Palmprint identification using restricted fusion

2008-2009 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

Acceptors in undoped gallium antimonide

Undoped GaSb materials were studied by temperature dependent Hall (TDH) measurements and photoluminescence (PL). The TDH data reveals four acceptor levels (having ionization energies of 7meV, 32meV, 89meV and 123meV) in the as-grown undoped GaSb samples. The 32meV and the 89meV levels were attributed to the GaSb defect and the VGa-related defect. The Ga Sb defect was found to be the important acceptor responsible for the p-type nature of the present undoped GaSb samples because of its abundance and its low ionization energy. This defect was thermally stable after the 500°C annealing. Similar to the non-irradiated samples, the 777meV and the 800meV PL signals were also observed in the electron irradiated undoped GaSb samples. The decrease of the two peaks' intensities with respect to the electron irradiation dosage reveals the introduction of a non-radiative defect during the electron irradiation process, which competes with the transition responsible for the 777meV and the 800meV PL peaks.published_or_final_versio

Hoxb3 negatively regulates Hoxb1 expression in mouse hindbrain patterning

The spatial regulation of combinatorial expression of Hox genes is critical for determining hindbrain rhombomere (r) identities. To address the cross-regulatory relationship between Hox genes in hindbrain neuronal specification, we have generated a gain-of-function transgenic mouse mutant Hoxb3 Tg using the Hoxb2 r4-specific enhancer element. Interestingly, in r4 of the Hoxb3 Tg mutant where Hoxb3 was ectopically expressed, the expression of Hoxb1 was specifically abolished. The hindbrain neuronal defects of the Hoxb3 Tg mutant mice were similar to those of Hoxb1 -/- mutants. Therefore, we hypothesized that Hoxb3 could directly suppress Hoxb1 expression. We first identified a novel Hoxb3 binding site S3 on the Hoxb1 locus and confirmed protein binding to this site by EMSA, and by in vivo ChIP analysis using P19 cells and hindbrain tissues from the Hoxb3 Tg mutant. We further showed that Hoxb3 could suppress Hoxb1 transcriptional activity by chick in ovo luciferase reporter assay. Moreover, in E10.5 wildtype caudal hindbrain, where Hoxb1 is not expressed, we showed by in vivo ChIP that Hoxb3 was consistently bound to the S3 site on the Hoxb1 gene. This study reveals a novel negative regulatory mechanism by which Hoxb3 as a posterior gene serves to restrict Hoxb1 expression in r4 by direct transcriptional repression to maintain the rhombomere identity. © 2011 Elsevier Inc.postprin

Phosphorylation of nucleophosmin at threonine 234/237 is associated with HCC metastasis

Hepatocellular carcinoma (HCC) is frequently complicated by the occurrence of intrahepatic and extrahepatic metastases, leading to poor prognosis. To improve the prognosis for HCC patients, there is an urgent need to understand the molecular mechanisms of metastasis in HCC. Since protein Serine/Threonine phosphorylation emerges to be an important posttranslational modification critical in signaling process associated with cell proliferation, survival and metastasis, we employed a pair of primary tumor-derived and corresponding lung-metastatic counterparts (PLC/PRF/5-PT and PLC/PRF/5-LM) and aimed to identify these changes using CelluSpot Serine/Threonine kinase peptide array. Upon analysis, we found phosphorylated level of nucleophosmin (NPM) at Threonine 234/237 (p-NPM-Thr234/237) had remarkably high level in metastatic HCC cells (PLC-LM) than the corresponding primary HCC cell line (PLC-PT). Similar observation was observed in another match primary and their metastatic counterparts (MHCC-97L and MHCC-97H). By immunohistochemical staining, p-NPM-Thr234/237 was consistently found to be preferentially expressed in metastatic HCCs when compared with primary HCC in 28 HCC cases (p < 0.0001). By overexpressing Flag-tagged NPM and its phosphorylation site mutant (Thr234/237A) into low p-NPM-Thr234/237 expressing cells (Hep3B and Huh7) using a lentiviral based approach, we demonstrated that p-NPM-Thr234/237 is critical in invasion and migration of HCC cells, and this effect was mediated by cyclin-dependent kinase 1 (CDK1). Wild-type NPM was found to physically interact with a metastatic gene, ROCK2, and defective in Thr234/237 phosphorylation decreased its binding affinity, resulting in decrease in ROCK2 mediated signaling pathway. Identification of CDK1/p-NPM/ROCK2 signaling pathway provides a novel target for molecular therapy against HCC metastasis.published_or_final_versio

Polysaccharopeptide enhanced the anti-cancer effect of gamma-tocotrienol through activation of AMPK

BACKGROUND: Prostate cancer (PCa) frequently relapses after hormone ablation therapy. Unfortunately, once progressed to the castration resistant stage, the disease is regarded as incurable as prostate cancer cells are highly resistant to conventional chemotherapy. METHOD: We recently reported that the two natural compounds polysaccharopeptide (PSP) and Gamma-tocotrienols (gamma-T3) possessed potent anti-cancer activities through targeting of CSCs. In the present study, using both prostate cancer cell line and xenograft models, we seek to investigate the therapeutic potential of combining gamma-T3 and PSP in the treatment of prostate cancer. RESULT: We showed that in the presence of PSP, gamma-T3 treatment induce a drastic activation of AMP-activated protein kinase (AMPK). This was accompanied with inactivation of acetyl-CoA carboxylase (ACC), as evidenced by the increased phosphorylation levels at Ser 79. In addition, PSP treatment also sensitized cancer cells toward gamma-T3-induced cytotoxicity. Furthermore, we demonstrated for the first time that combination of PSP and gamma-T3 treaments significantly reduced the growth of prostate tumor in vivo. CONCLUSION: Our results indicate that PSP and gamma-T3 treaments may have synergistic anti-cancer effect in vitro and in vivo, which warrants further investigation as a potential combination therapy for the treatment of cancer.published_or_final_versio

Nitrogen doped-ZnO/n-GaN heterojunctions

Nitrogen-doped ZnO nanorods were prepared by electrodeposition using two different Zn precursors (zinc nitrate and zinc acetate), while all other growth conditions (dopant precursor, concentration, growth temperature, and bias) were identical. We have shown that the precursor used affects the properties of the ZnO nanorods, and that the presence of rectifying properties in n-GaN/N:ZnO heterojunctions is strongly related to the use of nitrate precursor for ZnO growth. The difference in the properties of ZnO obtained from two precursors is attributed to the differences in native defect and impurity concentrations, which could affect the electronic properties of the samples. © 2011 American Institute of Physics.published_or_final_versio

Improved outcome of acute lymphoblastic leukaemia treated by delayed intensification in Hong Kong children: HKALL 97 study

Objective. To study the outcome of children with acute lymphoblastic leukaemia who were treated using a protocol including one or two delayed intensifications. Design. Prospective single-arm multicentre study. Setting. Five designated children cancer units of the Hospital Authority of Hong Kong. Patients. Children aged between 1 and 17.9 years with newly diagnosed acute lymphoblastic leukaemia seen from November 1997 to December 2002. Intervention. Chemotherapy was modified from a German Berlin-Frankfurt-Muenster 95 (BFM95) protocol that included a delayed intensification similar to the induction phase repeated 5 months after diagnosis. High-risk patients were given double delayed intensification. Main outcome measures. Overall survival and event-free survival of the whole group and the three risk groups (standard-, intermediate-, and high-risk groups), and comparison with historical controls. Results. A total of 171 patients were recruited with a median age at diagnosis of 5.57 years (range, 1.15-17.85 years). The induction remission rate was 95.3% and non-leukaemia mortality during remission was 2.3%. At 4 years, the relapse rate of this (HKALL97) study was significantly lower than that of the HKALL93 study (15.7 vs 37.3%; P<0.001). The 4-year overall survival of HKALL97 and HKALL93 studies were 86.5% and 81.8%, respectively (P=0.51). The 4-year event-free survival for HKALL 97 and HKALL93 studies were 79% and 65%, respectively (P=0.007). Nonetheless the difference of event-free survival was most remarkable in the intermediate-risk group: 75.6% and 53.1% for HKALL97 and HKALL93 studies, respectively (P=0.06). Conclusion. A more intensive delayed consolidation phase improved the outcome for children with acute lymphoblastic leukaemia by reducing relapses at 4 years. The early treatment complications were manageable and non-leukaemia mortality during remission remained low.published_or_final_versio

Solution-based growth of ZnO nanorods for light-emitting devices: Hydrothermal vs. electrodeposition

ZnO nanorods have been grown by two inexpensive, solution-based, low-temperature methods: hydrothermal growth and electrodeposition. Heterojunction n-ZnO nanorods/p-GaN light-emitting diodes have been studied for different nanorod growth methods and different preparation of the seed layer. We demonstrate that both the nanorod properties and the device performance are strongly dependent on the growth method and seed layer. All the devices exhibit light emission under both forward and reverse bias, and the emission spectra can be tuned by ZnO nanorod deposition conditions. Electrodeposition of rods or a seed layer results in yellow emission, while conventional hydrothermal growth results in violet emission. © The Author(s) 2010. This article is published with open access at Springerlink.com.published_or_final_versionSpringer Open Choice, 01 Dec 201

Gallium vacancy in GaSb studied by positron lifetime spectroscopy and photoluminescence

Positron lifetime technique and photoluminescence (PL) were employed to study the vacancy type defects in p-type Zn-doped and undoped GaSh samples. In the positron lifetime study, Ga vacancy related defect was identified in these materials and it was found to anneal out at temperature of about 350°C. For the PL measurement on the as-grown undoped sample performed at 10 K, a transition peak having a photon energy of about 777 meV was observed. This transition peak was observed to disappear after a 400°C annealing. Our results is consistent with the general belief that the 777 meV transition is related to the V GaGa sb defect, which is the proposed residual acceptor of GaSb.published_or_final_versio

Identification of the Rheumatoid Arthritis Shared Epitope Binding Site on Calreticulin

Background: The rheumatoid arthritis (RA) shared epitope (SE), a major risk factor for severe disease, is a five amino acid motif in the third allelic hypervariable region of the HLA-DRb chain. The molecular mechanisms by which the SE affects susceptibility to – and severity of- RA are unknown. We have recently demonstrated that the SE acts as a ligand that interacts with cell surface calreticulin (CRT) and activates innate immune signaling. In order to better understand the molecular basis of SE-RA association, here we have undertaken to map the SE binding site on CRT. Principal Findings: Surface plasmon resonance (SPR) experiments with domain deletion mutants suggested that the SE binding site is located in the P-domain of CRT. The role of this domain as a SE-binding region was further confirmed by a sulfosuccinimidyl-2-[6-(biotinamido)-2-(p-azido-benzamido) hexanoamido] ethyl-1,3-dithiopropionate (sulfo-SBED) photoactive cross-linking method. In silico analysis of docking interactions between a conformationally intact SE ligand and the CRT P-domain predicted the region within amino acid residues 217–224 as a potential SE binding site. Site-directed mutagenesis demonstrated involvement of residues Glu 217 and Glu 223- and to a lesser extent residue Asp 220- in cell-free SPR-based binding and signal transduction assays. Significance: We have characterized here the molecular basis of a novel ligand-receptor interaction between the SE and CRT. The interaction represents a structurally and functionally well-defined example of cross talk between the adaptive an