Psoriasis is a chronic inflammation-associated skin disorder featured by excessive proliferation and abnormal differentiation of keratinocytes. Here, we intended to investigate the role of circular RNA 0061012 (circ_0061012) in psoriasis progression. The expression of circ_0061012, SLMO2-ATP5E readthrough (SLMO2-ATP5E) messenger RNA (mRNA), microRNA-194-5p (miR-194-5p) and GRB2 associated binding protein 1 (GAB1) mRNA was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation and metastasis were analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell assays. Western blot assay was used to measure the protein levels of Ki67, matrix metallopeptidase 9 (MMP9) and GAB1. Dual-luciferase reporter assay and RNA immune co-precipitation (RIP) assay were used to verify the interaction between miR-194-5p and circ_0061012 or GAB1. Circ_0061012 abundance was significantly enhanced in lesional skin samples from psoriasis patients than that in normal skin specimens from healthy volunteers. Interleukin-22 (IL-22) treatment increased the expression of circ_0061012 in a dose-dependent manner. Circ_0061012 silencing alleviated IL-22-induced promoting effects in the proliferation, migration and invasion of HaCaT cells. Circ_0061012 interacted with miR-194-5p, and miR-194-5p knockdown counteracted circ_0061012 silencing-mediated influences in IL-22-induced HaCaT cells. GAB1 was a target of miR-194-5p in HaCaT cells, and miR-194-5p hampered proliferation and metastasis which were induced by IL-22 partly through targeting GAB1. Circ_0061012 elevated the expression of GAB1 through sponging miR-194-5p in HaCaT cells. Circ_0061012 accelerated IL-22-induced proliferation and metastasis in HaCaT cells through enhancing GAB1 expression via sponging miR-194-5p in psoriasis.

目的 探讨自血疗法联合雷公藤多苷(tripterygium wilfordii polyglycosidium,TWP)治疗银屑病血热证的疗效.方法 观察银屑病1组(寻常型银屑病血热证患者30例,TWP治疗8周)和2组(寻常型银屑病血热证患者30例,自血疗法联合TWP治疗8周)治疗前后的银屑病面积和严重程度指数(Psoriasis Area and Severity Index,PASI)评分变化,并比较2组的愈显效率.结果 治疗前,2组PASI评分无统计学差异(P>0.05);治疗后,2组的PASI评分均较各组治疗前显著降低(P均<0.05),且2组的PASI评分明显低于1组(P<0.01);银屑病1组和2组的愈显率分别为56.67％和83.33％,组间差异有显著性(P<0.05).结论 自血疗法联合TWP治疗寻常型银屑病血热证疗效显著,安全经济.

Objective: To detect the expression level of microRNA-155 (miR-155) and to determine the relationship with the imbalance of T-helper 17 cell/regulatory T cell (Th17/Treg) in the patients with cutaneous lichen planus (CLP).Methods: The expression of miR-155, retinoid-acid receptor-related orphan receptor gamma (RORγt), interleukin-17A (IL-17A), forkhead box P3 (Foxp3) and IL-10 in peripheral blood of 33 patients with CLP and 25 normal controls were detected by TaqMan probe.Results: Compared with the normal controls, the expression levels of miR-155, RORγt, Foxp3 and IL-17A were higher and the level of IL-10 expression was lower in the CLP patients with CLP (P<0.05).The level of miR-155 expression was positively correlated with the expression levels of of RORγt, Foxp3 and IL-17A in the patients with CLP (Ps<0.001).There was no correlation between the expression level of miR-155 and IL-10.Conclusion: The miR-155-upregulation existed in the CLP patients may be associated with the imbalance of Th17/Treg.

药源性血小板减少症( drug induced thrombocytopenia,DITP)是由某些药物引起周围血液中血小板计数减少而导致的出血性疾病. 当药物所致血小板计数<100×109 个/L时可诊断为血小板减少症,重症可致血小板计数<5. 0×109个/L.DITP常见临床表现为自发性皮肤和黏膜出血,以四肢为多,常伴鼻出血或齿龈出血,出血严重者可致贫血;颅内出血少见,一旦发生,预后不良,是导致死亡的主要原因. 我们调查了 2015 年 1—12月本院使用万古霉素治疗的儿童住院患者213例,年龄0 ～14 岁,男性133 例,女性80例,男女比例为33 : 20. 观察其使用万古霉素前最近一次、使用万古霉素期间及停药后1～3d血小板计数,其中治疗后出现 DITP 的患者有 13 例, DITP 发生率为 6. 10％ ( 13/213 ). 对213例患者用药前、后和48例同龄健康儿童的血小板计数进行了统计学分析, 13例DITP患者用药后血小板计数明显下降(t=4. 528,P=0.001),200 例非DITP患者用药后血小板计数无明显变化(t=0. 074,P=0. 941),结果见表1.13例患者万古霉素停药后,血小板计数均恢复到治疗前水平.

Objective Toexplore the expression and significance of microRNA-155 (miR-155) in psoriasis vulgaris. Methods Areal-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) method with TaqMan probe technology was performed to detect miR-155 expression in skin lesion area and nonskinlesionalarea of 35 patients with psoriasis vulgaris , compared with that of 30 normal controls. The correlations among miR-155 expression, psoriasis area and severity index (PASI) score and Interleukin-17A(IL-17A)expression were studied. Results The expressions of miR-155 and IL-17A in lesional and non-lesionalgroups were higher than that of control group (all P < 0.01). Also expressions in lesional skin were higher than non-lesional skin (both P < 0.01). In skin lesion group, significant positive correlations existed betweenmiR-155 or IL-17A expression and PASI score as well as miR-155 and IL-17A expression (all P < 0.05). Conclusions Up-expression of miR-155 was relevant to psoriasis development , which is related withthe hyperfunctionof Th17 cells in psoriasis.

Transforming growth factor (TGF)-β signaling plays an important role in the pathogenesis of psoriasis. CD109, a novel TGF-β co-receptor, which inhibits TGF-β signaling by enhancing Smad7-dependent degradation of TGF-β type I receptor (TGF-β RI), is abnormally expreβsed in psoriasis. To date, the expreβsion of Smad7 and the correlation between CD109 and Smad7 expreβsion in psoriasis have not been fully elucidated. This study was designed to investigate the expreβsion and the correlation of CD109 and TGF-β signaling aβsociated proteins in psoriasis and their roles in the pathogenesis of psoriasis. Thirty-two psoriasis specimens were subjected to immunohistochemical staining for CD109, Smad7, TGF-β RI and Ki67. Ten normal skin (NS) specimens served as controls. The positive expression rate (% positive cells) of Smad7 and Ki67 in psoriasis was significantly higher than in NS (62.6%±19.9% vs. 17.2%±4.4%, and 50.7%±14.3% vs. 19.5%±3.2%, respectively, P<0.001), and the expression levels of CD109 and TGF-β R? were reduced significantly in psoriasis as compared with NS (8.1%±6.7% vs. 35.8%±6.7% and 27.3%±3.4% vs. 3.0%±3.4%, respectively, P<0.001). There were significantly negative correlations between CD109 and Smad7 (r=-0.831, P<0.01). These findings indicated that CD109 might play a certain role in the pathogenesis of psoriasis. Lower expression of CD109 and TGF-β RI was highly correlated with higher expression of Smad7 and Ki67, suggesting that CD109 may induce the pathogenesis of psoriasis through Smad7-mediated degradation of TGF-β RI, and lead to the termination of TGF-β signaling.

Objective To explore the expression alteration and significance of inteleukin (IL)-37 in pso-riasis valguris (PV) patients. Methods Patients with PV had been treated with oral acitretin for 8 weeks. PASI score, ELISA and qRT-PCR were used to exam the data of 38 patients (PV group) and 32 controls (control group). Results IL-37 in PV group was significantly higher than that in control group (P < 0.001) and IL-37 changed slightly after 4 weeks of treatment(P > 0.05) but decreased obviously after 8 weeks(P < 0.001). Signif-icant correlations existed among PASI scores, IL-37, IFN-γ and IL-17, as well as among IL-37 and IFN-γ, IL-17 (P < 0.05). Conclusions The increase of IL-37 is relevant to PV development and is associated with pa-tients’ conditions, IFN-γ and IL-17 but the alteration of IL-37 is not related with IL-4.

报告1例浅表血管黏液瘤.患者女,17岁.外阴出现有蒂肿物2年,无自觉症状,肿物突然弥漫性红肿1d,微痛.皮肤科检查:外阴阴蒂包皮一有蒂鸡蛋大红色肿物,质韧,无触痛,有蒂部位可见勒痕及裂隙.皮损组织病理检查:表皮高度水肿,表皮内水疱,真皮及皮下组织中见境界不清的黏液状沉积物,阿辛蓝染色阳性,可见数量不等的梭形、星形等肿瘤细胞和丰富的小血管腔,稀疏散在少量中性粒细胞、淋巴细胞和上皮细胞索.免疫组化检查:FactorⅧ、波形蛋白(vimentin)、CD34和CD44均阳性.

目的 探讨本中心引起儿童泌尿系统感染的常见病原菌的分布以及耐药情况,为临床合理选用抗菌药物提供参考.方法 回顾性分析本医疗中心2012年1月-2013年12月2463例泌尿系统感染患儿中段尿标本培养及药敏检测结果.结果 2463例患儿中段尿标本共培养病原菌479株,阳性率为19.45％.其中革兰阴性杆菌309株(64.51％),革兰阳性球菌138株(28.81％),真菌32株(6.68％,主要为白假丝酵母菌).分离率前7位的病原菌依次为大肠埃希菌(36.53％)、肺炎克雷伯菌(12.73％)、粪肠球菌(D群) (12.32％)、屎肠球菌(D群)(10.23％)、真菌(6.68％)、铜绿假单胞菌(5.22％)、奇异变形菌(3.13％),革兰氏阴性杆菌以大肠埃希菌和肺炎克雷伯菌为主,其中产超广谱β-内酰胺酶菌株125株,比例高达71.42％;革兰阳性球菌以肠球菌(D群)为主,金黄色葡萄球菌检出率为2.30％,其中耐甲氧西林株占27.27％.结论 大肠埃希菌仍为儿童泌尿系统感染的主要病原菌,且存在多重耐药菌感染情况,革兰氏阳性球菌有增多的趋势;明确病原菌种类及药敏结果,对临床合理应用抗菌药物治疗儿童泌尿系统感染有重要意义.

自提倡成分输血以来,我院的成分输血率逐年提高,总的输血合理率达到了相关管理规定的要求.但由于观念更新不够、对输血不良反应的危害性认识不足等原因,部分科室和医生仍习惯输注血浆用于扩容、补充蛋白、补充营养等,导致血浆输注合理率较低.JCI标准的理念是最大限度地实现可达到的标准,以患者为中心,建立相应的政策、制度和流程以鼓励持续不断的质量改进并符合当地的文化.

The deubiquitinating enzyme ubiquitin specific peptidase 15 (USP15) is regarded as a regulator of TGFβ signaling pathway. This process depends on Smad7, the inhibitory factor of the TGFβ signal, and type I TGFβ receptor (TβR-I), one of the receptors of TGFβ. The expression level of USP15 seems to play vital roles in the pathogenesis of many neoplasms, but so far there has been no report about USP15 in psoriasis. In this study, immunohistochemical staining of USP15, TβR-I and Smad7 was performed in 30 paraffin-embedded psoriasis specimens and 10 normal specimens to investigate the expression of USP15, TβR-I and Smad7 in psoriasis and to explore the relevance among them. And USP15 small interfering RNA (USP15 siRNA) was used to transfect Hacat cells to detect the mRNA expression of TβR-I and Smad7. Of 30 cases of psoriasis in active stage, 28, 24 and 26 cases were positive for USP15, TβR-I and Smad7 staining, respectively. The positive rates of USP15 and Smad7 were significantly higher in psoriasis specimens than in normal skin specimens (44.1%±26.0% vs. 6.1%±6.6%, 47.2%±27.1% vs. 6.6%±7.1%), and positive rate of TβR-I (20.3%±22.2%) in psoriasis was lower than that in normal skin specimens (46.7%±18.2%). There was a significant positive correlation between USP15 and Smad7 expression, and significant negative correlations between USP15 and TβR-expression, an I d between TβR- and Smad7 expression I in psoriasis. After transfection of USP15 siRNA in Hacat cells, the expression of TβR-mRNA was up I -regulated and that of Smad7 was down-regulated. It is concluded that USP15 may play a role in the pathogenesis of psoriasis through regulating the TβR-I/Smad7 pathway and there may be other cell signaling pathways interacting with USP15 to take part in the development of psoriasis.

Objective To discuss the expressions and clinical significance of p53 and p33ING1b in human psoriasis and basal cell carcinoma (BCC). Methods Immunohistochemistry EnVision technique was used to detect the expressions of p53 and p33ING1b in samples of 36 psoriasis vulgaris, 28 BCC and 14 normal skins. Results The expression of p53 increased while p33ING1b had a degressive expression in the control group, the psoriasis group and the BCC group. It was found significant statistical difference between the two groups (all P < 0.05). Prominent positive correlation between p53 and p33ING1b were found in both psoriasis group and BCC group (all P<0.05). Conclusions p53 coacts with p33ING1b at local lesions of abnormal proliferative diseases . It′s one of the most prominent mechanisms contributing to deviant cell proliferation.

As one of the most serious types of psoriasis, pathogenesis of erythrodermic psoriasis (EP) is unclear so far. In this study, we aimed to detect the levels of Th1/Th2 cytokine-associated transcription factors and T-lymphocyte clone in peripheral blood mononuclear cells (PBMCs) derived from EP patients, and gene expression level of T-bet/GATA-3 in skin lesion. The potential role of Th1/Th2 reaction pattern played in the pathogenesis of EP was also discussed. Serum levels of IFN-γ, IL-2, IL-4 and IL-10 were quantified by ELISA among 16 EP patients, 20 psoriasis vulgaris (PV) patients and 15 healthy controls. The expression levels of T-bet/GATA-3 in the skin lesion and PBMCs were examined by real-time qPCR. The ratio of Th1/Th2 was measured by flow cytometry. The levels of IFN-γ, IL-2, IL-4 and IL-10 were higher in EP patients than in the healthy controls. The levels of IL-4 and IL-10 were 69.44±11.45 and 12.62±4.57 pg/mL, respectively, in EP patients, significantly higher than those in PV patients and healthy controls (P<0.05). Flow cytometry revealed the levels of both Th1 and Th2 in PBMCs from EP patients were higher than those in healthy controls, and the Th1/Th2 ratio was dramatically lower than in PV patients (P<0.01). The ratios of IFN-γ/IL-4 and T-bet/GATA-3 in EP patients were both less than 1.0, suggesting a reversal when compared with the other two groups. Our study indicated that the EP patients exerted a Th1/Th2 bidirectional response pattern, and the balance of Th cell subsets inclines to Th2, which might be one of the important mechanisms of EP pathogenesis.

Objective:To detect the expression of IL-36, p38 mitogen-activated protein kinase ( p-p38) pathway and Th17 cytokine in lichen planus. Methods:Immunohistochemistry EnVision technique was used to detect the expression of IL-36γ, p-p38 and IL-17A in 58 patients with lichen planus and 19 controls. Re-sults:The expression of IL-36γ, p-p38 and IL-17A was higher in the patients’ lesion of lichen planus ( the positive rates were 86.21%, 79.31% and 94.83%) than in control group (the positive rates were 68.42%, 15.79% and 63.16%) ( all P<0.01) . In lichen planus group, there were positive correlations between the ex-pression of IL-36γand p-p38 ( P<0.001) , and between the expression of IL-36γand IL-17A ( P<0.001) . Significant difference was also observed between the two cytokines’ expression grade ( P<0.05) . Conclusion:p38MAPK pathway and Th17 cytokine may be involved in the pathogenesis of lichen planus.

皮肤平滑肌瘤较少见,病因尚不明确,多发性者更为罕见.现将武汉市协和医院皮肤科确诊1例多发性皮肤平滑肌瘤报告如下. 1 病历摘要 患者男,54岁.右小腿起结节20余年,渐增多,于2010年10月21日就诊.患者20年前无明显诱因于右小腿胫前出现大小不等结节,肤色或淡红色,无明显自觉症状,皮疹渐增多.近七八年渐出现疼痛感,曾在当地就诊,未明确诊断,未予处理.

孤立性胶原瘤是一种由胶原纤维组成的结缔组织痣,临床表现为无自觉症状的单发性结节或斑块.1996 年由Gautam 等[1]首先报告.现报告我科诊治的1 例孤立性胶原瘤.

患者女,18岁.因右腘窝丘疹伴瘙痒3年,于2011年5月来我科就诊.3年前无明显诱因患者右侧腘窝出现粟粒大红色角化性丘疹,后逐渐融合成暗红色斑片,表面覆有鳞屑,伴轻度瘙痒,症状常于夏季加重,曾在多家外院就诊,诊断为"银屑病""体癣""湿疹"等.口服和外用多种西药和中药(具体成分不详)无明显效果.起病以来,患者一般情况尚可,既往未使用局部外用制剂,否认家族中有类似疾病患者.否认其他病史.

This study examined the correlation of the expression of interleukin-36 (IL-36), a novel member of interleukin-1 (IL-1) family, with p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways in psoriasis vulgaris skin lesions. The expression levels of IL-36α, IL-36β, IL-36Γ, phosphorylated p38 MAPK, and NF-κBp65 were detected in the skin tissues of 38 psoriasis patients and 17 healthy control subjects by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting. The cytokine expression levels were compared between the psoriasis group and the control group. A correlation analysis between cytokine proteins was performed in the psoriasis group. Results showed that the expression levels of IL-36a, IL-36β, IL-36Γ, phosphorylated p38 MAPK and NF-κBp65 in the psoriasis group were significantly higher than those in the control group (P<0.001). In the psoriasis group, the IL-36 cytokine expression was positively correlated with phosphorylated p38 MAPK and NF-κBp65 expression (P<0.05). A significant positive correlation was also found between the phosphorylated p38 MAPK and NF-κBp65 expression (P<0.01). It was concluded that the increased IL-36 expression is correlated with p38 MAPK and NF-κB pathways in psoriasis vulgaris skin lesions. All the three factors may be jointly involved in the pathogenesis and local inflammatory response of psoriasis.

目的:评价白花丹素联合肿瘤坏死因子相关凋亡诱导配体(TRAIL)对诱导人黑素瘤A375细胞的凋亡的影响.方法:采用MTT法检测白花丹素和TRAIL对人黑素瘤A375细胞的作用.流式细胞术Annexin V-FITC/PI染色法检测不同给药方案对细胞凋亡的影响.用直接免疫荧光染色结合流式细胞术检测细胞表面死亡受体TRAIL-R 1/DR4,TRAIL-R2/DR5用药前后的表达变化.结果:白花丹素对A375细胞的抑制作用随药物浓度的提高而增强.白花丹素和TRAIL单用或联用可以诱导细胞凋亡,联合用药有协同作用,联合用药组显著高于单独用药组(P＜0.01).白花丹素作用A375细胞24 h后,死亡受体TRAIL-R 1/DR4和TRAIL-R2/DR5在细胞表面表达明显上调(P＜0.05,P＜0.01).结论:白花丹素联合TRAIL可协同抑制细胞生长,其机制可能与白花丹素诱导细胞表面的死亡受体DR4、DR5表达上调有关.

The expression of the interferon regulatory factor 4 (IRF-4) and the IRF-4-binding pro-tein (IBP) in psoriatic skin lesions was investigated. The expression of IRF-4 and IBP in skin lesions of 20 patients with psoriasis vulgaris were immunohistochemically dectected. Normal skin from 10 healthy people was used as normal control. The study showed that expression of IRF-4 was increased significantly in keratinocytes and inflammatory cells in the lesions of psoriasis vulgaris than that in the normal control. The detection revealed that IBP expression in keratinocytes, lymphocytes, hair follicles, and sebaceous glands in normal skin was significantly lower than that in the lesions of pso-riasis vulgaris (P0.05). Both IRF-4 and IBP might be involved in the pathogenesis of psoriasis vul-garis.