Acne vulgaris is a common chronic inflammatory skin disorder with a multifactorial pathogenesis involving genetic predisposition, hormonal regulation, microbial factors, and the cutaneous immune microenvironment. In recent years, psychosocial influences and their association with acne onset and progression have drawn increasing attention. Chronic stress may disturb immune homeostasis via neuroendocrine regulatory pathways and thereby contribute to acne pathophysiology. However, the molecular mechanisms by which chronic stress modulates acne development and exacerbation remain unclear. In the present study, we established a chronic stress-induced murine model of acne to characterize stress-related behavioral alterations, skin histopathological changes, serum corticosterone levels, and inflammatory mediators profiles in both serum and skin tissue. We further performed transcriptomic profiling to identify differentially expressed genes and to elucidate candidate regulatory pathways and molecular targets. Our findings indicate that chronic stress indeed contributes to the pathological progression of acne. However, stress hormones do not appear to directly drive inflammatory worsening. Instead, transcriptomic analysis indicated that chronic stress may play an important role in complex neuroendocrine-metabolic-immune interactions involved in acne exacerbation. These preliminary results provide experimental evidence exploring the role of chronic stress in acne pathogenesis and suggest potential targets for acne prevention and treatment.

BACKGROUND:Systemic lupus erythematosus (SLE) is characterized by complex immune dysregulation, including abnormalities in macrophage polarization. Pyrroloquinoline quinone (PQQ) has been reported to exert anti-inflammatory and immunoregulatory effects in various disease models, but its role in SLE remains unclear. OBJECTIVE:To evaluate the therapeutic effects of PQQ in SLE and SLE-associated diffuse alveolar hemorrhage (DAH) and to assess its impact on macrophage activation. METHODS:Pristane-induced DAH mice and lupus-prone MRL/lpr mice were used to assess in vivo efficacy. Single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing (bulk RNA-seq) analyses were performed to characterize immune remodeling and explore underlying mechanisms. RAW264.7 macrophages were used to examine the inhibitory effects of PQQ on M1 macrophage polarization. RESULTS:PQQ alleviated lung injury in SLE-DAH mice and reduced splenomegaly, autoantibodies, renal inflammation, and systemic cytokines in MRL/lpr mice. Flow cytometry and scRNA-seq consistently demonstrated reductions in inflammatory macrophage populations. Bulk RNA-seq further indicated that PQQ modulated inflammatory pathways associated with macrophage activation. Moreover, PQQ significantly reduced the expression of inflammatory mediators (IL-6, TNF-α, and IL-1β), inhibited M1 macrophage polarization, and decreased the production of oxidative stress-associated indicators (ROS and NO) in LPS/IFN-γ-stimulated RAW264.7 cells. Finally, PQQ regulated ERK/MAPK signaling, which contributed to the attenuation of inflammatory responses. CONCLUSION:PQQ attenuates SLE and its pulmonary complication DAH by regulating macrophage polarization and may serve as a potential immunomodulatory therapeutic candidate.

This study aims to comprehensively analyze the intricate relationship between unsaturated fatty acids (UFAs, particularly omega-3 and omega-6 UFAs) and acne, from their clinical therapeutic effects to their underlying genetic regulatory mechanisms, to elucidate the role of UFAs in acne pathogenesis. Clinical evidence synthesis: we systematically reviewed randomized controlled trials (RCTs) to evaluate the impact of UFA supplementation on acne treatment outcomes. Genetic analysis: two-sample Mendelian randomization (MR) analysis we used to investigate causal relationships between serum UFA metabolites and acne, identifying potential key regulatory enzymes. The synthesis of these RCT studies confirmed that UFA supplementation improved acne conditions. MR analysis revealed causal links between three serum UFA metabolites and acne, with dihomo-gamma-linolenic acid (DGLA) (OR = 8.457; 95

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterised by chronic inflammation and immune dysregulation, with neutrophils playing a critical role in disease pathogenesis. In this study, we elucidated the involvement of the CXCL2-PI3K/AKT/NF-κB signalling axis in the abnormal activation of neutrophils in SLE using transcriptome analysis and functional experiments. Transcriptomic profiling revealed that CXCL2 expression is significantly upregulated in SLE patients, contributing to the activation of key inflammatory pathways and the expression of pro-inflammatory cytokines and chemokines. In vitro and in vivo experiments confirmed that CXCL2 promotes the transcription of inflammatory factors by activating the PI3K/AKT/NF-κB pathway, and inhibitors targeting this signalling axis effectively reduced inflammation. Furthermore, neutrophils from SLE patients exhibited a 'pre-activated' state under CXCL2 stimulation, potentially due to epigenetic or metabolic alterations. The functional relevance of CXCL2 was further validated in vivo, where knockout of CXCL2 or depletion of neutrophils reduced tissue damage and inflammatory responses. This study highlights the importance of the CXCL2-PI3K/AKT/NF-κB signalling axis in SLE and suggests that targeting CXCL2 or neutrophil-specific markers could provide novel therapeutic strategies for managing SLE. Future research should explore the heterogeneity of neutrophil subpopulations in SLE and the role of metabolic reprogramming in exacerbating inflammation, further refining potential targeted therapies.

Infantile hemangioma (IH), a common vascular tumor, occurs in childhood; however, its pathogenesis has not been fully elucidated. In the present study, the roles and detailed mechanisms of long non‑coding RNA (lncRNA) NEAT1 in the progression of hemangioma were further explored. The NEAT1‑interacting proteins were selected by analyzing the catRAPID database and lactate dehydrogenase B (LDHB) was predicted to bind with NEAT1. The binding between NEAT1 and LDHB was validated using an RNA immunoprecipitation assay and it was further found that knocking down NEAT1 expression destabilized LDHB by regulating the proteasome pathway. The knocking down of lncRNA NEAT1 also inhibited cellular protein lactylation and downregulated β‑catenin. Furthermore, blockade of lactylation via 2‑DG and oxamate attenuated the viability and colony formation of hemangioma cells. NEAT1 promoted the lactylation of H3K18 in the promoter region of β‑catenin, and blockade of lactylation downregulated β‑catenin expression in hemangioma cells. The lactyltransferases alanyl‑tRNA synthetase 1 and P300 were regulated by NEAT1 and also positively regulated β‑catenin. The levels of β‑catenin mRNA and H3K18 lactylation were also found to be elevated in IH tissues. Taken together, the results of the present study revealed that lncRNA NEAT1, which is upregulated in hemangioma, binds with and stabilizes LDHB, subsequently elevates the levels of cellular lactate and H3K18 lactylation, potentiates β‑catenin transcription and ultimately enhances the proliferation of hemangioma cells.

目的 探讨小儿手指挛缩性瘢痕激光治疗经验.方法 采用自身前后对照研究方法,选取 2021 年 12 月至2022 年 12 月,昆明市儿童医院皮肤科收治的 30 例手指挛缩性瘢痕患儿.其中 17 例瘢痕外观色红、充血明显,使用脉冲染料激光(PDL,585 nm)联合超脉冲CO2 点阵激光进行治疗;13 例肤色瘢痕单独使用超脉冲CO2 点阵激光进行治疗.每例患儿治疗 3 次,每次治疗间隔 2 个月.治疗前、治疗后分别采用温哥华瘢痕评分量表(VSS)对瘢痕情况进行评分,并记录治疗前后受累关节活动度的变化以及不良反应发生情况,治疗结束 8 周后进行疗效评价.结果 所有病例治疗后与治疗前相比,VSS评分均明显下降(P＜0.05),受累关节活动度明显优于首次治疗前(P＜0.05).疗效评价结果显示,显效 19 例、有效 8 例、无效 3 例,显效率 63.3%,有效率 90.0%.治疗区域治疗后均未观察到水疱、感染、增生性瘢痕形成等不良反应.结论 激光治疗小儿手指挛缩性瘢痕效果明显,相关并发症少,值得临床推广.

BACKGROUND Purpura annularis telangiectodes of Majocchi (PATM), also known as Majocchi, is a rare subclass of pigmented purpuric dermatoses. The etiology of PATM is unknown, but it seems more common in children and young women. The skin lesions are mostly symmetrical ring-shaped reddish-brown macules on the lower limbs. CASE SUMMARY A 9-year-old girl, who has received treated in our department, presented with reddish-brown ring-shaped rash on both lower limbs that had been present for 6 mo. These lesions, red brownish annular or petaloid patches, were mostly found on ankles and lower limber, which do not fade when adding pressure and no feel of infiltration and no atrophy when touching those lesions. Pathological examination showed deposition of hemosiderin in papillary dermis. However, dermoscopy showed the pigmentation in the center as well as the lavender patches on the edge of lesion. The child was thus diagnosed with PATM. After diagnosis, we suggested the patient avoid strenuous exercise. she was given vitamin C tablets for oral and mometasone furoate cream for external use. Follow-up examinations and treatment continue to support the clinical diagnosis to date. CONCLUSION This is the first report of investigating PATM using dermoscopy, which can differentiate PATM from other diseases due to its unique microscopic feature under dermoscopy. Although PATM is harmless, it still requires long-term follow-up. Moreover, dermoscopy technique can be applied for observation of multi-site lesions and correlated with histopathology. Thus, we believe this approach could be generalized for future diagnosis of PATM.

Dear Editor, A 2-month-old female infant was admitted to the hospital for “annular erythema, scales, and trophy in facial area and body for 1 month.” The baby had no history of fever, external drug treatment, or oral drug therapy during the disease course. The infant's gestational age was 39 + 3 weeks, and her body weight was 3100 g at birth. She received breast feeding exclusively and had no history of intrauterine hypoxia or birth asphyxia. The prenatal examinations of her mother showed normal findings, who reported no history of gestational hypertension, diabetes, or syphilis. No relevant family history was reported. Dermatological examinations showed annular erythema with different sizes (range of dimeter, 0.5–1.5 cm) at facial area and body of the baby, of which the edges were slightly raised, and the color decreased when pressed. Fine yellow-white scales were found in several skin lesions, and atrophy was detected at the center (Figure 1A,B). The infant's liver function examination revealed that the total bilirubin level was 21.5 (normal, 3.4–17.7) μmol/L, and the direct bilirubin level was 6.3 (normal, 0–3.4) μmol/L; in addition, the other indicators also showed no abnormality. Treponema pallidum antibody was negative (−), electrocardiograph showed nodal tachycardia (heart rate, 156 bpm). Echocardiography displayed patent foramen ovale (approximately 3.5 mm). Examination of antinuclear antibodies (ANA) in the baby revealed the following results: ANA (−), natural anti-Sjogren's syndrome A 60kDa (SSA-60) (++), anti-52 kDa human Ro ribonucleoprotein antibody (Ro-52)(−), anti-Sjogren's syndrome B antiboy (SSB antibody) (−), and anti-doubl-strand deoxyribonucleic acid (ds-DNA antibody) (−). The mother reported no clinical manifestations of connective tissue diseases, such as Sjogren's syndrome (SS) and systemic lupus erythematosus (SLE), and the results of ANA examination could be summarized as follows: ANA (+, titer 1:80), extractable nuclear antigens (ENA antibody) (+), Ro-52 antibody (−), SSA-60 antibody (+), SSB antibody (−), and ds-DNA antibody (−). The patient's dermoscopy showed light red background, disappearing of skin surface texture, and whitish structureless areas, and dispersed irregular linear or reticular vascular structures (Figure 2). Reflectance confocal microscopy (RCM) revealed focal spongiotic edema in the spinous layer of skin lesion, and inflammatory cells with the high refraction migrated to epidermis. The dermal-epidermal junction was full of inflammatory cells, which made the junction unclear. Besides, hemangiectasis and infiltration of various highly refractive inflammatory cells were found at the level of the superficial dermis (Figure 3). High-frequency ultrasound (HFUS) examination showed that the epidermis was thickened, and a hypoechoic zone appeared at the dermal-epidermal junction and superficial dermis, and the boundary was unclear (Figure 4). Combined with clinical and laboratory tests, the infant was diagnosed with neonatal lupus erythematosus (NLE). Due to the laboratory tests and her physical condition, we only required the baby strict sun protection without any special treatment. Five months later, the lesion was disappeared (Figure 1C), and her antinuclear antibody examination was negative. It is noteworthy that NLE is a rare autoimmune disease with the incidence of approximately 1/20 000,1 which was firstly reported by McCuistion and Schoch in 1954. At present, it is generally considered that maternal lupus-associated autoantibodies are passively transferred to fetus through placenta.2 Although 30%–50% of mothers have no symptoms before delivery, SSA or SSB antibody is detected in maternal serum.3 In some cases, the fetal antibodies are not fully consistent with maternal antibodies, and several studies reported the delivery of babies with NLE from mothers with negative antibodies. These findings indicate that maternal antibody transmission is not the only cause of NLE.3 The baby reported here was found with annular erythema of different sizes at facial area, scalp, and body at 1 month after birth. Although no clinical symptom was found in the mother, serum SSA-60 antibody in both baby and mother was positive, which was in agreement with the American College of Rheumatology (ACR) diagnostic criteria for NLE (2014 edition).4 SSA antibody includes two subtypes of SSA-60 and SSA-52/TRIM21 antibodies, while SSA-60 antibody is closely associated with SLE and SS. In addition, SSA-60-positive antibody could be the only indicator in some cases of SLE, which has especially a high specificity in patients with cutaneous lupus erythematosus.5 The pathological manifestations of NLE are similar to subacute lupus erythematosus, mainly including epidermal atrophy, liquefaction of basal cells, and dermal and perivascular infiltration of lymphocytes.6 Due to the possible risks of anesthesia and surgery, this baby's family refused pathological examination. Therefore, dermatoscopy, RCM, and HFUS examinations were used for the assessment of skin lesions in the baby. Dermatoscopy showed disappearing of texture on skin surface and whitish structureless areas, as well as focal hemangiectasis. HFUS examination revealed a hypoechoic zone at the dermal-epidermal junction and superficial dermis. RCM showed unclear dermal-epidermal junction, hemangiectasis, and infiltration of various highly refractive inflammatory cells at the level of epidermis, dermal-epidermal junction and superficial dermis. The manifestations of the three measurements were highly in agreement with the pathological manifestations of NLE. To date, no study has concentrated on skin imaging in NLE patients. As pathological examinations could not be performed for newborns, noninvasive examinations by dermatoscopy, RCM, and HFUS have a high consistency with histopathological examinations and play important roles in the early diagnosis and differential diagnosis of NLE. The authors thank Hong Shu for guiding them to analyze cases. This study is supported by Yunnan Key Laboratory of Children's Major Disease Research; Yunnan Province Clinical Research Center for Children's Health and Disease. The authors declare that there is no conflict of interest. Yunnan Key Laboratory of Children's Major Disease Research; Yunnan Province Clinical Research Center for Children's Health and Disease Data are available upon request from the authors.

皮肤影像学技术如皮肤镜、反射式共聚焦显微镜及皮肤甚高频超声等越来越多地应用于红斑鳞屑性疾病的诊断与鉴别诊断.皮肤型红斑狼疮临床表现多样,应用皮肤影像学技术可提高临床诊断率,其无创性及可重复性在诊断、鉴别诊断及预后随访中有较大优势.本文就皮肤影像学技术在皮肤型红斑狼疮中应用的研究进展作一综述.

硬化性苔藓(lichen sclerosus,LS)由法国学者Hal-lopeau于1887年首次提出,Darier[1]于1889年发表了第一篇相关论文,LS是一种病因及发病机制尚未明确的慢性炎症介导的萎缩性疾病,发病年龄主要集中在青春期前幼女及绝经后妇女,呈双峰分布.本病好发于女性外生殖器及肛周,病程缓慢,并伴有剧烈瘙痒,后期可出现局部萎缩、功能障碍以及继发恶性病变[2-4],因此,早期诊断、规范治疗及长期随访对于患者的预后尤其重要.皮肤影像学包括皮肤镜、反射式共聚焦显微镜(RCM)、甚高频超声,通过无创的检测手段对患者皮疹进行纵向及横向的动态评估,对于患者的早期诊断、治疗随访有明显优势,我们对近半年我科确诊的女童会阴部LS临床特征及皮肤影像学下表现进行归纳总结.

In this paper, we report the case of an 11-year-old child with multiple hyperpigmented spots with atrophy on the back, which was finally diagnosed as atrophying tinea versicolor, by dermoscopic and histopathological examination. Atrophying tinea versicolor is a rare type of pityriasis versicolor, and the mechanism of its atrophy is thought to be the result of apoptosis of keratin-forming cells and inhibition of keratin-forming cell proliferation caused by Malassezia itself, which stimulates the synthesis of inflammatory cytokines in the stratum corneum. The article reports for the first time on its characteristic dermoscopic manifestations, but further extensive studies are needed.

紫色色杆菌是一种机会致病菌，常存在于热带及亚热带的土壤和水中。紫色色杆菌偶尔可引起哺乳动物包括人类的严重化脓性感染或败血症，病死率极高，预后差。我院皮肤科门诊诊治了1例紫色色杆菌感染患儿，现将结果报告如下。1 病历摘要患儿女，10岁。因左下肢溃疡及红肿6 d，发热3 d，于2019年8月19日至我院急诊及皮肤科门诊就诊。

BACKGROUND:Membranous aplasia cutis congenita (MACC) presents at birth characterized by oval epidermis defect. Skin lesions with MACC have various clinic manifestations. In recent years, the usefulness of trichoscopy (scalp dermoscopy) has been reported for hair loss diseases. However, the dermoscopic features of MACC were mostly reported by case reports.OBJECTIVES:To summarized the obvious dermoscopic characteristics of MACC.MATERIALS & METHODS:These 56 cases met the clinical diagnostic criteria for MACC without forceps delivery complications or other birth injuries. To find the dermoscopic characteristics of MACC by summarizing 56 infants' dermoscopic pictures.RESULTS:The dermoscopic manifestation of MACC are characterized by hair follicle openings and hair deficiency in the center of skin lesions, translucent epidermis, hair root and hair bulb arranged along the margins of skin lesion.CONCLUSION:The typical dermoscopic characteristics of MACC could help clinicians to early diagnose and differential diagnosis.

Background. Aberrant DNA methylation patterns are of increasing interest in the study of psoriasis mechanisms. This study aims to screen potential diagnostic indicators affected by DNA methylation for psoriasis based on bioinformatics using multiple machine learning algorithms and to preliminarily explore its molecular mechanisms. Methods. GSE13355, GSE14905, and GSE73894 were collected from the gene expression omnibus (GEO) database. Differentially expressed genes (DEGs) and differentially methylated region- (DMR-) genes between psoriasis and control samples were combined to obtain differentially expressed methylated genes. Subsequently, a protein-protein interaction (PPI) network was established to analyze the interaction between differentially expressed methylated genes. Moreover, the hub genes of psoriasis were screened by the least absolute shrinkage and selection operator (LASSO), Random Forest (RF), and Support Vector Machine (SVM), which were further performed single-gene gene set enrichment analysis (GSEA) to clarify the pathogenesis of psoriasis. The druggable genes were predicted using DGIdb. Finally, the expressions of hub genes in psoriasis lesions and healthy controls were detected by immunohistochemistry (IHC) and quantitative real-time PCR (RT-qPCR). Results. In this study, a total of 767 DEGs and 896 DMR-genes were obtained. Functional enrichment showed that they were significantly associated with skin development, skin barrier function, immune/inflammatory response, and cell cycle. The combined transcriptomic and DNA methylation data resulted in 33 differentially expressed methylated genes, of which GJB2 was the final identified hub gene for psoriasis, with robust diagnostic power. IHC and RT-qPCR showed that GJB2 was significantly higher in psoriasis samples than those in healthy controls. Additionally, GJB2 may be involved in the development and progression of psoriasis by disrupting the body’s immune system, mediating the cell cycle, and destroying the skin barrier, in addition to possibly inducing diseases related to the skeletal aspects of psoriasis. Moreover, OCTANOL and CARBENOXOLONE were identified as promising compounds through the DGIdb database. Conclusion. The abnormal expression of GJB2 might play a critical role in psoriasis development and progression. The genes identified in our study might serve as a diagnostic indicator and therapeutic target in psoriasis.

目的 观察PDL联合超脉冲CO2点阵激光治疗儿童增生性瘢痕的临床疗效.方法 选取增生性瘢痕患儿45例,使用脉冲染料激光(PDL,585 nm)联合CO2点阵激光进行治疗,每例患儿治疗4次,每次治疗间隔8周.治疗前、后分别采用温哥华瘢痕评分量表(VSS)对患儿增生性瘢痕进行评分,并用皮肤镜及高频皮肤超声对瘢痕血管数量、厚度进行测量.治疗结束后8周评价疗效.结果 本组患儿中显效27例、有效13例、无效5例,有效率88.9％.将治疗前与治疗后的VSS评分、皮损厚度、皮肤镜评分进行对比,差异均有统计学意义(P<0.05).所有患儿在激光治疗及用药后均未出现皮肤水疱、破溃等严重不良反应.结论 PDL联合超脉冲CO2点阵激光治疗儿童增生性瘢痕安全、有效.

目的:总结5例传染性软疣样表现的先天自愈性朗格汉斯细胞组织细胞增生症临床特征、皮肤镜下表现及组织病理学特点.方法 :采用回顾性分析对昆明医科大学附属昆明市儿童医院皮肤科5例传染性软疣样表现的先天自愈性朗格汉斯细胞组织细胞增生症患儿的临床资料、皮肤镜图片、组织病理及免疫组化染色资料进行分析总结.结果 :5例患儿中,男3例,女2例,平均发病月龄为4.5个月,平均病程2.1个月.所有患儿皮肤镜下表现有2种,丘疹区在皮肤镜偏振光下可见淡红色及肤色类圆形结构区,部分中央见云雾状黄白色或褐色鳞屑,浸润法下边缘红色背景褪色呈白色环.白色萎缩区在皮肤镜偏振光下可见边界清楚的白色背景中央紫红色或褐色结构区.浸润法下中央紫红色或褐色结构区不能褪色.组织病理学表现为弥漫性浸润或灶性浸润的淋巴细胞、组织细胞及嗜酸性粒细胞,并可见胞质丰富、淡伊红染色的单核样细胞,核呈椭圆形或肾形,部分可见核沟.免疫组化中朗格汉斯细胞组织细胞S-100蛋白、CD1a、Langerin均阳性.结论 :该病临床少见,容易被误诊,结合皮肤镜下特点可初步判断,提高病检率,依靠组织病理学及免疫组织化学染色讲行确诊,该病有可能转化为系统性朗格汉斯细胞组织细胞增生症,需长期随访.

Background Syringocystadenoma papilliferum (SCAP) represents a rare, noncancerous adnexal tumor predominantly presenting at birth or in early childhood. Case summary In this study, a 35-day-old girl was admitted to Kunming Children's Hospital in October 2019 due to a lesion in the right frontotemporal region since birth. The surface of the lesion was bright red, granular, and papillary and easily bled upon touch, with about 1.5 cm × 4 cm in size. A subcutaneous mass was felt at the base of the lesion, with a size of about 3 cm × 5 cm. Dermatoscopy showed that the skin lesion was lobular and crumby. The lesion center was reddish or white, while the edges were white or yellowish band-like. There were polymorphic vascular structures and white radial streaks in the lesion, with some vascular clusters scattered. Pathological examination showed papilloma-like hyperplasia of the epidermis, with the epidermis partly sinking into the dermis to form several cystic depressions. Combining clinical and histopathological features, the child was diagnosed with SCAP. Follow-up is ongoing, and surgical resection will be performed. Conclusion This was a special clinical manifestation of SCAP, which complements the clinical manifestations of the disease and provides new insights for the diagnosis and differentiation of neonatal skin tumors.

目的 观察56例瘢痕患儿采用皮肤镜和高频超声检查的图像特征.方法 临床未经治疗的几类瘢痕患儿,每例皮损先后行皮肤镜及高频超声(频率50MHZ)检查,记录并统计各项图像特征.结果 56例瘢痕患者中,增生型瘢痕28例,皮肤镜下可见淡红(21例)或淡黄色背景(7例)、分支状血管(25例);高频超声下可见表皮变薄(24例)、真皮层增厚(28例)、回声不均(22例),可见线条状强回声(23例).瘢痕疙瘩10例,皮肤镜下可见淡红色背景(9例)、网状血管(8例);高频超声下可见表皮变薄(7例)、真皮层增厚(10例),可见线条状强回声紊乱(8例).浅表型瘢痕11例,皮肤镜下可见褐色色素沉着(10例)、分支状血管(8例);高频超声下表皮稍变薄(9例),真皮层基本正常(10例).凹陷型瘢痕7例,皮肤镜下可见肤色背景(6例),中央无结构区(5例);高频超声下可见表皮正常(6例),真皮层萎缩(7例).结论 结合临床表现,皮肤镜和高频超声的图像特征可能为瘢痕的治疗及疗效评估提供帮助.

目的 探讨云南地区婴幼儿血管瘤发病的危险因素.方法 随机选择确诊为IH的婴幼儿患者994例,与994名同年龄同地区的儿童进行对照研究.由专业调查员对其父母进行面对面的问卷调查(包括父母接触环境,职业,产前和国产期的特点).数据采用SPSS 19.0软件处理,采用二分类Logistic回归对所有变量进行单因素和多因素回归分析(向前LR,进入标准0.05,剔除标准0.10),检验水准a=0.05.结果 对以上单因素回归分析选出的11个相关因素进行分析.正相关危险因素7个,性别(OR=2.641,95％ CI:2.147～3.249)、保胎药(OR=2.797,95％CI:2.172～3.602)、孕期病毒感染(OR=10.233,95％ CI:2.521～41.536)、室内外环境有害暴露(OR=2.038,95％ CI:1.426～2.911)、母亲职业有害暴露(OR=3.396,95％ CI:1.886～6.115)、宫内室息(OR=15.060,95％CI:6.215～36.489)、脐带绕颈(OR=4.067,95％CI:3.050～5.422).负相关危险因素4个,足月(OR=0.507,95％ CI:0.348～0.741)、高龄产妇(OR=0.233,95％ CI:0.161～0.339)、头胎(OR=0.433,95％ CI:0.346～0.542)、滋补品(OR=0.550,95％ CI:0.391～0.772).结论 本研究发现IH发病和父母孕前和孕期部分环境因素相关(孕前和怀孕早期预防流产的孕激素治疗)之间有密切的关系.

Systemic lupus erythematosus (SLE) is a severe autoimmune disease and the pathogenesis remains incompletely understood. This study aimed to investigate the role of miR-125b in the pathogenesis of SLE and explore the underlying mechanism. Compared to healthy controls, the expression of miR-125b decreased in peripheral blood mononuclear cells (PBMCs) of SLE patients. In addition, PBMCs exposed to ultraviolet B had lower miR-125b level compared to those unexposed to radiation. We identified UV radiation resistance associated gene (UVRAG) as a target of miR-125b. Jurkat cells treated with miR-125b-5p agomir showed reduced levels of ATG7, Beclin-1 and LC3 II and decreased autophagy. In contrast, Jurkat cells treated with miR-125b-5p antagomir showed increased levels of ATG7, Beclin-1 and LC3 II and increased autophagy. Furthermore, Jurkat cells transfected with UVRAG expression vector showed higher expression of ATG7, Beclin-1 and LC3 II and increased autophagy. Conversely, cells transfected with UVRAG siRNA had lower expression of ATG7, Beclin-1 and LC3 II and decreased autophagy. Taken together, our data demonstrate that Ultraviolet B radiation can downregulate miR-125b-5p and increase UVRAG expression and autophagy activity in PBMCs of SLE patients. These findings help explain how ultraviolet B exacerbates SLE and suggest that UVRAG is a potential therapeutic target for SLE.