Seamless global connectivity in 6G requires a 3-dimensional network (or 3D network) that unifies terrestrial and non-terrestrial networks (NTN), which encompasses aerial and satellite networks to provide connectivities for a mass number of devices in industrial IoT. Even though computing resources in 3D networks can be used for computation offloading, scheduling communication and computing resources in such a highly dynamic and resource-constrained environment is challenging. This paper addresses the challenge by identifying research questions regarding resource allocation, considering handover dynamics and energy efficiency. Subsequently, we highlight the current status of our studies towards an intelligent scheduling strategy in softwarized 3D networks.
The 14-3-3 family of proteins is genetically linked to several psychiatric disorders, including schizophrenia. Our 14-3-3 functional knockout (FKO) mice, as well as other 14-3-3 knockout models, have been shown to exhibit behavioral endophenotypes related to schizophrenia. While specific forebrain regions, such as the prefrontal cortex (PFC) and hippocampus (HP), have been implicated in schizophrenic pathophysiology, the role of these brain regions in the top-down control of specific schizophrenia-associated behaviors has not been examined. Here, we used an adeno-associated virus (AAV) delivered shRNA to knock down the expression of the 14-3-3-inhibitor transgene, thus selectively restoring the function of 14-3-3 in the forebrain of the 14-3-3 FKO mice, we found that injection of the AAV-shRNA into both the PFC and the HP is necessary to attenuate psychomotor activity of the 14-3-3 FKO mice. Furthermore, we found that acute inhibition of 14-3-3, through the delivery of an AAV expressing the 14-3-3 inhibitor to both the PFC and HP, can trigger psychomotor agitation. Interestingly, when assessing the two brain regions separately, we determined that AAV-mediated expression of the 14-3-3 inhibitor specifically within the HP alone is sufficient to induce several behavioral deficits including hyperactivity, impaired associative learning and memory, and reduced sensorimotor gating. In addition, we show that post-synaptic NMDA receptor levels are regulated by acute 14-3-3 manipulations. Taken together, findings from this study directly link 14-3-3 inhibition in specific forebrain regions to certain schizophrenia-associated endophenotypes.
Data sets for manuscript, "14-3-3 proteins promote synaptic localization of N-methyl d-aspartate receptors (NMDARs) in mouse hippocampal and cortical neurons"
Precise segmentation of wheat spikes from a complex background is necessary for obtaining image-based phenotypic information of wheat traits such as yield estimation and spike morphology. A new instance segmentation method based on a Hybrid Task Cascade model was proposed to solve the wheat spike detection problem with improved detection results. In this study, wheat images were collected from fields where the environment varied both spatially and temporally. Res2Net50 was adopted as a backbone network, combined with multi-scale training, deformable convolutional networks, and Generic ROI Extractor for rich feature learning. The proposed methods were trained and validated, and the average precision (AP) obtained for the bounding box and mask was 0.904 and 0.907, respectively, and the accuracy for wheat spike counting was 99.29%. Comprehensive empirical analyses revealed that our method (Wheat-Net) performed well on challenging field-based datasets with mixed qualities, particularly those with various backgrounds and wheat spike adjacence/occlusion. These results provide evidence for dense wheat spike detection capabilities with masking, which is useful for not only wheat yield estimation but also spike morphology assessments.
The future Tactile Internet with Human in the Loop (TaHiL) [1] enables a perceived real-time interaction between a human and a remote physical or virtual object. Human intention needs to be inferred from data captured by sensors throughout the body and even the brain. Therefore, the prediction can happen already in a machine attached to the human body (or so-called a Body Computing Hub, BCH). This human-machine coaugmentation requires Tactile electronics [2] with extreme requirements, such as ultra-small, stretchable, and ultra-low-energy consumption, allowing for sensing at extremely low latency. However, for a human to interact with a real or virtual object across the globe, tactile electronics require tight integration with softwarised networks [3] , wireline or wireless, with extremely low latency. Such networks can also bring the computing capability to human's proximity, such as a network edge, by leveraging Network Function Virtualization (NFV) and Software-Defined Networking (SDN). Even though critical, the integration between tactile electronics in a body area network (BAN) and external softwarised networks is uncovered in the literature. This paper explores vital connections between tactile electronics and fully softwarised networks, focusing on adapting all layers from electronics to network and application.
The aspect-oriented software architectural weaving mechanism, to integrate aspectual components that encapsulate crosscutting behaviors and features into components and connectors constituting Software Architecture (SA), contributes to analyze and verify overall behaviors and quality attributes of SA. This paper proposes a new kind of weaving process and rules, which offer the measure to transform the unwoven SA model into the woven SA model. The unwoven SA model is described in a special aspect-oriented architecture description language, called AC2-ADL, and specifies the locations, times and constrains of injection. Then a woven SA model only containing components and connectors is acquired after weaving, and easier to analyze and verify.
Abstract Background Alzheimer’s disease (AD) is the memory‐related neurodegenerative disorder, contributing to 70% of the cases globally. Synaptic dysfunction is a well‐known early event that causes progressive cognitive decline in AD. The latest AD therapeutics on the forefront only offer a moderate symptomatic relief with significant off‐target effects. Therefore, understanding the mechanism for AD pathogenesis and developing novel therapeutic targets are urgently needed. Our lab has recently reported an anomalistic increase in phospholipase D isoform 1 (PLD1), that breakdown phospholipids in AD postmortem brain samples, compared to control subjects. Moreover, the effect of elevated PLD1 driven by amyloid‐β and tau deposits has been well‐established in wild type and in 6‐month‐old 3xTg‐AD model mice. In the present study, we assess the novel role of PLD1 in modulating cellular mechanisms involved in synaptic dysfunction in AD. Method Here, we studied the spatial and temporal expression of PLD1 in 3xTg‐AD model mice, treated with a small molecule PLD1 inhibitor (VU0155069), in an age‐dependent manner. Furthermore, the brain‐region specific mechanisms of PLD1 were evaluated by utilizing adeno‐associated viral 2 (AAV2) vectors via intracerebroventricular route in 18‐ and 24‐month‐old wild‐type and 3xTg‐AD model mice. Following VU0155069/AAV2 administration, the mice cohorts were subjected to behavioral studies specific to learning and memory, such as Y‐maze, novel object recognition (NOR), and elevated plus maze. Synaptic dysfunctions were studied using high frequency stimulation long‐term potentiation (HFS‐LTP), by conventional electrophysiology and multi‐electrode array (MEA). Finally, the synaptic strength in frozen synaptosomal (P2) fractions was determined by previously standardized novel in vitro assay called the Fluorescence‐Assisted Single Synaptosome‐Long Term Potentiation (FASS‐LTP). Morphological changes in the synapse were assessed using ImageJ and IMARIS following Golgi‐Cox staining, a gold standard for measuring dendritic spine integrity. To deduce the underlying mechanisms, we used brain spheroids developed from human tissue to test the effects of PLD1 inhibition. Result In WT aged mice we noted differential effects of PLD1 over expression and attenuation. Additionally, we corroborate our results with diseased aging seen in 3xTg‐AD using pharmacological and molecular approaches with AAV2 vectors. Conclusion Our research provides a novel insight into how PLD1 contributes to progressive functional deficits associated with synaptic dysfunction by impinging on critical cellular signaling events compromised in early and late stages of Alzheimer’s disease.
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