The impact of injury on match running performance following the return to competitive match-play over two consecutive seasons in elite European soccer players

Based on the assessment and diagnosis, the rest period following a moderate/severe injury may lead to deconditioning for the injured player and therefore an association with a prolonged rehabilitation, re-conditioning and return to sport is observed post-injury. The aim of the present study was to assess the impact of all injuries on match running performance following the return to competitive match-play over two consecutive seasons in elite European soccer players. A retrospective analysis was conducted utilizing data related to a player’s injury and match running performance. A club physiotherapist consistently recorded availability and injury data in a standardized format. Linear mixed modelling analysis revealed no difference between PRE and POST1, POST2, and POST3 for total distance, running distance, high-intensity distance, and sprint distance (all p >0.05). Although, maximum speed was significantly (p<0.05) lower in POST1 and POST2 when compared to PRE, in both cases with a large (ES = 1.88) effect. No significant difference was observed for maximum speed between PRE and POST3 (p=0.07). There were very low correlations between the number of days absent and changes in maximum speed between POST1 and PRE (r = 0.09, 95% CI -0.42 to 0.56), and POST2 and PRE (r = 0.10, 95% CI -0.42 to 0.57), respectively. In conclusion, no variation in distance variables were found regardless of one, two or three matches post-injury compared to pre-injury status. Moreover, maximum speed was lower during the first three matches post-injury, although the mean value was slightly lower. Finally, a low correlation between absent days and maximum speed loss between pre-injury and following one and two matches were foun

Randomized investigation of the bioavailability of fluoride in saliva after administration of sodium fluoride, amine fluoride and fluoride containing bioactive glass dentifrices

Witten/Herdecke University

In silico mining identifies IGFBP3 as a novel target of methylation in prostate cancer

Promoter hypermethylation is central in deregulating gene expression in cancer. Identification of novel methylation targets in specific cancers provides a basis for their use as biomarkers of disease occurrence and progression. We developed an in silico strategy to globally identify potential targets of promoter hypermethylation in prostate cancer by screening for 5′ CpG islands in 631 genes that were reported as downregulated in prostate cancer. A virtual archive of 338 potential targets of methylation was produced. One candidate, IGFBP3, was selected for investigation, along with glutathione-S-transferase pi (GSTP1), a well-known methylation target in prostate cancer. Methylation of IGFBP3 was detected by quantitative methylation-specific PCR in 49/79 primary prostate adenocarcinoma and 7/14 adjacent preinvasive high-grade prostatic intraepithelial neoplasia, but in only 5/37 benign prostatic hyperplasia (P<0.0001) and in 0/39 histologically normal adjacent prostate tissue, which implies that methylation of IGFBP3 may be involved in the early stages of prostate cancer development. Hypermethylation of IGFBP3 was only detected in samples that also demonstrated methylation of GSTP1 and was also correlated with Gleason score ⩾7 (P=0.01), indicating that it has potential as a prognostic marker. In addition, pharmacological demethylation induced strong expression of IGFBP3 in LNCaP prostate cancer cells. Our concept of a methylation candidate gene bank was successful in identifying a novel target of frequent hypermethylation in early-stage prostate cancer. Evaluation of further relevant genes could contribute towards a methylation signature of this disease

IGFBP3 Colocalizes with and Regulates Hypocretin (Orexin)

Background: The sleep disorder narcolepsy is caused by a vast reduction in neurons producing the hypocretin (orexin) neuropeptides. Based on the tight association with HLA, narcolepsy is believed to result from an autoimmune attack, but the cause of hypocretin cell loss is still unknown. We performed gene expression profiling in the hypothalamus to identify novel genes dysregulated in narcolepsy, as these may be the target of autoimmune attack or modulate hypocretin gene expression. Methodology/Principal Findings: We used microarrays to compare the transcriptome in the posterior hypothalamus of (1) narcoleptic versus control postmortem human brains and (2) transgenic mice lacking hypocretin neurons versus wild type mice. Hypocretin was the most downregulated gene in human narcolepsy brains. Among many additional candidates, only one, insulin-like growth factor binding protein 3 (IGFBP3), was downregulated in both human and mouse models and coexpressed in hypocretin neurons. Functional analysis indicated decreased hypocretin messenger RNA and peptide content, and increased sleep in transgenic mice overexpressing human IGFBP3, an effect possibly mediated through decrease