ライフサイエンスコーパス: DN

1 dominant negative form of the IP(3)R (IP(3)R(DN)).

2 les from patients with diabetic nephropathy (DN).

3 njury in patients with diabetic nephropathy (DN).

4 terise its function in diabetic nephropathy (DN).

5 site in progression of diabetic nephropathy (DN).

6 to treat patients with diabetic nephropathy (DN).

7 njury in patients with diabetic nephropathy (DN).

8 nociceptive C fibres in diabetic neuropathy (DN).

9 to nerve damage in diabetic polyneuropathy (DN).

10 pha2 dominant negative expressing mice (AMPK-DN).

11 flozin might be useful for the prevention of DN.

12 contributor of renal function impairment in DN.

13 sting a potential biomarker for prognosis of DN.

14 arriers affects microvascular homeostasis in DN.

15 function and preserve glomerular function in DN.

16 cultured in serum from patients with DM and DN.

17 o classify renal biopsies from patients with DN.

18 lpha is an attractive therapeutic target for DN.

19 sin system inhibition to slow progression of DN.

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

21 ediator of progressive kidney dysfunction in DN.

22 Cs has the potential to treat and ameliorate DN.

23 athways were elevated in individuals without DN.

24 ovel renal-specific GLUT2 inhibitors against DN.

25 hat contribute to peripheral nerve injury in DN.

26 that the activation of DGK would ameliorate DN.

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

28 e (QoL) in patients with and without painful DN.

29 in PTECs and downregulated in patients with DN.

30 sfunction through MAPK and eNOS signaling in DN.

31 -ANP convertase Corin in the pathogenesis of DN.

32 drial dysfunction was first observed in ADCA-DN.

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

34 erformed in 51 patients with T2D (23 without DN, 28 with DN) and 10 control subjects without diabetes

35 rial-whole-cell Footvax vaccine induced anti-Dn-ACP and anti-Dn-MIP antibodies.

36 he presence of two homologous ACP domains in Dn-ACP with potent C-type lysozyme inhibitor function, a

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

38 ved biochemical and histological features of DN along with reduced mitochondrial fission and diminish

39 CD4(-) CD8(-) double-negative (DN) alphabeta T cells with innate-like properties repres

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

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

42 However, DN and CSM B cells develop through unique differentiatio

43 sequencing was performed on peripheral blood DN and CSM B cells of HC and MS patients (n = 3 each).

44 Shared clones were found between DN and CSM B cells, although >95% of the clones were uni

45 orded intracranial electroencephalogram from DN and FPCN electrodes implanted in individuals undergoi

46 We found increased connectivity between DN and FPCN(A) during internally directed attention comp

47 enhanced theta band connectivity between the DN and FPCN(A) is a core electrophysiological mechanism

48 attention states in the connectivity between DN and FPCN(B).

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

50 mpared to those in diabetic patients without DN and healthy controls, and positively correlated with

51 ADCA-DN and HSN-IE are rare neurodegenerative syndromes cause

52 To unveil the effects of kallistatin on DN and its underlying mechanism, we crossed transgenic m

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

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

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

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

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

58 NMT1 mutations in fibroblasts from four ADCA-DN and two HSN-IE patients.

59 examined the theta power correlation between DN and two subsystems of the FPCN as a function of atten

60 51 patients with T2D (23 without DN, 28 with DN) and 10 control subjects without diabetes.

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

62 ing evidence implicates the default network (DN) and frontoparietal control network (FPCN)(4); howeve

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

64 erulonephritis (MPGN), diabetic nephropathy (DN) and obesity-related glomerulopathy (ORG), while the

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

66 is a site of injury in diabetic nephropathy (DN), and progressive renal tubulointerstitial fibrosis i

67 which quantify the structural progression of DN, and a recurrent network architecture which processes

68 ons to obtain four cell populations: NN, NH, DN, and DH.

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

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

71 ether, high levels of kallistatin exacerbate DN at least partly by inducing RAS overactivation and hy

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

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

74 DN B cells are Ag experienced, as shown by somatic hyper

75 Thus, DN B cells arise in HC and MS patients via a common deve

76 notypic analysis indicated a mature state of DN B cells by low CD5, CD10, and CD38 expression.

77 DN B cells from HC and MS patients showed similar phenot

78 h unique differentiation pathways, with most DN B cells representing an earlier maturation state.

79 the origin and selection characteristics of DN B cells were studied in MS patients and healthy contr

80 IgD(-)CD27(-) double negative (DN) B cells with proinflammatory characteristics are abn

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

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

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

84 e anaerobic bacterium Dichelobacter nodosus (Dn) causes footrot in ruminants, a debilitating and high

85 Nu-alpha-GalCer, which effectively increased DN CD38(hi) NKT cell numbers.

86 r-resident CD11b(-)CD103(-) double-negative (DN) cDCs to proliferate and differentiate into cDC1s in

87 erentiate from CD4(-)CD8(-) double-negative (DN) cell to CD4(+)CD8(+) double-positive (DP) cell.

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

89 Mucosal Deltagamma NKp44(+) and Deltagamma DN cells were similarly associated with protection and d

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

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

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

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

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

95 has been achieved by studying rare de novo (DN) coding variants.

96 ficantly increased in diabetic patients with DN compared to those in diabetic patients without DN and

97 stribution in plasma of patients with DM and DN compared with healthy control subjects.

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

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

100 metabolic disease typically characterized by DN damage.

101 tions in CYP27A1, typically characterized by DN damage.

102 variants in OCD contribute to risk and that DN damaging variants in approximately 335 genes contribu

103 Furthermore, genes harboring DN damaging variants in OCD are enriched for those repor

104 We estimate that 34% of DN damaging variants in OCD contribute to risk and that

105 igh-confidence risk genes, each containing 2 DN damaging variants in unrelated probands: CHD8 and SCU

106 gene discovery in OCD via identification of DN damaging variants.

107 ring liver regeneration, coincidentally with DN-DBC1 downregulation and the appearance of full length

108 DN-DBC1 is also found in vivo in mouse and human tissues

109 Interestingly, DN-DBC1 is cleared once quiescent cells re-enter to the

110 ion after partial hepatectomy, we found that DN-DBC1 is down-regulated in vivo during regeneration.

111 er partial hepatectomy, suggesting that DBC1/DN-DBC1 transitions play a role in normal cell cycle pro

112 roteolytically cleaved, producing a protein (DN-DBC1) that misses the S1-like domain and no longer bi

113 We propose that quiescent cells express DN-DBC1, which either replaces or coexist with the full-

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

115 At the molecular level, DN-DISC1 and Delta(9)-THC synergistically activated the

116 Selective expression of DN-DISC1 in astrocytes and adolescent treatment with Del

117 he cognitive abnormalities were prevented in DN-DISC1 mice exposed to Delta(9)-THC by simultaneous ad

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

119 inant-negative disrupted in schizophrenia 1 (DN-DISC1) selectively in astrocytes to evaluate the mole

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

121 ficients of individual driver mutations from dN/dS estimates.

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

123 ever the link, in somatic evolution, between dN/dS values and fitness coefficients is missing.

124 study provides the theoretical link between dN/dS values and selective coefficients in somatic evolu

125 o of non-synonymous to synonymous mutations (dN/dS) has become a popular method to detect selection i

126 o (4.83) of nonsynonymous versus synonymous (dN/dS) mtDNA mutations with high statistical significanc

127 nd the ratio of nonsynonymous to synonymous (dN/dS) substitutions of minor variants confirmed no appa

128 exhibit a strong molecular clock with omega (dN/dS) suggesting strong purifying selection.

129 on-synonymous to synonymous mutation ratios (dN/dS).

130 old) were biopsied after the detection of a dn DSA, 65.3 months (median) after kidney transplantatio

131 DN EGFR in these cells led to recruitment of the autopha

132 The autophagy inhibitor 3-MA prevented DN EGFR mice from exhibiting reduced CNS invasion.

133 s led to reduced parasite loads in mice with DN EGFR.

134 i in brain endothelial cells were reduced by DN EGFR.

135 FR] >30 mL/min/1.73 m(2)), and patients with DN (eGFR <30 mL/min/1.73 m(2)).

136 thelial cells expressed a dominant negative (DN) EGFR (inhibits EGFR signaling) exhibited diminished

137 diabetes mellitus (DM) with or without early DN (estimated glomerular filtration rate [eGFR] >30 mL/m

138 Flies with neuronal expression of IP(3)R(DN) exhibit flight deficits.

139 he cell surface and are loss of function and DN for cellular responses to IL-6, IL-11, LIF, and OSM.

140 n through expression of a dominant negative (DN) form of the fission protein [dynamin-related protein

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

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

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

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

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

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

147 sities were measured in the dentate nucleus (DN), globus pallidus (GP), crus anterior of capsula inte

148 Patients with painful compared to painless DN, had comparable neurophysiology and vibration percept

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

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

151 Expression of IP(3)R(DN) helped identify key flight-modulating dopaminergic n

152 nduced renal injury in diabetic nephropathy (DN). However, the role and regulation of proximal tubula

153 ), 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

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

155 ) and CRTH2(-)IL7Ralpha(-) (double-negative [DN]) human blood and lung cells.

156 of developmental markers on peripheral blood DN, IgD(-)CD27(+) class-switched memory (CSM) and IgD(+)

157 rom 8 unrelated kindreds with AD-HIES due to DN IL6ST mutations.

158 scriptomic analysis of CRTH2, IL7Ralpha, and DN ILCs confirmed the expression of mRNA for type 2 tran

159 cy of type 2 cytokine-positive IL7Ralpha and DN ILCs were similar to that of CRTH2 ILCs in the blood

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

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

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

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

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

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

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

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

168 ate mitochondrial fission and progression of DN in vivo, and highlight the stimulus-specific conseque

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

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

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

172 ess-mediated apoptosis, which might occur in DN, in db/db mice.

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

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

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

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

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

178 Diabetic nephropathy (DN) is one of the leading causes of mortality in diabeti

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

180 Its role in diabetic nephropathy (DN) is uncertain.

181 anced capacity reduced PI sensitivity, while DN-KRAS and DN-NRAS did the opposite.

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

183 DN likely gene disrupting and predicted damaging missens

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

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

186 The DN/MCP SI ratio increased linearly with the amount of ga

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

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

189 In DM and AMPK-DN mice, the inhibitory effect of SF-PreCon upon p38 act

190 SF-PreCon decreased MI/R injury in AMPK-DN mice.

191 f ERK1/2, a pro-survival MAPK in DM and AMPK-DN mice.

192 Footvax vaccine induced anti-Dn-ACP and anti-Dn-MIP antibodies.

193 lysozyme inhibitor function, and homology of Dn-MIP to other putative cell-surface and membrane-ancho

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

195 unfolded protein response activation, while DN mutations increased both.

196 We estimated the contribution of DN mutations to OCD risk and the number of genes involve

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

198 irus expands a CD4(-)CD8(-) double-negative (DN) natural killer T (NKT) cell subpopulation that prote

199 We showed that DN NKT cells with high CD38 expression produced IFN-gamm

200 NKT cells with that of suppressive Valpha14 DN NKT cells.

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

202 ty reduced PI sensitivity, while DN-KRAS and DN-NRAS did the opposite.

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

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

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

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

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

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

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

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

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

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

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

217 52, P < 0.001), with a closer correlation in DN patients (r = -0.66, P < 0.001).

218 of intracellular TCRbeta(+) cells within the DN population and increased DN4 cell death.

219 paired in MFN2 knockdown cells, whereas DRP1-DN-promoted fusion resulted in faster cytosolic Ca(2+) i

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

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

222 pathway through overexpression of DN-Ras or DN-Raf.

223 signaling pathway through overexpression of DN-Ras or DN-Raf.

224 Corin and ANP expression in DN rat kidneys and high-glucose-treated HK-2 cells was a

225 ant reduction in Corin and ANP expression in DN rat kidneys.

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

227 Diabetic nephropathy (DN) remains the leading cause of end-stage renal disease

228 (CA) (G12V/G13D/Q61H), or dominant-negative (DN) (S17N)-KRAS and -NRAS, or BRAF-V600E.

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

230 propensities were revealed at the deamidated DN site compared to the native NN motif for terminal and

231 TFIIS(DN) slowed elongation rates genome-wide by half, suggest

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

233 High donor number (DN) solvents in Li-O(2) batteries that dissolve superoxi

234 DN STAT3 and IL6ST mutations thus appear to underlie cli

235 S) is typically caused by dominant-negative (DN) STAT3 mutations.

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

237 ding osteopontin and osteocalcin, whilst the DN subset presented a transcriptionally 'intermediate' B

238 45-CD271+CD56-CD146-(termed double-negative, DN) subsets, and CD45+CD271-hematopoietic-lineage cells

239 hannels, by expression of dominant negative (DN) subunits, leads to changes in circadian locomotor ac

240 gions where termination is enhanced by TFIIS(DN), suggesting that backtracked pol II is a favorable s

241 e correlation between kallistatin levels and DN, suggesting a potential biomarker for prognosis of DN

242 However, the mechanisms regulating DN T cell homeostasis and responses to external danger s

243 We found both DN T cell subsets in normal and cancerous human kidneys,

244 DN T cells are a unique unconventional thymic-derived T

245 Moreover, we provide evidence that DN T cells can differentiate in MHC-deficient mice.

246 n in frequency or absolute numbers of kidney DN T cells due to impaired activation, proliferation, in

247 -cell receptor excision circles confirm that DN T cells from lupus-prone mice and patients with SLE u

248 le, which in turn provokes the generation of DN T cells from self-reactive CD8(+) T cells.

249 The remaining DN T cells in beta2m knockout mice mainly comprised a pr

250 t MHC-independent thymic selection can yield DN T cells that are distinct from NKT, gammadelta T, muc

251 Using reporter mouse strains, we show that DN T cells transit through the immature CD4(+)CD8(+) (do

252 DN T cells, a unique population of kidney T cells, depen

253 etween the loss of MZMs and the expansion of DN T cells, and indicate possible strategies to prevent

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

255 lass I and II molecules in regulating kidney DN T cells.

256 apoptosis, and loss of an NK1.1(+) subset of DN T cells.

257 ) DN thymocytes are precursors to peripheral DN T cells.

258 Mature double negative (DN) T cells are a population of alphabeta T cells that l

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

260 D4(-)CD8(-)TCRalphabeta(+), double-negative (DN) T cells, in mouse secondary lymphoid organs.

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

262 abled GCGR deubiquitination, whereas a Rab5a DN that blocks trafficking at early endosomes eliminated

263 Furthermore, a Rab4a dominant negative (DN) that blocks trafficking at recycling endosomes enabl

264 cells using a dominant-negative TFIIS (TFIIS(DN)) that inhibits RNA cleavage and stabilizes backtrack

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

266 al lymphocytes, we find that mature CD5(low) DN thymocytes are precursors to peripheral DN T cells.

267 m leukemic NHD13/NP23 mice demonstrated that DN thymocytes could transmit AML, and limiting dilution

268 In contrast to CD5(high) DN thymocytes that preferentially yield TCRalphabeta(+)

269 Instead, we show that in DN thymocytes WNK1 transduces pre-TCR signals via OXSR1

270 tively regulates CXCL12-induced migration in DN thymocytes.

271 Transplantation of CD4-CD8- double negative (DN) thymocytes (which were also negative for Mac1 and Gr

272 uired for the transition of double negative (DN) thymocytes through the beta-selection checkpoint and

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

274 Ratios of DN to pons and GP to CA were calculated, and univariable

275 ge range, 25-73 years), the dentate nucleus (DN)-to-middle cerebral peduncle (MCP) SI ratio showed a

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

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

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

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

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

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

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

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

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

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

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

287 Further, the GRK2-DN transgene dramatically accelerates oncogene-initiated

288 ve G protein-coupled receptor kinase 2 (GRK2-DN) transgene diminishes AR and AR target gene expressio

289 flight-dependence mechanism differs between DN types.

290 Here we identify two descending neuron (DN) types that control landing and contribute to visuomo

291 with painful (n = 78) and painless (n = 62) DN underwent assessment of large and small nerve fibre f

292 (184 trios after quality control), comparing DN variant frequencies with 777 previously sequenced una

293 ncy of CD95(+) and IgA(+) cells was lower in DN versus CSM B cells.

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

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

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

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

298 nd miR-126 increased in EVs of patients with DN, whereas miR-660 increased in the Ago-2 fraction and

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

300 ty of these miRs for microvascular injury in DN, while carrier-specific miRs can improve endothelial