Deep Learning the Effects of Photon Sensors on the Event Reconstruction Performance in an Antineutrino Detector

We provide a fast approach incorporating the usage of deep learning for evaluating the effects of photon sensors in an antineutrino detector on the event reconstruction performance therein. This work is an attempt to harness the power of deep learning for detector designing and upgrade planning. Using the Daya Bay detector as a benchmark case and the vertex reconstruction performance as the objective for the deep neural network, we find that the photomultiplier tubes (PMTs) have different relative importance to the vertex reconstruction. More importantly, the vertex position resolutions for the Daya Bay detector follow approximately a multi-exponential relationship with respect to the number of PMTs and hence, the coverage. This could also assist in deciding on the merits of installing additional PMTs for future detector plans. The approach could easily be used with other objectives in place of vertex reconstruction

The association between S100A13 and HMGA1 in the modulation of thyroid cancer proliferation and invasion

Additional file 5: Figure S3. Lentivirus-mediated S100A13 knockdown was utilized to detect the effect on migration capability with scratch-wound assays in TPC1 cell

Induction and Suppression of Innate Antiviral Responses by Hepatitis A Virus

Hepatitis A virus (HAV) belongs to the family Picornaviridae. It is the pathogen of acute viral hepatitis caused by fecal-oral transmission. RNA viruses are sensed by pathogen-associated pattern recognition receptors (PRRs) such as Toll-like receptor 3 (TLR3), retinoic acid-inducible gene I (RIG-I), and melanoma differentiation-associated gene 5 (MDA5). PRR activation leads to production of type 1 interferon (IFN-α/β), serving as the first line of defense against viruses. However, HAV has developed various strategies to compromise the innate immune system and promote viral propagation within the host cells. The long coevolution of HAV in hosts has prompted the development of effective immune antagonism strategies that actively fight against host antiviral responses. Proteases encoded by HAV can cleave the mitochondrial antiviral signaling protein (MAVS, also known as IPS-1, VISA, or Cardif), TIR domain- containing adaptor inducing IFN-β (TRIF, also known as TICAM-1) and nuclear factor-κB (NF-κB) essential modulator (NEMO), which are key adaptor proteins in RIG-I-like receptor (RLR), TLR3 and NF-κB signaling, respectively. In this mini-review, we summarize all the recent progress on the interaction between HAV and the host, especially focusing on how HAV abrogates the antiviral effects of the innate immune system