No abstract

The effect of intensive dynamic back extensor exercises for patients with chronic low back pain was investigated in a controlled clinical trial in which chronic low back pain patients underwent a 3-month intensive training program with a total of 30 sessions. The 105 patients were divided into 3 groups: a treatment group, an alternative group which underwent 1/5 of the treatment group's exercise program per session, and an alternative group in which treatment consisted of thermotherapy, massage and mild exercise. Regardless of whether the treatment outcome is assessed qualitatively or quantitatively, a statistically significant, favorable difference was found between the results for the treatment group and for the alternative groups at conclusion and at the 3-month follow-up. It appeared from the quantitative assessment that patients in the treatment group who completed the training program at least once a week for the entire 1-year follow-up period were the only patients with a significantly better back status after 1 year compared to the time of inclusion. Irrespective of sex, age, duration and degree of severity of back trouble, or of pre-existing sciatica or pathological findings upon X-ray of the spine, patients obtained a favorable result from the training program. The therapy was found to be without risk, but patients with clinical signs of current lumbar nerve root compression or radiological signs of spondylolysis or halisteresis of the spine were excluded from the study.

PRDM proteins are tissue-specific transcription factors often deregulated in diseases, particularly in cancer where different members have been found to act as oncogenes or tumor suppressors. PRDM5 is a poorly characterized member of the PRDM family for which several studies have reported a high frequency of promoter hypermethylation in cancer types of gastrointestinal origin. We report here the characterization of Prdm5 knockout mice in the context of intestinal carcinogenesis. We demonstrate that loss of Prdm5 increases the number of adenomas throughout the murine small intestine on an Apc Min background. By using the genome-wide ChIP-seq (chromatin immunoprecipitation (ChIP) followed by DNA sequencing) and transcriptome analyses we identify loci encoding proteins involved in metabolic processes as prominent PRDM5 targets and characterize monoacylglycerol lipase (Mgll) as a direct PRDM5 target in human colon cancer cells and in Prdm5 mutant mouse intestines. Moreover, we report the downregulation of PRDM5 protein expression in human colon neoplastic lesions. In summary, our data provide the first causal link between Prdm5 loss and intestinal carcinogenesis, and uncover an extensive and novel PRDM5 target repertoire likely facilitating the tumor-suppressive functions of PRDM5.