tbuckley/cabot-search huggingface dataset:
Surgical Treatment for Stable Angina Pectoris
Authors: Virendra S. Mathur, Gene A. Guinn, Lakis C. Anastassiades, Robert A. Chahine, Ferenc L. Korompai, Alfredo C. Montero, Robert J. Luchi
Journal: New England Journal of Medicine (1975)

To evaluate the role of coronary bypass treatment of stable angina, 72 patients were randomly divided into surgical and medical groups. They were followed with treadmill tests and repeat catheterization. Anginal symptoms decreased or disappeared in 89 per cent of those operated on and 65 per cent of those not operated on, but more of the former than of the latter became asymptomatic: 69 vs. 11 per cent respectively (p smaller than 0.01). Exercise tolerance time improved significantly (p smaller than 0.001) in both groups, but more in the group operated on, plus 78 per cent vs. plus 48 per cent, p smaller than 0.05. During a 28-month follow-up period, fewer cardiac complications occurred in the patients operated on--14 vs. 34 (p smaller than 0.02). Mortality was 9 per cent in the patients operated on and 14 per cent in those not operated on; this difference is not significant. The results indicate that improvement, though demonstrable in both groups, is greater with surgery, and quality of life during the first 28 months is better in patients who are operated on.
320 3.5-Diethoxycarbonyl-1.4-dihydrocollidine (DDC) feeding induces cholestasis, chronic inflammatory bile duct damage and biliary fibrosis in mice
Authors: U. Stöger, E. Fickert, A. Fuchsbichler, T. Moustafa, J. Gumhold, D. Silbert, K. Zatloukal, H. Denk, M. Trauner
Journal: Journal of Hepatology (2006)
Transmission of HTLV-II
Authors: Terence Chorba
Journal: JAMA (1986)

To the Editor.—  A recent article by Robert-Guroff et al 1 reported a high prevalence of antibodies specific for human T-cell lymphotropic virus type II (HTLV-II) in intravenous drug users studied in New York City. Serological evidence of infection with this virus has also been reported among intravenous drug users in Britain. 2 These are alarming reports, because HTLV-II has only been isolated in a total of four patients, two of whom were members of groups considered at risk for infection with hepatitis B virus and HTLV-III: one was a known intravenous drug user 3 and one was a patient with severe hemophilia A. 4 Although the role of HTLV-II in human disease remains obscure, the observation of a high prevalence of antibodies to HTLV-II in intravenous drug users and the fact that two of the four persons from whom HTLV-II has been isolated had multiple potential exposures to blood-borne
Chronic Pancreatitis Pain Pattern and Severity Are Independent of Abdominal Imaging Findings
Authors: C. Mel Wilcox, Dhiraj Yadav, Tian Ye, Timothy B. Gardner, Andres Gelrud, Bimaljit S. Sandhu, Michele D. Lewis, Samer Al-Kaade, Gregory A. Cote, Christopher E. Forsmark, Nalini M. Guda, Darwin L. Conwell, Peter A. Banks, Thiruvengadam Muniraj, Joseph Romagnuolo, Randall E. Brand, Adam Slivka, Stuart Sherman, Stephen R. Wisniewski, David C. Whitcomb, Michelle A. Anderson
Journal: Clinical Gastroenterology and Hepatology (2014)
Regular versus irregular inflection: A question of levels
Authors: Alessandro Laudanna
Journal: Behavioral and Brain Sciences (1999)

When referring to the organization of the mental lexicon, the distinction between combinatorial rules and lexical listing for regularly versus irregularly inflected words should be further developed to account for subregular morphological processes. Moreover, the distinction may be more or less appropriate depending on the lexical component under consideration, and it is subject to interplay with other factors that are relevant in determining the representational structure of the lexical system.
THE INFLUENCE OF PROLAPSE OF THE KIDNEY ON THE PRODUCTION OF DISEASE OF THE FEMALE PELVIC ORGANS.
Authors: AUGUSTIN H. GOELET
Journal: JAMA (1902)

Prolapse of the kidney may cause or maintain disease of the female pelvic organs by interfering with the return circulation from the pelvis and producing pelvic congestion. This may be brought about chiefly in two ways: The renal artery being less yielding than the other structures constituting the renal pedicle, dragging upon it by the kidney crowds the aorta over against the vena cava and distorts that great channel of return circulation when it is the right kidney that is prolapsed. When the displaced kidney reaches a certain point in its descent it is situated immediately in front of the ovarian vein as it ascends to empty into the vena cava just below the renal vein on the right or into the left renal vein on the left side. Hence, pressure backward upon the kidney, as from corsets, or clothing at the waist, or from accumulation of gas or feces
The Place of Angiotensin-Converting Enzyme Inhibition in the Treatment of Cardiovascular Diseases
Authors: Haralambos Gavras
Journal: New England Journal of Medicine (1988)

Elsewhere in this issue, Williams updates the pharmacology of angiotensin-converting enzyme inhibitors.1 The development of this class of drugs is a prime example of how a serendipitous finding — the observation that a Brazilian snake venom contained kininase-inactivating factors2 — was taken up by basic scientists, who showed its physiologic relevance by defining the relations between vasoactive peptide hormones and their enzymatic degradation.3 This led biochemists to purify and characterize the active compounds and use them to design and synthesize drugs targeting the specific enzymatic system.4 Physiologists and clinical researchers then used them to investigate the role of the renin–angiotensin . . .
ST-segment elevation and ventricular fibrillation without coronary spasm by intracoronary injection of acetylcholine and/or ergonovine maleate in patients with Brugada syndrome
Authors: Takashi Noda, Wataru Shimizu, Atsushi Taguchi, Kazuhiro Satomi, Kazuhiro Suyama, Takashi Kurita, Naohiko Aihara, Shiro Kamakura
Journal: Journal of the American College of Cardiology (2002)
Ongoing activation of autoantigen-specific B cells in primary biliary cirrhosis
Authors: Jun Zhang, Weici Zhang, Patrick S.C. Leung, Christopher L. Bowlus, Sandeep Dhaliwal, Ross L. Coppel, Aftab A. Ansari, Guo-Xiang Yang, Jinjun Wang, Thomas P. Kenny, Xiao-Song He, Ian R. Mackay, Eric M. Gershwin
Journal: Hepatology (2014)

The serologic hallmark of primary biliary cirrhosis (PBC), the antimitochondrial response to the E2 component of the pyruvate dehydrogenase complex (PDC-E2), has unique features, including continuous high titers of immunoglobulin M (IgM) and IgG reactivity throughout all stages of disease, capable not only of target enzyme inhibition, but also crossreactive with chemical xenobiotics that share molecular homology with the inner lipoyl domain of PDC-E2; such chemicals have been proposed as potential etiological agents. We used flow cytometry and enzyme-linked immunospot assay (ELISPOT) to examine B-cell subsets in 59 subjects, including 28 with PBC, 13 with primary sclerosing cholangitis (PSC), and 18 healthy controls. Strikingly, in PBC, although there were no significant differences in B-cell phenotype subpopulations, 10% of the total IgG and IgA plasmablast population and 23% of the IgM plasmablast population were uniquely reactive with PDC-E2, detected in the CXCR7+CCR10low plasmablast population. In contrast, plasmablast reactivity to a control antigen, tetanus toxoid, was minimal and similar in all groups. Additionally, we isolated plasmablast-derived polyclonal antibodies and compared reactivity with plasma-derived antibodies and noted a distinct noncirculating tissue source of xenobiotic crossreacting antibodies. The high levels of autoantigen specific peripheral plasmablasts indicate recent activation of naive or memory B cells and a continuous and robust activation. The presence of CXCR7+CCR10low PDC-E2-specific ASCs suggests a mechanistic basis for the migration of circulating antigen specific plasmablasts to the mucosal epithelial ligands CXCL12 and CCL28. Conclusion : Our findings suggest a sustained rigorous B-cell response in PBC, likely activated and perpetuated by cognate autoantigen. (Hepatology 2014;60:1708–1716)
Gastric tumour-derived ANGPT2 regulation by DARPP-32 promotes angiogenesis
Authors: Zheng Chen, Shoumin Zhu, Jun Hong, Mohammed Soutto, DunFa Peng, Abbes Belkhiri, Zekuan Xu, Wael El-Rifai
Journal: Gut (2015)

<h3>Objective</h3> Overexpression of dopamine and cAMP-regulated phosphoprotein, Mr 32000 (DARPP-32), and its truncated isoform (t-DARPP) are associated with gastric tumorigenesis. Herein, we investigated the role of DARPP-32 proteins in regulating angiopoietin 2 (ANGPT2) and promoting tumour angiogenesis. <h3>Design</h3> Quantitative real-time RT-PCR, immunoblotting, luciferase reporter, immunofluorescence, immunohistochemistry and angiogenesis assays were applied to investigate the regulation of angiogenesis by DARPP-32 proteins. <h3>Results</h3> Overexpression of DARPP-32 significantly increased the mRNA and protein levels of ANGPT2 in gastric cancer cells. The overexpression of DARPP-32 T34A mutant or the N-terminal truncated isoform, t-DARPP, led to similar effects ruling out the T34-dependent regulation of protein phosphatase 1 activity in regulating ANGPT2. DARPP-32 proteins induced a secreted form of ANGPT2, which was detectable in the media, functionally active, and able to induce angiogenesis, measured by the human umbilical vein endothelial cells tube formation assay. Antibody blocking of the secreted ANGPT2 abrogated its function. To identify the mechanism by which DARPP-32 regulates ANGPT2, we examined the activities of NF-κB and signal transducer and activator of transcription 3 (STAT3), known regulators of angiogenesis. The results ruled out NF-κB and showed induction of STAT3 phosphorylation, activation and nuclear localisation. Inhibition or knockdown of STAT3 significantly attenuated the induction of ANGPT2 by DARPP-32 proteins. In vivo xenograft models demonstrated that overexpression of DARPP-32 promotes angiogenesis and tumour growth. Analyses of human gastric cancer tissues showed a strong correlation between DARPP-32 and ANGPT2. <h3>Conclusions</h3> Our novel findings establish the role of DARPP-32-STAT3 axis in regulating ANGPT2 in cancer cells to promote angiogenesis and tumorigenesis.
Two instances of large genome profile picobirnavirus occurrence in Argentinian infants with diarrhea over a 26-year period (1977–2002)
Authors: Miguel O. Giordano, Gisela Masachessi, Laura C. Martinez, Patricia A. Barril, Leonardo J. Ferreyra, María B. Isa, Silvia V. Nates
Journal: Journal of Infection (2008)
Statin Use and Brain Hemorrhage
Authors: Marco A. Gonzalez-Castellon, Randolph S. Marshall
Journal: JAMA Neurology (2014)

The relationship between statin use and intracerebral hemorrhage (ICH) has not been definitively established. Studies show both benefit and detriment. Statins may decrease the level of platelet aggregation and thrombogenesis and thus worsen an ICH, but they also modulate the immune system, inhibit the inflammatory process, and improve cerebral blood flow, promoting neuroprotection and tissue recovery. Despite physiological and clinical evidence on both sides of the argument, the idea that statins should be avoided whenever brain hemorrhage is involved has permeated stroke practice. Indeed, early and more recent epidemiological studies have shown a convincing inverse association between low levels of low-density lipoprotein cholesterol and the risk of hemorrhagic stroke. 1 Whether this association can be applied to patients treated with statins is less clear. Is the fear of statin use for ICH justified? What is the basis on which clinicians have come to avoid statins for their hemorrhage risk, and how should this information guide our practice in light of newer evidence? Part of the confusion arises from a lack of clarity of the association between statin use and hemorrhage under different ICH etiologies. The pathophysiology may be quite different if the brain hemorrhage occurs in the setting of ischemic stroke vs after thrombolytic therapy, in hypertensive ICH, or in other conditions such as amyloid angiopathy. In the last decade, 2 large randomized trials suggested an association between treatment with statins and increased risk of ICH in the setting of acute ischemic stroke. The 2004 Heart Protection Study, 2 a large multicenter, randomized trial of simvastatin 40 mg vs placebo for patients with dyslipidemia and cerebrovascular disease, coronary disease, some other occlusive coronary disease, diabetes mellitus, or treated hypertension showed a nonsignificant increase in the rate of hemorrhagic stroke (1.3% of patients who received 40 mg of simvastatin vs 0.7% of patients who received placebo) in the treatment arm of patients who had a prior cerebrovascular event. The 2008 Stroke Prevention by Aggressive Reduction in Cholesterol Levels trial 3 showed that hemorrhagic stroke was more frequent among those treated with atorvastatin calcium (unadjusted hazard ratio, 1.68 [95% CI, 1.09-2.69]) than among those who received placebo, although hemorrhagic stroke as an entry level event, male sex, and advanced age at baseline accounted for 86% of the increased risk of hemorrhage. Two additional clinical studies 4,5 have shown no evidence of increased
Mouse Model for Hereditary Hemorrhagic Telangiectasia Has a Generalized Vascular Abnormality
Authors: Evelyn Torsney, Richard Charlton, Austin G. Diamond, John Burn, James V. Soames, Helen M. Arthur
Journal: Circulation (2003)

Background— Mutations in endoglin or activin like kinase-1, both involved in the endothelial transforming growth factor-β signaling pathway, cause the autosomal dominant bleeding disorder hereditary hemorrhagic telangiectasia. We and others have reported mouse models for this disease that share the characteristic phenotype of dilated vessels and sporadic hemorrhage. The reasons for the variable phenotype in hereditary hemorrhagic telangiectasia are not understood. Methods and Results— After a detailed immunohistochemical analysis of 129/Ola mice, which are heterozygous for a targeted deletion in the endoglin gene, we observed intrinsic abnormalities in the vascular walls throughout the cutaneous vasculature. Postcapillary venules were dilated, and up to 70% of the vascular wall had no smooth muscle cells. The supporting layers of collagens and elastin were irregular, with thin areas, adding to the fragility of these vessels. A variable hemorrhagic phenotype was observed in which local bleeding is associated not only with fragile vessels but also with regions of inflammation. Conclusions— These findings have relevance to our understanding of the molecular basis of vascular integrity in a wide range of diseases.
Consciousness does not seem to be linked to a single neural mechanism
Authors: Carlo Umiltà, Marco Zorzi
Journal: Behavioral and Brain Sciences (1995)

Abstract On the basis of neuropsychological evidence, it is clear that attention should be given a role in any model (or conjecture) of consciousness. What is known about the many instances of dissociation between explicit and implicit knowledge after brain damage suggests that conscious experience might not be linked to a restricted area of the brain. Even if it were true that there is a single brain area devoted to consciousness, the subicular area would seem to be an unlikely possibility.
Apolipoprotein B-dependent hepatitis C virus secretion is inhibited by the grapefruit flavonoid naringenin
Authors: Yaakov Nahmias, Jonathan Goldwasser, Monica Casali, Daan van Poll, Takaji Wakita, Raymond T. Chung, Martin L. Yarmush
Journal: Hepatology (2008)

Hepatitis C virus (HCV) infects over 3% of the world population and is the leading cause of chronic liver disease worldwide. HCV has long been known to associate with circulating lipoproteins, and its interactions with the cholesterol and lipid pathways have been recently described. In this work, we demonstrate that HCV is actively secreted by infected cells through a Golgi-dependent mechanism while bound to very low density lipoprotein (vLDL). Silencing apolipoprotein B (ApoB) messenger RNA in infected cells causes a 70% reduction in the secretion of both ApoB-100 and HCV. More importantly, we demonstrate that the grapefruit flavonoid naringenin, previously shown to inhibit vLDL secretion both in vivo and in vitro, inhibits the microsomal triglyceride transfer protein activity as well as the transcription of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase and acyl-coenzyme A:cholesterol acyltransferase 2 in infected cells. Stimulation with naringenin reduces HCV secretion in infected cells by 80%. Moreover, we find that naringenin is effective at concentrations that are an order of magnitude below the toxic threshold in primary human hepatocytes and in mice.These results suggest a novel therapeutic approach for the treatment of HCV infection.
Doctors' distinction awards suspended in Scotland
Authors: B. Christie
Journal: BMJ (2010)

Distinction awards for senior doctors have become one of the first casualties in the fight to rein in public spending in Scotland.

No new awards will be made next year and the value of existing awards will be frozen for the second year running. The Scottish government has already described the distinction awards system as outdated and says that a “fairer system” that rewards a wider range of health professionals is needed. The Doctors’ and Dentists’ Review Body is carrying out a UK review of the …
Bortezomib-Induced Skin Lesions
Authors: Mariëtte J Agterof, Douwe H Biesma
Journal: New England Journal of Medicine (2005)

A 62-year-old woman had progression of multiple myeloma despite many therapies, including an autologous hematopoietic stem-cell transplantation. Infusions of bortezomib (1.3 mg per square meter of body-surface area) were administered as an intravenous bolus twice weekly for 2 weeks, followed by a 10-day rest period. During the second treatment cycle, a purpuric rash, which was not associated with fever or itching, developed on the patient's trunk, back, hands, and face. A biopsy specimen of the skin lesion revealed a leukocytoclastic vasculitis. The patient was treated with 20 mg of prednisone, and the rash resolved. The rash recurred with subsequent cycles . . .
Novel Therapeutic Strategy to Treat Brain Ischemia
Authors: Munehisa Shimamura, Naoyuki Sato, Kazuo Oshima, Motokuni Aoki, Hitomi Kurinami, Satoshi Waguri, Yasuo Uchiyama, Toshio Ogihara, Yasufumi Kaneda, Ryuichi Morishita
Journal: Circulation (2004)

Background— Although cerebral occlusive disease leads to cerebral ischemic events, an effective treatment has not yet been established. An ideal therapeutic approach to treat ischemia might have both aspects of enhancement of collateral formation and prevention of neuronal death. Hepatocyte growth factor (HGF) is a potent angiogenic factor that also acts as a neurotrophic factor. Thus, in this study, we examined the therapeutic effects of HGF on brain injury in a rat permanent middle cerebral artery occlusion model. Methods and Results— Gene transfer into the brain was performed by injection of human HGF gene with hemagglutinating virus of Japan–envelope vector into the cerebrospinal fluid via the cisterna magna. Overexpression of the HGF gene resulted in a significant decrease in the infarcted brain area as assessed by triphenyltetrazolium chloride staining, whereas rats transfected with control vector exhibited a wide area of brain death after 24 hours of ischemia. Consistently, the decrease in neurological deficit was significantly attenuated in rats transfected with the HGF gene at 24 hours after the ischemic event. Stimulation of angiogenesis was also detected in rats transfected with the HGF gene compared with controls. Of importance, no cerebral edema or destruction of the blood-brain barrier was observed in rats transfected with the HGF gene. Conclusions— Overall, the present study demonstrated that overexpression of the HGF gene attenuated brain ischemic injury in a rat model, without cerebral edema, through angiogenic and neuroprotective actions. In particular, the reduction of brain injury by HGF may provide a new therapeutic option to treat cerebrovascular disease.
Toward Decoding the Principles of Cancer Metastasis Circuits
Authors: Mingyang Lu, Mohit Kumar Jolly, Jose' Onuchic, Eshel Ben-Jacob
Journal: Cancer Research (2014)

Understanding epithelial-mesenchymal transitions (EMT) during cancer metastasis remains a major challenge in modern biology. Recent observations of cell behavior together with progress in mapping the underlying regulatory genetic networks led to new understandings of carcinoma metastasis. It is now established that the genetic network that regulates the EMT also enables an epithelial-mesenchymal hybrid phenotype. These hybrid cells possess mixed carcinoma epithelial and mesenchymal characteristics that enable specialized capabilities such as collective cell migration. On the gene network perspective, a four-component decision unit composed of two highly interconnected chimeric modules--the miR34/SNAIL and the miR200/ZEB mutual-inhibition feedback circuits--regulates the coexistence of and transitions between the different phenotypes. Here, we present a new tractable theoretical framework to model and decode the underlying principles governing the operation of the regulatory unit. Our approach connects the knowledge about intracellular pathways with observations of cellular behavior and advances toward understanding the logic of cancer decision-making. We found that the miR34/SNAIL module acts as an integrator while the miR200/ZEB module acts as a three-way switch. Consequently, the combined unit can give rise to three phenotypes (stable states): (i) a high miR200 and low ZEB, or (1, 0) state; (ii) a low miR200 and high ZEB, or (0, 1) state; and (iii) a medium miR200 and medium ZEB, or (½, ½) state. We associate these states with the epithelial, mesenchymal, and hybrid phenotypes, respectively. We reflect on the consistency between our theoretical predictions and recent observations in several types of carcinomas and suggest new testable predictions. See all articles in this Cancer Research section,
THE STATE HOSPITAL TRAINING SCHOOL FOR PSYCHIATRIC NURSING
Authors: DONALD A. LAIRD
Journal: American Journal of Psychiatry (1921)

The function of institutions for the ill of mind has changed from the custodial to the remediable. An adequately equipped nursing staff is one of the chief means by which this new function can be realized. This nursing staff should be composed of those prepared primarily to care for mental patients, that is, psychiatric nurses. Psychiatric nurses should receive interpretative psychiatric training. It has been questioned if the State Hospital Training School is preparing nurses for psychiatric duty as efficiently as might be done with the practically unlimited facilities available. Nurses would be better equipped to aid in the rehabilitation of the patients if more emphasis were placed on the psychiatric phases of their training and if the content of the psychiatric courses was less a matter of disease entities and symptoms but aimed more at bringing the nurse into a psychological understanding of the socalled abnormal mental conditions. Any efficient psychiatric training under the conditions in which the state hospital nurse is placed must begin intensively with the pupil's entry into the service. As now organized the State Hospital Training School is not satisfying these desiderata. This is a field well meriting thoughtful consideration and this contribution should not be looked upon as a piece of radical and destructive criticism. The positions taken are justified and highly pragmatic and are presented in a constructive attitude with the hope that in them the hospital executive may find a stimulus to a readjustment of his training courses to the end that better educational values may be established, and that the state hospital nurse may genuinely aid in enabling her patients to adjust themselves to the situations of life.