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Biomedical subjects

N Guo

Publications and source records attributed to N Guo.

At least 73 records · Page 4Linked to original sources
PubMed1995

Mouse surfactant protein-D. cDNA cloning, characterization, and gene localization to chromosome 14.

Surfactant protein-D (SP-D) is a collectin found associated with surfactant in the lung. SP-D has also been functionally characterized as an opsonin for diverse microorganisms and a chemoattractant for phagocytic cells. To determine the structure of mouse SP-D, we isolated and characterized clones from a B6/CBAF1J strain lung cDNA library using a PCR-derived genomic probe. The deduced sequence predicts a 19-amino acid signal sequence, a 25-amino acid long NH2 terminus with two cysteines, followed by an uninterrupted collagen domain with 59 Gly-X-Y repeats. Next, a short "neck" domain of 28 amino acids, with a potential to form trimeric alpha-helical coiled coil is found ending in a COOH-terminal 125-amino acid carbohydrate recognition domain. The mature mouse SP-D protein of 355 amino acids shows strong homology to rat (92% identity), human (76%), and bovine (72%) SP-D amino acid sequences. Northern blot and RT-PCR analysis revealed that the mouse SP-D gene is expressed predominantly in lung and, surprisingly, also in heart, stomach, and kidney but not in brain. In contrast, mouse surfactant protein-A (SP-A) mRNA expression was found to be restricted to lung. Human lung and stomach, but not heart or liver, were found to express SP-D mRNA, as determined by PCR. The mouse SP-D gene (Sftp4) has been localized to chromosome 14 (to a region syntenic to human chromosome 10), closely linked to the genes for other collagenous lectins, mannose-binding protein-A (MbI1), and SP-A (Sftp1).

Amino Acid Sequence↗
PubMed1995

Receptor mechanisms mediating clozapine-induced c-fos expression in the forebrain.

The atypical antipsychotic clozapine produces distinctly different regional patterns of c-fos expression in rat forebrain than does the prototypical neuroleptic haloperidol. While haloperidol-induced c-fos expression appears to be mediated by its D2 dopamine receptor antagonist properties, the mechanisms by which clozapine increases c-fos expression remain uncertain. Using a combination of brain lesion, pharmacological and immunohistochemical techniques, the present study sought to determine the receptor mechanisms by which clozapine increases the number of Fos-like immunoreactive neurons in various regions of the forebrain. To test whether serotonergic and/or noradrenergic systems are involved in clozapine-induced c-fos expression, rats received either 5,7-dihydroxytryptamine lesions of the medial forebrain bundle or 6-hydroxydopamine lesions of the dorsal noradrenergic bundle two weeks prior to clozapine (20 mg/kg) injections. Neither type of lesion affected clozapine-induced c-fos expression in the rat forebrain, suggesting that neither serotonergic nor noradrenergic mechanisms are involved in this action of clozapine. In another experiment, the 5-hydroxytryptamine2 receptor antagonist ritanserin (5 mg/kg), either alone or in combination with haloperidol (1 mg/kg), failed to mimic the pattern of c-fos expression produced by clozapine. This suggests that clozapine's antagonist actions at 5-hydroxytryptamine2 receptors cannot explain the unique pattern of regional c-fos expression produced by this compound. To determine whether the blockade of subtypes of the D2 dopamine receptor family may contribute to clozapine's effects, the dopamine receptor agonists quinpirole and 7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OH-DPAT) were injected 15 min prior to clozapine. Quinpirole produced a small but significant decrease in clozapine-induced c-fos expression in the medial prefrontal cortex, had larger effects in the lateral septum, and blocked clozapine's actions in the nucleus accumbens and major island of Calleja. Pretreatment with 7-OH-DPAT attenuated clozapine-induced c-fos expression in the nucleus accumbens and lateral septum, completely blocked the expression in the major island of Calleja, but was without effect in the medial prefrontal cortex. Given the different affinities of quinpirole and 7-OH-DPAT for D2, D3 and D4 receptors, these data suggest that clozapine-induced increases in c-fos expression in the nucleus accumbens, major island of Cajella and lateral septal nucleus are due to antagonist actions of this antipsychotic at D3 dopamine receptors. They also indicate that while antagonist actions at D4 receptors may contribute, the primary mechanisms by which clozapine increases c-fos expression in the medial prefrontal cortex remain to be determined.

Animals↗
PubMed1995

[Ondansetron in the prophylaxis of acute emesis induced by supra-high single dose total body irradiation (TBI)].

One hundred sixteen cases of leukemia patients received supra-high single dose TBI for bone marrow transplantation (BMT) with total a radiation dosage of 700-770 Gy at about 5cGy/min. Seventy patients were given ondanstron (8mg) plus dexamethasone (DXM, 10mg) for prophylaxis of TBI-induced acute nausea and vomiting, 46 patients were given paspertin (10mg) plus dexamethasone (10mg) as controls. The clinical results showed that ondansetron plus DXM achieved complete or major control of vomiting in 59/70 (84%) of cases and there was little or no nausea in 61/70 (87%), while paspertin plus DXM achieved complete or major control of vomiting only in 9/46 (20%) of cases and little or no nausea in 5/46 (11%). It is concluded that ondansetron has significantly greater advantage over paspertin in the control of acute emesis induced by TBI.

Adult↗
PubMed1995

[Karyotype analysis of Candida species by PFGE and its use in classicification].

Electrophoretic karyotype in 7 medically important Candida species was analyzed by pulsed-field gel electrophoresis. The chromosomal DNAs of the Candida species were separated into 4-10 bamds ranging in size from 0.5-2.8 Mb. These patterns were species-specific, so the electrophoretic karyotype can be used as a genotype basis for classification and identification of Candida species.

Candida↗
PubMed1994

[The adherence reaction between Candida and cultured cell in vitro].

The adherence reaction between Candida and cultured cells in vitro was studied. After the comparison between two fungal phases, two different ratios of cells to fungi and two different incubation temperature, we found that the better adhesion condition is at 37 degrees C, with a concentration of cell to fungi of 1:200 and with the Candida albicans in the germ tube phase. We also found 4 different materials that could inhibit C. albicans adherence.

Animals↗
PubMed1993

Activated T-cell adhesion to thrombospondin is mediated by the alpha 4 beta 1 (VLA-4) and alpha 5 beta 1 (VLA-5) integrins.

T lymphocytes utilize adhesion receptors in a regulated manner to interact with other cells and with components of the extracellular matrix. These cell-cell and cell-matrix interactions serve a critical role in T cell recognition of foreign Ag and in the migration of T cells to various anatomic sites in vivo. Thrombospondin is an extracellular matrix protein that is transiently expressed at high concentration in damaged and inflamed tissue. Given recent evidence implicating a role for the extracellular matrix in modulating T-cell migration and function, we analyzed T-lymphocyte interactions with thrombospondin. We show here that CD4+ T cells specifically adhere to thrombospondin predominantly via the 70 kDa core region of the thrombospondin molecule. Antibody blocking and affinity chromatography analysis suggest that T-cell adhesion to thrombospondin involves three distinct receptors: an activation-independent receptor that mediates adhesion of resting T cells, and the alpha 4 beta 1 and alpha 5 beta 1 integrins, which mediate a rapid increase in adhesion to thrombospondin upon activation. These three molecules appear to be novel thrombospondin receptors, as other receptors previously implicated in the adhesion of nonlymphoid cells to thrombospondin appear not to be involved in T-cell/thrombospondin interactions. The up-regulation of alpha 4 beta 1 and alpha 5 beta 1 functional activity upon activation is associated with the preferential adhesion of memory T cells to thrombospondin. Our results thus define three novel thrombospondin receptors, and provide additional evidence that extracellular matrix proteins play an important role in lymphocyte migration into, and retention in, inflammatory sites.

CD4-Positive T-Lymphocytes↗
PubMed1993

Inhibition of fibronectin binding and fibronectin-mediated cell adhesion to collagen by a peptide from the second type I repeat of thrombospondin.

The platelet and extracellular matrix glycoprotein thrombospondin interacts with various types of cells as both a positive and negative modulator of cell adhesion, motility, and proliferation. These effects may be mediated by binding of thrombospondin to cell surface receptors or indirectly by binding to other extracellular matrix components. The role of peptide sequences from the type I repeats of thrombospondin in its interaction with fibronectin were investigated. Fibronectin bound specifically to the peptide Gly-Gly-Trp-Ser-His-Trp from the second type I repeat of thrombospondin but not to the corresponding peptides from the first or third repeats or flanking sequences from the second repeat. The two Trp residues and the His residue were essential for binding, and the two Gly residues enhanced the affinity of binding. Binding of the peptide and intact thrombospondin to fibronectin were inhibited by the gelatin-binding domain of fibronectin. The peptide specifically inhibited binding of fibronectin to gelatin or type I collagen and inhibited fibronectin-mediated adhesion of breast carcinoma and melanoma cells to gelatin or type I collagen substrates but not direct adhesion of the cells to fibronectin, which was inhibited by the peptide Gly-Arg-Gly-Asp-Ser. Thus, the fibronectin-binding thrombospondin peptide Gly-Gly-Trp-Ser-His-Trp is a selective inhibitor of fibronectin-mediated interactions of cells with collagen in the extracellular matrix.

Amino Acid Sequence↗
PubMed1993

A strain of urease negative Cryptococcus neoformans isolated from the environment in China.

This is the first report of a strain of urease negative Cryptococcus neoformans isolated from the environment in China. The colonies of this isolate showed brown pigmentation on cornmeal agar with 300 micrograms/ml caffeic acid, but failed to hydrolyze urea. Microbiological identification and pathogenicity tests in mice confirmed this as a strain of C. neoformans. A similar strain had reportedly been isolated from an AIDS patient.

Animals↗
PubMed1992

Scopolamine attenuates haloperidol-induced c-fos expression in the striatum.

Haloperidol increases the expression of Fos, the protein product of the proto-oncogene c-fos, in some parts of the central nervous system. Haloperidol also produces catalepsy in rodents and extrapyramidal side effects in humans, both of which are reduced by muscarinic receptor antagonists. In order to gain insight into the neurochemical and neuroanatomical substrates of haloperidol-induced catalepsy we examined the effects of the muscarinic receptor antagonist scopolamine on haloperidol-induced Fos expression in the striatum, nucleus accumbens and lateral septal nucleus. At a dose that reduced the cataleptic effect of haloperidol, scopolamine decreased the neuroleptic-induced Fos expression in the striatum and lateral septal nucleus but not the nucleus accumbens. These results indicate that haloperidol may increase c-fos expression in medium spiny striatal neurons indirectly by enhancing striatal acetylcholine release. They are also consistent with the hypothesis that neuroleptic-induced increases in striatal c-fos expression are predictive of extrapyramidal side effects produced by these compounds.

Animals↗
PubMed1992

Characterization and localization of glutathione binding sites on cultured astrocytes.

Glutathione (GSH) binding sites found in brain white matter in a previous study using biotinylated GSH (Third IBRO World Congress Neurosci. Abstr., 1991, P59.17) suggested that there might GSH receptors on glial cells. In the present study, radioligand receptor assays were performed on cultured astrocytes using [35S]GSH. Scatchard analyses of saturation binding of [35S]GSH revealed two binding sites: Kd1 = 2.0 +/- 0.1 nM, Bmax1 = 89.5 +/- 1.5 fmole/2.2 x 10(5) cells and Kd2 = 12.8 +/- 0.4 nM, Bmax2 = 187.7 +/- 2.4 fmol/2.2 x 10(5) cells. The saturable and displacible high affinity [35S]GSH binding we have observed suggests that this binding is not due to GSH sequestration by uptake sites or to the association of GSH with GSH S-transferases or GSH peroxidases which have Kds in the microM range. Colloidal gold and immunofluorescence double labelling were used to visualize the binding sites at the cellular level. Positive colloidal gold decoration further suggests that these labelled binding sites are membrane receptors on astrocytes.

Animals↗
PubMed1992

Glutathione: new candidate neuropeptide in the central nervous system.

The physiological significance of glutathione in the mammalian central nervous system is still uncertain, although some evidence indicates that it may be an important regulatory peptide. In the present study, the distribution and characteristics of glutathione binding sites in the brain have been studied. Biotinyl-glutathione was synthesized as a probe to detect glutathione binding sites in the CNS. Specific glutathione binding sites in the brain were largely localized to the white matter, suggesting the presence of glutathione receptors on neuroglial cells. The colloidal gold technique and immunofluorescence double staining allowed the visualization of the receptor at the cellular level and thus demonstrated that there are glutathione receptors on cultured astrocytes. Glutathione applied to cultured astrocytes elicited increased levels of intracellular inositol-1,4,5-trisphosphate, suggesting that glutathione receptors were coupled to phospholipase C. The localization of glutathione receptors on astrocytes and the activation of a second messenger system by glutathione suggest that glutathione may be a neuropeptide in the central nervous system.

Animals↗
PubMed1991

Immunoprecipitation of membrane proteins from rat basophilic leukemia cells by the antiganglioside monoclonal antibody AA4.

In previous studies, mAb AA4 inhibited IgE binding, induced rapid morphologic changes, and blocked histamine release in rat basophilic leukemia (RBL-2H3) cells. It bound to two novel derivatives of ganglioside GD1b (Ag I and Ag II) that appear to be present only in rat mast cells. The present study demonstrates the importance of gangliosides Ag I and Ag II for binding of mAb AA4 to intact cells. We also investigated the presence of gangliosides Ag I and Ag II and proteins immunoprecipitated with mAb AA4 in the parental and four variant cell lines. In comparison with the parental RBL-2H3, two variant cell lines had very low (0.5% and 2.0%) and two others had intermediate levels (9% and 18%) of 125I-AA4 binding. mAb AA4 inhibited 125I-IgE binding to the parental RBL-2H3 cells and to only one variant with intermediate amounts of gangliosides Ag I and Ag II. Therefore, there are variations in the proximity of these gangliosides to the high affinity IgE receptor (Fc epsilon RI) among different cell lines. mAb AA4 immunoprecipitated proteins of 50 to 60, 120, and 135 kDa from 125I-surface labeled cells. These were different from the subunits of Fc epsilon RI. The amount of gangliosides Ag I and Ag II in cell extracts correlated with the number of mAb AA4 binding sites on the cell surface and with the quantity of proteins precipitated from the different cell lines. Thus, these membrane proteins appear to be associated with gangliosides Ag I and Ag II. The binding of mAb AA4 to the surface gangliosides could induce intracellular changes through transmembrane signaling by these proteins.

Animals↗
PubMed1991

[Protective effect of glycyrrhizine in mice with systemic Candida albicans infection and its mechanism].

We proved that a Chinese herb extract--Glycyrrhizine, the sweet component of Licorice root--protected mice from Candida albicans infection in doses of 0.5 mg/(kg.d) for 15-20 d. After administration of the above doses, the mortality rate of infected mice was decreased from 100% to 65%; the survival time was extended from 6.76 +/- 1.95 to 10.99 +/- 7.24 days after infection with lethal spores; and the toxic symptoms were also alleviated. The mechanism of protection is probably related to several factors, such as plasma opsonin activity promotion, enhancement of NK cell activity, increasing levels of plasma SOD, etc. All of this indicates that GCZ might be used as an accessory drug in the treatment of severe fungal infection.

Animals↗
PubMed1990

Oxidative DNA and RNA damage in rat liver due to acetoxime: similarity to effects of 2-nitropropane.

Acetoxime (ACO) and 2-nitropropane (2-NP), both industrially important chemicals and known hepatocarcinogens in rats, induced increased levels of 8-hydroxy-guanine in liver DNA and RNA of male Sprague-Dawley and F344 rats after either oral or i.p. administration. Both compounds also produced qualitatively the same patterns of other apparent modifications of liver DNA and RNA nucleosides, discernible by HPLC with electrochemical detection. Six hours after administration, the effects of 2-NP on liver nucleic acids were more pronounced in F344 rats than in Sprague-Dawley rats, suggesting that 2-NP may prove to be a stronger carcinogen in the F344 strain. The effects of ACO, a weaker carcinogen than 2-NP, were less than those of the nitroalkane in both rat strains. These results suggest that the hepatocarcinogenicity of ACO, like that of 2-NP, may depend on increased generation of reactive oxygen species capable of producing DNA and RNA base damage in rat liver. In addition, the data support the hypothesis that the hepatocarcinogenicity of ACO depends on its partial in vivo N-oxidation to 2-NP.

Administration, Oral↗
PubMed1990

Sex and organ differences in oxidative DNA and RNA damage due to treatment of Sprague-Dawley rats with acetoxime or 2-nitropropane.

The hepatocarcinogens 2-nitropropane and acetoxime have previously been found to induce a specific and qualitatively identical pattern of base damage in rat liver DNA and RNA, including the induction of increased levels of 8-hydroxyguanine. Because both 2-nitropropane and acetoxime are weaker carcinogens in female rats than male rats, we examined the ability of these chemicals to induce this pattern of damage in liver and kidney nucleic acids of male and female Sprague-Dawley rats 6 and 18 h after administration. Significantly lower levels of 8-hydroxydeoxyguanosine, 8-hydroxyguanosine and other presumed modified nucleosides discernible by high-performance liquid chromatography with electrochemical detection were found in liver nucleic acids of female rats at both time points. In addition, minimal alteration of nucleic acids was observed in the kidney, which is not a target organ for the carcinogenicity of either 2-nitropropane (2-NP) or acetoxime (ACO). These results support the hypothesis that the specific DNA alterations observed are relevant to the hepatocarcinogenicity of 2-NP and ACO.

Alkanes↗