Interventions to Promote More Effective Balance-Recovery Reactions in Industrial Settings: New Perspectives on Footwear and Handrails

“Change-in-support” balance-recovery reactions that involve rapid stepping or reaching movements play a critical role in preventing falls. Recent geriatrics studies have led to new interventions to improve ability to execute these reactions effectively. Some of these interventions have the potential to reduce fall risk for younger persons working in industrial settings. In this paper, we review research pertaining to two such interventions: 1) balance-enhancing footwear insoles designed to improve stepping reactions, and 2) proximity-triggered handrail cueing systems designed to improve reach-to-grasp reactions. The insole has a raised ridge around the perimeter that is intended to improve balance control by providing increased stimulation of sensory receptors on the footsole in situations where loss of balance may be imminent. The cueing system uses flashing lights and/or verbal prompts to attract attention to the handrail and ensure that the brain registers its location, thereby facilitating more rapid and accurate grasping of the rail if and when sudden loss of balance occurs. Results to date support the efficacy of both interventions in geriatric populations. There is also some evidence that these interventions may improve balance control in younger persons; however, further research is needed to confirm their efficacy in preventing falls in industrial settings

Relationships Effecting College Students’ Perception of Family Influence Impacting their Health and Lifestyle

The purpose of this cross-sectional, nonexperimental descriptive design study was to determine college students’ perception of family influence impacting their health and lifestyle. The sample included 120 college students in a faithbased institution and each student completed a Likert-type survey (4-point agreement scale) that investigated their perception of health, and the degree of influence peers and family had on their health. This second data analysis reports correlations between variables and group differences related to health perceptions and behaviours. The strongest correlation is between ‘family demonstration of positive health habits’ and ‘personal health practices being like my families’ (r = 0.671, p \u3c 0.01), a moderate relationship supported by other weaker positive correlations to specific health outcomes. Negative correlations between ‘my friends display more positive health habits than family’ and both ‘family has influenced my idea of health’ and ‘my health practices are similar to my family’ indicate the potential for other contextual factors to effect family impact. While differences relating to health influence and outcomes between groups formed by age, gender, ethnicity, family structure and religion were found, the variable related to most healthy lifestyle transmission elements was ‘My family demonstrates positive health habits’. Recommendations supporting improved societal health are offered, together with suggestions for further research. Group classifications that are fixed but might inform interactions with elements of cohorts are identified, together with group memberships which might be changed to enhance health options. Caution in the generalisation of these findings is advised due to the explained limitations of this study

The potential shared role of inflammation in insulin resistance and schizophrenia:a bidirectional two-sample mendelian randomization study

BACKGROUND: Insulin resistance predisposes to cardiometabolic disorders, which are commonly comorbid with schizophrenia and are key contributors to the significant excess mortality in schizophrenia. Mechanisms for the comorbidity remain unclear, but observational studies have implicated inflammation in both schizophrenia and cardiometabolic disorders separately. We aimed to examine whether there is genetic evidence that insulin resistance and 7 related cardiometabolic traits may be causally associated with schizophrenia, and whether evidence supports inflammation as a common mechanism for cardiometabolic disorders and schizophrenia. METHODS AND FINDINGS: We used summary data from genome-wide association studies of mostly European adults from large consortia (Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC) featuring up to 108,557 participants; Diabetes Genetics Replication And Meta-analysis (DIAGRAM) featuring up to 435,387 participants; Global Lipids Genetics Consortium (GLGC) featuring up to 173,082 participants; Genetic Investigation of Anthropometric Traits (GIANT) featuring up to 339,224 participants; Psychiatric Genomics Consortium (PGC) featuring up to 105,318 participants; and Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium featuring up to 204,402 participants). We conducted two-sample uni- and multivariable mendelian randomization (MR) analysis to test whether (i) 10 cardiometabolic traits (fasting insulin, high-density lipoprotein and triglycerides representing an insulin resistance phenotype, and 7 related cardiometabolic traits: low-density lipoprotein, fasting plasma glucose, glycated haemoglobin, leptin, body mass index, glucose tolerance, and type 2 diabetes) could be causally associated with schizophrenia; and (ii) inflammation could be a shared mechanism for these phenotypes. We conducted a detailed set of sensitivity analyses to test the assumptions for a valid MR analysis. We did not find statistically significant evidence in support of a causal relationship between cardiometabolic traits and schizophrenia, or vice versa. However, we report that a genetically predicted inflammation-related insulin resistance phenotype (raised fasting insulin (raised fasting insulin (Wald ratio OR = 2.95, 95% C.I, 1.38–6.34, Holm-Bonferroni corrected p-value (p) = 0.035) and lower high-density lipoprotein (Wald ratio OR = 0.55, 95% C.I., 0.36–0.84; p = 0.035)) was associated with schizophrenia. Evidence for these associations attenuated to the null in multivariable MR analyses after adjusting for C-reactive protein, an archetypal inflammatory marker: (fasting insulin Wald ratio OR = 1.02, 95% C.I, 0.37–2.78, p = 0.975), high-density lipoprotein (Wald ratio OR = 1.00, 95% C.I., 0.85–1.16; p = 0.849), suggesting that the associations could be fully explained by inflammation. One potential limitation of the study is that the full range of gene products from the genetic variants we used as proxies for the exposures is unknown, and so we are unable to comment on potential biological mechanisms of association other than inflammation, which may also be relevant. CONCLUSIONS: Our findings support a role for inflammation as a common cause for insulin resistance and schizophrenia, which may at least partly explain why the traits commonly co-occur in clinical practice. Inflammation and immune pathways may represent novel therapeutic targets for the prevention or treatment of schizophrenia and comorbid insulin resistance. Future work is needed to understand how inflammation may contribute to the risk of schizophrenia and insulin resistance

A Quantitative System for Studying Metastasis Using Transparent Zebrafish

Metastasis is the defining feature of advanced malignancy, yet remains challenging to study in laboratory environments. Here, we describe a high-throughput zebrafish system for comprehensive, in vivo assessment of metastatic biology. First, we generated several stable cell lines from melanomas of transgenic mitfa-BRAF[superscript V600E];p53[superscript −/−] fish. We then transplanted the melanoma cells into the transparent casper strain to enable highly quantitative measurement of the metastatic process at single-cell resolution. Using computational image analysis of the resulting metastases, we generated a metastasis score, μ, that can be applied to quantitative comparison of metastatic capacity between experimental conditions. Furthermore, image analysis also provided estimates of the frequency of metastasis-initiating cells (∼1/120,000 cells). Finally, we determined that the degree of pigmentation is a key feature defining cells with metastatic capability. The small size and rapid generation of progeny combined with superior imaging tools make zebrafish ideal for unbiased high-throughput investigations of cell-intrinsic or microenvironmental modifiers of metastasis. The approaches described here are readily applicable to other tumor types and thus serve to complement studies also employing murine and human cell culture systems.National Institutes of Health (U.S.) (Directors New Innovator Award DP2CA186572 and K08AR055368)Melanoma Research Alliance (Young Investigator Award)American Association for Cancer Research/American Society of Clinical Oncology (Young Investigator Award)Memorial Sloan-Kettering Cancer Center. Alan and Sandra Gerry Metastasis Research InitiativeHoward Hughes Medical Institut

Physical Activity-Related Policy and Environmental Strategies to Prevent Obesity in Rural Communities: A Systematic Review of the Literature, 2002-2013

Citation: Meyer, M. R. U., Perry, C. K., Sumrall, J. C., Patterson, M. S., Walsh, S. M., Clendennen, S. C., . . . Valko, C. (2016). Physical Activity-Related Policy and Environmental Strategies to Prevent Obesity in Rural Communities: A Systematic Review of the Literature, 2002-2013. Preventing Chronic Disease, 13, 24. doi:10.5888/pcd13.150406Additional Authors: Valko, C.Introduction Health disparities exist between rural and urban residents; in particular, rural residents have higher rates of chronic diseases and obesity. Evidence supports the effectiveness of policy and environmental strategies to prevent obesity and promote health equity. In 2009, the Centers for Disease Control and Prevention recommended 24 policy and environmental strategies for use by local communities: the Common Community Measures for Obesity Prevention (COCOMO); 12 strategies focus on physical activity. This review was conducted to synthesize evidence on the implementation, relevance, and effectiveness of physical activity-related policy and environmental strategies for obesity prevention in rural communities. Methods A literature search was conducted in PubMed, PsycINFO, Web of Science, CINHAL, and PAIS databases for articles published from 2002 through May 2013 that reported findings from physical activity-related policy or environmental interventions conducted in the United States or Canada. Each article was extracted independently by 2 researchers. Results Of 2,002 articles, 30 articles representing 26 distinct studies met inclusion criteria. Schools were the most common setting (n = 18 studies). COCOMO strategies were applied in rural communities in 22 studies; the 2 most common COCOMO strategies were "enhance infrastructure supporting walking" (n = 11) and " increase opportunities for extracurricular physical activity" (n = 9). Most studies (n = 21) applied at least one of 8 non-COCOMO strategies; the most common was increasing physical activity opportunities at school outside of physical education (n = 8). Only 14 studies measured or reported physical activity outcomes (10 studies solely used self-report); 10 reported positive changes. Conclusion Seven of the 12 COCOMO physical activity-related strategies were successfully implemented in 2 or more studies, suggesting that these 7 strategies are relevant in rural communities and the other 5 might be less applicable in rural communities. Further research using robust study designs and measurement is needed to better ascertain implementation success and effectiveness of COCOMO and non-COCOMO strategies in rural communities

UBVRI Light Curves of 44 Type Ia Supernovae

We present UBVRI photometry of 44 type-Ia supernovae (SN Ia) observed from 1997 to 2001 as part of a continuing monitoring campaign at the Fred Lawrence Whipple Observatory of the Harvard-Smithsonian Center for Astrophysics. The data set comprises 2190 observations and is the largest homogeneously observed and reduced sample of SN Ia to date, nearly doubling the number of well-observed, nearby SN Ia with published multicolor CCD light curves. The large sample of U-band photometry is a unique addition, with important connections to SN Ia observed at high redshift. The decline rate of SN Ia U-band light curves correlates well with the decline rate in other bands, as does the U-B color at maximum light. However, the U-band peak magnitudes show an increased dispersion relative to other bands even after accounting for extinction and decline rate, amounting to an additional ~40% intrinsic scatter compared to B-band.Comment: 84 authors, 71 pages, 51 tables, 10 figures. Accepted for publication in the Astronomical Journal. Version with high-res figures and electronic data at http://astron.berkeley.edu/~saurabh/cfa2snIa

Expression of Normally Repressed Myosin Heavy Chain 7b in the Mammalian Heart Induces Dilated Cardiomyopathy

In mammals, muscle contraction is controlled by a family of 10 sarcomeric myosin motors. The expression of one of its members, MYH7b, is regulated by alternative splicing, and while the protein is restricted to specialized muscles such as extraocular muscles or muscle spindles, RNA that cannot encode protein is expressed in most skeletal muscles and in the heart. Remarkably, birds and snakes express MYH7b protein in both heart and skeletal muscles. This observation suggests that in the mammalian heart, the motor activity of MYH7b may only be needed during development since its expression is prevented in adult tissue, possibly because it could promote disease by unbalancing myocardial contractility. Methods and Results We have analyzed MYH7b null mice to determine the potential role of MYH7b during cardiac development and also generated transgenic mice with cardiac myocyte expression of MYH7b protein to measure its impact on cardiomyocyte function and contractility. We found that MYH7b null mice are born at expected Mendelian ratios and do not have a baseline cardiac phenotype as adults. In contrast, transgenic cardiac MYH7b protein expression induced early cardiac dilation in males with significantly increased left ventricular mass in both sexes. Cardiac dilation is progressive, leading to early cardiac dysfunction in males, but later dysfunction in females. Conclusions The data presented show that the expression of MYH7b protein in the mammalian heart has been inhibited during the evolution of mammals most likely to prevent the development of a severe cardiomyopathy that is sexually dimorphic.</p

Cardiac Fibroblasts Mediate a Sexually Dimorphic Fibrotic Response to beta-Adrenergic Stimulation

Background Biological sex is an important modifier of cardiovascular disease and women generally have better outcomes compared with men. However, the contribution of cardiac fibroblasts (CFs) to this sexual dimorphism is relatively unexplored. Methods and Results Isoproterenol (ISO) was administered to rats as a model for chronic &beta;‐adrenergic receptor (&beta;‐AR)‐mediated cardiovascular disease. ISO‐treated males had higher mortality than females and also developed fibrosis whereas females did not. Gonadectomy did not abrogate this sex difference. To determine the cellular contribution to this phenotype, CFs were studied. CFs from both sexes had increased proliferation in vivo in response to ISO, but CFs from female hearts proliferated more than male cells. In addition, male CFs were significantly more activated to myofibroblasts by ISO. To investigate potential regulatory mechanisms for the sexually dimorphic fibrotic response, &beta;‐AR mRNA and PKA (protein kinase A) activity were measured. In response to ISO treatment, male CFs increased expression of &beta;1‐ and &beta;2‐ARs, whereas expression of both receptors decreased in female CFs. Moreover, ISO‐treated male CFs had higher PKA activity relative to vehicle controls, whereas ISO did not activate PKA in female CFs. Conclusions Chronic in vivo &beta;‐AR stimulation causes fibrosis in male but not female rat hearts. Male CFs are more activated than female CFs, consistent with elevated fibrosis in male rat hearts and may be caused by higher &beta;‐AR expression and PKA activation in male CFs. Taken together, our data suggest that CFs play a substantial role in mediating sex differences observed after cardiac injury. </div

Le FORUM, Vol. 39 No. 1

https://digitalcommons.library.umaine.edu/francoamericain_forum/1044/thumbnail.jp

The potential shared role of inflammation in insulin resistance and schizophrenia: A bidirectional two-sample mendelian randomization study

Background: Insulin resistance predisposes to cardiometabolic disorders, which are commonly comorbid with schizophrenia and are key contributors to the significant excess mortality in schizophrenia. Mechanisms for the comorbidity remain unclear, but observational studies have implicated inflammation in both schizophrenia and cardiometabolic disorders separately. We aimed to examine whether there is genetic evidence that insulin resistance and 7 related cardiometabolic traits may be causally associated with schizophrenia, and whether evidence supports inflammation as a common mechanism for cardiometabolic disorders and schizophrenia. Methods and findings: We used summary data from genome-wide association studies of mostly European adults from large consortia (Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC) featuring up to 108,557 participants; Diabetes Genetics Replication And Meta-analysis (DIAGRAM) featuring up to 435,387 participants; Global Lipids Genetics Consortium (GLGC) featuring up to 173,082 participants; Genetic Investigation of Anthropometric Traits (GIANT) featuring up to 339,224 participants; Psychiatric Genomics Consortium (PGC) featuring up to 105,318 participants; and Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium featuring up to 204,402 participants). We conducted two-sample uni- and multivariable mendelian randomization (MR) analysis to test whether (i) 10 cardiometabolic traits (fasting insulin, high-density lipoprotein and triglycerides representing an insulin resistance phenotype, and 7 related cardiometabolic traits: low-density lipoprotein, fasting plasma glucose, glycated haemoglobin, leptin, body mass index, glucose tolerance, and type 2 diabetes) could be causally associated with schizophrenia; and (ii) inflammation could be a shared mechanism for these phenotypes. We conducted a detailed set of sensitivity analyses to test the assumptions for a valid MR analysis. We did not find statistically significant evidence in support of a causal relationship between cardiometabolic traits and schizophrenia, or vice versa. However, we report that a genetically predicted inflammation-related insulin resistance phenotype (raised fasting insulin (raised fasting insulin (Wald ratio OR = 2.95, 95% C.I, 1.38–6.34, Holm-Bonferroni corrected p-value (p) = 0.035) and lower high-density lipoprotein (Wald ratio OR = 0.55, 95% C.I., 0.36–0.84; p = 0.035)) was associated with schizophrenia. Evidence for these associations attenuated to the null in multivariable MR analyses after adjusting for C-reactive protein, an archetypal inflammatory marker: (fasting insulin Wald ratio OR = 1.02, 95% C.I, 0.37–2.78, p = 0.975), high-density lipoprotein (Wald ratio OR = 1.00, 95% C.I., 0.85–1.16; p = 0.849), suggesting that the associations could be fully explained by inflammation. One potential limitation of the study is that the full range of gene products from the genetic variants we used as proxies for the exposures is unknown, and so we are unable to comment on potential biological mechanisms of association other than inflammation, which may also be relevant. Conclusions: Our findings support a role for inflammation as a common cause for insulin resistance and schizophrenia, which may at least partly explain why the traits commonly co-occur in clinical practice. Inflammation and immune pathways may represent novel therapeutic targets for the prevention or treatment of schizophrenia and comorbid insulin resistance. Future work is needed to understand how inflammation may contribute to the risk of schizophrenia and insulin resistance