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AIMTo assess the role of three-dimensional endoanal ultrasound (3D-EAUS) for morphological assessment of the anal sphincter of female patients with chronic proctalgia (CP).METHODSIn this unmatched case control study, 30 consecutive female patients with CP and 25 normal women (control group) were enrolled. 3D-EAUS was performed in all subjects. Thickness and length of internal anal sphincter (IAS), thickness of puborectalis muscle (PR), length of the external anal sphincter (EAS) plus PR, and puborectalis angle were measured and compared between the two groups.RESULTSPatients with CP had significantly shorter IAS length and greater PR thickness, as compared to those in normal individuals (26.28 ± 3.59 mm vs 28.87 ± 4.84 mm, P < 0.05 and 9.67 ± 1.57 mm vs 8.85 ± 0.97 mm, P < 0.05, respectively). No significant between-group differences were observed with respect to IAS thickness and the EAS plus PR length (P > 0.05). Puborectalis angle in the CP group was significantly decreased, both in resting (88.23° ± 1.81° vs 89.94° ± 2.07° in control group, P < 0.05) and straining (88.47° ± 3.32° vs 90.72° ± 1.87° in control group, P < 0.05) phases, which suggest the presence of paradoxical contraction of PR in patients with CP. In the CP group, no significant difference in puborectalis angle was observed between the resting and straining phases (88.23° ± 1.81° vs 88.47° ± 3.32° respectively, P > 0.05).CONCLUSIONThe association of greater PR thickness and paradoxical contraction of PR with CP suggest their potential value as markers of CP.

Background Caudatin is extracted from radix cynanchi bungei and has an inhibitory effect on cancer progression. The study aims to reveal the impacts of hsa_circ_0060927 on Caudatin‐mediated colorectal cancer (CRC) development and the underneath mechanism. Methods The expression levels of hsa_circ_0060927, microRNA‐421 (miR‐421) and miR‐195‐5p were detected by quantitative real‐time reverse transcription‐polymerase chain reaction. The protein expression was analyzed by Western blot or immunohistochemistry assay. Cell viability and proliferation were analyzed by 3‐(4,5)‐dimethylthiahiazo (‐z‐y1)‐3,5‐di‐phenytetrazoliumromide or 5‐Ethynyl‐29‐deoxyuridine assay. Cell apoptosis was quantified by flow cytometry analysis. Cell migration and invasion were investigated by transwell assay. The putative associations among hsa_circ_0060927, miR‐421 and miR‐195‐5p were predicted by the starbase online database, and identified by dual‐luciferase reporter, RNA pull‐down and RNA immunoprecipitation (RIP) assays. The impacts of Caudatin treatment on tumor growth in vivo were revealed by a xenograft tumor model assay. Results Hsa_circ_0060927 expression was significantly upregulated, whereas miR‐421 and miR‐195‐5p were downregulated in CRC tissues and cells compared with control groups. Hsa_circ_0060927 expression was closely associated with lymph node metastasis and tumor‐node‐metastasis stage. Caudatin treatment significantly decreased hsa_circ_0060927 expression but increased miR‐421 and miR‐195‐5p expression. Caudatin exposure suppressed CRC cell proliferation, migration and invasion, and induced cell apoptosis; however, hsa_circ_0060927 overexpression hindered these impacts. Additionally, hsa_circ_0060927 was associated with miR‐421/miR‐195‐5p. Depletion of miR‐421 or miR‐195‐5p attenuated the influences of hsa_circ_0060927 silencing on CRC development. Furthermore, Caudatin treatment repressed tumor growth in vivo. Conclusion Caudatin inhibited CRC cell malignancy through the hsa_circ_0060927/miR‐421/miR‐195‐5p pathway, which provided a potential therapeutic agent for CRC.

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