Objective To observe the relationship of the Janus kinase-signal transducers and activator of transcription pathway and neurogenesis in the lateral ventricle subventricular zone(SVZ) and choroid plexus of neonatal rats with periventricular leukomalacia(PVL).Methods PVL models were established by right common carotid artery ligation followed by 4 h 60 mL/L oxygen exposure in 2-day-rat;the neonatal rats performed a sham operation,without hypoxia-ischemia were used as control group.The rats were sacrificed at 0 h,3 h,6 h,12 h,1 d,3 d and 7 d after hypoxic-ischemic(HI),and brain tissues were collected,immunohistochemistry was used to detect the expression of P-STAT3 and Nestin in the subventricular zone and choroid plexus.Results Very low expressions of P-STAT3 and Nestin were observed in lateral ventricle SVZ and choroid plexus in control group.The expression levels of P-STAT3 and Nestin increased significantly after HI,peaked at 1 d and 3 d separately,and remained at a higher level at 7 d after HI,demonstrating significant differences at each time point compared with those in control group(Pa

We isolated polyA~+ mRNA direcdy from tumor tissue of ovarian carcinoma using Oligotex~(TM) Direct mRNA Kit (QIAGEN) to synthesize the first and second strand cDNA. The ds-cDNA termini were blunted with pfu DNA poly-rnerase. The blunted cDNAs were added EcoR I adaptor, and then were digested by Xho I . Small cDNA molecules(

In order to build a high-quality teaching group with excellent academics,strong innovation and comprehensive ability, the School of Public Health of CQUMS pays much attention to training young teachers,encouraging them to further their study and scientific research abilities as well as improving their comprehensive abilities.

Gastroesophageal reflux disease( GERD)is caused by dysfunction of lower esophageal sphincter( LES), which allows the contents of stomach and duodenum to reflux into esophagus. Currently,medical and surgical therapies are the main treatment for GERD,but patients need to take life-long acid suppression and the surgical treatment has the risks of potential side effects. Endolumenal therapy as a minimally invasive approach to GERD can safely and effectively relieve the symptoms of GERD,especially Stretta radiofrequency procedure,transoral noninvasive fundoplication( TIF ) and LinX reflux management system. This article reviewed the advances in study on endolumenal therapy for GERD.

Staphylococcus aureus,an important foodborne pathogen,can contaminate foods through variety of ways and produce enterotoxin that may cause Staphylococcal food poisoning.In addition to food safety problems,Staphylococcus aureus could also cause clinical infection.The study of its pathogenicity is not only beneficial to prevent and control foodborne diseases,but also provide a new point for clinical treatment.This paper analyzes the types and characteristics of common strains of Staphylococcus aureus in food,and summaries the effect of food processing on pathogenicity and the methods for pathogenicity research in order to provide reference for the related study on pathogenicity of Staphylococcus aureus.

Adult ; Arsenic Poisoning ; pathology ; Chronic Disease ; Hemosiderin ; metabolism ; Hemosiderosis ; metabolism ; pathology ; Humans ; Hypertension, Portal ; chemically induced ; metabolism ; pathology ; Liver Cirrhosis ; chemically induced ; metabolism ; pathology ; Male ; Pancytopenia ; chemically induced ; metabolism ; pathology ; Splenomegaly ; chemically induced ; metabolism ; pathology

Objective To investigate the effects of interferon-γ (IFN-γ) on interleukin-10 (IL-10) and mononuclear macrophages in a mouse model of gallbladder cancer.Methods Mouse models of gallbladder cancer were constructed by inoculating the human gallbladder cancer cell line GBC-SD subcutaneously in 20 BALB/C mice,and then all the mice were randomly divided into the IFN-γ group and the control group (10 mice in each group).Murine recombinant IFN-γ (0.1 mL,1 × 105 kU/L,diluted with normal saline) was injected into the tumors in the IFN-γgroup,and normal saline was injected into the tumors in the control group.The expression of IL-10 was detected by ELISA,and the numbers of CD14 + cells (mononuclear macrophages),CD64 + cells (M1 macrophages) and CD206+ cells (M2 macrophages) were counted by the immunohistochemistry.All data were analyzed using the Student's t test.Results The mouse models of gallbladder cancer were successfully constructed 1 week later.Nine mice survived in the IFN-γ group,and 7 mice survived in the control group.The tumor weight was (518 ± 138)mg in the IFN-γ group and (669 ± 128)mg in the control group,with a significant difference between the 2 groups (t =2.240,P ＞ 0.05).The volume of the tumor was (456 ± 172)mm3 in the IFN-γ group and (505 ± 146)mm3 in the control group,with no significant difference between the 2 groups (t =1.503,P ＞ 0.05).The concentration of IL-10 was (58 ± 16) μg/g in the IFN-γgroup,which was significantly lower than (102 ± 45) μg/g in the control group (t =2.796,P ＜ 0.05).The number of mononuclear macrophages was 81 ± 16 in the IFN-γ group,which was significantly greater than 50 ± 21 in the control group; the number of M1 macrophages was 66 ± 12 in the IFN-γ group,which was significantly greater than 9 ± 4 in the control group ; the number of M2 macrophages was 15 ± 4 in the IFN-γgroup,which was significantly lower than 40 ± 14 in the control group (t =3.214,13.127,6.914,P ＜ 0.05).Conclusions IFN-γ could decrease the concentration of IL-10 in the tumor microenvironment,and it could induce the mononuclear macrophage to infiltrate into the stroma of the gallbladder cancer cells,and most of the monocytes and macrophages were differentiate to M1 macrophages.Gallbladder neoplasms; Interleukin-10; Interferon-γ; Mononuclear macrophages

Objective:To investigate the effect of basic fibroblast growth factor(bFGF) on the proliferation of gingiva-derived mesenchymal stem cells(GMSCs) in vitro.Methods:GMSCs were isolated from healthy gingival tissue samples and identified.GMSCs of passage 4 were treated by bFGF at 0,0.5,1,5,10,20 ng/ml respectively for 1-9 d.The proliferation of the cells was evaluated using CCK-8 kit.Results:bFGF at 0.5-20 ng/ml increased GMSCs proliferation.0.5-10 ng/ml of bFGF showed dose and time dependant proliferation promoting effect on GMSCs.Conclusion:bFGF can increase GMSCs proliferation ability in a dose and time dependant manner.

Objective To explore the mechanism ofJiedu Qingfei Mixture for airway mucus hypersecretion of rat models with chronic obstructive pulmonary disease (COPD).Methods Airway instilling lipopolysaccharide combining fuming method was used to establish COPD models. Forty clean level Wistar strain rats were randomly divided into blank control group, model group,Jiedu Qingfei group, and clarithromycin group. Model group, Jiedu Qingfei group, and clarithromycin group were given normal saline,Jiedu Qingfei Mixture, and clarithromycin by gavage respectively, while the blank control group was raised normally for 30 d. All rats were killed on the 31st day for taking lung tissue (6 rats from each group were chosen randomly). Pathological changes of lung tissue and mucous glands hyperplasia were observed by HE staining method. NE and MUC5AC mRNA expression on lung tissue were detected by RT-PCR method. Protein expressions of NE and MUC5AC on pulmonary tissue and airway epithelium were detected by immunohistochemical method.Results Compared with blank control group, mucous glands hyperplasia on airway epithelium, mRNA expression of NE and MUC5AC in lung tissue, and protein expressions of NE and MUCA5C on airway epithelium in the model group significantly increased (P<0.05,P<0.01). Compared with model group, mucous glands hyperplasia on airway epithelium inJiedu Qingfei group significantly decreased (P<0.01), as same as clarithromycin group;Jiedu Qingfei group showed better effects on down-regulating NE and MUC5AC mRNA expression in lung tissue compared with clarithromycin group. MUC5AC protein expression on airway epithelium inJiedu Qingfei group significantly decreased (P<0.05), as same as clarithromycin group.Jiedu Qingfei group and clarithromycin group had no difference on NE protein expression in airway epithelium compared with model group.Conclusion Jiedu Qingfei group Mixture can reduce airway mucus hypersecretion of COPD by down-regulating MUC5AC expression through neutrophil elastase.

Objective To observe the effects of Qingjin Huatan Decoction on EGFR/MAPK signaling pathway of airway mucus hypersecretion rats with chronic obstructive pulmonary disease (COPD). Methods Intratracheal instillation of LPS combined with smudging method was used to establish COPD airway mucus hypersecretion rat models. Experimental rats were randomly divided into blank group, model group, Qingjin Huatan Decoction group and clarithromycin group. The blank group was normally fed, while the other three groups were given NS, Qingjin Huatan Decoction, and clarithromycin respectively for gavage, once a day for 30 days. All rats were killed on the 31st day, and pathological changes of lung tissue and mucous glands hyperplasia were observed by HE staining method. The gene expressions of EGFR and MUC5AC in lung tissue were detected by RT-PCR method. The protein expressions of P-EGFR, P-ERK, P-JNK, P-p38 and MUC5AC in pulmonary tissue and airway epithelium were detected by immunohistochemical method. Results Compared with the blank group, mucous glands hyperplasia on airway epithelium, protein expressions of P-EGFR, P-ERK, P-JNK, P-p38 and MUC5AC on airway epithelium significantly increased in the model group (P<0.01); gene expression of MUC5AC of lung tissue increased (P<0.05). Compared with the model group, mucous glands hyperplasia on airway epithelium, P-p38, P-ERK and MUC5AC protein expression on airway epithelium in Qingjin Huatan Decoction group significantly decreased (P<0.05, P<0.01); the protein expression of P-JNK increased significantly (P<0.01). EGFR and MUC5AC mRNA in lung tissue in Qingjin Huatan Decoction group decreased significantly (P<0.01). Conclusion Qingjin Huatan Decoction can reduce airway mucus hepersecrection of COPD by inhibiting ERK and p38 signal pathway on EGFR downstream.