Heterologous survey of 130 DNA transposons in human cells highlights their functional divergence and expands the genome engineering toolbox.

Experimental studies on DNA transposable elements (TEs) have been limited in scale, leading to a lack of understanding of the factors influencing transposition activity, evolutionary dynamics, and application potential as genome engineering tools. We predicted 130 active DNA TEs from 102 metazoan genomes and evaluated their activity in human cells. We identified 40 active (integration-competent) TEs, surpassing the cumulative number (20) of TEs found previously. With this unified comparative data, we found that the Tc1/mariner superfamily exhibits elevated activity, potentially explaining their pervasive horizontal transfers. Further functional characterization of TEs revealed additional divergence in features such as insertion bias. Remarkably, in CAR-T therapy for hematological and solid tumors, Mariner2_AG (MAG), the most active DNA TE identified, largely outperformed two widely used vectors, the lentiviral vector and the TE-based vector SB100X. Overall, this study highlights the varied transposition features and evolutionary dynamics of DNA TEs and increases the TE toolbox diversity.

Knockout of nuclear receptor HR38 gene impairs pupal-adult development in silkworm Bombyx mori.

Nuclear receptors are ligand-regulated transcription factors that play important role in regulating insect metamorphosis through the ecdysone signalling pathway. In this study, we investigated the nuclear receptor HR38 gene in Bombyx mori (BmHR38), belonging to the NR4A subfamily. BmHR38 mRNA was highly expressed in the head and epidermis at the pupal stage. The expression of the BmHR38 gene was influenced by different doses of 20E at different times. A BmHR38 deletion mutant silkworm was generated using the clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 system. Compared with the wild-type B. mori, the BmHR38 deletion mutant resulted in abnormal development during the pupal stage, leading to either failed eclosion or the formation of abnormal adult wings. After silencing of BmHR38 in the pupal stage, the phenotype of pupa or moth had no significant change, but it did result in reduced egg production. The mRNA levels of USP, E75 and E74 were significantly increased, while the transcript levels of FTZ-F1 were suppressed after RNA interference. Furthermore, interference with BmHR38 also inhibited the expressions of chitin metabolism genes, including Chs1, Chs2, Chi, Chi-h and CDA. Our results suggest that BmHR38 is essential for pupal development and pupa-adult metamorphosis in B. mori by regulating the expression of NRs and chitin metabolism genes.

Sulfate sensitivity of aquatic organism in soft freshwaters explored by toxicity tests and species sensitivity distribution.

Elevated concentrations of sulfate in waterways are observed due to various anthropogenic activities. Elevated levels of sulfate can have harmful effects on aquatic life in freshwaters: sulfate can cause osmotic stress or specific ion toxicity in aquatic organisms, especially in soft waters where Ca2+ and Mg2+ concentrations are low. Formerly, chronic toxicity test data in soft water have been scarce. The chronic and acute sulfate toxicity tests conducted with aquatic organisms from 10 families across various trophic levels in this study multiplied the number of tests conducted in soft freshwater conditions and enabled derivation of the species sensitivity distribution (SSD) and sulfate hazardous concentrations for soft freshwaters. The cladoceran Daphnia longispina and freshwater snail Lymnaea stagnalis were the most sensitive to sulfate among the studied species. Harmful effects on the reproduction of D. longispina were observed at 49 mg SO4 /L while growth of L. stagnalis was inhibited at 217 mg SO4 /L. Most studied organisms tolerated high sulfate concentrations: the median of chronic effective concentrations (EC10 or LC10) was 1008 mg/L for all the species tested in this study. Based on the species sensitivity distribution of the studied species the hazardous concentration for 5 % of aquatic organism (HC5) in soft waters was 117-194 mg SO4/L. Different data set combinations were used to demonstrate the data variability in SSD-based HC5 estimates. The lowest values were produced from combining biotest results from the present study and earlier literature, while the highest values were calculated from the present study only. The derived chronic no-effect concentrations (PNEC) varied between 39 and 65 mg SO4/L.

Voluntary Exercise to Reduce Anxiety Behaviour in Traumatic Brain Injury Shown to Alleviate Inflammatory Brain Response in Mice.

Traumatic brain injury is a leading cause of neuroinflammation and anxiety disorders in young adults. Immune-targeted therapies have garnered attention for the amelioration of TBI-induced anxiety. A previous study has indicated that voluntary exercise intervention following TBI could reduce neuroinflammation. It is essential to determine the effects of voluntary exercise after TBI on anxiety via inhibiting neuroinflammatory response. Mice were randomly divided into four groups (sham, TBI, sham + voluntary wheel running (VWR), and TBI + VWR). One-week VWR was carried out on the 2nd day after trauma. The neurofunction of TBI mice was assessed. Following VWR, anxiety behavior was evaluated, and neuroinflammatory responses in the perilesional cortex were investigated. Results showed that after one week of VWR, neurofunctional recovery was enhanced, while the anxiety behavior of TBI mice was significantly alleviated. The level of pro-inflammatory factors decreased, and the level of anti-inflammatory factors elevated. Activation of nucleotide oligomerization domain-like thermal receptor protein domain associated protein 3 (NLRP3) inflammasome was inhibited significantly. All these alterations were consistent with reduced microglial activation at the perilesional site and positively correlated with the amelioration of anxiety behavior. This suggested that timely rehabilitative exercise could be a useful therapeutic strategy for anxiety resulting from TBI by targeting neuroinflammation.

Leptin Promotes the Proliferation and Neuronal Differentiation of Neural Stem Cells through the Cooperative Action of MAPK/ERK1/2, JAK2/STAT3 and PI3K/AKT Signaling Pathways.

The potential of neural stem cells (NSCs) for neurological disorders the treatment has relied in large part upon identifying the NSCs fate decision. The hormone leptin has been reported to be a crucial regulator of brain development, able to influence the glial and neural development, yet, the underlying mechanism of leptin acting on NSCs' biological characteristics is still poorly understood. This study aims to investigate the role of leptin in the biological properties of NSCs. In this study, we investigate the possibility that leptin may regulate the NSCs' fate decision, which may promote the proliferation and neuronal differentiation of NSCs and thus act positively in neurological disorders. NSCs from the embryonic cerebral cortex were used in this study. We used CCK-8 assay, ki67 immunostaining, and FACS analysis to confirm that 25-100 ng/mL leptin promotes the proliferation of NSCs in a concentration-dependent pattern. This change was accompanied by the upregulation of p-AKT and p-ERK1/2, which are the classical downstream signaling pathways of leptin receptors b (LepRb). Inhibition of PI3K/AKT or MAPK/ERK signaling pathways both abolished the effect of leptin-induced proliferation. Moreover, leptin also enhanced the directed neuronal differentiation of NSCs. A blockade of the PI3K/AKT pathway reversed leptin-stimulated neurogenesis, while a blockade of JAK2/STAT3 had no effect on it. Taken together, our results support a role for leptin in regulating the fate of NSCs differentiation and promoting NSCs proliferation, which could be a promising approach for brain repair via regulating the biological characteristics of NSCs.

Investigating the dynamic decoupling relationship between regional social economy and lake water environment: The application of DPSIR-Extended Tapio decoupling model.

The water environmental problems associated with rapid socioeconomic growth have drawn widespread attention from the government and the public. Revealing the decoupling mechanism between the social economy and lake water environment has become an important breakthrough point to seek the pathways of sustainable economic development. To investigate the decoupling process of the social economy‒lake water environmental system, this study proposes a comprehensive evaluation model, which integrates the Driving force-Pressure-State-Impact-Response (DPSIR) model, projection pursuit method, and Tapio decoupling model; and then applies it to the case study of Hefei City and Lake Chaohu in China in 2021-2035. Three typical scenarios of current, social economy, and water environment are designed and simulated using the DPSIR model to evaluate the dynamic decoupling relationships under various development patterns. We found that the DPSIR indexes had a fluctuating upward trend from 2009 to 2020, with a synchronous improvement trend of the social economy and lake water environment. Meanwhile, the Tapio decoupling analysis showed that the decoupling relationships between socioeconomic driver forces, response strategies and the status of lake water environment was mostly strongly decoupled and weakly decoupled during 2009-2020. However, there was still an inconsistency between the improvement rate of the lake water environment and the increase rate of the response strategies. During the 2021-2035 simulation period, the DPSIR indexes of all scenarios depicts an overall increasing trend. The decoupling states of S&I-D&P and S&I-R generally tend to be consistent under three regulation scenarios. Among them, the water environment scenario outperforms other scenarios, and the social economy scenario performs worst. Overall, the decoupling of the social economy and lake water environment can attribute to both the transformation of socioeconomic development patterns and the increase of water environmental protection efforts.

SERS enhancement induced by the Se vacancy defects in ultra-thin hybrid phase SnSex nanosheets.

Improving the photo-induced charge transfer (PICT) efficiency by adjusting the energy levels difference between adsorbed probe molecules and substrate materials is a key factor for boosting the surface enhanced Raman scattering (SERS) based on the chemical mechanism (CM). Herein, a new route to improve the SERS activity of two-dimensional (2D) selenium and tin compounds (SnSex, 1 ≤ x ≤ 2) by the hybrid phase materials is researched. The physical properties and the energy band structure of SnSex were analyzed. The enhanced SERS activity of 2D SnSex can be attribute to the coupling of the PICT resonance caused by the defect energy levels induced by Se vacancy and the molecular resonance Raman scattering (RRS). This established a relationship between the physical properties and SERS activity of 2D layered materials. The resonance probe molecule, rhodamine (R6G), which is used to detect the SERS performance of SnSex nanosheets. The enhancement factor (EF) of R6G on the optimized SnSe1.35 nanosheets can be as high as 2.6 × 106, with a detection limit of 10-10 M. The SERS result of the environmental pollution, thiram, shows that the SnSex nanosheets have a practical application in trace SERS detection, without the participation of metal particles. These results demonstrate that, through hybrid phase materials, the SERS sensitivity of 2D layered nanomaterials can be improved. It provides a kind of foreground non-metal SERS substrate in monitoring or detecting and provide a deep insight into the chemical SERS mechanism based on 2D layered materials.

Maternal high-salt diet during pregnancy impairs synaptic plasticity and memory in offspring.

Excess salt intake harms the brain health and cognitive functions, but whether a maternal high-salt diet (HSD) affects the brain development and neural plasticity of offspring remains unclear. Here, using a range of behavioral tests, we reported that the offspring of maternal HSD subjects exhibited short- and long-term memory deficits, especially in spatial memory in adulthood. Moreover, impairments in synaptic transmission and plasticity in the hippocampus were observed in adult offspring by using in vivo electrophysiology. Consistently, the number of astrocytes but not neurons in the hippocampus of the offspring from the HSD group were significantly decreased, and ERK and AKT signaling pathways involved in neurodevelopment were highly activated only during juvenile. In addition, the expression of synaptic proteins decreased both in juvenile and adulthood, and this effect might be involved in synaptic dysfunction. Collectively, these data demonstrated that the maternal HSD might cause adult offspring synaptic dysfunction and memory loss. It is possibly due to the reduction of astrocytes in juvenile.

SERS Sensing Using Graphene-Covered Silver Nanoparticles and Metamaterials for the Detection of Thiram in Soil.

Multilayer hyperbolic metamaterial (HMM)-based SERS substrates have received special consideration because they accommodate various propagation modes such as surface plasmonic polaritons (SPP). However, the SPP modes are difficult to generate in HMM due to their weak electric field enhancement. In this article, we designed novel SERS substrates consisting of graphene-covered AgNPs and HMM. The graphene-covered AgNPs work as an external coupling structure for hyperbolic metamaterials due to this structure exhibiting significant plasmonic effects as well as unique optical features. The localized surface plasmonic resonance (LSPR) of the graphene-covered AgNPs excited the SPP and thus formed a strong hot spot zone in the nanogap area of the graphene. The Raman experiment was performed using rhodamine 6G (R6G) and crystal violet (CV), which showed high stability and a maximum enhancement factor of 2.12 × 108. The COMSOL simulation further clarified that enhanced SERS performance was due to the presence of monolayer graphene and provided an atomically flat surface for organic molecules in a more controllable manner. Interestingly, the proposed SERS structure carries out quantitative detection of thiram in soil and can satisfy the basic environmental need for pesticide residue in the soil.

Rifaximin protects SH-SY5Y neuronal cells from iron overload-induced cytotoxicity via inhibiting STAT3/NF-κB signaling.

Acute or chronic liver disease-caused liver failure is the cause of hepatic encephalopathy (HE), characterized by neuropsychiatric manifestations. Liver diseases potentially lead to peripheral iron metabolism dysfunction and surges of iron concentration in the brain, contributing to the pathophysiological process of degenerative disorders of the central nervous system. In this study, the mechanism of rifaximin treating HE was investigated. Ferric ammonium citrate (FAC)-induced iron overload significantly reduced the proliferation and boosted the apoptosis in SH-SY5Y cells through increasing reactive oxygen species (ROS) levels and inducing iron metabolism disorder. Rifaximin treatment could rectify the FAC-induced iron overload and lipopolysaccharide (LPS)-induced iron deposition, therefore, effectively protecting SH-SY5Y cells from ROS-induced cell injury and apoptosis. Signal transducer and activator of transcription 3 (STAT3)/nuclear factor-kappa B (NF-κB) signaling is involved in the protective function of rifaximin against LPS-induced iron deposition. The therapeutic effect of rifaximin on HE associated with acute hepatic failure in mouse model was ascertained. In conclusion, Rifaximin could effectively protect SH-SY5Y cells against injury caused by iron overload through the rectification of the iron metabolism disorder via the STAT3/NF-κB signaling pathway.

A longitudinal study of cardiac structure and function using echocardiography in patients undergoing peritoneal dialysis.

BACKGROUND: Peritoneal dialysis (PD) can be associated with abnormal cardiac structure and function and increased mortality risk. Therefore, in this study, we analyzed the cardiac structure and function dynamic changes using echocardiography during the first 2 years of PD therapy. We also assessed its associations with all-cause mortality risk after 2 years of follow-up. METHODS: End-stage renal disease (ESRD) patients that have started PD from 2011 to 2017, and had echocardiography at baseline and years 1 and 2, were included in this study. Echocardiographic parameters were compared between baseline and year 2. Multivariable Cox models were used to estimate the association between echocardiographic parameters changes and all-cause mortality risk. RESULTS: We finally enrolled 72 PD patients in this study. The mean right ventricular diameter (RVD) increased from baseline (18.31 mm) to year 1 (18.75 mm) and year 2 (19.65 mm). We also observed a significant decrease in cardiac output (CO) between baseline and year 2. Additionally, a slight decrease trend in ejection fraction (EF) was observed. Finally, every 1 % increase in RVD was associated with a 68.2 % higher mortality risk after dialysis (HR, 1.682; 95 % CI, 1.017-2.783). CONCLUSIONS: Our results demonstrated a susceptibility for deteriorated right cardiac structure and function during the first 2 years of PD treatment. Also, higher all-cause mortality risk was observed after 2 years of PD. Altogether, these results highlighted the need for additional focus on regular echocardiographic examinations during long-term PD management. TRIAL REGISTRATION: The PD-CRISC cohort, registered with the Chinese Clinical Trial Registry ( ChiCTR1900023565 ).

gcMeta: a Global Catalogue of Metagenomics platform to support the archiving, standardization and analysis of microbiome data.

Meta-omics approaches have been increasingly used to study the structure and function of the microbial communities. A variety of large-scale collaborative projects are being conducted to encompass samples from diverse environments and habitats. This change has resulted in enormous demands for long-term data maintenance and capacity for data analysis. The Global Catalogue of Metagenomics (gcMeta) is a part of the 'Chinese Academy of Sciences Initiative of Microbiome (CAS-CMI)', which focuses on studying the human and environmental microbiome, establishing depositories of samples, strains and data, as well as promoting international collaboration. To accommodate and rationally organize massive datasets derived from several thousands of human and environmental microbiome samples, gcMeta features a database management system for archiving and publishing data in a standardized way. Another main feature is the integration of more than ninety web-based data analysis tools and workflows through a Docker platform which enables data analysis by using various operating systems. This platform has been rapidly expanding, and now hosts data from the CAS-CMI and a number of other ongoing research projects. In conclusion, this platform presents a powerful and user-friendly service to support worldwide collaborative efforts in the field of meta-omics research. This platform is freely accessible at https://gcmeta.wdcm.org/.

LncRNA DRAIC inhibits proliferation and metastasis of gastric cancer cells through interfering with NFRKB deubiquitination mediated by UCHL5.

BACKGROUND: Long non-coding RNA (lncRNA) as a widespread and pivotal epigenetic molecule participates in the occurrence and progression of malignant tumors. DRAIC, a kind of lncRNA whose coding gene location is on 15q23 chromatin, has been found to be weakly expressed in a variety of malignant tumors and acts as a suppressor, but its characteristics and role in gastric cancer (GC) remain to be elucidated. METHODS: Sixty-seven primary GC tissues and paired paracancerous normal tissues were collected. Bioinformatics is used to predict the interaction molecules of DRAIC. DRAIC and NFRKB were overexpressed or interfered exogenously in GC cells by lentivirus or transient transfection. Quantitative real-time PCR (qPCR) and western blotting were used to evaluate the expression of DRAIC, UCHL5 and NFRKB. The combinations of DRAIC and NFRKB or UCHL5 and NFRKB were verified by RNA-IP and Co-IP assays. Ubiquitination-IP and the treatment of MG132 and CHX were used to detect the ubiquitylation level of NFRKB. The CCK-8 and transwell invasion and migration assays measured the proliferation, migration and invasion of GC cells. RESULTS: DRAIC is down-regulated in GC tissues and cell lines while its potential interacting molecules UCHL5 and NFRKB are up-regulated, and DRAIC is positively correlated with NFRKB protein instead of mRNA. Lower DRAIC and higher UCHL5 and NFRKB indicated advanced progression of GC patients. DRAIC could increase NFRKB protein significantly instead of NFRKB mRNA and UCHL5, and bind to UCHL5. DRAIC combined with UCHL5 and attenuated binding of UCHL5 and NFRKB, meanwhile promoting the degradation of NFRKB via ubiquitination, and then inhibited the proliferation and metastasis of GC cells, which can be rescued by oeNFRKB. CONCLUSION: DRAIC suppresses GC proliferation and metastasis via interfering with the combination of UCHL5 and NFRKB and mediating ubiquitination degradation.

An analysis of the "Half-Perc" versus open surgical placement method for a peritoneal dialysis catheter: a non-inferiority cohort study.

BACKGROUND: Most end-stage renal disease (ESRD) patients undergo open surgical techniques for peritoneal dialysis (PD) catheter placement. An alternative method to PD catheter implantation is the half-percutaneous ("Half-Perc") technique based on a modified trocar that is performed by a nephrologist. The single-center, retrospective, observational, cohort study presented here aimed to compare the effects of the "Half-Perc" technique with the traditional open surgery on peritoneal catheter insertion. METHODS: From January 2015 to January 2018, 240 ESRD patients who received initial PD catheter placement were divided into two groups based on the "Half-Perc" technique or open surgery. All patients were followed up for 365 days or until loss of initial PD catheter or death. Prism 5 software was used to analyze baseline characteristics, operation-related parameters, mechanical complications and clinical outcomes. RESULTS: The "Half-Perc" technique showed shorter operation time, shorter incision length, lower postoperative pain scores and quick initiation of the PD program compared to the open surgery. After the 365-day follow-up, the "Half-Perc" group showed a higher rate of catheter dysfunction (4% versus 0.9%) that was corrected by conservative treatment in most patients and a lower rate of peritonitis (4% versus 9.6%) but mechanical complications and clinical outcomes did not differ between the two groups. There was also no significant difference based on overall patient mortality or catheter removal. One-year initial catheter survival and true catheter survival were not statistically different between the groups. CONCLUSION: The "Half-Perc" placement of the PD catheter using a modified metal trocar appears to be a non-inferior alternative method and carries minimal invasiveness and risk compared to open surgical placement.

Neural stem cell-derived factors inhibit the growth and invasion of U87 stem-like cells in vitro.

Glioma is one of the most common and aggressive tumors in the brain. Significant attention has been paid to the potential use of neural stem/progenitor cells (NSCs/NPCs) as delivery vehicles to cure gliomas. However, whether the NSCs/NPCs or the factors they produced could make a contribution still remains to be seen. In this study, we focused on the inhibitory effects of the factors produced by NSCs/NPCs on the biological behavior of the glioma stem-like cell in vitro. The human glioma cell line U87 was selected and the U87 stem-like cells were addressed. After being cultured in the NSC condition medium (NSC-CM), the viability and proliferation of U87 stem-like cells were significantly reduced. The invasion of U87 stem-like cells and the migration of U87 cells were also significantly decreased. However, no significant change was observed in regard to the astrocytic differentiation of U87 stem-like cells. These indicated that NSCs/NPCs produced some factors and had an inhibitory effect on the growth and invasion but not the terminal differentiation of U87 stem-like cells. It is worth paying attention to NSCs/NPCs as a high-potential candidate for glioma treatment.

miR-374a/Myc axis modulates iron overload-induced production of ROS and the activation of hepatic stellate cells via TGF-ß1 and IL-6.

The transformation of hepatic stellate cells (HSCs) to activated myofibroblasts plays a critical role in the progression of hepatic fibrosis, while iron-catalyzed production of free radical, including reaction and active oxygen (ROS), and activation and transformation of HSC into a myofibroblasts has been regarded as a major mechanism. In the present study, we attempted to investigate the mechanism of iron overload in hepatic fibrosis from the perspective of regulating HSC activation via oxidative stress and miR-374a/Myc axis. FAC stimulation significantly increased ROS production and TGF-ß1 and IL-6 release dose-dependently in hepatocytes. miR-374a could target Myc, a co-transcription factor of both TGF-ß1 and IL-6, to negatively regulate Myc expression; FAC stimulation significantly suppressed miR-374a expression, whereas the suppressive effect of FAC stimulation on miR-374a expression could be reversed by ROS inhibitor NAC, indicating that miR-374a could be modulated by iron overload-induced ROS. Via targeting Myc, miR-374a overexpression significantly reduced FAC-induced increases in TGF-ß1 and IL-6 levels within L02 cells, whereas the effects of miR-374a overexpression were significantly attenuated via Myc overexpression. Finally, miR-374a overexpression attenuated FAC-induced activity of HSCs by decreasing α-SMA and Collagen I levels whereas Myc overexpression enhanced FAC-induced activity of HSCs by increasing α-SMA and Collagen I levels; the effects of miR-374a overexpression could also be significantly reversed by Myc overexpression, indicating that miR-374a suppresses the activation of HSCs by inhibiting Myc to reduce FAC-induced increases in TGF-ß1 and IL-6 release. In conclusion, we demonstrate a novel mechanism of miR-374a/Myc axis modulating iron overload-induced production of ROS and the activation of HSCs via TGF-ß1 and IL-6.

[Research on the Construction of SPD Intelligent Logistics].

This paper introduced the workflow and use effect of SPD intelligent logistics supply chain management system in medical consumables management, analyzed the problems encountered in the process of hospital introduction of SPD management mode, and used PDCA principle to promote the hospital SPD before and after. using the PDCA principle to SPD before and after the introduction in such aspects as propaganda, information, system, safety management process continuously improve, in order to enhance the level of hospital consumables lean management and provide the reference for the introduction of the management system of hospital.

LncRNA Snhg12/IGFBP3 axis is involved in liver fibrosis by promoting the proliferation and activation of mouse hepatic stellate cells.

Liver fibrosis is a persistent damage repair response triggered by various injury factors, which leads to an abnormal accumulation of extracellular matrix within liver tissue samples. The current clinical treatment of liver fibrosis is currently ineffective; therefore, elucidating the mechanism of liver fibrogenesis is of significant importance. Herein, the function and related mechanisms of lncRNA Snhg12 within hepatic fibrosis were investigated. Snhg12 expression was shown to be increased in mouse hepatic fibrotic tissue samples, and Snhg12 knockdown suppressed hepatic pathological injury and down-regulated the expression levels of fibrosis-associated proteins. Mechanistically, Snhg12 played a role in the early activation of mouse hepatic stellate cells (mHSCs) based on bioinformatics analysis, and Snhg12 was positively correlated with Igfbp3 expression. Further experimental results demonstrated that Snhg12 knockdown impeded mHSCs proliferation and activation and also downregulated the protein expression of Igfbp3. Snhg12 could interact with IGFBP3 and boost its protein stability, and overexpression of Igfbp3 partially reversed the inhibition of mHSCsproliferation and activation by the knockdown of Snhg12. In conclusion, LncRNA Snhg12 mediates liver fibrosis by targeting IGFBP3 and promoting its protein stability, thereby promoting mHSC proliferation and activation. Snhg12 has been identified as an underlying target for treating liver fibrosis.

Microglia-Astrocyte Interaction in Neural Development and Neural Pathogenesis.

The interaction between microglia and astrocytes exhibits a relatively balanced state in order to maintain homeostasis in the healthy central nervous system (CNS). Disease stimuli alter microglia-astrocyte interaction patterns and elicit cell-type-specific responses, resulting in their contribution to various pathological processes. Here, we review the similarities and differences in the activation modes between microglia and astrocytes in various scenarios, encompassing different stages of neural development and a wide range of neural disorders. The aim is to provide a comprehensive understanding of their roles in neural development and regeneration and guiding new strategies for restoring CNS homeostasis.

A Protein Asteroid with PIN Domain in Silkworm Bombyx mori Is Involved in Anti-BmNPV Infection.

Nuclease is a type of protein that degrades nucleic acids, which plays an important role in biological processes, including RNA interference efficiency and antiviral immunity. However, no evidence of a link between nuclease and Bombyx mori nucleopolyhedrovirus (BmNPV) infection in silkworm B. mori has been found. In this study, a protein asteroid (BmAst) containing the PIN domain and XPG domain was identified in silkworm B. mori. BmAst gene was highest expressed in hemocytes and fat body of the 5th instar larvae, and high expression in the pupa stage. The transcriptional levels of the BmAst gene in 5th instar larvae were significantly induced by BmNPV or dsRNA. After knocking down BmAst gene expression by specific dsRNA, the proliferation of BmNPV in B. mori was increased significantly, whereas the survival rate of larvae was significantly lower when compared with the control. Our findings indicate that BmAst is involved in silkworm resistance to BmNPV infection.