tbuckley/cabot-search huggingface dataset:
Diagnostic Reasoning
Authors: Paul F. Griner
Journal: Annals of Internal Medicine (2018)

Letters15 May 2018Diagnostic ReasoningPaul F. Griner, MDPaul F. Griner, MDUniversity of Rochester Medical Center, Rochester, New York (P.F.G.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/L18-0011 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:I commend Simpkin and colleagues (1) for their initiatives to improve the competence of internal medicine trainees in the diagnostic process. Although they note that “the foundation of the diagnostic process is the patient's medical history and the physical examination,” their recommendations for rebuilding the focus on diagnostic reasoning do not seem to address weaknesses in these critically important first steps. Deficiencies among trainees in performing a good history and physical examination are well-documented (2). Personal observations of residents performing physical examinations more recently suggest that these deficiencies persist. They include auscultation of the heart and lungs ...References1. Simpkin AL, Vyas JM, Armstrong KA. Diagnostic reasoning: an endangered competency in internal medicine training. Ann Intern Med. 2017;167:507-8. [PMID: 28892818]. doi:10.7326/M17-0163 LinkGoogle Scholar2. Sharma S. A single-blinded, direct observational study of PGY-1 interns and PGY-2 residents in evaluating their history-taking and physical-examination skills. Perm J. 2011;15:23-9. [PMID: 22319412] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: University of Rochester Medical Center, Rochester, New York (P.F.G.)Disclosures: The author has disclosed no conflicts of interest. The form can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=L18-0011. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoDiagnostic Reasoning: An Endangered Competency in Internal Medicine Training Arabella L. Simpkin , Jatin M. Vyas , and Katrina A. Armstrong Diagnostic Reasoning Arabella L. Simpkin , Jatin M. Vyas , and Katrina A. Armstrong Diagnostic Reasoning David M. Mitchell Diagnostic Reasoning Liliana Grigorita , Andreea Stan , and Boban Thomas Metrics 15 May 2018Volume 168, Issue 10Page: 750-751KeywordsAuscultationConflicts of interestDiagnostic medicineDisclosureHeartLungsMedical educationReasoningReflexes ePublished: 15 May 2018 Issue Published: 15 May 2018 Copyright & PermissionsCopyright © 2018 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Abstract 57: Pharmacologic Inhibition of BK Channels Affects Cardiac Function
Authors: Nishi H Patel, Justin H Johannesen, Sumanta K Goswami, Devasena Ponnalagu, Andrew R Kohut, Harpreet Singh
Journal: Circulation Research (2017)

Calcium and voltage activated potassium channels (BK) are ubiquitously distributed, and have been shown to play roles in cardioprotection and cardiac function. To date, however, the effect of BK channel activation or inhibition in cardiac cells has only been studied using in vitro or ex vivo models. In this study, for the first time we demonstrate the role of BK channels on cardiac function in vivo using an antagonist, Paxilline. Male Sprague Dawley rats had an initial echocardiogram to establish baseline values of cardiac function. Afterwards, the femoral vein was isolated and rats injected with either DMSO or Paxilline of various concentrations ranging from 2 ng/mL/kg to 500 μg/mL/kg. Echocardiograms were then repeated 30 seconds, 15 minutes, and 24 hours after injection. Some rats at higher drug dosage suffered cardiac arrest within 15 minutes. In a separate experiment, a pressure transducer was inserted into the left ventricle (LV) via cannulation of the carotid artery. LV Developed Pressure (LVDP) and Heart Rate (HR) were continuously recorded as rats were infused with DMSO or Paxilline via the femoral vein. In agreement with BK null mutant mice, we found that rats receiving Paxilline had a significant decrease in HR compared to controls, as BK is known to play a role in SA nodal cells. In rats that lived, the transient decrease in HR averaged ~26.20%. Rats receiving Paxilline also had diminished Ejection Fraction (EF) ranging from 26.53% to 100% fold-decrease compared to controls. The decrease in EF occurred in a dose dependent manner, with rats receiving higher doses (&gt; 13 ng/mL/kg) of Paxilline typically suffering cardiac arrest within 15 minutes. Measurements using pressure transduction of the LV showed results similar to those rats assessed using echocardiography, with a significant decrease in LVDP ranging from 36.9% to 100% decrease. Rats that received lower doses (&lt;4 ng/mL/kg) of Paxilline showed improvement in their cardiac function back to baseline by 24 hours post injection, suggesting that the effects we observed are transient and that BK inhibition is reversible. We have shown that inhibition of BK is detrimental to cardiac function, suggesting that BK channels in cardiac tissue are not only functional but essential to maintain normal cardiac function.
Hepatic iron and zinc concentrations after portacaval shunting for nonalcoholic cirrhosis
Authors: P Adams
Journal: Hepatology (1994)

Hepatic iron and zinc concentrations were determined in 26 consecutive nonalcoholic cirrhotic patients who had previously undergone portacaval shunting and then liver transplantation and 37 control patients. Stainable iron was graded on a scale of 0 to 4; 11 shunt patients and 3 control patients had grade 2 to 4 iron staining. Mean hepatic iron concentration was significantly increased (20.1 ± 4.1 μmol/gm) in the shunt group compared with the control group (9.1 ± 2.3 μmol/gm) (normal value, < 35 μmol/gm) (p = 0.015, Student's t test). Mean hepatic iron index (hepatic iron/age) was 0.5 ± 0.10 in the shunt group and 0.19 ± 0.04 in the control group (p = 0.002). One shunt patient had a hepatic iron index of greater than 2. Hepatic zinc was not significantly different between the shunt group (2.42 ± 0.18 μmol/gm) and the control group (2.56 ± 0.14 μmol/gm). Serial biopsy specimens were analyzed in 17 cases (6 shunt, 11 controls), and the mean annual rate of iron accumulation was significantly greater in shunt patients (4.75 μmol/gm/yr) than in control cases (0.93 μmol/gm/yr, p = 0.037). Although increased stainable iron was ccmmon after portacaval shunting, quantitative iron analysis demonstrated increased hepatic iron concentrations in only 6 of 26 shunt patients and 3 of 37 control patients (p = 0.14, x2 test). Quantitative hepatic iron analysis demonstrated in this study that portacaval shunt patients have far less accumulated iron than hemochromatosis patients and are unlikely to have tissue injury resulting from iron overload. (Hepatology 1994;19:101-105).
Endogenous HMGB1 regulates autophagy
Authors: Daolin Tang, Rui Kang, Kristen M. Livesey, Chun-Wei Cheh, Adam Farkas, Patricia Loughran, George Hoppe, Marco E. Bianchi, Kevin J. Tracey, Herbert J. Zeh, Michael T. Lotze
Journal: The Journal of Experimental Medicine (2010)
Severe measles in immunocompromised patients
Authors: L. J. Kaplan
Journal: JAMA (1992)

<h3>Objectives.</h3> —To describe the severity of measles in immunocompromised hosts and to assess preventive and therapeutic modalities. <h3>Data Sources.</h3> —Patients admitted to two academic medical centers between September 1989 and December 1990 and English language references obtained by MEDLINE from 1963 to 1991. Bibliographies were used to identify reports prior to 1963. <h3>Study Selection.</h3> —We identified nine immunocompromised patients with measles. Further analysis was based on 35 patients from two cohort studies of measles in oncology patients and 24 reported cases of measles in human immunodeficiency virus (HIV)—infected patients. <h3>Data Extraction.</h3> —Clinical data are presented from the nine patients we treated. Information concerning measles complications, presence of rash, use of prophylactic immunoglobulin, and therapeutic measures was extracted from the literature. <h3>Data Synthesis.</h3> —Of our nine patients, eight developed severe complications and two died. Two patients had no rash. In combining our patients with those from the literature, severe complications occurred in about 80%. The case fatality rate for severe measles was about 70% for oncology patients and about 40% for HIV-infected patients. Rash was absent in about 30%. The efficacy of prophylactic or therapeutic measures could not be assessed due to the small number of patients. However, we observed a rapid defervescence following administration of ribavirin. Vaccinated, HIV-infected patients had a lower mortality rate than those not previously vaccinated (<i>P</i>=.06). <h3>Conclusions.</h3> —Measles is a severe illness in immunocompromised patients, and the absence of rash is frequent. While treatment is supportive, ribavirin requires further study. Measles vaccine may be efficacious in HIV-infected patients. Vaccination of oncology patients should be reassessed. (<i>JAMA</i>. 1992;267:1237-1241)
Sorafenib administered using a high-dose, pulsatile regimen in patients with advanced solid malignancies: Results of a phase I exposure escalation study.
Authors: Lemonitsa H. Mammatas, Anthe S. Zandvliet, Maria Rovithi, Richard J. Honeywell, Eleonora L. Swart, Godefridus J. Peters, Catharina Wilhelmina Menke, Henk M.W. Verheul
Journal: Journal of Clinical Oncology (2018)

e14560 Background: Sorafenib is an oral multikinase inhibitor prescribed at a standard fixed dose of 400 mg twice daily. Increased sorafenib exposure is associated with improved efficacy, but toxicity limits further increase of this continuous schedule. We found preclinical antitumor activity of high dose, pulsatile sorafenib exposure on tumor cells. Therefore, we translated this approach into a phase I clinical trial for further evaluation (NCT02636426). Due to large interpatient variability at a fixed dose and decreased absorption at higher doses sorafenib, we applied personalized dose titration in this trial. Methods: High-dose sorafenib was administered once weekly in exposure escalation cohorts. Drug monitoring was performed in weeks 1-3 and doses were adjusted to achieve a predefined target plasma AUC0-12h starting with 25-50 mg/L/h, analogous to the continuous schedule. Patients were treated in cohorts of 3-6 patients. Toxicities were graded according to CTCAEv4.0 and responses were evaluated according to RECIST1.1. Results: 17 patients with progressive metastatic malignancies were included and received a median of 7 weekly cycles (range 1-24). Most common adverse events were fatigue (71%), nausea/vomiting (both 53%) and diarrhea (29%). Exposure limiting toxicity was observed in 1/6 patients treated in cohort 75-100 mg/L/h (3600 mg/week) consisting of grade 5 biliary tract perforation, while in 2/3 patients in cohort 125-150 mg/L/h (both 2800 mg/week) we observed grade 3 duodenal perforation and grade 5 multiorgan failure. Personalized dose titration resulted in a mean difference between observed and target AUC0-12h of 4% (SD ± 32%) in week 3 compared to 39% (SD ± 53%) in week 1 (P = 0.06) using a fixed starting dose. Stable disease was seen in 2 patients for a duration of 2.9 and 5.3 months. Conclusions: High-dose, pulsatile sorafenib treatment induced severe toxicity in the 4th exposure cohort of 125-150 mg/L/h. At that point the phase I study was terminated because of these early toxicities and disappointing efficacy without the possibility to further increase the pulsatile exposure needed to explore the potential benefit of this alternative approach. Clinical trial information: NCT02636426.
Inverse association of dietary calcium with systolic blood pressure in young children
Authors: M. W. Gillman
Journal: JAMA (1992)

<h3>Objective.</h3> —To investigate the association of dietary calcium with blood pressure in young children. <h3>Design.</h3> —Cohort. <h3>Setting.</h3> —General community. <h3>Subjects.</h3> —Eighty-nine boys and girls, aged 3 to 6 years, from The Framingham Children's Study. <h3>Measurements.</h3> —During the first year of the study, we derived nutrient data from multiple food diaries (a mean of 9.6 days of recording for each subject). At the beginning of the second year of the study, we obtained anthropometric data and up to five blood pressure readings (mean, 4.5) on each child at a single sitting. <h3>Results.</h3> —The range of subjects' average daily calcium intake was 4.9 to 19.6 mmol per 4200 kJ, with a mean of 12.8 mmol per 4200 kJ. Subjects' average systolic blood pressure ranged from 73 to 129 mm Hg, with a mean of 95.9 mm Hg; for diastolic blood pressure, the range was 37 to 78 mm Hg, mean 54.6 mm Hg. Multiple linear regression analysis, adjusted for the effects of sex, height, body mass index, and heart rate, showed that for each increment of 2.5 mmol of dietary calcium per 4200 kJ per day, systolic blood pressure was 2.27 mm Hg lower (95% confidence interval, 0.63 to 3.91 mm Hg; P =.008). We found no such association for diastolic blood pressure. <h3>Conclusion.</h3> —Dietary calcium is inversely related to systolic blood pressure in young children. (<i>JAMA</i>. 1992;267:2340-2343)
The Cost of Health.
Journal: JAMA (1952)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Autopsy-determined causes of death after cardiac valve replacement
Authors: F. J. Schoen
Journal: JAMA (1983)

We reviewed records of 378 patients who died after cardiac valve replacement and underwent autopsy at The Methodist Hospital, Houston, from 1962 through 1979. Patients were divided according to postoperative interval at death: within 30 days (early) or 30 days to ten years (late). Early deaths (279 patients) were due almost exclusively to cardiovascular abnormalities or operative complications (94%). Only 6% of early deaths were caused by prosthesis-associated complications. In contrast, late deaths (99 patients) were valve related in 47% of cases, including complete thrombotic occlusion or systemic thromboembolism (21%), prosthetic valve endocarditis (14%), valve dehiscence (6%), anticoagulation-related hemorrhage (3%), and mechanical degeneration (2%). Nine percent of late deaths were unrelated to cardiovascular disease. Thus, while early deaths primarily reflected the severity of preexisting or associated cardiovascular disease, prosthesis-associated complications were an important cause of late death after cardiac valve replacement. (<i>JAMA</i>1983;249:899-902)
Phase I and Pharmacokinetic Study of Imatinib Mesylate in Patients With Advanced Malignancies and Varying Degrees of Liver Dysfunction: A Study by the National Cancer Institute Organ Dysfunction Working Group
Authors: Ramesh K. Ramanathan, Merrill J. Egorin, Chris H.M. Takimoto, Scot C. Remick, James H. Doroshow, Patricia A. LoRusso, Daniel L. Mulkerin, Jean L. Grem, Anne Hamilton, Anthony J. Murgo, Douglas M. Potter, Chandra P. Belani, Michael J. Hayes, Bin Peng, S. Percy Ivy
Journal: Journal of Clinical Oncology (2008)

Purpose To develop dosing guidelines and to evaluate the pharmacokinetics of imatinib in patients with liver dysfunction (LD). Patients and Methods Patients (N = 89) with varying solid tumors and liver function were stratified into four groups according to serum total bilirubin and AST and were treated with escalating doses of imatinib. Plasma and urine were assayed for concentrations of imatinib and its active metabolite, CGP74588 . Results In the mild LD group, dose-limiting toxicity, specifically nausea/vomiting and fatigue, occurred in two patients at the 600 mg/d dose level. In the moderate and severe LD groups, the maximal dose evaluated was 300 mg/d. Grade 3 to 4 toxicities consisted primarily of liver function test elevations (24%), nausea/vomiting (10%), fatigue (6%), and edema (5%). After the first imatinib dose, the mean (± SD) dose-normalized areas under the plasma concentration-time curve from time 0 to infinity (AUC 0-∞ ) were 162 ± 155, 171 ± 72, 182 ± 157, and 185 ± 172 (μg/mL × h)/mg for normal, mild, moderate, and severe LD groups, respectively. Renal excretion of imatinib was less than 10% of the total dose in all groups. Conclusion Imatinib exposure (as measured by the dose-normalized AUC) did not differ between patients with normal liver function and those with LD. The maximal recommended dose of imatinib for patients with mild LD is 500 mg/d. Dosing guidelines for patients with moderate and severe LD remain undetermined.
THE SURGERY OF EPILEPTOGENIC LESIONS
Journal: JAMA (1964)

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
Der endemische Kropf.
Journal: JAMA (1913)

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
PROTEIN RESERVES AND THE NITROGEN MINIMUM
Journal: JAMA (1928)

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
Autoimmune hemolytic anemia due to levodopa therapy
Authors: M. C. Territo
Journal: JAMA (1973)

A 67-year-old white man developed Coombs test-positive hemolytic anemia secondary to levodopa therapy for Parkinson disease. The initial episode of anemia occurred after 11 months and 660 gm of drug exposure. A warm autoantibody directed against the Rh locus was found in the patient's serum and on his erythrocytes. On discontinuance of levodopa therapy, the autoimmune hemolytic anemia abated.
THE PLEA OF HYPNOTISM IN CRIMINAL CASES.
Journal: JAMA (1895)

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