Depressive symptoms have been in the limelight for many kinds of people, but few studies have explored positive resources for combating depressive symptoms among Chinese nurses. The purpose of this study is to explore the association between work-family conflict (WFC) and depressive symptoms among Chinese female nurses, along with the mediating and moderating role of psychological capital (PsyCap) in this relationship. This cross-sectional study was completed during the period of September and October 2013. A questionnaire that consisted of the Center for Epidemiologic Studies Depression Scale, the Work-Family Conflict scale and the Psychological Capital Questionnair scale was distributed to nurses in Shenyang, China. A total of 824 individuals (effective response rate: 74.9%) participated. Asymptotic and resampling strategies explored the mediating role of PsyCap in the relationship between WFC and depressive symptoms. Hierarchical linear regression analyses were performed to explore the moderating role of PsyCap. Both WFC and family-work conflict (FWC) were positively related with depressive symptoms. PsyCap positively moderated the relationship of WFC with depressive symptoms. Self-efficacy and hope positively moderated the relationship of WFC with depressive symptoms. PsyCap partially mediated the relationship of FWC with depressive symptoms. Hope and optimism partially mediated the relationship of FWC with depressive symptoms. Work-family conflict, as the risk factor of depressive symptoms, can increase nurses’ depressive symptoms, and PsyCap is a positive resource to combat nurses’ depressive symptoms. PsyCap can aggravate the effects of WFC on depressive symptoms and FWC can impact PsyCap to increase nurses’ depressive symptoms.

Intestinal barrier dysfunction occurs in critical illnesses and involves the inflammatory and hypoxic injury of intestinal epithelial cells. Researchers are still defining the underlying mechanisms and evaluating therapeutic strategies for restoring intestinal barrier function. The anti-inflammatory drug, emodin, has been shown to exert a protective effect on intestinal barrier function; however, its mechanisms of action remain unknown. In this study, we investigated the protective effects of emodin on intestinal barrier function and the underlying mechanisms in intestinal epithelial cells challenged with lipopolysaccharide (LPS) and hypoxia/reoxygenation (HR). To induce barrier dysfunction, Caco-2 monolayers were subjected to HR with or without LPS treatment. Transepithelial electrical resistance and paracellular permeability were measured to evaluate barrier function. The expression of the tight junction (TJ) proteins, zonula occludens (ZO)-1, occludin, and claudin-1, as well as that of hypoxia-inducible factor (HIF)-1α, phospho-IκB-α, phospho-nuclear factor (NF)-κB p65 and cyclooxygenase (COX)-2 was determined by western blot analysis. The results revealed that emodin markedly attenuated the decrease in transepithelial electrical resistance and the increase in paracellular permeability in the Caco-2 monolayers treated with LPS and subjected to HR. Emodin also markedly alleviated the damage caused by LPS and HR (manifested by a decrease in the expression of the TJ protein, ZO-1), and inhibited the expression of HIF-1α, IκB-α, NF-κB and COX-2 in a dose-dependent manner. In conclusion, our data suggest that emodin attenuates LPS-and HR-induced intestinal epithelial barrier dysfunction by inhibiting the HIF-1α and NF-κB signaling pathways and preventing the damage caused to the TJ barrier (shown by the decrease in the expression of ZO-1).

Silybin is one of the main flavonoids produced by milk thistle, which has been used in the treatment of liver diseases. In this study, we examined the protective effects and possible mechanisms of action of silybin in lipopolysaccharide (LPS)-induced lung injury and inflammation. Pre-treatment of mice with silybin significantly inhibited LPS-induced airway inflammatory cell recruitment, including macrophages, T cells and neutrophils. The production of cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in bronchoalveolar fluid and serum was also decreased following treatment with silybin. Elevated cytokine mRNA levels induced by LPS in lung tissue were all suppressed by silybin and lung histological alterations were also improved. In addition, experiments using cells indicated that silybin significantly decreased the mRNA levels and secretion of IL-1β and TNF-α in THP-1 cells. Moreover, the mechanisms responsible for these effects were attributed to the inhibitory effect of silybin on nuclear factor-κB (NF-κB) signaling and NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. The data form our study thus support the utility of silybin as a potential medicine for the treatment of acute lung injury-associated inflammation and pathological changes. Silybin exerts protective effects against lung injury by regulating NF-κB signaling and the NLRP3 inflammasome activation.

Introduction Carbapenem-resistant gram-negative bacteria (CR-GNB) can cause life-threatening infections among abdominal solid organ transplantation (ASOT) recipients. This study aimed to investigate the epidemiology and drug susceptibility of CR-GNB pathogens and identity the risk factors associated with 90-day crude mortality of CR-GNB infections among ASOT recipients. Methods We retrospectively reviewed the clinical characteristics, drug resistance rate, and risk factors associated with mortality in CR-GNB infections among ASOT recipients between August 1, 2013, and August 1, 2020. The Cox regression model was performed to identify the independent risk factors for mortality. Results During the 8-year period, CR-GNB infections occurred in 153 of 1452 (10.5%) recipients, and 23 of 153 (15.0%) patients died. The most common pathogen was Acinetobacter baumannii ( n = 47). The drug resistance rate of CR-GNB pathogens was relatively low to tigecycline (33.3%) and high to other categories (> 60%). There was a significant increasing trend in drug resistance to tigecycline as time went on (from 24 to 40%, P = 0.04). The independent risk factors for mortality were mechanical ventilation (hazard ratio 7.40, 95% confidence interval 2.69–20.38, P < 0.001), septic shock (hazard ratio 7.41, 95% confidence interval 2.86–19.23, P < 0.001), and platelet count < 50,000/mm 3 (hazard ratio 4.00, 95% confidence interval 1.49–10.76, P = 0.006). Conclusion CR-GNB is widespread with high prevalence and mortality rates among ASOT recipients. Mechanical ventilation, septic shock, and low platelet count represent three independent risk factors related to the mortality of ASOT recipients with CR-GNB infection. We suggest that tigecycline may be used under rigorous management because of the significant increasing risk of drug resistance. Supplementary Information The online version contains supplementary material available at 10.1007/s40121-021-00411-z.

ObjectivesTo explore the efficacy of Chinese herbal formula compared with donepezil 5mg/day in patients with mild Alzheimer’s disease (AD).MethodsPatients with mild AD meeting the criteria were randomized into Chinese herbal formula Yishen Huazhuo decoction (YHD) group and donepezil hydrochloride (DH) group during the 24-week trial. The outcomes were measured by ADAS-cog, MMSE, ADL, and NPI with linear mixed-effect models.Results144 patients were randomized. The mean scores of ADAS-cog and MMSE in both YHD group and DH group both improved at the end of the 24-week treatment period. The results also revealed that YHD was better at improving the mean scores of ADAS-cog and MMSE than DH. Linear mixed-effect models with repeated measures showed statistical significance in time × group interaction effect of ADAS-cog and also in time × group interaction effect of MMSE. The data showed YHD was superior to DH in improving the scores and long term efficacy.ConclusionsOur study suggests that Chinese herbal formula YHD is beneficial and effective for cognitive improvement in patients with mild AD and the mechanism might be through reducing amyloid-β (Aβ) plaque deposition in the hippocampus.Trial RegistrationChinese Clinical Trial Registry ChiCTR-TRC-12002846