Family function, self-efficacy, care hours per day, closeness and benefit finding among stroke caregivers in China: A moderated mediation model.

AIMS AND OBJECTIVES: The aim of this study was to explore the moderated mediation mechanism of the relationships among family function, self-efficacy, care hours per day, closeness and benefit finding in family caregivers of patients with stroke in China. BACKGROUND: Benefit finding can provide a new means of resolving depression among family members caring for an ill loved one. However, current research has paid little attention to the benefit finding of family caregivers of stroke patients in China. DESIGN: A cross-sectional study. METHODS: Three hundred fifty family caregivers of patients with stroke were recruited from community service centres and hospitals in Zhengzhou, China. The participants completed the family APGAR index, caregiver benefit finding scale and Chinese general self-efficacy scale during a study conducted in 2017. Descriptive analyses and a moderated mediation model were computed. Reporting adhered to the STROBE checklist. RESULTS: A total of 311 family caregivers completed this study. Closeness between family caregivers and patients with stroke moderated the relationship between family function and caregiver benefit finding. Self-efficacy partially mediated the relationship between family function and caregiver benefit finding; moreover, care hours per day moderated the mediation. CONCLUSION: This study shows important factors associated with benefit finding in family caregivers of patients with stroke. This indicates elements that could help improve benefit finding intervention programmes for family caregivers of patients with stroke. RELEVANCE TO CLINICAL PRACTICE: The findings in our study provide valuable information on benefit finding and indicate some interventions to improve the mental health of family caregivers of stroke patients.

Characteristics of inflammatory factors and lymphocyte subsets in patients with severe COVID-19.

To investigate the inflammatory factors and lymphocyte subsets which play an important role in the course of severe coronavirus disease 2019 (COVID-19). A total of 27 patients with severe COVID-19 who were admitted to Tongji Hospital in Wuhan from 1 to 21 February 2020 were recruited to the study. The characteristics of interleukin-1ß (IL-1ß), IL-2 receptor (IL-2R), IL-6, IL-8, IL-10, tumor necrosis factor-α (TNF)-α, C-reactive protein (CRP), serum ferritin and procalcitonin (PCT), and lymphocyte subsets of these patients were retrospectively compared before and after treatment. Before treatment, there was no significant difference in most inflammatory factors (IL-1ß, IL-2R, IL-6, IL-8, IL-10, CRP, and serum ferritin) between male and female patients. Levels of IL-2R, IL-6, TNF-α, and CRP decreased significantly after treatment, followed by IL-8, IL-10, and PCT. Serum ferritin was increased in all patients before treatment but did not decrease significantly after treatment. IL-1ß was normal in most patients before treatment. Lymphopenia was common among these patients with severe COVID-19. Analysis of lymphocyte subsets showed that CD4+ and particularly CD8+ T lymphocytes increased significantly after treatment. However, B lymphocytes and natural killer cells showed no significant changes after treatment. A pro-inflammatory response and decreased level of T lymphocytes were associated with severe COVID-19.

MicroRNA-29a-3p Prevents Drug-Induced Acute Liver Failure through Inflammation-Related Pyroptosis Inhibition.

OBJECTIVE: Little is known about the role of microRNA-29a-3p (miR-29a-3p) in inflammation-related pyroptosis, especially in drug-induced acute liver failure (DIALF). This study aimed to identify the relationship between miR-29a-3p and inflammation-related pyroptosis in DIALF and confirm its underlying mechanisms. METHODS: Thioacetamide (TAA)- and acetaminophen (APAP)-induced ALF mouse models were established, and human samples were collected. The expression levels of miR-29a-3p and inflammation and pyroptosis markers were measured by quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, or immunochemical staining in miR-29a-3p knock-in transgenic mouse (MIR29A(KI/KI)) DIALF models. In addition, RNA sequencing was conducted to explore the mechanisms. RESULTS: MiR-29a-3p levels were decreased in TAA- and APAP-induced DIALF models. MiR-29a-3p prevented DIALF caused by TAA and APAP. RNA sequencing and further experiments showed that the protective effect of miR-29a-3p on DIALF was mainly achieved through inhibition of inflammation-related pyroptosis, and the inhibition was dependent on activation of the PI3K/AKT pathway. In addition, miR-29a-3p levels were reduced, and pyroptosis was activated in both peripheral blood mononuclear cells and liver tissues of DIALF patients. CONCLUSION: The study supports the idea that miR-29a-3p inhibits pyroptosis by activating the PI3K/AKT pathway to prevent DIALF. MiR-29a-3p may be a promising therapeutic target for DIALF.