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Biomedical subjects

Yu Zhang

Publications and source records attributed to Yu Zhang.

At least 55 records · Page 3Linked to original sources
PubMed2007

Addition of antioxidant of bamboo leaves (AOB) effectively reduces acrylamide formation in potato crisps and French fries.

The present study was to demonstrate the efficiency of antioxidant of bamboo leaves (AOB) on the reduction of acrylamide during thermal processing and to summarize the optimal level of AOB applied in potato-based products. Potato crisps and French fries were immersed into different contents of AOB solution, and the frying processing parameters were optimized. The acrylamide content was determined by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The sensory evaluation was performed in double blind manner. Our results showed that nearly 74.1% and 76.1% of acrylamide in potato crisps and French fries was reduced when the AOB addition ratio was 0.1% and 0.01% (w/w), respectively. The maximum inhibitory rate was achieved when the immersion time was designed as 60 s. Sensory evaluation results showed that the crispness and flavor of potato crisps and French fries processed by AOB solution had no significant difference compared to normal potato matrixes (P > 0.05) when the AOB addition ratio was <0.5% (w/w). These results suggested that AOB could significantly reduce acrylamide formation in potato-based foods and keep original crispness and flavor of potato matrixes. This study could be regarded as a pioneer contribution on the reduction of acrylamide in various foods by natural antioxidants.

Acrylamide↗
PubMed2007

Hyrtiosal, a PTP1B inhibitor from the marine sponge Hyrtios erectus, shows extensive cellular effects on PI3K/AKT activation, glucose transport, and TGFbeta/Smad2 signaling.

Protein tyrosine phosphatase 1B (PTP1B) negatively regulates insulin signaling, and PTP1B inhibitors have been seen as promising therapeutic agents against obesity and type 2 diabetes. Here we report that the marine natural product hyrtiosal, from the marine sponge Hyrtios erectus, has been discovered to act as a PTP1B inhibitor and to show extensive cellular effects on PI3K/AKT activation, glucose transport, and TGFbeta/Smad2 signaling. This inhibitor wad able to inhibit PTP1B activity in dose-dependent fashion, with an IC(50) value of 42 microM in a noncompetitive inhibition mode. Further study with an IN Cell Analyzer 1000 cellular fluorescence imaging instrument showed that hyrtiosal displayed potent activity in abolishing the retardation of AKT membrane translocation caused by PTP1B overexpression in CHO cells. Moreover, it was found that this newly identified PTP1B inhibitor could dramatically enhance the membrane translocation of the key glucose transporter Glut4 in PTP1B-overexpressed CHO cells. Additionally, in view of our recent finding that PTP1B was able to modulate insulin-mediated inhibition of Smad2 activation, hyrtiosal was also tested for its capabilities in the regulation of Smad2 activity through the PI3K/AKT pathway. The results showed that hyrtiosal could effectively facilitate insulin inhibition of Smad2 activation. Our current study is expected to supply new clues for the discovery of PTP1B inhibitors from marine natural products, while the newly identified PTP1B inhibitor hyrtiosal might serve as a potential lead compound for further research.

Animals↗
PubMed2007

Role of indenter material and size in veneer failure of brittle layer structures.

The roles of indenter material and size in the failure of brittle veneer layers in all-ceramic crown-like structures are studied. Glass veneer layers 1 mm thick bonded to alumina layers 0.5 mm thick on polycarbonate bases (representative of porcelain/ceramic-core/dentin) are subject to cyclic contact loading with spherical indenters in water (representative of occlusal biting environment). Two indenter materials-glass and tungsten carbide-and three indenter radii-1.6, 5.0, and 12.5 mm-are investigated in the tests. A video camera is used to follow the near-contact initiation and subsequent downward propagation of cone cracks through the veneer layer to the core interface, at which point the specimen is considered to have failed. Both indenter material and indenter radius have some effect on the critical loads to initiate cracks within the local Hertzian contact field, but the influence of modulus is weaker. The critical loads to take the veneer to failure are relatively insensitive to either of these indenter variables, since the bulk of the cone crack propagation takes place in the contact far field. Clinical implications of the results are considered, including the issue of single-cycle overload versus low-load cyclic fatigue and changes in fracture mode with loading conditions.

Aluminum Oxide↗
PubMed2007

[Reproduction of a rat model of disseminated intravascular coagulation accompanied by multiple organ injuries].

OBJECTIVE: To reproduce a rat model of disseminated intravascular coagulation (DIC) accompanied by multiple organ dysfunction syndrome (MODS) induced by endotoxin. METHODS: Twenty-four healthy Wistar rats were randomly divided into four groups: control group, low dosage lipopolysaccharide (LPS) group, middle dosage LPS group, and high dosage LPS group (each n=6). Rats of each group were given different dosages of normal saline (1.4 ml/kg, 2.8 ml/kg), low dosages LPS [1.4 mg/kg (56 microg/kg), 2.8 ml/kg (112 microg/kg)], middle dosages LPS [1.4 mg/kg(98 microg/kg), 2.8 ml/kg (196 microg/kg)] and high dosages LPS [1.4 ml/kg (196 microg/kg), 2.8 ml/kg (392 microg/kg)] respectively twice 12 hours apart through femoral vein intubation injection. Blood platelet (PLT) count, coagulation function, D-dimer, fibrinogen (Fbg), antithrombin III (AT-III) blood glucose (Glu), biochemistry indexes including aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were determined before and after LPS challenge, and histopathologic changes of lung, liver and kidney were observed 4 hours after the second injection. RESULTS: The rats in high dosage LPS group died 4 hours later, and the rats in low and middle dosage LPS groups survived after double LPS challenge. The results of blood PLT, D-dimer, Fbg, Glu, AST, ALT, ALP, LDH, coagulation function of activated partial thromboplastin time, prothrombin time and level of anti-thrombin III in middle dosage LPS group were significantly different compared with those of control group (P<0.05 or P<0.01). Obvious changes in histopathology were found in major organs such as lung, kidney and liver. CONCLUSION: Double intravenous LPS challenge (98 microg/kg and 196 microg/kg) in rats can reproduce a rat model with DIC accompanied by multiple organ injuries.

Animals↗
PubMed2006

RSC mobilizes nucleosomes to improve accessibility of repair machinery to the damaged chromatin.

Repair of DNA double-strand breaks (DSBs) protects cells and organisms, as well as their genome integrity. Since DSB repair occurs in the context of chromatin, chromatin must be modified to prevent it from inhibiting DSB repair. Evidence supports the role of histone modifications and ATP-dependent chromatin remodeling in repair and signaling of chromosome DSBs. The key questions are, then, what the nature of chromatin altered by DSBs is and how remodeling of chromatin facilitates DSB repair. Here we report a chromatin alteration caused by a single HO endonuclease-generated DSB at the Saccharomyces cerevisiae MAT locus. The break induces rapid nucleosome migration to form histone-free DNA of a few hundred base pairs immediately adjacent to the break. The DSB-induced nucleosome repositioning appears independent of end processing, since it still occurs when the 5'-to-3' degradation of the DNA end is markedly reduced. The tetracycline-controlled depletion of Sth1, the ATPase of RSC, or deletion of RSC2 severely reduces chromatin remodeling and loading of Mre11 and Yku proteins at the DSB. Depletion of Sth1 also reduces phosphorylation of H2A, processing, and joining of DSBs. We propose that RSC-mediated chromatin remodeling at the DSB prepares chromatin to allow repair machinery to access the break and is vital for efficient DSB repair.

Chromatin↗
PubMed2006

Recruitment of histone deacetylase 4 by transcription factors represses interleukin-5 transcription.

The critical role of IL-5 (interleukin-5) in eosinophilic inflammation implicates it as a therapeutic target for allergic diseases. The aim of the present study was to elucidate the molecular basis for the involvement of reversible histone acetylation in IL-5 transcriptional regulation. We provide evidence that HDAC4 (histone deacetylase 4) and p300, a known HAT (histone acetyltransferase), reversibly controlled the activity of the IL-5 promoter in vivo and in vitro, with a concurrent alteration of histone H3 acetylation status at the promoter regions. The nucleo-cytoplasmic shuttling of HDAC4 was shown to play an important role in the suppressive function of HDAC4 in IL-5 gene expression. Point mutation and reporter ChIP (chromatin immunoprecipitation) studies determined that the four transcription factors binding on the IL-5 promoter, i.e. C/EBPbeta (CAAT/enhancer-binding protein beta), GATA3 (GATA binding protein 3), NFAT (nuclear factor of activated T cells) and YY1 (Yin and Yang 1), were essential for the recruitment of HDAC4. Consistent with these observations, HDAC4 was found to form protein complexes with GATA3 and YY1, and to co-exist in the nuclei with GATA3. We propose that the unique regulatory mechanism of IL-5 gene transcription involves the reversible histone modification catalysed by HDAC4 and p300, which are recruited by the transcription factors. The dynamic balance in IL-5 transcriptional regulation is achieved through interactions among HATs/HDACs, histones and transcription factors. These data contribute to understanding the molecular mechanisms of IL-5 regulation, which is crucial to the development of new therapeutic strategies for IL-5-related allergic diseases.

Binding Sites↗
PubMed2006

Amplification and overexpression of CTTN (EMS1) contribute to the metastasis of esophageal squamous cell carcinoma by promoting cell migration and anoikis resistance.

Gain of chromosome 11q13 is a common event in esophageal squamous cell carcinoma (ESCC). The cortactin gene (CTTN, also EMS1), located at 11q13, plays a pivotal role in coupling membrane dynamics to cortical actin assembly. This gene has been implicated in the motility of several types of cells. In the present study, we found that the amplification and overexpression of the CTTN gene was associated with lymph node metastasis in ESCC. Functional analysis by small interfering RNA-mediated silencing of CTTN revealed that in addition to the effect on cell migration, CTTN influenced cell invasiveness by anoikis resistance. In vivo assay showed that inhibition of CTTN expression also decreased tumor growth and lung metastasis of ESCC cells. At the molecular level, we showed for the first time that the protective role of CTTN in anoikis resistance was correlated with the activation of the phosphatidylinositol 3-kinase/Akt pathway. Overall, the data suggest that CTTN is an oncogene in the 11q13 amplicon and exerts functions on tumor metastasis in ESCC.

Anoikis↗
PubMed2006

S-chiral sulfinamides as highly enantioselective organocatalysts.

Easily accessible chiral sulfinamide 2 has been developed as the first highly efficient and enantioselective organocatalyst relying solely on a chiral sulfur center for stereochemical induction. In the presence of 20 mol % of 2, a broad range of N-aryl ketimines 1 were reduced by trichlorosilane to produce amines 3 in high yield and enantioselectivity. [reaction: see text]

Amines↗
PubMed2006

Inhibition of adenovirus-mediated human MAGE-D1 on angiogenesis in vitro and in vivo.

MAGE-D1 is a member of the MAGE family of proteins, and functions as an adaptor that mediates multiple signaling pathways. The current study for the first time provides evidence for a role of MAGE-D1 in the negative regulation of angiogenic activity in vitro and in vivo models. Our findings showed that MAGE-D1 over-expression significantly suppressed the angiogenic key events such as endothelial cell migration and invasion, adhesion on collagen I substrate, and in vitro differentiation into tube-like structures under both normoxic and hypoxic conditions. MAGE-D1 over-expression also inhibited in vivo angiogenesis in Matrigel plugs that were implanted subcutaneously in mice. With further experiments, we revealed that MAGE-D1 over-expression disrupted actin cytoskeleton organization and lamellipodia formation, and down-regulated HIF-1-dependent gene expression in endothelial cells under hypoxic conditions. These findings demonstrate a new function of MAGE-D1 in the regulation of angiogenesis and provide new insight into the ability of MAGE-D1 to suppress the growth and angiogenic response of endothelial cells by interfering with HIF-1-dependent gene expression, and actin cytoskeleton reorganization, suggesting that MAGE-D1 might be a novel inhibitor of angiogenesis in vitro and in vivo.

Actins↗
PubMed2006

Huntingtin inhibits caspase-3 activation.

Huntington's disease results from a mutation in the HD gene encoding for the protein huntingtin. The function of huntingtin, although beginning to be elucidated, remains largely unclear. To probe the prosurvival function of huntingtin, we modulate levels of wild-type huntingtin in a number of cellular and in vivo models. Huntingtin depletion resulted in caspase-3 activation, and overexpression of huntingtin resulted in caspase-3 inhibition. Additionally, we demonstrate that huntingtin physically interacts with active caspase-3. Interestingly, mutant huntingtin binds active caspase-3 with a lower affinity and lower inhibitory effect on active caspase-3 than does wild-type huntingtin. Although reduction of huntingtin levels resulted in caspase-3 activation in all conditions examined, the cellular response was cell-type specific. Depletion of huntingtin resulted in either overt cell death, or in increased vulnerability to cell death. These data demonstrate that huntingtin inhibits caspase-3 activity, suggesting a mechanism whereby caspase-mediated huntingtin depletion results in a detrimental amplification cascade leading to further caspase-3 activation, resulting in cell dysfunction and cell death.

Animals↗
PubMed2006

Repeated use of MAP decomposition residues for the removal of high ammonium concentration from landfill leachate.

The residues of magnesium ammonium phosphate (MAP) decomposed by heating under alkali conditions were repeatedly used as the sources of phosphate and magnesium for the removal of high ammonium concentration from landfill leachate. Up to 96% of ammonium in MAP powder could be released under the following conditions: NH4(+):OH- molar ratio, 1:1; temperature, 90 degrees C; heating time, 2 h. Fourier transform infrared spectra and X-ray diffraction analysis of MAP before and after heating demonstrated that MAP was mainly transformed to amorphous magnesium sodium phosphate (MgNaPO4), which makes it possible for the NH4(+) to replace Na+ in MgNaPO4 to form more stable struvite. Successful ammonium removal was achieved by using the MAP decomposition residues as the sole phosphate and magnesium sources. The ammonium removal decreased gradually following the increase of MAP reuse cycles, and in the 6th cycle, ammonium removals of 84% and 62% were achieved for synthetic wastewater and landfill leachate, respectively. Analysis of the surfaces of MAP powders acquired at different reuse cycles using scanning electron microscopy with energy dispersive X-ray suggested that the existence of calcium, kalium and aluminum ions in landfill leachate might have inhibited the formation of MAP through competition with ammonium ions for phosphate ions. It is estimated that reuse of MAP for 3 cycles could save about 44% chemical costs.

China↗
PubMed2006

Chiral multinuclear macrocyclic polyamine complexes: synthesis, characterization and their interaction with plasmid DNA.

A series of multinuclear macrocyclic polyamine metal (Zn(2+), Cu(2+), Co(2+)) complexes containing chiral dipeptide linkage were synthesized and used as artificial nuclease enzyme model. The interaction between the complexes and plasmid DNA (pUC19) was studied, and the results revealed that these complexes could act as powerful catalysts for the cleavage of plasmid DNA under physiological conditions.

Catalysis↗
PubMed2006

Human TFDP3, a novel DP protein, inhibits DNA binding and transactivation by E2F.

The two known DP proteins, TFDP1 and -2, bind E2Fs to form heterodimers essential for high affinity DNA binding and efficient transcriptional activation/repression. Here we report the identification of a new member of the DP family, human TFDP3. Despite the high degree of sequence similarity, TFDP3 is apparently distinct from TFDP1 in function. Although TFDP3 retained the capacity to bind to E2F proteins, the resulting heterodimers failed to interact with the E2F consensus sequence. In contrast to the stimulatory effect of TFDP1, TFDP3 inhibited E2F-mediated transcriptional activation. Consistent with this observation, we found that ectopic expression of TFDP3 impaired cell cycle progression from G(1) to S phase instead of facilitating such a transition as TFDP1 does. Sequence substitution analysis indicated that the DNA binding domain of TFDP3 was primarily responsible for the lack of DNA binding ability of E2F-TFDP3 heterodimers and the inhibition of E2F-mediated transcriptional activation. Fine mapping further revealed four amino acids in this region, which were critical for the functional conversion from activation by TFDP1 to suppression by TFDP3. In conclusion, these studies identify a new DP protein and a novel mechanism whereby E2F function is regulated.

Amino Acid Sequence↗
PubMed2006

Identification of chromosome aberrations in esophageal cancer cell line KYSE180 by multicolor fluorescence in situ hybridization.

Analysis of chromosomal changes in esophageal squamous cell carcinoma (ESCC) can illuminate the molecular mechanisms underlying the development and progression of this cancer, which is among the 10 most common malignant tumors. Cell lines are better suited than surgical samples for chromosome analysis in this cancer. This study used multicolor fluorescence in situ hybridization (M-FISH) to characterize the molecular cytogenetics of ESCC in cell line KYSE180. Two pools of 12-color whole-chromosome painting probes were designed, and two rounds of FISH were performed on the same metaphase spreads. Loss of DNA copy number was observed at 4p, 5q, 6q, 9, 10p, 12p, 13, 14p, 15p, 18p, 18q, 20, 22, and Y. Chromosomal gains and translocations occurred at the entire or part of 1, 2p, 3, 4p, 5p, 5q, 6p, 7, 8, 10q, 11, 12q, 14q, 16, 17q, 19, and Xp. Seven derivative chromosomes (5, 8, 12, 14, 14, 14, and 17) presented complex translocations, each involving three or four chromosomes. No chromosomes 9, 13, or Y were detected. These results add significant information to the existing karyotype description of KYSE180 and provide detailed cytogenetic background data for appropriate use of the cell line.

Carcinoma, Squamous Cell↗
PubMed2006

Calmodulin is essential for angiogenesis in response to hypoxic stress in endothelial cells.

Angiogenesis, the formation of new blood vessels that is regulated by hypoxia, is a critical process for the growth and spread of tumors. Multiple phases of this process, including migration, adhesion, and formation of new capillary tubes, are needed for optimal tumor growth. Here, a new regulatory function for Ca2+-CaM in the vascular endothelium is described. Ca2+-CaM activation induced by hypoxia in endothelial cells is essential for angiogenic cellular responses. Inhibition of Ca2+-CaM activity suppressed endothelial cell migration, adhesion on collagen I substrate, invasion and impaired in vitro endothelial cell differentiation into tube-like structures. We also reported that CaM is co-distributed with the actin structures in the lamellipodia in migrating cells, whereas the actin cytoskeleton rearrangement induced by hypoxia was disrupted and HIF-1 transcriptional activity was decreased when treated with CaM antagonists into cultures. These data indicate that Ca2+-CaM activation is more closely associated with the regulation of angiogenic key events, especially in response to hypoxic stress.

Actins↗
PubMed2006

Simulation of Brugada syndrome using cellular and three-dimensional whole-heart modeling approaches.

Brugada syndrome (BS) is a genetic disease identified by an abnormal electrocardiogram (ECG) (mainly abnormal ECGs associated with right bundle branch block and ST-elevation in right precordial leads). BS can lead to increased risk of sudden cardiac death. Experimental studies on human ventricular myocardium with BS have been limited due to difficulties in obtaining data. Thus, the use of computer simulation is an important alternative. Most previous BS simulations were based on animal heart cell models. However, due to species differences, the use of human heart cell models, especially a model with three-dimensional whole-heart anatomical structure, is needed. In this study, we developed a model of the human ventricular action potential (AP) based on refining the ten Tusscher et al (2004 Am. J. Physiol. Heart Circ. Physiol. 286 H1573-89) model to incorporate newly available experimental data of some major ionic currents of human ventricular myocytes. These modified channels include the L-type calcium current (I(CaL)), fast sodium current (I(Na)), transient outward potassium current (I(to)), rapidly and slowly delayed rectifier potassium currents (I(Kr) and I(Ks)) and inward rectifier potassium current (I(Ki)). Transmural heterogeneity of APs for epicardial, endocardial and mid-myocardial (M) cells was simulated by varying the maximum conductance of I(Ks) and I(to). The modified AP models were then used to simulate the effects of BS on cellular AP and body surface potentials using a three-dimensional dynamic heart-torso model. Our main findings are as follows. (1) BS has little effect on the AP of endocardial or mid-myocardial cells, but has a large impact on the AP of epicardial cells. (2) A likely region of BS with abnormal cell AP is near the right ventricular outflow track, and the resulting ST-segment elevation is located in the median precordium area. These simulation results are consistent with experimental findings reported in the literature. The model can reproduce a variety of electrophysiological behaviors and provides a good basis for understanding the genesis of abnormal ECG under the condition of BS disease.

Action Potentials↗
PubMed2006

Acoustic analyses of sustained and running voices from patients with laryngeal pathologies.

In this paper, we investigated the acoustic characteristics of sustained and running vowels from normal subjects and patients with laryngeal pathologies. Perturbation methods (including jitter and shimmer), signal-to-noise ratio (SNR), and nonlinear dynamic methods (such as correlation dimension and second-order entropy) were used to analyze sustained and running vowels. We found that the sustained vowels and running voices from normal subjects and patients with laryngeal pathologies had low-dimensional dynamic characteristics. For sustained vowels, the analyses of jitter, shimmer, correlation dimension, and second-order entropy revealed significant differences between normal and pathological voices. For running voices, jitter and shimmer did not statistically discriminate between normal and pathological voices, but a significant difference was found for SNR, correlation dimension, and second-order entropy. The results suggest that nonlinear dynamic analysis and traditional SNR analysis may be valuable for the analysis of sustained and running vowels; perturbation analysis may be applicable for the analysis of sustained vowels but should be applied with caution for running voice analysis.

Adult↗