[ABSTRACT]OBJECTIVETo investigate the relationships between the characteristics of the upper airway anatomy, including the basis nasi, and the severity of obstructive sleep apnea hypopnea syndrome(OSAHS). METHODSFifty OSAHS patients and 40 normal subjects received three-dimensional CT scan and poly somnography(PSG). Variables between the two groups were compared. The association between the PSG parameters and the upper airway anatomic features were analyzed. RESULTSThere were significant differences in several CT variables between OSAHS patients and normal subjects(P<0.05), including the minimal lateral airway dimension and the minimal cross-sectional airway area of both velopharynx and glossopharynx, the minimal anterior-posterior airway dimension of velopharynx, and the airway width of basis nasi. The result of logistic regression analysis suggested that the minimal cross-sectional airway area of velopharynx and the airway width of basis nasi were significant predictors of the OSAHS(P<0.05, the values of the odds ratio were 0.978 and 0.589). The correlation analysis suggested that the airway width and the airway area of basis nasi both correlated significantly with several CT variables of pharynx(P<0.05), among these results, the correlation coefficents between these two variables and the mCSA of velopharynx were 0.536 and 0.425 respectively. CONCLUSIONNarrowed basis nasi and velopharynx might be important anatomical features in OSAHS patients. There are correlations between the characteristics of basis nasi and the anatomy of pharyngeal airway.

Objective To observe the effect of panretinal photocoagulation (PRP) on the expression of cyclooxygenase-2 (COX-2),vascular endothelial cell growth factor (VEGF) in epiretinal membrane of proliferative diabetic retinopathy (PDR).Methods A total of 35 patients (35 eyes) with PDR and underwent plana vitrectomy were enrolled in this study.The patients were divided into non-PRP group (19 patients,19 eyes) and PRP group (16 patients,16 eyes) depends on if they had received PRP before surgery.The epiretinal membranes stripped during operation were collected for pathological examination.The histopathological features was observed by haematoxylin and eosin stain.The expression of CD34,COX-2 and VEGF,and microvessel density (MVD) were measured by immunohistochemistry method.Results Many new dispersed capillary blood vessels were found in the thick epiretinal membranes of nonPRP group,while scattered small blood vessels were found in the relatively thin epiretinal membranes of PRP group.MVD value was (7.42± 1.39) in the non-PRP group and (4.56± 1.22) in the PRP group,which was lower than the non-PRP group (t=6.41,P＜0.01).The expression of CD34,COX-2 and VEGF in the tissues of epiretinal membrane in PRP group were obviously lower than the non-PRP group (t=6.147,5.944,7.445;P＜0.01).Conclusion PRP can effectively inhibit the expression of COX-2 and VEGF in epiretinal membrane of PRP patients.

Objective To investigate the therapeutic effects and mechanisms of curcumin derivatives C66 treatment on hepatic fibrosis .Methods Thirty three C57BL/6J mice were randomly divided into 3 groups:normal control group ,model control group and curcumin derivatives C66 treatment group .Nine mice in normal control group were fed with water and food .Hepatic fibrosis model was induced in 24 mice by intraperitoneal injection of 40% carbon tetrachloride at a dose of 4 mL/kg for the first time ,followed by 2 mL/kg twice a week for 6 weeks . At week 6 ,6 mice were randomly selected to perform pathological examination to evaluate whether the hepatic fibrosis were successfully induced .Mice with hepatic fibrosis were randomized into model control group and curcumin derivatives C66 treatment group with 9 mice in each group .From week 6 on ,mice in the treatment group were lavaged with curcumin derivatives C66 at a dosage of 10 mg ·/(kg · d) .The rest mice were administered with equivalent dosage of 0 .5% carboxymethylcellulose sodium .Serum alanine aminotransferase (ALT) ,aspartate aminotransferase (AST ) and liver hydroxyproline ( Hyp ) contents were detected , and the semi‐quantitative analysis of liver fibrosis was performed by pathological examination in hepatic tissue by hematoxylin and eosin (HE) and Masson staining .The expressions of collagen Ⅰ ,α‐smooth muscle actin (α‐SMA) mRNA and collagen Ⅰ ,α‐SMA ,nuclear factor‐kappa B p65 (NF‐κB p65) ,inhibitor kappa B alpha (IκBα) protein in each group were detected by quantitative real‐time polymerase chain reaction (RT‐PCR) and Western blot .Data were analyzed with one‐way ANOVA analysis .Results The serum levels of ALT and AST in model control group ,C66 treatment group and normal control group were (202 .71 ± 19 .66 ) U/L , (233 .42 ± 23 .97 ) U/L ;(102 .00 ± 11 .04 ) U/L , (120 .87 ± 13 .83 ) U/L ;(36 .66 ± 6 .37) U/L and (43 .33 ± 8 .08)U/L ,respectively .The differences between model and normal control group were both significant (t=23 .96 and 22 .39 ,respectively ;both P<0 .05) .The C66 treatment group showed significantly lower levels of serum ALT and AST in contrast with model control group (t =11 .56 and 10 .52 ,respectively ;both P<0 .05) .Compared to the model control group ,hepatic Hyp contents in normal control group and C66 treatment group were significantly different (t= 17 .50 , P< 0 .05;t=11 .45 ,P<0 .05) .Collagen Ⅰand α‐SMA mRNA expressions in C66 treatment group were remarkably lower in contrast with that in model control group (t= 7 .23 and 7 .95 ,respectively ;both P< 0 .05) . Protein levels of Collagen Ⅰ ,α‐SMA and NF‐κB p65 decreased in C66 treatment group ,while IκBαincreased significantly (all P<0 .05) .Conclusion The application of C66 can contribute to the regression of liver fibrosis and the mechanism may rely on the regulation of NF‐κB expression .

Objective To explore the effect of inhibiting placental growth factor ( PIGF ) by small interfering RNA ( siRNA) on migration, invasion and chemoresistance of human pancreatic cancer cell line PANC1.Methods Three specific siRNAs targeting PIGF (siRNA-PIGF) were designed.PANC1 cells were transfected with siRNA-PIGF by liposome transfection using untransfected cells as blank controls and nonspecific siRNA ( siRNA-NC) transfected cells as negative controls .The PIGF mRNA and protein expression was examined by real-time RT-PCR and ELISA.MTT method was used to assess the inhibition rate of chemotherapeutic reagents on cell proliferation .The abilities of migration and invasion were evaluated by Transwell assay.Results The inhibition rate of PIGF mRNA in PANC1 cells transfected by 3 siRNA-PIGF were (64.38 ±8.92)%, (70.48 ±7.72)% and (81.25 ±6.02)%, which was lowest in siRNA-PIGF-3 transfected cells.The expression of PIGF mRNA in PANC1 cells were decreased by (63.72 ±8.20)%at 24 h after siRNA-PIGF transfection compared with siRNA-NC transfected cells;and the level of PIGF protein in the supernatant of cultured PANC1 cells was lowered by (42.92 ±1.34)% compared with siRNA-NC transfected cells and by (46.25 ±3.64)% compared with untransfected cells at 48h after transfection, which all had significant difference .There was no statistical difference between untransfected and siRNA-NC transfected cells.After 3 ng/L gemicitabine treatment , the inhibition rate of cell proliferation in siRNA-PIGF group was even higher than that in siRNA-NC and untransfected group [(44.35 ±5.05)% vs(34.29 ±3.60)% and (31.01 ±1.08)%;both P<0.05], and no significant difference was not observed after 5-FU and adriamycin treatment.In migration and invasion assay , the number of transmembrane cells from siRNA-PIGF group was 38.1%and 28.2%of that from siRNA-NC group and 40.8% and 36.2% of that from untransfected group , which had statistical difference (all P<0.05).Conclusions PIGF silencing could significantly suppress the migration and invasion of PANC 1 cells and improve the sensitivity to gemicitabine .

Aim To establish phlegm and blood stasis, qi-stag-nation and blood stasis, phlegm turbid+qi-stagnation and blood stasis model in rats and to study the characteristics of animal models with different blood stasis. Methods SD rats were ran-domly divided into normal group, high fat diet group, chronic unpredictable mild stress group ( CUMS ) and high fat diet +chronic unpredictable mild stress group. Different states of blood stasis rat models were established by corresponding factors for 6 weeks. Indexes of weight, open field behavior, serum lipids and corticosterone were monitored dynamically at the 2 nd, 4 th, 6 th weeks. At the end of the experiment(6th week), the heart func-tion was detected by small animal ultrasound and the left ventric-ular intubation. The blood rheology indexes were detected by the viscosity tester and red blood cell deformation/aggregation test instrument. Results Compared with the normal group, blood stasis could be induced by high fat diet and chronic unpredicta-ble mild stress, introducing the influence of different degree on animal behavior, blood lipids, heart function and blood viscosi-ty. When the two factors were superimposed, the changes of the indexes about blood stasis were the most significant. Perform-ance as: compared with normal control group, a significant re-duction was observed in body weight ( P < 0. 01 ); horizontal movement, vertical movement and movement time were reduced (P<0. 01 or P<0. 05) at the 2 nd week;at the 2 nd and 4 th week, serum corticosterone was increased ( P <0. 01 or P <0. 05) as well as TG at the 4 th and 6 th week (P<0. 01); at the 6 th week, velocity of blood was slowed down ( P<0. 01 );left ventricular anterior wall and posterior wall thickness at end-systolic was increased ( P<0. 01 or P<0. 05 ); left ventricular diastolic index was increased ( P<0. 01 ); the maximum rate of myocardial contraction was decreased ( P < 0. 05 ); the whole blood viscosity was increased ( P<0. 01 ) . Conclusions Blood stasis could be formed by high fat diet and chronic unpredictable mild stress, which has different characteristics. When the two factors are superimposed, the abnormal behavior, blood viscosi-ty, heart function, blood lipid and other indexes of the animal could obviously appear, which can provide the basis for the stud-y of blood stasis syndrome and related drugs.

This paper introduces the structure and the equipment of special artificial environmental and experimental chamber and its basic operating requirements. In compliance with the national standard and safety management, the safety, effectiveness and controllability of the chamber are described.

Experimental pathology is an important part of life science research associated with animal experiment. Acquisition and fixation of optimum specimen and subsequent section of paraffin embedded tissue and dyeing are key factors playing important role in reliability, authenticity of pathological diagnosis.This paper summarizes the problems encountered in pathological section making of animal experiment and it correspond solutions.

Inflammation is the basic pathological process of a variety of diseases, which involved in the occurrence and development of female infertility-related diseases, especially in bacteria and viruses infection of reproductive system, resulting in infertility. However, inflammatory reactions and factors also exist in normal physiological processes, such as endometrial morphologic changes in menstrual cycles, follicle genesis, ovulation, luteinization, pregnancy, etc. In addition, inflammation is also involved in the occurrence of some reproductive endocrine and metabolic diseases, such as obesity, endometriosis, polycystic ovary syndrome and so on. In the past, the understanding to inflammation in reproductive system was mostly limited to the inflammatory diseases and resulted in fertility decline or sterility, infertility, and other problems, which was not comprehensive. This review summarized the normal physiological inflammation and disease-related inflammation in the reproductive system, and described the evaluation of inflammatory state, as well as relevant prevention and treatment suggestions.

The thalamus plays an important role in the process of production of memory and emotion. Patients with thalamic stroke have memory and emotional disorders. Memory disorders are mainly manifested in the generation of hallucinatory memory and amnesia, while emotional disorders are mainly manifested in the effect of negative emotions.

Objective To investigate the effect of myeloid-derived growth factor ( MYDGF) on the secretion of glucagon-like peptide 1 ( GLP-1) in type 2 diabetic mice and its mechanism. Methods A type 2 diabetes model was established by injecting streptozotocin into C57BL/6J wild type ( WT) mice and MYDGF knockout ( KO) mice, which were divided into diabetic group ( WT-D, KO-D) and non-diabetic group ( WT-ND, KO-ND) . Six weeks later, the relevant indicators were detected. Next, those mice were divided into wild-type diabetes group (WT-GFP), wild-type diabetes MYDGF intervention group (WT-MYDGF), knockout type diabetes group (KO-GFP), and knockout type MYDGF intervention group ( KO-MYDG ) according to whether or not the AAV-MYDGF intervention was performed. The wild-type non-diabetic mice were used as a blank control group to observe the effects of MYDGF on biochemical indexes, GLP-1 secretion, and mitogen-activated protein kinase kinase ( MEK)/extracellular regulated protein kinases ( ERK) signal pathway in mice. Results After 6 weeks of intervention, there was no significant difference in the glucose and lipid metabolism indexes between WT-ND and KO-ND groups ( P>0.05) . Compared with WT-D group, fasting plasma glucose (FPG), HbA1C, and blood lipid levels in KO-D group were increased, while gcg, pc3 mRNA, and GLP-1 secretion levels were decreased (all P<0.05). Compared with the WT-GFP group, FPG, HbA1C , and blood lipid levels were decreased in WT-MYDGF group, while gcg and pc3 mRNA, and GLP-1 secretion levels were increased (all P<0.05). KO group revealed a result similar to that in WT group after MYDGF intervention. Western blotting showed that the phosphorylation level of ERK1/2 was lowered in KO diabetic mice compared with WT diabetic mice, which was enhanced in WT and KO mice after MYDGF intervention. Conclusions MYDGF promotes the secretion of GLP-1 by activating MEK/ERK signaling pathway, thereby delaying the development of diabetes.