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1.
Healthc Q ; 26(2): 6-8, 2023 Jul.
Article in English | MEDLINE | ID: mdl-37572064

ABSTRACT

Canadians are living longer and as they do so, the number of people living with life-limiting illnesses, such as cancer or kidney disease, is growing. Consequently, supporting and improving access to palliative care are goals of Canada's various health sectors. This article uses Canadian Institute for Health Information data from multiple healthcare sectors to investigate how many Canadians receive palliative care in their last year of life, how access to palliative care has changed in the past five years and what barriers to access still exist.


Subject(s)
Neoplasms , Palliative Care , Humans , Health Services Accessibility , Canada
2.
Healthc Q ; 22(4): 10-12, 2020 Jan.
Article in English | MEDLINE | ID: mdl-32073385

ABSTRACT

Federal, provincial and territorial governments endorsed agreements in August of 2017 to focus on the shared health priorities of home, community, mental health and addictions care (Government of Canada 2017). The related $11 billion federal investment over a 10-year period aims to improve access for Canadians to effective and appropriate services in these areas (Government of Canada 2019).


Subject(s)
Health Services Accessibility/statistics & numerical data , Hospitalization/statistics & numerical data , Mental Disorders , Substance-Related Disorders , Adolescent , Adult , Aged , Canada , Child , Community Health Services/statistics & numerical data , Emergency Service, Hospital/statistics & numerical data , Female , Home Care Services/statistics & numerical data , Humans , Length of Stay/statistics & numerical data , Male , Middle Aged , Substance-Related Disorders/mortality
3.
Healthc Q ; 22(2): 10-12, 2019 Jul.
Article in English | MEDLINE | ID: mdl-31556372

ABSTRACT

Harms related to opioid use (whether prescribed or obtained illicitly) represent a growing cause of concern in developed countries, including Australia and Canada.This report examines the characteristics of opioid-related care visits to emergency departments (EDs) or hospital admissions and groups them into five distinct harm profiles. These profiles and their respective distributions illustrate how opioid-related harms differ across care settings in Canada. Opioid dependence and accidental poisoning were the more prominent types of harm seen in EDs, with a rate of 39.2 and 38.0 visits per 100,000 population, respectively. Within the in-patient population, rates of hospital stays were comparatively higher (26.8 per 100,000) for adverse drug reactions compared to other opioid-related harms. In addition to differing patterns in care settings, these harm groups differed on length of hospital stay, types of care received, other drugs involved and demographic variables such as age, gender and income.


Subject(s)
Analgesics, Opioid/adverse effects , Drug Overdose/epidemiology , Opioid-Related Disorders/epidemiology , Adult , Age Factors , Australia/epidemiology , Canada/epidemiology , Emergency Service, Hospital/statistics & numerical data , Female , Hospitalization/statistics & numerical data , Humans , Male , Middle Aged
4.
Healthc Q ; 19(2): 10-12, 2016.
Article in English | MEDLINE | ID: mdl-27700967

ABSTRACT

Good primary care is essential for the effective management of patients with chronic conditions in the community and to ensure their care is well coordinated with other parts of the system. The Commonwealth Fund 2015 International Health Policy Survey compares the views and experiences of primary care physicians in 11 countries including Canada. The survey found nearly all (98%) primary care doctors across countries treat patients with complex needs in their practice. However, when examining questions on chronic disease management and coordination of care with other providers, Canadian results are mixed compared to the international average, and show variation at the provincial level. Opportunities likely exist to learn from other countries that have a more systematic approach to primary care delivery.


Subject(s)
Chronic Disease/therapy , Physicians, Primary Care , Primary Health Care , Canada , Comorbidity , Continuity of Patient Care , Delivery of Health Care/methods , Female , Humans , Male , Surveys and Questionnaires
7.
Diabetes ; 59(10): 2588-96, 2010 Oct.
Article in English | MEDLINE | ID: mdl-20522597

ABSTRACT

OBJECTIVE: Autoimmune target tissues in type 1 diabetes include pancreatic ß-cells and peri-islet Schwann cells (pSC)--the latter active participants or passive bystanders in pre-diabetic autoimmune progression. To distinguish between these alternatives, we sought to suppress pSC autoimmunity by transgenic expression of the negative costimulatory molecule B7-H1 in NOD pSC. RESEARCH DESIGN AND METHODS: A B7-H1 transgene was placed under control of the glial fibrillary acidic protein (GFAP) promoter. Transgenic and wild-type NOD mice were compared for transgene PD-1 affinities, diabetes development, insulitis, and pSC survival. Mechanistic studies included adoptive type 1 diabetes transfer, B7-H1 blockade, and T-cell autoreactivity and sublineage distribution. RESULTS: Transgenic and endogenous B7-H1 bound PD-1 with equal affinities. Unexpectedly, the transgene generated islet-selective CD8(+) bias with accelerated rather than suppressed diabetes progression. T-cells of diabetic transgenics transferred type 1 diabetes faster. There were no earlier pSC losses due to conceivable transgene toxicity, but transgenic pSC loss was enhanced by 8 weeks, preceded by elevated GFAP autoreactivity, with high-affinity T-cells targeting the major NOD K(d)-GFAP epitope, p253-261. FoxP3(+) regulatory T- and CD11c(+) dendritic cell pools were unaffected. CONCLUSIONS: In contrast with transgenic B7-H1 in NOD mouse ß-cells, transgenic B7-H1 in pSC promotes rather than protects from type 1 diabetes. Here, ectopic B7-H1 enhanced the pathogenicity of effector T-cells, demonstrating that pSC can actively impact diabetes progression-likely through modification of intraislet T-cell selection. Although pSC cells emerge as a new candidate for therapeutic targets, caution is warranted with regard to the B7-H1-PD1 axis, where B7-H1 overexpression can lead to accelerated autoimmune disease.


Subject(s)
Antigens, CD/genetics , Diabetes Mellitus, Type 1/genetics , Insulin-Secreting Cells/physiology , Animals , Antigens, CD/analysis , Antigens, CD/metabolism , B7-1 Antigen/genetics , B7-H1 Antigen , Dendritic Cells/immunology , Diabetes Mellitus, Type 1/pathology , Gene Expression , Glial Fibrillary Acidic Protein/genetics , Glial Fibrillary Acidic Protein/metabolism , Histocytochemistry , Humans , Islets of Langerhans/pathology , Lymphocyte Activation , Membrane Glycoproteins/genetics , Mice , Mice, Inbred NOD , Mice, Transgenic , Peptides/genetics , Promoter Regions, Genetic , Surface Plasmon Resonance , T-Lymphocytes/immunology , T-Lymphocytes/physiology
8.
Eur J Immunol ; 39(9): 2629-35, 2009 Sep.
Article in English | MEDLINE | ID: mdl-19662632

ABSTRACT

Obesity is associated with numerous inflammatory conditions including atherosclerosis, autoimmune disease and cancer. Although the precise mechanisms are unknown, obesity-associated rises in TNF-alpha, IL-6 and TGF-beta are believed to contribute. Here we demonstrate that obesity selectively promotes an expansion of the Th17 T-cell sublineage, a subset with prominent pro-inflammatory roles. T-cells from diet-induced obese mice expand Th17 cell pools and produce progressively more IL-17 than lean littermates in an IL-6-dependent process. The increased Th17 bias was associated with more pronounced autoimmune disease as confirmed in two disease models, EAE and trinitrobenzene sulfonic acid colitis. In both, diet-induced obese mice developed more severe early disease and histopathology with increased IL-17(+) T-cell pools in target tissues. The well-described association of obesity with inflammatory and autoimmune disease is mechanistically linked to a Th17 bias.


Subject(s)
Colitis/immunology , Encephalomyelitis, Autoimmune, Experimental/immunology , Interleukin-17/immunology , Obesity/complications , Obesity/immunology , T-Lymphocytes, Helper-Inducer/immunology , Animals , Colitis/etiology , Disease Models, Animal , Encephalomyelitis, Autoimmune, Experimental/etiology , Glycoproteins/pharmacology , Interleukin-6/immunology , Interleukin-6/metabolism , Male , Mice , Mice, Inbred C57BL , Myelin-Oligodendrocyte Glycoprotein , Peptide Fragments/pharmacology , T-Lymphocytes, Helper-Inducer/drug effects , Trinitrobenzenesulfonic Acid/pharmacology
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