tbuckley/cabot-search huggingface dataset:
The Magic Mountain
Authors: T. Rutten
Journal: BMJ (2009)

The Magic Mountain tells the story of Hans Castorp, an “ordinary young man.” At the beginning of the novel Hans is on his way from Hamburg to Davos to visit his cousin, who is being treated for a lung complaint at one of the Swiss resort’s sanatoriums. As the tale unfolds, Hans’s intended three week visit turns into a seven year stint at the sanatorium, which ends only when Hans is catapulted into the Flanders battlefields at the outbreak of the first world war. 

To this day The Magic Mountain ranks among the best selling titles of its German publisher, Fischer Verlag, which recently reissued the novel in a new edition with a separate volume of detailed annotations.1 The swiftly commissioned English translation, published in 1927, as well as Mann’s considerable international reputation2 (he was awarded the Nobel prize for literature in 1929), no doubt contributed to the book’s early worldwide success. Variously labelled a bildungsroman or a tuberculosis or sanatorium novel, and in terms of genre classified as an intellectual novel, it soon attracted doctors and patients as readers and, indeed, early critics. As recently …
Prevention of Exercise-induced Asthma by Indoramin
Authors: S. Bianco, J. P. Griffin, P. L. Kamburoff, F. J. Prime
Journal: BMJ (1974)

Indoramin, an alpha-adrenoceptor blocking drug, has been found to prevent the occurrence of exercise-induced bronchoconstriction. Evidence is provided in two cases that this was not due to the antihistamine properties of indoramin.
GW25-e1524 SIRT1-Mediated Epigenetic Downregulation of Plasminogen Activator Inhibitor-1 Prevents Vascular Endothelial Replicative Senescence
Authors: Chen Houzao, Wan Yanzhen, Gao Peng, Zhou Shuang, Zhang Zhuqin, Hao Delong, Lian Lishan, Li Yongjun, Liu Depei
Journal: Journal of the American College of Cardiology (2014)
Interleukin-18 levels suggest different inflammatory pathways in unstable angina
Authors: Luigi M. Biasucci, Matteo Santamaria, Dominick J. Angiolillo, Giobanna Di Giannuario, Giulia Aguzzi, Maria Elena Lombardi, Donatella Lomaglio, Giobanna Liuzzo, Attilio Maseri, Charles A. Dinarello, Filippo Crea
Journal: Journal of the American College of Cardiology (2003)
Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation
Authors: Marc A.R.C. Daemen, Cornelis van ‘t Veer, Geertrui Denecker, Vincent H. Heemskerk, Tim G.A.M. Wolfs, Matthias Clauss, Peter Vandenabeele, Wim A. Buurman
Journal: Journal of Clinical Investigation (1999)

Ischemia followed by reperfusion leads to severe organ injury and dysfunction. Inflammation is considered to be the most important cause of tissue injury in organs subjected to ischemia. The mechanism that triggers inflammation and organ injury after ischemia remains to be elucidated, although different causes have been postulated. We investigated the role of apoptosis in the induction of inflammation and organ damage after renal ischemia. Using a murine model, we demonstrate a relationship between apoptosis and subsequent inflammation. At the time of reperfusion, administration of the antiapoptotic agents IGF-1 and ZVAD-fmk (a caspase inactivator) prevented the early onset of not only renal apoptosis, but also inflammation and tissue injury. Conversely, when the antiapoptotic agents were administered after onset of apoptosis, these protective effects were completely abrogated. The presence of apoptosis was directly correlated with posttranslational processing of the endothelial monocyte-activating polypeptide II (EMAP-II), which may explain apoptosis-induced influx and sequestration of leukocytes in the reperfused kidney. These results strongly suggest that apoptosis is a crucial event that can initiate reperfusion-induced inflammation and subsequent tissue injury. The newly described pathophysiological insights provide important opportunities to effectively prevent clinical manifestations of reperfusion injury in the kidney, and potentially in other organs.
The role of single cell derived vascular resident endothelial progenitor cells in the enhancement of vascularization in scaffold-based skin regeneration
Authors: Ziyang Zhang, Wulf D. Ito, Ursula Hopfner, Björn Böhmert, Mathias Kremer, Ann K. Reckhenrich, Yves Harder, Natalie Lund, Charli Kruse, Hans-Günther Machens, José T. Egaña
Journal: Biomaterials (2011)
Abstract 1722: Multidrug resistant P-glycoprotein mediates through Src-EGFR cascade to attenuate DNA-PK-mediated DNA repair
Authors: Pei-Chih Lee, Tsann-Long Su, Te-Chang Lee
Journal: Cancer Research (2011)

Abstract We have synthesized several novel bifunctional alkylating derivatives of 3a-aza-cyclopenta[a]inden (BO-1012, BO-1005, BO-1099, and BO-1101) and demonstrated that they were more cytotoxic to multidrug resistant (MDR) cells, such as KBvin10, KBtax50, and CEM/VBL, than their parental cells. Using xenograft model, we confirmed that BO-1012 was more effective to suppress the growth of MDR KBvin10 cells in nude mice than to the parental KB cells. To explore the possible mechanism, we revealed that KBvin10 and CEM/VBL MDR cells have significantly lower repair activity than KB and CEM parental cells. Our results also showed that reduced repair activity in KBvin10 cells was likely due to the defective in translocation of DNA-PK, a component of repair machinery of non-homologous end-joining, from cytosol into nucleus. Furthermore, we found that BO-1012 could activate Src kinase and trigger nuclear transport of EGFR in parental cells but not in MDR cells. Inhibition of Src resulted in suppression of BO-1012-induced EGFR translocation and consequently sensitized the parental cells to BO-1012. On the contrary, Src activation induced by BO-1012 was revived in MDR cells by using siRNA to reduce the expression of P-glycoprotein (P-gp). Meanwhile, P-gp silencing also facilitated the EGFR translocation and DNA repair in MDR cells treated with BO-1012. Taken together, our results demonstrated that overexpression of P-gp in MDR cells mediates through inhibition of Src-EGFR pathway to attenuate the DNA-PK-mediated repair. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1722. doi:10.1158/1538-7445.AM2011-1722
Intramural myocardial shortening in hypertensive left ventricular hypertrophy with normal pump function.
Authors: L C Palmon, N Reichek, S B Yeon, N R Clark, D Brownson, E Hoffman, L Axel
Journal: Circulation (1994)

BACKGROUND In hypertensive left ventricular hypertrophy (LVH), intrinsic myocardial systolic function may be normal or depressed. Magnetic resonance tagging can depict intramural myocardial shortening in vivo. METHODS AND RESULTS Tagged left ventricular magnetic resonance images were obtained in 30 hypertensive subjects with LVH (mean LV mass index, 142 +/- 41 g/m) and normal ejection fraction (mean, 64 +/- 9%) using spatial modulation of magnetization. In 26 subjects, circumferential myocardial shortening (%S) was compared with results obtained in 10 normal subjects at endocardium, midwall, and epicardium on up to 4 short-axis slices each. Similarly, in 10 subjects, midwall long-axis shortening at basal, midventricular, and apical sites was compared with results obtained in 12 normal volunteers. Circumferential %S was reduced in hypertensive subjects. Mean shortening was 29 +/- 6% at the endocardium in hypertensive subjects versus 44 +/- 6% in normal subjects (P = .0001); 20 +/- 6% at the midwall versus 30 +/- 6% (P = .0001); and 13 +/- 5% at the epicardium versus 21 +/- 5% (P = .0002). However, the transmural gradient in percent shortening from endocardium to epicardium in hypertensive subjects paralleled that in normal subjects. The normal base-to-apex gradient in circumferential %S was absent in LVH. In contrast to normal subjects, circumferential %S showed regional heterogeneity in hypertensive subjects, being maximal in the lateral wall and least in the inferior wall. Longitudinal shortening was also uniformly depressed in hypertensive subjects: 10 +/- 9% at the base versus 21 +/- 6% in normal subjects (P = .0001); 14 +/- 8% at the midventricle versus 18 +/- 3% (P = .03); and 14 +/- 8% at the apex versus 18 +/- 4% (P = .04). CONCLUSIONS In hypertensive LVH with normal pump function, intramural circumferential and longitudinal myocardial shortening are depressed.
P83FAs mediate cardiac hypertrophic response to exercise
Authors: S Brix, A Foryst-Ludwig, J Salatzki, E Januszewicz, M Rothe, E Kershaw, U Kintscher
Journal: Cardiovascular Research (2014)

We have previously showed that both exercise-induced lipolytic activity in adipose tissue and cardiac hypertophic response to training were significantly reduced in adipose tissue specific -ATGL-KO mice (atATGL-KO) mice. It was accompanied by the absence of plasma fatty acid increases in those mice. To identify the underlying mechanisms of physiological cardiac hypertrophy mediated by variations of plasma lipid concentrations in atATGL-KO mice, we performed a comprehensive analysis of circulating lipid species using Rapid Resolution HPLC/ Tandem MS. Selected fatty acids, such as C16:1 (palmitoleic acid), were increased in trained wt mice but not in atATGL-KO mice, whereas others were similarly regulated in both genotypes. To investigate the role of FAs in vitro we stimulated murine cardiomyocytic HL-1 cells with a FA-mixture containing C14:0, C16:0 and C16:1 (equimolar concentrations as determined in post-exercise serum), or with C16:1 alone, and analyzed cellular hypertrophy. The FA-mixture, and more importantly, C16:1 alone effectively induced cardiomyocyte hypertrophy in exercise-relevant plasma concentrations, suggesting that C16:1 liberated from adipose tissue serves as molecular mediator of training-induced cardiac hypertrophic. Moreover, the mRNA expression of the atrial natriuretic factor (ANF) and beta-cardiac myosin heavy chain isogene (beta-MHCH), both markers of pathological hypertrophy, was not increased under C16:1-stimulation. Collectively, our data provide the first evidence that the adipose tissue – heart crosstalk involving AT-lipolysis, cardiac FA-uptake, and FA-mediated cardiac hypertrophy determines the morphological adaptation of the exercising heart. Palmitoleic acid, released from adipose tissue in an ATGL-dependent manner, serve as molecular mediators of exercise-induced cardiac hypertrophy.
Regulation of Na,K-ATPase gene expression by thyroid hormone in rat cardiocytes.
Authors: T Kamitani, U Ikeda, S Muto, K Kawakami, K Nagano, Y Tsuruya, A Oguchi, K Yamamoto, Y Hara, T Kojima
Journal: Circulation Research (1992)

Synthesis and activity of the enzymatic equivalent of the sodium pump, Na,K-ATPase, are regulated by thyroid hormone in responsive tissues. The purpose of this study was to determine whether triiodothyronine (T3) regulates the level of the messenger RNA (mRNA) coding for Na,K-ATPase alpha- and beta-subunits in the heart. The expression of Na,K-ATPase mRNAs in in vitro myocardial cells was directly assayed by Northern and slot blot hybridization using Na,K-ATPase alpha- and beta-isoform-specific cDNA probes. Exposure of cultured neonatal rat cardiocytes to 10(-8) M T3 resulted in 1) threefold to fourfold increase in alpha 1- and beta 1-mRNA accumulation, with a maximum elevation at 48 hours, 2) sevenfold increase in alpha 2-mRNA accumulation with a peak elevation at 72 hours, and 3) transient threefold increase in alpha 3-mRNA within the first 24 hours followed by a deinduction thereafter. The increase in alpha 1-mRNA accumulation by T3 occurred over the physiological T3 concentration range with an EC50 of 5 x 10(-10) M. This was associated with a twofold increase in alpha 1-subunit protein accumulation and an increase in Na,K-ATPase transport activity. The half-life of alpha 1-mRNA analyzed by actinomycin D chase was less than 3 hours and was not affected by T3. Transfection experiments with the luciferase reporter gene revealed that thyroid hormone response sequences are located within the 5'-flanking regions of each alpha-isoform gene.(ABSTRACT TRUNCATED AT 250 WORDS)
Corticotropin-releasing hormone, proopiomelanocortin, and glucocorticoid receptor gene expression in adrenocorticotropin-producing tumors in vitro.
Authors: T Suda, F Tozawa, I Dobashi, N Horiba, N Ohmori, M Yamakado, M Yamada, H Demura
Journal: Journal of Clinical Investigation (1993)

To differentiate between ectopic ACTH syndrome and Cushing's disease, gene expression of corticotropin-releasing hormone (CRH), proopiomelanocortin (POMC), and glucocorticoid receptor was examined in 10 pituitary adenomas (Cushing's disease) and in 10 ectopic ACTH-producing tumors. CRH increased plasma ACTH levels in all patients with Cushing's disease and in five patients with ectopic ACTH syndrome whose tumors contained CRH and CRH mRNA. In five CRH nonresponders, CRH was not detected in tumors that contained no CRH mRNA or that contained only long-size CRH mRNA. Dexamethasone (Dex) decreased plasma ACTH levels in all patients with Cushing's disease and in three patients with ectopic ACTH-producing bronchial carcinoid. These tumors contained glucocorticoid receptor mRNA. CRH increased and Dex decreased ACTH release and POMC mRNA levels in pituitary adenoma and bronchial carcinoid cells. PMA increased POMC mRNA levels only in carcinoid cells. These results reveal characteristics of ectopic ACTH-producing tumors: long-size CRH mRNA and PMA-induced POMC gene expression. In addition, there are two ectopic ACTH syndrome subtypes: tumors containing ACTH with CRH (CRH responder) and tumors without CRH. Dex decreases ACTH release and POMC mRNA levels in some bronchial carcinoids. Therefore, CRH and Dex tests have limited usefulness in differentiating between Cushing's disease and ectopic ACTH syndrome.
Control of Cyclin D1 and Breast Tumorigenesis by the EglN2 Prolyl Hydroxylase
Authors: Qing Zhang, Jinming Gu, Lianjie Li, Jiayun Liu, Biao Luo, Hiu-Wing Cheung, Jesse S. Boehm, Min Ni, Christoph Geisen, David E. Root, Kornelia Polyak, Myles Brown, Andrea L. Richardson, William C. Hahn, William G. Kaelin, Archana Bommi-Reddy
Journal: Cancer Cell (2009)
Risks of Morbidity and Mortality in Dialysis Patients Undergoing Coronary Artery Bypass Surgery
Authors: Jean Y. Liu, Nancy J. O. Birkmeyer, John H. Sanders, Jeremy R. Morton, Horace F. Henriques, Stephen J. Lahey, Richard W. Dow, Christopher Maloney, Anthony W. DiScipio, Robert Clough, Bruce J. Leavitt, Gerald T. O’Connor
Journal: Circulation (2000)

Background —Although dialysis patients are undergoing CABG with increasing frequency, large studies specifically comparing patient characteristics and procedure-related risks in this population have not been performed. Methods and Results —We conducted a regional prospective cohort study of 15 500 consecutive patients undergoing CABG in northern New England from 1992 to 1997. We used multiple logistic regression analysis to examine associations between preoperative dialysis-dependent renal failure and postoperative events and to adjust for potentially confounding variables. The 279 dialysis-dependent renal failure patients (1.8%) were 4.4 times more likely to experience in-hospital mortality than were other CABG patients (12.2% versus 3.0%, respectively; P &lt;0.001). Dialysis-dependent renal failure patients were older and had more comorbidities and more severe cardiac disease than did other CABG patients. After adjusting for these factors in multivariate analysis, however, dialysis-dependent renal failure patients remained 3.1 times more likely to die after CABG (adjusted odds ratio [OR] 3.1, 95% CI 2.1 to 4.7; P &lt;0.001). Dialysis-dependent renal failure patients compared with other CABG patients also had a substantially increased risk of postoperative mediastinitis (3.6% versus 1.2%, respectively; adjusted OR 2.4, 95% CI 1.2 to 4.7; P =0.011) and postoperative stroke (4.3% versus 1.7%, respectively; adjusted OR 2.1, 95% CI 1.1 to 3.9; P =0.016), even after controlling for potentially confounding variables. Risks of reexploration for bleeding were similar for patients with and without dialysis-dependent renal failure. Conclusions —Preoperative dialysis-dependent renal failure is a strong independent risk factor for in-hospital mortality and mediastinitis after CABG.
Coal gas and the brain.
Authors: H. Matthew, A. T. Proudfoot
Journal: BMJ (1968)

BRITIsHrehabilitation situation that the more severely incapacitated are treated alongside the less handicapped, as this not only constitutes a stimulus to the patients but also to the staff engaged in this work.This review of the present situation is un- doubtedly timely, and one must hope sincerely that the obvious points emerging from it will neither be ignored nor be given the implica- tion that a rash of rehabilitation centres is required.Such rapid expansion is neither economically possible nor entirely desirable.The growth of rehabilitation requires to be carefully planned not only on a regional basis but as part of a carefully designed national policy.
Incidental Finding of Autosomal Dominant Polycystic Kidney Disease With Liver Involvement on Tc-99m Sestamibi Scintigraphy
Authors: Chih-Yung Chang, Ko-Han Lin, Yum-Kung Chu, Cheng-Pei Chang, Ren-Shyan Liu, Shih-Jen Wang
Journal: Clinical Nuclear Medicine (2011)

Autosomal dominant polycystic kidney disease is a systemic hereditary disease characterized by renal cysts and sometimes involvement of the liver. We present a 65-year-old woman with autosomal dominant polycystic kidney disease on regularly hemodialysis who recently experienced intermittent right upper quadrant abdominal pain and elevated intact parathyroid hormone for more than a year. She was referred for double-phase Tc-99m sestamibi scintigraphy, under the impression of hyperparathyroidism. Apart form increased uptake in the right thyroid bed, the images showed a large photon-deficient area in the upper portion of the abdomen corresponding to the liver.
Triphasic decline of hepatitis C virus RNA during antiviral therapy
Authors: Harel Dahari, Ruy M. Ribeiro, Alan S. Perelson
Journal: Hepatology (2007)

Abstract When patients chronically infected with hepatitis C virus (HCV) are placed on antiviral therapy with pegylated interferon (IFN)-α or IFN-α plus ribavirin (RBV), HCV RNA generally declines in a biphasic manner. However, a triphasic decline has been reported in a subset of patients. A triphasic decline consists of a first phase (1-2 days) with rapid virus load decline, followed by a “shoulder phase” (4-28 days) in which virus load decays slowly or remains constant, and a third phase of renewed viral decay. We show that by including the proliferation of both uninfected and infected cells, a viral kinetic model can account for a triphasic HCV RNA decay. The model predicts that a triphasic decline occurs only in patients in which a majority of hepatocytes are infected before therapy. The shoulder phase does not represent the intrinsic death rate of infected cells, but rather the third phase slope is close to the intrinsic death rate of infected cells when overall drug efficacy is close to 1. Conclusion: Triphasic responses can be predicted from a generalization of existent viral kinetic models through the inclusion of homeostatic proliferation of hepatocytes. This generalized model can also explain the viral kinetics seen in flat partial responders. Finally, the enhanced third phase in patients treated with IFN-α in combination with RBV versus patients treated with IFN-α alone can be explained by a mutagenic effect of RBV against HCV. (HEPATOLOGY 2007;46:16–21.)
Improved performance of urinary biomarkers of acute kidney injury in the critically ill by stratification for injury duration and baseline renal function
Authors: Zoltán H. Endre, John W. Pickering, Robert J. Walker, Prasad Devarajan, Charles L. Edelstein, Joseph V. Bonventre, Christopher M. Frampton, Michael R. Bennett, Qing Ma, Venkata S. Sabbisetti, Vishal S. Vaidya, Angela M. Walcher, Geoffrey M. Shaw, Seton J. Henderson, Maryam Nejat, John B.W. Schollum, Peter M. George
Journal: Kidney International (2011)
Author's reply to Bernard and Grayson
Authors: R. Chou
Journal: BMJ (2012)

Bernard and Grayson both suggest that an editorial on drugs for sciatica/radiculopathy should have addressed surgery and epidural steroid injections.1 2 However, both my editorial and the systematic review it commented on focused on the benefits and harms of systemic drugs.3 4 Other types of treatment for sciatica, including surgery and epidural steroids, have been …
Hypercalcemia: A Possible Cause for Elevated Serum Lysozyme Levels
Authors: IRA M. GOLDSTEIN
Journal: Annals of Internal Medicine (1976)

Letters1 April 1976Hypercalcemia: A Possible Cause for Elevated Serum Lysozyme LevelsIRA M. GOLDSTEIN, M.D., F.A.C.P., JAN K. HORN, B.S., HOWARD B. KAPLAN, M.S., ROY SOBERMAN, M.D., GERALD WEISSMANN, M.D.IRA M. GOLDSTEIN, M.D., F.A.C.P.Search for more papers by this author, JAN K. HORN, B.S.Search for more papers by this author, HOWARD B. KAPLAN, M.S.Search for more papers by this author, ROY SOBERMAN, M.D.Search for more papers by this author, GERALD WEISSMANN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-84-4-445 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptLysozyme is a normal constituent of the cytoplasmic granules (lysosomes) of human peripheral blood polymorphonuclear leukocytes (1). We have recently found that these cells can be stimulated to release, or secrete, a portion of their lysozyme activity when exposed to ionized calcium (at concentrations as low as 0.01 mM) (2, 3). Since it was possible that conditions for such lysozyme release could occur in vivo, we elected to study serum lysozyme activity in patients with various disorders associated with hypercalcemia.Serum samples were obtained from 16 patients with hypercalcemia (6 with primary hyperparathyroidism and 10 with nonhematologic malignancies). Total serum...References1. SPITZNAGELDALLDORFLEFFELL JFM: Character of azurophil and specific granules purified from human polymorphonuclear leukocytes. Lab Invest 30:774-785, 1974 MedlineGoogle Scholar2. GOLDSTEINHORNKAPLAN IJH: Calcium-induced lysozyme secretion from human polymorphonuclear leukocytes. Biochem Biophys Res Comm 60:807-812, 1974 CrossrefMedlineGoogle Scholar3. GOLDSTEINHOFFSTEINWEISSMAN ISG: Influence of divalent cations upon complement-mediated enzyme release from human polymorphonuclear leukocytes. J Immunol 115:665-670, 1975 MedlineGoogle Scholar4. Worthington Enzyme Manual. Freehold, New Jersey, Worthington Biochemical Corporation, 1972, p. 100 Google Scholar5. RUBIN R: The role of calcium in the release of neurotransmitter substances and hormones. Pharmacol Rev 22:389-428, 1970 MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York University Medical Center 550 First Ave. New York, New York 10016 Belle vue Hospital Center (Dr. Soberman) 27th St. and First Ave. New York, New York 10016 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySerum and tissue lysozyme in leprosyLysozyme and HypercalcaemiaP. J. PHILLIPS, R. W. PAIN, J. LLOYDLysozyme from Bone?REUBIN EISENSTEIN, M.D., KLAUS E. KUETTNER, PH.D. 1 April 1976Volume 84, Issue 4Page: 445-446KeywordsAttentionBloodCalciumCellsHypercalcemiaHyperparathyroidismLysosomesLysozymeNeutrophils ePublished: 1 December 2008 Issue Published: 1 April 1976 PDF downloadLoading ...