Search PubMed⌕ Search

Biomedical subjects

H Xiong

Publications and source records attributed to H Xiong.

At least 55 records · Page 3Linked to original sources
PubMed1999

Regulation of nerve growth factor release by nitric oxide through cyclic GMP pathway in cortical glial cells.

In the present study, we found that S-nitroso-N-acetyl-DL-penicillamine, a spontaneous nitric oxide (NO) generator, dose-dependently inhibited basal nerve growth factor (NGF) release from mixed glial cells. To elucidate the function of endogenous NO in the regulation of NGF release, the mixed glial cells were stimulated with lipopolysaccharide (LPS) or LPS plus interferon-gamma (IFNgamma). The results showed that LPS alone induced NGF release and moderate NO production. However, costimulation with LPS plus IFNgamma greatly enhanced NO production but significantly suppressed LPS-induced NGF release. When N(G)-monomethyl-L-arginine, an NOS inhibitor, was added to the culture, the suppression of NGF release by IFNgamma was significantly reduced. Quantitative reverse transcription-polymerase chain reaction demonstrated S-nitroso-N-acetyl-DL-penicillamine was also able to inhibit the LPS-induced NGF mRNA expression. To understand the different contributions of astroglia and microglia to this phenomenon, both cell types were purified. We found purified astroglia produced high amounts of NGF but low amounts of NO. However, purified microglia produced a large amount of NO but very low amounts of NGF after stimulation with LPS or LPS plus IFNgamma. Our data also indicated the second messenger cyclic GMP, but not cyclic AMP, was able to inhibit basal NGF release. In vivo experiments confirmed that NGF protein level was significantly enhanced in rats treated with L-N(omega)-nitro-arginine methyl ester and in endothelial NO synthase mutant mice. Taken together, we conclude NO derived mainly from microglia down-regulates NGF release from astroglia at the transcriptional level by stimulating cyclic GMP pathway.

Animals↗
PubMed1999

Induction of protective T cells against Listeria monocytogenes in mice by immunization with a listeriolysin O-negative avirulent strain of bacteria and liposome-encapsulated listeriolysin O.

Only listeriolysin O (LLO)-producing strains of Listeria monocytogenes generate protective immunity in mice. Based on the findings that endogenous gamma interferon (IFN-gamma) production was induced only by such strains and that purified LLO could induce IFN-gamma from NK cells, we have postulated that LLO may play a pivotal role in the induction of Th1-type protective T cells, which are highly dependent on IFN-gamma. In this study, mice were immunized with L. monocytogenes ATCC 15313, an LLO-nonproducing avirulent strain, along with LLO encapsulated in liposome (LLO-liposome). LLO-liposome was highly potent in the induction of various cytokines, including IFN-gamma. Immunization of mice with either LLO-liposome or the viable strain ATCC 15313 alone did not induce protection against challenge infection. In contrast, the combination of LLO-nonproducing bacteria plus LLO-liposome induced a significant level of protective immunity mediated mainly by Th1-type cells capable of producing a large amount of IFN-gamma in an antigen-specific manner. The protection afforded by the combination was not dependent on LLO-specific cytotoxic T cells. These results support the idea that the inability of an LLO-nonproducing avirulent strain or killed bacteria to induce the generation of protective T cells is due not to the lack of a central T-cell epitope(s) but to the lack of ability to induce the production of endogenous cytokine during the early stage of immunization; the results also suggest that an appropriate use of LLO at least in an animal model may be effective in the induction of antigen-specific Th1-dependent protective immunity to various kinds of intracellular parasitic bacteria.

Adoptive Transfer↗
PubMed1999

Soluble HIV-1 infected macrophage secretory products mediate blockade of long-term potentiation: a mechanism for cognitive dysfunction in HIV-1-associated dementia.

It is generally accepted that viral and cellular products from immune competent mononuclear phagocytes (MP) (brain macrophages and microglia) underlie the neuropathogenesis of HIV-1-associated dementia (HAD). What remains unanswered, however, is the composition of and mechanisms for such MP-induced neurological dysfunctions. In attempts to address these issues culture fluids from HIV-1ADA-infected monocyte-derived macrophages (MDMs) (depleted or enriched with progeny virus) were placed onto the CA1 area of rat hippocampal brain slices (the site of mammalian learning and memory) and neuronal long-term potentiation (LTP) assayed. LTP was induced by high frequency stimulation (HFS). Lipopolysaccharide (LPS) served as a surrogate macrophage activator. Synaptic strength was assayed by the initial slope of evoked field excitatory postsynaptic potentials (EPSPs). Synaptic potentiation following HFS was observed in slices incubated with uninfected (control) MDM culture fluids. The magnitude of the LTP response was 150.2 +/- 21.10% compared to basal levels (n=6). Synaptic strength was enhanced in virus-infected (135.7+/-28.9%, n=8) and LPS-activated MDM (123.3+/-5.1%, n=7) but at lower levels than controls. The lowest levels of LTP were in brain slices incubated with virus-infected and LPS-activated MDM fluids at (109.5+/-9.9% n=12). Interestingly, bath application of progeny HIV-1 virions showed minimal LTP effects. Virus-infected, LPS-activated MDM fluids, with progenyvirus, reduced synaptic strength but were not statistically different than replicate culture fluids depleted of virus. In contrast, IL-1beta and quinolinic acid, significantly diminished synaptic strength. These results, taken together, suggest that soluble HIV-1-infected MDM secretory products, but not virus per se, significantly affect LTP. This electrophysiological system, which monitors neuronal function following cell exposure to HIV-1 infected materials could provide a novel testing ground for therapeutics designed to protect brain function in HAD.

AIDS Dementia Complex↗
PubMed1999

[Three dimensional finite element analysis of effects on composite resin for filling in various cavity margin design].

OBJECTIVE: To evaluate the stress distribution of different angles of cavity margins with composite resin filling. METHODS: The stress distributions of different angles of cavity margins of class I cavity of molars were analyzed by the method of three dimensional finite element. The cavity was filled with composite resin and the stress vertical force and lateral force was calculated. RESULTS: In the 5 designed different cavity margin angles, the vertical forces and lateral forces were 18.757 MPa and 22.309 MPa respectively when the angle is 90 degrees; when the angles were 75 degrees and 60 degrees, they were 10.580 MPa, 14.265 MPa and 9.025 MPa, 13.230 MPa respectively. The vertical forces and lateral forces produced by the surface of composite resin while being stressed were up to 18.757 MPa and 22.309 MPa. The forces of the second layer evidently reduced to 2.586 MPa and 6.8 MPa. CONCLUSION: When fill the molars with resin in clinic, the angles of cavity margins should be prepared with the slopes of 60 degrees to 75 degrees.

Composite Resins↗
PubMed1999

[Experimental study on anti-cancer effect of Cantharidine derivatives and platinum complex].

OBJECTIVE: To certify the anti-tumor effects of the four Cantharidine derivatives and platinum complex on transplanted tumor in mice to search for new anti-tumor drugs. METHODS: Complex of four Cantharidine derivatives (Dpt 1-15, Dpt 5-10, Dpt 12-3 and Dpt6-2) and platinum were given to tumor beating mice of transplanted S180 sarcoma, H22 solid hepatocarcinoma and ascites hepatocarcinoma through intraperitoneal or intravenous injection, and the effect of treatment on tumor weight and survival of animal were observed. Cisplatin was used as positive control and 0.9% normal saline used as negative control. All data were treated with t test. RESULTS: All the four complex had anti-tumor effect. The inhibition rate of Dpt5-10 and Dpt1-15 on S180 sarcoma and H22 solid hepatocarcinoma and the survival prolongation rate of Dpt5-10 on H22 ascites hepatocarcinoma were similar to those of cisplatin. The toxicity of effective dose of Dpt1-15 was rather high. CONCLUSIONS: Cantharidine derivatives and platinum complex is new effective anti-tumor drug, among them the Dpt5-10 is the most effective one. Further study for improving the solubility of drug is necessary and study the difference of cross resistance between the new complex and cisplatinum.

Animals↗
PubMed1998

Subunit epsilon of the Escherichia coli ATP synthase: novel insights into structure and function by analysis of thirteen mutant forms.

Structural models of subunit epsilon of the ATP synthase from Escherichia coli have been determined recently by NMR [Wilkens et al. (1995) Nat. Struct. Biol. 2, 961-967] and by X-ray crystallography [Uhlin et al. (1997) Structure 5, 1219-1230], revealing a two-domain protein. In this study, six new epsilon mutants were constructed and analyzed: Y63A, D81A, T82A, and three truncated mutants, tr80(S), tr94(LAS), and tr117(AS). Seven mutants constructed previously were also analyzed: E31A, E59A, S65A, E70A, T77A, R58A, and D81A/R85A. Subunits were purified by isoelectric focusing from extracts of cells that overproduced these 13 mutants. F1 was prepared lacking subunit epsilon by immobilized-Ni affinity chromatography. Three mutants, E70A, S65A, and E31A, showed somewhat higher affinities and extents of inhibition than the wild type. Three mutants, T82A, R85A, and tr94(LAS), showed both lower affinities and extents of inhibition, over the concentration range tested. Two showed no inhibition, D81A and tr80(S). The others, T77A, Y63A, E59A, and tr117(AS), showed lower affinities than wild type, but the extents of inhibition were nearly normal. Results indicate that the C-terminal domain of subunit epsilon contributes to inhibition of ATP hydrolysis, but it is not necessary for ATP-driven proton translocation. Interactions with subunit gamma are likely to involve a surface containing residues S65, E70, T77, D81, and T82, while residues R85 and Y63 are likely to be important in the conformation of subunit epsilon.

Adenosine Triphosphate↗
PubMed1998

Identification of a two EF-hand Ca2+ binding domain in lobster skeletal muscle ryanodine receptor/Ca2+ release channel.

The lobster skeletal muscle Ca2+ release channel, known also as the ryanodine receptor, is composed of four polypeptides of approximately 5000 amino acids each, like its mammalian counterparts. Clones encoding the carboxy-terminal region of the lobster ryanodine receptor were isolated from a lobster skeletal muscle cDNA library. Analysis of the deduced 1513 carboxy-terminal amino acid sequence suggests a cytoplasmic Ca2+ binding domain consisting of two EF-hand Ca2+ binding motifs (amino acid residues 594-656). The Ca2+ binding properties of this domain were assessed by preparing bacterial fusion proteins with sequences from the lobster Ca2+ binding domain and the corresponding sequences of the rabbit cardiac and skeletal muscle ryanodine receptors. The lobster skeletal muscle fusion protein bound 45Ca2+ in Ca2+ overlays, and bound two Ca2+ under equilibrium binding conditions with a Hill dissociation constant (KH) of 0.9 mM and coefficient (nH) of 1.4. Rabbit skeletal and cardiac fusion proteins bound two Ca2+ with KHs of 3.7 and 3.8 mM and nHs of 1.1 and 1.3, respectively. Similar to results previously reported for the mammalian RyRs, the lobster RyR was activated by micromolar Ca2+ and inhibited by millimolar Ca2+, as determined in single-channel and [3H]ryanodine binding measurements. These results suggest that the two EF-hand Ca2+ binding domain of the lobster Ca2+ release channel as well as the corresponding regions of the mammalian channels may play a role in Ca2+ inactivation of sarcoplasmic reticulum Ca2+ release.

Amino Acid Sequence↗
PubMed1998

Administration of killed bacteria together with listeriolysin O induces protective immunity against Listeria monocytogenes in mice.

It is known that only listeriolysin O (LLO)-producing Listeria monocytogenes strains are able to induce protective immunity, but the underlining relationship between LLO produced by virulent strains and generation of protective immunity in the infected host remains poorly understood. In the present study, it was found that LLO gene expression was only detected in the mice infected with virulent strain which was able to induce protective immunity, while non-virulent strains or killed bacteria were not able to generate protective immunity. When mice were immunized with LLO plus killed bacteria in the presence of incomplete Freund's adjuvant, the protective immunity was partially generated, and adoptive transfer experiment confirmed that this protection was antigen specific. Reverse-transcription polymerase chain reaction revealed that LLO plus killed bacteria induced the expression of interferon-gamma (IFN-gamma) and interleukin-12 (IL-12). Our results also showed CD4+ T cells were the principal cells constituting protective immunity. Taken together, it may be concluded that LLO produced from virulent strains of L. monocytogenes was essential for the generation of protective immunity, and that LLO plus killed bacteria induced IFN-gamma and IL-12 expression which resulted in the generation of protective immunity.

Adoptive Transfer↗
PubMed1998

Killing mechanism of Listeria monocytogenes in activated macrophages as determined by an improved assay system.

Exposure of Listeria monocytogenes to gentamicin 5 mg/L for 4 h resulted in the killing of most extracellular bacteria, but had no effect on the survival of bacteria inside macrophages. Higher concentrations of gentamicin caused a reduction in the number of intracellular bacteria. This effect was associated with cellular uptake of gentamicin, but was unaffected by activation of macrophages by interferon-gamma and lipopolysaccharide. In experiments in which exposure to gentamicin 5 mg/L for 4 h was used to kill extracellular bacteria, killing by activated macrophages was impaired when O2- production was inhibited by superoxide dismutase, but not when nitric oxide production was blocked by NG-monomethyl-L-arginine. These data suggest that the reactive oxygen intermediates are more important than nitric oxide in the killing of L. monocytogenes, at least in macrophages activated in vitro.

Animals↗
PubMed1998

The contributions of reactive oxygen intermediates and reactive nitrogen intermediates to listericidal mechanisms differ in macrophages activated pre- and postinfection.

The contribution of reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI) to the killing of Listeria monocytogenes by macrophages activated by addition of spleen cells from listeria-immune mice plus specific antigen was examined. When macrophages were infected with L. monocytogenes and then spleen cells were added, there was not as big a difference in listericidal activity between macrophages cultured with normal spleen cells and those cultured with immune spleen cells as expected. In this culture system, RNI was mainly involved in the macrophage intracellular killing. In macrophages first activated and then infected, a significant level of enhanced killing was observed. Blockade of ROI production drastically affected the enhanced killing ability, while inhibition of RNI production had a negligible effect. Thus, the contributions of ROI and RNI to listericidal mechanisms of macrophages were different between macrophages activated at pre- and postinfection stages.

Animals↗
PubMed1998

Spraying chicken skin with selected chemicals to reduce attached Salmonella typhimurium.

Aqueous solutions of 5% and 10% trisodium phosphate (TSP), 0.1% and 0.5% cetylpyridinium chloride (CPC), 1% and 2% lactic acid (LA), and 0.1% and 0.5% grapefruit seed extract (DF-100) were evaluated in prechill spraying for reducing Salmonella typhimurium attached on chicken skins. Chicken skins were inoculated with S. typhimurium and then sprayed with the selected chemical solutions for 30 sec at 206 kPa and 20 degrees C. After chemical spraying, the skins were rinsed by spraying tap water for 30 sec. Each skin was stomached in buffered peptone water (BPW) for 1 min. The stomaching water was then diluted serially, inoculated onto both xylose lysine tergitol (XLT4) agar and Aerobic Plate Count (APC) Petrifilm, and incubated for 24 hr at 37 degrees C. The results showed that the numbers of Salmonella on the chicken skins after the chemical spraying were significantly lower than those without spray (P < 0.05). The CPC reduced Salmonella by 1.5 to 1.9 log10. TSP resulted in a 2.1 to 2.2 log10 reduction of Salmonella and DF-100 produced a 1.6 to 1.8 log10 reduction of Salmonella. The LA had a number of Salmonella with a 2.2 log10 reduction. The 0.5% CPC resulted a significantly greater reduction in Salmonella than 0.1% CPC. There were no significant differences in Salmonella reduction between different concentrations of the other three chemicals.

Animals↗
PubMed1998

[The expression of CD11a and CD11b on leucocytes in cerebral thrombosis].

This study sought to understand the mechanism for the increased adhesion of leucocytes and endothelial cells in ischemic stroke. 20 patients with acute cerebral thrombosis and 20 healthy subjects as controls for expression of CD11a and CD11b (adhesion molecules on surface of leucocytes) were tested in vitro by flow cytometry (FCM) method. The results showed that compared with the control group, the patient group had significantly higher rates for expression of CD11a on monocytes, granulocytes and lymphocytes (P < 0.05). The CD11b expression in the patient group was positively elevated on monocytes and granulocytes (P < 0.05), but it was of lower positive rate on lymphocytes and no statistical difference was noted between the patient and control groups. These indicate that the expression of CD11a and CD11b on leucocytes increases in cerebral ischemic damage; thus adhesion of leucocytes and endothelial cells obviously increases. This change may aggravate post-ischemic delayed neuronal death.

Adult↗
PubMed1998

[Sevoflurane (SEVOrane) as an inhalation anesthetic in dogs in comparison with halothane and isoflurane].

1969 Sevofluran was synthesized and in December 1995 licensed for clinical use in Germany. The low blood/gas partition coefficient is responsible for the fast uptake and elimination of sevoflurane. Sevoflurane does not irritate the airway. In human medicine no side effect of liver- and kidney function have been seen after sevofluran anaesthesia. There is low cardiovascular and respiratory depression caused by sevoflurane. In this study the use of sevoflurane in dogs should be tested and compared with isoflurane and halothane anaesthesia. All dogs were premedicated with /-methadon and diazepam. No significant depression of the cardiovascular system was seen. Neither kidney-nor hepatotoxic side effects could be found after sevoflurane, isoflurane and halothane anaesthesia. After sevoflurane anaesthesia the dogs woke up quietly and without any excitation and were able to stand on average ten minutes earlier after sevoflurane anaesthesia than after isoflurane and 85 minutes earlier than after halothane anaesthesia.

Anesthesia, Inhalation↗
PubMed1997

Processing of mammalian and plant S-adenosylmethionine decarboxylase proenzymes.

S-Adenosylmethionine decarboxylase (AdoMetDC) is a pyruvoyl enzyme, and the pyruvate is formed in an intramolecular reaction that cleaves a proenzyme precursor and converts a serine residue into pyruvate. The wild type potato AdoMetDC proenzyme processed much faster than the human proenzyme and did not require putrescine for an optimal rate of processing despite the presence of three acidic residues (equivalent to Glu11, Glu178, and Glu256) that were demonstrated in previous studies to be required for the putrescine activation of human AdoMetDC proenzyme processing (Stanley, B. A., Shantz, L. M., and Pegg, A. E. (1994) J. Biol. Chem. 269, 7901-7907). A fourth residue that is also needed for the putrescine stimulation of human AdoMetDC proenzyme processing was identified in the present studies, and this residue (Asp174) is not present in the potato sequence. The site of potato AdoMetDC proenzyme processing was found to be Ser73 in the conserved sequence, YVLSESS, which is the equivalent of Ser68 in the human sequence. Replacement of the serine precursor with threonine or cysteine by site-directed mutagenesis in either the potato or the human AdoMetDC proenzyme did not prevent processing but caused a significant reduction in the rate. Although the COOH-terminal regions of the known eukaryotic AdoMetDCs are not conserved, only relatively small truncations of 8 residues from the human protein and 25 residues from the potato proenzyme were compatible with processing. The maximally truncated proteins show no similarity in COOH-terminal amino acid sequence but each contained 46 amino acid residues after the last conserved sequence, suggesting that the length of this section of the protein is essential for maintaining the proenzyme conformation needed for autocatalytic processing.

Adenosylmethionine Decarboxylase↗
PubMed1997

Persistent production of interferon-gamma (IFN-gamma) and IL-12 is essential for the generation of protective immunity against Listeria monocytogenes.

IFN-gamma and IL-12 are believed to be important in the host defence against Listeria infection in mice. However, the relationship between these two cytokines and generation of protective immunity remains poorly understood. In the present study, it was found that at least 4 days of immunizing infection were required for the generation of protective immunity against L. monocytogenes. Protective immunity was generated only by immunizing infection with virulent strain. Even repeated injections of avirulent strain failed to induce protective immunity. When the immunizing infection was terminated with antibiotics, generation of protective immunity and IFN-gamma-producing ability was impaired, while expression of IFN-gamma and IL-12 was also impaired. The mutual relationship between IFN-gamma and IL-12 in L. monocytogenes infection was analysed in vitro. After neutralization of IL-12, IFN-gamma production was completely blocked and IFN-gamma expression was also inhibited. In contrast, there was no change of IL-12 expression after neutralization of IFN-gamma. Taking all facts into consideration, it may be concluded that persistent production of IFN-gamma induced by persistent production of IL-12 during immunizing infection is essential for the generation of protective immunity against L. monocytogenes.

Animals↗
PubMed1997

[Detection of hepatitis C virus markers in colostrum].

OBJECTIVE: To evaluate the possibility of hepatitis C virus (HCV) transmission through lactation by detection of HCV markers in colostrum. METHODS: Anti-HCV IgG, anti-HCV IgA and anti-HCV IgM antibodies in colostrum and sera were detected by indirect enzyme linked immunosorbent assay (ELISA), and HCV RNA was tested by reverse-transcription polymerase chain reaction simultaneously. RESULTS: Among 35 samples of colostrum from puerperants with anti-HCV IgG-positive sera, anti-HCV IgA, anti-HCV IgG, and anti-HCV IgM were detected in 19, 6 and 1 samples respectively. Fourteen of the 35 sera samples were HCV RNA-positive, and only 2 of colostrum samples showed HCV RNA-positive. A significant difference (P < 0.01) was found between the HCV RNA positive rates of sera and colostrum. CONCLUSIONS: IgA was the predominant anti-HCV antibodies in the colostrum from puerperants with anti-HCV IgG-positive sera. The HCV RNA-positive rate of sera was markedly higher than that of colostrum. It is presumed that puerperants with anti-HCV IgG-positive sera, especially those with both anti-HCV IgA-positive and HCV RNA-positive colostrum, are most likely to transmit HCV through lactation and cause their infants to be infected by HCV.

Adult↗