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1.
Indian J Exp Biol ; 2006 Mar; 44(3): 193-202
Article in English | IMSEAR | ID: sea-57532

ABSTRACT

The bactericidal activity of polymorphonuclear leucocyte (PMNL) against infection stimulates cytoskeletal changes accompanied with alteration in adhesion and locomotion. Microfilaments, the motile apparatus is known to regulate these changes by polymerization of monomeric G-actin to fibrous F-actin. PMNL from chronic myeloid leukemia (CML) patients have been reported to be defective in locomotion in response to synthetic peptide, n-formyl-methionyl-leucyl-phenylalanine (fMLP) but the mechanism leading to defective locomotion and their spatial reorganization remains unclear. Therefore, in order to study the cause of defective motility of PMNL from CML patients the spatial distribution and reorganization of microfilaments and microtubules in response to fMLP have been examined by transmission electron (TEM) and scanning electron microscopy (SEM). Under SEM, the PMNL-CML surface appeared smoother with reduced ruffling resulting in rounding off cells with lesser polarized morphology. Unstimulated PMNL from normal as well as CML subjects showed shorter and fewer microtubules and evenly distributed microfilaments as compared to fMLP stimulated PMNL. It is proposed that the cause of defective locomotion was due to reduced surface activity as a consequence of altered cytoskeletal configuration. This phenomenon seems to be related to impaired functional appendages and as a whole led to the defective cell motility and hence reduced chemotaxis in PMNL from CML patients.


Subject(s)
Cell Death , Cell Movement , Cytoskeleton/pathology , Gold , Granulocytes/pathology , Humans , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology , Microscopy, Electron, Scanning , Microscopy, Electron, Transmission , Microscopy, Immunoelectron , Myosin Subfragments/metabolism
2.
Acta bioquím. clín. latinoam ; 30(3): 231-44, sept. 1996.
Article in Spanish | LILACS | ID: lil-207539

ABSTRACT

Con el transcurso del tiempo surgen mejores alternativas terapéuticas para los pacientes que sufren de infarto agudo de miocardio (IAM), enfermedad considerada en nuestro país como una de los principales causas de muerte; esto hace que el Laboratorio deba evolucionar permanentemente hacia la utilización de nuevas prácticas que sean cada vez más sensibles y específicas para poder realizar un diagnóstico precoz. En el presente trabajo se pretende realizar una revisión sobre los análisis de laboratorio históricamente más frecuentemente utilizados, así como también efectuar una actualización sobre los nuevos parámetros en estudio para el diagnóstico de IAM


Subject(s)
Humans , Biomarkers/blood , Myocardial Infarction/diagnosis , Aspartate Aminotransferases , Creatine Kinase , Creatine , Enzymes , Interleukin-6 , Interleukins , Interleukins , L-Lactate Dehydrogenase , Biomarkers/analysis , Myocardial Infarction/therapy , Myoglobin , Myosin Subfragments , Myosins , Phosphopyruvate Hydratase , Phosphorylases , C-Reactive Protein , Troponin
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