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As a financial instrument and a crucial component of the environmental governance system, the comprehensive impacts of green credit on both the economy and the environment remain unclear. This study examines Chinese provincial data from 2001 to 2018 and employs multiple models to assess the dynamic effects of green credit on carbon productivity. The findings indicate a significant positive influence of green credit on carbon productivity within local and surrounding areas. Furthermore, the promotion effect of green credit on carbon productivity is mainly through energy structure transformation, upgrading of industrial structure and green technology innovation. Interestingly, when considering the spatiotemporal aspect, we observe an initial marginal negative impact of green credit on carbon productivity, which subsequently transitions to a positive effect. The regions demonstrating the highest positive impacts of green credit are primarily concentrated in the southwestern region rich in renewable energy and the economically developed eastern coastal region. [ABSTRACT FROM AUTHOR]

Background: Respiratory syncytial virus (RSV) causes the most common type of severe lower respiratory tract infection worldwide, and the fusion (F) protein is a target for neutralizing antibodies and vaccine development. This study aimed to investigate the immunogenicity and efficacy of an mRNA-based RSV vaccine with an F protein sequence. Methods: We designed an mRNA construct encoding a modified RSV F protein, which was further developed into an LNP-encapsulated mRNA vaccine (LVRNA007). LVRNA007 was administered to mice and cotton rats, followed by immunogenicity analysis and viral challenge studies. Protection of rodents from the viral infection was evaluated based on the presence of the virus in the lung and pathological examination of respiratory tissues. Results: LVRNA007 induced robust humoral and cellular immune responses in both mice and cotton rats, with neutralization antibody levels in the immunized animals maintained at high levels for over one year. Vaccination of LVRNA007 also protected the rodents from RSV challenge, judged by the much decreased virus titer and the pathological score in the lung tissue. In addition, no vaccine-enhanced disease (VED) phenomenon was observed with LVRNA007 vaccination. Conclusions: Based on the preclinical immunogenicity and efficacy data, LVRNA007 could be a potential promising vaccine for prophylaxis of RSV infection. [ABSTRACT FROM AUTHOR]

Background: Intervertebral disc degeneration (IVDD) is a major cause of low back pain (LBP), worsened by chronic inflammatory processes associated with aging. Tumor necrosis factor alpha (Tnf‐α) and its receptors, Tnf receptor type 1 (Tnfr1) and Tnf receptor type 2 (Tnfr2), are upregulated in IVDD. However, its pathologic mechanisms remain poorly defined. Methods: To investigate the role of Tnfr in IVDD, we generated global Tnfr1/2 double knockout (KO) mice and age‐matched control C57BL/6 male mice, and analyzed intervertebral disc (IVD)‐related phenotypes of both genotypes under physiological conditions, aging, and lumbar spine instability (LSI) model through histological and immunofluorescence analyses and μCT imaging. Expression levels of key extracellular matrix (ECM) proteins in aged and LSI mice, especially markers of cell proliferation and apoptosis, were evaluated in aged (21‐month‐old) mice. Results: At 4 months, KO and control mice showed no marked differences of IVDD‐related parameters. However, at 21 months of age, the loss of Tnfr expression significantly alleviated IVDD‐like phenotypes, including a significant increase in height of the nucleus pulposus (NPs) and reductions of endplates (EPs) porosity and histopathological scores, when compared to controls. Tnfr deficiency promoted anabolic metabolism of the ECM proteins and suppressed ECM catabolism. Tnfr loss largely inhibited hypertrophic differentiation, and, in the meantime, suppressed cell apoptosis and cellular senescence in the annulus fibrosis, NP, and EP tissues without affecting cell proliferation. Similar results were observed in the LSI model, where Tnfr deficiency significantly alleviated IVDD and enhanced ECM anabolic metabolism while suppressing catabolism. Conclusion: The deletion of Tnfr mitigates age‐related and LSI‐induced IVDD, as evidenced by preserved IVD structure, and improved ECM integrity. These findings suggest a crucial role of Tnf‐α/Tnfr signaling in IVDD pathogenesis in mice. Targeting this pathway may be a novel strategy for IVDD prevention and treatment. [ABSTRACT FROM AUTHOR]