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The evaluation or metrology of commercial bank management efficiency is the core of its effective management. The existing management efficiency of commercial banks adopts evaluation scheme rather than metrology. There are four shortcomings with the evaluation scheme, the evaluation is a ranking of advantages and/or disadvantages, all objects should participate in the evaluation, the evaluation results are valid only for the evaluated objects, and the evaluation results lack the metrology benchmark of the object domain. To address this issue, the paper presents a method to determine the benchmark of management efficiency, which is similar to the unit "meter" in the metrology of "length" and the unit "scale" in the metrology of "management efficiency". Firstly, the method of cluster analysis is used to solve the problem of attribute metrology base of management efficiency metrology. Based on the master of certain attribute data of commercial bank management efficiency metrology, cluster analysis is carried out onto the attribute data, and its characteristics and patterns are mined to determine the candidate benchmark set. Secondly, in the candidate datum set, k-means method is used to determine the metrology attribute datum to obtain the general metrology attributes. Finally, the absolute metrology of management efficiency is carried out for any commercial bank according to the benchmark, and the validity and feasibility of the benchmark are verified with an example. In such a way, the deficiencies of four aspects of evaluation are solved. Such a strategy can be adapted to different banks at any different time for their respective measurement, which extends the clustering statistical methods for attribute datum determination. The results can be applied to some other fields wherein object metrology is the basic task.

INTRODUCTION:Non-intubated anesthesia (NIA) has been proposed for video-assisted thoracoscopic surgery (VATS), although how the benefit-to-risk of NIA compares to that of intubated general anesthesia (IGA) for certain types of patients remains unclear. Therefore, the aim of the present meta-analysis was to understand whether NIA or IGA may be more beneficial for patients undergoing VATS. METHODS:A systematic search of Cochrane Library, Pubmed and Embase databases from 1968 to April 2019 was performed using predefined criteria. Studies comparing the effects of NIA or IGA for adult VATS patients were considered. The primary outcome measure was hospital stay. Pooled data were meta-analyzed using a random-effects model to determine the standard mean difference (SMD) with 95% confidence intervals (CI). RESULTS AND DISCUSSION:Twenty-eight studies with 2929 patients were included. The median age of participants was 56.8 years (range 21.9-76.4) and 1802 (61.5%) were male. Compared to IGA, NIA was associated with shorter hospital stay (SMD -0.57 days, 95%CI -0.78 to -0.36), lower estimated cost for hospitalization (SMD -2.83 US, 95% CI -4.33 to -1.34), shorter chest tube duration (SMD -0.32 days, 95% CI -0.47 to -0.17), and shorter postoperative fasting time (SMD, -2.76 days; 95% CI -2.98 to -2.54). NIA patients showed higher levels of total lymphocytes and natural killer cells and higher T helper/T suppressor cell ratio, but lower levels of interleukin (IL)-6, IL-8 and C-reactive protein (CRP). Moreover, NIA patients showed lower levels of fibrinogen, cortisol, procalcitonin and epinephrine. CONCLUSIONS:NIA enhances the recovery from VATS through attenuation of stress and inflammatory responses and stimulation of cellular immune function.

Background: Tumor metastasis is driven by malignant cells and stromal cell components of the tumor microenvironment. Cancer stem cells (CSCs) are thought to be responsible for metastasis by altering the tumor microenvironment. Epithelial-mesenchymal transition (EMT) processes contribute to specific stages of the metastatic cascade, promoted by cytokines and chemokines secreted by stromal cell components in the tumor microenvironment. C-C chemokine receptor 7 (CCR7) interacts with its ligand, chemokine ligand 21(CCL21), to mediate metastasis in some cancer cells lines. This study investigated the role of CCL21/CCR7 in promoting EMT and metastasis of cluster of differentiation 133+ (CD133+) pancreatic cancer stem-like cells. Methods: Panc-1, AsPC-1, and MIA PaCa-2 pancreatic cancer cells were selected because of their aggressive invasive potentials. CCR7 expression levels were examined in total, CD133+ and CD133− cell fractions by Immunofluorescence analysis and real time-quantitative polymerase chain reaction (RT-qPCR). The role of CCL21/CCR7 in mediating metastasis and survival of CD133+ pancreatic cancer stem-like cells was detected by Transwell assays and flow cytometry, respectively. EMT and lymph node metastasis related markers (E-cadherin, N- cadherin, LYVE-1) were analyzed by western blot. CCR7 expression levels were analyzed by immunohistochemical staining and RT-qPCR in resected tumor tissues, metastatic lymph nodes, normal lymph nodes and adjacent normal tissues from patients with pancreatic carcinoma. Results: CCR7 expression was significantly increased in CD133+ pancreatic cancer stem-like cells, resected pancreatic cancer tissues, and metastatic lymph nodes, compared with CD133− cancer cells, adjacent normal tissues and normal lymph nodes, respectively. CCL21/CCR7 promoted metastasis and survival of CD133+ pancreatic cancer stem-like cells and regulated CD133+ pancreatic cancer stem-like cells metastasis by modulating EMT and Erk/NF-κB pathway. Conclusions: These results indicate a specific role for CCL21/CCR7 in promoting EMT and metastasis in CD133+ pancreatic cancer stem-like cells. Furthermore the data also indicated the potential importance of developing therapeutic strategies targeting cancer stem-like cells and CCL21/CCR7 for reducing metastasis. [ABSTRACT FROM AUTHOR]

Microcystin-LR (MCLR) is the most common cyanotoxin in contaminated aquatic systems. MCLR inhibits protein phosphatases 1 and 2A, leading to liver damage and tumor formation. MCLR is relatively stable owing to its cyclic structures. The combined UV/H2O2 technology can degrade MCLR efficiently. The second-order rate constant of the reaction between MCLR and hydroxyl radical (·OH) is 2.79(±0.23)×1010 M−1 s−1 based on the competition kinetics model using nitrobenzene as reference compound. The probable degradation pathway was analyzed through liquid chromatography mass spectrometry. Results suggested that the major destruction pathways of MCLR were initiated by ·OH attack on the benzene ring and diene of the Adda side chain. The corresponding aldehyde or ketone peptide residues were formed through further oxidation. Another minor destruction pathway involved ·OH attack on the methoxy group of the Adda side chain, followed by complete removal of the methoxy group. The combined UV/H2O2 system is a promising technology for MCLR removal in contaminated aquatic systems. [ABSTRACT FROM AUTHOR]

B-1 cells are innate-like cells that play important roles in host defense against infection. However, the function of B-1 cells in fungi infection remains unclear. Previously we produced IgH transgenic mice TgVH3B4 with VH derived from a natural antibody 3B4 that can identify C. albicans, and found that TgVH3B4 mice were resistant to intraperitoneal (i. p.) and intravenous C. albicans infection. Most of the peritoneal cavity (PEC) B-1 cells in TgVH3B4 mice express transgenic BCR that binds C. albicans. In the present study, we explored the response of B-1 cells to C. albicans infection by applying i. p. inoculation of fungi in TgVH3B4 mice. We found that C. albicans was cleared more efficiently in TgVH3B4 mice after i. p. inoculation than that of littermate control. The level of C. albicans-reactive IgM in PEC of TgVH3B4 mice was much higher than that of control, and the number of B-1a B cells was also elevated in TgVH3B4 mice, which was mainly due to enhanced proliferation of B-1 cells. Additionally, numbers of C. albicans-specific B cells increased greatly in TgVH3B4 mice after C. albicans inoculation. Our data suggested that in situ IgM production and clonal expansion of B-1 cells in PEC participate in host defense against C. albicans infection. [ABSTRACT FROM AUTHOR]

B-1 cells are innate-like cells that play important roles in host defense against infection. However, the function of B-1 cells in fungi infection remains unclear. Previously we produced IgH transgenic mice TgVH3B4 with VH derived from a natural antibody 3B4 that can identify C. albicans, and found that TgVH3B4 mice were resistant to intraperitoneal (i. p.) and intravenous C. albicans infection. Most of the peritoneal cavity (PEC) B-1 cells in TgVH3B4 mice express transgenic BCR that binds C. albicans. In the present study, we explored the response of B-1 cells to C. albicans infection by applying i. p. inoculation of fungi in TgVH3B4 mice. We found that C. albicans was cleared more efficiently in TgVH3B4 mice after i. p. inoculation than that of littermate control. The level of C. albicans-reactive IgM in PEC of TgVH3B4 mice was much higher than that of control, and the number of B-1a B cells was also elevated in TgVH3B4 mice, which was mainly due to enhanced proliferation of B-1 cells. Additionally, numbers of C. albicans-specific B cells increased greatly in TgVH3B4 mice after C. albicans inoculation. Our data suggested that in situ IgM production and clonal expansion of B-1 cells in PEC participate in host defense against C. albicans infection.

Background: Tumor antigen (TA)-targeted monoclonal antibody (mAb) immunotherapy can be effective for the treatment of a broad range of cancer etiologies; however, these approaches have demonstrated variable clinical efficacy for the treatment of patients with prostate cancer (PCa). An obstacle currently impeding translational progress has been the inability to quantify the mAb dose that reaches the tumor site and binds to the targeted TAs. The coupling of mAb to nanoparticle-based magnetic resonance imaging (MRI) probes should permit in vivo measurement of patient-specific biodistributions; these measurements could facilitate future development of novel dosimetry paradigms wherein mAb dose is titrated to optimize outcomes for individual patients., Methods: The prostate stem cell antigen (PSCA) is broadly expressed on the surface of prostate cancer (PCa) cells. Anti-human PSCA monoclonal antibodies (mAb 7F5) were bound to Au/Fe(3)O(4) (GoldMag) nanoparticles (mAb 7F5@GoldMag) to serve as PSCA-specific theragnostic MRI probe permitting visualization of mAb biodistribution in vivo. First, the antibody immobilization efficiency of the GoldMag particles and the efficacy for PSCA-specific binding was assessed. Next, PC-3 (prostate cancer with PSCA over-expression) and SMMC-7721 (hepatoma cells without PSCA expression) tumor-bearing mice were injected with mAb 7F5@GoldMag for MRI. MRI probe biodistributions were assessed at increasing time intervals post-infusion; therapy response was evaluated with serial tumor volume measurements., Results: Targeted binding of the mAb 7F5@GoldMag probes to PC-3 cells was verified using optical images and MRI; selective binding was not observed for SMMC-7721 tumors. The immunotherapeutic efficacy of the mAb 7F5@GoldMag in PC-3 tumor-bearing mice was verified with significant inhibition of tumor growth compared to untreated control animals., Conclusion: Our promising results suggest the feasibility of using mAb 7F5@GoldMag probes as a novel paradigm for the detection and immunotherapeutic treatment of PCa. We optimistically anticipate that the approaches have the potential to be translated into the clinical settings.