266 research outputs found

    (E)-3-Bromo-N′-(2-chloro­benzyl­idene)benzohydrazide

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    The title compound, C14H10BrClN2O, was synthesized by the reaction of 2-chloro­benzaldehyde with an equimolar quantity of 3-bromo­benzohydrazide in methanol. The mol­ecule displays an E configuration about the C=N bond. The dihedral angle between the two benzene rings is 13.0 (2)°. In the crystal structure, mol­ecules are linked through inter­molecular N—H⋯O hydrogen bonds, forming chains propagating along the c axis

    The mediating effect of body mass index on the relationship between cigarette smoking and atopic sensitization in Chinese adults

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    Background: It is unclear whether the relationship between cigarette smoking and atopy is mediated by body fat mass, such as the Body Mass Index (BMI). We assessed the mediating role of BMI on the relationship between smoking and atopy in Chinese adults. Methods: A hospital-based case-control study of 786 atopic cases and 2771 controls was conducted in adults aged 18 years or older from March 2010 to September 2014 in Harbin, China. Mediation models were used to estimate the indirect effects of smoking on atopic sensitization through BMI. Results: Compared to non-smokers, light smokers and moderate smokers had a lower risk of inhalant allergen sensitization. The indirect effect of smoking and sensitization to aeroallergens were only observed in light smokers (point estimate, -0.026; 95% CI, -0.062 to -0.004). The mediating roles of BMI on the relationships between smoking and other types of allergic sensitization were not statistically significant. Conclusion: BMI appeared to partially mediate the effect of light smoking on sensitization to aeroallergens. However, considering the other harmful health effects of cigarette smoking, the effective method to lower the incidence of atopy would be to decrease body fat mass by physical exercise and employing other more healthy ways of living rather than smoking

    (E)-3-Bromo-N′-(2-hydr­oxy-1-naphthyl­idene)benzohydrazide

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    The title compound, C18H13BrN2O2, was synthesized by the reaction of 2-hydr­oxy-1-naphthaldehyde with an equimolar quantity of 3-bromo­benzohydrazide in methanol. The dihedral angle between the benzene ring and the naphthyl ring system is 18.3 (2)°. An intra­molecular O—H⋯N hydrogen bond is observed between the phenolate O and imine N atoms. In the crystal structure, mol­ecules are linked through inter­molecular N—H⋯O and C—H⋯O hydrogen bonds, forming a chain running along [101]

    (E)-N′-(3,5-Dibromo-2-hydroxy­benzyl­idene)-2-methoxy­benzohydrazide

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    The title compound, C15H12Br2N2O3, was synthesized by the reaction of 3,5-dibromo-2-hydroxy­benzaldehyde with an equimolar quantity of 2-methoxy­benzohydrazide in methanol. The dihedral angle between the two benzene rings is 3.4 (2)° and intra­molecular O—H⋯N and N—H⋯O hydrogen bonds are observed in the mol­ecule. The crystal studied was an inversion twin with a 0.513 (19):0.487 (19) domain ratio

    (E)-3-Bromo-N′-(5-bromo-2-hydroxy­benzyl­idene)benzohydrazide

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    The title compound, C14H10Br2N2O2, was synthesized by the reaction of 5-bromo­salicylaldehyde with an equimolar quantity of 3-bromo­benzohydrazide in methanol. The dihedral angle between the two benzene rings is 10.5 (4)°. In the crystal structure, mol­ecules are linked through inter­molecular N—H⋯O hydrogen bonds to form chains parallel to the c axis, and an intra­molecular O—H⋯N inter­action also occurs

    PITX2C loss-of-function mutations responsible for idiopathic atrial fibrillation

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    OBJECTIVE: This study aimed to identify novel PITX2c mutations responsible for idiopathic atrial fibrillation. METHODS: A cohort of 210 unrelated patients with idiopathic atrial fibrillation and 200 unrelated, ethnically matched healthy individuals used as controls were recruited. The whole coding exons and splice junctions of the PITX2c gene, which encodes a paired-like homeobox transcription factor required for normal cardiovascular morphogenesis, were sequenced in 210 patients and 200 control subjects. The causative potentials of the identified mutations were automatically predicted by MutationTaster and PolyPhen-2. The functional characteristics of the PITX2c mutations were explored using a dual-luciferase reporter assay system. RESULTS: Two novel heterozygous PITX2c mutations (p.Q105L and p.R122C) were identified in 2 of the 210 unrelated patients with idiopathic atrial fibrillation. These missense mutations were absent in the 400 control chromosomes and were both predicted to be pathogenic. Multiple alignments of PITX2c protein sequences across various species showed that the altered amino acids were highly evolutionarily conserved. A functional analysis demonstrated that the mutant PITX2c proteins were both associated with significantly reduced transcriptional activity compared with their wild-type counterparts. CONCLUSION: The findings of this study associate PITX2c loss-of-function mutations with atrial fibrillation, supporting the hypothesis that dysfunctional PITX2c confers enhanced susceptibility to atrial fibrillation and suggesting potential implications for early prophylaxis and allele-specific therapy for this common arrhythmia
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