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1  0 to 20, with higher scores indicating more severe disease).
2 te changes in probability of presenting with severe disease.
3  of the mechanisms by which EBOV causes such severe disease.
4 ategy for management for these patients with severe disease.
5 mary causative agents and has been linked to severe disease.
6 rus (ZIKV) has recently caused epidemics and severe disease.
7 nt strains and has been associated with more severe disease.
8 ficant protection, and does not wane against severe disease.
9 , particularly for patients with moderate-to-severe disease.
10 were significantly elevated in patients with severe disease.
11  1 (HSV-1) infects most people and can cause severe disease.
12 n the revascularization cohort reported more severe disease.
13 e symptomatic, and 500,000 cases progress to severe disease.
14 ct agent with the potential to quickly cause severe disease.
15 ribute to decreased microcirculatory flow in severe disease.
16 m 0 to 3, with higher scores indicating more severe disease.
17 f intravascular hemolysis were not higher in severe disease.
18 gh RSV genomic load was associated with more-severe disease.
19 ime to peak viremia are useful predictors of severe disease.
20 sease outcomes and to identify predictors of severe disease.
21 its stability (L299P and G267S), may predict severe disease.
22 1 genotype are strongly associated with more severe disease.
23 rlier disease onset was associated with less severe disease.
24 34% FN in moderate, and 16% FP and 51% FN in severe disease.
25 ession was used to evaluate risk factors for severe disease.
26 lade, Ic3, was significantly associated with severe disease.
27 hildren with acute onset of symptoms or less severe disease.
28 e and the need to be cautious in the face of severe disease.
29 y EHEC virulence determinant contributing to severe disease.
30 tural and remodeling changes associated with severe disease.
31 s admitted to hospital with warning signs or severe disease.
32 ccinated with MVA-H7-Sh2 were protected from severe disease.
33 n models were used to model risk factors for severe disease.
34 r outcomes than do patients with moderate or severe disease.
35 high IL-4/IFN-gamma ratio is associated with severe disease.
36 ort toward patients with more severe or less severe disease.
37 uding the large cholinergic interneurons, in severe disease.
38 ) were found to be independent predictors of severe disease.
39 ion within multiple organs, often leading to severe disease.
40  resulting in enhanced viral replication and severe disease.
41 se mice with B cells but no secreted Ig have severe disease.
42 ively) in both IL28B SNPs is associated with severe disease.
43 atients were admitted to hospital because of severe disease.
44  are the treatment of choice for moderate to severe disease.
45 ricted population of infants at high risk of severe disease.
46 hen the individual is more likely to develop severe disease.
47 highly virulent pathogens capable of causing severe disease.
48  the host response as a major contributor to severe disease.
49 ach, especially in patients with moderate-to-severe disease.
50 ances that drive a mild clinical course to a severe disease.
51 IAV) infection are typically associated with severe disease.
52 ement of eczema in children with moderate to severe disease.
53  upper respiratory tract and rarely produces severe disease.
54 ctions that place infected hosts at risk for severe disease.
55 e (mean, 68 years), chronically ill, and had severe disease.
56 fest later in life, from mild dysfunction to severe disease.
57 present, then the subject tends to have more severe disease.
58           Measles is a highly contagious and severe disease.
59 oropharyngeal candidiasis, resulting in more severe disease.
60 veloped diarrhea, 7 experiencing moderate to severe disease.
61  (13R(+/+)) and develop early onset and more severe disease.
62 aphical region, and was associated with more severe disease.
63 nd with a powerful new means to combat these severe diseases.
64 , and some of the transporters are linked to severe diseases.
65 s (GPCRs) are important targets for treating severe diseases.
66  been suggested to have an impact in several severe diseases.
67  2 years of life, with a minority developing severe disease (1%-3% hospitalized).
68 n indication for antibiotic prescription was severe disease (57%, 103/182 prescriptions), while it wa
69  in childhood, particularly in patients with severe disease accompanied by atopy, fatigue, and sleep
70       Almost 50% of patients had moderate-to-severe disease activity as reported by Urticaria Activit
71 th or treatment failure were the presence of severe disease (adjusted odds ratio [aOR], 4.96; 95% con
72 er viral coinfection was not associated with severe disease, ADV coinfection had increased odds of li
73 ocytes in necrotizing enterocolitis (NEC), a severe disease affecting premature infants, remain unkno
74 wborns are significantly more susceptible to severe disease after infection with herpes simplex virus
75 We estimated the relative risks of death and severe disease among MERS-CoV patients in the Middle Eas
76 ections among young children and can lead to severe disease among some infants.
77 impossible to predict which patients develop severe disease and are in need of aggressive treatment.
78                                  Miners with severe disease and available lung tissue were identified
79 rains with TPS2 and/or TPS3 resulted in less severe disease and better outcomes than infection with s
80                   Influenza infection causes severe disease and death in humans.
81 stridium difficile infection (CDI) can cause severe disease and death, especially in older adults.
82        The virus has the capability to cause severe disease and death, especially in young children.
83 as A(H5N1) and A(H7N9) subtypes, have caused severe disease and deaths in humans, raising public heal
84 D8(+) T cells resulted in significantly more severe disease and failure to clear the virus.
85 s a major health concern, often resulting in severe disease and hospitalization.
86             Pulmonary embolism (PE) can be a severe disease and is difficult to diagnose, given its n
87    Nonobese NAFLD patients tend to have less-severe disease and may have a better prognosis than obes
88 uman cytomegalovirus (HCMV) infection causes severe disease and mortality in immunocompromised indivi
89 omes, especially in patients presenting with severe disease and requiring intravenous corticosteroids
90 ) include the occurrence of more frequent or severe disease and risk factors shifts associated with c
91 e to injectable artesunate for management of severe disease and seasonal malaria chemoprevention wher
92    The elderly host is highly susceptible to severe disease and treatment failure in Clostridium diff
93  in the --350/-50-kb region 5' of SOX9 cause severe disease and whereby SOX9 expression is specified
94 ds, which can result in delayed diagnosis of severe diseases and inappropriate referrals.
95 ding the processes that are underlying these severe diseases and the mechanisms of ciliogenesis in ge
96  I to V, with higher classes indicating more severe disease) and elevated circulating concentrations
97 ment score of 3 (higher scores indicate more severe disease), and a psoriatic plaque of at least 2 cm
98 eveloped warning signs, three (4%) developed severe disease, and 35 had uncomplicated dengue; the oth
99 otal, 51.1% patients were considered to have severe disease, and 9.2% died.
100 mutations present at a younger age with more severe disease, and are at increased risk of death, and
101  known to have more persistent disease, more severe disease, and greater risk of food allergies and e
102  plays a critical role in the development of severe disease, and there is increasing evidence that cy
103 s before baseline, had currently moderate to severe disease, and were methotrexate treatment-naive.
104 rder to develop countermeasures against this severe disease, animal models that accurately recapitula
105                                              Severe disease appears to be more associated with extrav
106  tailor treatment so that children with less severe disease are given shorter regimens, and weekly do
107 oung infants are particularly susceptible to severe disease as a result of influenza virus infection.
108 ly cornea verticillata, correlates with more severe disease as indicated by FOS-MSSI scores in paedia
109    FGFR1 is a principal cause for these less severe diseases as well.
110 ommon nosocomial pathogen capable of causing severe diseases associated with significant morbidity an
111                               Eyes with more severe disease at baseline were also more likely to have
112                          Among patients with severe disease at baseline, those who reported mild or m
113 ophylactic treatment for infants at risk for severe disease because of respiratory syncytial virus (R
114 roved the predictive ability with respect to severe disease beyond that of individual questionnaire i
115        As expected, RAG2(-/-) mice developed severe disease but effectively cleared Pneumocystis and
116           Their use was associated with more severe disease but not with increased use of botulinum t
117 a are able to replicate in mammals and cause severe disease but with limited transmission.
118 cytokine concentrations correlated with more-severe disease, but patients with low CSF leukocytes and
119 responds to traditional medications, whereas severe disease can be refractory to inhaled corticostero
120 herwise healthy patients with other forms of severe disease caused by Candida, Trichophyton, Phialoph
121  Hopefully, new research, such as studies of severe diseases caused by miRNA malfunction, will benefi
122  influenza A(H7N9) infection often developed severe disease causing respiratory failure.
123 RT1 activation, a synergistic suppression of severe disease compared with TNFalpha blockade alone occ
124 t Rai(+/+) mice, these cells promoted a more severe disease compared with wild-type encephalitogenic
125 ay a central role in the development of more severe disease complications, such as mitten deformities
126 en between 5 and 10 years of age have a more severe disease course than adolescents, our analysis als
127 s amenable to exon 51 skipping showed a more severe disease course than those amenable to any exon sk
128  The ELF test distinguished between mild and severe disease defined by clinical outcome (transplantat
129 ients fulfilled the criteria for GBS and had severe disease (defined as not being able to walk unaide
130         All 4 patients with pulmonary edema (severe disease) demonstrated dorsal brainstem restricted
131 from female-enriched multiplex families with severe disease, enhancing the detection of key autism ge
132 antimalarial molecule able to interfere with severe-disease etiology at multiple levels through speci
133  with asthma, dysanapsis was associated with severe disease exacerbations (HR, 1.95; 95% CI, 1.38-2.7
134 The short-term mortality among patients with severe disease exceeds 30%.
135                    RSV-infected infants with severe disease exhibited a high GATA3/T-bet ratio, which
136 tive marker to identify patients at risk for severe disease exists.
137  persistent or transient QT prolongation and severe disease expression of exercise-induced cardiac ar
138  CR9114 have been shown to protect mice from severe disease following challenge with H1N1 and H5N1 an
139 expression (MDA5(-/-) mice) experienced more severe disease following MHV infection, with reduced sur
140 ts enable us to predict age distributions of severe disease for future pandemics and demonstrate that
141 nfection confers lifelong protection against severe disease from novel hemagglutinin (HA) subtypes in
142                                Patients with severe disease had higher viremia than those with modera
143 cted, such antibody-dependent enhancement of severe disease has not been shown to occur in humans.
144 protein C receptor (EPCR) is associated with severe disease has suggested new mechanisms of pathology
145                         Patients who develop severe disease have considerable mortality.
146 omparative molecular profiles of mild versus severe disease have not been performed.
147 tients with asthma, in particular those with severe disease, have an increased risk of venous thrombo
148 asthmatic patients, in particular those with severe disease, have increased risk of pulmonary embolis
149 riasis were classified as having moderate-to-severe disease if they had been prescribed psoralen, met
150  antibodies are able to protect infants from severe disease, if administered prophylactically.
151 0 to 10,000 times the dose required to cause severe disease in 2 days with WT A12.
152 wn to enhance viral replication in vitro and severe disease in animal models.
153 elioidosis and glanders, respectively, cause severe disease in both humans and animals.
154  a highly prevalent virus capable of causing severe disease in certain populations.
155 s associated with a 60% reduction in odds of severe disease in children aged 7 months-6 years in mult
156 djusted FOS-MSSI total score indicating more severe disease in children with eye findings versus thos
157  is a highly contagious pathogen that causes severe disease in dogs and wildlife.
158 , the etiologic agent of melioidosis, causes severe disease in humans and animals.
159 h virus (NiV) is a paramyxovirus that causes severe disease in humans and animals.
160 er 1 select agent that causes melioidosis, a severe disease in humans and animals.
161 RVFV) is an emerging pathogen that can cause severe disease in humans and animals.
162  avian influenza viruses are associated with severe disease in humans and are a pandemic threat.
163  avian influenza viruses are associated with severe disease in humans and continue to be a pandemic t
164 er from their fruit bat reservoirs can cause severe disease in humans and livestock.
165 ility to cross the species barrier and cause severe disease in humans and other mammal species as pig
166                  Most ebolaviruses can cause severe disease in humans and other primates, with high c
167                          While EBOV causes a severe disease in humans characterized by a dysregulated
168 es are important zoonotic pathogens, causing severe disease in humans globally.
169          The vector-borne flaviviruses cause severe disease in humans on every inhabited continent on
170 CE Multiple New World arenaviruses can cause severe disease in humans, and some geographic overlap ex
171 ), emerged in China in early 2013 and caused severe disease in humans, with infections occurring most
172 h farmed freshwater fish, capable of causing severe disease in humans.
173 ], and Chikungunya virus [CHIKV]) that cause severe disease in humans.
174 are related to zoonotic pathogens that cause severe disease in humans.
175                SFTSV has been shown to cause severe disease in humans.
176 viruses can spread between mammals and cause severe disease in humans.
177                     HCMV infection can cause severe disease in immunocompromised adults and infants i
178 rtunistic nosocomial pathogen that can cause severe disease in immunocompromised individuals.
179          This persistent infection can cause severe disease in immunocompromised people and is epidem
180          Gammaherpesvirus infection leads to severe disease in immunosuppressed populations.
181 , or both, in siblings; the manifestation of severe disease in infancy; the presence of comorbid deve
182 icrovascular dysfunction are associated with severe disease in knowlesi malaria and likely contribute
183 ted H5N2 and H5N8 viruses were able to cause severe disease in mice only at high doses.
184     Repeated low-dose challenges caused more severe disease in mice, associated with higher viral loa
185 ine backbone could regain virulence to cause severe disease in mice.
186 eloped double-stranded DNA virus that causes severe disease in newborns and immunocompromised patient
187      Baseline characteristics indicated more severe disease in nonresponders.
188 e and middle-income countries have looked at severe disease in people presenting for care, and there
189 riginal antigenic sin) in the development of severe disease in secondary dengue infections.
190 asite densities involved in the induction of severe disease in target organs.
191 ld inflammation in mono-associated mice, but severe disease in the presence of a microbiota, demonstr
192 viruses can cross species barriers and cause severe disease in their new hosts.
193 rus (HIV) infection because it can result in severe disease in this population.
194 mergence of pathogen strains that cause more severe disease in unvaccinated hosts.
195 ally, rotavirus was the most common cause of severe disease in young children globally.
196 V can infect multiple host species and cause severe diseases in human.
197 d by high rates of abortion in ruminants and severe diseases in humans.
198 n risk factors that are associated with more severe disease include consumption of fresh produce, con
199 the pathological hallmark of a wide range of severe diseases including Alzheimer's and Parkinson's di
200 squito-transmitted flavivirus that can cause severe disease, including congenital birth defects durin
201 rhagic Escherichia coli (EHEC) can result in severe disease, including hemorrhagic colitis and the he
202 d-type, claudin-2-deficient mice experienced severe disease, including increased mucosal colonization
203 er immunologic control of infection and more severe disease, including mucosal leishmaniasis.
204 a group of emerging pathogens that can cause severe diseases, including cancers in immunosuppressed i
205 s, the Congo Basin strain is associated with severe disease, increased mortality, and increased human
206 oes not address the needs of those with less severe disease, inducible urticarias, idiopathic histami
207 eason for the association of Stx2a with more severe disease is because Stx2a crosses the intestinal b
208                                              Severe disease is complicated by spontaneous preterm del
209                      The defining feature of severe disease is increased capillary permeability, whic
210 irus (DENV)-infected individuals progress to severe disease is poorly understood.
211 rial respiratory infections, development of (severe) disease is preceded by asymptomatic colonization
212                   Preeclampsia, particularly severe disease, is associated with ASD and DD.
213 mall proportion of patients with asthma have severe disease, it accounts for the majority of morbidit
214 -8/-6/-1) than those who continued to report severe disease (Kruskal-Wallis, P </= .0003 for all).
215 tibody-dependent enhancement may explain the severe disease manifestations associated with recent ZIK
216 her flaviviruses, possibly resulting in more severe disease manifestations in flavivirus immune vacci
217                                         With severe disease manifestations including microcephaly, co
218   In infants, Bordetella pertussis can cause severe disease, manifested as pronounced leukocytosis, p
219                                              Severe disease may occur in the young, in the elderly, i
220 ils to identify a patient subgroup with more severe disease, more frequent exacerbations, and increas
221                               Notably, for a severe disease mutant involving an R155C substitution th
222 62) had a worse prognosis than those without severe disease (n=113; median survival 8.0 years, 95% CI
223 lescents, and of those affected, moderate to severe disease occurs in 20%.
224 on is particularly relevant because the most severe disease occurs within the first 6 months of life,
225 showing a reduction in the incidence rate of severe disease of 45% (95% CI 5%-68%, p = 0.031).
226 radenitis suppurativa (HS) is a frequent and severe disease of the skin, characterized by recurrent o
227 cases of E. coli meningitis, risk factors of severe disease or death were preterm birth, severe hypog
228 strains to determine factors associated with severe disease or death.
229 sk of death or treatment failure if they had severe disease or were underweight.
230 recent history, with two events resulting in severe disease outbreaks in human populations.
231  0 to 39, with higher scores indicating more severe disease) over a 3-year period, as assessed by mea
232 omain subclasses was higher in patients with severe disease (P < .05).
233 -point higher probability of presenting with severe disease (P < 0.001) than white patients.
234  16 wild-type mice developed weight loss and severe disease (p < 0.01).
235 ulature, or cytoadhesion, is associated with severe disease pathology such as multiple organ failure
236 mune-prone strains consistently develop more severe disease pathology.
237 mune dysregulation in these cells relates to severe disease pathology.
238                   We hypothesize that a more severe disease phenotype could be the result of 1) an ea
239  knockout mice displayed a dramatically more severe disease phenotype than wild-type mice after intra
240 mpasses a disease spectrum with mild to very severe disease phenotypes whose traditional common chara
241 nset parkinsonism characterized by rapid and severe disease progression and early cognitive decline;
242 LAR criteria, and had prognostic factors for severe disease progression, including a positive rheumat
243 provide an effective prognostic indicator of severe disease progression.
244 , and LateVal30Met FAP showed more rapid and severe disease progression; onset of gait disorders was
245 ; all mutations have known associations with severe diseases, ranging from congenital or perinatal le
246 y 2010 to December 2015 for similar cases of severe disease reactivation after ceasing fingolimod tre
247 igh SVR12 rate (85%) including patients with severe disease recurrence and F3-4 cirrhosis.
248 s universal, with some individuals suffering severe disease recurrence.
249 sment is important to identify patients with severe disease-related damage who should avoid pregnancy
250 antimicrobials in returning travelers, where severe disease requires empirical treatment prior to rec
251 30, and >30 blisters for mild, moderate, and severe disease, respectively).
252 , -0.53, and -0.51 dB in mild, moderate, and severe disease, respectively.
253 infections range from subclinical illness to severe disease resulting in death, with symptoms being r
254 e self-limited infections, but can result in severe disease, secondary bacterial pneumonias, and deat
255  results showed that patients at an advanced severe disease stage had a higher frequency of terminall
256 asite Ags was observed in patients at a less severe disease stage.
257 ion, early inflammation, as well as mild and severe disease stages, could be distinguished.
258  0 to 12, with higher scores indicating more severe disease; subscores range from 0 to 3, with higher
259  identify patients with chance of developing severe diseases such as gastric cancer, rather than the
260      It can be an important manifestation of severe diseases such as necrotizing enterocolitis (NEC)
261 e virus are able to infect neurons and cause severe disease, such as encephalitis, or infection of br
262 marily topical corticosteroids and, for more severe disease, systemic immunosuppressants.
263 d anti-La identify patients with SS and more severe disease than anti-SP1, anti-CA6, and anti-PSP.
264    Patients with BRAF(V600E) manifested more severe disease than did those with wild-type BRAF.
265 ible to viral infections and experience more severe disease than do adults.
266 s present with a distinct phenotype and more severe disease than older children and adults.
267 termine if they indeed identify SS with less severe disease than patients expressing anti-Ro and anti
268 tx2a-producing STEC are associated with more severe disease than strains producing both Stx1a and Stx
269  produce only Stx2a are associated with more severe disease than strains producing Stx1a and Stx2a.
270 4-specific Th17-polarized cells induced more severe disease than Th1-polarized cells.
271 measures showed that the PKD1 group had more severe disease than the PKD2 group, whereas the NMD grou
272 hronic inflammation, which often causes more severe disease than the virus infection itself.
273 that neutrophil-depleted mice developed more severe disease than their wild-type counterparts, sugges
274 ed SLE, IL-17F-deficient mice developed less severe disease than wild-type mice, with respect to surv
275 lasmodium falciparum infection can result in severe disease that is associated with elevated inflamma
276                             For infants with severe disease, the insufficient available data suggest
277 ductive fitness for de novo variants causing severe disease, the likelihood of finding these as stand
278                          Consistent with the severe disease, the numbers of IFNgamma- and IL-17-produ
279  the central nervous system leads to several severe diseases, the definitive diagnostic means are lac
280 thrombocytopenia is typical of both mild and severe diseases, the mechanism triggering platelet reduc
281 s have reduced mortality in individuals with severe disease, they have had limited efficacy in amelio
282 phy (SMA) ranges from a neonatal-onset, very severe disease to an adult-onset, milder form.
283              BTV is the causative agent of a severe disease transmitted between ruminants by biting m
284                    HCMV infection results in severe disease upon immunosuppression and is a leading c
285 linical diagnosis of alcoholic hepatitis and severe disease were randomly assigned to one of four gro
286 h mild psoriasis and 12,290 with moderate-to-severe disease) were included in the analysis.
287 espiratory virus is not associated with more severe disease when compared to RSV alone in this study.
288 bacterium capable of causing a wide range of severe diseases when it gains access to underlying tissu
289 e variant of ASCC1 is associated with a more severe disease, which could have clinical value for asse
290 rbidity were risk factors for both death and severe disease, while cases arising in Saudi Arabia were
291 ntify those acute pancreatitis patients with severe disease who would benefit from aggressive treatme
292  are capable of infecting humans and causing severe disease with a high mortality rate.
293 al mutations in MYBPC3 in the literature had severe disease with death or heart transplant during the
294 matic infections for Reston virus (RESTV) to severe disease with fatal outcomes for EBOV.
295 haracteristics: (i) 'multi-panallergen PFS': severe disease with frequent allergic comorbidities and
296                                    Three had severe disease with multiple hospitalisations and compli
297  uncommon O serogroup strains (P = .014) and severe disease with O7 serogroup (P = .034) and PapGII a
298 nts with infection and at risk of developing severe disease with organ dysfunction remains a difficul
299 one belonging to cc11 and is associated with severe disease with unusual clinical presentations.
300                      Marburg virus can cause severe disease, with up to 90% human lethality.

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