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Biomedical subjects

M Huang

Publications and source records attributed to M Huang.

At least 19 recordsLinked to original sources
PubMed2007

Bioinspired design of dental multilayers.

This paper considers the use of bioinspired functionally graded structures in the design of dental multi-layers that are more resistant to sub-surface crack nucleation. Unlike existing dental crown restorations that give rise to high stress concentration, the functionally graded layers (between crown materials and the joins that attach them to dentin) are shown to promote significant reductions in stress and improvements in the critical crack size. Special inspiration is drawn from the low stress concentrations associated with the graded distributions in the dentin-enamel-junction (DEJ). The implications of such functionally graded structures are also discussed for the design of dental restorations.

Biomechanical Phenomena↗
PubMed2007

Creep induced rate effects on radial cracks in multilayered structures.

This paper considers foundation and epoxy creep induced loading rate effects on radial cracks in multilayered structures. These include top layers of glass or silicon that are bonded to polycarbonate foundations with epoxy. The creep properties of the epoxy join and the polycarbonate foundation are determined using compression experiments and spring-dashpot models. The measured creep parameters are then incorporated into an analytical mechanics model, and finite element simulations are used to predict the effects of creep on the critical loads for radial cracking at different loading rates. The models suggest that the combined effects of creep and slow crack growth must be considered in the predictions of the critical loads required for radial cracking in the systems containing glass top layers. Since slow crack growth does not occur in silicon, the model considering the creep effect is used to predict the critical loads for radial cracking in the systems containing silicon top layers. In both of the structures, analytical solutions are obtained for bi-layer structures and finite element simulations are used for tri-layer structures. Our results show that the analytical solutions obtained by bi-layer structures provide good estimations for tri-layer structures when the epoxy thickness is less than 100 mum. The predictions obtained for both systems are shown to provide improved predictions by comparing with experimental results reported by Lee et al. [J. Am. Ceram. Soc., 2002, 85(8), 2019-2024]. In both systems, the modeling of join/substrate creep is shown to be important for the accurate prediction of loading rate effects on radial cracking.

Ceramics↗
PubMed2006

Measurement of the asymmetry in the decay Omega+-->LamdaKappa+-->rhopi+Kappa+.

The asymmetry in the rho angular distribution in the sequential decay Omega+-->LamdaKappa+-->rhopi+Kappa+. has been measured to be alphaOmegaalphaLamda=[+1.16+/-0.18(stat)+/-0.17(syst)]x10(-2) using 1.89x10(6) unpolarized Omega+ decays recorded by the HyperCP (E871) experiment at Fermilab. Using the known value of alphaLamda, and assuming that alphaLamda=-alphaLamda, alphaOmega=[-1.81+/-0.28(stat)+/-0.26(syst)]x10(-2). A comparison between this measurement of alphaOmegaalphaLamda and recent measurements of alphaOmegaalphaLamda made by HyperCP shows no evidence of a violation of CP symmetry.

Journal Article↗
PubMed2006

Oncolytic adenovirus-mediated transfer of the antisense chk2 selectively inhibits tumor growth in vitro and in vivo.

Screening and identifying molecules target to checkpoint pathways has fostered the development of checkpoint-based anticancer strategies. Among these targets, inhibition of chk2 may induce cell death for tumors whose growth depends on enhanced chk2 activity. However, improvement of the potency and specificity of such therapeutics remains a major challenge. To resolve this problem, we constructed M3, a novel recombinant adenovirus with a 27-bp deletion in E1A CR2 region by which to realize tumor-specific replication, and an 829-bp of antisense chk2 fragment inserted into the E3 coding region. In this design, M3 exploited the native adenovirus E3 promoters to express antisense chk2 cDNA in a viral replication-dependent fashion, and preferentially silenced the chk2 gene in tumor cells. In vitro and in vivo assays confirmed that downregulated chk2 expression induced by M3 infection was tumor-specific and virus replication-dependent. Furthermore, systemic administration of M3 combined with a low dose of cisplatin cured 75% (9/12) of orthotopic hepatic carcinoma mouse models that were otherwise resistant to cisplatin. Our results indicated that the upcoming development in this field would improve the antitumor efficacy and maximize the synergistic effect of oncolytic viruses administered with traditional chemotherapy or radiotherapy.

Adenoviridae↗
PubMed2006

RhoB facilitates c-Myc turnover by supporting efficient nuclear accumulation of GSK-3.

The small GTPase RhoB suppresses cancer in part by limiting cell proliferation. However, the mechanisms it uses to achieve this are poorly understood. Recent studies link RhoB to trafficking of Akt, which through its regulation of glycogen synthase kinase-3 (GSK-3) has an important role in controlling the stability of the c-Myc oncoprotein. c-Myc stabilization may be a root feature of human tumorigenesis as it phenocopies an essential contribution of SV40 small T antigen in human cell transformation. In this study we show that RhoB directs efficient turnover of c-Myc in established or transformed mouse fibroblasts and that the attenuation of RhoB which occurs commonly in human cancer is a sufficient cause to elevate c-Myc levels. Increased levels of c-Myc elicited by RhoB deletion increased the proliferation of nullizygous cells, whereas restoring RhoB in null cells decreased the stability of c-Myc and restrained cell proliferation. Mechanistic analyses indicated that RhoB facilitated nuclear accumulation of GSK-3 and GSK-3-mediated phosphorylation of c-Myc T58, the critical site for ubiquitination and degradation of c-Myc. RhoB deletion restricted nuclear localization of GSK-3, reduced T58 phosphorylation, and stabilized c-Myc. These effects were not associated with changes in phosphorylation or localization of Akt, however, differences were observed in phosphorylation and localization of the GSK-3 regulatory Akt-related kinase, serum- and glucocorticoid-inducible protein kinase (SGK). The ability of RhoB to support GSK-3-dependent turnover of c-Myc offers a mechanism by which RhoB acts to limit the proliferation of neoplastically transformed cells.

Animals↗
PubMed2006

E2F-HDAC complexes negatively regulate the tumor suppressor gene ARHI in breast cancer.

ARHI is a maternally imprinted tumor suppressor gene whose expression is markedly downregulated in breast cancer. Reactivation of ARHI expression in breast cancer cells is associated with increased histone H3 acetylation and decreased lysine 9 methylation of histone H3. An ARHI promoter segment that spanned bases -420 to +58 (designated the P2 region) exhibits significantly higher promoter activity in normal cells than in cancer cells. To better understand the molecular mechanisms contributing to this differential transcriptional activity, we sought to identify transcription factors that bind to the P2 region of the ARHI promoter and regulate its activity. Sequence analysis and oligonucleotide competition in electrophoretic mobility shift assays identified an A2 fragment containing an E2F-binding site. Using specific antibodies in supershift assays, we have shown that anti-E2F1 and 4 antibodies can supershift the A2-protein complexes, whereas anti-E2F2 and 6 antibodies cannot, demonstrating that the A2 fragment interacts with specific members of the E2F family proteins. When compared with normal breast epithelial cells, breast cancer cells have significantly elevated expression of E2F1, 4 and increased E2F DNA-binding activity. Moreover, chromatin immunoprecipitation experiments revealed that both E2F1 and 4 bind to the ARHI promoter in breast cancer cells in vivo. This binding was reduced when the cells were treated with the histone deacetylase (HDAC) inhibitor--trichostatin A (TSA). When SKBr3 cells were cotransfected with an ARHI/luciferase reporter and E2F-expression vectors, E2F1 and 4 reduced ARHI promoter activity 2-3-fold, and this reduction could be reversed by TSA treatment. The negative regulation by E2F-HDAC complexes could also be reduced by small interfering RNA of E2F1 and 4. While the retinoblastoma protein, pRB, alone had no effect on ARHI promoter activity, repression by E2F1, but not E2F4, was enhanced by the coexpression of pRB. Taken together, our results suggest that E2F1, 4 and their complexes with HDAC play an important role in downregulating the expression of the tumor suppressor gene ARHI in breast cancer cells.

Acetylation↗
PubMed2006

Iodide sensitizes genetically modified non-small cell lung cancer cells to ionizing radiation.

While external ionizing radiation has been used for treating non-small cell lung cancer (NSCLC), improved efficacy of this modality would be an important advance. Ectopic expression of the sodium iodide symporter (NIS) and thyroperoxidase (TPO) genes in NSCLC cells facilitated concentration of iodide in NSCLC cells, which markedly induced apoptosis in vitro and in vivo. Pre-incubation of the NIS/TPO-modified NSCLC cells in iodide followed by ionizing radiation generates bystander tumoricidal effects and potently enhances tumor cell killing. This iodide-induced bystander effect is associated with enhanced gap junction intercellular communication (GJIC) activity and increased connexin-43 (Cx43) expression. Thus, iodide may serve as an enhancer to markedly improve the efficacy of radiation therapy in combined therapeutic modalities.

Apoptosis↗
PubMed2006

RhoB in cancer suppression.

RhoB is a mainly endosomal small GTPase that regulates actin organization and vesicle trafficking. Expression of RhoB is elevated rapidly by many stimuli, including growth factors, cytokines, and genotoxic stress. In cancer, RhoB can limit cell proliferation, survival, invasion, and metastasis, and during malignant progression its levels are attenuated commonly. In support of its role as a negative modifier of cancer progression, targeted deletion of RhoB in mice can increase tumor formation initiated by Ras mutation. How RhoB acts to suppress different aspects of cancer pathophysiology has emerged as a question of significant interest.

Actins↗
PubMed2005

Interfacial failure of a dental cement composite bonded to glass substrates.

OBJECTIVES: To measure the interfacial fracture toughness and investigate failure mechanisms of dental cements bound to soda-lime glasses elastically equivalent to dental ceramics, as loading angle changes from 0 to 20 degrees . METHODS: Two half-circle glass discs received surface treatment were bound using dental cement (3M RelyXTM ARC BLBL) to make Brazil-nut sandwich specimens for interfacial toughness testing. Before bonding the two half-circle glass disks, 8% hydrofluoric acid (HF) was applied on the surfaces to bond for 2 min, washed thoroughly for 1 min under tap water and air dried. The surfaces were further treated using silane primer Monobond-s (Vivadent, Liechtenstein) for 60s and air dried. Interfacial toughness as a function of mode mixity was measured using an Instron testing machine by changing loading angels from 0 to 20 degrees . The interfacial fracture surfaces were examined using SEM and EDX to determine the failure modes when loading angles change. RESULTS: Interfacial toughness increases from approximately 1 to 8 J/m/m when loading angle increases from 0 to approximately 20 degrees . Increasing deformation and fracture in dental cement occur when loading angle increases. SIGNIFICANCES: Increasing interfacial toughness can be attributed to more deformation and fracture of dental cement when loading angle increases. Brazil-nut sandwich samples are shown to provide a promising alternative method to evaluate bond strength and interfacial failure for dental restoration. Research was supported by NIH (NYU/PHS No. F5262-07).

Acid Etching, Dental↗
PubMed2005

Irradiation-induced magnetism in carbon nanostructures.

Nitrogen (15N) and carbon (12C) ion implantations with implant energy of 100 keV for different doses were performed on nanosized diamond (ND) particles. Magnetic measurements on the doped ND show ferromagnetic hysteresis behavior at room temperature. The saturation magnetization (M(s)) in the case of 15N implanted samples was found to be higher compared to the 12C implanted samples for dose sizes greater than 10(14) cm(-2). The role of structural modification or defects along with the carbon-nitrogen (C-N) bonding states for the observed enhanced ferromagnetic ordering in 15N doped samples is explained on the basis of x-ray photoelectron spectroscopy measurements.

Journal Article↗
PubMed2005

Search for the lepton-number-violating decay Xi(-)-->pmu(-)mu(-).

A sensitive search for the lepton-number-violating decay Xi(-)-->pmu(-)mu(-) has been performed using a sample of approximately 10(9) Xi(-) hyperons produced in 800 GeV/c p-Cu collisions. We obtain B(Xi(-)-->pmu(-)mu(-))<4.0x10(-8) at 90% confidence, improving on the best previous limit by 4 orders of magnitude.

Journal Article↗
PubMed2005

Search for DeltaS = 2 nonleptonic hyperon decays.

A sensitive search for the rare decays Omega(-)--> Lambdapi(-) and Xi(0)--> ppi(-) has been performed using data from the 1997 run of the HyperCP (Fermilab E871) experiment. Limits on other such processes do not exclude the possibility of observable rates for |DeltaS| = 2 nonleptonic hyperon decays, provided the decays occur through parity-odd operators. We obtain the branching-fraction limits B(Omega(-)-->Lambdapi(-)) < 2.9 x 10(-6) and B(Xi(0)--> ppi(-)) < 8.2 x 10(-6), both at 90% confidence level.

Journal Article↗
PubMed2005

Evidence for the decay sigma+ --> pmu+ mu-.

We report the first evidence for the decay Sigma(+)-->pmu(+)mu(-) from data taken by the HyperCP (E871) experiment at Fermilab. Based on three observed events, the branching ratio is B(Sigma(+)-->pmu(+)mu(-))=[8.6(+6.6)(-5.4)(stat)+/-5.5(syst)]x10(-8). The narrow range of dimuon masses may indicate that the decay proceeds via a neutral intermediate state, Sigma(+)-->pP(0),P0-->mu(+)mu(-) with a P0 mass of 214.3+/-0.5 MeV/c(2) and branching ratio B(Sigma(+)-->pP(0),P0-->mu(+)mu(-))=[3.1(+2.4)(-1.9)(stat)+/-1.5(syst)]x10(-8).

Journal Article↗
PubMed2005

Role of dietary salt intake in posttransplant hypertension with tacrolimus-based immunosuppression.

Dietary salt is an important contributor to hypertension in the general population. While its role in cyclosporine-induced hypertension is minimal, its role in tacrolimus-based immunosuppression has not been defined. We measured the 24-hour urine sodium excretion as an estimate of intake in a group of stable renal transplant recipients on tacrolimus (N = 143) who had serum creatinine fluctuations <20% during the preceding 3 months. Average clinic-measured blood pressure (BP) from before and after the 24-hour urine collection was computed. Patients with recent changes in antihypertensive medications were excluded. Average systolic BP was 126 +/- 14 and diastolic BP 76 +/- 7 mm Hg. Urine sodium was 162.6 +/- 70 mmol/d (range 50 to 351), and the sodium/creatinine ratio was 15.4 +/- 6.4. There was no correlation between urine sodium excretion and either systolic or diastolic BP (R = 0.07 and R = 0.05, P = NS) or the sodium/creatinine and systolic/diastolic BP (R = 0.13, R = 0.11, P = NS). By multiple linear regression only weight and urine protein were independently associated with both systolic BP (P < .0001 for each) and diastolic BP (P < .05 for each). In conclusion, there is no appreciable influence of dietary salt intake on BP under tacrolimus-based immunosuppression. Restricting dietary salt intake in these patients cannot be recommended at the current time.

Analysis of Variance↗
PubMed2005

Detection of apoptosis-specific autoantibodies directed against granzyme B-induced cleavage fragments of the SS-B (La) autoantigen in sera from patients with primary Sjögren's syndrome.

The objective of this study was to detect autoantibodies against granzyme B cleavage products in sera from patients with primary Sjögren's syndrome (SS). Cell lysates derived from human salivary gland (HSG) cell lines were incubated with granzyme B. The susceptibility to the generation of cleavage fragments of SS autoantigens was assayed by immunoblotting using sera from 57 primary SS patients, 17 primary SS patients with malignant lymphoma (ML), 28 systemic lupus erythematosus (SLE) patients, and 20 healthy controls. A 27 kD protein was recognized by serum autoantibodies in 8 (14.0%) of 57 primary SS patients, 5 (29.4%) of 17 SS patients with ML, 2 (7.1%) of 28 SLE patients, but not in 20 normal subjects. This protein was recognized by anti-SSB (La) monoclonal antibodies. Granzyme B-treated recombinant La protein was also shown to migrate as a discrete 27 kD protein by SDS PAGE. Blocking studies demonstrated the existence of an apoptosis-specific B cell epitope present in sera from 2 of 8 primary SS patients and in 2 of 5 primary SS patients with ML which recognized the 27 kD protein. Granzyme B-induced La fragments are generated during cytotoxicity in vitro. This is the first report describing autoantibodies in sera from primary SS patients that specifically recognize fragments of the La protein that are produced by the granzyme B protease.

Adult↗