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1 ung contusions tended to be posterior (60%), crescentic (50%), or amorphous (45%) and have confluent
2 angiitis, MPO-ANCA, higher serum creatinine, crescentic and sclerotic classes, and higher Brix score
3 ith small flakes, microblades, and retouched crescentic and trapezoidal tools, probably projectile el
4 ar-Kyoto rats with bovine GBM also induced a crescentic anti-GBM GN with an increase of renal cortica
5 ized with rabbit IgG, induced an accelerated crescentic anti-GBM GN.
6 cumulation and renal injury in experimental, crescentic anti-GBM nephritis.
7   Minor terminal fields were identified in a crescentic column of the lateral PAG, as well as in the
8 izumab may have a place in the management of crescentic dense deposit disease.
9 litting margin (stage 1), an inward detached crescentic flap lying on the anterior lens (stage 2), a
10 al evidence alone (such as the presence of a crescentic fluke), information on their soft parts has h
11 el to each other rather than in star-like or crescentic forms--are the most abundant type of desert s
12 onstrated to be involved in animal models of crescentic glomerulonephritis (cGN) and are potential ta
13 ocal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CGN) remain poorly unders
14                                              Crescentic glomerulonephritis (Crgn) is a complex diseas
15                                              Crescentic glomerulonephritis (Crgn) is a complex disord
16                          Treatment of acute, crescentic glomerulonephritis (GN) consists of unspecifi
17                                              Crescentic glomerulonephritis (GN) is a devastating dise
18  and Th17 cells are also the main drivers of crescentic glomerulonephritis (GN), the most severe form
19 phages to progressive renal injury in murine crescentic glomerulonephritis (GN).
20 that ANCA cause pauci-immune necrotizing and crescentic glomerulonephritis (NCGN) and systemic small
21 evidence that MPO-ANCA cause necrotizing and crescentic glomerulonephritis (NCGN) and vasculitis.
22                              Necrotizing and crescentic glomerulonephritis (NCGN) occurs in all syndr
23  elucidated ANCA-IgG induced necrotizing and crescentic glomerulonephritis (NCGN), pathogenesis of AN
24  development of pauci-immune necrotizing and crescentic glomerulonephritis (NCGN).
25 o ANCA-associated vasculitis and necrotizing crescentic glomerulonephritis (NCGN).
26                                 Pauci-immune crescentic glomerulonephritis (PICGN) is a major cause o
27 ly progressive glomerulonephritis/idiopathic crescentic glomerulonephritis (RPGN/ICG), IgA nephropath
28 ronounced in females, which developed severe crescentic glomerulonephritis accompanied by heavy prote
29  microscopic polyangiitis or necrotizing and crescentic glomerulonephritis achieve remission with the
30 city of Th17 cells in a mouse model of acute crescentic glomerulonephritis and in a mouse chronic mod
31  dose of 1600 microg/kg induced pauci-immune crescentic glomerulonephritis and lung hemorrhage in all
32 400 microg/kg of myeloperoxidase resulted in crescentic glomerulonephritis and lung hemorrhage in all
33                                              Crescentic glomerulonephritis and lung hemorrhage were M
34 s model so that all animals reliably develop crescentic glomerulonephritis and lung hemorrhage.
35 f patients with pauci-immune necrotizing and crescentic glomerulonephritis and systemic small vessel
36 both glomerular and interstitial fibrosis in crescentic glomerulonephritis and that neutralization of
37 microscopic polyangiitis and necrotizing and crescentic glomerulonephritis associated with antineutro
38 l, illustrate that TLR4 stimulation triggers crescentic glomerulonephritis by effects on both the ada
39  the role of SPARC in mediating experimental crescentic glomerulonephritis by inducing passive nephro
40    We hypothesized that the MDM2 would drive crescentic glomerulonephritis by NF-kappaB-dependent glo
41 ion is effective in reducing the severity of crescentic glomerulonephritis even when treatment is sta
42 early along the mouse GBM in vivo, eliciting crescentic glomerulonephritis in Fcgr2b(-/-) mice suscep
43  and the deterioration of kidney function in crescentic glomerulonephritis in mice.
44 ty of collagen-induced arthritis in mice and crescentic glomerulonephritis in rats, in part by decrea
45 everal susceptibility loci, Crgn1-Crgn7, for crescentic glomerulonephritis in the Wistar Kyoto (WKY)
46 ndance resulting from experimentally induced crescentic glomerulonephritis in these rats.
47                                     Inducing crescentic glomerulonephritis in two Pax2Cre reporter mo
48       The residual genetic susceptibility to crescentic glomerulonephritis in WKY.LCrgn1,2 rats assoc
49                                              Crescentic glomerulonephritis is an important cause of h
50                                              Crescentic glomerulonephritis is characterized by vascul
51 he migration of leukocytes into glomeruli in crescentic glomerulonephritis is fundamental to pathogen
52                                  Concomitant crescentic glomerulonephritis led to an initial mistaken
53  These azotemic EGF-deficient mice developed crescentic glomerulonephritis linked to HB-EGF/EGFR hype
54  kidney and lung basement membranes, neither crescentic glomerulonephritis nor alveolitis ensued, lik
55 WKY) rat strain, we have identified multiple crescentic glomerulonephritis QTL (Crgn) and positionall
56  MC1R null-mutant mice developed more severe crescentic glomerulonephritis than wild-type mice, marke
57 plenocytes into immune-deficient mice caused crescentic glomerulonephritis that could be completely b
58              Ranging from autoimmune-induced crescentic glomerulonephritis to HIV infection-induced c
59                               In these mice, crescentic glomerulonephritis was induced with a previou
60     Renal biopsy demonstrated a pauci-immune crescentic glomerulonephritis with 14 cellular crescents
61  control IgG developed focal necrotizing and crescentic glomerulonephritis with a paucity of glomerul
62 inin-521 in female Wistar-Kyoto rats induced crescentic glomerulonephritis with linear IgG deposits a
63 ematopoietic stem cell disorders, attenuated crescentic glomerulonephritis with recovery of kidney fu
64 CR1 also promoted influx of DC precursors in crescentic glomerulonephritis, a DC-dependent aggressive
65 apsing glomerulopathy variant), pauci-immune crescentic glomerulonephritis, acute interstitial nephri
66 atment experiment, all rats developed florid crescentic glomerulonephritis, and control rats showed m
67 li were also noted in amyloidosis, diabetes, crescentic glomerulonephritis, and diffuse endocapillary
68 604Glyfs*2), recurrent bacterial infections, crescentic glomerulonephritis, and end-stage renal failu
69 ome, idiopathic pauci-immune necrotizing and crescentic glomerulonephritis, and related and overlappi
70            With the emergence of necrotizing/crescentic glomerulonephritis, approximately 0.15% of re
71 splenocytes developed severe necrotizing and crescentic glomerulonephritis, granulomatous inflammatio
72       Excluding pauci-immune necrotizing and crescentic glomerulonephritis, IgG4 immunohistochemistry
73                   Moreover, in patients with crescentic glomerulonephritis, IL-26 is expressed by ren
74  ANCA-positive patients with necrotizing and crescentic glomerulonephritis, including 69 with evidenc
75 e's syndrome (GPS) develop severe autoimmune crescentic glomerulonephritis, kidney failure, and lung
76 or and found increased life span, suppressed crescentic glomerulonephritis, reduced spleen size, and
77       Kidney biopsy revealed necrotizing and crescentic glomerulonephritis, similar to primary ANCA-G
78 toplasmic antibody (ANCA) vasculitis-induced crescentic glomerulonephritis, to identify common diseas
79 iquely susceptible to experimentally induced crescentic glomerulonephritis.
80 elerating glomerulosclerosis in experimental crescentic glomerulonephritis.
81 (PEC) are major constituents of crescents in crescentic glomerulonephritis.
82 oto (WKY) rat shows marked susceptibility to crescentic glomerulonephritis.
83  of renal injury in an experimental model of crescentic glomerulonephritis.
84 s approach is effective in the prevention of crescentic glomerulonephritis.
85 proaches may be worth investigating in human crescentic glomerulonephritis.
86 amined the effect of an antibody to VLA-1 in crescentic glomerulonephritis.
87 ll type targeted in ANCA-induced necrotizing crescentic glomerulonephritis.
88  was associated with a poor outcome in human crescentic glomerulonephritis.
89 ng the kidneys, where they cause necrotizing crescentic glomerulonephritis.
90 e as the pre-emptive treatment in abrogating crescentic glomerulonephritis.
91 kade by nutlin-3a ameliorated all aspects of crescentic glomerulonephritis.
92 izations were needed to induce a necrotizing/crescentic glomerulonephritis.
93 autoimmune glomerulonephritis or necrotizing/crescentic glomerulonephritis.
94 corticoids, renal function in a rat model of crescentic glomerulonephritis.
95 sion of crescentic lesions in a patient with crescentic glomerulonephritis.
96 murine anti-MPO Abs derived from Spontaneous Crescentic Glomerulonephritis/Kinjoh mice.
97                                              Crescentic GN (cGN) is an aggressive form of immune-medi
98         T-cell infiltration is a hallmark of crescentic GN (cGN), often caused by ANCA-associated vas
99 h1 cells are central pathogenic mediators of crescentic GN (cGN).
100 Cs belong to the CD11b(+) subset and promote crescentic GN (cGN).
101 exes within glomerular capillary walls cause crescentic GN (CrGN).
102 t endothelial NF-kappaB mediates necrotizing crescentic GN (NCGN) and provides a specific treatment t
103 asmic antibody (ANCA)-associated necrotizing crescentic GN (NCGN) is incompletely understood.
104                              Necrotizing and crescentic GN (NCGN) with a paucity of glomerular immuno
105 A-associated vasculitis features necrotizing crescentic GN (NCGN), and ANCA-activated neutrophils con
106  phagocytes cause vasculitis and necrotizing crescentic GN (NCGN).
107           Here, using a mouse model of acute crescentic GN (nephrotoxic nephritis), we identified CD4
108 sociated crescentic GN and a murine model of crescentic GN (nephrotoxic nephritis).
109 etic nephropathy, 19; immune complex GN, 12; crescentic GN (vasculitis), 6; hemolytic uremic syndrome
110                               DBA/1 mice had crescentic GN 11 wk postimmunization with alpha3(IV)NC1.
111 the kidneys of patients with ANCA-associated crescentic GN and a murine model of crescentic GN (nephr
112 the kidneys of patients with ANCA-associated crescentic GN and colocalize with CXCR3(+) effector T ce
113 tions, we used a mouse model of experimental crescentic GN and double Foxp3mRFP IL-10eGFP reporter mi
114 Furthermore, biTregs appear to contribute to crescentic GN and hence may be novel therapeutic targets
115 e response and tissue injury in experimental crescentic GN and show that miR-155 is a potential thera
116 hlight the suppressive functions of Tregs in crescentic GN and suggest the importance of Treg-derived
117 ls, which have been shown to protect against crescentic GN and which require IKK2.
118 the kidneys of patients with ANCA-associated crescentic GN as opposed to patients with acute bacteria
119  samples from patients with various forms of crescentic GN for myeloperoxidase and neutrophils, measu
120                    All biopsy specimens with crescentic GN had extracellular glomerular myeloperoxida
121  membrane (GBM) antibody (Ab) GN, a model of crescentic GN in the WKY rat, and whether the effects of
122  ex vivo and were protective in experimental crescentic GN in vivo.
123 othelial cell damage in vitro, as well as on crescentic GN severity and antigen-specific T cell react
124 n in ANCA-associated vasculitis, may enhance crescentic GN through antigen-specific T and B cell acti
125 ced: nephrotoxic nephritis (NTN, a model for crescentic GN), pyelonephritis, and acute endotoxemic ki
126  NFkappaB-inducing kinase IKK2 can attenuate crescentic GN, a severe DC- and Th cell-dependent kidney
127  are key effectors of disease progression in crescentic GN, acting to regulate parenchymal cell popul
128 hrombotic microangiopathies, necrotizing and crescentic GN, acute tubular necrosis, and infective pye
129  evidenced by the development of necrotizing crescentic GN, albuminuria, renal impairment, and accumu
130 mbotic microangiopathy, one had pauci-immune crescentic GN, and another had global as well as segment
131 diseases, including diabetic kidney disease, crescentic GN, and dose-dependent direct podocyte toxici
132 ically target Th17 cells in murine and human crescentic GN, and suggest the kidney-specific action of
133                                In a model of crescentic GN, BTLA signaling effectively restrained nep
134 o the pathogenesis of human and experimental crescentic GN, but the cell types that produce IL-17A in
135 c cells (DCs) are protective early in murine crescentic GN, but the mechanisms underlying this protec
136                               In preclinical crescentic GN, delayed myeloperoxidase inhibition suppre
137 ephrotoxic nephritis (NTN), a mouse model of crescentic GN, in Btla -deficient ( BtlaKO ) mice and wi
138 ced nephrotoxic nephritis, a mouse model for crescentic GN, in mice lacking T cell-specific IL-6Ra.
139 antineutrophil cytoplasmic antibody-mediated crescentic GN, lupus nephritis, type I membranoprolifera
140                                    In murine crescentic GN, Mif-deficient mice were almost completely
141 udies suggest a role for Tregs in modulating crescentic GN, the underlying mechanisms are not well un
142                      Using a murine model of crescentic GN, we explored the effects of the CCL18 muri
143                Here, using a murine model of crescentic GN, we found that CD4(+) T cells, gammadelta
144                      Using a murine model of crescentic GN, we show that the pathogenic TH17/IL-17 im
145 nephritis (GN) as well as from patients with crescentic GN, with the aim of identifying potential ren
146 r a novel adjunctive therapeutic approach in crescentic GN.
147 he kidney in the early stage of experimental crescentic GN.
148 ted in kidneys of patients with two forms of crescentic GN.
149 phages through days 15 and 20 of progressive crescentic GN.
150 ferative, acute proliferative/exudative, and crescentic GN.
151 re) x Cxcr3(fl/fl)) and induced experimental crescentic GN.
152 r of diseases such as human and experimental crescentic GN.
153 d IL-17F drives renal tissue injury in acute crescentic GN.
154 e nephrotoxic nephritis (NTN) model of acute crescentic GN.
155 e nephrotoxic nephritis (NTN) model of acute crescentic GN.
156 hose in sera of patients with other forms of crescentic GN.
157 ctivity and renal relapse in ANCA-associated crescentic GN.
158 to understand its potential role in treating crescentic GN.
159 ted vasculitis is the most frequent cause of crescentic GN.
160 y samples from patients with ANCA-associated crescentic GN.
161 atients with newly diagnosed ANCA-associated crescentic GN.
162  observed in biopsy samples of patients with crescentic GN.
163  in the nephrotoxic nephritis (NTN) model of crescentic GN.
164 ne disease, including human and experimental crescentic GN.
165 econdary lymphoid tissue in a mouse model of crescentic GN.
166 nd contributing to the immunopathogenesis of crescentic GN.
167 t microscopy demonstrated pale pink, oval to crescentic intracytoplasmic inclusions with a predilecti
168 th membranous nephropathy and crescents, the crescentic lesion may be due to a distinct, separate dis
169  and molecular interactions occurring during crescentic lesion onset and evolution.
170 n progenitors concomitant with regression of crescentic lesions in a patient with crescentic glomerul
171 re 91% for focal, 69% for mixed, and 64% for crescentic (log-rank P<0.0001).
172 e Internet after a renal biopsy demonstrated crescentic, necrotizing glomerulonephritis and linear de
173 ice treated with nephrotoxic serum to induce crescentic nephritis (rapidly progressive GN), this gene
174 munity, was necessary for the development of crescentic nephritis in this model.
175 ation and the progression to fibrosis during crescentic nephritis we have developed and characterized
176 marked reduction in albuminuria, severity of crescentic nephritis, and number of glomerular macrophag
177 e identified a novel therapeutic approach in crescentic nephritis, that of glucocorticoid antagonism,
178 estigate its role in GN in a murine model of crescentic nephritis, the authors induced nephrotoxic ne
179 B- and T-cell epitopes in EAG and can induce crescentic nephritis.
180  important role in the inflammatory phase of crescentic nephritis.
181 ated glomerular parietal epithelial cells in crescentic nephritis.
182                       Patients classified as crescentic or mixed, however, had worse survival when th
183 e classified as absent, pinpoint, flattened, crescentic, or ellipsoidal flow.
184 categorizes patients as having focal, mixed, crescentic, or sclerotic GN.
185 by immunofluorescence (IF) without a diffuse crescentic pattern.
186 study of modern cryptochirid domicile shape (crescentic pit, circular-oval pit, or a true gall) shows
187                                              Crescentic pits in corals occur not only in the Western
188 ridae fam. nov. Nine Pleistocene corals with crescentic pits originate from Florida (USA), and single
189 tochirids in the fossil record through their crescentic pits, typical for certain cryptochirids, in W
190                                              Crescentic rapidly progressive glomerulonephritis (RPGN)
191                                           In crescentic RPGN the role of cellular rather than humoral
192 ion in 22 patients (75.9%) with a pattern of crescentic thickening in 19 (86.4%).
193 branous glomerulopathy, 1 was diagnosed with crescentic transformation of lupus nephritis, 1 was diag
194 ent's slowly progressive GN underwent severe crescentic transformation, leading to rapidly progressiv

 
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