tbuckley/cabot-search huggingface dataset:
Problem Solving in Clinical Medicine: From Data to Diagnosis.
Authors: Paul Cutler
Journal: Annals of Internal Medicine (1985)

Compatibility: BlackBerry[registered] OS 4.1 or Higher / iPhone/iPod Touch 2.0 or Higher /Palm OS 3.5 or higher / Palm Pre Classic / Symbian S60, 3rd edition (Nokia) / Windows Mobile[trademark] Pocket PC (all versions) / Windows Mobile Smartphone / Windows 98SE/2000/ME/XP/Vista/Tablet PC.
Measuring Functional Status and Disability in Older AdultsMeasuring Functional Status and Disability in Older Adults
Authors: Saralyn H. Allaire
Journal: JAMA (2003)

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
Abstract 73: Targeting KDR mutations in lung adenocarcinoma
Authors: Susan M. Mockus, Christopher S. Potter, Grace A. Stafford, Guruprasad Ananda, Douglas Hinerfeld, Gregory J. Tsongalis
Journal: Cancer Research (2015)

Abstract KDR, also known as VEGFR2, is a target of several VEGFR inhibitors, however, only bevacizumab, which targets the VEGF ligand, is FDA approved for lung cancer. Since an activating mutation in KDR was identified in 70% of lung adenocarcinoma patients we sought to identify the number of available clinical trials targeting KDR in lung adenocarcinomas and/or solid tumors, thereby increasing therapeutic options and treatment accessibility for these patients. DNA from thirteen lung cancer FFPE samples was sequenced on Illumina HiSeq 2500 or MiSeq sequencers using a CLIA-certified 358-gene targeted sequencing assay. FASTQ files generated from Illumina's CASAVA software were submitted to a Clinical Genome Analytics (CGA) data analysis pipeline to perform automated read quality assessment, alignment, and variant calling. Clinical reports were written for each sample through extensive literature and clinicaltrials.gov searches. Thirteen lung biopsies were obtained and subdivided based on pathology reports, into 10 lung adenocarcinomas, 1 mixed NSCLC/SCLC, 1 small cell carcinoma, and 1 squamous carcinoma. KDR Q472H was identified in 7/10 lung adenocarcinomas and 1/1 mixed NSCLC/SCLC, but not in the small or squamous cell carcinomas. KDR encodes Vegfr-2, a receptor tyrosine kinase overexpressed in a variety of solid tumors. KDR Q472H is an activating missense mutation, which increases phosphorylation and activation of Vegfr-2, thereby promoting increased microvessel density in lung tumor tissues. At the time of clinical report writing, there were a total of 47 actively recruiting clinical trials targeting KDR and 4 trials requiring the patient to have a molecular alteration of KDR. Further breakdown of these trials identified the use of 33 off-label VEGFR inhibitors, 5 investigational pan-VEGFR inhibitors, and 5 investigational specific KDR (VEGFR2) inhibitors. Next-generation sequencing of 358 genes from lung cancer biopsies identified a common KDR activating mutation, Q472H, in 70% of lung adenocarcinomas. Searching clincialtrials.gov by pan-VEGFR and specific KDR inhibitors identified 47 actively recruiting trials, thus increasing the accessible repertoire of treatment options for lung adenocarcinoma patients. Citation Format: Susan M. Mockus, Christopher S. Potter, Grace A. Stafford, Guruprasad Ananda, Douglas Hinerfeld, Gregory J. Tsongalis. Targeting KDR mutations in lung adenocarcinoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 73. doi:10.1158/1538-7445.AM2015-73
Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease
Authors: Minghua Chen, Victor O. Ona, Mingwei Li, Robert J. Ferrante, Klaus B. Fink, Shan Zhu, Jie Bian, Lei Guo, Laurie A. Farrell, Steve M. Hersch, Wendy Hobbs, Jean-Paul Vonsattel, Jang-Ho J. Cha, Robert M. Friedlander
Journal: Nature Medicine (2000)
Abstract 10072: Ischemic Preconditioning Attenuates No-Reflow by Enhancing the Phosphorylation of eNOS at Ser 1179 and Ser 635 via PKA Pathway
Authors: Yue-Jin Yang
Journal: Circulation (2010)

Aims: To investigate whether ischemic preconditioning (IPC) protects hearts from myocardial ischemia-reperfusion injury and no-reflow by enhancing the activity of endothelial nitric oxide synthase (eNOS) via protein kinase A (PKA) pathway. Methods and Results: In 90-minute ischemia and 3-hour reperfusion model, Minipigs were randomly assigned to 5 groups: (1) Sham; (2) Control; (3) IPC; (4) IPC+H-89 (1.0μg kg−1 min−1, an inhibitor of PKA); (5) H−89. Compared with control group, IPC significantly decreased the activity of creatine kinase (CK) and myeloperoxidase (MPO) (P<0.05), but H-89 suppressed this effect. The infarct size reduced from 78.5% to 31.3% and 50.4% in IPC and IPC+H-89 group respectively (P<0.05), and the size of no-reflow decreased from 48.6% to 9.7%, 27.3% and 29.5% in IPC, IPC+H-89 and H-89 group respectively (P<0.05). IPC increased the activity of PKA and NOS, and the expression of PKA, Thr 198 p-PKA, Ser1179 p-eNOS and Ser 635 p-eNOS in no-reflow myocardium; while H-89 completely ...
The Immunology of Malignant Disease.
Authors: Jules E. Harris, Joseph G. Sinkovics
Journal: Annals of Internal Medicine (1977)

cer patients are considered, while features of host defense and human malignant neoplasms are discussed in general terms. The chapter on Immunology of Tumors in Experimental Animals reviews the antigens found in virus-induced and chemically induced tumors, as well as embryonal antigens of tumors.  reactions to tumors and experimental approaches to immunotherapy are discussed. The chapter on Immune Deficiency States Associated With Hu-
Microscopic diagnosis of sodium acetate-acetic acid-formalin-fixed stool samples for helminths and intestinal protozoa: a comparison among European reference laboratories
Authors: J. Utzinger, S. Botero-Kleiven, F. Castelli, P.L. Chiodini, H. Edwards, N. Köhler, M. Gulletta, M. Lebbad, M. Manser, B. Matthys, E.K. N'Goran, E. Tannich, P. Vounatsou, H. Marti
Journal: Clinical Microbiology and Infection (2009)
Tropical Medicine in the United States.
Authors: Alfred C. m. D. Reed
Journal: JAMA (1930)

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
Interorgan ammonia and amino acid metabolism in metabolically stable patients with cirrhosis and a TIPSS
Authors: Steven W. M. Olde Damink, Rajiv Jalan, Doris N. Redhead, Peter C. Hayes, Nicolaas E. P. Deutz, Peter B. Soeters
Journal: Hepatology (2002)

Ammonia is central to the pathogenesis of hepatic encephalopathy. This study was designed to determine the quantitative dynamics of ammonia metabolism in patients with cirrhosis and previous treatment with a transjugular intrahepatic portosystemic stent shunt (TIPSS). We studied 24 patients with cirrhosis who underwent TIPSS portography. Blood was sampled and blood flows were measured across portal drained viscera, leg, kidney, and liver, and arteriovenous differences across the spleen and the inferior and superior mesenteric veins. The highest amount of ammonia was produced by the portal drained viscera. The kidneys also produced ammonia in amounts that equaled total hepatosplanchnic area production. Skeletal muscle removed more ammonia than the cirrhotic liver. The amount of nitrogen that was taken up by muscle in the form of ammonia was less than the glutamine that was released. The portal drained viscera consumed glutamine and produced ammonia, alanine, and citrulline. Urea was released in the splenic and superior mesenteric vein, contributing to whole-body ureagenesis in these cirrhotic patients. In conclusion, hyperammonemia in metabolically stable, overnight-fasted patients with cirrhosis of the liver and a TIPSS results from portosystemic shunting and renal ammonia production. Skeletal muscle removes more ammonia from the circulation than the cirrhotic liver. Muscle releases excessive amounts of the nontoxic nitrogen carrier glutamine, which can lead to ammonia production in the portal drained viscera (PDV) and kidneys. Urinary ammonia excretion and urea synthesis appear to be the only way to remove ammonia from the body.
Assessing Exposure to Toxic Gases in Bhopal—Reply
Authors: Daya R. Varma, Nishant Ranjan, Satinath Sarangi, Steve Holleran, Rajasekhar Ramakrishnan
Journal: JAMA (2004)

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
Drug Treatment of Lipid Disorders
Authors: Robert H. Knopp
Journal: New England Journal of Medicine (1999)

Arteriosclerosis of the coronary and peripheral vasculature is the leading cause of death among men and women in the United States1 and worldwide.2 In 1992, for example, cardiovascular disease accounted for 38 percent of deaths from all causes among men and 42 percent of all deaths among women in Washington State3; nationwide, the mortality rate for cardiovascular disease is approximately 50 percent.4 Mechanisms of AtherogenesisCentral to the pathogenesis of arteriosclerosis is the deposition of cholesterol in the arterial wall.5,6 Nearly all lipoproteins are involved in this process, including cholesterol carried by very-low-density lipoprotein (VLDL),7,8 remnant lipoprotein, . . .
A modified, improved, easy and fast technique for split-thickness skin grafting
Authors: M. Kneilling, H. Breuninger, W. Schippert, H.M. Häfner, M. Moehrle
Journal: British Journal of Dermatology (2011)

Large nonhealing ulcers and wounds frequently pose a great therapeutic challenge to clinicians and often require skin grafting. Various skin grafting methods are available to cover large skin defects that fail to epithelize. These methods include the use of small pinch grafts, full-thickness punch grafts, large-sized full-thickness grafts and split-thickness grafts. Large-sized full-thickness and split-thickness skin grafting requires expertise to produce cosmetically acceptable results and prevent cobblestoning, unlike small pinch and full-thickness punch grafts.To describe a modified technique of split-thickness skin grafting that can be considerably faster than alternative methods.We describe a method for split-thickness skin grafting using tumescent anaesthesia at the donor site and an electrodermatome and a polyurethane membrane without sutures at the site of the skin defect.Since 1997, we have practised a modified, improved, quick and easy split-thickness skin grafting method to cover large skin defects at the extremities. Complete healing is usually achieved 4-6 weeks after the split-thickness skin transplantation, and long-term results are aesthetically successful.We provide a sophisticated modified split-thickness skin graft procedure that has been practised for many years and provides cosmetically acceptable results while saving time.
Abstract 17866: Assessment of Echo-Attenuated Plaque by Optical Coherence Tomography and its Impact on Post-procedural CK-MB Elevation in Elective Stent Implantation
Authors: Tetsumin Lee, Taishi Yonetsu, Kentarou Takahashi, Kenji Koura, Ginga Yamamoto, Keiichi Hishikari, Hideomi Fujiwara, Tsunekazu Kakuta
Journal: Circulation (2010)

Background:  Recent intravascular ultrasound (IVUS) studies have described atherosclerotic plaques with echo attenuation (EA) without associated bright echoes that are correlated with no-reflow phenomenon after percutaneous coronary intervention (PCI). We investigated echo-attenuated plaques by optical coherence tomography (OCT) and evaluated their impact on post-PCI creatine kinase-MB (CK-MB) elevation in patients with elective stent implantation.   Methods and Results:  We studied 135 native de novo culprit coronary lesions in 135 patients with normal pre-PCI CK-MB levels (28: unstable angina; 107: stable angina) who underwent IVUS and OCT examinations before elective stent implantation. The lesions were divided into two groups based on the presence or absence of EA and OCT findings were compared. We then determined predictors of post-PCI CK-MB elevation. Further, angioscopic examination was performed in 12 lesions with EA. EA was found in 47 (34.8%) lesions, and was associated with higher frequencies of OCT-derived thin-capped fibroatheroma (TCFA; EA: 51.1% vs. non-EA: 21.6%, P    Conclusions:  Atherosclerotic plaques with EA were associated with characteristics considered to be high-risk. OCT examination showed a significant additive predictive value to the presence of EA for post-PCI CK-MB elevation.
Abstract 18525: Effects of Statin Therapy on Ascending Aorta Aneurysms Growth: a Propensity-matched Analysis of 828 Patients
Authors: Emiliano Angeloni, Simone Refice, Angelo Vitaterna, Paola Lombardo, Michele Pirelli, Giovanni Melina, Riccardo Sinatra
Journal: Circulation (2014)

Introduction: Pleiotropic effects of statins have been advocated for remodelling of the vascular wall. Hypothesis: Whether statin therapy influences the growth rate of ascending aorta (AA) aneurysms. Methods: A total of 1348 patients was referred to our outpatient clinic for initial AA ectasia from September 2005 to December 2010. A propensity score was built to perfectly match (1:1) patients administered (Group A) or not (Group B) with statin therapy. Clinical and echocardiographic follow-up was 100% completed at 3 years after the first visit. Treatment groups were investigated for differences in AA maximum diameter, furthermore rates of survival free from death and/or complications were assessed by Kaplan-Meyer analysis. Results: Finally, two fairly-comparable groups of 414 patients each were obtained (Propensity model c-statistic 0.84, p&lt;0.0001). No significant differences were noted in baseline characteristics, mean AA diameters were 40.9±2.6 mm and 40.7±2.5 mm in Group A and B, respectively. At 3-years, similar rates of hypertension control (84±9% vs. 83±11%) were found, whilst growth rate of AA diameter was +22.3±9.4 mm in Group A (+7.4 mm/year) and +26.5±8.4 mm (+8.8 mm/year) in Group B (p=0.0001). Three-year survival free from the composite outcome (death, dissection/rupture, need for operative repair) was found to be significantly improved in Group A (64±4%) rather than in Group B (53±5%), with a log-rank p=0.002 (HR 0.41, 95%CI 0.37 to 0.48). Conclusions: In this study, statin treatment is associated with reduced growth rate of ascending aorta aneurysms. The latter resulted in better survival free from complications for patients receiving statins.
Notice of Retraction: “Multiple Sclerosis and Epstein-Barr Virus” (
Authors: Alberto Ascherio, Mark Rubertone, Donna Spiegelman, Lynn Levin, Kassandra Munger, Charles Peck, Evelyne Lennette
Journal: JAMA (2005)

issue of JAMA 1 due to the discovery of a data error.The article was based on a nested case-control study in which we examined the relation between antibody titers against Epstein-Barr virus (EBV) and risk of developing multiple sclerosis (MS).To protect confidentiality, only the investigators at the Department of Defense Serum Repository (DoDSR) had access to the link between serum aliquots provided for serological analyses and case-control status or other covariates.Laboratory results were therefore sent to the DoDSR, where they were linked with the covariates of interest, and sent back to the other study investigators as an electronic file stripped of unique identifiers.Although the personnel linking the data at the DoDSR are highly trained and experienced in handling the huge database comprising millions of records, we discovered that in this instance the matching between laboratory results and remaining data were done incorrectly, apparently because of incorrect sorting of one of the files.We have now repeated our analyses on the correctly matched data.With one exception, there were no errors in the case/control assignment of the samples.Several dates of blood collection, however, were erroneously assigned, obscuring important temporal variations in antibody titers among the cases.Overall, analyses of the correct data still support the strong and highly significant association between anti-EB nuclear antigen titers and risk of MS as we originally reported, but it has become apparent that this association is strongly modified by age.Antibody titers of cases and controls were virtually identical in samples collected before age 20 years.However, while titers in controls remained constant, antibody titers of the cases increased, reaching a maximum between ages 25 and 29 years, followed by a plateau.As discussed in the article based on the corrected data, 2 this is a new and important finding that may be critical to the understanding of the relation between EBV and MS.We apologize for the inconvenience caused to
Blood Pictures: An Introduction to Clinical Hæmatology.
Authors: Cecil. Price-Jones
Journal: JAMA (1933)

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