tbuckley/cabot-search huggingface dataset:
Epithelium of mouse yolk sac placenta lacks H-2 complex alloantigens.
Authors: E L Parr, R V Blanden, R S Tulsi
Journal: The Journal of Experimental Medicine (1980)

The only fetal cell membrane exposed to the mother in the mouse yolk sac placenta is the apical membrane of the endodermal epithelial cells. In yolk sac preparations in vitro, this apical membrane was exposed to reagents or cells in the incubation medium. By using several techniques we were not able to detect fetal major histocompatibility complex (MHC) antigens in this membrane. Immunoferritin labeling with and without prefixation and after neurominidase and trypsin digestion indicated that the apical membrane could contain no more than approximately 1% of the H-2 complex antigens that were present on peritoneal macrophages. Incubation of yolk sac preparations in anti-H-2 complex antiserum and complement had no cytotoxic effect on the endodermal epithelium, nor did incubation in an excess of alloreactive lymphocytes. Dissociated preparations of prefixed yolk sac contained endodermal epithelial cells and vascular endothelial cells whose entire surface membranes were exposed to the medium. H-2-complex antigens were not detected by immunoferritin labeling in either the apical or the laterobasal membrane of the yolk sac endoderm, but they were present in low density on the vascular endothelium. Also, incubation of unfixed, dissociated cells in anti-H-2-complex serum and complement had no detectable cytotoxic effect on endodermal epithelial cells. These observations indicate that H-2 antigens are sparse or absent in both the apical and laterobasal membranes of endodermal epithelial cells. The deficiency of MHC antigens in the apical membrane may account for the failure of sensitized females to reject the yolk sac, whereas the composition of the laterobasal membrane is probably less important to maternal-fetal relations. The present observations are consistent with labeling studies of adult-lining epithelial cells, which indicate that self-marker MHC molecules are absent from the apical membranes oriented toward the outside world and variably expressed in the laterobasal self-side membranes. It is suggested that the corresponding exclusion of fetal self-marker molecules from the apical membranes of some kinds of placental epithelia would deprive the mother of target sites for an alloimmune reaction at the maternal-fetal interface.
A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction.
Authors: C H Luo, Y Rudy
Journal: Circulation Research (1991)

A mathematical model of the membrane action potential of the mammalian ventricular cell is introduced. The model is based, whenever possible, on recent single-cell and single-channel data and incorporates the possibility of changing extracellular potassium concentration [K]o. The fast sodium current, INa, is characterized by fast upstroke velocity (Vmax = 400 V/sec) and slow recovery from inactivation. The time-independent potassium current, IK1, includes a negative-slope phase and displays significant crossover phenomenon as [K]o is varied. The time-dependent potassium current, IK, shows only a minimal degree of crossover. A novel potassium current that activates at plateau potentials is included in the model. The simulated action potential duplicates the experimentally observed effects of changes in [K]o on action potential duration and rest potential. Physiological simulations focus on the interaction between depolarization and repolarization (i.e., premature stimulation). Results demonstrate the importance of the slow recovery of INa in determining the response of the cell. Simulated responses to periodic stimulation include monotonic Wenckebach patterns and alternans at normal [K]o, whereas at low [K]o nonmonotonic Wenckebach periodicities, aperiodic patterns, and enhanced supernormal excitability that results in unstable responses ("chaotic activity") are observed. The results are consistent with recent experimental observations, and the model simulations relate these phenomena to the underlying ionic channel kinetics.
River Blindness Trial
Authors: Joan Stephenson
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 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
Performance of US Citizen Candidates on the January 1974 ECFMG Examination
Authors: Aims C. McGuinness
Journal: JAMA (1974)

A total of 663 candidates who were citizens of the United States at time of entry into a medical school outside of the United States or Canada took the January 1974 ECFMG examination. Of these candidates, 237 (35.7%) passed the examination. This compares with a worldwide pass rate of 40.7% for all 18,765 candidates in that examination. It was found that candidates in the last two years of medical school were more successful than those who had already graduated, and that the highest pass rate was found among those taking the examination for the first time. Because of factors such as changes in the curricula of foreign schools, considerable shifts in student populations among the various schools were observed. (<i>JAMA</i>229:431-434, 1974)
Late Reactions in Food-Allergic Children after Double-Blind, Placebo-Controlled Food Challenges
Authors: Jacquelien Saleh-Langenberg, Bertine M.J. Flokstra-de Blok, Nahlah AlAgla, Boudewijn J. Kollen, Anthony E.J. Dubois
Journal: Journal of Allergy and Clinical Immunology (2015)
Follow-up of Patients With Breast Cancer-Reply
Authors: Marco Rosselli Del Turco
Journal: JAMA (1994)

<h3>In Reply.</h3> —Dr Cocconi and Dr Yun Ryo ask some questions concerning whether the results of the two trials on follow-up of breast cancer can be transferred to clinical practice. The main issue raised by Cocconi relates to the need for continuous reassessment of the frequency of follow-up according to the evolution of medical therapy and assessment of its efficacy based on "tumor burden," while he also agrees that currently it is safe to use conservative follow-up for routine clinical care. However, we strongly believe that the efficacy of any new treatment modality in breast cancer relapses detected early should be assessed in controlled trials before advocating any intensive follow-up regimen. We would like to clarify to Yun Ryo that the study was designed to evaluate the different impact on overall survival of two different follow-up regimens offered to study participants for 5 years. On the other hand, follow-up was
The Debt and the Cash Flow of Residents: I. The Grim Present
Authors: James W. Marshall
Journal: JAMA (1990)

<h3>To the Editor.—</h3> The article regarding student loan indebtedness<sup>1</sup>overlooked several issues we "new" physicians must face. Having attended school from 1981 through 1985, I was influenced in my borrowing by several factors that later changed. Foremost among these were income averaging and tax deductibility of student loans. When my residency was complete and all deferments were past, so too was any hope of obtaining any tax breaks from the huge debt incurred for obtaining my degree. It seems paradoxical to penalize students and starting practitioners with ever-increasing tuition and longer residencies, while eliminating methods of off-setting debts our predecessors enjoyed. At least the present trainees know not to expect any break from the federal government. It's a sad day when a board-certified internist in his second year of practice is turned down by four banks (including the one holding my Health Education Assistance Loan [HEAL]) for a car
A double-blind, randomized, comparative study of DysportR vs. BotoxR in primary palmar hyperhidrosis
Authors: M. Simonetta Moreau, C. Cauhepe, J.P. Magues, J.M. Senard
Journal: British Journal of Dermatology (2003)

Intradermal injections of type A botulinum toxin have been reported to reduce excessive sweating in patients with primary palmar hyperhidrosis. Two preparations are commercially available in Europe: Botox (Allergan; 100 U per vial) and Dysport (Beaufour Ipsen Biotech; 500 U per vial), which are not bioequivalent. A few studies have tried to find an appropriate conversion factor between the two preparations in dystonic patients but results remain controversial.To compare the efficacy of Botox and Dysport in palmar hyperhidrosis using a conversion factor of 1 : 4.In a double-blind, randomized study, eight patients with severe primary palmar hyperhidrosis received in the same session intradermal injections of Dysport in one palm and Botox in the other, after regional median and ulnar nerve blocks. Quantification of sweat production was performed by Minor's iodine starch test at baseline, 1, 3 and 6 months after the treatment. Subjective assessment of sweat production was performed using a visual analogue scale.The mean +/- SD number of injection sites (28 +/- 1), mean volume of reconstituted solution injected (2.8 mL) and mean sweating area at baseline (BSA) were similar in each palm group. The mean +/- SD dose injected was 69.3 +/- 3.1 U for the Botox-treated palms and 283.7 +/- 11.3 U for the Dysport-treated palms (1 : 4). At 1 month, Minor's test revealed significant decreases in mean sweating area for each preparation (Dysport palms: -78.6% vs. BSA, P = 0.0002; Botox palms: -56.6% vs. BSA, P = 0.003). The percentage of decrease was more pronounced in Dysport palms compared with Botox palms but the difference did not reach statistical significance. At 3 months, the decrease in sweating area remained significant for Dysport palms (-69.4% vs. BSA, P = 0.008) but not for Botox palms (-48.8% vs. BSA). Self-evaluation showed a similar amount of improvement in both palm groups at 1 and 3 months (77% and 75% for Dysport; 68% and 72% for Botox). Local side-effects were more frequent in Dysport palms (weakness of thumb-index pinch in four cases, lasting 8-30 days) than in Botox palms (weakness of thumb-index pinch in two cases, lasting 15-21 days). The mean duration of positive effect was similar: 17 weeks in Dysport (range 8-32) and 18 weeks in Botox palms (range 8-32).Using a conversion factor of 1 : 4, the efficacy of Botox and Dysport injections was similar. However, there was a trend towards a larger improvement after Dysport treatment but with a higher incidence of adverse effects.
Hereditary angioedema: A decade of human C1-inhibitor concentrate therapy
Authors: Henriette Farkas, László Jakab, György Temesszentandrási, Beáta Visy, György Harmat, George Füst, Gábor Széplaki, Béla Fekete, István Karádi, Lilian Varga
Journal: Journal of Allergy and Clinical Immunology (2007)
Regulation of Matrix Metalloproteinase Activity in Ischemic Tissue by Interleukin-10
Authors: Jean-Sébastien Silvestre, Ziad Mallat, Radia Tamarat, Micheline Duriez, Alain Tedgui, Bernard I. Levy
Journal: Circulation Research (2001)

We have previously shown that deficiency in the anti-inflammatory cytokine interleukin-10 (IL-10) is responsible for enhanced angiogenesis after hindlimb ischemia. This study examined the putative involvement of matrix metalloproteinase (MMP) activation in this process. Ischemia was produced by artery femoral occlusion in both C57BL6 IL-10(+/+) and IL-10(-/-) mice. Angiographic vessel density and laser Doppler perfusion data at day 28 showed significant improvement in ischemic/nonischemic leg ratio by, respectively, 1.8-fold and 1.4-fold in IL-10(-/-) mice compared with IL-10(+/+) mice. This was associated with an increase in vascular endothelial growth factor (VEGF) protein content in the ischemic hindlimb. Three days after ischemia, gelatin zymography showed a significant increase in both pro- and active forms of MMP-2 and MMP-9 in ischemic hindlimbs of IL-10(-/-) mice compared with IL-10(+/+) mice (P<0.01). This increase in MMP activity in IL-10(-/-) mice was completely inhibited by treatment with BB-94 (5 mg/kg IP), a specific MMP inhibitor. Furthermore, increases in both vessel density and blood perfusion indexes at day 28 in IL-10(-/-) mice were abolished after treatment with BB-94 (0.78+/-0.06 versus 1.17+/-0.09 and 0.62+/-0.02 versus 0.88+/-0.04, for vessel density and blood perfusion ratio, respectively, in IL-10(-/-) mice treated with BB-94 versus untreated IL-10(-/-) mice, P<0.05). In contrast, BB-94 treatment did not affect the rise in VEGF protein content. These findings in IL-10(-/-) mice underscore the critical role of MMP activation, in a context of increased VEGF expression, in promoting ischemia-induced angiogenesis.
Clinicopathologic and molecular features in cutaneous extranodal natural killer–/T-cell lymphoma, nasal type, with aggressive and indolent course
Authors: Isabella Fried, Monika Artl, Carlo Cota, Hansgeorg Müller, Elvira Bartolo, Sebastiana Boi, Concetta Chiarelli, Esmeralda Vale, Matthias Schmuth, Thomas Wiesner, Michael R. Speicher, Lorenzo Cerroni
Journal: Journal of the American Academy of Dermatology (2014)
Riociguat for Patients With Pulmonary Hypertension Caused by Systolic Left Ventricular Dysfunction
Authors: Diana Bonderman, Stefano Ghio, Stephan B. Felix, Hossein-Ardeschir Ghofrani, Evangelos Michelakis, Veselin Mitrovic, Ronald J. Oudiz, Francis Boateng, Andrea-Viviana Scalise, Lothar Roessig, Marc J. Semigran
Journal: Circulation (2013)

Background— Pulmonary hypertension caused by systolic left ventricular dysfunction is associated with significant morbidity and mortality; however, no treatment is approved for this indication. We hypothesized that riociguat, a novel soluble guanylate cyclase stimulator, would have beneficial hemodynamic effects in patients with pulmonary hypertension caused by systolic left ventricular dysfunction. Methods and Results— Overall, 201 patients with heart failure resulting from pulmonary hypertension caused by systolic left ventricular dysfunction were randomized to double-blind treatment with oral placebo or riociguat (0.5, 1, or 2 mg 3 times daily) for 16 weeks in 4 parallel arms. The primary outcome was the placebo-corrected change from baseline at week 16 in mean pulmonary artery pressure. Although the decrease in mean pulmonary artery pressure in the riociguat 2 mg group (−6.1±1.3 mm Hg; P &lt;0.0001 versus baseline) was not significantly different from placebo ( P =0.10), cardiac index (0.4 L·min −1 ·m −2 ; 95% confidence interval, 0.2–0.5; P =0.0001) and stroke volume index (5.2 mL·m −2 ; 95% confidence interval, 2.0–8.4; P =0.0018) were significantly increased without changes in heart rate or systemic blood pressure compared with placebo. Both pulmonary (−46.6 dynes·s −1 ·cm −5 ; 95% confidence interval, –89.4 to –3.8; P =0.03) and systemic vascular resistance (−239.3 dynes·s −1 ·cm −5 ; 95% confidence interval, –363.4 to –115.3; P =0.0002) were significantly reduced with riociguat 2 mg. Riociguat reduced the Minnesota Living With Heart Failure score ( P =0.0002). Discontinuation of treatment was similar between treatment groups. Conclusions— Although the primary end point of the study was not met, riociguat was well tolerated in patients with pulmonary hypertension caused by systolic left ventricular dysfunction and improved cardiac index and pulmonary and systemic vascular resistance. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01065454.
P337Homozygous founder mutation in desmocollin-2 causes arrhythmogenic cardiomyopathy
Authors: A Lorenzon, B Bauce, I Rigato, K Pilichou, M De Bortoli, M Calore, C Basso, D Corrado, G Thiene, A Rampazzo
Journal: Cardiovascular Research (2014)

Purpose. Dominant mutations in genes encoding desmosomal proteins are reported to cause arrhythmogenic cardiomyopathy (AC), a heart muscle disease associated with ventricular arrhythmias, heart failure and risk of sudden death. Recessive mutations in the same genes most frequently cause cardiocutaneous syndromes. We present here a clinical and genetic study of 4 apparently unrelated AC families in which the cardiac-restricted phenotype is determined by a homozygous Desmocollin-2 (DSC2) mutation. Methods. We performed an exon-by-exon analysis of the DSC2 gene on 80 unrelated Italian index patients diagnosed affected with AC according to revised 2010 Task Force criteria. Segregation of the detected DSC2 mutation was studied and haplotypes were reconstructed to determine whether this mutation was recurrent or founder. To evaluate the pathogenic potentials of the DSC2 mutation, full-length wild-type and mutated cDNAs were cloned in eukaryotic expression vectors to obtain a fusion protein with green fluorescence protein (GFP); constructs were transfected in HL-1 cells. Results. We identified the p.D179G homozygous mutation in DSC2 gene in 4 (5%) out of 80 Italian index cases. One of them resulted to carry an additional PKP2 frameshift mutation. Haplotype analysis revealed a conserved haplotype among all DSC2 mutation carriers, strongly indicating a common founder. A severe form of biventricular cardiomyopathy with typical electrical features of AC was diagnosed in all homozygous mutation carriers, whereas heterozygous family members were clinically asymptomatic. In vitro functional studies on HL-1 cells showed that DSC2-GFP-D179G protein correctly localizes at the intercalated discs. Conclusions. This is the first founder homozygous mutation in DSC2 gene invariably associated with a severe AC phenotype in the Italian population. These findings could be important for risk stratification and mutation screening strategy.
Research Ethics Committees in Africa: Authors' Reply
Authors: Nancy E Kass, Adnan Ali Hyder, Ademola Ajuwon, John Appiah-Poku, Nicola Barsdorf, Dya Eldin Elsayed, Mantoa Mokhachane, Bavon Mupenda, Paul Ndebele, Godwin Ndossi, Bornwell Sikateyo, Godfrey Tangwa, Paulina Tindana
Journal: PLoS Medicine (2007)

Each of these programs has a different focus and both
Abstract 4546: COX-2 inhibitors arrest prostate cancer cell cycle progression by downregulation of kinetochore/centromere proteins
Authors: Jared Bieniek, Chandra Childress, Matthew Swatski, Wannian Yang
Journal: Cancer Research (2014)

Abstract Epidemiologic studies likewise revealed a decreased incidence of prostate cancer in patients taking non-steroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors. Previous in vitro studies have shown that inhibition of cyclooxygenase-2 (COX-2) arrests cancer cell growth. However, the molecular mechanism underlying the growth arrest effect of COX-2 inhibition remains elusive. In this study, we demonstrated that treatment with the COX-2 inhibitors celecoxib and CAY10404 significantly inhibited prostate cancer LNCaP cell proliferation. Flow cytometric analysis confirmed the cell cycle arrested at the G2/M phase and immunofluorescent staining indicated that inhibition of COX-2 prevented the cells from entering into mitosis. Further biochemical analysis showed that inhibition of COX-2 induced a dramatic down-regulation of key proteins in the kinetochore/centromere assembly, such as ZWINT, Cdc20, Ndc80, CENP-A, Bub1 and Plk1. Furthermore, the EP1 receptor antagonist SC51322 produced similar effects to the COX-2 inhibitors on LNCaP cell proliferation and down-regulation of kinetochore/centromere proteins, which did not occur in the EP2, EP3 and EP4 receptor antagonists, suggesting the COX-2 inhibitors arrest the cell proliferation and down-regulate kinetochore/centromere proteins through inactivation of the EP1 receptor. Our studies indicate that inhibition of COX-2 can arrest prostate cancer cell growth through inactivation of the EP1 receptor signaling and down-regulation of kinetochore / centromere proteins. Citation Format: Jared Bieniek, Chandra Childress, Matthew Swatski, Wannian Yang. COX-2 inhibitors arrest prostate cancer cell cycle progression by downregulation of kinetochore/centromere proteins. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4546. doi:10.1158/1538-7445.AM2014-4546
Diminished Clostridium difficile toxin A sensitivity in newborn rabbit ileum is associated with decreased toxin A receptor.
Authors: R Eglow, C Pothoulakis, S Itzkowitz, E J Israel, C J O'Keane, D Gong, N Gao, Y L Xu, W A Walker, J T LaMont
Journal: Journal of Clinical Investigation (1992)

Human infants are relatively resistant to Clostridium difficile-associated diarrhea and colitis compared to adults. In that toxin A is the major cause of intestinal damage with this organism, we compared toxin A receptor binding and biological effects in newborn vs adult rabbit ileum. Purified toxin A (M(r) 308 kD) was labeled with tritium or biotin with full retention of biologic activity. Appearance of specific toxin A brush border (BB) binding was strongly age dependent with minimal [3H]toxin A specific binding at 2 and 5 d of life, followed by gradual increase in binding to reach adult levels at 90 d. Absence of toxin A binding sites in newborn and presence in adult rabbits was confirmed by immunohistochemical studies using biotinylated toxin A. Toxin A (50 ng to 20 micrograms/ml) inhibited protein synthesis in 90-d-old rabbit ileal loops in a dose-dependent fashion. In contrast, inhibition of protein synthesis in 5-d-old rabbit ileum occurred only at the highest toxin A doses (5 and 20 micrograms/ml) and at all doses tested was significantly less than the adult rabbit ileum. In addition, toxin A (5 micrograms/ml) caused severe mucosal damage in adult rabbit ileal explants but had no discernable morphologic effect on 5-d-old rabbit intestine. Our data indicate that newborn rabbit intestine lacks BB receptors for toxin A. The absence of the high-affinity BB receptor for toxin A in the newborn period may explain lack of biologic responsiveness to purified toxin, and the absence of disease in human infants infected with this pathogen.
Nuclear Medicine Imaging in a Case of Hyperfunctioning Parathyroid Carcinoma Associated With a Parathyroid Adenoma
Authors: LUCA CERIANI, LUCA C. GIOVANELLA, MAURIZIO SALVADORE, GIUSEPPINA RONCARI
Journal: Clinical Nuclear Medicine (1995)

This report describes a rare case of parathyroid carcinoma associated with an adenoma. Nuclear imaging provided the most specific information about localization of the primary carcinoma and cervical metastasis, but failed to demonstrate evidence of a parathyroid adenoma. This could be explained by a partial inhibition of hormonal biosynthesis due to the high level of circulating parathormone produced by the carcinoma.
Flow cytometric disease monitoring in multiple myeloma: the relationship between normal and neoplastic plasma cells predicts outcome after transplantation
Authors: Andy C. Rawstron, Faith E. Davies, Ranjit DasGupta, A. John Ashcroft, Russell Patmore, Mark T. Drayson, Roger G. Owen, Andrew S. Jack, J. Anthony Child, Gareth J. Morgan
Journal: Blood (2002)