tbuckley/cabot-search huggingface dataset:
Sensitivity of Mammography and Physical Examination of the Breast for Detecting Breast Cancer
Authors: Mary Jane Hicks
Journal: JAMA (1979)

Mammography and physical examination of the breast are evaluated as screening instruments for detecting breast cancer based on local biopsy data obtained from women enrolled in a national breast cancer screening program. One hundren thirteen cancers (15.5%) of women who underwent biopsy) were detected. The individual sensitivities of mammography and physical examination for detecting breast cancer are 62% and 24%, respectively. The sensitivity of the two methods combined is 75% (85 of 113). Thirty-seven cancers were in situ or minimally invasive (less than or equal to 1 cm in greatest dimension). Eighty-one percent (30 of 37) of these small cancers were detected by screening, and they comprised 35% (30 of 85) of all cancers detected by mammography, physical examination, or both. Improved survival is anticipated due to this high rate of discovery of small cancers.
Air pollution and blood markers of cardiovascular risk.
Authors: J Schwartz
Journal: Environmental Health Perspectives (2001)

Recent studies have linked air pollution to tens of thousands of premature cardiovascular deaths per year. The mechanisms of such associations remain unclear. In this study we examine the association between blood markers of cardiovascular risk and air pollution in a national sample of the U.S. population. Air pollution concentrations were merged to subjects in the Third National Health and Nutrition Examination Survey (NHANES III) in the United States, and the association with fibrinogen levels and counts of platelets and white blood cells were examined. The subjects in NHANES III are a representative sample of the U.S. population. Regressions controlled for age, race, sex, body mass index, current smoking, and number of cigarettes per day. The complex survey design was dealt with using mixed models with a random sampling site effect. In single-pollutant models, PM(10) (particulate matter with a mass median aerodynamic diameter less than 10 microm) was associated with all three outcomes (p< 0.05): Sulfur dioxide (SO(2)) was significantly associated only with white cell counts, nitrogen dioxide (NO(2)) with platelet counts and fibrinogen, and ozone with none of the outcomes. In two-pollutant models, PM(10) remained a significant predictor of white cell counts controlling for SO(2) but not vice versa. PM(10) was marginally significant in a model for platelet counts with NO(2), and the sign of the NO(2) coefficient was reversed. These results were stable with control for indoor exposures (wood stoves, environmental tobacco smoke, gas stoves, fireplaces), dietary risk factors (saturated fat, alcohol, caffeine intake, n-3 fatty acids), and serum cholesterol. The magnitude of the effects are modest [e.g., 13 microg/dL fibrinogen for an interquartile range (IQR) change in PM(subscript)10(/subscript), 95% confidence interval (CI) 4.6-22.1 mg/dL]. However, the odds ratio of being in the top 10% of fibrinogen for the same IQR change was 1.77 (95% CI 1.26-2.49). These effects provide considerable biologic plausibility to the mortality studies. PM(10), but not gaseous air pollutants, is associated with blood markers of cardiovascular risk, and this may explain epidemiologic associations with early deaths.
Surgical Clerkship
Authors: Charles G. Child
Journal: JAMA (1967)

Most clinical educators agree that for many years the clinical clerkship has been, and probably still is for that matter, their most important pedagogic method for instructing medical students in medicine and surgery. In this day of crisis and ferment in medical education, the clinical clerkship, along with other traditional systems of medical teaching, is properly being examined and reevaluated. Is the clerkship as useful as it has been? Should it be retained? Should a substitute be devised for it? Should it be modified? Efforts to answer these basic questions may be simplified by considering the clerkship's original nature and why it was introduced into medical school curricula in the first place. This should provide a reasonable background against which to examine the clerkship today. In course, some understanding may be achieved of why the surgical clerkship has apparently fallen on bad times and even amongst thieves. There are some,
Pricing for Orphan Drugs
Authors: Brian P. O’Sullivan, David M. Orenstein, Carlos E. Milla
Journal: JAMA (2013)

Cystic fibrosis (CF) is an inherited condition that affects approximately 30 000 individuals in the United States.1 Rare genetic diseases such as CF are increasingly seen as unique niche markets for pharmaceutical companies. An unsustainable price structure for novel drugs developed by pharmaceutical companies for this rare condition and others is developing. In January 2012, the US Food and Drug Administration approved Vertex Pharmaceuticals� drug ivacaftor (Kalydeco) for use in a subpopulation of patients with CF who carry a specific genetic mutation, G551D. Ivacaftor is the first drug that treats the underlying molecular defect in CF, and its introduction illustrates an application of personalized medicine. The development program that led to the discovery of this drug was firmly grounded and incrementally built on the many contributions made during at least 3 decades by a highly supportive community built by and around patients and their families affected by this disease. The work of the CF community has been used as an example of how to advance discovery toward a cure for rare conditions in partnership with industry
Therapeutic Strategy in Clinical Immunology
Authors: Robert S. Schwartz
Journal: New England Journal of Medicine (1969)

THE control of disease by immunologic means began in 1796, when Edward Jenner inoculated James Phipps with cowpox. Immunologic prophylaxis still flourishes, and the discovery that passive immunization prevents erythroblastosis1 is its latest triumph. Early in this century Clemens von Pirquet initiated another branch of immunology by establishing the principle that antibodies can be injurious. The central issues of clinical immunology, formulated in terms of these momentous discoveries, are the production of desired immunity and the elimination of undesired immune reactions. It is with the latter that this review is concerned.Normal Immune ResponsesStudies of the immune response are . . .
Photothermal ablation of tumor cells using a single-walled carbon nanotube–peptide composite
Authors: Yasuhiko Hashida, Hironori Tanaka, Shuwen Zhou, Shigeru Kawakami, Fumiyoshi Yamashita, Tatsuya Murakami, Tomokazu Umeyama, Hiroshi Imahori, Mitsuru Hashida
Journal: Journal of Controlled Release (2013)
Meningitis caused by Campylobacter fetus ssp jejuni.
Authors: R Norrby, R V McCloskey, G Zackrisson, E Falsen
Journal: BMJ (1980)

Differences in serum ampicillin concentrations among patients under constant-rate infusion Continuous infusion of a drug at a constant rate is supposed to main- tain its serum concentration at a constant and predictable level.We investigated the truth of this in patients treated with ampicillin for severe purulent meningitis.
POU Domain Factors in the Neuroendocrine System: Lessons from Developmental Biology Provide Insights into Human Disease*
Authors: Bogi Andersen, Michael G. Rosenfeld
Journal: Endocrine Reviews (2001)

POU domain factors are transcriptional regulators characterized by a highly conserved DNA-binding domain referred to as the POU domain. The structure of the POU domain has been solved, facilitating the understanding of how these proteins bind to DNA and regulate transcription via complex protein-protein interactions. Several members of the POU domain family have been implicated in the control of development and function of the neuroendocrine system. Such roles have been most clearly established for Pit-1, which is required for formation of somatotropes, lactotropes, and thyrotropes in the anterior pituitary gland, and for Brn-2, which is critical for formation of magnocellular and parvocellular neurons in the paraventricular and supraoptic nuclei of the hypothalamus. While genetic evidence is lacking, molecular biology experiments have implicated several other POU factors in the regulation of gene expression in the hypothalamus and pituitary gland. Pit-1 mutations in humans cause combined pituitary hormone deficiency similar to that found in mice deleted for the Pit-1 gene, providing a striking example of how basic developmental biology studies have provided important insights into human disease.
Caring for the World: A Guidebook to Global Health Opportunities
Authors: Samuel Y. Sessions
Journal: JAMA (2009)

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
Splenic Uptake of Both Technetium-99m Diphosphonate and Technetium-99m Sulfur Colloid in Sickle Cell Beta?? Thalassemia
Authors: LARRY L. HECK, GEOFFREY M. BRITTIN
Journal: Clinical Nuclear Medicine (1989)

A 19-year-old black woman with sickle cell betaº thalassemia had experienced more than 100 hospital admissions for sickle cell crisis and aseptic necrosis of both femoral heads. Her spleen was enlarged threefold and accumulated both radiocolloid and bone-seeking agent on two occasions, demonstrating an exception to the rule in sickle cell anemia that spleens that take up bone-seeking agents demonstrate functional asplenia. In the context of fever, left upper quadrant pain, and splenomegaly, the pattern of calcification in the patient's spleen as revealed in ultrasound and CT studies suggested possible abscess and led to unnecessary splenectomy. The nuclear medicine studies did not support this diagnosis. Nuclear medicine physicians should not be misled by splenic findings of sickle cell thalassemia (and possibly of other heterozygous sickle cell disorders) that differ from those of the more familiar homozygous sickle cell anemia.
Activation of TRPV1 by Dietary Capsaicin Improves Endothelium-Dependent Vasorelaxation and Prevents Hypertension
Authors: Dachun Yang, Zhidan Luo, Shuangtao Ma, Wing Tak Wong, Liqun Ma, Jian Zhong, Hongbo He, Zhigang Zhao, Tingbing Cao, Zhencheng Yan, Daoyan Liu, William J. Arendshorst, Yu Huang, Martin Tepel, Zhiming Zhu
Journal: Cell Metabolism (2010)
Follow-up Endoscopic Study of Gastric Mucosal Changes Secondary to Gastric Ulcer
Authors: F. Chang, T. Saito, S. Ashizawa
Journal: Endoscopy (1978)

A long-term follow-up gastrocamera photographic study of 481 patients with gastric ulcer was conducted at intervals of 3 weeks to 6 months. It showed that gastric ulcers could remain healed for 2 months to 6 years of observation, yet, recurrence of ulceration occurred in 79% including 18% with multiple occurences. Gastric polyp developed in 8 patients whose initial gastrophotography showed no such lesion in the original study. Furthermore, 7 cancers of the stomach developed at sites away from the initial benign ulcer foci. Six of these cases proved to be mucosal cancer and one was an advanced cancer. In 5 of 7 cases of malignancy, the cancer occurred distal to the initial ulcer foci and anaplastic adenocarcinoma was seen in 3 of these. The others were well differentiated adenocarcinomas. No correlation was found among histopathological type of cancer, depth of malignant invasion, location of the new growth or gastric juice acidity in these 7 cases of malignancy. It is concluded that a thorough and routine gastroscopic examination is indicated for all sorts of gastric disorders whether they are initial or follow-up cases.
Concanavalin A induces perforin-mediated but not Fas-mediated hepatic injury
Authors: Y Watanabe
Journal: Hepatology (1996)

Concanavalin A (Con A) induces T-cell-mediated hepatic injury in vivo, although Con A-stimulated lymphocytes are not cytotoxic to normal hepatocytes in vitro. This contradiction makes the mechanism of Con A-induced hepatitis elusive. In this study, we demonstrate that Con A but not tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), or actinomycin D (ActD) induced the susceptibility of hepatocytes to activated autologous lymphocyte cytotoxicity. Con A sensitized hepatocytes within 30 minutes after the stimulation in a dose-dependent fashion. The cytotoxicity was dose-dependently inhibited by either a Con A ligand, alpha-methyl mannoside, or a perforin inhibitor, concanamycin A (CMA), but not by anti-Fas ligand antiserum. In addition, Con A-treated hepatocytes were not sensitive to autologous activated lymphocytes from a perforin-deficient mouse, while hepatocytes from lpr mice were sensitized by Con A. In fact, Con A did not induce liver injury in perforin-deficient mice within the concentration employed in this study. Therefore, we conclude that the cytotoxicity was mediated through perforin/granzymes but not through the Fas/Fas ligand pathway. The cytotoxicity was inhibited by anti-intercellular adhesion molecule-1 (ICAM-1)/LFA-1 antibodies, but not by anti-VCAM-1/VLA-4 antibodies, both in vitro and in vivo. The cytotoxicity appears to be caused by CD8+ T cells; however, the cytokines from activated CD4+ T cells play a critical role in the pathogenesis of the hepatitis in vivo, because administration of anti-IFN-gamma antibodies inhibited the occurrence of the hepatitis. In conclusion, Con A-induced hepatitis is thought to be dominantly mediated by a perforin-dependent pathway through ICAM-1/LFA-1 interaction.
THE FUTURE CHEMIST.Read in the Section of Materia Medica and Pharmacy, at the Forty-second Annual Meeting of the American Medical Association, held at Washington, D. C., May, 1891.
Authors: CHAS. T. P. FENNEL
Journal: JAMA (1891)

When I was invited to undertake the honorable task of presenting a paper on this memorable occasion, the beginning of a new era for physicians and pharmacists, I felt a hesitancy in accepting, being cognizant of my unfitness to select and consider a subject worthy of, and of equal importance to, both professions. The beginning of a new era! American medicine has extended her arms and taken unto herself American pharmacy. The vocabulary of the English language is inadequate to express the gratitude due to the American Medical Association. Henceforth, the two professions go hand in hand; and if we are only content to await the harvest of the seed that has been sown, our granaries will, in good time, be filled with golden grain. All nations reverence antiquity. Historians have ever been ambitious of tracing back their subjects to the most remote antiquity. Writers on medicine and allied
Common Bile Duct Obstruction and Cholangiohepatitis in Clonorchiasis
Authors: Walter G. Sullivan
Journal: JAMA (1980)

This report describes a patient with common bile duct obstruction and cholangiohepatitis. Patients with clonorchiasis are usually asymptomatic and treatment is limited to complications. Treatment consists of cholecystectomy, choledochotomy, and T-tube drainage. A bypass procedure is indicated in cases of heavy infestation and recurrent disease.
THE PATHOGENESIS OF EXPERIMENTAL COLITIS, AND THE RELATION OF COLITIS IN ANIMALS AND MAN
Authors: Simon Flexner, J. Edwin Sweet
Journal: The Journal of Experimental Medicine (1906)

1. The facts described in this paper are intended to bear upon the pathogenesis of colitis in man and animals. 2. The toxin of the Shiga dysentery bacillus is liberated from the bacillus through the process of autolysis. 3. In rabbits the toxin is not absorbed directly in an active form by the gastro-intestinal tract; in man, however, absorption of an active poison does take place from the intestine. 4. The toxin is excreted in rabbits, and probably in man as well by the intestine, chiefly probably by the large intestine, which being injured by the act of elimination, reacts by the development of inflammation, etc. 5. In rabbits the characteristic action of the toxin depends upon the integrity of the biliary secretion into the intestine. When the bile is prevented from entering the intestine, either by ligature and section of the duct or by establishment of a biliary fistula, no lesions whatever of the large intestine appear, or they are inconsiderable in extent. 6. The loss of toxin through a biliary fistula does not prevent in rabbits the lethal effects which are caused, apparently, by a nervous poison. The tying off of the bile duct seems to prevent the passage of the toxin, in amounts sufficient to cause the large intestinal lesions, into the blood. The liver, therefore, in this condition tends to hold back the toxin from the general circulation. 7. The peculiar effects of the toxin on the large intestine in rabbits is not produced at once, but would appear to depend upon successive acts of excretion of the poison by the bowel. 8. The establishment of biliary fistula reduces the intensity of action of corrosive sublimate upon the large intestine in rabbits; and the lesions of ricin poisoning in these animals are also modified by this operation. 9. Dysentery toxin is destroyed by peptic digestion, and also, though probably more slowly, by tryptic digestion. The absence of power of the toxin to cause poisoning in rabbits when it is brought directly into the lumen of the intestine, is not explained by the destructive action of trypsin. 10. The character of the histological changes in the caecum of rabbits caused by the dysentery toxin points to an action upon the substance and not primarily upon the surface of the intestine.
Risk among gastroenterologists of acquiring Helicobacter pylori infection: case-control study
Authors: P. Hildebrand
Journal: BMJ (2000)

It has been suggested that endoscopists are at increased risk of Helicobacter pylori infection, but the results of the different studies have been contradictory. 1 2 Part of the explanation for the controversy may be the fact that these were cross sectional epidemiological studies rather than prospective ones with long term follow up. The mode of transmission of H pylori infection is gastric/oral to oral or fecal to oral, and the human gastric mucosa serves as the main reservoir for the bacterium. As many patients undergoing endoscopy are positive for H pylori , gastroenterologists are likely to be exposed to infected saliva and gastric juice, and this could increase their risk of acquiring H pylori infection.

This prospective study aimed to investigate whether gastroenterologists have a higher risk than …
B cell stimulatory factor 1 (interleukin 4) is sufficient for the proliferation and differentiation of lectin-stimulated cytolytic T lymphocyte precursors.
Authors: J D Pfeifer, D T McKenzie, S L Swain, R W Dutton
Journal: The Journal of Experimental Medicine (1987)

In this report, we demonstrate that IL-4 is sufficient to stimulate both the proliferation and differentiation of Lyt-2+, Ia- splenic CTL precursors stimulated with the mitogenic lectin Con A. The response to IL-4 and Con A was not dependent on a putative endogenous production of IL-2 within the cultures, as demonstrated by an absence of an inhibitory effect by an anti-IL-2-R blocking mAb. Our results indicate that IL-2 and IL-4 can support an equivalent proliferative response by lectin-stimulated Lyt-2+ T lymphocytes, while IL-4 is more efficacious in stimulating their differentiation into mature cytolytically active cells.
Role of Afadin in Vascular Endothelial Growth Factor– and Sphingosine 1-Phosphate–Induced Angiogenesis
Authors: Hideto Tawa, Yoshiyuki Rikitake, Motonori Takahashi, Hisayuki Amano, Muneaki Miyata, Seimi Satomi-Kobayashi, Mitsuo Kinugasa, Yuichi Nagamatsu, Takashi Majima, Hisakazu Ogita, Jun Miyoshi, Ken-ichi Hirata, Yoshimi Takai
Journal: Circulation Research (2010)

Angiogenesis contributes to physiological and pathological conditions, including atherosclerosis. The Rap1 small G protein regulates vascular integrity and angiogenesis. However, little is known about the effectors of Rap1 involved in angiogenesis. It is not known whether afadin, an adherens junction protein that connects immunoglobulin-like adhesion molecule nectins to the actin cytoskeleton and binds activated Rap1, plays a role in angiogenesis.We investigated the role of endothelial afadin in angiogenesis and attempted to clarify the underlying molecular mechanism.Treatment of human umbilical vein endothelial cells (HUVECs) with vascular endothelial growth factor (VEGF) and sphingosine 1-phosphate (S1P) induced the activation of Rap1. Activated Rap1 regulated intracellular localization of afadin. Knockdown of Rap1 or afadin by small interfering RNA inhibited the VEGF- and S1P-induced capillary-like network formation, migration, and proliferation, and increased the serum deprivation-induced apoptosis of HUVECs. Knockdown of Rap1 or afadin decreased the accumulation of adherens and tight junction proteins to the cell-cell contact sites. Rap1 regulated the interaction between afadin and phosphatidylinositol 3-kinase (PI3K), recruitment of the afadin-PI3K complex to the leading edge, and the activation of Akt, indicating the involvement of Rap1 and afadin in the PI3K-Akt signaling pathway. Binding of afadin to Rap1 regulated the activity of Rap1 in a positive-feedback manner. In vivo, conditional deletion of afadin in mouse vascular endothelium using a Cre-loxP system impaired the VEGF- and S1P-induced angiogenesis.These results demonstrate a novel molecular mechanism by which Rap1 and afadin regulate the VEGF- and S1P-induced angiogenesis.
Review: Ultrasonography screening reduces long-term abdominal aortic aneurysm–related mortality
Authors: A.C. Felix Burden
Journal: Annals of Internal Medicine (2014)

Source Citation Guirguis-Blake JM, Beil TL, Senger CA, Whitlock EP. Ultrasonography screening for abdominal aortic aneurysms: a systematic evidence review for the U.S. Preventive Services Task Force. Ann Intern Med. 2014;160:321-329. 24473919
1044-61 Creatine kinase-MB enzyme elevation after percutaneous coronary interventions using sirolimus-eluting stents
Authors: Goran Stankovic, Dejan Orlic, Ioannis Iakovou, Nicola Corvaja, Giuseppe Sangiorgi, Alaide Chieffo, Flavio Airoldi, Matteo Montorfano, Mauro Carlino, Giancarlo Vitrella, Iassen Michev, Antonio Colombo
Journal: Journal of the American College of Cardiology (2004)