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SUMMARY OBJECTIVE To report the surgical procedures and efficacy of using medial plantar venous flap for the repair of soft tissue defects of the fingers. Methods From March 2010 to April 2012, medial plantar venous flaps were harvested to repair the wounds of 31 fingers in 29 cases. Among them, there were 13 middle fingers with defects at the tips in 11 cases, 7 fingers with defects in the dorsal part in 7 cases, and 11 fingers with defects in the finger pulp in 11 cases. The size of the defects ranged from 1.2cm×1.5 cm to 2.5cm × 3.5cm. Medial plantar venous flaps of 1.5cm × 2cm – 3×4 cm were harvested. Full-thickness skin grafts were adopted for the donor areas. RESULTS All 31 flaps survived, except for 1 flap with arterial crisis and 2 cases with venous crisis. These conditions were timely corrected by secondary anastomosis of artery and vein and the flaps survived. The wounds and the donor areas achieved healing by the first intention. All grafted skins survived. Postoperative follow-up was conducted for 26 fingers in 24 cases for 4-12 months, excluding 5 cases with lost follow-up. The dorsal part of the damaged fingers had normal morphology, and the skin color and texture were similar to those of the normal skin. After the repair of defects in the fingertip and pulp, fingerprints appeared, and the protective sensation was restored. CONCLUSION The soft tissue defects of the fingers can be satisfactorily repaired with medial plantar venous flap, and little damage is caused to the donor area. This method is proven effective for the repair of soft tissue defects of the fingers.

Objective. To investigate the effects of berberine (Berb) on dexamethasone- (Dex-) induced injury of human tendon cells and its potential mechanism. Methods. CCK-8 assay was used to explore the appropriate concentration of Dex-induced injury of tendon cells and the doses of Berb attenuates Dex cytotoxicity; cell wound healing assay was used to detect the effects P < 0.05 of Berb and Dex on the migration ability of tendon cells; flow cytometry was used to measure cell apoptosis; DCF DA fluorescent probe was used to measure the ROS activity of cells. Western blotting was used to detect the expression of phenotype related factors including smooth muscle actin α (SMA-α), type I collagen (Col I), col III, apoptosis-related factors, caspase-3, cleaved caspase-3, caspase-9, cleaved caspase-9, and PI3K/AKT. Results. CCK-8 assay showed that 1–100 μM Dex significantly inhibited the proliferation of tendon cells in a concentration-dependent manner P < 0.05 , where the inhibitory effect of 100 μM Dex was most significant P < 0.005 , and the pretreatment of 150, 200 μM Berb could reverse those inhibitions (all P < 0.05 ). Compared with the control group, Dex significantly inhibited cell migration P < 0.05 , while Berb pretreatment could enhance cell migration P < 0.05 . Flow cytometry and ROS assay showed that Dex could induce apoptosis and oxidative stress response of tendon cells (all P < 0.05 ), while Berb could reverse those responses P < 0.05 . Western blot showed that Dex could inhibit the expression of the col I and III as well as α-SMA (all P < 0.05 ) and enhance the expression of apoptosis-related factors including cleaved caspase-3 and cleaved caspase-9 (all P < 0.05 ). Besides, Dex could also inhibit the activation of the PI3K/AKT signaling pathway (all P < 0.05 ), thus affecting cell function, while Berb treatment significantly reversed the expression of those above proteins (all P < 0.05 ). Conclusion. Berb attenuated DEX induced reduction of proliferation and migration, oxidative stress, and apoptosis of tendon cells by activating the PI3K/AKT signaling pathway and regulated the expression of phenotype related biomarkers in tendon cells. However, further studies are still needed to clarify the protective effects of Berb in vivo.

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Objective. To investigate the effect of Mn3O4 nanoparticles (Mn3O4NPs) on inflammatory factors induced by lipopolysaccharide (LPS) in human tendon cells and its mechanism. Methods. The Mn3O4NPs were synthesized by a hydrothermal method. RT-qPCR was used to detect the expression levels of miRNAs related to inflammation in human tendon cells. The expression level of NLRP1 (NOD-like receptor containing pyrin domain 1) was measured by Western blotting. ELISA assay was used to measure the level of TNF-α, IL-1β, IL-4, and IL-10. The relationship between miR-181a-5p and NLRP1 was verified by dual-luciferase reporter assay. Results. Mn3O4NPs produced in this study were brown spherical particles with an average size of 7-10 nm. Mn3O4NP treatment significantly reduced the levels of TNF-α and IL-1β but increased the levels of IL-4 and IL-10 in the human tendon cells induced by LPS. In addition, Mn3O4NP treatment remarkably increased the expression level of miR-181a-5p. NLRP1 is one of the targets of miR-181a-5p, and miR-181a-5p downregulated its expression. Further study showed that Mn3O4NPs could alleviate the inflammatory response of human tendon cells induced by LPS by upregulating miR-181a-5p and thus downregulating the expression of NLRP1. Conclusion. Mn3O4NPs affect the expression of inflammatory cytokines in the human tendon cells induced by LPS by modulating the molecular axis of miR-181a-5p/NLRP1.