[Time-related expression of adhesive proteins and other markers of age of injuries]. / K casovým relacím exprese adhezivních bílkovin a dalsích markeru stárí poranení.

UNLABELLED: In addition to evidence of the vital reaction it is important from the forensic aspect to assess the age of wounds, in particular in wounds with a short time of survival. To both can contribute detection of adhesive molecules, identified in recent years, possibly in combination with other markers of early stages of reparative inflammation. The submitted paper comprises the results of investigation of 465 skin wounds. The investigated samples were obtained from necroptic material, excision from wounds of treated patients and from experimental injuries in mice. Assessment of the age of injuries by means of endothelial adhesive molecules was made in paraffin sections after transfer into Varioclave and using the ABC techniqueref.. In human material a strong positive reaction of ICAM-1 was observed first after 1 and a half hours and latest after 3 and a half days, in P-selectin first after 3 mins., latest after 7 hours, in E-selectin first after 1 hour and latest after 17 days, in VCAM-1 first after 3 hours and latest 3 and a half days after the development of the injury. Expression of L-selectin was not typical for the injury. In skin injuries of mice positive immunohistochemical reactions were found as a rule sooner than in skin injuries of humans. Fibronectin was detected in paraffin sections from 70 skin wounds of dissected subjects immunohistochemically by the indirect immunoperoxidase reaction and by the use of the ABC technique labelled with alkaline phosphatase. Positive evidence was observed first after 5 minutes and latest after 8 hours. CONCLUSION: Detection of a rise of expression of ICAM-1, VCAM-1 and P- and E. selectin and the formation of basic netlike fibronectin structures improves the assessment of the age of wounds with a short survival period.

DNA adducts and human atherosclerotic lesions.

It has been hypothesized that mutational events may be involved in the atherogenetic process and that at least a portion of atherosclerotic plaques may be the results of monoclonal proliferation of a single mutated smooth muscle cell (SMC). Therefore, atherosclerosis may be similar to carcinogenesis and may have an environmental etiology. We have analyzed bulky-aromatic DNA adducts in human thoracic aortas from male subjects, aged between 30-60 years, who died suddenly or accidentally, and who had been examined by autopsy within 24 h after death. We found significantly (P < 0.001) higher DNA adduct levels in the samples from subjects with frequent atherosclerotic changes in the whole body ("Cases", N = 76) compared with those having few atherosclerotic changes ("Controls", N = 57). We also observed a significantly elevated weight of heart and plasma levels of total and LDL cholesterol in "Cases" vs "Controls". Significant differences in DNA adduct levels between smokers and nonsmokers were observed in "Controls" only. Multivariate linear regression analyses with age-adjusted data confirmed a significant influence of LDL cholesterol (P < 0.001), vitamin A (P < 0.01), smoking behavior (P < 0.05; evaluated as plasma cotinine levels) and NAT2 genotypes (P < 0.05) on bulky-aromatic DNA adduct levels. The induction of DNA adducts suggests that alterations at the DNA level may contribute to the development of atherosclerosis. Furthermore, atherogenesis and carcinogenesis may share a similar etiology, i.e. genotoxic action of environmental chemicals.