Objective To observe the effects of recombinant human bone morphogenetic protein-2 (rhBMP-2) on patients with type A thoracolumbar fractures treated by pedicle screw fixation via dorsal-approach and vertebral body bone graft.Methods A retrospective case-control study was conducted to analyze the clinical data of 64 patients with type A thoracolumbar fractures treated from June 2012 to July 2015.The patients were divided into control group (32 cases) and research group (32 cases) according to the random number table.There were 22 males and 10 females aged (48.2 ± 11.2)years old in control group.The injury was located at T11 in 2 cases,T12 in 4,L1 in 9,L2 in 7,L3 in 7 and L4 in 3 in control group.There were 24 males and 8 females aged (50.7 ± 11.4) years old in research group.The injury was located at T11in 2 cases,T12in 4,L1in 8,L2 in 8,L3 in 7 and L4 in 3.The control group was treated with posterior pedicle screw reduction,internal fixation and allograft cancellous bone grafting through pedicle of vertebral arch.The research group was treated with rhBMP-2 (mixed with cancellous bone implants) on the basis of the control group.The time of operation,the amount of bleeding during operation,the volume of postoperative bleeding,the amount of postoperative drainage,the recovery of the injured vertebra,the Lane-Sandhu score,the time of fracture healing,and the postoperative complications were compared.Results There was no difference between two groups on operation time,amount of bleeding during operation or amount of postoperative drainage (P ＞ 0.05).No difference existed in two groups about Cobb angle and injured vertebral leading edge height at one week after operation (P ＞ 0.05).At the time of last follow-up (12 months),in research group,Cobb angle was lower while injured vertebral leading edge height was much higher than that of control group (P ＜ 0.05),both of which were better than before (P ＜ 0.05).At 12 months after surgery,the lost Cobb angle of [(2.0 ± 0.7) °] and lost height of injured vertebral leading edge [(3.2 ± 1.0) ％] were smaller than those in control group [(5.6 ± 1.7) ° and (6.8 ± 2.4) ％ respectively] (P ＜ 0.05).The Lane-Sandhu score and healing time of fracture in research group were (8.9 ± 0.8) points and (6.9 ± 0.9) months,which were better than that (6.8 ±0.8)points and (8.4 ± 1.6)months in control group respectively (P＜0.05).The complication rate of research group was lower than that of control group,with no significant difference (P ＞ 0.05).Conclusion Compared with simple vertebral bone graft,posterior thoracolumbar vertebrae pedicle screw fixation with vertebral bone graft and hBMP-2 treatment for type A thoracolumbar fractures can restore vertebral stability,shorten the time of fracture healing and reduce the incidence of complications.

Objective To investigate the effect of continuous positive airway pressure(CPAP)during one lung ventilation on pulmonary function in patients undergoing video-assisted thoracoscopic repair of atrial septal defect.Methods Twenty ASA Ⅱ patients of both sexes,aged 16-30 yr,weighing 41-64 kg,scheduled for video-assisted thoracoscopic repair of atrial septal defect,were randomly divided into 2 groups(n = 10 each): control group and CPAP group.One lung ventilation(VT 8 ml/kg,RR 12-16 bpm,I:E 1:2,PETCO2 35-40 mm Hg)was perform in both groups.CPAP(6 cm H2O)was perform during one lung ventilation in group CPAP.The oxygenation index,pulmonary compliance and airway pressure were recorded during operation.The cardiovascular events,hyoxemia and extubation time were recorded.Results The oxygenation index and pulmonary compliance were significantly higher,extubation time was shorter,and the incidence of hyoxemia was lower in CPAP group than in control group(P ＜ 0.01).The airway pressure was in the normal range in both groups.No cardiovascular events was found in both groups.Conclusion CPAP(6cm H2O)during one lung ventilation can improve the pulmonary function in patients undergoing video-assisted thoracoscopic repair of atrial septal defect.

Objective To investigate the impact of aging and weight bearing on cartilage endplate morphology and chondrocyte apoptosis in rats. Methods The bipedal rat model (n=45) was developed by forelimb amputation and special breeding methods. The normal rats of the same age served as the control group (n=40). When the rats became 3, 6, 9, and 12 months old, 8 rats randomly selected from each group were sacrificed and paraffin-embedded mid-sagittal sections of the L4-5 spine were obtained. Sections were stained with hematoxylin and eosin and the TUNEL procedure was performed. The numbers of apoptotic cells and viable cells in the cartilage endplates of the intervertebral discs were counted, the thickness of the cartilage endplate was measured and the degree of impairment of the cartilage endplate was evaluated. Results Apoptosis first appeared in the cartilage endplate, then increased with aging and resulted in a remarkable decrease in cell density. The apoptotic rate of chondrocytes within the cartilage endplate of the bipedal rat model group was significantly higher than the control group at the 6-month time point. A statistically significant difference was observed in the bipedal rat model group between the 6-month time point and 9-month time point (P<0.05). Correlation analyses indicated that there was a highly negative correlation between the number of the viable cells of the cartilage endplate and the degree of the cartilage endplate degeneration (r=-0.97, P<0.05). Compared with the naturally aged group, the bipedal rat model group experienced more severe degeneration in the structure of the cartilage endplate, more obvious thickening of the cartilage endplate's calcified layer, and more defects in the structure of the cartilage. Conclusions Besides aging, weight bearing is probably a key factor of the increase of chondrocyte apoptosis and the degeneration of vertebral cartilage endplate.

The PDB culture medium was selected to ferment the endophyte strain, and the secondary metabolites of endophytic fungi Penicillium polonicum were studied. Combined application of Sephadex LH-20, ODS and HPLC chromatographies over the ethyl acetate extract of the fermented culture led to the isolation of 6 compounds. By spectral methods, the structures were elucidated as [3, 5-dihydroxy-2-(7-hydroxy-octanoyl)]-ethylphenylacetate (1), (3, 5-dihydroxy-2- octanoyl)-ethyl phenylacetate (2), (5, 7-di- hydroxy-9-heptyl)-isobenzo pyran-3-one (3), 3-(hydroxymethyl) 4-(1E)-1- propen-1-yl-(1R, 2S, 5R, 6S)-7-oxabicyclo [4.1.0] hept-3-ene-2, 5-diol (4), (E)-2-methoxy-3-(prop-1-enyl) phenol (5) and p-hydroxylphenylethanol (6).
Biological Factors ; chemistry ; metabolism ; Endophytes ; chemistry ; isolation & purification ; metabolism ; Fabaceae ; microbiology ; Fermentation ; Penicillium ; chemistry ; isolation & purification ; metabolism ; Secondary Metabolism

Objective To analyse the suspected hereditary non-polyposis colorectal cancer (HNPCC) in mismatch repair protein (MMR) expression of hMLH1 and hMSH2. Methods Immunohistochemical staining method was used for the detection of hMLH1 and hMSH2 protein expression in 193 cases suspected HNPCC patients, the deletion of MMR proteins was identified as highly suspected HNPCC cases. Results Of the 193 patients with suspected HNPCC hMLH1/hMSH2 abnormal expression rate was 29.02%; ≤30 years old was 40%, 31 ~ 40 years old was 28.05%, 41 ~ 50 years old was 28.71%,3 suspected HNPCC showed the deletion of hMLH1/hMSH2 protein expression at the same time ,; In the right colon , the left half colon and rectal anomaly detection rates were 40.74%, 32.65%and 18.89%; hMLH1/hMSH2 deletion was 46.15%with family history. Conclusions The deletion of MMR protein is closely related to age,site and family history in suspected HNPCC, and the deletion of hMLH1 is an important factor to induce early-set colorectal cancer. The deletion of hMLH1/hMSH2 at the same time indicates that hMLH1/hMSH2 genes may play important role in the incidence of HNPCC.

Teachers should have a good understanding of characteristic of Pathology Practical Training and enhance language communication competence,especially the expression ability in medical English.Meanwhile,it is essential for teachers to establish harmonious relationship with international students.

The glycosylation heterogeneity of recombinant human pro-urokinase (pro-UK) was assessed using ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). Firstly, the source of heterogeneity was determined by measuring the M_r of intact protein before and after N-deglycosylation. Glycosylation sites and the proportion of O-glycopeptides then were determined at the peptide level. Finally, the N-glycans were confirmed and quantified using the N-glycan profile. Results show that the structural heterogeneity of pro-UK is mainly caused by glycosylation. All T₁₈ were fucosylated, and 6.4% of S_138/139 was O-glycosylated with two kinds of oligosaccharides with a ratio of 6.0% and 0.4% respectively. All N₃₀₂ positions were N-glycosylated by more than ten types of glycans, among which A2F and A3F accounted for 80% of the total. The assessment of glycosylation heterogeneity of pro-UK will provide a reference for quality standardization.

BACKGROUND:Previous studies have indicated that ulinastatin can inhibit RANKL-induced osteoclastogenesis on RAW264.7 cells and also lower matrix metal oproteinase-9 expression and activity. However, it remains be unclear whether ulinastatin has the intervention effect on polymethyl methacrylate (PMMA)-induced MC3T3-E1 mouse preosteoblast apoptosis or not. ＜br> OBJECTIVE:To explore the intervention role of ulinastatin on the PMMA-induced MC3T3-E1 mouse preosteoblast apoptosis and its effects on type I col agen, osteocalcin, matrix metal oproteinase-2 mRNA expression. ＜br> METHODS:MC3T3-E1 mouse preosteoblasts at passages 6 and 7 were divided into four groups:blank group (only cultured MC3T3-E1 mouse preosteoblast), PMMA-induced group (MC3T3-E1 mouse preosteoblast+1 g/L PMMA bone cement suspension), low dose ulinastatin group (MC3T3-E1 mouse preosteoblast+1 g/L PMMA bone cement suspension+500 U/mL ulinastatin) and high dose ulinastatin group (MC3T3-E1 mouse preosteoblast+1 g/L PMMA bone cement suspension+5 000 U/mL ulinastatin). MTT method was adopted to detect the proliferation activity of proliferative activity of MC3T3-E1 mouse preosteoblast;alizarin red staining method was used to observe mineralization nodules of MC3T3-E1 mouse preosteoblast among different groups;the change of apoptosis rate for MC3T3-E1 cells was detected by flow cytometry analysis;semi-quantitative RT-PCR was taken to analyze type I col agen, osteocalcin, matrix metal oproteinase-2 mRNA expression level in MC3T3-E1 mouse preosteoblasts among different groups. ＜br> RESULTS AND CONCLUSION:Compared with the blank group, PMMA significantly inhibited the proliferation activity of MC3T3-E1 mouse preosteoblast (P＜0.05), and however significantly promoted cells apoptosis (P＜0.05). After addition of different concentrations of ulinastatin (500, 5 000 U/mL), the proliferation activity of MC3T3-E1 mouse preosteoblasts significantly raised (P＜0.05), and cells apoptosis rate significantly decreased (P＜0.05), showing the dose and time-dependent relation. Type I col agen and osteocalcin mRNA expression levels both significantly decreased after co-culture in PMMA group compared with the blank group (P＜0.05), matrix metal oproteinase-2 mRNA expression level, however, significantly increased (P＜0.05). After intervention with 5000 U/mL ulinastatin, type I col agen and osteocalcin mRNA expression levels both significantly increased, while matrix metal oproteinase-2 mRNA expression level significantly decreased (P＜0.05). PMMA group showed no obvious mineralization nodules. Yet, mineralization nodules were formed in the blank group, high and low dose ulinastatin groups. These results indicate that ulinastatin could have the inhibitory effect on the PMMA-induced MC3T3-E1 mouse preosteoblast apoptosis, and it could promote type I col agen and osteocalcin mRNA expression and yet suppress matrix metal oproteinase-2 mRNA expression.

Objective To study whether ferulic acid can promote healing on chronic ischemic wounds and its possible mechanisms.Methods 40 male New Zealand white rabbits were randomly divided into 4 groups:vaseline group,ischemic control group,5％ ferulic acid group and recombinant bovine basic fibroblast growth factor for external use (rb-bFGF) group.Gross wounds were carefully observed and HE staining was used to observe the wound healing and immumohistochemical staining to observe the expression of the VEGF and CD31.The RNA was extracted to detect the expression of VEGF and HIF-1a by real-time PCR.Results The general observation and the HE staining of each specimen 11 days after operation all indicated that the duration of wound healing of the 5 ％ ferulic acid group was similar to that of the rb-bFGF group and markedly shorter than the ischemic control group and the vaseline smear group.The result of the immunohistochemical staining indicated that the content of the VEGF and CD31 expression of the 5 ％ ferulic acid groups and the rb-bFGF group made lit tle difference,but there was markedly less VEGF and CD31 in ischemic control group and the vaseline smear group.The result of the PCR showed that expression level of VEGF and HIF-1α in the 5 ％ fer ulic acid group was similar to that in the rb bFGF group and the vaseline smear group,but was obviously more than that of the ischemic control group and the vaseline smear group (P ＜ 0.05).Conclusions Ferulic acid can promote angiogenesis by increasing VEGF and HIF-1α which are closely related to angiogenesis and then promote the healing of chronic wounds.

OBJECTIVETo investigate the therapeutic effect of IL-6 mAb on experimental autoimmune myocarditis (EAM) in rats, and search the mechanism of the role of IL-6, helper T cells 17 (Th17) and regulative T cells (Treg) in EAM pathogenesis.

METHODSThirty-four Lewis rats were divided into three groups randomly, i.e. control group (n = 6), EAM group (n = 12), and IL-6 mAb intervention group (n = 16). Rats in EAM group and IL-6 mAb intervention group were injected intracutaneously with myosin to establish EAM model. Rats in IL-6 mAb intervention group were injected intraperitoneally with 1 mg IL-6 mAb on 1st, 7th to 20th day after cardiac myosin immune injection. Myocardial inflammation was examined by HE stain, Masson stain, and TdT assay (TUNEL reaction) on 21st and 84th day after IL-6 mAb therapy in order to assess the therapeutic role. Spleen cells were analyzed by flow cytometry to illustrate Th17 and Treg cells? number and function. The serum concentration of IL-6, IL-10, IL-17, and TGF-beta in each group was measured by ELISA, concentration of STAT3, RORgammat, and Foxp3 mRNA in each group was determined with RT-PCR. Spleen cells derived from EAM were stimulated by IL-6 mAb in vitro, and the concentration of IL-10, IL-17 and TGF-beta was measured by ELISA.

RESULTSInflammation score, fibrosis score, and apoptosis index in IL-6 mAb intervention group were significantly decreased as compared with those in EAM group (P < 0.01). The number of Th17 and Treg cells in EAM group on the 21st day (experimental acute peak stage) were increased, and those in intervention group on the 21st day were significantly inhibited (P < 0.01). The concentration of serum IL-6, IL-10, IL-17 and TGF-beta in intervention group on the 21st day was decreased dramatically in comparison with that in EAM group on the same day (P < 0.01). The levels of peripheral blood STAT3, RORgammat, Foxp3 mRNA in intervention group on the 21st day was decreased significantly as compared with that in EAM group (P < 0.01). The expression of IL-10, IL-17 and TGF-beta was increased significantly (P < 0.01) by stimulation of IL-6 mAb on spleen cells derived from EAM in vitro.

CONCLUSIONSIL-6 mAb could neutralize IL-6, and ameliorate myocarditis and reduce heart autoimmune responses. IL-6 mAb has significantly protective effects on EAM by suppressing Th17 and Treg cells.

Animals ; Antibodies, Monoclonal ; therapeutic use ; Autoimmune Diseases ; drug therapy ; immunology ; Disease Models, Animal ; Forkhead Transcription Factors ; metabolism ; Interleukin-10 ; metabolism ; Interleukin-17 ; metabolism ; Interleukin-6 ; immunology ; Male ; Myocarditis ; drug therapy ; immunology ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; metabolism ; Rats ; Rats, Inbred Lew ; STAT3 Transcription Factor ; metabolism ; Th17 Cells ; immunology ; Transforming Growth Factor beta1 ; metabolism