Objective:To establish a model for the study of tooth initiation and early development by in vitro culture of mouse mandibular arch . Methods:42 mandibular arches of 11dpc fatal mouse were dissected and cultured in Trowell organ culture system for 11 days.Regular histologic observation was performed to observe the initiation and development of tooth.Results: Mandibular arches grew well in Trowell culture system.The initiation and early development of tooth was found.The explants maintained to cap stage.On day 11,necrosis of the cultured mandibular arches was observed and the culture was ended. Conclusion:In vitro cultured mandibular arch can be used as a model for the study of tooth initiation and early development.

Purpose To investigate the effects of intervention with Tanakan on anterior ocular segment in diabetic retinopathy (DR) after retinal photocoagulation. Methods Prospective random controlled study was performed on 72 patients (72 eyes) with ultrasound biomicroscopy (UBM),by obtaining and quantitatively analyzing the changes of anterior ocular segment including anterior chamber, anterior chamber angle, ciliary body and choroids before and the 3rd day and the 7th day after retinal photocoagulation. Results Three days after photocoagulation, significant elevated IOP and narrowed chamber angle were observed in control group and 4 eyes (11.11%) in Tanakan group (P

Randomized sampling-based questionnaire among 2000 community residents and personal contact with selected populations were conducted.Based on incidence or clinical featuxes of dermatosis and venereal diseases and recognition-related impact factor analyses,we provided evidence for community-based health education and behavior intervention.Our findings showed that itching was the most common skin disease,and fungous infection displayed an increasing trend.Viral diseases increased significantly in recent years.Patients failed to understand the skin diseases,although they partly had some misleading information about venereal diseases.Health care providers should perform more health education and behavior interventions regarding dermatosis and venereal diseases for community residents to improve their health condition or quality of life.

Gastrointestinal Neoplasms ; pathology ; Humans ; Neoplasm Recurrence, Local ; surgery ; Postoperative Period

Objective To study the appearance of skin mucous glycoprotein in vitro on the activity of human lung cancer cells A549. Methods Used alkali extraction and DEAE-52 ion exchange chromatography and Sephadex G-100 gel chromatography purification salamander mucous glycoprotein; Salamander mucous glycoprotein inhibition of human lung cancer cells A549 was detected by MTT colorimetric method in vitro.ResuIts It showed that the total sugar content in the appearance of mucus was 4.23%, the relatively pure glycoprotein component, by SDS protein electrophoresis tests, it contained a single glycoprotein component, its molecular weight was about 30 kDa.With glycoprotein pure concentration increased from 1,10, 20,40μg/mL, the glycoprotein inhibition rate of A549 cells increased; when the glycoprotein concentration was 40 μg/mL, for 24 h action, the inhibition rate of A549 cells was up to 85.66 %, while the role of 48 h, the inhibition rate of A549 cells was up to 92.32%.Inhibition effect of mucus glycoprotein on A549 cell compared with positive control drug, had significant difference.ConcIusion Salamander mucus glycoproteins of human lung cancer cells has obvious inhibitory effect, can provide theoretical basis for the development of lung cancer drug resistance.

Objective To study the influence of carboxymethyl-chitosan(CM-chitosan)on chondro- cyte apoptosis induced by recombinant human interleukin-1?(rhIL-1?)and explore its mechanism.Methods Rabbit chondrocytes were isolated and cultured.Chondrocytes were pretreated with different concentrations of CM-chitosan for 1 h,then 10 ng/ml IL-1?were added into the culture medium.After 24 h,the apoptotic rates of chondrocytes were measured by flow cytometry with AnnexinⅤ-FITC and PI staining.The morphology of nuclei was observed by fluorescent microscopy with Hoechst 33342 staining.The mitochondrial membrane po- tentials were tested by confocal laser scanning microsocopy with Rhodamine-123 and ATP contents were mea- sured by luciferase reaction.Results CM-chitosan could inhibit chondrocyte apoptosis and restore the func- tion of mitochondria induced by IL-113 in a dose-dependent manner.Conclusion CM-ehitosan can inhibit chondrocyte apoptosis by protecting mitochondrial function.

Objective To evaluate the role of ERK1/2 signaling pathway in mitigation of myocardial ischemia-reperfusion (I/R) injury by diazoxide postconditioriing in rats.Methods Sixty adult male SpragueDawley rats,aged 3 months,weighing 240-260 g,were randomly divided into 5 groups (n =12 each) using a random number table:sham operation group (S group),I/R group,vehicle group (Ⅴ group),diazoxide postconditioning group (D group),and ERK1/2 signaling pathway inhibitor U0126 group (U group).Myocardial I/R was produced by occlusion of left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion.In V and D groups,0.4％ DMSO and diazoxide 7 mg/kg (in 1 ml 0.4％ DMSO) were administrated,respectively,through the femoral vein at the onset of the reperfusion.In U group,U0126 was given through the femoral vein at 10 min before reperfusion,and the following procedures were similar to those previously described in group D.At 120 min of reperfusion,myocardial specimens were obtained for detection of myocardial infarct size,cell apoptosis (using TUNEL),and expression of ERK1/2 mRNA (by RT-PCR),total ERK1/2 (t-ERK1/2) and phosphorylated ERK1/2 (p-ERK1/2) (by Western blot).Apoptosis index was calculated.Results Compared with S group the myocardial infarct size and apoptosis index were significantly increased in the other groups,the expression of ERK1/2 mRNA and p-ERK1/2 was down-regulated in I/R,V and U groups,and no significant change was found in the expression of ERK1/2 mRNA and p-ERK1/2 in Dgroup.Compared with I/R group,the myocardial infarct size and apoptosis index we re significantly decrcaed,and the expression of ERK1/2 mRNA and p-ERK1/2 was up-regulated in D group,and no significant change was foundin the parameters mentioned above in V and U groups.Compared with D group,the myocardial infarct sizeand apoptosis index were significantly increased,and the expression of ERK1/2 mRNA and p-ERK1/2 was down-regulated in U group.There was no significant difference in t-ERK1/2 expression between five groups.Conclusion Diazoxide postconditioning mitigates myocardial I/R injury possibility through activating ERK1/2 signaling pathway in rats.

Objective To evaluate the relationship between extracelluar signal?regulated protein kinase 1∕2 (ERK1∕2) and signal transducer and activator of transcription 3 (STAT3) signaling pathways involving in cardioprotection induced by diazoxide postconditioning in rats. Methods Sixty adult male Sprague?Dawley rats, aged 3 months, weighing 240-260 g, were randomly divided into 5 groups ( n=12 each) using a random number table: sham operation group ( SH group ) , ischemia?reperfusion ( I∕R ) group, diazoxide postconditioning group ( D group ) , ERK1∕2 inhibitor U0126 group ( U group ) , and STAT3 inhibitor Stattic group ( St group) . Myocardial I∕R was produced by occlusion of anterior descending branch of the coronary artery followed by 120 min reperfusionIn I∕R and D groups, 0?4% dimethyl sulfoxide 1 ml and 7 mg∕kg diazoxide ( in 1 ml of 0?4% dimethyl sulfoxide) was injected through the femoral vein at the onset of reperfusionIn U and St groups, U0126 100 μg∕kg and Stattic 500 μg∕kg were injected through the femoral vein at 10 min before reperfusion, and the other procedures were similar to those previously described in group DAt 120 min of reperfusion, the rats were sacrificed, and myocardial specimens were obtained from the left ventricle for determination of myocardial infarct size, cell apoptosis, and ERK1, ERK2 and STAT3 mRNA expression ( real?time PCR), and phosphorylated ERK1∕2 ( p?ERK1∕2) and phosphorylated STAT3 (p?STAT3) (using Western blot). Apoptosis index (AI) was calculated. Results Compared with group S, the myocardial infarct size and AI were significantly increased, and the expression of ERK1, ERK2 and STAT3 mRNA, p?ERK1∕2 and p?STAT3 was down?regulated in group I∕R. Compared with group I∕R, the myocardial infarct size and AI were significantly decreased, and the expression of ERK1, ERK2 and STAT3 mRNA, p?ERK1∕2 and p?STAT3 was up?regulated in group D. Compared with group D, the myocardial infarct size and AI were significantly increased in U and S groups, the expression of ERK1, ERK2 and STAT3 mRNA, p?ERK1∕2 and p?STAT3 was down?regulated in group U, and the expression of STAT3 mRNA and p?STAT3 was down?regulated, and no significant change was found in ERK1 and ERK2 mRNA and p?ERK1∕2 expression in group S. Conclusion STAT3 signaling pathway is located downstream of ERK1∕2 signaling pathway in the mechanism by which diazoxide postconditioning reduces myocardial I∕R injury in rats.

Objective To investigate the effect of hydromorphone postconditioning on ischemiareperfusion (I/R) injury in isolated rat hearts and the role of mitochondial permeability transition pore (mPTP).Methods Male Sprague-Dawley rats, aged 2-3 months, weighing 250-320 g, were used in the study.The rats were heparinized and anesthetized with intraperitoneal 10％ chloral hydrate 350 mg/kg.The hearts were excised, and perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 36.5-37.5 ℃.Forty isolated rat hearts were randomly divided into 4 groups (n=10 each)using a random number table: control group (group C), group I/R, hydromorphone postconditioning group (group H), and hydromorphone postconditioning + mPTP opener lonidamine group (group HL).Group C was continuously perfused with K-H solution for 120 min.Group I/R was perfused with K-H solution for 30 min, the perfusion was then suspended for 30 min, and group I/R was perfused with K-H solution for another 30 min.Group H was perfused with K-H solution for 30 min, the perfusion was then suspended for 30 min, and group H was perfused with K-H solution containing 0.3 μmol/L hydromorphone for 10 min, and then with K-H solution for 50 min.Group HL was perfused with K-H solution for 30 min, the perfusion was then suspended for 30 min, and group HL was perfused with K-H solution containing 0.3 μmol/L hydromorphone and 30 μmol/L lonidamine for 10 min, and then with K-H solution for 50 min.At 30 min of equilibration (T0), and 30 and 60 min of reperfusion (T2,3), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP) , ±dp/dtmax, heart rate (HR), and coronary flow (CF) were measured.The concentrations of lactic dehydrogenase (LDH), creatine kinase-MB (CK-MB) , and troponin-T (Tn-T) in the coronary effluent were determined at T0 and T3.The coronary effluent was collected at T0 and 15 min of reperfusion (T1),nicotinamide-adenine dinucleotide (NAD+) concentrations were measured using enzyme-linked immunosorbent assay to reflect the degree of mPTP opening.The myocardial infarct size was determined at T3 by TTC staining.Results Compared with group C, LVDP, HR, ±dp/dtmax and CF were significantly decreased, and LVEDP was increased at T2,3, and the concentrations of LDH, CK-MB and Tn-T in the coronary effluent, myocardial infarct size at T3, and NAD+ concentrations in the coronary effluent at T1 were increased in group I/R (P＜0.05).Compared with I/R and HL groups, LVDP, ±dp/dt CF and HR were significantly increased, and LVEDP was decreased at T2,3, and the concentrations of LDH, CK-MB and Tn-T in the coronary effluent, myocardial infarct size at T3, and NAD+ concentrations in the coronary effluent at T1 were decreased in group H (P＜0.05).Conclusion Hydromorphone postconditioning can reduce myocardial I/R injury in isolated rat hearts, and the mechanism is related to inhibition of mPTP opening.

Objective To evaluate the role of signal transducer and activator of transcription 3 (STAT3) signaling pathway in the reduction of myocardial ischemia-reperfusion (I/R) injury by diazoxide postconditioning in rats.Methods Sixty adult male Sprague-Dawley rats,aged 3 months,weighing 240-260 g,were randomly divided into 5 groups (n =12 each):sham operation group (S group),I/R group,vehicle group (V group),diazoxide postconditioning group (D group),and STAT3 signaling pathway inhibitor Stattic group (St group).Myocardial I/R was produced by 30 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion.In V and D groups,0.4％ dimethyl sulfoxide and 7 mg/kg diazoxide (in 1 ml of 0.4％ dimethyl sulfoxide) were injected through the femoral vein at the onset of reperfnsion,respetively.In St group,Stattic was injected through the femoral vein 10 min before reperfusion,and the other procedures were the same as those in D group.The infarct size (IS) and myocardial apoptosis were detected by TTC staining and TUNEL,respectively.Apoptotic index (AI) was calculated.STAT3 mRNA expression in myocardial tissues was detected using RT-PCR.Western blot was used to detect the phosphorylation of STAT3.Results Compared with S group,the IS and AI were significantly increased and the expression of STAT3 mRNA and phosphorylation of STAT3 were decreased in I/R group (P ＜ 0.05).Compared with I/R group,the IS and AI were significantly decreased and the expression of STAT3 mRNA and phosphorylation of STAT3 were increased in D group (P ＜ 0.05).There was no significant difference in IS,AI,expression of STAT3 mRNA and phosphorylation of STAT3 between V group and St group (P ＞0.05).Compared with group D,the IS and AI were significantly increased and the expression of STAT3 mRNA and phosphorylation of STAT3 were decreased in St group (P ＜ 0.05).Conclusion STAT3 signaling pathway is involved in the reduction of myocardial I/R injury by diazoxide postconditioning in rats.