A Kinase Chaperones Hepatitis B Virus Capsid Assembly and Captures Capsid Dynamics in vitro

The C-terminal domain (CTD) of Hepatitis B virus (HBV) core protein is involved in regulating multiple stages of the HBV lifecycle. CTD phosphorylation correlates with pregenomic-RNA encapsidation during capsid assembly, reverse transcription, and viral transport, although the mechanisms remain unknown. In vitro, purified HBV core protein (Cp183) binds any RNA and assembles aggressively, independent of phosphorylation, to form empty and RNA-filled capsids. We hypothesize that there must be a chaperone that binds the CTD to prevent self-assembly and nonspecific RNA packaging. Here, we show that HBV capsid assembly is stalled by the Serine Arginine protein kinase (SRPK) binding to the CTD, and reactivated by subsequent phosphorylation. Using the SRPK to probe capsids, solution and structural studies showed that SRPK bound to capsid, though the CTD is sequestered on the capsid interior. This result indicates transient CTD externalization and suggests that capsid dynamics could be crucial for directing HBV intracellular trafficking. Our studies illustrate the stochastic nature of virus capsids and demonstrate the appropriation of a host protein by a virus for a non-canonical function

Training strategy for a lightweight countermeasure model for automatic speaker verification

The countermeasure (CM) model is developed to protect Automatic Speaker Verification (ASV) systems from spoof attacks and prevent resulting personal information leakage. Based on practicality and security considerations, the CM model is usually deployed on edge devices, which have more limited computing resources and storage space than cloud-based systems. This work proposes training strategies for a lightweight CM model for ASV, using generalized end-to-end (GE2E) pre-training and adversarial fine-tuning to improve performance, and applying knowledge distillation (KD) to reduce the size of the CM model. In the evaluation phase of the ASVspoof 2021 Logical Access task, the lightweight ResNetSE model reaches min t-DCF 0.2695 and EER 3.54%. Compared to the teacher model, the lightweight student model only uses 22.5% of parameters and 21.1% of multiply and accumulate operands of the teacher model.Comment: ASVspoof202

Energy and nitrogenous waste from glutamate/glutamine catabolism facilitates acute osmotic adjustment in non-neuroectodermal branchial cells

Maintenance of homeostasis is one of the most important physiological responses for animals upon osmotic perturbations. Ionocytes of branchial epithelia are the major cell types responsible for active ion transport, which is mediated by energy-consuming ion pumps (e.g., Na+-K+-ATPase, NKA) and secondary active transporters. Consequently, in addition to osmolyte adjustments, sufficient and immediate energy replenishment is essenttableial for acclimation to osmotic changes. In this study, we propose that glutamate/glutamine catabolism and trans-epithelial transport of nitrogenous waste may aid euryhaline teleosts Japanese medaka (Oryzias latipes) during acclimation to osmotic changes. Glutamate family amino acid contents in gills were increased by hyperosmotic challenge along an acclimation period of 72 hours. This change in amino acids was accompanied by a stimulation of putative glutamate/glutamine transporters (Eaats, Sat) and synthesis enzymes (Gls, Glul) that participate in regulating glutamate/glutamine cycling in branchial epithelia during acclimation to hyperosmotic conditions. In situ hybridization of glutaminase and glutamine synthetase in combination with immunocytochemistry demonstrate a partial colocalization of olgls1a and olgls2 but not olglul with Na+/K+-ATPase-rich ionocytes. Also for the glutamate and glutamine transporters colocalization with ionocytes was found for oleaat1, oleaat3, and olslc38a4, but not oleaat2. Morpholino knock-down of Sat decreased Na+ flux from the larval epithelium, demonstrating the importance of glutamate/glutamine transport in osmotic regulation. In addition to its role as an energy substrate, glutamate deamination produces NH4+, which may contribute to osmolyte production; genes encoding components of the urea production cycle, including carbamoyl phosphate synthetase (CPS) and ornithine transcarbamylase (OTC), were upregulated under hyperosmotic challenges. Based on these findings the present work demonstrates that the glutamate/glutamine cycle and subsequent transepithelial transport of nitrogenous waste in branchial epithelia represents an essential component for the maintenance of ionic homeostasis under a hyperosmotic challenge

Artists in Residence Recital

Program listing performers and works performed

Pancreatic Tail Cancer with Sole Manifestation of Left Flank Pain: A Very Rare Presentation

Pancreatic cancer is sometimes called a “silent disease” because it often causes no symptoms in the early stage. The symptoms can be quite vague and various depending on the location of cancer in the pancreas. The anatomic site distribution is 78% in the head of the pancreas, 11% in the body, and 11% in the tail. Pancreatic cancer is rarely detected in the early stage, and it is very uncommon to diagnose pancreatic tail cancer during an emergency department visit. The manifestation of pancreatic tail cancer as left flank pain is very rare and has seldom been identified in the literature. We present a case of pancreatic tail cancer with the sole manifestation of dull left flank pain. Having negative findings on an ultrasound study initially, this female patient was misdiagnosed as having possible acute gastritis, urolithiasis or muscle strain after she received gastroendoscopy and colonofiberscopy. Her symptoms persisted for several months and she visited our emergency department due to an acute exacerbation of a persistent dull pain in the left flank area. Radiographic evaluation with computed tomography was performed, and pancreatic tail tumor with multiple metastases was found unexpectedly. We review the literature and discuss this rare presentation of pancreatic tail cancer

Acute immune thrombocytopenic purpura in an adolescent with 2009 novel H1N1 influenza A virus infection

AbstractAlthough both leukopenia and thrombocytopenia are not uncommon hematological findings among patients with novel 2009 H1N1 influenza virus infection, immune thrombocytopenic purpura has rarely been shown to be associated with this novel influenza A infection. Here, we describe a previously healthy adolescent who presented with fever, influenza-like symptoms and acute onset of generalized petechiae and active oral mucosa bleeding on the third day of his illness. Severe leukopenia and thrombocytopenia were found. There was neither malignancy nor blast cells found by bone marrow aspiration. Real-time reverse transcriptase polymerase chain reaction was positive for novel 2009 H1N1 influenza infection. Novel influenza-associated atypical immune thrombocytopenic purpura was diagnosed. The patient recovered uneventfully after oseltamivir and methylprednisolone therapy

Regular Black Hole Interior Spacetime Supported by Three-Form Field

In this paper, we show that a minimally coupled 3-form endowed with a proper potential can support a regular black hole interior. By choosing an appropriate form for the metric function representing the radius of the 2-sphere, we solve for the 3-form field and its potential. Using the obtained solution, we construct an interior black hole spacetime which is everywhere regular. The singularity is replaced with a Nariai-type spacetime, whose topology is $\text{dS}_2 \times \text{S}^2$, in which the radius of the 2-sphere is constant. So long as the interior continues to expand indefinitely, the geometry becomes essentially compactified. The 2-dimensional de Sitter geometry appears despite the negative potential of the 3-form field. Such a dynamical compactification could shed some light on the origin of de Sitter geometry of our Universe, exacerbated by the Swampland conjecture. In addition, we show that the spacetime is geodesically complete. The geometry is singularity-free due to the violation of the null energy condition.Comment: 13 pages, 6 figures. Updated to match the published versio