2 results
A longer diagnostic interval is a risk for depression in amyotrophic lateral sclerosis
- Jashelle Caga, Eleanor Ramsey, Anne Hogden, Eneida Mioshi, Matthew C. Kiernan
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- Journal:
- Palliative & Supportive Care / Volume 13 / Issue 4 / August 2015
- Published online by Cambridge University Press:
- 19 August 2014, pp. 1019-1024
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- Article
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Objective:
Recognizing depressive symptoms in patients with amyotrophic lateral sclerosis (ALS) remains problematic given the potential overlap with the normal psychological responses to a terminal illness. Understanding mental health and disease-related risk factors for depression is key to identifying psychological morbidity. The present study aimed to determine the prevalence of depressive symptoms in ALS and to explore mental health and disease-related risk factors for depression.
Method:Structured medical and psychiatric history questionnaires and a validated depression scale (Depression, Anxiety, Stress Scale–21) were completed by 27 ALS patients (60% female; 59% limb onset; age 65.11 ± SE 2.21) prior to their initial review at a multidisciplinary clinic. Physical function was assessed with the Amyotrophic Lateral Sclerosis Functional Rating Scale (ALSFRS–R).
Results:At the time of initial assessment, 44% of patients had a previous psychiatric history, although the majority (62%) reported no symptoms of depression. The mean ALSFRS–R score was 37.78 ± SE 1.22, with an average diagnostic interval of 16.04 ± SE 2.39 months. Logistic regression analysis revealed that the length of the diagnostic interval alone predicted depressive symptoms (χ2(3, n = 26) = 9.21, Odds Ratio (OR) = 1.12, p < 0.05.
Significance of Results:The illness experiences of ALS patients rather than established mental health risk factors influence the manifestation of depressive symptoms in the early stages of the disease, with clinical implications for the assessment and treatment of psychological morbidity. Patients with lengthy diagnostic intervals may be prime targets for psychological assessment and intervention, especially in the absence of ALS-specific tests and biomarkers.
Tenascin: an extracellular matrix protein associated with bone growth
- Edited by P. T. Loughna, Royal Veterinary College, London, J. M. Pell
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- Book:
- Molecular Physiology of Growth
- Published online:
- 19 January 2010
- Print publication:
- 10 October 1996, pp 87-98
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- Chapter
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Summary
Introduction
Bone growth, whether longitudinal or appositional, requires a source of differentiated osteoblasts capable of secreting the proteins of bone matrix. Thus, factors influencing both the proliferation and differentiation of osteoblast precursors are important for bone growth. Cells of the osteoblast lineage respond to many environmental influences including soluble factors (hormones, growth factors) and mechanical loading. The proteins of the extracellular matrix, as well as having important structural roles in bone, may also be important local regulators of bone cell function, and may act as long-term insoluble mediators of the actions of soluble factors or load.
In recent years, it has been demonstrated that extracellular matrix proteins, acting through cell-surface receptors such as integrins, can have potent specific effects on cell behaviour, being able to influence cell proliferation, migration and differentiation. The extracellular matrix protein tenascin-C is of particular interest in bone development and growth because of its selective association with the developing skeleton. Tenascin-C (hereafter referred to simply as ‘tenascin’) is a member of the tenascin gene family, composed of at least four members (Chiquet-Ehrismann, Hagios & Matsumoto, 1994). Tenascin is a large hexameric glycoprotein with disulphide-linked subunits, each consisting of several structural domains, including epidermal growth factor-like repeats, fibronectin type III repeats and a fibrinogen-like terminal domain (Fig. 1; Spring, Beck & Chiquet-Ehrismann, 1989). Alternative splicing of the tenascin gene results in the existence of differently sized subunits, the number of possible subunits varying between species. The larger splice variants differ from the smaller variants by the presence of additional fibronectin type III repeats.