Tyrosine phosphorylation is a key post-translational mechanism that regulates cellular processes and maintains homeostasis.Aberrant changes in tyrosine phosphorylation are often associated with disease states such as metabolicdisorders,cancer and cardiovascular disease.Protein tyrosine phosphatases (PTPs) are the enzyme family that regulates protein phosphorylation level of tyrosine residues in the cellular processes and signaling ways.So far,scientists have discovered 112 kinds of human PTPs.Among them,PTP1B is widely and clearly studied.Recently,as an enzyme that play a role in oncogenesis,PTP1B has been wildey studied by scientists.Here,we highlight the relationship between protein tyrosine phosphatase 1B and hematologic neoplasms.

Objective To investigate the expression and the roles of Angiopoietin 1(ang-1) and Angiopoietin 2(ang-2) in the endometrium of women with abnormal bleeding after medical abortion. Methods Analyzing endometrial pathological change of 1087 patients with abnormal bleeding after medical abortion in early pregnancy,and the endometrial specimens from 40 patients were randomly chosen for the study. The endometrial specimens from 20 women without abnormal bleeding after medical abortion were used as control group.Immunohistochemistry was used to detect the levels of Ang-1 and Ang-2 proteins in endometria. Results The percentage of patients with both the residul decidua and villus was 80.5%; positive immunoreactive signals of Ang-1 and Ang-2 were found in the endometrial glandular epithelium, stromal cells and the endothelial cells of vessels; the expression rate of Ang-1 and Ang-2 in the patients with abnormal bleeding were higher than that in the control group(P

0.05). The mortality in group A was obviously higher than that in group AI ( P

Acupuncture Therapy ; Adult ; Humans ; Male ; Myopathies, Structural, Congenital ; therapy

Objective To construct recombinent retroviral vectors containsins the expression sequence of hIL-4,and detect the expression of target genes.Methods Design the primer with restrictive enzyme spot and amplify target gene by PCR from plasmid including hIL-4 gene.Clone the target gene into retroviral vector pLXSN,and identify the aquired plasmid by sequencing.Transfect human synoviocytes with acquired virus in vitro.Detect the protein expresssion by western blotting.Results We successfully constructed the recombinant retrovirus-rRV-hIL-4.The hIL-4 gene was transduced into human synoviocytes by recombinant retrovirus in vitro.The protein expression of genes was detected by Western blotting.Conclusion Recombinant retrovirus rRV-hIL-4 is constructed successfully.The hIL-4 gene is transduced successfully into the human synoviocytes in vitro and the transduced synoviocytes can express hIL-4 protein.

Objective:To investigate the effect of mycophenolate mofetil(MMF)on proliferation and apoptosis of cyst-lining epithelial cells in patients with autosomal dominant polycystic kidney disease(ADPKD),and to compare its effect with that of rapamycin(RAPA)in vitro.Methods: Primary cultured cyst-lining epithelial cells were treated with MMF and RAPA at different concentrations(0,0.005,0.05,0.5,5 ?g/ml)for 48 h or 72 h.The inhibitory effects of them on the cells were evaluated by MTT assay;the cell cycle distribution and apoptotic ratio were determined by flow cytometry.The morphological changes of cyst-lining epithelial cells were observed under transmission electron microscope.Results: Both MMF and RAPA significantly inhibited the proliferation of cyst-lining epithelial cells in a dose-and time-dependent manner.After 48 h treatment,the cells were blocked at S phase by MMF and at G0/G1 phase by RAPA.Both drugs induced cell apoptosis,with the maximal apoptotic rate being(5.53?0.27)% for MMF and(4.36?0.10)% for PAPA.Typical morphological changes of apoptotic cells were observed under electron microscope.Conclusion: MMF can effectively inhibit proliferation and induce apoptosis of cyst-lining epithelial cells,but its inhibitory effect is weaker than that of RAPA.

In order to adapt to the requirements of modem medical knowledge and skills for higher medical workers,and to cultivate medical students' molecular medicine quality and comprehensive ability,Weifang Medical University broke the boundaries of disciplines and constructed experimental course group in molecular medicine based on the ideas of curriculum group construction.Molecular medical knowledge was integrated into the teaching process of experimental course group,experimental teaching content system was reasonably integrated and optimized,high quality teaching team was set up,multi-level experimental teaching platform was built and student-centered teaching mode was implemented to explore the experimental teaching approach which helped medical students to form systematic molecular medicine knowledge structure and ability structure.

Objective To observe the impact of heparanase on glomerular endothelium glycocalyx during sepsis and to investigate the prevention of glycocalyx injury.Methods C57/BL6 mice were injected with lipopolysaccharide (LPS) or tumor necrosis factor-α(TNF-o) and sacrificed one hour later.Glomerular endothelium glycocalyx traced with lanthanum was observed by transmission electron microscope(TEM).Western blotting was used to observe heparanse protein expression of renal cortex tissue.Human renal glomerular endothelial cells (HRGECs) were stimulated with TNF-α and active heparanase protien expression was detected by Western blotting.Mice were administrated with heparin sodium or heparinase Ⅲ and renal endothelium glycocalyx was observed by TEM.Urine during twenty-four hours was collected to measure urinary albumin and creatinine.The ratio of albumin to creatinine was calculated and compared among groups.Results The glomerular endothelium glycocalyx of LPS group and TNF-α group was degradated and the one of podocyte was integrated.Renal cortex tissue heparanase protein expression was significantly increased since one hour after LPS injection (P ＜ 0.01).The protein expression of activited heparanase of HRGECs which were stimulated with TNF-α was increased (P ＜ 0.05).Administration of heparin sodium which could inhibit the activity of heparanase could prevent the glycocalyx form degradation.The ratio of urine albumin to creatinine of heparin sodium group was decreased compared with LPS group (P ＜ 0.05) and the ratio of heparinase Ⅲ group was higher than control group(P ＜ 0.01) as a result of degradation of glomerular endothelium glycocalyx.Conclusions During the early stage of sepsis,TNF-α can induce glomerular endothelium heparanase to increase and active,and consequently the glycocalyx is degradated which leads to albuminuria.Inhibition of heparanase can protect glomerular endothelium glycocalyx and prevent albuminuria.

Objective To explore the role of Hippo pathway in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD),and find potential targets for drug therapy.Methods By means of immunofluorescence staining,Western blotting,Real-time PCR,the differences of sublocalization,expression and phosphorylation level about Hippo pathway molecules in Han:SPRD (cy/+) and ADPKD patients compared with the control were observed.Knockdown Yes kinaseassociated protein (YAP),transcriptional coactivator with PDZ binding motif (TAZ) and large tumor suppressor kinase1 (LATS1) in cystic lining epithelium cell line WT9-12 were took by siRNA interference,and then their effects on cell proliferation,apoptosis and cell cycle were assessed.Results In cystic lining epithelium of Han:SPRD(cy/+),decreased expression of LATS1 and increased expression of YAP were found compared with the control,and the immunofluorescence of YAP was distributed both in cytoplasm and nucleus,while distribution and expression level of TAZ were without significant variance.Abnormal mRNA expressions of Hippo pathway components in ADPKD patients were found (P ＜ 0.05).Down-regulation of LATS1 in WT9-12 cells could prohibit phosphorylation of YAP,and prompted proliferation and cell division.Knockdown YAP in WT9-12 cells could inhibited cell proliferation by arresting cell cycle in G0/G1 phase,but down-regulating TAZ showed no significant differences in proliferation and cell cycle.Conclusions Altered Hippo signaling exists in ADPKD,and YAP activation may be one leading cause of autosomal dominant polycystic kidney disease onset.In vitro,knockdown YAP in WT9-12 cells can inhibit cell proliferation by arresting cell cycle and depressing cell division,suggesting the expression level and activity of YAP are potential targets for ADPKD treatment.