Intracerebral hemorrhage (ICH) is a common and devastating disease affecting millions of people worldwide annually. Exaggerated inflammation and apoptosis are two pivotal pathological processes for secondary brain injury after ICH. Quercetin, a flavonoid widely distributed in various herbs, fruits and vegetables, has been proved to improve neuronal functional recovery in spinal cord injury rats. However, the efficacy of quercetin in caring for post-ICH brain injury has not been investigated. In the present study, we established an ICH model by injecting type VII bacterial collagenase (0.5U) into the central striatum of male Sprague-Dawley rats. The animals were randomized to four groups: sham-operation group; ICH + vehicle group; ICH + 5 mg/kg quercetin group; and ICH + 50 mg/kg quercetin group. The expression levels of IL-1β, IL-4, IL-6 and TNF-α in the brain tissue were assayed by Real-time PCR, ELISA and Western Blot, and cell apoptosis was assayed by TUNEL and caspase-3 staining 3 days after model establishment. It was found that the lesion volume, the brain water content, the expression levels of the four inflammation markers and the number of apoptotic cells were reduced significantly in ICH rats receiving quercetin, especially in 50 mg/kg quercetin group. These results confirmed the therapeutic efficacy of quercetin in repairing brain injury, probably by inhibiting inflammatory response and apoptosis, thus promoting nerve functional restoration.

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Transplanted human umbilical cord mesenchymal stem cells (hUC-MSCs) have exhibited considerable therapeutic potential for traumatic brain injury (TBI). However, how hUC-MSCs migrating to the injury region and the mechanism of hUC-MSCs promoting functional recovery after TBI are still unclear. In this study, we investigated whether stromal cell-derived factor-1 (SDF-1) was involved in the hUC-MSCs migration and the possible mechanisms that might be involved in the beneficial effect on functional recovery. In vitro experiments demonstrated that SDF-1 induces a concentration-dependent migration of hUC-MSCs. Furthermore, pre-treatment with the CXCR4-specific antagonist AMD3100 significantly prevented the migration of hUC-MSCs in vitro. We found that the expression of SDF-1 increased significantly around the damaged area. Transplanted hUC-MSCs were localized to regions where SDF-1 was highly expressed. Additionally, our results showed that hUC-MSCs-treated animals showed significantly improved functional recovery compared with controls. In hUC-MSCs-transplanted group, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells were decreased and BrdU-positive cells were significantly increased compared with control group, more of BrdU-positive cells co-localized with GFAP. These suggest that SDF-1 plays an important role in the migration of hUC-MSCs to the damaged area and hUC-MSCs are beneficial for functional recovery after TBI.

Clinical laboratory, and treatment data of inpatients with laboratory-confirmed COVID-19 were collected and analyzed. Outcomes of patients with and without pre-existing diabetes were compared. The associations of diabetes history and/or FBG levels with mortality were analyzed. Multivariate cox regression analysis on the risk factors associated with mortality in patients with COVID-19 was performed. Results: A total of 941 hospitalized patients with COVID-19 were enrolled in the study. There was a positive relationship between pre-existing diabetes and the mortality of patients who developed COVID-19 (21 of 123 [17.1%] vs 76 of 818 [9.3%]; P = 0.012). FBG !7.0 mmol/L was an independent risk factor for the mortality of COVID-19 regardless of the presence or not of a history of diabetes (hazard ratio, 2.20 [95% CI, 1.21-4.03]; P = 0.010). Conclusions: We firstly showed FBG !7.0 mmol/L predicted worse outcome in hospitalized patients with COVID-19 independent of diabetes history. Our findings indicated screening FBG level is an effective method to evaluate the prognosis of patients with COVID-19.

Baicalein could serve as a promising agent for treatment of HPSs and a selective ALK5 inhibitor.

The domestic surgical robot system which was verified as safe and effective through these trials. The proposed design method is an effective way to solve some of drawbacks that exist in the former generations of the da Vinci surgical system.

The pathogenesis and therapy of hypertrophic scars (HS) have not yet been established. The aim of the present study was to investigate the potential effect of naringenin on HS and its underlying mechanisms. The mouse model of HS was prepared by a mechanical stretch device and then treated with naringenin at various concentrations. Histological studies were performed to evaluate scar hypertrophy by hematoxylin and eosin, as well as Masson's trichrome staining. The activation of HS fibroblasts was determined based on reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blotting and immunohistochemical staining. Following observing the retention of inflammation cells by immunohistochemistry, the cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and transforming growth factor (TGF)-β1, mRNA and protein levels were quantitated by RT-qPCR, ELISA and western blotting methods. As a result, naringenin significantly inhibited the formation of HS in a concentration-dependent manner. In addition, naringenin inhibited fibroblast activation and inflammatory cell recruitment. In addition, mRNA and protein expression levels of TNF-α, IL-1β, IL-6 and TGF-β1 were downregulated following naringenin treatment. The current study highlighted a new pharmacological activity of naringenin on HS. The mechanism of action of naringenin was associated with the inhibition of fibroblast activation and local inflammation. These results suggested that naringenin may serve as a novel agent for treatment of HS.

Obesity is associated with increased risks of diverse diseases; brown adipose tissue (BAT) can increase energy expenditure and protect against obesity by increasing the decomposition of white adipose tissue (WAT) to enhance the non-coupled oxidative phosphorylation of fatty acid in adipocytes and contributes to weight loss. However, BAT is abundant in only small rodents and newborn humans, but not in adults. PRDM16 is a key factor that induces the differentiation of skeletal muscle precursors to brown adipocytes and simultaneously inhibits myogenic differentiation. In the present study, we set insulin-induced skeletal muscle satellite cells (SMSCs) adipogenic differentiation model, as confirmed by the contents of adipogenic markers PRDM16, UCP1 and PGC1α and myogenic markers MyoD1 and MyoG. We selected miR-499 as candidate miRNA, which might regulate PRDM16 to affect SMSCs adipogenic differentiation. Possibly through directly binding to PRDM16 3'-UTR, miR-499 negatively regulated PRDM16 expression and hindered SMSCs adipogenic differentiation by reducing adipogenic markers PRDM16, UCP1 and PGC1α and increasing myogenic markers MyoD1 and MyoG. PRDM16 overexpression could partially reverse the effect of miR-499 on the above markers and SMSCs adipogenic differentiation. Taken together, miR-499/PRDM16 axis can affect the balance between SMSC myogenic and adipogenic differentiation, targeting miR-499 to rescue PRDM16 expression, thus promoting SMSCs adipogenic differentiation may be a promising strategy for obesity treatment.