Search

A planar gate U-shaped (PGU) channel silicon-on-insulator (SOI) lateral insulated gate bipolar transistor (LIGBT) featuring divided gates (G1 and G2) is proposed, which aims to suppress the gate voltage (VG) overshoot and improve the di/dt controllability. In the conventional PGU structure, the hole accumulating and the electric potential rising in the JFET region leads to a displacement current to overcharge the gate during the turn-on transient. Two gate connection modes (Mode A and B) for the proposed PGU structure are discussed. Mode A with a grounded G2 can effectively enhance the VG stability, however, degenerating the on-state voltage (VON). Mode B shields the displacement current by a pre-charged G2. G2 is driven with a separate gate resistor to the main gate G1, which results in an improved di/dt controllability without deteriorating VON. When adjusted for the same turn-on loss of 5.28mJ/cm2, the di/dt of the proposed PGU structure with mode B is 74% lower than that of the conventional PGU structure.

In this paper, five types of superjunction (SJ) configurations are investigated in the silicon-on-insulator lateral insulated-gate bipolar transistor (SOI-LIGBT). technology computer aided design simulations are carried out to give insight into the mechanism for improving turn-off loss ( ${E} _{ \mathrm{\scriptscriptstyle OFF}}$ ) by adopting SJ in the drift region of SOI-LIGBT. In mechanism revealing, collector–emitter voltage rising during the inductive load turn-off is divided into two phases: slow rising phase (SRP) and rapid rising phase (RRP). It is found that the depletion accompanying with carrier extraction in the drift region and at the collector is responsible for the SRP and RRP, respectively, and accordingly, the difference of turn-off transient among the five types of SJ configurations is clarified. Moreover, reduced ${E} _{ \mathrm{\scriptscriptstyle OFF}}$ can be realized by lowering the transition voltage from SRP to RRP ( ${V} _{\text {A}}$ ). Low electric potential from the emitter side can be delivered to the collector side through the undepleted regions in P-pillar, which largely determine ${V} _{\text {A}}$ . According to the above-mentioned mechanism, an optimization strategy and a novel SJ SOI-LIGBT with composite P-pillar are proposed for the first time. The proposed SJ SOI-LIGBT achieves an ${E} _{ \mathrm{\scriptscriptstyle OFF}}~76.3$ % lower than the conventional SOI-LIGBT at ON-state voltage drop of ~1.41 V.

A novel 500-V rated silicon-on-insulator lateral insulated-gate bipolar transistor (SOI-LIGBT), featuring a W-shaped n-typed buffer and p-typed composite collectors, is proposed for the first time in this paper. The composite collectors which consist of a high-doped p+ layer and a low-doped p− layer can maintain a high level of collector-side hole injection in ON-state; the low-doped p− layer combining with the W-shaped buffer provides a low barrier path for electron extraction during turn-off; thus, high current capability and high turn-off speed can be realized at the same time. The measurement results show that 67.3% decrease in turn-off time can be obtained at the expense of only 6.3% of current capability. Compared with the standard SOI-LIGBT, no additional processing steps or process modifications are required for the proposed SOI-LIGBT. The low-doped p− collector is formed simultaneously with the emitter-side p-well while the W-shaped buffer is formed by diffusion overlapping of two neighboring windows. At 125 °C, the proposed SOI-LIGBT exhibits an ON-state voltage drop of 2.48 V, a saturated current density of 420 A/cm2, a turn-off time of $>4~\mu \text{s}$ , allowing significant improvements in power loss, operating frequency, and ruggedness for single-chip intelligent power ICs.

The effects of quercetin liposomes (Q-PEGL) on streptozotocin (STZ)-induced diabetic nephropathy (DN) was investigated in rats. Male Sprague Dawley rats were used to establish a STZ induced DN model. DN rats randomly received one of the following treatments for 8 weeks: blank treatment (DN), free quercetin (Que), pegylated liposomes (PEGL) and pegylated quercetin liposomes (Q-PEGL). A group of healthy rats served as the normal control. The fasting blood glucose (FBG), body weights (BWs), renal hypertrophy index (rHI), serum and urine biochemistry, renal histopathology, oxidative stress and immunohistochemical measurements of AGEs were analyzed to compare the effect of different treatments. Que and Q-PEGL significantly improved DN biochemistry and pathological changes, although the treated rats still had some symptoms of DN. The therapeutic effect of Q-PEGL surpassed that of Que. Pegylated quercetin liposomes allow maintaining higher quercetin concentrations in plasma than non-encapsulated quercetin. In conclusion the use of quercetin liposomes allows to reduce disease symptoms in a rat model of DN.

In this paper, the off-state avalanche stability is investigated and a time-dependent avalanche instability is observed at −40°C in SOI lateral IGBT. Combining results from measurements with those from TCAD simulations, the mechanism for avalanche instability is revealed. Two optimization schemes are proposed to suppress or eliminate the unstable avalanche phenomenon. The unstable avalanche can be suppressed by employing a thick buried oxide layer and V CE shift can be reduced from 54V to 11V. Another scheme is that replacing P-type substrate by N-type substrate, and then V CE shift can be completely eliminated.

The text watermarking is a feasible method to protect the copyright from being copied and tampered. In this paper, a text zero-watermarking algorithm is proposed based on the connection between the Chinese characters and the Chinese phonetic alphabets. According to the predefined interval threshold, the proposed algorithm extracts the characteristics of the text content by valuing on the basis of the custom of Chinese phonetic alphabets. After being chaotic transformed, the algorithm combines the text characteristics with the embedded watermarking information in the Chinese text. The experimental results show that the watermarking’s capability of preventing tampering is up to 0.1%, which demonstrates the strong robustness and resistance to aggressive behavior of the algorithm.

Objective A new view is proposed for the mechanism of exercise prevention and improvement of chronic disease, that exercise may play a role by promoting the expression of anti-aging protein α-Klotho. Methods By means of literature review and prospective analysis, this paper summarizes the research status of the application of exercise in the prevention and improvement of chronic diseases and the effects of anti-aging protein α-Klotho on chronic cardiovascular disease, diabetes, chronic kidney disease and cancer and other chronic diseases and the effect of exercise on the expression of plasma α-Klotho and its possible mechanism. The research prospects of exercise to interfere with chronic diseases by promoting the expression of α-Klotho are envisioned Results (1) At present, the incidence and mortality of chronic diseases are high on a global scale. With the development of aging, chronic diseases will cause a serious economic burden and great waste of resources. Therefore, research on how to prevent and treat chronic diseases related to aging and lifestyle has become a top priority. Strong evidence suggests that exercise is an economical and efficient way to slow down the progress of some chronic diseases and to control symptoms such as diabetes, chronic kidney disease, heart failure, cardiovascular disease, and so on. However, we have not fully understood the cellular and molecular mechanisms underlying the effects of exercise.(2) α-Klotho is an anti-aging protein that regulates calcium and phosphorus metabolism, inhibits Wnt signaling, inhibits oxidative stress, and inhibits tumor and fibrosis. It has been proved to play an important role in the occurrence and development of chronic diseases such as chronic cardiovascular disease, diabetes, chronic kidney disease, tumor and other chronic diseases.(3) Exercise has been proved to be effective in promoting the expression of plasma α-Klotho protein, and the degree of response may be related to physical fitness and age. However, the mechanism of exercise to promote the expression of α-Klotho protein has not been reported. Combined with the existing research results, it is presumed that it may be related to DNA methylation, Peroxisome proliferator-activated receptor gamma(PPARγ) signal transduction and vitamin D receptor. Conclusions Exercise has gradually become an important way to intervene in chronic diseases, but the lack of understanding of its mechanism hinders the development of exercise in the field of prevention and treatment of chronic diseases. It is found that exercise can promote the expression of plasma α-Klotho protein, and the expression of α-Klotho protein will be beneficial to the prevention and improvement of chronic diseases such as chronic cardiovascular disease, diabetes, chronic kidney disease and tumor. Therefore, it is speculated that promoting the expression of α-Klotho may be one of the mechanisms of exercise prevention and improvement of chronic diseases, but there is still a research gap on the mechanism of exercise promoting α-Klotho expression. In addition, the current research on the expression of plasma α-Klotho is aimed at healthy people, and the effect of exercise on the expression of α-Klotho in chronic diseases, such as chronic cardiovascular disease, diabetes, chronic kidney disease, is also needed to be studied more. The study of the mechanism of exercise prevention and improvement of chronic diseases provides a theoretical basis for the selection and formulation of related exercise programs, and may provide new ideas for the development of new drugs for chronic diseases. Therefore, studies on exercise to interfere with chronic diseases by promoting the expression of α-Klotho have good research prospects.

When an electron is scattered by a tightly-focused laser beam in vacuum, the intensity gradient is a critical factor to influence the electron dynamics, for example, the electron energy exchange with the laser fields as have been explored before [P.X.Wang et al.,J. Appl. Phys. 91, 856 (2002]. In this paper, we have further investigated its influence upon the electron high-harmonic generation (HHG) by treating the spacial gradient of the laser intensity as a ponderomotive potential. Based upon perturbative QED calculations, it has been found that the main effect of the intensity gradient is the broadening of the originally line HHG spectra. A one-to-one relationship can be built between the beam width and the corresponding line width. Hence this finding may provides us a promising way to measure the beam width of intense lasers in experiments. In addition, for a laser pulse, we have also studied the different influences from transverse and longitudinal intensity gradients upon HHG.

The expression of nearly all smooth muscle genes are controlled by serum response factor binding sites in their promoter regions. However, SRF alone is not sufficient for regulating smooth muscle cell development. It associates with other cardiovascular specific cofactors to regulate smooth muscle gene expression. Previously, we showed that the transcription co-factor CRP2 was a regulator of smooth muscle gene expression. Here, we report that CSRP2BP, a coactivator for CRP2, is a histone acetyltransferase and a driver of smooth muscle gene expression. CSRP2BP directly interacted with SRF, CRP2 and myocardin. CSRP2BP synergistically activated smooth muscle gene promoters in an SRF-dependent manner. A combination of SRF, GATA6 and CRP2 required CSRP2BP for robust smooth muscle gene promoter activity. Knock-down of Csrp2bp in smooth muscle cells resulted in reduced smooth muscle gene expression. We conclude that the CSRP2BP histone acetyltransferase is a coactivator for CRP2 that works synergistically with SRF and myocardin to regulate smooth muscle gene expression.

Serum response factor (SRF), a cardiac enriched transcription factor, is required for the appearance of beating sarcomeres in the heart. SRF may also direct the expression of microRNAs (miRs) that inhibit the expression of cardiac regulatory factors. The recent knockout of miR-1-2, an SRF gene target, showed defective heart development, caused in part by the induction of GATA6, Irx4/5, and Hand2, that may alter cardiac morphogenesis, channel activity and cell cycling. SRF and co-factors play an obligatory role in cardiogenesis, as major determinants of myocyte differentiation not only by regulating the biogenesis of muscle contractile proteins but also by driving the expression of silencer miRNA.

Myocardin, a serum response factor (SRF)-dependent cofactor, is a potent activator of smooth muscle gene activity but a poor activator of cardiogenic genes in pluripotent 10T1/2 fibroblasts. Posttranslational modification of GATA4, another myocardin cofactor, by sumoylation strongly activated cardiogenic gene activity. Here, we found that myocardin's activity was strongly enhanced by SUMO-1 via modification of a lysine residue primarily located at position 445 and that the conversion of this residue to arginine (K445R) impaired myocardin transactivation. PIAS1 was involved in governing myocardin activity via its E3 ligase activity that stimulated myocardin sumoylation on an atypical sumoylation site(s) and by its physical association with myocardin. Myocardin initiated the expression of cardiac muscle-specified genes, such as those encoding cardiac alpha-actin and alpha-myosin heavy chain, in an SRF-dependent manner in 10T1/2 fibroblasts, but only in the presence of coexpressed SUMO-1/PIAS1. Thus, SUMO modification acted as a molecular switch to promote myocardin's role in cardiogenic gene expression.

With the improvement of request in diesel engine dynamic performance, economical efficiency and emission behavior, test technology of diesel engine has gained extensive attention, which has become one of the hot points in the domestic and international relevant research fields. Among the performance parameters of diesel engine, the instantaneous speed signal contains relevant information about diesel engine combustion and working conditions. As researches show, the instantaneous speed can be used to detect the diesel engine cylinder compression pressure, working nonuniform, combustion difference and other working character. Therefore, the study of instantaneous speed has gradually become a significant technology of non-contact detection. In this paper, the algorithm of instantaneous speed signal is successfully realized under specific sampling frequency. Furthermore, the change law of instantaneous speed curve is compared under different rotate speed. At last, fuel supply of one cylinder is cut off to imitate the misfire fault of diesel engine, and then the fault is successfully diagnosed through the analysis of instantaneous speed. Thus, both the algorithm realization of instantaneous speed and the conclusion related to misfire fault diagnosis can be used to various kinds of diesel engines, which have important project application value. Keywords-Fault Diagnosis; Diesel Engine; Instantaneous Speed; Data Sampling; Test

The vitellogenin receptor (VtgR) belongs to the low density lipoprotein receptor (LDLR) gene family. It mediates the uptake of vitellogenin (Vtg) in oocyte development of oviparous animals. In this study, we cloned and characterized two forms of Oreochromis aureus VtgR. Northern analysis showed that VtgR was specifically expressed in ovarian tissues. However, reverse transcription-PCR indicates that either there are trace levels of expression of VtgR or a homolog of LDLR exists in nonovarian tissues. The VtgR is highly homologous to the very low density lipoprotein receptor. To better understand the mechanism by which similar structural modules in the ligand-binding domain bind different ligands, we used the yeast two-hybrid system to screen for the minimal interaction motifs in Vtg and VtgR. The amino-terminal region of the lipovitellin I domain of Vtg interacts with the ligand-binding domain of VtgR. The first three ligand-binding repeats of the receptor were found to be essential for ligand binding. Computational analysis of the binding sequence indicates that Vtg has a similar receptor-binding region to apolipoprotein (apo) E and apoB. Site-directed mutagenesis of this region indicates electrostatic interaction between Vtg and its receptor. Sequence analysis suggests the coevolution of receptor-ligand pairs for the LDLR/apo superfamily and suggests that the mode of binding of LDLR/very low density lipoprotein receptor to apoB and apoE is inherited from the electrostatic attraction of VtgR and Vtg.

Receptor-associated late transducer (RALT) is a feedback inhibitor of epidermal growth factor receptor signaling. RALT has been shown previously to be induced in the ischemic heart and to promote cardiomyocyte apoptosis in vitro. However, the role of RALT in cardiac hypertrophy remains unclear. We hypothesized that forced expression of RALT in the murine heart would protect the heart against cardiac hypertrophy in vivo. We investigated the effect of cardiac overexpression of rat RALT on cardiac hypertrophy induced by angiotensin II and isoproterenol in RALT transgenic mice and wild-type littermates. The extent of cardiac hypertrophy was assessed by 2D and M-mode echocardiography as well as by molecular and pathological analyses of cardiac samples. Constitutive expression of rat RALT in cardiac myocytes of murine heart attenuated both hypertrophic and inflammatory responses and preserved cardiac function. These beneficial effects were associated with the attenuation of the epidermal growth factor receptor–dependent cascade that was triggered by angiotensin II and isoproterenol stimulation. Additional evidence demonstrated that RALT expression blocked fibrosis in vivo and collagen synthesis in vitro. Therefore, cardiac overexpression of RALT improves cardiac function and inhibits maladaptive hypertrophy, inflammation, and fibrosis through attenuating epidermal growth factor receptor–dependent signaling.

SummaryMicroRNAs (miRNAs) are genomically encoded small RNAs used by organisms to regulate the expression of proteins generated from messenger RNA transcripts. The in vivo requirement of specific miRNAs in mammals through targeted deletion remains unknown, and reliable prediction of mRNA targets is still problematic. Here, we show that miRNA biogenesis in the mouse heart is essential for cardiogenesis. Furthermore, targeted deletion of the muscle-specific miRNA, miR-1-2, revealed numerous functions in the heart, including regulation of cardiac morphogenesis, electrical conduction, and cell-cycle control. Analyses of miR-1 complementary sequences in mRNAs upregulated upon miR-1-2 deletion revealed an enrichment of miR-1 “seed matches” and a strong tendency for potential miR-1 binding sites to be located in physically accessible regions. These findings indicate that subtle alteration of miRNA dosage can have profound consequences in mammals and demonstrate the utility of mammalian loss-of-function models in revealing physiologic miRNA targets.

The vitellogenin receptor (VtgR) belongs to the low density lipoprotein receptor (LDLR) gene family. It mediates the uptake of vitellogenin (Vtg) in oocyte development of oviparous animals. In this study, we cloned and characterized two forms of Oreochromis aureus VtgR. Northern analysis showed that VtgR was specifically expressed in ovarian tissues. However, reverse transcription-PCR indicates that either there are trace levels of expression of VtgR or a homolog of LDLR exists in nonovarian tissues. The VtgR is highly homologous to the very low density lipoprotein receptor. To better understand the mechanism by which similar structural modules in the ligand-binding domain bind different ligands, we used the yeast two-hybrid system to screen for the minimal interaction motifs in Vtg and VtgR. The amino-terminal region of the lipovitellin I domain of Vtg interacts with the ligand-binding domain of VtgR. The first three ligand-binding repeats of the receptor were found to be essential for ligand binding. Computational analysis of the binding sequence indicates that Vtg has a similar receptor-binding region to apolipoprotein (apo) E and apoB. Site-directed mutagenesis of this region indicates electrostatic interaction between Vtg and its receptor. Sequence analysis suggests the coevolution of receptor-ligand pairs for the LDLR/apo superfamily and suggests that the mode of binding of LDLR/very low density lipoprotein receptor to apoB and apoE is inherited from the electrostatic attraction of VtgR and Vtg.

In this paper, a detailed numerical comparison of the high-harmonic generation (HHG) from free electrons in intense laser fields in both classical and semi-classical frameworks has been presented. These two frameworks have been widely used in the literature. It has been found that the HHG spectra display distinct quantitative differences for high-energy electrons. In some special situations, qualitative differences appear. Even if the radiation reaction is included in the electron classical dynamics, no consistent result can be obtained. Hence it should be of critical importance to submit the present HHG theory for high-precision experimental tests, which can help us not only to justify the present theories, but also to check the QED predictions in the high-intensity regime.

In this paper, the spontaneous bremsstrahlung emission from an electron scattered by two fixed nuclei in an intense laser field is investigated in detail based upon the Volkov state and the Dirac-Volkov propagator. It has been found that the fundamental harmonic spectrum from the electron radiation exhibits distinctive fringes, which is dependent not only upon the internucleus distance and orientation but also upon the initial energy of the electron and the laser intensity. By analyzing the differential cross section, we are able to explain these effects in terms of interference among the electron scattering by the nuclei. These results could have promising applications in probing the atomic or molecular dressed potentials in intense laser fields.

Production of positron-electron (e+e−) pairs in an intense laser pulse is investigated by solving the Dirac equation with analytical and numerical methods. We observe that the probability of the pair production will firstly decrease slowly as the pulse length τ becomes shortened. Then it will increase until τ is reduced to the Compton time τc = /(mec) ≈ 1.29 × 10−21s and finally decrease exponentially to zero. Hence, for a prominent pair production, we not only require that the electric field strength should be higher than the the Schwinger critical value Ecr = m2c3/(e) ≈ 1.32 × 1016 V/cm, but also that the pulse duration τ should be larger than τc. The latter is shown to be related to momentum requirement for the transition. For fields with different pulse lengths, the phase and chirp influences upon the pair production are also explored.