Objective To observe the suppressive effect of combination of tissue plasminogen activator(t-PA),heparin and homoharringtonine on the formation of proliferative vitreoretinopathy (PVR) after vitreoretinal surgery. Methods Forty-three cases (44 eyes)of complicated retinal detachment who receivedvitreoretinal surgery were divided into 2 groups.Twenty cases(20 eyes)in group A were treated by intravitreal injection of above mentioned drugs at the end of operation,while no intraocular injection of drugs given in 23cases(24 eyes)in group B.The mean follow-up period was 7.9 months. Result The rate of recurrent PVR in group A was 15.8%(3 of 19),and 45.5%(10 of 22) in group B (P

Epithelial mesenchymal transition (EMT) is a process of normal cell physiological development, in which epithelial cells transform into mesenchyme cells through a specific program. EMT plays a key role in inflammatory reaction, cell development, tumor invasion, and metastasis and has an interrelation with prostate cancer stem cells. Recent researches show the involvement of EMT in the development and metastasis of prostate cancer. This article reviews the specific roles and action mechanisms of EMT in the progression of prostate cancer.
Biomedical Research ; Cell Differentiation ; Disease Progression ; Epithelial Cells ; physiology ; Epithelial-Mesenchymal Transition ; physiology ; Humans ; Male ; Mesenchymal Stromal Cells ; Neoplastic Stem Cells ; physiology ; Prostatic Neoplasms ; pathology

Adenoma ; pathology ; Carcinoma ; pathology ; Carcinoma in Situ ; pathology ; Gastric Mucosa ; pathology ; Humans ; Neoplasm Invasiveness ; Precancerous Conditions ; pathology ; Stomach Neoplasms ; classification ; pathology

OBJECTIVE: To explore the effect of traditional Chinese herbal medicine (TCM) for nourishing liver and kidney, clearing meridians and removing toxic substances, on the neurobehavioral manifestations and the activity of the dopamine D2 receptor in rat with levodopa-induced dyskinesias (LID). METHODS: The rat model of Parkinson's disease (PD) was established by injecting 6-hydroxydopamine (6-OHDA) into right substantia nigra of brain, then, the model of LID in rat was produced by injecting levodopa (LD) and benserazide for 4 weeks. The rats were divided into normal control group, 4-week LD treated group, 4-week LD plus TCM treated group, 8-week LD treated group, and 8-week LD plus TCM treated group, and the effect of the TCM on neurobehavioral manifestations was observed. The radioligand binding assay (RLBA) and Scatchard drawing were used to measure the maximal binding capacity of receptor (Bmax) and equilibrium dissociation constant (KD) of the dopamine D2 receptor in corpora striatum. RESULTS: Compared with the 4-week LD treated group and 8-week LD treated group, TCM could decrease abnormal involuntary movement scores of the rats with LID; the RLBA revealed that the dopamine D2 receptor Bmax significantly increased (P<0.05, P<0.01) and the KD significantly decreased (P<0.05). CONCLUSION: TCM can improve the activity of the dopamine D2 receptor and relieve the symptoms of LID.

Objective To examine the effect of Pu-Erh tea extract(PTE) on genes expression of lipogenesis in white adipose tissue of rats fed high fat diet.Method Thirty male SD rats were randomly divided into three groups(n=10):the control group(basal diet);the high fat group(high fat diet);the PTE group(high fat diet + Pu-Erh tea extract).Body weight and adipose tissue were measured.Expression of genes regulating lipid metabolism was assessed in adipose tissue.Results PTE supplementation prevented diet-induced increases in body weight and adipose tissue.Diacylglycerol acyltransferase-1(DGAT1),stearoyl-CoA desalurase-1(SCD1) and sterol regulatory element binding protein-1c(SREBP-1c) mRNA levels were markedly decreased in adipose tissue of rats fed PTE.Conclusion This study shows for the first time that Pu-Erh tea extract prevents diet-induced obesity,and this effect is partly mediated via a direct influence on adipose tissue.

BACKGROUND:Human umbilical cord mesenchymal stem cel s are considered as novel seed cel s in bone tissue engineering. Cryopreservation is an effective method for storing cel s for a long time.
OBJECTIVE:To explore whether umbilical cord mesenchymal stem cel s of cryopreservation could be induced to differentiated into osteoblasts.
METHODS:Mesenchymal stem cel s were isolated from the Wharton’s jel y of human umbilical cord tissue by the tissue explant adherent method. Morphology of primitive cel s was observed by inverted microscopy. Immunophenotypes and cel cycle of umbilical cord mesenchymal stem cel s were measured using flow cytometry. After frozen storage for 6 months, the second passage of umbilical cord mesenchymal stem cel s was thawed and subcultured to passage 12. Upon induction with osteogenic inductive medium, the osteogenic ability of passage 12 of umbilical cord mesenchymal stem cel was evaluated by alkaline phosphatase activity, the immunofluorescent analysis of osteocalcin and bone sialoprotein and the assay of alizarin red staining separately.
RESULTS AND CONCLUSION:Primary umbilical cord mesenchymal stem cel s displayed a typical fibroblast-like morphology. Flow cytometry showed that the cultured cel s expressed high levels of the mesenchymal stem cel s surface markers CD73, CD105 and CD90, but did not express hematopoietic cel s surface markers CD34 and CD45. The survival rate of umbilical cord mesenchymal stem cel s after resuscitation was 90%. The cel cycle analysis indicated that 75%of the cel s of passage 8 were in G 0/G 1 phase and 25%in S+G 2 M phase. Passage 12 cel s treated with osteogenic inductive medium displayed a higher alkaline phosphatase activity compared with control cel s (P<0.01). Moreover, the cel s, induced in osteogenic inductive medium, were positive for osteocalcin and bone sialoprotein staining and formed the mineralized nodules. Umbilical cord mesenchymal stem cel s stil maintain their biological characteristics after cryopreservation, and can be induced into osteoblasts with osteogenic inductive medium.

Objective To determine the effects of Che A and CheY proteins of Campylobacter jejuni regulating the bacterial chemotaxis in vitro and colonization in vivo. Methods By using pET42a plasmid and E. coli BL21DE3 as expression vector and expression strain, respectively, prokaryotic expression systems of cheA and cheY genes of C. jejuni strain NCTC11168 was constructed. Rabbits were immunized with the target recombinant expression proteins, rCheA and rCheY, to prepare the antisera. rCheA-IgG and rCheY-IgG in the antisera were separated using DEAE-52 ion exchange column. pBluescript- II -SK was applied to construct suicide plasmid which used to generate cheA gene knock-out mutant (cheA-). A chemotaxis model in vitro of C. jejuni based on DOC-HAP, the chemotactic ability of cheA' mutant as well as the effect of rCheA-IgG and closantel inhibiting the bacterial chemotaxis were demonstrated. The phosphorylation levels of CheA and CheY after DOC treatment were examined by using either rCheA-IgG or CheY-IgG capture method. The difference of colonization ability between cheA- mutant and wild-type of C. jejuni in mice were checked and then compared. Results The constructed prokaryotic expression systems could efficiently express rCheA and rCheY. The data from PCR and sequencing confirmed the cheA gene knock out from cheA- mutant chromosome. cheA- mutant lost its chemotactic ability towards DOC. Both the rCheA-IgG and closantel could inhibit the chemotaxis of wild-type of C. jejuni (P < 0.05 ). When treatment of DOC, the phosphorylation levels of CheA and CheY in wild-type of C. jejuni rapidly decreased (P < 0. 05 ). The colonization ability in murine jejunum of cheA- mutant was also lower than that of the wild-type ( P<0.05 ) . Conclusion Chemotaxis-associated two-component signaling system (Che-TCSS) of C. jejuni are composed of CheA and CheY, and the two proteins are activated by dephosphorylation. CheA in the Che-TCSS play a critical role in chemotaxis in vitro and colonization in vivo of C. jejuni, and this protein can be used as a target for developing novel anti- C. jejuni drugs.

Background Diabetic retinopathy (DR) is a common ocular complication of diabetes,and its pathogenesis is associated with a variety of factors.c-Jun N terminal kinase (JNK),one of the genes involving in apoptosis,plays an important role in the pathology of diabetes,and relative research is catching increasing interests in recent years.Objective This study was to quantify the expression of JNK3 in retinas of DR murine.Methods Forty-eight SPF male C57BL/6 mice were randomly divided into the diabetes group and the normal control group.Diabetic mouse models were establishend by intraperitoneal injection of 1％ streptozocin (STZ) dissolved by sodium citrate buffer,and equvilant volume of sodium citrate buffer was used in the same way in the mice of the control mice.The left eyeballs were obtained 2,4,8 weeks after modeling and the retinas were collected.Real-time quantitaive PCR was perfored to detect the expression of JNK3 mRNA in retinas.The use and care of the experimental mice complied with the Administration of Experimental Animals in Kunming Medical College.Results Blood glucose levels were significantly higher in 2,4,8 weeks after modeling in the diabetic group compared with the normal control group (t=-5.675,-5.498,-5.347,all at P＜0.01).The relative expression levels of JNK3 mRNA (A value) in the retinas were significantly different between the groups at various time points (Fgroup =102.345,P＜0.05 ; Ftime =131.679,P＜ 0.05).The relative expression levels of JNK3 mRNA in the retinas were 3.21 ±0.14 and 5.43 ±O.37 in 4 and 8 weeks after modeling in the diabetic group,which were significantly elevated in comparison with the normal control group (2.54±0.42 versus 2.26±0.67) (t =4.073,23.399,both at P＜0.05).Compared with the second week and fourth week,the relative expression levels of JNK3 mRNA in the retinas in the eighth week were significantly raised in the diabetic group (t =10.756,16.857,both at P ＜ 0.05).Conclusions JNK3 expression in the retina upregulates in diabtic mice in a time-dependent manner.JNK3 is paopably involved in the pathogenesis and development of DR.

0.05),but that MFI and/or PPC of CAR in the 2 types cells markedly increased compared with lymphocytes in the same group(Pa

Objective To explore the relationship of Helicobacter pylori (Hp) infection and carotid plaques in patients with coronary heart disease and analyze the related factors of carotid plaques.Methods This study enrolled 209 patients.13C-urea breath test (13C-UBT) was used to assess Hp infection.Based on the results of 13C-UBT,patients were divided into infection-positive group (101 patients) and infection-negative group (108 patients).The incidence of carotid plaques was detected by color Doppler,and plasma homocysteine (Hcy),total cholesterol (TC),low density lipoprotein cholesterol (LDL-C),fibrinogen (Fbg),high sensitivity C reactive protein (hs-CRP) were measured and compared.Results The incidence of carotid plaques in infection-positive group(69.31％,70/101) was higher than that in infection-negative group (55.56％,60/108),and there was significant difference (P =0.040).There was significant difference in hs-CRP between infection-positive group and infection-negative group [(3.91 ± 1.91) mg/L vs.(2.65 ± 1.15)mg/L] (P =0.041).There were no significant difference in Hcy,TC,LDL-C,Fbg between infection-positive group and infection-negative group (P ＞ 0.05).Logistic regression analysis showed that Hp infection was correlated with carotid plaques in patients with coronary heart disease.The severity of Hp infection had no significant effect on the incidence of carotid plaques.Conclusions Hp infection-positive patients with coronary heart disease may have a higher incidence of carotid plaque,regardless of Hcy,LDL-C,Fbg and TC level.This study shows that Hp is correlated with carotid plaque.The severity of Hp infection has no significant effect on the incidence of carotid plaque.