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Tong Zhou

Publications and source records attributed to Tong Zhou.

At least 37 records · Page 2Linked to original sources
PubMed2006

A point-process model for rapid identification of post-translational modifications.

Post-translational modifications (PTMs) are very important to biological function, and yet are notoriously difficult to detect and identify, especially in a high-throughput manner. Most of the existing approaches rely on exhaustive searches which are highly time consuming and thus are currently limited to handling of a few types of PTMs. In this paper, we present a point-process model that aims to find the optimal mass shifts to maximize the spectra alignment between an experimental MS/MS spectrum and a candidate theoretical spectrum, through cross-correlation calculation, yields a rapid search for all types of PTMs in a blind mode, i.e., without giving the types of the searching PTMs in advance. The test results show that our new approach's performance is comparable to or better than the other blind search methods, but is more efficient computationally and simpler in its concept.

Algorithms↗
PubMed2006

[DNA damage and oncogenic protein expression induced by cadmium].

OBJECTIVE: To explore the DNA damage and the expression of oncogenic protein induced by cadmium in vitro (human cells) and in vivo in rats. METHODS: The colony formation assay and the MTT assay were employed to determine the cytotoxicity of cadmium. The DNA damage and the cell cycle were measured by the comet assay and the flow cytometry, respectively. The western bolt and the X-Gal staining were also used to determine the change of oncogenic protein and the senescent marker. RESULTS: The cadmium inhibited the proliferation of cells and induced DNA damage significantly not only in human cultured cells but also in vivo animal cells. The comet rate increased from 6.1% in the control group to 23.2% in 200 microM cadmium treatment group (P < 0.01). The comet rate increased in all organs of male rats with the increase of dosage, and there were significant difference between treatment the groups and the control group in kidney and ventral prostate (P < 0.05). Furthermore, the cadmium blocked the cell cycle progression. At the same time, the expression of c-myc, c-Jun and beta-Gal were increased by cadmium. CONCLUSION: The cadmium could induce DNA damage and block the cell cycle, and further cause senescence, and death. However, the cadmium induced the DNA damage and the oncogenic protein expression may be the important factors to cause cancer.

Animals↗
PubMed2005

Synonymous codon usage in environmental chlamydia UWE25 reflects an evolutional divergence from pathogenic chlamydiae.

Publication of the complete genome sequence for the Acanthamoeba sp. endosymbiont UWE25 has illuminated the evolution history of chlamydiae. In this study, the codon usage bias in UWE25 and five other species of pathogenic chlamydiae was calculated. It was found that genomic composition constraints are the major source of codon usage variation in UWE25. This result is different from the former observation in pathogenic chlamydiae, whose genomic base composition is more unbiased. Four other factors, such as strand-specific mutational bias, natural selection acting at the level of translation, hydropathy level of each protein and the conservation level of amino acids also have influence in shaping the codon usage in these six species to some extent. Further analysis suggests that the high stability of the UWE25 genome partially account for the difference in codon usage pattern between environmental and pathogenic chlamydiae. Moreover, our results imply that the replicational selection pressure in pathogenic chlamydiae is stronger than that in UWE25. Analyzing the codon usage pattern in the environmental chlamydia and comparing it with that of the pathogenic chlamydiae may provide clues how the chlamydiae have evolved from their common ancestor.

Amino Acids↗
PubMed2005

Anti-tumor activity of TRA-8 anti-death receptor 5 (DR5) monoclonal antibody in combination with chemotherapy and radiation therapy in a cervical cancer model.

OBJECTIVES: There is substantial evidence that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) causes apoptosis via activation of death receptors 4 and 5 (DR4 and DR5). We sought to determine the therapeutic potential of TRA-8 (anti-DR5 monoclonal antibody) in combination with chemotherapy and radiation therapy in a cervical cancer model. METHODS: DR5 expression in 7 human cervical cancer cell lines was analyzed by indirect immunofluorescence using murine TRA-8 in combination with flow cytometry. Cell lines were treated with TRA-8 alone or in combination with cisplatin, topotecan, or radiation, and cytotoxicity assays were performed. Mice were inoculated with ME-180 cancer cells and treated with different combinations of therapy. Animals receiving antibody were injected intraperitoneally with 200 microg of TRA-8. Animals received 9 Gy 60Co radiation divided into 3 fractions and 3 intraperitoneal doses of cisplatin (6 mg/kg) 1 h before radiation. A similar experiment was performed using topotecan (2 mg/kg) as the chemotherapeutic agent. RESULTS: DR5 was expressed to a varying degree on the cervical cancer cell lines. Combination treatment with TRA-8 and chemotherapy or radiation resulted in synergistic cytotoxicity in vitro. In vivo, combination therapy with TRA-8, cisplatin, and radiation produced tumor growth inhibition that was significantly greater than the other groups. Similar results were seen in combination studies with topotecan. CONCLUSIONS: These data suggest that DR5 is a good target for activation of the apoptotic pathway. Monoclonal antibodies such as TRA-8 may play an important role in the development of an effective treatment strategy for patients with advanced cervical cancer.

Animals↗
PubMed2005

Evolutionary dynamics and highly optimized tolerance.

We develop a numerical model of a lattice community based on Highly Optimized Tolerance (HOT), which relates the evolution of complexity to robustness tradeoffs in an uncertain environment. With the model, we explore scenarios for evolution and extinction which are abstractions of processes which are commonly discussed in biological and ecological case studies. These include the effects of different habitats on the phenotypic traits of the organisms, the effects of different mutation rates on adaptation, fitness, and diversity, and competition between generalists and specialists. The model exhibits a wide variety of microevolutionary and macroevolutionary phenomena which can arise in organisms which are subject to random mutation, and selection based on fitness evaluated in a specific environment. Generalists arise in uniform habitats, where different disturbances occur with equal frequency, while specialists arise when the relative frequency of different disturbances is skewed. Fast mutators are seen to play a primary role in adaptation, while slow mutators preserve well-adapted configurations. When uniform and skewed habitats are coupled through migration of the organisms, we observe a primitive form of punctuated equilibrium. Rare events in the skewed habitat lead to extinction of the specialists, whereupon generalists invade from the uniform habitat, adapt to their new surroundings, ultimately leading their progeny to become vulnerable to extinction in a subsequent rare disturbance.

Adaptation, Physiological↗
PubMed2005

Low level, long-term inorganic arsenite exposure causes generalized resistance to apoptosis in cultured human keratinocytes: potential role in skin co-carcinogenesis.

Inorganic arsenic is a human carcinogen that targets the skin. Carcinogenesis is a multistep process in which acquired apoptotic resistance is a common event and prior work in non-skin cells shows acquired resistance to apoptosis occurs with chronic arsenite exposure. In the present study, when HaCaT cells, an immortalized, non-tumorigenic human keratinocyte cell line, were continuously exposed to low-level inorganic arsenite (as sodium arsenite; 100 nM) for 28 weeks, the cells acquired a generalized resistance to apoptosis. This included resistance to apoptosis induced by acute high concentrations of arsenite, ultraviolet A (UVA) irradiation, and several chemotherapeutic compounds (cisplatin, etoposide and doxorubicin). These arsenite-tolerant (As-TL) cells showed similar levels of UVA-induced reactive oxygen species (ROS) and oxidative DNA damage when compared to passage match control cells. Because cellular apoptosis is dependent on the balance between proapoptotic and survival pathways, the roles of protein kinase B (PKB), a key antiapoptotic molecule, in this acquired apoptotic resistance were investigated. Stimulation of apoptosis markedly decreased nuclear phosphorylated PKB (P-PKB) levels in control cells, but As-TL cells showed greatly increased stability of nuclear P-PKB. Pretreatment of the As-TL cells with LY294002 or Wortmannin, which specifically inhibit PKB phosphorylation, completely blocked apoptotic resistance in As-TL cells, indicating acquired apoptotic resistance is associated with increased stability of nuclear P-PKB. Because arsenic and UV irradiation are co-carcinogenic in mouse skin, resistance to UV-induced apoptosis in As-TL cells may allow UV-damaged cells to escape normal cell population controls and initiate the carcinogenic cascade. The observation that As-TL cells show no lessening of UV-induced genotoxicity supports this possibility.

Apoptosis↗
PubMed2005

Analysis of synonymous codon usage in H5N1 virus and other influenza A viruses.

In this study, we calculated the codon usage bias in H5N1 virus and performed a comparative analysis of synonymous codon usage patterns in H5N1 virus, five other evolutionary related influenza A viruses and a influenza B virus. Codon usage bias in H5N1 genome is a little slight, which is mainly determined by the base compositions on the third codon position. By comparing synonymous codon usage patterns in different viruses, we observed that the codon usage pattern of H5N1 virus is similar with other influenza A viruses, but not influenza B virus, and the synonymous codon usage in influenza A virus genes is phylogenetically conservative, but not strain-specific. Synonymous codon usage in genes encoded by different influenza A viruses is genus conservative. Compositional constraints could explain most of the variation of synonymous codon usage among these virus genes, while gene function is also correlated to synonymous codon usages to a certain extent. However, translational selection and gene length have no effect on the variations of synonymous codon usage in these virus genes.

Base Composition↗
PubMed2005

A Brownian dynamics study on the self-diffusion of charged tracers in dilute polyelectrolyte solutions.

Brownian dynamics simulations with hydrodynamic interactions are conducted to investigate the self-diffusion of charged tracer particles in a dilute solution of charged polymers, which are modeled by bead-spring chains. The Debye-Hückel approximation is used for the electrostatic interactions. The hydrodynamic interactions are implemented by the Ewald summation of the Rotne-Prager tensor. Our simulations find that the difference in short- and long-time diffusivities is very slight in uncharged short-chain solutions. For charged systems, to the contrary, the difference becomes considerable. The short-time diffusivity is found to increase with increasing chain length, while an opposite behavior is obtained for the long-time diffusivity. The former is attributed to the hydrodynamic screening among beads in a same chain due to the bead connectivity. The latter is explained by the memory effect arising from the electrostatic repulsion and chain length. The incorporation of hydrodynamic interactions improves the agreement between the simulation prediction and the experimental result.

Journal Article↗
PubMed2005

Role of adhesion molecules and dendritic cells in rat hepatic/renal ischemia-reperfusion injury and anti-adhesive intervention with anti-P-selectin lectin-EGF domain monoclonal antibody.

AIM: To investigate the role of P-selectin, intercellular adhesion molecule-1 (ICAM-1) and dendritic cells (DCs) in liver/kidney of rats with hepatic/renal ischemia-reperfusion injury and the preventive effect of anti-P-selectin lectin-EGF domain monoclonal antibody (anti-PsL-EGFmAb) on the injury. METHODS: Rat models of hepatic and renal ischemia-reperfusion were established. The rats were then divided into two groups, one group treated with anti-PsL-EGFmAb (n = 20) and control treated with saline (n = 20). Both groups were subdivided into four groups according to reperfusion time (1, 3, 6 and 24 h). The sham-operated group (n = 5) served as a control group. DCs were observed by the microscopic image method, while P-selectin and ICAM-1 were analyzed by immunohistochemistry. RESULTS: P-selectin increased significantly in hepatic sinusoidal endothelial cells and renal tubular epithelial cells 1 h after ischemia-reperfusion, and the expression of ICAM-1 was up-regulated in hepatic sinusoid and renal vessels after 6 h. CD1a(+)CD80(+)DCs gradually increased in hepatic sinusoidal endothelium and renal tubules and interstitium 1 h after ischemia-reperfusion, and there was the most number of DCs in 24-h group. The localization of DCs was associated with rat hepatic/renal function. These changes became less significant in rats treated with anti-PsL-EGFmAb. CONCLUSION: DCs play an important role in immune pathogenesis of hepatic/renal ischemia-reperfusion injury. Anti-PsL-EGFmAb may regulate and inhibit local DC immigration and accumulation in liver/kidney.

Animals↗
PubMed2005

Extreme cytotoxicity and susceptibility to hprt mutagenesis in Ku-deficient xrs-6 cells treated with bleomycin in plateau phase.

In an attempt to determine the possible role of Ku-dependent end joining in mutagenesis resulting from DNA double-strand breaks, mutations induced by bleomycin at the hprt locus in plateau phase normal CHO-K1 and Ku-deficient xrs-6 cells were examined. Plateau phase xrs-6 cells were 500-fold more sensitive to chronic bleomycin treatment than were CHO-K1 cells. XRCC4-deficient XR-1 cells were approximately 100-fold and DNA-PKcs-deficient XR-C1 and V-3 cells 15- to 30-fold more sensitive than CHO-K1 cells. These hypersensitivities are much greater than those previously reported for acute treatments with bleomycin or ionizing radiation. While the induced mutation frequencies at comparable levels of survival were slightly lower in xrs-6 cells, mutations were induced by bleomycin at much lower concentrations in xrs-6 than in CHO-K1 cells. For both cell lines bleomycin treatment resulted in a marked increase in the incidence of complete hprt deletions, while point mutations in hprt cDNA were rare. The results suggest that bleomycin-induced double-strand breaks tend to generate very large deletions in both cell lines and that this effect occurs at much lower levels of double-strand breaks in Ku-deficient than in normal cells.

Animals↗
PubMed2005

Deficiency in 3'-phosphoglycolate processing in human cells with a hereditary mutation in tyrosyl-DNA phosphodiesterase (TDP1).

Tyrosyl-DNA phosphodiesterase (TDP1) is a DNA repair enzyme that removes peptide fragments linked through tyrosine to the 3' end of DNA, and can also remove 3'-phosphoglycolates (PGs) formed by free radical-mediated DNA cleavage. To assess whether TDP1 is primarily responsible for PG removal during in vitro end joining of DNA double-strand breaks (DSBs), whole-cell extracts were prepared from lymphoblastoid cells derived either from spinocerebellar ataxia with axonal neuropathy (SCAN1) patients, who have an inactivating mutation in the active site of TDP1, or from closely matched normal controls. Whereas extracts from normal cells catalyzed conversion of 3'-PG termini, both on single-strand oligomers and on 3' overhangs of DSBs, to 3'-phosphate termini, extracts of SCAN1 cells did not process either substrate. Addition of recombinant TDP1 to SCAN1 extracts restored 3'-PG removal, allowing subsequent gap filling on the aligned DSB ends. Two of three SCAN1 lines examined were slightly more radiosensitive than normal cells, but only for fractionated radiation in plateau phase. The results suggest that the TDP1 mutation in SCAN1 abolishes the 3'-PG processing activity of the enzyme, and that there are no other enzymes in cell extracts capable of processing protruding 3'-PG termini. However, the lack of severe radiosensitivity suggests that there must be alternative, TDP1-independent pathways for repair of 3'-PG DSBs.

Cell Line↗
PubMed2005

Expression and occupancy of BAFF-R on B cells in systemic lupus erythematosus.

OBJECTIVE: To determine whether receptors for B lymphocyte stimulator (BLyS) are altered on B cells of patients with systemic lupus erythematosus (SLE). METHODS: Total available receptors for BLyS were measured by analysis of binding of recombinant soluble BLyS to peripheral blood B cells in 36 SLE patients, 29 healthy controls, and 10 disease controls. Antibodies to the receptors BAFF-R, BCMA, and TACI were used to define expression of the individual BLyS receptors on subsets of B cells in blood, spleen, and tonsils. Two different antibodies to BAFF-R, which were differentially sensitive to BAFF-R occupancy, were used to compare BAFF-R on B cells in an additional 20 healthy subjects and 25 SLE patients. Assays of B cell survival after stimulation in vitro were used to determine the sensitivity of B cells to exogenous BLyS. RESULTS: Total available receptors for BLyS were decreased in patients with SLE, independent of changes of subsets in the blood in these patients. The decrease correlated with changes in disease activity. Although total surface BAFF-R was not significantly different between healthy controls and SLE patients, BAFF-R was occupied in SLE patients. B cells from these patients were less responsive to exogenous BLyS. CONCLUSION: BAFF-R is consistently occupied on blood B cells in SLE. Occupancy of BAFF-R on blood B cells is likely to contribute to disease mechanisms in SLE and could serve as a biomarker of disease activity. Targeting BLyS as a therapeutic strategy will require overcoming the persistent binding of BLyS to BAFF-R.

Adult↗
PubMed2005

[Correlation of polymorphisms of UDP-glucuronosyltransferase 1A7 gene to genetic susceptibility of lung cancer].

BACKGROUND & OBJECTIVE: UDP-glucuronosyltransferase 1A7 (UGT1A7) plays an important role in detoxification through catalyzing combination of glucuronic acid and tobacco carcinogens, including benzo [alpha] pyrene, nitrosamine, and heterocyclic amine PhIP, therefore, inactivates the carcinogens. This study was to examine the correlation of polymorphisms of UGT1A7 gene to genetic susceptibility of lung cancer. METHODS: Polymorphisms of UGT1A7 gene at 12-131 and 208 sites in peripheral lymph cells of 312 patients and 317 age- and sex-matched controls were detected by polymerase chain reaction-denaturized high performance liquid chromatography (PCR-DHPLC) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP); the correlation of these polymorphisms to genetic susceptibility of lung cancer was analyzed. RESULTS: Compared with the UGT1A7*1/*1 genotype carriers, the UGT1A7*3/*1 genotype carriers had a 1.80-fold increased risk of lung adenocarcinoma [adjusted odds ratio (OR), 1.80; 95% confidence interval (CI), 1.03-3.12], the UGT1A7*3 genotype carriers had a 1.59-fold increased risk of lung adenocarcinoma (adjusted OR, 1.59; 95% CI, 0.96-2.63). The UGT1A7 polymorphisms had no correlation with risk of lung squamous cell carcinoma. CONCLUSION: UGT1A7 gene polymorphisms may increase the genetic susceptibility of lung adenocarcinoma in Chinese.

Adenocarcinoma↗
PubMed2005

[A preliminary study on the role of anti-atrial fibrillation pacemaker in the prevention of atrial tachyarrhythmia].

OBJECTIVE: To investigate the effect of anti-atrial fibrillation of Philos DDDR pacemaker on atrial tachyarrhythmia. METHODS: Thirty-eight patients with sick sinus syndrome and paroxysmal atrial fibrillation (AF) were implanted with Philos DDDR pacemaker. After implantation, auto-Mode-Switch (AMS) function was switched "on" and AF preventive algorithms were "off" in all cases. The number of AMS, atrial premature beats, heart rate and the percentage of atrial and ventricular pacing were recorded by pacemaker diagnostic function for one-month after procedure. AF preventive algorithms function with "middle" (approx 8 bpm) was then switched on and the same parameters as above from the database of pacemaker diagnostic function were collected for additional one month. RESULTS: The symptoms of dizziness, dyspnoea, and palpitation in the majority of patients were dramatically improved regardless of whether the AF preventive algorithms function was switched "on" or "off" after pacemaker implantation. There were no significant clinical changes in most patients when AF preventive algorithms were "on". However, 5 cases (13.2%) had palpitations and short of breath. These symptoms were relieved by changing the algorithms from "middle to slight (approx 4 bpm)". When AF preventive algorithms were switched on, atrial premature beats were reduced significantly (P < 0.05) with a dramatic increase in atrial pacing percentage and heart rate (P < 0.05). However, there was no significant difference in AMS (P > 0.05) between the two groups of AF preventive algorithms function switching "on" and "of", indicating that atrial tachyarrhythmias were not inhibited by anti-atrial fibrillation pacemaker. CONCLUSION: This study suggested that atrial fibrillation and atrial tachycardia were not reduced by implantation of an anti-atrial fibrillation Philos DDDR pacemaker, although atrial premature beats decreased significantly with increasing atrial pacing percentage when AF preventive algorithms were in "middle" and "slight".

Aged↗
PubMed2004

Cadmium at a non-toxic dose alters gene expression in mouse testes.

The testes are important targets of cadmium (Cd)-induced toxicity and carcinogenicity in rodents. Exposure to Cd at environmentally relevant low levels is a significant human health concern, but the effects of Cd on the rodent testes at doses that do not cause overt lesions are poorly defined. We used cDNA microarray and quantitative real-time RT-PCR assays to determine gene expression profiles in the testes of CD-1 mice 12-72 h after a single s.c. injection of 5 micromol/kg CdCl2. This dose of Cd did not produce overt histopathological changes, but clearly altered the expression of some genes that are likely to be important in toxicity responses. The most significant changes in gene expression occurred 24 h after treatment, corresponding to when the highest level of Cd was detected in the testes. Increased expression of the C-myc and Egr1 genes strongly suggests acute stress responses. Repressed expression of cell cycle-regulated cyclin B1 and CDC2 proteins indicates a potential for causing G2/M arrest and disturbance of meiosis. Decreased expression of pro-apoptotic genes, particularly Casp3, and DNA repair genes possibly contributes to Cd-induced carcinogenesis. These results indicate that changes in gene expression occur well before overt effects of Cd-induced testicular toxicity and carcinogenicity are apparent.

Animals↗
PubMed2004

Role of soluble Fas ligand in autoimmune diseases.

AIM: To investigate the role of soluble Fas ligand in autoimmune diseases. METHODS: RT-PCR was performed to amplify sFasL cDNA from the total RNA extracted from activated human peripheral blood lymphocytes. DNA fragments were cloned into PCR vector. After sequenced, sFasL gene fragments were inserted into pQE-31 vector and expressed in E. Coli M15 respectively. Proteins were purified through affinity chromatography column with ligand of 6XHis tag and identified by SDS-PAGE and Western blot. Mice were immunized with sFasL protein and specific anti-serum was harvested 6 wk after immunization. Monoclonal anti-human FasL antibody was made from the immunized mice. Serum level of sFasL in different patients was detected using anti-FasL antibodies from the immunized mice. RESULTS: The protein expressed was 24 ku by SDS-PAGE electrophrosis. The protein was specially bound to anti-human FasL antibody by Western blot analysis. The sFasL protein could induce Jurket cell apoptosis in vitro. The concentration of serum sFasL in patients with autoimmune diseases was higher than that in normal individuals. sFasL could reduce arthritis in collagen induced arthritis (CIA) mice model by subcutaneous injection. CONCLUSION: sFasL may be involved in either induction of apoptosis or autoimmune diseases. Furthermore, sFasL may have potential application in treatment of autoimmune diseases.

Animals↗
PubMed2004

Inactivation of PTEN is associated with increased angiogenesis and VEGF overexpression in gastric cancer.

AIM: To investigate the expression of PTEN/MMAC(1)/TEP(1) and vascular endothelial growth factor (VEGF), their roles in biologic behavior and angiogenesis and their association in gastric cancer. METHODS: Immunohistochemical staining was used to evaluate the expression of PTEN, VEGF and microvascular density (MVD) on paraffin-embedded sections in 70 patients with primary gastric cancer and 24 patients with chronic superficial gastritis (CSG). Expression of PTEN, VEGF and MVD were compared with clinicopathological features of gastric cancer. The relationship between expression of PTEN, VEGF and MVD as well as the relationship between PTEN and VEGF expression in cancer cells were investigated. RESULTS: PTEN expression significantly decreased (t = 3.98, P<0.01) whereas both VEGF expression and MVD significant increased (t = 4.29 and 4.41, respectively, both P<0.01) in gastric cancer group compared with CSG group. PTEN expression was significantly down-regulated (t = 1.95,P<0.05) whereas VEGF expression (t = 2.37, P<0.05) and MVD (t = 3.28, P<0.01) was significantly up-regulated in advanced gastric cancer compared with early-stage gastric cancer. PTEN expression in gastric cancer showed a negative association with lymph node metastasis (t = 3.91, P<0.01), invasion depth (t = 1.95, P<0.05) and age (t = 4.69, P<0.01). MVD in PTEN-negative gastric cancer was significantly higher than that in PTEN-positive gastric cancer (t = 3.69, P<0.01), and there was a negative correlation between PTEN expression and MVD (gamma= -0.363, P<0.05). VEGF expression was positively associated with invasion depth (especially with serosa invasion, t = 4.69, P<0.01), lymph node metastasis (t = 2.31, P<0.05) and TNM stage (t = 3.04, P<0.01). MVD in VEGF-positive gastric cancer was significantly higher than that in VEGF-negative gastric cancer (t = 4.62, P<0.01), and there was a positive correlation between VEGF expression of and MVD (gamma= 0.512, P<0.05). VEGF expression in PTEN-negative gastric cancer was significantly stronger than that in PTEN-positive gastric cancer (t = 2.61, P<0.05), and there was a significantly negative correlation between the expression of VEGF and PTEN (gamma= -0.403, P<0.05). CONCLUSION: Our results imply that inactivation of PTEN gene and over-expression of VEGF contribute to the neovascularization and progression of gastric cancer. PTEN-related angiogenesis might be attributed to its up-regulation of VEGF expression. PTEN and VEGF could be used as the markers reflecting the biologic behaviors of tumor and viable targets in therapeutic approaches to inhibit angiogenesis of gastric cancers.

Adult↗