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Biomedical subjects

J Shao

Publications and source records attributed to J Shao.

At least 109 records · Page 6Linked to original sources
PubMed1997

A selective cyclooxygenase 2 inhibitor suppresses the growth of H-ras-transformed rat intestinal epithelial cells.

BACKGROUND & AIMS: Constitutive expression of cyclooxygenase 2 (COX-2) has been found in 85% of colorectal cancers. Ras mutations are found in 50% of colorectal adenocarcinomas. The aim of this study was to determine the role of COX-2 in ras-induced transformation in rat intestinal epithelial (RIE) cells. METHODS: Cell growth was determined by cell counts. The expression of COX-2 was examined by Northern and Western analyses. For tumorigenicity assays, cells were inoculated into dorsal subcutaneous tissue of athymic nude mice. DNA-fragmentation assays were performed to detect apoptosis. RESULTS: The expression of COX-2 was increased in RIE-Ras cells at both messenger RNA (9-fold) and protein (12-fold) levels. Prostaglandin I2 levels were elevated 2.15-fold in RIE-Ras cells. Serum deprivation further increased COX-2 expression 3.8-fold in RIE-Ras cells. Treatment with a selective COX-2 antagonist (SC58125) inhibited the growth of RIE-Ras cells through inhibition of cell proliferation and by induction of apoptosis. SC-58125 treatment reduced the colony formation in Matrigel by 83.0%. Intraperitoneal administration of SC-58125 suppressed RIE-Ras tumor growth in nude mice by 60.3% in 4 weeks. SC-58125 treatment also induced apoptosis in RIE-Ras cells as indicated by increased DNA fragmentation. CONCLUSIONS: Overexpression of COX-2 may contribute to tumorigenicity of ras-transformed intestinal epithelial cells. Selective inhibition of COX-2 activity inhibits growth of ras-transformed intestinal epithelial cells and induces apoptosis.

Animals↗
PubMed1997

Mannan-binding lectin in the sub-Saharan HIV and tuberculosis epidemics.

Inherited deficiency of mannan-binding lectin (MBL) has been shown to predispose to infections. Conversely, it has also been suggested that MBL might facilitate the uptake of certain intracellular microbes. The aim of this study was to investigate whether MBL plays a role in the HIV and tuberculosis epidemics in Africa. Thus, the authors determined the MBL serum concentration in 173 HIV infected patients (150 with concomitant tuberculosis), 94 patients with tuberculosis without being HIV infected, and 113 controls from Tanzania. The frequency of MBL deficiency was significantly increased in HIV infected patients compared with controls (12.1% and 3.5%, respectively). The frequency of patients deficient of MBL did not differ between controls and HIV negative patients with tuberculosis. However, HIV negative patients with tuberculosis had significantly higher MBL levels than both controls and HIV infected patients with or without tuberculosis. These results indicate that low levels of MBL are associated with increased risk of sexually transmitted HIV infection in Africans. By contrast, high levels of MBL may be involved in the pathogenesis of tuberculosis in immunocompetent individuals.

Adolescent↗
PubMed1997

N-(4-hydroxyphenyl)retinamide induces apoptosis in T lymphoma and T lymphoblastoid leukemia cells.

We demonstrate that N-(4-hydroxyphenyl)-all-trans-retinamide (4-HPR), a synthetic retinoic acid (RA) derivative, is a potent and selective inducer of apoptosis in malignant T lymphoid cells, but has little effect on normal lymphoid cells of the thymus or spleen. 4-HPR and its stereoisomer, 9-cis-4-HPR, are 50 to > 150 times more potent than 7 other retinoids in killing CEM-C7 human T lymphoblastoid leukemia cells and P1798-C7 murine T lymphoma cells. 4-HPR's apoptotic action requires the intact molecule bearing both the retinoid moiety and the hydroxyphenol ring; 4-HPR remains unmetabolized after uptake into CEM-C7 and P1798-C7 cells for up to 24 hours. We also show that glucocorticoid (GC)-resistant variants are equally susceptible to 4-HPR as are GC-sensitive cells. Thus, 4-HPR may be potentially important as a new chemotherapeutic drug for use as alternative to, or in combination with, conventional drugs for treating lymphoid malignancies.

Aminophenols↗
PubMed1997

[Simulation of a decoupling generalized predictive control algorithm for temperature-humidity system].

A decoupling generalized predictive control algorithm was presented in this paper. This algorithm was proposed to control the temperature-humidity system of a practical air-conditioning environmental chamber. By introducing absolute humidity as an intermediate variable, temperature and humidity of the system can be decoupled. Then the two decoupled systems are controlled by generalized predictive control (GPC) algorithm at different sample rates. Many simulation experiments demonstrated the effectiveness of the algorithm. Besides, decoupling of temperature and humidity will be extremely helpful to the application of GPC on the real system. This is also the effective method to control the temperature and humidity system.

Air Conditioning↗
PubMed1997

Cyclooxygenase-2 induction and transforming growth factor beta growth inhibition in rat intestinal epithelial cells.

Rat intestinal epithelial cells (RIE-1) permanently transfected with the prostaglandin endoperoxide synthase 2 (also referred to as cyclooxygenase-2; COX-2) gene exhibit decreased cyclin D1 levels, decreased cdk4-associated kinase activity, and delayed G1 cell cycle progression, which represents a phenotype similar to that which follows transforming growth factor beta (TGF-beta) treatment. In the current study, we have found that addition of TGF-beta 1 to the parental RIE-1 cells (designated RIE-P) caused a rapid induction of COX-2 mRNA and protein. COX-2 protein levels progressively increased and reached peak levels 6 h after TGF-beta 1 addition. Cyclin D1 was decreased by 74% at 6 h and was undetectable 24 h after addition of TGF-beta 1. In RIE cells transfected with the COX-2 antisense expression vector (RIE-AS cells), TGF-beta 1 induction of COX-2 protein was reduced greater than 90%. Addition of TGF-beta 1 did not reduce the abundant cyclin D1 protein expression in the RIE-AS cells, unlike the effect in RIE-P cells. TGF-beta 1 treatment reduced peak [3H]thymidine incorporation by 60% and delayed G1/S-phase transition by at least 4 h in the RIE-P cells. In contrast, S-phase entry occurred at 16 h in RIE-AS cells and was not altered by TGF-beta 1 treatment. Restoration of cyclin D1 expression by transfection of the cyclin D1 cDNA under transcriptional control of the cytomegalovirus promoter/enhancer in the COX-2-overexpressing (RIE-S) cells decreased the time required for S-phase entry by at least 4 h and increased the peak level of [3H]thymidine incorporation. Taken together, the results demonstrate that TGF-beta 1 strongly induces COX-2 at both the mRNA and protein levels and suggest that this induction of COX-2 is involved in the down-regulation of cyclin D1 and inhibition of cell growth caused by TGF-beta 1 in rat intestinal epithelial cells.

Animals↗
PubMed1996

CIF, an essential cofactor for TFIID-dependent initiator function.

The core promoters for mammalian protein-coding genes often contain a TATA box, an initiator (Inr) element, or both of these control elements. The TFIID complex is essential both for TATA activity and for the activity of a common class of Inr elements characterized by an approximate consensus sequence PyPyA+1NT/APyPy. Although the complete set of proteins required for basal TATA-mediated transcription has been established, the requirements for TFIID-dependent Inr activity remain undefined. In this study we set out to reconstitute Inr activity with purified and recombinant general transcription factors. For this analysis, Inr activity was measured as the ability of an Inr to enhance the strength of a core promoter containing an upstream TATA box. Inr activity was not detected in reactions containing TFIIB, RAP30, RAP74, RNA polymerase II, and either TBP or TFIID, even though these factors were sufficient for TATA-mediated transcription from supercoiled templates. By use of a complementation assay, a factor that imparts Inr activity was identified. This factor, named CIF, stimulated Inr activity in reactions containing the TFIID complex, but activity was not detected with TBP. Further characterization of CIF suggested that it contains multiple components. Functional and immunological experiments demonstrated that one of the CIF components is the mammalian homolog of Drosophila TAF(II)150, which is not tightly associated with mammalian TFIID. These results reveal significant differences in the factor requirements for basal TATA and Inr activity. Further elucidation of these differences is likely to explain the need for the core promoter heterogeneity found within protein-coding genes.

Animals↗
PubMed1996

G1 delay in cells overexpressing prostaglandin endoperoxide synthase-2.

Colorectal cancer is the second leading cause of death from cancer in the United States. Continuous use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to reduce the risk of colorectal cancer in humans by 40-50%. Patients with familial adenomatous polyposis who take NSAIDs, such as sulindac, undergo a regression of intestinal adenomas. Rodents exposed to carcinogens that cause colon cancer have a 50-60% reduction in the size and number of colonic tumors when treated continuously with NSAIDs. One common target for these drugs is prostaglandin endoperoxide synthase, also referred to as cyclooxygenase (COX). We and others have shown recently that COX-2 levels are increased dramatically in 85-90% of human colorectal adenocarcinomas and in 40-50% of colonic adenomas. We prepared intestinal epithelial cells that express the COX-2 gene permanently and found that they have altered adhesion properties and resist undergoing apoptosis. We report here that these cells also have a 3-fold increase in the duration of G1, lower levels of cyclin D1 protein, and a marked decrease in retinoblastoma kinase activity associated with cyclin-dependent kinase 4. The delay in G1 transit may relate to the resistance of these cells to undergo programmed cell death, which could affect their tumorigenic potential.

Adenoma↗
PubMed1996

Immunoregulation of lupus-like NZB/W F1 mice by anti-murine IL-1 alpha, IL-6 antibodies.

Anti-murine IL-1 alpha, IL-6 antibodies were intra-peritoneally injected to the lupus-like NZB/W F1 mice of 4 months with the dosage of 10 micrograms per day for three days and then per month for three months. The mice were killed at the age of 11 months. The results showed that the treatment of the dosage could not absolutely prevent lupus nephritis--it could alleviate proteinuria, obviously reduce the levels of serum IL-1 alpha and inhibit the secretion of IL-1 alpha by celiac macrophage. As to the level of IL-6 and TNF-alpha no significant change was observed.

Animals↗
PubMed1996

Tetrasomy 8 detected by interphase cytogenetics in a child with acute lymphocytic leukemia.

Tetrasomy 8 is a rare clonal anomaly in human acute leukemia. Here we present a case of a 7-year-old boy with acute lymphoblastic leukemia (ALL) displaying a tetrasomy 8 clone that could not be detected by conventional cytogenetics. In this study, bone marrow and peripheral blood cells were collected at five different diagnostic stages and analyzed by double targeted fluorescence in situ hybridization (FISH) with centromeric DNA probes for chromosomes 7, 8, 9, and 12. FISH analysis revealed a significant increase in tetrasomy 8 frequency, but not in other chromosomes examined. A smaller increase in trisomy 8 was also detected. At one stage over 60% of the cells were hyperdiploid with 40% being tetrasomic. The size of the tetrasomic clone changed during the course of the disease. The hyperdiploid frequencies of chromosome 8 detected by interphase FISH analysis in bone marrow and peripheral blood were similar. Our findings indicate the utility of FISH analysis in cytogenetic monitoring of leukemia patients and further show that tetrasomy 8 may play a specific role in a subtype of ALL.

Aneuploidy↗
PubMed1996

Delayed-type hypersensitivity testing in Tanzanian adults with HIV infection.

Delayed-type hypersensitivity (DTH) testing and total lymphocyte counts as measures of cell-mediated immune function were assessed for medical patients in Dar es Salaam, Tanzania. DTH testing was performed with the Multitest CMI device which simultaneously administers seven antigens. Of 201 patients completing DTH testing, 90 were HIV seropositive. Anergy occurred more frequently among HIV-seropositive patients (39 of 90) as compared with HIV-seronegative patients (17 of 111). DTH skin test reactivity, measured by anergy, the number of positive antigens, and the combined DTH response induration, was significantly related to the clinical stage of HIV disease. Median total lymphocyte counts were significantly lower in HIV-seropositive patients than in HIV-seronegative patients (1,130 vs. 1,680 lymphocytes x 10(6)/L). Total lymphocyte counts decreased with increasing severity of HIV disease. In multivariable analysis, the number of positive antigens in DTH testing and lymphopenia significantly predicted HIV infection. The findings suggest that DTH testing and total lymphocyte counts may be useful, inexpensive tests of immune function in African patients with HIV disease.

Adult↗
PubMed1996

HIV-1 proviral DNA sequences of env gp41 PCR amplificates from Tanzania.

The polymerase chain reaction (PCR) and direct DNA sequencing were used to detect and characterize selected regions of the HIV-1 proviral genome in whole blood samples from Tanzania. Specific PCR amplification products were obtained in gag and/or env (gp41) regions from 15 of the 19 HIV-1 seropositive samples investigated. Env regions from 12 different amplificates were further characterized using the dideoxy sequencing method. Preliminary results indicate that, despite scattered nucleotide mismatches, HIV-1 gp41 amino acid sequences from Tanzania conform to the 1990 Los Alamos African consensus sequence and resemble the HIV-1 subtype A or D consensus sequences in the characterized regions.

Amino Acid Sequence↗
PubMed1996

[Study of immunoregulation by interleukin-1 receptor antagonist in NZB/W F1 mice].

OBJECTIVE: It is known that the development of systemic lupus erythematosus (SLE) is associated with the highly activated B cells. Interleukin-1 (IL-1) can obviously promote the proliferation and secretive activity of B cells. Moreover, interleukin-1 receptor antagonist (IL-1ra) can block the effect of IL-1 by specifically combining with IL-1 receptor, we, therefore studied the immunoregulative action of IL-1ra in lupus-like NzB/w F1 mice to detect any possible way to prevent lupus nephritis. METHODS: 12 femal NZB/W F1 mice of 13 weeks (Weight: 30-35 g) were divided randomly into 2 groups. Each mouse in the treated group was intraperitoneally injected with IL-1ra once per 2 weeks for 3 times by the dosage of 100 micrograms (0.1 ml) per time, while in the control group injected with 0.1 ml normal saline. All the mice were killed at the age of 9 months and the immunologic function was detected. RESULTS: This dosage could not prevent absolutely the development of lupus nephritis, but the renal damage was alleviated and the urine protein decreased. Moreover, it could improve the immunofunction by significantly reducing the levels of serum IL-1 alpha and obviously increasing the activities of NK cells and IL-2 induced by ConA in mononuclear cells of spleen. There was no significant difference on the levels of serum IL-6 and TNF-alpha between the treated group and control group. CONCLUSION: IL-1ra has certain regulatory effect on the immunologic function of lupus-like NZB/W F1 mice.

Animals↗
PubMed1996

[The molecular cloning and sequencing of the cobra serum antitoxic protein gene].

In the previous study the authors found at least one peptide of 39 amino acid residues of several purified tryptic-fragments of the cobra serum antitoxic protein (CSAP), whose sequence had shown certain correlation with the rat serum albumin. For further clarification of the toxin-binding activity of CSAP in relation with its corresponding structure, the cDNA gene library of cobra liver cells was established and DNA primers were designed according to the known amino acid sequences of the tryptic peptides of CSAP. The specific probes were prepared and the specific clone was screened out from the library by PCR. Finally, the CSAP cDNA was sequenced from its sub-clones. Then the complete amino acid sequence of CSAP was elucidated. It is a polypeptide chain of 614 amino acid residues with a molecular size of 69.8 KDa. In comparing the whole sequence of CSAP, especially its signal peptide, with mammalian serum albumins, the authors have come to realize that CSAP is just the cobra serum albumin (CSA).

Amino Acid Sequence↗