Impact of financial development and economic growth on energy consumption: A panel vector autoregressive analysis for the comparison of G7 and top 10 emerging market economies

The aim of this paper is to investigate the relationship between energy consumption, financial development, and economic growth in the case of the G7 economies and emerging market economies. To this end, the role of the banking sector, as well as data from both the stock and the bond market, are explicitly used to proxy financial development. It is used the panel VAR method for the data period from 1990 to 2015. The results illustrate that there is a positive link between the stock market development and energy consumption in both G7 and top 10 emerging market economies in the long run. Also, while banking sector development in G7 countries decreases energy consumption in the long run, increases it in emerging market economies. Another aspect of the results is the determination of the energy-enhancing effect of the bond market development in the G7 countries. Moreover, while the results once again emphasize the existence of the link between financial development and energy consumption, they differ in terms of developed and developing countries

Telomerase activity in patients with stage 2–5D chronic kidney disease

Background: Molecular mechanisms of increased cardiovascular mortality in chronic kidney disease (CKD) associated with biological age are not well understood. Recent studies support the hypothesis that common factors responsible for this phenomenon are cellular aging and telomere dysfunction. Objectives: The purpose of this study was to investigate the relation between telomerase activity and CKD stages. Methods: The study included 120 patients who were followed-up for CKD stage 2–5D, composed of 30 patients of each stage and 30 healthy volunteers without any known disease who were admitted to our hospital for routine check-ups. Telomerase activity in peripheral blood mononuclear cells (PBMC) was measured using the TRAP assay. Results: A significant difference was observed for telomerase activity in PBMC between groups. The detected levels were lowest in the healthy control group (0.15 ± 0.02), and highest in CKD stage 5D patients (0.23 ± 0.04). In CKD patients, telomerase activity in PBMC was positively correlated with the CKD stage, serum creatinine, potassium and parathormone levels, and negatively correlated with estimated glomerular filtration rate (eGFR), body mass index (BMI), platelet count and serum calcium levels. According to the linear regression analysis, independent predictors for high telomerase activity in CKD patients were eGFR and BMI. Conclusion: Telomerase activity in PBMC increases with advancing CKD stage in CKD patients. Increased telomerase activity in PBMC is associated with eGFR and BMI

The Canine copper toxicosis gene <i>MURR1</i> is not implicated in the pathogenesis of Wilson disease

Background It has recently been demonstrated that the Wilson disease (WD) protein directly interacts with the human homolog of the MURR1 protein in vitro and in vivo, and that this interaction is specific for the copper transporter. The aim of the present study was to clarify the role of MURR1 in the pathogenesis of WD as well as in other WD-like disorders of hepatic copper metabolism of unknown origin. Methods Using the single-strand conformation polymorphism (SSCP) method followed by sequencing, we analyzed the 5′ untranslated region (UTR) and three exons of the MURR1 gene in three groups of patients: 19 wd patients in whom no mutations were detected in the ATP7B gene, 53 wd patients in whom only one mutation in the ATP7B gene was found, and 34 patients in whom clinical and laboratory data suggested a WD-like disorder of hepatic copper metabolism of unknown origin. Results We  detected in these patients six rare nucleotide substitutions, namely one splice-site consensus sequence and one missense and four silent nucleotide substitutions. All substitutions except one were found in the heterozygous state. No difference in the frequencies of the various substitutions was observed between patients and controls. Conclusions These data suggest that the MURR1 gene and its protein product are unlikely to play a primary role in the pathogenesis of Wilson disease. More extensive studies with larger numbers of clinically homogeneous patients should be carried out to establish whether nucleotide alterations in the MURR1 gene may have a role in causing WD or WD-like disorders or act as modifying factors in the phenotype variability in WD.</br