tbuckley/cabot-search huggingface dataset:
Abstract 18756: Association of Morphologic Variability with 6-Month Mortality in a General Cohort of Intensive Care Unit Patients: Results from the MIMICII Database
Authors: Chih-Chun Chia, Mohammed Saeed, Collin Stultz, John Guttag, Zeeshan Syed
Journal: Circulation (2012)

Background: Morphologic variability (MV) has been previously shown to identify patients at increased risk of mortality following acute coronary syndrome in retrospective analyses of randomized controlled clinical trial data. We assessed the relationship of MV and mortality in a general cohort of intensive care unit (ICU) patients. Methods: MV was calculated for ICU patients within the MIMICII database. Data from all ICU admissions with at least 10 hours of continuous ECG sampled at 9-bit quantization or greater during the first 24 hours were used (n=359). Patients were dichotomized into risk groups at the highest quartile. The primary endpoint was in-hospital or 6-month post-discharge mortality previously determined in MIMICII from the Social Security Death Index (n=83). Results: MV was associated with mortality on univariate analysis and in multivariate models adjusted for the Simplified Acute Physiology Score (SAPS) and the Sequential Organ Failure Assessment (SOFA) Score (Table). These results were consistent when the multivariate models were further adjusted for the Elixhauser comorbidity scores of cardiac arrhythmia and congestive heart failure (adjusted hazard ratio 2.46; 95% CI 1.30 - 4.66; p=0.005). The model constructed for the overall cohort using SAPS and SOFA showed improved discrimination and reclassification when MV was added (IDI 0.022, p=0.027; NRI 0.349, p=0.008). Conclusions: MV has value in risk stratification of the general cohort of ICU patients and provides complementary information to existing ICU scoring systems.
Low glucose metabolism during brain stimulation in older Down's syndrome subjects at risk for Alzheimer's disease prior to dementia
Authors: P Pietrini, A Dani, M L Furey, G E Alexander, U Freo, C L Grady, M J Mentis, D Mangot, E W Simon, B Horwitz, J V Haxby, M B Schapiro
Journal: American Journal of Psychiatry (1997)

Down's syndrome is characterized by the genetically programmed accumulation of substantial Alzheimer's disease neuropathology after age 40 and the development of early dementia years later, providing a unique human model to investigate the preclinical phases of Alzheimer's disease. Older nondemented adults with Down's syndrome show normal rates of regional cerebral glucose metabolism at rest before the onset of dementia, indicating that their neurons maintain function at rest. The authors hypothesized that an audiovisual stimulation paradigm, acting as a stress test, would reveal abnormalities in cerebral glucose metabolism before dementia in the neocortical parietal and temporal areas most vulnerable to Alzheimer's disease.Regional cerebral glucose metabolism was assessed by means of positron emission tomography (PET) with [18F]fluorodeoxyglucose in eight younger (mean age = 35 years, SD = 2) and eight older (mean age = 50, SD = 7) healthy, nondemented adults with trisomy 21 Down's syndrome. PET scans were performed at rest and during audiovisual stimulation in the same scanning session. Levels of general intellectual functioning and compliance were similar in the two groups.At rest the two groups showed no difference in glucose metabolism in any cerebral region. In contrast, during audiovisual stimulation the older subjects with Down's syndrome had significantly lower glucose metabolic rates in the parietal and temporal cortical areas.Abnormalities in cerebral metabolism during stimulation appeared in the first cortical regions typically affected in Alzheimer's disease. These results indicate that a stress test paradigm can detect metabolic abnormalities in the preclinical stages of Alzheimer's disease despite normal cerebral metabolism at rest.
Abstract 14692: Loss of Myeloid Related Protein (MRP)-8/14 Augments B7 molecule Expression and Exacerbates Cardiac Allograft Rejection
Authors: Koichi Shimizu, Viviane Z Rocha, Eduardo J Folco, Richard N Mitchell, Peter Libby, Daniel I Simon, Kevin J Croce
Journal: Circulation (2010)

MRP-8/14 complexes regulate myeloid cell function and inflammatory responses, and serve as serum markers for allograft rejection. Despite functioning as putative pro-inflammatory mediator, the path...
Abstract 3787: Three-Dimensional Electrical Mapping During Endocardial and Epicardial Cardiac Resynchronization Therapy
Authors: Marc Strik, Arne van Hunnik, Marion Kuiper, Anniek Lampert, Caroline J van Deursen, Leonard M Rademakers, Angelo Auricchio, Frits W Prinzen
Journal: Circulation (2009)

Introduction: We previously demonstrated that endocardial (ENDO) left ventricular (LV) pacing for cardiac resynchronization therapy improves LV pump function compared to conventional epicardial (EP...
Understanding Ventricular Remodeling after Correction of Mitral Regurgitation: Thinking Volumetrically
Authors: Hartzell V. Schaff
Journal: Circulation (2011)

Early after correction of mitral valve (MV) regurgitation, systolic function of the left ventricle (LV) declines, but the underlying mechanisms of this phenomenon are unknown. Most studies in this area have analyzed LV function at one week postoperatively or later. In a retrospective study from our Clinic, Enriquez-Sarano et al. reported a decline in LV ejection fraction (EF) from 62% to 52% ( P &lt;0.001) in 217 patients with organic mitral regurgitation who were studied within the first year after MV replacement or repair. This decline was due to decreased left ventricular end-diastolic dimension (LVEDD) and minimal change in left ventricular end-systolic dimension (LVESD). Surgical investigators have compared the outcomes for different techniques of MV replacement and studies indicate that decline in EF may be mitigated by chordal preservation. It has been suggested that early postoperative measurements of cardiac geometry and function are confounded by the effects of global ischemia, reperfusion, and myocardial protection. Indeed, some clinicians have suggested that reduced EF early after MV repair results from myocardial dysfunction that, in turn, is related to poor myocardial protection. In addition, cardiac loading conditions change dramatically early after operation. We speculated that a postoperative decline in LV systolic indexes (eg, EF, FAC, and FS) may be interpreted as a volumetric adjustment of the heart to the correction of mitral regurgitation rather than as postoperative LV dysfunction due to impaired myocardial contractility, and clinical studies support this hypothesis. Soon after MV repair, the LV remodels gradually. Very early after correction of mitral regurgitation, the LVESD increases, preventing an acute increase in forward stroke volume. Within the next few postoperative days, the LVEDD begins to decrease and the LVESD changes accordingly to maintain a normal forward stroke volume; the remodeling occurs when neurohumoral mechanisms of the body adapt to the new hemodynamic milieu. This progression of remodeling may explain why some investigators have observed unchanged LV systolic and decreased diastolic size on the first postoperative echocardiogram about a week after MV repair.
Toric phakic intraocular lens
Authors: H.Burkhard Dick, Jorge Alió, Marco Bianchetti, Camille Budo, Bern Jurriën Christiaans, M.Alaa El-Danasoury, José L Güell, Jörg Krumeich, Monika Landesz, Fransico Loureiro, Gregorius P.M Luyten, Antonio Marinho, Mohamed Saleh Rahhal, Oliver Schwenn, Raimund Spirig, Urs Thomann, Jan Venter
Journal: Ophthalmology (2002)
Childhood-onset psychosis: evolution and comorbidity [clinical conference]
Authors: J Gartner, S Weintraub, G A Carlson
Journal: American Journal of Psychiatry (1997)

E dward was a 12-year-old child with a lifelong history of serious problems in behavior, mood, and reality testing. Elucidating his psychotic disorder was especially difficult because his attention deficits and disruptive behavior were more prominent to his caretakers than his psychotic symptoms, which were initially tenuous and intermittent. Disentangling symptoms required obtaining records from many sources as well as careful and systematic questioning of Edward and his parents. Edward’s case was like the blind men describing the elephant; each of the programs and professionals he encountered had to deal with what was in front of them. In fact, the entire longitudinal perspective was necessary to put the picture together. In addition, the psychotic spectrum symptoms that did occur did not meet the full criteria for a particular psychosis, and even when criteria were met, diagnosis was not entirely satisfactory. Finally, Edward was very sensitive to psychosocial stressors, further complicating our understanding of his psychopathology. In the end, Edward’s case points out that we are confronted with disorders that are probably evolving and that there are limitations to our current nosology. There is as yet no satisfactory resolution of his diagnosis.
Abstract B116: Modeling of early to invasive stages of pancreatic cancer progression with an iPSC-like line from human pancreatic ductal adenocarcinoma
Authors: Jungsun Kim, Kenneth S. Zaret
Journal: Cancer Research (2015)

Abstract Pancreatic ductal adenocarcinoma (PDAC) has one of the worst prognoses of any human malignancy. When human PDAC cells are injected into immunodeficient animals, they create tumors of the late stage from which they were derived. We hypothesized that if human PDAC cells were converted to pluripotency and then allowed to differentiate back into pancreatic tissue, they might undergo early stages of cancer. Although most induced pluripotent stem cell (iPSC) lines that we generated from PDAC were not of the expected cancer genotype, one PDAC iPS-like line, 10–22 cells, conferred the highly disrupted cancer genome of the starting tumor epithelial population. When 10-22 iPS-like cells are injected into immunodeficient mice, they generate pancreatic intraepithelial neoplasia (PanIN) precursors that progress to the invasive stage PDAC. Using this unique system, we established serum-free cultures of human PanIN lesions from immunodeficient mice injected with 10-22 cells and analyzed the proteome of secreted and released proteins. The live human PanIN explants secrete or release proteins from many genes that are known to be expressed in human pancreatic cancer progression and that predicted an HNF4a network achieved in intermediate-stage lesions from new clinical samples. Recent studies show that the PanIN cells progress to metastases at longer time. The 10-22 cell line is being engineered with near-infrared fluorescent protein under the control of the ductal K19 promoter so that populations can be retrieved by FACS for transcriptome analysis as well as tumor progression and regression in response to drugs can be monitored in vivo. We are now assessing the secreted or released proteins from early lesions grown in mice as diagnostic markers for human PDAC prognosis. Thus, rare events allow iPSC technology to provide a live human cell model of early pancreatic cancer and insights into disease progression. Citation Format: Jungsun Kim, Kenneth S. Zaret. Modeling of early to invasive stages of pancreatic cancer progression with an iPSC-like line from human pancreatic ductal adenocarcinoma. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr B116.
Three Patients with Full Facial Transplantation
Authors: Orlando Guntinas-Lichius, Mira Finkensieper
Journal: New England Journal of Medicine (2012)

Sum m a r yUnlike conventional reconstruction, facial transplantation seeks to correct severe deformities in a single operation.We report on three patients who received full-face transplants at our institution in 2011 in operations that aimed for functional restoration by coaptation of all main available motor and sensory nerves.We enumerate the technical challenges and postoperative complications and their management, including single episodes of acute rejection in two patients.At 6 months of followup, all facial allografts were surviving, facial appearance and function were improved, and glucocorticoids were successfully withdrawn in all patients.
Abstract 4364: Gender-Specific Regulation of Ncx in Human Heart Failure
Authors: Constance E Mash, Wendy E Sweet, Christine S Moravec
Journal: Circulation (2008)

We and others have previously reported increased protein levels of the sarcolemmal sodium-calcium exchanger (NCX) in failing (F) vs non-failing (NF) human hearts. In the non-failing cardiomyocyte, NCX transports calcium out of the cell following contraction, in an amount roughly equal to that which enters the cell through L type calcium channels upon depolarization. In the face of decreased sarcoplasmic reticulum calcium ATPase (SERCA) function in the F human heart, up-regulation of NCX is thought to be a compensatory change, helping to prevent calcium overload. It has also been demonstrated that NCX may work in reverse mode in F heart cells, providing for increased calcium influx during the action potential plateau. Recent studies have suggested that over-expression of NCX has different functional consequences in male and female animal hearts during metabolic inhibition as well as ischemia/reperfusion injury, yet studies demonstrating up-regulation of NCX in F human hearts have largely pooled male and female hearts. We have measured NCX and SERCA in a population of male and female F and NF human hearts. Nine patients were studied per group. F hearts were explanted from cardiac transplant recipients with diagnosis of dilated cardiomyopathy and NF hearts from unmatched organ donors. Immunoblotting was used to quantify NCX and SERCA, normalized to actin. NCX was increased in both male and female F hearts as compared to NF hearts, but the increase was proportionately greater in the male population (Normalized values: Male F 3.30 vs NF 1.0; Female F 2.60 vs NF 1.0). Comparison of NF hearts from males and females, however, demonstrated that levels of NCX protein are consistently higher in female than male hearts (Female NF 2.18 vs Male 1.0). SERCA protein was decreased in both male and female F hearts to equal degrees as compared to both groups of NF hearts (Male F 0.65 vs NF 1.0; Female F 0.65 vs NF 1.0), with no difference in NF levels between males and females (female NF 1.1 vs Male 1.0). These data suggest that NCX is regulated differently in male and female F human hearts, which may play a role in the ability of the heart to preserve adequate calcium cycling during cardiac dysfunction.
Long-Term Outcome in Patients Treated With Sirolimus-Eluting Stents in Complex Coronary Artery Lesions
Authors: Henning Kelbæk, Lene Kløvgaard, Steffen Helqvist, Jens F. Lassen, Lars R. Krusell, Thomas Engstrøm, Hans E. Bøtker, Erik Jørgensen, Kari Saunamäki, Samir Aljabbari, Per Thayssen, Anders Galløe, Gunnar V.H. Jensen, Leif Thuesen
Journal: Journal of the American College of Cardiology (2008)
Abstract 8784: Mechanisms of Recurrent Spontaneous Ventricular Fibrillation in a Rabbit Model of Electrical Storm
Authors: Mitsunori Maruyama, Su-Kiat Chua, Tomohiko Ai, Hyung-Wook Park, Young-Soo Lee, Mark J Shen, Po-Cheng Chang, Shien-Fong Lin, Peng-Sheng Chen
Journal: Circulation (2011)

Introduction: Electrical storm (ES) is defined as recurrent spontaneous ventricular fibrillation (SVF) within a short period of time. The mechanism of ES remains unclear. Objective: To develop a model of ES in normal rabbit ventricles and to test the hypothesis that ATP-sensitive K + current ( I KATP ) activation underlies the mechanisms of ES. Methods and Results: Intracellular Ca 2+ (Ca i ) and membrane voltage were optically mapped in 32 Langendorff-perfused rabbit ventricles. At baseline, no SVF was observed after 5 attempts of the VF-defibrillation episodes. During the post-shock period, isoproterenol (0.3 μ mol/L) heterogeneously shortened 50% recovery of action potential duration (APD 50 ) while lowering [K + ] o during isoproterenol infusion prolonged Ca i transient duration (Ca i TD 50 ). Increased difference between Ca i TD and APD (ΔCa i TD 50 -APD 50 ) lead to late phase 3 early afterdepolarization, triggered activity and SVF. In 11 (69%) of 16 SVF episodes, the VF originated from a focal site with maximal or next to maximal ΔCa i TD 50 -APD 50 (Figure A). The focal wavefronts developed wavebreak at sites with large voltage gradient, leading to SVF. Suppression of I Ca,L with nifedipine (10 μ mol/L) reliably prevented ES when given before, but not after, the development of SVF. I KATP blockade with glibenclamide (5 μ mol/L) prolonged post-shock APD 50 and suppressed ES in all ventricles (Figure B). An I Kr blocker E-4031 (1 μ mol/L) failed to terminate ES. The lactate concentration did not increase after 5 VF episodes. Conclusions: VF during beta-adrenergic stimulation causes non-ischemic activation of I KATP and abbreviated APD 50 . Low [K + ] o increases Ca i TD 50. These two factors synergistically enlarge the postshock ΔCa i TD 50 -APD 50 and induce late phase 3 afterdepolarization, triggered activity, wavebreaks and recurrent SVF (electrical storm). I KATP blockade effectively prolongs post-shock APD 50 and suppresses ES.
3D Echocardiography to Evaluate Right Atrial Pressure in Acutely Decompensated Heart Failure
Authors: Ayan R. Patel, Alawi A. Alsheikh-Ali, Jayanta Mukherjee, Antonietta Evangelista, Dima Quraini, Linda J. Ordway, Jeffrey T. Kuvin, David DeNofrio, Natesa G. Pandian
Journal: JACC. Cardiovascular imaging (2011)
丙泊酚注射痛的预防——研究充分，但管理不足
Authors: 马爽, 虞雪融
Journal: BMJ (2011)

丙泊酚是一种可以提供镇静或麻醉的镇静催眠药，广泛应用于手术室、重症监护室和急诊科。丙泊酚起效快，易于滴定式使用，麻醉复苏过程平稳，并有诸如预防恶心及呕吐等其他优点，因此在临床中得以广泛应用，这并不令人感到吃惊。
Abstract 4394: Chronic Administration of Urocortin 2 Prevents the Development of Heart Failure in an Animal Model of Hypertensive Heart Disease
Authors: Silvia Meili-Butz, Marco Studer, Dietlinde John, Christian Morandi, Matthias Pfisterer, Peter Buser, Wylie W Vale, Kirk L Peterson, Marijke Brink, Thomas Dieterle
Journal: Circulation (2008)

Background: Recently, novel corticotropin-releasing factor (CRF)-related peptides named Urocortin (Ucn) 1, 2, and 3 were described. Available data suggest that the Ucns are part of a peripheral CRF system modulating cardiovascular function and mediating cardiovascular responses to stress. Chronic Ucn2 administration induced sustained blood pressure lowering and prevented the development of left ventricular hypertrophy (LVH) in an animal model of hypertensive heart disease. However, no data are available whether chronic administration of Ucn2 may prevent the progression from LVH to heart failure. Methods: Experiments were performed in Dahl salt-sensitive rats. Animals were fed a high salt diet containing 4% NaCl to induce arterial hypertension, LVH, and heart failure. From the phase of LVH on (after 7 weeks of high salt diet), animals were injected with either Ucn2 at a dose of 2.5 μg/kg body weight or vehicle b.i.d. Animals underwent repetitive tail cuff blood pressure measurements and echocardiographic analysis of LV dimension and function at baseline (prior to first injection of Ucn2) and after 5 weeks of b.i.d. treatment with Ucn2. Results: Results are given in the following table as mean (± SD). No differences in heart weight/body weight ratios between Ucn2- and vehicle treated animals were found after 5 weeks of treatment. Conclusion: Chronic CRF receptor stimulation by Ucn2 in the severely hypertensive Dahl salt-sensitive rat, an animal model of hypertensive heart disease, prevents the progression from LVH to LV dilatation and the deterioration of LV function. Thus, chronic administration of Ucn2 might represent a novel approach to the prevention of heart failure.
A randomized trial of atropine regimens for treatment of moderate amblyopia in children
Authors: Michael X Repka, Susan A Cotter, Roy W Beck, Raymond T Kraker, Eileen E Birch, Donald F Everett, Richard W Hertle, Jonathan M Holmes, Graham E Quinn, Nicholas A Sala, Mitchell M Scheiman, David R Stager, David K Wallace
Journal: Ophthalmology (2004)
Can antidepressants cause mania and worsen the course of affective illness?
Authors: T A Wehr, F K Goodwin
Journal: American Journal of Psychiatry (1987)

Several investigators have recently challenged the belief that antidepressants can precipitate mania or rapid cycling between mania and depression. With one exception, there appear to be no placebo-controlled studies of switches into mania in bipolar patients during antidepressant treatment. Patients most likely to switch into mania during antidepressant therapy have probably been excluded from maintenance treatment studies and are probably overrepresented in studies at special research facilities. On balance, the available evidence suggests that some bipolar patients become manic, and a few experience rapid cycling, when they are treated with antidepressants. The prevention of these responses will require further research on risk factors and on the antimanic efficacy of coadministered lithium or other mood stabilizers.
Abstract 916: Molecular and Functional Identification of a New Pathogenic Mechanism in Hypertrophic Cardiomyopathy: Mutations in JPH2-encodeded Jynctophilin-2
Authors: J. M Bos, Karin B Batalden, Noah Weisleder, David J Tester, Steve R Ommen, Moonsun Hwang, Jianjie Ma, Michael J Ackerman
Journal: Circulation (2006)
Plasma viscosity, fibrinogen, white cell count, and cardiovascular risk factors.
Authors: R H Jay, M W Rampling, D J Betteridge
Journal: Circulation (1992)

Although these preliminary data appear to be promising, the Brugada criteria should be applied with caution to patients who present with wide-complex tachycardia while receiving IC antiar- rhythmic agents.Whether they will be as specific in such patients as they are in the drug-free state awaits further investigation.