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ABSTRACT:
PROVIDER: PRJNA1145505 | ENA |
REPOSITORIES: ENA
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Project description:This was a retrospective comparison study of SNP-based preimplantation genetic screening (SNP-PGS) and FISH-based preimplantation genetic diagnosis (FISH-PGD) for 575 couples in total with chromosome translocations, including 169 couples treated by SNP-PGS between October 2011 and August 2012, and 406 couples treated by FISH- PGD between January 2005 and October 2011. In total, 773 blastocysts obtained from 169 couples were biopsied and frozen, embryo transfer was carried out on the balanced embryos. The PGS results and pregnancy outcomes were compared with those of FISH-PGD for 406 translocation carriers with 3,968 embryos biopsied on day 3. Of the 773 biopsied blastocysts, reliable SNP-PGS results were obtained for 717 (92.76%). For Robertsonian translocation carriers, the rate of normal/balanced embryos, embryos with translocation-related abnormalities, and embryos with abnormalities unrelated to a translocation were 57.80%, 23.39% and 18.81%, respectively. In reciprocal translocation carriers, the rate of normal/balanced embryos, embryos with translocation-related abnormalities and embryos with abnormalities unrelated to translocation were 35.47%, 52.10% and 12.42%, respectively. There was no significant differences in patient age, basal endocrine level and the average number of retrieved oocytes and good quality day 3 embryos before biopsy in the SNP-PGS group compared with the FISH-PGD group. The number of embryos biopsied in the FISH-PGD group was higher than in the SNP-PGS group. However, the pregnancy rate with successful delivery per oocyte retrieval and the implantation rate were both lower in the FISH-PGD group than in the SNP-PGS group. The spontaneous abortion rate was higher in the FISH-PGD group than in the SNP-PGS group.
2013-03-11 | GSE44994 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. The BioProject ID on this superSeries record also encompasses a genome sequencing project under BioProject PRJNA213010.
2014-05-29 | GSE50585 | GEO
Project description:This was a retrospective comparison study of SNP-based preimplantation genetic screening (SNP-PGS) and FISH-based preimplantation genetic diagnosis (FISH-PGD) for 575 couples in total with chromosome translocations, including 169 couples treated by SNP-PGS between October 2011 and August 2012, and 406 couples treated by FISH- PGD between January 2005 and October 2011. In total, 773 blastocysts obtained from 169 couples were biopsied and frozen, embryo transfer was carried out on the balanced embryos. The PGS results and pregnancy outcomes were compared with those of FISH-PGD for 406 translocation carriers with 3,968 embryos biopsied on day 3. Of the 773 biopsied blastocysts, reliable SNP-PGS results were obtained for 717 (92.76%). For Robertsonian translocation carriers, the rate of normal/balanced embryos, embryos with translocation-related abnormalities, and embryos with abnormalities unrelated to a translocation were 57.80%, 23.39% and 18.81%, respectively. In reciprocal translocation carriers, the rate of normal/balanced embryos, embryos with translocation-related abnormalities and embryos with abnormalities unrelated to translocation were 35.47%, 52.10% and 12.42%, respectively. There was no significant differences in patient age, basal endocrine level and the average number of retrieved oocytes and good quality day 3 embryos before biopsy in the SNP-PGS group compared with the FISH-PGD group. The number of embryos biopsied in the FISH-PGD group was higher than in the SNP-PGS group. However, the pregnancy rate with successful delivery per oocyte retrieval and the implantation rate were both lower in the FISH-PGD group than in the SNP-PGS group. The spontaneous abortion rate was higher in the FISH-PGD group than in the SNP-PGS group. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from trophectoderm cells.
2013-03-11 | E-GEOD-44994 | biostudies-arrayexpress
Project description:Granulomas are organized immune cell aggregates formed in response to chronic infection or antigen persistence. The bacterial pathogen Yersinia pseudotuberculosis (Yp) blocks innate inflammatory signalling and immune defence, inducing neutrophil-rich pyogranulomas (PGs) within lymphoid tissues. Here we uncover that Yp also triggers PG formation within the murine intestinal mucosa. Mice lacking circulating monocytes fail to form defined PGs, have defects in neutrophil activation and succumb to Yp infection. Yersinia lacking virulence factors that target actin polymerization to block phagocytosis and reactive oxygen burst do not induce PGs, indicating that intestinal PGs form in response to Yp disruption of cytoskeletal dynamics. Notably, mutation of the virulence factor YopH restores PG formation and control of Yp in mice lacking circulating monocytes, demonstrating that monocytes override YopH-dependent blockade of innate immune defence. This work reveals an unappreciated site of Yersinia intestinal invasion and defines host and pathogen drivers of intestinal granuloma formation.
2022-02-07 | GSE194334 | GEO
Project description:In the effort to identify novel, relevant prognostic factors for the clinical monitoring of patients affected by squamous cell carcinomas of the oral cavity (SCCOC) we have pursued a molecular screening at the gene and protein level on 166 surgical specimens derived from patients with an accessible clinical history and >2 years follow-up. The screening was focalized on cell surface proteoglycans (PGs) based upon the assumption that altered expression of individual or groups of PGs may predict disease course and therapeutic response, and thereby allow for a clusterization of patients in discrete subsets. The 11 PGs contemplated in the screening and including syndecan-1-4 (SDC1-SDC4), glypican-1-6 (GPC1-GPC6) and NG2, were found to be transcribed at variable levels and with a decreasing frequencies SDC1>SDC4>SDC2>SDC3>GPC4>GPC3>GPC1 >GPC5>CSPG4>GPC6>GPC2. SCCOC cells de novo transcribed GPC2, GPC5 and NG2 and regulated all SDCs, GPC1, -3, -4 and -6, suggesting that an altered surface profile of PG is a characterizing trait of these tumor cells In situ distributional analysis of these PGs on a total of 149 cases revealed many fewer lesions actually translated the molecules which were detected with a frequency range of 14% (SDC2) to 92% (SDC1). Noteworthy was, however, that SDC2 was present in the intra-lesional stroma and in association with neovessels in all the cases, suggesting that this specific PG was a key element of stromal fibroblasts and angiogenic structures. Poor translational efficacy of several of the PGs was accompanied by an apparent retention of the molecules within the cytoplasm of SCCOC cells. This finding suggest that modulated expression of cell surface PGs may be a representative secondary event in SCCOC and that these carcinoma cells do not mount up an effective intracellular machinery for proper shuttling and membrane incorporation of the PGs.
2013-11-01 | GSE33788 | GEO
Project description:BioProject Replaced by BioProject PRJNA622920
| PRJNA622916 | ENA
Project description:The Golgi stress response is a homeostatic mechanism that augments the functional capacity of the Golgi apparatus when Golgi function becomes insufficient (Golgi stress). Three response pathways of the Golgi stress response have been identified in mammalian cells, the TFE3, HSP47 and CREB3 pathways, which augment the capacity of specific Golgi functions such as N-glycosylation, anti-apoptotic activity and pro-apoptotic activity, respectively. On the contrary, glycosylation of proteoglycans (PGs) is another important function of the Golgi, although the response pathway upregulating expression of glycosylation enzymes for PGs in response to Golgi stress remains unknown. Here, we found that expression of glycosylation enzymes for PGs was induced upon insufficiency of PG glycosylation capacity in the Golgi (PG-Golgi stress), and that transcriptional induction of genes encoding glycosylation enzymes for PGs was independent of the known Golgi stress response pathways and ER stress response. Promoter analyses of genes encoding these glycosylation enzymes revealed the novel enhancer element PGSE, which regulates their transcriptional induction upon PG-Golgi stress. From these observations, the response pathway we discovered is a novel Golgi stress response pathway, which we have named the PG pathway.
2018-09-14 | GSE119909 | GEO