10年早产儿及新生儿结果分析

目的 探讨早产儿的发生因素和对母儿的影响及防治。方法 收集１９８９年１月至１９９８年１２月,１０年中我院住院分娩的全部早产病例８１６例,按产５年和后５年分为两组进行回顾性分析。结果 前组早产数为５３４例,早产发生率为３．２０％;后组早产数为２８２例,发生率为３．０５％,两组发生率对比无统计学差异（Ｐ〉０．０５）。其流行病学调查显示在职业、流动人口数和产前检查方面两组对比有极其显著性差异（Ｐ〈０．０     

应用抗粘灵气雾剂预防腹腔术后粘连的实验研究

目的：为临床外科寻找简便易行有效的预防腹腔术后粘连的新方法和药物：方法：用白及、黄芪等多味中药制成抗粘灵气雾剂，通过对60只家免盲肠部分切除制造实验动物模型，并对其创面进行活体药物喷涂。结果：抗粘灵气雾剂预防腹腔术后粘连效果良好，总有效率86．67％，与对照组比较，有非常显著差异（P〈0．01）。结论：抗粘灵气雾剂预防腹腔术后粘连有效，且方法简便易行，从而可为临床外科领域提供高效。价廉的木申抗粘连药物。     

以组蛋白去乙酰化酶为靶标的抗癌药物研发进展

基因表达的精确控制是细胞增殖分化和器官正常生长和发育的基础。基因转录和激活程序依赖于组蛋白乙酰化酶(histone acetylase，HAT)和组蛋白去乙酰化酶(histone deacetylase，HDAC)的协同作用。当HDAC过度表达并被转录因子募集，就会导致特定基因的不正常抑制，从而导致癌症及其他疾病。目前以HDAC作为抗癌靶点的研究方兴未艾，现综述HDAC类似蛋白(HDLP)的晶体结构和当前存在的HDAC抑制剂的作用机制、结构种类、研发状况和构效关系，以及新的HDAC抑制剂CS055的研发策略。     

经会阴四维盆底超声动态成像对初产妇膀胱膨出疾病分级与分型的临床价值

目的 探讨经会阴四维盆底超声动态成像对初产妇膀胱膨出疾病分级与分型的临床价值。方法 选取西安市第三医院2018年1月~2018年6月收治的盆底功能障碍性疾病（膀胱膨出）初产妇92例为研究对象,根据产妇的分娩方式分为经阴道分娩组（n=46）及剖宫产组（n=46）。在静息、屏气向下用力动作（Valaslva）及缩肛状态下观察两组患者膀胱尿道及盆膈裂孔的超声成像变化,测量膀胱相关参数数值并进行膀胱膨出Green分型。 结果 两组产妇经会阴盆底超声参数比较中,静止期BSD、尿道膀胱后角比较,差异均无统计学意义（均 P＞0.05）;剖宫产组产妇张力期BSD、尿道膀胱后角及膀胱颈移动度、尿道旋转角均明显小于经阴道分娩组产妇（均 P＜0.05）。 经阴道分娩组产妇膀胱膨出Green分型中,Ⅰ型6例（13.04%）,Ⅱ型26例（56.52%）,Ⅲ型14例（30.43%）;剖宫产组产妇膀胱膨出Green分型中,Ⅰ型14例（30.43%）,Ⅱ型23例（50.00%）,Ⅲ型9例（19.56%）。经阴道分娩组Ⅰ型膀胱膨出者明显少于剖宫产组,差异有统计学意义（P＜0.05）;而两组产妇Ⅱ型、Ⅲ型膀胱膨出例数比较,差异无统计学意义（P＞0.05）。结论 经会阴四维盆底超声检查可清楚显示盆底解剖结构,有效区分不同分娩方式产妇的盆底Green类型,为临床制定治疗方案提供可靠的影像学资料。     

Whole-exome sequencing identifies novel mutations in genes responsible for retinitis pigmentosa in 2 nonconsanguineous Chinese families

AIM: To detect the pathogenetic mutations responsible for nonsyndromic autosomal recessive retinitis pigmentosa (RP) in 2 nonconsanguineous Chinese families. METHODS: The clinical data, including detailed medical history, best corrected visual acuity (BCVA), slit-lamp biomicroscope examination, fundus photography, optical coherence tomography, static perimetry, and full field electroretinogram, were collected from the members of 2 nonconsanguineous Chinese families preliminarily diagnosed with RP. Genomic DNA was extracted from the probands and other available family members; whole-exome sequencing was conducted with the DNA samples provided by the probands, and all mutations detected by whole-exome sequencing were verified using Sanger sequencing in the probands and the other available family members. The verified novel mutations were further sequenced in 192 ethnicity matched healthy controls. RESULTS: The patients from the 2 families exhibited the typical symptoms of RP, including night blindness and progressive constriction of the visual field, and the fundus examinations showed attenuated retinal arterioles, peripheral bone spicule pigment deposits, and waxy optic discs. Whole-exome sequencing revealed a novel nonsense mutation in FAM161A (c.943A>T, p.Lys315*) and compound heterozygous mutations in RP1L1 (c.56C>A, p.Pro19His; c.5470C>T, p.Gln1824*). The nonsense c.5470C>T, p.Gln1824* mutation was novel. All mutations were verified by Sanger sequencing. The mutation p.Lys315* in FAM161A co-segregated with the phenotype, and all the nonsense mutations were absent from the ethnicity matched healthy controls and all available databases. CONCLUSION: We identify 2 novel mutations in genes responsible for autosomal recessive RP, and the mutation in FAM161A is reported for the first time in a Chinese population. Our result not only enriches the knowledge of the mutation frequency and spectrum in the genes responsible for nonsyndromic RP but also provides a new target for future gene therapy.     

Granulocyte-macrophage colony-stimulating factor protects mice against hepatocellular carcinoma by ameliorating intestinal dysbiosis and attenuating inflammation

BACKGROUND Hepatocellular carcinoma(HCC) is the third leading cause of cancer mortality worldwide. The gut microbiota can help maintain healthy metabolism and immunity. Granulocyte-macrophage colony-stimulating factor(GM-CSF) is a critical factor in promoting health and homeostasis; it promotes intestinal immunity, stimulates bone marrow precursors to generate macrophage colonies, and enhances the antibacterial and antitumor activity of circulating monocytes. As such, GM-CSF may protect against HCC development by regulating immunity as well as intestinal microecology.AIM To investigate the impact of GM-CSF on the gut microbiome and metabolic characteristics of HCC.METHODS Thirty-six male BALB/c nude mice were divided into three groups: Control(n = 10), HCC(n = 13), and HCC + GM-CSF(GM-CSF overexpression, n = 13). We utilized HCC cells to establish orthotopic transplantation tumor models of HCC with normal and over-expressing GM-CSF. Liver injury, immune inflammatory function and intestinal barrier function were evaluated. The fecal microbiome and metabolome were studied using 16S rRNA absolute quantification sequencing and gas chromatography-mass spectrometry.RESULTS GM-CSF overexpression significantly affected the gut microbiome of mice with HCC and resulted in a high abundance of organisms of the genera Roseburia, Blautia and Butyricimonass, along with a significant reduction in Prevotella, Parabacteroides, Anaerotruncus, Streptococcus, Clostridium, and Mucispirillum. Likewise, GM-CSF overexpression resulted in a substantial increase in fecal biotin and oleic acid levels, along with a prominent decrease in the fecal succinic acid, adenosine, fumaric acid, lipoic acid, and maleic acid levels. Correlation analysis revealed that the intestinal microbiota and fecal metabolites induced by GM-CSF were primarily involved in pathways related to reducing the inflammatory response, biotin metabolism, and intestinal barrier dysfunction.CONCLUSION GM-CSF can protect against HCC development by regulating immunity and modulating the abundance of specific intestinal microorganisms and their metabolites. This study provides new insights into the therapeutic approaches for HCC.     

Xuezhikang ameliorates contrast media-induced nephropathy in rats via suppression of oxidative stress,inflammatory responses and apoptosis

Background: The aim of this study was to assess the preventive effect of xuezhikang (XZK) to replace atorvastatin on the contrast media-induced acute kidney injury (CI-AKI).

Methods: The male Sprague–Dawley rats were divided into five groups: group 1 (sham), injected with normal saline; group 2 (XZK), treated with XZK; group 3 contrast media (CM), injected with CM; group 4 (CM?+?ATO), injected with CM?+?pretreatment with atorvastatin; group 5 (CM?+?XZK), injected with CM?+?pretreatment with XZK. Twenty-four hours after injection with normal saline or CM, the blood sample and the kidneys were collected for the measurement of biochemical parameters, oxidative stress markers, nitric oxide production, inflammatory parameters, as well as renal histopathology and apoptosis detection.

Results: Our results indicated that XZK restored the renal function by reducing serum blood urea nitrogen (BUN) and serum creatinine (Scr), depressing renal malondialdehyde (MDA), increasing renal NO production, decreasing TNF-ɑ and IL-6 expression, attenuating renal pathological changes and inhibiting the apoptosis of renal tubular cells.

Conclusion: XZK’s therapeutic effect is similar, or even better than atorvastatin at the same effectual dose in some parts.     

甘露聚糖肽预防慢性阻塞性肺疾病急性发作的单盲、随机双模拟临床研究

目的评价甘露聚糖肽预防慢性阻塞性肺疾病(COPD)急性发作的临床效果及安全性。方法采用多中心、单盲、随机对照方法,试验组给予常规治疗,如解痉、祛痰、抗感染治疗,加用甘露聚糖肽胶囊(30 mg/d),对照1组加用安慰剂(30 mg/d),对照2组加用泛福舒7 mg/d,隔日服用,疗程为3个月,随访12个月评价患者的COPD急性发作情况及机体免疫功能。结果共240例患者入选,每组各80例,甘露聚糖肽显著减少COPD急性发作感染次数、发作天数、抗生素应用天数、住院天数及圣乔治呼吸问卷评分,显著改善肺功能指标第1秒用力呼气容积(FEV1)、用力肺活量(FVC)及CD3+、CD4+、CD4+/CD8+、IgA水平及6 min步行距离,与安慰剂比较具有统计学差异(P<0.05);与泛福舒相似,不具有统计学差异(P>0.05)。结论甘露聚糖肽可减少反复呼吸道发生COPD急性发作,提高肺功能指标及机体;免疫功能,提高患者的生活质量,不良反应轻微。     

人原发性直肠恶性淋巴瘤裸小鼠原位移植模型的建立及其生物学特性

目的:建立人原发性直肠恶性淋巴瘤裸小鼠原位移植模型,探讨其生物学特性.方法:采用人直肠原发性恶性淋巴瘤术中的新鲜瘤组织块植入裸鼠的直肠黏膜层内,观察原位移植的成瘤率,移植瘤的侵袭和转移率.进行形态学(光镜、电镜、免疫组织化学),染色体核型,流式细胞分析.结果:依据WHO新的分类标准,建成1株人直肠原发性(非霍奇金B细胞性)恶性淋巴瘤裸鼠原位移植模型HRBL-0305.移植瘤组织病理学为(非霍奇金B细胞性)高度恶性淋巴瘤;免疫组织化学示CD19,CD20,CD22,CD45阳性,CD3,CD7阴性.染色体众数56-69条,流式细胞DI值为1.57-1.61,均为异倍体.HRBL-0305已传至31代;共移植裸鼠187只.其肿瘤移植生长率和液氮冻存复苏成活率均为100.0%,肝转移率为45.4%,淋巴结和腹腔种植转移率均为38.0%,移植瘤在裸鼠的直肠内自主侵袭性生长,发生血液、淋巴转移和腹腔内种植性转移,移植瘤组织病理学,超微结构的观察,流式细胞DNA含量测定及染色体核型的分析,表明与人源直肠恶性淋巴瘤细胞相一致.结论:HRBL-0305是首次成功建立的人直肠原发性恶性淋巴瘤裸鼠原位移植模型,完整地重现了人直肠原发性恶性淋巴瘤的自然临床病理过程,且转移模式与临床患者相似,为研究直肠恶性淋巴瘤的生物学特性和治疗提供了理想动物模型平台.