Objective To analyze the risk factors for traumatic cerebral venous sinus occlusion (CVSO)and to investigate the strategies of early diagnosis of traumatic CVSO. Methods The clinical data of 212 patients with moderate to severe closed traumatic brain injury from January 2012 to December 2015 were analyzed retrospectively. Logistic regression analysis was used to evaluate the risk factors for traumatic CVSO. Results Of the 212 patients with traumatic brain injury, 16.5%(35/212) patients had CVSO. Ten patients had CVSO of thrombotic type (typeⅠ), 16 patients had CVSO of compression type (typeⅡ), and 9 patients had CVSO of mixed type (typeⅢ). Logistic regression analysis showed that skull fracture (OR = 8.141; 95%CI: 3.224-20.840) and epidural hematoma of crossing venous sinus (OR = 3.179; 95%CI: 1.470-7.037) were the risk factors for CVSO, and the former was more significantly correlated with CVSO. Female gender was the risk factor for CVSO typeⅠ(OR =10.425; 95%CI: 1.831-30.053), epidural hematoma of crossing venous sinus was the risk factor for CVSO typeⅡ(OR = 5.766; 95%CI: 1.885-18.197), and skull fracture, epidural hematoma of crossing venous sinus, and the previous history of vein thrombosis was the risk factors for CVSO type Ⅲ(OR =18.005, 4.596, 11.394; 95%CI: 2.021-58.836, 1.144-19.525, 1.436-46.558). Conclusions In the early diagnosis of traumatic CVSO, the crossing venous sinus fracture line and epidural hematoma should be given attention. Attention should be paid to the history of venous thrombosis. MR venography and CT venography contributes to early diagnosis of CVSO.

Objective To investigate the roles of the chemokine receptor CXCR3 and its ligand I-TAC in the pathogenesis of immune thrombocytopenic purpura (ITP).Methods A total of 48 ITP patients were enrolled in this study:30 with newly diagnosed or relapse ITP and 18 in remission after treatment,and 24 healthy volunteers were as controls.IFNγ and I-TAC in plasma were detected by ELISA.The mRNA expression of CXCR3 in the peripheral blood mononuclear cells (PBMNCs) was determined by quantitative RT-PCR.Results The IFNγ level in the plasma of ITP patients before the treatment was obviously increased than those in the remission group and controls[ (71.45 ± 17.62)ng/L vs (36.94 ±14.86 )ng/L and (25.28 ± 12.85 )ng/L,all P ＜ 0.05 ]and those in the remission group was higher than in the controls ( P ＜ 0.05 ).In contrast,there were no statistic differences of the levels of I-TAC among the three groups[ (455.56 ± 144.70 ) ng/L,( 488.24 ± 164.70 ) ng/L and ( 382.97 ± 167.43 ) ng/L,P ＞0.05 ].Both ITP patients before the treatment and remission groups expressed more CXCR3 mRNA [ 6.76(3.03,37.00),1.76 (0.45,14.18 ) vs 0.12 ( 0.04,0.28 ),P ＜ 0.05 ].After effective therapy,CXCR3mRNA expression decreased,while it was still higher than that in the controls.Conclusions Our data demonstrate that Th1 cytokine (IFNγ) dominance is reflected in ITP.Simultaneously,the CXCR3 + cell may play a role in cell-mediated immunity through chemotaxis in ITP.

Objective:To investigate the expression of SHIP1 in the patients with acute myeloid leukemia and its effect on the apoptosis of human leukemia cells.Methods:The expression of SHIP1 in the bone marrow of patients with acute myeloid leukemia was detected by Westem blot.U937 cells was transfected with SHIP1 expression vector (pEGFP-SHIP1 group) and empty vector control (pEGFP group) respectively,U937 cells without transfection were used as the control group.Flow cytometry was used to detect the apoptosis of the cells,the expression of SHIP1,Bcl-2,Bax,Akt,p-Akt were detected by western blot.Results:The expression of SHIP1 in the bone marrow of patients with acute myeloid leukemia was significantly lower than that of the normal human bone marrow SHIP 1 (P＜0.01).The SHIP1 and Bax expressions as well as the apoptotic rate ofpEGFP-SHIP1 group were significantly higher than those of the control group(P＜0.01),while the Bcl-2 and p-Akt expressions were significantly lower than those in the control group(P＜0.01).Conclusions:SH-P1 expression was down regulated in the bone marrow of patients with acute myeloid leukemia.SHIP1 could promote the apoptosis of human leukemia cells via Akt signaling pathway.