Publications by authors named "Dave Schwinn Gao"

Itaconate plays a prominent role in anti-inflammatory effects and has gradually been ushered as a promising drug candidate for treating inflammatory diseases. However, its significance and underlying mechanism for inflammatory pain remain unexplored. In the current study, we investigated the effects and mechanisms of Dimethyl Itaconate (DI, a derivative of itaconate) on Complete Freund's adjuvant (CFA)-induced inflammatory pain in a rodent model.

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The spinal cord (SC) is crucial for a myriad of somatosensory, autonomic signal processing, and transductions. Understanding the SC vascular structure and function thus plays an integral part in neuroscience and clinical research. However, the dense layers of myelinated ascending axons on the dorsal side inconveniently grant the SC tissue with high optical scattering property, which significantly hinders the imaging depth of the SC vasculature in vivo.

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Epilepsy is an abnormal brain state that may be induced by synchronous neuronal activation and also abnormalities in energy metabolism or the oxygen supply vascular system. Neurovascular coupling (NVC), the relationship between neuron, capillary, and penetrating artery, remains unexplored on a fine-scale with respect to the pathology process after acute temporal lobe epilepsy (TLE). Here we use two-photon microscopy (TPM) to provide high temporal-spatial resolution imaging to identify changes in NVC during spontaneous and electro-stimulated (ES) states in awake mice.

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The metabolite itaconate has both anti-inflammatory and immunomodulatory effects. However, its influence on chronic pain is unclear. Here, we demonstrated that intraperitoneal injection of the itaconate derivative dimethyl itaconate (DI) alleviated chronic pain symptoms, such as allodynia and hyperalgesia, in spinal nerve ligation (SNL) and inflammatory pain models.

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Opioids are the last option for the pharmacological treatment of neuropathic pain, but their antinociceptive effects are limited. Decreased mu opioid receptor (MOR) expression in the peripheral nervous system may contribute to this. Here, we showed that nerve injury induced hypermethylation of the gene promoter and an increased expression of methyl-CpG binding protein 2 (MeCP2) in injured dorsal root ganglion (DRG).

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Nerve injury-induced changes of gene expression in dorsal root ganglion (DRG) are critical for neuropathic pain genesis. However, how these changes occur remains elusive. Here we report the down-regulation of zinc finger protein 382 (ZNF382) in injured DRG neurons after nerve injury.

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Metabolites have recently been found to be involved in significant biological regulation and changes. Itaconate, an important intermediate metabolite isolated from the tricarboxylic acid cycle, is derived from cis-aconitate decarboxylation mediated by immune response gene 1 in mitochondrial matrix. Itaconate has emerged as a key autocrine regulatory component involved in the development and progression of inflammation and immunity.

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Nerve injury-induced gene expression change in the spinal cord is critical for neuropathic pain genesis. RNA N-methyladenosine (mA) modification represents an additional layer of gene regulation. We showed that spinal nerve ligation (SNL) upregulated the expression of matrix metallopeptidase 24 (MMP24) protein, but not mRNA, in the spinal cord neurons.

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It has been reported that the incidence of recurrent laryngeal nerve (RLN) injury is higher in an operational procedure in the thyroid and parathyroid region. Elevating voice pitch is achieved by the cricothyroid contraction, which in turn is innervated by the external branch of the superior laryngeal nerve (EBSLN). Due to the subtle nature and clinical variability of EBSLN damage, diagnosis may be difficult.

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Rationale: Renal Fanconi syndrome (FS) is a rare complication of monoclonal gammopathy. It is characterized by the impairment of renal proximal tubular function leading to normoglycemic glycosuria, aminoaciduria, hypophosphatemia, hypouricemia and proximal renal tubular acidosis. Renal impairment in monoclonal gammopathy, without fulfilling the criteria of multiple myeloma, is categorized as monoclonal gammopathy of renal significance (MGRS).

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