tbuckley/cabot-search huggingface dataset:
The exercise addiction inventory: a quick and easy screening tool for health practitioners: Table 1
Authors: M D Griffiths, A Szabo, A Terry
Journal: British Journal of Sports Medicine (2005)

Background: Exercise addiction is not routinely screened for probably because available instruments take a long time to administer, their scoring may be complicated, and their interpretation is not always obvious. A new psychometric instrument has been developed that is capable of identifying people affected by, or at risk of, exercise addiction: the exercise addiction inventory (EAI). A preliminary report showed the EAI had good reliability and validity. Objectives: To test further the EAI’s psychometric properties and show that it would be quick and simple to administer by general practitioners. Methods: A sample of 200 habitual exercisers were given the EAI and two existing exercise addiction scales (obligatory exercise questionnaire; exercise dependence scale). Two weeks later, another sample of 79 exercisers were administered the EAI to determine the test-retest reliability of the questionnaire. Results: The original data from the preliminary report were reanalysed to determine the split half correlation of the EAI. This was found to be 0.84 (Guttman split-half coefficient). A correlation between weekly frequency of exercising and EAI scores was also determined, and it was found that the two variables shared 29% of the variance ( r 2 = 0.29). The test-retest reliability of the scale was found to be very good (0.85). Conclusions: The EAI is a valid and reliable tool which would be capable of helping general practitioners to quickly and easily identify people affected by, or at risk of, exercise addiction.
Lymphocyte surface marker expression in rheumatic diseases: evidence for prior activation of lymphocytes in vivo.
Authors: M D Smith, P J Roberts-Thomson
Journal: Annals of the Rheumatic Diseases (1990)

Expression of major histocompatibility complex (MHC) class II and other lymphocyte activation markers on peripheral blood and synovial fluid T lymphocytes from patients with rheumatoid arthritis (RA), psoriatic arthritis, and Reiter9s syndrome were measured and the mean fluorescence intensities of these antigens were assessed. Increased expression of MHC class II antigens of synovial fluid T lymphocytes is not unique to RA, though it is quantitatively greater on RA synovial fluid T cells. There was less expression of other lymphocyte activation markers (4F2, transferin receptor) and a marked discordance between the expression of these markers and the interleukin 2 receptor (IL2r). Synovial fluid T lymphocytes contain a subpopulation of larger cells expressing MHC class II and other lymphocyte activation antigens with the exception of the IL2r. Mean fluorescence intensity of CD3 and CD4 antigens on synovial fluid T lymphocytes was decreased in all three patient groups, suggesting prior in vivo exposure of synovial fluid T lymphocytes to an unknown antigen.
Mechanisms and treatment of cardiovascular disease in Williams-Beuren syndrome
Authors: Barbara R. Pober, Mark Johnson, Zsolt Urban
Journal: Journal of Clinical Investigation (2008)

Williams-Beuren syndrome (WBS) is a microdeletion disorder caused by heterozygous loss of approximately 1.5-Mb pairs of DNA from chromosome 7. Patients with WBS have a characteristic constellation of medical and cognitive findings, with a hallmark feature of generalized arteriopathy presenting as stenoses of elastic arteries and hypertension. Human and mouse studies establish that defects in the elastin gene, leading to elastin haploinsufficiency, underlie the arteriopathy. In this review we describe potential links between elastin expression and arteriopathy, possible explanations for disease variability, and current treatment options and their limitations, and we propose several new directions for the development of nonsurgical preventative therapies based on insights from elastin biology.
Four Clusters were Identified in Abruptly-Increasing Neonates and Infants with Food Protein-Induced Gastrointestinal Syndrome, A Report of Japanese Patients
Authors: I. Nomura, H. Morita, N. Ito, T. Fukuie, N. Ohtsuka, S. Hosokawa, M. Watanabe, A. Terada, H. Hoshina, T. Takamasu
Journal: Journal of Allergy and Clinical Immunology (2011)
Glioma Cell Populations Grouped by Different Cell Type Markers Drive Brain Tumor Growth
Authors: Lars Prestegarden, Agnete Svendsen, Jian Wang, Linda Sleire, Kai Ove Skaftnesmo, Rolf Bjerkvig, Tao Yan, Lasse Askland, Andreas Persson, Per Øystein Sakariassen, Per Øyvind Enger
Journal: Cancer Research (2010)

Although CD133 has been proposed as a marker for brain tumor-initiating cells, studies show that a tumorigenic potential exists among CD133(-) glioma cells as well. However, it is not established whether the ability of CD133(-) cells to form tumors is a property confined to a small subpopulation, rather than a common trait associated with most glioma cell types. Thus, we used lentiviral vectors expressing green fluorescent protein under lineage-specific promoters to identify CD133(-) glioma cells expressing Nestin, glial fibrillary acidic protein (GFAP), and neuron-specific enolase (NSE). Flow cytometry analysis showed the presence of CD133(-) subpopulations expressing these markers in glioma cell lines and in primary cultures from human glioblastoma (GBM) biopsies. Moreover, analysis of cell cycle distribution showed that subgroups expressing Nestin, GFAP, and NSE uniformly contained actively cycling cells, when cultured in serum-containing medium and stem cell medium. These subpopulations were fluorescence-activated cell sorted from CD133(-) U373 glioma cells and implanted intracerebrally in severe combined immunodeficient mice. Moreover, we implanted Nestin-, GFAP-, and NSE-positive glioma cells sorted from a human GBM biopsy, following removal of CD133-positive cells. All the CD133(-) subpopulations produced tumors, with no significant differences in survival or tumor take rates. However, there was a trend toward lower take rates for CD133(-) glioma subpopulations expressing GFAP and NSE. These findings suggest that the ability to form tumors may be a general trait associated with different glioma cell phenotypes, rather than a property limited to an exclusive subpopulation of glioma stem cells.
Transmural repolarisation in the left ventricle in humans during normoxia and ischaemia
Authors: Peter Taggart, Peter M.I Sutton, Tobias Opthof, Ruben Coronel, Richard Trimlett, Wilfred Pugsley, Panny Kallis
Journal: Cardiovascular Research (2001)

Background: Studies in isolated tissues and myocytes show different repolarisation properties in subepicardium, midmyocardium and subendocardium. Whether these differences are present in vivo and are relevant to humans has been the subject of controversy. Our objectives were (1) to ascertain whether transmural repolarisation gradients are present in humans, (2) to determine whether the greater sensitivity of subepicardial cells to ischaemia in vitro is manifest during early ischaemia in humans in vivo. Methods and results: We studied 21 patients during routine coronary artery surgery. Unipolar activation recovery intervals (ARI) were recorded from five transmural locations between subepicardium and subendocardium in the left ventricular wall. A pacing protocol spanned a range of cycle lengths from a cycle length of 300 ms to the maximum permitted by the intrinsic atrial activity. Following the onset of cardiopulmonary bypass recordings were obtained before (control) and during a 3-min period of global ischaemia. During control transmural ARIs were homogeneous between 300 and 1500 ms (ventricular pacing) and 750 and 1500 ms (atrial spontaneous beats). During ischaemia, ARIs shortened similarly at all transmural electrode sites and transmural homogeneity was maintained. Conclusions: Transmural repolarisation differences within the ventricular wall of the human heart were absent at cycle lengths within the physiological range but also during prolonged cycles. During early (global) ischaemia repolarisation changed equally in subepicardial and subendocardial regions and transmural homogeneity of repolarisation was preserved.
Monocyte Chemotactic Protein-4 (MCP-4; CCL-13) and the CC chemokine Receptor 3 (CCR3) in Sputum of Asthmatic Children
Authors: Y.M. El-Gamal, N.M. Heshmat, K.S. Awwad, M.H.M. Ezzat, M.M. Abd Al-Aziz, Z.M. El-Gabbas
Journal: Journal of Allergy and Clinical Immunology (2007)
A Small-Molecule Smoothened Agonist Prevents Glucocorticoid-Induced Neonatal Cerebellar Injury
Authors: Vivi M. Heine, Amelie Griveau, Cheryl Chapin, Philip L. Ballard, James K. Chen, David H. Rowitch
Journal: Science Translational Medicine (2011)

A Sonic hedgehog–Smoothened signaling agonist can protect against brain injury in mice caused by glucocorticoids, which are given to treat chronic lung disease in preterm infants.
Saturated phosphatidic acids mediate saturated fatty acid–induced vascular calcification and lipotoxicity
Authors: Masashi Masuda, Shinobu Miyazaki-Anzai, Audrey L. Keenan, Kayo Okamura, Jessica Kendrick, Michel Chonchol, Stefan Offermanns, James M. Ntambi, Makoto Kuro-o, Makoto Miyazaki
Journal: Journal of Clinical Investigation (2015)

Recent evidence indicates that saturated fatty acid–induced (SFA-induced) lipotoxicity contributes to the pathogenesis of cardiovascular and metabolic diseases; however, the molecular mechanisms that underlie SFA-induced lipotoxicity remain unclear. Here, we have shown that repression of stearoyl-CoA desaturase (SCD) enzymes, which regulate the intracellular balance of SFAs and unsaturated FAs, and the subsequent accumulation of SFAs in vascular smooth muscle cells (VSMCs), are characteristic events in the development of vascular calcification. We evaluated whether SMC-specific inhibition of SCD and the resulting SFA accumulation plays a causative role in the pathogenesis of vascular calcification and generated mice with SMC-specific deletion of both Scd1 and Scd2. Mice lacking both SCD1 and SCD2 in SMCs displayed severe vascular calcification with increased ER stress. Moreover, we employed shRNA library screening and radiolabeling approaches, as well as in vitro and in vivo lipidomic analysis, and determined that fully saturated phosphatidic acids such as 1,2-distearoyl-PA (18:0/18:0-PA) mediate SFA-induced lipotoxicity and vascular calcification. Together, these results identify a key lipogenic pathway in SMCs that mediates vascular calcification.
D<scp>IETARY AND</scp> G<scp>ENETIC</scp> E<scp>FFECTS ON</scp> L<scp>OW</scp>-D<scp>ENSITY</scp> L<scp>IPOPROTEIN</scp> H<scp>ETEROGENEITY</scp>
Authors: Ronald M Krauss
Journal: Annual Review of Nutrition (2001)

▪ Abstract We have tested whether differences in distribution and dietary responsiveness of low-density lipoprotein (LDL) subclasses contribute to the variability in the magnitude of LDL-cholesterol reduction induced by diets low in total and saturated fat and high in carbohydrate. Our studies have focused on a common, genetically influenced metabolic profile, characterized by a predominance of small, dense LDL particles (subclass pattern B), that is associated with a two- to threefold increase in risk for coronary artery disease. We have found that healthy normolipidemic individuals with this trait show a greater reduction in LDL cholesterol and particle number in response to low-fat, high-carbohydrate diets than do unaffected individuals (subclass pattern A). Moreover, such diets result in reduced LDL particle size, with induction of pattern B in a substantial proportion of pattern A men. Recent studies have indicated that this response is under genetic influence. Future identification of the specific genes involved may lead to improved targeting of dietary therapies aimed at reducing cardiovascular disease risk.
Measurement of Cremophor EL Following Taxol: Plasma Levels Sufficient to Reverse Drug Exclusion Mediated by the Multidrug-Resistant Phenotype
Authors: Lorraine Webster, Martha Linsenmeyer, Michael Millward, Carmel Morton, James Bishop, David Woodcock
Journal: JNCI Journal of the National Cancer Institute (1993)

Paclitaxel (Taxol) is the first of a new class of cytotoxic agents with activity against tumors resistant to other drugs. For clinical use, paclitaxel is currently formulated in a vehicle of 50% ethanol and 50% polyethoxylated surfactant Cremophor EL (Cremophor). We have previously shown that Cremophor will block the P-glycoprotein drug efflux pump responsible for the multidrug-resistant phenotype. Overexpression of P-glycoprotein is one mechanism of in vitro resistance to a number of currently used cytotoxic agents including paclitaxel.Our aim was to develop a bioassay to measure plasma levels of Cremophor and to determine whether or not plasma levels of Cremophor achieved during paclitaxel therapy are sufficient to inhibit the activity of the P-glycoprotein.All patients studied had histologically proven, advanced ovarian carcinoma with measurable or evaluable disease and had received at least one prior platinum-containing regimen. The bioassay used flow cytometry to measure the increase in equilibrium intracellular daunorubicin levels in multidrug-resistant human T-cell leukemia cells (CEM/VLB100) in the presence of a series of concentrations of Cremophor. Levels of Cremophor were measured in plasma from 21 patients after a 3-hour infusion of 135 or 175 mg/m2 paclitaxel. Both dose levels were given following premedication with oral dexamethasone, intravenous promethazine hydrochloride, and intravenous cimetidine. The Cremophor bioassay involved incubation of CEM/VLB100 cells (5 x 10(5)) for 1 hour with 2 micrograms/mL daunorubicin in 0.5 mL HL-1 medium plus 0.5 mL plasma prior to flow cytometric analysis. Pretreatment plasma was used to derive a standard curve for the effect of Cremophor on equilibrium daunorubicin levels. All measurements were done in triplicate.In vitro experiments indicated that, for maximal inhibition of P-glycoprotein activity, concentrations of Cremophor of 0.1% (vol/vol) were required. At the end of a 3-hour infusion of paclitaxel, plasma levels of Cremophor in 19 of 21 patients were 0.1% or higher and 0.09% in the remaining two. Concentrations of 5-20 microM paclitaxel dissolved in ethanol without Cremophor did not inhibit P-glycoprotein in this assay.The concentrations of Cremophor measured in plasma drawn from patients after a 3-hour infusion of paclitaxel at 135 or 175 mg/m2 were found to be sufficient to inhibit P-glycoprotein activity in vitro.The efficacy of paclitaxel against some tumors may be aided by its administration in a vehicle solution containing Cremophor in quantities that reach concentrations in the plasma sufficient to reverse multidrug resistance of neoplastic cells.
A Hotspot of Gene Order Rearrangement by Tandem Duplication and Random Loss in the Vertebrate Mitochondrial Genome
Authors: Diego San Mauro, David J. Gower, Rafael Zardoya, Mark Wilkinson
Journal: Molecular Biology and Evolution (2005)

Most reported examples of change in vertebrate mitochondrial (mt) gene order could be explained by a tandem duplication followed by random loss of redundant genes (tandem duplication–random loss [TDRL] model). Under this model of evolution, independent loss of genes arising from a single duplication in an ancestral species are predicted, and remnant pseudogenes expected, intermediate states that may remain in rearranged genomes. However, evidence for this is rare and largely scattered across vertebrate lineages. Here, we report new derived mt gene orders in the vertebrate “WANCY” region of four closely related caecilian amphibians. The novel arrangements found in this genomic region (one of them is convergent with the derived arrangement of marsupials), presence of pseudogenes, and positions of intergenic spacers fully satisfy predictions from the TDRL model. Our results, together with comparative data for the available vertebrate complete mt genomes, provide further evidence that the WANCY genomic region is a hotspot for gene order rearrangements and support the view that TDRL is the dominant mechanism of gene order rearrangement in vertebrate mt genomes. Convergent gene rearrangements are not unlikely in hotspots of gene order rearrangement by TDRL.
Identification and Referral of Families at High Risk for Cancer Susceptibility
Authors: K. M. Sweet
Journal: Journal of Clinical Oncology (2002)

PURPOSE: Obtainment of family history and accurate assessment is essential for the identification of families at risk for hereditary cancer. Our study compared the extent to which the family cancer history in the physician medical record reflected that entered by patients directly into a touch-screen family history computer program. PATIENTS AND METHODS: The study cohort consisted of 362 patients seen at a comprehensive cancer center ambulatory clinic over a 1-year period who voluntarily used the computer program and were a mixture of new and return patients. The computer entry was assessed by genetics staff and then compared with the medical record for corroboration of family history information and appropriate physician risk assessment. RESULTS: Family history information from the medical record was available for comparison to the computer entry in 69%. It was most often completed on new patients only and not routinely updated. Of the 362 computer entries, 101 were assigned to a high-risk category. Evidence in the records confirmed 69 high-risk individuals. Documentation of physician risk assessment (ie, notation of significant family cancer history or hereditary risk) was found in only 14 of the high-risk charts. Only seven high-risk individuals (6.9%) had evidence of referral for genetic consultation. CONCLUSION: This study demonstrates the need to collect family history information on all new and established patients in order to perform adequate cancer risk assessment. The lack of identification of patients at highest risk seems to be directly correlated with insufficient data collection, risk assessment, and documentation by medical staff.
CALCIUM AND PHOSPHORUS HOMEOSTASIS IN THE PARATHYROIDECTOMIZED DOG; EVALUATION BY MEANS OF ETHYLENEDIAMINE TETRAACETATE AND CALCIUM TOLERANCE TESTS*
Authors: Peter H. Sanderson, Foster Marshall, Richard E. Wilson
Journal: Journal of Clinical Investigation (1960)

In an experiment designed to determine whether or not homografts of parathyroid tissue would survive and function in millipore diffusion chambers, Wilson, Zollinger, Mahan and Brooks (1) subjected female mongrel dogs to parathyroidectomy either in two stages or as a single procedure.Twelve animals with trans- plants survived the acute postoperative period with its attendant severe hypocalcemia, but all re- quired intensive parenteral calcium support for periods ranging from 19 to 78 days.This supportive therapy could eventually be stopped, and 11 of these dogs were perfectly well in all respects for two to five months prior to removal of their transplants.The range of the serum calcium level was 9 to 11 mg per 100 ml in six of them, and 7 to 8 mg per 100 ml in the other five.How- ever, after all of the millipore chambers were re- moved, there was little or no alteration in their clinical status or their serum calcium levels.The dogs were followed for two and one-half to four months after the chambers were excised, and the only shift in the level of serum calcium that oc- curred was in one dog, which, with a serum cal- cium initially in the 7 to 8 mg per 100 ml range, was later able to maintain a consistent value of 9.0 mg per 100 ml.
Prevalence of atopic dermatitis, asthma, allergic rhinitis, and hand and contact dermatitis in adolescents. The Odense Adolescence Cohort Study on Atopic Diseases and Dermatitis
Authors: C.G. Mortz, J.M. Lauritsen, C. Bindslev-Jensen, K.E. Andersen
Journal: British Journal of Dermatology (2001)

Atopic diseases are common in children and adolescents. However, epidemiological knowledge is sparse for hand eczema and allergic contact dermatitis in this age group. Furthermore, no population-based studies have evaluated the prevalence of atopic diseases and hand and contact dermatitis in the same group of adolescents.To assess prevalence measures of atopic dermatitis (AD), asthma, allergic rhinitis and hand and contact dermatitis in adolescents in Odense municipality, Denmark.The study was carried out as a cross-sectional study among 1501 eighth grade school children (age 12-16 years) and included questionnaire, interview, clinical examination and patch testing.The lifetime prevalence of AD was 21.3% (girls 25.7% vs. boys 17.0%, P < 0.001) using predefined questionnaire criteria. The 1-year period prevalence of AD was 6.7% and the point prevalence 3.6% (Hanifin and Rajka criteria). In the interview the lifetime prevalence of inhalant allergy was estimated as 17.7% (6.9% allergic asthma, 15.7% allergic rhinitis). The lifetime prevalence of hand eczema based on the questionnaire was 9.2%, the 1-year period prevalence was 7.3% and the point prevalence 3.2%, with a significant predominance in girls. A significant association was found both between AD and inhalant allergy, and between AD and hand eczema using lifetime prevalence measures. The point prevalence of contact allergy was 15.2% (girls 19.4% vs. boys 10.3%, P < 0.001), and present or past allergic contact dermatitis was found in 7.2% (girls 11.3% vs. boys 2.5%). Contact allergy was most common to nickel (8.6%) and fragrance mix (1.8%).High prevalence figures were found for atopic diseases, hand eczema and allergic contact dermatitis, and the diseases were closely associated. A considerable number of adolescents still suffers from AD, and a considerable sex difference was noted for hand eczema and allergic contact dermatitis. Nickel allergy and perfume allergy were the major contact allergies. In the future this cohort of eighth grade school children will be followed up with regard to the course and development of atopic diseases, hand eczema and contact dermatitis.
Protein kinase C is activated in glomeruli from streptozotocin diabetic rats. Possible mediation by glucose.
Authors: P A Craven, F R DeRubertis
Journal: Journal of Clinical Investigation (1989)

Glomerular inositol content and the turnover of polyphosphoinositides was reduced by 58% in 1-2 wk streptozotocin diabetic rats. Addition of inositol to the incubation medium increased polyphosphoinositide turnover in glomeruli from diabetic rats to control values. Despite the reduction in inositol content and polyphosphoinositide turnover, protein kinase C was activated in glomeruli from diabetic rats, as assessed by an increase in the percentage of enzyme activity associated with the particulate cell fraction. Total protein kinase C activity was not different between glomeruli from control and diabetic rats. Treatment of diabetic rats with insulin to achieve near euglycemia prevented the increase in particulate protein kinase C. Moreover, incubation of glomeruli from control rats with glucose (100-1,000 mg/dl) resulted in a progressive increase in labeled diacylglycerol production and in the percentage of protein kinase C activity which was associated with the particulate fraction. These results support a role for hyperglycemia per se in the enhanced state of activation of protein kinase C seen in glomeruli from diabetic rats. Glucose did not appear to increase diacylglycerol by stimulating inositol phospholipid hydrolysis in glomeruli. Other pathways for diacylglycerol production, including de novo synthesis and phospholipase C mediated hydrolysis of phosphatidylcholine or phosphatidyl-inositol-glycan are not excluded.