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PurposeThis paper discusses how the features of blockchain technology impact supply chain transparency through the lens of the information security triad (confidentiality, integrity and availability). Ultimately, propositions are developed to encourage future research in supply chain applications of blockchain technology.Design/methodology/approachPropositions are developed based on a synthesis of the information security and supply chain transparency literature. Findings from text mining of Twitter data and a discussion of three major blockchain use cases support the development of the propositions.FindingsThe authors note that confidentiality limits supply chain transparency, which causes tension between transparency and security. Integrity and availability promote supply chain transparency. Blockchain features can preserve security and increase transparency at the same time, despite the tension between confidentiality and transparency.Research limitations/implicationsThe research was conducted at a time when most blockchain applications were still in pilot stages. The propositions developed should therefore be revisited as blockchain applications become more widely adopted and mature.Originality/valueThis study is among the first to examine the way blockchain technology eases the tension between supply chain transparency and security. Unlike other studies that have suggested only positive impacts of blockchain technology on transparency, this study demonstrates that blockchain features can influence transparency both positively and negatively.

Background The role of CIA‐II has been clarified in several types of tumors; however, whether dysregulated CIA‐II expression is also involved in the pathophysiology of lower‐grade glioma (LGG) remains undisclosed. Methods A comprehensive pan‐cancer analysis of the expression patterns and prognostic significance of CIA‐II in miscellaneous tumors was undertaken. Subsequently, a detailed bioinformatics analysis was executed to identify putative correlations between CIA‐II expression and clinical features, prognosis, biological functions, immunological characteristics, genomic alterations, and chemotherapeutics in LGG. In vitro studies were implemented to examine the potential roles of CIA‐II in LGG. Results CIA‐II expression was found to be abnormally elevated in a variety of tumors, including LGG. Additionally, patients with LGG with higher CIA‐II expression owned worse prognosis. Importantly, the results declared that CIA‐II expression was an independent prognostic indicator for LGG. Moreover, the expression of CIA‐II was tightly interrelated with immune cell infiltration, gene mutations, and chemotherapeutics in LGG. In vitro studies revealed that CIA‐II was increased and strongly related to the cell proliferation in LGG. Conclusion CIA‐II may be an independent prognostic factor and a serviceable therapeutic target in LGG. CIA‐II expression was an independent prognostic indicator for LGG. Moreover, the expression of CIA‐II was tightly interrelated with immune cell infiltration, gene mutations, and chemotherapeutics in LGG. In vitro studies revealed that CIA‐II was increased and strongly related to the cell proliferation in LGG.

The Cia-Cia language, which is spoken by around 79.000 people in the Bau-Bau area of Buton Island, does not have its own writing system. In 2009, the Korean alphabet, Hangeul, was approved by the Bau-Bau city government for transcribing Cia-Cia, owing to the similarity of phonemes in Korean to those in Cia-Cia. This research aimed to compare the acoustics of monophthongs in the Korean and Cia-Cia languages with an experimental phonetic approach and to discuss writing system problems in Cia-Cia when adopting the Korean writing system. Based on the classification, the Cia-Cia vowels /i, e, a, u, and o/ are equivalent to the Korean vowels /이 ([i]), 에 ([e]), 아 ([a]), 우 ([u]), 오 ([o])/.  However, there are two Korean vowels that have no Cia-Cia equivalents namely, /으/ ([ɨ]) and /어/ ([ə]). In general, the vowel equivalents between the two languages have significant differences in terms of their acoustic characteristics. Nonetheless, unlike other vowel equivalents, the Cia-Cia vowel /u/ and Korean vowel /우/ ([u]) when pronounced show similar phonetic features in terms of position and oral cavity opening level. In contrast, the Cia-Cia vowel /a/ and Korean vowel /아/ ([a]) when pronounced is shown to have the same oral cavity opening level, but different tongue positions. The use of the vowel /으/ ([ɨ]) in Hangeul's writing in transcribing particular Cia-Cia words is a unique feature of Korean grammar. This renders some transcriptions different from the pronunciation of the source Cia-Cia word. This is because of the limitations of Korean syllables, which, unlike Cia-Cia words, are not able to be written as double consonants.

Rheumatoid arthritis (RA) is a chronic, heterogeneous autoimmune disease. Its high disability rate has a serious impact on society and individuals, but there is still a lack of effective and reliable diagnostic markers and therapeutic targets for RA. In this study, we integrated RA patient information from three GEO databases for differential gene expression analysis. Additionally, we also obtained pan-cancer-related genes from the TCGA and GTEx databases. For RA-related differential genes, we performed functional enrichment analysis and constructed a weighted gene co-expression network (WGCNA). Then, we obtained 490 key genes by intersecting the significant module genes selected by WGCNA and the differential genes. After using the RanddomForest, SVM-REF, and LASSO three algorithms to analyze these key genes and take the intersection, based on the four core genes (BTN3A2, CYFIP2, ST8SIA1, and TYMS) that we found, we constructed an RA diagnosis. The nomogram model showed good reliability and validity after evaluation, and the ROC curves of the four genes showed that these four genes played an important role in the pathogenesis of RA. After further gene correlation analysis, immune infiltration analysis, and mouse gene expression validation, we finally selected CYFIP2 as the cut-in gene for pan-cancer analysis. The results of the pan-cancer analysis showed that CYFIP2 was closely related to the prognosis of patients with various tumors, the degree of immune cell infiltration, as well as TMB, MSI, and other indicators, suggesting that this gene may be a potential intervention target for human diseases including RA and tumors.

Programmed cell death is a vital biological process for multicellular organisms to maintain cellular homeostasis, which is regulated in a complex manner. Over the past several years, apart from apoptosis, which is the principal mechanism of caspase-dependent cell death, research on non-apoptotic forms of programmed cell death has gained momentum. p53 is a well characterized tumor suppressor that controls cell proliferation and apoptosis and has also been linked to non-apoptotic, non-canonical cell death mechanisms. p53 impacts these non-canonical forms of cell death through transcriptional regulation of its downstream targets, as well as direct interactions with key players involved in these mechanisms, in a cell type- or tissue context-dependent manner. In this review article, we summarize and discuss the involvement of p53 in several non-canonical modes of cell death, including caspase-independent apoptosis (CIA), ferroptosis, necroptosis, autophagic cell death, mitotic catastrophe, paraptosis, and pyroptosis, as well as its role in efferocytosis which is the process of clearing dead or dying cells.

Objective Rheumatoid arthritis (RA) is a chronic inflammatory condition that, despite available approaches to manage the disease, lacks an efficient treatment and timely diagnosis. Using the most advanced omics technique, metabolomics and proteomics approach, we explored varied metabolites and proteins to identify unique metabolite-protein signatures involved in the disease pathogenesis of RA. Methods Untargeted metabolomics ( n  = 20) and proteomics ( n  = 60) of RA patients’ plasma were carried out by HPLC/LC-MS/MS and SWATH, respectively and analyzed by Metaboanalyst. The targets of metabolite retrieved by PharmMapper were matched with SWATH data, and joint pathway analysis was carried out. An in-vitro study of metabolites in TNF-α induced SW982 cells was conducted by Western, RT-PCR, scratch, and ROS scavenging assay. The effect of GUDCA was also evaluated in the CIA rat model. Results A Total of 82 metabolites and 231 differential proteins were revealed. Porphyrin and chlorophyll pathway and its metabolite Glycoursodeoxycholic acid (GUDCA) was found to be significantly altered. In vitro analysis has shown that GUDCA reduces inflammation thus offering protection against ROS production and cell proliferation. PharmMapper analysis revealed that GUDCA was significantly linked with identified SWATH proteins insulin like growth factor-1(IGF1), and Transthyretin (TTR) and it upregulates the expression of IGF1 and downregulates the expression of TTR in both in vitro and in vivo models. Conclusion GUDCA was found to possess antioxidative, antiproliferative properties and an effective anti-inflammatory property at a low dosage. It may be considered as a potential therapeutic option for reducing the inflammatory parameters associated with RA. Graphical Abstract

Recent studies have shown the significance of metabolic reprogramming in immune and stromal cell function. Yet, the metabolic reconfiguration of RA macrophages (MΦs) is incompletely understood during active disease and in crosstalk with other cell types in experimental arthritis. This study elucidates a distinct regulation of glycolysis and oxidative phosphorylation in RA MΦs compared to fibroblast (FLS), although PPP (Pentose Phosphate pathway) is similarly reconfigured in both cell types. 2-DG treatment showed a more robust impact on impairing the RA M1 MΦ-mediated inflammatory phenotype than IACS-010759 (IACS, complexli), by reversing ERK, AKT and STAT1 signaling, IRF8/3 transcription and CCL2 or CCL5 secretion. This broader inhibitory effect of 2-DG therapy on RA M1 MΦs was linked to dysregulation of glycolysis (GLUT1, PFKFB3, LDHA, lactate) and oxidative PPP (NADP conversion to NADPH), while both compounds were ineffective on oxidative phosphorylation. Distinctly, in RA FLS, 2-DG and IACS therapies constrained LPS/IFNγ-induced AKT and JNK signaling, IRF5/7 and fibrokine expression. Disruption of RA FLS metabolic rewiring by 2-DG or IACS therapy was accompanied by a reduction of glycolysis (HIF1α, PFKFB3) and suppression of citrate or succinate buildup. We found that 2-DG therapy mitigated CIA pathology by intercepting joint F480+iNOS+MΦ, Vimentin+ fibroblast and CD3+T cell trafficking along with downregulation of IRFs and glycolytic intermediates. Surprisingly, IACS treatment was inconsequential on CIA swelling, cell infiltration, M1 and Th1/Th17 cytokines (IFN-γ/IL-17) and joint glycolytic mediators. Collectively, our results indicate that blockade of glycolysis is more effective than inhibition of complex 1 in CIA, in part due to its effectiveness on the MΦ inflammatory phenotype.

Rheumatoid arthritis (RA) is a chronic and systemic autoimmune disease of unknown etiology. The most common form of this disease is chronic inflammatory arthritis, which begins with inflammation of the synovial membrane of the affected joints and eventually leads to disability of the affected limb. Despite significant advances in RA pharmaceutical therapies and the availability of a variety of medicines on the market, none of the available medicinal therapies has been able to completely cure the disease. In addition, a significant percentage (30–40%) of patients do not respond appropriately to any of the available medicines. Recently, mesenchymal stromal cells (MSCs) have shown promising results in controlling inflammatory and autoimmune diseases, including RA. Experimental studies and clinical trials have demonstrated the high power of MSCs in modulating the immune system. In this article, we first examine the mechanism of RA disease, the role of cytokines and existing medicinal therapies. We then discuss the immunomodulatory function of MSCs from different perspectives. Our understanding of how MSCs work in suppressing the immune system will lead to better utilization of these cells as a promising tool in the treatment of autoimmune diseases.