UVA1对人工皮肤成纤维细胞光损伤的影响

目的探讨不同UVA1照射剂量对人工皮肤真皮细胞形态及细胞活性的影响,为建立人工皮肤光损伤模型提供依据。方法以不同剂量UVA1（0J／cm^2-80J／cm^2）照射人工皮肤,通过HE染色,从形态学上观察经UVA1照射后真皮成纤维细胞数量的变化,通过MTT法检测真皮成纤维细胞的活性。结果HE染色示真皮成纤维细胞的数量随UVA1剂量的增大而减少,于真皮浅层较为明显;MTT法示与0J／cm^2组相比,20J／cm^2和30J／cm^2UVA1照射人工皮肤时成纤维细胞活性未受到明显的抑制（P〉0．05）．UVA1剂量大于40J／cm^2时细胞活性下降明显（P〈0．05,P〈0．001）,呈剂量依赖性。结论UVA1照射剂量大于40J／cm^2是造成人工皮肤真皮成纤维细胞光损伤的始剂量。     

咪喹莫特对瘢痕疙瘩成纤维细胞增殖和胶原产生的影响

目的 探讨咪喹莫特对瘢痕疙瘩成纤维细胞增殖和胶原产生的影响.方法 从手术切除的瘢痕疙瘩组织中培养成纤维细胞,加入不同浓度的咪喹莫特作用后,观察细胞的形态学变化,MTT法检测细胞的活性.免疫组化和蛋白免疫印迹法检测咪喹莫特对瘢痕疙瘩成纤维细胞Ⅰ型、Ⅲ型前胶原产生的影响.结果 在10～100μg/mL范围内,咪喹莫特能显著抑制瘢痕疙瘩成纤维细胞的增殖,且存在剂量和时间依赖性;进一步检测到咪喹莫特作用后瘢痕疙瘩成纤维细胞Ⅰ型、Ⅲ型前胶原表达减弱.结论 咪喹莫特能有效抑制瘢痕疙瘩成纤维细胞的增殖和Ⅰ型、Ⅲ型前胶原的产生.     

阿魏酸保护人成纤维细胞光源性氧化损伤的研究

目的观察阿魏酸是否可以保护人成纤维细胞,抑制长波紫外线（UVA）辐射对其所致的氧化损伤。方法加入200μg/mL阿魏酸孵育培养的成纤维细胞4h后,以5、10J／cm^2的UVA照射细胞,照光后继续培养24h。以四甲基偶氮唑蓝还原法（MTT）法检测细胞活性,比色法检测细胞上清液中的超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）和丙二醛（MDA）含量变化。结果接受UVA照射后,成纤维细胞出现不同程度的增殖活性下降,活性下降程度与辐射强度成正比：阿魏酸干预处理可使细胞活性明显恢复。UVA照射组的SOD和GSH—Px水平明显下降、而MDA则明显上升：经阿魏酸预处理的细胞上清液中SOD和GSH—Px活性显著增加,而MDA水平明显下降（P〈0．05）。结论阿魏酸可明显保护人成纤维细胞免于UVA损伤,其具体机制可能与抑制氧化损伤和增强细胞抗氧化能力有关。     

人参皂苷Rg1对UVB损伤PG12及成纤维细胞的保护作用

目的研究人参皂苷Rg1对中波紫外线（UVB）损伤皮肤成纤维细胞以及作为皮肤神经细胞模型的PC12细胞的保护作用。方法实验分为UVB模型组、UVB＋Rg1三个不同浓度保护组、对照组,分别以60mJ／cm^2、100mJ／cm^2强度UVB造成培养的皮肤成纤维细胞、皮肤神经细胞模型PC12（神经元化）细胞损伤,用MTT法检测细胞增殖活性,酶生化法检测光损伤前后细胞培养上清SOD活性、MDA含量。结果强度为60mJ／cm^2、100mJ／cm^2的中波紫外线分别可以造成体外培养的人皮肤成纤维细胞、神经元化PC12细胞增殖活性降低,细胞培养上清SOD活性降低,MDA含量升高,与UVB模型组相比均P〈0．05。给定浓度范围的Rg1能增加细胞的增殖活性,增加细胞培养上清SOD活性、降低MDA含量。结论紫外线可以造成体外培养的人皮肤成纤维细胞及PC12细胞氧化损伤,人参皂苷Rg1对损伤的细胞具有一定保护作用,其机制可能与它的抗氧化、增强细胞活力有关     

染料木素对UVA诱导成纤维细胞急性光损伤的防护作用

目的：明确染料木素对UVA诱导成纤维细胞急性光损伤的防护作用。方法：将体外培养的成纤维细胞分为空白对照组,UVA照射对照组及UVA+染料木素（0.01,0.1,1,10,100umol/L）组。采用CCK8法测定细胞增殖情况,流式细胞术检测细胞凋亡情况, RT-PCR检测Sirt1mRNA的表达水平。结果：与UVA组比较,UVA+0.01,0.1,1,10 μmol/L染料木素组细胞增值活性及Sirt1mRNA表达明显升高,细胞凋亡率降低（均P<0.05）;而UVA+100μmol/L染料木素,细胞凋亡率无明显差异（P>0.05）;结论：0.01～10μmol/L染料木素对UVA诱导成纤维细胞的急性光损伤有防护作用。     

咪喹莫特对人皮肤鳞状细胞癌SCL-1细胞增殖和端粒酶活性的影响

目的 探讨咪喹莫特对人皮肤鳞状细胞癌SCL-1细胞增殖及端粒酶活性的影响。方法 使用噻唑蓝（MTT）法检测药物处理后细胞生长抑制情况，细胞克隆形成试验检测药物处理后细胞增殖能力变化，倒置显微镜观察药物作用前后细胞形态改变；端粒酶重复序列扩增-酶联免疫吸附法（TRAP-ELISA）检测细胞端粒酶活性变化；细胞免疫组化和实时定量RT-PCR技术检测端粒酶活性相关c-Myc基因表达情况。结果 咪喹莫特能明显抑制SCL-1细胞增殖，并存在浓度依赖性。培养48 h时，0，0.05，0.10，0.15和0.20 g/L咪喹莫特组细胞增殖抑制率分别为0，31.3% ± 3.19%，44.7% ± 4.21%，49.2% ± 3.71%和71.6% ± 3.24%。咪喹莫特作用SCL-1细胞48 h，端粒酶活性随药物浓度增高呈显著的递减关系。48 h时，0.05和0.15 g/L咪喹莫特组c-Myc mRNA和蛋白表达均低于空白对照组（P ＜ 0.05）。结论 咪喹莫特可明显抑制SCL-1细胞的增殖，降低c-Myc基因表达，下调SCL-1肿瘤细胞端粒酶活性，可能是其抗癌作用的机制之一。     

不同培养条件对皮肤角质形成细胞和成纤维细胞增殖的影响

目的观察含不同血清浓度培养基对皮肤角质形成细胞和成纤维细胞体外活性的影响。方法体外培养、扩增皮肤角质形成细胞和成纤维细胞,按3×10^5／ml的密度接种于96孔板,加入含不同血清浓度的K-SFM培养基培养。并用MTY比色法观察细胞活性。结果应用K—SFM＋10％FBS组培养基培养成纤维细胞与DMEM＋10％FBS为对照组培养细胞的活性影响相同（P〉0．05）;应用K-SFM＋1％FBS培养基培养角质形成细胞与K—SFM为对照组培养细胞的活性影响相同（P〉0．05）;结论在构建人工皮肤体外模型时,角质形成细胞和成纤维细胞可分别加用含1％FBS、10％FBS的K—SFM培养基进行培养。     

阿维A酸对系统性硬皮病患者成纤维细胞增殖及分泌TGF—β1的影响

目的：确定阿维A酸对系统性硬皮病患者皮肤成纤维细胞增殖及分泌转化生长因子β1（TGF-β1）的影响。方法：原代培养系统性硬皮病（SSc）患者皮肤成纤维细胞（FB），使用不同浓度的阿维A酸作用48h，四甲基偶氮唑盐（M1T）方法及ELISA法测定阿维A酸对成纤维细胞增殖及分泌TGF-β1的影响。结果：阿维A酸可明显抑制患者皮肤成纤维细胞的增殖，显著减少成纤维细胞TGF-β1的分泌，并具有浓度依赖性。与空白对照组相比，差异有显著性（P〈0．05）。结论：阿维A酸对SSc皮肤成纤维细胞的增殖及TGF—β1的分泌均有显著抑制作用，为其治疗硬皮病提供了理论基础。     

黄芩甙治疗银屑病的机制研究

目的 探讨黄芩甙治疗银屑病的可能机制。方法 以体外培养的角质形成细胞、成纤维细胞、外周血单个核细胞为对象，不同浓度黄芩甙处理细胞后，用MTT比色分析法反映细胞增殖变化，流式细胞仪测定细胞周期分布。结果 1．5～96μg／mL黄芩甙对成纤维细胞显示一定的抑制作用，并呈时间和剂量依赖关系，而该浓度范围对良性角质形成细胞株HaCaT细胞无明显影响，且外周血单个核细胞活力在此浓度不受影响。流式细胞仪检测细胞周期分布变化，成纤维细胞随药物浓度的升高，G0-G1期细胞比例逐渐增高，G2M、S期细胞比例降低；而HaCaT无明显细胞周期分布变化。结论 一定浓度的黄芩甙可通过阻滞成纤维细胞周期发挥抑制增殖作用，进而影响表皮角质形成细胞生长，是其治疗银屑病的可能机制之一。     

咖啡因可保护UVB致人皮肤成纤维细胞的损伤

目的：确定咖啡因对中波紫外线（UVB）照射致体外培养人皮肤成纤维细胞氧化损伤的防护作用.方法：分离培养人成纤维细胞,分为空白对照组、咖啡因组、UVB照射组、UVB照射＋咖啡因组,UVB照射剂量为30 mJ/cm2.用MTT法检测细胞增殖活性,酶生化比色法检测细胞丙二醛（MDA）含量、超氧化物歧化酶（SOD）及谷胱甘肽过氧化物酶（GSH-Px）活性.结果：UVB照射前后用咖啡因处理能使成纤维细胞存活率提高、MDA产生减少,酶的活性增强.结论：咖啡因对UVB照射损伤成纤维细胞具有一定保护性作用,其机制可能与抑制氧化损伤和增强抗氧化能力有关.     

New fillers for the new man

ABSTRACT:  Two new collagen-based lidocaine-containing dermal fillers, ArteSense™/ArteFill™ (Artes Medical, San Diego, CA) and Evolence® (Colbar LifeScience Ltd., Herzliya, Israel), have proved to be of particular interest to men, many of whom seek a long-lasting or permanent correction. ArteFill™ has been available in the United States since 2006, and it is expected that Evolence® will reach the American market in 2008. The properties of the two products will be described, and experience based on the administration of many hundreds of syringes of both products by a Canadian dermatologist will be detailed here, with tips and precautions to optimize patient outcomes.     

Outcomes and adverse effects of ablative vs nonablative lasers for skin resurfacing: A systematic review of 1093 patients

It is generally believed that ablative laser therapies result in prolonged healing and greater adverse events when compared with nonablative lasers for skin resurfacing. To evaluate the efficacy of ablative laser use for skin resurfacing and adverse events as a consequence of treatment in comparison to other modalities, a PRISMA‐compliant systematic review (Systematic Review Registration Number: 204016) of twelve electronic databases was conducted for the terms “ablative laser” and “skin resurfacing” from March 2002 until July 2020. Studies included meta‐analyses, randomized control trials, cohort studies, and case reports to facilitate evaluation of the data. All articles were evaluated for bias. The search strategy produced 34 studies. Of 1093 patients included in the studies of interest, adverse events were reported in a total of 106 patients (9.7%). Higher rates of adverse events were described in nonablative therapies (12.2% ± 2.19%, 31 events) when compared with ablative therapy (8.28% ± 2.46%, 81 events). 147 patients (13.4%) reported no side effects, 68 (6.22%) reported expected, transient self‐resolving events, and five (0.046%) presented with hypertrophic scarring. Excluding transient events, ablative lasers had fewer complications overall when compared with nonablative lasers (2.56% ± 2.19% vs 7.48% ± 3.29%). This systematic review suggests ablative laser use for skin resurfacing is a safe and effective modality to treat a range of pathologies from photodamage and acne scars to hidradenitis suppurativa and posttraumatic scarring from basal cell carcinoma excision. Further studies are needed, but these results suggest that ablative lasers are a superior, safe, and effective modality to treat damaged skin.     

Genetic alterations in RAS‐regulated pathway in acral lentiginous melanoma

Studies integrating clinicopathological and genetic features have revealed distinct patterns of genomic aberrations in Melanoma. Distributions of BRAF or NRAS mutations and gains of several oncogenes differ among melanoma subgroups, while 9p21 deletions are found in all melanoma subtypes. In the study, status of genes involved in cell cycle progression and apoptosis was evaluated in a panel of 17 frozen primary acral melanomas. NRAS mutations were found in 17% of the tumors. In contrast, BRAF mutations were not found. Gains of AURKA gene (20q13.3) were detected in 37.5% of samples, gains of CCND1 gene (11q13) or TERT gene (5p15.33) in 31.2% and gains of NRAS gene (1p13.2) in 25%. Alterations in 9p21 were identified in 69% of tumors. Gains of 11q13 and 20q13 were mutually exclusive, and 1p13.2 gain was associated with 5p15.33. Our findings showed that alterations in RAS‐related pathways are present in 87.5% of acral lentiginous melanomas.     

Self‐resolving superficial primary cutaneous mucormycosis in a 7‐week‐old infant

A 7‐week‐old girl, born at 30 weeks' gestational age, presented to clinic for evaluation of a crop of vesicular lesions that were noted after removal of a bandage that had been in place for 4 days. A punch biopsy of the lesion revealed fungal elements that were later identified as Rhizopus spp. The lesion began to self‐resolve, and no further treatment was needed, with full resolution of the lesion by 1 month after presentation. Clinicians should be aware of the variable presentations of mucormycosis and consider fungal infection in the differential diagnosis when evaluating vulnerable patients with skin eruptions.     

Pathogenic role of IL-17 in psoriasis and psoriatic arthritis

Psoriasis is a chronic inflammatory skin disorder resulting from a complex network of cytokines and chemokines produced by various immune cell types and tissue cells. Emerging evidence suggests a central role of IL-17 and IL-23/T17 axis in the pathogenesis of psoriasis, giving a rationale for using IL-17-blocking agents as therapeutics.Three agents targeting IL-17 signaling are being studied in Phase III clinical trials: secukinumab and ixekizumab (IL-17 neutralizing agents), and brodalumab (IL-17 receptor antagonist). Preliminary results are highly promising for all anti-IL17 agents, creating fair expectations on this class of agents as the new effective therapeutic approach for the treatment of psoriasis.