Publications by authors named "He Qianru"

Ischemia and hypoxia caused by vascular injury intensify nerve damage. Skin precursor-derived Schwann cells have demonstrated an accelerated in vivo prevascularization of tissue-engineered nerves. Furthermore, extracellular vesicles from skin precursor-derived Schwann cells (SKP-SC-EVs) show the potential in aiding peripheral nerve regeneration.

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Radiofrequency ablation (RFA) is an effective treatment for hepatocellular carcinoma (HCC), but the recurrence rate remains high due to angiogenesis in residual cancer cells. We used thermal stimulation to simulate the post-RFA microenvironment. The expression profile of circRNAs between normal control HCC cell-derived exosomes and exosomes after heat stimulation were analyzed by RNA sequencing.

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Article Synopsis
  • Gastrointestinal stromal tumors (GIST) are the most common type of mesenchymal tumors in the GI tract, with uncertain malignant potential, prompting the need for improved predictive models for recurrence-free survival (RFS).
  • A study involving 254 patients who underwent surgery for GIST utilized radiomics and deep learning to create multiple predictive models, with a multimodal model showing the best performance in predicting RFS.
  • The findings indicated significant differences in RFS between high and low-risk groups, suggesting a connection between tumor cell morphology and prognosis, thus supporting the use of advanced modeling techniques in clinical decision-making.
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Extracellular vesicles from skin-derived precursor Schwann cells (SKP-SC-EVs) promote neurite outgrowth in culture and enhance peripheral nerve regeneration in rats. This study aimed at expanding the application of SKP-SC-EVs in nerve grafting by creating a chitosan/PLGA-based, SKP-SC-EVs-containing tissue engineered nerve graft (TENG) to bridge a 40-mm long sciatic nerve defect in dogs. SKP-SC-EVs contained in TENGs significantly accelerated the recovery of hind limb motor and electrophysiological functions, supported the outgrowth and myelination of regenerated axons, and alleviated the denervation-induced atrophy of target muscles in dogs.

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JOURNAL/nrgr/04.03/01300535-202501000-00035/figure1/v/2024-05-14T021156Z/r/image-tiff Our previous study found that rat bone marrow-derived neural crest cells (acting as Schwann cell progenitors) have the potential to promote long-distance nerve repair. Cell-based therapy can enhance peripheral nerve repair and regeneration through paracrine bioactive factors and intercellular communication.

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Brachial plexus injury (BPI) with motor neurons (MNs) damage still remain poor recovery in preclinical research and clinical therapy, while cell-based therapy approaches emerged as novel strategies. Previous work of rat skin precursor-derived Schwann cells (SKP-SCs) provided substantial foundation for repairing peripheral nerve injury (PNI). Given that, our present work focused on exploring the repair efficacy and possible mechanisms of SKP-SCs implantation on rat BPI combined with neurorrhaphy post-neurotomy.

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G protein-coupled receptor 37-like 1 (GPR37L1) is an orphan GPCR with largely unknown functions. Here, we report that Gpr37l1/GRP37L1 ranks among the most highly expressed GPCR transcripts in mouse and human dorsal root ganglia (DRGs) and is selectively expressed in satellite glial cells (SGCs). Peripheral neuropathy induced by streptozotoxin (STZ) and paclitaxel (PTX) led to reduced GPR37L1 expression on the plasma membrane in mouse and human DRGs.

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Nerve injury often leads to severe dysfunction because of the lack of axon regeneration in adult mammal. Intriguingly a series of extracellular vesicles (EVs) have the obvious ability to accelerate the nerve repair. However, the detailed molecular mechanisms to describe that EVs switch neuron from a transmitter to a regenerative state have not been elucidated.

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G protein coupled receptor 37-like 1 (GPR37L1) is an orphan GPCR and its function remains largely unknown. Here we report that GPR37L1 transcript is highly expressed compared to all known GPCRs in mouse and human dorsal root ganglia (DRGs) and selectively expressed in satellite glial cells (SGCs). Peripheral neuropathy following diabetes and chemotherapy by streptozotocin and paclitaxel resulted in downregulations of surface GPR37L1 in mouse and human DRGs.

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Article Synopsis
  • Sensory systems develop after birth through the refinement of connections between neurons, especially in the spinal cord's dorsal horn where adjustments occur in response to activity.
  • Microglia, the brain's immune cells, play a crucial role in this process by removing excess A-fiber terminals in the early postnatal weeks; without this action, normal sensory refinement is hindered.
  • When microglial activity is disrupted, it leads to persistent changes in sensitivity to touch, causing lasting hypersensitivity due to the retention of unnecessary A-fiber projections in the dorsal horn.
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Cutaneous metastases of ovarian cancer are rare and often have poor prognosis. We report a case of a 62-year-old woman with recurrent low-grade serous ovarian cancer, who presented with lung, brain, and multiple skin (nasal and anterior chest wall) metastases approximately six months after the initial diagnosis. In this case, Nijmegen breakage syndrome carrier status caused by RAD50 heterozygous mutation and previous bevacizumab therapy could be the predisposing factor for cutaneous metastases.

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Programmed death protein 1 (PD-1) and its ligand PD-L1 constitute an immune checkpoint pathway. We report that neuronal PD-1 signaling regulates learning/memory in health and disease. Mice lacking PD-1 (encoded by Pdcd1) exhibit enhanced long-term potentiation (LTP) and memory.

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Extracellular vesicles (EVs) show potential as a therapeutic tool for peripheral nerve injury (PNI), promoting neurological regeneration. However, there are limited data on the spatio-temporal trafficking and biodistribution of EVs. In this study, we introduce a new non-invasive near-infrared fluorescence imaging strategy based on glucose-conjugated quantum dot (QDs-Glu) labeling to target and track EVs in a sciatic nerve injury rat model in real-time.

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Background: Colorectal cancer (CRC) is the second most common cause of cancer-related death (9.4% of the 9.9 million cancer deaths).

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Excessive inflammation has been implicated in autism spectrum disorder (ASD), but the underlying mechanisms have not been fully studied. SHANK3 is a synaptic scaffolding protein and mutations of are involved in ASD. Shank3 expression in dorsal root ganglion sensory neurons also regulates heat pain and touch.

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Functional reconstruction after peripheral nerve injury depends on the ability of the regenerated sensory and motor axons to re-innervate the suitable target organs. Therefore, it is essential to explore the cellular mechanisms of peripheral nerve-specific regeneration. In a previous study, we found that sensory and motor fibroblasts can guide Schwann cells to migrate towards the same phenotype.

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Our understanding of neuropathic itch is limited due to a lack of relevant animal models. Patients with cutaneous T cell lymphoma (CTCL) experience severe itching. Here, we characterize a mouse model of chronic itch with remarkable lymphoma growth, immune cell accumulation, and persistent pruritus.

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The peripheral nervous system has remarkable regenerative capabilities. Schwann cells and fibroblasts are known to play crucial roles in these processes. In this study, we delineated the differential effects of peripheral nerve fibroblasts and cardiac fibroblasts on Schwann cells.

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In resected non-small cell lung cancer (NSCLC), ALK rearrangements are associated with worse recurrence-free survival (RFS) than other driver genes. In addition, the micropapillary pattern of NSCLC is associated with a poor prognosis. In recent years, crizotinib tyrosine kinase inhibitors (TKIs) have been widely used to treat patients with advanced NSCLC with ALK fusion.

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Anaplastic lymphoma kinase () gene rearrangement is an essential driver mutation identified in approximately 5% of non-small cell lung cancers (NSCLCs). The results of clinical trials have demonstrated the impressive efficacy of ALK tyrosine kinase inhibitors (ALK-TKIs). Besides the classic fusions, a growing list of gene fusion partners for in NSCLC have been identified with heterogeneous clinical responses to ALK-TKIs.

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