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Notes: Metamorphic field gradients were determined across the entire amphibolite grade Central Alps (c. 50×100 km). P–T  were calculated from 116 samples acquired from our own field work, from samples provided to us by others, and from rocks with mineral compositions described in the literature. Only fluid-conserved equilibria were used to determine P–T . The use of an internally consistent thermodynamic database and mineral solid solution models makes the results robust and reduces relative errors. The results are presented in contour maps. Temperature increases from 500 to 550 °C along the limit of amphibolite grade metamorphism in the north and west, to c. 675 °C toward the south at the Insubric line near the town of Bellinzona. Maximum recorded pressures of c. 7 kbar are in a central region c. 20 km north of the Insubric line, and decrease both to the north (5.5 kbar) and south (4.5 kbar). The P–T  results indicate that there is a relatively large area that reached conditions in the sillimanite stability field but developed neither sillimanite nor fibrolite; this is interpreted as a result of kinetic constraints on nucleation and growth because of the small amounts of thermal overstep (〈40 °C) of the kyanite-sillimanite phase boundary. Comparison of P–T  conditions with carbonate isograds in the region indicate that fluids present during metamorphism were not dominated by a homogeneous external source. Examination of the two-dimensional distribution of pressure and temperature in the context of thermal and tectonic models indicates that two thermal pulses affected the Central Alps during the Tertiary. In the second, heat affected only the southern parts of the area and overprinted the previously established P–T  gradients.

Notes: Objective: To review the human and veterinary literature on the role of the vascular endothelial cell in health, as well as during hypoxic and inflammatory disease states.Data sources: Data from human and veterinary literature were reviewed through a Pubmed search and a manual search of the references listed in articles covering some aspect of vascular endothelial cell function.Human data synthesis: The development of techniques that allow the maintenance and growth of endothelial cells in culture has produced an explosion of new research in the area of endothelial cell physiology. This plethora of data has revealed the critical role that vascular endothelial cells play in both health and disease states. Interspecies variations can occur with respect to the vascular endothelial cell physiology and its response to pathologic conditions.Veterinary data synthesis: There is a paucity of information regarding the role of the vascular endothelial cell in health or disease of small animals. Many human studies use species cared for by veterinarians, providing information that may be applied to small animals and that may be used to construct future studies.Conclusion: An organ system itself, the vascular endothelium is an essential component of all organs in the body. The endothelial cell lining functions to maintain selective permeability between the blood and the tissue it supplies, regulate vascular tone, sustain blood fluidity through regulation of coagulation, and modulate interaction of leukocytes with the interstitium and inflammatory reactions. During disease states, the endothelial cell functions locally to limit the boundaries of the disease process. If these functions are not controlled, they can become a part of the pathogenic process, contributing to blood stasis and thrombosis, potentiation of local inflammation and interstitial edema formation, subsequent tissue hypoxia, and multiple organ dysfunction. Pharmacological investigations targeting the modulation of endothelial function during disease states have not yet advanced treatment protocols. Since all critically ill animals are at risk for some degree of endothelial cell dysfunction, treatment regimens should focus on promoting capillary blood flow and tissue oxygen delivery.

Notes: The reliability, rapidity, and safety of nonsurgical, transatrial pericardial access for local cardiac therapy have been demonstrated in healthy animals. Since many patients take aspirin or have increased right-sided pressures, we evaluated the procedure's safety under these conditions. Transatrial pericardial access was performed in anesthetized pigs following aspirin administration (162 mg po, n = 6) or during experimental pulmonary artery hypertension (n = 4 different animals) and required only 3 minutes following guide catheter positioning. Platelet aggregability testing with arachidonic acid confirmed aspirin effectiveness. Mean pericardial fluid hematocrit was 0.1 ± 0.1% after 2 days of aspirin therapy and 1.9 ± 1.1% at sacrifice 24 hours later (NS). Mean pericardial fluid hematocrit was 1.0 ± 0.5% after 45 minutes of pulmonary artery hypertension and 4.3 ± 0.8% at sacrifice 30 minutes later (NS). Histologic analysis in both groups revealed a small thrombus and localized inflammation at the site of puncture. Neither aspirin use nor pulmonary artery hypertension causes significant bleeding into the pericardial space following transatrial access and thus does not preclude this route for local cardiac drug delivery.

Notes: Protein kinase C (PKC) isozymes transduce signals from cell surface receptors and thereby regulate important cellular functions in skin including keratinocyte growth and differentiation. Overexpression of individual PKC isozymes results in aberrant cell growth and in certain instances tumorigenicity. PKC is implicated in tumour promotion in mouse skin. Abnormal expression of PKC has been reported in several human cancers. We have, therefore, investigated expression of PKC-α and -β in basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) by immunohistochemistry. Sections were stained with specific antibodies to PKC-α, PKC-β, CDla, T cells, B cells and dermal dendritic cells (factor XIIIa), using an immunoperoxidase technique, PKC-α and PKC-β were not detected in tumour cells in BCCs or SCCs. In SCCs, PKC-β immunostaining revealed positively stained inflammatory and dendritic cells scattered through the stroma: PKC-α immunostaining was essentially negative. In contrast, in BCCs, PKC-α+ and PKC-β+ dendritic and spindle-shaped cells were observed in the stroma, immediately adjacent to the tumour islands. Double-labelling experiments showed that a proportion (approximately 20%) of PKC-β+ dendritic cells also expressed factor XIIIa. BCCs depend on stroma for growth: PKC regulates expression of type IV collagenase and stromelysis III and interactions between tumour and stroma may be important in determining tumour invasion and metastasis, Therefore, overexpression of PKC-α and -β by stromal dendritic cells in BCCs suggests that PKC activation may be involved in stromal/tumour interactions in these tumours.