Search Results (205)

Carbon (C) sequestration and nitrogen (N) and phosphorus (P) accumulation in urban forest green spaces are significant for global climate regulation and alleviating nutrient pollution. However, the effects of management and conservation practices across different urban forest vegetation types on soil C, N, and P contents and stoichiometric ratios remain largely unexplored. We selected forest soils from Guangzhou, a major Metropolis in China, as our study area. Soil samples were collected from two urban secondary forests that naturally regenerated after disturbance (108 samples) and six urban forest parks primarily composed of artificially planted woody plant communities (72 samples). We employed mixed linear models and variance partitioning to analyze and compare soil C, N, and P contents and their stoichiometry and its main driving factors beneath suburban forests and urban park vegetation. These results exhibited that soil pH and bulk density in urban parks were higher than those in suburban forests, whereas soil water content, maximum storage capacity, and capillary porosity were higher in urban forests than in urban parks. Soil C, N, and P contents and their stoichiometry (except for N:P ratio) were significantly higher in suburban forests than in urban parks. Multiple analyzes showed that soil pH had the most pronounced negative influence on soil C, N, C:N, C:P, and N:P, but the strongest positive influence on soil P in urban parks. Soil water content had the strongest positive effect on soil C, N, P, C:N, and C:P, while soil N:P was primarily influenced by the positive effect of soil non-capillary porosity in suburban forests. Overall, our study emphasizes that suburban forests outperform urban parks in terms of carbon and nutrient accumulation, and urban green space management should focus particularly on the impact of soil pH and moisture content on soil C, N, and P contents and their stoichiometry. Full article

Background: Lower phylogenetic species are known to rebuild cut-off caudal parts with regeneration of the central nervous system (CNS). In contrast, CNS regeneration in higher vertebrates is often attributed to immaturity, although this has never been conclusively demonstrated. The emergence of stem cells and their effective medical applications has intensified research into spinal cord regeneration. However, despite these advances, the impact of clinical trials involving spinal cord-injured (SCI) patients remains disappointingly low. Long-distance regeneration has yet to be proven. Methods: Our study involved a microsurgical dorsal myelotomy in fetal rats. The development of pioneering long primary afferent axons during early gestation was examined long after birth. Results: A single cut triggered the intrinsic ability of the dorsal root ganglion (DRG) neurons to reprogram. Susceptibility to hypoxia caused the axons to stop developing. However, the residual axonal outgrowth sheds light on the intriguing temporal and spatial events that reveal long-distance CNS regeneration. The altered phenotypes displayed axons of varying lengths and different features, which remained visible throughout life. The previously designed developmental blueprint was crucial for interpreting these enigmatic features. Conclusions: This research into immaturity enabled the exploration of the previously impenetrable domain of early life and the identification of a potential missing link in CNS regeneration research. Central axon regeneration appeared to occur much faster than is generally believed. The paradigm provides a challenging approach for exhaustive intrauterine reprogramming. When the results demonstrate pre-clinical effectiveness in CNS regeneration research, the transformational impact may ultimately lead to improved outcomes for patients with spinal cord injuries. Full article

Extracellular vesicles (EVs) are bilayer lipid membrane particles that are released by every cell type. These secretions are further classified as exosomes, ectosomes, and microvesicles. They contain biomolecules (RNAs, proteins, metabolites, and lipids) with the ability to modulate various biological processes and have been shown to play a role in intercellular communication and cellular rejuvenation. Various studies suggest exosomes and/or microvesicles as a potential platform for drug delivery. EVs may deliver lipids and nucleotides directly to an injury site in an axon, promoting growth cone stabilization and membrane expansion as well as repair, thus positively modulating adult axon regeneration. In this review, we will provide a perspective on the metabolite composition of EVs in adult axonal regeneration relevant to the central nervous system (CNS), specifically that pertaining to the optic nerve. We will present an overview of the methods for isolation, enrichment, omics data analysis and quantification of extracellular vesicles with the goal of providing direction for future studies relevant to axon regeneration. We will also include current resources for multi-omics data integration relevant to extracellular vesicles from diverse cell types. Full article

Traumatic injuries to the peripheral (PNS) and central nervous systems (CNS) trigger distinct regenerative responses, with the PNS displaying limited regenerative capacity and the CNS remaining largely refractory. Recent research highlights the role of epigenetic modifications, particularly histone acetylation, in modulating the gene expression programs that drive axonal regeneration. This review synthesizes current findings on post-translational histone modifications, focusing on histone acetyltransferases (HATs), histone deacetylases (HDACs), and epigenetic readers, in addition to their impact on neuronal and non-neuronal cells following injury. While HATs like p300/CBP and PCAF promote the expression of regeneration-associated genes, HDAC inhibition has been shown to facilitate neurite outgrowth, neuroprotection, and functional recovery in both PNS and CNS models. However, HDAC3, HDAC5, and HDAC6 demonstrate context- and cell-type-specific roles in both promoting and limiting regenerative processes. The review also highlights cell-specific findings that have been scarcely covered in the previous literature. Thus, the immunomodulatory roles of epigenetic regulators in microglia and macrophages, their involvement in remyelination via Schwann cells and oligodendrocytes, and their impact on astrocyte function are within the scope of this review. Closely considering cell-context specificity is critical, as some targets can exert opposite effects depending on the cell type involved. This represents a major challenge for current pharmacological therapies, which often lack precision. This complexity underscores the need to develop strategies that allow for cell-specific delivery or target regulators with converging beneficial effects across cell types. Such approaches may enhance regenerative outcomes after CNS or PNS injury. Full article

The central nervous system (CNS) is highly susceptible to damage due to its limited ability to regenerate. Injuries to the CNS, whether from trauma, ischemia, or neurodegenerative diseases, disrupt both cellular and vascular structures, leading to immediate (primary) and subsequent (secondary) damage. Primary damage involves the physical disruption of cells and blood vessels, weakening the blood–brain barrier (BBB) and triggering excitotoxicity and calcium overload. Secondary damage develops over hours to days and is marked by ionic imbalance, mitochondrial dysfunction, oxidative stress, and chronic inflammation, which further aggravates tissue damage. Inflammation plays a dual role: acute inflammation helps in repair, while chronic inflammation accelerates neurodegeneration. Microglia and astrocytes play key roles in this inflammatory response, with M1-like microglia promoting pro-inflammatory responses and M2-like microglia supporting anti-inflammatory and repair processes. Neurodegenerative diseases are characterized by the accumulation of misfolded proteins such as Tau, amyloid-beta, TDP-43, and α-synuclein, which impair cellular function and lead to neuronal loss. Neurodegenerative diseases are characterized by the accumulation of misfolded proteins and influenced by genetic risk factors (e.g., APOE4, TARDBP). Despite the CNS’s limited regenerative abilities, processes like synaptogenesis, neurogenesis, axonal regeneration, and remyelination offer potential for recovery. Therapeutic approaches aim to target inflammatory pathways, enhance repair mechanisms, and develop neuroprotective treatments to counter excitotoxicity, oxidative stress, and apoptosis. Advances in stem cell therapy, gene therapy, and personalized medicine hold promise for improving outcomes. Future research should focus on combining strategies, utilizing advanced technologies, and conducting translational studies to bridge the gap between preclinical research and clinical application. By better understanding and leveraging the complex processes of CNS injury and repair, researchers hope to develop effective therapies to restore function and enhance the quality of life for individuals with CNS disorders. Full article

Demyelination in the central nervous system (CNS) disrupts neuronal communication and promotes neurodegeneration. Despite the widespread use of cuprizone-induced demyelination models to study myelin injury and repair, the mechanisms underlying oligodendrocyte apoptosis and regeneration are poorly understood. This study investigated the dynamic cellular and molecular changes that occur during demyelination and remyelination, with a focus on glial cell responses, blood-brain barrier (BBB) integrity, and neuroimmune interactions. C57BL/6J mice exposed to cuprizone exhibited weight loss, sensorimotor deficits, and cognitive decline, which were reversed during remyelination. Histological and immunofluorescence analyses revealed reduced myelin protein levels, including myelin basic protein (MBP) and myelin-associated glycoprotein (MAG), and decreased oligodendrocyte populations during demyelination, with recovery during repair. The BBB permeability increases during demyelination, is associated with the decreased expression of tight junction proteins (ZO-1, Occludin), and normalizes during remyelination. Single-cell RNA sequencing revealed dynamic shifts in glial cell populations and upregulated Psap-Gpr37l1 signaling. Neuroimmune activation and oxidative stress peak during demyelination, characterized by elevated ROS, MDA, and immune cell infiltration, followed by recovery. Transcriptomic profiling revealed key inflammatory pathways (JAK-STAT, NF-κB) and hub genes associated with demyelination and repair. These findings provide insights into myelin repair mechanisms and highlight potential therapeutic targets for treating demyelinating diseases. Full article

In the adult central nervous system (CNS), myelin regeneration primarily occurs through the differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes. In men, declining testosterone levels accelerate the progression of multiple sclerosis (MS), while in women, menopause worsens MS-related disability. We previously demonstrated that functional testes and testosterone are required for the spontaneous remyelination of a focal lysolecithin (LPC)-induced demyelinating lesion in the spinal cords of male mice. Testosterone-dependent myelin repair was dependent on the induction of the chemokine receptor CXCR4 in astrocytes that repopulated the lesion and on cooperation between androgen-receptor signaling and CXCR4 signaling. In the present study, we investigated whether ovaries and estradiol have a comparable key role in female mice. Ovariectomy prevents, the appearance of astrocytes, while treatment with estradiol enhances astrocyte numbers and promotes remyelination by oligodendrocytes within the LPC-demyelinated lesion. Unlike testosterone, estradiol did not induce CXCR4 expression, and its effects remained unaffected by the CXCR4 inhibitor AMD3100. As was seen with testosterone treatment, the presence of astrocytes and myelinating oligodendrocytes within the LPC lesion of estradiol-treated females prevented the incursion of Schwann cells. These findings highlight estradiol’s crucial role in CNS remyelination in females, providing a strong rationale for estrogen-replacement therapy in estrogen-deficient and menopausal women with MS. Full article

The long-interspersed elements (LINE-1; L1) represent the main active family of retrotransposons in the human organism, comprising approximately 17% of its content. L1 sequence codifies for the two proteins involved in its retrotransposition: ORF1p, an RNA binding protein, and ORF2p, endowed with endonuclease and reverse transcriptase activity. The vast majority of L1 copies are inactive, with only a small percentage retaining their retrotransposition capacity, posing a threat to the organism due to its mutagenic potential. To mitigate such risks, mammals have evolved intricate regulatory mechanisms, including heterochromatin formation and RNA degradation pathways. Age-related diminution in these regulatory pathways may be particularly important within the Central Nervous System (CNS), where cellular regeneration is limited, and genomic integrity is critical for lifelong function. Here, we describe an age-associated upregulation of ORF1p in the mouse brain, indicating a potential role of L1 activity in aging. We further demonstrate the presence of ORF1p across diverse CNS cell types, including neurons, oligodendrocytes and microglia. Notably, we observe a correlation between ORF1p presence and microglial activation, a hallmark of neuroinflammation, during aging. This study advances our understanding of L1 dynamics in the CNS and underscores the significance of L1 in age-related neurological changes. Full article

Background: In tissue engineering, developing injectable hydrogels with tailored mechanical and bioactive properties remains a challenge. This study introduces an injectable hydrogel composite for soft tissue regeneration, composed of oxidized alginate (OA) and N-succinyl chitosan (NSC) cross-linked via Schiff base reaction, reinforced with graphene oxide (GOx) and cyclic arginylglycylaspartic acid (c-RGD). The objective was to create a multifunctional platform combining injectability, bioactivity, and structural stability. Methods: The OA/NSC/GOx-cRGD hydrogel was synthesized through Schiff base cross-linking (aldehyde-amine reaction). Characterization included FTIR (C=N bond at 1650 cm⁻¹), Raman spectroscopy (D/G bands at 1338/1567 cm⁻¹), SEM (porous microstructure), and rheological analysis (shear-thinning behavior). In vitro assays assessed fibroblast viability (MTT) and macrophage TNF-α secretion (ELISA), while ex-vivo injectability and retention were evaluated using chicken cardiac tissue. Results: The hydrogel exhibited shear-thinning behavior (viscosity: 10 to <1 Pa·s) and elastic-dominated mechanics (G′ > G″), ensuring injectability. SEM revealed an interconnected porous structure mimicking native extracellular matrix. Fibroblast viability remained ≥95%, and TNF-α secretion in macrophages decreased by 80% (30 vs. 150 pg/μL in controls), demonstrating biocompatibility and anti-inflammatory effects. The hydrogel adhered stably to cardiac tissue without leakage. Conclusions: The OA/NSC/GOx-cRGD composite integrates injectability, bioactivity, and structural stability, offering a promising scaffold for tissue regeneration. Its modular design allows further functionalization with peptides or growth factors. Future work will focus on translational applications, including scalability and optimization for dynamic biological environments. Full article

Neuroplasticity, the ability of the nervous system to adapt structurally and functionally in response to environmental interactions and injuries, is a cornerstone of recovery in the central (CNS) and peripheral nervous systems (PNS). This review explores the mechanisms underlying neuroplasticity, focusing on the dynamic roles of cellular and molecular processes in recovery from nervous system injuries. Key cellular players, including Schwann cells, oligodendrocytes, and neural stem cells, are highlighted for their contributions to nerve repair, myelination, and regeneration. Advances in therapeutic interventions, such as electrical stimulation, bioluminescent optogenetics, and innovative nerve grafting techniques, are discussed alongside their potential to enhance recovery and functional outcomes. The molecular underpinnings of plasticity, involving synaptic remodeling, homeostatic mechanisms, and activity-dependent regulation of gene expression, are elucidated to illustrate their role in learning, memory, and injury repair. Integrating emerging technologies and therapeutic approaches with a foundational understanding of neuroplasticity offers a pathway toward more effective strategies for restoring nervous system functionality after injury. Full article

Repulsive guidance molecule-a (RGMa) has emerged as a significant therapeutic target in a variety of neurological disorders, including neurodegenerative diseases and acute conditions. This review comprehensively examines the multifaceted role of RGMa in central nervous system (CNS) pathologies such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, neuromyelitis optica spectrum disorder, spinal cord injury, stroke, vascular dementia, auditory neuropathy, and epilepsy. The mechanisms through which RGMa contributes to neuroinflammation, neuronal degeneration, and impaired axonal regeneration are herein discussed. Evidence from preclinical studies associate RGMa overexpression with negative outcomes, such as increased neuroinflammation and synaptic loss, while RGMa inhibition, particularly the use of agents like elezanumab, has shown promise in enhancing neuronal survival and functional recovery. RGMa’s responses concerning immunomodulation and neurogenesis highlight its potential as a therapeutic avenue. We emphasize RGMa’s critical role in CNS pathology and its potential to pave the way for innovative treatment strategies in neurological disorders. While preclinical findings are encouraging so far, further clinical trials are needed to validate the safety and efficacy of RGMa-targeted therapies. Full article

Spinal cord injury (SCI) affects millions of people worldwide. One of the main challenges of rehabilitation strategies is re-training and enhancing the plasticity of the spinal circuitry that was preserved or rebuilt after the injury. The serotonergic system appears to be crucial in these processes, since recent studies have reported the capability of serotonergic (5-HT) axons for axonal sprouting and regeneration in response to central nervous system (CNS) trauma or neurodegeneration. We took advantage of tryptophan hydroxylase 2 knockout (TPH2 KO) rats, lacking serotonin specifically in the brain and spinal cord, to study the role of the serotonergic system in the recovery of sensorimotor function after SCI. In the present work, we compared the rate of sensorimotor recovery of TPH2 KO and wild-type (WT) female rats after SCI (lateral hemisection at the T8 spinal level). SCI caused severe motor impairments in the ipsilateral left hindlimb, the most pronounced in the first week after the hemisection with gradual functional recovery during the following 3 weeks. The results demonstrate that TPH2 KO rats have less potential to recover motor functions since the degree of sensorimotor deficit in the tapered beam walking test (TBW) and ladder walking test (LW) was significantly higher in the TPH2 KO group in comparison to the WT animals in the 3rd and 4th weeks after SCI. The recovery dynamics of the hindlimb muscle tone and voluntary movements was in agreement with the restoration of motor performance in TBW and LW. Compound muscle action potential analysis in the gastrocnemius (GM) and tibialis (TA) muscles of both hindlimbs after electrical stimulation of the sciatic nerve or lumbar region (L5–L6) of the spinal cord indicated slower recovery of sensorimotor pathways in the TPH2 KO group versus their WT counterparts. In general, the observed results confirm the significance of central serotonergic mechanisms in the recovery of sensorimotor functions in rats and the relevance of the TPH2 KO rat model in studying the role of the 5-HT system in neurorehabilitation. Full article

Many seedlings and a few young trees have recently been observed in Pinus yunnanensis forests, reducing the natural regeneration ability and succession. Shade treatments were applied to potted 1-year-old P. yunnanensis seedlings, and the shade net was opened at noon to simulate light patches. We used four treatments, i.e., 80% shade with 1 h light at noon (T80-1), 80% shade all the time (T80), 95% shade with 1 h light at noon (T95-1), and 95% shade all the time (T95), and a control (natural light). We analyzed the effects of light patches on the growth and C:N:P stoichiometry of P. yunnanensis seedlings. (1) Shading significantly inhibited seedling growth, with height increments reduced by 29.59% and 47.40% under T80 and T95, respectively, and basal diameter increments decreased by 10.97% and 14.41%. (2) Shading reduced biomass across organs, with total biomass under T95 being only 39.02% of CK, but midday light patches alleviated this inhibition (T80-1 total biomass increased by 137.90% compared to T80). (3) Under high shading (T95), seedlings prioritized photosynthetic product allocation to aboveground parts (needle biomass proportion reached 58.01%), while light patches (T80-1) enhanced coarse root biomass (137.90% higher than T80). (4) Shading significantly increased needle C:N and C:P ratios (T95 increased by 69.01% and 129.93% compared to CK, respectively), with N:P > 16 indicating phosphorus limitation; light patches (T80-1) reduced N:P to 14–16, mitigating co-limitation by N and P. The study demonstrates that P. yunnanensis seedlings adopt conservative strategies under shading by adjusting biomass allocation and stoichiometry to adapt to low-light conditions, while midday light patches enhance photosynthetic efficiency and nutrient utilization. We recommend forest thinning to increase understory light patches, thereby improving natural regeneration and promoting sustainable forest management of P. yunnanensis forests. These findings highlight the importance of light management in P. yunnanensis forests to enhance regeneration by regulating understory light patches. Full article

Graphite-phase carbon nitride (CN) has the advantages of high stability, non-toxicity, and harmlessness in degrading antibiotic pollutants in water. How to achieve the reduction of its electron-hole complexation efficiency as well as the improvement of its recyclability, while at the same time ensuring these advantages, is the focus of this paper. In this study, modified magnetic particles selected from coal gasification slag were used as carriers, which were compounded with CN and then subjected to a simple roasting process to obtain composite magnetic photocatalysts (MCN) with different ratios. The introduction of porous magnetic carriers increased the specific surface area of MCN, provided more active sites, and effectively improved the migration ability and redox capacity of CN carriers. Among them, 50% MCN showed excellent photodegradation performance, and the removal rate of tetracycline reached 82% within 60 min, which was much higher than that of CN. 50% MCN has a saturated magnetisation intensity of 1.55 emu·g⁻¹, which can be regenerated after recycling using a magnetic field, and the degradation efficiency of tetracycline is still more than 70% after five cycles, indicating that 50% MCN has good stability. This work demonstrates that magnetic gasification slag as a modified carrier can effectively promote the separation of photogenerated electron-hole pairs of graphite-phase carbon nitride, which provides a reference for the resourceful utilisation of coal gasification slag, as well as for the construction of g-C₃N₄-based photocatalysts with highly efficient and stable photodegradation activity. This work exemplifies how waste-derived materials can advance photocatalyst design, addressing both efficiency and sustainability challenges in water treatment. Full article

Wildfires are frequently observed in watersheds with a Mediterranean climate and seriously affect vegetation, soil, hydrology, and ecosystems as they cause abrupt changes in land cover. Assessing wildfire effects, as well as the recovery process, is critical for mitigating their impacts. This paper presents a geospatial analysis approach that enables the investigation of wildfire effects on vegetation, soil, and hydrology. The prediction of regeneration potential and the period needed for the restoration of hydrological behavior to pre-fire conditions is also presented. To this end, the catastrophic wildfire that occurred in August 2021 in the wider area of Varybobi, north of Athens, Greece, is used as an example. First, an analysis of the extent and severity of the fire and its effect on the vegetation of the area is conducted using satellite imagery. The history of fires in the specific area is then analyzed using remote sensing data and a regrowth model is developed. The effect on the hydrological behavior of the affected area was then systematically analyzed. The analysis is conducted in a spatially distributed form in order to delineate the critical areas in which immediate interventions are required for the rapid restoration of the hydrological behavior of the basin. The period required for the restoration of the hydrological response is then estimated based on the developed vegetation regrowth models. Curve Numbers and post-fire runoff response estimations were found to be quite similar to those derived from measured data. This alignment shows that the SCS-CN method effectively reflects post-fire runoff conditions in this Mediterranean watershed, which supports its use in assessing hydrological changes in wildfire-affected areas. The results of the proposed approach can provide important data for the restoration and protection of wildfire-affected areas. Full article