Whole-genome analysis of animal A- and B-type cyclins.

BACKGROUND: Multiple A- and B-type cyclins have been identified in animals, but their study is complicated by varying degrees of functional redundancy. A non-essential phenotype may reflect redundancy with a known or as yet unknown gene. Complete sequencing of several animal genomes has allowed us to determine the size of the mitotic cyclin gene family and therefore to start to address this issue. RESULTS: We analyzed the Caenorhabditis elegans, Drosophila melanogaster and Homo sapiens genomes to identify known and novel A- and B-type cyclin genes and distinguish them from related pseudogenes. We find only a single functional A-type cyclin gene in invertebrates but two in vertebrates. In addition to the single functional cyclin A gene, the C. elegans genome contains numerous cyclin A pseudogenes. In contrast, the number and relationship of B-type cyclins varies considerably between organisms but all contain at least one cyclin B1-like gene and a cyclin B3 gene. CONCLUSIONS: There are three conserved families of mitotic cyclins in animals: A-, B3- and B-type. The precise number of genes within the A- and B-type families varies in different organisms, possibly as an adaptation to their distinct developmental strategies.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Whole-genome analysis of animal A- and B-type cyclins

BACKGROUND: Multiple A- and B-type cyclins have been identified in animals, but their study is complicated by varying degrees of functional redundancy. A non-essential phenotype may reflect redundancy with a known or as yet unknown gene. Complete sequencing of several animal genomes has allowed us to determine the size of the mitotic cyclin gene family and therefore to start to address this issue. RESULTS: We analyzed the Caenorhabditis elegans, Drosophila melanogaster and Homo sapiens genomes to identify known and novel A- and B-type cyclin genes and distinguish them from related pseudogenes. We find only a single functional A-type cyclin gene in invertebrates but two in vertebrates. In addition to the single functional cyclin A gene, the C. elegans genome contains numerous cyclin A pseudogenes. In contrast, the number and relationship of B-type cyclins varies considerably between organisms but all contain at least one cyclin B1-like gene and a cyclin B3 gene. CONCLUSIONS: There are three conserved families of mitotic cyclins in animals: A-, B3- and B-type. The precise number of genes within the A- and B-type families varies in different organisms, possibly as an adaptation to their distinct developmental strategies

Tris(1,10-Phenanthroline)Cobalt(II) Triiodide

The asymmetric unit of the title compound, [Co(C12H8N2)3](I3)2, contains one [Co(1,10-phenanthroline)3]2+ cation, half each of two centrosymmetric triiodide anions, and one complete triiodide anion. The title compound was synthesized solvothermally from Co(NO3)2, 1,10-phenanthroline, and SnI2, where the SnI2 reagent serves only as a source of I atoms

Tetrakis[2-(2-Pyridyl)Pyridinium] Tetra-μ\u3csub\u3e3\u3c/sub\u3e-Iodo-Hexa-μ\u3csub\u3e2\u3c/sub\u3e-Iodo-Dodecaiodohexabismuthate and Bis[Tris(2,2\u27-Bipyridine)Ruthenium(II)] Di-μ\u3csub\u3e4\u3c/sub\u3e-Iodo-Octa-μ\u3csub\u3e2\u3c/sub\u3e-Iodo-Dodecaiodohexabismuthate

Crystals of the title compounds were grown solvothermally in an ethanol-water solvent mixture using ruthenium triiodide, 2,2\u27-bipyridine and bismuth triiodide as starting materials. Tetrakis[2-(2-pyridyl)pyridinium] tetra-3-iodo-hexa-2-iodo-dodecaiodohexabismuthate, (C10H9N2)4[Bi6I22], crystallizes in the triclinic space group P and is the major reaction product. The asymmetric unit of this compound consists of half a centrosymmetric [Bi6I22]4- anion and two independent 2,2\u27-bipyridinium cations. The minor product of the reaction is bis[tris(2,2\u27-bipyridine)ruthenium(II)] di-4-iodo-octa-2-iodo-dodecaiodohexabismuthate, [Ru(C10H8N2)3]2[Bi6I22], which also crystallizes in the triclinic space group P. For this compound, the asymmetric unit consists of one full [Ru(2,2\u27-bipyridine)3]2+ cation and half a centrosymmetric [Bi6I22]4- anion. Although both compounds contain a centrosymmetric [Bi6I22]4- anion, the polyhedral arrangement of the distorted BiI6 octahedra in the two compounds is quite different, and the anion of the latter compound has not previously been observed in iodobismuthate chemistry. Formula: (C10H9N2)4[Bi6I22] and [Ru(C10H8N2)3][Bi6I22

Referral for specialist follow-up and its association with post-discharge mortality among patients with systolic heart failure (from the National Heart Failure Audit for England and Wales)

For patients admitted with worsening heart failure, early follow-up after discharge is recommended. Whether outcomes can be improved when follow-up is done by cardiologists is uncertain. We aimed to determine the association between cardiology follow-up and risk of death for patients with heart failure discharged from hospital. Using data from the National Heart Failure Audit (England & Wales), we investigated the effect of referral to cardiology follow-up on 30-day and one-year mortality in 68 772 patients with heart failure and a reduced left ventricular ejection fraction (HFREF) discharged from 185 hospitals between 2007 to 2013. The primary analyses used instrumental variable analysis complemented by hierarchical logistic and propensity matched models. At the hospital level, rates of referral to cardiologists varied from 6% to 96%. The median odds ratio (OR) for referral to cardiologist was 2.3 (95% confidence interval [CI] 2.1, 2.5), suggesting that, on average, the odds of a patient being referred for cardiologist follow-up after discharge differed approximately 2.3 times from one randomly selected hospital to another one. Based on the proportion of patients (per region) referred for cardiology follow-up, referral for cardiology follow-up was associated with lower 30-day (OR 0.70; CI 0.55, 0.89) and one-year mortality (OR 0.81; CI 0.68, 0.95) compared with no plans for cardiology follow-up (i.e., standard follow-up done by family doctors). Results from hierarchical logistic models and propensity matched models were consistent (30-day mortality OR 0.66; CI 0.61, 0.72 and 0.66; CI 0.58, 0.76 for hierarchical and propensity matched models, respectively). For patients with HFREF admitted to hospital with worsening symptoms, referral to cardiology services for follow-up after discharge is strongly associated with reduced mortality, both early and late