Exact image reconstruction on PI-lines from minimum data in helical cone-beam CT

The development of accurate and efficient algorithms for image reconstruction from helical cone-beam projections remains a subject of active research. In the last few years, a number of quasi-exact and exact algorithms have been developed. Among them, the Katsevich algorithms are of filtered backprojection type and thus possess computational advantages over other existing exact algorithms. In this work, we propose an alternative approach to reconstructing exactly an image from helical cone-beam projections. Based on this approach, we develop an algorithm that requires less data than do the existing quasi-exact and exact algorithms, including the Katsevich algorithms. Our proposed algorithm is also of filtered backprojection type with one-dimensional filtering performed along a PI-line in image space. Therefore, it is (at least) computationally as efficient as the Katsevich algorithms. We have performed a preliminary numerical study to demonstrate and validate the proposed algorithm using computer-simulation data. The implication of the proposed approach and algorithm appears to be significant in that they can naturally address the long object problem as well as the super-short scan problem and, most importantly, in that they provide the opportunity to reconstruct images within any selected region of interest from minimum data, allowing the use of detector with a reduced size, the selection of a minimum number of rotation angles and thus the reduction of radiation dose delivered to the imaged subject.     

糖代谢异常对冠心病合并慢性心力衰竭的影响

目的探讨冠心病合并慢性心力衰竭（CHF）患者糖代谢异常的流行情况,以及糖代谢异常和CHF的严重程度的关系。方法研究对象分别来自北京、上海等7个城市,52家医院心内科,连续入选2005年6月至9月间所有符合CHF诊断标准的冠心病住院患者,共收集1009例,其中有效病例1004例。调查内容包括口服糖耐量试验、糖化血红蛋白、空腹血糖和血脂等;心功能分级使用美国纽约心脏病学会（NYHA）心功能分级。结果1004例患者中,过去确诊为糖尿病420（42％）例,新诊断为糖尿病175（17％）例,糖耐量异常208（21％）例,正常201（20％）例。心功能等级随着糖代谢异常程度的增加而增加[等级相关系数（L）=0．17,P=0．001]。多因素logistic回归分析发现,调整年龄等因素后,过去确诊为糖尿病、新诊断为糖尿病和IGT患严重CHF的OR值分别为1．7（95％CI：1．2～2．4）、1．4（95％CI：0．9～2．1）和1．2（95％CI：0．7～1．7）。结论CHF患者的糖代谢异常患病率较高。糖代谢异常和CHF的症状轻重相关,糖代谢异常者患严重CHF的危险性比血糖正常者高。     

Misdiagnosis: cardiac metastasis presented as a pseudo-infarction on electrocardiography

Most tumor invasion into the heart is nonspecific and clinically silent. Myocardium metastasis rarely mimics a myocardial infarction. In this case, a cardiac metastasis from a squamous cell carcinoma presented with both persistent ST elevation and paroxysmal supraventricular tachycardia. The secondary lesion was located in the anterior wall and lateral wall of the left ventricle and induced electrocardiographic changes imitating an acute myocardial infarction.     

早老素1基因在转染CHO细胞中的表达及其与γ-分泌酶的关系

目的 研究早老素1(PS1)在淀粉样前体蛋白(APP)加工生成β-淀粉样多肽(Ap)过程中的作用及其与γ-分泌酶的关系。方法构建APP和PSI双基因稳定转染的中国仓鼠卵巢(CHO)细胞株,应用免疫沉淀和印迹、脉冲追踪及ELISA方法,检测PS1的表达和代谢半衰期,分析对Aβ分泌的影响及与γ-分泌酶功能的关系。结果PS1转染的CHO细胞(APP-PSI)表达的主要是相对分子质量为45000的全长PS1蛋白,其半衰期短于1h,而其活性片段的N-末端片段和C-末端片段则相对稳定,半衰期接近16h。突变型PS1(M146L)转染细胞分泌的Ap总量与野生型PS1转染细胞没有明显差别,但分泌的Aβ亚型Ap142是未转染PS1或野生型PS1转染细胞分泌的将近2倍。结论 PS1参与了APP加工生成Aβ的过程,突变型PS1(M16L)导致Aβ142的分泌增加,提示PS1可能就是预期的γ-分泌酶。     

伴玻璃样间质的透明细胞癌二例

例1男,76岁。因双下肢浮肿2个月余,声嘶1周于2000年3月12日入院。体检:一般情况差,左颈部触及肿大淋巴结约2cm×2cm大小,血生化检查提示肾功能及呼吸功能衰竭,后因呼吸困难作气管插管时舌根部见一菜花状肿瘤约3.0cm×2.5cm大小,行颈淋巴结及舌根部肿瘤活检术。术后1个月患者死于慢性肾炎所致肾功能及呼吸功能衰竭。病理检查:切除淋巴结大小2cm×2cm,切面灰白色,质硬。舌根部肿瘤大小3.0cm×2.5cm,表面呈菜花状,切面灰白色,质硬。镜下观察:舌根部肿瘤细胞形态较一致,排列呈互相吻合的小梁状、岛状或片状。巢间有大量玻璃样变的纤维性间质。瘤…     

Enhancing growth human endothelial cells on Arg-Gly-Asp (RGD) embedded poly (epsilon-caprolactone) (PCL) surface with nanometer scale of surface disturbance

To explore the application of PCL for the engineering of soft tissues, the PCL surface was first embedded in an amphiphilic moiety and then grafted with RGD peptide to enhance the growth rate of human endothelial cells (HUVEC) on the surface. To graft cell-adhesive peptide RGD on the PCL surface, the PCL surface was first etched by the selected solvent with only nanometer-scale of surface disturbance, and simultaneously embedded with DSPE-PEG [di-stearoyl-phosphatidyl-ethanolamine-methoxy-poly (ethylene glycol)] moiety. Then the PCL-PEG surface was photochemically grafted by GRGD to form PCL-PEG-RGD surface. PCL and the modified surfaces were characterized by surface morphology, surface disturbance, contact angles, ATR-FTIR functional group analysis, and the growth rate of HUVEC. The surface disturbances of PCL and the modified surfaces were examined by atomic force microscope (AFM) and presented by the topography and a roughness parameter, Ra. The Ra values were 16.4 +/- 3.0, 34.8 +/- 1.6, and 12.8 +/- 0.3 nm (n = 3) for PCL, PCL-PEG, and PCL-PEG-RGD surfaces, respectively. The topographies of the surfaces and Ra values indicated that the PCL modified technique developed by this study resulted in only nanometer scale of surface disturbance. In addition to reducing surface disturbances, reducing contact angle from 73.7 degrees +/- 0.4 (n = 3) for the PCL surface to 56.9 degrees +/- 4.0 (n = 3) for the PCL-PEG surface, and the ATR-FTIR transmission spectra at 1660 cm(-1) for shoulder of amine I of PCL-PEG-RGD surface both confirmed the successful modification of PCL surfaces. HUVECs adhered well and grew on the PCL-PEG-RGD surface after 36 h incubation, whereas other surfaces did not support growth. Moreover, the viability for the relative growth rate of HUVECs on the PCL-PEG-RGD surface analyzed by MTT assay showed 8.5 times greater growth than that of the unmodified one. In conclusion, a PCL-PEG-RGD surface for enhancing the growth rate of HUVECs has been prepared by a new technique that caused only a nanometer-scale of surface disturbance. This technique and the PCL-PEG-RGD surface could be further applied to engineer soft tissues.     

The neuroprotective effects of K252a through inhibiting MLK3/MKK7/JNK3 signaling pathway on ischemic brain injury in rat hippocampal CA1 region

It has been well documented that the activation of c-Jun N-terminal protein kinase (JNK) pathway and caspase-3 signal are involved in the delayed neuronal cell death in cerebral ischemia. In this study, we first detected the activation pattern of JNK signaling including mixed lineage kinase (MLK)3, mitogen-activated protein kinase kinase (MKK)7 and JNK3 in hippocampal CA1 and CA3/DG regions at various time points after 15 min of ischemia. These results indicated that cerebral ischemia induced the continuous activation of MLK3/MKK7/JNK3 cascade, which all had two active waves only in the CA1 region. We also detected the phosphorylation of JNK substrates c-Jun and Bcl-2, and the activation of a key protease of caspase-3 in CA1 region, which only had one active peak, respectively. Because K252a has recently been shown to be a potent inhibitor of MLK3 activity both in vivo and in vitro, we further examined the possible effects and mechanism of this interesting drug in cerebral ischemia. In our present paper, we found that administration of K252a 20 min prior to ischemia inhibited MLK3/MKK7/JNK3 signaling, Bcl-2 phosphorylation, the activation of c-Jun and caspase-3, but had no significant effects on these protein expressions. Additionally, pretreatment of K252a significantly increased the number of the surviving CA1 pyramidal cells at 5 days of reperfusion. Our results suggest that K252a play a neuroprotective role in ischemic injury via inhibition of the JNK pathway, involving the death effector of caspase-3. Thus, JNK signaling may eventually emerge as a prime target for novel therapeutic approaches to treatment of ischemic stroke, and K252a may serve as a potential and important neuroprotectant in therapeutic aspect in ischemic stroke.