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.
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.
Chacin-Bonilla L.,University of Zulia
Revista Medica de Chile | Year: 2013
The description of Entamoeba dispar, and the recovery of Entamoeba moshkovskii from humans had a major impact in the epidemiology and clinical management of amebiasis. Infections range from asymptomatic colonization to hemorrhagic colitis and extra-intestinal diseases. Only a minority of amebiasis patients progress to the development of disease. Recent studies suggest that susceptibility to infection, and its outcome is influenced by the host, parasite genotype, and environment. The identification of Entamoeba histolytica is based on the detection of specific antigens by ELISA and DNA in stool and other clinical samples. Several diagnostic tests have been developed, including polymerase chain reaction, the technique of choice, for the detection and differentiation of E. histolytica, E. dispar, and E. moshkovskii. Combination of serologic tests with detection of the parasite DNA by PCR or antigen by ELISA offers the best approach to diagnosis. However, these techniques are impractical for clinical laboratories of developing countries. Clinicians must follow the guidelines of the World Health Organization to avoid unnecessary treatments. This review describes and discusses recent advances in amebiasis with emphasis in the clinical aspects and management of infection.
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.
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.
Castejon O.J.,University of Zulia
Folia Neuropathologica | Year: 2012
Cortical biopsies of patients with the diagnosis of complicated brain trauma, congenital hydrocephalus, brain vascular anomaly, and brain tumour are studied with the electron microscope using cortical biopsies of different cortical brain regions to analyze the alterations of endothelial junctions, and their participation in the pathogenesis of human brain oedema. In moderate oedema, most endothelial tight junctions are structurally closed and intact, while in some cases of severe oedema, the opening of tight endothelial junctions is observed. In very severe brain oedema, a considerable enlargement of interjunctional pockets of extracellular space is also seen suggesting that in highly increased cerebrovascular permeability, the endothelial junctions are open in their entire extent, and that an intercellular or paracellular route through interendothelial clefts for transferring haematogenous oedema fluid from blood to the capillary basement membrane and the brain parenchyma is formed, contributing to the formation of brain oedema. High intensity brain trauma, seizures, osmotic forces, hypoxic conditions, and alteration of tight junctions proteins would explain the opening of endothelial junctions in severe and complicated brain oedema. In congenital hydrocephalus, the capillary wall shows evident signs of blood-brain barrier dysfunction characterized by closed and open interendothelial junctions, increased endothelial vesicular and vacuolar transport, thin and fragmented basement membrane with areas of focal thickening, and discontinuous perivascular astrocytic end-feet. The perivascular space is notably dilated and widely communicated with the enlarged extracellular space in the neuropil, showing the contribution of damaged endothelial junction to the formation of interstitial or hydrocephalic brain oedema. Altered expression of tight junction proteins could cause a blood-brain barrier breakdown following brain injury and hypoxic conditions leading to brain oedema. The results are compared with those found in experimental brain oedema. Some controversial results are also described.
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.
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.
Arismendi-Morillo G.,University of Zulia
Biochimica et Biophysica Acta - Bioenergetics | Year: 2011
Gliomas still represent a serious and discouraging brain tumor; despite of the diversity of therapeutic modalities, the prognosis for patients is still poor. Understanding the structural and functional characteristics of the vascular microenvironment in gliomas is essential for the design of future therapeutic strategies. This review describes and analyzes the electron microscopy morphology of the mitochondrial network in human gliomas and their vascular microenvironment. Heterogeneous mitochondrial network alterations in glioma cells and in microvascular environment are implicated directly and indirectly in the processes linked to hypoxia-tolerant and hypoxia-sensitive cells phenotype, effects of the hypoxia-inducible factor-1α, increased expression of several glycolytic protein isoforms as well as fatty acid synthase, and survivin. The prevalent existence of partial or total cristolysis observed suggests that oxidative phosphorylation is severely compromised. A mixed therapy emerged as the most appropriate. This article is part of a Special Issue entitled: Bioenergetics of Cancer. © 2010 Elsevier B.V. All rights reserved.
Cabrera F M.I.,University of Zulia
Ecological Modelling | Year: 2011
Our understanding of predator-prey systems has progressed in recent decades mainly due to the ability to test models in chemostats. This study aimed to develop a deterministic model using differential equations to reproduce the dynamics of the interaction of a predator and a prey in a two stage chemostat focusing in the proposed previous prey dependent model of Fussmann et al. (2000) [Fussmann, G.F., Ellner, S.P., Shertzer, K.W., Hairston Jr., N.G., 2000. Crossing the Hopf bifurcation in a live predator-prey system. Science 290, 1358-1360]. The main problem with that model, but parameterized with the values obtained in this study (particularly the concentration of nutrient), was that the temporal trajectory of both the prey and the predator showed very high peaks that eventually led to the extinction of predator in all cases. In the same way the experimental time series obtained in this study does not exhibit the behavior predicted by the model of Fussman et al. On the contrary, as prey density increases, the system actually becomes more stable. Finally, the model that best explained the behavior of the predator and prey in the chemostat, at medium to high dilution rates, was the ratio dependent (algae-nitrogen) model with mutual interference measured in the chemostat (rotifer-alga) and that incorporated the age structure of the predator. Qualitative analysis of the dynamic behavior enabled evaluation of coexistence at equilibrium, coexistence on limit cycles, extinction of the predator or extinction of both populations. © 2010 Elsevier B.V.
Maestre G.E.,University of Zulia |
Maestre G.E.,Columbia University
Current Neurology and Neuroscience Reports | Year: 2012
The numbers and proportions of elderly are increasing rapidly in developing countries, where prevalence of dementia is often high. Providing cost-effective services for dementia sufferers and their caregivers in these resourcepoor regions poses numerous challenges; developing resources for diagnosis must be the first step. Capacity building for diagnosis involves training and education of healthcare providers, as well as the general public, development of infrastructure, and resolution of economic and ethical issues. Recent progress in some low-to-middle-income countries (LMICs) provides evidence that partnerships between wealthy and resource-poor countries, and between developing countries, can improve diagnostic capabilities. Without the involvement of the mental health community of developed countries in such capacity-building programs, dementia in the developing world is a disaster waiting to happen. © Springer Science+Business Media, LLC 2012.