ライフサイエンスコーパス: DN

1 to the development of diabetic nephropathy (DN).

2 e mechanisms underlying diabetic neuropathy (DN).

3 to treat patients with diabetic nephropathy (DN).

4 mplications, including diabetic nephropathy (DN).

5 omerulopathy (ORG) and diabetic nephropathy (DN).

6 y-proven, mild and moderate dysplastic nevi (DN).

7 e with FSGS and type 2 diabetic nephropathy (DN).

8 in the pathogenesis of diabetic neuropathy (DN).

9 s been associated with diabetic nephropathy (DN).

10 to the pathogenesis of diabetic nephropathy (DN).

11 ersible progression of diabetic nephropathy (DN).

12 njury in patients with diabetic nephropathy (DN).

13 in PTECs and downregulated in patients with DN.

14 lysis changing the mechanism from ANDN to AN+DN.

15 ithout DN and those with histologic signs of DN.

16 c mice, causing insulin unresponsiveness and DN.

17 ide analysis of the PNS of a rodent model of DN.

18 helin-1 are essential for the development of DN.

19 contribute to the glycemic memory effect in DN.

20 c Chop(-/-) mice that showed protection from DN.

21 he clinical characteristics of patients with DN.

22 n of CDK2 associates with the development of DN.

23 ites in 9.9% of excised and 9.4% of resected DN.

24 nflammatory microRNA, in the pathogenesis of DN.

25 ), has been implicated in the progression of DN.

26 cyte B7-1 for the prevention or treatment of DN.

27 a novel therapy to improve renal outcomes in DN.

28 to Drp1 as a potential therapeutic target in DN.

29 therapeutic target and a novel biomarker of DN.

30 m in miR-146a(-/-) mice leads to accelerated DN.

31 sion, on the pathogenesis and progression of DN.

32 rrelation between Li(+)-O2(-) solubility and DN.

33 nsulin resistance, podocyte dysfunction, and DN.

34 recently emerged as important regulators of DN.

35 al and histological features associated with DN.

36 significant improvements in key features of DN.

37 of action of endothelin receptor blockers in DN.

38 targeting strategies to treat proteinuria in DN.

39 anti-inflammatory noncoding RNA modulator of DN.

40 nctions have to be considered jointly in the DN.

41 revent podocyte apoptosis and progression of DN.

42 sin system inhibition to slow progression of DN.

43 re not associated with an SI increase in the DN.

44 Cs has the potential to treat and ameliorate DN.

45 athways were elevated in individuals without DN.

46 ovel renal-specific GLUT2 inhibitors against DN.

47 hat contribute to peripheral nerve injury in DN.

48 lpha is an attractive therapeutic target for DN.

49 that the activation of DGK would ameliorate DN.

50 f RTN1A and ER stress in podocyte injury and DN.

51 rs led to a small thymus, a double negative (DN)1/DN2 thymocyte transition block, and an accumulation

52 with Bifidobacterium animalis subsp. lactis DN-173010 versus a placebo yogurt, followed by a 5-day n

53 Among 590 positive-margin DN, 191 were reexcised and 399 clinically observed witho

54 nger than 60 y with peripheral expansions of DN (8/41) and CD21(low) (9/41) B cells compared with age

55 better treatments for diabetic nephropathy (DN), a debilitating renal complication.

56 ghted signal enhancement was observed in the DN after multiple macrocyclic GBCA injections.

57 The lateral cerebellum (hemispheres and DN) also participates in modulating goal directed gaze b

58 unc-1(dn) alters a stomatin-like protein that regulates unc-9

59 DN and CD21(low) B cell frequencies were further increas

60 prevalence and functional characteristics of DN and CD21(low) B cells in multiple sclerosis (MS) pati

61 Increased frequencies of DN and CD21(low) B cells were found in the cerebrospinal

62 loproteinase (MMP)-1/2/9 genes compared with DN and double-positive (DP) subpopulations.

63 Conclusion Changes in SI of the DN and GP that are independent of the administration of

64 ochondrial morphology and the progression of DN and point to Drp1 as a potential therapeutic target i

65 uerarin in an experimental model of advanced DN and provide a molecular mechanism by which puerarin e

66 ding hypotheses for further investigation in DN and providing a workflow with potential applications

67 ess plays a major role in podocyte injury in DN and RTN1A might be a key regulator of ER stress in po

68 that the decreased connectivity between the DN and the left caudate nucleus could play a role in bal

69 eme duration of diabetes (l50 years) without DN and those with histologic signs of DN.

70 od and neural responses to heartbeats in the DN and thus directly support theories grounding selfhood

71 ctomy (Unx) as a murine model of progressive DN and treated mice with tauroursodeoxycholic acid (TUDC

72 Patients with diabetic nephropathy (DN) and autosomal-dominant polycystic kidney disease (AD

73 Recently, IgD(-)CD27(-) (double negative, DN) and CD21(-)CD11c(+) (CD21(low)) B cells were describ

74 ensity (SI) increase in the dentate nucleus (DN) and globus pallidus (GP) in relation to the middle c

75 Recurrent de novo (DN) and likely gene-disruptive (LGD) mutations contribut

76 is an early feature of diabetic nephropathy (DN) and predicts its progression.

77 ), number (Tb.N), connectivity density (Conn.Dn), and by increased separation (Tb.Sp) in trabecular b

78 allidus (GP), thalamus (T), dentate nucleus (DN), and pons (P) were measured on unenhanced T1-weighte

79 n energy of Li(+) trended with donor number (DN), and varied greater than that of O2 (-) ions, which

80 ncreased in the glomeruli of mouse models of DN, and mesangial cells treated with transforming growth

81 erentiation transcription factors in memory, DN, and naive B cells in SLE show elevated levels of Aio

82 Using a DN approach and RNA interference knockdown, we demonstra

83 seemingly disparate functional roles of the DN are functionally coupled, in line with theories propo

84 late effects (>130 ms) in other nodes of the DN, as well as FPN and SN.

85 hy (DN) may be involved in the generation of DN-associated peptides in urine.

86 A dominant-negative (dn) atypical PKM selectively reversed associative LTF, w

87 tors BAFF, IL-2, and IL-21 induce memory and DN B cell activation and differentiation has implication

88 ereas SLE patients exhibit elevated BAFF and DN B cells and reduced IL-21.

89 The majority of DN B cells had an IgG(+) memory phenotype, whereas CD21(

90 Further, DN B cells produced proinflammatory and cytotoxic cytoki

91 DN B cells showed similar (MS patients) or increased (he

92 d memory-like CD27(-)IgD(-) double-negative (DN) B cells, but not CD27(-)IgD(+) naive B cells.

93 ed B7-1 expression in human and experimental DN before embarking on clinical studies of the use of B7

94 as been highlighted in diabetic nephropathy (DN), but little is known about the underlying molecular

95 onists have emerged as a novel treatment for DN, but the mechanisms underlying the protective effect

96 Thus, PKM2 activation may protect against DN by increasing glucose metabolic flux, inhibiting the

97 chromatin reorganization and progression of DN by modulating its target Msk2, a histone kinase, and

98 each form of LTF is sensitive to a distinct dn calpain expressed in the postsynaptic neuron.

99 y, these data suggest TCR signal strength in DN cells directly impacts on subsequent DP cell differen

100 Adoptive transfer of splenic DN cells gives rise to CD8alphaalpha cells in the gut, e

101 ion, both displayed weaker TCR signalling in DN cells, an inefficient DN-to-DP transition, and reduce

102 that display altered TCR signal strength in DN cells, which correlates with altered generation of un

103 n mice with increased TCR signal strength in DN cells.

104 example in CD4((-))CD8((-)) double negative (DN) cells, impact on later fate decisions is presently u

105 Associative LTF is blocked by dn classical calpain, whereas non-associative LTF is blo

106 electively reversed associative LTF, while a dn classical PKM selectively reversed non-associative LT

107 KEY POINTS: A cerebellar dentate nuclei (DN) contribution to volitional oculomotor control has re

108 hat heartbeat-evoked responses (HERs) in the DN covary with the self-relatedness of ongoing spontaneo

109 CTX patients with DN damage showed less precise saccades with longer laten

110 metabolic disease typically characterized by DN damage.

111 tions in CYP27A1, typically characterized by DN damage.

112 Laparoscopic DN decreased the need for intraoperative blood transfusi

113 ession, with adjustment for sex, age, HbA1c, DN, diabetes duration, smoking, systolic blood pressure,

114 and loss of BDNF surge in the hippocampus of DN-DISC mice, but not in wild-type mice.

115 on of BDNF in the hippocampus of THC-treated DN-DISC1 mice prevented the impairment in recognition me

116 Wild-Type and dominant-negative-DISC1 (DN-DISC1) mice were injected with THC (10 mg/kg) or vehi

117 S) activity, known to predict progression of DN, downregulated CDK2 (cyclin-dependent kinase 2).

118 The estimated dN/dS < 1 in the concatenated protein-coding genes sugge

119 be a better approach than the commonly used dN/dS metric for identifying functionally significant ge

120 nonymous to synonymous evolutionary changes (dN/dS ratio) located a region of overlapping reading fra

121 for which evolutionary rates and selection (dN/dS) can be estimated, and systematically characterize

122 Finally, using a dN/dS-based test in a phylogenetic framework, we searche

123 n the medial temporal lobe components of the DN evoked relatively late effects (>130 ms) in other nod

124 cimens from patients with established ORG or DN expressed significantly less TGR5 mRNA, and levels in

125 mitochondrial fission in the early stages of DN formation and eventual mitochondrial degeneration at

126 acmid DNA or viral bacmid DNA that expressed DN forms of ESCRT-I and ESCRT-III components.

127 nd that overexpression of dominant-negative (DN) forms of NSF or knockdown of the expression of NSF,

128 ng down or overexpressing dominant negative (DN) forms of the components of ESCRT-I and ESCRT-III com

129 se-dead [p38(KD)] and dominant-negative [p38(DN)] forms of p38alpha.

130 urther, we demonstrate a strong link between dN frequencies in RNA and the balance of dNTPs and ribon

131 miR-146a-5p and hsa-miR-30a-5p distinguished DN from all other conditions except IgAN.

132 d 162 individuals with diabetic nephropathy (DN) from the outpatient clinic at Steno Diabetes Center.

133 pre-identified nodes of the default network (DN), frontoparietal network (FPN), and salience network

134 networks of the brain, the default network (DN), frontoparietal network (FPN), and salience network

135 ens from patients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membranoproliferative

136 Compared with control glomeruli, DN, FSGS, IgAN, and MPGN glomeruli exhibited differentia

137 Compared with control proximal tubules, DN, FSGS, IgAN, and MPGN proximal tubules had differenti

138 we generated dnTGF-betaRII/galectin-3(-/-) (dn/Gal3(-/-)) mice, which showed impaired inflammasome a

139 ther surgery; 170 reexcised and 304 observed DN had available follow-up data, with mean (SD) follow-u

140 The default network (DN) has been consistently associated with self-processin

141 The default network (DN) has been consistently associated with self-related c

142 ve surgical approaches to donor nephrectomy (DN) has been driven by the potential advantages for the

143 In ADL, unc-1(dn) has effects opposite to those of tetanus toxin light

144 ling in development of diabetic nephropathy (DN) has not been studied.

145 ), vasculitis (HR, 0.66; 95% CI, 0.61-0.70), DN (HR, 0.50; 95% CI, 0.47-0.52), ADPKD (HR, 0.85; 95% C

146 ], vasculitis [HR, 0.85; 95% CI, 0.76-0.94), DN [HR, 0.73; 95% CI, 0.69-0.77]).

147 enriched CD133(-)/EpCAM(-) (double negative, DN), Huh-7 cells underwent a transwell selection for met

148 maller amounts of the desnitro-imidacloprid (DN-IMD, 16% yield) product, and gaseous nitrous oxide (N

149 ibitors (PDE5is) exert protective effects in DN improving perivascular inflammation.

150 and LPAR3 antagonist, affects development of DN in endothelial nitric oxide synthase-knockout db/db m

151 thus provides a unique opportunity to study DN in human oculomotor control.

152 We showed that VtE can ameliorate DN in mice and that DGKalpha is involved in the VtE-indu

153 In conclusion PDE5i slows the progression of DN in mice, improving hemodynamic parameters and vessel

154 ssion and rescued key pathologic features of DN in mice.

155 t could be used to detect the involvement of DN in other cerebellar disorders.

156 en reported that vitamin E (VtE) ameliorates DN in rat by activating DGK, and we recently reported th

157 mitochondrial fission affects progression of DN in vivo is unknown.

158 involved in the VtE-induced amelioration of DN in vivo remains unknown.

159 involved in the VtE-induced amelioration of DN in vivo, suggesting that DGKalpha is an attractive th

160 Our study confirms the relevant role of DN in voluntary aspects of oculomotion and delineates sp

161 investigated the VtE-induced amelioration of DN in wild-type (DGKalpha(+/+)) and DGKalpha-deficient (

162 Expression of unc-1(dn) in RMG hub neurons, ADL or ASK pheromone-sensing neu

163 tive type II TGF-beta receptor (TGF-beta-RII-DN) in the posterior left atrium in a canine heart failu

164 to the pathogenesis of diabetic nephropathy (DN) in which evidence suggests that metabolic events in

165 Targeting early features of DN, including renal extracellular matrix accumulation (E

166 re discussed, including the possibilities of dN incorporation in RNA as a contributing factor in vira

167 with significant stress-induced variation of dN incorporation.

168 is not induced in podocytes of patients with DN, independent of disease stage, or BTBR ob/obmice, a m

169 nctions could be functionally coupled in the DN, inspired by theories according to which selfhood is

170 ults were related to the presence/absence of DN involvement and compared with those of healthy subjec

171 These saccadic abnormalities related to DN involvement but were independent of global and region

172 The saccadic abnormalities related to DN involvement were independent of global and regional b

173 ents, with and without brain MRI evidence of DN involvement, with a set of healthy subjects.

174 ns, than either controls or patients without DN involvement.

175 Relevance to human DN is also demonstrated.

176 NAs in the regulation of inflammation during DN is poorly understood.

177 al biomarker for tubular oxidative injury in DN is unknown.

178 Diabetic nephropathy (DN) is a major cause of end-stage renal disease, and the

179 (cerebellar hemispheres and dentate nuclei, DN) is less well understood.

180 Diabetic nephropathy (DN) is one of vascular complications of diabetes and is

181 Diabetic nephropathy (DN) is the leading cause of CKD in the Western world.

182 Diabetic Nephropathy (DN) is the leading cause of end-stage renal disease.

183 Diabetic nephropathy (DN) is the leading cause of ESRD worldwide.

184 Diabetic nephropathy (DN) is the major cause of end-stage renal disease worldw

185 hin the SN sites, whereas stimulation of the DN led to sustained responses in later time windows (85-

186 We report an 11-fold increase in the odds of DN LGD mutations compared with expectation under an exom

187 We identify novel DN LGD recurrences (GIGYF2, MYT1L, CUL3, DOCK8 and ZNF29

188 berrantly expressed in diabetic nephropathy (DN) may be involved in the generation of DN-associated p

189 Results DN/MCP (rho = 0.51, P < .0001) and DN-to-pons (rho = 0.4

190 DN/MCP and DN-to-pons ratios were significantly differen

191 DN/MCP, DN-to-pons, GP-to thalamus, and GP-to-cerebrospi

192 BAFF and Aiolos may prime CD27(+) memory and DN memory-like B cells to become Ab-producing plasmablas

193 elated orphan receptor gammat-Cre x RARalpha-DN mice had reduced numbers of NCR(-) and NCR(+) ILC3 su

194 These studies suggest that in early DN, miR-146a upregulation exerts a protective effect by

195 role of puerarin by employing an accelerated DN model, STZ-induced diabetes in the endothelial nitric

196 n DN, was investigated using zymography in a DN mouse model confirming the predictions.

197 knockdown (KD) or PRAS40 dominant-negative (DN) mutant overexpression blocks not only TGF-alpha- but

198 te, approximately 4% of ASD patients carry a DN mutation in one of just 29 autism risk genes.

199 (GIGYF2, MYT1L, CUL3, DOCK8 and ZNF292) and DN mutations in previous ASD candidates (ARHGAP32, NCOR1

200 The most prevalent gene for recurrent DN mutations is SCN2A (1.1% of patients) followed by CHD

201 icroRNAs in a second cohort of patients with DN (n=19) and FSGS (n=21).

202 21) to diabetic patients with no evidence of DN (normoalbuminuric, n = 118).

203 The presence of DN NSF also moderately reduced trafficking of the viral

204 The presence of a DN NSF protein resulted in low-efficiency entry of BV an

205 y analysis of infections in cells expressing DN NSF revealed that progeny nucleocapsids were retained

206 In cells expressing DN NSF, entering virions were trapped in the cytoplasm o

207 between baseline normalized SI (nSI) in the DN (nSIDN) and the average change in nSIDN of all postba

208 ths from melanoma arising from biopsy-proven DN occurred through the latest dermatology follow-up.

209 ignal intensity (SI) of the dentate nucleus (DN) of the pediatric brain on nonenhanced T1-weighted ma

210 ignal intensity (SI) of the dentate nucleus (DN) on unenhanced T1-weighted magnetic resonance (MR) im

211 e visual enhancement of the dentate nucleus (DN) on unenhanced T1-weighted magnetic resonance (MR) im

212 individual neurons using dominant-negative (dn) or constitutively-active (ca) forms of nuclear-local

213 pression of the dominant-negative Rac1 (Rac1 DN), or the specific Rac1 inhibitor NSC23766 greatly inh

214 number of GBCA doses was correlated with the DN:P ratio for the nontreated brain tumor group (P < .00

215 Results DN:P ratio for the radiation therapy group was greater t

216 reated brain tumor group demonstrated higher DN:P ratios than the nontreated brain tumor group for nu

217 GP:T and DN:P SI ratios were compared between groups by using the

218 Our results suggest that DN participate in voluntary behaviour, such as the execu

219 hese recent advances in our understanding of DN pathogenesis are paving the way for critical mechanis

220 We compared urinary peptide profiles of DN patients (macroalbuminuric, n = 121) to diabetic pati

221 nocytes (PBMs) and renal biopsy tissues from DN patients and then analysed the relationship between p

222 ntly increased in PBMs and kidney tissues of DN patients.

223 All living DN performed from June 1963 through December 2014 at the

224 ons of interest (ROIs): the dentate nucleus (DN), pons, substantia nigra (SN), pulvinar thalami, and

225 cations of targeting lnc-MGC for controlling DN progression.

226 (Number of GBCA applications: DN: r = -0.254, P = .31; pons: r = -0.097, P = .65; SN:

227 P = .75; total amount of administered GBCA: DN: r = 0.091, P = .72; pons: r = 0.106, P = .62; SN: r

228 r proteins and a panel of dominant negative (DN) Rab GTPases involved in TGN-endosome trafficking ste

229 PDE5i treatment prevented the development of DN-related hypertension (P < 0.001), the increase of uri

230 therapeutic benefit afforded by puerarin in DN remained inconclusive.

231 ith controls, dogs treated with pUBC-TGFbeta-DN-RII demonstrated an attenuated increase in conduction

232 ctionated and less organized in pUBc-TGFbeta-DN-RII versus pUBc-LacZ dogs.

233 tive TGF-beta type II receptor (pUBc-TGFbeta-DN-RII; n=9) or control vector (pUBc-LacZ; n=12), follow

234 enzyme in the cytosolic deoxyribonucleoside (dN) salvage pathway, is an important therapeutic and pos

235 last examination for the presence of visual DN signal enhancement.

236 n, whereas non-associative LTF is blocked by dn small optic lobe (SOL) calpain.

237 SN activity predominant in early windows and DN stimulation affecting the network in later windows.

238 DN T cells also made up a large fraction of the T cell c

239 Our results indicate that DN T cells are an important subset of the resident alpha

240 ithin the first 3-24 hours after IRI, kidney DN T cells expanded significantly and upregulated expres

241 king leads to downregulation of IFN-gamma by DN T cells from patients with Chagas heart disease, whic

242 on via CD1d is associated with activation of DN T cells in Chagas disease and that CD1d blocking lead

243 Given the importance of DN T cells in immunoregulatory processes and their poten

244 h a striking decrease in the accumulation of DN T cells in the kidneys and secondary lymphoid organs.

245 and functionally characterized murine kidney DN T cells in the steady state and in response to IRI.

246 Unlike CD4(+) and CD8(+) T cells, DN T cells in the steady state expressed high levels of

247 In adoptive transfer experiments, DN T cells significantly protected recipients from AKI b

248 showed an association with the activation of DN T cells, as well as with worse ventricular function i

249 and murine lupus including the expansion of DN T cells, decreased IL-2, and increased IL-17 producti

250 tional profile of Trypanosoma cruzi-specific DN T cells.

251 out the pathophysiologic functions of kidney DN T cells.

252 xpression of interferon gamma (IFN-gamma) by DN T cells.

253 gen presentation led to a clear reduction of DN T-cell activation and a decrease in the expression of

254 LL4 Notch ligand to CD4/CD8 double-negative (DN) T cell progenitors, and reduced expression of NOTCH1

255 Double-negative (DN) T cells are important sources of inflammatory and an

256 ly identified CD4(-)CD8(-) (double-negative; DN) T cells as an important subset of alphabeta T cell r

257 eas T follicular helper and double negative (DN) T cells significantly expanded.

258 xpression and masquerade as double-negative (DN) TCRalphabeta(hi) thymocytes.

259 Outcomes were compared among 4 DN techniques.

260 imary outcome was the proportion of biopsied DN that progressed to histologically confirmed invasive

261 esponses to heartbeats in two regions of the DN, the ventral precuneus and the ventromedial prefronta

262 st GFR decline and attenuates development of DN through multiple mechanisms.

263 Although these DN thymocytes fail to re-express coreceptors after OP9-D

264 itlisting (HRs vs IgAN, ranged from 0.49 for DN to 0.92 for membranous nephropathy or ADPKD) than by

265 tests were used to compare SI and SI ratios (DN to pons, GP to thalamus) between case patients and co

266 e in Gli-1/2 gene expression levels from DP, DN to TS subpopulations, which was consistent with eleva

267 r TCR signalling in DN cells, an inefficient DN-to-DP transition, and reduced contribution of TCRalph

268 tor for DN-to-pons ratio = 0.09 and that for DN-to-MCP ratio = 0.12).

269 ncrease (0.10 for DN-to-pons ratio; 0.27 for DN-to-MCP ratio).

270 to-pons ratio: -0.0032 +/- 0.0154, P = .248; DN-to-MCP ratio: -0.0011 +/- 0.0093, P = .521), and one-

271 to-pons ratio: -0.0012 +/- 0.0101, P = .436; DN-to-MCP ratio: 0.0007 +/- 0.0088, P = .604), and one-s

272 fferences were calculated for DN-to-pons and DN-to-middle cerebellar peduncle (MCP) ratios by subtrac

273 amination were calculated for DN-to-pons and DN-to-middle cerebellar peduncle (MCP) ratios in a regio

274 Results DN/MCP (rho = 0.51, P < .0001) and DN-to-pons (rho = 0.41, P = .0001) ratios correlated pos

275 SI ratio differences were calculated for DN-to-pons and DN-to-middle cerebellar peduncle (MCP) ra

276 and last MR examination were calculated for DN-to-pons and DN-to-middle cerebellar peduncle (MCP) ra

277 ROI and no group differences were found when DN-to-pons and GP-to-pulvinar ratios were compared (DN-t

278 ainst an SI ratio increase (Bayes factor for DN-to-pons ratio = 0.09 and that for DN-to-MCP ratio = 0

279 ons and GP-to-pulvinar ratios were compared (DN-to-pons ratio in case mean, 1.0083 +/- 0.0373 [standa

280 ean, 1.0083 +/- 0.0373 [standard deviation]; DN-to-pons ratio in control mean, 1.0183 +/- 0.01917; P

281 erences did not differ significantly from 0 (DN-to-pons ratio: -0.0012 +/- 0.0101, P = .436; DN-to-MC

282 erences did not differ significantly from 0 (DN-to-pons ratio: -0.0032 +/- 0.0154, P = .248; DN-to-MC

283 dence against an SI ratio increase (0.10 for DN-to-pons ratio; 0.27 for DN-to-MCP ratio).

284 DN/MCP and DN-to-pons ratios were significantly different between c

285 DN/MCP, DN-to-pons, GP-to thalamus, and GP-to-cerebrospinal flui

286 trategies, we studied protective factors for DN using proteomics on glomeruli from individuals with e

287 Laparoscopic DN was associated with a higher probability of left kidn

288 Conclusion No increase of the SI in the DN was found after a mean of 8.6 serial injections of th

289 tive sample of 1473 histologically confirmed DN was identified using surgical pathology databases at

290 Signal intensity (SI) in the DN was normalized to the SI of the pons, and a one-sampl

291 Visually appreciable enhancement in the DN was observed on contrast-optimized images in two pati

292 MP-2 and MMP-9, predicted to be decreased in DN, was investigated using zymography in a DN mouse mode

293 sing a murine model of diabetic nephropathy (DN), we performed an unbiased RNA-sequencing (RNA-seq) a

294 Several symptoms of DN were ameliorated by VtE treatment in the DGKalpha(+/+

295 propose a novel functional framework for the DN, where self-processing is coupled with physiological

296 dministrations and the increase of SI in the DN, which is likely due to gadolinium retention.

297 and Relevance: In cases of mild and moderate DN with microscopically positive margins and no concerni

298 Affairs medical center with biopsy-confirmed DN with positive histologic margins diagnosed from May 1

299 ciated melanoma in biopsied mild or moderate DN with positive histologic margins that were clinically

300 e, we further hypothesized that TGF-beta-RII-DN would lead to increased fractionation and decreased o