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1 plotype had reduced plasma MIF levels during acute disease.
2 on in children with malaria, but only during acute disease.
3 e functions that change during the course of acute disease.
4 t recipients receiving prophylaxis to reduce acute disease.
5 ced IFN-gamma does not alter the severity of acute disease.
6 ) are required for the development of severe acute disease.
7 , while infection with JHM.IA resulted in no acute disease.
8 ection, is not essential for inflammation in acute disease.
9 ntioxidant protection (R =.48; p =.00067) in acute disease.
10 in inducing specific CD8+ T cells during the acute disease.
11 r, but only a subset went on to develop more acute disease.
12 on recovered normally from passively induced acute disease.
13 eath (AICD) in the spontaneous recovery from acute disease.
14 d IL-10 (Ad-5/IL-10) reduced the severity of acute disease.
15 se, and the mice recovered more quickly from acute disease.
16 3 billion just for those found to be free of acute disease.
17 with rapid, high-level viral replication and acute disease.
18 required for the in vitro properties or for acute disease.
19 irectly related to signs and symptoms during acute disease.
20 9 exhibited a high prevalence of ANCA during acute disease.
21 pha, interleukin-10, and interferon-gamma in acute disease.
22 fection having completely recovered from the acute disease.
23 obability approaching 0% for those with mild acute disease.
24 om the qRT-PCR analysis done in blood during acute disease.
25 navirus 2 (SARS-CoV-2) can cause chronic and acute disease.
26 s acquired or correlate with protection from acute disease.
27 lbeit developing quicker after recovery from acute disease.
28 , by components of plasma from patients with acute disease.
29 polysaccharide I (CPS I) to virulence during acute disease.
30 38), as previously reported in a cohort with acute disease.
31 oup and none in the combined group developed acute disease.
32 er from cognitive impairment long time after acute disease.
33 e analyzed to identify the major features of acute disease.
34 e encephalitis (JE) is a vaccine-preventable acute disease.
35 amsters, a species particularly sensitive to acute disease.
36 of long-term residency within the horse post-acute disease.
37 -17A's ability to induce Th2 inflammation in acute disease.
38 y higher in the CNS at remission than during acute disease.
39 fever with renal syndrome (HFRS) is a severe acute disease.
40 ere also reduced in Panx1 KO EAE mice during acute disease.
41 1 does not contribute to the pathogenesis of acute disease.
42 enal fibrosis in mouse models of chronic and acute disease.
43 al, unknown trigger is needed to bring about acute disease.
44 o obtain CSF was performed 1.5-7 years after acute disease.
45 ng virus-host interactions in persistent and acute disease.
46 midine is also effective in a mouse model of acute disease.
47 ntly lower than those found in patients with acute disease.
48 nt the high-level bacteremia associated with acute disease.
49 r novel, host cell-focused therapies against acute diseases.
50 tus of the individual and early diagnosis of acute diseases.
51 ing a key strategy in addressing chronic and acute diseases.
52 tic indicator or predicting other chronic or acute diseases.
53 uses may be implicated in chronic as well as acute diseases.
54 tions are linked to multiple degenerative or acute diseases.
55 ilable in six patients and were decreased in acute disease (0.29 +/- 0.02 g/L) compared with convales
56 tive colitis during the study period: 73 for acute disease, 18 for advanced age and/or comorbidities,
57 f transferrin was significantly increased in acute disease (36.9% +/- 2.5%) compared with convalescen
58 issue activation in the head and neck during acute disease, a generalised pattern of peripheral lymph
59 gly, BIO 5192 treatment begun at the peak of acute disease accelerated entrance into disease remissio
60 nstructed from MRI-is highly associated with acute disease activity, both in the studied mouse models
63 cue fibrotic disease after the resolution of acute disease, addressing a current unmet need in the cl
64 tients with COVID-19 with severe or moderate acute disease, after recovery, and prepandemic healthy i
66 six types of EEHV in blood of elephants with acute disease, although EEHV1A is the predominant pathog
67 on of T(H)1-associated genes was detected in acute disease, although some were significantly upregula
68 iphasic disease, with T(H)2 predominating in acute disease and a switch to T(H)1 characterizing chron
69 tudinal profiling of immune responses during acute disease and following recovery in children who dev
70 riven classical pathway stimulus during both acute disease and in many patients during clinical remis
71 CD4 and CD8(+) T cells were detected during acute disease and maintained to 12 years, but these decl
73 ile therapeutics with potential for limiting acute disease and promoting bacterial decolonization.
74 ation, immunosuppression, or parturition) to acute disease and recrudescence from persistent SVA infe
75 le, as indicated by blocking and reversal of acute disease and reduced number of relapses and diminis
77 s may contribute to the clinical features of acute disease and represents a potential novel target fo
78 useful marker for leukemia in patients with acute disease and suggest a role for CREB in leukemogene
79 f drugs targeting short course therapies for acute diseases and towards long-term treatment of chroni
80 ticipate actively in the pathogenesis of the acute disease, and harbor the virus chronically, allowin
81 of T and B cell genes) persisted beyond the acute disease, and immune dysregulation was greatly impa
82 ecific imaging modality for the diagnosis of acute disease, and it helps in the management and progno
83 asma exchange, and pulse cyclophosphamide in acute disease, and strategies to prevent relapse over th
86 oals infused with nonimmune plasma developed acute disease associated with high levels of the predomi
87 e brain during several neurodegenerative and acute diseases associated with infiltration of periphera
88 ed with improved management of patients with acute disease because it accurately predicts short-term
89 Ab's between 26 and 35 weeks of age reversed acute disease, blocked chronic disease, and extended the
91 tomegalovirus (CMV) prophylaxis prevents the acute disease but its impact on subclinical infection an
93 n at this position (T81W) produced a similar acute disease but was attenuated for the development of
95 sets tolerized to MOG were protected against acute disease, but after tolerization treatment a lethal
96 e activated and initiate regeneration during acute disease, but lose this ability during the chronic
100 may have direct application in prevention of acute disease caused by intracellular bacterial pathogen
101 Chikungunya virus (CHIKV) infection causes acute disease characterized by fever, rash and arthralgi
102 -/- mice suffered an early and a more severe acute disease characterized by incomplete recovery when
104 plasmids that were originally isolated from acute-disease, chronic-disease, and severely attenuated
105 the treated group) and significantly reduced acute disease (clinical index of 4.3 +/- 0.7 in the untr
106 hould be considered a chronic rather than an acute disease condition, and have implications for the m
109 tation (SBMT), when performed at the peak of acute disease (day 14), prevented glial scarring and ame
112 ither CD28 peptide mimic administered during acute disease dramatically improved clinical signs of EA
114 disease initiation or during remission from acute disease effectively blocks the expression of the i
117 ion in experimentally infected equids during acute disease episodes and during asymptomatic infection
120 ntries, resulting in detailed reports of the acute disease following EBOV infection as well as descri
121 nstrates the benefit of antiviral therapy of acute disease for long-term respiratory health.IMPORTANC
123 ical data analysis phenotypes differentiated acute disease from health and acute cardiorespiratory ex
124 ponders (group A, n=11) and untreated active/acute disease (group B, n=9) and compared to Caucasian h
127 infection usually results in a self-limiting acute disease; however, in infected pregnant women, it i
128 ANCE Hepatitis E is usually a self-resolving acute disease; however, in pregnant women, HEV infection
129 t also play an early role in protection from acute disease.IMPORTANCE Syrian hamsters are in use as a
130 these cell types in vitro and in vivo during acute disease in a mouse model of S. aureus craniotomy i
131 S-CoV-2 IgG antibodies, distinguishable from acute disease in children but with antibody levels simil
132 osoma cruzi, can reactivate and cause severe acute disease in immunocompromised patients such as thos
133 aemocanis is a blood pathogen that may cause acute disease in immunosuppressed or splenectomized dogs
134 redominant sites of virus replication during acute disease in infected equids and serve as resilient
136 length or secreted gD2 significantly reduced acute disease in mice and guinea pigs (both P<.001) and
137 alphavirus chikungunya virus (CHIKV), cause acute disease in millions of people and utilize potent m
138 nged with group I isolates, mild to moderate acute disease in response to group V isolates, and no ac
144 ev region from the avirulent parent, induced acute disease in two animals, while a similar infectious
146 infections, including bacteraemia and other acute diseases in adults and immunocompromised individua
147 chronic diseases or can reactivate to cause acute diseases in AIDS patients or patients receiving im
148 cting contagion and the immediate outcome of acute diseases in previously healthy individuals is larg
150 r cycle length and consisted of five states: acute disease, indeterminate disease, cardiomyopathy wit
151 e most advanced in development are targeting acute disease indications such as stroke, myocardial inf
165 sease phase but increase significantly after acute disease onset on cardiomyocyte death and fibrotic
166 10, and 15 to examine the effect of RvD1 on acute disease or administered the same dose on days 60,
167 154 antibody treatment at either the peak of acute disease or during remission effectively blocked cl
168 contrast, Ab treatment either at the peak of acute disease or during remission exacerbated disease re
169 blood cells were isolated during the initial acute disease or from asymptomatic animals and analyzed
171 r VB families revealed their presence during acute disease or relapses but, with the exception of VB1
172 ere depleted immediately before the onset of acute disease, or during the chronic stage, a striking a
173 d to P. vivax infection; in the remaining 4, acute diseases other than malaria were found to be the c
174 ogle Trends was most suitable for monitoring acute disease outbreaks at the regional level in high-in
175 n to modulate immune responses and influence acute disease outcomes, suggesting that mTreg recall may
179 ease who do not meet the case definition for acute disease pose a low infection risk to health-care p
180 and IL-10(-)CD8 T cells interconvert during acute disease, possibly based on recent Ag exposure.
181 V-specific T-cell responses generated during acute disease predominantly target ORF2, but decline in
183 osis of leptospirosis are still lacking, and acute disease presents with nonspecific symptomatology a
184 sease: Improving Global Outcomes (KDIGO) and Acute Disease Quality Initiative (ADQI) criteria were us
186 Here, we provide recommendations from the Acute Disease Quality Initiative consensus meeting, whic
187 ssified as acute kidney disease according to Acute Disease Quality Initiative definition and 44 patie
190 dult patients that was developed at the 34th Acute Disease Quality Initiative meeting, which convened
191 agement and follow-up of PrAKI from the 32nd Acute Disease Quality Initiative meeting, which involved
196 prognostic cohort study of 3606 adults with acute diseases referred to 5 tertiary care hospitals in
197 ranscriptional and cytokine responses during acute disease reflected dominant type I/II interferon si
198 n contrast, uPAR-/- mice had a delayed, less acute disease reflected in delayed infiltration of infla
199 r endogenous myelin epitopes released during acute disease, reflecting a critical role for epitope sp
205 Hantavirus pulmonary syndrome (HPS) is an acute disease resulting from infection with any one of a
206 f convergent evolution in isolates from post-acute disease samples as a result of niche adaptation to
207 parable age and sex hospitalized for another acute disease (SARS-CoV-2 negative), and (c) healthy con
209 with higher tissue susceptibility had worse acute disease severity, higher acute inflammatory marker
210 x (MHC) class I, and perforin contributed to acute disease signs at 8 days postinfection (p.i.).
211 ients with anti-NMDAR encephalitis after the acute disease stage and 25 healthy control subjects unde
212 st patients are severely affected during the acute disease stage, but long-term functional recovery i
213 often severe, and usually persist beyond the acute disease stage, interfering with patients' recovery
215 ui within the horse is defined by short-term acute disease, strangles, followed by long-term infectio
216 d highly specific enrichment patterns in all acute disease subgroups, for example, selective enrichme
219 The introduction of vaccination against acute diseases such as measles induced a dramatic declin
222 ylori) is responsible for various chronic or acute diseases, such as stomach ulcers, dyspepsia, pepti
223 arameters and in a guinea pig fever model of acute disease, suggesting a difference in virulence pote
224 nsory, neurons.IMPORTANCE Stress exacerbates acute disease symptoms resulting from HSV-1 and HSV-2 in
232 iated hepatitis (AH) is a clinically severe, acute disease that afflicts only a fraction of patients
234 ntration of Legionella pneumophila causes an acute disease that is resolved by innate immune response
235 d adaptive immune activation pathways during acute disease that, despite reduced immunosuppressant us
237 features, including the rapid development of acute disease, the episodic nature of chronic disease, t
239 iruses affect host physiology beyond causing acute disease, thereby giving rise to the concept that t
245 A, USA) in Malawian NTS cases (n=106) during acute disease was correlated with genotype by linear reg
247 genic events are required for progression to acute disease, we crossed hMRP8p210BCR/ABL mice to apopt
248 like the T-cell infiltrates that peak during acute disease, we found that microglia activation persis
250 those isolated from naive mice or mice with acute disease, were able to endogenously present a varie
252 ease in response to group V isolates, and no acute disease when infected with group IV and VI isolate
253 ein-reactive cells infiltrate the CNS during acute disease, whereas affinities during remission, rela
254 ely related to known genotypes from cases of acute disease, whereas the seven loci (4.0 kb) obtained
255 and CCL5, were prominently expressed during acute disease, whereas transcripts for CXCL9, CXCL10, an
256 high level of HIV gene expression developed acute disease which resulted in premature death, and mic
257 le was seen in pediatric patients during the acute disease, which resolved at the subacute and conval
258 UL19/UL47 adenovirus groups developed severe acute disease, while 2/8 animals in the gC2/gD2-only gro
259 play an important role in protection against acute disease, while both CD4 T cells and antibodies are
260 la pertussis is the etiological agent of the acute disease whooping cough in infants and young childr
262 n that causes source-originated epidemics of acute disease with a case fatality rate thought to vary
265 tand breath metabolite network enrichment in acute disease, with a view to gaining mechanistic insigh
266 nce was significantly associated with severe acute disease, with probability of persistence in this p
268 20%) was characterized by a more aggressive acute disease within the 48 hours preceding ICU admissio