文心兰类原球茎的愈伤组织诱导及其植株再生

该研究首次以文心兰的类原球茎( protocorm-like bodies, PLBs)为外植体进行愈伤组织诱导及其植株再生培养,并分析了不同浓度的TDZ和2,4-D配比对愈伤组织增殖的影响。结果表明：以1/2MS为基本培养基,添加1 mg.L-1 TDZ与3 mg.L-12,4-D,从接种的 PLBs上可以诱导出乳白色的、较疏松的愈伤组织,诱导频率达到100％。愈伤组织继代培养时,在2,4-D浓度为0.5~2.0 mg.L-1的范围内,其增殖主要受TDZ浓度的影响,TDZ浓度从1.0 mg.L-1降低到0.5 mg.L-1,愈伤组织鲜重增殖倍数显著增加,由最低的4.50倍增加到最高的6.04倍。愈伤组织增殖的最适培养基为1/2MS ＋0.5 mg.L-1 TDZ ＋1.0 mg.L-12,4-D。将在最适愈伤组织增殖培养基上继代培养约1个月的愈伤组织转移到T2培养基(3.5 g.L-1花宝1号＋20 g.L-1红薯＋25 g.L-1香蕉＋1 g.L-1 tryptone ＋20 g.L-1蔗糖＋3.5 g.L-1 phytagel)上,黑暗培养1个月后,每克鲜重的愈伤组织约诱导出1328.67个PLBs。将诱导出的PLBs转移到新鲜的T2培养基上光照培养1个月,萌发率为90.12％。而将小植株转移到添加1 g.L-1活性炭的1/2MS培养基上,成苗率达到100％。该研究结果成功建立了文心兰的高频愈伤组织诱导及其植株再生体系,为文心兰基因工程育种提供了一个高效、稳定的转化受体系统。     

Genes important for survival or reproduction in Varroa destructor identified by RNAi

The Varroa mite,(Varroa destructor),is the worst threat to honey bee health worldwide.To explore the possibility of using RNA interference to control this pest, we determined the effects of knocking down various genes on Varroa mite survival and reproduction.Double-stranded RNA (dsRNA)of six candidate genes (Da,Pros26S,RpL8, RpL11,RpPO and RpS13)were synthesized and each injected into Varroa mites,then mite survival and reproduction were assessed.Injection of dsRNA for Da (Daughterless)and Pros26S (Gene for proteasome 26S subunit adenosine triphosphatase)caused a significant reduction in mite survival,with 3.57%±1.94% and 30.03%±11.43% mites surviving at 72 h post-inj ection (hpi),respectively.Control mites injected with green fluorescent protein (GFP)-dsRNA showed survival rates of 81.95%±5.03% and 82.36 ±2.81%,respectively. Injections of dsRNA for four other genes (RpL8,RpL11,RpPO and RpS13)did not affect survival significantly,enabling us to assess their effect on Varroa mite reproduction.The number of female offspring per mite was significantly reduced for mites injected with dsRNA of each of these four genes compared to their GFP-dsRNA controls.Knockdown of the target genes was verified by real-time polymerase chain reaction for two genes important for reproduction (RpL8,RpL11)and one gene important for survival (Pros26S). In conclusion,through RNA interference,we have discovered two genes important for mite survival and four genes important for mite reproduction.These genes could be explored as possible targets for the control of Varroa destructor in the future.     

急性缺血性脑卒中患者血清GAL3、CXCL12水平与病情严重程度和预后的关系研究

目的:探讨急性缺血性脑卒中(AIS)患者血清半乳糖凝集素3(GAL3)、血清趋化因子12(CXCL12)水平与病情严重程度和预后的关系。方法:选取成都市第五人民医院于2016年2月～2018年9月期间接收的AIS患者138例为观察组,另选取同期来该院行健康体检的志愿者60例为对照组。其中观察组根据美国国立卫生研究所中风量表(NIHSS)评分分为轻症组(n=42,4分),中症组(n=61,4～15分),重症组(n=35,15分),根据改良RABKIN量表(m RS)评分分为预后良好组(n=82)和预后不良组(n=56)。比较对照组、观察组的血清GAL3、CXCL12水平,分析不同NIHSS得分、不同预后的血清GAL3、CXCL12水平,采用Pearson相关性分析血清GAL3、CXCL12水平与NIHSS评分、m RS评分的相关性。结果:观察组血清GAL3、CXCL12水平均显著高于对照组,差异有统计学意义(P0.05)。重症组、中症组AIS患者血清GAL3、CXCL12水平高于轻症组,且重症组高于中症组,差异有统计学意义(P0.05)。预后不良组的AIS患者血清GAL3、CXCL12水平均高于预后良好组,差异有统计学意义(P0.05)。Pearson相关性分析结果可知,血清GAL3、CXCL12水平与NIHSS评分、m RS评分均呈正相关(P0.05)。结论:AIS患者的血清GAL3、CXCL12水平均异常升高,且其升高程度与AIS患者病情严重程度及预后息息相关。     

老年冠心病患者血清Lp-PLA2、hs-CRP、IL-27及MMP-9水平与Gensini积分的相关性研究*

目的:探讨老年冠心病患者血清脂蛋白相关磷脂酶A2(Lp-PLA2)、高敏C反应蛋白(hs-CRP)、白细胞介素-27(IL-27)及基质金属蛋白酶-9(MMP-9)水平与Gensini积分的相关性。方法:选取2015年10月至2018年2月我院收治的冠心病患者142例为研究对象,将所有患者按照不同的冠心病类型分为不稳定型心绞痛(UAP)组54例、稳定型心绞痛(SAP)组40例和急性心肌梗死(AMI)组48例。同时根据患者Gensini积分将其分为轻度47例、中度51例和重度44例。比较不同冠心病类型、不同严重程度的Lp-PLA2、hs-CRP、IL-27、MMP-9水平及Gensini积分,并分析冠心病患者上述指标水平与Gensini积分的相关性。结果:AMI组患者Lp-PLA2、hs-CRP、IL-27、MMP-9水平及Gensini积分均高于UAP组和SAP组,且UAP组高于SAP组(P0.05)。重度患者Lp-PLA2、hs-CRP、IL-27、MMP-9水平及Gensini积分均高于中度和轻度患者,且中度患者高于轻度患者(P0.05)。经Spearman相关性分析结果显示,冠心病患者Lp-PLA2、hs-CRP、IL-27、MMP-9水平与Gensini积分均呈正相关(P0.05)。结论:老年冠心病患者Lp-PLA2、hs-CRP、IL-27及MMP-9水平与患者冠状动脉病变Gensini积分均呈正相关。临床根据Lp-PLA2、hs-CRP、IL-27及MMP-9水平的变化,有助于评估老年冠心病患者的病情严重程度。     

基于专利信息分析的中国3D生物打印技术发展与产业化研究*

目的:基于专利信息对我国3D生物打印技术的发展态势进行分析。方法:本文基于incopat和TDA两大专利分析平台对中国3D生物打印的专利发展态势从专利统计分析与专利计量分析两个维度进行了跨库组合分析,总结了我国3D生物打印技术的专利前沿动态特征。结果:研究发现,中国3D生物打印技术从2013年起进入专利激增态势,中国作为潜在技术市场的国际竞争日趋激烈,本文还从专利申请人、技术领域分布、专利文本关键词聚类、专利价值、专利合作等方面进行了深度挖掘分析。结论:最后,结合对中国3D生物打印专利申请人的专利产业化案例深度分析与专利特征总结,为中国3D生物打印技术发展与产业化提供参考建议。     

生长抑素联合双歧杆菌四联活菌治疗急性胰腺炎的效果及对肠粘膜屏障功能的影响

目的:探究生长抑素联合双歧杆菌四联活菌治疗急性胰腺炎的效果及对肠粘膜屏障功能的影响。方法:选取2015年8月～2018年8月我院收治的急性胰腺炎患者98例,根据患者入院先后顺序分为两组。对照组患者给予生长抑素治疗,观察组在对照组的基础上联合双歧杆菌四联活菌片治疗。比较两组患者的临床治疗效果,临床症状和指标的恢复时间及胃肠动力的恢复情况,治疗前后D-乳酸、二胺氧化酶(DAO)和尿乳果糖和甘露醇的比值(L/M)水平的变化。结果:治疗后,观察组患者的总有效率显著高于对照组(P0.05),腹痛、腹胀、腹膜刺激征、血淀粉酶和尿淀粉酶恢复正常时间均显著短于对照组(P0.05)。治疗后,两组患者的血清D-乳酸、DAO和L/M水平均较治疗前显著下降,且观察组以上指标均显著低于对照组(P0.05)。此外,观察组患者的腹内压显著低于对照组,肠鸣音恢复时间显著短于对照组,胃肠减压引流量显著低于对照组(P0.05)。结论:与单用生长抑素相比,生长抑素联合双歧杆菌四联活菌可更迅速缓解急性胰腺炎患者的临床症状及指标,恢复胃肠动力,并显著改善患者的肠粘膜屏障功能,利于患者的康复。     

药物注射联合针刀治疗肩周炎临床疗效及安全性分析

为探讨针刀联合曲安奈德、正清风痛宁、利多卡因治疗肩周炎的临床疗效及安全性分析,本研究选取2016年1月至2017年12月来东南大学附属中大医院疼痛科就诊肩周炎患者120例,随机数字表法分为药物治疗组40例(曲安奈德+正清风痛宁+利多卡因+臭氧治疗),针刀治疗组40例,综合治疗组40例(曲安奈德+正清风痛宁+利多卡因+臭氧+针刀治疗),对比分析各组治疗前后肩关节功能评分、视觉模拟评分法(visual analogue score, VAS)评分、不良反应发生率。结果显示,组内比较,3组治疗后VAS和肩关节功能评分与治疗前比较,差异具有统计学意义(p<0.001)。组间比较,治疗前3组VAS和肩关节功能评分比较,差异不具有统计学意义;综合治疗组各时间点VAS评分均低于药物及针刀治疗组,综合治疗组肩关节功能评分在治疗后1个月和2个月高于药物及针刀治疗组,差异具有统计学意义(p<0.001)。3组的不良反应发生率,差异不具有统计学意义(p>0.05)。综上所述,针刀治疗联合曲安奈德、正清风痛宁、利多卡因及臭氧在关节腔及关节周围注射治疗肩周炎安全有效,值得在临床中推广应用。     

Transplantation of adult spinal cord grafts into spinal cord transected rats improves their locomotor function

Grafted embryonic central neural tissue pieces can recover function of hemisected spinal cord in neonatal rats and promote axonal growth in adults. However, spinal cord segments from adults have not been used as donor segments for allogeneic transplantation. Here, we utilized adult spinal cord tissue grafts(aSCGs) as donor constructs for repairing complete spinal cord injury(SCI). Moreover, to provide a favourable microenvironment for SCI treatment, a growth factor cocktail containing three growth factors(brain-derived neurotrophic factor, neurotrophin-3 and vascular endothelial growth factor), was applied to the aSCG transplants. We found that the locomotor function was significantly improved 12 weeks after transplantation of aSCGs into the spinal cord lesion site in adult rats. Transplantation of aSCGs combined with these growth factors enhanced neuron and oligodendrocyte survival and functional restoration. These encouraging results indicate that treatment of complete SCI by transplanting aSCGs, especially in the presence of growth factors, has a positive effect on motor functional recovery, and therefore could be considered as a possible therapeutic strategy for SCI.     

Association of interleukin‐27 gene polymorphisms with susceptibility to HIV infection and disease progression

Interleukin‐27 (IL‐27) gene polymorphisms are linked to infectious disease susceptibility and IL‐27 plasma level is associated with HIV infection. Therefore, we aimed to investigate the association between IL‐27 polymorphisms and susceptibility to HIV infection and disease progression. A total of 300 patients with HIV infection (48 long‐term nonprogressors and 252 typical progressors) and 300 healthy controls were genotyped for three IL‐27 polymorphisms, rs17855750, rs181206, rs40837 which were performed by using multiple single nucleotide primer extension technique. Significant association was found between IL‐27 rs40837 polymorphisms with susceptibility to HIV infection (AG vs AA: adjusted OR = 1.60, 95% CI, 1.11‐2.30, P = 0.012; AG+GG vs AA: adjusted OR = 1.44, 95% CI, 1.02‐2.03, P = 0.038) and disease progression (LTNP: AG vs AA: adjusted OR = 2.33, 95% CI, 1.13‐4.80, P = 0.021; TP: AG vs AA: adjusted OR = 1.50, 95% CI, 1.04‐2.24, P = 0.030). Serum IL‐27 levels were significantly lower in cases compared to controls (P < 0.001). There were lower serum IL‐27 levels in TPs than in LTNPs (P < 0.001). We further found that LTNPs with rs40837 AG or GG genotype had lower serum IL‐27 levels than with AA genotype (P < 0.05). The CD4⁺T counts in cases were significantly lower than controls (P < 0.001). In contrast, individuals with rs40837 AG genotype had lower CD4⁺T counts than with AA genotype in cases (P < 0.05). In addition, CD4⁺T counts in TPs were significantly lower than LTNPs (P < 0.001). IL‐27 rs40837 polymorphism might influence the susceptibility to HIV infection and disease progression probably by regulating the level of serum IL‐27 or the quantity of CD4⁺T.     

MicroRNA‐488 inhibits endometrial glandular epithelial cell proliferation,migration, and invasion in endometriosis mice via Wnt by inhibiting FZD7

Endometriosis is a chronic inflammatory syndrome and nearly 6%‐10% of women are affected by it during the reproductive period. Previous studies have proved that microRNAs (miRNAs) are implicated in the pathogenesis of ovarian endometriosis. In this study, we aimed to investigate that restored miR‐488 would effectively inhibit the development of endometriosis. The microarray‐based data analysis was performed to screen endometriosis‐related differentially expressed genes (DEGs). The mouse model in endometriosis syndrome was established by being subcutaneously injected with Estradiol benzoate, and the ectopic endometrial tissues and normal endometrial tissues were collected. Additionally, the endometrial glandular epithelial cells were extracted from the endometrial glandular epithelial tissues from normal and endometriosis mice. In order to examine the role of miR‐488 in mice with endometriosis, we measured miR‐488 expression and expression levels of Frizzled‐7 (FZD7), cyclinD1, β‐catenin, and c‐Myc in vivo and in vitro. Finally, we detected the effect of miR‐488 on cell proliferation, apoptosis, migration and invasion in vitro. FZD7 was upregulated in human endometriosis. The data showed higher expression levels of FZD7, β‐catenin, c‐Myc and cyclinD1, and lower miR‐488 expression in mouse endometrial tissues. FZD7 was the target gene of miR‐488. Furthermore, elevated miR‐488 in isolated mouse endometrial glandular endometrial cells inhibited FZD7, the translocation of β‐catenin to nucleus, the activation of Wnt pathway, and the cell proliferation, migration and invasion. Collectively, these findings indicated that up‐regulated miR‐488 may reduce the proliferation, migration and invasion of endometrial glandular epithelial cells through inhibiting the activation of Wnt pathway by down‐regulating FZD7.