Objective To delineate the current research landscape,emerging hotspots,and frontiers re-garding the relationship between the oral microbiome and digestive system diseases.Methods We retrieved publications from the Web of Science Core Collection database using topic-specific queries on"oral microbi-ome"and"digestive diseases."Bibliometric analysis was performed using VOSviewer,CiteSpace,and the"bibliometrix"package in R for data mining and visualization.Results A total of 1228 eligible articles were included.Analysis revealed that research on the correlation between oral microbiota and digestive system diseases will remain a global hotspot.Academic institutions dominated the publications,with centralized institutional distribution and team-based collaboration,though overall collaboration networks remained fragmented.Geo-graphically,the United States emerged as the leading contributor,followed by China and the United Kingdom.While China-U.S.collaborations were prominent,China's engagement with other regions remained limited.Current research hotspots focus on the interplay between oral microbiota and gut microbiota,inflam-matory bowel disease(IBD),and digestive system tumors.Conclusions Research in this field demonstrates high activity and diversity.Studies on the associations of oral microbiota with gut microbiota,IBD,and diges-tive system tumors(particularly esophageal,gastric,pancreatic,and colorectal cancers)remain prominent.Future studies should prioritize elucidating underlying mechanisms and innovating in biomarker discovery and application.However,insufficient collaboration and resource-sharing among institutions currently hinder pro-gress in this field.

Objective To delineate the current research landscape,emerging hotspots,and frontiers re-garding the relationship between the oral microbiome and digestive system diseases.Methods We retrieved publications from the Web of Science Core Collection database using topic-specific queries on"oral microbi-ome"and"digestive diseases."Bibliometric analysis was performed using VOSviewer,CiteSpace,and the"bibliometrix"package in R for data mining and visualization.Results A total of 1228 eligible articles were included.Analysis revealed that research on the correlation between oral microbiota and digestive system diseases will remain a global hotspot.Academic institutions dominated the publications,with centralized institutional distribution and team-based collaboration,though overall collaboration networks remained fragmented.Geo-graphically,the United States emerged as the leading contributor,followed by China and the United Kingdom.While China-U.S.collaborations were prominent,China's engagement with other regions remained limited.Current research hotspots focus on the interplay between oral microbiota and gut microbiota,inflam-matory bowel disease(IBD),and digestive system tumors.Conclusions Research in this field demonstrates high activity and diversity.Studies on the associations of oral microbiota with gut microbiota,IBD,and diges-tive system tumors(particularly esophageal,gastric,pancreatic,and colorectal cancers)remain prominent.Future studies should prioritize elucidating underlying mechanisms and innovating in biomarker discovery and application.However,insufficient collaboration and resource-sharing among institutions currently hinder pro-gress in this field.

Colorectal cancer is a common clinical malignant tumor. As the main therapeutic method of colorectal cancer, radiotherapy has a good inhibitory effect on tumor progression. In recent years, because of its good physical and biological advantages, carbon ion has shown better clinical efficacy than traditional radiotherapy in the treatment of local recurrence or distant metastasis of colorectal cancer. In this article, basic and clinical studies related to the efficacy of carbon ion therapy for the recurrence of colorectal cancer in recent years were reviewed, aiming to provide theoretical basis for preventing and reducing adverse reactions after radiotherapy and prolonging the survival of colorectal cancer patients.

Objective To compare the effect of different size needle gauges to the degenerative response in rat caudal discs.Methods A total of 40 Sprague Dawley (SD) rats,level 5/6,7/8 and 9/10 interverbral discs of rat caudal spine were punctured with 18 or 21 or 25-gauge needles respectively.Radiographs and magnetic resonance imaging (MRI) were obtained at 1,2,4 and 6 weeks postsurgery.At each time point,ten rats from each group were sacrificed for histological analysis.Real-time fluorescent quantitative polymerase chain reaction (qPCR) was used to examine mRNA expression level.Results Significant differences were identified in the disc height index (DHI ％) and MRI grade between 18 G and normal group,MRI grade,histological score between 21 G and normal group at 2,4,and 6 weeks postsurgery.Significant differences were also identified in the histological score and mRNA expression levels between 18 G and normal group,alcian blue stain and hypoxia inducible factor-1α (HIF-1 α) mRNA expression level between 21G and normal group at all time point postsurgery.Significant differences existed in DHI％,type Ⅱ collagen and aggrecan mRNA expression levels between 21 G and normal group,all type mRNA expression levels between 25 G and normal group at 4,6 weeks.There were significant differences in MRI grade and histological score between 25 G and normal group at 6 weeks.Significant differences existed in almost all parameters compared between 18 G and 25 G at all time point.There were significant differences in DHI％,MRI grade,histological score and HIF-1α mRNA expression levels between 18 G and 21 G at 4,6 weeks.There were significant differences in type Ⅱ collagen and aggrecan mRNA expression levels between 18 G and 21 G at all time point.Significant differences exist in DHI％ and HIF-1α mRNA expression level between 21 G and 25 G at 6 weeks.Compared with the 25 G group,the DHI％ and Pfirrmann scores and the pathological score of each time at 2,4 and 6 weeks after operation in 18 G group have significant difference (P ＜ 0.05).Conclusions The middle size needle (21G) is better to induce disc degeneration.The 2-week time point may be the better time frame to further experimental treatments.

Objective To compare the clinical results of percutaneous endoscopic interlaminar discectomy (PEID) and percutaneous endoscopic transforaminal discectomy (PETD) in L5/S1 disc herniation.Methods A total of 102 patients with L5/S1 disc herniation in our hospital from September 2014 to June 2016 were enrolled in this study.Fifty-two patients underwent percutaneous endoscopic interlaminar discectomy (PEID group) and 50 patients underwent percutaneous endoscopic transforaminal discectomy (PETD group).The surgical effectiveness was assessed according to Visual Analog Scale (VAS),Oswestry Disability Index (ODI),and modified MacNab criteria.The frequencies of intraoperative radiation exposure,operation time and complication rates were compared between the groups.Results All the patients completed follow up with a mean of 15.0 months (range,10-20 months).In the PEID group,the mean operation time was 44-72 (58.3 ± 12.0)minutes and the intraoperative frequencies of radiation exposure were 3-6(3.8 ±2.1)seconds.For the PETD group,the mean operation time was 52-96(82.4 ± 16.0) minutes and the intraoperative radiation time was 13-34 (24.1 ± 10.1) seconds.There were significant differences in operation time and radiation frequency between the two groups (P ＜ 0.05).The postoperative VAS and ODI were obviously improved in both groups when compared with preoperation (P ＜ 0.05),but there were no significant differences between the two groups (P ＞ 0.05).There was no statistically significant difference considering the satisfactory rates according to the MacNab criteria between PEID group (96.1％) and PETD group (96.0％).Conclusions The treatment of L5/S1 disc herniation through lamina or intervertebral foramen approach is both effective.PEID can significantly reduce the frequencies of intraoperative radiation exposure and operation time.

Objective To explore the effect and mechanism of microRNA (miR)-17-5p on the invasion and metastasis of hepatocellular carcinoma (HCC) cells. Methods Expression of miR-17-5p in the normal human L-02 hepatocyte and QGY-7703 HCC cells was detected by RT-PCR. QGY-7703 HCC cells were transfected by miR-17-5p mimic and mimic control respectively. Influence of miR-17-5p on the invasion and metastasis ability of HCC cells was detected using Transwell assay and scratch test. Target gene of miR-17-5p was confirmed by bioinformatic analysis, and its expression in HCC cells was detected by Western blot. After siRNA silenced by target gene, the invasion and metastasis ability of HCC cells were observed. Comparison of microRNA in the two kinds of cells was conducted by t test. Results Expression level of miR-17-5p in HCC cells was 0.16±0.04, significantly lower than 1.01±0.19 in normal L-02 hepatocytes (t=-9.67, P<0.05). Number of trans-membrane cells and metastasis rate of HCC cells transfected by miR-17-5p mimic were respectively 36±4 and (5.37±0.15) mm/d, significantly lower than 62±7 and (7.50±0.01) mm/d of control group (t=-15.40, -32.00; P<0.05). Bioinformatic analysis showed that AKT3 was the key target gene of miR-17-5p, and the expression of AKT3 in HCC cells was obviously higher than that of normal hepatocyte. Number of trans-membrane cells and metastasis rate of HCC cells transfected by siRNA-AKT3 were respectively 13±3 and (4.13±0.15) mm/d, significantly lower than 58±3 and (7.23±0.25) mm/d of control group (t=-17.88, -53.69; P<0.05). Conclusion miR-17-5p inhibits the invasion and metastasis ability of HCC cells through targeting effect on AKT3.

BACKGROUND:Statins can promote the mRNA expression of bone morphogenetic protein 2, aggrecan and type II col agen in intervertebral disc cel s, and they also can reverse the phenotype of dedifferentiated nucleus pulposus cel s to slow disc degeneration process. OBJECTIVE:To review the research progress of simvastatin modulating the biological characteristics and mobilizing endogenous stem cel s for the repair of intervertebral disc degeneration. METHODS:The first author retrieved the PubMed and CNKI databases for relevant articles published before January 2016 using the key words of“disc degeneration factor, Simvastatin AND stem cel s, endogenous stem cel s AND disc degeneration”in English and Chinese, respectively. Initial y, 102 relevant articles were retrieved, but only 48 articles were included in result analysis fol owing elimination of duplicate studies.RESULTS AND CONCLUSION:By summarizing a large number of studies on the treatment of intervertebral disc degeneration worldwide, we found that simvastatin may modulate the biological characteristics and function of nucleus pulposus mesenchymal stem cel s via promoting the expression of hypoxia-inducible factor 1αfor the endogenous stem cel-based therapy of intervertebral disc degeneration.

Objective To establish a NOD/SCID mouse model with human immune reconstitution and observe its immune response to human triple-negative breast cancer xenograft. Methods Twenty-four NOD/SCID mice without immune leakage were subjected to cyclophosphamide (CTX) treatment 3 days prior to immune reconstitution with human peripheral blood mononuclear cell (PBMC) injection and subcutaneous transplantation of human triple-negative breast cancer MDA-MB-231 cells, CTX treatment and PBMC injection without tumor cell transplantation, MDA-MB-231 cell transplantation only, or no treatments. The tumor growth and immune responses of the mice were observed at regular intervals. Results Compared with the tumor-bearing mice, the tumor-bearing mice with immune reconstitution showed prolonged incubation period of tumor formation, slower tumor growth rate and increased survival rate. Human IgG and CD3+T cells were detected in the peripheral blood of the mice 1 week after human PBMC injection. The percentage of CD3+T cells in the spleen cells was 55.3%at 9 weeks in tumor-bearing mice with immune reconstitution and 52.7% in tumor-bearing mice without immune reconstitution. The spleen index of the tumor-bearing mice with immune reconstitution was much higher than that in mice with only immune reconstitution and the control mice (9.64 vs 3.82±0.31 and 1.51±0.14 mg/g). Conclusion A stable NOD/SCID mouse model with immune reconstitution has been established successfully, which shows immune responses to triple-negative breast cancer xenografts and allows studies of immunological therapy study of triple-negative breast cancer.

Objective To establish a NOD/SCID mouse model with human immune reconstitution and observe its immune response to human triple-negative breast cancer xenograft. Methods Twenty-four NOD/SCID mice without immune leakage were subjected to cyclophosphamide (CTX) treatment 3 days prior to immune reconstitution with human peripheral blood mononuclear cell (PBMC) injection and subcutaneous transplantation of human triple-negative breast cancer MDA-MB-231 cells, CTX treatment and PBMC injection without tumor cell transplantation, MDA-MB-231 cell transplantation only, or no treatments. The tumor growth and immune responses of the mice were observed at regular intervals. Results Compared with the tumor-bearing mice, the tumor-bearing mice with immune reconstitution showed prolonged incubation period of tumor formation, slower tumor growth rate and increased survival rate. Human IgG and CD3+T cells were detected in the peripheral blood of the mice 1 week after human PBMC injection. The percentage of CD3+T cells in the spleen cells was 55.3%at 9 weeks in tumor-bearing mice with immune reconstitution and 52.7% in tumor-bearing mice without immune reconstitution. The spleen index of the tumor-bearing mice with immune reconstitution was much higher than that in mice with only immune reconstitution and the control mice (9.64 vs 3.82±0.31 and 1.51±0.14 mg/g). Conclusion A stable NOD/SCID mouse model with immune reconstitution has been established successfully, which shows immune responses to triple-negative breast cancer xenografts and allows studies of immunological therapy study of triple-negative breast cancer.