FMCW Laser Fuze Structure with Multi-Channel Beam Based on 3D Particle Collision Scattering Model under Smoke Interference.

In the environment of smoke and suspended particles, the accurate detection of targets is one of the difficulties for frequency-modulated continuous-wave (FMCW) laser fuzes to work properly in harsh conditions. To weaken and eliminate the significant influence caused by the interaction of different systems in the photon transmission process and the smoke particle environment, it is necessary to increase the amplitude of the target echo signal to improve the signal-to-noise ratio (SNR), which contributes to enhancing the detection performance of the laser fuze for the ground target in the smoke. Under these conditions, the particle transmission of photons in the smoke environment is studied from the perspective of three-dimentional (3D) collisions between photons and smoke particles, and the modeling and Unity3D simulation of FMCW laser echo signal based on 3D particle collision is conducted. On this basis, a laser fuze structure based on multiple channel beam emission is designed for the combined effect of particle features from different systems and its impact on the target characteristics is researched. Simulation results show that the multiple channel laser emission enhances the laser target echo signal amplitude and also improves the anti-interference ability against the combined effects of multiple particle features compared with the single channel. Through the validation based on the laser prototype with four-channel beam emitting, the above conclusions are supported by the experimental results. Therefore, this study not only reveals the laser target properties under the 3D particle collision perspective, but also reflects the reasonableness and effectiveness of utilizing the target characteristics in the 3D particle collision mode to enhance the detection performance of FMCW laser fuze in the smoke.

Modulated Radio Frequency Stealth Waveforms for Ultra-Wideband Radio Fuzes.

The increasingly complex electromagnetic environment of modern warfare and the proliferation of intelligent jamming threaten to reduce the survival rate of radio fuzes on the battlefield. Radio frequency (RF) stealth technology can fundamentally improve the anti-interception and reconnaissance capabilities of radio fuzes, thereby lessening the probability of them being intercepted, recognized, and jammed by the enemy. In this paper, an RF stealth waveform based on chaotic pulse-position modulation is proposed for ultra-wideband (UWB) radio fuzes. Adding a perturbation signal based on the Tent map ensures that the chaotic sequences have sufficiently long periods despite hardware byte limitations. Measuring the approximate entropy and sequence period shows that the Tent map with the addition of perturbation signals can maintain good randomness under byte constraints, closely approximating the Tent map with ideal precision. Simulations verify that the proposed chaotic mapping used to modulate the pulse position of an ultra-wideband radio fuze signal results in superior detection, anti-interception, and anti-jamming performance.

Active Ingredients and Mechanism of Gegen Qinlian Decoction in the Treatment of Diabetic Cardiomyopathy: A Network Pharmacology Study.

BACKGROUND: Diabetic cardiomyopathy (DCM) is a common diabetes complication with limited medications. Gegen Qinlian decoction (GQD) has been used in the treatment of diabetes and its related complications in China for several decades. OBJECTIVE: In this study, network pharmacology was employed to predict the active ingredients, key targets, and pathways involved in the treatment of DCM by GQD and to validate it by animal experiments. METHODS: The active ingredients of GQD were retrieved from TCMSP and published literature. DCM-related gene targets were searched in Drugbank, Genecards, Disgenet, and OMIM disease databases. Protein-protein interaction networks were constructed using the STRING database and Cytoscape. GO analysis and KEGG pathway enrichment analysis were performed using the Metascape platform. Moreover, a diabetic mouse model was established to evaluate the therapeutic effects of GQD by measuring serum biochemical markers and inflammation levels. Finally, the expression of predicted key target genes was determined using real-time quantitative PCR. RESULTS: A total of 129 active ingredients were screened from GQD. Moreover, 146 intersecting genes related to DCM were obtained, with key targets, including AKT1, TNF, IL6, and VEGFA. Lipid and atherosclerosis, AGE-RAGE, PI3K-AKT, and MAPK pathways were identified. Blood glucose control, decreased inflammatory factors, and serum CK-MB levels were restored after GQD intervention, and the same occurred with the expressions of PPAR-γ, AKT1, APOB, and GSK3B genes. CONCLUSION: Quercetin, kaempferol, wogonin, 7-methoxy-2-methyl isoflavone, and formononetin may exert major therapeutic effects by regulating key factors, such as AKT1, APOE, and GSK3B, in the inflammatory reaction, glycolipid oxidation, and glycogen synthesis related signaling pathways.

Virtual Simulation of the Effect of FMCW Laser Fuse Detector's Component Performance Variability on Target Echo Characteristics under Smoke Interference.

The laser transmitter and photoelectric receiver are the core modules of the detector in a laser proximity fuse, whose performance variability can affect the accuracy of target detection and identification. In particular, there is no study on the effect of detector's component performance variability on frequency-modulated continuous-wave (FMCW) laser fuse under smoke interference. Therefore, based on the principles of particle dynamic collision, ray tracing, and laser detection, this paper builds a virtual simulation model of FMCW laser transmission with the professional particle system of Unity3D, and studies the effect of performance variability of laser fuse detector components on the target characteristics under smoke interference. Simulation results show that the difference in the performance of the fuse detector components causes the amplitude variation and peak migration of the beat signal spectrum, and the change in the visibility of the smoke can also affect the results, which indicates that the factors affecting the signal-to-noise ratio (SNR) of the echo signal are related to the smoke interference and performance variability of the detector. The proposed simulation model is supported by experimental results, which reflect the reliability of the proposed findings. Therefore, this study can be used for the optimization of the parameters in the laser fuse antismoke interference to avoid false alarms.

Boundary force exerted on spatial solitons in cylindrical strongly nonlocal media.

We investigate the propagation of spatial solitons in cylindrical strongly nonlocal media by a method of image beam of light. The dynamic force of the soliton steering resulting from the boundary effect is equivalent to the force between the soliton beam and the image beam. The trajectory of the soliton is analytically studied, which is in good agreement with the experimental results.

Identification of a novel alternative splicing variant of RGS5 mRNA in human ocular tissues.

Regulator of G protein signaling (RGS) proteins act as GTPase-activating proteins (GAPs) for Galpha subunits and negatively regulate G protein-coupled receptor signaling. Using RGS5 gene-specific RT-PCR, we have identified a novel alternative splicing variant of RGS5 mRNA in human ocular tissues. The alternative splicing of RGS5 mRNA occurred at position +44 (GenBank NM_003617), spliced out 174 bp (+44 to +218 bp) of the coding region, and encoded an RGS5s protein with a 108 amino acid N-terminal deletion. This study is the first to document alternative splicing of an RGS5 gene. We therefore studied RGS5 and RGS5s mRNA distribution in human tissues. In the eye, RGS5s was found to be highly expressed in the ciliary body and trabecular meshwork. It was also expressed in the kidney, brain, spleen, skeletal muscle and small intestine, but was not detectable in the liver, lung, heart. RGS5s was not found in monkey and rat ocular tissues, indicating species specificity for the eye. Comparing the recombinant RGS5 and RGS5s expression in HEK293/EBNA cells, RGS5s was present almost exclusively in the cytosolic fraction, whereas RGS5 was present in both membrane and cytosolic fractions. The data suggest that the N-terminal of RGS5 may be important for protein translocation to the cell membrane. Both RGS5 and RGS5s antagonized the rapid phosphorylation of p44/42 MAP kinase induced by Galphai coupled cannibinoid receptor-1 activation. RGS5, but not RGS5s, inhibited the Ca2+ signaling initiated by activation of Galphaq coupled angiotensin II receptors (AT1) and prostaglandin FP receptors. Cotransfection of RGS5s with RGS5 resulted in the blockade of RGS5 actions with respect to inhibition of the signal transduction initiated by activation of both AT1 and FP receptor, suggesting that RGS5s may contain functional domains that compete with RGS5 in the regulation of the Galphaq coupled AT1 and FP receptors. The unique expression pattern, cellular localization and functions of RGS5s suggest that RGS5s may play a critical role in the regulation of intracellular signaling pathways.

Upregulation of orphan nuclear receptor Nur77 following PGF(2alpha), Bimatoprost, and Butaprost treatments. Essential role of a protein kinase C pathway involved in EP(2) receptor activated Nur77 gene transcription.

1. Using gene chip technology, we first identified that PGF(2alpha) (FP agonist) and Butaprost (EP(2) agonist) induced about a five-fold upregulation of Nur77 mRNA expression in hFP-HEK 293/EBNA and hEP(2)-HEK293/EBNA cells. Northern Blot analysis revealed that PGF(2alpha)- and Butaprost-induced upregulation of Nur77 expression are dose- and time-dependent. 2. Both PGF(2alpha) and Butaprost upregulated Nur77 gene expression through the protein kinase C (PKC) pathway. These data are the first showing a link between EP(2) receptor stimulation and protein kinase C activation. Calcineurin was found to be involved downstream of the PKC pathway in PGF(2alpha)-induced Nur77 expression, but not in Butaprost-induced Nur77 expression. 3. We also used Nur77 as a marker gene to compare the effects of PGF(2alpha), Butaprost, and Bimatoprost (a prostamide) on Nur77 expression in human primary trabecular meshwork and ciliary smooth muscle (SM) cells, which are target cells for antiglaucoma drugs. The results showed that PGF(2alpha) and Butaprost, but not Bimatoprost, induced upregulation of Nur77 expression in human TM cells. PGF(2alpha), but not Bimatoprost, dramatically induced upregulation of Nur77 mRNA expression in human ciliary SM cells, whereas Butaprost slightly upregulated Nur77 mRNA expression in SM cells. 4. Nur77 promoter deletion analysis indicated that PGF(2alpha), but not Bimatoprost, activated Nur77 promoter-luciferase reporter in hFP-HEK 293/EBNA cells. Butaprost was less efficacious in inducing Nur77 promoter-luciferase reporter activity in hEP(2)-HEK293/EBNA cells relative to PGF(2alpha) in the comparable assay. The data for Nur77 promoter functional analysis were matched to the Northern blot analysis. 5. It appears that PGF(2alpha) and Butaprost activate Nur77 transcription mechanisms through the activation of FP and EP(2) receptor-coupled signaling pathways, whereas Bimatoprost stimulates neither FP nor EP(2) receptors.

Microglial apolipoprotein E and astroglial apolipoprotein J expression in vitro: opposite effects of lipopolysaccharide.

Apolipoprotein E (apoE) and apoJ are lipid carriers produced in the brain primarily by glial cells. A variety of glial-activating stimuli induce a parallel upregulation of both apolipoproteins expression in vivo and in vitro. To further characterize the cell type and mechanisms by which apoE and apoJ expression are upregulated in activated glia, mixed glial cultures from neonatal rat cortex were treated with the endotoxin lipopolysaccharide (LPS). LPS induced dose-dependent increases in apoJ and decreases in apoE expression and secretion with maximum effects at 1-10 ng/mL and 0.1-1 microg/mL, respectively. Experiments with enriched astroglial and microglial cultures demonstrated that apoE and apoJ expression are predominantly microglial and astroglial, respectively. Given the pivotal role that nuclear factor-kappa B (NF-kappa B) plays in glial activation, we assessed its possible role in mediating apoE and apoJ expression by activated glia. LPS robustly increased NF-kappa B activation in mixed glial cultures. Two NF-kappa B inhibitors, aspirin (10 mM) and MG-132 (0.1 microM), blocked basal apoE and apoJ secretion as well as LPS-induced apoJ secretion. These data demonstrate that glial apoE and apoJ expression are independently regulated by LPS in microglia and astroglia, respectively, and that activated microglia are the predominant source of apoE in mixed glial cultures. The transcription factor NF-kappa B appears to be a critical mediator of LPS-stimulated apoJ expression from astroglia.

Comparison of prostaglandin F2alpha, bimatoprost (prostamide), and butaprost (EP2 agonist) on Cyr61 and connective tissue growth factor gene expression.

Connective tissue growth factor (CTGF) and Cyr61 (cysteine-rich angiogenic protein 61) are members of the CCN gene family that encode multifunctional, extracellular matrix-associated signaling proteins. Because the mechanism of action of certain anti-glaucoma drugs involves extracellular matrix remodeling of ocular ciliary muscle, with a resultant increase in drainage of aqueous humor from the eye, we compared the effects of three pharmacologically distinct ocular hypotensive agents on Cyr61 and CTGF gene expression. Thus, prostaglandin F2alpha (PGF2alpha) (FP receptor agonist), Butaprost (EP2 receptor agonist), and Bimatoprost (a prostamide) were compared. Using Affymetrix gene chip technology, we first identified that PGF2alpha dramatically up-regulated Cyr61 and CTGF mRNA expression in HEK 293/EBNA cells (hFP-HEK 293/EBNA). Northern blot further confirmed the Cyr61 and CTGF up-regulation is in a dose- and time-dependent manner. PGF2alpha-induced up-regulation of Cyr61 appeared to exclusively involve the Rho pathway, and up-regulation of CTGF was via multiple intracellular pathways. Because prostamide receptors are, to date, defined only at the pharmacological level, Bimatoprost effects on Cyr61 and CTGF were studied in the isolated feline iris sphincter preparation, a tissue highly responsive to prostamides. Both PGF2alpha and Bimatoprost up-regulated Cyr61 mRNA expression in the cat iris tissue. Only PGF2alpha up-regulated CTGF mRNA expression in the cat iris. Therefore, PGF2alpha and Bimatoprost appear to interact with different receptors populations in the cat iris, according to their markedly different effects on CTGF. Activation of prostaglandin EP2 receptors (Gs-coupled) also up-regulated Cyr61 but not CTGF mRNA expression in the isolated cat iris. Similar data were observed in human primary ciliary smooth muscle cells. Thus, despite quite different signal transduction pathways, FP receptor stimulation up-regulates CTGF and Cyr61. The prostamide analog Bimatoprost and an EP2-selective agonist affects only Cyr61.