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Assessment of glutamatergic synaptic transmission and plasticity in brain slices: relevance to bioelectronic approaches
Eric H. Chang;Samantha T. Carreiro;Stephen A. Frattini;Patricio T. Huerta
Academic Journal Academic Journal | Bioelectronic Medicine, Vol 5, Iss 1, Pp 1-12 (2019) TCD affiliated users click here for access
Abstract Background Glutamatergic neurons represent the largest neuronal class in the ... more
Assessment of glutamatergic synaptic transmission and plasticity in brain slices: relevance to bioelectronic approaches
Bioelectronic Medicine, Vol 5, Iss 1, Pp 1-12 (2019)
Abstract Background Glutamatergic neurons represent the largest neuronal class in the brain and are responsible for the bulk of excitatory synaptic transmission and plasticity. Abnormalities in glutamatergic neurons are linked to several brain disorders and their modulation represents a potential opportunity for emerging bioelectronic medicine (BEM) approaches. Here, we have used a set of electrophysiological assays to identify the effect of the pyrimidine nucleoside uridine on glutamatergic systems in ex vivo brain slices. An improved understanding of glutamatergic synaptic transmission and plasticity, through this type of examination, is critical to the development of potential neuromodulation strategies. Methods Ex vivo hippocampal slices (400 μm thick) were prepared from mouse brain. We recorded field excitatory postsynaptic potentials (fEPSP) in the CA1’s stratum radiatum by stimulation of the CA3 Schaeffer collateral/commissural axons. Uridine was applied at concentrations (3, 30, 300 μM) representing the physiological range present in brain tissue. Synaptic function was studied with input-output (I-O) functions, as well as paired-pulse facilitation (PPF). Synaptic plasticity was studied by applying tetanic stimulation to induce post-tetanic potentiation (PTP), short-term potentiation (STP) and long-term potentiation (LTP). Additionally, we determined whether uridine affected synaptic responses carried solely by n-methyl-d-aspartate receptors (NMDARs), particularly during the oxygen-glucose deprivation (OGD) paradigm. Results The presence of uridine altered glutamatergic synaptic transmission and plasticity. We found that uridine affected STP and LTP in a concentration-dependent manner. Low-dose uridine (3 μM) had no effect, but higher doses (30 and 300 μM) impaired STP and LTP. Moreover, uridine (300 μM) decreased NMDAR-mediated synaptic responses. Conversely, uridine (at all concentrations tested) had a negligible effect on PPF and basal synaptic transmission, which is mediated primarily by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). In addition, uridine (100 μM) exerted a protective effect when the hippocampal slices were challenged with OGD, a widely used model of cerebral ischemia. Conclusions Using a wide set of electrophysiological assays, we identify that uridine interacts with glutamatergic neurons to alter NMDAR-mediated responses, impair synaptic STP and LTP in a dose-dependent manner, and has a protective effect against OGD insult. This work outlines a strategy to identify deficits in glutamatergic mechanisms for signaling and plasticity that may be critical for targeting these same systems with BEM device-based approaches. To improve the efficacy of potential neuromodulation approaches for treating brain dysfunction, we need to improve our understanding of glutamatergic systems in the brain, including the effects of modulators such as uridine.

Subject terms:

Uridine - Nucleoside - LTP - Synaptic plasticity - Glutamate - NMDA - Medical technology - R855-855.5

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Directory of Open Access Journals
The entity : five centuries of secret Vatican espionage / Eric Frattini
Printed Book | 2010
Available at Santry Stacks (place request) (PB-335-738)
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Santry Stacks (place request) PB-335-738 IN
Holland-Frei Cancer Medicine / Robert C. Bast, Jr., Carlo M. Croce, William N. Hait, Waun Ki Hong, Donald W. Kufe, Martine Piccart-Gebhart, Raphael E. Pollock, Ralph R. Weichselbaum, Hongyang Wang, James F. Holland
e-Books (UK eLD) | 2017

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The Journal of Human Resources Referees Volume 54.
Academic Journal Academic Journal | Journal of Human Resources. Fall2019, Vol. 54 Issue 4, p1182-1187. 6p. TCD affiliated users click here for access
The Journal of Human Resources Referees Volume 54.
Journal of Human Resources. Fall2019, Vol. 54 Issue 4, p1182-1187. 6p.

Subject terms:

Human capital

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Business Source Complete
Usefulness of a multiplying factor in predicting the final number of victims during a mass casualty incident
Olga Maurin;Michel Bignand;Daniel Jost;Stéphane Travers;Stéphane Raclot;Jul...
Electronic Resource Electronic Resource | European journal of emergency medicine, Volume 24:Number 5(2017). TCD affiliated users click here for access
Objective: Whenever a mass casualty incident (MCI) occurs, it is essential to anticipa... more
Usefulness of a multiplying factor in predicting the final number of victims during a mass casualty incident
European journal of emergency medicine, Volume 24:Number 5(2017).
Objective: Whenever a mass casualty incident (MCI) occurs, it is essential to anticipate the final number of victims to dispatch the adequate number of ambulances. In France, the custom is to multiply the initial number of prehospital victims by 2–4 to predict the final number. However, no one has yet validated this multiplying factor (MF) as a predictive tool. We aimed to build a statistical model to predict the final number of victims from their initial count. Methods: We observed retrospectively over 30 years of MCIs triggered in a large urban area. We considered three types of events: explosions, fires, and road traffic accidents. We collected the initial and final numbers of victims, with distinction between deaths, critical victims (T1), and delayed or minimal victims (T2–T3). The MF was calculated for each category of victims according to each type of event. Using a Poisson multivariate regression, we calculated the incidence risk ratio (IRR) of the final number of T1 as a function of the initial deaths and the initial T2–T3 counts, while controlling for potential confounding variables. Results: Sixty-eight MCIs were included. The final number of T1 increased with the initial incidence of deaths [IRR: 1.8 (1.4–2.2)], the initial number of T2–T3 being greater than 12 [IRR: 1.6 (1.3–2.1)], and the presence of one or more explosion [IRR: 1.4 (1.1–1.8)]. Conclusion: The MF seems to be an appealing decision-making tool to anticipate the need for ambulance resources. In explosive MCIs, we recommend multiplying T1 by 1.4 to estimate final count and the need for supplementary advanced life support teams.

Subject terms:

Europe - emergency medical services - mass casualty incident - triage - Emergency medicine - Medical emergencies - Emergency medical services - Emergencies - Emergency Medical Services - Emergency Medicine

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Electronic Legal Deposit
The Entity is a primer in fast-and-shallow writing.
Jones, Arthur
Review Review | National Catholic Reporter. 2/6/2009, Vol. 45 Issue 8, p7a-7a. 2/3p. TCD affiliated users click here for access
The article reviews the book "The Entity: Five Centuries of Secret Vatican Espionage,"... more
The Entity is a primer in fast-and-shallow writing.
National Catholic Reporter. 2/6/2009, Vol. 45 Issue 8, p7a-7a. 2/3p.
The article reviews the book "The Entity: Five Centuries of Secret Vatican Espionage," by Eric Frattini, translated by Dick Cluster.

Subject terms:

ENTITY: Five Centuries of Secret Vatican Espionage, The (Book) - FRATTINI, Eric - NONFICTION - CATHOLIC Church government

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Academic Search Complete

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THE ENTITY: Five Centuries of Secret Vatican Espionage.
Review Review | Kirkus Reviews. 11/15/2008, Vol. 76 Issue 22, p1187-1187. 1/3p. TCD affiliated users click here for access
The article reviews the book "The Entity: Five Centuries of Secret Vatican Espionage,"... more
THE ENTITY: Five Centuries of Secret Vatican Espionage.
Kirkus Reviews. 11/15/2008, Vol. 76 Issue 22, p1187-1187. 1/3p.
The article reviews the book "The Entity: Five Centuries of Secret Vatican Espionage," by Eric Frattini.

Subject terms:

ENTITY: Five Centuries of Secret Vatican Espionage, The (Book) - FRATTINI, Eric - ESPIONAGE - NONFICTION

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Academic Search Complete

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USP18 is a significant driver of memory CD4 T-cell reduced viability caused by type I IFN signaling during primary HIV-1 infection.
Dagenais-Lussier, Xavier;Loucif, Hamza;Cadorel, Hugo;Blumberger, Juliette;I...
Academic Journal Academic Journal | PLoS Pathogens. 10/28/2019, Vol. 15 Issue 10, p1-32. 32p. TCD affiliated users click here for access
The loss of Memory CD4 T-cells (Mem) is a major hallmark of HIV-1 immuno-pathogenesis ... more
USP18 is a significant driver of memory CD4 T-cell reduced viability caused by type I IFN signaling during primary HIV-1 infection.
PLoS Pathogens. 10/28/2019, Vol. 15 Issue 10, p1-32. 32p.
The loss of Memory CD4 T-cells (Mem) is a major hallmark of HIV-1 immuno-pathogenesis and occurs early during the first months of primary infection. A lot of effort has been put into understanding the molecular mechanisms behind this loss, yet they still have not been fully identified. In this study, we unveil the unreported role of USP18 in the deleterious effects of sustained type I IFN signaling on Mem, including HIV-1-specific CD4 T-cells. We find that interfering with IFN-I signaling pathway in infected patients, notably by targeting the interferon-stimulated gene USP18, resulted in reduced PTEN expression similar to those observed in uninfected control donors. We show that AKT activation in response to cytokine treatment, T-cell receptor (TcR) triggering, as well as HIV-1 Gag stimulation was significantly improved in infected patients when PTEN or USP18 were inhibited. Finally, our data demonstrate that higher USP18 in Mem from infected patients prevent proper cell survival and long-lasting maintenance in an AKT-dependent manner. Altogether, we establish a direct role for type I IFN/USP18 signaling in the maintenance of total and virus-specific Mem and provide a new mechanism for the reduced survival of these populations during primary HIV-1 infection. In this study, we expend our knowledge of how type I interferons (IFN-I) leads to memory CD4 T-cell defective survival by unveiling the molecular mechanism behind such impairments, placing USP18 at its center. Our data further deciphers the specific USP18-related mechanism that is responsible for such impairments by implicating AKT inhibition in a PTEN-dependent manner. Our findings also point to a potential use of neutralizing anti-interferon α/β receptor antibodies to rescue the defective memory CD4 T-cell survival during HIV-1 infection, even in HIV-1 specific CD4 T-cell. To conclude, our findings provide the characterization of the molecular pathway leading to disturbances caused by sustained IFN-I signaling which occurs early during primary HIV-1 infection, complementing current knowledge which placed sustained IFN-I signaling as detrimental to the host during this infection. [ABSTRACT FROM AUTHOR]

Subject terms:

INFECTION - INTERFERON receptors - TYPE I interferons - CD8 antigen - MEMORY loss - RECEPTOR antibodies - MEMORY

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Intrinsic Resistance to EGFR-Tyrosine Kinase Inhibitors in EGFR-Mutant Non-Small Cell Lung Cancer: Differences and Similarities with Acquired Resistance.
Santoni-Rugiu, Eric;Melchior, Linea C.;Urbanska, Edyta M.;Jakobsen, Jan N.;...
Academic Journal Academic Journal | Cancers. Jul2019, Vol. 11 Issue 7, p923-923. 1p. TCD affiliated users click here for access
Activating mutations in the epidermal growth factorreceptor gene occur as early cancer... more
Intrinsic Resistance to EGFR-Tyrosine Kinase Inhibitors in EGFR-Mutant Non-Small Cell Lung Cancer: Differences and Similarities with Acquired Resistance.
Cancers. Jul2019, Vol. 11 Issue 7, p923-923. 1p.
Activating mutations in the epidermal growth factorreceptor gene occur as early cancer-driving clonal events in a subset of patients with non-small cell lung cancer (NSCLC) and result in increased sensitivity to EGFR-tyrosine-kinase-inhibitors (EGFR-TKIs). Despite very frequent and often prolonged clinical response to EGFR-TKIs, virtually all advanced EGFR-mutated (EGFRM+) NSCLCs inevitably acquire resistance mechanisms and progress at some point during treatment. Additionally, 20–30% of patients do not respond or respond for a very short time (<3 months) because of intrinsic resistance. While several mechanisms of acquired EGFR-TKI-resistance have been determined by analyzing tumor specimens obtained at disease progression, the factors causing intrinsic TKI-resistance are less understood. However, recent comprehensive molecular-pathological profiling of advanced EGFRM+ NSCLC at baseline has illustrated the co-existence of multiple genetic, phenotypic, and functional mechanisms that may contribute to tumor progression and cause intrinsic TKI-resistance. Several of these mechanisms have been further corroborated by preclinical experiments. Intrinsic resistance can be caused by mechanisms inherent in EGFR or by EGFR-independent processes, including genetic, phenotypic or functional tumor changes. This comprehensive review describes the identified mechanisms connected with intrinsic EGFR-TKI-resistance and differences and similarities with acquired resistance and among clinically implemented EGFR-TKIs of different generations. Additionally, the review highlights the need for extensive pre-treatment molecular profiling of advanced NSCLC for identifying inherently TKI-resistant cases and designing potential combinatorial targeted strategies to treat them. [ABSTRACT FROM AUTHOR]

Subject terms:

LUNG cancer -- Diagnosis - LUNG cancer -- Genetic aspects - PROTEIN-tyrosine kinase inhibitors - DRUG resistance in cancer cells - LUNG cancer - MUTATION (Biology) - TUMOR classification - PHENOTYPES - TREATMENT effectiveness - DISEASE progression - GENE expression profiling - THERAPEUTIC use

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Academic Search Complete
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