Editorial: World Health Organisation 'Healthy Life Expectancy in 191 Countries, 1999' - What of the future?

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Complement, immunoglobulin and creatine kinase response in black and white males after muscle-damaging exercise

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Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways

It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers

Non-allergic activation of eosinophils after strenuous endurance exercise

Objective. To determine the effect of prolonged endurance exercise on the serum concentrations of eosinophil cationic protein (ECP), immunoglobulin E (IgE) and upper respiratory tract symptoms (URTS).Design. In 11 healthy, experienced volunteers (6 males, 5 females, age 43 ± 9.8 years) the serum concentrations of ECP and IgE were measured, 24 hours prior to projected finishing time, immediately post exercise (IPE), and 3 h, 24 h, and 72 h after an ultramarathon (90 km). Self-reported URTS were also recorded for 14 days after the race. ECP was measured using radioimmunoassay and IgE using the Alastat Microplate Total IgE kit. The after-exercise values were corrected for plasma volume changes, which were calculated from haematocrit and haemoglobin values. Serum concentrations of ECP and IgE were analysed using an analysis of variance (ANOVA) comparing values with before-exercise levels. Level of significance was set at p ≤ 0.05.Results. ECP was significantly elevated at 72 hours (+52%), whilst IgE was not significantly altered after the ultramarathon. There were no reported URTS for the 14 days after the race.Conclusion. The eosinophil is a pro-inflammatory leukocyte involved in bronchial hyperreactivity and allergic inflammation of the airways. IgE is associated with allergic diseases such as asthma and rhinitis. Serum ECP is a sensitive marker of eosinophil activation. The result provides evidence for the non-allergic activation of blood eosinophils during prolonged endurance exercise. Whether this indicates exercise or environmentally induced airway inflammation, or a role for ECP in muscle /tissue repair, are hypotheses that require additional research

Alterations in acute-phase reactants (CRP, rheumatoid factor, complement, Factor B, and immune complexes) following an ultramarathon

Objectives. The human body initiates an acute phase response (APR) in response to a wide range of homeostatic disturbances. This complex series of reactions serves to activate repair processes and prevent ongoing tissue damage. An important aspect of the APR is the de novo synthesis of acute phase proteins (APP), many of which have not been thoroughly investigated. Main outcome measures. Alterations in CRP (C-reactive protein), C1est, C3, C4, C6, rheumatoid factor (RF) and Factor B were determined before and after an ultramarathon. Data were analysed using a one-way analysis of variance comparing values to pre-exercise levels. Significance was set at p < 0.05. Design. Venepunctures were performed on athletes participating in an ultramarathon (90 km) 24 hours before, immediately post-exercise (IPE), and 3h, 24h and 72h after the race. Serum was stored at –80°C until analysed. CRP levels in serum were assessed using the N Latex CRP kit. The levels of circulating immune complexes (CIC) were determined using particle-enhanced nephelometry. Complement proteins C1est, C3, C4 and RF were measured using laser nephelometry. C6 and Factor B were determined by radial immunodiffusion. Results. CRP was significantly elevated IPE (58%), 3h post (77%), 24h post (87%) and 72h post (69%). Pre-race CRP levels were above the normative range (5.10 ± 3.08 mg/l), C6 was significantly elevated (p < 0.05) at 24h post (7.8%) and 72h post (8.8%) exercise. Factor B was significantly elevated (p < 0.05) at 72h post exercise (12.8%). RF was significantly elevated at 72h post exercise (6.7%). Conclusion. Significant increases in selected acutephase reactants occur several days after the exercise event. In addition, as indicated by elevated resting levels of CRP, the athletes began the race with some degree of inflammation, presumably as a result of the cumulative training and racing mileage in preparation for the ultramarathon

Immunoglobulin responses to a repeated bout of downhill running

Objective: To examine the effect of downhill running on immunoglobulin responses. Method: Eleven untrained men performed 2 x 60 minute bouts of downhill running (-13.5% gradient), at a speed eliciting 75% of their VO2PEAK on a level grade. Two runs were spaced 14 days apart. Serum samples were collected before, after, and every hour for 12 hours and every 24 hours for six days. Serum total creatine kinase and immunoglobulin isotypes and subclasses were measured, and results were analysed using a repeated measures analysis of variance (12 hour period, 2 x 14; 24 hour intervals, 2 x 6, p≤0.05). Results: There was a significant interaction effect for creatine kinase (activity lower after run 2 than after run 1, 6-24 h) and exercise effect, with the serum concentrations of IgG1, IgG2, IgG4, and IgE lower, and IgM higher, after run 2. Conclusion: Lower concentrations of IgG1, lgG2, and IgE after run 2 may reflect a dampened autoimmune inflammatory response to autoantigens and enhanced autoontigen clearance mediated by the upregulation of IgM