tbuckley/cabot-search huggingface dataset:
Comparison of Near-Patient Capillary Glucose Measurement and a Risk Assessment Questionnaire in Screening for Type 2 Diabetes in a High-Risk Population in Rural India
Authors: Georgia E. Ritchie, Andre Pascal Kengne, Rohina Joshi, Clara Chow, Bruce Neal, Anushka Patel, Sophia Zoungas
Journal: Diabetes Care (2010)

To assess the utility of a point-of-care (POC) capillary blood glucose measurement as compared with routine clinical parameters in predicting undiagnosed diabetes in a low-resource rural India setting.Nine hundred and ninety-four participants aged >30 years and stratified by age and sex were randomly selected from 20 villages in India. A clinical questionnaire, sampling for laboratory venous fasting plasma glucose (FPG), and POC capillary blood glucose assay were performed simultaneously. Diabetes diagnosis was based on the World Health Organization (WHO) definition using FPG. The capacity of the POC glucose to predict the presence of diabetes was assessed and compared with the questionnaire using area under the receiver operating characteristic curves (AUCs).The AUC for POC glucose alone in predicting diabetes was 0.869 (95% CI 0.810-0.929). This was significantly better (P < 0.001 for AUC comparison) than the models based upon clinical variables alone (AUC for the best clinical model including age, BMI, hypertension, waist circumference: 0.694 [95% CI 0.621-0.766]). POC glucose appropriately reclassified the risk of up to one-third of participants ranked according to the clinical models. Adding the clinical variables to the POC glucose assay did not significantly improve the discriminatory capability beyond that achieved with the POC glucose measurement alone (all P > 0.37).POC glucose testing appears to be a simple and reliable tool for identifying undiagnosed diabetes in a high-risk, resource-poor rural population. However, studies evaluating the cost effectiveness of introducing POC glucose testing are needed prior to widespread implementation.
Complexity of CEBPA Dysregulation in Human Acute Myeloid Leukemia
Authors: Thomas Pabst, Beatrice U. Mueller
Journal: Clinical Cancer Research (2009)

The transcription factor CCAAT enhancer binding protein alpha (CEBPA) is crucial for normal development of granulocytes. Various mechanisms have been identified how CEBPA function is dysregulated in patients with acute myeloid leukemia (AML). In particular, dominant-negative mutations located either at the N- or the C terminus of the CEBPA gene are observed in roughly 10% of AML patients, either in the combination on separate alleles or as sole mutation. Clinically significant complexity exists among AML with CEBPA mutations, and patients with double CEBPA mutations seem to have a more favorable course of the disease than patients with a single mutation. In addition, myeloid precursor cells of healthy carriers with a single germ-line CEBPA mutation evolve to overt AML by acquiring a second sporadic CEBPA mutation. This review summarizes recent reports on dysregulation of CEBPA function at various levels in human AML and therapeutic concepts targeting correction of CEBPA activity. The currently available data are persuasive evidence that impaired CEBPA function contributes directly to the development of AML, whereas restoring CEBPA function represents a promising target for novel therapeutic strategies in AML.
Phospholipid metabolism in cardiomyopathic hamster heart cells.
Authors: H Kawaguchi, M Shoki, H Sano, T Kudo, H Sawa, H Okamoto, Y Sakata, H Yasuda
Journal: Circulation Research (1991)

We demonstrated that the activities of phosphatidylinositide-specific phospholipase C, inositol 1,4,5-trisphosphate (IP3) kinase, and IP3 phosphatase were enhanced in cardiomyopathic hamster hearts (BIO 14.6 and BIO 53.58) in comparison to control hamsters (F1b). Release of both arachidonic acid and prostacyclin was markedly enhanced by norepinephrine in the cardiomyopathic hamsters. Phospholipase C in heart has high substrate specificity to phosphatidylinositol. IP3 production was markedly enhanced in the cardiomyopathic hamsters. We also determined the intracellular calcium concentration, which was higher in BIO 53.58 hamsters than in BIO 14.6 hamsters at 5-20 weeks of age. There was no significant difference in the intracellular calcium level between F1b and BIO 14.6 hamsters at 5 weeks of age. These results suggest that phosphatidylinositol turnover stimulated by norepinephrine may produce high intracellular calcium levels in both BIO 14.6 and BIO 53.58 myocytes. In addition, in BIO 53.58 hamsters, some mechanism such as the sarcoplasmic reticulum, which controls the intracellular calcium level, may deteriorate in function. We concluded from these results that a prolonged high intracellular calcium level may lead to the death of BIO 53.58 myocytes.
Smoking and inflammation: evidence for a synergistic role in chronic disease
Authors: Annsofi Johannsen, Cristiano Susin, Anders Gustafsson
Journal: Periodontology 2000 (2013)

Tobacco smoking is the most important preventable risk factor for periodontitis; however, the underlying biological mechanisms responsible for the detrimental effects of smoking on periodontal health remain largely unclear. It is also well established that smoking has a negative impact on several inflammatory diseases, including rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease. The aim of this paper was to review smoking-related changes in local and systemic host responses with a focus on cellular and molecular effects that could explain a hyperinflammatory response leading to periodontal destruction. Biological mechanisms that may be common to periodontal disease and other chronic inflammatory diseases were also explored, together with gene-smoking interactions. An epidemiologic perspective on the burden of smoking on periodontal health and the potential for smoking cessation is also presented. Tobacco smoking seems to induce changes ranging from decreased leukocyte chemotaxis to decreased production of immunoglobulins. Smoking also seems to cause a stronger inflammatory reaction with an increased release of potentially tissue-destructive substances (e.g. reactive oxygen species, collagenase, serine proteases and proinflammatory cytokines). These findings support a hypothesis that periodontitis is a hyperinflammatory condition rather than a hypo-inflammatory condition.
Telomere Length Abnormalities Occur Early in the Initiation of Epithelial Carcinogenesis
Authors: Alan K. Meeker, Jessica L. Hicks, Christine A. Iacobuzio-Donahue, Elizabeth A. Montgomery, William H. Westra, Theresa Y. Chan, Brigitte M. Ronnett, Angelo M. De Marzo
Journal: Clinical Cancer Research (2004)

Abstract Purpose: Telomeres help maintain chromosomal integrity. Dysfunctional telomeres can cause genetic instability in vitro and an increased cancer incidence in telomerase knock out mouse models. We recently reported that telomere shortening was a prevalent alteration in human prostate, pancreas, and breast cancer precursor lesions. In the present study, we address whether the previous findings are broadly applicable to human epithelial cancer precursors in general. Experimental Design: Surgical specimens of epithelial cancer precursor lesions from the urinary bladder, esophagus, large intestine, oral cavity, and uterine cervix were examined using a recently developed technique for direct in situ telomere length assessment in formalin-fixed human tissue specimens. Results: Widespread telomere length abnormalities were nearly universal (97.1% of cases) in the preinvasive stages of human epithelial carcinogenesis in all sites examined in this series, with telomere shortening the predominant abnormality (88.6% of cases). Conclusions: Telomere length abnormalities appear to be one of the earliest and most prevalent genetic alterations acquired in the multistep process of malignant transformation. These findings support a model whereby telomere dysfunction induces chromosomal instability as an initiating event in many, perhaps most, human epithelial cancers. Together with previous findings from the prostate and pancreas, the percentage of intraepithelial neoplasia lesions showing telomere length abnormalities is 95.6%. The implications of these findings include the potential that telomere length assessment in situ may be a widely useful biomarker for monitoring disease prevention strategies and for improved early diagnosis.
Increased Arteriovenous Oxygen Difference After Physical Training in Coronary Heart Disease
Authors: JEAN-MARIE R. DETRY, MICHEL ROUSSEAU, GENEVIEVE VANDENBROUCKE, FUSAKO KUSUMI, LUCIEN A. BRASSEUR, ROBERT A. BRUCE
Journal: Circulation (1971)

A preliminary study of 12 male patients (mean age, 47.8 years) with coronary heart disease (six with angina pectoris and six with prior myocardial infarction but without angina) was conducted according to a common protocol in Seattle, Washington, and Louvain, Belgium. Maximal oxygen intake (V o o2 max) and hemodynamic studies at rest and at two or three levels of submaximal exercise in the upright position were obtained before and after a 3-month physical training program that involved three sessions of 45 min/week. "V o o2 max" increased 22.5% ( P &lt; 0.0001) with physical training. Changes in maximal heart rate occurred in the patients with angina (+8.4%) but not in those without angina (+0.8%). At rest and at each submaximal exercise, heart rate, mean blood pressure, and cardiac output decreased after training, whereas stroke volume was unchanged and arterio-mixed venous oxygen (A-V o o2 ) difference increased. The pressure-rate product and the left ventricular work decreased after training. The classic posttraining bradycardia was compensated not by a higher stroke volume but by an increased A-V o o2 difference which resulted from both a higher arterial oxygen content and an increased peripheral oxygen extraction. The latter was more apparent when exercises of the same relative intensity were compared. Thus, benefits with physical training in coronary patients result at submaximal exercise level from enhanced arterial oxygen content and peripheral extraction and secondarily from lower hemodynamic stress on ischemic myocardium. Increased maximal A-V o o2 difference probably explains most of the increase in "V o o2 max" with physical training in coronary patients not limited by angina pectoris.
Oral D-4F Causes Formation of Pre-β High-Density Lipoprotein and Improves High-Density Lipoprotein–Mediated Cholesterol Efflux and Reverse Cholesterol Transport From Macrophages in Apolipoprotein E–Null Mice
Authors: Mohamad Navab, G.M. Anantharamaiah, Srinivasa T. Reddy, Susan Hama, Greg Hough, Victor R. Grijalva, Alan C. Wagner, Joy S. Frank, Geeta Datta, David Garber, Alan M. Fogelman
Journal: Circulation (2004)

These studies were designed to determine the mechanism of action of an oral apolipoprotein (apo) A-I mimetic peptide, D-4F, which previously was shown to dramatically reduce atherosclerosis in mice.Twenty minutes after 500 microg of D-4F was given orally to apoE-null mice, small cholesterol-containing particles (CCPs) of 7 to 8 nm with pre-beta mobility and enriched in apoA-I and paraoxonase activity were found in plasma. Before D-4F, both mature HDL and the fast protein liquid chromatography fractions containing the CCPs were proinflammatory. Twenty minutes after oral D-4F, HDL and CCPs became antiinflammatory, and there was an increase in HDL-mediated cholesterol efflux from macrophages in vitro. Oral D-4F also promoted reverse cholesterol transport from intraperitoneally injected cholesterol-loaded macrophages in vivo. In addition, oral D-4F significantly reduced lipoprotein lipid hydroperoxides (LOOH), except for pre-beta HDL fractions, in which LOOH increased.The mechanism of action of oral D-4F in apoE-null mice involves rapid formation of CCPs, with pre-beta mobility enriched in apoA-I and paraoxonase activity. As a result, lipoprotein LOOH are reduced, HDL becomes antiinflammatory, and HDL-mediated cholesterol efflux and reverse cholesterol transport from macrophages are stimulated.
A two-gene expression ratio predicts clinical outcome in breast cancer patients treated with tamoxifen
Authors: Xiao-Jun Ma, Zuncai Wang, Paula D Ryan, Steven J Isakoff, Anne Barmettler, Andrew Fuller, Beth Muir, Gayatry Mohapatra, Ranelle Salunga, J.Todd Tuggle, Yen Tran, Diem Tran, Ana Tassin, Paul Amon, Wilson Wang, Wei Wang, Edward Enright, Kimberly Stecker, Eden Estepa-Sabal, Barbara Smith, Jerry Younger, Ulysses Balis, James Michaelson, Atul Bhan, Karleen Habin, Thomas M Baer, Joan Brugge, Daniel A Haber, Mark G Erlander, Dennis C Sgroi
Journal: Cancer Cell (2004)
The Care and Feeding of Children: A Catechism for the Use of Mothers and Children's Nurses
Authors: L E Holt
Journal: JAMA (1934)

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
Randomised controlled trial of Alexander technique lessons, exercise, and massage (ATEAM) for chronic and recurrent back pain
Authors: P. Little, G. Lewith, F. Webley, M. Evans, A. Beattie, K. Middleton, J. Barnett, K. Ballard, F. Oxford, P. Smith, L. Yardley, S. Hollinghurst, D. Sharp
Journal: BMJ (2008)

To determine the effectiveness of lessons in the Alexander technique, massage therapy, and advice from a doctor to take exercise (exercise prescription) along with nurse delivered behavioural counselling for patients with chronic or recurrent back pain.Factorial randomised trial.64 general practices in England.579 patients with chronic or recurrent low back pain; 144 were randomised to normal care, 147 to massage, 144 to six Alexander technique lessons, and 144 to 24 Alexander technique lessons; half of each of these groups were randomised to exercise prescription.Normal care (control), six sessions of massage, six or 24 lessons on the Alexander technique, and prescription for exercise from a doctor with nurse delivered behavioural counselling.Roland Morris disability score (number of activities impaired by pain) and number of days in pain.Exercise and lessons in the Alexander technique, but not massage, remained effective at one year (compared with control Roland disability score 8.1: massage -0.58, 95% confidence interval -1.94 to 0.77, six lessons -1.40, -2.77 to -0.03, 24 lessons -3.4, -4.76 to -2.03, and exercise -1.29, -2.25 to -0.34). Exercise after six lessons achieved 72% of the effect of 24 lessons alone (Roland disability score -2.98 and -4.14, respectively). Number of days with back pain in the past four weeks was lower after lessons (compared with control median 21 days: 24 lessons -18, six lessons -10, massage -7) and quality of life improved significantly. No significant harms were reported.One to one lessons in the Alexander technique from registered teachers have long term benefits for patients with chronic back pain. Six lessons followed by exercise prescription were nearly as effective as 24 lessons.National Research Register N0028108728.
Fat middle section is less healthy than being obese, say researchers
Authors: J. Wise
Journal: BMJ (2015)

People who are of normal weight but fat around their middle have a greater chance of dying early than those who are overweight or obese but with a normal fat distribution, a large study published in the Annals of Internal Medicine has shown.1

The US study included 15 184 adults with a mean age of 45 from the third National Health and Nutrition Examination Survey (NHANES III). …
The Endogenous CXXC Motif Governs the Cadmium Sensitivity of the Renal Na+/Glucose Co-Transporter
Authors: Xiaobing Xia, Gang Wang, Yanchun Peng, Ming-Gene Tu, Jimmy Jen, Hongqing Fang
Journal: Journal of the American Society of Nephrology (2005)

Cadmium (Cd2+) poisoning causes severe renal disorders manifested by defects in reabsorptive transport of various compounds. It is reported here that the renal brush-border membrane Na+/glucose co-transporter-1 (SGLT1) is a molecular target for Cd2+ toxicity. In micromolar concentrations, Cd2+ acted as a noncompetitive, partial inhibitor of methyl-D-glucopyranoside uptake in vesicles from COS-7 cells transiently expressing SGLT1. In contrast, only a modest effect in the closely related Na+/myo-inositol co-transporter-1 (SMIT1) was observed. The factor responsible for this difference was the CXXC motif (X can be any residue) at the cytoplasmic end of the eighth transmembrane segment (TM8) of SGLT1. Thus, a mutational transfer of this motif conveyed Cd2+ sensitivity to SMIT1. Moreover, mimicking the inhibitory effect of Cd2+, the biarsenical molecule FlAsH-EDT2 strongly inhibited the SGLT1 that had an engineered tetracysteine motif at the cytoplasmic end of TM8. The experiments also showed that covalent binding of the sulfhydryl reactive biotin-PEO-maleimide to the SGLT1 wild type but not to the mutant lacking the CXXC motif was suppressed by Cd2+. Taken together, these results suggest that in SGLT1, Cd2+ binding to the CXXC motif induces conformational changes that cause a partial inhibition of d-glucose transport.
Intravenous pulse cyclophosphamide therapy in Crohn's disease and ulcerative colitis.
Authors: Z Barta, L Toth, G G Szabo, G Szegedi, M Zeher
Journal: Gut (2004)

The management of refractory severe inflammatory bowel disease (IBD) is still unresolved. We read with interest the article by Stallmach et al on the safety and efficacy of intravenous pulse cyclophosphamide in acute steroid refractory IBD ( Gut 2003; 52 :377–82).

In common with other disease, the aims of therapy in IBD fall into three categories:



1.  induction of remission;

2.  maintenance of remission; and

3.  prevention of relapse, all of which should be undertaken with minimal mortality and morbidity …
Developmental model for the pathogenesis of testicular carcinoma in situ: genetic and environmental aspects
Authors: Ewa Rajpert-De Meyts
Journal: Human Reproduction Update (2006)

Carcinoma in situ testis (CIS), also known as intratubular germ cell neoplasia (ITGCN), is a pre-invasive precursor of testicular germ cell tumours, the commonest cancer type of male adolescents and young adults. In this review, evidence supporting the hypothesis of developmental origin of testicular germ cell cancer is summarized, and the current concepts regarding aetiology and pathogenesis of this disease are critically discussed. Comparative studies of cell surface proteins (e.g. PLAP and KIT), some of the germ cell-specific markers (e.g. MAGEA4, VASA, TSPY and NY-ESO-1), supported by studies of regulatory elements of the cell cycle (e.g. p53, CHK2 and p19-INK4d) demonstrated a close similarity of CIS to primordial germ cells and gonocytes, consistent with the pre-meiotic origin of CIS. Recent gene expression profiling studies showed that CIS cells closely resemble embryonic stem cells (ESCs). The abundance of factors associated with pluripotency (NANOG and OCT-3/4) and undifferentiated state (AP-2γ) may explain the remarkable pluripotency of germ cell neoplasms, which are capable of differentiating to various somatic tissue components of teratomas. Impaired gonadal development resulting in the arrest of gonocyte differentiation and retention of its embryonic features, associated with an increasing genomic instability, is the most probable model for the pathogenesis of CIS. Genomic amplification of certain chromosomal regions, e.g. 12p, may facilitate survival of CIS and further invasive progression. Genetic studies, have so far not identified gene polymorphisms predisposing to the most common non-familial testicular cancer, but this research has only recently begun. Association of CIS with other disorders, such as congenital genital malformations and some forms of impaired spermatogenesis, all rising in incidence in a synchronous manner, led to the hypothesis that CIS might be a manifestation of testicular dysgenesis syndrome (TDS). The aetiology of TDS including testicular cancer remains to be elucidated, but epidemiological trends suggest a primary role for environmental factors, probably combined with genetic susceptibility.
Stromal Cells Protect against Acute Tubular Injury via an Endocrine Effect
Authors: Baoyuan Bi, Roland Schmitt, Malika Israilova, Hitoshi Nishio, Lloyd G. Cantley
Journal: Journal of the American Society of Nephrology (2007)

Emerging evidence suggests that the intravenous injection of bone marrow–derived stromal cells (BMSC) improves renal function after acute tubular injury, but the mechanism of this effect is controversial. In this article, we confirm that intravenous infusion of male BMSC reduced the severity of