Time to speed up, not slow down: A narrative review on the importance of community-based physical activity among older people

Introduction: There is now substantial evidence that physical activity reduces the risk of falls and physical disability in later life. Despite encouragement, many older adults are not accruing the health benefits of an active lifestyle. The purpose of this review is to provide an update on the literature specifically highlighting the benefits of regular physical activity (PA) for older adults in the community setting. Methods: An exploratory, narrative review was constructed from peer-reviewed journal articles after a literature database search involving Google Scholar, SPORTDiscus, and PubMed. We considered all types of article and study design written in English language and published with a date range set between 2002 to 2018. Results: A multitude of benefits related to the effects of physical activity with older adults were recognised in the literature search. Two overarching thematical dimensions were formed to represent the findings of this review: 1) functional ability and independence, and 2) psychological health and social connectedness. Our findings showed that community-based group exercise programmes have been found to positively enhance older adult’s physical function, improving mobility and flexibility. The primary components related to successful ageing are: 1) The absence of disease and disability, 2) the maintenance of physical and cognitive function, and 3) continued involvement in social activities. Discussion: While the prescription and community-based programmes for older adults vary in format, structure and effectiveness, it is perhaps more important to promote the general concept of encouraging as many individuals to participate and adhere to sustained PA in later life, particularly as so many benefits are accrued from simply taking part

Examining the New-Member Effect to an Established Community-Based Physical Activity Program for Older Adults in England

Community-based group physical activity programs promote exercise opportunities for older people. The aim of this study was to examine the short-term, new participant effect after joining Vitality, a community-based group physical activity program available in the East of England for older adults. Two independent groups of participants were assessed before and after an 8 week period: a group recruited from the ‘Vitality’ program (VP) (n 15, age: Age = 69.4 ± 6.4 y), and; a non-intervention control (CON) group (n 14, age: 64.5 ± 5.8 y). Assessment outcomes included basic physical health measures, a fitness test battery, and three psychological scales. The VP group recorded statistically significant improvements on the following outcomes: body mass (VP: −1.39 kg/CON: −0.2 kg), body mass index (VP: −1.5 kg/CON: −0.2 kg), 6 min walk (VP: +42.81 m/CON: −0.45 m), 30 s sit-to-stand (VP: −1.7 s/CON: −0.7 s), the chair sit-and-reach (VP: +3.12 cm/CON: +1.90 cm), and the 30 s arm curl test (VP: + 2 reps/CON: +0.9 reps). No significant differences were found with the other outcomes assessed. New members to the Vitality program achieved several physical and functional benefits without regression on any aspects of physical or psychological health

Jersey cattle in Africa: From the Breed's Documented Past to a Profit Index-Linked Future

The aim of this paper was to review the documented reports of the Jersey breed in Africa; and the suitability of the breed for a dairy profit index relevant for the future of Rwanda's dairy development programmes. We extended our review of available reports on the Jersey breed to various African countries to deliver on our main objective of providing relevant knowledge to support long term genetic improvement plans that could be customised to any targeted countries based on the productions systems, constraints, national policies and the local socioeconomic development targets. Through extensive research the authors have confirmed a presence for the Jersey breed across the majority of the continent of Africa, whether current or historic, as a pure breed or used in cross breeding programmes

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

A pilot study exploring performance based emotional intelligence in anorexia nervosa

Previous research has demonstrated that people with anorexia nervosa (AN) experience difficulties in processing emotional states and affective information. Recent explanatory and treatment models of AN and other eating disorders (EDs) hypothesise that these difficulties may contribute to the maintenance of EDs and influence outcome. However, much of the existing literature is based on self-report data, experimental tasks that have questionable ecological validity, and has often not adequately explored potentially confounding effects of IQ and current affective distress. The current study sought to build on existing research and explore emotional processing in AN using a theoretically derived, performance-based measure of emotional intelligence (El). Specifically, this study explored the abilities of people with AN to identify emotions in themselves and others, to understand emotional meaning, use emotions to facilitate thought, and manage their own and others' emotions through their behaviour. A cross-sectional design was employed. Thirty two women with AN and 32 age- and IQ-matched healthy control (HC) women were compared regarding their performance on the Mayer-Salovey-Caruso Emotional Intelligence Test (MSCEIT), along with measures of EO symptomatology, indices of clinical severity, anxiety and depression, social functioning, and the Big Five personality dimensions. Results indicated that women with AN demonstrated El scores within the broadly average range compared to normative data, but exhibited significantly lower overall El compared to HCs in the current study. The two groups did not differ with regard to specific branches of El. El in people with AN was not related to EO symptomatology or indices of illness severity, but it was with anxiety and Agreeableness. Regression analyses indicated that both anxiety and Agreeableness significantly predicted El over and above diagnostic status. The current study suggests that people with AN may not experience particular difficulties in their abilities to reason about emotions and use emotional knowledge to guide their behaviour. Anxiety was highlighted as important in influencing El. 4EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Implementation of a Thue-Mahler equation solver

A practical algorithm for solving an arbitrary Thue-Mahler equation is presented, and its correctness is proved. Methods of algebraic number theory are used to reduce the problem of solving the Thue-Mahler equation to the problem of solving a finite collection of related Diophatine equations having parameters in an algebraic number field. Bounds on the solutions of these equations are computed by employing the theory of linear forms in logarithms of algebraic numbers. Computational Diophantine approximation techniques based on lattice basis reduction are used to reduce the upper bounds to the point where a direct enumerative search of the solution space becomes possible. Such an enumerative search is carried out with the aid of a sieving procedure to finally determine the complete set of solutions of the Thue-Mahler equation. The algorithm is implemented in full generality as a function in the Magma computer algebra system. This is the first time a completely general algorithm for solving Thue-Mahler equations has been implemented as a computer program.Science, Faculty ofMathematics, Department ofGraduat