Exploration of the association between chronic periodontal disease and erectile dysfunction from a population‐based view point

[[abstract]]Several cross‐sectional studies have indicated an association between chronic periodontal disease (CPD) and cardiovascular disease and metabolic syndrome. Erectile dysfunction (ED) also shares pathological mechanisms with these diseases. Using a nationwide population‐based data set, we examined the association between ED and CPD and assessed the effect of dental extraction (DE) on ED prevalence in different aged CPD populations in Taiwan. We identified 5105 patients with ED and randomly selected 10 210 patients as controls. Of these patients, 2617 (17.09%) were diagnosed with CPD according to the index data: 1196 (23.43%) in the ED group and 1421 (13.92%) in the control group. After adjusting for comorbid factors, patients with ED were more likely to have been diagnosed with prior CPD than controls (OR = 1.79, 95% CI = 1.64–1.96, P < 0.001). Moreover, the association was much stronger in the populations aged less than 30 years (OR = 2.13, 95% CI = 1.23–3.70, P < 0.001) and more than 59 years (OR = 2.27, 95% CI = 1.99–2.59, P < 0.001). Dental extraction seems to attenuate damage to the penile endothelial beds caused by CPD‐related inflammation and overcame the process of ED in the middle‐aged and older populations

Novel multi-spin-state linear hexanickel complexes Ni-6(11+) and their singly oxidized products Ni-6(12+) with 1,8-naphthyridine-based ligands: Tuning the redox properties of the metal string

The new ligand, 2,7-bis(alpha-pyrimidylamino)- 1,8-naphthyridine (H(2)bpmany), was prepared by the reaction of 2,7-dichloro-1,8-naphthyridine with 2-aminopyrimidine in the presence of sodium tert-butoxide under palladium-catalyzed conditions. The linear hexanickel Ni-6(11+) complexes [Ni-6(mu(6)-bpmany)(4)X-2]Cl (X = Cl (1); X = NCS (2)) and their singly oxidized products [Ni-6(P-6-bpmany)(4)X-2](BF4)(2) (X = Cl (3); X = NCS (4)) have been synthesized, and compounds 1, 2 and 4 have been crystallographically characterized. The crystal structures of the Ni-6(11+) complexes show remarkably short Ni-Ni distances (ca. 2.22 angstrom), clearly indicative of partial metal-metal bonding in the mixed-valence Ni-2(3+) unit. This is also verified by the axial X-band EPR spectra of the complexes in solution. Magnetic susceptibility measurements reveal that the Ni-6(11+) complexes exhibit anti ferromagnetic interactions (J = -47 cm(-1)) between the terminal Ni2+ ion and the central Ni-2(3+) unit, and the Ni-6(12+) complexes exhibit weak antiferromagnetic interactions (J = -5 cm(-1)) between the two terminal Ni2+ ions. The cyclic voltammograms display three reversible redox waves at E-1/2((1)) = +0.87, E-1/2((2)) = -0.02 and E-1/2((3)) = -0.46 V for 1, and E-1/2((1)) = +0.96, E-1/2((2)) = -0.01, and E-1/2((3)) = -0.41 V for 2. The relatively low potentials of E-1/2((2)) suggest that the Ni-6(11+) complexes can be easily converted to their Ni-6(12+) forms. (c) 2007 Elsevier Ltd. All rights reserved

Oxidation of linear trinuclear ruthenium complexes Ru-3(dpa)(4)Cl-2 and Ru-3(dpa)(4)(CN)(2) : Synthesis, structures, electrochemical and magnetic properties

The neutral, monocationic, and dicationic linear trinuclear ruthenium compounds [Ru-3(dpa)(4)(CN)(2)], [Ru-3(dpa)(4)(CN)(2)][BF4], [Ru-3(dpa)(4)Cl-2]- [BF4], and [Ru-3(dpa)(4)Cl-2][BF4](2) (dpa = the anion of dipyridylamine) have been synthesized and characterized by various spectroscopic techniques. Cyclic voltammetric and spectroelectrochemical studies on the neutral and oxidized compounds are reported. These compounds undergo three successive metal-centered one-electron-transfer processes. X-ray structural studies reveal a symmetrical Ru-3 unit for these compounds. While the metal-metal bond lengths change only slightly, the metal-axial ligand lengths exhibit a significant decrease upon oxidation of the neutral complex. The electronic configuration of the Ru-3 unit changes as the axial chloride ligands are replaced by the stronger &quot;pi-acid&quot; cyanide axial ligands. Magnetic measurements and H-1 NMR spectra indicate that [Ru-3(dpa)(4)Cl-2] and [Ru-3(dpa)(4)Cl-2][BF4](2) are in a spin state of S = 0 and [Ru-3-(dpa)(4)Cl-2][BF4], [Ru-3(dpa)(4)(CN)(2)], and [Ru-3(dpa)(4)(CN)(2)][BF4] are in spin states of S=1/2, 1, and 3/2, respectively. These results are consistent with molecular orbital (MO) calculations

Histamine(2)-Receptor Antagonists Are an Alternative to Proton Pump Inhibitor in Patients Receiving Clopidogrel

BACKGROUND & AIMS: Previous observational studies reported that concomitant use of clopidogrel and proton pump inhibitors (PPIs) in patients with prior acute coronary syndrome (ACS) was associated with adverse cardiovascular outcomes. We investigated whether H-2-receptor antagonist (H(2)RA) is an alternative to PPI in patients with ACS. METHODS: We conducted a population- based retrospective cohort study of 6552 patients in Taiwan discharged for ACS between 2002 and 2005. Patients were divided into 5 cohorts: clopidogrel plus H2RA (n = 252), clopidogrel plus PPI (n = 311), clopidogrel alone (n = 5551), H(2)RA alone (n = 235), and PPI alone (n = 203). The primary outcome was rehospitalization for ACS or all-cause mortality within 3 month of rehospitalization. RESULTS: The 1-year cumulative incidence of the primary outcome was 26.8% (95% CI: 21.5%-33.0%) in the clopidogrel plus H(2)RA cohort and 33.2% (95% CI: 27.8%-39.4%) in the clopidogrel plus PPI cohort, compared with 11.6% (95% CI: 10.8%-12.5%) in the clopidogrel alone cohort (P < .0001). No significant difference was observed between the PPI alone cohort (11.0%; 95% CI: 7.1%-16.8%), the H(2)RA alone cohort (11.8%; 95% CI: 8.2%-16.8%), and the clopidogrel alone cohort in terms of the primary outcome. The number needed to harm was 7 with concomitant H(2)RA and 5 with concomitant PPI. On multivariate analysis, concomitant H(2)RA and PPI were independent risk factors predicting adverse outcomes (adjusted hazard ratios, 2.48 and 3.20, respectively; P < .0001). CONCLUSIONS: Concomitant use of clopidogrel and H(2)RA or PPI after hospital discharge for ACS is associated with increased risk of adverse outcomes

An Extended Metal Chain with the 2,7-Bis(dipyridyldiamino)-1,8-naphthyridine (H(4)bdpdany) Ligand - The Longest Even-Numbered Metal Chain Complex

A decanickel extended metal atom chain (EMAC) complex with a new pyridyl-and naphthyridyl-modulated ligand (H(4)bdpdany) was synthesized. Analysis of the crystal structure of complex [Ni-10(mu(10)-bdpdany)(4)(NCS)(2)](PF6)(2) (1) shows that all of the bdpdany(4-)ligands bind the metal in an all-syn conformation, and structural data reveals short Ni center dot center dot center dot Ni distances in the range 2.36-2.23 angstrom. Temperature-dependent magnetic measurements performed on two independent high-spin nickel(II) ions of complex [Ni-10(mu(10)-bdpdany)(4)(NCS)(2)](PF6)(2) (1) demonstrate that the metal chain is antiferromagnetic. The longer distance between the two terminal high-spin nickel(II) ions relative to those in tetranickel and hexanickel strings causes a decrease in the magnitude of the antiferromagnetic interaction

The candidate tumor suppressor gene BLU, located at the commonly deleted region 3p21.3, is an E2F-regulated, stress-responsive gene and inactivated by both epigenetic and genetic mechanisms in nasopharyngeal carcinoma

10.1038/sj.onc.1207632Oncogene23274793-4806ONCN

Phenotypes, genotypes and disease susceptibility associated with gene copy number variations: complement C4 CNVs in European American healthy subjects and those with systemic lupus erythematosus

A new paradigm in human genetics is high frequencies of inter-individual variations in copy numbers of specific genomic DNA segments. Such common copy number variation (CNV) loci often contain genes engaged in host-environment interaction including those involved in immune effector functions. DNA sequences within a CNV locus often share a high degree of identity but beneficial or deleterious polymorphic variants are present among different individuals. Thus, common gene CNVs can contribute, both qualitatively and quantitatively, to a spectrum of phenotypic variants. In this review we describe the phenotypic and genotypic diversities of complement C4 created by copy number variations of RCCX modules (RP-C4-CYP21-TNX) and size dichotomy of C4 genes. A direct outcome of C4 CNV is the generation of two classes of polymorphic proteins, C4A and C4B, with differential chemical reactivities towards peptide or carbohydrate antigens, and a range of C4 plasma protein concentrations (from 15 to 70 mg/dl) among healthy subjects. Deliberate molecular genetic studies enabled development of definitive techniques to determine exact patterns of RCCX modular variations, copy numbers of long and short C4A and C4B genes by Southern blot analyses or by real-time quantitative PCR. It is found that in healthy European Americans, the total C4 gene copy number per diploid genome ranges from 2 to 6: 60.8% of people with four copies of C4 genes, 27.2% with less than four copies, and 12% with more than four copies. Such a distribution is skewed towards the low copy number side in patients with systemic lupus erythematosus (SLE), a prototypic autoimmune disease with complex etiology. In SLE, the frequency of individuals with less than four copies of C4 is significantly increased (42.2%), while the frequency of those with more than four copies is decreased (6%). This decrease in total C4 gene copy number in SLE is due to increases in homozygous and heterozygous deficiencies of C4A but not C4B. Therefore, it is concluded that lower copy number of C4 is a risk factor for and higher gene copy number of C4 is a protective factor against SLE disease susceptibility

Clinical variability in distal spinal muscular atrophy type 1 (DSMA1): determination of steady-state IGHMBP2 protein levels in five patients with infantile and juvenile disease

Distal spinal muscular atrophy type 1 (DSMA1) is caused by mutations in the immunoglobulin mu-binding protein 2 (IGHMBP2) gene. Patients with DSMA1 present between 6 weeks and 6 months of age with progressive muscle weakness and respiratory failure due to diaphragmatic palsy. Contrary to this "classic" infantile disease, we have previously described a DSMA1 patient with juvenile disease onset. In this paper, we present (1) a second juvenile case and (2) the first study of DSMA1 on protein level in patients with infantile (n = 3) as well as juvenile (n = 2) disease onset observing elevated residual steady-state IGHMBP2 protein levels in the patients with late onset DSMA1 as compared to those with classic DSMA1. Mutation screening in IGHMBP2 revealed two patients compound heterozygous for a novel missense mutation (c.1478C-->T; p.T493I) and another previously described mutation. In lymphoblastoid cells of both patients, steady-state IGHMBP2 protein levels were reduced. In comparison to wild-type IGHMBP2, the p.T493I variant protein had an increased tendency to aggregate and spontaneously degrade in vitro. We verified a change in the physicochemical properties of the p.T493I variant which may explain the pathogenicity of this mutation. Our data further suggest that the age of onset of DSMA1 is variable, and we discuss the effect of residual IGHMBP2 protein levels on the clinical course and the severity of the disease