Experimental study of tendon healing early phase: is IGF-1 expression influenced by platelet rich plasma gel?

BACKGROUND: It is well established that growth factors play a critical role in the healing process of connective tissues. To our knowledge, there are no studies in literature concerning the influence of PRP on growth factors expression. HYPOTHESIS: The aim of this study was to assess the effect of a single application of platelet rich plasma (PRP) gel in a patellar tendon defect on the spatial and temporal expression of Insulin-like Growth Factor 1 (IGF-1) during tendon healing. MATERIALS AND METHODS: Twenty-four animals were randomized to receive PRP (PRPFast, Bioteck) in a gel form (PRP group) and 24 to serve as untreated controls (Control group). A defect of 3 mm x 10 mm was surgically created on the tendon under general anaesthetic and in the PRP group, PRP gel was applied to fill the tendon defect whereas no treatment was applied in the control group. Six animals (12 limbs) from each treatment-group were sacrificed after one, two, three and four weeks following treatment. Histological and immunohistochemical staining were performed. RESULTS: Histology revealed a faster healing process in the tendons of PRP group in comparison with the controls. In the first 2 weeks of healing, IGF-1 was found intracellularly in various type cells, whereas in the last 2 weeks of healing, IGF-1 was detected mainly in tenocytes. Both cytoplasmic and nuclear expressions were present, whereas the larger amounts of immunoexpression were localized in both epitenon and endotenon. A superior expression of IGF-1 was seen in PRP group compared with controls (p<0.0001) in both the epitenon and endotenon at each time point except at 4th week of healing where a superior expression of IGF-1 was shown in the endotenon of control group, compared to the PRP group (p<0.0001). CONCLUSION: PRP may improve tendon defect healing by overexpression of IGF-1. LEVEL OF EVIDENCE: Laboratory control animal study.

ANP concentrations during interchanging DDD-VVI pacing modes in patients with retrograde ventriculoatrial conduction.

The main reason for the pacemaker syndrome during VVI pacing is the existence of ventriculoatrial conduction (V-AC). Twenty-five patients with a permanent DDD pacemaker and ventriculoatrial conduction were included in the study. IN those patients the hemodynamic changes were evaluated in relation to ANP plasma concentration changes during different modes of pacing. After a resting period of 30 minutes in the supine position ANP plasma concentration and blood pressure were evaluated: a) under DDD atrioventricular pacing at 90/min and for 30 minutes and b) under VVI pacing at 90/min and for 30 minutes. A decrease of systolic blood pressure by 12.77% (P < 0.0001) and diastolic blood pressure by 10.50% (P < 0.0001) was noticed during VVI pacing. ANP was increased during VVI pacing by 215.95% (P < 0.0001). It was observed that the acute transition from DDD to VVI pacing leads to a 3-fold increase in the levels of plasma ANP; this may be partially responsible for the pathogenesis of the haemodynamic changes during VVI pacing mediated through the direct hypotensive effect in addition to the coincidence of atrial and ventricular contraction. This study also proves the role of the increased systolic stress of atrial myocardium for the increased ANP secretion.

The effect of trimetazidine on reperfusion arrhythmias in acute myocardial infarction.

The study aims to evaluate the effect of trimetazidine in reducing reperfusion arrhythmias in patients with acute myocardial infarction after successful thrombolysis. A total of 169 patients were included in the study, 83 of whom received trimetazidine orally at an initial dose of 60 mg followed by 20 mg tid for 5 days. These patients formed the study group (group T) while the remaining 86, the control group (group C). Successful thrombolysis by clinical and electrocardiographic criteria was observed in 53 patients of group T and in 55 patients of group C. Reperfusion arrhythmias were observed in 16 patients in group T (30.1%) and in 31 in group C (56.3%). This difference was statistically significant. Serious ventricular arrhythmias (sustained ventricular tachycardia, ventricular fibrillation) were observed in 1 patient of group T (1.8%) and in 6 patients of group C (10.9%). This difference was also statistically significant. It is concluded that trimetazidine administration can reduce the rate of reperfusion arrhythmias. This conclusion should be confirmed by larger clinical trials in order to give to the clinical results a stronger statistical power.

A new glucose 6-phosphate dehydrogenase variant (G6PD Thessaloniki) in a patient with idiopathic myelofibrosis.

A new deficient glucose 6-phosphate dehydrogenase (G6PD) variant, G6PD Thessaloniki, which was found in the red blood cells of a 70-year-old woman who had idiopathic myelofibrosis, is described. G6PD Thessaloniki had a low Michaelis constant (Km) for G6P (20 microM), high Km for NADP (10.1 microM), normal pH optimum, reduced heat stability, decreased electrophoretic mobility (96-98% of the normal), increased 2-deoxy-G6P and decreased galactose 6-phosphate utilization. Several other enzymatic activities measured in the patient's red blood cells were normal. Studies of red blood cell survival and glucose utilization gave evidence of haemolysis caused by defective glucose utilization by the pentose phosphate pathway. The only son of the patient had normal G6PD in his red blood cells. In an attempt to investigate the origin of G6PD Thessaloniki, heat stability tests of G6PD extracted from the patient's skin have been performed.