OBJECTIVETo explore an exercise method for the prevention and treatment of the patients with shoulder and back fasciitis.

METHODSFrom 2006.8 to 2008.3, 120 patients with shoulder and back fasciitis were randomly divided into control group (n = 60, including 21 females and 39 males, the average age was (47.0 +/- 12.0) years, and the average course of disease was (14.1 +/- 12.0) months) and treatment group (n = 60,including 19 females and 41 males, the average age was (43.7 +/- 9.9) years, and the average course of disease was (16.4 +/- 13.4) months). The patients in the control group received massage therapy and the ones in the treatment group were treated with massage therapy and horizontal bar exercise. After 3 weeks treatment, the curative effects of the patients in two groups were observed. All the patients were followed up for 6 to 26 months, the recurrence were observed.

RESULTSAfter 3 weeks treatment, the scores of pain, sense of heaviness, strip sign, tenderness, shoulder and back function of the patients in two groups had significant differences compared with those before treatment (all P < 0.01). After treatment, the scores of pain, sense of heaviness, strip sign, tenderness, shoulder and back function of the patients in the treatment group were lower than those in the control group (P < 0.05). After 6 to 26 months following-up, the rate of recurrence in the treatment group was lower than that in the control group (P < 0.01).

CONCLUSIONHorizontal bar exercise is a simple, no expense and effective method in the prevention and treatment of shoulder and back fasciitis, which can improve the effect of the treatment and reduce the rate of recurrence.

Adult ; Back Pain ; etiology ; prevention & control ; therapy ; Exercise Therapy ; methods ; Fasciitis ; prevention & control ; therapy ; Female ; Humans ; Male ; Middle Aged ; Shoulder Pain ; etiology ; prevention & control ; therapy ; Treatment Outcome

This study was purposed to characterize the genomic distribution of the binding sites for AML1-ETO fusion protein on chromosome 2, 9 and 19, and to further gain insights into the characteristics of transcriptional regulation by AML1-ETO in acute myeloid leukemia so as to provide theoretical basis for the development of targeted therapy and optimization for treatment. Chromatin immunoprecipitation (ChIP) coupled with high density tiling arrays (chip), also known as ChIP-chip, was utilized in this study. ChIP-DNA enriched by an anti-ETO antibody and total genomic DNA of Kasumi cells were hybridized to tiling arrays, tiled through chromosome 2, 9 and 19. The ChIP enriched regions were identified using a model based analytical tool (MAT). Genomic distribution of the ChIP regions was analyzed using publicly available CEAS web server. The Gene Ontology (GO) enrichment analysis was performed to excavated the biological significance. The results indicated that a total of 588 enriched regions were identified on chromosome 2, 9 and 19 by the anti-ETO antibody. A number of the identified regions were located within enhancers (48.86%) or introns (37.35%), much smaller fractions were within proximal promoters (5.96%) or exons (5.49%). Functional enrichment analysis showed that cell proliferation and signal transduction biological pathways were enriched in potential genes of AML-ETO. It is concluded that half of the AML1-ETO binding sites are located within known transcriptional regulatory regions (promoter, 5' UTR and enhancer), while almost another half were within the sequences which were not previously reported as regulatory regions. The potential target molecular network of AML1-ETO is involved in several essential biological processes.
Base Sequence ; Binding Sites ; Cell Line, Tumor ; Chromosomes, Human, Pair 21 ; Chromosomes, Human, Pair 8 ; Core Binding Factor Alpha 2 Subunit ; genetics ; metabolism ; DNA-Binding Proteins ; metabolism ; Genome, Human ; Humans ; Leukemia, Myeloid, Acute ; genetics ; Oncogene Proteins, Fusion ; genetics ; metabolism ; Promoter Regions, Genetic ; RUNX1 Translocation Partner 1 Protein ; Translocation, Genetic