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Acne inversa/hidradenitis suppurativa is a chronic, recurrent, inflammatory skin disease that affects the pilosebaceous units, causinfollicular occlusion. The etiology and pathogenesis of acne inversa/hidradenitis suppurativa involves internal and external factors such as genetic susceptibility, inflammation and immunity, microorganisms, obesity, and smoking. acne inversa/hidradenitis suppurativa is difficult to treat, and the current aim of treatment is to control the frequency and duration of disease flares and improve the quality of life. Treatment protocols for acne inversa/hidradenitis suppurativa should be selected based on the disease severity grade. Medical treatments include antibiotics, retinoids, biologics, immunosuppressive agents, and antiandrogen agents. Adjuvant treatments include surgery and laser/light therapies. This consensus aims to further standardize the diagnosis and treatment procedures of acne inversa/hidradenitis suppurativa in China to facilitate its diagnosis and treatment.

HS1-associated protein X-1 (Hax-1) is a novel intracellular protein and recent studies suggested that it is an anti-apoptotic factor in different tumors. Hax-1 expression was upregulated in various metastatic tumors and cancer cell lines, including melanoma. To understand the role of Hax-1 in melanoma development and progression, we constructed Hax-1 short interfering RNA (siRNA) expression vectors to downregulate Hax-1 expression in a human melanoma A375 cell line. One of the two Hax-1 RNA interference (RNAi) constructs significantly reduced melanoma cell viability, which was due to induction of apoptosis in A375 cells. Molecularly, the induced apoptosis through downregulation of Hax-1 expression was mediated by activation of caspase-3 and poly-ADP-ribose polymerase (PARP) enzymatic activity in A375 cells. The data indicate that Hax-1 plays a role in suppression of apoptosis and promotion of melanoma cell growth, suggesting that this Hax-1 siRNA has a therapeutic indication in control of melanoma.

To explore the role of Bmi-1 gene in the proliferation of squamous carcinoma cells and whether the silencing Bmi-1 can inhibit the growth of squamous cell carcinomas cells.The expressions of Bmi-1 in primary cultured Fibroblasts, karatinocyte cell line Hacat,squamous carcinoma cell line A431, and ECA109 were detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis. Recombinant plasmid inserted with Bmi-1 gene short hairpin RNA (shRNA) expression vector PGPU6/GFP/Neo-shBmi-1 was constructed and transfected into ECA109 cells with control set. After transfection for 48 and 72 hours,the mRNA and protein levels of Bmi-1 were examined with RT-PCR and Western blot analysis, respectively. The proliferation of the ECA109 cells was evaluated by MTT method and flow cytometry.Bmi-1 was highly expressed in A431 and ECA109 cells than in Fibroblast cells and Hacat cells. The mRNA and protein expressions of Bmi-1 were significantly silenced in ECA109 cells after recombinant expression vector PGPU6/GFP/Neo-shBmi-1 transfection (P0.05). Compared with the control groups,the proliferation of ECA109 transfected with PGPU6/GFP/Neo-shBmi-1 was significantly inhibited (P0.05), and cells in G1 phase increased while in S phase decreased (P0.05).Bmi-1 is involved in the proliferation of squamous carcinoma cells. After the silencing of Bmi-1 expression,the proliferation ECA109 cells is suppressed due to the altered cell cycle.

Background The term angiokeratoma refers to a group of unrelated diseases with similar histopathologic features. Four clinical variants of angiokeratoma have been described. However, it is not known whether some variants of angiokeratoma are of lymphatic origin, and an immunohistochemical study of lymphatic markers has not been previously performed. Methods We performed an immunohistochemical study of angiokeratomas using lymphatic markers. Fifteen cases of angiokeratoma corporis diffusum, 10 cases of Fordyce angiokeratoma, 10 cases of Mibelli angiokeratoma and 10 cases of solitary angiokeratoma were examined by immunohistochemical analysis using CD31, D2-40, Prox1 and Wilms' tumor 1 (WT-1). Results The vessels of angiokeratoma corporis diffusum, Fordyce angiokeratoma and solitary angiokeratoma were usually focally positive for D2-40 and positive for Prox1, whereas the vessels of Mibelli angiokeratoma were negative for D2-40 and positive for Prox1. Conclusions The results suggest lymphatic derivation of angiokeratoma corporis diffusum, Fordyce angiokeratoma and solitary angiokeratoma. However, the derivation of Mibelli angiokeratoma could not be determined based on the present immunohistochemical results.

To study the expression of integrin beta1 in squamous cell carcinoma (SCC) and explore the relationship between stem cell marker and SCC.The expressions of integrin beta1 in SCC tissues and SCC cell strain A431 were detected with immunohistochemical methods and cell staining method. The differentiation of SCC cells were induced with all-trans-retinoic acid (ATRA). The changes of integrin beta1 levels before and after induction were detected with RT-PCR.In highly differentiated SCC tissues, integrin beta1 was constantly expressed in the basal-like cells in the edge of tumor; some cells inside arranged as island also showed positive integrin beta1 expression. In poorly differentiated SCC tissues, island-like integrin beta1-positive cells remarkably increased and distributed in a diffuse way. In SCC A431 cells, integrin beta1 was expressed unevenly in tumor cells. After treatment by ATRA, level of integrin beta1 mRNA in A431 cells significantly decreased compared with untreated control (P0.05), and the ratios between the intensity values of integrin beta1 to beta-actin were 0.071 +/- 0.025 and 0.029 +/- 0.018 at 24 h and 48 h, respectively, whereas in controls were 0.148 +/- 0.027 and 0.136 +/- 0.011 (P0.05).Integrin beta1 is heterogeneously expressed in both SCC tissues and SCC A431 cells. The expression of Integrin beta1 decreases when the differentiation level of tumor cells increase, indicating that integrin beta1 is closely related with the initiation of SCC and potential cancer stem cells in SCC.

To identify the localization of hair follicles stem cell (HFSC) in different stages of hair and explore the differentiating capacity of HFSC into epidermis in vitro.HFSC were detected by K19 immunostaining in normal human skin. Then, the isolated HFSC through enzyme digestion were seeded on dermal equivalent (DE) and cultured between the air-liquid interfaces for 14 days. Skin-equivalents was harvested and used for evaluation.HFSC mainly located in outer root sheet in hair follicle and human anagen hair follicles containing two distinct reservoirs for K19-positive cells located in the bulge and bulb of the follicle. These two reservoirs fused in line of outer root sheets during the catagen-telogen transition phase and individualized again in the newly forming anagen hair follicle. Based on DE, growing HFSC built a multilayered and confined epidermis.HFSC located in outer root sheets can promote hair cycle and differentiate into epidermis in vitro.

To investigate effects of bcl-2 fully phosporothioated antisense oligodeoxynucleotide(bcl-2 ASODN) on proliferation and apoptosis of human melanoma A375 cell, and its possible mechanism.Proliferation and apoptosis of A375 cell with bcl-2 ASODN treatment were evaluated by MTT colorimetric assay, laser scanning confocal microscope (LSCM), TUNEL and Annexin V/propidium iodide(PI), and the level of bcl-2 mRNA expression in A375 cell was detected by RT-PCR before and after being treated by bcl-2 ASODN.MTT assay demonstrated that bcl-2 ASODN could inhibit the proliferation of the cells in both time and concentration dependent manner. Characteristic morphologic apoptosis changes were observed by LSCM after incubated with bcl-2 ASODN for 48 h. Most nucleus were labeled in brown by TUNEL in ASODN group, but not markedly labeled both in SODN and control group. The apoptosis rate of A375 cells in 30 micromol/L bcl-2 ASODN group was significantly higher than that in bcl-2 SODN and in control group. The bcl-2 ASODN-induced apoptosis of A375 cells, which was accompanied by declined expression of bcl-2 mRNA was distinctly lower than that in SODN and control groups.These results suggest that bcl-1 ASODN can not only inhibit proliferation but also induce apoptosis of human melanoma A375 cells in vitro, and the apoptosis-induced mechanism is down-regulating expression of bcl-2 mRNA.

Background: There are few studies on the abnormal morphology of Langerhans cells (LCs) in condyloma acuminatum (CA) lesions and the essence of the abnormal morphology of LCs in CA lesions is still not well elucidated. The aim of this study was to further investigate the morphological features of LCs in CA lesions. Methods: CD1a+ LCs in 13 CA lesions and in 13 normal controls were labeled using immunohistochemistry and examined by light microscopy. Ultrastructural investigation on LCs in six CA lesions and in six normal controls was performed by electron microscopy. Results: Compared with those in normal controls, most CD1a+ LCs in CA lesions exhibited dysplastic dendrities and abnormal distribution. The number of CD1a+ LCs in CA lesions (26.31 ± 18.84) was statistically lower (p < 0.001) than that in normal controls (72.00 ± 27.40). Electron microscopy showed that the number of Birbeck granules within lesional LCs (4.00 ± 2.94) was significantly decreased (p < 0.001) than that within normal LCs (10.80 ± 4.78). The ultrastructures of most lesional LCs displayed degenerative changes. Conclusions: The morphology of most LCs in CA lesions shows degenerative changes, which suggest that these LCs have been functionally impaired.