绝经综合征评定量表的试测与调适研究

目的：在绝经综合征评定量表建立过程中,对量表进行语言和形式等调适。方法：在绝经综合征患者和更年期非绝经综合征人群进行了3次绝经综合征评定量表3个试测版本小样本的试测,考察量表的语言、形式、回答方式等。结果与结论：根据每次试测的结果,对量表进行了调整,使量表在语言、格式等各个方面更适合受试人群回答,保证了获取信息量的准确性及量表的可行性。     

UBE2C promotes the progression of pancreatic cancer and glycolytic activity via EGFR stabilization-mediated PI3K-Akt pathway activation

BackgroundPancreatic cancer (PC) is among the most prevalent and deadliest endocrine tumors, yet the mechanisms governing its pathogenesis remain to be fully clarified. While ubiquitin-conjugating enzyme E2C (UBE2C) has been identified as an important oncogene in several cancers, its importance in PC has yet to be established.MethodsUBE2C expression in PC tumor samples and cell lines was examined via quantitative real-time polymerase chain reaction (qRT-PCR), while appropriate commercial kits were used to assess lactate production, ATP generation, and the uptake of glucose.ResultsUBE2C was found to be upregulated in PC patient tumors and correlated with poorer survival outcomes. In PC cell lines, the silencing of this gene suppressed the malignant activity of cells, thus supporting its identification as an oncogene in this cancer type. Mechanistically, UBE2C was found to promote enhanced matrix metalloproteinase (MMP) protein expression via activating the PI3K-Akt pathway. Moreover, it was found to bind to the epidermal growth factor receptor (EGFR), stabilizing it and driving additional PI3K-Akt pathway activation. UBE2C knockdown in PC cells impaired their uptake of glucose and their ability to produce lactate and ATP.ConclusionsIn conclusion, the results of this study support a role for UBE2C as a driver of metastatic PC progression owing to its ability to bind to EGFR and to induce signaling via the PI3K-Akt pathway.     

痤疮患者皮肤敏感性的临床分析与治疗

目的:分析痤疮患者的皮肤敏感情况并观察疗效.方法:以2018年1月至2019年5月河南大学第一附属医院皮肤科门诊收治的73例痤疮患者为对象,所有患者行敏感性测验(乳酸测验),将38例乳酸测验阴性者作为皮肤非敏感组,将35例乳酸测验阳性者作为皮肤敏感组,两组患者均给予抗炎等相同的治疗,观察疗效并分析两组患者治疗后的临床相...     

地塞米松对脓毒血症鼠Peyer小结Tfh细胞的影响

目的：测定脓毒血症鼠Peyer小结内滤泡辅助性T细胞（T follicular helper,Tfh）的变化,分析地塞米松（dexamethasone,Dex）对脓毒血症Tfh细胞的可能作用。方法：昆明小鼠诱导脓毒血症模型,模型诱导成功后随机分2组,脓毒血症组（SE组,n=12）、脓毒血症＋Dex处理组（DE组,n=12）。另设对照组（NC组,n=12）。测定血清白介素-6（interleukin-6,IL-6）、降钙素原（procalcitonin,PCT）、中性粒细胞明胶酶相关载脂蛋白（neutrophil gelatinase-associated lipocalin,NGAL）水平。Peyer小结Ⅰ型1-磷酸鞘氨醇（Sphingosine 1-Phosphate 1,S1P1）、CXC趋化因子配体13（CXC chemokine ligand 13,CXCL13）免疫组化染色。Western blot分别检测Peyer小结IL-21、程序性死亡分子-1（programmed death 1,PD-1）、胞嘧啶脱氨酶（enzyme activation-induced cytidine deaminase,AID）蛋白的表达。流式细胞仪测定3组Peyer小结Tfh细胞占T淋巴细胞的百分率。结果：与NC组相比,SE组血清IL-6（19.7±5.20 vs 10.7±3.60 ng·L~（-1））、PCT（1.56±0.92 vs 0.31±0.09μg·L~（-1））、NGAL（0.44±0.11 vs 0.35±0.09 mg·L（-1））升高（P〈0.05或0.01）,Peyer小结S1P1（0.22±0.06 vs 0.14±0.04）、CXCL13（0.25±0.07 vs 0.15±0.04）的表达增加（P〈0.01）,IL-21（0.60±0.08 vs 0.35±0.08）、PD-1（0.30±0.04 vs 0.20±0.05）、AID（0.23±0.05 vs 0.18±0.03）蛋白的表达亦升高（P〈0.05或0.01）,Tfh细胞占T淋巴细胞（8.30±2.00 vs 5.69 vs 1.64%）的百分率升高（P〈0.01）。Dex治疗可降低SE鼠血清IL-6（19.7±5.20 vs 12.8±3.40 ng·L~（-1））、PCT（1.56±0.92 vs 0.71±0.44μg·L~（-1））水平（P〈0.05或0.01）,降低Peyer小结S1P1（0.22±0.06 vs 0.17±0.05）、CXCL13（0.25±0.07 vs 0.19±0.06）的表达（P〈0.05或0.01）,下调Peyer小结IL-21（0.60±0.08 vs 0.48±0.09）、PD-1（0.30±0.04 vs 0.26±0.06）、AID（0.23±0.05 vs0.19±0.04）蛋白的表达（P〈0.05）,降低Tfh细胞占T淋巴细胞（8.30±2.00 vs 6.56±1.59%）的百分率（P〈0.05）。结论：Peyer小结Tfh细胞可能参与脓毒血症的发病机制,Dex抑制Peyer小结Tfh的活化,对Peyer小结微环境起保护作用。     

下咽癌肉瘤临床病理特征的研究

目的:探讨下咽癌肉瘤的临床病理学特征、诊断和鉴别诊断。方法:报道1例经病理证实的下咽癌肉瘤患者的临床资料,结合文献复习进行分析。结果:患者通过手术切除病变,病理检查证实为鳞状细胞癌横纹肌肉瘤,术后行放化疗,恢复良好,随访18个月无复发。结论:下咽癌肉瘤是一种极为罕见的恶性肿瘤,具有特征性的组织病理学、免疫组织化学及临床特点,需与肉瘤样癌、喉癌的放疗反应等相鉴别。下咽癌肉瘤的治疗应首选手术切除。对局部晚期、术后残留、肉眼切除范围欠安全的头颈部癌肉瘤患者应行放疗并及时随访。     

雏鸡耳蜗中的一氧化氮合成酶分布

应用冰冻切片组织化学技术，以还原型尼克酰胺腺嘌呤二核苷酸磷酸-黄递酶特异性地确定一氧化氮合成酶（NOS）在小鸡耳蜗中存在，观察其分布情况，发现听毛细胞底部颗粒较集中，染色深，毛细胞周围亦有散在颗粒，基底乳头近端与远端染色强弱相似。阳性反应神经纤维连接毛细胞底部。螺旋神经节细胞胞浆中有大量的蓝色颗粒，细胞核无着色，这些细胞大小均匀，呈圆形或椭圆形，周围有多量阳性神经纤维，提示可能为神经性NOS。血管盖内皮细胞胞浆中酶活性较强。对这些分布特点和意义进行了讨论。     

INTRABEAM实施乳腺癌术中放疗系统临床应用观察(附20例报告)

目的:评价INTRABEAM术中放射治疗系统临床应用的安全性和优势.方法:INTRABEAM对20例保乳手术患者实施术中瘤床放疗,均为单次照射每次20Gy,施用器规格为4.5cm(范围1.5-5.0cm),治疗持续时间35.5-51分钟.结果:术中照射治疗后有3例发生治疗区局部积液,经抽吸并加压包扎后愈合,乳房水肿1例.结论:INTRABEAM术中放射治疗系统近期无明显毒副作用,INTRABEAM术中放射治疗系统是一项安全良好耐受性技术,病人乐于接受.     

Inhibiting DNA methylation alleviates cisplatin-induced hearing loss by decreasing oxidative stress-induced mitochondria-dependent apoptosis via the LRP1–PI3K/AKT pathway

Cisplatin-related ototoxicity is a critical side effect of chemotherapy and can lead to irreversible hearing loss. This study aimed to assess the potential effect of the DNA methyltransferase (DNMT) inhibitor RG108 on cisplatin-induced ototoxicity. Immunohistochemistry, apoptosis assay, and auditory brainstem response (ABR) were employed to determine the impacts of RG108 on cisplatin-induced injury in murine hair cells (HCs) and spiral ganglion neurons (SGNs). Rhodamine 123 and TMRM were utilized for mitochondrial membrane potential (MMP) assessment. Reactive oxygen species (ROS) amounts were evaluated by Cellrox green and Mitosox-red probes. Mitochondrial respiratory function evaluation was performed by determining oxygen consumption rates (OCRs). The results showed that RG108 can markedly reduce cisplatin induced damage in HCs and SGNs, and alleviate apoptotic rate by protecting mitochondrial function through preventing ROS accumulation. Furthermore, RG108 upregulated BCL-2 and downregulated APAF1, BAX, and BAD in HEI-OC1 cells, and triggered the PI3K/AKT pathway. Decreased expression of low-density lipoprotein receptor-related protein 1 (LRP1) and high methylation of the LRP1 promoter were observed after cisplatin treatment. RG108 treatment can increase LRP1 expression and decrease LRP1 promoter methylation. In conclusion, RG108 might represent a new potential agent for preventing hearing loss induced by cisplatin via activating the LRP1-PI3K/AKT pathway.KEY WORDS: Cisplatin, DNMT, Apoptosis, Hair cell, Spiral ganglion neurons, RG108, Mitochondrial dysfunction, ROS     

智能代理在网络课程监控中的应用模式研究

网络课程作为终身教育学习资源的一种,越来越受到人们的重视.在网络课程中,是否具备良好的监控能力,是影响学习者学习效果的关键因素.而目前的网络监控普遍存在智能程度不高问题,无法满足网络监控的需要.该文将智能代理技术与电子学档结合起来对网络课程进行监控,以期对今后网络课程监控方面的研究提供一些帮助.