Woodsguerrero6373

This paper presents a robust phase unwrapping algorithm based on a particle-Kalman filter for wrapped fringe patterns by combining a particle filter and an extended Kalman filter, which formulates the phase unwrapping problem of wrapped fringe patterns as an optimal state estimation problem under the frame of the particle-Kalman filter. First, a state space equation for state variables is extended to the second order of Taylor series, and a local phase gradient estimator based on a modified matrix pencil model is used to obtain the first-order and second-order phase gradient information required by the extended state space equation, which is conducive to enhancing the phase unwrapping accuracy of the proposed procedure. Second, the initial estimate of unwrapped phase is obtained through applying an efficient phase unwrapping program based on a particle filter to unwrap noisy wrapped pixels. Finally, the initial estimate of unwrapped phase obtained by the particle filter is taken as the predicted estimate of state variables and further processed by the extended Kalman filter to obtain the final estimate of unwrapped phase. In addition, an efficient quality-guided strategy that has been demonstrated well is used to guarantee that the particle-Kalman filter efficiently and accurately unwraps wrapped pixels along a suitable path. Results obtained with synthetic data and experimental data demonstrate the effectiveness of the proposed method and show that this new approach can obtain more acceptable solutions from noisy wrapped fringe patterns, with respect to some of the most commonly used methods.

Although dysregulated adaptive immune response has been considered as the main culprit for systemic lupus erythematosus (SLE), emerging studies have indicated that innate immunity, functioning upstream of adaptive immunity, acts as an important trigger of autoimmune diseases and promotes SLE development. Here, we have reviewed the most recent findings to highlight the influence of neutrophils on SLE pathogenesis.

Neutrophils participate in SLE development mainly via promoting self-antigen exposure and autoantibody production, advocating the release of type I interferons (IFNs) and other pro-inflammatory cytokines, and mediating systemic tissue injury. A recent study revealed that neutrophil ferroptosis exerts a strong pathogenic effect in SLE, and that dysregulated innate immunity is adequate to disrupt the homeostasis of immune tolerance.

Insights into the pathogenic role of neutrophils in SLE will contribute to a more comprehensive understanding of this disease and may propose novel clinical targets for accurate diagnosis and precision medicine.

Insights into the pathogenic role of neutrophils in SLE will contribute to a more comprehensive understanding of this disease and may propose novel clinical targets for accurate diagnosis and precision medicine.The purpose of this report is to provide guidance to users of NCHS data in the selection of modeling options when using the NCI Joinpoint regression software to analyze trends. This report complements another report, "National Center for Health Statistics Guidelines for Analysis of Trends." Considerations are presented for selecting the modeling options, with examples illustrating the choices. The tradeoffs and consequences of choosing the various modeling options using data from NCHS data systems are discussed.encounters.

Asthma is a heterogeneous common respiratory disease that remains poorly understood. The established genetic associations fail to explain the high estimated heritability, and the prevalence of asthma differs between populations and geographic regions. Robust association analyses incorporating different genetic ancestries and whole-genome sequencing data may identify novel genetic associations.

We performed family-based genome-wide association analyses of childhood-onset asthma based on whole-genome sequencing (WGS) data for the 'The Genetic Epidemiology of Asthma in Costa Rica' study (GACRS) and the Childhood Asthma Management Program (CAMP). Based on parent-child trios with children diagnosed with asthma, we performed a single variant analysis using an additive and a recessive genetic model and a region-based association analysis of low-frequency and rare variants.

Based on 1180 asthmatic trios (894 GACRS trios and 286 CAMP trios, a total of 3540 samples with WGS data), we identified three novel genetinked genes. Furthermore, region-based analyses suggest independent potential low-frequency/rare variant associations on 8p22. Follow-up analyses are needed to understand the functional mechanisms and generalizability of these associations.Advanced nursing practice model for head and neck cancer A practice development project Abstract. Background Head and neck cancer confronts patients and their families with big challenges due to complex treatments as well as changes in vital functions and appearance. They require multifaceted support and benefit from coordinated, interprofessional collaboration and advanced nursing practice. Problem/aim In a tertiary head and neck cancer center, a coordinating contact person was missing for patients, families and the care team. Therefore, a project was launched to develop an advanced nursing practice program. Methods Methods included an advanced nursing practice concept, approaches for practice development, and action research. The project consisted of four phases Stakeholder analysis and literature review were followed by the definition of the advanced nursing practice program, which was then tested during a pilot phase, and evaluated using structural/process data and stakeholder interviews. Results Evidence-based, continuous, person-centered care was improved across the care continuum for patients/families. The nurses' expertise was supported and the collaboration with internal/external clinicians was facilitated. Patients/families valued the continuity offered by the advanced practice nurse. Discussion The methodological approaches supported a goal-oriented approach; especially participatory practice development helped to address employees' concerns. Limitations/transfer To date, a sustainable program cannot yet be warranted. For similar projects, an approach with stakeholder analysis, multidisciplinary focus, and early evaluation planning is recommended.Spinal muscular atrophy (SMA) is a fatal neuromuscular disease caused by homozygous deletions or mutations of the SMN1 gene. SMN2 is a paralogous gene of SMN1 and a modifying gene of SMA. A better understanding of how SMN2 exon 7 splicing is regulated helps discover new therapeutic targets for SMA therapy. Based on an antisense walk method to map exonic and intronic splicing silencers (ESSs and ISSs) in SMN2 exon 7 and the proximal regions of its flanking introns, we identified one ISS (ISS6-KH) at upstream of the branch point site in intron 6. By using mutagenesis-coupled RT-PCR with SMN1/2 minigenes, immunochromatography, over-expression, and siRNA-knockdown, we found this ISS consists of a bi-partite hnRNP A1 binding cis-element and a poly-U sequence located between the proximal hnRNP A1 binding site (UAGCUA) and the branch site. Both HuR and hnRNP C1 proteins promote exon 7 skipping through the poly-U stretch. Mutations or deletions of these motifs lead to efficient SMN2 exon 7 inclusion comparable to SMN1 gene. Furthermore, we identified an optimal antisense oligonucleotide (ASO) that binds the intron 6 ISS and causes striking exon 7 inclusion in the SMN2 gene in patient fibroblasts and SMA mouse model. Our findings demonstrate that this novel ISS plays an important role in SMN2 exon 7 skipping and highlight a new therapeutic target for SMA therapy.SUPT16H encodes the large subunit of the FACT complex, which functions as a nucleosome organizer during transcription. We identified two individuals from unrelated families carrying de novo missense variants in SUPT16H. The probands exhibit global developmental delay, intellectual disability, epilepsy, facial dysmorphism, and brain structural abnormalities. We used Drosophila to characterize these two variants, p.T171I and p.G808R. Loss of the fly ortholog, dre4, causes lethality at an early developmental stage. RNAi-mediated knockdown of dre4 in either glia or neurons causes severely reduced eclosion and longevity. Tissue-specific knockdown of dre4 in the eye or wing leads to the loss of these tissues whereas overexpression of SUPT16H has no dominant effect. Moreover, expression of the reference SUPT16H significantly rescues the loss-of-function phenotypes in the nervous system as well as wing and eye. In contrast, expression of SUPT16H p.T171I or p.G808R rescue the phenotypes poorly, indicating that the variants are partial loss-of-function alleles. While previous studies argued that the developmental arrest caused by loss of dre4 is due to impaired ecdysone production in the prothoracic gland, our data show that dre4 is required for proper cell growth and survival in multiple tissues in a cell-autonomous manner. Altogether, our data indicate that the de novo loss-of-function variants in SUPT16H are indeed associated with developmental and neurological defects observed in the probands.How ancestry-associated genetic variance affects disparities in the risk for polygenic diseases and influences the identification of disease-associated genes warrant a deeper understanding. Dansylcadaverine clinical trial We hypothesized that the discovery of genes associated with polygenic diseases may be limited by overreliance on single-nucleotide polymorphism (SNP)-based genomic investigation, since most significant variants identified in genome-wide SNP association studies map to introns and intergenic regions of the genome. To overcome such potential limitation, we developed a gene-constrained and function-based analytical method centered on high-risk variants (hrV) that encode frameshifts, stopgains, or splice site disruption. We analyzed the total number of hrV per gene in populations of different ancestry, representing a total of 185 934 subjects. Using this analysis, we developed a quantitative index of hrV (hrVI) across 20 428 genes within each population. We then applied hrVI analysis to the discovery of genes associated with type 2 diabetes mellitus (T2DM), a polygenic disease with ancestry-related disparity. HrVI profiling and gene-to-gene comparisons of ancestry-specific hrV between the case (20 781 subjects) and control (24 440 subjects) populations in the T2DM national repository identified 57 genes associated with T2DM, 40 of which were discoverable only by ancestry-specific analysis. These results illustrate how function-based and ancestry-specific analysis of genetic variations can accelerate the identification of genes associated with polygenic diseases. Besides T2DM, such analysis may facilitate our understanding of the genetic basis for other polygenic diseases that are also greatly influenced by environmental and behavioral factors, such as obesity, hypertension, and Alzheimer's disease.The rapid development of artificial intelligence places high demands on human-machine interfaces. Various types of huma-machine interfaces have been implemented, including smart keyboards, electronic skins, and wearable motion sensors. Handwriting behavior has a high degree of interaction freedom, and handwriting characteristics offer high-security standards for human-machine systems. Herein, we propose a portable smart pen integrated with triboelectric displacement vector sensors to trace handwriting trajectories for human-machine interactions and biometric identification. A triboelectric pressure sensor array is evenly distributed along the pen case to sense displacement vectors, and an additional triboelectric sensor is placed on top of the pen to detect vertical force. By leveraging the resin pen refill as a tribopositive material and a nanowired polyethylene tribonegative layer attached to a Cu electrode, triboelectric signals are generated during the writing/moving process. The calculation and analysis of the sensor signals enable the recognition of handwritten patterns, including Latin letters and Arabic numerals.