帕金森病是全球第二大神经退行性疾病，其根本病理特征为中脑黑质多巴胺能神经元的退变死亡。目前临床一线治疗主要采用左旋多巴替代疗法，然而疗效有限且副作用显著。以补充多巴胺能神经元为基础的细胞替代疗法，能够从根本上解决神经元丢失的问题，具有长远的临床意义。细胞替代治疗的细胞最早来自于胎儿腹侧中脑组织，随着重编程技术的不断发展，已逐步转向人类胚胎干细胞和诱导多能干细胞体外分化的前体细胞。同时，直接在体内重编程，将胶质细胞转分化为多巴胺能神经元，也是一种具有应用潜力的策略。本文系统总结了近年来帕金森病细胞替代疗法的进展和面临的挑战，旨在为该疾病治疗新策略的研究提供参考和启示。

       Parkinson’s disease（PD）is the second most prevalent neurodegenerative disorder worldwide，characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta．Traditional treatments，primarily involving levodopa for dopamine replacement，offer limited efficacy and associated with significant side effects．Cell  replacement therapies aimed at replenishing dopaminergic neurons provide a promising long-term solution to neuronal loss，with  substantial clinical significance．The initial successful cellular source for transplantation in PD research was fetal ventral mesencephalic tissue．Nevertheless，advancements in  reprogramming technologies have increasingly favored the use of human embryonic stem cells and induced pluripotent stem cells．Additionally，direct in vivo reprogramming，converting glial cells into dopaminergic neurons，has emerged as an alternative strategy for cell replacement therapy．This  review  systematically  summarizes the  recent advances and challenges in cell replacement therapies for PD，with the aim of providing insights and guidance for the development of novel therapeutic strategies for the PD．

目的 明确亚甲基四氢叶酸还原酶（MTHFR）C677T、A1298C基因多态性与成人患者使用大剂量甲氨蝶呤（MTX）治疗急性淋巴细胞白血病（ALL）毒性反应和24、48、72 h MTX血药浓度关系。方法 收集2014年6月—2020年6月就诊于新疆医科大学第一附属医院成人急性淋巴细胞白血病75例患者血样检测MTHFR C677T及A1298C基因多态性, 根据抗癌药物常见毒性反应分级标准对毒性反应进行分级,采用非条件Logistic回归分析MTHFR C677T、A1298C基因多态性与HD-MTX毒性反应及血药浓度的关系。结果 MTHFR 677TT型发生贫血风险显著高于CC型（P=0.027, OR=4.694, 95%CI：1.195~18.438）; 未发现MTHFR C677T与白细胞减少、血小板计数减少、中性粒细胞计数减少、淋巴粒细胞计数减少、骨髓抑制、谷丙转氨酶升高、谷草转氨酶升高、肝功能损伤、急性肾损伤及黏膜损伤、24 h、48 h及72 h MTX血药浓度有相关性（P>0.05）; 未发现MTHFR A1298C与HD-MTX毒性反应及血药浓度有相关性（P>0.05）。结论 MTHFR C677T基因多态性与成人急性淋巴细胞白血病患者大剂量MTX化学治疗后血液毒性存在相关性。

Objective To determine the relationship among C677T and A1298C gene polymorphisms of methyltetrahydrofolate reductase（MTHFR）and adult acute lymphocytic leukemia（ALL）, the relationship between the toxicity of high-dose methotrexate（HD-MTX）after chemotherapy and the MTX blood concentration of 24 h, 48 h and 72 h in patients with ALL．Methods Blood samples were collected from 75 adult patients with ALL who were treated at the First Affiliated Hospital of Xinjiang Medical University from June 2014 to June 2020．The samples were used to detect the genetic polymorphisms of MTHFR C677T and A1298C, and the toxic reactions were graded according to the common toxic reaction classification criteria of anti-cancer drugs．Unconditional Logistic regression was used to analyze the relationship between MTHFR C677T and A1298C gene polymorphisms and HD-MTX toxic reactions and blood drug concentration．Results The risk of anemia in MTHFR 677TT was significantly higher than that in CC type（P=0.027, OR=4.694, 95% CI：1.195-18.438）．No correlation was found between MTHFR C677T and leukopenia, thrombocytopenia, neutropenia, lymphogranulocytopenia, bone marrow suppression, elevated alanine aminotransferase, elevated aspartate aminotransferase, liver function injury, acute kidney injury and mucosal injury, 24 h, 48 h and 72 h MTX plasma concentrations（>0.05）．No correlation was found among MTHFR A1298C and HD-MTX toxicity and blood concentration（P>0.05）．Conclusions MTHFR C677T gene polymorphism is associated with hematotoxicity after HD-MTX chemotherapy in adult patients with ALL．

目的 观察辅助性T17细胞（Th17）与调节性T细胞（Treg）比值与2型糖尿病（T2DM）患者胰岛素抵抗及胰岛β细胞功能的关系。方法 纳入2022年4月—2023年4月在贵州医科大学第二附属医院内分泌科住院及健康体检人群各100例, 分为糖耐量正常组（NGT组, n=100）和T2DM组（n=100）, 分别测定糖化血红蛋白（HbA1c）、空腹血糖（FPG）、甘油三酯（TG）等生化指标, 电化学发光法测定空腹胰岛素（FINS）, 稳态模型计算胰岛β细胞功能指数（HOMA-β）、胰岛素抵抗指数（HOMA-IR）及胰岛素敏感指数（HOMA-ISI）。流式细胞术检测Th17、Treg水平。HOMA-IR、HOMA-β和HOMA-ISI的影响因素采用多元线性回归分析。结果 与NGT组相比, T2DM组BMI、FPG、HbA1c、LDL-C 、TG、TC、FINS、HOMA-IR、Th17及Th17/Treg水平均升高（P<0.01）, HDL-C、HOMA-β、HOMA-ISI、Treg水平均降低, 且差异有统计学意义（P<0.01）。Th17与BMI（r=0.251, P<0.001）及HOMA-IR（r=0.305, P<0.001）呈正相关; 与HOMA-β（r=-0.204, P<0.001）及HOMA-ISI（r=-0.359, P<0.001）呈负相关。Treg与HOMA-ISI之间呈正相关（r=0.170, P=0.008）, 而与HOMA-IR呈负相关（r=-0.153, P=0.017）; Th17/Treg与BMI（r=0.332, P<0.001）及HOMA-IR（r=0.374, P<0.001）;与HOMA-β（r=-0.249, P<0.001）及HOMA-ISI（r=-0.427, P<0.001）呈负相关。多元线性回归分析显示, Th17/Treg是HOMA-IR（β=5.915）升高及HOMA-ISI（β=-2.557）下降的影响因素（P<0.01）。结论 Th17/Treg可能通过影响胰岛素抵抗、降低胰岛素敏感性参与T2DM的发生。

Objective To explore the relationship among the proportion of helper T17 cells（Th17）to regulatory T cells（Treg）, insulin resistance, and the function of islet beta cells．Methods One hundred cases of hospitalized patients and 100 cases of health check-ups people in the Department of Endocrinology of the Second Affiliated Hospital of Guizhou Medical University from April 2022 to April 2023 were included．Patients were divided into normal glucose tolerance group（NGT group, n=100）and type 2 diabetes mellitus group（T2DM group, n=100）．The biochemical indexes of HbA1c, fasting blood glucose（FPG）, triglyceride（TG）and fasting insulin（FINS）were determined by electrochemiluminescence．Islet beta cell function index（HOMA-β）, insulin resistance index（HOMA-IR）and insulin sensitivity index（HOMA-ISI）were calculated in homeostasis model．The levels of Th17 and Treg were detected by flow cytometry．Spearman was used to analyze the correlation between indicators, and multiple linear regression analysis was used to analyze the influencing factors of HOMA-IR, HOMA-β and HOMA-ISI．Results In contrast to the NGT group, the T2DM group exhibited elevated levels of BMI, FPG, HbA1c, LDL-C, TG, TC, FINS, HOMA-IR, Th17 and Th17/Treg, with these variances being signifincantly different（P<0.01）．There was a notable reduction in the levels of HDL-C,HOMA-β,HOMA-ISI,Treg,with those changes being significantly different（P<0.01）．Th17 was positively correlated with BMI（r=0.251, P<0.001）and HOMA-IR（r=0.305, P<0.001）, it was negatively correlated with HOMA-β（r=-0.204, P<0.001）and HOMA-ISI（r=-0.359, P<0.001）．Treg was positively correlated with HOMA-ISI（r=0.170, P=0.008）, while it was negatively correlated with HOMA-IR（r=-0.153, P=0.017）．The ratio of Th17/Treg was positively correlated with BMI（r=0.332, P<0.001）and HOMA-IR（r=0.374, P<0.001）, it was negatively correlated with HOMA-β（r=-0.249, P<0.001）and HOMA-ISI（r=-0.427, P<0.001）．Multiple linear regression analysis showed that Th17/Treg was an influential factor in the increase of HOMA-IR（β=5.915）and the decrease of HOMA-ISI（β=-2.557）（P<0.01）．Conclusions Th17/Treg may be involved in the development of T2DM by affecting insulin resistance and reducing insulin sensitivity．

目的 探讨卵巢癌化学治疗（化疗）耐药与焦孔素E（GSDME）基因的甲基化是否有关, 以及地西他滨是否可以通过去甲基化使GSDME蛋白表达水平升高从而逆转卵巢癌化疗耐药。方法 顺铂逆浓度梯度构建SKOV-3卵巢癌耐顺铂细胞株（SKOV-3/DDP）; CCK8法检测耐药前后细胞株的半抑制浓度（IC₅₀）; 实时荧光定量甲基化特异性PCR法检测两组细胞中GSDME基因的甲基化水平; Wetern Blot检测两组细胞中GSDME的表达水平。将耐药细胞株用不同质量浓度的地西他滨处理,重复上述实验, 检测地西他滨处理前后细胞的IC₅₀、GSDME基因的甲基化水平及GSDME蛋白的表达程度。结果 与SKOV-3细胞相比, SKOV-3/DDP中GSDME基因的甲基化水平升高（P<0.01）, 同时GSDME蛋白的表达水平降低（P<0.001）; 随着地西他滨作用浓度的升高, 耐药细胞中GSDME基因的甲基化程度逐渐降低, 蛋白的表达水平逐渐升高, 细胞的IC₅₀逐渐降低：在用0.5 μg/mL地西他滨处理耐药细胞后GSDME基因的甲基化水平虽然降低（P<0.01）, 但是此时蛋白的表达水平及耐药细胞的IC₅₀均无明显改变（P>0.05）; 当地西他滨的浓度增加到1.0 μg/mL时蛋白的表达水平才明显升高（P<0.05）, 而此时细胞的IC₅₀仍未见明显降低（P>0.05）; 待药物浓度达到1.5 μg/mL时, 细胞的IC₅₀才表现出明显的下降趋势（P<0.05）。结论 GSDME的表达与卵巢癌的化疗耐药密切相关, GSDME的高甲基化水平致使其低表达可促进卵巢癌的化疗耐药。但地西他滨可以通过去甲基化使卵巢癌耐药细胞中GSDME的表达水平升高, 从而增加卵巢癌细胞对化疗药物的敏感性, 进而逆转卵巢癌化疗耐药。

Objective To explore whether drug resistance in ovarian cancer is associated with gasdermin E（GSDME） methylation, and to explore whether decitabine can reverse ovarian cancer chemoresistance by increasing GSDME protein expression levels through demethylation．Methods The cisplatin-resistant cell line（SKOV-3/DDP）was constructed by inverse concentration gradient of cisplatin．Semi-inhibitory concentration（IC₅₀）of cell lines after drug resistance was detected using the CCK8 assay．Real-time fluorescence quantitative methylation-specific PCR was used to detect the methylation level of GSDME gene in the two groups of cells．Wetern Blot was used to detect the expression level of GSDME in the two groups of cells．Drug-resistant cell lines were treated with different concentrations of the demethylating drug decitabine．Experiments above were repeated to detect the methylation degree of IC₅₀ and GSDME genes and the expression level of GSDME protein in drug-resistant cells before and after decitabine treatment．Results Compared with SKOV-3 cells, the methylation level of GSDME gene in SKOV-3/DDP was significantly increased（P<0.01）, while the expression level of GSDME protein was significantly decreased（P<0.001）．With the increase of decitabine concentration, the methylation degree of GSDME gene in drug-resistant cells was gradually decreased, the expression level of protein was gradually increased, and the IC₅₀ of cells was gradually decreased：the methylation level of GSDME gene was decreased after 0.05 μg/mL decitabine treatment（P<0.01）, but there were no significant changes in protein expression level and IC₅₀ of drug-resistant cells（P>0.05）．The protein expression level was significantly increased when the concentration of local citabine was increased to 0.10 μg/mL（P<0.05）, while the IC50 of the cells was not significantly decreased（P>0.05）．When the drug concentration reached 0.15 μg/mL, he IC₅₀ of the cells showed a significant downward trend（P<0.05）．Conclusions The expression of GSDME is closely related to chemoresistance in ovarian cancer, and the low expression of GSDME due to its high methylation level can promote chemoresistance in ovarian cancer．However, decitabine can increase the expression level of GSDME in drug-resistant ovarian cancer cells through demethylation,thereby increasing the sensitivity of ovarian cancer cells to chemotherapeutic drugs, and then reversing the chemoresistance of ovarian cancer．

目的 研究靶向NKG2A抑制剂抗头颈部鳞状细胞癌（HNSCC）的作用。方法 应用GEO和TCGA数据库分析NKG2A及其配体HLA-E单细胞表达情况、与患者预后以及免疫微环境的相关性。构建HNSCC皮下抑制瘤模型,流式细胞技术检测化学治疗（化疗）对免疫检测点NKG2A表达的影响。动物实验验证NKG2A抑制剂以及NKG2A抑制剂联合多西他赛化疗的抗肿瘤作用。结果 NKG2A（KLRC1）主要表达在NK细胞,少量表达在T淋巴细胞。HNSCC肿瘤高表达NKG2A/HLA-E（P<0.01）,与患者不良预后密切相关;肿瘤微环境中NKG2A/HLA-E与多个免疫细胞浸润以及免疫检测点表达密切相关（P<0.01）。动物实验显示化疗能上调T、B淋巴细胞表达免疫检查点NKG2A的表达水平（P<0.01）;化疗的基础上联合NKG2A抑制剂能更有效地介导抗肿瘤作用（P=0.013）。结论 化疗基础上联合NKG2A抑制剂能更有效地介导抗肿瘤作用,为探索HNSCC临床新策略提供实验和理论基础。

Objective To investigate the anti-tumor effects of NKG2A inhibitor on head and neck squamous cell carcinoma（HNSCC）．Methods The single-cell expression of NKG2A ,its ligand HLA-E and their correlations with patient prognosis and immune microenvironment were analyzed in GEO and TCGA databases．The subcutaneous tumor model of HNSCC was constructed,and the effects of chemotherapy on the expression of NKG2A on T and B lymphocytes were detected by flow cytometry．Animal experiments were used to confirmed the anti-tumor effects of NKG2A inhibitor and NKG2A inhibitors combined with docetaxel．Results NKG2A（KLRC1）was mainly expressed in NK cells,and a small amount was expressed in T lymphocytes．The high expression of NKG2A/HLA-E in HNSCC tumors（P<0.01）were closely related to poor prognosis．NKG2A/HLA-E in tumor microenvironment were closely related to the infiltration of multiple immune cells and the expression of immune checkpoints（P<0.01）．Animal experiments showed that chemotherapy could up-regulate the expression of NKG2A in T and B lymphocytes（P<0.01）．Chemotherapy in combination with NKG2A inhibitor could mediate more effective antitumor effects in HNSCC（P=0.013）．Conclusions Combined with NKG2A inhibitor on the basis of chemotherapy can mediate more effective anti-tumor effects,and this study may provide experimental and theoretical basis for exploring new clinical strategies of HNSCC．

目的 检测微小RNA（miR）在人黑色素瘤中的表达情况,研究miR-412通过抑制性别确定区Y框转录因子6（SOX6）的表达影响黑色素瘤细胞增殖及侵袭能力的变化。方法 癌症基因组图谱（TCGA）数据库分析发现miR-412在黑色素瘤中异常表达,为研究其表达与肿瘤的相关性,采用Transwell小室,非锚定独立生长实验分析miR-412对黑色素瘤细胞增殖及侵袭能力的影响。软件预测SOX6可能为其靶向基因,采用荧光素酶报告分析及Western blot实验检测SOX6与miR-412的靶向调节情况。结果 TCGA数据库分析黑色素瘤组织中miR-412表达水平高于正常对照组,表达越高,生存时间越短。Transwell小室,非锚定独立生长实验显示miR-412过表达后促进细胞增殖及侵袭能力,而下调miR-412后抑制黑色素瘤细胞增殖及侵袭能力;通过靶点预测miR-412结合SOX6基因3’-非翻译区（UTR）,导致SOX6蛋白因miR-412表达增高而下调;同时在miR-412下调的细胞中抑制SOX6表达可恢复黑色素瘤细胞的增殖及侵袭能力。结论 miR-412过表达后促进黑色素瘤细胞增殖及侵袭能力,反之则抑制黑色素瘤细胞增殖及侵袭能力。 miR-412通过靶向调控SOX6影响黑色素瘤细胞增殖及侵袭,提示miR-412在黑色素瘤的发病过程中起重要作用,是潜在的治疗靶点。

Objective To assess the expression of miR-412 in human melanoma and investigate how miR-412 modulates melanoma cell proliferation and invasive capacity by inhibiting SRY-Box Transcription Factor 6,（SOX6） expression．Methods Analysis of the TCGA（The Cancer Genome Atlas）database identified aberrant miR-412 expression in melanoma．To explore its relevance to tumorigenesis,we conducted Transwell chamber and non-adherent independent growth assays to examine the effects of miR-412 on melanoma cell proliferation and invasion．Software predictions highlighted SOX6 as a potential target gene．We performed luciferase reporter assays and Western blot experiments to elucidate the regulatory interactions between SOX6 and miR-412．Results TCGA database analysis revealed significantly elevated miR-412 expression levels in melanoma tissues compared to the normal control group．Moreover,higher miR-412 expression correlated with shorter survival times．Functional assays using Transwell chambers and non-adherent independent growth assays demonstrated that overexpressing miR-412 enhanced cell proliferation and invasive capabilities．Conversely,reducing miR-412 expression restrained these attributes in melanoma cells． Target prediction analysis indicated that miR-412 binds to the 3’-UTR region of SOX6,resulting in decreased SOX6 protein levels due to increased miR-412 expression．Intriguingly,inhibiting SOX6 expression concurrently amplified the proliferation and invasive potential of melanoma cells,which was initially dampened by miR-412 downregulation．Conclusions Elevated miR-412 expression augments melanoma cell proliferation and invasive capabilities,while its suppression diminishes these traits．Through its targeted regulation of SOX6,miR-412 exerts a significant influence on melanoma cell proliferation and invasion．These findings underscore the pivotal role of miR-412 in melanoma pathogenesis and underscore its potential as a promising therapeutic target．

脊髓损伤是一种高致残性中枢神经系统疾病,目前缺乏有效的治疗措施。干细胞组织工程兴起和神经调控技术的发展,给脊髓损伤的治疗带来新的希望。目前,多项针对脊髓损伤的干细胞相关治疗项目的临床研究已在全球注册,干细胞疗法是脊髓损伤领域的研究热点,具有良好的应用前景。而神经调控技术一直在临床上脊髓损伤后的康复治疗中发挥着重要作用,特别是靶向神经调控技术近年在脊髓损伤治疗方面取得突破性进展。有研究尝试联合干细胞疗法和神经调控技术应用治疗脊髓损伤,试图取得更好的效果。本文综述了干细胞疗法和神经调控技术在脊髓损伤治疗中的研究进展,旨在探讨其作用效果、修复机制、应用前景以及面临的问题,进一步为脊髓损伤的基础研究和临床转化提供参考。

Spinal cord injury is a highly disabling disease of the central nervous system without effective treatment to date．With the rise of stem cell and tissue engineering,and the breakthrough of neuromodulation technology,it brings new hope to the treatment of spinal cord injury．At present,a number of clinical studies on stem cell-related treatment projects for spinal cord injury have been registered worldwide,which has become a research hotspot．Neuromodulation technology has been playing an important role in the clinical rehabilitation of spinal cord injury．Especially,breakthroughs have been made in the treatment of spinal cord injury by targeted neuromodulation technology in recent years,which is encouraging．Some studies have attempted to combine stem cell therapy and neuromodulation technology to treat spinal cord injuries in an attempt to achieve better effect．This review summarizes the research progress of stem cell therapy and neuromodulation technology in the treatment of spinal cord injury,with the aim of discussing their effect,repair mechanisms,application prospect and various problems to face,and providing further reference for the basic research and clinical transformation of spinal cord injury．

目的 总结儿童嗜酸细胞性胃肠炎（EG）的临床表现、内镜检查和病理学特点、治疗和预后。方法 回顾性分析2019年1月—2022年12月滨州医学院附属医院儿科确诊的48例EG患儿临床资料,包括临床症状、实验室检查、影像学检查、内镜和病理学检查、治疗和随访情况。结果 48例患儿中,男26例（54.17%）,女22例（45.83%）,中位年龄7.8岁,20例（41.67%）患儿有过敏史或家族史,临床症状主要有腹痛（34例,70.83%）、腹泻（18例,37.5%）和腹胀（12例,25%）。外周血嗜酸性粒细胞（EOS）升高36例（75%）,血清总IgE升高14例（29.17%）。48例行胃镜检查,最常见的表现是黏膜充血水肿（32例,66.67%）、点状红斑（28例,58.33%）和糜烂（22例,45.83%）,28例行结肠镜检查,表现为黏膜充血水肿（18例,64.29%）、点状红斑（15例,53.57%）和结节样隆起（12例,42.86%）。黏膜组织病理表现为大量EOS浸润,主要累及十二指肠降部、胃窦和回肠末端。所有患儿均采用饮食干预的治疗,6例（12.5%）单纯饮食干预治疗后好转,16例（33.33%）孟鲁司特钠、酮替芬、奥美拉唑治疗后好转,26例（54.17%）联合泼尼松治疗后好转,随访10个月~3年,8例（16.67%）停药后复发,再次治疗后好转。结论 儿童EG临床症状和内镜表现多样化、缺乏特异性,内镜下黏膜组织病理检查有助于确诊。大多数患儿外周血EOS升高,饮食干预和糖皮质激素治疗效果显著,但存在复发的可能,需长期维持治疗和随访。

Objective To summarize the clinical manifestations,endoscopic and pathological features,treatment and prognosis of eosinophilic gastroenteritis（EG）in children．Methods A retrospective analysis was carried out on clinical data of 48 patients with EG diagnosed at the Department of Pediatrics of Binzhou Medical University Hospital from January 2019 to December 2022,including clinical symptoms,laboratory examination,imaging examination,endoscopic and pathological examination,treatment and follow-up．Results A total of 48 patients were included in the analysis,including 26 males（54.17%）and 22 females（45.83%）,with the median age of 7.8 years（7 months to 13 years）．Twenty patients（41.67%）had a history or family history of allergy．The most clinical symptoms were abdominal pain（34 cases,70.83%）,diarrhea（18 cases,37.5%）and abdominal distension（12 cases,25%）．Peripheral blood eosinophils（EOS）increased in 36 cases（75%）,and the serum total IgE increased in 14 cases（29.17%）．48 cases underwent gastroscopy,the most common manifestations were mucosal hyperemia and edema（32 cases,66.67%）,punctate erythema（28 cases,58.33%）and erosion（22 cases,45.83%）．Twenty-eight cases underwent colonoscopy,the manifestations were mucosal hyperemia and edema（18 cases,64.29%）,spotted erythema（15 cases,53.57%）and nodular eminence（12 cases,42.86%）．Mucosal histopathology showed a large number of EOS infiltration,mainly involving the descending duodenum,gastric antrum and terminal ileum．All children were treated with dietary intervention,6 cases（12.5%）were improved after simple diet intervention,16 cases（33.33%）were improved after treatment with montelukast,ketotifen,omeprazole,26 cases（54.17%）were improved after combined treatment with prednisone acetate．Followed up for 10 months to 3 years,8 cases（16.67%）relapsed after drug withdrawal and improved after retreatment．Conclusions The clinical symptoms and endoscopic manifestations of EG in children are diverse and lack of specificity,endoscopic mucosal histopathological examination is helpful for diagnosis．The EOS in peripheral blood of most children increased,diet intervention and glucocorticoid therapy are effective,but there is a possibility of recurrence,which need long-term maintenance treatment and follow-up．

目的 探讨微RNA-29b（miR-29b）对子宫内膜癌细胞增殖、迁移和侵袭的影响。方法 子宫内膜癌HEC-1-B细胞分为miR-29b模拟物组（MM组）、miR-29b阻遏物组（MR组）和阴性对照物组（MNC组）,分别转染miR-29b拟似物、miR-29b阻遏物和miR-29b阴性对照物,每组设置6个复孔。以实时定量逆转录PCR检测miR-29b表达,以水溶性四氮唑（WST-1）检测miR-29b对HEC-1-B子宫内膜癌细胞增殖的影响,以Transwell小室检测HEC-1-B子宫内膜癌细胞迁移和侵袭的影响,以Western blot法检测磷酸酶张力蛋白同源物（PTEN）-蛋白激酶 B（AKT）通路蛋白表达水平。结果 MNC组、MM组、MR组miR-29b相对表达量分别为（2 032.1±873.4）、（19 272.8±2 087.9）、（472.7±105.6）,组间比较差异有统计学意义（P<0.05）。MM组0、3、5、7 d时OD值分别为（0.32±0.06）、（0.53±0.08）、（1.13±0.12）和（1.92±0.14）,MNC组0、3、5、7 d时OD值分别为（0.34±0.09）、（0.71±0.08）、（1.67±0.21）和（3.49±0.24）,MR组0、3、5、7 d时OD值分别为（0.38±0.09）、（0.84±0.18）、（2.43±0.24）和（5.67±0.15）,3组0 d时OD值比较差异无统计学意义（P=0.216）,三组3 d、5 d、7 d时OD值比较差异存在统计学意义（P<0.001）。MNC组、MM组和MR组迁移细胞数分别为（403.9±23.8）（102.6±15.7）和（685.7±46.8）个,上述3组侵袭细胞数分别为（82.1±12.7）（38.2±10.6）和（124.6±21.6）个,MM组和MNC组上述指标比较差异均有统计学意义（P<0.05）,MR组和MM组上述指标比较差异均有统计学意义（P<0.05）。MNC组、MM组、MR组PTEN蛋白相对表达量分别为（0.25±0.08）、（0.69±0.11）、（0.11±0.05）,上述3组p-AKT蛋白相对表达量分别为（0.58±0.10）、（0.13±0.06）和（0.79±0.08）,上述3组AKT蛋白相对表达量分别为（0.38±0.09）、（0.37±0.11）和（0.37±0.08）,MM组与MNC组PTEN、p-AKT水平比较差异有统计学意义（P<0.05）,AKT水平比较差异无统计学意义（P>0.05）;MR组与MNC组、MM组PTEN、p-AKT水平比较差异有统计学意义（P<0.05）,AKT水平比较差异无统计学意义（P>0.05）。结论 过表达miR-29b对子宫内膜癌细胞增殖、迁移和侵袭具有抑制作用,靶向PTEN-AKT可能是其重要作用途径。

Objective To investigate the effects of microRNA-29b on proliferation,migration and invasion of endometrial cancer cells．Methods The endometrial cancer HEC-1-B cells were divided into micro29b mimetic group（MM group）,micro29b repressor group（MR group）and negative control group（MNC group）,and the micro29b mimetic,micro29b repressor and micro29b negative control were transfected into each group,six compound holes with each group．The real-time quantitative reverse transcription polymerase chain reaction（RT-PCR）was used to detect the expression of mi29b,WST-1 was used to detect the effect of mi29b on the proliferation of HEC-1-B endometrial cancer cells,Transwell chamber was used to detect the migration and invasion of HEC-1-B endometrial cancer cells,and Western blot was used to detect the expression level of PTEN-AKT pathway protein．Results The relative expression levels of microRNA-29b in MNC group,MM group and MR group were（2 032.1±873.4）,（19 272.8±2 087.9）and（472.7±105.6）,respectively,and there were significant differences between groups（P<0.05）．OD values of MM group at 0 d,3 d,5 d and 7 d were（0.32±0.06）,（0.53±0.08）,（1.13±0.12）and（1.92±0.14）respectively．The OD values of MNC group at 0,3,5 and 7 days were（0.34±0.09）,（0.71±0.08）,（1.67±0.21）and（3.49±0.24）respectively．The OD values of MR group at 0 d,3 d,5 d and 7 d were（0.38±0.09）,（0.84±0.18）,（2.43±0.24）and（5.67±0.15）respectively．There was no significant difference in OD value between the three groups on day 0 （P=0.216）．There were significant differences in OD value between the three groups on day 3,day 5 and day 7（P<0.001）．The number of migrating cells in MNC group,MM group and MR group were（403.9±23.8）cells,（102.6±15.7）cells and（685.7±46.8）cells,respectively．The number of invasive cells in the above three groups were（82.1±12.7）cells,（38.2±10.6）cells and（124.6±21.6）cells．There were significant differences in the above indexes between MM group and MNC group（P<0.05）,also between MR group and MM group（P<0.05）．The relative expression levels of PTEN protein in MNC group,MM group and MR group were（0.25±0.08）,（0.69±0.11）and（0.11±0.05）．The relative expression levels of p-AKT protein in the above three groups were（0.58±0.10）,（0.13±0.06）and（0.79±0.08）．The relative expression levels of AKT protein in the above three groups were（0.38±0.09）,（0.37±0.11）and（0.37±0.08）,respectively．Compared with MNC group,the levels of PTEN and p-AKT in MM group had statistical significance（P<0.05）,but there was no statistical difference in AKT level（P>0.05）．Compared with MNC group and MM group,the levels of PTEN and p-AKT in MR group had statistical significance（P<0.05）,and there was no statistical difference in AKT level（P>0.05）．Conclusions Overexpression of microRNA-29b can inhibit the proliferation,migration and invasion of endometrial cancer cells,and targeting PTEN-AKT may be an important pathway．

弥漫性大B细胞淋巴瘤（DLBCL）是最常见的高度异质性非霍奇金淋巴瘤（NHL）,不同的疾病阶段或临床亚型预后不尽相同。放射治疗作为无交叉耐药的理想局部治疗技术,应用于DLBCL可有效改善患者预后。初治DLBCL通过放射治疗联合化学治疗、免疫治疗等综合治疗可使约60%~70%患者疾病缓解。对于不同预后影响因素,如年龄、肿瘤体积、淋巴结外侵犯等,联合放射治疗也可取得更佳疗效。在复发性/难治性DLBCL的治疗中,自体造血干细胞移植（ASCT）和嵌合抗原受体T细胞免疫治疗（CAR-T）是目前的研究热点,而放射治疗无论是作为ASCT与CAR-T术前的桥接治疗或失败后的挽救性治疗均有助改善患者预后。随着放射治疗技术的日益优化,放射治疗在综合治疗方案中扮演着越来越重要的角色。

Diffuse large B-cell lymphoma（DLBCL）is a highly heterogeneous type of non-Hodgkin lymphoma（NHL）and its prognosis is different for different disease stages or clinical subtypes．Radiation therapy（RT）is a local treatment technique that does not cause cross-resistance and can effectively improve the prognosis of patients with DLBCL．When combined with chemotherapy and immunotherapy,RT can alleviate the disease in more than 60% of patients．Furthermore,RT can achieve better results for different prognostic factors such as age,tumor volume and external nodal invasion．For treating relapsed / refractory DLBCL,autologous stem cell transplantation（ASCT）and chimeric antigen receptor T cell immunotherapy（CAR-T）are currently being researched,while RT can help as bridging therapy before ASCT and CAR-T or salvage therapy after failure．With the increasing optimization of technology,radiotherapy plays an increasingly important role in combined treatment options．