Legislative Documents

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Enhanced Lifetime of Cyanine Salts in Dilute Matrix Luminescent Solar Concentrators via Counterion Tuning

Organic luminophores offer great potential for energy harvesting and light emission due to tunable spectral properties, strong luminescence, high solubility, and excellent wavelength selectivity. To realize their full potential, the lifetimes of luminophores must extend to many years under illumination. Many organic luminophores, however, have a tendency to degrade and undergo rapid photobleaching, leading to the perception of intrinsic instability of organic molecules. In this work, we demonstrate that by exchanging the counterion of a heptamethine cyanine salt the photostability and corresponding lifetime of dilute cyanine salts can be enhanced by orders of magnitude from 10 h to an extrapolated lifetime of greater than 65,000 h under illumination. To help correlate and comprehend the underlying mechanism behind this phenomenon, the water contact angle and binding energy of each pairing were measured and calculated. We find that increased water contact angle, and therefore increasing hydrophobicity, generally correlates to improved lifetimes. Similarly, a lower absolute binding energy between cation and anion correlates to increased lifetimes. Utilizing the binding energy formalism, we predict the stability of a new anion and experimentally verify it with good consistency. Moving forward, these factors could be used to rapidly screen and identify highly photostable organic luminophore salt systems for a range of energy harvesting and light-emitting applications

Enhanced Electroluminescence Efficiency in Metal Halide Nanocluster Based Light Emitting Diodes through Apical Halide Exchange

Metal halide nanoclusters represent an attractive class of molecular building blocks for the design of functional materials with superior optical properties that can be utilized in a range of applications. Here, we demonstrate red and near-infrared light emitting diodes with a maximum external quantum efficiency >1%, utilizing phosphorescent octahedral molybdenum iodide nanoclusters. Efficiency improvement in these devices is realized by substituting heavier ligands in the apical nanocluster position that lead to the improvement in photoluminescence and exciton formation efficiencies in the nanoclusters. These results highlight how modulation of nanocluster salts with key terminal ligands has a profound effect on photoluminescence as well as electrical injection

data_sheet_3_Sialic Acid Metabolism: A Key Player in Breast Cancer Metastasis Revealed by Metabolomics.xlsx

<p>Metastatic breast cancer is currently incurable. It has recently emerged that different metabolic pathways support metastatic breast cancer. To further uncover metabolic pathways enabling breast cancer metastasis, we investigated metabolic differences in mouse tumors of differing metastatic propensities using mass spectrometry-based metabolomics. We found that sialic acid metabolism is upregulated in highly metastatic breast tumors. Knocking out a key gene in sialic acid metabolism, Cmas, inhibits synthesis of the activated form of sialic acid, cytidine monophosphate-sialic acid and decreases the formation of lung metastases in vivo. Thus, the sialic acid pathway may be a new target against metastatic breast cancer.</p

image_4_Sialic Acid Metabolism: A Key Player in Breast Cancer Metastasis Revealed by Metabolomics.jpeg

<p>Metastatic breast cancer is currently incurable. It has recently emerged that different metabolic pathways support metastatic breast cancer. To further uncover metabolic pathways enabling breast cancer metastasis, we investigated metabolic differences in mouse tumors of differing metastatic propensities using mass spectrometry-based metabolomics. We found that sialic acid metabolism is upregulated in highly metastatic breast tumors. Knocking out a key gene in sialic acid metabolism, Cmas, inhibits synthesis of the activated form of sialic acid, cytidine monophosphate-sialic acid and decreases the formation of lung metastases in vivo. Thus, the sialic acid pathway may be a new target against metastatic breast cancer.</p

image_6_Sialic Acid Metabolism: A Key Player in Breast Cancer Metastasis Revealed by Metabolomics.jpeg

<p>Metastatic breast cancer is currently incurable. It has recently emerged that different metabolic pathways support metastatic breast cancer. To further uncover metabolic pathways enabling breast cancer metastasis, we investigated metabolic differences in mouse tumors of differing metastatic propensities using mass spectrometry-based metabolomics. We found that sialic acid metabolism is upregulated in highly metastatic breast tumors. Knocking out a key gene in sialic acid metabolism, Cmas, inhibits synthesis of the activated form of sialic acid, cytidine monophosphate-sialic acid and decreases the formation of lung metastases in vivo. Thus, the sialic acid pathway may be a new target against metastatic breast cancer.</p

image_1_Sialic Acid Metabolism: A Key Player in Breast Cancer Metastasis Revealed by Metabolomics.jpeg

<p>Metastatic breast cancer is currently incurable. It has recently emerged that different metabolic pathways support metastatic breast cancer. To further uncover metabolic pathways enabling breast cancer metastasis, we investigated metabolic differences in mouse tumors of differing metastatic propensities using mass spectrometry-based metabolomics. We found that sialic acid metabolism is upregulated in highly metastatic breast tumors. Knocking out a key gene in sialic acid metabolism, Cmas, inhibits synthesis of the activated form of sialic acid, cytidine monophosphate-sialic acid and decreases the formation of lung metastases in vivo. Thus, the sialic acid pathway may be a new target against metastatic breast cancer.</p

image_8_Sialic Acid Metabolism: A Key Player in Breast Cancer Metastasis Revealed by Metabolomics.jpeg

<p>Metastatic breast cancer is currently incurable. It has recently emerged that different metabolic pathways support metastatic breast cancer. To further uncover metabolic pathways enabling breast cancer metastasis, we investigated metabolic differences in mouse tumors of differing metastatic propensities using mass spectrometry-based metabolomics. We found that sialic acid metabolism is upregulated in highly metastatic breast tumors. Knocking out a key gene in sialic acid metabolism, Cmas, inhibits synthesis of the activated form of sialic acid, cytidine monophosphate-sialic acid and decreases the formation of lung metastases in vivo. Thus, the sialic acid pathway may be a new target against metastatic breast cancer.</p

image_5_Sialic Acid Metabolism: A Key Player in Breast Cancer Metastasis Revealed by Metabolomics.jpeg

<p>Metastatic breast cancer is currently incurable. It has recently emerged that different metabolic pathways support metastatic breast cancer. To further uncover metabolic pathways enabling breast cancer metastasis, we investigated metabolic differences in mouse tumors of differing metastatic propensities using mass spectrometry-based metabolomics. We found that sialic acid metabolism is upregulated in highly metastatic breast tumors. Knocking out a key gene in sialic acid metabolism, Cmas, inhibits synthesis of the activated form of sialic acid, cytidine monophosphate-sialic acid and decreases the formation of lung metastases in vivo. Thus, the sialic acid pathway may be a new target against metastatic breast cancer.</p

table_2_Sialic Acid Metabolism: A Key Player in Breast Cancer Metastasis Revealed by Metabolomics.xlsx

<p>Metastatic breast cancer is currently incurable. It has recently emerged that different metabolic pathways support metastatic breast cancer. To further uncover metabolic pathways enabling breast cancer metastasis, we investigated metabolic differences in mouse tumors of differing metastatic propensities using mass spectrometry-based metabolomics. We found that sialic acid metabolism is upregulated in highly metastatic breast tumors. Knocking out a key gene in sialic acid metabolism, Cmas, inhibits synthesis of the activated form of sialic acid, cytidine monophosphate-sialic acid and decreases the formation of lung metastases in vivo. Thus, the sialic acid pathway may be a new target against metastatic breast cancer.</p