Health Students’ Attitudes towards Disability

Background: Individuals with disabilities remain one of the most socially excluded segments of the population, constantly fighting for equal rights and social inclusion. Disability is not an easy subject for health professionals to deal with, in part because it crosses many professional and cultural boundaries.Objective: The aim of this research is to analyze and understand the various attitudes toward people with disabilities, amongst the final year medical, midwifery and nursing students and to compare the three health departments on their students’ attitudes.Methods: A questionnaire-based electronic survey was directed to all medical, midwifery and nursing students registered at two big universities in Athens, Greece (n=190). The time frame was decided to encompass a month window (from 2nd May to 2nd June 2021).Results: The Nursing students in the study showed overall a better attitude towards disabled people. Our research mainly indicates the fact that in general, there is need to prioritize training in both theoretical and practical fields through alterations in all three university departments’ curricula.Conclusions: Undergraduates Health Students (of Nursing, Midwifery and Medicine) generally present a lack of awareness, familiarity and experience towards disabled people. Numerous reasons seemed to influence health professional’s attitudes to people with a disability including their age, gender, nationality, education, years of experience, general knowledge regarding a disability and the level and nature of their training. This research clearly illustrates the importance of improving how universities’ undergraduate curricula address disabilities in an effort to inspire upcoming health professionals

The dual role of LSD1 and HDAC3 in STAT5-dependent transcription is determined by protein interactions, binding affinities, motifs and genomic positions

STAT5 interacts with other factors to control transcription, and the mechanism of regulation is of interest as constitutive active STAT5 has been reported in malignancies. Here, LSD1 and HDAC3 were identified as novel STAT5a interacting partners in pro-B cells. Characterization of STAT5a, LSD1 and HDAC3 target genes by ChIP-seq and RNA-seq revealed gene subsets regulated by independent or combined action of the factors and LSD1/HDAC3 to play dual role in their activation or repression. Genes bound by STAT5a alone or in combination with weakly associated LSD1 or HDAC3 were enriched for the canonical STAT5a GAS motif, and such binding induced activation or repression. Strong STAT5 binding was see

Gene therapy approaches to evaluate neuroprotection from oxidation stress in experimental models of amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by the loss of upper and lower motor neurons, with no effective treatment to date. Only 5-10% of ALS cases are familial, of which 20% are caused by missense mutations in the gene encoding Cu/Zn superoxide dismutase 1 (SOD I). Although ALS has a multi-factorial aetiology, oxidative stress is hypothesized to be one of the key pathogenic mechanisms. It is thus proposed that manipulation of the expression of anti- oxidant genes may serve as a therapeutic strategy for the protection of motor neurons. It has been previously found that three specific anti-oxidant genes (PTGR 1 /L TB4DH - prostaglandin reductase I / leukotriene B4 12-hydroxydehydrogenase, PRDX3 - peroxiredoxin 3, and NRF2 - nuclear factor erythroid 2-related factor 2) are down- regulated in the presence of mutant SOD 1. The main aim of this project is to alter the expression of the target genes using viral vectors and study the effect on the vulnerability of cells expressing mutant SOD I both in vitro and in vivo. Lentiviral vectors expressing each of the three target genes were tested in the NSC34 cell line (hybrid cell line of mouse motor neurons and neuroblastoma), and the oxidative stress levels as well as cell survival was measured in wild type cells and cells stably expressing the human SOD I gene incorporating the ALS-causing G93A mutation. In the ALS tissue culture model, stable over-expression was achieved, and two of the genes showed cytoprotective properties. Virally delivered PTGR I exhibited no significant effect on oxidation stress levels or cell survival, and as such this gene was not investigated further. However, cells over-expressing either PRDX3 or NRF2 showed a significant decrease in endogenous oxidation stress levels by 40% and 50% respectively compared to controls, whereas cell survival was increased by 30%. These two genes were taken forward to the ALS mouse model, in which intramuscular injections of adeno-associated virus serotype 6 expressing either of the target genes were administered at a pre-symptornatic stage. Behavioural tests and quantitative readouts of motor function allowed the investigation of this therapeutic strategy. However no significant effect was seen in survival, disease onset or disease progression. Quantification of the efficiency of viral delivery showed that only 5% of the lumbar motor neurons were transduced through retrograde transport accounting for the absence of a therapeutic effect. These results suggest that such a delivery is not sufficient to induce a therapeutic effect, and a more widespread CNS delivery is needed.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Sex-specific transcriptional profiles identified in β-thalassemia patients

β-thalassemia comprises a group of heterogeneous autosomal recessive hereditary anemias characterized by the reduction or absence of β-globin chain synthesis, and it is a highly prevalent disease affecting 1.5% of the global population. Three different clinical conditions are recognized in patients with β-thalassemia minor (trait) being the asymptomatic form, β-thalassemia major (TM) being the most severe form of the disease and β-thalassemia intermedia (TI) presenting with variable severity. Despite extensive characterization of the genetic basis of disease pathogenesis, currently the classification of patients relies on the severity of symptoms and HbF levels regardless of the underlying genotype. Thus, the aim of the study was to develop an approach for patient stratification based on gene expression, pinpoint the targets that dictate each phenotype and provide a framework for the development of therapeutic strategies focused on these targets. To this end, we have analysed the gene expression profiles of TI, TM and healthy individuals using RNA-seq (NCBI, GSE117221) and we have studied the differentially expressed genes (DEGs) and pathways irrespective to patient genotype. Interestingly, after analysis of various confounding factors, we identified gender differences in the patients’ expression profiles suggesting that males and females are differentially affected by β-thalassemia. Thus, taking gender into account might benefit prognosis, diagnosis, stratification and therapeutic management of the disease