Structures of ethylenediaminetetraacetato (3-) metal complexes. I complexes with Co, Mg and Cd metals

(I): Hexaaquacobalt(II) aqua[ethylenediaminetetraacetato(3-)]cobaltate(II) dihydrate, [Co(H2O)6][Co(C10H13N2O8)(H2O)]2.2H2O (Ibis): Hexaaquamagnesium(II) aqua[ethylenediaminetetraacetato(3-)]magnesiate(II) dihydrate, [Mg(H2O)6][Mg(C10H13N2O8)(H2O)]2.2H2O (II):Tetraaquabis{aqua[ethylenediaminetetraacetato(3-)]cadmium(II)-O-O'}Cadmium(II) tetrahydrate

Structures of ethylenediaminetetraacetato (3-) metal complexes. I complexes with Co, Mg and Cd metals

(I): Hexaaquacobalt(II) aqua[ethylenediaminetetraacetato(3-)]cobaltate(II) dihydrate, [Co(H2O)6][Co(C10H13N2O8)(H2O)]2.2H2O (Ibis): Hexaaquamagnesium(II) aqua[ethylenediaminetetraacetato(3-)]magnesiate(II) dihydrate, [Mg(H2O)6][Mg(C10H13N2O8)(H2O)]2.2H2O (II):Tetraaquabis{aqua[ethylenediaminetetraacetato(3-)]cadmium(II)-O-O'}Cadmium(II) tetrahydrate

Structures of ethylenediaminetetraacetato (3-) metal complexes. I complexes with Co, Mg and Cd metals

(I): Hexaaquacobalt(II) aqua[ethylenediaminetetraacetato(3-)]cobaltate(II) dihydrate, [Co(H2O)6][Co(C10H13N2O8)(H2O)]2.2H2O (Ibis): Hexaaquamagnesium(II) aqua[ethylenediaminetetraacetato(3-)]magnesiate(II) dihydrate, [Mg(H2O)6][Mg(C10H13N2O8)(H2O)]2.2H2O (II):Tetraaquabis{aqua[ethylenediaminetetraacetato(3-)]cadmium(II)-O-O'}Cadmium(II) tetrahydrate

Targeting microglial KATP channels to treat neurodegenerative diseases: a mitochondrial issue

Neurodegeneration is a complex process involving different cell types and neurotransmitters. A common characteristic of neurodegenerative disorders is the occurrence of a neuroinflammatory reaction in which cellular processes involving glial cells, mainly microglia and astrocytes, are activated in response to neuronal death. Microglia do not constitute a unique cell population but rather present a range of phenotypes closely related to the evolution of neurodegeneration. In a dynamic equilibrium with the lesion microenvironment, microglia phenotypes cover from a proinflammatory activation state to a neurotrophic one directly involved in cell repair and extracellular matrix remodeling. At each moment, the microglial phenotype is likely to depend on the diversity of signals from the environment and of its response capacity. As a consequence, microglia present a high energy demand, for which the mitochondria activity determines the microglia participation in the neurodegenerative process. As such, modulation of microglia activity by controlling microglia mitochondrial activity constitutes an innovative approach to interfere in the neurodegenerative process. In this review, we discuss the mitochondrial KATP channel as a new target to control microglia activity, avoid its toxic phenotype, and facilitate a positive disease outcome.

Targeting microglial KATP channels to treat neurodegenerative diseases: a mitochondrial issue

Neurodegeneration is a complex process involving different cell types and neurotransmitters. A common characteristic of neurodegenerative disorders is the occurrence of a neuroinflammatory reaction in which cellular processes involving glial cells, mainly microglia and astrocytes, are activated in response to neuronal death. Microglia do not constitute a unique cell population but rather present a range of phenotypes closely related to the evolution of neurodegeneration. In a dynamic equilibrium with the lesion microenvironment, microglia phenotypes cover from a proinflammatory activation state to a neurotrophic one directly involved in cell repair and extracellular matrix remodeling. At each moment, the microglial phenotype is likely to depend on the diversity of signals from the environment and of its response capacity. As a consequence, microglia present a high energy demand, for which the mitochondria activity determines the microglia participation in the neurodegenerative process. As such, modulation of microglia activity by controlling microglia mitochondrial activity constitutes an innovative approach to interfere in the neurodegenerative process. In this review, we discuss the mitochondrial KATP channel as a new target to control microglia activity, avoid its toxic phenotype, and facilitate a positive disease outcome.

Structure and function of RecA-DNA complexes.

While the E. coli RecA protein has been the most intensively studied enzyme of homologous recombination, the unusual RecA-DNA filament has stood alone until very recently. It now appears that this protein is part of a universal family that spans all of biology, and the filament that is formed by the protein on DNA is a universal structure. With RecA's role in recombination given new and greatly increased significance, we focus in this review on the energetics of the RecA-mediated strand exchange and the relation between the energetics and recombination spanning heterologous inserts.

Evolutionary and dispersal history of Eurasian house mice Mus musculus clarified by more extensive geographic sampling of mitochondrial DNA.

We examined the sequence variation of mitochondrial DNA control region and cytochrome b gene of the house mouse (Mus musculus sensu lato) drawn from ca. 200 localities, with 286 new samples drawn primarily from previously unsampled portions of their Eurasian distribution and with the objective of further clarifying evolutionary episodes of this species before and after the onset of human-mediated long-distance dispersals. Phylogenetic analysis of the expanded data detected five equally distinct clades, with geographic ranges of northern Eurasia (musculus, MUS), India and Southeast Asia (castaneus, CAS), Nepal (unspecified, NEP), western Europe (domesticus, DOM) and Yemen (gentilulus). Our results confirm previous suggestions of Southwestern Asia as the likely place of origin of M. musculus and the region of Iran, Afghanistan, Pakistan, and northern India, specifically as the ancestral homeland of CAS. The divergence of the subspecies lineages and of internal sublineage differentiation within CAS were estimated to be 0.37-0.47 and 0.14-0.23 million years ago (mya), respectively, assuming a split of M. musculus and Mus spretus at 1.7 mya. Of the four CAS sublineages detected, only one extends to eastern parts of India, Southeast Asia, Indonesia, Philippines, South China, Northeast China, Primorye, Sakhalin and Japan, implying a dramatic range expansion of CAS out of its homeland during an evolutionary short time, perhaps associated with the spread of agricultural practices. Multiple and non-coincident eastward dispersal events of MUS sublineages to distant geographic areas, such as northern China, Russia and Korea, are inferred, with the possibility of several different routes.

Caspase-2 activation in the absence of PIDDosome formation.

PIDD (p53-induced protein with a death domain [DD]), together with the bipartite adapter protein RAIDD (receptor-interacting protein-associated ICH-1/CED-3 homologous protein with a DD), is implicated in the activation of pro-caspase-2 in a high molecular weight complex called the PIDDosome during apoptosis induction after DNA damage. To investigate the role of PIDD in cell death initiation, we generated PIDD-deficient mice. Processing of caspase-2 is readily detected in the absence of PIDDosome formation in primary lymphocytes. Although caspase-2 processing is delayed in simian virus 40-immortalized pidd(-/-) mouse embryonic fibroblasts, it still depends on loss of mitochondrial integrity and effector caspase activation. Consistently, apoptosis occurs normally in all cell types analyzed, suggesting alternative biological roles for caspase-2 after DNA damage. Because loss of either PIDD or its adapter molecule RAIDD did not affect subcellular localization, nuclear translocation, or caspase-2 activation in high molecular weight complexes, we suggest that at least one alternative PIDDosome-independent mechanism of caspase-2 activation exists in mammals in response to DNA damage.

No longitudinal mitochondrial DNA sequence changes in HIV-infected individuals with and without lipoatrophy.

The potential for mitochondrial (mt) DNA mutation accumulation during antiretroviral therapy (ART), and preferential accumulation in patients with lipoatrophy compared with control participants, remains controversial. We sequenced the entire mitochondrial genome, both before ART and after ART exposure, in 29 human immunodeficiency virus (HIV)-infected Swiss HIV Cohort Study participants initiating a first-line thymidine analogue-containing ART regimen. No accumulation of mtDNA mutations or deletions was detected in 13 participants who developed lipoatrophy or in 16 control participants after significant and comparable ART exposure (median duration, 3.3 and 3.7 years, respectively). In HIV-infected persons, the development of lipoatrophy is unlikely to be associated with accumulation of mtDNA mutations detectable in peripheral blood.

Oligonucleotide-polyethylenimine complexes targeting retinal cells: structural analysis and application to anti-TGFbeta-2 therapy.

PURPOSE: The aim of this study was to characterize oligonucleotide-polyethylenimine (ODN/PEI) complex preparation for potential transfection of retinal cells in vitro and in vivo. METHODS: The effect of medium preparation [HEPES-buffered saline (HBS), water] on particle size and morphology was evaluated. Cultured Lewis rat retinal Müller glial (RMG) cells were transfected using fluorescein isothiocyanate (FITC)-ODN/PEI complexes specifically directed at transforming growth factor beta (TGFbeta)-2. Efficacy of transfection was evaluated using confocal microscopy, and regulation of gene expression was assayed using quantitative real-time RT-PCR and ELISA assay. One, 24, and 72 h after injection of FITC-ODN/PEI complexes into the vitreous of rat eyes, their distribution was analyzed on eye sections. RESULTS: Complexes prepared in HBS were smaller than complexes prepared in pure water and presented a core-shell structure. These particles showed a high cellular internalization efficacy, along with a significant and specific down-regulation of TGFbeta-2 expression and production in RMG cells, correlating with specific inhibition of cell growth at 72 h. In vivo, complexes efficiently transfect retinal cells and follow a transretinal migration at 24 h. After 72 h, ODN seems to preferentially target RMG cells without inducing any detectable toxicity. CONCLUSIONS: Specific down-regulation of TGFbeta-2 expression using ODN/PEI complexes may have potential interest for the treatment of retinal diseases associated with glial proliferation.

Migration of dissolved organic carbon in biochars and biochar-mineral complexes

The objective of this work was to determine the contribution of dissolved organic carbon (DOC) from a biochar mineral complex (BMC), so as to better understand the interactions between DOC, biochar, clay, and minerals during thermal treatment, and the effects of BMC on amended soils. The BMC was prepared by heating a mixture of a H3PO4-treated saligna biochar from Acacia saligna, clays, other minerals, and chicken manure. The BMC was applied to a sandy loam soil in Western Australia, where wheat was grown. Liquid chromatography-organic carbon detection (LC-OCD) tests were carried out on water extracts from the untreated biochar, the BMC, the BMC-amended soil, and on a control soil to measure the DOC concentration. LC-OCD tests provide a fingerprint of the DOC, which allows the fractions of DOC to be determined. Thermal processing enhanced the reaction of the A. saligna biochar with manure, clays and minerals, and affected the distribution of the DOC fractions. Notably, the process leads to immobilization of hydrophobic DOC and to an increase in the concentration of low-molecular-weight neutrals in the BMC. The application of the BMC to soil increases the DOC in the amended soil, especially the biopolymer fraction.

Anthracene-tethered ruthenium(II) arene complexes as tools to visualize the cellular localization of putative organometallic anticancer compounds.

Anthracene derivatives of ruthenium(II) arene compounds with 1,3,5-triaza-7-phosphatricyclo[3.3.1.1]decane (pta) or a sugar phosphite ligand, viz., 3,5,6-bicyclophosphite-1,2-O-isopropylidene-α-d-glucofuranoside, were prepared in order to evaluate their anticancer properties compared to the parent compounds and to use them as models for intracellular visualization by fluorescence microscopy. Similar IC(50) values were obtained in cell proliferation assays, and similar levels of uptake and accumulation were also established. The X-ray structure of [{Ru(η(6)-C(6)H(5)CH(2)NHCO-anthracene)Cl(2)(pta)] is also reported.

Mitochondrial control region and microsatellite data show low genetic variability in reared senegalese sole, Solea senegalensis. Preliminary data

Peer reviewed