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Preeclampsia (PE) is a hypertensive complication of pregnancy. Its cause is still unknown and it could be a risk factor for future ophthalmic problems. Retinal vascular bed alterations have been described as a consequence of PE, suggesting a retinopathy. Factors related to angiogenesis and vascular permeability, such as vascular endothelial growth factor (VEGF) and pigment epithelium derived factor (PEDF) or components of the renin angiotensin aldosterone system (RAAS), prorrenin/renin receptor ((P)RR) and angiotensin II type I receptor (AT1R) have been located in the retina, participating in other retinopathies, but it is unknown if they could participate in PE. Our aim was to elucidate whether VEGF, PEDF, (P)RR and AT1R could be modified during PE and during hypertension induced in rats with a history of PE. We used female Wistar rats and subrrenal aortic coarctation to induce PE, and after delivery, we induced a second hit by Nω-nitro-L-arginine methyl ester (L-NAME) administration. We measured blood pressure, proteinuria and pups development. In both models, eye fundal exploration and immunoblot for VEGF, PEDF, (P)RR and AT1R were performed. We found that the development of hypertension occurred faster in previously PE rats than in normal animals. VEGF, PEDF, (P)RR and AT1R were increased in PE, but in L-NAME-induced hypertension only (P)RR and AT1R were altered. Eye fundal data indicated that PE induced a level I retinopathy, but L-NAME induced a faster and more severe retinopathy in previously PE animals compared to previously normal pregnancy rats. These results indicate that PE predisposes to development of a faster and more severe retinopathy after a second hit. They also suggest that VEGF and PEDF seem to participate only in PE retinopathy, but in both models, RAAS components seem to have a more critical participation.

Craniopharyngiomas (CPs) are cystic, encapsulated, slow-growing epithelial tumors. CPs can be aggressive forms invading and resorting surrounding structures of adjacent brain tissue, where Rosenthal fibers (RFs) are expressed. The aim of this study was to investigate the ultrastructure of these fibers in human biopsies and compare it with an experimental toxic model produced by the cortical infusion of the oil cyst fluid ("Oil machinery" fluid or OMF) from CPs to rats. For this purpose, the CPs from ten patients were examined by light and electron microscopy. OMF was administered to rats intracortically. Immunohistochemical detection of glial fibrillary acidic protein (GFAP) and vimentin was assessed. In both freshly obtained CPs and rat brain tissue, the presence of abundant cellular debris, lipid-laden macrophages, reactive gliosis, inflammation and extracellular matrix destruction were seen. Ultrastructural results suggest focal pathological disturbances and an altered microenvironment surrounding the tumor-brain junction, with an enhanced presence of RFs in human tumors. In contrast, in the rat brain different degrees of cellular disorganization with aberrant filament-filament interactions and protein aggregation were seen, although RFs were absent. Our immunohistochemical findings in CPs also revealed an enhanced expression of GFAP and vimentin in RFs at the peripheral, but not at the central (body) level. Through these findings we hypothesize that the continuous OMF release at the CPs boundary may cause tissue alterations, including damaging of the extracellular matrix, and possibly contributing to RFs formation, a condition that was not possible to reproduce in the experimental model. The presence of RFs at the CPs boundary might be considered as a major criterion for the degree of CPs invasiveness to normal tissue. The lack of RFs reactivity in the experimental model reveals that the invasive component of CPs is not present in the OMF, although the fluid per se can exert tissue damage.

NADPH-diaphorase activity has been considered as a nitric oxide synthase (NOS) marker. Therefore, the presence of NADPH-d activity in Entamoeba histolytica suggests that they have NOS activity. The aim of this work was to provide support for this contention. The amebic culture medium or amebic purified proteins induced relaxation of endothelium-denuded rat aortic rings pre-contracted with phenylephrine (10(-6) M), which was inhibited when the amebas were incubated with NG-monomethyl-L-arginine or aminoguanidine (NOS inhibitors), or by pretreatment of the aortic rings with methylene blue. L-Arginine reverted the L-NAME inhibitory effect. In addition, trophozoites produce NO in culture and they have proteins which were recognized by antibodies specific to NOS and show activity of NO synthase. In conclusion, our results provide evidence about the production of NO by trophozoites. This molecule may be responsible for the relaxation elicited by the amebic culture medium and may participate in the pathogenesis of the invasive amebiasis. Index Descriptors and Abbreviations: Entamoeba histolytica; NO, nitric oxide; NOS, nitric oxide synthase; iNOS, inducible nitric oxide synthase; ecNOS, endothelial nitric oxide synthase; NADPH-d, NADPH-diaphorase enzyme; beta-NADPH, beta-nicotinamide-adenine dinucleotide; L-NAME, N-omega-nitro-L-arginine methyl ester hydrochloride; NBT, nitobluetetrazolium; PBS, phosphate-buffered saline; EDTA, ethylenediaminetetraacetic acid; SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis