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Objectives To investigate the effectiveness of a futsal-specific warm-up to reduce injuries in amateur teams. Design Quasi-experimental. Setting Two futsal centres followed over one season using a specific report card. Participants 878 teams (Intervention group, n = 458; Control group, n = 420) of both genders and three age groups (U13, U17, adults). Intervention A futsal-specific warm-up consisting of cardiovascular exercises, dynamic stretches, and game-related skills. Main outcome measures The incidence rate and severity of all injuries, lower extremity (LE) injuries and contact injuries. A multivariate Poisson regression analysis was used to compare between-group rates. Results The rate of all injuries was lower in the intervention group (rate ratio (RR) = 0.72, 95% CI = 0.59 to 1.06), yet not significant. There was a significantly lower rate of contact injuries in the intervention group (RR = 0.68, 95% CI = 0.51 to 0.98). Subgroup analysis, based on the warm-up adherence of intervention teams (low, intermediate, high), showed a lower rate of all injuries (RR = 0.52, 95% CI = 0.29 to 0.97), and LE injuries (RR = 0.32, 95% CI = 0.14 to 0.81) in the high compared to low adherence group. Conclusion A futsal-specific warm-up can reduce the rate of contact injuries in amateur players. With high adherence the rate of all injuries and LE injuries may also reduce.

BackgroundTrigger finger (TF), a painful condition involving a finger flexor tendon, is a common problem with a prevalence of ~2-3% in the general population. However, the TF prevalence is higher among diabetic patients-ranges from 6.7% to 10%. We have analyzed the expression of the extracellular matrix, inflammation, and epigenetic related genes in diabetic and non-diabetes TF. We hypothesized that Diabetes condition induces alter the expression of epigenetic modification genes in diabetic patients and one of the underlying determinants for more prevalence of TF in diabetic patients.MethodTissues from the fingers of patients with symptomatic trigger fingers were collected. We had three groups: carpal tunnel syndrome (as a control), trigger finger, and diabetic trigger finger. A quantitative real-time polymerase chain reaction was performed. The gene expression of Extracellular matrix (ECM) components [COL-I, COL-II, COL-X, Aggrecan], DNA methyltransferases enzymes (DNMT1, DNMT3), growth factors (TGF-b, IGF), and Histone deacetylase enzymes (HDAC1, HDAC2) were evaluated in all groups.ResultsThe mRNA expression of COL-I, COL-II, Aggrecan was significantly higher in the pully A1 of diabetic patients (p= 0.0164, p=0.0351, p=0.0399, respectively) as compared to non-diabetic TF patients. Diabetes was associated with a significant increase in the DNMT3 expression compared to non-diabetic TF patients (p=0.0485). HDAC1 and HDAC2 gene expression were up-regulated in diabetic TF than non-diabetic TF.ConclusionThe chronic state of hyperglycemia induces epigenetic modification of gene expressions in trigger fingers. This seems to have a significant impact on the development, recurrence, and progression of trigger finger in diabetic patients.

Trigger finger is a common yet vastly understudied fibroproliferative hand pathology, severely affecting patients’ quality of life. Consistent trauma due to inadequate positioning within the afflicted finger’s tendon/pulley system leads to cellular dysregulation and eventual fibrosis. While the genetic characteristics of the fibrotic tissue in the trigger finger have been studied, the pathways that govern the initiation and propagation of fibrosis are still unknown. The complete gene expression profile of the trigger finger has never been explored. Our study has used the Nanostring nCounter gene expression assay to investigate the molecular signaling involved in trigger finger pathogenesis. We collected samples from patients undergoing trigger finger (n = 4) release surgery and compared the gene expression to carpal tunnel tissue (n = 4). Nanostring nCounter analysis identified 165 genes that were differentially regulated, 145 of these genes were upregulated, whereas 20 genes were downregulated. We found that several collagen genes were significantly upregulated, and a regulatory matrix metalloproteinase (MMP), MMP-3, was downregulated. Bioinformatic analysis revealed that several known signaling pathways were dysregulated, such as the TGF-β1 and Wnt signaling pathways. We also found several novel signaling pathways (e.g., PI3K, MAPK, JAK-STAT, and Notch) differentially regulated in trigger finger. The outcome of our study helps in understanding the molecular signaling pathway involved in the pathogenesis of the trigger finger.

This report describes a 21-year-old man, a semiprofessional football (soccer) player, with a navicular stress fracture. It highlights the difficulty in diagnosing the condition and the complications arising from inadequate management. The case discusses the optimal management of these stress fractures and the detrimental role of weight-bearing recovery. The diagnosis of navicular stress fractures is challenging, and a high index of suspicion is required. The available literature indicates that limited weightbearing is not an appropriate treatment for navicular stress injuries. Non-weight-bearing (NWB) cast immobilisation for 6–8 weeks appears to be the gold standard treatment; however, open reduction with internal fixation (ORIF) has similar success rates and an equal return-to-play time but should also be followed by a period of NWB. NWB cast immobilisation for 6 weeks remains a good second option at any time following failed limited weight-bearing activity.