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1 eactive periosteal bone formation around the nidus.
2 (RFA) to create a quantifiable prothrombotic nidus.
3 l shunts between arteries and veins within a nidus.
4 position, avoiding direct penetration of the nidus.
5 and microbial survival within the infectious nidus.
11 y, dimensions, and temporal stability of the nidus are determined largely by pathogen natural history
14 id osteoma in relation to the native cortex, nidus area, nidus calcification area and attenuation at
17 n relation to the native cortex, nidus area, nidus calcification area and attenuation at CT, and nidu
20 esis by altering the destiny of CEP55 from a nidus for abscission to an integral component of the int
21 as the potential to function physically as a nidus for appositional new bone growth in alveolar socke
23 Contaminated vascular devices can act as a nidus for bloodstream infection and systemic pathogen di
29 dard permanent electronic hardware acts as a nidus for infection: bacteria form biofilms along percut
32 smooth muscle cells (VSMCs), form the first nidus for mineralization and fetuin-A, a potent circulat
35 low numbers of cryptococci that can become a nidus for re-activation disease during immunodeficient s
36 rcation periodontal breakdown may serve as a nidus for recolonization and disease recurrence or for t
38 Thus, although the ChEL domain provides a nidus for Tg dimerization, interactions of upstream Tg r
39 onic, persistent SGs that appear to act as a nidus for the aggregation of disease-related proteins.
41 table protective environment and acting as a nidus for the dissemination of large numbers of microorg
43 rmed stem cells represent a potential common nidus for the primary cancer and the recurrent cancer th
44 aggregates readily and appears to provide a nidus for the subsequent aggregation of A beta 40, resul
47 tion of A beta (template-independent initial nidus formation) and deposition of A beta (template-depe
50 alcification area and attenuation at CT, and nidus mineralization ratio (percentage of the calcificat
55 significantly increased CBF in the presumed nidus of arteriovenous malformation causing haemorrhage
60 central memory responses that can clear the nidus of initial virus-infected cells at mucosal surface
66 ave been present on the platelet core at the nidus of the injury, bound proteins were not evident on
72 aracterization consisted of arterial feeder, nidus size, and venous drainage type identification comp
75 , MR imaging depicted an absence of residual nidus vascularity in 32 (76%) of the 42 patients who wer
77 es of osteoid osteoma (edema, hyperemia, and nidus vascularization) were considered at baseline and a