Abstract With field effect transistor (FET) sustained to downscale to sub‐10 nm nodes, performance degradation originates from short channel effects (SCEs) degradation and power consumption increment attributed to inhibition of supply voltage (VDD) scaling down proportionally caused by thermionic limit subthreshold swing (SS) (60 mV dec −1 ) pose substantial challenges for today's semiconductor industry. To further sustain the Moore's law life, incorporation of new device concepts or new materials are imperative. 2D materials are predicted to be able to combat SCEs by virtue of high carrier mobility maintainability regardless of thickness thinning down, dangling bonds free surface and atomic thickness, which contributes to super gate electrostatic controllability. To overcome increasing power dissipation problem, new device structures including negative capacitance FET (NCFET), tunnel FET (TFET), dirac source FET (DSFET) and the like, which show superiority in decreasing VDD by lowering SS below thermionic limit of 60 mV dec −1 have been brought out. The combination of 2D materials and ultralow steep slope device structures holds great promise for low power‐dissipation electronics, which encompass both suppressed SCEs and reduced VDD simultaneously, leading to improved device performance and lowered power dissipation.
Some transcription factors (TFs) can form liquid-liquid phase separated (LLPS) condensates. However, the functions of these TF condensates in 3D genome organization and gene regulation remain elusive. In response to methionine (met) starvation, budding yeast TF Met4 and a few co-activators, including Met32, induce a set of genes involved in met biosynthesis. Here, we show that the endogenous Met4 and Met32 form co-localized puncta-like structures in yeast nuclei upon met depletion. Recombinant Met4 and Met32 form mixed droplets with LLPS properties in vitro . In relation to chromatin, Met4 puncta co-localize with target genes, and at least a subset of these target genes is clustered in 3D in a Met4-dependent manner. A MET3pr -GFP reporter inserted near several native Met4 binding sites becomes co-localized with Met4 puncta and displays enhanced transcriptional activity. A Met4 variant with a partial truncation of an intrinsically disordered region (IDR) shows less puncta formation, and this mutant selectively reduces the reporter activity near Met4 binding sites to the basal level. Overall, these results support a model where Met4 and co-activators form condensates to bring multiple target genes into a vicinity with higher local TF concentrations, which facilitates a strong response to methionine depletion.
Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system. MS pathogenesis is closely related to the environment, genetic, and immune system, but the underlying interactions have not been clearly elucidated. This study aims to unveil the genetic basis and immune landscape of MS pathogenesis with bioinformatics.
Various treatments of giant cell tumor of bone (GCTB) included in curettages and resections and with adjuvant are exerted, but the best treatment is controversial. The aim of the study was the identification of individual risk factors after various treatments in GCTB. A total of 179 patients treated for GCTB between 1998 and 2010 were concluded in the retrospective study. All patients were treated with intralesional curettage, extensive curettage, or wide resection. Mean follow-up was 60.2 ± 18.7 months (36~112 months). Age, gender, tumor location, Campanacci grade, soft tissue extension, pathological features, and surgical methods were performed to univariate Kaplan-Meier survival analysis and multivariate Cox regression analysis. The local recurrence rates of intralesional curettage (41.9 %) and extensive curettage (19.0 %) were significantly higher than that of wide resection (7.7 %). The higher risk of local recurrence was found for soft tissue extension (hazard = 7.921, 95 % CI 1.107~56.671), compared with no statistical significances between gender, location, Campanacci grade, pathologic fracture, and local recurrences, which were shown by Kaplan-Meier analysis. However, recurrence-free survival (RFS) of patients younger than 30 was significantly lower than that of patients older than 30. The RFS of pathologic fracture patients with soft tissue extension was significantly lower than that of pathologic fracture patients without soft tissue extension. Multivariate Cox regression analysis indicated that the independent variable that contributed to recurrence-free survival was soft tissue extension and surgical methods. The RFS of extensive curettage had no statistically significant difference with wide resection and was significantly higher than that of intralesional curettage. Use of high-speed burring and bone cement significantly decreased the local recurrence rate. Age (below 30 years), gender, tumor location, Campanacci grade, and pathologic fracture have no statistically significant influence on local recurrences. Soft tissue extension and intralesional curettage of surgical methods increased the RFS. The results of the present study suggested that compared with curettage and wide section, treatment of GCTB by extensive curettage could provide the favorable local control and functional recovery.
Some transcription factors (TFs) can form liquid-liquid phase separated (LLPS) condensates. However, the functions of these TF condensates in 3D genome organization and gene regulation remain elusive. In response to methionine (met) starvation, budding yeast TF Met4 and a few co-activators, including Met32, induce a set of genes involved in met biosynthesis. Here, we show that the endogenous Met4 and Met32 form co-localized puncta-like structures in yeast nuclei upon met depletion. Recombinant Met4 and Met32 form mixed droplets with LLPS properties in vitro . In relation to chromatin, Met4 puncta co-localize with target genes, and at least a subset of these target genes are clustered in 3D in a Met4-dependent manner. A MET3pr -GFP reporter inserted near several native Met4 binding sites becomes co-localized with Met4 puncta and displays enhanced transcriptional activity. A Met4 variant with a partial truncation of an intrinsically disordered region (IDR) shows less puncta formation, and this mutant selectively reduces the reporter activity near Met4 binding sites to the basal level. Overall, these results support a model where Met4 and co-activators form condensates to bring multiple target genes into a vicinity with higher local TF concentrations, which facilitates a strong response to methionine depletion.
Abstract BackgroundOsteoarthritis (OA) is an age-related chronic inflammatory and degenerative changes that carries heavy burden for individuals and the society. The specific mechanism of OA still remains unclear today, which requires new methods and technologies to achieve some new breakthrough. Bioinformatics technology is a novel method to extract genetic information from many diseases. In this study, we aims at screening out some key genes to help to illuminate the pathogenesis of OA to help to diagnosis and cure it.Objective and MethodsBioinformatics technology was used to screen some key target genes that were closely related to OA and nervous system, and by using qRT-PCR to preliminary verify the results.ResultsIn this work, we analysis three gene expression profiles, GSE114007, GSE51588, and GSE55457, that downloaded from the Gene Expression Omnibus database (GEO). At last, a total of 878 DEGs were identified with dataset GSE114007 (P<0.05 and |logFC|>1.5), consisting of 495 up-regulated genes and 383 down-regulated genes between the osteoarthritis and normal cartilage tissues. And by combining with the screened results of GSE51588 and GSE55457, finally, three genes, HES1, JUN, and IRE2, which were closely correlated with the nervous system that may help to diagnosis and cure osteoarthritis in the future were identified, and the result of qRT-PCR preliminary confirmed our finding.ConclusionHES1, JUN, and IRE2 were three potential genes related to osteoarthritis and nervous system that may help to diagnosis and cure OA.
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