Erratum: Addendum: Validation of the digital health literacy assessment among the university students in China.

[This corrects the article DOI: 10.3389/fpubh.2023.1294183.].

Soliton and dispersive wave generation with third-order dispersion and temporal boundary.

We investigate the pulse evolution and energy conservation condition at the temporal boundary under third-order dispersion. When the fundamental soliton crosses the temporal boundary and forms two reflected pulses and one transmitted pulse, the power of the transmitted pulse first increases and then decreases as the incident spectrum shifts toward the blue side. If the transmitted spectrum lies in the anomalous group-velocity dispersion region, second-order soliton is formed and dispersive wave is radiated. We present a modified phase-matching condition to predict the resonance frequencies. The predicted results are in good agreement with the results obtained by numerically solving the nonlinear Schrödinger equation.

TGR5-mediated lateral hypothalamus-dCA3-dorsolateral septum circuit regulates depressive-like behavior in male mice.

Although bile acids play a notable role in depression, the pathological significance of the bile acid TGR5 membrane-type receptor in this disorder remains elusive. Using depression models of chronic social defeat stress and chronic restraint stress in male mice, we found that TGR5 in the lateral hypothalamic area (LHA) predominantly decreased in GABAergic neurons, the excitability of which increased in depressive-like mice. Upregulation of TGR5 or inhibition of GABAergic excitability in LHA markedly alleviated depressive-like behavior, whereas down-regulation of TGR5 or enhancement of GABAergic excitability facilitated stress-induced depressive-like behavior. TGR5 also bidirectionally regulated excitability of LHA GABAergic neurons via extracellular regulated protein kinases-dependent Kv4.2 channels. Notably, LHA GABAergic neurons specifically innervated dorsal CA3 (dCA3) CaMKIIα neurons for mediation of depressive-like behavior. LHA GABAergic TGR5 exerted antidepressant-like effects by disinhibiting dCA3 CaMKIIα neurons projecting to the dorsolateral septum (DLS). These findings advance our understanding of TGR5 and the LHAGABA→dCA3CaMKIIα→DLSGABA circuit for the development of potential therapeutic strategies in depression.

Super-enhancer-driven LIF promotes the mesenchymal transition in glioblastoma by activating ITGB2 signaling feedback in microglia.

BACKGROUND: The mesenchymal (MES) subtype of glioblastoma (GBM) is believed to be influenced by both cancer cell-intrinsic alterations and extrinsic cellular interactions, yet the underlying mechanisms remain unexplored. METHODS: Identification of microglial heterogeneity by bioinformatics analysis. Transwell migration, invasion assays, and tumor models were used to determine gene function and the role of small molecule inhibitors. RNA sequencing, chromatin immunoprecipitation, and dual-luciferase reporter assays were performed to explore the underlying regulatory mechanisms. RESULTS: We identified the inflammatory microglial subtype of tumor-associated microglia (TAM) and found that its specific gene ITGB2 was highly expressed in TAM of MES GBM tissues. Mechanistically, the activation of ITGB2 in microglia promoted the interaction between the SH2 domain of STAT3 and the cytoplasmic domain of ITGB2, thereby stimulating the JAK1/STAT3/IL-6 signaling feedback to promote the MES transition of GBM cells. Additionally, microglia communicated with GBM cells through the interaction between the receptor ITGB2 on microglia and the ligand ICAM-1 on GBM cells, while an increased secretion of ICAM-1 was induced by the proinflammatory cytokine LIF. Further studies demonstrated that inhibition of CDK7 substantially reduced the recruitment of SNW1 to the super-enhancer of LIF, resulting in transcriptional inhibition of LIF. We identified notoginsenoside R1 as a novel LIF inhibitor that exhibited synergistic effects in combination with temozolomide. CONCLUSIONS: Our research reveals that the epigenetic-mediated interaction of GBM cells with TAM drives the MES transition of GBM and provides a novel therapeutic avenue for patients with MES GBM.

Acidification-Induced Micronano Mechanical Properties and Microscopic Permeability Enhancement Mechanism of Coal.

An acid solution improves the pore-plugging problem in hydraulic fracturing, which in turn improves the permeability of the coal seam. The study aimed to investigate the effect of mixed acid on the micronano mechanical properties and permeability of the coal seam. The surface morphology of acidified coal was analyzed from the micronano scale using atomic force microscopy (AFM) and scanning electron microscopy. Additionally, the micronano scale mechanical characteristics of acidified coal were examined using the mechanical mode in an atomic force microscope. Furthermore, the complexity and connectivity of the micronano pores of samples were investigated using the low-temperature nitrogen adsorption and mercury intrusion porosimetry methods and the fractal theory. The results indicated that the surface minerals of acidified coal were dissolved, loosening the coal and increasing the complexity of the pore structure. Mineral deformation and pore deformation weakened the mechanical properties of coal at the micronano scale, and the mean elastic modulus of acidified coal (B# and E#) decreased by 28.78 and 25.66% compared to that of raw coal. The acid solution effectively enlarged the pore diameter, transitioning from micropores to mesopores and macropores, and the total pore volume of acidified coal increased by 1.88 times and 1.25 times, Kn increased from 0.064 to 0.581 and 0.37, respectively. The type of methane diffusion in the diffusion pores changed from Knudsen diffusion to transition-type diffusion. The tortuosity of the pore structure of acidified coal decreased, the fractal dimension of the tortuosity of the pore structure decreased, and the permeability increased by nearly three times. The research results indicate that the mechanical properties of coal decrease after acidification and that the microstructural changes can promote methane migration (diffusion-seepage), which can provide theoretical guidance for coalbed methane extraction in low-permeability coal reservoirs.

Mice lacking Astn2 have ASD-like behaviors and altered cerebellar circuit properties.

Astrotactin 2 (ASTN2) is a transmembrane neuronal protein highly expressed in the cerebellum that functions in receptor trafficking and modulates cerebellar Purkinje cell (PC) synaptic activity. We recently reported a family with a paternally inherited intragenic ASTN2 duplication with a range of neurodevelopmental disorders, including autism spectrum disorder (ASD), learning difficulties, and speech and language delay. To provide a genetic model for the role of the cerebellum in ASD-related behaviors and study the role of ASTN2 in cerebellar circuit function, we generated global and PC-specific conditional Astn2 knockout (KO and cKO, respectively) mouse lines. Astn2 KO mice exhibit strong ASD-related behavioral phenotypes, including a marked decrease in separation-induced pup ultrasonic vocalization calls, hyperactivity and repetitive behaviors, altered social behaviors, and impaired cerebellar-dependent eyeblink conditioning. Hyperactivity and repetitive behaviors were also prominent in Astn2 cKO animals. By Golgi staining, Astn2 KO PCs have region-specific changes in dendritic spine density and filopodia numbers. Proteomic analysis of Astn2 KO cerebellum reveals a marked upregulation of ASTN2 family member, ASTN1, a neuron-glial adhesion protein. Immunohistochemistry and electron microscopy demonstrates a significant increase in Bergmann glia volume in the molecular layer of Astn2 KO animals. Electrophysiological experiments indicate a reduced frequency of spontaneous excitatory postsynaptic currents (EPSCs), as well as increased amplitudes of both spontaneous EPSCs and inhibitory postsynaptic currents (IPSCs) in the Astn2 KO animals, suggesting that pre- and postsynaptic components of synaptic transmission are altered. Thus, ASTN2 regulates ASD-like behaviors and cerebellar circuit properties.

Mesenchymal stem cells-derived extracellular vesicle-incorporated H19 attenuates cardiac remodeling in rats with heart failure.

Cardiac remodeling is manifested by hypertrophy and apoptosis of cardiomyocytes, resulting in the progression of cardiovascular diseases. Long noncoding RNAs (lncRNAs) serve as modifiers of cardiac remodeling. In this study, we aimed to explore the molecular mechanism of H19 shuttled by mesenchymal stem cells (MSC)-derived extracellular vesicles (EV) in cardiac remodeling upon heart failure (HF). Using the GEO database, H19, microRNA (miR)-29b-3p, and CDC42 were screened out as differentially expressed biomolecules in HF. H19 and CDC42 were elevated, and miR-29b-3p was decreased after MSC-EV treatment in rats subjected to ligation of the coronary artery. MSC-EV alleviated myocardial injury in rats with HF. H19 downregulation exacerbated myocardial injury, while miR-29b-3p inhibitor alleviated myocardial injury. By contrast, CDC42 downregulation aggravated the myocardial injury again. PI3K/AKT pathway was activated by MSC-EV. These findings provide insights into how H19 shuttled by EV mitigates cardiac remodeling through a competitive endogenous RNA network regarding miR-29b-3p and CDC42.

Prognostic impact of absolute peripheral blood NK cell count after four cycles of R-CHOP-like regimen treatment in patients with diffuse large B cell lymphoma.

As a subtype of lymphocyte, natural killer (NK) cell is the first line of defense that shows a strong function in tumor immunotherapy response and clinical outcomes. The current study aims to investigate the prognostic influence of peripheral blood absolute NK cell count after four cycles of rituximab combined with cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) treatment (NKCC4) in diffuse large B cell lymphoma (DLBCL) patients. A total of 261 DLBCL patients treated with R-CHOP from January 2018 to September 2022 were enrolled. The low NKCC4 was observed in patients who died during the study period compared with survival individuals. A NKCC4 < 135 cells/µl had a remarkable negative influence in overall survival and progression-free survival (PFS) compared to a NKCC4 ≥ 135 cells/µl (p < 0.0001 and p < 0.0004, respectively). In addition, the OS and PFS were synergistically lower in a NKCC4 < 135 cells/µl group among DLBCL patients with GCB type or high IPI. In conclusion, this study indicates NCKK4 as a valuable marker in clinical practice and provides an insight for combination treatment of R-CHOP to improve outcomes of DLBCL patients.

Advances in neural circuits of innate fear defense behavior. / å ˆå¤©æ€§ææƒ§é˜²å¾¡è¡Œä¸ºçš„ç¥žç»å›žè·¯ç ”ç©¶è¿›å±•.

Fear, a negative emotion triggered by dangerous stimuli, can lead to psychiatric disorders such as phobias, anxiety disorders, and depression. Investigating the neural circuitry underlying congenital fear can offer insights into the pathophysiological mechanisms of related psychiatric conditions. Research on innate fear primarily centers on the response mechanisms to various sensory signals, including olfactory, visual and auditory stimuli. Different types of fear signal inputs are regulated by distinct neural circuits. The neural circuits of the main and accessory olfactory systems receive and process olfactory stimuli, mediating defensive responses like freezing. Escape behaviors elicited by visual stimuli are primarily regulated through the superior colliculus and hypothalamic projection circuits. Auditory stimuli-induced responses, including escape, are mainly mediated through auditory cortex projection circuits. In this article, we review the research progress on neural circuits of innate fear defensive behaviors in animals. We further discuss the different sensory systems, especially the projection circuits of olfactory, visual and auditory systems, to provide references for the mechanistic study of related mental disorders.

Inhibitory effects of hinokitiol on the development and pathogenicity of Colletotrichum gloeosporioides.

Postharvest anthracnose of mango fruit caused by Colletotrichum gloeosporioides is a devastating fungal disease, which causes tremendous quality deterioration and economic losses. Hinokitiol, an environmentally friendly natural compound, is effective in controlling a variety of postharvest fungal diseases. However, there is still a lack of research on the inhibitory effect of hinokitiol on C. gloeosporioides and its possible modes of action. In the present study, the activity of hinokitiol against C. gloeosporioides and its potential mechanisms involved have been investigated. We found that hinokitiol treatment could effectively inhibit the virulence of C. gloeosporioides to harvested mango fruit. After treatment with 8 mg/L hinokitiol, the mycelial growth of C. gloeosporioides was completely inhibited. When the concentration of hinokitiol reached 9 mg/L, the spore germination rate of C. gloeosporioides decreased to 2.43% after 9 h of cultivation. The inhibitory effect is mainly due to the attenuation in cell viability, and impairment in plasma membrane followed by leakage of cytoplasmic contents such as nucleic acids, proteins, and soluble carbohydrates, which ultimately leads to the destruction of cell structure. Furthermore, hinokitiol suppressed the expression of pathogenicity-related genes, leading to reduced infection activity. Collectively, these results suggest that hinokitiol may be an excellent bio-fungicides for the management of mango anthracnose.

1D Chiral Enantiomer Lead-Free Perovskites Induced Chiralopical Activity and Photoelectric Response.

Chirality is a fascinating geometrical concept with widespread applications in biology, chemistry, and materials. Incorporating chirality into hybrid perovskite materials can induce novel physical properties (chiral optical activity, nonlinear optics, etc.). Hybrid lead-free or lead-substituted perovskite materials, as representatives of perovskites, have been widely used in fields such as photovoltaics, sensors, catalysis, and detectors. However, the successful introduction of chirality into hybrid lead-free perovskites, which can enable their potential applications in areas such as circularly polarized light photodetectors, memories, and spin transistors, remains a challenging research topic. Here, we synthesized two new chiral lead-free perovskites, [(R)-2-methylpiperazine][BiI5] and [(S)-2-methylpiperazine][BiI5]. The material possesses a perovskite structure with a one-dimensional (1D) arrangement, denoted as ABX5. This structure is composed of chiral cations, specifically methylpiperazine, and endless chains of [BiI3] along the a-axis. These chains are assembled from distorted coplanar [BiI5]2- octahedra. The testing results revealed that (R)-1 and (S)-1 have narrow band gaps (Eg-R = 2.016 eV, Eg-S = 1.964 eV), high photoelectric response, and long carrier lifetime [R = 4.94 µs (τ), S = 7.85 µs (τ)]. It is worth noting that 1D chiral lead-free perovskites (R)-1 and (S)-1, which are synthesized in this study with narrow band gaps, high photoelectric response, and long carrier lifetime, have the potential to serve as alternative materials for the perovskite layer in future iterations of lead-free perovskite solar cells. Moreover, this research will inspire the preparation of multifunctional, lead-free perovskites.

Antifungal activity of star anise extract against Penicillium roqueforti and Aspergillus niger for bread shelf life.

Because star anise is underutilized in the baking sector and the antifungal targets are unclear, this study aimed to investigate the antifungal effect and mechanism of star anise extract (SAE) on spoilage fungi in bread. SAE was prepared by ethanol extraction and 31 substances were identified by GC-MS, among which trans-anethole (62.62%), estragole (7.82%) and linalool (4.66%) were the major components. The antifungal activity of SAE and the three main components against Penicillium roqueforti and Aspergillus niger were determined by using the Oxford cup method and the sesqui-dilution method. The inhibition zones were 9.88 mm and 15.09 mm, while the minimum inhibitory concentrations were 125.00 µL/mL and 31.25 µL/mL. Trans-anethole and estragole both showed antifungal activity against Penicillium roqueforti and Aspergillus niger, while linalool only showed antifungal activity against Aspergillus niger. Propidium iodide and fluorescein diacetate staining analysis, leakage of cellular components (nucleic acids and proteins) and rise in ergosterol content indicated that SAE disrupted the integrity and permeability of the cell membrane. Malondialdehyde was increased after SAE treatment, indicating that SAE caused lipid peroxidation in the cell membrane, further confirming that it disrupted the cell membrane. At the same time, SAE interacted with membrane proteins and altered their conformation, resulting in cell membrane dysfunction. Finally, the shelf life test showed that SAE extended the shelf life of the bread by up to 6 days. In general, this study highlights the antifungal effect of SAE against Penicillium roqueforti and Aspergillus niger, which indicated that SAE can be used as an antifungal agent to extend the shelf life of bread.

Influences of Evolution of Pore Structures in Tectonic Coal under Acidization on Methane Desorption.

Experiments on corrosion reactions of pulverized coal with monomeric and polymeric (mixed) acid solutions reveal that monomeric acids are listed in a descending order as HF, HCl, and CH3COOH according to their corrosion effects on tectonic coal collected in Faer Coal Mine (Liupanshui City, Guizhou Province, China). In addition, the optimal mixing ratio of mixed acids is 6% HCl + 6% HF + 3% CH3COOH + 2% KCl. The mineral grains filled in pores in coal samples treated with mixed acid solutions are dissolved, so the porosity increases. The volumes of transition pores and mesopores are obviously affected by acidization, and some transition pores are transformed into mesopores and macropores to form dissolved pores. At the same time, inkbottle-shaped pores reduce, while slit pores or open pores increase. The coal samples after acidization show a higher aromatization degree and an increased relative content of oxygen-containing functional groups, with a generally lower hydroxyl content, so the methane (CH4) adsorption capacity of coal declines, which promotes CH4 desorption. The control effect of pore structures after acidization reactions on CH4 desorption was revealed from perspectives of the diffusion coefficient (Kn), adsorption volume (ω), average pore-throat ratio (PT), and average sinuosity (τav). That is, CH4 molecules in tectonic coal after acidization turn from Knudsen diffusion to transitional diffusion, the adsorption volume of CH4 molecules shrinks, the average pore-throat ratio decreases, and the average sinuosity reduces, which promotes CH4 desorption from tectonic coal.

Piper nigrum Extract Inhibits the Growth of Human Colorectal Cancer HT-29 Cells by Inducing p53-Mediated Apoptosis.

Colorectal cancer (CRC) is a prevalent malignancy of the digestive tract with the second highest mortality rate globally. Piper nigrum is a widely used traditional medicinal plant, exhibiting antitumor activity against various tumor cells. At present, research on the effect of Piper nigrum on CRC is limited to in vitro cytotoxicity, lacking comprehensive mechanism investigations. This study aimed to explore the inhibitory effect and mechanism of Piper nigrum extract (PNE) on HT-29 cells. Firstly, we identified the chemical components of PNE. Then, MTT assay, colony formation assay, JC-1 staining, and flow cytometry were used to analyze the effect of PNE on HT-29 cells in vitro. A xenograft model, histopathological examination, immunohistochemistry, and western blot were used to evaluate the tumor growth inhibitory activity and mechanism of PNE in vivo. The results indicated that PNE could inhibit cell proliferation and colony formation, reduce mitochondrial membrane potential, induce cell apoptosis in vitro, and inhibit tumor growth in vivo. Furthermore, PNE could regulate p53 and its downstream proteins, and subsequently activate the caspase-3 pathway. In summary, PNE probably induced apoptosis of HT-29 cells through the mitochondrial pathway mediated by p53. All these results suggested that PNE might be a potential natural-origin anti-CRC drug candidate.

Neurodevelopmental risk and adaptation as a model for comorbidity among internalizing and externalizing disorders: genomics and cell-specific expression enriched morphometric study.

BACKGROUND: Comorbidity is the rule rather than the exception for childhood and adolescent onset mental disorders, but we cannot predict its occurrence and do not know the neural mechanisms underlying comorbidity. We investigate if the effects of comorbid internalizing and externalizing disorders on anatomical differences represent a simple aggregate of the effects on each disorder and if these comorbidity-associated cortical surface differences relate to a distinct genetic underpinning. METHODS: We studied the cortical surface area (SA) and thickness (CT) of 11,878 preadolescents (9-10 years) from the Adolescent Brain and Cognitive Development Study. Linear mixed models were implemented in comparative and association analyses among internalizing (dysthymia, major depressive disorder, disruptive mood dysregulation disorder, agoraphobia, panic disorder, specific phobia, separation anxiety disorder, social anxiety disorder, generalized anxiety disorder, post-traumatic stress disorder), externalizing (attention-deficit/hyperactivity disorder, oppositional defiant disorder, conduct disorder) diagnostic groups, a group with comorbidity of the two and a healthy control group. Genome-wide association analysis (GWAS) and cell type specificity analysis were performed on 4468 unrelated European participants from this cohort. RESULTS: Smaller cortical surface area but higher thickness was noted across patient groups when compared to controls. Children with comorbid internalizing and externalizing disorders had more pronounced areal reduction than those without comorbidity, indicating an additive burden. In contrast, cortical thickness had a non-linear effect with comorbidity: the comorbid group had no significant CT differences, while those patient groups without comorbidity had significantly higher thickness compare to healthy controls. Distinct biological pathways were implicated in regional SA and CT differences. Specifically, CT differences were associated with immune-related processes implicating astrocytes and oligodendrocytes, while SA-related differences related mainly to inhibitory neurons. CONCLUSION: The emergence of comorbidity across distinct clusters of psychopathology is unlikely to be due to a simple additive neurobiological effect alone. Distinct developmental risk moderated by immune-related adaptation processes, with unique genetic and cell-specific factors, may contribute to underlying SA and CT differences. Children with the highest risk but lowest resilience, both captured in their developmental morphometry, may develop a comorbid illness pattern.

The small peptide VISP1 acts as a selective autophagy receptor regulating plant-virus interactions.

Selective macroautophagy/autophagy is tightly regulated by cargo receptors that recruit specific substrates to the ATG8-family proteins for autophagic degradation. Therefore, identification of selective receptors and their new cargoes will improve our understanding of selective autophagy functions in plant development and stress responses. We have recently demonstrated that the small peptide VISP1 acts as a selective autophagy receptor to mediate degradation of suppressors of RNA silencing (VSRs) of several RNA and DNA viruses. Moreover, VISP1 induces symptom recovery through fine-tuning the balance of plant immunity and virus pathogenicity. Our findings provide new insights into the double-edged sword roles of selective autophagy in plant-virus interactions.

The Effects and Mechanisms of PBM Therapy in Accelerating Orthodontic Tooth Movement.

Malocclusion is one of the three major diseases, the incidence of which could reach 56% of the imperiled oral and systemic health in the world today. Orthodontics is still the primary method to solve the problem. However, it is clear that many orthodontic complications are associated with courses of long-term therapy. Photobiomodulation (PBM) therapy could be used as a popular way to shorten the course of orthodontic treatment by nearly 26% to 40%. In this review, the efficacy in cells and animals, mechanisms, relevant cytokines and signaling, clinical trials and applications, and the future developments of PBM therapy in orthodontics were evaluated to demonstrate its validity. Simultaneously, based on orthodontic mechanisms and present findings, the mechanisms of acceleration of orthodontic tooth movement (OTM) caused by PBM therapy were explored in relation to four aspects, including blood vessels, inflammatory response, collagen and fibers, and mineralized tissues. Also, the cooperative effects and clinical translation of PBM therapy in orthodontics have been explored in a growing numbers of studies. Up to now, PBM therapy has been gaining popularity for its non-invasive nature, easy operation, and painless procedures. However, the validity and exact mechanism of PBM therapy as an adjuvant treatment in orthodontics have not been fully elucidated. Therefore, this review summarizes the efficacy of PBM therapy on the acceleration of OTM comprehensively from various aspects and was designed to provide an evidence-based platform for the research and development of light-related orthodontic tooth movement acceleration devices.

NPFR regulates the synthesis and metabolism of lipids and glycogen via AMPK: Novel targets for efficient corn borer management.

RNA biopesticides are regarded as "the third revolution in the history of pesticides" due to their extensive advantages such as precision, high efficiency, green, pollution-free, etc. In the current study, two target genes encoding neuropeptide F receptor (NPFR) and AMP-activated protein kinase (AMPK), which are essential for insect feeding, cellular energy homeostasis and nutrient availability, were selected to design RNA pesticides. We achieved high RNA interference (RNAi) efficiency of npfr via a star polycation nanocarrier-based double-stranded RNA (dsRNA) delivery system. The food consumption of Ostrinia furnacalis is largely suppressed, which leads to a good protective effect on corn leaves. We determined the mechanism of the above genes. NPFR binds to the Gα protein and activates the intracellular second messengers cAMP and Ca2+, which in turn phosphorylate AMPK to regulate the synthesis and metabolism of lipids and glycogen. We then adopted a highly efficient bacteria-based expression system for the production of large amounts of dsRNA segments targeting npfr and ampk simultaneously and subsequently complexed them with nanocarriers to develop a novel dual-target RNA pesticide. Our RNA nanopesticide dramatically inhibits larval feeding, growth and development, and its controlling effect is even better than that of the widely used anti-feedant azadirachtin.