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San Carlos del Zulia, Venezuela

The University of Zulia , is a public university whose main campus is located in the city of Maracaibo, Venezuela. LUZ is one of the largest and most important universities of Venezuela.The University of Zulia has three campuses: two in Zulia State, in the cities of Maracaibo and Cabimas; and one in the city of Punto Fijo, located in Falcón State) Wikipedia.


Castejon O.J.,University of Zulia
Folia Neuropathologica | Year: 2013

The endothelial vacuolar and vesicular transports in traumatic human brain oedema have been reviewed and compared with experimental brain oedema in order to establish their role in both oedema formation and oedema resolution. Normal or "non-activated" and "activated" capillaries are found. The activated capillaries showed predominantly an enhanced abluminally orientated vesicular transport by means of small, medium and large uncoated and clathrin coated vesicles, as well as the presence of endothelial tubular structures. Activation of the endothelial nuclear zone is featured by the increased amount of micropinocytotic vesicles. Vesicles internalizing to the hypertrophic Golgi complex, lysosomes and multivesicular bodies are observed. The protein vacuolar transport is predominant in most cortical capillaries. A wide spectrum of endothelial cell mechanisms is observed increasing the vesicular and vacuolar transport, such as deep invaginations of the luminal surface, large coated vesicles, tubular structures, and transient and incomplete transendothelial channels formed either by chained plasmalemmal vesicles or elongated protein-containing vacuoles. Uncoated vesicles are seen surrounding lysosomes. Vesicular transport might be discriminated between abluminally orientated or transendothelial transport (oedema formation) and intraendothelial transport (oedema resolution) directed towards cell lysosomes to be degraded by lysosomal enzymes. The transendothelial passage via large vacuoles is mainly caused by macromolecular protein transport. Source


Chacin-Bonilla L.,University of Zulia
Acta Tropica | Year: 2010

Cyclospora cayetanensis is an intestinal coccidian protozoon that has emerged as an important cause of endemic or epidemic diarrhoeal illness in children and adults worldwide. Humans appear to be the only natural hosts. However, the role of animals as natural reservoirs is uncertain but of increasing concern. Human-to-human spread of the parasite occurs indirectly via the environment through oocysts in contaminated water, food or soil. In endemic areas, risk factors associated with the infection include contaminated water or food, contact with soil or animals, type of sanitation and low socioeconomic status. Infections linked to soil contact provide reasons to believe that this route of spread may be more common than realised in disadvantaged community settings. C. cayetanensis is an important cause of traveller's diarrhoea and numerous large foodborne outbreaks associated with the globalisation of the food supply and importation of fruits and vegetables from developing countries have occurred. Waterborne outbreaks have also been reported. Implementation of measures to prevent or control the spread of Cyclospora oocysts in the environment is critical. In endemic areas, the most important steps to prevent infection are improving environmental sanitation and health education. Significant gaps remain in our understanding of the epidemiology of human cyclosporiasis that highlight the need for continued research in several aspects of C. cayetanensis. © 2010 Elsevier B.V. Source


Rodriguez-Iturbe B.,University of Zulia
Clinical and Experimental Nephrology | Year: 2010

This review examines the participation of immunocompetent cells that accumulate in tubulointerstitial areas of the kidney in the pathogenesis of sodium-sensitive hypertension. Tubulointerstitial inflammation is a universal feature in experimental models of sodium-sensitive hypertension, and the suppression of inflammation and its constant companions, oxidative stress and renal angiotensin II activity, ameliorates or prevents hypertension. Human studies also support the association between renal inflammation and hypertension. The proinflammatory effects of a high sodium diet and the mechanisms by which renal inflammation induces sodium retention are discussed. It is suggested that autoimmune reactivity may play a role in the development and maintenance of renal inflammation in hypertensive states. © 2010 Japanese Society of Nephrology. Source


Castejon O.J.,University of Zulia
Folia Neuropathologica | Year: 2011

In human traumatic brain oedema pericytes exhibit remarkable oedematous changes, increased vacuolar and vesicular transport, transient transpericytal channels, and tubular structures demonstrating pericyte brain barrier dysfunction. They show nuclear invaginations, actin and myosin-like filaments, and coupled interaction with endothelial cells through the macula occludens. Some pericytes display hypertrophic and necrotic changes, and phagocytic capacity. Hypertrophic pericytes induce basement membrane splitting. Degenerated pericytes exhibit lacunar enlargement of endoplasmic reticulum, dense osmiophilic bodies, glycogen granules, vacuolization, oedematous Golgi apparatus, and pleomorphic mitochondria. Certain micropinocytotic vesicles are orientated to the Golgi complex and multivesicular bodies, suggesting that pericytes play some role in oedema resolution. Source


Castejon O.J.,University of Zulia
Folia Neuropathologica | Year: 2014

The capillary basement membranes are examined in severe traumatic brain injuries, vascular malformation, congenital hydrocephalus and brain tumours. They exhibit homogeneous and nodular thickening, vacuolization, rarefaction, reduplication, and deposition of collagen fibers. Their average thickness varied according to the aetiology and severity of brain oedema. In moderate brain oedema the thickness ranged from 71.97 to 191.90 nm in width, and in patients with severe brain oedema it varied from 206.66 to 404.22 nm. The basement membrane complex appears apparently intact in moderate oedema, and shows glio-basal dissociation in severe oedema. In areas of highly increased cerebro-vascular permeability, the basement membrane shows matrix disorganization, reduplication, and bifurcations protruding toward the endothelial cells, and acting as abluminal transcapillary channels. In regions of total brain necrosis, its structural stability is lost showing loosening, dissolution and rupture. Basement membrane swelling is due to overhydration of its protein-complex glycoprotein matrix. The thickening, rarefaction and vacuolization are induced by the increased vacuolar and vesicular transendothelial transport. The degenerated basement membrane areas exhibit a finely granular precipitate interpreted as protein, proteoglycan, glycoprotein, and agrin degraded matrix. Source

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