Traumatic brain injury(TBI)is mostly caused by motor vehicle traffic accidents or competitive sports,with high mortality and disability.TBI mainly includes primary injury and secondary injury.Primary injuries were caused directly by external forces.Secondary injuries include brain edema,excitotoxic effect of neuron cells,oxidative stress and neuroinflammation,etc.Effective intervention of secondary injury not only helps to improve the prognosis of patients with TBI,but also reduces the risk of Parkinson's disease and other neurodegenerative diseases related to TBI.Autophagy is one of approaches to regulate homeostasis in cells,and autophagy dysfunction has been found in several neurodegenerative diseases and TBI.It is speculated that autophagy dysfunction may play an important role in TBI and explain why patients with TBI have higher risk of neurodegenerative disease.Discovering the role of autophagy in the pathological mechanism of TBI may provide new targets for TBI clinical treatment and cognitive impairment prevention in patients with TBI.

Objective To explore the value of inflammatory markers in predicting paroxysmal sympathetic hyperactivity(PSH)after traumatic brain injury(TBI).Methods A total of 84 TBI patients who were admitted to The Second Affiliated Hospital of Naval Medical University(Second Military Medical University)from Dec.2016 to Nov.2020 were retrospectively analyzed.They were classified into PSH group(n=41)and non-PSH group(n=43)according to whether PSH occurred during hospitalization.The baseline data and laboratory results of the 2 groups were collected and compared.Kendall correlation analysis was used to analyze the correlation between inflammatory markers and the occurrence of PSH after TBI,and receiver operating characteristic(ROC)curve was used to analyze the predictive value of inflammatory markers to PSH.Results There were no significant differences in baseline data,including age,gender,or Glasgow coma scale score,between the 2 groups(all P＞0.05).Compared with patients in the non-PSH group,the neutrophil to lymphocyte ratio(NLR),platelet to lymphocyte ratio(PLR),systemic immune-inflammation index(SII),neutrophils and leukocytes in the PSH group were significantly increased(all P＜0.05).NLR,SII and neutrophil were positively correlated with PSH(r=0.360,0.308,0.289;all P＜0.01),with the corresponding ROC area under curve values being 0.752,0.716 and 0.702,respectively.Conclusion NLR,SII and neutrophils have a value in predicting the occurrence of PSH after TBI.

Craniocerebral injury with seawater immersion is a special kind of compound injury, with low temperature, high permeability, high alkali, high salt content, and bacterial infection being the main causes. The injury is also characterized with complex damage mechanisms, difficulty to treat, and poor prognosis. At present, the damage mechanisms of craniocerebral injury with seawater immersion are mainly studied by establishing the experimental animal models at the levels of tissue, cell, organelle, molecule, etc. However, the craniocerebral injury with seawater immersion is more complex than the simple onshore craniocerebral injury, therefore, a stable disease model is not easy to construct. Most researches on the specific injury mechanisms are relatively single and one-sided, with many different views in existence, and the damage mechanisms of craniocerebral injury with seawater immersion have hitherto not been clear. The authors reviewed the research progress in the damage mechanisms of craniocerebral injury with seawater immersion, in order to promote the in-depth study of the mechanism of craniocerebral injury with seawater immersion and provide reference for its clinical treatment.

Posttraumatic stress disorder (PTSD), the most common mental illness after patients suffer physically or emotionally from traumatic events, can cause persistently strong, painful and terrible avoidance symptoms, emotional and cognitive changes, causing psychologically strong stimulation and heavy burden to patients and even leading to some extreme behavioral reactions. Traumatic brain injury (TBI) is an important factor in the occurrence of PTSD, both of which shares many similar pathological overlaps, and may coexist and interact with each other. The hippocampus and amygdala play a central role in the pathogenesis of PTSD, but the specific cellular and molecular and neural circuit mechanisms are still unclear. About two-thirds of the patients still meet the diagnostic criteria for PTSD after psychotherapy. However, the current treatment methods are complicated and not unified, and patients treated with medications may have adverse drug reactions, poor treatment outcomes and recurrence. Therefore, it is of great significance to further clarify the occurrence and development of PTSD in TBI patients. The authors reviewed the research progress of the pathogenesis and treatment of PTSD in TBI patients, so as to provide reference for the related research and treatment of PTSD in TBI patients.

Objective To investigate the relationship of chronic sleep deprivation and high fat diet with laryn-gopharyngeal reflux (LPRD) .Methods A total of 16 rats were randomly divided into the experimental group and control group .Modified multiplatform water surface method and high fat diet (containing 35％ fat) were used in the experimental group rats .The rats in the control group had free sleep and normal feed .The upper gastrointestinal tract pH monitoring with double detectors was used to record the changes of pH in the both rats for 10 hours .The reflux index ,the times of re-flux with pH<4 and the longest duration of reflux were selected and converted into data of 24 hours .The three indexes of the experiment group were compared to those of the control group .Results There was no animal death during the model construction .The rats in the experimental group were irritable .There was no difference of rats weight in both groups before and after the experiment(P>0 .05) .The median of reflux index ,times of reflux with pH<4 and the longest duration of reflux of pharyngeal pH 2 detector in the rats of the experimental group were 21 .07 ,27 .25 and 61 .11 ,respectively .Those of the control group were 1 .25 ,0 .95 and 8 .44 ,respectively .Above three index of the experimental group increased obviously and the difference was statistically significant when compared to those of the control (P<0 .05) .It was suggested that LPRD might appear in the experimental group rats .The median of reflux index and the times of reflux with pH < 4 of esophageal pH1 detector in the rats of the experimental group were 15 .87 and 96 .67 ,displaying an increase when compared to those of the control group (26 .25 and 5 .6) .The differ-ences were statistically significant(P<0 .05);but the median of the longest duration of reflux in pH1 detector of the experimental group rats was 26 .25 ,failing to show statistical difference compared to that of the control group (5 .6) (P>0 .05) .Conclusion Chronic sleep deprivation and high fat diet may play an important role in the pathogenesis of LPRD .This animal model may be a new vector to study LPRD .