Carbon Monoxide Levels Produced by Propane/Isobutane Canister Stoves inside a Tent.

INTRODUCTION: Improper use of camp stoves in enclosed spaces has resulted in fatalities from carbon monoxide (CO) poisoning. Prior research has focused on the CO output of stoves burning white gas, unleaded gas, or kerosene. Stoves burning an isobutane/propane fuel have not been investigated and are the focus of this study. METHODS: Three stoves utilizing isobutane/propane fuel were used to heat a pot of water inside a 3-season tent under controlled settings. Multiple runs with each stove were performed, and CO measurements, in parts per million (ppm), were recorded at 1-min intervals for a total of 15 min using a RAE Systems gas monitor. Data are reported as mean with SD. Repeated measures analysis of variance was utilized to examine changes over time. Statistical significance was set at P<0.05. RESULTS: There was a statistically significant main effect of time and CO level, F (14, 168)=7.6, P<0.001. There was a statistically significant difference between-subjects effect of stove group F (2, 12)=8.6, P=0.005, indicating that CO levels were different depending on the stove. Tukey's post-hoc analyses revealed that stove A had the highest CO levels. The average level of stove A was statistically significantly higher than that of stove B and stove C, with a mean CO level difference of 79 ppm (95% CI, 3-156), P=0.043 and 117 ppm (95% CI, 40-194), P=0.004, respectively. CONCLUSIONS: Stoves utilizing isobutane/propane fuel can produce unsafe CO levels and should not be used in enclosed spaces.

Lineage tracing reveals the dynamic contribution of Hes1+ cells to the developing and adult pancreas.

Notch signaling regulates numerous developmental processes, often acting either to promote one cell fate over another or else to inhibit differentiation altogether. In the embryonic pancreas, Notch and its target gene Hes1 are thought to inhibit endocrine and exocrine specification. Although differentiated cells appear to downregulate Hes1, it is unknown whether Hes1 expression marks multipotent progenitors, or else lineage-restricted precursors. Moreover, although rare cells of the adult pancreas express Hes1, it is unknown whether these represent a specialized progenitor-like population. To address these issues, we developed a mouse Hes1(CreERT2) knock-in allele to inducibly mark Hes1(+) cells and their descendants. We find that Hes1 expression in the early embryonic pancreas identifies multipotent, Notch-responsive progenitors, differentiation of which is blocked by activated Notch. In later embryogenesis, Hes1 marks exocrine-restricted progenitors, in which activated Notch promotes ductal differentiation. In the adult pancreas, Hes1 expression persists in rare differentiated cells, particularly terminal duct or centroacinar cells. Although we find that Hes1(+) cells in the resting or injured pancreas do not behave as adult stem cells for insulin-producing beta (ß)-cells, Hes1 expression does identify stem cells throughout the small and large intestine. Together, these studies clarify the roles of Notch and Hes1 in the developing and adult pancreas, and open new avenues to study Notch signaling in this and other tissues.