コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 s in hospitalized patients with COVID-19 and hyperinflammation.
2 tates imbalanced immune responses and tissue hyperinflammation.
3 ncrease antiviral responses while curtailing hyperinflammation.
4 c lymphohistiocytosis (HLH) is a syndrome of hyperinflammation.
5 of novel therapeutic targets for modulating hyperinflammation.
6 te chemoattactant protein-1, consistent with hyperinflammation.
7 the prevention of XIAP deficiency-associated hyperinflammation.
8 ion leads to EBV reactivation and subsequent hyperinflammation.
9 ice, the loss of PIP4K2C leads to late onset hyperinflammation.
10 patients with severe COVID-19 pneumonia and hyperinflammation.
11 as a critical regulator of SARS-CoV-2-evoked hyperinflammation.
12 ome describing patients with severe systemic hyperinflammation.
13 s, and targeted therapeutics in the field of hyperinflammation.
14 for revolutionizing the clinical aspects of hyperinflammation.
15 or critical COVID-19 disease accompanied by hyperinflammation.
16 Covid-19) pneumonia is often associated with hyperinflammation.
17 and develop chronic infections that trigger hyperinflammation.
18 he rationale for an IL-18-driven subclass of hyperinflammation.
19 ednisolone in severe COVID-19 pneumonia with hyperinflammation.
20 me characterized by immune dysregulation and hyperinflammation.
21 s interleukin-1beta production, resulting in hyperinflammation.
22 er frequently associated with a nonresolving hyperinflammation.
23 leading to an increased bacterial burden and hyperinflammation.
24 (FHL4), a life-threatening disease of severe hyperinflammation.
25 cases by infectious agents, leads to severe hyperinflammation.
26 y characterized by initial cytokine-mediated hyperinflammation.
27 (MOF) may result from overwhelming systemic hyperinflammation.
28 rity of infections, autoimmune features, and hyperinflammation.
29 , a life-threating condition associated with hyperinflammation.
30 r PAMPs and DAMPs as the main contributor to hyperinflammation.
31 endotypes marked by immune dysregulation and hyperinflammation.
32 -2 antigens into the bloodstream, leading to hyperinflammation.
33 COVID-19 pneumonia is often associated with hyperinflammation.
35 g in response to TLR4 activation, leading to hyperinflammation, a hallmark of cystic fibrosis (CF) di
37 and plant fibers can dramatically reduce the hyperinflammation and also the infiltration by neutrophi
38 d by immune dysregulation with granulomatous hyperinflammation and autoimmunity, with relatively norm
39 s are not completely known, it is clear that hyperinflammation and coagulopathy contribute to disease
40 oach to treat organ dysfunction arising from hyperinflammation and cytokine storm by processing immun
41 reported to have protective benefits against hyperinflammation and cytokine storm syndrome, condition
43 lower respiratory tract infection-associated hyperinflammation and death, as observed in COVID-19.
45 mpt HLH-directed therapy in SD patients with hyperinflammation and evolving multiorgan failure at ris
46 with a homologous mutation exhibited similar hyperinflammation and greater susceptibility to collagen
47 The mechanisms linking systemic infection to hyperinflammation and immune dysfunction in sepsis are p
49 3 deficiency in mice, the mechanisms driving hyperinflammation and immunodeficiency are incompletely
50 hreatening syndrome, characterized by severe hyperinflammation and immunopathological manifestations
52 Fatal H7N9 infections are characterized by hyperinflammation and increased cellular infiltrates in
53 hat loss of neutrophil Shp1 in mice produced hyperinflammation and lethal pulmonary hemorrhage in ste
58 induce maladaptive effects and contribute to hyperinflammation and progression of cardiovascular dise
59 Two severe complications of LCH are systemic hyperinflammation and progressive neurodegeneration.
61 -19 patients consecutively hospitalized with hyperinflammation and respiratory failure (oxygen therap
62 therapeutic option in COVID-19 patients with hyperinflammation and respiratory failure, also on mecha
64 ue-resident trained macrophages that prevent hyperinflammation and restore tissue homeostasis followi
66 iver of life-threatening innate and adaptive hyperinflammation and support the rationale for an IL-18
69 ugh hyperoxia alone attenuated the postshock hyperinflammation and thereby tended to improve visceral
71 tem plays a substantial role in creating the hyperinflammation and thrombotic microangiopathy that ap
72 o the maladaptive immune response that fuels hyperinflammation and thrombotic microangiopathy, thereb
74 iew of the molecular mechanisms underpinning hyperinflammation and underscores the potential of omics
75 the proteome would reflect heterogeneity in hyperinflammation and vascular injury, and further ident
76 LR hyporesponsiveness may be associated with hyperinflammation and/or excessive or prolonged stimulat
77 nhancement of infection, and reduced risk of hyperinflammation, and (iii) streamlined antibody-like p
78 kely to result from increased mucus density, hyperinflammation, and defective bacterial killing could
79 alleviate oxidative stress, cytokine storm, hyperinflammation, and diminish the risk of organ failur
82 increase in children presenting with fever, hyperinflammation, and multiorgan dysfunction frequently
83 reduce programmed cell death and associated hyperinflammation, and restore functioning alveoli in CO
85 that CD80/86 signaling is essential for this hyperinflammation, and that blocking this proinflammator
86 rized by defective cellular cytotoxicity and hyperinflammation, and the only cure known to date is he
87 bility of many pathogenic antigens to induce hyperinflammation, and the previously identified role of
88 thal hemorrhagic shock, hyperoxia attenuated hyperinflammation, and thereby showed a favorable trend
89 al-acquired lung infections characterized by hyperinflammation, antibiotic resistance, and high morbi
90 hain (IFNAR1) in a child with fatal systemic hyperinflammation, apparently provoked by live-attenuate
91 hain (IFNAR1) in a child with fatal systemic hyperinflammation, apparently provoked by live-attenuate
95 gents to further elucidate the importance of hyperinflammation as a factor contributing to severe COV
96 ysis in mice with lipopolysaccharide-induced hyperinflammation, as well as in ex vivo human sepsis mo
97 ulated immune reaction involving features of hyperinflammation, as well as protracted immune suppress
100 nflammation that intensifies virally induced hyperinflammation associated with SARS-CoV-2 infection.
101 ation in a patient with severe infancy-onset hyperinflammation associated with signs of fulminant hem
102 ions including susceptibility to infections, hyperinflammation, autoimmunity, and lymphoproliferation
103 with increases in neutrophil senescence and hyperinflammation, broad inflammatory cytokine signaling
104 In sepsis, M1 macrophages can compensate for hyperinflammation by acquiring an M2-like immunosuppress
108 nsgenic (Il18tg) mice developed cachexia and hyperinflammation comparable to Prf1-/- mice, albeit wit
109 ID-19 is a systemic illness characterized by hyperinflammation, cytokine storm, and elevations of car
111 mechanical ventilation [IMV]), and systemic hyperinflammation defined by increased blood concentrati
112 e inflammation caused by excess lipoxins and hyperinflammation driven by excess leukotriene B(4).
113 hypomorphic mutation in SLP76 tones down the hyperinflammation due to STX11 deletion, resulting in a
116 agy as a means of limiting IL-1beta-mediated hyperinflammation during periods of cellular stress.
117 ard macrophages, is critical for suppressing hyperinflammation during the first 3 h of endotoxemia.
118 lying pathophysiological processes including hyperinflammation, endothelial damage, thrombotic microa
120 (February 25, 2020, to March 30, 2020) with hyperinflammation (ferritin >=1000 ng/mL and/or C-reacti
124 ctive response to infection while preventing hyperinflammation, gene expression in innate immune cell
126 eoxygenase (IDO), was proposed as a cause of hyperinflammation in CGD and this pathway has been consi
131 evels have been proposed to reflect systemic hyperinflammation in patients admitted to the intensive
132 However, whether it contributes to pulmonary hyperinflammation in patients with coronavirus disease 2
134 a contribution of IL-18 to inflammation and hyperinflammation in sepsis and MAS, we sought to study
135 We demonstrated that pulmonary and systemic hyperinflammation in severe COVID-19 are associated with
137 characterized by persistent hypothermia and hyperinflammation in the most severely affected mice.
138 ding the pathophysiology of autoimmunity and hyperinflammation in these disorders may also permit mor
139 responses to inflammatory stimuli to prevent hyperinflammation in vivo, yet whether STAT3 mediates pa
140 phic placental response to ZIKV and observed hyperinflammation in ZIKV-exposed male offspring followi
141 is associated with immune dysregulation and hyperinflammation, including elevated interleukin-6 leve
150 ed type I interferon activity and a state of hyperinflammation leading to acute respiratory distress
152 or repression activity of Miz1, resulted in hyperinflammation, lung injury and greater mortality in
153 wever, in CF airways, the Ca(2+)(i)-mediated hyperinflammation may be ineffective in promoting the er
156 mococcal infections can lead to uncontrolled hyperinflammation of the tissue along with substantial t
157 The patients displayed various types of hyperinflammation, often triggered by viral infection or
158 h the bone marrow of young mice did not show hyperinflammation or early bacteremia in response to K.
161 is poorly described, and the degree to which hyperinflammation or specific tissue injury contributes
162 hese children and adult patients with severe hyperinflammation present with a constellation of sympto
163 Neutrophil-specific Shp1 disruption leads to hyperinflammation, pulmonary hemorrhage, and increased m
165 Consequently, Ncl depletion causes aberrant hyperinflammation, resulting in a severe lethality in re
166 acterized by unchecked immune activation and hyperinflammation, resulting in end-organ tissue damage
167 ansgenic IL-18 production caused spontaneous hyperinflammation specifically characterized by CD8 T-ce
168 egy may also hold promise for treating acute hyperinflammation, such as observed in coronavirus disea
169 ryopyrin, a protein implicated in hereditary hyperinflammation syndromes, and was termed PAN2 for PAA
170 in CR3 and CR4 predispose to the maladaptive hyperinflammation that characterizes severe sepsis with
171 lyses may indicate specific populations with hyperinflammation that could benefit from pacritinib, al
172 ive care units, and patients who survive the hyperinflammation that develops early during sepsis late
173 p1 has the potential to fine tune neutrophil hyperinflammation that is central to the pathogenesis of
174 initial insult and coincides with a stage of hyperinflammation that is followed by a condition of inn
178 ry response syndrome transition implies that hyperinflammation triggers acute sepsis mortality, where
179 rrhagic shock-induced tissue hypoxia induces hyperinflammation, ultimately causing multiple organ fai
184 eptic mice by controlling both infection and hyperinflammation, whereas survival are only 50-60% with
185 viral replication phase is often followed by hyperinflammation, which can lead to acute respiratory d
186 -1beta secretion contributed to the observed hyperinflammation, which decreased upon caspase-1 inhibi
188 atory response that turned to an exaggerated hyperinflammation with the onset of severe pneumonia.