医学图像光线投影体绘制中一种改进的快速算法

光线投影算法是体绘制算法中图像效果比较好的方法，但存在运算量大，绘制速度慢的问题。为此本文提出了一种新的光线投影体绘制的加速算法，利用重采样点在两坐标系中的矩阵变换特性。减少矩阵运算量，加快重采样计算过程，并且通过将Bresenham算法扩展至三维，利用包围盒技术避免对空体元的采样，从而加速了光线投影的效率。实验结果表明改进后的加速算法，既能保证绘制质量，又能显著减少计算量，提高体绘制的速度。     

IL-1α及与IL-11、LIF和GDNF联合诱导胚鼠皮质、中脑神经干细胞向多巴胺神经元分化的比较

为比较皮质和中脑来源的神经干细胞(NSCs)定向分化为多巴胺神经元的情况,应用无血清和单克隆培养技术,分别从皮质和中脑组织中分离克隆、扩增NSCs,然后分成3组诱导分化:①对照组用10%胎牛血清诱导分化;②IL-1α组在10%胎牛血清的基础上加IL-1α诱导分化;③联合因子组在10%胎牛血清的基础上加IL-1α、IL-11、LIF及GDNF进行诱导分化。用酪氨酸羟化酶(TH)免疫组化染色检测多巴胺神经元。在100倍镜下随机取5个视野,计数每个视野中的TH阳性神经元数;并用图像分析软件处理TH阳性神经元的胞体面积和细胞周长;用STATA7.0统计软件进行统计处理。结果显示,皮质对照组中仅见极少的TH阳性神经元(0.25±0.163),中脑对照组中见少量TH阳性神经元(2±0.378);而皮质IL-1α组有较多的TH阳性神经元(15.5±0.866),中脑IL-1α组中的TH阳性神经元则为皮质IL-1α组的150%(22.875±1.517);皮质联合因子组中的TH阳性神经元数(25.75±0.940)与中脑联合因子组中的TH阳性神经元数(28.875±2.125)接近,无显著差异。胞体面积和细胞周长的结果显示出IL-1α组和联合因子组大于对照组、而联合因子组又优于IL-1α组的趋势。上述结果提示,中脑来源的NSCs本身具有一定的分化为多巴胺神经元的区域特异性,而皮质来源的NSCs在IL-1α、IL-11、LIF及GDNF等细胞因子的诱导下可改变其区域特异性而分化为较多较为成熟的多巴胺神经元。     

大鼠失血性休克对内毒素诱导TNFα产生的影响及其分子机制

笔者观察了大鼠失血性休克（ＨＳ）对内毒素诱导肿瘤坏死因子α（ＴＮＦα）产生的影响及其细胞来源，并结合休克后组织内脂多糖结合蛋白（ＬＢＰ）ｍＲＮＡ的表达变化，对其分子机制进行了初步分析。研究结果显示，静脉注射ＬＰＳ后９０ｍｉｎ，ＨＳ＋ＬＰＳ组血浆ＴＮＦα水平分别较ＨＳ组高２０倍（Ｐ＜０．０１），ＬＰＳ组高２．７倍（Ｐ＜０．０５）；休克和复苏后，外周血白细胞产生ＴＮＦα的能力明显受抑，而肝Ｋｕｐｆｅｒ＇ｓ细胞产生ＴＮＦα的能力却明显增强；休克后不仅肝组织内ＬＢＰｍＲＮＡ表达增多，肺、肾组织内ＬＢＰｍＲＮＡ也相继表达增加。研究结果提示，失血性休克能显著增敏内毒素诱导ＴＮＦα的产生作用，其机制可能与休克后组织内ＬＢＰ表达上调有关，组织巨噬细胞群（如Ｋｕｐｆｅｒ细胞）可能是休克后细胞因子产生的主要来源。     

新型MAO钛基生物材料的血液相容性研究

目的初步评价新型钛基材料的血液相容性。方法采用新西兰大白兔新鲜全血,抗凝后分别与实验组和阳性对照、阴性对照组接触,用紫外-可见光分光光度计比色,评价各组的溶血率。实验符合国际化标准组织规定要求。结果新型微弧氧化钛基材料直接接触溶血率为0.79％,符合医用材料的溶血率不大于5％的要求。结论新型钛基材料具有良好的血液相容性。     

军团菌MOMPS基因的克隆并在原核系统中表达

以军团菌DNA为模板，PCR扩增获得军团菌主要外膜蛋白基因（Major outer membrane protein gene，ompS），与原核表达质粒pUC18定向重组，构建重组质粒，转化大肠杆菌BL21，并用限制性酶酶切分析、聚合酶链式反应、核酸序列分析、十二烷基磺酸钠-聚丙烯酰胺凝胶电泳、Western印迹进行鉴定。实验结果表明我们扩增出了军团菌914bp的ompS基因，成功构建了重组质粒pLPompS，并在原核系统中得到了表达。     

壳聚糖醋酸溶液对凝血作用的研究

研究了不同脱乙酰度和不同分子量壳聚糖醋酸溶液的凝血作用。发现壳聚糖醋酸溶液使抗凝血液中红细胞发生了明显的聚集和变形。通过不同分子量和脱乙酰度壳聚糖的促红细胞聚集实验,证明了低脱乙酰度壳聚糖(60%~70%)使红细胞聚集效果更好,分子量在105~106范围内作用不十分明显。对血液的凝血酶时间(TT)、凝血酶原时间(PT)、活化部分促凝血酶原激酶时间(APTT)和纤维蛋白原浓度(FIB)的测定结果验证了壳聚糖醋酸溶液凝血机理不依赖于血小板和常规“瀑布”凝血机制。     

Pleiotropic genomic variants at 17q21.31 associated with bone mineral density and body fat mass: a bivariate genome-wide association analysis

Osteoporosis and obesity are two severe complex diseases threatening public health worldwide. Both diseases are under strong genetic determinants as well as genetically correlated. Aiming to identify pleiotropic genes underlying obesity and osteoporosis, we performed a bivariate genome-wide association (GWA) meta-analysis of hip bone mineral density (BMD) and total body fat mass (TBFM) in 12,981 participants from seven samples, and followed by in silico replication in the UK biobank (UKB) cohort sample (N = 217,822). Combining the results from discovery meta-analysis and replication sample, we identified one novel locus, 17q21.31 (lead SNP rs12150327, {"type":"entrez-nucleotide","attrs":{"text":"NC_000017.11","term_id":"568815581"}}NC_000017.11:g.44956910G > A, discovery bivariate P = 4.83 × 10⁻⁹, replication P = 5.75 × 10⁻⁵) at the genome-wide significance level (ɑ = 5.0 × 10⁻⁸), which may have pleiotropic effects to both hip BMD and TBFM. Functional annotations highlighted several candidate genes, including KIF18B, C1QL1, and PRPF19 that may exert pleiotropic effects to the development of both body mass and bone mass. Our findings can improve our understanding of the etiology of osteoporosis and obesity, as well as shed light on potential new therapies.Subject terms: Genome-wide association studies, Gene expression profiling     

Systemic autoimmune disease induced by dendritic cells that have captured necrotic but not apoptotic cells in susceptible mouse strains

Systemic lupus erythematosus (SLE) is an autoimmune disorder of a largely unknown etiology. Anti-double-stranded (ds) DNA antibodies are a classic hallmark of the disease, although the mechanism underlying their induction remains unclear. We demonstrate here that, in both lupus-prone and normal mouse strains, strong anti-dsDNA antibody responses can be induced by dendritic cells (DC) that have ingested syngeneic necrotic (DC/nec), but not apoptotic (DC/apo), cells. Clinical manifestations of lupus were evident, however, only in susceptible mouse strains, which correlate with the ability of DC/nec to release IFN-gamma and to induce the pathogenic IgG2a anti-dsDNA antibodies. Injection of DC/nec not only accelerated disease progression in the MRL/MpJ-lpr/lpr lupus-prone mice but also induced a lupus-like disease in the MRL/MpJ-+/+ wild-type control strain. Immune complex deposition was readily detectable in the kidneys, and the mice developed proteinuria. Strikingly, female MRL/MpJ-+/+ mice that had received DC/nec, but not DC/apo, developed a 'butterfly' facial lesion resembling a cardinal feature of human SLE. Our study therefore demonstrates that DC/nec inducing a Th1 type of responses, which are otherwise tightly regulated in a normal immune system, may play a pivotal role in SLE pathogenesis.     

Protective efficacy in chickens, geese and ducks of an H5N1-inactivated vaccine developed by reverse genetics

We generated a high-growth H5N1/PR8 virus by plasmid-based reverse genetics. The virulence associated multiple basic amino acids of the HA gene were removed, and the resulting virus is attenuated for chickens and chicken eggs. A formalin-inactivated oil-emulsion vaccine was prepared from this virus. When SPF chickens were inoculated with 0.3 ml of the vaccine, the hemagglutinin-inhibition (HI) antibody became detectable at 1 week post-vaccination (p.v.) and reached a peak of 10log2 at 6 weeks p.v. then slowly declined to 4log2 at 43 weeks p.v. Challenge studies performed at 2, 3 and 43 weeks p.v. indicated that all of the chickens were completely protected from disease signs and death. Ducks and geese were completely protected from highly pathogenic H5N1 virus challenge 3 weeks p.v. The duration of protective immunity in ducks and geese was investigated by detecting the HI antibody of the field vaccinated birds, and the results indicated that 3 doses of the vaccine inoculation in geese could induce a 34 weeks protection, while 2 doses induced more than 52 weeks protection in ducks. We first reported that an oil-emulsion inactivated vaccine derived from a high-growth H5N1 vaccine induced approximately 10 months of protective immunity in chickens and demonstrated that the oil-emulsion inactivated avian influenza vaccine is immunogenic for geese and ducks. These results provide useful information for the application of vaccines to the control of H5N1 avian influenza in poultry, including chickens and domestic waterfowl.