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1 e tuberculous granulation tissue surrounding caseous and liquefied pulmonary foci and cavities, we fo
5 ary sarcoma, 2; myxoma, 4; fibroelastoma, 1; caseous calcification of mitral annulus, 3; and thrombus
10 r and local tissue environment, resulting in caseous granulomas with incomplete bacterial sterilizati
11 cell alpha-chemoattractant) within solid and caseous granulomas, and there was only minimal expressio
12 lli in low-oxygen microenvironments, such as caseous granulomas, has been hypothesized to have the po
14 xin production leads to development of large caseous lesions, and in infective endocarditis, increase
18 ys a major role in the liquefaction of solid caseous material and in the subsequent cavity formation.
21 in tuberculosis immunopathology, leading to caseous necrosis and compromising the immune response, r
23 from intense granulomatous inflammation with caseous necrosis for infection with type C to minimal in
24 l tenet of tuberculosis pathogenesis is that caseous necrosis leads to extracellular matrix destructi
25 egates of leukocytes and a greater degree of caseous necrosis than those from JH2-2-infected mice.
27 ion of those from inbred rabbits showed more caseous necrosis, more visible bacilli, and fewer mature
28 Zebrafish tuberculous granulomas undergo caseous necrosis, similar to human tuberculous granuloma
29 n of human matrix metalloproteinase 1 causes caseous necrosis, the pathological hallmark of human tub
31 was done and dilated bile ducts filled with caseous necrotic material were seen intra-operatively.
32 into preexisting granulomas, including their caseous (necrotic) centers, through specific mycobacteri
33 le adduct formation surrounding necrotic and caseous regions of pulmonary granulomas by immunohistoch
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