Mild traumatic brain injury (MTBI) is defined as a mild brain trauma resulting in a short loss of consciousness and alteration of mental status. It may also occasionally develop persistent and pro-gressive symptoms. It has been confirmed that MTBI causes changes of anatomic structures in central nervous systemand biomarkers in the body fluid. How ever, there is no sufficient research on relevance among threshold for the brain injury, individual vulnerability and duration of disturbance of conscious-ness. Furthermore, there are no reliable diagnostic methods to establish w hether a blow to the head is sufficient to cause the brain injury. T his review provides references for biomarkers in cerebrospinal fluid and blood associated w ith T B I. It also provides application status and potential prospects for further as-sessment and diagnosis of MTBI.

This study investigated the role of reactive oxygen species (ROS) in the pathogenesis of triptolide-induced renal injury in vivo. Rats were randomly divided into 4 groups (n=5 in each): triptolide group in which the rats were intraperitoneally injected with triptolide solution at a dose of 1 mg/kg of body weight on day 8; control group in which the rats received a single intraperitoneal injection of 0.9% physiological saline on day 8; vitamin C group in which the rats were pretreated with vitamin C by gavage at a dose of 250 mg/kg of body weight per day for 7 days before the same treatment as the control group on day 8; triptolide+vitamin C group in which the rats were first subjected to an oral administration of vitamin C at a dose of 250 mg/kg of body weight per day for 7 days, and then to the same treatment as the triptolide group on day 8. All the rats were sacrificed on day 10. Blood samples were collected for detection of plasma creatinine (Pcr) and plasma urea nitrogen (PUN) concentrations. Both kidneys were removed. The histological changes were measured by haematoxylin-eosin (HE) staining. The production of ROS was determined by detecting the fluorescent intensity of the oxidation-sensitive probe rhodamine 123 in renal tissue. Renal malondialdehyde (MDA) content was measured to evaluate lipid peroxidation level in renal tissue. TUNEL staining was performed to assess apoptosis of renal tubular cells. Renal expression of apoptosis-related proteins Bcl-2, Bax, Bid, Bad, Fas and FasL, as well as corresponding encoding genes were assessed by Western Blotting and real-time PCR. The results showed that triptolide treatment promoted the generation of a great amount of ROS, up-regulated the expression of Bax, Bid, Bad, Fas and FasL at both protein and mRNA levels, as well as the ratio of Bax to Bcl-2, and caused the apoptosis of renal tubular cells and renal injury. However, pretreatment with an antioxidant, vitamin C, significantly reduced the generation of ROS and effectively inhibited the triptolide-induced apoptosis of renal tubular cells and renal injury. It was concluded that ROS plays a critical role in triptolide-induced apoptosis of renal tubular cells and renal injury. The protective administration of vitamin C may help alleviate triptolide-induced renal injury and nephrotoxicity.

Objective:To analyze the prognostic factors of robot-assisted radical cystectomy (RARC).Methods:The clinical data of 224 patients underwent RARC from December 2014 to December 2018 in Nanjing Drum Hospital were reviewed. There were 193 males and 31 females, aged 36-92 years, with mean of 68 years. There were 7 patients(3.1%)undergoing neoadjuvant chemotherapy, the ASA scores of 125 patients (55.8%) were more than 2, and the mean body mass index was 23.4(15.4-35.5)kg/m 2. All patients were treated with RARC, with 72(32.1%) patients undergoing intraoperative blood transfusion. Kaplan-Meier method was used to analyze recurrence-free survival rate (RFS), cancer-specific survival rate (CSS) and overall survival rate (OS). Cox multivariate risk ratio model was used to evaluate the correlation between survival outcome and perioperative and pathological factors in patients treated with RARC. Results:For pathological status, there were 82 of ≤T 1, 64 of T 2, 57 of T 3 and 21 of T 4. Of all the patients, 49(21.9%) had lymph node metastasis, 12(5.4%) had positive surgical margin, 82(36.6%) had lymphovascular invasion(LVI), and 41(18.3%) underwent adjuvant chemotherapy. Follow-up time was between 11-60 months, and the median follow-up time was 24 months. The 5-year cumulative OS, RFS and CSS were 57.15%, 48.84% and 59.60%, respectively. Univariate Cox regression analysis showed that T stage( HR=5.764, 95% CI 1.926-17.249, P=0.002; HR=4.086, 95% CI 1.611-10.364, P=0.003; HR=9.391, 95% CI 2.118-41.637, P=0.003), N stage( HR=6.446, 95% CI 3.438-12.087, P<0.001; HR=5.661, 95% CI 3.086-10.385, P<0.001; HR=5.980, 95% CI 2.982-11.992, P<0.001), LVI( HR=3.319, 95% CI 2.008-5.486, P<0.001; HR=2.894, 95% CI 1.782-4.701, P<0.001; HR=3.471, 95% CI 2.017-5.974, P<0.001), American Society of Anesthesia (ASA)score( HR=2.888, 95% CI 1.619-5.150, P<0.001; HR=1.765, 95% CI 1.060-2.940, P=0.029; HR=2.612, 95% CI 1.424-4.792, P=0.002), body mass index( HR=0.886, 95% CI 0.819-0.957, P=0.002; HR=0.885, 95% CI 0.819-0.955, P=0.002; HR=0.862, 95% CI 0.792-0.938, P=0.001), age( HR=1.580, 95% CI 1.250-1.997, P<0.001; HR=1.362, 95% CI 1.088-1.705, P=0.007; HR=1.530, 95% CI 1.190-1.968, P=0.001) and intraoperative blood transfusion( HR=1.899, 95% CI 1.160-3.108, P=0.011; HR=2.218, 95% CI 1.371-3.587, P=0.001; HR=2.227, 95% CI 1.312-3.782, P=0.003) were significantly related to survival outcome. Multivariate Cox regression analysis showed that T stage( HR=4.506, 95% CI 1.433-14.175, P=0.01; HR=3.159, 95% CI 1.180-8.454, P=0.022; HR=7.810, 95% CI 1.674-36.444, P=0.009), N stage( HR=6.096, 95% CI 2.981-12.467, P<0.001; HR=5.368, 95% CI 2.683-10.740, P<0.001; HR=5.539, 95% CI 2.497-12.288, P<0.001) and ASA score( HR=6.180, 95% CI 2.371-16.110, P<0.001; HR=2.702, 95% CI 1.175-6.215, P=0.019; HR=6.471, 95% CI 2.290-18.286, P<0.001) were independent predictors of RFS, CSS and OS, and adjuvant chemotherapy( R=0.434, 95% CI 0.202-0.930, P=0.032) could only predict OS. Conclusion:T stage, N stage and ASA were main independent predictors of postoperative survival outcomes, and adjuvant chemotherapy was independent predictor of OS.

This study investigated the role of reactive oxygen species (ROS) in the pathogenesis of triptolide-induced renal injury in vivo.Rats were randomly divided into 4 groups (n=5 in each):triptolide group in which the rats were intraperitoneally injected with triptolide solution at a dose of 1 mg/kg of body weight on day 8; control group in which the rats received a single intraperitoneal injection of 0.9％ physiological saline on day 8; vitamin C group in which the rats were pretreated with vitamin C by gavage at a dose of 250 mg/kg of body weight per day for 7 days before the same treatment as the control group on day 8; triptolide+vitamin C group in which the rats were first subjected to an oral administration of vitamin C at a dose of 250 mg/kg of body weight per day for 7 days,and then to the same treatment as the triptolide group on day 8.All the rats were sacrificed on day 10.Blood samples were collected for detection of plasma creatinine (Pcr) and plasma urea nitrogen (PUN) concentrations.Both kidneys were removed.The histological changes were measured by haematoxylin-eosin (HE)staining.The production of ROS was determined by detecting the fluorescent intensity of the oxidation-sensitive probe rhodamine 123 in renal tissue.Renal malondialdehyde (MDA) content was measured to evaluate lipid peroxidation level in renal tissue.TUNEL staining was performed to assess apoptosis of renal tubular cells.Renal expression of apoptosis-related proteins Bcl-2,Bax,Bid,Bad,Fas and FasL,as well as corresponding encoding genes were assessed by Western Blotting and real-time PCR.The results showed that triptolide treatment promoted the generation of a great amount of ROS,up-regulated the expression of Bax,Bid,Bad,Fas and FasL at both protein and mRNA levels,as well as the ratio of Bax to Bcl-2,and caused the apoptosis of renal tubular cells and renal injury.However,pretreatment with an antioxidant,vitamin C,significantly reduced the generation of ROS and effectively inhibited the triptolide-induced apoptosis of renal tubular cells and renal injury.It was concluded that ROS plays a critical role in triptolide-induced apoptosis of renal tubular cells and renal injury.The protective administration of vitamin C may help alleviate triptolide-induced renal injury and nephrotoxicity.