937 research outputs found
Variational Speech Waveform Compression to Catalyze Semantic Communications
We propose a novel neural waveform compression method to catalyze emerging
speech semantic communications. By introducing nonlinear transform and
variational modeling, we effectively capture the dependencies within speech
frames and estimate the probabilistic distribution of the speech feature more
accurately, giving rise to better compression performance. In particular, the
speech signals are analyzed and synthesized by a pair of nonlinear transforms,
yielding latent features. An entropy model with hyperprior is built to capture
the probabilistic distribution of latent features, followed with quantization
and entropy coding. The proposed waveform codec can be optimized flexibly
towards arbitrary rate, and the other appealing feature is that it can be
easily optimized for any differentiable loss function, including perceptual
loss used in semantic communications. To further improve the fidelity, we
incorporate residual coding to mitigate the degradation arising from
quantization distortion at the latent space. Results indicate that achieving
the same performance, the proposed method saves up to 27% coding rate than
widely used adaptive multi-rate wideband (AMR-WB) codec as well as emerging
neural waveform coding methods
Wireless Deep Speech Semantic Transmission
In this paper, we propose a new class of high-efficiency semantic coded
transmission methods for end-to-end speech transmission over wireless channels.
We name the whole system as deep speech semantic transmission (DSST).
Specifically, we introduce a nonlinear transform to map the speech source to
semantic latent space and feed semantic features into source-channel encoder to
generate the channel-input sequence. Guided by the variational modeling idea,
we build an entropy model on the latent space to estimate the importance
diversity among semantic feature embeddings. Accordingly, these semantic
features of different importance can be allocated with different coding rates
reasonably, which maximizes the system coding gain. Furthermore, we introduce a
channel signal-to-noise ratio (SNR) adaptation mechanism such that a single
model can be applied over various channel states. The end-to-end optimization
of our model leads to a flexible rate-distortion (RD) trade-off, supporting
versatile wireless speech semantic transmission. Experimental results verify
that our DSST system clearly outperforms current engineered speech transmission
systems on both objective and subjective metrics. Compared with existing neural
speech semantic transmission methods, our model saves up to 75% of channel
bandwidth costs when achieving the same quality. An intuitive comparison of
audio demos can be found at https://ximoo123.github.io/DSST
Pulmonary embolism after cesarean section and successful treatment with early application of extracorporeal membrane oxygenation system and anticoagulant agents
Chromosomal imbalances in nasopharyngeal carcinoma: a meta-analysis of comparative genomic hybridization results
Nasopharyngeal carcinoma (NPC) is a highly prevalent disease in Southeast Asia and its prevalence is clearly affected by genetic background. Various theories have been suggested for its high incidence in this geographical region but to these days no conclusive explanation has been identified. Chromosomal imbalances identifiable through comparative genomic hybridization may shed some light on common genetic alterations that may be of relevance to the onset and progression of NPC. Review of the literature, however, reveals contradictory results among reported findings possibly related to factors associated with patient selection, stage of disease, differences in methodological details etc. To increase the power of the analysis and attempt to identify commonalities among the reported findings, we performed a meta-analysis of results described in NPC tissues based on chromosomal comparative genomic hybridization (CGH). This meta-analysis revealed consistent patters in chromosomal abnormalities that appeared to cluster in specific "hot spots" along the genome following a stage-dependent progression
Population phylogenomic analysis of mitochondrial DNA in wild boars and domestic pigs revealed multiple domestication events in East Asia
A fine-grained mitochondrial DNA phylogenomic analysis was conducted in domestic pigs and wild boars, revealing that pig domestication in East Asia occurred in the Mekong and the middle and downstream regions of the Yangtze river
Lentivirus-mediated RNA interference targeting the H19 gene inhibits cell proliferation and apoptosis in human choriocarcinoma cell line JAR
BACKGROUND: H19 is a paternally imprinted gene that has been shown to be highly expressed in the trophoblast tissue. Results from previous studies have initiated a debate as to whether noncoding RNA H19 acts as a tumor suppressor or as a tumor promotor in trophoblast tissue. In the present study, we developed lentiviral vectors expressing H19-specific small interfering RNA (siRNA) to specifically block the expression of H19 in the human choriocarcinoma cell line JAR. Using this approach, we investigated the impact of the H19 gene on the proliferation, invasion and apoptosis of JAR cells. Moreover, we examined the effect of H19 knockdown on the expression of insulin-like growth factor 2 (IGF2), hairy and enhancer of split homologue-1 (HES-1) and dual-specific phosphatase 5 (DUSP5) genes. RESULTS: H19 knockdown inhibited apoptosis and proliferation of JAR cells, but had no significant impact on cell invasion. In addition, H19 knockdown resulted in significant upregulation of HES-1 and DUSP5 expression, but not IGF2 expression in JAR cells. CONCLUSIONS: The finding that H19 downregulation could simultaneously inhibit proliferation and apoptosis of JAR cells highlights a putative dual function for H19 in choriocarcinoma and may explain the debate on whether H19 acts as a tumor suppressor or a tumor promotor in trophoblast tissue. Furthermore, upregulation of HES-1 and DUSP5 may mediate H19 downregulation-induced suppression of proliferation and apoptosis of JAR cells
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