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This study develops a multi‐stage stochastic model to forecast the issuance of green bonds using the Filtered Historical Simulation (FHS) method to identify the most cost‐effective conditions for issuing these bonds amid various risk factors. Drawing on historical yield data and financial metrics of corporate green bonds from December 2014 to June 2023, the model considers fluctuating elements such as risk probabilities, financial risks in worst‐case scenarios, and liquidity risks at upcoming issuance moments. Our findings reveal the model's effectiveness in pinpointing the lowest possible costs of issuing new green bond portfolios in the future, while also addressing expected financial risk, risk occurrence probability, and liquidity issues. The results provide issuers with the insights needed to accurately time the market, tailor bond maturities according to a corporation's future risk profile, and enhance liquidity management. Notably, our model indicates that refining the estimated probability of future risk occurrences can lead to significant savings in green bond issuance costs. This approach allows for adaptable bond issuance strategies, addresses inherent debt, and enables detailed risk management, offering substantial benefits for green enterprises navigating the complexities of future financial landscapes. [ABSTRACT FROM AUTHOR]

Clostridium perfringens (C. perfringens), a Gram-positive bacterium, produces a variety of toxins and extracellular enzymes that can lead to disease in both humans and animals. Common symptoms include abdominal swelling, diarrhea, and intestinal inflammation. Severe cases can result in complications like intestinal hemorrhage, edema, and even death. The primary toxins contributing to morbidity in C. perfringens-infected intestines are CPA, CPB, CPB2, CPE, and PFO. Amongst these, CPB, CPB2, and CPE are implicated in apoptosis development, while CPA is associated with cell death, increased intracellular ROS levels, and the release of the inflammatory factor IL-18. However, the exact mechanism by which PFO toxins exert their effects in the infected gut is still unidentified. This study demonstrates that a C. perfringens PFO toxin infection disrupts the intestinal epithelial barrier function through in vitro and in vivo models. This study emphasizes the notable influence of PFO toxins on intestinal barrier integrity in the context of C. perfringens infections. It reveals that PFO toxins increase ROS production by causing mitochondrial damage, triggering pyroptosis in IPEC-J2 cells, and consequently resulting in compromised intestinal barrier function. These results offer a scientific foundation for developing preventive and therapeutic approaches against C. perfringens infections. [ABSTRACT FROM AUTHOR]

Zoonoses are diseases and infections naturally transmitted between humans and vertebrate animals. They form the dominant group of diseases among emerging infectious diseases and represent critical threats to global health security. This dilemma is largely attributed to our insufficient knowledge of the pathogenesis regarding zoonotic spillover. Long non-coding RNAs (lncRNAs) are transcripts with limited coding capacity. Recent technological advancements have enabled the identification of numerous lncRNAs in humans, animals, and even pathogens. An increasing body of literature suggests that lncRNAs function as key regulators in zoonotic infection. They regulate immune-related epigenetic, transcriptional, and post-transcriptional events across a broad range of organisms. In this review, we discuss the recent research progress on the roles of lncRNAs in zoonoses. We address the classification and regulatory mechanisms of lncRNAs in the interaction between host and zoonotic pathogens. Additionally, we explore the surprising function of pathogen-derived lncRNAs in mediating the pathogenicity and life cycle of zoonotic bacteria, viruses, and parasites. Understanding how these lncRNAs influence the zoonotic pathogenesis will provide important therapeutic insights to the prevention and control of zoonoses. [ABSTRACT FROM AUTHOR]