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At least 469 records · Page 26
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

Taking into Account Interelement Interference in X-Ray Fluorescence Analysis of Thin Two-Layer Ti/V Systems

We propose a new method for determining the thickness of layers in x-ray fluorescence analysis of two-layer Ti/V systems, using easily fabricated standardized film layers obtained by sputter deposition of titanium on a polymer film substrate. We have calculated correction factors taking into account the level of attenuation for the intensity of the primary emission from the x-ray tube and the analytical line for the element of the bottom layer in the top layer, and the enhancement of the fluorescence intensity for the top layer by the emission of atoms in the bottom layer.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2013

Interference of silibinin with IGF-1R signalling pathways protects human epidermoid carcinoma A431 cells from UVB-induced apoptosis

Highlights: ► Silibinin protects A431 cells from UVB irradiation-induced apoptosis. ► Up-regulation of the IGF-1R-JNK/ERK pathways by UVB induces cell apoptosis. ► Silibinin inhibits IGF-1R pathways to repress caspase-8-mediated apoptosis. -- Abstract: Ultraviolet B (UVB) from sunlight is a major cause of cutaneous lesion. Silibinin, a traditional hepatic protectant, elicits protective effects against UVB-induced cellular damage. In A431 cells, the insulin-like growth factor-1 receptor (IGF-1R) was markedly up-regulated by UVB irradiation. The activation of the IGF-1R signalling pathways contributed to apoptosis of the cells rather than rescuing the cells from death. Up-regulated IGF-1R stimulated downstream mitogen-activated protein kinases (MAPKs), such as c-Jun N-terminal kinases (JNK) and extracellular signal-regulated protein kinases 1/2 (ERK1/2). The subsequent activation of caspase-8 and caspase-3 led to apoptosis. The activation of IGF-1R signalling pathways is the cause of A431 cell death. The pharmacological inhibitors and the small interfering RNA (siRNA) targeting IGF-1R suppressed the downstream activation of JNK/ERK-caspases to help the survival of the UVB-irradiated A431 cells. Indeed, silibinin treatment suppressed the IGF-1R-JNK/ERK pathways and thus protected the cells from UVB-induced apoptosis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2014

Liver X receptors interfere with the deleterious effect of diethylstilbestrol on testicular physiology

Highlights: • Part of the neonatal effect of DES on testis needs the presence of Lxrα/β. • Some DES-induced pathways are blocked in Lxr-deficient mice. • Lxr-deficient mice analysis defines DES-target genes protected by Lxr. - Abstract: Liver X receptors LXRα (NR1H3) and LXRβ (NR1H2) are transcription factors belonging to the nuclear receptor superfamily, activated by specific oxysterols, oxidized derivatives of cholesterol. These receptors are involved in the regulation of testis physiology. Lxr-deficient mice pointed to the physiological roles of these nuclear receptors in steroid synthesis, lipid homeostasis and germ cell apoptosis and proliferation. Diethylstilbestrol (DES) is a synthetic estrogen considered as an endocrine disruptor that affects the functions of the testis. Various lines of evidences have made a clear link between estrogens, their nuclear receptors ERα (NR3A1) and ERβ (NR3A2), and Lxrα/β. As LXR activity could also be regulated by the nuclear receptor small heterodimer partner (SHP, NR0A2) and DES could act through SHP, we wondered whether LXR could be targeted by estrogen-like endocrine disruptors such as DES. For that purpose, wild-type and Lxr-deficient mice were daily treated with 0.75 μg DES from days 1 to 5 after birth. The effects of DES were investigated at 10 or 45 days of age. We demonstrated that DES induced a decrease of the body mass at 10 days only in the Lxr-deficient mice suggesting a protective effect of Lxr. We defined three categories of DES-target genes in testis: those whose accumulation is independent of Lxr; those whose accumulation is enhanced by the lack of both Lxrα/β; those whose accumulation is repressed by the absence of Lxrα/β. Lipid accumulation is also modified by neonatal DES injection. Lxr-deficient mice present different lipid profiles, demonstrating that DES could have its effects in part due to Lxrα/β. Altogether, our study shows that both nuclear receptors Lxrα and Lxrβ are not only basally important for testicular physiology but could also have a preventive effect against estrogen-like endocrine disruptors.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Loss of zebrafish Smyd1a interferes with myofibrillar integrity without triggering the misfolded myosin response

Highlights: • Smyd1a is expressed in fast-twitch skeletal as well as heart muscle. • Loss-of smyd1b can be compensated by overexpression of smyd1a. • Smyd1a and smyd1b are part of different transcriptional regulatory mechanisms. Sarcomeric protein turnover needs to be tightly balanced to assure proper assembly and renewal of sarcomeric units within muscle tissues. The mechanisms regulating these fundamental processes are only poorly understood, but of great clinical importance since many cardiac and skeletal muscle diseases are associated with defective sarcomeric organization. The SET- and MYND domain containing protein 1b (Smyd1b) is known to play a crucial role in myofibrillogenesis by functionally interacting with the myosin chaperones Unc45b and Hsp90α1. In zebrafish, Smyd1b, Unc45b and Hsp90α1 are part of the misfolded myosin response (MMR), a regulatory transcriptional response that is activated by disturbed myosin homeostasis. Genome duplication in zebrafish led to a second smyd1 gene, termed smyd1a. Morpholino- and CRISPR/Cas9-mediated knockdown of smyd1a led to significant perturbations in sarcomere structure resulting in decreased cardiac as well as skeletal muscle function. Similar to Smyd1b, we found Smyd1a to localize to the sarcomeric M-band in skeletal and cardiac muscles. Overexpression of smyd1a efficiently compensated for the loss of Smyd1b in flatline (fla) mutant zebrafish embryos, rescued the myopathic phenotype and suppressed the MMR in Smyd1b-deficient embryos, suggesting overlapping functions of both Smyd1 paralogs. Interestingly, Smyd1a is not transcriptionally activated in Smyd1b-deficient fla mutants, demonstrating lack of genetic compensation despite the functional redundancy of both zebrafish Smyd1 paralogs.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2025

Kinetic and structural evidence for specific DMSO interference with reversible binding of uncharged bis-oximes to hAChE and their reactivation kinetics of OP-hAChE

The structural basis of inhibitory effect of organic solvent dimethyl sulfoxide (DMSO) on human acetylcholinesterase (EC 3.1.1.7; hAChE) was inferred from the effect of DMSO on kinetics of reversible inhibition of uncharged, heterocyclic bis-oximes to hAChE, from DMSO effect on rates of reactivation of inactive organophosphate (OP)-hAChE conjugates by bis-oximes and by X-ray structures of bis-oxime and DMSO binding to hAChE. Here, the reversible inhibition constant of DMSO for hAChE in 0.1 M phosphate buffer pH 7.4 at 22 °C, was K i = (0.32 ± 0.04) % (or 45 ± 5 mM). The K i of the bis-oxime LG-703 for hAChE was 3.2-fold larger in 1 % DMSO, consistent with direct competition between LG-703 and DMSO. The X-ray structure of the LG-703∗hAChE complex (PDB ID: 6U3P) shows DMSO and LG-703 bound to individual hAChE monomers, LG-703 in the chain A and DMSO in the chain B. In the co-crystallization both small molecules were present at a similar excess over their corresponding K i values for hAChE (7.8-fold for DMSO and 6.5-fold for LG-703) and formation of two different complexes (DMSO∗hAChE and LG-703∗hAChE), in the same crystal, appears consistent with inhibition kinetics. Furthermore, rates of reactivation of paraoxon-inhibited hAChE (POX-hAChE) and of VX-hAChE by LG-703 and by a novel heterocyclic bis-oxime LG-1922 were reduced 2 – 3-fold in DMSO, consistent with observation of the active-center-bound DMSO molecules in the newly solved structure of the LG-1922∗POX-hAChE complex presented here and in our POX-hAChE structure (PDB ID: 8DT2) showing obstruction of the reactivator access to the conjugated P atom.

Acetylcholinesterase inhibition↗
DOE OSTI2015

Time series monitoring of water quality and microalgal diversity in a tropical bay under intense anthropogenic interference (SW coast of the Bay of Bengal, India)

In recent decades, material fluxes to coastal waters from various land based anthropogenic activities have significantly been enhanced around the globe which can considerably impact the coastal water quality and ecosystem health. Hence, there is a critical need to understand the links between anthropogenic activities in watersheds and its health. Kakinada Bay is situated at the SW part of the Bay of Bengal, near to the second largest mangrove cover in India with several fertilizer industries along its bank and could be highly vulnerable to different types of pollutants. However, virtually, no data is available so far reporting its physicochemical status and microalgal diversity at this bay. In order to fill this gap, we conducted three time series observations at a fixed station during January, December and June 2012, at this bay measuring more than 15 physical, chemical and biological parameters in every 3 h over a period of 36 h in both surface (0 m) and subsurface (4.5 m) waters. Our results clearly depict a strong seasonality between three sampling months; however, any abnormal values of nutrients, biological oxygen demand or dissolved oxygen level was not observed. A Skeletonema costatum bloom was observed in December which was probably influenced by low saline, high turbid and high Si input through the river discharge. Otherwise, smaller diatoms like Thalassiosira decipiens, Thalassiothrix frauenfeldii, and Thalassionema nitzschioides dominated the bay. It is likely that the material loading can be high at the point sources due to intense anthropogenic activities, however, gets diluted with biological, chemical and physical processes in the offshore waters. - Highlights: • No signature of enormous nutrient loading was observed over the diel cycle • Dissolved oxygen and BOD concentrations did not show any exceptional trend • Diatoms dominated more than 90% of the total phytoplankton communities • A Skeletonema Costatum (a centric diatom) bloom was noticed during December • No indication of pollution was noticed in terms of the parameters measured.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2013

Sensitization of Tumor to {sup 212}Pb Radioimmunotherapy by Gemcitabine Involves Initial Abrogation of G2 Arrest and Blocked DNA Damage Repair by Interference With Rad51

Purpose: To elucidate the mechanism of the therapeutic efficacy of targeted α-particle radiation therapy using {sup 212}Pb-TCMC-trastuzumab together with gemcitabine for treatment of disseminated peritoneal cancers. Methods and Materials: Mice bearing human colon cancer LS-174T intraperitoneal xenografts were pretreated with gemcitabine, followed by {sup 212}Pb-TCMC-trastuzumab and compared with controls. Results: Treatment with {sup 212}Pb-TCMC-trastuzumab increased the apoptotic rate in the S-phase-arrested tumors induced by gemcitabine at earlier time points (6 to 24 hours). {sup 212}Pb-TCMC-trastuzumab after gemcitabine pretreatment abrogated G2/M arrest at the same time points, which may be associated with the inhibition of Chk1 phosphorylation and, in turn, cell cycle perturbation, resulting in apoptosis. {sup 212}Pb-TCMC-trastuzumab treatment after gemcitabine pretreatment caused depression of DNA synthesis, DNA double-strand breaks, accumulation of unrepaired DNA, and down-regulation of Rad51 protein, indicating that DNA damage repair was blocked. In addition, modification in the chromatin structure of p21 may be associated with transcriptionally repressed chromatin states, indicating that the open structure was delayed at earlier time points. Conclusion: These findings suggest that the cell-killing efficacy of {sup 212}Pb-TCMC-trastuzumab after gemcitabine pretreatment may be associated with abrogation of the G2/M checkpoint, inhibition of DNA damage repair, and chromatin remodeling.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2022

Reduction of detection limit and quantification uncertainty due to interferent by neural classification with abstention

Many measurements in the physical sciences can be cast as counting experiments, where the number of occurrences of a physical phenomenon informs the prevalence of the phenomenon's source. Often, detection of the physical phenomenon (termed signal) is difficult to distinguish from naturally occurring phenomena (termed background). In this case, the discrimination of signal events from background can be performed using classifiers, and they may range from simple, threshold-based classifiers to sophisticated neural networks. These classifiers are often trained and validated to obtain optimal accuracy, however we show that the optimal accuracy classifier does not generally coincide with a classifier that provides the lowest detection limit, nor the lowest quantification uncertainty. Here, we present a derivation of the detection limit and quantification uncertainty in the classifier-based counting experiment case. We also present a novel abstention mechanism to minimize the detection limit or quantification uncertainty a posteriori. We illustrate the method on two data sets from the physical sciences, discriminating Ar-37 and Ar-39 radioactive decay from non-radioactive events in a gas proportional counter, and discriminating neutrons from gammas in an inorganic scintillator and report results therefrom.

46 INSTRUMENTATION RELATED TO NUCLEAR SCIENCE AND ↗