ライフサイエンスコーパス: cytokine storm

1 into the bloodstream, causing the so-called "cytokine storm".

2 ponse leading to a potentially catastrophic "cytokine storm".

3 ng systemic inflammatory response, termed a 'Cytokine Storm'.

4 ce resulted in induction of rapid and lethal cytokine storm.

5 tory syndromes characterized by uncontrolled cytokine storm.

6 n thought to drive excessive inflammation in cytokine storm.

7 icity involve strain selection and a massive cytokine storm.

8 event where virus-specific T cells induce a cytokine storm.

9 participants who all developed a devastating cytokine storm.

10 rimental aspects of the influenza-associated cytokine storm.

11 g, indicating a common pathway inhibition of cytokine storm.

12 stemic uncontrolled inflammatory response or cytokine storm.

13 mechanisms that are important in initiating cytokine storm.

14 tics for infectious disease characterized by cytokine storm.

15 g endothelial cells as central regulators of cytokine storm.

16 gn therapies to attenuate a COVID-19-related cytokine storm.

17 entify new proteins involved in triggering a cytokine storm.

18 e them to be eliminated by a proinflammatory cytokine storm.

19 nsplantation to avoid the adverse effects of cytokine storm.

20 -mediated conditions are frequently termed a cytokine storm.

21 ding of similar conditions associated with a cytokine storm.

22 ociated with improved survival and decreased cytokine storm.

23 hyperactivation that has been described as a cytokine storm.

24 e to study the effects of CAR T-cell-induced cytokine storm.

25 y responses can lead to a potentially lethal cytokine storm.

26 driven by hyperactive cytokine release, or a cytokine storm.

27 mic or local inflammation with presence of a cytokine storm.

28 is by limiting the scope and duration of the cytokine storm.

29 nd can even be used for the COVID-19-related cytokine storm.

30 endoplasmic reticulum (ER) stress and robust cytokine storm.

31 COVID-19 outcomes are attributed to classic cytokine storm.

32 e circulating biomarkers associated with the cytokine storm.

33 haracterized by robust T-cell activation and cytokine storm.

34 ase 2019 in intensive care units suffer from cytokine storm.

35 d proinflammatory cytokines, consistent with cytokine storm.

36 flammation, vascular leak, organ damage, and cytokine storm.

37 ication of immune dysregulation resulting in cytokine storm.

38 uspected infection has also been viewed as a cytokine storm.

39 ers are altered as a result of infection and cytokine storm.

40 n immune responses, such as autoimmunity and cytokine storm.

41 The secondary outcome was the occurrence of cytokine storm.

42 inating NLRP3-driven pyroptosis and the sHLH cytokine storm.

43 ere clinical outcomes and the development of cytokine storm.

44 L-6 and IP-10 levels, two key players in the cytokine storm.

45 tory distress syndrome (ARDS) triggered by a cytokine storm.

46 mmatory acute stage of COVID-19 results in a cytokine storm.

47 with excessive cytokine release known as the cytokine storm.

48 lammatory mediators, representing an ongoing cytokine storm.

49 ift hyperinflammatory response typified by a cytokine storm.

50 othelial barrier disruption and uncontrolled cytokine storm.

51 y mediators implicated in the TSS-associated cytokine storm.

52 anced vascular permeability, likely due to a cytokine storm.

53 hat resulted in an elevated pro-inflammatory cytokine storm.

54 tivation in BALB/c mice was accompanied by a cytokine storm.

55 (high) monocytes and neutrophils and fuels a cytokine storm.

56 tress response and subsequent eicosanoid and cytokine storms.

57 s that adequately reduce the burden of these cytokine storms.

58 overly exuberant immune response, termed a "cytokine storm," accompanies virus-induced acute respira

59 ced hyperinflammatory response that leads to cytokine storm, acute respiratory distress syndrome (ARD

60 ma (HCC) tumor growth via an "eicosanoid and cytokine storm." AFB(1)-generated debris up-regulates cy

61 A cytokine storm also occurred, with GVHD-specific secreti

62 Whether human cytokine storm also plays a similar role is not clear.

63 CoV-2 induced weight loss, clinical signs, a cytokine storm, an eicosanoid storm, and severe lung inf

64 e inflammation and respiratory disease, with cytokine storm and acute respiratory distress syndrome i

65 This implies a connection between the cytokine storm and altered B cell phenotype and function

66 ir potent activation of T cells leading to a cytokine storm and consequently vascular leakage, shock,

67 e patients with severe Covid-19 experience a cytokine storm and display evidence of inflammasome acti

68 In cynomolgus monkeys, no serious cytokine storm and hepatotoxicity are observed after ATG

69 disorder characterized by a life-threatening cytokine storm and immunopathology.

70 targeting viral entry, replication, and the cytokine storm and is associated with beneficial outcome

71 according to the receipt of tocilizumab for cytokine storm and matched to controls using propensity

72 ld identify those patients at higher risk of cytokine storm and most likely to benefit from IL-1B-neu

73 anti-CD28 antibody TGN1412 caused a massive cytokine storm and multiorgan failure in six healthy hum

74 ases are mild; severe disease often involves cytokine storm and organ failure.

75 ines with neutralizing antibodies blunts the cytokine storm and protects the host.

76 pe, TLR7-knockout mice had attenuated plasma cytokine storm and reduced lung and hepatic injury after

77 mmune disorders, from autoimmune diseases to cytokine storm and shock.

78 okines and cytokines, which triggers harmful cytokine storms and hyper-thrombotic responses.

79 cyRIIIa responses but also amplifies brewing cytokine storms and immune-mediated pathologies.

80 maRIIIa responses but also amplifies brewing cytokine storms and immune-mediated pathologies.

81 nhibition of CeA GABAergic neurons mitigated cytokine storms and improved survival rates in lethal pn

82 immunity can elicit autoimmune side effects, cytokine storms and other toxicities.

83 s of acute and chronic inflammation, such as cytokine storms and rheumatoid arthritis.

84 Severe COVID-19 patients may experience a "cytokine storm" and associated organ damage characterize

85 combination therapy induces an intratumoral "cytokine storm" and extensive lymphocyte infiltration.

86 e of the nucleocapsid protein in triggering "cytokine storms" and severe COVID-19 that led to hospita

87 acerbated proinflammatory cytokines release (cytokine storm) and loss of T lymphocytes (leukopenia) c

88 evidence of drug-induced hypercytokinemia or cytokine storm, and at higher doses, some indication of

89 rum, in infections, inflammatory conditions, cytokine storm, and cancer.

90 lated with the severity of COVID-19 disease, cytokine storm, and changes in myeloid cell subsets.

91 ammatory diseases including atherosclerosis, cytokine storm, and chronic autoimmune disease.

92 verted the molecular signature of sepsis for cytokine storm, and deregulated inflammatory reaction an

93 illness characterized by hyperinflammation, cytokine storm, and elevations of cardiac injury biomark

94 injury (ALI) characterized by vascular leak, cytokine storm, and infiltration of mononuclear cells in

95 ication in lung and nasal turbinate tissues, cytokine storm, and lung pathology.

96 ungs and nasal turbinates, body weight loss, cytokine storm, and lung pathology.

97 profound, aberrant myeloid cell activation, cytokine storm, and lymphopenia, with unknown immunopath

98 y lymphopenia, breach in vascular integrity, cytokine storm, and multiorgan failure.

99 also contribute to inflammatory cell death, cytokine storm, and organ damage in severe COVID-19 path

100 aberrant cell death can induce inflammation, cytokine storm, and pathology, making it a central molec

101 ivity impairs bacterial clearance, elicits a cytokine storm, and precipitates septic shock.

102 ory mechanisms of TLR responses relevant for cytokine storm, and suggest targeting the TBK1-IKKepsilo

103 adaptive immune response, characterized by a cytokine storm, and that it is triggered by prior SARS-C

104 oRNA combination therapy triggered transient cytokine storms, and (3) delivery of microRNA-122 and an

105 notypes, e.g. unusual neurological symptoms, cytokine storms, and blood clots were explored.

106 erapy, which triggers inflammatory cascades, cytokine storms, and EC dysfunction leading to acute lun

107 severity (aOR, 1.79; 95% CI, 1.36-2.35) and cytokine storm (aOR, 2.32; 95% CI, 1.42-3.79).

108 s untreated) had worse COVID-19 severity and cytokine storm (aOR, 3.33; 95% CI, 1.38-8.01, and aOR, 4

109 of sepsis include the inflammation-mediated cytokine storm, apoptosis-driven lymphopenia, and prolon

110 suggest that strain selection and a massive cytokine storm are major factors behind increased pathog

111 While eicosanoid and cytokine storms are well-characterized in infection and

112 However, uncontrolled inflammation and the "cytokine storm" are hallmarks of immunopathology in seve

113 ood and Drug Administration for treatment of cytokine storm associated with chimeric antigen receptor

114 Although the cytokine storm associated with GVHD leads to expression

115 a, pneumonia, and septicemia and averted the cytokine storm associated with septic infection but had

116 oles in the initiation and regulation of the cytokine storm associated with severe influenza.

117 ctivity, chloroquine might also mitigate the cytokine storm associated with severe pneumonia caused b

118 d with systemic inflammation often termed a "cytokine storm." Because interleukin-1 (IL-1) blocks the

119 llular restriction factor and suppression of cytokine storm: both aimed at long-term latency and host

120 y that is independent of NF-kappaB triggered cytokine storm but dependent on cellular egress.

121 Induction of a cytokine storm by blocking the interaction of NK inhibit

122 agonist significantly inhibited PVM-elicited cytokine storm by blunting the PVM-specific CD8(+) T cel

123 pattern recognition receptors initiating the cytokine storm by extensive cross-talk.

124 sfunction arising from hyperinflammation and cytokine storm by processing immune cells in an extracor

125 ells infiltrated into the lung, initiating a cytokine storm by their production of gamma interferon (

126 ith the observation that COVID-19 triggers a cytokine storm capable of injuring the endothelium and d

127 -A4, Sema3A (semaphorin 3A), exacerbates the cytokine storm caused by TLR agonists and bacterial seps

128 a preponderant role in the development of a cytokine storm causing fatal consequences in coronavirus

129 t-onset Still's disease (AOSD), and COVID-19 cytokine storm (CCS) are characterized by markedly eleva

130 cute inflammatory phase of GVHD, attenuating cytokine storm, CD8+ T-cell proliferation/activation, an

131 D4(+)T cell compartment, high viremia, and a cytokine storm characterize the early days after HIV inf

132 ses including COVID-19 are associated with a cytokine storm characterized by high interleukin-6 (IL-6

133 These pathogenic T cells initiated a cytokine storm characterized by high levels of tumor nec

134 onchoalveolar lavage fluid, and an augmented cytokine storm, compared with S1SP-treated mice on a con

135 ogressors (RDPs) had earlier and more robust cytokine storms, compared with slow disease progressors

136 ar, induction of high levels of interferon ("cytokine storms"), coupled with evasion of its effects,

137 Cytokine storm (CS) is a hyperinflammatory syndrome caus

138 Cytokine storms (CSs) are associated with various pathol

139 is believed to contribute to the pathogenic cytokine storm described in severe dengue patients, but

140 Cytokine storm describes a life-threatening, systemic in

141 marrow transplantation where an inflammatory cytokine storm dominates.

142 evented the debris-stimulated eicosanoid and cytokine storm, down-regulated ER stress genes, and prom

143 sease (iMCD) is a rare and poorly-understood cytokine storm-driven inflammatory disorder.

144 Cytokine storm due to COVID-19 can cause high morbidity

145 ctively), suggesting the faster and stronger cytokine storm during AHI could promote disease progress

146 The cytokine storm during influenza virus infection, whereby

147 ether, these data reveal a mechanism for the cytokine storm during SARS-CoV-2 infection and suggest t

148 tors and metabolic reprogramming that drives cytokine storm during sepsis.

149 Cytokine storm during severe COVID-19 infection increase

150 Cytokine storm during viral infection is a prospective p

151 intranasal/inhaled routes to mitigate acute cytokine storm effects.

152 The resulting CSF "cytokine storm", elicited from peripherally derived and

153 The dysregulated sepsis-induced cytokine storm evoked during systemic infection consists

154 virus infection, robust cytokine production (cytokine storm), excessive inflammatory infiltrates, and

155 onal symptoms to a hyperinflammatory state ("cytokine storm") followed by acute respiratory distress

156 ncluding IL-6 and IFN-gamma, contribute to a cytokine storm formerly known as "toxemia." A more preci

157 ecific CD4 T cells and was associated with a cytokine storm, generalized inflammation, and multi-orga

158 Cytokine storm has been postulated as one of the major c

159 During the COVID-19 pandemic, research on "cytokine storms" has been reinvigorated in the field of

160 el genetic and immunotherapeutic triggers of cytokine storm have been identified.

161 Systemic inflammation accompanied by a "cytokine storm," hemostasis alterations and severe vascu

162 nous administration of AVIDs did not trigger cytokine storm, hepatotoxicity, or thrombocytopenia.

163 ressed secretion of HMGB1, reduced the human cytokine storm, human lymphocyte apoptosis, and rescued

164 Antioxidants alleviate oxidative stress, cytokine storm, hyperinflammation, and diminish the risk

165 mall airways, successfully demonstrating the cytokine storm, immune cell activation, epithelial cell

166 infection of Kupffer cells and the following cytokine storm.IMPORTANCE Immunocompromised human patien

167 uced acute respiratory distress syndrome and cytokine storm in a murine model.

168 trigger the development of MIS-C as well as cytokine storm in adult COVID-19 patients, with importan

169 odulatory interventions aimed at controlling cytokine storm in AHI may be beneficial to slow eventual

170 A unique feature of the cytokine storm in coronavirus disease 2019 (COVID-19) is

171 verproduction of reactive oxygen species and cytokine storm in COVID-19 is essential to counteract th

172 ics analyses demonstrated a massive systemic cytokine storm in COVID-MDR compared with the relatively

173 volved in endothelial barrier disruption and cytokine storm in experimental lung injury.

174 A hyperinflammatory state referred to as cytokine storm in its severest form has been marked by e

175 the use of tocilizumab for the management of cytokine storm in patients with COVID-19.

176 tial mechanism for the increased M -mediated cytokine storm in patients with T2D in response to COVID

177 tection demonstrates that BR therapy reduces cytokine storm in plasma and ELISA demonstrates reduced

178 Overall, this study characterized the cytokine storm in severe COVID-19 and provides insights

179 ce, TLR7 antagonism reduces diverse types of cytokine storm in severe influenza.

180 2 transgenic mice produced a modest TH1/2/17 cytokine storm in the lung and spleen that peaked by day

181 Severe pneumonia is predominantly caused by cytokine storms in the lung, but whether this process is

182 in conjunction with alphaCD40/IL-2 prevented cytokine storms in young obese mice and protected from l

183 cytokine production in vitro and blunts the "cytokine storm" in endotoxemic mice by reducing levels o

184 on factors owing to hepatocellular necrosis, cytokine storm, increased permeability by vascular endot

185 ory state that is further propelled with the cytokine storm induced by SARS-CoV-2 infection or the lo

186 uch as Campath) and severe (such as TGN1412) cytokine storm-inducing drugs.

187 in severe cases of COVID-19, contributing to cytokine storm, inflammation, long-COVID, and other comp

188 ecan-1-null mice from the magnified systemic cytokine storm, inflammatory tissue injury, and death.

189 Inflammation markers were suggestive of cytokine storm (interleukin-6 median, 135 pg/mL) and mac

190 Cytokine storm is a broad term for a phenomenon with div

191 Inflammatory cytokine storm is a known cause for acute respiratory di

192 ests that diseases in which amplification of cytokine storm is a significant pathological component c

193 The cytokine storm is an intensified, dysregulated, tissue-i

194 Importantly, the cytokine storm is chemically treatable with specific ago

195 n contrast to influenza infection, where the cytokine storm is initiated early by the innate immune s

196 nia virus of mice (PVM), a model of RSV, the cytokine storm is initiated late in infection by the ada

197 rome coronavirus 2 (SARS-CoV-2) is variable, cytokine storm is observed in a subset of symptomatic in

198 g SARS-CoV-2 infection and suggests that the cytokine storm is primarily responsible for morbidity an

199 alth burden due to sepsis and the associated cytokine storm is substantial.

200 An excessive immune response known as cytokine storm is the hallmark of severe COVID-19.

201 proinflammatory cytokines, but whether this cytokine storm is the main cause of fatality or is a con

202 during H5N1 influenza virus infection, the "cytokine storm" is hypothesized to be the main cause of

203 kewise, the utility of a broad term such as "cytokine storm" is that it reflects a convergence on a s

204 ne release syndrome (CRS), commonly known as cytokine storm, is an acute systemic inflammatory respon

205 ession and inflammatory gene dysregulation ("cytokine storm"), leading to systemic damage and often d

206 table approach for the effective blunting of cytokine storm, leading to the improvement of clinical a

207 rrant systemic inflammatory reaction, named "cytokine storm," leads to a detrimental impairment of th

208 e all significantly elevated, resulting in a cytokine storm-like phenotype.

209 IL-1B is a key mediator of the cytokine storm linked to high morbidity and mortality fr

210 sponse phase that includes an eicosanoid and cytokine storm, lung inflammation and respiratory failur

211 RS-CoV-2) pneumonia patients indicate that a cytokine storm may increase morbidity and mortality.

212 A systemic cytokine storm may promote activation of Mo/Mac and cyto

213 tion, most likely by reducing TLR4-dependent cytokine storm mediated by damage-associated molecular p

214 s while showing similar activities, and (ii) cytokine storm-mediated pro-inflammation (e.g. acute res

215 ent cardiac dysfunction and death in a mouse cytokine-storm model.

216 beneficial, an excessive activation leads to cytokine storms, multiple organ failure, and even death.

217 Thus, superantigens induce a cytokine storm not only by mediating the interaction bet

218 nt in the rats did not reproduce the massive cytokine storm observed following TGN1412 administration

219 OVID-MDR compared with the relatively milder cytokine storm observed in DRESS, while MDR did not exhi

220 tes to lower pathogenicity by preventing the cytokine storm observed in EBOV infection.

221 drome (SIRS) and confirm the hypothesis that cytokine storm occurs as a result of HTRs.

222 We conclude that the cytokine storm of HLH is marked by distinctive T-cell ac

223 Cytokine storm of influenza virus infection is initiated

224 evere dengue has long been associated with a cytokine storm of unclear origin.

225 onment is triggered by a chemotherapy-driven cytokine storm or through direct effects of certain chem

226 remia, sepsis, and parasitosis, limiting the cytokine storm, organ damage/dysfunction, pathogen sprea

227 S) are 2 similar diseases characterized by a cytokine storm, overwhelming inflammation, multiorgan dy

228 egulates multiple ARDS GWAS genes related to cytokine storm, oxidation, and coagulation in lung micro

229 With cytokine storm playing a role in the pathogenesis of a w

230 ons uncovered the prominent direct role that cytokine storm plays in the pathogenesis, morbidity, and

231 Mouse models support the hypothesis that 'cytokine storm' plays an important role in the pathogene

232 The characteristic cytokine storm produced upon alpha-GalCer activation was

233 The virus-induced cytokine storm puts the immune system in overdrive at th

234 Current bioassays that detect cytokine storm responses in vitro rely on endothelial ce

235 t need for human tissue bioassays to predict cytokine storm responses to biologics.

236 tosis, Prf-deficient infants suffer a fatal "cytokine storm" resulting from macrophage overactivation

237 Plasma exchange mitigates cytokine storm, reverses organ failure, and could improv

238 uires identification of key mediators of the cytokine storm's initial wave.

239 IPA analysis showed that pathogen-induced cytokine storm signaling pathway, phagosome formation, a

240 y-IgE interaction model, including TREM1 and cytokine storm signaling.

241 A hyperinflammatory 'cytokine storm' state termed macrophage activation syndr

242 by dramatically increased bacterial burden, cytokine storm, striking histological abnormalities, and

243 TMA syndromes overlap with those released in cytokine storm, suggesting close connections between ine

244 ndromes converge upon an IL15/IL15RA-centric cytokine storm, suggestive of shared proximal pathways o

245 Cytokine storm syndrome (CSS) has generally been describ

246 mic juvenile idiopathic arthritis (sJIA) and cytokine storm syndrome (CSS), a potentially fatal compl

247 ne dysregulation, in some cases resulting in cytokine storm syndrome and acute respiratory distress s

248 e activation syndrome (MAS) is a devastating cytokine storm syndrome complicating many inflammatory d

249 ses increased proliferation of T cells and a cytokine storm syndrome in vivo.

250 lays a previously unappreciated role in sHLH/cytokine storm syndrome pathogenesis by preventing macro

251 The Clinical Trial of the Use of Anakinra in Cytokine Storm Syndrome Secondary to COVID-19 (ANA-COVID

252 tive conditioning regimen is hindered by the cytokine storm syndrome triggered by anti-CD3 and the hi

253 uces cytokine production and ameliorates the cytokine storm syndrome triggered by anti-CD3.

254 cases of the disease and has been labeled a 'cytokine storm syndrome' (CSS).

255 ctive benefits against hyperinflammation and cytokine storm syndrome, conditions that are associated

256 lymphohistiocytosis (sHLH), a severe form of cytokine storm syndrome, is the emergence of overactivat

257 Despite descriptions of COVID-19 as a cytokine storm syndrome, levels of circulating cytokines

258 istress syndrome (ARDS) that may progress to cytokine storm syndrome, organ dysfunction, and death.

259 atory distress syndrome that may progress to cytokine storm syndrome, organ dysfunction, and death.

260 ated HLH within a larger umbrella concept of cytokine storm syndrome.

261 hohistiocytosis (HLH) is a potentially fatal cytokine storm syndrome.

262 ality is associated with patients developing cytokine storm syndrome.

263 lood inflammatory parameters, reminiscent of cytokine storm syndrome.

264 Cytokine storm syndromes (CSS) are severe hyperinflammat

265 Cytokine storm syndromes (CSSs) are potentially fatal hy

266 Since the first textbook devoted to cytokine storm syndromes (CSSs) was published in 2019, t

267 Cytokine storm syndromes (CSSs), including hemophagocyti

268 Cytokine storm syndromes such as hemophagocytic lymphohi

269 Cytokine storm syndromes, such as familial hemophagocyti

270 tal role in the inflammatory response during cytokine storm syndromes.

271 markers for distinguishing between different cytokine storm syndromes.

272 factor and interferon-gamma) critical to the cytokine storm that amplifies expansion of donor APCs an

273 e immune cell population responsible for the cytokine storm that has been shown, in T2D, to promote e

274 Bacterial infection triggers a cytokine storm that needs to be resolved to maintain the

275 xcessive inflammatory response depicted in a cytokine storm that results from invasive bacterial, fun

276 -19 induces a robust, extended inflammatory "cytokine storm" that contributes to an increased morbidi

277 eads to the severe immune dysregulation and "cytokine storm" that is characteristic of fatal ebolavir

278 al emphasis on the principal features of the cytokine storm the mechanisms underlying this intense sy

279 rheumatoid arthritis and influenza-mediated "cytokine storm." The molecular mechanism of these anti-i

280 This "cytokine storm" then acts on T cells in the graft, promp

281 For over two decades, we have embraced the cytokine storm theory to explain sepsis, severe sepsis a

282 SASP factors can contribute to a 'cytokine storm', tissue-destructive immune cell infiltra

283 erized by a type I interferon (IFN-I)-driven cytokine storm, TLR7 antagonist treatment leaves epithel

284 s to better characterize the contribution of cytokine storm to COVID-19 pathophysiology.

285 and peripheral inflammatory responses (i.e., cytokine storm) to infection, which might produce neuroi

286 ge responses and probably contributes to the cytokine storms triggered by SARS-CoV-2.

287 Foetal cytokine storm (two or more pro-inflammatory cytokines >

288 ore likely to contribute to the pathological cytokine storm underlying STSS.

289 tion leads to severe disease associated with cytokine storm, vascular dysfunction, coagulation, and p

290 hough no difference in COVID-19 severity and cytokine storm was found in the IO group compared with t

291 The typical cytokine storm was present, with levels of interferon ga

292 In contrast to a "cytokine storm," we observe reduced proinflammatory gene

293 f proinflammatory cytokines and chemokines ('cytokine storm'), which can cause organ damage and even

294 d complications, such as lymphocytopenia and cytokine storm, which are associated with the severity o

295 lead to an aberrant inflammatory response or cytokine storm, which contributes to the severity of ill

296 e respiratory syndrome coronavirus 2-induced cytokine storm, which drives acute respiratory distress

297 dysregulated immune responses that trigger a cytokine storm with associated immunoparesis.

298 fraction of T cell pools to set in motion a "cytokine storm" with severe and sometimes life-threateni

299 Central to its pathogenesis is a cytokine storm, with markedly increased levels of numero

300 hrough altered T-bet dominance to dampen the cytokine storm without impeding the generation of memory