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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]
  • Note of appreciation / Note de reconnaissance
    • Abstract: Biochemistry and Cell Biology, e-First Articles.

      Citation: Biochemistry and Cell Biology
      PubDate: 2018-02-01T01:26:25Z
      DOI: 10.1139/bcb-2018-0003
  • 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
  • Developmental neurotoxic effects of a low dose of TCE on a 3-D neurosphere
    • Authors: M.E. Abdraboh, S.H. Abdeen, M. Salama, M. El-Husseiny, Y.M. El-Sherbini, N.M. Eldeen
      Pages: 50 - 56
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 1, Page 50-56, February 2018.
      Trichloroethylene (TCE) is one of the industrial toxic byproducts that now persist in the air, soil, and water. Several studies have already illustrated the toxic effect of high doses of TCE on the biological functions of several organs. This study aims to highlight the toxic impact of a low dose of TCE (1 μmol/L) on the development of rat neural stem cells (NSCs). The subventricular zones (SVZ) of rat pup’s brains were collected and minced, and the harvested cells were cultured in the presence of neural growth factors B27/N2 to develop neurospheres. The cells were then exposed to a dose of 1 μmol/L TCE for 1 or 2 weeks. The outcomes indicated a remarkable inhibitory effect of TCE on the differentiation capacity of NSCs, which was confirmed by down-regulation of the astrocyte marker GFAP The inhibitory effect of TCE on the proliferation of NSCs was identified by the reductions in neurosphere diameter, Ki67 expression, and cell cycle arrest at the G1/S phase. Immunolabelling with annexin V indicated the proapoptotic effect of TCE exposure. PCR results revealed a TCE-mediated suppression of the expression of the antioxidant enzyme SOD1. This paper illustrates, for the first time, a detailed examination of the toxic effects of an environmentally low dose of TCE on NCSs at the transcriptional, translational, and functional levels.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-17T07:00:00Z
      DOI: 10.1139/bcb-2017-0089
  • Mechanistic effect of human umbilical cord blood derived mesenchymal stem
           cells on the submandibular salivary gland in ovariectomized rats
    • Authors: Zienab A. Gouda, Mohamed E. Ali Khalifa, Sally M. Shalaby, Samia Hussein
      Pages: 57 - 67
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 1, Page 57-67, February 2018.
      We performed this study to understand the effect of human umbilical cord blood derived mesenchymal stem cells (hUCB-MSCs) on the submandibular gland after bilateral ovariectomy. For this, 21 adult female rats were distributed equally among 3 groups: the sham-operated group (SHAM); the ovariectomized group (OVX); and the OVX group that received repeated intravenous injections of the hUCB-MSCs (OVX + hUCB-MSCs). We used reverse transcription – PCR to analyze for the gene expression of AQPs 3, 4, 5, and BMP-6. The cellular localization and expression of human CD105, human CD34, proliferating nuclear antigen (PCNA), single-stranded DNA (ss-DNA), caspase 3, AQP1, and α smooth muscle actin (α-SMA) were determined immunohistochemically. In the OVX group, a significant decrease in the gene expression of AQP3, AQP4, and BMP6, as well as the acinar area % was detected, while area % of granular convoluted tubules (GCTs) showed a significant increase. A significant decrease in area % staining positively for AQP1 and α-SMA was noted. An obvious improvement in the structure of the submandibular gland was demonstrated in the group injected with hUCB-MSCs, as well as a significant increase in the gene expression of AQP3, AQP4, and BMP6. The acinar and GCT area %, as well as the different measured markers, were relatively normal. This demonstrates that E2-deficiency induces structural changes to the submandibular gland. Moreover, a definite amelioration of the structure and function of the submandibular gland was detected after the administration of hUCB-MSCs.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-16T07:00:00Z
      DOI: 10.1139/bcb-2017-0196
  • Characterization of a thermostable endoglucanase from Cellulomonas fimi
    • Authors: Hirak Saxena, Bryan Hsu, Marc de Asis, Mirko Zierke, Lyann Sim, Stephen G. Withers, Warren Wakarchuk
      Pages: 68 - 76
      Abstract: Biochemistry and Cell Biology, Volume 96, Issue 1, Page 68-76, February 2018.
      Bacteria in the genus Cellulomonas are well known as secretors of a variety of mesophilic carbohydrate degrading enzymes (e.g., cellulases and hemicellulases), active against plant cell wall polysaccharides. Recent proteomic analysis of the mesophilic bacterium Cellulomonas fimi ATCC484 revealed uncharacterized enzymes for the hydrolysis of plant cell wall biomass. Celf_1230 (CfCel6C), a secreted protein of Cellulomonas fimi ATCC484, is a novel member of the GH6 family of cellulases that could be successfully expressed in Escherichia coli. This enzyme displayed very little enzymatic/hydrolytic activity at 30 °C, but showed an optimal activity around 65 °C, and exhibited a thermal denaturation temperature of 74 °C. In addition, it also strongly bound to filter paper despite having no recognizable carbohydrate binding module. Our experiments show that CfCel6C is a thermostable endoglucanase with activity on a variety of β-glucans produced by an organism that struggles to grow above 30 °C.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-05T07:00:00Z
      DOI: 10.1139/bcb-2017-0150
  • 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
  • MMS19 localizes to mitochondria and protects the mitochondrial genome from
           oxidative damage
    • Authors: Rui Wu, Qunsong Tan, Kaifeng Niu, Yuqi Zhu, Di Wei, Yongliang Zhao, Hongbo Fang
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      MMS19 localizes to the cytoplasmic and nuclear compartments involved in transcription and nucleotide excision repair (NER). However, whether MMS19 localizes to mitochondria, where it plays a role in maintaining mitochondrial genome stability, remains unknown. In this study, we provide the first evidence that MMS19 is localized in the inner membrane of mitochondria and participates in mtDNA oxidative damage repair. MMS19 knockdown led to mitochondrial dysfunctions including decreased mtDNA copy number, diminished mtDNA repair capacity, and elevated levels of mtDNA common deletion after oxidative stress. Immunoprecipitation – mass spectrometry analysis identified that MMS19 interacts with ANT2, a protein associated with mitochondrial ATP metabolism. ANT2 knockdown also resulted in a decreased mtDNA repair capacity after oxidative damage. Our findings suggest that MMS19 plays an essential role in maintaining mitochondrial genome stability.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-16T07:00:00Z
      DOI: 10.1139/bcb-2017-0149
  • Liver X receptor α is targeted by microRNA-1 to inhibit cardiomyocyte
           apoptosis through a ROS-mediated mitochondrial pathway
    • Authors: Yongxia Cheng, Dawei Zhang, Min Zhu, Ying Wang, Sufen Guo, Biao Xu, Guangyu Hou, Yukuan Feng, Guibo Liu
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Diabetic cardiomyopathy (DCM) is defined as ventricular dysfunction occurring independently of a recognized cause such as hypertension or coronary artery disease. Liver X receptor α (LXRα), a subtype of ligand-activated transcription factors LXRs, has been considered as a potential pharmacological target in the pathogenesis of cardiovascular and metabolic diseases. However, the potential mechanism of how LXRα is regulated in cardiomyocytes is still unclear. This study investigated the effect of activating LXRα with GW3965 on cardiomyocyte apoptosis and its upstream regulator in glucose-induced H9C2 cells. Our data indicated that GW3965 up-regulated the expression of LXRα, inhibited cardiomyocyte apoptosis, and altered the apoptosis-related proteins in glucose-induced H9C2 cells. In addition, GW3965 restored the mitochondrial membrane potential level and decreased the ROS production induced by glucose. Moreover, LXRα was confirmed as a direct target of microRNA-1 (miR-1) that was involved in cardiomyocyte apoptosis of DCM, and overexpression of miR-1 abrogated the inhibiting effect of GW3965 on glucose-induced apoptosis in H9C2 cells. This study highlights an important role of LXRα in the development of DCM and brings new insights into the complex mechanisms involved in the pathogenesis of DCM.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-12T07:00:00Z
      DOI: 10.1139/bcb-2017-0154
  • 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
  • Cardiac actin changes in the actomyosin interface have different effects
           on myosin duty ratio
    • Authors: Haidun Liu, Mary Henein, Maria Anillo, John F. Dawson
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Hypertrophic cardiomyopathy (HCM) is an inherited cardiovascular disease (CD) that commonly causes an increased size of cardiomyocytes in the left ventricle. The proteins myosin and actin interact in the myocardium to produce contraction through the actomyosin ATPase cycle. The duty ratio (r) of myosin is the proportion of the actomyosin ATPase cycle that myosin is bound to actin and does work. A common hypothesis is that HCM mutations increase contraction in cardiac sarcomeres; however, the available data are not clear on this connection. Based on previous work with human α-cardiac actin (ACTC), we hypothesize that HCM-linked ACTC variants with alterations near the myosin binding site have an increased r, producing more force. Myosin duty ratios using human ACTC variant proteins were calculated with myosin ATPase activity and in-vitro motility data. We found no consistent changes in the duty ratio of the ACTC variants, suggesting that other factors are involved in the development of HCM when ACTC variants are present.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-10-03T07:00:00Z
      DOI: 10.1139/bcb-2017-0136
  • LncRNA SNHG1 enhances cell proliferation, migration, and invasion in
           cervical cancer
    • Authors: Yang Liu, Yanling Yang, Lei Li, Yuan Liu, Peng Geng, Guilin Li, Hongjuan Song
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Objective: This study investigated the effects of lncRNA SNHG1 on the proliferation, migration, and invasiveness of cervical cancer cells. Methods: Three pairs of cervical cancer tissue samples and their corresponding adjacent samples were analyzed using Human LncRNA Microarray V3.0 chip for differential analysis. The expression of SNHG1 in cervical cancer cell lines was verified by qRT–PCR. CCK8 assays and colony formation assays were used to study the changes in cell proliferation. Cell migration and Transwell assays were used to study changes in cell migration and invasiveness. Results: SNHG1 was highly expressed in cervical cancer tissues and cervical cancer cell lines. SNHG1 siRNA could knock-down the expression level of SNHG1 in cervical cancer cell lines HeLa and C33-A. After knock-down of SNHG1, cell proliferation and migration as well as invasiveness in HeLa and C-33A cells decreased. Conclusion: LncRNA SNHG1 promotes the development of cervical cancer cells.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-09-20T07:00:00Z
      DOI: 10.1139/bcb-2017-0188
  • Efficacy of hyperthermia in human colon adenocarcinoma cells is improved
           by auraptene
    • Authors: Mahdi Moussavi, Farhang Haddad, Maryam M. Matin, Mehrdad Iranshahi, Fatemeh B. Rassouli
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Colon adenocarcinoma is one of the most common cancers worldwide, and resistance to current therapeutic modalities is a serious drawback in its treatment. Auraptene is a natural coumarin with considerable anticancer effects. The goal of this study was to introduce a novel combinatorial approach for treatment against colon adenocarcinoma cells. To do so, HT29 cells were pretreated with nontoxic auraptene and then hyperthermia was induced. Afterwards, the viability of the cells was assessed, changes induced in the cell cycle were analyzed, and the expression patterns of candidate genes were studied. Results from the MTT assay demonstrated significant (p < 0.01) decreases in cell viability when 20 μg/mL auraptene was used for 72 h, heat shock was induced, and cells were allowed to recover for 24 h. Flow cytometry analysis also indicated considerable changes in the distribution of cells between the sub-G1/G1 and G2/M phases of cell cycle after the combinatorial treatment. Real-time RT–PCR studies revealed significant (p < 0.01) up-regulation of P21 in the cells pretreated with auraptene after heat shock, whereas no significant change was observed in HSP27 expression. Our findings not only indicate, for the first time, that the efficacy of hyperthermia was improved by auraptene pretreatment, but also suggest that this coumarin could be used in the future to achieve more effective therapeutic outcomes.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-09-15T07:00:00Z
      DOI: 10.1139/bcb-2017-0146
  • Portal vein ligation alters coding and noncoding gene expression in rat
    • Authors: Bin Li, Yan Zhu, Lei Xie, Shuyang Hu, Shupeng Liu, Xiaoqing Jiang
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Portal vein occlusion increases the resectability of initially unresectable liver cancer by inducing hypertrophy in non-occluded liver lobes. However, the mechanisms of how portal vein occlusion induces hepatic hypertrophy remain unclear. A cDNA microarray was used to identify the gene expression signatures of ligated (LLLs) and nonligated liver lobes (NLLLs) at different time points after portal vein ligation (PVL). The results of a bioinformatics analysis revealed that LLLs and NLLLs displayed different gene expression profiles. Moreover, the expression levels of both coding and noncoding RNA were different between LLLs and NLLLs at different time points after PVL. A series test of cluster analysis revealed that the No. 22 and No. 5 expression patterns, which showed altered expression at 24 h and maintained this altered expression over the following 14 days, had the lowest P values and the highest number of differentially expressed genes in both the LLLs and NLLLs. The results of a GO analysis showed the activation of hypoxia pathways in LLLs and the activation of cell proliferation and cell-cycle pathways in NLLLs, suggesting the involvement of these pathways in PVL-induced hepatic hypertrophy and regeneration. These results provide insight into the molecular mechanisms underlying hepatic hypertrophy and regeneration induced by portal vein occlusion, and they identify potential targeting pathways that can promote the clinical application of PVL in liver cancer therapy.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-08-24T07:00:00Z
      DOI: 10.1139/bcb-2017-0070
  • 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
  • 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
  • MiR-129-5p suppresses gastric cancer cell invasion and proliferation by
           inhibiting COL1A1
    • Authors: Quan Wang, Jinhai Yu
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Gastric cancer (GC) is one of the most lethal cancers worldwide. In this study, we aimed to explore the role of miR-129-5p, a newly identified miR-129 member, in GC cells as well as the potential mechanism of action. The results of reverse transcription – qualitative polymerase chain reaction (RT–qPCR) and Western Blot showed that miR-129 was downregulated in GC cells compared with normal ones. Using MTT, colony formation, wound healing assay, and a Transwell assay, we evaluated the proliferation, migration, and invasion abilities of transfected cells, and confirmed miR-129-5p as a tumor suppressor in GC. After a microarray analysis comparing different gene expressions in miR-129-5p transfected SGC-7901 cells, COL1A1 was selected for biggest fold-change and potential target of miR-129-5p predicted by TargetScan. Measured by RT–qPCR and Western blot, COL1A1 turned out to be upregulated in GC tissues and cells. We further confirmed the targeting relationship between miR-129-5p and COL1A1 by dual luciferase assay. By manipulating the expression of COL1A1 in SGC-7901 cells, cell proliferation, migration, and invasion were examined and the tumor-promoting function of COL1A1 was validated. Moreover, co-transfection of miR-129-5p mimics and COL1A1 attenuated the tumor-promoting effects induced by a single-transfection of COL1A1, and miR-129-5p inhibitor counteracted the tumor-suppressing effects of COL1A1 siRNA. Collectively, the data demonstrate the important functions of the miR-129-5p–COL1A1 axis in GC: miR-129-5p suppresses GC cell proliferation, migration, and invasion, by selectively inhibiting COL1A1. This study provides new therapeutic targets for the clinical treatment of GC.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-05-08T07:00:00Z
      DOI: 10.1139/bcb-2016-0254
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