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Biomedical subjects

Y Peng

Publications and source records attributed to Y Peng.

At least 37 records · Page 2Linked to original sources
PubMed2004

Biological nitrogen removal in SBR bypassing nitrate generation accomplished by chlorination and aeration time control.

A novel control strategy for biological nitrogen removal with high nitrite built-up through chlorine dosage was studied. In the biological nitrogen removal process operated in a bench-scale sequencing batch reactor, dose of chlorine of 0.2 mg/l in the form of sodium hypochlorite was applied after the COD was depleted. The aerobic phase switched to an anoxic phase shortly after the ammonium was completely biotically oxidized. Nitrite accumulation was stably achieved which was attributed to the chlorination and the lag-time of nitrification. With the time control, stable 100% conversion of nitrite could also be sustained even under the absence of chlorine for at least 20 days. The nitrite oxidizer should have been killed rather than been suppressed in this study. For engineering applications, the advantages of the nitrification/denitrification via nitrite can compensate the cost of chlorine dosage. Combined with the aeration time control, it is feasible to apply chlorination in a biological nitrogen removal process in SBRs.

Bioreactors↗
PubMed2003

Simplified thermal lattice Boltzmann model for incompressible thermal flows.

Considering the fact that the compression work done by the pressure and the viscous heat dissipation can be neglected for the incompressible flow, and its relationship with the gradient term in the evolution equation for the temperature in the thermal energy distribution model, a simplified thermal energy distribution model is proposed. This thermal model does not have any gradient term and is much easier to be implemented. This model is validated by the numerical simulation of the natural convection in a square cavity at a wide range of Rayleigh numbers. Numerical experiments showed that the simplified thermal model can keep the same order of accuracy as the thermal energy distribution model, but it requires much less computational effort.

Journal Article↗
PubMed2003

Numerical simulation of natural convection in a concentric annulus between a square outer cylinder and a circular inner cylinder using the Taylor-series-expansion and least-squares-based lattice Boltzmann method.

In this paper, natural convective heat transfer in a horizontal concentric annulus between a square outer cylinder and a heated circular inner cylinder is numerically studied using the Taylor-series-expansion and least-squares-based lattice Boltzmann method (TLLBM). The TLLBM is used to extend the current thermal model to more practical applications. Since the TLLBM is basically a meshless approach and can be applied to any complex geometry, we can easily use it to solve the complex thermal problem accurately and effectively. The present method is validated by comparing its numerical results with available data in the literature, and very good agreement has been achieved.

Journal Article↗
PubMed2003

Non-filamentous sludge bulking caused by a deficiency of nitrogen in industrial wastewater treatment.

Deficiency in the nutrient supply such as nitrogen usually results in activated sludge bulking and this phenomenon often takes place in the industrial wastewater treatment plants with activated sludge process. The effects of nitrogen deficiency on activated sludge bulking were studied specially in some experiments carried out in a sequencing batch reactor fed with brewing process wastewater in this paper. The experimental results showed that the sludge settled properly at an influent BOD/N value of 100/4. When the value of BOD/N was 100/3, filaments had an excessive growth at one time during the reaction process. Afterwards, the number of filamentous bacteria began to reduce and simultaneously an excessive growth of viscous Zoogloea with high percentage of moisture was observed and non-filamentous activated sludge bulking occurred. When the influent BOD/N value was 100/2, the excessive growth of filamentous microorganisms could not be observed at all times and the sludge characterization was similar to the case in which BOD/N value was 100/3. When the value of influent BOD/N was 100/0.94, more serious non-filamentous bulking occurred. Furthermore, the effects of nitrogen deficiency on the nitrogen sources and phosphorus sources utilization rate and the COD removal rate were investigated in the experiments.

Beer↗
PubMed2002

Neural inhibition by c-Jun as a synergizing factor in bone morphogenetic protein 4 signaling.

The transcription factor, activator protein 1 (AP-1) complexes (c-Jun and c-Fos heterodimers) has been shown to interact with transforming growth factor beta signaling in mammalian cells and Drosophila embryo. Here we show that c-Jun alone is involved in the anti-neuralizing activity of bone morphogenetic protein 4, a transforming growth factor beta superfamily member, in Xenopus neurogenesis. Co-injection of mRNAs encoding c-jun and a dominant negative bone morphogenetic protein receptor completely inhibits dominant negative bone morphogenetic protein receptor-induced neuralization and reverses the epidermal fate in the animal cap. Surprisingly, a dominant negative c-Jun does not induce neural tissue in the animal cap, but it synergizes with dominant negative bone morphogenetic protein receptor for neural induction. Temporal analysis using a dexamethasone-inducible c-Jun shows that exogenous c-Jun activity must be turned on before or at stage 11 to fulfill the anti-neuralizing effect. Neural inhibition by c-Jun does not occur until stage 13 suggesting that c-Jun probably acts by suppressing neural maintenance rather than neural initiation. This is also supported by the fact that c-Jun does not inhibit expression of the neural-initializing gene Zic-r1 but the neural cofactor Sox2, and that ectopic expression of Sox2 attenuates the anti-neuralizing effect of c-Jun. Finally, we display that the c-Jun effect is enhanced by an auto-regulatory loop between c-Jun and bone morphogenetic protein. These studies suggest that c-Jun/AP-1 is a converging point in both the fibroblast growth factor and transforming growth factor beta signaling pathways. Based on our findings, we propose that c-Jun synergizes with bone morphogenetic protein 4 signaling to inhibit neural development in Xenopus ectoderm.

Animals↗
PubMed2001

Inhibition of MDM2 by hsp90 contributes to mutant p53 stabilization.

Stabilization and overexpression are hallmarks of mutant p53 found in nearly 50% of human tumors. Mutations in the conformation-sensitive core domain of p53 often lead to association with molecular chaperones such as hsp70 and hsp90. Inhibition of hsp90 function accelerates mutant p53 degradation. We recently found that expression of p53 core domain mutants inhibits MDM2 degradation, suggesting that mutant p53 can modulate MDM2 functions. In this report, we show that mutant p53 mediates formation of MDM2-p53-hsp90 complexes. Release of MDM2 from the p53-hsp90 complex after DNA damage restores MDM2 but not p53 turnover, whereas dissociation of hsp90 by geldanamycin increases the degradation of both MDM2 and mutant p53. Mutant p53 degradation after hsp90 inhibition requires MDM2 expression. The interaction between MDM2 and hsp90 is disrupted by the 2A10 antibody, which recognizes a site on MDM2 important for binding to alternative reading frame (ARF). Expression of mutant p53 prevents MDM2 from binding ARF and accumulating in the nucleolus in an hsp90-dependent fashion. These results suggest that hsp90 recruited by mutant p53 conceals the ARF-binding site on MDM2 and inhibits its ubiquitin-protein isopeptide ligase function, resulting in the stabilization of both mutant p53 and MDM2.

Benzoquinones↗
PubMed2001

Testing for the presence of cured patients: a simulation study.

An important but difficult problem in clinical trials is to determine the presence of cured patients when long-term survivors are observed. The likelihood ratio test has been studied for this purpose in the gamma mixture model. However, its asymptotic null distribution is not readily available due to a violation of boundary conditions in the standard asymptotic theory. In this paper, a simulation study is employed to examine a proposed asymptotic null distribution of the likelihood ratio test. We find that the distribution can also be used to approximate the asymptotic null distribution of the likelihood ratio test in the Weibull and log-normal mixture models when the censoring rate is not too light. However, the simulation study also shows that null distribution of the likelihood ratio test deviates significantly from the suggested distribution under moderate sample sizes when the censoring rate is small or the hazard rate is large. Consequently caution is needed in this case to determine the presence of cured patients. Finally, the results are used to confirm the presence of cured patients in a leukaemia study.

Bone Marrow Transplantation↗
PubMed2001

Activation of p53 by roscovitine-mediated suppression of MDM2 expression.

The p53 tumor suppressor is regulated by the MDM2 oncoprotein. Overexpression of MDM2 maintains p53 at low levels and contributes to the functional inactivation of p53 in a subset of tumors. We found that treatment with roscovitine and olomoucin, which were originally developed as cyclin-dependent kinase (CDK) inhibitors, can efficiently stabilize and activate nuclear p53 in tumor cells with MDM2 amplification or cytoplasmic p53. These inhibitors block the degradation of p53 without affecting p53-MDM2 binding and the nuclear shuttling function of p53 and MDM2. Roscovitine also induces stabilization of the p53 Ala-315 mutant, indicating that it does not act by regulating the CDK phosphorylation of serine 315. Roscovitine induces down-regulation of MDM2 expression at both protein and mRNA levels. Ectopic expression of MDM2 can abrogate the ability of roscovitine to induce p53 stabilization. Low concentrations of roscovitine cooperate with the DNA-damaging agent camptothecin to activate p53 in a synergistic fashion. These results show that the small molecule CDK inhibitors can be used to activate p53 through their potent inhibitory effect on MDM2 expression and may be useful as sensitizing agents for other DNA-damaging drugs.

Cell Compartmentation↗
PubMed2001

Association of tyrosine phosphatase SHP-2 with F-actin at low cell densities.

SHP-2 is an intracellular SH2 domain-containing protein-tyrosine phosphatase with an essential role in cell signaling. Here we demonstrate that localization of SHP-2 is regulated by cell density in a cell adhesion-dependent manner. When cells were plated at low densities, SHP-2 was distributed in Triton X-100-insoluble fractions, whereas it was totally soluble when cells were plated at high densities or when low density cells approached confluency. In all cases, the total protein level of SHP-2 was not changed. Fluorescent cell staining revealed that SHP-2 was co-localized with actin stress fibers to the cell peripheral at low cell densities but was diffused in the entire cytoplasm at high cell densities. Transient transfection of cells with truncated forms of SHP-2 demonstrated that the catalytic domain of the enzyme was responsible for the density-regulated distribution of SHP-2, but the catalytic activity was not required. An in vitro co-sedimentation study demonstrated direct binding of full-length and SH2 domain-truncated forms of SHP-2 to F-actin. The data indicate that SHP-2 is regulated by cell density and that it may have a role in assembling and disassembling of the actin network.

3T3 Cells↗
PubMed2001

ATF-7, a novel bZIP protein, interacts with the PRL-1 protein-tyrosine phosphatase.

We have identified a novel basic leucine zipper (bZIP) protein, designated ATF-7, that physically interacts with the PRL-1 protein-tyrosine phosphatase (PTPase). PRL-1 is a predominantly nuclear, farnesylated PTPase that has been linked to the control of cellular growth and differentiation. This interaction was initially found using the yeast two-hybrid system. ATF-7 is most closely related to members of the ATF/CREB family of bZIP proteins, with highest homology to ATF-4. ATF-7 homodimers can bind specifically to CRE elements. ATF-7 is expressed in a number of different tissues and is expressed in association with differentiation in the Caco-2 cell model of intestinal differentiation. We have confirmed the PRL-1.ATF-7 interaction and mapped the regions of ATF-7 and PRL-1 important for interaction to ATF-7's bZIP region and PRL-1's phosphatase domain. Finally, we have determined that PRL-1 is able to dephosphorylate ATF-7 in vitro. Further insight into ATF-7's precise cellular roles, transcriptional function, and downstream targets are likely be of importance in understanding the mechanisms underlying the complex processes of maintenance, differentiation, and turnover of epithelial tissues.

Activating Transcription Factors↗
PubMed2001

Stabilization of the MDM2 oncoprotein by mutant p53.

MDM2 is a short-lived protein that regulates p53 degradation. We report here that transient coexpression of MDM2 and several p53 hotspot mutants resulted in stabilization and increased expression of MDM2. Ectopic expression of the mutant p53(175H) allele by recombinant adenovirus infection or stable transfection also stabilized endogenous MDM2 in p53-null cells. A panel of human tumor cell lines expressing different endogenous mutant p53 alleles also contained stabilized nuclear MDM2 at elevated levels when compared with p53-null cells. MDM2 was present in complexes with mutant p53 in tumor cells, and stabilization of MDM2 required direct binding to mutant p53. These results reveal a novel property of mutant p53 and a unique feature of tumors with p53 missense mutations. Accumulation of stable MDM2 may contribute to tumorigenesis through its p53-independent transforming functions.

Humans↗
PubMed2001

Identification of apoptosis-inhibiting gene in Leucania separata nuclear polyhedrosis virus.

A novel gene lsp40 from leucania separata nuclear polyhedrosis virus (LsNPV) which was homologous to the p35 gene from Autographa californica Nuclear Polyhedrosis Virus (AcNPV) was localized in the EcoRV-5.5 kb fragment of LsNPV genome DNA and was sequenced. The open reading frame (ORF) of lsp40 was 906 bp long and encoded an approximately 40 kDa peptide consisting of 302 amino acid residues. The Isp40 shares 80.4% and 70.4% identity of nucleotide and amino acid sequence, respectively, to the AcNPV-p35 gene. The identity in promoters of both genes was as high as 100%. It was found that there were two TATA and GC boxes, three ACGT motifs for initiation of early gene transcription and one typical TTAAG core sequence for initiation of late gene transcription at both gene's 5' end, and two AATAAA tail signals at 3' end. The Isp40 started to express 2 hours after being transfected into the Ls cells to produce an approximately 40 kDa protein. The expression of the lsp40 gene might also inhibit the apoptosis of the Ls cells induced by removing serum. The expression of lsp40 in Vero cells delayed the apoptosis of the Vero cells induced by poliovirus infection. The lsp40 gene rescued vAcAnh (a kind of AcNPV p35-deletion mutant) in the Sf9 cells resulting in inhibition of the apoptosis and production of polyhedra. All these data suggested that the lsp40 gene was a homologous and functional gene similar to AcNPV p35 gene.

Amino Acid Sequence↗
PubMed2001

Analysis of telomerase processivity: mechanistic similarity to HIV-1 reverse transcriptase and role in telomere maintenance.

The key protein subunit of the telomerase complex, known as TERT, possesses a reverse transcriptase (RT)-like domain that is conserved in enzymes encoded by retroviruses and retroelements. Structural and functional analysis of HIV-1 RT suggests that RT processivity is governed, in part, by the conserved motif C, motif E, and a C-terminal domain. Mutations in analogous regions of the yeast TERT were found to have anticipated effects on telomerase processivity in vitro, suggesting a great deal of mechanistic and structural similarity between TERT and retroviral RTs, and a similarity that goes beyond the homologous domain. A close correlation was uncovered between telomerase processivity and telomere length in vivo, suggesting that enzyme processivity is a limiting factor for telomere maintenance.

Catalytic Domain↗
PubMed2001

Variation in adenovirus transgene expression between BALB/c and C57BL/6 mice is associated with differences in interleukin-12 and gamma interferon production and NK cell activation.

The innate immune response against replication-defective adenoviruses (Ad) is poorly defined. We and others have previously observed striking differences in the rate at which the Ad vector itself or the virus encoding a variety of transgenes is eliminated in different mouse strains. Here, we report that Ad infection of BALB/ mice is associated with sixfold-higher levels of serum alanine aminotransferase and that Ad transgenes induce two- to threefold-higher levels of intrahepatic NK cells and NK activity compared to C57BL/6 mice. The increase in NK activation in BALB/c mice was associated with approximately 4-fold higher level of mRNA expression of a newly described NKG2 receptor activator, H-60, as well as increased expression of interleukin-12 and gamma interferon mRNAs in BALB/c mice compared to C57BL/6 mice. NK depletion in BALB/c mice or defective NK function in C3H beige mice extended transgene expression compared to their appropriate controls, and attenuation of NK together with CD8 T-cell function had a synergistic effect. These findings indicate that there are intrinsic differences in the innate immune responses of different mouse strains to Ad and Ad transgenes and that NK cells, in cooperation with CD8 T cells, play a pivotal role in the early extinction of transgene expression in BALB/c mice.

Adenoviruses, Human↗
PubMed2001

ET(B) receptor activation causes exocytic insertion of NHE3 in OKP cells.

Endothelin-1 (ET-1) activates sodium/hydrogen exchanger 3 (NHE3) in opossum kidney clone P (OKP) cells expressing ET(B) receptors. ET-1 (10(-8) M) caused a two- to threefold increase in apical membrane NHE3 (assessed by surface biotinylation), in the absence of a change in total cellular NHE3. A maximal effect was achieved within 15 min. The increase in apical NHE3 was not blocked by cytochalasin D but was blocked by latrunculin B, which also prevented the ET-1-induced increase in NHE3 activity. Endocytic internalization of NHE3, measured as protection of biotinylated NHE3 from the membrane-impermeant, sulfhydryl-reducing agent MesNa was minimal within 35 min and was not regulated by ET-1. Exocytic insertion of NHE3, measured as the appearance of biotinylated NHE3 after the blockade of reactive sites with sulfo-NHS-acetate, was increased in response to ET-1. These studies demonstrate that ET-1 induces net trafficking of NHE3 to the apical membrane that is mediated by enhanced exocytic insertion and is required for increased NHE3 activity.

Alkaline Phosphatase↗