Spatial organization of detector neurons in the caudo-medial part of the frog tectum opticum

Investigation of the spatial organization of detector neurons of the frog tectum opticum showed that these neurons are mainly in the nuclear layers. When responding to a photic stimulus they form a mosaic of groups of synergically excited cells separated by inhibited or nonresponding neurons. Inhibited neurons are much more numerous than excited. Different photic stimuli (shaped or diffuse) evoke the appearance of mosaics of different structure; mosaics connected with different forms of detection are to a considerable degree stratified.Rostov State University. Research Institute of Neurocybernetics, Rostov-on-Don. Translated from Neirofiziologiya, Vol. 5, No. 5, pp. 468–475, September–October, 1973.     

Exploring the conformation of bilirubins with natural and unnatural analogues: use of positional and bridged isomers of bilirubin IXalpha.

Unlike bilirubin IXalpha (1), the isomers bilirubin IXdelta (2) and neobilirubin IXbeta (3) do not require conjugation with glucuronic acid in order to be excreted. A conformational analysis employing an optimized Monte Carlo method and a mixed Monte Carlo stochastic dynamics reveals that isomer 2 exhibits a structure more closed than the well known 'ridge-tile' conformation of 1. The change in the position of both propionic acid chains causes the loss of at least four hydrogen bonds. On the other hand, the change in the configuration of the distal dipyrrinone and the blockage of the lactamic nitrogen by the presence of a bridge in isomer 3 results in an open and more elongated structure, where the chance of hydrogen bond formation in this region is obliterated. The resulting molecular models for these compounds are consistent with 1H NM R, UV-vis, and TLC data.     

根施甜菜碱对镍胁迫下小麦幼苗生长生理的影响

以普通小麦品种‘轮选988’为材料,采用溶液培养法,研究了根施不同浓度甜菜碱(1.0、2.0、3.0、4.0、5.0、10.0、15.0、20.0mmol·L~(-1))对镍(100μmol·L~(-1) NiSO_4)胁迫下小麦根系生长的影响,以及4.0mmol·L~(-1)甜菜碱处理镍胁迫幼苗根系相关抗逆生理生化指标的变化。结果表明:(1)与不施加镍对照相比,镍胁迫下小麦幼苗的根长、株高、鲜重和干重分别显著降低了14.7%、11.7%、15.0%和16.7%。(2)与单独镍胁迫处理相比,小麦幼苗的根长、株高、鲜重和干重均随着根施甜菜碱的浓度逐渐增加且呈先升后降的趋势,并以4.0mmol·L~(-1)外源甜菜碱处理效果较佳。(3)与单独镍胁迫处理相比较,在4.0mmol·L~(-1)外源甜菜碱处理下,小麦幼苗根系超氧化物歧化酶(SOD)、过氧化物酶(POD)、过氧化氢酶(CAT)和抗坏血酸过氧化物酶(APX)活性分别升高了284.7%、40.3%、82.9%和20.4%,超氧阴离子自由基(O-·2)含量、过氧化氢(H_2O_2)含量和丙二醛(MDA)含量分别显著降低了50.6%、38.4%和40.6%,可溶性糖含量及游离脯氨酸(Pro)含量分别显著降低了19.2%、45.4%,而根系活力大幅上升了358.0%。研究认为,根施适宜浓度外源甜菜碱可显著增强小麦幼苗根系的抗氧化能力,恢复根系活力,从而有效减弱镍胁迫对小麦幼苗生长的伤害。     

Surface N balances and reactive N loss to the environment from global intensive agricultural production systems for the period 1970-2030

Data for the historical years 1970 and 1995 and the FAO-Agriculture Towards 2030 projection are used to calculate N inputs (N fertilizer, animal manure, biological N fixation and atmospheric deposition) and the N export from the field in harvested crops and grass and grass consumption by grazing animals. In most industrialized countries we see a gradual increase of the overall N recovery of the intensive agricultural production systems over the whole 1970-2030 period. In contrast, low N input systems in many developing countries sustained low crop yields for many years but at the cost of soil fertility by depleting soil nutrient pools. In most developing countries the N recovery will increase in the coming decades by increasing efficiencies of N use in both crop and livestock production systems. The surface balance surplus of N is lost from the agricultural system via different pathways, including NH3 volatilization, denitrification, N2O and NO emissions, and nitrate leaching from the root zone. Global NH3-N emissions from fertilizer and animal manure application and stored manure increased from 18 to 34 Tg·yr-1 between 1970 and 1995, and will further increase to 44 Tg·yr-1 in 2030. Similar developments are seen for N2O-N (2.0 Tg·yr-1 in 1970, 2.7 Tg·yr-1 in 1995 and 3.5 Tg·yr-1 in 2030) and NO-N emissions (1.1 Tg·yr-1 in 1970, 1.5Tg·yr-1 in 1995 and 2.0 Tg·yr-1 in 2030).     

Climate and prevalence of atopic eczema in 6- to 7-year-old school children in Spain. ISAAC PhASE III

Atopic eczema (AE) is a chronic skin disease. Recent reports indicate that the worldwide prevalence of AE is increasing and that various environmental factors are implicated in its aetiology. Climatic conditions have been related with AE prevalence, and Spain has varying climatic conditions. The aim of this study is to document the possible climatic influence on the prevalence of AE in schoolchildren aged 6–7 years in three different climatic regions in Spain. We conducted a cross-sectional population-based survey of 28,394 schoolchildren aged 6–7 years from 10 Spanish centres in three different climatic regions. The mean participation rate was 76.5%. AE prevalence was assessed using the International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire and the Spanish Academy of Dermatology criteria used in Spain to diagnose AE. The data, including annual temperature, precipitation, relative humidity and the annual number of sunny hours per climatic region, were obtained from the Spanish National Institute of Meteorology. Different AE prevalences were found in all three climatic regions studied: Atlantic, 32.9; Mediterranean 28.3; and Continental 31.2 per 100 children studied (p < 0.005). AE was positively associated with precipitation and humidity, and was negatively associated with temperature and the number of sunny hours. The results show that AE is significantly dependent on meteorological conditions.     

Lectinomics II. A highway to biomedical/clinical diagnostics

The review assesses current status and attempts to forecast trends in the development of lectin biorecognition technology. The progressive trend is characterized scientometrically and reflects the current transient situation, when standard low-throughput lectin-based techniques are being replaced by a novel microarray-based techniques offering high-throughput of detection. The technology is still in its infancy (validation phase), but already shows promise as an efficient tool to decipher the enormous complexity of the glycocode that influences physiological status of the cell. Further enhancement in robustness and flexibility of lectin microarrays is predicted by using recombinant and artificial lectins that will render production of lectin microarrays cost-effective and more affordable. Mass spectrometry is expected to play an important role to characterize the binding profile of new lectins. Differences in glycan recognition by lectins and anti-carbohydrate antibodies are given on a molecular basis, and strong and weak points of both biorecognition molecules in diagnosis are briefly discussed.     

Isocitrate dehydrogenase 1 R132C mutation occurs exclusively in microsatellite stable colorectal cancers with the CpG island methylator phenotype

The CpG Island Methylator Phenotype (CIMP) is fundamental to an important subset of colorectal cancer; however, its cause is unknown. CIMP is associated with microsatellite instability but is also found in BRAF mutant microsatellite stable cancers that are associated with poor prognosis. The isocitrate dehydrogenase 1 (IDH1) gene causes CIMP in glioma due to an activating mutation that produces the 2-hydroxyglutarate oncometabolite. We therefore examined IDH1 alteration as a potential cause of CIMP in colorectal cancer. The IDH1 mutational hotspot was screened in 86 CIMP-positive and 80 CIMP-negative cancers. The entire coding sequence was examined in 81 CIMP-positive colorectal cancers. Forty-seven cancers varying by CIMP-status and IDH1 mutation status were examined using Illumina 450K DNA methylation microarrays. The R132C IDH1 mutation was detected in 4/166 cancers. All IDH1 mutations were in CIMP cancers that were BRAF mutant and microsatellite stable (4/45, 8.9%). Unsupervised hierarchical cluster analysis identified an IDH1 mutation-like methylation signature in approximately half of the CIMP-positive cancers. IDH1 mutation appears to cause CIMP in a small proportion of BRAF mutant, microsatellite stable colorectal cancers. This study provides a precedent that a single gene mutation may cause CIMP in colorectal cancer, and that this will be associated with a specific epigenetic signature and clinicopathological features.