Objective To study the lymphatic microvessel density of keloid and correlation of invasive growth.Methods Invasive part,proliferative part and peripheral normal skin of keloid patients (n=10) were collected by surgical excision,and normal skin of keloid and non-keloid patients as control.Lymphatic vessel density of different parts of keloid and normal skin were investigated by immunohistochemical staining using the lymphatic endothelium specific marker D2-40.Results There were no significant differences between lymphatic microvessel density of peripheral normal skin of keloid (12.563 ±1.803) n/mm2 and normal skin of non-keloid patients (11.071 ± 2.645) n/mm2 (t=1.389,P＞0.05); Lymphatic microvessel density of invasive part of keloid (27.315 ± 7.430) n/mm2 was significantly higher than those of proliferative part of keloid (17.375± 6.221) n/mm2 and normal skin (12.563±1.803) n/mm2 (x2 =16.8,P＜0.01); there were significant differences between proliferative parts of keloid and normal skin (t=2.276,P＜0.05).Conclusions Lymphatic microvessel density increase in the invasive part of keloid may have a certain relationship with invasive growth.

To introduce the diagnosis and treatment of one male case with accessory breast. The patient was a 27-year-old male. An additional nipple on the left posterior axillary line was found on birth, which enlarged and became darken since adolescence. The clinical diagnosis was accessory breast, and a complete surgical excision was performed. Pathological examination proved the diagnosis of accessory breast.

Tetrandrine(TET),a natural bisbenzyl isoquinoline alkaloid extracted from Stephania tetrandra S.Moore,has diverse pharmacological effects.However,its effects on melanoma remain unclear.Cellular prolif-eration assays,multi-omics analyses,and xenograft models were used to determine the effect of TET on melanoma.The direct target of TET was identified using biotin-TET pull-down liquid chromatograph-mass spectrometry(LC-MS),cellular thermal shift assays,and isothermal titration calorimetry(ITC)analysis.Our findings revealed that TET treatment induced robust cellular autophagy depending on activating transcription factor 6(ATF6)-mediated endoplasmic reticulum(ER)stress.Simultaneously,it hindered autophagic flux by inducing cytoskeletal protein depolymerization in melanoma cells.TET treatment resulted in excessive accumulation of reactive oxygen species(ROS)and simultaneously triggered mitophagy.Sirtuin 5(SIRT5)was ultimately found to be a direct target of TET.Mechanistically,TET led to the degradation of SIRT5 via the ubiquitin(Ub)-26S proteasome system.SIRT5 knockdown induced ROS accumulation,whereas SIRT5 overexpression attenuated the TET-induced ROS accumula-tion and autophagy.Importantly,TET exhibited anti-cancer effects in xenograft models depending on SIRT5 expression.This study highlights the potential of TET as an antimelanoma agent that targets SIRT5.These findings provide a promising avenue for the use of TET in melanoma treatment and underscore its potential as a therapeutic candidate.