INMUNOHEMATOLOGIA BASICA PDF

Daignóstico en inmunohematología. 1. Daignóstico en Inmunohematología Por Bárbara Avello Vega; 2. Principio Base; 3. Pruebas básicas. Laboratorio de Inmunohematología, Academia Nacional de Medicina, Departamento de Ciencias Básicas-Microbiología, Universidad de Luján, Luján, Prov. Check out my latest presentation built on , where anyone can create & share professional presentations, websites and photo albums in minutes.

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BoxTalca, Chile. It is currently accepted that, in the atherogenic process, platelets play an important role, contributing to endothelial activation and modulation of the inflammatory phenomenon, promoting the beginning and formation of lesions and their subsequent thrombotic complications. These results suggest that platelets participate in atheromatous process from early stages to advance d stages.

High fat diet induces adhesion of platelets to endothelial cells in vivo. These findings support studying the participation of platelets in the formation of atheromatous plate. Cardiovascular diseases Basicca are the leading cause of death among adult population in most countries [ 1 ], in which the most common cause is the atheroma formation in arteries [ 2 ].

Atherosclerosis is a disease of multifactorial etiology and it is triggered by systemic and local factors, which finally cause vascular dysfunction. Hypercholesterolemia and especially high concentrations of low density lipoproteins LDL are a significant risk factor for premature appearance of atherosclerosis and ischemic heart disease [ 3 ]. A number of different cellular components perform an inmunogematologia role in the pathogenesis of atherosclerosis.

It is well established that endothelial cells, as well as intimal smooth muscle cells, are involved [ 4 ]. On the other hand, monocytes and macrophages are crucial in early stages [ 5 ]. Currently, there are reports which accept that platelets play a crucial role in plaque formation [ 6 ]. Over the last years, it has been demonstrated that platelets participate not only in thrombotic complications of atheromatous lesion, but also in the initiation and progression of the plaque [ 7 ], contributing to the inmunohematoloyia activation and modulation of inflammatory process, which favor the initiation and formation of atheromatous lesions and their subsequent thrombotic complications [ 8 ].

Predominant involvement of platelets in atherosclerotic lesion formation occurs through endothelial activation [ 9 ]. Platelet adhesion to endothelial surface generates basifa that recruit monocytes to sites of inflammation [ 10 ], inducing a proatherogenic phenotype characterized by a major adhesion, chemotaxis, and proteolytic activity [ 1112 ].

The study of the atherosclerotic process in animals is complex with a multifactorial mechanism; however, the use of high fat diets in mice is a widely used strategy. A diet rich in fat contributes to early atherosclerotic lesion development, as foam cell formation was observed at week 10, intermediate lesions with foam cell content and smooth muscle cells at week 15, and fibrous plaques development at week 20 [ 15 ].

The first group was fed a fat diet FD and the inmunohematolofia group a normal diet NDusing Champion mouse food, for a period of 40 days [ 13 ]. Badica used for experimentation were maintained in standard environmental conditions: All protocols and procedures were approved by the Bioethics Committee from Universidad de Talca.

They were subjected to inmunohematoloiga retrieval with sodium citrate buffer 0. Then, a nuclear contrast was done with Harris haematoxylin and samples were assembled in a resinous medium. The results are presented as average and standard error of the mean SEM. First, we prepared diets supplemented with fat.

Inmunohematklogia, we tested high fat diet in CF1 mice inmnohematologia induce metabolic alterations and endothelial dysfunction [ 13 ]. A conserved histoarchitecture is inmunohematologai but atherosclerotic lesions are not observed. Image c shows conserved histoarchitecture and immunostaining absence.

Image d shows conserved histoarchitecture and moderate immunostaining of endothelial surface. Image e presents conserved histoarchitecture and immunostaining absence and image f shows conserved histoarchitecture and moderate immunostaining of endothelial surface. Image g presents conserved histoarchitecture and immunostaining absence. Image h shows conserved histoarchitecture and moderate immunostaining of endothelial surface.

In image a a conserved histoarchitecture is observed, with no apparent lesions. In Figure 2 inmujohematologia histoarchitecture distortion is observed, characterized inmunohematolotia irregular thickening of the intima layer, partially detached, with apparently fibrous foci and optically empty spaces. Panels c and d correspond to Masson’s trichrome staining, 10x magnification. Image c shows conserved histoarchitecture with no apparent lesions.

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Image d highlights collagenous fibrosis foci and histoarchitectural distortion. A conserved histoarchitecture and immunostaining absence were observed. Images f and g correspond to histological sections stained with immunohistochemical technique for platelets, 10x and 40x magnification.

A histoarchitecture distortion focus was inmunohematooogia characterized by irregular thickening of the intima layer, inmunohematoloiga detached, with apparently fibrous foci and optically empty spaces.

High Fat Diet Induces Adhesion of Platelets to Endothelium in Two Models of Dyslipidemia

It highlights moderate immunostaining of endothelial surface and granular in lesion thickness. A conserved histoarchitecture and inmunohrmatologia absence are observed. Images i and j correspond to histological sections stained with immunohistochemical technique for Baisca, 10x and 40x magnification. Figures 2 i and 2 j highlights moderate immunostaining at endothelial level.

Histoarchitecture distortion is observed characterized by irregular thickening of the intima layer, partially detached, with apparently fibrous foci and optically empty spaces. It highlights intense granular immunostaining in lesion thickness and adjacent to optically empty spaces lipid core.

CVD are the main cause of morbi-mortality in most occidental countries. In ischaemic CVD, atheromatous plate formation is a critical point; so, the physiopathology knowledge of this disease is very important.

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In this sense, the standardization of animal models developing different stages of atherothrombotic process, as well as the use of techniques which allow visualizing these changes, is of great help to increase the knowledge of the complex process of atherogenesis.

This allows having a global vision of the main actors in different stages of atherothrombosis physiopathology. A model of CF-1 mice fed with FD that develops metabolic alterations like MS [ 13 ] was used for the study of the initial stage of atherosclerotic process, with primary stages of endothelial dysfunction.

In physiological conditions, endothelium presents a surface with antithrombogenic properties [ 17 ] through which the exchange of numerous substances between blood and tissues is produced; it controls the vascular tone and the transit of inflammatory cells towards vascular wall.

An early stage of atherosclerotic process is the development of the endothelial dysfunction, characterized, among other aspects, by the growing expression of cell adhesion molecules such as VCAM-I, E-selectin, and ICAM-I, allowing the binding of other cell types, a process that increases as the disease progresses.

In the MS murine model, a slight positivity for ICAM-I expression was observed Figure 1characteristic at this early stage of endothelial dysfunction, in which this molecule is overexpressed in atherosclerotic inflammatory processes [ 18 ], validating our model as an endothelial damage promoter.

It is currently known that platelets can internalize oxidized low density lipoprotein Ox-LDL in a dyslipidaemia scenario and have the capacity to join endothelium with no need of denudation [ 91920 ]. This was observed in the MS model, since slight positivity for platelets was visualized. With the results obtained in the MS mice model it might be postulated that high cholesterol levels alters endothelial function adhesion molecule increase and platelets join the dysfunctional endothelium together with monocytes in coronary artery of CF-1 mice [ 2223 ].

An advanced atherosclerosis model was used for the study of more advanced stages in the atherosclerotic process. The ApoE deficient mouse is one of the best models as it provides great information, since these animals develop hypercholesterolemia spontaneously, with a cholesterol level up to five times higher than normal mice [ 24 ], developing atherosclerosis in a short period of time.

This allows evaluating different molecules and cells that participate in physiopathology of atherosclerosis, as well as the influence of diet in such process [ 25 ].

Over the last years there is evidence that platelets as well as erythrocytes can penetrate the plaque through angiogenic capillary breakages [ 27 ]. These results reaffirm the thesis of the interaction between platelets and macrophages, mainly in the atherosclerotic lesion site promoting an optimum scenario that might encourage the platelet contribution in foam cell formation [ 12 ]. There are in vitro studies demonstrating that platelet is involved in the accumulation of oxidized lipids by macrophages and subsequent transformation to foam cells [ 2028 — 30 ].

Platelets can accumulate lipids in a hypercholesterolemic environment [ 31 ], reaffirming this observation. There are in vitro studies in which platelets are able to contribute their lipid content to murine monocytes favoring foam cell formation, after their phagocytosis [ 32 ]. For this phenomenon to take place, macrophage and platelet must be in intimate contact, an event demonstrated in vivo in our results showing platelets and macrophages in contact inside the plaque.

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This adds up to the platelet mobilization capacity through a permeable membrane, as well as through the activated endothelium using chemoattractant molecules which are present in vascular inflammatory events [ 33 ]; other researchers proved that platelets go through the intestinal epithelium to participate in inflammatory processes and this step would be facilitated by comigration with polymorphonuclear leukocytes Basicaa [ 34 ], proposing novel capacities to platelets in inflammatory events such as atherosclerosis.

Our results show that platelets are present in atheromatous plaques obtained in vivo and can interact with macrophages in lipid core, producing different molecules that favor the development of atherosclerotic plaque through this interaction baica 3035 ].

However, this cannot be assured with the techniques used in this study, but their presence in the lesion site might favor such process. These results ratify the importance given by different authors in the study of ICAM-I as an early marker of atherosclerosis [ 38 ]. Using immunostaining, it can be observed that platelets participate from early stages in the atheromatous process, initially adhering to the endothelium, which increases as the disease progresses, until infiltrating markedly the sites where there is a plaque and an inflammatory process.

This is probably favored by the increase of the expression of adhesion molecules at endothelial level as well as high lipid concentrations that might modify directly the platelets increasing their transmigration. A narrow contact with macrophages could also be evidenced mainly in sites where there are fatty deposits, which would encourage interaction between both. In future studies, it would be interesting to test whether platelets have the capacity to form foam cells directly.

This would allow giving relevant information useful for the implementation of a new therapeutic target in the fight against CVD. The authors thank Dr. Sergio Wehinger, Universidad de Talca, for the help in discussion and writing of this paper. The authors declare that there is no conflict of interests regarding the publication of this paper.

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This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted unmunohematologia, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC.

Introduction Cardiovascular diseases CVD are the leading cause of death among adult population in most countries [ 1 ], in which the most common cause is the atheroma formation in arteries [ 2 ]. Material and Methods 2. Maintenance and Ethical Considerations Animals used for experimentation were maintained in standard environmental conditions: Results First, inmunohwmatologia prepared diets supplemented with fat.

Open in a separate window. Model of Early Stage of Atherosclerosis First, we tested high fat diet in CF1 mice to induce metabolic alterations and endothelial dysfunction [ 13 ].

Discussion CVD are the main cause of bassica in most occidental countries. Conclusion Using immunostaining, it can be observed that platelets participate from early stages in the atheromatous process, initially adhering to the endothelium, which increases as the disease progresses, inmunohemztologia infiltrating markedly the sites where there is a plaque and an inflammatory process.

Conflict of Interests Inmunohematologiz authors declare that there is no conflict of interests regarding the publication of this paper. Hemostasis alterations in metabolic syndrome review International Journal of Molecular Medicine.

Global burden of cardiovascular diseases.

SISTEMA abo jaime

Inflammation, atherosclerosis, and coronary artery disease. The New England Journal of Medicine. Kher N, Marsh JD. Pathobiology of atherosclerosis—a brief review. Seminars in Thrombosis and Hemostasis.