tbuckley/cabot-search huggingface dataset:
Abstract 3207: Curcumin induces pancreatic cancer cell death by targeting IAPs
Authors: Carlos J. Diaz Osterman, Malyn May Asuncion Valenzuela, Heather R. Ferguson Bennit, Salma Khan, Nathan R. Wall
Journal: Cancer Research (2014)

Abstract Background Pancreatic cancer has among the highest mortality rates compared to other cancer types, with 94% of patients dying within five years of diagnosis. Contributing to the high mortality rate, patients with pancreatic cancer do not present significant symptoms until the disease is advanced. Moreover, treatment strategies have not improved substantially over the last decade. For this reason, a recent trend has led toward focusing on the use of herb-derived compounds, such as curcumin (turmeric derivative), to explore alternative treatments that will improve current pancreatic cancer therapy. Objective The objectives of this study were (1) to determine the effects of curcumin on pancreatic cancer cell metabolism, viability, cell cycle and morphology, and (2) to determine the mechanism by which curcumin induces cell death in pancreatic cancer cells by analyzing intracellular expression levels of inhibitor of apoptosis proteins (IAPs). Design/method Pancreatic adenocarcinoma cell lines (Panc-1 and MiaPaCa-2) were used to assess the effects of curcumin in pancreatic cancer. Effects on metabolism, viability and cell cycle were assayed by Alamar Blue, Trypan Blue and Propidium Iodide (PI) staining/flow cytometry (FACSCalibur). Morphological imaging was performed using Hoffman Modulation microscopy. Apoptosis was detected by Annexin V/PI flow cytometry (MACSQuant) and the expression of IAPs was assessed by Western blot. Results These data show that curcumin decreases pancreatic cancer cell metabolism and viability. Cell cycle stages were arrested in pancreatic cancer cells treated with curcumin compared to the non-treated controls. Apoptotic cells were detected by microscopy and confirmed by Annexin V/PI staining with subsequent flow cytometry analysis. IAPs levels are reduced in pancreatic cancer cell lines treated with curcumin compared to non-treated controls. Conclusion These results demonstrate that pancreatic adenocarcinoma cell lines are sensitive to curcumin treatment. Moreover, curcumin's possible mechanism of action is inducing apoptosis by targeting IAPs. Collectively, these data suggest a potential role for curcumin in pancreatic cancer therapy. Citation Format: Carlos J. Diaz Osterman, Malyn May Asuncion Valenzuela, Heather R. Ferguson Bennit, Salma Khan, Nathan R. Wall. Curcumin induces pancreatic cancer cell death by targeting IAPs. [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 3207. doi:10.1158/1538-7445.AM2014-3207
646 THE CONTROL OF HBV REPLICATION THAT LEADS TO HBEAG LOSS DOES NOT PREVENT THE EMERGENCE OF PRE-CORE DEFECTIVE VARIANTS IN GENOTYPE D INFECTED CHILDREN
Authors: P. Colombatto, C. Barbera, F. Bortolotti, A.M. Maina, F. Moriconi, P. Calvo, M. Baldi, F. Oliveri, F. Bonino, M.R. Brunetto
Journal: Journal of Hepatology (2008)
Teaching Hospital Costs
Authors: Robert Mechanic, Kevin Coleman, Allen Dobson
Journal: JAMA (1998)

Context.—As the managed care environment demands lower prices and a greater focus on primary care, the high cost of teaching hospitals may adversely affect their ability to carry out academic missions.Objective.—To develop a national estimate of total inpatient hospital costs related to graduate medical education (GME).Design.—Using Medicare cost report data for fiscal year 1993, we developed a series of regression models to analyze the relationship between inpatient hospital costs per case and explanatory variables, such as case mix, wage levels, local market characteristics, and teaching intensity (the ratio of interns and residents to beds).Setting and Participants.—A total of 4764 nonfederal, general acute care hospitals, including 1014 teaching hospitals.Major Outcome Measures.—Actual direct GME hospital costs and estimated indirect GME-related hospital costs based on the statistical relationship between teaching intensity and inpatient costs per case.Results.—In 1993, academic medical center (AMC) costs per case were 82.9% higher than those for urban nonteaching hospitals (actual cost per case, $9901 vs $5412, respectively). Non-AMC teaching hospital costs per case were 22.5% higher than those for nonteaching hospitals (actual cost per differences in case, $6630 vs $5412, respectively). After adjustment for case mix, wage levels, and direct GME costs, AMCs were 44% more expensive and other teaching hospitals were 14% more costly than nonteaching hospitals. The majority of this difference is explained by teaching intensity. Total estimated US direct and indirect GME-related costs were between $18.1 billion and $22.8 billion in 1997. These estimates include some indirect costs, not directly educational in nature, related to clinical research activities and specialized service capacity.Conclusions.—The cost of teaching hospitals relative to their nonteaching counterparts justifies concern about the potential financial impact of competitive markets on academic missions. The 1997 GME-related cost estimates provide a starting point as public funding mechanisms for academic missions are debated. The efficiency of residency programs, their consistency with national health workforce needs, financial benefits provided to teaching hospitals, and ability of AMCs to maintain higher payment rates are also important considerations in determining future levels of public financial support.
Sexual knowledge and attitudes of general practitioners in Wessex.
Authors: M Elstein, A D Gordon, M S Buckingham
Journal: BMJ (1977)

A survey of the sexual attitudes and knowledge of general practitioners in Wessex found that GP trainees and those in practice for less than 10 years were less conservative and better informed than doctors in practice for 20 years or more, The results suggest that the attitudes of the doctors are determined by their early environmental influences rather than their clinical experience.
The eradication of gonorrhoea
Authors: C. Bignell
Journal: BMJ (1994)

The continued global survival of Neisseria gonorrhoeae is inevitable because of its immunobiology,1 the seeming lack of natural or acquired immunity, human sexual behaviour, and the frequency of asymptomatic infection. Nevertheless, endemic gonorrhoea could be eradicated from Britain in the 1990s. Sweden has achieved this public health goal, and many other developed countries report dramatic reductions in incidence.2 In Britain reported cases of gonorrhoea have declined every year since 1977, with a particularly big decrease in 1987. Many health districts have already achieved the nationally set target for 1995 of fewer than 49 cases per 100 000 population aged 15-64.3 Geographical variation in the incidence of gonorrhoea in England is, however, considerable, with some urban areas still substantially above this target.4

Has any one factor been decisive in recent successes in controlling gonorrhoea? Certainly, radical innovations in treatment cannot take the credit. Effective drugs have been available throughout the rise and fall in the incidence of gonococcal infection during the 1960s, 1970s, and 1980s. Effective treatment is, however, a key component in control and has required some major …
Influences on Prescribing Practices
Authors: Richard A. Moore
Journal: JAMA (1984)

<h3>To the Editor.—</h3> The recent article by Schaffner et al<sup>1</sup>appears to indicate that the physicians in the study had a greater influence on prescribing behavior than did the pharmacist. However, there may be an unrecognized source of bias in this study that could have influenced the results. The physician counselors were described in part as "senior physicians in part-time practice." The pharmacist drug educator was described as "a recent honors pharmacy graduate." Since the educational visit lasted less than 15 minutes, it seems reasonable that factors such as physical appearance had a role in the influence of the interventions. The physicians must have differed markedly in physical appearance from the pharmacist. The physician counselors surely had the appearance of clinicians with many years of experience. On the other hand, the pharmacist must have appeared still "wet behind the ears" with very little clinical experience because of his youth.
Abstract 2417: The INHERIT EGFR study: Investigating hereditary risk from T790M.
Authors: Geoffrey R. Oxnard, Elizabeth J. Root, Alicia Sable-Hunt, Irene Rainville, Suzanne E. Dahlberg, Jennifer C. Heng, David M. Jackman, Pasi A. Janne, Judy E. Garber
Journal: Cancer Research (2013)

Abstract Background: The EGFR T790M mutation, commonly associated with acquired resistance to EGFR kinase inhibitors, has also been described rarely as a germline mutation in association with familial lung cancer. In collaboration with the Addario Lung Cancer Medical Institute (www.ALCMI.net), we initiated a prospective trial to identify patients and families carrying germline EGFR mutations in order to characterize their lung cancer risk. Preliminary data: In a prior study (GR Oxnard et al, JTO, 2012), it was identified that patients with lung cancers found to harbor EGFR T790M at diagnosis have a 50% chance of carrying an underlying germline T790M mutation. This suggests that by focusing on patients already identified to carry T790M in their cancer, it is possible to enrich for a germline mutation that may be otherwise too rare to study prospectively. Subject eligibility: The following groups are eligible: (1) Patients with a cancer (lung or other) harboring an EGFR T790M mutation on tumor genotyping; lung cancers that acquired EGFR T790M only following treatment with an EGFR kinase inhibitor are ineligible. (2) First-degree relatives of patients found to carry a germline EGFR mutation. (3) Patients who already are known to carry a germline EGFR mutation on prior testing. Subjects are referred to cohort 1 based upon genotyping results from academic centers, oncology practices, or partnering commercial laboratories (e.g. Response Genetics, Los Angeles, CA). Trial design: Subjects may present at a participating cancer center or may participate remotely through a study website (www.Dana-Farber.org/T790Mstudy). Eligible patients submit a saliva and/or blood specimen for central testing in a CLIA lab. After counseling, patients carrying germline EGFR mutations have the option of inviting first-degree relatives to participate. Genetic counseling is coordinated at the participating center or offered over the phone. Chest CT scans are collected from germline carriers and analyzed centrally to study nodule prevalence and characteristics. Patients are then clinically followed for 2 years. Funding: Supported by grants from the Conquer Cancer Foundation of ASCO and the Bonnie J. Addario Lung Cancer Foundation. Citation Format: Geoffrey R. Oxnard, Elizabeth J. Root, Alicia Sable-Hunt, Irene Rainville, Suzanne E. Dahlberg, Jennifer C. Heng, David M. Jackman, Pasi A. Janne, Judy E. Garber. The INHERIT EGFR study: Investigating hereditary risk from T790M. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2417. doi:10.1158/1538-7445.AM2013-2417
Evidence of Carotid Artery Wall Hypertrophy in Homozygous Homocystinuria
Authors: Jean-Louis Megnien, Jérôme Gariepy, Jean-Marie Saudubray, Jean-Marc Nuoffer, Nicolas Denarie, Jaime Levenson, Alain Simon
Journal: Circulation (1998)

Background —We aimed to determine whether intima-media thickness (IMT) was increased in the carotid artery of subjects with homocystinuria to better understand the in vivo contribution of homocysteine to early atherogenesis. Methods and Results —We investigated ultrasonographically the right common carotid artery in 14 subjects with homozygous homocystinuria aged 3 to 34 years (mean, 13 years) and in 15 of their heterozygous parents aged 32 to 47 years (mean, 41 years) by comparison with 2 control groups of 15 healthy subjects of the same age. Far-wall IMT and lumen diameter were measured with a computerized program, and the cross-sectional area of the intima-media complex (CSA-IMC) was calculated from IMT and diameter. Comparison with their respective controls, adjusted for body surface area or height, showed that homozygotes had greater IMT ( P &lt;0.001) and CSA-IMC ( P &lt;0.05) and smaller diameter ( P &lt;0.05), whereas heterozygotes had values similar to their controls. Multivariate analysis of the arterial parameters with age, body surface area (or height), and plasma total homocysteine in the homozygous and heterozygous groups combined showed that IMT was related to age ( P &lt;0.05) and homocysteine ( P &lt;0.01), diameter was related to body surface area ( P &lt;0.001) or height ( P &lt;0.05), and CSA-IMC was related to age ( P &lt;0.05), body surface area ( P &lt;0.05) (but not height), and homocysteine ( P &lt;0.05). Conclusions —Homozygous homocystinuria was associated with common carotid wall hypertrophy, whereas heterozygous disease was not. Such hypertrophy may reflect a smooth muscle proliferation induced by hyperhomocysteinemia and represent a promising target for testing vascular effects of therapeutic measures to lower homocysteine.
Myocardial collagen, the effects of right ventricular hypertrophy and its involution induced by changes in atmospheric pressure
Authors: P. G. CASPARI, M. NEWCOMB, K. GIBSON, P. HARRIS
Journal: Cardiovascular Research (1978)

Journal Article Myocardial collagen, the effects of right ventricular hypertrophy and its involution induced by changes in atmospheric pressure Get access P. G. CASPARI, P. G. CASPARI 1 From the Cardiothoracic Institute, University of London 1Present address: Department of Cardiology, The Royal North Shore Hospital of Sydney, St Leonards, NSW 2065, Australia. Search for other works by this author on: Oxford Academic PubMed Google Scholar M. NEWCOMB, M. NEWCOMB From the Cardiothoracic Institute, University of London Search for other works by this author on: Oxford Academic PubMed Google Scholar K. GIBSON, K. GIBSON From the Cardiothoracic Institute, University of London Search for other works by this author on: Oxford Academic PubMed Google Scholar P. HARRIS P. HARRIS From the Cardiothoracic Institute, University of London Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 12, Issue 3, March 1978, Pages 173–178, https://doi.org/10.1093/cvr/12.3.173 Published: 01 March 1978
Bariatric Surgery and Diabetes
Authors: Jonathan Q. Purnell, David R. Flum
Journal: JAMA (2009)

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
Screening for cervical cancer in developing countries.
Authors: M. M. Soe
Journal: BMJ (1992)

cholecystectomy, however, is generally done by one person, and it is difficult for anyone other than the operating surgeon to observe what is taking place.How do Baxter and O'Dwyer propose to teach the minilaparotomy procedure to surgeons in training, particularly iffuture trainees have little or no experience with the open operation?Perhaps the most pressing reason for leaving minilaparotomy cholecystectomy out of the equation at this stage is that it is not yet recognised as a routine procedure.
Non–high-density lipoprotein cholesterol (non-HDL-C) as a predictor of cardiovascular mortality in patients with end-stage renal disease
Authors: Yoshiki Nishizawa, Tetsuo Shoji, Ryusuke Kakiya, Yoshihiro Tsujimoto, Tsutomu Tabata, Eiji Ishimura, Tatsuya Nakatani, Takami Miki, Masaaki Inaba
Journal: Kidney International (2003)
REVIEW OF HOSPITAL PATIENTS WITH ALT&gt;1000 IU/L
Authors: A McDonough, Z Galvin, J Ryan, M T O'Neill, H Fitzpatrick, S Stewart
Journal: Gut (2013)

<h3>Introduction</h3> There are many potential causes for an ALT&gt;1000 IU/L, the commonest being ischaemia, drug induced liver injury (DILI) and viral hepatitis. There are however many other potential causes, and, more recently, acute endemic hepatitis E (HEV) has been identified in some of these patients. <h3>Aims/Background</h3> Our aim was to establish the causes of ALT&gt;1000 IU/L in patients in a large teaching hospital. We also wanted to determine the number of patients in whom a cause was not found, and how many of these had been checked for HEV. <h3>Method</h3> All ALT values over a two-year period (2010/11) were examined. Those with an ALT&gt;1000 IU/L were identified and their investigations/notes reviewed. All data was annonymised and recorded in a dedicated electronic database. <h3>Results</h3> 182 patients (57% male and 43% female) with an ALT&gt;1000 IU/L were identified. The mean age for males versus females was 47+/−18 years versus 62+/−18 years (p=0.001). The most common causes of an ALT&gt;1000 IU/L were ischaemic hepatitis, (n=111, (61%)), DILI, (n=30, (16.5%)) and viral hepatitis, (n=22, (12.1%)). The remaining causes included choledocholithiasis (n=8) and autoimmune hepatitis (n=3). No cause was identified for 8 patients. Of these, none had HEV IgM checked. 35.7% (n=65) died during this admission, 54.9%(n=100) were discharged home and 9.3% (17) were not admitted. <h3>Conclusion</h3> This review confirms that ischaemic liver injury is the commonest cause of ALT&gt;1000 IU/L in hospital inpatients. Ischaemia, DILI and viral hepatitis account for almost 90% of presentations. Only 5% of patients had no aetiology identified. This number may be significantly lower if all had had HEV IgM checked.
Terminology used in article on cloning was incorrect
Authors: P. Millard
Journal: BMJ (2001)

EDITOR—The myth that stem cells developed by cloning will be genetically similar to the adult needs to be exposed. Scientifically, the statements in the box in Mayor's news article are wrong.1 The Donaldson report (page 23, para 2.28) states “animals born from cell nuclear replacement are not exactly identical to the animal cell whose cell nucleus was used in the …
Effects of Ischemia on Left Ventricular Apex Rotation
Authors: Carol A. Gibbons Kroeker, John V. Tyberg, Rafael Beyar
Journal: Circulation (1995)

Background Left ventricular (LV) twist has been defined as the counterclockwise rotation of the ventricular apex with respect to the base during systole. We recently showed that, since base rotation is minimal, measurement of apex rotation reflects the dynamics of LV twist. Since ischemia is known to affect endocardial and epicardial fiber force and shortening and therefore the transmural balance of torsional moments, we hypothesized that ischemia has a significant effect on apex-rotation amplitude and on untwisting during the isovolumic relaxation (IVR) period. Methods and Results With an optical device coupled to the LV apex, apex rotation was recorded simultaneously with LV pressure, ECG, LV segment length, and minor-axis diameters in 16 open-chest dogs. Ischemia was caused by a 1- to 2-minute snare occlusion of either the left anterior descending (LAD) or circumflex (LCx) arteries. LAD ischemia had a pronounced effect on apex rotation: an increase in apex-rotation amplitude attributed to subendocardial dysfunction at 10 seconds of ischemia; maximum apex rotation occurring later (during the IVR period) throughout the ischemia; a paradoxical relaxation pattern of initial untwisting followed by twisting and untwisting during the IVR period with ischemia; and a decrease in the amplitude of apex rotation with ischemia, possibly due to transmural dysfunction. LCx occlusion had similar effects on apex rotation, except that apex-rotation amplitude was not increased at 10 seconds of occlusion and the amplitude of apex rotation did not decrease with severe ischemia. Under control preischemic conditions, a linear relationship between apex rotation and segment length was observed during ejection and a different, steeper relationship during IVR. With regionally ischemic segments, this relationship became nonlinear for both ejection and IVR. Conclusions Both LAD and LCx ischemia had profound effects on the dynamics of apex rotation. A paradoxical relaxation pattern occurred with ischemia. We suggest that these observations are due to changes in the dynamic transmural balance of torsional moments that determine LV twist.
Mode of Action of Antirheumatic Drugs
Authors: J. N. McArthur, P. D. Dawkins, M. J. H. Smith, E. B. D. Hamilton
Journal: BMJ (1971)

The concentrations of free and protein-bound L-tryptophan were measured in sera from normal subjects, patients with rheumatoid arthritis, pregnant women, and patients with jaundice. In the patients with rheumatoid arthritis receiving treatment with one or more antirheumatic drugs the percentage of the amino-acid bound to the circulating proteins was significantly depressed and in one patient returned to normal when therapy was stopped. Pregnancy and jaundice were also associated with raised free tryptophan and decreased bound tryptophan concentrations and bilirubin displaced the amino-acid from its binding sites on human serum proteins in vitro. It is suggested the behaviour of tryptophan mimics that of certain peptides which protect susceptible tissues against chronic inflammatory insults.