Agenda 2030: Measuring Progress in the Montenegro’s National Strategy for Sustainable Development through SDG Indicators

The Government of Montenegro nationalized 2030 Agenda on Sustainable Development by adopting the National Strategy for Sustainable Development (NSSD) in 2016, together with a corresponding Action Plan for its implementation. The NSSD is umbrella, horizontal and long-term development strategy of Montenegro that relates not only to environment and economics, but also to human resources, valuable social capital that should ensure prosperous development, recommendations for establishing the framework of financing and governance for sustainable development. The NSSD represents strategic framework for the transposition of the UN sustainable development goals (SDGs) and its indicators into national context. The NSSD Action plan, divided into 6 thematic areas with 30 strategic goals of sustainable development of Montenegro and their 102 measures and 601 sub-measures, represents very complex mechanism for monitoring and reporting about achieving the UN sustainable development goals (SDGs) in Montenegro. Hence, measuring progress in the NSSD implementation is the focus of this research. Effective measuring of the progress in the NSSD implementation could be achieved under the following preconditions: developed coordination mechanism for reporting, methodology of designing indicators, IT support for data collection and reporting, and strengthening of inter-linkages between the EU agenda and UN 2030 Agenda

Serbian consumer law: Out with the old, in with the new

The is a pre-print version (prior to acceptance/ pre-refereeing). Copyright © 2019 by SAGE Publication

Governance and Growth in the Western Balkans: A SVAR Approach

The quality of economic governance is one of the prerequisites for sustainable and faster economic development of the Western Balkan countries, having in mind their historical background, dissolution of the ex-Yugoslavia, specific economic circumstances during the transition recession of the 1990s, slow economic recovery at the beginning of the twenty-first century, strong impact of the global financial and economic crisis, and long and complexed path towards the European Union (EU). The main research problem in this paper is examining the dynamic relationships among government effectiveness, inflation, and GDP across Albania, Bosnia and Hercegovina, Kosovo, Montenegro, North Macedonia, and Serbia. We employ the Worldwide Governance Indicators of the World Bank, namely, the Governance Effectiveness Indicator, as one of the six broad dimensions of governance. Using a structural VAR approach, we examine the time-varying effects of economic governance shocks on inflation and economic growth dynamics for each of the Western Balkan (WB) countries in the period of January 2006 to December 2018. Our findings allow the WB policymakers to understand the impact of institutional strength involved in identifying the onset of sustainable development dynamics and the EU integration process in WB better and develop more effective government regulations that can be employed nationally

Functional effects of schizophrenia-linked genetic variants on intrinsic single-neuron excitability: A modeling study

Background: Recent genome-wide association studies (GWAS) have identified a large number of genetic risk factors for schizophrenia (SCZ) featuring ion channels and calcium transporters. For some of these risk factors, independent prior investigations have examined the effects of genetic alterations on the cellular electrical excitability and calcium homeostasis. In the present proof-of-concept study, we harnessed these experimental results for modeling of computational properties on layer V cortical pyramidal cell and identify possible common alterations in behavior across SCZ-related genes. Methods: We applied a biophysically detailed multi-compartmental model to study the excitability of a layer V pyramidal cell. We reviewed the literature on functional genomics for variants of genes associated with SCZ, and used changes in neuron model parameters to represent the effects of these variants. Results: We present and apply a framework for examining the effects of subtle single nucleotide polymorphisms in ion channel and Ca2+ transporter-encoding genes on neuron excitability. Our analysis indicates that most of the considered SCZ- related genetic variants affect the spiking behavior and intracellular calcium dynamics resulting from summation of inputs across the dendritic tree. Conclusions: Our results suggest that alteration in the ability of a single neuron to integrate the inputs and scale its excitability may constitute a fundamental mechanistic contributor to mental disease, alongside with the previously proposed deficits in synaptic communication and network behavior

Human apoB contributes to increased serum total apo(a) level in LPA transgenic mice

Background The Lp(a) lipoprotein (Lp(a)) consists of the polymorphic glycoprotein apolipoprotein(a) (apo(a)), which is attached by a disulfide bond to apolipoprotein B (apoB). Apo(a), which has high homology with plasminogen, is present only in primates and hedgehogs. However, transgenic mice and rabbits with high serum apo(a) levels exist. Liver is the main site for apo(a) synthesis, but the site of removal is uncertain. To examine differences between transgenic mice expressing the LPA gene and mice capable of forming Lp(a) particles, LPA -YAC transgenic mice and hAPOB transgenic mice were crossed and their offspring examined. Results Comparison of LPA -YAC with LPA -YAC/hAPOB transgenic mice showed that LPA -YAC/hAPOB transgenic mice have higher serum total apo(a) and total cholesterol level than mice lacking the hAPOB gene. However, hepatic apo(a) mRNA level was higher in LPA -YAC transgenic mice than in LPA -YAC/hAPOB transgenic mice. Feeding of a high-cholesterol/high-fat diet to male LPA -YAC transgenic mice with or without the hAPOB gene resulted in reduced serum total apo(a) and hepatic apo(a) mRNA level. Conclusion In conclusion, the higher serum total apo(a) level in LPA -YAC/hAPOB transgenic mice than in LPA -YAC transgenic mice is not caused by increased apo(a) synthesis. Lower hepatic apo(a) mRNA level in LPA -YAC/hAPOB than in LPA -YAC transgenic mice may suggest that the increase in total apo(a) level is a result of apo(a) accumulation in serum. Furthermore, observed higher serum total cholesterol level in LPA -YAC/hAPOB transgenic mice than either in wild type or LPA -YAC transgenic mice may further suggest that human APOB transgenicity is a factor that contributes to increased serum total apo(a) and cholesterol levels. Our results on reduced serum total apo(a) and hepatic apo(a) mRNA levels in HCHF fed male LPA -YAC transgenic mice confirm earlier findings in females, and show that there are no sex difference in mechanisms for lowering apo(a) level in response to HCHF feeding

Bivariate causal mixture model quantifies polygenic overlap between complex traits beyond genetic correlation.

Accumulating evidence from genome wide association studies (GWAS) suggests an abundance of shared genetic influences among complex human traits and disorders, such as mental disorders. Here we introduce a statistical tool, MiXeR, which quantifies polygenic overlap irrespective of genetic correlation, using GWAS summary statistics. MiXeR results are presented as a Venn diagram of unique and shared polygenic components across traits. At 90% of SNP-heritability explained for each phenotype, MiXeR estimates that 8.3 K variants causally influence schizophrenia and 6.4 K influence bipolar disorder. Among these variants, 6.2 K are shared between the disorders, which have a high genetic correlation. Further, MiXeR uncovers polygenic overlap between schizophrenia and educational attainment. Despite a genetic correlation close to zero, the phenotypes share 8.3 K causal variants, while 2.5 K additional variants influence only educational attainment. By considering the polygenicity, discoverability and heritability of complex phenotypes, MiXeR analysis may improve our understanding of cross-trait genetic architectures

Cross-tissue eQTL enrichment of associations in schizophrenia.

The genome-wide association study of the Psychiatric Genomics Consortium identified over one hundred schizophrenia susceptibility loci. The number of non-coding variants discovered suggests that gene regulation could mediate the effect of these variants on disease. Expression quantitative trait loci (eQTLs) contribute to variation in levels of mRNA. Given the co-occurrence of schizophrenia and several traits not involving the central nervous system (CNS), we investigated the enrichment of schizophrenia associations among eQTLs for four non-CNS tissues: adipose tissue, epidermal tissue, lymphoblastoid cells and blood. Significant enrichment was seen in eQTLs of all tissues: adipose (β = 0.18, p = 8.8 × 10−06), epidermal (β = 0.12, p = 3.1 × 10−04), lymphoblastoid (β = 0.19, p = 6.2 × 10−08) and blood (β = 0.19, p = 6.4 × 10−06). For comparison, we looked for enrichment of association with traits of known relevance to one or more of these tissues (body mass index, height, rheumatoid arthritis, systolic blood pressure and type-II diabetes) and found that schizophrenia enrichment was of similar scale to that observed when studying diseases in the context of a more likely causal tissue. To further investigate tissue specificity, we looked for differential enrichment of eQTLs with relevant Roadmap affiliation (enhancers and promoters) and varying distance from the transcription start site. Neither factor significantly contributed to the enrichment, suggesting that this is equally distributed in tissue-specific and cross-tissue regulatory elements. Our analyses suggest that functional correlates of schizophrenia risk are prevalent in non-CNS tissues. This could be because of pleiotropy or the effectiveness of variants affecting expression in different contexts. This suggests the utility of large, single-tissue eQTL experiments to increase eQTL discovery power in the study of schizophrenia, in addition to smaller, multiple-tissue approaches. Our results conform to the notion that schizophrenia is a systemic disorder involving many tissues