戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

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 a potential therapeutic for the treatment of anthrax.
2  a life-saving, postexposure therapy against anthrax.
3 nthracis spores causes gastrointestinal (GI) anthrax.
4 f Bacillus anthracis, the causative agent of anthrax.
5 se of 10(4)B. anthracis cells for inhalation anthrax.
6    Bacillus anthracis can cause inhalational anthrax.
7 ll mutant is avirulent in a murine model for anthrax.
8 f Bacillus anthracis, the causative agent of anthrax.
9  of all common manifestations of the disease anthrax.
10 prominent clinical manifestation of systemic anthrax.
11 n Bacillus anthracis, the causative agent of anthrax.
12  depletion in a murine model of inhalational anthrax.
13 affected for virulence in a murine model for anthrax.
14 ities may enhance the management of systemic anthrax.
15 herapeutic VNAs and/or diagnostic agents for anthrax.
16 t Bacillus anthracis infection, the agent of anthrax.
17 ere originally submitted for tests to detect anthrax.
18 llus anthracis spores initiates inhalational anthrax, a life-threatening infection.
19 ity of elephants and springbok to mount anti-anthrax adaptive immune responses is still equivocal, ou
20 of bacilli from the thoracic cavity to cause anthrax after inhalation challenge with spores.
21                      Bacillus anthracis, the anthrax agent, is a member of the Bacillus cereus sensu
22   Bacillus anthracis, the causative agent of anthrax and a potential weapon of bioterrorism, grows ra
23 ive bacterium that is the causative agent of anthrax and a potential weapon of bioterrorism.
24 es that target events in the pathogenesis of anthrax and may potentially augment antimicrobials are b
25 , and polio, and biological threats, such as anthrax and plague.
26 nti-protective antigen antibodies to prevent anthrax and suggest that lethal factor is the dominant t
27 masome in cells is triggered by a toxin from anthrax and that it initiates caspase-1 activation and r
28 ich serves as a simulant of B. anthracis (or anthrax) and which possesses a peptidoglycan (sugar)-ric
29 nst Shiga, botulinum, Clostridium difficile, anthrax, and ricin toxins.
30 ith other computation models of inhalational anthrax, and using the resulting information towards ext
31 -linked immunosorbent assays to measure anti-anthrax antibody titres and developed three increasingly
32 k and 3-52% of elephants had measurable anti-anthrax antibody titres, depending on the model used.
33 orrhagic clinical manifestations of systemic anthrax are unlikely to be caused by the direct binding
34 ible human risk assessments for inhalational anthrax associated with exposure to a low number of bact
35                                              Anthrax-associated shock is closely linked to lethal tox
36 ential adjunctive agents in the treatment of anthrax-associated shock.
37  plays a central role in the pathogenesis of anthrax-associated shock.
38 asive and received a final stimulus when the anthrax attack occurred in the United States in 2001.
39  Japanese religious cult sought to launch an anthrax attack on Tokyo.
40 en a top bioterrorism concern since the 2001 anthrax attacks in the USA.
41 ortant to learn from the lessons of the 2001 anthrax attacks, including the critical role of clinicia
42  determined by testing blood spiked with non-anthrax bacterial isolates or by testing blood samples d
43  of exposure to lethal concentrations of the anthrax bacterium, Bacillus anthracis, for grazing anima
44 e to category BSL 3 and 4 pathogens, such as anthrax, bubonic plague, Ebola and Marburg fever.
45 vity against Gram-positive bacteria, such as anthrax, but also shows activity against selected Gram-n
46 apsule may contribute to the pathogenesis of anthrax by suppressing the responses of immune cells and
47 63), C2IIa, and Ib channels (B components of anthrax, C2, and iota toxins, respectively).
48 h Bacillus anthracis, the causative agent of anthrax, can lead to persistence of lethal secreted toxi
49 ly important sapronoses, such as cholera and anthrax, can sustain an epidemic in a host population.
50         We follow pathogen concentrations at anthrax carcass sites and waterholes for five years and
51         Here we show that the dynamics of an anthrax-causing agent, Bacillus cereus biovar anthracis,
52 ivity, and is selectively active against the anthrax-causing organism.
53 d may be used as a safe oral vaccine against anthrax challenge.
54 easily at high protonation state through the anthrax channel (and the varphi clamp), the initial perm
55 l factor (LF) N-terminal segment through the anthrax channel.
56                                              Anthrax continues to generate concern as an agent of bio
57  sperm protamine, that effectively inhibited anthrax cytotoxic protease and demonstrated that they al
58 demonstrated that the course of inhalational anthrax disease and the resulting pathology in guinea pi
59 g bacterium Bacillus anthracis causes lethal anthrax disease in humans and animals.
60 pores that upon germination can cause lethal anthrax disease in humans.
61 the course and manifestation of experimental anthrax disease induced under controlled conditions in t
62                                              Anthrax disease is caused by a toxin consisting of prote
63  significant importance with respect to both anthrax disease progression, spore detection for biodefe
64 on of bas0520, a gene recently implicated in anthrax disease progression.
65 Bacillus anthracis, the etiological agent of anthrax disease, as the model pathogen.
66   Bacillus anthracis, the causative agent of anthrax disease, is lethal owing to the actions of two e
67 er proteins with known or potential roles in anthrax disease.
68  and lipid mediators in host survival during anthrax disease.
69 e to reassess the mechanisms of inhalational anthrax dissemination, since it is this form of anthrax
70 cellent levels of detection and accuracy for anthrax DNA can be achieved using PNA probes with suitab
71       Despite this, our current knowledge of anthrax ecology is largely limited to arid ecosystems, w
72 alysis by the adenylyl cyclase domain of the anthrax edema factor toxin was simulated using the empir
73                                          The anthrax edema toxin (ET) of Bacillus anthracis is compos
74 get, mitogen-activated protein kinase 1, and anthrax edema toxin fails to increase intracellular cycl
75 lar, the technique is capable of identifying anthrax endospores inside a sealed paper envelope.
76 tform, particularly for vaccines such as for anthrax, for which rapid induction of protective immunit
77   Bacillus anthracis, the causative agent of anthrax, forms an S-layer atop its peptidoglycan envelop
78 and real-time PCR for diagnosis of cutaneous anthrax from clinical swabs of cutaneous lesions.
79      Biological weapons such as smallpox and anthrax had the potential to cause a national catastroph
80 nes required for Bacillus anthracis to cause anthrax have been acquired recently by horizontal gene t
81 nthracis infections cause maturation of anti-anthrax immunity.
82  such as Bacillus anthracis, causal agent of anthrax in humans and animals.
83 rats, and 24-hour postprophylaxis of inhaled anthrax in mice.
84 d toxins in the pathogenesis of inhalational anthrax in rabbits by comparing infection with the Ames
85  efficacy of medical countermeasures against anthrax in support of licensure under the FDA's "Animal
86         As physicians involved in diagnosing anthrax in the index case and alerting authorities, we o
87 thophysiology, and pathology of inhalational anthrax in this animal model following nose-only aerosol
88 y to confer post-exposure protection against anthrax in vivo.
89 opathologic findings typical of disseminated anthrax included suppurative (heterophilic) inflammation
90               In vivo, we found that 100% of anthrax-infected rabbits survived when treated with cAb2
91 o investigate risk factors in an outbreak of anthrax infection among Scottish heroin users.
92 xtravascular fluid collection characterizing anthrax infection clinically.
93                     Furthermore, in a murine anthrax infection model, 15d-PGJ2 reversed anthrax letha
94 r methicillin-resistant S. aureus (MRSA) and anthrax infection, respectively.
95 nd their roles in initial and late stages of anthrax infection.
96  virulence in a murine model of inhalational anthrax infection.
97 mproved survival of mice in a spore model of anthrax infection.
98 vaccine component and therapeutic target for anthrax infections but also an excellent model system fo
99 rophages are critical for the development of anthrax infections, as spores are thought to use macroph
100 te that zebra in ENP often survive sublethal anthrax infections, encounter most B. anthracis in the w
101 acis, the bacterial pathogen responsible for anthrax infections.
102 to understand events initiating inhalational anthrax infections.
103 els of leak-associated infections, including anthrax, influenza, malaria, and sepsis.
104 ive tool for the analysis of the kinetics of anthrax intoxication and ultimately drug discovery.
105 et spore germination or downstream events in anthrax intoxication are also under investigation.
106 gainst the TEM8 extracellular domain blocked anthrax intoxication, inhibited tumor-induced angiogenes
107                                              Anthrax is a globally important animal disease and zoono
108                                              Anthrax is a life-threatening disease caused by infectio
109  over three decades, we show that rainforest anthrax is a persistent and widespread cause of death fo
110                                              Anthrax is a serious bacterial disease of man and animal
111                        Despite the fact that anthrax is an ancient and emerging zoonotic infectious d
112             The rabbit model of inhalational anthrax is an important tool in the assessment of potent
113         The ability of B. anthracis to cause anthrax is attributed to the plasmid-encoded A/B-type to
114                                 Inhalational anthrax is caused by inhalation of Bacillus anthracis sp
115                                              Anthrax is caused by the spore-forming, gram-positive ba
116                                 Inhalational anthrax is caused by the sporulating bacterium Bacillus
117 e clinical laboratory diagnosis of cutaneous anthrax is generally established by conventional microbi
118                        Gastrointestinal (GI) anthrax is the most prevalent form of naturally acquired
119          The infectious agent of the disease anthrax is the spore of Bacillus anthracis.
120 major role for toxins in the pathogenesis of anthrax is to enable the organism to overcome innate hos
121   Bacillus anthracis, the causative agent of anthrax, is a potential bioterrorism agent.
122   Bacillus anthracis, the causative agent of anthrax, is a well known bioterrorism agent.
123                                           GI anthrax led to significant inhibition of immunoglobulins
124 tigen (PA) is essential for the transport of anthrax lethal and edema toxins into human cells.
125   Therefore, we have examined the effects of anthrax lethal and edema toxins on human platelets.
126  an anti-cancer fusion protein consisting of anthrax lethal factor (LF) and the catalytic domain of P
127                                              Anthrax lethal factor (LF) enters the cytosol through po
128                        The metalloproteinase anthrax lethal factor (LF) is secreted by Bacillus anthr
129 ensin RTD-1 is a noncompetitive inhibitor of anthrax lethal factor (LF) protease (IC50 = 390 +/- 20 n
130            They bind protein toxins, such as anthrax lethal factor (LF), and kill bacteria, including
131 ly to its ability to kill S. aureus, inhibit anthrax lethal factor (LF), bind gp120 of HIV-1, dimeriz
132   Certhrax shares 31% sequence identity with anthrax lethal factor from Bacillus anthracis; however,
133                      Finally, the pathogen's anthrax lethal factor is required to establish lethal in
134 ication of this platform to detection of the anthrax lethal factor sequence.
135                                         Like anthrax lethal factor, Certhrax was found to require pro
136 structural similarities and differences with anthrax lethal factor.
137 e 60-fold more toxic to mammalian cells than anthrax lethal factor.
138 crophages pre-exposed to a sublethal dose of anthrax lethal toxin (LeTx) are refractory to subsequent
139 ages expressing a functional NLRP1b prevents anthrax lethal toxin (LeTx)-induced caspase-1 autoproteo
140 his BaPGN-induced response was suppressed by anthrax lethal toxin (LT) and edema toxin (ET), with the
141 ethal owing to the actions of two exotoxins: anthrax lethal toxin (LT) and oedema toxin (ET).
142                                          The anthrax lethal toxin (LT) enters host cells and enzymati
143                                              Anthrax lethal toxin (LT) is an A-B type toxin secreted
144           These two proteins combine to form anthrax lethal toxin (LT), whose proximal targets are mi
145  pathology associated with administration of anthrax lethal toxin (LT).
146                                 We find that anthrax lethal toxin fails to cleave its target, mitogen
147                        The immunosuppressive anthrax lethal toxin impairs NK gamma interferon (IFN-ga
148                    Engineered tumor-targeted anthrax lethal toxin proteins have been shown to strongl
149  and also reduces the detrimental effects of anthrax lethal toxin, diphtheria toxin, cholera toxin, P
150 omes by their respective activating signals, anthrax lethal toxin, nigericin, and flagellin.
151 screen to identify host factors required for anthrax lethal toxin-induced cell death.
152  provided almost complete protection against anthrax lethal toxin-induced cytotoxicity and death in m
153  provided protection against NLRP1-dependent anthrax lethal toxin-mediated cell death and prevented N
154 e anthrax infection model, 15d-PGJ2 reversed anthrax lethal toxin-mediated NLRP1-dependent resistance
155 th specific antibody prior to treatment with anthrax lethal toxin.
156 th specific antibody prior to challenge with anthrax lethal toxin.
157 d increased the survival of cells exposed to anthrax lethal toxin.
158 ated with the NALP1b inflammasome activator, anthrax lethal toxin.
159 all molecules was screened for inhibitors of anthrax lethal toxin.
160 flammasome activation by either flagellin or anthrax lethal toxin.
161  sufficient to confer macrophage survival to Anthrax lethal toxin.
162  anthracis spores made after one of the 2001 anthrax letter attacks.
163 ion may also protect humans from respiratory anthrax-like death.
164 XO1-like virulence plasmid cause respiratory anthrax-like disease in humans, particularly in welders.
165             As the pathogenesis of B. cereus anthrax-like disease in mice is dependent on pagA1 and P
166 eus G9241 contributes to the pathogenesis of anthrax-like disease in mice.
167  that had been isolated from a fatal case of anthrax-like disease.
168 ver, some recent isolates cause inhalational anthrax-like diseases and death.
169 ereus strains and enable the pathogenesis of anthrax-like diseases.
170       Bacillus cereus G9241, which caused an anthrax-like infection, has two virulence plasmids, pBCX
171 was isolated from a welder suffering from an anthrax-like inhalation illness.
172            We identified Certhrax, the first anthrax-like mART toxin from the pathogenic G9241 strain
173 ilated, instrumented canines challenged with anthrax LT were assigned to no treatment (controls), hem
174  screening patients for meningitis during an anthrax mass casualty incident.
175 re essential for successful management of an anthrax mass casualty incident.
176 d as a 4-item assessment tool for use during anthrax mass casualty incidents.
177 of 363 (36%) cases with systemic anthrax met anthrax meningitis criteria.
178                                              Anthrax meningitis is a common manifestation of B. anthr
179 r on admission had a sensitivity for finding anthrax meningitis of 89% (83%) in the adult (pediatric)
180                                  Survival of anthrax meningitis was predicted by treatment with a bac
181                                              Anthrax meningitis was unlikely in the absence of any of
182 inical diagnostic and prognostic factors for anthrax meningitis.
183  thirty-two of 363 (36%) cases with systemic anthrax met anthrax meningitis criteria.
184 ined from immunized alpacas and screened for anthrax neutralizing activity in macrophage toxicity ass
185 , rather than being solely a lethal disease, anthrax often occurs as a sublethal infection in some su
186 of a model ligand, the protective antigen of anthrax on the gold surface, is monitored in real-time w
187 ch as the Amerithrax incident of 2001 or the anthrax outbreaks in Russia and Sweden in 2016, critical
188  evaluated using lesion swabs from cutaneous anthrax outbreaks, the SETS yielded culture-negative, PC
189 pproach to a particular case-blockage of the anthrax PA(63) channel by a multicharged cyclodextrin de
190  of the Bacillus cereus group, including the anthrax pathogen, contains a 2D-crystalline basal layer,
191                                The genes for anthrax pathogenesis are located on two large virulence
192 nea pig, which has been used extensively for anthrax pathogenesis studies and anthrax vaccine potency
193 elegans is a useful infection model to study anthrax pathogenesis.
194 pecificity and efficiency of the re-directed anthrax pore for transport of TccC3 toxin and establishe
195 he sensitive, specific and easy detection of anthrax protective antigen (PA) toxin in picogram concen
196 gh pores in the endosomal membrane formed by anthrax protective antigen.
197 A; mPA) which cannot bind to the two natural anthrax receptors.
198 nc hydrolase that is chiefly responsible for anthrax-related cell death.
199   Bacillus anthracis, the causative agent of anthrax, relies on multiple virulence factors to subvert
200 ow these molecular events lead to death from anthrax remains poorly understood, but published reports
201   Bacillus anthracis, the causative agent of anthrax, replicates as chains of vegetative cells by reg
202 posed that the dissemination of inhalational anthrax required spores to be transported from the lumen
203  augment NK cell function in early stages of anthrax should be further explored in animal models as a
204  JMO-G1, was fully protective against lethal anthrax spore infection in mice as a single dose.
205                                              Anthrax spores can be aerosolized and dispersed as a bio
206           Through use of the postal service, anthrax spores were widely disseminated, including to ho
207 ted from challenge with 200 LD50 aerosolized anthrax spores.
208                       Working in the natural anthrax system of Etosha National Park, Namibia, we coll
209 ly more zebras responding immunologically to anthrax than have previous studies using less comprehens
210 hrax dissemination, since it is this form of anthrax that is most lethal and of greatest concern when
211 f entry for Bacillus anthracis in inhalation anthrax, the deadliest form of the disease.
212 s, our studies show the potential of VNAs as anthrax therapeutics.
213 rming bacterium, is such a pathogen, causing anthrax through a combination of bacterial infection and
214 tive activity against the causative agent of anthrax toxicity.
215                                           As anthrax toxin (Atx) accesses the cytosol, the purpose of
216 e detection of B. anthracis by using atxA an anthrax toxin activator gene.
217 ate talin-1 are exploited for association of anthrax toxin and its principal receptor, CMG2, with hig
218              The three protein components of anthrax toxin are nontoxic individually, but they form a
219  We investigated the ratchet mechanism using anthrax toxin as a model.
220 encodes a host membrane protein exploited by anthrax toxin as a principal receptor, dramatically alte
221 doing so we targeted a protease component of anthrax toxin as well as host proteases exploited by thi
222 ages and human lymphoblastoid cells affected anthrax toxin binding, internalization, and sensitivity.
223        The protective antigen (PA) moiety of anthrax toxin binds to cellular receptors and mediates t
224 ted by the protective antigen (PA) moiety of anthrax toxin by more than four orders of magnitude, wit
225  We used our method to prepare two different anthrax toxin cargo proteins: one containing an (alpha)t
226 tency in cell assays and protected mice from anthrax toxin challenge with much better efficacy than t
227 ways to the neutralizing activity of an anti-anthrax toxin chimeric mAb.
228 on-antimicrobial drugs with activity against anthrax toxin components; and agents that inhibit bindin
229                               The tripartite anthrax toxin consists of protective antigen, lethal fac
230                        Protective antigen of anthrax toxin forms a pore through which the two catalyt
231                                              Anthrax toxin forms one such machine through the self-as
232 regulator AtxA controls transcription of the anthrax toxin genes and capsule biosynthetic operon.
233 ing the protective antigen (PA) component of anthrax toxin genetically fused to a dendritic cell (DC)
234 clonal antibody that effectively neutralizes anthrax toxin in an unknown mechanism.
235 e polypeptide-based polyvalent inhibitors of anthrax toxin in which multiple copies of an inhibitory
236                                              Anthrax toxin is a tripartite toxin comprised of the pro
237                                              Anthrax toxin is a tripartite virulence factor produced
238                                              Anthrax toxin is an intracellularly acting toxin in whic
239                                              Anthrax toxin is an intracellularly acting toxin where s
240                                              Anthrax toxin is composed of three proteins, a transloca
241 er as a fusion to the N-terminal fragment of anthrax toxin lethal factor or when naturally delivered
242                            We generated anti-anthrax toxin mAbs with specific Fc domain variants with
243  engagement, with minimal protection against anthrax toxin observed in FcgammaR-deficient mice follow
244 l blockers of three binary bacterial toxins: anthrax toxin of Bacillus anthracis, C2 toxin of Clostri
245 molysin pore from Staphylococcus aureus, the anthrax toxin pore and the 1.2-MDa mouse mechanosensitiv
246 ting in a corresponding increase in AtxA and anthrax toxin production.
247                                              Anthrax toxin protective antigen (PA) delivers its effec
248  Bacillus anthracis structural genes for the anthrax toxin proteins and biosynthetic operon for capsu
249 ure supernatant directly cleaved each of the anthrax toxin proteins as well as an additional secreted
250                                          The anthrax toxin proteins were secreted from the mutant str
251                     Here, we have identified anthrax toxin receptor 1 (ANTXR1) as the receptor for SV
252                                          The anthrax toxin receptor 1 (ANTXR1) has been identified as
253  this corresponded with the higher levels of anthrax toxin receptor 1 (ANTXR1) in these cells than in
254 r endothelial marker 8 (TEM8), also known as anthrax toxin receptor 1 (ANTXR1), is a highly conserved
255 tasis of other membrane proteins as CFTR and anthrax toxin receptor 2, two poor folders involved in s
256         Here we generated cell-type-specific anthrax toxin receptor capillary morphogenesis protein-2
257 ls would be protected from anthrax toxins if anthrax toxin receptor expression was effectively silenc
258                                        Thus, anthrax toxin receptor-targeted RNAi has the potential t
259 lular matrix binding protein that is also an anthrax toxin receptor.
260                                        Thus, anthrax toxin receptors in mouse and human macrophages w
261 nthrax toxins enter cells via two identified anthrax toxin receptors: tumor endothelial marker 8 (TEM
262 nd edema factor, which are the components of anthrax toxin, and other proteins with known or potentia
263                                              Anthrax toxin, comprising protective antigen, lethal fac
264                                              Anthrax toxin, comprising three proteins-protective anti
265  Protective antigen (PA), a key component of anthrax toxin, mediates the entry of lethal factor (LF)
266 acis protective antigen (PA), a component of anthrax toxin, results in significantly augmented protec
267             B. cereus strain G9241 expresses anthrax toxin, several polysaccharide capsules, and the
268 nhanced the in vitro and in vivo activity of anthrax toxin-neutralizing antibodies.
269 terium's major virulence factors are (a) the anthrax toxins and (b) an antiphagocytic polyglutamic ca
270 ltaatxA1 mutant produced lower levels of the anthrax toxins and no hyaluronic acid capsule.
271     This review focuses on the activities of anthrax toxins and their roles in initial and late stage
272 ter stages of infection, when high levels of anthrax toxins are present.
273                                          The anthrax toxins are three polypeptides-protective antigen
274                      We also showed that the anthrax toxins did not play a role in persistence.
275                                              Anthrax toxins enter cells via two identified anthrax to
276 ized that host cells would be protected from anthrax toxins if anthrax toxin receptor expression was
277           This review focuses on the role of anthrax toxins in pathogenesis.
278 be caused by the direct binding and entry of anthrax toxins into human platelets.
279 aracterized a new set of 15 VHHs against the anthrax toxins that act by binding to the edema factor (
280 s with high activity and specificity for the anthrax toxins.
281 inst the protective antigen component of the anthrax toxins.
282 g-targeted pathology would be beneficial for anthrax treatment.
283 Certhrax resides in the mART domain, whereas anthrax uses a metalloprotease mechanism.
284 d as an adjuvant for a candidate vaccine for anthrax using recombinant protective Ag (rPA) from Bacil
285 tant of a nonencapsulated, toxigenic strain (anthrax vaccine absorbed [AVA]) whose primary protective
286                                              Anthrax vaccine adsorbed (AVA) immunization raised antib
287 healthy subjects following immunization with Anthrax Vaccine Adsorbed (AVA).
288                            The U.S.-licensed anthrax vaccine is made from an incompletely characteriz
289 nsively for anthrax pathogenesis studies and anthrax vaccine potency testing, is a good candidate for
290  protective Ag of Bacillus anthracis in both anthrax vaccine-adsorbed vaccinees and nonvaccinees with
291                    Improving next-generation anthrax vaccines is important to safeguard citizens and
292 sired characteristic of vaccines, especially anthrax vaccines, which must be stockpiled for large-sca
293 (rPA)--the major component of new-generation anthrax vaccines--affects vaccine immunogenicity, we cre
294 entially allowing a prolonged circulation of anthrax virulence factors such as EF during infection.
295    Though we found that adaptive immunity to anthrax wanes rapidly, subsequent and frequent sublethal
296 er understand the pathogenesis of DIC during anthrax, we compared the effects of 24-hour infusions of
297 del appeared to describe rabbit inhalational anthrax well.
298 sks (CR) computational model of inhalational anthrax where data was collected from NZW rabbits expose
299 Bacillus anthracis is the causative agent of anthrax, which is associated with a high mortality rate.
300 enge of guinea pigs resulted in inhalational anthrax with death occurring between 46 and 71 h postcha
301  and requires more aggressive treatment than anthrax without meningitis.

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top