Analysis of factors influencing onset and survival of patients with severe acute pancreatitis: A clinical study.

OBJECTIVES: Acute pancreatitis (AP) is an inflammatory disease of the pancreas, and the prognosis of severe AP (SAP) is poor. The study aimed to identify promising biomarkers for predicting the occurrence and survival outcome of SAP patients. MATERIALS AND METHODS: Two hundred and forty AP patients were retrospectively recruited, in which 72 cases with SAP. Blood test was done for collection of laboratory indicators. After treatment, the mortality of patients was recorded. RESULTS: Patients in the SAP group had higher intensive care unit admissions and longer hospital stays (p < .001). Among laboratory parameters, significantly high values of C-reactive protein (CRP), triglycerides and glucose (TyG) index, Von willebrand factor antigen (vWF:Ag) and D-dimer were found in SAP groups relative to non-SAP ones. Receiver operating characteristic curve indicated the good performance of CRP, TyG index, vWF:Ag and D-dimer in SAP diagnosis. Among all SAP cases, 51 survived while 21 died. TyG index (odds ratio [OR] = 6.914, 95% confidence interval [CI] = 1.193-40.068, p = .028), vWF:Ag (OR = 7.441, 95% CI = 1.236-244.815, p = .028), and D-dimer (OR = 7.987, 95% CI = 1.251-50.997, p = .028) were significantly related to survival outcome of SAP patients by multiple logistic regression analysis. Both TyG index and vWF showed favorable efficiency in predicting overall prognosis. The area under the curve for the multivariate model (PRE = -35.908 + 2.764 × TyG + 0.021 × vWF:Ag) was 0.909 which was greater than 0.9, indicating its excellent performance in prognosis prediction. CONCLUSION: CRP, TyG index, vWF:Ag, and D-dimer values on admission may be potential clinical predictors of the development of SAP. Moreover, TyG index and vWF:Ag may be helpful to predict survival outcome.

Recent advances in super-resolution optical imaging based on aggregation-induced emission.

Super-resolution imaging has rapidly emerged as an optical microscopy technique, offering advantages of high optical resolution over the past two decades; achieving improved imaging resolution requires significant efforts in developing super-resolution imaging agents characterized by high brightness, high contrast and high sensitivity to fluorescence switching. Apart from technical requirements in optical systems and algorithms, super-resolution imaging relies on fluorescent dyes with special photophysical or photochemical properties. The concept of aggregation-induced emission (AIE) was proposed in 2001, coinciding with unprecedented advancements and innovations in super-resolution imaging technology. AIE probes offer many advantages, including high brightness in the aggregated state, low background signal, a larger Stokes shift, ultra-high photostability, and excellent biocompatibility, making them highly promising for applications in super-resolution imaging. In this review, we summarize the progress in implementation methods and provide insights into the mechanism of AIE-based super-resolution imaging, including fluorescence switching resulting from photochemically-converted aggregation-induced emission, electrostatically controlled aggregation-induced emission and specific binding-regulated aggregation-induced emission. Particularly, the aggregation-induced emission principle has been proposed to achieve spontaneous fluorescence switching, expanding the selection and application scenarios of super-resolution imaging probes. By combining the aggregation-induced emission principle and specific molecular design, we offer some comprehensive insights to facilitate the applications of AIEgens (AIE-active molecules) in super-resolution imaging.

Photoplastic Transformation Based on Dynamic Covalent Chemistry.

The magical fantasy of decades-old transformer characters is becoming closer to scientific reality, as transformable materials can change their shapes in response to thermal, mechanical, electrical, and chemical stimuli. However, precise and prompt control of plastic shaping remains to be wanted. Photoresponsive materials provide a promising alternative for rapid optomechanical shaping with limited success. Here, we report a new class of photoplastic transformation based on dynamic covalently crosslinked polytriazole (PTA) networks, in which crosslinking points are comprised of photocleaveable hexaarylbiimidazole (HABI). Upon sub-500 nm light irradiation, HABI is dissociated into two triphenylimidazole radicals (TPIRs) followed by spontaneous recombination back to the initial state. This photoswitching effect is demonstrated to generate nonthermal shape change in the PTA-HABI gel network at will upon light stimulus. A unique photoalignment phenomenon has also been discovered which can form oriented nanoscale patterning in the PTA-HABI gel network upon laser irradiation. The solvent-free PTA-HABI elastomer exhibits photoenhanced automatic self-healing properties at temperatures ranging from 25 °C to freezing points, which is attributed to the dynamic equilibrium between TPIRs and HABI. A photoplastic spring is fabricated and exhibits photoswitchable plastic behavior, i.e., a reversible transformation between plastic strain and elastic strain upon light irradiation. HABI-based polymer networks, including solvated gel and solvent-free elastomer, are promising as smart materials for nonthermal photoactivated shape changing, transformation, and self-healing applications.

Cadherin-11 is inactivated due to promoter methylation and functions in colorectal cancer as a tumour suppressor.

Background: The cadherin-11 (CDH11, OB-cadherin) gene is a member of the cadherin family and is located on chromosome 16q22.1. Previous studies have revealed that cadherins play significant roles in the development of many human malignancies. Increasing evidence has identified CDH11 as a functional tumour suppressor, which is commonly silenced by promoter methylation, but the functions of this gene in colorectal cancer (CRC) have been unclear. Methods: The CDH11 expression in primary CRC tissues and cell lines was investigated by qRT-PCR, RT-PCR and immunohistochemistry. The promoter methylation status of CDH11 was measured by methylation-specific PCR (MSP). Cell proliferation assay, colony formation assay, flow cytometry analysis, wound-healing assay, transwell assay and in vivo experiments were used to investigate the function of CDH11 in CRC. The mechanisms of CDH11 also were explored by western blots. Results: Our study suggests that CDH11 downregulation in CRC due to its promoter methylation and induced cell cycle arrest in G0/G1 phase and apoptosis, suppressing tumor cell proliferation, colony formation, migration and invasion by affecting the NF-kB signaling pathway. Conclusion: Overall, CDH11 may be considered as a functional tumour suppressor gene (TSG) in CRC, CDH11 has the potential to serve as a valuable prognostic marker for colorectal cancer.

Expression patterns of E2F transcription factors and their potential prognostic roles in breast cancer.

E2Fs, as a family of pivotal transcription factors, have been implicated in multiple biological functions in human cancer; however, the expression and prognostic significance of E2Fs in breast cancer remains unknown. In the present study, the mRNA expression patterns of E2Fs in breast cancer were investigated with Oncomine and The Cancer Genome Atlas data. Prognostic values of E2Fs for patients with breast cancer were determined using the Kaplan-Meier plotter database. The results strongly indicated that E2F1, E2F2, E2F3, E2F5, E2F7 and E2F8 were overexpressed in patients with breast cancer, whereas E2F4 and E2F6 exhibited no expression difference between patients with cancer and healthy controls. In survival analyses, elevated E2F1, E2F3, E2F5, E2F7 and E2F8 expression levels were significantly associated with lower overall survival, relapse-free survival (RFS), distant metastasis-free survival (DMFS) or post-progression survival for patients with breast cancer. Furthermore, high expression of E2F4 indicated improved RFS but reduced DMFS. Subgroup analyses based on four clinicopathological factors further revealed that E2Fs were associated with the prognosis of patients with breast cancer in an estrogen receptor-, progesterone receptor-, human epidermal growth factor 2- and lymph node status-specific manner. These data indicated that E2Fs may serve as promising biomarkers and therapeutic targets for breast cancer.

Zinc-finger protein 545 is inactivated due to promoter methylation and functions as a tumor suppressor through the Wnt/ß-catenin, PI3K/AKT and MAPK/ERK signaling pathways in colorectal cancer.

The transcription factor, zinc-finger protein 545 (ZNF545), that belongs to the Kruppel-associated box zinc-finger protein (KRAB-ZFP) family, acts as a tumor suppressor and is inactivated by promoter methylation in cancers such as nasopharyngeal carcinoma, breast cancer, and gastric cancer, but its role in colorectal cancer (CRC) is unknown. The purpose of this study was to characterize the ZNF545 expression, methylation status, biological function, and related molecular mechanisms in CRC. The results showed that ZNF545 was expressed in adult normal colorectal tissues, but downregulated or silenced in CRC cell lines, and this mechanism was reversed by demethylation treatment with 5-aza-2'-deoxycytidine and trichostatin A. The results also showed that the expression of ZNF545 in primary CRC tissues was significantly downregulated compared to adjacent tissues (p<0.05). Overexpression of ZNF545 caused CRC cell cycle arrest and apoptosis, suppressed cell proliferation, and suppressed colony formation and migration in vitro, showing that ZNF545 can function as a tumor suppressor. This function was also shown in nude mice. Furthermore, Wnt/ß­catenin, phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT), and mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) signaling pathways participated in the regulation of ZNF545 in CRC cells. Together, the results suggested that ZNF545 functions as a tumor suppressor in CRC and is frequently inactivated by promoter methylation.

The transcription levels and prognostic values of seven proteasome alpha subunits in human cancers.

Proteasome alpha subunits (PSMAs) have been shown to participate in the malignant progression of human cancers. However, the expression patterns and prognostic values of individual PSMAs remain elusive in most cancers. In the present study, we investigated the mRNA expression levels of seven PSMAs in different kinds of cancers using Oncomine and The Cancer Genome Atlas (TCGA) databases. The prognostic significance of PSMAs was also determined by Kaplan-Meier Plotter and PrognScan databases. Combined with Oncomine and TCGA, the mRNA expression levels of PSMA1-7 were significantly upregulated in breast, lung, gastric, bladder and head and neck cancer compared with normal tissues. Moreover, only PSMA6 and PSMA5 were not overexpressed in colorectal and kidney cancer, respectively. In survival analyses based on Kaplan-Meier Plotter, PSMA1-7 showed significant prognostic values in breast, lung and gastric cancer. Furthermore, potential correlations between PSMAs and survival outcomes were also observed in ovarian cancer, colorectal cancer and melanoma by Kaplan-Meier Plotter and PrognScan. These data indicated that PSMAs might serve as novel biomarkers and potential therapeutic targets for multiple human cancers. However, further studies are needed to explore the detailed biological functions and molecular mechanisms involved in tumor progression.

Epigenetic identification of ZNF545 as a functional tumor suppressor in multiple myeloma via activation of p53 signaling pathway.

The KRAB-zinc-finger protein ZNF545 was recently identified as a potential suppressor gene in several tumors. However, the regulatory mechanisms of ZNF545 in tumorigenesis remain unclear. In this study, we investigated the expression and roles of ZNF545 in multiple myeloma (MM). ZNF545 was frequently downregulated in MM tissues compared with non-tumor bone marrow tissues. ZNF545 expression was silenced by promoter methylation in MM cell lines, and could be restored by demethylation treatment. ZNF545 methylation was detected in 28.3% of MM tissues, compared with 4.3% of normal bone marrow tissues. ZNF545 transcriptionally activated the p53 signaling pathway but had no effect on Akt in MM, whereas ectopic expression of ZNF545 in silenced cells suppressed their proliferation and induced apoptosis. We therefore identified ZNF545 as a novel tumor suppressor inhibiting tumor growth through activation of the p53 pathway in MM. Moreover, tumor-specific methylation of ZNF545 may represent an epigenetic biomarker for MM diagnosis, and a potential target for specific therapy.