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We have studied differences in the number of Drosophila pseudoobscura produced in a culture when the flies differ with respect to two alleles (F and S) at the Mdh-2 locus, which codes for a malate dehydrogenase enzyme. The studies were done at low and at high density in two- and three-genotype combinations (S/S, F/F and S/F), with one-genotype cultures as controls.--Density affects the fitness of the Mdh-2 genotypes. Different genotypes are differently affected, and the genotype of the competitors also makes a difference on the fitness of a given genotype. When three genotypes are present in a culture, particularly at high density, intergenotypic competition is less intense than intragenotypic competition at several frequency combinations. That is, there is "overcompensation": the three genotypes together exploit the environmental resources better than one genotype alone.--The fitness of the genotypes is frequency dependent in both two-genotype and three-genotype combinations. An inverse relationship between frequency and fitness is observed at high density. This may lead to a stable polymorphism, because the fitness of a genotype increases as its frequency decreases.--Forty independent strains, sampled from a natural population, were used in the experiments. This ensures that more than 95% of the variation present in the genome in the natural population is also present in the experimental cultures. It also ensures that the genetic background on the Mdh-2 alleles is randomized in the same way as it is in nature. However, the possibility remains that Mdh-2 alleles in nature are nonrandomly associated with alleles at closely linked loci. If linkage disequilibrium is present in the experiments because it exists in nature, then the observed effects (such as frequency-dependent selection) would affect the Mdh-2 locus in nature as well.

The phase evolution in a calcium phosphate glass with the molar ratio [CaO]/[P2O5] < 1, to which 6.4 mol% TiO2 and 10 mol% Al2O3 were added as nucleation agents, was studied. The results indicate that the primary phase β-Ca2P2O7 is formed during surface nucleation and crystallization which are dominant at T < 930°C. No presence of metastable calcium phosphates was registered during the formation of the primary phase. The growth of β-Ca2P2O7 crystals occurs on the faceted crystal/glass interface with dendritic morphology at a crystal growth rate that is independent of time. The kinetics of β-Ca2P2O7 crystal growth are characterised by a growth activation energy of Ea = 426 ± 15 kJ/mol. The parameters of the unit cell of the β-Ca2P2O7 phase decrease with increasing temperature. The secondary TiP2O7 and AlPO4 phases are formed by volume nucleation and crystallization. The temperature of the maximum nucleation rate was determined to be Tn = 690°C, and it is higher than the transformation temperature Tg. In the temperature interval T < 930°C secondary phases appear during long annealing times. At T > 930°C glass volume crystallization is dominant. [ABSTRACT FROM AUTHOR]

During the latest outbreak of the gypsy moth in Serbia (2009-2014), some areas of Central Serbia were particularly endangered, and one of them was Krusevac region, where the forests give way to orchards in the pattern resembling the tiger's skin. Since the number of the laid egg masses in the autumn 2013 guaranteed the defoliation of both forest tree species and agricultural crops, and the presence of E. maimaigo, in Central Serbia had already been determined, at 30 selected plots the assisted spread of it was performed, through the introduction of the infectious inoculum in the beech and oak forests which border the orchards. Since there was dealt with the living organism--fungus, which is particularly susceptible to the weather conditions (temperature and air humidity, as well as the precipitation), and under the conditions of the global warming and great drought, the special recipe for the preparation of inoculum was made. In the following year the mass epizootic of the gypsy moth caterpillars, of the younger instars (L2 and L3), occurred, which implies that E. maimaiga caused the crash of the outbreak of this most harmful species of the defoliating insects of the forests and orchards.

Introduction: Occlusive vascular diseases take the first places on lists of diseases in general population today. In spite of this, all risk factors which contribute to development of these diseases are not yet known. Recent studies have shown that homocysteine plays a critical role in it and is established as a new risk factor. WHAT IS HOMOCYSTEINE?: Homocysteine is a sulfur containing amino acid formed in the metabolism of methionine. Reference values of homocysteine in circulation and different forms in plasma are described. HYPERHOMOCYSTEINEMIA--A RISK FACTOR: Homocysteine was associated with atherosclerosis and occlusive vascular disease in 1960s for the first time. Since then, many studies--prospective and retrospective, have confirmed the role of hyperhomocysteinemia as a risk factor in 42% of patients with cerebrovascular disease, 28% with peripheral vascular and 30% with coronary artery disease. The Physician's Health Study, a prospective study in which 15,000 male physicians took part, revealed that increase in homocysteine concentration of 1.7 mumol/l above normal values was associated by threefold higher risk for myocardial infarction. The risk for carotid artery stenosis also increases with elevation of homocysteine concentration. Hyperhomocysteinemia is associated with poor prognosis in patients with angiographically established coronary disease. Stroke, venous thromboembolism, and atherosclerosis in chronic renal failure are some of the complications of hyperhomocysteinemia., Causes of Hyperhomocysteinemia: Hyperhomocysteinemia has numerous genetic and nongenetic etiologic factors. Cystathionine synthase deficiency, methylenetetrahydrofolate reductase deficiency and defects in the synthesis of cobalamin cofactors are genetically determined. Nutritional factors such as B12, folate or B6 vitamin deficiency, cofactors in homocysteine metabolism, lead to hyperhomocysteinemia., Mechanisms of Homocysteine Action: Atherogenic propensity of homocysteine is related to endothelial dysfunction, blood thrombocyte aggregation changes in factors of coagulation. Oxidative stress is involved, but the exact mechanism is still unknown., Conclusion: Hyperhomocysteinemia is established as an important risk factor for occlusive vascular diseases. Reduction in homocysteine concentration can be achieved by supplementation of B-group vitamins, cofactors in homocysteione metabolism. Is it going to be effective in reducing cardiovascular risks remains to be seen.

Introduction: Homocystinuria is a rare, congenital, autosomal-recessive, metabolic disease biochemically characterized by homocysteinemia and homocystinuria and by multi-system clinical disorders. It is a biochemical abnormality of methionine metabolism caused either by transulfuration pathway disorders or by disorders of homocysteine remethilation into methionine and as such it can be a result of numerous specific and different genetic lesions., Case Report: Homocystinuria is most commonly caused by deficiency of cystationine beta synthetase enzyme which catalyses the synthesis of cystathionine from homocysteine and serine in the methinione pathway. This results in accumulation of homocysteine and methionine in plasma and leads to excretion of excessive urinary homocysteine. Depending on specific property of the mutant enzyme molecule some patients respond to very high doses of pyridoxine with decreases of methionine and homocystine and some not. Pyridoxine responsiveness is based on the presence of small residual activity of cystathionine beta synthetase which is not present in nonresponsive patients. Homocystinuria due to cystathionine beta-synthase (CBS) deficiency is characterized by numerous different clinical abnormalities, but changes in four organ systems are dominant (eye, skeletal, central nervous and vascular system)., Case Description: Six years ago a six year-old boy was admitted to the hospital with vision problems. Ophthalmologic examination revealed a lens dislocation and because of many stigmates the child was sent to endocrinologist. The child had a marfanoid stature, with pectus carinatum and genu valgum, ataxic gait with motoric discoordination, muscle tone which ranged from hypotonia to hypertonia of extrapvramidal type and low intellectual abilities. A simple cyanide-nitroprusside test of patient's urine was positive suggesting homocystinuria. The diagnosis was established after plasma and urine amino acid analysis by HPLC. Concentration of homocystine and methionine were 52 mumol/l and 57 mumol/l in plasma and 249 mumol/du and 55 mumol/du in urine, respectively. After four months of treatment with pyridoxine there were not any significant changes in plasma homocysteine and methionine, but at the same time decrease in urine of these two amino acids were more than 2.5 times higher. This confirms that the patient has a pyridoxine-responsive type of homocystinuria and the dose was increased to 60 mg/day and 600 mg/day. This results in further decline of homocysteine and methionine in plasma and urine which persists up to now (for six years).

Myelin basic protein (MBP) is a major myelin constituent produced by oligodendrocytes in the central nervous system (CNS). Expression of MBP was considered to be a marker for oligodendrocyte differentiation and myelination in the developing CNS. In this study, expression of myelin basic protein (MBP) and its messenger RNA (mRNA) was examined in human embryos and fetuses ranging in age from 5 to 20 gestational weeks (g.w.). We were able to demonstrate that MBP antibody labels cells in both human nervous and non-nervous tissues beginning from early embryonic life (5-6 g.w.). MBP positive (MBP+) cells were rounded, with either no cell processes or only 1-2 short processes, and were located in caudal regions of the CNS. MBP+ cells were also observed in the non-nervous tissue, such as leptomeninges, choroid plexus, and connective tissues. A number of MBP+ cells in nervous and non-nervous tissues were morphologically similar to macrophages and showed a positive reaction to macrophage-microglia markers: lectin (RCA-1) and the monoclonal antibody (EBM-11) to human macrophage antigen CD68, whereas they were negative for neuronal, astroglial, or marker for oligodendrocyte progenitors. At the same embryonic age, 5 g.w. and onward, the MBP mRNA was observed in the CNS by in situ hybridization. The results of this study show that MBP immune reaction is spread in a large area of the CNS prior to myelin appearance. In addition, for the first time it has been demonstrated that the same population of cells could be labelled with both MBP and macrophage markers. These results indicate that MBP, or MBP-related proteins, could represent a link between the immune and nervous system during early development. Thus, besides the well established role in myelination, these proteins might have an additional and still unknown function in development.

Homocystinuria is a rare autosomal recessive disease characterized by homocystinuria and multisystemic clinical disorders. The term denotes a biochemical abnormality of methionine metabolism caused both by transsulfuration pathway disorders and remethylation of homocysteine into methionine, and as such it can be a result of numerous specific and different genetic lesions. Homocystinuria is most commonly caused by deficiency of cystathionine beta-synthase (CBS) activity (EC 4.2.1.22). In this lesion, depending on specific characteristics of mutant enzyme molecules, in regard to existence of residual activity, responsive and nonresponsive homocystinuria can be differed regarding clinical response to high doses of pyridoxine. Although there are numerous different clinical abnormalities, changes on four organ systems are dominant. The most common symptoms of homocystinuria include lens dislocation, vascular disorders, skeletal abnormalities and mental retardation. Laboratory findings are the first diagnostic procedure, while determination of enzymatic activity is a direct parameter for making diagnosis. Prenatal diagnosis and early detection are extremely important for the course and prognosis of the disease as they enable application of currently available therapy as soon as possible. The presently available therapy can, only in such cases, prevent occurrence of serious clinical symptoms, prevent their advancement to some extent or improve reversible clinical manifestations.