Lin28b is an RNA-binding protein that inhibits biogenesis of let-7 microRNAs. LIN28B is overexpressed in diverse cancers, yet a specific role in the molecular pathogenesis of colon cancer has yet to be elucidated. We have determined that human colon tumors exhibit decreased levels of mature let-7 isoforms and increased expression of LIN28B. In order to determine LIN28B's mechanistic role in colon cancer, we expressed LIN28B in immortalized colonic epithelial cells and human colon cancer cell lines. We found that LIN28B promotes cell migration, invasion, and transforms immortalized colonic epithelial cells. In addition, constitutive LIN28B expression increases expression of intestinal stem cell markers LGR5 and PROM1 in the presence of let-7 restoration. This may occur as a result of Lin28b protein binding LGR5 and PROM1 mRNA, suggesting that a subset of LIN28B functions are independent of its ability to repress let-7. Our findings establish a new role for LIN28B in human colon cancer pathogenesis, and suggest LIN28B post-transcriptionally regulates LGR5 and PROM1 through a let-7 independent mechanism.
In a population-based study in California, we found that following S-colo, rates of serious GI adverse events were low but clinically relevant, and that rates of myocardial infarction, stroke, and serious pulmonary events were no higher than after low-risk comparator procedures. Rates of myocardial infarction are similar to, but rates of stroke are higher than, those reported for the general population.
A method is described for the catheterization of the carotid of the rat which permits blood volume determinations to be made on unanesthetized animals. The cell volume (P32) and plasma volume (T-1824) were measured simultaneously on the day after catheterization. The average Fcells factor was 0.739 (S.D., 0.053) in 11 normal rats and 0.726 (S.D., 0.041) in 10 splenectomized rats. In 50 unanesthetized normal rats the plasma volume averaged 3.90 ml/100 gm body weight. The blood and cell volumes calculated by using the Fcells factor of 0.74 and the separately determined plasma trapping' factor of 0.95 averaged 5.93 ml/ 100 gm and 2.14 ml/100 gm, respectively. These values agree closely with those determined from the simultaneous measurement of cell and plasma volumes and also with the values obtained on 27 normal rats under ether.
The use of liquid biofuels has expanded over the past decade in response to policies such as the U.S. Renewable Fuel Standard (RFS) that promote their use for transportation. One rationale is the belief that biofuels are inherently carbon neutral, meaning that only productionrelated greenhouse gas (GHG) emissions need to be tallied when comparing them to fossil fuels. This assumption is embedded in the lifecycle analysis (LCA) modeling used to justify and administer such policies. LCA studies have often found that crop-based biofuels such as corn ethanol and biodiesel offer at least modest net GHG reductions relative to petroleum fuels. Data over the period of RFS expansion enable empirical assessment of net CO 2 emission effects. This analysis evaluates the direct carbon exchanges (both emissions and uptake) between the atmosphere and the U.S. vehicle-fuel system (motor vehicles and the physical supply chain for motor fuels) over 2005-2013. While U.S. biofuel use rose from 0.37 to 1.34 EJ/yr over this period, additional carbon uptake on cropland was enough to offset only 37 % of the biofuel-related biogenic CO 2 emissions. This result falsifies the assumption of a full offset made by LCA and other GHG accounting methods that assume biofuel carbon neutrality. Once estimates from the literature for process emissions and displacement effects including land-use change are considered, the conclusion is that U.S. biofuel use to date is associated with a net increase rather than a net decrease in CO 2 emissions.
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