Can COVID-19 mark a tipping point for home-based telework? Conflict between untact technology and rigid institutions in Korea

BackgroundPreviously, Korea showed a passive attitude toward home-based telework; however, this stance rapidly changed after the COVID-19 pandemic. Sustaining home-based telework entails adjusting productivity conditions, introducing performance-based evaluations, and modifying employment rules, as required by the Korean Labor Standards Act, which demand the consent of most workers. This study aims to explore the societal and institutional shifts necessary for ongoing home-based telework post-pandemic.MethodsThis study discusses the sustainability of home-based work based on survey data and materials from institutions and previous research. It used data from the Workplace Panel Survey provided by the Korea Labor Institution for 3 years (2015, 2017, and 2019) to examine the status of home-based work and business responses. It also addresses legal issues related to changes in working conditions and worker-management agreements resulting from telework implementation. Legal aspects of telework are explained using relevant sections of Korea’s labor laws.ResultsTo establish home-based telework as a working method relevant to the Fourth Industrial Revolution after the pandemic, essential discussions are needed regarding its fundamental applicability to specific job sectors. Moreover, to activate home-based telework without deteriorating working conditions, achieving agreement between workers and management is imperative. However, legal complexities necessitate systemic changes for effective resolution. For the sustainable continuity of telework, a blend of societal awareness and institutional transformations is indispensable.DiscussionThe growth of home-based telework through untact technology expansion is hindered by inflexible Korean labor laws, judicial precedents, and worker-management relations. The absence of necessary legal and organizational changes could lead Korea to revert to pre-pandemic norms or slow implementation. Initially prevalent in IT, home-based telework has expanded across sectors due to the pandemic. Leading the “new normal,” companies creatively enhance productivity through telework, but rigid systems and outdated cultures could impede post-pandemic progress.ConclusionThe study highlights the need for forward-looking institutional changes and adaptation to advancing technology. It provides valuable insights for organizations and policymakers to optimize work dynamics and enhance employee and employer well-being in the post-COVID-19 era

TCF/β-catenin plays an important role in HCCR-1 oncogene expression

<p>Abstract</p> <p>Background</p> <p>Oncogene <it>HCCR-1 </it>functions as a negative regulator of the p53 and contributes to tumorigenesis of various human tissues. However, it is unknown how <it>HCCR-1 </it>contributes to the cellular and biochemical mechanisms of human tumorigenesis.</p> <p>Results</p> <p>In this study, we showed how the expression of <it>HCCR-1 </it>is modulated. The luciferase activity assay indicated that the <it>HCCR-1 </it>5'-flanking region at positions -166 to +30 plays an important role in <it>HCCR-1 </it>promoter activity. Computational analysis of this region identified two consensus sequences for the T-cell factor (TCF) located at -26 to -4 (Tcf1) and -136 to -114 (Tcf2). Mutation at the Tcf1 site led to a dramatic decrease in promoter activity. Mobility shift assays (EMSA) revealed that nuclear proteins bind to the Tcf1 site, but not to the Tcf2 site. LiCl, Wnt signal activator by GSK-3β inhibition, significantly increased reporter activities in wild-type Tcf1-containing constructs, but were without effect in mutant Tcf1-containing constructs in HEK/293 cells. In addition, endogenous <it>HCCR-1 </it>expression was also increased by treatment with GSK-3β inhibitor, LiCl or AR-A014418 in HEK/293 and K562 cells. Finally, we also observed that the transcription factor, TCF, and its cofactor, β-catenin, bound to the Tcf1 site.</p> <p>Conclusion</p> <p>These findings suggest that the Tcf1 site on the <it>HCCR-1 </it>promoter is a major element regulating <it>HCCR-1 </it>expression and abnormal stimulation of this site may induce various human cancers.</p

Infection-related and lifestyle-related cancer burden in Kampala, Uganda: Projection of the future cancer incidence up to 2030

OBJECTIVES: In Uganda, infection-related cancers have made the greatest contribution to cancer burden in the past; however, burden from lifestyle-related cancers has increased recently. Using the Kampala Cancer Registry data, we projected incidence of top five cancers, namely, Kaposi sarcoma (KS), cervical, breast and prostate cancer, and non-Hodgkin\u27s lymphoma (NHL) in Uganda. DESIGN: Trend analysis of cancer registry data. SETTING: Kampala Cancer Registry, Uganda. MAIN OUTCOME MEASURE: Cancer incidence data from 2001 to 2015 were used and projected to 2030. Population data were obtained from the Uganda Bureau of Statistics. Age-standardised incidence rates (ASRs) and their trends over the observed and projected period were calculated. Percentage change in cancer incidence was calculated to determine whether cancer incidence changes were attributable to cancer risk changes or population changes. RESULTS: It was projected that the incidence rates of KS and NHL continue to decrease by 22.6% and 37.3%, respectively. The ASR of KS was expected to decline from 29.6 per 100 000 population to 10.4, while ASR of NHL was expected to decrease from 7.6 to 3.2. In contrast, cervical, breast and prostate cancer incidence were projected to increase by 35.3%, 57.7% and 33.4%, respectively. The ASRs of cervical and breast were projected to increase up to 66.1 and 48.4 per 100 000 women. The ASR of prostate cancer was estimated to increase from 41.6 to 60.5 per 100 000 men. These changes were due to changes in risk factors and population growth. CONCLUSION: Our results suggest a rapid shift in the profile of common cancers in Uganda, reflecting a new trend emerging in low/middle-income countries. This change in cancer spectrum, from infection-related to lifestyle-related, yields another challenge to cancer control programmes in resource-limited countries. Forthcoming cancer control programmes should include a substantial focus on lifestyle-related cancers, while infectious disease control programmes should be maintained

Multiscale, multimodal analysis of tumor heterogeneity in IDH1 mutant vs wild-type diffuse gliomas.

Glioma is recognized to be a highly heterogeneous CNS malignancy, whose diverse cellular composition and cellular interactions have not been well characterized. To gain new clinical- and biological-insights into the genetically-bifurcated IDH1 mutant (mt) vs wildtype (wt) forms of glioma, we integrated data from protein, genomic and MR imaging from 20 treatment-naïve glioma cases and 16 recurrent GBM cases. Multiplexed immunofluorescence (MxIF) was used to generate single cell data for 43 protein markers representing all cancer hallmarks, Genomic sequencing (exome and RNA (normal and tumor) and magnetic resonance imaging (MRI) quantitative features (protocols were T1-post, FLAIR and ADC) from whole tumor, peritumoral edema and enhancing core vs equivalent normal region were also collected from patients. Based on MxIF analysis, 85,767 cells (glioma cases) and 56,304 cells (GBM cases) were used to generate cell-level data for 24 biomarkers. K-means clustering was used to generate 7 distinct groups of cells with divergent biomarker profiles and deconvolution was used to assign RNA data into three classes. Spatial and molecular heterogeneity metrics were generated for the cell data. All features were compared between IDH mt and IDHwt patients and were finally combined to provide a holistic/integrated comparison. Protein expression by hallmark was generally lower in the IDHmt vs wt patients. Molecular and spatial heterogeneity scores for angiogenesis and cell invasion also differed between IDHmt and wt gliomas irrespective of prior treatment and tumor grade; these differences also persisted in the MR imaging features of peritumoral edema and contrast enhancement volumes. A coherent picture of enhanced angiogenesis in IDHwt tumors was derived from multiple platforms (genomic, proteomic and imaging) and scales from individual proteins to cell clusters and heterogeneity, as well as bulk tumor RNA and imaging features. Longer overall survival for IDH1mt glioma patients may reflect mutation-driven alterations in cellular, molecular, and spatial heterogeneity which manifest in discernable radiological manifestations

CHD7 Mutational Analysis and Clinical Considerations for Auditory Rehabilitation in Deaf Patients with CHARGE Syndrome

BACKGROUND: Otologic manifestations are one of the most consistent findings of CHARGE syndrome found in more than 90%. Since genetic analysis of the CHD7 gene has rarely been performed in previous reports dealing with ear abnormalities, the genotypic spectrum of CHD7 mutations was analyzed in deaf patients with CHARGE syndrome, and the clinical considerations concerning auditory rehabilitation were investigated. METHODS: Nine Korean patients with CHARGE syndrome showing profound hearing loss and semicircular canal aplasia were included. All 38 exons of CHD7 were analyzed by direct sequencing. For splice site variations, in silico and exon-trapping analyses were performed to verify the pathogenicity of nucleotide variations. Clinical features and the outcome of auditory rehabilitation were also analyzed. RESULTS: Eight of 9 patients revealed alterations of the CHD7 gene including 3 frameshift, 2 nonsense, 2 splice site, and 1 missense mutations. Five of 9 patients were clinically diagnosed as atypical CHARGE syndrome but demonstrated various mutations of the CHD7 gene. One familial case showed intra-familial variability. Radiologic findings suggesting cochleovestibular nerve deficiency were identified in most of the patients. Of the 8 patients who underwent cochlear implantation, 5 patients demonstrated favorable outcome. Larger diameter of the cochleovestibular nerve on imaging and absence of severe mental retardation were factors related to better outcome after cochlear implantation rather than the type of CHD7 mutations. Auditory brainstem implantation was performed in two patients who did not benefit from cochlear implantation. CONCLUSIONS: Genetic analysis of the CHD7 gene should be performed in cases with semicircular canal aplasia even when other typical features of CHARGE syndrome are absent. For auditory rehabilitation in CHARGE syndrome, cochlear implantation should be strongly recommended in selected cases with favorable prognostic factors. Auditory brainstem implantation may be a viable option in patients with CHARGE syndrome who have failed to benefit from cochlear implantation

Oncoprotein HCCR-1 expression in breast cancer is well correlated with known breast cancer prognostic factors including the HER2 overexpression, p53 mutation, and ER/PR status

<p>Abstract</p> <p>Background</p> <p>Oncoprotein HCCR-1 functions as a negative regulator of the p53 and contributes breast tumorigenesis. The serum HCCR-1 assay is useful in diagnosing breast cancer and mice transgenic for HCCR developed breast cancers. But it is unknown how <it>HCCR-1 </it>contributes to human breast tumorigenesis.</p> <p>Methods</p> <p>Oncogene HCCR-1 expression levels were determined in normal breast tissues, breast cancer tissues and cancer cell lines. We examined whether HCCR-1 protein expression in breast cancer is related to different biological characteristics, including ER, PR, p53 genotype, and HER2 status in 104 primary breast cancer tissues using immunohistochemical analyses.</p> <p>Results</p> <p>HCCR-1 was upregulated in breast cancer cells and tissues compared with normal breast tissues. In this study, overexpression of HCCR-1 was well correlated with known breast cancer prognostic markers including the presence of steroid receptors (ER and PR), p53 mutation and high HER2 overexpression. HCCR-1 was not detected in the ER-negative, PR-negative, p53 negative and low HER2 breast cancer tissues. These data indicate that the level of HCCR-1 in breast cancer tissues is relatively well correlated with known breast cancer factors, including the HER2 overexpression, p53 mutation, and ER/PR status.</p> <p>Conclusion</p> <p>Determination of HCCR-1 levels as options for HER2 testing is promising although it needs further evaluation.</p

Epithelial TGFβ engages growth-factor signalling to circumvent apoptosis and drive intestinal tumourigenesis with aggressive features

The pro-tumourigenic role of epithelial TGFβ signalling in colorectal cancer (CRC) is controversial. Here, we identify a cohort of born to be bad early-stage (T1) colorectal tumours, with aggressive features and a propensity to disseminate early, that are characterised by high epithelial cell-intrinsic TGFβ signalling. In the presence of concurrent Apc and Kras mutations, activation of epithelial TGFβ signalling rampantly accelerates tumourigenesis and share transcriptional signatures with those of the born to be bad T1 human tumours and predicts recurrence in stage II CRC. Mechanistically, epithelial TGFβ signalling induces a growth-promoting EGFR-signalling module that synergises with mutant APC and KRAS to drive MAPK signalling that re-sensitise tumour cells to MEK and/or EGFR inhibitors. Together, we identify epithelial TGFβ signalling both as a determinant of early dissemination and a potential therapeutic vulnerability of CRC’s with born to be bad traits