简介：摘要胸腺瘤是起源于胸腺上皮细胞的肿瘤，是一种具有良性细胞学特征、恶性生物学行为的肿瘤，国内外文献有对胸腺瘤远处转移的报道，常见的转移部位有肺、肝、纵隔等，发生于腹壁的转移罕见报道，且没有有效的治疗方法。本文就1例B2/B3混合型胸腺瘤腹壁转移病例进行报告，并回顾国内外相关文献报道，总结晚期转移性胸腺瘤的治疗方法。通过对腹壁转移灶的放疗，联合GM-CSF的应用，患者腹壁病灶退缩明显且不良反应轻微。该病例为合并肌无力的晚期转移性胸腺瘤的患者提供了新的治疗手段。

简介：AbstractStroke is a devastating disease that occurs when a blood vessel in the brain is either blocked or ruptured, consequently leading to deficits in neurological function. Stroke consistently ranked as one of the top causes of mortality, and with the mean age of incidence decreasing, there is renewed interest to seek novel therapeutic treatments. The Scavenger Receptor Class B type 1 (SR-B1) is a multifunctional protein found on the surface of a variety of cells. Research has found that that SR-B1 primarily functions in an anti-inflammatory and antiatherosclerotic capacity. In this review, we discuss the characteristics of SR-B1 and focus on its potential correlation with the modifiable risk factors of stroke. SR-B1 likely has an impact on stroke through its interaction with smoking, diabetes mellitus, diet, physical inactivity, obesity, hypercholesterolemia, atherosclerosis, coronary heart disease, hypertension, and sickle cell disease, all of which are critical risk factors in the pathogenesis of stroke.

简介：摘要目的研究miR-125b-1-3p在轮状病毒(rotavirus)复制过程中的作用和调控机制。方法将MA104细胞中的miR-125b-1-3p分别上调和下调后感染轮状病毒，通过RT-PCR分析miR-125b-1-3p的表达情况和轮状病毒拷贝数；免疫荧光分析miR-125b-1-3p对轮状病毒蛋白表达情况的影响；Western blot分析miR-125b-1-3p参与调控的相关蛋白表达情况。结果轮状病毒感染细胞后，miR-125b-1-3p的表达水平明显上调，上调miR-125b-1-3p后，轮状病毒的VP7、NSP3基因拷贝数下降，下调miR-125b-1-3p后，轮状病毒的VP7、NSP3基因拷贝数明显升高；上调miR-125b-1-3p的表达水平后轮状病毒蛋白荧光数下降，下调miR-125b-1-3p后，病毒蛋白荧光数增加；轮状病毒感染细胞16 h后PI3K/Akt通路活性受到抑制，上调miR-125b-1-3p能够抑制PI3K/Akt通路的活化。结论miR-125b-1-3p通过调控PI3K/Akt通路抑制轮状病毒的复制。研究结果为探讨miR-125b-1-3p和PI3K/Akt通路之间的具体调控机制研究提供了实验基础，为轮状病毒抗感染治疗提供了靶点。

简介：摘要目的探讨B7-H3在弥漫大B细胞淋巴瘤（DLBCL）中的表达及其预后意义。方法采用免疫组织化学法对2013年5月至2019年5月于临沂市中心医院初诊的103例DLBCL患者的石蜡包埋肿瘤组织进行检测。分析B7-H3蛋白的表达与DLBCL患者临床病理特征及与无进展生存（PFS）和总生存（OS）的关系，采用Cox比例风险模型分析影响患者PFS和OS的因素。结果DLBCL患者B7-H3蛋白阳性率为68.0%（70/103）。患者性别、年龄、临床分期、国际预后指数（IPI）评分、治疗效果、B症状、病理类型等临床病理特征分层患者间B7-H3蛋白阳性率差异均无统计学意义（均P>0.05）。所有患者的5年PFS率和5年OS率分别为24%和32%，B7-H3阴性患者和阳性患者的5年PFS率分别为47%和14%（P<0.01），5年OS率分别为50%和24%（P<0.001）。多因素Cox回归分析显示B7-H3阳性为DLBCL患者PFS（HR=2.685，95%CI 1.503~4.789，P=0.001）和OS（HR=2.262，95% CI 1.248~4.098，P=0.007）不良影响因素。结论B7-H3的中高强度表达可能与DLBCL患者预后不良有关。

简介：AbstractBackground:Long non-coding RNA (lncRNA) actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) functions as a competing endogenous RNA to regulate target genes expression by sponging microRNAs (miRs) to play cancer-promoting roles in cancer stem cells. However, the regulatory mechanism of AFAP1-AS1 in cervical cancer (CC) stem cells is unknown. The present study aimed to provide a new therapeutic target for the clinical treatment of CC.Methods:Hyaluronic acid receptor cluster of differentiation 44 variant exon 6 (CD44v6)(+) CC cells were isolated by flow cytometry (FCM). Small interfering RNAs of AFAP1-AS1 (siAFAP1-AS1) were transfected into the (CD44v6)(+) cells. The levels of AFAP1-AS1 were measured by quantitative real-time PCR (qRT-PCR). Sphere formation assay, cell cycle analysis, and Western blotting were used to detect the effect of siAFAP1-AS1. RNA pull-down and luciferase reporter assay were used to verify the relationship between miR-27b-3p and AFAP1-AS1 or vascular endothelial growth factor (VEGF)-C.Results:CD44v6(+) CC cells had remarkable stemness and a high level of AFAP1-AS1. However, AFAP1-AS1 knockdown with siAFAP1-AS1 suppressed the cell cycle transition of G(1)/S phase and inhibited self-renewal of CD44v6(+) CC cells, the levels of the stemness markers octamer-binding transcription factor 4 (OCT4), osteopontin (OPN), and cluster of differentiation 133 (CD133), and the epithelial-mesenchymal transition (EMT)-related proteins Twist1, matrix metalloprotease (MMP)-9, and VEGF-C. In the mechanism study, miR-27b-3p/VEGF-C signaling was demonstrated to be a key downstream of AFAP1-AS1 in the CD44v6(+) CC cells.Conclusions:LncRNA AFAP1-AS1 knockdown inhibits the CC cell stemness by upregulating miR-27b-3p to suppress VEGF-C.

简介：AbstractBackground:Intracerebral hemorrhage (ICH) is fatal and detrimental to quality of life. Clinically, options for monitoring are often limited, potentially missing subtle neurological changes. Integrin β 1 (ITGB1) and β 3 (ITGB3) are the main components of integrin family receptors, which regulate the formation and stability of blood vessels. This study explored the relationship between the expression of ITGB1 and ITGB3 in intracerebral hemorrhage (ICH) to analyze their functional and clinical relevance.Methods:The expression of ITGB1 and ITGB3 in ICH was accomplished by immunohistochemical (IHC) staining and western blotting (WB) analysis, respectively.Results:Furthermore, the results demonstrated that ITGB1 was expressed in ICH tissues, but ITGB3 was not expressed in ICH tissues.Conclusions:In summary, the clinical progression of ICH was related to the expression of ITGB1. ITGB1 may be a potential biomarker and contribute to the treatment of ICH.

简介：摘要例1，男，6岁，因间断鼻衄4年余入院，血常规提示血小板减少，低浓度瑞斯脱霉素诱导血小板聚集阳性，血管性血友病因子（vWF）基因c.3916C>T（p.R1306 W）杂合错义突变。例2，女，8日龄，因血小板减少5 d入院，予以人免疫球蛋白输注无效，低浓度瑞斯脱霉素诱导血小板聚集阳性，vWF基因c.3946G>A（p.V1316M）杂合错义突变，为自发突变。例3，因间断鼻衄3年余入院，血常规提示血小板减少，外院予丙种球蛋白、糖皮质激素治疗效果不佳，低浓度瑞斯脱霉素诱导血小板聚集阳性，vWF基因c.3946G>A（p.V1316M）杂合错义突变，为自发突变。3例患儿均确诊为血管性血友病。例1及例3应用含血管性血友病因子的人血源性凝血因子Ⅷ可止血，血小板可升至正常。

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简介：AbstractBackground:Degree of mucosal recovery is an important indicator for evaluating the therapeutic effects of drugs in treatment of inflammatory bowel disease (IBD). Increasing evidences has proved that tight junction (TJ) barrier dysfunction is one of the pathological mechanisms of IBD. The aim of this study was to observe whether enhancement of TJ can decrease colitis recurrence.Methods:Eighty C57BL/6 mice were randomly divided into four groups including normal group, colitis group, sulfasalazine (SASP) treated group, and traditional Chinese drug salvianolic acid B (Sal B) treated group. Colitis was established in mice by free drinking water containing dextran sulfate sodium, after treatments by SASP and Sal B, recombinant human interleukin-1β (IL-1β) was injected intraperitoneally to induce colitis recurrence.Results:Compared with sham control, cell apoptosis in colitis group was increased from 100.85 ± 3.46% to 162.89 ± 11.45% (P = 0.0038), and TJ dysfunction marker myosin light chain kinase (MLCK) was also significantly increased from 99.70 ± 9.29% to 296.23 ± 30.78% (P = 0.0025). The increased cell apoptosis was reversed by both SASP (125.99 ± 8.45% vs. 162.89 ± 11.45%, P = 0.0059) and Sal B (104.27 ± 6.09% vs. 162.89 ± 11.45%, P = 0.0044). High MLCK expression in colitis group was reversed by Sal B (182.44 ± 89.42% vs. 296.23 ± 30.78%, P = 0.0028) but not influenced by SASP (285.23 ± 41.04% vs. 296.23 ± 30.78%, P > 0.05). The recurrence rate induced by recombinant human IL-1β in Sal B-treated group was significantly lower than that in SASP-treated group.Conclusions:These results suggested a link between intestinal mucosal barrier dysfunction, especially TJ barrier dysfunction, and colitis recurrence. The TJ barrier dysfunction in remission stage of colitis increased the colitis recurrence. This study might provide potential treatment strategies for IBD recurrence.

简介：摘要患儿8月龄起病以脾脏、淋巴结和腮腺肿大为突出表现，伴反复发热、窦肺感染、贫血和血小板减少，外周血多克隆性B细胞增殖。基因检出半胱天冬酶募集结构域11基因第5外显子新发杂合变异（c.368C>T，p.G123D），父母为野生型，诊断NF-κB相关B细胞增殖和T细胞失能性疾病。经10年利妥昔单抗治疗，淋巴增殖控制良好。

简介：摘要目的探讨急性胰腺炎(Acute pancreatitis, AP)患者早期血清中载脂蛋白B/载脂蛋白A1( apolipoprotein B/apolipoprotein A1, Apo B/A1)、微管相关蛋白1-轻链3(microtubule-associated protein 1-light chain 3, MAP1-LC3)及细胞间黏附分子-1(intercellular adhesion molecule-1, ICAM-1)水平对AP患者病情的早期评估价值。方法收集2019年1月至2020年8月安徽医科大学第二附属医院急诊外科诊治的AP患者资料。同时还收集了入院24 h内的AP患者血清。根据患者病情严重程度分为非重症AP(non-severe acute pancreatitis, Non-SAP)组(n=315例)和重症AP(severe acute pancreatitis, SAP)组(n=98例)，并收集60例体检健康者作为非特异性对照(non-specific control, NC)组。利用单因素方差分析比较3组间Apo B/A1、MAP1-LC3和ICAM-1水平的差异,并利用Pearson相关性分析分析其与AP病情严重程度的相关性。采用受试者工作曲线(receiver operating characteristic curve, ROC)来预测上述指标在评估病情严重程度中的灵敏度与特异度。结果AP组患者早期Apo B/A1、MAP1-LC3和ICAM-1水平均显著高于NC组(P<0.05)，SAP组Apo B/A1、MAP1-LC3和ICAM-1水平分别为(2.21±1.40)、(0.92±0.29) ng/mL和(235.57±54.50) ng/mL高于Non-SAP组的(0.96±0.34)、(0.48±0.24) ng/mL和(120.28±61.69) ng/mL，差异有统计学意义(P<0.05)。Pearson相关性分析显示以上指标与入院后首次Ranson评分呈正相关(P<0.05)，其中ICAM-1与AP病情严重程度相关性最高(r=0.519)。ROC示Apo B/A1、MAP1-LC3、ICAM-1及联合检测的受试者工作特征曲线下面积(area under the receiver operating characteristic curve, AUROC)分别为0.769、0.811、0.828和0.938。结论AP患者入院24 h内血清Apo B/A1、MAP1-LC3和ICAM-1水平与AP病情严重程度明显相关，对早期预测AP的病情严重程度有一定的临床意义。

简介：摘要目的检测β-1，3-N-乙酰氨基葡萄糖氨基转移酶3（B3GNT3）在胰腺癌组织中的表达情况，分析其临床意义。方法采用生物信息学的方法分析B3GNT3在胰腺癌组织及癌旁正常组织中的mRNA水平，并分析其表达与胰腺癌患者的生存率间的关系。回顾性分析78例接受手术治疗的胰腺癌患者的临床病理资料。采用免疫组化法检测胰腺癌组织和癌旁正常组织中的B3GNT3蛋白表达水平，分析其与肾透明细胞癌患者临床病理特征的关系。结果生物信息学分析结果显示，B3GNT3的mRNA在胰腺癌组织中显著高表达，并与患者总生存率和无病生存率显著相关。免疫组化结果表明，B3GNT3在胰腺癌组织中的表达明显高于癌旁正常组织。B3GNT3在胰腺癌组织中的高表达与肿瘤分期、肿瘤大小及淋巴结的转移情况相关（均P<0.05），而与年龄、性别、肿瘤分级无关（均P>0.05）。结论B3GNT3在胰腺癌的进展演变中发挥重要作用，有望成为胰腺癌重要的治疗靶点和一个潜在的生物标志物。

简介：摘要免疫治疗在肿瘤生物学研究中至关重要，并在肿瘤靶向治疗中取得了重大进展。B7-H3（CD276）是B7家族的一个免疫关卡抑制剂，与CTLA4、PD-1和CD28等许多免疫相关因子相互作用。尽管B7-H3的受体是什么尚不明确，但确定其在多种肿瘤中过度表达。起初，有研究结果认为B7-H3可协同刺激免疫反应，但最新的研究结果表明，其在T细胞上有协同抑制作用，从而导致肿瘤细胞的免疫逃避。因此，B7-H3的过度表达与肿瘤患者的预后不良有关，且在体外实验中已证实与肿瘤的侵袭和转移有关。此外，有结果表明，除了免疫调节作用外，B7-H3还能直接影响上皮恶性肿瘤进展。旨在描述不同恶性肿瘤中B7-H3的作用、与其他免疫因子的关系以及在恶性肿瘤进展中的非免疫学功能。在肿瘤治疗中靶向B7-H3可减少肿瘤细胞增殖、抑制肿瘤进展和转移，因此这可能会改善治疗方案和取得更好的临床治疗效果。

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简介：摘要本文报道右侧海绵窦区B细胞性淋巴瘤1例。患者女，53岁，因右眼肿胀伴眼睑下垂1个月余入院。CT表现为右侧海绵窦一类圆形稍高密度软组织影，病灶邻近的蝶窦上侧窦壁骨质破坏；MRI表现为右侧海绵窦区包绕颈内动脉的不规则软组织信号影，T1WI及T2WI呈等信号，增强扫描病变呈明显均匀强化。最终病理诊断为海绵窦区B细胞性淋巴瘤。

简介：摘要弥漫大B细胞淋巴瘤(DLBCL)是最常见的淋巴瘤亚型，发病率随增龄增加，但部分老年患者由于高龄、体能状态差、并发症多等原因不能耐受一线标准方案R-CHOP(利妥昔单抗＋环磷酰胺＋阿霉素＋长春新碱＋泼尼松)的治疗。老年综合评估可判断适合标准剂量R-CHOP的老年患者；还有一些减低毒性方案可尝试；各类新型药物的出现也为老年DLBCL治疗提供了新的选择。

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简介：摘要高迁移率族蛋白B1(HMGB1)是一类广泛存在于细胞内的核蛋白，当机体受到应激刺激时从细胞中释放或分泌，在细胞的存活/死亡途径中起关键作用。HMGB1具有巨大的生物学功能，是炎性疾病和肿瘤等重大疾病的主要调节因子。HMGB1与肿瘤细胞的增殖、分化、迁移、凋亡及耐药关系密切。随着对HMGB1研究的不断深入，发现其在乳腺癌的发生、发展、转移及耐药中扮演重要角色。结合HMGB1研究现状，探讨其在乳腺癌中的表达，可为临床探索新的治疗方案提供依据。

简介：摘要探讨PIM1基因与黏膜相关边缘区B细胞淋巴瘤的发病机制及相关治疗。对1例PIM1基因阳性的黏膜相关边缘区B细胞淋巴瘤患者的相关实验室检查、影像学、病理学结果及治疗情况进行回顾性分析，并复习相关文献。患者使用R-CHOP 方案治疗，效果较好。黏膜相关淋巴组织（mucosa associated lymphoid tissue，MALT）淋巴瘤是一种惰性淋巴瘤。PIM1在调节正常造血细胞和造血系统恶性肿瘤细胞的增殖和分化中起着重要作用。