Objective:This study aims to investigate the impact of socioeconomic status on cognitive function in older adults, while analyzing the mediating role of health-related social determinants.The findings will provide a foundation for the implementation of an active aging strategy.Methods:Utilizing data from the China Health and Retirement Longitudinal Study(CHARLS)2020, this study employed multiple linear regression analysis to investigate the relationship between socioeconomic status and cognitive function among older adults.A multiple mediation model was applied to evaluate the mediating effects of health-related social determinants on the association between socioeconomic status and cognitive function, with these mediation effects assessed using the Bootstrap method.Results:The results of the multiple linear regression analysis indicated that socioeconomic status significantly positively influences cognitive function in older adults.Factors such as younger age, male gender, Han ethnicity, and urban residence were associated with higher cognitive scores.The mediation analysis demonstrated that, of the total effect of socioeconomic status on cognitive function, health status accounted for 1.564%, individual lifestyle for 14.820%, social support networks for 2.719%, living conditions for 1.632%, and other social structural factors for 1.496%.In the multiple mediation model, a total of 17.945% of the effect of socioeconomic status on cognitive function in older adults was jointly mediated by health-related social determinants.Conclusions:Socioeconomic status is a critical determinant of cognitive impairment among older adults in China.To address this issue, comprehensive interventions should be implemented to promote the equitable distribution of economic and social resources, reduce socioeconomic disparities, and mitigate health inequalities, thereby enhancing the overall cognitive function of disadvantaged groups.Preventive measures and strategies aimed at improving health status, encouraging healthy lifestyle choices, strengthening social support networks, enhancing living conditions, and optimizing social structural factors could serve as essential intervention points to improve the cognitive function of older adults with lower socioeconomic status.

Objective:This study aims to investigate the impact of socioeconomic status on cognitive function in older adults, while analyzing the mediating role of health-related social determinants.The findings will provide a foundation for the implementation of an active aging strategy.Methods:Utilizing data from the China Health and Retirement Longitudinal Study(CHARLS)2020, this study employed multiple linear regression analysis to investigate the relationship between socioeconomic status and cognitive function among older adults.A multiple mediation model was applied to evaluate the mediating effects of health-related social determinants on the association between socioeconomic status and cognitive function, with these mediation effects assessed using the Bootstrap method.Results:The results of the multiple linear regression analysis indicated that socioeconomic status significantly positively influences cognitive function in older adults.Factors such as younger age, male gender, Han ethnicity, and urban residence were associated with higher cognitive scores.The mediation analysis demonstrated that, of the total effect of socioeconomic status on cognitive function, health status accounted for 1.564%, individual lifestyle for 14.820%, social support networks for 2.719%, living conditions for 1.632%, and other social structural factors for 1.496%.In the multiple mediation model, a total of 17.945% of the effect of socioeconomic status on cognitive function in older adults was jointly mediated by health-related social determinants.Conclusions:Socioeconomic status is a critical determinant of cognitive impairment among older adults in China.To address this issue, comprehensive interventions should be implemented to promote the equitable distribution of economic and social resources, reduce socioeconomic disparities, and mitigate health inequalities, thereby enhancing the overall cognitive function of disadvantaged groups.Preventive measures and strategies aimed at improving health status, encouraging healthy lifestyle choices, strengthening social support networks, enhancing living conditions, and optimizing social structural factors could serve as essential intervention points to improve the cognitive function of older adults with lower socioeconomic status.

Objective:To explore the relationship of sleep quality and sleep duration with hypertension among adults aged 30-79 years old in Guangzhou.Methods:According to multi-stage stratified cluster sampling, 12 747 residents aged 30-79 years old were sampled and surveyed in Guangzhou from January 2018 to March 2019. Data on general demographic characteristics, sleep quality, sleep duration and hypertension were collected through questionnaire survey, the Pittsburgh sleep quality index (PSQI) and physical examination. Multivariate logistic regression models were used to analyze the putative association between sleep quality, sleep duration and hypertension. Restrictive cubic spline curve was used to draw the dose-response relationship curve between sleep quality, sleep time and hypertension.Results:The mean age of the subjects was (52.68±12.17) years, the prevalence of hypertension was 36.6% (4 664/12 747), the average score of PSQI was (4.70±2.88), and the average sleep time was (7.00±1.32) hours. The prevalence of hypertension was positively associated with the PSQI score. Compared to the subjects with a score less than 3, OR (95% CI) of hypertension with a PSQI score of 3-5, 5-8, ≥9 were 1.14 (1.02-1.27), 1.17 (1.03-1.34), 1.41 (1.21-1.64), respectively. The relationship between sleep duration and hypertension appeared U-shaped. Compared with 6 to 8 hours sleep duration, both sleep duration<6 hours with OR(95% CI) of 1.27(1.12-1.43) or >8 hours with OR(95% CI) of 1.20(1.05-1.38) was associated with hypertension. Conclusion:Both poor sleep quality, longer or shorter sleep duration were responsible for increased risk of cognitive impairment in older Chinese.

Objective:To explore the relationship of sleep quality and sleep duration with hypertension among adults aged 30-79 years old in Guangzhou.Methods:According to multi-stage stratified cluster sampling, 12 747 residents aged 30-79 years old were sampled and surveyed in Guangzhou from January 2018 to March 2019. Data on general demographic characteristics, sleep quality, sleep duration and hypertension were collected through questionnaire survey, the Pittsburgh sleep quality index (PSQI) and physical examination. Multivariate logistic regression models were used to analyze the putative association between sleep quality, sleep duration and hypertension. Restrictive cubic spline curve was used to draw the dose-response relationship curve between sleep quality, sleep time and hypertension.Results:The mean age of the subjects was (52.68±12.17) years, the prevalence of hypertension was 36.6% (4 664/12 747), the average score of PSQI was (4.70±2.88), and the average sleep time was (7.00±1.32) hours. The prevalence of hypertension was positively associated with the PSQI score. Compared to the subjects with a score less than 3, OR (95% CI) of hypertension with a PSQI score of 3-5, 5-8, ≥9 were 1.14 (1.02-1.27), 1.17 (1.03-1.34), 1.41 (1.21-1.64), respectively. The relationship between sleep duration and hypertension appeared U-shaped. Compared with 6 to 8 hours sleep duration, both sleep duration<6 hours with OR(95% CI) of 1.27(1.12-1.43) or >8 hours with OR(95% CI) of 1.20(1.05-1.38) was associated with hypertension. Conclusion:Both poor sleep quality, longer or shorter sleep duration were responsible for increased risk of cognitive impairment in older Chinese.

Objective: To examine the effects of ethyl pyruvate (EP) on mitochondrial dynamics and cell apoptosis in lipopolysaccharide (LPS)-induced human kidney-2 (HK-2) cells. Methods: HK-2 cells were divided into three groups: HK-2 cells were challenged with LPS (800 μg/L) for 24 hours as LPS group, or LPS mixed with EP (0.25 mmol/L) for 24 hours as EP group. Cells were incubated with normal saline for 24 hours as control group. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and intracellular adenosine triphosphate (ATP) were detected by enzyme linked immunosorbent assay (ELISA). JC-1 staining and Annexin V-fluorescein isothiocyanate/propidium iodide (FITC/PI) assays were used to evaluate mitochondrial membrane potential and cell apoptosis, respectively. Western Blot was used to evaluate the protein expressions of mitochondrial dynamics, including death-associated protein kinase 2 (DAPK-2), mitofusin (Mfn-1 and Mfn-2), and apoptotic associated biomarkers, including caspase-3, caspase-9, Bcl-2, Bcl-xL, cytochrome C (Cyt C), and DNA repair enzyme poly ADP-ribose polymerase (PARP). Results: Compared with the NC group, MDA, IL-6, TNF-α of LPS group were significantly increased, the expression of SOD, mitochondrial membrane potential and ATP level were significantly decreased, the expression of mitochondrial fission protein DAPK-2 was significantly increased, and mitochondrial fusion proteins Mfn-1 and Mfn-2 were significantly decreased, cell apoptosis and apoptotic protein caspase-3, caspase-9 and Cyt C were increased, and anti-apoptotic protein Bcl-2, Bcl-xL, PARP were significantly decreased. Compared with the LPS group, the oxidative activities and inflammatory factors above were inhibited in EP group [MDA (μmol/L): 12.35±2.21 vs. 45.95±1.76, SOD (kU/L): 54.68±1.42 vs. 40.73±1.60, IL-6 (ng/L): 67.87±2.61 vs. 338.92±20.91, TNF-α (ng/L): 19.23±1.80 vs. 180.69±6.51], mitochondrial membrane potential and ATP level were significantly increased [mitochondrial membrane potential: (99.43±0.25)% vs. (69.40±0.75)%, ATP (×10⁶ RLU): 0.19±0.01 vs. 0.12±0.05], the expression of mitochondrial fission protein was significantly decreased (DAPK-2/β-actin: 0.03±0.01 vs. 0.61±0.02), mitochondrial fusion proteins were significantly increased (Mfn-1/β-actin: 0.43±0.04 vs. 0.17±0.01, Mfn-2/β-actin: 0.201±0.004 vs. 0.001±0.001), percentage of cell apoptosis was significantly decreased [(5.25±0.17)% vs. (34.42±0.64)%], the expressions of apoptotic proteins were significantly decreased (caspase-3/β-actin: 0.25±0.15 vs. 1.76±0.01, caspase-9/β-actin: 0.09±0.02 vs. 1.52±0.12, Cyt C/β-actin: 0.001±0.001 vs. 0.350±0.030), and the expressions of anti-apoptotic proteins and PARP were significantly increased (Bcl-2/β-actin: 0.500±0.010 vs. 0.009±0.004, Bcl-xL/β-actin: 0.550±0.010 vs. 0.009±0.001, PARP/β-actin: 0.94±0.01 vs. 0.16±0.13), with statistically significant differences (all P < 0.05). Conclusions There are enhanced mitochondrial fission and diminished mitochondrial fusion in LPS-induced HK-2 cells. EP can protect mitochondria functions by regulate mitochondrial dynamics, and reducethe apoptosis of LPS-induced HK-2 cells.

OBJECTIVE: To examine the effects of ethyl pyruvate (EP) on mitochondrial dynamics and cell apoptosis in lipopolysaccharide (LPS)-induced human kidney-2 (HK-2) cells. METHODS: HK-2 cells were divided into three groups: HK-2 cells were challenged with LPS (800 μg/L) for 24 hours as LPS group, or LPS mixed with EP (0.25 mmol/L) for 24 hours as EP group. Cells were incubated with normal saline for 24 hours as control group. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and intracellular adenosine triphosphate (ATP) were detected by enzyme linked immunosorbent assay (ELISA). JC-1 staining and Annexin V-fluorescein isothiocyanate/propidium iodide (FITC/PI) assays were used to evaluate mitochondrial membrane potential and cell apoptosis, respectively. Western Blot was used to evaluate the protein expressions of mitochondrial dynamics, including death-associated protein kinase 2 (DAPK-2), mitofusin (Mfn-1 and Mfn-2), and apoptotic associated biomarkers, including caspase-3, caspase-9, Bcl-2, Bcl-xL, cytochrome C (Cyt C), and DNA repair enzyme poly ADP-ribose polymerase (PARP). RESULTS: Compared with the NC group, MDA, IL-6, TNF-α of LPS group were significantly increased, the expression of SOD, mitochondrial membrane potential and ATP level were significantly decreased, the expression of mitochondrial fission protein DAPK-2 was significantly increased, and mitochondrial fusion proteins Mfn-1 and Mfn-2 were significantly decreased, cell apoptosis and apoptotic protein caspase-3, caspase-9 and Cyt C were increased, and anti-apoptotic protein Bcl-2, Bcl-xL, PARP were significantly decreased. Compared with the LPS group, the oxidative activities and inflammatory factors above were inhibited in EP group [MDA (μmol/L): 12.35±2.21 vs. 45.95±1.76, SOD (kU/L): 54.68±1.42 vs. 40.73±1.60, IL-6 (ng/L): 67.87±2.61 vs. 338.92±20.91, TNF-α (ng/L): 19.23±1.80 vs. 180.69±6.51], mitochondrial membrane potential and ATP level were significantly increased [mitochondrial membrane potential: (99.43±0.25)% vs. (69.40±0.75)%, ATP (×10⁶ RLU): 0.19±0.01 vs. 0.12±0.05], the expression of mitochondrial fission protein was significantly decreased (DAPK-2/β-actin: 0.03±0.01 vs. 0.61±0.02), mitochondrial fusion proteins were significantly increased (Mfn-1/β-actin: 0.43±0.04 vs. 0.17±0.01, Mfn-2/β-actin: 0.201±0.004 vs. 0.001±0.001), percentage of cell apoptosis was significantly decreased [(5.25±0.17)% vs. (34.42±0.64)%], the expressions of apoptotic proteins were significantly decreased (caspase-3/β-actin: 0.25±0.15 vs. 1.76±0.01, caspase-9/β-actin: 0.09±0.02 vs. 1.52±0.12, Cyt C/β-actin: 0.001±0.001 vs. 0.350±0.030), and the expressions of anti-apoptotic proteins and PARP were significantly increased (Bcl-2/β-actin: 0.500±0.010 vs. 0.009±0.004, Bcl-xL/β-actin: 0.550±0.010 vs. 0.009±0.001, PARP/β-actin: 0.94±0.01 vs. 0.16±0.13), with statistically significant differences (all P < 0.05). CONCLUSIONS There are enhanced mitochondrial fission and diminished mitochondrial fusion in LPS-induced HK-2 cells. EP can protect mitochondria functions by regulate mitochondrial dynamics, and reducethe apoptosis of LPS-induced HK-2 cells.
Apoptosis ; Humans ; Kidney ; Lipopolysaccharides ; Mitochondrial Dynamics/drug effects* ; Protective Agents/pharmacology* ; Pyruvates/pharmacology*

Objective: To investigate the MUC1 specific immune response enhanced by thmosinal (Tα1) using MUC1-MBP as the specific antigen, and to discuss the feasibility of MUC1-MBP as an adjuvant. Methods: The C57BL/6 mice were randomly divided into normal saline group, MUC1-MBP + BCG group and MUC1-MBP + Tα1 group. The T cellular immune activities, MUC1 special antibody and subclass, anti-tumor effect of Tα1 combined with MUC1-MBP were detected. 4-7 d after the 3rd immunization, the spleen indexes of the mice in various groups were measured; the lymphocyte proliferation response was used to detect the stimulate index (SI) of the mice in various groups; the levels of specific cytokines IFN-γ, IL-2, IL-4 and IL-10 in the supernatant of spleen cells of the mice were detected by ELISA; the level of serum MUC1-specific antibody was detected by ELISA. The C57BL/6 mice were inoculated with B16-MUC1 7 d after the last immunization and the survival of the mice was observed. Results: Compared with normal saline group, the spleen index and SI of the mice in MUCl-MBP+Tα1 and MUC1-MBP+BCG groups were significantly increased (P< 0.05 or P<0.01); the specific SI of MUC1 were significantly increased (P< 0.05). Compared with normal saline group, the levels of IFN-y and IL-2 in the supernatant of spleen cells of the mice in MUC1-MBP+BCG group were obviously increased (P<0.05); the levels of IL-4 and IL-10 were slightly increased, but there were no significant differences (P>0.05); compared with normal saline group, the level of IL-4 in MUCl-MBP+Tal group was obviously increased (P< 0.01); the levels of IFN-γ, IL-2 and IL-10 were slightly increased, but there were no significant differences (P>0.05). The titer of MUC1 specific antibody was increased with the increase of concentration of Tα1. The antibody subtype detection results showed that compared with normal saline group, the level of IgG1 in MUCl-MBP + BCG group was significantly increased (P< 0.05 or P< 0.01), and the level of IgG2a had no obvious change. The tumor prevention experiment results showed that compared with normal saline group, the survival rates of the mice in MUC1-MBP+BCG group and MUCl-MBP + Tal group had no significant differences. Conclusion: MUC1-MBP combined with Tα1 prefers to Th2 immune responses in the mice. It indicates that Tα1 can be used as an adjuvanted preventive vaccines, but not suitable for therapeutic vaccines.

Objective:To study the inductive effect of recombinant MUC1-MBP fusion protein combined with R848 on the immune activity of T cells in the mice,and to provide experimental basis for searching the suitable adjuvants of recombinant MUC1-MBP fusion protein.Methods:A total of 21 C57BL/6 mice were randomly divided into control group(treat with normal saline),MUC1-MBP+R848 group (treated with MUC1-MBP+R848),and MUC1-MBP+baillus calmette guerin(BCG) group(treated with MUC1-MBP+BCG)(n=7).After immunized for 4-7 d,the spleen tissue was taken and the spleen indexes of the mice in various groups were measured;the stimmulus index(SI) of the mice was detected by lymphocyte proliferation response;the levels of tumor necrosis factor-γ(TNF-γ) and interleukin-4(IL-4) were detected by ELISA method;the proprotions of T lymphocyte subsets in spleen cells were analyzed by flow cytometry.Results:Compared with control group,the spleen indexes,SI,and TNF-γ levels of the mice in MUC1-MBP+ R848 and MUC1-MBP+BCG groups were significantly increased (P<0.05 or P<0.01);the indexes metioned above of the mice in MUC1-MBP+ R848 were higher than those in MUC1-MBP+BCG group;the IL-4 levels had no significant difference(P>0.05).Compared with control group,the proprotions of CD3+T,CD4+T,and CD8+ T cells of the mice in MUC1-MBP+ R848 group and MUC1-MBP+BCG group were significantly increased(P<0.05 or P<0.01).Conclusion:Both MUC1-MBP fusion protein combined with R848 and BCG can induce the Th1 type of immune activity in the mice,and R848 is the potential candidate adjuvant for MUC1-MBP.

BACKGROUNDMany studies have shown that continuous renal replacement therapy (CRRT) could clean lactate and treat the hyper-lactatemia. On the contrary, some other studies found that filter lactate clearance only accounted for a very small part of total lactate clearance and the hemofilter's contribution to the overall lactate clearance was negligible. The objective of this study was to evaluate the effects of various doses of continuous veno-venous hemofiltration (CVVH) on plasma lactate elimination in critically ill patients.

METHODSPatients were divided into three groups according to their incipient plasma lactate concentration. Group A: lactate ≤ 2 mmol/L, group B: lactate 2-5 mmol/L, group C: lactate ≥ 5 mmol/L. Three different doses (20 ml × kg(-1)× h(-1), 35 ml × kg(-1)× h(-1) and 45 ml × kg(-1)× h(-1)) of CVVH were applied to critically ill patients who experiencing CVVH. The concentrations of plasma lactate in pre-(A), post-dialyzer (V) sites and ultrafiltrate were measured after each dosage of CVVH was carried out for 30 minutes. Rate of lactate clearance by the filter (RLC) and filter lactate clearance (FLC) and Lactate-Sieving Coefficient (LSC) were calculated under different circumstances, including different doses of CVVH and different incipient lactate levels.

RESULTSFifteen patients were enrolled and 104 blood samples were drawn and lactate concentrations were measured in this study. RLC was found increased ((9.36 ± 9.73) mmol/h, (13.92 ± 12.56) mmol/h and (16.52 ± 12.71) mmol/h, P < 0.05 respectively) with the dose of CVVH increased. RLC was also increased ((3.46 ± 1.46), (10.38 ± 5.50) and (24.53 ± 14.69) mmol/h, P < 0.05 respectively) with the incipient lactate increased. FLC was increased ((1.95 ± 0.63), (2.95 ± 0.74) and (3.45 ± 0.54) L/h, P < 0.05 respectively) with the dose of CVVH increased. There was no significant difference of LSC in different doses of CVVH and different incipient lactate levels.

CONCLUSIONSPlasma lactate can be eliminated by CVVH and different doses of CVVH affect the rate of lactate clearance in critically ill patients.

Adult ; Aged ; Aged, 80 and over ; Critical Illness ; Female ; Hemofiltration ; Humans ; Lactic Acid ; blood ; Male ; Middle Aged