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The mechanisms of the harmful cardiovascular effects of small particulate matter are incompletely understood. Endothelial progenitor cells (EPCs) predict outcome of patients with vascular disease. The aim of our study was to examine the effects of diesel exhaust particles (DEP) on EPC and on the associated vascular damage in mice. C57Bl/6 mice were exposed to DEP. 2 μg DEP/day was applicated intranasally for 3 weeks. Exposure to DEP reduced DiLDL/lectin positive EPC to 58.4 ± 5.6 % ( p < 0.005). Migratory capacity was reduced to 65.8 ± 3.9 % ( p < 0.0001). In ApoE mice, DEP application reduced the number of EPC to 75.6 ± 6.4 % ( p < 0.005) and EPC migration to 58.5 ± 6.8 % ( p < 0.005). Neoangiogenesis was reduced to 39.5 ± 14.6 % ( p < 0.005). Atherogenesis was profoundly increased by DEP treatment (157.7 ± 18.1 % vs. controls, p < 0.05). In cultured human EPC, DEP (0.1-100 μg/mL) reduced migratory capacity to 25 ± 2.6 % ( p < 0.001). The number of colony-forming units was reduced to 8.8 ± 0.9 % ( p < 0.001) and production of reactive oxygen species was elevated by DEP treatment ( p < 0.001). Furthermore, DEP treatment increased apoptosis of EPC (to 266 ± 62 % of control, p < 0.05). In a blood-brain barrier model, DEP treatment impaired endothelial cell integrity during oxygen-glucose deprivation ( p < 0.001). Diesel exhaust particles impair endothelial progenitor cell number and function in vivo and in vitro. The reduction in EPC was associated with impaired neoangiogenesis and a marked increase in atherosclerotic lesion formation. [ABSTRACT FROM AUTHOR]

The family of toll-like receptors (TLRs) plays a central role in the cutaneous immune defense system. To date, different TLRs have been found on several major cell populations of the skin, such as keratinocytes, fibroblasts, antigen-presenting cells, and melanocytes. Activation of TLRs leads, via different intracellular signaling pathways, to the production of proinflammatory stimuli, and is considered a danger signal that should transform the skin in to the functional state of defense. However, TLRs have also been implicated in tissue homeostasis and renewal. Within the group of TLRs, two types have been identified: surface-expressed TLRs, which are predominantly active against bacterial cell wall compounds; and intracellular receptors, which preferentially recognize virus-associated pattern molecules. In addition, surface-expressed receptors trigger phagocytotic and maturation signals, while the intracellular TLRs lead to the induction of antiviral genes. Our review aims to outline the importance of TLRs in the pathogenesis of numerous skin diseases and the potential of TLR agonists as a treatment option for various skin diseases. [ABSTRACT FROM AUTHOR]

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Copyright of Der Hautarzt is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Recently we demonstrated that lack of mecA transcription was responsible for the decreased methicillin resistance phenotype of strongly slime-negative Staphylococcus epidermidis phase variants [Mempel M, Feucht H, Ziehbuhr W, Endres M, Laufs R, Grüter L (1994) Antimicrob Agents Chemother 38:1251-1255]. In the present study we compared the beta-lactam susceptibility and the slime production capacity of 60 phenotypic variants of S. epidermidis parent strain RP62A identified by their colony morphology on congo red agar. We could show that the variable degree of slime production is linked to different levels of β-lactam susceptibility in intermediate-stage phase variants. The increased deltahemolysin production of slime-negative phase variants may indicate an accessory gene regulator-like control. [ABSTRACT FROM AUTHOR]

Copyright of Der Hautarzt is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The article discusses the formation of an abdominal postoperative pyoderma gangrenosum (PPG), a rare and rapidly developing complication of surgical procedures, following a laparoscopic sigmoidectomy. It cites the case of a 39-year-old patient with a progressive ulceration at the lower abdomen that occurred after a laparoscopic sigmoid resection. Moreover, it examines the diagnosis of PPG.

Copyright of Der Hautarzt is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)