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Journal Cover Biochemistry and Cell Biology
  [SJR: 0.859]   [H-I: 76]   [15 followers]  Follow
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 0829-8211 - ISSN (Online) 1208-6002
   Published by NRC Research Press Homepage  [21 journals]
  • A global research collaboration on fetal alcohol spectrum disorder
    • Authors: Heather Medwick, Albert E. Chudley
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page vii-viii, April 2018.

      Citation: Biochemistry and Cell Biology
      PubDate: 2018-04-10T06:22:56Z
      DOI: 10.1139/bcb-2018-0088
  • Special issue on fetal alcohol spectrum disorder
    • Authors: Abraham Fainsod, Geoff Hicks
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page v-vi, April 2018.

      Citation: Biochemistry and Cell Biology
      PubDate: 2018-04-10T05:59:56Z
      DOI: 10.1139/bcb-2018-0087
  • Effects of prenatal alcohol exposure (PAE): insights into FASD using mouse
           models of PAE
    • Authors: Berardino Petrelli, Joanne Weinberg, Geoffrey G. Hicks
      Pages: 131 - 147
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 131-147, April 2018.
      The potential impact of prenatal alcohol exposure (PAE) varies considerably among exposed individuals, with some displaying serious alcohol-related effects and many others showing few or no overt signs of fetal alcohol spectrum disorder (FASD). In animal models, variables such as nutrition, genetic background, health, other drugs, and stress, as well as dosage, duration, and gestational timing of exposure to alcohol can all be controlled in a way that is not possible in a clinical situation. In this review we examine mouse models of PAE and focus on those with demonstrated craniofacial malformations, abnormal brain development, or behavioral phenotypes that may be considered FASD-like outcomes. Analysis of these data should provide a valuable tool for researchers wishing to choose the PAE model best suited to their research questions or to investigate established PAE models for FASD comorbidities. It should also allow recognition of patterns linking gestational timing, dosage, and duration of PAE, such as recognizing that binge alcohol exposure(s) during early gestation can lead to severe FASD outcomes. Identified patterns could be particularly insightful and lead to a better understanding of the molecular mechanisms underlying FASD.
      Citation: Biochemistry and Cell Biology
      PubDate: 2018-01-25T08:00:00Z
      DOI: 10.1139/bcb-2017-0280
  • Translating to the Community (T2C): a protocol paper describing the
           development of Canada’s first social epigenetic FASD biobank
    • Authors: Brenda Elias, Ana Hanlon-Dearman, Betty Head, Geoffrey G. Hicks
      Pages: 275 - 287
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 275-287, April 2018.
      Translating to the Community (T2C) is a social biorepository designed to advance new diagnostic tools and realign community–clinical processes, with the aim to mitigate the short- and long-term impacts of fetal alcohol spectrum disorder (FASD) as well as prenatal alcohol exposure and its co-morbidities and behaviors. In this paper, we describe the evolution of this repository as a new translational partnership to advance a precision-medicine approach to FASD. Key to its evolution was a partnership between academic researchers, Indigenous communities, families, and a regional diagnostic clinic. We further describe the rationale for social biobanking, the type of banking, ethical engagement of families, communities, and clinics, their roles in repository design, governance, translation, and research activities, types of data collected from families, and how the study data are managed, reported, and accessed. The repository design includes biological samples, social-contextual health-survey data, and clinical data (which are linkable to administrative data) from community and clinical cohorts of diagnosed children, children prenatally exposed but not diagnosed, children suspected to have had a prenatal exposure, and related siblings, biological parents, and unrelated children and their parents. From these cohorts and families, potential studies drawing on this data will shed light on various risk factors, social and biological pathways, and service utilization issues, with the aim to implement primary and secondary prevention and intervention strategies.
      Citation: Biochemistry and Cell Biology
      PubDate: 2018-03-15T07:00:00Z
      DOI: 10.1139/bcb-2017-0278
  • Copy number variation in fetal alcohol spectrum disorder
    • Authors: Mehdi Zarrei, Geoffrey G. Hicks, James N. Reynolds, Bhooma Thiruvahindrapuram, Worrawat Engchuan, Molly Pind, Sylvia Lamoureux, John Wei, Zhouzhi Wang, Christian R. Marshall, Richard F. Wintle, Albert E. Chudley, Stephen W. Scherer
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Fetal alcohol spectrum disorder (FASD) is characterized by a combination of neurological, developmental, and congenital defects that may occur as a consequence of prenatal alcohol exposure. Earlier reports showed that large chromosomal anomalies may link to FASD. Here, we examined the prevalence and types of copy number variations (CNVs) in FASD cases previously diagnosed by a multidisciplinary FASD team in sites across Canada. We genotyped 95 children with FASD and 87 age-matched, typically developing controls on the Illumina Human Omni2.5 SNP (single nucleotide polymorphisms) array platform. We compared their CNVs with those of 10 851 population controls to identify rare CNVs (
      Citation: Biochemistry and Cell Biology
      PubDate: 2018-03-13T07:10:33Z
      DOI: 10.1139/bcb-2017-0241
  • Xenopus embryos to study fetal alcohol syndrome, a model for environmental
    • Authors: Abraham Fainsod, Hadas Kot-Leibovich
      Pages: 77 - 87
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 77-87, April 2018.
      Vertebrate model systems are central to characterize the outcomes of ethanol exposure and the etiology of fetal alcohol spectrum disorder (FASD), taking advantage of their genetic and morphological closeness and similarity to humans. We discuss the contribution of amphibian embryos to FASD research, focusing on Xenopus embryos. The Xenopus experimental system is characterized by external development and accessibility throughout embryogenesis, large clutch sizes, gene and protein activity manipulation, transgenesis and genome editing, convenient chemical treatment, explants and conjugates, and many other experimental approaches. Taking advantage of these methods, many insights regarding FASD have been obtained. These studies characterized the malformations induced by ethanol including quantitative analysis of craniofacial malformations, induction of fetal growth restriction, delay in gut maturation, and defects in the differentiation of the neural crest. Mechanistic, biochemical, and molecular studies in Xenopus embryos identified early gastrula as the high alcohol sensitivity window, targeting the embryonic organizer and inducing a delay in gastrulation movements. Frog embryos have also served to demonstrate the involvement of reduced retinoic acid production and an increase in reactive oxygen species in FASD. Amphibian embryos have helped pave the way for our mechanistic, molecular, and biochemical understanding of the etiology and pathophysiology of FASD.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-25T07:00:00Z
      DOI: 10.1139/bcb-2017-0219
  • Diving into the world of alcohol teratogenesis: a review of zebrafish
           models of fetal alcohol spectrum disorder
    • Authors: Yohaan Fernandes, Desire M. Buckley, Johann K. Eberhart
      Pages: 88 - 97
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 88-97, April 2018.
      The term fetal alcohol spectrum disorder (FASD) refers to the entire suite of deleterious outcomes resulting from embryonic exposure to alcohol. Along with other reviews in this special issue, we provide insight into how animal models, specifically the zebrafish, have informed our understanding of FASD. We first provide a brief introduction to FASD. We discuss the zebrafish as a model organism and its strengths for alcohol research. We detail how zebrafish has been used to model some of the major defects present in FASD. These include behavioral defects, such as social behavior as well as learning and memory, and structural defects, disrupting organs such as the brain, sensory organs, heart, and craniofacial skeleton. We provide insights into how zebrafish research has aided in our understanding of the mechanisms of ethanol teratogenesis. We end by providing some relatively recent advances that zebrafish has provided in characterizing gene-ethanol interactions that may underlie FASD.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-08-17T07:00:00Z
      DOI: 10.1139/bcb-2017-0122
  • The avian embryo as a model for fetal alcohol spectrum disorder
    • Authors: George R. Flentke, Susan M. Smith
      Pages: 98 - 106
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 98-106, April 2018.
      Prenatal alcohol exposure (PAE) remains a leading preventable cause of structural birth defects and permanent neurodevelopmental disability. The chicken (Gallus gallus domesticus) is a powerful embryological research model, and was possibly the first in which the teratogenicity of alcohol was demonstrated. Pharmacologically relevant exposure to alcohol in the range of 20–70 mmol/L (20–80 mg/egg) disrupt the growth of chicken embryos, morphogenesis, and behavior, and the resulting phenotypes strongly parallel those of mammalian models. The avian embryo’s direct accessibility has enabled novel insights into the teratogenic mechanisms of alcohol. These include the contribution of IGF1 signaling to growth suppression, the altered flow dynamics that reshape valvuloseptal morphogenesis and mediate its cardiac teratogenicity, and the suppression of Wnt and Shh signals thereby disrupting the migration, expansion, and survival of the neural crest, and underlie its characteristic craniofacial deficits. The genetic diversity within commercial avian strains has enabled the identification of unique loci, such as ribosome biogenesis, that modify vulnerability to alcohol. This venerable research model is equally relevant for the future, as the application of technological advances including CRISPR, optogenetics, and biophotonics to the embryo’s ready accessibility creates a unique model in which investigators can manipulate and monitor the embryo in real-time to investigate the effect of alcohol on cell fate.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-12T07:00:00Z
      DOI: 10.1139/bcb-2017-0205
  • Detrimental effects of alcohol exposure around conception: putative
    • Authors: J.I. Kalisch-Smith, K.M. Moritz
      Pages: 107 - 116
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 107-116, April 2018.
      In western countries, alcohol consumption is widespread in women of reproductive age, and in binge quantities. These countries also continue to have high incidences of unplanned pregnancies, with women often reported to cease drinking after discovering their pregnancy. This suggests the early embryo may be highly exposed to the detrimental effects of alcohol during the periconception period. The periconception and pre-implantation windows, which include maturation of the oocyte, fertilisation, and morphogenesis of the pre-implantation embryo, are particularly sensitive times of development. Within the oviduct and uterus, the embryo is exposed to a unique nutritional environment to facilitate its development and establish de-novo expression of the genome through epigenetic reprogramming. Alcohol has wide-ranging effects on cellular stress, as well as hormonal, and nutrient signalling pathways, which may affect the development and metabolism of the early embryo. In this review, we summarise the adverse developmental outcomes of early exposure to alcohol (prior to implantation in animal models) and discuss the potential mechanisms for these outcomes that may occur within the protected oviductal and uterine environment. One interesting candidate is reduced retinoic acid synthesis, as it is implicated in the control of epigenetic reprogramming and cell lineage commitment, processes that have adverse consequences for the formation of the placenta, and subsequently, fetal programming.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-11-07T08:00:00Z
      DOI: 10.1139/bcb-2017-0133
  • Pre-implantation alcohol exposure and developmental programming of FASD:
           an epigenetic perspective
    • Authors: Lisa-Marie Legault, Virginie Bertrand-Lehouillier, Serge McGraw
      Pages: 117 - 130
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 117-130, April 2018.
      Exposure to alcohol during in-utero development can permanently change the developmental programming of physiological responses, thereby increasing the risk of neurological illnesses during childhood and later adverse health outcomes associated with fetal alcohol spectrum disorder (FASD). There is an increasing body of evidence indicating that exposure to alcohol during gestation triggers lasting epigenetic alterations in offspring, long after the initial insult; together, these studies support the role of epigenetics in FASD etiology. However, we still have little information about how ethanol interferes with the fundamental epigenetic reprogramming wave (e.g., erasure and re-establishment of DNA methylation marks) that characterizes pre-implantation embryo development. This review examines key epigenetic processes that occur during pre-implantation development and especially focus on the current knowledge regarding how prenatal exposure to alcohol during this period could affect the developmental programming of the early stage pre-implantation embryo. We will also outline the current limitations of studies examining the in-vivo and in-vitro effects of alcohol exposure on embryos and underline the next critical steps to be taken if we want to better understand the implicated mechanisms to strengthen the translational potential for epigenetic markers for non-invasive early detection, and the treatment of newborns that have higher risk of developing FASD.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-31T07:00:00Z
      DOI: 10.1139/bcb-2017-0141
  • Competition between ethanol clearance and retinoic acid biosynthesis in
           the induction of fetal alcohol syndrome
    • Authors: Yehuda Shabtai, Abraham Fainsod
      Pages: 148 - 160
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 148-160, April 2018.
      Several models have been proposed to explain the neurodevelopmental syndrome induced by exposure of human embryos to alcohol, which is known as fetal alcohol spectrum disorder (FASD). One of the proposed models suggests a competition for the enzymes required for the biosynthesis of retinoic acid. The outcome of such competition is development under conditions of reduced retinoic acid signaling. Retinoic acid is one of the biologically active metabolites of vitamin A (retinol), and regulates numerous embryonic and differentiation processes. The developmental malformations characteristic of FASD resemble those observed in vitamin A deficiency syndrome as well as from inhibition of retinoic acid biosynthesis or signaling in experimental models. There is extensive biochemical and enzymatic overlap between ethanol clearance and retinoic acid biosynthesis. Several lines of evidence suggest that in the embryo, the competition takes place between acetaldehyde and retinaldehyde for the aldehyde dehydrogenase activity available. In adults, this competition also extends to the alcohol dehydrogenase activity. Ethanol-induced developmental defects can be ameliorated by increasing the levels of retinol, retinaldehyde, or retinaldehyde dehydrogenase. Acetaldehyde inhibits the production of retinoic acid by retinaldehyde dehydrogenase, further supporting the competition model. All of the evidence supports the reduction of retinoic acid signaling as the etiological trigger in the induction of FASD.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-05T07:00:00Z
      DOI: 10.1139/bcb-2017-0132
  • Thiamin deficiency on fetal brain development with and without prenatal
           alcohol exposure
    • Authors: Olena Kloss, N.A. Michael Eskin, Miyoung Suh
      Pages: 169 - 177
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 169-177, April 2018.
      Adequate thiamin levels are crucial for optimal health through maintenance of homeostasis and viability of metabolic enzymes, which require thiamine as a co-factor. Thiamin deficiency occurs during pregnancy when the dietary intake is inadequate or excessive alcohol is consumed. Thiamin deficiency leads to brain dysfunction because thiamin is involved in the synthesis of myelin and neurotransmitters (e.g., acetylcholine, γ-aminobutyric acid, glutamate), and its deficiency increases oxidative stress by decreasing the production of reducing agents. Thiamin deficiency also leads to neural membrane dysfunction, because thiamin is a structural component of mitochondrial and synaptosomal membranes. Similarly, in-utero exposure to alcohol leads to fetal brain dysfunction, resulting in negative effects such as fetal alcohol spectrum disorder (FASD). Thiamin deficiency and prenatal exposure to alcohol could act synergistically to produce negative effects on fetal development; however, this area of research is currently under-studied. This minireview summarizes the evidence for the potential role of thiamin deficiency in fetal brain development, with or without prenatal exposure to alcohol. Such evidence may influence the development of new nutritional strategies for preventing or mitigating the symptoms of FASD.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-09-15T07:00:00Z
      DOI: 10.1139/bcb-2017-0082
  • The role of folic acid and selenium against oxidative damage from ethanol
           in early life programming: a review
    • Authors: Luisa Ojeda, Fátima Nogales, Luisa Murillo, Olimpia Carreras
      Pages: 178 - 188
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 178-188, April 2018.
      There are disorders in children, covered by the umbrella term “fetal alcohol spectrum disorder” (FASD), that occur as result of alcohol consumption during pregnancy and lactation. They appear, at least in part, to be related to the oxidative stress generated by ethanol. Ethanol metabolism generates reactive oxygen species and depletes the antioxidant molecule glutathione (GSH), leading to oxidative stress and lipid and protein damage, which are related to growth retardation and neurotoxicity, thereby increasing the incidence of FASD. Furthermore, prenatal and postnatal exposure to ethanol in dams, as well as increasing oxidation in offspring, causes malnutrition of several micronutrients such as the antioxidant folic acid and selenium (Se), affecting their metabolism and bodily distribution. Although abstinence from alcohol is the only way to prevent FASD, it is possible to reduce its harmful effects with a maternal dietary antioxidant therapy. In this review, folic acid and Se have been chosen to be analyzed as antioxidant intervention systems related to FASD because, like ethanol, they act on the methionine metabolic cycle, being related to the endogenous antioxidants GSH and glutathione peroxidase. Moreover, several birth defects are related to poor folate and Se status.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-17T07:00:00Z
      DOI: 10.1139/bcb-2017-0069
  • Maternal iron nutriture as a critical modulator of fetal alcohol spectrum
           disorder risk in alcohol-exposed pregnancies
    • Authors: Kaylee K. Helfrich, Nipun Saini, Pamela J. Kling, Susan M. Smith
      Pages: 204 - 212
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 204-212, April 2018.
      Alcohol consumption during pregnancy places the fetus at risk for permanent physical, cognitive, and behavioral impairments, collectively termed fetal alcohol spectrum disorder (FASD). However, prenatal alcohol exposure (PAE) outcomes vary widely, and growing evidence suggests that maternal nutrition is a modifying factor. Certain nutrients, such as iron, may modulate FASD outcomes. Untreated gestational iron deficiency (ID) causes persistent neurodevelopmental deficits in the offspring that affect many of the same domains damaged by PAE. Although chronic alcohol consumption enhances iron uptake and elevates liver iron stores in adult alcoholics, alcohol-abusing premenopausal women often have low iron reserves due to menstruation, childbirth, and poor diet. Recent investigations show that low iron reserves during pregnancy are strongly associated with a worsening of several hallmark features in FASD including reduced growth and impaired associative learning. This review discusses recent clinical and animal model findings that maternal ID worsens fetal outcomes in response to PAE. It also discusses underlying mechanisms by which PAE disrupts maternal and fetal iron homeostasis. We suggest that alcohol-exposed ID pregnancies contribute to the severe end of the FASD spectrum.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-10T07:00:00Z
      DOI: 10.1139/bcb-2017-0206
  • Skeletal muscle and fetal alcohol spectrum disorder
    • Authors: Semone B. Myrie, Mark A. Pinder
      Pages: 222 - 229
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 222-229, April 2018.
      Skeletal muscle is critical for mobility and many metabolic functions integral to survival and long-term health. Alcohol can affect skeletal muscle physiology and metabolism, which will have immediate and long-term consequences on health. While skeletal muscle abnormalities, including morphological, biochemical, and functional impairments, are well-documented in adults that excessively consume alcohol, there is a scarcity of information about the skeletal muscle in the offspring prenatally exposed to alcohol (“prenatal alcohol exposure”; PAE). This minireview examines the available studies addressing skeletal muscle abnormalities due to PAE. Growth restriction, fetal alcohol myopathy, and abnormalities in the neuromuscular system, which contribute to deficits in locomotion, are some direct, immediate consequences of PAE on skeletal muscle morphology and function. Long-term health consequences of PAE-related skeletal abnormalities include impaired glucose metabolism in the skeletal muscle, resulting in glucose intolerance and insulin resistance, leading to an increased risk of type 2 diabetes. In general, there is limited information on the morphological, biochemical, and functional features of skeletal abnormalities in PAE offspring. There is a need to understand how PAE affects muscle growth and function at the cellular level during early development to improve the immediate and long-term health of offspring suffering from PAE.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-11-01T07:00:00Z
      DOI: 10.1139/bcb-2017-0118
  • Global prevalence of alcohol use and binge drinking during pregnancy, and
           fetal alcohol spectrum disorder
    • Authors: Svetlana Popova, Shannon Lange, Charlotte Probst, Gerrit Gmel, Jürgen Rehm
      Pages: 237 - 240
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 237-240, April 2018.
      Alcohol use during pregnancy is an established cause of fetal alcohol spectrum disorder (FASD), with heavy drinking during pregnancy being explicitly linked to fetal alcohol syndrome (FAS). This paper presents recent estimates of the prevalence of: (i) any amount of alcohol use during pregnancy; (ii) one or more binge drinking episode(s) (4 or more standard drinks on a single occasion) during pregnancy; (iii) FAS; and (iv) FASD among the general population globally and by World Health Organization region. It is apparent, based on the presented estimates, that alcohol use and binge drinking occur frequently among pregnant women in many countries and as a result, FASD is a prevalent alcohol-related developmental disability. Urgent action is required around the globe to eliminate prenatal alcohol exposure and prevent future children, adolescents, and adults from having FASD.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-08-23T07:00:00Z
      DOI: 10.1139/bcb-2017-0077
  • Understanding and managing sleep disruption in children with fetal alcohol
           spectrum disorder
    • Authors: Ana Hanlon-Dearman, Maida Lynn Chen, Heather Carmichael Olson
      Pages: 267 - 274
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 2, Page 267-274, April 2018.
      Accumulating evidence has revealed high rates of sleep disruption among children with fetal alcohol spectrum disorder (FASD). Multiple animal and clinical studies have found a clear association between sleep problems and prenatal alcohol exposure, and recent research is beginning to characterize the types and extent of sleep disruption in FASD. Nevertheless, sleep disruption in children with FASD often goes unrecognized or is treated without referring to an evidence base. Children’s disrupted sleep interferes with parental sleep and increases caregiver burden, which is of particular importance for families raising children with FASD, a group with very high levels of caregiving stress. The literature supporting an association between sleep problems and deficits in emotional, behavioral, and cognitive function in children is compelling, but needs further investigation in children with FASD. This paper will review the current state of knowledge on sleep in FASD and recommend a rational approach to sleep interventions for affected children and their families.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-04T07:00:00Z
      DOI: 10.1139/bcb-2017-0064
  • Emerging branches of the N-end rule pathways are revealing the sequence
           complexities of N-termini dependent protein degradation
    • Authors: Mohamed A. Eldeeb, Luana C.A. Leitao, Richard P. Fahlman
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      The N-end rule links the identity of the N-terminal amino acid of a protein to its in vivo half-life, as some N-terminal residues confer metabolic instability to a protein via their recognition by the cellular machinery that targets them for degradation. Since its discovery, the N-end rule has generally been defined as set of rules of whether an N-terminal residue is stabilizing or not. However, recent studies are revealing that the N-terminal code of amino acids conferring protein instability is more complex than previously appreciated, as recent investigations are revealing that the identity of adjoining downstream residues can also influence the metabolic stability of N-end rule substrate. This is exemplified by the recent discovery of a new branch of N-end rule pathways that target proteins bearing N-terminal proline. In addition, recent investigations are demonstrating that the molecular machinery in N-termini dependent protein degradation may also target proteins for lysosomal degradation, in addition to proteasome-dependent degradation. Herein, we describe some of the recent advances in N-end rule pathways and discuss some of the implications regarding the emerging additional sequence requirements.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-12-18T08:00:00Z
      DOI: 10.1139/bcb-2017-0274
  • Savitzky–Golay smoothing and differentiation for polymerase chain
           reaction quantification
    • Authors: Charles Gaudreault, Joanny Salvas, Joël Sirois
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      In quantitative PCR (qPCR), replicates can minimize the impact of intra-assay variation; however, inter-assay variations must be minimized to obtain a robust quantification method. The method proposed in this study uses Savitzky–Golay smoothing and differentiation (SGSD) to identify a derivative-maximum-based cycle of quantification. It does not rely on curve modeling, as is the case with many existing techniques. PCR fluorescence data sets challenged for inter-assay variations (different thermocycler units, different reagents batches, different operators, different standard curves, and different labs) were used for the evaluation. The algorithm was compared with a four-parameter logistic model (4PLM) method, the Cy0 method, and the threshold method. The SGSD method compared favourably with all methods in terms of inter-assay variation. SGSD was statistically different from the 4PLM (P = 0.03), Cy0 (P = 0.05), and threshold (P = 0.004) methods on relative error comparison basis. For intra-assay variations, SGSD outperformed the threshold method (P = 0.005) and equalled the 4PLM and Cy0 methods (P > 0.05) on relative error basis. Our results demonstrate that the SGSD method could potentially be an alternative to sigmoid modeling based methods (4PLM and Cy0) when PCR data are challenged for inter-assay variations.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-11-30T08:00:00Z
      DOI: 10.1139/bcb-2016-0194
  • An enhanced chemoenzymatic method for loading substrates onto carrier
           protein domains
    • Authors: Tiia Kittilä, Max J. Cryle
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Non-ribosomal peptide synthetase (NRPS) machineries produce many medically relevant peptides that cannot be easily accessed by chemical synthesis. Thus, understanding NRPS mechanism is of crucial importance to allow efficient redesign of these machineries to produce new compounds. During NRPS-mediated synthesis, substrates are covalently attached to peptidyl carrier proteins (PCPs), and studies of NRPSs are impeded by difficulties in producing PCPs loaded with substrates. Different approaches to load substrates onto PCP domains have been described, but all suffer from difficulties in either the complexity of chemical synthesis or low enzymatic efficiency. Here, we describe an enhanced chemoenzymatic loading method that combines 2 approaches into a single, highly efficient one-pot loading reaction. First, d-pantetheine and ATP are converted into dephospho-coenzyme A via the actions of 2 enzymes from coenzyme A (CoA) biosynthesis. Next, phosphoadenylates are dephosphorylated using alkaline phosphatase to allow linker attachment to PCP domain by Sfp mutant R4-4, which is inhibited by phosphoadenylates. This route does not depend on activity of the commonly problematic dephospho-CoA kinase and, therefore, offers an improved method for substrate loading onto PCP domains.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-11-24T08:00:00Z
      DOI: 10.1139/bcb-2017-0275
  • Postnatal nutritional treatment of neurocognitive deficits in fetal
           alcohol spectrum disorder
    • Authors: A. Bastons-Compta, M. Astals, V. Andreu, E. Navarro, O. Garcia-Algar
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Ethanol is the most important teratogen agent in humans. Prenatal alcohol exposure can lead to a wide range of adverse effects, which are broadly termed as fetal alcohol spectrum disorder (FASD). The most severe consequence of maternal alcohol abuse is the development of fetal alcohol syndrome, defined by growth retardation, facial malformations, and central nervous system impairment expressed as microcephaly and neurodevelopment abnormalities. These alterations generate a broad range of cognitive abnormalities such as learning disabilities and hyperactivity and behavioural problems. Socioeconomic status, ethnicity, differences in genetic susceptibility related to ethanol metabolism, alcohol consumption patterns, obstetric problems, and environmental influences like maternal nutrition, stress, and other co-administered drugs are all factors that may influence FASD manifestations. Recently, much attention has been paid to the role of nutrition as a protective factor against alcohol teratogenicity. There are a great number of papers related to nutritional treatment of nutritional deficits due to several factors associated with maternal consumption of alcohol and with eating and social disorders in FASD children. Although research showed the clinical benefits of nutritional interventions, most of work was in animal models, in a preclinical phase, or in the prenatal period. However, a minimum number of studies refer to postnatal nutrition treatment of neurodevelopmental deficits. Nutritional supplementation in children with FASD has a dual objective: to overcome nutritional deficiencies and to reverse or improve the cognitive deleterious effects of prenatal alcohol exposure. Further research is necessary to confirm positive results, to determine optimal amounts of nutrients needed in supplementation, and to investigate the collective effects of simultaneous multiple-nutrient supplementation.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-11-01T07:00:00Z
      DOI: 10.1139/bcb-2017-0085
  • Inhibiting polo-like kinase 1 enhances radiosensitization via modulating
           DNA repair proteins in non-small-cell lung cancer
    • Authors: Da Yao, Peigui Gu, Youyu Wang, Weibin Luo, Huiliang Chi, Jianjun Ge, Youhui Qian
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      To assure faithful chromosome segregation, cells make use of the spindle assembly checkpoint, which can be activated in aneuploid cancer cells. In this study, the efficacies of inhibiting polo-like kinase 1 (PLK1) on the radiosensitization of non-small-cell lung cancer (NSCLC) cells were studied. Clonogenic survival assay was performed to identify the effects of the PLK1 inhibitor on radiosensitivity within NSCLC cells. Mitotic catastrophe assessment was used to measure the cell death and histone H2AX protein (γH2AX) foci were utilized to assess the DNA double-strand breaks (DSB). The transcriptome was analyzed via unbiased profiling of microarray expression. The results showed that the postradiation mitotic catastrophe induction and the DSB repair were induced by PLK1 inhibitor BI-6727, leading to an increase in the radiosensitivity of NSCLC cells. BI-6727 in combination with radiation significantly induced the delayed tumor growth. PLK1-silenced NSCLC cells showed an altered mRNA and protein expression related to DNA damaging, replication, and repairing, including the DNA-dependent protein kinase (DNAPK) and topoisomerase II alpha (TOPO2A). Furthermore, inhibition of PLK1 blocked 2 important DNA repair pathways. To summarize, our study showed PLK1 kinase as an option in the therapy of NSCLC.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-17T07:00:00Z
      DOI: 10.1139/bcb-2017-0063
  • Role of the TSLP–DC–OX40L pathway in asthma pathogenesis and
           airway inflammation in mice
    • Authors: Shuang Feng, Li Zhang, Xu-Hua Bian, Ying Luo, Guang-Hui Qin, Rui-Ming Shi
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      This study aimed to explore the effect of the TSLP–DC–OX40L pathway in asthma pathogenesis and airway inflammation in mice. For this, 65 male BALF/c mice were distributed among the control, asthma, immunoglobulin G (IgG) + asthma (IgG, 500 μg/500 μL, intratracheal injection of 50 μL each time), LY294002 (OX40L inhibitor) + asthma (intratracheal injection of 2 mg/kg LY294002), and anti-TSLP + asthma (intratracheal injection of 500 μg/500 μL TSLP antibody, 50 μL each time) groups. ELISA was applied to measure the serum levels of immunoglobulin E (IgE), ovalbumin (OVA)-sIgE, interleukin-4 (IL-4), IL-5, IL-13, and interferon-γ (IFN-γ); flow cytometry was employed to detect Treg cells and dendritic cell (DC) and lymphopoiesis. RT–qPCR and Western blot assays were used to measure the levels of TSLP, OX40L, T-bet, GATA-3, NF-κB, p38, and ERK. Treatment with LY294002 and anti-TSLP resulted in increases in the numbers of total cells, eosinophils, neutrophils, and lymphocytes in the bronchoalveolar lavage fluid; total serum levels of IgE, OVA-sIgE, IL-4, IL-5, and IL-13; levels of DC cells; lymphopoiesis; and levels of TSLP, OX40L, GATA-3, NF-κB, p38, and ERK, whereas there were decreases in the levels of IFN-γ and CD4+CD25+Treg cells; CD4+Foxp3+Treg cells; and T-bet. The TSLP–DC–OX40L pathway may contribute to asthma pathogenesis and airway inflammation by modulating the levels of CD4+CD25+Treg cells and inflammatory cytokines.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-12T07:00:00Z
      DOI: 10.1139/bcb-2017-0126
  • The Manitoba Youth Justice Program: empowering and supporting youth with
           FASD in conflict with the law
    • Authors: S. Longstaffe, A.E. Chudley, M.K. Harvie, T. Markesteyn, D. Neault, T. Brown
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Fetal alcohol spectrum disorder (FASD) describes a constellation of physical, cognitive, neurologic, and behavioral impairments resulting from prenatal exposure to alcohol. FASD is recognized as being one of the most common causes of preventable brain injury in children. There had long been concerns that some youth in conflict with the law may be affected with FASD given repetitive patterns of offending and apparent lack of understanding of the consequences of their actions. In 2004, funding was received from Justice Canada for a pilot project with a cross-departmental steering committee working together to determine a best way of working across systems to provide FASD assessments to these youth. It was recognized that provision of timely FASD assessments would allow the court to provide more meaningful sentences taking into account the youth’s strengths and challenges and enhance the changes of decreased recidivism and increased changes of rehabilitation. This paper describes the basic science around FASD and its diagnosis, provides a history of the FASD Youth Justice Program, and reports on legal issues, structure, statistics, accomplishments, and ongoing future challenges.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-04T07:00:00Z
      DOI: 10.1139/bcb-2017-0078
  • miR-96 targets SOX6 and promotes proliferation, migration, and invasion of
           hepatocellular carcinoma
    • Authors: Zhengwei Li, Ying Wang
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Recent research suggested that microRNA 96 (miR-96) might function as an oncogene in several types of cancers. Therefore, the purpose of this study was to probe into the mechanism of miR-96 in hepatocellular carcinoma (HCC) cells. HCC tissues and non-tumorous tissues, HCC cell lines, and healthy cell lines were all involved in this study. Quantitative real-time PCR (qRT-PCR) and Western blot were used to detect miR-96 and SOX6 mRNA and protein expressions. The direct regulation of miR96 on SOX6 was confirmed by luciferase reporter assays. Cell proliferation and growth were determined by MTT (3-(4,5-dimethyl–2-thiazolyl)–2,5-diphenyl–2-H-tetrazolium bromide) assay and colony formation assay. Wound healing and transwell assay were employed for migration and invasion analyses. Finally, SPSS 21.0 and GraphPad 7.0 were applied for statistical analyses. In HCC tissues, miR-96 was highly expressed while SOX6 was lowly expressed. The overexpression of miR-96 reversely inhibited the expression of SOX6, contributing to the promotion of the biological functions of HCC cells. miR-96 could promote cell proliferation, migration, and invasion in HCC by targeting SOX6.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-09-11T07:00:00Z
      DOI: 10.1139/bcb-2017-0183
  • Age-related differences in neuropsychological assessment of fetal alcohol
           spectrum disorder: a cross-sectional study
    • Authors: Nicole M. Taylor, Leah N. Enns
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      This cross-sectional study examined 6 key areas of neuropsychological functioning (cognitive, academic, attention, executive function, adaptive skills) comparing adolescents and school-age children with prenatal alcohol exposure (PAE). The aims were: (i) to examine which neuropsychological measures were predictive of an FASD diagnosis in adolescents and school-age children with PAE, and (ii) to compare the neuropsychological performance of adolescents and children diagnosed with FASD. Hierarchical logistic regressions determined that the Full-Scale IQ, Verbal Comprehension and Perceptual Reasoning indices, basic reading and math skills, adaptive functioning at school, and components of executive functioning (dependent on age) improved the probability of an accurate FASD diagnosis in both groups: 9.1% to 19.2% for adolescents and 10.9% to 19.4% for school-age children (61.5%–80.9% correct classifications overall). For the age comparison analyses (ANOVAs/MANOVAs), a significant difference was observed in the cognitive domain, as well as with basic math skills (trend) in the sample diagnosed with FASD, with lower scores observed for adolescents across these measures. These findings provide further evidence for age differences in neuropsychological assessment as well as increased neuropsychological difficulties in adolescence by comparison with childhood with FASD. Longitudinal studies will be needed to make further inferences about developmental changes in neuropsychological functioning in FASD.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-08-10T07:00:00Z
      DOI: 10.1139/bcb-2017-0081
  • FASD: folic acid and formic acid — an unholy alliance in the alcohol
           abusing mother
    • Authors: Bhushan M. Kapur, Marta Baber
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Alcohol consumption during pregnancy remains a significant cause of preventable birth defects and developmental disabilities; however, the mechanism of toxicity remains unclear. Methanol is present as a congener in many alcoholic beverages and is formed endogenously. Because ethanol is preferentially metabolized over methanol, it has been found in the sera and cerebro-spinal fluid of alcoholics. Toxicity resulting from methanol has been attributed to formic acid. Formic acid is present in significantly higher quantities in the biofluids of alcoholics. These higher levels can be cytotoxic and cause neuronal cell death. However, the adverse effects can be mitigated by adequate levels of hepatic folic acid, because formic acid elimination depends on folic acid. During pregnancy, folate concentrations are at least 2-fold higher in cord blood then in maternal blood, owing to increased folate requirements. The reverse has been demonstrated in pregnancies with alcohol abuse, suggesting downregulation of folate transporters and low fetal folate levels. Moreover, formic acid can cross the placenta and its adverse effects can be mitigated by folic acid. Thus, the combination of low fetal folate levels and presence of formic acid form a potent cytotoxic combination that may play a significant role in the etiology of fetal alcohol spectrum disorder.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-08-09T07:00:00Z
      DOI: 10.1139/bcb-2017-0079
  • Diagnosis of fetal alcohol spectrum disorder: current practices and future
    • Authors: Albert E. Chudley
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      This paper discusses the current state of knowledge and practice for diagnosing fetal alcohol spectrum disorder (FASD). The strengths and challenges of different models of diagnosis are compared. Some models require a team approach for evaluation, while other approaches assume that a clinician in his or her office provides a diagnosis based on a review of the patient’s medical and social history, behaviour, and physical examination. The author reviews the emergence of new information from recent advances in genetics, imaging, and electrophysiology that has the potential to lead to changes in practice and improved reliability of an FASD diagnosis.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-07-26T07:00:00Z
      DOI: 10.1139/bcb-2017-0106
  • Metabolomics and fetal alcohol spectrum disorder
    • Authors: Erin M. Goldberg, Michel Aliani
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Fetal alcohol spectrum disorder (FASD) is a major public health issue that encompass an array of physical, neurological, and behavioral effects due to alcohol consumption during pregnancy. The classical biomarkers of FASD that are currently used lack sensitivity and specificity, and as such there is an opportunity through the use of novel metabolomics analysis to identify new biomarkers to identify those at risk for FASD, which could more effectively aid in early intervention. The focus of this minireview is to identify current work that is being done in the field of metabolomics in FASD in utero, and to highlight promising metabolites that could act as biomarkers in the future. We will conclude with suggestions for further research, as there is a large gap of knowledge in this particular area of metabolomics.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-07-07T07:00:00Z
      DOI: 10.1139/bcb-2017-0080
  • MicroRNA-34a protects myocardial cells against ischemia–reperfusion
           injury through inhibiting autophagy via regulating TNFα expression
    • Authors: Haifeng Shao, Lili Yang, Li Wang, Bozan Tang, Jian Wang, Qiang Li
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Background: ischemia–reperfusion (I/R) is a consequence of restored blood supply after myocardial infarction. Myocardial I/R injury can be alleviated by reducing autophagy in heart tissue. MicroRNA-34a (miR-34a) has been shown to regulate autophagy in a renal model of I/R, but it is not known whether it can protect cardiac tissues from I/R injury. This study investigated how miR-34a protects myocardial cells from I/R injury by inhibiting autophagy via regulation of tumor necrosis factor α (TNFα). Methods: we constructed an I/R model in vivo using Langendorff perfusion, and we constructed an in vivo model by treating neonatal rat cardiomyocytes (NRCMs) with hypoxia–reoxygenation (H/R method). Transfected adenoviral-overexpressed miR-34a mimics and controlled NRCMs after H/R. We analyzed cell viability using the MTT assay and a cell counting kit-8 (CCK-8) assay. Changes in the rate of apoptosis were detected by flow cytometry. We investigated the effect mechanisms of miR-34a with Western blot and luciferase assays. Results: miR-34a expression decreased after in vivo reperfusion of the myocardial cells and heart tissues of neonatal rats. MiR-34a reduced apoptosis of the NRCMs and autophagy levels, simultaneously, after H/R injury. Further, miR-34a decreased the expression of Lc3-II and p62, indicating that miR-34a reduces myocardial I/R injury by decreasing TNFα expression. Conclusion: miR-34a can inhibit autophagy levels after I/R by targeting TNFα, thereby reducing myocardial injury.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-05-25T07:00:00Z
      DOI: 10.1139/bcb-2016-0158
  • Prevalence of externalizing disorders and Autism Spectrum Disorders among
           children with Fetal Alcohol Spectrum Disorder: systematic review and
    • Authors: Shannon Lange, Jürgen Rehm, Evdokia Anagnostou, Svetlana Popova
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Owing to their central nervous system impairments, children with Fetal Alcohol Spectrum Disorder (FASD) commonly exhibit externalizing behaviours such as hyperactivity, impulsivity, and (or) delinquency. The purpose of this study was to estimate the prevalence of neurodevelopmental disorders with prominent externalizing behaviours, namely Attention-Deficit Hyperactivity Disorder (ADHD), Conduct Disorder (CD), Oppositional Defiant Disorder (ODD), as well as Autism Spectrum Disorders (ASD) among children with FASD. A comprehensive systematic literature search was performed, followed by disorder-specific random-effects meta-analyses. Of the disorders investigated, ADHD was found to be the most common co-morbid disorder among children with FASD (52.9%), followed by ODD (12.9%), CD (7.0%), and ASD (2.6%). When compared with the general population of the USA, these rates are notably higher: 15 times higher for ADHD, 2 times higher for ASD, 3 times higher for CD, and 5 times higher for ODD. The results call attention to the need for identifying a distinct neurodevelopmental profile to aid in the accurate identification of children with FASD and the discrimination of FASD from certain idiopathic neurodevelopmental disorders.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-05-18T07:00:00Z
      DOI: 10.1139/bcb-2017-0014
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