Comparison of normalisation methods for surface-enhanced laser desorption and ionisation (SELDI) time-of-flight (TOF) mass spectrometry data

Background  

Mass spectrometry for biological data analysis is an active field of research, providing an efficient way of high-throughput proteome screening. A popular variant of mass spectrometry is SELDI, which is often used to measure sample populations with the goal of developing (clinical) classifiers. Unfortunately, not only is the data resulting from such measurements quite noisy, variance between replicate measurements of the same sample can be high as well. Normalisation of spectra can greatly reduce the effect of this technical variance and further improve the quality and interpretability of the data. However, it is unclear which normalisation method yields the most informative result.     

Maternal prenatal depressive symptoms predict infant NR3C1 1F and BDNF IV DNA methylation

Prenatal maternal psychological distress increases risk for adverse infant outcomes. However, the biological mechanisms underlying this association remain unclear. Prenatal stress can impact fetal epigenetic regulation that could underlie changes in infant stress responses. It has been suggested that maternal glucocorticoids may mediate this epigenetic effect. We examined this hypothesis by determining the impact of maternal cortisol and depressive symptoms during pregnancy on infant NR3C1 and BDNF DNA methylation. Fifty-seven pregnant women were recruited during the second or third trimester. Participants self-reported depressive symptoms and salivary cortisol samples were collected diurnally and in response to a stressor. Buccal swabs for DNA extraction and DNA methylation analysis were collected from each infant at 2 months of age, and mothers were assessed for postnatal depressive symptoms. Prenatal depressive symptoms significantly predicted increased NR3C1 1F DNA methylation in male infants (β = 2.147, P = 0.044). Prenatal depressive symptoms also significantly predicted decreased BDNF IV DNA methylation in both male and female infants (β = −3.244, P = 0.013). No measure of maternal cortisol during pregnancy predicted infant NR3C1 1F or BDNF promoter IV DNA methylation. Our findings highlight the susceptibility of males to changes in NR3C1 DNA methylation and present novel evidence for altered BDNF IV DNA methylation in response to maternal depression during pregnancy. The lack of association between maternal cortisol and infant DNA methylation suggests that effects of maternal depression may not be mediated directly by glucocorticoids. Future studies should consider other potential mediating mechanisms in the link between maternal mood and infant outcomes.     

The relation between mitogen activated protein kinase (MAPK) pathway and different genes expression in patients with beta Thalassemia

Backgroundβ-thalassemia is an inherited hemoglobinopathy resulting in quantitative changes in the β-globin chain. Understanding the molecular basis of that disorder requires studying the expression of genes controlling the pathways that affect the erythropoietic homeostasis especially the MAPK pathway. The MAPKs are a family of serine/threonine kinases that play an essential role in connecting cell-surface receptors to DNA in the nucleus of the cell.Aimto study the effect of expression of GNAI2, DUSP5 and ARRB1 genes on MAPK signaling pathway in pediatric patients with beta thalassemia.MethodsForty children with beta thalassemia major (TM), forty children with beta thalassemia intermedia (TI) and forty age and gender matched healthy controls were enrolled in this study. Detection of GNAI2, DUSP5 and ARRB1 mRNA expression was done by real time polymerase chain reaction (RT-PCR).Resultsrevealed increased expression of ARRB1 (Arrestin Beta 1) gene, and decreased expression of both GNAI2 (Guanine nucleotide-binding protein G (i) subunit alpha-2) and DUSP5 (Dual specificity protein phosphatase 5) genes in both patient groups than control groups respectively.ConclusionsChange in the rate of expression of ARRB1, GNAI2 and DUSP5 may have a role in the pathogenesis of abnormal hematopoiesis in cases of β thalassemia through affecting the MAPK pathway.