Formation Mechanism of Microbial Diversity in Artificial Intelligence Devices due to Intermediate Disturbance by Low-Dose UV Radiation for Complementary Medicine.

The development of artificial intelligence devices in the complementary medicine field is rapid and the surface microbial diversity pollution was found with periodic low-dose ultraviolet radiation (LDUVR). Since artificial intelligence devices do not have enough different types of substrates for microbial communities, it is unclear how the great microbial diversity can emerge and persist, as this clearly defies the competitive exclusion principle of ecology. In this study, the 5 most common genera in the artificial intelligence devices, Escherichia, Pseudomonas, Streptococcus, Staphylococcus and Aeromonas have been sampled without and with periodic LDUVR, respectively. A new hypothesis was put up to clarify the construction and maintenance process of high microbiological diversity in artificial intelligence devices by comparing and evaluating the variations between the dynamic response characteristics of their relative abundances in the two scenarios as follows: the periodic LDUVR can be regarded as an adverse factor with intermediate disturbance, causing stronger microbial stochastic growth responses (SGR) which would inevitably give rise to stronger random variation of the other important processes tightly correlated with SGR, such as intra- and interspecific competition process, and substrates production and consumption process, which could effectively diminish the auto- and cross-correlation of stochastic processes of microbial populations, alleviating the intra- and inter-specific competitions. In artificial intelligence devices with LDUVR, these crucial succession processes can propel the microbial communities to generate and sustain a high species diversity. Finally, thorough Monte Carlo simulations were used to thoroughly confirm the idea. This research can build the theoretical groundwork, offer fresh viewpoints, and suggest potential microbial prevention strategies for the succession of microbial communities in LDUVR.

[Matrine alleviates N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric mucosal damage in rats and its mechanism].

Objective To investigate the effect of matrine on gastric mucosal injury induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in rats and its mechanism. Methods A total of 75 Wister rats were randomly divided into a control group, a model group and three matrine-treated groups (100, 150 and 200 mg/kg). Except for the control group, the other groups were treated with MNNG to establish the models of gastric mucosal injury in the rats. After the models were successfully established, the rats in the three matrine-treated groups were administrated 100, 150, 200 mg/kg matrine, respectively, for successive 45 days. After the last administration, the body mass, daily intake of drinking water and dietary of rats were measured. And then the tissue samples were collected after the rats were sacrificed. The levels of interleukin 1ß (IL-1ß), IL-4, interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α) were measured by ELISA in gastric mucosa. HE staining was used to observe the pathological changes of gastric mucosa tissue. Immunohistochemical staining was performed to evaluate the expression of vascular endothelial growth factor C (VEGF-C) and vascular endothelial growth factor receptor 3 (VEGFR3) in gastric mucosa. The protein levels of Bcl2, BAX, caspase-3, cytochrome C (Cyt-C), Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor κB p65 (NF-κB p65) were determined by Western blotting. Results The body mass, daily intake of drinking water and dietary increased in matrine-treated rats in comparison with the model group. In addition, compared with the model group, matrine significantly reduced the expression levels of VEGF-C, VEGFR3, BAX, caspase-3, Cyt-C, TLR4, MyD88 and NF-κB p65, and increase Bcl2 protein level in the gastric mucosa tissues. Conclusion Matrine can reduce gastric mucosal damage induced by MNNG in rats, which is related to the down-regulation of VEGF-C/VEGFR3 and NF-κB/TLR4 signaling pathway.

Expression and clinical significance of autophagic protein LC3B and EMT markers in gastric cancer.

BACKGROUND AND AIM: Gastric cancer (GC) is a fatal malignancy with high rate of recurrence and metastasis. Here, we investigated the correlations between the expression of autophagic protein LC3B and 2 epithelial-mesenchymal transition-related proteins (E-cadherin and Vimentin) and the clinicopathological factors and prognosis of patients with GC. MATERIALS AND METHODS: The expression of LC3B, E-cadherin, and Vimentin in GC samples (110 cases) and paracarcinoma tissues (40 cases) was analyzed using the Oncomine databases and further detected by immunohistochemistry. The correlations among these markers expression and clinicopathological features in GC were analyzed. The patients were followed for survival analysis. RESULTS: Compared to the nontumor tissues, the expression of LC3B and Vimentin proteins were significantly elevated in GC tissues, but the E-cadherin expression was decreased (all p<0.05). Interestingly, LCB expression was positively correlated with Vimentin (r=0.320, p=0.001) and negatively associated with E-cadherin expression (r= -0.484, p<0.001) in GC. The expression of these markers was closely related to tumor differentiation, T classification, TNM stage, and lymph node metastasis (all p<0.05). Furthermore, survival analyses and screening Kaplan-Meier plotter database revealed that GC patients with high LC3B and Vimentin expression levels had a poorer clinical outcome than those with low expression. Conversely, high E-cadherin expression was linked with favorable overall survival (all p<0.05, log-rank test). Multivariate survival analysis demonstrated that LC3B, E-cadherin, and Vimentin expression were independent prognostic factors of GC patients. CONCLUSION: LC3B, E-cadherin, and Vimentin may play an important role in the tumorigenesis of GC, and these marker expressions may serve as additional prognostic indicators for overall survival of patients. The interactions of autophagy and epithelial-mesenchymal transition in GC merits further investigation.