目的 探讨α-平滑肌肌动蛋白(α-SMA)在结直肠癌组织中的表达情况及其与结直肠癌患者临床特征和预后的关系.方法 选取103例结直肠癌患者的结直肠癌组织标本,采用免疫组织化学染色法检测结直肠癌组织中α-SMA的表达情况,分析α-SMA表达与结直肠癌患者临床特征及预后的关系.结果 103例结直肠癌患者中,α-SMA高表达患者25例,α-SMA低表达患者78例.不同性别、年龄、肿瘤部位、病理类型、TNM分期、微卫星稳定性情况结直肠癌患者结直肠癌组织中α-SMA的表达情况比较,差异均无统计学意义(P﹥0.05).α-SMA低表达结直肠癌患者的无病生存结局优于α-SMA高表达的患者(P﹤0.05).TNM分期为Ⅲ期的结直肠癌患者中,α-SMA高表达患者的3年累积无病生存率为30.8％,低于α-SMA低表达患者的75.0％(P﹤0.05).结论 α-SMA在结直肠癌组织中的表达情况与结直肠癌患者的无病生存期较短有关,可能参与结直肠癌的发生、发展,可作为结直肠癌的生物标志物.

PD-1/PD-L1通路可通过多种机制产生免疫抑制作用,介导肿瘤免疫逃逸.目前针对PD-1/PD-L1通路的研究已成为近几年的热点.区别于传统的化疗及放疗,抗PD-1/抗PD-L1药物介导的免疫靶向治疗,能更加有效地调动机体本身的抗肿瘤免疫能力,改善免疫微环境,在肺癌、黑色素瘤、胃癌等恶性肿瘤治疗中取得了显著效果.但目前抗PD-1/抗PD-L1药物治疗并非所有患者均能获益,部分患者存在原发性耐药,有的患者出现继发性耐药.本文就抗PD-1/PD-L1药物治疗的耐药机制作一综述.

The proband was a 29 years old male presenting with papule and pustule on face for 9 years, ag￣gravating for 4 years. There were 7 patients ( 4 males and 3 females) out of 15 members of 3 generations in this family and the age at onset was all around puberty. The clinical and pathological features were in accord￣ance with the diagnosis of hidradenitis suppurativa.

Objective:To investigate the effects of CXCL12 on the biological behavior of human melanoma M14 cell line. Methods:The human melanoma M14 cell line was incubated or induced by different concentra￣tions of CXCL12 ( 0,10,50,100,200 ng/mL) . The Cell Counting Kit-8 ( CCK8) , transwell migration and in￣vasion assay were used to evaluate the proliferation, migration, and invasion of M14 cells. The Western blot was used to detect the protein expression of ERK, p-ERK, AKT, and p-AKT of M14 cells treated with 100 ng/mL CXCL12 at different times ( 0, 5, 10, 20, 30, 60 min) . Results: CXCL12 promoted the prolifera￣tion, migration and invasion of M14 cells, and the activation of the ERK and AKT signaling pathways. Conclusion:CXCL12 may be associated with the progression of melanoma.

Objective To screen microRNAs(miRNAs)related to early mycosis fungoides(MF). Methods A high?throughput miRNA PCR array was used to determine miRNA expression profiles in skin lesions of 6 patients with early MF (early MF group) and 6 patients with lichen planus (control group), followed by screening of differentially expressed miRNAs between the two groups. Then, real?time fluorescence?based quantitative PCR(RT?qPCR)was performed to verify the differentially expressed miRNAs in lesional specimens from 13 patients with early MF and 13 patients with eczema or lichen planus, as well as in Myla cells and normal human T?lymphocytes. Results The high?throughput miRNA PCR array showed that the expressions of hsa?miR?378a?5p, hsa?miR?107 and hsa?miR?302c?3p were significantly higher in the early MF group than in the control group(all P<0.05). For skin lesions, the results from RT?qPCR were similar to those from the miRNA array assay. Compared with normal human peripheral blood T?lymphocytes, Myla cells showed significantly increased expressions of hsa?miR?378a?5p and hsa?miR?107, which was consistent with the results from the miRNA array assay. However, no significant difference was observed in the expression of hsa?miR?302c?3p between the two kinds of cells. Conclusion MiRNA expression profiles in early MF are different from those in inflammatory skin diseases.

患者女,58岁.面颈部橘红色斑块5年.皮肤科情况:面部.尤其右眼眶周围和颈部融合性橘红色斑块、结节.皮损边界清楚,部分皮疹边缘可见红晕.血清免疫电泳示单克隆IgG k轻链.组织病理:表面萎缩变薄,真皮全层弥漫性组织细胞,泡沫细胞及多核巨细胞浸润,部分区域可见散在淋巴细胞浸润,未见明显渐进性坏死.诊断为无渐进坏死性黄色肉芽肿伴IgG κ型副球蛋白血症.

Objective To measure expressions of chemokine receptor 4 (CXCR4) and CXCR7 in cutaneous malignant melanoma (CMM) and pigmented nevus tissues,and to explore their correlations with pathological features.Methods Skin specimens were obtained from the lesions of 40 patients with CMM (CMM group) and 40 patients with pigmented nevus (pigmented nevus group).An immunohistochemical study was performed to measure expressions of CXCR4 and CXCR7 in these specimens.Results In the CMM group,8 (20.0％) and 6 (15.0％) specimens were negative (-),5 (12.5％) and 4 (10.0％) mildly positive (+),13 (32.5％) and 9 (22.5％) moderately positive (++),14 (35.0％) and 21 (52.2％) strongly positive (+++),for CXCR4 and CXCR7 respectively.Of the pigmented nevus specimens,20 (50.0％) and 14 (35.0％) were negative (-),17 (42.5％) and 25 (62.5％) mildly positive (+),3 (7.5％) and 1 (2.5％) moderately positive (++),for CXCR4 and CXCR7 respectively,but none was strongly positive (+++) for either of them.There were significant differences in the expressions of CXCR4 and CXCR7 between the CMM group and pigmented nevus group (U =317,256.5,respectively,both P ＜ 0.01).The expression of CXCR4 was significantly higher in non-acral than in acral melanomas (U =38,P ＜ 0.05),higher in Clark's level Ⅲ-V than in Ⅰ-Ⅱ melanomas (U =116,P ＜ 0.05),and higher in melanoma tissues from patients with lymphatic metastasis than in those without (U =16.5,P ＜ 0.05),but similar among patients of different age or gender,and among melanomas with different Breslow thickness,degrees of ulceration or lymphocytic infiltration (all P ＞ 0.05).No significant difference was observed in the expression of CXCR7 among patients of different age,gender,or among melanomas with different degrees of ulceration or lymphocytic infiltration,or between melanoma tissues from patients with lymphatic metastasis and those without (all P ＞ 0.05),but it was significantly higher in non-acral than in acral melanomas (U =64,P ＜ 0.05),higher in melanomas with Breslow thickness ＞ 1.00 mm than in those ≤ 1.00 mm (U =81.5,P ＜ 0.05),and higher in Clark's level Ⅲ-Ⅴ than in Ⅰ-Ⅱ melanomas (U =60.5,P ＜ 0.05).Conclusion Both CXCR4 and CXCR7 are expressed to different extents in CMM and pigmented nevus tissues,suggesting that they may participate in the occurrence and development of CMM.

Psoriasis is a chronic inflammatory proliferative skin disease induced by aberrant cellular immunity under the interactive effect between polygenic and environmental factors.The exact pathogenesis of psoriasis remains unclear,and interleukin-17 (IL-17) is currently considered to play a critical role in it by stimulating the proliferation and aberrant activation of keratinocytes.Three newly developed biological agents targeting the interleukin-17 pathway have been used to treat psoriasis in clinical trials or practice,including secukinumab and ixekizumab that directly antagonize IL-17A,as well as brodalumab that inhibits downstream signal molecules of the IL-17 signaling pathway by antagonizing IL-17RA.They have proved to be effective and safe in the treatment of psoriasis vulgaris and psoriatic arthritis in clinical trials,and provided new choices for the treatment of psoriasis.However,there is still a need for long-term evaluation of their safety.

医院档案室的安全管理工作一直以来均是档案管理的重要工作内容，如何做好医院档案室的安全管理工作对于管理人员来说是一项不可推卸的重要职责。本文主要针对如何做好医院档案室的安全管理工作展开论述，提出了若干具体对策：安装监控设备、坚决杜绝火源、杜绝非人因素以及建立安全制度。希望通过本文可以进一步给相关人员以安全管理经验方面的启示。

目的 探讨22例乳房Paget病患者的临床表现和组织病理改变.方法 所有标本均来自2010-2013年医院门诊就诊者,分析其临床资料、苏木素-伊红(HE)及免疫组化染色结果、随访信息.结果 22例乳房Paget病患者均为女性,平均年龄55岁(35～83岁),平均病程3.4年(0.5～15年),均为单侧发病,14例(64％)累及乳头.组织病理改变显示,15例患者表现为大细胞型,5例表现为小细胞型,2例表现为大细胞型并小细胞型.14例呈全层分布模式,6例呈经典分布模式,腺泡样分布模式和腺泡样并棘层松解分布模式各l例.22例患者在乳腺外科均确诊为乳腺癌.第1年随访中失访9例,2例发生全身广泛转移而死亡,11例行广泛切除术后随访至今未见复发.结论 乳房Paget病与乳腺癌关系密切,一经诊断需及时至乳腺外科就诊,高度警惕转变成乳腺癌.临床上大部分患者乳头受累,组织病理学上可见到不同的细胞类型及分布模式,其临床意义尚不明确.

皮肌炎(dermatomyositis,DM)以累及皮肤、横纹肌为特征的自身免疫性结缔组织病.DM临床表现复杂多样,而直观或可触及的皮损有助于临床诊断与鉴别诊断,某些皮损与潜在的内脏损害、恶性肿瘤、实验室检查指标异常及预后有关,现就皮肌炎伴发的皮损及其意义进行概述.

Objective:To detect the effects of levocetirizine on the expression of CD86 and production of IL-8 by monocyte-derived dendritic cells ( MoDC) . Methods: Monocytes were isolated from healthy volunteers and were induced into monocyte-derived dendritic cells (MoDC). MoDC was cultured with histamine and levocetirizine separately. The secretion of CD86 and IL-8 by MoDC in the co-cultures was detected by FACS and ELSIA methods, separately. Results: In the culture with histamine, the secretion of CD86 cells and IL-8 was increased,while in the culture with levocetirizine the secretion of CD86 cells and IL-8 was reduced (P<0.05). However, this suppressive effect varied in different subjects. Conclusions: Levocetirizine can suppress the increase of CD86 cells and IL-8 secretion after histamine stimulation. The clinical treatment with levocetirizine should be individually.

OBJECTIVE:To study the mechanism of resistance and its reversal to 2', 2'-difluorodeoxycytidine (gemcitabine) in a pancreatic cancer cell line SW1990.METHODS:Immunohistochemistry and RT-PCR techniques were used to investigate the mechanism of drug resistance. Salvicine (SAL) was used to reverse the drug resistance in a gemcitabine-resistant pancreatic cancer cell line (SW1990-GEM). RT-PCR, flow cytometry and MTT assay were employed to evaluate the effect of reversing drug resistance by salvicine.RESULTS:SW1990-GEM cells showed weak expression of P-glycoprotein (P-gp) revealed by immunohistochemistry, while its parental SW1990 cells were negative. Both cell lines did not express multidrug-resistance-related protein (MRP). As compared to the parental SW1990 cells, the mRNA expression of deoxycytidine kinase (dCK) was decreased while that of ribonucleotide reductase (RR) and mdr-1 was increased. With a concentration of 4 nmol/L, at one hr and 24 hr after SAL treatment, there was no change in mdr-1 mRNA expression, and the IC(50) of gemcitabine was 121.36 micromol/L and 121.64 micromol/L, respectively. However, when the concentration of SAL was increased to 30, 60, and 90 nmol/L, there was a dose-dependent down-regulation of mdr-1 mRNA expression in SW1990-GEM cells. The accumulation of rhodamine 123 was concomitantly increased, and the IC(50) of gemcitabine was correspondingly decreased.CONCLUSION:The resistance to gemcitabine of a pancreatic cancer cell line is due to decreased expression of dCK and increased expression of RR and mdr-1. Salvicine, only in toxic concentrations, can reverse the drug resistance by down-regulating mdr-1 gene and P-gp expression.