Discovery of a Novel CSF-1R Inhibitor with Highly Improved Pharmacokinetic Profiles and Superior Efficacy in Colorectal Cancer Immunotherapy.

Blocking CSF-1/CSF-1R pathway has emerged as a promising strategy to remodel tumor immune microenvironment (TME) by reprogramming tumor-associated macrophages (TAMs). In this work, a novel CSF-1R inhibitor C19 with a highly improved pharmacokinetic profile and in vivo anticolorectal cancer (CRC) efficiency was successfully discovered. C19 could effectively reprogram M2-like TAMs to M1 phenotype and reshape the TME by inducing the recruitment of CD8+ T cells into tumors and reducing the infiltration of immunosuppressive Tregs/MDSCs. Deeper mechanistic studies revealed that C19 facilitated the infiltration of CD8+ T cells by enhancing the secretion of chemokine CXCL9, thus significantly potentiating the anti-CRC efficiency of PD-1 blockade. More importantly, C19 combined with PD-1 mAb could induce durable antitumor immune memory, effectively overcoming the recurrence of CRC. Taken together, our findings suggest that C19 is a promising therapeutic option for sensitizing CRC to anti-PD-1 therapy.

TFEB overexpression through GFAP promoter disrupts neuronal lamination by dysregulating neurogenesis during embryonic development.

INTRODUCTION: Transcription factor EB (TFEB), a key regulator of autophagy and lysosomal biogenesis, has diverse roles in various physiological processes. Enhancing lysosomal function by TFEB activation has recently been implicated in restoring neural stem cells (NSCs) function. Overexpression of TFEB can inhibit the cell cycle of newborn cortical NSCs. It has also been found that TFEB regulates the pluripotency transcriptional network in mouse embryonic stem cells independent of autophagy lysosomal biogenesis. This study aims to explore the effects of TFEB activation on neurogenesis in vivo through transgenic mice. METHODS: We developed a GFAP-driven TFEB overexpression mouse model (TFEB GoE) by crossing the floxed TFEB overexpression mice and hGFAP-cre mice. We performed immunohistochemical and fluorescence staining on brain tissue from newborn mice to assess neurogenesis changes, employing markers such as GFAP, Nestin, Ki67, DCX, Tbr1 and Neun to trace different stages of neural development and cell proliferation. RESULTS: TFEB GoE mice exhibited premature mortality, dying at 10-20 days after birth. Immunohistochemical analysis revealed significant abnormalities, including disrupted hippocampal structure and cortical layering. Compared to control mice, TFEB GoE mice showed a marked increase in radial glial cells (RGCs) in the hippocampus and cortex, with Ki67 staining indicating these cells were predominantly in a quiescent state. This suggests that TFEB overexpression suppresses RGCs proliferation. Additionally, abnormal distributions of migrating neurons and mature neurons were observed, highlighted by DCX, Tbr1 and Neun staining, indicating a disruption in normal neurogenesis. CONCLUSION: This study, using transgenic animals in vivo, revealed that GFAP-driven TFEB overexpression leads to abnormal neural layering in the hippocampus and cortex by dysregulating neurogenesis. Our study is the first to discover the detrimental impact of TFEB overexpression on neurogenesis during embryonic development, which has important reference significance in future TFEB overexpression interventions in NSCs for treatment.

Supercritical water oxidation for the treatment and utilization of organic wastes: Factor effects, reaction enhancement, and novel process.

Supercritical water oxidation (SCWO) has been regarded as a new and efficient technology for the harmless treatment and energy utilization of organic wastes, resulting in the quickly homogeneous oxidation between organics and oxidizers and the former being wholly degraded into small environment-friendly green molecules such as H2O and N2 and inorganic salts. This paper systematically analyzed the influencing behavior and mechanisms of the reaction factors, such as temperature, pressure, residence time, oxidant type, oxidation coefficient, and the concentration and pH values of the raw material, on the treatment effect of organic wastes. For most organic wastes, the SCWO conditions at 550 °C with a residence time of 1min and an oxidation coefficient of 100% can meet the removal rate of more than 99%. To further enhance the degradation rate of organics, the principles, implementation cases, and related equipment components of general enhancement technologies of supercritical water oxidation were discussed, such as fractional oxygen injection, auxiliary fuel co-oxidation, and hydrothermal flame-assisted degradation. This paper proposes a novel supercritical flame-assisted oxidation process in which the reactor performs preheating, corrosion protection, and desalination functions. The use of additive-enhanced oxidation, segmented oxidation, and supercritical hydrothermal flame-assisted oxidation has achieved good results in the complicated treatment process of brutal degradation of organic matter.

CSF1R inhibition reprograms tumor-associated macrophages to potentiate anti-PD-1 therapy efficacy against colorectal cancer.

PD-1 blockade therapy has made great breakthroughs in treatment of multiple solid tumors. However, patients with microsatellite-stable (MSS) colorectal cancer (CRC) respond poorly to anti-PD-1 immunotherapy. Although CRC patients with microstatellite instability (MSI) or microsatellite instability-high (MSI-H) can benefit from PD-1 blockade therapy, there are still some problems such as tumor recurrence. Tumor-associated macrophages (TAMs), most abundant immune components in tumor microenvironment (TME), largely limit the therapeutic efficacy of anti-PD-1 against CRC. The CSF1/CSF1R pathway plays a key role in regulating macrophage polarization, and blocking CSF1R signaling transduction may be a potential strategy to effectively reprogram macrophages and remodel TME. Here, we found that increasing expression of CSF1R in macrophages predicted poor prognosis in CRC cohort. Furthermore, we discovered a novel potent CSF1R inhibitor, PXB17, which significantly reprogramed M2 macrophages to M1 phenotype. Mechanically, PXB17 significantly blocked activation of PI3K/AKT/mTORC1 signaling, resulting in inhibition of cholesterol biosynthesis. Results from 3D co-culture system suggested that PXB17-repolarized macrophages could induce infiltration of CD8+ T lymphocytes in tumors and improve the immunosuppressive microenvironment. In vivo, PXB17 significantly halted CRC growth, with a stronger effect than PLX3397. In particular, PXB17 potently enhanced therapeutic activity of PD-1 mAb in CT-26 (MSS) model and prevented tumor recurrence in MC-38 (MSI-H) model by promoting formation of long-term memory immunity. Our study opens a new avenue for CSF1R in tumor innate and adaptive anti-tumor immunomodulatory activity and suggests that PXB17 is a promising immunotherapy molecule for enhancing the efficacy of PD-1 mAb or reducing tumor recurrence of CRC.

High salt diet exacerbates cognitive deficits and neurovascular abnormalities in APP/PS1 mice and induces AD-like changes in wild-type mice.

High salt diet (HSD) is a risk factor of hypertension and cardiovascular disease. Although clinical data do not clearly indicate the relationship between HSD and the prevalence of Alzheimer's disease (AD), animal experiments have shown that HSD can cause hyperphosphorylation of tau protein and cognition impairment. However, whether HSD can accelerate the progression of AD by damaging the function of neurovascular unit (NVU) in the brain is unclear. Here, we fed APP/PS1 mice (an AD model) or wild-type mice with HSD and found that the chronic HSD feeding increased the activity of enzymes related to tau phosphorylation, which led to tau hyperphosphorylation in the brain. HSD also aggravated the deposition of Aß42 in hippocampus and cortex in the APP/PS1 mice but not in the wild-type mice. Simultaneously, HSD caused the microglia proliferation, low expression of Aqp-4, and high expression of CD31 in the wild-type mice, which were accompanied with the loss of pericytes (PCs) and increase in blood brain barrier (BBB) permeability. As a result, wild-type mice fed with HSD performed poorly in Morris Water Maze and object recognition test. In the APP/PS1 mice, HSD feeding for 8 months worsen the cognition and accompanied the loss of PCs, the activation of glia, the increase in BBB permeability, and the acceleration of calcification in the brain. Our data suggested that HSD feeding induced the AD-like pathology in wild-type mice and aggravated the development of AD-like pathology in APP/PS1 mice, which implicated the tau hyperphosphorylation and NVU dysfunction.

In-Plane Ferrielectric Order in van der Waals ß'-In2Se3.

van der Waals ferroic materials exhibit rich potential for implementing future generation functional devices. Among these, layered ß'-In2Se3 has fascinated researchers with its complex superlattice and domain structures. As opposed to ferroelectric α-In2Se3, the understanding of ß'-In2Se3 ferroic properties remains unclear because ferroelectric, antiferroelectric, and ferroelastic characteristics have been separately reported in this material. To develop useful applications, it is necessary to understand the microscopic structural properties and their correlation with macroscopic device characteristics. Herein, using scanning transmission electron microscopy (STEM), we observed that the arrangement of dipoles deviates from the ideal double antiparallel antiferroelectric character due to competition between antiferroelectric and ferroelectric structural ordering. By virtue of second-harmonic generation, four-dimensional STEM, and in-plane piezoresponse force microscopy, the long-range inversion-breaking symmetry, uncompensated local polarization, and net polarization domains are unambiguously verified, revealing ß'-In2Se3 as an in-plane ferrielectric layered material. Additionally, our device study reveals analogous resistive switching behaviors of different types owing to polarization switching, defect migration, and defect-induced charge trapping/detrapping processes.

The role of JAK/STAT signaling pathway in cerebral ischemia-reperfusion injury and the therapeutic effect of traditional Chinese medicine: A narrative review.

Cerebral ischemia is a cerebrovascular disease with symptoms caused by insufficient blood or oxygen supply to the brain. When blood supplied is restored after cerebral ischemia, secondary brain injury may occur, which is called cerebral ischemia-reperfusion injury (CIRI). In this process, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway plays an important role. It mediates neuroinflammation and participates in the regulation of physiological activities, such as cell proliferation, differentiation, and apoptosis. After CIRI, M1 microglia is activated and recruited by the damaged tissue. The inflammatory factors are produced by M1 microglia through the JAK/STAT pathway, eventually leading to cell apoptosis. Meanwhile, the JAK2/STAT3 signaling pathway and the expression of lipocalin-2 and caspase-3 could increase. In the pathway, phosphorylated JAK2 and phosphorylated STAT3 function of 2 ways. They not only promote the proliferation of neurons, but also affect the differentiation direction of neural stem cells by further acting on the Notch signaling pathway. Recently, traditional Chinese medicine (TCM) is a key player in CIRI, through JAK2, STAT3, STAT1 and their phosphorylation. Therefore, the review focuses on the JAK/STAT signaling pathway and its relationship with CIRI as well as the influence of the TCM on this pathway. It is aimed at providing the basis for future clinical research on the molecular mechanism of TCM in the treatment of CIRI.

Effect of acupuncture on BDNF signaling pathways in several nervous system diseases.

In recent years, the understanding of the mechanisms of acupuncture in the treatment of neurological disorders has deepened, and considerable progress has been made in basic and clinical research on acupuncture, but the relationship between acupuncture treatment mechanisms and brain-derived neurotrophic factor (BDNF) has not yet been elucidated. A wealth of evidence has shown that acupuncture exhibits a dual regulatory function of activating or inhibiting different BDNF pathways. This review focuses on recent research advances on the effect of acupuncture on BDNF and downstream signaling pathways in several neurological disorders. Firstly, the signaling pathways of BDNF and its function in regulating plasticity are outlined. Furthermore, this review discusses explicitly the regulation of BDNF by acupuncture in several nervous system diseases, including neuropathic pain, Parkinson's disease, cerebral ischemia, depression, spinal cord injury, and other diseases. The underlying mechanisms of BDNF regulation by acupuncture are also discussed. This review aims to improve the theoretical system of the mechanism of acupuncture action through further elucidation of the mechanism of acupuncture modulation of BDNF in the treatment of neurological diseases and to provide evidence to support the wide application of acupuncture in clinical practice.

2D Ferroionics: Conductive Switching Mechanisms and Transition Boundaries in Van der Waals Layered Material CuInP2 S6.

The recently unfolded ferroionic phenomena in 2D van der Waals (vdW) copper-indium-thiophosphate (CuInP2 S6 or CIPS) have received widespread interest as they allow for dynamic control of conductive switching properties, which are appealing in the paradigm-shift computing. The intricate couplings between ferroelectric polarization and ionic conduction in 2D vdW CIPS facilitate the manipulation and dynamic control of conductive behaviors. However, the complex interplays and underlying mechanisms are not yet fully explored and understood. Here, by investigating polarization switching and ionic conduction in the temperature and applied electric field domains, it is discovered that the conducting mechanisms of CIPS can be divided into four distinctive states (or modes) with transitional boundaries, depending on the dynamics of Cu ions in the material. Further, it demonstrates that dynamically-tunable synaptic responsive behavior can be well implemented by governing the working-state transition. This research provides an in-depth, quantitative understanding of the complex phenomena of conductive switching in 2D vdW CIPS with coexisting ferroelectric order and ionic disorder. The developed insights in this work lay the ground for implementing high-performance, function-enriched devices for information processing, data storage, and neuromorphic computing based on the 2D ferroionic material systems.

Experiences Shape Hippocampal Neuron Morphology and the Local Levels of CRHR1 and OTR.

The dorsal hippocampus is involved in behavioral avoidance regulation. It is unclear how experiences such as the neonatal stress of maternal deprivation (MD) and post-weaning environmental enrichment (EE) affect avoidance behavior and the dorsal hippocampal parameters, including neuronal morphology, corticotrophin-releasing hormone (CRH) signaling, and oxytocin receptor (OTR) level. In male BALB/c mice, we found that MD impaired avoidance behavior in the step-on test compared to non-MD and EE rearing conditions could alleviate that partially. MD increased neuronal branches in the CA1 but decreased synaptic connection levels in the CA2, CA3, and DG. Meanwhile, MD increased the CA1's OTR levels, which negatively correlated with nucleus densities. MD also increased the CA1's and CA2's CRH levels, which positively correlated with CRHR1 levels. However, MD statistically elevated the CA3's CRH receptor 1 (CRHR1) levels, which negatively correlated with nucleus densities and, probably, synaptic connection levels in the CA3. The additive effects of MD and EE maintained similar CRH levels and CRHR1 levels as well as OTR levels in the hippocampal areas as the additive of non-MD and non-EE. However, the presence of MD and EE still decreased the CA1's neuronal branches and the CA2's and DG's synaptic connection levels. The study illustrates how MD and EE affect avoidance behaviors, hippocampal neuron morphology, and CRH and OTR levels. The results indicate that the late-life environmental improvement partially restores the alterations in dorsal hippocampal areas induced by early life stress.

Quality and microbial diversity of homemade bread packaged in cinnamaldehyde loaded poly(lactic acid)/konjac glucomannan/wheat gluten bilayer film during storage.

The current study aimed to reveal the changes in quality and microbial diversity of bread at 25 °C, and to analyze the activity of antifungal bilayer film on maintaining the quality of bread during 10 days of storage. Antifungal bilayer film prepared with cinnamaldehyde loaded polylactic acid/konjac glucomannan/wheat gluten (PLA/KGM/WG-CIN) was used to preserve bread samples fermented at different times. The changes in the morphology, moisture state, texture properties and microbiological analysis of bread were investigated during the storage. Analysis of microbial diversity of bread samples showed a clear decrease in the abundance of the main spoilage fungi (Aspergillus and Penicillium) in samples packed with PLA/KGM/WG-CIN film. The PLA/KGM/WG-CIN film effectively prevented moisture from evaporation, maintained the texture properties, retarded the growth of fungi, and reduced the fungi diversity during the storage. Results suggest a large potential of PLA/KGM/WG-CIN film to ensure the quality and safety of bread products.

Single-Transistor Neuron with Excitatory-Inhibitory Spatiotemporal Dynamics Applied for Neuronal Oscillations.

Brain-inspired neuromorphic computing systems with the potential to drive the next wave of artificial intelligence demand a spectrum of critical components beyond simple characteristics. An emerging research trend is to achieve advanced functions with ultracompact neuromorphic devices. In this work, a single-transistor neuron is demonstrated that implements excitatory-inhibitory (E-I) spatiotemporal integration and a series of essential neuron behaviors. Neuronal oscillations, the fundamental mode of neuronal communication, that construct high-dimensional population code to achieve efficient computing in the brain, can also be demonstrated by the neuron transistors. The highly scalable E-I neuron can be the basic building block for implementing core neuronal circuit motifs and large-scale architectural plans to replicate energy-efficient neural computations, forming the foundation of future integrated neuromorphic systems.

Effects of maternal deprivation and environmental enrichment on anxiety-like and depression-like behaviors correlate with oxytocin system and CRH level in the medial-lateral habenula.

The medial-lateral habenula (LHbM)'s role in anxiety and depression behaviors in female mice remains unclear. Here, we used neonatal maternal deprivation (MD) and post-weaning environmental enrichment (EE) to treat female BALB/c offspring and checked anxiety-like and depression-like behaviors as well as the corticotropin-releasing hormone (CRH), oxytocin receptor (OTR), estrogen receptor-beta (ERß) levels in their LHbM at adulthood. We found that MD enhanced state anxiety-like behaviors in the elevated plus-maze test, and EE caused trait anxiety-like behaviors in the open field test and depression-like behaviors in the tail suspension test. The immunochemistry showed that MD reduced OT immunoreactive neuron numbers in the hypothalamic paraventricular nucleus but increased OTR levels in the LHbM; EE increased CRH levels in the LHbM but decreased OTR levels in the LHbM. The additive effects of EE and MD maintained the behavioral parameters, OT-ir neuronal numbers, CRH levels, and OTR levels similar to the additive of non-MD and non-EE. The correlation analysis showed that CRH levels correlated with synaptic connection levels, OTR levels correlated with nucleus densities, and ERß levels correlated with Nissl body levels and body weights in female mice. Neither MD nor EE affected ERß levels in the LHbM. Together, the study revealed the relationships between behaviors and neuroendocrine and neuronal alterations in female LHbM and the effects of experiences including MD and EE on them.

Potential Gut Microbiota Features for Non-Invasive Detection of Schistosomiasis.

The gut microbiota has been identified as a predictive biomarker for various diseases. However, few studies focused on the diagnostic accuracy of gut microbiota derived-signature for predicting hepatic injuries in schistosomiasis. Here, we characterized the gut microbiomes from 94 human and mouse stool samples using 16S rRNA gene sequencing. The diversity and composition of gut microbiomes in Schistosoma japonicum infection-induced disease changed significantly. Gut microbes, such as Bacteroides, Blautia, Enterococcus, Alloprevotella, Parabacteroides and Mucispirillum, showed a significant correlation with the level of hepatic granuloma, fibrosis, hydroxyproline, ALT or AST in S. japonicum infection-induced disease. We identified a range of gut bacterial features to distinguish schistosomiasis from hepatic injuries using the random forest classifier model, LEfSe and STAMP analysis. Significant features Bacteroides, Blautia, and Enterococcus and their combinations have a robust predictive accuracy (AUC: from 0.8182 to 0.9639) for detecting liver injuries induced by S. japonicum infection in humans and mice. Our study revealed associations between gut microbiota features and physiopathology and serological shifts of schistosomiasis and provided preliminary evidence for novel gut microbiota-derived features for the non-invasive detection of schistosomiasis.

Corrigendum: Potential gut microbiota features for non-invasive detection of schistosomiasis.

[This corrects the article DOI: 10.3389/fimmu.2022.941530.].

Synergistic effects of hIAPP and Aß1-42 impaired the olfactory function associated with the decline of adult neurogenesis in SVZ.

According to many in the field，the prevalence of Alzheimer's disease (AD) in type II diabetes (T2DM) populations is considerably higher than that in the normal population. Human islet amyloid polypeptide (hIAPP) is considered to be a common risk factor for T2DM and AD. Preliminary observations around T2DM animal model show that the decrease of adult neural stem cells (NSCs) in the subventricular zone (SVZ) is accompanied by olfactory dysfunction. Furthermore, impaired olfactory function could serve as to an early predictor of neurodegeneration，which is associated with cognitive impairment. However, the synergistic effects between hIAPP and amyloid-beta (Aß) 1-42 in the brain and the neurodegeneration remains to be further clarified. In this study, olfactory capacity, synaptic density, status of NSC in SVZ, and status of newborn neurons in olfactory bulb (OB) were assessed 6 months after stereotactic injection of oligomer Aß1-42 into the dens gyrus (DG) of hIAPP-/+ mice or wild-type homogenous mice. Our results set out that Aß42 and amylin co-localized into OB and raised Aß42 deposition in hIAPP-/+ mice compared with wild-type brood mice. In addition, 6 months after injection of Aß1-42 in hIAPP-/+ mice, these mice showed increased olfactory dysfunction, significant loss of synapses, depletion of NSC in SVZ, and impaired cell renewal in OB. Our present study suggested that the synergistic effects between hIAPP and Aß1-42 impairs olfactory function and was associated with decreased neurogenesis in adults with SVZ.

Relationship between serum insulin-like growth factor 1 levels and ischaemic stroke: a systematic review and meta-analysis.

OBJECTIVE: To assess the association of insulin-like growth factor 1 (IGF-1) with the risk of incident ischaemic stroke and outcome after ischaemic stroke. DESIGN: A systematic review of primary studies. SETTING: Hospitals in Western Sweden, Italy, China and Denmark. METHODS: A search was carried out in eligible studies in electronic databases (PubMed, Scopus, Embase, China National Knowledge Infrastructure and Web of Science) updated to 29 December 2020. The relevant data were extracted in order to conduct the meta-analysis. Review Manager V.5.2 was used to pool data and calculate the mean difference (MD) and its 95% CI. Heterogeneity, subgroup analysis, sensitivity analysis and publication bias were also performed in this meta-analysis. RESULTS: A total of 2277 patients were included in 17 studies. This meta-analysis indicated that higher serum IGF-1 levels were significantly correlated with less risk of ischaemic stroke (MD=-45.32 95% CI -63.70 to -26.94], p < 0.00001, I2=99%) and better improvement of outcome after ischaemic stroke (MD=27.52, 95% CI 3.89 to 51.14, p=0.02, I2=96%). According to subgroup analysis, heterogeneity comes from country, sample size, male and the time from symptom onset to blood collection. Sensitivity analysis showed that there was no significant influence of any individual study on the pooled MD. The effect of high heterogeneity on result credibility was eliminated when four included studies were merged (MD=-30.32, 95% CI -36.52 to -24.11, p< 0.00001, I2=0%). Moreover, no potential publication bias was discovered in this meta-analysis. CONCLUSION: Higher serum IGF-1 was significantly correlated with a lower risk of ischaemic stroke. In view of the high degree of heterogeneity, it may need more studies to confirm the prognostic value of serum IGF-1 levels in ischaemic stroke and explore the sources of heterogeneity.

Bacillus subtilis Attenuates Hepatic and Intestinal Injuries and Modulates Gut Microbiota and Gene Expression Profiles in Mice Infected with Schistosoma japonicum.

Parasitic infection can induce pathological injuries and impact the gut microbiota diversity and composition of the host. Bacillus subtilis is a nonpathogenic and noninvasive probiotic bacterium for humans and other animals, playing an important role in improving the host immune system's ability to respond to intestinal and liver diseases and modulating gut microbiota. However, whether B. subtilis can impact biological functions in Schistosoma japonicum-infected mice is unclear. This study used oral administration (OA) of B. subtilis to treat mice infected with S. japonicum. We evaluated changes in the gut microbiota of infected mice using 16 S rRNA gene sequencing and differentially expressed gene profiles using transcriptome sequencing after OA B. subtilis. We found that OA B. subtilis significantly attenuated hepatic and intestinal pathological injuries in infected mice. The gut microbiota of mice were significantly altered after S. japonicum infection, while OA B. subtilis remodel the diversity and composition of gut microbiomes of infected mice. We found that the S. japonicum-infected mice with OA B. subtilis had an overabundance of the most prevalent bacterial genera, including Bacteroides, Enterococcus, Lactobacillus, Blautia, Lachnoclostridium, Ruminiclostridium, and Enterobacter. Transcriptomic analysis of intestinal tissues revealed that OA B. subtilis shaped the intestinal microenvironment of the host responding to S. japonicum infection. Differentially expressed genes were classified into KEGG pathways between S. japonicum-infected mice and those without included cell adhesion molecules, intestinal immune network for IgA production, hematopoietic cell lineage, Fc epsilon RI signaling pathway, Th1 and Th2 cell differentiation, Th17 cell differentiation, calcium signaling pathway, Fc gamma R-mediated phagocytosis, chemokine signaling pathway, phospholipase D signaling pathway, NF-kappa B signaling pathway, B cell receptor signaling pathway, pancreatic secretion, and phagosome. In conclusion, our findings showed that OA B. subtilis alleviates pathological injuries and regulates gene expression, implying that B. subtilis supplementation may be a potential therapeutic strategy for schistosomiasis. Our study may highlight the value of probiotics as a beneficial supplementary therapy during human schistosomiasis, but further studies are needed.

Exploring Low Power and Ultrafast Memristor on p-Type van der Waals SnS.

Memristor devices that exhibit high integration density, fast speed, and low power consumption are candidates for neuromorphic devices. Here, we demonstrate a filament-based memristor using p-type SnS as the resistive switching material, exhibiting superlative metrics such as a switching voltage ∼0.2 V, a switching speed faster than 1.5 ns, high endurance switching cycles, and an ultralarge on/off ratio of 108. The device exhibits a power consumption as low as ∼100 fJ per switch. Chip-level simulations of the memristor based on 32 × 32 high-density crossbar arrays with 50 nm feature size reveal on-chip learning accuracy of 87.76% (close to the ideal software accuracy 90%) for CIFAR-10 image classifications. The ultrafast and low energy switching of p-type SnS compared to n-type transition metal dichalcogenides is attributed to the presence of cation vacancies and van der Waals gap that lower the activation barrier for Ag ion migration.