Kochia [Bassia scoparia (L.) A.J. Scott] is an invasive tumbleweed in the North American Great Plains that is difficult to manage in croplands and ruderal areas due to widespread resistance to up to four herbicide sites of action, including auxin mimics (Herbicide Resistance Action Committee [HRAC] Group 4) and inhibitors of acetolactate synthase (HRAC Group 2), photosystem II (HRAC Group 5), and 5-enolpyruvylshikimate-3-phosphate synthase (HRAC Group 9). Poor B. scoparia control with protoporphyrinogen oxidase (PPO)-inhibiting (HRAC Group 14) herbicides was noted in a brown mustard [Brassica juncea (L.) Czern.] field near Kindersley, SK, Canada, in 2021. Similar observations were made in a sunflower (Helianthus annuus L.) field near Mandan, ND, USA, and in research plots near Minot, ND, USA, in 2022. Whole-plant dose–response experiments were conducted to determine whether these B. scoparia accessions were resistant to the PPO-inhibiting herbicides saflufenacil and carfentrazone and the level of resistance observed. All three B. scoparia accessions were highly resistant to foliar-applied saflufenacil and carfentrazone compared with two locally relevant susceptible accessions. The Kindersley accession exhibited 57- to 87-fold resistance to saflufenacil and 97- to 121-fold resistance to carfentrazone based on biomass dry weight at 21 d after treatment (DAT). Similarly, the Mandan accession exhibited 204- to 321-fold resistance to saflufenacil and 111- to 330-fold resistance to carfentrazone, while the Minot accession exhibited 45- to 71-fold resistance to saflufenacil and 88- to 264-fold resistance to carfentrazone. Substantial differences in visible control at 7 and 21/28 DAT were also observed between the putative-resistant and susceptible accessions. This study represents the first confirmations of PPO inhibitor–resistant B. scoparia globally and the fifth herbicide site of action to which B. scoparia has evolved resistance. It also documents this issue present at three locations in the Northern Great Plains region that occur up to 790 km apart and on both sides of the Canada/U.S. border.

OBJECTIVES/GOALS: Our lab previously identified a population of vascular smooth muscle (SMC)-derived progenitor cells (AdvSca1-SM) which expand robustly in response to disease and can differentiate into multiple cell types. We now aim to define the role of these AdvSca1-SM cells in atherosclerotic plaque progression. METHODS/STUDY POPULATION: Goal one uses SMC lineage tracing mice and a model of atherosclerosis to track reprogramming of SMCs to AdvSca1-SM cells in the setting of disease. Arteries are analyzed using flow cytometry and immunofluorescence to quantify changes in number of mature SMCs and AdvSca1-SM cells. Goal two uses AdvSca1-SM lineage tracing mice with high cholesterol-induced atherosclerosis and plaque neovascularization. Arteries are analyzed to quantify expansion of AdvSca1-SM cells, subsequent re-differentiation into mature SMC, endothelial cells, or macrophages, and contribution to plaque neovascularization. Mechanistic findings from both goals are being investigated in diseased human coronary arteries. RESULTS/ANTICIPATED RESULTS: Flow cytometry from SMC lineage tracing mice revealed a 7- to 13-fold expansion of AdvSca1-SM cells in carotid arteries (p<0.001) and aortas (p = 0.03) after 6 weeks of western diet; no differences in macrophage numbers were observed. Additional SMC and AdvSca1-SM cell lineage tracing mice are on atherogenic diets to assess early and advanced atherosclerosis. We predict that AdvSca1-SM cells will contribute to macrophage accumulation as well as plaque neovascularization in the setting of severe atherosclerosis. Translational relevance of mechanisms driving SMC reprogramming and AdvSca1-SM cell contribution to plaque progression are being applied to studies of diseased human coronary arteries. DISCUSSION/SIGNIFICANCE OF IMPACT: Our data suggest a role for AdvSca1-SM cells in atherosclerosis. Ongoing work will clarify the mechanisms driving plaque-associated AdvSca1-SM expansion and define the ultimate fates of these cells. In vivo modulation of this process could provide the basis for future anti-atherosclerotic therapies. CONFLICT OF INTEREST DESCRIPTION: AD - CCTSI TOTTS TL1TR002533; SL - 18POST34030397 from the American Heart Association; AJ – no conflicts; KS - 1F31HL147393 from the National Heart, Lung, and Blood Institute, NIH; MM – no conflicts; RT – no conflicts; KSM – no conflicts; RAN - R01CA236222 from the National Cancer Institute, NIH, and 2018-03 from the Lungevity Foundation; and MCMW-E - R01 HL121877 from the National Heart, Lung, and Blood Institute, NIH, and 25A8679 from the Chernowitz Foundation.

Using airborne and spaceborne high-resolution digital elevation models and laser altimetry, we present estimates of interannual and multi-decadal surface elevation changes on the Bering Glacier system, Alaska, USA, and Yukon, Canada, from 1972 to 2006. We find: (1) the rate of lowering during 1972–95 was 0.9 ± 0.1 m a−1; (2) this rate accelerated to 3.0 ± 0.7 m a−1 during 1995–2000; and (3) during 2000–03 the lowering rate was 1.5 ± 0.4 m a−1. From 1972 to 2003, 70% of the area of the system experienced a volume loss of 191 ± 17 km3, which was an area-average surface elevation lowering of 1.7 ± 0.2 m a−1. From November 2004 to November 2006, surface elevations across Bering Glacier, from McIntosh Peak on the south to Waxell Ridge on the north, rose as much as 53 m. Up-glacier on Bagley Ice Valley about 10 km east of Juniper Island nunatak, surface elevations lowered as much as 28 m from October 2003 to October 2006. NASA Terra/MODIS observations from May to September 2006 indicated muddy outburst floods from the Bering terminus into Vitus Lake. This suggests basal–englacial hydrologic storage changes were a contributing factor in the surface elevation changes in the fall of 2006.

The length-scales at which thermal transport crosses from the diffusive to ballistic regime are of much interest particularly in the design and improvement of nano-structured materials. In this work, we demonstrate that the departure from diffusive transport has been observed in Si and GaAs using an optical transient thermal grating technique where an arbitrary, experimentally set length scale can be imposed on a material. In a transient thermal grating experiment, crossed laser pulses interfere creating a well-defined periodic absorption and temperature profile. A probe beam is diffracted from this transient grating and length-scale dependent thermal transport properties can be determined from the signal decay. As the length scale is decreased to lengths shorter than the mean free paths of heat carrying phonons, quasi-ballistic heat transport effects become apparent allowing us to map out length scales and mean free paths relevant to nondiffusive thermal transport in Si and GaAs.

One of the key problems in microfabrication and especially nanofabrication applied to biology is materials selection. Proper materials must have mechanical stability and the ability to hermetically bond to other surfaces, yet not bind biological molecules. They must also be wettable by water and have good optical properties. In this article, we review some of the attempts to find materials for micro- and nanofluidic systems in biological applications that satisfy these rather conflicting constraints.We discuss the materials properties that make poly (dimethylsiloxane) or non-elastomeric materials more or less suitable for particular applications in biology. We also explore the effects and the importance of surface treatments for integrating biological objects into microfabricated and nanofabricated fluidic devices.

First year mathematics undergraduates entering British universities are often very unprepared for the kind of proof activities that occur throughout undergraduate degree programmes. Their previous experiences of the idea of proof are frequently limited to situations where the ‘proof’ is simply an extended chain of calculations or algebraic manipulations. In fact, this is well-illustrated by their approach to proof by induction, where they can carry out the mechanical details of the inductive step, but have no understanding of why proof by induction works, nor what status the initialisation step and the inductive hypothesis have in the proof. There is no real grasp of what it means to prove that some assertion is true. Much time, in consequence, is spent in the first years of mathematics degree courses up and down the country attempting to bring about this understanding.

Diana runs from A to B with speed u and then from B to C with speed v. Eric runs from A to C with speed w. They start together and finish together.

If we now draw three lines from a point O, with OP parallel to AB and of length u, OQ parallel to BC and of length v and OR parallel to AC and of length w, then we find P, Q and R are collinear.

It is not difficult to construct a proof of the theorem so that is left as an exercise for the reader.

A familiar result is that in any group of six people there are three who either all know each other or are all strangers to each other. This can be reformulated to say that, if six points are marked on a piece of paper and every pair of points is joined by a red or blue line, then there will be a monochromatic triangle, i.e. one which is all red or all blue. This result is related to a theorem which the Cambridge philosopher Frank Ramsey proved in 1930.