Estimating the Potential Health Care Cost-Savings from a Flax-Based Treatment for Hypertension.

Hypertension contributes to the increase in health care spending in Canada through two primary mechanisms. First, it directly increases costs, as individuals with hypertension require medical care to manage the condition. Second, it indirectly raises expenses by serving as a risk factor for numerous chronic diseases, leading to increased health care utilization among those affected.

variants in the non-coding spliceosomal snRNA gene are a frequent cause of syndromic neurodevelopmental disorders.

Around 60% of individuals with neurodevelopmental disorders (NDD) remain undiagnosed after comprehensive genetic testing, primarily of protein-coding genes. Increasingly, large genome-sequenced cohorts are improving our ability to discover new diagnoses in the non-coding genome. Here, we identify the non-coding RNA as a novel syndromic NDD gene.

SARCOPTIC MANGE IN FREE-RANGING NORTH AMERICAN PORCUPINES IN NEW YORK STATE.

Sarcoptic mange causes pruritic and crusting dermatitis in a large number of mammalian species with varying population impacts. Between 2016 and 2022, 15 North American porcupines () were diagnosed with sarcoptic mange at Cornell University's Janet L. Swanson Wildlife Hospital in Ithaca, New York.

Prognostic factors in major depressive disorder: comparing responders and non-responders to Repetitive Transcranial Magnetic Stimulation (rTMS), a naturalistic retrospective chart review.

Aim: Repetitive transcranial magnetic stimulation (rTMS) is widely utilized as an effective treatment for major depressive disorder (MDD) with varying response rates. Factors associated with better treatment outcome remain scarce. This naturalistic retrospective chart review hopes to shed light on easily obtainable and measurable predictive factors for patients referred to rTMS.

Cardiovascular disease and the risk of dementia: a survival analysis using administrative data from Manitoba.

Objectives: Recent research has shown that cardiovascular disease (CVD) raises the risk of dementia and other forms of cognitive decline. Generally, these studies are unable to model the time of diagnosis of CVD in their analyses and treat CVD as a time-fixed variable. Our objective was to assess the risk of being diagnosed with dementia for individuals diagnosed with CVD when CVD is time-dependent.

Examining differences in diet quality between Canadian Indigenous and non-Indigenous adults: results from the 2004 and 2015 Canadian Community Health Survey Nutrition Surveys.

Objectives: The Truth and Reconciliation Commission includes a call to action to close gaps in health outcomes, including type 2 diabetes, of which diet quality must be considered an important mediator. The objectives of this study were to compare diet quality between off-reserve Indigenous and non-Indigenous adults in 2004 and 2015, and examine food security as a predictor of diet quality.

Methods: We employed a repeated cross-sectional design using the 2004 and 2015 Canadian Community Health Surveys-Nutrition.

Demographic and Clinical Presentations of Youth using Enhanced Mental Health Services in Six Indigenous Communities from the ACCESS Open Minds Network.

Objective: In many Indigenous communities, youth mental health services are inadequate. Six Indigenous communities participating in the ACCESS Open Minds (AOM) network implemented strategies to transform their youth mental health services. This report documents the demographic and clinical presentations of youth accessing AOM services at these Indigenous sites.

Clustering patients and caregivers for technology design: A step prior to the design of an innovative technological device for the detection of epileptic seizures.

Aims: Seizure detection using heart rate variability, from a detailed analysis by deep learning analysis system, may help patients with epilepsy to manage their symptoms. This exploratory study aims to identify patient and caregiver groups, according to acceptability factors.

Methods: Two versions of the same questionnaire were designed to survey quality of life, self-efficacy, and patients with epilepsy and caregivers on seizure detection acceptability using a patch, after watching a video that described a patch connected to a companion application.

Diet quality among Indigenous and non-Indigenous children and youth in Canada in 2004 and 2015: a repeated cross-sectional design.

Objective: The objectives were to describe changes in diet quality between off-reserve Indigenous and non-Indigenous children and youth from 2004 to 2015 and examine the association between food security and diet quality.

Design: We utilised a repeated cross-sectional design using both the 2004 and 2015 nutrition-focused Canadian Community Health Surveys, including 24-h dietary recall. Diet quality was estimated according to the Healthy Eating Index (HEI).

The financial impact of cancer on Canadian young adults.

Purpose: To explore the financial impact of cancer in young adults (YAs) compared to matched non-cancer peers.

Methods: Five hundred seventy-five YAs from the Young Adults with Cancer in their Prime (YACPRIME) study reported on out-of-pocket cancer costs and missed work. YA cancer survivors were compared to matched peers without cancer on key financial indices based on current age (< 35 vs.

Impact of Age, Menopause, and Obesity on Oxylipins Linked to Vascular Health.

Objective: Cardiovascular disease, a major cause of mortality and morbidity, exhibits sexual dimorphism since the onset of cardiovascular disease occurs later in women than in men. The loss of cardioprotection in older women may be due to an increase in arterial stiffness after menopause. Free fatty acid metabolites of polyunsaturated fatty acids, called oxylipins, are known to impact vessel function and may be responsible for the vascular benefits of polyunsaturated fatty acids.

O brother how art thou: Propensity to report self-assessed unmet need.

Research investigating self-assessed unmet need (SUN) has taken the reports from surveys as given and subsequently attempted to discover patterns in inequality of access to healthcare. This requires the yet untested assumption that, given a certain level of care and demand, the likelihood of reporting unmet need does not vary across socioeconomic/demographic status (SEDS), be satisfied. Using an administrative dataset spanning 2001 to 2011 comprised of sufferers of a set of conditions that suggest unmet need (n = 3300) we evaluate the proposition that, given health status and care received, the propensity to report unmet need does not vary along SEDS.

The 18th Rocky Mountain Virology Association Meeting.

This autumn, approximately 100 scientists and students from the Rocky Mountain area along with invited speakers attended the 18th annual meeting of the Rocky Mountain Virology Association that was held at the Colorado State University Mountain Campus. The two-day gathering featured 31 talks and 33 posters all of which focused on specific areas of current virology and prion protein research. Since the keynote presentation focused on the oligoadenylate synthetase-ribonuclease L pathway the main area of focus was on host⁻virus interactions, however other areas of interest included virus vectors, current models of virus infections, prevention and treatment of virus infections, separate sessions on RNA viruses and prion proteins, and a special talk highlighting various attributes of targeted next-generation sequencing.

Endotoxin tolerance from lipopolysaccharide pretreatment induces nuclear factor-kappaB alterations not present in C3H/HeJ mice.

Background: Lipopolysaccharide (LPS) activation of macrophage (MO) cytokine secretion requires activation and translocation of nuclear factor-kappaB (NF-kappaB). Endotoxin tolerance induced in LPS-responsive C3H/HeN MOs by LPS pretreatment results in decreased tumor necrosis factor (TNF) secretion and altered NF-kappaB activation. C3H/HeJ MOs have a genetic defect that renders them tolerant to LPS activation.

Defective lipopolysaccharide-dependent ERK 1/2 activation in endotoxin tolerant murine macrophages is reversed by direct protein kinase C stimulation.

Lipopolysaccharide (LPSp) pretreatment inhibits TNF secretion in endotoxin-tolerant macrophages via alterations in signal transduction pathways of LPS activation (LPSa). Protein kinase C inhibitors prevent TNF release in response to LPSa and direct protein kinase C activation with phorbol myristate acetate (PMA) restores TNF secretion after LPSp. In the current experiments the effect of protein kinase C modulation on LPSa-stimulated ERK 1/2 activation was investigated.

Macrophage TNF secretion in endotoxin tolerance: role of SAPK, p38, and MAPK.

Purpose: Endotoxin (LPS) activation of macrophages results in phosphorylation of mitogen-activated protein kinases (MAPK), stress-activated protein kinases (SAPK), and p38 kinase. LPS pretreatment inhibits subsequent LPS-stimulated MAPK activation and TNF release and both were reversed if macrophages were treated with phorbol myristate acetate (PMA) before LPS stimulation. In this study we sought to determine if SAPK and p38 tyrosine kinases are required for TNF production and if LPS pretreatment alters their activation.

In vitro macrophage endotoxin tolerance: defective in vitro macrophage map kinase signal transduction after LPS pretreatment is not present in macrophages from C3H/HeJ endotoxin resistant mice.

Altered endotoxin (LPS) signal transduction in macrophages (Mphi) may mediate development of organ dysfunction in sepsis. C3H/HeJ Mphi have a specific genetic defect that renders them "tolerant" to in vitro LPS activation. LPS tolerance can be induced in normal C3H/HeN Mphi following in vitro LPS pretreatment.

Lipopolysaccharide pretreatment produces macrophage endotoxin tolerance via a serum-independent pathway.

Background: Lipopolysaccharide activation (LPSa) of macrophages is thought to occur via a CD14-dependent mechanism with a requirement for the serum factor, lipopolysaccharide binding protein. LPS-stimulated, CD14-dependent signal transduction is associated with phosphorylation of mitogen-activated protein kinase (MAPK), nuclear factor-kappaB (NF-kappaB) translocation, and secretion of tumor necrosis factor (TNF) and interleukin-1 (IL-1). Macrophage endotoxin tolerance after low-dose LPS pretreatment (LPSp) is characterized by inhibition of LPSa-stimulated TNF and augmentation of IL-1 secretion.

Protein kinase C regulates macrophage tumor necrosis factor secretion: direct protein kinase C activation restores tumor necrosis factor production in endotoxin tolerance.

Background: Macrophages pretreated in vitro with endotoxin (LPSp) secrete less tumor necrosis factor (TNF) in response to a second LPS activating (LPSa) stimulus. Protein kinase C (PKC) is required for TNF secretion in a macrophage stimulated with LPSa. In these experiments we examined the role of PKC in TNF signal transduction in naive and tolerant macrophages.

In vivo endotoxin tolerance: impaired LPS-stimulated TNF release of monocytes from patients with sepsis, but not SIRS.

In vitro pretreatment of human monocytes (MO) with low-dose lipopolysaccharide (LPSp) inhibits TNF release in response to subsequent LPSa activation. Septic patients are often indistinguishable from patients with systemic inflammatory response syndrome (SIRS). We hypothesized that in vivo exposure to "septic" stimuli impairs subsequent LPSa-stimulated MO TNF production in vitro.

LPS pretreatment reprograms macrophage LPS-stimulated TNF and IL-1 release without protein tyrosine kinase activation.

Pretreatment of macrophages with low-dose endotoxin (LPSp) profoundly alters cytokine release in response to subsequent LPSa activation. These qualitative and quantitative alterations in cytokine release have been termed macrophage reprogramming. Macrophage activation by LPS is thought to occur via a mechanism involving an early protein tyrosine kinase (PTK) phosphorylation step.

Role of calcium in lipopolysaccharide-stimulated tumor necrosis factor and interleukin-1 signal transduction in naive and endotoxin-tolerant murine macrophages.

Objective: Dysregulated macrophage cytokine production may predispose to organ failure during sepsis. Macrophages pretreated in vitro with low-dose endotoxin (LPSp) become "tolerant" to subsequent lipopolysaccharide (LPS) activation (LPSa), characterized by inhibition of tumor necrosis factor (TNF) and augmentation of interleukin-1 (IL-1). To understand cytokine dysregulation we examined the Ca2+ dependence of TNF and IL-1 signal transduction to LPSa and whether it was altered by LPSp.

Discordant reprogramming of LPS-stimulated cytokine gene transcription and secretion by macrophages after LPS pretreatment.

Dysregulated macrophage (Mphi) cytokine release occurs during systemic inflammation and may predispose to organ failure. We showed that Mphis pretreated (PreRx) in vitro with low-dose LPSp are "reprogrammed" to release less TNF and more IL-1 in response to subsequent LPS activation (LPSa). The effects of this LPSp "reprogramming" on Mphi cytokine gene transcription were investigated in the present study.

Reprogrammed macrophage tumor necrosis factor and interleukin-1 release with inflammatory pretreatment: differential regulation by endotoxin and zymosan.

Objective: To determine whether different reprogrammed alterations in endotoxin (lipopolysaccharide, LPS)-stimulated tumor necrosis factor (TNF) and interleukin-1 (IL-1) release are seen following pretreatment with endotoxin (LPSp) or pretreatment with the particulate inflammatory stimulus zymosan.

Methods: Murine peritoneal macrophages (M phi) pretreated for 24 hours in vitro with medium, LPSp, zymosan, latex beads, or killed Escherichia coli. After 24 hours M phi were restimulated with medium, LPSa, zymosan, latex beads, or E.

Mechanisms of reprogrammed macrophage endotoxin signal transduction after lipopolysaccharide pretreatment.

Background: Dysregulation of macrophage tumor necrosis factor (TNF) and interleukin-(IL-1) release results from repetitive lipopolysacharride (LPS) stimulation. In this study we investigated the mechanisms of LPS pretreatment (LPSp) signal transduction producing altered LPS-activated (LPSa) cytokine release.

Methods: Murine macrophages were treated with medium alone, actinomycin D, cycloheximide, a protein kinase C inhibitor (H7), or the nitric oxide synthase inhibitor L-NMA.