The luminescent bacteria bioassay has been commonly used in the detection of environmental pollutants. Compared with traditional chemical and other biological detection methods, the luminescent bacteria bioassay has many demonstrated advantages such as a sensitive response, low cost, high efficiency, and environmental friendliness. The traditional luminescent bacteria bioassay has poor reproducibility and cannot achieve undisturbed soil testing, and the use of leach liquor also affects the results. This paper reviews the research progress and existing issues for the traditional luminescent bacteria bioassay used in the detection of soil pollutants. The luminescence mechanisms and detection principles of three commonly used luminescent bacteria, i.e., Vibrio fischeri, Photobacterium phosphoreum, and Vibrio qinghaiensis, are discussed and compared. In addition, two new luminescent bacteria bioassays are introduced to detect soil pollutants. One method is based on recombinant luminescent bacteria obtained with a gene-modification technique. This method can realize specific detection and enhance sensitivity, but it still cannot achieve undisturbed soil detection. The other method involves using magnetic nanoparticle (MNP)-based biosensors made from luminescent bacteria and MNPs. It can realize the accurate detection of the biological toxicity of the combined pollutants in soil without disturbing the soil’s integrity. This study shows that MNP-based biosensors have good application prospects in soil pollution detection, but the mechanism behind their utility still needs to be investigated to realize their popularization and application.
Background: Pancreatic cancer is an aggressive type of cancer with poor prognosis, short survival rate, and high mortality. Drug resistance is a major cause of treatment failure in the disease. MiR-331-3p has been reported to play an important role in several cancers. We previously showed that miR-331-3p is upregulated in pancreatic cancer and promotes pancreatic cancer cell proliferation and epithelial-to-mesenchymal transition–mediated metastasis by targeting ST7L. However, it is uncertain whether miR-331-3p is involved in drug resistance. Methods: We investigated the relationship between miR-331-3p and pancreatic cancer drug resistance. As part of this, microRNA mimics or inhibitors were transfected into pancreatic cancer cells. Quantitative polymerase chain reaction was used to detect miR-331-3p expression, and flow cytometry was used to detect cell apoptosis. The Cell Counting Kit-8 assay was used to measure the IC50 values of gemcitabine in pancreatic cancer cells. The expression of multidrug resistance protein 1, multidrug resistance-related protein 1, breast cancer resistance protein, β-Catenin, c-Myc, Cyclin D1, Bcl-2, and Caspase-3 was evaluated by Western blotting. Results: We confirmed that miR-331-3p is upregulated in gemcitabine-treated pancreatic cancer cells and plasma from chemotherapy patients. We also confirmed that miR-331-3p inhibition decreased drug resistance by regulating cell apoptosis and multidrug resistance protein 1, multidrug resistance-related protein 1, and breast cancer resistance protein expression in pancreatic cancer cells, whereas miR-331-3p overexpression had the opposite effect. We further demonstrated that miR-331-3p effects in drug resistance were partially reversed by ST7L overexpression. In addition, overexpression of miR-331-3p activated Wnt/β-catenin signaling in pancreatic cancer cells, and ST7L overexpression restored activation of Wnt/β-catenin signaling. Conclusions: Taken together, our data demonstrate that miR-331-3p contributes to drug resistance by activating Wnt/β-catenin signaling via ST7L in pancreatic cancer cells. These data provide a theoretical basis for new targeted therapies in the future.
Pathogenic E.coli was infused into the cavity of uterus by uterine horn cannulation in the experiment,and then a pathological model of endometritis was established.As a result,the E.coli just existed in the uterine veins blood for a short time.There were significant increase of WBC in the uterine veins blood and the jugular veins blood.Comparing with the jugular veins blood,there were more leukomonocytes and less neutrophils in the uterine veins blood.There was obvious lesion on the endometrium,and the uterine wall infiltrated with inflammatory cells,and the microvilli and cilia of endothelial cell exfoliated largely or partly.
Pancreatic cancer (PC) is a highly invasive tumor with a poor prognosis, short overall survival rate and few chemotherapeutic choices. Despite the importance of finding ways to treat pancreatic cancer, the mechanisms of tumor progression have not been fully elucidated. microRNA-455-3p (miR-455-3p) has been reported to play an important role in several cancers, but its function in pancreatic cancer remains unclear. To investigate the biological functions, miRNAs mimics or inhibitors were transfected into pancreatic cancer cells. Flow cytometry was used to detect cell apoptosis. Wound healing and Transwell assays were employed to observe cell invasion and migration abilities. The expression of Bcl-2, Bax, caspase-3, E-cadherin, N-cadherin, Snail, β-Catenin, c-Myc and Cyclin D1 were evaluated by qPCR and Western blot. We confirmed that inhibition of miR-455-3p decreases cell apoptosis and increases cell migration, invasion and EMT of pancreatic cancer, whereas forced overexpression of miR-455-3p has the opposite effect. Furthermore, we demonstrated that the tumor suppression effects of miR-455-3p were partially reversed by TAZ overexpression. In addition, miR-455-3p led to inactivation of Wnt/β-catenin signaling in pancreatic cancer cells, and TAZ overexpression restored the inhibition of Wnt/β-catenin signaling. Taken together, our data demonstrated that miR-455-3p functions as an important tumor suppressor that suppresses the Wnt/β-catenin signaling pathway via TAZ to inhibit tumor progression in pancreatic cancer. We conclude that the miR-455-3p/TAZ/Wnt axis may be a potential therapeutic target for pancreatic cancer.
Abstract Background Certain members of the Procollagen-lysine 2-oxyglutarate 5-dioxygenase (PLOD) family have been identified to play a role in tumor metastasis and progression. Materials & Methods The association between PLOD expression and overall survival (OS) rates was assessed utilizing the Kaplan-Meier survival curve. The correlation between gene expression and patient OS rate was determined utilizing a univariate or multivariate Cox proportional hazards regression model or log-rank test to evaluate the difference in OS rates. The infiltration levels of stromal cells and immune cells in different tumors were analyzed utilizing the stromal-immune-ESTIMATE score. Results Our results showed that PLOD1, PLOD2, and PLOD3 were predominantly upregulated in cancer cells, and the expression of PLOD family members frequently correlated with the OS of cancer patients. All PLOD genes exhibited significant associations with immune infiltration subtypes, as well as different levels of stromal cell infiltration and tumor cell stemness. Furthermore, our research demonstrated that the PLOD gene might contribute to drug resistance in cancer cells. Conclusion Our study indicated that PLOD was primarily associated with more aggressive cancer characteristics and potentially contributed to tumor metastasis and tumorigenesis, leading to a poorer prognosis.
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