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Small and medium-sized enterprises (SMEs) were an important part of China's economy, but they faced challenges to growth due to financing difficulties. Government subsidies are considered as a potential way to address this problem. This study aims to assess the effectiveness of the Chinese government's subsidy program aimed at improving the accessibility of financing for SMEs. We analyze a comprehensive dataset of Chinese firms' subsidy programs from 2011 to 2020. We classify subsidies into unconditional and conditional categories and use fixed-effects regression models to control for the effects of time and between-group variation to more accurately assess the effectiveness of government subsidies. In addition, we use a PSM-DID model to reduce the effect of selectivity bias to more accurately estimate the causal effect of subsidies on financing strategies. We also use a mediated effects model to help understand the mechanisms by which different types of subsidies affect financing strategies. The results show that government subsidies can significantly improve SMEs' financing ability, but different types of subsidies produce subtle differences. Conditional subsidies support debt financing mainly through incentives, while unconditional subsidies help SMEs improve their equity financing ability through information effects. Furthermore, we find that over-reliance on a single subsidy type may reduce its effectiveness, suggesting a complex relationship between government intervention and SME financing. Thus, well-designed policies are crucial for promoting SMEs and fostering economic growth. [ABSTRACT FROM AUTHOR]

The interrelated side reactions and dendrites growth severely destabilize the electrode/electrolyte interfaces, resulting in the difficult application of aqueous Zn ion batteries (AZIBs). Hydrophobic protective layer possesses natural inhibition ability for side reactions. However, the conventional protective layer with plane structure is difficult to attain joint regulation of side reaction and Zn nucleation. Herein, a novel three‐dimensional (3D) electrically conductive and hydrophobic (3DECH) interface is elaborated to enable stable Zn anode. The as‐prepared 3DECH interface presents a uniform 3D morphology with hydrophobic property, large specific surface area, abundant zincophilic sites, and excellent electroconductivity. Therefore, the 3DECH interface achieves uniform nucleation and dendrite‐free deposition from synergetic benefits: (1) increased nucleation sites and reduced local current density through the special 3D structure and (2) uniform electric potential distribution and rapid Zn2+ transport due to the electroconductive alloy chemistry, thus coupling the hydrophobic property to obtain a highly reversible Zn anode. Consequently, the modified anode achieves a superior coulombic efficiency of 99.88% over 3500 cycles, and the pouch cells using modified anode and LiMn2O4 (LMO) cathode retain a capacity of 84 mAh g−1 after 700 cycles at a reasonable depth discharge of 36%, without dendrite piercing and "dead Zn." [ABSTRACT FROM AUTHOR]

Aims: Dexmedetomidine (DEX) has been reported to alleviate hypoxic–ischemic brain damage (HIBD) in neonates. This study aimed to investigate whether DEX improves cognitive impairment by promoting hippocampal neurogenesis via the BDNF/TrkB/CREB signaling pathway in neonatal rats with HIBD. Methods: HIBD was induced in postnatal day 7 rats using the Rice‐Vannucci method, and DEX (25 μg/kg) was administered intraperitoneally immediately after the HIBD induction. The BDNF/TrkB/CREB pathway was regulated by administering the TrkB receptor antagonist ANA‐12 through intraperitoneal injection or by delivering adeno‐associated virus (AAV)‐shRNA‐BDNF via intrahippocampal injection. Western blot was performed to measure the levels of BDNF, TrkB, and CREB. Immunofluorescence staining was utilized to identify the polarization of astrocytes and evaluate the levels of neurogenesis in the dentate gyrus of the hippocampus. Nissl and TTC staining were performed to evaluate the extent of neuronal damage. The MWM test was conducted to evaluate spatial learning and memory ability. Results: The levels of BDNF and neurogenesis exhibited a notable decrease in the hippocampus of neonatal rats after HIBD, as determined by RNA‐sequencing technology. Our results demonstrated that treatment with DEX effectively increased the protein expression of BDNF and the phosphorylation of TrkB and CREB, promoting neurogenesis in the dentate gyrus of the hippocampus in neonatal rats with HIBD. Specifically, DEX treatment significantly augmented the expression of BDNF in hippocampal astrocytes, while decreasing the proportion of detrimental A1 astrocytes and increasing the proportion of beneficial A2 astrocytes in neonatal rats with HIBD. Furthermore, inhibiting the BDNF/TrkB/CREB pathway using either ANA‐12 or AAV‐shRNA‐BDNF significantly counteracted the advantageous outcomes of DEX on hippocampal neurogenesis, neuronal survival, and cognitive improvement. Conclusions: DEX promoted neurogenesis in the hippocampus by activating the BDNF/TrkB/CREB pathway through the induction of polarization of A1 astrocytes toward A2 astrocytes, subsequently mitigating neuronal damage and cognitive impairment in neonates with HIBD. [ABSTRACT FROM AUTHOR]

The commercial application of lithium (Li) metal anode is hindered by the growth of Li dendrites. Here, we develop a multidimensional composite structure composed of Co3O4/NiO heterojunction particles and reduced graphene oxide (rGO) nanosheets, that allows Li to nucleate and deposit selectively in one direction. Among, two transition metal oxides (TMOs) without lithiophilicity are transformed into lithiophilic species due to the rich phase boundaries and high Li adsorption energies on interfaces, which can provide uniform active sites and reduce nucleation overpotential for Li deposition. Meanwhile, the rGO substrate with high electrical conductivity and large specific surface area can form a conductive network between TMOs and alleviate volume expansion caused by Li deposition. Benefitting from the synergistic effect of the heterojunctions and carbon substrate, the Co3O4/NiO‐rGO regulates the local current density and enables the dendrite‐free Li plating/stripping behavior. At a current density of 1 mA cm−2, the Li metal anode with the Co3O4/NiO‐rGO host exhibits remarkable electrochemical performance, consistently maintaining high Coulombic efficiency (>93.8%) over 1000 cycles. Additionally, the full cells matched with LiFePO4 cathode also display high rate capability of 130 mAh g−1 at 1 C and stable cycling life over 500 cycles. [ABSTRACT FROM AUTHOR]

Background: Quantitative detection of glucose-6-phosphate dehydrogenase (G6PD) is commonly done to screen for G6PD deficiency. However, current reference intervals (RIs) of G6PD are unsuitable for evaluating G6PD-activity levels with local populations or associating G6PD variants with hemolysis risk to aid clinical decision-making. We explored appropriate RIs and clinical decision limits (CDLs) for G6PD activity in individuals from Guangzhou, China., Methods: We enrolled 5,852 unrelated individuals between 2020 and 2022 and screened their samples in quantitative assays for G6PD activity. We conducted further investigations, including G6PD genotyping, thalassemia genotyping, follow-up analysis, and statistical analysis, for different groups., Results: In Guangzhou, the RIs for the G6PD activities were 11.20-20.04 U/g Hb in male and 12.29-23.16 U/g Hb in female. The adjusted male median and normal male median (NMM) values were 15.47 U/g Hb and 15.51 U/g Hb, respectively. A threshold of 45% of the NMM could be used as a CDL to estimate the probability of G6PD variants. Our results revealed high hemolysis-risk CDLs (male: <10% of the NMM, female: <30% of the NMM), medium hemolysis-risk CDLs (male: 10%-45% of the NMM, female: 30%-79% of the NMM), and low hemolysis-risk CDLs (male: ≥ 45% of the NMM, female: ≥ 79% of the NMM)., Conclusions: Collectively, our findings contribute to a more accurate evaluation of G6PD-activity levels within the local population and provide valuable insights for clinical decision-making. Specifically, identifying threshold values for G6PD variants and hemolysis risk enables improved prediction and management of G6PD deficiency, ultimately enhancing patient care and treatment outcomes.

MEX3A is an RNA-binding protein that mediates mRNA decay through binding to 3' untranslated regions. However, its role and mechanism in clear cell renal cell carcinoma remain unknown. In this study, we found that MEX3A expression was transcriptionally activated by ETS1 and upregulated in clear cell renal cell carcinoma. Silencing MEX3A markedly reduced clear cell renal cell carcinoma cell proliferation in vitro and in vivo . Inhibiting MEX3A induced G1/S cell-cycle arrest. Gene set enrichment analysis revealed that E2F targets are the central downstream pathways of MEX3A. To identify MEX3A targets, systematic screening using enhanced cross-linking and immunoprecipitation sequencing, and RNA-immunoprecipitation sequencing assays were performed. A network of 4,000 genes was identified as potential targets of MEX3A. Gene ontology analysis of upregulated genes bound by MEX3A indicated that negative regulation of the cell proliferation pathway was highly enriched. Further assays indicated that MEX3A bound to the CDKN2B 3' untranslated region, promoting its mRNA degradation. This leads to decreased levels of CDKN2B and an uncontrolled cell cycle in clear cell renal cell carcinoma, which was confirmed by rescue experiments. Our findings revealed that MEX3A acts as a post-transcriptional regulator of abnormal cell-cycle progression in clear cell renal cell carcinoma., Competing Interests: The authors declare no competing interests., (© 2021 The Author(s).)