Translation, cultural adaptation and validation of the Chinese version of the Carer Support Needs Assessment Tool for family caregivers of cancer patients receiving home-based hospice care.

BACKGROUND: Family caregivers need to be supported in caring for patients at the end of life, but practical tools to assess their support needs have been missing in China. So this study aimed to culturally adapt and validate the Carer Support Needs Assessment Tool (CSNAT). METHODS: Cross-cultural adaptation of the original CSNAT for a Chinese setting was performed according to Brislin's translation guidelines. A pilot study was conducted with 15 Chinese family caregivers of cancer patients receiving hospice home care and 5 medical staff. A cross-sectional survey of 205 family caregivers was conducted from December 2018 to May 2019 at a home-based hospice care institute in Shenzhen, China. The validation procedure comprised the establishment of (1) content validity by a group of six experts; (2) face validity by 15 family caregivers; (3) criterion validity by calculating Spearman's correlations between the CSNAT and caregiving burden, caregiving preparedness and quality of life scales; (4) internal consistency using Cronbach's alpha. RESULTS: The CSNAT demonstrated good face validity and good content validity. CSNAT scores showed clear positive correlations with caregiving burden and negative correlations with preparedness for caregiving and quality of life. Internal consistency was high (Cronbach's alpha = 0.899), although such reliability testing is not recommended for this tool. CONCLUSIONS: The Chinese version of the CSNAT is a valid tool that is appropriate for identifying needs of family caregivers of cancer patients in home-based hospice care.

Talin mechanotransduction in disease.

Talin protein (Talin 1/2) is a mechanosensitive cytoskeleton protein. The unique structure of the Talin plays a vital role in transmitting mechanical forces. Talin proteins connect the extracellular matrix to the cytoskeleton by linking to integrins and actin, thereby mediating the conversion of mechanical signals into biochemical signals and influencing disease progression as potential diagnostic indicators, therapeutic targets, and prognostic indicators of various diseases. Most studies in recent years have confirmed that mechanical forces also have a crucial role in the development of disease, and Talin has been found to play a role in several diseases. Still, more studies need to be done on how Talin is involved in mechanical signaling in disease. This review focuses on the mechanical signaling of Talin in disease, aiming to summarize the mechanisms by which Talin plays a role in disease and to provide references for further studies.

Low shear stress induces inflammatory response via CX3CR1/NF-κB signal pathway in human umbilical vein endothelial cells.

Low shear stress (LSS) has been reported to induce atherosclerosis. However, the molecular mechanisms underlying inflammation induced by LSS are still poorly understood. The objective of our study is the comprehensive identification of molecular circuitry involved in low shear stress-induced inflammation in human umbilical vein endothelial cells (HUVECs) through protein profiling and cell function experiment. In this study, Western blotting analyses revealed a significant increase in the expression of CX3CR1, nucleusP65, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and Interleukin-6 (IL-6), while the expression of cytosolic P65 and IκB has significantly decreased in HUVECs treated with low shear stress. CX3CR1 Sh-RNA was use to reveal its effect on LSS-induced inflammation. Further, specific NF-κB P65 inhibitors pyrrolidinedithiocarbamate (PDTC) were used to reveal the downstream NF-κB P65 exclusively involved in LSS-induced inflammation in HUVECs, this effect can be abrogated by CX3CR1 sh-RNA and NF-κB inhibitors. Monocyte adhesion assay and scratch test revealed low shear stress to promotes adhesion of monocytes and migration of cells, this effect can be abrogated by CX3CR1 sh-RNA and NF-κB inhibitors. LSS was involved in the expression of adhesion molecules and chemokines, which are important for the initiation of endothelial inflammation-related atherosclerosis. Therefore, the cell signaling pathways activated by LSS in endothelial cells may represent therapeutic targets of atherosclerosis.

Promising remedies for cardiovascular disease: Natural polyphenol ellagic acid and its metabolite urolithins.

BACKGROUND: Cardiovascular disease (CVD) is a significant worldwide factor contributing to human fatality and morbidity. With the increase of incidence rates, it is of concern that there is a lack of current therapeutic alternatives because of multiple side effects. Ellagic acid (EA), the natural polyphenol (C14H6O8), is abundant in pomegranates, berries, and nuts. EA and its intestinal microflora metabolite, urolithins, have recently attracted much attention as a potential novel "medicine" because of their wide pharmacological properties. PURPOSE: This study aimed to critically analyze available literature to summarize the beneficial effects of EA and urolithins, and highlights their druggability and therapeutic potential in various CVDs. METHODS: We systematically studied research and review articles between 1984 and 2022 available on various databases to obtain the data on EA and urolithins with no language restriction. Their cardiovascular protective activities, underlying mechanism, and druggability were highlighted and discussed comprehensively. RESULTS: We found that EA and urolithins may exert preventive and curative effects on CVD with negligible side effects and possibly regulate lipid metabolism imbalance, pro-inflammatory factor production, vascular smooth muscle cell proliferation, cardiomyocyte apoptosis, endothelial cell dysfunction, and Ca2+ intake and release. Potentially, this may lead to the prevention and amelioration of atherosclerosis, hypertension, myocardial infarction, cardiac fibrosis, cardiomyopathy, cardiac arrhythmias, and cardiotoxicities in vivo. Several molecules and signaling pathways are associated with their therapeutic actions, including phosphatidylinositol 3-kinase/protein kinase B, mitogen-activated protein kinase, NF-κB, nuclear factor erythroid-2 related factor 2, sirtuin1, miRNA, and extracellular signal-regulated kinase 1/2. CONCLUSION: In vitro and in vivo studies shows that EA and urolithins could be used as valid candidates for early prevention and effective therapeutic strategies for various CVDs.