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Isolation and characterization of stromal progenitor cells from ascites of patients with epithelial ovarian adenocarcinoma

<p>Abstract</p> <p>Background</p> <p>At least one-third of epithelial ovarian cancers are associated with the development of ascites containing heterogeneous cell populations, including tumor cells, inflammatory cells, and stromal elements. The components of ascites and their effects on the tumor cell microenvironment remain poorly understood. This study aimed to isolate and characterize stromal progenitor cells from the ascites of patients with epithelial ovarian adenocarcinoma (EOA).</p> <p>Methods</p> <p>Seventeen ascitic fluid samples and 7 fresh tissue samples were collected from 16 patients with EOA. The ascites samples were then cultured in vitro in varying conditions. Flow cytometry and immunocytochemistry were used to isolate and characterize 2 cell populations with different morphologies (epithelial type and mesenchymal type) deriving from the ascites samples. The in vitro cell culture model was established using conditional culture medium.</p> <p>Results</p> <p>The doubling times of the epithelial type and mesenchymal type cells were 36 h and 48 h, respectively, indicating faster growth of the epithelial type cells compared to the mesenchymal type cells. Cultured in vitro, these ascitic cells displayed the potential for self-renewal and long-term proliferation, and expressed the typical cancer stem/progenitor cell markers CD44^high, CD24^low, and AC133⁺. These cells also demonstrated high BMP-2, BMP4, TGF-β, Rex-1, and AC133 early gene expression, and expressed EGFR, integrin α₂β₁, CD146, and Flt-4, which are highly associated with tumorigenesis and metastasis. The epithelial type cells demonstrated higher cytokeratin 18 and E-cadherin expression than the mesenchymal type cells. The mesenchymal type cells, in contrast, demonstrated higher AC133, CD73, CD105, CD117, EGFR, integrin α₂β₁, and CD146 surface marker expression than the epithelial type cells.</p> <p>Conclusion</p> <p>The established culture system provides an in vitro model for the selection of drugs that target cancer-associated stromal progenitor cells, and for the development of ovarian cancer treatments.</p

Sibling recurrence risk ratio analysis of the metabolic syndrome and its components over time

BACKGROUND: The purpose of this study was to estimate both cross-sectional sibling recurrence risk ratio (λ(s)) and lifetime λ(s )for the metabolic syndrome and its individual components over time among sibships in the prospectively followed-up cohorts provided by the Genetic Analysis Workshop 13. Five measures included in the operational criteria of the metabolic syndrome by the Adult Treatment Panel III were examined. A method for estimating sibling recurrence risk with correction for complete ascertainment was used to estimate the numerator, and the prevalence in the whole cohort was used as the denominator of λ(s). RESULTS: Considerable variability in the λ(s )was found in terms of different time-points for the cross-sectional definition, the times of fulfilling the criterion for lifetime definition, and different components. Obesity and hyperglycemia had the highest cross-sectional λ(s )of the five components. Both components also had the largest slopes in the linear trend of the lifetime λ(s). However, the magnitudes of the lifetime λ(s )were similar to that of the mean cross-sectional λ(s), which were <2. The results of nonparametric linkage analysis showed only suggestive evidence of linkage between one marker and lifetime diagnosis of low high-density lipoprotein cholesterol and metabolic syndrome, respectively. CONCLUSION: The λ(s )of the metabolic syndrome and its components varies substantially across time, and the λ(s )of lifetime diagnosis was not necessarily larger than that of a cross-sectional diagnosis. The magnitude of λ(s )does not predict well the maximum LOD score of linkage analysis

Artificial Intelligence and Human Error Prevention: A Computer Aided Decision Making Approach: Technical Report No. 4: Survey and Analysis of Research on Learning Systems from Artificial Intelligence

Coordinated Science Laboratory was formerly known as Control Systems LaboratoryU.S. Department of Transportation / DOT FA79WA-4360 ABFederal Aviation Administratio

Melatonin acts synergistically with pazopanib against renal cell carcinoma cells through p38 mitogen-activated protein kinase-mediated mitochondrial and autophagic apoptosis

Background Mounting evidence indicates that melatonin has possible activity against different tumors. Pazopanib is an anticancer drug used to treat renal cell carcinoma (RCC). This study tested the anticancer activity of melatonin combined with pazopanib on RCC cells and explored the underlying mechanistic pathways of its action. Methods The 786-O and A-498 human RCC cell lines were used as cell models. Cell viability and tumorigenesis were detected with the MTT and colony formation assays, respectively. Apoptosis and autophagy were assessed using TUNEL, annexin V/propidium iodide, and acridine orange staining with flow cytometry. The expression of cellular signaling proteins was investigated with western blotting. The in vivo growth of tumors derived from RCC cells was evaluated using a xenograft mouse model. Results Together, melatonin and pazopanib reduced cell viability and colony formation and promoted the apoptosis of RCC cells. Furthermore, the combination of melatonin and pazopanib triggered more mitochondrial, caspase-mediated, and LC3-II-mediated autophagic apoptosis than melatonin or pazopanib alone. The combination also induced higher activation of the p38 mitogen-activated protein kinase (p38MAPK) in the promotion of autophagy and apoptosis by RCC cells than melatonin or pazopanib alone. Finally, tumor xenograft experiments confirmed that melatonin and pazopanib cooperatively inhibited RCC growth in vivo and predicted a possible interaction between melatonin/pazopanib and LC3-II. Conclusion The combination of melatonin and pazopanib inhibits the growth of RCC cells by inducing p38MAPK-mediated mitochondrial and autophagic apoptosis. Therefore, melatonin might be a potential adjuvant that could act synergistically with pazopanib for RCC treatment

Ring finger protein 39 genetic variants associate with HIV-1 plasma viral loads and its replication in cell culture

BACKGROUND: The human immunodeficiency virus (HIV-1) exploits host proteins to complete its life cycle. Genome-wide siRNA approaches suggested that host proteins affect HIV-1 replication. However, the results barely overlapped. RING finger protein 39 (RNF39) has been identified from genome-wide association studies. However, its function during HIV-1 replication remains unclear. METHODS AND RESULTS: We investigated the relationship between common RNF39 genetic variants and HIV-1 viral loads. The effect of RNF39 protein knockdown or overexpression on HIV-1 replication was then investigated in different cell lines. Two genetic variants were associated with HIV-1 viral loads. Patients with the ht1-GG/GG haplotype presented lower RNF39 expression levels and lower HIV-1 viral load. RNF39 knockdown inhibited HIV-1 expression. CONCLUSIONS: RNF39 protein may be involved in HIV-1 replication as observed in genetic studies on patients with HIV-1 and in in vitro cell cultures

SCUBA-2 Ultra Deep Imaging EAO Survey (STUDIES). II. Structural Properties and Near-infrared Morphologies of Faint Submillimeter Galaxies

We present structural parameters and morphological properties of faint 450 μm selected submillimeter galaxies (SMGs) from the JCMT Large Program, STUDIES, in the COSMOS-CANDELS region. Their properties are compared to an 850 μm selected and a matched star-forming samples. We investigate stellar structures of 169 faint 450 μm sources (S 450 = 2.8–29.6 mJy; S/N > 4) at z 2 mJy) and more extended than the star-forming galaxies in the same redshift range. For the stellar mass and SFR-matched sample at z sime 1 and z sime 2, the size differences are marginal between faint SMGs and the matched galaxies. Moreover, faint SMGs have similar Sérsic indices and projected axis ratios as star-forming galaxies with the same stellar mass and SFR. Both SMGs and the matched galaxies show high fractions (~70%) of disturbed features at z sime 2, and the fractions depend on the SFRs. These suggest that their star formation activity is related to galaxy merging and the stellar structures of SMGs are similar to those of star-forming galaxies. We show that the depths of submillimeter surveys are approaching the lower luminosity end of star-forming galaxies, allowing us to detect galaxies on the main sequence

First Data Release of the Hyper Suprime-Cam Subaru Strategic Program

The Hyper Suprime-Cam Subaru Strategic Program (HSC-SSP) is a three-layered imaging survey aimed at addressing some of the most outstanding questions in astronomy today, including the nature of dark matter and dark energy. The survey has been awarded 300 nights of observing time at the Subaru Telescope and it started in March 2014. This paper presents the first public data release of HSC-SSP. This release includes data taken in the first 1.7 years of observations (61.5 nights) and each of the Wide, Deep, and UltraDeep layers covers about 108, 26, and 4 square degrees down to depths of i~26.4, ~26.5, and ~27.0 mag, respectively (5sigma for point sources). All the layers are observed in five broad bands (grizy), and the Deep and UltraDeep layers are observed in narrow bands as well. We achieve an impressive image quality of 0.6 arcsec in the i-band in the Wide layer. We show that we achieve 1-2 per cent PSF photometry (rms) both internally and externally (against Pan-STARRS1), and ~10 mas and 40 mas internal and external astrometric accuracy, respectively. Both the calibrated images and catalogs are made available to the community through dedicated user interfaces and database servers. In addition to the pipeline products, we also provide value-added products such as photometric redshifts and a collection of public spectroscopic redshifts. Detailed descriptions of all the data can be found online. The data release website is https://hsc-release.mtk.nao.ac.jp/.Comment: 34 pages, 20 figures, 7 tables, moderate revision, accepted for publication in PAS