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1 neys, with increases in the proliferation of peritubular (1 wk) and glomerular (2 wk) endothelial cel
2 are disorder characterized by glomerular and peritubular amorphous deposits of a truncated monoclonal
3                 Human, but not murine, renal peritubular and glomerular capillaries constitutively ex
4  obese ZSF1 animals showed regression of the peritubular and glomerular microvasculature, accompanied
5                   Once established, both the peritubular and interstitial macrophage populations exhi
6 r mineral had values between those of normal peritubular and intertubular dentin.
7  The aging rats also displayed focal loss of peritubular capillaries (as noted by focally decreased R
8  In ACR, no more than trace C4d was found in peritubular capillaries (P < 0.0001 versus AHR), and no
9 etection of the C4d complement product along peritubular capillaries (PC) may indicate humoral reject
10 d by determining whether C4d is deposited in peritubular capillaries (PTC) and whether it correlates
11 r of layers of basement membrane (BM) around peritubular capillaries (PTC) can be used in a cohort of
12                            C4d deposition in peritubular capillaries (PTC) of renal allografts has be
13 odies (DSA) and complement C4d deposition in peritubular capillaries (PTC).
14 graft function (DGF) and to an early loss of peritubular capillaries (PTC).
15                         Deposition of C4d in peritubular capillaries (PTCs) has been shown to be a se
16 nic kidney diseases, leads to rarefaction of peritubular capillaries (PTCs), promoting secondary isch
17                                    Injury to peritubular capillaries and capillary basement membrane
18 irus infection and were more frequent within peritubular capillaries and glomeruli from antibody-medi
19 scular cells and how these cells detach from peritubular capillaries and migrate to the interstitial
20 Additionally, we found endothelial damage in peritubular capillaries and vasa recta.
21                                 Human kidney peritubular capillaries are particularly susceptible to
22 o cases was the absence of C4d deposition in peritubular capillaries as well as the absence of C1q-bi
23 dy (DSA) and histologic evidence of AMR with peritubular capillaries C4d deposition.
24 ury, with a relative loss of staining of the peritubular capillaries compared with young rats.
25                   Although C4d deposition in peritubular capillaries has been identified as a strong
26 d deposited prominently and diffusely in the peritubular capillaries in all AHR biopsies (16 of 16).
27 y-implicated in the progressive attrition of peritubular capillaries in areas of tubular atrophy and
28 ition and thrombosis in renal glomerular and peritubular capillaries in association with a fall in he
29                     Endothelial cells of the peritubular capillaries in grafts with ABMR expressed fa
30                 We explored the integrity of peritubular capillaries in relation to expression of vas
31 s are also related to the presence of C4d in peritubular capillaries in TG biopsies.
32                            C4d deposition in peritubular capillaries is a specific marker for the pre
33 loss, the optimal cutoff for the fraction of peritubular capillaries needed to establish a positive s
34   Diffuse C4d deposition was detected in the peritubular capillaries of 6 of 48 (13%) biopsies.
35 ecificity the endothelium of the fenestrated peritubular capillaries of the kidney and those of the i
36 operfusion of L-arginine (10[-3] M) into the peritubular capillaries reduced the maximum TGF response
37                            The percentage of peritubular capillaries staining positively for C4d was
38 anism for this epidemiologic link is loss of peritubular capillaries triggering chronic hypoxia.
39                        Fascin1 expression in peritubular capillaries was also induced in a rat model
40                       The presence of C4d in peritubular capillaries was an independent risk factor f
41 ndothelial cell adhesion molecule-expressing peritubular capillaries was preceded by marked decreases
42 e higher in NRs, whereas Banff-C4d scores of peritubular capillaries were increased in the Rs.
43                               Glomerular and peritubular capillaries were increased with endothelial
44 sensitive AR, and widespread C4d deposits in peritubular capillaries were present in 18 of these 19 (
45 scopy revealed dilation of renal tubules and peritubular capillaries within 20 minutes of RCM applica
46 asured in double-perfused tubules (lumen and peritubular capillaries) by manipulating the applied tra
47 of the basement membranes (glomerular and/or peritubular capillaries) in milder forms of injury.
48  had acute graft dysfunction, neutrophils in peritubular capillaries, and a concurrent positive cross
49 IgM, and C5b-9 were scored in the glomeruli, peritubular capillaries, and arterioles.
50 ohistochemistry and evaluated on arterioles, peritubular capillaries, glomeruli, and tubular basement
51 jury as evidenced by reduced C4d staining in peritubular capillaries, microcirculation inflammation,
52 e increased pericytes around kidney cortical peritubular capillaries, perhaps an indirect consequence
53 ion, Nec-1 prevented RCM-induced dilation of peritubular capillaries, suggesting a novel role unrelat
54  of rejection had widespread C4d deposits in peritubular capillaries, suggesting a pathogenic role of
55 ted with preservation or accelerated loss of peritubular capillaries, suggesting no significant pro-a
56 howed gp-Fy in the endothelium of glomeruli, peritubular capillaries, vasa recta, and the principal c
57 ficiency causes dysmorphogenesis of cortical peritubular capillaries, with adjacent cells expressing
58  in association with immature glomerular and peritubular capillaries.
59 C3d) deposition was diffuse and prominent in peritubular capillaries.
60  microcirculation, especially with regard to peritubular capillaries.
61 optosis in arteries, tubules, glomeruli, and peritubular capillaries.
62  antibodies (0 of 8); 27% had neutrophils in peritubular capillaries.
63 epithelium and occasionally, in contact with peritubular capillaries.
64 dr/Vegfr2) is largely restricted to adjacent peritubular capillaries.
65  with a striking reduction in the density of peritubular capillaries.
66 HLA) cause graft injury identified by C4d in peritubular capillaries.
67 e Banff components glomerulitis (g), C4d, g+ peritubular capillaritis (ptc) and acute composite score
68                            Recently, diffuse peritubular capillaritis (ptc) has been suggested to ind
69                         Glomerulitis (g) and peritubular capillaritis (ptc) scores were independently
70 ined by the addition of glomerulitis (g) and peritubular capillaritis (ptc) scores) to assess long-te
71 nd lower glomerulitis, but similar levels of peritubular capillaritis and C4d deposition.
72 ) at diagnosis and changes in GFR (P<0.001), peritubular capillaritis Banff score (P=0.002), and DSA
73 mmation was prevalent, with glomerulitis and peritubular capillaritis found in 60.0% and 47.6% of 1-y
74                                              Peritubular capillaritis scores 1, 2, and 3 were present
75 glomerulitis, interstitial inflammation, and peritubular capillaritis scores were also significantly
76                                              Peritubular capillaritis was detected in 50% (76% mononu
77  microvascular injury scores (glomerulitis + peritubular capillaritis), were less in the TLN-treated
78 biopsy (glomerulitis, 6.1% vs. 32%, P=0.003; peritubular capillaritis: 13% vs. 40%, P=0.0009).
79 inical and molecular significance of minimal peritubular capillary (PTC) and isolated glomerular C4d+
80 whether, on electron microscopy examination, peritubular capillary (PTC) basement membrane multilayer
81 for allograft dysfunction, were assessed for peritubular capillary (PTC) C4d and CD55 expression.
82 ediated rejection, which is characterized by peritubular capillary (PTC) deposition of C4d.
83 atient with hemoglobin SC disease who showed peritubular capillary and vasa recta thrombi and capilla
84                                       Severe peritubular capillary basement membrane multilayering (P
85                                              Peritubular capillary basement membrane multilayering on
86 complement pathway, it was hypothesized that peritubular capillary C4d deposition might distinguish t
87           These results suggest that diffuse peritubular capillary C4d deposition without rejection i
88 teria, including capillaritis, glomerulitis, peritubular capillary C4d deposition, and donor-specific
89         In ABO-incompatible grafts, however, peritubular capillary C4d is often present on protocol b
90 ic associations and clinical implications of peritubular capillary C4d staining from long-term renal
91 nsitivity and specificity by the presence of peritubular capillary C4d staining on renal biopsy and d
92                                              Peritubular capillary C4d staining was negative in all c
93                                         Rare peritubular capillary C4d staining was present in 50% of
94 y-one patients (group A) had strong, diffuse peritubular capillary C4d staining without histologic ev
95 tients (group B) had negative or weak, focal peritubular capillary C4d staining.
96  degree of microcirculation inflammation and peritubular capillary C4d staining.
97 onents correlated with the g score, DSA, and peritubular capillary C4d+.
98 r endothelium, resulting in the formation of peritubular capillary C4d.
99                                  The loss of peritubular capillary density and caliber at week 8 clos
100 h mice to visualize, analyze, and quantitate peritubular capillary dynamics after AKI.
101 kidney, TNFR1 is expressed in glomerular and peritubular capillary EC, and some tubular cells, and co
102 ely associated with CD31- and Tie-2-positive peritubular capillary endothelia, and some of the alpha
103 was also associated with more glomerular and peritubular capillary endothelial cell loss in associati
104 us vehicle, P < 0.05), a twofold increase in peritubular capillary endothelial cell proliferation (1.
105 nal unit, formed by resident macrophages and peritubular capillary endothelial cells, which monitors
106             Damage to tubular epithelium and peritubular capillary endothelium also was seen.
107 herefrom perturb normal interactions between peritubular capillary endothelium and pericyte-like fibr
108     Additionally, HIFD significantly reduced peritubular capillary erythrocyte congestion and improve
109 i1(+) kidney pericytes in the maintenance of peritubular capillary health, and the consequences of pe
110 ated rejection manifests with glomerular and peritubular capillary inflammation and transplant glomer
111 ial, mononuclear cell infiltrates; prominent peritubular capillary inflammatory cell margination; pat
112  be the consequence of ischemia secondary to peritubular capillary injury and altered eNOS expression
113                    Ang-1 therapies attenuate peritubular capillary loss in adult models of tubulointe
114 nti-angiogenic effects leading to aggravated peritubular capillary loss.
115       Glomerular CD68+ cells correlated with peritubular capillary multilamellation, and similarly, t
116  was associated with a higher density of the peritubular capillary network in the corticomedullary ju
117                       Integrity of the renal peritubular capillary network is an important limiting f
118 alk by Vegfa is essential for maintenance of peritubular capillary networks in kidney.
119 e AKI, we measured a 40%+/-7.4% reduction in peritubular capillary number (P<0.05) and a 36%+/-4% dec
120  genetically labeled endothelia, we compared peritubular capillary number and size after moderate AKI
121  organ level, trametinib completely restored peritubular capillary perfusion in the kidney.
122 calized E-selectin to the endothelium of the peritubular capillary plexus.
123  vehicle, P < 0.01), a threefold decrease in peritubular capillary rarefaction (P < 0.01), and a twof
124                                              Peritubular capillary rarefaction is hypothesized to con
125                   We detected glomerular and peritubular capillary rarefaction, macrophage infiltrati
126 igger transient tubular injury and permanent peritubular capillary rarefaction.
127 ata show that in long-term renal allografts, peritubular capillary staining for C4d occurs in approxi
128                                       C4d in peritubular capillary walls distinguishes AHR from ACR,
129 surfaces of endothelial cells in glomerular, peritubular capillary, and arterial renal sites of matur
130 teomic study using cultured human testicular peritubular cells (HTPCs) i.e. the cells, which form thi
131 nding effects of erythropoietin induction in peritubular cells and unwarranted extrarenal effects.
132                              Thus testicular peritubular cells, via PEDF, may prevent vascularization
133  and (4) GSH can be secreted intact from the peritubular compartment into the tubular lumen.
134                                              Peritubular complement C3d staining was also similar in
135      This study supports the hypothesis that peritubular dentin is a non-collagenous tissue and is th
136 al areas contained distorted tubules without peritubular dentin or intratubular mineral.
137 in the dentin intertubular matrix, while the peritubular dentin remained without response.
138                                              Peritubular dentin values were unaltered in transparent
139                   CRS decreased podocyte and peritubular endothelial cell killing associated with col
140 of diabetic nephropathy with proteinuria and peritubular extracellular matrix production.
141 ephritis and with spontaneous glomerular and peritubular fibrin deposition in the nephritic kidney.
142 fibrin within the glomeruli and by decreased peritubular inflammation.
143                                        Renal peritubular interstitial fibroblast-like cells are criti
144 ediated (HIF-2-mediated) induction of EPO in peritubular interstitial fibroblast-like cells, which se
145 sion is activated by tissue hypoxia in renal peritubular interstitial fibroblasts and, to a lesser ex
146 ive myofibroblasts dramatically increased in peritubular interstitial spaces 48 hours after Habu veno
147 essels and fewer F4/80 positive cells in the peritubular interstitium.
148 beta prominently immunolocalized in cortical peritubular locations.
149  interstitial macrophage population, whereas peritubular macrophages are exclusively seeded postnatal
150 sure, EOCs not only attenuated mesangial and peritubular matrix expansion, as well as tubular apoptos
151 d with hypoxia and oxidant generation in the peritubular microenvironment and a decrease in glomerula
152 l hemodynamics and oxidant generation in the peritubular microenvironment using the murine cecal liga
153 ed, purified, and characterized human kidney peritubular microvascular endothelial cells (HKMECs) and
154  receptor-positive Leydig, Sertoli, and some peritubular myoepithelial cells express SUMO-1, findings
155 us epithelium delimited by Sertoli cells and peritubular myoid (PM) cells.
156 sis, but the role for androgen signaling via peritubular myoid (PTM) cells is contentious.
157                 The basal lamina produced by peritubular myoid and Sertoli cells is disrupted, leadin
158 o maintain normal Sertoli cells function and peritubular myoid cell contractility, thus ensuring norm
159           Furthermore, there were defects in peritubular myoid cell contractility-related genes such
160 out mouse with the AR gene deleted in testis peritubular myoid cells (PM-AR-/y).
161  to maintain the differentiated phenotype of peritubular myoid cells (PTMCs) in prepubertal life; (2)
162 erentiation by regulating the development of peritubular myoid cells and the formation of intact test
163                             BrdU labeling of peritubular myoid cells is low, consistent with decrease
164 ence for the requirement of functional AR in peritubular myoid cells to maintain normal Sertoli cells
165 known as Pept1, was predominantly present in peritubular myoid cells, interstitial Leydig cells, vasc
166                       However, the number of peritubular myoid cells, which normally surround the tes
167  (AR) on the Sertoli cells, Leydig cells and peritubular myoid cells.
168 lized to clusters of Leydig cells and select peritubular myoid cells.
169 is similar to the IC50 for PAH inhibition of peritubular ochratoxin A uptake in tubule suspensions an
170 High DSA levels and positive C4d staining of peritubular or glomerular capillaries were present at th
171                                        Thus, peritubular OTA uptake into all segments of the proximal
172                               Application of peritubular ouabain (0.1 mM) significantly increased (P
173 in tubule suspensions and the Km, values for peritubular PAH uptake.
174 P<0.001) for a 62%+/-2.2% reduction in total peritubular perfusion (P<0.01).
175                                Whereas total peritubular perfusion and number of capillaries did not
176           A precise definition of changes in peritubular perfusion would help test this hypothesis by
177  severity of acute injury and future loss of peritubular perfusion, demonstrate that reduced capillar
178                          The identity of the peritubular population of cells with mesenchymal phenoty
179 opoiesis and is predominantly synthesized by peritubular renal interstitial fibroblast-like cells, wh
180   Leydig cells, which normally reside in the peritubular space and extend from the coelomic surface t
181                    The normal renal cortical peritubular space contains fenestrated capillaries, whic
182 d capillaries and adjacent cells in cortical peritubular spaces in mutant neonate kidneys.
183 Epifluorescence microscopy was used to study peritubular transport of the fluorescent mycotoxin ochra
184 apacity of this pathway for OTA suggest that peritubular uptake may be a significant avenue for the e
185     Several lines of evidence indicated that peritubular uptake of OTA in S2 segments was effectively
186 nge of Km values previously reported for the peritubular uptake of PAH.
187 ntravital two-photon imaging revealed prompt peritubular vasodilation after fluvoxamine treatment, wh
188  and in platelets adherent in glomerular and peritubular vessels.

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