Design and Implementation of Machine Tool Life Inspection System Based on Sound Sensing.

The main causes of damage to industrial machinery are aging, corrosion, and the wear of parts, which affect the accuracy of machinery and product precision. Identifying problems early and predicting the life cycle of a machine for early maintenance can avoid costly plant failures. Compared with other sensing and monitoring instruments, sound sensors are inexpensive, portable, and have less computational data. This paper proposed a machine tool life cycle model with noise reduction. The life cycle model uses Mel-Frequency Cepstral Coefficients (MFCC) to extract audio features. A Deep Neural Network (DNN) is used to understand the relationship between audio features and life cycle, and then determine the audio signal corresponding to the aging degree. The noise reduction model simulates the actual environment by adding noise and extracts features by Power Normalized Cepstral Coefficients (PNCC), and designs Mask as the DNN's learning target to eliminate the effect of noise. The effect of the denoising model is improved by 6.8% under Short-Time Objective Intelligibility (STOI). There is a 3.9% improvement under Perceptual Evaluation of Speech Quality (PESQ). The life cycle model accuracy before denoising is 76%. After adding the noise reduction system, the accuracy of the life cycle model is increased to 80%.

[Mechanism of regulation of hepatoma cell cycle by XPD/P44 subcomplex : an in vitro experiment].

OBJECTIVE: To explore the effects of xeroderma pigmentosum group D(XPD)/P44 subcomplex on the cell cycle of the hepatoma cells. METHODS: Human hematoma cells of the line SMMC-7721 were cultured and transfected with human XPD gene by Lipofectamine and 2 strains with stably transfected plasmid pEGFG-N2 and stably transfected recombinant plasmid pEGFG-N2/XPD were selected. After stably transfection,the antisense oligonucleotides of P44 were added to treat the stably transfected cells. The cells were divided into 6 groups: Group (1) (control group), Group (2) transfected with the blank plasmid pEGFP-N2, Group (3) transfected with the recombinant plasmid pEGFP-N2/XPD, Group (4) transfected with ASODN complementary to the translation initiation site of pEGFP-N2/XPD, Group (5) transfected with antisense oligodeoxynucleotides (ASODN) complementary to the translation terminal site of pEGFP-N2/XPD, and Group (6) transfected with ASODN complementary to the translation exon5 site of pEGFP-N2/XPD. The expression levels of wild-type P44, XPD, cdk7, cdk2, c-myc, and cdc25A were detected by RT-PCR and Western blotting. The cell growth and the cell cycle were examined by MTT and flow cytometry (FCM). RESULTS: The P44 and XPD mRNA expression levels of Group (4) were significantly higher than those of Groups (1) and (2) (both P < 0.01). Western blotting indicated that the changes of P44 and XPD protein expression levels were consistent with those of their mRNAs respectively; while the mRNA and protein expression levels of cdk7, cdk2, c-myc, and cdc25A were all decreased. MTF method showed that the hepatoma cells grew slowly, FCM showed that the number of the cells arrested at the G1 stage of Group (3) were higher than those of Groups (1) and (2). After the blockage of P44 gene expression, the expression levels of XPD mRNA and protein were decreased. The XPD mRNA and protein expression levels of Groups (4), (5), and (6) were significantly higher than those of Group (3) (all P < 0.01). The mRNA and protein expression levels of cdk7, cdk2, c-myc, and cdc25A were upregulated. MT method indicated that cells grew fast. FCM showed that the numbers of the cells arrested at the G1 stage of Group (4), (5), and (6) were all lower than that of Group ((3) The expression levels of cell cycle regulatory genes including cdk7, cdk2, c-myc, and cdc25A were markedly decreased,the hepatoma cells grew slowly; after the blockage of P44 gene expression the expression levels of XPD mRNA and protein were decreased, whereas the expression levels of the cell cycle regulatory genes mentioned above were enhanced, and the hepatoma cells grew faster. CONCLUSION: XPD gene inhibits the proliferation and promotes the apoptosis of hepatoma cells. The expression of XPD may be regulated by its molecular partner P44. XPD/P44 subcomplex is involved in the regulation of DNA damage checkpoint.

Inhibitory effects of antisense oligodeoxynucleotide on expression of vascular endothelia growth factor by human hepatocarcinoma cells.

BACKGROUND: It is widely recognized that the growth of solid tumor depends on angiogenesis. Vascular endothelia growth factor (VEGF) is an endothelial cell-specific mitogen that promotes angiogenesis in solid tumor. Inhibition of angiogenesis is considered a promising approach for cancer therapy, and treatments including administration of antisense drugs and RNA interference for the VEGF gene are geared to the suppression of tumor angiogenesis. METHODS: As a new approach for gene therapy of hepatocellular carcinoma (HCC), four groups of antisense oligodeoxynucleotide (ASODN) (A-Cap, A-AUG, A-UGA and A-Exon-3) were used to block the expression of VEGF, then VEGF mRNA and protein were detected by RT-PCR and Western blot. RESULTS: After treatment with ASODN, the relative VEGF mRNA levels of A-Cap, A-AUG, A-UGA, and A-Exon-3 were decreased significantly to (32+/-9)%, (63+/-1)%, (86+/-3)%, and (70+/-5)%, respectively(F=64.18, P<0.001). The relative VEGF protein levels of A-Cap, A-AUG, A-UGA and A-Exon-3 were decreased significantly to (41+/-5)%, (59+/-3)%, (88+/-7)%, and (79+/-9)% respectively (F=60.64, P<0.001). CONCLUSIONS: Among the four ASODNs, the ASODN for Cap structure showed the strongest inhibitory effect and that for A-UGA, the least (P<0.05 ). The inhibitory effect of ASODN on the expression of VEGF proteins was similar to that of VEGF mRNA expression.

[Study on thermal treatment schedule of leucite microcrystallization to reinforce dental glass ceramics].

OBJECTIVE: To explore the thermal treatment schedule of leucite microcrystallization to reinforce dental glass ceramics. METHODS: After component analysis and selection, the raw material were treated by different temperature schedules. The products were analyzed by polaring microscope and X-ray diffractometer to determine the appropriate thermal treatment schedule. RESULTS: The temperature of melting, nuclearing and crystalizing was 1,600 degrees C, 1,200 degrees C and 1,500 degrees C. Leucite microcrystals dispersed in the glass matrix evenly and the size of leucite particle was about 0.8 micro m. CONCLUSION: Leucite can be microcrystalized according to an appropriate thermal treatment schedule.