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These data suggest possible involvement of intracellular Ca2+-dependent mechanism(s) in acute lethal toxin exposure-elicited cardiomyocyte contractile inhibitory responses.
For acute lethal toxin challenge in vivo, mice were injected intraperitoneally with anthrax lethal toxin (2 µg/g body weight, LF+PA at 1∶2 ratio) and were sacrificed under anesthesia (ketamine/xylazine: 3∶1, 1.32 mg/kg, i.p.,) at 2, 4 and 18 hrs after lethal toxin injection.
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Anthrax lethal factor (LF) is a Zn+2-dependent metalloprotease that cleaves several MAPK kinases and is responsible for the lethality of anthrax lethal toxin (LT).
Acute in vitro exposure (2 hrs) of lethal toxin displayed a concentration-dependent (0.05 – 50 nM) prolongation in resting cell length and decrease in peak shortening [14] as well as maximal velocity of shortening/relengthening (± dL/dt) in freshly isolated cardiomyocytes.
Hamsters, unlike mice, appear acutely sensitive to the toxins, with animals succumbing to an acute lethal disease between 24 48 h following oral challenge.
The toads release a lethal toxin from glands on their heads when they are attacked.
A letter addressed to Barack Obama has been found to contain a lethal toxin, the FBI revealed.
But the strain E. coli 0157 H7 produces a lethal toxin and can cause severe diarrhea, kidney failure and even death.
Lethal toxin may also alter vascular smooth muscle function [30].
Protective antigen (PA) and lethal factor (LF) are the two components of anthrax lethal toxin.
Pulmonary dissection is an acute, lethal disease to patients.
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