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Biomedical subjects

Y Jiang

Publications and source records attributed to Y Jiang.

At least 703 records · Page 39Linked to original sources

Effect of intracerebral microinjection of naloxone on acupuncture- and morphine-analgesia in the rabbit.

Although there are unequivocal evidences indicating the participation of endogenous opiate-like substances in acupuncture analgesia, their exact sites of action remain to be elucidated. From the results of localization studies by injecting minute amount of narcotic antagonist naloxone into discrete brain areas and assessing its effect on acupuncture analgesia in rabbits it is concluded that nuclei accumbens, amygdala, habenula and periaquaductal grey are the strategic sites for endogenous opioids to exert their analgesic effect. These brain areas are also of extreme importance for the realization of morphine analgesia.

Acupuncture Therapy↗

A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease.

Much evidence indicates that abnormal processing and extracellular deposition of amyloid-beta peptide (A beta), a proteolytic derivative of the beta-amyloid precursor protein (betaAPP), is central to the pathogenesis of Alzheimer's disease (reviewed in ref. 1). In the PDAPP transgenic mouse model of Alzheimer's disease, immunization with A beta causes a marked reduction in burden of the brain amyloid. Evidence that A beta immunization also reduces cognitive dysfunction in murine models of Alzheimer's disease would support the hypothesis that abnormal A beta processing is essential to the pathogenesis of Alzheimer's disease, and would encourage the development of other strategies directed at the 'amyloid cascade'. Here we show that A beta immunization reduces both deposition of cerebral fibrillar A beta and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of A beta in the brain. This implies that either a approximately 50% reduction in dense-cored A beta plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic A beta species.

Alzheimer Disease↗

Oral immunization with a live recombinant attenuated Salmonella typhimurium protects mice against Toxoplasma gondii.

The natural site of infection for T. gondii is the mucosal surface of the intestine, so the protective immunity obtained after natural infection with T. gondii points to the importance of developing a vaccine that stimulates mucosal defences. In this study, an aroA- and aroD- attenuated strain of Salmonella typhimurium (BRD509) has been used to deliver the recombinant eukaryotic plasmid pSAG(1-2)/CTA2/B expressing a multi-antigenic gene encoding SAG1 and SAG2 of T. gondii linked to A2/B subunits of cholera toxin as a candidate oral T. gondii vaccine. Immunoblot analysis showed compound gene expression in HeLa cells in vitro and intragastric immunization of mice with the recombinant salmonella resulted in the induction of humoral and Th1 type cellular immune responses and afforded protection against RH strain T. gondii challenge. Anti-T. gondii IgG values increased markedly in the BRD509/pSAG(1-2)-CTA2/B immunized group; these values were significantly higher than those in the negative controls (P = 0.008). With CTA2/B genetic adjuvant, the T. gondii-specific response was predominantly Th1, indicating that the CTA(2)/B genetic adjuvant was able to overcome the strong Th2-bias of the antigen (IgG2a >> IgG1). Antigen-specific T cell proliferative responses and CTL activity were significantly enhanced when cholera toxin CTA2/B genetic adjuvant was used (P = 0.009; P = 0.006). Culture supernatants from antigen-stimulated splenocytes from mice in these groups were also examined by ELISA for Th1- and Th2-type cytokines; mean IFN-gamma levels produced after oral immunization with BRD509/pSAG(1-2)-CTA2/B were about nine-fold higher than after immunization with BRD509/pSAG(1-2) (P = 0.007). On the other hand, the levels of IL-4 were low for all groups and no increase was seen in the presence of CTA2/B genetic adjuvant. When the immunized mice were intraperitoneally challenged with 10(3) tachyzoites of the highly virulent RH strain, the survival time of the mice immunized with BRD509/pSAG(1-2)-CTA2/B was markedly longer than other groups (P = 0.003) and a 40% survival rate was achieved. This is the first report that demonstrates that an oral attenuated salmonella DNA vaccine can induce protective immunity against the acute phase of T. gondii infection.

Adjuvants, Immunologic↗

Characterization of Bovidae sex-determining gene SRY.

In mammals, testis determination is under the control of the sex-determining gene SRY. This Y-linked gene encodes a protein with a DNA binding domain similar to those found in high-mobility-group proteins. Here we report the cloning and sequences of the SRY genes of yak and Chinese native cattle. Our data show that SRY genes in Bovidae are less divergent, especially in the coding and 3' regions.

3' Untranslated Regions↗

Effect of beta-chemokines on human immunodeficiency virus type 1 replication, binding, uncoating, and CCR5 receptor expression in human monocyte-derived macrophages.

OBJECTIVES: We examined the effect and time of addition of beta-chemokines on human immunodeficiency virus type 1 (HIV-1) replication, binding, and uncoating in human macrophages and measured CCR5 receptor expression during virus binding and uncoating. METHODS: Macrophages were treated with beta-chemokines before infection, at infection, or postinfection, and virus replication was determined by p24 antigen level. Binding and uncoating of 35[S]-methionine-labeled HIV-1 was measured. CCR5 expression was determined by flow cytometry. RESULTS: The beta-chemokines potently inhibited virus replication. The strongest inhibition occurred when cultures were pretreated and maintained with beta-chemokines. Beta-chemokines also caused strong inhibition of viral uncoating and a considerable decrease in CCR5 expression during uncoating. CONCLUSIONS: CCR5 receptors appear to be internalized and recycled to the cell surfaces during HIV entry. The down-regulation of CCR5 expression by beta-chemokines during virus uncoating probably accounts for the reduction in virus uncoating (entry) and hence in virus replication.

CD4 Antigens↗

Vascular dementia, with special reference to its vascular and immunological events.

Vascular dementia (VaD) is an poorly defined entity; it relates to different vascular mechanisms and different changes in the brain and has different clinical manifestations with different etiologies. From the pathogenetic and therapeutic point of view, we tried to find some practical events that could help identify VaD. We combined critical review with our own clinical and laboratory experience and found that some vascular, nonvascular, and immunological components are involved in the pathogenesis and treatment of VaD. We concluded that although the definition, etiology, clinical manifestation, laboratory data, and treatment are still controversial, it is useful to find some common, key points in the pathogenesis and treatment of VaD.

Dementia, Vascular↗

Use of the monoclonal antibody M30 for detecting HSG cell apoptosis.

An immunocytochemical method using a monoclonal antibody (MoAb), M30, which reacts with the product resulting from the cleavage of cytokeratin 18 by activated caspase, was applied to detect the apoptosis of human salivary gland tumor (HSG) cells induced by epigallocatechin gallate (EGCG), gallic acid (GA) and sodium ascorbate (SA). EGCG, GA and SA dose-dependently induced HSG cell death. Immunoreactive products were significantly observed in the cytoplasm of HSG cells after treatment with all these compounds. The reactions occurred with lower concentrations of these agents and after shorter treatment times, in comparison with DNA fragmentation detected by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method. These results suggest that immunocytochemical staining with the MoAb M30 may be useful for detecting the apoptosis-inducing activities of various chemical compounds.

Antibodies, Monoclonal↗

Induction of apoptosis by flavones, flavonols (3-hydroxyflavones) and isoprenoid-substituted flavonoids in human oral tumor cell lines.

Various flavones, flavonols (3-hydroxyflavones) and isoprenoid-substituted flavones (flavonols) were investigated for their cytotoxic activity. Most of these compounds were more cytotoxic against human oral squamous cell carcinoma and salivary gland tumor cell lines than human gingival fibroblasts. The cytotoxic activity of flavonoids was generally higher than that of tannin-related compounds. Flavonoids induced apoptotic cell death characterized by DNA fragmentation (as identified by TUNEL method) and activation of caspase(s) (as identified by degradation products of cytokeratin 18 with M30 monoclonal antibody). ESR spectroscopy revealed that higher concentrations of flavonoids produced radicals under alkaline conditions. However, not all of them enhanced the radical intensity of sodium ascorbate, suggesting that the redox potential of flavonoids differs considerably from samples to samples. Catalase failed to eliminate the cytotoxic activity of flavonoids, reducing the possibility of the involvement of hydrogen peroxide for the cytotoxicity induction by them.

Apoptosis↗

Interaction between chlorogenic acid and antioxidants.

The interaction between chlorogenic acid (CGA) and antioxidants was investigated by two different parameters: radical intensity and cytotoxicity induction. ESR spectroscopy shows that CGA produced radicals under alkaline condition. The CGA radical was scavenged by 100-300-fold lower concentrations of sodium ascorbate or N-acetyl-l-cysteine (NAC), whereas the ascorbate radical was not completely scavenged by CGA. The cytotoxic activity of CGA against human oral tumor cells (HSC-2, HSG) was completely eliminated by lower concentrations of sodium ascorbate or NAC, whereas that of sodium ascorbate or NAC was only slightly reduced by CGA. The present study demonstrated that CGA induces cytotoxicity by its radical-mediated oxidation mechanism and suggests the applicability of ESR spectroscopy for the screening of drug to drug interaction.

Acetylcysteine↗