[Pulmonary localization of hairy cell leukemia].
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Biomedical subjects
Publications and source records attributed to J Bayle.
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In vitro, LSLCL is expressed by numerous myeloid, promyelocytic, and T or B lymphoblastoid cell lines. In vivo, LSLCL is strongly expressed in bone marrow and only faintly in lymphoid organs. We show here that, in bone marrow, LSLCL is detected: (i) concentrated in the cytoplasm of immature neutrophils but not in myeloblasts nor in mature neutrophils, (ii) in extracellular bone marrow fluid. Besides, numerous cDNAs, similar to LSLCL (identity of 93-99%), are found in 'expressed sequence tags' databases from various origins, mostly fetal and undifferentiated tumour tissues. Since LSLCL and various closely related cDNAs are expressed at definite stages of cellular maturation processes, we hypothesize that this class of proteins could play an important role in the control of cellular differentiation.
Our objective was to study the influence of HIV infection of polymorphonuclear leukocytes (PMN) on transepithelial migration. To date, reports of functional PMN chemotaxis in AIDS are contradictory. This is the first attempt to assess this function via an in vitro model allowing transmigration of neutrophils through an intestinal epithelial barrier. PMN were isolated from 45 HIV-infected patients and 45 healthy volunteers. PMN transmigration across T84 epithelial cells was initiated by applying either various concentrations of formyl-met-leu-phe peptide (f-MLP) or interleukin-8 and assayed by quantification of myeloperoxidase activity. CD11b, CD18, and CD47 expression on PMN was compared before and after transepithelial migration by flow cytometry analysis. CD11b expression was studied by electron microscopy. Apoptosis of transmigrated HIV PMN and control PMN was investigated by morphology and DNA fragmentation characterization. Compared to control PMN, HIV PMN exhibited a decrease in transepithelial migration that directly correlated with CD4+ counts. Basal and transepithelial migration-mediated expression of CD11b, CD18, and CD47 were unmodified in HIV PMN compared to control PMN. Electron microscopy labeling confirmed no difference in CD11b expression on HIV and control PMN. The index of apoptosis in transmigrated HIV PMN and control PMN was identical. These data provide evidence of a defect in the f-MLP-induced chemotaxis of PMN from HIV-infected patients across an intestinal epithelial barrier. This defective migration is not due to a quantitative modification of CD11b, CD18 and CD47 on HIV PMN suggesting a more subtle alteration. The impairment in the transmigration function may contribute in vivo to an increased susceptibility to intestinal bacterial infection in HIV-infected patients.
BACKGROUND: Young patients who experience cardiovascular events may have raised levels of homocysteine. There may be several causes for this hyperhomocysteinemia. CASE REPORT: Cerebrovascular disease occurred in a 40-year-old female smoker with hyperhomocysteinemia. This patient subsequently had several episodes of thromboembolism involving the brain and lower limb arteries. Prothrombin concentration was difficult to control with antivitamin K anticoagulants. Investigations to identify a genetic cause of hyperhomocysteinemia revealed that she was homozygous for the C677T mutation on the methylenetetrahydrofolate reductase gene. There was no G1691A mutation of the factor V gene, a risk factor for familial thrombosis. Supplementation with folic acid successfully halted episodes of thromboembolism (follow-up 2 years) and prothrombin levels stabilized under treatment. DISCUSSION: The C677T mutation, which is common in the general population (15.7%), cannot explain the effect of folate supplementation alone. Other mutations affecting homocysteine metabolism could have a potentializing effect on vascular events.
An evaluation of the new automated hematology analyzer was performed in comparison with the Coulter STKS on 1,694 blood samples coming from the different departments of Nice University Hospital. The Cobas Vega showed very satisfactory results in terms of repeatability, reproducibility and linearity. Correlation with the STKS was excellent with the exception of the following parameters: red blood cell distribution index and the absolute values for eosinophils and basophils. Two qualities were particularly appreciable: absence of leukocyte carryover, and stability of the complete blood count and leukocyte differential count over a long period. Analysis of qualitative flags showed that the overall blood smear review rate was 47% for the Cobas Vega, not forgetting that optical microscopy detects 37% of all abnormalities. The STKS's review rate was 49.5%. Flags commonly concerned the granulocytic lineage, 61% for the STKS and 48% for the Vega, with a false positive rate of 43.4% for the STKS compared with 22% for the Vega. The opposite phenomenon was observed with the flag for atypical lymphocytes which represented 11% of flags for the STKS and 25.6% for the Vega, with a false positive rate of 25.5% for the STKS and 34% for the Cobas Vega. This may be explained by the fact that lymphocyte abnormalities sometimes generated "granulocytic" flags on the STKS. Studies of the false negative rate carried out using light microscopy on 505 blood samples without flags on either system, detected the presence of a slight myelemia, and a few hyperbasophilic lymphocytes or plasmocytes in 18.6% of all cases. Finally, the Cobas Vega's practicality was greatly appreciated and there was no trouble with breakdowns throughout the whole period of its use.
Glanzmann's thrombasthenia (GT) is a hereditary platelet disorder resulting from a quantitative or qualitative deficiency of the major platelet membrane complex GPIIb-IIIa (CD41) required for platelet aggregation. We investigated by flow cytometry, the expression of CD41, fibrinogen, and of two platelet activation-related antigens, CD62 and CD63, (i) before and after activation of platelets by PMA, and (ii) on the surface and within the cytoplasm of resting platelets, after permeabilization by saponin. Platelets from a series of normal subjects and from nine members of two GT families, were reacted with FITC-conjugated antibodies and analyzed on a flow cytometer. Fluorescence intensities measured on normal and GT platelets were quantified by using calibrated beads. Results showed lack of both GPIIb-IIIa and fibrinogen, on the platelet surface and also within the cytoplasm in five of these GT patients, whereas GPIIb-IIIa and fibrinogen remained normal in the four other cases. However, CD62 and CD63 antigenic levels were found within normal range for all members of these families, after PMA stimulation and also after platelet permeabilization. This work therefore showed that the lack of CD41 in GT, which causes strong disturbance of platelet aggregation, may not be associated with the deficiency of activation pathways.
The authors described an assay procedure for the determination of free and total carnitine in red blood cells. This method is based on ultrafiltration of the broken red blood cells in Centrisart filter, by centrifugation. Free and total carnitine in ultrafiltrates is determined by the spectrophotometric method of Cederblad and Coll., adapted to Cobas-Fara. They evaluated the procedure linearity, reproductability and analytical recovery. Comparison with precipitate protein procedure showed that results correlated well. The advantages of this original assay include simplicity, increase rapidity, lower cost of reagents and mainly improved reproductability.
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Although carnitine levels and carnitine therapy have been extensively studied in dialysis patients, the pathophysiology of L-carnitine is poorly understood. The usual therapeutic dose is 20-30 mg/kg, resulting in dramatic increases of circulating levels above the normal values. Guided by studies on its lipidic effect and by our experience of its action on haematocrit, we propose the use of 2-3 mg/kg of L-carnitine in future prospective studies.
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We have undertaken the cytogenetic monitoring of 39 adult patients treated for de novo acute myeloid leukemia (AML) by intensive chemotherapy. We describe this monitoring in seven patients in continuous complete clinical and morphologic remission (CR) of AML. Although in CR, these patients exhibit the emergence of cytogenetically abnormal clones. Abnormalities observed include monosomy 7, del(20)(q11), partial trisomy 1q, and 6p12-22 rearrangements. They correspond to well-known chromosomal rearrangements commonly found in myelodysplasia (MDS), and myeloproliferative syndromes (MPS), as well as AML. Present as the sole detected chromosomal change, they preceded by months the onset of overt leukemia or MDS. In some cases, the abnormal clone showed a proliferative advantage (some patients exhibited up to 100% of abnormal bone marrow metaphases in subsequent analyses). AML relapse, when it occurred, was associated with a different chromosomal modification. Altogether the question arises, whether the abnormalities pointed out in our study (monosomy 7, del(20)(q11), partial trisomy for the long arm of chromosome 1 (q21qter), 6p12-22 rearrangements), and seen after chemotherapy, mark preleukemic cells or not, and whether they participate indirectly, or not at all in the leukemic process.
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Specific morphological and histochemical changes serve to define stages of differentiation during terminal myeloid maturation. The development of the hybridoma technology has allowed generation of monoclonal antibodies selectively reactive with antigenic determinants expressed in the hematopoietic system by myeloid cells at specific stages of differentiation. Here, the characterization by one of these antibodies i.e. GO35 (CD17) which shows myeloid specificity, was reported on blastic cells from 30% of acute lymphoid leukemia cases investigated (8/25). This monoclonal antibody may prove useful in the subclassification of atypical lymphoproliferative disorders including "hybrid leukemias" and serve as a possible prognostic factor for a therapy.
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