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Biomedical subjects

H Jiang

Publications and source records attributed to H Jiang.

At least 685 records · Page 38Linked to original sources
PubMed1985

Regulation of a liver plasma membrane phosphoinositide phosphodiesterase by guanine nucleotides and calcium.

Rat liver plasma membranes are enriched in a Ca2+-dependent phosphodiesterase active on phosphatidylinositol 4,5-P2 and phosphatidylinositol 4-P, but not phosphatidylinositol. Inositol-P3 is the first product of the reaction, but is rapidly degraded. Micromolar concentrations of GTP and its nonhydrolyzable analogues stimulate the reaction, whereas GDP, GMP and other nucleoside triphosphates are inactive. GTP and its analogues decrease the requirement of the reaction for Ca2+ and also increase its activity at saturating Ca2+. These results support the hypothesis that guanine nucleotides and a guanine nucleotide binding regulatory protein are involved in coupling the receptors for Ca2+-mediated agonists to the breakdown of plasma membrane phosphatidylinositol 4,5-P2.

Animals↗
PubMed1985

A preliminary study on the mechanism of neonatal allotransplantation tolerance. Participation of suppressor cells in the mediation of neonatal allotransplantation tolerance.

Using a method from Billingham, an animal model of the neonatal allotransplantation tolerance of SWI to C57BL inbred mice was established and the mechanism of neonatal tolerance established by us was preliminarily studied. Our experiment indicates that the clonal deletion theory is not the unique explanation for the neonatal tolerance and a peripheral active inhibitory mechanism including suppressor cells may participate in mediating and maintaining the neonatal tolerance. The suppressor cells in the neonatal tolerance are radioresistant, but rather sensitive to mitomycin C treatment. These results suggest that suppressor cell population may be nonhomogenous. Further studies about this problem are needed.

Animals↗
PubMedDate not supplied

Child survivors of parental death from cancer or suicide: depressive and behavioral outcomes.

Depressive symptoms, social competence, and behavior problems of prepubescent children bereaved within 18 months of parental death from cancer (57 families, 64 children) or suicide (11 families, 16 children) were compared. Most children reported normative levels of depressive symptoms. Children whose parents died from suicide, compared with those whose parents died from cancer, reported significantly more depressive symptoms, involving negative mood, interpersonal problems, ineffectiveness, and anhedonia. Parental reports of children's competence and behavior were similar to a normative sample of children and did not differ between the children bereaved by parental cancer or suicide. Additional research should focus on other factors, such as family psychopathology, stresses, and impact of stigma, which may influence the course of bereaved children.

Achievement↗
PubMedDate not supplied

Inhibition of luminol and lucigenin chemiluminescence by reducing organic compounds.

The effect of 22 reducing organic compounds on the chemiluminescent intensities and spectra of luminol-H(2)O(2)-Co(2+) and lucigenin-H(2)O(2)-Co(2+) reactions were examined. Many of the reductants inhibit the two chemiluminescent systems to different extents in the presence and absence of Co(2+). The magnitude of inhibition by reducing organic compounds is related to their molecular structure and reducing properties. The mechanism of chemiluminescent inhibition by reducing organic compounds is probably due to the reaction between reductants and radical intermediates of chemiluminescent reaction. Based on the inhibition of luminol and lucigenin chemiluminescence by reducing organic compounds, the possibility of analytical application was explored. Some reductants are detectable at picomolar levels.

Acridines↗
PubMedDate not supplied

Mutation analysis of hereditary multiple exostoses in the Chinese.

Hereditary multiple exostoses (EXT; MIM 133700) is an autosomal dominant bone disorder. It is genetically heterogeneous with at least three chromosomal loci: EXT1 on 8q24.1, EXT2 on 11p11, and EXT3 on 19p. EXT1 and EXT2, the two genes responsible for EXT1 and EXT2, respectively, have been cloned. Recently, three other members of the EXT gene family, named the EXT-like genes (EXTL: EXTL1, EXTL2, and EXTL3), have been isolated. EXT1, EXT2, and the three EXTLs are homologous with one another. We have identified the intron-exon boundaries of EXTL1 and EXTL3 and analyzed EXT1, EXT2, EXTL1, and EXTL3, in 36 Chinese families with EXT, to identify underlying disease-related mutations in the Chinese population. Of the 36 families, five and 12 family groups have mutations in EXT1 and EXT2, respectively. No disease-related mutation has been found in either EXTL1 or EXTL2, although one polymorphism has been detected in EXTL1. Of the 15 different mutations (three families share a common mutation in EXT2), 12 are novel. Most of the mutations are either frameshift or nonsense mutations (12/15). These mutations lead directly or indirectly to premature stop codons, and the mutations generate truncated proteins. This finding is consistent with the hypothesis that the development of EXT is mainly attributable to loss of gene function. Missense mutations are rare in our families, but these mutations may reflect some functionally crucial regions of these proteins. EXT1 is the most frequent single cause of EXT in the Caucasian population in Europe and North America. It accounts for about 40% of cases of EXT. Our study of 36 EXT Chinese families has found that EXT1 seems much less common in the Chinese population, although the frequency of the EXT2 mutation is similar in the Caucasian and Chinese populations. Our findings suggest a possibly different genetic spectrum of this disease in different populations.

China↗
PubMedDate not supplied

PG490-88, a new immunosuppressant, effectively prevents acute and chronic rejection in rat renal allografts.

PG490-88 is a semisynthetic derivative of the novel compound PG490 (triptolide) purified from a Chinese herb. It has been shown to prolong acute allograft survival in multiple experimental organ transplant models. However, the effect of PG490-88 on prevention of acute and chronic renal allograft rejection has not been determined. Kidneys of ACI or F344 rats were transplanted into bilaterally nephrectomized LEW recipients as the acute or chronic allograft rejection models, respectively. Treatment of LEW recipients with PG490-88 significantly prolonged ACI kidney graft survival in a dose-dependent manner when compared with the untreated allograft controls. LEW recipients of F344 kidney grafts who received PG490-88 for 90 days with a brief course of low-dose FK506 showed normal serum creatinine levels and markedly reduced histological changes of chronic rejection at day 90 after transplantation. These results suggest that PG490-88 significantly prolongs kidney allograft survival in an acute rejection model and prevents chronic allograft rejection in rats.

Acute Disease↗
PubMedDate not supplied

Tumor-derived recognition factor (TDRF) induces production of TNF-alpha by murine macrophages, but requires synergy with IFN-gamma alone or in combination with IL-2 to induce nitric oxide synthase.

A constitutively produced soluble activity, designated tumor-derived recognition factor (TDRF), from L1210, P815 and EL4 tumor targets, was previously shown to synergize with interferon-gamma (IFN-gamma) and subactivating concentrations of interleukin-2 (IL-2) to induce murine macrophage production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) for cytotoxicity of the target of origin. Another study had suggested that TDRF upregulated both TNF-alpha receptor (TNF-alpha R) and IFN-gamma receptor (IFN-gamma R) mRNA synthesis, as well as increased TNF-alpha and IFN-gamma binding to their receptors. In the present study, we have further characterized the concentration-dependent macrophage activating potential of TDRF alone and in synergy with IFN-gamma or IFN-gamma and subactivating concentrations of IL-2. Higher concentrations of TDRF acted independently on inflammatory C3H FeJ mouse macrophage to induce expression of TNF-alpha mRNA and release of TNF-alpha, but failed to induce nitric oxide synthase (NOS) mRNA expression and NO generation. At lower concentrations, TDRF synergized with either IFN-gamma alone or in combination with IL-2 to stimulate a dose-related increase in the expression of TNF-alpha mRNA and secretion of TNF-alpha, as well as increased induction of NOS mRNA and cytotoxic NO generation by macrophage. MCA tumor targets which did not produce TDRF activity were killed by macrophage that had been activated by exogenously added L1210-derived TDRF in synergy with IFN-gamma or in combination with subactivating concentrations of IL-2, but not by TDRF alone. Taken together, our results indicate that TDRF acted independently in a dose-dependent fashion to induce macrophage synthesis and release of TNF-alpha, but in the absence of IFN-gamma or in combination with IL-2 failed to induce the NOS enzyme which was necessary for cytotoxic NO generation. Thus TDRF appears to be a sufficient second signal for IFN-gamma-primed macrophage or alternatively a sufficient third signal for IFN-gamma and IL-2 treated macrophage to culminate the activation process for NOS mRNA synthesis and NO-mediated tumor cytotoxicity.

Animals↗
PubMedDate not supplied

The effect of interferon beta-1b on cytokine-induced adhesion molecule expression.

Interferon beta-1b (IFN beta-1b) (Betaseron) has been recently shown to alter the course of multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system (CNS) where migration of activated lymphocytes across the blood-brain barrier (BBB) is a critical step in the pathogenesis of this disease. Magnetic resonance imaging (MRI) studies performed on patients treated with IFN beta-1b showed a remarkable effect on the BBB as determined by a reduction in the number of gadolinium enhancing lesions, a measure of BBB leakiness. Since adhesion molecules (AM) induced on endothelial cells (EC) play an important role in T-cell migration into the CNS, the objective of this study was to examine the effect of IFN beta-1b on the expression of the AM, ICAM-1, V-CAM and E-selection induced on EC by IFN-gamma, TNF-alpha, or IL-1 beta. Primary cultures of human umbilical vein EC (HUVEC) were used, which under basal conditions expressed low levels of AM. IFN beta-1b (1-1000IU/ml) had minimal effect on basal expression of AM on HUVEC, but AM could be substantially upregulated by IFN-gamma, IL-1 beta or TNF-alpha. The effect of IFN beta-1b on AM expression induced by IFN-gamma, IL-1 beta or TNF-alpha was slightly additive. It is concluded that IFN beta-1b does not downregulate the inducible expression of ICAM-1, V-CAM or E-selectin on HUVEC. These findings suggest alternate mechanisms for the effect of IFN beta-1b on the BBB in MS.

Adjuvants, Immunologic↗
PubMedDate not supplied

Hypoxia-inducible factor 1alpha (HIF-1alpha) correlated with tumor growth and apoptosis in ovarian cancer.

The aims of this study were to investigate the hypoxia-inducible factor 1alpha (HIF-1alpha) protein inhibition and tumor growth by a molecular target of rapamycin inhibitor, rapamycin, in xenogeneic transplant model of ovarian cancer and to study the correlation of apoptosis with HIF-1alpha and vascular endothelial growth factor (VEGF) expression. Four groups of female nude mice were inoculated subcutaneous with SKOV-3 cells and treated with vehicle, rapamycin, paclitaxel, or rapamycin plus paclitaxel. The expressions of HIF-1alpha and VEGF and microvessel density (MVD) were assessed by immunohistochemistry. While messenger RNA (mRNA) expression of Glut1, bcl-2, and VEGF was studied by reverse transcription-polymerase chain reaction, and apoptosis of tumor cells was determined by terminal deoxynucleotidyl biotin-dUTP nick end labeling (TUNEL). The HIF-1alpha was expressed in epithelial ovarian cancer. There was a significant correlation between HIF-1alpha protein expression and VEGF or MVD. Tumor burden treated with rapamycin alone, rapamycin plus paclitaxel, and paclitaxel alone was reduced (47.91%, 51.03%, and 31.75%, respectively) compared with controls. The expression of HIF-1alpha was inhibited, and apoptotic index of tumor cell increased in rapamycin and rapamycin plus paclitaxel group. HIF-1alpha may upregulate VEGF expression both in mRNA and protein level. There is a positive correlation between HIF-1alpha and MVD. Rapamycin inhibits expression of HIF-1alpha and suppresses ovarian tumor growth. Our data suggested that a combination of HIF-1alpha inhibitor and chemotherapy could provide an effective approach for inhibiting tumor growth in ovarian cancer.

Actins↗
PubMedDate not supplied

NGF stimulation of erk phosphorylation is impaired by a point mutation in the transmembrane domain of trkA receptor.

The nerve growth factor (NGF) trkA receptor is a transmembrane glycoprotein composed of a large extracellular ligand-binding region connected to the cytoplasmic tyrosine kinase region by a single transmembrane domain (TMD). To explore the role of TMD in the process of receptor activation, we substituted the hydrophobic amino-acid residue valine 432 with the charged amino-acid glutamic acid (designated V432E mutant) by utilizing in vitro site-directed mutagenesis. NIH 3T3 cells lacking endogenous NGF receptors were stably transfected with a pRc/CMV vector carrying either wild-type (trkA) or mutated (V432E) receptors. Stable transfectants were shown, using 125I-NGF binding and Western-blot analysis, to express the trkA recombinant receptors. Scatchard analysis revealed similar affinity for NGF in wild-type and V432E receptors. Although the level of basal trkA receptor tyrosine phosphorylation was higher in the mutant than in the wild-type, NGF stimulation of WT 11 and V432E transfectants resulted in a rapid increase in receptor tyrosine phosphorylation and of its intracellular adaptor protein SHC. In contrast to WT 11, V432E mutants showed very low levels of NGF-, and moderate levels of FGF-induced erks phosphorylation, respectively. Collectively, these findings suggest that a single substitution (V432E) in the trkA TMD results in a selective impairment of trkA-mediated erks signaling pathway.

3T3 Cells↗
PubMedDate not supplied

An enhanced electrical impedance imaging algorithm for hyperthermia applications.

Electrical impedance imaging is a technique which is under investigation as a noninvasive method of tracking subsurface temperature distributions and/or associated cellular response during hyperthermia. In previous work, a finite element image reconstruction algorithm for converting surface potential distributions recorded at discrete electrode positions into spatial maps of conductivity values was developed. This paper reports on a series of significant improvements in the basic image reconstruction approach. Specifically, the ability to recover both the resistive and capacitive components of tissue electrical impedance have been incorporated. In addition, the image enhancement schemes of (1) total variation minimization, (2) dual meshing, and (3) spatial low-pass filtering, have been added. Through a series of simulation studies involving both phantom-like and clinically-relevant geometries having discrete regions and continuously-varying electrical property profiles, a significantly improved ability to recover spatial images of electrical properties in the impedance imaging context is demonstrated. The results show that the new algorithm is much more tolerant of measurement noise with levels up to 1% causing relatively modest degradations in image quality (compared to 0.1% which was needed previously in order to produce high quality images). The recovered electrical properties, themselves, both resistive and capacitive, are also found to be quantitative in value with errors in the 10-20% range occurring in the majority of cases, although deviations can reach 40% or more when noise levels as high as 10% are used. Temperature estimation simulations show that maximum temperature errors are significantly reduced (to approximately 2 degrees C relative to more than 10 degrees C in previous thermal simulations) with the new algorithm; however, temperature accuracies of better than 0.5 degree C on average are still found to be difficult to achieve with electrical impedance imaging even when the enhanced image reconstruction approach is used.

Algorithms↗