Search PubMed⌕ Search

Biomedical subjects

Dexin Zhang

Publications and source records attributed to Dexin Zhang.

7 recordsLinked to original sources
PubMed2006

MG7 mimotope-based DNA vaccination for gastric cancer.

Gastric cancer is still one of the leading causes of cancer-related death worldwide. Prevention and treatment of gastric cancer through vaccination has been difficult owing to lack of a specific target and poor immunity. A number of vaccination strategies have been used to augment immune responses against gastric cancer and some progress has been made. In a series of studies, the authors have focused on gastric cancer vaccination approaches based on MG7 mimotopes, which are mimicry epitopes selected from phage-displayed oligopeptide libraries with a gastric cancer cell-specific monoclonal antibody, MG7-Ab. Strategies employed in these studies include viral or plasmid vectors in combination with carrier sequence or unmethylated CpG with synthetic peptides in nanoemulsion. The results demonstrated that MG7 mimotopes could effectively and specifically induce both cellular and humoral immune reactions and in vivo antitumor responses. In particular, a four-MG7 mimotope DNA vaccine was found to elicit much stronger antitumor immune responses in mice compared with its single-mimotope counterpart. These encouraging findings might pave the way for the development of novel MG7 antigen-based vaccination approaches for human gastric cancer. The review also discusses other immune-enhancing vaccination strategies for gastric cancer.

Animals↗
PubMed2005

Expressions and clinical significances of angiopoietin-1, -2 and Tie2 in human gastric cancer.

The roles of angiopoietins in gastric cancer progression are still not fully understood. In this study the expressions of angiopoietin-1 (Ang-1), -2 (Ang-2) were compared by immunohistochemistry in 53 gastric cancer and 23 normal gastric mucosa samples. Results revealed that Ang-2 expression was significantly increased in gastric cancer tissues (74%) and was correlated with higher TNM stage, lymph node metastasis as well as distance metastasis. The expression of Ang-1 was also elevated in cancerous tissues (66%) and significantly associated with differentiation degree. In addition, Ang-2 as well as its receptor Tie2 expressions were higher in 12 pairs of gastric cancer tissue samples than those in corresponding adjacent samples by Western blot, while Ang-1 expression showed great heterogeneity. Furthermore, the expressions of Ang-1 and Ang-2 were almost positive in eight gastric cancer cell lines. Among them, AGS expressed both Ang-2 and a relatively moderate amount of Ang-2(443), a novel splice form of Ang-2, while others showed only Ang-2 mRNA expression.

Angiopoietin-1↗
PubMed2004

Efficient iris recognition by characterizing key local variations.

Unlike other biometrics such as fingerprints and face, the distinct aspect of iris comes from randomly distributed features. This leads to its high reliability for personal identification, and at the same time, the difficulty in effectively representing such details in an image. This paper describes an efficient algorithm for iris recognition by characterizing key local variations. The basic idea is that local sharp variation points, denoting the appearing or vanishing of an important image structure, are utilized to represent the characteristics of the iris. The whole procedure of feature extraction includes two steps: 1) a set of one-dimensional intensity signals is constructed to effectively characterize the most important information of the original two-dimensional image; 2) using a particular class of wavelets, a position sequence of local sharp variation points in such signals is recorded as features. We also present a fast matching scheme based on exclusive OR operation to compute the similarity between a pair of position sequences. Experimental results on 2255 iris images show that the performance of the proposed method is encouraging and comparable to the best iris recognition algorithm found in the current literature.

Algorithms↗
PubMed2003

Widespread inosine-containing mRNA in lymphocytes regulated by ADAR1 in response to inflammation.

Adenosine-to-inosine (A-to-I) RNA editing is a post-transcriptional modification of pre-mRNA catalysed by an RNA-specific adenosine deaminase (ADAR). A-to-I RNA editing has been previously reported in the pre-mRNAs of brain glutamate and serotonin receptors and in lung tissue during inflammation. Here we report that systemic inflammation markedly induces inosine-containing mRNA to approximately 5% of adenosine in total mRNA. Induction was the result of up-regulation of A-to-I RNA editing as both dsRNA editing activity and ADAR1 expression were increased in the spleen, thymus and peripheral lymphocytes from endotoxin-treated mice. Up-regulation of ADAR1 was confirmed in vitro in T lymphocytes and macrophages stimulated with a variety of inflammatory mediators including tumour necrosis factor-alpha and interferon-gamma. A late induction of RNA editing was detected in concanavalin A-activated splenocytes stimulated with interleukin-2 in vitro. Taken together, these data suggest that a large number of inosine-containing mRNAs are produced during acute inflammation via up-regulation of ADAR1-mediated RNA editing. These events may affect the inflammatory and immune response through modulation of protein production.

Acute Disease↗
PubMed2002

Characterization of a murine model of endotoxin-induced acute lung injury.

Endotoxin-induced microvascular lung injury in mice is a commonly used experimental model of the acute respiratory distress syndrome (ARDS). The present paper aimed to characterize this popular model in a comprehensive and systematic fashion. Male C57bl/6 mice (n = 5) were administered an LD55 dose of E. coli endotoxin (15 mg/kg, i.p.), and lungs were harvested at several time points and evaluated for injury as well as for expression of a variety of inflammatory mediators. Endotoxin induced many features characteristic of acute microvascular lung injury. These included early (1-2 h) expression of inflammatory mediators (IL-1alpha, IL-1beta, IL-4, IL-6, IL-10, TNF-alpha, interferon-alpha, interferon gamma, and MCP-1) and leukocyte accumulation in lung tissue (lung myeloperoxidase activity 18.5 +/- 7.8 U/g tissue, P < 0.05), followed by pulmonary edema (lung water content index 17.4% +/- 2.5%, P < 0.05) and mortality. Histopathological evaluation of lung tissue was compatible with these findings. The characterization of this murine model of endotoxin-induced microvascular injury will facilitate its utilization in ARDS research.

Animals↗
PubMed2002

MOB-1 and TNF-alpha interact to induce microvascular lung injury.

We have recently identified the alpha-chemokine mob-1 as a highly inducible gene in several rat models of microvascular lung injury, whose expression was suppressed by inhibition of tumor necrosis TNF-alpha (TNF-alpha). This work provides further insight into the relationship between mob-1 and TNF-alpha in the development of lung injury assessed by pulmonary edema and leukosequestration. First, pulmonary mob-1 and TNF-alpha were upregulated in animals subjected to lung injury produced by the intratracheal administration of recombinant TNF-alpha and recombinant mob-1, respectively. Second, mob-1 inhibition by intratracheal anti-mob-1 antibody attenuated lung injury induced by recombinant TNF-alpha. Third, pretreatment with anti-TNF-alpha monoclonal antibody administered intratracheally abrogated recombinant mob-1-induced microvascular lung injury. In vitro, mob-1 and TNF-alpha increased each other's production in RAW 264.7 cells and mob-1 or TNF-alpha inhibition prevented endotoxin-induced upregulation of TNF-alpha or mob-1, respectively, from these cells. Together, these data suggest that mob-1 and TNF-alpha interact to promote lung inflammation.

Animals↗