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Articles by Y Tang
Total Records ( 7 ) for Y Tang
  N. R Dean , J. R Newman , E. E Helman , W Zhang , S Safavy , D.M Weeks , M Cunningham , L. A Snyder , Y Tang , L Yan , L. R McNally , D. J Buchsbaum and E. L. Rosenthal
 

Purpose: Extracellular matrix metalloprotease inducer (EMMPRIN) is a tumor surface protein that promotes growth and is overexpressed in head and neck cancer. These features make it a potential therapeutic target for monoclonal antibody (mAb)–based therapy. Because molecular therapy is considered more effective when delivered with conventional cytotoxic agents, anti-EMMPRIN therapy was assessed alone and in combination with external beam radiation.

Experimental Design: Using a murine flank model, loss of EMMPRIN function was achieved by transfection with a small interfering RNA against EMMPRIN or treatment with a chimeric anti-EMMPRIN blocking mAb. Cytokine expression was assessed for xenografts, tumor cells, fibroblasts, and endothelial cells.

Results: Animals treated with anti-EMMPRIN mAb had delayed tumor growth compared with untreated controls, whereas treatment with combination radiation and anti-EMMPRIN mAb showed the greatest reduction in tumor growth (P = 0.001). Radiation-treated EMMPRIN knockdown xenografts showed a reduction in tumor growth compared with untreated knockdown controls (P = 0.01), whereas radiation-treated EMMPRIN–expressing xenografts did not show a delay in tumor growth. Immunohistochemical evaluation for Ki67 and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) resulted in a reduction in proliferation (P = 0.007) and increased apoptosis in anti-EMMPRIN mAb–treated xenografts compared with untreated controls (P = 0.087). In addition, we provide evidence that EMMPRIN suppression results in decreased interleukin 1β (IL-1β), IL-6, and IL-8 cytokine production, in vitro and in vivo.

Conclusions: These data suggest that anti-EMMPRIN antibody inhibits tumor cell proliferation in vivo and may represent a novel targeted treatment option in head and neck squamous cell carcinoma.

  Y Tang , S Zheng and A. Chen
 

Nonalcoholic steatohepatitis (NASH) is commonly found in patients with obesity and is often accompanied with abnormally elevated levels of plasma leptin, i.e. hyperleptinemia. A relatively high population of NASH patients develops hepatic fibrosis, even cirrhosis. Hepatic stellate cells (HSCs) are the major effector cells during liver fibrogenesis and could be activated by leptin. The antioxidant curcumin, a phytochemical from turmeric, has been shown to suppress HSC activation in vitro and in vivo. This project is to evaluate the effect of curcumin on leptin-induced HSC activation and to elucidate the underlying mechanisms. We hypothesize that curcumin abrogates the stimulatory effect of leptin on HSC activation by interrupting leptin signaling and attenuating leptin-induced oxidative stress. Curcumin eliminates the stimulatory effects of leptin on regulating expression of genes closely relevant to HSC activation. Curcumin interrupts leptin signaling by reducing phosphorylation levels of leptin receptor (Ob-R) and its downstream intermediators. In addition, curcumin suppresses gene expression of Ob-R in HSCs, which requires the activation of endogenous peroxisome proliferator-activated receptor- and de novo synthesis of glutathione. In conclusion, our results demonstrate that curcumin abrogates the stimulatory effect of leptin on HSC activation in vitro by reducing the phosphorylation level of Ob-R, stimulating peroxisome proliferator-activated receptor- activity, and attenuating oxidative stress, leading to the suppression of Ob-R gene expression and interruption of leptin signaling. These results provide novel insights into therapeutic mechanisms of curcumin in inhibiting HSC activation and intervening liver fibrogenesis associated with hyperleptinemia in NASH patients.

  Y Nishimori , K Iida , M Furusawa , Y Tang , K Tokuyama , S Nagai and Y. Nishiyama
 

Nishimori, Y., Iida, K., Furusawa, M., Tang, Y., Tokuyama, K., Nagai, S., and Nishiyama, Y. 2009. The development and evaluation of a three-dimensional, echo-integration method for estimating fish-school abundance. – ICES Journal of Marine Science, 66: 1037–1042.

A three-dimensional, echo-integration method (3DEI) which uses scanning-sonar observations of a fish school to estimate its backscattering cross section (bss = Nbs) was developed. Coupled with a modelled estimate of the average backscattering cross section of individual fish (bs), the 3DEI theoretically allows estimation of the number of fish in a school (N). To test the practicality of the method, measurements were made of a metal sphere simulating fish, and several spheres simulating a fish school. The 3DEI correctly measured the bss of each target. Next, the 3DEI was applied to echo data from a herring school in the Norwegian Sea, to estimate its bss. Several values of bs were estimated with a prolate-spheroid model, each assuming different distributions of fish orientations relative to the sonar beam. Dividing the 3DEI-estimated bss by these modelled bs shows that the resulting estimates of N were closer to the skipper's estimate than those estimated using the apparent school volume. The 3DEI measurements of bss, modelled bs, and resulting accuracy of N depend largely on the assumed orientations of the fish relative to the acoustic beam.

  Y Tang , Y Nishimori and M. Furusawa
 

Tang, Y., Nishimori, Y., and Furusawa, M. 2009. The average three-dimensional target strength of fish by spheroid model for sonar surveys. – ICES Journal of Marine Science, 66: 1176–1183.

When surveying fish schools by sonar, the fish are insonified from various directions. Because the fish target strength (TS) has three-dimensional directivity, according to its orientation relative to the sonar beam, the TS must be appropriately averaged. By connecting the geometries of the sonar beam and the fish body, the relationship between the apparent orientation of fish, as viewed by the sonar, and the actual orientation in space is derived. Using this relationship, equations for calculating the three-dimensional-averaged TS (<TS>3D) are presented. A prolate-spheroid, modal-series, scattering model is then used to determine the characteristics of <TS>3D against various parameters, such as fish attitudes, fish length, sonar frequency, and method of beam scanning. The model is evaluated with two boundary conditions at the spheroid surface: a gas-fluid boundary relevant to fish with a swimbladder, and a fluid-fluid boundary relevant to fish without a swimbladder. The results reveal that <TS>3D varies greatly with the horizontal aspect (yaw angle), but only slightly with the vertical aspect (pitch angle) of the fish. The difference in <TS>3D between the side-on aspect and the end-on (head or tail) aspect increases with the ratio of the fish length to the acoustic wavelength.

  K Tao , N Qian , Y Tang , Z Ti , W Song , D Cao and K. Dou
  Objective

A disintegrin and metalloprotease-9 has been involved in the carcinogenesis of various solid tumors. However, its role in hepatocellular carcinoma remains unknown. The aim of this study was to investigate the clinicopathological and prognostic relevance of a disintegrin and metalloprotease-9 by immunohistochemistry.

Methods

The expression profile of a disintegrin and metalloprotease-9 in association with the clinicopathological factors was determined by immunohistochemical analysis in hepatocellular carcinoma patients, and its potential prognostic value was investigated by comparing the survival rate between a disintegrin and metalloprotease-9-positive and a disintegrin and metalloprotease-9-negative patients.

Results

Hepatocellular carcinoma tissues with positive a disintegrin and metalloprotease-9 expression were larger and less differentiated than those with negative expression (P = 0.02 and 0.008, respectively). Portal venous invasion, hepatic venous invasion, bile duct invasion and intrahepatic metastasis were detected significantly more frequently in a disintegrin and metalloprotease-9-positive group (P = 0.009, 0.01, 0.03 and 0.02, respectively). In addition, high -fetoprotein levels were significantly associated with the expression of a disintegrin and metalloprotease-9 in hepatocellular carcinoma (P = 0.01). Moreover, a disintegrin and metalloprotease-9-positive group had significantly poorer outcomes than a disintegrin and metalloprotease-9-negative group (P = 0.01) and was an independent prognostic factor for overall survival.

Conclusions

A disintegrin and metalloprotease-9 is over-expressed in hepatocellular carcinoma tissues, consistent with findings in other tumor entities, and is an independent prognostic marker of overall survival following hepatectomy. Further studies are needed to investigate the precise function of a disintegrin and metalloprotease-9 in the progression of hepatocellular carcinoma.

  Y Tang , E. A Scheef , Z Gurel , C. M Sorenson , C. R Jefcoate and N. Sheibani
 

We have recently shown that deletion of constitutively expressed CYP1B1 is associated with attenuation of retinal endothelial cell (EC) capillary morphogenesis (CM) in vitro and angiogenesis in vivo. This was largely caused by increased intracellular oxidative stress and increased production of thrombospondin-2, an endogenous inhibitor of angiogenesis. Here, we demonstrate that endothelium nitric oxide synthase (eNOS) expression is dramatically decreased in the ECs prepared from retina, lung, heart, and aorta of CYP1B1-deficient (CYP1B1–/–) mice compared with wild-type (CYP1B1+/+) mice. The eNOS expression was also decreased in retinal vasculature of CYP1B1–/– mice. Inhibition of eNOS activity in cultured CYP1B1+/+ retinal ECs blocked CM and was concomitant with increased oxidative stress, like in CYP1B1–/– retinal ECs. In addition, expression of eNOS in CYP1B1–/– retinal ECs or their incubation with a nitric oxide (NO) donor enhanced NO levels, lowered oxidative stress, and improved cell migration and CM. Inhibition of CYP1B1 activity in the CYP1B1+/+ retinal ECs resulted in reduced NO levels and attenuation of CM. In contrast, expression of CYP1B1 increased NO levels and enhanced CM of CYP1B1–/– retinal ECs. Furthermore, attenuation of CYP1B1 expression with small interfering RNA proportionally lowered eNOS expression and NO levels in wild-type cells. Together, our results link CYP1B1 metabolism in retinal ECs with sustained eNOS activity and NO synthesis and/or bioavailability and low oxidative stress and thrombospondin-2 expression. Thus CYP1B1 and eNOS cooperate in different ways to lower oxidative stress and thereby to promote CM in vitro and angiogenesis in vivo.

 
 
 
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