Fabrication of a Highly Efficient Wood-Based Solar Interfacial Evaporator with Self-Desalting and Sterilization Performance.

Solar interfacial evaporation based on wood-derived materials has been considered a promising strategy for desalination and wastewater purification. Herein, we adopted delignified wood (DW) as the water transport substrate and lignosulfonate (LS)-modified narrow-band gap semiconductor nickel disulfide (NiS2) as the light-absorbing agent (LS-NiS2) to fabricate a high-efficiency evaporator (LS-NiS2@DW). On the one hand, the high absorbance (>95%) within a broad wavelength range and excellent photothermal conversion efficiency of LS-NiS2 endow efficient solar energy utilization. On the other hand, the hydrophilicity of DW facilitates water activation, which results in a lower evaporation enthalpy of LS-NiS2@DW (1274.4 kJ kg-1) than that of pure water. By combining LS-NiS2 and DW, LS-NiS2@DW achieved an evaporation rate as high as 2.80 kg m-2 h-1 under one sun irradiation (1 kW m-2), and the evaporation efficiency reached 87.4%. Notably, LS-NiS2@DW exhibits a high evaporation rate (2.42-2.69 kg m-2 h-1) in simulated seawater for 24 h with no salt crystals formed on the surface. Moreover, LS-NiS2@DW shows high antibacterial activity with about 90% reduction in bacterial survival rate. This work could provide new perspectives for the design of a high-efficiency wood-based photothermal evaporator.

Effects of Simo decoction on gastric motility of diabetic rats.

BACKGROUND: To investigate the effects of simo decoction (SMD) on the gastric motility of diabetic rats. METHODS: Diabetic rats were gavaged with various doses of SMD (0.15, 1.5, and 3.0 ml/kg/d) or saline, and their blood glucose levels and body weight were monitored. Gastric emptying and antral motility were assessed by phenol red retention and contractions of antral strips, respectively. The levels of substance P (SP), vasoactive intestinal peptide (VIP), and neurogenic nitric oxide synthase (nNOS) in the gastric antrum were determined by real-time polymerase chain reaction and Western blot. RESULTS: Gastric emptying was delayed in diabetic rats (p < 0.01 vs. non-diabetic controls) but accelerated after SMD administration (p < 0.01). The contractions of antral strips were reduced in diabetic rats (p < 0.01 vs. non-diabetic controls) but improved after SMD intervention (p < 0.05). The mRNA expressions of SP, VIP, and nNOS in diabetic rats were downregulated compared with non-diabetic controls (all p < 0.01). Simo decoction treatment did not affect the expression of these factors in diabetic rats. The protein levels of SP, VIP, and nNOS in diabetic rats were decreased (p < 0.01), increased (p < 0.01), and comparable (p > 0.05), respectively, in comparison with non-diabetic controls. Simo decoction administration increased SP protein expression (p < 0.01) and decreased the levels of VIP (p < 0.01) and nNOS (p < 0.01) in diabetic rats. CONCLUSIONS: Simo decoction improved gastric dysmotility of diabetic rats possibly by upregulating SP and downregulating VIP and nNOS.

Apathy as a Risky Neuropsychiatric Syndrome of Progression From Normal Aging to Mild Cognitive Impairment and Dementia: A Systematic Review and Meta-Analysis.

Background: Apathy has been suggested as a potential predictor of mild cognitive impairment (MCI) progression to dementia. Whether it might predict the transition from normal cognitive function to cognitive impairment has been less studied. The current study aimed to provide a comprehensive summary of the evidence on the association between apathy and the transition from normal cognitive function to cognitive impairment. Methods: We searched the PubMed, Embase, and Web of Science databases for longitudinal prospective cohort studies that evaluated apathy at baseline in the cognitively normal population and had cognitive impairment as the outcome. Random effects models were used, and heterogeneity was explored with stratification. The stability of the synthesized result was indicated using sensitivity analysis by excluding one study each time and recalculating the overall effect. Results: Ten studies comprising 26,195 participants were included. Apathy status was available for 22,101 participants. Apathy was present in 1,803 of 22,101 participants (8.16%). Follow-up ranged from 1 to 13 years. The combined odds ratio (OR) of cognitive impairment for patients with apathy was 2.07 (95% CI: 1.43-2.99; I2 = 86%), and the combined hazard ratio was 2.70 (95% CI: 1.38-5.27; I2 = 94%). The OR meta-analyses for different conversion outcomes were MCI (OR = 3.38, 95% CI: 1.57-7.28; I2 =71%), cognitive decline (OR = 1.27, 95% CI: 0.81-2.00; I2 = 64%) and dementia (OR = 2.12, 95% CI: 1.32-3.41; I2 = 86%). Subgroup analysis suggested that the association between apathy and cognitive impairment changed with age, depression adjustments, apathy measurement, and follow-up time. Conclusions: Apathy was associated with a greater than 2-fold increased risk of progression to cognitive impairment in the cognitively normal population. Future interventions targeting apathy management in the general population may reduce the risk of cognitive impairment.

Sedum sarmentosum Total Flavonoids Alleviate Schistosomiasis-Induced Liver Fibrosis by Altering TGF-ß1 and Smad7 Expression.

OBJECTIVES: Schistosomiasis is a parasitic disease that affects over 142 million people worldwide. The main causes of death of schistosomiasis include liver granuloma and secondary hepatic cirrhosis resulting from severe fibrosis. Despite intensive research, controlling liver fibrosis associated with schistosomiasis remains challenging. Sedum sarmentosum total flavonoid (SSTF) is a promising agent to reduce liver fibrosis with an unknown mechanism. Thus, the objectives of this study are to validate its effect on the liver fibrosis caused by schistosomiasis and to explore the underlying molecular mechanism. METHODS: Sixty male Sprague-Dawley rats were randomly divided into six groups: one group of normal control and five groups of liver fibrosis induced by schistosomiasis japonica with or without SSTF or colchicine treatment, the latter serving as the positive control. Liver tissues from each animal were harvested to observe the degree and grade of hepatic fibrosis. We also measured the expression of transforming growth factor-beta 1 (TGF-ß1) and Smad7 using RT-qPCR, Western blot, and immunohistochemistry. RESULTS: Compared with the untreated model group, groups treated with SSTF at all three tested doses had significantly reduced hepatic fibrosis (P < 0.05). Each dose of SSTF also significantly reduced TGF-ß1 protein expression and mRNA levels in the liver tissues (P < 0.05). In contrast, the middle and high doses of SSTF significantly increased Smad7 protein expression and mRNA levels (P < 0.05). Immunohistochemistry showed that each dose of SSTF reduced TGF-ß1 protein expression (P < 0.05). CONCLUSION: Our results demonstrated that SSTF alleviated schistosomiasis japonica-induced hepatic fibrosis by inhibiting the TGF-ß1/Smad7 pathway.

The Influence of Bifidobacterium bifidum and Bacteroides fragilis on Enteric Glial Cell-Derived Neurotrophic Factors and Inflammasome.

Enteric glial cells (EGCs) and enteric glial-derived neurotrophic factor (GDNF) are directly involved in intestinal inflammation. In this study, we sought to examine the possible mechanisms for how Bifidobacterium bifidum (B.b.) and Bacteroides fragilis (B.f.) influence EGC regulation. In this study, lipopolysaccharide (LPS) and interferon-γ (IFN-γ) were used as exogenous stimuli of EGCs to establish an intestinal inflammation model. After stimulation with LPS and IFN-γ, B.b. and B.f. supernatants were used to activate EGCs and to examine EGC immune mechanisms. For this purpose, qRT-PCR, western blotting, and laser scanning confocal microscopy (LSCM) were used to detect the expression of NLRP3, NLRP6, NGF, NT-3, IL-18, IL-1ß, and caspase-1. We found that EGCs, after stimulation with LPS and IFN-γ, could express NLRP3, NLRP6, NT-3, NGF, IL-18, IL-1ß, and caspase-1 through LSCM. In intestinal inflammation, B.b. and B.f. could trigger an increase in NGF and NT-3 expression in EGCs in order to protect the intestine. Furthermore, B.b. and B.f. could upregulate NLRP3 expression in EGCs and promote an inflammatory response. B.b. had a dual regulatory role in EGC NLRP6 expression, while B.f. inhibited NLRP6 protein expression. Moreover, B.b. could decrease the expression of IL-18, IL-1ß, and caspase-1 in EGCs in order to inhibit the inflammatory response. Contrary to this, B.f. could upregulate IL-18, IL-1ß, and caspase-1 expression in EGCs in order to promote the inflammatory response. B.b. and B.f. can influence the expression of NGF, NT-3, NLRP3, NLRP6, IL-18, IL-1ß, and caspase-1 in EGCs in order to inhibit or promote intestinal inflammation.