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  • Resultat 14411-14420 av 595675
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14411.
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14412.
  • Wamala, S. P, et al. (författare)
  • Women's exposure to early and later life socioeconomic disadvantage and coronary heart disease risk : the Stockholm Female Coronary Risk Study
  • 2001
  • Ingår i: International Journal of Epidemiology. - Karolinska Inst, Dept Publ Hlth Sci, Div Prevent Med, S-17176 Stockholm, Sweden. Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA. : OXFORD UNIV PRESS. - 0300-5771 .- 1464-3685. ; 30:2, s. 275-284
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Measures of low socioeconomic position have been associated with increased risk for coronary heart disease (CHD) among women. A more complete understanding of this association is gained when socioeconomic position is conceptualized from a life course perspective where socioeconomic position is measured both in early and later life. We examined various life course socioeconomic indicators in relation to CHD risk among women. Methods The Stockholm Female Coronary Risk Study is a population-based case-control study, in which 292 women with CHD aged less than or equal to 65 years and 292 age-matched controls were investigated using a wide range of socioeconomic, behavioural, psychosocial and physiological risk factors. Socioeconomic disadvantage in early life (large family size in childhood, being born last, low education), and in later life (housewife or blue-collar occupation at labour force entry blue-collar occupation at examination, economic hardships prior to examination) was assessed. Results Exposure to early (OR = 2.65, 95% CI : 1.12-6.54) or later (OR = 5.38, 95% CI : 2.01-11.43) life socioeconomic disadvantage was associated with increased CHD risk as compared to not being exposed. After simultaneous adjustment for marital status and traditional CHD risk factors, early and later socioeconomic disadvantage, exposure to three instances of socioeconomic disadvantage in early life was associated with an increased CHD risk of 2.48 (95% CI:0.90-6.83) as compared to not being exposed to any disadvantage. The corresponding adjusted risk associated with exposure to later life disadvantage was 3.22 (95% CI : 1.02-10.53). Further analyses did not show statistical evidence of interaction effects between early and later life exposures (P = 0.12), although being exposed to both resulted in a 4.2-fold (95% CI: 1.4-12.1) increased CHD risk. Exposure to cumulative socioeconomic disadvantage (combining both early and later life), across all stages in the life course showed strong, graded associations with CHD risk after adjusting for traditional CHD risk factors. Stratification of cumulative disadvantage by body height showed that exposure to more than three periods of cumulative socioeconomic disadvantage had a 1.7- (95% CI : 0.9-3.2) and 1.9-(95% CI : 1.0-7.7) fold increased CHD risk for taller and shorter women, respectively. The combination of both short stature and more than two periods of cumulative socioeconomic disadvantage resulted in a 4.4-fold (95% CI : 1.7-9.3) increased CHD risk. Conclusions Both early and later exposure to socioeconomic disadvantage were associated with increased CHD risk in women. Later life exposure seems to be more harmful for women's cardiovascular health than early life exposure to socioeconomic disadvantage. However, being exposed to socioeconomic disadvantage in both early and later life magnified the risk for CHD in women. Cumulative exposure to socioeconomic disadvantage resulted in greater likelihood of CHD risk, even among women who were above median height. In terms of better understanding health inequalities among women, measures of socioeconomic disadvantage over the life course are both conceptually and empirically superior to using socioeconomic indicators from one point in time.
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14413.
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14414.
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14415.
  • Wang, F. H., et al. (författare)
  • Determination of conjugation efficiency of antibodies and proteins to the superparamagnetic iron oxide nanoparticles by capillary electrophoresis with laser-induced fluorescence detection
  • 2003
  • Ingår i: Journal of nanoparticle research. - 1388-0764 .- 1572-896X. ; 5:02-jan, s. 137-146
  • Tidskriftsartikel (refereegranskat)abstract
    • The method based on capillary electrophoresis with laser-induced fluorescence detection (CE/LIF) was developed for determination of magnetic iron oxide nanoparticles (hydrodynamic diameters of 100 nm) functionalized with molecules containing primary amino groups. The magnetic nanoparticles with carboxylic or aminopropyltrimethoxysilane groups at their surface were conjugated to the model proteins ( bovine serum albumin, BSA; streptavidin or goat anti-rabbit immunoglobulin G, IgG) using carbodiimide as a zero-length cross-linker. The nanoparticle-protein conjugates ( hydrodynamic diameter 163 - 194 nm) were derivatized with naphthalene-2,3- dicarboxaldehyde reagent and separated by CE/LIF with a helium - cadmium laser ( excitation at 442 nm, emission at 488 nm). The separations were carried out by using a fused-silica capillary ( effective length 48 cm, inner diameter 75 mum) and 100 mM sodium borate buffer ( pH 9.2), the potential was 30 kV. The detection limit for BSA-conjugate was 1.3 pg/10 nl, i.e. about 20 amol. The present method provides an efficient and fast tool for sensitive determination of the efficacy of biomolecular functionalization of magnetic nanoparticles. The CE/LIF technique requires only negligible sample volumes for analysis, which is especially suitable for controlling the process of preparation of functionalized nanoparticles with unique properties aimed to be used for diagnostic or therapeutic purposes.
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14416.
  • Wang, F. H., et al. (författare)
  • Magnetic resonance tracking of nanoparticle labelled neural stem cells in a rat's spinal cord
  • 2006
  • Ingår i: Nanotechnology. - : IOP Publishing. - 0957-4484 .- 1361-6528. ; 17:8, s. 1911-1915
  • Tidskriftsartikel (refereegranskat)abstract
    • Neural stem cells isolated from an adult rat's spinal cord were loaded with superparamagnetic gold-coated monocrystalline iron oxide nanoparticles (Au-MION) intended for use as contrast enhancers in magnetic resonance imaging (MRI). A dose-dependent attenuation of MRI signals was observed for Au-MION down to 0.001 mu gFe/mu l and for nanoparticle-loaded clusters of only 20 cells. The labelled cells were infused into the spinal cord of anaesthetized rats and tracked by MRI at 1 h, 48 h and 1 month post-injection. Histological analysis revealed that MRI signals correlated well with gold-positive staining of transplanted cells. The present results show that Au-MION exerts powerful contrast-enhancing properties and may represent novel MRI labels for labelling and tracking the transplanted cells in vivo.
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14417.
  • Wang, Hong, et al. (författare)
  • Norbin Is an Endogenous Regulator of Metabotropic Glutamate Receptor 5 Signaling
  • 2009
  • Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 326:5959, s. 1554-1557
  • Tidskriftsartikel (refereegranskat)abstract
    • Metabotropic glutamate receptor 5 (mGluR5) is highly expressed in the mammalian central nervous system (CNS). It is involved in multiple physiological functions and is a target for treatment of various CNS disorders, including schizophrenia. We report that Norbin, a neuron-specific protein, physically interacts with mGluR5 in vivo, increases the cell surface localization of the receptor, and positively regulates mGluR5 signaling. Genetic deletion of Norbin attenuates mGluR5-dependent stable changes in synaptic function measured as long-term depression or long-term potentiation of synaptic transmission in the hippocampus. As with mGluR5 knockout mice or mice treated with mGluR5-selective antagonists, Norbin knockout mice showed a behavioral phenotype associated with a rodent model of schizophrenia, as indexed by alterations both in sensorimotor gating and psychotomimetic-induced locomotor activity.
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14418.
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14419.
  • Wang, Jianpu, 1957-, et al. (författare)
  • Effects of endothelin receptor antagonism on acute lung injury induced by chlorine gas
  • 2006
  • Ingår i: Critical Care Medicine. - 0090-3493 .- 1530-0293. ; 34:6, s. 1731-1737
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To test the hypothesis that the endothelin system is involved in chlorine gas-induced lung injury.DESIGN: Experimental study.SETTING: Academic research laboratory.SUBJECTS: Twenty-four domestic juvenile pigs.INTERVENTIONS: Anesthetized, ventilated pigs were exposed to chlorine gas (400 parts per million in air) for 20 mins and then randomly allocated to four groups (n = 6 in each group). The tezosentan pretreatment group received the dual endothelin receptor antagonist tezosentan 20 mins before and hyperoxic gas (Fio2 0.6) after chlorine gas exposure. The tezosentan postinjury treatment group received hyperoxic gas after chlorine gas exposure and tezosentan 60 mins later. Animals in the oxygen group received hyperoxic gas after chlorine gas exposure. Pigs in the fourth group (air) were ventilated with room air (Fio2 0.21) throughout the experiment.MEASUREMENTS AND MAIN RESULTS: Hemodynamics, gas exchange, lung mechanics, and plasma endothelin-1 were evaluated for 6 hrs. Chlorine gas exposure induced an increase in circulating endothelin-1 by 90% (p < .05). The acute chlorine gas-induced rise in pulmonary vascular resistance was partly blocked by tezosentan pretreatment (p < .001). Tezosentan postinjury treatment also decreased pulmonary vascular resistance to levels significantly lower than in the air and oxygen groups (p < .001). Recovery of peak airway pressure was better in the tezosentan-treated groups than in the air group. There were significant linear relationships between circulating endothelin-1 and pulmonary vascular resistance (r = .47, p < .001) and endothelin-1 and peak airway pressure (r = .41, p < .001). These relationships were modified by tezosentan.CONCLUSIONS: Tezosentan modified chlorine gas-induced pulmonary dysfunction, indicating that the endothelin system is involved in this mode of acute lung injury.
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14420.
  • Wang, J. H., et al. (författare)
  • Pulmonary edema in the transurethral resection syndrome induced with mannitol 5%
  • 2009
  • Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley-Blackwell. - 0001-5172 .- 1399-6576. ; 53:8, s. 1094-1096
  • Tidskriftsartikel (refereegranskat)abstract
    • Two patients developed the transurethral resection (TUR) syndrome after having absorbed mannitol 5% during TUR of the prostate. Both developed pulmonary edema and became severely hypoatremic (lowest serum sodium 99 and 97 mmol/l, respectively). Hypertonic saline was infused to raise the serum sodium level and plasma volume expansion used to combat hypotension. One patient also required positive-pressure ventilation and intravenous administration of norepinephrine. Both patients recovered completely.
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