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H-C Huang

Publications and source records attributed to H-C Huang.

At least 19 recordsLinked to original sources
PubMed2006

Thymosin beta4 triggers an epithelial-mesenchymal transition in colorectal carcinoma by upregulating integrin-linked kinase.

The epithelial-mesenchymal transition (EMT) is crucial for the invasion and metastasis of many epithelial tumors including colorectal carcinoma (CRC). In the present study, a scattering and fibroblastic morphology with reduced intercellular contacts was found in the SW480 colon cancer cells overexpressing the gene encoding thymosin beta4 (Tbeta4), which was accompanied by a loss of E-cadherin as well as a cytosolic accumulation of beta-catenin, two most prominent markers of EMT. Whereas E-cadherin downregulation was likely to be accounted by a ZEB1-mediated transcriptional repression, the accumulation of beta-catenin was a result of glycogen synthase kinase-3beta inactivation mediated by integrin-linked kinase (ILK) and/or its downstream effector, Akt. Intriguingly, ILK upregulation in Tbeta4-overexpressing SW480 cells seemed to be attributed mainly to a stabilization of this kinase by complexing with particularly interesting new Cys-His protein (PINCH) more efficiently. In the meantime, a strong correlation between the expression levels of Tbeta4, ILK and E-cadherin in CRC patients was also revealed by immunohistochemical analysis. Taken together, these data suggest a novel role of Tbeta4 in promoting CRC progression by inducing an EMT in tumor cells via upregulating ILK and consequentially its signal transduction.

Adaptor Proteins, Signal Transducing↗
PubMed2006

C2GnT-M is downregulated in colorectal cancer and its re-expression causes growth inhibition of colon cancer cells.

Changes in carbohydrates on the cell surface are associated with tumor malignancy. The mucin-type core 2 beta-1,6-N-acetylglucosaminyltransferase (C2GnT-M) is highly expressed in the gastrointestinal tract and catalyses the formation of core 2, core 4, and blood group I branches on O-glycans. In the present study, we evaluated the role of C2GnT-M in colorectal cancer. C2GnT-M downexpression was observed in 73.6% of the primary tumors from colorectal cancer patients (39 of 53) analysed by cancer profiling array. Consistently, the majority of colon cancer cell lines and primary colon tumors expressed lower levels of C2GnT-M than did normal colon tissues by RT-PCR. HCT116 cells stably transfected with C2GnT-M inhibited expression of the core 1 structure, Galbeta1,3GalNAcalpha1-Ser/Thr, on the cell surface. Moreover, C2GnT-M expression suppressed cell adhesion, motility, and invasion as well as colony formation ability. The growth of C2GnT-M-transfected HCT116 and SW480 cells was dramatically suppressed, and the cell death induced by C2GnT-M was demonstrated by an increase in the annexin V-positive cells. Interestingly, C2GnT-M inhibited cell adhesion to collagen IV and fibronectin, and decreased tyrosine phosphorylation of paxillin, indicating that the changes in cancer behavior may be partly mediated by integrin-signaling pathways. Tumor growth in vivo was also significantly suppressed by C2GnT-M in the xenografts of nude mice. These results demonstrate that C2GnT-M is frequently downregulated in colorectal cancer and suppresses colon cancer cell growth.

Animals↗
PubMed2006

Ras modulation of superoxide activates ERK-dependent fibronectin expression in diabetes-induced renal injuries.

Although previous studies have demonstrated that diabetic nephropathy is attributable to early extracellular matrix accumulation in glomerular mesangial cells, the molecular mechanism by which high glucose induces matrix protein deposition remains not fully elucidated. Rat mesangial cells pretreated with or without inhibitors were cultured in high-glucose or advanced glycation end product (AGE) conditions. Streptozotocin-induced diabetic rats were given superoxide dismutase (SOD)-conjugated propylene glycol to scavenge superoxide. Transforming growth factor (TGF)-beta1, fibronectin expression, Ras, ERK, p38, and c-Jun activation of glomerular mesangial cells or urinary albumin secretion were assessed. Superoxide, not nitric oxide or hydrogen peroxide, mediated high glucose- and AGE-induced TGF-beta1 and fibronectin expression. Pretreatment with diphenyliodonium, not allopurinol or rotenone, reduced high-glucose and AGE augmentation of superoxide synthesis and fibronection expression. High glucose and AGEs rapidly enhanced Ras activation and progressively increased cytosolic ERK and nuclear c-Jun activation. Inhibiting Ras by manumycin A reduced the stimulatory effects of high glucose and AGEs on superoxide and fibronectin expression. SOD or PD98059 pretreatment reduced high-glucose and AGE promotion of ERK and c-Jun activation. Exogenous SOD treatment in diabetic rats significantly attenuated diabetes induction of superoxide, urinary albumin excretion, 8-hydroxy-2'-deoxyguanosine, TGF-beta1, and fibronectin immunoreactivities in renal glomerular mesangial cells. Ras induction of superoxide activated ERK-dependent fibrosis-stimulatory factor and extracellular matrix gene transcription of mesangial cells. Reduction of oxidative stress by scavenging superoxide may provide an alternative strategy for controlling diabetes-induced early renal injury.

Animals↗
PubMed2006

Transvascular dissemination of Porphyromonas gingivalis from a sequestered site is dependent upon activation of the kallikrein/kinin pathway.

BACKGROUND AND OBJECTIVE: Epidemiological evidence implicates a connection between human periodontitis and systemic diseases. One possible mechanism involves the direct dissemination of periodontopathogens to the target organs through the circulation. The aim of this work was to define the mechanism used by Porphyromonas gingivalis for dissemination from a sequestered infection site. MATERIAL AND METHODS: BALB/c mice were subcutaneously infected with P. gingivalis via use of a mouse chamber model. Tissue fluids from various sites were collected and cultured to determine the presence of P. gingivalis. Evans Blue dye was used to measure the dissemination ability of P. gingivalis. Kinin-associated molecules were introduced into mice, and their effects on bacterial dissemination and mouse pathology were monitored. RESULTS: P. gingivalis strain A7436 caused remote lesions and septicemia with severe cachexia, resulting in animal death. Intrachamber challenge with A7436 resulted in vascular permeability enhancement (VPE), as measured by the systemic infiltration of Evans Blue dye into chamber fluids. VPE was blocked by kininase and kinin receptor antagonist and enhanced by exogenous bradykinin and kininase inhibitor. Live bacteria were recovered from the subcutaneous perichamber and abdominal spaces (spreading), and from the blood (disseminating) of infected mice. Both kininase and kinin receptor antagonist reduced animal mortality as a result of infection with strain A7436 and decreased the number of bacteria recoverable from the blood, but they were not associated with bacterial spreading. CONCLUSIONS: The results suggest that activation of the kinin system is involved in the breach of the vascular barrier that permits dissemination of P. gingivalis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

X-ray absorption spectroscopy study of a copper-containing material after thermal treatment.

Thermal immobilization of copper contaminant in a copper-containing solid material collected from local copper smelting and foundry area is investigated in the present work. X-ray absorption spectroscopy (XAS) and X-ray diffraction (XRD) are employed for copper speciation. XAS results indicate that cupric hydroxide is the major copper species in the solid material dried at 105 degrees C. After being subjected to a 500 degrees C thermal process, cupric hydroxide still remains as the main copper species, but some Cu(II) is chemically reduced to Cu(I). More cupric hydroxide is progressively converted to Cu(I) as the sample was heated at 1100 degrees C than that heated at 500 degrees C. The sample heated at 500 degrees C is in its original powder form. However, thermal treatment at 1100 degrees C transforms the powder into a hardened granule-like form that is much bigger in size and difficult to be ground into powders. The sample is sintered with the sparingly soluble cuprous oxide and elemental copper being encapsulated inside. Toxicity characteristic leaching procedure (TCLP) results depict that amount of copper leached from the sample (containing 133,000 mg copper kg-1) heated at 1100 degrees C for 2 h is considerably minor, being 367 mg copper kg-1.

Copper↗
PubMed2004

Evidence for direct CP violation in B0-->K+pi- decays.

We report evidence for direct CP violation in the decay B0-->K+pi(-) with 253 fb(-1) of data collected with the Belle detector at the KEKB e(+)e(-) collider. Using 275x10(6) BB pairs we observe a B-->K+/-pi(-/+) signal with 2140+/-53 events. The measured CP violating asymmetry is A(CP)(K+pi(-))=-0.101+/-0.025(stat)+/-0.005(syst), corresponding to a significance of 3.9sigma including systematics. We also search for CP violation in the decays B+-->K+pi(0) and B+-->pi(+)pi(0). The measured CP violating asymmetries are A(CP)(K+pi(0))=0.04+/-0.05(stat)+/-0.02(syst) and A(CP)(pi(+)pi(0))=-0.02+/-0.10(stat)+/-0.01(syst), corresponding to the intervals -0.05<A(CP)(K+pi(0))<0.13 and -0.18<A(CP)(pi(+)pi(0))<0.14 at 90% confidence level.

Journal Article↗
PubMed2004

Evidence for B+-->omegal+nu.

We have searched for the decay B+-->omegal(+)nu (l=e or mu) in 78 fb(-1) of Upsilon(4S) data (85x10(6)BB events) accumulated with the Belle detector. The final state is fully reconstructed using the omega decay into pi(+)pi(-)pi(0), combined with detector hermeticity to estimate the neutrino momentum. A signal of 414+/-125 events is found in the data, corresponding to a branching fraction of (1.3+/-0.4+/-0.2+/-0.3)x10(-4), where the first two errors are statistical and systematic, respectively. The third error reflects the estimated form-factor uncertainty.

Journal Article↗
PubMed2004

Search for the lepton-flavor-violating decay tau- -->micro-eta at Belle.

We have searched for the lepton flavor violating decay tau(-)-->micro(-)eta using a data sample of 84.3 fb(-1) accumulated with the Belle detector at KEK. The eta meson was detected through the decay modes: eta-->gammagamma and pi(+)pi(-)pi(0). No signal candidates are found, and we obtain an upper limit for the branching fraction B(tau(-)-->micro(-)eta)<3.4 x 10(-7) at the 90% confidence level.

Journal Article↗
PubMed2004

Observation of B+-->psi(3770)K+.

We report the first observation of the decay B+-->psi(3770)K+ where the psi(3770) is reconstructed in the D0(-)D(0) and D+D- decay channels. The obtained branching fraction is B(B+-->psi(3770)K+)=(0.48+/-0.11+/-0.07)x10(-3). We have measured the branching fraction for the decay B+-->D0(-)D0K+ to be (1.17+/-0.21+/-0.15)x10(-3) and set a 90% confidence level upper limit of 0.90 x 10(-3) for the decay B+-->D+D-K+. We also present the results of a search for possible decays to D(-)D and D0(-)D(0)pi(0) of the recently observed X(3872) particle. The analysis is based on 88 fb(-1) of data collected at the Upsilon(4S) resonance by the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider.

Journal Article↗
PubMed2004

Upper bound on the decay tau-->microgamma from the Belle detector.

We have performed a search for the lepton-flavor-violating decay tau-->microgamma using a data sample of 86.3 fb(-1) accumulated by the Belle detector at KEK. No evidence for a signal is seen, and we set an upper limit for the branching fraction of B(tau-->microgamma)<3.1 x 10(-7) at the 90% confidence level.

Journal Article↗
PubMed2004

Observation of B(+)-->pppi+, B0-->ppK0, and B(+)-->ppK(*+).

We report the first observation of a b-->u type charmless baryonic B decay, B+-->pppi(+), as well as b-->s type B0-->ppK0 and B+-->ppK(*+) decays. The analysis is based on a 78 fb(-1) data sample recorded on the Upsilon(4S) resonance with the Belle detector at KEKB. We find B(B+-->pppi(+))=(3.06(+0.73)(-0.62)+/-0.37)x10(-6), B(B0-->ppK0)=(1.88(+0.77)(-0.60)+/-0.23)x10(-6), and B(B+-->ppK(*+))=(10.3(+3.6+1.3)(-2.8-1.7))x10(-6). We also update B(B+-->ppK+)=(5.66(+0.67)(-0.57)+/-0.62)x10(-6) and present an upper limit on B(B0-->ppK(*0)) at the 90% confidence level. A common feature of the observed decay modes is threshold peaking in baryon pair invariant mass.

Journal Article↗
PubMed2004

Observation of the radiative decay D0-->phigamma.

We report the observation of the decay D0-->phigamma with a statistical significance of 5.4sigma in 78.1 fb(-1) of data collected by the Belle experiment at the KEKB e+e- collider. This is the first observation of a flavor-changing radiative decay of a charmed meson. The Cabibbo- and color-suppressed decays D0-->phipi(0), phieta are also observed for the first time. We measure branching fractions B(D0-->phigamma)=[2.60(+0.70)(-0.61)(stat)+0.15-0.17(syst)] x 10(-5), B(D0-->phipi(0))=[8.01+/-0.26(stat)+/-0.47(syst)] x 10(-4), and B(D0-->phieta)=[1.48+/-0.47(stat)+/-0.09(syst)] x 10(-4).

Journal Article↗
PubMed2004

Measurement of /V(ub)/ using inclusive B-->X(u)lnu decays with a novel X(u)-reconstruction method.

We report the measurement of an inclusive partial branching fraction for charmless semileptonic B decay and the extraction of /V(ub)/. Candidates for B-->X(u)lnu are identified with a novel X(u) reconstruction method based on neutrino reconstruction via missing 4-momentum and a technique called "simulated annealing." Based on 86.9 fb(-1) of data taken with the Belle detector, we obtain DeltaB(B-->X(u)lnu;M(X)<1.7 GeV/c2,q2>8.0 GeV2/c2)=[7.37+/-0.89(stat)+/-1.12(syst)+/-0.55(b-->c)+/-0.24(b-->u)]x10(-4) and determine |V(ub)|=[4.66+/-0.28(stat)+/-0.35(syst)+/-0.17(b-->c)+/-0.08(b-->u)+/-0.58(theory)]x10(-3).

Journal Article↗
PubMed2004

Observation of radiative B-->phi K gamma decays.

The radiative decay B-->phi K gamma is observed for the first time. The branching fraction for the charged B--->phi K- gamma decay mode is measured to be B(B--->phi K- gamma)=(3.4+/-0.9+/-0.4)x10(-6). The photon energy distribution for the B--->phi K- gamma decay is presented. The signal for the neutral B(0)-->phi K(0)gamma decay mode is not statistically significant and an upper limit, B(B(0)-->phi K(0)gamma)<8.3x10(-6) at 90% C.L., is set. The analysis is based on a data set of 90 fb(-1) collected by the Belle experiment at the e(+)e(-) asymmetric collider KEKB.

Journal Article↗
PubMed2004

Measurements of the D(sJ) resonance properties.

We report measurements of the properties of the D(+)(sJ)(2317) and D(+)(sJ)(2457) resonances produced in continuum e(+)e(-) annihilation near sqrt[s]=10.6 GeV. The analysis is based on an 86.9 fb(-1) data sample collected with the Belle detector at KEKB. We determine the masses to be M(D(+)(sJ)(2317))=2317.2+/-0.5(stat)+/-0.9(syst) MeV/c(2) and M(D(+)(sJ)(2457))=2456.5+/-1.3(stat)+/-1.3(syst) MeV/c(2). We observe the radiative decay mode D(+)(sJ)(2457)-->D(+)(s)gamma and the dipion decay mode D(+)(sJ)(2457)-->D(+)(s)pi(+)pi(-) and determine their branching fractions. No corresponding decays are observed for the D(sJ)(2317) state. These results are consistent with the spin-parity assignments of 0(+) for the D(sJ)(2317) and 1(+) for the D(sJ)(2457).

Journal Article↗
PubMed2004

Lack of detrimental effects of nitric oxide inhibition in bile duct-ligated rats with hepatic encephalopathy.

BACKGROUND: The pathogenetic mechanisms of hepatic encephalopathy (HE) are not fully understood. Vasodilatation induced by nitric oxide (NO) may be involved in the development of HE. There is no comprehensive data concerning the effects of NO inhibition on HE in chronic liver disease. METHODS: Male Sprague-Dawley rats weighing 240-270 g at the time of surgery were selected for experiments. Secondary biliary cirrhosis was induced by bile duct ligation (BDL). Counts of movements were compared between BDL rats and rats receiving a sham operation. In another series of experiments, BDL rats received either Nomega-nitro-L-arginine methyl ester (L-NAME, 25 mg kg-1 day-1 in tap water) or tap water (control) from the 36th to 42nd days after BDL. Besides motor activities, plasma levels of tumour necrosis factor (TNF)-alpha and nitrate/nitrite, liver biochemistry tests and haemodynamics were determined after treatment. RESULTS: Compared with the sham-operated rats, the total, ambulatory and vertical movements were significantly decreased in the BDL rats (P </= 0.001). The L-NAME group had a significantly higher mean arterial pressure than that of the control group (119.0 +/- 2.5 mmHg vs. 97.3 +/- 2.8 mmHg, P = 0.002). However, the counts of motor activities, plasma levels of TNF-alpha and nitrate/nitrite, and serum biochemistry tests were not significantly different between the L-NAME and control groups. CONCLUSIONS: Bile duct ligation may induce HE evidenced by a decrease in motor activities. However, chronic L-NAME administration did not have significantly detrimental or therapeutic effects on the severity of encephalopathy in BDL rats.

Animals↗
PubMed2004

Effects of endothelin-1 on portal-systemic collaterals of common bile duct-ligated cirrhotic rats.

BACKGROUND/AIMS: Endothelin-1 (ET-1) may induce intrahepatic vasoconstriction and consequently increase portal pressure. Endothelin-1 has been shown to exert a direct vasoconstrictive effect on the collateral vessels in partially portal vein-ligated rats with a high degree of portal-systemic shunting. This study investigated the collateral vascular responses to ET-1, the receptors in mediation and the regulation of ET-1 action by nitric oxide and prostaglandin in cirrhotic rats with a relatively low degree of portal-systemic shunting. METHODS: The portal-systemic collaterals of common bile duct-ligated (BDL) cirrhotic rats were tested by in situ perfusion. The concentration-response curves of collaterals to graded concentrations of ET-1 (10(-10)-10(-7) m) with or without BQ-123 (ET(A) receptor antagonist, 2 x 10(-6) m), BQ-788 (ET(B) receptor antagonist, 10(-7) m) or both were recorded. In addition, the collateral responses to ET-1 with preincubation of N(omega)-nitro-L-arginine (NNA, 10(-4) M), indomethacin (INDO, 10(-5) M) or in combination were assessed. RESULTS: Endothelin-1 significantly increased the perfusion pressures of portal-systemic collaterals. The ET-1-induced constrictive effects were inhibited by BQ-123 or BQ-123 plus BQ-788 but not by BQ-788 alone. The inhibitory effect was greater in the combination group. Pretreatment of NNA or NNA plus INDO equivalently enhanced the response of ET-1 while pretreatment of INDO alone exerted no effect. CONCLUSION: Endothelin-1 has a direct vasoconstrictive effect on the collaterals of BDL cirrhotic rats, mainly mediated by ET(A) receptor. Endogenous nitric oxide may play an important role in modulating the effects of ET-1 in the portal-systemic collaterals of BDL cirrhotic rats.

Animals↗