Tao J

OpenAlex Profile
2
EM Publications
8
h-index
(648 citations, 30 total works)

Research Topics

Lung Cancer Treatments and Mutations (21) Medical Imaging and Pathology Studies (16) RNA modifications and cancer (13) Cancer, Hypoxia, and Metabolism (8) Lung Cancer Research Studies (3)

Erythromelalgia Publications

CT-guided Chemical Lumbar Sympathectomy in the Treatment of Cold Hypersensitivity in the Hands and Feet.

Tao J, Zhu J, Wang T, He Q, Luo G , et al.
Pain physician •

Cold hypersensitivity in the hands and feet is a common clinical symptom in Asian women. Currently, treatment of cold hypersensitivity in the hands and feet is still limited to traditional Chinese medicine, mainly herbal medicine. However, many patients with cold hypersensitivity in the hands and feet in China are not satisfied with the therapeutic effect of herbal medicine, and took medication for a longer time. Chemical lumbar sympathectomy is widely used in the treatment of plantar hyperhidrosis, diabetic foot, recalcitrant erythromelalgia, and other diseases. This study was conducted to evaluate the short-term as well as long-term efficacy, complications, and patient satisfaction of chemical lumbar sympathectomy during treatment cold hypersensitivity in the hands and feet. A retrospective, observational study. Department of Anesthesiology and Pain Medicine, Jiaxing, China. A retrospective study of 72 patients with cold hypersensitivity in the hands and feet who received chemical lumbar sympathectomy treatment in our hospital from January 2015 to October 2018 was conducted. The heart rate, non-invasive blood pressure, oxygen saturation, visual analog scale, perfusion index, and plantar temperature were monitored and recorded in before treatment (T1) and after treatment (T2) groups. The patients were followed up on day 1, at week 1, 1 month, 3 months, 6 months, one year, and 2 years after operation for satisfaction, complications, and recurrence. There were no significant differences in heart rate, non-invasive blood pressure, and oxygen saturation between T1 and T2 groups (P > 0.05). Perfusion index and plantar temperature in T2 group were remarkably higher than T1 group, and the difference was statistically significant (P < 0.01). The visual analog scale score of the T2 group was significantly reduced (P < 0.01). Of all the patients who underwent chemical lumbar sympathectomy, the postoperative therapeutic effect was effective in 63 cases (87.5%) and ineffective in 9 cases (12.5%). Among the effective patients, the postoperative curative effect was shown to be excellent in 47 cases and improved in 16 cases. According to the follow-up results at day 1, 1 week, 1 month, 3 months, 6 months, 1 year, and 2 years after operation, the satisfaction rate was 87.5%, 87.5%, 81.9%, 61.1%, 52.7%, 41.6%, and 34.7%, respectively. There were no serious complications observed and 23 patients relapsed after two years. Multivariate logistic regression analysis results showed that the effect of visual analog scale (OR = 7.312, 95% CI: 1.598 - 33.646, P = 0.011) and plantar temperature (OR = 0.470, 95% CI: 0.288 - 0.766, P = 0.002) on therapeutic effect showed has statistical significance; the effect of gender (OR = 0.654, 95% CI: 0.134 - 3.181, P = 0.599), age (OR = 0.975, 95% CI: 0.916 - 1.039, P = 0.441), perfusion index (OR = 0.710, 95% CI: 0.367 - 1.375, P = 0.310), and disease course (OR = 1.019, 95% CI: 0.997 - 1.042, P = 0.088) on therapeutic effect showed no statistical significance. The effect of gender (OR = 0.451, 95% CI 0.131 - 1.554, P = 0.207), age (OR = 0.961, 95% CI 0.912 - 1.013, P = 0.141), and course of disease (OR = 1.006, 95% CI 0.997 - 1.015, P = 0.203) on postoperative recurrence showed no statistical significance. The nonrandomized, single-center, small sample size, retrospective design is a major limitation of this study. Chemical lumbar sympathectomy is a valid treatment option for cold hypersensitivity in hands and feet, and computed tomography-guided percutaneous puncture chemical lumbar sympathectomy has the advantages of high success rate, less invasion, less complications, and repeatablity.

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Insensitivity to Pain upon Adult-Onset Deletion of Nav1.7 or Its Blockade with Selective Inhibitors.

Shields SD, Deng L, Reese RM, Dourado M, Tao J , et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience •

Strong human genetic evidence points to an essential contribution of the voltage-gated sodium channel Nav1.7 to pain sensation: loss of Nav1.7 function leads to congenital insensitivity to pain, whereas gain-of-function mutations in the gene that encodes Nav1.7 cause painful neuropathies, such as inherited erythromelalgia, a syndrome characterized by episodic spontaneous pain. Selective Nav1.7 channel blockers thus hold promise as potential painkillers with improved safety and reduced unwanted side effects compared with existing therapeutics. To determine the maximum effect of a theoretically perfectly selective Nav1.7 inhibitor, we generated a tamoxifen-inducible KO mouse model enabling genetic deletion of Nav1.7 from adult mice. Electrophysiological recordings of sensory neurons from these mice following tamoxifen injection demonstrated the loss of Nav1.7 channel current and the resulting decrease in neuronal excitability of small-diameter neurons. We found that behavioral responses to most, but surprisingly not all, modalities of noxious stimulus are abolished following adult deletion of Nav1.7, pointing toward indications where Nav1.7 blockade should be efficacious. Furthermore, we demonstrate that isoform-selective acylsulfonamide Nav1.7 inhibitors show robust analgesic and antinociceptive activity acutely after a single dose in mouse pain models shown to be Nav1.7-dependent. All experiments were done with both male and female mice. Collectively, these data expand the depth of knowledge surrounding Nav1.7 biology as it relates to pain, and provide preclinical proof of efficacy that lays a clear path toward translation for the therapeutic use of Nav1.7-selective inhibitors in humans. Loss-of-function mutations in the sodium channel Nav1.7 cause congenital insensitivity to pain in humans, making Nav1.7 a top target for novel pain drugs. Targeting Nav1.7 selectively has been challenging, however, in part due to uncertainties in which rodent pain models are dependent on Nav1.7. We have developed and characterized an adult-onset Nav1.7 KO mouse model that allows us to determine the expected effects of a theoretically perfect Nav1.7 blocker. Importantly, many commonly used pain models, such as mechanical allodynia after nerve injury, appear to not be dependent on Nav1.7 in the adult. By defining which models are Nav1.7 dependent, we demonstrate that selective Nav1.7 inhibitors can approximate the effects of genetic loss of function, which previously has not been directly established.

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