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1.
Chinese Journal of Preventive Medicine ; (12): 516-521, 2023.
Artigo em Chinês | WPRIM | ID: wpr-984766

RESUMO

Objective: To investigate the relationship between hemoglobin and serum uric acid in adults with various glucose metabolism status. Methods: The demographic data and biochemical indicators of the adult population who had received physical examination in the Second Medical Center of the PLA General Hospital from January 2018 to December 2021 were collected. The subjects were divided into two groups according to the level of serum uric acid: the normal uric acid group and the hyperuricemia group. The relationship between hemoglobin (stratified into four levels of Q1 to Q4 by the quartile) and serum uric acid was quantified by using Pearson correlation and logistic regression analysis. The effects of age and glucose metabolism status on the relationship between hemoglobin and serum uric acid were analyzed. Results: A total of 33 183 adults were enrolled with age (50.6±10.0) years. The level of hemoglobin in the normal uric acid group (142.61±14.24) g/L was significantly lower than that in the hyperuricemia group [(151.79±11.24) g/L, P<0.001]. Univariate Pearson correlation analysis showed that hemoglobin was positively associated with serum uric acid (r=0.444, P<0.001). After adjusting for related confounding factors, multivariate logistic regression analysis showed that hemoglobin was associated with serum uric acid, and the OR values (95%CI) of hemoglobin Q2 to Q4 group were 1.29 (1.13-1.48), 1.42 (1.24-1.62) and 1.51 (1.32-1.72), respectively (Ptrend<0.001) when compared with hemoglobin Q1 group. Subgroup analysis and hierarchical interaction analysis suggested that with the increase of hemoglobin, the serum uric acid in the age<60 years subgroup, normal glucose subgroup and prediabetes subgroup increased gradually (Ptrend<0.05 and Pinteraction<0.001). Conclusion: The association between hemoglobin and serum uric acid in adults is affected by age and glucose metabolism status.


Assuntos
Humanos , Adulto , Pessoa de Meia-Idade , Ácido Úrico , Hiperuricemia/epidemiologia , Hemoglobinas , Estado Pré-Diabético , Glucose , Fatores de Risco
2.
Chinese Journal of Stomatology ; (12): 155-161, 2022.
Artigo em Chinês | WPRIM | ID: wpr-935842

RESUMO

Objective: To detect gene mutation in patients with hypohidrotic ectodermal dysplasia (HED) by using whole exome sequencing, to analyze the pathogenicity of the mutations, and to provide reference for the genetic diagnosis of HED patients. Methods: Peripheral blood genomic DNA was extracted from each of the HED patients and their family members collected in Peking University School and Hospital of Stomatology from August 2016 to August 2021. Whole exome sequencing and sanger sequencing were performed to detect gene mutations. Functions of the rare variants after the database filtering were analyzed by bioinformatics tools. Results: Three reported mutations of ectodysplasin A (EDA) gene (c.2T>C, c.161A>G, c.467G>A) and a mutation of ectodysplasin A receptor (EDAR) gene (c.871G>A) were detected by whole genome sequencing in four HED patients, and were verified by Sanger sequencing in four HED families. The EDAR gene mutation founded in this research was reported in HED patients for the first time. Bioinformatics tools predicted that the mutations of EDA gene detected in this study were highly species conserved and disease-causing. The combined annotation dependent depletion (CADD) scores of EDA gene mutations c.2T>C, c.161A>G and c.467G>A were 22.5, 26.3 and 25.5 respectively, and the genomic evolutionary rate profiling (GERP) scores were 2.16, 2.26 and 2.18 respectively. The EDAR gene mutation c.871G>A detected in this study was species conserved and possibly disease-causing. The CADD and GERP scores of EDAR gene mutation c.871G>A were 22.0 and 1.93 respectively. Conclusions: Three reported mutations of EDA gene and a previously unreported mutation of EDAR gene were detected in four HED families. Different mutations of EDA gene and EDAR gene could make different influence on the protein function and lead to the occurrence of HED.


Assuntos
Humanos , Displasia Ectodérmica/genética , Displasia Ectodérmica Anidrótica Tipo 1/genética , Receptor Edar/genética , Mutação , Linhagem , Sequenciamento do Exoma
3.
Academic Journal of Second Military Medical University ; (12): 201-205, 2017.
Artigo em Chinês | WPRIM | ID: wpr-838370

RESUMO

Objective To investigate the protective effect of lithium chloride (LiCl)-activated Wnt/beta-catenin signaling pathway on glucocorticoid-induced bone loss. Methods C57BL6/J mice were randomly divided into 3 groups. osteoporosis (OP) group and LiCl group were injected intraperitoneally once daily with dexamethasone (50 mg kg). while control group was injected with normal saline. LiCl group was given LiCl (200 mg kg) through water administration. After 5 weeks of treatment, mice were sacrificed within 24 h. Anti-active hela-catenin antibody was used in immuno his to chemical staining to detect the activity of Wnt/beta-cat enin signaling pathway, tone morphology was observed by UK siaining. Meanwhile. bone histomorphometrical parameters were analyzed by microCT. Bone formation and bone resorption of different groups were detected by calcein labeling and TRAP siaining. respectively. Results The protein level of active beta-calenin was higher in LiCl group compared with OP group, tone histomorphometrical parameters including the trabecular bone volume as a percentage of total volume (BV/TV). bone mineral density (HMD), trabecular number (Tb. N) and trabecular space (Tb. Sp) were all significantly improved in LiCl group- even though obvious difference existed lieiween LiCl group and control group (P<0. 05). Calcein labeling showed that new hone formation was markedly improved in LiCl group, but was still lower than that in control group, tone resorption was not significantly changed among three groups as indicated by TRAP siaining. Conclusion LiCl administration effectively activates Wnt/β-catenin signaling pathway in vivo* which improve new bone formation and rescue glucocorticoid-induced bone loss.

4.
China Biotechnology ; (12)2006.
Artigo em Chinês | WPRIM | ID: wpr-685713

RESUMO

A review of studies on the influence of impurities on protein crystallization is given.The possible sources of impurities and its effect on the protein crystallization are presented.The effects of impurities on protein crystallization,including nucleation,macroscopic morphologies,microscopic surface morphologies,growth rates,kinetics,quality,and repartitioning of impurities are reviewed.

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