tbuckley/cabot-search huggingface dataset:
CD4+ T Cell Help Impairs CD8+ T Cell Deletion Induced by Cross-presentation of Self-Antigens and Favors Autoimmunity
Authors: Christian Kurts, Francis R. Carbone, Megan Barnden, Effrossini Blanas, Janette Allison, William R. Heath, Jacques F.A.P. Miller
Journal: The Journal of Experimental Medicine (1997)

Self-antigens expressed in extrathymic tissues such as the pancreas can be transported to draining lymph nodes and presented in a class I–restricted manner by bone marrow-derived antigen-presenting cells. Such cross-presentation of self-antigens leads to CD8+ T cell tolerance induction via deletion. In this report, we investigate the influence of CD4+ T cell help on this process. Small numbers of autoreactive OVA-specific CD8+ T cells were unable to cause diabetes when adoptively transferred into mice expressing ovalbumin in the pancreatic β cells. Coinjection of OVA-specific CD4+ helper T cells, however, led to diabetes in a large proportion of mice (68%), suggesting that provision of help favored induction of autoimmunity. Analysis of the fate of CD8+ T cells indicated that CD4+ T cell help impaired their deletion. These data indicate that control of such help is critical for the maintenance of CD8+ T cell tolerance induced by cross-presentation.
Calcium- and CaMKII-dependent chloride secretion induced by the microsomal Ca(2+)-ATPase inhibitor 2,5-di-(tert-butyl)-1,4-hydroquinone in cystic fibrosis pancreatic epithelial cells.
Authors: A C Chao, K Kouyama, E K Heist, Y J Dong, P Gardner
Journal: Journal of Clinical Investigation (1995)

Microsomal Ca(2+)-ATPase inhibitors such as thapsigargin (THG), cyclopiazonic acid (CPA) and 2,5-di-(tert-butyl)-1,4-hydroquinone (DBHQ) have been shown to inhibit Ca2+ reuptake by the intracellular stores and increase cytosolic free Ca2+ ([Ca2+]i). DBHQ is a commercially available non-toxic synthetic compound chemically unrelated to THG and CPA. In this study, we tested the feasibility of utilizing DBHQ to improve Cl- secretion via the Ca(2+)-dependent pathway, in the cystic fibrosis (CF)-derived pancreatic epithelial cell line CFPAC-1. DBHQ stimulated 125I efflux and mobilized intracellular free Ca2+ in a dose-dependent manner. The maximal effects were seen at concentrations of 25-50 microM. DBHQ (25 microM) caused a short-term rise in [Ca2+]i in the absence of ambient Ca2+, and a sustained elevation of [Ca2+]i in cell monolayers bathed in the efflux solution (1.2 mM Ca2+), which was largely attenuated by Ni2+ (5 mM). Bath-application of DBHQ induced an outwardly-rectifying whole-cell Cl- current, which was abolished by pipette addition of BAPTA (5 mM) or CaMK [273-302] (20 microM), an inhibitory peptide of multifunctional Ca2+/calmodulin-dependent protein kinase (CaMKII). Pretreatment of monolayers of CFPAC-1 cells with DBHQ for 4-5 min significantly increased the Ca(2+)-independent or autonomous activity of CaMKII assayed in the cell homogenates. Thus, DBHQ appears to enhance Cl- channel activity via a Ca(2+)-dependent mechanism involving CaMKII. Pretreatment of CFPAC-1 cells with up to 50 microM DBHQ for 6 h did not cause any detectable change in cell viability and did not significantly affect the cell proliferation rate. These results suggest that appropriate selective microsomal Ca(2+)-ATPase inhibitors may be therapeutically useful in improving Cl- secretion in CF epithelial cells.
Special Communication From the National Institutes of Health
Authors: Craig K. Wallace
Journal: JAMA (1987)

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
Is Therapeutic Hypothermia a Risk Factor for Stent Thrombosis?
Authors: Sandra O. Rosillo, Esteban Lopez-de-Sa, Angel M. Iniesta, Fernando de Torres, Susana del Prado, Juan R. Rey, Eduardo Armada, Raúl Moreno, José L. López-Sendón
Journal: Journal of the American College of Cardiology (2013)
The Feyrter cell in hypoxia
Authors: H. Moosavi, P. Smith, D. Heath
Journal: Thorax (1973)

<b>Moosavi, H., Smith, P., and Heath, D. (1973).</b><i>Thorax,</i><b>28,</b> 729-741. <b>The Feyrter cell in hypoxia.</b> It is clear that the bronchial tree has functions beyond the mere conduction of air into the alveolar spaces. In addition to the familiar ciliated respiratory epithelial cells the bronchus is lined by non-ciliated Clara and Feyrter cells. In the present study we investigated the histological and ultrastructural features of the bronchial argyrophilic (Feyrter) cell of the neonatal rat. On electron microscopy this cell has all the features of an APUD cell which is associated with the secretion of polypeptide hormones. It bears a close ultrastructural resemblance to the chief cell of the carotid body and shows the same changes in its membrane-bound bodies on exposure to chronic hypoxia. These are strong grounds for believing that the bronchi and bronchioles have either a chemoreceptor or an endocrine function in the neonatal period.
Doctors should carry out more biopsies on secondary breast cancers, researchers say
Authors: N. Hawkes
Journal: BMJ (2013)

Ten “critical gaps” in breast cancer research need to be filled if further substantial progress is to be made in preventing and treating the disease, a team of British researchers has concluded.

Among the most important, say lead authors Sue Eccles and Alastair Thompson, is better provision of biopsy material from patients in whom the cancer has spread, since secondary cancers can differ in important ways from primaries. 

Thompson, of the University of Dundee, told a press conference at the Science Media Centre in London, “We have only begun to appreciate the heterogeneity of cancers in the past five years, but only a very small percentage of patients with secondaries have biopsies. There’s been a reluctance to put patients through biopsies, but knowing …
Dermoscopy and Confocal Microscopy of Nested Melanoma of the Elderly
Authors: Caterina Longo, Iris Zalaudek, Simonetta Piana, Giovanni Pellacani, Aimilios Lallas, Camilla Reggiani, Giuseppe Argenziano
Journal: JAMA Dermatology (2013)

Nested melanoma of the elderly is a newly identified histopathologic variant of superficial spreading melanoma, characterized by intraepidermal large nests. However, the clinical, dermoscopic, and confocal aspects have been depicted only partially.In our cases series, nested melanoma was a flat, irregularly shaped lesion with variably pigmented and irregularly distributed globules on dermoscopic examination. Confocal microscopy revealed the presence of a "clod" pattern made of large compact nests with variable atypia. These findings correlated well with histopathologic features.Nested melanoma of the elderly should be included in the differential diagnosis when a flat pigmented lesion, showing dermoscopically an irregular globular pattern, is seen in a patient older than 60 years.
SYMPTOMATOLOGY OF VALVULAR HEART DISEASE IN CHILDREN.
Authors: FREDERICK A. PACKARD
Journal: JAMA (1900)

When the subject of the symptomatology of heart disease in children was assigned to me in the program of the meeting I considered that there was not much to be said regarding it. I find that there is in reality less to be said than I had calculated, as an analysis of case histories has convinced me more even than was the case before, that heart disease, especially in children, has no symptomatology, or rather that there can be said to be no group of symptoms pointing to the heart when so large a proportion of children show signs of heart lesions without the existence of any symptoms indicating their existence. Consideration of the only method of even suspecting the presence or absence of heart disease in children has been allotted to another member of the society; I refer to physical diagnosis. By careful physical examination alone can we be
Hyperkalemia and Trimethoprim-Sulfamethoxazole
Authors: Chatrchai Watanakunakorn
Journal: Annals of Internal Medicine (1996)

Letters1 November 1996Hyperkalemia and Trimethoprim-SulfamethoxazoleChatrchai Watanakunakorn, MDChatrchai Watanakunakorn, MDSt. Elizabeth Health Center Youngstown, OH 44501.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-9-199611010-00019 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In their recent report, Alappan and colleagues [1] do not state clearly whether theirs was a prospective clinical study or a concurrent or retrospective chart review project. If this was a prospective clinical study, no mention was made of approval by an institutional review board or of written informed consent by patients.In their Methods section, the authors stated that “the charts of these patients were reviewed prospectively in the hospital.” They further stated thatserum potassium, sodium, and chloride concentrations; serum carbon dioxide content; anion gap; blood urea nitrogen level; and serum creatinine level were measured ...REFERENCE1. Alappan R, Perazella MA, Buller GK. Hyperkalemia in hospitalized patients treated with trimethoprim-sulfamethoxazole. Ann Intern Med. 1996; 124:316-20. Google Scholar Author, Article, and Disclosure InformationAuthors: Chatrchai Watanakunakorn, MDAffiliations: St. Elizabeth Health Center Youngstown, OH 44501. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 November 1996Volume 125, Issue 9Page: 778KeywordsBlood urea nitrogenCarbon dioxideChartsChloridesCreatinineInstitutional review boardsPotassiumProspective studiesRetrospective studiesSodium ePublished: 15 August 2000 Issue Published: 1 November 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Cardiomyocyte-restricted peroxisome proliferator-activated receptor-δ deletion perturbs myocardial fatty acid oxidation and leads to cardiomyopathy
Authors: Lihong Cheng, Guoliang Ding, Qianhong Qin, Yao Huang, William Lewis, Nu He, Ronald M Evans, Michael D Schneider, Florence A Brako, Yan Xiao, Yuqing E Chen, Qinglin Yang
Journal: Nature Medicine (2004)
Pleural effusion as a cause of right ventricular diastolic collapse.
Authors: K Vaska, L S Wann, K Sagar, H S Klopfenstein
Journal: Circulation (1992)

We hypothesized, after seeing several suggestive clinical examples, that a process leading to a large bilateral pleural effusion in the presence of an otherwise insignificant pericardial effusion could result in right ventricular diastolic collapse (RVDC) as seen by two-dimensional echocardiography. This noninvasive marker for hemodynamically significant cardiac tamponade occurs when pericardial fluid is under pressure. Therefore, RVDC resulting from a large pleural effusion would represent a false-positive indication of cardiac tamponade caused by excessive pericardial fluid.Seven spontaneously breathing dogs were chronically instrumented to measure ascending aortic, right atrial, intrapericardial, intrapleural, left atrial, and pulmonary artery pressures and cardiac output. Intravascular volume was adjusted before each experiment to the euvolemic range with saline solution. The onset of RVDC was observed in each animal by two-dimensional echocardiography during seven paired episodes of tamponade induced by infusions of warm saline into the pericardial space alone and, after drainage of the pericardial fluid and complete recovery, into the pleural space in the presence of a small pericardial effusion. The onset of RVDC occurred at the same intrapericardial (8.17 versus 9.47 mm Hg) and right atrial (7.41 versus 7.46 mm Hg) blood pressures regardless of whether it was produced by an intrapericardial or an intrapleural effusion but began in expiration during the former and in inspiration during the latter. Intrapericardial pressure increased in the same manner as intrapleural pressure during intrapleural saline infusion. Nevertheless, cardiac output and aortic blood pressure were better preserved, and at the onset of RVDC, the pulmonary artery systolic blood pressure was higher (p less than 0.0001) and the degree of pulsus paradoxus lower (p less than 0.01) with intrapleural infusion.These results indicate that a large bilateral pleural effusion can elevate intrapericardial pressure sufficiently to cause RVDC and, perhaps, lead to misdirected therapy of an otherwise insignificant pericardial effusion.
Women's experiences of breast and ovarian cancer
Authors: T S. Epstein
Journal: BMJ (2005)

reliably recorded 2 and is a good proxy for social class in Hong Kong.As data on cases and controls were derived from the same proxy, reporting bias should be minimal. 2If our results are not due to residual confounding, they provide further evidence that the dose-response associations between passive smoking and stroke and all cause mortality are likely to be causal.We thank W L Cheung for help with analysis; the Immigration Department of the Government of the Hong Kong
Biotransformation of xenobiotics in human intestinal mucosa
Authors: H. P. Hoensch, R. Hutt, F. Hartmann
Journal: Environmental Health Perspectives (1979)

Drug-metabolizing enzymes, especially monooxygenases, play a major role in biotransformation and detoxification of many foreign compounds including environmental carcinogens. Although largely localized in the liver they are also found in the small intestine, which is the portal of entry of dietary toxins. Therefore cytochrome P-450 content as well as monooxygenase (7-ethoxycoumarin O-deethylase) and NADPH-cytochrome c reductase activities were determined in surgical specimens of the human small intestine and in jejunal biopsy material obtained from patients by use of a hydraulic biopsy instrument. Microsomes were prepared from surgical material; these ranged in P-450 content from 30 to 120 pmole/mg protein and in monooxygenase activity from 60 to 110 pmole/min-mg protein. In the 20,000g supernatant of the homogenized biopsy material, monooxygenase activity was undetectable in patients who had total villous atrophy, and low enzyme rates were found when the mucosa showed a partial villous atrophy. The mucosal monooxygenase activity of patients with normal jejunal histology and steatorrhea was significantly higher than in mucosa with villous atrophy but was only half of that observed in normal controls. These eight control patients had normal histology and no malassimilation. Our results suggest that monooxygenase activity in the human small intestine is dependent on the morphological integrity of the mucosa and that in normal mucosa the enzyme rates are reduced when malassimilation is present.
In Vivo Adenovirus-Mediated Gene Transfer Via the Pulmonary Artery of Rats
Authors: Susan K. Schachtner, Jonathan J. Rome, Robert F. Hoyt, Kurt D. Newman, Renu Virmani, David A. Dichek
Journal: Circulation Research (1995)

Abstract Gene transfer into the pulmonary vasculature has the potential to be a powerful technique for both investigation of pulmonary pathophysiology and development of genetic therapies for pulmonary vascular disease. To evaluate the potential for in vivo pulmonary arterial gene transfer, we infused adenoviral vectors into the left pulmonary artery of Sprague-Dawley and cotton rats. Access to the left pulmonary artery was obtained by a percutaneous transcatheter approach or through thoracotomy and pulmonary arteriotomy. With the thoracotomy approach, both pulmonary arterial inflow and pulmonary venous outflow were occluded during vector infusion and throughout a subsequent 20-minute dwell period. The success of gene transfer was assessed by staining for evidence of recombinant gene expression in lungs excised at time points ranging from 48 to 72 hours after virus infusion. With the thoracotomy technique, pulmonary gene transfer was successful in 15% of surviving Sprague-Dawley rats and 30% of surviving cotton rats. Percutaneous catheter-based pulmonary gene transfer was not successful. In rats with pulmonary gene transfer, 1% to 8% of total left lung cells expressed the recombinant gene. Recombinant gene expression was found in endothelial cells (0.2% to 18% of total transduced cells), smooth muscle cells (0% to 3%), macrophages (1% to 7%), airway epithelial cells (2% to 50%), and alveolar epithelial cells (38% to 94%). Investigation of the low rate of successful gene transfer in individual animals suggested that insufficient physical contact between the virions and pulmonary cells was the most likely cause. In vivo gene transfer into the rat pulmonary vasculature can be accomplished with adenovirus vectors. The overall efficiency is low, however, and pulmonary arterial infusion of the vectors results in gene transfer primarily into nonvascular cells.
Alveolar macrophage deficiency in osteopetrotic mice deficient in macrophage colony-stimulating factor is spontaneously corrected with age and associated with matrix metalloproteinase expression and emphysema
Authors: Yoko Shibata, Zsuzsanna Zsengeller, Kazuhisa Otake, Nades Palaniyar, Bruce C. Trapnell
Journal: Blood (2001)
Chinese avian influenza
Authors: E Walker, P Christie
Journal: BMJ (1998)

Influenza viruses are unique among respiratory viruses in exhibiting “drift,” which is change in surface antigens as a result of host immunological pressure. In addition, influenza A viruses exhibit “shift”—which is the genetic intermingling of human strains with animal or bird strains, resulting in completely new viruses of pandemic potential. This makes the production of long lasting comprehensive vaccines impossible and continual monitoring for the appearance of new strains essential. Moreover, unlike infections transmitted through blood, food, or water, those transmitted through the respiratory tract are difficult to control through public health measures apart from vaccination and in controlled situations such as laboratories or under barrier protection conditions. Hence the current interest in so called Chinese …
Abstract 5254: Dependence of Beta-3 Adrenergic Signaling on the Adipokine Leptin in Cardiac Myocytes
Authors: Jill E Larson, Ronghua Yang, Karen Miller, Alexander Phan, Lili A Barouch
Journal: Circulation (2008)

Introduction: The adipokine leptin modulates cardiac contractility via a NO-dependent mechanism. Beta-3 adrenergic receptors (B3AR) negatively regulate B-adrenergic signaling via NO and are dependent on leptin for normal expression in adipocytes, making B3AR an attractive candidate for crosstalk with leptin in the heart. Accordingly, we tested the hypothesis that cardiac B3AR signaling is dependent on leptin and is severely diminished in leptin-deficient ob/ob mice. Methods and Results: We studied fura-loaded isolated cardiac myocytes (n=11–25 cells/strain) from B3 −/− , ob/ob , and their respective background strains of WT mice (FVB and C57BL6) with a combined treatment of the nonspecific B-agonist isoproterenol (ISO) and the B3-specific agonist BRL37344 (BRL). Continuous administration of ISO “primes” cells to elicit a maximal response from subsequent B3-specific stimulation. Stepwise increases in BRL produced dose-dependent reductions of sarcomere shortening and calcium transients in myocytes from both WT strains. Negative inotropic effects of BRL were absent in B3 −/− as expected. Importantly, effects of BRL were markedly diminished in ob/ob myocytes. To confirm that B3AR signaling is dependent on leptin, we performed qPCR of B3AR mRNA in WT and ob/ob myocardial extracts. B3AR mRNA levels were indeed decreased by 78±5% (n=4–5 hearts) in ob/ob vs. WT, and 4 weeks of in vivo leptin repletion restored B3AR mRNA in ob/ob to WT levels. Conclusions: These findings demonstrate a novel role for leptin in cardiac myocyte physiology, specifically, leptin dependence of B3AR signaling. Our results offer new insight into the mechanisms of obesity-related cardiac dysfunction.
Coordinated Surgical-Chemical Therapy of Cancer
Authors: Frances E. Knock
Journal: JAMA (1963)

FOR CHEMOTHERAPY of cancer, much work has been done on antimetabolites for deoxyribonucleic acid (DNA) but little on attack at the protein associated with DNA. Yet, by analogy with viruses, such an attack on protein coat of nucleic acid may be fruitful, since viral nucleic acid stripped of protein coat can drop in activity to 1/1000 of that of native nucleic acid with intact protein coat. Deliberate attack on the protein coat of DNA is therefore being studied for coordinated surgicalchemical therapy of human cancer.  The protein associated with DNA stains more intensely for protein-sulfhydryl groups than does any other part of the dividing cell. All steps of the mitotic cycle can be delineated by histological stains which react only with sulfhydryl groups. Also, the potent sulfhydryl inhibitor oxophenarsine rapidly causes profound damage to the mitotic apparatus, Roosa and De Lamater1found in studies on mouse tumors.  Therefore,