ライフサイエンスコーパス: target organ

1 sequestration) or harmful (toxin delivery to target organs).

2 to this functional state upon infiltrating a target organ.

3 g of the laparoscope and registration of the target organ.

4 tion responding to hemodynamic injury in the target organ.

5 zed by ectopic lymphoid follicles within the target organ.

6 eactive T cells in the intestine, a key GVHD target organ.

7 essly integrate and restore functions of the target organ.

8 in an ongoing adaptive immune response in a target organ.

9 by many autoimmune TCRs are abundant in the target organ.

10 f beryllium-responsive CD4(+) T cells in the target organ.

11 le sclerosis in which T(EM) are found in the target organ.

12 epertoire compares between the periphery and target organ.

13 toantigen to other antigens expressed in the target organ.

14 n of pathogenic self-reactive T cells in the target organ.

15 on the electrical stimulation pattern of the target organ.

16 tigen provokes an inflammatory lesion in the target organ.

17 s was long lasting and localized only in the target organ.

18 be eliminated or diverted from reaching the target organ.

19 y directly applying it to specimens from the target organ.

20 contribute to the pathogenic damaging of the target organ.

21 80(+) cells ("F4/80(+) cells") in metastatic target organs.

22 g from the CNS to the periphery to reach the target organs.

23 tor T cells, and lymphocytic infiltration of target organs.

24 ntially play a role in inflamed hypoxic GvHD target organs.

25 lammatory infiltrate into the peritoneum and target organs.

26 3 ligand-mediated lymphocyte infiltration of target organs.

27 , cytokine production, and migration to GVHD target organs.

28 nd gastrointestinal tract as primary CBLB502 target organs.

29 -effector cells (Teffs) that migrate to GVHD target organs.

30 whether putative dysfunction exists only in target organs.

31 butes to the trafficking of WT Tconv to GVHD target organs.

32 ability to be activated by self-antigens in target organs.

33 ated by altered trafficking of Tconv to GVHD target organs.

34 nd glucuronidated forms that are exported to target organs.

35 for both Tregs and Tconv to migrate to GVHD target organs.

36 induced an increased metastatic activity to target organs.

37 in extravasation and homing of leukocytes to target organs.

38 ty because of activated T cells infiltrating target organs.

39 that favor successful colonization of distal target organs.

40 opulation, and are present in all major GVHD target organs.

41 pathways that are co-expressed in IMIDs and target organs.

42 nucleases and enable distribution to desired target organs.

43 pread from the inoculation site to secondary target organs.

44 MX001 acts by reducing Ad replication in key target organs.

45 within aggregated lipid rafts guides them to target organs.

46 es to host tissues and by direct toxicity to target organs.

47 r RBP and mediates vitamin A uptake in these target organs.

48 early effector migration to GVHD parenchymal target organs.

49 ffect needed to control virus infectivity in target organs.

50 uencing whole-body metabolism via effects on target organs.

51 he colonization and growth of tumor cells in target organs.

52 ite the presence of intact hair cells in the target organs.

53 tion for T cells, especially in non-lymphoid target organs.

54 y of COX-2, similar to inflammatory cells in target organs.

55 ppressor cells (MDSCs) were enriched in GVHD target organs.

56 sturbs fluid homeostasis and host defense in target organs.

57 ive fragments with resulting inflammation in target organs.

58 cells and plasma cells invade and persist in target organs.

59 orable microenvironment in the stroma of the target organs.

60 undergo metastatic reactivation in multiple target organs.

61 in the body to attain therapeutic effects at target organs.

62 ic catheters and confer specific delivery to target organs.

63 ons during metastasis of cancer to different target organs.

64 minate to cause systemic infection and reach target organs.

65 ever, remain unclear and differ depending on target organs.

66 cle structure affects biodistribution to off-target organs.

67 invaded locally, intravasated and lodged in target organs.

68 cer cells that is invasive and can spread to target organs.

69 volved in the induction of severe disease in target organs.

70 and maintenance of CD4+ effector T cells in target organs.

71 anded in vivo and invaded lymphatic and GVHD target organs.

72 e variants act in sympathetically innervated target organs.

73 n, which in turn cause insulin resistance in target organs.

74 othelium could improve cell retention within targeted organs.

75 e, whereas WT virus is readily detectable in target organs 30 d after infection, some variants fail t

76 itrite bioactivation by myoglobin within the target organ abrogated the cardioprotection by rIPC.

77 The major target organs affected are skin, lungs, and liver.

78 with an improved control of viral titers in target organs after the development of the specific immu

79 proliferation of T cells in situ within the target organ, an effect that would be expected to restra

80 echanisms of how these cells recognize their target organ and induce sustained inflammation are incom

81 ut not necessarily all, CD8(+) Teff into the target organ and suggest a novel approach to achieve tra

82 e, suggesting that the genetic origin of the target organ and/or its innate immune cells is critical

83 s, and antibodies promote dysfunction of the target organs and cause damage.

84 kines, followed by decreased inflammation in target organs and increment in parasite burden.

85 e of the most-reduced transcripts in several target organs and is hypothesized to have a causal role

86 its diverse metabolic functions in multiple target organs and its ability to act as an autocrine, pa

87 l peptides studied, with saturable uptake in target organs and low uptake by nontarget tissues other

88 kely elicits systemic molecular responses in target organs and may contribute to whole-plant stress t

89 TERM P-PMO treatment reduced viral titers in target organs and protected mice against virus-induced t

90 r, these cells migrate to and expand in GVHD target organs and secondary lymphoid tissues.

91 to rapidly innervate and arborize into final target organs and then slow but not halt their growth to

92 appears that in the absence of Nmnat2, major target organs and tissues (e.g., muscle) are not functio

93 bility of T-bet(-/-) T cells to migrate into target organs and to produce Th1-related cytokines.

94 s by which viruses kill susceptible cells in target organs and ultimately produce disease in the infe

95 reactive T cells, leading to inflammation of target organs and, ultimately, autoimmune disease.

96 e majority of sporozoites do not reach their target organs, and in the mammalian host, they initiate

97 the delivery of the therapeutic cells to the target organs are getting more and more into the focus o

98 come dormant and how and why tumors recur in target organs are not well understood.

99 switch of homeostasis rather than a passive target organ as hitherto conceived.

100 ow that a similar process takes place in the target organ, as both alpha and beta cells within pancre

101 t tissues or organs before the injury of the target organ, attempts to invoke adaptive responses that

102 d in experimental endocarditis infections by target organ bacterial counts.

103 inhibited lymphoid infiltrates in different target organs based on the Y RNA and TLR status of the m

104 nic functions of CD4(+) T cells within their target organ but not in lymphoid tissues during EAE.

105 at strategies aimed not at target tissues or target organs but rather at restoring the quality and qu

106 infiltration into graft-versus-host reaction target organs, but decreased the functional activity of

107 Autoreactive T cells infiltrating the target organ can possess a broad TCR affinity range.

108 contributions to good health that all 36 VDR target organs can provide.

109 etic ganglia (TSG) and transaxonal spread to target organs cause human visceral disease.

110 ether biomarkers can identify silent cardiac target organ damage (cTOD) in a primary prevention popul

111 inflammation (C-reactive protein [CRP]), and target organ damage (urine albumin-creatinine ratio).

112 ss of circadian BP change has been linked to target organ damage and accelerated kidney function loss

113 of this study was to determine hypertensive target organ damage and adverse cardiovascular outcomes

114 Patients with PA more frequently displayed target organ damage and cardiovascular events compared w

115 pressure with antihypertensive drugs reduces target organ damage and prevents cardiovascular disease

116 vation of a cellular immune response, or off-target organ damage by BNP116.I-1c gene therapy in pigs.

117 orenal adverse remodeling, contribute to the target organ damage found in hypertension, heart failure

118 T(1) receptors may have divergent effects on target organ damage in hypertension.

119 risk score was significantly associated with target organ damage in multiple tissues but with minor e

120 ely discrepant effects on blood pressure and target organ damage in this disorder.

121 blood pressure, presence of risk factors and target organ damage subjects were divided into 4 groups:

122 toring, is associated with increased risk of target organ damage, cardiovascular disease, and mortali

123 ture of blood pressure and assess effects on target organ damage, we analyzed 128,272 SNPs from targe

124 ssion and may play a role in smoking-induced target organ damage.

125 recruitment as a key step in development of target organ damage.

126 ediators of smoking-induced inflammation and target organ damage.

127 xcretion might be involved in cardiovascular target organ damage.

128 one and consequent cardiac, renal, and brain target organ damage.

129 m cytokine production in vivo, and prevented target organ damage.

130 ents are in treating hypertension-associated target organ damage.

131 l activation and differentiation, as well as target organ damage.

132 xtensive transcriptomic changes that lead to target-organ damage and smoking-related diseases.

133 Subtle target-organ damage such as left-ventricular hypertrophy

134 ient screening test for hypertension-related target-organ damage.

135 of T helper 1 and T helper 17 cells in GVHD target organs, demonstrating that blockade of IL-6 signa

136 These findings suggest a target organ-derived neurotrophin suppresses development

137 ong recognized that only a limited subset of target organs develop clinically overt metastases.

138 While viral replication in target organs did not differ between sigma1s(-) and sigm

139 een drugs exist with respect to reduction of target-organ disease and prevention of major cardiovascu

140 t role in regulating TSP-1 production in the target organ during acute inflammation.

141 The kidney is the target organ during infection and whose control is large

142 tivity of immune pathology within individual target organs during GVHD.

143 their concomitant roles at protein levels in target organs during human allergic disease have not bee

144 tension, and AKI is a frequent form of acute target organ dysfunction, particularly in those with bas

145 e microvasculature is necessary to reach its target organs (e.g., adipose and muscle tissues) and is

146 of action, block of related channels in non-target organs, e.g. the heart, can result in major and p

147 eveal that Cdk5 activity is increased in key target organs early after allo-HCT.

148 d NK cells led to far greater viral loads in target organs early after infection compared with nondep

149 ficant metabolic and cytoskeleton changes in target organ ECs in gene array and proteomic analyses.

150 inephrine contributed to neuronal control of target organ effector cells.

151 and the effect of treating inflammation in a target organ (eg, the skin) on vascular diseases.

152 trafficking of IFNgammaR(-/-) Tconv to GVHD target organs, especially the gastrointestinal (GI) trac

153 cells effectively eliminates B cells in the target organ even though thyroid B cells have decreased

154 e effects of AT1 receptor stimulation in the target organ, exogenous administration of AT2 receptor a

155 perior potency and very good oral as well as target organ exposure in rats.

156 cific with the kidney cortex being the major target organ, followed by the heart and the liver.

157 abolic process, which makes it an attractive target organ for gene therapy.

158 The kidney is a target organ for human cytomegalovirus (hCMV) in such pa

159 previously showed that the brain was a major target organ for infection in mice that are transgenic f

160 Although the liver is a major target organ for RA, no data exist on global expression

161 ducing skin as a nonconventional, peripheral target organ for regulation by TSH.

162 The liver serves as a target organ for several important pathogens, including

163 The eye is an excellent target organ for such cell-based therapeutics due to its

164 the thymus, gut, brain and other tissues as target organs for consideration in developing a new unde

165 nor cells significantly reduced systemic and target organ GVHD severity, and CCR1 expression on both

166 tically reduced the severity of systemic and target organ GVHD.

167 nts and their pharmacological sensitivity in target organs has proved difficult.

168 Although actions of the RAS in a variety of target organs have the potential to promote high blood p

169 e aggressive goals (<130 mm Hg), we observed target organ heterogeneity in that the risk of stroke co

170 case of cortisol) circulating levels of the target-organ hormones.

171 ge in the acute and chronic GVHD overlapping target organs (i.e., skin and lung); they also markedly

172 I and phosphorylated SMAD3) increases in the target organs, i.e., kidneys, of these mice as they age

173 own-regulate immune complex formation in the target organ in individuals with circulating pathogenic

174 is an important but previously unrecognized target organ in SLE with neutrophil-mediated IFN activat

175 ex steroid concentrations and bioactivity on target organs in mice expressing a human SHBG transgene.

176 y of interactions between adipose tissue and target organs in obesity and the resulting clinical impl

177 lar to WT T cells and accumulated in SLO and target organs in similar numbers as WT T cells.

178 ed virus (AAV), thereby allowing delivery to target organs in vivo.

179 Because the liver is one of the primary target organs in VL, unraveling the mechanisms governing

180 ding the ability to accurately visualize the target organ, in particular during laparoscopic surgery.

181 Enhanced TGF-beta in target organs, in turn, can lead to dysregulated tissue

182 ic mucosa invade and metastasize to specific target organs including the intestinal lymph nodes, live

183 rgan can activate protective pathways in the target organ, including the heart and brain.

184 by decreases in numbers of effector cells in target organs, including mast cells, basophils, eosinoph

185 , excess dietary sodium can adversely affect target organs, including the blood vessels, heart, kidne

186 egulated in graft-versus-host disease (GVHD) target organs, including the colon, liver, and lung.

187 f remote ischemic preconditioning in various target organs, including the kidneys.

188 tissue-protective effects of rIPC in various target organs, including the kidneys.

189 ors that favor their accumulation in certain target organs, including the skin and gut.

190 that immune cells become activated and enter target organs, including the vasculature and the kidney,

191 t cGVHD manifestations in a wide spectrum of target organs, including those with mucosal surfaces.

192 ese findings suggest that controlling remote target organ inflammation (eg, in the skin) may improve

193 Last, modulation of target organ inflammation (eg, skin) was associated with

194 ion and role of systemic IL-22 in modulating target organ inflammation.

195 ext is sufficient to induce autoimmunity and target organ injury consistent with MCTD.

196 With prolonged obesity and development of target organ injury, especially renal injury, obesity-as

197 g the entry of autoreactive T cells to their target organ is important in autoimmunity because this e

198 An important target organ is the brain, but even though their effects

199 nd to vascular surfaces and extravasate into target organs is an underappreciated, yet essential step

200 Efficient delivery of cells to target organs is critical to improving their effectivene

201 selective inducers of autophagy function in target organs is expected to maximize clinical benefits

202 rafficking of immature DC from blood to GVHD target organs is likely to be regulated by chemokine rec

203 prolonged ischemia/reperfusion injury of the target organ, is an adaptational response that protects

204 he absence of immune cell infiltrates in the target organ (islets and the brain tissue).

205 ectively control autoimmune reactions in the target organ, it may also be necessary to control tissue

206 cells producing IFN-gamma and IL-17 in GVHD target organs, leading to reduction of GVHD and improved

207 a noninvasive method to visualize T1D at the target organ level in patients with active insulitis.

208 ress potential bioactivity at intestinal and target organs level.

209 Whether target organs liberate chemokines to recruit these fibro

210 Host-type dendritic cells from the GVHD target organs liver and spleen or skin- and gut-draining

211 tion showed that neutrophil migration in the target organ lung was significantly reduced in the prese

212 (BP) increased Cdc25B protein levels in the target organ, lung.

213 3, hearing loss segregates without any other target-organ manifestations of CAPS.

214 We report that, in the absence of distal target organs, molecular guidance cues can mediate the g

215 of the gastrointestinal (GI) tract, the GVHD target organ most associated with nonrelapse mortality (

216 ntestinal tract (LGI) and liver are the GVHD target organs most associated with treatment failure and

217 We demonstrate that the BM is a major target organ of GVHD in an informative clinically releva

218 rophages accumulated in the kidney, the main target organ of infection, and formed direct contacts wi

219 r center of amino acids as well as the prime target organ of insulin.

220 ntering large amounts of self-antigen in the target organ of the autoimmune disease.

221 ify global transcriptomic differences in the target organ of the virus between chicken lines that dif

222 Although the fetal lung is a major target organ of the virus, HCMV lung pathogenesis has re

223 lls in blood, secondary lymphoid organs, and target organs of aGvHD after BMT showed significantly re

224 scriptional map of immune activation in DENV target organs of an immunocompetent host and supports th

225 re-like reactions are well-documented in the target organs of autoimmune diseases.

226 dly accumulated in the liver and spleen, the target organs of intracellular infection.

227 dence suggests that the kidneys are not only target organs of many diseases but also can strikingly a

228 hin the peripheral lymphoid compartments and target organs of mice with experimental autoimmune encep

229 Na/K-ATPase was significantly reduced in the target organs of Niemann-Pick type C mice where the intr

230 carried the pups to term, and viral loads in target organs of pups were analyzed.

231 me to WNV-infected cells and infiltrate into target organs of Tlr7(-/-) mice.

232 elies on the recruitment of monocytes to the target organ or tumor and functioning therein as a parac

233 itis without affecting p65 expression in off-target organs or eliciting a humoral response after seri

234 Migration of donor-derived T cells into GVHD target organs plays an essential role in the development

235 sting its potential clinical application for target organ protection in hypertensive cardiovascular d

236 dards should analyze exposure information by target organ, rather than for a single chemical only or

237 o survive, upregulates adhesion molecules in target organs, recruits immune cells capable of entrappi

238 One reason for the impaired target organ reinnervation is degradation of motor endpl

239 mary afferent sensory neurons that innervate target organs release inflammatory neuropeptides in the

240 VDR, has broadened at least 9-fold from the target organs required for calcium homeostasis (intestin

241 The SUVmax and SUVmean of healthy target organs, residual primary tumor, and up to 5 lesio

242 EPCR interaction reduced infiltration in the target organ, resulting in impaired prometastatic activi

243 pansion, activation, and migration into GVHD target organs, resulting in effective prevention of GVHD

244 which expand in the periphery and infiltrate target organs, resulting in tissue damage.

245 anterior pituitary hormones, whereas altered target-organ sensitivity and hormone metabolism result i

246 differences in chemokine expression within a target organ shape the spatial pattern and composition o

247 eneic transplantation mainly in GVHD typical target organs skin, liver, and intestines, whereas no an

248 clinical symptoms in one or more of the main target organs (skin, liver, gastrointestinal tract) and

249 The mechanisms by which these target organ-specific mAbs bypass the requirements for e

250 sets in the activation, effector phases, and target organ specificity of acute GVHD.

251 ly that analysis of a more readily evaluable target organ such as skin might shed light on mechanisms

252 sition and inflammatory cell infiltration in target organs such as kidneys and brain lead to complica

253 g through its cognate receptor in peripheral target organs such as liver, muscle, and adipose tissue

254 local autocrine and paracrine factors within target organs such as the heart modulate AMPK is unknown

255 ause T-cell activation and infiltration into target organs such as the vessel and the kidney, which p

256 The anatomical location of various target organs, such as brain, pancreas, and prostate, ma

257 vo and fail to productively infect important target organs, such as the heart or pancreas.

258 r alloreactive T cells trafficking into GVHD target organs, such as the intestines and skin.

259 ied first by presentation timing and then by target organ systemic toxicity and included early (<6 hr

260 ring particular windows of susceptibility in target organ systems.

261 on windows of susceptibility for particular target organ systems.

262 emination of human cytomegalovirus (HCMV) to target organ systems.

263 quired for entry of cells into inflamed GVHD target organs that lack expression of NKG2D ligands reco

264 tuberculosis during infection of the primary target organ, that is, the lungs of susceptible individu

265 ges that facilitate their migration into the target organ, the eye.

266 n controlling herpesvirus replication in the target organ, the lung, and does so by evoking a strong

267 expressed during Mtb infection in the major target organ, the lung, and must be capable of eliciting

268 kedly augment damage in a prototypical cGVHD target organ, the salivary gland.

269 at efficiently infiltrate the tumor-burdened target organ; therapeutic efficacy; heightened ratios of

270 In graft-versus-host disease (GVHD) target organs, three recipient CD11b(+) cell subsets (Gr

271 y acid, glucose, and phosphate metabolism in target organs through activating FGF receptors (FGFR1-4)

272 of vaccines based on synthetic materials to target organs, tissues, cells or intracellular compartme

273 on and therapeutic results demonstrated high target organ to nontarget organ ratios of radioactivity

274 i-inflammatory cytokines such as TGF-beta in target organs to counter inflammation.

275 y interrogating transcriptional responses of target organs to MSC therapy.

276 dogs for up to 3 months with no significant target-organ toxicities observed.

277 chniques to evaluate candidate biomarkers of target organ toxicity and to expedite the development of

278 duced sox9b expression levels and subsequent target organ toxicity are unknown.

279 aP exposure leads to dramatic differences in target-organ toxicity and tumor type as a function of do

280 killer (NK) cells, reducing the risk of off-target-organ toxicity.

281 he disseminated tumor cells recruited to the target organs undergo mesenchymal-to-epithelial transiti

282 ional response to infection in multiple DENV target organs using a mouse model of disease.

283 nate from the initial infection focus to the target organs usually through the blood vasculature.

284 Biopsy of target organs (usually skin, skeletal muscles or kidneys

285 educed CMV transmission, with 23.5% infected target organs versus 75.9% in the control group.

286 signaling pathway that are delivered to the target organ via the phloem stream.

287 Absorbed dose estimates for all target organs were determined using MIRD schema with OLI

288 cell numbers and homing in lymphoid and GVHD target organs were not considerably affected in MDSC-tre

289 Target organs were related to routes of metabolism and e

290 eactive T cells can become pathogenic in the target organ where high concentrations of antigen and/or

291 The gill was the main target organ where immature and mature poxvirus particle

292 settings, intestinal Th17 cells migrate into target organs, where they contribute to pathology.

293 orphological and functional abnormalities in target organs, which may act as inciting events for leuk

294 o inhibit T-effector cell trafficking to the target organ, while antigen-specific iTregs primarily pr

295 tly combining an endogenous peptide from the target organ with a synthetic small molecule inhibitor i

296 e heart was identified as the most sensitive target organ with rapid onset of extensive platelet aggr

297 The lung was a primary target organ with serosanguinous pleural effusions, intr

298 ATAK cells accumulated in target organs with distinct profiles, depending on the m

299 Vegf induced differential gene expression in target organs, with Il10 and Mmp8 displaying consistent

300 hich achieve high drug concentrations in the target organ, would more effectively treat respiratory i