalapril in Patients With Chronic Heart Failure
Authors: Milton Packer, Robert M. Califf, Marvin A. Konstam, Henry Krum, John J. McMurray, Jean-Lucien Rouleau, Karl Swedberg
Journal: Circulation (2002)

Background— Combined inhibition of the angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP) may produce greater benefits in heart failure than ACE inhibition alone. Methods and Results— We randomly assigned 5770 patients with New York Heart Association class II to IV heart failure to double-blind treatment with either the ACE inhibitor enalapril (10 mg BID, n=2884) or to the ACE-NEP inhibitor omapatrilat (40 mg once daily, n=2886) for a mean of 14.5 months. The primary end point—the combined risk of death or hospitalization for heart failure requiring intravenous treatment—was used prospectively to test both a superiority and noninferiority hypothesis (based on the effect of enalapril in the Studies of Left Ventricular Dysfunction [SOLVD] Treatment Trial). A primary end point was achieved in 973 patients in the enalapril group and in 914 patients in the omapatrilat group (hazard ratio 0.94; 95% CI: 0.86 to 1.03, P =0.187)—a result that fulfilled prespecified criteria for noninferiority but not for superiority. The omapatrilat group also had a 9% lower risk of cardiovascular death or hospitalization ( P =0.024) and a 6% lower risk of death ( P =0.339). Post hoc analysis of the primary end point with the definition used in the SOLVD Treatment Trial (which included all hospitalizations for heart failure) showed an 11% lower risk in patients treated with omapatrilat (nominal P =0.012). Conclusion— Omapatrilat reduces the risk of death and hospitalization in chronic heart failure but was not more effective than ACE inhibition alone in reducing the risk of a primary clinical event. Between-group differences in favor of omapatrilat observed in secondary and post hoc analyses warrant further study.
Case-Control Study of Childhood Acute Lymphoblastic Leukemia and Residential Radon Exposure
Authors: J H Lubin, M S Linet, J D Boice, J Buckley, S M Conrath, E E Hatch, R A Kleinerman, R E Tarone, S Wacholder, L L Robison
Journal: JNCI Journal of the National Cancer Institute (1998)

Background: Several ecologic analyses have shown significant positive associations between mean indoor radon concentrations and risk of leukemia at all ages (acute myeloid leukemia and chronic lymphocytic leukemia) and for children (all leukemia, acute myeloid leukemia, and acute lymphoblastic leukemia [ALL]). As part of an age-matched, case-control study of childhood ALL in the United States, we investigated the association between the incidence of ALL in children under age 15 years and indoor radon exposure. Methods: Radon detectors were placed in current and previous homes of subjects where they resided for 6 months or longer. Children were included in analyses if radon measurements covered 70% or more of the 5-year period prior to diagnosis for case subjects (or from birth for case subjects under age 5 years) and the corresponding reference dates for control subjects. Radon levels could be estimated for 97% of the exposure period for the eligible 505 case subjects and 443 control subjects. Results: Mean radon concentration was lower for case subjects (65.4 becquerels per cubic meter [Bqm−3]) than for control subjects (79.1 Bqm−3). For categories less than 37, 37–73, 74–147, and 148 or more Bqm−3 of radon exposure, relative risks based on matched case-control pairs were 1.00, 1.22, 0.82, and 1.02, respectively, and were similar to results from an unmatched analysis. There was no association between ALL and radon exposure within subgroups defined by categories of age, income, birth order, birth weight, sex, type of residence, magnetic field exposure, parental age at the subject's birth, parental occupation, or parental smoking habits. Conclusions: In contrast to prior ecologic studies, the results from this analytic study provide no evidence for an association between indoor radon exposure and childhood ALL.
Individual Differences and Social Influences on the Neurobehavioral Pharmacology of Abused Drugs
Authors: M. T. Bardo, J. L. Neisewander, T. H. Kelly
Journal: Pharmacological Reviews (2013)

The interaction of drugs with biologic targets is a critical area of research, particularly for the development of medications to treat substance use disorders. In addition to understanding these drug-target interactions, however, there is a need to understand more fully the psychosocial influences that moderate these interactions. The first section of this review introduces some examples from human behavioral pharmacology that illustrate the clinical importance of this research. The second section covers preclinical evidence to characterize some of the key individual differences that alter drug sensitivity and abuse vulnerability, related primarily to differences in response to novelty and impulsivity. Evidence is presented to indicate that critical neuropharmacological mechanisms associated with these individual differences involve integrated neurocircuits underlying stress, reward, and behavioral inhibitory processes. The third section covers social influences on drug abuse vulnerability, including effects experienced during infancy, adolescence, and young adulthood, such as maternal separation, housing conditions, and social interactions (defeat, play, and social rank). Some of the same neurocircuits involved in individual differences also are altered by social influences, although the precise neurochemical and cellular mechanisms involved remain to be elucidated fully. Finally, some speculation is offered about the implications of this research for the prevention and treatment of substance abuse.