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Subtypes of microglia/macrophage regulate the inflammation in the opposite direction during ischemic stroke. JAK2/STAT3 signaling pathway participates in the development of stroke-related inflammation via ischemic stimulation. However, the relationship between JAK2/STAT3 pathway and microglia/macrophage phenotype transformation is unclear.This study established a transient middle cerebral artery occlusion (tMCAO) model in male STAT3For the conditioned STAT3-KO mice, the infarction was significantly increased after MCAO, accompanied by the aggravation of neurological deficit. Higher expression of iNOS and CD16/32 than Arg-1, Ym-1, and CD206 in vivo and in vitro, and decreased p-STAT3/STAT3 ratio in STAT3Collectively, these results reveal that JAK2/STAT3 signaling pathway regulates the microglia/macrophage polarization (skewing toward the M2 polarization) during the CIRI, thus alleviating brain damage. Therefore, approaches targeting JAK2/STAT3 activation are promising therapies for ischemic stroke.

Autophagy has been described to be both protective and pathogenic in cerebral ischemia/reperfusion (I/R) injury. The underlying association between autophagy and ferroptosis in ischemic stroke has not yet been clearly investigated. The purpose of this study was to explore the role of autophagy-related gene 5 (ATG5) in experimental ischemic stroke. After injection of ATG5 shRNA lentivirus, mice underwent surgery for transient middle cerebral artery occlusion (MCAO)-induced focal cerebral ischemia. The infarct volume, neurological function, apoptosis, reactive oxygen species (ROS), autophagy, and ferroptosis levels were evaluated. After MCAO, ATG5-knockdown mice had a smaller infarct size and fewer neurological deficits than wild-type mice. The levels of apoptosis and ROS in ischemic mouse brains were alleviated through ATG5 knockdown. The expression of LC3 I/II was reduced through ATG5 knockdown after MCAO. Additionally, the expression of beclin1 and LC3 II was increased after I/R, but the increase was counteracted by preconditioning with ATG5 knockdown. After ischemic stroke, the levels of Fe

The past decade has witnessed unprecedented medical progress, which has translated into cardiac surgery being increasingly common and safe. However, complications such as postoperative delirium remain a major concern. Although the pathophysiological changes of delirium after cardiac surgery remain poorly understood, it is widely thought that inflammation and oxidative stress may be potential triggers of delirium. The development of delirium following cardiac surgery is associated with perioperative risk factors. Multiple interventions are being explored to prevent and treat delirium. Therefore, research on the potential role of biomarkers in delirium as well as identification of perioperative risk factors and pharmacological interventions are necessary to mitigate the development of delirium.

Glioma is the common, most aggressive and poorest prognostic tumor type in the brain. More and more biomarkers associated with glioma treatment, prognosis, and immunity are being discovered. Here, we aimed to explore the underlying biological functions and prognostic predictive value of Apolipoprotein L4 (APOL4) in glioma. We downloaded the expression data of APOL4 and clinical information from several databases and used R software for preprocessing. The clinical significance of APOL4 in a glioma outcome was explored by the Cox regression analysis and Kaplan–Meier survival analysis. In addition, immune infiltrates and microenvironmental indicators were assessed by CIBERSORT and TIMER. GO and KEGG analyses were used to analyze the potential functions of APOL4 in gliomas. APOL4 expression was increased in glioma specimens compared to normal tissues and correlated dramatically with the WHO grade. A survival analysis showed a shorter overall survival (OS) in glioma patients with APOL4 overexpression, and a Cox regression analysis showed that APOL4 was an independent prognostic factor for the OS of glioma patients. GSEA, GO, and KEGG enrichment analyses showed remarkable enrichment in immune-related pathways. APOL4 expression was positively correlated with immune infiltration (including DC cells, neutrophils, CD8+ T cells, B cells, macrophages, CD4+ T cells, etc.) and microenvironmental parameters (including immune, stromal, and ESTIMATE scores) in gliomas. Glioma patients with a higher expression of APOL4 may be more sensitive to immune checkpoint inhibitors (ICI). In conclusion, these findings suggest that APOL4 is associated with the tumor grade and immune infiltrates; APOL4 may be a new and potential biomarker for therapeutic and prognostic evaluations that may further suggest the therapeutic efficacy of immunotherapy.

Glioma is the most common primary brain tumor in the human brain. The present study was designed to explore the expression of PIMREG in glioma and its relevance to the clinicopathological features and prognosis of glioma patients. The correlations of PIMREG with the infiltrating levels of immune cells and its relevance to the response to immunotherapy were also investigated. PIMREG expression in glioma was analyzed based on the GEO, TCGA, and HPA databases. Kaplan–Meier survival analysis was used to examine the predictive value of PIMREG for the prognosis of patients with glioma. The correlation between the infiltrating levels of immune cells in glioma and PIMREG was analyzed using the CIBERSORT algorithm and TIMRE database. The correlation between PIMREG and immune checkpoints and its correlation with the patients’ responses to immunotherapy were analyzed using R software and the GEPIA dataset. Cell experiments were conducted to verify the action of PIMREG in glioma cell migration and invasion. We found that PIMREG expression was upregulated in gliomas and positively associated with WHO grade. High PIMREG expression was correlated with poor prognosis of LGG, prognosis of all WHO grade gliomas, and prognosis of recurrent gliomas. PIMREG was related to the infiltration of several immune cell types, such as M1 and M2 macrophages, monocytes and CD8+ T cells. Moreover, PIMREG was correlated with immune checkpoints in glioma and correlated with patients’ responses to immunotherapy. KEGG pathway enrichment and GO functional analysis illustrated that PIMREG was related to multiple tumor- and immune-related pathways. In conclusion, PIMREG overexpression in gliomas is associated with poor prognosis of patients with glioma and is related to immune cell infiltrates and the responses to immunotherapy.

Based on residents’ food consumption data from 31 provinces in China from 2015–2021, this study analyzes the deviation in food consumption from nutrition targets and the spatial distribution characteristics of urban and rural residents in China from 2015–2021, and finds that there are irrationalities in the structure of food consumption of Chinese residents as well as regional differences in consumption. The food consumption of Chinese residents deviates from the recommended values of the Chinese Food Guide Pagoda to a certain extent, with large differences between urban and rural areas and provinces. Therefore, a new concept of food security with nutrition as the target should be established to guide residents’ food consumption scientifically and rationally, and to adopt focused attention and targeted measures for regions with serious imbalances in food consumption.

Grains account for a large proportion of the diet of rural residents in Tibet. The lack of selenium (Se) and zinc (Zn) threatens the population’s nutrition and health. However, the intakes of selenium and zinc in grains remains unclear. To clarify the nutritional status of selenium and zinc consumed from staple grains of residents along the Yarlung Zangbo River in Tibet, 341 grain samples and 242 urine samples were collected, and 244 food frequency questionnaires were completed along the Yarlung Zangbo River in 2020–2021. The results showed that the selenium concentrations of 88.5% of self-produced tsampa and 80.8% of self-produced flour were lower than the grain selenium threshold (

Glioblastoma (GBM) is an aggressive primary brain tumor with a poor prognosis following conventional therapeutic interventions. Moreover, the blood–brain barrier (BBB) severely impedes the permeation of chemotherapy drugs, thereby reducing their efficacy. Consequently, it is essential to develop novel GBM treatment methods. A novel kind of pericyte immunotherapy known as chimeric antigen receptor T (CAR-T) cell treatment uses CAR-T cells to target and destroy tumor cells without the aid of the antigen with great specificity and in a manner that is not major histocompatibility complex (MHC)-restricted. It has emerged as one of the most promising therapy techniques with positive clinical outcomes in hematological cancers, particularly leukemia. Due to its efficacy in hematologic cancers, CAR-T cell therapy could potentially treat solid tumors, including GBM. On the other hand, CAR-T cell treatment has not been as therapeutically effective in treating GBM as it has in treating other hematologic malignancies. CAR-T cell treatments for GBM have several challenges. This paper reviewed the use of CAR-T cell therapy in hematologic tumors and the selection of targets, difficulties, and challenges in GBM.

Ischemic stroke is an acute cerebrovascular disease characterized by sudden interruption of blood flow in a certain part of the brain, leading to serious disability and death. At present, treatment methods for ischemic stroke are limited to thrombolysis or thrombus removal, but the treatment window is very narrow. However, recovery of cerebral blood circulation further causes cerebral ischemia/reperfusion injury (CIRI). The endoplasmic reticulum (ER) plays an important role in protein secretion, membrane protein folding, transportation, and maintenance of intracellular calcium homeostasis. Endoplasmic reticulum stress (ERS) plays a crucial role in cerebral ischemia pathophysiology. Mild ERS helps improve cell tolerance and restore cell homeostasis; however, excessive or long-term ERS causes apoptotic pathway activation. Specifically, the protein kinase R-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6), and inositol-requiring enzyme 1 (IRE1) pathways are significantly activated following initiation of the unfolded protein response (UPR). CIRI-induced apoptosis leads to nerve cell death, which ultimately aggravates neurological deficits in patients. Therefore, it is necessary and important to comprehensively explore the mechanism of ERS in CIRI to identify methods for preserving brain cells and neuronal function after ischemia.

The role of ferroptosis in ischemic stroke has been hotly debated recently, but the mechanism is not clearly clarified. It has been reported that the NLRP3 inflammasome is essential for the progression of ischemic stroke. Whether the ferroptosis after ischemic stroke mediated by the activation of NLRP3 inflammasome is still not reported. In this study, we investigated the effect of NLRP3 deficiency on ferroptosis following cerebral ischemia-reperfusion injury (CIRI) in vivo and in vitro.In vivo, we used C57BL/6J mice and NLRP3Three days after MCAO, the NLRP3Inhibition of the NLRP3 inflammasome alleviates CIRI by inhibiting ferroptosis and inflammation, possibly through a mechanism of the Keap1-Nrf2 pathway.

Stroke is a disease with high incidence, mortality and disability rates. It is also the main cause of adult disability in developed countries. Stroke is often caused by small emboli on the inner wall of the blood vessels supplying the brain, which can lead to arterial embolism, and can also be caused by cerebrovascular or thrombotic bleeding. With the exception of recombinant tissue plasminogen activator (rt-PA), which is a thrombolytic drug used to recanalize the occluded artery, most treatments have been demonstrated to be ineffective. Stroke can also induce peripheral organ damage. Most stroke patients have different degrees of injury to one or more organs, including the lung, heart, kidney, spleen, gastrointestinal tract and so on. In the acute phase of stroke, severe inflammation occurs in the brain, but there is strong immunosuppression in the peripheral organs, which greatly increases the risk of peripheral organ infection and aggravates organ damage. Nonneurological complications of stroke can affect treatment and prognosis, may cause serious short-term and long-term consequences and are associated with prolonged hospitalization and increased mortality. Many of these complications are preventable, and their adverse effects can be effectively mitigated by early detection and appropriate treatment with various medical measures. This article reviews the pathophysiological mechanism, clinical manifestations and treatment of peripheral organ injury after stroke.

A systematic understanding of the potential contribution of the neighbourhood in explaining health inequalities remains an under-researched area. To quantify the importance of the neighbourhood in explaining health, by conducting pooled cross-sectional investigations of 49,602 adult participants, this study has hierarchically examined the magnitude of neighbourhood heterogeneity in different health outcomes in five Chinese provinces from 2010 to 2016. We found significant neighbourhood heterogeneity in both self-reported health and mental health with neighbourhood explaining 2.37% to 22.7% of the total variance. The majority of neighbourhood heterogeneity remained significant, with a range between 2.66% to 19.16% after individual attributes were considered. The magnitudes of neighbourhood heterogeneity in health were different across provinces, with Guangdong being the highest, followed by Shanghai and Henan, followed by Gansu and ended by Liaoning. There was a slightly descending trend in neighbourhood heterogeneity in health from 2010 to 2016. There remained unexplained significant and increased spatiotemporal variations in neighbourhood heterogeneity in health, after neighbourhood socioeconomic and sociodemographic attributes were considered. Both the compositional and contextual factors of neighbourhood heterogeneity in health were conditional on broader contextual backgrounds. Our study is the first of its kind in systematically investigating neighbourhood heterogeneity in health using provincially representative data from China's national database. Our findings have strengthened the groundwork for studies linking the neighbourhood to health and provided the framework for future studies to assess neighbourhood heterogeneity in health in consideration to broader contexts.

The air micro- and nanobubbles on a silicon wafer surface, generated by ethanol–water exchange method in THF solution, are found with anomalous small contact angles on the gas side due to the pinni...

The crystallization process of a droplet of tetrahydrofuran (THF) solution on a silicon wafer is studied based on the in situ observation with a high-resolution atomic force microscope. On the basi...

This paper is an extension of known results of Pesin’s entropy formula and SRB measures for random compositions of infinite-dimensional mappings to the continuous-time setting of stochastic flows. Consider a stochastic flow ϕ on a separable infinite dimensional Hilbert space preserving a probability measure μ, which is supported on a random compact set K. We show that if ϕ is C2 (on K) and satisfies some mild integrable conditions of the differentials, then Pesin’s entropy formula holds if μ has absolutely continuous conditional measures along the unstable manifolds. The converse is also true under an additional condition on K when the system has no zero Lyapunov exponent.

Cyclin-dependent kinase regulatory subunit 2 (CKS2) is a potential prognostic marker and is overexpressed in various cancers. This study analyzed sequencing and clinical data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus, with external validation using the Chinese Glioma Genome Atlas (CGGA) data. CKS2 expression in the normal brain and tumor tissue was compared. cBioPortal and MethSurv were utilized to scrutinize the prognostic value of CKS2 methylation. Gene set enrichment examination and single-sample gene set enrichment analysis were employed to explore the potential biological functions of CKS2. Cell viability, colony formation, and transwell assays were conducted to evaluate the influence of CKS2 on glioma cell proliferation and invasion. Compared with normal brain tissue, the expression of CKS2 was upregulated in glioma samples (p < 0.001). Multivariate data analysis from TCGA and CGGA indicated that increased expression of CKS2 was an independent risk factor for the prognosis of overall survival in glioma patients. CKS2 methylation was negatively associated with CKS2 expression. Patients with CKS2 hypomethylation had worse overall survival compared with patients with CKS2 methylation, as suggested by the analysis of both TCGA and CGGA datasets. The expression level of CKS2 is closely related to tumor immunity, including the correlation of tumor immune cell infiltration, immune score, and co-expression of multiple immune-related genes. In addition, CKS2 is associated with several immune checkpoints and responses to the chemotherapy drug cisplatin. CKS2 knockdown impeded the expansion and aggression of glioma cell lines. The changes in CKS2 expression may provide a novel prognostic biomarker that can be used to improve patient overall survival rates.

The clinical success of cisplatin ushered in a new era of the application of metallodrugs. When it comes to practice, however, drug resistance, tumor recurrence, and drug systemic toxicity make it implausible to completely heal the patients. Herein, we successfully transform an electron acceptor [1, 2, 5]thiadiazolo[3,4

Previous research linking social capital to child nutritional status primarily constitutes cross-sectional studies. To investigate whether a longitudinal relationship exists, by conducting fixed-effects analyses with 16,977 repeatedly measured observations of 6193 children from the 2012, 2014, 2016, and 2018 China Family Panel Studies, this study explored the longitudinal effects of neighborhood participation, bonding trust, and bridging trust on the BMI-for-age z-score (BAZ) and BMI categories of school-aged children, differentiating between urban and rural residence. We found an increasing average BAZ, a decreasing prevalence of underweight, an increasing prevalence of overweight/obesity, and a reducing urban/rural gap in nutritional status. The levels of social capital components descended faster in the urban area. Bonding trust was predictive of a lower BAZ, a higher likelihood of being underweight, and a lower likelihood of being overweight/obese. Bridging trust was predictive of a higher BAZ. The longitudinal effects of bonding trust were significant among only the rural children. Our findings indicate that neighborhood social capital may impose causal impacts on the nutritional status of children. To effectively improve child nutritional status, a more empathetic governmental approach that promotes a more supportive distal social environment is needed.

As one of the most important physical parameters of seawater, salinity is essential to study climatological change, to trace seawater masses and to model ocean dynamics. The traditional way to conduct salinity measurement in hydrographical observation is to use a standard conductivity-temperature-depth (CTD) probe where the salinity determination is based on a measurement of electrical conductivity. This article describes some developments of recent years that could lead to a new generation of instruments for the determination of salinity in seawater. Salinity determination with optical salinity sensor based on the refractive index measurement have been extensively studied. Different ways to conduct refractive index measurements are summarized, including measurements based on beam deviation, light wave mode coupling and swelling of surface coating material, among which the optical fiber sensors are promising candidates for further commercialization. Complementary to the above-mentioned direct measurement salinity point sensors, seismic observation takes advantages of large scale multichannel seismic data to retrieve the ocean salinity with high lateral resolution of ∼10 m. This work provide comprehensive information in the techniques related to the marine salinity measurement.

Recent studies showed that molecule interacting with CasL2 (MICAL2) could be a novel tumor growth factor, and it is closely associated with tumor growth and invasion. However, the role it plays in glioblastoma (GBM) and its potential mechanisms are currently unknown. Our study is designed to identify the effect of MICAL2 on GBM cells and the potential mechanisms behind it. Here, we found that MICAL2 interacts with TGF receptor-type I (TGFRI) and promotes the proliferation and migration of glioblastoma through the TGF-β/p-Smad2/EMT-like signaling pathway. MICAL2-knockdown inhibited the proliferation of glioblastoma cells, which was related to cell cycle arrest and downregulation of DNA replication. The invasion abilities of U87 and U251 cells were reduced after the knockdown of MICAL2. MICAL2 promoted the growth of GBM in nude mice. High MICAL2 predicts poor outcome of GBM patients. MICAL2 could be identified as a novel promising therapeutic target for human GBM.

Background and purpose Stroke is associated with high disability and mortality rates and increases the incidence of organ-related complications. Research has revealed that the outcomes and prognosis of stroke are regulated by the state of the intestinal microbiota. However, the possibility that the manipulation of the intestinal microbiota can alter sex-related stroke outcomes remain unknown. Methods To verify the different effects of microbiota from different sexes on stroke outcomes, we performed mouse fecal microbiota transplantation (FMT) and established a model of ischemic stroke. Male and female mice received either male or female microbiota through FMT. Ischemic stroke was triggered by MCAO (middle cerebral artery occlusion), and sham surgery served as a control. Over the next few weeks, the mice underwent neurological evaluation and metabolite and inflammatory level detection, and we collected fecal samples for 16S ribosomal RNA analysis. Results We found that when the female mice were not treated with FMT, the microbiota (especially the Firmicutes-to-Bacteroidetes ratio) and the levels of three main metabolites tended to resemble those of male mice after experimental stroke, indicating that stroke can induce an ecological imbalance in the biological community. Through intragastric administration, the gut microbiota of male and female mice was altered to resemble that of the other sex. In general, in female mice after MCAO, the survival rate was increased, the infarct area was reduced, behavioral test performance was improved, the release of beneficial metabolites was promoted and the level of inflammation was mitigated. In contrast, mice that received male microbiota were much more hampered in terms of protection against brain damage and the recovery of neurological function. Conclusion A female-like biological community reduces the level of systemic proinflammatory cytokines after ischemic stroke. Poor stroke outcomes can be positively modulated following supplementation with female gut microbiota.

BackgroundInflammatory responses play a multiphase role in the pathogenesis of cerebral ischemic stroke (IS). Ruxolitinib (Rux), a selective oral JAK 1/2 inhibitor, reduces inflammatory responses via the JAK2/STAT3 pathway. Based on its anti-inflammatory and immunosuppressive effects, we hypothesized that it may have a protective effect against stroke. The aim of this study was to investigate whether inhibition of JAK2 has a neuroprotective effect on ischemic stroke and to explore the potential molecular mechanisms.MethodsRux, MCC950 or vehicle was applied to middle cerebral artery occlusion (MCAO) mice in vivo and an oxygen-glucose deprivation/reoxygenation (OGD/R) model in vitro. After 3 days of reperfusion, neurological deficit scores, infarct volume and brain water content were assessed. Immunofluorescence staining and western blots were used to measure the expression of NLRP3 inflammasome components. The infiltrating cells were investigated by flow cytometry. Proinflammatory cytokines were assessed by RT-qPCR. The expression of the JAK2/STAT3 pathway was measured by western blots. Local STAT3 deficiency in brain tissue was established with a lentiviral vector carrying STAT3 shRNA, and chromatin immunoprecipitation (ChIP) assays were used to investigate the interplay between NLRP3 and STAT3 signaling.ResultsRux treatment improved neurological scores, decreased the infarct size and ameliorated cerebral edema 3 days after stroke. In addition, immunofluorescence staining and western blots showed that Rux application inhibited the expression of proteins related to the NLRP3 inflammasome and phosphorylated STAT3 (P-STAT3) in neurons and microglia/macrophages. Furthermore, Rux administration inhibited the expression of proinflammatory cytokines, including TNF-α, IFN-γ, HMGB1, IL-1β, IL-2, and IL-6, suggesting that Rux may alleviate IS injury by inhibiting proinflammatory reactions via JAK2/STAT3 signaling pathway regulation. Infiltrating macrophages, B, T, cells were also reduced by Rux. Local STAT3 deficiency in brain tissue decreased histone H3 and H4 acetylation on the NLRP3 promoter and NLRP3 inflammasome component expression, indicating that the NLRP3 inflammasome may be directly regulated by STAT3 signaling. Rux application suppressed lipopolysaccharide (LPS)-induced NLRP3 inflammasome secretion and JAK2/STAT3 pathway activation in the OGD/R model in vitro.ConclusionJAK2 inhibition by Rux in MCAO mice decreased STAT3 phosphorylation, thus inhibiting the expression of downstream proinflammatory cytokines and the acetylation of histones H3 and H4 on the NLRP3 promoter, resulting in the downregulation of NLRP3 inflammasome expression.

Ischemic stroke is one of the main issues threatening human health worldwide, and it is also the main cause of permanent disability in adults. Energy consumption and hypoxia after ischemic stroke leads to the death of nerve cells, activate resident glial cells, and promote the infiltration of peripheral immune cells into the brain, resulting in various immune-mediated effects and even contradictory effects. Immune cell infiltration can mediate neuronal apoptosis and aggravate ischemic injury, but it can also promote neuronal repair, differentiation and regeneration. The central nervous system (CNS), which is one of the most important immune privileged parts of the human body, is separated from the peripheral immune system by the blood-brain barrier (BBB). Under physiological conditions, the infiltration of peripheral immune cells into the CNS is controlled by the BBB and regulated by the interaction between immune cells and vascular endothelial cells. As the immune response plays a key role in regulating the development of ischemic injury, neutrophils have been proven to be involved in many inflammatory diseases, especially acute ischemic stroke (AIS). However, neutrophils may play a dual role in the CNS. Neutrophils are the first group of immune cells to enter the brain from the periphery after ischemic stroke, and their exact role in cerebral ischemia remains to be further explored. Elucidating the characteristics of immune cells and their role in the regulation of the inflammatory response may lead to the identification of new potential therapeutic strategies. Thus, this review will specifically discuss the role of neutrophils in ischemic stroke from production to functional differentiation, emphasizing promising targeted interventions, which may promote the development of ischemic stroke treatments in the future.

Efficient suppression of common-mode noises (CMNs) is significant for the performance of interferometric fiber-optic sensor system. To suppress CMNs, a reference interferometer is normally required as noise canceller. In this paper, we firstly report a detailed correlation analysis between the outputs of the sensing and reference interferometers. By using a band-limited noise decomposing method, we show that the correlation coefficient of the two interferometer outputs is a strong function over their mean phase difference, which appears as the limiting factor of the CMN suppression effect. Based on the analysis, we propose a novel CMN suppression technique by locking the mean phase value of the sensing interferometer using a reference interferometer with a 3 × 2 coupler. Experimental results show that our technique can increase the correlation coefficient between the outputs of sensing and reference interferometers by 6% (to 0.93) and reduce its standard deviation by $\sim$ 70% compared to traditional method. The CMNs suppression factor is measured as $-$ 8.49 dB in the frequency range from 300 Hz to 1 kHz, comparing to $\sim -$ 6 dB achieved by traditional method of simple subtraction. Our results set a new benchmark on the noise level of interferometric fiber-optic sensors.

A radar is an important part of an air defense and combat system. It is of great significance to military defense to improve the effectiveness of radar state monitoring and the accuracy of fault diagnosis during operation. However, the complexity of radar equipment’s structure and the uncertainty of the operating environment greatly increase the difficulty of fault diagnosis in real life situations. Therefore, a Bayesian network diagnosis method based on multi-source information fusion technology is proposed to solve the fault diagnosis problems caused by uncertain factors such as the high integration and complexity of the system during the process of fault diagnosis. Taking a fault of a radar receiver as an example, we study 2 typical fault phenomena and 21 fault points. After acquiring and processing multi-source information, establishing a Bayesian network model, determining conditional probability tables (CPTs), and finally outputting the diagnosis results. The results are convincing and consistent with reality, which verifies the effectiveness of this method for fault diagnosis in radar receivers. It realizes device-level fault diagnosis, which shortens the maintenance time for radars and improves the reliability and maintainability of radars. Our results have significance as a guide for judging the fault location of radars and predicting the vulnerable components of radars.

The nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome is a member of the NLR family of inherent immune cell sensors. The NLRP3 inflammasome can detect tissue damage and pathogen invasion through innate immune cell sensor components commonly known as pattern recognition receptors (PRRs). PRRs promote activation of nuclear factor kappa B (NF-κB) pathways and the mitogen-activated protein kinase (MAPK) pathway, thus increasing the transcription of genes encoding proteins related to the NLRP3 inflammasome. The NLRP3 inflammasome is a complex with multiple components, including an NAIP, CIITA, HET-E, and TP1 (NACHT) domain; apoptosis-associated speck-like protein containing a CARD (ASC); and a leucine-rich repeat (LRR) domain. After ischemic stroke, the NLRP3 inflammasome can produce numerous proinflammatory cytokines, mediating nerve cell dysfunction and brain edema and ultimately leading to nerve cell death once activated. Ischemic stroke is a disease with high rates of mortality and disability worldwide and is being observed in increasingly younger populations. To date, there are no clearly effective therapeutic strategies for the clinical treatment of ischemic stroke. Understanding the NLRP3 inflammasome may provide novel ideas and approaches because targeting of upstream and downstream molecules in the NLRP3 pathway shows promise for ischemic stroke therapy. In this manuscript, we summarize the existing evidence regarding the composition and activation of the NLRP3 inflammasome, the molecules involved in inflammatory pathways, and corresponding drugs or molecules that exert effects after cerebral ischemia. This evidence may provide possible targets or new strategies for ischemic stroke therapy.

Objective: The current study was to explore whether meisoindigo was effective in suppressing proliferation and inducing apoptosis of human glioblastoma multiforme U87 cells and to explore its possible mechanisms. Method: Morphological changes were observed by light microscopy. Cell counting kit-8 (CCK-8) assay was performed to detect cellular proliferation. Apoptosis was monitored by flow cytometry. Akt, phospho-Akt, PI3K, p65, phospho-p65 and apoptosis-related proteins caspase-3 and caspase-9 were examined by Western blotting assays. Immunofluorescence was used to evaluate level of P65 expression in cells. Result: Meisoindigo inhibited the proliferation of U87 cells, and the inhibitory effect increased in a dose dependent manner. Moreover, meisoindigo exposure triggered an increase in the level of caspase-3 and caspase-9, supporting its role in the activation of apoptosis. Furthermore, meisoindigo reduced the expression of PI3K, Akt, phospho-Akt, NF-κB, p65 and phospho-p65 in U87 cells, and displacement of p65 from the nucleus to the cytoplasm. Conclusion: Meisoindigo inhibits proliferation and induces apoptosis of U87 cells, probably through down-regulating the PI3K/Akt pathway and reducing nuclear translocation of NF-κB p65.

Background The importance of social and economic capital as predictors of health is widely documented, yet the complexity of interactions between them and effects on older people’s health is still unclear. Combining the material and psychosocial explanations of health, this study explores the potential interactions between social and economic capital in influencing older adults’ health in urban and rural China. Methods Using data from the China Family Panel Survey, physical and mental health in 2018 were regressed on social and economic capital indicators in 2016, controlling for sociodemographic characteristics of 3535 respondents aged 65 and older. Rothman’s synergy index was calculated to investigate potential interaction effects. Results Economic hardships were significantly related to both self-reported health and mental health. Neighborhood cohesion and social participation were significantly associated with mental health for all, bonding trust was significantly associated with mental health for urban older people. We found no significant associations between social capital components and self-reported health. There was an interaction effect between low neighborhood cohesion and economic hardships, and between low social participation and economic hardships, creating an increased burden of poor mental health. The interaction effect between low bonding trust and economic hardships on mental health was apparent only among urban older people. Conclusions Geographical settings are important factors in the complexity between social and economic capital in affecting older health. Intervention efforts directed towards reducing simultaneously multiple dimensions of deprivation, such as poverty, social exclusion, social isolation, could be helpful in improving older people’s health. In materially deprived places, policies to promote health equity by improving social capital but without eliminating poverty may be less effective.

BackgroundEvidence shows that inflammatory responses play multiphasic roles in stroke pathogenesis. Ruxolitinib (Rux), a selective oral JAK 1/2 inhibitor, is efficacious in COVID-19 by reducing inflammation via the JAK2/STAT3 pathway. MethodsHere, we investigated whether JAK2 inhibition has neuroprotective effects against ischemic stroke (IS) in MCAO mice in vivo and in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model, and explored the potential molecular mechanisms. Rux was applied to MCAO mice. Immunofluorescence staining, RT-qPCR, and western blots were used to measure the expression of NLRP3 inflammation components and proinflammatory cytokines as well as JAK2/STAT3 pathway. Local STAT3 deficiency in brain tissue was established to investigate the interplay between NLRP3 and STAT3 signaling.ResultsRux treatment obviously improved neurological scores, decreased the infarct size and ameliorated cerebral edema 3 days after stroke. In addition, immunofluorescence staining and western blots showed that Rux application inhibited the expression of NLRP3 inflammasome components, proteins related to the NLRP3 inflammasome and phosphorylated STAT3 (p-STAT3) in neurons. Furthermore, Rux administration inhibited the expression of proinflammatory cytokines, including TNF-α, IFN-γ, HMBG1, IL-1β, IL-2, and IL-6 in middle cerebral artery occlusion (MCAO) model mice, suggesting that Rux may alleviate IS injury by inhibiting proinflammatory reactions via JAK2/STAT3 signaling pathway regulation. Local STAT3 deficiency decreased histone H3 and H4 acetylation on the NLRP3 promoter and the NLRP3 inflammasome component expression, indicating that the NLRP3 inflammasome may be directly regulated by STAT3 signaling. Finally, the effect of Rux on the NLRP3 inflammasome was further assessed in a HT22 cell OGD/R model in vitro. Rux application markedly suppressed lipopolysaccharide (LPS)-induced NLRP3 inflammasome secretion and JAK2/STAT3 pathway activation in vitro the in OGD/R HT22 cell model.ConclusionJAK2 inhibition by Rux in MCAO mice decreased STAT3 phosphorylation, thus inhibiting downstream proinflammatory cytokines and H3 and H4 acetylation on the NLRP3 promoter, resulting in downregulation of NLRP3 inflammasome component expression.

Through considerable effort in research and clinical studies, the immune system has been identified as a participant in the onset and progression of brain injury after ischaemic stroke. Due to the involvement of all types of immune cells, the roles of the immune system in stroke pathology and associated effects are complicated. Past research concentrated on the functions of monocytes and neutrophils in the pathogenesis of ischaemic stroke and tried to demonstrate the mechanisms of tissue injury and protection involving these immune cells. Within the past several years, an increasing number of studies have elucidated the vital functions of T cells in the innate and adaptive immune responses in both the acute and chronic phases of ischaemic stroke. Recently, the phenotypes of T cells with proinflammatory or anti-inflammatory function have been demonstrated in detail. T cells with distinctive phenotypes can also influence cerebral inflammation through various pathways, such as regulating the immune response, interacting with brain-resident immune cells and modulating neurogenesis and angiogenesis during different phases following stroke. In view of the limited treatment options available following stroke other than tissue plasminogen activator therapy, understanding the function of immune responses, especially T cell responses, in the post-stroke recovery period can provide a new therapeutic direction. Here, we discuss the different functions and temporal evolution of T cells with different phenotypes during the acute and chronic phases of ischaemic stroke. We suggest that modulating the balance between the proinflammatory and anti-inflammatory functions of T cells with distinct phenotypes may become a potential therapeutic approach that reduces the mortality and improves the functional outcomes and prognosis of patients suffering from ischaemic stroke.

Investigating the spatial epidemic dynamics of COVID-19 is crucial in understanding the routine of spatial diffusion and in surveillance, prediction, identification and prevention of another potential outbreak. However, previous studies attempting to evaluate these spatial diffusion dynamics are limited. Using city as the research unit and spatial association analysis as the primary strategy, this study explored the changing primary risk factors impacting the spatial spread of COVID-19 across Chinese cities under various diffusion assumptions and throughout the epidemic stage. Moreover, this study investigated the characteristics and geographical distributions of high-risk areas in different epidemic stages. The results empirically indicated rapid intercity diffusion at the early stage and primarily intracity diffusion thereafter. Before countermeasures took effect, proximity, GDP per capita, medical resources, outflows from Wuhan and intercity mobility significantly affected early diffusion. With speedily effective countermeasures, outflows from the epicenter, proximity, and intracity outflows played an important role. At the early stage, high-risk areas were mainly cities adjacent to the epicenter, with higher GDP per capita, or a combination of higher GDP per capita and better medical resources, with more outflow from the epicenter, or more intercity mobility. After countermeasures were effected, cities adjacent to the epicenter, or with more outflow from the epicenter or more intracity mobility became high-risk areas. This study provides an insightful understanding of the spatial diffusion of COVID-19 across cities. The findings are informative for effectively handling the potential recurrence of COVID-19 in various settings.

The special fiber-optic microseismic monitoring system has been successfully developed by Peking university and Xinjiang oilfield company. It has performed 7 monitor-ing tasks from 2016 to 2019, providing ideal interpretations of induced fracture. (tel: +86 138 0108 9536, e-mail: zhang min@pku.edu.cn)