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1.
CMAJ Open ; 9(2): E413-E423, 2021.
Article in English | MEDLINE | ID: mdl-33863800

ABSTRACT

BACKGROUND: Canada lags behind other countries with respect to wait times for specialist physician and allied health professional consultations. We conducted a systematic review to assess the effects of a single-entry model on waiting time, referral volume and the satisfaction of patients and health care providers. METHODS: We searched MEDLINE, Embase, Cochrane CENTRAL and CINAHL databases from inception to December 2019. We included studies from countries in the Organisation for Economic Co-operation and Development that reported on the effects of a single-entry model on the time between referral to first assessment by a specialist physician or allied health professional, termed wait time 1 (WT1). Patient volume and the satisfaction of providers and patients were secondary outcomes. We conducted a narrative synthesis using descriptive statistics. RESULTS: Of the 4637 citations identified, 17 met the eligibility criteria, and we included 10 of these in the final analysis. All of the included studies reported an absolute reduction in WT1 after implementation of the single-entry model. The average percent reduction in WT1 across specialties was greatest for surgical referrals (57%) and urgent internal medicine referrals (40%). Higher initial WT1 was associated with a greater absolute reduction in WT1 after implementation of the single-entry model (p = 0.002). Patient and provider satisfaction with the single-entry model was high in all studies. The effect estimates from all included studies were at high risk of bias. INTERPRETATION: Single-entry models were associated with an absolute reduction in time from referral from primary care to consultation. These models represent a promising option to improve access to a range of health services, but there is a need for rigorous prospective evaluations to inform policy. PROSPERO REGISTRATION: CRD42018100395.


Subject(s)
Health Services Accessibility/standards , Referral and Consultation , Time-to-Treatment/standards , Waiting Lists , Humans , Models, Organizational , Quality Improvement , Referral and Consultation/organization & administration , Referral and Consultation/standards
2.
Methods Mol Biol ; 1752: 1-9, 2018.
Article in English | MEDLINE | ID: mdl-29564757

ABSTRACT

Genotyping is an invaluable tool for identifying organisms carrying genetic variations including insertions and deletions. This method involves the extraction of DNA from animal tissue samples and subsequent amplification of genomic regions of interest by polymerase chain reaction (PCR). The amplified products are analyzed by agarose gel electrophoresis based on their size.


Subject(s)
DNA/genetics , Genotype , Animals , Electrophoresis, Agar Gel , Mice , Polymerase Chain Reaction
3.
Development ; 144(11): 1976-1987, 2017 06 01.
Article in English | MEDLINE | ID: mdl-28455378

ABSTRACT

Defective fetoplacental vascular maturation causes intrauterine growth restriction (IUGR). A transcriptional switch initiates placental maturation, during which blood vessels elongate. However, the cellular mechanisms and regulatory pathways involved are unknown. We show that the histone methyltransferase G9a, also known as Ehmt2, activates the Notch pathway to promote placental vascular maturation. Placental vasculature from embryos with G9a-deficient endothelial progenitor cells failed to expand owing to decreased endothelial cell proliferation and increased trophoblast proliferation. Moreover, G9a deficiency altered the transcriptional switch initiating placental maturation and caused downregulation of Notch pathway effectors including Rbpj Importantly, Notch pathway activation in G9a-deficient endothelial progenitors extended embryonic life and rescued placental vascular expansion. Thus, G9a activates the Notch pathway to balance endothelial cell and trophoblast proliferation and coordinates the transcriptional switch controlling placental vascular maturation. Accordingly, G9A and RBPJ were downregulated in human placentae from IUGR-affected pregnancies, suggesting that G9a is an important regulator in placental diseases caused by defective vascular maturation.


Subject(s)
Histocompatibility Antigens/metabolism , Histone-Lysine N-Methyltransferase/metabolism , Placenta/blood supply , Receptors, Notch/metabolism , Signal Transduction , Animals , Cell Movement/genetics , Cell Proliferation , Down-Regulation/genetics , Embryo, Mammalian/metabolism , Embryo, Mammalian/ultrastructure , Embryonic Development/genetics , Endothelial Cells/cytology , Endothelial Cells/metabolism , Female , Fetal Growth Retardation/genetics , Gene Expression Regulation, Developmental , Histocompatibility Antigens/genetics , Histone-Lysine N-Methyltransferase/genetics , Humans , Immunoglobulin J Recombination Signal Sequence-Binding Protein/genetics , Immunoglobulin J Recombination Signal Sequence-Binding Protein/metabolism , Mice , Organogenesis/genetics , Placenta/cytology , Placenta/ultrastructure , Pregnancy , Signal Transduction/genetics , Stem Cells/cytology , Stem Cells/metabolism , Transcription, Genetic , Trophoblasts/cytology , Trophoblasts/metabolism
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