Slow relaxation of the magnetization in high-nuclearity Ln-complexes

By the surface modification strategy, a novel high-nuclearity lanthanide complex with a discrete structure, Er₂₆I(μ₃-OH)₂₀(μ₃-O)₆(NO₃)₉(IN)₃₃(OH)₃(H₂O)₃₃ (noted Er₂₆, HIN = isonicotinic acid), has been prepared under hydrothermal conditions. The magnetic properties of Er₂₆ and two analogue dysprosium assemblies Dy₃₀I(μ₃-OH)₂₄(μ₃-O)₆(NO₃)₉(IN)₄₁(OH)₃(H₂O)₃₈ (noted Dy₂₆-I) and Dy₂₆I(μ₃-OH)₂₀(μ₃-O)₆(NO₃)₉(IN)_31.25(OH)_4.75(H₂O)_41.75 (noted Dy₂₆-II) have been studied. The results show that the slow relaxation of the magnetization is newly found in Dy₂₆-I constructed from {Dy₂₆} and {Dy₄} cluster units. The {Dy₄} units in Dy₂₆-I, the relative orientation of the complex or the inter-molecular interactions between {Dy₂₆} cores might play an important role in the origin of this magnetic behavior.     

Phage response to CRISPR-encoded resistance in Streptococcus thermophilus

Clustered regularly interspaced short palindromic repeats (CRISPR) and their associated genes are linked to a mechanism of acquired resistance against bacteriophages. Bacteria can integrate short stretches of phage-derived sequences (spacers) within CRISPR loci to become phage resistant. In this study, we further characterized the efficiency of CRISPR1 as a phage resistance mechanism in Streptococcus thermophilus. First, we show that CRISPR1 is distinct from previously known phage defense systems and is effective against the two main groups of S. thermophilus phages. Analyses of 30 bacteriophage-insensitive mutants of S. thermophilus indicate that the addition of one new spacer in CRISPR1 is the most frequent outcome of a phage challenge and that the iterative addition of spacers increases the overall phage resistance of the host. The added new spacers have a size of between 29 to 31 nucleotides, with 30 being by far the most frequent. Comparative analysis of 39 newly acquired spacers with the complete genomic sequences of the wild-type phages 2972, 858, and DT1 demonstrated that the newly added spacer must be identical to a region (named proto-spacer) in the phage genome to confer a phage resistance phenotype. Moreover, we found a CRISPR1-specific sequence (NNAGAAW) located downstream of the proto-spacer region that is important for the phage resistance phenotype. Finally, we show through the analyses of 20 mutant phages that virulent phages are rapidly evolving through single nucleotide mutations as well as deletions, in response to CRISPR1.     

Identification of a rosette-like agent as Sphaerothecum destruens, a multi-host fish pathogen

A recent threat to European fish diversity was attributed to an infectious pathogen, a rosette-like intracellular parasite carried by invasive cyprinids. Here we show that the emerging rosette-like agent is Sphaerothecum destruens, originally found to be responsible for disease outbreaks in salmon in the United States. Sequencing of the ribosomal internal transcribed spacer (ITS) DNA highlights some level of geographical isolation. Unlike the situation in the United States, its occurrence in invasive fishes presents a risk of spread from wild invasive populations to sympatric populations of susceptible native fish and as such represents a risk for fisheries, as movement of fish for stocking purposes is common practice.     

Human APOBEC1 cytidine deaminase edits HBV DNA

David D. Derse, Ph.D., Head of the Retrovirus Gene Expression Section in the HIV Drug Resistance Program at the National Cancer Institute-Frederick (NCI-Frederick), passed away on October 9, 2009, a scant six weeks after being diagnosed with liver cancer. It was with great sadness that family, friends, and colleagues gathered together for his memorial service on Saturday, October 17, 2009, at the Middletown United Methodist Church in Maryland. As a NCI scientist since 1986, Dave studied the molecular mechanisms of infection and replication of a number of different types of retroviruses. Dave became an internationally known expert on human T cell lymphotrophic viruses type 1 and 2 (HTLV-1 and HTLV-2) and served on the editorial boards of Virology and Retrovirology. His most recent studies focused on the mechanisms of HTLV-1 virion morphogenesis, transmission, and replication.     

Genetic Editing of HBV DNA by Monodomain Human APOBEC3 Cytidine Deaminases and the Recombinant Nature of APOBEC3G

Hepatitis B virus (HBV) DNA is vulnerable to editing by human cytidine deaminases of the APOBEC3 (A3A-H) family albeit to much lower levels than HIV cDNA. We have analyzed and compared HBV editing by all seven enzymes in a quail cell line that does not produce any endogenous DNA cytidine deaminase activity. Using 3DPCR it was possible to show that all but A3DE were able to deaminate HBV DNA at levels from 10⁻² to 10⁻⁵ in vitro, with A3A proving to be the most efficient editor. The amino terminal domain of A3G alone was completely devoid of deaminase activity to within the sensitivity of 3DPCR (∼10⁻⁴ to 10⁻⁵). Detailed analysis of the dinucleotide editing context showed that only A3G and A3H have strong preferences, notably CpC and TpC. A phylogenic analysis of A3 exons revealed that A3G is in fact a chimera with the first two exons being derived from the A3F gene. This might allow co-expression of the two genes that are able to restrict HIV-1Δvif efficiently.     

Immobilisation of DNA to polymerised SU-8 photoresist

SU-8 is an epoxy-based photosensitive resist, which is currently used for a large variety of MEMS and lab-on-a-chip applications. Here, we demonstrate a one-step process to functionalize SU-8 with DNA probes. The immobilisation procedure relies on direct coupling of DNA to SU-8 and resulted in surfaces with functional capture probe densities of approximately 10 fmol/mm(2) as determined by hybridisation assays with fluorescent labelled target molecules. A comparable density of functional capture probes was measured on commercial aldehyde coated glass. DNA probes did not decrease in hybridisation performance after 10 min incubation in water at 98 degrees C prior to hybridisation, indicating a covalent bond between DNA and SU-8. Finally, DNA microarrays of high quality were obtained on SU-8 by contact printing of probe solution directly on SU-8 demonstrating a simple method for the implementation of microarrays in microsystems.     

Tooth Enamel Microstructure of Living and Extinct Hyracoids Reveals Unique Enamel Types Among Mammals

Among medium- to large-sized terrestrial ‘ungulates,’ there is often a relationship between increasing body size, correlated changes in diet, and increased complexity of the enamel microstructures [notably the development of Hunter-Schreger bands (HSB)]. An exhaustive survey of the enamel microstructures of living and extinct Hyracoidea demonstrates, however, that the Schmelzmuster within this order of mammals is generally one-layered and formed by radial enamel despite a large range of body sizes and dietary adaptations; HSB are remarkably absent. Radial enamel is characteristic of early diverging hyracoids, as well as more derived members of the extinct families Geniohyidae and Pliohyracidae, and the extant Procaviidae. Only some large ‘Saghatheriidae,’ and all members of the family Titanohyracidae, developed a more complex enamel microstructure (i.e., with prisms decussating), a unique condition among Mammalia that we name ‘bundled enamel’ (BE). This structure is reminiscent to some degree of both the ‘Pyrotherium enamel’ and the ‘3D enamel’ of proboscideans. Hyracoids with BE represented a major component of the diversity of mid- to large-sized herbivores during the Paleogene in Africa. Like HSB, which are developed by most other ‘ungulates,’ the BE is regarded as a device for resisting propagation of cracks during mastication. Hyracoids never developed however the ‘modified radial enamel’ that is characteristic of most large and hypsodont perissodactyls and artiodactyls that entered Africa during the Miocene.     

Decreased sarcolipin protein expression and enhanced sarco(endo)plasmic reticulum Ca2+ uptake in human atrial fibrillation

Sarcolipin (SLN), a key regulator of cardiac sarco(endo)plasmic reticulum (SR) Ca(2+) ATPase, is predominantly expressed in atria and mediates β-adrenergic responses. Studies have shown that SLN mRNA expression is decreased in human chronic atrial fibrillation (AF) and in aortic banded mouse atria; however, SLN protein expression in human atrial pathology and its role in atrial SR Ca(2+) uptake are not yet elucidated. In the present study, we determined the expression of major SR Ca(2+) handling proteins in atria of human AF patients and in human and in a mouse model of heart failure (HF). We found that the expression of SR Ca(2+) uptake and Ca(2+) release channel proteins are significantly decreased in atria but not in the ventricles of pressure-overload induced HF in mice. In human AF and HF, the expression of SLN protein was significantly decreased; whereas the expressions of other major SR Ca(2+) handling proteins were not altered. Further, we found that the SR Ca(2+) uptake was significantly increased in human AF. The selective downregulation of SLN and enhanced SR Ca(2+) uptake in human AF suggest that SLN downregulation could play an important role in abnormal intracellular Ca(2+) cycling in atrial pathology.     

Aqua bridge cleavage and metal ion extrusion by thiocyanate anions in a dicopper complex

Reaction of the imidazolidinyl phenolate-based ligand, H₃L [(2-(2′-hydroxyphenyl)-1,3-bis[4-(2-hydroxyphenyl)-3-azabut-3-enyl]-1,3-imidazolidine)] with Cu(ClO₄)₂·6H₂O produces an aqua-bridged cationic reactant complex [Cu₂(μ-H₂O)(μ-L)][ClO₄]·1.5H₂O (1·1.5H₂O). Solution phase interaction of 1·1.5H₂O with SCN⁻ anions in 1:1 molar ratio leads to [Cu₂(μ-L)(NCS)]·2H₂O (2·2H₂O) that does not possess anymore the reactive aqua bridge but instead a terminal SCN⁻ anion coordinated only to one Cu^II ion. Whereas in 1:2 molar ratio, partial extrusion of the Cu^II ions takes place to generate in situ [Cu(NCS)₃(OH₂)]⁻ anions. These complex anions then quantitatively replace anions in 1·1.5H₂O via ‘anion metathesis’ and concurrently remove the aqua bridge by coordination of linear MeCN to one of the Cu^II ions to give [Cu₂(μ-L)(CH₃CN)][Cu(NCS)₃(OH₂)] (3). The literature unknown [Cu(NCS)₃(OH₂)]⁻ anion forms an intimate H-bonded assembly with the cationic part of 3 to yield a novel [Cu₃] isosceles triangle. The precursor complex is known as antiferromagnetic whereas in 2·2H₂O, the Cu^II (S = 1/2) ions in a dinuclear entity exhibit ferromagnetic interactions (J/k_B = +15.0 K and g = 2.22) to yield an S_T = 1 spin ground state in good agreement with the M versus H data below 8 K.     

New template reactions of salicylaldehyde S-methyl-isothiosemicarbazone with 2-formylpyridine promoted by Ni(II) or Cu(II) metal ions

The template reaction between salicylaldehyde S-methyl-isothiosemicarbazone and 2-formylpyridine in presence of nickel(II) or copper(II) salts yields two new coordination compounds with general formula [NiL¹]₂(1) and [CuL²]₂(2) (L¹ = the dianionic (N¹-salicylidene)(N⁴-(hydroxy(pyridin-2-yl)methyl) S-methyl-isothiosemicarbazide) ligand and L² = the doubly deprotonated (N¹-salicylidene)(N⁴-(picolinoyl) S-methyl-isothiosemicarbazide) ligand). In the complex 1, the formed L¹ ligand appears as result of an addition reaction of the precursors, while for 2 a redox mechanism is implicated in the formation of L². Despite the fact that the initial organic precursors are the same, the resulting ligands obtained in the template reaction are different. In 1, the Ni(II) metal ion adopts a square-planar geometry and the [NiL¹] units are forming dimerized chains through weak Ni···Ni interactions (3.336 and 3.632 Å). In 2, the Cu(II) metal ions adopt a square-pyramidal geometry and form dinuclear species through weak Cu···O (phenoxo) interactions. The magnetic susceptibility measurements of the complexes reveal the diamagnetic nature of 1 as expected for a square planar Ni(II) complex and a paramagnetic behavior for 2 with weak intra-dimer antiferromagnetic interaction (J/k_B = −2.1(1) K).