Objective To investigate the expression of aquaporin-4 (AQP4) in contused brain and contralateral side and correlation of AQP4 level with brain edema.Methods A total of 70 health adult SD rats were divided into sham operation group (n =10) and brain contusion group (n =60) according to the random number table.Except for no impact in sham operation group,the remaining operations were the same in both groups.Ten rats in brain contusion group were separately sacrificed at 1,6,24,48 and 72 hours,and 7 days.Pathological changes in brain tissues of rats were detected and immunohistochemistry staining and Western-blot were used to measure AQP-4 expression.Results There were no abnormalities of brain tissue structure in sham operation group with AQP4 expressed mainly in glial cells and vascular endothelial cells.With respect to the injured side in brain contusion group,mixed brain edema that consisted of angioedema and cellular edema occurred along with tissue necrosis,massive inflammatory cell infiltration,and microgial proliferation.AQP4 was apparently expressed in gliocytes and vascular endothelial cells,which showed a fall at 1 hour,the lowest at 6 hours,the peak at 24 hours,slow fall at 48 hours,a second peak at 72 hours,and then a fall until 7 days.Level of AQP4 other than that at 1 hour had significant difference compared with sham operation group (P ＜ 0.01).Whereas the contralateral side in brain contusion group showed no pathological abnormalities at 1 hour,but cellular edema emerged at 6 hours followed by mixed brain edema mainly characterized as cellular edema at 24 hours,continued cellular edema but alleviated angioedema at 48 and 72 hours,and alleviated cellular edema at day 7.AQP4 was up-regulated in gliocytes and vascular endothelial cells,which decreased at 1 hour (1.313 ± 0.01),minimized at 6 hours (0.922 ± 0.03),peaked at 24 hours (2.848 ± 0.020),fell at 48 hours,peaked again at 72 hours (2.662 ± 0.02) and fell to almost normal level at day 7.By contrast with sham operation group,level of AQP4 had significant difference other than that at 1 hour and 7 days (P ＜ 0.01).Conclusions After brain contusion,angioedema and subsequent cellular edema emerge in the contused side.Pathological changes are delayed in non-contused side with cellular edema ahead of angioedema.Level of AQP4 is closely related with traumatic brain edema.

OBJECTIVEThis study aims to test the accuracy and precision of iWitness photogrammetry for measuring the facial tissues of mannequin head.

METHODSUnder ideal circumstances, the 3D landmark coordinates were repeatedly obtained from a mannequin head using iWitness photogrammetric system with different parameters, to examine the precision of this system. The differences between the 3D data and their true distance values of mannequin head were computed.

RESULTSOperator error of 3D system in non-zoom and zoom status were 0.20 mm and 0.09 mm, and the difference was significant (P 0.05). Image captured error of 3D system was 0.283 mm, and there was no significant difference compared with the same group of images (P>0.05). Error of 3D systen with recalibration was 0.251 mm, and the difference was not statistically significant compared with image captured error (P>0.05). Good congruence was observed between means derived from the 3D photos and direct anthropometry, with difference ranging from -0.4 mm to +0.4 mm.

CONCLUSIONThis study provides further evidence of the high reliability of iWitness photogrammetry for several craniofacial measurements, including landmarks and inter-landmark distances. The evaluated system can be recommended for the evaluation and documentation of the facial surface.

The individual variability should be considered in precision medicine-prevention and treatment strategies.Medical research using genomics, proteomics, metabolomics, systems analyses, and other modern tools has made big progress.In 2002, the members of the Complex-Trait Consortium proposed to develop a new mouse genetics resource called the Collaborative Cross (CC).The CC is a genetic reference panel of recombinant inbred lines of mice, designed for the dissection of complex traits and gene networks.It will provide a powerful measure for functional studies of biological networks, which will be essential to understand the intricacies of disease processes.

Objective To observe the effect of ulinastatin on the expression of interleukin 15 (IL-15), connective tissue growth factor (CTGF) and malondialdehyde (MDA) in rat peritoneal mesothelial cells (RPMCs) induced by high glucose. Methods RPMCs were isolated, cultured and passaged by trypsin, then identified. The third generation of cultured RPMCs were used in the experiment. RPMCs were divided into normal control group, high glucose (1.5%, 2.5%, 4.25%) for 6 hours and 12 hours, high glucose (2.5%) for 3, 6, 12, 24 hours or ulinastatin (160, 320, 640U/ml) for 12 hours. IL-15 mRNA was detected by real-time PCR. IL-15 and CTGF protein in supernatants was detected by ELISA. MDA protein was detected by TBAS. Results Compared with the control group, the expression of IL-15, CTGF and MDA was significantly increased in the groups stimulated by high glucose (P＜0.05) in dose- and time-dependent manner. Ulinastatin could significantly decrease the expression of IL-15, CTGF and MDA induced by high glucose in dosedependent manner both in protein and gene levels (P＜0.05). Conclusions High glucose can up-regulate the expression of IL-15, CTGF and MDA in RPMCs. Ulinastatin can reverse these changes.

Objective To study the effect of periodontitis on rats with chronic bacterial prostatitis. Methods A total of 80 male rats were randomly divided into the 4 weeks group (n=40) and the 8 weeks group (n=40), and then the two groups were randomly divided into the normal control group (N=10), the periodontitis group (PE=10), the chronic bacterial prostatitis group (CBP=10), and the peri-odontitis+chronic bacterial prostatitis group (CBP+PE=10) respectively. The pathological changes, inflammation score, level of TNF-αand IL-1β, and indicators of periodontal of all rats were observed. Results In the 4 weeks group, the indicators of periodontal in PE group and CBP+PE group were higher than that in N group and CBP group (P<0. 05), but there was no significant difference between PE group and CBP+PE group as well as between the N group and the CBP group (P>0. 05). The pathological changes, inflammation score,TNF-αlevel ,IL-1 β level in CBP+PE group and CBP group were higher than that in N group and PE group (P<0. 05), while there was no sing-nificant difference between N group and PE group as well as between CBP+PE group and CBP group (P>0. 05). In the 8 weeks group, the indicators of periodontal in PE group and CBP+PE group were higher than that in N group and CBP group (P<0. 05), but there was no sig-nificant difference between PE group and CBP+PE group as well as between the N group and the CBP group (P>0. 05). The pathological changes, inflammation score, TNF-α level , IL-1 β level in CBP +PE group and CBP group were higher than that in N group and PE group (P<0. 05),while there was no singnificant difference between N group and PE group (P>0. 05). The pathological changes, inflam-mation score,TNF-α level ,IL-1 β level in CBP+PE group were higher than those in the CBP group (P<0. 05). Compared between 4 weeks group and 8 weeks group, there was no obvious difference in N group in terms of periodontal indexes. Periodontal indexes in 8 weeks PE group was higher than that in 4 weeks PE group (P<0. 05), but there was no significant difference prostate tissue pathology, inflamma-tion score,TNF-α level,IL-1βlevel (P>0. 05). Pathology, inflammation score,TNF-αlevel, IL-1βlevel in 8 weeks CBP group were low-er compared to 4 weeks CBP group (P<0. 05), and there was no significant difference between the indexes of periodontal (P>0. 05). Prostate tissue pathology, inflammation score, TNF-αlevel, IL-1βlevel in 8 weeks CBP+PE group were lower than that in 4 weeks CBP+PE group (P<0. 05), but indicators of periodontal in 8 weeks CBP+PE group were higher than 4 weeks CBP+PE group (P<0. 05). Conclusion Chronic bacterial prostatitis combined with periodontitis can inhibit self-healing tendency of chronic bacterial prostatitis of rats and keep rats in chronic inflammatory phase.

patients received thoracic surgery. Methods Fifty patients underwent radical resection of pulmonary carcinoma were divided into DP group ( dexmedetomidine infusion by micro pumo and parecoxib 40 mg through intravenous injection) and DN group ( dexmedetomidine infusion by micro pumo and nomal saline 5mL through intravenous injection). The time for spontaneous breath,eye opening and extubation after the oper-ation were recorded. The mimi-mental state examination ( MMSE) was used to assess the cognitive function. The concentration of protein S100β and IL-6,TNF-α were determined at 1 d before operation and 1 h,24 h after the operation. Results The difference of time for spon-taneous breath,eye opening,extubation and preoperative values of MMSE between two groups were not statistically significant(P>0. 05). MMSE scores at 1 d,3 d and 5 d after operation in group DN were lower than those in group DP (P<0. 05). The values of S100β、IL-6、TNF-α at 1 h and 24 h after operation in group DN were higher than that in group DP (P< 0. 05). Conclusion Dexmedetomidine com-bined with parecoxib can decrease the incidence of postoperative cognitive dysfunction in elderly patients underwent thoracic surgery,and the mechanism of which may be related to the downregulation of serum inflammatory factors.

Objective To explore the relationship between the damage of neuromyelitis optica (NMO) astrocytes (AS) and the onset of NMO, and investigate the relevance of AS damage with the severity of the patients with functional defect. Methods The levels of aquaprin4-antibody (AQP4 -Ab), glial fibrillary acidic protein (GFAP), apolipoprotein(ApoE),interleukins-6(IL-6), interleukins-10(IL-10), tumor necrosis factor-α(TNF-α) in cerebrospinal fluid (CSF ) and serum of 30 acute NMO patients were tested by means of ELISA. The results were later compared with control group. And analysis of the relevance of the various index of the levels in CSF with the CSF AQP4-Ab level, the acute phase expanded disability status scale(EDSS) score of the NMO group were made. Results (1)The NMO group in CSF and serum AQP4-Ab, GFAP, IL-6 levels were higher than the control group (P < 0.05), and ApoE, IL-10 levels were lower than the control group (P < 0.05). (2)The CSF GFAP, ApoE, IL-6 in NMO group is higher than the serum (P < 0.05), and CSF AQP4-Ab, IL-10 levels were lower than the serum ( P < 0 . 05 ) . ( 3 ) The CSF GFAP , IL-6 levels and the CSF AQP4-Ab level were positively correlated (r=0.749, r=0.526, P<0.05), and the CSF ApoE, IL-10 levels were negatively correlated with CSF AQP4-Ab level(r = -0.571, r = -0.676, P < 0.05). (4)The CSF AQP4-Ab, GFAP, IL-6 levels and the acute phase EDSS score were positively correlated (P < 0.05), the CSF ApoE, IL-10 levels were negatively correlated with the acute phase EDSS score (P < 0.05). Conclusion The AS damage exists in the NMO and the damage severity may correlate with patient function defect. AQP4-Ab, GFAP, IL-6 may play important roles in the onset of NMO and the disease aggravating. The decrease of the ApoE and IL-10 may exacerbate NMO damage.

Objective To investigate the protective effect of 1,25-(OH) 2D3 on radiation-induced bone marrow microenvironment injury and to explore the related molecular mechanism.Methods Sixty 7-week old male BALB/c mice were randomly divided into control group without any treatment; radiation group exposed to 6.0 Gy 60Co γ-rays with DMSO,and 1,25-(OH)2 D3 + radiation group treated with 1,25-(OH)2D32.5 μg/kg dissolved in DMSO each day and 6 Gy of γ-rays.The body weight and peripheral white blood cells,femur bone marrow histology,and the proportion of adipocyte area were measured.The expression of peroxisome proliferator-activated receptor-gamma (PPARγ) was detected immunohistochemistrically at 8 d after irradiation.Results After irradiation,the number of white blood cells and the body weight decreased obviously,and the percentage of adipocyte area was increased significantly.Compared with radiation group,1,25-(OH)2D3 reduced the decrease rate of body weight (t =-2.23,-2.34,P ＜ 0.05),partly recovered the number of white blood cells at 4 or 8 d after irradiation(t =-4.99,-4.46,P ＜ 0.05),and reduced the proportion of adipocyte area (t =-3.75,-2.10,P ＜ 0.05).With immunohistochemistrical assay,it was found that 1,25-(OH) 2D3 inhibited adipogenesis by reducing the expression of PPARγ.Conclusions 1,25-(OH) 2 D3 decreases radiationinduced adipogenesis and hence protects the bone marrow microenvironment from radiation damage.

Objective To investigate the wake-promoting effect of vagus nerve stimulation (VNS) on coma rats after traumatic brain in-jury (TBI), and the related mechanism. Methods A total of 168 healthy Sprague-Dawley rats were randomly divided into blank group, TBI group, antagonist group and VNS group, 42 rats in each group. The latter three groups were established TBI model with impact, and the rats in coma at least 30 minutes were included. VNS group accepted VNS, the antagonist group were injected intralateroventricularly Orexin A receptor 1 (OXR1) antagonist SB334867, and TBI group accepted sham VNS. Their behaviors were observed to determine the level of con-sciousness six, twelve and 24 hours after intervention, while the expression ofγ-aminobutyric acid b1 receptor (GABAb1R) in prefrontal cortex was detected with immunohistochemistry and Western blotting. Results There were 42 rats in the blank group, 11 rats in TBI group, 13 rats in the antagonist group, and 28 rats in VNS group awakened finally. The expression of GABAb1R in prefrontal cortex ranged as TBI group, antagonist group, blank group and VNS group from more to less twelve and 24 hours after intervention under Western blotting (F>60.412, P<0.001), and it ranged as TBI group, antagonist group, VNS group and blank group under immunohistochemistry (H=15.121, P=0.002), with no significant difference among time points (H=3.028, P=0.220). Conclusion VNS can promote waking from coma in rats after TBI, which may relate with the decrease of GABAb1R in prefrontal cortex that induced by Orexin A.

AIM:To investigate the effect of cyclopamine on Hedgehog (HH) signaling, phenotypic transfor-mation and matrix accumulation induced by aristolochic acid (AA) in renal tubular epithelial cell NRK-52E.METHODS:NRK-52E cells were randomly divided into control group (treated with solvent only), AA group (treated with AA at con-centrations of 1, 5, 10 mg/L) and cyclopamine group (treated with AA at concentration of 10 mg/L plus cyclopamine at concentrations of 1, 5, 10μmol/L).After cultured for 24 h, the mRNA expression of Ptch1, Smo,α-SMA, E-cadherin, ZO-1, BMP-7, type I collagen and type III collagen was quantified by real-time PCR.The protein levels of Shh and TGF-β1 were detected by ELISA .Immunofluorescence staining was used to evaluate the expression of Ptch 1, Smo,α-SMA, E-cadherin and type III collagen in the NRK-52E cells.RESULTS: AA increased the expression of TGF-β1, α-SMA and type III collagen, decreased the expression of E-cadherin and ZO-1 protein, and down-regulated the expression of Ptch1, Shh and Smo mRNA in the NRK-52E cells, indicating that AA activated HH signaling , and phenotypic transformation and matrix accumulation occurred in AA-treated NRK-52E cells.Treatment with cyclopamine inhibited HH signaling by decrea-sing Smo expression and increasing Ptch 1 expression.Moreover, cyclopamine also down-regulated the expression of TGF-β1,α-SMA, type I collagen and III collagen , and up-regulated the expression of BMP-7, ZO-1 and E-cadherin.CON-CLUSION:AA induces phenotypic transformation and matrix accumulation in renal tubular epithelial cells , which can be inhibited by cyclopamine treatment .The possible mechanism is that cyclopamine suppresses the activation of HH signaling , resulting in the reduction of epithelial-to-mesenchymal transition and matrix deposition .