患者男, 41岁, 因全身反复发生鳞屑性红斑、丘疹、斑块16年, 泛发加重伴发热7 d就诊。16年前患者全身出现皮疹, 初发4年未行治疗。12年前, 患者因皮疹反复发作于当地医院就诊, 口服甲氨蝶呤, 用药期间出现肝功能异常, 予停药并对症处理, 后逐渐好转。8年前劳累后皮疹复发加重, 当地医院给予环孢素口服, 用药后血压持续升高, 环孢素逐渐减量, 继续治疗, 最终病情好转。此后患者长期外用糖皮质激素(简称激素)药膏封包, 皮疹时轻时重, 无明显季节性。7 d前, 受凉后全身皮肤出现潮红肿胀、脱屑, 局部发生脓疱伴发热, 最高达40 ℃。无关节疼痛。既往高血压病史1年。入院体检:体温38.2 ℃, 血压150/75 mmHg(1 mmHg = 0.133 kPa), 体重110 kg, 向心性肥胖;双下肢、足背重度凹陷性水肿, 余无明显异常。皮肤科情况:全身弥漫性潮红肿胀、脱屑, 局限性脓疱、脓湖形成;指(趾)甲角化过度性增厚、浑浊、变形, 局部呈不同程度顶针样改变;银屑病面积和严重程度指数(psoriasis area and severity index, PASI)67.1, 体表面积(body surface area, BSA)评分95%(图1A ～ 1C)。四肢近心端和腹部、前胸多发紫红色膨胀纹。实验室检查:血常规示白细胞12.5 × 109/L[参考值:(3.5 ～ 9.5) × 109/L, 下同], 中性粒细胞比例0.812(0.40 ～ 0.75), C反应蛋白234.81 mg/L(0 ～ 10 mg/L), 血清淀粉样蛋白A 440.46 mg/L(0 ～ 10 mg/L);血尿酸722 μmol/L(135 ～ 425 μmol/L), 甘油三酯2.39 mmol/L(0.56 ～ 1.71 mmol/L), 动脉粥样硬化指数4.288(<4), 血钾3.25 mmol/L(3.50 ～ 5.30 mmol/L), IgE 1 370.00 IU/ml(<100 IU/ml), 降钙素原0.326 ng/ml(<0.046 ng/ml), 红细胞沉降率67.0 mm/1 h(0 ～ 15.0 mm/1 h);乙肝病毒抗原抗体、肿瘤标志物(神经元特异性烯醇化酶、癌胚抗原、甲胎蛋白、总前列腺特异性抗原、游离前列腺特异性抗原、细胞角蛋白19片段、游离前列腺特异抗原/总前列腺特异抗原、糖类抗原125、糖类抗原19-9、糖类抗原72-4、铁蛋白)、结核感染T细胞实验、风疹病毒、巨细胞病毒、EB病毒、单纯疱疹病毒1型等检查结果均阴性。胸部计算机断层扫描示双肺尖小叶间隔增厚, 双肺轻度间质性改变, 双侧胸腔积液并肺组织膨胀不全。

OBJECTIVE:By presenting a case study on multiple instances of Bowen's disease and the consistent use of narrow-band ultraviolet B (NB-UVB) phototherapy over a three-year period, our aim is to enhance the comprehension of domestic clinicians regarding the disease. Additionally, we seek to review existing literature, encouraging dermatologists to consider clinical secondary primary lesion diagnoses.METHOD:Our approach involves analyzing a diagnosed case of multiple Bowen's disease, examining clinical manifestations, histopathology, imaging results, and treatment methods related to NB-UVB phototherapy. We aim to facilitate discussion and understanding through a comprehensive literature analysis.RESULTS:An elderly male with a 30-year history of psoriasis vulgaris initiated continuous NB-UVB therapy three years ago. A year later, he developed red patches and plaques with distinct borders and scaly surfaces on his face, trunk, lower extremities, and scrotum. Histopathological examination confirmed Bowen's disease. Treatment involved liquid nitrogen cryotherapy, with no recurrence observed during the one-year follow-up.CONCLUSION:This case highlights that Bowen's disease, typically solitary, can manifest as multiple instances, especially in individuals with a history of psoriasis vulgaris. While NB-UVB stands as the primary treatment for psoriasis vulgaris, caution is warranted due to the potential risk of skin tumor induction with prolonged high-dose usage. Clinicians should be vigilant in monitoring and assessing the long-term implications of such therapies.

Melanoma is a malignant tumor that originates from melanocytes. The incidence of melanoma is increasing worldwide, partially because of its insensitivity to radiotherapy or chemotherapy. Therefore, effective treatments for melanoma are urgently required. In this study, we employed folic acid-modified sulfasalazine long-circulating liposomes (FA-SSZ-Lips) to precisely target drug delivery to melanoma cells, eliciting ferroptosis effectively. The synthesized FA-SSZ-Lips were characterized as small spheres of a double-layer membrane, a particle size of 110.1 nm, and a zeta-potential of -22.8 +/- 0.66 mV. FA-SSZ-Lips are effective drug carriers with SSZ-loading ratio and SSZ release rate of 6.2 +/- 0.10%, and 72.63 +/- 1.40%, respectively. The liposomes enhanced SSZ solubility, and the folic acid modifications increased the liposome targeting to melanoma cells. Compared with SSZ alone, FA-SSZ-Lips more strongly inhibited B16F10 cell growth, significantly disrupted the intracellular redox balance, and induced ferroptosis. After treatment, considerable differences were observed in the tumor volumes between FA-SSZ-Lips and phosphate-buffered saline control groups. The tumor growth-inhibition value of the FA-SSZ-Lips group reached 70.09%. Thus, FA-SSZ-Lips exhibited favorable antitumor effects in vitro and in vivo and are a promising strategy for melanoma treatment.

BACKGROUND Tofacitinib is an oral Janus kinase（JAK） inhibitor that is currently approved by the United States Food and Drug Administration for the treatment of rheumatoid arthritis（RA）. Varicella zoster virus reactivation leading to herpes zoster（HZ） is an adverse effect of this drug; however, recurrent HZ at the same site is a rare clinical condition.CASE SUMMARY A 70-year-old female RA patient had undergone 1-year of tofacitinib treatment（10 mg daily）. About 1 mo after initiation of oral tofacitinib, she developed blisters on the left flank and abdomen and was diagnosed with HZ; antiviral therapy with acyclovir was resolutory. However, 5 d prior to presentation at our hospital, erythema and blisters with severe pain recurred at the same site. Small clustered blisters and bullous were visible on the left lumbar abdomen and perineum, with a pain score of 8（visual analogue scale）. Antiviral, nutritional supplement, analgesic and other treatments led to healing but over an atypically long period（approximately 26 d, vs approximately 1 wk）. HZ is a common and serious adverse reaction of JAK inhibitors, but it rarely recurs. Our patient’s experience of HZ recurrence at the same site, with a wider affected area, more severe pain and longer healing period, is inconsistent with previous reports.CONCLUSION Same-anatomical site HZ recurrence may occur during oral tofacitinib treatment, with more severe clinical manifestations than in the initial occurrence.

BACKGROUND:JAK2/STAT3 pathway is involved in the development and progression of melanoma once DNA damage is caused by environment and genetic factors.OBJECTIVE:Here, we aimed to identify novel inhibitor of JAK2/STAT3 pathway and reveal the underlying mechanisms.METHODS:Eighty MedChemExpress compounds were screened by using STAT3-Luc reporter in A375 cells. Podocarpusflavone A (PCFA) was identified as an inhibitor of STAT3, which was further verified in four melanoma cell lines. The anti-melanoma effects and mechanism of PCFA were examined and explored in melanoma cells and mouse xenograft models by using Western blot and cell-counting kit-8 assay.RESULTS:PCFA exhibited potent inhibitory effects on melanoma both in vitro and in vivo. PCFA inhibited the activation of STAT3 through suppressing the phosphorylation of JAK2, and then restrained cell cycle and induced apoptosis of melanoma cells.CONCLUSION:PCFA inhibits melanoma growth via the inhibition of JAK2/STAT3 pathway, which provides a promising therapeutic strategies of melanoma treatment.

Background: The impact of NBUVB on the cutaneous microbiota of vitiligo patients remains to be fully elucidated. Methods: To characterize the cutaneous microbiota in vitiligo patients, cutaneous samples from 60 patients with vitiligo and after NBUVB irradiation were profiled using the Illumina MiSeq platform. Alpha diversity estimations revealed higher microbiota diversity in samples from patients with lesional skin. Beta diversity (Principal Component Analysis (PCA)) analysis showed that the bacterial community structure segregated differently between different groups. Results: There was a statistically significant increase in the Sobs, ACE, and Chao indices in the NB group compared with NF group, as determined by t-test. The alpha diversity have no significant difference between NF and DB group. At the phylum level, Firmicutes, Proteobacteria and Actinobacteria were the most predominant phyla. Propionibacterium and Pseudomonas were the most predominant genera in each group. In addition, Staphylococcus, Bacillus and Prevotella were enriched in DF group compared to DB group. Propionibacterium was enriched in DB group compared to DF group. Conclusions: Our studies indicate differences in microbial community dynamics of the lesional and non-lesional sites of vitiligo subjects, with greater diversity and higher association between microbial communities of the unaffected site. And NBUVB irradiation might eliminate these differences.

Our study aimed to identify the key genes and upstream regulators in vitiligo. To screen the pathogenic genes of vitiligo, an integrated analysis was performed by using the microarray datasets in vitiligo derived from the Gene Expression Omnibus (GEO) database. The functional annotation and potential pathways of differentially expressed genes (DEGs) were further explored by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. We constructed a vitiligo-specific transcriptional regulatory network to identify crucial transcriptional factors that target the DEGs in vitiligo. From two GEO datasets, we identified 1863 DEGs (744 downregulated DEGs and 1,119 upregulated DEGs [false discovery rate < 0.05, |Combined.ES| > 1]) between lesional tissues and nonlesional tissues. GO and KEGG analyses revealed that ubiquitin-mediated proteolysis and the endoplasmic reticulum were significantly enriched pathways for DEGs. The expressions of premelanosome (PMEL), melan-A (MLANA), dopachrome tautomerase (DCT), SRY-boxtranscription factor 10 (SOX10), tyrosinase-related protein 1 (TYRP1), and melanocortin 1 receptor (MC1R) were shown to be involved in the pathogenesis of vitiligo. We concluded that PMEL, MLANA), DCT, SOX10, TYRP1, and MC1R may play a role in vitiligo, among which TYRP1 and MC1R are regulated by forkhead box J2 (FOXJ2). Our finding may contribute to the development of new potential biomarkers, reveal the underlying pathogenesis of vitiligo, and identify novel therapeutic targets for vitiligo.

Renal ischemia/reperfusion injury is a main cause of acute kidney injury (AKI) triggering an inflammatory response associated with infiltrating macrophages. Lipocalin-2 (Lcn2) levels correlate positively and protect against renal ischemia/reperfusion injury. However, the mechanisms remain unclear. The aim of study was to investigate the protective mechanisms of Lcn2 on renal ischemia/reperfusion injury. We found that Lcn2 deficiency significantly aggravated renal injury as evidenced by higher serum creatinine, more severe morphological injury, and increased tubular epithelial cell death in mice. We also observed that attenuated autophagy in Lcn2(-/-) mice, as autophagy markers LC3 II level was significantly decreased and p62 was increased in the Lcn2(-/-) mice after I/R, compared with that of wild type. Mechanistically, we found that recombinant Lcn2 attenuated hypoxia-induced apoptosis in proximal tubule epithelial cells in vitro, and downregulation of HIF-1 alpha blunted Lcn2-induced autophagy and enhanced apoptosis. In addition, the Lcn2 attenuated NF-kappa b subunit p65 activation under hypoxia conditions. Thus, our findings provide a better understanding of the protective role of Lcn2 in kidney ischemia/reperfusion injury and suggest that Lcn2 may be a promising therapeutic target for treating patients with AKI.

目的 评价自拟扶正祛疣汤治疗尖锐湿疣临床疗效.方法 96例患者随机分为治疗组和对照组,2组患者均采用CO2激光祛除疣体,创面外用龙珠软膏;治疗组每日口服自拟扶正祛疣汤,并局部熏洗,20 min/次,2次/d,连用1个月.治疗后每月进行随访,治疗结束后3个月判定痊愈率和复发率.结果 治疗组痊愈率优于对照组,复发率低于对照组(P＜0.05).结论 扶正祛疣汤治疗尖锐湿疣可提高疗效,降低复发率,不良反应小.

目的评价自拟扶正祛疣汤治疗尖锐湿疣临床疗效。方法 96例患者随机分为治疗组和对照组,2组患者均采用CO2激光祛除疣体,创面外用龙珠软膏;治疗组每日口服自拟扶正祛疣汤,并局部熏洗,20 min/次,2次/d,连用1个月。治疗后每月进行随访,治疗结束后3个月判定痊愈率和复发率。结果治疗组痊愈率优于对照组,复发率低于对照组(P<0.05)。结论扶正祛疣汤治疗尖锐湿疣可提高疗效,降低复发率,不良反应小。

目的:探讨在男性患者尿道内注入利多卡因对导尿术的影响。方法:将60例男性患者随机分为对照组和实验组各30例,对照组采用常规导尿术,实验组插尿管前尿道内注入2%利多卡因5ml,记录两组插尿管后1min、5min、10min心率(HR)、无创平均动脉血压(NIMBP)、呼吸(RR)、疼痛、插管成功率及尿道损伤情况。结果:插尿管后1min、5min各观察指标比较有极显著性差异(P<0.01),插管10min后两组各观察指标比较有显著性差异(P<0.05)。对照组疼痛表现、重复插尿管及尿道损伤例数多于实验组(P<0.01)。结论:尿道内注入利多卡因可提高男性患者插尿管成功率,减轻尿道损伤程度,减少并发症的发生。

糖尿病(DM)为慢性终身性疾病,患者需在复杂的社会生活中进行治疗,患者对疾病的态度及其对治疗经过的认识与DM控制有很大影响,掌握一定的DM知识和自我管理技能是患者实现有效病情控制的基础.因此,加强对DM患者的管理及教育是DM治疗中不容忽视的一个重要方面.我科对2003年2月-2005年2月收治的糖尿病进行了健康教育,收到了良好效果,现将体会报告如下.