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Biomedical subjects

Zhen Chen

Publications and source records attributed to Zhen Chen.

45 records · Page 3Linked to original sources

Concurrent hyperglycemia does not influence the long-term prognosis of unresectable hepatocellular carcinomas.

AIM: The association has been established between the disorder of carbohydrate metabolism and liver cancer. However, little is known regarding the impact of concurrent hyperglycemia on prognosis of hepatocellular carcinoma (HCC). The present study aimed at solving this problem. METHODS: A total of 225 patients included in this study, were admitted from January 1998 to December 2001 for an unresectable HCC proven by histological and imaging examinations. Most of the patients received interventional treatment, radiation and biotherapy. Response was evaluated by computerized tomography (CT) scan conducted 4-6 weeks following completion of the treatment, and then every 3 months. Survival was calculated from the beginning of treatment using the Kaplan-Meier method. Pretreatment, treatment and follow-up variables with possible prognostic significance were analyzed. A stepwise multivariate analysis was performed using the Cox regression model, and a prognostic index was obtained. RESULTS: No differences were observed in survival parameters between the patients with and without hyperglycemia, median survival times of the patients were being 26+/-3.46 months and 29.5+/-2.04 months, respectively, and the 3-year survival rate was 8.36 % and 9.62 %, respectively. The univariate analysis indicated that there were several survival-associated variables including serum AFP level, clinical stage, Child-Pugh grade, method of treatment, size and number of tumor nodule (s). However, only the clinical stage, Child-Pugh grade and the treatment procedure were proved to be independent prognostic factors in the multivariate analysis. CONCLUSION: This study indicates that hyperglycemia does not influence the long-term prognosis of HCC, and concurrent hyperglycemia should not be considered as an unfavorable prognostic factor during the treatment of patients with HCC.

Carcinoma, Hepatocellular↗

[A new alkaloid from Opuntia vulgaris].

AIM: To study the chemical constituents of the stems of Opuntia vulgaris Mill(Cactaceae). METHODS: The compounds of Opuntia vulgaris were isolated by chromatography of Amberlite Dowex 50 and silica gel, and identified by means of UV, IR, MS, 1D and 2D NMR. RESULTS: Three compounds were isolated and identified as: opuntin B(I), 4-hydroxyproline(II) and tyrosine(III). CONCLUSION: Compound I is a new alkaloid.

Hydroxyproline↗

Inhibition of digestive enzyme activities by copper in the guts of various marine benthic invertebrates.

Digestive systems of deposit and suspension feeders can be exposed to high concentrations of copper (Cu) by ingestion of contaminated sediments. We assessed a potential impact of this Cu exposure on digestive enzyme activities in a wide range of benthic organisms by monitoring enzyme activities in their gut fluids during in vitro titrations with dissolved Cu, which mimics Cu solubilization from sediments. Increasing Cu inhibited digestive protease activities at threshold values, which varied widely among organisms, from 8 microM for an echinoderm to 0.4 M for an echiuran. More Cu was required to inhibit proteases in guts containing higher amino acid concentrations because strong Cu-binding sites on amino acids prevent Cu interaction with the enzymatically active sites. Threshold Cu concentrations were similar for proteases, esterases, lipases, and alpha- and beta-glucosidases, suggesting the same inhibition mechanism. Copper was less effective at inhibiting enzymes at lower pH, suggesting that protons can compete with Cu ion for binding to enzymatically active sites or that enzyme conformation is less vulnerable to Cu inhibition at lower pH. These results lead to the counterintuitive conclusion that deposit feeders with low enzyme activity, low amino acid concentration, and high pH values are most vulnerable to harm from sedimentary Cu by this mechanism, although they solubilize less sedimentary Cu than their counterparts with high enzyme activity, high amino acid concentrations, and low gut pH. In general, digestive systems of echinoderms may therefore be more susceptible to Cu contamination than those of polychaetes, with various other phyla showing intermediate susceptibilities. If threshold Cu values are converted to solid-phase sedimentary Cu concentrations, the thresholds are at least consistent with Cu loadings that have been observed to lead to biological impacts in the field.

Animals↗

Comparison of antitumor effect of recombinant L-asparaginase with wild type one in vitro and in vivo.

AIM: To investigate the antitumor effect of recombinant L-asparaginase on the growth of several tumors such as P388, L1210, hepatocellular carcinoma (Heps), K562, P815, and sarcoma 180 (S180). METHODS: Tumor cells (K562, L1210, and P815) were cultured in vitro and the morphology of those cells was observed with inverse microscope and transmission electron microscope. MTT assay was performed to measure the cell proliferation and inhibition rate. DNA content was assayed by flow cytometry. According to protocols of transplant tumor research, mice were transplanted with tumor cells L1210, P388, Heps, and S180. The survival rate and weight of tumor were observed after the treatment of test drugs. RESULTS: The antitumor effects of L-asparaginase were observed in vitro with tumor cells K562, L1210, and P815 (P <0.01). In vivo experiments showed that ip administration of L-asparaginase significantly increased the survival rate and life span of mice with P388 or L1210 tumor cells (P <0.01). Tumor growth induced with Heps was also significantly suppressed. Furthermore, significant suppression of tumor growth was observed in mice induced with Heps and S180 by iv administration of L-asparaginase. CONCLUSION: Recombinant L-asparaginase markedly inhibited tumors tested in this study and the results strongly suggest that recombinant L-asparaginase has great potential for clinical treatment of these tumors.

Animals↗

Novel Method to Prepare Dihydroxy Permethylated beta-Cyclodextrin Isomeric Intermediates for Bifunctional Enzyme Mimics.

Natural beta-cyclodextrin was treated with 3.5 equiv of tert-butyldimethylsilyl chloride and then with NaH and MeI in the same reaction vessel to give a mixture of oligosilyl-substituted permethylated beta-cyclodextrins. The mixture was treated with NH(4)F and the resulting 6(A),6(D)-(1), 6(A),6(C)-(2), and 6(A),6(B)-(3) dihydroxy permethylated beta-cyclodextrins were isolated in 7.6-8.9% yields by two silica gel chromatographic separations. The structures of 1-3 were verified by comparison of spectral properties with a known diol (2) or preparing known derivatives (1 and 3). This is a superior way to prepare and isolate dihydroxy permethylated beta-cyclodextrin intermediates for bifunctional enzyme mimics.

Journal Article↗

New Type of Polymeric Indium Tellurides: Low-Temperature Synthesis and Structure Characterization of [M(en)(3)]In(2)Te(6) (M = Fe, Zn) and alpha- and beta-[Mo(3)(en)(3)(&mgr;(2)-Te(2))(3)(&mgr;(3)-Te)(&mgr;(3)-O)]In(2)Te(6).

Crystal growth of metal tellurides and tellurometalates employing solvothermal reactions at temperatures below 200 degrees C have resulted in four new indium tellurium phases, [Fe(en)(3)](In(2)Te(6)) (I), [Zn(en)(3)](In(2)Te(6)) (II), and alpha- and beta-[Mo(3)(en)(3)(&mgr;(2)-Te(2))(3)(&mgr;(3)-Te)(&mgr;(3)-O)]In(2)Te(6) (III-alpha and III-beta). Single crystal X-ray diffraction analyses show that I and II are isostructural and belong to the orthorhombic crystal system, space group P2(1)()2(1)()2(1)() (No. 19). Compound I: a = 11.654 (1) Å, b = 12.968(2) Å, c = 16.273(2) Å, Z = 4. Compound II: a = 11.662(2) Å, b = 12.948(2) Å, c = 16.285(1) Å, Z = 4. The two polymorphs III-alpha and III-beta crystallize in the monoclinic system. Compound III-alpha: a = 11.815(2) Å, b = 21.769(3)Å, c = 14.498(4) Å, beta = 95.43(2) degrees, Z = 4, space group P2(1)()/c (No. 14). Compound III-beta: a = 22.154(3) Å, b = 11.550(2)Å, c = 14.230(2) Å, beta = 99.05(1) degrees, Z = 4, space group P2(1)()/a (No. 14). All four are Zintl compounds containing novel one-dimensional polymeric chains of [(In(2)Te(6))(2)(-)] that can be described as alternating fused five-membered rings [(In(3+))(2)(Te(2)(2)(-))(Te(2)(-))], joined at the In atoms.

Journal Article↗

Self-Inclusion Complexes Derived from Cyclodextrins: Synthesis and Characterization of 6(A),6(B)-Bis-O-[p-(allyloxy)phenyl]-Substituted beta-Cyclodextrins.

The syntheses, structures, and spectroscopic properties of 6(A),6(B)-bis-O-[p-(allyloxy)phenyl]-substituted beta-cyclodextrins have been investigated. Selective activation of the 6(A),6(B)-hydroxy groups was carried out by treating heptakis(2,3-di-O-methyl)-beta-cyclodextrin (1) with 2,4-dimethoxybenzene-1,5-disulfonyl chloride to give 6(A),6(B)-bissulfonate ester 2 in a yield of only 3%. This material was treated with sodium p-(allyloxy)phenoxide in DMF to form 6(A),6(B)-bis-O-[p-(allyloxy)phenyl]-heptakis(2,3-di-O-methyl)-beta-cyclodextrin (3), which had two isomers. One (3A) has the two p-(allyloxy)phenyl arms directed away from the cyclodextrin cavity, and the other (3B) has one of the p-(allyloxy)phenyl groups through the cavity to form a self-inclusion complex. When either 3A or 3B was treated with methyl iodide and sodium hydride, the resulting permethylated 6(A),6(B)-bis-O-[p-(allyloxy)phenyl]heptakis(2,3-di-O-methyl)-6(C),6(D),6(E),6(F),6(G)-penta-O-methyl-beta-cyclodextrin (4) was composed of two isomers, in which 4B is a self-inclusion complex. 3A and 3B also can be converted into a mixture of 3A and 3B in strong base but not when melted in the absence of base. 4A and 4B do not isomerize. Detailed 1D and 2D NMR spectroscopic studies were carried out to characterize the structures of these new compounds, and molecular mechanics techniques were used to explain the experimental facts.

Journal Article↗

Transient increased expression of VEGF and MMP-1 in a rat liver tumor model after hepatic arterial occlusion.

BACKGROUND/AIMS: This study investigates the influence of hepatic arterial occlusion (HAO) on blood perfusion of transplanted cancer in rat's liver, and the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-1 (MMP-1) and explores the mechanisms involved in transcatheter arterial embolization (TAE)-induced metastasis of liver cancer preliminarily. METHODOLOGY: Walker 256 carcinosarcoma was transplanted into rat's liver to create the liver cancer model. Hepatic arterial ligation (HAL) was used to block the hepatic arterial blood supply and simulate TAE. Rats bearing tumor were divided into three groups: control, laparotomy control, and HAL groups. Blood perfusion of tumor was analyzed by a Hoechst 33342 labeling assay. The level of serum VEGF was assayed by ELISA; and the expression of VEGF and MMP-1 mRNA was detected by in situ hybridization. RESULTS: Two days after HAL, the number of Hoechst 33342 labeled cells which represent the blood perfusion of the tumor directly and hypoxia of tumor indirectly in the HAL group decreased significantly compared with that in the control group (329.1+/-29.3 vs. 383.6+/-19.2, P<0.01). The level of serum VEGF in the HAL group increased significantly compared with that of the control group (92.5+/-43.9 pg/mL vs. 54.9+/-19.3 pg/mL, P<0.05). The expression of VEGF and MMP-1 mRNA in the tumor tissue of the HAL group increased significantly compared with that of the control and the laparotomy control groups (P<0.05). The blood perfusion data of the tumor, represented by number of Hoechst 33342 labeled cells, showed an inverse correlation with the expression of VEGF mRNA in tumor tissue (P<0.05). While 6 days after HAL, the blood perfusion of tumor in HAL group decreased and the expression of VEGF and MMP-1 increased only slightly, not significantly, compared with that in the control group. CONCLUSIONS: In conclusion, blockage of hepatic arterial blood supply results in transient decreased blood perfusion and increased expression of metastasis-associated genes VEGF and MMP-1 of transplanted liver cancer in rats. Decreased blood perfusion and hypoxia may be the major reason for up-regulated expression of VEGF. Better understanding of the mechanisms involved with TAE-induced metastasis may lead to the enhancement of the long-term effects of TAE for liver cancer.

Animals↗