Prenatal diagnosis of caudal regression with heterotaxy syndrome: “A mermaid with a broken heart”

Caudal regression syndrome (CRS) is a rare congenital malformation with varying degrees of early gestational developmental failure. It is characterized by agenesis of the sacrum and lumbar spine, with lower limb neurological deficit and accompanying deformities of the pelvis, lower extremities, genitourinary, and gastrointestinal systems. We report a case of CRS associated with rare complex congenital heart defect, that is, heterotaxy syndrome, diagnosed prenatally.     

神经内科护理中康复护理对于脑卒中后偏瘫患者的预后观察研究

目的:本次研究分析在脑卒中后偏瘫患者护理中采用神经内科护理对患者预后效果的观察。方法:本次研究样本选取莒南县中医医院100例脑卒中后偏瘫患者,研究时间从2018年3月-2019年3月,按照护理方式进行对比,试验组患者采用神经内科护理,对照组患者采用常规护理,对比两组患者护理结果。结果:对比两组患者肢体运动功能评分,分析得知,试验组患者出院后肢体功能评分明显较高,两组对比存在统计学标准(P<0.05);对比两组患者日常生活能力量表(Activities of Daily Living,ADL)评分,分析得知,试验组患者出院后ADL评分明显较高,两组对比存在统计学标准(P<0.05);对比两组患者预后生活质量评分,分析得知,试验组患者预后生活质量评分较高,两组对比符合统计学标准(P<0.05)。结论:通过此次研究得知,在脑卒中后偏瘫患者护理中采用神经内科护理,能对患者肢体功能与神经功能进行明显改善,还能进一步提高患者生活质量。     

恩度治疗小细胞肺癌脑转移瘤瘤周水肿1例报告及文献复习

目的:探讨治疗脑转移瘤瘤周水肿的方法。方法:总结1例小细胞肺癌脑转移患者的临床资料及恩度治疗脑转移瘤瘤周水肿的效果，并对治疗脑水肿相关文献进行复习。结果:恩度抗血管生成治疗小细胞肺癌脑转移瘤瘤周水肿有很好的临床效果，能够控制脑水肿，减轻临床症状，提高生活质量。结论:恩度可以作为治疗脑转移瘤瘤周水肿的有效药物选择。     

Protective role of histone deacetylase 4 from ultraviolet radiation-induced DNA lesions

Ultraviolet B (UVB) exposure is a core factor that leads to skin disease or carcinogenesis through the insufficient repair of DNA lesions. UVB-induced DNA lesions are mainly removed by the nucleotide excision repair (NER) mechanism. The expression of histone deacetylase 4 (HDAC4) is altered in the skin upon UVB exposure, indicating its possible implication in UVB-induced DNA lesions repair. Here, we investigated the role of HDAC4 in the NER removal of the main classes of UVB-induced DNA lesions consisting of cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs). We found that UVB irradiation increased HDAC4 expression at both the mRNA and protein levels. HDAC4 interacted with NER factor XPC, which played an important role in effectively removing the UVB-induced DNA lesions. This study provides an understanding of the HDAC4 function in DNA repair, which will allow the development of efficient strategies to protect the skin from UVR-induced diseases.     

Effects and long‐term follow‐up of using umbilical cord blood–derived mesenchymal stromal cells in pediatric patients with severe BK virus‐associated late‐onset hemorrhagic cystitis after unrelated cord blood transplantation

This is a retrospective study to evaluate the efficacy and safety of umbilical cord blood–derived mesenchymal stromal cells (MSCs) for the treatment of pediatric patients with severe BK virus–associated late‐onset hemorrhagic cystitis (BKV‐HC) after unrelated cord blood transplantation (UCBT). Thirteen pediatric patients with severe BKV‐HC from December 2013 to December 2015 were treated with MSCs. The number of MSCs transfused in each session was 1 × 10⁶/kg once a week until the symptoms improved. The median follow‐up time was 1432 (89‐2080) days. The median frequency of MSC infusion was 2 (1‐3), with eight cured cases and five effective cases; the total efficacy rate was 100%. The copy number of urine BKV DNA was 4.43 (0.36‐56.9) ×10⁸/mL before MSC infusion and 2.67 (0‐56.3) ×10⁸/mL after MSC infusion; the difference was not significant (P = .219). There were no significant differences in the overall survival, disease‐free survival, and the incidence of relapse and acute and chronic graft‐versus‐host disease between the MSC infusion group and non‐MSC infusion group. There was also no significant difference in the cytomegalovirus, Epstein‐Barr virus (EBV), and fungal and bacterial infection rates between the two groups. Although umbilical cord blood–derived MSCs do not reduce the number of BKV DNA copies in the urine, the cells have a high efficacy rate and minimal side effects in treating severe BKV‐HC after UCBT among pediatric patients. MSCs do not affect the rates of relapse, long‐term infection, or survival of patients with leukemia.     

临床医学专业“5+3”一体化本科全程导师制创新人才培养的实践与探索

以培养创新型人才为目标，大连医科大学制定实施了“5+3”创新人才培养改革方案，以导师制培养为载体，在医学本科教育全过程中，制定分阶段创新能力培养体系，涵盖课程、讲座、实验设计、论文等基本科研能力训练，强化本科生科研能力培养。通过对首届“5+3”学生阶段性培养成果的统计学分析发现，“5+3”学生发表中文期刊、SCI，主持国家级创新项目、省级创新项目的比例均显著高于普通5年制学生，差异具有统计学意义（P<0.05）。虽然实施过程中存在一些问题和不足，但以导师制为核心的科研基础训练对提高学生科研思维和创新能力效果显著，对培养医学创新型人才具有可实施性。     

lncRNA MALAT1靶向miR-150对口腔鳞癌细胞增殖和凋亡的影响及分子机制

目的:研究MALAT1对口腔鳞癌细胞SCC-25增殖、凋亡的影响，并探讨其机制。方法:运用qRT-PCR检测人口腔鳞癌细胞SCC-25、人永生化口腔上皮细胞HIOEC中MALAT1和miR-150的mRNA表达；将si-con组（转染si-con）、si-MALAT1组（转染si-MALAT1）、miR-150组（转染miR-150 mimics）、miR-con组（转染miR-con）、si-MALAT1+anti-miR-con组（si-MALAT1和anti-miR-con共转染）、si-MALAT1+anti-miR-150组（si-MALAT1和anti-miR-150共转染），均以脂质体法转染至SCC-25细胞；MTT法检测各组细胞的增殖；流式细胞术检测各组细胞的凋亡；双荧光素酶报告基因检测实验检测各组细胞的荧光活性。结果:与人永生化口腔上皮HIOEC细胞（Normal组）相比，口腔鳞癌SCC-25细胞（Tumor组）中MALAT1表达显著上调，miR-150显著下调（P＜0.05）；敲减MALAT1、过表达miR-150均可抑制SCC-25细胞增殖，促进凋亡；MALAT1靶向miR-150。抑制miR-150逆转了敲减MALAT1对口腔鳞癌细胞的增殖抑制和凋亡促进作用。结论:MALAT1可促进口腔鳞癌细胞增殖并抑制凋亡，其机制可能与靶向miR-150有关，可为口腔鳞癌的治疗提供新靶点。     

A novel lncRNA-LINC01116 regulates tumorigenesis of glioma by targeting VEGFA

Brain glioma is the most common malignant tumor of the central nervous system, and one of the leading causes of death in patients with intracranial tumors. The clinical outcome of glioma is usually poor due to abundant vascularity, fast growth and susceptibility of invasion to normal brain tissues. Our microarray study showed that lncRNA-LINC01116 was significantly upregulated in glioma tissues and played an important role in cell proliferation, cycle, migration, invasion and angiogenesis. In addition, vascular endothelial growth factor (VEGFA) may be the major target genes in the downstream of lncRNA-LINC01116. Dual luciferase assay showed that LINC01116 and VEGFA both contained a miR-31-5p binding site, and LINC01116 could regulate the expression of VEGFA through competitive absorption of miR-31-5p. RNA immunoprecipitation indicated that LINC01116 and VEGFA were present in the miR-31-5p-RISC complex, and biotinylated miR-31-5p pull-down assay suggested that there was a competitive relationship between LINC01116 and VEGFA to bind with miR-31-5p. Collectively, our study has identified a novel lncRNA-LINC01116 and clarified the role and mechanism of LINC01116 in the tumorigenesis of glioma. LINC01116 may prove to be a potential target for the clinical diagnosis and treatment of glioma.