ライフサイエンスコーパス: end organ

1 pe is a functionally distinct mechanosensory end organ.

2 er with specialized skin cells that form the end-organ.

3 that IFN-I may be acting at the level of the end-organ.

4 mmunity may be exercised at the level of the end-organ.

5 ithelia in the organ of Corti and vestibular end organs.

6 /auchene and zigzag, serve as mechanosensory end organs.

7 ying the diverse functions of cutaneous LTMR end organs.

8 s, epithelial dilation with abnormal sensory end organs.

9 emically comparable to developing vestibular end organs.

10 and functional development of the vestibular end organs.

11 ensity were not found in the other inner ear end organs.

12 a clinical biomarker for the blood supply to end organs.

13 trajectories to innervate their appropriate end organs.

14 han the detection range of the corresponding end organs.

15 forming units found in the blood and several end-organs.

16 The absence of consistent end organ abnormalities in many chronic pain syndromes h

17 ion, which seeks to reduce the expression of end-organ allergic disease in children with established

18 eptibilities, adaptive immune responses, and end-organ alterations (particularly in airway mucous cel

19 eptibilities, adaptive immune responses, and end-organ alterations (particularly in airway mucous cel

20 ls to obtain therapeutic control of targeted end organs and effectors.

21 thways, allowing better visualization of the end organs and peripheral nerves.

22 evidence indicates that auditory/vestibular end organs and subsets of hair cells therein rely on dis

23 d by distinct combinations of mechanosensory end organs and the low-threshold mechanoreceptors (LTMRs

24 Adenoviruses (Ads) cause a wide array of end-organ and disseminated diseases in severely immunosu

25 al cardiovascular pathologies resides at the end organ, and is coupled to impairment of cyclic nucleo

26 patient's prognosis, hemodynamic stability, end organ, and neurologic status.

27 upport the notion that peripheral vestibular end organs are not passive transducers of head movements

28 thelium of the organ of Corti and vestibular end organs as well as in cells of the spiral ganglion.

29 o 1.5 x 10(6)-fold) viral loads in blood and end organs compared to N13R10.

30 hronic, relentless disease in which delay of end-organ complications is the major treatment goal, GI

31 anding of the pathophysiology and downstream end-organ complications of disordered mineral metabolism

32 chromogranin A (CHGA) polymorphisms predict end-organ complications of hypertension, such as end-sta

33 iable clinical course, many patients develop end-organ complications that are associated with signifi

34 wever, limited insight has been gained as to end-organ complications.

35 tential treatment for diabetic patients with end-organ complications.

36 so-occlusive events drive the development of end-organ complications.

37 results in worsening functional capacity and end-organ compromise.

38 en lipid accumulation was uncoupled from its end-organ consequences in IL-17RA(-/-) mice, which exhib

39 The CMR LGE may represent the end-organ consequences of sustained adrenergic activatio

40 The Merkel disc, a main type of tactile end organ consisting of Merkel cells (MCs) and Abeta-aff

41 Merkel discs are tactile end organs consisting of Merkel cells and Abeta-afferent

42 In this observational study, we assessed end organ damage and clinical symptoms with special focu

43 microL for more than 6 months are at risk of end organ damage and should be referred for specialized

44 is report suggest that EFE represents severe end organ damage associated with IVDA and portends poor

45 ecelerate the aging process as well as blunt end organ damage from obesity.

46 te that neutrophils are primary mediators of end organ damage in a novel humanized lupus mouse model,

47 er cell derangement in exacerbating postburn end organ damage in alcohol-exposed mice.

48 SDMA) predict and potentially contribute to end organ damage in cardiovascular diseases.

49 to induce erythrocyte sickling and eventual end organ damage in sickle cell disease (SCD).

50 rk of epithelial cell damage and can lead to end organ damage including renal failure.

51 receptor blocker on intermediate markers of end organ damage, and long-term end point trials are pla

52 oimmunity should be considered distinct from end organ damage.

53 ed macrophages, neutrophils, and significant end organ damage.

54 ncreased salt sensitivity, inflammation, and end organ damage.

55 oplasmacytic infiltration but no evidence of end-organ damage (anemia, constitutional symptoms, hyper

56 a significant improvement in SCD-associated end-organ damage (nephropathy, pulmonary hypertension, p

57 The patient suffered no end-organ damage and achieved a positive outcome, discha

58 but often-beneficial effects in ameliorating end-organ damage and blood pressure elevation in experim

59 there was no association between DM without end-organ damage and BRVO (aHR, 0.92; CI, 0.81-1.04; P =

60 This observational study assessed end-organ damage and clinical symptoms during dose reduc

61 vidence that increased KCC activity worsened end-organ damage and diminished survival in sickle cell

62 ate and adaptive immune system contribute to end-organ damage and dysfunction in hypertension.

63 utcomes of adverse drug events can result in end-organ damage and even death.

64 these cells may prove beneficial in reducing end-organ damage and preventing consequences of hyperten

65 lar protein deposition disease that leads to end-organ damage and related symptoms and requires a tis

66 of IL-2 to lupus-prone mice protects against end-organ damage and suppresses inflammation by dually l

67 reatable vascular risk factor, how it causes end-organ damage and vascular events is poorly understoo

68 contributes to the chronic inflammation and end-organ damage associated with the disease; however, i

69 ase progression requiring the development of end-organ damage attributable to multiple myeloma and bi

70 sease severity was important; enrollees with end-organ damage caused by HTN had a 107% increased haza

71 Both HTN and end-organ damage from DM contribute to arteriosclerosis,

72 2; CI, 0.81-1.04; P = 0.2), individuals with end-organ damage from DM had a 36% increased hazard of B

73 d with patients without DM, individuals with end-organ damage from DM have a heightened risk of CRVO,

74 Individuals with end-organ damage from hypertension (HTN) or diabetes mel

75 0.002), and patients with DM complicated by end-organ damage had 52% lower odds of having KCN (adjus

76 The presence of hypertensive end-organ damage has been demonstrated in hypertensive c

77 onally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic fac

78 ression MIF alleles also are associated with end-organ damage in different autoimmune diseases.

79 er in attenuating this measure of myocardial end-organ damage in hypertensive patients with LV hypert

80 nsights on the genetics of susceptibility to end-organ damage in lupus glomerulonephritis have been d

81 e cells in the kidney and the development of end-organ damage in patients and animal models with sodi

82 ous system and promote T-cell activation and end-organ damage in peripheral tissues.

83 terial pathogens, but may also contribute to end-organ damage in sepsis.

84 rs of systemic intravascular coagulation and end-organ damage in septic mice.

85 he severity of BP elevation and hypertensive end-organ damage in several animal models.

86 , cause not only insulin resistance but also end-organ damage in the form of nonalcoholic fatty liver

87 tivation, subsequent T-cell infiltration and end-organ damage in the kidney in the development of hyp

88 nk to the high rates of death as a result of end-organ damage in the months after recovery from pneum

89 he association between aprotinin and serious end-organ damage indicates that continued use is not pru

90 nclusions are that, in most cases, patients' end-organ damage is expected to either stabilise or impr

91 rove evaluation techniques, and determine if end-organ damage is reversible with proper therapy.

92 fective therapy exists but is ineffective if end-organ damage is severe.

93 ular signaling response that leads to target end-organ damage may be a more viable therapeutic strate

94 lar disease (CVD) are both manifestations of end-organ damage of the metabolic syndrome.

95 s, cardiovascular, hepatic, and reproductive end-organ damage or disease.

96 countries with CVD or diabetes mellitus with end-organ damage receiving proven medications.

97 nvestigate incidence of and risk factors for end-organ damage resulting in registration on a waiting

98 ssment for the presence of comorbidities and end-organ damage should be emphasized.

99 c ADAMTS13 replacement decreases the risk of end-organ damage such as ischemic stroke and resolved pr

100 development of blood pressure elevation and end-organ damage that occur on delayed exposure to mild

101 row plasma cells, or both, in the absence of end-organ damage was used to define light-chain smoulder

102 ac arrest myocardial dysfunction, attenuated end-organ damage, and improved neurologic outcome and su

103 rombin is a powerful modifier of SCD-induced end-organ damage, and present a novel therapeutic target

104 ove our understanding of pathophysiology and end-organ damage, and, furthermore, open doors to its ev

105 icular (LV) hypertrophy, a marker of cardiac end-organ damage, is associated with an increased risk o

106 Progressive end-organ damage, partly related to a systemic vasculopa

107 e renal disease, embolic events resulting in end-organ damage, renovascular complications, or hyperte

108 Long-term, there is a risk of end-organ damage, seen in 75% of patients with late diag

109 atic multiple myeloma and the development of end-organ damage.

110 ity and hypertension as well as hypertensive end-organ damage.

111 f primary bone marrow disease with secondary end-organ damage.

112 rteries, which leads to arteriosclerosis and end-organ damage.

113 d into a debilitating disorder with emerging end-organ damage.

114 sens systolic hypertension and its attendant end-organ damage.

115 sis model in vivo to determine mortality and end-organ damage.

116 inically-relevant metabolic disturbances and end-organ damage.

117 dial infarction, thrombocytopenia, and other end-organ damage.

118 uroretinal disorder as an indicator of other end-organ damage.

119 ular hypertrophy, vascular inflammation, and end-organ damage.

120 oduction and facilitating the development of end-organ damage.

121 otypes may protect from ensuing inflammatory end-organ damage.

122 elopment of sepsis-related sequelae, such as end-organ damage.

123 to smaller distal arteries, causing ischemic end-organ damage.

124 tory and profibrotic cascades culminating in end-organ damage.

125 at IMT levels below thresholds for clinical end-organ damage.

126 pair, progressive fibrogenesis, and eventual end-organ damage.

127 NZB genes and induces significantly greater end-organ damage.

128 her B cell lymphoproliferative disorder with end-organ damage.

129 lf dsDNA and induce dsDNA autoantibodies and end-organ damage.

130 tion, hemoglobin A1C level, insulin use, and end-organ damage.

131 elial dysfunction, and increases the risk of end-organ damage.

132 s have been shown to ameliorate hypertensive end-organ damage.

133 iple myeloma (MM) and represents a marker of end-organ damage; it is used to establish the diagnosis

134 t in part, emerge through extrinsic, sensory end organ-derived signals.

135 egaly, intrarenal leukocyte trafficking, and end organ disease in a murine model of lupus.

136 approach for prevention of CMV syndrome and end organ disease.

137 as an increased frequency of age-associated end-organ disease (e.g. cardiovascular complications, ca

138 of viral load correlate with development of end-organ disease and are moderated by pre-existing natu

139 n or reduction in DNAemia and CMV-associated end-organ disease and/or the cessation or reduced use of

140 Cytomegalovirus end-organ disease can be prevented by giving ganciclovir

141 te quantitative nucleic acid testing in some end-organ disease categories.

142 munity, but this may not suffice to engender end-organ disease in lupus.

143 t are key to the prevention and treatment of end-organ disease in this population and critical to the

144 BK virus (BKV) infection causing end-organ disease remains a formidable challenge to the

145 However, HCMV can cause end-organ disease that results in death in the immunosup

146 the ability to provide transplants or other end-organ disease treatment, 3) cultural differences tha

147 ry of ischemic heart disease), valvular, and end-organ disease were followed up for the adverse compo

148 MV viremia requiring antiviral treatment, or end-organ disease), nonrelapse mortality, and severe (gr

149 0.01) including relapsing-viremia episodes, end-organ disease, and CMV resistance to therapy, as wel

150 ejection, allograft dysfunction, significant end-organ disease, and mortality.

151 disease, severe liver disease, diabetes with end-organ disease, chronic renal failure, and dementia)

152 rug because of CMV antigen or DNA detection, end-organ disease, or any other cause.

153 excess clotting on tissue function leads to end-organ disease.

154 g the development of inflammation-associated end-organ disease.

155 on is a lifesaving therapy for patients with end-organ disease.

156 emia and clinical or laboratory findings) or end-organ disease.

157 expression contributes to the development of end organ diseases such as HIV-1-associated CNS disease.

158 e persistent inflammation that leads to many end-organ diseases in adults.Despite viral suppression,

159 ld, likely due to 1) differences in rates of end-organ diseases, 2) economic differences in the abili

160 etic activation may contribute to, or worsen end-organ diseases, and reduce the possibility of ventri

161 lar disease, cancer, osteoporosis, and other end-organ diseases.

162 ally related to the premature onset of other end-organ diseases.

163 Thus, OS-dependent metabolic and end organ dysfunction of aging may result from life-long

164 End organ dysfunction, particularly liver and kidney, is

165 morbidities without a resulting increase in end organ dysfunction.

166 GVHD remain inadequate and commonly lead to end-organ dysfunction and opportunistic infection.

167 ained systolic blood pressure <90 mm Hg with end-organ dysfunction ascribed to the hypotension.

168 atory response to infection characterized by end-organ dysfunction distant from the primary site of i

169 poperfusion probably account for much of the end-organ dysfunction in African patients with severe se

170 sitemia (<10%), and were less likely to have end-organ dysfunction other than their splenic involveme

171 n some instances, and the high prevalence of end-organ dysfunction that affects the pharmacokinetic a

172 strategy combining a code for infection and end-organ dysfunction was more sensitive in identifying

173 dices of global illness severity, markers of end-organ dysfunction, and profiles of hemodynamic insta

174 cate into the systemic circulation and cause end-organ dysfunction, including renal dysfunction.

175 ic leak was associated with the incidence of end-organ dysfunction, mortality, reoperation, and hospi

176 The main outcomes were 30-day mortality, end-organ dysfunction, reoperation, prolonged hospitaliz

177 ogy are related to pulmonary endothelial and end-organ dysfunction, suggesting a mechanistic link bet

178 requiring two ICD-9 codes for infection and end-organ dysfunction.

179 noverlapping with respect to their cutaneous end organs (e.g., hair follicles), with Abeta rapidly ad

180 ge," may be a useful method to quantify the "end organ" effect of exposure to these various risks.

181 ure), lack of effect on regression of target end organ effects like left ventricular hypertrophy and

182 End-organ effects are diverse, resulting in both cogniti

183 This global functionality explains how large end-organ effects can be induced through modest individu

184 2 receptor genes expressed in the gustatory end organs enable bony vertebrates (Euteleostomi) to rec

185 scade activation, and fibrosis predict these end-organ events.

186 eficiency virus (HIV)-infected patients with end organ failure can safely receive an organ transplant

187 spitalized patients who had Covid-19 without end-organ failure in a 1:1 ratio to receive either LY-Co

188 tunity to improve survival for patients with end-organ failure through greater access to organ transp

189 advances in understanding the mechanisms of end-organ failure, and modulation of the inflammatory re

190 -year childhood cancer survivors with severe end-organ failure.

191 spitalized patients who had Covid-19 without end-organ failure.

192 le midshipman use the saccule as the primary end organ for hearing to detect and locate "singing" mal

193 patterns of SCG connections, restoration of end organ function would be expected.

194 status, biomarkers, symptoms, hospital stay, end organ function, and mortality have all been employed

195 nucleotide variation in microRNAs can affect end-organ function and stress response.

196 tion cluster, diastolic-hemodynamic cluster, end-organ function cluster, vital-sign cluster, complete

197 diate both pancreatic beta-cell function and end-organ function offers the opportunity to develop the

198 End-organ function was assessed using magnetic resonance

199 mance status of 2 or less, and with adequate end-organ function were eligible to participate.

200 Eligible patients had adequate end-organ function, an Eastern Cooperative Oncology Grou

201 1 (RECIST v1.1), adequate haematological and end-organ function, and no autoimmune disease or active

202 ECIST v1.1), and adequate haematological and end-organ function.

203 ia In Solid Tumors version 1.1, and adequate end-organ function.

204 unt less than 10 x 10(9) per L, and adequate end-organ function.

205 al seed sequence modifies mRNA targeting and end-organ function.

206 factor-1 in injured tissue leads to improved end-organ function.

207 p performance status of 0 or 1, and adequate end-organ function.

208 eviously treated solid tumours, and adequate end-organ function.

209 eria in Solid Tumors version 1.1, and normal end-organ function.

210 r findings provide insights into how tactile end-organs function and have clinical implications for t

211 urgery outweigh the significant benefits for end-organ health.

212 Sex hormone dysregulation and altered end-organ hormone sensitivity might explain this organ-s

213 omplex, and hemodynamically diverse state of end-organ hypoperfusion that is frequently associated wi

214 thelin-1 (ET-1) on cholinergic mechanisms of end-organs (i.e. skin blood vessels and sweat glands) fo

215 sepsis database the earliest measurement of end organ impairment, tqSOFA, performed poorly at identi

216 End-organ impairment has received relatively little rese

217 rves in invertebrates to complicated tactile end organs in mammals.

218 nical stimuli activate specialized cutaneous end organs in the bill, innervated by trigeminal afferen

219 plasticity.SIGNIFICANCE STATEMENT Vestibular end organs in the inner ear receive efferent inputs from

220 te activation, and infection-mediated innate end-organ inflammation.

221 e euthanized and inflammatory responses, and end organ injuries were assessed.

222 ccumulation alone is not responsible for the end organ injury in cystinosis.

223 mbotic microangiopathy (TMA), and widespread end organ injury.

224 ex hormones have been shown to modulate some end-organ injury after shock, post-T/HS BM dysfunction h

225 may play an important role in sepsis-related end-organ injury and dysfunction, especially in the hear

226 ies, aGVHD diagnosis is typically made after end-organ injury and often requires invasive tests and t

227 mics, decrease myocardial damage, and reduce end-organ injury from prolonged hypoperfusion.

228 in GCs and EF, are major contributors to the end-organ injury in systemic autoimmunity.

229 End-organ injury is evident, illustrated by the presence

230 Development of end-organ injury on ECMO and longer ECMO duration were a

231 ion and diagnosis of aHUS as the recovery of end-organ injury present appears to be related to the ti

232 to be high MIF producers develop accelerated end-organ injury.

233 ys, proinflammatory cytokine production, and end-organ injury.

234 and protected lupus-prone MRL/Lpr mice from end-organ injury.

235 nvolvement when compared to patients without end-organ involvement (P = 0.023, P = 0.005, and P = 0.0

236 by cold temperatures and that has different end-organ involvement and increased intracellular signal

237 as more than 1500 cells per microliter with end-organ involvement and no recognized secondary cause.

238 h those without DM (P = 0.45), patients with end-organ involvement from DM had a 27% increased hazard

239 y, risk of neurodevelopmental impairment and end-organ involvement with fungal infections in the neon

240 le (MS) and Golgi tendon organ (GTO) sensory end organs is critical for normal motor control, but how

241 anglia are predetermined to innervate select end-organs is unknown.

242 ntimal destruction, arterial thrombosis, and end-organ ischemia.

243 rienced more neurological symptoms and other end-organ ischemic events than those without dissection.

244 a of 1.5 x 10(9)/L or higher and evidence of end organ manifestations attributable to the eosinophili

245 erized by marked peripheral eosinophilia and end organ manifestations attributable to the eosinophili

246 ccurately describe the clinical sequelae and end-organ manifestations of RHF.

247 has resulted largely from therapies treating end-organ manifestations.

248 oninvasive control of the nervous system and end-organs may enable safer and more effective treatment

249 d in Ex16 rats, implicating both central and end-organ mechanisms in vagal enhancement.

250 d dehydrogenase type 1 (11betaHSD1) performs end-organ metabolism of glucocorticoids (GCs) by catalyz

251 ted therapeutics aimed at reducing the major end-organ morbidities of chronic SF.

252 tructive sleep apnea (OSA) leads to multiple end-organ morbidities that are mediated by the cumulativ

253 ntly present, is associated with substantial end-organ morbidities that primarily but not exclusively

254 impact of PAD upon microvascular flow in the end-organ, muscle, remains unknown.

255 Because the kidney is the major end organ of FGF23 action, we hypothesized that it relea

256 demonstration of TH-ir terminals in the main end organ of hearing in a nonmammalian vertebrate sugges

257 ously an inaccessible, but highly important, end organ of the brain.

258 well as in the adrenal medulla (AM), a major end organ of the sympathetic nervous system.

259 h CGRP staining was absent in the vestibular end-organs of null (-/-) mice, cholinergic staining appe

260 utside the cardiac vasculature, resulting in end-organ optic nerve ischaemia.

261 inability to meet metabolic requirements of end organs or skeletal muscle.

262 ion, hematological abnormalities, markers of end-organ or right ventricular dysfunction, and lack of

263 ompass all connections from sensory input to end-organ output across the entire animal, information t

264 us nephritis (LN) is a potentially dangerous end organ pathology that affects upwards of 60% of lupus

265 n, pLVAD support was able to safely maintain end-organ perfusion despite extended periods of hemodyna

266 highly morbid condition in which inadequate end-organ perfusion leads to death if untreated.

267 r mechanical circulatory support to maintain end-organ perfusion until transplantation or recovery.

268 d skin sympathetic nerve activity (SSNA) and end-organ peripheral vascular responsiveness are unclear

269 suggests that the non-neuronal components of end organs play an active role in signaling to LTMRs and

270 Animal models demonstrating end-organ protection in C3-deficient mice and evidence o

271 t is CD39 deletion on NK cells that provides end-organ protection, which is comparable to that seen i

272 Volatile agents may possess important end-organ protective properties mediated via cytoprotect

273 hways directly connecting sensory neurons to end organs; recurrent and reciprocal connectivity among

274 Thus, loss of USH2A in corpuscular end-organs reduced mechanoreceptor sensitivity as well a

275 nce to the development of cGN is mediated by end organ resistance to damage.

276 hat increases in activity do not result from end-organ resistance but rather from lowered urinary ATP

277 temic autoimmunity, end-organ responses, and end-organ resistance to damage are also critical in dete

278 lts from compromised ATP release rather than end-organ resistance: ENaC in Cx30(-/-) mice responds to

279 In addition, studies of end-organ responses provide new targets for therapeutic

280 e that in addition to systemic autoimmunity, end-organ responses, and end-organ resistance to damage

281 chemoreflex function show congruence in the end-organ responses.

282 ation are mediated, in part, by increases in end-organ responsiveness to efferent sympathetic outflow

283 rcholesterolaemic older adults by increasing end-organ responsiveness to sympathetic outflow during p

284 ark of sepsis, resulted in underperfusion of end organs, resulting in their damage.

285 hogenic role in the pernicious metabolic and end-organ sequelae of obesity.

286 noclonal gammopathy, immune suppression, and end-organ sequelae.

287 ons; (ii) patients with a positive biopsy in end organs, such as the lung or stomach; (iii) symptomat

288 nts such as the initial fluid resuscitation, end-organ support, pain management, nutrition support, a

289 role in both propagation of autoimmunity and end-organ targeting.

290 iology: how are signals processed in sensory end organs, taste buds?

291 To evaluate the end-organs, taste buds and a class of putative taste rec

292 Meissner corpuscles are mechanosensory end organs that densely occupy mammalian glabrous skin.

293 Neurobiotin labeling of the main auditory end organ, the saccule, combined with tyrosine hydroxyla

294 tion not only in lymphoid organs but also in end organs, thereby preventing the break in tolerance.

295 Significantly, end-organ tissue injury was not significantly different

296 has let mammals develop complicated tactile end organs to enable sophisticated sensory tasks, includ

297 ransport of a lipophilic dye from peripheral end organs to the dorsal medulla shows that fibers from

298 levels may provide a potential biomarker for end-organ vulnerability.

299 ferents carry signals from single vestibular end organs, whereas secondary afferents from vestibular

300 lood is delivered from the left ventricle to end organs with each cardiac cycle (200 million litres o