Effect of endothelial responses on sepsis-associated organ dysfunction.

ABSTRACT: Sepsis-related organ dysfunction is associated with increased morbidity and mortality. Previous studies have found that the endothelium plays crucial roles in maintaining the vascular permeability during sepsis, as well as in regulating inflammation and thrombosis. During sepsis, endothelial cells may release cytokines, chemokines, and pro-coagulant factors, as well as express adhesion molecules. In general, endothelial responses during sepsis typically inhibit bacterial transmission and coordinate leukocyte recruitment to promote bacterial clearance. However, excessive or prolonged endothelial activation can lead to impaired microcirculation, tissue hypoperfusion, and organ dysfunction. Given the structural and functional heterogeneity of endothelial cells in different organs, there are potential differences in endothelial responses by organ type, and the risk of organ damage may vary accordingly. This article reviews the endothelial response observed in sepsis and its effects on organ function, summarizes current progress in the development of therapeutic interventions targeting the endothelial response, and discusses future research directions to serve as a reference for researchers in the field.

Research trends in nutritional interventions for stroke: a bibliometric analysis and literature review.

Background: Over the past 23 years, there has been a thorough analysis of literature concerning nutritional interventions, nutrients, and feeding approaches related to stroke. Furthermore, a scientific knowledge map was established, elucidating the current state of research, examining its development and trends, and offering new research viewpoints for the future. This study aimed to investigate global and emerging research trends in nutritional interventions for stroke from 2000 to 2023 through bibliometric analysis. Methods: A bibliometric analysis of literature from the Core Collection of Scientific Networks for the years 2000-2022 was conducted. CiteSpace, VOSviewer, and bibliometric graphical software were used to identify major contributors to publications, including authors, countries, institutions, journals, references, and keywords. Results: The bibliometric analysis yielded a total of 464 publications. This is a gradually increasing number in terms of the number of publications during the study period. China had the highest number of publications. Clinical Nutrition" was the journal with the highest number of relevant publications, and the most commonly used keywords were "stroke," "nutrition" and "malnutrition." Conclusion: These analyses reveal research trends in nutritional therapy for stroke from 2000 to 2023 and point to prospective research frontiers. This study provides a deeper understanding of what nutritional treatment of stroke entails and provides guidance and support for future research in this area.

Effects of low frequency repetitive transcranial magnetic stimulation on motor recovery in subacute stroke patients with different motor evoked potential status: a randomized controlled trial.

Objectives: To explore the effects of low-frequency repetitive transcranial magnetic stimulation (LF-rTMS) on motor function and cortical excitability in stroke patients with different motor evoked potential (MEP) status. Methods: A total of 80 stroke patients were enrolled in this randomized controlled trial and divided into two groups according to MEP status (- or +) of lesioned hemisphere. Then, each group was randomly assigned to receive either active or sham LF-rTMS. In addition to conventional rehabilitation, all participants received 20 sessions of rTMS at 1 Hz frequency through the active or the sham coil over 4 weeks. Fugl-Meyer Assessment (FMA), National Institutes of Health Stroke Scale (NIHSS), Shoulder Abduction Finger Extension (SAFE) and Barthel Index (BI), bilateral resting motor threshold (rMT), amplitude of Motor evoked potential (MEP) and Central Motor Conduction Time (CMCT), and Interhemispheric asymmetry (IHA) were blindly assessed at baseline, 4 weeks and 8 weeks after treatment, respectively. Results: At 4 weeks after intervention, FMA and NIHSS changed scores in 1 Hz MEP(+) group were significantly higher than those in the other three groups (p < 0.001). After receiving 1 Hz rTMS, stroke patients with MEP(+) showed significant changes in their bilateral cortical excitability (p < 0.05). At 8 weeks after intervention, 1 Hz MEP(+) group experienced higher changes in NIHSS, FMA, SAFE, and BI scores than other groups (p < 0.001). Furthermore, 1 Hz rTMS intervention could decrease unaffected cortical excitability and enhance affected cortical excitability of stroke patients with MEP(+) (p < 0.05). The correlation analysis revealed that FMA motor change score was associated with decreased unaffected MEP amplitude (r = -0.401, p = 0.010) and decreased affected rMT (r = -0.584, p < 0.001) from baseline, which was only observed in the MEP(+) group. Conclusion: The effects of LF-rTMS on motor recovery and cortical excitability were more effective in stroke patients with MEP than those with no MEP.

Long-term performance and mechanism of in-situ biogenetic sulfidated zero-valent iron for enhanced nitrate reduction.

The biogenetic sulfidation of zero-valent iron (BS-ZVI) by sulfate-reducing bacteria (SRB) has been demonstrated to enhance the reactivity of ZVI. However, long-term performance of BS-ZVI and related mechanism were still unknown. Therefore, columns containing sponge iron and SRB are built to prepare BS-ZVI in-situ and study its long-term performance. Over 80 % of NO3‾ was reduced to NH4+ by in-situ BS-ZVI within 140 days, which was higher than the sole ZVI treatment (40 %-60 %). The bonding of ZVI and FeSx was in-situ firstly and finally loaded on ZVI. The reduction of Fe(III) by S(-II) and SRB contributed to the formation of FeSx, which improved the electrons transfer. Moreover, BS-ZVI enhanced the enzymes activity of SRB, thus accelerating the metabolic transformation of lactic acid to acetic acid. The accumulation of acetic acid enhanced the removal efficiency of NO3‾ through the dissolution of passivation layer. Overall, this study demonstrated a reactivity enhancement of ZVI through biogenetic sulfidation, which provided a new alternative method for the remediation of groundwater.

Astrocytic neuroligin 3 regulates social memory and synaptic plasticity through adenosine signaling in male mice.

Social memory impairment is a key symptom of many brain disorders, but its underlying mechanisms remain unclear. Neuroligins (NLGs) are a family of cell adhesion molecules essential for synapse development and function and their dysfunctions are linked to neurodevelopmental and neuropsychiatric disorders, including autism and schizophrenia. Although NLGs are extensively studied in neurons, their role in glial cells is poorly understood. Here we show that astrocytic deletion of NLG3 in the ventral hippocampus of adult male mice impairs social memory, attenuates astrocytic Ca2+ signals, enhances the expression of EAAT2 and prevents long-term potentiation, and these impairments are rescued by increasing astrocyte activity, reducing EAAT2 function or enhancing adenosine/A2a receptor signaling. This study has revealed an important role of NLG3 in astrocyte function, glutamate homeostasis and social memory and identified the glutamate transporter and adenosine signaling pathway as potential therapeutic strategies to treat brain disorders.

Repetitive Transcranial Magnetic Stimulation Alleviates MPTP-Induced Parkinson's Disease Symptoms by Regulating CaMKII-CREB-BMAL1 Pathway in Mice Model.

Background: Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive neuromodulation technique that shows promise for the treatment of Parkinson's disease (PD). However, there is still limited understanding of the optimal stimulation frequencies and whether rTMS can alleviate PD symptoms by regulating the CaMKII-CREB-BMAL1 pathway. Methods: A PD mouse model was induced intraperitoneally with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and treated with 1 Hz, 5 Hz, and 10 Hz rTMS. The neurological function, survival of dopaminergic neurons, and protein levels of Tyrosine hydroxylase (TH), α-synuclein(α-syn), and brain-derived neurotrophic factor (BDNF) in the striatum were measured to determine the optimal stimulation frequencies of rTMS treatment in PD mice. The levels of melatonin, cortisol, and the circadian rhythm of Brain and muscle ARNT-like 1 (BMAL1) in PD model mice were detected after optimal frequency rTMS treatment. Additionally, KN-93 and Bmal1siRNA interventions were used to verify that rTMS could alleviate PD symptoms by regulating the CaMKII-CREB-BMAL1 pathway. Results: Administration of 10 Hz rTMS significantly improved neurological function, increased the protein levels of TH and BDNF, and inhibited abnormal aggregation of a-syn. Furthermore, administration of 10 Hz rTMS regulated the secretion profile of cortisol and melatonin and reversed the circadian arrhythmia of BMAL1 expression. After the KN-93 intervention, the MPTP+rTMS+KN-93 group exhibited decreased levels of P- Ca2+/calmodulin-dependent protein kinase II (CaMKII)/CaMKII, P-cAMP-response-element-binding protein (CREB)/CREB, BMALI, and TH. After Bmal1siRNA intervention, the protein levels of BMAL1 and TH were significantly reduced in the MPTP+10 Hz+ Bmal1siRNA group. At the same time, there were no significant changes in the proportions of P-CaMKIIα/CaMKIIα and P-CREB/CREB expression levels. Finally, immunohistochemical analysis showed that the number of TH-positive neurons was high in the MPTP+10 Hz group, but decreased significantly after KN-93 and Bmal1siRNA interventions. Conclusion: Treatment with 10 Hz rTMS alleviated MPTP-induced PD symptoms by regulating the CaMKII-CREB-BMAL1 pathway. This study provides a comprehensive perspective of the therapeutic mechanisms of rTMS in PD.

Grey modelling and real-time forecasting for the approximate non-homogeneous white exponential law BDS clock bias sequences.

Precise forecasting of satellite clock bias is crucial for ensuring service quality and enhancing the efficiency of real-time precise point positioning (PPP).The grey model with many benefits is an excellent choice for predicting real-time clock bias. However, the absolute prediction error of a small number of satellites is very high in actual forecasting process. In order to address this issue, a non-homogeneous white exponential law grey model has been constructed specifically for predicting clock bias sequences with non-homogeneous class ratio approximating constants. Considering that any model is difficult to apply to different kinds of satellite clocks and clock bias signals, an adaptive selection strategy for forecast model is proposed to ensure more excellent prediction accuracy. Afterwards, a prediction scenario based on the observed products of the BeiDou satellite navigation system (BDS) is created to demonstrate the effectiveness of the approach described in this article. The outcomes of the method are then compared with those of a single grey model and the ultra-rapid predicted products. The outcomes demonstrate that this strategy's prediction accuracy is less than 1 ns/day and that its prediction uncertainty is much decreased, which may improve data selection for real-time applications like real-time kinematics (RTK) and PPP.

Autism-associated neuroligin 3 deficiency in medial septum causes social deficits and sleep loss in mice.

Patients with autism spectrum disorder (ASD) frequently experience sleep disturbance. Genetic mutations in the neuroligin 3 (NLG3) gene are highly correlative with ASD and sleep disturbance. However, the cellular and neural circuit bases of this correlation remain elusive. Here, we found that the conditional knockout of Nlg3 (Nlg3-CKO) in the medial septum (MS) impairs social memory and reduces sleep. Nlg3 CKO in the MS caused hyperactivity of MSGABA neurons during social avoidance and wakefulness. Activation of MSGABA neurons induced social memory deficits and sleep loss in C57BL/6J mice. In contrast, inactivation of these neurons ameliorated social memory deficits and sleep loss in Nlg3-CKO mice. Sleep deprivation led to social memory deficits, while social isolation caused sleep loss, both resulting in a reduction in NLG3 expression and an increase in activity of GABAergic neurons in the MS from C57BL/6J mice. Furthermore, MSGABA-innervated CA2 neurons specifically regulated social memory without impacting sleep, whereas MSGABA-innervating neurons in the preoptic area selectively controlled sleep without affecting social behavior. Together, these findings demonstrate that the hyperactive MSGABA neurons impair social memory and disrupt sleep resulting from Nlg3 CKO in the MS, and achieve the modality specificity through their divergent downstream targets.

Association between the triglyceride-glucose index and carotid artery plaque burden in patients with primary hypertension: A cross-sectional study.

BACKGROUND: Studies have shown an association between the triglyceride-glucose (TyG) index and carotid artery plaque (CAP). However, the relationship between the TyG index and plaque burden in individuals with primary hypertension remains uncertain. Our study specifically aimed to explore this relationship among primary hypertension patients. METHODS: This study involved 5,153 hospitalized patients diagnosed with primary hypertension who were undergoing treatment at the Affiliated Hospital of Jiangxi University of Chinese Medicine. We utilized multivariate logistic regression, penalized spline regression, and generalized additive models to assess the association between the TyG index and CAP burden. RESULTS: There were 2,400 patients with primary hypertension in all. The multivariate study, which took into account all covariables, showed a positive correlation between the TyG index and CAP (OR: 1.25, 95% CI: 1.04-1.5). When the TyG index was evaluated as quartiles, the risk of CAP in the Q3 and Q4 levels of the TyG index were 1.4 (95% CI: 1.03-1.91) and 1.54 (95% CI: 1.11-2.14) times greater than in the Q1 level after adjusting for all covariables (P for trend < .05). Regardless of whether the TyG index was used as a continuous variable or a categorical variable, it has no significant association with the risk of single plaque after adjusting for all confounders (p ≥ .05). The TyG index was found to be substantially correlated with the presence of multiple plaques when analyzed as a continuous variable (OR: 1.32, 95% CI: 1.09-1.59, p = .004). When the TyG index was evaluated as quartiles, the adjusted OR in Q3 and Q4 were 1.49 (95% CI: 1.06-2.1) and 1.67 (95% CI: 1.16-2.41), respectively, with Q1 as reference (P for trend = .005). The relationship between the TyG index and the presence of multiple plaques is also consistent in all subgroups. CONCLUSION: The TyG index is positively associated with the presence of multiple plaques in patients with primary hypertension, whereas no association is found between the TyG index and the presence of a single carotid plaque.

[Basic research in sepsis: advances and challenges].

Although the understanding of sepsis has evolved from "sepsis 1.0" to "sepsis 3.0", and the consensus on clinical management of sepsis has been continuously updated, the incidence rate and mortality of sepsis remain high. Therefore, in-depth investigation of the pathogenesis and related influencing factors of sepsis is of great significance for revealing the nature of sepsis and improving the clinical outcome of sepsis patients. This review will focus on the key issues in the basic research of sepsis, and summarize the recent advances and challenges in this field, mainly including genetic polymorphism, microorganisms, high-mobility group box 1 (HMGB1), endothelial dysfunction, immunotherapy, and biomarkers, aiming to provide new insights for the diagnosis and treatment of sepsis.

A Series of Lanthanide Coordination Polymers as Luminescent Sensors for Selective Detection of Inorganic Ions and Nitrobenzene.

Seven new lanthanide coordination polymers, namely [Ln(cpt)3H2O)]n(Ln = La (1), Pr (2), Sm (3), Eu (4), Gd (5), Dy (6), and Er (7)), which were synthesized under hydrothermal conditions using 4'-(4-(4-carboxyphenyloxy)phenyl)-4,2':6',4'-tripyridine (Hcpt) as the ligand. The crystal structures of these seven complexes were determined using single-crystal X-ray diffraction, and they were found to be isostructural, crystallizing in the triclinic P1- space group. The Ln(III) ions were nine-coordinated with tricapped trigonal prism coordination geometry. The Ln(III) cations were coordinated by carboxylic and pyridine groups from (cpt)- ligands, forming one-dimensional ring-chain structures. Furthermore, the luminescent properties of complexes 1-7 were investigated using fluorescent spectra in the solid state. The fluorescence sensing experiments demonstrated that complex 4 exhibits high selectivity and sensitivity for detecting Co2+, Cu2+ ions, and nitrobenzene. Moreover, complex 3 shows good capability for detecting Cu2+ ions and nitrobenzene. Additionally, the sensing mechanism was also thoroughly examined through theoretical calculations.

Therapeutic effect of nicotinamide mononucleotide on Alzheimer's disease through activating autophagy and anti-oxidative stress.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the deposition of ß-amyloid (Aß) plaques and neurofibrillary tangles composed of tau protein in the brain. These neuropathological hallmarks contribute to cognitive impairment by inducing neuronal loss in the cerebral cortex and hippocampus. Unfortunately, current therapeutic approaches only target symptomatic relief and do not impede disease progression. Nicotinamide mononucleotide (NMN), a precursor of nicotinamide adenine dinucleotide (NAD+), has emerged as a promising candidate for the treatment of age-related neurodegenerative disorders. NMN supplementation could restore NAD+ levels, thereby alleviating neuronal damage and slowing the progression of AD and other aging-associated diseases. AD is closely associated with autophagic impairment and oxidative stress. Our in vivo experiments demonstrated that NMN could ameliorate pathological and behavioral impairments in AD mice. Specifically, NMN enhanced autophagy and promoted p-tau clearance. Meanwhile, NMN could activate the Nrf2/Keap1/NQO1 pathway, thereby reducing the oxidative stress. Immunofluorescence results demonstrated that NMN could alleviate neuronal damage in AD mice. Furthermore, in vitro results showed that the p-tau clearance and antioxidant stress effects of NMN were suppressed by autophagy inhibitor, chloroquine (CQ) or bafilomycin A1 (BafA1), in Aß-induced PC12 cells. Lastly, when Nrf2 was knocked down, the antioxidant stress, autophagy enhancement, and p-tau clearance effects of NMN were all inhibited. In conclusion, our research indicates that NMN exerts therapeutic effect against AD by activating autophagy and the Nrf2/Keap1/NQO1 pathway through a mutual regulating mechanism of autophagy and antioxidative stress. These findings highlight the promising potential of NMN for the treatment of AD.

Clinical Application of Artificial Intelligence in the Ultrasound Classification of Hepatic Cystic Echinococcosis.

Hepatic cystic echinococcosis (HCE) is a zoonotic disease that occurs when the larvae of Echinococcus granulosus parasitize the livers of humans and mammals. HCE has five subtypes, and accurate subtype classification is critical for choosing a treatment strategy. To evaluate the clinical utility of artificial intelligence (AI) based on convolutional neural networks (CNNs) in the classification of HCE subtypes via ultrasound imaging, we collected ultrasound images from 4,012 HCE patients at the First Affiliated Hospital of Xinjiang Medical University between 2008 and 2020. Specifically, 1,820 HCE images from 967 patients were used as the training and validation sets for the construction of the AI model, and the remaining 6,808 images from 3,045 patients were used as the test set to evaluate the performance of the AI models. The 6,808 images were randomly divided into six groups, and each group contained equal proportions of the five subtypes. The data of each group were analyzed by a resident physician. The accuracy of HCE subtype classification by the AI model and by manual inspection was compared. The AI HCE classification model showed good performance in the diagnosis of subtypes CE1, CE2, CE4, and CE5. The overall accuracy of the AI classification (90.4%) was significantly greater than that of manual classification by physicians (86.1%; P <0.05). The CNN can better identify the five subtypes of HCE on ultrasound images and should help doctors with little experience in more accurately diagnosing HCE.

Multiclassification of Hepatic Cystic Echinococcosis by Using Multiple Kernel Learning Framework and Ultrasound Images.

To properly treat and care for hepatic cystic echinococcosis (HCE), it is essential to make an accurate diagnosis before treatment. OBJECTIVE: The objective of this study was to assess the diagnostic accuracy of computer-aided diagnosis techniques in classifying HCE ultrasound images into five subtypes. METHODS: A total of 1820 HCE ultrasound images collected from 967 patients were included in the study. A multi-kernel learning method was developed to learn the texture and depth features of the ultrasound images. Combined kernel functions were built-in Support Vector Machine (MK-SVM) for the classification work. The experimental results were evaluated using five-fold cross-validation. Finally, our approach was compared with three other machine learning algorithms: the decision tree classifier, random forest, and gradient boosting decision tree. RESULTS: Among all the methods used in the study, the MK-SVM achieved the highest accuracy of 96.6% on the fused feature set. CONCLUSION: The multi-kernel learning method effectively learns different image features from ultrasound images by utilizing various kernels. The MK-SVM method, which combines the learning of texture features and depth features separately, has significant application value in HCE classification tasks.

Hydrogen Sulfide Protects against Rat Ischemic Brain Injury by Promoting RhoA Phosphorylation at Serine 188.

The protective role of hydrogen sulfide against cerebral ischemia-reperfusion injury involves the inhibition of the RhoA-/Rho-associated coiled-coil kinase (ROCK) pathway. However, the specific mechanism remains elusive. This study investigates the impact of hydrogen sulfide on RhoA phosphorylation at serine 188 (Ser188) in vivo, aiming to test the hypothesis that hydrogen sulfide exerts neuroprotection by enhancing RhoA phosphorylation at Ser188, subsequently inhibiting the RhoA/ROCK pathway. Recombinant RhoAwild-pEGFP-N1 and RhoAS188A-pEGFP-N1 plasmids were constructed and administered via stereotaxic injection into the rat hippocampus. A rat global cerebral ischemia-reperfusion model was induced by bilateral carotid artery ligation to elucidate the neuroprotective mechanisms of hydrogen sulfide. Both RhoAwild-pEGFP-N1 and RhoAS188A-pEGFP-N1 plasmids expressed RhoAwild and RhoAS188A proteins, respectively, in rat hippocampal tissues, alongside the intrinsic RhoA protein. Systemic administration of the exogenous hydrogen sulfide donor sodium hydrosulfide led to an increase in Ser188 phosphorylation of transfected RhoAwild and intrinsic RhoA protein within the hippocampus. However, this effect was not observed in tissues transfected with RhoAS188A. Sodium hydrosulfide-mediated RhoA phosphorylation correlated with decreased RhoA and ROCK2 activity in rat hippocampal tissues. Furthermore, sodium hydrosulfide administration reduced cerebral ischemia-reperfusion-induced neuronal damage and apoptosis in rat hippocampal tissues transfected with RhoAwild. However, this neuroprotective effect was attenuated in rats transfected with RhoAS188A. These findings suggest that the neuroprotective mechanism of hydrogen sulfide against cerebral ischemia/reperfusion injury involves increased RhoA phosphorylation at Ser188. Promoting this phosphorylation may represent a potential intrinsic therapeutic target for ischemic stroke.

MoMkk1 and MoAtg1 dichotomously regulating autophagy and pathogenicity through MoAtg9 phosphorylation in Magnaporthe oryzae.

Autophagy is a central biodegradation pathway critical in eliminating intracellular cargo to maintain cellular homeostasis and improve stress resistance. At the same time, the key component of the mitogen-activated protein kinase cascade regulating cell wall integrity signaling MoMkk1 has an essential role in the autophagy of the rice blast fungus Magnaporthe oryzae. Still, the mechanism of how MoMkk1 regulates autophagy is unclear. Interestingly, we found that MoMkk1 regulates the autophagy protein MoAtg9 through phosphorylation. MoAtg9 is a transmembrane protein subjected to phosphorylation by autophagy-related protein kinase MoAtg1. Here, we provide evidence demonstrating that MoMkk1-dependent MoAtg9 phosphorylation is required for phospholipid translocation during isolation membrane stages of autophagosome formation, an autophagic process essential for the development and pathogenicity of the fungus. In contrast, MoAtg1-dependent phosphorylation of MoAtg9 negatively regulates this process, also impacting growth and pathogenicity. Our studies are the first to demonstrate that MoAtg9 is subject to MoMkk1 regulation through protein phosphorylation and that MoMkk1 and MoAtg1 dichotomously regulate autophagy to underlie the growth and pathogenicity of M. oryzae.IMPORTANCEMagnaporthe oryzae utilizes multiple signaling pathways to promote colonization of host plants. MoMkk1, a cell wall integrity signaling kinase, plays an essential role in autophagy governed by a highly conserved autophagy kinase MoAtg1-mediated pathway. How MoMkk1 regulates autophagy in coordination with MoAtg1 remains elusive. Here, we provide evidence that MoMkk1 phosphorylates MoAtg9 to positively regulate phospholipid translocation during the isolation membrane or smaller membrane structures stage of autophagosome formation. This is in contrast to the negative regulation of MoAtg9 by MoAtg1 for the same process. Intriguingly, MoMkk1-mediated MoAtg9 phosphorylation enhances the fungal infection of rice, whereas MoAtg1-dependant MoAtg9 phosphorylation significantly attenuates it. Taken together, we revealed a novel mechanism of autophagy and virulence regulation by demonstrating the dichotomous functions of MoMkk1 and MoAtg1 in the regulation of fungal autophagy and pathogenicity.

Neuroprotective effects of galectin­1 on cerebral ischemia/reperfusion injury by regulating oxidative stress.

Oxidative stress contributes to the pathology of cerebral ischemia/reperfusion (I/R) injury. Galectin-1 has shown an anti-oxidative stress effect. The present study investigated whether this anti-oxidative stress effect can account for the neuroprotective actions of galectin-1 induced by cerebral I/R injury. A cerebral I/R injury model was created in C57Bl/6 mice by transient occlusion of the middle cerebral artery, after which the mice were treated with galectin-1 for 3 days. Infarct volumes were measured. A rotarod test and neurological deficit score assessment was performed to evaluate the neurological deficits. Oxidative stress was evaluated by measuring the levels of reactive oxygen species (ROS) and lipid peroxidation malondialdehyde (MDA), while the anti-oxidative stress status was assessed by measuring molecules such as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidation enzyme (GSH-Px) in the ischemic cerebral hemisphere of mice. The inflammatory cytokines, including Interleukin 1 (IL-1), IL-6 and tumor necrosis factor alpha (TNF-α) were measured, and the expression of microglia was evaluated by immunohistochemistry in the ischemic cerebral hemisphere of mice. Galectin-1 treatment ameliorated neurological deficits and reduced infarct volumes in the mice model with cerebral I/R injury. Moreover, it was demonstrated that galectin-1 can significantly alleviate cerebral I/R injury in the ischemic cerebral hemisphere by decreasing the production of ROS and MDA, but increasing the production of CAT, SOD and GSH-Px. Galectin-1 treatment decreased microglia expression, and IL-1, IL-6 and TNF-α levels in the ischemic cerebral hemisphere of mice. Galectin-1 could improve the outcome of cerebral I/R injury by alleviating oxidative stress. Moreover, the neuroprotective effect of galectin-1 in cerebral ischemia could be related to its anti-oxidative stress effect.

Low Contact Resistance Organic Single-Crystal Transistors with Band-Like Transport Based on 2,6-Bis-Phenylethynyl-Anthracene.

Contact resistance has become one of the main bottlenecks that hinder further improvement of mobility and integration density of organic field-effect transistors (OFETs). Much progress has been made in reducing contact resistance by modifying the electrode/semiconductor interface and decreasing the crystal thickness, however, the development of new organic semiconductor materials with low contact resistance still faces many challenges. Here, 2,6-bis-phenylethynyl-anthracene (BPEA) is found, which is a material that combines high mobility with low contact resistance. Single-crystal BEPA OFETs with a thickness of ≈20 nm demonstrated high mobility of 4.52 cm2 V-1 s-1, contact resistance as low as 335 Ω cm, and band-like charge transport behavior. The calculated compatibility of the EHOMO of BPEA with the work function of the Au electrode, and the decreased |EHOMO-ΦAu| with the increase of external electric field intensity from source to gate both contributed to the efficient charge injection and small contact resistance. More intriguingly, p-type BPEA as a buffer layer can effectively reduce the contact resistance, improve the mobility, and meanwhile inhibit the double-slope electrical behavior of p-channel 2,6-diphenyl anthracene (DPA) single-crystal OFETs.

Full-Length Transcriptome Sequencing and Comparative Transcriptomic Analyses Provide Comprehensive Insight into Molecular Mechanisms of Flavonoid Metabolites Biosynthesis in Styphnolobium japonicum.

Styphnolobium japonicum L. is a commonly consumed plant in China, known for its medicinal and nutritional benefits. This study focuses on the medicinal properties influenced by flavonoid metabolites, which vary during flower development. Utilizing full-length transcriptome sequencing on S. japonicum flowers, we observed changes in gene expression levels as the flowers progressed through growth stages. During stages S1 and S2, key genes related to flavonoid synthesis (PAL, 4CL, CHS, F3H, etc.) exhibited heightened expression. A weighted gene co-expression network analysis (WGCNA) identified regulatory genes (MYB, bHLH, WRKY) potentially involved in the regulatory network with flavonoid biosynthesis-related genes. Our findings propose a regulatory mechanism for flavonoid synthesis in S. japonicum flowers, elucidating the genetic underpinnings of this process. The identified candidate genes present opportunities for genetic enhancements in S. japonicum, offering insights into potential applications for improving its medicinal attributes.