Recurrent skin ulcer cross-repair and sensory reconstruction in a WRN gene mutational patient

Abstract: A 37-year-old man complained of a refractory posterior malleolar ulceration on his left ankle. He was diagnosed with Werner syndrome according to the progeroid clinical features and genetic testing. To approach the ulceration, a free flow-through right anterolateral thigh perforator flap with anterolateral thigh cutaneous nerve was harvested. One year later, he was readmitted due to a new ulceration on his right ankle. We harvested the left anterolateral thigh perforator flap with anterolateral thigh cutaneous nerve to reconstruct the defect. After one more year of follow-up, there was no recurrence of ulcers, and the sensation of the flap recovered partially after 6 months. We conclude that free flow-through anterolateral thigh perforator flap is a feasible choice for the repair of foot ulcers in Werner syndrome.

Anticancer activity and mechanism of apoptosis induced by Amaranthus spinosus L. extract in HepG2 cells / 中国药理学通报

Aim To investigate the anticancer activity and the mechanism of the apoptosis induced by Ama-ranthus spinosus L. extract ( ASE ) in human hepatic carcinoma cell line HepG2 . Methods Alamar blue assay was used for detecting the influence of ASE on the proliferation of the cancer cells. The morphological changes of cells were observed under inverted micro-scope and Hoechst 33258 stainning. The apoptosis of HepG2 cells was detected by flow cytometry. Western blot and caspase-3 activity kit were used to detect the protein expression in HepG2 cells. The specific inhibi-tor of caspase-9 and caspase-3 ( Z-LEHD-FMK and Ac-DEVD-CHO) was used to validate the signal transduc-tion pathyway. Results The results indicated that the cell proliferation was inhibited by ASE,especicially the HepG2 cells. The HepG2 cells showed obvious apop-totic characteristics. Flow cytometry analysis further validated the apoptosis of HepG2 cells. The expression of Bcl-2 and survivin was downreagulated in HepG2 cells treated with ASE, and Bax, caspase-9, caspase-3, Apaf-1 and PARP were upregualted. Besides, the caspase-3 activity was also increased. Z-LEHD-FMK and Ac-DEVD-CHO significantly increased the cell vi-abilty of HepG2 cells induced by ASE. Conclusion These results confirm that ASE induces the apoptosis of HepG2 through mitochondria-mediated pathway.