The binding of Chlamydia trachomatis and zinc to McCoy cells (mouse fibroblasts)

Summary Zinc was found to have profoundly different effects upon the infection of McCoy cells (mouse fibroblasts) by two strains ofChlamydia trachomatis dependent upon the time and concentration of zinc exposure. Radiolabeled zinc-65 became McCoy cell-associated in a manner independent of incubation temperature, but highly dependent on incubation time and zinc concentration. This effect was maximal after 30 to 60 minutes of incubation. Correspondingly, incubation of a chlamydia inoculant with McCoy cells and supplemental zinc (10^–5 to 10^–4M) for 1 h was associated with significantly (approximately twofold) more binding of the chlamydia to the McCoy cells compared with control media (8×10^–6M Zn). More prolonged incubation of the chlamydia and McCoy cells with supplemental zinc was associated with significantly fewer chlamydia inclusions. Concentrations of 5×10^–4M zinc or higher were also found to be toxic to the McCoy cells after 48 h of incubation. Brief exposure to supplemental zinc may augment infection of cells by chlamydia: however, more prolonged exposure to the same concentrations of zinc lessens cellular infection by chlamydia.

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Bindung von Chlamydia trachomatis und Zink an McCoy-Zellen

Zusammenfassung Der Einfluß von Zink auf die Infektion von McCoy-Zellen (Mäusefibroblasten) durchChlamydia trachomatis erwies sich bei zwei getesteten Stämmen als außerordentlich abhängig von der Inkubationszeit und Zinkkonzentration. Die Anlagerung von radioaktiv markiertem Zink-65 an McCoy-Zellen erfolgte unabhängig von der Inkubationstemperatur, doch wurde sie von der Inkubationszeit und Zinkkonzentration stark beeinflußt. Nach 30 bis 60 Minuten Inkubationszeit war dieser Effekt am stärksten ausgeprägt. Entsprechend war die einstündige Inkubation eines Inokulum von Chlamydien mit McCoy-Zellen bei erhöhter Zugabe von Zink (10^–5 bis 10^–4M) mit einer signifikant höheren (etwa zweifachen) Bindungsrate von Chlamydien and McCoy-Zellen assoziiert als in Kontrollmedium (8×10^–6M Zn). Wenn die Inkubation von Chlamydien und McCoy-Zellen unter erhöhter Zinkkonzentration über einen noch längeren Zeitraum erfolgte, waren signifikant weniger Chlamydien-Einschlußkörperchen nachzuweisen. Nach 48stündiger Inkubation erwiesen sich Zinkkonzentrationen von 5×10^–4M oder darüber als toxisch für McCoy-Zellen. Eine kurzzeitige Inkubation in erhöhter Zinkkonzentration kann die Infektion von Zellen durch Chlamydien verstärken; bei längerer Expositionszeit gegenüber denselben Zinkkonzentrationen nimmt die Infektion von Zellen durch Chlamydien hingegen ab.

     

退化性脊椎病变前方入路手术适应证探讨

目的：探讨退化性脊椎病变前方入路手术的适应证，方法：回顾性分析142例接受过前方手术的病例，根据不同病情，划分出不同组别，。分别讨论其预后，结果：总体疗效评价优等者占82％，一般者占15％，不好者占3％，结论：总结出4项适应证；（1）椎间盘突出症，尤其是中央型突出者以及椎间盘伴有过渡型腰骶变形者。（2）脊椎骨关节病变为主的病灶。（3）I度脊前倾滑脱症者，或其合并有椎间盘病变者。（4）曾接受椎间盘手术，因残余的软骨压迫导致严重的临床症状者。     

Use of a Sterile, Disposable, Radiation-Absorbing Shield Reduces Occupational Exposure to Scatter Radiation During Pectoral Device Implantation

The aim of this study was to demonstrate the effectiveness of a radiation-absorbing shield in reducing physicians' occupational radiation exposure during pectoral device implantation. A sterile, disposable, lead-free radiation-absorbing surgical drape containing x-ray attenuation material was evaluated. Twenty procedures used the radiation absorbing drape, and 20 were performed without the shielding. Radiation exposure was measured using thermoluminescent dosimetry collar badges. Use of the protective shield was associated with a time adjusted 80% reduction in radiation dose (0.009 mrem/s with shielding vs 0.047 mrem/s without shielding, P < 0.05) to the physician performing the procedures. The radiation-absorbing surgical drape did not interfere with technical performance nor add procedural time, and all procedures were successfully completed. This study demonstrates that a sterile, disposable, radiation-absorbing drape provides a convenient means of augmenting conventional radiation shielding. Use of this protective shielding greatly reduces operators' occupational exposure to scatter radiation during pectoral device implantation without compromising sterility or procedural technique. (PACE 2004; 27[Pt. I]:726–729)     

The Toxicity of Dimethylamine in F-344 Rats and B6C3F1 Mice following a 1-Year Inhalation Exposure

The Toxicity of Dimethylamine in F-344 Rats and B6C3F1 Micefollowing a 1-Year Inhalation Exposure (1985). BUCKLEY, L. A.,MORGAN, K. T., SWENBERG, J. A., JAMES, R. A., HAMM, T. E., JR.,and BARROW, C. S. Fundam. Appl. Toxicol. 5, 341–352. Dimethylamineis a widely used commodity chemical, for which there are fewchronic toxicity data. Male and female F-344 rats and B6C3F1mice were exposed by inhalation to 0, 10, 50, or 175 ppm dimethylamine(DMA) for 6 hr/day, 5 days/week for 12 months. Groups of 9–10male and female rats and mice were necropsied after 6 and 12months of exposure. No male mice were sacrificed at 12 monthsdue to a high incidence of early deaths in that group. The meanbody weight gain of rats and mice exposed to 175 ppm DMA wasdepressed to approximately 90% of control after 3 weeks of exposure.The only other treatment-related changes were concentration-relatedlesions in the nasal passages. Two distinct locations in thenose were affected: the respiratory epithelium in the anteriornasal passages, and the olfactory epithelium, especially thatlining the anterior dorsal meatus. There was focal destructionof the anterior nasoturbinate and nasal septum, local inflammation,and focal squamous metaplasia of the respiratory epitheliumin rats and mice. Mild goblet cell hyperplasia was observedonly in rats. The olfactory epithelium exhibited extensive lossof sensory cells with less damage to sustentacular cells. Therewas also loss of olfactory nerves, hypertrophy of Bowman's glands,and distension of the ducts of these glands by serocellulardebris in regions underlying degenerating olfactory epithelium.At the 175-ppm exposure level, rats had more extensive olfactorylesions than mice, with hyperplasia of small basophilic cellsadjacent to the basement membrane being present in rats butnot mice. After 12 months of exposure to 10 ppm DMA, minimalloss of olfactory sensory cells and their axons in olfactorynerve bundles was observed in the nasal passages of a few ratsand mice. These results indicate that the olfactory sensorycell is highly sensitive to the toxic effects of DMA, with minorlesions being produced in rodents even at the current thresholdlimit value of 10 ppm.     

Characterization of the specificity and duration of T cell tolerance to intranasally administered peptides in mice: a role for intramolecular epitope suppression

Mucosal administration of antigens in experimental animals leads to the induction of peripheral T cell tolerance. We have previously reported that in H-2b mice, intranasal (i.n.) or oral administration of a peptide containing the immunodominant T cell epitope will down-regulate the function of CD4+ T cells reactive with Der P 1, a major target antigen in both B and T cell responses to house dust mite. In the present study we have investigated the tolerogenicity of peptides containing both dominant and subdominant determinants when given i.n. to nalve mice. Induction of tolerance by the nasally administered immunodominant peptide leads to a diminution in all T cell-derived cytokines and modulation of delayed-type hypersensitivity responses, but IgE production did not seem to be affected, furthermore the induction of T cell tolerance was stable, lasting beyond 6 months. We have also examined the specificity of intramolecular epitope suppression which is a feature of mucosal tolerance induced by nasally administered peptides and demonstrate that regulatory CD4+ T cells may exert their suppressive effect by linked recognition of epitopes on the same or neighbouring antigen-presenting cells.