tbuckley/cabot-search huggingface dataset:
Emotional Impairment in Internal Medicine House Staff
Authors: Charles L. Pelton
Journal: JAMA (1986)

To the Editor.—  I was very pleased to read the two articles 1,2 on  impairment of physicians in the March 7, 1986, issue of JAMA . Thank you for presenting this material and recognizing that physicians do indeed have problems with   As a physician who was once emotionally impaired, I involve myself in the treatment of   I am now teaching others how to get the information they need and how to apply it in their personal as well as their professional lives.  However, I would like clarification of what the authors mean by emotional impairment. I know what  impairment meant for me, my wife, and my children, but I do not know what it means to the authors.  I also wish to point out that the health care profession is being promoted as an adversary system, based on pathology and fault finding, similar to our
Localization of Islet-1–Positive Cells in the Healthy and Infarcted Adult Murine Heart
Authors: Florian Weinberger, Dennis Mehrkens, Felix W. Friedrich, Mandy Stubbendorff, Xiaoqin Hua, Jana Christina Müller, Sonja Schrepfer, Sylvia M. Evans, Lucie Carrier, Thomas Eschenhagen
Journal: Circulation Research (2012)

The transcription factor Islet-1 is a marker of cardiovascular progenitors during embryogenesis. The isolation of Islet-1-positive (Islet-1(+)) cells from early postnatal hearts suggested that Islet-1 also marks cardiac progenitors in adult life.
Sacred Space: Stories from a Life in Medicine
Authors: Herbert M. Swick
Journal: Annals of Internal Medicine (1998)

Medical Writings15 April 1998Sacred Space: Stories from a Life in MedicineHerbert M. Swick, MDHerbert M. Swick, MDUniversity of Kansas School of Medicine, Kansas City, KansasSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-128-8-199804150-00035 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Cleaveland C. 210 pages. Philadelphia: American Coll Physicians; 1998. $21.95. ISBN 0943126649. Order phone 800-523-1546.Field of medicine: General medicine.Format: Hardcover book.Audience: Although written principally for a lay audience, this book will also interest medical students and physicians.Purpose: The author hopes to convey “the very essence of medical care” through stories of his patients and teachers. His observations define the “sacred space” that has at its center a sick person, as depicted by Sir Luke Fildes in his famous painting, “The Doctor.”Content: The book is a series of short vignettes. Most are drawn from the author's ... Author, Article, and Disclosure InformationAffiliations: University of Kansas School of Medicine, Kansas City, Kansas PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 April 1998Volume 128, Issue 8Page: 699KeywordsMedical conditions ePublished: 15 August 2000 Issue Published: 15 April 1998 Copyright & PermissionsCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Severe Diarrhea in Pneumococcal Bacteremia
Authors: Jean-Michel Guerin
Journal: JAMA (1987)

To the Editor.—  In a recent letter, Del Rio and McGowan 1 report a case of watery diarrhea occurring during pneumococcal septicemia. This occurrence is not unusual. During the period from Jan 1,1979, to Dec 31,1986, we treated in an intensive care unit 86 patients who had severe pneumococcal septicemia. In seven (8%) cases there was severe watery diarrhea.  Report of Cases.— Case 1.—  A 56-year-old man with alcoholic cirrhosis had bilateral pneumonia and was hypotensive. He had profuse acute diarrhea, was leukoneutropenic, and had disseminated intravascular coagulation. Streptococcus pneumoniae was grown from all blood cultures. Despite treatment with penicillin G, the patient died 12 hours later.  Case 2.—  An 84-year-old hypertensive man was in a febrile coma. He had no pneumonia, but did have severe watery diarrhea. Streptococcus pneumoniae grew from blood and cerebrospinal fluid (CSF) cultures. He died six days later, having shown a flat electroencephalogram, despite
Contribution of increased mitochondrial free Ca2+ to the mitochondrial permeability transition induced bytert-butylhydroperoxide in rat hepatocytes
Authors: Aaron M. Byrne, John J. Lemasters, Anna-Liisa Nieminen
Journal: Hepatology (1999)

Previously, we showed that the oxidant chemical, tert –butylhydroperoxide ( t –BuOOH), induces a mitochondrial permeability transition (MPT) in intact hepatocytes, causing lethal cell injury. Here, we investigated the role of mitochondrial free Ca 2+ in t –BuOOH cytotoxicity to 1–day–cultured rat hepatocytes using confocal microscopy of autofluorescence and parameter–indicating fluorophores. t –BuOOH (100 μmol/L) caused an early increase of mitochondrial free Ca 2+ , as assessed by confocal microscopy of Rhod–2 fluorescence. Increased mitochondrial Ca 2+ was followed by onset of the MPT, as evidenced by permeation of cytosolic calcein into mitochondria and loss of the mitochondrial membrane potential-indicating dye, tetramethylrhodamine methylester. Preincubation with an intracellular Ca 2+ chelator (BAPTA–AM and its derivatives) partially blocked the late phase of mitochondrial NAD(P)H oxidation after t –BuOOH, but failed to prevent the early oxidation of mitochondrial NAD(P)H. Ca 2+ chelation also prevented the increase of mitochondrial Ca 2+ , generation of mitochondrial reactive oxygen species (ROS), onset of the MPT, and subsequent cell death. Confocal images showed that protection occurred when loading of the Ca 2+ chelator was predominantly mitochondrial. The antioxidant, desferal, also diminished increased mitochondrial Ca 2+ after t –BuOOH and prevented cell death. We conclude that oxidative stress induced by t –BuOOH enhances mitochondrial Ca 2+ uptake, leading to increased matrix Ca 2+ , increased ROS formation, onset of the MPT, and cell death.
New Device for Procedures on Diseased Bypass Grafts
Authors: Bernard A. Schwetz
Journal: JAMA (2001)

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
PD5-1-2: A phase I/II study of concurrent hypofractionated chemoradiotherapy using concomitant boost by 3D-conformal or intensity modulated radiotherapy for patients with stage III non-small cell lung cancer: preliminary results of Korean Radiation Oncology Group (KROG) Study- 0301
Authors: Sung-Ja Ahn, Hong Ryull Pyo, Woong Sub Koom, Tae Hyun Kim, Ji-Youn Han, Hung Tae Kim, Jin Soo Lee, Kwan Ho Cho, Kyu-Sik Kim, Young-Chul Kim
Journal: Journal of Thoracic Oncology (2007)
In vivo RNAi-mediated silencing of TAK1 decreases inflammatory Th1 and Th17 cells through targeting of myeloid cells
Authors: Gabriel Courties, Virginia Seiffart, Jessy Presumey, Virginie Escriou, Daniel Scherman, Jochen Zwerina, Gisela Ruiz, Natalia Zietara, Jadwiga Jablonska, Siegfried Weiss, Andrea Hoffmann, Christian Jorgensen, Florence Apparailly, Gerhard Gross
Journal: Blood (2010)
Norethisterone oenanthate as an injectable contraceptive.
Authors: R H Gray
Journal: BMJ (1979)

The World Health Organizations Special Program of Research Development and Research Training in Human Reproduction is presently conducting a multinational randomized comparative controlled clinical trial of depot-medroxyprogesterone acetate (DMPA) and norethisterone oenanthate (NET-OEN) in 11 countries.  The injections of NET-OEN are given at 8 weekly intervals for the first 6 months of therapy and then 50% of the NET-OEN subjects are randomly assigned to a 12 weekly injection schedule;  the remaining 50% continue on the 8 weekly regimen.  By August 1 1978 1186 subjects had received NET-OEN and 13344 women months of experience had been accumulated.  There have been a number of pregnancies among women receiving NET-OEN at 8 week intervals in contrast to the results presented by Giwa-Osagie and colleagues.  In addition the termination rates for amenorrhea among subjects receiving 8 weekly NET-OEN injections is substantially higher than that reported by Giwa-Osagie et al. and higher than the rates observed in a previous World Health Organization trial.
Coexpression of erythropoietin and heme oxygenase genes in Hep3B cells
Authors: John D. Lutton, Margaret O. Griffin, Miki Nishimura, Richard D. Levere, Attallah Kappas, Nader G. Abraham, Shigeki Shibahara
Journal: Hepatology (1993)

Exposure of Hep3B cells to metalloporphyrins (tinprotoporphyrin and heme) or cobalt chloride resulted in the production of a significant number of heme oxygenase transcripts, erythropoietin transcripts or both, as indicated by in situ hybridization. Exposure to heme 10 mumol/L resulted in a 30-fold to 40-fold increase in cells expressing erythropoietin messenger RNA (erythropoietin-positive cells) by 6 hr; this increased level remained elevated for 24 hr. Tin-protoporphyrin (10 mumol/L) produced an eightfold to 10-fold increase in erythropoietin RNA within 40 min. This value then returned to control levels by 60 min. Exposure to cobalt chloride (100 mumol/L) resulted in a 20-fold to 30-fold increase in erythropoietin expression for 5 to 20 min, returning to control by 40 min. Additionally, nuclear runoff assays demonstrated that the increase in heme oxygenase or erythropoietin messenger RNA accumulation by cobalt chloride appeared to be a result of stimulated transcription of the heme oxygenase and erythropoietin genes. However, the pattern for heme oxygenase messenger RNA induction was different from that for erythropoietin expression. Heme produced an immediate expression of heme oxygenase RNA (50-fold within 5 min) and a second sustained response during the next 24 hr. Tin-protoporphyrin also produced an immediate response (40-fold within 5 min) and remained elevated (20-fold) for 6 hr. Cobalt chloride produced a 22-fold increase within 20 min and returned to the control value by 1 hr. Thus both erythropoietin and heme oxygenase genes appear to be expressed after treatment with tin-protoporphyrin, heme or cobalt chloride; however, the time and patterns of expression are different.(ABSTRACT TRUNCATED AT 250 WORDS)
Liver function tests in workers with occupational exposure to polychlorinated biphenyls (PCBs): comparison with yusho and yu-cheng.
Authors: A Fischbein
Journal: Environmental Health Perspectives (1985)

The results of liver function tests in a population manufacturing capacitors and transformers are presented. Two clinical field examinations were performed, one in 1976 when PCBs were still used in the manufacturing of the electrical equipment and one at the end of 1979, 2.5 years after discontinuation of PCBs use. A low prevalence of abnormal liver function tests was found and mean values for all tests were within normal laboratory ranges. At the initial examination, weak, but statistically significant correlations were found between log LDH and plasma levels of log HPCB (higher chlorinated congeners of polychlorinated biphenyls) and log TPCB (total polychlorinated biphenyls) among the female workers, while log gamma-GTP correlated significantly only with log HPCB among the male workers. A significant increase to abnormal levels of gamma-GTP was noted at the follow-up examination in both male and female workers, and preliminary results indicate significant correlations between gamma-GTP and serum levels of PCBs among the male workers. These findings are in accordance with previously reported data on populations occupationally exposed to PCBs, but differ from hepatic biochemistry findings in accidental poisonings due to ingestion of cooking oil contaminated with PCBs and related compounds, i.e., polychlorinated dibenzofurans (PCDFs) and polychlorinated quaterphenyls (PCQs). Hence, the importance of considering the related compounds as etiologic factors in PCB poisoning is emphasized.
Abstract P6-07-28: Assessment of T stage in the multiple breast carcinomas
Authors: G Gong, J-H Jo, HJ Lee, J Kang
Journal: Cancer Research (2012)

Abstract Background: Tumor size is an important predictor of nodal metastasis, recurrence, distant metastasis in invasive breast carcinomas. T stage assignment of the multiple simultaneous ipsilateral breast carcinomas is based on the largest tumor with the suffix “(m)” to indicate multiplicity in the AJCC staging, and sum of the sizes should not be used. The aim of this study is to compare current AJCC staging and two test models using the aggregate of all tumor foci and the aggregate of all tumor volume in the single and multiple breast carcinomas. Methods: We reviewed original pathologic reports of 1145 consecutive patients with invasive ductal carcinoma, 2003–2004. 131 (11.4%) patients had multiple masses. Three factors were used to compare T stages; (1) the greatest dimension of the largest invasive component (T), (2) the aggregate of all tumor foci (TA), and (3) the aggregate of all tumor volume (TV). T stage follows AJCC (7th ed, 2010) system. TA and TV were categorized as followings: TA1 &amp;lt; 2cm, 2cm ≤ TA2 &amp;lt; 5cm and TA3 ≥ 5cm; TV1 &amp;lt; 8cm³ (average diameter &amp;lt; 2cm), 8 cm³ ≤ TV2 &amp;lt; 125cm³ and TV3 ≥ 125cm³ (average diameter ≥ 5cm). Clinicopathologic parameters were analyzed according to T stage. Results: Axillary lymph node metastasis was more common in the cases with multiple masses (64/131, 48.9%) than single mass (397/1014, 39.2%) and the number of the metastatic lymph node was also higher in multiple cases. Multiple breast carcinomas tended to show frequent recurrence, and disease specific death compared with the single cases in the same stage. (p &amp;lt; 0.05) Among 606 cases of T1, 34 cases were reclassified to TA2 and in 487 cases of the T2, 23 cases were reclassified to TA3. TV also showed reclassification of the cases. Multiplicity, T stage, TA stage, and TV stage were significant factors for nodal positivity in the univariate analysis (p &amp;lt; 0.05). Nodal positivity was remained in the multivariate analysis for recurrence and disease specific death, but the other factors were not significant for nodal involvement, recurrence and disease specific death. Conclusion: Multiple breast carcinomas has adverse patients' outcome than single carcinoma with same T stage of AJCC system and a better staging method is required to cover multiple carcinomas. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P6-07-28.
Effect of two randomised exercise programmes on bone mass of healthy postmenopausal women.
Authors: R Chow, J E Harrison, C Notarius
Journal: BMJ (1987)

The effect of two structured exercise programmes on the bone mass of 48 healthy postmenopausal white women aged 50-62 was studied after one year. Volunteers were randomised to group 1 (control), group 2 (aerobic exercise), or group 3 (aerobic and strengthening exercises). Before and after the training programme each subject had evaluations of bone mass (determined by neutron activation analysis and expressed as calcium bone index) and maximum oxygen uptake attained on a multistage exercise treadmill test. After one year both exercise groups had higher levels of fitness and greater bone mass than controls. Mean values (2 SEM) for changes in the calcium bone index were -0.011 (0.037), 0.039 (0.035), and 0.066 (0.036) for groups 1, 2, and 3, respectively. Analysis of variance on the observed data and analysis of covariance adjusting changes to the initial mean value for the whole group showed significant differences between each exercise group and the controls but no difference between the exercise groups themselves. Both exercise groups showed a significant improvement in maximum oxygen uptake. This study suggests that exercise may modify bone loss in healthy postmenopausal women.
An incidental finding in a preoperative chest radiograph
Authors: G. Currie, K. Fraser, D. R. Miller, M. Chetty
Journal: BMJ (2011)

An 88 year old woman who had never smoked was found to have a left lower zone mass on chest radiography before elective total knee replacement for osteoarthritis. Other than weight loss, she had no other symptoms. Her medical history included hypertension and anterior resection for Dukes’s A rectal cancer complicated by postoperative deep vein thrombosis eight years earlier; she had no history of tuberculosis. Cardiorespiratory and abdominal examinations (other than a scar) were normal; performance status was 1. Routine blood tests and carcinoembryonic antigen were normal and negative, respectively. Chest and abdominal computed tomography was performed (figs 1⇓ and 2⇓), with abnormalities noted only within the thorax.



Fig 1 Computed tomography of the chest 





Fig 2 Computed tomography of the chest (at a different level from that of fig 1)





### 1 What does performance status measure?

#### Short answer

The Eastern Co-operative Oncology Group/World Health Organization performance status is used widely in patients with cancer to measure their general wellbeing and ability to perform (or otherwise) daily living activities.

#### Long answer

Performance status is often used as a general guide to help …
Abstract 3341: TGFβ/ TNFα-mediated epithelial-mesenchymal transition generates breast cancer stem cells with a claudin-low phenotype
Authors: Michael K. Asiedu, James N. Ingle, Marshall D. Behrens, Derek C. Radisky, Keith L. Knutson
Journal: Cancer Research (2011)

Abstract Breast cancer recurrence is believed to be caused by a potently tumorigenic sub-population of cancer cells possessing stem cell attributes of resistance to chemotherapy, radiation and other forms of treatment. Recently, we and others have reported the generation of breast cancer stem cell (BCSC) characteristics by inducers of epithelial to mesenchymal transition (EMT). Both EMT and acquisition of BCSC properties are therefore important steps in cancer progression, although the physiological process by which BCSCs arise in vivo remains unclear. We show here that exposure to TGFβ and TNFα induces a stable BCSC phenotype, characterized by self-renewal, greatly increased tumorigenicity, and increased resistance to oxaliplatin, etoposide and paclitaxel. We further found that the TGFβ/TNFα-derived cells showed downregulated expression of Claudins 3, 4 and 7 and the luminal marker KRT18, demonstrating a shift to the claudin low molecular subtype, a recently identified breast cancer subtype characterized by the expression of mesenchymal and stem cell-associated markers and correlation with poor prognosis. Furthermore, pathway analyses of the generated BCSCs showed deregulation of a number of breast cancer-associated genes and pathways including inflammatory cytokine and receptors, chemokines, homeobox, hedgehog, notch and metastases genes. These results confirm the role of EMT and BCSCs in resistance of breast cancer to conventional chemotherapy and identify novel target genes and pathways for validation as potential therapeutic targets. Our demonstration that stable BCSCs can be produced by specific microenvironmental signals also provides a valuable tool for studying cancer stem cells, as well as a means for screening potential cancer drugs for efficacy of targeting cancer stem cells to prevent recurrence. 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 3341. doi:10.1158/1538-7445.AM2011-3341
Mechanisms and models of TDP-43 proteinopathies
Authors: Leonard Petrucelli
Journal: Molecular Neurodegeneration (2012)

Background Abnormal distribution, modification and aggregation of transactivation response DNA-binding protein 43 (TDP43) are the hallmarks of multiple neurodegenerative diseases, especially frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis (ALS). Results To explore the pathogenic properties of mutant forms of TDP-43, we generated and characterized two mouse lines expressing human TDP-43 carrying the M337V mutation (hTDP-43M337V). We found hTDP-43M337V was expressed primarily in the nuclei of neurons in the brain and spinal cord, intranuclear and cytoplasmic phosphorylated TDP43 aggregates were frequently detected, and the levels of TDP-43 LMW products of ~25 kDa and ~35 kDa species were also increased. Overexpression of hTDP-43M337V dramatically down regulated the levels of mouse TDP-43 (mTDP-43) protein and RNA, indicating TDP-43 levels are tightly controlled in mammalian systems. TDP43M337V mice displayed reactive gliosis, widespread ubiquitination, chromatolysis, gait abnormalities, and early lethality. Abnormal cytoplasmic mitochondrial aggregates and abnormal phosphorylated tau were also detected in the mice. Conclusion While overexpression of hTDP-43 in wild-type TDP-43 and TDP-43M337V mouse models produces similar phenotypes, our results suggest that overexpression of the hTDP-43M337V can cause neuronal dysfunction due to its effect on a number of cell organelles and proteins, such as mitochondria and TDP-43, that are critical for neuronal activity.
A man with rust coloured urine and normocytic anaemia
Authors: Sarah Case, Thomas J Johnston, Michael O'Sullivan, Will Thomas, Oliver J Wiseman
Journal: BMJ (2015)

A 65 year old man presented to the emergency department with a 10 day history of dark urine, general malaise, and progressive shortness of breath. He had a history of rheumatic heart disease and had been on warfarin since he had a metallic mitral valve replacement in 1984. He was a retired teacher, drank a minimal amount of alcohol, and was a non-smoker. He had no family history of cancer.

On examination he was jaundiced with a sinus tachycardia (120 beats/min) and a pansystolic murmur. His other vital signs were normal. On examination, his other systems were normal except for mild suprapubic tenderness, as were the results of a digital rectal examination.

His urine was rust coloured (fig 1⇓) with no blood clots. Urine dipstick was positive for blood (3+), protein (3+), and leucocytes (3+), but negative for nitrites. No red blood cells or casts were noted during microscopy.



Fig 1 Patient’s urine on admission



The table⇓ shows the results of his initial laboratory investigations. A peripheral blood film showed red cell fragments, polychromasia, and normal platelets (a representative smear is shown in fig 2⇓). The results of chest radiography, computed tomography of the kidneys, and ultrasound of the urinary tract were also unremarkable. Serial sepsis screens and three sets of blood cultures for endocarditis were all negative.

View this table:

Laboratory test results on admission





Fig 2 A representative blood film showing red cell fragments (arrows)





### 1. What are the causes of dark urine?

#### Answer

Haematuria, menstrual contamination, haemoglobinuria, and myoglobinuria will cause dark urine that is positive for blood on urine dipstick testing. Red cells …