Dengue viruses induce cell proliferation and morphological changes of endothelial cells.

Replication of dengue viruses (type 1, 2, 3 and 4) in vitro in endothelial cells from human umbilical cord vein was demonstrated by virus titers and immunofluorescent antibody studies. Both showed highest peak at Day 6 after inoculation and declined to origin at Day 14. Some of the cultured endothelial cells detached from the culture well. Most of these floating cells were rarely viable as shown by failure in trypan blue exclusion whereas the adhering cells are mostly viable. More frequent and higher intensity of immunofluorescent positive cells were found in the detached cells as compared to adhering cells. The virus titers in the supernatant and in the adhering cell population were comparable, although floating cells were maximally 26.2% of the total cultured endothelial cells. Many floating cells and occasional adhering cells had numerous blebs on their surface. Endothelial cell proliferation was markedly increased after virus inoculation as compared with the control. Increased number of mitotic cells was also observed in the dengue virus-endothelial cell culture. Comparing among the four types, dengue type 4 induced highest peaks of cell proliferation and cell mitosis at Day 10 after inoculation. Dengue type 2 had the highest virus titers both in adhering cells and in supernatant at Day 6 as compared with other types.

Corroboración bioquímica del compromiso endotelial en la preeclampsia severa

En este estudio prospectivo de casos y controles se investigó si las concentraciones elevadas de fibronectina celular plasmática informadas previamente en mujeres preeclámpticas reflejan probablemente disfunción endotelial. Nosotros encontramos además mayores concentraciones plasmáticas materias de fibronectina celular, mayores niveles de factor de von Willerbrand, activador tisular del plasinógeno e inhibidor -1 del activador del plasinógeno en el plasma materno, ofreciendo una corrobación bioquímica de disfunción endotelial en la preeclampsia severa

Placenta humana chagásica: alteración estructural y citoquímica de vasos sanguíneos / Human chagasic placenta: structural and cytochemical changes of blood vessels

Diversos autores han demostrado que los vasos sanguíneos coronarios pueden tener alguna participación en la patogenia de las alteraciones cardíacas en la enfermedad de Chagas. El objetivo del presente trabajo fue detectar alteraciones estructurales y citoquímicas en vasos sanguíneos de placentas humanas a término mediante microscopía óptica y electrónica, considerando la posibilidad de su participación en la patogenia del pasaje transplacentario del agente causal del Chagas. En dos de seis placentas chagásicas provenientes de embarazadas a término con serologías positivas para enfermedad de Chagas, se halló estrechamiento u oclusión de vasos fetales de las vellosidades coriales con aspecto hialinizado de sus paredes mediante microscopía óptica y actividad de fosfatasa ácida aumentada en el endotelio vascular mediante ultracitoquímica. El estrechamiento de la luz vascular mediante ultracitoquímica. El estrechamiento de la luz vascular podría deberse a la participación del músculo liso y del endotelio.

Endothelial tissue pathological alterations demonstrated in mice naturally infected with sarcocystis

Comparative electron microscopical study showed a spectrum of cytopathological changes ranging from exudative to obstructive inflammation of the vascular endothelium in mice naturally infected with sarcocystis. The endothelial cells changes were characteristic of necrotizing vasculitis and ischemic injury indicating loss of metabolic integrity and impaired perfusion. Signs of chronic inflammation and reflecting macrophage-lymphocyte interaction were also, evident. The fact that the endothelial affection was not a consistent feature in all infected mice, indicates that such cytopathological alterations may often be temporary and repairable or more likely genetically predisposed

Endotelio e plaquetas na doenca vaso-oclusiva pulmonar / Endothelium and platelets in pulmonary vascular obstructive disease

A doenca vaso-oclusiva pulmonar e a resultante final de uma serie de alteracoes estruturais que ocorrem na parede dos vasos, sobretudo arteriais, habitualmente designadas por remodelagem vascular. Todos os elementos celulares, incluindo componentes da matriz extra-celular, estao direta ou indiretamente envolvidas no processo. Tem sido enfatizada a importancia fisiopatologica de mecanismos interativos envolvendo a parede vascular e elementos do sangue circulante. Estudos recentes, incluindo dados do nosso laboratorio, indicam a ocorrencia de importante alteracoes estruturais e funcionais das celulas endoteliais nesta sindrome. Paralelamente, tem sido cada vez mais ressaltado o papel das plaquetas, cujo envolvimento direto no processo vaso-oclusivo ja se encontra plenamente estabelecido. A presente revisao tem por objetivo discutir alteracoes estruturais e funcionais envolvendo celulas endoteliais e plaquetas na doenca vaso-oclusiva pulmonar, com enfase para os mecanismos interativos

So-called sclerosing hemangioma of the lung: two cases report with ultrastructural study

Sclerosing hemangiomas of the lung are benign neoplasms of uncertain histogenesis. We analysed two cases of sclerosing hemangiomas of the lung with histochemistry and electron microscopy. They had a variegated histologic appearance characterized by an admixture of solid, hemorrhagic, papillary and sclerotic lesions. Characteristic uniform round cells, unique to this tumor, were found within the stroma in all lesions. In the electron microscopic examination, we found Weibel-Palade bodies like small bodies in the tumor cells. We suspect hypothesis originating in the endothelial cell can not be completely excluded yet. Sclerosing hemangioma is a distinct clinicopathologic entity and should be distinguished from other benign neoplasms or inflammatory lesions of the lung.

Electron microscopy of the human brain in cerebral malaria.

Ultrastructure of erythrocytes infected with Plasmodium falciparum in human brain, obtained 3 hours post mortem revealed gross distortion of host red cells with abnormality of the red cell surface. The superficial alterations of the parasitized cells as knob-like protrusion appear to be the sites of attachment to vascular endothelium. There was evidence of platelets sticking to the injured endothelium. The endothelial vesicular membrane is in close adhesion to the parasitized red cell, and also to the platelets involved in this mechanism. Thus, explaining the sequestration of parasitized red cell and obstruction in cerebral microcirculation, cerebral oedema and low peripheral platelet count. The was no evidence of inflammation, fibrin or thrombus formation observed in our studies.

Electron microscopic study of the vascular endothelial cell in dengue hemorrhagic fever.

Electron microscopic studies were performed from skin biopsies taken from patients aged between 1-14 years suffering from dengue hemorrhagic fever. Several capillaries showed marked distortion, but severely damaged vessels were not observed in this study. In many cases, however, swelling of a single endothelial cell was noted. This was characterized by a rarefaction of the cytoplasm and formation of the plasma membrane which extruded into lumen and narrowed it. In many vessels examined, these blebs became detached from the endothelium and were found free within the capillary lumen. Myelin figures were often observed in such vessels. Mitochondria in the swollen endothelial cells often showed contraction of the inner compartments. Although, most of the endothelial junctional complexes were intact, several gap formations, in vascular wall were observed. Vacuolation of the cytoplasm and increase in the pinocytotic vesicles in endothelial cells which represented transport of plasma fluids from the capillary to the pericapillary space were quite evident. In no case did there seem to be marked alternation of the basement membrane of the capillary. The morphological alterations observed in this study only suggest the non-specific response of the dermal capillaries. These findings were similar to the findings observed in capillaries after being subjected to heat or ischemia.