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Vascular endothelial growth factor (VEGF) has been well documented to stimulate cell proliferation and differentiation; however, we have observed that copper (Cu)-induced regression of heart hypertrophy was VEGF-dependent. The present study was undertaken to test the hypothesis that Cu causes alterations in the distribution of VEGF receptors (VEGFRs) in hypertrophic cardiomyocytes so that it switches the signalling pathway from stimulation of cell growth to reversal of cell hypertrophy.', 'Primary cultures of neonatal rat cardiomyocytes were exposed to phenylephrine (PE) at a final concentration of 100 microM in cultures for 48 h to induce cell hypertrophy. The hypertrophic cardiomyocytes were exposed to copper sulfate at a final concentration of 5 microM in cultures for 24 h with a concomitant presence of PE. Flow cytometry, gene silencing, and ELISA procedures were used to analyse the changes in VEGFRs and their relationship with regression of cardiomyocyte hypertrophy. Cu did not change the concentration of VEGF in culture media, but increased the ratio of VEGFR-1 to VEGFR-2 two-fold. Gene silencing of VEGFR-2, in the absence of Cu addition, reversed PE-induced cardiomyocyte hypertrophy, which was suppressed by an anti-VEGF antibody. Gene silencing of VEGFR-1 blocked Cu-induced regression of cell hypertrophy and decreased the activity of cGMP-dependent protein kinase-1 (PKG-1). A PKG-1 antagonist, Rp-8-pCPT-cGMPS, blocked both Cu- and VEGFR-2 gene silencing-induced regression of cardiomyocyte hypertrophy.
Is copper-induced regression of cardiomyocyte hypertrophy associated with enhanced vascular endothelial growth factor receptor-1 signalling pathway?

The 6-min walk test (6MWT) has prognostic value in various pulmonary disorders including idiopathic pulmonary fibrosis (IPF). We determined the individual prognostic accuracy of distance walked and oxygen saturation during the 6MWT in patients with IPF. We defined a new composite index, the distance-saturation product (DSP), which is the product of distance walked and lowest oxygen saturation during the 6-min walk test. We compared the performance of the DSP to the individual 6MWT parameters in predicting mortality.', 'We evaluated pulmonary function tests, 6-min walk parameters and the DSP between survivors and non-survivors. The ability of each measure to discriminate outcomes was determined by receiver operator curves.', '81 patients (48 survivors, 33 non-survivors) were included. Pulmonary function tests were similar and did not correlate with survival. Desaturation was greater (89.4% versus 83.7%, P<0.001) and distance walked was lower (406.9 versus 181.3m, P = 0.005) in non-survivors. The DSP was significantly lower among non-survivors (364.8 versus 153.5m%, P < 0.001) and predicted mortality more accurately than either individual 6MWT component (P = 0.035 versus desaturation, P=0.040 versus distance). A DSP <200 m% was associated with a seven-fold greater risk of 12-month mortality and an 18.0% shorter median survival compared with a DSP > 200 m% (P < 0.001).
Does the distance-saturation product predict mortality in idiopathic pulmonary fibrosis?

Pacemaker lead implantation can cause thrombosis, which can be associated with serious local morbidity and complicated by pulmonary embolism. Few reliable estimates of the incidence of thrombosis have been reported. The contribution of established risk factors to venous thrombosis in patients with implanted pacemaker leads is unknown.', 'One hundred forty-five consecutive patients n = 145) underwent routine clinical and Doppler ultrasound evaluation for thrombosis before and 3, 6, and 12 months after lead implantation. Established risk factors for venous thrombosis were assessed in detail for all patients. Clinical outcome, including clinically manifest thrombosis, pulmonary embolism, associated pacemaker lead infection, complicated reinterventions, and death, was evaluated. Thrombosis was observed in 34 (23%) of 145 patients. Thrombosis did not cause any signs or symptoms in 31 patients but resulted in overt clinical symptoms in 3 patients. The absence of anticoagulant therapy, use of hormone therapy, and a personal history of venous thrombosis were associated with an increased risk of thrombosis. The risk of thrombosis increased in the presence of multiple pacemaker leads compared to a single lead.
Does incidence and risk factors of early venous thrombosis associated with permanent pacemaker lead?