Project description:As an adaptive response to the environment, oaks have evolved long taproots that increase their ability to acquire water. Taproots penetrate deeper layers of soil and send out absorptive roots that can then uptake water from these layers. This ability enables taproots to supply trees with water better. Unfortunately, the applied agrotechnical procedures during seedlings production in container nurseries damage the oaks' taproot, leading to changes in the root system structure. That changes may make the seedlings more responsive to chronic or periodic episodes of severe drought. In turn, seedlings that containers do not restrict roots growth, i.e. grown in rhizotron, may elongate because they are not subjected to air-pruning. Despite their significant role, little is known about the internal factors (specific genes) and their interactions that regulate taproot elongation in oaks seedlings. Thus, our study aimed to determine the potential genes regulating growth, cessation and physiology of taproot and check whether there is a difference in the expression level of the genes involved in root development. For this purpose, we performed next-generation sequencing (NGS), taproots and lateral roots, which allowed us to obtain a complete picture of the transcriptomes. Our findings of taproot growth regulations can be used to improve trees production in forest nurseries.
Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage.
Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage.