The objective of this research work was to explore the scope, structure and quality of production and use of domestic wheat in the RS. The subject of the research was to determine the production of wheat in the Republic of Srpska, the needs for seed wheat, determine the amount imported, and to identify measures to increase domestic production of seed wheat and to reduce imports. The analysis of commercial wheat production in the period 2006-2010 showed that the production took place in the average area of ​​44,017.6 ha, with an average yield of 3.28 t/ha and total production of 145,591 t. The highest level of wheat production was recorded in 2007 when it was 172,481 t, and a minimum production was in 2010 when it was 84,647 t. In the Republic of Srpska in 2010, the area under wheat amounted to 33,641 ha, which required about 8,410 tonnes of wheat seed, and only 4.27% of the quantities of seed wheat needed for the RS market were produced in the RS, the rest came from imports. According to the Indirect Taxation Administration data, the Republic of Srpska imported 125 t of wheat seed in 2009. The quantities of imported wheat vary considerably from year to year and are influenced by the weather in the sowing season and the prices on the market. Analysis of seed wheat in period 2006-2010 showed that the seed wheat occupied an average area of ​​128.8 ha, with the average yield of 4.06 t/ha and the total average production of 514.2 tonnes. The highest production was recorded in 2008 when it was 656.25 tonnes, and the lowest in 2010, 359.4 tonnes. Demand for wheat seed of the Republic of Srpska, based on five-year average, amounts to 13,205 tonnes, in which the domestic production share is 514 tonnes or 3.9%. The value of domestic wheat seed production in this period was BAM 393,616, and the value of missing quantities of seeds that are imported is BAM 9,824,152, based on the domestic price.

INTRODUCTION Hospital infections (HIs), which are frequently associated with hospital treatment, increase morbidity, mortality and treatment costs. The aim of this study was to establish the incidence of HIs in a neurological intensive care unit (nICU), and to determine the most prevalent causative agents and risk factors for HIs. METHODOLOGY A cross-sectional study with nested case-control design was conducted between 1 July 2009 and 30 June 2010 at an 18-bed neurological intensive care unit at the Clinical Center Kragujevac, Serbia. RESULTS In total, 537 patients were enrolled in the study, with 6,549 patient-days. There were 89 patients with 101 HIs. The incidence of patients with HIs was 16.57%, and incidence of HIs was 18.81%, while density of HIs was 15.42 per 1,000 patient-days. The most frequent anatomical sites of HIs were urinary tract (73.27%), blood (10.89%), and skin and soft tissues (10.89%). The following risk factors were identified: co-morbidity (OR=3.9; 95% CI=1.9-7.9), surgical intervention in the last 30 days (OR=5.6; 95% CI=1.5-20.4), urinary bladder catheterization longer than seven days (OR=3.8; 95% CI=1.8-8.2), value of Glasgow coma scale ≤ 9 (OR=3.7; 95% CI=1-6.9), and longer hospital stay (OR=1.1; 95% CI=1.1-1.2). CONCLUSIONS Hospitalization in an nICU bears high risk of HIs, especially of urinary tract infections caused by Gram-negative bacteria, in patients with longer hospital stay or co-morbidities, and in those who have had surgical interventions or prolonged use of a urinary bladder catheter. Special attention should be paid to these patients to prevent HIs.

To evaluate cytotoxicity of experimental conventional and resin modified glass-ionomer cements on UMR-106 osteoblast cell cultures and cell cultures of NIH(3)T(3) mouse fibroblasts specimens were prepared for every experimental material and divided into: group 1.Conventional glass-ionomer cements: GC Fuji IX GP Fast, GC Fuji Triage and Ketac Silver; group 2. Resin modified glass-ionomer cements: GC Fuji II LC, GC Fuji Plus and Vitrebond; group 3. Positive control was presented by specimens of composite Vit-l-ecence® and negative control-group 4. was presented by α-minimum essential medium for UMR-106 - osteoblast-like cells and Dulbecco's Modified Eagle's Medium for NIH(3)T(3) mouse fibroblast cells. Both cell cultures were exposed to 10% of eluate of each single specimen of each experimental material. Experimental dishes were incubated for 24 h. Cell metabolism was evaluated using methyltetrazolium assay. Kruskal-Wallis test and Tukey-Kramer post hoc test for the materials evaluated on NIH(3)T(3) mouse fibroblast cells, as well as UMR-106 osteoblast-like cells showed significantly more cytotoxicity of RMGICs, predominantly Vitrebond to both GICs and composite- Vit-l-ecence®.The lowest influence on cell's metabolism on UMR-106 osteoblas-like cells was shown by Ketac Silver and the lowest influence on cell's metabolism on NIH(3)T(3) mouse fibroblast cells was shown by Fuji IX GP Fast. Statistical evaluation of sensitivity of cell lines UMR-106 osteoblast-like cells and NIH(3)T(3) mouse fibroblast cells, using Mann-Whitney test, showed that NIH(3)T(3) mouse fibroblast cells were more sensitive for the evaluation of cytotoxicity of dental materials.

Large scale genetic association meta-analyses showed that neurocan (NCAN) gene polymorphism rs1064395 is susceptibility locus for bipolar disorder. These studies also included patients with bipolar disorder originated from Bosnia and Herzegovina. Followed by theory of shared genetic elements between bipolar disorder and schizophrenia susceptibility, other studies explored several genetic factors with schizophrenia vulnerability as well. In this work, authors investigated the association between previously confirmed bipolar disorder genetic risk factor- neurocan with schizophrenia in a population sample of Bosnia and Herzegovina. Ethical aspects of this research were assessed by Ethics Committee of Clinical Center University of Sarajevo. Blood samples for DNA extraction were taken from the total of 86 patients and healthy individuals who previously signed informed consent. Genotyping for rs 1064395 was done using direct sequencing method. A case-control analysis of common genetic polymorphism within neurocan gene and schizophrenia status in a consecutively sampled patient cohort have been done using Fisher-exact test with odds-ratio calculation. No statistically significant allele and genotype association with disease status was found (p>0.05). Our finding supports the fact that large-scale genetic association studies approach need to be employed when detecting the variants with small additive effect in phenotypes with complex ethiology.

Although the mechanism of Aβ action in the pathogenesis of Alzheimer’s disease (AD) has remained elusive, it is known to increase the expression of the antagonist of canonical wnt signalling, Dickkopf-1 (Dkk1), whereas the silencing of Dkk1 blocks Aβ neurotoxicity. We asked if clusterin, known to be regulated by wnt, is part of an Aβ/Dkk1 neurotoxic pathway. Knockdown of clusterin in primary neurons reduced Aβ toxicity and DKK1 upregulation and, conversely, Aβ increased intracellular clusterin and decreased clusterin protein secretion, resulting in the p53-dependent induction of DKK1. To further elucidate how the clusterin-dependent induction of Dkk1 by Aβ mediates neurotoxicity, we measured the effects of Aβ and Dkk1 protein on whole-genome expression in primary neurons, finding a common pathway suggestive of activation of wnt–planar cell polarity (PCP)–c-Jun N-terminal kinase (JNK) signalling leading to the induction of genes including EGR1 (early growth response-1), NAB2 (Ngfi-A-binding protein-2) and KLF10 (Krüppel-like factor-10) that, when individually silenced, protected against Aβ neurotoxicity and/or tau phosphorylation. Neuronal overexpression of Dkk1 in transgenic mice mimicked this Aβ-induced pathway and resulted in age-dependent increases in tau phosphorylation in hippocampus and cognitive impairment. Furthermore, we show that this Dkk1/wnt–PCP–JNK pathway is active in an Aβ-based mouse model of AD and in AD brain, but not in a tau-based mouse model or in frontotemporal dementia brain. Thus, we have identified a pathway whereby Aβ induces a clusterin/p53/Dkk1/wnt–PCP–JNK pathway, which drives the upregulation of several genes that mediate the development of AD-like neuropathologies, thereby providing new mechanistic insights into the action of Aβ in neurodegenerative diseases.

The major purpose of this paper is to present a way of solving problems through so-called visual planning and programming using object-oriented concepts. This paper describes the process of UML modeling for solving the traveling salesman problem using one of the metaheuristic-genetic algorithms. The analysis and problem solving in this way has many advantages just because it provides a clear definition of requirements and specific plan that we will later use to create specific applications. This is a good way to resolve because the UML describes the source code, models help to visualize the system as it is or what it should be and allow you to determine the structure and behavior of the system. Static and dynamic diagrams implemented in developing tools for modeling, as well as a description of specific applications and testing are mentioned. With this approach we describe modeling tool that can be used in the development of specific solutions and a way of establishing explicit links between concepts and execution code.