tbuckley/cabot-search huggingface dataset:
The Lumleian Lectures on Inflammation
Authors: J. B. Sanderson
Journal: BMJ (1882)

I FEEL that I need some apology for coming before the College with a subject which has been frequently discussed already, and about which it may be presumed that I have nothing new to say.I cannot promise that it will not be so; for I have no new doctrine of inflammation to advance, no great discovery to relate.In what I shall have to say to-day of the nature of the process of inflammation, it will be my purpose to strengthen the position I have taken with reference to the subject on former occasi.ns, and particularly in my essay on Inflammation published in 1870, and in the lectures I gave in the theatre of the University of London seven years ago.*In my second lecture, I intend to enter on a question which, though not new, has attained of late years a significance which it did not before possess-that of the retiology of inflammation-that is, the discussion of the various agencies which, either as principal or accessory causes, may be concerned in its origin.And, lastly, I desire, in my third lecture, to bring our modern knowledge into comparison and harmony with the teaching of those who have thouight and observed best on the subject, from Hunter to our own times.i. Inflammation is the Phzysiological Effect of the Damcaz,e donle to a Tisste wthen it is inijured.-Thedefinition which in our epoch has
Influence of Atrial Fibrillation on Outcome Following Mitral Valve Repair
Authors: Eric Lim, Clifford W. Barlow, A. Reza Hosseinpour, Christopher Wisbey, Kate Wilson, Willis Pidgeon, Susan Charman, John B. Barlow, Francis C. Wells
Journal: Circulation (2001)

Background To investigate the outcome of patients in atrial fibrillation (AF) following mitral valve repair, clinical and echocardiographic follow-up was undertaken in 400 consecutive patients who underwent mitral valvuloplasty from 1987 to 1999. Methods and Results The main indications for surgery were degenerative (81.4%), endocarditis (7.1%), rheumatic (6.6%), ischemic (4.6%), and traumatic (0.3%) mitral valve disease. After excluding 6 paced patients and 1 patient in nodal rhythm, we compared the outcomes of 152 patients in AF against 241 patients in sinus rhythm. For patients in AF versus those in sinus rhythm, more AF patients were older (mean age 67.2±8.8 versus 61.9±11.8 years, respectively; P &lt;0.001), more were assigned to a poorer New York Heart Association (NYHA) class (77.6% versus 66.0% in NYHA III/IV, respectively; P =0.01), and more demonstrated impaired ventricular function (78.9% versus 46.2% with moderate or severe impairment, respectively; P &lt;0.001). For patients in AF versus those in sinus rhythm, there was no difference in 30-day mortality (2.0% versus 2.1%, respectively; P =0.95), repair failure (5.4% versus 3.6%, respectively; P =0.41), stroke (5.4% versus 2.2%, respectively; P =0.11), or endocarditis (2.3% versus 0.9%, respectively; P =0.27) on follow-up at a median of 2.8 years (interquartile range 1.1 to 6.0). On echocardiography, the proportion of patients with mild regurgitation or worse was 13.3% (AF patients) versus 10.8% (patients in sinus rhythm) ( P =0.70). Patients in AF versus those in sinus rhythm had lower survival at 3 years (83% versus 93%, respectively) and 5 years (73% versus 88%, respectively). Univariate analysis identified factors affecting survival as AF ( P =0.002), age &gt;70 years ( P =0.041), and poor ventricular function ( P &lt;0.001). However, by use of a multivariate model, only poor ventricular function remained significant ( P =0.01). Conclusions AF does not affect early outcome or durability of mitral repair. The onset of AF may be indicative of disease progression because of its association with poor left ventricular function.
Medical Education, Registration and Hospital Service
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 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
Identification of Putative Gene Based Markers of Renal Toxicity
Authors: Rupesh P. Amin, Alison E. Vickers, Frank Sistare, Karol L. Thompson, Richard J. Roman, Michael Lawton, Jeffrey Kramer, Hisham K. Hamadeh, Jennifer Collins, Sherry Grissom, Lee Bennett, C. Jeffrey Tucker, Stacie Wild, Clive Kind, Victor Oreffo, John W. Davis II, Sandra Curtiss, Jorge M. Naciff, Michael Cunningham, Raymond Tennant, James Stevens, Bruce Car, Timothy A. Bertram, Cynthia A. Afshari
Journal: Environmental Health Perspectives (2004)

Renal toxicity commonly occurs after administration of xenobiotics and a variety of pharmaceutical agents.The process is typically initiated by a toxic injury to tubular epithelial cells in various nephron segments or by injury to specific cell types in the glomerulus.The initial injury is often followed by cellular proliferation and repair that attempts to restore normal renal function (Toback 1992).Changes in the expression of mRNA specifically expressed in the injured kidney cells are some of the earliest events that accompany renal injury.This is accompanied by changes in the expression of other genes that contribute either to cellular repair or recovery of renal function or in those that mediate fibrosis and further pathology of the kidney (Matejka 1998;Norman et al. 1988;Safirstein et al. 1990).For example, elevations in the expression of heme oxygenase I (HO-1), kidney injury molecule-1 (KIM-1), clusterin, thymosin beta 4, osteopontin, and several growth factors have been reported in various models of renal injury (Hammerman 1998a(Hammerman , 1998b;;
Abstract 4734: Response of bladder and colon cancer cells to combined treatment with bromodomain and histone deacetylase inhibitors
Authors: Michael A. Lea, Niyati Patel, Charles desBordes
Journal: Cancer Research (2019)

Abstract Since bromodomains of proteins bind acetylated histone lysine side chains while histone deacetylase inhibitors increase the level of histone acetylation, it seemed possible that bromodomain inhibitors might counteract some cellular responses to the action of histone deacetylase inhibitors. We have examined this possibility in bladder and colon cancer cells treated with combinations of bromodomain and histone deacetyalase inhibitors. Actions on growth and on the induction of alkaline phosphatase activity by histone deacetylase inhibitors were investigated. Compounds studied were the bromodomain inhibitors JQ1, I-BET763, olinone and RVX208 and the histone deacetylase inhibitors butyrate, RGFP966 and valproate. The cells studied were ones in which alkaline phosphatase activity is induced by histone deacetylase inhibitors. They were bladder cancer lines 5637, HT1197 and HT1376 and colon cancer lines Caco-2 and HT29. The combination that most clearly showed decreased induction of alkaline phosphatase activity by a bromodomain inhibitor was butyrate plus JQ1. If this action represents blocking combination of bromodomain-containing transcription factors with acetylated histones one might anticipate that inhibitory effects of histone deacetylase inhibitors on growth might be mitigated by combination with bromodomain inhibitors. However, the tendency was for additive effects on growth inhibition in accord with some data in the literature. Of the bromodomain inhibitors that were studied, JQ1 was the most effective as a growth inhibitor and olinone was the least effective. The mechanism for additive effects of bromodomain and histone deacetylase inhibitors on growth remains to be defined but antagonistic effects on cell differentiation appear possible. Citation Format: Michael A. Lea, Niyati Patel, Charles desBordes. Response of bladder and colon cancer cells to combined treatment with bromodomain and histone deacetylase inhibitors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4734.
Correction
Journal: BMJ (1961)

the lower limit for fertility is regarded as something above 20 million per ml., provided volume, motility, and morphology are satisfactory.Many conceptions have been known to occur when the sperm density has been less than 5 million per ml.There is no upper limit to the normal sperm count, but, provided the density exceeds 20 million per ml., mere increase in numbers does not appear to result in enhanced fertility.(3) Water is a perfectly satisfactory diluent for counting sperms, though, of course, if counts of moving sperms are required, a physiological diluent such as normal saline or Baker's1 medium must be used, since water immediately kills sperms.Some (e.g., Farris2) consider that the total number of moving sperms in the ejaculate provides the best assessment of male fertility.It is not necessary to use a stain for sperm counting, though for observations on sperm morphology stained smears are required.
SODIUM DISPOSSESSED
Journal: JAMA (1961)

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
Psychiatrie.
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
ERCP for primary sclerosing cholangitis (PSC): An acceptable risk? (Dutch Multicenter PSC study group). Div. of GI &amp; Hepatology, Academic Medical Center, University of Amsterdam, NL, and The University of Alabama at Birmingham, USA
Journal: Hepatology (1995)

To determine the mechanism of action by which angiotensin-converting enzyme (ACE) inhibitors lower hematocrit in patients with posttransplant erythrocytosis, indices of red blood cell production and red blood cell destruction were obtained serially for 6 months from 10 renal transplant patients receiving treatment with enalapril for this problem. Before treatment, five patients had an elevated red blood cell mass, four had plasma volume contraction, and one had both. The mean hemoglobin concentration decreased by 2 g/dL (range, 0.5 to 3.3 g/dL), from 17 ± 1 g/dL to 15 ± 1 g/dL (P = 0.001) following 6 months of enalapril therapy. Similarly, the mean hematocrit decreased by 8% (range, 3% to 12%), from 52% ± 2% to 44% ± 3% (P = 0.001) during the same period. The mean reticulocyte count tended to decrease, although the change was not significant. The red blood cell mass decreased dramatically by 15% to 50%, from 32 ± 9 mL/kl to 23 ± 4 mL/kg (P = 0.008). Although serial erythropoietin levels declined steadily in two patients, there was no consistent change in the other patients. Mean levels decreased modestly, from 20 ± 11 mU/mL at baseline to 12 ± 5 mU/mL at 6 months, a change that was not statistically significant. Mean levels at each time point were not statistically different from the mean pretreatment value. Furthermore, during enalapril therapy, there was no correlation between mean circulating erythropoietin level and mean hematocrit (r = 0.43, P = 0.20) or hemoglobin concentration (r = 0.36, P = 0.30) or between changes in these parameters. Indices of red blood cell destruction, including haptoglobin, billrubin, and lactic dehydrogenase, were unchanged by enalapril therapy, as was calculated plasma volume at the beginning and end of the study. The current data suggest that enalapril improves posttransplant erythrocytosis by impairing red blood cell production without affecting red blood cell destruction or plasma volume. Furthermore, hematocrit decreased in most patients without a concomitant decrease in circulating erythropoietin levels. These results suggest that an inhibition of erythropoietin synthesis is not an essential component of the mechanism by which angiotensin-converting enzyme inhibitors lower hematocrit in most patients with posttransplant erythrocytosis. An inhibitory effect (ie, erythropoietin resistance) at the level of the bone marrow appears more likely, a hypothesis that would have to be proven by ferrokinetic studies in patients or by direct studies of erythropoiesis in vitro.
Cryptococcal Prostatitis
Authors: Marion H. Brooks
Journal: JAMA (1965)

SYSTEMIC CRYPTOCOCCOSIS (torulosis) is not as rare as was once believed. There were 286 cases reported in the English literature alone between 1950 and 1960.<sup>1</sup>Infection with<i>Cryptococcus neoformans</i>is most often associated with hematologic malignancies, steroid therapy, sarcoidosis, diabetes mellitus, tuberculosis, rheumatoid disease, cirrhosis, or some other debilitating illness. It usually involves the central nervous system. Although the lungs, skin, bones, adrenals, kidneys, and occasionally other organs have been affected, involvement of the prostate has been rarely observed. This report deals with a patient in whom cryptococcosis was diagnosed early by histological and bacteriological study of the prostate gland. <h3>Report of a Case</h3> This 31-year-old white man had Hodgkin's disease diagnosed by lymph node biopsy in 1956. Over the ensuing seven years, he was treated with x-radiation to all nodebearing areas, mechlorethamine hydrochloride, cyclophosphamide, Elderfield pyrimidine mustard, vinblastine sulfate, and hexamethylmelamine. In 1959, an acquired spherocytic hemolytic anemia
HLA typing for bone marrow transplantation. New polymerase chain reaction-based methods
Authors: A. B. Begovich
Journal: JAMA (1995)

BONE MARROW transplantation, first introduced into clinical practice in the 1960s, has now become an accepted form of therapy for a variety of hematologic malignancies as well as a number of other cancers, inherited blood disorders, immunodeficiency syndromes, and certain metabolic diseases.<sup>1,2</sup>In general, the purpose of bone marrow transplantation is to (1) replace malignant or genetically defective hematopoietic stem cells with healthy, fully functional stem cells; (2) allow the cancer patient to survive the high-dose radiation and/or chemotherapy required to destroy the malignant cells; and (3) in the case of certain cancers, provide a source of immunocompetent cells that can destroy any residual malignant cells (graft vs leukemia effect).<sup>3-5</sup>The clinical procedure of bone marrow transplantation involves the destruction of the patient's own marrow by irradiation and/or chemotherapy followed by the infusion of healthy bone marrow obtained from another individual (an allogeneic transplant). In cases of solid
236P Comparing chemo-radiotherapy with 5-fluorouracil and cisplatin versus thoracoscopic esophagectomy for cStage II-III esophageal squamous cell carcinoma
Authors: T. Kashiwada, Y. Harada, Y. Yoda, H. Noshiro, N. Aragane, S. Kimura
Journal: Annals of Oncology (2016)
Metaplasia of bronchial epithelium. Effect of age, sex, and smoking
Authors: D. M. Spain
Journal: JAMA (1970)

In 500 apparently "healthy" adults who died suddenly and unexpectedly and who lived and worked within the environs of a large urban area noted for its air pollution, autopsy studies revealed that 50% of all adult nonsmokers had metaplasia of their tracheobronchial epithelium. Metaplasia was present in 70% of male cigarette smokers. Women in each category revealed half the frequency of metaplasia present in the men. Metaplasia was present in less than 20% of men under the age of 30 years, rose to a peak of 80% at age 50 years, and gradually declined in frequency after the age of 60 years.
The Dietary of Health and Disease for the Use of Dietitians, Nurses and Instructors in the Sciences that Pertain to Nutrition.
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
TUBERCULOUS RHEUMATISM.
Journal: JAMA (1905)

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
Predicting the carcinogenicity of chemicals in humans from rodent bioassay data.
Authors: G Goodman, R Wilson
Journal: Environmental Health Perspectives (1991)

Regulatory agencies currently rely on rodent carcinogenicity bioassay data to predict whether or not a given chemical poses a carcinogenic threat to humans. We argue that it is always more useful to know a chemical's carcinogenic potency (with confidence limits) than to be able to say only qualitatively that it has been found to be a carcinogen. In a typical bioassay, a chemical is administered to groups of 50 to 100 rodents at the highest feasible level (the maximum tolerated dose) and rarely at less than 1/10 this dose in order to maximize the statistical significance of any increase in tumors that might result. Recently, much experimental work has focused on the mechanisms by which site-specific toxicity arising from chronic administration at the maximum tolerated dose may lead to carcinogenicity. Extrapolation of high-dose results to low doses does not take into consideration the possibility of a threshold dose, below which the carcinogenic potency is much lower or even zero. Threshold dose-response phenomena may be much more relevant to the etiology of cancer in the rodent bioassays than was earlier realized; if so, there is an even greater need for establishing dose-dependent potency estimates. The emphasis of this review is on the interspecies comparison of high-dose potencies. The qualitative and quantitative comparison of carcinogenicities between mice and rats and between rodents and humans is reviewed and discussed. We conclude that there is a good qualitative (yes/no) correlation for both the rat/mouse and the rodent/human comparison. There is also a good correlation of the carcinogenic potencies between rats and mice, and the upper limits on potencies in humans are consistent with rodent potencies for those chemicals for which human exposure data are available. For the rodent/human comparison, the best estimate of the interspecies potency factor is lognormally distributed around 1 when the potencies in both species are measured in units of (mg/kg-day)-1.
Gastrointestinal Hemorrhage (Excluding Peptic Ulcer and Esophageal Varices)
Authors: Irving B. Brick, Harold J. Jeghers
Journal: New England Journal of Medicine (1955)

THE two most common causes of gastrointestinal bleeding, peptic ulcer of the stomach and duodenum and esophageal varices secondary to portal cirrhosis of the liver, account for approximately 85 per cent of cases in which the etiology is known and have been the subject of an extensive literature. On the other hand, causes of gastrointestinal bleeding noted clinically less frequently tend to be neglected in the literature, except in sporadic case reports of a single entity. The importance of knowledge of these uncommon lesions is accentuated in individual cases in which massive gastrointestinal bleeding occurs but in which the usual . . .