The exciting encounter between lncRNAs and radiosensitivity in IR-induced DNA damage events.

Radiation therapy is a commonly used tool in cancer management due to its ability to destroy malignant tumors. Mechanically, the efficacy of radiotherapy mainly depends on the inherent radiosensitivity of cancer cells and surrounding normal tissues, which mostly accounts for molecular dynamics associated with radiation-induced DNA damage. However, the relationship between radiosensitivity and DNA damage mechanism deserves to be further probed. As the well-established RNA regulators or effectors, long noncoding RNAs (lncRNAs) dominate vital roles in modulating ionizing radiation response by targeting crucial molecular pathways, including DNA damage repair. Recently, emerging evidence has constantly confirmed that overexpression or inhibition of lncRNAs can greatly influence the sensitivity of radiotherapy for many kinds of cancers, by driving a diverse array of DNA damage-associated signaling cascades. In conclusion, this review critically summarizes the recent progress in the molecular mechanism of IR-responsive lncRNAs in the context of radiation-induced DNA damage. The different response of lncRNAs when IR exposure. IR exposure can trigger the changes in expression pattern and subcellular localization of lncRNAs that influences the different radiology processes.

D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome.

This article aims to investigate the protection of the intestine from ionizing radiation-induced injury by using D-galactose (D-gal) to alter the gut microbiome. In addition, this observation opens up further lines of research to further increase therapeutic potentials. Male C57BL/6 mice were exposed to 7.5 Gy of total body irradiation (TBI) or 13 Gy of total abdominal irradiation (TAI) in this study. After adjustment, D-gal was intraperitoneally injected into mice at a dose of 750 mg/kg/day. Survival rates, body weights, histological experiments and the level of the inflammatory factor IL-1ß were observed after TBI to investigate radiation injury in mice. Feces were collected from mice for 16S high-throughput sequencing after TAI. Furthermore, fecal microorganism transplantation (FMT) was performed to confirm the effect of D-gal on radiation injury recovery. Intraperitoneally administered D-gal significantly increased the survival of irradiated mice by altering the gut microbiota structure. Furthermore, the fecal microbiota transplanted from D-gal-treated mice protected against radiation injury and improved the survival rate of recipient mice. Taken together, D-gal accelerates gut recovery following radiation injury by promoting the growth of specific microorganisms, especially those in the class Erysipelotrichia. The study discovered that D-gal-induced changes in the microbiota protect against radiation-induced intestinal injury. Erysipelotrichia and its metabolites are a promising therapeutic option for post-radiation intestinal regeneration.

Nondestructive Testing of Local Incomplete Brazing Defect in Stainless Steel Core Panel Using Pulsed Eddy Current.

Stainless steel core panel is a novel structure for fast modular building, but its brazing foils are susceptible to defects due to the difficulty of precisely controlling the brazing process. An automated, nondestructive testing technique is highly desirable for quick inspection of the brazing defects buried in the stainless-steel core panel. In this paper, pulsed eddy current testing (PECT) was employed to inspect local incomplete brazing defects. Finite element simulation and experiment verification were conducted to investigate the feasibility and effectiveness of the proposed method. The peak value of the PECT signal was found to be sensitive to the presence of the defect. With the aid of an industrial robotic arm, line and two-dimensional scans were performed of the PECT probe above the panel specimen. The prefabricated incomplete brazing foil was successfully imaged as a notched ring, whose opening coincides with the physical length of the missing brazing. The proposed method shows potential to serve as an effective tool for in-line or off-line automated nondestructive testing of the brazing defects in stainless steel core panels.

Elevated BTG2 improves the radiosensitivity of non-small cell lung cancer (NSCLC) through apoptosis.

BACKGROUND: To identify radio-responsive genes and explore the biological function of encoded proteins in non-small cell lung cancer (NSCLC). METHODS: Radio-responsive genes in irradiated H460 cells were screened from microarray data deposited in the Gene Expression Omnibus (GEO) database. A quantitative real time polymerase chain reaction assay was used to detect the expression of candidate radio-responsive genes in irradiated cells. CCK-8 assay, EDU assay, clone formation assay, immunofluorescence and flow cytometry were conducted to evaluate the biological function of B cell translocation gene 2 (BTG2) in NSCLC. RESULTS: Bioinformatic analysis using GES20549 showed that BTG2 was a radio-responsive gene in irradiated H460 cells. The mRNA expression level of BTG2 was lower in H460 cells compared with that in BEAS-2B normal lung epithelial cells. BTG2 expression was elevated upon IR exposure, in a dose-dependent but not a time-dependent manner. CCK-8 and EDU assays revealed that BTG2 overexpression inhibited the growth rate of irradiated cells. Clone formation showed that elevated BTG2 promoted DNA damage of irradiated H460 cells. The number of γ-H2AX foci induced by DNA damage was also markedly increased upon BTG2 overexpression. Flow cytometry showed that BTG2 increased IR-induced cell apoptosis. CONCLUSIONS: BTG2 may be a novel radio-responsive factor and a promising therapeutic target for radiotherapy of NSCLC.

Increased activation of cGAS-STING pathway enhances radiosensitivity of non-small cell lung cancer cells.

BACKGROUND: Radiotherapy is an effective therapeutic approach widely used clinically in non-small cell lung cancer (NSCLC), but radioresistance remains a major challenge. New and effective radiosensitizing approaches are thus urgently needed. The activation of DNA-sensing cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway has become an attractive therapeutic target, but the relationship between activation of cGAS-STING pathway and radiosensitization of NSCLC cells remains unknown. METHODS: Considering low expression of cGAS-STING pathway genes in NSCLC, including STING, we used an activator (STING agonist, dimeric amidobenzimidazole [diABZI]) of cGAS-STING pathway and increased activation factor (DNA double strand breaks) of cGAS-STING pathway to respectively reinforce the activation of cGAS-STING pathway in NSCLC cells. We then investigated the effect of increased activation of cGAS-STING pathway on the proliferation of H460 and A549 cells by CCK-8 and colony formation assays, and revealed the underlying mechanism. RESULTS: We found that both diABZI and the increased DNA double strand breaks could sensitize NSCLC cells to irradiation. Mechanically, our results showed that the increased activation of cGAS-STING pathway enhanced radiosensitivity by promoting apoptosis in NSCLC cells. CONCLUSION: Taken together, we concluded that diABZI could be used as a radiosensitizer in NSCLC cells, and targeting the activation of cGAS-STING pathway has a potential to be a new approach for NSCLC radiosensitizing.

Identification of Key Genes and Pathways Associated With Irradiation in Breast Cancer Tissue and Breast Cancer Cell Lines.

Radiotherapy is mainly a traditional treatment for breast cancer; however, the key genes and pathways in breast cancer associated with irradiation are not clear. In this study, we aimed to explore the messenger RNA expression changes between preradiation and postradiation breast cancer. The gene expression data set (GSE59733) was downloaded from Gene Expression Omnibus database. According to |log2FC (fold change) | ≥ 1 and with false discovery rate adjusted P value <.05, differentially expressed genes (DEGs) were screened and annotated by R programming software. The protein-protein interaction (PPI) network was conducted through STRING database, and subnetworks and hub genes were extracted by plug-in in Cytoscape. A total of 82 DEGs (74 upregulated and 8 downregulated genes) were identified. These DEGs mainly enriched in an intrinsic apoptotic signaling pathway and G-protein-coupled receptor binding. What's more, tumor necrosis factor signaling pathway and interleukin 17 signaling pathway abnormally activated in postradiation tumor samples. Two characteristic subnetworks and 3 hub genes (FOS, CCL2, and CXCL12) were strongly distinguished in PPI network. Moreover, the expression level of the hub genes was confirmed in irradiated MCF-7 cell and SUM-159 cell using quantitative real-time polymerase chain reaction assay. These findings imply that these hub genes may play momentous function in breast cancer to irradiation.

Gut Microbiota Metabolite Fights Against Dietary Polysorbate 80-Aggravated Radiation Enteritis.

Radiation therapy is a cornerstone of modern management methods for malignancies but is accompanied by diverse side effects. In the present study, we showed that food additives such as polysorbate 80 (P80) exacerbate irradiation-induced gastrointestinal (GI) tract toxicity. A 16S ribosomal RNA high-throughput sequencing analysis indicated that P80 consumption altered the abundance and composition of the gut microbiota, leading to severe radiation-induced GI tract injury. Mice harboring fecal microbes from P80-treated mice were highly susceptible to irradiation, and antibiotics-challenged mice also represented more sensitive to radiation following P80 treatment. Importantly, butyrate, a major metabolite of enteric microbial fermentation of dietary fibers, exhibited beneficial effects against P80 consumption-aggravated intestinal toxicity via the activation of G-protein-coupled receptors (GPCRs) and maintenance of the intestinal bacterial composition in irradiated animals. Moreover, butyrate had broad therapeutic effects on common radiation-induced injury. Collectively, our findings demonstrate that P80 are potential risk factors for cancer patients during radiotherapy and indicate that butyrate might be employed as a therapeutic option to mitigate the complications associated with radiotherapy.

LncRNA HOTAIR enhances breast cancer radioresistance through facilitating HSPA1A expression via sequestering miR-449b-5p.

BACKGROUND: Breast cancer (BRCA) is the leading cause of cancer-related death in women worldwide. Pre- and postoperative radiotherapy play a pivotal role in BRCA treatment but its efficacy remains limited and plagued by the emergence of radiation resistance, which aggravates patient prognosis. The long noncoding RNA (lncRNA)-implicated mechanisms underlying radiation resistance are rarely reported. The aim of this study was to determine whether lncRNA HOX transcript antisense RNA (HOTAIR) modulated the radiosensitivity of breast cancer through HSPA1A. METHODS: A Gammacell 40 Exactor was used for irradiation treatment. Bioinformatic tools and luciferase reporter assay were adopted to explore gene expression profile and demonstrate the interactions between lncRNA, miRNA and target mRNA 3'-untranslated region (3'-UTR). The expression levels of certain genes were determined by real-time PCR and western-blot analyses. in vitro and in vivo functional assays were conducted by cell viability and tumorigenicity assays. RESULTS: The levels of oncogenic lncRNA HOTAIR were positively correlated with the malignancy of BRCA but reversely correlated with the radiosensitivity of breast cancer cells. Moreover, the expression levels of HOTAIR were positively associated with those of heat shock protein family A (Hsp70) member 1A (HSPA1A) in clinical BRCA tissues and HOTAIR upregulated HSPA1A at the mRNA and protein levels in irradiated BRCA cells. Mechanistically, miR-449b-5p restrained HSPA1A expression through targeting the 3'-UTR of HSPA1A mRNA, whereas HOTAIR acted as a competing sponge to sequester miR-449b-5p and thereby relieved the miR-449b-5p-mediated HSPA1A repression. Functionally, HOTAIR conferred decreased radiosensitivity on BRCA cells, while miR-449b-5p overexpression or HSPA1A knockdown abrogated the HOTAIR-enhanced BRCA growth under the irradiation exposure both in vitro and in vivo. CONCLUSIONS: LncRNA HOTAIR facilitates the expression of HSPA1A by sequestering miR-449b-5p post-transcriptionally and thereby endows BRCA with radiation resistance. KEY POINTS: Therapeutically, HOTAIR and HSPA1A may be employed as potential targets for BRCA radiotherapy. Our findings shed new light into the mechanism by which lncRNAs modulate the radiosensitivity of tumors.

Gut microbiota-derived indole 3-propionic acid protects against radiation toxicity via retaining acyl-CoA-binding protein.

BACKGROUND: We have proved fecal microbiota transplantation (FMT) is an efficacious remedy to mitigate acute radiation syndrome (ARS); however, the mechanisms remain incompletely characterized. Here, we aimed to tease apart the gut microbiota-produced metabolites, underpin the therapeutic effects of FMT to radiation injuries, and elucidate the underlying molecular mechanisms. RESULTS: FMT elevated the level of microbial-derived indole 3-propionic acid (IPA) in fecal pellets from irradiated mice. IPA replenishment via oral route attenuated hematopoietic system and gastrointestinal (GI) tract injuries intertwined with radiation exposure without precipitating tumor growth in male and female mice. Specifically, IPA-treated mice represented a lower system inflammatory level, recuperative hematogenic organs, catabatic myelosuppression, improved GI function, and epithelial integrity following irradiation. 16S rRNA gene sequencing and subsequent analyses showed that irradiated mice harbored a disordered enteric bacterial pattern, which was preserved after IPA administration. Notably, iTRAQ analysis presented that IPA replenishment retained radiation-reprogrammed protein expression profile in the small intestine. Importantly, shRNA interference and hydrodynamic-based gene delivery assays further validated that pregnane X receptor (PXR)/acyl-CoA-binding protein (ACBP) signaling played pivotal roles in IPA-favored radioprotection in vitro and in vivo. CONCLUSIONS: These evidences highlight that IPA is a key intestinal microbiota metabolite corroborating the therapeutic effects of FMT to radiation toxicity. Owing to the potential pitfalls of FMT, IPA might be employed as a safe and effective succedaneum to fight against accidental or iatrogenic ionizing ARS in clinical settings. Our findings also provide a novel insight into microbiome-based remedies toward radioactive diseases. Video abstract.

[Prokaryotic expression, purification and characterization of tissue inhibitor of metalloproteinase-2].

Tissue inhibitor of metalloproteinases-2 (TIMP-2) inhibits tumor migration and invasion. Obtaining TIMP-2 protein is conducive to a comprehensive and in-depth study of its function and mechanism in tumorigenesis and development. We collected human TIMP-2 protein through prokaryotic expression in vitro. We expressed, purified and characterized human TIMP-2 protein. First, the human TIMP-2 gene was cloned from the cDNA obtained by reverse transcription of total RNA of human lung cancer A549 cells, and constructed to pET28a vector. The recombinant plasmid pET28a-TIMP-2 was transformed into Escherichia coli BL21(DE3) after restriction endonuclease digestion and sequencing analysis. The expression of TIMP-2 protein was induced by isopropyl-ß-D-thiogalactoside (IPTG), and the expression conditions were optimized. After purification by nickel affinity column, the fusion protein His-TIMP-2 was identified by Western blotting method and its biological activity was detected by gelatin zymography. The fusion protein His-TIMP-2 existed in the form of inclusion body in E. coli. In a certain range, the concentration of IPTG had no significant effect on the expression amount of His-TIMP-2. But in this expression system, induction temperature and time were the key parameters, and the expression amount of His-TIMP-2 in E. coli increased with the increase of induction temperature. The purified and refolded fusion protein could effectively inhibit the activity of matrix metalloproteinases expressed by human lung cancer A549 cells. The acquisition of active fusion protein lays a foundation for further study of the function and mechanism of human TIMP-2, and is of great significance for tumor therapy.

Sexual Dimorphism of Gut Microbiota Dictates Therapeutics Efficacy of Radiation Injuries.

Accidental or iatrogenic ionizing radiation exposure precipitates acute and chronic radiation injuries. The traditional paradigm of mitigating radiotherapy-associated adverse side effects has ignored the gender-specific dimorphism of patients' divergent responses. Here, the effects of sexual dimorphism on curative efficiencies of therapeutic agents is examined in murine models of irradiation injury. Oral gavage of simvastatin ameliorates radiation-induced hematopoietic injury and gastrointestinal tract dysfunction in male mice, but adversely deteriorates these radiation syndromes in female animals. In a sharp contrast, feeding animals with high-fat diet (HFD) elicites explicitly contrary results. High-throughput sequencing of microbial 16S rRNA, host miRNA, and mRNA shows that simvastatin or HFD administration preventes radiation-altered enteric bacterial taxonomic structure, preserves miRNA expression profile, and reprogrammes the spectrum of mRNA expression in small intestines of male or female mice, respectively. Notably, faecal microbiota transplantation of gut microbes from opposite sexual donors abrogates the curative effects of simvastatin or HFD in respective genders of animals. Together, these findings demonstrate that curative efficiencies of therapeutic strategies mitigating radiation toxicity might be dependent on the gender of patients, thus simvastatin or HFD might be specifically useful for fighting against radiation toxicity in a sex-dependent fashion partly based on sex-distinct gut microbiota composition in preclinical settings.

Amelioration of whole abdominal irradiation-induced intestinal injury in mice with 3,3'-Diindolylmethane (DIM).

Ionizing radiation-induced intestinal injury is a catastrophic disease with limited effective therapies. 3,3'-Diindolylmethane (DIM), a potent antioxidant agent, has previously been shown to ameliorate hematopoietic injury in a murine model of total body radiation injury, but its effects on ionizing radiation-induced intestinal damage are not clear. Here, we demonstrate that administration of DIM not only protects mice against whole abdominal irradiation (WAI)-induced lethality and weight loss but also ameliorates crypt-villus structural and functional injury of the small intestine. In addition, treatment with DIM significant enhances WAI-induced reductions in Lgr5+ ISCs and their progeny cells, including lysozyme+ Paneth cells, Villin+ enterocytes and Ki67+ instantaneous amplifying cells, thus promoting small intestine repair following WAI exposure. Notably, the expression of Nrf2 increased, while the number of apoptotic cells and the expression of γH2AX decreased in the small intestines of DIM-treated mice compared to mice treated with vehicle following WAI. In vitro, we demonstrated that DIM protected human intestinal epithelial cell-6 (HIEC-6) against ionizing radiation, leading to increased cell vitality. Mechanistically, the radioprotective effect of DIM was likely attributable to its anti-DNA damage effects in irradiated HIEC-6 cells. Moreover, these changes were related to reduction in reactive oxygen species (ROS) levels and increased the activities of antioxidant enzymatic in irradiated HIEC-6 cells. Additionally, the DIM radioprotective effects on the intestine resulted in the restoration of the WAI-shifted gut bacteria composition in mice. Collectively, our findings demonstrate that the beneficial properties of DIM mitigate intestinal radiation injury, which provides a novel strategy for improving the therapeutic effects of irradiation-induced intestinal injury.

Cordycepin sensitizes breast cancer cells toward irradiation through elevating ROS production involving Nrf2.

Radiation therapy toward malignancies is often ineffective owing to radioresistance of cancer cells. On the basis of anti-tumor properties of cordycepin, we examined the effects of cordycepin on sensitizing breast cancer cells toward radiotherapy. Cordycepin administration promoted G2/M arrest and apoptosis of MCF-7 and MDA-MB-231 cells resulting in restraining the proliferation of the cells in vitro and in vivo following irradiation. Mechanistic investigations showed that the breast cancer cells cultured with cordycepin harbored higher levels of intracellular reactive oxygen species (ROS) and incremental numbers of γ-H2AX foci after irradiation exposure. Importantly, cordycepin treatment down-regulated the expression levels of Nuclear factor erythroid 2-related factor (Nrf2) and a series of downstream genes, such as heme oxygenase-1 (HO-1), to enhance ROS in breast cancer cells exposed to irradiation. Together, our observations demonstrate that cordycepin treatment sensitizes breast carcinoma cells toward irradiation via Nrf2/HO-1/ROS axis. Thus, our findings provide novel insights into the function and the underlying mechanism of cordycepin in radiotherapy, and suggest that cordycepin might be employed as a radiosensitizer during radiotherapy toward breast cancer in a pre-clinical setting.

Low dose irradiation facilitates hepatocellular carcinoma genesis involving HULC.

Irradiation exposure positive correlates with tumor formation, such as breast cancer and lung cancer. However, whether low dose irradiation induces hepatocarcinogenesis and the underlying mechanism remain poorly defined. In the present study, we reported that low dose irradiation facilitated the proliferation of hepatocyte through up-regulating HULC in vitro and in vivo. Low dose irradiation exposure elevated HULC expression level in hepatocyte. Deletion of heightened HULC erased the cells growth accelerated following low dose irradiation exposure. CDKN1, the neighbor gene of HULC, was down-regulated by overexpression of HULC following low dose irradiation exposure via complementary base pairing, resulting in promoting cell cycle process. Thus, our findings provide new insights into the mechanism of low dose irradiation-induced hepatocarcinogenesis through HULC/CDKN1 signaling, and shed light on the potential risk of low dose irradiation for the development of hepatocellular carcinoma in pre-clinical settings.

Research on two-port network of wavelet transform processor using surface acoustic wavelet devices and its application.

The goal of this research is to study two-port network of wavelet transform processor (WTP) using surface acoustic wave (SAW) devices and its application. The motive was prompted by the inconvenience of the long research and design cycle and the huge research funding involved with traditional method in this field, which were caused by the lack of the simulation and emulation method of WTP using SAW devices. For this reason, we introduce the two-port network analysis tool, which has been widely used in the design and analysis of SAW devices with uniform interdigital transducers (IDTs). Because the admittance parameters calculation formula of the two-port network can only be used for the SAW devices with uniform IDTs, this analysis tool cannot be directly applied into the design and analysis of the processor using SAW devices, whose input interdigital transducer (IDT) is apodized weighting. Therefore, in this paper, we propose the channel segmentation method, which can convert the WTP using SAW devices into parallel channels, and also provide with the calculation formula of the number of channels, the number of finger pairs and the static capacitance of an interdigital period in each parallel channel firstly. From the parameters given above, we can calculate the admittance parameters of the two port network for each channel, so that we can obtain the admittance parameter of the two-port network of the WTP using SAW devices on the basis of the simplification rule of parallel two-port network. Through this analysis tool, not only can we get the impulse response function of the WTP using SAW devices but we can also get the matching circuit of it. Large numbers of studies show that the parameters of the two-port network obtained by this paper are consistent with those measured by network analyzer E5061A, and the impulse response function obtained by the two-port network analysis tool is also consistent with that measured by network analyzer E5061A, which can meet the accuracy requirements of the analysis of the WTP using SAW devices. Therefore the two-port network analysis tool discussed in this paper has comparatively higher theoretical and practical value.

Temperature compensation of the SAW yarn tension sensor.

The objective of this research was to investigate the possibility of the temperature compensation for the surface acoustic wave (SAW) yarn tension sensor. The motivation for this work was prompted by the oscillation frequency of the SAW yarn tension sensor varying with the temperature. In this paper, we deduce the functional relationship between the temperature variation and the oscillation frequency shift caused by the temperature. This functional relationship and the temperature sensor are used to get the oscillation frequency shift caused by the temperature, so that we can use the oscillation frequency shift caused by the temperature to implement the temperature compensation of the SAW yarn tension sensor. In this paper, we also get the relative error of the temperature compensation. The theoretical and experimental results confirm that this temperature compensation method can implement the temperature compensation of the SAW yarn tension sensor.

A novel optimal sensitivity design scheme for yarn tension sensor using surface acoustic wave device.

In this paper, we propose a novel optimal sensitivity design scheme for the yarn tension sensor using surface acoustic wave (SAW) device. In order to obtain the best sensitivity, the regression model between the size of the SAW yarn tension sensor substrate and the sensitivity of the SAW yarn tension sensor was established using the least square method. The model was validated too. Through analyzing the correspondence between the regression function monotonicity and its partial derivative sign, the effect of the SAW yarn tension sensor substrate size on the sensitivity of the SAW yarn tension sensor was investigated. Based on the regression model, a linear programming model was established to gain the optimal sensitivity of the SAW yarn tension sensor. The linear programming result shows that the maximum sensitivity will be achieved when the SAW yarn tension sensor substrate length is equal to 15 mm and its width is equal to 3mm within a fixed interval of the substrate size. An experiment of SAW yarn tension sensor about 15 mm long and 3mm wide was presented. Experimental results show that the maximum sensitivity 1982.39 Hz/g was accomplished, which confirms that the optimal sensitivity design scheme is useful and effective.

Implementing wavelet inverse-transform processor with surface acoustic wave device.

The objective of this research was to investigate the implementation schemes of the wavelet inverse-transform processor using surface acoustic wave (SAW) device, the length function of defining the electrodes, and the possibility of solving the load resistance and the internal resistance for the wavelet inverse-transform processor using SAW device. In this paper, we investigate the implementation schemes of the wavelet inverse-transform processor using SAW device. In the implementation scheme that the input interdigital transducer (IDT) and output IDT stand in a line, because the electrode-overlap envelope of the input IDT is identical with the one of the output IDT (i.e. the two transducers are identical), the product of the input IDT's frequency response and the output IDT's frequency response can be implemented, so that the wavelet inverse-transform processor can be fabricated. X-112(0)Y LiTaO(3) is used as a substrate material to fabricate the wavelet inverse-transform processor. The size of the wavelet inverse-transform processor using this implementation scheme is small, so its cost is low. First, according to the envelope function of the wavelet function, the length function of the electrodes is defined, then, the lengths of the electrodes can be calculated from the length function of the electrodes, finally, the input IDT and output IDT can be designed according to the lengths and widths for the electrodes. In this paper, we also present the load resistance and the internal resistance as the two problems of the wavelet inverse-transform processor using SAW devices. The solutions to these problems are achieved in this study. When the amplifiers are subjected to the input end and output end for the wavelet inverse-transform processor, they can eliminate the influence of the load resistance and the internal resistance on the output voltage of the wavelet inverse-transform processor using SAW device.

Solution to the influence of the MSSW propagating velocity on the bandwidths of the single-scale wavelet-transform processor using MSSW device.

The objective of this research was to investigate the possibility of solving the influence of the magnetostatic surface wave (MSSW) propagating velocity on the bandwidths of the single-scale wavelet transform processor using MSSW device. The motivation for this work was prompted by the processor that -3dB bandwidth varies as the propagating velocity of MSSW changes. In this paper, we present the influence of the magnetostatic surface wave (MSSW) propagating velocity on the bandwidths as the key problem of the single-scale wavelet transform processor using MSSW device. The solution to the problem is achieved in this study. we derived the function between the propagating velocity of MSSW and the -3dB bandwidth, so we know from the function that -3dB bandwidth of the single-scale wavelet transform processor using MSSW device varies as the propagating velocity of MSSW changes. Through adjusting the distance and orientation of the permanent magnet, we can implement the control of the MSSW propagating velocity, so that the influence of the MSSW propagating velocity on the bandwidths of the single-scale wavelet transform processor using MSSW device is solved.

A novel compensation method of insertion losses for wavelet inverse-transform processors using surface acoustic wave devices.

The objective of this research was to investigate the possibility of compensating for the insertion losses of the wavelet inverse-transform processors using SAW devices. The motivation for this work was prompted by the processors which are of large insertion losses. In this paper, the insertion losses are the key problem of the wavelet inverse-transform processors using SAW devices. A novel compensation method of the insertion losses is achieved in this study. When the output ends of the wavelet inverse-transform processors are respectively connected to the amplifiers, their insertion losses can be compensated for. The bandwidths of the amplifiers and their adjustment method are also given in this paper.