Bibliometric insights into the evolution of uranium contamination reduction research topics: Focus on microbial reduction of uranium.

Confronting the threat of environment uranium pollution, decades of research have yielded advanced and significant findings in uranium bioremediation, resulting in the accumulation of tremendous amount of high-quality literature. In this study, we analyzed over 10,000 uranium reduction-related papers published from 1990 to the present in the Web of Science based on bibliometrics, and revealed some critical information on knowledge structure, thematic evolution and additional attention. Methods including contribution comparison, co-occurrence and temporal evolution analysis are applied. The results of the distribution and impact analysis of authors, sources, and journals indicated that the United States is a leader in this field of research and China is on the rise. The top keywords remained stable, primarily focused on chemicals (uranium, iron, plutonium, nitrat, carbon), characters (divers, surfac, speciat), and microbiology (microbial commun, cytochrome, extracellular polymeric subst). Keywords related to new strains, reduction mechanisms and product characteristics demonstrated the strongest uptrend, while some keywords related to mechanism and performance were clearly emerging in the past 5 years. Furthermore, the evolution of the thematic progression can be categorized into three stages, commencing with the discovery of the enzymatic reduction of hexavalent uranium to tetravalent uranium, developing in the groundwater remediation process at uranium-contaminated sites, and delving into the research on microbial reduction mechanisms of uranium. For future research, enhancing the understanding of mechanisms, improving uranium removal performance, and exploring practical applications can be considered. This study provides unique insights into microbial uranium reduction research, providing valuable references for related studies in this field.

Performance and mechanisms exploration of nano zinc oxide (nZnO) on anaerobic decolorization by Shewanella oneidensis MR-1.

Although the ecological safety of nanomaterials is of widespread concern, their current ambient concentrations are not yet sufficient to cause serious toxic effects. Thus, the nontoxic bioimpact of nanomaterials in wastewater treatment has attracted increasing attention. In this study, the effect of nano zinc oxide (nZnO), one of the most widely used nanomaterials, on the anaerobic biodegradation of methyl orange (MO) by Shewanella oneidensis MR-1 was comprehensively investigated. High-dosage nZnO (>0.5 mg/L) caused severe toxic stress on S. oneidensis MR-1, resulting in the decrease in decolorization efficiency. However, nZnO at ambient concentrations could act as nanostimulants and promote the anaerobic removal of MO by S. oneidensis MR-1, which should be attributed to the improvement of decolorization efficiency rather than cell proliferation. The dissolved Zn2+ was found to contribute to the bioeffect of nZnO on MO decolorization. Further investigation revealed that low-dosage nZnO could promote the cell viability, membrane permeability, anaerobic metabolism, as well as related gene expression, indicating that nZnO facilitated rather than inhibited the anaerobic wastewater treatment under ambient conditions. Thus, this work provides a new insight into the bioeffect of nZnO in actual environment and facilitates the practical application of nanomaterials as nanostimulants in biological process.

Shaoyao decoction attenuates DSS-induced ulcerative colitis, macrophage and NLRP3 inflammasome activation through the MKP1/NF-κB pathway.

BACKGROUND: Shaoyao decoction (SYD), a traditional Chinese medicine prescription that originated in the Jin-Yuan Dynasty, has shown effects in treating ulcerative colitis. However, the underlying mechanism is unclear. We combined network pharmacology with molecular biology technology to detect the mechanism underlying the effect of SYD on ulcerative colitis. We combined network pharmacology with molecular biology technology to detected the further mechanism in SYD effect on ulcerative colitis. PURPOSE: In this study, we investigated the mechanism by which SYD exerts a protective effect against ulcerative colitis in vivo and in vitro. STUDY DESIGN AND METHODS: We focused on two aspects of the mechanism by which SYD relieves ulcerative colitis, regulation of the MAPK cascade and the NF-κB signaling pathway, through analysis of the "active ingredient-target-disease" network followed by GO enrichment and KEGG pathway analysis according to network pharmacology. Mice with ulcerative colitis underwent 5% dextran sulfate sodium (DSS), and the RAW 264.7 cell model was used to identify important targets. RESULTS: We found that after 5% DSS treatment, the inflammation indexes and the expression of NLRP3-related proteins were increased concomitant with the loss of mucins and occludin. Treatment with SYD (2.25 g/kg, BW) significantly improved the expression of mucins and occludin after DSS at the protein and transcriptional levels. Furthermore, SYD treatment significantly reduced NF-κB P65 and P38 expression, thus exerting a great antinecrotic effect, as revealed by TUNEL staining and Western blotting. The beneficial effects of SYD were almost canceled by NSC 95397 (an inhibitor of mitogen-activated protein kinase phosphatase-1 (MKP1)) after DSS treatment in vivo or LPS treatment in vitro. In addition, treatment with SYD reduced caspase-1 activity and rescued the release of ASC and GSDMD, thus inhibiting the assembly of NLRP3 and maintaining the integrity of the intestinal barrier. We also conducted in vitro experiments in the LPS-induced RAW 264.7 cell model and found that cells incubated with 1 mg/ml SYD for 24 h possessed the highest cell viability. Next, we incubated 1 mg/ml SYD for 24 h after treatment with 1 µg/ml LPS for 6 h. We showed that 1 mg/ml SYD displayed anti-inflammatory and anti-necrotic effects through the NLRP3, NF-κB P65 and P38 pathways, and the effects of SYD were also inhibited by 10 nM NSC 95397. CONCLUSION: These results demonstrate that SYD has protective effects against ulcerative colitis and alleviates pyroptosis by inhibiting the MKP1/NF-κB/NLRP3 pathway.

MT-α-glucan from the fruit body of the maitake medicinal mushroom Grifola frondosa (higher Basidiomyetes) shows protective effects for hypoglycemic pancreatic ß-cells.

The hypoglycemic effect of an α-glucan (designated here as MT-α-glucan) from the fruit body of the Maitake medicinal mushroom, Grifola frondosa, on a murine type 2 diabetes mellitus (T2DM) model was evaluated. Body weight and levels of fasting plasma glucose, glycosylated hemoglobin, triglycerides, cholesterol, free fatty acid, nitric oxide (NO), NO synthase, inducible NO synthase, and hepatic malondialdehyde content decreased significantly when MT-α-glucan was administered to T2DM mice. The content of serum insulin, hepatic glycogen, and reduced glutathione and the activity of superoxide dismutase and glutathione peroxidase increased significantly when MT-α-glucan was administered to T2DM mice. Histopathological changes of the pancreas were ameliorated in the treatment group. These data suggest that MT-α-glucan has a hypoglycemic effect on T2DM mice, which might be related to its protective effect of pancreatic ß-cells exerted by decreasing levels of factors that destroy ß-cells, such as oxidative stress and NO synthesis.

Hypoglycemic and hypolipidemic activities of MT-α-glucan and its effect on immune function of diabetic mice.

The hypoglycemic and hypolipidemic effect of an α-glucan (designed here as MT-α-glucan) from fruit body of maitake (Grifola frondosa) on diabetic mouse model induced by streptozotocin and high-fat-diet were evaluated, and its effect on immune function of diabetic mice was investigated. Treatment with MT-α-glucan (300 or 100 mg kg(-1)) could decrease the levels of fasting plasma glucose, triglycerides, cholesterol, free fatty acid, the proliferative response of macrophages and IL-1, NO production by macrophages significantly. Treatment with MT-α-glucan could increase the serum insulin, the proliferative response and IL-2 production of splenocytes induced by ConA significantly. Ultrastructural changes of pancreatic ß-cells were ameliorated in the treatment group. These data suggest that MT-α-glucan has hypoglycemic and hypolipidemic effect on the diabetic mice model, which might be related to its benefit effect on immune reactions involved in pathogenesis of diabetes mellitus, leading to attenuate the degree of injured ß-cells of the pancreatic islets.