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- Pedro, L M, et al.
(författare)
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Placa de ateroma da bifurcacao carotidea: como identificar a lesao "activa"?
- 1999
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Ingår i: Revista portuguesa de cardiologia : orgao oficial da Sociedade Portuguesa de Cardiologia = Portuguese journal of cardiology : an official journal of the Portuguese Society of Cardiology. ; 18:7, s. 699-708
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Tidskriftsartikel (refereegranskat)abstract
- The identification of carotid atheromatous plaques associated to a higher neurologic risk may be important in therapeutic decision making for asymptomatic patients and symptomatic patients with 50%-70% stenosis. The introduction of high-definition ultrasonography (HDU) and computer-assisted image analysis provides the possibility of a standard, objective and detailed characterization of the structure of the carotid plaque. The aim of this study is to analyse the relationship between the ultrasonographic characteristics of a group of plaques and the risk of associated cerebrovascular events and cerebral infarction. MATERIAL: One hundred carotid bifurcation plaques (in 68 patients) were studied for the presence of ipsilateral cerebrovascular events. In 61 patients (87 plaques), a correlation with CT scan for the presence of cerebral infarction was possible. METHOD: The lesions were studied by HDU (ATL-HDI 3000) and digitalized for computer-assisted standardization of the image. The analysis included the appreciation of the histogram of the image gray-scale pixel distribution by use of commercial software Adobe Photoshop 3.0. The parameters analysed for global echogenicity were the median of the histogram and the percentage of percentile 40 hypoechogenic pixels (40). Statistical analysis was made with STATA 4.0 software with categorical variables analysed by chi-square and Fisher's exact test and continuous variables analysed by variance analysis and Student's t test. RESULTS: Thirty eight (38%) plaques were symptomatic and 34 (39.1%) were associated to cerebral infarction. The degree of stenosis was > 70% in 51%; between 50 and 69% in 27% and < 50% in 22%. The mean of the median and P40 values was 33.9 and 60.3% in the symptomatic and 46.8 (p = 0.005) and 46.6% (p = 0.001) in the asymptomatic plaques respectively. In the plaques associated to cerebral infarction, it was 32.7 and 61.6% respectively, and in the ones with negative CT scan, it was 44.6 (p = 0.005) and 48.1% (p = 0.002). The mean of the median in the plaques vs. degree of stenosis was: > 70%--33.3; 50-69%--45.1; < 49%--57.7 (p < 0.001). In the series the cut-off point for the median value was 32 and for P40 it was 43 (for any degree of stenosis): G1--plaques < 32 (echolucent); G2--plaques > 32 (echogenic). In G1 symptoms occurred in 60% of the plaques and in 26% of the plaques in G2 (p = 0.0001). CT scan was positive in 66% of the echolucent plaques and in 25% of the echogenic plaques (p = 0.0238). CONCLUSION: 1. The more echolucent plaques are associated with a significantly higher neurological risk. 2. The plaques associated with higher degrees of stenosis are more echolucent. 3. The use of a standard and objective methodology in the analysis of the echographic structure of carotid plaques is important and limits the known intra and inter-observer variability of subjective appreciation.
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| 2. |
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| 3. |
- Colucci, Francesco, et al.
(författare)
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Apoptosis resistance of nonobese diabetic peripheral lymphocytes linked to the Idd5 diabetes susceptibility region
- 1997
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 94:16, s. 8670-8674
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Tidskriftsartikel (refereegranskat)abstract
- Defects in lymphocyte apoptosis may lead to autoimmune disorders and contribute to the pathogenesis of type 1 diabetes. Lymphocytes of nonobese diabetic (NOD) mice, an animal model of autoimmune diabetes, have been found resistant to various apoptosis signals, including the alkylating drug cyclophosphamide. Using an F2 intercross between the apoptosis-resistant NOD mouse and the apoptosis-susceptible C57BL/6 mouse, we define a major locus controlling the apoptosis-resistance phenotype and demonstrate its linkage (logarithm of odds score = 3.9) to a group of medial markers on chromosome 1. The newly defined gene cannot be dissociated from Ctla4 and Cd28 and in fact marks a 20-centimorgan region encompassing Idd5, a previously postulated diabetes susceptibility locus. Interestingly, we find that the CTLA-4 (cytotoxic T lymphocyte-associated antigen 4) and the CD28 costimulatory molecules are defectively expressed in NOD mice, suggesting that one or both of these molecules may be involved in the control of apoptosis resistance and, in turn, in diabetes susceptibility.
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| 4. |
- Colucci, Francesco, et al.
(författare)
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Programmed cell death in the pathogenesis of murine IDDM : resistance to apoptosis induced in lymphocytes by cyclophosphamide
- 1996
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Ingår i: Journal of Autoimmunity. - : Elsevier. - 0896-8411 .- 1095-9157. ; 9:2, s. 271-276
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Tidskriftsartikel (refereegranskat)abstract
- The non-obese diabetic (NOD) mouse displays several immune related defects, each of which could potentially contribute to the immunopathogenesis of diabetes that spontaneously develops in these mice. The reported resistance of NOD-lymphocytes to several apoptosis-inducing signals constitutes one such factor. Apoptosis plays a key role in the homeostasis of the immune system, as a means of selecting lymphocyte repertoires both in primary lymphoid organs and in the periphery; distortions in the apoptotic machinery may therefore be hypothesized to be implicated in the pathogenesis of autoimmune disorders. We now report that cyclophosphamide constitutes an apoptosis signal to peripheral lymphocytes and we provide evidence that NOD B cells as well as both CD4 and CD8 T cells display resistance to cyclophosphamide-induced apoptosis. These observations support the notion that apoptosis resistance in NOD mice exists at various levels, and suggest that the CY-sensitive lymphoid population, believed to play an important role in inhibiting the disease in diabetes resistant NOD mice (particularly males), may be controlled by mechanisms that are mediated by apoptosis.
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