Killing Activity of Clostocin O

Clostocin O is a phage tail-like bacteriocin produced by Clostridium saccharoperbutylacetonicum Nl–4. One particle of clostocin O had an activity to kill one sensitive organism. Clostocin O had also the lytic activity, but this lytic activity was not an essential action of clostocin O, because clostocin O was able to show a sufficient killing activity even under the condition to inhibit its lytic activity. The biosynthesis of macromolecules (protein, RNA and DNA) in sensitive organisms was inhibited by clostocin O infection. The amounts of macro-molecules of the infected organisms were held at the initial level.     

Killing cells by targeting mitosis

Cell cycle deregulation is a common feature of human cancer. Tumor cells accumulate mutations that result in unscheduled proliferation, genomic instability and chromosomal instability. Several therapeutic strategies have been proposed for targeting the cell division cycle in cancer. Whereas inhibiting the initial phases of the cell cycle is likely to generate viable quiescent cells, targeting mitosis offers several possibilities for killing cancer cells. Microtubule poisons have proved efficacy in the clinic against a broad range of malignancies, and novel targeted strategies are now evaluating the inhibition of critical activities, such as cyclin-dependent kinase 1, Aurora or Polo kinases or spindle kinesins. Abrogation of the mitotic checkpoint or targeting the energetic or proteotoxic stress of aneuploid or chromosomally instable cells may also provide further benefits by inducing lethal levels of instability. Although cancer cells may display different responses to these treatments, recent data suggest that targeting mitotic exit by inhibiting the anaphase-promoting complex generates metaphase cells that invariably die in mitosis. As the efficacy of cell-cycle targeting approaches has been limited so far, further understanding of the molecular pathways modulating mitotic cell death will be required to move forward these new proposals to the clinic.     

Killing Babies: Hrdy on the Evolution of Infanticide

Sarah Hrdy argues that women (1) possess a reproductive behavioral strategy including infanticide, (2) that this strategy is an adaptation and (3) arose as a response to stresses mothers faced with the agrarian revolution. I argue that while psychopathological and cultural evolutionary accounts for Hrdy's data fail, her suggested psychological architecture for the strategy suggests that the behavior she describes is really only the consequence of the operation of practical reasoning mechanism(s) – and consequently there is no reproductive strategy including infanticide as such, nor could the alleged strategy be sufficiently mosaic to count as an adaptation. What might count as an adaptation is a ‘window’ before bonding that permits practical reasoning about the reproductive value of infants and hence variable maternal investment, and which, contra (3) arose early in hominid history due to a combination of increases in infant dependency and increased human abilities for conditional practical reasoning.     

Killing of Cells in Bacterial Colonies

Bacterial colonies grown on membrane filters and transferred to plates of inhibitor-containing medium decrease in number of total viable colony-forming cells. The decrease in viable cell count occurs in direct proportion to the concentration of inhibitor present and the length of time the colonies are exposed to the inhibitor, suggesting that the kinetics of cell kill approximate a first-order chemical reaction.     

Killing, letting die and the bare difference argument

I believe that there is no intrinsic moral difference between killing and letting die. That is, there is no difference that depends solely on the distinction between an act and an omission. I also believe that we can reasonably establish this thesis by appeal to the Bare Difference Argument. The form of this argument involves considering two imaginary cases in which there are no morally relevant differences present, save the bare difference that one is a case of killing and one a case of letting die. But in the pair of cases under consideration this bare difference makes no moral difference. Hence it cannot be that the bare difference between killing and letting die is in itself a morally important difference.
Winston Nesbitt has recently argued that the Bare Difference Argument fails because "the examples produced typically possess a feature which makes their use in this context illegitimate, and that when modified to remove this feature, they provide support for the view which they were designed to undermine". I argue that Nesbitt misunderstands the logic of the Bare Difference Argument and that accordingly his objections are mistaken.     

Killing bacterial spores by organic hydroperoxides

Killing of wild-type spores of Bacillus subtilis by t-butyl hydroperoxide, cumene hydroperoxide and peracetic acid was not through DNA damage, as shown by the absence of mutations in the survivors and the identical sensitivity of spores of strains with or without a recA mutation. In contrast, B. subtilis spores (termed α⁻β⁻) lacking the DNA protective α/β-type small, acid-soluble spore proteins (SASP) were more sensitive to t-butyl hydroperoxide and cumene hydroperoxide, and their killing was in large part through DNA damage, as shown by the high frequency of mutations in the survivors and the greater sensitivity of α⁻β⁻ recA spores. Analysis of t-butyl hydroperoxide-treated spores showed that generation of DNA damage in α⁻β⁻ spores was more rapid than in wild-type spores; α/β-type SASP also protected against DNA strand breakage in vitro caused by t-butyl hydroperoxide. α/β-Type SASP appeared to play no role in protection of spores from killing by peracetic acid; wild-type and α⁻β⁻ spores exhibited identical peracetic acid sensitivity and their killing by this agent appeared to be not through DNA damage. Received 17 December 1996/ Accepted in revised form 13 March 1997