Social factors influencing utilization of home care in community-dwelling older adults: a scoping review

Background: Older adults want to live at home as long as possible, even in the face of circumstances that limit their autonomy. Home care services reflect this emergent preference, allowing older adults to ‘age in place’ in familiar settings rather than receiving care for chronic health conditions or ageing needs in an institutionalized setting. Numerous social factors, generally studied in isolation, have been associated with home care utilization. Even so, social circumstances are complex and how these factors collectively influence home care use patterns remains unclear. Objectives: To provide a broad and comprehensive overview of the social factors influencing home care utilization; and to evaluate the influence of discrete social factors on patterns of home care utilization in community-dwelling older adults in high-income countries. Methods: A scoping review was conducted of six electronic databases for records published between 2010 and 2020; additional records were obtained from hand searching review articles, reference lists of included studies and documents from international organisations. A narrative synthesis was presented, complemented by vote counting per social factor, harvest plots and an evaluation of aggregated findings to determine consistency across studies. Results: A total of 2,365 records were identified, of which 66 met inclusion criteria. There were 35 discrete social factors grouped into four levels of influence using a socio-ecological model (individual, relationship, community and societal levels) and grouped according to outcome of interest (home care propensity and intensity). Across all studies, social factors consistently showing any association (positive, negative, or equivocal in pattern) with home care propensity were: age, ethnicity/race, self-assessed health, insurance, housing ownership, housing problems, marital status, household income, children, informal caregiving, social networks and urban/rural area. Age, education, personal finances, living arrangements and housing ownership were associated with home care intensity, also with variable patterns in utilization. Additional community and societal level factors were identified as relevant but lacking consistency across the literature; these included rurality, availability of community services, methods of financing home care systems, and cultural determinants. Conclusion: This is the first literature review bringing together a wide range of reported social factors that influence home care utilization. It confirms social factors do influence home care utilization in complex interactions, distinguishes level of influences at which these factors affect patterns of use and discusses policy implications for home care reform

Amelioration of the neuroinhibitory local environment after ischemic injury through in situ astrocyte-to-neuron conversion

Ischemic injury in central nervous system (CNS) often causes severe neuronal loss and activates glial cells. We showed earlier that NeuroD1-mediated astrocyte-to-neuron (AtN) conversion can regenerate a substantial proportion of neurons (~40% of the total) and reconstruct the ischemic injured neural circuits. In this study, we focus on glial changes and blood vessel recovery following AtN conversion. Specifically, we found that ectopic expression of NeuroD1 in the reactive astrocytes after ischemic injury significantly reduced glial reactivity, as shown by less hypertrophic morphology, along with reduced secretion of neuroinhibitory factors such as CSPG and LCN2. As for microglia, we found less amoeboid shape of reactive microglia with reduced inflammatory factors such as IL-1β, TNFα. Moreover, blood vessels in the injured areas were repaired after AtN conversion and the blood-brain-barrier structure was restored. Whole tissue transcriptome sequencing identified significantly reduced reactive astrocyte genes and proinflammatory genes, as well as an upregulation of neurogenesis pathway and angiogenesis genes. Together, we demonstrate that NeuroD1-mediated astrocyte-to-neuron (AtN) conversion can alleviate glial scarring and inflammation to create a more neuropermissive micro-environment for functional recovery

Amphetamine-evoked c- fos mRNA expression in the caudate-putamen: the effects of DA and NMDA receptor antagonists vary as a function of neuronal phenotype and environmental context

Dopamine (DA) and glutamate neurotransmission is thought to be critical for psychostimulant drugs to induce immediate early genes (IEGs) in the caudate-putamen (CPu). We report here, however, that the ability of DA and glutamate NMDA receptor antagonists to attenuate amphetamine-evoked c- fos mRNA expression in the CPu depends on environmental context. When given in the home cage, amphetamine induced c- fos mRNA expression predominately in preprodynorphin and preprotachykinin mRNA-containing neurons (Dyn-SP+ cells) in the CPu. In this condition, all of the D1R, D2R and NMDAR antagonists tested dose-dependently decreased c- fos expression in Dyn-SP+ cells. When given in a novel environment, amphetamine induced c- fos mRNA in both Dyn-SP+ and preproenkephalin mRNA-containing neurons (Enk+ cells). In this condition, D1R and non-selective NMDAR antagonists dose-dependently decreased c- fos expression in Dyn-SP+ cells, but neither D2R nor NR2B-selective NMDAR antagonists had no effect. Furthermore, amphetamine-evoked c- fos expression in Enk+ cells was most sensitive to DAR and NMDAR antagonism; the lowest dose of every antagonist tested significantly decreased c- fos expression only in these cells. Finally, novelty-stress also induced c- fos expression in both Dyn-SP+ and Enk+ cells, and this was relatively resistant to all but D1R antagonists. We suggest that the mechanism(s) by which amphetamine evokes c- fos expression in the CPu varies depending on the stimulus (amphetamine vs. stress), the striatal cell population engaged (Dyn-SP+ vs. Enk+ cells), and environmental context (home vs. novel cage).Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66272/1/j.1471-4159.2003.01815.x.pd

Strengthening a One Health approach to emerging zoonoses

Given the enormous global impact of the COVID-19 pandemic, outbreaks of highly pathogenic avian influenza in Canada, and manifold other zoonotic pathogen activity, there is a pressing need for a deeper understanding of the human-animal-environment interface and the intersecting biological, ecological, and societal factors contributing to the emergence, spread, and impact of zoonotic diseases. We aim to apply a One Health approach to pressing issues related to emerging zoonoses, and propose a functional framework of interconnected but distinct groups of recommendations around strategy and governance, technical leadership (operations), equity, education and research for a One Health approach and Action Plan for Canada. Change is desperately needed, beginning by reorienting our approach to health and recalibrating our perspectives to restore balance with the natural world in a rapid and sustainable fashion. In Canada, a major paradigm shift in how we think about health is required. All of society must recognize the intrinsic value of all living species and the importance of the health of humans, other animals, and ecosystems to health for all

Activity pacing for osteoarthritis symptom management: study design and methodology of a randomized trial testing a tailored clinical approach using accelerometers for veterans and non-veterans

<p>Abstract</p> <p>Background</p> <p>Osteoarthritis (OA) is a prevalent chronic disease and a leading cause of disability in adults. For people with knee and hip OA, symptoms (e.g., pain and fatigue) can interfere with mobility and physical activity. Whereas symptom management is a cornerstone of treatment for knee and hip OA, limited evidence exists for behavioral interventions delivered by rehabilitation professionals within the context of clinical care that address how symptoms affect participation in daily activities. Activity pacing, a strategy in which people learn to preplan rest breaks to avoid symptom exacerbations, has been effective as part of multi-component interventions, but hasn't been tested as a stand-alone intervention in OA or as a tailored treatment using accelerometers. In a pilot study, we found that participants who underwent a tailored activity pacing intervention had reduced fatigue interference with daily activities. We are now conducting a full-scale trial.</p> <p>Methods/Design</p> <p>This paper provides a description of our methods and rationale for a trial that evaluates a tailored activity pacing intervention led by occupational therapists for adults with knee and hip OA. The intervention uses a wrist accelerometer worn during the baseline home monitoring period to glean recent symptom and physical activity patterns and to tailor activity pacing instruction based on how symptoms relate to physical activity. At 10 weeks and 6 months post baseline, we will examine the effectiveness of a tailored activity pacing intervention on fatigue, pain, and physical function compared to general activity pacing and usual care groups. We will also evaluate the effect of tailored activity pacing on physical activity (PA).</p> <p>Discussion</p> <p>Managing OA symptoms during daily life activity performance can be challenging to people with knee and hip OA, yet few clinical interventions address this issue. The activity pacing intervention tested in this trial is designed to help people modulate their activity levels and reduce symptom flares caused by too much or too little activity. As a result of this trial, we will be able to determine if activity pacing is more effective than usual care, and among the intervention groups, if an individually tailored approach improves fatigue and pain more than a general activity pacing approach.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov: <a href="http://www.clinicaltrials.gov/ct2/show/NCT01192516">NCT01192516</a></p

Depressive Symptoms in Children with Chronic Kidney Disease

To assess depression in children with chronic kidney disease (CKD) and to determine associations with patient characteristics, intellectual and educational levels, and health related quality of life (HRQoL)

Ensembl’s 10th year

Ensembl (http://www.ensembl.org) integrates genomic information for a comprehensive set of chordate genomes with a particular focus on resources for human, mouse, rat, zebrafish and other high-value sequenced genomes. We provide complete gene annotations for all supported species in addition to specific resources that target genome variation, function and evolution. Ensembl data is accessible in a variety of formats including via our genome browser, API and BioMart. This year marks the tenth anniversary of Ensembl and in that time the project has grown with advances in genome technology. As of release 56 (September 2009), Ensembl supports 51 species including marmoset, pig, zebra finch, lizard, gorilla and wallaby, which were added in the past year. Major additions and improvements to Ensembl since our previous report include the incorporation of the human GRCh37 assembly, enhanced visualisation and data-mining options for the Ensembl regulatory features and continued development of our software infrastructure

Report on ISCTM consensus meeting on clinical assessment of response to treatment of cognitive impairment in schizophrenia

Funding for this manuscript was provided by the International Society for CNS Clinical Trials and Methodology.Dr Keefe currently or in the past 3 years has received investigator-initiated research funding support from the Department of Veteran's Affair, Feinstein Institute for Medical Research, GlaxoSmithKline, National Institute of Mental Health, Novartis, Psychogenics, Research Foundation for Mental Hygiene, Inc., and the Singapore National Medical Research Council. He currently or in the past 3 years has received honoraria, served as a consultant, or advisory board member for Abbvie, Akebia, Amgen, Asubio, AviNeuro/ChemRar, BiolineRx, Biogen Idec, Biomarin, Boehringer-Ingelheim, Eli Lilly, EnVivo/FORUM, GW Pharmaceuticals, Janssen, Lundbeck, Merck, Minerva Neurosciences, Inc., Mitsubishi, Novartis, NY State Office of Mental Health, Otsuka, Pfizer, Reviva, Roche, Sanofi/Aventis, Shire, Sunovion, Takeda, Targacept, and the University of Texas South West Medical Center. Dr Keefe receives royalties from the BACS testing battery, the MATRICS battery (BACS Symbol Coding), and the Virtual Reality Functional Capacity Assessment Tool. He is also a shareholder in NeuroCog Trials, Inc. and Sengenix. Dr Haig is a full-time employee of Abbvie. Dr Marder has received consulting fees from Abbvie, Genentech, Roche, Lundbeck, Pfizer, Otsuka, Takeda, and Boeringer Ingelheim. He has received research support from Amgen, Sunovion, and Synchroneuron. Dr Harvey has received consulting fees from Abbvie, Boehringer Ingelheim, Forest Labs, Forum Pharma, Genentech, Otsuka America, Roche Pharma, Sunovion Pharma, and Takeda Pharma during the past year. He also received contract research support from Genentech. Dr Dunayevich for the past 3 years has been a full-time employee and stockholder of Amgen. Dr Medalia in the past 3 years has received research funding support from Sunovion. Dr Medalia has also currently or in the past 3 years received honoraria or served as consultant for Dainippon Sumitomo Pharma Co., Ltd., Otsuka, and Takeda Pharmaceuticals U.S.A., Inc. Dr Davidson has received research grant support and/or travel support and/or speaker fees and/or consultancy fees from Lundbeck, Eli Lilly, Servier, Abbott, Minerva and holds stocks in CTR and BiolineRx. Dr Lombardo is a full-time employee of FORUM Pharmaceuticals. Dr Bowie reports receiving grant support from Pfizer. He has also been a consultant for Lundbeck, Otsuka, Abbvie, and Takeda. Dr Buchanan reports: Advisory Board: Abbvie, Amgen, EnVivo, Roche; Consultant: Abbvie, Amgen, Bristol Myers Squibb, EnVivo, Omeros; DSMB member: Pfizer. Dr Bugarski -Kirola is a full-time employee of Hoffmann-La Roche Ltd. Dr Carpenter in the past 2 years has been a consultant to Roche/Genetech. Dr Dago in the last 3 years has received honoraria from Lundbeck, Forest Pharmaceuticals, Otsuka, Pam Labs, and Astra Zeneca for lectures given in promotion of their psychotropic medications. Dr Durand in the past year has been a consultant and received honoraria from Teva Pharmaceuticals. Dr Gold receives royalty payments from the BACS. He also has served as a consultant for Amgen, Hoffman LaRoche, and Lundbeck. Dr Hooker has served as a consultant and is currently a Co-Investigator on an NIH SBIR grant with PositScience Corporation. Dr Loebel is an employee of Sunovion Pharmaceuticals. Dr McGurk reports receiving consulting fees from Abbvie and EnVivo Pharmaceuticals. Dr Pinkham in the past year has received consulting fees from Otsuka America Pharmaceutical, Inc.The following authors have declared that there are no conflicts of interest in relation to the subject of this study: Drs Csernansky, Frese, Goff, Kopelowic, Opler, and Stern. (International Society for CNS Clinical Trials and Methodology; Department of Veteran's Affair; Feinstein Institute for Medical Research; GlaxoSmithKline; National Institute of Mental Health; Novartis; Psychogenics; Research Foundation for Mental Hygiene, Inc.; Singapore National Medical Research Council; Abbvie; Genentech; Roche; Lundbeck; Pfizer; Otsuka; Takeda; Boeringer Ingelheim; Amgen; Sunovion; Synchroneuron; Boehringer Ingelheim; Forest Labs; Forum Pharma; Otsuka America; Roche Pharma; Sunovion Pharma; Takeda Pharma; Eli Lilly; Servier; Abbott; Minerva; BACS; EnVivo Pharmaceuticals; Otsuka America Pharmaceutical, Inc.)Published versio

KrasP34R and KrasT58I mutations induce distinct RASopathy phenotypes in mice.

Somatic KRAS mutations are highly prevalent in many cancers. In addition, a distinct spectrum of germline KRAS mutations causes developmental disorders called RASopathies. The mutant proteins encoded by these germline KRAS mutations are less biochemically and functionally activated than those in cancer. We generated mice harboring conditional KrasLSL-P34Rand KrasLSL-T58I knock-in alleles and characterized the consequences of each mutation in vivo. Embryonic expression of KrasT58I resulted in craniofacial abnormalities reminiscent of those seen in RASopathy disorders, and these mice exhibited hyperplastic growth of multiple organs, modest alterations in cardiac valvulogenesis, myocardial hypertrophy, and myeloproliferation. By contrast, embryonic KrasP34R expression resulted in early perinatal lethality from respiratory failure due to defective lung sacculation, which was associated with aberrant ERK activity in lung epithelial cells. Somatic Mx1-Cre-mediated activation in the hematopoietic compartment showed that KrasP34R and KrasT58I expression had distinct signaling effects, despite causing a similar spectrum of hematologic diseases. These potentially novel strains are robust models for investigating the consequences of expressing endogenous levels of hyperactive K-Ras in different developing and adult tissues, for comparing how oncogenic and germline K-Ras proteins perturb signaling networks and cell fate decisions, and for performing preclinical therapeutic trials