132 research outputs found
High Activity Mutants of Butyrylcholinesterase for Cocaine Hydrolysis
Butyrylcholinesterase (BChE) polypeptide variants of the presently-disclosed subject matter have enhanced catalytic efficiency for (−)-cocaine, as compared to wild-type BChE. Pharmaceutical compositions of the presently-disclosed subject matter include a BChE polypeptide variant having an enhanced catalytic efficiency for (−)-cocaine. A method of the presently-disclosed subject matter for treating a cocaine-induced condition includes administering to an individual an effective amount of a BChE polypeptide variant, as disclosed herein, to lower blood cocaine concentration
High Activity Mutants of Butyrylcholinesterase for Cocaine Hydrolysis
Butyrylcholinesterase (BChE) polypeptide variants of the presently-disclosed subject matter have enhanced catalytic efficiency for (−)-cocaine, as compared to wild-type BChE. Pharmaceutical compositions of the presently-disclosed subject matter include a BChE polypeptide variant having an enhanced catalytic efficiency for (−)-cocaine. A method of the presently-disclosed subject matter for treating a cocaine-induced condition includes administering to an individual an effective amount of a BChE polypeptide variant, as disclosed herein, to lower blood cocaine concentration
High Activity Mutants of Butyrylcholinesterase for Cocaine Hydrolysis
Butyrylcholinesterase (BChE) polypeptide variants of the presently-disclosed subject matter have enhanced catalytic efficiency for (−)-cocaine, as compared to wild-type BChE. Pharmaceutical compositions of the presently-disclosed subject matter include a BChE polypeptide variant having an enhanced catalytic efficiency for (−)-cocaine. A method of the presently-disclosed subject matter for treating a cocaine-induced condition includes administering to an individual an effective amount of a BChE polypeptide variant, as disclosed herein, to lower blood cocaine concentration
Delay-Compound-Compensation Control for Photoelectric Tracking System Based on Improved Smith Predictor Scheme
Imprint of the stochastic nature of photon emission by electrons on the proton energy spectra in the laser-plasma interaction
The impact of stochasticity effects (SEs) in photon emissions on the proton
energy spectra during laser-plasma interaction is theoretically investigated in
the quantum radiation-dominated regime, which may facilitate SEs experimental
observation. We calculate the photon emissions quantum mechanically and the
plasma dynamics semiclassically via two-dimensional particle-in-cell
simulations. An ultrarelativistic plasma generated and driven by an
ultraintense laser pulse head-on collides with another strong laser pulse,
which decelerates the electrons due to radiation-reaction effect and results in
a significant compression of the proton energy spectra because of the charge
separation force. In the considered regime the SEs are demonstrated in the
shift of the mean energy of the protons up to hundreds of MeV. This effect is
robust with respect to the laser and target parameters and measurable in soon
available strong laser facilities
A novel HCC prognosis predictor PDSS1 affects the cell cycle through the STAT3 signaling pathway in HCC
Decaprenyl diphosphate synthase subunit 1 (PDSS1) is closely related to a variety of human diseases, but its expression pattern and biological function in HCC have not been studied to date.MethodsThe expression level of PDSS1 was analyzed using the TCGA and GEO databases. The relationships between PDSS1 and patient clinicopathological characteristics were verified based on TCGA clinical data. Additionally, the co-expressed genes of PDSS1were investigated and Gene Set Enrichment Analysis (GSEA) was conducted using LinkedOmics. Next, the association between PDSS1 and immune infiltration was determined using version 1.34.0 of the GSVA package. EdU assay, colony-formation assay, transwell assay, wound-healing assay, and flow cytometry analysis were used to assess the effect of PDSS1 on the cell phenotype.ResultsPDSS1 was upregulated in HCC compared with adjacent tissues. High PDSS1 in HCC was associated with poor overall survival, disease-specific survival, and progress-free interval. Results suggested that PDSS1 may activate multiple oncogenic pathways in HCC, especially those involved in the cell cycle. The expression of PDSS1 was significantly related to Th2 cells, TFH, T helper cells, NK CD56bright cells, cytotoxic cells, DC, CD8 T cells, and neutrophils. PDSS1 knockdown inhibited cell proliferation, cell cycle, migration and invasion. Furthermore, PDSS1 acted as an oncogene through the STAT3 signaling pathway.ConclusionOur study reveals that a high level of PDSS1 is significantly correlated with poor patient prognosis and immune cell infiltration in HCC. PDSS1 may be a novel biomarker and potential therapeutic target for HCC
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