Inter-Ethnic/Racial Facial Variations: A Systematic Review and Bayesian Meta-Analysis of Photogrammetric Studies

Background Numerous facial photogrammetric studies have been published around the world. We aimed to critically review these studies so as to establish population norms for various angular and linear facial measurements; and to determine inter-ethnic/racial facial variations. Methods and Findings A comprehensive and systematic search of PubMed, ISI Web of Science, Embase, and Scopus was conducted to identify facial photogrammetric studies published before December, 2014. Subjects of eligible studies were either Africans, Asians or Caucasians. A Bayesian hierarchical random effects model was developed to estimate posterior means and 95% credible intervals (CrI) for each measurement by ethnicity/race. Linear contrasts were constructed to explore inter-ethnic/racial facial variations. We identified 38 eligible studies reporting 11 angular and 18 linear facial measurements. Risk of bias of the studies ranged from 0.06 to 0.66. At the significance level of 0.05, African males were found to have smaller nasofrontal angle (posterior mean difference: 8.1°, 95% CrI: 2.2°–13.5°) compared to Caucasian males and larger nasofacial angle (7.4°, 0.1°–13.2°) compared to Asian males. Nasolabial angle was more obtuse in Caucasian females than in African (17.4°, 0.2°–35.3°) and Asian (9.1°, 0.4°–17.3°) females. Additional inter-ethnic/racial variations were revealed when the level of statistical significance was set at 0.10. Conclusions A comprehensive database for angular and linear facial measurements was established from existing studies using the statistical model and inter-ethnic/racial variations of facial features were observed. The results have implications for clinical practice and highlight the need and value for high quality photogrammetric studies.published_or_final_versio

Validity and reliability of the Chinese critical thinking disposition inventory

2004-2005 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Gene expression profiling identifies distinct molecular subgroups of leiomyosarcoma with clinical relevance

YesBackground: Soft tissue sarcomas are heterogeneous and a major complication in their management is that the existing classification scheme is not definitive and is still evolving. Leiomyosarcomas, a major histologic category of soft tissue sarcomas, are malignant tumours displaying smooth muscle differentiation. Although defined as a single group, they exhibit a wide range of clinical behaviour. We aimed to carry out molecular classification to identify new molecular subgroups with clinical relevance. Methods: We used gene expression profiling on 20 extra-uterine leiomyosarcomas and cross-study analyses for molecular classification of leiomyosarcomas. Clinical significance of the subgroupings was investigated. Results: We have identified two distinct molecular subgroups of leiomyosarcomas. One group was characterised by high expression of 26 genes that included many genes from the sub-classification gene cluster proposed by Nielsen et al. These sub-classification genes include genes that have importance structurally, as well as in cell signalling. Notably, we found a statistically significant association of the subgroupings with tumour grade. Further refinement led to a group of 15 genes that could recapitulate the tumour subgroupings in our data set and in a second independent sarcoma set. Remarkably, cross-study analyses suggested that these molecular subgroups could be found in four independent data sets, providing strong support for their existence. Conclusions: Our study strongly supported the existence of distinct leiomyosarcoma molecular subgroups, which have clinical association with tumour grade. Our findings will aid in advancing the classification of leiomyosarcomas and lead to more individualised and better management of the disease.Alexander Boag Sarcoma Fund

Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells

Epstein-Barr virus (EBV) is implicated in the pathogenesis of multiple human tumours of lymphoid and epithelial origin. The virus infects and immortalizes B cells establishing a persistent latent infection characterized by varying patterns of EBV latent gene expression (latency 0, I, II and III). The CDK1 activator, Response Gene to Complement-32 (RGC-32, C13ORF15), is overexpressed in colon, breast and ovarian cancer tissues and we have detected selective high-level RGC-32 protein expression in EBV-immortalized latency III cells. Significantly, we show that overexpression of RGC-32 in B cells is sufficient to disrupt G2 cell-cycle arrest consistent with activation of CDK1, implicating RGC-32 in the EBV transformation process. Surprisingly, RGC-32 mRNA is expressed at high levels in latency I Burkitt's lymphoma (BL) cells and in some EBV-negative BL cell-lines, although RGC-32 protein expression is not detectable. We show that RGC-32 mRNA expression is elevated in latency I cells due to transcriptional activation by high levels of the differentially expressed RUNX1c transcription factor. We found that proteosomal degradation or blocked cytoplasmic export of the RGC-32 message were not responsible for the lack of RGC-32 protein expression in latency I cells. Significantly, analysis of the ribosomal association of the RGC-32 mRNA in latency I and latency III cells revealed that RGC-32 transcripts were associated with multiple ribosomes in both cell-types implicating post-initiation translational repression mechanisms in the block to RGC-32 protein production in latency I cells. In summary, our results are the first to demonstrate RGC-32 protein upregulation in cells transformed by a human tumour virus and to identify post-initiation translational mechanisms as an expression control point for this key cell-cycle regulator

Field Emission Properties and Fabrication of CdS Nanotube Arrays

A large area arrays (ca. 40 cm2) of CdS nanotube on silicon wafer are successfully fabricated by the method of layer-by-layer deposition cycle. The wall thicknesses of CdS nanotubes are tuned by controlling the times of layer-by-layer deposition cycle. The field emission (FE) properties of CdS nanotube arrays are investigated for the first time. The arrays of CdS nanotube with thin wall exhibit better FE properties, a lower turn-on field, and a higher field enhancement factor than that of the arrays of CdS nanotube with thick wall, for which the ratio of length to the wall thickness of the CdS nanotubes have played an important role. With increasing the wall thickness of CdS nanotube, the enhancement factorβdecreases and the values of turn-on field and threshold field increase

Circulating CD133+VEGFR2+ and CD34+VEGFR2+ cells and arterial function in patients with beta-thalassaemia major

Arterial dysfunction has been documented in patients with beta-thalassaemia major. This study aimed to determine the quantity and proliferative capacity of circulating CD133+VEGFR2+ and CD34+VEGFR2+ cells in patients with beta-thalassaemia major and those after haematopoietic stem cell transplantation (HSCT), and their relationships with arterial function. Brachial arterial flow-mediated dilation (FMD), carotid arterial stiffness, the quantity of these circulating cells and their number of colony-forming units (CFUs) were determined in 17 transfusion-dependent thalassaemia patients, 14 patients after HSCT and 11 controls. Compared with controls, both patient groups had significantly lower FMD and greater arterial stiffness. Despite having increased CD133+VEGFR2+ and CD34+VEGFR2+ cells, transfusion-dependent patients had significantly reduced CFUs compared with controls (p = 0.002). There was a trend of increasing CFUs across the three groups with decreasing iron load (p = 0.011). The CFUs correlated with brachial FMD (p = 0.029) and arterial stiffness (p = 0.02), but not with serum ferritin level. Multiple linear regression showed that CFU was a significant determinant of FMD (p = 0.043) and arterial stiffness (p = 0.02) after adjustment of age, sex, body mass index, blood pressure and serum ferritin level. In conclusion, arterial dysfunction found in patients with beta-thalassaemia major before and after HSCT may be related to impaired proliferation of CD133+VEGFR2+ and CD34+VEGFR2+ cells

Prevalence of Cataract Surgery and Visual Outcomes in Indian Immigrants in Singapore: The Singapore Indian Eye Study

10.1371/journal.pone.0075584PLoS ONE810-POLN

Template Route to Chemically Engineering Cavities at Nanoscale: A Case Study of Zn(OH)2 Template

A size-controlled Zn(OH)2 template is used as a case study to explain the chemical strategy that can be executed to chemically engineering various nanoscale cavities. Zn(OH)2 octahedron with 8 vertices and 14 edges is fabricated via a low temperature solution route. The size can be tuned from 1 to 30 μm by changing the reaction conditions. Two methods can be selected for the hollow process without loss of the original shape of Zn(OH)2 template. Ion-replacement reaction is suitable for fabrication of hollow sulfides based on the solubility difference between Zn(OH)2 and products. Controlled chemical deposition is utilized to coat an oxide layer on the surface of Zn(OH)2 template. The abundant hydroxyl groups on Zn(OH)2 afford strong coordination ability with cations and help to the coating of a shell layer. The rudimental Zn(OH)2 core is eliminated with ammonia solution. In addition, ZnO-based heterostructures possessing better chemical or physical properties can also be prepared via this unique templating process. Room-temperature photoluminescence spectra of the heterostructures and hollow structures are also shown to study their optical properties

TSPY potentiates cell proliferation and tumorigenesis by promoting cell cycle progression in HeLa and NIH3T3 cells

BACKGROUND: TSPY is a repeated gene mapped to the critical region harboring the gonadoblastoma locus on the Y chromosome (GBY), the only oncogenic locus on this male-specific chromosome. Elevated levels of TSPY have been observed in gonadoblastoma specimens and a variety of other tumor tissues, including testicular germ cell tumors, prostate cancer, melanoma, and liver cancer. TSPY contains a SET/NAP domain that is present in a family of cyclin B and/or histone binding proteins represented by the oncoprotein SET and the nucleosome assembly protein 1 (NAP1), involved in cell cycle regulation and replication. METHODS: To determine a possible cellular function for TSPY, we manipulated the TSPY expression in HeLa and NIH3T3 cells using the Tet-off system. Cell proliferation, colony formation assays and tumor growth in nude mice were utilized to determine the TSPY effects on cell growth and tumorigenesis. Cell cycle analysis and cell synchronization techniques were used to determine cell cycle profiles. Microarray and RT-PCR were used to investigate gene expression in TSPY expressing cells. RESULTS: Our findings suggest that TSPY expression increases cell proliferation in vitro and tumorigenesis in vivo. Ectopic expression of TSPY results in a smaller population of the host cells in the G(2)/M phase of the cell cycle. Using cell synchronization techniques, we show that TSPY is capable of mediating a rapid transition of the cells through the G(2)/M phase. Microarray analysis demonstrates that numerous genes involved in the cell cycle and apoptosis are affected by TSPY expression in the HeLa cells. CONCLUSION: These data, taken together, have provided important insights on the probable functions of TSPY in cell cycle progression, cell proliferation, and tumorigenesis