hTERT extends proliferative lifespan and prevents oxidative stress-induced apoptosis in human lens epithelial cells.

Purpose: Telomerase is a specialized polymerase that catalyzes synthesis of telomeres in most eukaryotes. When introduced into somatic cells, it extends the proliferative lifespan and prevents replicative senescence. Whether it has similar functions in lens epithelial cells, especially in human lens epithelial cells (HLECs) remains to be determined.

Levels of polychlorinated biphenyls in 1,4-dichlorobenzene mothballs.

Although polychlorinated biphenyls (PCBs) are globally recognized pollutant, an understanding of their resources as by-products in chemical industry is poorly investigated. This paper presents data from a study that was conducted in order to determine the extent of PCBs in 1,4-dichlorobenzene( p-DCB) mothballs. Total PCBs and dioxin-like PCBs were detected in five mothball samples.

Human telomerase reverse transcriptase immortalizes bovine lens epithelial cells and suppresses differentiation through regulation of the ERK signaling pathway.

Telomerase is a specialized reverse transcriptase that extends telomeres of eukaryotic chromosomes. The functional telomerase complex contains a telomerase reverse transcriptase catalytic subunit and a telomerase template RNA. We have previously demonstrated that human telomerase reverse transcriptase (hTERT) catalytic subunit is functionally compatible with a telomerase template RNA from rabbit.

[Expression of calprotectin in colon mucosa and fecal of patients with ulcerative colitis].

Objective: To investigate the correlation between the disease activity of ulcerative colitis (UC) and the immunohistochemical distribution of calprotectin in colon mucosa,as well as the levels of calprotectin in fecal.

Methods: Monoclonal antibody against calprotectin was used to investigate the distribution of these proteins in colon mucosa from 42 patients with ulcerative colitis and 20 healthy controls. ELISA assay was used to measure the concentrations of calprotectin in fecal.

Effects of a plasmid expressing antisense tissue inhibitor of metalloproteinase-1 on liver fibrosis in rats.

Background: No efficient therapy for liver fibrosis has been available. This study was aimed to provide evidence that the introduction of a plasmid expressing antisense tissue inhibitor of metalloproteinase-1 (TIMP-1) into a rat model of immunologically induced liver fibrosis can result in the increased activity of interstitial collagenase, thus enhancing the degradation of collagen.

Methods: Real-time nested polymerase chain reaction (RT-Nested-PCR) and gene recombination techniques were used to construct a rat antisense TIMP-1 recombinant plasmid that can be expressed in eukaryotic cells.

[Eukaryotic expression and biological activities of anti-p185 erbB2 mouse/human chimeric antibody].

Objective: Overexpression of the HER2/neu oncogene is a frequent molecular event in multiple human cancers. Being a cancer antigen, p185(erbB2) is an ideal target for immunotherapy. In order to decrease the immunogenicity of mouse anti-p185(erbB2) monoclonal antibody in human cancer therapy, we constructed the eukaryotic expression vector of anti-p185(erbB2) chimeric monoclonal antibody and verified expression of the chimeric antibody in CHO-dhfr(-) cell.

Formation of PCDD/Fs from heating polyethylene with metal chlorides in the presence of air.

This paper investigated the effect of inorganic chlorine on the formation of PCDD/Fs from heating polyethylene (PE) in the presence of air. There was an increase in the formation of PCDD/Fs with an increasing amount of metal chlorides except NaCl, which was not observed to have any effects on the formation of PCDD/Fs without the presence of catalysts. Although the levels of PCDD/Fs formation in this study have no relevance to full scale municipal solid waste incineration, the results of the present experiments can aid understanding of the mechanisms of the formation of PCDD/Fs from heating PE in the presence of metal chlorides.

Blockage of transforming growth factor beta receptors prevents progression of pig serum-induced rat liver fibrosis.

Aim: To test the hypothesis that introduction of antisense T beta R I and T beta R II eukaryotic expressing plasmids into a rat model of immunologically induced liver fibrosis might block the action of TGF-beta (1) and halt the progression of liver fibrosis.

Methods: RT-Nest-PCR and gene recombination techniques were used to construct rat antisense T beta R I and T beta R II recombinant plasmids which could be expressed in eukaryotic cells. The recombinant plasmids and empty vector (pcDNA3) were encapsulated by glycosyl-poly-L-lysine and then transducted into rats of pig serum-induced liver fibrosis model.

[Effects of antisense transforming growth factor beta receptor-II (TGFbetaRII) expressing plasmid on experimental liver fibrosis].

Objective: To study the effects of antisense transforming growth factor beta receptor-II (TGFbetaRII) expressing plasmid on experimental liver fibrosis.

Methods: RT-Nest-PCR and gene recombinant techniques were used to construct the rat antisense TGFbetaRII recombinant plasmid which can be expressed in eukaryotic cells. Thirty-six male SD rats were randomly distributed into five groups: 10 in experimental liver fibrosis model induced by pig-serum as disease control group; 10 in antisense TGFbetaRII transfection as treatment group; 10 in pCDNA3 transfection as treatment control group and 6 in normal control group.

Inhibition on the production of collagen type I, III of activated hepatic stellate cells by antisense TIMP-1 recombinant plasmid.

Aim: To investigate the inhibition effects on the production of collagen type I, III secreted by activated rat hepatic stellate cells (rHSCs) by antisense tissue inhibitors of metalloproteinase 1 (TIMP-1) recombinant plasmid through elevating interstitial collagenase activity.

Methods: rHSCs were extracted from normal rat liver by pronase and collagenase digestion and purified by centrifugal elutriation, and were cultured on plastic dishes until they were activated to a myofibroblastic phenotype after 7-10 days. RT-Nest-PCR and gene recombinant techniques were used to construct the rat antisense TIMP-1 recombinant plasmids which can express in eucaryotic cells.