tbuckley/cabot-search huggingface dataset:
AN EVALUATION OF THE TREATMENT OF PROBLEM CHILDREN AS DETERMINED BY A FOLLOW-UP STUDY
Authors: Howard W. Potter, Henriette R. Klein
Journal: American Journal of Psychiatry (1937)

To recapitulate, this is a report of the outcome of 175 problem children whose maladjustment in the majority of instances was so severe that it necessitated hospitalization. No case included in this report had been out of the hospital for less than one year; well over half of the patients had been out three years or more. So far as the treatment accorded is concerned, it may be said that it was widely conceived and was both extensive and intensive except for those 64 cases belonging to the Organic reaction group. There were 64 cases in the organic reaction group; ten of these were making a satisfactory social adjustment at the time of the follow-up contact. We wish to state, however, that for administrative reasons, we found it inadvisable to attempt a long term treatment of these cases. More adequate treatment might have resulted in a larger number of social recoveries. The results in the situational reaction group (conduct disorders, personality and habit problems and psychoneuroses) were gratifying, as 55 out of a total of 97 were making a good social adjustment when the follow-up contact was made. The percentage of children making a satisfactory social adjustment was definitely higher in the psychoneurotic group. It is our impression that children who have superior intelligence, who are in the prepubertal years (10 to 13), who show a definite response to treatment during the first six months, and whose parents, although having faulty attitudes, are free from well defined neurosis or psychosis, have the better prognosis. The outcome of the schizophrenic reaction group is exceedingly poor; only 1 out of 14 has made an at all satisfactory readjustment; the remainder became progressively worse. This certainly emphasizes the constitutional inadequacy factor, whatever it may be, in those cases which we call schizophrenia in children.
Effects of candesartan and propranolol combination therapy versus propranolol monotherapy in reducing portal hypertension
Authors: Jae Hyun Kim, Jung Min Kim, Youn Zoo Cho, Ji Hoon Na, Hyun Sik Kim, Hyoun A Kim, Hye Won Kang, Soon Koo Baik, Sang Ok Kwon, Seung Hwan Cha, Young Ju Kim, Moon Young Kim
Journal: Clinical and Molecular Hepatology (2014)

Background/Aims Angiotensin receptor blockers (ARBs) inhibit activated hepatic stellate cell contraction and are thought to reduce the dynamic portion of intrahepatic resistance. This study compared the effects of combined treatment using the ARB candesartan and propranolol versus propranolol monotherapy on portal pressure in patients with cirrhosis in a prospective, randomized controlled trial. Methods Between January 2008 and July 2009, 53 cirrhotic patients with clinically significant portal hypertension were randomized to receive either candesartan and propranolol combination therapy (26 patients) or propranolol monotherapy (27 patients). Before and 3 months after the administration of the planned medication, the hepatic venous pressure gradient (HVPG) was assessed in both groups. The dose of propranolol was subsequently increased from 20 mg bid until the target heart rate was reached, and the candesartan dose was fixed at 8 mg qd. The primary endpoint was the HVPG response rate; patients with an HVPG reduction of >20% of the baseline value or to <12 mmHg were defined as responders. Results The mean portal pressure declined significantly in both groups, from 16 mmHg (range, 12-28 mmHg) to 13.5 mmHg (range, 6-20 mmHg) in the combination group (P<0.05), and from 17 mmHg (range, 12-27 mmHg) to 14 mmHg (range, 7-25 mmHg) in the propranolol monotherapy group (P<0.05). However, the medication-induced pressure reduction did not differ significantly between the two groups [3.5 mmHg (range, -3-11 mmHg) vs. 3 mmHg (range, -8-10 mmHg), P=0.674]. The response rate (55.6% vs. 61.5%, P=0.435) and the reductions in mean blood pressure or heart rate also did not differ significantly between the combination and monotherapy groups. Conclusions The addition of candesartan (an ARB) to propranolol confers no benefit relative to classical propranolol monotherapy for the treatment of portal hypertension, and is thus not recommended. Keywords: Portal hypertension; Angiotensin receptor blocker; Non-selective beta blocker; Cirrhosis; Hepatic venous pressure gradient
GW25-e3208 The Mechanism of Tongxinluo Capsule on Coronary Micrangium Spasm: inflammation, micrangium basement membrane and collagen remodeling
Authors: Xiao Li, Ping Jiang, Xiang-dong Xu, Hai-qing Lin, Yong Zhang, Xue Wang, Yue-hua Jiang
Journal: Journal of the American College of Cardiology (2014)
Diagnosis and Treatment of Drug Dependence of the Barbiturate Type
Authors: ABRAHAM WIKLER
Journal: American Journal of Psychiatry (1968)

The basic principles in treatment of patients suspected of, or known to be, physically dependent on barbiturates, nonbarbiturate sedatives, and/or "minor tranquilizers" are: stabilization on pentobarbital in daily amounts and frequency of dosage sufficient to completely suppress barbiturate-type abstinence phenomena and produce minimal signs of barbiturate intoxication; and progressive reduction of pentobarbital dosage at the rate of not more than 100 mg. a day after three to five days of stabilization.
Human Leukocyte Antigen Associations in Occupational Asthma Induced by Isocyanates
Authors: C. E. MAPP, A. BALBONI, R. BARICORDI, L. M. FABBRI
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

Section:ChooseTop of pageAbstract <<ANTIBODY-MEDIATED HYPERSE...CELL-MEDIATED HYPERSENSIT...GENETIC MECHANISMS IN OCC...ReferencesCITING ARTICLES
Studies of T- and B-Cell Interactions in Adult Patients with Combined Immunodeficiency
Authors: T. Morito, A. D. Bankhurst, R. C. Williams
Journal: Journal of Clinical Investigation (1980)

Cellular interactions involved in the pathogenesis of hypogammaglobulinemia were studied in six patients with common variable immunodeficiency. Amounts of immunoglobulin (Ig)G and IgM in the supernate of pokeweed mitogen-stimulated cocultures of normal and immunodeficient mononuclear cells were measured by radioimmunoassays. Mononuclear cells from three of six patients inhibited Ig production of normal B cells (P < 0.005). When purified patient and normal T cells were added to B cells in various autologous or allogeneic combinations, it was observed that immunodeficient T cells (AT) from four patients suppressed normal IgM synthesis. Allogeneic normal T cells did not provide help for B cells from these same immunodeficient patients. In two patients, autologous T cells were able to help autologous B-cell IgM synthesis in vitro. In five patients, AT cells inhibited normal B-cell IgG synthesis. Removal of T cells bearing Ia determinants or T cells with Fc-IgG receptors did not diminish the suppressive effect of AT cells on normal B-cell Ig synthesis. Addition of indomethacin, a prostaglandin synthetase inhibitor, did not abrogate the suppressive effect of immunodeficient mononuclear cells. Addition of hydrocortisone succinate (10 μM) did reverse the suppressive effect of AT cells on IgM production in one patient; however, no in vitro reversal of suppressor cell effect was recorded in five. Suppression by immune-deficient T cells was eliminated by 2,000 rad of x-ray irradiation in three patients. After x-ray irradiation immunedeficient T cells could function as helpers of normal B cells.
Reply from Authors re: Suzanne Biehn Stewart, Shelby D. Reed, Judd W. Moul. Will the Future of Health Care Lead to the End of the Robotic Golden Years? Eur Urol 2014;65:325–7
Authors: Jim C. Hu, Stephen J. Freedland, Brent K. Hollenbeck, Yair Lotan, William T. Lowrance, Joel B. Nelson, Christian Bolenz
Journal: European Urology (2013)
Meta-Analysis of Breast Cancer Outcomes in Adjuvant Trials of Aromatase Inhibitors Versus Tamoxifen
Authors: Mitch Dowsett, Jack Cuzick, Jim Ingle, Alan Coates, John Forbes, Judith Bliss, Marc Buyse, Michael Baum, Aman Buzdar, Marco Colleoni, Charles Coombes, Claire Snowdon, Michael Gnant, Raimund Jakesz, Manfred Kaufmann, Francesco Boccardo, Jon Godwin, Christina Davies, Richard Peto
Journal: Journal of Clinical Oncology (2009)

Purpose To conduct meta-analyses of randomized trials of aromatase inhibitors (AIs) compared with tamoxifen either as initial monotherapy (cohort 1) or after 2 to 3 years of tamoxifen (cohort 2). Materials and Methods Data submitted to the Early Breast Cancer Trialists' Collaborative Group were used in separate meta-analyses of two cohorts. Primary analyses involve postmenopausal women with tumors reported to be estrogen receptor positive. Log-rank P values are two-sided. Results Cohort 1 comprised 9,856 patients with a mean of 5.8 years of follow-up. At 5 years, AI therapy was associated with an absolute 2.9% (SE = 0.7%) decrease in recurrence (9.6% for AI v 12.6% for tamoxifen; 2P &lt; .00001) and a nonsignificant absolute 1.1% (SE = 0.5%) decrease in breast cancer mortality (4.8% for AI v 5.9% for tamoxifen; 2P = .1). Cohort 2 comprised 9,015 patients with a mean of 3.9 years of follow-up. At 3 years from treatment divergence (ie, approximately 5 years after starting hormonal treatment), AI therapy was associated with an absolute 3.1% (SE = 0.6%) decrease in recurrence (5.0% for AI v 8.1% for tamoxifen since divergence; 2P &lt; .00001) and an absolute 0.7% (SE = 0.3%) decrease in breast cancer mortality (1.7% for AI v 2.4% for tamoxifen since divergence; 2P = .02). There was no convincing heterogeneity in the proportional recurrence reduction with respect to age, nodal status, tumor grade, or progesterone receptor status and no indication of an increase in nonbreast deaths with AIs in either cohort. Conclusion AIs produce significantly lower recurrence rates compared with tamoxifen, either as initial monotherapy or after 2 to 3 years of tamoxifen. Additional follow-up will provide clearer information on long-term survival.
A predictive model of treatment outcome in patients with chronic HCV infection using IL28B and PD-1 genotyping
Authors: Jose Ramón Vidal-Castiñeira, Antonio López-Vázquez, Rebeca Alonso-Arias, Marco Antonio Moro-García, Pablo Martinez-Camblor, Santiago Melón, Jesús Prieto, Rosario López-Rodriguez, Paloma Sanz-Cameno, Luis Rodrigo, Rosa Pérez-López, Ramón Pérez-Álvarez, Carlos López-Larrea
Journal: Journal of Hepatology (2012)
Ontogeny of Fc receptors and complement receptor (CR3) during human myeloid differentiation.
Authors: H B Fleit, S D Wright, C J Durie, J E Valinsky, J C Unkeless
Journal: Journal of Clinical Investigation (1984)

Two different Fc receptors for IgG (Fc gamma R) have been identified on human leukocytes: a high avidity receptor (Fc gamma Rhi) present on monocytes but not on neutrophils, and a low avidity receptor (Fc gamma Rlo) present on neutrophils but not on monocytes. Fc gamma Rlo can be inhibited and the receptor precipitated by monoclonal antibody 3G8. We have used this monoclonal antibody to study the course of Fc gamma Rlo appearance on bone marrow cells, leukocytes of patients with chronic myelogenous leukemia (CML), and HL-60 and U937 cells induced to differentiate with agents such as dimethyl sulfoxide (DMSO), retinoic acid, phorbol myristate acetate, and lymphokine. We report that Fc gamma Rlo is a late differentiation antigen, first expressed at the metamyelocyte stage. Since precursors to metamyelocytes bear Fc gamma R, and the promyelocyte line HL-60 bears Fc gamma Rhi, there must be a progressive loss of Fc gamma Rhi during myeloid differentiation and the reciprocal expression of Fc gamma Rlo. Results of immunoprecipitation and polyacrylamide gel analysis of the proteins are consistent with these results. We have also studied the receptor for the C3bi complement component (CR3), which is blocked and immunoprecipitated by monoclonal antibody OKM10. During DMSO-driven differentiation of HL-60 cells, we find that CR3 is induced on all cells, whereas Fc gamma Rlo is induced on only 24% of cells, suggesting that CR3 appears earlier during differentiation than Fc gamma Rlo does.
Role of transiently altered sarcolemmal membrane permeability and basic fibroblast growth factor release in the hypertrophic response of adult rat ventricular myocytes to increased mechanical activity in vitro.
Authors: D Kaye, D Pimental, S Prasad, T Mäki, H J Berger, P L McNeil, T W Smith, R A Kelly
Journal: Journal of Clinical Investigation (1996)

One of the trophic factors that has been implicated in initiating or facilitating growth in response to increased mechanical stress in several tissues and cell types is basic fibroblast growth factor (bFGF; FGF-2). Although mammalian cardiac muscle cells express bFGF, it is not known whether it plays a role in mediating cardiac adaptation to increased load, nor how release of the cytosolic 18-kD isoform of bFGF would be regulated in response to increased mechanical stress. To test the hypothesis that increased mechanical activity induces transient alterations in sarcolemmal permeability that allow cytosolic bFGF to be released and subsequently to act as an autocrine and paracrine growth stimulus, we examined primary isolates of adult rat ventricular myocytes maintained in serum-free, defined medium that were continually paced at 3 Hz for up to 5 d. Paced myocytes, but not nonpaced control cells, exhibited a "hypertrophic" response, which was characterized by increases in the rate of phenylalanine incorporation, total cellular protein content, and cell size. These changes could be mimicked in control cells by exogenous recombinant bFGF and could be blocked in continually paced cells by a specific neutralizing anti-bFGF antibody. In addition, medium conditioned by continually paced myocytes contained significantly more bFGF measured by ELISA and more mitogenic activity for 3T3 cells, activity that could be reduced by a neutralizing anti-bFGF antibody. The hypothesis that transient membrane disruptions sufficient to allow release of cytosolic bFGF occur in paced myocytes was examined by monitoring the rate of uptake into myocytes from the medium of 10-kD dextran linked to fluorescein. Paced myocytes exhibited a significantly higher rate of fluoresceinlabeled dextran uptake. These data are consistent with the hypothesis that nonlethal, transient alterations in sarcolemmal membrane permeability with release of cytosolic bFGF is one mechanism by which increased mechanical activity could lead to a hypertrophic response in cardiac myocytes.
CRITICISMS ON REMARKS IN THE DISCUSSION OF DR. CLARKE'S 1 PAPER ON DISPLACEMENT OF THE UTERUS.
Authors: FRANKLIN H. MARTIN
Journal: JAMA (1897)

In imagination, two days ago, I sat in this hall as an inexperienced practitioner of medicine, seeking for some light on the subject of displacements of the uterus, which might be afforded me by the discussion of Dr. Clarke's excellent paper by the many gynecologists present. The discussion, hesitatingly begun, waxed eloquent, grew aggressive and, in the vortex of its climax, many voices of learned men were heard. To me, in my capacity of an imaginary beginner, confusion existed in my mind at the commencement of the discussion, but when the discussion grew in proportions, my mind became a whirlwind of conflicting emotions, because of the many positive, not to be appealed from, opinions, of a diametrically opposite character thundered at us from as many different distinguished specialists. The discussion was begun, as all hot discussions on gynecologic subjects are begun in Philadelphia, by one of the big four of
Effect of Cigarette Smoking on Outcome After Thrombolytic Therapy for Myocardial Infarction
Authors: Cindy L. Grines, Eric J. Topol, William W. O’Neill, Barry S. George, Dean Kereiakes, Harry R. Phillips, Jeffrey D. Leimberger, Lynn H. Woodlief, Robert M. Califf
Journal: Circulation (1995)

Background Smoking is known to be a strong risk factor for premature atherosclerosis, myocardial infarction, and sudden cardiac death. Unexpectedly, in the reperfusion era, investigators have reported that patients who smoke have a more favorable prognosis after thrombolysis compared with nonsmokers. Since smoking is associated with a relatively hypercoagulable state, we hypothesized that the coronary occlusion responsible for infarction may be primarily thrombotic, with improved outcome relating to enhanced patency or the absence of a residual stenosis after thrombolytic therapy. Methods and Results To examine this issue, we evaluated 1619 patients treated with TPA, urokinase, or both in six consecutive myocardial infarction trials, of whom 878 (54%) were currently smoking. Patients underwent 90-minute and predischarge catheterizations, which were quantified blinded to the patients’ smoking status. As expected, baseline fibrinogen (2.8 [2.5, 3.6] versus 2.7 [2.4, 3.5] g/dL, P =.003) and hematocrit (44% [41%, 47%] versus 43% [40%, 45%], P =.0001) levels were greater in smokers. Although there were no differences between smokers and nonsmokers with regard to 90-minute patency (73% versus 74%), smokers were more likely to have TIMI-3 flow (41.1% versus 34.6%, P =.034), with a larger minimum lumen diameter of the infarct stenosis both acutely (0.82 [0.51, 1.11] versus 0.72 [0.43, 1.04] mm, P =.0432) and at follow-up (1.2 [0.8, 1.74] versus 1.0 [0.7, 1.5], P =.002). Although smokers tended to have reduced in-hospital mortality compared with nonsmokers in univariate analysis (4.0% versus 8.9%, P =.0001), after adjustment for baseline differences between smokers and nonsmokers in age (54 [47, 62] versus 60 [54, 68] years, P &lt;.0001), inferior infarct location (60% versus 53%, P &lt;.0001), three-vessel disease (16% versus 22%, P &lt;.001), and baseline ejection fraction (53% [44%, 60%] versus 50% [42%, 58%], P =.0069), smoking history was of no independent prognostic significance. Conclusions Therefore, smokers have a relatively hypercoagulable state, documented by increased hematocrit and fibrinogen levels. Quantitative coronary angiographic analysis suggests that the mechanism of infarction in smokers is more often thrombosis of a less critical atherosclerotic lesion compared with nonsmokers. Enhanced perfusion status, as well as favorable baseline clinical and angiographic characteristics, may be responsible for the more benign prognosis of current smokers.
Abstract B71: Syndecan-1 promotes breast cancer metastasis by modulating tissue stiffness
Authors: Colleen L. Chute, Patricia Keely, Caroline Alexander, Andreas Friedl
Journal: Cancer Research (2013)

Abstract Tumor-stroma interactions are integral to breast cancer progression and metastasis. It has been well established that women with dense breast tissue have increased risk of developing breast cancer as compared to women with less dense breast tissue; it has also been documented that a stiffer extracellular matrix (ECM) can promote tumor cell invasion both in vitro and in vivo. Our lab has previously shown that Syndecan-1 (Sdc1), a cell surface heparan sulfate proteoglycan, regulates the in vitro organization of a fibroblast-constructed ECM that thus creates an invasion-permissive microenvironment. Therefore, we sought to characterize the role of stromal Sdc1 in cancer progression in vivo. Using the 4T1 model of late stage metastatic breast cancer in both Sdc1 wild-type (WT) and Sdc1 knock-out (KO) mice, we assayed for tumor metastasis from orthotopic tumor cell implants. Sdc1 deficiency in the host did not influence the primary tumor weight or growth rate, but significantly reduced the incidence and the number of metastatic lesions (p&amp;lt;0.001, p&amp;lt;0.0001, respectively). In an effort to dissect out the mechanism by which loss of stromal Sdc1 is inhibiting metastasis, we analyzed the tumor microenvironment for the presence of specific cell types and structural differences. There was no difference in the recruitment of macrophages, the activation of fibroblasts, angiogenesis, or the structure or deposition of collagen between 4T1-induced tumors in the Sdc1 WT and Sdc1 KO mice. Interestingly, preliminary data suggest the tumors from the Sdc1 WT mice are significantly stiffer than the tumors from Sdc1 KO mice, as measured by atomic force microscopy. To determine whether Sdc1 was influencing later stages of metastasis we injected tumor cells via tail vein to specifically assay extravasation and metastatic outgrowth. After 2 weeks, all mice assayed had metastatic lesions but the Sdc1 WT mice had significantly more numerous and larger lesions (p&amp;lt;0.004, p&amp;lt;0.05, respectively). These data indicate that the presence of stromal Sdc1 promotes tumor cell outgrowth in the metastatic target organ, but may not play as large a role in tumor cell extravasation based on the finding that all mice assayed had metastatic lesions. These results further suggest that Sdc1 influences breast cancer metastasis by promoting increased tissue stiffness, which promotes tumor cell invasion and tumor outgrowth at secondary metastatic target organs, and ultimately promotes formation of metastatic lesions. Citation Format: Colleen L. Chute, Patricia Keely, Caroline Alexander, Andreas Friedl. Syndecan-1 promotes breast cancer metastasis by modulating tissue stiffness. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr B71.
Serum Lectin-Like Oxidized LDL Receptor-1 Levels for the Detection and Evaluation of the Left Ventricular Systolic Heart Failure
Authors: Feyzullah Beşli, Sümeyye Güllülü, Saim Sağ, Ebru Açıkgöz, Mesut Keçebaş, Bülent Özdemir, Aysel Aydın Kaderli, Tunay Şentürk, İbrahim Baran, Emre Sarandöl, Ali Aydınlar
Journal: Journal of the American College of Cardiology (2013)
Cooking for a New Earth: A New Approach to Home Cooking That Promotes Wholesome Eating and Healthy Living
Authors: John La Puma
Journal: JAMA (1993)

<b>American Heart Association Low-Fat, Low-Cholesterol Cookbook</b>, edited by Scott M. Grundy and Mary Winston, 340 pp, $21, ISBN 0-8129-1783-9, paper $13, 0-8129-1982-3, New York, NY, Times Books, 1989. <b>American Heart Association Cookbook</b>, edited by Mary Winston, 5th ed, 643 pp, $25, ISBN 0-8129-1895-9, paper $14, ISBN 0-8129-2282-4, New York, NY, Times Books, 1991. <b>Eat More, Weigh Less: Dr Dean Ornish's Life Choice Program for Losing Weight Safely While Eating Abundantly</b>, by Dean Ornish, 425 pp, $25, ISBN 0-06-016838-2, New York, NY, HarperCollins, 1993. <b>Great Good Food: Luscious Lower Fat Cooking</b>, by Julee Rosso, 574 pp, with illus, $29, ISBN 0-517-59645-8, paper, $19, ISBN 0-517-88122-5, New York, NY, Crown, 1993. While our biochemical base may help us tell a micelle from an HDL, few physicians are chefs, and even fewer can help patients choose a low-fat diet without a nutritionist and a stack of pamphlets. These five authors have sought to