The Need for Effective Early Behavioral Family Interventions for Children with Attention Deficit Hyperactivity Disorder (ADHD)

There is a pressing need for the development of effective early family intervention programs for children showing Attention Deficit Hyperactivity Disorder (ADHD) behaviours with Conduct Disorder (CD) or Oppositional Defiant Disorder (ODD) behaviours. Previous research has indicated that children with ADHD are at risk of developing comorbid CD or ODD behaviours. In addition, it has been shown that ODD or CD behaviours in childhood tend to persist and to have adverse effects on later social adjustment. However, ODD or CD behaviours are not necessary concomitants of ADHD, and it has been demonstrated that behavioural intervention can have both short- and long term beneficial effects for children showing early signs of ODD or CD behaviours. In short term, behavioural family interventions may be able to reduce oppositional behaviour, particularly in the preschool years. In the long term, early intervention has shown to reduce the incidence of later antisocial behaviour in children at risk for this developmental trajectory. In this paper, it will be argued that behavioural family interventions have not been effectively utilised or promulgated in the community for children with ADHD despite the demonstrated efficacy of these types of interventions. A model of a multilevel system of intervention that can be tailored to the individual family’s needs is presented

Fyn kinase regulates microglial neuroinflammatory responses in cell culture and animal models of parkinson’s disease

Sustained neuroinflammation mediated by resident microglia is recognized as a key pathophysiological contributor to many neurodegenerative diseases, including Parkinson’s disease (PD), but the key molecular signaling events regulating persistent microglial activation have yet to be clearly defined. In the present study, we examined the role of Fyn, a non-receptor tyrosine kinase, in microglial activation and neuroinflammatory mechanisms in cell culture and animal models of PD. The well-characterized inflammogens LPS and TNFɑ rapidly activated Fyn kinase in microglia. Immunocytochemical studies revealed that activated Fyn preferentially localized to the microglial plasma membrane periphery and the nucleus. Furthermore, activated Fyn phosphorylated PKCδ at tyrosine residue 311, contributing to an inflammogen-induced increase in its kinase activity. Notably, the Fyn-PKCδ signaling axis further activated the LPSand TNFɑ-induced MAP kinase phosphorylation and activation of the NFB pathway, implying that Fyn is a major upstream regulator of proinflammatory signaling. Functional studies in microglia isolated from wild-type (Fyn) and Fyn knock-out (Fyn) mice revealed that Fyn is required for proinflammatory responses, including cytokine release as well as iNOS activation. Interestingly, a prolonged inflammatory insult induced Fyn transcript and protein expression, indicating that Fyn is upregulated during chronic inflammatory conditions. Importantly, in vivo studies using MPTP, LPS, or 6-OHDA models revealed a greater attenuation of neuroinflammatory responses in Fyn and PKCδ mice compared with wild-type mice. Collectively, our data demonstrate that Fyn is a major upstream signaling mediator of microglial neuroinflammatory processes in PD

A prospective study to evaluate the incidence of difficult endotracheal intubation in thyroid surgery

BACKGROUND: Thyroid swelling has been considered a risk factor for difficult direct laryngoscopy and intubation. Airway management in thyroid swelling patients poses Unique challenges and one should be thoroughly prepared for any anticipated or unpredicted difficult airway. Airway management in general population has been widely studied. But very few studies have been done on airway management in thyroid swelling patients. Thus it will be useful to find the incidence of difficult endotracheal intubation in thyroid surgeries . OBJECTIVES: A prospective study to evaluate the incidence of difficult endotracheal intubation in thyroid surgery. Selection criteria: Elective adult thyroid surgery patients requiring general endotracheal Anaesthesia. Males and Females.whose, ASA physical status 1-II, Age 18 years of age and older, Who have given valid informed consent. DATA ANALYSIS: It is a prospective study conducted in the department of anaesthesiology, Madras Medical college, Chennai..100 adult patients satisfying inclusion criteria were enrolled in this study. Body mass index, thyromental distance, interincisor distance , Retrognathia , neck mobility, tracheal deviation and compression were evaluated for all thyroid swelling patients who satisfy the inclusion criteria and the incidence of difficult endotracheal intubation was analysed using Intubation Difficulty Scale. Duration of intubation and trauma during intubation were also noted. RESULTS: It is concluded that the incidence of difficult endotracheal intubation in thyroid surgery is less. In this study population, no specific predictive factors were found to be associated with difficult endotracheal intubation in thyroid swelling. CONCLUSION: The incidence of difficult endotracheal intubation in thyroid surgery is less. This correlates with the results of previous studies done on difficult endotracheal intubation in thyroid surgeries

A Study to Assess the Effectiveness of Structured Teaching Programme on Knowledge regarding care of preterm babies among parents at Neonatal Intensive Care Unit, Institute of Obstetrics and Gynaecology and Government Hospital for Women and Children at Egmore, Chennai

Babies born before the gestational age of 37 weeks and weighing less than 2.5 grams are considered premature. Prematurity accounts for the largest number of admissions to NICUs and most common direct cause of newborn mortality. The goals of the preterm care are to promote normal growth and development and minimize morbidity and mortality. The care of preterm is a great challenge to parents. The baby cannot survive alone without a care taker. TITLE: “A study to assess the effectiveness of structured teaching programme on knowledge regarding care of preterm babies among parents at Neonatal Intensive care unit, Institute of Obstetrics and Gynaecology and Government Hospital for Women and Children at Egmore, Chennai -08.” OBJECTIVES: 1. To assess the knowledge on care of preterm babies among parents. 2. To evaluate the effectiveness of structured teaching programme on knowledge regarding care of preterm babies among parents. 3. To find out the association between the post-test knowledge of parents on preterm care with demographic var iables. MATERIALS AND METHODS: This study was conducted with 60 samples (parents of preterm babies) in quantitative approach, Pre experimental one group pretest posttest design, convenient sampling technique. Pre -existing knowledge was assessed by using semi Structured questionnaires. After the pre-test, Structured teaching programme was given regarding care of preterm babies.After7 days post-test was conducted by using same tool. RESULTS: The findings of the study revealed that there is a statistical significance in knowledge on care of preterm babies which shows the effectiveness of structured teaching programme with calculated paired ‘t’ test value of t=23.05, P=0.001 level. CONCLUSION: The knowledge of the parents regarding care of preterm babies improved significantly after they had undergone the structured teaching programme. The structured teaching programme found to be effective in improving the knowledge on care of preterm among the parents of preterm babies

Environmental neurotoxin dieldrin induces apoptosis via caspase-3-dependent proteolytic activation of protein kinase C delta (PKCdelta): Implications for neurodegeneration in Parkinson's disease

BackgroundIn previous work, we investigated dieldrin cytotoxicity and signaling cell death mechanisms in dopaminergic PC12 cells. Dieldrin has been reported to be one of the environmental factors correlated with Parkinson's disease and may selectively destroy dopaminergic neurons.MethodsHere we further investigated dieldrin toxicity in a dopaminergic neuronal cell model of Parkinson's disease, namely N27 cells, using biochemical, immunochemical, and flow cytometric analyses.ResultsIn this study, dieldrin-treated N27 cells underwent a rapid and significant increase in reactive oxygen species followed by cytochrome c release into cytosol. The cytosolic cytochrome c activated caspase-dependent apoptotic pathway and the increased caspase-3 activity was observed following a 3 hr dieldrin exposure in a dose-dependent manner. Furthermore, dieldrin caused the caspase-dependent proteolytic cleavage of protein kinase C delta (PKCδ) into 41 kDa catalytic and 38 kDa regulatory subunits in N27 cells as well as in brain slices. PKCδ plays a critical role in executing the apoptotic process in dieldrin-treated dopaminergic neuronal cells because pretreatment with the PKCδ inhibitor rottlerin, or transfection and over-expression of catalytically inactive PKCδ(K)³⁷⁶(R), significantly attenuates dieldrin-induced DNA fragmentation and chromatin condensation.ConclusionTogether, we conclude that caspase-3-dependent proteolytic activation of PKCδ is a critical event in dieldrin-induced apoptotic cell death in dopaminergic neuronal cells

Protein kinase D1 (PKD1) activation mediates a compensatory protective response during early stages of oxidative stress-induced neuronal degeneration

<p>Abstract</p> <p>Background</p> <p>Oxidative stress is a key pathophysiological mechanism contributing to degenerative processes in many neurodegenerative diseases and therefore, unraveling molecular mechanisms underlying various stages of oxidative neuronal damage is critical to better understanding the diseases and developing new treatment modalities. We previously showed that protein kinase C delta (PKCδ) proteolytic activation during the late stages of oxidative stress is a key proapoptotic signaling mechanism that contributes to oxidative damage in Parkinson's disease (PD) models. The time course studies revealed that PKCδ activation precedes apoptotic cell death and that cells resisted early insults of oxidative damage, suggesting that some intrinsic compensatory response protects neurons from early oxidative insult. Therefore, the purpose of the present study was to characterize protective signaling pathways in dopaminergic neurons during early stages of oxidative stress.</p> <p>Results</p> <p>Herein, we identify that protein kinase D1 (PKD1) functions as a key anti-apoptotic kinase to protect neuronal cells against early stages of oxidative stress. Exposure of dopaminergic neuronal cells to H₂O₂or 6-OHDA induced PKD1 activation loop (PKD1S744/748) phosphorylation long before induction of neuronal cell death. Blockade of PKCδ cleavage, PKCδ knockdown or overexpression of a cleavage-resistant PKCδ mutant effectively attenuated PKD1 activation, indicating that PKCδ proteolytic activation regulates PKD1 phosphorylation. Furthermore, the PKCδ catalytic fragment, but not the regulatory fragment, increased PKD1 activation, confirming PKCδ activity modulates PKD1 activation. We also identified that phosphorylation of S916 at the C-terminal is a preceding event required for PKD1 activation loop phosphorylation. Importantly, negative modulation of PKD1 by the RNAi knockdown or overexpression of PKD1^S916Aphospho-defective mutants augmented oxidative stress-induced apoptosis, while positive modulation of PKD1 by the overexpression of full length PKD1 or constitutively active PKD1 plasmids attenuated oxidative stress-induced apoptosis, suggesting an anti-apoptotic role for PKD1 during oxidative neuronal injury.</p> <p>Conclusion</p> <p>Collectively, our results demonstrate that PKCδ-dependent activation of PKD1 represents a novel intrinsic protective response in counteracting early stage oxidative damage in neuronal cells. Our results suggest that positive modulation of the PKD1-mediated compensatory protective mechanism against oxidative damage in dopaminergic neurons may provide novel neuroprotective strategies for treatment of PD.</p

Synthesis and Characterization of ZnO-MMT Nanocomposite for Antibacterial Activity Studies

ZnO oxide Nanoparticle and ZnO oxide with Montmorillonite nanocomposite were prepared by an environmentally friendly, efficient, and&nbsp; inexpensive method that was synthesized using the chemical method. ZnO nanoparticles as an effective antibacterial material were immobilized on the surface of montmorillonite (MMT). The objectives of this paper are to summarize our research activities in (a) developing processes to dispersenanomaterials (undoped and doped zinc oxide powders) in the polymers matrix, (b) using X-ray diffraction (XRD), Fourier Transform Infra-Red Spectroscopy (FT-IR), Scanning Electron Microscopy (SEM) and Thermo Gravimetric Analysis (TGA) techniques to characterize polymer matrix structures, (c) studying structure-property relationship of these types of new materials, and (d) evaluating the antibacterial performance of these materials for different applications. The results showed that the ZnO nanocomposite was uniformly dispersed in the polymer matrix and the particles remained their average size (20 - 150 nm) before incorporation into the polymer matrix. Keywords: Zinc Oxide nanoparticle, Montmorillonite, FTIR, Antibacterial activit

Mitochondrial stress-induced H4K12 hyperacetylation dysregulates transcription in Parkinson’s disease

Aberrant epigenetic modification has been implicated in the pathogenesis of Parkinson’s disease (PD), which is characterized by the irreversible loss of dopaminergic (DAergic) neurons. However, the mechanistic landscape of histone acetylation (ac) in PD has yet to be fully explored. Herein, we mapped the proteomic acetylation profiling changes at core histones H4 and thus identified H4K12ac as a key epigenomic mark in dopaminergic neuronal cells as well as in MitoPark animal model of PD. Notably, the significantly elevated H4K12ac deposition in post-mortem PD brains highlights its clinical relevance to human PD. Increased histone acetyltransferase (HAT) activity and decreased histone deacetylase 2 (HDAC2) and HDAC4 were found in experimental PD cell models, suggesting the HAT/HDAC imbalance associated with mitochondrial stress. Following our delineation of the proteasome dysfunction that possibly contributes to H4K12ac deposition, we characterized the altered transcriptional profile and disease-associated pathways in the MitoPark mouse model of PD. Our study uncovers the axis of mitochondrial impairment-H4K12ac deposition-altered transcription/disease pathways as a neuroepigenetic mechanism underlying PD pathogenesis. These findings provide mechanistic information for the development of potential pharmacoepigenomic translational strategies for PD

Synthesis and Characterization of ZnO-MMT Nanocomposite for Antibacterial Activity Studies

ZnO oxide Nanoparticle and ZnO oxide with Montmorillonite nanocomposite were prepared by an environmentally friendly, efficient, and inexpensive method that was synthesized using the chemical method. ZnO nanoparticles as an effective antibacterial material were immobilized on the surface of montmorillonite (MMT). The objectives of this paper are to summarize our research activities in (a) developing processes to disperse nanomaterials (undoped and doped zinc oxide powders) in the polymers matrix, (b) using X-ray diffraction (XRD), Fourier Transform Infra-Red Spectroscopy (FT-IR), Scanning Electron Microscopy (SEM) and Thermo Gravimetric Analysis (TGA) techniques to characterize polymer matrix structures, (c) studying structure-property relationship of these types of new materials, and (d) evaluating the antibacterial performance of these materials for different applications. The results showed that the ZnO nanocomposite was uniformly dispersed in the polymer matrix and the particles remained their average size (20 - 150 nm) before incorporation into the polymer matrix