The effect of vitamin D supplementation on the muscle damage after eccentric exercise in young men: a randomized, control trial.

BACKGROUND: Vitamin D contributes to the optimal functioning of muscles. This study was designed to determine the modulating effect of vitamin D supplementation on the degree of muscle cell damage caused by eccentric exercise in young men. METHODS: 60 male volunteers (20-24 years old) taking part in this study were divided in two groups - with suboptimal (S) and optimal (O;) 25(OH)D plasma levels. These groups were randomly subdivided into groups with vitamin D supplementation (experimental: SE and OE) and controls (SC and OC). Before the supplementation (Test I) and after 3 months (Test II), participants were subjected to two rounds of eccentric exercise tests on a declined treadmill (running speed corresponded 60% VO2peak determined in each subject in incremental exercise test). During each test, blood samples used for determination of 25(OH)D, Il-1ß, myoglobin (Mb) levels and CK, LDH activity were taken at three timepoints: before the test, 1 h and 24 h after it ended. After distribution normality testing (Saphiro-Wilk test), statistical analyses were performed. Non-parametric: Kruskal-Wallis test and the Wilcoxon test were applied, and the Dunn-Bonferroni test as a post-hoc test. RESULTS: In all groups, after 3 months, higher concentrations of 25(OH)D were indicated (SE p = 0.005; SC p = 0.018; OE p = 0.018; OC p = 0.028). SE and SC groups showed higher baseline concentrations of Il-1ß and significantly higher concentrations of this interleukin after 1 h compared to groups with an optimal 25(OH)D level. After supplementation, the SE group reacted with a similar jump in concentration of Il-1ß as the OC and OE groups. The change after 1 h after exercise in Test II was significantly different from that from Test I (p = 0.047) in SE group. Lower Mb concentrations indicated 1 h after exercise in Test II for SC and SE groups were indicated. CK activity did not differentiate the studied groups. Plasma calcium and phosphate disorders were also not indicated. CONCLUSIONS: The study has shown that vitamin D doses determined from the plasma concentration of 25(OH)D of individuals to match their specific needs can significantly reduce muscle cell damage induced by eccentric exercise.

Interferon-beta is a key regulator of proinflammatory events in experimental autoimmune encephalomyelitis.

BACKGROUND: Interferon (IFN)-ß is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined. OBJECTIVES: Our objective was to characterize the role of IFN-ß in immune regulation in experimental autoimmune encephalomyelitis (EAE). METHODS: IFN-ß(+/+) and IFN-ß(-/-) mice were immunized with myelin oligodendrocyte glycoprotein peptide in the presence or absence of IFN-ß, to induce EAE. Disease pathogenesis was monitored in the context of incidence, time of onset, clinical score, and immune cell activation in the brains, spleens and lymph nodes of affected mice. RESULTS: Compared with IFN-ß(+/+) mice, IFN-ß(-/-) mice exhibited an earlier onset and a more rapid progression of EAE, increased numbers of CD11b(+) leukocytes infiltrating affected brains and an increased percentage of Th17 cells in the central nervous system and draining lymph nodes. IFN-ß treatment delayed disease onset and reduced disease severity. Ex vivo experiments revealed that the lack of IFN-ß results in enhanced generation of autoreactive T cells, a likely consequence of the absence of IFN-ß-regulated events in both the CD4(+) T cells and antigen-presenting dendritic cells. Gene expression analysis of IFN-ß-treated bone marrow macrophages (CD11b(+)) identified modulation of genes affecting T cell proliferation and Th17 differentiation. CONCLUSIONS: We conclude that IFN-ß acts to suppress the generation of autoimmune-inducing Th17 cells during the development of disease as well as modulating pro-inflammatory mediators.

Interferons and viruses: signaling for supremacy.

Interferon (IFN)-alpha and IFN-beta are critical mediators of host defense against microbial challenges, directly interfering with viral infection and influencing both the innate and adaptive immune responses. IFNs exert their effects in target cells through the activation of a cell-surface receptor, leading to a cascade of signaling events that determine transcriptional and translation regulation. Understanding the circuitry associated with IFN-mediated signal transduction that leads to a specific biological outcome has been a major focus of our laboratory. Through the efforts of graduate students, postdoctoral fellows, a skilled research technologist, and important collaborations with investigators elsewhere, we have provided some insights into the complexity of the IFN system-and the elegance and simplicity of how protein-protein interactions define biological function.

Bone and joint pathology in fluoride-exposed workers.

Clinical and radiological investigations were performed for 2,258 aluminum workers exposed to fluoride for an average of 17.6 yr (standard deviation = 7.6). Changes in bone and joints were presented in detail in three groups: (1) exposed up to 5 yr (135 cases), (2) exposed from 6-32 yr (1,463 cases), and (3) retired workers (660 cases). A semiquantitative assessment of early fluorosis was introduced. A 20.2% incidence of fluorosis was found, but, according to Roholm, only 1.05% was in stage I. The disease was mainly in the pre-stages of O and OI. A close relationship between the occurrence of fluorosis and the time and degree of fluoride exposure was found. The difficulties in diagnosing skeletal fluorosis result from the questionable sensitivity of the x-ray techniques and from the nonspecificity of the associated symptoms. A quantitative method to assess osteosclerosis and bone structure alteration is needed.