tbuckley/cabot-search huggingface dataset:
Cancer chemoprevention and therapy by monoterpenes.
Authors: M N Gould
Journal: Environmental Health Perspectives (1997)

Monoterpenes are found in the essential oils of many plants including fruits, vegetables, and herbs. They prevent the carcinogenesis process at both the initiation and promotion/progression stages. In addition, monoterpenes are effective in treating early and advanced cancers. Monoterpenes such as limonene and perillyl alcohol have been shown to prevent mammary, liver, lung, and'other cancers. These compounds have also been used to treat a variety of rodent cancers, including breast and pancreatic carcinomas. In addition, in vitro data suggest that they may be effective in treating neuroblastomas and leukemias. Both limonene and perillyl alcohol are currently being evaluated in phase I clinical trials in advanced cancer patients. The monoterpenes have several cellular and molecular activities that could potentially underlie their positive therapeutic index. The monoterpenes inhibit the isoprenylation of small G proteins. Such inhibitions could alter signal transduction and result in altered gene expression. The results of a new gene expression screen-subtractive display-have identified or confirmed several up- or downregulated genes in regressing mammary carcinomas. For example, these regressing tumors overexpress the mannose 6-phosphate/IGF II receptor. The product of the gene both degrades the mammary tumor mitogen IGF II and activates the cytostatic factor TGF-beta. These and other alterations in the gene expression of mammary carcinomas lead to a G1 cell cycle block, followed by apoptosis, redifferentiation, and finally complete tumor regression in which tumor parenchyma is replaced by stromal elements. It is likely that monoterpenes prevent mammary cancer during their progression stage by mechanisms similar to those that occur during therapy. In contrast, prevention of mammary cancer by polycyclic hydrocarbons such as 7,12-dimethylbenz[a]anthracene occur by the induction of detoxifying phase II hepatic enzymes.
Carabin Protects Against Cardiac Hypertrophy by Blocking Calcineurin, Ras, and Ca <sup>2+</sup> /Calmodulin-Dependent Protein Kinase II Signaling
Authors: Malik Bisserier, Magali Berthouze-Duquesnes, Magali Breckler, Florence Tortosa, Loubina Fazal, Annélie de Régibus, Anne-Coline Laurent, Audrey Varin, Alexandre Lucas, Maxime Branchereau, Pauline Marck, Jean-Nicolas Schickel, Claudine Deloménie, Olivier Cazorla, Pauline Soulas-Sprauel, Bertrand Crozatier, Eric Morel, Christophe Heymes, Frank Lezoualc’h
Journal: Circulation (2014)

Background— Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and is regulated by various signaling pathways. However, the molecular mechanisms that negatively regulate these signal transduction pathways remain poorly understood. Methods and Results— Here, we characterized Carabin, a protein expressed in cardiomyocytes that was downregulated in cardiac hypertrophy and human heart failure. Four weeks after transverse aortic constriction, Carabin-deficient (Carabin −/− ) mice developed exaggerated cardiac hypertrophy and displayed a strong decrease in fractional shortening (14.6±1.6% versus 27.6±1.4% in wild type plus transverse aortic constriction mice; P &lt;0.0001). Conversely, compensation of Carabin loss through a cardiotropic adeno-associated viral vector encoding Carabin prevented transverse aortic constriction–induced cardiac hypertrophy with preserved fractional shortening (39.9±1.2% versus 25.9±2.6% in control plus transverse aortic constriction mice; P &lt;0.0001). Carabin also conferred protection against adrenergic receptor–induced hypertrophy in isolated cardiomyocytes. Mechanistically, Carabin carries out a tripartite suppressive function. Indeed, Carabin, through its calcineurin-interacting site and Ras/Rab GTPase–activating protein domain, functions as an endogenous inhibitor of calcineurin and Ras/extracellular signal-regulated kinase prohypertrophic signaling. Moreover, Carabin reduced Ca 2+ /calmodulin-dependent protein kinase II activation and prevented nuclear export of histone deacetylase 4 after adrenergic stimulation or myocardial pressure overload. Finally, we showed that Carabin Ras–GTPase–activating protein domain and calcineurin-interacting domain were both involved in the antihypertrophic action of Carabin. Conclusions— Our study identifies Carabin as a negative regulator of key prohypertrophic signaling molecules, calcineurin, Ras, and Ca 2+ /calmodulin-dependent protein kinase II and implicates Carabin in the development of cardiac hypertrophy and failure.
The erythemal action spectrum and deoxyribonucleic acid repair synthesis in xeroderma pigmentosum
Authors: C.A. RAMSAY, F. GIANNELLI
Journal: British Journal of Dermatology (2006)

The reactions to monochromatic radiation of the skin of ten patients with xeroderma pigmentosum were investigated, and eight were abnormal. The abnormalities consisted of papular and vesicular reactions and delay in the development of the minimal erythema dose reaction with wavelengths principally in the 290-320 nm range. Three patients were too young for full action spectra to be obtained but of those patients in whom all wavelengths were tested only one showed a reaction to radiation above 320 nm and this was at 340 nm only. In only one patient was the minimal erythema dose at 300 nm at 24 h lower than normal. In six patients the repair synthesis of deoxyribonucleic acid after ultraviolet radiation was estimated. Reduced levels were seen in five but repair was normal in one patient. The patient with normal repair also had normal reactions to monochromatic radiation. The abnormal reaction of the skin to artificial radiation and the abnormal deoxyribonucleic acid repair synthesis may enable the diagnosis of xeroderma pigmentosum to be made at a very early age. In one of the patients the diagnosis was made at the age of 6 months in a child with photosensitivity but with no other clinical signs of the disease. It is suggested that, by making the diagnosis as early as possible and by protecting the skin from natural sunlight, cutaneous malignancies may be prevented.
Efficient construction of producer cell lines for a SIN lentiviral vector for SCID-X1 gene therapy by concatemeric array transfection
Authors: Robert E. Throm, Annastasia A. Ouma, Sheng Zhou, Anantharaman Chandrasekaran, Timothy Lockey, Michael Greene, Suk See De Ravin, Morvarid Moayeri, Harry L. Malech, Brian P. Sorrentino, John T. Gray
Journal: Blood (2009)
Human thymus antigen: Characterization and its expression on human leukemias
Authors: Junichiro Fujimoto, Yoshifumi Ishii, Hirofumi Koshiba, Akihiro Matsuura, Minoru Ogasawara, Toshimitsu Uede, Kokichi Kikuchi
Journal: American Journal of Hematology (1981)

Specific anti-human thymus xenoantiserum (ATS) was utilized for characterizing a human thymus antigen (HTA) preferentially expressed on human thymocytes. Binding of ATS with different cell types was studied by immunofluorescence and immunoperoxidase techniques, as well as by radioimmunoprecipitation (RIP) followed by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). ATS reacted selectively with the majority (87%) of human thymocytes among normal lymphoid cell populations tested. In the thymus, HTA was expressed largely on cortical thymocytes but not on those cells located in the thymic medulla. When 20 cases of different types of lymphatic leukemias were studied with ATS, HTA was found on acute lymphoblastic leukemia cells rosetting with sheep erythrocytes (T-ALL) but not on other lymphatic leukemia cases, including chronic lymphocytic leukemia cells rosetting with sheep red blood cells (T-CLL). SDS-PAGE analysis of immunoprecipitates formed between ATS and radiolabeled cell-surface components of human thymocytes demonstrated that ATS bound a 48,000-molecular-weight component that could be adsorbed to Sepharose 4B coupled with Les culinaris hemagglutinin and could be labeled by periodate-tritiated borohydride, indicating that HTA is a sialoglycoprotein. Similar antigen molecules were also precipitated by ATS from T-ALL cells but not from other lymphatic leukemia cells. Five T-ALL-derived cell lines were tested with ATS by immunofluorescence and by RIP and SDS-PAGE, but only two cell lines (MOLT-3 and P12/Ich) possessed HTA molecules on their cell membrane.
Salmeterol attenuates the inflammatory response in asthma and decreases the pro-inflammatory cytokine secretion of dendritic cells
Authors: Zhenli Hu, Ruohua Chen, Zhijian Cai, Lei Yu, Yang Fei, Lixia Weng, Jinghan Wang, Xiahui Ge, Tianyi Zhu, Jianli Wang, Chong Bai
Journal: Cellular and Molecular Immunology (2012)
COMPARISON OF TRANSFEMORAL AND TRANSAPICAL AORTIC VALVE REPLACEMENT: RESULTS OF THE GERMAN REGISTRY ON TRANSCATHETER AORTIC VALVE IMPLANTATIONS
Authors: Ulrich Gerckens, Harald Mudra, Gerhard C. Schuler, Ralf Zahn, Horst Sievert, Raimund Erbel, Rainer Hambrecht, Georg Nickenig, Karl-Eugen Hauptmann, Christoph Naber, Hans Rainer Figulla, Stefan Sack, Jochen Senges, Lutz Buellesfeld, Eberhard Grube
Journal: Journal of the American College of Cardiology (2010)
Serial prothrombin time as prognostic indicator in paracetamol induced fulminant hepatic failure.
Authors: P M Harrison, J G O'Grady, R T Keays, G J Alexander, R Williams
Journal: BMJ (1990)

OBJECTIVE--To find out whether changes in the daily prothrombin time are of prognostic importance in patients with paracetamol induced fulminant hepatic failure. DESIGN--Retrospective study. SETTING--The Liver Unit, King9s College Hospital, London. PATIENTS--150 Consecutive patients with paracetamol induced fulminant hepatic failure admitted between October 1986 and February 1989. MAIN OUTCOME MEASURE--Death. RESULTS--Of the 150 patients, 72 (48%) died. In all, 34 of the 37 (92%) patients with a peak prothrombin time of greater than or equal to 180 seconds died as did 20 of the 41 (49%) with a time of 130-179 seconds, nine of the 25 (36%) with a time of 90-129 seconds, and nine of the 47 (19%) with a time of less than 90 seconds. Of the 42 patients with a continuing rise in prothrombin time between days 3 and 4 after overdose, 39 died (93%) compared with 21 of the 96 (22%) in whom the prothrombin time fell. CONCLUSIONS--These data indicate that a continued increase in prothrombin time on day 4 after overdose and a peak prothrombin time of greater than or equal to 180 seconds identify at an early stage those patients with a less than 8% chance of survival. Liver transplantation should be considered in patients meeting either of these criteria.
ACTH Secretion from a Functioning Pheochromocytoma
Authors: Richard F. Spark, Peter B. Connolly, Doreen S. Gluckin, Robert White, Barry Sacks, Lewis Landsberg
Journal: New England Journal of Medicine (1979)

A PATIENT with hypertension, hirsutism, hyperglycemia, hypokalemic alkalosis and a transient paranoid psychosis was found to have hypercortisolism and increased excretion of catecholamines secondary to an ACTH-secreting pheochromocytoma. Fluctuations in plasma ACTH levels coincided with variations in urinary catecholamine excretion, suggesting that a common factor regulated peptide and catecholamine secretion in this patient. Adrenal-vein sampling revealed fourfold elevations in left-adrenal-vein ACTH and 10-fold elevations in left-adrenal-vein norepinephrine, when these values were compared with samples from the right adrenal vein and peripheral blood. After surgical removal of the left adrenal gland, urinary catecholamine levels returned to the normal range, whereas levels . . .
Critical Care Evidence—New Directions
Authors: John J. Marini, Jean-Louis Vincent, Djillali Annane
Journal: JAMA (2015)

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
Generalized peritonitis due to spontaneous intraperitoneal rupture of pyeonephrosis.
Authors: I. B. Tiwari
Journal: BMJ (1966)

Acute Non-specific syndrome; it has also been described in Reiter's disease (Csonka and Oates, 1957).It is important to exclude other common causes of pericarditis such as rheumatic fever, myocardial infarction, collagen disorders, and neoplastic disease.All patients in the present series were given purely supportive therapy with analgesics and bed rest.No antibiotics or corticosteroids were used, and all patients made relatively rapid and uneventful recoveries. SummaryNineeteen cases of acute non-specific pericarditis are presented, the majority of which were seen in one hospital within one year.It would appear that the illness is much more common than previous reports would indicate.The importance of differentiating acute non-specific pericarditis from myocardial infarction is discussed.Pericarditis can be diagnosed only when either a pericardial friction rub is heard or the electro- cardiograph shows S-T segment elevation without pathological Q-waves or S-T segment depression in the reciprocal leads.Premonitory chest pain is an important finding in acute non- specific pericarditis.The blood sedimentation rate is usually accelerated, but a neutrophilia in the peripheral blood film occurs in less than half the cases.All the present cases made a uniformly good recovery.
Abstract 437: A putative role of hypoxia in development of de novo chemoresistance
Authors: Ariosto S. Silva, Robert A. Gatenby
Journal: Cancer Research (2010)

Abstract In this work we built a computational model that explores the concept of hypoxia induced de novo chemoresistance. We propose that the hypoxic regions of solid tumors not only protect tumor cells from chemotherapy (environmental resistance) but also are the birthplace of de novo multidrug phenotypically chemoresistant cells. These phenotypically resistant cells would be rare in an untreated tumor due to hypoxia and low external pH (pHe) induced quiescence in the environment where they grow. These cells, however, would be subject to a selective pressure for survival by disruption of apoptotic pathways and overexpression of hypoxia-inducible factors which are known to activate multidrug resistance genes, among other pro-survival mechanisms. Tumor cells under chronic hypoxic conditions are also subject to higher genetic instability than tumor cells in normoxia, due in part to the decrease in the expression of homologous recombination proteins, what could also increase the rate of evolution towards a multi-drug chemoresistant phenotype. In the presence of therapy, the sensitive cells (environmentally or phenotypically) are removed from the tumor, reducing hypoxia, normalizing pHe and allowing the phenotypically chemoresistant subpopulation of cells to grow and re-populate the tumor. This work extends our recent chemoresistance model by adding a representation of HIF-1alpha gene, whose response to hypoxia may change due to mutation from varying thresholds until constant activation or deactivation. The expression of this gene is linked to survival in low pHe, expression of multidrug resistance gene (MDR-1) and glycolysis. Our simulations show that HIF-1alpha expression is selected towards constitutive activation due to its increase in glycolysis and low pHe resistance, which in turn increase tumor survival and invasion. Multi-drug resistance is also increased in such cells as a consequence of the selection for these two phenotypes. This work proposes a mechanism for development of chemoresistance in absence of drug which is different from acquired resistance since the selection for this phenotype is not imposed by the drug itself but as side effect of the selection for survival in hypoxia and low pHe. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 437.
Efficacy and Safety of Antioxidant Treatment With α-Lipoic Acid Over 4 Years in Diabetic Polyneuropathy
Authors: Dan Ziegler, Phillip A. Low, William J. Litchy, Andrew J.M. Boulton, Aaron I. Vinik, Roy Freeman, Rustem Samigullin, Hans Tritschler, Ullrich Munzel, Joachim Maus, Klemens Schütte, Peter J. Dyck
Journal: Diabetes Care (2011)

To evaluate the efficacy and safety of α-lipoic acid (ALA) over 4 years in mild-to-moderate diabetic distal symmetric sensorimotor polyneuropathy (DSPN). RESEARCH DESIGN AND METHODS In a multicenter randomized double-blind parallel-group trial, 460 diabetic patients with mild-to-moderate DSPN were randomly assigned to oral treatment with 600 mg ALA once daily (n = 233) or placebo (n = 227) for 4 years. Primary end point was a composite score (Neuropathy Impairment Score [NIS]-Lower Limbs [NIS-LL] and seven neurophysiologic tests). Secondary outcome measures included NIS, NIS-LL, nerve conduction, and quantitative sensory tests (QSTs).Change in primary end point from baseline to 4 years showed no significant difference between treatment groups (P = 0.105). Change from baseline was significantly better with ALA than placebo for NIS (P = 0.028), NIS-LL (P = 0.05), and NIS-LL muscular weakness subscore (P = 0.045). More patients showed a clinically meaningful improvement and fewer showed progression of NIS (P = 0.013) and NIS-LL (P = 0.025) with ALA than with placebo. Nerve conduction and QST results did not significantly worsen with placebo. Global assessment of treatment tolerability and discontinuations due to lack of tolerability did not differ between the groups. The rates of serious adverse events were higher on ALA (38.1%) than on placebo (28.0%).Four-year treatment with ALA in mild-to-moderate DSPN did not influence the primary composite end point but resulted in a clinically meaningful improvement and prevention of progression of neuropathic impairments and was well tolerated. Because the primary composite end point did not deteriorate significantly in placebo-treated subjects, secondary prevention of its progression by ALA according to the trial design was not feasible.
Pulsed doppler echocardiographic measurement of beat-to-beat changes in stroke volume in dogs.
Authors: R M Steingart, J Meller, J Barovick, R Patterson, M V Herman, L E Teichholz
Journal: Circulation (1980)

Measurement of stroke volume by pulsed Doppler echocardiography has not been validated against a reference method in vivo. We compared Doppler systolic frequency shift integrals with electromagnetic flowmeter stroke volume in seven open-chest dogs. A pulsed Doppler echocardiographic transducer was held on the aortic arch with the sample volume in the ascending aorta. Stroke volume was varied by epinephrine or pentobarbital infusions, fluid administration or inferior vena caval construction. Linear regression analysis of stroke volume vs Doppler systolic frequency shift integrals revealed strong correlations and intercepts close to zero (tau = 0.74-0.096, rho less than 0.001). Minor changes in transducer position did not influence Doppler frequency shift integrals substantially. Therefore, pulsed Doppler echocardiography served as an excellent measurement of stroke volume changes in model. However, serious limitations are presented that may limit its clinical application.
Noninvasive Assessment of Exercise-Related Intramyocellular Acetylcarnitine in Euglycemia and Hyperglycemia in Patients With Type 1 Diabetes Using 1H Magnetic Resonance Spectroscopy
Authors: Andreas Boss, Roland Kreis, Stefan Jenni, Michael Ith, Jean-Marc Nuoffer, Emanuel Christ, Chris Boesch, Christoph Stettler
Journal: Diabetes Care (2010)

OBJECTIVE Intramyocellular acetylcarnitine (IMAC) is involved in exercise-related fuel metabolism. It is not known whether levels of systemic glucose influence IMAC levels in type 1 diabetes. RESEARCH DESIGN AND METHODS Seven male individuals with type 1 diabetes performed 120 min of aerobic exercise at 55–60% of Vo2max randomly on two occasions (glucose clamped to 5 or 11 mmol/l, identical insulinemia). Before and after exercise, IMAC was detected by 1H magnetic resonance spectroscopy in musculus vastus intermedius. RESULTS Postexercise levels of IMAC were significantly higher than pre-exercise values in euglycemia (4.30 ± 0.54 arbitrary units [a.u.], P &amp;lt; 0.001) and in hyperglycemia (2.44 ± 0.53 a.u., P = 0.01) and differed significantly according to glycemia (P &amp;lt; 0.01). The increase in exercise-related levels of IMAC was significantly higher in euglycemia (3.97 ± 0.45 a.u.) than in hyperglycemia (1.71 ± 0.50 a.u.; P &amp;lt; 0.01). CONCLUSIONS The increase in IMAC associated with moderate aerobic exercise in individuals with type 1 diabetes was significantly higher in euglycemia than in hyperglycemia.
Myeloma and benign intracranial hypertension.
Authors: R. J. Davenport, R. E. Cull
Journal: BMJ (1992)

control.The indicators of prostaglandin metabolism are related to the HbAI concentrations- namely, to the different stages of diabetic control.It is reasonable to suppose that the uncontrolled diabetic state and the shift in the balance of two antagonistic prostaglandins towards pathogenic direction might have a role in diabetic microangiopathy.Our observations support the authors' opinion.
Measurement of Renin Activity — When Is It Useful?
Authors: Gordon H. Williams
Journal: New England Journal of Medicine (1976)

Since the discovery of renin by Tigerstedt and Bergman 80 years ago, controversy has surrounded its role in the diagnosis and management of the hypertensive patient.1 For many years even its existence was questioned. In the 1930's a boost in its popularity occurred when Goldblatt demonstrated that renal-artery constriction produced hypertension.2 This discovery led several groups to postulate that renin was the factor responsible for the hypertension and that a similar cause- and-effect relation might exist in man.3 However, several years passed before refinements in the measurement of renin permitted assessment of this hypothesis. Initially, proponents enthusiastically proclaimed that renin . . .