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Background and purpose:Brucellosis is a disease with zoonotic and transmissible world wide distribution which, often becomes chronic with high rate of recurrence. Since the immune responses during brucellosis have not been studied profoundly, therefore in this study cytokine production in the patients suffering from brucellosis and in healthy individuals has been evaluated.
Materials and methods: 14 with acute and 13 with chronic brucellosis (mean age of 38.03+18.2 years) and 22 healthy individuals matched for age( mean age of 35.33+21) were recruted for the study. Diluted boiled samples were cultured in presence of either mitigen, heat inactivated brucella melitensis Rev-1 strain or medium alone. ÏL-12. Ïl-10, Ïl-13 and ÏFN- γ were measured by specific sandwich ËLÏSÂ and blastogenic responses of lymphocytes were also counted by liquid scintillation counter (LTT).
Results: Ïnterferon-y production and specific proliferative responses were significantly diminished in chronic brucellosis compared to the acute patients (P<0.05). Ïn contrast. ÏL-12 production in whole blood culture of chronic patients was higher than that of acute patients (P<0.05). ÏL-10 production was also augmented in chronic patients, which had no relation with ÏFN- γ production.
Çonclusion: Findings indicate that brucella- spectific cytokine patterns observed in patients with brucellosis differ between acute and chronic plases of the disease. Âlso the results suggest that diminished production of Th1 cytokines and T cell blastogenic responses may be due to lack of T cell responses to brucella antigens,in patents suffering from chronic brucellosis.

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Background and Purpose: Conventionally, the architecture of the artery wall is based upon the close-packed smooth muscle cells, endothelial and adventitial cells in both sides of internal elastic lamina (IEL). However, the adventitia and endothelium are now viewed as key players in vascular growth and repair. Recent work raises fundamental questions about the cellular heterogeneity of arteries, time course, triggering of normal and pathological re-modeling.
Materials and Methods: Twelve wild type mice were employed. After killing with CO2 inhalation, dissected mesenteric arteries were removed and cleaned with adipose tissue. Arteries were mounted in the perfusion pressure myograph under normal pressure (70mmHg) in Kreb’s solution, which bubbled with 95% O2 and 5% CO2 to pH 7.4, at 37°C. After staining with fluorescent ligands (Syto 13) for nuclei and (DIO 1µM) for cytoplasm, arteries were scanned with the Laser Scanning Co focal Microscopy (LSCM) under (488nm/515nm), (484nm/501nm) and (543nm/580nm) Argon-Helium ion laser wavelength.
Results: Three dimensional images of computer observation suggest that there may be a close relationship between the helical organization of smooth muscle cells and the underlying pattern of endothelial cells (myoendothelial connection).
Conclusion: Tight junctions between cells must be broken and remade during the remodeling process. This suggests a carefully controlled defensive structure for intra-cellular connections, that is capable of withstanding the acute stresses of normal function, but which must be capable of modification to adapt to a new state, when the bio-physical conditions dictate. Endothelial mosaicism related to spiral arrangements of underlying smooth muscle cells, are associated with the functional cell connections. Taken together, these issues provide an exciting new phase in understanding the physiological modeling of the vascular wall, producing a new view of the dynamic nature of vascular structure.