tbuckley/cabot-search huggingface dataset:
Endoscopic studies of dyspepsia in a general practice.
Authors: M W Gear, R J Barnes
Journal: BMJ (1980)

In an urban general practice serving 7800 patients, all patients presenting over five and a half years with dyspepsia lasting more than two weeks were investigated by fibreoptic endoscopy and cholecystography, and many by barium meal. Of the 393 patients with dyspepsia, 346 completed the investigation: 180 had specific disease of the oesophagus, stomach, duodenum, or gall bladder, including six with carcinoma. Al further 67 had mucosal disease, and only 99 patients had no abnormality. After the first year the number of patients presenting annually and the percentage of patients with specific lesions remained constant. The annual incidence for patients with dyspepsia was about 1% and for patients with specific lesions 0.4%, suggesting that each year those who became symptom free (either spontaneously or because of treatment) were balanced by a similar number who developed symptoms. In contrast to the conclusions of other workers that an "open-access" endoscopy service could not be justified because the number of patients with specific lesins fell during their survey, we suggest that such endoscopy services are indeed worth while for providing an accurate diagnosis of dyspepsia.
The last wish of a patient with end stage chronic obstructive pulmonary disease
Authors: D. J A Janssen, T. P G Alsemgeest, G. A M Widdershoven, E. F M Wouters, J. M G A Schols, M. A Spruit
Journal: BMJ (2008)

At her explicit request, euthanasia allowed a 55 year old woman in the Netherlands with end stage chronic obstructive pulmonary disease to end her life
Abstract 1585: Loss of CDK5 sensitizes ovarian cancer cells to paclitaxel by enhancing intracellular retention
Authors: Ahmed A. Ahmed, Xiao-Feng Le, Zhen Lu, Maggie Mao, Abigail Aiken, Robert C. Bast
Journal: Cancer Research (2010)

Abstract In order to improve the efficacy of paclitaxel in treatment of ovarian cancer, we have performed a kinome siRNA library screen to identify kinases that regulate paclitaxel sensitivity. CDK5 was one of kinase targets that could modulate paclitaxel sensitivity in SKOv3 cells. Unlike typical cyclin dependent kinases, CDK5 does not have a clearly defined role in the regulation of the cell cycle. CDK5 is required for the regulation of neuronal synaptic vesicular transport in the brain through phosphorylation of Munc 18, a key regulator of vesicular exocytosis. In this report, we aimed to explore the mechanisms by which CDK5 potentiate paclitaxel activity. We found that eighteen ovarian cancer cell lines expressed variable CDK5 levels measured by quantitative real time PCR and Western blotting. Basal levels of CDK5 in ovarian cancer cell lines appeared not to correlate with paclitaxel sensitivity. We used immunoprecipitation of CDK5 and in vitro kinase assays using 32P-ATP and observed that paclitaxel treatment of SKOv3 cells resulted in a profound (&amp;gt;20 fold) increase in CDK5 activity. Selective depletion of CDK5 using 4 individual siRNAs in SKOv3, TOV112 and DOV13 ovarian cancer cells lines resulted in a significant increase in paclitaxel-induced cytotoxicity as measured by cell viability assays. In addition, loss of CDK5 resulted in a significant increase in paclitaxel-mediated induction of caspase 3/7 activation in the ovarian cancer cell lines SKOv3, ES2, OVAR429 and DOV13. Remarkably, the magnitude of sensitization was directly proportional (p&amp;lt;0.001) to the dose of paclitaxel used. Knockdown of CDK5 did not enhance microtubule stabilization or increase paclitaxel-induced mitotic arrest. Instead, CDK5 depletion in SKOv3 cells resulted in a significant (p&amp;lt;0.001) increase in retention of fluorescent-tagged paclitaxel. This effect was similar to but independent from the effect of inhibition of trans-membrane pumps using verapamil, suggesting that the two mechanisms act in parallel. Indeed, knockdown of CDK5 in combination with verapamil resulted in greater intracellular retention of paclitaxel in SKOv3 cells. Consequently, we conclude that depletion of CDK5 results in decreased paclitaxel exocytosis leading to increased cytotoxicity to ovarian cancer cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1585.
Histopathological analysis and clinical correlation of drug reaction with eosinophilia and systemic symptoms (DRESS)
Authors: M.-H. Chi, R.C.-Y. Hui, C.-H. Yang, J.-Y. Lin, Y.-T. Lin, H.-C. Ho, W.-H. Chung, T.-T. Kuo
Journal: British Journal of Dermatology (2013)

Background Drug reaction with eosinophilia and systemic symptoms (DRESS) is a severe cutaneous adverse drug reaction. However, its histopathological features have not been well defined. Objectives To identify the clinicohistopathological findings of DRESS, and analyse the cutaneous histopathological changes observed in DRESS compared with those observed in maculopapular exanthema (MPE). Methods In a retrospective study, conducted at Chang Gung Memorial Hospital (Taiwan) between 2001 and 2011, we compared the clinicohistopathological features of 32 patients with probable/definite DRESS (defined by the RegiSCAR scoring system) with those of 17 patients with MPE. Results The major pathological changes observed in patients with DRESS included dyskeratosis (97%), epidermal spongiosis (78%), interface vacuolization (91%), perivascular lymphocytic infiltration (97%) and eosinophilic infiltration (72%). Many pathological features were common to both MPE and DRESS. However, severe dyskeratosis, epidermal spongiosis and severe interface vacuolization were significantly more prominent in cases of DRESS (P < 0·05). The presence of severe dyskeratosis was significantly associated with the clinical severity of renal impairment (P = 0·01). Conclusions The severe dyskeratosis detected in patients with DRESS may correlate with a greater extent of systemic involvement compared with that noted in MPE. However, the histopathological changes associated with DRESS are not entirely specific.
Reduction of myocardial reperfusion injury by intravenous adenosine administered during the early reperfusion period.
Authors: C J Pitarys, R Virmani, H D Vildibill, E K Jackson, M B Forman
Journal: Circulation (1991)

Adenosine influences the function of several cell types thought to be involved in the pathogenesis of myocardial reperfusion injury. We have previously demonstrated that intracoronary administration of adenosine enhances myocardial salvage 24 hours after reperfusion. To determine if these beneficial effects could be obtained during a prolonged period of reperfusion using an intravenous route of administration, 22 closed-chest dogs were subjected to 90 minutes of proximal left anterior descending coronary artery occlusion and 72 hours of reperfusion. Animals randomly received either intravenous adenosine (0.15 mg/kg/min) or an equal volume of Ringer's lactate during the first 150 minutes of reperfusion. The area at risk was defined in vivo with Monastral blue, and infarct size was measured histologically with Mallory's trichrome stain. Serial global and regional ventricular function were determined with contrast ventriculography and analyzed using a computerized radial shortening method. Biopsies were obtained from the central ischemic zone to assess endothelial ultrastructure and capillary obstruction. No significant effects in heart rate or blood pressure were noted during adenosine infusion. Transmural collateral blood flow during ischemia was similar in the groups. Infarct size expressed as a percentage of the anatomical area at risk was significantly less in the adenosine-treated group (35.3 +/- 4.3% in controls versus 17.1 +/- 4.3% in treated animals, p less than 0.01). A progressive decrease in transmural blood flow was noted in control animals during reperfusion, resulting in a significant reduction at 3 hours compared with the preocclusion value (0.69 +/- 0.11 ml/min/g [at baseline versus 0.45 +/- 0.10 ml/min/g at 3 hours, p less than 0.05]). In contrast, flow in adenosine animals at 3 hours was similar to baseline values (0.91 +/- 0.15 ml/min/g at baseline versus 0.98 +/- 0.14 ml/min/g at 3 hours, p = NS) and was significantly higher (p less than 0.05) than the control group. Radial shortening in the ischemic zone was significantly improved at 3 (-2.6 +/- 2.8% in controls versus 11.6 +/- 3.3% in treated animals, p less than 0.01) and 72 hours (5.5 +/- 2.0% in controls versus 17.3 +/- 3.5% in treated animals, p less than 0.01) after reperfusion in treated animals. Electron microscopy showed reduced neutrophil and erythrocyte plugging of capillaries with relative preservation of endothelial cell structure in the adenosine group.(ABSTRACT TRUNCATED AT 400 WORDS)
Return of the postcode lottery
Authors: J. Graham, S. Guglani, S. Elyan, S. Falk, J. Braybrooke, T. Roques
Journal: BMJ (2010)

Many of the issues arising from changes to NHS drug pricing in 2014 already apply to the Interim Cancer Drugs Fund.1 The government’s initial pledge of £50m up to April 2011 has been followed by a proposal for …
MerTK is required for apoptotic cell–induced T cell tolerance
Authors: Mark A. Wallet, Pradip Sen, Rafael R. Flores, Yaming Wang, Zuoan Yi, Yingsu Huang, Clayton E. Mathews, H. Shelton Earp, Glenn Matsushima, Bo Wang, Roland Tisch
Journal: The Journal of Experimental Medicine (2008)

Self-antigens expressed by apoptotic cells (ACs) may become targets for autoimmunity. Tolerance to these antigens is partly established by an ill-defined capacity of ACs to inhibit antigen-presenting cells such as dendritic cells (DCs). We present evidence that the receptor tyrosine kinase Mer (MerTK) has a key role in mediating AC-induced inhibition of DC activation/maturation. Pretreatment of DCs prepared from nonobese diabetic (NOD) mice with AC blocked secretion of proinflammatory cytokines, up-regulation of costimulatory molecule expression, and T cell activation. The effect of ACs on DCs was dependent on Gas6, which is a MerTK ligand. NOD DCs lacking MerTK expression (NOD.MerTKKD/KD) were resistant to AC-induced inhibition. Notably, autoimmune diabetes was exacerbated in NOD.MerTKKD/KD versus NOD mice expressing the transgenic BDC T cell receptor. In addition, β cell–specific CD4+ T cells adoptively transferred into NOD.MerTKKD/KD mice in which β cell apoptosis was induced with streptozotocin exhibited increased expansion and differentiation into type 1 T cell effectors. In both models, the lack of MerTK expression was associated with an increased frequency of activated pancreatic CD11c+CD8α+ DCs, which exhibited an enhanced T cell stimulatory capacity. These findings demonstrate that MerTK plays a critical role in regulating self-tolerance mediated between ACs, DCs, and T cells.
Functional heterogeneity in allospecific cytotoxic T lymphocyte clones. I. CTL clones express strong anti-self suppressive activity.
Authors: M H Claësson, R G Miller
Journal: The Journal of Experimental Medicine (1984)

Five out of five allo-specific cytotoxic T lymphocyte (CTL) clones tested strongly suppressed the development of CTLs directed against the H-2 haplotype of the CTL clone and independent of the H-2 specificity recognized by the CTL clone. This was shown by including 100-1,000 cells from the five clones in one way mixed lymphocyte reaction (MLR) cultures in which the stimulator cells were of the same H-2 type as the CTL cells. When these cultures were assayed for cytotoxicity against the stimulator cell haplotype, the cytotoxic activity was decreased in a CTL cell dose-dependent manner by 50 to more than 90%. Suppression was usually not observed in MLR cultures where the CTL-H-2 type was identical with the responder cells or was different from both the responder or stimulator cells. Suppression was demonstrated not to be due to "cold" target inhibition at the time of cytotoxicity assay. Even if the added CTL were completely removed after 48-72 h of culture, significant suppression was obtained. Suppressive ability did not appear to be correlated with the level of allo-specific cytotoxic activity present in the CTL clones, but might involve direct killing of MLR precursor cells by cells in the added CTL clones. The suppression observed here, which is anti-self from the point of view of the added CTL clone, appears to be triggered by precursor cells in the MLR responder population recognizing MHC determinants on cells from the added CTL clone. This peculiar type of suppression, in which the regulator regulates on being recognized, has been christened the veto phenomenon and may play a role in maintenance of self tolerance.
Depression in cancer patients. An approach to differential diagnosis and treatment
Authors: J. R. Peteet
Journal: JAMA (1979)

Despite recent attention to death and dying, many questions remain about the diagnosis and treatment of depression in cancer patients. To provide a framework for effective treatment, this article distinguishes the following types of depression: (1) transient stress reactions, (2) major psychiatric disturbances requiring prompt attention, and (3) other depressive reactions. Depressions in the third general category, comprising the majority, are often mismanaged because of characterological, interpersonal, and organic factors receive insufficient attention. Understanding of such factors provides a basis for rational intervention with both patients and their families. (<i>JAMA</i>241:1487-1489, 1979)
Identifying Livestock-Associated Methicillin-Resistant<i>Staphylococcus aureus</i>in the United States
Authors: Eli N. Perencevich, Robert Skov, Jan Kluytmans
Journal: JAMA Internal Medicine (2014)

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Letter by Dai et al Regarding Article, “Cardiac Resynchronization Therapy in Patients With Heart Failure and a QRS Complex &lt;120 Milliseconds: The Evaluation of Resynchronization Therapy for Heart Failure (LESSER-EARTH) Trial”
Authors: Hailong Dai, Xuefeng Guang, Zhicheng Xiao
Journal: Circulation (2013)

We read with interest the article by Thibault et al. 1 Their study was interrupted prematurely by the Data Safety and Monitoring Board because of futility and safety concerns.In our opinion, according to their experimental design, the results of the study are inevitable for several reasons.First, this study did not include mechanical dyssynchrony in eligibility criteria.Several reports suggest that QRS duration is not correlated with mechanical dyssynchrony, that the main predictor of responsiveness to CRT is mechanical dyssynchrony, and that CRT may be helpful in patients with echocardiographic evidence of mechanical dyssynchrony and narrow QRS. 2 However, if mechanical dyssynchrony is not used in patients with narrow QRS, CRT may worsen or provoke dyssynchrony in patients with little or no dyssynchrony to begin with.Second, left ventricular (LV) lead position was not optimized.The LV stimulation site appears to be a crucial factor for successful CRT.Optimal LV lead position may theoretically be defined by the positioning of the LV pacing lead coincident with the latest activated areas of the LV.A match between LV lead position and the site of the latest mechanical activation resulted in a better echocardiographic response after CRT. 3 Third, atrioventricular and interventricular optimization was not done after CRT.The response in patients who receive CRT can be influenced by the programmed atrioventricular and interventricular delay because appropriate atrioventricular interval timing may convert an underresponder to improved status and because appropriate interventricular interval is thought to improve CRT performance by altering the activation front and possibly compensating for suboptimal lead position.How to improve CRT responder rate in heart failure patients with narrow QRS (combining different and complementary parameters of dyssynchrony, optimizing LV lead position, atrioventricular and interventricular, etc) will be our research direction in the future.
Diastolic Murmur Caused by Coronary Artery Stenosis
Authors: TSUNG O. CHENG
Journal: Annals of Internal Medicine (1970)

Two patients had diastolic murmur caused by coronary artery stenosis. In both the diastolic murmur was associated with a severe, localized narrowing of the proximal left anterior descending artery demonstrated by selective coronary cinearteriography. The murmur disappeared after acute myocardial infarction involving the area of distribution by the stenosed coronary artery. Although mid-diastolic timing of the murmur combined with an accentuated first sound may lead to an erroneous diagnosis of mitral stenosis, several distinguishing features, including its response to amyl nitrite inhalation, help to differentiate. A stenosed coronary artery is a cause of diastolic murmur.
Video surveillance uncovers parental child abuse
Authors: J. Wise
Journal: BMJ (1997)

Evidence of child abuse carried out by parents has been uncovered by secret video cameras hidden in two hospitals, according to a report by Professor David Southall in which he calls for sweeping changes in Britain's approach to child protection.

The report, which is to be published in Pediatrics on 3 November, is based on covert video surveillance of 39 children admitted to hospital after recurrent episodes of losing consciousness, going blue, or stopping breathing. There was strong suspicion that the children were in serious danger of life threatening abuse by a parent …
Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase
Authors: Elmar Jaeckel, Ludger Klein, Natalia Martin-Orozco, Harald von Boehmer
Journal: The Journal of Experimental Medicine (2003)

Experiments in nonobese diabetic (NOD) mice that lacked expression of glutamic acid decarboxylase (GAD) in β cells have suggested that GAD represents an autoantigen essential for initiating and maintaining the diabetogenic immune response. Several attempts of inducing GAD-specific recessive tolerance to support this hypothesis have failed. Here we report on successful tolerance induction by expressing a modified form of GAD under control of the invariant chain promoter resulting in efficient epitope display. In spite of specific tolerance insulitis and diabetes occurred with normal kinetics indicating that GAD is not an essential autoantigen in the pathogenesis of diabetes.
Validation of a Pseudomonas aeruginosa porcine model of septic shock
Authors: Thomas Rimmelé, Abdulnasser Assadi, Farida Benatir, Emmanuel Boselli, Catherine Kaminski, Florence Arnal, Corinne Lambert, Joëlle Goudable, Dominique Chassard, Bernard Allaouchiche
Journal: Journal of Infection (2005)
Nonvisualization of the Left Lobe of the Liver Due to Atrophy or Aplasia
Authors: P TODD MAKLER, ERROL LEWIS, ROBERT CANTOR, N DAVID CHARKES, LEON S. MALMUD
Journal: Clinical Nuclear Medicine (1980)

Aplasia or atrophy of the left lobe of the liver may result in a liver scan appearance easily misinterpreted as showing evidence of tumor involvement. Three illustrative cases of the phenomenon are presented.
Hyperfibrinolysis increases the risk of gastrointestinal hemorrhage in patients with advanced cirrhosis
Authors: Francesco Violi, Domenico Ferro, Stefania Basili, Claudio Quintarelli, Mirella Saliola, Cesare Alessandri, Corrado Cordova, Francesco Balsano
Journal: Hepatology (1992)

Sixty-one patients with different degrees of liver failure, 23 with Child-Pugh class B and 38 with Child-Pugh class C, were studied and observed for 3 yr. Coagulation index analysis showed significantly lower values of prothrombin activity, more prolonged activated partial thromboplastin time, higher bilirubin and fibrinogen degradation products values in class C patients. Among all patients, 28 had fibrinogen degradation products values greater than 10 μg/ml, and in these patients a hyperfibrinolytic state was confirmed by higher values of circulating plasminogen activator antigen (17.3 ± 8.7 ng/ml vs. 5.41 ± 1.9 ng/ml; p < 0.0001) and activity (6.6 ± 2.1 IU/ml vs. 1.92 ± 1.12 IU/mi; p < 0.0001) and significantly lower plasminogen activator inhibitor antigen (6.4 ± 3.5 ng/ml vs. 15.8 ± 5.6 ng/ml; p < 0.0001) and activity (3.6 ± 2.2 IU/ml vs. 8.5 ± 3.9 IU/ml; p < 0.0001). Patients with positive fibrinogen degradation products had higher serum bilirubin (6 ± 4 mg/dl vs. 2 ± 2 mg/dl; p < 0.0001) and lower fibrinogen (156 ± 52 mg/dl vs. 194 ± 62 mg/dl; p < 0.02) than patients without hyperfibrinolysis. During the follow-up period, 41 patients died, 22 from fatal gastrointestinal hemorrhage and 19 from liver failure. Thirty patients experienced fatal (22 patients) and nonfatal (8 patients) gastrointestinal hemorrhage. Patients with positive fibrinogen degradation products or class C had a higher risk of gastrointestinal bleeding than patients with negative fibrinogen degradation products (odds ratio = 8) or class B (odds ratio = 3.5), respectively. Cox's multiple regression model showed that positive fibrinogen degradation products was the best bleeding predictor (β coefficient = 3.9 ± 0.7 S.E.M., p < 0.001). This study indicates that in cirrhosis the presence of hyperfibrinolysis should be regarded as an important warning sign of gastrointestinal bleeding. (Hepatology 1992;15:672–676).