Revealing the Magic of Skele-Gro

This paper investigates the extent to which Skele-Gro increases the rate of normal bone growth by comparing the regrowth of Harry’s arm bones to the rate of regeneration of bone in a fracture. The amount of energy provided by Skele-Gro is also determined. We find that the rate of bone growth is at least 90 times greater than that of a fracture repair and that the amount of energy that Skele-Gro supplies to do this is a minimum of 133,050 kcal. The lower estimate of Skele-Gro’s power output is therefore 6443 W

Did Mark Watney make it Home from Mars?

At the conclusion of the 2015 film ‘The Martian’ astronaut Mark Watney cuts a hole in his space suit, and uses the escaping air as a mini thruster in order to make it to his rescuers. This paper finds that the air would not provide enough force to propel Watney with enough acceleration to make it home

AHI-1 interacts with BCR-ABL and modulates BCR-ABL transforming activity and imatinib response of CML stem/progenitor cells

Chronic myeloid leukemia (CML) represents the first human malignancy successfully treated with a tyrosine kinase inhibitor (TKI; imatinib). However, early relapses and the emergence of imatinib-resistant disease are problematic. Evidence suggests that imatinib and other inhibitors may not effectively eradicate leukemic stem/progenitor cells, and that combination therapy directed to complimentary targets may improve treatment. Abelson helper integration site 1 (Ahi-1)/AHI-1 is a novel oncogene that is highly deregulated in CML stem/progenitor cells where levels of BCR-ABL transcripts are also elevated. Here, we demonstrate that overexpression of Ahi-1/AHI-1 in murine and human hematopoietic cells confer growth advantages in vitro and induce leukemia in vivo, enhancing effects of BCR-ABL. Conversely, RNAi-mediated suppression of AHI-1 in BCR-ABL–transduced lin−CD34+ human cord blood cells and primary CML stem/progenitor cells reduces their growth autonomy in vitro. Interestingly, coexpression of Ahi-1 in BCR-ABL–inducible cells reverses growth deficiencies exhibited by BCR-ABL down-regulation and is associated with sustained phosphorylation of BCR-ABL and enhanced activation of JAK2–STAT5. Moreover, we identified an AHI-1–BCR-ABL–JAK2 interaction complex and found that modulation of AHI-1 expression regulates phosphorylation of BCR-ABL and JAK2–STAT5 in CML cells. Importantly, this complex mediates TKI response/resistance of CML stem/progenitor cells. These studies implicate AHI-1 as a potential therapeutic target downstream of BCR-ABL in CML

Targeting Primitive Chronic Myeloid Leukemia Cells by Effective Inhibition of a New AHI-1BCR-ABL-JAK2 Complex

This is a pre-copyedited, author-produced version of an article accepted for publication in JNCI: Journal of the National Cancer Institute following peer review. The version of record Chen, M., et al. (2013). "Targeting Primitive Chronic Myeloid Leukemia Cells by Effective Inhibition of a New AHI-1–BCR-ABL–JAK2 Complex." JNCI: Journal of the National Cancer Institute 105(6): 405-423. is available online at: https://doi.org/10.1093/jnci/djt006This work was funded by the Canadian Cancer Society (grant 700289), in part by the Canadian Institutes of Health Research, the Leukemia & Lymphoma Society of Canada, and the Cancer Research Society (XJ), the Canadian Cancer Society Research Institute (AE, XJ, CE), Cancer Research UK Programme grant C11074/A11008 (TLH), the Glasgow Experimental Cancer Medicine Centre, which is funded by Cancer Research UK and by the Chief Scientist’s Office (Scotland), and Cancer Research UK grant C973/A9894 (JP, JS). M. Chen was supported by a fellowship from Lymphoma Foundation Canada, and P. Gallipoli was supported by Medical Research Council grant G1000288. X. Jiang was a Michael Smith Foundation for Health Research Scholar

Effect of noxious stimulation upon antipredator responses and dominanace status in rainbow trout

A potentially painful experience may modify normal behavioural responses. To gauge the importance of pain relative to predation or social status, we presented competing stimuli, a predator cue or an unfamiliar social group, to two groups of noxiously treated rainbow trout, Oncorhynchus mykiss. In the predator cue experiment, fish were classified as bold or shy. Noxiously stimulated fish did not show antipredator responses, suggesting that pain is the imperative. In the social status experiment, noxiously stimulated fish held individually and undisturbed showed an increase in respiration rate and plasma cortisol. As a comparison, we used the dominant or subordinate fish in a group as the noxiously stimulated fish. After the noxious treatment, we returned this test fish to a familiar or unfamiliar social group. Neither dominants nor subordinates showed a negative change in physiology compared to their controls. However, in a familiar group the dominant was much less aggressive, suggesting a behavioural impairment in response to noxious stimulation. In an unfamiliar group, no reduction of aggression was seen, suggesting that maintaining dominance status took priority over showing signs of pain. These findings may reflect an ability to prioritize motivational drivers in fish, and as such provides evidence for central processing of pain rather than merely showing a nociceptive reflex

Effect of Noxious Stimulation Upon Antipredator Responses and Dominance Status in Rainbow Trout

A potentially painful experience may modify normal behavioural responses. To gauge the importance of pain relative to predation or social status, we presented competing stimuli, a predator cue or an unfamiliar social group, to two groups of noxiously treated rainbow trout, Oncorhynchus mykiss. In the predator cue experiment, fish were classified as bold or shy. Noxiously stimulated fish did not show antipredator responses, suggesting that pain is the imperative. In the social status experiment, noxiously stimulated fish held individually and undisturbed showed an increase in respiration rate and plasma cortisol. As a comparison, we used the dominant or subordinate fish in a group as the noxiously stimulated fish. After the noxious treatment, we returned this test fish to a familiar or unfamiliar social group. Neither dominants nor subordinates showed a negative change in physiology compared to their controls. However, in a familiar group the dominant was much less aggressive, suggesting a behavioural impairment in response to noxious stimulation. In an unfamiliar group, no reduction of aggression was seen, suggesting that maintaining dominance status took priority over showing signs of pain. These findings may reflect an ability to prioritize motivational drivers in fish, and as such provides evidence for central processing of pain rather than merely showing a nociceptive reflex