A study of sleep quality and occupational fatigue among healthcare providers who work shift duty in emergency department, Hospital Universiti Sains Malaysia in the year 2014

Health care workers generally are under tremendous stress. This is especially true in the emergency department where the Emergency Medical Services (EMS) workers are constantly under significant pressure with regard to health care and responsibilities. Healthcare providers in Emergency Department are required to deliver critical around-the-clock or “24/7” operational care to a variety of patients. The emergency department (ED) presents a real risk factor for cases of burnout because it generates more stress than any other department (O. Fernández Martínez and García, 2007). This is evidenced by increased pressure on health care, patients demanding a reduction in waiting time, long working hours, few breaks and a lack of cooperation from patients and their families. EMS workers are constantly and increasingly faced with difficult clinical cases and workloads that are taxing physically, mentally and emotionally. There are also lots of civil and legal responsibility associated with medical work, residents are frequently at risk and in potentially dangerous situations, constantly feeling rushed and harassed (O. Fernández Martínez and García, 2007).Providing quality health care services requires EMS providers to attend to details critical for life, such as monitoring of changing vital signs, administering the correct type and dose of medications, and in general, making crucial decisions to achieve optimal patient care. They are regularly required to problem-solve delicate and complex issues, inan independent, self-governing and timely fashion. They are also required to perform clinical skills, procedures and driving with professionalism and care. Their management is crucial during treatment of critical patients, where skills are paramount and errors in judgment or lapses in concentration could end up having fatal consequences (Frank Archer, 2012)

SASS v.2.1: Anthropometric Spreadsheet and Database for the IRIS

This report is the user\u27s manual of SASS v.21, the Spreadsheet Anthropometric Scaling System (version 2.1). It describes the usage of SASS, a spreadsheet-like system which allows flexible interactive access to all anthropometric variables needed to size a computer-based human figure, described structurally by a PEABODY file. Data that may be accessed is organized into the following groups : segment dimension ( girth ), joint limits, center of mass, and strength, all of which work based on statistical population data. SASS creates generic computer-based human figures based on this data. SASS also is an anthropometric database and interactive query system that works upon anthropometric data of real individuals. Scaled computer-based human figures created by SASS can be displayed directly, and interactively changed, within the Jack software

The Use of Rasch Model to Create Adaptive Practices in e-Learning Systems

While different approaches were developed to create computerized adaptive practices for e-learning systems, we show that exploiting Rasch models to create adaptive practices can be a new promising approach. Rasch analysis enables us to find a mathematical model to analyze students’ answers to exam questions by representing students’ abilities and questions difficulty levels on the same scale. In this paper, we introduce a novel algorithm to generate adaptive practices based on the Rasch analysis of students’ performance in an initial assessment. This approach enables us to generate adaptive practices that consider not only the student’s ability and his previous performance but also the difficulty level of each question. We also present results from a preliminary field experiment that we have conducted using an online learning system that implements this algorithm. The potential advantages of this approach and the practical contributions are discussed

HNF4A Haploinsufficiency in MODY1 Abrogates Liver and Pancreas Differentiation from Patient-Derived Induced Pluripotent Stem Cells.

Maturity-onset diabetes of the young 1 (MODY1) is a monogenic diabetes condition caused by heterozygous HNF4A mutations. We investigate how HNF4A haploinsufficiency from a MODY1/HNF4A mutation influences the development of foregut-derived liver and pancreatic cells through differentiation of human induced pluripotent stem cells from a MODY1 family down the foregut lineage. In MODY1-derived hepatopancreatic progenitors, which expressed reduced HNF4A levels and mislocalized HNF4A, foregut genes were downregulated, whereas hindgut-specifying HOX genes were upregulated. MODY1-derived hepatocyte-like cells were found to exhibit altered morphology. Hepatic and β cell gene signatures were also perturbed in MODY1-derived hepatocyte-like and β-like cells, respectively. As mutant HNF4A (p.Ile271fs) did not undergo complete nonsense-mediated decay or exert dominant negativity, HNF4A-mediated loss of function is likely due to impaired transcriptional activation of target genes. Our results suggest that in MODY1, liver and pancreas development is perturbed early on, contributing to altered hepatic proteins and β cell defects in patients

Skin models for cutaneous melioidosis reveal Burkholderia infection dynamics at wound's edge with inflammasome activation, keratinocyte extrusion and epidermal detachment.

Funder: Research Centre of Excellence, Mechanobiology InstituteFunder: National Research FoundationFunder: Cambridge-NUS Global Alliance FundABSTRACTMelioidosis is a serious infectious disease endemic in Southeast Asia, Northern Australia and has been increasingly reported in other tropical and subtropical regions in the world. Percutaneous inoculation through cuts and wounds on the skin is one of the major modes of natural transmission. Despite cuts in skin being a major route of entry, very little is known about how the causative bacterium Burkholderia pseudomallei initiates an infection at the skin and the disease manifestation at the skin known as cutaneous melioidosis. One key issue is the lack of suitable and relevant infection models. Employing an in vitro 2D keratinocyte cell culture, a 3D skin equivalent fibroblast-keratinocyte co-culture and ex vivo organ culture from human skin, we developed infection models utilizing surrogate model organism Burkholderia thailandensis to investigate Burkholderia-skin interactions. Collectively, these models show that the bacterial infection was largely limited at the wound's edge. Infection impedes wound closure, triggers inflammasome activation and cellular extrusion in the keratinocytes as a potential way to control bacterial infectious load at the skin. However, extensive infection over time could result in the epidermal layer being sloughed off, potentially contributing to formation of skin lesions

HNF4A haploinsufficiency in MODY1 abrogates liver and pancreas differentiation from patient-derived induced pluripotent stem cells

Maturity-onset diabetes of the young 1 (MODY1) is a monogenic diabetes condition caused by heterozygous HNF4A mutations. We investigate how HNF4A haploinsufficiency from a MODY1/HNF4A mutation influences the development of foregut-derived liver and pancreatic cells through differentiation of human induced pluripotent stem cells from a MODY1 family down the foregut lineage. In MODY1-derived hepatopancreatic progenitors, which expressed reduced HNF4A levels and mislocalized HNF4A, foregut genes were downregulated, whereas hindgut-specifying HOX genes were upregulated. MODY1-derived hepatocyte-like cells were found to exhibit altered morphology. Hepatic and β cell gene signatures were also perturbed in MODY1-derived hepatocyte-like and β-like cells, respectively. As mutant HNF4A (p.Ile271fs) did not undergo complete nonsense-mediated decay or exert dominant negativity, HNF4A-mediated loss of function is likely due to impaired transcriptional activation of target genes. Our results suggest that in MODY1, liver and pancreas development is perturbed early on, contributing to altered hepatic proteins and β cell defects in patients.publishedVersio

Molar root-incisor malformation: considerations of diverse developmental and etiologic factors

Objective. The objective of this study was to evaluate the variation in the condition referred to as molar root-incisor malformation (MRIM) and elucidate the distribution of affected teeth. This study further aimed to identify associated environmental stressors. Study Design. Individuals were identified through retrospective review of dental radiographs and through referral to the investigators. Histologic evaluation included examination of mineralized and decalcified sections of affected first permanent molar teeth. Results. Thirty cases of MRIM were identified, with all having affected first permanent molars with dysplastic root formation. The primary second molars were affected in 57% of the cases, with permanent anterior teeth being involved in 40% of the cases. A variety of medical conditions were associated with MRIM, the most common being neurologic. Several affected individuals reported no significant past medical history or environmental stressors. Conclusions. The etiology of MRIM remains unclear, and this unique developmental defect of the first permanent molar roots appears to occur in populations throughout the world. Clinicians identifying the MRIM phenotype should carefully evaluate the permanent incisors for associated developmental defects that could result in pulpal necrosis.OAIID:RECH_ACHV_DSTSH_NO:220160000011512001RECH_ACHV_FG:RR00200001ADJUST_YN:EMP_ID:A080446CITE_RATE:1.262FILENAME:1-s2.0-S2212440315011992-main.pdfDEPT_NM:치의학과EMAIL:[email protected]_YN:YFILEURL:https://srnd.snu.ac.kr/eXrepEIR/fws/file/d112ef1e-7a5b-4713-bb11-0fb377291141/linkCONFIRM:

Risk Factors, Molecular Epidemiology and Outcomes of Ertapenem-Resistant, Carbapenem-Susceptible Enterobacteriaceae: A Case-Case-Control Study

Background: Increasing prevalence of ertapenem-resistant, carbapenem-susceptible Enterobacteriaceae (ERE) in Singapore presents a major therapeutic problem. Our objective was to determine risk factors associated with the acquisition of ERE in hospitalized patients; to assess associated patient outcomes; and to describe the molecular characteristics of ERE. Methods: A retrospective case-case-control study was conducted in 2009 at a tertiary care hospital. Hospitalized patients with ERE and those with ertapenem-sensitive Enterobacteriaceae (ESE) were compared with a common control group consisting of patients with no prior gram-negative infections. Risk factors analyzed included demographics; co-morbidities; instrumentation and antibiotic exposures. Two parallel multivariate logistic regression models were performed to identify independent variables associated with ERE and ESE acquisition respectively. Clinical outcomes were compared between ERE and ESE patients. Results: Twenty-nine ERE cases, 29 ESE cases and 87 controls were analyzed. Multivariate logistic regression showed that previous hospitalization (Odds ratio [OR], 10.40; 95 % confidence interval [CI], 2.19–49.20) and duration of fluoroquinolones exposure (OR, 1.18 per day increase; 95 % CI, 1.05–1.34) were unique independent predictors for acquiring ERE. Duration of 4 th-generation cephalosporin exposure was found to predict for ESE acquisition (OR, 1.63 per day increase; 95 % CI, 1.05– 2.54). In-hospital mortality rates and clinical response rates were significantly different between ERE and ESE groups