Natural Products Improve Organ Microcirculation Dysfunction Following Ischemia/Reperfusion-and Lipopolysaccharide-Induced Disturbances:Mechanistic and Therapeutic Views

Microcirculatory disturbances are complex processes caused by many factors,including abnormal vasomotor responses,decreased blood flow velocity,vascular endothelial cell injury,altered leukocyte and endothelial cell interactions,plasma albumin leakage,microvascular hemorrhage,and thrombosis.These disturbances involve multiple mechanisms and interactions among mechanisms that can include energy metabolism,the mitochondrial respiratory chain,oxidative stress,inflammatory factors,adhesion molecules,the cytoskeleton,vascular endothelial cells,caveolae,cell junctions,the vascular basement membrane,neutrophils,monocytes,and platelets.In clinical practice,aside from drugs that target abnormal vasomotor responses and platelet adhesion,there continues to be a lack of multi-target drugs that can regulate the complex mechanistic links and interactions underlying microcirculatory disturbances.Natural products have demonstrated obvious positive therapeutic effects in treating ischemia/reperfusion(I/R)-and lipopolysaccharide(LPS)-induced microcirculatory disturbances.In recent years,numerous research papers on the improvement of microcirculatory function by natural products have been published in international journals.In 2008 and 2017,the first listed author of this review was invited to publish reviews in the journal of Pharmacology&Therapeutics on the improvement of microcirculatory disturbances and organ injury induced by I/R using Salvia miltiorrhiza ingredients and other natural components of compounded Chinese medicine,respectively.This review systematically summarizes the effects,targets of action,and mechanisms of natural products regarding improving I/R-and LPSinduced microcirculatory disturbances and tissue injury.Based on this summary,scientific proposals are suggested for the discovery of new drugs to improve microcirculatory disturbances in disease.

Uncertainties of ENSO-related Regional Hadley Circulation Anomalies within Eight Reanalysis Datasets

El Nino-Southern Oscillation(ENSO),the leading mode of global interannual variability,usually intensifies the Hadley Circulation(HC),and meanwhile constrains its meridional extension,leading to an equatorward movement of the jet system.Previous studies have investigated the response of HC to ENSO events using different reanalysis datasets and evaluated their capability in capturing the main features of ENSO-associated HC anomalies.However,these studies mainly focused on the global HC,represented by a zonal-mean mass stream function(MSF).Comparatively fewer studies have evaluated HC responses from a regional perspective,partly due to the prerequisite of the Stokes MSF,which prevents us from integrating a regional HC.In this study,we adopt a recently developed technique to construct the three-dimensional structure of HC and evaluate the capability of eight state-of-the-art reanalyses in reproducing the regional HC response to ENSO events.Results show that all eight reanalyses reproduce the spatial structure of HC responses well,with an intensified HC around the central-eastern Pacific but weakened circulations around the Indo-Pacific warm pool and tropical Atlantic.The spatial correlation coefficient of the three-dimensional HC anomalies among the different datasets is always larger than 0.93.However,these datasets may not capture the amplitudes of the HC responses well.This uncertainty is especially large for ENSO-associated equatorially asymmetric HC anomalies,with the maximum amplitude in Climate Forecast System Reanalysis(CFSR)being about 2.7 times the minimum value in the Twentieth Century Reanalysis(20CR).One should be careful when using reanalysis data to evaluate the intensity of ENSO-associated HC anomalies.

Exendin-4 and linagliptin attenuate neuroinflammation in a mouse model of Parkinson's disease

Use of glucagon-like peptide-1 receptor agonist or dipeptidyl peptidase 4 inhibitor has been shown to lower the incidence of Parkinson's disease in patients with diabetes mellitus.Therefore,using these two treatments may help treat Parkinson's disease.To further investigate the mechanisms of action of these two compounds,we established a model of Parkinson's disease by treating mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and then subcutaneously injected them with the glucagon-like peptide-1 receptor agonist exendin-4 or the dipeptidyl peptidase 4 inhibitor linagliptin.We found that both exendin-4 and linagliptin reversed motor dysfunction,glial activation,and dopaminergic neuronal death in this model.In addition,both exendin-4 and linagliptin induced microglial polarization to the anti-inflammatory M2 phenotype and reduced pro-inflammatory cytokine secretion.Moreover,in vitro experiments showed that treatment with exendin-4 and linagliptin inhibited activation of the nucleotide-binding oligomerization domain-and leucine-rich-repeat-and pyrin-domaincontaining 3/caspase-1/interleukin-1βpathway and subsequent pyroptosis by decreasing the production of reactive oxygen species.These findings suggest that exendin-4 and linagliptin exert neuroprotective effects by attenuating neuroinflammation through regulation of microglial polarization and the nucleotidebinding oligomerization domain-and leucine-rich-repeat-and pyrin-domain-containing 3/caspase-1/interleukin-1βpathway in a mouse model of Parkinson's disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.Therefore,these two drugs may serve as novel anti-inflammatory treatments for Parkinson's disease.

Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis

Emodin,a substance extracted from herbs such as rhubarb,has a protective effect on the central nervous system.However,the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown.In this study,a rat model of experimental autoimmune encephalomyelitis was established by immune induction to simulate multiple sclerosis,and the rats were intraperitoneally injected with emodin(20 mg/kg/d)from the day of immune induction until they were sacrificed.In this model,the nucleotide-binding domain-like receptor family pyrin domain containing 3(NLRP3)inflammasome and the microglia exacerbated neuroinflammation,playing an important role in the development of multiple sclerosis.In addition,silent information regulator of transcription 1(SIRT1)/peroxisome proliferator-activated receptor-alpha coactivator(PGC-1α)was found to inhibit activation of the NLRP3 inflammasome,and SIRT1 activation reduced disease severity in experimental autoimmune encephalomyelitis.Furthermore,treatment with emodin decreased body weight loss and neurobehavioral deficits,alleviated inflammatory cell infiltration and demyelination,reduced the expression of inflammatory cytokines,inhibited microglial aggregation and activation,decreased the levels of NLRP3 signaling pathway molecules,and increased the expression of SIRT1 and PGC-1α.These findings suggest that emodin improves the symptoms of experimental autoimmune encephalomyelitis,possibly through regulating the SIRT1/PGC-1α/NLRP3 signaling pathway and inhibiting microglial inflammation.These findings provide experimental evidence for treatment of multiple sclerosis with emodin,enlarging the scope of clinical application for emodin.

DNA hypomethylation promotes learning and memory recovery in a rat model of cerebral ischemia/reperfusion injury

Cerebral ischemia/reperfusion injury impairs learning and memory in patients.Studies have shown that synaptic function is involved in the formation and development of memory,and that DNA methylation plays a key role in the regulation of learning and memory.To investigate the role of DNA hypomethylation in cerebral ischemia/reperfusion injury,in this study,we established a rat model of cerebral ischemia/reperfusion injury by occlusion of the middle cerebral artery and then treated the rats with intraperitoneal 5-aza-2′-deoxycytidine,an inhibitor of DNA methylation.Our results showed that 5-aza-2′-deoxycytidine markedly improved the neurological function,and cognitive,social and spatial memory abilities,and dose-dependently increased the synaptic density and the expression of SYP and SHANK2 proteins in the hippocampus in a dose-dependent manner in rats with cerebral ischemia/reperfusion injury.The effects of 5-aza-2′-deoxycytidine were closely related to its reduction of genomic DNA methylation and DNA methylation at specific sites of the Syp and Shank2 genes in rats with cerebral ischemia/reperfusion injury.These findings suggest that inhibition of DNA methylation by 5-aza-2′-deoxycytidine promotes the recovery of learning and memory impairment in a rat model of cerebral ischemia/reperfusion injury.These results provide theoretical evidence for stroke treatment using epigenetic methods.

Exosome-transported IncRNA H19 regulates insulin-like growth factor-1 via the H19/let-7a/insulin-like growth factor-1 receptor axis in ischemic stroke

LncRNA(long non-coding RNA) H19 is a transcript of the H19 gene that is expressed during embryogenesis.We previously discove red a role for circular lncRNA H19 in the onset and prognosis of cerebral ischemic stroke.In this study,we used serum from patients with ischemic stroke,and mouse and cell culture models to elucidate the roles of plasma and neuronal exosomes in the regulatory effect of lncRNA H19 on insulin-like growth factor-1 and its mechanism in ischemic stroke,using western blotting,quantitative real-time polymerase chain reaction,and enzyme-linked immunosorbent assays.Plasma exosomal IncRNA H19 was negatively associated with blood levels of insulin-like growth factor-1 in samples from patients with cerebral ischemic stroke.In a mouse model,levels of exosomal IncRNA H19 were positively correlated with plasma and cerebral lncRNA H19.In a cell co-culture model,we confirmed that IncRNA H19 was transported from neuro ns to astrocytes by exosomes to induce downregulation of insulin-like growth factor-1 through the H19/let-7 a/insulin-like growth factor-1 receptor axis.This study provides the first evidence for the transpo rtation of IncRNA H19 by exosomes and the relationship between IncRNA H19 and insulinlike growth factor-1.

Insight to the enhanced microwave absorption of porous N-doped carbon driven by ZIF-8:Competition between graphitization and porosity

Porous carbon-based materials are promised to be lightweight dielectric microwave absorbents.Deeply understanding the influence of graphitization grade and porous structure on the dielectric parameters is urgently required.Herein,utilizing the low boiling point of Zn,porous N-doped carbon was fabricated by carbonization of ZIF-8(Zn)at different temperature,and the microwave absorption performance was investigated.The porous N-doped carbon inherits the high porosity of ZIF-8 precursor.By increasing the carbonization temperature,the contents of Zn and N elements are decreased;the graphitization degree is improved;however,the specific surface area and porosity are increased first and then decreased.When the carbonization temperature is 1000°C,the porous N-doped carbon behaves enhanced microwave absorption.With an ultrathin thickness of 1.29 mm,the ideal RL reaches-50.57 dB at 16.95 GHz and the effective absorption bandwidth is 4.17 GHz.The mechanism of boosted microwave absorption is ascribed to the competition of graphitization and porosity as well as N dopants,resulting in high dielectric loss capacity and good impedance matching.The porous structure can prolong the pathways and raise the contact opportunity between microwaves and porous carbon,causing multiple scattering,interface polarization,and improved impedance matching.Besides,the N dopants can induce electron polarization and defect polarization.These results give a new insight to construct lightweight carbon-based microwave absorbents by regulating the graphitization and porosity.

Prognostic scores in primary biliary cholangitis patients with advanced disease

BACKGROUND Due to the chronic progressive disease characteristics of primary biliary cholangitis(PBC),patients with advanced PBC should not be ignored.Most prognostic score studies have focused on early stage PBC.AIM To compare the prognostic value of various risk scores in advanced PBC to help PBC patients obtain more monitoring and assessment.METHODS This study considered patients diagnosed with PBC during hospitalization between 2015 and 2021.The clinical stage was primarily middle and late,and patients usually took ursodeoxycholic acid(UDCA)after diagnosis.The discriminatory performance of the scores was assessed with concordance statistics at baseline and after 1 year of UDCA treatment.Telephone follow-up was conducted to analyze the course and disease-associated outcomes.The follow-up deadline was December 31,2021.We compared the risk score indexes between those patients who reached a composite end point of death or liver transplantation(LT)and those who remained alive at the deadline.The combined performance of prognostic scores in estimating the risk of death or LT after 1 year of UDCA treatment was assessed using Cox regression analyses.Predictive accuracy was evaluated by comparing predicted and actual survival through Kaplan-Meier analyses.RESULTS We included 397 patients who were first diagnosed with PBC during hospitalization and received UDCA treatment;most disease stages were advanced.After an average of 6.4±1.4 years of follow-up,82 patients had died,and 4 patients had undergone LT.After receiving UDCA treatment for 1 year,the score with the best discrimination performance was the Mayo,with a concordance statistic of 0.740(95%confidence interval:0.690-0.791).The albumin-bilirubin,GLOBE,and Mayo scores tended to overestimate transplant-free survival.Comparing 7 years of calibration results showed that the Mayo score was the best model.CONCLUSION The Mayo,GLOBE,UK-PBC,and ALBI scores demonstrated comparable discriminating performance for advanced stage PBC.The Mayo score showed optimal discriminatory performance and excellent predictive accuracy.

Constraint-induced movement therapy enhances angiogenesis and neurogenesis after cerebral ischemia/reperfusion

Constraint-induced movement therapy after cerebral ischemia stimulates axonal growth by decreasing expression levels of Nogo-A,RhoA,and Rho-associated kinase(ROCK)in the ischemic boundary zone.However,it remains unclear if there are any associations between the Nogo-A/RhoA/ROCK pathway and angiogenesis in adult rat brains in pathological processes such as ischemic stroke.In addition,it has not yet been reported whether constraint-induced movement therapy can promote angiogenesis in stroke in adult rats by overcoming Nogo-A/RhoA/ROCK signaling.Here,a stroke model was established by middle cerebral artery occlusion and reperfusion.Seven days after stroke,the following treatments were initiated and continued for 3 weeks:forced limb use in constraint-induced movement therapy rats(constraint-induced movement therapy group),intraperitoneal infusion of fasudil(a ROCK inhibitor)in fasudil rats(fasudil group),or lateral ventricular injection of NEP1-40(a specific antagonist of the Nogo-66 receptor)in NEP1-40 rats(NEP1-40 group).Immunohistochemistry and western blot assay results showed that,at 2 weeks after middle cerebral artery occlusion,expression levels of RhoA and ROCK were lower in the ischemic boundary zone in rats treated with NEP1-40 compared with rats treated with ischemia/reperfusion or constraint-induced movement therapy alone.However,at 4 weeks after middle cerebral artery occlusion,expression levels of RhoA and ROCK in the ischemic boundary zone were markedly decreased in the NEP1-40 and constraint-induced movement therapy groups,but there was no difference between these two groups.Compared with the ischemia/reperfusion group,modified neurological severity scores and foot fault scores were lower and time taken to locate the platform was shorter in the constraint-induced movement therapy and fasudil groups at 4 weeks after middle cerebral artery occlusion,especially in the constraint-induced movement therapy group.Immunofluorescent staining demonstrated that fasudil promoted an immune response of nerve-regeneration-related markers(BrdU in combination with CD31(platelet endothelial cell adhesion molecule),Nestin,doublecortin,NeuN,and glial fibrillary acidic protein)in the subventricular zone and ischemic boundary zone ipsilateral to the infarct.After 3 weeks of constraint-induced movement therapy,the number of regenerated nerve cells was noticeably increased,and was accompanied by an increased immune response of tight junctions(claudin-5),a pericyte marker(a-smooth muscle actin),and vascular endothelial growth factor receptor 2.Taken together,the results demonstrate that,compared with fasudil,constraint-induced movement therapy led to stronger angiogenesis and nerve regeneration ability and better nerve functional recovery at 4 weeks after cerebral ischemia/reperfusion.In addition,constraint-induced movement therapy has the same degree of inhibition of RhoA and ROCK as NEP1-40.Therefore,constraint-induced movement therapy promotes angiogenesis and neurogenesis after cerebral ischemia/reperfusion injury,at least in part by overcoming the Nogo-A/RhoA/ROCK signaling pathway.All protocols were approved by the Institutional Animal Care and Use Committee of China Medical University,China on December 9,2015(approval No.2015 PS326 K).

Pathways of Influence of the Northern Hemisphere Mid–high Latitudes on East Asian Climate: A Review

This paper reviews recent progress made by Chinese scientists on the pathways of influence of the Northern Hemisphere mid-high latitudes on East Asian climate within the framework of a“coupled oceanic-atmospheric(land-atmospheric or seaice-atmospheric)bridge”and“chain coupled bridge”.Four major categories of pathways are concentrated upon,as follows:Pathway A—from North Atlantic to East Asia;Pathway B—from the North Pacific to East Asia;Pathway C—from the Arctic to East Asia;and Pathway D—the synergistic effects of the mid-high latitudes and tropics.In addition,definitions of the terms“combined effect”,“synergistic effect”and“antagonistic effect”of two or more factors of influence or processes and their criteria are introduced,so as to objectively investigate those effects in future research.

Recent Progress in Studies of the Variabilities and Mechanisms of the East Asian Monsoon in a Changing Climate

Located in a monsoon domain,East Asia suffers devastating natural hazards induced by anomalous monsoon behaviors.East Asian monsoon(EAM)research has traditionally been a high priority for the Chinese climate community and is particularly challenging in a changing climate where the global mean temperature has been rising.Recent advances in studies of the variabilities and mechanisms of the EAM are reviewed in this paper,focusing on the interannual to interdecadal time scales.Some new results have been achieved in understanding the behaviors of the EAM,such as the evolution of the East Asian summer monsoon(EASM),including both its onset and withdrawal over the South China Sea,the changes in the northern boundary activity of the EASM,or the transitional climate zone in East Asia,and the cycle of the EASM and the East Asian winter monsoon and their linkages.In addition,understanding of the mechanism of the EAM variability has improved in several aspects,including the impacts of different types of ENSO on the EAM,the impacts from the Indian Ocean and Atlantic Ocean,and the roles of mid-to high-latitude processes.Finally,some scientific issues regarding our understanding of the EAM are proposed for future investigation.

Neuroprotective mechanisms ofε-viniferin in a rotenone-induced cell model of Parkinson's disease:significance of SIRT3-mediated FOXO3 deacetylation

Trans-(-)-ε-viniferin(ε-viniferin)has antioxidative and anti-inflammatory effects.It also has neuroprotective effects in Huntington's disease by activating the SIRT3/LKB1/AMPK signaling pathway;however,it remains unknown whetherε-viniferin also has a neuroprotective role in Parkinson's disease.A Parkinson's disease cell model was induced by exposing SH-SY5 Y cells to 3.0μM rotenone for 24 hours,and cells were then treated with 1.0μMε-viniferin for 24 hours.Treatment withε-viniferin upregulated SIRT3 expression,which promoted FOXO3 deacetylation and nuclear localization.ε-Viniferin also increased ATP production and decreased reactive oxygen species production.Furthermore,ε-viniferin treatment alleviated rotenone-induced mitochondrial depolarization and reduced cell apoptosis,and restored the expression of mitochondrial homeostasis-related proteins.However,when cells were transfected with SIRT3 or FOXO3 shRNA prior to rotenone andε-viniferin treatment,these changes were reversed.The results from the present study indicate thatε-viniferin enhances SIRT3-mediated FOXO3 deacetylation,reduces oxidative stress,and maintains mitochondrial homeostasis,thus inhibiting rotenone-induced cell apoptosis.ε-Viniferin may therefore be a promising treatment strategy for Parkinson's disease.

MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway

Apoptosis is an important programmed cell death process involved in ischemia/reperfusion injury.MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ischemia and reperfusion injury.However,whether miR-670 can regulate cell growth and death in cerebral ischemia/reperfusion and the underlying mechanism are poorly understood.In this study,we established mouse models of transient middle artery occlusion and Neuro 2a cell models of oxygen-glucose deprivation and reoxygenation to investigate the potential molecular mechanism by which miR-670 exhibits its effects during cerebral ischemia/reperfusion injury both in vitro and in vivo.Our results showed that after ischemia/reperfusion injury,miR-670 expression was obviously increased.After miR-670 expression was inhibited with an miR-670 antagomir,cerebral ischemia/reperfusion injury-induced neuronal death was obviously reduced.When miR-670 overexpression was induced by an miR-670 agomir,neuronal apoptosis was increased.In addition,we also found that miR-670 could promote Yap degradation via phosphorylation and worsen neuronal apoptosis and neurological deficits.Inhibition of miR-670 reduced neurological impairments after cerebral ischemia/reperfusion injury.These results suggest that microRNA-670 aggravates cerebral ischemia/reperfusion injury through the Yap pathway,which may be a potential target for treatment of cerebral ischemia/reperfusion injury.The present study was approved by the Institutional Animal Care and Use Committee of China Medical University on February 27,2017(IRB No.2017PS035K).

Influence of the NAO on Wintertime Surface Air Temperature over East Asia:Multidecadal Variability and Decadal Prediction

In this paper,we investigate the influence of the winter NAO on the multidecadal variability of winter East Asian surface air temperature(EASAT)and EASAT decadal prediction.The observational analysis shows that the winter EASAT and East Asian minimum SAT(EAmSAT)display strong in-phase fluctuations and a significant 60-80-year multidecadal variability,apart from a long-term warming trend.The winter EASAT experienced a decreasing trend in the last two decades,which is consistent with the occurrence of extremely cold events in East Asia winters in recent years.The winter NAO leads the detrended winter EASAT by 12-18 years with the greatest significant positive correlation at the lead time of 15 years.Further analysis shows that ENSO may affect winter EASAT interannual variability,but does not affect the robust lead relationship between the winter NAO and EASAT.We present the coupled oceanic-atmospheric bridge(COAB)mechanism of the NAO influences on winter EASAT multidecadal variability through its accumulated delayed effect of~15 years on the Atlantic Multidecadal Oscillation(AMO)and Africa-Asia multidecadal teleconnection(AAMT)pattern.An NAO-based linear model for predicting winter decadal EASAT is constructed on the principle of the COAB mechanism,with good hindcast performance.The winter EASAT for 2020-34 is predicted to keep on fluctuating downward until~2025,implying a high probability of occurrence of extremely cold events in coming winters in East Asia,followed by a sudden turn towards sharp warming.The predicted 2020/21 winter EASAT is almost the same as the 2019/20 winter.

Ghrelin alleviates 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells

Ghrelin is a neuropeptide that has various physiological functions and has been demonstrated to be neuroprotective in a number of neurological disease models.However,the underlying mechanisms of ghrelin in Parkinson’s disease remain largely unexplored.The current study aimed to study the effects of ghrelin in a 6-hydroxydopamine(6-OHDA)-induced Parkinson’s disease model and evaluate the potential underlying mechanisms.In the present study,we treated an SH-SY5 Y cell model with 6-OHDA,and observed that pretreatment with different concentrations of ghrelin(1,10,and 100 nM)for 30 minutes relieved the neurotoxic effects of 6-OHDA,as revealed by Cell Counting Kit-8 and Annexin V/propidium iodide(PI)apoptosis assays.Reverse transcription quantitative polymerase chain reaction and western blot assay results demonstrated that 6-OHDA treatment upregulatedα-synuclein and lincRNA-p21 and downregulated TG-interacting factor 1(TGIF1),which was predicted as a potential transcription regulator of the gene encodingα-synuclein(SNCA).Ghrelin pretreatment was able to reverse the trends caused by 6-OHDA.The Annexin V/PI apoptosis assay results revealed that inhibiting eitherα-synuclein or lincRNA-p21 expression with small interfering RNA(siRNA)relieved 6-OHDA-induced cell apoptosis.Furthermore,inhibiting lincRNA-p21 also partially upregulated TGIF1.By retrieving information from a bioinformatics database and performing both double luciferase and RNA immunoprecipitation assays,we found that lincRNA-p21 and TGIF1 were able to form a double-stranded RNA-binding protein Staufen homolog 1(STAU1)binding site and further activate the STAU1-mediated mRNA decay pathway.In addition,TGIF1 was able to transcriptionally regulateα-synuclein expression by binding to the promoter of SNCA.The Annexin V/PI apoptosis assay results showed that either knockdown of TGIF1 or overexpression of lincRNA-p21 notably abolished the neuroprotective effects of ghrelin against 6-OHDA-induced neurotoxicity.Collectively,these findings suggest that ghrelin exerts neuroprotective effects against 6-OHDA-induced neurotoxicity via the lincRNA-p21/TGIF1/α-synuclein pathway.

Synergistic effect of total ionizing dose on single event effect induced by pulsed laser microbeam on SiGe heterojunction bipolar transistor

The synergistic effect of total ionizing dose（TID） on single event effect（SEE） in SiGe heterojunction bipolar transistor（HBT） is investigated in a series of experiments. The SiGe HBTs after being exposed to 60 Co g irradiation are struck by pulsed laser to simulate SEE. The SEE transient currents and collected charges of the un-irradiated device are compared with those of the devices which are irradiated at high and low dose rate with various biases. The results show that the SEE damage to un-irradiated device is more serious than that to irradiated SiGe HBT at a low applied voltage of laser test. In addition, the g irradiations at forward and all-grounded bias have an obvious influence on SEE in the SiGe HBT, but the synergistic effect after cutting off the g irradiation is not significant. The influence of positive oxide-trap charges induced by TID on the distortion of electric field in SEE is the major factor of the synergistic effect. Moreover, the recombination of interface traps also plays a role in charge collection.

Neuropsychiatric issues after stroke: Clinical significance and therapeutic implications

A spectrum of neuropsychiatric disorders is a common complication from stroke.Neuropsychiatric disorders after stroke have negative effects on functional recovery,increasing the rate of mortality and disability of stroke survivors.Given the vital significance of maintaining physical and mental health in stroke patients,neuropsychiatric issues after stroke have raised concerns by clinicians and researchers.This mini-review focuses on the most common non-cognitive functional neuropsychiatric disorders seen after stroke,including depressive disorders,anxiety disorders,post-traumatic stress disorder,psychosis,and psychotic disorders.For each condition,the clinical performance,epidemiology,identification of the therapeutic implication,and strategies are reviewed and discussed;the main opinions and perspectives presented here are based on the latest controlled studies,meta-analysis,or updated systematic reviews.In the absence of data from controlled studies,consensus recommendations were provided accordingly.

Adaptive beamforming and phase bias compensation for GNSS receiver

Adaptive antenna arrays have been used to mitigate the interference on global navigation satellite system（GNSS） receivers. The performance of interference mitigation depends on the beamforming algorithms adopted by the antenna array. However,the adaptive beamforming will change the array pattern in realtime, which has the potential to introduce phase center biases into the antenna array. For precise applications, these phase biases must be mitigated or compensated because they will bring errors in code phase and carrier phase measurements. A novel adaptive beamforming algorithm is proposed firstly, then the phase bias induced by the proposed algorithm is estimated, and finally a compensation strategy is addressed. Simulations demonstrate that the proposed beamforming algorithm suppresses effectively the strong interference and improves significantly the capturing performance of GNSS signals. Simultaneously, the bias compensation method avoids the loss of the carrier phase lock and reduces the phase measurement errors for GNSS receivers.

Borrower’s default and self-disclosure of social media information in P2P lending

Background:We examine the signaling effect of borrowers’social media behavior,especially self-disclosure behavior,on the default probability of money borrowers on a peer-to-peer(P2P)lending site.Method:We use a unique dataset that combines loan data from a large P2P lending site with the borrower’s social media presence data from a popular social media site.Results:Through a natural experiment enabled by an instrument variable,we identify two forms of social media information that act as signals of borrowers’creditworthiness:(1)borrowers’choice to self-disclose their social media account to the P2P lending site,and(2)borrowers’social media behavior,such as their social network scope and social media engagement.Conclusion:This study offers new insights for screening borrowers in P2P lending and a novel usage of social media information.

Decadal Indian Ocean Dipolar Variability and Its Relationship with the Tropical Pacific

A robust decadal Indian Ocean dipolar variability （DIOD） is identified in observations and found to be related to tropical Pacific decadal variability （TPDV）. A Pacific Ocean-global atmosphere （POGA） experiment, with fixed radiative forcing, is conducted to evaluate the DIOD variability and its relationship with the TPDV. In this experiment, the sea surface temperature anomalies are restored to observations over the tropical Pacific, but left as interactive with the atmosphere elsewhere. The TPDV-forced DIOD, represented as the ensemble mean of 10 simulations in POGA, accounts for one third of the total variance. The forced DIOD is triggered by anomalous Walker circulation in response to the TPDV and develops following Bjerknes feedback. Thermocline anomalies do not exhibit a propagating signal, indicating an absence of oceanic planetary wave adjustment in the subtropical Indian Ocean. The DIOD-TPDV correlation differs among the 10 simulations, with a low correlation corresponding to a strong internal DIOD independent of the TPDV. The variance of this internal DIOD depends on the background state in the Indian Ocean, modulated by the thermocline depth off Sumatra/Java.