The production and removal of anaerobic metabolites from flooded tree roots with special reference to 'Pinus contorta'

The production and removal of anaerobiotic compounds, principally ethanol from flooded tree roots was examined in lodgepole pine (Pinus contorta) from known provenances. Contrary to earlier suggestions, the gaseous pathway, with ethanol exiting from the tree through the lenticels, removes only a very small proportion (less than 0.2%) of the ethanol generated in the flooded roots. The transpiration stream provides the major route for ethanol transport from the roots. Although the lenticels do not contribute significantly to the removal of ethanol from tree roots, analysis of the gas exiting from them provides a sensitive indicator of the existence of oxygen within roots. Within the xylem sap and root tissue, changes in ethanol, amino acid (alanine, alpha amino butyrate and glutamine) and organic acid (malate and shikimate) composition under flooded conditions were analysed and discussed. For example during flooding glutamine (the major constituent amino acid) was shown to decrease, and alanine and alpha amino butyrate to increase. From the data obtained it was concluded that the health and the metabolism of the root tissue during flooding can be diagnosed by examination of the xylem sap

Older Adults in Service to Society

Older Adults in Service to Societ

A Study of Municipal Funding of Nonprofit Agencies for the City of College Station, Texas

The City of College Station funds nonprofit agencies through a program called Outside Agency Funding because the nonprofits provide services not offered by the city. In working to streamline the application, review, and monitoring of this funding, it became clear that there is no standard method outlined and packaged for municipal governments to use as a guide or best practice in funding nonprofit agencies. This capstone project developed a guide for municipal governments that fund nonprofit agencies

Thermal Runaway of Li-Ion Cells: How Internal Dynamics, Mass Ejection, and Heat Vary with Cell Geometry and Abuse Type

Thermal runaway of lithium-ion batteries can involve various types of failure mechanisms each with their own unique characteristics. Using fractional thermal runaway calorimetry and high-speed radiography, the response of three different geometries of cylindrical cell (18650, 21700, and D-cell) to different abuse mechanisms (thermal, internal short circuiting, and nail penetration) are quantified and statistically examined. Correlations between the geometry of cells and their thermal behavior are identified, such as increasing heat output per amp-hour (kJ Ah-1) of cells with increasing cell diameter during nail penetration. High-speed radiography reveals that the rate of thermal runaway propagation within cells is generally highest for nail penetration where there is a relative increase in rate of propagation with increasing diameter, compared to thermal or internal short-circuiting abuse. For a given cell model tested under the same conditions, a distribution of heat output is observed with a trend of increasing heat output with increased mass ejection. Finally, internal temperature measurements using thermocouples embedded in the penetrating nail are shown to be unreliable thus demonstrating the need for care when using thermocouples where the temperature is rapidly changing. All data used in this manuscript are open access through the NREL and NASA Battery Failure Databank

The role of ERK5 in endothelial cell function

Extracellular-signal-regulated kinase 5 (ERK5), also termed big MAPK1 (BMK1), is the most recently discovered member of the mitogen-activated protein kinase (MAPK) family. It is expressed in a variety of tissues and is activated by a range of growth factors, cytokines and cellular stresses. Targeted deletion of Erk5 in mice has revealed that the ERK5 signalling cascade is critical for normal cardiovascular development and vascular integrity. In vitro studies have revealed that, in endothelial cells, ERK5 is required for preventing apoptosis, mediating shear-stress signalling and regulating tumour angiogenesis. The present review focuses on our current understanding of the role of ERK5 in regulating endothelial cell function

Targeting the MAPK7/MMP9 axis for metastasis in primary bone cancer

From Springer Nature via Jisc Publications RouterHistory: received 2020-03-17, rev-recd 2020-05-24, accepted 2020-06-23, registration 2020-06-24, pub-electronic 2020-07-13, online 2020-07-13, pub-print 2020-08-13Publication status: PublishedFunder: Friends of RosieFunder: THRT, Big C, Paget's AssociationAbstract: Metastasis is the leading cause of cancer-related death. This multistage process involves contribution from both tumour cells and the tumour stroma to release metastatic cells into the circulation. Circulating tumour cells (CTCs) survive circulatory cytotoxicity, extravasate and colonise secondary sites effecting metastatic outcome. Reprogramming the transcriptomic landscape is a metastatic hallmark, but detecting underlying master regulators that drive pathological gene expression is a key challenge, especially in childhood cancer. Here we used whole tumour plus single-cell RNA-sequencing in primary bone cancer and CTCs to perform weighted gene co-expression network analysis to systematically detect coordinated changes in metastatic transcript expression. This approach with comparisons applied to data collected from cell line models, clinical samples and xenograft mouse models revealed mitogen-activated protein kinase 7/matrix metallopeptidase 9 (MAPK7/MMP9) signalling as a driver for primary bone cancer metastasis. RNA interference knockdown of MAPK7 reduces proliferation, colony formation, migration, tumour growth, macrophage residency/polarisation and lung metastasis. Parallel to these observations were reduction of activated interleukins IL1B, IL6, IL8 plus mesenchymal markers VIM and VEGF in response to MAPK7 loss. Our results implicate a newly discovered, multidimensional MAPK7/MMP9 signalling hub in primary bone cancer metastasis that is clinically actionable

Genome assembly and population genomic analysis provide insights into the evolution of modern sweet corn.

Sweet corn is one of the most important vegetables in the United States and Canada. Here, we present a de novo assembly of a sweet corn inbred line Ia453 with the mutated shrunken2-reference allele (Ia453-sh2). This mutation accumulates more sugar and is present in most commercial hybrids developed for the processing and fresh markets. The ten pseudochromosomes cover 92% of the total assembly and 99% of the estimated genome size, with a scaffold N50 of 222.2 Mb. This reference genome completely assembles the large structural variation that created the mutant sh2-R allele. Furthermore, comparative genomics analysis with six field corn genomes highlights differences in single-nucleotide polymorphisms, structural variations, and transposon composition. Phylogenetic analysis of 5,381 diverse maize and teosinte accessions reveals genetic relationships between sweet corn and other types of maize. Our results show evidence for a common origin in northern Mexico for modern sweet corn in the U.S. Finally, population genomic analysis identifies regions of the genome under selection and candidate genes associated with sweet corn traits, such as early flowering, endosperm composition, plant and tassel architecture, and kernel row number. Our study provides a high-quality reference-genome sequence to facilitate comparative genomics, functional studies, and genomic-assisted breeding for sweet corn

Targeting the MAPK7/MMP9 axis for metastasis in primary bone cancer

Metastasis is the leading cause of cancer related death. This multistage process involves contribution from both tumour cells and the tumour stroma to release metastatic cells into the circulation. Circulating tumour cells (CTCs) survive circulatory cytotoxicity, extravasate and colonise secondary sites effecting metastatic outcome. Reprogramming the transcriptomic landscape is a metastatic hallmark but detecting underlying master regulators that drive pathological gene expression is a key challenge, especially in childhood cancer. Here we used whole tumour plus single cell RNA sequencing in primary bone cancer and CTCs to perform weighted gene co-expression network analysis to systematically detect coordinated changes in metastatic transcript expression. This approach with comparisons applied to data collected from cell line models, clinical samples and xenograft mouse models revealed MAPK7/MMP9 signalling as a driver for primary bone cancer metastasis. RNAi knockdown of MAPK7 reduces proliferation, colony formation, migration, tumour growth, macrophage residency/polarisation and lung metastasis. Parallel to these observations were reduction of activated interleukins IL1B, IL6, IL8 plus mesenchymal markers VIM and VEGF in response to MAPK7 loss. Our results implicate a newly discovered, multidimensional MAPK7/MMP9 signalling hub in primary bone cancer metastasis that is clinically actionable