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1.
Environmental Health and Preventive Medicine ; : 42-42, 2021.
Article in English | WPRIM | ID: wpr-880360

ABSTRACT

BACKGROUND@#Little is known about the effects of environmental cobalt exposure on insulin resistance (IR) in the general adult population. We investigated the association between cobalt concentration and IR.@*METHODS@#A total of 1281 subjects aged more than 20 years with complete blood cobalt data were identified from the National Health and Nutrition Examination Survey (NHANES) 2015-2016 cycle. Blood cobalt levels were analyzed for their association with IR among all populations and subgroups by sex. Regression coefficients and 95% confidence intervals (CIs) of blood cobalt concentrations in association with fasting glucose, insulin and homeostatic model assessment of insulin resistance (HOMA-IR) were estimated using multivariate linear regression after adjusting for age, sex, ethnicity, alcohol consumption, body mass index, education level, and household income. A multivariate generalized linear regression analysis was further carried out to explore the association between cobalt exposure and IR.@*RESULTS@#A negative association between blood cobalt concentration (coefficient = - 0.125, 95% CI - 0.234, - 0.015; P = 0.026) and HOMA-IR in female adults in the age- and sex-adjusted model was observed. However, no associations with HOMA-IR, fasting glucose, or insulin were found in the overall population. In the generalized linear models, participants with the lowest cobalt levels had a 2.74% (95% CI 0.04%, 5.50%) increase in HOMA-IR (P for trend = 0.031) compared with subjects with the highest cobalt levels. Restricted cubic spline regression suggested that a non-linear relationship may exist between blood cobalt and HOMA-IR.@*CONCLUSIONS@#These results provide epidemiological evidence that low levels of blood cobalt are negatively associated with HOMA-IR in female adults.


Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Young Adult , Cobalt/blood , Cross-Sectional Studies , Environmental Pollutants/blood , Homeostasis , Insulin/blood , Insulin Resistance , Nutrition Surveys , Sex Factors , United States
2.
Journal of Central South University(Medical Sciences) ; (12): 958-963, 2010.
Article in Chinese | WPRIM | ID: wpr-814372

ABSTRACT

OBJECTIVE@#To explore the role of IL-21 in the pathogenesis of myasthenia gravis (MG) and its influence on the the class switch of anti-AChR antibodies.@*METHODS@#Blood was taken from 26 patients and 18 healthy controls, and the expression of IL-21R mRNA in peripheral blood mononuclear cells (PBMCs) was detected by RT-PCR. The expression of IL-21R on B lymphocytes was measured by flow cytometry, while the concentrations of serum IL-21 and the levels of anti-AChR-IgG and its isotype IgG(1), IgG(2), and IgG(3) were tested by ELISA.@*RESULTS@#The serum concentration of IL-21 in the MG group was higher than that in the control group (31.686±8.499 pg/mL, 15.147±6.366 pg/mL) and the difference was significant (P0.05). Compared with the control group, the expression of IL-21R on B lymphocytes also increased in the MG group (P0.05). Expression of IL-21R mRNA in the PBMCs showed no correlation with the level of serum anti-AChR-IgG and its isotype IgG(1), IgG(2), and IgG(3), respectively(P>0.05); however the expression of IL-21R in B lymphocytes showed positive correlation with anti-AChR-IgG and it's isotype IgG(1) and IgG(3) (P0.05).@*CONCLUSION@#IL-21 might induce the class switch of anti-AChR antibodies to IgG(1) and IgG(3) isotype through IL-21R on B lymphocytes which promotes the pathogenesis of the MG.


Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Young Adult , Autoantibodies , Classification , Allergy and Immunology , Immunoglobulin Class Switching , Allergy and Immunology , Immunoglobulin G , Classification , Interleukins , Blood , Genetics , Myasthenia Gravis , Blood , Allergy and Immunology , RNA, Messenger , Blood , Genetics , Receptors, Cholinergic , Allergy and Immunology , Receptors, Interleukin-21 , Blood , Genetics
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