tbuckley/cabot-search huggingface dataset:
Reply:
Authors: Stephen P. Hunt, Hiroshi Kiyama, Andrew J. H. Smith, Christa Laurence
Journal: Hepatology (2007)

In a recent letter, Drs. Liu and Cui state that "The current terminology used for mammalian Reg family genes/proteins is very confusing and should be unified with debates." According to the article, Reg2, also called RegIIIb, is the mouse homolog of human hepatocarcinoma-intestine-pancreas/pancreatic associated protein (HIP/PAP), whose cDNA has been cloned in different species under different names: human HIP/PAP or Reg3A; rat Reg2, PAPI, or peptide 23; mouse Reg2/RegIIIb; and hamster islet neogenesis associated protein or INGAP. The target gene could be, respectively, Reg2, Reg3a, Reg3b or INGAP.1 This is impossible because they represent independent genes encoding unique proteins, assuming only one gene was targeted. To clarify the terminology, Table 1 compares the nomenclature and clarifies the homologies of the various members of the Reg family. We believe that the confusion is due to the mixed usage of Arabic numerals (2 and 3) and Roman numerals (I, II, and III) adopted in previous papers. The table by Liu and Cui uses Arabic numerals, but in original articles, the usages are a mixture of Arabic and Roman. In any event, we agree the terminology is inconvenient (see Namikawa et al.2 and Namikawa et al.3). Stephen P. Hunt*, Hiroshi Kiyama , Andrew J. H. Smith , Christa Laurence§, * Department of Anatomy and Developmental Biology, University College London, London, UK, Department of Anatomy and Neurobiology, Osaka City University, Graduate School of Medicine, Osaka, Japan, Gene Targeting Laboratory, Institute for Stem Cell Research, University of Edinburgh, Edinburgh, UK, § MCU-PH, Service de Biochimie Métabolique, Hôpital Necker Enfants Malades, Paris, France.
Population-based norms for the Mini-Mental State Examination by age and educational level
Authors: R. M. Crum
Journal: JAMA (1993)

<h3>Objective.</h3> —To report the distribution of Mini-Mental State Examination (MMSE) scores by age and educational level. <h3>Design.</h3> —National Institute of Mental Health Epidemiologic Catchment Area Program surveys conducted between 1980 and 1984. <h3>Setting.</h3> —Community populations in New Haven, Conn; Baltimore, Md; St Louis, Mo; Durham, NC; and Los Angeles, Calif. <h3>Participants.</h3> —A total of 18 056 adult participants selected by probability sampling within census tracts and households. <h3>Main Outcome Measures.</h3> —Summary scores for the MMSE are given in the form of mean, median, and percentile distributions specific for age and educational level. <h3>Results.</h3> —The MMSE scores were related to both age and educational level. There was an inverse relationship between MMSE scores and age, ranging from a median of 29 for those 18 to 24 years of age, to 25 for individuals 80 years of age and older. The median MMSE score was 29 for individuals with at least 9 years of schooling, 26 for those with 5 to 8 years of schooling, and 22 for those with 0 to 4 years of schooling. <h3>Conclusions.</h3> —Cognitive performance as measured by the MMSE varies within the population by age and education. The cause of this variation has yet to be determined. Mini-Mental State Examination scores should be used to identify current cognitive difficulties and not to make formal diagnoses. The results presented should prove to be useful to clinicians who wish to compare an individual patient's MMSE scores with a population reference group and to researchers making plans for new studies in which cognitive status is a variable of interest. (<i>JAMA</i>. 1993;269:2386-2391)
Editorial Board
Authors: Stavroula Kousta, Katja Brose, Rolf Van Der Sanden, Loek De Weerd, Philip Patenall, R Adolphs, R Baillargeon, D Chalmers, N Chater, J Cohen, J Driver, A Engel, R French, A Friederici, M Goodale, M Hauser, R Jackendoff, P Johnson-Laird, S Kosslyn, N Logothetis, J Mcclelland, L Nadel, S Pinker, Z Pylyshyn, T Robbins, S Shamma, A Wagner, V Walsh, D Wolpert
Journal: Trends in Cognitive Sciences (2009)
Congenital 6‐phosphogluconate dehydrogenase (6PGD) deficiency associated with chronic hemolytic anemia in a Spanish family
Authors: J.Ll. Vives Corrons, D. Colomer, A. Pujades, A. Rovira, M. Aymerich, A. Merino, J. Ll. Aguilar i Bascompte
Journal: American Journal of Hematology (1996)

Clinical and metabolic studies were performed in four members of a Spanish family with partial (50%) 6 phosphogluconate dehydrogenase (6PGD) deficiency. In all cases the activities of 6 phosphogluconolactone (6PGL) and glutathione reductase (GR) were normal, and the molecular characterization performed in the partially purified 6PGD from the propositus showed normal kinetic and electrophoretic patterns. Two females (the propositus and her sister) suffered from a well-compensated chronic nonspherocytic hemolytic anemia (CNSHA) and exhibited decreased RBC glutathione (GSH) stability with increased oxidative susceptibility, defined by enhanced malonyldialdehyde (MDA) generation “in vitro.” The other two members of the family (the propositus's mother and brother) were clinically asymptomatic. In the propositus and her sister, RBC metabolism exhibited a markedly abnormal concentration of glycolytic intermediates, mainly characterized by striking increases in fructose 1,6 bisphosphate (50-fold), dihydroxiacetone-phosphate (20-fold) and glyceraldehyde 3-phosphate (tenfold). Although the precise mechanism of the hemolysis in the two patients is unknown, the enhanced oxidative threat observed in their RBCs may interfere in some way with the glycolytic pathway function, leading to a marked increase in certain metabolic intermediates located before the glyceraldehyde 3 phosphate dehydrogenase (GA3PD) step. Since it seems that GA3PD half-life is modulated by fluctuations of the cytosolic redox status, an “in situ” approach was simulated by using permeabilized RBCs. In these conditions, GA3PD activity was significantly lower in the propositus and her sister than in the asymptomatic members of the family and the simultaneous normal control. © 1996 Wiley-Liss, Inc.
Erratum: CALM/AF10-positive leukemias show upregulation of genes involved in chromatin assembly and DNA repair processes and of genes adjacent to the breakpoint at 10p12
Authors: M A Mulaw, A Krause, A J Deshpande, L F Krause, A Rouhi, R La Starza, A Borkhardt, C Buske, C Mecucci, W-D Ludwig, C Lottaz, S K Bohlander
Journal: Leukemia (2012)
Concanavalin A induces perforin-mediated but not Fas-mediated hepatic injury
Authors: Y Watanabe, M Morita, T Akaike
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 α (TNF–α), interferon γ (IFN–γ), 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, α–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–γ 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.
A Better Knowledge of Genetics Urged
Journal: JAMA (1965)

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
Irradiated Candy
Authors: G. G. Liddle
Journal: JAMA (1967)

<h3>To the Editor:—</h3> Among the by-products of atomic energy, irradiated carbohydrates have become a formidable reality. Even before the days of apocalyptic prophesies of fallout from exploded A-bombs, irradiation of culture media by ultraviolet light had been shown to alter staphylococci grown on such media. The overworked fruit fly has taken up some of the research burden by undergoing suitable mutation, when his food is irradiated, but he has been mutating for research biology for many years, and this is not very exciting. Food plants have been found to get sticky chromosomes when fed irradiated carbohydrates, and their anaphase fragments lag. Irradiated glucose is found toxic to mammalian cells, which don't grow well on this dietary ingredient. Now, investigators from Michigan report chromosome damage in mammalian cells fed irradiated sucrose (<i>Nature</i><b>221</b>:1254, 1966). This irradiated candy does not provoke changes radically different from those observed in directly irradiated cells.
Bronchopulmonary Dysplasia
Journal: Thorax (1989)

ness, again when applied to the whole population of asth- matic individuals, leads to a disproportionate increase in the proportion of those with severe disease.The probable validity of the second assumption can be illustrated (figure) by comparing childhood asthma prevalence in England and New Zealand (EA Mitchell, HR Anderson, unpublished study).The lifetime prevalence of wheeze in Auckland, New Zealand, is 18-5% higher than in South West Thames, England (25-6% v 21-6%), the prevalence of wheeze in the last 12 months 32-1% higher (14-8% v 11-2%), and the prevalence of wheeze in the last month 87-5% higher (7 7% v 4-1%).Thus there is a difference in the distribution ofasthma severity between the two countries.Could this be produced by New Zealand's higher asthma drug consumption2 and the promotion of maintenance beta agonists?Dr Gregg speculates that "pan-adrenoceptor" agonists may be superior to selective beta2 agonists in relieving and preventing mucosal oedema.These drugs were effective when used intermittently for acute severe asthma.The hypothesis, however, relates to long term regular use.The recent report suggesting that fenoterol, a less selective beta2 agonist, might increase the risk of death in patients with asthma3 indicates the need for caution before returning to even less selective adrenoceptor agonists.
From the editor
Authors: George deStevens
Journal: Medicinal Research Reviews (1981)

Medicinal Research Reviews will provide a forum for critical reviews of all aspects of research addressing the study of disease states and the consequent development of therapeutic agents.It will feature developments in specific areas of medicinal research, including the total review of the history leading up to introduction of a new pharmaceutical.Although several well known volumes and series are devoted to developments in the therapeutic area, these are usually of an encyclopedic nature and cover the field in a broad sense.Medicinal Research Reviews, as a quarterly publication, will be able to cover the most recent developments in the area and will emphasize timely publication.In addition, articles about new concepts and hypotheses concerning innovative approaches to drug design, new methods, and new biological principles associated with drug discovery will be encouraged in the journal.
Fertility Specialists Seeking Better Recipe for In Vitro Fertilization
Authors: Chris Anne Raymond
Journal: JAMA (1988)

ON THE HORIZON are several developments that, if widely implemented, could presage higher and more predictable birth rates at in vitro fertilization clinics. Some of those discussed at the last meeting of the American Fertility Society in Reno, Nev, included the following: • Predictors of response to follicular stimulation. Research conducted at the Jones Institute for Reproductive Medicine at the Eastern Virginia Medical School, Norfolk, suggests that women who respond to exogenous gonadotropins with a very high surge of either luteinizing hormone (LH) or folliclestimulating hormone (FSH) will not conceive. By this criterion, about 60% of women are nonresponders. These women, once identified, may avoid stimulation failure by being pretreated with gonadotropin releasing hormone (Gn-RH) agonists. • Synthetic Gn-RH agonists. Gn-RH agonists bind tightly to receptors in the pituitary gland. Initially, this stimulates the pituitary to release FSH and LH. Continuous administration, however, suppresses endogenous gonadotropin levels, through a process
Predicting return of erectile function following external beam radiotherapy or brachytherapy for prostate cancer using EPIC-CP.
Authors: Stephen A. Mihalcik, Jonathan Chipman, Martin G. Sanda, Irving D. Kaplan, Catrina Crociani, Peter Chang
Journal: Journal of Clinical Oncology (2016)

87 Background: EPIC-CP (Expanded Prostate Cancer Index Composite for Clinical Practice) is a one page, 16-item questionnaire designed and validated to measure patient-reported health related quality of life in prostate cancer (PC) patients at the point of care in the clinical setting. We previously developed and externally validated models predictive of intact sexual function (i.e. achieving an erection firm enough for intercourse) at two years following external beam radiation (EBRT) or brachytherapy (BT) using EPIC-26, the parent tool from which EPIC-CP was derived. We aimed to enable the use of these models in clinical practice by recalibrating them for use with EPIC-CP. Methods: Using a previously described multicenter longitudinal cohort (PROST-QA), we identified 217 men treated with EBRT and 230 with BT with complete sexual domain and model covariate information. We used the established covariates predictive of functional erections in the EPIC-26-based models (baseline sexual score, neoadjuvant hormonal therapy, and baseline PSA for EBRT, and baseline sexual score, age, race, and BMI for BT) to recalibrate the multivariable logistic regression models for use with EPIC-CP. We examined Pearson residuals to determine goodness of fit and compared the individual predictions based on the revised models with those generated by the EPIC-26-based models. Results: The recalibrated EPIC-CP-based models demonstrated excellent discrimination (AUC 0.81 for EBRT, AUC 0.87 for BT). Odds ratio estimates for the EPIC-CP models changed by no more than 0.2 from their EPIC-26 counterparts, and remained statistically significant. EPIC-CP and EPIC-26-based predictions had good concordance: the mean ± SD difference in predicted probability between EPIC-26 and EPIC-CP models was 0.0 ± 0.08 in each treatment group. Predicted probabilities were within 15.4% and 15.8% for 95% of the subjects treated with EBRT and BT, respectively. Conclusions: EPIC-CP-based nomograms predicting erectile function two years after EBRT or BT are in good agreement with established EPIC-26-based tools and offer an easily applied and accurate prediction regarding a common and impactful side effect of PC treatment.
Specialty Abstracts
Journal: JAMA (1990)

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Transactions of Indiana State Medical Society.
Journal: JAMA (1899)

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
Warner's Pocket Medical Dictionary of today, comprising pronunciation and definition of 10,000 essential words and terms used in medicine and associated sciences
Journal: JAMA (1897)

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
Bone Tumors
Authors: Howard L. Steinbach
Journal: JAMA (1978)

Part 6 of volume 5 of the<i>Encyclopedia of Medical Radiology</i>is a handsome book with spine and corners bound in maroon leather. The pages are thick and glossy, and most illustrations are large and superbly reproduced. The price of the book reflects its quality. The text is in English, with English references at the end of each of the 15 sections. In addition, there is an author index of 37 pages and English-German and German-English indexes of 45 pages each at the end of the book. An unusual and welcome feature is a chapter on "High Resolution Radiographic Techniques for the Detection and Study of Skeletal Neoplasms," by Genant and Doi, in which the benefits of optical and roentgenographic magnification are discussed in detail. As would be expected in a book written by many individuals, there is considerable variation in the detail described and space used in the discussion
Atrial fibrillation while chewing nicotine gum
Authors: N. A. Rigotti
Journal: JAMA (1986)

<h3>To the Editor.—</h3> Since 1984, nicotine chewing gum has been widely prescribed by physicians to aid cigarette smokers attempting to give up their habit. Many smokers who could benefit from smoking cessation have cardiovascular disease. Whether they can safely use the gum has not been established, because there are no published reports of gum use in cardiac patients. We report here a man with known cardiovascular disease who developed atrial fibrillation while chewing nicotine gum. <h3>Report of a Case.—</h3> A 52-year-old male smoker with known coronary artery disease sought help in order to stop smoking. He had smoked three packs of cigarettes per day for 35 years and made several unsuccessful attempts to quit. Following coronary artery bypass surgery in 1981 he did not smoke for three years, but relapsed during a time of stress. When seen, he was smoking one pack of low-tar and nicotine cigarettes daily, had rare