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1 NGAL and IL-18 quantiles also predicted graft recovery u
2 NGAL blockade may be a novel therapeutic approach for th
3 NGAL can inhibit erythroid cell production, leading to a
4 NGAL depicted CIN in patients who received iodinated con
5 NGAL expression and intensity was evaluated separately.
6 NGAL expression correlated with negative hormone recepto
7 NGAL expression did not correlate with pCR in the full p
8 NGAL expression was required for MMP-9 activity and tumo
9 NGAL improved the C-statistic (0.835 to 0.842) for predi
10 NGAL induced apoptosis via caspase 3 activation and up-r
11 NGAL is a glycoprotein released by damaged renal tubular
12 NGAL is a novel marker best known for its role in rapidl
13 NGAL is a potential biomarker for the early detection of
14 NGAL is significantly increased in patients with myocard
15 NGAL is transcriptionally regulated by NFkappaB, and S2R
16 NGAL together with creatinine clearance plus MCP-1 was a
17 NGAL was analytically superior to traditional AKI biomar
18 NGAL was detected in 42.2% of the breast carcinomas in t
19 NGAL-expressing neutrophils and CD3(+) T cells were in c
20 NGAL-knockout mice had attenuated proteinuria and improv
21 utcomes and urinary concentrations of KIM-1, NGAL, 8-OHdG, and F2-isoprostane controlling for sex, ag
23 ve urine biomarkers of kidney injury (IL-18, NGAL, KIM-1, L-FABP, and albumin) and five plasma biomar
28 dase], KIM-1 [kidney injury molecule-1], and NGAL [neutrophil gelatinase-associated lipocalin]) were
30 levels of IL-1beta, MMP-3, MMP-8, MMP-9, and NGAL compared with the other study groups, strengthening
34 We determined the plasma levels of CysC and NGAL in 429 patients hospitalized for acute decompensati
37 elated anemia, and the ErbB2, NF-kappaB, and NGAL pathways may serve as potential therapeutic targets
39 ated with persistently high NGAL levels, and NGAL was an independent predictive factor of AKI progres
40 human DKK3, BMP1, vasorin, neogenin, MIA and NGAL treatment increased cellular quiescence in both C4-
41 y of renal damage in NGAL wild-type mice and NGAL-knockout mice following induction of nephrotoxic ne
42 rating cells, and cytokines in wild-type and NGAL-deficient chimeric mice with anti-MPO antibody-indu
45 e oxidation current upon the binding between NGAL and its antibody is obtained when compared to an un
47 n the fine-tuning of the interaction between NGAL and its cellular receptor or in a biochemical mecha
48 erminants underlying the interaction between NGAL and its cellular receptor remain largely unknown.
49 Tight correlations were observed between NGAL expression, renal histopathology, and urine NGAL ex
51 9), decreased expression of injury biomarker NGAL (P = .012), improved microvascular perfusion on con
55 onstrate an important role for CD4(+) T cell NGAL as a mechanism by which CD4(+) T cells mediate AKI
56 l CVD risk factors and creatinine clearance, NGAL was a significant predictor of CVD mortality (hazar
59 de (NT-proBNP) and C-reactive protein (CRP), NGAL remained an independent predictor of each outcome.
62 iltration rate <60 ml/min/1.73 m(2), a first NGAL <150 ng/ml indicated a low likelihood of adverse ev
64 Peak NGAL was more predictive than the first NGAL, but neither added significant diagnostic utility o
66 ansfer of NGAL-deficient CD4(+) T cells from NGAL KO mice into CD4 KO or WT mice led to worse renal f
70 elimination by Cox regression analysis, high NGAL remained an independent predictor of all-cause mort
71 zation was associated with persistently high NGAL levels, and NGAL was an independent predictive fact
73 In the HIV-transgenic mouse model of HIVAN, NGAL mRNA was abundant in dilated, microcystic segments
75 te with pCR in the full population, however, NGAL expression and staining intensity were significantl
76 relatively high levels of lipocalin 2 (human NGAL) induced suppression of hematopoiesis in spleen and
78 onformational stability of recombinant human NGAL and the solution phase binding properties of six mo
81 ceiving wild-type bone marrow, as well as in NGAL/IL-17A-deficient chimeras compared with NGAL-defici
82 we compared the severity of renal damage in NGAL wild-type mice and NGAL-knockout mice following ind
83 metabolites was associated with increases in NGAL (beta = 0.13 [95% CI: 0.05, 0.21], p = 0.001), KIM-
87 trinsic neutrophil functions were similar in NGAL-deficient and wild-type neutrophils, whereas T cell
90 Similarly, following nephritis induction, NGAL injection significantly exacerbated nephritis and d
94 neutrophil protease genes (MMP8, OLFM4, LCN2/NGAL, LTF, PRTN3, MPO) and also of 5 genes involved in t
95 expressed by osteoblasts, while MIA, LECT1, NGAL and PEDF are expressed by other calvarial cells.
97 neutrophil gelatinase-associated lipocalin (NGAL) and podocalyxin, concomitant with upregulated rena
98 neutrophil gelatinase-associated lipocalin (NGAL) can predict development of renal dysfunction (RD),
99 /neutrophil gelatinase-associated lipocalin (NGAL) complex is also significantly increased in AVM tis
102 neutrophil gelatinase-associated lipocalin (NGAL) has emerged an early marker protein, predicative o
103 neutrophil gelatinase-associated lipocalin (NGAL) in a large population of patients with ST-segment
104 Neutrophil gelatinase-associated lipocalin (NGAL) is a 25-kDa secreted acute phase protein, which is
105 Neutrophil gelatinase-associated lipocalin (NGAL) is a diagnostic marker of intrinsic kidney injury
106 Neutrophil gelatinase-associated lipocalin (NGAL) is a novel renal biomarker that may predict WRF in
107 Neutrophil gelatinase-associated lipocalin (NGAL) is a secreted glycoprotein expressed in a variety
108 Neutrophil gelatinase-associated lipocalin (NGAL) is an early marker of acute kidney injury (AKI).
109 neutrophil gelatinase-associated lipocalin (NGAL) is developed by the immobilization of rabbit polyg
110 Neutrophil gelatinase-associated lipocalin (NGAL) is expressed and secreted by immune cells, hepatoc
111 neutrophil gelatinase-associated lipocalin (NGAL) levels and cardiovascular and all-cause mortality
112 neutrophil gelatinase associated lipocalin (NGAL) was found to be involved in 1alpha,25(OH)2D3 and M
114 neutrophil gelatinase-associated lipocalin (NGAL) were found in diseased groups compared with the he
115 neutrophil gelatinase-associated lipocalin (NGAL) were the most robust markers but were not superior
116 neutrophil gelatinase-associated lipocalin (NGAL)), which is expressed in the distal nephron, has be
118 neutrophil gelatinase-associated lipocalin (NGAL), a marker of tubular injury, to determine whether
119 neutrophil gelatinase-associated lipocalin (NGAL), a novel marker of renal tubular damage, in patien
120 neutrophil gelatinase-associated lipocalin (NGAL), an iron-binding protein up-regulated in response
122 neutrophil gelatinase associated lipocalin (NGAL), combined with contemporary biomarkers such as N-t
123 neutrophil gelatinase-associated lipocalin (NGAL), IL-18, and kidney injury molecule-1 (KIM-1) as bi
124 neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), kidney injury molecule-1
125 neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1) and endothelin-1
126 neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), IL-18, and live
127 neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), IL-18, and live
128 neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver-type fatt
129 neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1, serum creatinine, and c
130 neutrophil gelatinase-associated lipocalin (NGAL), monomeric NGAL (mNGAL), interleukin-18, and stand
131 neutrophil gelatinase-associated lipocalin (NGAL), or plasma NGAL could identify which patients woul
132 neutrophil gelatinase-associated lipocalin (NGAL), or plasma NGAL could identify which patients woul
133 neutrophil gelatinase-associated lipocalin (NGAL), which is a new diagnostic marker of acute kidney
135 neutrophil gelatinase-associated lipocalin (NGAL); each measurement was on the day of AKI diagnosis
136 neutrophil gelatinase-associated lipocalin (NGAL, also known as LCN2) and its cellular receptor (LCN
137 neutrophil gelatinase-associated lipocalin [NGAL]) and oxidative stress (8-hydroxy-2'-deoxyguanosine
138 neutrophil gelatinase-associated lipocalin [NGAL]) is an antimicrobial host defense factor produced
139 (neutrophil gelatinase-associated lipocalin [NGAL], interleukin [IL]-18, liver fatty acid-binding pro
140 neutrophil gelatinase-associated lipocalin, NGAL), kidney growth, and glomerulosclerosis, however, w
144 isease (hazard ratio [per SD increase in log NGAL]=1.45 [1.22-1.72]; P<0.001 and hazard ratio=1.51 [1
146 elayed graft function (highest versus lowest NGAL tertile relative risk, 1.21; 95% confidence interva
147 regulation of urinary kidney injury markers (NGAL and KIM-1) and renal Interleukin-6 and Ngal mRNA ob
151 inase-associated lipocalin (NGAL), monomeric NGAL (mNGAL), interleukin-18, and standard biomarkers we
154 bone marrow-derived, presumably neutrophil, NGAL protects from ANCA-induced NCGN by downregulating T
156 rve analysis suggested that the abilities of NGAL or IL-18 to predict dialysis within 1 wk were moder
159 cation improvement (>0) with the addition of NGAL was 18% (p = 0.02); the integrated discrimination i
161 With ML, the AKI predictive capability of NGAL was further enhanced when combined with NT-proBNP o
163 n, the sensor is tested for the detection of NGAL in human urine, and the results correspond well wit
166 ic antibodies stimulates local expression of NGAL, which plays a crucial role in the pathogenesis of
167 Pgrmc1) markedly regulated the expression of NGAL/LCN2 (neutrophil gelatinase-associated lipocalin/li
168 or has been constructed by immobilization of NGAL capture antibodies to electropolymerized aniline de
172 ed growth inhibition for CCA as knockdown of NGAL decreased Ki-67 expression in SNU308 cells and rend
173 nt of serum creatinine, and higher levels of NGAL and ET-1 were associated with a higher EVKP score (
174 xPC-3, and Capan-2) expressed high levels of NGAL but moderately to poorly differentiated PaCa cells
175 In multivariate analysis, elevated levels of NGAL or IL-18 predicted the need for dialysis after adju
180 g creatinine, sensitivity and specificity of NGAL for detecting acute injury were 0.900 (95% CI, 0.73
182 These data show that marked upregulation of NGAL accompanies HIVAN and support further study of uNGA
184 Conclusion: These results support the use of NGAL in clinical practice within the context of a diagno
186 These pleiotropic functions mainly rely on NGAL's siderophore-mediated iron transport properties.
188 ce with bone marrow from either wild-type or NGAL-deficient mice; we also transplanted irradiated MPO
189 Finally, MIAPaCa-2 cells overexpressing NGAL reduced tumor volume (P = 0.012), local and distant
190 Compared with K562 cells, overexpressing NGAL in K562 led to a higher apoptosis rate and an atrop
192 surement of urinary biomarkers, particularly NGAL in combination with functional perfusion parameters
194 first NGAL was a better predictor than peak NGAL, but similar to the first creatinine (areas under t
200 95% confidence interval=1.3-9.1), and plasma NGAL (odds ratio=7.7, 95% confidence interval=2.6-22.5).
201 clusion, urine IL-18, urine NGAL, and plasma NGAL associate with subsequent AKI and poor outcomes amo
202 highest quintiles of urine IL-18 and plasma NGAL associated with 6.8-fold and 5-fold higher odds of
203 Elevated urine IL-18 and urine and plasma NGAL levels associated with longer length of hospital st
208 w cystatin C (median cut-off), higher plasma NGAL levels were independently associated with an increa
212 , urine IL-18 and urine NGAL, but not plasma NGAL, associate with subsequent AKI and poor outcomes am
214 inase-associated lipocalin (NGAL), or plasma NGAL could identify which patients would develop AKI and
215 inase-associated lipocalin (NGAL), or plasma NGAL could identify which patients would develop AKI and
218 d with the clinical model alone, with plasma NGAL performing the best (category-free net reclassifica
219 In univariate survival analysis, positive NGAL expression and strong staining intensity correlated
228 There was a significant difference in serum NGAL between healthy children (median 80 ng/mL, interqua
230 owed high sensitivity and specificity (serum NGAL: area under the curve, 0.995; 95% confidence interv
232 untreated tissue microarray showed specific NGAL staining in resected PaCa specimens (P = 0.0167).
236 The results show that in low-risk subgroups, NGAL was found to be a predictive marker for pCR after N
238 GAL has been sparked by the observation that NGAL is massively upregulated after renal tubular injury
241 o-simulated ischemia/reperfusion showed that NGAL-deficient CD4(+) T cells express higher levels of I
242 re neutrophils, and recent data suggest that NGAL may also be involved in the development of atherosc
245 in the absence of renal injury, induced the NGAL gene, but not MCP-1, suggesting the possibility of
248 , we show that ErbB2 overexpression leads to NGAL upregulation, which is dependent on nuclear factor-
254 fidence interval [CI]: 0.868, 0.992; urinary NGAL: area under the curve, 0.992; 95% CI: 0.925, 1.000)
259 ipient characteristics, higher donor urinary NGAL concentrations associated with recipient delayed gr
260 al function demonstrated that higher urinary NGAL and L-FABP concentrations associated with slightly
261 ry had a significantly elevated mean urinary NGAL level compared with the other kidney function group
262 th stable allograft function, median urinary NGAL concentration was 7.8 ng/mL (interquartile range, 3
266 As a readily available parameter, urinary NGAL may guide differential diagnosis and initial therap
267 In multiple logistic regression, urinary NGAL level was highly predictive of clinical outcomes, i
275 e highest quintiles of urine IL-18 and urine NGAL associated with 6.9- and 4.1-fold higher odds of AK
281 hat kidney NGAL expression, as well as urine NGAL levels, were significantly increased in mice with n
282 duced AKI occurred at 6 hours for both urine NGAL (>/=20 ng/mL; 97% negative predictive value and 27%
283 nclusion, among prevalent KTRs, higher urine NGAL, KIM-1, and IL-18 levels independently and differen
286 ents (validation set), no patient with urine NGAL <20 ng/mL or sNGAL <179 ng/mL at 6 hours developed
287 redictor of response to NACT and to validate NGAL as a prognostic factor for clinical outcome in pati
289 stly improved the prediction of DGF, whereas NGAL, serum creatinine, and the creatinine reduction rat
291 We undertook this study to determine whether NGAL is instrumental in the pathogenesis of nephritis, i
293 ay represent an important mechanism by which NGAL may contribute to the loss of cartilage matrix prot
294 at day 3 did not provide any benefit; while NGAL is also associated with short-term mortality, it fa
297 intrinsically disordered and interacts with NGAL preferentially in its apo state to form a fuzzy com
299 immunity was increased in chimeric mice with NGAL-deficient neutrophils with more renal infiltrating