tbuckley/cabot-search huggingface dataset:
Atrial Therapies Reduce Atrial Arrhythmia Burden in Defibrillator Patients
Authors: Paul A. Friedman, Barbara Dijkman, Eduardo N. Warman, H. Amy Xia, Rahul Mehra, Marshall S. Stanton, Stephen C. Hammill
Journal: Circulation (2001)

Background Approximately 25% of patients who receive an implantable cardioverter-defibrillator (ICD) to treat ventricular tachyarrhythmias have documented atrial tachyarrhythmias before implantation. This study assessed the ability of device-based prevention and termination therapies to reduce the burden of spontaneous atrial tachyarrhythmias. Methods and Results Patients with a standard indication for the implantation of an ICD and 2 episodes of atrial tachyarrhythmias in the preceding year received a dual-chamber ICD (Medtronic 7250 Jewel AF) that uses pacing and shock therapies for prevention and/or termination of atrial tachyarrhythmias. In a multicenter trial, patients were randomized to 3-month periods with atrial therapies “on” or “off” and subsequently crossed over. Analysis was performed on the 52 of 269 patients who had episodes of atrial tachyarrhythmia and had ≥30 days of follow-up with atrial therapies on and off. The atrial therapies resulted in a reduction of atrial tachyarrhythmia burden from a mean of 58.5 to 7.8 h/mo. A paired analysis (Wilcoxon signed-rank test) showed that the median difference in burden (1.1 h/mo) was highly significant ( P =0.007). When the subgroup of 41 patients treated only with atrial pacing therapies was analyzed, the reduction in burden persisted ( P =0.01). Conclusions In this study, patients with a standard ICD indication and atrial tachyarrhythmias had a significant reduction in atrial tachyarrhythmia burden with use of atrial pacing and shock therapies.
Integrating Complementary Medicine Into Cardiovascular Medicine
Authors: John H.K. Vogel, Steven F. Bolling, Rebecca B. Costello, Erminia M. Guarneri, Mitchell W. Krucoff, John C. Longhurst, Brian Olshansky, Kenneth R. Pelletier, Cynthia M. Tracy, Robert A. Vogel, Robert A. Vogel, Jonathan Abrams, Jeffrey L. Anderson, Eric R. Bates, Bruce R. Brodie, Cindy L. Grines, Peter G. Danias, Gabriel Gregoratos, Mark A. Hlatky, Judith S. Hochman, Sanjiv Kaul, Robert C. Lichtenberg, Jonathan R. Lindner, Robert A. O’Rourke, Gerald M. Pohost, Richard S. Schofield, Samuel J. Shubrooks, Cynthia M. Tracy, William L. Winters
Journal: Journal of the American College of Cardiology (2005)
Immune Escape and Survival Mechanisms in Circulating Tumor Cells of Colorectal Cancer
Authors: Gunnar Steinert, Sebastian Schölch, Thomas Niemietz, Naoki Iwata, Sebastián A. García, Bianca Behrens, Anita Voigt, Matthias Kloor, Axel Benner, Ulrich Bork, Nuh N. Rahbari, Markus W. Büchler, Nikolas H. Stoecklein, Jürgen Weitz, Moritz Koch
Journal: Cancer Research (2014)

Abstract The prognosis of colorectal cancer is closely linked to the occurrence of distant metastases. Systemic dissemination is most likely caused by circulating tumor cells (CTC). Despite the fundamental role of CTC within the metastatic cascade, technical obstacles have so far prevented detailed genomic and, in particular, phenotypic analyses of CTC, which may provide molecular targets to delay or prevent distant metastases. We show here a detailed genomic analysis of single colorectal cancer–derived CTC by array comparative genomic hybridization (aCGH), mutational profiling, and microsatellite instability (MSI) analysis. Furthermore, we report the first gene expression analysis of manually selected colorectal cancer–derived CTC by quantitative real-time PCR (qRT-PCR) to investigate transcriptional changes, enabling CTC to survive in circulation and form distant metastases. aCGH confirmed the tumor cell identity of CellSearch-isolated colorectal cancer–derived CTC. Mutational and MSI analyses revealed mutational profiles of CTC to be similar, but not identical to the corresponding tumor tissue. Several CTC exhibited mutations in key genes such as KRAS or TP53 that could not be detected in the tumor. Gene expression analyses revealed both a pronounced upregulation of CD47 as a potential immune-escape mechanism and a significant downregulation of several other pathways, suggesting a dormant state of viable CTC. Our results suggest mutational heterogeneity between tumor tissue and CTC that should be considered in future trials on targeted therapy and monitoring of response. The finding of upregulated immune-escape pathways, which may be responsible for survival of CTC in circulation, could provide a promising target to disrupt the metastatic cascade in colorectal cancer. Cancer Res; 74(6); 1694–704. ©2014 AACR.
Refutation of the myth of the female athlete triad
Authors: L Di Pietro, N Stachenfeld
Journal: British Journal of Sports Medicine (2006)

We are pleased to respond to Refutation of “the myth of the female athlete triad” by Loucks; however, to respond in a point-by-point manner to each and every issue of contention would prove quite tiresome, and, more than likely, futile. Therefore, our response will focus on the more general issues of science and language, with particular attention to the translation (ie, application) of laboratory findings into practice and then into policy intended to affect collective behaviours. In doing so, we wish to remind the reader that there are guidelines governing the delicate balance between science and practice. We have described these guidelines previously with regard to the triad,1 and wish to reiterate that they were developed to prevent practitioners, policy makers and regulators from reacting either too hastily to incomplete science or too slowly to sound science. We continue to maintain that the science pertaining to the female athlete triad is less than complete. Therefore, any attempt to influence practice or policy with regard to the triad should be made with extreme caution, as these efforts may be misguided at this time.

Loucks et al 2–5 have made a landmark contribution to women’s health by identifying a mechanism (low energy availability, independent of exercise stress) by which exercise disrupts leutinising hormone pulsatility. That this mechanism was identified using the …
Risk Factors for Pilot Fatalities in General Aviation Airplane Crash Landings
Authors: Paul S. Rostykus
Journal: JAMA (1998)

Most pilots survive airplane crash landings in small airplanes. Factors associated with pilot death have not been well studied.To identify factors associated with fatalities in general aviation airplane crash landings.Case-control study.The United States.All pilots in general aviation crash landings of airplanes with 10 seats or fewer, from 1983 through 1992.Pilot death.Pilots died in 437 (5.2%) of 8411 crash landings. A fire or explosion on the ground was strongly associated with pilot death (relative risk [RR], 20.4; 95% confidence interval [CI], 15.5-26.9), adjusted for pilot age, pilot flight hours, type of landing gear, and the filing of an instrument flight plan. Pilots who failed to use both lap belt and shoulder harness were more likely to die (adjusted RR, 6.8; 95% CI, 1.8-25.5), as were those who used only the lap belt (adjusted RR, 1.7; 95% CI, 1.3-2.2), compared with pilots who used both restraints.Pilots may be able to reduce their risk of death in a crash landing by using lap and shoulder restraints.
Overlapping Genetic and Environmental Influences on Nonsuicidal Self-injury and Suicidal Ideation
Authors: Dominique F. Maciejewski, Hanneke E. Creemers, Michael T. Lynskey, Pamela A. F. Madden, Andrew C. Heath, Dixie J. Statham, Nicholas G. Martin, Karin J. H. Verweij
Journal: JAMA Psychiatry (2014)

Nonsuicidal self-injury (NSSI) and suicidal self-injury are very harmful behaviors and are associated with several psychiatric disorders. In the recently developed fifth edition of the DSM, NSSI and suicidal behavior disorder are for the first time introduced as conditions in their own right instead of symptoms of other psychiatric disorders. It is unclear to what extent NSSI and suicidal self-injury share the same underlying biological mechanisms and are influenced by the same environmental factors.To determine the relative importance of genetic and environmental influences on the variation in NSSI and suicidal ideation and their covariation.Classical twin design using a sample of 10,678 male and female adult twins (mean [SD] age, 32.76 [6.99] years) from the Australian Twin Registry, a population-based twin registry. Between 1996 and 2009, the twins participated in semistructured telephone interviews that primarily focused on psychiatric disorders.Lifetime presence of self-reported NSSI and suicidal ideation. RESULTS The prevalences of NSSI and suicidal ideation were 4.7% and 26.5%, respectively, and individuals who engaged in self-harm were much more likely to report suicidal ideation (odds ratio = 8.39; 95% CI, 6.84-10.29). Results from a bivariate genetic model indicated that genetic factors explain a substantial part of the variance in both NSSI (37% for men and 59% for women) and suicidal ideation (41% for men and 55% for women), while residual influences (including nonshared environmental influences and measurement error) explain the remainder of the variance. Shared (family) environment did not seem to play a role. Moreover, both behaviors were strongly correlated (r = 0.49 for men and 0.61 for women), and this correlation was largely explained by overlapping genetic influences (76% for men and 62% for women), whereas residual influences accounted for the remainder of the phenotypic correlation.Results indicated that the substantial correlation between NSSI and suicidal ideation is largely driven by overlapping genetic factors, suggesting that the 2 behaviors share similar biological underpinnings. Overlapping residual influences also explain part of the covariance between the 2 traits. Future research should further investigate which genetic and environmental influences underlie the vulnerability to NSSI and suicidal ideation.
Bone disease in chronic childhood cholestasis. I. vitamin D absorption and metabolism†
Authors: James E. Heubi, Bruce W. Hollis, Bonny Specker, Reginald C. Tsang
Journal: Hepatology (1989)

Metabolic bone disease is common in children and adults with chronic cholestasis. We evaluated baseline vitamin D (vitamin D 2 and D 3 ), 25-OH vitamin D 2 and D 3 , 1,25(OH) 2 vitamin D, vitamin D-binding protein, bone mineral content and dietary mineral content in six children (mean age: 12.1 years) with cholestasis since infancy. Absorption of 25-OH vitamin D 3 and vitamin D 2 was evaluated by measuring serial serum concentrations after a test dose. Bone mineral content was reduced by &gt;2 S.D. in five of six subjects compared to age-specific controls; none had radiographic evidence of rickets but all had osteopenia. Dietary Ca and P content in the subjects was comparable to the recommended daily allowance for age-specific children. Baseline serum vitamin D 2 concentrations were undetectable in all but one cholestatic subject despite oral supplementation with 2,500 to 50,000 IU per day vitamin D 2 . Baseline serum 25-OH vitamin D was 33.2 ± 6.0 ng per ml (mean ± S.E.) and comparable to our laboratory norms (15 to 50 ng per ml). Serum 1,25(OH) 2 vitamin D and “free” 1,25(OH) 2 vitamin D were both significantly (p&lt;0.05) reduced compared to controls. A significantly blunted rise and reduced area under the absorption curve (both p&lt;0.001) after 1,000 IU per kg vitamin D 2 was found in cholestatic children (0.8 ng ± 0.5 ng per ml and 18.0 ± 14.3 ng hr per ml, respectively) compared to controls (59.5 ± 10.0 ng per ml and 1,780 ± 253 ng hr per ml, respectively). The peak change and area under the absorption curve for 25-OH vitamin D 3 from baseline after 10 μg per kg 25-OH vitamin D 3 was significantly reduced (both p&lt;0.05) in cholestatic children (60.2 ± 13.8 ng per ml and 751.5 ± 189.9 ng hr per ml, respectively) compared to controls (151.6 ± 30.7 ng per ml and 2,021 ± 472 ng hr per ml, respectively). We conclude that despite severe vitamin D malabsorption, normal serum 25-OH vitamin D concentrations in cholestatic children most likely result from sunlight-stimulated endogenous vitamin D synthesis. Use of oral 25-OH vitamin D should be considered in cholestatic children because its absorption is less impaired than vitamin D.
Early Antiretroviral Therapy and Mortality among HIV-Infected Infants
Authors: Avy Violari, Mark F. Cotton, Diana M. Gibb, Abdel G. Babiker, Jan Steyn, Shabir A. Madhi, Patrick Jean-Philippe, James A. McIntyre
Journal: New England Journal of Medicine (2008)

In countries with a high seroprevalence of human immunodeficiency virus type 1 (HIV-1), HIV infection contributes significantly to infant mortality. We investigated antiretroviral-treatment strategies in the Children with HIV Early Antiretroviral Therapy (CHER) trial.HIV-infected infants 6 to 12 weeks of age with a CD4 lymphocyte percentage (the CD4 percentage) of 25% or more were randomly assigned to receive antiretroviral therapy (lopinavir-ritonavir, zidovudine, and lamivudine) when the CD4 percentage decreased to less than 20% (or 25% if the child was younger than 1 year) or clinical criteria were met (the deferred antiretroviral-therapy group) or to immediate initiation of limited antiretroviral therapy until 1 year of age or 2 years of age (the early antiretroviral-therapy groups). We report the early outcomes for infants who received deferred antiretroviral therapy as compared with early antiretroviral therapy.At a median age of 7.4 weeks (interquartile range, 6.6 to 8.9) and a CD4 percentage of 35.2% (interquartile range, 29.1 to 41.2), 125 infants were randomly assigned to receive deferred therapy, and 252 infants were randomly assigned to receive early therapy. After a median follow-up of 40 weeks (interquartile range, 24 to 58), antiretroviral therapy was initiated in 66% of infants in the deferred-therapy group. Twenty infants in the deferred-therapy group (16%) died versus 10 infants in the early-therapy groups (4%) (hazard ratio for death, 0.24; 95% confidence interval [CI], 0.11 to 0.51; P<0.001). In 32 infants in the deferred-therapy group (26%) versus 16 infants in the early-therapy groups (6%), disease progressed to Centers for Disease Control and Prevention stage C or severe stage B (hazard ratio for disease progression, 0.25; 95% CI, 0.15 to 0.41; P<0.001). Stavudine was substituted for zidovudine in four infants in the early-therapy groups because of neutropenia in three infants and anemia in one infant; no drugs were permanently discontinued. After a review by the data and safety monitoring board, the deferred-therapy group was modified, and infants in this group were all reassessed for initiation of antiretroviral therapy.Early HIV diagnosis and early antiretroviral therapy reduced early infant mortality by 76% and HIV progression by 75%. (ClinicalTrials.gov number, NCT00102960.)
Sickle cell acute chest syndrome associated with parvovirus B19 infection: Case series and review
Authors: Elizabeth A. Lowenthal, Alan Wells, Peter D. Emanuel, Rick Player, Josef T. Prchal
Journal: American Journal of Hematology (1996)

Acute Chest Syndrome (ACS) continues to be a major source of morbidity and mortality among patients with sickle cell disease. It is characterized by the presence of pleutitic chest pain, fever, rales on lung auscultation, and pulmonary infiltrates on chest X-ray [Castro et al: Blood 84:643–649, 1994]. The pathophysiology of this disorder remains poorly understood leading to the descriptive term "Acute Chest Syndrome" designated by Charache et al. [Arch Intern Med 139:67–69, 1979]. Typical bacterial pathogens are seldom isolated in adults, although they play a significant role in the pathogenesis of this entity in children. Until recently, the technology to accurately study viral infection as a precipitating cause of ACS has been unavailable. Parvovirus B19 is being increasingly recognized as an important human pathogen, and has been established as the cause of transient "aplastic crisis" in patients with sickle cell disease [Saarlen et al: Blood 67:11411–11417, 1986; Young: Sem Hematol 25:159–172, 1988]. We present three patients with hemoglobin SC variant of sickle cell disease who developed ACS in association with acute parvovirus B19 infection, one of which died of respiratory failure. Parvovirus B19 infection was established by polymerase chain reaction for parvovirus B19 DNA, and the presence of parvovirus B19 specific IgM antibodies. These cases suggest that parvovirus B19 may be associated with more than self-limited illness in patients with sickle cell disease, and that this ubiquitous virus may merit further study as a precipitating cause of ACS. © 1996 Wiley-Liss, Inc.
TOXIC EPIDERMAL NECROLYSIS AND MALIGNANT LYMPHOMA
Authors: I. W. CALDWELL, P. R. MONTGOMERY, R. D. G. PEACHEY
Journal: British Journal of Dermatology (1967)

Journal Article TOXIC EPIDERMAL NECROLYSIS AND MALIGNANT LYMPHOMA Get access I. W. CALDWELL, M.D., M.R.C.P., I. W. CALDWELL, M.D., M.R.C.P. Royal South Hants Hospital, Southampton Search for other works by this author on: Oxford Academic Google Scholar P. R. MONTGOMERY, M.R.C.P., P. R. MONTGOMERY, M.R.C.P. Royal Hampshire County Hospital, Winchester Search for other works by this author on: Oxford Academic Google Scholar R. D. G. PEACHEY, M.R.C.P. R. D. G. PEACHEY, M.R.C.P. Royal Hampshire County Hospital, Winchester Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 79, Issue 5, 1 May 1967, Pages 287–292, https://doi.org/10.1111/j.1365-2133.1967.tb11493.x Published: 01 May 1967
IgG3 Levels in Patients with Chronic Membranoproliferative Glomerulonephritis
Authors: R. A. Thompson
Journal: BMJ (1972)

In patients with membranoproliferative glomerulonephritis a higher proportion of the serum IgG was IgG3 than in normal subjects, patients with other types of renal disease, or patients with non-renal diseases. Though having a lower mean serum IgG than normal their mean serum IgG3 was raised. This tendency was more pronounced in the hypocomplementaemic patients with the disorder than in those with a normal level of serum complement.
On the proper treatment of connectionism
Authors: Paul Smolensky
Journal: Behavioral and Brain Sciences (1988)

Abstract A set of hypotheses is formulated for a connectionist approach to cognitive modeling. These hypotheses are shown to be incompatible with the hypotheses underlying traditional cognitive models. The connectionist models considered are massively parallel numerical computational systems that are a kind of continuous dynamical system. The numerical variables in the system correspond semantically to fine-grained features below the level of the concepts consciously used to describe the task domain. The level of analysis is intermediate between those of symbolic cognitive models and neural models. The explanations of behavior provided are like those traditional in the physical sciences, unlike the explanations provided by symbolic models. Higher-level analyses of these connectionist models reveal subtle relations to symbolic models. Parallel connectionist memory and linguistic processes are hypothesized to give rise to processes that are describable at a higher level as sequential rule application. At the lower level, computation has the character of massively parallel satisfaction of soft numerical constraints; at the higher level, this can lead to competence characterizable by hard rules. Performance will typically deviate from this competence since behavior is achieved not by interpreting hard rules but by satisfying soft constraints. The result is a picture in which traditional and connectionist theoretical constructs collaborate intimately to provide an understanding of cognition.
Detection of Hepatitis-Associated Antigen and Anti-HAA
Authors: Edwin J. Hacker
Journal: JAMA (1973)

A highly sensitive radioimmunoassay (RIA) is compared to counterimmunoelectrophoresis (CEP) in detection of hepatitis-associated antigen (HAA) and antibody in healthy adults, volunteer blood donors, and patients with acute and chronic liver disease. Three hundred twentysix sera were screened. Counterimmunoelectrophoresis failed to demonstrate HAA in any of the 100 control subjects and 105 volunteer donors, whereas RIA revealed a 1% and 2% incidence, respectively. In the same two groups, RIA demonstrated a 10% and 21% incidence of anti-HAA; only one of these subjects had anti-HAA by CEP.  Radioimmunoassay approximately doubled the rate of detection of antigen in parenterally transmitted, sporadic, and chronic active hepatitis. Hepatitis-associated antigen, when found in chronic persistent hepatitis, was present in large amounts and detectable by both techniques.
Intestinal lipid absorption in the nephrotic rat.
Authors: W D Paulson, C N Torres-Rivera, L Gray, P Tso
Journal: Journal of the American Society of Nephrology (1996)

There is limited data on intestinal lipid absorption in the nephrotic syndrome. This study investigated whether the efficiency of intestinal lipid absorption is altered in nephrotic lymph-fistula rats. The nephrotic syndrome was induced in nine Sprague-Dawley rats by an i.v. injection of puromycin aminonucleoside in saline; seven control rats received saline only. At 10 to 14 days after injection, the main intestinal lymph duct was cannulated for collection of lymph. The duodenum was also cannulated and a fasting saline-glucose solution was infused overnight at 3 mL/h. The next day, the infusate was changed to a lipid emulsion that contained (14C) cholesterol and (3H)triglyceride (triolein) that was infused at 3 mL/h for 8 h. During the last hour of fasting and during the lipid infusion, lymph flow in the Nephrotic group averaged 0.6 mL/h higher than the Control group (P = 0.02). No significant differences were found between the two groups in recovery of infused radioactive cholesterol (P = 0.37) or triglyceride (P = 0.38) from the gastrointestinal lumen, small intestinal mucosa, or lymph. Lymphatic output of chemically measured cholesterol was also similar (P = 0.96). These results suggest that mucosal uptake and lymphatic output of cholesterol and triglyceride are not altered in the nephrotic syndrome.
The interaction of macrophage and non-macrophage tropic isolates of HIV-1 with thymic and tonsillar dendritic cells in vitro.
Authors: P U Cameron, M G Lowe, F Sotzik, A F Coughlan, S M Crowe, K Shortman
Journal: The Journal of Experimental Medicine (1996)

Dendritic cells isolated from thymus and tonsil were tested for susceptibility to HIV-1 strains that are tropic for macrophages or for T cell lines. DCs were purified by cell sorting and before infection expressed high levels of CD4 and HLA-DR and lacked markers for T, B, NK cells, or macrophages. Viral entry and reverse transcription was found after pulsing with strains of HIV-1 that could infect macrophages. During the first 36 h the PCR signals for gag sequences increased in DCs and macrophages. In contrast little if any viral DNA was found after pulsing macrophages or DCs with HIV-1 that was able to infect T cell lines. DCs pulsed with HIV-1 were able to transmit infection to responding T cells during an allogeneic or superantigen response. Selection for virus able to infect lymphoid DCs and other DCs expressing CD4 and its transfer to T cells during subsequent immune responses may provide a mechanism for the observed predominance of macrophage-tropic HIV-1 after in vivo transmission.
Familial extensive idiopathic bilateral pleural fibrosis
Authors: E. Azoulay, B. Paugam, M-F. Heymann, M. Kambouchner, A Haloun, D. Valeyre, J-P. Battesti, A. Tazi
Journal: European Respiratory Journal (1999)

The authors report three sisters with bilateral isolated apical pleural fibrosis of unknown origin, which did not respond to empirical antituberculosis therapy and oral corticosteroids. The disease evolved in an unrelenting fashion producing pleural fibrosis at the lung bases and leading to the death of two sisters and to lung transplantation in the other one. There was no history of other familial disease or consanguinity. The particular features of these cases and the differences from other reports of apparently cryptogenic pleural fibrosis are outlined.