Two planarization approaches of the oxide-filled trench isolation have been evaluated. Results show that the oxidefilled shallow-trench isolation technology based on a chemical-mechanical polishing (CMP) process is difficult to control and has a poor uniformity. It also results in a dishing effect in wide field regions. On the other hand, a new planarization process can achieve an excellent uniformity and fully planar surface by using a combination of a masking polysilicon layer based on a CMP process, selective wet etching for oxide refill on active regions, short-time CMP process for oxide refill, and reactive ion etching etchback. Results also show that the high breakdown yield of the gate oxide and the low leakage current of the nt/p junction diodes with the novel planarization process demonstrates extremely low defect density from this process. This new process is a very promising candidate for oxide-filled shallow-trench isolation.
INTRODUCTION: Alzheimer's disease (AD) blood tests are likely to become increasingly important in clinical practice, but need to be evaluated in diverse groups before use in the general population. METHODS: This study enrolled a community-based sample of older adults in the Saint Louis, Missouri, USA area. Participants completed a blood draw, AD8® dementia screening interview, Montreal Cognitive Assessment (MoCA), and survey about their perceptions of the blood test. A subset of participants completed additional blood collection, amyloid PET, MRI, and Clinical Dementia Rating® (CDR). RESULTS: Of the 859 participants enrolled in this ongoing study, 20.6% self-identified as Black or African American. The AD8 and MoCA correlated moderately with the CDR. The blood test was well-accepted by the cohort, but perceived more positively by White and highly educated individuals. DISCUSSION: Studying an AD blood test in a diverse population is feasible, and may accelerate accurate diagnosis and implementation of effective treatments.
INTRODUCTIONAlzheimer's disease (AD) blood tests are likely to become increasingly important in clinical practice, but they need to be evaluated in diverse groups before use in the general population.METHODSThis study enrolled a community‐based sample of older adults in the St. Louis, Missouri, USA area. Participants completed a blood draw, Eight‐Item Informant Interview to Differentiate Aging and Dementia (AD8®), Montreal Cognitive Assessment (MoCA), and survey about their perceptions of the blood test. A subset of participants completed additional blood collection, amyloid positron emission tomography (PET), magnetic resonance imaging (MRI), and Clinical Dementia Rating (CDR®).RESULTSOf the 859 participants enrolled in this ongoing study, 20.6% self‐identified as Black or African American. The AD8 and MoCA correlated moderately with the CDR. The blood test was well accepted by the cohort, but it was perceived more positively by White and highly educated individuals.DISCUSSIONStudying an AD blood test in a diverse population is feasible and may accelerate accurate diagnosis and implementation of effective treatments.HIGHLIGHTS
A diverse group of older adults was recruited to evaluate a blood amyloid test.
The enrollment rate was high and the blood test was well accepted by participants.
Cognitive impairment screens have moderate performance in a diverse population.
Alzheimer's disease blood tests are likely to be feasible for use in real‐world settings.
The transcription factor RUNX1 is mutated in familial platelet disorder with associated myeloid malignancy (FPDMM) and in sporadic myelodysplastic syndrome and leukemia. RUNX1 was shown to regulate inflammation in multiple cell types. Here we show that RUNX1 is required in granulocyte–monocyte progenitors (GMPs) to epigenetically repress two inflammatory signaling pathways in neutrophils: Toll-like receptor 4 (TLR4) and type I interferon (IFN) signaling. RUNX1 loss in GMPs augments neutrophils’ inflammatory response to the TLR4 ligand lipopolysaccharide through increased expression of the TLR4 coreceptor CD14. RUNX1 bindsCd14and other genes encoding proteins in the TLR4 and type I IFN signaling pathways whose chromatin accessibility increases when RUNX1 is deleted. Transcription factor footprints for the effectors of type I IFN signaling—the signal transducer and activator of transcription (STAT1::STAT2) and interferon regulatory factors (IRFs)—were enriched in chromatin that gained accessibility in both GMPs and neutrophils when RUNX1 was lost. STAT1::STAT2 and IRF motifs were also enriched in the chromatin of retrotransposons that were derepressed in RUNX1-deficient GMPs and neutrophils. We conclude that a major direct effect of RUNX1 loss in GMPs is the derepression of type I IFN and TLR4 signaling, resulting in a state of fixed maladaptive innate immunity.
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