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1 n the degree of interstitial fibrosis in the corticomedullary junction.
2 ed in tubular cells of the outer medulla and corticomedullary junction.
3 ed kidneys and on active reabsorption in the corticomedullary junction.
4 ure thymocytes exit via blood vessels at the corticomedullary junction.
5 in the cortex and is most abundant near the corticomedullary junction.
6 eys in one fetus showed tubular cysts at the corticomedullary junction and diffuse effacement of the
7 itic cells and macrophages were found at the corticomedullary junction and in foci in the thymic cort
8 of the peritubular capillary network in the corticomedullary junction and increased numbers of bone
9 d kidney size, cysts are concentrated at the corticomedullary junction, and tubulointerstitial fibros
11 revealed increased apoptotic cells near the corticomedullary junction in lymphoid follicles and in t
12 is a major cause of tubular necrosis in the corticomedullary junction of isolated perfused kidneys,
13 ed predominantly in intestinal villi and the corticomedullary junction of the kidney, whereas guanyli
16 rring in 10.3 +/- 9.5% and 32.3 +/- 17.8% of corticomedullary-junction tubules by conventional light
17 situ by thymic epithelium in the cortex and corticomedullary junction, two locations at which VCAM-1
18 , in situ apoptosis in the cortex and at the corticomedullary junction was responsible for a synchron
19 the boundary between DP and SP thymocytes at corticomedullary junctions was disrupted and medullary s
20 ce revealed extensive ischemic injury at the corticomedullary junction, whereas kidneys from sham HO-
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