ライフサイエンスコーパス: glomerular tuft

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1 s had uniform characteristics throughout the glomerular tuft.

2 rine fashion once these cells migrate to the glomerular tuft.

3 ving one primary dendrite bearing a terminal glomerular tuft.

4 ificant recruitment of labeled PECs onto the glomerular tuft.

5 cells were observed in structures resembling glomerular tufts.

6 al cell infiltrates but were rare within the glomerular tufts.

7 from extensive areas of adhesion between the glomerular tuft and capsule to invest the tubular neck.

8 Reduced proliferation in glomerular tuft and increased apoptosis in perivascular

9 e [Ca(2)(+)]i resulted in contraction of the glomerular tuft and increased capillary albumin permeabi

10 and PENT were detected in the proliferative glomerular tufts and crescents.

11 otein was detected in podocytes in collapsed glomerular tufts and in glomerular pseudocrescents.

12 ory nerve stimulation at the site of origin (glomerular tuft) and to determine its attenuation along

13 although there was no difference in the mean glomerular tuft area among groups.

14 protein-positive podocyte nuclear number and glomerular tuft area was studied.

15 ous casts, number of ED-1-positive cells per glomerular tuft area, and interstitial fibrosis.

16 trix area, calculated as a fraction of total glomerular tuft area, and plasma creatinine were signifi

17 ted in healthy mice, about two-thirds of the glomerular tufts became LacZ positive during the regener

18 In summary, detection of PECs on the glomerular tuft by immunostaining improves the different

19 In conclusion, repopulation of the glomerular tuft by parietal cells may represent a compen

20 preparations, although minor differences in glomerular tuft contractility and macula densa cell calc

21 ed in capillaries of the nephrogenic cortex, glomerular tufts, cortical interstitium, and medulla inc

22 erent arterioles, LacZ-positive cells in the glomerular tuft did not express renin.

23 he vascular stalk and are recruited onto the glomerular tuft during infancy to adolescence in mice an

24 ue to reduced glomerular podocyte number and glomerular tuft enlargement.

25 tor cells of the Bowman's capsule invade the glomerular tuft exclusively in proliferative disorders.

26 A subset of labeled cells within the glomerular tuft expressed the podocyte markers Wilms tum

27 In summary, failure of podocytes to match glomerular tuft growth in response to growth signaling t

28 y showed strong and specific staining of the glomerular tufts in a distribution that mimicked that of

29 een fluorescent protein-positive area in the glomerular tufts increased after mesangial injury.

30 nied by proteinuria and widespread segmental glomerular tuft injury.

31 ignificant increase in the percentage of the glomerular tufts occupied by ECM in diabetic WT compared

32 nificant difference in the percentage of the glomerular tufts occupied by ECM relative to nondiabetic

33 and central neurons lack the characteristic glomerular tufting of their arbors.

34 tribution along Bowman's capsule, within the glomerular tuft, or in both locations.

35 l epithelial cells (PECs) migrating onto the glomerular tuft participate in the formation of focal se

36 tric analysis confirmed the mismatch between glomerular tuft volume and total podocyte volume (number

37 erent locations on dendritic branches in the glomerular tuft was relatively narrow and appeared to be

38 in the scars, Bowman's space was dilated and glomerular tufts were degenerated.

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