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G Yang

Publications and source records attributed to G Yang.

At least 361 records · Page 20Linked to original sources
PubMed1996

[Subcellular location of blood group substances ABH using transmission electron microscopical immunocytochemistry technique].

The subcellular location of blood group substances ABH was studied by using transmission electron microscopical immunocytochemistry. The cells were the epithelial cells of both mucous membranes and glands of normal human stomach, duodenum and transverse colon. Both cellular ultrastructure and antigens should be well preserved in transmission electron microscopical immunocytochemistry. In this paper, various fixatives, embedding media and immunostaining methods were investigated and compared. The results indicate that the solution containing 2% paraformaldehyde and 0.2% glutaraldehyde (2PG) is the best fixative and Epon 812 medium is the best embedding medium for preserving ABH antigens and protecting cellular ultrastructure. Post-embedding immunogold staining technique is superior to pre-embedding immunoperoxidase staining.

ABO Blood-Group System↗
PubMed1996

[The role of p53 gene during the development of human oral malignant lesions: a comparative study of p53 gene mutation with P53 protein positive immunostaining].

In order to increase the sensitivity to immunostaining in formalinfixed, paraffin-embedded tissues, we developed an immunohistochemical method by microwave heating of tissue sections instead of trypsin digestion. The results of this study showed that there was no positive P53 protein reaction in normal and hyperplastic mucousa of human mouth, whereas 90% (27/30) of cases with dysplasia, 61% (30/49) of oral squamous cell carcinomas and 86% (13/15) of regional metastatic lymph nodes were positive. And all positive reactions were localized in nuclei. Comparison of these positive results of p53 gene mutation detected by silver staining method with the results by polymerase chain reaction-single strand conformation polymorphism analysis did not reveal matched results, especially during the precancerous period. The authors analysed the causes of difference not only by methodology, but also by cell groups which had different genetic changes in tissues of precancerous lesions.

Carcinoma, Squamous Cell↗
PubMed1996

[The relationship of non-Hodgkin's lymphoma with P16 protein expression].

The expression of P16 protein was examined in 45 cases of non-Hodgkin's lymphoma (NHL), 4 cases of reactive hyperplasia of lymph node (RHLN) and 6 cases of normal spleen with immunohistochemical staining. Positive reaction of P16 protein was observed in some lymphocytes of RHLN and splenic nodule and around splenic sinus. The positive rate of P16 protein expression in NHL was 37.8% (17/45). The positive rates of P16 protein expression for the low intermadiate- and high-grade malignancy groups were 66.7% (10/15), 37.5% (6/16) and 7.1% (1/14) respectively. There was a significant difference between the low malignancy NHL and the high malignancy NHL (P < 0.005) in expression rate of P16 protein. It suggests that P16 protein expression may be one of the important parameters in estimating the prognosis of patients with NHL.

Adolescent↗
PubMed1996

[Expression of P16 protein in pancreatic carcinoma].

In order to investigate the prognostic value of P16 protein in the prediction for patient with pancreatic carcinoma, we examined the expression of P16 protein in 50 cases of pancreatic carcinoma by immunohistochemical staining. The results showed that P16 protein positive rate was 56% (28/50) and the immunoreaction was in the cytoplasm of cancer cell. The expression of P16 protein did not correlate with histological grade, but with lymph node metastasis (P < 0.05). Our results indicate that P16 protein expression may be a promising predictor for the prognosis of patients with pancreatic carcinoma, i.e. carcinoma being positive for P16 protein may have a better prognosis than the negative one.

Carcinoma, Ductal, Breast↗
PubMed1996

[Renin-angiotension system--stress hormone response system].

Angiotensin II (A II) was significantly increased in both acutely and chronically stressed animals as found in brain, heart, blood vessels and adrenal glands. After running a race, the plasma A II contents of sportsmen similar to cortisol increased markedly too. In the chronical stress-hypertensive animals, the contents of circulating A II and tissue A II were increased quite lastingly. It was also found that the high concentration of A II may stimulate the adrenal gland secreting glucosteroid, and increase of tissue A II may be faciliated by the activation of beta adrenergic receptors. On basis of the above finding, we tend to assume that A II is a stress hormone and the renin angiotension system (RAS) is a stress hormone responses system. Morever there exists a close relation between RAS and two classic stress hormone response systems, i.e. the hypothalamus-pituitary-adrenal cortex system and the sympathetic-adrenal medulla system.

Angiotensin II↗
PubMed1996

[The role of P53 gene in the development of oral squamous cell carcinoma: study of P53 gene mutation by silver staining polymerase chain reaction-single strand conformation polymorphism].

It is widely accepted that the inactivation of P53 tumor suppressor gene is related to the tumorigenesis of many cancers. The study on P53 tumor suppressor gene has become a hotspot in molecular oncology. But until now, the reports on the research of the role of P53 gene in the tumorigenesis and prognosis of oral squamous cell carcinoma are scarce. So, two studies have been carried out. (1) A silver staining method of polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis was established by detecting the mobility shifts of the DNA bands of the products of PCR of mutant P53 gene plasmid and the Sup F mutants which had been proved to have point mutation by DNA sequencing in shuttle vector plasmid pS 189 mutagenesised by N-methyl-N-nito-N-nitosoguanidine (MNNG). For the method is non-radiation with high sensitive, it has applicable value. (2) By silver staining PCR-SSCP system, tissues from normal oral mucoas membrane to metastatic oral squamous cell carcinoma (OSCC) were analyzed and the results showed that tissues from 53% oral precancerous lesions and 65% OSCC had abnormal SSCP bands and the abnormal frequency of metastatic cancers was higher than that of nonmetastatic ones. These suggest that P53 gene mutation plays some role on the process of initiation, development and metastasis of OSCC.

Adult↗
PubMed1996

[Effect of leaf picking on the output of radix Astragali seu Hedysari].

Based on an orthogonal design, the experiments have shown that proportion and time of leaf picking are the major factors to influence the thickness and output of Radix Astragali seu Hedysari. If the proportion is extended and the time is delayed, both the thickness and output of the roots will be reduced accordingly. The output will not change much if the time is set on around June 15 each year and the proportion is taken 1 out of 3.

Fabaceae↗
PubMed1996

Clustered p53 immunostaining: a novel pattern associated with prostate cancer progression.

Abnormal p53 protein accumulation is typically defined as present when greater than 5 or 10% of cancer cells stain positively. We present a novel approach whereby immunopositivity is defined when 15 or more cells within a 300 x 400-micrometer(2) field exhibit p53 protein accumulation; a feature that we have called "clustered" staining. We assessed p53 immunostaining of moderately differentiated, clinically localized prostate cancers derived from two patient groups: those without cancer recurrence 5 years after radical prostatectomy, and those in whom cancer had recurred following radical prostatectomy. Clustered p53 immunopositivity was present in 10 (63%) of 16 patients in the recurrent group and in only 7 (21%) of 33 in the nonrecurrent group. Clustered p53 staining was clearly associated with cancer recurrence (P < 0.01). This refinement of a commonly used assay may help define the biological aggressiveness of a cancer.

Humans↗
PubMed1996

Reduced levels of transforming growth factor beta receptor type II in human prostate cancer: an immunohistochemical study.

In previous studies we demonstrated that the growth of human prostatic adenocarcinoma is associated with aberrant accumulation of transforming growth factor (TGF) beta1, a growth factor that has been shown to be a potent inhibitor of epithelial cell proliferation. We investigated the expression of TGF-beta receptor II (TGFbetaR-II) in benign prostate tissue and in prostate cancer using standard immunohistochemical techniques. Quantitation of immunopositivity for TGFbetaR-II was assessed on a visual analogue scale ranging from 0 (absence of staining) to 4+ (intensely positive staining). All of the benign glandular epithelia stained intensely, either 3+ or 4+, representative of the ubiquitous nature of TGFbetaR-II in normal tissue. Overall, staining was reduced in prostate cancer sections, and there was progressively diminished staining as the histological grade of the cancer increased (P < 0.01, Kruskal-Wallis test). This immunohistochemical study indicates that a decline in the levels of TGFbetaR-II is correlated with advancing histological aggressiveness of the cancer and suggests that aberrant TGFbetaR-II function may play a role in human prostate carcinogenesis.

Aged↗
PubMed1995

Multiple lineages of tumors express a common tumor antigen, P1A, but they are not cross-protected.

Whether tumors of different lineages share common Ags is a critical issue for understanding anti-tumor immune responses and for designing Ag-specific tumor immunotherapy. Because of lack of cross-protection among individually derived tumors, it has been proposed that tumor Ags are specific for individual tumors. Here we show that lack of cross-protection is not due to lack of a shared tumor Ag. Thus, a plasmocytoma J558 transfected with the costimulatory molecule B7 activates a cross-reactive CTL response in vivo. The major Ag recognized by the cross-reactive CTL is P1A, which is expressed in mastocytoma P815, plasmocytoma J558, and fibrosarcoma Meth A. Surprisingly, no significant cross-protection can be detected among P1A-expressing tumors after immunization with either P1A-expressing or B7-transfected P815 cells. Our results demonstrate that multiple lineages of tumors are not cross-protected even though they share a tumor Ag that can be recognized by CTL. These results have important implications for tumor immunotherapy.

Amino Acid Sequence↗
PubMed1995

In vivo gene therapy with p53 or p21 adenovirus for prostate cancer.

We introduced the gene for wild-type human p53 or p21, a critical downstream mediator of p53-induced growth suppression, into a p53-deficient mouse prostate cancer cell line using a recombinant adenoviral vector (Ad5CMV-p53 or Ad5CMV-p21). Elevated levels of endogenous mouse p21 mRNA provided evidence for the functional activity of virally transduced p53. Functional activity of viral-transduced p21 was demonstrated through immunoprecipitation of cellular protein extracts, which showed that the viral-transduced p21 associates with cyclin-dependent kinase 2 and was sufficient to down-regulate the activity of the cyclin-dependent kinase by approximately 65%. In vitro growth assays revealed significantly higher growth suppression after Ad5CMV-p21 infection compared to Ad5CMV-p53. In vivo studies in syngeneic male mice with established s.c. prostate tumors demonstrated that the rate of growth and final tumor volume were reduced to a much greater extent in mice that received intratumor injection of Ad5CMV-p21 compared to Ad5CMV-p53. In addition, the survival of host animals bearing tumors that were infected with Ad5CMV-p21, but not Ad5CMV-p53, was significantly extended. These data suggest that Ad5CMV-p21 may be effective as a therapeutic agent for prostate cancer.

Adenoviridae↗
PubMed1995

In vitro priming of tumor-reactive cytolytic T lymphocytes by combining IL-10 with B7-CD28 costimulation.

Naive spleen cells from syngeneic mice generated tumor-reactive CTL following three cycles of in vitro culturing with IL-10 and cells from the P815 mouse mastocytoma that expressed the B7-1 or B7-2 costimulator. Unpurified as well as CD8-enriched naive splenocytes could be used for priming. The in vitro primed CTL were CD8+, and their recognition was MHC class I restricted. Both IL-10 and B7-transfected P815 cells were required for the priming. However, a combination of exogenous IL-10 and IL-2 in the presence of B7-negative wild-type P815 cells also induced tumor-reactive CTL. Injection of the neutralizing anti-IL-10 mAb JES-2A5 into mice reduced their ability to mount a primary CTL response after immunization with B7-1+ P815 cells, and inclusion of this mAb in the in vitro cultures inhibited a secondary CTL response. Adoptive transfer of the in vitro primed CTL had a therapeutic effect in mice with P815 established as an ascites tumor. Our results underscore an important role of IL-10 in the induction of a tumor-specific CTL response.

Animals↗
PubMed1995

Flow cytometric detection of human immunodeficiency virus type 1 proviral DNA by the polymerase chain reaction incorporating digoxigenin- or fluorescein-labeled dUTP.

Serological assays are routinely used in the laboratory diagnosis of human immunodeficiency virus type-1 (HIV-1) infection, but the polymerase chain reaction (PCR) is ultimately the most sensitive and direct method for establishing definitive diagnosis. As an alternative to the conventional radioactive PCR procedure we have developed and evaluated a pair of rapid nonradioisotopic flow cytometric detection methods. Using heminested PCR we directly incorporated fluorescein-12-dUTP (fluo-dUTP) or digoxigenin-11-dUTP (dig-dUTP) into the PCR-amplicons. The labeled amplicons were hybridized with biotinylated antisense and sense probes, followed by capture of the hybrid DNA using streptavidin-coated beads which were finally analyzed in a flow cytometer by 1) direct detection of the fluorescence intensity of the amplicons incorporating fluo-dUTP and 2) immunodetection of the amplicons incorporating dig-dUTP by anti-digoxigenin IgG labeled with fluorescein isothiocyanate (FITC). Although both assays were functionally comparable with radiolabeled probe in reliably detecting as low as five copies of HIV-1 proviral DNA sequences, the immunodetection of dig-dUTP consistently yielded higher mean channel fluorescence and gave a stable signal over an extended period of 12-14 weeks. In testing a panel of 20 pedigreed PBMC specimens from blood donors with or without HIV-1 infection, the results of both flow cytometric assays were identical with those of the conventional radioactive procedure. Therefore, we conclude that the dig-dUTP incorporation in amplicons, hybridization with a pair of sense-antisense biotinylated probes and immunodetection of hybrids by flow cytometric analyses is the nonisotopic method of choice for PCR-diagnosis of HIV-1 infection.

Base Sequence↗
PubMed1995

Antitumor immunity elicited by tumor cells transfected with B7-2, a second ligand for CD28/CTLA-4 costimulatory molecules.

We have examined the role of the B7-2 costimulatory molecule, a second ligand for CD28/CTLA-4 counter-receptors, in the induction of antitumor immunity. A plasmid containing murine B7-2 cDNA was transfected into the immunogenic mouse mastocytoma P815 of DBA/2 origin. In contrast to the lethal growth of the wild-type (wt) P815 tumor, B7-2-positive (B7-2+) P815 cells inoculated into syngeneic mice regressed, and immunization of mice with such tumor cells protected them against the challenge of wt P815 tumor. Depletion of CD8+, but not of CD4+, lymphocytes in vivo by specific Abs abolished the regression of B7-2+ P815 tumors. CD8+ cytolytic T cells could be generated from mice immunized with B7-2+ P815. They were found to be MHC class I-restricted and specific for the P815 tumor. In contrast, transfection of the B7-2 gene into the nonimmunogenic MCA102 fibrosarcoma of C57BL/6 origin induced neither tumor regression nor protective immunity. Co-expression on MCA102 cells of B7-2 together with the related costimulator B7-1 also failed to induce immunity to MCA102 tumor. Our results indicate that transfection of B7-2 into tumor cells can improve host response to some tumors, and that the effects seen are similar to those previously observed for B7-1.

Abatacept↗
PubMed1995

Loss of p53 function leads to metastasis in ras+myc-initiated mouse prostate cancer.

To study the interactions between dominantly acting oncogenes and tumor suppressor genes we used p53 'knockout' mouse urogenital sinus tissue for retroviral transduction of ras and myc in the mouse prostate reconstitution (MPR) model system. Epithelial hyperplasia was observed in all wild-type p53 MPRs with one small focal cancer and no evidence of metastasis. Prostatic cancer was found in 100% of the heterozygous and homozygous p53 mutant MPRs with metastatic deposits in 95% of the mice. The pattern of metastasis was remarkably similar to that in human prostate cancer with gross metastatic deposits in the lung, lymph nodes, bone and liver of many animals. Progression of carcinomas in the ras+myc-initiated heterozygous p53 mutant MPRs was invariably associated with either complete loss, partial deletion or loss of expression of the wild-type p53 allele. Southern blotting analysis of proviral-cellular DNA junction fragments in primary carcinomas and cell lines derived from metastatic deposits revealed that metastases do not necessarily seed out from the most abundant clone in the primary carcinoma.

Alleles↗
PubMed1995

Trichodiene synthase. Substrate specificity and inhibition.

The substrate specificity of the sesquiterpene synthase trichodiene synthase was examined by determining the Vmax and Km parameters for the natural substrate, trans,trans-farnesyl diphosphate (1), its stereoisomer, cis,trans-farnesyl diphosphate, and the tertiary allylic isomer, (3R)-nerolidyl diphosphate (3), using both the native fungal and recombinant enzymes. A series of farnesyl diphosphate analogs, 15, 16, 20, 7, 8, and 9, was also tested as inhibitors of trichodiene synthase. 10-Fluorofarnesyl diphosphate (15) was the most effective competitive inhibitor, with a K1 of 16 nM compared to the Km for 1 of 87 nM, while the ether analog of farnesyl diphosphate, 8, an extremely potent inhibitor of squalene synthase, showed only modest inhibition of trichodiene synthase, with a K1/Km of 70.

Binding, Competitive↗