Objective Uterine intravenous leiomyomatosiswas a rare type of uterus tumors.Because of the lack of knowledge about the ultrasonic patterns of this kind of disease,misdiagnosis frequently happens.Reviewing the cases and relevant researcheswas helpful to understand the disease and figure it out inultrasonic images.Methods Six cases of patients with uterine intravenous leiomyomatosis were reviewed which werehospitalized in Beijing Obstetrics and Gynecology Hospital during 2014 to 2016.All of the patients underwentultrasound examinations before surgery.The ultrasound findings,clinical presentations and pathological features of the 6 patients were evaluated.Results In 6 patients with uterine intravenous leiomyomatosis,3 cases were solid tumors,located in the cervix region and para uterine region,withirregular veinvascular inside;3 cases performance as multiple tumorlocated in dilated uterine vein,active tumor embolus were found in inferior vena cavain one of the 3 cases.Conclusions Uterine intravenous leiomyomatosisis found to be a solid mass located in the cervix region and para uterine region.The internal fissure of solid tumor is an important feature.Tumor extending to the iliac vein and inferior vena cava in some cases.Thusit is hard to be diagnosed before surgery by ultrasonography.Moreover,transvaginal ultrasound combined with inferior vena cava ultrasonography and echocardiography has a more obvious advantage in the diagnosis of the uterine intravenous leiomyomatosis.

Objective: In this study, we used HepG2 human hepatocellular carcinoma cells to study the effects of Compound Xishu Granule (CXG) on cell proliferation, apoptosis, and the cell cycle in vitro. We also used a xenograft tumor model to study the anti-tumor effects of CXG and related mechanisms in vivo.Methods: The effect of CXG on cell viability was measured using Cell Counting Kit-8 and a colony for-mation assay. The effect of CXG on apoptosis and the cell cycle was analyzed using flow cytometry. The in vivo anti-tumor effect of CXG was assessed by measuring the volume change in xenograft tumors after drug administration. The CXG anti-tumor mechanism was studied using western blotting assay to detect cell cycle and apoptotic associated proteins. Results: CXG suppressed HepG2 cell proliferation in a time-and dose-dependent manner in vitro. Colony formation experiments showed that CXG administration for 24 h significantly reduced HepG2 cell for-mations (P<.01). Flow cytometric analysis showed that CXG treatment for 48 h promoted apoptosis and blocked HepG2 cells in the G2/M phase. Western blotting results showed that Bax was significantly up-regulated and Bcl-2 was down-regulated in graft tumor tissues and HepG2 cells after CXG administra-tion, which increased the Bax/Bcl-2 ratio. PLK1, CDC25C, CDK1, and Cyclin B1 expression were up-regulated. CXG had a good inhibitory effect on graft tumor growth in vivo. Conclusion: CXG has good anti-tumor effects in vitro and in vivo. In vitro, CXG promoted HepG2 cell apoptosis and induced G2/M phase arrest. In vivo, CXG significantly inhibited graft tumor growth. The CXG mechanism in treating hepatocellular carcinoma may be that CXG can induce abnormal apoptotic and cell cycle associated protein expression, leading to mitotic catastrophe and apoptosis.

Background and purpose:Colorectal cancer(CRC)is one of the major malignant tumors threatening human health worldwide,with long-term high incidence and mortality rate.Potassium channel modulatory factor 1(KCMF1)is a member of the E3 ubiquitin ligase family.It binds to target proteins through the RING domain and participates in the regulation of a variety of biological processes in vivo.However,the function of KCMF1 in CRC remains unclear.This study aimed to investigate the expression level of E3 ubiquitin ligase KCMF1 in colorectal tumor,and to explore the effects of KCMF1 on the proliferation of CRC cells and its underlying molecular mechanism.Methods:The The Cancer Genome Atlas(TCGA)and Genotype-Tissue Expression(GTEx)databases were used to analyze the expression level of KCMF1 in CRC tissues and adjacent tissues and the association between the KCMF1 expression and the prognosis of CRC patients.Furthermore,immunohistochemical staining was performed to detect the protein level of KCMF1 in 90 paired human CRC tissues and adjacent non-tumor tissues.Lentiviral shRNA delivery system was employed to specifically target the KCMF1 gene(shKCMF1)in HCT116 and HCT15 CRC cell lines.The effects of KCMF1 knockdown on cell proliferation,apoptosis and cell cycle distribution were assessed by methyl thiazoyl terazolium(MTT)assay,colony formation assay,Western blot and flow cytometry.Changes in the transcriptional profile in HCT116 cells upon KCMF1 knockdown were identified by RNA sequencing(RNA-Seq),and the affected signaling pathways were evaluated by bioinformatics analysis.Real-time fluorescence quantitative polymerase chain reaction(RTFQ-PCR),Western blot,luciferase reporter assay and cell immunofluorescence assay were utilized to validate the alteration of the affected signaling pathway.Results:The TCGA and GTEx databases and IHC results showed that the mRNA and protein expression levels of KCMF1 in CRC tissues were significantly upregulated compared with adjacent tissues(P＜0.01).KCMF1 expression level was negatively correlated with the survival time of patients with CRC(P＜0.01),and was positively associated with CRC clinical stage(P＜0.05).Compared with control cells,KCMF1 knockdown significantly inhibited the proliferation of HCT116 and HCT15 cells(P＜0.001),induced cell apoptosis(P＜0.001),and led to cell cycle arrest in G1 phase(P＜0.01).RNA-Seq analysis showed that KCMF1 was involved in the regulation of several signaling pathways,including nuclear factor-κB(NF-κB)signaling pathway.KCMF1 knockdown reduced the transcription levels of the target genes of NF-κB signaling pathway,including BCL-XL,XIAP and CIAP(P＜0.05),and suppressed the expression of phosphorylated p65 and nuclear translocation of p65(P＜0.01).Meanwhile,the activity of NF-κB reporter was reduced in tumor cells upon KCMF1 knockdown(P＜0.01).Conclusion:The expression of KCMF1 is significantly upregulated in human CRC tissues and positively associated with advanced clinical stage and poor prognosis.KCMF1 may promote the proliferation of CRC cells by activating the NF-κB signaling pathway.KCMF1 may be a potential new therapeutic target for CRC.

Shengyang Yiweitang is one of the first 100 classical prescriptions published by the National Administration of Traditional Chinese Medicine. It originated from the Clarifying Doubts about Damage from Internal and External Causes by physician LI Dongyuan of Jin dynasty， and is composed of Astragali Radix， Ginseng Radix et Rhizoma， Glycyrrhizae Radix et Rhizoma， Atractylodis Macrocephalae Rhizoma， Poria， Pinelliae Rhizoma， Citri Reticulatae Pericarpium， Angelicae Pubescentis Radix， Saposhnikoviae Radix， Notopterygii Rhizoma et Radix， Bupleuri Radix， Paeoniae Radix Alba， Alismatis Rhizoma， and Coptidis Rhizoma. With the effects of replenishing Qi， promoting Yang， clearing heat and removing dampness， Shengyang Yiweitang is used to treat spleen-stomach weakness and dampness-heat accumulation syndrome. Using bibliometrics， the authors systematically sorted out the source，composition， dosage， preparation， efficacy， indications， principle of composition， origin and processing of drugs，and modern clinical application of the prescription， and explored its history and key information. Additionally， it was found that Shengyang Yiweitang was widely used in modern clinical practice and was suitable for multisystem diseases， of which digestive system （264） was the most common， accounting for 41.71%， followed by urogenital system （57， 9.00%） and nervous system （48， 7.58%）. Although the treatment scope was wide， the pathogenesis of the diseases in traditional Chinese medicine belongs to "spleen-stomach weakness"， which fully reflected Li's academic thought of "internal injury of spleen and stomach leads to various diseases". The key information of Shengyang Yiweitang was determined by summarizing the relevant ancient books and modern literature， so as to provide accurate reference for its rational clinical application and further research and development.