脾脏血管性病变与淋巴瘤CT鉴别诊断

目的 运用CT区分脾脏血管性病变与淋巴瘤。方法 回顾性分析20例经手术、穿刺病理学检查证实的脾脏病变的发病年龄、性别、脾脏指数、病变大小、数目、有无液化、钙化、强化幅度、强化方式等特征,并进行统计学分析。结果 20例脾脏病变中,11例血管性病变(6例海绵状血管瘤,3例窦岸细胞血管瘤,2例硬化性血管瘤样结节性转化),9例淋巴瘤;两组间发病年龄、病变大小、数目、有无液化、钙化等差异无统计学意义;两组间脾脏指数、动脉期强化幅度差异具有统计学意义(P＜0.05)。5例海绵状血管瘤呈不均匀性强化,1例呈渐进性填充式强化,2例窦岸细胞血管瘤呈“雀斑征”,1例硬化性血管瘤样结节性转化呈“辐轮征”;9例淋巴瘤实质部分均呈均匀、轻中度强化。结论 脾脏血管性病变与淋巴瘤CT表现不同,CT有助于明确诊断。     

miR-26b通过调节Notch1信号通路参与原发性肝细胞肝癌侵袭的机制研究

目的:探讨miR-26b参与原发性肝细胞肝癌（HCC）侵袭的机制。方法:在细胞培养液中培养人肝细胞系HL-7702和HCC细胞各系Hepb-3、HuH-7、MHCC97-L、MHCC97-H。实时荧光定量PCR法（qRT-PCR）检测miR-26b的表达水平；用miR-26b mimics、miR-26b inhibitors和Notch1-siRNA分别转染HCC细胞；MTT实验检测转染后HCC细胞的活力；采用Western blot检测Notch1受体蛋白表达水平的变化；Transwell小室测定不同处理后的HCC细胞的侵袭能力。结果:人正常肝细胞系HL-7702和HCC细胞系Hepb-3、HuH-7、MHCC97-L、MHCC97-H中的miR-26b相对表达含量随其侵袭和迁移能力的升高而依次下降；抑制miR-26b的表达，Notch1受体蛋白表达明显增高，而此时HCC细胞的侵袭性显著增强；相反，上调miR-26b的表达，Notch1受体蛋白表达明显降低，而HCC细胞侵袭性显著下降；miR-26b可能通过调控Notch1信号通路调节HCC细胞侵袭性。结论:miR-26b通过负调控Notch1信号通路抑制HCC细胞侵袭能力，为HCC侵袭的机制奠定了理论基础，miR-26b可能成为HCC治疗的新靶点。     

T3、T4期结直肠癌淋巴结转移危险因素分析

目的探讨T3、T4期结直肠癌患者淋巴结转移危险因素,为临床诊疗提供参考。方法回顾性分析2008年1月至2017年12月在空军军医大学西京消化病医院行结直肠癌根治术的1112例T3、T4期结直肠癌患者的临床病理资料,分析淋巴结转移状态与临床病理因素及肿瘤标志物的相关性,应用logistic多因素回归法分析淋巴结转移的相关危险因素。结果单因素分析结果显示,性别、年龄、肿瘤部位分层的结直肠癌患者间淋巴结转移率差异均无统计学意义(均P>0.05),淋巴结转移率在不同肿瘤长径[<5 cm和≥5 cm分别为37.75%(211/559)、52.26%(289/553),χ^2=23.666,P<0.01]、大体类型[浸润、溃疡、蕈伞、隆起分别为37.04%(20/54)、47.52%(432/909)、34.33%(23/67)、69.51%(57/82),χ^2=13.787,P=0.003]、分化程度[高、中、低分化分别为34.11%(102/299)、49.00%(317/647)、48.80%(81/166),χ^2=19.771,P<0.01]、错配修复缺陷(dMMR)[是和否分别为26.34%(64/243)、50.17%(436/869),χ^2=43.996,P<0.01]、神经侵犯[是和否分别为48.17%(421/874)、33.20%(79/238),χ^2=16.954,P<0.01]、脉管侵犯[是和否分别为79.16%(338/427)、23.65%(162/685),χ^2=327.493,P<0.01]以及术前癌胚抗原(CEA)[阳性(≥5 mg/ml)和阴性(<5 mg/ml)分别为52.87%(249/471)、39.16%(251/641),χ^2=20.162,P<0.01]和CA199[阳性(≥35 U/ml)和阴性(<35 U/ml)分别为59.33%(124/209)、41.64%(376/903),χ^2=21.465,P<0.01]分层患者间差异均有统计学意义。logistic多因素回归分析显示,脉管侵犯和术前CA199阳性是T3、T4期结直肠癌患者淋巴结转移独立危险因素(OR=13.006,95%CI 9.329~17.276,P<0.01;OR=2.194,95%CI 1.513~3.181,P<0.01),dMMR阳性是淋巴结转移的保护性因素(OR=0.279,95%CI 0.190~0.411,P<0.01)。结论脉管侵犯是T3、T4期结直肠癌患者淋巴结转移的主要危险因素。术前肿瘤标志物CA199的检测可以作为预测T3、T4期结直肠癌患者淋巴结转移状态的指标,一定程度上可为诊疗方案的制订提供参考。     

Necroptotic TNFα-Syndecan 4-TNFα Vicious Cycle as a Therapeutic Target for Preventing Temporomandibular Joint Osteoarthritis

Temporomandibular joint osteoarthritis (TMJOA) is a chronic degenerative disease for which the underlying mechanism still remains unclear. Compared with apoptosis and autophagy, necroptosis causes greater harm to tissue homeostasis by releasing damage-associated molecular patterns (DAMPs). However, the role of necroptosis and downstream key DAMPs in TMJOA is unknown. Here, rodent models of TMJOA were established by the unilateral anterior crossbite (UAC). Transmission electron microscopy (TEM) and immunohistochemistry of receptor interacting protein kinase 3 (RIPK3)/phosphorylation of mixed lineage kinase domain-like protein (pMLKL) were conducted to evaluate the occurrence of necroptosis in vivo. The therapeutic effects of blocking necroptosis were achieved by intra-articularly injecting RIPK3 or MLKL inhibitors and using RIPK3 or MLKL knockout mice. In vitro necroptosis of condylar chondrocyte was induced by combination of tumor necrosis factor alpha (TNFα), second mitochondria-derived activator of caspases (SMAC) mimetics and carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]- fluoromethylketone (z-VAD-fmk). The possible DAMPs released by necroptotic chondrocytes were screened by quantitative proteomics and blocked by specific antibody. Translucent cytosol, swollen organelles, and ruptured cell membranes, features of necroptosis, were frequently manifested in chondrocytes at the early stage of condylar cartilage degeneration in TMJOA, which was accompanied by upregulation of RIPK3/pMLKL. Inhibiting or knocking out RIPK3/MLKL significantly prevented cartilage degeneration. DAMPs released by necroptotic condylar chondrocytes, such as syndecan 4 (SDC4) and heat shock protein 90 (HSP90), were verified. Furthermore, blocking the function of SDC4 significantly attenuated the expression of TNFα in cartilage and synovium, and accordingly increased cartilage thickness and reduced synovial inflammation. Thus, the necroptotic vicious cycle of TNFα-SDC4-TNFα contributes to cartilage degeneration and synovitis, and can serve as a potential therapeutic target for treating TMJOA. © 2022 American Society for Bone and Mineral Research (ASBMR).     

血小板第4因子对放射损伤小鼠骨髓基质细胞周期的影响

目的探讨血小板第4因子（platelet factor 4,PF4）对5.0 Gy γ射线全身照射小鼠的骨髓基质细胞（bone marrow stromal cells,BMSCs）的保护作用,进一步探讨PF4对造血的辐射防护机制.方法30只雄性小鼠随机分为3组：①放射组,②PF4保护组,③对照组.小鼠照射前分别于26和20 h腹腔内注射PF4,每次剂量50 μg/kg.于照射后3 d取骨髓细胞体外培养,分别计数培养后3、7和14 d的骨髓基质细胞集落（CFU-F）;在培养后10 d流式细胞仪检测细胞周期.结果3组中,照射组3 d的CFU-F数量与PF4保护组差异无统计学意义,7和14 d的CFU-F数量PF4保护组较照射组明显增加.流式细胞仪检测结果表明3组中照射组G0＋G1期细胞明显高于其余两组,S,G2＋M期细胞明显低于其余两组.结论PF4对照射小鼠的骨髓基质细胞有保护作用,促进造血重建.     

耳穴脉冲刺激对Oddi括约肌张力及肌电活动的影响

目的　探讨耳穴脉冲电刺激治疗胆石症 ,胆绞痛的机制 .方法　选用 15条成年杂种犬 ,进行耳穴体表脉冲刺激与缩胆素 (CCK)对在体狗胆囊张力 ,Oddi括约肌张力及肌电活动影响的对比研究 .结果　耳穴脉冲电刺激对胆囊张力无明显影响 [(1.2 7± 0 .2 6 ) k Pa与 (1.2 4± 0 .2 2 ) k Pa,P<0 .0 5 ],CCK注射液能明显提高胆囊张力 [(1.2 7± 0 .2 6 ) k Pa与 (1.91± 0 .39) k Pa,P<0 .0 5 ],CCK注射液能明显降低Oddi括约肌张力 [(2 .2 4± 0 .5 5 ) k Pa与 (1.5 8± 0 .5 6 ) k Pa,P>0 .0 5 ]及肌电活动 .结论　耳穴脉冲电刺激同 CCK一样 ,均对 Oddi括约肌的张力有显著的降低作用 ,并减少 Oddi括约肌的肌电峰电位爆发波的频率与电压值 ,推测其对胆绞痛有治疗作用 ,并有助于胆结石的排石过程 .     

庆大霉素对豚鼠前庭上皮IGF-1及其受体表达的影响

目的：研究庆大霉素对豚鼠前庭上皮胰岛素样生长因子-1（insulin-like growth factor-1，IGF-1）及其受体（insulin-like growth factor-1 receptor，EGF-1R）表达的影响，并探讨其生物学特性。方法：采用免疫组织细胞化学方法，以抗IGF-1及IGF-1R抗体为标记物，检测庆大霉素损伤后豚鼠前庭上皮自发修复期IGF-1及IGF-1R的表达变化和分布特点；采用Brdu体内标记和抗Brdu抗体免疫组化染色，检测庆大霉素损伤后豚鼠前庭上皮增殖的变化。结果：IGF-1及IGF-1R在正常成年豚鼠前庭上皮细胞中有低水平表达，庆大霉素损伤后，其表达增多。在1d组IGF-1及IGF-1R表达最强，其后逐渐减少。在正常对照组中无Brdu阳性细胞。各实验组均观察到Brdu阳性细胞，7d组最多。结论：庆大霉素损伤后，豚鼠前庭上皮IGF-1及IGF-1R表达增强，其时程变化与细胞增殖活动密切相关。IGF-1在豚鼠前庭上皮损伤后的细胞增殖中可能起重要信号转导作用。