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The Beishan orogen is part of the Neoproterozoic to early Mesozoic Central Asian Orogenic System in central Asia that exposes ophiolitic complexes, passive-margin strata, arc assemblages, and Precambrian basement rocks. To better constrain the tectonic evolution of the Beishan orogen, we conducted field mapping, U-Pb zircon dating, whole-rock geochemical analysis, and Sr-Nd isotopic analysis. The new results, when interpreted in the context of the known geological setting, show that the Beishan region had experienced five phases of arc magmatism at ca. 1450-1395 Ma, ca. 1071-867 Ma, ca. 542-395 Ma, ca. 468-212 Ma, and ca. 307-212 Ma. In order to explain the geological, geochemical, and geochronological data from the Beishan region, we present a tectonic model that involves the following five phases of deformation: (1) Proterozoic rifting that separated the North Beishan block from the Greater North China craton that led to the opening of the Beishan Ocean, (2) early Paleozoic north-dipping subduction (ca. 530- 430 Ma) of the Beishan oceanic plate associated with back-arc extension followed by collision between the North and South Beishan microcontinental blocks, (3) northward slab rollback of the south-dipping subducting Paleo-Asian oceanic plate at ca. 450-440 Ma along the northern margin of the North Beishan block that led to the formation of a northward-younging extensional continental arc (ca. 470-280 Ma) associated with bimodal igneous activity, which indicates that the westward extension of the Solonker suture is located north of the Hongshishan-Pengboshan tectonic zone, (4) Late Carboniferous opening and Permian north-dipping subduction of the Liuyuan Ocean in the southern Beishan orogen, and (5) Mesozoic-Cenozoic intracontinental deformation induced by the final closure of the Paleo-Asian Ocean system in the north and the Tethyan Ocean system in the south. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC) is a common malignancy worldwide, which is especially prevalent in Asia. Elucidating the molecular basis of HCC is crucial to develop targeted diagnostic tools and novel therapies. Recent studies have identified AT-rich interactive domain-containing protein 1A (ARID1A) as a broad-spectrum tumor suppressor. We evaluated the clinical implications of decreased ARID1A expression in HCC, and investigated the mechanisms of ARID1A-mediated tumor suppression. Methods: Quantitative PCR, western blotting, immunohistochemical analysis of ARID1A mRNA and protein expression was conducted in 64 paired HCC and adjacent non-tumorous tissues. ARID1A function was evaluated in vitro in MHCC-97H and Huh7 HCC cell lines, and in vivo in a xenografted HCC tumor model. Results: ARID1A mRNA and protein expression were significantly decreased in HCC tissues, and decreased expression was significantly associated with overall metastasis, including local lymph node and distant metastasis, and poor prognosis. ARID1A knockdown promoted HCC cell migration and invasion in vitro, whereas overexpression of ARID1A inhibited migration and invasion. E-cadherin levels were closely correlated with ARID1A expression, suggesting a role in migration and invasion. In addition, ARID1A and E-cadherin (CDH1) expression were found to be regulated in a coordinated fashion in HCC samples. Furthermore, ARID1A knockdown significantly increased HCC tumor growth and lung metastasis in vivo. Conclusions: ARID1A served as an important tumor suppressor. Decreased expression of ARID1A was associated with tumor progression, metastasis, and reduced overall survival in mice and humans. ARID1A could represent a promising candidate therapeutic target for HCC. [ABSTRACT FROM AUTHOR]

Background: Esophageal Squamous Cell Carcinoma (ESCC) is a major subtype of esophageal cancer causing significant morbility and mortality in Asia. Mechanism of initiation and progression of this disease is unclear. Tumor initiating cells (TICs) are the subpopulation of cells which have the ability to self-renew, as well as, to drive initiation and progression of cancer. Increasing evidence has shown that TICs exist in a variety of tumors. However, the identification and characterization of TICs in esophageal carcinoma has remained elusive. Methodology/Principal Findings: to identify TICs in ESCC, ESCC cell lines including two primary cells were used for screening suitable surface marker. Then colony formation assay, drug resistant assay and tumorigenicity assay in immune deficient mice were used to characterize TICs in ESCC. We found that just the CD44 expression correlated with tumorigenicity in ESCC cell lines. And then induced differentiation of ESCC cells by all-trans retinoic acid treatment led to decreased expression of CD44. The FACS isolated cell subpopulations with high CD44 expression showed increased colony formation and drug resistance in vitro, as well as significantly enhanced tumorigenicity in NOD/SICD mice, as compared to the low expressing CD44 ESCC cells. Conclusions/Significance: our study has discovered a novel TIC surface marker, CD44, which can be utilized to enrich efficiently the TICs in ESCC. These findings will be useful for further studies of these cells and exploring therapeutic approaches. [ABSTRACT FROM AUTHOR]

Human immunodeficiency virus type 1 (HIV-1) CRF08_BC and CRF07_BC are two major recombinants descended from subtypes B' and C. Despite their massive epidemic impact in China, their migration patterns and divergence times remain unknown. Phylogenetic and population genetic analyses were performed on 228 HIV-1 sequences representing CRF08_BC, CRF07_BC, and subtype C strains from different locations across China, India, and Myanmar. Genome-specific rates of evolution and divergence times were estimated using a Bayesian Markov chain Monte Carlo framework under various evolutionary models. CRF08_BC originated in 1990.3 (95% credible region [CR], 1988.6 to 1991.9) in Yunnan province before spreading to Guangxi (south) and Liaoning (northeast) around 1995. Inside Guangxi region, the eastward expansion of CRF08_BC continued from Baise city (west) to Binyang (central) between 1997 and 1998 and later spread into Pingxiang around 1999 in the south, mainly through injecting drug users. Additionally, CRF07_BC diverged from its common ancestor in 1993.3 (95% CR, 1991.2 to 1995.2) before crossing the border into southern Taiwan in late 1990s. Phylogenetic analysis indicates that both CRF08_BC and CRF07_BC can trace their origins to Yunnan. The parental Indian subtype C lineage likely entered China around 1981.2 (95% CR, 1976.7 to 1985.9). Using a multiple unlinked locus model, we also showed that the dates of divergence calculated in this study may not be significantly affected by intrasubtype recombination among different lineages. This is the first phylodynamic study depicting the spatiotemporal dynamics of HIV/AIDS in East Asia. [ABSTRACT FROM AUTHOR]