The future of artificial hibernation medicine:protection of nerves and organs after spinal cord injury

Spinal cord injury is a serious disease of the central nervous system involving irreversible nerve injury and various organ system injuries.At present,no effective clinical treatment exists.As one of the artificial hibernation techniques,mild hypothermia has preliminarily confirmed its clinical effect on spinal cord injury.However,its technical defects and barriers,along with serious clinical side effects,restrict its clinical application for spinal cord injury.Artificial hibernation is a futureoriented disruptive technology for human life support.It involves endogenous hibernation inducers and hibernation-related central neuromodulation that activate particular neurons,reduce the central constant temperature setting point,disrupt the normal constant body temperature,make the body adapt"to the external cold environment,and reduce the physiological resistance to cold stimulation.Thus,studying the artificial hibernation mechanism may help develop new treatment strategies more suitable for clinical use than the cooling method of mild hypothermia technology.This review introduces artificial hibernation technologies,including mild hypothermia technology,hibernation inducers,and hibernation-related central neuromodulation technology.It summarizes the relevant research on hypothermia and hibernation for organ and nerve protection.These studies show that artificial hibernation technologies have therapeutic significance on nerve injury after spinal co rd injury through inflammatory inhibition,immunosuppression,oxidative defense,and possible central protection.It also promotes the repair and protection of res pirato ry and digestive,cardiovascular,locomoto r,urinary,and endocrine systems.This review provides new insights for the clinical treatment of nerve and multiple organ protection after spinal cord injury thanks to artificial hibernation.At present,artificial hibernation technology is not mature,and research fa ces various challenges.Neve rtheless,the effort is wo rthwhile for the future development of medicine.

IL-17A-dependent gut microbiota is essential for regulating diet-induced disorders in mice

The gut microbiota plays a key role in obesity and related metabolic disorders, and multiple factors including diet, host genotype, and age regulate it. Many studies have examined the contribution of extrinsic factors to the regulation of the gut microbiota, but the importance of the host genetic constitution cannot be ignored. Interleukin 17A(IL-17A), a pro-inflammatory cytokine, is important in the defense against infection and diseases. Here, we investigated the association among IL-17, a high-fat diet(HFD), and the gut microbiota. Mice deficient in IL-17A were resistant to diet-induced obesity and related diseases. Compared with the Ⅱ-17^(-/-)mice, wild-type(WT) mice challenged with HFD showed obvious weight fluctuations, such as those seen in type 2 diabetes, and hematological changes similar to those associated with metabolic syndrome. However, housing WT mice and Ⅱ-17a^(-/-)mice together significantly alleviated these symptoms in the WT mice. A metagenomic analysis of the mouse feces indicated that the microbial community compositions of these two groups differed before HFD feeding. The HFD mediated shifts in the gut microbial compositions, which were associated with the mouse phenotypes.We also identified potentially beneficial and harmful species present during this period, and drew networks of the most abundant species. A functional analysis indicated pathway changes in the WT and Ⅱ-17a^(-/-)mice when fed the HFD. Collectively, these data underscore the importance of the host factor IL-17 A in shaping and regulating the gut microbiota, which conversely, influences the host health.