We aimed to evaluate levels of amino-terminal pro-brain natriuretic peptid (NT-proBNP) in prediction of left ventricular ejection fraction (LVEF) in heart failure patients. Prospective study on 60 consecutive patients with symptoms and signs of heart failure was performed. Blood samples for NT-proBNP analysis was taken from all test subjects and echocardiography was also done in all of them. According to LVEF value, patients were divided into four groups; those with <or=30%, 31 to 39%, 40 to 49% and >or=50%. NT-proBNP values correlated with LVEF value. Regression analysis was used to evaluate how well NT-proBNP values predict LVEF. We used Receiver Operating Characteristic Curve calculation to evaluate diagnostic performance of NT-proBNP in estimation of LVEF. Average value of NT-proBNP in test group was 3191.69+/-642.89 pg/ml (p<0.001). Average value of NT-proBNP decreased with higher LVEF categories with significant (p<0.001) and high negative correlation (r= -0,75). Stepwise multivariate linear regression analysis showed that logarithmic value of NT-proBNP was excellent predictor of LVEF value (p<0.05). Model equation based on regression analysis was LVEF=88.645-15.311 x log (NT-proBNP). Predictive model for LVEF yielded from regression analysis had sensitivities of 98% and 81%, specificities of 20% and 90%, positive predictive values of 86% and 78% and negative predictive values of 67% and 92% for predicting patients with LVEF<50% and LVEF<40%, respectively. There was negative linear correlation between NT-proBNP and LVEF. NT-proBNP was excellent predictor of LVEF value (p<0.05).

Diagnosis and management of patients with SLE (Systemic Lupus Eritematosus), autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), involves specific diagnostic tests, such as IFA-AMA, IFA anti-dsDNA and immunoblotting for the detection of autoantibodies for specific autoantigens (mitochondria, dsDNA, M2, LKM-1, LC-1, SLA/LP). We established specific correlation between the detected autoantibodies and corresponding clinical findings. The total of 813 serum specimens were probed with IFA-anti-dsDNA, 98 of which tested positive. We also performed dilution analysis to the end point for all the positive specimens. Numerous specimens were tested by IFA, AMA and immunoblotting.

Since its foundation in 1992, the Croatian Medical Journal (CMJ) has followed the strict standards of quality in the scientific publishing. However, the Journal has been aware that its specific position demands more than just following the already established rules. From the very beginning, the Journal declared an “author-helpful policy,” stating that “journal editors should have a major role in training authors in science communication, especially in smaller and developing scientific communities. Journal authors usually send scientifically acceptable but poorly prepared articles and it is a pity to lose valid data because of their poor presentation.” (1,2). In brief, the editors and editorial staff of the CMJ have been well aware that the skills of scientific reporting and publishing in our academic community are not developed and that valuable research results and valid data are being lost because of poor presentation. To be perfectly honest, ten years ago this statement looked like a nice promise, one of the many we in academic medicine learnt not to take too seriously.

The signaling mechanisms downstream of growth factor-stimulated proliferation in myeloid leukemia cells have not yet been fully elucidated. Recent evidence suggests that alternate pathways to the mitogen-activated protein kinase cascade are required. We have previously shown that Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) activates cytosolic phospholipase A2 (cPLA2), which is involved in the proliferation of vascular smooth muscle cells. In the present study, the contribution of this pathway was investigated in the proliferation of U-937 myeloid leukemia cells. In U-937 cells, fetal bovine serum (FBS)-induced proliferation was attenuated by CaM kinase II inhibitor KN-93 but not by its inactive analog KN-92. Inhibitors of cPLA2 (methyl arachidonyl fluorophosphonate and arachidonyl trifluoromethyl ketone) also reduced proliferation of U-937 cells. FBS-induced proliferation was also attenuated by cotransfection with cPLA2 antisense oligonucleotides. These results suggest a role for CaM kinase II and cPLA2 in the proliferation of U-937 cells. FBS stimulated CaM kinase II and cPLA2 activities in a time-dependent manner. Moreover, FBS-stimulated phosphorylation and activation of cPLA2 activation was inhibited by KN-93. FBS-stimulated phosphorylation of CaM kinase II was blocked by KN-93 but not by cPLA2 inhibitors, suggesting that CaM kinase II activates cPLA2. The products of phospholipid hydrolysis produced by cPLA2, lysophosphatidylcholine but not arachidonic acid, increased [3H]thymidine incorporation in U-937 cells. These data suggest that exposure of U-937 cells to FBS promotes phosphorylation and activation of CaM kinase II, leading to stimulation of cPLA2 and generation of lysophosphatidylcholine and resultant proliferation of these cells.