then spread to the entire body including limbs. It was itchy. The family are originally from Quebec and had been residing in Ireland for the past 2 years in relation to the father's occupation. Contact with infectious disease and recent travel were denied. He had never been hospitalised and had no medical diagnoses .His mother was adamant that all vaccinations were up to date and included the Varicella vaccine at one year of age in Canada. He had no known allergies and was not taking any medications.On examination he had multiple vesicular and pustular lesions with an erythematous base. Some lesion had necrotic centres. There were some vesicles on his lower lip, buccal mucosa and also on the throat.His WCC was 2.08, Neutrophils 0.73, Lymphocytes 0.73, CRP 20. Influenza, RSV and Monospot were negative.He was initially treated with IV Augmentin and Flucloxacillin for a presumed diagnosis of Impetigo. More lesions appeared over his trunk and abdomen over the subsequent 24 hours although he was not systemically unwell. The Dermatologist made a clinical diagnosis of 'Chicken Pox'. He was discharged home on an immunocompetent dose of oral acyclovir pending results of skin swab, throat swabs and Varicella titre.At follow up one week later he was clinically well with multiple healing lesions. His Varicella titres were high confirming a diagnosis of Varicella Zoster infection. His mother brought with her his vaccination records from Canada which showed that he had received only one dose of the Varicella vaccine and had missed the booster. This is in contrast to his siblings who were fully vaccinated and did not develop Varicella despite close contact. Conclusion Common conditions are common. Vaccines can fail. Parents should be encouraged to keep detailed records of all vaccinations including boosters and to follow through with booster vaccines when indicated.
Objectives To characterise the novel growth-promoting or suppressive actions of selected Oxovanadium-Response genes, here coded as BRG1-5, and putative suppressor gene PTPRH, through gain/loss-of-function assays and enzyme inhibitory assays in Neuroblastoma cells. Methods SiRNA and plasmid of the genes were transfected into Neuroblastoma cells; Cell morphology was studied by microscopy, and quantitation of growth was done through resazurin assays. Inhibitors of glycosaminoglycan synthesis, thought to be upstream of BRG3, were assayed using resazurin to check the involvement of glycosaminoglycan signaling in Neuroblastoma cell survival. Results BRG3 and BRG1 SiRNA transfections generated statistically significant reductions in cell growth on IMR32 (P=0.000, P=0.004) and Kelly (P=0.000, P=0.001) Neuroblastoma cells. BRG3 and BRG1 plasmid transfection induced growth suppression or promotion, respectively, to varying degrees in 293T, IMR32 and Kelly. PTPRH induced growth suppression (p=0.001). Additionally, the genes had morphological effects on transfected cells. BRG3 protein was located on microtubules during mitosis, BRG1 was located in round, elongated protrusions, potentially invadopodia. Glycosaminoglycan synthesis inhibitor 4MU significantly reduced cell survival, with EC50 (SD) in Kelly, IMR32, SKNSH cells of 0.45 mM (0.037), 0.32 mM (0.086), and 0.11 mM (0.054), respectively. These results indicate that Glycosaminoglycan signaling protein BRG3 is of particular interest to pursue as a therapeutic target. Conclusion This study identified the growth-promoting and suppressing effects of the novel genes in Neuroblastoma and confirmed the morphological location of the proteins in some Neuroblastoma cell lines. In addition, it estimated the response to Glycosaminoglycan synthesis inhibitor and calculated the EC 50. This Glycosaminoglycan pathway, potentially acting via BRG3, could present a route for defining a new target treatment for Neuroblastoma. The novel BRG3 data may be of particular interest, since BRG3 is implicated in other cancers, but not so far in Neuroblastoma.
engagement and recovery within medical treatment plans. Stimulants (e.g. methylphenidate) are first line licensed medications for ADHD, and selective norepinephine reuptake inhibitors (e.g. atomoxetine) and alpha-2A adrenergic receptor agonists (e.g. guanfacine) are second line. At least 85% of children respond to stimulants, and only require alternative medications due to poor tolerance profiles.European Union member states classify narcotics according to United Nation conventions, and stimulant medications are classified as controlled drugs. This means that they have strict prescribing rules, which if not adhered to results in delayed dispensing, continued impairment, and increased demands on already stretched clinical resources. In Ireland ADHD is treated by tertiary mental health services, however in many European countries, paediatricians take a lead role in ADHD treatment. Aim This study examines the knowledge of trainee doctors in Ireland of the prescribing restrictions of stimulant medications, and the alternative non controlled medications used to treat ADHD. Method A questionnaire was designed to capture the current knowledge and prescribing habits of Irish trainee doctors on the 4 commonly used ADHD medications i.e. methylphenidate based, amphetamine based, atomoxetine and guanfacine. The percentage of correct answers were calculated, and Chi squared testing used. Results 47 questionnaires were completed and returned with a response rate of 57.5%. The majority of doctors knew that stimulants were controlled and how to prescribe these, however only one third of doctors distinguished correctly that the other 2 drug classes were not controlled, and similarly did not know how to prescribe them. Conclusion There is a knowledge gap amongst trainee doctors around prescribing for ADHD. Mainly for the non-controlled medication options, but also on specific points around prescribing the controlled stimulant medications. We hope that this identified gap in knowledge can be filled with targeted teaching; supporting doctors to become informed, competent and comfortable in prescribing for this common childhood illness.Background and aim Institute of Obstetricians and Gynaecologists (RCPI) guideline for preterm prelabour rupture of the membranes (PPROM) recommends the administration of antenatal corticosteroids for women who are 24 to 36 weeks pregnant with anticipated preterm labour. It reduces the risks of respiratory distress syndrome, intraventricular haemorrhage and necrotizing enterocolitis. Recommended steroid is 12 mg of intramuscular Betamethasone given 24 hours apart and at least 24 hours before delivery. This study determined the level of adherence to the guidelines. Methodology Mothers who presented in preterm prelabour rupture of membranes between 1/1/2015 and 31/12/2018 were incorporated into this study. Mothers were evaluated for
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