Enhancing solid-phase extraction of tetracyclines with a hybrid biochar sorbent: A comparative study of chlorella and bamboo biochars.

Biochar, a sustainable sorbent derived from pyrolyzed biomass, has garnered attention for its efficacy in solid-phase extraction (SPE) of antibiotics, with a particular focus on tetracyclines (TCs). Despite its recognized potential, the intricate separation mechanisms operative in biochar-based SPE systems have not been fully deciphered. This investigation contrasts chlorella biochar against commercial bamboo biochar, harnessing an array of analytical methodologies-microstructure characterization, adsorption thermodynamics, competitive adsorption kinetics, H+ back titration, and selectivity adsorption studies-complemented by a Box-Behnken design for the optimization of chlorella/bamboo-SPE and subsequent application in the analysis of animal-derived foodstuffs. The study unveils that a hybrid sorbent, integrating nitrogen-doped microporous chlorella biochar with mesoporous bamboo biochar in a 95/5 mass ratio, markedly diminishes irreversible adsorption while enhancing selectivity, surpassing the performance of single biochar SPE systems. The elucidated separation mechanisms implicate a partition model, propelled by oxygen-rich functional groups on chlorella biochar and the rapid adsorption kinetics of bamboo biochar, all orchestrated by electrostatic interactions within the mixed biochar framework. Moreover, the synergy of mixed biochar-SPE with high-performance liquid chromatography (HPLC) demonstrates exceptional proficiency in detecting TCs in animal viscera, evidenced by recovery rates spanning 80.80 % to 106.98 % and RSDs ranging from 0.24 % to 14.69 %. In essence, this research not only sheds light on the multifaceted factors influencing SPE efficiency but also propels the use of biochar towards new horizons in environmental monitoring and food safety assurance.

Neural Correlates of Early-Life Urbanization and Their Spatial Relationships with Gene Expression, Neurotransmitter, and Behavioral Domain Atlases.

Previous neuroimaging research has established associations between urban exposure during early life and alterations in brain function and structure. However, the molecular mechanisms and behavioral relevance of these associations remain largely unknown. Here, we aimed to address this question using a combined analysis of multimodal data. Initially, we calculated amplitude of low-frequency fluctuations (ALFF) and gray matter volume (GMV) using resting-state functional and structural MRI to investigate their associations with early-life urbanization in a large sample of 511 healthy young adults. Then, we examined the spatial relationships of the identified neural correlates of early-life urbanization with gene expression, neurotransmitter, and behavioral domain atlases. Results showed that higher early-life urbanization scores were correlated with increased ALFF of the right fusiform gyrus and decreased GMV of the left dorsal medial prefrontal cortex and left precuneus. Remarkably, the identified neural correlates of early-life urbanization were spatially correlated with expression of gene categories primarily involving immune system process, signal transduction, and cellular metabolic process. Concurrently, there were significant associations between the neural correlates and specific neurotransmitter systems including dopamine, acetylcholine, and serotonin. Finally, we found that the ALFF correlates were associated with behavioral terms including "perception," "sensory," "cognitive control," and "reasoning." Apart from expanding existing knowledge of early-life urban environmental risk for mental disorders and health in general, our findings may contribute to an emerging framework for integrating social science, neuroscience, genetics, and public policy to respond to the major health challenge of world urbanization.

Brain Structural and Functional Damage Network Localization of Suicide.

BACKGROUND: Extensive neuroimaging research on brain structural and functional correlates of suicide has produced inconsistent results. Despite increasing recognition that damage in multiple different brain locations that causes the same symptom can map to a common brain network, there is still a paucity of research investigating network localization of suicide. METHODS: To clarify this issue, we initially identified brain structural and functional damage locations in relation to suicide from 63 published studies with 2135 suicidal and 2606 nonsuicidal individuals. By applying novel functional connectivity network mapping to large-scale discovery and validation resting-state functional magnetic resonance imaging datasets, we mapped these affected brain locations to 3 suicide brain damage networks corresponding to different imaging modalities. RESULTS: The suicide gray matter volume damage network comprised widely distributed brain areas primarily involving the dorsal default mode, basal ganglia, and anterior salience networks. The suicide task-induced activation damage network was similar to but less extensive than the gray matter volume damage network, predominantly implicating the same canonical networks. The suicide resting-state activity damage network manifested as a localized set of brain regions encompassing the orbitofrontal cortex and middle cingulate cortex. CONCLUSIONS: Our findings not only may help reconcile prior heterogeneous neuroimaging results, but also may provide insights into the neurobiological mechanisms of suicide from a network perspective, which may ultimately inform more targeted and effective strategies to prevent suicide.

Neurexins control the strength and precise timing of glycinergic inhibition in the auditory brainstem.

Neurexins play diverse functions as presynaptic organizers in various glutamatergic and GABAergic synapses. However, it remains unknown whether and how neurexins are involved in shaping functional properties of the glycinergic synapses, which mediate prominent inhibition in the brainstem and spinal cord. To address these issues, we examined the role of neurexins in a model glycinergic synapse between the principal neuron in the medial nucleus of the trapezoid body (MNTB) and the principal neuron in the lateral superior olive (LSO) in the auditory brainstem. Combining RNAscope with stereotactic injection of AAV-Cre in the MNTB of neurexin1/2/3 conditional triple knockout mice, we showed that MNTB neurons highly express all isoforms of neurexins although their expression levels vary remarkably. Selective ablation of all neurexins in MNTB neurons not only reduced the amplitude but also altered the kinetics of the glycinergic synaptic transmission at LSO neurons. The synaptic dysfunctions primarily resulted from an impaired Ca2+ sensitivity of release and a loosened coupling between voltage-gated Ca2+ channels and synaptic vesicles. Together, our current findings demonstrate that neurexins are essential in controlling the strength and temporal precision of the glycinergic synapse, which therefore corroborates the role of neurexins as key presynaptic organizers in all major types of fast chemical synapses.

Metabolomics and lipidomics combined with serum pharmacochemistry uncover the potential mechanism of Huang-Lian-Jie-Du decoction alleviates atherosclerosis in ApoE-/- mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Atherosclerosis (AS) is one of the main cardiovascular diseases (CVDs) leading to an increase in global mortality, and its key pathological features are lipid accumulation and oxidative stress. Huang-Lian-Jie-Du decoction (HLJDD), a representative formula for clearing heat and detoxifying, has been shown to reduce aortic lipid plaque and improve AS. However, multiple components and multiple targets of HLJDD pose a challenge in comprehending its comprehensive mechanism in the treatment of AS. AIM OF THE STUDY: This study was designed to illustrate the anti-AS mechanisms of HLJDD in an apolipoprotein E-deficient (ApoE-/-) mouse model from a metabolic perspective. MATERIALS AND METHODS: ApoE-/- mice were kept on a high-fat diet (HFD) to induce AS. Serum total cholesterol (TC), total triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels were determined to evaluate the influence of HLJDD on dyslipidemia. Oil red O was used to stain mouse aortic lipid plaques, and hematoxylin and eosin (HE) staining was used to assess the pathological changes in the aortic roots. Metabolomics and lipidomics combined with serum pharmacochemistry were performed to research the HLJDD mechanism of alleviating AS. RESULTS: In this study, HLJDD treatment improved serum biochemical levels and histopathological conditions in AS mice. A total of 6 metabolic pathways (arginine biosynthesis, glycerophospholipid, sphingolipid, arachidonic acid, linoleic acid, and glycerolipid metabolism) related to 25 metabolic biomarkers and 41 lipid biomarkers were clarified, and 22 prototype components migrating to blood were identified after oral administration of HLJDD. CONCLUSION: HLJDD improved AS induced by HFD in ApoE-/- mice. The effects of HLJDD were mainly attributed to regulating lipid metabolism by regulating the metabolic pathways of glycerophospholipids, sphingolipids, arachidonic acid, linoleic acid, and glycerolipids and reducing the levels of oxidative stress by upregulating arginine biosynthesis.

Investigating the anti-atherosclerotic effects and potential mechanism of Dalbergia odorifera in ApoE-deficient mice using network pharmacology combined with metabolomics.

Dalbergia odorifera (DO) is a precious rosewood species in Southern Asia, and its heartwood is used in China as an official plant for invigorating blood circulation and eliminating stasis. This study aims to evaluate the efficacy of DO on atherosclerosis (AS), and further explore its active components and potential mechanisms. The apolipoprotein-E (ApoE)-deficient mice fed a high-fat diet were used as model animals, and the pathological changes in mice with or without DO treatment were compared to evaluate the pharmacodynamics of DO on AS. The mechanisms were preliminarily expounded by combining with metabolomics and network pharmacology. Moreover, the bioactive components and targets were assessed by cell experiments and molecular docking, respectively. Our findings suggested that DO significantly modulated blood lipid levels and alleviated intimal hyperplasia in atherosclerotic-lesioned mice, and the mechanisms may involve the regulation of 18 metabolites that changed during the progression of AS, thus affecting 3 major metabolic pathways and 3 major signaling pathways. Moreover, the interactions between 16 compounds with anti-proliferative effect and hub targets in the 3 signaling pathways were verified using molecular docking. Collectively, our findings preliminarily support the therapeutic effect of DO in atherosclerosis, meanwhile explore the active constituents and potential pharmacological mechanisms, which is conducive to its reasonable exploitation and utilization.