Knowledge In Renal Nutrition Of Medical Doctors And Nursing Staff

Diet prescription for hospitalized renal patients should be individualized and based on their nutritional status and biochemical profiles. However the practice of ordering a ‘renal diet’ which consists of low protein, low salt, low potassium and low phosphate for all renal patients is common in the acute hospital setting. A total of 49 medical doctors were interviewed on their diet prescription practices for renal patients. In addition, a questionnaire was distributed to 488 nurses to assess their knowledge in renal nutrition. 68% of house officers (first year residents) reported that a ‘renal diet’ should be low in protein, salt, potassium, phosphate but only 38% of medical officers reported the same. While 100% of medical doctors stated that renal patients are at risk of compromised nutrition, only 45% of them would refer all renal patients to a dietitian. 47% of nurses believed that ‘renal diet’ low in potassium, salt, phosphate and protein should be prescribed to all patients with chronic renal failure. Only 38% of nurses were aware of the need for higher protein diet for patients on dialysis. In conclusion, there is a need to improve the knowledge of medical doctors and nursing staff in renal nutrition

Factors influencing the implementation, adoption, use, sustainability and scalability of mLearning for medical and nursing education: a systematic review protocol

Background: mLearning is increasingly presented as an attractive novel educational strategy for medical and nursing education. Yet, evidence base for its effectiveness or factors which influence use, success, implementation or adoption are not clear. We aim to synthesise findings from qualitative studies to provide insight into the factors (barriers and facilitators) influencing adoption, implementation and use of mobile devices for learning in medical and nursing education. The review also aims to identify factors or actions which are considered to optimise the experience and satisfaction of educators and learners in using mobile technologies for medical and nursing education and to identify strategies for improving mLearning interventions for medical and nursing education. / Methods: A systematic search will be conducted across a range of databases for studies describing or evaluating the experiences, barriers, facilitators and factors pertaining to the use of mLearning for medical and nursing education. The framework synthesis approach will be used to organise and bring different components of the results together. The confidence in the qualitative review findings will be assessed using the CERQual approach. / Discussion: This study will contribute to the planning and design of effective mLearning and the development of mLearning guidelines for medical and nursing education. / Systematic review registration: PROSPERO CRD4201603541

Additional file 2: of Factors influencing the implementation, adoption, use, sustainability and scalability of mLearning for medical and nursing education: a systematic review protocol

PRISMA-P (Preferred Reporting Items for Systematic review and Meta-Analysis Protocols) 2015 checklist: recommended items to address in a systematic review protocol. (DOC 82 kb

Integrative epigenomic and high-throughput functional enhancer profiling reveals determinants of enhancer heterogeneity in gastric cancer

10.1186/s13073-021-00970-3GENOME MEDICINE13

Multi-region sampling with paired sample sequencing analyses reveals sub-groups of patients with novel patient-specific dysregulation in Hepatocellular Carcinoma

Abstract Background Conventional differential expression (DE) testing compares the grouped mean value of tumour samples to the grouped mean value of the normal samples, and may miss out dysregulated genes in small subgroup of patients. This is especially so for highly heterogeneous cancer like Hepatocellular Carcinoma (HCC). Methods Using multi-region sampled RNA-seq data of 90 patients, we performed patient-specific differential expression testing, together with the patients’ matched adjacent normal samples. Results Comparing the results from conventional DE analysis and patient-specific DE analyses, we show that the conventional DE analysis omits some genes due to high inter-individual variability present in both tumour and normal tissues. Dysregulated genes shared in small subgroup of patients were useful in stratifying patients, and presented differential prognosis. We also showed that the target genes of some of the current targeted agents used in HCC exhibited highly individualistic dysregulation pattern, which may explain the poor response rate. Discussion/conclusion Our results highlight the importance of identifying patient-specific DE genes, with its potential to provide clinically valuable insights into patient subgroups for applications in precision medicine

Dynamic phenotypic heterogeneity and the evolution of multiple RNA subtypes in hepatocellular carcinoma: the PLANET study

Intra-tumor heterogeneity (ITH) is a key challenge in cancer treatment, but previous studies have focused mainly on the genomic alterations without exploring phenotypic (transcriptomic and immune) heterogeneity. Using one of the largest prospective surgical cohorts for hepatocellular carcinoma (HCC) with multi-region sampling, we sequenced whole genomes and paired transcriptomes from 67 HCC patients (331 samples). We found that while genomic ITH was rather constant across stages, phenotypic ITH had a very different trajectory and quickly diversified in stage II patients. Most strikingly, 30% of patients were found to contain more than one transcriptomic subtype within a single tumor. Such phenotypic ITH was found to be much more informative in predicting patient survival than genomic ITH and explains the poor efficacy of single-target systemic therapies in HCC. Taken together, we not only revealed an unprecedentedly dynamic landscape of phenotypic heterogeneity in HCC, but also highlighted the importance of studying phenotypic evolution across cancer types.National Medical Research Council (NMRC)National Research Foundation (NRF)Published versionThis work is supported in part by the Singapore National Medical Research Council grants (TCR/015-NCC/2016, CIRG18may-0057l, NMRC/CSA-SI/0018/2017, and NMRC/ OFIRG/0064/2017) and the National Research Foundation, Singapore (NRF-NRFF2015-04). W.Z. is supported in part by the National Key R&D Program of China (2018YFC1406902 and 2018YFC0910400), the National Natural Science Foundation of China (31970566), and the Strategic Priority Research Program of the Chinese Academy of Sciences (XDPB17). H.Y. is supported by the National Natural Science Foundation of China (32000407)

Genomic and epigenomic <i>EBF1</i> alterations modulate<i> TERT</i> expression in gastric cancer

Transcriptional reactivation of telomerase catalytic subunit (TERT) is a frequent hallmark of cancer, occurring in 90% of human malignancies. However, specific mechanisms driving TERT reactivation remain obscure for many tumor types and in particular gastric cancer (GC), a leading cause of global cancer mortality. Here, through comprehensive genomic and epigenomic analysis of primary GCs and GC cell lines, we identified the transcription factor early B cell factor 1 (EBF1) as a TERT transcriptional repressor and inactivation of EBF1 function as a major cause of TERT upregulation. Abolishment of EBF1 function occurs through 3 distinct (epi)genomic mechanisms. First, EBF1 is epigenetically silenced via DNA methyltransferase, polycomb-repressive complex 2 (PRC2), and histone deacetylase activity in GCs. Second, recurrent, somatic, and heterozygous EBF1 DNA-binding domain mutations result in the production of dominant-negative EBF1 isoforms. Third, more rarely, genomic deletions and rearrangements proximal to the TERT promoter remobilize or abolish EBF1-binding sites, derepressing TERT and leading to high TERT expression. EBF1 is also functionally required for various malignant phenotypes in vitro and in vivo, highlighting its importance for GC development. These results indicate that multimodal genomic and epigenomic alterations underpin TERT reactivation in GC, converging on transcriptional repressors such as EBF1

Genomic and epigenomic EBF1 alterations modulate TERT expression in gastric cancer

Transcriptional reactivation of telomerase catalytic subunit (TERT) is a frequent hallmark of cancer, occurring in 90% of human malignancies. However, specific mechanisms driving TERT reactivation remain obscure for many tumor types and in particular gastric cancer (GC), a leading cause of global cancer mortality. Here, through comprehensive genomic and epigenomic analysis of primary GCs and GC cell lines, we identified the transcription factor early B cell factor 1 (EBF1) as a TERT transcriptional repressor and inactivation of EBF1 function as a major cause of TERT upregulation. Abolishment of EBF1 function occurs through 3 distinct (epi)genomic mechanisms. First, EBF1 is epigenetically silenced via DNA methyltransferase, polycomb-repressive complex 2 (PRC2), and histone deacetylase activity in GCs. Second, recurrent, somatic, and heterozygous EBF1 DNA-binding domain mutations result in the production of dominant-negative EBF1 isoforms. Third, more rarely, genomic deletions and rearrangements proximal to the TERT promoter remobilize or abolish EBF1-binding sites, derepressing TERT and leading to high TERT expression. EBF1 is also functionally required for various malignant phenotypes in vitro and in vivo, highlighting its importance for GC development. These results indicate that multimodal genomic and epigenomic alterations underpin TERT reactivation in GC, converging on transcriptional repressors such as EBF1