tbuckley/cabot-search huggingface dataset:
MEDICAL MOTION PICTURES
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
Effect of lamivudine on morphology and function of mitochondria in patients with chronic hepatitis B
Authors: P Honkoop
Journal: Hepatology (1997)

Nucleoside analogues can induce mitochondrial dysfunction leading to severe clinical syndromes. Lamivudine, a new nucleoside analogue, is an active inhibitor of hepatitis B viral replication without apparent clinical toxicity. To assess subclinical mitochondrial toxicity, we studied the morphology and function of the mitochondrial system in 15 patients treated with lamivudine. Morphology was investigated by routine histological evaluation and electron-microscopic studies of mitochondria in liver biopsy specimens. Mitochondrial function was assessed by 2-keto[1-14C] isocaproic acid decarboxylation (KICA breath test) and by measuring the activity in liver biopsy specimens of the mitochondrial enzymes encoded by nuclear and mitochondrial DNA (mt-DNA) (complex I and IV) as well as a mitochondrial and a cytosolic enzyme both encoded by nuclear DNA only (complex II and lactic dehydrogenase [LDH]). All 15 patients underwent a liver biopsy before treatment and a KICA breath test before and during treatment; 13 agreed to undergo a repeat liver biopsy during lamivudine treatment. Liver tissue with no or minimal fibrotic changes from 7 patients treated for 6 months with lamivudine was suitable for assessment of the mitochondrial enzyme activity. We observed no signs of toxicity by routine histological or electron-microscopic evaluation. KICA breath tests revealed no differences in either peak exhalation or the area under the curve from 0 to 60 minutes between healthy controls (3.0% and 19.3%), untreated patients with chronic hepatitis B (3.4% and 19.3%), and patients treated with lamivudine (3.1% and 20.6%). The activities of the mt-DNA-encoded enzymes remained normal after lamivudine therapy. Unexpectedly a significant decrease in the activity of nuclear-DNA-encoded enzymes in patients with chronic hepatitis B in comparison with normal controls was found. The mean activity of complex II dropped from 45.3 to 20.0 µmol · min−1, that of lactic dehydrogenase from 106 to 44 µmol · min−1 (Wilcoxon rank sum; P < .05). In conclusion, no subclinical signs of mitochondrial toxicity resulting from lamivudine therapy for 6 months were observed.
Abstract 15483: Functional Relevance of Rare GUCY1A3 Variants in Patients Affected by Premature Myocardial Infarction
Authors: Jana Wobst, Tan A Dang, Thorsten Kessler, Simon von Ameln, Stephanie Tennstedt, Christian Hengstenberg, Jeanette Erdmann, Heribert Schunkert
Journal: Circulation (2015)

Introduction: Myocardial infarction (MI) is the main complication of coronary artery disease (CAD). Recently, a locus tagging the GUCY1A3 gene has been shown to be genome-wide significantly associated with CAD. GUCY1A3 encodes the α1 subunit of the soluble guanylyl cyclase (sGC), a heterodimer composed of α1 and β1 subunits. Activated by nitric oxide (NO) the sGC produces cGMP. cGMP mediates various cellular functions including vasodilatation and inhibition of platelet aggregation. Besides this common variant, our group also identified rare variants in the coding sequence of GUCY1A3 associated with CAD/MI. Aim: We aimed to investigate the functional implication of rare variants found in CAD/MI patients regarding expression level, dimerization capability and enzymatic activity. Methods and Results: Employing whole-exome sequencing our group identified two rare GUCY1A3 variants in two extended families with a high prevalence of premature CAD/MI (Erdmann et al Nature 2013). Sequencing the respective exons in further 252 young MI patients led to the identification of seven additional rare variants. Effects on protein level were investigated by Western blotting after overexpression in HEK cells. Except for one of the variants, all dimerized with β1 shown by co-immunoprecipitation. One of the α1 variants exhibited significantly decreased protein levels compared to wild type α1 while another showed significantly increased protein levels. The amounts of β1 subunits correlated with those of α1 in all cases. sGC enzymatic activity was assessed by measuring cGMP by radioimmunoassay after stimulating overexpressed HEK cells with NO. Three of the variants demonstrated significantly decreased cGMP production at every time point tested. cGMP levels only correlated in part with the observed protein levels. Conclusion and Outlook: We identified nine rare variants in the coding sequence of GUCY1A3 and demonstrated some of them leading to altered protein levels as well as diminished activity. As both mechanisms in the end influence the capacity of cGMP formation, this appears to be a possible mechanism for GUCY1A3 leading to atherosclerosis and MI. Future studies will focus on mRNA abundance and protein degradation to uncover the reason for altered protein levels.
Lvmphedema Praecox
Journal: JAMA (1963)

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
THE GOLD-HEADED CANE
Authors: J. H. T.
Journal: JAMA (1960)

The hallmark of the carriage trade of medical practice in England in the 18th century was the gold-headed cane. The story of the ascendancy through five generations of practitioners of one eminent cane is recounted, with many asides, by a supposedly anonymous editor speaking for the cane. My copy of "The Gold-Headed Cane" is a second edition published in 1828, presumably with no editor,<sup>1</sup>The boards probably are original; less than one square inch of the back strip was salvaged by the book binder who refurbished the monograph in its present state. The salvaged scrap includes a portion of the title. A zinc etching of the botanical gardens of Chelsea is reproduced on the flyleaf. The 1864 edition edited by William Munk was published by Longmans, Green and Co. A reprinting of the volume in 1915 carries a foreword by William Osler and a title page, with William MacMichael as
Toxic epidermal necrolysis. A step forward in treatment
Authors: D. M. Heimbach
Journal: JAMA (1987)

Toxic epidermal necrolysis is an uncommon but severe form of epidermal sloughing with associated mucositis. Treated in a general hospital, it carries a high mortality (25% to 70%) and substantial long-term morbidity. If the patient is referred early to a burn center, where it can be treated with biologic dressings and intensive support care, the mortality can be reduced below 20% and there may be negligible long-term morbidity. We describe 19 patients so treated, with three deaths and no long-term complications. (<i>JAMA</i>1987;257:2171-2175)
The effects of bicarbonate on blood coagulation
Authors: D. W. Wong
Journal: JAMA (1980)

The anticoagulant effects of sodium and potassium bicarbonate were investigated with use of fresh human whole blood obtained from normal healthy volunteers. Results from prothrombin and thrombin clotting time determinations demonstrated that bicarbonate can interfere with the clotting process. Clinical data obtained from patients who received intravenous administration of sodium bicarbonate supported these findings. (<i>JAMA</i>244:61-62, 1980)
Reply
Authors: David Pereyra, Patrick Starlinger
Journal: Hepatology (2018)

Potential conflict of interest: Nothing to report. We thank Pang et al. for their interest in our study. In our recent publication, we observed that von Willebrand factor antigen (vWF‐Ag) seems to be critically involved in liver regeneration after liver resection in humans. Indeed, we agree that vWF‐Ag might be involved in mechanisms with potentially opposing effects. In fact, this is nicely demonstrated within our present study: while patients with high preoperative levels of vWF‐Ag were found to have an increased risk for postoperative complications, an increase in vWF‐Ag during the very early phase of liver regeneration seemed to be required to allow for adequate postoperative liver regeneration. In this context, preoperative levels of vWF‐Ag presumably reflect the degree of parenchymal damage and portal hypertension. In contrast, the initial vWF‐Ag burst during early liver regeneration seems to be central for induction and success of platelet‐mediated liver regeneration, which is in line with experimental data.1 Similar to its involvement in liver disease and regeneration, there is evidence for both a protumorigenic and an antitumorigenic property of vWF‐Ag.2 While Pang and coworkers specifically referred to hepatocellular carcinoma, current literature describes vWF‐Ag as a modulator in a variety of malignant neoplasms.3 Still, the underlying pathophysiologic mechanisms seem to be similar for nearly all investigated entities. In summary, studies show an antiangiogenic role of vWF‐Ag supposedly as a consequence of negative interaction with receptors for vascular endothelial growth factor. Further, a direct proapoptotic effect of vWF‐Ag could be shown. Most puzzling, however, is the function of vWF‐Ag in tumor metastasis: while a prometastatic role of vWF‐Ag, most likely through augmentation of tumor cell binding on platelets and endothelial cells, was independently shown by several studies, experimental data revealed an increased metastatic potential for transplanted tumor cells in vWF‐deficient mice. Based on the available data, one has to acknowledge the probability of opposing functions of vWF‐Ag. As we recently reported on the bivalent role of a key molecule of liver regeneration,4 a similar involvement of vWF‐Ag in patients undergoing liver surgery is indeed conceivable. Still, there is a lack of human data in regard to functional properties of vWF‐Ag in tissue regeneration and cancer. Thus, we fully agree with Pang et al. and encourage further work on the pathophysiologic involvement of vWF‐Ag in this area. Author names in bold designate shared co‐first authorship.
Socialized Medicine
Authors: Edward Palmer
Journal: JAMA (1965)

<h3>To the Editor:—</h3> A recent communication in the Dec 28, 1964, issue ofThe Journalby E. Grey Dimond (The Long Range Alternative to Socialized Medicine is Academic Medicine,<b>190</b>:1118) is a worthwhile plea for a program of continuing medical education and supervision of the practitioner, but its connection to socialized medicine is elusive. There are those who are so devoted to medicine that they are unaware there is more to medical practice than "academic medicine." That we should omit all interest in and consideration of the economics of medical practice and devote ourselves solely to the care of patients is very noble; but we should not forget that the recent history of compulsory medical practice overseas is one where the medical profession has been at the mercy of the government. As members of a profession participating in free enterprise, we should be most concerned with its survival and
Members of the House of Delegates
Journal: JAMA (1986)

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
LATENT TUBERCULOSIS IN CHILDHOOD.
Journal: JAMA (1906)

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
Conference on Medical Reform: Fifth Meeting of the Delegates, Tuesday, February 9, 1841
Authors: None Forbes
Journal: BMJ (1841)

mons, and he trusted that clauses would be soon0 introduced, or attempted to be introduced, se- curing a better remuneration to that part of the medical profession that was called upon to attend the poor.He hoped that every gentleman would feel the importance of signing petitions on this subject.The resolution was so concise, and yet so explanatory, that he need not say anything further on the subject.R. L. Purching, Esq. of Walthamstow, seconded the resolution.The Chairman explained that the clauses re- ferred to embraced, first, the size of districts, by limiting those which were now too extensive; se- condly, they also contended for the abolition of the system of " tender;" thirdly, they provided for something like a remuneration to poor-law me- dical officers.He had that evening been informed by Mr. Bottomley of Croydon,
Erratum: NLRP12 attenuates colon inflammation by maintaining colonic microbial diversity and promoting protective commensal bacterial growth
Authors: Liang Chen, Justin E Wilson, Mark J Koenigsknecht, Wei-Chun Chou, Stephanie A Montgomery, Agnieszka D Truax, W June Brickey, Christopher D Packey, Nitsan Maharshak, Glenn K Matsushima, Scott E Plevy, Vincent B Young, R Balfour Sartor, Jenny P-Y Ting
Journal: Nature Immunology (2017)
Effect of Glutathione S-Transferase M1 Polymorphisms on Biomarkers of Exposure and Effects
Authors: Radim J. Sram
Journal: Environmental Health Perspectives (1998)

Genotypes responsible for interindividual differences in ability to activate or detoxify genotoxic agents are recognized as biomarkers of susceptibility.Among the most studied genotypes are human glutathione transferases.The relationship of genetic susceptibility to biomarkers of exposure and effects was studied especially in relation to the genetic polymorphism of glutathione S-transferase Ml (GSTM1).For this review papers reporting the effect of GSTM1 genotype on DNA adducts, protein adducts, urine mutagenicity, Comet assay parameters, chromosomal aberrations, sister chromatid exchanges (SCE), micronuclei, and hypoxanthine-guanine phosphoribosl transferase mutations were assessed.Subjects in groups occupationally exposed to polycyclic aromatic hydrocarbons, benzidine, pesticides, and 1,3-butadiene were included.As environmentally exposed populations, autopsy donors, coal tar-treated patients, smokers, nonsmokers, mothers, postal workers, and firefighters were followed.From all biomarkers the effect of GSTM1 and N-acetyl transferase 2 was seen in coke oven workers on mutagenicity of urine and of glutathione S-transferase Ti on the chromosomal aberrations in subjects from 1,3-butadiene monomer production units.Effects of genotypes on DNA adducts were found from lung tissue of autopsy donors and from placentas of mothers living in an air-polluted region.The GSTM1 genotype affected mutagenicity of urine in sm6kers and subjects from polluted regions, protein adducts in smokers, SCE in smokers and nonsmokers, and Comet assay parameters in postal workers.A review of all studies on GSTM1 polymorphisms suggests that research probably has not reached the stage where results can be interpreted to formulate preventive measures.The relationship between genotypes and biomarkers of exposure and effects may provide an important guide to the risk assessment of human exposure to mutagens and carcinogens.
Smoking and cervical cancer
Authors: D. F. Austin
Journal: JAMA (1983)

Elsewhere in this issue (p 499), Trevathan and colleagues report an association between cigarette smoking and both dysplasia and carcinoma in situ of the uterine cervix. Initially hypothesized in 1977 by Winkelstein,<sup>1</sup>the association of invasive cervical cancer and carcinoma in situ with smoking has now been reported by almost every retrospective<sup>2-6</sup>and prospective<sup>7,8</sup>study in which the investigators sought to detect such a relationship. Trevathan et al now confirm the existence of the same relationship in cervical carcinoma in situ and in its premalignant precursor, dysplasia. Both the work of Trevathan et al and of Lyon et al<sup>9</sup>may be considered second-generation studies because they were undertaken with the primary intent of testing the validity of the previously reported association. Both studies substantiated the association and both found a particularly strong effect from smoking at an early age. Both groups suggest, as a possible biologic
Organophosphorus Poisoning
Authors: JOHN S. TOBIN
Journal: Annals of Internal Medicine (1978)

Letters and Corrections1 October 1978Organophosphorus PoisoningJOHN S. TOBIN, M.D.JOHN S. TOBIN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-89-4-579_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: I wish to comment on the report "Late Onset of Neuromuscular Block in Organophosphorus Poisoning" by Gadoth and Fisher in the May 1978 issue (Ann Intern Med 88:654-655, 1978).The case described is not, in my opinion, a case of organophosphate intoxication, for the following reasons.Labored breathing is not one of the early signs of this syndrome. The signs and symptoms of organophosphate intoxication are clearcut. The earliest are lightheadedness, dizziness, headache, and weakness, with hyperhydrosis, pallor, nausea, and blurring of vision. Respiratory depression is a late finding and is due to dysfunction of respiratory musculature....References1. NAMBA T, NOLTE C, JACKREL G, and GROB D: Poisoning due to organophosphate insecticides. Am J Med 50:475-492, 1971 CrossrefMedlineGoogle Scholar2. TCHERNILAS J: Poisoning with organophosphorus insecticides in Israel. Doctoral thesis. The University of Tel Aviv Medical School, April 1970 Google Scholar3. WADIA R, SADAGOPAN C, AMIN R, and SARDESAI H: Neurological manifestations of organophosphorus insecticides poisoning. J Neurol Neurosurg Psychiatry 37:841-847, 1974 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: JOHN S. TOBIN, M.D. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1978Volume 89, Issue 4 Page: 579-579 Keywords Breathing Headaches Intoxication Nausea Neuromuscular blockade Signs and symptoms Vision ePublished: 1 December 2008 Issue Published: 1 October 1978 PDF downloadLoading ...
Corrigendum
Journal: BMJ (1931)

the provision of his board and domestic service, can properly be taken into account when estimating what is the appropriate fraction of the total domestic expenses to be taken into account for the y-ear in question as the pro- fessional rather than the domestic cost of the whole.Motor Car Allowance "MW.J. C." bought an " X " car in 1929 for £135 and was allowed £27 depreciation thereon as for 1930-31.In November, 1930, he sold the car for £45 an(d bought a " Y " car for £C110.What should he claim in the accounts which he is sending in for the 1931-32 assessment?*** (1) Obsolescence allowance-that is, £135 -£27-£45=£63-as a professional expense of the year 1930, and(2) depreciation allowance for 1931-32 at 20 per cent. of £110=£22.
SI Units
Authors: E. Armitage, R. Burwood, D. A. Chamberlain, T. A. Copp, G. Deutsch, P. Hall-Smith, A. Harden, B. Hogbin, J. Horley, R. P. Juniper, E. Keat, P. A. Lane-Roberts, B. A. Lathan, D. R. Levinson, A. Macfarlane, B. Measday, D. Melcher, B. R. P. Murray, C. E. Quin, J. Rees, D. Reid, C. Riley, D. S. T. C. Roberts, P. Sharpstone, J. Sheldon, P. G. Somerville, J. R. R. Spurrell, A. Trafford, J. de Winter, P. A. D. Williams
Journal: BMJ (1975)