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871.
CARMEL M. HUGHES ABDALAZIZ AL‐GHADEER MARY McCLEAN JAMES C. McELNAY 《The International journal of pharmacy practice》2001,9(Z1):61-61
□ No specific health‐elated quality of life (HRQL) measure exists for patients receiving continuous ambulatory peritoneal dialysis (CAPD) □ This study assessed evaluated the use of the kidney disease questionnaire (KDQ) which has been specifically designed for haemodialysis patients in those undergoing CAPD □ Confirmatory factor analysis was used to assess the validity and reliability of the KDQ which was administered by interview to 41 CAPD patients □ Many of the items in the five dimensions of the KDQ demonstrated high factor loadings, thus indicating good representation of the associated dimension; good reliability scores were also reported □ The KDQ may be a useful measure of HRQL in CAPD patients 相似文献
872.
The spectrum of mutations in UBE3A causing Angelman syndrome 总被引:5,自引:1,他引:4
Fang P; Lev-Lehman E; Tsai TF; Matsuura T; Benton CS; Sutcliffe JS; Christian SL; Kubota T; Halley DJ; Meijers-Heijboer H; Langlois S; Graham JM Jr; Beuten J; Willems PJ; Ledbetter DH; Beaudet AL 《Human molecular genetics》1999,8(1):129-135
Angelman syndrome (AS) is characterized by mental retardation, absence of
speech, seizures and motor dysfunction. AS is caused by maternal deletions
for chromosome 15q11-q13, paternal uniparental disomy (UPD), imprinting
defects or loss-of-function mutations in the UBE3A locus which encodes
E6-AP ubiquitin-protein ligase. The UBE3A gene is imprinted with paternal
silencing in human brain and similar silencing of the Ube3a locus in
Purkinje cells and hippocampal neurons in the mouse. We have sequenced the
major coding exons for UBE3A in 56 index patients with a clinical diagnosis
of AS and a normal DNA methylation pattern. The analysis identified
disease-causing mutations in 17 of 56 patients (30%) including 13
truncating mutations, two missense mutations, one single amino acid
deletion and one stop codon mutation predicting an elongated protein.
Mutations were identified in six of eight families (75%) with more than one
affected case, and in 11 of 47 isolated cases (23%); no mutation was found
in one family with two siblings, one with a typical and one with an
atypical phenotype. Mutations were de novo in nine of the 11 isolated
cases. An amino acid polymorphism of threonine substituted for alanine at
codon 178 was identified, and a 3 bp length polymorphism was found in the
intron upstream of exon 8. In all informative cases, phenotypic expression
was consistent with imprinting with a normal phenotype when a mutation was
on the paternal chromosome and an AS phenotype when a mutation was on the
maternal chromosome. Laboratory diagnosis and genetic counseling for AS are
complex, and mutation analysis is valuable in clinically typical AS
patients with a normal methylation analysis.
相似文献
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Correlation of SARS-CoV-2 Subgenomic RNA with Antigen Detection in Nasal Midturbinate Swab Specimens
Katherine Immergluck Mark D. Gonzalez Jennifer K. Frediani Joshua M. Levy Janet Figueroa Anna Wood Beverly B. Rogers Jared ONeal Roger Elias-Marcellin Allie Suessmith Julie Sullivan Raymond F. Schinazi Ahmed Babiker Anne Piantadosi Miriam B. Vos Greg S. Martin Wilbur A. Lam Jesse J. Waggoner 《Emerging infectious diseases》2021,27(11):2887
Among symptomatic outpatients, subgenomic RNA of severe acute respiratory syndrome coronavirus 2 in nasal midturbinate swab specimens was concordant with antigen detection but remained detectable in 13 (82.1%) of 16 nasopharyngeal swab specimens from antigen-negative persons. Subgenomic RNA in midturbinate swab specimens might be useful for routine diagnostics to identify active virus replication. 相似文献
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Fiberoptic Contact‐Force Sensing Electrophysiological Catheters: How Precise Is the Technology? 下载免费PDF全文
879.
Contributions of endothelial and neuronal nitric oxide synthases to cerebrovascular responses to hyperoxia. 总被引:4,自引:0,他引:4
D N Atochin I T Demchenko J Astern A E Boso C A Piantadosi P L Huang 《Journal of cerebral blood flow and metabolism》2003,23(10):1219-1226
Hyperoxia causes a transient decrease in CBF, followed by a later rise. The mediators of these effects are not known. We used mice lacking endothelial or neuronal nitric oxide synthase (NOS) isoforms (eNOS-/- and nNOS-/- mice) to study the roles of the NOS isoforms in mediating changes in cerebral vascular tone in response to hyperoxia. Resting regional cerebral blood flow (rCBF) did not differ between wild type (WT), eNOS-/- mice, and nNOS-/- mice. eNOS-/- mice showed decreased cerebrovascular reactivities to NG-nitro-L-arginine methyl ester (L-NAME), PAPA NONOate, acetylcholine (Ach), and SOD1. In response to hyperbaric oxygen (HBO2) at 5 ATA, WT and nNOS-/- mice showed decreases in rCBF over 30 minutes, but eNOS-/- mice did not. After 60 minutes HBO2, rCBF increased more in WT mice than in eNOS-/- or nNOS-/- mice. Brain NO-metabolites (NOx) decreased in WT and eNOS-/- mice within 30 minutes of HBO2, but after 45 minutes, NOx rose above control levels, whereas they did not change in nNOS-/- mice. Brain 3NT increased during HBO2 in WT and eNOS-/- but did not change in nNOS-/- mice. These results suggest that modulation of eNOS-derived NO by HBO2 is responsible for the early vasoconstriction responses, whereas late HBO2-induced vasodilation depends upon both eNOS and nNOS. 相似文献
880.