纳米羟基磷灰石/硫酸钙复合人工骨顺铂缓释系统注射液的制备与研究

目的研制可注射α-CSH-nano-HA/PHBV-PEG顺铂释药系统,为骨转移瘤提供新型的局部药物缓释系统。方法α-CSH-nano-HA/PHBV-PEG载顺铂制成可注射用α-CSH-nano-HA/PHBV-PEG cis-platinum缓释微球,研究其结构、释药特性、可注射性以及力学性能。结果(1)第1、3、5、7天缓释微球的释药浓度分别为97.5、90.7、83.2、68.5μg/mL,第7天后趋于稳定。(2)可注射α-CSH-nano-HA/PHBV-PEG顺铂释药系统在液固比为0.7时可注射性强,与此同时缓释药系统随着液固比的增大凝固时间延长。结论α-CSH-nano-HA/PHBVPEG顺铂释药系统具有良好的注射性能和缓释作用。     

手性修饰氧化石墨衍生物对小鼠成神经瘤细胞活性的影响

目的比较手性修饰的氧化石墨(GO)衍生物对小鼠成神经瘤细胞N2a活性的影响。方法倒置荧光显微镜观察N2a细胞形态,MTT法检测N2a细胞的活性。结果在0.1~0.4μmol/L浓度GO衍生物对N2a细胞活性影响呈浓度相关,其中0.4μmol/L的GO衍生物对N2a细胞生长状况最好;L-型GO(L-GO)和D-型GO(D-GO)促N2a细胞增殖率分别为94%和52%,二者差异有统计学意义(P0.01)。结论手性修饰的GO衍生物在0.1~0.4μmol/L能促进N2a细胞生长,L-GO促进N2a细胞生长活性比D-GO强。     

16S rDNA测序技术在婴儿肠道微生态研究中的应用

目的探讨16SrDNA测序技术在新生儿、婴儿肠道微生态研究中的应用。方法于生后3天、1月、6月、1岁时收集2例健康婴儿粪便标本共8份,提取细菌总DNA,以Illumina Hiseq 2000为测序平台,采用新一代高通量16SrDNA宏基因组测序技术对V6可变区测序,并进行生物信息分析(物种分类和丰度分析;多样性分析)。结果 8份样品共产生原始测序数据为1 027.47 Mbp,Unique tags序列数量均值为58630,OTU数量63~209;优势菌门为Proteobacteria和Firmicutes;在科水平,1%的物种1个月之内2~4种,6月后达7~10种;1号婴儿一直以Enterobacteriaceae占优势,2号婴儿优势菌群包括Enterobacteriaceae、Lachnospiraceae、Streptococcaceae和Bacteroidaceae;4个时间点的npShannon和Simpson指数分别为1.17、1.29、2.16、2.51和0.43、0.40、0.26、0.14。结论 16SrDNA测序技术能满足新生儿、婴儿肠道微生态研究需求;新生儿、婴儿粪便中含丰富细菌基因组;细菌物种丰度及分类存在个体差异;从出生到1岁,婴儿肠道菌群结构趋向复杂和多样。     

Prevalence and specificity of red-blood-cell antibodies in a multiethnic South and East Asian patient population and influence of using novel MUT+Mur+ kodecytes on its detection

Background and Objectives Appropriate screening for irregular red‐cell antibodies is essential for ensuring transfusion compatibility and for antenatal management of mothers at risk of haemolytic disease of the foetus and newborn. Screening for all relevant antibodies is, however, limited by screening cells that do not express antigens present in the patient and donor population. Technology to artificially incorporate antigens into red cells is currently available and may be an option for customizing screening cells. Materials and Methods We sought to identify retrospectively the changing patterns of alloantibody prevalence in our multiethnic population on change of screening cells. Antibody screening records of 143 501 patients tested from 2004 to 2010 were retrieved and divided into two groups: period‐1 (2004–2008) and period‐2 (2009–2010). During period‐1, standard screening cells were used while in period‐2, MUT+Mur+ KODE^? transformed red cells (kodecytes) were used. Results Four per cent of samples tested during period‐2 were positive on antibody screening compared to 3·2% in period‐1. Specific antibodies, excluding anti‐D, were identified in 1·66% and 1·52% of patients in period‐2 and ‐1, respectively. When confined to antibodies of clinical significance only, period‐2 showed higher alloantibody prevalence of 1·16% as compared to 0·66% in period‐1. Antibodies to glycophorin variants of MNS (vMNS) were more commonly detected while antibodies to Lewis antigens declined during period‐2. Conclusion Antibodies to vMNS antigens are common in South and East Asian populations and are often missed when using standard screening cells. Use of specifically engineered screening cells to express red‐cell antigens artificially is beneficial in detecting the diverse alloantibodies present in our population.     

暂时冠桥材料抗压强度的体外实验研究

目的:对比分析5种暂时冠桥材料的抗压强度。方法:参照标准制作直径4 mm,高6 mm的圆柱形试件50个,甲基丙烯酸酯即自凝树脂(A组)、Integrity(B组)、Luxatemp(C组)、Temphase(D组)、Protem 3 Garan(tE组)5种暂时冠桥材料试件各10个,采用万能材料试验机测定其抗压强度,并进行统计分析。结果:A组抗压强度(210.28±20.07)MPa,显著低于其余4组(P<0.05),E组抗压强度最高(304.55±24.50)MPa,B、C、D组间无统计学差异(P>0.05),B、D、E组间也无显著性差异(P>0.05),C组和E组间抗压强度差异有统计学意义(P<0.05)。结论:5种暂时冠桥材料抗压强度间存在较大差异,Bis-acryl类材料较甲基丙烯酸酯类材料抗压强度高。     

宝石CT能谱成像测定甲状腺含碘量的初步探讨

目的 利用宝石CT能谱成像技术测量正常甲状腺含碘量,计算甲状腺与胸锁乳突肌含碘量的碘比值,为高碘或缺碘性甲状腺疾病诊断提供参考依据.方法 采用美国GE公司生产的宝石CT,对来自潍坊医学院的226例怀疑颈部或颈椎疾病患者进行能谱扫描,扫描范围包括甲状腺,胸锁乳突肌.其中男119例,女107例,年龄18 ～ 77岁,平均年龄(46±17)岁.将扫描数据传至AW 4.4工作站,利用GSI Viewer软件处理,找出甲状腺与胸锁乳突肌的最佳对比噪声比及其所对应的单能量图像,在碘基图像上测量甲状腺左右叶、两侧胸锁乳突肌含碘量,计算二者含碘量比值.结果 甲状腺左右叶总含碘量为(1.5233±0.4318)mg/cm3,其中左叶为(1.5230±0.4271)mg/cm3,右叶为(1.5236±0.4365)mg/cm3,二者比较差异无统计学意义(t=0.0084,P＞0.05).男性甲状腺含碘量为(1.6395±0.4105)mg/cm3,女性为(1.4238±0.3832) mg/cm3,二者比较差异有统计学意义(t=3.4743,P＜0.01).甲状腺与胸锁乳突肌含碘量的碘比值为96.6271±33.2442,其中男性比值为94.6250±37.3621,女性比值为98.0000±29.0737,二者比较差异无统计学意义(t=0.3817,P＞0.05).随年龄增长甲状腺含碘量呈逐渐下降趋势,组间比较差异有统计学意义(F=9.66,P＜ 0.01);其中＜40岁组[(1.7256±0.4631) mg/cm3]甲状腺含碘量高于40～60岁组[(1.4517±0.3643 )mg/cm3]和＞60岁组[(1.4368±0.3465)mg/cm3,q值分别为5.6195、5.4158,P均＜0.0l].结论 宝石CT能谱成像能测定甲状腺含碘量,反映人体碘水平,对高碘或缺碘性甲状腺疾病诊断有重要指导意义.     

指侧方静脉动脉化再植末节断指

目的：探讨指侧方静脉动脉化再植末节断指的疗效。方法2007年3月至2012年4月,收治末节断指患者34例,均在正常指动脉多次吻合失败后行静脉动脉化。20例采用指侧方静脉动脉化再植,将近端指动脉与远端指侧方静脉吻合（A组）;14例采用指腹静脉动脉化再植,用近端指动脉与远端指腹静脉吻合（B组）。结果 A组患者末节断指全部成活,创面均Ⅰ期愈合;B组中有4例坏死。本组中有27例随访6～14个月（A组18例,B组9例）。 A组再植末节断指指腹饱满,指体无明显萎缩,B组指体轻度萎缩;A组指甲长度（15.6±2.7） mm,长于B组（11.9±2.2） mm;A组DIPJ活动度（62±4）°,大于B组（45±3）°;A组两点分辨觉（4.6±0.3） mm,小于B组（7.4±0.6） mm;A组再植断指感觉测定为S（3.49±0.33）,高于B组S（2.47±0.44）;手指各关节活动度参照TAM标准：A组优良率94.4%,B组优良率87.5%,两组优良率比较差异无统计学意义（P=0.534）。结论指侧方静脉动脉化是正常供血失败后的末节断指再植的有效方法。     

Skeletal muscle α-actin diseases (actinopathies): pathology and mechanisms

Mutations in the skeletal muscle α-actin gene (ACTA1) cause a range of congenital myopathies characterised by muscle weakness and specific skeletal muscle structural lesions. Actin accumulations, nemaline and intranuclear bodies, fibre-type disproportion, cores, caps, dystrophic features and zebra bodies have all been seen in biopsies from patients with ACTA1 disease, with patients frequently presenting with multiple pathologies. Therefore increasingly it is considered that these entities may represent a continuum of structural abnormalities arising due to ACTA1 mutations. Recently an ACTA1 mutation has also been associated with a hypertonic clinical presentation with nemaline bodies. Whilst multiple genes are known to cause many of the pathologies associated with ACTA1 mutations, to date actin aggregates, intranuclear rods and zebra bodies have solely been attributed to ACTA1 mutations. Approximately 200 different ACTA1 mutations have been identified, with 90 % resulting in dominant disease and 10 % resulting in recessive disease. Despite extensive research into normal actin function and the functional consequences of ACTA1 mutations in cell culture, animal models and patient tissue, the mechanisms underlying muscle weakness and the formation of structural lesions remains largely unknown. Whilst precise mechanisms are being grappled with, headway is being made in terms of developing therapeutics for ACTA1 disease, with gene therapy (specifically reducing the proportion of mutant skeletal muscle α-actin protein) and pharmacological agents showing promising results in animal models and patient muscle. The use of small molecules to sensitise the contractile apparatus to Ca²⁺ is a promising therapeutic for patients with various neuromuscular disorders, including ACTA1 disease.