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This paper is concerned with the stabilization of complex-valued stochastic coupled systems possessing multiple time delays and regime-switching jump diffusion (RSJD) via periodically intermittent control. Moreover, most of the existing results about RSJD are considered in real-valued cases, which is extended to complex-valued cases in this paper. Combining the Lyapunov method with the graph theory, some sufficient conditions can be obtained, which reflect that the realization of stability is related to stochastic disturbance strength, coupling strength and control rate. Additionally, the theoretical results are applied to complex-valued stochastic coupled oscillators with multiple time delays and RSJD. In the end, some simulation results are presented to demonstrate the validity and availability of the theoretical results.

In this paper, two linearized Galerkin finite element methods, which are based on the L1 approximation and the WSGD operator, respectively, are proposed to solve the nonlinear fractional Rayleigh-Stokes problem. In order to obtain the unconditionally optimal error estimate, we firstly introduce a time-discrete elliptic equation, and derive the unconditional error estimate between the exact solution and the solution of the time-discrete system in H 2 -norm. Secondly, we obtain the boundedness of the fully discrete finite element solution in L ∞ -norm through the more detailed study of the error equation. Then, the optimal L 2 -norm error estimate is derived for the fully discrete system without any restriction conditions on the time step size. Finally, some numerical experiments are presented to confirm the theoretical results, showing that the two linearized schemes given in this paper are efficient and reliable.

Quantifying canopy biophysical parameters is critical to agricultural research and farm management. In this study, strawberry dry biomass and leaf area were modeled statistically using high spatial and temporal resolution imagery. A mobile field data acquisition system was used to acquire thousands of very high resolution (~0.5 mm) close-range images seven times throughout the strawberry growing season. Ortho-mosaics and dense point clouds were generated through Structure from Motion (SfM) and used in Object-Based Image Analysis (OBIA) at the sub-leaf level to extract canopy structure variables such as planimetric canopy area, canopy average height, and canopy smoothness metric. Regression analysis was carried out using these image-derived canopy variables as predictors to model leaf area ( R 2 = 0.79; ten-fold cross-validation RMSE = 0.056 m2) and dry biomass ( R 2 = 0.84; ten-fold cross-validation RMSE = 7.72 g) obtained through destructive measurements. Results indicate consistent predictive power through the season and across 17 strawberry genotypes. The study showed that the canopy smoothness metric developed in this study as an indicator of canopy density could complement other variables (planimetric canopy area, canopy average height) that describe canopy geometric properties.

A sequence of Cr-modified CeZr2Ox catalysts were synthesized through the co-precipitation way and applied in selective catalytic reduction (SCR) of NOx with ammonia. The optimal catalyst (Cr1CeZr2Ox) exhibited the excellent NH3-SCR activity and high SO2 resistance. From the characterization results, Cr species in Cr1CeZr2Ox could suppress the formation of ZrO2 crystals, which could also contribute to stronger surface acidity and reducibility. Besides, more Ce3+ and surface adsorbed oxygen species were observed on Cr1CeZr2Ox catalyst. On the basis of in situ DRIFT experiments, it could be confirmed that the NH3-SCR process on Cr1CeZr2Ox was promoted through Langmuir-Hinshelwood (L-H) mechanism. Besides, the improved NO oxidation and more ad-NOx and ad-NH3 also played a vital role for the superior low-temperature SCR activity of Cr1CeZr2Ox.

Removal of NO and Hg0 simultaneously was achieved on Nb-modified MnTiOx catalyst. Experimental results revealed that high NO conversion (>95%) and Hg0 oxidation (>95%) in 200–300 °C were available on Mn0.15Nb0.02TiOx catalyst with a GHSV of 108,000 h−1. The excellent catalytic performance of Mn0.15Nb0.02TiOx catalyst should be originated from its high reducibility and massive surface chemisorbed oxygen species. Moreover, the introduction of Nb into MnTiOx catalyst greatly enhanced its resistance to SO2 and H2O. Neither gaseous Hg0 nor HgO formed on catalyst surface could affect the NH3-SCR reaction. NO had a promotion effect on Hg0 oxidation, while NH3 was detrimental to Hg0 oxidation owing to the inhibited adsorption of Hg0 by NH3. Under SCR reaction conditions, an inhibition impact on Hg0 oxidation could be detected, but this negative effect could be avoided by using more catalyst sample.

Spinal cord paralysis is relatively common after surgical repair of thoraco-abdominal aortic aneurysm (TAAA) and its etiology is unknown. The present study was designed to examine the histopathology of the disease and investigate whether miR-155 ablation would reduce spinal cord ischemic damage and delayed hindlimb paralysis induced by aortic cross-clamping (ACC) in our mouse model. The loss of locomotor function in ACC-paralyzed mice correlated with the presence of extensive gray matter damage and central cord edema, with minimal white matter histopathology. qRTPCR and Western blotting showed that the spinal cords of wild-type ACC mice that escaped paralysis showed lower miR-155 expression and higher levels of transcripts encoding Mfsd2a, which is implicated in the maintenance of blood-brain barrier integrity. In situ based testing demonstrated that increased miR-155 detection in neurons was highly correlated with the gray matter damage and the loss of one of its targets, Mfsd2a, could serve as a good biomarker of the endothelial cell damage. In vitro, we demonstrated that miR-155 targeted Mfsd2a in endothelial cells and motoneurons and increased endothelial cell permeability. Finally, miR-155 ablation slowed the progression of central cord edema, and reduced the incidence of paralysis by 40%. In sum, the surgical pathology findings clearly indicated that the epicenter of the ischemic-induced paralysis was the gray matter and that endothelial cell damage correlated to Mfsd2a loss is a good biomarker of the disease. MiR-155 targeting therefore offers new therapeutic opportunity for edema caused by traumatic spinal cord injury and diagnostic pathologists, by using immunohistochemistry, can clarify if this mechanism also is important in other ischemic diseases of the CNS, including stroke.

In this paper, we propose a fully discrete stabilized multiphysics finite element method by the pressure projection method to solve the polymer gel model. To reveal the multi-physical process of the polymer gel model, we reformulate the polymer gel model by introducing a new variable to get a new multi-field problem, then we propose the fully discrete stabilized multiphysics finite element method using the simplest equal order element of P 1 − P 1 − P 1 without the discrete inf–sup condition to solve the new reformulated system, and we prove that the new method not only has no ”locking” phenomenon, but also preserves some energy conservation laws. Also, we prove that the stabilized multiphysics finite element method has optimal convergence order. Finally, we give the numerical example to verify the theoretical results.

Spinal cord injury (SCI) damages supraspinal control over spinal autonomic circuitry. As a result, normally innocuous visceral or somatic stimuli (e.g. distended bladder or bowel) trigger pathological dysautonomia caused by uncontrolled reflex activation of sympathetic circuitry. In this report we show that remarkable structural remodeling and synaptic plasticity occurs within spinal autonomic circuitry and that this increases the frequency of autonomic dysreflexia (AD), a life-threatening condition of episodic vascular hypertension that develops progressively in SCI animals and people. We also prove that maladaptive plasticity can be prevented if SCI mice are treated with human equivalent doses of the FDA-approved drug, gabapentin (GBP) before the onset of plasticity. Although GBP is used clinically to treat pain or spasticity after symptom onset, we tested the hypothesis that GBP would prevent maladaptive plasticity if it were used as a prophylactic therapy, starting before the onset of a critical period of enhanced synaptogenesis with maintenance dosing continued for up to 35d post-injury. Using this novel treatment regimen, we show that prophylactic GBP successfully blocks multi-segmental excitatory synaptogenesis within spinal autonomic lamina, abolishes sprouting of autonomic neurons that innervate immune organs and also the sensory afferents that trigger pain and AD. Functionally, this treatment protocol delays the onset and decreases the frequency of spontaneous AD, confers resistance to experimentally induced AD, and protects mice from SCI-induced immune suppression. These data show that GBP could be repurposed as a prophylactic therapy in at-risk individuals with a high-level SCI to prevent the pathological effects of autonomic dysfunction.

SUMMARY After spinal cord injury (SCI), normally innocuous visceral or somatic stimuli can trigger uncontrolled reflex activation of sympathetic circuitry, causing pathological dysautonomia. We show that remarkable structural remodeling and plasticity occur within spinal autonomic circuitry, creating abnormal sympathetic reflexes that promote dysautonomia. However, when mice are treated early after SCI with human-equivalent doses of the US Food and Drug Administration (FDA)-approved drug gabapentin (GBP), it is possible to block multi-segmental excitatory synaptogenesis and abolish sprouting of autonomic neurons that innervate immune organs and sensory afferents that trigger pain and autonomic dysreflexia (AD). This “prophylactic GBP” regimen decreases the frequency and severity of AD and protects against SCI-induced immune suppression. These benefits persist even 1 month after stopping treatment. GBP could be repurposed to prevent dysautonomia in at-risk individuals with high-level SCI., In Brief Brennan et al. show that α2δ−1 calcium channel subunits drive remarkable structural reorganization of autonomic circuitry and autonomic dysfunction after spinal cord injury. Early (prophylactic) post-injury treatment with gabapentin, an FDA-approved drug, prevents α2δ−1-dependent structural changes and autonomic dysfunction. Prophylactic gabapentin could be repurposed clinically for at-risk individuals., Graphical Abstract

High-quality three dimensional seismic data integrated with well data are used to identify, interpret and assess the significance of mass transport deposits (MTDs) to the evolution of the Kaiping Sag, Zhu-II depression, Pearl River Mouth Basin (northern South China Sea). Diagnostic features observed in 3D and 2D reflection seismic profiles document a multifarious mass movement history spanning from the Middle Miocene to the Quaternary period. MTDs in the Kaiping Sag were composite and multi-event units involving the entire spectra of mass transport processes. The diagnostic fingerprints of MTDs includes chaotic to transparent acoustic facies, and significant amounts of basal erosion grooves in the middle part of basal shear surfaces. We decipher for the first time that tectonic events, sea level fluctuations slope instability and/or volcanism may control the southwest decreasing distribution of MTDs in the Kaiping Sag. Knowledge regarding the seismic identification characteristics, the spatial and temporal distribution of MTDs, along with a better understanding of their underlying geological processes is valuable for providing new insights on the tectono-stratigraphic evolution of the Kaiping Sag.

We devise second-order accurate, unconditionally uniquely solvable and unconditionally energy stable schemes for the nonlocal Cahn-Hilliard (nCH) and nonlocal Allen-Cahn (nAC) equations for a large class of interaction kernels. We present numerical evidence that both schemes are convergent. We solve the nonlinear equations resulting from discretization using an efficient nonlinear multigrid method and demonstrate the performance of our algorithms by simulating nucleation and crystal growth for several different choices of interaction kernels.

Folate deficiency is considered a risk factor for many diseases such as cancer, congenital heart disease and neural tube defects (NTDs). There is a pressing need for more methods of detecting folate and its main metabolites in the human body. Here, we developed a simple, fast and sensitive ultraperformance liquid chromatography tandem mass spectrometry (UPLC/MS/MS) method for the simultaneous quantifications of folate metabolites including folic acid, 5-methyltetrahydrofolate (5-MeTHF), 5-formyltetrahydrofolate (5-FoTHF), homocysteine (Hcy), S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH). The method was validated by determining the linearity (r(2)0.998), sensitivity (limit of detection ranged from 0.05 to 0.200ng/mL), intra- and inter-day precision (both CV6%) and recovery (each analyte was90%). The total analysis time was 7min. Serum samples of NTD-affected pregnancies and controls from a NTD high-risk area in China were analyzed by this method, the NTD serum samples showed lower concentrations of 5-MeTHF (P0.05) and 5-FoTHF (P0.05), and higher concentrations of Hcy (P0.05) and SAH (P0.05) compared with serum samples from controls, consistent with a previous study. These results showed that the method is sensitive and reliable for simultaneous determination of six metabolites, which might indicate potential risk factors for NTDs, aid early diagnosis and provide more insights into the pathogenesis of NTDs.

It is widely believed that microglia and monocyte-derived macrophages (collectively referred to as central nervous system (CNS) macrophages) cause excitotoxicity in the diseased or injured CNS. This view has evolved mostly from in vitro studies showing that neurotoxic concentrations of glutamate are released from CNS macrophages stimulated with lipopolysaccharide (LPS), a potent inflammogen. We hypothesized that excitotoxic killing by CNS macrophages is more rigorously controlled in vivo, requiring both the activation of the glutamate/cystine antiporter (system x(c)(-)) and an increase in extracellular cystine, the substrate that drives glutamate release. Here, we show that non-traumatic microinjection of low-dose LPS into spinal cord gray matter activates CNS macrophages but without causing overt neuropathology. In contrast, neurotoxic inflammation occurs when LPS and cystine are co-injected. Simultaneous injection of NBQX, an antagonist of AMPA glutamate receptors, reduces the neurotoxic effects of LPS+cystine, implicating glutamate as a mediator of neuronal cell death in this model. Surprisingly, neither LPS nor LPS+cystine adversely affects survival of oligodendrocytes or oligodendrocyte progenitor cells. Ex vivo analyses show that redox balance in microglia and macrophages is controlled by induction of system x(c)(-) and that high GSH:GSSG ratios predict the neurotoxic potential of these cells. Together, these data indicate that modulation of redox balance in CNS macrophages, perhaps through regulating system x(c)(-), could be a novel approach for attenuating injurious neuroinflammatory cascades.

PDGF-BB induces a rapid, sustained increase in intracellular calcium levels in U-1242 MG cells. We used several calcium channel blockers to identify the types of channels involved. L channel blockers (verapamil, nimodipine, nicardipine, nitrendipine and taicatoxin) had no effect on PDGF-BB induced alterations in intracellular calcium. Blockers of P, Q and N channels (ω-agatoxin-IVA, ω-conotoxin MVIIC and ω-conotoxin GVIA) also had no effect. This indicates that these channels play an insignificant role in supplying the Ca 2+ necessary for PDGF stimulated events in U-1242 MG cells. However, a T channel blocker (NDGA) and the non-specific (NS) calcium channel blockers (FFA and SK&F 9365) abolished PDGF-induced increases in intracellular calcium. This indicates that PDGF causes calcium influx through both non-specific cationic channels and T channels. To study the participation of intracellular calcium stores in this process, we used thapsigargin, caffeine and ryanodine, all of which cause depletion of intracellular calcium stores. The PDGF effect was abolished using both thapsigargin and caffeine but not ryanodine. Collectively, these data indicate that in these human glioma cells PDGF-BB induces release of intracellular calcium from caffeine- and thapsigargin-sensitive calcium stores which in turn lead to further calcium influx through both NS and T channels.

Neurotrophic factors have been proposed as a therapeutic treatment for traumatic brain and spinal cord injury. The present study determined whether exogenous administration of one such factor, brain-derived neurotrophic factor (BDNF), could effect behavioral recovery and/or histopathological changes after spinal cord injury. Adult rats received a mild or moderate contusion injury or complete transection of the mid-thoracic spinal cord. Immediately thereafter, they were infused intrathecally with vehicle or BDNF for 28 days. Behavioral recovery was evaluated for 6 weeks after injury, at which time the rats were sacrificed and the spinal cord tissue was examined histologically. The infusion of BDNF resulted in acute stimulation of hindlimb activity. These effects included activation of alternating airstepping in injured rats when the hindlimbs were unloaded as well as slight improvements in the rate of recovery in open field locomotion score. BDNF infusion was also associated with enhanced growth of cholinergic fibers at the injury epicenter, but did not affect white matter sparing or density of serotonergic axons at or below the injury site. Based on immunohistochemical detection of BDNF protein distribution, these described effects are likely to be mediated by the activation of cells and axons within the central injury region and the along the peripheral rim of the spinal cord. Together, these findings demonstrate that the exogenous infusion of BDNF after spinal trauma can influence postinjury outcome through mechanisms that include acute stimulation of hindlimb activity and neuritogenesis at the injury site.

The accurate calibration of Fura-2 fluorescence in living cells is dependent upon the apparent dissociation constant (Kd) of Fura-2 for Ca2+. If Ca-EGTA calibration buffers are used to construct an in vitro calibration curve, then the calculated value of the apparent Ca-EGTA association constant (K'CaEGTA) will have an important influence on the Kd of Fura-2 and thus the calculated free [Ca2+] in cells. In order to simulate experimental conditions, the individual proton and Ca2+ association constants for EGTA in these experiments were adjusted for both ionic strength and temperature using a semi-empirical form of the Debye-Huckel limiting law and the Van't Hoff isochore, respectively, as described by Harrison and Bers. The modified individual binding constants were then employed in the calculation of K'CaEGTA using the SPECS computer program of Fabatio. At pH = 7.05, ionic strength = 0.15 M, temp = 20 degrees C, K'CaEGTA = 3.232 x 10(6) M-1; at pH = 6.84, temp = 36 degrees C, K'CaEGTA = 1.652 x 10(6) M-1. These values differed substantially from those obtained with unadjusted individual association constants. Calibration buffers of varying [Ca2+] were prepared using the corrected values of K'CaEGTA, and Fura-2 fluorescence ratios were measured during superfusion of these buffers in the experimental chamber at both 20 degrees C and 37 degrees C. The Kd of Fura-2 for Ca2+ was determined to be 236 nM at 20 degrees C and 285 nM at 37 degrees C, utilizing the value of K'CaEGTA adjusted by the method of Harrison and Bers.(ABSTRACT TRUNCATED AT 250 WORDS)