Meta-analysis and systematic review of the relationship between sex and the risk or incidence of poststroke aphasia and its types.

OBJECTIVE: To analyse and discuss the association of gender differences with the risk and incidence of poststroke aphasia (PSA) and its types, and to provide evidence-based guidance for the prevention and treatment of poststroke aphasia in clinical practice. DATA SOURCES: Embase, PubMed, Cochrane Library and Web of Science were searched from January 1, 2002, to December 1, 2023. STUDY SELECTION: Including the total number of strokes, aphasia, the number of different sexes or the number of PSA corresponding to different sex. DATA EXTRACTION: Studies with missing data, aphasia caused by nonstroke and noncompliance with the requirements of literature types were excluded. DATA SYNTHESIS: 36 papers were included, from 19 countries. The analysis of 168,259 patients with stroke and 31,058 patients with PSA showed that the risk of PSA was 1.23 times higher in female than in male (OR = 1.23, 95% CI = 1.19-1.29, P < 0.001), with a prevalence of PSA of 31% in men and 36% in women, and an overall prevalence of 34% (P < 0.001). Analysis of the risk of the different types of aphasia in 1,048 patients with PSA showed a high risk in females for global, broca and Wenicke aphasia, and a high risk in males for anomic, conductive and transcortical aphasia, which was not statistically significant by meta-analysis. The incidence of global aphasia (males vs. females, 29% vs. 32%) and broca aphasia (17% vs 19%) were higher in females, and anomic aphasia (19% vs 14%) was higher in males, which was statistically significant (P < 0.05). CONCLUSIONS: There are gender differences in the incidence and types of PSA. The risk of PSA in female is higher than that in male.

Exercise Preconditioning Protects against Acute Cardiac Injury Induced by Lipopolysaccharide Through General Control Nonderepressible 2 Kinase.

Exercise preconditioning may protect against cardiac injury induced by lipopolysaccharide (LPS), but the mechanism is unresolved. The aim of this study is to explore whether the general control nonderepressible 2 (GCN2) kinase gene is associated with the protective effect of exercise preconditioning. Eight-week-old male C57BL/6J (n = 40) and GCN2 knockout (KO) (n = 40) mice were divided into four groups: control, LPS (L), exercise preconditioning (E), and exercise preconditioning LPS (EL). Mice in the exercise groups performed exercise for eight weeks. After exercise, all mice were given an equal volume of LPS or saline (10 µg/g). We measured the cardiac function using echocardiography and then collected heart tissue. Exercise preconditioning improved cardiac inflammation (interleukin-6, tumor necrosis factor α) and cardiac dysfunction (ejection fraction, fraction shortening) in C57 mice induced by LPS and also decreased the expression levels of GCN2, phosphorylation of eukaryotic translation initiation factor 2α (p-eIF2α), and activating transcription factor 4 (ATF4). Moreover, GCN2 KO decreased inflammation and cardiac dysfunction induced by LPS in sedentary mice. The inflammation and cardiac dysfunction in the GCN2 KO EL group were lower than in the C57 EL group, and the expression of GCN2, p-eIF2α, and ATF4 in the GCN2 KO EL group was lower than in the C57 EL group. Exercise preconditioning alleviated cardiac injury induced by LPS. GCN2 KO also improved cardiac injury. Exercise preconditioning promoted the effect of GCN2 KO in alleviating cardiac injury, and the GCN2 and eIF2α/ATF4 pathways play an important role in the process.