757 research outputs found
Perceptual snoring as a basis for a psychoacoustical modeling and clinical patient profiling
Purpose The perceptual burden and social nuisance for mainly the co-sleeper can affect the relationship between snorer and bedpartner. Mandibular advancement devices (MAD) are commonly recommended to treat sleep-related breathing such as snoring or sleep apnea. There is no consensus about the definition of snoring particularly with MAD, which is essential for assessing the effectiveness of treatment. We aimed to stablish a notion of perceptual snoring with MAD in place. Methods Sound samples, each 30 min long, were recorded during in-home, overnight, automatic mandibular repositioning titration studies in a population of 29 patients with obstructive sleep apnea syndrome (OSAS) from a clinical trial carried out to validate the MATRx plus. Three unspecialized and calibrated raters identified sound events and classified them as noise, snore, or breathing as well as providing scores for classification certainty and annoyance. Data were analyzed with respect to expiration-inspiration, duration, annoyance, and classification certainty. Results A Fleiss' kappa (>0.80) and correlation duration of events (>0.90) between raters were observed. Prevalence of all breath sounds: snore 55.6% (N = 6398), breathing sounds 31.7% (N = 3652), and noise 9.3% (N = 1072). Inspiration occurs in 88.3% of events, 96.8% contained at least on expiration phase. Snore and breath events had similar duration, respectively 2.58s (sd 1.43) and 2.41s (sd 1.22). Annoyance is lowest for breathing events (8.00 sd 0.98) and highest for snore events (4.90 sd 1.92) on a VAS from zero to ten. Conclusion Perceptual sound events can be a basis for analysis in a psychosocial context. Perceived snoring occurs during both expiration as well as inspiration. Substantial amount of snoring remains despite repositioning of the mandible aimed at the reduction of AHI-ODI
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Clinical and serological features of systemic sclerosis in a multicenter African American cohort: Analysis of the genome research in African American scleroderma patients clinical database.
Racial differences exist in the severity of systemic sclerosis (SSc). To enhance our knowledge about SSc in African Americans, we established a comprehensive clinical database from the largest multicenter cohort of African American SSc patients assembled to date (the Genome Research in African American Scleroderma Patients (GRASP) cohort).African American SSc patients were enrolled retrospectively and prospectively over a 30-year period (1987-2016), from 18 academic centers throughout the United States. The cross-sectional prevalence of sociodemographic, clinical, and serological features was evaluated. Factors associated with clinically significant manifestations of SSc were assessed using multivariate logistic regression analyses.The study population included a total of 1009 African American SSc patients, comprised of 84% women. In total, 945 (94%) patients met the 2013 American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) classification criteria for SSc, with the remaining 64 (6%) meeting the 1980 ACR or CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia) criteria. While 43% were actively employed, 33% required disability support. The majority (57%) had the more severe diffuse subtype and a young age at symptom onset (39.1 ± 13.7 years), in marked contrast to that reported in cohorts of predominantly European ancestry. Also, 1 in 10 patients had a severe Medsger cardiac score of 4. Pulmonary fibrosis evident on computed tomography (CT) chest was present in 43% of patients and was significantly associated with anti-topoisomerase I positivity. 38% of patients with CT evidence of pulmonary fibrosis had a severe restrictive ventilator defect, forced vital capacity (FVC) ≤50% predicted. A significant association was noted between longer disease duration and higher odds of pulmonary hypertension, telangiectasia, and calcinosis. The prevalence of potentially fatal scleroderma renal crisis was 7%, 3.5 times higher than the 2% prevalence reported in the European League Against Rheumatism Scleroderma Trials and Research (EUSTAR) cohort.Our study emphasizes the unique and severe disease burden of SSc in African Americans compared to those of European ancestry
Generalized Interpolation Material Point Approach to High Melting Explosive with Cavities Under Shock
Criterion for contacting is critically important for the Generalized
Interpolation Material Point(GIMP) method. We present an improved criterion by
adding a switching function. With the method dynamical response of high melting
explosive(HMX) with cavities under shock is investigated. The physical model
used in the present work is an elastic-to-plastic and thermal-dynamical model
with Mie-Gr\"uneissen equation of state. We mainly concern the influence of
various parameters, including the impacting velocity , cavity size , etc,
to the dynamical and thermodynamical behaviors of the material. For the
colliding of two bodies with a cavity in each, a secondary impacting is
observed. Correspondingly, the separation distance of the two bodies has a
maximum value in between the initial and second impacts. When the
initial impacting velocity is not large enough, the cavity collapses in a
nearly symmetric fashion, the maximum separation distance increases
with . When the initial shock wave is strong enough to collapse the cavity
asymmetrically along the shock direction, the variation of with
does not show monotonic behavior. Our numerical results show clear indication
that the existence of cavities in explosive helps the creation of ``hot
spots''.Comment: Figs.2,4,7,11 in JPG format; Accepted for publication in J. Phys. D:
Applied Physic
Presymptomatic risk assessment for chronic non-communicable diseases
The prevalence of common chronic non-communicable diseases (CNCDs) far
overshadows the prevalence of both monogenic and infectious diseases combined.
All CNCDs, also called complex genetic diseases, have a heritable genetic
component that can be used for pre-symptomatic risk assessment. Common single
nucleotide polymorphisms (SNPs) that tag risk haplotypes across the genome
currently account for a non-trivial portion of the germ-line genetic risk and
we will likely continue to identify the remaining missing heritability in the
form of rare variants, copy number variants and epigenetic modifications. Here,
we describe a novel measure for calculating the lifetime risk of a disease,
called the genetic composite index (GCI), and demonstrate its predictive value
as a clinical classifier. The GCI only considers summary statistics of the
effects of genetic variation and hence does not require the results of
large-scale studies simultaneously assessing multiple risk factors. Combining
GCI scores with environmental risk information provides an additional tool for
clinical decision-making. The GCI can be populated with heritable risk
information of any type, and thus represents a framework for CNCD
pre-symptomatic risk assessment that can be populated as additional risk
information is identified through next-generation technologies.Comment: Plos ONE paper. Previous version was withdrawn to be updated by the
journal's pdf versio
Predicting biochemical recurrence and prostate cancer-specific mortality after radical prostatectomy: comparison of six prediction models in a cohort of patients with screening- and clinically detected prostate cancer
Objectives
To perform a comparison and external validation of three
models predicting biochemical recurrence (BCR) and three
models predicting prostate cancer (PCa)-specific mortality
(PCSM) in a screening setting, i.e. patients with screeningdetected PCa (S-PCa) and in those with clinically detected
PCa (C-PCa).
Subjects and Methods
We retrospectively evaluated 795 men with S-PCa, from the
European Randomized Study of Screening for Prostate
Cancer, Rotterdam, and 1123 men with C-PCa initially
treated with RP. The discriminative ability of the models was
assessed according to the area under the curve (AUC) of the
receiver-operating characteristic, and calibration was assessed
graphically using calibration plots.
Results
The median (interquartile range [IQR]) follow-up for the SPCa group was 10.4 (6.8–14.3) years and for the C-PCa group
it was 8.8 (4.8–12.9) years. A total of 123 men with S-PCa
(15%) and 389 men with C-PCa (35%) experienced BCR. Of
the men with S-PCa and BCR, 24 (20%) died from PCa and 29
(23%) died from other causes. Of the men with C-PCa and
BCR, 68 (17%) died from PCa and 105 (27%) died from other
causes. The discrimination of the models predicting BCR or
PCSM was higher for men with S-PCa (AUC: BCR 0.77–0.84,
PCSM 0.60–0.77) than for the men with C-PCa (AUC: BCR
0.75–0.79, PCSM 0.51–0.68) as a result of the similar patient
characteristics of the men with S-PCa in the present study and
those of the cohorts used to develop these models. The risk of
BCR was typically overestimated, while the risk of PCSM was
typically underestimated.
Conclusion
Prediction models for BCR showed good discrimination and
reasonable calibration for both men with S-PCa and men
with C-PCa, and even better discrimination for men with SPCa. For PCSM, the ev
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Data for Genetic Analysis Workshop (GAW) 15 Problem 2, Genetic Causes of Rheumatoid Arthritis and Associated Traits
For Genetic Analysis Workshop 15 Problem 2, we organized data from several ongoing studies designed to identify genetic and environmental risk factors for rheumatoid arthritis. Data were derived from the North American Rheumatoid Arthritis Consortium (NARAC), collaboration among Canadian researchers, the European Consortium on Rheumatoid Arthritis Families (ECRAF), and investigators from Manchester, England. All groups used a common standard for defining rheumatoid arthritis, but NARAC also further selected for a more severe phenotype in the probands. Genotyping and family structures for microsatellite-based linkage analysis were provided from all centers. In addition, all centers but ECRAF have genotyped families for linkage analysis using SNPs and these data were additionally provided. NARAC also had additional data from a dense genotyping analysis of a region of chromosome 18 and results from candidate gene studies, which were provided. Finally, smoking influences risk for rheumatoid arthritis, and data were provided from the NARAC study on this behavior as well as some additional phenotypes measuring severity. Several questions could be evaluated using the data that were provided. These include comparing linkage analysis using single-nucleotide polymorphisms versus microsatellites and identifying credible regions of linkage outside the HLA region on chromosome 6p13, which has been extensively documented; evaluating the joint effects of smoking with genetic factors; and identifying more homogenous subsets of families for whom genetic susceptibility might be stronger, so that linkage and association studies may be more efficiently conducted
Data for Genetic Analysis Workshop (GAW) 15 Problem 2, genetic causes of rheumatoid arthritis and associated traits
For Genetic Analysis Workshop 15 Problem 2, we organized data from several ongoing studies designed to identify genetic and environmental risk factors for rheumatoid arthritis. Data were derived from the North American Rheumatoid Arthritis Consortium (NARAC), collaboration among Canadian researchers, the European Consortium on Rheumatoid Arthritis Families (ECRAF), and investigators from Manchester, England. All groups used a common standard for defining rheumatoid arthritis, but NARAC also further selected for a more severe phenotype in the probands. Genotyping and family structures for microsatellite-based linkage analysis were provided from all centers. In addition, all centers but ECRAF have genotyped families for linkage analysis using SNPs and these data were additionally provided. NARAC also had additional data from a dense genotyping analysis of a region of chromosome 18 and results from candidate gene studies, which were provided. Finally, smoking influences risk for rheumatoid arthritis, and data were provided from the NARAC study on this behavior as well as some additional phenotypes measuring severity. Several questions could be evaluated using the data that were provided. These include comparing linkage analysis using single-nucleotide polymorphisms versus microsatellites and identifying credible regions of linkage outside the HLA region on chromosome 6p13, which has been extensively documented; evaluating the joint effects of smoking with genetic factors; and identifying more homogenous subsets of families for whom genetic susceptibility might be stronger, so that linkage and association studies may be more efficiently conducted
I Believe, Therefore I Do
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Autoimmune and autoinflammatory mechanisms in uveitis
The eye, as currently viewed, is neither immunologically ignorant nor sequestered from the systemic environment. The eye utilises distinct immunoregulatory mechanisms to preserve tissue and cellular function in the face of immune-mediated insult; clinically, inflammation following such an insult is termed uveitis. The intra-ocular inflammation in uveitis may be clinically obvious as a result of infection (e.g. toxoplasma, herpes), but in the main infection, if any, remains covert. We now recognise that healthy tissues including the retina have regulatory mechanisms imparted by control of myeloid cells through receptors (e.g. CD200R) and soluble inhibitory factors (e.g. alpha-MSH), regulation of the blood retinal barrier, and active immune surveillance. Once homoeostasis has been disrupted and inflammation ensues, the mechanisms to regulate inflammation, including T cell apoptosis, generation of Treg cells, and myeloid cell suppression in situ, are less successful. Why inflammation becomes persistent remains unknown, but extrapolating from animal models, possibilities include differential trafficking of T cells from the retina, residency of CD8(+) T cells, and alterations of myeloid cell phenotype and function. Translating lessons learned from animal models to humans has been helped by system biology approaches and informatics, which suggest that diseased animals and people share similar changes in T cell phenotypes and monocyte function to date. Together the data infer a possible cryptic infectious drive in uveitis that unlocks and drives persistent autoimmune responses, or promotes further innate immune responses. Thus there may be many mechanisms in common with those observed in autoinflammatory disorders
How Can We Improve Patient-Clinician Communication for Men Diagnosed with Prostate Cancer?
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