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Biomedical subjects

J D García Palomo

Publications and source records attributed to J D García Palomo.

12 recordsLinked to original sources
PubMed1991

[General pathogenesis of diffuse alveolar-interstitial pulmonary disease].

Diffuse alveolar-interstitial lung disease is a syndrome characterized, amongst others, by a common pathogenic scheme. The different phases of its pathogenesis are reviewed in this work. First of all, the concept of alveolitis is described, indicating its characteristics and general consequences of this lesion. Secondly, the different agents which could lead to the destruction of alveolar and interstitial structures, especially those of macrophagic origin, are reviewed. Next, the different types of granulomas, cells of which they are formed, and their general production mechanism are described. Finally the concept of lung fibrosis are reviewed, studying the different processes which lead to increased collagen in the interstitial tissue, specially chemotaxis and fibroblastic proliferative factors.

Humans↗
PubMed1989

[HIV infection and monocyte function].

An study of the non-specific function of monocyte in 14 IVDU (intravenous drug-users) was carried out in order to assess the role of HIV in the pathogenesis of monocyte function alteration in this population. Two separate groups were formed depending on whether they were infected with HIV or not. In comparison with the control group, the decreases of the adherence and of chemotaxis found were similar to that previously described. No differences were observed between both groups. Finally, the meaning of these results is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[The action of naloxone on monocyte chemotaxis in heroin addicts].

Intravenous (I.V.) drug users possess a decrease of the monocyte chemotaxis directly related to drug usage. We study the effects of naloxone on monocyte chemotaxis in I.V. drug users, evaluating the chemotactic index and the cellular level of cAMP. The incubation of monocytes with naloxone did not modify the chemotactic index nor the cellular levels of cAMP, the first remaining low and the second high, this being statistically significant compared with the control group. We comment on the possible causes of naloxone's lack of effect and we suggest the role of cAMP in causing the chemotactic defect in this group of patients.

Chemotaxis, Leukocyte↗
PubMedDate not supplied

Leukocyte chemotaxis.

Monocyte chemotaxis is a function of mononuclear phagocytic system cells that enables migration toward the focus of infection and inhibition of microorganism growth and proliferation. In this paper we review the chemotactic phenomena following Becker's scheme that distinguishes three phases: recognition, transduction and the effector phase. The recognition phase is comprised of the interaction of a chemotactic agent with a receptor located on the cell surface. We cite the multiple chemoattractant presently known, and the mechanisms that regulate this phase, "up-regulation" and "down-regulation" phenomena, and the presence of receptors in low and high-affinity states. The transduction phase comprises all biochemical events produced after internalization of the attractant-receptor complex, whose purpose is triggering the cell motor apparatus. The key event in beginning movement is the increase of cytosol calcium. Alterations in membrane phosphoinositols constitute the initial transductor mechanism in chemotaxis, inositol-triphosphate and diacylglycerol behaving as second messengers. We review the diverse functions of these phospholipids, as well as we do a graphic representation of these (fig 1). Motor phase comprises the movement of the cell toward the chemotactic gradient through activation of the motor cell apparatus. We describe the intervening elements, actin and its regulatory proteins acumentin and gelsolin, actin-fixing protein, myosin and microtubuli, and the four phases of locomotion mechanism: reversible adherence, pseudopode emission, cell polarity and movement that results from an alternance between gel and sol states.

Calcium↗
PubMedDate not supplied

Depression of monocyte chemotaxis in intravenous drug abusers (IDA): cell alteration.

Intravenous drug abusers (IDA) show an important immunological dysfunction that plays a key role in pathogenesis of infections found in these patients. A defective adherence and chemotaxis has been described at the level of mononuclear phagocytic system (MPS). In this paper, we center on defective chemotaxis. In the face of a chemotactic alteration, the first step is trying to locate the alteration as humoral or cellular; we have used the work sheme proposed by Yousif-Kadaru. Serum of IDA and controls, E. Coli endotoxin-activated and non-activated were used as attractants. Chemotaxis was studied by the morphologic method of Snyderman. Attractant capacity of E. Coli endotoxin activated serum was 55.93 +/- 10.88, similar to that of controls, 59 +/- 10.58. The same was true for non-activated serum, 42.5 +/- 16.8 compared to 44.67 +/- 19.54. That means, according with the scheme proposed, that the alteration is localized in the cell. Some factors that could participate in the pathogenesis of the motor defect are commented in the discussion. The elevation in immunocomplexes titer observed in IDA could depress monocyte chemotaxis, but the defect would be humoral. A deficit in chemotactic factor could be discarded because its production capacity is preserved in IDA. Liver disease, both acute and chronic, is one of the most frequent medical complications in these patients. The cellular localization of depression eliminates any participation in the pathogenesis of chemotactic alteration.

Chemotaxis, Leukocyte↗
PubMedDate not supplied

[Monocyte chemotaxis: critical evaluation of 2 methods of quantification].

The mononuclear phagocytic system (Mo) possesses a series of well defined functions regarding both its circulatory components--monocytes--and histiocytic macrophages. These functions--antimicrobial defense, elimination of cellular particles or detritus, immunological interaction with lymphocytes cells, antitumoral defense and control of granulopoiesis--require chemotaxis and phagocytosis or preceding steps. Although knowledge of these functional aspects is continually becoming better--always assured by advances obtained in the study of the function and pathology of polymorphonuclear cells--, an authentic pathology of monocyte chemotaxis as an independent clinical entity doesn't exist. This is attributed to of these cells. The techniques currently in use differ not only in their methodology but also in their bases and thus the results obtained by various authors are not generally comparable. All this led us to do a comparative study, in control subjects, between two techniques which explore the chemotactic capacity of monocytes from peripheral blood. The chemotactic capacity of monocytes from peripheral blood in control subjects, measured by two distinct quantification methods, were studied: Radioanalytic Method (monocytes tagged with 99 mTc) and a morphological method (counting the number of monocytes per field in immersion). The results obtained from both techniques were very similar, the existence of significant differences in cell behavior with exposure to the different chemotactic substances used could not be demonstrated. These results are commented on.

Adult↗
PubMedDate not supplied

Monocyte functional defects in rheumatoid arthritis.

Monocytes derived from peripheral blood of patients with rheumatoid arthritis (RA) had a marked defect in their chemotactic and phagocytic activity. The chemotactic defect resides at a cellular level, while the phagocytic defect is serum-dependent. Both defects could be of importance in the pathogenicity of RA and the susceptibility to infection such patients show. Finally, monocytes were found to have a negative influence over spontaneous cytotoxicity mediated by T lymphocytes.

Arthritis, Rheumatoid↗