tbuckley/cabot-search huggingface dataset:
Expression of nitric oxide synthase in the human nasal mucosa.
Authors: K Furukawa, D G Harrison, D Saleh, H Shennib, F P Chagnon, A Giaid
Journal: American Journal of Respiratory and Critical Care Medicine (1996)

The nasal mucosa plays an important role in defense of the lung against harmful agents. It has been suggested that this is partly mediated by the production of nitric oxide (NO). We have investigated the localization of the messenger ribonucleic acids (MRNAs) for human endothelial NO synthase (Type III NOS) and inducible NO synthase (Type II NOS) and the immunoreactivities of these enzymes in human nasal mucosa by immunohistochemistry, in situ hybridization, and reduced nicotinamide adenine diphosphate (NADPH) diaphorase histochemistry. Inferior nasal turbinates were obtained from 27 patients at the time of surgery for local disease. Strong immunostaining for Type III NOS was localized to vascular endothelium, surface epithelium, and submucosal glands in all subjects. Moderate immunostaining for Type II NOS was seen in surface epithelium; glandular, inflammatory, and vascular endothelial cells; and smooth-muscle cells in the specimens from patients with chronic rhinitis only. In situ hybridization showed expression of the mRNA for Type III NOS in similar sites to those shown by immunohistochemistry, whereas the mRNA for Type II NOS was predominantly localized to inflammatory cells. The sites of NOS expression were further confirmed by NADPH histochemical staining. These findings demonstrate the cellular expression of NOS in the human nasal mucosa and suggest a possible role for Types II and III NO synthase in the regulation of blood flow, nasal secretion, and ciliary movement in health and disease.
Late follow-up of patients submitted to subtotal splenectomy
Authors: Andy Petroianu, Vivian Resende, Rodrigo Gomes Da Silva
Journal: International Journal of Surgery (2006)

Over the past 21 years, we have performed more than 200 subtotal splenectomies, in which the upper splenic pole vascularized only by the gastrosplenic pole vascularized only by the gastrosplenic vessels is preserved, to treat different pathologic conditions. A meticulous follow-up of the postoperative results of this procedure is of fundamental importance. All patients undergoing subtotal splenectomy were invited to be reviewed. A total of 86 patients who had undergone surgery 1–20 years ago were gathered; the surgical procedure was performed for one of the following conditions: portal hypertension due to schistosomiasis (n = 43), trauma (n = 31), Gaucher's disease (n = 4), myeloid hepatosplenomegaly due to myelofibrosis (n = 3), splenomegalic retarded growth and sexual development (n = 2), severe pain due to splenic ischemia (n = 2) and pancreatic cystadenoma (n = 1). Patients underwent a hematological examination, an immunological assessment, abdominal ultrasonography, computed tomography, scintigraphy and endoscopy. Increased white blood cell count and platelets were the only hematological abnormalities. No immunological deficit was found. Esophageal varices were still present in patients who underwent surgery because of portal hypertension although without rebleeding. The ultrasound, tomography and scintigraphy examinations confirmed the presence of functional splenic remnants without significant size alteration. Subtotal splenectomy seems to be a safe procedure that can be useful in treating conditions involving the spleen. The functions of the splenic remnants are preserved during long periods of time.
EARLY POSTOPERATIVE INTESTINAL OBSTRUCTION.
Authors: C. C. FREDERICK
Journal: JAMA (1907)

Postoperative ileus, unfortunately, is one of the serious sequels of abdominal operations which all who have had an extended experience have often been called on to treat. Among the earliest papers treating of this subject exhaustively in this country are those of such excellence from the pen of Dr. Rohé<sup>1</sup>in 1894 and Dr. Marcy<sup>2</sup>in 1896. That intestinal obstruction is common following abdominal sections of all kinds can readily be proved by the reported statistics from various sources. There are reports of single cases by the hundreds. But there are also collected and analyzed series of cases which prove more that is needed in a discussion of our topic. Sir Spencer Wells (Finney) in 1,000 ovariotomies reported 11 cases which he diagnosed, all dead without operation. McWilliams<sup>3</sup>collects a series of 86 secondary operations for postoperative obstruction from various sources, all occurring in the small intestine.
Abstract 945: Inhibition of T-type calcium channels sensitizes ovarian cancer cell growth and metastasis to platinum-based chemotherapy.
Authors: Eli V. Casarez, Lloyd Gray, Amir A. Jazaeri, Jill K. Slack-Davis
Journal: Cancer Research (2013)

Abstract The inability to successfully treat women with ovarian cancer is due in large part to the advanced stage of disease at diagnosis and the development of platinum resistance. T-type calcium channels have recently garnered interest as potential targets for the treatment of many cancers. We investigated the hypothesis that inhibiting T-type calcium channels would sensitize ovarian cancer cells to platinum based chemotherapy using cell culture and mouse models. Sequential treatment of cultured ovarian cancer cell lines or primary cells obtained from patients with mibefradil followed by carboplatin showed a dose-dependent decrease in cell number that was greater than observed with either drug alone. Importantly, treatment of platinum-resistant tumor cells with mibefradil followed by carboplatin also decreased cell number. Moreover, either simultaneous administration of both drugs or treatment with carboplatin followed by mibefradil did not alter cellular response to carboplatin. Based on these findings, we tested the effect of mibefradil and carboplatin in a mouse model of peritoneal ovarian cancer metastasis with platinum-resistant ovarian cancer cells. Tumor-bearing mice were subjected to 3 cycles of Interlaced TherapyTM, which consists of 5 days of mibefradil treatment followed by one dose of carboplatin and 2 days off. We found that while neither drug alone significantly affected tumor growth compared to control, the mice that received the dual treatment had a dramatic reduction in tumor burden. Together, the data provide pre-clinical evidence supporting the use of T-type calcium channel blockers with platinum-based chemotherapy to treat ovarian cancer. Citation Format: Eli V. Casarez, Lloyd Gray, Amir A. Jazaeri, Jill K. Slack-Davis. Inhibition of T-type calcium channels sensitizes ovarian cancer cell growth and metastasis to platinum-based chemotherapy. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 945. doi:10.1158/1538-7445.AM2013-945
Presentation of numerous viral peptides to mouse major histocompatibility complex (MHC) class I-restricted T lymphocytes is mediated by the human MHC-encoded transporter or by a hybrid mouse-human transporter.
Authors: J W Yewdell, F Esquivel, D Arnold, T Spies, L C Eisenlohr, J R Bennink
Journal: The Journal of Experimental Medicine (1993)

The major histocompatibility complex-encoded transporter associated with antigen processing (TAP) is required for the efficient presentation of cytosolic antigens to class I-restricted T cells. TAP is thought to be formed by the interaction of two gene products, termed TAP1 and TAP2. We find that TAPs consisting either of human subunits, or mouse TAP1 and human TAP2, facilitate the presentation of numerous defined viral peptides to mouse class I-restricted T cells. As human and mouse TAP2 and TAP1 differ in 23 and 28% of their residues, respectively, this indicates that TAP1 and TAP2 can form a functional complex with partners considerably different from those they coevolved with. Moreover, these findings indicate that widely disparate TAPs facilitate delivery of the same peptides to class I molecules. These findings suggest that TAP polymorphism does not greatly influence the types of peptides presented to the immune system.
Caregiving in Alzheimer Dementia
Authors: Kingsley M. Stevens
Journal: Annals of Internal Medicine (1991)

Letters15 January 1991Caregiving in Alzheimer DementiaKingsley M. Stevens, MDKingsley M. Stevens, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-114-2-168_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors:Alzheimer disease is the most devastating disease of the 1990s because it destroys not only the patient but at least one caretaker. The destruction is slow—almost without end. Even when institutional care is required, the caretaker does not escape. Walsh and colleagues (1) studied length of survival in patients with Alzheimer disease. Their stated objective was to increase the prevalence of Alzheimer disease through increasing survival time! This approach to treating Alzheimer disease is not unique to these authors; management of Alzheimer disease in the United States focuses on keeping these patients physically healthy. The tacit assumption...Reference1. Walsh J, Welch H, and Larson E. Survival of outpatients with Alzheimer-type dementia. Ann Intern Med. 1990;113:429-34. LinkGoogle Scholar1. Walsh J, Welch H, and Larson E. Survival of outpatients with Alzheimer-type dementia. Ann Intern Med. 1990;113:429-34. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Kingsley M. Stevens, MDAffiliations: State University of New York at Stony Brook Stony Brook, NY 11794 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 January 1991Volume 114, Issue 2Page: 168-168KeywordsAlzheimer diseaseDementia ePublished: 1 December 2008 Issue Published: 15 January 1991 PDF downloadLoading ...
The Reading Retreat
Authors: Gerald I. Plitman
Journal: JAMA (1976)

<h3>To the Editor.—</h3> I have read with interest the article by Libby et al (233:797, 1975) entitled, "Help Stamp Out Mandatory Continuing Education!," followed by Dr Mangun's editorial comments (233:816, 1975). I quite agree that any system of enforced mandatory education would likely become onerous and would be greeted with apathy if not outright resistance. I believe there is a new concept in continuing education—a reading retreat.<sup>1</sup>This type of learning experience has been inaugurated by the Tennessee region of the American College of Physicians during the past 2 1/2 years. The basic emphasis here is on reading and not on a pedantic teacher-student relationship through didactic presentations. The course subjects chosen have been various subspecialty areas of internal medicine, a separate day devoted to each subject. Experts in the field begin the workday with a "Meet-the-Professor, What's-New, What's-Important" session to introduce the material. The remainder of the attendees'
Biosynthesis of somatostatin in canine fundic D cells.
Authors: T Chiba, J Park, T Yamada
Journal: Journal of Clinical Investigation (1988)

The observation that virtually all of the somatostatin-like immunoreactivity in the stomach consists of somatostatin-14 (S14), to the exclusion of somatostatin-28 (S28), suggests a unique pattern of prosomatostatin posttranslational processing. In order to examine the mechanisms by which S14 is produced from its precursor in the stomach, we investigated the biosynthesis of somatostatin in isolated canine fundic D cells. D cells pulse-labeled with [35S]cysteine revealed a cycloheximide inhibitable time-dependent incorporation of radioactivity into S14. A small fraction of radioactivity was incorporated into S28 but not into larger precursors. However, when the cells were incubated with monensin (1 microM), incorporation of radioactivity into a presumed somatostatin precursor was noted. Upon transfer of [35S]cysteine prelabeled cells to radioactivity-free medium, no conversion of S28 to S14 could be detected and the decrease of labeled S14 in cells correlated with a complimentary increase in the culture medium. Exogenous somatostatin inhibited somatostatin biosynthesis in a fashion that could be blocked by pertussis toxin pretreatment. Stimulation of prelabeled D cells with tetradecanoyl phorbol 13-acetate (10(-7) M) or forskolin (10(-4) M) for 2 h resulted in release of 41 and 33% of the newly synthesized radioactive S14, respectively, while only 9 and 6% of the total cell content of radioimmunoassayable somatostatin was secreted. These data suggest that: (a) somatostatin is synthesized in fundic D cells primarily as S14, (b) S14 is produced by rapid processing of a larger precursor but there is little, if any, conversion of S28 to S14, (c) somatostatin biosynthesis is autoregulated, and (d) newly synthesized S14 is preferentially released from D cells in response to stimulation.
Immunoregulatory changes induced by total lymphoid irradiation. II. Development of thymus-leukemia antigen-positive and -negative suppressor T cells that differ in their regulatory function.
Authors: D P King, S Strober
Journal: The Journal of Experimental Medicine (1981)

BALB/c mice treated with total lymphoid irradiation (TLI) develop non-antigen-specific suppressor cells of the adoptive secondary antibody response and of the mixed leukocyte reaction. Suppressors of the adoptive anti-DNP response were eliminated by incubation of spleen cells with anti-Thy-1.2 or anti-thymus-leukemia (TL) antiserum and complement before cell transfer. Thymectomy before TLI prevented the appearance of the latter suppressor cells. On the other hand, suppressors of the MLR were eliminated by incubation of spleen cells with anti-Thy-1.2 but not anti-TL antiserum and complement. Thymectomy before TLI did not prevent their subsequent development. Thus, two subpopulations of suppressor T cells that differ in the expression of the TL surface antigen, dependence on the presence of the thymus, and in regulatory functions develop after TLI. The TL+, thymus-dependent cell suppresses the adoptive antibody response, and the TL-, thymus-independent cell suppresses the MLR.
Effects of fiber characteristics on lung deposition, retention, and disease.
Authors: M Lippmann
Journal: Environmental Health Perspectives (1990)

There is abundant epidemiologic evidence that asbestos fibers can cause lung fibrosis (asbestosis), bronchial cancer, and mesothelioma in humans, as well as limited evidence for such effects in workers exposed to slag and rockwool fibers. Epidemiological evidence for human disease from inhalation exposures to conventional fibrous glass is negative. While health concerns based on the morphological and toxicological similarities between man-made fibers and asbestos are warranted, it is important to note that most of the toxicological evidence for glass fiber toxicity in laboratory animals is based on nonphysiological exposures such as intratracheal instillation or intraperitoneal injection of fiber suspensions. Man-made fibers have produced lung fibrosis and mesotheliomas in such tests, albeit at much lower yields than asbestos. For all durable mineral fibers, critical length limits must be exceeded to warrant concern about chronic toxicity; i.e., 2 microns for asbestosis, 5 microns for mesothelioma, and 10 microns for lung cancer. Fiber width must be less than 0.1 microns for mesothelioma, and larger than this limit for asbestosis and lung cancer. The human health risks for most fibrous glass products are either low or negligible for a variety of reasons. First, most commercial fibrous glass products have mean fiber diameters of approximately 7.5 microns, which results in mean aero-dynamic diameters approximately 22 microns. Thus, most glass fibers, even if dispersed into the air, do not penetrate into the lung to any great extent. Second, the small fraction of smaller diameter fibers that do penetrate into the lungs are not persistent within the lungs for most fibrous glass products due to mechanical breakage into shorter lengths and overall dissolution.(ABSTRACT TRUNCATED AT 250 WORDS)
A study of the effect of saliva on the concentration of mucin in gastric juice and its possible relationship to the aetiology of peptic ulcer.
Authors: S L Malhotra
Journal: Gut (1967)

This interesting paper suggests that the consistency of food affects the quality of gastric mucus derived from swallowed saliva, foods needing much mastication stimu- lating a high salivary output.Salivary mucus, by augmenting gastric mucus, may help to protect against peptic ulceration.
Comparison of early dobutamine stress echocardiography, exercise treadmill testing, and hospital admission for management of patients presenting to the emergency department with chest pain: a multicenter international randomized study
Authors: Luigi P. Badano, Nizal Sarraf-Zadegan, Mara Baldassi, Giorgio Scaffidi, Apostolos Karavidas, Vitas Vysniauskas, Baris Ilerigelen, Costantino Astarita, Gianni Pettinati, Alessandro Desideri, Marco Ghidina, Dario Gregori, Paolo M. Fioretti
Journal: Journal of the American College of Cardiology (2002)
Myocardial temperature reduction attenuates necrosis after prolonged ischemia in rabbits
Authors: S Hale
Journal: Cardiovascular Research (1998)

Previously we observed that a large reduction in infarct size was attained by cooling the risk region of the heart, either before or early after the onset of a 30-min coronary artery occlusion. While this is a standard duration of ischemia used in the rabbit model of infarction, it may not reflect the situation of patients who are reperfused late. The effects of regional hypothermia with a longer duration of ischemia, and when the intervention is applied later, are unknown. This study tests the hypothesis that a local reduction in cardiac temperature protects myocardium during prolonged ischemia (2 h) even if begun well after coronary artery occlusion.Anesthetized rabbits received 2 h of coronary artery occlusion and 3 h of reperfusion. Rabbits were randomly assigned to a treated group: topical myocardial cooling starting 30 min after coronary occlusion (n = 14), or control group, no intervention (n = 12). Myocardial temperature in the risk zone, hemodynamics and regional myocardial blood flow were measured.Ischemic zone temperature was similar in both groups at 30 min post occlusion, but the cooling maneuver produced a reduction in temperature in the risk region of the treated group such that myocardial temperature was reduced an average of 10 degrees C between 30 and 60 min of coronary artery occlusion. Myocardial temperature in the control group remained within 0.3 degree C of baseline during coronary artery occlusion and into reperfusion. Core temperatures were similar in both groups. Hemodynamic parameters and collateral blood flow during occlusion were also equivalent in both groups. After 120 min of coronary occlusion, necrosis in the control group comprised 72 +/- 3% of the ischemic risk region. However, in cooled hearts, infarct size, expressed as a fraction of the risk region was significantly lower. Infarct size in this group averaged 59 +/- 3% of the risk region (p < 0.004 vs. controls), and thus cooling resulted in a salvage of approximately 18% of the risk region.These results show that reducing myocardial temperature protects ischemic myocardium during a long duration of ischemia even if initiated after coronary artery occlusion.
What Is the Enemy in CME, Conflicts of Interest or Bias?
Authors: Bernard Lo, Chelsea Ott
Journal: JAMA (2013)

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
Open Clinical Trials
Authors: Jeffrey M. Drazen, Stephen Morrissey, Gregory D. Curfman
Journal: New England Journal of Medicine (2007)

On September 27, 2007, President Bush signed into law the Food and Drug Administration Revitalization Act, which aims to improve the FDA's ability to ensure the safety of the nation's drugs and medical devices. The legislation not only reauthorizes the user-fee mechanism that has been part of the agency's funding since 1992, but also increases the agency's overall financial resources. Although the user-fee approach to funding has been controversial because the fees are paid by the pharmaceutical industry, which the FDA is charged with regulating, legislators believed that user fees provide a stable monetary base that is crucial to the . . .