Ixodes dammini: Induced skin lesions in guinea pigs and rabbits compared to erythema chronicum migrans in patients with lyme arthritis

Erythematous skin lesions occurred in rabbits 2 days after being fed upon by larvae or nymphs of the tick, Ixodes dammini. Similar lesions occurred in guinea pigs 7 days after a primary infestation with either larvae or nymphs. Host resistance to secondary feeding by larvae was demonstrated in guinea pigs and rabbits. Host resistance to secondary feeding by nymphs was seen in guinea pigs, but not in rabbits. Guinea pigs developed resistance to nymphs after being previously fed upon twice by larvae. All skin lesions in resistant guinea pigs contained large accumulations of basophils (49–76% of cells) with smaller (20–33%), but significant, numbers of eosinophils. These responses were characteristic of strong cutaneous basophil hypersensitivity reactions. Primary and secondary lesions in rabbits fed upon by larvae contained mostly mononuclear cells (46–52%) and moderate numbers (16–30%) of basophils and eosinophils. Primary and secondary lesions in rabbits fed upon by nymphs had few (3–11%) basophils and eosinophils and were dominated by mononuclear cells (73–86%). Thus, acquired resistance in guinea pigs and rabbits was associated with cutaneous basophil and eosinophil responses and the lack of resistance of rabbits to nymphs was associated with erythematous lesions dominated by mononuclear cells. The mononuclear nature of rabbit lesions induced by nymphal feeding was similar to that seen in erythema chronicum migrans in Lyme arthritis patients who are thought to have been fed upon by I. dammini nymphs. This study confirms the cutaneous basophil hypersensitivity characteristics of lesions in guinea pigs resistant to ticks and demonstrates a relationship between the mononuclear cell response of rabbits to nymphal I. dammini and the cellular response seen in patients with erythema chronicum migrans and Lyme arthritis.     

Transformation of MMC-E epithelial cells by acute 3611-MSV: inhibition of collagen synthesis and induction of novel polypeptides

Mouse embryo epithelial cells MMC-E were transformed by novel fibrosarcoma-inducing murine sarcoma virus 3611-MSV. The cells were analyzed for the production and deposition of pericellular glycoproteins by immunofluorescence and by radioactive metabolic and cell surface labeling techniques followed by analysis in polyacrylamide gels and fluorography. The pericellular fibronectin matrix was lost, but unlike in virus-transformed fibroblastic cells, the production of fibronectin was not affected. The major differences detected were decrease in collagen production and initiation of synthesis of two major glycoproteins with Mr 58,000 and 60,000. Cell surface carbohydrate labeling indicated that after 3611-MSV transformation the cells expressed Mr 100,000 and 68,000 polypeptides. The present and previous results show that viral transformation of epithelial cells induces different transformed phenotypes that are associated with distinct alterations in pericellular glycoproteins.     

Ultrastructural changes at gap junctions between lesioned crayfish axons

Summary In crayfish, the severed distal segment of single lateral giant axon (SLGA) often survives for at least 10 months after lesioning if this segment retains a septal region of apposition with an adjacent, intact SLGA. In control (unsevered) SLGAs, this septal region usually contains gap junctions and 50–60 nm vesicles near the axolemma of both SLGAs. From 1–14 days after lesioning, the distal segment of a severed SLGA undergoes obvious ultrastructural changes in mitochondria and neurotubular organization compared to control SLGAs or to adjacent, intact SLGAs in the same animal. Gap junctions are very difficult to locate in severed SLGAs within 24 h after lesioning. From two weeks to ten months after lesioning, the surviving stumps of severed SLGAs often appear remarkably normal except that structures normally associated with the presence of gap junctions remain very difficult to find.These and other data suggest that SLGA distal segments receive trophic support from adjacent, intact SLGAs. The mechanism of this support probably could not be via diffusion across gap junctions between intact and severed SLGAs since gap junctions largely disappear after lesioning. However, trophic maintenance could occur via the exocytotic — pinocytotic action of 50–60 nm vesicles which are always present on both sides of the septum between an intact SLGA and a severed SLGA distal segment.This work was supported by NIH research grant NS-14412 and and RCDA 00070 to G.D.B.     

Selection of malignant melanoma variant cell lines for ovary colonization

Murine melanoma line B16-F1, which shows some specificity for metastatic organ colonization of lung but rarely metastasizes to ovary, was used to select variant cell lines with increased preference for experimental ovary metastasis. Ovary-colonizing melanoma cell lines were sequentially selected in syngeneic C57BL/6 mice by repeated intravenous administration and surgical recovery of ovarian melanoma tumors for tissue culture. After ten selections for experimental ovary metastasis, line B16-010 was established which formed experimental metastatic ovary tumors in almost every test animal. In tissue culture B16–010 cells grew in circular in circular colonies with rounded, smooth cell peripheries compared to B16-F1 cells which were flatter, grew in irregular patterns, and exhibited long cellular projections. Ovary-selected B16 lines contained less melainin pigment (B16-010 < B16-05 < B16-01 ? B16-F1) compared to the parental melanoma line. Together with previous cloning and selection data, these results are consistent with the preexistence of highly malignant cells in the parental tumor population that possess the ability to metastasize to specific organs.     

The surface morphology of normal and malignant rat liver epithelial cells in culture

Summary A direct comparison has been made between normal parenchymal cells cultured from rat liver and malignant cells from both a rat liver tumor and a spontaneously transformed line derived from the parent rat culture. In all nondividing cells there was a 3- to 5-fold increase in the population of surface microvilli on the malignant cells compared to the normal cells. Notable variations in overall morphology were also observed when cells were incubated in arginine-deficient medium. During the course of this work T. D. Allen and P. T. Iype were supported by grants from the Medical Research Council and Cancer Research Campaign, and M. J. Murphy, Jr. was supported by a Special Fellowship of the Leukemia Society of America, Inc. and the Jean Shaland Fund.     

siRNA沉默整合素beta1 基因对子宫内膜癌细胞侵袭、转移的影响

目的：探讨siRNA 沉默整合素茁1 基因对子宫内膜癌细胞侵袭、转移的影响。方法：选取子宫内膜癌ECC-1细胞系(ER阳性) 和KLE细胞系(ER阴性)，分别转染Integrin beta1 siRNA 质粒(Integrin beta1 siRNA 组)、无义序列siRNA质粒(无义序列对照组)和空载 质粒(空载对照组)，利用实时荧光定量PCR 检测各组细胞中Integrin 茁1 mRNA的表达，Western blot 检测各组细胞中Integrin beta1、 beta-catenin 和C-Myc 蛋白的表达，Transwell 小室检测各组细胞迁移和侵袭能力，MTT 法检测各组细胞的增殖情况。结果：Integrin beta1 siRNA 组ECC-1 细胞和KLE 细胞中Integrin beta1 mRNA 和蛋白相对表达量均低于无义序列对照组和空载对照组(P<0.05)； Integrin beta 1 siRNA组ECC-1 细胞和KLE细胞中beta-catenin 蛋白和C-Myc 蛋白相对表达量均低于无义序列对照组和空载对照组， 差异均有统计学意义(P<0.05)；Integrin beta1 siRNA组ECC-1 细胞和KLE 细胞中迁移细胞数和侵袭细胞数均低于无义序列对照组 和空载对照组(P<0.05)；Integrin beta1 siRNA 组ECC-1细胞和KLE 细胞的A 值均低于无义序列对照组和空载对照组(P<0.05)。结 论：特异性抑制Integrin beta1 基因可抑制子宫内膜癌细胞迁移、侵袭和增殖，可能与抑制Wnt信号传导有关。     

Monostotic fibrous dysplasia in the temporal bone: A late prehistoric occurrence

Fibrous dysplasia, characterized by benign osteolytic and osteoblastic lesions may involve one or several bones. Recent investigators have suggested that it may be merely a phase of what have previously been thought to be several different bone disease. Isolated fibrous dysplasia in the temporal bone is infrequent. Several reports of this disease have appeared in the literature of paleopathology, but none involved only the temporal bone. Monostotic involvement of the right temporal bone was discovered in the skull of an adult male recovered from an archeological site dating from the Late Mississippian period (A. D. 1,350–A. D. 1,650). It will provide an opportunity for preliminary documentation of the antiquity of this disease in the southeastern portion of the United States.     

人滋养细胞表面抗原（Trop-2）在病变子宫内膜中表达的研究

摘要 目的：探讨人滋养细胞表面抗原（trophoblast cell-surface antigens2,Trop-2）在病变子宫内膜中的表达及其临床相关性。方法：采用免疫组化法检测100例正常子宫内膜或病变子宫内膜组织中Trop-2蛋白的表达,其中单纯增生子宫内膜患者26例,复杂或不典型增生子宫内膜患者34例,子宫内膜腺癌患者20例,对照组为20例增生期子宫内膜患者。结果：免疫组织化学法研究结果显示,Trop-2蛋白在正常增生子宫内膜和单纯性增生子宫内膜中几乎不表达,在复杂或不典型增生子宫内膜组织中以及子宫内膜腺癌呈阳性表达。主要分布在细胞膜上,阳性率分别为35.29 %和65.00 %,经过对比子宫内膜癌组的阳性表达率显著高于复杂型或伴不典型增生子宫内膜组的阳性表达率（P<0.05）,且复杂型或伴不典型增生子宫内膜组的阳性表达率显著高于单纯性增生子宫内膜组（P<0.05）,其表达水平随内膜病变程度的加重而升高,呈正相关关系（P＜0.05）。结论：Trop-2蛋白在子宫内膜病变中的表达与其严重程度一致,可反映子宫内膜病变的发生发展,或可作为判断其严重程度的指标。     

肺炎支原体感染对川崎病的影响及机制探讨

目的分析肺炎支原体感染对川崎病的影响及其机制,以期指导临床诊疗。方法回顾性分析2013年8月至2018年8月我科住院的496例川崎病患儿临床资料,其中合并肺炎支原体感染组193例,未合并肺炎支原体感染组303例。应用倾向评分匹配法1∶1校正2组的年龄、性别、是否为不完全型川崎病、是否使用糖皮质激素、丙种球蛋白使用时间、丙种球蛋白使用方法和阿司匹林初始剂量,比较2组患儿的总发热天数、冠状动脉直径、冠状动脉扩张发生率、冠状动脉瘤发生率和丙种球蛋白无反应发生率。结果川崎病合并肺炎支原体感染组男性患儿多,更易发生颈部淋巴结肿大,年龄、中性粒细胞百分比、血沉和低密度脂蛋白高于川崎病未合并肺炎支原体感染组,血钾、血钙、高密度脂蛋白和白蛋白低于川崎病未合并肺炎支原体感染组,差异有统计学意义(均P<0.05)。应用倾向评分匹配法1∶1配对后发现,川崎病合并肺炎支原体感染组患儿总发热时间更长[8(6~10)d vs 7(6~9)d,Z=-2.089,P<0.05),冠状动脉直径值更大[(2.81±0.81)mm vs(2.63±0.45)mm,t=2.532,P<0.05],冠状动脉瘤发生率更高(5.5% vs 1.1%,χ²=5.516,P<0.05)。结论肺炎支原体感染可能引起川崎病患儿脂质代谢及电解质的紊乱,其炎症反应更强,持续时间更长,对冠状动脉损伤更大。