[摘 要] 目的：探讨核仁小RNA（snoRNA）71A通过TLR3/PD-L1通路对食管鳞状细胞癌（ESCC）细胞增殖、迁移及侵袭能力的影响。方法：qPCR检测52例ESCC患者的配对肿瘤组织、癌旁组织，以及人ESCC细胞中SNORA71A的表达情况。将反义寡核苷酸（SNORA71A-ASO-29、SNORA71A-ASO-102和NC-ASO）或小干扰RNA（siTLR3、siTLR3-NC）分别转染至人ESCC TE-1细胞，分别记为SNORA71A-ASO1组、SNORA71A-ASO2组、NC-ASO组及siTLR3组、siNC组。另外将过表达质粒pcDNA3.1-SNORA71A和pcDNA3.1空载体质粒分别转染至TE-1细胞，分别记为SNORA71A组和Vector组。细胞功能学实验（MTS实验、划痕愈合实验，以及Transwell侵袭实验）评估各组细胞在敲低或过表达SNORA71A后增殖、迁移和侵袭能力的变化。高通量转录组测序筛选SNORA71A下游作用靶基因，基因本体论（GO）和京都基因与基因组百科全书（KEGG）功能富集分析预测SNORA71A下游作用靶基因可能参与的生物学过程和信号通路。qPCR检测测序筛选出的下游作用靶基因TLR3在ESCC组织以及细胞中的表达。同时，qPCR和WB检测TE-1细胞在敲低或过表达TLR3后PD-L1 mRNA和蛋白质表达变化。细胞功能学实验检测TLR3敲低对SNORA71A所促进的TE-1细胞恶性生物行为（增殖、迁移、侵袭）的影响。结果：在52例ESCC患者的肿瘤组织以及ESCC细胞中SNORA71A表达均呈高水平（P < 0.01或P < 0.05）。敲低SNORA71A抑制TE-1细胞增殖、迁移和侵袭（P < 0.01或P < 0.05），过表达SNORA71A则促进TE-1细胞增殖、迁移和侵袭（P < 0.01或P < 0.05）。高通量转录组测序筛选到TLR3为SNORA71A下游作用靶基因。TLR3在ESCC组织以及TE-1细胞中呈低表达（P < 0.01或P < 0.05）。TLR3正向调控PD-L1 mRNA和蛋白质表达（P < 0.01或P < 0.05）。细胞功能学实验中，TLR3可以部分削弱SNORA71A对PD-L1表达的调控（P < 0.01）。结论：SNORA71A通过调控TLR3/PD-L1通路调节TE-1细胞增殖、迁移和侵袭。

Purpose: Lateral cephalograms are conventionally used for landmark identification and cephalometric analysis, butexpose patients to ionizing radiation. Magnetic resonance imaging (MRI) is increasingly employed to evaluate various tissue types, with dental-dedicated MRI (ddMRI) emerging as a promising modality in clinical dentistry. High-quality MRI could offer a radiation-free alternative for orthodontic diagnosis and treatment planning. This pilot study aimed to evaluate the reliability of ddMRI for 2-dimensional (2D) orthodontic cephalometric landmark identification and annotation. Materials and Methods: Thirteen volunteers (7 men, 6 women; mean age 33±5.2 years) underwent ddMRI. Threeindependent raters identified 2D cephalometric landmarks and annotated their positions on the same ddMRI datasetstwice. The 3D Slicer application was used to identify key orthodontic cephalometric landmarks on multiplanar reconstruction images in the sagittal plane. Intra-rater and inter-rater reproducibility were assessed using intraclass correlation coefficients (ICCs), and reliability was evaluated by nominal differences in linear distance (mm) between annotated points. Results: Intra-rater ICCs ranged from 0.909 to 0.999, and inter-rater ICCs ranged from 0.988 to 0.999, indicating excellent intra- and inter-rater reliability. Bland-Altman plots were used to display mean differences (mm) and limits of agreement (±1.96 standard deviations) between annotations to assess potential biases. Conclusion ddMRI is a feasible imaging modality for 2D orthodontic landmark identification. Based on intra- andinter-rater reproducibility values, ddMRI demonstrates high reliability in identifying key orthodontic cephalometric landmarks, providing a radiation-free alternative for orthodontic diagnosis and treatment planning.

Background/Aims: Systemic Inflammation (SI) is considered a key mechanism in disease progression and development of complications in decompensated liver cirrhosis. SI is mainly driven by portal hypertension and bacterial translocation. Transjugular intrahepatic portosystemic shunt (TIPS) insertion represents an effective treatment for portal hypertension. This study aims to investigate the impact of TIPS insertion on SI and bacterial translocation. Methods: We prospectively included 59 cirrhotic patients undergoing TIPS insertion. Blood samples were collected at TIPS insertion and follow-up (FU) 1, 3, 6, and 12 months thereafter. At all time points, we performed a comprehensive analysis of SI including 43 soluble inflammatory markers (SIMs), and surrogates of bacterial translocation (sCD14, sCD163). To investigate long-term kinetics of SI, C-reactive protein (CRP) and white blood cells (WBC) were retrospectively analyzed in a cohort of 177 patients up to 3 years after TIPS insertion. Results: At TIPS insertion, 30/43 SIMs, sCD14, and sCD163 measured significantly higher in cirrhotic patients compared to healthy controls. By FU6 25 SIMs and sCD14 measured at significantly lower levels compared to baseline. Interestingly, in patients with TIPS indication of refractory ascites, IL-6 decreased to levels documented in earlier stages of cirrhosis. In long-term follow-up, CRP levels significantly decreased after TIPS insertion, which translated into lower mortality in Cox regression analysis (HR 0.968, p=0.042). Notably, patients with residual ascites post-TIPS showed significantly higher CRP and IL-6 levels across all follow-ups compared to patients with resolved ascites. Conclusions Decreasing portal hypertension via TIPS insertion leads to a significant attenuation of SI and bacterial translocation over time.

Thermal analysis technology has emerged as a pivotal tool for the identification and quality control of traditional Chinese medicine （TCM） owing to its advantages of high sensitivity and capability for simultaneous multi-parameter detection. The application progress on thermogravimetric analysis （TGA）, differential thermal analysis （DTA）, and differential scanning calorimetry （DSC） in four key areas: authenticity identification of herbal medicines, optimization of processing techniques, evaluation of extract thermal stability, and construction of quality evaluation systems were summarized. Thermal analysis technology enables rapid authentication of medicinal materials by establishing a thermal fingerprint. When integrated with hyphenated techniques （e.g., FTIR and GC-MS）, it facilitates in-depth analysis of compositional differences in complex matrices. In Future, the development of thermal analysis databases and multi-technology integration will be expected to further promote the standardization of TCM quality control.

Background/Aims: Systemic Inflammation (SI) is considered a key mechanism in disease progression and development of complications in decompensated liver cirrhosis. SI is mainly driven by portal hypertension and bacterial translocation. Transjugular intrahepatic portosystemic shunt (TIPS) insertion represents an effective treatment for portal hypertension. This study aims to investigate the impact of TIPS insertion on SI and bacterial translocation. Methods: We prospectively included 59 cirrhotic patients undergoing TIPS insertion. Blood samples were collected at TIPS insertion and follow-up (FU) 1, 3, 6, and 12 months thereafter. At all time points, we performed a comprehensive analysis of SI including 43 soluble inflammatory markers (SIMs), and surrogates of bacterial translocation (sCD14, sCD163). To investigate long-term kinetics of SI, C-reactive protein (CRP) and white blood cells (WBC) were retrospectively analyzed in a cohort of 177 patients up to 3 years after TIPS insertion. Results: At TIPS insertion, 30/43 SIMs, sCD14, and sCD163 measured significantly higher in cirrhotic patients compared to healthy controls. By FU6 25 SIMs and sCD14 measured at significantly lower levels compared to baseline. Interestingly, in patients with TIPS indication of refractory ascites, IL-6 decreased to levels documented in earlier stages of cirrhosis. In long-term follow-up, CRP levels significantly decreased after TIPS insertion, which translated into lower mortality in Cox regression analysis (HR 0.968, p=0.042). Notably, patients with residual ascites post-TIPS showed significantly higher CRP and IL-6 levels across all follow-ups compared to patients with resolved ascites. Conclusions Decreasing portal hypertension via TIPS insertion leads to a significant attenuation of SI and bacterial translocation over time.

Background/Aims: Systemic Inflammation (SI) is considered a key mechanism in disease progression and development of complications in decompensated liver cirrhosis. SI is mainly driven by portal hypertension and bacterial translocation. Transjugular intrahepatic portosystemic shunt (TIPS) insertion represents an effective treatment for portal hypertension. This study aims to investigate the impact of TIPS insertion on SI and bacterial translocation. Methods: We prospectively included 59 cirrhotic patients undergoing TIPS insertion. Blood samples were collected at TIPS insertion and follow-up (FU) 1, 3, 6, and 12 months thereafter. At all time points, we performed a comprehensive analysis of SI including 43 soluble inflammatory markers (SIMs), and surrogates of bacterial translocation (sCD14, sCD163). To investigate long-term kinetics of SI, C-reactive protein (CRP) and white blood cells (WBC) were retrospectively analyzed in a cohort of 177 patients up to 3 years after TIPS insertion. Results: At TIPS insertion, 30/43 SIMs, sCD14, and sCD163 measured significantly higher in cirrhotic patients compared to healthy controls. By FU6 25 SIMs and sCD14 measured at significantly lower levels compared to baseline. Interestingly, in patients with TIPS indication of refractory ascites, IL-6 decreased to levels documented in earlier stages of cirrhosis. In long-term follow-up, CRP levels significantly decreased after TIPS insertion, which translated into lower mortality in Cox regression analysis (HR 0.968, p=0.042). Notably, patients with residual ascites post-TIPS showed significantly higher CRP and IL-6 levels across all follow-ups compared to patients with resolved ascites. Conclusions Decreasing portal hypertension via TIPS insertion leads to a significant attenuation of SI and bacterial translocation over time.

[摘 要] 目的：基于生物信息学分析和体内、体外实验研究长链非编码RNA00511（LINC00511）敲减对非小细胞肺癌细胞增殖、凋亡、侵袭等恶性生物学行为的影响，并初步探究其作用机制。方法：通过基因表达谱交互分析（GEPIA）数据库分析LINC00511在非小细胞肺癌的表达水平，及其与患者肿瘤分期、生存期等临床特征、肿瘤细胞恶性生物学行为有关基因的相关性；利用shRNA慢病毒载体构建LINC00511敲减的H1299肺癌细胞株，克隆形成实验、划痕愈合实验和流式细胞术分别检测对H1299细胞增殖、迁移、细胞周期和凋亡能力的影响，qRT-PCR检测相关调控基因表达，WB法检测肿瘤相关蛋白的表达；构建裸鼠皮下移植瘤模型，取瘤组织进行免疫组织化学实验检测Ki67表达情况。结果：GEPIA数据库分析表明LINC00511在非小细胞肺癌组织中表达水平升高，且与该病的临床分期情况相关（P < 0.05），LINC00511与肺癌中CASP3、CCNB1、CDK4等多种基因表达均有相关性（P < 0.01）；LINC00511敲减可抑制细胞的克隆形成和迁移能力、促进肺癌细胞凋亡并影响细胞周期进展（P < 0.05，P < 0.01）；LINC00511敲减可下调肺癌细胞CCNB、CDK4、TGF-β1基因的表达（P < 0.01），对CCND1、VEGFA基因表达无明显影响，LINC00511敲减可抑制细胞内MMP9、CTNNB1表达，上调CASP3的表达（P < 0.05，P < 0.01）；裸鼠体内实验证实，LINC00511敲减可抑制移植瘤体组织内Ki67的表达（P < 0.01）。结论：LINC00511在非小细胞肺癌组织中呈高表达，与肺癌临床分期和多种基因表达具有相关性，LINC00511敲减可能通过影响相关基因、蛋白的表达，抑制肺癌H1299细胞的恶性生物学行为。

[摘 要] 目的：探讨多结节非小细胞肺癌（NSCLC）组织中的驱动基因突变情况与临床病理特征的关系，为多结节NSCLC患者治疗提供分子诊断依据。方法：本研究共纳入2018年1月至2023年10月间云南省肿瘤医院分子诊断中心检测的121例多结节NSCLC患者的253个肺结节肿瘤组织标本，以第二代测序（NGS）技术或扩增阻滞突变系统PCR（ARMS-PCR）技术检测多结节NSCLC 组织中驱动基因突变情况，分析其与患者临床病理特征的关系，比较不同结节间肺癌驱动基因的突变异质性。结果：与非“宣威”NSCLC相比，“宣威”多结节NSCLC患者驱动基因突变具有显著的地域特点，表现在“宣威”患者具有较低（20%）的EGFR敏感突变（L858R、19-del）及较高（27.26%）的EGFR少见突变（主要为G719/S768I、G719）；“宣威”多结节NSCLC患者的KRAS突变率（27.27%）亦显著高于非“宣威”患者突变率（12.59%）（P<0.05）。此外，“宣威”多结节NSCLC患者驱动基因突变不一致率高达69.23%，远高于非“宣威”患者驱动基因突变不一致率（55.07%）（P<0.05）。结论：“宣威”多结节NSCLC患者具有较高的EGFR少见突变及KRAS突变率，同一患者不同病灶之间存在更高的驱动基因突变异质性，本研究将为“宣威”多结节NSCLC的诊疗策略提供更多的选择。

[摘 要] 目的：探究SOX9通过上调长链非编码RNA LINC01503的表达对喉鳞状细胞癌（LSCC）细胞的增殖、迁移、侵袭及肿瘤干细胞干性的影响。方法： 常规培养人LSCC细胞AMC-HN-8、TU177、TU212和TU686，用转染试剂将敲减序列及其对照核酸（si-SOX9-NC、si-SOX9#1、 si-SOX9#2、si-LINC01503-NC、si-LINC01503#1、si-LINC01503#2）或过表达质粒及其对照核酸（pcDNA3.1-SOX-NC、pcDNA3.1-SOX-oe、pcDNA3.1-LIN01503-NC和pcDNA3.1-LIN01503-oe）分别转染至TU177细胞或TU686细胞，记为si-SOX9-NC组、si-SOX9#1组、si-SOX9#2组、si-LINC01503-NC组、si-LINC01503#1组、si-LINC01503#2组；pcDNA3.1-SOX9-NC组、pcDNA3.1-SOX9-oe组、pcDNA3.1-LINC01503-NC组、pcDNA3.1-LINC01503-oe组、si-SOX9-NC + pcDNA3.1-LINC01503-NC组和si-SOX9 + pcDNA3.1-LINC01503-oe组。qPCR法检测SOX9 mRNA和LINC01503 在各组细胞中的表达，生物信息学分析SOX9与LINC0503启动子区的结合位点，双萤光素酶报告基因实验和染色质免疫共沉淀实验验证SOX9与LINC01503启动子区是否直接结合，WB法检测SOX9的敲减效率及LINC01503对TU177和TU686细胞干性标志物表达的影响，MTS法检测各组细胞的增殖活力，划痕愈合和Transwell小室实验检测各组细胞的迁移能力，克隆形成实验检测各组细胞的克隆形成能力。结果：SOX9在各种LSCC细胞中呈高表达（均P < 0.05），数据库数据分析显示，在头颈部鳞状细胞癌中，SOX9与LINC01503表达呈正相关（R = 0.12，P = 0.005 9）；SOX9可与LINC01503启动子区直接结合并促进其转录表达（均P < 0.05）；敲减LINC01503可明显抑制TU177细胞的增殖、迁移、侵袭（均P < 0.05），过表达LINC01503明显促进TU686细胞增殖、迁移、侵袭的能力（均P < 0.05），提高TU686细胞克隆形成能力和细胞干性标志物分子CD133、OCT4、SOX2的mRNA和蛋白水平表达（均P < 0.05），敲减LINC01503则均可抑制TU686细胞的克隆形成和细胞干性标志物的表达（均P < 0.05）；敲减SOX9均可明显抑制TU177细胞的增殖、迁移和侵袭能力，降低其干性细胞标志物的表达（均P < 0.05），同时过表达LINC01503则可部分逆转敲减SOX9对TU177细胞恶性生物学行为和干性标志物表达的抑制作用（均P < 0.05）。结论：SOX9和LINC01503在LSCC细胞中呈高表达，SOX9可能通过上调LINC01503表达提高LSCC细胞增殖、转移和侵袭能力和肿瘤干细胞干性。