tbuckley/cabot-search huggingface dataset:
Smoking Status and Health Care Costs in the Perioperative Period
Authors: David O. Warner, Bijan J. Borah, James Moriarty, Darrell R. Schroeder, Yu Shi, Nilay D. Shah
Journal: JAMA Surgery (2014)

Cigarette smoking adds an estimated $100 billion in annual incremental direct health care costs nationwide. Cigarette smoking increases complication risk in surgical patients, but the potential effects of smoking status on perioperative health care costs are unclear.To test the hypothesis that current and former smoking at the time of admission for inpatient surgery, compared with never smoking, are independently associated with higher incremental health care costs for the surgical episode and the first year after hospital discharge.This population-based, propensity-matched cohort study, with cohort membership based on smoking status (current smokers, former smokers, and never smokers) was performed at Mayo Clinic in Rochester (a tertiary care center) and included patients at least 18 years old who lived in Olmsted County, Minnesota, for at least 1 year before and after the index surgery.Undergoing an inpatient surgical procedure at Mayo Clinic hospitals between April 1, 2008, and December 31, 2009.Total costs during the index surgical episode and 1 year after hospital discharge, with the latter standardized as costs per month. Costs were measured using the Olmsted County Healthcare Expenditure and Utilization Database, a claims-based database including information on medical resource use, associated charges, and estimated economic costs for patients receiving care at the 2 medical groups (Mayo Clinic and Olmsted Medical Center) that provide most medical services within Olmsted County, Minnesota.Propensity matching resulted in 678 matched pairs in the current vs never smoker grouping and 945 pairs in the former vs never smoker grouping. Compared with never smokers, adjusted costs for the index hospitalization did not differ significantly for current or former smokers. However, the adjusted costs in the year after hospitalization were significantly higher for current and former smokers based on regression analysis (predicted monthly difference of $400 [95% CI, $131-$669] and $273 [95% CI, $56-$490] for current and former smokers, respectively).Compared with never smokers, health care costs during the first year after hospital discharge for an inpatient surgical procedure are higher in both former and current smokers, although the cost of the index hospitalization is not affected by smoking status.
Physicians confront the apocalypse. The American medical profession and the threat of nuclear war
Authors: P. Boyer
Journal: JAMA (1985)

IN THE resurgence of nuclear weapons activism and cultural awareness that swept the United States in the early 1980s, physicians figured prominently. The Australian pediatrician Helen Caldicott gained national visibility as president of the 30,000-member Physicians for Social Responsibility. Dean Howard Hiatt, of the Harvard School of Public Health; psychiatrist John Mack, of Harvard Medical School; H. Jack Geiger, of the City College of New York School of Biomedical Education; and Yale psychiatrist Robert Lifton were influential voices in the antinuclear cause. In<i>The Final Epidemic: Physicians and Scientists on Nuclear War</i>,<sup>1</sup>and<i>Last Aid: The Medical Dimensions of Nuclear War</i>,<sup>2</sup>medical leaders spoke out on this issue.<i>The Journal of the American Medical Association</i>published major articles on aspects of the subject, including the role of the medical profession in preventing nuclear holocaust.<sup>3,4</sup> This article seeks to place this activism in historical context. Focusing on the
Dual Regulation by Apurinic/Apyrimidinic Endonuclease-1 Inhibits Gastric Epithelial Cell Apoptosis during <i>Helicobacter pylori</i> Infection
Authors: Ranajoy Chattopadhyay, Asima Bhattacharyya, Sheila E. Crowe
Journal: Cancer Research (2010)

Human apurinic/apyrimidinic endonuclease-1 (APE-1), a key enzyme involved in repair of oxidative DNA base damage, is an important transcriptional coregulator. We previously reported that Helicobacter pylori infection induces apoptosis and increases APE-1 expression in human gastric epithelial cells (GEC). Although both the DNA repair activity and the acetylation-mediated transcriptional regulation of APE-1 are required to prevent cell death, the mechanisms of APE-1-mediated inhibition of infection-induced apoptosis are unclear. Here, we show that short hairpin RNA-mediated stable suppression of APE-1 results in increased apoptosis in GEC after H. pylori infection. We show that programmed cell death involves both the caspase-9-mediated mitochondrial pathway and the caspase-8-dependent extrinsic pathway by measuring different markers for both the pathways. Overexpression of wild-type APE-1 in APE-1-suppressed GEC reduced apoptosis after infection; however, overexpression of the DNA repair mutant or the nonacetylable mutant of APE-1 alone was unable to reduce apoptosis, suggesting that both DNA repair and acetylation functions of APE-1 modulate programmed cell death. We show for the first time that the DNA repair activity of APE-1 inhibits the mitochondrial pathway, whereas the acetylation function inhibits the extrinsic pathway during H. pylori infection. Thus, our findings establish that the two different functions of APE-1 differentially regulate the intrinsic and the extrinsic pathway of H. pylori-mediated GEC apoptosis. As proapoptotic and antiapoptotic mechanisms determine the development and progression of gastritis, gastric ulceration, and gastric cancer, this dual regulatory role of APE-1 represents one of the important molecular strategies by H. pylori to sustain chronic infection.
Flegel’s disease treated with psoralen ultraviolet A
Authors: S.M. Cooper, S. George
Journal: British Journal of Dermatology (2000)

Flegel’s disease is an uncommon condition which causes asymptomatic keratotic papules on the limbs. It usually develops in the fourth or fifth decade. Therapeutic options are limited to emollients, topical 5‐fluorouracil and retinoids, but none of these treatments is consistently helpful. We report a patient with Flegel’s disease who responded to psoralen ultraviolet A treatment.
Comparison of acute myeloid leukemia occurring de novo or preceded by a myelodysplastic stage: Differences in cellular DNA content
Authors: S. Widell, G. Auer, R. Hast, P. Reizenstein
Journal: American Journal of Hematology (1993)

Abstract The DNA content of bone marrow cells in patients with acute leukemia preceded by a myelodysplastic stage (MDS‐AML) was compared to that in patients with de novo AML. We studied granulocytes, lymphocytes, monocytes, and blasts/promyelocytes from Feul‐gen‐stained bone marrow smears of 11 patients with de novo AML, ten patients with MDS‐AML, and 13 apparently healthy controls. The mean amount of DNA per cell (DNA index; Dl) in each cell population was determined using a digital video‐based imageanalyzing system (CAS‐100). Analysis of variance (F test) showed a significant difference in the DNA content between de novo AML on one hand and MDS‐AML and controls on the other as regards to blasts/promyelocytes ( P &lt; 0.01), lymphocytes ( P &lt; 0.05), and monocytes ( P &lt; 0.01), respectively. In three of 11 (27%) patients with de novo AML, a lower than normal limit Dl was found both in immature and mature bone marrow cells. Patients with MDS‐AML had those of Dl values similar to normal controls. In consequence, a significantly reduced mean Dl was found in patients with de novo AML in blasts/promyelocytes ( P &lt; 0.01), and monocytes ( P &lt; 0.05) compared to both normal controls and MDS‐AML. Together with data published separately, suggesting differences in granulocyte morphology, clonality, and HLA‐DR expression, these data suggest biological differences between the two diseases. © 1993 Wiley‐Liss, Inc.
An automatic device for freeze-clamping of cardiac tissue within a fraction of the contraction cycle
Authors: T. PODZUWEIT, T. J. van der WERFF, O. BRICKNELL, A. KAY
Journal: Cardiovascular Research (1978)

An automatic quick-freeze clamping device has been developed. Opposed pneumatic pistons fitted with aluminium caps previously cooled in liquid nitrogen are used to compress a portion (100 to 200 mg) of the myocardium to a 0.15 to 0.20 mm thick wafer, cooling the tissue from 37°C to -15°C within 10 ms. The clamp is triggered electronically from the R-wave of the ECG. This tissue fixation by freezing within 10 ms is sufficiently rapid to study oscillations of myocardial metabolite levels during the contraction cycle of isolated perfused hearts of small mammals such as the rat and guinea pig whose rate is 4 to 5 beats per second.
Achilles tendon thickness and ischemic heart disease in familial hypercholesterolemia
Authors: H. Mabuchi, R. Tatami, T. Haba, K. Ueda, R. Ueda, S. Ito, T. Karnetani, J. Koizurni, S. Miyarnoto, M. Ohta, R. Takeda, T. Takegoshi, H. Takeshita
Journal: Metabolism (1978)
A CASE OF SCLEREMA NEONATORUM
Authors: W. G. Nash
Journal: BMJ (1924)

SCLE,REMIA NEONATORUM appears to be sufficiently uncommon in Great Britain to render the following case worthy of record.A female infant, aged 2 months, was first seen by me on January 11th, 1924.The father, aged 44, and the motlher, aged 33, had for some years resided on the Gold Coast.This was their first child.The mother about a month after she became pregnant came to England suffering from bacilluria, and this was still present in February, 1924.The father denied any history of syphilis.The child was born in South Devon on November 9th, 1923, and at birth weighed 8 lb. 3 oz.It is possible she was a ten months baby.At birth she was blue owing to compression of the cord.A few days after birth oedema was noticed, and this gradually increased in hardness and extent.She was artificially fed from birth.On November 28th it was noted that the arms above the elbows were very hard and the buttocks very hard and lumpy.This hardness continued to increase until the whole of the back and all the extremities were involved.On January 10th, 1924, when she came to Bedford, the hardness at the back of the neck wvas getting less.It was noticed that the
Oesophagomyotomy for achalasia of the cardia.
Authors: C Sariyannis, K S Mullard
Journal: Thorax (1975)

Experience of 48 cases of achalasia of the cardia, treated by oesophagomyotomy, and of three cases of failed 9Heller9 operation, treated by jejunal interposition, is recorded. Some technical details and the results are discussed.
Risk for Life-Threatening Cardiac Events in Patients With Genotype-Confirmed Long-QT Syndrome and Normal-Range Corrected QT Intervals
Authors: Ilan Goldenberg, Samuel Horr, Arthur J. Moss, Coeli M. Lopes, Alon Barsheshet, Scott McNitt, Wojciech Zareba, Mark L. Andrews, Jennifer L. Robinson, Emanuela H. Locati, Michael J. Ackerman, Jesaia Benhorin, Elizabeth S. Kaufman, Carlo Napolitano, Pyotr G. Platonov, Silvia G. Priori, Ming Qi, Peter J. Schwartz, Wataru Shimizu, Jeffrey A. Towbin, G. Michael Vincent, Arthur A.M. Wilde, Li Zhang
Journal: Journal of the American College of Cardiology (2010)
Interleukin-2 Therapy in Patients with HIV Infection
Authors: The INSIGHT–ESPRIT Study Group and SILCAAT Scientific Committee
Journal: New England Journal of Medicine (2009)

Used in combination with antiretroviral therapy, subcutaneous recombinant interleukin-2 raises CD4+ cell counts more than does antiretroviral therapy alone. The clinical implication of these increases is not known.We conducted two trials: the Subcutaneous Recombinant, Human Interleukin-2 in HIV-Infected Patients with Low CD4+ Counts under Active Antiretroviral Therapy (SILCAAT) study and the Evaluation of Subcutaneous Proleukin in a Randomized International Trial (ESPRIT). In each, patients infected with the human immunodeficiency virus (HIV) who had CD4+ cell counts of either 50 to 299 per cubic millimeter (SILCAAT) or 300 or more per cubic millimeter (ESPRIT) were randomly assigned to receive interleukin-2 plus antiretroviral therapy or antiretroviral therapy alone. The interleukin-2 regimen consisted of cycles of 5 consecutive days each, administered at 8-week intervals. The SILCAAT study involved six cycles and a dose of 4.5 million IU of interleukin-2 twice daily; ESPRIT involved three cycles and a dose of 7.5 million IU twice daily. Additional cycles were recommended to maintain the CD4+ cell count above predefined target levels. The primary end point of both studies was opportunistic disease or death from any cause.In the SILCAAT study, 1695 patients (849 receiving interleukin-2 plus antiretroviral therapy and 846 receiving antiretroviral therapy alone) who had a median CD4+ cell count of 202 cells per cubic millimeter were enrolled; in ESPRIT, 4111 patients (2071 receiving interleukin-2 plus antiretroviral therapy and 2040 receiving antiretroviral therapy alone) who had a median CD4+ cell count of 457 cells per cubic millimeter were enrolled. Over a median follow-up period of 7 to 8 years, the CD4+ cell count was higher in the interleukin-2 group than in the group receiving antiretroviral therapy alone--by 53 and 159 cells per cubic millimeter, on average, in the SILCAAT study and ESPRIT, respectively. Hazard ratios for opportunistic disease or death from any cause with interleukin-2 plus antiretroviral therapy (vs. antiretroviral therapy alone) were 0.91 (95% confidence interval [CI], 0.70 to 1.18; P=0.47) in the SILCAAT study and 0.94 (95% CI, 0.75 to 1.16; P=0.55) in ESPRIT. The hazard ratios for death from any cause and for grade 4 clinical events were 1.06 (P=0.73) and 1.10 (P=0.35), respectively, in the SILCAAT study and 0.90 (P=0.42) and 1.23 (P=0.003), respectively, in ESPRIT.Despite a substantial and sustained increase in the CD4+ cell count, as compared with antiretroviral therapy alone, interleukin-2 plus antiretroviral therapy yielded no clinical benefit in either study. (ClinicalTrials.gov numbers, NCT00004978 [ESPRIT] and NCT00013611 [SILCAAT study].)
Periostin Is Required for Maturation and Extracellular Matrix Stabilization of Noncardiomyocyte Lineages of the Heart
Authors: Paige Snider, Robert B. Hinton, Ricardo A. Moreno-Rodriguez, Jian Wang, Rhonda Rogers, Andrew Lindsley, Fang Li, David A. Ingram, Donald Menick, Loren Field, Anthony B. Firulli, Jeffery D. Molkentin, Roger Markwald, Simon J. Conway
Journal: Circulation Research (2008)

The secreted periostin protein, which marks mesenchymal cells in endocardial cushions following epithelial–mesenchymal transformation and in mature valves following remodeling, is a putative valvulogenesis target molecule. Indeed, periostin is expressed throughout cardiovascular morphogenesis and in all 4 adult mice valves (annulus and leaflets). Additionally, periostin is expressed throughout the fibrous cardiac skeleton and endocardial cushions in the developing heart but is absent from both normal and/or pathological mouse cardiomyocytes. Periostin ( peri lacZ ) knockout mice exhibit viable valve disease, with neonatal lethality in a minority and latent disease with leaflet abnormalities in the viable majority. Surviving peri lacZ -null leaflets are truncated, contain ectopic cardiomyocytes and smooth muscle, misexpress the cartilage proteoglycan aggrecan, demonstrate disorganized matrix stratification, and exhibit reduced transforming growth factor-β signaling. Neonatal peri lacZ nulls that die (14%) display additional defects, including leaflet discontinuities, delamination defects, and deposition of acellular extracellular matrix. Assessment of collagen production, 3D lattice formation ability, and transforming growth factor-β responsiveness indicate periostin-deficient fibroblasts are unable to support normal valvular remodeling and establishment of a mature cardiac skeleton. Furthermore, pediatric stenotic bicuspid aortic valves that have lost normal extracellular matrix trilaminar stratification have greatly reduced periostin. This suggests that loss of periostin results in inappropriate differentiation of mesenchymal cushion cells and valvular abnormalities via a transforming growth factor-β–dependent pathway during establishment of the mature heart. Thus, peri lacZ knockouts provide a new model of viable latent valve disease.
Bronchoesophageal Fistula and Fatal Hemoptysis After Bevacizumab-Containing Chemotherapy Without Radiation in Lung Cancer
Authors: Jens Schreiber, Nadine Waldburg
Journal: Journal of Clinical Oncology (2012)

Introduction There are several reports on tracheoesophageal fistula formation and related morbidity and mortality in patients with lung cancer treated with chemoradiotherapy and bevacizumab. We draw attention to a recent patient in whom bronchoesophageal fistula and fatal hemoptysis developed after the first course of treatment of a pulmonary adenocarcinoma with platinum-based chemotherapy containing bevacizumab without radiotherapy.
Exercise-induced silent myocardial ischemia and coronary morbidity and mortality in middle-aged men
Authors: Jari A Laukkanen, Sudhir Kurl, Timo A Lakka, Tomi-Pekka Tuomainen, Rainer Rauramaa, Riitta Salonen, Jaakko Eränen, Jukka T Salonen
Journal: Journal of the American College of Cardiology (2001)
Cardiac-Specific Overexpression of Cyclin-Dependent Kinase 2 Increases Smaller Mononuclear Cardiomyocytes
Authors: Hai-Sun Liao, Peter M. Kang, Hirotaka Nagashima, Naohito Yamasaki, Anny Usheva, Bo Ding, Beverly H. Lorell, Seigo Izumo
Journal: Circulation Research (2001)

Cyclin-dependent kinase 2 (cdk2) plays a critical role in the G1- to S-phase checkpoint of the cell cycle. Adult cardiomyocytes are believed to withdraw from the cell cycle. To determine whether forced overexpression of cdk2 results in altered cell-cycle regulation in the adult heart, we generated transgenic mice specifically overexpressing cdk2 in hearts. Transgenic hearts expressed high levels of both cdk2 mRNA and catalytically active cdk2 proteins. Cdk2 overexpression significantly increased the levels of cdk4 and cyclins A, D3, and E. There was an increase in both DNA synthesis and proliferating cell nuclear antigen levels in the adult transgenic hearts. The ratio of heart weight to body weight in cdk2 transgenic mice was significantly increased in neonatal day 2 but not in adults compared with that of wild-type mice. Analysis of dispersed individual adult cardiomyocytes showed a 5.6-fold increase in the proportion of smaller mononuclear cardiomyocytes in the transgenic mice. Echocardiography revealed that transgenic heart was functionally normal. However, adult transgenic ventricles expressed beta-myosin heavy chain and atrial natriuretic factor. Surgically induced pressure overload caused an exaggerated maladaptive hypertrophic response in transgenic mice but did not change the proportion of mononuclear cardiomyocytes. The data suggest that overexpression of cdk2 promotes smaller, less-differentiated mononuclear cardiomyocytes in adult hearts that respond in an exaggerated manner to pressure overload.
Splenic lymphoma with villous lymphocytes, associated with type II cryoglobulinemia and HCV infection: a new entity?
Authors: David Saadoun, Felipe Suarez, François Lefrere, Françoise Valensi, Xavier Mariette, Achille Aouba, Caroline Besson, Bruno Varet, Xavier Troussard, Patrice Cacoub, Oliver Hermine
Journal: Blood (2004)
NADPH oxidase-dependent redox signalling in cardiac hypertrophy, remodelling and failure
Authors: C MURDOCH, M ZHANG, A CAVE, A SHAH
Journal: Cardiovascular Research (2006)

Markers of increased oxidative stress are known to be elevated following acute myocardial infarction and in the context of chronic left ventricular hypertrophy or heart failure, and their levels may correlate with the degree of contractile dysfunction or cardiac deficit. An obvious pathological mechanism that may account for this correlation is the potential deleterious effects of increased oxidative stress through the induction of cellular dysfunction, energetic deficit or cell death. However, reactive oxygen species have several much more subtle effects in the remodelling or failing heart that involve specific redox-regulated modulation of signalling pathways and gene expression. Such redox-sensitive regulation appears to play important roles in the development of several components of the phenotype of the failing heart, for example cardiomyocyte hypertrophy, interstitial fibrosis and chamber remodelling. In this article, we review the evidence supporting the involvement of reactive oxygen species and redox signalling pathways in the development of cardiac hypertrophy and heart failure, with a particular focus on the NADPH oxidase family of superoxide-generating enzymes which appear to be especially important in redox signalling.
Donor-Specific Antibodies Adversely Affect Kidney Allograft Outcomes
Authors: Sumit Mohan, Amudha Palanisamy, Demetra Tsapepas, Bekir Tanriover, R. John Crew, Geoffrey Dube, Lloyd E. Ratner, David J. Cohen, Jai Radhakrishnan
Journal: Journal of the American Society of Nephrology (2012)

The effect of low titers of donor-specific antibodies (DSAs) detected only by sensitive solid-phase assays (SPAs) on renal transplant outcomes is unclear. We report the results of a systematic review and meta-analysis of rejection rates and graft outcomes for renal transplant recipients with such preformed DSAs, defined by positive results on SPA but negative complement-dependent cytotoxicity and flow cytometry crossmatch results. Our search identified seven retrospective cohort studies comprising a total of 1119 patients, including 145 with isolated DSA-SPA. Together, these studies suggest that the presence of DSA-SPA, despite a negative flow cytometry crossmatch result, nearly doubles the risk for antibody-mediated rejection (relative risk [RR], 1.98; 95% confidence interval [CI], 1.36–2.89; P<0.001) and increases the risk for graft failure by 76% (RR, 1.76; 95% CI, 1.13–2.74; P=0.01). These results suggest that donor selection should consider the presence of antibodies in the recipient, identified by the SPA, even in the presence of a negative flow cytometry crossmatch result.