Résumé
INTRODUCTION@#Due to COVID-19 pandemic, many have shifted into working at home which led to physical inactivity. This may cause musculoskeletal discomfort, chronic disease, muscle atrophy and spinal imbalance due to improper and prolonged sitting posture. Since mobile devices are relatively available for most of the office workers, there were still a lack of evidence-based mobile applications that can counteract the inactivity through exercises, which led to the researchers to create an application called SitMate that consists of evidence-based exercises which aimed to prevent musculoskeletal discomfort among a business process outsourcing company Workforce Management Personnel (BPO-WMP).@*METHODS@#Eleven participants (18-40 years old) full-time, work-from-home BPO-WMP were randomized into Treatment Group(TG)(n=6) and Control Group (CG)(n=5). The TG received one month intervention with the use of SitMate Application containing relaxation exercises, range of motion exercises and stretching exercises, and notifications for postural correction while the CG continued their usual working schedule.@*RESULTS@#There were no significant differences between two groups on all body parts that were measured using the Cornell Musculoskeletal Discomfort Questionnaire, and no significant differences in the intragroup pre-test and post-test scores on all body parts between TG and CG. For the intra-group post-test of the TG, there were noted improvements on the hip/buttock, right shoulder, upper back (median = 0) and right wrist (median = 1.5). There was also a noted increase in discomfort on the neck (median = 1.5) and lower back (median = 3). For the post-test of the CG, there were noted improvements on the right shoulder, right wrist (median = 0) and lower back (median = 1.5).@*CONCLUSION@#This study has shown that the SitMate application does not effectively reduce the prolonged sitting-related discomfort among the personnel after 1 month of intervention.
Sujets)
Applications mobiles , Mode de vie sédentaire , Lombalgie , PostureRésumé
Background & objectives: The amount of foetal haemoglobin that persists in adulthood affects the clinical severity of haemoglobinopathies including β-thalassaemia major and sickle cell anaemia (SCA). The present study was undertaken to analyse β-thalassaemia as well as SCA patients for the single nucleotide polymorphism (SNP), rs11886868 (T/C) in BCL11A gene and to evaluate the association between this polymorphism and severity of β-thalassaemia major and SCA. Methods: A total of 620 samples (420 β-thalassaemia major and 200 SCA cases) were analysed before blood transfusion using basic screening tests like complete blood analysis and osmotic fragility and further confirmed by high performance liquid chromatography (HPLC), amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) and reverse dot blot techniques. All patients were transfusion dependent. Patients with β-thalassaemia and SCA were classified into mild, moderate, severe according to the severity score based on Hb levels, age of onset, age at which patients received their first blood transfusion, the degree of growth retardation and splenectomy. β-thalassaemia as well as SCA patients were analysed for the SNP, rs11886868 (T/C) in BCL11A gene and association between this polymorphism and severity of β-thalassaemia major as well as SCA was evaluated. Results: There was a significant difference in genotypic and allelic frequencies of BCL11A gene polymorphism between mild and moderate and mild and severe cases in both the groups. A significant (P<0.001) difference was observed in the mean HbF levels between the three genotypes in different severity groups. HbF levels were found to be high in CC genotype bearing individuals followed by TC and TT in β-thalassaemia major as well as SCA. Interpretation & conclusions: This study confirms that the T/C variant (rs11886868) of the BCL11A gene causing downregulation of BCL11A gene expression in adult erythroid precursors results in the induction of HbF and ameliorates the severity of β-thalassaemia as well as SCA.