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Eun-Sook Park,
Yong Kwang Park,
Chanyoung Shin,
Seung Hwa Park,
Sung Hyun Ahn,
Doo Hyun Kim,
Keo-Heun Lim,
So Young Kwon,
Kwang Pyo Kim, Sung-Il Yang,
Baik L Seong,
Kyun-Hwan Kim
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ABSTRACT: Liver regeneration after liver damage caused by toxins and pathogens is critical for liver homeostasis. Retardation of liver proliferation was reported in hepatitis B virus (HBV) X protein (HBx)-transgenic mice. However, the underlying mechanism of the HBx-mediated disturbance of liver regenerationis unknown.We investigated the molecular mechanismof the inhibition of liver regeneration using liver cell lines and a mouse model. The mouse model of acute HBV infection was established by hydrodynamic injection of viral DNA.Liver regeneration after partial hepatectomy was significantly inhibited in the HBV DNA-treatedmice. Mechanism studies have revealed that the expression of urokinase-type plasminogen activator (uPA), which regulates the activation of hepatocyte growth factor (HGF), was significantly decreased in the liver tissues of HBV or HBx-expressing mice. The down-regulation of uPA was further confirmed using liver cell lines transiently or stably transfected with HBx and the HBV genome. HBx suppresseduPA expression through the epigenetic regulationof the uPA promoter in mice liver tissues and human liver cell lines. Expression of HBx strongly induced hyper-methylation of the uPA promoter byrecruiting DNA methyltransferase (DNMT) 3A2.Conclusions:Taken together,these resultssuggest that infection of HBV impairs liver regeneration throughthe epigenetic dysregulation of liver regeneration signals by HBx. (HEPATOLOGY 2013.).
Hepatology 03/2013; · 11.66 Impact Factor
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Se Jin Jeon,
Seol-Heui Han, Sung-Il Yang,
Ji Woong Choi,
Kyoung Ja Kwon,
Seung Hwa Park,
Hahn Young Kim,
Jae Hoon Cheong,
Jong Hoon Ryu,
Kwang Ho Ko,
David G Wells,
Chan Young Shin
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ABSTRACT: J. Neurochem. (2012) 123, 226-238. ABSTRACT: Fragile X syndrome (FXS), the most common single genetic cause of mental retardation and autistic spectrum disease, occurs when FMR1 gene is mutated. FMR1 encodes fragile X mental retardation protein (FMRP) which regulates translation of mRNAs playing important roles in the development of neurons as well as formation and maintenance of synapses. To examine whether FMRP regulates cell viability, we induced apoptosis in rat primary cortical neurons with glutamate in vitro and with middle cerebral artery occlusion (MCAO) in striatal neurons in vivo. Both conditions elicited a rapid, but transient FMRP expression in neurons. This up-regulated FMRP expression was abolished by pre-treatment with PI3K and Protein Kinase B (Akt) inhibitors: LY294002, Akt inhibitor IV, and VIII. Reduced FMRP expression in vitro or in vivo using small hairpin Fmr1 virus exacerbated cell death by glutamate or MCAO, presumably via hypophosphorylation of Akt and reduced expression of B-cell lymphoma-extra large (Bcl-xL). However, over-expression of FMRP using enhanced green fluorescent protein (eGFP)-FMRP constructs alleviated cell death, increased Akt activity, and enhanced Bcl-xL production. The pro-survival role of Akt-dependent up-regulation of FMRP in glutamate-stimulated cultured neuron as well as in ischemic brain may have a clinical importance in FXS as well as in neurodegenerative disorders and traumatic brain injury.
Journal of Neurochemistry 07/2012; 123(2):226-238. · 4.06 Impact Factor
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Se Jin Jeon,
So Young Rhee,
Jong Hoon Ryu,
Jae Hoon Cheong,
Kyungja Kwon, Sung-Il Yang,
Seung Hwa Park,
Jongmin Lee,
Hahn Young Kim,
Seol-Heui Han,
Kwang Ho Ko,
Chan Young Shin
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ABSTRACT: As a member of neurotrophin family, brain derived neurotrophic factor (BDNF) plays critical roles in neuronal development, differentiation, synaptogenesis, and neural protection from the harmful stimuli. There have been reported that adenosine A2(A) receptor subtype is widely distributed in the brain regions, such as hippocampus, striatum, and cortex. Adenosine A2(A) receptor is colocalized with BDNF in brain regions and the functional interaction between A2(A) receptor stimulation and BDNF action has been suggested. In this study, we investigated the possibility that the activation of A2(A) receptor modulates BDNF production in rat primary cortical neuron. CGS21680, an adenosine A2(A) receptor agonist, induced BDNF expression and release. An antagonist against A2(A) receptor, ZM241385, prevented CGS21680-induced increase in BDNF production. A2(A) receptor stimulation induced the activation of Akt-GSK-3β signaling pathway and the blockade of the signaling pathway with specific inhibitors abolished the increase in BDNF production, possibly via modulation of ERK1/2-CREB pathway. The physiological roles of A2(A) receptor-induced BDNF production was demonstrated by the protection of neurons from the excitotoxicity and increased neurite extension as well as synapse formation from immature and mature neurons. Taken together, activation of A2(A) receptor regulates BDNF production in rat cortical neuron, which provides neuro-protective action.
Neurochemical Research 07/2011; 36(12):2259-69. · 2.24 Impact Factor
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ABSTRACT: Prenatal exposure to valproic acid (VPA) induces neural tube defects and impairment in social behaviors related to autistic spectrum disorder in newborns, which make it a useful animal model of autism. In this study, we compared the effects of different time window of prenatal valproic acid exposure for inducing the altered social behaviors relevant to autism from embryonic day 7 to embryonic day 15 in Sprague-Dawley rats to determine the critical periods for the impairment. Compared to E7, E9.5 and E15 exposure, VPA exposure at E12 showed most significant changes in behaviors over control animals with reduced sociability and social preference. E9.5 exposure to valproic acid showed strong reproductive toxicity including decrease in the number of live birth. In general, exposure at E15 showed only marginal effects on reproduction and social behaviors. Finally, VPA-exposed rats at E12 were more sensitive to electric shock than VPA-exposed rats at any other periods. These results suggested that E12 is the critical period in rats when valproate exposure has prominent effects for inducing the altered social behavior similar to human autistic behavior.
Toxicology Letters 03/2011; 201(2):137-42. · 3.23 Impact Factor
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ABSTRACT: Fragile X syndrome (FXS), the most commonly inherited mental retardation and single gene cause of autistic spectrum disorder, occurs when the Fmr1 gene is mutated. The product of Fmr1, fragile X linked mental retardation protein (FMRP) is widely expressed in HeLa cells, however the roles of FMRP within HeLa cells were not elucidated, yet. Interacting with a diverse range of mRNAs related to cellular survival regulatory signals, understanding the functions of FMRP in cellular context would provide better insights into the role of this interesting protein in FXS. Using HeLa cells treated with etoposide as a model, we tried to determine whether FMRP could play a role in cell survival.
Apoptotic cell death was induced by etoposide treatment on Hela cells. After we transiently modulated FMRP expression (silencing or enhancing) by using molecular biotechnological methods such as small hairpin RNA virus-induced knock down and overexpression using transfection with FMRP expression vectors, cellular viability was measured using propidium iodide staining, TUNEL staining, and FACS analysis along with the level of activation of PI3K-Akt pathway by Western blot. Expression level of FMRP and apoptotic regulator BcL-xL was analyzed by Western blot, RT-PCR and immunocytochemistry.
An increased FMRP expression was measured in etoposide-treated HeLa cells, which was induced by PI3K-Akt activation. Without FMRP expression, cellular defence mechanism via PI3K-Akt-Bcl-xL was weakened and resulted in an augmented cell death by etoposide. In addition, FMRP over-expression lead to the activation of PI3K-Akt signalling pathway as well as increased FMRP and BcL-xL expression, which culminates with the increased cell survival in etoposide-treated HeLa cells.
Taken together, these results suggest that FMRP expression is an essential part of cellular survival mechanisms through the modulation of PI3K, Akt, and Bcl-xL signal pathways.
Journal of Biomedical Science 02/2011; 18:17. · 2.01 Impact Factor
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ABSTRACT: Abstract Background Fragile X syndrome (FXS), the most commonly inherited mental retardation and single gene cause of autistic spectrum disorder, occurs when the Fmr1 gene is mutated. The product of Fmr1, fragile X linked mental retardation protein (FMRP) is widely expressed in HeLa cells, however the roles of FMRP within HeLa cells were not elucidated, yet. Interacting with a diverse range of mRNAs related to cellular survival regulatory signals, understanding the functions of FMRP in cellular context would provide better insights into the role of this interesting protein in FXS. Using HeLa cells treated with etoposide as a model, we tried to determine whether FMRP could play a role in cell survival. Methods Apoptotic cell death was induced by etoposide treatment on Hela cells. After we transiently modulated FMRP expression (silencing or enhancing) by using molecular biotechnological methods such as small hairpin RNA virus-induced knock down and overexpression using transfection with FMRP expression vectors, cellular viability was measured using propidium iodide staining, TUNEL staining, and FACS analysis along with the level of activation of PI3K-Akt pathway by Western blot. Expression level of FMRP and apoptotic regulator BcL-xL was analyzed by Western blot, RT-PCR and immunocytochemistry. Results An increased FMRP expression was measured in etoposide-treated HeLa cells, which was induced by PI3K-Akt activation. Without FMRP expression, cellular defence mechanism via PI3K-Akt-Bcl-xL was weakened and resulted in an augmented cell death by etoposide. In addition, FMRP over-expression lead to the activation of PI3K-Akt signalling pathway as well as increased FMRP and BcL-xL expression, which culminates with the increased cell survival in etoposide-treated HeLa cells. Conclusions Taken together, these results suggest that FMRP expression is an essential part of cellular survival mechanisms through the modulation of PI3K, Akt, and Bcl-xL signal pathways.
Journal of Biomedical Science. 01/2011;
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Keo-Heun Lim,
Kyun-Hwan Kim,
Seong Il Choi,
Eun-Sook Park,
Seung Hwa Park,
Kisun Ryu,
Yong Kwang Park,
So Young Kwon, Sung-Il Yang,
Han Chu Lee,
In-Kyung Sung,
Baik L Seong
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ABSTRACT: Hepatitis B virus (HBV) infection is one of the major causes of hepatocellular carcinoma (HCC) development. Hepatitis B virus X protein (HBx) is known to play a key role in the development of hepatocellular carcinoma (HCC). Several cellular proteins have been reported to be over-expressed in HBV-associated HCC tissues, but their role in the HBV-mediated oncogenesis remains largely unknown. Here, we explored the effect of the over-expressed cellular protein, a ribosomal protein S3a (RPS3a), on the HBx-induced NF-κB signaling as a critical step for HCC development. The enhancement of HBx-induced NF-κB signaling by RPS3a was investigated by its ability to translocate NF-κB (p65) into the nucleus and the knock-down analysis of RPS3a. Notably, further study revealed that the enhancement of NF-κB by RPS3a is mediated by its novel chaperoning activity toward physiological HBx. The over-expression of RPS3a significantly increased the solubility of highly aggregation-prone HBx. This chaperoning function of RPS3a for HBx is closely correlated with the enhanced NF-κB activity by RPS3a. In addition, the mutational study of RPS3a showed that its N-terminal domain (1-50 amino acids) is important for the chaperoning function and interaction with HBx. The results suggest that RPS3a, via extra-ribosomal chaperoning function for HBx, contributes to virally induced oncogenesis by enhancing HBx-induced NF-κB signaling pathway.
PLoS ONE 01/2011; 6(8):e22258. · 4.09 Impact Factor
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ABSTRACT: Akt regulates various cellular processes, including cell growth, survival, and metabolism. Recently, Akt's role in neurite outgrowth has also emerged. We thus aimed to identify neuronal function-related genes that are regulated by Akt.
We performed suppression subtractive hybridization on two previously established PC12 sublines, one of which overexpresses the wild-type (WT) form and the other, the dominant-negative (DN) form of Akt. These sublines respond differently to NGF's neuronal differentiation effect.
A variety of genes was identified and could be classified into several functional groups, one of which was developmental processes. Two genes involved in neuronal differentiation and function were found in this group. v-Maf musculoaponeurotic fibrosarcoma oncogene homolog K (MafK) induces the neuronal differentiation of PC12 cells and immature telencephalon neurons, and synaptotagmin I (SytI) is essential for neurotransmitter release. Another gene, syntenin-1 (Syn-1) was also recognized in the same functional group into which MafK and SytI were classified. Syn-1 has been reported to promote the formation of membrane varicosities in neurons. Quantitative reverse transcription polymerase chain reaction analyses show that the transcript levels of these three genes were lower in PC12 (WT-Akt) cells than in parental PC12 and PC12 (DN-Akt) cells. Furthermore, treatment of PC12 (WT-Akt) cells with an Akt inhibitor resulted in the increase of the expression of these genes and the improvement of neurite outgrowth. These results indicate that dominant-negative or pharmacological inhibition of Akt increases the expression of MafK, SytI, and Syn-1 genes. Using lentiviral shRNA to knock down endogenous Syn-1 expression, we demonstrated that Syn-1 promotes an increase in the numbers of neurites and branches.
Taken together, these results indicate that Akt negatively regulates the expression of MafK, SytI, and Syn-1 genes that all participate in regulating neuronal integrity in some way or another.
Journal of Biomedical Science 03/2010; 17:18. · 2.01 Impact Factor
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ABSTRACT: Abstract
Background
Akt regulates various cellular processes, including cell growth, survival, and metabolism. Recently, Akt's role in neurite outgrowth has also emerged. We thus aimed to identify neuronal function-related genes that are regulated by Akt.
Methods
We performed suppression subtractive hybridization on two previously established PC12 sublines, one of which overexpresses the wild-type (WT) form and the other, the dominant-negative (DN) form of Akt. These sublines respond differently to NGF's neuronal differentiation effect.
Results
A variety of genes was identified and could be classified into several functional groups, one of which was developmental processes. Two genes involved in neuronal differentiation and function were found in this group. v-Maf musculoaponeurotic fibrosarcoma oncogene homolog K (MafK) induces the neuronal differentiation of PC12 cells and immature telencephalon neurons, and synaptotagmin I (SytI) is essential for neurotransmitter release. Another gene, syntenin-1 ( Syn-1 ) was also recognized in the same functional group into which MafK and SytI were classified. Syn-1 has been reported to promote the formation of membrane varicosities in neurons. Quantitative reverse transcription polymerase chain reaction analyses show that the transcript levels of these three genes were lower in PC12 (WT-Akt) cells than in parental PC12 and PC12 (DN-Akt) cells. Furthermore, treatment of PC12 (WT-Akt) cells with an Akt inhibitor resulted in the increase of the expression of these genes and the improvement of neurite outgrowth. These results indicate that dominant-negative or pharmacological inhibition of Akt increases the expression of MafK , SytI , and Syn-1 genes. Using lentiviral shRNA to knock down endogenous Syn-1 expression, we demonstrated that Syn-1 promotes an increase in the numbers of neurites and branches.
Conclusions
Taken together, these results indicate that Akt negatively regulates the expression of MafK , SytI , and Syn-1 genes that all participate in regulating neuronal integrity in some way or another.
Journal of Biomedical Science. 01/2010;
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ABSTRACT: Protease-activated receptors (PARs) play important roles in the regulation of brain function such as neuroinflammation by transmitting the signal from proteolytic enzymes such as thrombin and trypsin. We and others have reported that a member of the family, PAR-2 is activated by trypsin, whose involvement in the neurophysiological process is increasingly evident, and is involved in the neuroinflammatory processes including morphological changes of astrocytes. In this study, we investigated the role of PAR-2 in the production of nitric oxide (NO) in rat primary astrocytes. Treatment of PAR-2 agonist trypsin increased NO production in a dose-dependent manner, which was mediated by the induction of inducible nitric-oxide synthase. The trypsin-mediated production of NO was mimicked by PAR-2 agonist peptide and reduced by either pharmacological PAR-2 antagonist peptide or by siRNA-mediated inhibition of PAR-2 expression, which suggests the critical role of PAR-2 in this process. NO production by PAR-2 was mimicked by PMA, a PKC activator, and was attenuated by Go6976, a protein kinase C (PKC) inhibitor. PAR-2 stimulation activated three subtypes of mitogen-activated protein kinases (MAPKs): extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. NO production by PAR-2 was blocked by inhibition of ERK, p38, and JNK pathways. PAR-2 stimulation also activated nuclear factor-kappaB (NF-kappaB) DNA binding and transcriptional activity as well as IkappaBalpha phosphorylation. Inhibitors of NF-kappaB pathway inhibited PAR-2-mediated NO production. In addition, inhibitors of MAPK pathways prevented transcriptional activation of NF-kappaB reporter constructs. These results suggest that PAR-2 activation-mediated NO production in astrocytes is transduced by the activation of MAPKs followed by NF-kappaB pathways.
Nitric Oxide 07/2009; 21(2):110-9. · 3.55 Impact Factor
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ABSTRACT: Glycogen synthase kinase (GSK)-3beta and extracellular signal-regulated kinase (ERK) regulate several cellular signaling pathways in common, including embryonic development, cell differentiation and apoptosis. In this study, we investigated whether GSK-3beta inhibition is involved in ERK activation, which affects the activation of NF-kappaB and induction of MMP-9 in cultured rat primary astrocytes. Here, we found that GSK-3beta inhibition using GSK-3beta inhibitor TDZD-8 increased the phosphorylation of GSK-3beta at Ser9 site as well as the phosphorylation of ERK1/2 and Akt at Ser473 site. In this condition, GSK-3beta inhibition increased MMP-9 but not MMP-2 activity in a concentration-dependent manner. In RT-PCR analysis, MMP-9 mRNA level was increased by GSK-3beta inhibition in a concentration-dependent manner. MMP-9 promoter reporter activity was similarly increased by GSK-3beta inhibition. Pretreatment of U-0126 (MEK1/2 inhibitor) completely abolished the GSK-3beta inhibition-induced phosphorylation of ERK1/2. U-0126 prevented GSK-3beta inhibition-mediated induction of MMP-9 reporter activity as well as the MMP-9 gene expression. The transcriptional activity of NF-kappaB was significantly increased by GSK-3beta inhibition, which was determined by nuclear translocation of NF-kappaB. Inhibition of ERK1/2 activity by U-0126 also completely blocked the nuclear translocation of NF-kappaB. Transfection of dominant negative plasmid (S9A) of GSK-3beta significantly decreased phosphorylation of ERK, MMP-9 expression and nuclear translocation of NF-kappaB by GSK-3beta inhibition as compared to wild type GSK-3beta. These data suggest that GSK-3beta inhibition mediates ERK1/2 activation followed by NF-kappaB activation, which directly regulates the induction of MMP-9 in rat primary astrocytes.
Brain Research 01/2008; 1186:12-20. · 2.73 Impact Factor
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ABSTRACT: Although ubiquitously expressed, the transcriptional factor CP2 also exhibits some tissue- or stage-specific activation toward certain genes such as globin in red blood cells and interleukin-4 in T helper cells. Because this specificity may be achieved by interaction with other proteins, we screened a peptide display library and identified four consensus motifs in numerous CP2-binding peptides: HXPR, PHL, ASR and PXHXH. Protein-database searching revealed that RE-1 silencing factor (REST), Yin-Yang1 (YY1) and five other proteins have one or two of these CP2-binding motifs. Glutathione S-transferase pull-down and coimmunoprecipitation assays showed that two HXPR motif-containing proteins REST and YY1 indeed were able to bind CP2. Importantly, this binding to CP2 was almost abolished when a double amino acid substitution was made on the HXPR sequence of REST and YY1 proteins. The suppressing effect of YY1 on CP2's transcriptional activity was lost by this point mutation on the HXPR sequence of YY1 and reduced by an HXPR-containing peptide, further supporting the interaction between CP2 and YY1 via the HXPR sequence. Mapping the sites on CP2 for interaction with the four distinct CP2-binding motifs revealed at least three different regions on CP2. This suggests that CP2 recognizes several distinct binding motifs by virtue of employing different regions, thus being able to interact with and regulate many cellular partners.
FEBS Journal 04/2005; 272(5):1265-77. · 3.79 Impact Factor
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ABSTRACT: CP2 is a member of a family of transcription factors that regulate genes involved in events from early development to terminal differentiation. In an effort to understand how it selects its target genes we carried out a database search, and located several CP2 binding motifs in the promoter region of bone morphogenetic protein-4 (BMP4). BMP4 is a key regulator of cell fate and body patterning throughout development. For the CP2 binding motifs in BMP4 promoter region to be relevant in vivo, CP2 and BMP4 should be expressed together. We found that CP2b and CP2c, two potent transcriptional activators, are expressed in a manner similar to BMP4 during osteoblast differentiation of C3H10T1/2 cells. In in vitro assays, the CP2 proteins bound to two CP2 binding motifs (-715 to -676 and -147 to -118) in the BMP4 promoter, and luciferase reporter assays indicated that this binding was essential for transcription of BMP4 during osteoblast differentiation. Taken together, our data indicate that CP2b and CP2c play important roles during bone development by activating BMP4 transcription.
Molecules and Cells 07/2004; 17(3):454-61. · 2.18 Impact Factor
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ABSTRACT: We consider the non-stationary or colored noise estimation by wavelet thresholding method. First, we propose node dependent thresholding for adaptation in colored or non-stationary noise. Next, we suggest a noise estimation method based on spectral entropy using histogram of intensity instead of estimation method based on median absolute deviation (MAD). We use a modified hard thresholding to alleviate time-frequency discontinuities. The proposed methods are evaluated on various noise conditions - white Gaussian noise, car interior noise, F-16 cockpit noise, pink noise, speech babble noise. We compare our proposed methods with the conventional one with level dependent thresholding based on MAD
Acoustics, Speech, and Signal Processing, 2002. Proceedings. (ICASSP '02). IEEE International Conference on; 02/2002
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ABSTRACT: In this paper, the authors propose an adaptive wavelet threshold
for noise cancellation. For this, they use a threshold value which
minimizes Bayesian risk. And using entropy, they part the noisy signal
into an unvoiced signal section and the other signal section is used to
apply each the threshold value for each section. Experimental results
show that proposed algorithm is more efficient
Industrial Electronics, 2001. Proceedings. ISIE 2001. IEEE International Symposium on; 02/2001
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ABSTRACT: In a real environment, additive noise will corrupt input speech for speech recognition. In this paper, the authors propose a noise suppression method on the wavelet packet domain as a front-end pre-processor for robust speech recognition. They focus on the enhancement of the formant characteristic to input speech. Suppose, one has observations y<sub>i</sub>=f(t<sub>i</sub>)+ σ·z<sub>i </sub>, i=0, 1, …, n-1, where f(t<sub>i</sub>) is the speech signal and z<sub>i</sub> is i.i.d. white Gaussian noise (AWGN). And assume that one has an available library L of orthogonal bases, such as wavelet packet bases. Using these assumptions, the authors enhance the formant characteristic as well as SNR by adjusting each node variance from adapted wavelet packet transform (AWPT) tree. Experimental result shows an enhancement of SNR from 3.58 dB to 8.66 dB. Also, phoneme recognition performance is improved more than 6%. It confirms the robustness of proposed noise suppression method against additive white Gaussian noise
Industrial Electronics, 2001. Proceedings. ISIE 2001. IEEE International Symposium on; 02/2001
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ABSTRACT: The speech signal is decomposed through adapted local
trigonometric transforms. The decomposed signal is classified by M
uniform sub-bands for each subinterval. The energy of each sub-band is
used as a speech feature. This feature is applied to vector quantisation
and the hidden Markov model. The new speech feature shows a slightly
better recognition rate than the cepstrum for speaker independent speech
recognition. The new speech feature also shows a lower standard
deviation between speakers than does the cepstrum
Electronics Letters 12/1998; · 0.96 Impact Factor
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ABSTRACT: For speaker-verification, we design a hybrid-recognizer composed
of conventional methods (such as HMM, MLP, and DTW) as pre-recognizer
and pitch-detection method through wavelet transforms as
post-recognizer. Conventional methods have respectively 3 classes of
feature vectors; LSF, cepstrum, and filter bank. The pitch carries
information about speaker identification, which is obtained by wavelet
analysis. Wavelet analysis has advantages over traditional Fourier
methods in analyzing physical situations where a signal contains
discontinuities and sharp spikes, etc. The pitches in speech analysis
are composed of impulses, so that a wavelet transform for detection of
the pitch period can be used. This system can analyze pitch period under
various noisy environments
Time-Frequency and Time-Scale Analysis, 1998. Proceedings of the IEEE-SP International Symposium on; 11/1998
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ABSTRACT: A real-time moving automotive vehicle identification system (AVIS)
has been developed for intelligent vehicle highway systems (IVHS). AVIS
consists of 3 major elements: invisible bar-code material, optical
scanner, and DSP board. The invisible bar-code material reflects only
the specific wavelength light (1500 nm). The optical scanner developed
can read the invisible bar-code data only at the corresponding
wavelength light. The TI TMS320C31 digital signal processing (DSP) board
has been implemented. The DSP board processes the bar-code data obtained
from the optical scanner through the invisible bar-code. The DSP board
operates at 33 MHz with the image processing algorithm which includes
error-detecting and error-correcting capabilities. The system has been
tested and the results show that the AVIS performed successfully. The
AVIS is expected to be applied to the non-stop toll gate and violation
enforcement system
Intelligent Vehicles '95 Symposium., Proceedings of the; 10/1995
