Sixty-six rabbits were divided into 2 groups, the control group and the experimental group. The latter was subdivided into 10 groups according to the time of observation after burn injury including 2nd-hour group to 30th-day group. Each group consisted of 6 animals. Specimens from the trachea and the lungs were examined with optical microscopy, scanning electron microscopy and transmission electron microscopy.No obvious lesion was seen in the specimens from the control. In the experimental group, various pathological changes began to appear from the 6th hour after injury. In the trachea and bronchi, congestion of varying degrees, edema, leucocytic infiltration, lodging, adhesion, breaking or separation of cilia, and increase of goblet cells and Clara cells in number weie found. In. the lungs, interstitial edema of varying degrees, accumulation and infiltration of neutro-phils in capillaries, pulmonary interstitium and alveolar spaces, decrease in num ber of type II pneumocytes and their lamellar bodies, vacuolization of lamellar bodies, and phagocytosis of lamellar bodies by macrophages were seen. Most prominent changes were shown on the 3rd day postburn, and they began to alleviate on the 7th day. The number of type II pneumocytes and their lamellar bodies gradually increased number. Some lesions still existed on the 30th day postburn but no significant fibrosis could be found. The occurrence and development of the main lesions and their significance were discussed.

Totally 79 obese children and 64 children with normal body weight were included in the present study.Serum apolipoprotein A5 (ApoA5) and leptin levels were determined by ELISA and fasting insulin by RIA.The clinical data including height,body weight,waist circumference,blood pressure,blood lipid,blood glucose,etc,were collected.Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated.The results showed that compared with normal weight children,both serum leptin and insulin levels were significantly raised in obese children [19.15 (13.01 ～ 25.08) ng/ml vs 3.29 (1.45 ～ 6.02) ng/ml and 15.44 (12.05 ～ 20.26) μg/L vs 10.12 (8.60 ～ 12.60) μg/L,both P＜0.01],while ApoA5 level was significantly lowered [134.5 (105.9 ～ 172.7) ng/ml vs 2005.9(164.3 ～ 265.3) ng/ml,P＜0.01].Serum ApoA5 was negatively correlated with serum leptin and insulin (both P＜0.01).

Objective To detect the expression level of human zinc finger 23 (ZNF23) in hepatocellular carcinoma tissue samples and HepG2 cell lines and investigate the relationship between hZNF23 expression and clinicopathological characteristics of HCC and cell apoptosis. Methods The expression levels of hZNF23 and GAPDH mRNA in 37 cases of HCC were measured by real-time RT-PCR. The association between the expression of hZNF23 and the clinicopathological characteristics of HCC was analyzed. Cultured HepG2 cells were divided into 4 groups ( control group, 1.25 μg/ml , 2.5 μg/ml and 5 μg/ml cisplatin)or 6 groups( control group, 1.25 μg/ml, 2.5 μg/ml, 5 μg/ml, 10 μg/ml and 20 μg/ml cisplatin). MTT method was employed to evaluate cell proliferation. Annexin V-FITC assay was used to assess percentage of apoptotic HepG2 cells. The expression levels of hZNF23 and GAPDH mRNA of HepG2 cells after apoptosis induced by cisplatin with a series of concentrations were measured by real-time RT-PCR.Results The median ( quartile1, quartile 3) expression levels of hZNF23 mRNA in 37 HCC tissue samples and adjacent tissue samples were 8.84 (3.59-15.05), 22.20 ( 13.85-42.90 ), respectively. There was significant difference ( U = 259.5, P ＜ 0.01 ). The median ( quartile1, quartile 3 ) expression levels of hZNF23 mRNA in cancer tissue samples with Edmondson stage Ⅰ + Ⅱ [12.80(4.80-19.50)] was much higher than those in stage Ⅲ + Ⅳ [5.01 ( 2.88-11.68 ), U = 99.00, P ＜ 0.05] The median ( quartile1,quartile 3 ) expression levels of hZNF23 mRNA in patients with and without hepatic cirrhosis were 9.92(3.80-15.25) , 3.21 (2.78-3.60), respectively. The median ( quartile1, quartile 3 ) expression levels of hZNF23 mRNA in HBV infection and non-infection patients was 9.09(3.72-15.25 ), 2.48 (1.79-12.10),respectively. There was no significant difference between groups with and without hepatic cirrhosis and between HBV infection and non-infection groups( U = 16. 00 and 24.00, P ＞0.05 ). MTT assay indicated that cisplatin significantly inhibited HepG2 cells proliferation in a dose-dependent manner. Annexin V-FITC/PI assay showed that HepG2 cells apoptosis rates were (0.9 ± 0.2 ) %, ( 4. 2 ± 0.3 ) %, ( 9.8 ± 4. 3 ) %,(23.0 ± 6.0)%, respectively. Cisplatin significantly induced HepG2 cells apoptosis in a dose-dependent manner( F = 27.89, P ＜ 0.01 ). The expression levels of hZNF23 mRNA in cisplatin groups [( 10.39 ±3.08) × 10-5, (24.10 ± 2.09) × 10-5, (6.90 ± 2.24) × 10-4] were significantly lower than that of the controlgroup[(94.80±1.80) ×10-5, F=6.027, P＜0.01]. Conclusions The expression level hZNF23 mRNA is related to Edmondson stage of HCC. The apoptosis effect of cisplatin on HepG2 cells may be associated with the upregulation of hZNF23.

BACKGROUND:The internal structures of the colagen-heparan sulfate scaffold and human nerve are very similar. OBJECTIVE: To explore thein vivo biocompatibility of colagen-heparin sulfate scaffold. METHODS:Forty pigs were randomly divided into two groups, 20 in each group: observation group and control group. Medulo-puncture needle was inserted 1.0 cm adjacent to the midline of anterior fontanele into the subarachnoid space, and then removed gradualy. Colagen-heparin sulfate scaffold was implanted into the observation group, and no treatment was given in the control group. Brain tissues were observed under transmission electron microscope, and cel apoptosis and Caspase-3 expression were detected at days 1, 3, 7, 14 and 30 after surgery. RESULTS AND CONCLUSION:Under the electron microscope, there were some damaged neurons in the observation group with the emergence of demyelination changes in the myelinated nerve fibers; positiveexpression of Caspase-3 protein was found at the junction between the brain tissue and scaffold as wel as within the scaffold, but no positive expression was found in the surrounding tissue. There was no cel apoptosis within 30 days after surgery except for individual apoptotic neurons both in the observation group and control group. The number of apoptotic cels in the observation group was higher than that in the control group at days 1, 3, 7, 14 days after surgery (P < 0.05), but there was no difference between the two groups at 30 days after surgery (P > 0.05). Caspase-3 protein expression was at a low state in the two groups, but the protein expression of Caspase-3 was higher in the observation group than the control group at days 3 and 7 after surgery (P < 0.05). These findings indicate that the colagen heparin sulfate scaffold has good biocompatibility in the porcine brain.

OBJECTIVE: To investigate the involvement of ephrinB2 in periodontal tissue remodeling in compression areas during orthodontic tooth movement and the effects of compressive force on EphB4 and ephrinB2 expression in osteoblasts and osteoclasts. METHODS: A rat model of experimental tooth movement was established to examine the histological changes and the localization of ephrinB2 in compressed periodontal tissues during experimental tooth movement. RAW264.7 cells and ST2 cells, used as precursor cells of osteoclasts and osteoblasts, respectively, were subjected to compressive force in vitro. The gene expression of EphB4 and ephrinB2, as well as bone-associated factors including Runx2, Sp7, NFATc1, and calcitonin receptor, were examined by quantitative real-time polymerase chain reaction (PCR). RESULTS: Histological examination of the compression areas of alveolar bone from experimental rats showed that osteoclastogenic activities were promoted while osteogenic activities were inhibited. Immunohistochemistry revealed that ephrinB2 was strongly expressed in osteoclasts in these areas. Quantitative real-time PCR showed that mRNA levels of NFATc1, calcitonin receptor, and ephrinB2 were increased significantly in compressed RAW264.7 cells, and the expression of ephrinB2, EphB4, Sp7, and Runx2 was decreased significantly in compressed ST2 cells. CONCLUSIONS: Our results indicate that compressive force can regulate EphB4 and ephrinB2 expression in osteoblasts and osteoclasts, which might contribute to alveolar bone resorption in compression areas during orthodontic tooth movement.
Animals ; Bone Resorption* ; Gene Expression ; Immunohistochemistry ; Models, Animal ; Osteoblasts* ; Osteoclasts* ; Rats ; Real-Time Polymerase Chain Reaction ; Receptors, Calcitonin ; RNA, Messenger ; Tooth Movement*

Objective To evaluate the effect of liberal transfusion versus restrictive transfusion strategies on the mortality rate of operative period and critically ill patients.Methods The domestic and abroad databases of WanFang Data,VIP,CBM,CNKI,Cochrane Library,PubMed,EMBASE,OVID and Web of Science were retrieved by computer.The randomized controlled trials(RCTs) on the effects of liberal blood transfusion versus restrictive blood transfusion strategies on the mortality were collected.The ¨Jadad scale¨ assessment tool provided by the Cochrane Collaboration was used to evaluate the quality of collected articles.Then the meta analysis was performed by using Review Manager(RevMan) version 5.3 software.Results Twenty-sevenRCTs involving 10 890 patients were included.The study indicated that there was no statistically significant difference between liberal transfusion group and restrictive transfusion group in the patients ' mortality[RR =0.97,95 ％ CI(0.83,1.13),P =0.69];the sub-group analysis showed that compared with the restrictive blood transfusion group,the liberal blood transfusion group could not effectively reduce the mortality of perioperative patients[RR=0.80,95 ％CI(0.62,1.03),P=0.08],and could not effectively reduce the mortality of critically ill patients[RR=1.09,95 ％CI(0.90,1.33),P =0.37].Conclusion The liberal blood transfusion can not significantly increase the survival rate of perioperative and critically ill patients compared with restrictive blood transfusion.

Sphingosine-1-phosphate(S1P)is a bioactive lipid that regulates a variety of physiological processes,including immune surveillance,immune cell transport,vascular development,and cell differentiation.S1P also plays an important role in regulating vascular function and balancing endothelial barrier homeostasis.The majority of S1P mole-cules are located in their chaperone proteins,such as apolipoprotein M or albumin.The chaperone protein is also a carrier and modulator of S1P molecules,and the combination of the two can protect the S1P structure.S1P-binding chaperone pro-tein selectively activates S1P receptor in the form of a complex that opens downstream pathways by coupling with different S1P receptor targets to exert its effects in vivo.The present review elucidates the metabolism and function of S1P,as well as the effect of chaperones on its function,and clarifies the regulation of S1P in vascular activity and pathogenesis of atherosclerosis.