To improve the accuracy of finite element method used in medicine field, it is necessary to build the finite element model including real structural information of tissues in human body. In this study, an edge extracting method was introduced on CT image of human body, and the method of building the two-dimensional finite element model from the extracted edges was then raised. Using the above methods, a finite element model of human body containing real structural information can be successfully made. The methods were used for many CT images of hospitals and tested to be simple, fast and adaptable. The study makes a good foundation for further finite element analysis based on medicine images.

Existing antidepressants exhibit delayed onset of action,which can decrease the compliance of the patients and enhance the risk of suicide.How to produce early-onset antidepressants with higher efficacy and lower adverse reactions has become a crucial point in the research of antidepressants.It has been demonstrated that selective 5-HT1Aantagonist,?2 antagonist and 5-HT2Aantagonist can accelerate the response of classic antidepressants.Furthermore,5-HT/NE dual reuptake inhibitor and 5-HT/NE/DA triple reuptake inhibitor can also produce early onset of action.Here,several reasons for the delayed onset of action and the progress in the development of early-onset antidepressants are reviewed.

Aim To study the activation of transcription factor cAMP response element binding protein(CREB)in the rat C6 glioma cells induced by bradykinin,and discuss its possible significance.Methods Immunocytochemistry and western-blot method were used to determine the phosphorylation of CREB after stimulated by 1 ?mol? L-1 bradykinin at various time points(0,5,10,15,20,30min).Results Bradykinin at 1 ?mol? L-1 induced phosphorylation of CREB inthe glioma cells at the indicated time points(0～30min)(P

The von willebrand factor (vWF) and angiotensin converting enzyme(ACE) were measured in asthmatic patients in stages of attack and remission, using ELISA and ultraviolet methods. The results showed that the vWF and ACE were (72.1 ? 58.3)%, and 22.9 ? 6.9U in the stage of attack, and (68.8 ? 42.1)% and 23.2? 7.9U in the stage of remission, respectively. All these values were significantly lower than that of healthy controls [(117.1 ? 50.30)% and 31.3 ? 9.3U, respectively, P

Objective Primitive neuroectodermal tumor (PNET) is a rare malignant small round cell tumor .This paper aimed to study the clinical and pathological features of primary pulmonary primitive neuroectodermal tumor . Methods We collected 2 cases of primary pulmonary PNET to review the clinical and pathological features .Immunohistochemical staining was used to detect immune mark-ers, and fluorescence in situ hybridization (FISH) was applied to detect EWS translocation. Results 2 patients were aged 33 years and 17 years.Microscopically, the tumor cell was composed of single small round cells in diffusion or in distribution of sheets or beams , with scant cytoplasm , oval or spindle-shaped nucleus , high mitotic count .Irregular tumor necrosis scattered in the tumor along with visi-ble rosette structure.Immunohistochemical study showed that the tumor cells were positive for CD 99, FLI-1 and Syn, while CKpan, EMA, Desmin, CgA, TTF1, CD34 were negative.EWS/FLI1 translocations were detected positive in both the cases .2 patients died 7 months and 32 months after operation , respectively . Conclusion Primary pulmonary PNET is rare , so the selection of appropriate im-mune markers (CD99, FLI-1, Syn) and FISH for the detection of EWS translocation helps to improve the accuracy of diagnosis .

Objective To study the mechanism of miR?200c in regulating RMP7?induced increases of blood?tumor barrier(BTB)permeability by targeting Ras homolog gene family member A(RhoA). Methods Endogenous expression of miR?200c was detected by real?time PCR in hu?man cerebral microvascular endothelial cell line hCMEC/D3(ECs)after RMP7 treatment. miR?200c mimic and miR?200c inhibitor were transfect?ed into GECs(ECs with U87 glioma cells co?culturing),respectively. Transfection efficiency of miR?200c mimic and miR?200c inhibitor were de?termined by real?time PCR. HRP flux and TEER assays revealed BTB permeability. The protein expression level of RhoA was assessed by West?ern blotting. The distribution of RhoA was assessed by immunofluorescence microscopy. RhoA luciferase assays were performed using the Dual?Lucif?erase reporter assay system. Results RMP7 significantly induced a decrease in miR?200c expression in GECs of BTB. miR?200c mimic and miR?200c inhibitor were successfully transfected into GECs. Overexpression of miR?200c inhibited endothelial leakage and restored normal transendo?thelial electric resistance values. Simultaneously ,overexpression of miR?200c significantly reduced the protein expression level of RhoA. In addi?tion,immunofluorescence analysis revealed that the distribution of RhoA in the cytoplasm and nuclei of GECs were decreased in miR?200c mimic group. RhoA was one of the direct targets of miR?200c with the specific binding site being located at the seed sequence. The results of miR?200c si?lencing were opposite to that of the miR?200c overexpression group. Conclusion miRNA?200c regulated RMP7?induced increases in BTB perme?ability by targeting RhoA.

Aim To investigate the signaling mecha-nisms in endothelial monocyte-activating polypeptide-Ⅱ( EMAP-Ⅱ)-induced increase in blood-tumor barri-er ( BTB ) permeability. Methods Relatively pure cerebral microvessel fragments were obtained from the cortex of 3-5 days old Wistar rats by using careful dis-section, enzyme digestion, and dextran centrifugation. Then, these fragments were seeded on dishes and cul-tured primarily. In vitro BTB models were constructed by co-cultivation of rat brain microvascular endothelial cells ( BMECs) with C6 glioma cells. Confluent mono-layers of co-cultured BMECs were divided randomly in-to 5 groups ( each n=6 ): control, EMAP-Ⅱ, H7 +EMAP-Ⅱ, C3 exoenzyme + EMAP-Ⅱ, and C3 ex-oenzyme + H7 + EMAP-Ⅱ groups. Transendothelial electric resistance values and horseradish peroxidase flux were measured to evaluate changes in the BTB permeability . The expression levels of tight junction-re-lated protein occludin and ZO-1 in BMECs were meas-ured by Western blot. Immunofluorescence was used to identify the expression and distribution of occludin and ZO-1 in BMECs. Also, Western blot were used to de-tect the expression levels of myosin light chain ( MLC) and phosphomyosin light chain ( pMLC ) in BMECs. Results Compared with control group, the BTB per-meability of EMAP-Ⅱ group was increased significant-ly. The expression levels of occludin and ZO-1 in BMECs were significantly decreased, accompanied with marked increase in the expression level of pMLC. These above-mentioned effects of EMAP-Ⅱ were sig-nificantly inhibited by pretreatment with H7 ( an inhib-itor of PKC ) or/and C3 exoenzyme ( an inhibitor of RhoA ) . Conclusion Signaling molecules PKC and RhoA play important roles in EMAP-Ⅱ-induced in-crease in BTB permeability; signaling pathways PKC-pMLC and RhoA-pMLC are involved in this process.

Objective To compare the clinical efficacy and radiologic changes between constrained and non-constrained titanium plate in anterior cervical corpectomy and fusion (ACCF) in elderly cervical spondylosis patients.Methods A total of 58 elderly cervical spondylosis patients who underwent ACCF were divided into group 1 (patients treated with constrained titanium plates,n =30) and group 2 (patients treated with non-constrained titanium plates,n=28).The Japanese Orthopedic Association (JOA) score,fusion rate,the loss of segmental height and cervical lordosis were recorded.The clinical efficacy and imaging features were compared between the two groups.Results The improvement rate of JOA score had no significant differences between group 1 and group 2 [(77.7±18.6)％ vs.(75.8±23.2)％,t=0.340,P＞0.05].At 3 months after operation,the fusion rate was higher in group 2 than in group 1 (89.3％ vs.63.3％,x2 =5.327,P＜0.05).At 3,6 and 12 months after operation,there were no significant differences in the loss of segmental cervical height and lordosis between group 1 and group 2 [(2.42±3.05)mm vs.(0.98±2.86)mm,(3.95±3.65)mm vs.(2.34±2.97)mm,(3.60±4.33)mm vs.(2.40±2.96)mm,(1.64±2.33)° vs.(0.66 ± ±2.14)°,(2.13∧±±3.79)° vs.(0.70±2.99)°,(2.39±4.26)° vs.(0.86±3.25)°,respectively,all P ＞0.05].Conclusions The clinical efficacy is similar in ACCF with the two types of titanium plates.The non-constrained titanium plate can increase the fusion rate in early time,but may aggravate the loss of segmental cervical height and lordosis,which should be used with caution in elderly osteoporosis patients.

Objective To investigate the effects of toll-like receptor 9 (TLR9) agonist CpG ODN2216 on the sensitivity of pancreatic cancer cell line PANC1's to gemcitabine.Methods The immunofluorescence staining method and Western blot method were used to examine the expression of TLR9 protein in PANC1 cells.The changes of sensitivity to gemcitabine after CpG ODN2216 treatment were examined by MTT assay.Results The TLR9 protein was highly expressed in PANC1 cells and the median inhibition concentration of gemcitabine against PANC1 cells was reduced from (1.23 ± 0.14) mg/L to (0.28 ± 0.13) mg/L after CpG ODN2216 treatment,and the difference between the two groups was statistically significant (P ＜0.01).After 0.01,0.10,1.00,10.00 mg/L gemcitabine treatment with CpG 0DN2216,the inhibition rates of PANC1 were (34.4 ±1.3)％,(43.5 ± 2.7)％,(76.3 ± 2.5)％,(95.3 ± 2.2)％ ; and without CpG ODN2216,the inhibition rates of PANC1 were (14.5 ± 0.9) ％,(23.5 ± 1.1) ％,(44.8 ± 1.4) ％,(63.6 ± 1.8) ％,and the difference between the two groups was statistically significant (P ＜ 0.01).Conclusions The sensitivity of PANC1 cells to gemcitabine can be enhanced by CpG ODN2216.

Background Elevated intraocular pressure leads to the loss of retinal ganglion cells and vigorous reaction of retinal glial cells.The expression of nestin in retinal glial cells secondary to hypertention and its significance are unclear.ObjectiveThis study aim to investigate the expression of nestin in retinal glial cells (RGCs) in ocular hypertention rats.Methods The ocular hypertention models were established by cauterizing the limbus-draining veins in the right eyes of 42 SD rats,and a conjunctival incision in the left eyes of the rats served as the sham group.The intraocular pressure (IOP) was measured with the Tono-Pen XL tonometer.The number of RGCs in the rats with ocular hypertention was counted.The expression of the nestin protein in RGCs was semi-quantitatively analyzed using Western by immunochemistry.Double immunofluorescence was carried out to evaluate the the confocal laser scaning microscope.Results Significant differences were found in the IOP between the model group and the sham group at various time points (P＜0.05).In 1 week to 3 weeks after operation,the number of RGCs significantly declined in the model group compared with the sham group (P＜0.05).Immunochemistry showed that from 2 hours through 1 week after operation,the expression of nestin was gradually enhanced in the model group in comparison with the sham group.Western blot revealed that the expression of the nestin protein reflected a similar tendency to that of immunofluorescence.The increased introcular pressure as manifested by the induced expression of nestin.Immunoelectron microscopy also confirmed the induced expression of nestin especially at their end-feet suggests a potential neuroprotective mechanism in neuronal degeneration.Nestin may be a useful biomarker for retinal injury study.