The neutron-neutron (n-n) scattering length is a fundamental parameter in nuclear physics; however, measurements are plagued with large uncertainties caused by neutron detector cross talk. Many experimentalists also rely upon computer code to calibrate their neutron detectors. Experiments give one of two different numbers but there is still no adequate explanation for this discrepancy. We have developed a new neutron detector expressly for the purpose of improving the n-n scattering length measurement. It offers two important advantages: 1) minimal cross talk and 2) high counting efficiency. We calibrated the detector from 1 MeV to 6 MeV at 1 MeV increments. We have shown that the computer code, MCNP, does not always give the correct detector efficiency, and that reliance upon this code for calibration could be a large factor for error in previous experiments. Preliminary tests show no cross talk between two like detectors and suggest that these detectors in a n-n scattering length measurement.

As the semiconductor industry grapples with escalating scaling challenges associated with the floating gate MOSFET, alternative memory technologies like Resistive Random Access Memory (ReRAM) are gaining prominence in the scientific community. Boasting a straightforward device structure, ease of fabrication, and compatibility with CMOS (Complementary Metal-oxide Semiconductor) Back-end of Line (BEOL), ReRAM stands as a leading candi- date for the next generation of non-volatile memory (NVM). ReRAM devices feature nanoionics-based filamentary switching, outperforming flash memory in terms of power consumption, scalability, retention, ON/OFF ratio, and endurance. Furthermore, integrating ReRAMs within the CMOS BEOL/low-k Cu interconnect system not only reduces latency between the connectivity constraints of logic and memory modules but also minimizes the chip footprint. However, investigations have revealed a significant concern surrounding ReRAMs—specifically, their electro-thermal reliability. This research provides evidence highlighting the critical influence of material properties, deposition effects, and thermal transport on the device's performance and reliability. Various material systems have undergone in this work scrutiny to comprehend the impact of intrinsic material properties such as thermal conductivity, specific heat capacity, thermal diffusivity, and deposition effects like surface roughness on the electroforming voltages of ReRAM devices. The reference device structure considered in this work is Cu/TaOx/Pt, which has been compared with alternative configurations involving metals like Ru and Co as potential substitutes for Pt. Additionally, a new vehicle has been introduced to quantify cell degradation resulting from thermal cross-talk in crossbar Resistive Random Access Memory (ReRAM) arrays. Furthermore, a novel methodology has been presented to predict cell degradation due to remote heating, taking into account the cell's location, the material properties of the device, and geometry of its electrodes. The experimental results presented in this study showcase filament rupture caused by remote heating, along with spontaneous filament restoration ensuing from the subsequent cooling of the ReRAM cell. / Doctor of Philosophy / As the demand for compact, high-speed logic-memory modules continues to surge, the diminishing silicon real estate in our gadgets poses a challenge in extending Moore's law to meet the scaling needs of the semiconductor device industry. To tackle this challenge, emerging memory technologies like Resistive Random Access Memory (ReRAM) are positioned as promising successors to flash memory. ReRAM devices offer distinct advantages over flash memory, showcasing superior power consumption, scalability, long retention, a high ON/OFF ratio, and good endurance. Their compatibility with current CMOS (Complementary Metal-oxide Semiconductor) technology facilitates seamless integration. However, a significant concern associated with ReRAMs is their electro-thermal reliability. This research delves into how material properties comprising a ReRAM device and fabrication factors, such as the surface roughness of the material, can impact the electrical and thermal reliability of a ReRAM cell. In this context, a novel methodology has been introduced to predict cell degradation within ReRAM crossbar arrays induced by thermal cross-talk, considering material properties and the geometry of the device. The new methodology has been thoroughly verified on manufactured ReRAM arrays with various composite electrodes. The study also presents experimental results demonstrating the rupture of cell filaments due to remote heating, along with instances of spontaneous filament restoration due to subsequent cooling.

Background: This bioinformatics study aimed to reveal potential cross-talk genes, related pathways, and transcription factors between periimplantitis and rheumatoid arthritis (RA). Methods: The datasets GSE33774 (seven periimplantitis and eight control samples) and GSE106090 (six periimplantitis and six control samples) were included from the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO). A differential expression analysis (p < 0.05 and |logFC (fold change)| ≥ 1) and a functional enrichment analysis (p < 0.05) were performed. Based on this, a protein–protein interaction (PPI) network was constructed by Cytoscape. RA-related genes were extracted from DisGeNET database, and an overlap between periimplantitis-related genes and these RA-related genes was examined to identify potential cross-talk genes. Gene expression was merged between two datasets, and feature selection was performed by Recursive Feature Elimination (RFE) algorithm. For the feature selection cross-talk genes, support vector machine (SVM) models were constructed. The expression of these feature genes was determined from GSE93272 for RA. Finally, a network including cross-talk genes, related pathways, and transcription factors was constructed. Results: Periimplantitis datasets included 138 common differentially expressed genes (DEGs) including 101 up- and 37 downregulated DEGs. The PPI interwork of periimplantitis comprised 1,818 nodes and 2,517 edges. The RFE method selected six features, i.e., MERTK, CD14, MAPT, CCR1, C3AR1, and FCGR2B, which had the highest prediction. Out of these feature genes, CD14 and FCGR2B were most highly expressed in periimplantitis and RA. The final activated pathway–gene network contained 181 nodes and 360 edges. Nuclear factor (NF) kappa B signaling pathway and osteoclast differentiation were identified as potentially relevant pathways. Conclusions: This current study revealed FCGR2B and CD14 as the most relevant potential cross-talk genes between RA and periimplantitis, which suggests a similarity between RA and periimplantitis and can serve as a theoretical basis for future research.

No description available.

No / Most inhibitory signals are mediated via γ-aminobutyric acid (GABA) receptors whereas glutamate receptors mediate most excitatory signals (Trends Neurosci 14:515–519, 1991; Annu Rev Neurosci 17:31–108, 1994). Many factors influence the regulation of excitatory and inhibitory synaptic inputs on a given neuron. One important factor is the subtype of neurotransmitter receptor present not only at the correct location to receive the appropriate signals but also their abundance at synapses (Pharmacol Rev 51: 7–61, 1999; Cold Spring Harb Perspect Biol 3, 2011). GABAB receptors are G-protein-coupled receptors and different subunits dimerise to form a functional receptor. GABAB receptor subunits are widely expressed in the brain and by assembling different isoform combinations and accessory proteins they produce variety of physiological and pharmacological profiles in mediating both inhibitory and excitatory neurotransmission. This chapter will describe the understanding of the molecular mechanisms underlying GABAB receptor regulation of glutamate and GABAA receptors and how they modulate excitatory and inhibitory neurotransmission.

The Thermal Radiation Group, a laboratory in the Department of Mechanical Engineering at Virginia Polytechnic Institute and State University, is currently working to develop a new technology for thermal radiation detectors. The Group is also studying the viability of replacing current Earth Radiation Budget radiometers with this new concept. This next-generation detector consists of a thermopile linear array thermal radiation detector. The principal objective of this research is to develop an optical model for the detector and its cavity. The model based on the Monte-Carlo ray-trace (MCRT) method, permits parametric studies to optimize the design of the detector cavity and the specification of surface optical properties. The model is realized as a FORTRAN program which permits the calculation of quantities related to the cross-talk among pixels of the detector and radiation exchange among surfaces of the cavity. An important capability of the tool is that it provides estimates of the discrete Green's function that permits partial correction for optical cross-talk among pixels of the array. / Master of Science

Les facteurs environnementaux que sont le Bisphénol A (BPA), un perturbateur endocrinien, et le Benzo[a]pyrène (B[a]P), un agent génotoxique, représentent un véritable enjeu parmi les facteurs de risques du cancer du sein associés à l'exposition environnementale. Nos objectifs sont d'explorer l'impact d'une exposition chronique à de faibles doses (10-10 M) de BPA et/ou de B[a]P sur l'agressivité de la lignée cellulaire pré-cancéreuse mammaire MCF10AT1 (immortelle, transformée, ER-, PR-, HER2-). Les buts principaux sont : (i) d'explorer si la combinaison de deux molécules possédant deux mécanismes d'action distincts conduit à un effet potentialisé par rapport à l'exposition aux molécules seules ; (ii) d'identifier et de prévenir les mécanismes moléculaires et cellulaires associés à cette exposition multiple. Nos résultats démontrent que l'exposition chronique des MCF10AT1 à de faibles doses de BPA et/ou de B[a]P induit un phénotype cellulaire agressif de façon temps-dépendant, avec un effet potentialisé pour la combinaison BPA+B[a]P, comparée aux molécules seules. Le phénotype observé est un phénotype acquis, car toujours présent 30 jours post-exposition. Nous avons également déterminé dans les cellules MCF10AT1 la présence et la fonctionnalité de deux récepteurs : le récepteur Aryl hydrocarbon (AhR) liant le B[a]P et le récepteur couplé à la protéine G (GPER1/GPR30) liant le BPA. D'un point de vue mécanistique, ces deux récepteurs sont impliqués dans le phénotype cellulaire agressif BPA et/ou B[a]P-dépendant, et notre travail révèle un nouveau cross-talk fonctionnel entre ces deux récepteurs. L'inhibition in vitro d'AhR et de GPR30 (inhibiteurs chimiques ou siRNA) permet de bloquer les effets délétères de l'exposition chronique au BPA et/ou au B[a]P. Enfin, l'analyse rétrospective de tumeurs primitives du sein ER-négatives démontre que la signature moléculaire GPR30/AhR possède une valeur de mauvais pronostic, alors que l'expression de GPR30 ou d'AhR n'en possède pas. L'ensemble de ces résultats souligne donc le rôle particulier que joue la présence concomitante d'AhR et de GPR30 dans des cellules précancéreuses/cancéreuses mammaires. En conclusion, nos résultats permettent d'identifier des cibles potentielles pour le développement de nouvelles stratégies préventives capables de bloquer la carcinogenèse mammaire due à l'exposition chronique au BPA et/ou B[a]P, et d'envisager des nouveaux biomarqueurs de cette exposition environnementale / Environmental factors such as Bisphenol A (BPA), an endocrine disruptor, and Benzo[a]pyrene (B[a]P), a genotoxic agent, represent a real issue among the environmental risk factors for breast cancer. Our objectives are to investigate the impact of chronic and low doses exposure to BPA (10-10 M) and/or B[a]P on the aggressiveness of the mammary pre-cancerous cell line MCF10AT1 (immortal, transformed, ER-, PR-, HER2-). The main aims are: (i) explore whether an exposure to the combination of two molecules with two distinct mechanisms of action has a greater impact than the molecules tested alone; (ii) identify and prevent the associated molecular and cellular mechanisms. Our results demonstrate that chronic exposure of MCF10AT1 to low doses of BPA and/or B[a]P induces an aggressive cell phenotype in a time-dependent manner, with a greater effect for (BPA + B[a]P) combination compared to single molecules. The observed phenotype is an acquired phenotype, as it still persists 30 days post-exposure. We also determined the presence and functionality of two receptors in the MCF10AT1 cells: the Aryl hydrocarbon receptor (AhR) binding B[a]P and the G binding protein receptor (GPER1 / GPR30) binding BPA. Mechanistically, these two receptors are involved in the BPA and/or B[a]P-induced aggressive phenotype, and our study reveals a new functional cross-talk/interplay between these two receptors. In vitro, the inhibition of AhR and GPR30 (chemical inhibitors or siRNA) can block the deleterious effects of chronic exposure to BPA and/or B[a]P. Finally, a retrospective analysis of primary ER-negatif subclass breast tumors demonstrates that the GPR30/AhR gene expression signature has a poor prognosis value, whereas GPR30 or AhR mRNA levels were poorly informative. All these results underline the particular role played by the concomitant presence of AhR and GPR30 in mammary precancerous/cancerous cells. In conclusion, our results allow us to identify potential targets for the development of new preventive strategies capable of blocking mammary carcinogenesis due to chronic exposure to BPA and/or B[a]P, and to consider new biomarkers for environmental exposure

The Smartphone is a technological innovation that has transformed for the better how billions of people live by enabling them to transcend time and space to remain socially connected to potentially millions of others despite being thousands of miles apart. Although smartphones help people connect from a distance, there has been much concern about how they affect face-to-face interactions. This study explored, drawing on Goffmanian concepts, how and why smartphones affect face-to-face encounters. The findings show there are three types of smartphone cross-talk: exclusive, semi-exclusive, and collaborative. With the addition of smartphone play and solo smartphone activity, interactants can engage in five different types of smartphone use during a social encounter. Smartphones can both disrupt and facilitate face-to-face encounters at any given time. A theory of cross-talk was created as an extension of Goffman’s work to help explain the phenomenon.

<p>The alpha-2 adrenergic receptor (α₂-AR) subfamily includes three different subtypes, α_2A-, α_2B- and α_2C-AR, all believed to exert their function through heterotrimeric G_i/o-proteins. The present study was undertaken in order to investigate subtype differences in terms of cellular response and to explore other potential signalling pathways of α₂-ARs.</p><p>Evidence is provided for a strong G_s-protein coupling capability of the α_2B-AR, leading to stimulation of adenylyl cyclase (AC). The difference between the α_2A- and α_2B-AR subtypes, in this respect, was shown to be due to differences in the second intracellular loops of the receptor proteins. Substitution of the second loop in α_2A-AR with the corresponding domain of α_2B-AR enrolled the chimeric α_2A/α_2B receptor with functional α_2B-AR properties. Dual G_i and G_s coupling can have different consequences for AC output. Using coexpression of receptors and G-proteins, it was shown that the ultimate cellular response of α_2B-AR activation is largely dependent on the ratio of G_i- to G_s-protein amounts in the cell. Also G_i- and G_o-proteins appear to have different regulatory influences on AC. Heterologous expression of AC2 together with G_i or G_o and the α_2A-AR resulted in receptor-mediated inhibition of protein kinase C-stimulated AC2 activity through G_o, whereas activation of G_i potentiated the activity. </p><p>α₂-ARs mobilize Ca²⁺ in response to agonists in some cell types. This response was shown to depend on tonic purinergic receptor activity in transfected CHO cells. Elimination of the tonic receptor activity almost completely inhibited the Ca²⁺ response of α₂-ARs.</p><p>In conclusion, α₂-ARs can couple to multiple G-proteins, including G_i, G_o and G_s. The cellular response to α₂-AR activation depends on which receptor subtype is expressed, which cellular signalling constituents are engaged (G-proteins and effectors), and the signalling status of the effectors (dormant or primed).</p>

The alpha-2 adrenergic receptor (α2-AR) subfamily includes three different subtypes, α2A-, α2B- and α2C-AR, all believed to exert their function through heterotrimeric Gi/o-proteins. The present study was undertaken in order to investigate subtype differences in terms of cellular response and to explore other potential signalling pathways of α2-ARs. Evidence is provided for a strong Gs-protein coupling capability of the α2B-AR, leading to stimulation of adenylyl cyclase (AC). The difference between the α2A- and α2B-AR subtypes, in this respect, was shown to be due to differences in the second intracellular loops of the receptor proteins. Substitution of the second loop in α2A-AR with the corresponding domain of α2B-AR enrolled the chimeric α2A/α2B receptor with functional α2B-AR properties. Dual Gi and Gs coupling can have different consequences for AC output. Using coexpression of receptors and G-proteins, it was shown that the ultimate cellular response of α2B-AR activation is largely dependent on the ratio of Gi- to Gs-protein amounts in the cell. Also Gi- and Go-proteins appear to have different regulatory influences on AC. Heterologous expression of AC2 together with Gi or Go and the α2A-AR resulted in receptor-mediated inhibition of protein kinase C-stimulated AC2 activity through Go, whereas activation of Gi potentiated the activity. α2-ARs mobilize Ca2+ in response to agonists in some cell types. This response was shown to depend on tonic purinergic receptor activity in transfected CHO cells. Elimination of the tonic receptor activity almost completely inhibited the Ca2+ response of α2-ARs. In conclusion, α2-ARs can couple to multiple G-proteins, including Gi, Go and Gs. The cellular response to α2-AR activation depends on which receptor subtype is expressed, which cellular signalling constituents are engaged (G-proteins and effectors), and the signalling status of the effectors (dormant or primed).