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AN ADAPTIVE MULTIRESOLUTION SPEECH ENHANCEMENT ALGORITHM BASED ON WAVELET TRANSFORM
基于小波变换的自适应多分辨率语音增强算法
Zheng Yuanjin,Li Lemin,Wen Maosheng,
郑元谨,李乐民,闻懋生
电子与信息学报 , 1998,
Abstract: In this paper, an adaptive multiresolution speech enhancement algorithm based on wavelet transform is put forward. It can make adaptive filtering to noise speech both at scales and among scales. So that the noise parts during the frequency intervals which decrease hearing quality mostly are reduced efficiently. Both the SNR and subject hearing quality of denoised speech are high and good.
Minimax Curve Fitting Method in Application of C-D Production Function—With the Grain Yield Data in China as the Example
Lemin Gu
Journal of Modern Agriculture , 2013,
Abstract: In the article, Minimax method of curve fitting under the principle of Chebyshev optimal approximation has been introduced; and C-D mathematical model under the principle of Cobb-Dauglas production function model is described. From the data processing perspective, five major factors that affect the grain products: (1) Consumption of chemical fertilizer; (2) Total sown area; (3) Areas affected; (4) Total agricultural machinery power; (5) the relationship between the total employed persons of primary industry and domestic grain products, carry on the fitting under the optimal approximation principle to the C-D mathematical model, and process the data above during the years of 1983-2011 in China. This new combination of optimal approximation result shows that the maximum absolute error of the description during 29 years on our country grain products does not surpass 986 ten thousand tons, and the maximum relative error of which is less than 2.1%. In this foundation, the explanation and the analysis of the data has been explained. Data analysis showed that Maximum error minimization can explain "the maximum risk minimization principle", as well constitutes the greatest possible range of grain security; and during 29 years from 1983 to 2011, China's grain yield growth mainly depends on the Consumption of chemical fertilizer and the Total Agricultural Machinery Power, where the Consumption of chemical fertilizer has a "positive" effects, while the Total Agricultural Machinery Power tends to dynamically saturated and belongs to theoretically "negative " i and does not constitute actual negative effects; in addition, the Total sown area is the largest of the "positive" effects, and the grain yield still may grow under the condition of the Total sown area does not increase, but the increase in the grain sown area will promote our country's grain yield rapidly; the Areas affected is "negative" impact factors of grain growth, whose absolute value is increased but the relative value in reduction. Along with the development of agriculture modernization , the Total employed persons of primary industry for grain growth influence has changed from "positive" to "negative" with limited influential degree, demonstrating its potential for development and improvement.
Insufficient Radiofrequency Ablation Promotes Angiogenesis of Residual Hepatocellular Carcinoma via HIF-1α/VEGFA
Jian Kong, Jinge Kong, Bing Pan, Shan Ke, Shuying Dong, Xiuli Li, Aimin Zhou, Lemin Zheng, Wen-bing Sun
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037266
Abstract: Background The mechanism of rapid growth of the residual tumor after radiofrequency (RF) ablation is poorly understood. In this study, we investigated the effect of hyperthermia on HepG2 cells and generated a subline with enhanced viability and dys-regulated angiogenesis in vivo, which was used as a model to further determine the molecular mechanism of the rapid growth of residual HCC after RF ablation. Methodology/Principal Findings Heat treatment was used to establish sublines of HepG2 cells. A subline (HepG2 k) with a relatively higher viability and significant heat tolerance was selected. The cellular protein levels of VEGFA, HIF-1α and p-Akt, VEGFA mRNA and secreted VEGFA were measured, and all of these were up-regulated in this subline compared to parental HepG2 cells. HIF-1α inhibitor YC-1 and VEGFA siRNA inhibited the high viability of the subline. The conditioned media from the subline exerted stronger pro-angiogenic effects. Bevacizumab, VEGFA siRNA and YC-1 inhibited proangiogenic effects of the conditioned media of HepG2 k cells and abolished the difference between parental HepG2 cells and HepG2 k cells. For in vivo studies, a nude mouse model was used, and the efficacy of bavacizumab was determined. HepG2 k tumor had stronger pro-angiogenic effects than parental HepG2 tumor. Bevacizumab could inhibit the tumor growth and angiogenesis, and also eliminate the difference in tumor growth and angiogenesis between parental HepG2 tumor and HepG2 k tumor in vivo. Conclusions/Significance The angiogenesis induced by HIF1α/VEGFA produced by altered cells after hyperthermia treatment may play an important role in the rapid growth of residual HCC after RF ablation. Bevacizumab may be a good candidate drug for preventing and treating the process.
High-density lipoprotein of patients with Type 2 Diabetes Mellitus upregulates cyclooxgenase-2 expression and prostacyclin I-2 release in endothelial cells: relationship with HDL-associated sphingosine-1-phosphate
Xunliang Tong, Hui Peng, Donghui Liu, Liang Ji, Chenguang Niu, Jun Ren, Bing Pan, Jianying Hu, Lemin Zheng, Yining Huang
Cardiovascular Diabetology , 2013, DOI: 10.1186/1475-2840-12-27
Abstract: Subjects with T2DM with or without proved large arteries atherosclerosis and normal controls (n=15 for each group) were recruited in the present study. HDL was isolated from the subjects by ultracentrifugation. The levels of HDL-associated S1P were determined by UPLC-MS/MS. The protective function of diabetic HDL and S1P was evaluated by measuring cyclooxygenase-2 (COX-2) expression and prostacyclin I-2 (PGI-2) release by human umbilical vein endothelial cells (HUVECs) using western blot and enzyme-linked immunosorbent assay (ELISA), respectively.The S1P levels in isolated HDL were significantly increased in T2DM subjects compared with controls (235.6 +/- 13.4 vs 195.0 +/- 6.4 ng/mg, P< 0.05). The diabetic HDL exerted greater protective effects on inducing COX-2 expression and PGI-2 release by HUVECs than those of control HDL (p < 0.05, p < 0.01, respectively). Pertussis toxin, a common inhibitor of G-couple protein receptors, and VPC 23019, an antagonist of S1P receptor 1 and 3 significantly attenuated HDL-induced COX-2 expression and PGI-2 release.Diabetic HDL carries higher level of S1P compared with normal HDL, which has the potential to contribute to protective effects on endothelial cells by inducing COX-2 expression and PGI-2 release. These findings provide a new insight of S1P function in T2DM patients, possibly leading to a new therapeutic target.
COMP-prohibitin 2 interaction maintains mitochondrial homeostasis and controls smooth muscle cell identity
Changtao Jiang,Chenfeng Mao,Fang Yu,Lemin Zheng,Meili Wang,Ming Zheng,Qingbo Xu,Qinghua Hu,Rui Xiao,Wei Kong,Yi Fu,Yingbao Wang,Yiting Jia
- , 2018, DOI: 10.1038/s41419-018-0703-x
Abstract: a Subcellular localization of COMP as demonstrated by confocal fluorescence microscopy. Mito-Tracker, TGN46 and ERp5 were used to indicate the mitochondria, Golgi complex and endoplasmic reticulum, respectively. Colocalization was evaluated on basis of the Pearson’s correlation coefficient and Manders’ overlap coefficient from 20–30 cells in 4 independent studies\. Scale bar？=？5？μm. b Cell fractionation prior to the western blot analysis of COMP expression. Tubulin and AIF were used as cytoplasmic and mitochondrial markers, respectively. c Mitochondria isolated from rat VSMCs were subjected to subfractionation prior to the identification of COMP by western blot. Tom40 and Cox1 were used as markers for the mitochondrial outer and inner membranes, respectively. Cytochrome c is a dynamic component of mitochondria and is present in both the inner membrane and intermembrane space. d Sequence of mitochondrial and non-mitochondrial cytoplasmic COMP. The potential common N-terminus of mitochondrial COMP and non-mitochondrial cytoplasmic COMP is in bold red. e The MS/MS spectrum of the peptide (GQIPLGGDLAPQMLR) that matches the N-terminal sequence of non-mitochondrial cytoplasmic and mitochondrial COMP. M mitochondria, ER endoplasmic reticulum, G golgi complex, C cytoplasm, M mitochondria, OMM outer mitochondrial membrane, IMS intermembrane space, IMM inner mitochondrial membrane, Matrix mitochondrial matri
Human Surfactant Protein A2 Gene Mutations Impair Dimmer/Trimer Assembly Leading to Deficiency in Protein Sialylation and Secretion
Yi Song, Guodong Fang, Haitao Shen, Hui Li, Wenbing Yang, Bing Pan, Guowei Huang, Guangyu Lin, Lian Ma, Belinda Willard, Jiang Gu, Lemin Zheng, Yongyu Wang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0046559
Abstract: Surfactant protein A2 (SP-A2) plays an essential role in surfactant metabolism and lung host defense. SP-A2 mutations in the carbohydrate recognition domain have been related to familial pulmonary fibrosis and can lead to a recombinant protein secretion deficiency in vitro. In this study, we explored the molecular mechanism of protein secretion deficiency and the subsequent biological effects in CHO-K1 cells expressing both wild-type and several different mutant forms of SP-A2. We demonstrate that the SP-A2 G231V and F198S mutants impair the formation of dimmer/trimer SP-A2 which contributes to the protein secretion defect. A deficiency in sialylation, but not N-linked glycosylation, is critical to the observed dimmer/trimer impairment-induced secretion defect. Furthermore, both mutant forms accumulate in the ER and form NP-40-insoluble aggregates. In addition, the soluble mutant SP-A2 could be partially degraded through the proteasome pathway but not the lysosome or autophagy pathway. Intriguingly, 4-phenylbutyrate acid (4-PBA), a chemical chaperone, alleviates aggregate formation and partially rescued the protein secretion of SP-A2 mutants. In conclusion, SP-A2 G231V and F198S mutants impair the dimmer/trimer assembly, which contributes to the protein sialylation and secretion deficiency. The intracellular protein mutants could be partially degraded through the proteasome pathway and also formed aggregates. The treatment of the cells with 4-PBA resulted in reduced aggregation and rescued the secretion of mutant SP-A2.
Trimethylamine‐N‐oxide promotes brain aging and cognitive impairment in mice
Aiping Zeng,Bing Pan,Changjie Liu,Huashan Hong,Lemin Zheng,Liang Ji,Mingming Zhao,Rui Zhan,Si Cheng,Xiaoyun Shi,Yilang Ke
- , 2018, DOI: 10.1111/acel.12768
Abstract:
Elevated Neurosteroids in the Lateral Thalamus Relieve Neuropathic Pain in Rats with Spared Nerve Injury
Feng-Yu Liu,Honghai Wu,Jia Liu,Lemin Zheng,Meng Zhang,Meng-Meng Zhou,Ming Yi,Yanning Hou,You Wan,Yun-Feng Li,Yuxin Yin
- , 2016, DOI: 10.1007/s12264-016-0044-7
Abstract: Mass spectrometry parameters for target neurosteroids
Diabetic HDL Is Dysfunctional in Stimulating Endothelial Cell Migration and Proliferation Due to Down Regulation of SR-BI Expression
Bing Pan, Yijing Ma, Hui Ren, Yubin He, Yongyu Wang, Xiaofeng Lv, Donghui Liu, Liang Ji, Baoqi Yu, Yuhui Wang, Y. Eugene Chen, Subramaniam Pennathur, Jonathan D. Smith, George Liu, Lemin Zheng
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0048530
Abstract: Background Diabetic HDL had diminished capacity to stimulate endothelial cell (EC) proliferation, migration, and adhesion to extracellular matrix. The mechanism of such dysfunction is poorly understood and we therefore sought to determine the mechanistic features of diabetic HDL dysfunction. Methodology/Principal Findings We found that the dysfunction of diabetic HDL on human umbilical vein endothelial cells (HUVECs) was associated with the down regulation of the HDL receptor protein, SR-BI. Akt-phosphorylation in HUVECs was induced in a biphasic manner by normal HDL. While diabetic HDL induced Akt phosphorylation normally after 20 minutes, the phosphorylation observed 24 hours after diabetic HDL treatment was reduced. To determine the role of SR-BI down regulation on diminished EC responses of diabetic HDL, Mouse aortic endothelial cells (MAECs) were isolated from wild type and SR-BI (？/？) mice, and treated with normal and diabetic HDL. The proliferative and migratory effects of normal HDL on wild type MAECs were greatly diminished in SR-BI (？/？) cells. In contrast, response to diabetic HDL was impaired in both types suggesting diminished effectiveness of diabetic HDL on EC proliferation and migration might be due to the down regulation of SR-BI. Additionally, SR-BI down regulation diminishes diabetic HDL’s capacity to activate Akt chronically. Conclusions/Significance Diabetic HDL was dysfunctional in promoting EC proliferation, migration, and adhesion to matrix which was associated with the down-regulation of SR-BI. Additionally, SR-BI down regulation diminishes diabetic HDL’s capacity to activate Akt chronically.
Hypochlorite-induced oxidative stress elevates the capability of HDL in promoting breast cancer metastasis
Bing Pan, Hui Ren, Xiaofeng Lv, Yangyu Zhao, Baoqi Yu, Yubin He, Yijing Ma, Chenguang Niu, Jinge Kong, Fangzhu Yu, Wen-bing Sun, Youyi Zhang, Belinda Willard, Lemin Zheng
Journal of Translational Medicine , 2012, DOI: 10.1186/1479-5876-10-65
Abstract: Human breast cancer cell lines were treated with normal and hypochlorite-oxidized HDL, and then cell metastasis potency in vivo and the abilities of migration, invasion, adhesion to HUVEC and ECM in vitro were examined. Integrin expression and PKC activity were evaluated, and PKC inhibitor and PKC siRNA was applied.We found hypochlorite-oxidized HDL dramatically promotes breast cancer cell pulmonary metastasis (133.4% increase at P < 0.0 l for MDA-MB-231 by mammary fat pad injection; 164.3% increase at P < 0.01 for MCF7 by tail vein injection) and hepatic metastasis (420% increase at P < 0.0 l for MDA-MB-231 by mammary fat pad injection; 1840% fold increase at P < 0.001 for MCF7 by tail vein injection) in nude mice, and stimulates higher cell invasion (85.1% increase at P < 0.00 l for MDA-MB-231; 88.8% increase at P < 0.00 l for MCF7;), TC-HUVEC adhesion (43.4% increase at P < 0.00 l for MDA-MB-231; 35.2% increase at P < 0.00 l for MCF7), and TC-ECM attachment (41.0% increase at P < 0.00 l for MDA-MB-231; 26.7% increase at P < 0.05 for MCF7) in vitro compared with normal HDL. The data also shows that the PKC pathway is involved in the abnormal actions of hypochlorite-oxidized HDL.Our study demonstrated that HDL under hypochlorite-induced oxidative stress stimulates breast cancer cell migration, invasion, adhesion to HUVEC and ECM, thereby promoting metastasis of breast cancer. These results suggest that HDL-based treatments should be considered for treatment of breast cancer patients.Breast cancer is the most common malignant neoplasm among women worldwide, and is one of the leading causes of cancer-related death [1]. Annually, about one million women are newly diagnosed with breast cancer and 400,000 patients die from the disease [2]. The etiology of breast cancer is multifactorial. It is suggested that oxidative stress which is responsible for protein, lipid and DNA damage plays an important role in the development and progression of breast cancer [3]. Hypochlorit
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