239 research outputs found

    Efficacy of flour fortification with folic acid in women of childbearing age in Iran

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    Background: Flour fortification with folic acid is one of the main strategies for improving folate status in women of childbearing age. No interventional trial on the efficacy of folic acid fortification has been conducted so far in Iran. Objectives: To study the effects of flour fortification with folic acid on any reduction in neural tube defects (NTDs) and folate status of women of childbearing age. Methods: In a longitudinal hospital-based study, 13,361 postpartum women were studied after admission for childbirth before and after fortification. In addition, two cross-sectional surveys were conducted before (2006) and after flour fortification (2008). The cluster sampling method was used and 580 women, 15-49 years old, were studied as a representative sample of Golestan province in the north of Iran. Fasting blood samples were collected to measure serum vitamin B 12, folate and plasma homocysteine. Sociodemographic data, health characteristics and dietary intake were determined. Results: The mean daily intakes of folate from natural food before and after flour fortification were 198.3 and 200.8 μg/day, respectively. The total folate intake increased significantly from 198.3 to 413.7 μg/day after fortification (p < 0.001). Folate intake increased by an average of 226 μg/day from fortified bread. The mean serum folate level increased from 13.6 to 18.1 nmol/l; folate deficiency decreased from 14.3 to 2.3% (p < 0.001). The incidence rate of NTDs declined by 31% (p < 0.01) in the post-fortification period (2.19 per 1,000 births; December 2007 to December 2008) compared to the pre-fortification period (3.16 per 1,000 births; September 2006 to July 2007). Conclusions: Implementation of mandatory flour fortification with folic acid can lead to a significant increase in serum folate and a significant decrease in NTDs. Copyright © 2011 S. Karger AG, Basel

    Arene C−H Bond Activation and Arene Oxidative Coupling by Cationic Palladium(II) Complexes

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    N,N‘-Diaryl-α-diimine-ligated Pd(II) dimethyl complexes (^(tBu)2^(Ar)DAB^(Me))PdMe_2 and {(CF_3)_2^(Ar)DAB^(Me)}PdMe_2 {^(tBu)2^(Ar)DAB^(Me): ArNC═(CH_3)−C(CH_3═NAr, Ar=3,5-di-tert-butylphenyl; (CF_3)_2^(Ar)DAB^(Me):Ar = 3,5-bis(trifluoromethyl)phenyl} undergo protonolysis with HBF_4(aq) in trifluoroethanol (TFE) to form cationic complexes [(α-diimine)Pd(CH_3)(H_2O)][BF_4]. The cations activate benzene C−H bonds at room temperature. Kinetic analyses reveal trends similar to those observed for the analogous platinum complexes:  the C−H activation step is rate-determining (KIE = 4.1 ± 0.5) and is inhibited by H_2O. The kinetic data are consistent with a mechanism in which benzene substitution proceeds by a solvent- (TFE-) assisted associative pathway. Following benzene C−H activation under 1 atm O_2, the products of the reaction are biphenyl and a dimeric μ-hydroxide complex, [(α-diimine)Pd(OH)]_2[BF_4]_2. The Pd(0) formed in the reaction is reoxidized by O_2 to the dimeric μ-hydroxide complex after the oxidative C−C bond formation. The regioselectivity of arene coupling was investigated with toluene and α,α,α-trifluorotoluene as substrates

    Effect of Different Factors on Proliferation of Antler Cells, Cultured In Vitro

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    Antlers as a potential model for bone growth and development have become an object of rising interest. To elucidate processes explaining how antler growth is regulated, in vitro cultures have been established. However, until now, there has been no standard method to cultivate antler cells and in vitro results are often opposite to those reported in vivo. In addition, many factors which are often not taken into account under in vitro conditions may play an important role in the development of antler cells. In this study we investigated the effects of the antler growth stage, the male individuality, passaged versus primary cultures and the effect of foetal calf serum concentrations on proliferative potential of mixed antler cell cultures in vitro, derived from regenerating antlers of red deer males (Cervus elaphus). The proliferation potential of antler cells was measured by incorporation of 3H thymidine. Our results demonstrate that there is no significant effect of the antler growth stage, whereas male individuality and all other examined factors significantly affected antler cell proliferation. Furthermore, our results suggest that primary cultures may better represent in vivo conditions and processes occurring in regenerating antlers. In conclusion, before all main factors affecting antler cell proliferation in vitro will be satisfactorily investigated, results of in vitro studies focused on hormonal regulation of antler growth should be taken with extreme caution

    Impact damage characteristics of carbon fibre metal laminates : experiments and simulation

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    In this work, the impact response of carbon fibre metal laminates (FMLs) was experimentally and numerically studied with an improved design of the fibre composite lay-up for optimal mechanical properties and damage resistance. Two different stacking sequences (Carall 3–3/2–0.5 and Carall 5–3/2–0.5) were designed and characterised. Damage at relatively low energy impact energies (≤30 J) was investigated using Ultrasonic C-scanning and X–ray Computed Tomography (X-RCT). A 3D finite element model was developed to simulate the impact induced damage in both metal and composite layers using Abaqus/Explicit. Cohesive zone elements were introduced to capture delamination occurring between carbon fibre/epoxy plies and debonding at the interfaces between aluminium and the composite layers. Carall 5–3/2–0.5 was found to absorb more energy elastically, which indicates better resistance to damage. A good agreement is obtained between the numerically predicted results and experimental measurements in terms of force and absorbed energy during impact where the damage modes such as delamination was well simulated when compared to non-destructive techniques (NDT)

    Cellular interference in craniofrontonasal syndrome: Males mosaic for mutations in the x-linked EFNB1 gene are more severely affected than true hemizygotes

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    Craniofrontonasal syndrome (CFNS), an X-linked disorder caused by loss-of-function mutations of EFNB1, exhibits a paradoxical sex reversal in phenotypic severity: females characteristically have frontonasal dysplasia, craniosynostosis and additional minor malformations, but males are usually more mildly affected with hypertelorism as the only feature. X-inactivation is proposed to explain the more severe outcome in heterozygous females, as this leads to functional mosaicism for cells with differing expression of EPHRIN-B1, generating abnormal tissue boundariesa process that cannot occur in hemizygous males. Apparently challenging this model, males occasionally present with a more severe female-like CFNS phenotype. We hypothesized that such individuals might be mosaic for EFNB1 mutations and investigated this possibility in multiple tissue samples from six sporadically presenting males. Using denaturing high performance liquid chromatography, massively parallel sequencing and multiplex-ligation-dependent probe amplification (MLPA) to increase sensitivity above standard dideoxy sequencing, we identified mosaic mutations of EFNB1 in all cases, comprising three missense changes, two gene deletions and a novel point mutation within the 5 untranslated region (UTR). Quantification by Pyrosequencing and MLPA demonstrated levels of mutant cells between 15 and 69. The 5 UTR variant mutates the stop codon of a small upstream open reading frame that, using a dual-luciferase reporter construct, was demonstrated to exacerbate interference with translation of the wild-type protein. These results demonstrate a more severe outcome in mosaic than in constitutionally deficient males in an X-linked dominant disorder and provide further support for the cellular interference mechanism, normally related to X-inactivation in females. © The Author 2013. Published by Oxford University Press. All rights reserved

    The autophagy protein Atg7 is essential for hematopoietic stem cell maintenance.

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    The role of autophagy, a lysosomal degradation pathway which prevents cellular damage, in the maintenance of adult mouse hematopoietic stem cells (HSCs) remains unknown. Although normal HSCs sustain life-long hematopoiesis, malignant transformation of HSCs leads to leukemia. Therefore, mechanisms protecting HSCs from cellular damage are essential to prevent hematopoietic malignancies. In this study, we crippled autophagy in HSCs by conditionally deleting the essential autophagy gene Atg7 in the hematopoietic system. This resulted in the loss of normal HSC functions, a severe myeloproliferation, and death of the mice within weeks. The hematopoietic stem and progenitor cell compartment displayed an accumulation of mitochondria and reactive oxygen species, as well as increased proliferation and DNA damage. HSCs within the Lin(-)Sca-1(+)c-Kit(+) (LSK) compartment were significantly reduced. Although the overall LSK compartment was expanded, Atg7-deficient LSK cells failed to reconstitute the hematopoietic system of lethally irradiated mice. Consistent with loss of HSC functions, the production of both lymphoid and myeloid progenitors was impaired in the absence of Atg7. Collectively, these data show that Atg7 is an essential regulator of adult HSC maintenance
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