Assessment of Medication Adherence Barriers in COPD Patients in A Secondary Care Teaching Hospital

Background: COPD is characterised by persistent airway obstruction in which better clinical outcome can be attained by appropriate management of disease. Adherence to COPD medication is poorly understood due to chronic nature of the disease. It is crucial to identify the barriers of non-adherence to build up and execute policies and interventions to upgrade medication adherence. Objective: To identify the predisposing barriers of medication adherence and to find the association between medication adherence and variables. Methods: A descriptive analytical study was conducted and data was collected from COPD outpatients. The Morisky Medication Adherence Scale was used to measure adherence and self-assessed questionnaire was employed to identify the predictors of poor adherence. Chi square test was carried out to find the relationship between medication adherence and variables such as age, gender, literacy, socioeconomic class, polypharmacy, delivery device and climate. Results: A total of 403 patients were involved in the study where 68% reported lower adherence. The most common adherence barriers found were forgetfulness (88%), intentional stoppage of medicines when symptoms improve (83%) and negligence towards medication (82%).A significant association was found between gender, literacy, socioeconomic class, polypharmacy, delivery device and climate. Conclusion: Adherence to medication regimen in COPD patients is poor, even though it is a preventable and a treatable disease. Well-structured education, training, counseling is required to overcome medication adherence particularly among illiterate and low socioeconomic class patients. The combined interventions should be used such as video clips demonstrations of inhaler technique should be given. Keywords: COPD, Morisky medication adherence scale, Chi square test

CHD8 Regulates Neurodevelopmental Pathways Associated with Autism Spectrum Disorder in Neural Progenitors

Truncating mutations of chromodomain helicase DNA-binding protein 8 (CHD8), and of many other genes with diverse functions, are strong-effect risk factors for autism spectrum disorder (ASD), suggesting multiple mechanisms of pathogenesis. We explored the transcriptional networks that CHD8 regulates in neural progenitor cells (NPCs) by reducing its expression and then integrating transcriptome sequencing (RNA sequencing) with genome-wide CHD8 binding (ChIP sequencing). Suppressing CHD8 to levels comparable with the loss of a single allele caused altered expression of 1,756 genes, 64.9% of which were up-regulated. CHD8 showed widespread binding to chromatin, with 7,324 replicated sites that marked 5,658 genes. Integration of these data suggests that a limited array of direct regulatory effects of CHD8 produced a much larger network of secondary expression changes. Genes indirectly down-regulated (i.e., without CHD8-binding sites) reflect pathways involved in brain development, including synapse formation, neuron differentiation, cell adhesion, and axon guidance, whereas CHD8-bound genes are strongly associated with chromatin modification and transcriptional regulation. Genes associated with ASD were strongly enriched among indirectly down-regulated loci (P < 10[superscript −8]) and CHD8-bound genes (P = 0.0043), which align with previously identified coexpression modules during fetal development. We also find an intriguing enrichment of cancer-related gene sets among CHD8-bound genes (P < 10[superscript −10]). In vivo suppression of chd8 in zebrafish produced macrocephaly comparable to that of humans with inactivating mutations. These data indicate that heterozygous disruption of CHD8 precipitates a network of gene-expression changes involved in neurodevelopmental pathways in which many ASD-associated genes may converge on shared mechanisms of pathogenesis.Simons FoundationNancy Lurie Marks Family FoundationNational Institutes of Health (U.S.) (Grant MH095867)National Institutes of Health (U.S.) (Grant MH095088)National Institutes of Health (U.S.) (Grant GM061354)March of Dimes Birth Defects FoundationCharles H. Hood FoundationBrain & Behavior Research FoundationAutism Genetic Resource ExchangeAutism Speaks (Organization)Pitt–Hopkins Research Foundatio

Suitability of self-organizing service composition approach for smart healthcare ecosystem: A study

Future IoT systems will be deployed in open environments where the functionality of millions of IoT devices that are heterogeneous will be abstracted. In such a large scale system manual service composition is not feasible and often erroneous. A self-organizing service composition is a well known approach to deal with the problems in IoT systems. In a self-organizing service composition, the service composition is a runtime and autonomous process and human intervention is minimal. The atomic components will interact among themselves in a decentralized manner to form complex composites according to a set of self-organizing rules. The features of a self-organizing software composition are aptly suitable for the IoT domain. Smart healthcare has provided affordable healthcare for patients and enables them to self manage emergencies. This paper aims to establish the suitability of a self-organizing service composition for the smart healthcare ecosystem with special focus on real time monitoring applications

Keratocystic odontogenic tumor: A case report and review of literature

Keratocystic odontogenic tumor (KCOT) has been identified as a "tumor" after observation of its biological behavior and genetic abnormalities consistent with neoplastic progression. In 2005, the World Health Organization (WHO) working group considered odontogenic keratocyst (OKC) to be a tumor and recommended the term KCOT, distinguishing the lesion from the orthokeratinizing variant, which is now considered an OKC or orthokeratinized odontogenic cyst. Very rarely, KCOTs can transform into more aggressive lesions such as ameloblastoma and primary intraosseous carcinoma (PIOSCC). In this paper, we present a case of KCOT involving the angle and ramus of the mandible, with histopathologic evidence of ameloblastomatous changes. We also discuss about the evolution of this lesion from a cyst to a tumor along with the latest updates of the entity