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Wu T.,Zhejiang University | Zhao W.-H.,Ning Xia Medical University | Dong Y.,Hangzhou Hospital of Zhejiang Chinese Peoples Armed Police Force | Song H.-X.,Zhejiang University | Li J.-H.,Zhejiang University
Archives of Physical Medicine and Rehabilitation | Year: 2016

Objective: To review the literature and assess the comparative effectiveness of ultrasound-guided (USG) versus computed tomography (CT)-/fluoroscopy-guided lumbar facet joint injections in adults. Data Sources: PubMed, Ovid MEDLINE, Ovid Embase, EBSCO, and Web of Science. Study Selection: Randomized or nonrandomized controlled trials comparing the clinical effectiveness between USG and CT-/fluoroscopy-guided injection techniques in patients with facet syndrome were included. Data Extraction: Two reviewers independently screened abstracts and full texts. The results of the mean procedure duration, decreased pain score, and Modified Oswestry Disability score after treatment were extracted and presented in the form of mean ± SD. Data Synthesis: There were 103 records screened; 3 studies were included, with a total of 202 adults with facet joint pain. There was no statistically significant difference between the 2 groups in pain score and Modified Oswestry Disability score after injection (weighted mean difference [WMD], .07; 95% confidence interval [CI], -.51 to .65; P=.80; I2=78%; WMD, -.55; 95% CI, -1.31 to .22; P=.16; I2=0%, respectively). There was also no statistically significant difference in the mean procedure duration between the 2 groups (standardized mean difference [SMD], .97; 95% CI, -1.01 to 2.94; P=.34; I2=97%). Conclusions: This review suggested that no significant differences in pain and functional improvement were noted between the USG and CT-/fluoroscopy-guided techniques in facet joint injection. USG injection is feasible and minimizes exposure of radiation to patients and practitioners in the lumbar facet joint injection process. © 2016 American Congress of Rehabilitation Medicine.


Lv D.,Ning Xia Medical University | Bai Z.,General Hospital of Ning Xia Medical University | Yang L.,First Peoples Hospital | Li X.,Ning Xia Medical University | Chen X.,General Hospital of Ning Xia Medical University
Environmental Toxicology and Pharmacology | Year: 2016

Some findings have suggested that the rescue of bupivacaine (BPV)-induced cardiotoxicity by lipid emulsion (LE) is associated with inhibition of mitochondrial permeability transition pore (mPTP). However, the mechanism of this rescue action is not clearly known. In this study, the roles of phosphoinositide 3-kinase (PI3K)/Akt and glycogen synthase kinase-3β (GSK-3β) in the molecular mechanism of LE-induced protection and its relationship with mPTP were explored. h9c2 cardiomyocytes were randomly divided into several groups: control, BPV, LE, BPV. +. LE. To study the effect of LE on mPTP, atractyloside (Atr, 20. μM, mPTP opener) and cyclosporine A (CsA, 10. μM, mPTP blocker) were used. To unravel whether LE protects heart through the PI3K/Akt/GSK-3β signaling pathway, cells were treated with LY294002 (LY, 30. μM, PI3K blocker) or TWS119 (TWS 10. μM, GSK-3β blocker). Later mitochondrial respiratory chain complexes, apoptosis, opening of mPTP and phosphorylation levels of Akt/GSK-3β were measured. LE significantly improved the mitochondrial functions in h9c2 cardiomyocytes. LE reversed the BPV-induced apoptosis and the opening of mPTP. The effect of LE was not only enhanced by CsA and TWS, but also abolished by Atr and LY. LE also increased the phosphorylation levels of Akt and GSK-3β. These results suggested that LE can reverse the apoptosis in cardiomyocytes by BPV and a mechanism of its action is inhibition of mPTP opening through the PI3K/Akt/GSK-3β signaling pathway. © 2016 Elsevier B.V.


Qiu D.,Fudan University | Qiu D.,Sun Yat Sen University | Hou L.,Fudan University | Hou L.,Sun Yat Sen University | And 6 more authors.
Respiratory Physiology and Neurobiology | Year: 2011

Therapeutic application of Asarum, a herbal medicine that has been used for centuries, reportedly causes acute respiratory disturbance. The responsible constituents, the sites of action, and the mechanisms involved in this side effect are unclear. We investigated the effects of β-asarone, a volatile constituent of Asarum, on neurotransmission in the medullary respiratory neuronal network using extracellular recording of the rhythmic hypoglossal activity and voltage clamp recordings of the postsynaptic activity of the airway preganglionic parasympathetic motoneurons (APPMs) in vitro. β-Asarone caused progressive decreases in the duration and area of the hypoglossal bursts in a concentration-dependent manner. The frequency and amplitude of the bursts were initially unaltered or temporarily increased, but were then inhibited progressively after prolonged exposure. As with the inhibition of the hypoglossal bursts, the tonic and the phasic excitatory and inhibitory postsynaptic currents in the APPMs were attenuated. These data suggest that the Asarum-caused acute respiratory disturbance involves β-asarone-induced inhibition of neurotransmission in the medullary respiratory neuronal network. © 2011 Elsevier B.V.


Zhou X.,Fudan University | Chen Y.,Fudan University | Ge D.,Fudan University | Yuan W.,Ning Xia Medical University | Wang J.,Fudan University
Experimental Physiology | Year: 2013

New Findings: • What is the central question of this study? Airway vagal preganglionic neurons (AVPNs) supply the essential excitatory drive to the postganglionic neurons, which dominate the neural control of the airway physiologically and play critical roles in the pathogenesis of some common airway disorders. AVPNs express multiple subunits of nicotinic acetylcholine receptors (nAChRs), but the influences of exogenous nicotine or endogenous acetylcholine are unknown. • What is the main finding and its importance? Nicotine and endogenous acetylcholine both cause a postsynaptic excitatory current in inspiratory- activated AVPNs, and enhance both the excitatory and inhibitory synaptic inputs. The overall effect of nicotine on inspiratory-activated AVPNs is excitatory. The nicotinic effects on inspiratory-activated AVPNs are mediated presynaptically by activation of α4β2 type of nAChRs and postsynaptically by activation of multiple nAChRs including α7 and α4β2 types. The airway vagal preganglionic neurons (AVPNs) supply the essential excitatory drive to the postganglionic neurons and dominate the neural control of the airway both physiologically and pathophysiologically. The AVPNs express multiple subunits of nicotinic acetylcholine receptors (nAChRs), but the influences of exogenous nicotine and endogenous acetylcholine are unknown. This study examined the effects of nicotine and endogenous acetylcholine on retrogradely labelled, functionally identified inspiratory-activated AVPNs (IA-AVPNs) using the patch-clamp technique. Nicotine (10 μmol l-1) significantly increased the frequency and amplitude of the spontaneous EPSCs of IA-AVPNs, and these effects were insensitive to methyllycaconitine (MLA, 100 nmol l-1), an antagonist of the α7 type of nAChR, but was prevented by dihydro-β-erythroidine (DHβE, 3 μmol l-1), an antagonist of the α4β2 type of nAChR. Nicotine caused a tonic inward current in IA-AVPNs, which was reduced by MLA or DHβE alone, but was not abolished by co-application of MLA and DHβE. Nicotine caused a significant increase in the frequency of GABAergic and glycinergic spontaneous IPSCs and significantly increased the amplitude of glycinergic spontaneous IPSCs, all of which were prevented by DHβE. Nicotine had no effects on the miniature EPSCs or miniature IPSCs following pretreatment with TTX. Under current clamp, nicotine caused depolarization and increased the firing rate of IA-AVPNs during inspiratory intervals. Neostigmine (10 μmol l-1), an acetylcholinesterase inhibitor, mimicked the effects of nicotine. These results demonstrate that nicotine and endogenous ACh enhance the excitatory and inhibitory synaptic inputs of IA-AVPNs and cause a postsynaptic excitatory current and that the nicotinic effects are mediated presynaptically by activation of the α4β2 type of nAChR and postsynaptically by activation of multiple nAChRs, including α7 and α4β2 types. © 2012 The Authors. Experimental Physiology © 2012 The Physiological Society.

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