945 resultados para National Institutes Of Health


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"Revised April 1979."

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"May 1988."

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"Papers given at a program held in National Library of Medicine on May 24-25, 1979"--p. iv.

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Bibliography: p. 205-211.

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Mode of access: Internet.

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On Cover 1970/71-1972/73: National Institutes of Health Statistical Reference Book of International Activities

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Background and Purpose - To assess the prevalence of premorbid undernutrition and its impact on outcomes 1 month after stroke. Methods - The study recruited from consecutive stroke admissions during a 10-month period. Premorbid nutritional status ( using the subjective global assessment [SGA]), premorbid functioning ( modified Rankin scale [MRS]), and stroke severity ( National Institutes of Health Stroke Scale [NIHSS] score) were assessed at admission. The associations between premorbid nutritional status, poor outcome ( defined as MRS greater than or equal to 3), and mortality were examined before and after adjustment for confounding variables, including age, gender, stroke risk factors, stroke severity, and admission serum albumin. Results - Thirty of 185 patients were assessed as having undernutrition at admission. Significant unadjusted associations were observed between undernutrition and poor outcome (odds ratio [OR], 3.4; 95% CI, 1.3 to 8.7; P = 0.01), and mortality (OR, 3.1, 95% CI, 1.3 to 7.7; P = 0.02) at 1 month. NIHSS, age, and premorbid MRS were also significantly associated with poor outcomes. After adjustment for these factors, the effect size of associations remained important but not significant ( poor outcome: OR, 2.4; 95% CI, 0.7 to 9.0, P = 0.18; mortality: OR, 3.2; 95% CI, 1.0 to 10.4, P = 0.05). Conclusions - Premorbid undernutrition, as assessed using the SGA, appears to be an independent predictor of poor stroke outcome. Stroke prevention strategies should target undernutrition in the population at risk for stroke to improve outcomes.

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Introduction. Potentially modifiable physiological variables may influence stroke prognosis but their independence from modifiable factors remains unclear. Methods. Admission physiological measures (blood pressure, heart rate, temperature and blood glucose) and other unmodifiable factors were recorded from patients presenting within 48 hours of stroke. These variables were compared with the outcomes of death and death or dependency at 30 days in multivariate statistical models. Results. In the 186 patients included in the study, age, atrial fibrillation and the National Institutes of Health Stroke Score were identified as unmodifiable factors independently associated with death and death or dependency. After adjusting for these factors, none of the physiological variables were independently associated with death, while only diastolic blood pressure (DBP) >= 90 mmHg was associated with death or dependency at 30 days (p = 0.02). Conclusions. Except for elevated DBP, we found no independent associations between admission physiology and outcome at 30 days in an unselected stroke cohort. Future studies should look for associations in subgroups, or by analysing serial changes in physiology during the early post-stroke period.

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A report from the National Institutes of Health defines a disease biomarker as a “characteristic that is objectively measured and evaluated as an indicator of normal biologic processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.” Early diagnosis is a crucial factor for incurable disease such as cancer and Alzheimer’s disease (AD). During the last decade researchers have discovered that biochemical changes caused by a disease can be detected considerably earlier as compared to physical manifestations/symptoms. In this dissertation electrochemical detection was utilized as the detection strategy as it offers high sensitivity/specificity, ease of operation, and capability of miniaturization and multiplexed detection. Electrochemical detection of biological analytes is an established field, and has matured at a rapid pace during the last 50 years and adapted itself to advances in micro/nanofabrication procedures. Carbon fiber microelectrodes were utilized as the platform sensor due to their high signal to noise ratio, ease and low-cost of fabrication, biocompatibility, and active carbon surface which allows conjugation with biorecognition moieties. This dissertation specifically focuses on the detection of 3 extensively validated biomarkers for cancer and AD. Firstly, vascular endothelial growth factor (VEGF) a cancer biomarker was detected using a one-step, reagentless immunosensing strategy. The immunosensing strategy allowed a rapid and sensitive means of VEGF detection with a detection limit of about 38 pg/mL with a linear dynamic range of 0–100 pg/mL. Direct detection of AD-related biomarker amyloid beta (Aβ) was achieved by exploiting its inherent electroactivity. The quantification of the ratio of Aβ1-40/42 (or Aβ ratio) has been established as a reliable test to diagnose AD through human clinical trials. Triple barrel carbon fiber microelectrodes were used to simultaneously detect Aβ1-40 and Aβ1-42 in cerebrospinal fluid from rats within a detection range of 100nM to 1.2μM and 400nM to 1μM respectively. In addition, the release of DNA damage/repair biomarker 8-hydroxydeoxyguanine (8-OHdG) under the influence of reactive oxidative stress from single lung endothelial cell was monitored using an activated carbon fiber microelectrode. The sensor was used to test the influence of nicotine, which is one of the most biologically active chemicals present in cigarette smoke and smokeless tobacco.

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Funding • The pooled data coordination team (PBoffetta, MH, YCAL) were supported by National Cancer Institute grant R03CA113157 and by National Institute of Dental and Craniofacial Research grant R03DE016611 • The Milan study (CLV) was supported by the Italian Association for Research on Cancer (Grant no. 10068). • The Aviano study (LDM) was supported by a grant from the Italian Association for Research on Cancer (AIRC), Italian League Against Cancer and Italian Ministry of Research • The Italy Multicenter study (DS) was supported by the Italian Association for Research on Cancer (AIRC), Italian League Against Cancer and Italian Ministry of Research. • The Study from Switzerland (FL) was supported by the Swiss League against Cancer and the Swiss Research against Cancer/Oncosuisse [KFS-700, OCS-1633]. • The central Europe study (PBoffetta, PBrenan, EF, JL, DM, PR, OS, NS-D) was supported by the World Cancer Research Fund and the European Commission INCOCOPERNICUS Program [Contract No. IC15- CT98-0332] • The New York multicentre study (JM) was supported by a grant from National Institute of Health [P01CA068384 K07CA104231]. • The study from the Fred Hutchison Cancer Research Center from Seattle (CC, SMS) was supported by a National Institute of Health grant [R01CA048996, R01DE012609]. • The Iowa study (ES) was supported by National Instituteof Health [NIDCR R01DE011979, NIDCR R01DE013110, FIRCA TW001500] and Veterans Affairs Merit Review Funds. • The North Carolina studies (AFO) were supported by National Institute of Health [R01CA061188], and in part by a grant from the National Institute of Environmental Health Sciences [P30ES010126]. • The Tampa study (PLazarus, JM) was supported by National Institute of Health grants [P01CA068384, K07CA104231, R01DE013158] • The Los Angeles study (Z-F Z, HM) was supported by grants from National Institute of Health [P50CA090388, R01DA011386, R03CA077954, T32CA009142, U01CA096134, R21ES011667] and the Alper Research Program for Environmental Genomics of the UCLA Jonsson Comprehensive Cancer Center. • The Houston study (EMS, GL) was supported by a grant from National Institute of Health [R01ES011740, R01CA100264]. • The Puerto Rico study (RBH, MPP) was supported by a grant from National Institutes of Health (NCI) US and NIDCR intramural programs. • The Latin America study (PBoffetta, PBrenan, MV, LF, MPC, AM, AWD, SK, VW-F) was supported by Fondo para la Investigacion Cientifica y Tecnologica (FONCYT) Argentina, IMIM (Barcelona), Fundaco de Amparo a‘ Pesquisa no Estado de Sao Paulo (FAPESP) [No 01/01768-2], and European Commission [IC18-CT97-0222] • The IARC multicentre study (SF, RH, XC) was supported by Fondo de Investigaciones Sanitarias (FIS) of the Spanish Government [FIS 97/ 0024, FIS 97/0662, BAE 01/5013], International Union Against Cancer (UICC), and Yamagiwa-Yoshida Memorial International Cancer Study Grant. • The Boston study (KKelsey, MMcC) was supported by a grant from National Institute of Health [R01CA078609, R01CA100679]. • The Rome study (SB, GC) was supported by AIRC (Italian Agency for Research on Cancer). • The US multicentre study (BW) was supported by The Intramural Program of the National Cancer Institute, National Institute of Health, United States. • The Sao Paolo study (V W-F) was supported by Fundacao de Ampara a Pesquisa no Estado de Sao Paulo (FAPESP No 10/51168-0) • The MSKCC study (SS, G-P Y) was supported by a grant from National Institute of Health [R01CA051845]. • The Seattle-Leo stud (FV) was supported by a grant from National Institute of Health [R01CA030022] • The western Europe Study (PBoffetta, IH, WA, PLagiou, DS, LS, FM, CH, KKjaerheim, DC, TMc, PT, AA, AZ) was supported by European Community (5th Frame work Programme) grant no QLK1-CT-2001- 00182. • The Germany Heidelberg study (HR) was supported by the grant No. 01GB9702/3 from the German Ministry of Education and Research.

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Funding was provided in part by the US National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) K23 AR061406 (Nelson); US National Institutes of Health (NIH)/NIAMS P60AR30701 (Jordan/Renner/Schwartz); US Centers for Disease Control/Association of Schools of Public Health S043 and S3486 (Jordan/Renner); K24-AR04884, P50-AR063043, and P50-AR060752 (Lane); and NIH/National Center for Advancing Translational Sciences KL2TR001109 (Golightly).

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Funding was provided in part by the US National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) K23 AR061406 (Nelson); US National Institutes of Health (NIH)/NIAMS P60AR30701 (Jordan/Renner/Schwartz); US Centers for Disease Control/Association of Schools of Public Health S043 and S3486 (Jordan/Renner); K24-AR04884, P50-AR063043, and P50-AR060752 (Lane); and NIH/National Center for Advancing Translational Sciences KL2TR001109 (Golightly).

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This work was supported by the National Institutes of Health (Grant Nos. R01DK093587 and R01DK101379 [to YX], R01DK092605 to [QT], R01DK078056 [to MM]), the Klarman Family Foundation (to YX), the Naman Family Fund for Basic Research (to YX), Curtis Hankamer Basic Research Fund (to YX), American Diabetes Association (Grant Nos. 7-13-JF-61 [to QW] and 1-15-BS-184 [to QT]), American Heart Association postdoctoral fellowship (to PX), Wellcome Trust (Grant No. WT098012 [to LKH]), and Biotechnology and Biological Sciences Research Council (Grant No. BB/K001418/1 [to LKH]). The anxiety tests (e.g., open-field test, light-dark test, elevated plus maze test) were performed in the Mouse Neurobehavior Core, Baylor College of Medicine, which was supported by National Institutes of Health Grant No. P30HD024064. PX and YH were involved in experimental design and most of the procedures, data acquisition and analyses, and writing the manuscript. XC assisted in the electrophysiological recordings; LV-T assisted in the histology study; XY, KS, CW, YY, AH, LZ, and GS assisted in surgical procedures and production of study mice. MGM, QW, QT, and LKH were involved in study design and writing the manuscript. YX is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. The authors report no biomedical financial interests or potential conflicts of interest.