Rabies, for which the mortality rate is almost 100%, is a zoonotic viral disease that can be transmitted via solid organs or tissue allotransplantation. Dozens of deaths from rabies via solid organs or tissues allotransplantation (ROTA) have been documented during the last decades. In 2015 and 2016, two cases of rabies virus transmission via solid organs or tissue allotransplantation were reported in China, which further underscore the risk and importance of this special type of rabies for organ transplant recipients. From 1978 to 2017, at least 13 cases of ROTA, causing dozens of deaths, have been reported worldwide, whether in the high-risk or low-risk countries of rabies. The reported incubation period of ROTA ranges from 11 days to more than 17 months, while the historical incubation period of rabies is generally considered to range from ~ 1 week to several years. The pathogenesis of ROTA is not clear, but the use of post-exposure prophylaxis (PEP) can play a protective role in the transplant recipients. We also summarize reports about ROTA in China, combined with the actual situation regarding work on rabies surveillance and elimination, and suggest countermeasures for the prevention and control of ROTA in the future. Understanding the significance of ROTA, screening the suspected organs, assessing the risk and protecting the related population will be effective way to prevent and control further occurrence of ROTA.

Objective: Obesity-induced precocious puberty presents serious health risks to adolescents. Building on our previous finding that epigallocatechin gallate (EGCG) exhibits a preventive effect on obesity-induced precocious puberty, the present study aims to elucidate the underlying molecular mechanisms. Methods: Female C57BL/6 mice were divided into four groups: control, normal diet + EGCG, high-fat diet (HFD), and HFD + EGCG. Body weight, vaginal opening time, and serum samples were analyzed to assess the effects of EGCG on obesity-induced precocious puberty, using serum metabolomics and molecular docking. Results: EGCG treatment significantly altered the serum metabolite profile, particularly affecting lipid metabolism. Glycerophospholipid metabolism emerged as the key pathway modulated by EGCG. Molecular docking identified phosphatidylserine decarboxylase, phospholipase D, and phosphatidylserine synthase as potential targets. Conclusion: EGCG prevents obesity-induced precocious puberty, an effect associated with the reshaping of lipid metabolism, with key enzymes in the glycerophospholipid metabolism serving as potential therapeutic targets. These findings provide a foundational hypothesis for further mechanistic investigation.