Publications by authors named "Yudan Gao"

JOURNAL/nrgr/04.03/01300535-202510000-00024/figure1/v/2024-11-26T163120Z/r/image-tiff The presence of endogenous neural stem/progenitor cells in the adult mammalian brain suggests that the central nervous system can be repaired and regenerated after injury. However, whether it is possible to stimulate neurogenesis and reconstruct cortical layers II to VI in non-neurogenic regions, such as the cortex, remains unknown.

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Genetic variations of signaling modulator protein LNK (also called SH2B3) are associated with relatively mild myeloproliferative phenotypes in patients with myeloproliferative neoplasms (MPN). However, these variations can induce more severe MPN disease and even leukemic transformation when co-existing with other driver mutations. In addition to the most prevalent driver mutation JAK2V617F, LNK mutations have been clinically identified in patients harboring CBL inactivation mutations, but its significance remains unclear.

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Attempts have been made to use cell transplantation and biomaterials to promote cell proliferation, differentiation, migration, and survival, as well as angiogenesis, in the context of brain injury. However, whether bioactive materials can repair the damage caused by ischemic stroke by activating endogenous neurogenesis and angiogenesis is still unknown. In this study, we applied chitosan gel loaded with basic fibroblast growth factor to the stroke cavity 7 days after ischemic stroke in rats.

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Persistent neurogenesis exists in the subventricular zone (SVZ) of the ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus in the adult mammalian brain. Adult endogenous neurogenesis not only plays an important role in the normal brain function, but also has important significance in the repair and treatment of brain injury or brain diseases. This article reviews the process of adult endogenous neurogenesis and its application in the repair of traumatic brain injury (TBI) or ischemic stroke, and discusses the strategies of activating adult endogenous neurogenesis to repair brain injury and its practical significance in promoting functional recovery after brain injury.

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Objective: To investigate the electrophysiological properties of pyramidal neurons in mouse motor cortex during the early postnatal development.

Methods: Thirty-six mice were randomly divided into postnatal 1-, 2-, 3-Week and 1-, 2-,3-Month groups (=6). Membrane properties, action potentials (AP) and spontaneous excitatory postsynaptic currents (sEPSCs) of motor cortex pyramidal neurons were recorded to evaluate the changes in the intrinsic electrophysilogical characteristics by using whole cell patch clamp.

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Available methods for differentiating stem cells into neurons require a large number of cytokines and neurotrophic factors, with complex steps and slow processes, and are inefficient to produce functional neurons and form synaptic contacts, which is expensive and impractical in clinical application. Here, we demonstrated a bioactive material, basic fibroblast growth factor (bFGF)-chitosan controlled release system, for facilitating neuronal differentiation from NSCs and the functional maturation of the induced neurons with high efficiency. We illustrated by immunostaining that the neurons derived from NSCs expressed mature immunomarkers of interneurons and excitatory neurons.

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Tumor-associated macrophages (TAMs) are highly heterogeneous and play vital roles in tumor progression. Here we adopted a C57BL/6 mouse model imitating the late-stage colorectal liver metastasis (CRLM) by Mc38 colorectal cancer cell injection via the portal vein. With serial sections of CRLM biopsies, we defined 7-9 days post-injection as the critical period for tumor neovascularization, which was initiated from the innate liver vessels via vessel cooption and extended by vascular mimicry and thereof growth of CD34cells.

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Activation of endogenous neurogenesis by bioactive materials enables restoration of sensory/motor function after complete spinal cord injury (SCI) via formation of new relay neural circuits. The underlying wiring logic of newborn neurons in adult central nervous system (CNS) is unknown. Here, we report neurotrophin3-loaded chitosan biomaterial substantially recovered bladder function after SCI.

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An implanted neurotrophin-3 (NT3)-chitosan scaffold can recruit endogenous neural stem cells to migrate to a lesion region and differentiate into mature neurons after adult spinal cord injury (SCI). However, the identities of these newborn neurons and whether they can form functional synapses and circuits to promote recovery after paraplegia remain unknown. By using combined advanced technologies, we revealed here that the newborn neurons of several subtypes received synaptic input from the corticospinal tract (CST), rubrospinal tract (RST), and supraspinal tracts.

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Spinal cord injury (SCI) is a severe damage usually leading to limb dysesthesia, motor dysfunction, and other physiological disability. We have previously shown that NT3-chitosan could trigger an acute SCI repairment in rats and non-human primates. Due to the negative effect of inhibitory molecules in glial scar on axonal regeneration, however, the role of NT3-chitosan in the treatment of chronic SCI remains unclear.

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Muscle spindles, an important proprioceptor scattered in the skeletal muscle, participate in maintaining muscle tension and the fine regulation of random movement. Although muscle spindles exist in all skeletal muscles, explanations about the distribution and morphology of muscle spindles remain lacking for the indetermination of spindle location across muscles. In this study, traditional time-consuming histochemical technology was utilized to determine the muscle spindle anatomical and morphological characteristics in the lower extremity skeletal muscle in C57BL/6 mice.

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Although autogenous nerve transplantation is the gold standard for treating peripheral nerve defects of considerable length, it still has some shortcomings, such as insufficient donors and secondary injury. Composite chitosan scaffolds loaded with controlled release of nerve growth factor can promote neuronal survival and axonal regeneration after short-segment sciatic nerve defects. However, the effects on extended nerve defects remain poorly understood.

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The repair of peripheral nerve injury is still a great challenge in clinic. Autologous nerve transplantation is the gold standard for the treatment of long-distance peripheral nerve defects, but this method remains associated with high morbidity of the donor site and lack of matching donor. In this study, a novel chitosan scaffold (CS) loaded with control-released basic fibroblast growth factor (bFGF) was used to repair 20 mm sciatic nerve defects in adult rat.

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Bone marrow mesenchymal stem cells undergo differentiation to different lineages with different efficiencies when induced by different factors. We added a bFGF-chitosan controlled release system (bFGF-CCRS) as an inducer into conditioned medium to facilitate the oriented differentiation of BMSCs into neural lineage cells (eventually mature neurons); furthermore, we synchronized BMSCs to the G0/G1 phase via serum starvation to observe the effect of the inducer on the differentiation direction and efficiency. The nonsynchronized group, chitosan alone (not loaded with bFGF) group, soluble bFGF group, and conditioned medium group served as controls, and we observed the dynamic process of differentiation of BMSCs into neural lineage cells at different time points after the beginning of coculture.

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Neural circuit reconstruction is the main target of functional restoration after adult spinal cord injury (SCI). The microenvironment after adult SCI is hostile to neural regeneration. Here, we designed a bFGF controlled releasing system (bFGF-CRS) by loading bFGF onto the sodium hyaluronate collagen scaffolds to modify the hostile microenvironment.

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The purpose of this study was to assess the pathological variation in white matter tracts in the adult severe thoracic contusion spinal cord injury (SCI) rat models combined with in vivo magnetic resonance imaging (MRI), as well as the effect of spared white matter (WM) quantity on hindlimb motor function recovery. 7.0T MRI was conducted for all experimental animals before SCI and 1, 3, 7, and 14 days after SCI.

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The present study was aimed to investigate the electrophysiological characteristics of hippocampal postnatal early development mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in rats. Forty-eight Wistar rats were divided into postnatal 0.5-, 1-, 2- and 3-month groups (n = 12).

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The present study aimed to explore the potential of the sodium hyaluronate-CNTF (ciliary neurotrophic factor) scaffold in activating endogenous neurogenesis and facilitating neural network re-formation after the adult rat spinal cord injury (SCI). After completely cutting and removing a 5-mm adult rat T8 segment, a sodium hyaluronate-CNTF scaffold was implanted into the lesion area. Dil tracing and immunofluorescence staining were used to observe the proliferation, differentiation and integration of neural stem cells (NSCs) after SCI.

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Article Synopsis
  • Mammals continually regenerate new neurons throughout their lives, particularly in specific brain regions like the dentate gyrus and subventricular zone.
  • Recent advancements have enhanced our understanding of spinal cord neural stem cells, especially ependymal cells, and their importance in adult spinal cord development.
  • The review discusses key topics such as adult neurogenesis, how ependymal cells respond to spinal cord injuries, their diversity, regulatory factors, and the specific environments that influence their activation and differentiation.
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Unlabelled: The traumatic brain injury (TBI) usually causes brain tissue defects, including neuronal death or loss, which ultimately results in dysfunction in some degree. The cell replacement therapy is now one of the most promising methods for such injury. There are currently various methods to induce the differentiation of stem cells into neurons, but all extremely complex, slow and unstable.

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The central nervous system (CNS) has very restricted intrinsic regeneration ability under the injury or disease condition. Innovative repair strategies, therefore, are urgently needed to facilitate tissue regeneration and functional recovery. The published tissue repair/regeneration strategies, such as cell and/or drug delivery, has been demonstrated to have some therapeutic effects on experimental animal models, but can hardly find clinical applications due to such methods as the extremely low survival rate of transplanted cells, difficulty in integrating with the host or restriction of blood-brain barriers to administration patterns.

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