13 results match your criteria: "B.C. Research Institute for Children's and Women's Health[Affiliation]"

Background: In recent years, decision makers in Canada and elsewhere have expressed a desire for more explicit, evidence-based approaches to priority setting. To achieve this aim within health care organizations, knowledge of both the organizational context and stakeholder attitudes towards priority setting are required. The current work adds to a limited yet growing body of international literature describing priority setting practices in health organizations.

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Introduction: Building on a survey of key decision-makers within the Provincial Health Services Authority (PHSA) of British Columbia, a process for prioritizing new service options within this organization for the 2005/06 budget cycle was developed and implemented by senior managers and researchers at the University of British Columbia.

Methods: A case study approach was taken in which development and implementation of the prioritization process was documented and feedback was obtained from decision-makers to evaluate the activity. Information from the literature was also used to identify areas for improvement.

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Chronic granulomatous disease: from genetic defect to clinical presentation.

Adv Exp Med Biol

September 2005

Department of Pediatrics, B C Research Institute for Children's and Women's Health, University of British Columbia, Vancouver, Canada.

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The in vivo actions of insulin-like growth factor-I (IGF-I) on the growth and development of the cerebral cortex were investigated in transgenic (Tg) mice that overexpress IGF-I in the brain, beginning as early as embryonic day (E) 13. Compared to non-Tg littermate controls, Tg mice at postnatal day (P) 12 exhibited significant increases in total cortical volume (31%) and in total neuron number (27%). The numerical density of neurons did not differ significantly between Tg and control mice, except in layer I.

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Expression of the sex hormone-binding globulin gene (SHBG) in the liver produces SHBG, which transports sex steroids in the blood. In rodents, the SHBG gene is also expressed in Sertoli cells giving rise to the testicular androgen-binding protein, which is secreted into the seminiferous tubule where it presumably controls testosterone action. Evidence that the SHBG gene functions in this way in the human testis is lacking, and mice containing a human SHBG transgene (shbg4) under the control of its own promoter sequence are characterized by SHBG gene expression in the liver but not in the testis.

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The depiction of car light beams in a child born completely blind.

Perception

September 2004

Human Early Learning Partnership, B C Research Institute for Children's and Women's Health, Biobehavioural Research Unit, University of British Columbia, 4480 Oak Street, L 480 Vancouver, British Columbia V6H 3Z4, Canada.

A 12-year-old child (DI) who was completely blind from birth, made a series of tactual (raised-lines) drawings of cars. Among them, there was the depiction of a 'fast car at night' in which DI drew beams of light projecting out of the car. We analyse this drawing, and the preceding ones.

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Type 1 diabetes is an autoimmune disease in which pancreatic beta-cells are destroyed by cytotoxic T-cells that recognize peptide epitopes presented by HLA class I molecules. The identification of human beta-cell epitopes may significantly improve the prospects for immunodiagnosis and immunotherapy in type 1 diabetes. Using algorithms to predict nonameric beta-cell peptides that would bind to the common HLA allele, HLA-A*0201, we identified a potential epitope from the leader sequence of islet amyloid polypeptide (human islet amyloid polypeptide [IAPP] precursor protein [preproIAPP] 5-13: KLQVFLIVL).

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Early pain in preterm infants. A model of long-term effects.

Clin Perinatol

September 2002

Centre for Community Child Health Research, Room L408, B.C. Research Institute for Children's and Women's Health, Department of Pediatrics, University of British Columbia, 4480 Oak Street, Vancouver, BC V6H 3V4, Canada.

There are multiple lines of evidence suggesting that in vulnerable prematurely born infants, repeated and prolonged pain exposure may affect the subsequent development of pain systems, as well as potentially contribute to alterations in long-term development and behavior. Multiple factors cumulatively contribute to altered developmental trajectories in such infants. These include characteristics of the developing organism (low tactile threshold, sensitization, rapid brain development), characteristics intrinsic to the infant (gestation, illness severity), characteristics of the experience in the neonatal intensive care unit (pain exposure and cumulative stress), and characteristics of the caregivers within their family and social context.

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Objective: Children with neurologic impairments have shown diminished pain response compared with control subjects; however, it remains unclear what mechanisms underlie this response or when it develops. If this were also true with premature infants who undergo neonatal intensive care, then infants with parenchymal brain injury (PBI) would be at increased risk of underrecognition and undertreatment of procedural pain. The purpose of this study was to determine whether infants with PBI display altered responses to acute procedural pain at 32 weeks' postconceptional age (PCA), compared with control subjects.

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Paternal uniparental disomy (UPD) for chromosome 15 (UPD15), which is found in approximately 2% of Angelman syndrome (AS) patients, is much less frequent than maternal UPD15, which is found in 25% of Prader-Willi syndrome patients. Such a difference cannot be easily accounted for if 'gamete complementation' is the main mechanism leading to UPD. If we assume that non-disjunction of chromosome 15 in male meiosis is relatively rare, then the gain or loss of the paternal chromosome involved in paternal and maternal UPD15, respectively, may be more likely to result from a post-zygotic rather than a meiotic event.

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More than 50% of spontaneous abortions (SAs) have abnormal chromosomes; the most common abnormalities are trisomy, sex chromosome monosomy, and polyploidy. Conventional cytogenetic analysis of SAs depends on tissue culturing and is associated with a significant tissue culture failure rate and contamination by maternally derived cells. Comparative genomic hybridization (CGH), in combination with flow cytometry (FCM), can detect numerical and unbalanced structural chromosomal abnormalities associated with SAs while avoiding the technical problems associated with tissue culture.

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Although maternal meiotic errors predominate in most studies of nonmosaic trisomy, studies of trisomy ascertained through confined placental mosaicism (CPM) have shown a high rate of somatic errors. However, origin of trisomy of many of the chromosomes involved in CPM has not been evaluated previously in cases ascertained through spontaneous abortions (SAs). Therefore, it was impossible to determine if the relative lack of meiotic errors in trisomy-CPM cases was a characteristic of the specific chromosome involved or due simply to ascertainment through a mosaic state.

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Bedside application of the Neonatal Facial Coding System in pain assessment of premature neonates.

Pain

June 1998

Centre for Community Child Health Research, B.C. Research Institute for Children's and Women's Health, Vancouver, BC V6H 3V4, Canada Department of Paediatrics, University of British Columbia, Vancouver, BC V6H 3V4, Canada B.C.'s Children's Hospital, Vancouver, BC V6H 3V4, Canada.

Assessment of infant pain is a pressing concern, especially within the context of neonatal intensive care where infants may be exposed to prolonged and repeated pain during lengthy hospitalization. In the present study the feasibility of carrying out the complete Neonatal Facial Coding System (NFCS) in real time at bedside, specifically reliability, construct and concurrent validity, was evaluated in a tertiary level Neonatal Intensive Care Unit (NICU). Heel lance was used as a model of procedural pain, and observed with n = 40 infants at 32 weeks gestational age.

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