Wall enhancement in MR vessel wall imaging is associated with inflammatory cell invasion, neovascularization, and the presence of vasa vasorum. Enhancement does not occur when histologic signs of inflammation are absent. Our results support the hypothesis that MR vessel wall imaging could provide valuable information for risk stratification.

Purpose Circumferential enhancement on MR vessel wall imaging has been proposed as a biomarker of a higher risk of rupture in intracranial aneurysms. Focal enhancement is frequently encountered in unruptured aneurysms, but its implication for risk stratification and patient management remains unclear. This study investigates the association of focal wall enhancement with hemodynamic and morphological risk factors and histologic markers of wall inflammation and degeneration. Methods Patients with an unruptured middle cerebral artery aneurysm who underwent 3D rotational angiography and 3T MR vessel wall imaging showing focal wall enhancement were included. Hemodynamic parameters were calculated based on flow simulations and compared between enhanced regions and the entire aneurysm surface. Morphological parameters were semiautomatically extracted and quantitatively associated with wall enhancement. Histological analysis included detection of vasa vasorum, CD34, and myeloperoxidase staining in a subset of patients. Results Twenty-two aneurysms were analyzed. Enhanced regions were significantly associated with lower AWSS, lower maxOSI, and increased LSA. In multivariate analysis, higher ellipticity index was an independent predictor of wall enhancement. Histologic signs of inflammation and degeneration and higher PHASES score were significantly associated with focal enhancement. Conclusion Focal wall enhancement is colocalized with hemodynamic factors that have been related to a higher rupture risk. It is correlated with morphological factors linked to rupture risk, higher PHASES score, and histologic markers of wall destabilization. The results support the hypothesis that focal enhancement could serve as a surrogate marker for aneurysm instability.

Papillomaviruses cause certain forms of human cancers, most notably carcinomas of the uterine cervix. In contrast to the well-established involvement of papillomavirus infection in the etiology of cervical carcinomas and in carcinomas of a rare hereditary condition, epidermodysplasia verruciformis, a causative role for cutaneous human papillomavirus types in the development of nonmelanoma skin cancer has not been proven. In order to better understand the functions of individual genes of cutaneous papillomavirus types, we generated transgenic mice carrying oncogene E6 of the Mastomys natalensis papillomavirus (MnPV), which causes keratoacanthomas of the skin in its natural host. In the present study, we demonstrate that under conditions of experimental two-stage skin carcinogenesis, fast-paced squamous cell carcinomas develop in nearly 100% of MnPV E6 transgenic mice in comparison to 10% in their nontransgenic littermates (log rank test; P < 0.0001). Therefore, we conclude that the MnPV E6 transgene favors the malignant progression of chemically induced tumors. Whereas an activating H-ras mutation is a consistent feature in benign and malignant tumors in wild-type mice, the majority of papillomas and keratoacanthomas and all squamous cell carcinomas obtained in MnPV E6 transgenic mice contain nonmutated ras alleles. These results indicate that the development of squamous cell carcinomas in MnPV E6 transgenic mice does not depend on an activated H-ras oncogene.Papillomaviruses are widely known to play a causative role in the development of tumors in humans. Certain genotypes cause mostly benign epidermal tumors in humans and animals. Another subgroup of genotypes, the so-called "high-risk" anogenital human papillomavirus (HPV) types, are causally involved in the development of malignant tumors, such as carcinoma of the cervix (17, 47, 49). The carcinogenic potential was first detected in 1935, when Rous and Bernard showed that inoculation into domestic rabbits of the filterable extracts from warts of cottontail rabbits was able to induce skin carcinomas (37). A direct involvement of cutaneous HPV types in the development of squamous cell carcinomas, one of the most frequent malignancies in humans of Caucasian origin, is suspected but still not proven (7, 34). The earliest hints of an involvement of specific HPV types in human skin cancer originated from studies of patients suffering from the very rare hereditary disease epidermodysplasia verruciformis (EV) (32,21). Only a limited number of HPV types, commonly referred to as EV-HPV types, such as HPV5, -8, and -14, are frequently detected in squamous cell carcinomas that develop in ϳ30% of cases within multiple flat warts in sun-exposed areas of the skin in such patients (25). More recent data suggested a role for EV-related papillomaviruses in the origin of skin cancer in immunosuppressed patients (39) and those with renal transplants (28). Thus, specific high-risk cutaneous HPV types comparable to carcinogenic anogenital HPV types have not been identified (48,49)...

Sulfatides are quantitatively prominent glycosphingolipids of rat kidney. In order to gain insight into their possible physiological significance in this organ, and their possible role in Heymann's nephritis, the main sulfatide components were localized immunohistochemically. The antibodies used recognized the sulfatides Sgal1, Stri1, Stri2, and Stet2a. Stri1 epitopes were expressed in the brush border of proximal tubuli, whereas Stri2-specific immuno staining was observed in cortical and medullar collecting ducts. Both Stri1 and Stri2 were also expressed by interstitial cells of the inner medulla. Stet2a was visualized in epithelia of the distal tubules of Henle's loop and the juxtaglomerular apparatus, including the macula densa. The mAb Sulph-I, that recognizes the SO3(-)-3Galbeta