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Highlights: The [W–O] group with strong adsorption capacity is introduced into CoP to fabricate a bi-functional catalyst towards HER and HzOR. The cell voltage of HzOR coupled electrolyzer with 6W–O–CoP/NF as both anode and cathode catalysts is 1.634 V lower than that of the water splitting system at 100 mA cm−2. A proof-of-concept self-powered H2 production system is assembled to realize the H2 evolution rate of 3.53 mmol cm−2 h−1. Hydrazine oxidation reaction (HzOR) assisted hydrogen evolution reaction (HER) offers a feasible path for low power consumption to hydrogen production. Unfortunately however, the total electrooxidation of hydrazine in anode and the dissociation kinetics of water in cathode are critically depend on the interaction between the reaction intermediates and surface of catalysts, which are still challenging due to the totally different catalytic mechanisms. Herein, the [W–O] group with strong adsorption capacity is introduced into CoP nanoflakes to fabricate bifunctional catalyst, which possesses excellent catalytic performances towards both HER (185.60 mV at 1000 mA cm−2) and HzOR (78.99 mV at 10,00 mA cm−2) with the overall electrolyzer potential of 1.634 V lower than that of the water splitting system at 100 mA cm−2. The introduction of [W–O] groups, working as the adsorption sites for H2O dissociation and N2H4 dehydrogenation, leads to the formation of porous structure on CoP nanoflakes and regulates the electronic structure of Co through the linked O in [W–O] group as well, resultantly boosting the hydrogen production and HzOR. Moreover, a proof-of-concept direct hydrazine fuel cell-powered H2 production system has been assembled, realizing H2 evolution at a rate of 3.53 mmol cm−2 h−1 at room temperature without external electricity supply. [ABSTRACT FROM AUTHOR]

Endometriosis is an immune chronic inflammatory disease, and there are currently no more effective drugs for treating endometriosis due to its unknown etiology. Salbutamol is a β2-adrenergic receptor (β2AR) agonist commonly used to treat asthma by selectively activating β2 receptors on airway smooth muscle and leukocytes, exerting bronchial dilation and synergistic anti-inflammatory effects. In recent years, β2AR agonists have been used in endometriosis studies, and we speculate that salbutamol may have a therapeutic effect on endometriosis. The purpose of this research was to explore the therapeutic effect of salbutamol on endometriosis mice. The mouse endometriosis model was established and treated with different doses of salbutamol. Endometrial lesions were harvested for pathological diagnosis, immunohistochemistry (IHC), Masson staining, and toluidine blue analysis. We found that the number and size of endometriotic lesions were all significantly decreased after 3 weeks of treatment with different doses of salbutamol on endometriosis model mice (P < 0.05). After Salbutamol treatment, the amount of mast cells (toluidine blue) and macrophages (F4/80) in the lesions as well as the expressions of interleukin (IL)-1β, tumor necrosis factor (TNF)-ɑ, platelet-derived growth factor subunit B (PDGFB), CD31, transforming growth factor (TGF)-β, Masson staining, BCL2, TUBB3, substance P (SP), and nerve growth factor (NGF) were significantly reduced (P < 0.05). These results suggested that salbutamol could effectively treat endometriosis in mice by reducing immune inflammatory cells and factors, angiogenesis, and fibrosis, increasing apoptosis of endometriotic lesions, and decreasing neurogenesis. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a chronic joint disorder that causes cartilage degradation and subchondral bone abnormalities. Nangibotide, also known as LR12, is a dodecapeptide with considerable anti-inflammatory properties, but its significance in OA is uncertain. The aim of the study was to determine whether nangibotide could attenuate the progression of OA, and elucidate the underlying mechanism. In vitro experiments showed that nangibotide strongly inhibited TNF-α-induced osteogenic reduction, significantly enhanced osteoblast proliferation and prevented apoptosis in MC3T3-E1 cells. Male C57BL/6 J mice aged 2 months were randomly allocated to three groups: sham, ACLT, and ACLT with nangibotide therapy. Nangibotide suppressed ACLT-induced cartilage degradation and MMP-13 expression. MicroCT analysis revealed that nangibotide attenuated in vivo subchondral bone loss induced by ACLT. Histomorphometry results showed that nangibotide attenuated ACLT-induced osteoblast inhibition; TUNEL assays and immunohistochemical staining of cleaved-caspase3 further confirmed the in vivo anti-apoptotic effect of nangibotide on osteoblasts. Furthermore, we found that nangibotide exerted protective effects by suppressing TGF-β signaling mediated by Smad2/3 to restore coupled bone remodeling in the subchondral bone. In conclusion, the findings suggest that nangibotide might exert a protective effect on the bone-cartilage unit and maybe an alternative treatment option for OA. [ABSTRACT FROM AUTHOR]