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Biomedical subjects

Ping Ye

Publications and source records attributed to Ping Ye.

66 records · Page 4Linked to original sources
PubMed2003

The influence of apolipoprotein B and E gene polymorphisms on the response to simvastatin therapy in patients with hyperlipidemia.

OBJECTIVE: To investigate the effect of apolipoprotein B (apoB) and E (apoE) genetic variations on lipid profile at baseline (before treatment), and also on the subsequent response to simvastatin therapy. METHODS: Eighty-eight patients with hyperlipidemia were treated with simvastatin 5mg daily. The plasma levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), triglyceride (TG) and apo B were measured pre-treatment and at the end of the 4th, 8th and 12th post-treatment week. Polymorphisms of apoB at XbaI locus and apoE were determined by restriction fragment length polymorphism (RFLP). RESULTS: In all patients, relative frequencies of X- allele and X+ allele were 0.943 and 0.057 for apoB gene respectively. For apoE gene the relative frequency of epsilon2 allele was determined as 0.182, epsilon3 as 0.580 and epsilon4 as 0.238. The reduction in TC level was more prominent in patients carrying X- allele than in those with X+ allele following treatment (-23. 9% vs. -13. 6%, P < 0. 05). Compared with patients carrying epsilon3 or epsilon4 allele, those with epsilon2 allele showed a significantly higher percentage in reduction of apoB level after treatment (P < 0.05). CONCLUSION: The relative frequency of apoB X+ allele is high in patients with hyperlipidemia, in whom the TC-lowering efficacy is decreased following treatment of simvastatin. The relative frequencies of epsilon2 and epsilon4 are also high in hyperlipidemic patients, and the epsilon2 allele is associated with reduction in apoB level during lipid-relating therapy.

Aged↗
PubMed2002

The effects of different HIV type 1 strains on human thymic function.

Studies of HIV-1-infected humans indicate that the thymus can be infected by HIV-1. In some of these patients, there is a significant CD4(+) T cell decline and a faster disease progression. This phenomenon is more evident in pediatric patients who depend heavily on their thymus for generation of new T cells. We hypothesize that HIV-1 causes T cell regenerative failure within the thymus, which has a profound impact on disease progression. Building on our established human thymopoiesis model, we include dynamic interactions between different HIV-1 strains (R5 and X4) and thymocytes. Our results predict that thymic infection with different HIV-1 strains induces thymic dysfunction to varying degrees, contributing to differences in disease progression as observed in both HIV-1-infected children and adults. Thymic infection in children is more severe than in adults, particularly during X4 infection. This outcome is likely due to both a higher viral load and a more active thymus in pediatric patients. Our results also indicate that a viral strain switch from R5 to X4 induces further deterioration in thymopoiesis. We predict that both viral and host factors play key roles in controlling thymic infection, including strain virulence and health status of the thymus.

Acquired Immunodeficiency Syndrome↗
PubMed2002

Field testing of Schistosoma japonicum DNA vaccines in cattle in China.

Vaccines are needed to reduce the zoonotic reservoir of Schistosoma japonicum infection in bovines in China. We have developed two experimental DNA vaccines and have already shown these to be capable of inducing partial protection in water buffalo naturally exposed to the risk of S. japonicum infection in the field. We now report a similar field trial in cattle, the other major bovine reservoir host species in China. Groups of cattle were vaccinated with the VRSj28 vaccine or the VRSj23 vaccine, or, to test whether protection could be enhanced by combination vaccination, with both these DNA vaccines together. After vaccination, the cattle were exposed to natural infection in the field for a period of 54 days. Worm and egg counts carried out at the end of the experiment showed that each of the vaccine groups showed partial resistance, and that combined vaccination was not more effective than vaccination with the individual plasmids.

Animals↗
PubMed2002

Myelination is altered in insulin-like growth factor-I null mutant mice.

Increasing evidence indicates that insulin-like growth factor-I (IGF-I) has an important role in oligodendrocyte development. In this study, we examined myelination during postnatal development in IGF-I knock-out (KO) mice by assessing myelin staining, the expression of myelin basic protein (MBP) and proteolipid protein (PLP), two major myelin-specific proteins, and the number of oligodendrocytes and their precursors. For comparison, we also measured the expression of median subunit of the neuron-specific intermediate filament, M-neurofilament (M-NF), to obtain an index of the effects of IGF-I deficiency on neurons. We found that myelin staining, MBP and PLP expression, and the percentage of oligodendrocytes and their precursors are significantly reduced in all brain regions of developing IGF-I KO mice but are similar to controls in adult IGF-I KO mice. In contrast, the abundance of M-NF was decreased in both the developing and adult brain of IGF-I KO mice. We also found that IGF-II protein abundance is increased in the brains of IGF-I KO mice. Our data indicate, therefore, that myelination during early development is altered in the absence of IGF-I by mechanisms that involve a reduction in oligodendrocyte proliferation and development. Although neuronal actions cannot be excluded in the myelin normalization, the reduced axonal growth suggested by the reduced M-NF expression makes a role for neuronal factors less compelling. These data suggest that IGF-I plays a significant role in myelination during normal early development and that IGF-II can compensate in part for IGF-I actions on myelination.

Aging↗
PubMed2002

Deficient expression of insulin receptor substrate-1 (IRS-1) fails to block insulin-like growth factor-I (IGF-I) stimulation of brain growth and myelination.

To determine whether insulin receptor substrate-1 (IRS-1) is essential in mediating insulin-like growth factor-I (IGF-I) stimulation of brain growth and myelination in vivo, we cross-bred IGF-I transgenic (Tg) mice with IRS-1 null mutant (IRS-1(-/-)) mice and examined brain growth and expression of myelin-specific proteins in mice that overexpress IGF-I with or without IRS-1 expression. We found that while IGF-I overexpression stimulates a dramatic increase in brain weight (43%) by 7-8 weeks of age in the absence of IRS-1, it stimulates a greater increase (50%) with intact IRS-1 expression. To evaluate myelination we investigated IGF-I-stimulated expression of myelin basic protein (MBP) and proteolipid protein (PLP) in the cerebral cortex CTX and brainstem, and found similar increases in each region in IRS-1(-/-) and wild type mice. In studies using mixed glial cultures derived from IRS-1(-/-) mice, IGF-I also increased the abundance of MBP and PLP mRNA. To assess possible alternate mediators of IGF-I actions, we examined IRS-2 and IRS-4 and found that the abundance of each is increased in the CTX of IRS-1(-/-) mice and IGF-I Tg mice. Our results suggest that IRS-1 is not essential in IGF-I promotion of oligodendrocyte development and myelination, and that IRS-2 and IRS-4 may compensate for the loss of IRS-1 expression and function in the cells of oligodendrocyte lineage. Nonetheless, the finding that IGF-I stimulates brain growth less well in the absence of IRS-1 suggests that IRS-1-mediated signaling may be more central to IGF-I action in cells other than glia and oligodendrocytes.

Animals↗
PubMed2002

Reevaluation of T cell receptor excision circles as a measure of human recent thymic emigrants.

The human thymus exports newly generated T cells to the periphery. As no markers have been identified for these recent thymic emigrants (RTE), it is presently impossible to measure human thymic output. T cell receptor excision circles (TREC) have been recently used to assess thymic output during both health and disease. Using a mathematical model, we quantify age-dependent changes both in the number of RTE generated per day and in TREC concentration during an 80-year lifespan. Through analyses, we demonstrate that RTE and peripheral T cell division have the same potential to affect TREC concentration at any age in healthy people. T cell death also influences TREC concentration, but to a lesser extent. During aging, our results indicate that thymic involution primarily induces an age-dependent decline in TREC concentrations within both CD4(+) and CD8(+) T cell populations. We further apply this model for studying TREC concentration during HIV-1 infection. Our analyses reveal that a decrease in thymic output is the major contributor to the decline in TREC concentration within CD4(+) T cells, whereas both increased peripheral T cell division and decreased thymic output induce the decline in TREC concentration within CD8(+) T cells. Therefore, we suggest that T cell turnover should be examined together with TREC concentration as a measure of RTE. If peripheral T cell division remains relatively unchanged, then TREC concentration indeed reflects thymic output.

Adult↗
PubMed2002

[Expression of fusion proteins in beta(2)GP I gene-transfected HEp-2 cells and its clinical application].

OBJECTIVE: To establish an indirect immunofluorescent test so as to improve the sensitivity and specificity of examination of antibodies to beta(2)-glycoprotein. METHODS: Full-length beta(2)GP cDNA was obtained from human hepatocellular cancer cell line HepG2 by RT-PCR and cloned into the mammalian expression vector pEGFP-C1. The recombinant plasmid pEGFP-beta(2)GP was transfected into HEp-2 cells. RT-PCR, immunoblotting (IBT), confocal fluorescence microscopy, and indirect immunofluorescent test (IIF) were used to confirm the expression, localization, and antigenicity of fusion protein of green fluorescent protein (GFP). Serum specimens from 19 patients suspected as with secondary antiphospholipid syndrome (APS), 1 patient diagnosed as with primary APS, and 10 normal persons were detected with IIF-IgG-beta(2)GP1, ELISA-IgG-ACL, and ELISA-IgG-beta(2)GP I simultaneously. RESULTS: (1) The HEp-beta(2)GP I cells thus obtained retained their ability of expression of beta(2)GP-I-GFP for more than ten generations. This beta(2)GP-I-GFP showed the antigenicity of beta(2)GP-I with a characteristic feature. (2) Seven of the 20 serum specimens from APS patients showed characteristic immunofluorescent pattern. No serum specimen from normal persons showed immunofluorescent staining. The comparison of results of the three methods showed that the concordance between IIF-IgG-beta(2)GP I and ELISA-IgG-beta(2)GP I was the most perfect (Kappa = 0.886). (3) HEp-beta(2)GP I retained the immunofluorescent property of HEp-2 cell. CONCLUSION: As a new kind of substrate of IIF, beta(2)GP I transfectant can be used to detect anti-beta(2)GP-I antibodies. Transfeted HEp-2 cells keep the immunofluorescent property of HEp-2 cells in IFANA test and can be used as substrate for routine IFANA detection.

Antibodies, Antiphospholipid↗
PubMed2002

Measuring emigration of human thymocytes by T-cell receptor excision circles.

Recent advances in characterizing thymic function confirm the importance of thymus to T-cell diversity in the periphery of both children and adults during both health and disease. Lack of a marker to identify human recent thymic emigrants (RTEs) is the biggest hurdle to accurately characterizing and quantifying thymic output. T-cell receptor excision circles (TRECs) are used as an assay to measure RTE levels. Controversy exists, however, as to whether TREC concentrations reflect the number of RTEs or are mainly altered by peripheral T-cell division and death. In this review, we first summarize recent data on the human thymus and RTEs. On the basis of both experimental and mathematical analyses, we characterize factors that influence TREC dynamics in the periphery and elucidate primary elements that induce a decline in TREC concentrations during normal aging and HIV-1 infection. Our findings suggest that T-cell dynamics are key to the accuracy of TREC concentrations as a useful measurement of human RTEs.

Aging↗
PubMed2002

The increase in plasminogen activator inhibitor type-1 expression by stimulation of activators for peroxisome proliferator-activated receptors in human endothelial cells.

OBJECTIVE: [corrected] To investigate the effect of peroxisome proliferator-activated receptors (PPARs) activators on plasminogen activator inhibitor type-1 (PAI-1) expression in human umbilical vein endothelial cells and the possible mechanism. METHODS: Human umbilical vein endothelial cells (HUVECs) were obtained from normal fetus, and cultured conventionally. Then the HUVECs were exposed to test agents (linolenic acid, linoleic acid, oleic acid, stearic acid and prostaglandin J2 respectively) in varying concentrations with fresh media. RT-PCR and ELISA were applied to determine the expression of PPARs and PAI-1 in HUVECs. RESULTS: PPAR alpha, PPAR beta and PPAR gamma mRNA were detected by using RT-PCR in HUVECs. Treatment of HUVECs with PPARalpha and PPAR gamma activators--linolenic acid, linoleic acid, oleic acid and prostaglandin J2 respectively, but not with stearic acid could augment PAI-1 mRNA expression and protein secretion in a concentration-dependent manner. However, the mRNA expressions of 3 subclasses of PPAR with their activators in HUVECs were not changed compared with controls. CONCLUSION: HUVECs express PPARs. PPARs activators may increase PAI-1 expression in ECs, but the underlying mechanism remains unclear. Although PPARs expression was not enhanced after stimulated by their activators in ECs, the role of functionally active PPARs in regulating PAI-1 expression in ECs needs to be further investigated by using transient gene transfection assay.

Cells, Cultured↗
PubMed2002

Detection of autoantibodies in the serum of primary hepatocarcinoma patients.

OBJECTIVE: To study the significance of detecting autoantibodies in primary hepatocarcinoma (PHC) patients. METHODS: Autoantibodies were detected by indirect immunofluorescence assay. Antigens and antibodies of HBV were determined by enzyme immune assay. Antibody to HCV IgG was detected by enzyme-linked immunoabsorbent assay. RESULTS: The positive rate of autoantibody was 27.3% (38/139) in 139 PHC patients. The main type of autoantibodies in PHC was anti-nuclear antibody (36/38, 94.7%), others included anti-smooth muscle antibody(2/38, 5.3%), anti-mitochondria antibody (1/38, 2.6%), anti-midbody antibody (1/38, 2.6%, and anti-liver cell membrane antibody (2/38, 5.3%). CONCLUSIONS: Detecting autoantibodies in PHC patients is of significance in studying the mechanism of autoimmune reaction and etiology in PHC. The diversity of autoantibodies might result from a wide variety of etiological factors involved in PHC development, and from a wide variety of overexpressed or mutated proteins involved in repeated cycles of necrosis and regeneration in hepatocarcinoma development.

Adult↗
PubMedDate not supplied

Mutant mouse models of insulin-like growth factor actions in the central nervous system.

Insulin-like growth factor-I (IGF-I) and its cognate receptor, the type 1 IGF receptor (IGF1R), as well as high-affinity IGF binding proteins (IGFBP) that modulate IGF-I actions, are expressed throughout the course of brain development. These observations, taken together with studies in cultured neural cells demonstrating a variety of IGF-I growth-promoting activities, provide a strong argument for IGF-I having a central role in the growth and development of the CNS. This report reviews studies of brain development in mutant mice with alterations of IGF-I expression or action. Transgenic (Tg) mice overexpressing IGF-I postnatally exhibit brain overgrowth characterized by increased neuron and oligodendrocyte number, as well as marked increases in myelination. Mutant mice with ablated IGF-I and IGF1R expression, as well as those with overexpression of IGFBPs capable of inhibiting IGF actions, exhibit brain growth retardation with a variety of growth deficits. These studies confirm a role for IGF-I in neural development, and indicate that IGF-I stimulates neurogenesis and synaptogenesis, facilitates oligodendrocyte development, promotes neuron and oligodendrocyte survival, and stimulates myelination. Evidence from experiments in these mouse models also indicates that IGF-I has a role in recovery from neural injury.

Animals↗