tbuckley/cabot-search huggingface dataset:
Plasma Levels of Receptor for Advanced Glycation End Products, Blood Transfusion, and Risk of Primary Graft Dysfunction
Authors: Jason D. Christie, Chirag V. Shah, Steven M. Kawut, Nilam Mangalmurti, David J. Lederer, Joshua R. Sonett, Vivek N. Ahya, Scott M. Palmer, Keith Wille, Vibha Lama, Pali D. Shah, Ashish Shah, Ann Weinacker, Clifford S. Deutschman, Benjamin A. Kohl, Ejigayehu Demissie, Scarlett Bellamy, Lorraine B. Ware
Journal: American Journal of Respiratory and Critical Care Medicine (2009)

The receptor for advanced glycation end products (RAGE) is an important marker of lung epithelial injury and may be associated with impaired alveolar fluid clearance. We hypothesized that patients with primary graft dysfunction (PGD) after lung transplantation would have higher RAGE levels in plasma than patients without PGD.To test the association of soluble RAGE (sRAGE) levels with PGD in a prospective, multicenter cohort study.We measured plasma levels of sRAGE at 6 and 24 hours after allograft reperfusion in 317 lung transplant recipients at seven centers. The primary outcome was grade 3 PGD (Pa(O(2))/Fi(O(2)) < 200 with alveolar infiltrates) within the first 72 hours after transplantation.Patients who developed PGD had higher levels of sRAGE than patients without PGD at both 6 hours (median 9.3 ng/ml vs. 7.5 ng/ml, respectively; P = 0.028) and at 24 hours post-transplantation (median 4.3 ng/ml vs. 1.9 ng/ml, respectively; P < 0.001). Multivariable logistic regression analyses indicated that the relationship between levels of sRAGE and PGD was attenuated by elevated right heart pressures and by the use of cardiopulmonary bypass. Median sRAGE levels were higher in subjects with cardiopulmonary bypass at both 6 hours (P = 0.003) and 24 hours (P < 0.001). sRAGE levels at 6 hours were significantly associated with intraoperative red cell transfusion (Spearman's rho = 0.39, P = 0.002 in those with PGD), and in multivariable linear regression analyses this association was independent of confounding variables (P = 0.02).Elevated plasma levels of sRAGE are associated with PGD after lung transplantation. Furthermore, plasma sRAGE levels are associated with blood product transfusion and use of cardiopulmonary bypass.
Oxford Handbook of Emergency Medicine
Authors: Suzanne Dooley-Hash
Journal: JAMA (2012)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Induction of a deficiency of steroid delta 4-5 alpha-reductase activity in liver by a porphyrinogenic drug.
Authors: A Kappas, H L Bradlow, D R Bickers, A P Alvares
Journal: Journal of Clinical Investigation (1977)

The hepatic enzymes that catalyze drug oxidations and the reductive metabolism of steroid hormones to 5alpha-derivatives are localized in membranes of the endoplasmic reticulum. Phenobarbital, which exacerbates acute intermittent porphyria in man, induces drug-oxidizing enzymes in liver. Additionally, patients in whome the primary gene defect (uroporphyrinogen-I-synthetase deficiency) of acute intermittent porphyria has become clinically expressed have low levels of hepatic steroid delta4-5alpha-reductase activity. This 5alpha-reductase deficiency in acute intermittent porphyria leads to the disproportionate generation of 5beta-steroid metabolites from precursor hormones; such steroid metabolites have significant porphyria-inducing action experimentally. In this study the effects of phenobarbital on drug oxidation and steroid 5alpha-reduction in man were examined to determine if this drug could produce changes in steroid 5alpha-reductase activity which mimicked those seen in patients with acute intermittent porphyria. Metabolic studies with [14C]-testosterone and 11beta-[3H]hydroxyandrostenedione were carried out in five normal volunteers. In all five subjects phenobarbital administration (2 mg/kg/per day for 21 days) enhanced plasma removal of the test drugs antipyrine and phenylbutazone as expected; but in four subjects phenobarbital also substantially depressed 5alpha-metabolite formation from [14C]testosterone and resulted in a pattern of hormone biotransformation characterized by a high ratio of 5beta/5alpha-metabolite formation. Studies with 11beta-[3H]hydroxy-androstenedione in three subjects confirmed that phenobarbital produced this high 5beta/5alpha ratio of steroid metabolism by depressing 5alpha-reductase activity for steroid hormones in liver. The high ratio of 5beta/5alpha-metabolites formed in normals after drug treatment mimicks the high 5beta/5alpha-steroid metabolite ratio formed from endogenous hormones in acute intermittent porphyria. The proximate mechanism by which phenobarbital induces reciprocal changes in activities of the microsomal enzymes which catalyze drug oxidations and steroid 5alpha-reductions is not known. This action of phenobarbital raises the possibility, however, that certain drugs which provoke exacerbations of human porphyria may do so, in part, by producing deleterious shifts in the patterns of endogenous steroid hormone metabolism.
Methods for reducing lead exposure in young children and other risk groups: an integrated summary of a report to the U.S. Congress on childhood lead poisoning.
Authors: P Mushak, A F Crocetti
Journal: Environmental Health Perspectives (1990)

As part of a Congressionally mandated report on U.S. childhood lead poisoning prepared by the Federal government (U.S. Agency for Toxic Substances and Disease Registry [ATSDR]), the authors have analyzed the relative effectiveness of measures to reduce source-specific lead exposure of U.S. children. An integrated overview of this analysis is presented in this article. Two national actions, the Federally mandated phasedown of lead in gasoline by the U.S. Environmental Protection Agency and the voluntary phasedown of lead use in domestic food can production, are examples of centrally directed initiatives that have been relatively successful in limiting childhood lead exposure in the U.S. Efforts to abate lead-based paint exposure of children have largely failed. This is especially true for the nation's 21 million residential units with the highest lead content paint. Similarly, abatement of lead exposure from contaminated dusts and soils has generally been unsuccessful. Comprehensive measures to reduce lead exposure from drinking water in residences and public facilities, e.g., elementary schools, are only now being promulgated or implemented. The full extent of their effectiveness remains to be demonstrated. There are many miscellaneous but potentially severe exposure sources that are difficult to control but require attention, such as poorly glazed foodware and ethno-specific preparations.
Pulmonary Toxicity of Antineoplastic Drugs
Authors: Gerald Batist
Journal: JAMA (1981)

Pulmonary toxicity caused by antineoplastic drugs is becoming a more frequently recognized entity, and the number of drugs known or suspected of causing this disease is steadily increasing. In general, the initial clinical appearance includes both constitutional signs of malaise and fever, as well as pulmonary complaints. Some clinical signs may suggest a particular drug as the cause. The pathological condition also is generally nonspecific, but some clues may be present histologically that help define the causal agent. This is a review of the antineoplastic drugs that are associated with pulmonary toxicity. Clinical, laboratory, and pathological data are presented as useful information for practicing physicians. Although therapeutic maneuvers are limited, these are discussed with regard to each drug.
The Chromatin Remodeler Mi-2β Is Required for CD4 Expression and T Cell Development
Authors: Christine J Williams, Taku Naito, Pablo Gómez-del Arco, John R Seavitt, Susan M Cashman, Beverly De Souza, Xiaoqing Qi, Piper Keables, Ulrich H Von Andrian, Katia Georgopoulos
Journal: Immunity (2004)
Abstract 130: Deadly KISS, Kisspeptin10 interaction with osteoblasts and breast cancer metastastic cells
Authors: Kaitlyn E. Leahey, Danny R. Welch, Yu-Chi Chen, Karen M. Bussard, Andrea M. Mastro
Journal: Cancer Research (2014)

Abstract Current cancer research focuses on blockading metastasis with the hope of increasing patient survival and prognoses. This research has spurred an interest in metastasis suppressor genes, such as KISS-1, whose role in breast cancer remains controversial. This study focuses on the interactions among one of the proteolytic processing products of the Kiss1 protein (kisspeptin10, KP10), its receptor, KISS1R (GPR54, AXOR12), osteoblasts (bone forming cells), and bone-metastatic breast cancer cells, MDA-MB-231. Previous research suggests that treatment with KP10 reduces the ability of the cancer cells to invade a reconstituted basement membrane (Matrigel) and to migrate in response to osteosarcoma cells. The aim of this present study was to determine if KP10 affected the interaction of MC3T3-E1 osteoblasts and bone-metastatic breast cancer cells. Our laboratory had previously determined that osteoblasts exhibit an inflammatory response when treated with conditioned medium from breast cancer cells. This inflammatory response may contribute to cancer cell proliferation in the bone. This response has not yet been characterized in the presence of KP10. I hypothesized that KP10 would down regulate the inflammatory response of osteoblasts to breast cancer cells. MDA-MB-231 breast cancer cells express theKISS1R; therefore, these cells were treated with KP10 (10-100 nM, 2hr), the medium was collected, and the osteoblasts were treated with it. KP10 significantly decreased the inflammatory response of osteoblasts to breast cancer conditioned media indicated by decreased levels of IL-6 as determined by ELISA. This research has important implications because it provides insight into how KP10 may be acting on either the breast cancer cells or the bone cells. In my future research, I will continue to characterize how KP10 can be used to prevent proliferation or activation of breast cancer metastases in the bone. This work was supported by an undergraduate research grant from the Eberly College of Science of Penn State University. Citation Format: Kaitlyn E. Leahey, Danny R. Welch, Yu-Chi Chen, Karen M. Bussard, Andrea M. Mastro. Deadly KISS, Kisspeptin10 interaction with osteoblasts and breast cancer metastastic cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 130. doi:10.1158/1538-7445.AM2014-130
Use of tobacco, drugs, and alcohol among English children is falling
Authors: O. Mashta
Journal: BMJ (2010)

Smoking, drinking, and drug use among schoolchildren is on the decline, says a new report from the NHS Information Centre.

The annual survey of 7700 school pupils aged 11 to 15 in England found an overall downward trend in the age group, even though use among the 15 year olds has risen.

The percentage of 11 to 15 year olds who had ever taken drugs stood at 22% in 2009, down …
Sulphydryl blocker induced gastric damage is ameliorated by scavenging of free radicals.
Authors: F Karmeli, E Okon, D Rachmilewitz
Journal: Gut (1996)

Sulphydryl compounds and nitric oxide are essential in maintaining gastric mucosal integrity.To characterise the gastric damage induced by a sulphydryl blocker, to evaluate the role of nitric oxide in its pathogenesis, and to reveal its possible prevention by scavenging of free radicals.Gastritis was induced in rats by addition of iodoacetamide (0.1%) to the drinking water, with and without daily intragastric administration of TEMPOL. After death, the stomach was resected, washed, lesion area assessed, and mucosal inflammatory mediators, myeloperoxidase and nitric oxide synthase activities were determined.Administration of iodoacetamide induced gastric mucosal erosions present for up to two weeks. Myeloperoxidase activity was increased for up to seven days and nitric oxide synthase activity was significantly decreased for up to 14 days. Treatment for seven days with the free radical scavenger, TEMPOL, decreased by 68% the damage induced by iodoacetamide.Gastric damage induced by iodoacetamide, a sulphydryl alkylator, accompanied by inhibition of nitric oxide synthase activity shows the important contribution of sulphydryl compounds and nitric oxide to the maintenance of gastric mucosal integrity. Nitric oxide donation and scavenging of free radicals may be a novel approach to prevent gastric damage.
Activation of the Jak3 pathway is associated with granulocytic differentiation of myeloid precursor cells
Authors: Sushil G. Rane, James K. Mangan, Arshad Amanullah, Brian C. Wong, Renu K. Vora, Dan A. Liebermann, Barbara Hoffman, Xavier Graña, E. Premkumar Reddy
Journal: Blood (2002)
Nitric Oxide Inhibits Capacitative Cation Influx in Human Platelets by Promoting Sarcoplasmic/Endoplasmic Reticulum Ca <sup>2+</sup> -ATPase–Dependent Refilling of Ca <sup>2+</sup> Stores
Authors: Elena S. Trepakova, Richard A. Cohen, Victoria M. Bolotina
Journal: Circulation Research (1999)

Abstract —Nitric oxide (NO) is a potent inhibitor of thrombin-induced increase in cytoplasmic free Ca 2+ concentration and aggregation in platelets, but the precise mechanism of this inhibition is unclear. To measure Ca 2+ /Mn 2+ influx in intact platelets and to monitor Ca 2+ uptake into the stores in permeabilized platelets, fura-2 was used. In intact platelets, maximal capacitative Ca 2+ and Mn 2+ influx developed rapidly (within 30 s) after fast release of Ca 2+ from the stores with thrombin (0.5 U/mL) or slowly (within 5 to 10 minutes) following passive Ca 2+ leak caused by inhibition of sarcoplasmic/endoplasmic reticulum Ca 2+ -ATPase (SERCA) with 30 μmol/L 2,5-di-( tert -butyl)-1,4-benzohydroquinone (BHQ). NO (1 μmol/L) inhibited capacitative Ca 2+ and Mn 2+ influx independently of the time after thrombin application. In contrast, the effect of NO on BHQ-induced Ca 2+ and Mn 2+ influx was observed only during the first few minutes after BHQ application and completely disappeared when capacitative cation influx reached its maximum. In Ca 2+ -free medium, NO reduced the peak Ca 2+ rise caused by thrombin and significantly promoted Ca 2+ back-sequestration into the stores. Both effects disappeared in the presence of BHQ. Inhibition of guanylate cyclase with H-(1,2,4) oxadiazolo(4,3-a) quinoxallin-1-one (10 μmol/L) attenuated but did not prevent the effects of NO on cytoplasmic free Ca 2+ concentration. Inhibition of Ca 2+ uptake by mitochondria did not change the effects of NO. In permeabilized platelets, NO accelerated back-sequestration of Ca 2+ into the stores after inositol-1,4,5-trisphosphate–induced Ca 2+ release or after addition of Ca 2+ (1 μmol/L) in the absence of inositol-1,4,5-trisphosphate. The effect of NO depended on the initial rate of Ca 2+ uptake and on the concentration of ATP and was abolished by BHQ, indicating the direct involvement of SERCA. These data strongly support the hypothesis that NO inhibits store-operated cation influx in human platelets indirectly via acceleration of SERCA-dependent refilling of Ca 2+ stores.
China sets out new 10 year health plan for women and children
Authors: J. Parry
Journal: BMJ (2011)

China’s chief administrative body, the State Council, has set out a 10 year plan for children and women, laying out more than 100 goals in seven areas for women and five for children, including health, education, and social welfare. The goals are issued every 10 years, and the current ones run from 2011 to 2020.

The goals in the “outline for the development of Chinese women” are wide ranging, from the general, such as ensuring access to good basic healthcare, to the specific, such as targets on maternal mortality and hospital births. 

Maternal mortality in China stood at 38 deaths per 100 000 live births in 2009, show World …
Iron deficiency is a key determinant of health‐related quality of life in patients with chronic heart failure regardless of anaemia status
Authors: Josep Comín‐Colet, Cristina Enjuanes, Gina González, Ainhoa Torrens, Mercè Cladellas, Oona Meroño, Nuria Ribas, Sonia Ruiz, Miquel Gómez, José Maria Verdú, Jordi Bruguera
Journal: European Journal of Heart Failure (2013)

To evaluate the effect of iron deficiency (ID) and/or anaemia on health-related quality of life (HRQoL) in patients with chronic heart failure (CHF).We undertook a post-hoc analysis of a cohort of CHF patients in a single-centre study evaluating cognitive function. At recruitment, patients provided baseline information and completed the Minnesota Living with Heart Failure questionnaire (MLHFQ) for HRQoL (higher scores reflect worse HRQoL). At the same time, blood samples were taken for serological evaluation. ID was defined as serum ferritin levels <100 ng/mL or serum ferritin <800 ng/mL with transferrin saturation <20%. Anaemia was defined as haemoglobin ≤12 g/dL. A total of 552 CHF patients were eligible for inclusion, with an average age of 72 years and 40% in NYHA class III or IV. The MLHFQ overall summary scores were 41.0 ± 24.7 among those with ID, vs. 34.4 ± 26.4 for non-ID patients (P = 0.003), indicating worse HRQoL. When adjusted for other factors associated with HRQoL, ID was significantly associated with worse MLHFQ overall summary (P = 0.008) and physical dimension scores (P = 0.002), whereas anaemia was not (both P > 0.05). Increased levels of soluble transferrin receptor were also associated with impaired HRQoL (P ≤ 0.001). Adjusting for haemoglobin and C-reactive protein, ID was more pronounced in patients with anaemia compared with those without (P < 0.001).In patients with CHF, ID but not anaemia was associated with reduced HRQoL, mostly due to physical factors.
Endoscopic ultrasound-guided fine-needle aspiration biopsy coupled with<i>KRAS</i>mutation assay to distinguish pancreatic cancer from pseudotumoral chronic pancreatitis
Authors: B. Bournet, A. Souque, P. Senesse, E. Assenat, M. Barthet, N. Lesavre, A. Aubert, D. O'Toole, P. Hammel, P. Levy, P. Ruszniewski, M. Bouisson, J. Escourrou, P. Cordelier, L. Buscail
Journal: Endoscopy (2009)

Background and study aims: Differential diagnosis between pancreatic adenocarcinoma (PADC) and pseudotumoral forms of chronic pancreatitis remains difficult. Mutation of KRAS oncogene is present in 75 % to 95 % of PADC. This study aimed to evaluate whether the combined analysis of KRAS mutation with cytopathological findings from endoscopic ultrasound-guided fine-needle aspiration biopsy (EUS-FNAB) might improve discrimination between PADC and chronic pancreatitis.
Effects of oral verapamil in patients with atrioventricular reentrant tachycardia incorporating an accessory pathway.
Authors: D Wu, H C Kou, S J Yeh, F C Lin, J S Hung
Journal: Circulation (1983)

In 14 patients with atrioventricular reentrant tachycardia incorporating an accessory pathway, electrophysiologic studies were performed before and serially at 0.5--1-hour intervals for 6 hours after the fourth dose of 80 mg of oral verapamil given every 6 hours. Verapamil increased both the longest atrial paced cycle length producing type 1 atrioventricular block and the effective refractory period of the atrioventricular conduction system at all measurements. Before verapamil, sustained tachycardia could be induced in all 14 patients. After verapamil, six patients had induction of echo beats alone at all measurements, and in eight patients nonsustained or sustained tachycardia could be induced, particularly after the fourth hour. Follow-up study with oral verapamil at the same dosage in 13 patients for 7 +/- 5 months (+/- SD) revealed that the six patients with induction of echo beats alone have been free of symptomatic arrhythmia, while six of the remaining eight patients had occasional attacks of sustained tachycardia. Thus, oral verapamil increases atrioventricular nodal refractoriness, with an effect lasting up to 6 hours. Electrophysiologic study performed 5-6 hours after verapamil can be used to predict clinical responses in patients with atrioventricular reentrant tachycardia.
366 EFFICACY AND SAFETY OF TRANSARTERIAL CHEMOEMBOLIZATION IN RECURRENT HEPATOCELLULAR CARCINOMA AFTER CURATIVE SURGICAL RESECTION
Authors: J.W. Choi, S.H. Ahn, Y.H. Paik, C.K. Lee, K.S. Lee, B.S. Moon, K.-H. Han, C.Y. Chon, Y.M. Moon, D.Y. Kim
Journal: Journal of Hepatology (2008)
The aging oesophagus
Authors: JAN TACK, GASTON VANTRAPPEN
Journal: Gut (1997)

Diagnosing and treating gastrointestinal disorders in elderly patients requires that the physician be acquainted with both psychological and physical alterations induced by aging. Diseases of the oesophagus in elderly patients may be associated with the classic complaints of dysphagia, regurgitation, chest pain, and heartburn. However, atypical presentations are more common in this age group, and there is a greater likelihood of concurrent disease that may confound the interpretation of symptoms. Elderly patients are also more susceptible to complications that may accompany inadequately treated or long-standing oesophageal disease, such as aspiration, malnutrition or Barrett’s adenocarcinoma.

Oesophageal function in elderly patients has been studied in several cross-sectional studies. Only one prospective study on the effect of aging on oesophageal function was reported, in a rather young group of healthy volunteers.1 Earlier literature suggested a rather common degeneration of oesophageal function with aging. The term presbyoesophagus was proposed to describe an age related decrease in contractile amplitude, polyphasic waves in the oesophageal body, incomplete sphincter relaxation, and oesophageal dilatation.2 This notion has been abandoned more recently as it was felt that most motility disorders in old age are related to medical problems that accumulate during aging, such as diabetes mellitus, neurological disorders and the intake of numerous drugs. Investigations in healthy elderly people have shown only minor to mild alterations in oesophageal motility.

A gradual decrease in upper oesophageal sphincter (UOS) pressure occurs with age, with a delay in UOS relaxation after deglutition.3 4 Pharyngeal contraction pressures and pharyngo-oesophageal wave velocity are notably increased.3 4 The changes are attributed to increased resistance to flow across the UOS as a result of loss of compliance with age. The sensory threshold for the initiation of deglutition may also be increased with age.5 

With increasing age, there is a significantly increased …