Traumatic brain injury (TBI), particularly explosive blast-induced TBI (bTBI), has become the most prevalent injury among military personnel. The disruption of cognitive function is one of the most serious consequences of bTBI because its long-lasting effects prevent survivors fulfilling their active duty and resuming normal civilian life. However, the mechanisms are poorly understood and there is no treatment available. This study investigated the effects of adenosine A2A receptor (A2AR) on bTBI-induced cognitive deficit, and explored the underlying mechanisms. After being subjected to moderate whole-body blast injury, mice lacking the A2AR (A2AR knockout (KO)) showed less severity and shorter duration of impaired spatial reference memory and working memory than wild-type mice did. In addition, bTBI-induced cortical and hippocampal lesions, as well as proinflammatory cytokine expression, glutamate release, edema, cell loss, and gliosis in both early and prolonged phases of the injury, were significantly attenuated in A2AR KO mice. The results suggest that early injury and chronic neuropathological damages are important mechanisms of bTBI-induced cognitive impairment, and that the impairment can be attenuated by preventing A2AR activation. These findings suggest that A2AR antagonism is a potential therapeutic strategy for mild-to-moderate bTBI and consequent cognitive impairment.

Trauma is a life-threatening “modern disease”. The outcomes could only be optimized by cost-efficient and prompt trauma care, which embarks on the improvement of essential capacities and conceptual revolution in addition to the disruptive innovation of the trauma care system. According to experiences from the developed countries, systematic trauma care training is the cornerstone of the generalization and the improvement on the trauma care, such as the Advance Trauma Life Support (ATLS). Currently, the pre-hospital emergency medical services (EMS) has been one of the essential elements of infrastructure of health services in China, which is also fundamental to the trauma care system. Hereby, the China Trauma Care Training (CTCT) with independent intellectual property rights has been initiated and launched by the Chinese Trauma Surgeon Association to extend the up-to-date concepts and techniques in the field of trauma care as well to reinforce the generally well-accepted standardized protocols in the practices. This article reviews the current status of the trauma care system as well as the trauma care training.

In our previous studies, we occasionally found that high-dose glucocorticoids (GC) induced decrease in [Ca(2+)](i) in hypothalamus neurons. In previous articles, modulation of Ca(2+) channels by GC has been shown to contribute to the elementary regulation of several neuronal functions. However, little is known about the regulation of the Ca efflux pathways that counterbalance the Ca(2+) influx in neurons caused by high-dose GC. In this study, we demonstrate that a high-dose of GC (10 M dexamethasone) caused a 20% decrease in [Ca(2+)](i) within 2 s in cultured hypothalamic neurons; furthermore, we show that an antagonist of the GC receptor blocks this action. To ascertain the temporal sequence of relevant calcium transport mechanisms we selectively blocked the main calcium transporters, including sodium/calcium exchanger (NCX), plasma membrane calcium pumps (PMCA), and P-type Ca(2+)-ATPases of the sarcoplasmic reticulum (SERCA). The GC-induced [Ca(2+)](i) decrease disappeared completely when PMCA was blocked, but not when NCX and SERCA were blocked. These results suggest that high-dose GC (10(-6) M) rapidly decreases [Ca(2+)](i) by activating PMCA but not NCX or SERCA.

The adverse effects of antibiotics have attracted widespread attention, thus reducing the use of antibiotics in animal feed has become a very important issue in improving of the health of livestock. The effects of Enterococcus faecium ( E. faecium ) on growth performance and gut microbiota in weaned piglets were investigated in the present study. Piglets were randomly assigned to four treatments: a control group fed with a diet containing 75 mg/kg aureomycin (Diet 1 group) and three experimental groups fed with diets of 50 mg/kg aureomycin (Diet 2 group), 50 mg/kg aureomycin + 9 × 10 5 CFU/g E. faecium (Diet 3 group), or 50 mg/kg aureomycin + 1.2 × 10 6 CFU/g E. faecium (Diet 4 group). Their gut microbial communities were analyzed by sequencing the V3–V4 region of the 16SrRNA gene. The results showed that the final body weights and the average daily gain of the weaned piglets in the Diet 2 group were higher ( P = 0.05) than those in the Diet 1 or Diet 3 group. Decreasing trends ( P = 0.08) was observed in mortality rate in the Diet 3 and 4 group when compared with that in the Diet 1 group. Increases in the Sobs, Chao1, ACE, and Shannon indexes and a decrease in the Simpson index were observed at intervals from day 1 to 14 ( P < 0.05). The Sobs, Chao1, and ACE indexes in the Diet 3 group were the lowest on day 14 ( P < 0.05). The abundance of Bacteroidetes was increased and that of Proteobacteria was decreased from day 1 to 7, but both of them kept stable from day 7 to 14. Besides, the lowest abundance of Fusobacteria , Lentisphaerae , and Planctomycetes was observed on day 1 and the lowest abundance of Actinobacteria was observed on day 14 in the Diet 3 group ( P < 0.05). Overall, these results suggest that the antibiotics and E. faecium interventions result in different changes in the gut microbiota, and a reduced antibiotics diet supplemented with 1.2 × 10 6 CFU/g E. faecium does not affect the growth performance in weaned piglets. Electronic supplementary material The online version of this article (10.1186/s13568-019-0755-z) contains supplementary material, which is available to authorized users.