tbuckley/cabot-search huggingface dataset:
Impaired Physicians, Professional Psychotherapy, and Alcoholics Anonymous
Authors: David —
Journal: JAMA (1982)

<h3>To the Editor.—</h3> The description by Herrington et al (1982;247:2253) of their program for physicians with substance abuse was encouraging but disappointing. Despite their apparent success, they perpetuated two ideas that I believe are dangerous for physicians with this problem. These people are not helped by believing either that they are elite or that intellectual insight will set them free of their addiction. To excuse them from regular Alcoholics Anonymous (AA) meetings to attend a weekly "doctors' AA" group and to put them immediately into psychotherapy as they are just getting sober is to do them a disservice. I know. I am an alcoholic physician, sober through daily help from AA, happy and fully functional professionally. I went the same routes they describe—of special doctors' groups and psychiatry—and found these to reinforce my feelings of being different from the rest of the human race and therefore unable to follow their
Hemorrhagic pseudoaneurysm in a pancreatic pseudocyst after extracorporeal shock wave lithotripsy for pancreatolithiasis
Authors: Y. Nakagawa, T. Abe, M. Uchida, K. Inoue, R. Ogawa, K. Mizukami, T. Okimoto, M. Kodama, K. Murakami, T. Fujioka
Journal: Endoscopy (2011)

A 49-year-old man with a history of alcohol abuse and chronic pancreatitis was referred to our hospital for extracorporeal shock wave lithotripsy (ESWL) for pancreatolithiasis. Computed tomography (CT) revealed chronic pancreatitis with a pseudocyst (diameter, 30 mm) in the pancreatic tail and multiple pancreatic calculi ([Fig. 1 a, b]).
Author's views
Authors: S Finfer
Journal: BMJ (1994)

Patients with life threatening haemorrhage rarely refuse blood transfusions, but when they do staff face unfamiliar legal, medical, and ethical problems. At first the legal issues seem the easiest to resolve. Those on duty are obliged to provide treatment and to withhold transfusion.

We were fortunate that our patients were conscious and clearly understood that without blood they were likely to die. Had they arrived unconscious, as many trauma patients do, we would have had to determine their wishes. Patients may carry written instructions that they are …
Ending Extra Payment for “Never Events” — Stronger Incentives for Patients' Safety
Authors: Arnold Milstein
Journal: New England Journal of Medicine (2009)

On September 1, 2008, Medicare eliminated a long-standing presumption in its payment rules that, since hospitals were doing everything possible to prevent complications of treatment, taxpayers and patients should primarily bear the average cost consequences when complications occurred. A 2006 law, meant to motivate hospitals to accelerate improvement of patients' safety, constrains hospitals' ability to bill Medicare for a higher-paid diagnosis-related group when complications occur.1 The constraint applies only to hospital-acquired conditions deemed "reasonably preventable" through the use of evidence-based guidelines. These initially included eight complication categories: foreign objects left in the body after surgery, air emboli, infusion of incompatible . . .
358 COMPARING THE LONG-TERM OUTCOME OF HEPATITIS DELTA AND HBV MONOINFECTION: IS HDV-INFECTION REALLY WORSE?
Authors: B. Calle Serrano, A. Grosshennig, B. Heidrich, J. Jaroszewicz, J. Kirschner, B. Bremer, M. Cornberg, M.P. Manns, H. Wedemeyer
Journal: Journal of Hepatology (2011)
Validation of three-dimensional echocardiography for quantifying the extent of dyssynergy in canine acute myocardial infarction: Comparison with two-dimensional echocardiography
Authors: Peter M. Sapin, Gregory B. Clarke, Aasha S. Gopal, Mikel D. Smith, Donald L. King
Journal: Journal of the American College of Cardiology (1996)

Objectives. This study was designed to compare the accuracy of three- and two-dimensional echocardiography for quantifying the extent of abnormal wall motion in experimental acute myocardial infarction, as correlated with the pathologic determination of infarct size. Background. Two-dimensional echocardiographic estimations of the fraction of myocardium showing abnormal wall motion are often used as an index of infarct size even though they rely on image plane positioning and geometric assumptions that may not be valid. Three-dimensional echocardiographic reconstruction of the endocardial surface eliminates the need for these assumptions and may improve echocardiographic estimates of infarct size. Methods. Coronary ligation was performed in 14 open chest dogs, and echocardiographic imaging of the ventricle was performed 6 h later. Three-dimensional echocardiography used seven or eight spatially registered short-axis images to measure percent of endocardial surface and mass showing abnormal wall motion. Three two-dimensional echocardiographic methods using multiple, nonspatially registered images were evaluated. One method used seven or eight short-axis slices and a summation of discs algorithm for computing surface area. The second method used the same images and a conical model for the left ventricle. The third used basal, middle and apical short-axis plus apical four- and two-chamber views comparing summed endocardial lengths showing abnormal wall motion with the total of the endocardial dimensions, expressed as percent. The percent of left ventricular mass and surface area infarcted was determined by staining with triphenyltetrazolium chloride. Results. Three-dimensional echocardiographic measurements of endocardial surface area correlated more closely with infarct mass (r = 0.94, SEE ±3.6%) than did the two-dimensional method using the summation of discs algorithm (r = 0.85, SEE ±6.6%), the summation of conical sections algorithm (r = 0.82, SEE ±5.4%) or the method using summed endocardial lengths (r = 0.79, SEE ±7.4%). Limits of agreement analysis comparing mass showing abnormal wall motion with anatomic infarct mass and surface area showing abnormal wall motion with anatomic infarct surface area showed the smallest limits for three-dimensional echocardiography. Conclusions. Three-dimensional echocardiography is a more accurate means of noninvasively estimating myocardial infarct size in this canine model than two-dimensional echocardiography.
Conditioned medium from stimulated mononuclear leucocytes potentiates the ability of human neutrophils to damage human articular cartilage.
Authors: E J Bates, I C Kowanko, A Ferrante
Journal: Annals of the Rheumatic Diseases (1988)

Human neutrophils were able to degrade proteoglycan and inhibit its synthesis when incubated with human articular cartilage coated with heat aggregated immunoglobulin G. These effects were potentiated when culture medium conditioned by mononuclear leucocytes stimulated with killed Staphylococcus aureus was also present during the incubations. Neutrophils preincubated with this conditioned medium and washed before incubation with cartilage also showed an increased ability to degrade proteoglycan and inhibit its synthesis. The percentage of neutrophils binding to cartilage was significantly increased in the presence of this conditioned medium.
PATIENT-SPECIFIC SIMULATION OF RIGHT VENTRICLE OUTFLOW TRACT CONDUIT BALLOON ANGIOPLASTY USING CARDIAC MRI-DERIVED 3D VIRTUAL MODELS TO ASSESS THE RISK OF CORONARY ARTERY COMPRESSION DURING TRANSCATHETER PULMONARY VALVE REPLACEMENT
Authors: Puneet Bhatla, Sujata Chakravarti, Achiau Ludomirsky, Michael Argilla, Phillip Berman, Doff McElhinney, Vittoria Flamini
Journal: Journal of the American College of Cardiology (2015)
Abstract 159: Macrophage Migration Inhibitory Factor (MIF) enhances proliferation and expression of tumorigenic cytokines in a bladder cancer cell line
Authors: Shilpa Choudhary, James R. Pruitt, Thais M. Sielecki, Carol Pilbeam, John Arthur Taylor
Journal: Cancer Research (2012)

Abstract Background: MIF is a proinflammatory cytokine with regulatory properties over tumor suppressor proteins involved in bladder cancer. We have previously reported that the absence of MIF in transgenic mice or the use of a small molecule oral inhibitor of MIF (CPSI-1306, Cytokine PharmaSciences, Inc, King of Prussia, PA) leads to decreased angiogenesis and invasive potential in the BBN mouse model of bladder cancer. The objective of this study was to evaluate potential pathways of MIF activity in a cell culture model. Methods: High grade, metastatic HTB-5 bladder cancer cells were treated with rhMIF 1-100 ng/ml (CPSI). Measurements included cell counts, proliferation by 3H-thymidine incorporation (TdR), phosphorylated and total ERK by Western analysis and mRNA expression of TNF-α, IL-6, VEGF and CD74 (putative receptor for MIF) by real time PCR. CPSI-1306 (0.5-500 nM) was tested for its ability to decrease ERK phosphorylation. Results: MIF 100 ng/ml increased cell counts 2-fold (p&amp;lt;0.01) on culture days 2-4. MIF increased TdR, normalized to cell numbers, 30% (p&amp;lt;0.01). MIF (1-100 ng/ml) stimulated ERK phosphorylation in a dose dependent manner, which was abrogated by the addition of CPSI-1306 at doses above 5 nM. A specific inhibitor of ERK (PD98059, 50 μm) blocked the MIF stimulated increase in cell number. MIF treatment for 24 hrs increased mRNA expression of the agiogenic factor VEGF and the cytokine TNF-α 2-fold (p&amp;lt;0.01). IL-6 mRNA was unchanged. mRNA levels for the putative MIF receptor, CD74, increased 1.3 fold with treatment (p=0.01). Conclusion: MIF increased ERK phosphorylation, which was blocked by CPSI-1306, a small molecule inhibitor of MIF. MIF also increased cell proliferation via an ERK pathway. These data, along with the increased cytokine expression, provide a potential explanation for the decreased angiogenesis and invasion seen in our in vivo murine models using global knockout of MIF or CPSI-1306. This study is the first to begin to elucidate mechanistic pathways involved in MIFs role in bladder cancer and possible pathways involved in CPSI-1306 inhibition. Funding Source: ACS MRSG-08-270-01-CCE, NIH RO1DK48361 Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 159. doi:1538-7445.AM2012-159
Development of brucine-loaded microsphere/thermally responsive hydrogel combination system for intra-articular administration
Authors: Zhi-peng Chen, Wen Liu, Dan Liu, Yan-yu Xiao, Hong-xuan Chen, Jun Chen, Weidong Li, Hao Cai, Wei Li, Bao-chang Cai, Jinhuo Pan
Journal: Journal of Controlled Release (2012)
T-cadherin attenuates insulin-dependent signalling, eNOS activation, and angiogenesis in vascular endothelial cells
Authors: Maria Philippova, Manjunath B. Joshi, Dennis Pfaff, Emmanouil Kyriakakis, Kseniya Maslova, Paul Erne, Thérèse J. Resink
Journal: Cardiovascular Research (2012)

T-cadherin (T-cad) is a glycosylphosphatidylinositol-anchored cadherin family member. Experimental, clinical, and genomic studies suggest a role for T-cad in vascular disorders such as atherosclerosis and hypertension, which are associated with endothelial dysfunction and insulin resistance (InsRes). In endothelial cells (EC), T-cad and insulin activate similar signalling pathways [e.g. PI3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR)] and processes (e.g. angiogenesis). We hypothesize that T-cad is a regulatory component of insulin signalling in EC and therefore a determinant of the development of endothelial InsRes. We investigated T-cad-dependent effects on insulin sensitivity using human EC stably transduced with respect to T-cad overexpression or T-cad silencing. Responsiveness to insulin was examined at the level of effectors of the insulin signalling cascade, EC nitric oxide synthase (eNOS) activation, and angiogenic behaviour. Overexpression and ligation of T-cad on EC attenuates insulin-dependent activation of the PI3K/Akt/mTOR signalling axis, eNOS, EC migration, and angiogenesis. Conversely, T-cad silencing enhances these actions of insulin. Attenuation of EC responsiveness to insulin results from T-cad-mediated chronic activation of the Akt/mTOR-dependent negative feedback loop of the insulin cascade and enhanced degradation of the insulin receptor (IR) substrate. Co-immunoprecipitation experiments revealed an association between T-cad and IR. Filipin abrogated inhibitory effects of T-cad on insulin signalling, demonstrating localization of T-cad-insulin cross-talk to lipid raft plasma membrane domains. Hyperinsulinaemia up-regulates T-cad mRNA and protein levels in EC. T-cad expression modulates signalling and functional responses of EC to insulin. We have identified a novel signalling mechanism regulating insulin function in the endothelium and attribute a role for T-cad up-regulation in the pathogenesis of endothelial InsRes.
Candida and candidiasis
Authors: P. J. Kozinn
Journal: JAMA (1971)

To the Editor.—  The EDITORIAL Candidiasis: Colonization vs Infection ( 215 :285-286, 1971) presented the clinician's dilemma but few clues to its resolution. It quoted Ellis and Spivack's 12 cases of repeated candidemia and noted that six cases came to autopsy. Two cases were considered to be preterminal candidemia, in which no lesions were found at autopsy. Four cases showed widespread major organ candidiasis. Six patients got well, two with the aid of antifungal therapy. The absence of a fatality in these six cases does not disprove the presence of candidal infection. Major organ disease in four out of 12 cases with persistent candidemia should give serious pause to any clinician.  The review of Toala et al ( Arch Intern Med  126 :983, 1970) on the lack of significance of 371 Candida isolates from specimens submitted for bacteriological examination leads only to more befuddlement. Although Candida from any specimen should not be
Surgical Revascularization Is Associated With Maximal Survival in Patients With Ischemic Mitral Regurgitation
Authors: Anthony W. Castleberry, Judson B. Williams, Mani A. Daneshmand, Emily Honeycutt, Linda K. Shaw, Zainab Samad, Renato D. Lopes, John H. Alexander, Joseph P. Mathew, Eric J. Velazquez, Carmelo A. Milano, Peter K. Smith
Journal: Circulation (2014)

Background— The optimal treatment for ischemic mitral regurgitation remains actively debated. Our objective was to evaluate the relationship between ischemic mitral regurgitation treatment strategy and survival. Methods and Results— We retrospectively reviewed patients at our institution diagnosed with significant coronary artery disease and moderate or severe ischemic mitral regurgitation from 1990 to 2009, categorized by medical treatment alone, percutaneous coronary intervention, coronary artery bypass grafting (CABG), or CABG plus mitral valve repair or replacement. Kaplan-Meier methods and multivariable Cox proportional hazards analyses were performed to assess the relationship between treatment strategy and survival, with the use of propensity scores to account for nonrandom treatment assignment. A total of 4989 patients were included: medical treatment alone=36%, percutaneous coronary intervention=26%, CABG=33%, and CABG plus mitral valve repair or replacement=5%. Median follow-up was 5.37 years. Compared with medical treatment alone, significantly lower mortality was observed in patients treated with percutaneous coronary intervention (adjusted hazard ratio, 0.83; 95% confidence interval, 0.76–0.92; P =0.0002), CABG (adjusted hazard ratio, 0.56; 95% confidence interval, 0.51–0.62; P &lt;0.0001), and CABG plus mitral valve repair or replacement (adjusted hazard ratio, 0.69; 95% confidence interval, 0.57–0.82; P &lt;0.0001). There was no significant difference in these results based on mitral regurgitation severity. Conclusions— Patients with significant coronary artery disease and moderate or severe ischemic mitral regurgitation undergoing CABG alone demonstrated the lowest risk of death. CABG with or without mitral valve surgery was associated with lower mortality than either percutaneous coronary intervention or medical treatment alone.
Patient Survival and Instrument Performance With Permanent Cardiac Pacing
Authors: Lockhart B. McGuire
Journal: JAMA (1977)

Among 313 patients who received cardiac pacemakers between 1961 and 1973, there was a 65% survival rate after five years, a progressive decrease in premature pulse generator failures, and a low, stable incidence of electrode malfunction. Decreased survival among more recently paced patients was attributed to an evolution of the selection for pacing that favored older patients with associated diseases. Death due to unexpected pacing failure was extremely rare. Premature pulse generator failures decreased from 0.8 per 100 pacing months among early units to 0.06 per 100 months among units implanted during 1971 to 1973, when a prophylactic replacement policy was in effect. Electrode revisions were required at a frequency of 0.5 to 0.8 per 100 months in both epicardial and endocardial systems. Electrode failures may limit the predictive value of surveillance systems, since these rely on a change of pacing frequency or pulse width to indicate battery depletion. (<i>JAMA</i>237:558-561, 1977)
Whole-genome sequencing and comprehensive molecular profiling identify new driver mutations in gastric cancer
Authors: Kai Wang, Siu Tsan Yuen, Jiangchun Xu, Siu Po Lee, Helen H N Yan, Stephanie T Shi, Hoi Cheong Siu, Shibing Deng, Kent Man Chu, Simon Law, Kok Hoe Chan, Annie S Y Chan, Wai Yin Tsui, Siu Lun Ho, Anthony K W Chan, Jonathan L K Man, Valentina Foglizzo, Man Kin Ng, April S Chan, Yick Pang Ching, Grace H W Cheng, Tao Xie, Julio Fernandez, Vivian S W Li, Hans Clevers, Paul A Rejto, Mao Mao, Suet Yi Leung
Journal: Nature Genetics (2014)
Genes contributing to minimal residual disease in childhood acute lymphoblastic leukemia: prognostic significance of CASP8AP2
Authors: Christian Flotho, Elaine Coustan-Smith, Deqing Pei, Shotaro Iwamoto, Guangchun Song, Cheng Cheng, Ching-Hon Pui, James R. Downing, Dario Campana
Journal: Blood (2006)
Neurology and Trauma
Authors: Panayiotis Varelas
Journal: JAMA (2007)

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Specific binding of K- and I-region products of the H-2 complex to activated thymus-derived (T) cells belonging to different Ly subclasses.
Authors: Z Nagy, B E Elliott, M Nabholz
Journal: The Journal of Experimental Medicine (1976)

Responder cells [C57BL/6J X A.TL)F1 lymph node cells depleted of bursa equivalent-derived (B) cells by filtration through nylon wool columns] were activated against incompatible K-region and I-region products together under conditions where these antigens are presented on separate stimulator cells. The resulting T blasts were stained with different concentrations of antisera directed against incompatible stimulator K-region or I-region products, or both. We obtained results that strongly suggest that in these cultures each activated responder blast stains with antiserum directed against either K-region or I-region products, but not both. Responder blasts from the same cultures were treated with antiserum and complement (C) directed against either Ly-1.2 or Ly-2.2 T-cell-specific surface antigens. Anti-Ly-1.2 serum and C specifically eliminates virtually all responder blasts staining with antiserum directed against stimulator I-region products; whereas anti-Ly-2.2 serum reduces to background levels the proportion of cells staining with antiserum against stimulator K-region products. The results obtained suggest that T cells binding stimulator K-region and I-region products, respectively, belong to two different subclasses distinguishable by their Ly phenotypes. Possible explanations for this association of T- cell subclass and specificity are discussed.
T lymphocytes infiltrating the liver during chronic hepatitis C infection express a broad range of T-cell receptor beta chain diversity
Authors: Ines Vigan, Evelyne Jouvin-Marche, Vincent Leroy, Martine Pernollet, Stefania Tongiani-Dashan, Eve Borel, Elisabeth Delachanal, Maurice Colomb, Jean-Pierre Zarski, Patrice N. Marche
Journal: Journal of Hepatology (2003)
A Histone Deacetylase Inhibitor Enhances Recombinant Adeno-associated Virus-Mediated Gene Expression in Tumor Cells
Authors: Takashi Okada, Ryosuke Uchibori, Mayumi Iwata-Okada, Masafumi Takahashi, Tatsuya Nomoto, Mutsuko Nonaka-Sarukawa, Takayuki Ito, Yuhe Liu, Hiroaki Mizukami, Akihiro Kume, Eiji Kobayashi, Keiya Ozawa
Journal: Molecular Therapy (2006)

The transduction of cancer cells using recombinant adeno-associated virus (rAAV) occurs with low efficiency, which limits its utility in cancer gene therapy. We have previously sought to enhance rAAV-mediated transduction of cancer cells by applying DNA-damaging stresses. In this study, we examined the effects of the histone deacetylase inhibitor FR901228 on tumor transduction mediated by rAAV types 2 and 5. FR901228 treatment significantly improved the expression of the transgene in four cancer cell lines. The cell surface levels of alpha v integrin, FGF-R1, and PDGF-R were modestly enhanced by the presence of FR901228. These results suggest that the superior transduction induced by the HDAC inhibitor was due to an enhancement of transgene expression rather than increased viral entry. Furthermore, we characterized the association of the acetylated histone H3 in the episomal AAV vector genome by using the chromatin immunoprecipitation assay. The results suggest that the superior transduction may be related to the proposed histone-associated chromatin form of the rAAV concatemer in transduced cells. In the analysis with subcutaneous tumor models, strong enhancement of the transgene expression as well as therapeutic effect was confirmed in vivo. The use of this HDAC inhibitor may enhance the utility of rAAV-mediated transduction strategies for cancer gene therapy.