Severe fever with thrombocytopenia syndrome virus trends and hotspots in clinical research: A bibliometric analysis of global research.

Background: Since severe fever with thrombocytopenia syndrome virus (SFTSV) was first reported in 2009, a large number of relevant studies have been published. However, no bibliometrics analysis has been conducted on the literature focusing on SFTSV. This study aims to evaluate the research hotspots and future development trends of SFTSV research through bibliometric analysis, and to provide a new perspective and reference for future SFTSV research and the prevention of SFTSV. Methods: We retrieved global publications on SFTSV from the Web of Science Core Collection (WoSCC) and Scopus databases from inception of the database until 2022 using VOSviewer software and CiteSpace was used for bibliometric analysis. Results: The number of SFTSV-related publications has increased rapidly since 2011, peaking in 2021. A total of 45 countries/regions have published relevant publications, with China topping the list with 359. The Viruses-Basel has published the most papers on SFTSV. In addition, Yu et al. have made the greatest contribution to SFTSV research, with their published paper being the most frequently cited. The most popular SFTSV study topics included: (1) pathogenesis and symptoms, (2) characteristics of the virus and infected patients, and (3) transmission mechanism and risk factors for SFTSV. Conclusions: In this study, we provide a detailed description of the research developments in SFTSV since its discovery and summarize the SFTSV research trends. SFTSV research is in a phase of explosive development, and a large number of publications have been published in the past decade. There is a lack of collaboration between countries and institutions, and international collaboration and exchanges should be strengthened in the future. The current research hotpots of SFTSV is antiviral therapy, immunotherapy, virus transmission mechanism and immune response.

Expression of p-STAT3 and vascular endothelial growth factor in MNNG-induced precancerous lesions and gastric tumors in rats.

AIM: To investigate the dynamic expression of p-signal transducer and activator of transcription 3 (STAT3) and vascular endothelial growth factor (VEGF) in the formation of gastric tumors induced by drinking water containing N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in Wistar rats. METHODS: One hundred and twenty Wistar rats were randomly divided into two groups (60 in each group): Control group and Model group. The rats in each group were then randomly divided into three groups (20 in each group): C/M15, C/M25 and C/M40 (15, 25 and 40 represent the number of feeding weeks from termination). Rats in the control group received normal drinking water and rats in the model group received drinking water containing 100 µg/mL MNNG. Stomach tissues were collected at the end of the 15(th), 25(th) and 40(th) week, respectively, for microscopic measurement using hematoxylin and eosin staining. The expression of p-STAT3 and VEGF in different pathological types of gastric tissue, including normal, inflammation, atrophy, hyperplasia and gastric stromal tumor, was observed by immunohistochemistry and Western blot, and the corelation between p-STAT3 and VEGF was analyzed. RESULTS: (1) The expression of p-STAT3 in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor were significantly increased in the model group compared with the control group (2.5 ± 1.0, 2.75 ± 0.36, 6.2 ± 0.45, 5.67 ± 0.55 vs 0.75 ± 0.36, P = 0.026, 0.035, 0.001, 0.002, respectively); the expression of p-STAT3 in tissue with dysplasia was higher than that in samples with gastritis or atrophy (6.2 ± 0.45 vs 2.5 ± 1.0, P = 0.006; 6.2 ± 0.45 vs 2.75 ± 0.36, P = 0.005, respectively); however, the expression of p-STAT3 in gastritis and atrophy was not significantly different (P > 0.05); (2) the expression of VEGF in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor was significantly increased in the model group compared with normal gastric mucosa; and the expression of VEGF in tissue with dysplasia was higher than that in tissue with inflammation and atrophy (10.8 ± 1.96 vs 7.62 ± 0.25, P = 0.029; 10.8 ± 1.96 vs 6.26 ± 0.76, P = 0.033, respectively); similarly, the expression of VEGF in tissue with gastritis and atrophy was not significantly different (P > 0.05); and (3) the expression of VEGF was positively correlated with p-STAT3. CONCLUSION: p-STAT3 plays an important role in gastric cancer formation by regulating the expression of VEGF to promote the progression of gastric tumor from gastritis.