TASK DEFINITION: Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
PROBLEM: Context: To determine the mechanisms of Bacillus subtilis spore killing by and resistance to an acidic solution containing Fe(3+), EDTA, KI and ethanol termed the KMT reagent.', 'Wild-type B. subtilis spores were not mutagenized by the KMT reagent but the wild-type and recA spores were killed at the same rate. Spores (alpha(-)beta(-)) lacking most DNA-protective alpha/beta-type small, acid-soluble spore proteins were less resistant to the KMT reagent than wild-type spores but were also not mutagenized, and alpha(-)beta(-) and alpha(-)beta(-)recA spores exhibited nearly identical resistance. Spore resistance to the KMT reagent was greatly decreased if spores had defective coats. However, the level of unsaturated fatty acids in the inner membrane did not determine spore sensitivity to the KMT reagent. Survivors in spore populations killed by the KMT reagent were sensitized to killing by wet heat or nitrous acid and to high salt in plating medium. KMT reagent-killed spores had not released their dipicolinic acid (DPA), although these killed spores released their DPA more readily when germinated with dodecylamine than did untreated spores. However, KMT reagent-killed spores did not germinate with nutrients or Ca(2+)-DPA and were recovered only poorly by lysozyme treatment in a hypertonic medium.
Answer: The KMT reagent does not kill spores by DNA damage and a major factor in spore resistance to this reagent is the spore coat. KMT reagent treatment damages the spore's ability to germinate, perhaps by damaging the spore's inner membrane. However, this damage is not oxidation of unsaturated fatty acids.

SOLUTION: Do mechanisms of Bacillus subtilis spore killing by and resistance to an acidic Fe-EDTA-iodide-ethanol formulation?

PROBLEM: Context: Sit-to-stand tasks are commonly facilitated by modifying the initial position of the center of mass relative to the feet. It was hypothesized that modifications in the center of mass trajectory during sit-to-stand tasks altered the total body momentum at seat departure and redistributed the lower extremity net joint moments.', 'Between-task within-subject comparison was employed using a robust statistical method to accommodate for small sample size.', 'Six individuals performed four sit-to-stand tasks with systematic modifications in the initial center of mass position by varying the orientation of the lower extremity segments. The momentum of the center of mass and lower extremity net joint moments were quantified and compared.', 'Reducing the horizontal center of mass displacement significantly reduced horizontal total body momentum required at seat departure. Sit-to-stand tasks initiated with more horizontal shank and thigh positions required significantly greater knee and hip extensor net joint moments than those with more vertical shank and thigh positions. Sit-to-stand tasks initiated with vertical shank positions also required significantly greater hip extensor net joint moments as compared to those with more horizontal shank orientations.
Answer: When changes in initial center of mass position are made, alteration in center of mass horizontal momentum and the orientation of the lower extremity segments relative to the reaction force are observed. Consequently, mechanical demand imposed on the ankle, knee, and hip joint is redistributed. The magnitude of the net joint moments is dependent on the segment orientation, the reaction force, and the adjacent net joint moment.

SOLUTION: Does modifying center of mass trajectory during sit-to-stand tasks redistribute the mechanical demand across the lower extremity joints?

PROBLEM: Context: Defects of the mitochondrial genome (mtDNA) cause a series of rare, mainly neurological disorders. In addition, they have been implicated in more common forms of movement disorders, dementia and the ageing process. In order to try to model neuronal dysfunction associated with mitochondrial disease, we have attempted to establish a series of transmitochondrial mouse embryonic stem cells harbouring pathogenic mtDNA mutations.', 'Transmitochondrial embryonic stem cell cybrids were generated by fusion of cytoplasts carrying a variety of mtDNA mutations, into embryonic stem cells that had been pretreated with rhodamine 6G, to prevent transmission of endogenous mtDNA. Cybrids were differentiated into neurons and assessed for efficiency of differentiation and electrophysiological function.', 'Neuronal differentiation could occur, as indicated by expression of neuronal markers. Differentiation was impaired in embryonic stem cells carrying mtDNA mutations that caused severe biochemical deficiency. Electrophysiological tests showed evidence of synaptic activity in differentiated neurons carrying non-pathogenic mtDNA mutations or in those that caused a mild defect of respiratory activity. Again, however, neurons carrying mtDNA mutations that resulted in severe biochemical deficiency had marked reduction in post-synaptic events.
Answer: Differentiated neurons carrying severely pathogenic mtDNA defects can provide a useful model for understanding how such mutations can cause neuronal dysfunction.

SOLUTION:
Are transmitochondrial embryonic stem cells containing pathogenic mtDNA mutations compromised in neuronal differentiation?