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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.
19 ity of elephants and springbok to mount anti-anthrax adaptive immune responses is still equivocal, ou
22 Bacillus anthracis, the causative agent of anthrax and a potential weapon of bioterrorism, grows ra
24 es that target events in the pathogenesis of anthrax and may potentially augment antimicrobials are b
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
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
38 asive and received a final stimulus when the anthrax attack occurred in the United States in 2001.
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
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
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.
54 easily at high protonation state through the anthrax channel (and the varphi clamp), the initial perm
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
61 the course and manifestation of experimental anthrax disease induced under controlled conditions in t
63 significant importance with respect to both anthrax disease progression, spore detection for biodefe
66 Bacillus anthracis, the causative agent of anthrax disease, is lethal owing to the actions of two e
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
72 alysis by the adenylyl cyclase domain of the anthrax edema factor toxin was simulated using the empir
74 get, mitogen-activated protein kinase 1, and anthrax edema toxin fails to increase intracellular cycl
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
80 nes required for Bacillus anthracis to cause anthrax have been acquired recently by horizontal gene t
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
87 thophysiology, and pathology of inhalational anthrax in this animal model following nose-only aerosol
89 opathologic findings typical of disseminated anthrax included suppurative (heterophilic) inflammation
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
104 ive tool for the analysis of the kinetics of anthrax intoxication and ultimately drug discovery.
106 gainst the TEM8 extracellular domain blocked anthrax intoxication, inhibited tumor-induced angiogenes
109 over three decades, we show that rainforest anthrax is a persistent and widespread cause of death fo
117 e clinical laboratory diagnosis of cutaneous anthrax is generally established by conventional microbi
120 major role for toxins in the pathogenesis of anthrax is to enable the organism to overcome innate hos
126 an anti-cancer fusion protein consisting of anthrax lethal factor (LF) and the catalytic domain of P
129 ensin RTD-1 is a noncompetitive inhibitor of anthrax lethal factor (LF) protease (IC50 = 390 +/- 20 n
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,
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
149 and also reduces the detrimental effects of anthrax lethal toxin, diphtheria toxin, cholera toxin, P
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
164 XO1-like virulence plasmid cause respiratory anthrax-like disease in humans, particularly in welders.
173 ilated, instrumented canines challenged with anthrax LT were assigned to no treatment (controls), hem
179 r on admission had a sensitivity for finding anthrax meningitis of 89% (83%) in the adult (pediatric)
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,
192 nea pig, which has been used extensively for anthrax pathogenesis studies and anthrax vaccine potency
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
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
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
213 rming bacterium, is such a pathogen, causing anthrax through a combination of bacterial infection and
217 ate talin-1 are exploited for association of anthrax toxin and its principal receptor, CMG2, with hig
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.
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
228 on-antimicrobial drugs with activity against anthrax toxin components; and agents that inhibit bindin
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)
235 e polypeptide-based polyvalent inhibitors of anthrax toxin in which multiple copies of an inhibitory
241 er as a fusion to the N-terminal fragment of anthrax toxin lethal factor or when naturally delivered
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
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
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
257 ls would be protected from anthrax toxins if anthrax toxin receptor expression was effectively silenc
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
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
269 terium's major virulence factors are (a) the anthrax toxins and (b) an antiphagocytic polyglutamic ca
271 This review focuses on the activities of anthrax toxins and their roles in initial and late stage
276 ized that host cells would be protected from anthrax toxins if anthrax toxin receptor expression was
279 aracterized a new set of 15 VHHs against the anthrax toxins that act by binding to the edema factor (
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
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
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
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
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