Objective: To develop a polyvinylidene fluoride (PVDF)-based instrument which may be used to measure bite force in natural teeth as well as in denture. Methods: The PVDF film was used as transducer. Electricity amplifier, lowpass filter, secondary magnifier in metrical circuit, and collection with disposal system were employed to produce the instrument for bite force measurement. The demarcating system was MTS-858. The instrument was used to measure the dynamic force in laterotrusion in 9 volunteers with Angle I occlusion. Results: The instrument was produced.By the used of the instrument the peak value of bite force (N) in the 9 subjects was 277.3?78.4 on the main functional side (MFS) and 258.7?83.3 on the subfunctional side (SFS).The time(ms) needed in the four phases on MFS was 65.6?7.3,354.4?66.1,116.3?25.0 and 226.9?35.8;that on SFS 67.5?6.6,394.4?65.3,141.9?25.6 and 167.5?41.9,respectively.Conclusion: The new system is steady and sensitive for bite force measurement.

Objective To explore the relationship between the HBV‐DNA ,ALT ,AST and NO ,iNOS ,SOD levels in serum of patients with chronic hepatitis B(CHB) .Methods 24 patients with mild CHB ,30 patients with moderate CHB ,18 patients with se‐vere CHB and 30 healthy individuals were selected and set in group A ,B ,C and D ,respectively .The serum levels of HBV‐DNA , ALT ,AST ,NO ,iNOS ,and SOD were detected by FQ‐PCR and chemical analysis respectively .Results There were significant difference in the levels of ALT ,AST ,NO ,iNOS and SOD between group D and group A ,B and C (P<0 .05) .The serum level of ALT was positive relative to the levels of NO and iNOS(r=0 .487 ,0 .521 ,P<0 .05) ,and was negative relative to the level of SOD (r= -0 .574 ,P<0 .05) .The serum level of AST was positive relative to the levels of NO and iNOS(r=0 .453 ,0 .545 ,P<0 .05) , and was negative relative to the level of SOD(r= -0 .484 ,P<0 .05) .Conclusion With the increase of ALT and AST levels ,the levels of NO and iNOS increase ,and the level of SOD decreases simultaneously in CHB patients .It is suggested hepatocellular inju‐ry .

Objective To establish burn-induced esophageal lesion model by adding NaOH with different concentrations in rabbits, and investigate the effect of modified sijunzi decoction on the p53 and Bcl-2.Methods After injection with different concentrations of NaOH, esophagus was dissected and observed anatomically.Rabbits were given a gavage of modified Sijunzi decoction daily for 20 days, and then were injected with NaOH.Esophageal epithelium isolated from each group was observed by hematoxylin-eosin staining.p53 and Bcl-2 protein and mRNA expression was measured with western blot and qRT-PCR, respectively.Results The degree of corrosion of esophageal epithelium was positively correlated with the concentration of NaOH.p53 protein and mRNA levels were increased after NaOH challenge; this increase was inhibited by treatment with modified Sijunzi decoction.Additionally, NaOH decreased Bcl-2 protein and mRNA, which was attenuated by modified Sijunzi decoction.Conclusion Modified sijunzi decoction can relieve the esophageal alkali burning in a dose-dependent manner, suggesting that modified Sijunzi decoction may be a useful strategy to treat chemical injuries in esophageal tissue.

Objective To explore the etiologies and characteristics of esophageal motility in patients with non-obstructive dysphagia by esophageal high-resolution manometry (HRM).Methods From November 2011 to August 2015,233 patients with non-obstructive dysphagia diagnosed by HRM were retrospectively analyzed.All the patients received gastroendoscopy to exclude obstructive dysphagia.Results Among 233 patients with non-obstructive dysphagia,there were 160 cases of achalasia,38 cases of nonspecific esophageal motor disorder (13 cases of low amplitude peristalsis or absent peristalsis,seven cases of synchronous contraction or rapid contraction,three cases of distal esophageal spasm,six cases of increased resting upper esophageal sphincter pressure (UESP),three cases of reduced UESP,six cases of lower esophageal sphincter (LES) incomplete relaxation),five cases of gastroesophageal reflux disease,four cases of scleroderma,two cases of Jackhammer esophagus,and 24 cases with normal esophageal motility.Conclusions Achalasia is the most common cause of non-obstructive dysphagia,followed by nonspecific esophageal motor disorder.Esophageal HRM is an important method for the diagnosis of nonobstructive dysphagia,especially for unexplained dysphagia.

This article mainly discusses the psychological characteristics of patients in orthodontic practice on the view of medical ethics. To achieve good relationship and cooperation between doctors and patients, be helpful to lighten patients' burden and to complete treatment successfully by strengthening the ethical education on orthodontic doctors and right education on patients and giving psychological guidance.

Objective To explore the diagnosis value of narrow-band imaging magnifying endoscopy (NBI-ME) in the early esophageal cancer and precancerous lesions while estimating the quality,depth and treatment strategy.Methods One hundred and eleven cases of patients with suspected early esophageal cancer and precancerous lesions,who underwent ESD treatment,were selected as the study subjects.To estimate the diagnosis value of NBI-ME in the quality,depth and treatment strategy with pathological histology as gold standard.Results While estimating quality,there was no low grade intraepithelial neoplasia(LGIN) cases with NBI-ME.A total of 33 cases were diagnosed as high grade intraepithelial neoplasia(HGIN),including 30 cases of HGIN and 3 cases of LGIN after ESD treatment,and the other 78 cases were diagnosed as early esophageal cancer,including 5 cases of LGIN,22 cases of HGIN,and 51 cases of early esophageal cancer.Compared with the pathology results,the quality consistency of NBI-ME is general:K=0.498.While estimating depth,there was no LGIN cases with NBI-ME.A total of 33 cases were diagnosed as HGIN,including 30 cases of HGIN and 3 cases of LGIN after ESD treatment,67 cases were diagnosed as intramucosal carcinoma,including 5 cases of LGIN,22 cases of HGIN,30 cases of intramucosal carcinoma,and 10 cases of submucosal carcinoma after ESD treatment,and 11 cases were diagnosed as submucosal carcinoma.Compared with the pathology results,the depth consistency of NBI-ME is general:K=0.469.Most of the patients shoud be treated by ESD except 8 cases of LGIN.Conclusion The study shows general diagnosis value of NBI-ME in estimating quality,depth and treatment strategy of early esophageal cancer and precancerous lesions.

Objective In our previous work, the prevalence of anti-endothelial cell antibodies(AECA) in patients with systemic vasculitis and other autoimmune diseases was analyzed. AECA against a 47 000 endothelial cell antigen was found in patients of a variety of systemic vasculitis and systemic lupus erythematosus (SLE). It was suggested to be α-enolase by the combination of immunoblotting and proteomics methods. The aim of this work is to demonstrate that α-enolase is one of the targets of AECA, and to detect the prevalence of anti-α-enolase antibody in sera of patients with autoimmune disorders including systemic vasculitis. Methods The CDS of human Enol gene was amplified by polymerase chain reaction (PCR), with template of human placenta λzap express Cdna library. The product was then recombined with expression vector. After expression and purification from E.coli, the recombinant protein was analyzed by mass spee-trometry. The prevalence of anti-α-enolase antibody in patients with autoimmune disorders including systemic vasculitis was tested by Western blot and enzyme-linked immunosorbent assay (ELISA). Results The CDS of human Enol gene was subcloned to the expression vector. Recombinant human α-enolase was expressed and purified in E.coli. The recombinant protein was demonstrated to be his-tagged human a-enolase by mass spectrometry. Results of Dot-Blot revealed that the prevalence of anti-α-enolase antibody was 76.7% in systemic vasculitis [including 74.0% in Behcet's disease (BD), 81.5% in Takayasu artefitis (TA), 62.5% in Wegener's granulomatosus (WG), 92.3% in microscopic polyangitis (MPA) and 80.0% in Churg-Stranss syndrome (CSS)], 78.3% in SLE, 63.6% in Sjogren's syndrome (SS) and 78.9% in rheumatoid arthritis(RA). No positive signals were detected in sera of normal controls or patients with polymyositis/ dermatomyositis (PM/DM). There was no statistical significance among positive rates of anti-α-enolase antibody in systemic vasculitis, SLE, SS or RA patients. The prevalence of positive signals at the most extensive level (+++～++++) was 51.7% in patients with systemic vasculitis, 33.3% in SLE, 42.9% in SS and 20.0% in RA. There was statistical significant difference between RA and systemic vasculitis. Conclusion The identification of human α-enolase as one of the targets of AECA and its prevalence in a variety of autoimmune disorders will shed some light on the understanding of the pathogenesis of vascular injury in autoimmune diseases.

Objective To study expression and activation of p38 mitogen activated protein kinase (MAPK) in vascular endothelial cells dysfunction in preeclampsia. Methods From Sept. 2009 to Mar.2010, 54 pregnant women underwent deliveries in the First Affiliated Hospital of Chongqing Medical University were enrolled in this study, including 20 patients in mild preeclampsia group, 16 patients in severe preeclampsia group and 18 women with term cesarean section without perinatal complications as control group. Placental endothelial cells were labeled by CD34 to assay microvessel density (MVD) of each group. Immunohistochemical SP and western blot were used to detect localization and expression of p-p38 MAPK protein, respectively. The levels of sera soluble fms-like tyrosine kinase-1 (sFlt-1)and soluble endoglin(sEng) were measured by ELISA. Results ①The MVD of placenta were 103 ± 3 in control group, 81 ±5 in mild preeclampsia group and 63±4 in severe group, respectively, which showed statistical difference among each group (P＜0.05).②The expression of p38 MAPK protein were 0.84±0.05 in control group,0.90±0.14 in mild group and 0. 86 ±0.18 in severe group, which did not reach remarkable difference among each group (P＞0.05). The expression of p-p38 MAPK protein were 0.13±0.05 in control group,0.59±0.12 in mild group and 1.16±0.18 in severe group, which show statistical difference among each group(P＜0.05).(3) The localization of p-p38 was in trophoblast, endothelial cells and a few (5.2±0.3)and(10.9±0.4)μg/L in control group,(12.5±1.2) and (20.4±5.3)μg/L in mild group and (19.3±3.0) and (29. 5 ±3.7) μg/L in severe group. When drawing paired comparison in those p-p38 MAPK protein levels and the concentrations of serum sFlt-1, sEng in preeclampsia groups (r=0.68,P＜0.05;r=0.87,P＜0.05). Conclusions The remarkable activation of the p38 MAPK in the placenta of patients with preeclampsia induced the increased levels of sFlt-1 and sEng in maternal serum, which confer the injury of vascular endothelial cells that caused the significant decline of MVD in placentas. p38 MAPK signaling might be one of the key pathways in vascular endothelial cell dysfunction in preeclampsia.

Objective:To elucidate the characterization of CD8+T cell in H1N1 influenza vaccine for children.Methods:PBMCs were isolated from 31 children aged from 3 to 6 years old who had accepted H 1N1 influenza vaccine during December 2009 to January 2010.The lymphocytes were joined with the H 1N1 influenza vaccine as experimental group and cultured .The experiment set without vaccine group as control group .At last we detected the surface molecules by FCM .The CCK-8 assay was added to detecting cellular proliferation and cellular proliferation index were detected by CCK-8.Results: CD8+T cells of PBMC in the two groups were 13.41%and 9.41%,P>0.05.CD8+CD45RAA+naive T cells in the two groups were up to more than 80%,P>0.05.The proportion of CD8+CD45ROA+memory T cells in two groups were up to 17%-19%,P>0.05.Two subsets of CD8+CD45ROA+memory T cells :CCR7+and CD62L+single positive memory T cell subsets in the experimental group were significantly lower than that of the control group,P<0.05.The CCK-8 assay was added to detect cellular proliferation .Only 51.16% of which cellular proliferation index was greater than 0.8,with none was greater than 1 in this study.Conclusion:This study showed that the CD4+T cells were low-level,naive T cells (CD8+CD45RAA+)were higher,with antigen stimulation and response.H1N1 vaccination specific memory T cells were few in number , specific memory T cell subsets were diversity , control memory cells were the main phenotypic characteristics .Cellular proliferation index showed that the proliferation of specific CD 8+T cells vaccine was poor .

Purpose To investigate the location and distribution of EV71 receptors scavenger receptor class B member 2 ( SCARB2 ) and human P-selectin glycoprotein ligand-1 (PSGL-1) in lung tissues of fatal hand, foot and mouth disease (HFMD), healthy children and adults. Methods The expression of EV71 receptors SCARB2 and PSGL-1 was detected by using immunohistochemistry in lung tissues of 15 autopsies of HFMD, 3 of healthy children, 8 of healthy adults. Results SCARB2 distributed in bronchial, bronchioli ep-ithelia, alveolar epithelial cells and inflammatory cells among HFMD, healthy children and adults. No significant difference was noted of the positive rates of SCARB2 expression among these three groups (P>0. 05). PSGL-1 distributed in bronchial and bronchioli epi-thelium of adults, but no PSGL-1 expression was found in HFMD and healthy children. The positive rates of PSGL-1 were 100%, 0, 0 in bronchial and bronchioli epithelium among the three groups, respectively (P<0. 05). The positive rates of PSGL-1 were 100%, 66. 7%, 100% in inflammatory cells among HFMD, healthy children and adults, respectively. No significant difference was noted of PSGL-1 expression among the three groups (P>0. 05). Further, no PSGL-1 expression was observed in alveolar epithelia cells of all groups tested. Conclusions EV71 receptor SCARB2 distributes in bronchial, bronchioli, alveolar epithelial and inflammatory cells of HFMD. Meanwhile, PSGL-1 only distributes in inflammatory cells of HFMD, suggesting that SCARB2 possibly plays a role on HFMD infection.