GIST-AiTeR Speaker Diarization System for VoxCeleb Speaker Recognition Challenge (VoxSRC) 2023

This report describes the submission system by the GIST-AiTeR team for the VoxCeleb Speaker Recognition Challenge 2023 (VoxSRC-23) Track 4. Our submission system focuses on implementing diverse speaker diarization (SD) techniques, including ResNet293 and MFA-Conformer with different combinations of segment and hop length. Then, those models are combined into an ensemble model. The ResNet293 and MFA-Conformer models exhibited the diarization error rates (DERs) of 3.65% and 3.83% on VAL46, respectively. The submitted ensemble model provided a DER of 3.50% on VAL46, and consequently, it achieved a DER of 4.88% on the VoxSRC-23 test set.Comment: 2023 VoxSRC Track

Symplectic Embedding of a Massive Vector-Tensor Theory with Topological Coupling

In the symplectic Lagrangian framework we newly embed an irreducible massive vector-tensor theory into a gauge invariant system, which has become reducible, by extending the configuration space to include an additional pair of scalar and vector fields, which give the desired Wess-Zumino action. A comparision with the BFT Hamiltonian embedding approach is also done.Comment: LaTeX file, 23 page

Diosgenin Induces Apoptosis in HepG2 Cells through Generation of Reactive Oxygen Species and Mitochondrial Pathway

Diosgenin, a naturally occurring steroid saponin found abundantly in legumes and yams, is a precursor of various synthetic steroidal drugs. Diosgenin is studied for the mechanism of its action in apoptotic pathway in human hepatocellular carcinoma cells. Based on DAPI staining, diosgenin-treated cells manifested nuclear shrinkage, condensation, and fragmentation. Treatment of HepG2 cells with 40 μM diosgenin resulted in activation of the caspase-3, -8, -9 and cleavage of poly-ADP-ribose polymerase (PARP) and the release of cytochrome c. In the upstream, diosgenin increased the expression of Bax, decreased the expression of Bid and Bcl-2, and augmented the Bax/Bcl-2 ratio. Diosgenin-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of JNK, p38 MAPK and apoptosis signal-regulating kinase (ASK)-1, as well as generation of the ROS. NAC administration, a scavenger of ROS, reversed diosgene-induced cell death. These results suggest that diosgenin-induced apoptosis in HepG2 cells through Bcl-2 protein family-mediated mitochndria/caspase-3-dependent pathway. Also, diosgenin strongly generated ROS and this oxidative stress might induce apoptosis through activation of ASK1, which are critical upstream signals for JNK/p38 MAPK activation in HepG2 cancer cells