Skin Tissues(皮肤组织)研究综述
Skin Tissues 皮肤组织 - Here we report that in transgenic (Tg) mice expressing hamster cellular prion protein (PrPC) infected with the 263K prion, the prion-seeding activity becomes undetectable in the skin tissues of TC-5RW-treated Tg mice by both sPMCA and RT-QuIC assays, whereas such prion-seeding activity is readily detectable in the skin of untreated mice. [1] METHODS RNA-sequencing of skin tissues from rosacea patients and integrative analyses facilitated comprehensive exploration of lncRNA, mRNA, and miRNA networks. [2] Human epidermal keratinocytes (HEKs) from neonatal foreskin tissues were isolated and cultured. [3] The rat psoriasis model was established via imiquimod (IMQ) induction followed by verification of miR-383 and LCN2 expression in the skin tissues of the models. [4] In addition, through gene expression analysis of acne, rosacea and skin tissues of healthy individuals, we found a higher infiltration of Th1 and Th17 cells in acne lesions, relative to non-lesional skin areas of acne patients. [5] In this study, we found that acellular dermal matrix (ADM) bioink preserved the main extracellular matrix (ECM) components of the skin to promote cell growth, and gelatine methacrylamide (GelMA) bioink with tunable and sufficient mechanical properties was strong and elastic for skin tissues. [6] This study compared the Quick—DNA Fungal/Bacterial Miniprep Kit and CTAB methods and tested them across four samples of Chromodoris quadricolor gut and skin tissues. [7] Gills and skin tissues were prepared for histopathology and light and scanning electron microscopy. [8] Conclusion: The results of this study indicated that DM upregulated the expressions of HSP 90, iNOS, and VEGF in the skin tissues of diabetic rats and may impact the healing of skin wounds. [9] rubripes, the intestine, liver, and skin tissues of D. [10] Median δ13C and δ15N values in Sowerby's beaked whale bone, muscle, and skin tissues significantly differed between whales sampled from the east and west North Atlantic Ocean. [11] We performed single-cell RNA sequencing on skin tissues of T2DM patients and non-diabetics and identified the cell cluster of skin, single-cell subsets, and transcriptional characteristics of mast cells at a single-cell level. [12] METHODS Skin tissues of both healthy controls and SSc patients were detected the distribution of BMP-7. [13] The objectives of the current analyses are to develop the PKPD model for biomarkers (thymidine kinase 1 (TK1) in serum and phosphor-Rb (pRb) and Ki67 in skin tissues) related to CDK4/6 inhibition by palbociclib and to explore the relationship of the biomarker response with the efficacy endpoint (PFS). [14] A numerical analysis is performed to investigate the comparative contribution of the mechanisms responsible for electron gain and losses in laser-induced breakdown of the skin tissues. [15] Studies have shown that the concentration of AGEs is elevated in the skin tissues and not subcutaneous tissues in refractory diabetic wounds, which suggests there may be a causal relationship between the two. [16] Methods For hair growth experiment, shaved dorsal skins of C57BL/6 mice were topically applied with vehicle, RGO, RGO's major compounds, or minoxidil for consecutive 21 days and skin tissues were examined the hair growth promoting capacity. [17] On the other hand, TDDS with nanocarriers minimizing damage to the skin tissues has emerged together with the development of nanotechnology in recent years. [18] This conclusion is a promising finding for applying the selective photothermolysis in pathological subepithelial capillary structures which will ensure precise treatment with minimal damage to skin tissues. [19] In addition, under the guidance of NIR, Cu-GA-CA-PDA NRs can hinder the formation of inflammatory cells, reduce oxidative stress damage, accelerate the regeneration of skin tissues in S. [20] Background Epidermolysis bullosa is an inherited disease that causes bleeding blisters on the skin tissues and mucosal membranes. [21] After itch behaviour and ear-swelling response were monitored, serum, auricular lymph nodes, and skin tissues were collected to analyse immunocyte differentiation, cytokine determination, and histological changes. [22] KI67 expression and keratinocyte apoptosis at the skin tissues were, respectively, detected by Immunohistochemical analysis and TUNEL assay. [23] HMGB1 levels in the blood and its expression in skin tissues are increased in psoriasis, alopecia areata, dystrophic epidermolysis bullosa, and vitiligo. [24] They may also participate in other diseases, including pulmonary disorders and cancer, because CD1a-expressing dendritic cells are also located in non-skin tissues. [25] To provide enriched genomic resources and infer possible mechanisms underlying skin pigmentation, we performed a large-scale transcriptomic sequencing on 13 adult goldfish tissues, larvae at one- and three-days post hatch, and skin tissues with four different color pigmentation. [26] By comparing the histological sections of the skin with sunburn-induced damage of the skin tissues at the epidermal and dermal layers, the UV protection capabilities of all materials could be deduced and established. [27] After the skin tissues were homogenized overnight by enzymatic digestion using collagenase A, the skin homogenates were further processed by protein precipitation and phenyl-bonded solid phase extraction. [28] A total of 4 days after applying the zinc oxide, protective film or silicon dressing intervention, IAD scores and pH values in skin tissues were examined. [29] This study suggests that the cream formulated using CAVA can alleviate the damages caused by the UV-B-irradiation at a high level and safeguard the skin tissues. [30] Further results showed that cloves upregulate SOD1, SOD2, CAT, GSH, IL-10, IκB-α, AMPK, SIRT1, LKB1, PGC-1α, APPL1, and FoxO1 and downregulate NF-κB p65, TNF-α, IL-6, and mTOR mRNA expression in the skin tissues of UVB-damaged mice. [31] Moreover, the module was successfully applied to characterize melanoma in skin tissues based on the enhanced protein profiles. [32] Results The administration of PLD has been demonstrated to induce the histological damage of skin tissues including the destruction of collagen fibers and the induction of severe inflammation and apoptosis of epidermal cells. [33] Compared with IMQ-treated and PBS-treated mice, pGP3- and PGP3M-treated mice had less inflammatory cell infiltration in skin tissues and had significantly reduced IL-17A, IFN-γ, and IL-22 levels in serum. [34] Our results revealed a significant augmented expression of CD11b + CD11c + (pro-inflammatory DC) in peripheral blood mononuclear cells (PBMCs) and skin tissues of active vitiligo patients versus control and stable vitiligo group. [35] Previous studies have shown that some genes are expressed differentially in the skin tissues between the goats produced superior-quality and normal-quality brush hair. [36] As a result, redness and ulcers occur due to lacking oxygen and nutrients in the skin tissues, and these sites are often infected with microorganisms and, thus, become suppurative wounds, a condition commonly determined as pressure injuries. [37] Bacteria growth of infected secretions was checked on LB agar, and Hematoxylin and eosin (H&E) staining was performed for Histological analysis of skin tissues infected with bacteria after Madeng’ai and PBS (control) treatment. [38] The results showed that PVA materials mainly accumulated in the skin tissues of mice after dissolving and the concentration of PVA in the insertion sites gradually decreased and almost undetectable at 6 days after administration. [39] Differentially expressed genes in skin tissues at the initial site before and after scale development were analyzed and some key regulatory genes (Wnt3, Wnt6, Fgf8, Fgf10, Fgf16, Fgfr1a, Ihhb and BMP6) which are crucial for scale morphogenesis were selected. [40] The closest and most stable connections for different sites are the following indicators: blood leukocytes (negative dependence for affected bone, soft tissue and skin tissues), ESR (positive dependence for soft tissues), C-reactive protein (positive dependence for soft tissues and skin), agglutination with a polyvalent strain of Staphylococcus aureus (negative dependence for affected bones and skin). [41] We previously developed a red-green-blue camera-based spectral imaging method for the measurements of melanin concentration, oxygenated hemoglobin concentration (CHbO), deoxygenated hemoglobin concentration (CHbR), total hemoglobin concentration (CHbT) and tissue oxygen saturation (StO2) in skin tissues. [42] Furthermore, by comparing m6A-modified genes of the male Liaoning Cashmere Goat (M-LCG) and female Liaoning Cashmere Goat (F-LCG) skin tissues, we get 862 differentially expressed m6A-modified genes. [43] Numerous cell types have been used in 3D bioprinting to build cardiovascular, musculoskeletal, neural, hepatic, adipose and skin tissues. [44] Present empirical study analyses the thermal changes and the specific absorption rates (SAR) of brain, eye and skin tissues due to prolonged exposure to mobile phone radiation. [45] Skin cancer is basically the unnatural growth of skin tissues and it can be fatal. [46] AGE Pro developed by the Chinese Academy of Sciences uses the principle of positive correlation between fluorescence intensity of specific excitation/emission band and AGEs accumulation amount in skin tissues to invert the AGE level of subjects in vivo based on the obtained optical signals, to realize the risk and disease assessment of diabetes complications. [47] We further showed the presence of the MAL protein in HaCaT keratinocytes and HEKa and skin tissues, supporting the hypothesis that it is a key element in the mechanism of cytotoxicity of ETX. [48] RNA was extracted from skin tissues and WNT5A expression was quantified by RT-PCR. [49] Zinc is abundant in skin tissues, as zinc is required for the differentiation and proliferation of keratinocytes. [50]在这里，我们报告说，在表达用 263K 朊病毒感染的仓鼠细胞朊病毒蛋白 (PrPC) 的转基因 (Tg) 小鼠中，sPMCA 和 RT-QuIC 在 TC-5RW 处理的 Tg 小鼠的皮肤组织中检测不到朊病毒播种活性化验，而这种朊病毒播种活动很容易在未经处理的小鼠的皮肤中检测到。 [1] 方法 酒渣鼻患者皮肤组织的 RNA 测序和综合分析促进了对 lncRNA、mRNA 和 miRNA 网络的全面探索。 [2] 分离和培养来自新生儿包皮组织的人表皮角质形成细胞 (HEK)。 [3] 通过咪喹莫特 (IMQ) 诱导建立大鼠银屑病模型，然后验证模型皮肤组织中 miR-383 和 LCN2 的表达。 [4] 此外，通过对健康个体的痤疮、红斑痤疮和皮肤组织的基因表达分析，我们发现，相对于痤疮患者的非病变皮肤区域，痤疮病变中的 Th1 和 Th17 细胞浸润更高。 [5] 在这项研究中，我们发现脱细胞真皮基质 (ADM) 生物墨水保留了皮肤的主要细胞外基质 (ECM) 成分以促进细胞生长，并且具有可调节和足够机械性能的明胶甲基丙烯酰胺 (GelMA) 生物墨水对皮肤具有强韧和弹性组织。 [6] 本研究比较了 Quick-DNA Fungal/Bacterial Miniprep Kit 和 CTAB 方法，并在四个 Chromodoris quadricolor 肠道和皮肤组织样本中进行了测试。 [7] 为组织病理学和光学和扫描电子显微镜准备了鳃和皮肤组织。 [8] 结论：本研究结果表明，DM上调了糖尿病大鼠皮肤组织中HSP 90、iNOS、VEGF的表达，可能影响皮肤创面的愈合。 [9] 红葡萄、肠、肝和皮肤组织 D. [10] 索尔比喙鲸骨骼、肌肉和皮肤组织的中值 δ13C 和 δ15N 值在北大西洋东部和西部采样的鲸鱼之间存在显着差异。 [11] 我们对 T2DM 患者和非糖尿病患者的皮肤组织进行了单细胞 RNA 测序，并在单细胞水平上鉴定了皮肤细胞簇、单细胞亚群和肥大细胞的转录特征。 [12] 方法 健康对照和SSc患者的皮肤组织均检测到BMP-7的分布。 [13] 当前分析的目的是开发与 palbociclib 抑制 CDK4/6 相关的生物标志物（血清中的胸苷激酶 1 (TK1) 和皮肤组织中的磷-Rb (pRb) 和 Ki67）的 PKPD 模型，并探索与具有疗效终点 (PFS) 的生物标志物反应。 [14] 进行数值分析以研究负责电子增益和损失的机制在激光诱导的皮肤组织破裂中的比较贡献。 [15] 研究表明，在难治性糖尿病伤口中，皮肤组织中 AGEs 的浓度升高，而不是皮下组织，这表明两者之间可能存在因果关系。 [16] 方法 生发实验中，C57BL/6小鼠剃毛后背皮肤外用载体、RGO、RGO主要化合物或米诺地尔连续21天，检测皮肤组织促生毛能力。 [17] 另一方面，近年来随着纳米技术的发展，出现了具有纳米载体的TDDS，可最大限度地减少对皮肤组织的损伤。 [18] 这一结论对于在病理上皮下毛细血管结构中应用选择性光热作用是一个有希望的发现，这将确保对皮肤组织造成最小损伤的精确治疗。 [19] 此外，在 NIR 的引导下，Cu-GA-CA-PDA NRs 可以阻碍炎性细胞的形成，减少氧化应激损伤，加速金黄色葡萄球菌皮肤组织的再生。 [20] 背景大疱性表皮松解症是一种遗传性疾病，会导致皮肤组织和黏膜出现水疱出血。 [21] 监测瘙痒行为和耳肿胀反应后，收集血清、耳廓淋巴结和皮肤组织，分析免疫细胞分化、细胞因子测定和组织学变化。 [22] 免疫组化分析和TUNEL法分别检测皮肤组织KI67表达和角质形成细胞凋亡。 [23] 在银屑病、斑秃、营养不良性大疱性表皮松解症和白癜风中，血液中 HMGB1 水平及其在皮肤组织中的表达增加。 [24] 它们还可能参与其他疾病，包括肺部疾病和癌症，因为表达 CD1a 的树突状细胞也位于非皮肤组织中。 [25] 为了提供丰富的基因组资源并推断皮肤色素沉着的可能机制，我们对 13 种成年金鱼组织、孵化后 1 天和 3 天的幼虫以及具有四种不同颜色色素沉着的皮肤组织进行了大规模转录组测序。 [26] 通过比较皮肤的组织切片与晒伤引起的表皮和真皮层皮肤组织的损伤，可以推断和确定所有材料的紫外线防护能力。 [27] 通过使用胶原酶A的酶消化将皮肤组织匀浆过夜后，通过蛋白质沉淀和苯基键合固相萃取进一步处理皮肤匀浆。 [28] 在应用氧化锌、保护膜或硅敷料干预后总共 4 天，检查皮肤组织中的 IAD 评分和 pH 值。 [29] 这项研究表明，使用 CAVA 配制的面霜可以高水平地缓解 UV-B 照射造成的损伤，保护皮肤组织。 [30] 进一步的结果表明，丁香上调 SOD1、SOD2、CAT、GSH、IL-10、IκB-α、AMPK、SIRT1、LKB1、PGC-1α、APPL1 和 FoxO1，并下调 NF-κB p65、TNF-α、IL-6 , 和 mTOR mRNA 在 UVB 损伤小鼠皮肤组织中的表达。 [31] 此外，该模块已成功应用于基于增强的蛋白质谱表征皮肤组织中的黑色素瘤。 [32] 结果PLD的施用已被证明可诱导皮肤组织的组织学损伤，包括胶原纤维的破坏和表皮细胞的严重炎症和凋亡的诱导。 [33] 与 IMQ 处理和 PBS 处理的小鼠相比，pGP3 和 PGP3M 处理的小鼠皮肤组织中炎症细胞浸润较少，血清中 IL-17A、IFN-γ 和 IL-22 水平显着降低。 [34] 我们的研究结果显示，与对照组和稳定白癜风组相比，活动性白癜风患者外周血单个核细胞 (PBMC) 和皮肤组织中 CD11b + CD11c + (促炎 DC) 的表达显着增加。 [35] 先前的研究表明，山羊皮肤组织中的某些基因表达不同，从而产生了优质和正常质量的刷毛。 [36] 结果，由于皮肤组织缺氧和营养不足而出现红肿和溃疡，这些部位经常被微生物感染，从而变成化脓性伤口，这种情况通常被确定为压力性损伤。 [37] 在LB琼脂上检查感染分泌物的细菌生长情况，并进行苏木精和伊红（H＆E）染色，用于马登艾和PBS（对照）处理后感染细菌的皮肤组织的组织学分析。 [38] 结果表明，PVA物质溶解后主要在小鼠皮肤组织中蓄积，给药后6天插入部位的PVA浓度逐渐下降，几乎检测不到。 [39] 分析了鳞片发育前后初始部位皮肤组织中差异表达的基因，筛选出一些对鳞片形态发生至关重要的关键调控基因（Wnt3、Wnt6、Fgf8、Fgf10、Fgf16、Fgfr1a、Ihhb 和 BMP6）。 [40] 不同部位最接近和最稳定的联系是以下指标：血液白细胞（对受影响的骨骼、软组织和皮肤组织的负依赖）、ESR（对软组织的正依赖）、C反应蛋白（对软组织和皮肤组织的正依赖）皮肤），与金黄色葡萄球菌的多价菌株凝集（对受影响的骨骼和皮肤的负依赖性）。 [41] 我们之前开发了一种基于红-绿-蓝相机的光谱成像方法，用于测量黑色素浓度、含氧血红蛋白浓度 (CHbO)、脱氧血红蛋白浓度 (CHbR)、总血红蛋白浓度 (CHbT) 和组织氧饱和度 (StO2)皮肤组织。 [42] 此外，通过比较雄性辽宁绒山羊（M-LCG）和雌性辽宁绒山羊（F-LCG）皮肤组织的m6A修饰基因，我们得到了862个差异表达的m6A修饰基因。 [43] 许多细胞类型已用于 3D 生物打印，以构建心血管、肌肉骨骼、神经、肝脏、脂肪和皮肤组织。 [44] 目前的实证研究分析了由于长时间暴露于手机辐射而导致的大脑、眼睛和皮肤组织的热变化和特定吸收率 (SAR)。 [45] 皮肤癌基本上是皮肤组织的不自然生长，它可能是致命的。 [46] 中科院研制的AGE Pro利用特定激发/发射波段的荧光强度与皮肤组织中AGEs积累量正相关的原理，根据获得的光信号反演受试者体内AGE水平，实现糖尿病并发症的风险和疾病评估。 [47] 我们进一步证明了 HaCaT 角质形成细胞和 HEKa 和皮肤组织中存在 MAL 蛋白，支持了它是 ETX 细胞毒性机制中的关键因素的假设。 [48] 从皮肤组织中提取 RNA，并通过 RT-PCR 定量 WNT5A 的表达。 [49] 锌在皮肤组织中含量丰富，因为锌是角质形成细胞分化和增殖所必需的。 [50]
necrosis factor α
Histopathologically, inflammatory cell infiltration(ICI), edema and fibroblast proliferation density(FPD); immunohistochemically TNF-α(Tumor necrosis factor α), EphrinA1, EphrinB1, EphrinB2 and EphB4 antibodies were evaluated in the skin tissues obtained after the applications performed twice a day and lasting 7 days. [1] miR-125a in lesional and non-lesional skin tissues, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-17 mRNA expressions in lesional skin tissues were detected. [2] Although the invasion of larvae upregulated the abundance of RAGE ligands in host skin tissues, mRNA expression levels of tumor necrosis factor-α, cyclooxygenase-2, endothelial adhesion molecules vascular cell adhesion protein-1, intracellular adhesion molecule-1, and E-selectin were suppressed by endogenous venestatin. [3]组织病理学上，炎症细胞浸润（ICI）、水肿和成纤维细胞增殖密度（FPD）；免疫组织化学方法评估了每天两次应用并持续 7 天后获得的皮肤组织中的 TNF-α（肿瘤坏死因子 α）、EphrinA1、EphrinB1、EphrinB2 和 EphB4 抗体。 [1] 检测病变和非病变皮肤组织中miR-125a、病变皮肤组织中肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-1β、IL-6和IL-17 mRNA的表达。 [2] nan [3]
advanced glycation end
The authors apply Raman spectroscopy to detect advanced glycation end products in human skin and to classify skin tissues by means of their Raman spectra. [1] After that, collected ear skin tissues were subjected to the observation of melanocytes, investigation for antioxidative stress markers, and measurement of advanced glycation-end products (AGEs). [2] Background The accumulation of advanced glycation end products (AGEs) occurring in skin tissues can be measured as skin autofluorescence (SAF). [3]作者应用拉曼光谱检测人体皮肤中的高级糖基化终产物，并通过拉曼光谱对皮肤组织进行分类。 [1] 之后，对收集的耳部皮肤组织进行黑色素细胞的观察、抗氧化应激标志物的研究以及晚期糖基化终产物（AGEs）的测量。 [2] nan [3]
polymerase chain reaction
Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-211-5p in 15 cases of HS tissues and normal skin tissues, as well as its expression in human hypertrophic scar fibroblasts (hHSFs) and normal fibroblasts. [1] We have investigated the expression levels of lnc-H19, miR-214-5p and fibroblast growth factor 2 (FGF2) in KD skin samples and normal skin tissues as well as matched cells by real-time quantitative polymerase chain reaction (RT-qPCR) assay. [2] Immunohistochemistry (IHC), Western blot (WB), and real-time polymerase chain reaction (RT-PCR) were used to detect the protein and mRNA expression levels of VEGF-A and TGF-β1 in skin tissues after treatment with PPE. [3]方法 采用定量实时聚合酶链反应（qRT-PCR）检测miR-211-5p在15例HS组织和正常皮肤组织中的表达，以及在人肥厚性瘢痕成纤维细胞（hHSFs）和正常皮肤组织中的表达情况成纤维细胞。 [1] 我们通过实时定量聚合酶链反应 (RT-qPCR) 研究了 KD 皮肤样本和正常皮肤组织以及匹配细胞中 lnc-H19、miR-214-5p 和成纤维细胞生长因子 2 (FGF2) 的表达水平化验。 [2] nan [3]
Normal Skin Tissues
Methods To clarify whether adiponectin plays a role in the inflammation and fibrosis of keloid, 50 patients with keloid and 50 healthy subjects were enrolled, We examined the serum and mRNA expression levels of adiponectin, TGF-β1, CTGF, IL-6 and TNF-α in normal skin tissues and keloid tissues by ELISA and qPCR, respectively. [1] To better understand the regulatory network underlying psoriasis, we explored the landscape of chromatin accessibility by assay for transposase-accessible chromatin using sequencing (ATAC-seq) on 15 psoriatic, 9 nonpsoriatic, and 19 normal skin tissues, and the chromatin accessibility data were integrated with genomic, epigenomic, and transcriptomic datasets. [2] Primary skin amyloidosis is a chronic skin disease in which amyloid deposits in the normal skin tissues without involving other organs. [3] We separated keloid tissues and normal skin tissues from keloid patients, and found that the expression of myofibroblast markers, α-SMA, Collagen I and Collagen III was increased in the keloid tissues as compared with normal skin tissues. [4] The results revealed that Runx2 expression levels were upregulated in keloid tissues and primary HKFs compared with the normal skin tissues and human normal fibroblasts. [5] We found that EIF3H was obviously upregulated in MM tissues compared with normal skin tissues, which was correlated with tumor stage and risk of lymphatic metastasis. [6] Keloid tissues, keloid-surro unding tissues, and normal skin tissues were collected from patients, for primary fibroblast culture. [7] PATIENTS AND METHODS Gene expression profiles of SKCM samples and normal skin tissues were obtained from the Genotype-Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA) databases to identify differentially expressed OS genes. [8] In this study, we immunohistochemically examined Trop2 expression in 116 EMPD tissue samples and 10 normal skin tissues. [9] Here, we found that the expression of ITIH5 was decreased in melanoma tissues compared with normal skin tissues. [10] The expression levels of FOXM1 in psoriasis tissues and normal skin tissues were examined using qRT-PCR and western blot. [11] Although, in normal skin tissues, CD137 expression was observed in 1. [12] Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-211-5p in 15 cases of HS tissues and normal skin tissues, as well as its expression in human hypertrophic scar fibroblasts (hHSFs) and normal fibroblasts. [13] Similarly, MIR205HG levels were significantly higher melanoma tissues than adjacent normal skin tissues (n=30). [14] To investigate the lncRNA, circRNA and mRNA expression profiles, we performed RNA sequencing of human HS and normal skin tissues. [15] Methods: The expression of PKM2 in 62 cases of actinic keratoses (AK), 15 cases ofBowen´s diseases (BD), 66 cases of CSCC and 10 cases of normal skin tissues (NT) were detected by immunohistochemistry. [16] From October 2019 to January 2020, hypertrophic scar tissues from 6 patients with hypertrophic scar (2 males and 4 females, aged (34±11) years) and the remaining normal skin tissues from 6 patients with trauma (3 males and 3 females, aged (35±13) years) after skin flap transplantation were collected. [17] We have investigated the expression levels of lnc-H19, miR-214-5p and fibroblast growth factor 2 (FGF2) in KD skin samples and normal skin tissues as well as matched cells by real-time quantitative polymerase chain reaction (RT-qPCR) assay. [18] MIR503HG was upregulated and miR‐143‐3p was downregulated in HS versus normal skin tissues. [19] Thirty‐seven keloids and 37 normal skin tissues were collected, and the changes of circRNAs, microRNAs (miRNAs) and mRNAs in 3 keloids and 3 normal samples by high‐throughput sequencing were detected first. [20] In this report, we analyzed gene expression profiles of paired specimens of keratinocyte carcinomas with their matched normal skin tissues as the control. [21] In this report, we analyzed gene expression profiles of paired specimens of keratinocyte carcinomas with their matched normal skin tissues as the control. [22] In contrast, the MCPyV negative MCC, BCCs, SCCs and normal skin tissues all exhibited exclusive fully-spliced TrkA mRNA expression, associated with variable immunoreactivity for non-phosphorylated but not phosphorylated TrkA. [23] Data obtained from the GEPIA database and the Gene Expression Omnibus database showed a lower expression of PKP1 in melanoma tissues compared to normal skin tissues. [24] The obtained novel 2D-CNs not only present robust and localized multiple bacterial eradication capabilities with nearly 100% bactericidal efficiency at low concentrations but also possess rapid and safe skin wound disinfection via a short-time photothermal treatment without damaging normal skin tissues or causing accumulative toxicities, thus presenting great potential for broad-spectrum eradication of pathogenic bacteria. [25] We performed a circRNA microarray assay to determine circRNA expression in keloid and paired normal skin tissues. [26]方法 为明确脂联素是否在瘢痕疙瘩炎症和纤维化中发挥作用，选取 50 例瘢痕疙瘩患者和 50 名健康受试者，检测脂联素、TGF-β1、CTGF、IL-6 和 TNF-α 的血清和 mRNA 表达水平。分别通过ELISA和qPCR检测正常皮肤组织和瘢痕疙瘩组织中的α。 [1] 为了更好地了解银屑病背后的调控网络，我们通过对 15 个银屑病患者、9 个非银屑病患者和 19 个正常皮肤组织进行转座酶可及染色质测序 (ATAC-seq) 来探索染色质可及性的前景，并整合染色质可及性数据使用基因组、表观基因组和转录组数据集。 [2] nan [3] nan