Conversation-oriented ASR with multi-look-ahead CBS architecture

During conversations, humans are capable of inferring the intention of the speaker at any point of the speech to prepare the following action promptly. Such ability is also the key for conversational systems to achieve rhythmic and natural conversation. To perform this, the automatic speech recognition (ASR) used for transcribing the speech in real-time must achieve high accuracy without delay. In streaming ASR, high accuracy is assured by attending to look-ahead frames, which leads to delay increments. To tackle this trade-off issue, we propose a multiple latency streaming ASR to achieve high accuracy with zero look-ahead. The proposed system contains two encoders that operate in parallel, where a primary encoder generates accurate outputs utilizing look-ahead frames, and the auxiliary encoder recognizes the look-ahead portion of the primary encoder without look-ahead. The proposed system is constructed based on contextual block streaming (CBS) architecture, which leverages block processing and has a high affinity for the multiple latency architecture. Various methods are also studied for architecting the system, including shifting the network to perform as different encoders; as well as generating both encoders' outputs in one encoding pass.Comment: Submitted to ICASSP202

Transcriptional Repression of Cdc25B by IER5 Inhibits the Proliferation of Leukemic Progenitor Cells through NF-YB and p300 in Acute Myeloid Leukemia

The immediately-early response gene 5 (IER5) has been reported to be induced by γ-ray irradiation and to play a role in the induction of cell death caused by radiation. We previously identified IER5 as one of the 2,3,4-tribromo-3-methyl-1-phenylphospholane 1-oxide (TMPP)-induced transcriptional responses in AML cells, using microarrays that encompassed the entire human genome. However, the biochemical pathway and mechanisms of IER5 function in regulation of the cell cycle remain unclear. In this study, we investigated the involvement of IER5 in the cell cycle and in cell proliferation of acute myeloid leukemia (AML) cells. We found that the over-expression of IER5 in AML cell lines and in AML-derived ALDHhi (High Aldehyde Dehydrogenase activity)/CD34+ cells inhibited their proliferation compared to control cells, through induction of G2/M cell cycle arrest and a decrease in Cdc25B expression. Moreover, the over-expression of IER5 reduced colony formation of AML-derived ALDHhi/CD34+ cells due to a decrease in Cdc25B expression. In addition, over-expression of Cdc25B restored TMPP inhibitory effects on colony formation in IER5-suppressed AML-derived ALDHhi/CD34+ cells. Furthermore, the IER5 reduced Cdc25B mRNA expression through direct binding to Cdc25B promoter and mediated its transcriptional attenuation through NF-YB and p300 transcriptinal factors. In summary, we found that transcriptional repression mediated by IER5 regulates Cdc25B expression levels via the release of NF-YB and p300 in AML-derived ALDHhi/CD34+ cells, resulting in inhibition of AML progenitor cell proliferation through modulation of cell cycle. Thus, the induction of IER5 expression represents an attractive target for AML therapy