Licht- und elektronenmikroskopische Untersuchungen zur Histopathogenität vonMacracanthorhynchus hirudinaceus (Archiacanthocephala) in experimentell infizierten Hausschweinen

Zusammenfassung Die vonMacracanthorhynchus hirudinaceus verursachten Läsionen im Dünndarm von experimentell infizierten Hausschweinen (7 Tage p.i. und 84 Tage p.i.) wurden licht- und elektronenmikroskopisch untersucht. Die Würmer der 84 Tage alten Infektion waren tiefer in die Darmwand eingedrungen als die 7 Tage alten Würmer. Ihr Präsoma wurde von Entzündungsbzw. Bindegewebe umhüllt, das zahlreiche Plasmazellen enthielt. Bei 7 Tage alten Infektionen wurde noch keine Fibrose nachgewiesen. Eosinophilen-ähnliche Granulozyten, die an den Proboscishaken akkumulierten, herrschten in der Läsion vor. Eine osmiophile Gleitflüssigkeit, die offenbar an der Basis der Proboscishaken ausgeschieden wurde, schien eine stark antigene Wirkung auf die Leukozyten des Schweins auszuüben. In keinem Fall wurden Würmer angetroffen, die die gesamte Darmwand perforiert hatten, wie es in China bei Menschen beschrieben wurde.

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Light and electron microscopical investigation of the histopathogenicity ofMacracanthorhynchus hirudinaceus in experimentally infected swine

One and 12 weeks after infection the lesions in the small intestine of two domestic pigs caused byMacracanthorhynchus hirudinaceus were studied by means of light and electron microscopy. Worms of 7 d.p.i. were found to have penetrated with their presoma into the tunica propria and partly into the tunica muscularis where they had caused local mechanic destructions and heavy eosinophilic-like and hemorrhagic reactions. Most eosinophilic-like granulocytes were attracted to the proboscis hooks, at the base of which an osmiophilic substance apparently was excreted. Worms of 84 d.p.i. had penetrated with their proboscis deeply into the tunica muscularis. The presoma had become encapsulated by a solid capsule of necrotic/inflammatory tissue in its inner part and by filamentous connective tissue in its outer part. The predominant leucocytes in the inflammatory tissue now were plasma cells indicating a progressive immune reaction. No worms were found to have perforated the entire intestinal wall as was described from human patients in China.

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Unterstützt durch ein Stipendium der VR China für Herrn Bin Zhao     

高能重带电粒子束平均能量计算的一个简单公式

本文提出了一个计算高能重带电粒子束平衡能量的简单公式。在计算重带电粒子放射治疗剂量时，用此公式可获得与平均能量有关的物理量的解析表达式，用此公式计算了入射铝内10-MeV的质子束的平均能量，并与相应的实验数据作了比较，比较表明，本文提出的公式在相当大的能量范围内能够精确地预言重带电粒子的平均能量，此外，还计算了在水中在100-MeV、150-MeV和200-MeV的质子束的平均能量。     

结核性脑膜炎的CT诊断(附16例分析)

目的：通过分析16例结核性脑膜炎的CT表现及其产生的病理基础，提高对本病的认识和诊断水平。方法：16例结核性脑膜炎病人采用常规头颅CT扫描，对其影像及临床资料进行回顾性分析。结果：脑基底池、侧裂池变窄12例(75％)，合并密度增高8例(50％)；不同程度的脑积水14例(88％)；脑梗塞8例(50％)；结核瘤1例(6％)。结论：结核性脑膜炎的主要CT征象是脑基底池、侧裂池变窄，同时有不同程度的脑积水。如同时伴有脑结核瘤，可作出诊断。     

肢体缺血/再灌注后氧自由基与Bax蛋白、细胞凋亡的关系

目的　阐明氧自由基与Bax蛋白、细胞凋亡在大鼠肢体缺血 /再灌注不同时相中的变化规律及相互关系。方法　采用大鼠股动脉夹闭模型 ,阻断股动脉血流 5h后再灌注 ,设立缺血组、再灌注组 ,再灌注组设立 1,6 ,12 ,2 4h 4个检测时相 ,应用硫代巴比妥酸法测定肌肉组织中脂质过氧化产物丙二醛 (MDA)水平 ,应用免疫组化方法测定Bax蛋白表达的变化 ,应用原位末端标记法及电镜方法观察细胞凋亡现象。结果　随着再灌注时间的延长 ,MDA水平、Bax蛋白表达强度、细胞凋亡指数 (AI)进行性升高 ,且三者呈显著正相关。结论　氧自由基与细胞凋亡同时参与肢体再灌注损伤 ,氧自由基可能通过调节Bax蛋白表达促进细胞凋亡的发生。     

寰枕关节完全骨化2例伴先天脊柱裂1例

笔者在整理100余套散骨标本时,发现有两例寰枕关节完全骨化、愈合,其中1例伴有先天性脊柱裂,此类标本实属罕见,现将观察和测量结果报告如下:     

Brachydactyly type A3 is caused by a novel 13 bp HOXD13 frameshift deletion in a Chinese family

Brachydactyly type A (BDA) is defined as short middle phalanges of the affected digits and is subdivided into four types (BDA1‐4). To date, the molecular cause is unknown. However, there is some evidence that pathogenic variants of HOXD13 could be associated with BDA3 and BDA4. Here, we report a Chinese autosomal dominant BDA3 pedigree with a novel HOXD13 mutation. The affected individuals presented with an obviously shorter fifth middle phalanx. The radial side of the middle phalanx was shorter than the ulnar side, and the terminal phalanx of the fifth finger inclined radially and formed classical clinodactyly. Interestingly, the index finger was normal. The initial diagnosis was BDA3. However, the distal third and fourth middle phalanges were also slightly affected, resulting in mild radial clinodactyly. Both feet showed shortening of the middle phalanges, which were fused to the distal phalanges of the second to the fifth toes, as reported in BDA4. Therefore, this pedigree had combined BDA3 and atypical BDA4. By direct sequencing, a 13 bp deletion within exon 1 of HOXD13 (NM_000523.4: c.708_720del13; NP_000514.2: p.Gly237fs) was identified. The 13 bp deletion resulted in a frameshift and premature termination of HOXD13. This study provides further evidences that variants in HOXD13 cause BDA3‐BDA4 phenotypes.     

C and V proteins of Sendai virus target signaling pathways leading to IRF-3 activation for the negative regulation of interferon-beta production

We here report a molecular basis for downregulation of interferon (IFN)-beta production by V and C proteins of Sendai virus (SeV). The infection of HeLa cells with SeV poorly induced IFN-beta even if the expression of C/C' was disrupted. In contrast, when the expression of C/C'/Y1/Y2 or V/W was disrupted, SeV infection strongly induced IFN-beta production and significantly activated the interferon regulatory factor (IRF)-3 pathway. The independent expression of C or V inhibited the double-stranded (ds) RNA- or Newcastle disease virus (NDV)-induced activation of IRF-3 and NF-kappa B, as well as the IFN-beta promoter. This inhibitory effect was also observed when Y1, Y2, or a C-terminal half fragment (aa 85-204) of C was independently expressed. Phosphorylation and homodimer formation of IRF-3 were suppressed not only in cells infected with SeV capable of expressing both C/C'/Y1/Y2 (or Y1/Y2) and V/W, but also in HeLa cells constitutively expressing Y1. These results suggest that C, Y1, Y2, and V block signaling pathways leading to IRF-3 activation to downregulate IFN-beta production.     

Differential effects of Th1, monocyte/macrophage and Th2 cytokine mixtures on early gene expression for glial and neural-related molecules in central nervous system mixed glial cell cultures: neurotrophins, growth factors and structural proteins

Background  

In multiple sclerosis, inflammatory cells are found in both active and chronic lesions, and it is increasingly clear that cytokines are involved directly and indirectly in both formation and inhibition of lesions. We propose that cytokine mixtures typical of Th1 or Th2 lymphocytes, or monocyte/macrophages each induce unique molecular changes in glial cells.     

TRP超家族与肾脏

TRP(Transient receptor potentical)家族是非选择性阳离子通道家族，近来发现其与肾脏关系密切，如调节肾小管离子转运，肾脏微循环等。TRP通道异常可导致遗传性局灶节段硬化性肾病（FSGS），常染色体显性遗传多囊肾(ADPKD)，低镁血症继发低钙血症(HSH)等，对TRP通道的进一步研究将有助于临床肾脏病的防治。