Determinants influencing health-promoting behaviors in individuals at high risks of stroke: a cross-sectional study.

Background: Quit smoking, moderate drinking, exercise, and healthy eating habits are all known to decrease the risk of stroke. As a result, understanding the health behaviors of high risk groups for stroke is crucial. Health behavior is influenced by knowledge, social environment, and health beliefs. However, little research has been done on these relationships. For a better grasp of the relationships mentioned above, consider using the COM-B model (capability, opportunity, motivation, and behavior). The purpose of this study was to investigate the variables related to health behavior and to test the mediating effect of health beliefs. Methods: The cross-sectional study was carried out at a physical examination center of a tertiary hospital in Shanghai, China. 986 high-risk populations of stroke have been tested using the Health Behavior Scale (HBS-SP), Stroke Knowledge Questionnaire (SKQ), Health Beliefs Questionnaire (HBS), and Multidimensional Scale of Perceived Social Support (MSPSS). The structural equation modeling was used in this study. Results: The scores for MSPSS, SKQ, HBS, and HBS-SP were 60.64 ± 13.72, 26.60 ± 9.77, 157.71 ± 34.34, and 2.46 ± 0.41, respectively. The revised model fits well (approximate root mean square error = 0.042; comparative fit index = 0.946). The health behavior was obviously and positively correlated to social Support, stroke knowledge, and health beliefs. Moreover, health belief has a mediating effect on the relation of social support, stroke knowledge, and health behavior. Conclusion: Chinese high risk groups for stroke have a mediate level of health behaviors. Factors associated with health behaviors are knowledge of stroke, health beliefs, and social support. The COM-B-based model can be used to explain the health behavior of individuals at risk of stroke and to guide the formulation of effective health management programs.

The role of the D-dimer to fibrinogen ratio in the classification of cardioembolism and atherosclerotic stroke.

BACKGROUND: The D-dimer-to-fibrinogen ratio (DFR) is a good indicator of thrombus activity in thrombotic diseases, but its clinical role in acute ischaemic stroke (AIS) patients with different etiologies has not been studied. We evaluated the diagnostic value of the DFR for different subtypes of AIS. METHODS: We conducted a single-center retrospective study of 269 patients with AIS who were referred to our stroke center within 4.5 h from Jan 2017 to Oct 2019. Coagulation data including DFRs were compared among the different stroke subtypes, and a separate retrospective validation sample was utilized to evaluate the prediction efficiency of the DFR for subtype diagnosis. RESULTS: A higher DFR was observed in patients with cardioembolism than in those with large artery atherosclerosis (LAA) (odds ratio (OR) per 0.1 increase of the DFR: 1.49 [1.01-2.18]) after we adjusted for vascular risk factors. The diagnostic value of the DFR for detecting cardioembolism (AUC = 0.722, 95 % CI = 0.623-0.820) exceeded that of isolated D-dimer or fibrinogen. The validation sample (n = 117) further supported the notion that a diagnosis of cardioembolism was more common in patients with a DFR > 0.11 (multivariable risk ratio = 3.11[1.33-7.31], P = 0.009). CONCLUSION: High DFRs were associated with cardioembolism in patients with AIS. The utilization of DFR can be beneficial for distinguishing a cardiac embolic source from atherosclerotic stroke.

AKG Attenuates Cerebral Ischemia-Reperfusion Injury through c-Fos/IL-10/Stat3 Signaling Pathway.

Inflammation is dominant in the pathogenesis of ischemic stroke (IS). Alpha-ketoglutarate (AKG), according to previous studies, has demonstrated a variety of pharmacological effects such as antioxidation and inhibitive inflammation activities. However, whether AKG ameliorates cerebral ischemic injury, as well as the underlying molecular events, is still unclear. Therefore, the effect and underlying mechanisms of AKG on ischemic brain injury should be identified. The study established a cerebral ischemia-reperfusion (I/R) model in mice as well as an oxygen-glucose deprivation/reperfusion (OGD/R) model in SH-SY5Y cells, respectively. It was observed that AKG markedly suppressed infarction volume and neuronal injuries and improved the neurological score in vivo. Moreover, AKG reduced the inflammatory response and lowered the expression of proinflammatory cytokines. In vitro, AKG treatment strongly inhibited OGD/R-induced neuronal injury and the proinflammatory factors. It was also found that the increased SOD and GSH levels, as well as the lower ROS levels, showed that AKG reduced oxidative stress in OGD/R-treated SY-SY5Y cells. Mechanistically, AKG largely promoted IL-10 expression in ischemic brain injury and OGD/R-induced neuronal injury. Furthermore, IL-10 silencing neutralized the protective effect of AKG on inflammation. Notably, it was discovered that AKG could upregulate IL-10 expression by promoting the translocation of c-Fos from the cytoplasm to the nucleus. The results indicated that AKG demonstrated neuroprotection on cerebral ischemia while inhibiting inflammation through c-Fos/IL-10/stat3 pathway.