Objective: This study aims to investigate the research status and hotspots of surgical treatment for tremor in Parkinson’s disease (PD) from 2002 to 2022, utilizing bibliometric and visual analysis. Additionally, it aims to offer insights into future research trends in this field.Methods: This study collected publications on the surgical treatment of tremor in PD from 2002 to 2022 using the Web of Science (WOS) database. CiteSpace, VOSviewer, and Scimago Graphica were employed to quantify the number of publications and analyze the bibliographic information networks, including the contributions of countries/cities, authors, keywords, and co-cited references.Results: A total of 2,815 publications were included in the study, revealing that 541 scientific institutions experienced an increase in publications from 2002 to 2022. Michael Okun emerged as the most productive author, and the United States emerged as the leading hub for research. The study identified 772 keywords. Noteworthy citation bursts and long-term activity were observed in pallidotomy, bilateral stimulation, and focused ultrasound thalamotomy. The top 10 highly co-cited references comprised eight deep brain stimulation (DBS) studies (including two follow-up studies and six randomized controlled trials), one randomized controlled trial on focused ultrasound, and one consensus on tremor.Conclusion: This study uses an in-depth and systematic bibliometric and visualization analysis to visualize the evolution of research and identify emerging hotspots. The identified hotspots are as follows: Firstly, DBS has received significant attention and widespread recognition as a surgical treatment for tremor in PD. Secondly, there are various key aspects to consider in DBS, such as operative indications, operative targets, and surgical protocols. Lastly, magnetic resonance-guided focused ultrasound (MRgFUS) has emerged as a promising treatment option in the surgical management of tremor in Parkinson’s disease. This research also provides insights into the phenomenon of these hotspots, offering valuable prompts and reminders for further research.

Background. Inflammatory bowel disease (IBD) is becoming a global disease. A percentage of IBD patients will not react to therapy or will lose their response. Qu-Yu-Jie-Du Decoction (QYJD) is a traditional Chinese medicine formula commonly used for intestinal diseases. It has been reported that QYJD has an anti-inflammatory effect, but the mechanism is not fully understood. In this study, we mainly evaluated the anti-inflammatory effect of QYJD and explored the possible mechanisms. Methods. Twenty-four BALB/c mice were randomly divided into 4 groups according to their body weight, namely, the control group, the dextran sulfate sodium (DSS) group, the DSS+QYJD group, and the QYJD group. Mice were given 3 DSS drinking water freely, and at the same time, mice were given normal saline or QYJD (4.44mg/g/d), respectively. Mental state, faeces, and weight were recorded every day. On the 10th day, the mice were sacrificed and collected for investigation. The length of the mice colon was measured. Histological analysis was used to detect the morphological changes in the colon. Immunohistochemistry was used to measure the infiltration of macrophages (F4/80, CD163) and neutrophils (Ly6G). Colorimetry was used to detect the myeloperoxidase (MPO) activity of colon tissues. ELISA was utilized to detect associated inflammatory cytokines and chemokines in colon tissues. Results. QYJD alleviated the weight loss and colitis symptoms of mice caused by DSS. QYJD fought against the shortening of the intestine caused by DSS; that is, it improved the decline of intestinal compliance in mice and had a protective effect on colon tissues. The mechanisms were related to downregulating macrophages and neutrophils in colon tissues of infiltration. Besides, QYJD simultaneously reduced the activity of myeloperoxidase activity (MPO) and the contents of IL-1β, IL-6, TNF-α, TGF-β, CCL2, and CXCL2 in colon tissues. Conclusions. QYJD can ameliorate DSS-induced colitis in mice and the mechanism is connected with a reduction in neutrophil and macrophage infiltration.