Association between self-reported oral health and cognitive function among the community-dwelling elderly in Jinan, China: the mediating effect of life satisfaction.

Background: Deterioration of self-reported oral health and decline in cognitive function are two main adverse health outcomes experienced by the older adults. Little evidence was found on the psychosocial mechanism between self-reported oral health and cognitive function. This study explores the association between self-reported oral health and cognitive function and examines the mediating effect of life satisfaction among the community-dwelling elderly in Jinan, China. Methods: A total of 512 older individuals (60+) were included in the study. Cognitive function was assessed using the Chinese version of the Mini-Mental State Examination scale (MMSE), and self-reported oral health was measured using the Chinese version of the Geriatric Oral Health Assessment Index (GOHAI). Pearson correlation analysis was used to determine the relationship between self-reported oral health, life satisfaction, and cognitive function. Multivariate linear regression analysis was conducted to explore the possible effect of covariates. Structural equation modelling and Bootstrap analyses were conducted to verify the mediating role of life satisfaction. Results: The mean MMSE score was 25.65 ± 4.42. Better self-reported oral health was significantly associated with a higher level of life satisfaction, and those with higher life satisfaction experienced better cognitive function. Age, educational level and source of living expenses were found to be cofounding variables. Life satisfaction partially mediated the effect of self-reported oral health on cognitive function (95% confidence interval [CI]: 0.010 to 0.075). The mediating effect of life satisfaction accounted for 24% of the total effect. Conclusion: The level of cognitive function was relatively high. Self-reported oral health was positively associated with cognitive function, and the mediating effect of life satisfaction was proven to exist in the community-dwelling older individuals. Early screening for oral diseases and a greater focus on life satisfaction are recommended.

PREDICTIVE VALUE OF SOLUBLE PROGRAMMED CELL DEATH LIGAND-1 IN THE PROGRESSION OF SEPTIC PATIENTS TO CHRONIC CRITICAL ILLNESS IN THE INTENSIVE CARE UNIT: A PROSPECTIVE OBSERVATIONAL CLINICAL STUDY.

ABSTRACT: Background: As an immune marker, serum soluble programmed cell death ligand-1 (sPD-L1) is significantly increased in sepsis and is predictive of mortality. We investigated the prognostic value of sPD-L1 in postseptic immunosuppression and progression to chronic critical illness (CCI). Methods: Adults with sepsis in intensive care units (ICUs) for the first time were screened and assigned to either a CCI group (ICU stay ≥14 days with persistent organ dysfunction) or a rapid recovery (RAP) group based on clinical outcome. Data regarding basic admission information and clinical parameters were collected and compared across the two groups. Serum sPD-L1 levels were detected by enzyme-linked immunosorbent assay at admission and on the seventh day (D 7 ). Logistic regression analysis was used to determine the factors affecting septic patients' lymphocytopenia diagnosis on day 7 and CCI progression during hospitalization. The receiver operating characteristic curve and DeLong test were used to assess variable predictive power. Results: During the study period, a total of 166 septic patients were admitted to the ICU, and 91 septic patients were enrolled after screening. Compared with those in healthy individuals, the sPD-L1 levels in septic patients were significantly higher and positively correlated with traditional inflammatory markers and disease severity scores ( P < 0.05). In a multivariate regression analysis, sPD-L1 alone predicted lymphocytopenia on day 7 ( P < 0.05). In the sepsis cohort, 59 patients (64.8%) experienced RAP, and 32 patients (35.2%) developed CCI. Compared with the RAP group, the patients in the CCI group had a higher mean age, greater severity of disease, and higher mortality ( P < 0.05). D 7 -sPD-L1 remained higher in the CCI group, and the area under the curve that predicted the occurrence of CCI was equivalent to the APACHE II score, with areas under the curve of 0.782 and 0.708, respectively. Conclusions: The severity of infection and immunosuppression in sepsis may be linked to serum sPD-L1. D 7 -sPD-L1 is valuable in predicting the progression of CCI in patients.

Effects of childcare disagreement with children, social support, and health status on unmet healthcare-seeking behavior among the migrant older with children to Jinan, China.

Due to the acceleration of China's urbanization, the number of migrant older with children (MOC) continued to increase. This study aimed to clarify the effects of childcare disagreement with children, social support, and health status on unmet healthcare-seeking behavior among the MOC to Jinan, China. A cross-sectional study included 656 MOC (36.3% men and 63.7% women) using multi-stage cluster random sampling in Jinan, China. Childcare disagreement was evaluated by the differences between parents and grandparents on the diet, dressing, education, and childcare consumption. Social support was assessed using the social support rating scale (SSRS). Descriptive analysis, chi-squared test, and binary logistic regression were applied to analyze the association between childcare disagreement with children, social support, health status, and unmet healthcare-seeking behavior of the MOC. Approximately 41.3% of participants had unmet healthcare-seeking behavior. Logistic regression analysis showed that the MOC whose health status compared to last year get better were more likely to have unmet healthcare-seeking behavior, while who were women, had partial will of migration, hired a nanny, had smaller childcare disagreement with children on dressing, had smaller childcare disagreement with children on consumption, and had moderate social support, were less likely to experience unmet healthcare-seeking behavior. Recommendations were given to the government and family members to improve the health services-seeking behavior of the MOC.

Mediating effect of family support on the relationship between acculturation and loneliness among the migrant elderly following children in Jinan, China.

The total number of migrant elderly following children (MEFC) has gradually increased along with population aging and urbanization in recent decades in China. The purpose of this study was to investigate the mediating effect of family support on the relationship between acculturation and loneliness among the MEFC in Jinan, China. A total of 656 MEFC were selected by multistage cluster random sampling. Loneliness was measured using the short-form UCLA Loneliness Scale (ULS-8), while acculturation and family support were assessed using a self-designed questionnaire. Descriptive analysis, univariate analysis, and the structural equation model (SEM) were conducted to illustrate the relationship between the above indicators and loneliness. The average ULS-8 score of the MEFC was 12.82 ± 4.05 in this study. Acculturation of the MEFC exerted a negatively direct effect on loneliness and a positively direct effect on family support simultaneously, while family support exerted a negatively direct effect on loneliness. Family support partially mediated the relationship between acculturation and loneliness [95% CI: -0.079 to 0.013, p < 0.001], while the mediating effect of family support accounted for 14.0% of the total effect. The average ULS-8 score of 12.82 ± 4.05 implied a low level of loneliness in the MEFC in Jinan, China. Acculturation was found to be correlated with loneliness, while the mediating role of family support between acculturation and loneliness was established. Policy recommendations were provided to reduce loneliness and improve the acculturation and family support of the MEFC according to the findings above.

Heparin-binding protein (HBP) worsens the severity of pancreatic necrosis via up-regulated M1 macrophages activation in acute pancreatitis mouse models.

Acute pancreatitis (AP) is one of the most widespread clinical emergencies. Macrophages are the most common immune cells in AP pancreatic tissue and are closely associated with pancreatic necrosis and recovery. The level of heparin-binding protein (HBP) is closely linked to inflammation. In this study, we assessed the effect of HBP on AP tissue necrosis severity and whether HBP is associated with M1 macrophages in pancreatic necrosis. We observed the dynamic changes of HBP levels in the pancreas during acute inflammation in the caerulein-induced AP mice model. We used hematoxylin-eosin staining to evaluate pancreatic edema and necrosis, and to detect infiltration of macrophages by immunohistochemistry. Moreover, expressions of the maker and cytokines of macrophages, including inducible nitric oxide synthase (iNOS), and arginase 1 (Arg-1), interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) mRNA, were detected by real-time polymerase-chain reaction (RT-PCR). High levels of HBP in the pancreas were detected at 48 h, and heparin inhibited HBP expression in AP pancreatic tissue. Inhibiting HBP expression by injecting heparin before AP can alleviate pancreatic necrosis and inhibit F4/80 labeled M1 macrophage infiltration and IL-6, TNF-α, and iNOS mRNA expression. Clodronate liposome (CLDL) intraperitoneally treated mice showed no change in pancreatic HBP levels, but pancreatic macrophage-specific antigen F4/80 and TNF-α, IL-1ß, and IL-6 mRNA levels decreased after CLDL treatment. HBP is critical for pancreatic necrosis response in acute pancreatitis by increasing the infiltration of M1 macrophages and promoting the secretion of inflammatory factors, such as TNF-α, IL-6, IL-1ß, which can be reduced by heparin.

miR-20b suppresses mitochondrial dysfunction-mediated apoptosis to alleviate hyperoxia-induced acute lung injury by directly targeting MFN1 and MFN2.

Supplemental oxygen is commonly used to treat severe respiratory failure, while prolonged exposure to hyperoxia can induce acute lung injury characterized by the accumulation of reactive oxygen species (ROS) and pulmonary inflammation. Dysregulation of microRNAs contributes to multiple diseases, including hyperoxia-induced acute lung injury (HALI). In this study, we explored the roles of miR-20b in mediating the response of type II alveolar epithelial cells (ACE IIs) to hyperoxia and the potential underlying mechanisms. We found that miR-20b was significantly decreased in the lung tissues of HALI models and H2O2-treated ACE IIs. Hyperoxia induced the release of TNF-α, decreased the mitochondrial membrane potential, and led to excessive ROS production and cell apoptosis. Overexpression of miR-20b suppressed the hyperoxia-induced biological effects in ACE IIs. miR-20b negatively regulated the expression levels of Mitofusin 1 (MFN1) and MFN2, the two key proteins of mitochondrial fusion, via complementarily binding to the 3'-untranslated regions of mRNAs. Furthermore, both in vivo and in vitro, upregulation of MFN1 and MFN2 aggravated lung damage and cell apoptosis that were alleviated by miR-20b overexpression. These results provided new insights into the involvement of the miR-20b/MFN1/2 signaling pathway in HALI.

Heparin-Binding Protein Enhances NF-κB Pathway-Mediated Inflammatory Gene Transcription in M1 Macrophages via Lactate.

In early-stage sepsis, glucose metabolism is increased primarily through glycolysis in the inflammatory response of M1 macrophages. Heparin-binding protein (HBP) has been linked to sepsis, which can promote macrophage activation and inflammatory factor release. However, the mechanism by which glucose metabolism regulates the inflammatory response is unclear. We show that HBP contributes to sepsis by modulating the inflammatory response via lactate-dependent glycolysis in macrophages. Peritoneal macrophages from BALB/c mouse were treated with lipopolysaccharide (LPS). The expression of M1-related proinflammatory genes was investigated by PCR array. IL-1ß, iNOS, TNF-α, and IL-6 mRNA expression was determined by qRT-PCR. Intracellular lactate levels were measured using lactate assays. Nuclear factor-kappaB (NF-κB) activity was determined by electrophoretic mobility shift assays (EMSAs). TNF-α levels were measured by qRT-PCR. HBP enhanced inflammatory gene expression in mouse peritoneal macrophages and intracellular lactate accumulation and significantly increased LPS-stimulated NF-κB transcriptional activity and TNF-α expression through lactate. Lactate was essential for the HBP-induced increase in LPS-stimulated TNF-α expression. The critical role of lactate in HBP-induced NF-κB signaling was confirmed, as α-CHCA-mediated (MCT) suppression significantly inhibited NF-κB activity and TNF-α expression. HBP plays an important role in the initial inflammatory reaction, presumably by activating M1 macrophages, increasing lactate levels, and regulating proinflammatory factor release via NF-κB pathway activation.

Role of M2 Macrophages in Sepsis-Induced Acute Kidney Injury.

BACKGROUND: Sepsis is a major cause of acute kidney injury (AKI), with high rates of morbidity and mortality. M2 macrophages have been shown to play important roles in the secretion of anti-inflammatory and tissue repair mediators. In this study, we investigate the role of M2 macrophages in sepsis-induced AKI by depleting these cells in vivo through the systemic administration of liposomal clodronate (LC). METHODS: Male Sprague-Dawley rats were subjected to cecal ligation and puncture (CLP) or sham surgery. Biochemical and histological renal damage was assessed. Macrophage infiltration and M2 macrophage depletion were assessed by immunohistochemistry. RT-PCR was used to investigate the expression of the inducible nitric oxide synthase (iNOS), arginase 1 (Arg-1), and found in inflammatory zone 1 (FIZZ1) mRNAs. Western blots were performed to assay the tissue levels of interleukin-10 (IL-10) and tumor necrosis factor alpha (TNF-α). RESULTS: M2 macrophages were obviously detected 72 h after sepsis-induced AKI. Kidney injury was more severe, renal function was decreased, and blood creatinine and blood urea nitrogen (BUN) levels were higher after M2 macrophage depletion. M2 macrophage depletion significantly inhibited the proliferation of tubular cells. M2 macrophage depletion also downregulated IL-10 expression and increased TNF-α secretion during sepsis-induced AKI. CONCLUSIONS: M2 macrophages attenuate sepsis-induced AKI, presumably by upregulating IL-10 expression and suppressing TNF-α secretion.

Glucocorticoids offer protection against myocardial injury in a murine model of sepsis.

Sepsis is a serious infection-related complication that, in causing significant inflammation, often leads to myocardial injury. Severe inflammation, including in sepsis, is sometimes treated with exogenous glucocorticoids (GCs). Here, to explore the potential effect of GCs to protect against myocardial injury, we created a model of sepsis in rats by performing cecal ligation and puncture (CLP) in 96 rats randomly divided into sham-operated control (N=32), untreated sepsis (CLP, N=32), and GC-treated sepsis (N=32) groups. At 3, 6, 12, and 24 h after surgery, the changes in cardiac hemodynamic indexes, serum inflammatory response factor levels, and myocardial enzymes were measured, along with mitochondrial membrane potential in myocardial cells, apoptosis of myocardial cells, and the expression of nuclear factor kappa B (NF-κB p65) in myocardial tissues. Pathological changes in myocardial cells were also observed. Compared to the sham-operated group, CLP rats experienced deterioration of left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximum rate of left ventricular pressure rise (+dP/dtmax), and the maximum rate of left ventricular pressure drop (-dP/dtmax). CLP rats also had a rise in serum tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), cardiac troponin I (cTnI), creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and NF-κB p65 in myocardial tissues. The GCs-treated group had lower levels of these inflammatory response molecules than the CLP group, with the exception of anti-inflammatory cytokine interleukin-10 (IL-10), which was higher in the GC-treated rats than the CLP group at each time point post-surgery. Compared to the sham group, CLP rats had a rise in myocardial cell apoptosis and a drop in mitochondrial membrane potential in myocardial cells. In addition, GCs-treated rats had a marked drop in the myocardial cell apoptosis rate and a rise in the mitochondrial membrane potential compared to CLP rats. After intervention with GCs, the pathological changes in heart tissues were also reduced compared to those in the sepsis group. Based on these results, we conclude that exogenous GCs can inhibit a drop in myocardial mitochondrial membrane potential and inhibit myocardial cell apoptosis by blocking the activation of NF-κB, decreasing the generation of proinflammatory cytokines, and relieving inflammatory injury in heart tissues.

Polymorphism in Integrin ITGA2 is Associated with Ischemic Stroke and Altered Serum Cholesterol in Chinese Individuals.

BACKGROUND: Recent studies have reported contrasting results regarding the association of polymorphisms in two integrin genes, ITGA2 and ITGB3, with ischemic stroke. AIMS: The present study aimed to investigate the correlation between the ITGA2 C807T and ITGB3 T176C polymorphic loci with ischemic stroke, as well as plasma lipid and lipoprotein levels. STUDY DESIGN: Case control study. METHODS: Human venous blood samples were collected from patients admitted for ischemic stroke (n=350, 'patients') and healthy individuals (n=300, 'controls'). Blood was genotyped at these loci by polymerase chain reaction-restriction fragment length polymorphism. Plasma lipid and lipoprotein levels were measured by routine enzymatic, masking, and turbidimetry methods. RESULTS: As expected, total cholesterol, triglycerides, and low-density lipoprotein were all significantly higher in patients than in controls (p<0.05). Genotype and allele frequencies of ITGA2 C807T were significantly different between patients and controls (p<0.05), but no difference was detected in genotype or allele frequencies for ITGA3 T176C. For ITGA-2, the T allele conferred a 1.226 times higher relative risk of ischemic stroke than the C allele (odds ratio=1.226, 95% confidence interval=1.053-1.428). Similarly, total cholesterol was higher in T allele carriers than in non-carriers (p<0.05). CONCLUSION: ITGA2 C807T polymorphism is associated with ischemic stroke, with the T allele acting as a susceptibility allele that appears to confer increased cholesterol levels.

Correlation between interleukin-18 promoter -607C/A polymorphism and susceptibility to ischemic stroke

Single nucleotide polymorphisms in the promoter region of interleukin-18 (IL-18), an inflammatory cytokine, have been linked to susceptibility to many diseases, including cancer and immune dysfunction. Here, we explored the potential association between the IL-18 -607C/A (rs1946518) promoter region polymorphism and susceptibility to ischemic stroke (IS). This locus was amplified from peripheral blood samples of 386 IS patients (cases) and 364 healthy individuals (controls) by the polymerase chain reaction with sequence-specific primers. Significant differences were observed by the χ2 test in the -607C/A (rs1946518) genotype and allele frequencies between cases and controls (P < 0.05). Furthermore, after excluding for age, gender, smoking status, and hypertension, logistic regression indicated that IS susceptibility of -607C carriers increased 1.6 times (OR = 1.601, 95%CI = 1.148-2.233, P = 0.006) compared to -607A carriers. Additionally, similar increases in IS risk were noted for male patients or patients less than 65 years old. In conclusion, IL-18 -607C/A (rs1946518) promoter polymorphism is associated with IS susceptibility, and the C allele may confer increased IS risk.

Correlation between interleukin-18 promoter -607C/A polymorphism and susceptibility to ischemic stroke.

Single nucleotide polymorphisms in the promoter region of interleukin-18 (IL-18), an inflammatory cytokine, have been linked to susceptibility to many diseases, including cancer and immune dysfunction. Here, we explored the potential association between the IL-18 -607C/A (rs1946518) promoter region polymorphism and susceptibility to ischemic stroke (IS). This locus was amplified from peripheral blood samples of 386 IS patients (cases) and 364 healthy individuals (controls) by the polymerase chain reaction with sequence-specific primers. Significant differences were observed by the χ2 test in the -607C/A (rs1946518) genotype and allele frequencies between cases and controls (P < 0.05). Furthermore, after excluding for age, gender, smoking status, and hypertension, logistic regression indicated that IS susceptibility of -607C carriers increased 1.6 times (OR = 1.601, 95%CI = 1.148-2.233, P = 0.006) compared to -607A carriers. Additionally, similar increases in IS risk were noted for male patients or patients less than 65 years old. In conclusion, IL-18 -607C/A (rs1946518) promoter polymorphism is associated with IS susceptibility, and the C allele may confer increased IS risk.

Effect of aloe polysaccharide on caspase-3 expression following cerebral ischemia and reperfusion injury in rats.

Stroke is a leading cause of cardiovascular morbidity, economic and social burden and mortality. Novel approaches are needed to address stroke prevention and treatment. The purpose of this study was to explore the effects of aloe polysaccharide on caspase-3 expression following cerebral ischemia reperfusion injury in rats. Male Wistar rats were randomly divided into 5 groups (16 rats in each group): aloe polysaccharide, ginkgo leaf tablet, nimodipine, model and sham surgery groups. The rats were administered the appropriate drug or normal saline for 7 days by gavage. A rat model of cerebral ischemia and reperfusion injury was established using the middle cerebral artery occlusion (MCAO) model. Caspase-3 protein and mRNA expression levels in the cerebral cortex were detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Results showed that caspase-3 protein and mRNA expression levels in the cerebral cortex in the aloe polysaccharide, ginkgo leaf tablet and nimodipine groups were significantly lower compared with the model group and were higher than the sham surgery group (P<0.05). No significant difference was observed in caspase-3 protein and mRNA expression among the aloe polysaccharide, the ginkgo leaf tablet and the nimodipine groups (P>0.05). In conclusion, aloe polysaccharide has a protective effect on cerebral ischemia that may be due to the inhibition of neuronal cell apoptosis.

[The expression and significance of ANXA2 in human glioma].

AIM: to investigate the relation between the expression of ANXA2 in human glioma and its pathological grades, and research the possibility that if ANXA2 could be as a useful diagnostic marker for glioma. METHOD: Semi-quantity RT-PCR and immunohistochemistry were proceeded fro corresponding specimens to detect the level of ANXA2 and ANXA2mRNA. RESULTS: In RT-PCR, the expression level of ANXA2mRNA in glioma was higher than that in surrounding brain tissue. (P < 0.05), as the same, in immunohistochemistry, the expression level of ANXA2 in glioma is higher than that is surrounding brain tissues (P< 0.05). CONCLUSION: ANXA2 expression was much higher in glioma samples than in the surrounding brain tissues, and positive correlation between its expression and pathological grades was found. It could be used as an assistant diagnostic index for glioma.