tbuckley/cabot-search huggingface dataset:
Interventions Among Primary-Care Practitioners to Improve Care for Preventable Complications of Diabetes
Authors: Larry C Deeb, F Phillips Pettijohn, Jerry K Shirah, Garry Freeman
Journal: Diabetes Care (1988)

The National Diabetes Advisory Board recommends that diabetes prevention and control programs focus on the preventable complications of diabetes, i.e., visual impairment, lower-extremity problems, renal problems, ketoacidosis, and adverse outcomes of pregnancy. The Florida Diabetes Control Program chose to focus its efforts on the first three of these complications at the federal- and state-funded primary-care programs in Florida because these programs had access to targeted, public-sector patients and because of fiscal restraints that make the care provider the logical source of entry to the health-care system. This study sought to document the current level of care for complications of diabetes in primary-care settings, provide state-of-the-art professional education along with patient education, and evaluate changes in practice habits. Three intervention and three control primary-care centers were selected. Medical records in each center were reviewed over a 2-yr period. At intervention sites, retinopathy referrals increased from 9 to 43% (P less than .001), urinalyses increased from 69 to 94% (P less than .001), and examinations of lower extremities increased from 66 to 94% (P less than .001). There were no such changes in the control sites. Hypertension was diagnosed in nearly two-thirds of patients, and a last blood pressure of greater than 140 mmHg systolic or greater than 90 mmHg diastolic was present in 64% of the intervention group at yr 1 and declined to 56% at yr 2 (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
Developmental Twin Study of Attention Problems
Authors: Zheng Chang, Paul Lichtenstein, Philip J. Asherson, Henrik Larsson
Journal: JAMA Psychiatry (2013)

The genetic and environmental link between attention-deficit/hyperactivity disorder in childhood and the adult manifestation of the disorder is poorly understood because of a lack of longitudinal studies with cross-informant data.To explore the relative contribution of genetic and environmental influences on symptoms of attention problems from childhood to early adulthood.Analysis was conducted using longitudinal structural equation modeling with multiple informants.The Swedish Twin Study of Child and Adolescent Development.One thousand four hundred eighty twin pairs were prospectively followed up from childhood to young adulthood.Symptoms were obtained using parent and self-ratings of the Attention Problems Scale at ages 8 to 9, 13 to 14, 16 to 17, and 19 to 20 years.The best-fitting model revealed high heritability of attention problems as indexed by parent and self-ratings from childhood to early adulthood (h² = 0.77-0.82). Genetic effects operating at age 8 to 9 years continued, explaining 41%, 34%, and 24% of the total variance at ages 13 to 14, 16 to 17, and 19 to 20 years. Moreover, new sets of genetic risk factors emerged at ages 13 to 14, 16 to 17, and 19 to 20 years.The shared view of self- and informant-rated attention problems is highly heritable in childhood, adolescence, and early adulthood, suggesting that the previous reports of low heritability for attention-deficit/hyperactivity disorder in adults are best explained by rater effects. Both genetic stability and genetic innovation were present throughout this developmental stage, suggesting that attention problems are a developmentally complex phenotype characterized by both continuity and change across the life span.
Imaging human brown adipose tissue under room temperature conditions with 11C-MRB, a selective norepinephrine transporter PET ligand
Authors: Janice J. Hwang, Catherine W. Yeckel, Jean-Dominique Gallezot, Renata Belfort-De Aguiar, Devrim Ersahin, Hong Gao, Michael Kapinos, Nabeel Nabulsi, Yiyun Huang, David Cheng, Richard E. Carson, Robert Sherwin, Yu-Shin Ding
Journal: Metabolism (2015)
The actin regulator coronin 1A is mutant in a thymic egress–deficient mouse strain and in a patient with severe combined immunodeficiency
Authors: Lawrence R Shiow, David W Roadcap, Kenneth Paris, Susan R Watson, Irina L Grigorova, Tonya Lebet, Jinping An, Ying Xu, Craig N Jenne, Niko Föger, Ricardo U Sorensen, Christopher C Goodnow, James E Bear, Jennifer M Puck, Jason G Cyster
Journal: Nature Immunology (2008)
Expression of Excision Repair Cross-Complementation Group 1, Breast Cancer Susceptibility 1, and β III-Tubulin in Thymic Epithelial Tumors
Authors: Kyoichi Kaira, Masakuni Serizawa, Yasuhiro Koh, Satoru Miura, Rieko Kaira, Masato Abe, Kazuo Nakagawa, Yasuhisa Ohde, Takehiro Okumura, Tateaki Naito, Haruyasu Murakami, Toshiaki Takahashi, Haruhiko Kondo, Takashi Nakajima, Masahiro Endo, Nobuyuki Yamamoto
Journal: Journal of Thoracic Oncology (2011)
Synergistic Actions of Glucagon and Miniglucagon on Ca <sup>2+</sup> Mobilization in Cardiac Cells
Authors: Anne Sauvadet, Troy Rohn, Françoise Pecker, Catherine Pavoine
Journal: Circulation Research (1996)

Abstract It has been recently shown that the physiological processing of glucagon into its C-terminal (19-29) fragment, miniglucagon, by cardiac cells was essential for the contractile positive inotropic effect of the hormone. However, the mechanisms underlying the effects of miniglucagon remained undetermined. In the present study, we assessed the effects of miniglucagon on Ca 2+ homeostasis in embryonic chick ventricular myocytes. In quiescent cells, short-term applications of 0.1 nmol/L miniglucagon markedly increased the accumulation of 45 Ca into intracellular compartments resistant to digitonin lysis and sensitive to caffeine. Ca 2+ accumulation into the sarcoplasmic reticular (SR) store was further attested by fura 2 imaging studies on quiescent or prestimulated cells: miniglucagon potentiated Ca 2+ release from the SR compartment triggered by caffeine and evoked a rise in cytosolic Ca 2+ when applied on cells pretreated with 1 μmol/L thapsigargin, a specific inhibitor of the SR Ca 2+ pump. Glucagon alone produced a small cytosolic Ca 2+ signal that was considerably amplified by miniglucagon. The action of glucagon was mimicked by 8-bromo-cAMP and was blocked by isradipine, suggesting that it relied on the activation of L-type Ca 2+ channels, via phosphorylation. We conclude that the combined actions of miniglucagon and glucagon on Ca 2+ accumulation into SR stores and Ca 2+ release from the same stores are likely to support the positive inotropic effect elicited in vivo by glucagon on heart contraction.
The procoagulant effect of zinc on fibrin clot formation
Authors: Gerard Marx, Amiram Eldor
Journal: American Journal of Hematology (1985)

Abstract The influence of Zn +2 on fibrin clot formation was investigated by measuring its effect on the clotting times of fibrinogen exposed to thrombin. It was observed with either human or bovine thrombin that 0.01‐0.1 mM Zn +2 induced significant reductions of clotting times in a concentration‐dependent manner. The procoagulant effect of Zn +2 occurred in the presence of Ca +2 but was inhibited by metal chelating agents. Higher levels of Zn +2 (&gt; 0.2 mM final concentration) were required to accelerate thrombin‐induced clot formation in the presence of citrate or oxalate. Similarly with oxalated human plasma, &gt; 0.2 mM Zn +2 decreased the clotting time. Cations such as Mg +2 and Mn +2 caused little change in clotting times. As an extension of these findings, we examined the effect of Zn +2 on the in hibition of thrombin by antithrombin‐III (AT‐III). The presence of as little as 0.006 mM Zn +2 in an incubating mixture of thrombin and AT‐III severely reduced the inhibitory activity of AT‐III towards thrombin. It was observed that the relative intrinsic fluorescence emission of human thrombin decreased upon exposure to Zn +2 but was unaffected by Mg +2 or Mn +2 . It is suggested that Zn +2 can form a complex with thrombin, which results in altered reactivity towards fibrinogen and decreased inhibition by AT‐III.
The Natural History of Ventricular Septal Defect in Patients Surviving Infancy
Authors: DANIEL K. BLOOMFIELD
Journal: Circulation (1964)

It is now possible to synthesize the natural history of ventricular septal defect. Size is fundamental, and stemming from it, the smaller defects (groups 1 and 2) separate from the larger (groups 3, 4, and 5) immediately at birth. Apparent size may differ from real size, for defects may become partially closed by tricuspid valve leaflets, or be gradually obstructed by an enlarging aneurysm of the sinus of Valsalva. One instance has been observed in which a muscular defect was obstructed by a large papillary muscle. The reverse may also occur, i.e., a partially obstructed defect may enlarge as a blocking tricuspid leaflet detaches or tears.
Glimepiride Versus Metformin as Monotherapy in Pediatric Patients With Type 2 Diabetes
Authors: Michael Gottschalk, Thomas Danne, Aleksandra Vlajnic, José F. Cara
Journal: Diabetes Care (2007)

To compare the efficacy and safety of glimepiride versus metformin in pediatric subjects with type 2 diabetes inadequately controlled with diet and exercise alone or oral monotherapy.This 26-week, single-blind, active-controlled, multinational study randomized 285 subjects to receive glimepiride (1-8 mg once daily) or metformin (500-1000 mg twice daily) for 24 weeks. The primary end point was mean change in A1C from baseline to week 24. Safety was assessed by incidence of hypoglycemia and other adverse events.Significant reductions from baseline A1C were seen in both the glimepiride (-0.54%, P = 0.001) and metformin (-0.71%, P = 0.0002) groups. A total of 42.4% (56 of 132) and 48.1% (63 of 131) of subjects in the glimepiride and metformin groups, respectively, in the intent-to-treat population achieved A1C <7.0% at week 24. No significant differences were observed between groups in reductions in A1C and self-monitored blood glucose levels, changes in serum lipid concentrations, or hypoglycemia incidence. Significant differences were observed in mean changes from baseline in BMI between groups (0.26 kg/m(2) for glimepiride and -0.33 kg/m(2) for metformin; P = 0.003). The adjusted mean body weight increase was 1.97 kg for glimepiride and 0.55 kg for metformin (P = 0.005). A hypoglycemic episode with blood glucose <50 mg/dl (<2.8 mmol/l) was experienced by 4.9 and 4.2% of glimepiride- and metformin-treated subjects, respectively. A single severe hypoglycemic event occurred in each group.Glimepiride reduced A1C similarly to metformin with greater weight gain, and there was comparable safety over 24 weeks in the treatment of pediatric subjects with type 2 diabetes.
Bronchial responsiveness to histamine in wheezy infants.
Authors: A Prendiville, S Green, M Silverman
Journal: Thorax (1987)

Little is known about airway responsiveness in infancy. The bronchial response to incremental doses of nebulised histamine (to a maximum dose of 8 g/l) was measured in 11 wheezy infants with a mean age of 8.7 months. The study was repeated after a 30-40 minute recovery period in seven infants and again on a separate day in 10. The index of response was the provoking concentration of histamine that produced a 30% fall in the maximum expiratory flow at functional residual capacity (PC30), taken from partial forced expiratory flow-volume curves produced in a pressure jacket. Nine of 11 infants had a PC30 of less than 8 g/l. The response was consistent between tests in both the nine responders and the two who failed to respond at 8 g/l. The PC30 was lower in infants with more severe baseline airway obstruction. Spontaneous recovery after challenge was complete in 30 minutes in seven of eight infants studied. The highest doses of histamine caused changes in the configuration of the flow-volume curves and symptomatic cough and wheeze in addition to a change in forced flow rates. This study provides clear evidence of intrathoracic airway responsiveness to histamine in infancy.
Deaths from climate change will triple in next 20 years if inaction continues, warns report
Authors: Z. Kmietowicz
Journal: BMJ (2010)

The number of deaths attributable to climate change will reach one million a year by 2030—up from 350 000 this year—if efforts to limit worldwide rises in temperature are not speeded up, warns a new report.

Children in sub-Saharan Africa and south Asia will make up close to 80% of the casualties. Their deaths, from malnutrition, diarrhoeal disease, and malaria, are entirely preventable with better distribution of mosquito nets, rehydration solutions, and basic dietary and vitamin supplements, says the report, which has been produced jointly by Development Assistance Research Associates (DARA), a humanitarian research organisation, and the Climate Vulnerable Forum, a group of countries vulnerable to climate change, including the Maldives, Bangladesh, and Barbados.

Their report, the Climate Vulnerability Monitor , analyses the effects that climate change will have in 184 countries in the four key …
Protective effects of slow channel calcium antagonists on noradrenaline induced myocardial necrosis
Authors: G. L TODD, D. A STERNS, R. D PLAMBECK, C. S JOEKEL, R. S ELIOT
Journal: Cardiovascular Research (1986)

Catecholamine excess results in two distinct forms of coagulative myocytolysis, apparently due to increased membrane permeability followed by a large influx of calcium. To determine if three slow channel calcium antagonists, verapamil, nifedipine, and diltiazem, could reduce the calcium overload and prevent the development of noradrenaline induced acute myocardial contraction band lesions, 48 adult mongrel dogs in eight groups (n = 6) were continuously infused with saline alone, noradrenaline alone (4 micrograms X kg-1 X min-1), nifedipine (1 microgram X kg-1 X min-1), or other calcium blockers (10 micrograms X kg-1 X min-1) with saline or noradrenaline. After 15 minutes of pretreatment with a calcium antagonist, the antagonists were simultaneously infused with either saline or noradrenaline for 60 minutes. Nifedipine increased heart rate to the same degree as noradrenaline alone, whereas verapamil and diltiazem significantly suppressed the noradrenaline induced increases in heart rate. All three calcium antagonists reduced the increases in blood pressure and frequency of ventricular arrhythmias seen with noradrenaline alone. Only nifedipine produced a moderate increase in contractility (dP/dtmax) within 5 min and a pronounced synergistic increase when combined with noradrenaline. The effect of the other antagonists with noradrenaline was no different than the effect with noradrenaline alone. Contraction band lesions in the hearts of dogs in the saline and saline plus calcium antagonist groups were rare. The group receiving noradrenaline alone showed large numbers of the two predominant lesions: small paradiscal contraction band lesions and large holocytic contraction band lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac alpha-myosin heavy chains differ in their induction of myocarditis. Identification of pathogenic epitopes.
Authors: L Liao, R Sindhwani, L Leinwand, B Diamond, S Factor
Journal: Journal of Clinical Investigation (1993)

BALB/c mice develop autoimmune myocarditis after immunization with mouse cardiac myosin, whereas C57B/6 mice do not. To define the immunogenicity and pathogenicity of cardiac myosin in BALB/c mice, we immunized mice with different forms of cardiac myosin. These studies demonstrate the discordance of immunogenicity and pathogenicity of myosin heavy chains. The cardiac alpha-myosin heavy chains of BALB/c and C57B/6 mice differ by two residues that are near the junction of the head and rod in the S2 fragment of myosin. Myosin preparations from both strains are immunogenic in susceptible BALB/c as well as in nonsusceptible C57B/6 mice; however, BALB/c myosin induces a greater incidence of disease. To further delineate epitopes of myosin heavy chain responsible for immunogenicity and disease, mice were immunized with fragments of genetically engineered rat alpha cardiac myosin. Epitopes in the region of difference between BALB/c and C57B/6 (residues 735-1032) induce disease in both susceptible and nonsusceptible mice. The data presented here demonstrate that pathogenic epitopes of both mouse and rat myosin residue in the polymorphic region of the S2 subunit. In addition, these studies suggest that polymorphisms in the autoantigen may be part of the genetic basis for autoimmune myocarditis.
Abstract 3085: Overexpression of the <i>NOTCH3</i> intracellular domain alters neuroendocrine phenotype in carcinoid tumor cells
Authors: Renata Jaskula-Sztul, Ponghtep Pisarnturakit, Muthusamy Kunnimalaiyaan, Herbert Chen
Journal: Cancer Research (2010)

Abstract Introduction: There are four mammalian Notch receptors (Notch1-4), which exhibit unique and overlapping expression pattern and act as oncogenes or tumor suppressor genes depending on the cell and context type. We previously reported that Notch1 pathway is minimally active in neuroendocrine (NE) tumors. Furthermore, induction of the Notch1 signaling pathway by over- expression or by pharmacological treatment with valproic acid (VPA) and suberoyl bis-hydroxamic acid (SBHA) suppresses hormone secretion. However, the role of other Notch isoforms is not clear in carcinoid. In this study, we analyzed the presence of Notch isoforms and their regulatory role on chromogranin A (CgA), a clinically important NE marker, and achaete-scute complex-like1 (ASCL1), a known downstream target of Notch. Methods: Expression of four Notch isoforms was quantified by real time RT-PCR from parental BON cells (GI carcinoid) and VPA treated BON cells. pcDNA3.3 TOPO plasmid containing constitutively expressed human active portion of Notch3, NICD3, was transiently transfected into BON cells and the cell lysates were tested for the presence of NOTCH3. The levels of NE markers such as CgA and ASCL1 were analyzed by Western blot. Results: Gene expression analysis showed that the parental BON cells had very minimal levels of Notch1-3. Notch4 expression was not detected. In VPA treated cells, the levels of Notch1, 2 and 3 were increased significantly. Overall, the Notch3 expression level was higher than Notch1 and 2 in VPA treated cells. Importantly, there was a 60-fold induction of Notch3 expression in VPA treated cells compared to parental untreated cells. VPA treatment also resulted in a 15-fold and 20-fold increase for Notch1 and Notch2 respectively whereas Notch4 was not detected in these cells. The constitutive expression of NICD3 in BON cells resulted in a reduction in ASCL1 and CgA. Conclusions: Carcinoid tumor cells have a paucity of all Notch isoforms, including Notch3. For the first time, we demonstrate that Notch3 regulates the NE phenotype, and may play an important role in regulating carcinoid tumor progression. These findings warrant further investigation on targeting Notch3 for carcinoid cancer therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3085.
Effect of betamethasone on airway obstruction and bronchial response to salbutamol in prednisolone resistant asthma.
Authors: B Grandordy, N Belmatoug, A Morelle, D De Lauture, J Marsac
Journal: Thorax (1987)

Twelve patients with chronic severe asthma, having previously shown an FEV1 increase of less than 20% of the predicted value with prednisolone treatment (20-60 mg daily for 10 days), took part in a double blind crossover comparison of equipotent anti-inflammatory doses of betamethasone and prednisolone. Betamethasone (8 mg) and prednisolone (40 mg) were administered daily for 10 days with a washout period of 10 days between. In this first part of the study betamethasone was administered intramuscularly and prednisolone orally. Placebo injections and tablets were used. Mean FEV1 was not significantly different before each period. There was a significant increase in FEV1 while they were taking betamethasone but not prednisolone. Individual analysis of the data showed that FEV1 increased with betamethasone in nine patients and remained stable or decreased in three. During treatment with prednisolone baseline FEV1 increased moderately in three patients (FEV1 0.3, 0.5 and 0.6 l) and remained stable or decreased in nine. There was no significant difference between the bronchodilator responses to cumulative doses of inhaled salbutamol when they were measured immediately before, on the last day of treatment with each steroid, and between steroid treatment periods. The same protocol was followed four months later in five of the 12 patients but both drugs were administered orally on this occasion. Similar results were obtained. The greater effect of betamethasone on bronchial obstruction may be due to its longer biological half life or to some unidentified property of its metabolites. The bronchial response to inhaled beta 2 agonist appears not to be influenced by either steroid in these patients.
Mother-Infant Interactions in the First Year
Authors: Peter H. Wolff
Journal: New England Journal of Medicine (1976)

The folk wisdom of most cultures has celebrated the interaction between infant and mother as one of the decisive social relations in the human life cycle. It did not, however, become a legitimate topic for empirical research until the beginning of this century, so that the biologic and experiential determinants of an infant's social development are only now being documented in controlled observations. Research to date has nevertheless identified some of the essential elements that must be encompassed in any comprehensive theory of early social development.The observation of infants in their natural environment has disposed of the traditional prejudice . . .
Bradykinin-activated membrane-associated phospholipase C in Madin-Darby canine kidney cells.
Authors: D Portilla, J Morrissey, A R Morrison
Journal: Journal of Clinical Investigation (1988)

Previous studies have demonstrated that bradykinin stimulates the rapid release of inositol 1,4,5 trisphosphate (IP3) from membrane phosphatidylinositol 4,5 bisphosphate (PIP2) in Madin-Darby canine kidney (MDCK) cells. Since current evidence would suggest that the activation of phospholipase C (PLC) is mediated through a guanine nucleotide-binding protein in receptor-mediated activation of PLC, we evaluated the role of guanine nucleotide proteins in receptor-mediated (bradykinin-stimulated) activation of PLC in MDCK cells. Bradykinin at 10(-7) M produced a marked increase in IP3 formation within 10 s increasing from a basal level of 46.2 to 686.6 pmol/mg cell protein a 15-fold increase. Pretreatment of MDCK cells in culture with 200 ng/ml of pertussis toxin for 4 h reduced the bradykinin-stimulated response to 205.8 pmol/mg protein. A 41-kD protein substrate in MDCK membranes was ADP ribosylated in vitro in the presence of pertussis toxin. The ADP ribosylation in vitro was inhibited by pretreatment of the cells in culture with pertussis toxin. Membranes from MDCK cells incubated in the presence of [3H]PIP2/phosphatidyl ethanolamine liposomes demonstrated hydrolysis of [3H]PIP2 with release of [3H]IP3 when GTP 100 microM or GTP gamma S 10 microM was added. Bradykinin 10(-7) M added with GTP 100 microM markedly increased the rate of hydrolysis within 10 s, thus demonstrating a similar time course of PLC activation as intact cells. These results demonstrate that bradykinin binds to its receptor and activates a membrane-associated PLC through a pertussis toxin-sensitive, guanine nucleotide protein.