tbuckley/cabot-search huggingface dataset:
Perception of “Healthy” Body Weight by Patients With Diabetes
Authors: Kathleen McTigue, Rachel Hess, Cindy L. Bryce, Katharine Fitzgerald, Ellen Olshansky, Diane Sacco, Gary Fischer
Journal: Diabetes Care (2006)

Although weight management is important to diabetes treatment (1–3), obesity remains common among adults with diabetes (4). This may reflect the difficulty of promoting weight loss (5) or inattention to obesity management during routine clinical practice (6). Since self-management is a major tenet of diabetes care (4), patient understanding of weight-related health risk may be an important step toward setting healthy lifestyle goals and effective weight management. We sought to understand how well patients with diabetes who receive care in primary care practices could identify healthy body weight.

During a diabetes education initiative, a survey was mailed to 2,607 patients with diabetes from three university-based general medicine practices in a single urban area. It included questions on knowledge (diabetes knowledge test, general knowledge subscale [7]) and behaviors related to diabetes. Patients were also asked to report their current height and weight, and “the healthiest weight for your height.”

To ensure privacy, patients with diabetes were identified anonymously from the practices’ electronic medical records. Participant responses were anonymous; to avoid undue burden on nonresponders uninterested in participating, the University’s Institutional Review Board precluded multiple mailings.

Each participant’s current BMI (weight in kilograms divided by the square of height in meters [kg/m2]) was calculated. Likewise, perceived healthiest BMI was calculated from reported current height and “healthiest” weight. If the current BMI was higher …
Deep-sequencing identification of the genomic targets of the cytidine deaminase AID and its cofactor RPA in B lymphocytes
Authors: Arito Yamane, Wolfgang Resch, Nan Kuo, Stefan Kuchen, Zhiyu Li, Hong-wei Sun, Davide F Robbiani, Kevin McBride, Michel C Nussenzweig, Rafael Casellas
Journal: Nature Immunology (2010)
EUROSCOP, ISOLDE and the Copenhagen City Lung Study
Authors: P S. BURGE
Journal: Thorax (1999)

In some countries inhaled corticosteroids are widely prescribed for patients with chronic obstructive pulmonary disease (COPD), despite the lack of good studies to support their use. In the last 12 months these three important large, parallel group, placebo controlled studies have reported at scientific meetings but, at the time of going to press with this article, they have not been published. This review will give an individual view of what has been presented, and provide a basis for the assessment of the trials when they are published.

All three studies used similar definitions of COPD and excluded patients with a clinical diagnosis of asthma or significant bronchodilator responsiveness. The Copenhagen study also excluded those with a prednisolone response, which was found in only 5% of their otherwise unselected population. The Copenhagen study started with a random population survey which identified all those with an FEV1/VC ratio of <70%, irrespective of their FEV1. They have the least diseased group with a mean FEV1 of 85% predicted and include many subjects whose FEV1 was within the normal range; indeed, only 39% had an FEV1 of <80% predicted. The subjects in the ISOLDE study were mostly recruited from respiratory clinics and have the most

severe COPD with a mean FEV1 of 50% predicted. The EUROSCOP group is intermediate in severity with a mean FEV1 of 77% predicted.

The EUROSCOP subjects were all current smokers, having failed to quit in a three month period during the run in. The ISOLDE subjects had all been smokers, but only 48% were smoking at trial entry. The Copenhagen study did not have any entry criteria relating to smoking; 76% were current smokers.

The principal outcome measure for all three studies was longitudinal decline in FEV1. It …
Does long term use of psychiatric drugs cause more harm than good?
Authors: P. C. Gotzsche, A. H. Young, J. Crace
Journal: BMJ (2015)

We could stop almost all psychotropic drug use without deleterious effect, says <b>Peter C Gøtzsche</b>, questioning trial designs that underplay harms and overplay benefits. <b>Allan H Young</b> and <b>John Crace</b> disagree, arguing that evidence supports long term use
Quantitative Measurement and Prediction of Biophysical Response During Freezing in Tissues
Authors: John C. Bischof
Journal: Annual Review of Biomedical Engineering (2000)

▪ Abstract Cryopreservation and cryosurgery are important biomedical applications used to selectively preserve or destroy cellular systems through freezing. Studies using cryomicroscopy techniques, which allow the visualization of the freezing process in single cells, have shown that a drop in viability correlates with the extent of two biophysical events during the freezing process: (a) intracellular ice formation and (b) cellular dehydration. These same biophysical events operate in tissue systems; however, the inability to visualize and quantify the dynamics of the freezing process in tissues has hampered direct correlation of these events with freezing-induced changes in viability. This review highlights two new techniques that use freeze substitution and differential scanning calorimetry to provide dynamic freezing data in tissue. Characteristic dimensions and parameters extracted from these new data are then used in a predictive model of biophysical freezing response in several tissues, including liver and tumor. This approach promises to help guide improved design of both cryopreservation and cryosurgical applications of tissue freezing.
Spain is to lead on EU policy on organ donation and transplantation
Authors: A. Garcia Rada
Journal: BMJ (2011)

Spain will take the lead on improving the training of transplant coordinators under a European Union directive published last year aimed at setting uniform quality and safety standards and improving waiting times for transplants ( BMJ 2010;340:c2785, doi:10.1136/bmj.c2785).

The training programmes for transplant coordinators, organised by the Spanish National Transplant Organisation (ONT) together with the Andalusian Public Foundation for the Advancement of Technology and Professional Training, aims to expand the Spanish model of organ donation and transplantation, said Rafael Matesanz, director of ONT, at a conference at the Menendez Pelayo International University in Santander.

The training programmes will be based on a Spanish …
Microalbuminuria Is Common in Japanese Type 2 Diabetic Patients
Authors: Hiroki Yokoyama, Koichi Kawai, Masashi Kobayashi
Journal: Diabetes Care (2007)

Previous studies have reported a marked variation in the prevalence of microalbuminuria in type 2 diabetic patients ranging from 7 to 47% (1–13). The variation could arise from ethnic/genetic differences in susceptibility (3–11) and from methodological issues for investigating the prevalence, such as small-sized populations (3,12,13); single clinic–based studies (8,12); use of the dipstick method instead of quantitative determinations (4,5); or only a single measurement of urinary albumin excretion (UAE) (3–13), whereas multiple measurements have been recommended for years (14). In terms of investigating the prevalence of microalbuminuria in type 2 diabetic patients, we performed this study with the aim of investigating patients with a specific ethnicity (i.e., Japanese). The study had a large-sized population, a nationwide multicenter-based design, and a high proportion of data availability for clinical variables and for multiple measurements of UAE.

A cross-sectional study was conducted that included 29 medical clinics (i.e., general practitioners) or general/university-affiliated hospitals from different areas in Japan, using the same software to incorporate patient records, as a working study group. Known as the Japan Diabetes Clinical Data Management Study Group (15), this group consists of medical doctors who volunteered to dedicate daily standard clinical work to scientific analysis. The study was performed …
Electrophysiologic effects of intracellular lysophosphoglycerides and their accumulation in cardiac lymph with myocardial ischemia in dogs.
Authors: H Akita, M H Creer, K A Yamada, B E Sobel, P B Corr
Journal: Journal of Clinical Investigation (1986)

Lysophosphatidylcholine (LPC) accumulates in ischemic tissue, and exogenous LPC (20-100 microM) induces electrophysiologic alterations in vitro. However, to determine whether compartmentalization is critical, intracellular pressure microinjection of LPC was performed with simultaneous recording of the transmembrane action potential. Intracellular LPC in concentrations as high as 500 microM (n = 18), calculated based on calibration of injectate volume and cellular volume, did not induce electrophysiologic alterations. The concentrations and efflux of phospholipids and lysophospholipids were assessed in lymph obtained from the supracardiac lymph vessel in anesthetized dogs to assess the extent of extracellular accumulation. Prior to ischemia, phosphatidylcholine (PC) was the major phospholipid in lymph (79 +/- 2%) with substantial quantities of sphingomyelin (11 +/- 2%) and LPC (6 +/- 1%). With ischemia, the concentration of LPC increased by 18%, and net efflux of LPC increased by 24% (P less than 0.01) with no net efflux of PC or other assayed phospholipids. The calculated concentration of LPC increased from 84 to 197 microM in lymph within the ischemic region, a concentration sufficient to induce electrophysiologic derangements.
Paced QRS duration as a predictor for clinical heart failure events during right ventricular apical pacing in patients with idiopathic complete atrioventricular block: results from an observational cohort study (PREDICT‐HF)
Authors: Shaojie Chen, Yuehui Yin, Xianbin Lan, Zengzhang Liu, Zhiyu Ling, Li Su, Márcio Galindo Kiuchi, Xiaoli Li, Bin Zhong, Mitchell W. Krucoff
Journal: European Journal of Heart Failure (2012)
Limited effect of sulphasalazine treatment in reactive arthritis. A randomised double blind placebo controlled trial
Authors: C. Egsmose, T. M. Hansen, L. S. Andersen, J. M. Beier, L. Christensen, L. Ejstrup, N. D. Peters, D. M F M van der Heijde
Journal: Annals of the Rheumatic Diseases (1997)

To assess the efficacy and safety of sulphasalazine in reactive arthritis.Double blind placebo controlled trial of six months duration comparing sulphasalazine 2-3 g per day (n = 37) with matching placebo (n = 42) in adults with active reactive arthritis (age 19-57 years, median 34). Treatment response was evaluated once a month by changes in erythrocyte sedimentation rate (ESR), pain, peripheral arthritis, tender iliosacral joints, entesopathy, extra-articular manifestations, and working ability.15 patients in the sulphasalazine group and eight in the placebo group withdrew from the study prematurely. Adverse events, primarily gastrointestinal, were the main reason for withdrawal in the actively treated group. Intention-to-treat analyses showed significant improvements over time in both groups in ESR, pain, and number of swollen joints (P < 0.01). Number of days on sick leave decreased significantly in the sulphasalazine group only (P < 0.01). No significant differences between the two groups were present after six months. Among the patients completing the trial according to protocol, persistent complete remission had occurred within two months in five (23%) of the actively treated, but in no placebo treated patients (P = 0.013).Sulphasalazine seemed to improve only the very short term outcome of reactive arthritis. The possible beneficial effect of the drug should also be weighed against the risk of adverse events. Although these were mainly mild, almost 25% of the patients in the actively treated group gave up treatment for this reason.
Effects of Environmental Agents on the Attainment of Puberty: Considerations When Assessing Exposure to Environmental Chemicals in the National Children’s Study
Authors: Richard Y. Wang, Larry L. Needham, Dana B. Barr
Journal: Environmental Health Perspectives (2005)

The apparent decline in the age at puberty in the United States raises a general level of concern because of the potential clinical and social consequences of such an event. Nutritional status, genetic predisposition (race/ethnicity), and environmental chemicals are associated with altered age at puberty. The Exposure to Chemical Agents Working Group of the National Children's Study (NCS) presents an approach to assess exposure for chemicals that may affect the age of maturity in children. The process involves conducting the assessment by life stages (i.e., in utero, postnatal, peripubertal), adopting a general categorization of the environmental chemicals by biologic persistence, and collecting and storing biologic specimens that are most likely to yield meaningful information. The analysis of environmental samples and use of questionnaire data are essential in the assessment of chemicals that cannot be measured in biologic specimens, and they can assist in the evaluation of exposure to nonpersistent chemicals. Food and dietary data may be used to determine the extent to which nutrients and chemicals from this pathway contribute to the variance in the timing of puberty. Additional research is necessary in several of these areas and is ongoing. The NCS is uniquely poised to evaluate the effects of environmental chemicals on the age at puberty, and the above approach will allow the NCS to accomplish this task.
ECL-Cell Derived Gastric Cancer in Male Cotton Rats Dosed with the H2-Blocker Loxtidine
Authors: Reidar Fossmark, Tom C. Martinsen, Karin E. Bakkelund, Shiro Kawase, Helge L. Waldum
Journal: Cancer Research (2004)

Abstract Spontaneously hypergastrinemic cotton rats (Sigmodon hispidus) develop tumors that have the phenotype of an adenocarcinoma but most likely originate from the enterochromaffin-like (ECL) cells. Among inbred animals ∼50% of the females, but &amp;lt;1% of males develop spontaneous gastric carcinomas. Gastrin is the principle carcinogen in this model, as &amp;gt;4 months of hypergastrinemia results in carcinoma, but a gastrin receptor antagonist prevents carcinomas. Carcinomas can also be induced by partial corpectomy. In the present study, the insurmountable H2-receptor antagonist loxtidine (200 mg/kg/day) was given to male cotton rats for 6 months. The loxtidine-dosed animals developed hypergastrinemia, whereas control animals remained normogastrinemic. At termination, 4 of 5 cotton rats had cancer located to the oxyntic mucosa, whereas 1 animal had dysplasia. The gastric mucosa of all of the control animals was normal. In the dysplastic mucosa of loxtidine-dosed animals there was a marked increase in chromogranin A-positive cells, where numerous groups of cells also stained positive with the Sevier-Munger technique. In areas of high proliferation and cancer there were also histidine decarboxylase, chromogranin A, and Sevier-Munger-positive cells, altogether indicating an ECL cell origin of the tumors. This represents an interesting animal model where ECL cell-derived gastric cancer can be induced by pharmacological acid inhibition in 6 months.
Changes in myofibrillar activation and troponin C Ca2+ binding associated with troponin T isoform switching in developing rabbit heart.
Authors: J J McAuliffe, L Z Gao, R J Solaro
Journal: Circulation Research (1990)

Postnatal development of the mammalian heart is associated with changes in the population of isoforms of the thin filament proteins. We correlated the change in thin filament proteins, which occur in rabbit hearts between 5 days and 22 days of age, with changes in Ca2+ dependence of myofibrillar ATPase activity, force generation, and troponin C Ca2+ binding. The preparations derived from the 5-day-old animals exhibited a high molecular weight isoform of troponin T not found in the hearts of the 22-day-old animals. Other troponin T isoforms were also found to be present in different relative amounts. No other major differences in thin filament protein composition could be identified. Compared with the 5-day-old rabbit heart preparations, the ATPase activity of myofibrils from 22-day-old rabbit hearts exhibited a reduced Ca2+ sensitivity. The pCa50 (negative log of the half-maximal-activity free Ca2+) of the MgATPase activity was shifted by 0.15 pCa units with maturation. Maturation of the myofibrils was also associated with an increased effect of Mg2+ on pCa50. On increasing the Mg2+ from 2 to 10 mM at constant MgATP2-, the pCa50 of 5-day myofibrils was increased (shifted to the right) by 0.39 pCa units for 5-day-old rabbit hearts and 0.45 pCa units for 22-day-old rabbit hearts. Although similar changes in pCa50 of force developed by myofibrils were marginally significant, fibers from hearts of 5-day-old rabbits exhibited a greater Hill coefficient than hearts from 22-day-old rabbits (3.0 vs. 2.1). Despite the increased sensitivity of 5-day-old rabbit hearts to Ca2+, these hearts exhibited significantly less Ca2+ bound to myofibrillar troponin C than did the 22-day-old rabbit hearts. Moreover, the models that best described the Ca2+ binding data are different for the two age groups. Our data indicate that the Ca2+ activation and Ca2+ binding properties of myofibrillar troponin C are altered in developing cardiac myofibrils and that the changes in these properties may be influenced by changes in the troponin T isoforms present in the myofibril.
New Perspectives on Alzheimer's Disease
Authors: D L Price
Journal: Annual Review of Neuroscience (1986)

Significant progress has been made in refining diagnostic criteria for AD and in developing imaging approaches to exclude treatable disease and to assess some of the metabolic processes occurring in vivo in the brains of individuals with AD. However, as yet, no reliable diagnostic test is available. Although risk factors have been identified, the etiology of AD remains an enigma. The roles of familial, chromosomal, and genetic factors, toxins, and transmissible agents in the pathogenesis of this disease deserve intensive study. A variety of neurotransmitter systems are affected in the disease, and it seems likely that new approaches may identify additional systems at risk. Of particular importance will be studies on surviving neurons, since these cells will be targets for treatment. Neurons in certain parts of the brainstem, basal forebrain, amygdala, hippocampus, and neocortex show several types of cytoskeletal abnormalities, but mechanisms of cytoskeletal disorganization are not well understood, e.g. we do not have a clear idea of the sequence of cytoskeletal pathology, the time course of dysfunction of individual neurons, and consequences of these processes on cell function. In situ hybridization with radiolabeled nucleic acid probes and immunocytochemical approaches should provide information about levels of gene expression, protein compositions, and posttranslational modifications of normal and abnormal proteins in these cells. The relationships and sources of some of the abnormal proteins (e.g. those associated with PHF, 15-nm straight filaments, plaque amyloid, and vascular amyloid) can be clarified by new approaches of protein chemistry (purification and sequencing) and molecular biology (recombinant DNA techniques). Finally, investigations of animal models that recapitulate certain features of AD should provide new insights into the nature, mechanisms, and consequences of cellular pathology of specific systems. These models may be useful for imaging studies similar to those used in human patients and for developing and testing new therapeutic approaches that eventually may be useful for treating this all-too-common disorder of the central nervous system.
The long non-coding RNA ERIC is regulated by E2F and modulates the cellular response to DNA damage
Authors: Orit Feldstein, Tal Nizri, Tirza Doniger, Jasmine Jacob, Gideon Rechavi, Doron Ginsberg
Journal: Molecular Cancer (2013)

Abstract Background The human genome encodes thousands of unique long non-coding RNAs (lncRNAs), and these transcripts are emerging as critical regulators of gene expression and cell fate. However, the transcriptional regulation of their expression is not fully understood. The pivotal transcription factor E2F1 which can induce both proliferation and cell death, is a critical downstream target of the tumor suppressor, RB. The retinoblastoma pathway is often inactivated in human tumors resulting in deregulated E2F activity. Results Here, we report that lncRNA XLOC 006942, which we named ERIC, is regulated by E2F1 and, most probably, also E2F3. We show that expression levels of ERIC were elevated upon activation of exogenous E2F1, E2F3 or endogenous E2Fs. Moreover, knockdown of either E2F1 or E2F3 reduced ERIC levels and endogenous E2F1 binds ERIC’s promoter. Expression of ERIC was cell cycle regulated and peaked in G1 in an E2F1-dependent manner. Inhibition of ERIC expression increased E2F1-mediated apoptosis, suggesting that E2F1 and ERIC constitute a negative feedback loop that modulates E2F1 activity. Furthermore, ERIC levels were increased following DNA damage by the chemotherapeutic drug Etoposide, and inhibition of ERIC expression enhanced Etoposide -induced apoptosis. Conclusions Our data identify ERIC as a novel lncRNA that is transcriptionally regulated by E2Fs, and restricts apoptosis induced by E2F1, as well as by DNA damage.
CARDIAC RESYNCHRONIZATION THERAPY IN PATIENTS WITH ISCHEMIC HEART FAILURE AFTER BONE MARROW CELL TRANSPLANTATION
Authors: Evgeny Pokushalov, Aleksandr Romanov, Darya Prohorova, Sergey Artemenko, Aleksandr Cherniavskiy, Aleksandr Karaskov, Nabil Dib
Journal: Journal of the American College of Cardiology (2011)
DNA methylation profiles in monozygotic and dizygotic twins
Authors: Zachary A Kaminsky, Thomas Tang, Sun-Chong Wang, Carolyn Ptak, Gabriel H T Oh, Albert H C Wong, Laura A Feldcamp, Carl Virtanen, Jonas Halfvarson, Curt Tysk, Allan F McRae, Peter M Visscher, Grant W Montgomery, Irving I Gottesman, Nicholas G Martin, Art Petronis
Journal: Nature Genetics (2009)
Genetics of NIDDM
Authors: M Alan Permutt
Journal: Diabetes Care (1990)

This brief review discusses the current level of understanding of the role of genetic defects in the etiology of non-insulin-dependent diabetes mellitus (NIDDM) and the use of molecular-genetic methods for this study. Evidence for genetic susceptibility is strong, and defects in both insulin production and action are suspect. With restriction-fragment-length polymorphisms and genomic sequencing, various candidate loci are being evaluated. Evidence that multiple genes are involved is only circumstantial. If NIDDM is genetically heterogeneous and also influenced by environmental components, population associations and linkage analyses in families may not be as easily interpreted as for diseases involving single major gene defects.