In a tertiary care hospital, the prevalence of unrecognised PAD among patients hospitalised for non-PAD-related causes is high and the preventive CVD therapy rates are low. Hospitalisation is a good opportunity to detect PAD.
An infected aneurysm of the thoracic aorta due to mycobacterium tuberculosis is an unusual entity for which the classical treatment is antituberculosis chemotherapy and open-chest surgery. Recent improvements in endovascular treatments have led to their proposed use for infected aneurysms in patients for whom open surgery poses too high a risk. We report on a 68-year-old man with a tuberculous aortic aneurysm who had been treated with an endoprosthesis and antituberculosis chemotherapy. His clinical and radiological follow-up was uneventful and led to the discontinuation of pharmacological treatment after 16 months. However, a recurrence of the infection led to a fatal aortic rupture 4 months after discontinuation of therapy.
Together with increase of proliferation potential, the myelodysplastic syndromes are characterised by qualitative abnormalities of differentiation of myeloid precursors associated with increased intramedullary apoptosis, resulting in peripheral cytopenia.1 FAB and WHO classifications of these syndromes, widely used among hematologists, are relatively robust and simple, but omit immunophenotyping for diagnosis. Immunophenotypic abnormalities are frequent in myelodysplastic syndromes.2 Yet interpretation of flow cytometry remains complex, and often qualitative, being thus unable to give a black and white readout as molecular and cytogenetic techniques do. To simplify flow-
To our knowledge, this is the first real-world observational report highlighting the interest of statins for the prevention of stroke in the very special situation of CABG. Even though according to randomized trials coronary patients have a benefit from these drugs, a special level of interest should be directed towards those presenting the above-mentioned risk factors.
Outcomes of fulminant GCMs may differ from those of milder forms. In this context, heart transplant might likely be the only long-term survival option.
Background: The different B-cell subsets in human bone marrow result from a dynamic equilibrium between endogenous production, B-cell bone marrow reentry and terminal plasma cell differentiation. Our aim was to define and quantify the different medullary B-cell subsets.Methods: A series of 32 normal adult bone marrows plus 15 normal adult blood samples was studied by nine color flow cytometry (CD10, CD19, CD24, CD27, CD34, CD38, CD45, IgM, and IgD). With the Kaluza software radar plots, two 2D triple parametric histograms (CD10/CD34/CD45 and CD27/IgM/IgD) were set-up to identify six progenitor and five mature B-cell subsets.Results: Very early B-cell progenitors were CD19neg/CD10pos/CD34pos. B-cell progenitors were split into five subsets on the CD10/CD34/CD45 triple parametric histogram, sequentially ordered according to the loss of CD34 and CD10 and acquisition of surface IgM and IgD. CD19pos/CD38low mature B-cells were divided into four subsets on the CD27/IgM/IgD triple parametric histogram, with two stages of naïve B-cells and two CD27hi marginal zone and switched memory B-cell compartments. CD19pos/CD34neg/CD10low immature B-cells were the main bone marrow B-cell subset, accounting for one third of bone marrow B-cells. Transitional B-cells were the only immature bone marrow stage found in the blood. Compared to blood, the bone marrow was enriched in both marginal zone and switched B-cells.Conclusion: We provide the first analysis of 3D B-cell differentiation by multicolor flow cytometry leading to propose reference values for each bone marrow and blood B-cell compartment. This warrants further exploration of normal and pathological human B-cell maturation.
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