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1 ulate host translation and restrict WT mouse coronavirus infection.
2 ost, disease progression and transmission of coronavirus infection.
3 nd extent of myocardial damage caused by the coronavirus infection.
4 ting that multiple PARPs function to counter coronavirus infection.
5 tory response in diabetic M s in response to coronavirus infection.
6  enhances AAT inhibition of both TMPRSS2 and coronavirus infection.
7 ine safety and efficacy against heterologous coronavirus infection.
8  increased pathologic inflammation following coronavirus infection.
9 s and epidemiological history would indicate coronavirus infection.
10 on direction from the 3' viral genome during coronavirus infection.
11 he impact of sepsis as a comorbidity to beta-coronavirus infection.
12 ied to develop a potent inhibitor to prevent coronavirus infection.
13 er the age of five were at increased risk of coronavirus infection.
14 to evade host innate immune responses during coronavirus infection.
15 eam implications for interferon signaling in coronavirus infection.
16  which had been proved to be associated with coronavirus infection.
17 erase chain reaction scan-confirmed seasonal coronavirus infection.
18 rs <5 years of age were at increased risk of coronavirus infection.
19  to be diagnosed with a laboratory-confirmed coronavirus infection.
20 acterial/fungal coinfection in patients with coronavirus infection.
21 estigational drug for the treatment of human coronavirus infection.
22 RIPK3)-mediated inflammatory cell deathafter coronavirus infection.
23 new light on the immunopathogenesis of human coronavirus infection.
24 ic hypermutation (SHM) following neurotropic coronavirus infection.
25 , we consider a role for bacteria in shaping coronavirus infection.
26 ibitors was evaluated using a mouse model of coronavirus infection.
27 hin complex networks following influenza and coronavirus infection.
28 p40 mRNA rapidly increases after neurotropic coronavirus infection.
29 ns function in the context of a heterologous coronavirus infection.
30 NA expression increased in the CNS following coronavirus infection.
31 erapeutic and investigative potential toward coronavirus infection.
32 und has therapeutic potential for control of coronavirus infection.
33  illnesses were evaluated for rhinovirus and coronavirus infection.
34 hat ADP-ribosylation can effectively control coronavirus infection.
35 ses to have antiviral activity against human coronavirus infection.
36 drome coronavirus-2 (SARS-CoV-2) and broader coronavirus infection.
37 women), 87% of whom had laboratory-confirmed coronavirus infection.
38 ered SETDB2 and the inflammatory response to coronavirus infection.
39  to be diagnosed with a laboratory-confirmed coronavirus infection.
40  route, we define the role of interferons in coronavirus infection.
41 velopment of multitarget therapeutics toward coronavirus infections.
42 adapted SARS-CoV-2 BA.5, SARS-CoV and SHC014 coronavirus infections.
43 cluding those from individuals with seasonal coronavirus infections.
44 against coronavirus disease 2019 and related coronavirus infections.
45 orm for further multidisciplinary studies of coronavirus infections.
46 e most common comorbidities in patients with coronavirus infections.
47 her explains the ability of bats to tolerate coronavirus infections.
48 ndividuals, and 18 individuals with seasonal coronavirus infections.
49 lent SARS-CoV-2 3CL protease inhibitors, for coronavirus infections.
50 ole of metabolism during influenza virus and coronavirus infections.
51 mal species susceptible, and not, to certain coronavirus infections.
52 tanding PLpro deubiquitinating activities in coronavirus infections.
53 herapeutic approach against a broad range of coronavirus infections.
54 and not infants or individuals with previous coronavirus infections.
55 re promising arms for controlling the deadly coronavirus infections.
56 ith antiviral drugs used in the treatment of coronavirus infections.
57  the rapid clearance of SARS-CoV-2 and other coronavirus infections(1-3).
58  variable effects of interferons in treating coronavirus infections according to inflammatory status
59 tions are based on daily counts of confirmed coronavirus infections across all 401 German counties.
60 e described variability in genes involved in coronavirus infections across many different pig populat
61 ation in procedures with the risk of endemic coronavirus infection among HCP who participated in the
62 ation in procedures with the risk of endemic coronavirus infection among healthcare personnel who par
63 Rb and its interaction with Nsp15 can affect coronavirus infection and adds coronaviruses to a small
64  hidradenitis in both trials, in addition to coronavirus infection and diarrhoea in BE HEARD I, and o
65     Severe acute respiratory syndrome (SARS) coronavirus infection and growth are dependent on initia
66 somal acidification and various proteases to coronavirus infection and identifies an unexpected class
67             We identified 32 studies of SARS coronavirus infection and severe influenza.
68 matory cell death, PANoptosis, is induced by coronavirus infection and that impaired NLRP3 inflammaso
69 tic silencing of glutaminase enzymes reduces coronavirus infection and that newer members of two clas
70  Also, the role of innate immune response to coronavirus infection and the related therapeutic option
71 d show that glutaminase inhibitors can block coronavirus infection and thereby may represent a novel
72 ienced a relapse due to acute stress or post-coronavirus infection and/or vaccination.
73                                              Coronavirus infections and co-infections are highest amo
74 rs accounted for a significant proportion of coronavirus infections and may experience particularly h
75 y reflect the ability of the host to control coronavirus infections and respond to vaccination.
76 e highlight kinases that are associated with coronavirus infections and their inhibitors with antivir
77 rmation about the coronavirus, concern about coronavirus infection, and compliance are consistent cro
78 perimental severe acute respiratory syndrome coronavirus infection, and retrocyclin-1 protects mice f
79 f the immune system in severe cases of human coronavirus infection, and there is ample evidence that
80 estigate how age compromises defense against coronavirus infection, and whether a pro-longevity ketog
81  limited durability of antibody responses in coronavirus infections, and suggest that achieving herd
82 require LY6E for protection from respiratory coronavirus infection are unknown.
83                    Effective agents to treat coronavirus infection are urgently required, not only to
84 D-19 pandemic has highlighted treatments for coronavirus infection as an unmet medical need.
85                      Quantifying the risk of coronavirus infection associated with workplace activiti
86 acrophages are an important cell type during coronavirus infections because they "notice" the infecti
87 , murine CEACAM1a, are susceptible to murine coronavirus infection by a receptor-dependent pathway.
88 several mammalian species, including humans, coronavirus infection can modulate the host immune respo
89 a from the literature regarding the previous coronavirus infections can give some insights, more stud
90 owledge that coronavirus vaccines (and prior coronavirus infections) can confer broad protection agai
91                                              Coronavirus infection causes diffuse alveolar damage lea
92                                              Coronavirus infection causes tissue damage, which trigge
93             Extensive efforts in testing for coronavirus infection, combined with isolating infected
94                             Similarly, prior coronavirus infections conferred heterologous protection
95 s presenting clinical data for patients with coronavirus infection (defined as SARS-1, MERS, SARS-CoV
96       Characterizing the mechanisms by which coronavirus infection dictates pathogenesis or counters
97 apply this platform to influenza A virus and coronavirus infections, evaluating viral infection kinet
98 dle East respiratory syndrome-CoV, and other coronavirus infections express a nucleocapsid protein (N
99 s is essential to promote protection against coronavirus infection; however, the underlying mechanism
100 nt an important immunostrategy for combating coronavirus infections; however, for this strategy to su
101         Among 4,689 HCP-seasons, we detected coronavirus infection in 387 (8%).
102          Among 4689 HCP seasons, we detected coronavirus infection in 387 (8%).
103 25HC failed to suppress Zika virus and human coronavirus infection in ACAT-deficient cells, and Liste
104 lism or deep vein thrombosis, and history of coronavirus infection in analyses of venous thrombosis;
105  by vaccination is vital for protection from coronavirus infection in animal models.
106 on the efficacy of 3CLpro inhibitors against coronavirus infection in experimental animals.
107                                              Coronavirus infection in humans is usually associated to
108 contributes to the beneficial effects during coronavirus infection in mice.
109  checkpoint as a potential treatment against coronavirus infection in the aged.
110  following severe acute respiratory syndrome coronavirus infection in vivo.
111 inally, we define airway responses to common coronavirus infections in children, finding that these i
112 ulate outcomes of primary and secondary beta-coronavirus infections in hosts with variable susceptibi
113                                        Novel coronavirus infections in humans have steadily become mo
114 cilitate the design of antivirals to prevent coronavirus infections in the field.
115   Here, we present the molecular virology of coronavirus infection, including its entry into cells, i
116 operties of alisporivir in various models of coronavirus infection, including SARS-CoV-2.
117 an important role in protection against beta-coronavirus infections, including SARS-CoV-2, where they
118  workers experience significant burdens from coronavirus infections, including SARS-CoV-2.
119 oduction of proinflammatory cytokines during coronavirus infection independent of viral entry.
120                                  Neurotropic coronavirus infection induces expression of both beta in
121       Identification of host determinants of coronavirus infection informs mechanisms of viral pathog
122 e longevity and breath of immune response to coronavirus infection is crucial for the development of
123           Caring for patients with the novel coronavirus infection is placing great stress on health
124 elevance of apoptosis in the pathogenesis of coronavirus infections is unknown.
125 are not available for the treatment of human coronavirus infections, it is essential to understand th
126             There are currently no cures for coronavirus infections, making the prevention of infecti
127         Finally, we used an orthologous beta-coronavirus infection model and observed that genetic ab
128 t our hypothesis, we established a long-term coronavirus infection model of bat cells that are persis
129 ent phenotypes in human COVID-19 and a mouse coronavirus infection model.
130 ural cell biology that has been confused for coronavirus infection of cells, and rigorous criteria th
131 amples where GLS expression increases during coronavirus infection of host cells, and another where G
132 for severe acute respiratory syndrome (SARS) coronavirus infection of humans are needed to elucidate
133                                       Murine coronavirus infection of mice provides a useful model fo
134 on plays a pivotal role in defense following coronavirus infection of the CNS by enhancing innate imm
135 romoting innate defense mechanisms following coronavirus infection of the CNS.
136                                              Coronavirus infection of the murine central nervous syst
137  framework for studying the effects of prior coronavirus infection on neuron function.IMPORTANCE We d
138 re analyzed for expression of ACE2 and other coronavirus infection-related genes using microarray, RN
139 al of type I and type III interferons during coronavirus infection remains poorly defined, and opposi
140 lished host defense pathway, but its role in coronavirus infection remains unclear.
141 A H1N1, and Middle East respiratory syndrome coronavirus infection, require development of new antivi
142                 This decrease in SETDB2 upon coronavirus infection results in a decrease of the repre
143 protection measures and on the perception of coronavirus infection risk by our participants.
144 ), and observational studies of mask use and coronavirus infection risk were included.
145 as among the best characterized against SARS coronavirus infection, showing weight loss and other cli
146 ally, with respiratory mucosa as the initial coronavirus infection site, our findings are relevant to
147 pective, we will discuss what is known about coronavirus infection, some of the basic ultrastructural
148 FR) using the Office for National Statistics Coronavirus Infection Survey (ONS CIS) and the Real-time
149 mmunological imprinting by previous seasonal coronavirus infections that can potentially modulate the
150 e vaccines are protective against homologous coronavirus infection, the emergence of novel variants a
151 N responses have been associated with severe coronavirus infection, the extent to which the recently
152 imen has never been thoroughly evaluated for coronavirus infections, there is an urgent need to rapid
153 the impact of the STING signaling pathway on coronavirus infection using the human coronavirus OC43 (
154                         Although its role in coronavirus infection was previously undescribed, DYRK1A
155  the importance of these fatty acylations to coronavirus infection, we exposed infected cells to 2-br
156 rofibrinolytic phenotypes seen in vivo after coronavirus infection were MLL1-dependent despite blunte
157 he amounts of some cytokines released during coronavirus infection were significantly altered in the
158 tween SARS-CoV-2 and human host cells during coronavirus infection, where 403 high-confidence interac
159 oronavirus OC43 dominated the seasonal human coronavirus infections whereas parainfluenza 3 dominated
160 proteins such as IRAK1/4 in supporting human coronavirus infection, which can inform further drug dis
161                          Using a glia-tropic coronavirus infection, which is initiated in the brain b
162  mice susceptible to even a sublethal murine coronavirus infection, while the type III interferon def
163         The effective treatment strategy for coronavirus infections with immunopathological complicat
164 imeric spikes can prevent SARS-like zoonotic coronavirus infections with pandemic potential.

 
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