USING RAINBOW TROUT CELL LINES AS A MODEL FOR UNDERSTANDING THE INNATE ANTI-FV3 IMMUNE RESPONSE

Ranavirus infections are on the rise and have been implicated in numerous species die-offs across the globe. Frog virus 3 (FV3) is the type-species of the genus, yet the immune mechanisms governing susceptibility remain poorly understood. Arguably the most important immune response to infection is the type I interferon (IFN) response. Type I IFNs trigger an “antiviral state” in host cells via the production of numerous interferon-stimulated genes (ISGs) that act to inhibit virus replication in various way, including the induction of apoptosis. Apoptosis is an important antiviral defense mechanism to limit virus replication within infected cells. This study employed the use of two rainbow trout cell lines, RTgutGC (intestinal origin) and RTG-2 (gonadal origin), previously shown to differ in susceptibility to FV3, thereby providing an excellent model to study innate anti-FV3 immune responses. Time-lapse infection videos and cell viability assays were used to quantify differences in the extent of cell death over time. RTG-2 exhibited greater cell death at a lower virus titre, compared with RTgutGC. The mechanism of cell death was investigated via DAPI staining and DNA laddering to observe nuclear condensation and intranucleosomal fragmentation, respectively, both hallmarks of apoptosis. Both cells underwent apoptosis in response to FV3. Moreover, UV-inactivated FV3 exhibited similar apoptotic cell death, suggesting that FV3-induced apoptosis is independent of productive virus replication. Likewise, poly I:C induction of IFN and ISGs inhibited virus replication, but had no effect on FV3-induced cell death. Using real-time RT-PCR IFN, ISG, and viral transcript expression was examined in both cell lines. Surprisingly FV3 elicited an equally poor IFN and ISG response in both cell lines, and was only detectable at 72h post-infection. Even when UV-inactivated, FV3 did not elicit a significant IFN response. However, viral transcript expression appears to be greater in the highly susceptible RTG-2 cell line. Further investigation into this difference in susceptibility between cell lines revealed that RTG-2 exhibited greater viral entry and cellular metabolism, which may account for the enhanced level of infection. Thus, FV3 appears to exhibit virulence factors that are independent of replication, yet the mechanisms governing susceptibility appear to be the result of intrinsic cellular features that are IFN-independent

Dual separable feedback systems govern firing rate homeostasis.

Firing rate homeostasis (FRH) stabilizes neural activity. A pervasive and intuitive theory argues that a single variable, calcium, is detected and stabilized through regulatory feedback. A prediction is that ion channel gene mutations with equivalent effects on neuronal excitability should invoke the same homeostatic response. In agreement, we demonstrate robust FRH following either elimination of Kv4/Shal protein or elimination of the Kv4/Shal conductance. However, the underlying homeostatic signaling mechanisms are distinct. Eliminating Shal protein invokes Krüppel-dependent rebalancing of ion channel gene expression including enhanced slo, Shab, and Shaker. By contrast, expression of these genes remains unchanged in animals harboring a CRISPR-engineered, Shal pore-blocking mutation where compensation is achieved by enhanced IKDR. These different homeostatic processes have distinct effects on homeostatic synaptic plasticity and animal behavior. We propose that FRH includes mechanisms of proteostatic feedback that act in parallel with activity-driven feedback, with implications for the pathophysiology of human channelopathies

Unlocking the UK continental shelf electrification potential for offshore oil and gas installations: a power grid architecture perspective

Most of the UK Continental Shelf (UKCS) oil and gas (OG) installations have traditionally adopted in situ power generation, which is not only inefficient but also generating about 70% of the offshore CO2 emissions. The offshore wind and energy storage technologies for deep water are developing at a fast pace, enabling great opportunities for the OG installations located in the North Sea. In this paper, a pathway for the UKCS offshore OG installations electrification is introduced. The aim is to provide different power architectures that facilitate the OG installations' electrification, while benefiting from the existing and planned UK offshore wind power. Four hypothetical case studies (based on real data) were created, along the UKCS, where the corresponding power architectures were proposed. The selection of each architecture power component (e.g., transformers, converters and cables), as well as the transmission and distribution technology (e.g., AC or DC), is also provided and justified. Further, an overview cost estimation is carried out to predict the architecture capital cost. It is concluded that the four architectures can be mimicked not only along the UKCS but also worldwide, promoting the UKCS potential for a world-leading offshore energy hub and fostering the UK offshore wind-energy resources

HySenS data exploitation for urban land cover analysis

This paper addresses the use of HySenS airborne hyperspectral data for environmental urban monitoring. It is known that hyperspectral data can help to characterize some of the relations between soil composition, vegetation characteristics, and natural/artificial materials in urbanized areas. During the project we collected DAIS and ROSIS data over the urban test area of Pavia, Northern Italy, though due to a late delivery of ROSIS data only DAIS data was used in this work. Here we show results referring to an accurate characterization and classification of land cover/use, using different supervised approaches, exploiting spectral as well as spatial information. We demonstrate the possibility to extract from the hyperspectral data information which is very useful for environmental characterization of urban areas

A meta-analytic investigation of the role of reward on inhibitory control

Contemporary theories predict that Inhibitory Control (IC) can be improved when rewards are available for successfully inhibiting. In non-clinical samples empirical research has demonstrated some support, however 'null' findings have also been published. The aim of this meta-analysis was to clarify the magnitude of the effect of reward on IC, and identify potential moderators. Seventy-three articles (contributing k = 80 studies) were identified from Pubmed, PsychInfo and Scopus, published between 1997 - 2020, using a systematic search strategy. A random effects meta-analysis was performed on effect sizes generated from IC tasks which included rewarded and non-rewarded inhibition trials. Moderator analyses were conducted on clinical samples (vs 'healthy controls'), task type (Go/No-Go vs Stop Signal vs Flanker vs Simon vs Stroop vs Anti-Saccade), reward type (monetary vs points vs other), and age (adults vs children). The prospect of reward for successful inhibition significantly improved IC (SMD=0.429 (95% CI= 0.288, 0.570), I2=96.7%), compared to no reward conditions/groups. This finding was robust against influential cases and outliers. The significant effect was present across all IC tasks. There was no evidence the effect was moderated by type of reward, age or clinical samples. Moderator analyses did not resolve considerable heterogeneity. Findings suggest that IC is a transient state that fluctuates in response to motivations driven by reward. Future research might examine the potential of improving inhibitory control through rewards as a behavioural intervention