Search PubMed⌕ Search

Biomedical subjects

Xia Zhang

Publications and source records attributed to Xia Zhang.

100 records · Page 6Linked to original sources
PubMed2002

Relations between brain pathology and temporal lobe epilepsy.

Temporal lobe epilepsy, the most common type of epilepsy in adult humans, is characterized clinically by the progressive development of spontaneous recurrent seizures of temporal lobe origin and pathologically by hippocampal neuronal loss and mossy fiber sprouting. In this study, we sought to test the prominent hypothesis that neuronal loss and mossy fiber sprouting play a critical role in the genesis and progression of temporal lobe epilepsy. Rats receiving a single kainic acid injection experienced a single sustained episode of epileptic status with massive neuronal loss and mossy fiber sprouting, whereas rats receiving triple kainic acid injections experienced two priming episodes and one sustained episode of epileptic status with no detectable neuronal loss and mossy fiber sprouting. Early in the process of chronic seizure development, primed rats that failed to show detectable neuronal loss and mossy fiber sprouting exhibited a starting date and a frequency of spontaneous recurrent seizures similar to those of nonprimed rats that showed massive neuronal loss and mossy fiber sprouting. However, nonprimed rats displayed significantly prolonged episodes of spontaneous recurrent seizures over the whole process of chronic seizure development and more frequent severe seizures later in the process. Similar results were observed in both Fischer-344 and Wistar rats as well as in the rat pilocarpine preparation of temporal lobe epilepsy. These results fail to reveal a relation between neuronal loss-mossy fiber sprouting and the genesis of temporal lobe epilepsy but suggest that neuronal loss, mossy fiber sprouting, or both contribute to the intensification of chronic seizures.

Animals↗
PubMed2002

PPAR and immune system--what do we know?

Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear steroid receptor superfamily. Originally, the receptors were identified as critical controllers for several key enzymes that catalyze the oxidation of fatty acids. PPARs consist of three members: PPAR-alpha, PPAR-beta/delta, and PPAR-gamma. Among them, PPAR-gamma is essential for controlling thermogenesis and adipocyte differentiation. The ligands for PPAR-gamma include 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2)--a metabolite from the prostaglandin synthesis pathway, and "glitazones"--drugs utilized in the treatment of patients with diabetes. The precursors for prostaglandins are fatty acids consumed from diet and these precursors have long been postulated to have a regulatory role in immune functions. Emerging evidence indicates that PPAR-gamma and its ligands are indeed important for the modulation of immune and inflammatory reactions. In this review, we will spotlight the molecular mechanisms of receptor/ligand function and how they may regulate immune and inflammatory reactions. We also propose that PPAR-gamma and its endogenous ligands are participating factors for Type 1/Type 2 T and NK cell differentiation and development. Deciphering the mechanism of action of PPAR-gamma and its ligands may lead to a new therapeutic regiment for treatment of diseases involving dysfunction of the immune system.

Animals↗
PubMed2002

The role of NF-kappaB in the regulation of cell stress responses.

Nuclear factor-kappaB (NF-kappaB) is one of the key regulatory molecules in oxidative stress-induced cell activation. NF-kappaB is normally sequestered in the cytoplasm of nonstimulated cells and must translocate into the nucleus to regulate effector gene expression. A family of inhibitory proteins, IKBs, binds to NF-kappaB and masks its nuclear localization signal domain and therefore controls the translocation of NF-kappaB. Exposure of cells to extracellular stimuli that perturb redox balance results in rapid phosphorylation, ubiquitination, and proteolytic degradation of IkappaBs. This process frees NF-kappaB from the NF-KB/IKB complexes and enables NF-kappaB to translocate to the nucleus where it regulates gene transcription. Many effector genes including those encoding cytokines and adhesion molecules are in turn regulated by NF-kappaB. NF-kappaB is also an essential component of ionizing radiation (IR)-triggered signal transduction pathways that can lead to cell death or survival. The purpose of this review is to briefly summarize the recent progress in the studies of the role of reactive oxygen species (ROS), cytokines and ionizing radiation in NF-kappaB activation.

Animals↗
PubMed2002

[Expression and significance of P-glycoprotein, glutathione S-transferase-pi and Topoisomerase II in gastric carcinomas].

BACKGROUND & OBJECTIVE: Multi-drug resistance(MDR) is the most important failing reason of tumor chemotherapy, the substance that P-glycoprotein(P-gp), glutathione S-transferase-pi(GST-pi), Topoisomerase II (Topo II) etc was the fundamental substances producing MDR. Gastric carcinoma is the relatively familiar malignancy, the report was relatively fewness that the expression of P-gp, GST-pi and Topo II by means of immunohistochemistry were associated with in the gastric carcinomas of previously untreated patients. This study was designed to investigate the expression and significance of P-gp, glutathione S-transferase-pi(GST-pi) and Topoisomerase II(Topo II) in gastric carcinomas. METHODS: Seventy-five human gastric carcinomas of previously untreated patients were studied for the expression of P-gp, GST-pi and Topo II by means of immunohistochemistry. RESULTS: The expression of P-gp, GST-pi and Topo II were 76.0%, 85.3% and 68.0% in gastric carcinoma tissues. There was no significant relationship between the expression levels and age, sex, location of tumor and depth of tumor invasion. Positive rate was higher in glandular-form carcinoma than that in mucoid carcinoma, signet-ring cell carcinoma and poorly differentiated carcinoma (P < 0.05). There was a significant relationship between the lymph node involvement and the higher expression of P-gp, GST-pi, lower expression of Topo II. CONCLUSION: There is a correlation between the expression of P-gp, GST-pi, Topo II and histologic subtypes, the expression may also related to the differentiation and metastasis of the gastric carcinomas.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2002

Oral immunization of mice with attenuated Salmonella typhimurium expressing Helicobacter pylori urease B subunit.

OBJECTIVE: To establish attenuated Salmonella typhimurium producing Helicobacter pylori (H. pylori) urease subunit B (UreB) and determine whether it could be used as an oral vaccine against H. pylori. METHODS: H. pylori (SS1 strain) UreB gene fragment amplified by PCR was cloned into the prokaryotic expression vector pTC01 after sequencing, and then transformed into attenuated Salmonella typhimurium SL3261 to acquire SL3261/pTC01-UreB. The expression of H. pylori UreB in SL3261 was detected by Western blot. Twelve weeks after oral immunization of mice, antibody responses were evaluated using serum and intestinal fluid by ELISA assay. Interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) in the supernatant of spleen cells culture were also assessed by ELISA. In vitro stability of pTC01-UreB plasmid in SL3261 was confirmed by growing in Luria Broth (LB) medium to 80 generations. RESULTS: The UreB gene fragment amplified by PCR was consistent with the sequence of the H. pylori UreB as evidenced by sequence analysis. Enzyme digestion revealed that the correct pTC01-UreB was obtained. Western blot showed that a 61kDa protein was expressed in SL3261/pTC01-UreB, which could be recognized by anti-H. pylori UreB antiserum. After 80 generations of continuous culture, the recombinant plasmid pTC01-UreB was stable in SL3261 and had no obvious toxicity. Multiple oral immunizations with SL3261/pTC01-UreB could significantly induce H. pylori-specific mucosal IgA response as well as serum IgG response. Moreover, there were significant increases of IFN-gamma and IL-10 in the SL3261/pTC01-UreB group. Finally, no obvious side effects for mice and no change in gastric inflammation were observed. CONCLUSION: Attenuated Salmonella typhimurium expressing H. pylori UreB may be used as oral vaccine against H. pylori infection.

Administration, Oral↗
PubMed2002

[Structures and pharmacological activities of beesiosides O and P].

AIM: To investigate the chemical constituents of the rhizomes of Beesia calthaefolia native to China in order to obtain a more comprehensive understanding of its effective components. METHODS: Compounds were isolated by column chromatography with silica gel. Their structures were elucidated by spectral analysis and chemical evidence. Compounds identified were subjected to pharmacological evaluation. RESULTS: Two novel compounds were isolated and identified as (20S, 24S)-15 alpha-acetoxy-16 beta, 24; 20, 24-diepoxy-9, 19-cyclolanostane-3 beta, 25-diol-3-O-beta-D-xylopyranoside (I) and (20S, 24R)-15 alpha-acetoxy-9, 19-cyclolanostane-3 beta, 16 beta, 20, 24, 25-pentaol-3-O-beta-D-xylopyranoside (II), named beesioside O and beesioside P. CONCLUSION: Compounds I and II are new compounds. Compounds I exhibited immunosuppressive activity and could inhibit angiogenesis as well as inhibit the proliferation of osteoblast. Compound II displayed remarkable inhibition activity against calcium channel receptor.

Angiogenesis Inhibitors↗
PubMedDate not supplied

Effects of IL-7 and dexamethasone: induction of CD25, the high affinity IL-2 receptor, on human CD4+ cells.

Since we have previously shown that dexamethasone (Dex) enhances the proportion of murine Treg cells, we tested the effect of IL-7, a promoter of T cell survival, together with Dex on human CD4+CD25+ Treg cells in an in vitro setting. The results showed that IL-7 in concert with Dex markedly augmented the generation of CD4+CD25+ T cells. To discern the origin of the induced CD4+CD25+ T cells, MACS-purified CD4+CD25-, and CD4+CD25+ cells were cultured in the presence of Dex and/or IL-7 for 4 days. Although two thirds of CD4+CD25- T cells became CD4+CD25+ T cells, they had no suppressive activity. In contrast, the original CD4+CD25+ T cells maintained suppressive activity after Dex/IL-7 treatment, however, there was not a significant expansion in their cell number. Dex and IL-7 did not induce additional Treg cells, but additively induced the expression of the activation marker CD25 by CD4+CD25- T cells. This combination may provide a novel means of priming CD4 T cells to respond to IL-2 and may prove useful in up-regulation of normal immune responses in immune deficient diseases.

CD4-Positive T-Lymphocytes↗
PubMedDate not supplied

In vivo formation of salsolinol induced by high acetaldehyde concentration in rat striatum employing microdialysis.

AIMS: The in vivo formation of salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquionoline), an endogeneous condensation product of dopamine (DA) with acetaldehyde (AcH), was examined following the administration of cyanamide (CY) plus ethanol (EtOH) using microdialysis-high-performance liquid chromatography with electrochemical detection. METHODS: After the insertion of a microdialysis probe into the striatum, rats were treated with CY (a potent inhibitor of aldehyde dehydrogenase, 50 mg/kg), 4-methylpyrazole (4-MP, a strong inhibitor of alcohol dehydrogenase, 82 mg/kg), and CY + 4-MP, followed 1 h later by EtOH (1 g/kg), CY and 4-MP only by intraperitoneal administration. RESULTS: In the CY + EtOH group, salsolinol was detected in striatal dialysates and high AcH concentrations were found in the blood. The time course of changes in salsolinol concentrations correlated with blood AcH concentrations. In the other experimental groups, salsolinol in the dialysates and high AcH concentrations in the blood were not detected. CONCLUSIONS: These observations indicate that: (1) high AcH concentrations induce the formation of salsolinol in the rat striatum; (2) there is no effect of EtOH or AcH on striatal dialysate concentrations of DA and 5-hydroxytryptamine.

Acetaldehyde↗