基于地球网格剖分的球体3D-Voronoi图生成

球体3D-Voronoi图是球面Voronoi图向球体空间扩展产生的,可用于空间目标管理与空间行为建模。在全球空间网格剖分与编码基础上,提出了一种基于地球网格剖分的球体3D-Voronoi图生成算法。首先针对生长元为点集和全要素两种情况,分别给出了球体3D-Voronoi图的定义;然后阐述了基于活动像素生长的球体3D-Voronoi图生成算法的原理和具体实现步骤;最后以雷达探测威胁源和火力打击威胁源为生长元生成球体3D-Voronoi图,并提取边界网格,用于减少飞行器路径规划搜索网格范围,验证了算法的有效性。

均匀颜色空间中的免疫荧光图像分析

分析彩色免疫荧光图像可以获得细胞免疫信息,用于辅助研究和医疗诊断。视觉上图像前景荧光区域和背景之间存在明显的颜色差异,在CIE(L*,a*,b*)均匀颜色空间中利用该颜色差异给出了一种像素生长算法用于获取荧光区域。在区域提取的基础上,根据同一细胞不同区域之间的相关性初步识别细胞并计数。

复杂环境下的激光雷达目标物实时检测方法

目标物实时检测是自动驾驶决策控制的基础信息,保证了智能车安全可靠的行驶。针对现有的尤其是城市复杂场景下的基于三维点云的方法对地面点云去除不干净、目标物过分割欠分割等问题,提出一种基于激光雷达的智能车目标物实时检测方法。在分析三维点云数据特征的基础上,采用一维核密度估计和RANSAC（随机抽样一致性）的方法去除背景点云,然后通过将三维点云映射到二维图像域中,使用像素区域生长和连通区域标记的方法提取目标物,得到轴向矩形盒体作为目标物,完成智能车的目标物实时检测。实验证明,该方法将地面点云去除的非常干净,同时很好的保留了目标物点云,解决了绝大多数情况下的目标物过分割和欠分割问题,在自车前后各100m左右各20m的感兴趣区域内,目标物提取正确率为98%以上,纵向和横向检测距离偏差平均都在16cm内,算法运行时间在45ms/帧内。

基于密度-距离空间的红外引信抗噪声方法研究

目的通过简易的图像处理和目标检测方法,提高红外引信在复杂环境下的抗干扰能力。方法分析红外引信在复杂背景中的噪声类别,采用“密度–距离”空间方法与像素生长方法进行预处理和目标检测,赋予像素2种属性,并进行量化分析,确定灰度平坦区域中的红外候选目标,并通过像素生长方法筛选候选目标中的真实目标。结果计算在不同信噪比环境下算法的抗噪声干扰能力,当红外图像的SNR值在44.1~45.4时,算法检测效果理想。结论红外引信探测过程中的复杂背景和随机噪声都会降低图像质量,考虑到红外目标所占像素数少,极易受噪声影响,需要运用自适应简易算法提高检测准确性。该算法有良好的实时性和抗干扰能力,为红外引信在目标检测中的环境适应性提供了理论依据。

Insulin-like growth factor-1, IGF binding protein-3, and the risk of esophageal cancer in a nested case-control study

To assess the relationship between serum levels of insulin-like growth factor-1 (IGF1)/IGF-binding protein-3 (IGFBP3) and the risk of esophageal carcinoma.METHODSWe assessed the relationship between the serum levels of these molecules and the risk of esophageal cancer in a prospective, nested case-control study of participants from the Japan Collaborative Cohort Study. A baseline survey was conducted from 1988 to 1990. Of the 110585 enrolled participants, 35% donated blood samples. Those who had been diagnosed with esophageal cancer were considered cases for nested case-control studies. A conditional logistic model was used to estimate odds ratios for the incidence of esophageal cancer associated with serum IGF1 and IGFBP3 levels.RESULTSThirty-one cases and 86 controls were eligible for the present assessment. The molar ratio of IGF1/IGFBP3, which represents the free and active form of IGF1, was not correlated with the risk of esophageal carcinoma. A higher molar difference between IGFBP3 and IGF1, which estimates the free form of IGFBP3, was associated with a decreased risk of esophageal carcinoma (P = 0.0146), and people in the highest tertile had the lowest risk (OR = 0.107, 95%CI: 0.017-0.669). After adjustment for body mass index, tobacco use, and alcohol intake, the molar difference of IGFBP3-IGF1 was inversely correlated with the risk of esophageal carcinoma (P = 0.0150).CONCLUSIONThe free form of IGFBP3, which is estimated by this molar difference, may be inversely associated with esophageal cancer incidence.

Inhibition of N-methyl-N-nitrosourea-induced gastric tumorigenesis by Liuwei Dihuang Pill in db/db mice

AIM To investigate the inhibitory effect of Liuwei Dihuang Pill(LDP) on gastric tumorigenesis induced by N-methyl-N-nitrosourea(MNU) in diabetic mice.METHODS Four-week-old mice were divided into four groups: A, 12 db/m mice treated with MNU and saline, as the non-diabetic control; B, 12 db/db mice treated with MNU and saline, as the diabetic control; C, 12 db/db mice treated with MNU and metformin, as the positive control; and D, 12 db/db mice treated with MNU and LDP. MNU was administrated for 20 wk to induce gastric carcinogenesis. LDP was administrated for 10 wk for improvement of insulin resistance. Body weight and food intake were measured every week. Blood samples were collected for assays of fasting blood glucose, insulin, insulin-like growth factor(IGF)-1, adiponectin and leptin. Stomach tissues were collected for histopathological analysis, immunohistochemical staining of Ki67, quantitative reverse transcriptionpolymerase chain reaction and western blotting. RESULTS The incidence of MNU-induced gastric dysplasia was significantly elevated in diabetic(db/db) mice relative to the control(db/m) mice. The incidence of gastricdysplasia was significantly reduced by LDP with suppression of cell proliferation, as demonstrated by a decrease in Ki67 staining. Hyperglycemia, hyperinsulinemia and serum IGF-1 were inhibited by LDP. Expression of IGF-1 and insulin receptor m RNAs was decreased, phosphorylation of IGF-1 receptor and AKT protein was reduced in the stomach tissues by LDP. In addition, adiponectin was increased and leptin was decreased in the serum by LDP. CONCLUSION LDP decreased risk of gastric dysplasia in type 2 diabetic mice by down-regulation of IGF and insulin activity and correction of adipokines disorders.

Wound healing of intestinal epithelial cells

The intestinal epithelial cells(IECs) form a selective permeability barrier separating luminal content from underlying tissues.Upon injury,the intestinal epithelium undergoes a wound healing process.Intestinal wound healing is dependent on the balance of three cellular events;restitution,proliferation,and differentiation of epithelial cells adjacent to the wounded area.Previous studies have shown that various regulatory peptides,including growth factors and cytokines,modulate intestinal epithelial wound healing.Recent studies have revealed that novel factors,which include toll-like receptors(TLRs),regulatory peptides,particular dietary factors,and some gastroprotective agents,also modulate intestinal epithelial wound repair.Among these factors,the activation of TLRs by commensal bacteria is suggested to play an essential role in the maintenance of gut homeostasis.Recent studies suggest that mutations and dysregulation of TLRs could be major contributing factors in the predisposition and perpetuation of inflammatory bowel disease.Additionally,studies have shown that specific signaling pathways are involved in IEC wound repair.In this review,we summarize the function of IECs,the process of intestinal epithelial wound healing,and the functions and mechanisms of the various factors that contribute to gut homeostasis and intestinal epithelial wound healing.

Preparatory training attenuates drastic response of the insulin-like growth factor binding protein 1 at the point of maximal oxygen consumption in handball players

Background:Intensive exercise changes physiological need for glucose and several biochemical pathways responsible for its metabolism response.Among them are those which involve insulin,insulin-like growth factor(IGF-1),and IGF-binding proteins(IGFBPs).Different types and degrees of exercise,as well as an athlete's fitness,may induce a range of responses regarding concentrations and time needed for the alteration.The idea of the work was to find out whether and how insulin/IGF axis responds to additional physical activity in the already trained subjects and if so,is the adaptation potentially beneficial from the aspect of metabolic control.Methods:The effect of 4-week intensive training on campus(preparatory training) on the levels of insulin,IGF-1,and IGFBPs during maximal progressive exercise test(MPET) on a treadmill was compared to the results obtained during MPET conducted after a regular training season of a female elite handball team(n = 17,age:17 ± 1 years,height:171 ± 8 cm,weight:65 ± 8 kg,body mass index:22 ± 1 kg/m^2 at the beginning of the study;there were no significant changes at the end).Serum samples were obtained from players immediately before the test(basal),at the end of the test after reaching the point of maximal oxygen consumption(VO_(2max)),and after recovery.Results:The concentration of insulin decreased at VO_(2max),but remained higher in players after preparatory training(12.2 ± 2.5 m U/L vs.8.9 ± 4.4 m U/L,p = 0.049).The level of IGFBP-1 decreased in players at VO_(2max) in either case of training,but it remained much higher in tests performed after the preparatory regime than before(p = 0.029).Concentrations of IGF-1,IGFBP-2,-3,and-4 did not change significantly.Conclusion:The inverse relation between insulin and IGFBP-1 was lost during MPET,as these 2 molecules changed in the same direction.The results obtained suggest less severe stress-induced depression of insulin and IGFBP-1 after preparatory training.But another metabolic mechanism cannot be excluded,and that is potentially impaired insulin sensitivity resulting in higher level of IGFBP-1.