Eccentric hamstring strength is associated with age and duration of previous season hamstring injury in male soccer players

Background: Eccentric hamstring strength seems important in reducing the odds of future hamstring injuries. While age and previous injury are well-known risk factors for future hamstring injuries, the association of age and previous hamstring injury with eccentric hamstring strength in the following season is unknown.Purpose: To investigate the association of age and previous hamstring injury with preseason eccentric hamstring strength in soccer players, and to investigate the association between previous hamstring injury duration and preseason eccentric hamstring strength. Study design: Descriptive, cross-sectional studyMethods: A convenience sample of 284 male amateur soccer players (age 18-38 years) was included in the analyses. Self-reported information about previous season hamstring injury and its duration (three weeks or less; more than three weeks) was collected. Preseason eccentric hamstring strength was obtained during the Nordic hamstring exercise using a field-based device. Results: Age had a negative association with preseason eccentric hamstring strength with 0.9% reduction per year. Players with a previous hamstring injury duration of more than three weeks (n=27) had 13% lower preseason eccentric hamstring strength compared to players without previous hamstring injury. Conclusion: Older players have lower preseason eccentric hamstring strength than younger players. Players with a previous hamstring injury duration of more than three weeks have lower preseason eccentric hamstring strength than the rest of the players. These results highlight the need to monitor and address the identified weaknesses in eccentric hamstring strength in amateur soccer players, with specific emphasis on older players with a previous hamstring injury of longer duration

Reasons for poor follow-up of diabetic retinopathy patients after screening in Tanzania: a cross-sectional study

Diabetes is an emerging public health problem in sub-Saharan Africa. Diabetic retinopathy is the commonest microvascular complication of diabetes and is a leading cause of blindness, mainly in adults of working age. Follow-up is crucial to the effective management of diabetic retinopathy, however, follow-up rates are often poor in sub-Saharan Africa. The aim of this study was to assess the proportion of patients not presenting for follow-up and the reasons for poor follow-up of diabetic patients after screening for retinopathy in Kilimanjaro Region of Tanzania

G Protein-coupled Receptor Kinase 4 (GRK4) Regulates the Phosphorylation and Function of the Dopamine D3 Receptor*

During conditions of moderate sodium excess, the dopaminergic system regulates blood pressure and water and electrolyte balance by engendering natriuresis. Dopamine exerts its effects on dopamine receptors, including the dopamine D3 receptor. G protein-coupled receptor kinase 4 (GRK4), whose gene locus (4p16.3) is linked to essential hypertension, desensitizes the D1 receptor, another dopamine receptor. This study evaluated the role of GRK4 on D3 receptor function in human proximal tubule cells. D3 receptor co-segregated in lipid rafts and co-immunoprecipitated and co-localized in human proximal tubule cells and in proximal and distal tubules and glomeruli of kidneys of Wistar Kyoto rats. Bimolecular fluorescence complementation and confocal microscopy revealed that agonist activation of the receptor initiated the interaction between D3 receptor and GRK4 at the cell membrane and promoted it intracellularly, presumably en route to endosomal trafficking. Of the four GRK4 splice variants, GRK4-γ and GRK4-α mediated a 3- and 2-fold increase in the phosphorylation of agonist-activated D3 receptor, respectively. Inhibition of GRK activity with heparin or knockdown of GRK4 expression via RNA interference completely abolished p44/42 phosphorylation and mitogenesis induced by D3 receptor stimulation. These data demonstrate that GRK4, specifically the GRK4-γ and GRK4-α isoforms, phosphorylates the D3 receptor and is crucial for its signaling in human proximal tubule cells

D5 dopamine receptor decreases NADPH oxidase, reactive oxygen species and blood pressure via heme oxygenase-1

D(5) dopamine receptor (D(5)R) knock-out mice (D(5)(−/−)) have a higher blood pressure (BP) and higher reactive oxygen species (ROS) production than their D(5)R wild-type littermates (D(5)(+/+)). We tested the hypothesis that the high BP and increased ROS production in D(5)(−/−) mice may be caused by decreased heme oxygenase-1 (HO-1) expression and activity. We found that renal HO-1 protein expression and HO enzyme activity were decreased (65 and 50%, respectively) in D(5)(−/−) relative to D(5)(+/+) mice. A 24 h of administration of hemin, an HO-1 inducer, increased HO-1 expression and HO activity (6.8- and 1.9-fold, respectively) and normalized the increased ROS production and BP in D(5)(−/−) mice. Expression of HO-1 protein and HO activity were increased (2.3- and 1.5-fold, respectively) in HEK cells that heterologously expressed human wild-type D(5)R (HEK-hD(5)R), but not the empty vector-transfected HEK-293 cells. Fenoldopam (Fen), a D(5)R agonist, increased HO activity (3 h), HO-1 protein expression, HO-1 and D(5)R colocalization and co-immunoprecipitation in HEK-hD(5)R cells. Cellular NADPH oxidase activity was decreased by 35% in HEK-hD(5)R that was abrogated with silencing of the heme oxygenase 1 gene (HMOX1). HMOX1 siRNA also impaired the ability of Fen to decrease NADPH oxidase activity in HEK-hD(5)R cells. In summary, the D(5)R positively regulates HO-1 through direct protein/protein interaction in the short-term and by increasing HO-1 protein expression in the long-term. The impaired D(5)R regulation of HO-1 and ROS production contributes to the pathogenesis of hypertension in D(5)(−/−) mice