Bis(μ-9-anthracenemethano­lato)bis­[dimethyl­aluminium(III)]

The title complex, [Al2(CH3)4(C15H11O)2], is dimeric bridged through the O atoms of the 9-anthracenemethano­late anions. Each Al atom is tetra­coordinated by two bridging O atoms from two different 9-anthracenemethano­late ligands and by two C atoms from two methyl groups, forming a distorted tetra­hedral environment. The average Al—O bond distance in the Al2O2 core is 1.845 Å

Bis{1-[(E)-o-tolyl­diazen­yl]-2-naphtho­l­ato}copper(II)

In the title complex, [Cu(C17H13N2O)2], the CuII atom is tetra­coordinated by two N atoms and two O atoms from two bidentate 1-[(E)-o-tolyl­diazen­yl]-2-naphtho­late ligands, forming a slightly distorted square-planar environment. The two N atoms and two O atoms around the CuII atom are trans to each other, with an O—Cu—O bond angle of 177.00 (9)° and an N—Cu—N bond angle of 165.63 (10)°. The average distances between the CuII atom and the coordinated O and N atoms are 1.905 (2) and 1.995 (2)Å, respectively

Bis[μ-2-(2H-benzotriazol-2-yl)-4-methyl­phenolato]bis­[dimethyl­aluminium(III)]

The title complex, [Al2(CH3)4(C13H10N3O)2], is dimeric, bridged through the O atoms of the phenolate anions. The asymmetric unit contains one half of the mol­ecule and there is a crystallographic inversion centre in this mol­ecule. Each Al atom is penta­coordinated by one N atom and two bridging O atoms of two N,O-bidentate benzotriazolylphenolate ligands and by two C atoms from two methyl groups, forming a distorted trigonal–bipyramidal environment

Bis[2-(2H-benzotriazol-2-yl)-4-methyl-6-(phenyl­imino­methyl-κN)phenolato-κO]palladium(II)

In the title complex, [Pd(C20H15N4O)2], the PdII atom is tetra­coordinated by two N atoms and two O atoms from two bidentate imine–benzotriazole phenolate ligands, forming a square-planar environment. The asymmetric unit contains two half-mol­ecules in both of which the PdII atom lies on a centre of symmetry. The average distances between the PdII atom and the coordinated O and N atoms are 1.9831 (12) and 2.012 (2) Å, respectively

Type I IL-1 Receptor (IL-1RI) as Potential New Therapeutic Target for Bronchial Asthma

The IL-1R/TLR family has been receiving considerable attention as potential regulators of inflammation through their ability to act as either activators or suppressors of inflammation. Asthma is a chronic inflammatory disease characterized by airway hyperresponsiveness, allergic inflammation, elevated serum total, allergen-specific IgE levels, and increased Th2 cytokine production. The discovery that the IL-1RI–IL-1 and ST2–IL-33 pathways are crucial for allergic inflammation has raised interest in these receptors as potential targets for developing new therapeutic strategies for bronchial asthma. This paper discusses the current use of neutralizing mAb or soluble receptor constructs to deplete cytokines, the use of neutralizing mAb or recombinant receptor antagonists to block cytokine receptors, and gene therapy from experimental studies in asthma. Targeting IL-1RI–IL-1 as well as ST2–IL-33 pathways may promise a disease-modifying approach in the future

Molecular population genetics and gene expression analysis of duplicated CBF genes of Arabidopsis thaliana

<p>Abstract</p> <p>Background</p> <p><it>CBF/DREB </it>duplicate genes are widely distributed in higher plants and encode transcriptional factors, or CBFs, which bind a DNA regulatory element and impart responsiveness to low temperatures and dehydration.</p> <p>Results</p> <p>We explored patterns of genetic variations of <it>CBF1, -2</it>, and -<it>3 </it>from 34 accessions of <it>Arabidopsis thaliana</it>. Molecular population genetic analyses of these genes indicated that <it>CBF2 </it>has much reduced nucleotide diversity in the transcriptional unit and promoter, suggesting that <it>CBF2 </it>has been subjected to a recent adaptive sweep, which agrees with reports of a regulatory protein of <it>CBF2</it>. Investigating the ratios of K_a/K_sbetween all paired <it>CBF </it>paralogus genes, high conservation of the AP2 domain was observed, and the major divergence of proteins was the result of relaxation in two regions within the transcriptional activation domain which was under positive selection after <it>CBF </it>duplication. With respect to the level of <it>CBF </it>gene expression, several mutated nucleotides in the promoters of <it>CBF3 </it>and <it>-1 </it>of specific ecotypes might be responsible for its consistently low expression.</p> <p>Conclusion</p> <p>We concluded from our data that important evolutionary changes in <it>CBF1, -2</it>, and -<it>3 </it>may have primarily occurred at the level of gene regulation as well as in protein function.</p

Juvenile Dermatomyositis: A 20-year Retrospective Analysis of Treatment and Clinical Outcomes

BackgroundJuvenile dermatomyositis is a rare childhood multisystem autoimmune disease involving primarily the skin and muscles, and it may lead to long-term disability. This study aimed to describe the clinical course of juvenile dermatomyositis and determine if any early clinical or laboratory features could predict outcome.MethodsMedical charts of patients aged ≤18 years and diagnosed with juvenile dermatomyositis (according to the criteria of Bohan and Peter) at the Pediatric Department, National Taiwan University Hospital, between 1989 and 2009 were reviewed. The endpoints for disease assessment were complete clinical response and complete clinical remission. Cox's proportional hazards model was fitted to identify important predictors of complete clinical remission.ResultsA total of 39 patients with juvenile dermatomyositis were reviewed. Two-thirds were females, and the mean age at disease onset was 81.97 ± 46.63 months. The most common initial presentations were Gottron's papule (82.1%) and muscle weakness (82.1%). After excluding one patient with an incomplete record, the remaining 31 patients who had muscle weakness were analyzed; among them, 22 (70.97%) achieved complete clinical response, but only six (19.4%) achieved complete clinical remission. Multivariate analysis showed that female sex, negative Gowers' sign at disease onset, and positive photosensitivity at disease onset were favorable factors to achieve complete clinical remission. Moreover, covariate-adjusted survival curves were drawn for making predictions of complete clinical remission. Only 13 (33.33%) patients were symptom free at the end of follow up, whereas the other 26 suffered from different kinds of complications. None of them developed malignancy, but two (5.13%) patients died during the follow-up period.ConclusionFactors such as male sex and Gowers' sign were unlikely to favor the achievement of complete clinical remission in juvenile dermatomyositis. Certain complications cannot be avoided, and thus more effective treatments and monitoring strategies are needed for better control of juvenile dermatomyositis