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Dr Smita Nambiar-Mann
No full text<p>Dr Smita Nambiar-Mann is an Accredited Practising Dietitian with over 15 years of experience in clinical dietetics (private practice), research (industry and academia) and teaching.</p>
<p>Smita is passionate about paediatric nutrition, particularly in relation to the prevention of childhood obesity. Her career in dietetics began as a research dietitian for the Healthy Kids Queensland: Physical Activity and Nutrition Survey where she lead one of 5 teams to collect anthropometry, nutrition and physical activity information from children aged 5-17 years across the state. She was also the lead dietitian who trained research assistants on dietary data collection, and oversaw the entry and coding of over 2500 dietary records. Following this, she received the University of Queensland Joint Research Scholarship to complete a PhD. She used data from this survey to validate the waist-height ratio as a measure of abdominal adiposity in children and developed cut-offs to classify high abdominal adiposity. She used these new cut-offs to explore associations between the waist-height ratio and breastfeeding, consumption of non-core foods, parental perception of body weight and risk of metabolic syndrome. Throughout the PhD candidature, Smita kept up her clinical skills by managing her own private practice. She also worked as a research dietitian on another study called NOURISH. This RCT provided first-time mothers with anticipatory guidance on responsive feeding practices. Children were followed from birth to 5- years old and data on anthropometry, food intake, child eating behaviour and parental feeding practices were collected. Following completion of her PhD, Smita took on a postdoc position at QUT and coordinated the last two years of NOURISH and was involved in conducting two pilot studies - Eating in the Absence of Hunger and Nourish for Formula Feeders.</p>
<p>Most recently, Smita had the opportunity to take on an industry position in Singapore. In her role as a nutrition scientist, Smita advised on the dietary assessment component of clinical trials in Singapore and across Asia. She also developed simple dietary assessment tools for the company, to use in young children. One of these tools was a semi-quantitative food frequency questionnaire which was the first of its kind for Singapore. After 4 years abroad, Smita returned to Brisbane and commenced at QUT as a full-time academic. Smita predominantly teaches first-year units, and supervises Honours, Masters and PhD students. She was recently recognised as Fellow of the Higher Education Academy.</p>
<p>At QUT, Smita plans to continue research in paediatric nutrition where her skills in nutrition assessment, dietary methodology, child eating behaviours and parental feeding practices can be utilised.</p>
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Get PDFDr. Smita Modi talks about her staff and the fee structure.Asian StudiesHindi Urdu FlagshipSouth Asia Institut
Brain-Derived Neurotrophic Factor (BDNF) Produced by Human Umbilical Tissue-derived Cells (hUTC) Is Required for its Effect on Hippocampal Dendritic Differentiation
No full textThe potential for non-embryonic cells to promote differentiation of neuronal cells has therapeutic implications for regeneration of neurons damaged by stroke or injury and avoids many ethical and safety concerns. We assessed the capacity of human umbilical tissue-derived cells (hUTC) and human mesenchymal stromal cells (hMSC) to enhance differentiation of rodent hippocampal neurons. Coculture of hippocampal cells with hUTC or hMSC in transwell inserts for 3 days resulted in increase of several dendritic parameters including the number and length of primary dendrites. The effect of hUTC or hMSC on dendritic maturation was only apparent on neurons grown for two weeks in vitro prior to co-culture. Changes in dendritic morphology in the presence of hUTC were also accompanied by increased expression of the presynaptic marker synaptotagmin and the postsynaptic marker postsynaptic density protein 95kD (PSD95) suggesting that there may also be an increase in the number of synapses formed in the presence of hUTC. The effect of hUTC and hMSC on hippocampal cells in co-culture was comparable to those induced by treatment with recombinant human BDNF (rhBDNF) implying that a similar factor may be released from hUTC or hMSC. Analysis of hUTC conditioned medium by ELISA demonstrated that BDNF was indeed secreted. An antibody that blocks the actions of BDNF partially inhibited the actions of hUTC on dendritic morphology suggesting that BDNF is at least one of the factors secreted from the cells to promote dendritic maturation. These results indicate that hUTC secrete biologically active BDNF which can affect dendritic morphology.Peer reviewe
Early presynaptic and late postsynaptic components contribute independently to Brain-Derived Neurotrophic Factor-induced synaptic plasticity
No full textTrophin-induced synaptic plasticity consists of both presynaptic and postsynaptic processes. The potential interdependence of these mechanisms and their temporal relationships are undefined. The synaptic vesicle protein Rab3A is required for the early, initial 10 min phase, but not for the later phase of BDNF-enhanced transmission. We now examine the temporal distinction and mechanistic relationships between these phases of BDNF action. Rab3A mutant cells did not exhibit increased mEPSC frequency in response to BDNF in cell culture, indicating absence of the presynaptic component. In contrast, BDNF enhanced post-synaptic glutamate-induced current in the mutant neurons as in the wildtype, indicating that the postsynaptic component of the response was intact. Finally, the postsynaptic NMDA receptor subunit NR2B was phosphorylated at Tyr1472 by BDNF in Rab3A knockouts, as previously shown in wildtype. Our results are the first to demonstrate that presynaptic and postsynaptic components of BDNF-enhanced synaptic activity are independent and temporally distinct.Peer reviewe
Ceremony - Smita Sarkar, Timothy Schaefer, Richard Schaller
No full textGraduates Smita Sarkar, Timothy Schaefer, and Richard Schaller receive their hoods.https://scholarship.kentlaw.iit.edu/commencement_2013/1152/thumbnail.jp
Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice
No full textTraumatic brain injury (TBI) research has attained renewed momentum due to the increasing awareness of head injuries, which result in morbidity and mortality. Based on the nature of primary injury following TBI, complex and heterogeneous secondary consequences result, which are followed by regenerative processes 1,2. Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement 3,4. The resulting hematomas and lacerations cause a vascular response 3,5, and the morphological and functional damage of the white matter leads to diffuse axonal injury 6- 8. Additional secondary changes commonly seen in the brain are edema and increased intracranial pressure 9. Following TBI there are microscopic alterations in biochemical and physiological pathways involving the release of excitotoxic neurotransmitters, immune mediators and oxygen radicals 10-12, which ultimately result in long-term neurological disabilities 13,14. Thus choosing appropriate animal models of TBI that present similar cellular and molecular events in human and rodent TBI is critical for studying the mechanisms underlying injury and repair. Various experimental models of TBI have been developed to reproduce aspects of TBI observed in humans, among them three specific models are widely adapted for rodents: fluid percussion, cortical impact and weight drop/impact acceleration 1. The fluid percussion device produces an injury through a craniectomy by applying a brief fluid pressure pulse on to the intact dura. The pulse is created by a pendulum striking the piston of a reservoir of fluid. The percussion produces brief displacement and deformation of neural tissue 1,15. Conversely, cortical impact injury delivers mechanical energy to the intact dura via a rigid impactor under pneumatic pressure 16,17. The weight drop/impact model is characterized by the fall of a rod with a specific mass on the closed skull 18. Among the TBI models, LFP is the most established and commonly used model to evaluate mixed focal and diffuse brain injury 19. It is reproducible and is standardized to allow for the manipulation of injury parameters. LFP recapitulates injuries observed in humans, thus rendering it clinically relevant, and allows for exploration of novel therapeutics for clinical translation 20. We describe the detailed protocol to perform LFP procedure in mice. The injury inflicted is mild to moderate, with brain regions such as cortex, hippocampus and corpus callosum being most vulnerable. Hippocampal and motor learning tasks are explored following LFP.Peer reviewe
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[Guest with Smita Mehta]
No full textPhotograph of Smita Mehta (right) and an unidentified guest standing together in front of a UNT backdrop during the 2017 UNT College of Education's STAR Celebration. Mehta is a professor with the College of Education. The event is held annually to celebrate and recognize the recipients of scholarships in the College of Education
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[Smita Mehta with guest]
No full textPhotograph of Smita Mehta (left) and an unidentified guest standing together in front of a UNT backdrop during the 2017 UNT College of Education's STAR Celebration. Mehta is a professor with the College of Education. The event is held annually to celebrate and recognize the recipients of scholarships in the College of Education
Transcriptional profiling of brain-derived-neurotrophic factor-induced neuronal plasticity: a novel role for nociceptins in hippocampal neurite outgrowth
No full textBDNF exhibits a sequence of actions on neurons ranging from acute enhancement of transmission to long-term promotion of neurite outgrowth and synaptogenesis associated with learning and memory. The manifold effects of BDNF on neuronal modifications may be mediated by genomic alterations. We previously found that BDNF treatment acutely increases transcription of the synaptic vesicle protein, Rab3A, required for trophin-induced synaptic plasticity, as well as the peptide, VGF, which increases during learning (Thakker-Varia et al., 2001; Alder et al., 2003). To elucidate comprehensive transcriptional programs associated with short and long-term BDNF exposure, we now examine mRNA abundance and complexity using Affymetrix GeneChips in cultured hippocampal neurons. Consistent with the modulation of synaptic plasticity, BDNF treatment (3-6 hr) induced mRNAs encoding the synapse-associated proteins synaptojanin 2, neuronal pentraxin 1, septin 9 and ryanodine receptor 2. BDNF also induced expression of mRNAs encoding neuropeptides (6-12 hr), including prepronociceptin, neuropeptide Y and secretogranin. To determine whether these neuropeptides induced by BDNF mediate neuronal development, we examined their effects on hippocampal neurons. The four mature peptides derived from post-translational processing of the ppNociceptin propeptide induced the expression of several immediate early genes in hippocampal cultures, indicating neuronal activation. To examine the significance of activation, the effects of nociceptin (orphanin FQ) and nocistatin on neurite outgrowth were examined. Quantitative morphometric analysis revealed that nociceptin significantly increased both average neurite length and average number of neurites per neuron, while nocistatin had no effect on these parameters. These results reveal a novel role for nociceptin and suggest that these neuropeptide systems may contribute to the regulation of neuronal function by BDNF.Peer reviewe
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