Objective To provide a description of clinical manifestations, special imaging features and treatment of diffuse axonal injury(DAI).Methods Retrospective analysis of 32 cases of diffuse axonal injury.Result 87.5% patients were involved in traffic accident. All patients came into persistent comatose state immediately. 75% patients had abnormal CT scan findings. MRI showed more sensitive. It could reveal injury appearance of corpus callosum and brain stem clearly. Hypothermic therapy and calcium ion antagonist were used. Conclusions combination of clinical manifestations and special imaging features helped to diagnosis of DAI in early stage. Intensive care and preventing secondary brain injury were the important treatment points.

ObjectiveTo observe the effect of early rehabilitation on motor function, high-sensitivity C-reactive protein (hs-CRP), interleukin-1（IL-1） and interleukin-6（IL-6） in patients with acute cerebral infarction (ACI). Methods160 patients with ACI were randomly divided into rehabilitation group (n=80) and control group (n=80), who accepted early rehabilitation and routine medicine or medicine only, respectively. They were assessed with modified Edinburgh-Scandinavian Stroke Scale (MESSS) and their peripheral level of hs-CRP, IL-1 and IL-6 were detected before and 1, 2, 4, and 8 weeks after treatment. Results4 and 8 weeks after treatment, the level of hs-CRP, IL-1 and IL-6 were lower in rehabilitation group than in control group（P＜0.05）, as well as the scores of the MESSS （P＜0.01）. The incidence of improvement is more in rehabilitation group than in control group（P＜0.05）. ConclusionEarly rehabilitation can reduce the expression of hs-CRP, IL-1 and IL-6, and improve the neurological function in patients with ACI.

AIM: To establish an animal model of experimental autoimmune myocarditis (EAM) in BALB/c mice and to investigate the expression and significance of Toll-like receptor 3 in mouse EAM. METHODS: BALB/c mice were immunized with cardiac myosin extracted from porcine ventricular myocardium covered by complete freund's adjuvant (CFA) on 0 d and 7 d, then divided into immunized with CFA only. Serum and myocardium samples were collected at 14 d and 21 d after the first immunization. HE staining was used to identify the areas of inflammation. The myosin IgG antibody was examined by indirect ELISA assay. The changes of TLR3 protein and mRNA expression in myocardial tissue were measured by immunohistochemistry and real time-PCR. RESULTS: Compared to control group, immunohistochemistry results showed that there was positive expression of TLR3 in the myocardium of mice with EAM and the mRNA of TLR3 were more than 20 times (P<0.05). The expression of interferon beta mRNA in EAM group was more than 14 times as many as basal expression, that of tumor necrosis factor alpha was more than 18 times (P<0.05). CONCLUSION: The expression of Toll-like receptor 3 in myocardium is up-regulated in experimental autoimmune myocarditis. The inflammatory response to cardiac myosin may associate with the TLR3 signal transduction pathway.

Objective:　To study the changes and clinical significance of arginine vasopressin (AVP) and angiotensin II (AT-II) in patients with acute moderate and severe cerebral injury. 　　Methods:　The early plasma concentration was checked by radioimmunoassay in 47 cases of acute moderate and severe cerebral injury, 30 cases of non-cerebral injury and 30 healthy volunteers. 　　Results:　The early plasma concentrations of AVP (50.23 ng/L±15.31 ng/L) and AT-II (248.18 ng/L±82.47 ng/L) in cerebral injury group were higher than those in non-cerebral injury group (AVP for 30.91 ng/L±11.48 ng/L and AT-II for 120.67 ng/L±42.49 ng/L, P<0.01). The early plasma concentrations of AVP and AT-II in cerebral injury group were also obviously higher than those of the volunteers (AVP for 5.16 ng/L±4.23 ng/L and AT-II for 43.11 ng/L±16.39 ng/L, P<0.001). At the same time, the early plasma level of AVP (58.90 ng/L±18.12 ng/L) and AT-II (292.13 ng/L±101.17 ng/L) was higher in severe cerebral injured patients than moderate cerebral injured ones (AVP for 36.68 ng/L±12.16 ng/L and AT-II for 201.42 ng/L±66.10 ng/L, P<0.01). The early level of AVP and AT-II was negatively related to the GCS scales in acute cerebral injury. The early plasma concentrations of AVP (45.98 ng/L±13.48 ng/L) and AT-II (263.28 ng/L±80.23 ng/L) were lower in epidural hematoma group than those of subdural hematoma and cerebral injury group (AVP for 64.12 ng/L±15.56 ng/L and AT-II for 319.82 ng/L±108.11 ng/L, P<0.01). 　　Conclusions:　 AVP and AT-II may play an important role in pathophysiologic process in the secondary cerebral injury. The more severe the cerebral injury is, the higher the early level of AVP and AT-II will be. The early plasma level of AVP and AT-II may be one of the severity indexes of cerebral injury.