Secondary trisomy 1 q due to a reciprocal maternal translocation]

The authors report a case of partial trisomy 1 q due to a maternal balanced translocation : t(1 ; 4) (q 32 : p 16). The evocative malformations of trisomy 1 q and monosomy 4 p are discussed and compared to seven others from the literature. Then the interest of the chromosomical prenatal diagnosis and the significance of familial genetic studies are showed.     

Planktonic ecosystems. The effects of dystrophic conditions on structure and function in the gulf of fos

In the areas studied, an unusual structure and dynamic behavior was exhibited by the plankton ecosystems, due for the most part to industrial and natural effluents from the Rhǒne and Durance. The ecosystem was kept at a low state of maturity, which is characterized by frequent periods of intense multiplication by small species with high metabolic rates, such as the diatom, Skeletonema costatum, and the dinoflagellates, Exuviaella and Prorocentrum. Brackish water seems congenial to that type of proliferation. The turnover rate of these populations decreases as they become older and cell size increases. A lack of competition by species of the same genus is a characteristic of the photo-autotrophic organisms in these environments. Secondary production follows the same cycle as the primary production by the dinoflagellate population. Zooplankton species of the genus Acartia have periods of intensive development in these areas.     

Coding processes involved in the cortical representation of complex tactile stimuli

To understand how information is coded in the primary somatosensory cortex (S1) we need to decipher the relationship between neural activity and tactile stimuli. Such a relationship can be formally measured by mutual information. The present study was designed to determine how S1 neuronal populations code for the multidimensional kinetic features (i.e. random, time-varying patterns of force) of complex tactile stimuli, applied at different locations of the rat forepaw. More precisely, the stimulus localization and feature extraction were analyzed as two independent processes, using both rate coding and temporal coding strategies. To model the process of stimulus kinetic feature extraction, multidimensional stimuli were projected onto lower dimensional subspace and then clustered according to their similarity. Different combinations of stimuli clustering were applied to differentiate each stimulus identification process. Information analyses show that both processes are synergistic, this synergy is enhanced within the temporal coding framework. The stimulus localization process is faster than the stimulus feature extraction process. The latter provides more information quantity with rate coding strategy, whereas the localization process maximizes the mutual information within the temporal coding framework. Therefore, combining mutual information analysis with robust clustering of complex stimuli provides a framework to study neural coding mechanisms related to complex stimuli discrimination.     

Synthesis,characterization, and application of cy-dye- and alexa-dye-labeled hongotoxin(1) analogues. The first high affinity fluorescence probes for voltage-gated K+ channels

Hongotoxin(1) (HgTX(1)), a 39-residue peptide recently isolated from the venom of Centruroides limbatus, blocks the voltage-gated K+ channels K(v)1.1, K(v)1.2, and K(v)1.3 at picomolar toxin concentrations (Koschak, A., Bugianesi, R. M., Mitterdorfer, J., Kaczorowski, G. J., Garcia, M. L., and Knaus, H. G. (1998) J. Biol. Chem. 273, 2639-2644). In this report, we determine the three-dimensional structure of HgTX(1) using NMR spectroscopy (PDB-code: 1HLY). HgTX(1) was found to possess a structure similar to previously characterized K+ channel toxins (e.g. margatoxin) consisting of a three-stranded antiparallel beta-sheet (residues 2-4, 26-30, and 33-37) and a helical conformation (part 3(10) helix and part alpha helix; residues 10-20). Due to the importance of residue Lys-28 for high-affinity interaction with the respective channels, lysine-reactive fluorescence dyes cannot be used to label wild-type HgTX(1). On the basis of previous studies (see above) and our NMR data, a HgTX(1) mutant (HgTX(1)-A19C) was engineered, expressed, and purified. HgTX(1)-A19C-SH was labeled using sulfhydryl-reactive Cy3-, Cy5-, and Alexa-dyes. Pharmacological characterization of fluorescently labeled HgTX(1)-A19C in radioligand binding studies indicated that these hongotoxin(1) analogues retain high-affinity for voltage-gated K+ channels and a respective pharmacological profile. Cy3- and Alexa-dye-labeled hongotoxin(1) analogues were used to investigate the localization of K+ channels in brain sections. The distribution of toxin binding closely follows the distribution of K(v)1.2 immunoreactivity with the highest expression levels in the cerebellar Purkinje cell layer. Taken together, these results demonstrate that fluorescently labeled HgTX(1) analogues comprise novel probes to characterize a subset of voltage-gated K+ channels.     

MSCs—cells with many sides

The field of mesenchymal stromal cell (MSC) biology and clinical cellular therapy has grown exponentially over the last few decades. With discovery of multiple tissue specific sources of stromal cells, invariably being termed MSCs, and their increasing clinical application, there is a need to further delineate the true definition of a mesenchymal stromal cell and to recognise the inherit differences between cell sources; both their potential and limitations.In this review, we discuss the importance of considering every stromal cell source as an independent entity and the need to critically evaluate and appreciate the true phenotype of these cells and their safety when considering their use in novel cell therapies.     

Selection of fatty acid auxotrophs from the oleaginous yeast Cryptococcus curvatus and production of cocoa butter equivalents in batch culture

Summary A search was carried out for mutants, defective in the conversion of stearic acid to oleic acid in effort to improve the quality of lipids produced by Cryptococcus curvatus ATCC, 20509. Mutants were selected as unsaturated fatty acid (Ufa) auxotrophs. After treatment of parent organism with Ethyl methanesulfonate (EMS), 11 oleate-requiring auxotrophs were isolated. Only 3 of them were real unsaturated fatty acid (Ufa) mutants, while the other 8 were designated as fatty acid synthetase (Fas) mutants. The amount of saturated fatty acid (SFA) was about 65.2 % in the lipids extracted from an Ufa mutant named UfaM3 and it was significantly higher than that of the wild-type (WT) (46.6 %) and similar to that of cocoa butter (60.4 %).     

Astrocytic Gap Junctional Communication Decreases Neuronal Vulnerability to Oxidative Stress-Induced Disruption of Ca2+ Homeostasis and Cell Death

Abstract: We investigated the effect of uncoupling astrocytic gap junctions on neuronal vulnerability to oxidative injury in embryonic rat hippocampal cell cultures. Mixed cultures (neurons growing on an astrocyte monolayer) treated with 18-α-glycyrrhetinic acid (GA), an uncoupler of gap junctions, showed markedly enhanced generation of intracellular peroxides (2,7-dichlorofluorescein fluorescence), impairment of mitochondrial function [(dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction], and cell death (lactate dehydrogenase release) following exposure to oxidative insults (FeSO₄ and 4-hydroxynonenal). GA alone had little or no effect on basal levels of peroxides, mitochondrial function, or neuronal survival. Intercellular dye transfer analyses revealed extensive astrocyte-astrocyte coupling but no astrocyte-neuron or neuron-neuron coupling in the mixed cultures. Studies of pure astrocyte cultures and microscope analyses of neurons in mixed cultures showed that the increased oxidative stress and cell death in GA-treated cultures occurred only in neurons and not in astrocytes. Antioxidants (propyl gallate and glutathione) blocked the death of neurons exposed to FeSO₄/GA. Elevations of neuronal intracellular calcium levels ([Ca²⁺]_i) induced by FeSO₄ were enhanced in neurons in mixed cultures exposed to GA. Removal of extracellular Ca²⁺ and the L-type Ca²⁺ channel blocker nimodipine prevented impairment of mitochondrial function and cell death induced by FeSO₄ and GA, whereas glutamate receptor antagonists were ineffective. Finally, GA exacerbated kainate- and FeSO₄-induced injury to pyramidal neurons in organotypic hippocampal slice cultures. The data suggest that interastrocytic gap junctional communication decreases neuronal vulnerability to oxidative injury by a mechanism involving stabilization of cellular calcium homeostasis and dissipation of oxidative stress.