Objective To analyze the CT features of intestinal tumor obstruction, and explore its CT value.Methods CT manifestation and clinical materials of intestinal tumor obstruction proved by surgical findings or endoscopy biopsy in 35 cases were analyzed restrospectively, and compared with the results of surgery-pathology and endoscopy. Results CT findings were consistence with the results of surgery-pathology and endoscopy in 33 of 35 cases. The CT diagnostic accuracy of intestinal obstruction was 100%. And the accuracy of the cause was 94%, including colon carcinoma in 25, lyphoma in 5, gastrointestinal stromal tumor in 2, and lipoma in 3.Conclusion CT has unique advantage in examining intestinal tumor obstruction, not only for definiting the existence of the obstruction, but also locating the site of obstruction diagnosing the cause and chosing the appropriate treatment.

Liver fibrosis is primarily driven by the activation of hepatic stellate cells(HSCs),a process associated with ferroptosis.Ginsenoside Rb1(GRb1),a major active component extracted from Panax ginseng,inhibits HSC activation.However,the potential role of GRb1 in mediating HSC ferroptosis remains un-clear.This study examined the effect of GRb1 on liver fibrosis both in vivo and in vitro,using CCl4-induced liver fibrosis mouse model and primary HSCs,LX-2 cells.The findings revealed that GRb1 effectively inactivated HSCs in vitro,reducing alpha-smooth muscle actin(a-SMA)and type Ⅰ collagen(Col1A1)levels.Moreover,GRb1 significantly alleviated CCl4-induced liver fibrosis in vivo.From a mechanistic standpoint,the ferroptosis pathway appeared to be central to the antifibrotic effects of GRb1.Specifically,GRb1 promoted HSC ferroptosis both in vivo and in vitro,characterized by increased glutathione depletion,malondialdehyde production,iron overload,and accumulation of reactive oxygen species(ROS).Intriguingly,GRb1 increased Beclin 1(BECN1)levels and decreased the System Xc-key subunit SLC7A11.Further experiments showed that BECN1 silencing inhibited GRb1-induced effects on HSC ferroptosis and mitigated the reduction of SLC7A11 caused by GRb1.Moreover,BECN1 could directly interact with SLC7A11,initiating HSC ferroptosis.In conclusion,the suppression of BECN1 counteracted the effects of GRb1 on HSC inactivation both in vivo and in vitro.Overall,this study highlights the novel role of GRb1 in inducing HSC ferroptosis and promoting HSC inactivation,at least partly through its modulation of BECN1 and SLC7A11.