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Purpose: Business models define the activity system that an organization employs to create and capture value. As such, business models are essentially the application of strategic management. The term business model, however, suffers from definitional ambiguity which makes the construction of effective business models problematic. We argue that this ambiguity is largely due to a lack of clarity around value. This paper seeks to provide clarity around value and in doing so aid in the development of effective business models. Design: Theoretical paper that deconstructs value into use value and exchange value and develops these concepts. Findings: We deconstruct value into use value and exchange value to explain the micro-conditions of value creation and capture. In doing so, we also provide an explanation of how VRIN and non-VRIN resources can be traded for gain as well as opening up greater strategic options for managers in their development of business models. Originality / Value: Against the background of the study’s focus on BMI, its comparably broad literature basis, and its quantitative and qualitative analysis approach, which provides straightforward recommendations for future research, the study caters an original contribution to the field.

Many knowledge-intensive organizations (KIOs) have invested in tools and policies to enhance knowledge-sharing and application as this is crucial for their growth. The implementation of these tools results in multiple approaches for knowledge-sharing being available. This article reports on an empirical study of five global management consultancies investigating how consultants choose between these knowledge-sharing alternatives and the factors driving this choice. Our findings indicate that consultants base their decisions on both judging the anticipated benefits of the knowledge content and the associated process costs. Importantly, the criteria employed to assess these knowledge-sharing alternatives were different to that of the leadership. The use of different criteria resulted in the leadership championing tools and policies that the consultants did not perceive as valuable. The study contributes to the HRM and knowledge management literature, not only by surfacing criteria, yet to be discussed in the literature, used by the leadership and consultants of KIOs in determining which knowledge-sharing approach to use, but also by highlighting that when considering KM tools it was critical to take a multi-level approach as there may be some differences in rationales as to why some systems are used or not. [ABSTRACT FROM PUBLISHER]

DNA methylation has been implied to play a role in the immune dysfunction associated with inflammatory bowel disease (IBD) and the disease development of ulcerative colitis (UC). Changes of the DNA methylation and correlated gene expression in patient samples with inactive UC might reveal possible regulatory features important for further treatment options for UC. Targeted bisulfite sequencing and whole transcriptome sequencing were performed on mucosal biopsies from patients with active UC (UC, n = 14), inactive UC (RM, n = 20), and non-IBD patients which served as controls (NN, n = 11). The differentially methylated regions (DMRs) were identified by DMRseq. Correlation analysis was performed between DMRs and their nearest differentially expressed genes (DEGs). Principal component analysis (PCA) was performed based on correlated DMR regulated genes. DMR regulated genes then were functional annotated. Cell-type deconvolutions were performed based on methylation levels. The comparisons revealed a total of 38 methylation-regulated genes in inactive UC that are potentially regulated by DMRs (correlation p value < 0.1). Several methylation-regulated genes could be identified in inactive UC participating in IL-10 and cytokine signalling pathways such as IL1B and STAT3. DNA methylation events in inactive UC seem to be fine-tuned by the balancing pro- and anti- inflammatory pathways to maintain a prevailed healing process to restore dynamic epithelium homeostasis., (© 2024. The Author(s).)

Background: Heart rate variability (HRV) is a valuable indicator of autonomic nervous system integrity and can be a prognostic tool of COVID-19 induced myocardial affection. This study aimed to compare HRV indices between patients who developed myocardial injury and those without myocardial injury in COVID-19 patients who were admitted to intensive care unit (ICU)., Methods: In this retrospective study, the data from 238 COVID-19 adult patients who were admitted to ICU from April 2020 to June 2021 were collected. The patients were assigned to myocardial injury and non-myocardial injury groups. The main collected data were R-R intervals, standard deviation of NN intervals (SDANN) and the root mean square of successive differences between normal heartbeats (RMSSD) that were measured daily during the first five days of ICU admission., Results: The R-R intervals, the SDANN and the RMSSD were significantly shorter in the myocardial injury group than the non-myocardial group at the first, t second, third, fourth and the fifth days of ICU admission. There were no significant differences between the myocardial injury and the non-myocardial injury groups with regard the number of patients who needed mechanical ventilation, ICU length of stay and the number of ICU deaths., Conclusions: From the results of this retrospective study, we concluded that the indices of HRV were greatly affected in COVID-19 patients who developed myocardial injury., (© 2023. The Author(s).)

Severe ulcerative colitis (UC) is a potentially life-threatening disease with a potential colorectal cancer (CRC) risk. The aim of this study was to explore the relationship between transcriptomic and genome-wide DNA methylation profiles in a well-stratified, treatment-naïve severe UC patient population in order to define specific epigenetic changes that could be responsible for the grade of disease severity. Mucosal biopsies from treatment-naïve severe UC patients (n = 8), treatment-naïve mild UC (n = 8), and healthy controls (n = 8) underwent both whole transcriptome RNA-Seq and genome-wide DNA bisulfite- sequencing, and principal component analysis (PCA), cell deconvolutions and diverse statistical methods were applied to obtain a dataset of significantly differentially expressed genes (DEGs) with correlation to DNA methylation for severe UC. DNA hypo-methylation correlated with approximately 80% of all DEGs in severe UC when compared to mild UC. Enriched pathways of annotated hypo-methylated genes revealed neutrophil degranulation, and immuno-regulatory interactions of the lymphoid system. Specifically, hypo-methylated anti-inflammatory genes found for severe UC were IL10, SIGLEC5, CD86, CLMP and members of inflammasomes NLRP3 and NLRC4. Hypo-methylation of anti-inflammatory genes during severe UC implies an interplay between the epithelium and lamina propria in order to mitigate inflammation in the gut. The specifically DNA hypo-methylated genes found for severe UC can potentially be useful biomarkers for determining disease severity and in the development of new targeted treatment strategies for severe UC patients., Competing Interests: The authors have no competing interests.

Background: This study addresses whether existing specific transcriptional profiles can improve and support the current status of the definition of ulcerative colitis (UC) remission apart from the existing endoscopic, histologic, and laboratory scoring systems. For that purpose, a well-stratified UC patient population in remission was compared to active UC and control patients and was investigated by applying the next-generation technology RNA-Seq., Methods: Mucosal biopsies from patients in remission (n = 14), patients with active UC (n = 14), and healthy control patientss (n = 16) underwent whole-transcriptome RNA-Seq. Principal component analysis, cell deconvolution methods, gene profile enrichment, and pathway enrichment methods were applied to define a specific transcriptional signature of UC in remission., Results: Analyses revealed specific transcriptional signatures for UC in remission with increased expression of genes involved in O-glycosylation (MUC17, MUC3A, MUC5AC, MUC12, SPON1, B3GNT3), ephrin-mediated repulsion of cells (EFNB2E, EFNA3, EPHA10, EPHA1), GAP junction trafficking (TUBA1C, TUBA4A, TUBB4B, GJB3, CLTB), and decreased expression of several toll-like receptors (TLR1, TLR3, TLR5, TLR6)., Conclusions: This study reveals specific transcriptional signatures for remission. Partial restoration and improvement of homeostasis in the epithelial mucus layer and revival of immunological functions were observed. A clear role for bacterial gut flora composition can be implied. The results can be useful for the development of treatment strategies for UC in remission and may be useful targets for further investigations aiming to predict the outcome of UC in the future., (© 2020 Crohn’s & Colitis Foundation. Published by Oxford University Press on behalf of Crohn’s & Colitis Foundation.)

Background and Aims: The aim of this study was to investigate the genome-wide DNA methylation status in treatment-naïve ulcerative colitis [UC], and to explore the relationship between DNA methylation patterns and gene expression levels in tissue biopsies from a well-stratified treatment-naïve UC patient group., Methods: Mucosal biopsies from treatment-naïve patients [n = 10], and a healthy control group [n = 11] underwent genome-wide DNA bisulfite sequencing. Principal component analysis [PCA] and diverse statistical methods were applied to obtain a dataset of differentially methylated genes. DNA methylation annotation was investigated using the UCSC Genome Browser. Gene set enrichments were obtained using the Kyoto Encyclopaedia of Genes and Genomes [KEGG] and PANTHER., Results: Of all significantly differentially expressed genes [DEGs], 25% correlated with DNA methylation patterns; 30% of these genes were methylated at CpG sites near their transcription start site [TSS]. Hyper-methylation was observed for genes involved in homeostasis and defence, whereas hypo-methylation was observed for genes playing a role in immune response [i.e. chemokines and interleukins]. Of the differentially DNA methylated genes, 25 were identified as inflammatory bowel disease [IBD] susceptibility genes. Four genes [DEFFA6, REG1B, BTNL3, OLFM4] showed DNA methylation in the absence of known CpG islands., Conclusions: Genome-wide DNA methylation analysis revealed distinctive functional patterns for hyper-and hypo-methylation in treatment-naïve UC. These distinct patterns could be of importance in the development and pathogenesis of UC. Further investigation of DNA methylation patterns may be useful in the development of the targeting of epigenetic processes, and may allow new treatment and target strategies for UC patients.

Background and Aims: Ulcerative colitis [UC] is a chronic inflammatory disease that effects the gastrointestinal tract and is considered one of the most prominent and common forms of inflammatory bowel disease [IBD]. This study aimed to define and describe the entire transcriptomic landscape in a well-stratified, treatment-naïve UC patient population compared with control patients by using next-generation technology, RNA-Seq., Methods: Mucosal biopsies from treatment-naïve UC patients [n = 14], and healthy controls [n = 16] underwent RNA-Seq. Principal component analysis [PCA], cell deconvolution methods, and diverse statistical methods were applied to obtain and characterise a dataset of significantly differentially expressed genes [DEGs]., Results: Analyses revealed 1480 significantly DEGs in treatment-naïve UC when compared with controls. Cell populations of monocytes, T cells, neutrophils, B cells/ lymphoid cells, and myeloid cells were increased during inflammation, whereas the fraction of epithelial cells were reduced in UC, which is reflected by the DEGs; 79 DEGs were identified as IBD susceptibility genes, and 58 DEGs were expressed in a gender-specific manner. MUC5B, REG3A, DEFA5, and IL33 might be considered as colorectal cancer [CRC] risk factors following UC in males. AQP9 together with CLDN2 may have a role regulating tissue-specific physiological properties in tight junctions in UC. An additional functional role for AQP9 in the synthesis and/or the function of mucus can be implied., Conclusions: This study reveals new potential players in UC pathogenesis in general, and provides evidence for a gender-dependent pathogenesis for UC. These results can be useful for the development of personalised treatment strategies for UC in the future., (© European Crohn’s and Colitis Organisation (ECCO) 2017.)