Fatalism as a Mediator of the Association Between Family Resilience and Self-Management Among Patients with Chronic Wounds in China.

Purpose: The purpose of this study was to examine how fatalism acts as a mediator in the correlation between family resilience and self-management among patients with chronic wounds in China. Participants and Methods: This study used a cross-sectional research design. A total of 269 adult patients (18-94 years old) with chronic wounds residing in Wuxi, China participated in this study. Participants completed the Chinese version of the Walsh Family Resilience Questionnaire, 16-item Chinese version of the Fatalism Scale, and Self-Management Scale of Chronic Wound Patients. We conducted correlation and mediation analyses using SPSS 27.0 and PROCESS 4.0. Results: The results indicated family resilience was a significant positive predictor of self-management (ß = 0.7101, p < 0.0001), and the pathway between family resilience and self-management was partially mediated by fatalism (Effect = 0.1432, 95% confidence interval [0.0625, 0.2341]). Conclusion: The results indicated that incorporating spiritual interventions into future person-centered self-management programs could align with the motivation of patients with chronic wounds and their families, and reduce the negative impact of fatalism on health outcomes.

eCASH concept-based care for patients with small-area burns: a pilot randomized controlled trial.

BACKGROUND: Small-area burn is a common but specific type of injury that can still lead to serious complications if not managed properly. Researchers have introduced a number of interventions. OBJECTIVE: The objective of this study was to compare the effects of eCASH concept-based care (ie, eBCare) with those of standard treatment on wound healing in patients with small-area burns. METHODS: In this prospective randomized controlled trial, patients with small-area burns received either eBCare (n = 35) or standard burn treatment (n = 35) for 2 weeks. Pain, anxiety, heart rate, exudate, and wound area were measured during and after dressing changes. Scar color and thickness were assessed 4 years or longer after discharge. RESULTS: The eBCare group had a lower median pain score, anxiety score, and heart rate compared with the control group (P < .001). The eBCare group also had a higher median wound healing rate on day 14 than the control group (P < .05). At follow-up 4 years or more after discharge, the eBCare group had better scar color and thickness than the control group (P < .05). CONCLUSION: The use of eBCare reduced pain and anxiety, accelerated wound healing, and improved scar outcomes in patients with small-area burns, which suggests that eBCare may be a feasible option for this population.

Sequences of Seven Complete Genomes of Human Parvovirus B19.

We are reporting the sequences of seven complete genomes of parvovirus B19, which were extracted from human plasma specimens collected in the United States. The seven B19 genome sequences, which are 5,596 nucleotides long and include the inverted terminal repeats (ITRs), share an identity of 96.73%. Their ITRs can be grouped into two types that have two nucleotide mutations between each other.

TGF-ß3 Promotes MUC5AC Hyper-Expression by Modulating Autophagy Pathway in Airway Epithelium.

Mucus secretion accumulation in the airways may act as a contributing factor for the development of airflow limitation in severe fetal asthma patients. Accumulated evidences showed that transforming growth factor beta (TGF-ß) plays a regulatory role in airway remodeling including mucus hyper-secretion in asthma. However, the detailed molecular mechanisms of TGF-ß3 induced MUC5AC hyper-expression in airway epithelium remains unclear. Here, we demonstrated the pivotal roles of autophagy in regulation of MUC5AC hyper-production induced by TGF-ß3 in airway epithelium. Our experimental data showed that inhibiting autophagy pathway in repeated ovalbumin (OVA) exposed mice exhibited decreased airway hyper-response and airway inflammation, diminishing the expression of Muc5ac and TGF-ß3. Furthermore, our studies demonstrated that autophagy was induced upon exposure to TGF-ß3 and then mediated MUC5AC hyper-expression by activating the activator protein-1 (AP-1) in human bronchial epithelial cells. Finally, Smad2/3 pathway was involved in TGF-ß3-induced MUC5AC hyper-expressions by promoting autophagy. These data indicated that autophagy was required for TGF-ß3 induced airway mucous hyper-production, and that inhibition of autophagy exerted therapeutic benefits for TGF-ß3 induced airway mucus secretion.