The Effect of Tramadol Versus Sufentanil on Controlling Postoperative Pain for Men Who Smoke and Do Not Smoke: A Randomized Clinical Trial.

Background: Smoking behavior alters the analgesic threshold, which challenges postoperative pain management for patients who smoke.

Objectives: We aimed to assess the analgesic efficacy of tramadol versus sufentanil in relieving postoperative pain for patients who do and do not smoke who underwent a partial hepatectomy.

Study Design: Double-blinded randomized controlled trial.

Corrigendum: Role of MicroRNA-143 in Nerve Injury-Induced Upregulation of Dnmt3a Expression in Primary Sensory Neurons.

[This corrects the article DOI: 10.3389/fnmol.2017.

Differentially Expressed Genes in the Brain of Aging Mice With Cognitive Alteration and Depression- and Anxiety-Like Behaviors.

Despite the great increase in human lifespan with improved medical care, the physiological and pathological changes such as memory and cognitive disorders and associated anxiety and depression are major concern with aging. Molecular mechanisms underlying these changes are little known. The present study examined the differentially expressed genes (DEGs) and the genes with differentially expressed isoforms in three brain regions, anterior cingulate cortex (ACC), amygdala and hippocampus, throughout the lifespan of mice.

MicroRNA-330 Directs Downregulation of the GABAR2 in the Pathogenesis of Pancreatic Cancer Pain.

Pancreatic cancer is one of the most aggressive and deadly malignancies with a very poor prognosis. Pancreatic cancer-induced visceral pain is very common and is generally presented among the initial symptoms in patients; such pain is strongly associated with poor quality of life, impaired functional activity, and decreased survival. However, the principal neurobiological mechanisms of pain caused by pancreatic cancer have not been fully elucidated.

Wrist-ankle acupuncture attenuates cancer-induced bone pain by regulating descending pain-modulating system in a rat model.

Background: Cancer-induced bone pain (CIBP) presents a multiple-mechanism of chronic pain involving both inflammatory and neuropathic pain, and its pathogenesis is closely related to endogenous descending system of pain control. However, the action mechanism underlying the effects of wrist-ankle acupuncture (WAA) versus electroacupuncture (EA) on CIBP remains unknown.

Methods: Thirty-two Wistar rats were divided into sham, CIBP, EA-treated and WAA-treated groups.

Inhibition of Mast Cell Degranulation Relieves Visceral Hypersensitivity Induced by Pancreatic Carcinoma in Mice.

Cancer pain induced by pancreatic carcinoma is one of the most common symptoms and is difficult to endure, especially in the advanced stage. Evidence suggests that mast cells are recruited and degranulate in enteric disease-related visceral hypersensitivity. However, whether mast cells promote the visceral pain induced by pancreatic carcinoma remains unclear.

Intravenous Dexmedetomidine Combined with Ultrasound-Guided Rectus Sheath Block for Open Gastrectomy: a Prospective Randomized Trial.

Purpose: To compare the incidences of positive hemodynamic response (HR > 100 beats min or SBP > 160 mmHg) during abdominal exploration and moderate pain after surgery, when using dexmedetomidine infusion and rectus sheath block.

Methods: One hundred patients undergoing open gastrectomy were randomized to receive rectus sheath block with ropivacaine (Group B, n = 25), initial loading dose of 0.6 μg kg dexmedetomidine, followed by a continuous infusion of 0.

TET1 Overexpression Mitigates Neuropathic Pain Through Rescuing the Expression of μ-Opioid Receptor and Kv1.2 in the Primary Sensory Neurons.

Peripheral nerve injury downregulates the expression of the μ-opioid receptor (MOR) and voltage-gated potassium channel subunit Kv1.2 by increasing their DNA methylation in the dorsal root ganglion (DRG). Ten-eleven translocation methylcytosine dioxygenase 1 (TET1) causes DNA demethylation.

Posttraumatic stress disorder: from diagnosis to prevention.

Posttraumatic stress disorder (PTSD) is a chronic impairment disorder that occurs after exposure to traumatic events. This disorder can result in a disturbance to individual and family functioning, causing significant medical, financial, and social problems. This study is a selective review of literature aiming to provide a general outlook of the current understanding of PTSD.

Role of MicroRNA-143 in Nerve Injury-Induced Upregulation of Dnmt3a Expression in Primary Sensory Neurons.

Peripheral nerve injury increased the expression of the DNA methyltransferase 3A () mRNA and its encoding Dnmt3a protein in injured dorsal root ganglia (DRG). This increase is considered as an endogenous instigator in neuropathic pain genesis through epigenetic silencing of pain-associated genes (such as ) in injured DRG. However, how DRG DNMT3a is increased following peripheral nerve injury is still elusive.

Trypsin-protease activated receptor-2 signaling contributes to pancreatic cancer pain.

Pain treatment is a critical aspect of pancreatic cancer patient clinical care. This study investigated the role of trypsin-protease activated receptor-2 (PAR-2) in pancreatic cancer pain. Pancreatic tissue samples were collected from pancreatic cancer (n=22) and control patients (n=22).

G9a participates in nerve injury-induced Kcna2 downregulation in primary sensory neurons.

Nerve injury-induced downregulation of voltage-gated potassium channel subunit Kcna2 in the dorsal root ganglion (DRG) is critical for DRG neuronal excitability and neuropathic pain genesis. However, how nerve injury causes this downregulation is still elusive. Euchromatic histone-lysine N-methyltransferase 2, also known as G9a, methylates histone H3 on lysine residue 9 to predominantly produce a dynamic histone dimethylation, resulting in condensed chromatin and gene transcriptional repression.

Identification of Early RET+ Deep Dorsal Spinal Cord Interneurons in Gating Pain.

The gate control theory (GCT) of pain proposes that pain- and touch-sensing neurons antagonize each other through spinal cord dorsal horn (DH) gating neurons. However, the exact neural circuits underlying the GCT remain largely elusive. Here, we identified a new population of deep layer DH (dDH) inhibitory interneurons that express the receptor tyrosine kinase Ret neonatally.

Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury-induced Nociceptive Hypersensitivity.

Background: Peripheral nerve injury-induced gene alterations in the dorsal root ganglion (DRG) and spinal cord likely participate in neuropathic pain genesis. Histone methylation gates gene expression. Whether the suppressor of variegation 3-9 homolog 1 (SUV39H1), a histone methyltransferase, contributes to nerve injury-induced nociceptive hypersensitivity is unknown.

Dorsal root ganglion transcriptome analysis following peripheral nerve injury in mice.

Background: Peripheral nerve injury leads to changes in gene expression in primary sensory neurons of the injured dorsal root ganglia. These changes are believed to be involved in neuropathic pain genesis. Previously, these changes have been identified using gene microarrays or next generation RNA sequencing with poly-A tail selection, but these approaches cannot provide a more thorough analysis of gene expression alterations after nerve injury.

Inhibition of GAP-43 by propentofylline in a rat model of neuropathic pain.

Neural plasticity within the spinal nociceptive network may be fundamental to the chronic nature of neuropathic pain. The relation of growth-associated protein-43 (GAP-43), a protein involved in the nerve fiber growth and sprouting, to pain hypersensitivity has been investigated. Glial activation and inflammatory cytokines released by microglia and astrocytes are considered to be involved in the neural sprouting and plasticity.

Down-regulation of GAP-43 by inhibition of caspases-3 in a rat model of neuropathic pain.

Background: Neuropathic pain remains a prevalent and persistent clinical problem due to incomplete understanding of its pathogenesis.

Objective: The present study aimed to investigate the role of caspase-3 in the neuropathic pain in rats with chronic constriction injury (CCI).

Methods: SD rats were randomly assigned four groups (n=18 per group): sham group, normal saline group (NS group), Z-DEVD-FMK group (DEVD group) and RNA interference group (siRNA group).

Effect of recombinant adenovirus coding for endomorphin-2 on neuropathic pain in rats.

Objective: To construct a transgene expressing human endomorphin-2 by linking the signal peptide of mouse nerve growth factor (PN) to a human endomorphin-2 DNA sequence containing a short linker recognized by the protease FURIN and test the analgesic effect of endomorphin-2 on neuropathic pain.

Methods: The transgene was inserted into the cosmid pAxCAwt to generate PN-EM-2-pAxCAwt. The recombinant adenovirus Ad-PNEM2 was packaged and propagated in HEK293 cells.

Small interference RNA targeting TLR4 gene effectively attenuates pulmonary inflammation in a rat model.

Objective: The present study was to investigate the feasibility of adenovirus-mediated small interference RNA (siRNA) targeting Toll-like receptor 4 (TLR4) gene in ameliorating lipopolysaccharide- (LPS-) induced acute lung injury (ALI).

Methods: In vitro, alveolar macrophages (AMs) were treated with Ad-siTLR4 and Ad-EFGP, respectively, for 12 h, 24 h, and 48 h, and then with LPS (100 ng/mL) for 2 h, and the function and expression of TLR4 were evaluated. In vivo, rats received intratracheal injection of 300 μL of normal saline (control group), 300 μL of Ad-EGFP (Ad-EGFP group), or 300 μL of Ad-siTLR4 (Ad-siTLR4 group) and then were intravenously treated with LPS (50 mg/kg) to induce ALI.

Acute PAR2 activation reduces GABAergic inhibition in the spinal dorsal horn.

We investigated the mechanism underlying inhibition of spinal dorsal horn GABAergic neurotransmission to elucidate the role of protease-activated receptor-2 (PAR2). Initially, we confirmed that PAR2 agonist SL-NH(2) applied intrathecally produced mechanical hyperalgesia. Then we performed patch-clamp experiments in substantia gelatinosa neurons of spinal cord slice, and found that spontaneous inhibitory post-synaptic currents (sIPSCs) were significantly decreased in both frequency and amplitude when neurons were incubated with PAR2 agonist SL-NH(2) for a brief time period (2 min).

Suppression of acute morphine withdrawal syndrome by adenovirus-mediated β-endorphin in rats.

Background: Endogenous β-endorphin (β-EP) in the central nervous system (CNS) is decreased upon opioid addiction. The current study examined whether exogenous β-EP, delivered using an adenoviral vector into the CNS could attenuate morphine withdrawal syndrome in rats.

Methods: The model of opioid-dependent rats was set up by receiving subcutaneous injection of morphine using an escalating regimen for 6days (5, 10, 20, 40, 50, 60mg/kg, three times/day).

Intrathecal siRNA against Toll-like receptor 4 reduces nociception in a rat model of neuropathic pain.

Background: Neuropathic pain is characterized by hyperalgesia, allodynia and spontaneous pain. It often occurs as a result of injury to peripheral nerves, dorsal root ganglions (DRG), spinal cord, or brain. Recent studies have suggested that Toll-like receptor 4 (TLR4) might play a role in neuropathic pain.

Bilateral downregulation of Nav1.8 in dorsal root ganglia of rats with bone cancer pain induced by inoculation with Walker 256 breast tumor cells.

Background: Rapid and effective treatment of cancer-induced bone pain remains a clinical challenge and patients with bone metastasis are more likely to experience severe pain. The voltage-gated sodium channel Nav1.8 plays a critical role in many aspects of nociceptor function.