80 research outputs found

    Foot pain and foot health in an educated population of adults: results from the Glasgow Caledonian University Alumni Foot Health Survey

    Get PDF
    Abstract Background Foot pain is common amongst the general population and impacts negatively on physical function and quality of life. Associations between personal health characteristics, lifestyle/behaviour factors and foot pain have been studied; however, the role of wider determinants of health on foot pain have received relatively little attention. Objectives of this study are i) to describe foot pain and foot health characteristics in an educated population of adults; ii) to explore associations between moderate-to-severe foot pain and a variety of factors including gender, age, medical conditions/co-morbidity/multi-morbidity, key indicators of general health, foot pathologies, and social determinants of health; and iii) to evaluate associations between moderate-to-severe foot pain and foot function, foot health and health-related quality-of-life. Methods Between February and March 2018, Glasgow Caledonian University Alumni with a working email address were invited to participate in the cross-sectional electronic survey (anonymously) by email via the Glasgow Caledonian University Alumni Office. The survey was constructed using the REDCap secure web online survey application and sought information on presence/absence of moderate-to-severe foot pain, patient characteristics (age, body mass index, socioeconomic status, occupation class, comorbidities, and foot pathologies). Prevalence data were expressed as absolute frequencies and percentages. Multivariate logistic and linear regressions were undertaken to identify associations 1) between independent variables and moderate-to-severe foot pain, and 2) between moderate-to-severe foot pain and foot function, foot health and health-related quality of life. Results Of 50,228 invitations distributed, there were 7707 unique views and 593 valid completions (median age [inter-quartile range] 42 [31–52], 67.3% female) of the survey (7.7% response rate). The sample was comprised predominantly of white Scottish/British (89.4%) working age adults (95%), the majority of whom were overweight or obese (57.9%), and in either full-time or part-time employment (82.5%) as professionals (72.5%). Over two-thirds (68.5%) of the sample were classified in the highest 6 deciles (most affluent) of social deprivation. Moderate-to-severe foot pain affected 236/593 respondents (39.8%). High body mass index, presence of bunions, back pain, rheumatoid arthritis, hip pain and lower occupation class were included in the final multivariate model and all were significantly and independently associated with moderate-to-severe foot pain (p < 0.05), except for rheumatoid arthritis (p = 0.057). Moderate-to-severe foot pain was significantly and independently associated lower foot function, foot health and health-related quality of life scores following adjustment for age, gender and body mass index (p < 0.05). Conclusions Moderate-to-severe foot pain was highly prevalent in a university-educated population and was independently associated with female gender, high body mass index, bunions, back pain, hip pain and lower occupational class. Presence of moderate-to-severe foot pain was associated with worse scores for foot function, foot health and health-related quality-of-life. Education attainment does not appear to be protective against moderate-to-severe foot pain

    Plantar calcaneal spurs in older people: longitudinal traction or vertical compression?

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Plantar calcaneal spurs are common, however their pathophysiology is poorly understood. This study aimed to evaluate the prevalence and correlates of plantar calcaneal spurs in a large sample of older people.</p> <p>Methods</p> <p>Weightbearing lateral foot radiographs of 216 people (140 women and 76 men) aged 62 to 94 years (mean age 75.9, <smcaps>SD</smcaps> 6.6) were examined for plantar calcaneal and Achilles tendon spurs. Associations between the presence of spurs and sex, body mass index, radiographic measures of foot posture, self-reported co-morbidities and current or previous heel pain were then explored.</p> <p>Results</p> <p>Of the 216 participants, 119 (55%) had at least one plantar calcaneal spur and 103 (48%) had at least one Achilles tendon spur. Those with plantar calcaneal spurs were more likely to have Achilles tendon spurs (odds ratio [OR] = 2.0, 95% confidence interval [CI] 1.2 to 3.5). Prevalence of spurs did not differ according to sex. Participants with plantar calcaneal spurs were more likely to be obese (OR = 7.9, 95% CI 3.6 to 17.0), report osteoarthritis (OR = 2.6, 95% CI 1.6 to 4.8) and have current or previous heel pain (OR = 4.6, 95% CI 2.3 to 9.4). No relationship was found between the presence of calcaneal spurs and radiographic measures of foot posture.</p> <p>Conclusion</p> <p>Calcaneal spurs are common in older men and women and are related to obesity, osteoarthritis and current or previous heel pain, but are unrelated to radiographic measurements of foot posture. These findings support the theory that plantar calcaneal spurs may be an adaptive response to vertical compression of the heel rather than longitudinal traction at the calcaneal enthesis.</p

    Zinc uptake promotes myoblast differentiation via Zip7 transporter and activation of Akt signalling transduction pathway

    Get PDF
    [EN] Myogenic regeneration occurs through a chain of events beginning with the output of satellite cells from quiescent state, formation of competent myoblasts and later fusion and differentiation into myofibres. Traditionally, growth factors are used to stimulate muscle regeneration but this involves serious off-target effects, including alterations in cell homeostasis and cancer. In this work, we have studied the use of zinc to trigger myogenic differentiation. We show that zinc promotes myoblast proliferation, differentiation and maturation of myofibres. We demonstrate that this process occurs through the PI3K/Akt pathway, via zinc stimulation of transporter Zip7. Depletion of zinc transporter Zip7 by RNA interference shows reduction of both PI3K/Akt signalling and a significant reduction of multinucleated myofibres and myotubes development. Moreover, we show that mature myofibres, obtained through stimulation with high concentrations of zinc, accumulate zinc and so we hypothesise their function as zinc reservoirs into the cell.P.R. and R.S. acknowledges support from the Spanish Ministry of Economy and Competitiveness (MINECO) (MAT2015-69315-C3-1-R). P.R. acknowledges the Fondo Europeo de Desarrollo Regional (FEDER). CIBER-BBN is an initiative funded by the VI National R&D&I Plan 2008-2011, Iniciativa Ingenio 2010, Consolider Program, CIBER Actions and financed by the Instituto de Salud Carlos III with assistance from the European Regional Development Fund. R.S. acknowledges the support from the Spanish MECD through the PRX16/00208 grant. MSS acknowledges support from the European Research Council (ERC - HealInSynergy 306990) and the UK Engineering and Physical Sciences Research Council (EPSRC - EP/P001114/1)Mnatsakanyan, H.; Sabater I Serra, R.; Rico Tortosa, PM.; Salmerón Sánchez, M. (2018). Zinc uptake promotes myoblast differentiation via Zip7 transporter and activation of Akt signalling transduction pathway. Scientific Reports. 8:1-14. https://doi.org/10.1038/s41598-018-32067-0S1148Frontera, W. R. & Ochala, J. Skeletal muscle: a brief review of structure and function. Calcif. Tissue Int. 96, 183–195 (2015).Wolfe, R. R., Frontera, W. R. & Ochala, J. The underappreciated role of muscle in health and disease. Am. J. Clin. Nutr. 84, 475–82 (2006).Sciorati, C., Rigamonti, E., Manfredi, A. A. & Rovere-Querini, P. Cell death, clearance and immunity in the skeletal muscle. Cell Death Differ. 23, 927–937 (2016).Wang, Y. X. & Rudnicki, M. A. Satellite cells, the engines of muscle repair. Nat. Rev. Mol. Cell Biol. 13, 127–133 (2011).Yin, H., Price, F. & Rudnicki, M. A. Satellite cells and the muscle stem cell niche. Physiol. Rev. 93, 23–67 (2013).Dhawan, J. & Rando, T. A. Stem cells in postnatal myogenesis: Molecular mechanisms of satellite cell quiescence, activation and replenishment. Trends Cell Biol. 15, 666–673 (2005).Yun, K. & Wold, B. Skeletal muscle determination and differentiation: Story of a core regulatory network and its context. Curr. Opin. Cell Biol. 8, 877–889 (1996).Gharaibeh, B. et al. Biological approaches to improve skeletal muscle healing after injury and disease. Birth Defects Res. Part C Embryo Today Rev. 96, 82–94 (2012).Schiaffino, S. & Mammucari, C. Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models. Skelet. Muscle 1, 4 (2011).Sandri, M. Signaling in muscle atrophy and hypertrophy. Physiology (Bethesda). 23, 160–70 (2008).Karalaki, M., Fili, S., Philippou, A. & Koutsilieris, M. Muscle regeneration: cellular and molecular events. In Vivo 23, 779–96 (2009).Fujio, Y. et al. Cell cycle withdrawal promotes myogenic induction of Akt, a positive modulator of myocyte survival. Mol. Cell. Biol. 19, 5073–82 (1999).Wilson, E. M. & Rotwein, P. Control of MyoD function during initiation of muscle differentiation by an autocrine signaling pathway activated by insulin-like growth factor-II. J. Biol. Chem. 281, 29962–29971 (2006).Sun, L., Liu, L., Yang, X. & Wu, Z. Akt binds prohibitin 2 and relieves its repression of MyoD and muscle differentiation. J. Cell Sci. 117, 3021–3029 (2004).Milner, D. & Cameron, J. Muscle repair and regeneration: stem cells, scaffolds, and the contributions of skeletal muscle to amphibian limb regeneration. Curr. Top. Microbiol. Immunol. 367, 133–159 (2013).Liu, C. et al. PI3K/Akt signaling transduction pathway is involved in rat vascular smooth muscle cell proliferation induced by apelin-13. Acta Biochim Biophys Sin 42, 396–402 (2010).Eriksson, M., Taskinen, M. & Leppä, S. Mitogen Activated Protein Kinase-Dependent Activation of c-Jun and c-Fos is required for Neuronal differentiation but not for Growth and Stress Reposne in PC12 cells. J. Cell. Physiol. 207, 12–22 (2006).Arsic, N. et al. Vascular endothelial growth factor stimulates skeletal muscle regeneration in Vivo. Mol. Ther. 10, 844–854 (2004).Borselli, C. et al. Functional muscle regeneration with combined delivery of angiogenesis and myogenesis factors. Proc. Natl. Acad. Sci. USA 107, 3287–3292 (2010).Hanft, J. R. et al. Phase I trial on the safety of topical rhVEGF on chronic neuropathic diabetic foot ulcers. J. Wound Care 17(30–2), 34–7 (2008).Simón-Yarza, T. et al. Vascular endothelial growth factor-delivery systems for cardiac repair: An overview. Theranostics 2, 541–552 (2012).Briquez, P. S., Hubbell, J. A. & Martino, M. M. Extracellular Matrix-Inspired Growth Factor Delivery Systems for Skin Wound Healing. Adv. Wound Care 4, 479–489 (2015).Barthel, A., Ostrakhovitch, E. A., Walter, P. L., Kampkötter, A. & Klotz, L. O. Stimulation of phosphoinositide 3-kinase/Akt signaling by copper and zinc ions: Mechanisms and consequences. Arch. Biochem. Biophys. 463, 175–182 (2007).Ostrakhovitch, E. A., Lordnejad, M. R., Schliess, F., Sies, H. & Klotz, L.-O. Copper ions strongly activate the phosphoinositide-3-kinase/Akt pathway independent of the generation of reactive oxygen species. Arch. Biochem. Biophys. 397, 232–239 (2002).Kaur, K., Gupta, R., Saraf, S. A. & Saraf, S. K. Zinc: The metal of life. Compr. Rev. Food Sci. Food Saf. 13, 358–376 (2014).Coleman, J. E. Zinc proteins: enzymes, storage proteins, transcription factors, and replication proteins. Annu. Rev. Biochem. 61, 897–946 (1992).Fukada, T. & Kambe, T. Molecular and genetic features of zinc transporters in physiology and pathogenesis. Metallomics 3, 662–674 (2011).Murakami, M. & Hirano, T. Intracellular zinc homeostasis and zinc signaling. Cancer Sci. 99, 1515–1522 (2008).Hogstrand, C., Kille, P., Nicholson, R. I. & Taylor, K. M. Zinc transporters and cancer: a potential role for ZIP7 as a hub for tyrosine kinase activation. Trends Mol. Med. 15, 101–111 (2009).Kolenko, V., Teper, E., Kutikov, A. & Uzzo, R. Zinc and zinc transporters in prostate carcinogenesis. Nat. Rev. Urol. 10, 219–26 (2013).Myers, S. A., Nield, A., Chew, G. S. & Myers, M. A. The zinc transporter, Slc39a7 (Zip7) is implicated in glycaemic control in skeletal muscle cells. Plos One 8 (2013).Kambe, T., Tsuji, T., Hashimoto, A. & Itsumura, N. The Physiological, Biochemical, and Molecular Roles of Zinc Transporters in Zinc Homeostasis and Metabolism. Physiol. Rev. 95, 749–784 (2015).Jinno, N., Nagata, M. & Takahashi, T. Marginal zinc deficiency negatively affects recovery from muscle injury in mice. Biol. Trace Elem. Res. 158, 65–72 (2014).Taylor, K. M., Hiscox, S., Nicholson, R. I., Hogstrand, C. & Kille, P. Protein Kinase CK2 Triggers Cytosolic Zinc Signaling Pathways by Phosphorylation of Zinc Channel ZIP7. Sci. Signal. 5, ra11–ra11 (2012).Yamasaki, S. et al. Zinc is a novel intracellular second messenger. J. Cell Biol. 177, 637–45 (2007).Sumitani, S., Goya, K., Testa, J. R., Kouhara, H. & Kasayama, S. Akt1 and Akt2 differently regulate muscle creatine kinase and myogenin gene transcription in insulin-induced differentiation of C2C12 myoblasts. Endocrinology 143, 820–828 (2002).Ohashi, K. et al. Zinc promotes proliferation and activation of myogenic cells via the PI3K/Akt and ERK signaling cascade. Exp. Cell Res. 333, 228–237 (2015).Chesters, J. K. In Zinc in human biology 53, 109–118 (1989).Burattini, S. et al. C2C12 murine myoblasts as a model of skeletal muscle development: Morpho-functional characterization. Eur. J. Histochem. 48, 223–233 (2004).Mnatsakanyan, H. et al. Controlled Assembly of Fibronectin Nanofibrils Triggered by Random Copolymer Chemistry. ACS Appl. Mater. Interfaces 7, 18125–18135 (2015).Jeong, J. & Eide, D. J. The SLC39 family of zinc transporters. Molecular Aspects of Medicine 34, 612–619 (2013).Huang, L., Kirschke, C. P., Zhang, Y. & Yan, Y. Y. The ZIP7 gene (Slc39a7) encodes a zinc transporter involved in zinc homeostasis of the Golgi apparatus. J. Biol. Chem. 280, 15456–15463 (2005).Vallee, B. L. & Falchuk, K. H. The biochemical basis of zinc physiology. Physiological reviews 73 (1993).Ganju, N. & Eastman, A. Zinc inhibits Bax and Bak activation and cytochrome c release induced by chemical inducers of apoptosis but not by death-receptor-initiated pathways. Cell Death Differ. 10, 652–61 (2003).Chai, F., Truong-Tran, A. Q., Ho, L. H. & Zalewski, P. D. Regulation of caspase activation and apoptosis by cellular zinc fluxes and zinc deprivation: A review. Immunol. Cell Biol. 77, 272–278 (1999).Smith, P. J., Wiltshire, M., Furon, E., Beattie, J. H. & Errington, R. J. Impact of overexpression of metallothionein-1 on cell cycle progression and zinc toxicity. Am. J. Physiol. Cell Physiol. 295, C1399–C1408 (2008).Bozym, R. A. et al. Free zinc ions outside a narrow concentration range are toxic to a variety of cells in vitro. Exp. Biol. Med. (Maywood). 235, 741–50 (2010).Plum, L. M., Rink, L. & Hajo, H. The essential toxin: Impact of zinc on human health. Int. J. Environ. Res. Public Health 7, 1342–1365 (2010).Chen, C.-J. & Liao, S.-L. Zinc toxicity on neonatal cortical neurons: involvement of glutathione chelation. J. Neurochem. 85, 443–453 (2003).Chassot, A. A. et al. Confluence-induced cell cycle exit involves pre-mitotic CDK inhibition by p27Kip1 and cyclin D1 downregulation. Cell Cycle 7, 2038–2046 (2008).Spencer, S. L. et al. XThe proliferation-quiescence decision is controlled by a bifurcation in CDK2 activity at mitotic exit. Cell 155, 369–383 (2013).Walsh, K. & Perlman, H. Cell cycle exit upon myogenic differentiation. Curr. Opin. Genet. Dev. 7, 597–602 (1997).Puri, P. L. & Sartorelli, V. Regulation of muscle regulatory factors by DNA-binding, interacting proteins, and post-transcriptional modifications. Journal of Cellular Physiology 185, 155–173 (2000).Zammit, P. S., Partridge, T. A. & Yablonka-Reuveni, Z. The skeletal muscle satellite cell: the stem cell that came in from the cold. J Histochem Cytochem 54, 1177–1191 (2006).McCord, M. C. & Aizenman, E. The role of intracellular zinc release in aging, oxidative stress, and Alzheimer’s disease. Front. Aging Neurosci. 6, 1–16 (2014).Dirksen, R. T. Sarcoplasmic reticulum–mitochondrial through-space coupling in skeletal muscle. This paper is one of a selection of papers published in this Special Issue, entitled 14th International Biochemistry of Exercise Conference – Muscles as Molecular and Metabolic. Appl. Physiol. Nutr. Metab. 34, 389–395 (2009).Groth, C., Sasamura, T., Khanna, M. R., Whitley, M. & Fortini, M. E. Protein trafficking abnormalities in Drosophila tissues with impaired activity of the ZIP7 zinc transporter Catsup. Development 140, 3018–3027 (2013).Ellis, C. D. et al. Zinc and the Msc2 zinc transporter protein are required for endoplasmic reticulum function. J. Cell Biol. 166, 325–335 (2004).Koch, U., Lehal, R. & Radtke, F. Stem cells living with a Notch. Development 140, 689–704 (2013).Gardner, S., Anguiano, M. & Rotwein, P. Defining Akt actions in muscle differentiation. Am. J. Physiol. Physiol. 303, C1292–C1300 (2012).Knight, J. D. & Kothary, R. The myogenic kinome: protein kinases critical to mammalian skeletal myogenesis. Skelet. Muscle 1, 29 (2011).Roth, S. M. Genetic aspects of skeletal muscle strength and mass with relevance to sarcopenia. Bonekey Rep. 1, 1–7 (2012).Mebratu, Y. & Tesfaigzi, Y. How ERK1/2 Activation Controls Cell Proliferation and Cell Death Is Subcellular Localization the Answer? Cell Cycle 8, 1168–1175 (2009)

    Attitudes and behaviour predict women's intention to drink alcohol during pregnancy: the challenge for health professionals

    Get PDF
    Background. To explore women's alcohol consumption in pregnancy, and potential predictors of alcohol consumption in pregnancy including: demographic characteristics; and women's knowledge and attitudes regarding alcohol consumption in pregnancy and its effects on the fetus. Methods. We conducted a national cross-sectional survey via computer assisted telephone interview of 1103 Australian women aged 18 to 45 years. Participants were randomly selected from the Electronic White Pages. Pregnant women were not eligible to participate. Quotas were set for age groups and a minimum of 100 participants per state to ensure a national sample reflecting the population. The questionnaire was based on a Health Canada survey with additional questions constructed by the investigators. Descriptive statistics were calculated and logistic regression analyses were used to assess associations of alcohol consumption in pregnancy with participants' characteristics, knowledge and attitudes.Results. The majority of women (89.4%) had consumed alcohol in the last 12 months. During their last pregnancy (n = 700), 34.1% drank alcohol. When asked what they would do if planning a pregnancy (n = 1103), 31.6% said they would consume alcohol and 4.8% would smoke. Intention to consume alcohol in a future pregnancy was associated with: alcohol use in the last pregnancy (adjusted OR (aOR) 43.9; 95% Confidence Interval (CI) 27.0 to 71.4); neutral or positive attitudes towards alcohol use in pregnancy (aOR 5.1; 95% CI 3.6 to 7.1); intention to smoke in a future pregnancy (aOR 4.7; 95% CI 2.5 to 9.0); and more frequent and higher current alcohol consumption. Conclusions. Women's past pregnancy and current drinking behaviour, and attitudes to alcohol use in pregnancy were the strongest predictors of alcohol consumption in pregnancy. Targeted interventions for women at higher risk of alcohol consumption in pregnancy are needed to change women's risk perception and behaviour

    Patterns and associates of cognitive function, psychosocial wellbeing and health in the Lothian Birth Cohort 1936

    Get PDF
    BACKGROUND: Cognitive function, psychosocial wellbeing and health are important domains of function. Consistencies and inconsistencies in patterns of wellbeing across these domains may be informative about wellbeing in old age and the ways it is manifested amongst individuals. In this study we investigated whether there were groups of individuals with different profiles of scores across these domains. We also aimed to identify characteristics of any evident groups by comparing them on variables that were not used in identifying the groups. METHODS: The sample was the Lothian Birth Cohort 1936, which included 1091 participants born in 1936. They are a community-dwelling, narrow-age-range sample of 70-year-olds. Most had taken part in the Scottish Mental Survey 1947 at an average age of 11, making available a measure of childhood intelligence. We used latent class analysis (LCA) to explore possible profiles using 9 variables indicating cognitive functioning, psychosocial wellbeing and health status. Demographic, personality, and lifestyle variables – none of which were used in the LCA – were used to characterize the resulting profile groups. RESULTS: We accepted a 3-group solution, which we labeled High Wellbeing (65.3%), Low Cognition (20.3%), and Low Bio-Psychosocial (14.5%). Notably, the High Wellbeing group had significantly higher childhood IQ, lower Neuroticism scores, and a lower percentage of current smokers than the other 2 groups. CONCLUSION: The majority of individuals were functioning generally well; however, there was evidence of the presence of groups with different profiles, which may be explained in part in terms of cognitive ability differences. Results suggested that higher life-long intelligence, personality traits associated with less mental distress, and basic health practices such as avoiding smoking are important associates of wellbeing in old age

    Theories of schizophrenia: a genetic-inflammatory-vascular synthesis

    Get PDF
    BACKGROUND: Schizophrenia, a relatively common psychiatric syndrome, affects virtually all brain functions yet has eluded explanation for more than 100 years. Whether by developmental and/or degenerative processes, abnormalities of neurons and their synaptic connections have been the recent focus of attention. However, our inability to fathom the pathophysiology of schizophrenia forces us to challenge our theoretical models and beliefs. A search for a more satisfying model to explain aspects of schizophrenia uncovers clues pointing to genetically mediated CNS microvascular inflammatory disease. DISCUSSION: A vascular component to a theory of schizophrenia posits that the physiologic abnormalities leading to illness involve disruption of the exquisitely precise regulation of the delivery of energy and oxygen required for normal brain function. The theory further proposes that abnormalities of CNS metabolism arise because genetically modulated inflammatory reactions damage the microvascular system of the brain in reaction to environmental agents, including infections, hypoxia, and physical trauma. Damage may accumulate with repeated exposure to triggering agents resulting in exacerbation and deterioration, or healing with their removal. There are clear examples of genetic polymorphisms in inflammatory regulators leading to exaggerated inflammatory responses. There is also ample evidence that inflammatory vascular disease of the brain can lead to psychosis, often waxing and waning, and exhibiting a fluctuating course, as seen in schizophrenia. Disturbances of CNS blood flow have repeatedly been observed in people with schizophrenia using old and new technologies. To account for the myriad of behavioral and other curious findings in schizophrenia such as minor physical anomalies, or reported decreased rates of rheumatoid arthritis and highly visible nail fold capillaries, we would have to evoke a process that is systemic such as the vascular and immune/inflammatory systems. SUMMARY: A vascular-inflammatory theory of schizophrenia brings together environmental and genetic factors in a way that can explain the diversity of symptoms and outcomes observed. If these ideas are confirmed, they would lead in new directions for treatments or preventions by avoiding inducers of inflammation or by way of inflammatory modulating agents, thus preventing exaggerated inflammation and consequent triggering of a psychotic episode in genetically predisposed persons
    corecore