Search

Intelligent technology solutions have revolutionized banking and enhanced the overall efficiency of financial institutions worldwide. As banks endeavor to evolve into comprehensive financial service hubs, this study examines the impact of intelligent technology solutions on the efficiency of a sample of Chinese banks and analyzes efficiency trends over time based on two vectors affecting intelligent technology (enterprise-side innovation and consumer-side co-creation). The study builds upon the parameter non-frontier method (ACF) to measure efficiency and examines intelligent technology solutions and channel usage in China from 2007 to 2017. The results indicate that intelligent innovation and consumer co-creation within intelligent channels both have significant positive impacts on banking efficiency. Moreover, these impacts have gradually surpassed traditional banking innovations and consumer participation in traditional self-service channels. In some ways, consumer participation’s positive impact on banking efficiency is even greater than banks’ institutional innovation. Notably, the relative influence of intelligent innovation and consumer participation on bank efficiency has shifted, and customer participation now occupies a more important position. Based on these findings, banks would be well advised to develop intelligent technology solutions along two paths: enhancing institutional technology and supporting consumer participation.

BackgroundThis meta-analysis was dedicated to evaluating the safety and effectiveness of indocyanine green (ICG) -mediated fluorescence molecular imaging (FMI) technology in liver tumors resection.MethodsA literature search of PubMed, Embase databases, Cochrane Library, and Web of Science was performed to identify all clinical controlled studies exploring the effects of fluorescence imaging on liver tumors resection. Quality assessment and data extraction of studies were conducted independently by 3 reviewers. Mean difference (MD) and odds ratio (OR) with 95% confidence interval (CI) were calculated using a fixed-effects or random-effects model. The meta-analysis was performed with RevMan 5.3 software.Results14 retrospective cohort studies (RCSs) involving a total of 1227 patients were finally included. The results showed that Fluorescence-assisted liver tumors resection could improve the R0 resection rate (OR = 2.63; 95% CI: 1.46~4.73, p = 0.001), reduce overall complications (OR = 0.66; 95% CI: 0.44~0.97, p = 0.04), biliary fistula (OR = 0.20; 95% CI: 0.05~0.77, p = 0.02), intraoperative blood loss (MD = −70.76, 95% CI: −106.11 to −35.41; p < 0.0001), and shortens hospital stay (MD = −1.41, 95% CI: −1.90 to −0.92; p < 0.00001). There were no significant differences in the incidences of operative time (MD = −8.68, 95% CI: −18.59 to −1.22; p = 0.09), complications of grade III or above (OR = 0.73; 95% CI: 0.43~1.25, p = 0.26), liver failure (OR = 0.86; 95% CI: 0.39~1.89, p = 0.71), and blood transfusion (OR = 0.66; 95% CI: 0.42~1.03, p = 0.07).ConclusionCurrent evidence suggests that ICG-mediated FMI technology could enhance the clinical effectiveness of patients with liver tumors resection and is clinically worthy of promotion.Systematic review registrationPROSPERO, identifier CRD42022368387.

How much environmental pollution can be reduced by the efficient use of financial, natural, and energy resources in the current globalization. Thus, this study provides empirical evidence in support of the theoretical argument by investigating the impact of financial development, environmental assets, globalization, coal, natural gas, and sustainable carbon emissions in 32 developed countries from 1990 to 2018. Ecological degradation (estimated by carbon dioxide emissions) experienced a structural shift that was considerably more pronounced in 2000–2011 than in 1991–1998. A broad variety of econometric methodologies (such as the Chow test, Cross-country regression, and the Generalized Method of Moments (GMM)) were applied. As a consequence, environmental deterioration is strongly linked to economic development and urbanization, according to the findings. These nations’ ecological footprints are favorably influenced by financial development, environmental assets, and non-renewable energy, whereas globalization and sustainable sources have a negative impact. Environmental degradation may be slowed by combining globalization’s impact on financial growth with the conservation of natural resources such as renewable energy sources. In order to improve their economic and ecological resource frameworks, these nations will need to increase their use of solar and other renewable energy.

In recent years, the growth of cryptocurrency has undergone an enormous increase in cryptocurrency markets all around the world. Sadly, only insignificant heed has been paid to the unveiling of determinants of cryptocurrency adoption globally, particularly in emerging markets like Malaysia. The purpose of the study is to examine whether the application of deep learning-based dual-stage Partial Least Square-Structural Equation Modelling (PLS-SEM) & Artificial Neural Network (ANN) analysis enable better in-depth research results as compared to single-step PLS-SEM approach and to excavate factors which can predict behavioural intention to adopt cryptocurrency. The Unified Theory of Acceptance and Use of Technology 2 (UTAUT2) model were extended with the inclusion of trust and personnel innovativeness. The model was further validated by introducing a new path model compared to the original UTAUT2 model and the moderating role of personal innovativeness between performance expectancy and price value, with a sample of 314 respondents. Contrary to previous technology adoption studies that used PLS-SEM & ANN as single-stage analysis, this study further enhanced the analysis by applying a deep learning-based dual-stage PLS-SEM and ANN method. The application of deep learning-based dual-stage PLS-SEM & ANN analysis is a novel methodological approach, detecting both linear and non-linear associations among constructs. At the same time, it is regarded as a superior statistical approach as compared to traditional hybrid shallow SEM & ANN single-stage analysis. Also, sensitivity analysis provides normalised importance using multi-layer perceptron with the feed-forward-back-propagation algorithm. Furthermore, the deep learning-based dual-stage PLS-SEM & ANN revealed that trust proved to be the strongest predictor in driving user intention. The introduction of this new methodology and the theoretical contribution opens the vistas of the extant body of knowledge in technology-adoption related literature. This study also provides theoretical, practical and methodological contributions.

Summary We report that interleukin (IL)‐4 and IL‐10 can significantly up‐ or down‐regulate CXC chemokine receptor 4 (CXCR4) expression on CD4+ T lymphocytes, respectively. Stromal cell‐derived factor‐1α (SDF‐1α)‐induced CD4+ T‐lymphocyte chemotaxis was also correspondingly regulated by IL‐4 and IL‐10. IL‐4 and IL‐10 up‐ or down‐regulated CXCR4 mRNA expression in CD4+ T lymphocytes, respectively, as detected by real‐time quantitative reverse transcription–polymerase chain reaction (RT–PCR). Scatchard analysis revealed a type of CXCR4 with affinity (Kd ≈ 6·3 nm), and ≈ 70 000 SDF‐1α‐binding sites per cell, among freshly isolated CD4+ T lymphocytes, and two types of CXCR4 with different affinities (Kd1 ≈ 4·4 nm and Kd2 ≈ 14·6 nm), and a total of ≈ 130 000 SDF‐1α‐binding sites per cell, among IL‐4‐stimulated CD4+ T lymphocytes. The regulation of CXCR4 expression in CD4+ T lymphocytes by IL‐4 and IL‐10 could be blocked by a selective inhibitor of protein kinase (staurosporine) or by a selective inhibitor of cAMP‐ and cGMP‐dependent protein kinase (H‐8), indicating that these cytokines regulate CXCR4 on CD4+ T lymphocytes via both cAMP and cGMP signalling pathways. The fact that cyclosporin A or ionomycin were able to independently change the CXCR4 expression and block the effects of IL‐4 and IL‐10 on CXCR4 expression implied that the capacity of IL‐4 and IL‐10 to regulate CXCR4 on CD4+ T lymphocytes is not linked to calcium‐mobilization stimulation. These results indicate that the effects of IL‐4 and IL‐10 on the... [ABSTRACT FROM AUTHOR]

The reports on the origin of human CD8(+) Valpha24(+) T-cell receptor (TCR) natural killer T (NKT) cells are controversial. The underlying mechanism that controls human CD4 versus CD8 NKT cell development is not well-characterized. In the present study, we have studied total 177 eligible patients and subjects including 128 healthy latent Epstein-Barr-virus(EBV)-infected subjects, 17 newly-onset acute infectious mononucleosis patients, 16 newly-diagnosed EBV-associated Hodgkin lymphoma patients, and 16 EBV-negative normal control subjects. We have established human-thymus/liver-SCID chimera, reaggregated thymic organ culture, and fetal thymic organ culture. We here show that the average frequency of total and CD8(+) NKT cells in PBMCs from 128 healthy latent EBV-infected subjects is significantly higher than in 17 acute EBV infectious mononucleosis patients, 16 EBV-associated Hodgkin lymphoma patients, and 16 EBV-negative normal control subjects. However, the frequency of total and CD8(+) NKT cells is remarkably increased in the acute EBV infectious mononucleosis patients at year 1 post-onset. EBV-challenge promotes CD8(+) NKT cell development in the thymus of human-thymus/liver-SCID chimeras. The frequency of total (3% of thymic cells) and CD8(+) NKT cells ( approximately 25% of NKT cells) is significantly increased in EBV-challenged chimeras, compared to those in the unchallenged chimeras (

Background/aims: Mucosa-associated T-lymphocyte (MAIT) cells that are selectively accumulated in the intestinal mucosa may be involved in immune regulation. MAIT cells are determined by their Vα7.2-Jα33 (human)/Vα19-Jα33 (mice) invariant chain. The encoding DNA sequences of Human Jα33 and mouse Jα33 are identical. In order to study the role of MAIT cells in IBD we produced anti-Jα33 antibody to detect MAIT cells in TNBS induced IBD models., Methodology: Colitis was induced by TNBS in male BALB/c mice. Jα33+MAIT cells from normal mice were transferred into TNBS induced mice as donors. Colitis severity was evaluated clinically and histologically, under the condition of transferred Jα33+MAIT cells., Results: The mRNA and protein expression levels of MAIT aTCR in the colonic mucosa were decreased after TNBS administration; Jα33+MAIT cells were aggregated in spleen after TNBS administration. The disease activity index (DAI) which was determined by weight loss, stool consistency and intestinal bleeding, increased after TNBS administration. Transferred Jα33+MAIT cells significantly degrade the increase in the disease activity index scores., Conclusions: Taken together, the results indicated that the aggregation of Jα33+MAIT cells in intestinal mucosa improved TNBS-induced colitis. We conclude that Jα33+MAIT cells play a protective role in TNBS induced intestinal inflammation.

The underlying mechanism of the protective and suppressive role of NKT cells in human tumor immunosurveillance remains to be fully elucidated. We show that the frequencies of CD8(+) NKT cells in patients with EBV-associated Hodgkin's lymphoma or nasopharyngeal carcinoma are significantly lower than those in healthy EBV carriers. These CD8(+) NKT cells in tumor patients are also functionally impaired. In human-thymus-severe combined immunodeficient (hu-thym-SCID) chimeras, EBV challenge efficiently promotes the generation of IFN-gamma-biased CD8(+) NKT cells. These cells are strongly cytotoxic, drive syngeneic T cells into a Th1 bias, and enhance T-cell cytotoxicity to EBV-associated tumor cells. Interleukin-4-biased CD4(+) NKT cells are predominately generated in unchallenged chimeras. These cells are noncytotoxic, drive syngeneic T cells into a Th2 bias, and do not affect T-cell cytotoxicity. In humanized xenogeneic tumor-transplanted hu-thym-SCID chimeras, adoptive transfer with EBV-induced CD8(+) NKT cells significantly suppresses tumorigenesis by EBV-associated malignancies. EBV-induced CD8(+) NKT cells are necessary and sufficient to enhance the T-cell immunity to EBV-associated malignancies in the hu-thym-SCID chimeras. CD4(+) NKT cells are synergetic with CD8(+) NKT cells, leading to a more pronounced T-cell antitumor response in the chimeras cotransferred with CD4(+) and CD8(+) NKT cells. Thus, immune reconstitution with EBV-induced CD8(+) NKT cells could be a useful strategy in management of EBV-associated malignancies.

The source of IgA and the mechanism for deposition of IgA in the mesangium remain unknown for primary IgA nephropathy. Because CD19(+)CD5(+) B cells are important producers of IgA and contribute to several autoimmune diseases, they may play an important role in IgA nephropathy. In this study, flow cytometry, quantitative PCR, and confocal microscopy were used to assess the frequency, distribution, Ig production, CD phenotypes, cytokine production, and sensitivity to apoptosis of CD19(+)CD5(+) B cells in the peripheral blood, peritoneal fluid, and kidney biopsies of 36 patients with primary IgA nephropathy. All patients with IgA nephropathy were significantly more likely to have CD19(+)CD5(+) B cells in the peripheral blood, peritoneal fluid, and kidney biopsies than were five control subjects and 10 patients with active systemic lupus erythematosus. The 33 patients who had IgA nephropathy and responded to treatment demonstrated a significant decrease in CD19(+)CD5(+) B cells in the peripheral blood, peritoneal fluid, and kidney (all P < 0.01). In the three patients who had IgA nephropathy and did not respond to treatment, the frequency of CD19(+)CD5(+) B cells did not change. CD19(+)CD5(+) B cells isolated from patients with untreated IgA nephropathy expressed higher levels of IgA, produced more IFN-gamma, and were more resistant to CD95L-induced apoptosis than cells isolated from control subjects and patients with lupus; these properties reversed with effective treatment of IgA nephropathy. In conclusion, these results strongly suggest that CD19(+)CD5(+) B cells play a prominent role in the pathogenesis of primary IgA nephropathy.

Urticaria is a relatively common autoimmune/autoreactive skin disorder that may severely impair quality of life. Although rarely life-threatening, widespread urticaria and its associated angioedema can be an extremely disabling and difficult-to-treat condition. Patients may suffer symptoms such as pruritus and disfigurement due to wheals for years or decades. Urticaria is caused by cutaneous mast-cell degranulation attributed to immunological, non-immunological, and idiopathic causes. The last decade has seen some notable advances in the understanding of the etiology and pathogenesis of common forms of urticaria and their management. Furthermore, the wide diversity in urticaria subtypes has been identified and this reflects a partial understanding of the causes or factors that trigger it as well as the molecular and cellular mechanisms that are involved in its physiopathology. In addition, new instruments for diagnosing urticaria variants and for assessing quality of life in urticaria patients have been developed. Finally, several clinical trials have demonstrated the efficacy of novel treatment approaches for urticaria, while other therapeutic concepts are under development. The objective of this article was to review the literature to be able to offer the readers comprehensive and updated information on the basic etiological and physiopathological mechanisms and to make special emphasis on the current management of urticaria, thus promoting continuous medical education.

The significance of necrobiosis lipoidica (NL) includes its relationship with insulin-dependent diabetes mellitus, its tendency to break down into painful ulcers, an albeit tenuous association with squamous cell carcinoma and, by no means least, its cosmetic impact, occurring as it does on the shins of young and middle-aged women. Necrobiosis (degeneration of collagen) and granulomous inflammation are well-documented histological findings in NL; however, to see an asteroid body in an area of NL is rare. To the best of our knowledge, there is only one such report of NL described so far. We report the case of a NL patient whose histopathological examination revealed asteroid bodies. The patient had suffered persistent NL for a period of more than 2 years. She was successfully treated with dipyridamole plus intralesional triamcinolone and the lesions healed completely after 2 months of therapy. The patient has remained free of lesions since discontinuing therapy.

Interacting with T cells, cytokine-producing B cells play a critical protective role in autoimmune diseases. However, the interaction between malignant B and T cells remains to be fully elucidated. In a previous study, we have reported that ligation of CCL19-CCR7 and CXCL13-CXCR5 activates paternally expressed gene 10 (PEG10), resulting in an enhancement of apoptotic resistance in B-cell acute lymphocytic leukemia (B-ALL) CD23+CD5+ B cells. Here, we report that B-ALL CD23+CD5+ B cells produce IL-10 at high level, which can be further elevated by costimulation with CCL19 and CXCL13. CCL19/CXCL13-activated B-ALL CD23+CD5+ B cells, in turn, increase IL-10 expression in syngeneic CD8+ T cells in a B cell-derived IL-10-dependent manner and requiring a cell-cell contact. IL-10 secreted from B-ALL CD23+CD5+ B cells in vitro impairs tumor-specific CTL responses of syngeneic CD8+ T cells. The impairment of cytotoxicity of syngeneic CD8+ T cells is escalated by means of CCL19/CXCL13-induced up-regulation of IL-10 from B-ALL CD23+CD5+ B cells. Moreover, using a short hairpin RNA to knockdown PEG10, we provide direct evidence that increased expression of PEG10 in B-ALL CD23+CD5+ B cells is involved in malignant B-T cell interaction, contributing to the up-regulation of IL-10 expression, as well as to the impairment of cytotoxicity of syngeneic CD8+ T cells. Thus, malignant B-ALL CD23+CD5+ B cells play an immunoregulatory role in controlling different inflammatory cytokine expressions. IL-10 may be one of the critical cellular factors conferring B-ALL CD23+CD5+ B cells to escape from host immune surveillance.