The Relationship between Self-Efficacy,Functional Exercise Capacity and Physical Activity in People with COPD: A Systematic Review and Meta-Analyses

Abstract

The purpose of this study was to investigate the strength of the relationships between self-efficacy and (i) functional exercise capacity and (ii) physical activity in chronic obstructive pulmonary disease (COPD), and whether self-efficacy assessment type (i.e., COPD symptoms, exercise-task, exercise-barrier, general, falls) and physical activity assessment type (i.e., self-report vs. objective) are moderators. A systematic search of COPD and self-efficacy concepts was conducted using eight databases from inception to 23 January 2019. Studies were included if they provided correlation coefficients of the relationship between self-efficacy and functional exercise capacity or physical activity, were conducted in adults diagnosed with COPD, and were published in English-language journals. A total of 14 correlation coefficients were included in the self-efficacy and functional exercise capacity meta-analysis, and 16 in the self-efficacy and physical activity meta-analysis. Data were screened, reviewed, and extracted independently by two reviewers, with discrepancies resolved by a third reviewer. Stronger self-efficacy was associated with better functional exercise capacity (weighted r?=?0.38, 95%CI [0.25, 0.50]), and greater physical activity (weighted r?=?0.25, 95%CI [0.17, 0.34]). Exercise-task self-efficacy had the strongest relationship to functional exercise capacity (weighted r?=?0.64, 95% CI [0.51, 0.73]). For physical activity, the type of self-efficacy most strongly related was inconclusive. In COPD, self-efficacy has a relationship to functional exercise capacity and physical activity, the strength of which is influenced by the choice of self-efficacy measure. An understanding of these relationships will assist clinicians in selecting the self-efficacy measure most closely related to the outcome of interest.     

Schließlich sind wir doch alle behindert! Ein Beitrag zur Begegnung zwischen Menschen mit und ohne Behinderung

I discuss various viewpoints of physically disabled and nondisabled persons. I then question which views to preserve and which need to be changed as regards the subject of supervision of the physically disabled. I believe that illness and/or being physically disabled require different definitions and that for many physically disabled persons there is no either-or. In various theories it is asked how the physically disabled can be supported in their personal development, when it is maintained held that both disabled and non-disabled persons have the same mental and emotional conditions and requirements. The following theories will be considered: role theory, labeling theory, which holds to the idea of "self-fulfilling prophesy", the concept of the five pillars of identity, the expectations of self-effectiveness and of results and the theory of internal locus of control. It is a question of whether the physically disabled, like the nondisabled, should take the responsibility for their personal development upon themselves. In closing, I discuss where supervision can have a supportive effect in helping the physically disabled achieve greater personal development. Personal development improves the quality of life. Supervision for those who work with the physically disabled should contribute to reaching these goals.     

Massive Immune Hemolysis Caused by Anti-D After Dual Kidney Transplantation

Massive immune hemolysis due to passenger lymphocyte-derived anti-D has not been reported in renal transplantation. A 50-year-old (B-positive) male received a dual deceased-donor kidney transplant (B-negative) for diabetic renal failure. Two weeks post-transplant, the patient developed severe hemolytic anemia. The donor anti-D titer was 1:8. The recipient anti-D titer (zero pre-transplant) increased from 1:4 to 1:16 over 4 days. Rapid hemolysis caused severe anemia, minimum Hb = 4.2 g/dL, while selectively lysing the patient's autologous red cells during this time. The hemolytic anemia did not impair the allografts and subsided without monoclonal B-cell pharmacotherapy or apheresis. The anti-D titer decreased to barely detectable levels at four months and had cleared when checked 2 years post-transplant. Transfusion support subsided after two months. If complications of anemia can be avoided, the deleterious effects of hemolysis may be well tolerated by renal allografts using antigen negative transfusion alone.     

Human colonic goblet cells. Demonstration of distinct subpopulations defined by mucin-specific monoclonal antibodies.

We studied glycoprotein content of human colonic goblet cells, using a library of monoclonal antibodies (MAbs) directed against purified human colonic mucin (HCM). Using indirect immunofluorescence (IIF), we found that 17 of 23 anti-HCM MAbs stained some or all goblet cells of normal human colonic mucosa. We observed a variety of cellular staining patterns, including (a) diffuse (homogeneous) staining of intracellular mucin, (b) speckled (inhomogeneous) staining of mucin droplets, (c) peripheral staining of intracellular droplets, (d) cytoplasmic staining of goblet cells, and (e) apical (luminal) surface staining. Staining patterns were not associated with particular HCM species. In addition to variable patterns of IIF within individual cells, anti-HCM MAbs varied in the proportion of goblet cells stained. Some MAbs stained all goblet cells, while others stained a limited number of goblet cells. Although each goblet cell contained more than one type mucin, HCM species III, and IV and V appeared to exist in mutually exclusive goblet cell populations and it was possible to define at least seven subpopulations of goblet cells in colonic mucosa by their content of various combinations of HCM species. Anti-HCM MAbs stained goblet cells from other sites within the gastrointestinal tract to a varying extent. Anti-HCM MAbs also showed extensive cross-reactivity with rodent, rabbit, and monkey colonic mucosa. However, several anti-HCM MAbs stained only human colonic mucosa. These data show that human colonic mucosa contains discrete subpopulations of goblet cells that produce distinctive combinations of specific mucin glycoprotein species.     

N-acetylaspartate is an axon-specific marker of mature white matter in vivo: a biochemical and immunohistochemical study on the rat optic nerve.

Axonal pathology is a major cause of neurological disability in multiple sclerosis. Axonal transection begins at disease onset but remains clinically silent because of compensatory brain mechanisms. Noninvasive surrogate markers for axonal injury are therefore essential to monitor cumulative disease burden in vivo. The neuronal compound N-acetylaspartate, as measured by magnetic resonance spectroscopy, is currently the best and most specific noninvasive marker of axonal pathology in multiple sclerosis. The possibility has been raised, however, that N-acetylaspartate is expressed also by oligodendroglial lineage cells. In order to investigate N-acetylaspartate specificity for white matter axons, transected rat optic nerves were analyzed by high-performance liquid chromatography and immunohistochemistry. In transected adult nerves, N-acetylaspartate and N-acetyl aspartylglutamate decreased in concordance with axonal degeneration and were undetectable 24 days posttransection. Nonproliferating oligodendrocyte progenitor cells, oligodendrocytes, and myelin were abundant in these axon-free nerves. At 24 days posttransection, N-acetylaspartate was increased (42%; p = 0.02) in nontransected contralateral nerves. After transection at postnatal day 4, total N-acetylaspartate decreased by 80% (P14; p = 0.002) and 94% (P20; p = 0.003). In these developing axon-free nerves, 25 to 33% of oligodendrocyte progenitor cells were proliferating. These data validate magnetic resonance spectroscopy measurements of N-acetylaspartate as an axon-specific monitor of central nervous system white matter in vivo. In addition, the results indicate that neuronal adaptation can increase N-acetylaspartate levels, and that 5 to 20% of the N-acetylaspartate in developing white matter is synthesized by proliferating oligodendrocyte progenitor cells.