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Objective: The present study investigated the incidence of and risk factors for emergence agitation (EA) in adult patients after thoracoscopic lung surgery. Design: A retrospective case-control study. Setting: Single-center university hospital. Participants: The study comprised 1,950 adult patients who underwent elective lung surgery from January to December 2016. Interventions: None. Measurements and Main Results: Preoperative, surgical, and anesthesia-related data were collected. EA was assessed with the Riker Sedation-Agitation Scale and defined as a Riker score ≥5. Univariate analyses and multivariate logistic regression analysis were used to identify risk factors for EA. The incidence of EA was 14.1%. The results of the multivariate analysis showed that male sex (odds ratio [OR] 1.877, 95% confidence interval [CI] 1.341-2.627), age ≥65 years (OR 1.424, 95% CI 1.074-1.889), body mass index ≥24 kg/m2 (OR 1.409, 95% CI 1.070-1.856), American Society of Anesthesiologists physical status Ⅲ or Ⅳ (OR 2.654, 95% CI 1.189-5.924), cigarette smoking (OR 1.553, 95% CI 1.108-2.177), duration of surgery (OR 1.006, 95% CI 1.003-1.009), intraoperative tachycardia (OR 1.721, 95% CI 1.058-2.802), intraoperative hypotension (OR 1.636, 95% CI 1.064-2.514), intraoperative hypertension (OR 1.608; 95% CI 1.056-2.448), and rescue analgesia (OR 1.810, 95% CI 1.235-2.653) were independent risk factors for EA. However, wound infiltration (OR 0.679, 95% CI 0.507-0.908) and the use of dexmedetomidine (OR 0.663, 95% CI 0.490-0.869) appeared to be protective factors against EA. Conclusion: EA is a common complication after thoracoscopic lung surgery, especially within a certain population. Adequate perioperative management, which comprises wound infiltration, the maintenance of intraoperative hemodynamic stability, sufficient analgesia, and the use of dexmedetomidine, should be adopted to reduce the incidence of EA. [ABSTRACT FROM AUTHOR]

Orofacial neuropathic pain caused by trigeminal nerve injury is a debilitating condition with limited therapeutic options. Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels regulate neuronal excitability and are involved in the development and maintenance of chronic pain. However, the effect of HCN channel activity in the Gasserian ganglion on trigeminal neuropathic pain has not been examined. We evaluated nociceptive behaviors after microinjection of the HCN channel blockers ZD7288 or ivabradine into the Gasserian ganglion in rats with trigeminal nerve injury. Both blockers dose-dependently ameliorated evoked and spontaneous nociceptive behavior in rats with trigeminal neuropathic pain. Moreover, the clinically available HCN channel blocker ivabradine showed a prolonged antinociceptive effect. In the Gasserian ganglion, HCN1 and HCN2 are major HCN isoforms. After trigeminal nerve injury, the counts of HCN1 as well as HCN2 immuno-positive punctae were increased in the ipsilateral Gasserian ganglions. These results indicate that the increased HCN channel activity in the Gasserian ganglion directly contributes to neuropathic pain resulting from trigeminal nerve injury.Perspective: Trigeminal nerve damage-induced orofacial pain is severe and more resistant to standard pharmacological treatment than other types of neuropathic pain. Our study suggests that targeting HCN channel activities in the Gasserian ganglion may provide an alternative treatment of trigeminal neuropathy including trigeminal neuralgia. [ABSTRACT FROM AUTHOR]

The number of studies on trigeminal nerve injury using animal models remains limited. A rodent model of trigeminal neuropathic pain was first developed in 1994, in which chronic constriction injury (CCI) is induced by ligation of the infraorbital nerve (IoN). This animal model has served as a major tool to study trigeminal neuropathic pain. Unfortunately, the surgical procedure in this model is complicated and far more difficult than ligation of peripheral nerves (eg, sciatic nerve). The aim of this study was to improve on the current surgical procedure of IoN ligation to induce trigeminal neuropathic pain in rats. We show that the IoN can be readily accessed through a small facial incision. CCI can be induced by ligation of a segment at the distal IoN (dIoN). This dIoN-CCI procedure is simple, minimally invasive, and time-saving. Our data show that the dIoN-CCI procedure consistently induced acute as well as chronic nociceptive behaviors in rats. Daily gabapentin treatment attenuated mechanical allodynia and reduced face-grooming episodes in dIoN-CCI rats.Perspective: The orofacial pain caused by trigeminal nerve damage is severe and perhaps more debilitating than other types of neuropathic pain. However, studies on trigeminal neuropathic pain remain limited. This is largely because of the lack of proper animal models because of the complexity of the existing surgical procedures required to induce trigeminal nerve injury. Our improved dIoN-CCI model is likely to make it more accessible to study the cellular and molecular mechanisms of neuropathic pain caused by trigeminal nerve damage. [ABSTRACT FROM AUTHOR]

MicroRNAs are short 21-22 nucleotide single strand RNAs that are involved in post-transcriptional regulation of gene expression. Most microRNAs are first transcribed as long primary microRNAs and then undergo a two step-wise sequential processing to yield single-stranded mature microRNAs. It has been suggested that the loop region of primary microRNAs plays an important role in regulating microRNA biogenesis and target recognition. However, despite the fact that several single nucleotide polymorphisms have been identified in mature microRNA sequences and are related to human diseases, it remains unclear whether and how the single nucleotide polymorphisms in the loop regions of primary microRNAs would affect the biogenesis and function of microRNAs. Herein, we provide evidence that primary microRNAs loop nucleotides control the accuracy and efficiency of microRNA processing. Accordingly, we identified 32 single nucleotide polymorphisms in the loop regions of human primary microRNAs using bioinformatics, and further validated three loss-of-function and one gain-of-function single nucleotide polymorphisms using dual-luciferase assays. Thus, these results reveal a critical regulatory role encoded in the loop nucleotides of primary microRNAs for microRNA processing and function. [ABSTRACT FROM AUTHOR]

Abstract: A multiplex loop-mediated isothermal amplification-RFLP (mLAMP-RFLP) was developed and validated for simultaneous detection of Salmonella strains and Shigella strains in milk. In this system, two sets of LAMP primers were designed to specifically target invA of Salmonella spp. and ipaH of Shigella spp. Under isothermal conditions at 63°C, ladder pattern of DNA bands could be amplified within 60min in the presence of genomic DNAs of Salmonella strains and Shigella strains, which could be distinguished between Salmonella spp. and Shigella spp. simultaneously based on the different ladder pattern of DNA bands and subsequent restriction enzyme analysis. The overall analysis time was approximately 20h including the enrichment of the bacterial cells, which greatly saved detection time. The sensitivity of mLAMP was found to be 100fg DNA/tube with genomic DNAs of Salmonella strains and Shigella strains, comparatively, multiplex PCR was 1pg DNA/tube. The mLAMP allowed the detection of milk sample artificially contaminated by Salmonella strains and Shigella strains at initial inoculation levels of approximate 5CFU/10mL. In conclusion, the mLAMP described here can potentially facilitate simultaneous monitoring of Salmonella and Shigella in a large number of food samples, which could be used as a primary screening method and as a supplement to classical detection method. [Copyright &y& Elsevier]

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels regulate neuronal excitability in both peripheral and central nerve systems. Emerging evidence indicates that HCN channels are involved in the development and maintenance of chronic pain. However, the impact of HCN channel activity in the thalamus on chronic pain has not been examined. In this report, we evaluated the effect on nociceptive behaviors after infusion of a HCN channel blocker ZD7288 into the ventral posterolateral (VPL) nucleus of the thalamus in rats with neuropathic pain or monoarthritis. We show that ZD7288 dose-dependently attenuated mechanical allodynia and thermal hyperalgesia in rats with chronic pain. In the thalamus, immunoreactivity of both HCN1 and HCN2 subunits was increased in both rat models. These results suggest that the increased HCN channel activity in the thalamus of the ascending nociceptive pathway contributes to both chronic neuropathic and inflammatory pain conditions. [ABSTRACT FROM AUTHOR]

Inflammation is extremely important in the development of cerebral ischemia/reperfusion injury. Pannexin 1 (Panx1) channel has been reported to activate inflammasome in astrocytes and be involved in ischemic injury, but this damage effect is reversed by a Panx1 inhibitor—probenecid. However, the mechanism of probenecid protects against cerebral ischemia/reperfusion injury remains unclear. In present study, we hypothesized that probenecid protected astrocytes from ischemia/reperfusion injury in vitro by modulating the inflammasome. Primary cultured neocortical astrocytes were exposed to oxygen–glucose deprivation/reoxygenation (OGD/RX) and probenecid was added in this model. Viability and nuclear morphology of astrocytes, production of reactive oxygen species (ROS), protein expressions of NLRP3 (NOD-like receptor protein 3), caspase-1, and AQP4 (Aquaporins 4), as well as release of cellular HMGB1 and IL-1β were observed to evaluate the effect and mechanisms of probenecid on OGD/reoxygenated astrocytes. Probenecid did not affect cell viability at concentrations of 1, 5, 10, and 100 μM but induced significant astrocytes death at 500 μM. Probenecid inhibited cell death and ROS generation in astrocytes subjected to 6 h of OGD and 24 h of reoxygenation. The expression levels of NLRP3, caspase-1, and AQP4 increased after 6 h of OGD, but probenecid treatment attenuated this increase. Moreover, the extracellular release of IL-1β and HMGB1 from OGD/reoxygenated astrocytes increased significantly. However, treatment by probenecid resulted in substantial reduction of these proteins levels in extracellular space. In conclusion, The Panx1 inhibitor, probenecid, which was administered before OGD, provided protective effects on the OGD/reoxygenation model of cultured astrocytes by modulating inflammasome activity and downregulating AQP4 expression. [ABSTRACT FROM AUTHOR]

Study Objective: To determine the incidence of major complications in patients undergoing regional anesthesia (RA) in China.Design: Multicenter prospective survey.Setting: Eleven teaching hospitals in China.Patients and Interventions: A total of 106,569 patients undergoing RA from April 1, 2009, to April 30, 2011, were involved.Measurement: Information on patients, types of surgery, and RA techniques was collected with a standardized chart. After RA, the patients were followed up by an investigator in each center for 1 to 3 weeks according to the patient's condition. Data were integrated and analyzed with a structured query language server system.Main Results: Among the patients undergoing RA, 37 developed major complications, including Horner syndrome (n = 9; 0.84/10,000), recurrent laryngeal nerve blockade (n = 6; 0.56/10,000), cardiac arrest (n = 1; 0.09/10,000), hematoma (n = 2; 0.19/10,000), seizures (n = 5; 0.46/10,000), catheter break (n = 1; 0.09/10,000), paraplegia (n = 1; 0.09/10,000), cauda equina syndrome (n = 2; 0.19/10,000), and extensive neuraxial block (n = 10; 0.94/10,000). The incidence of major RA complications varied from 0.8/10,000 to 18.8/10,000 among centers and was highest in cervical plexum block. Plastic surgery had the highest incidence of complications (19.0/10,000), most of which were recurrent extensive neuraxial block. The total incidence of major RA complications was 3.47/10,000.Conclusion: This large, multicenter, prospective survey revealed the incidence of major complications after RA in China's hospitals. Although severe complication like cardiac arrest is rare, it is distressing and challenging. Hence, there is still a room to improve on daily basis to further reduce complications related to RA. [ABSTRACT FROM AUTHOR]

Abstract: Previous studies have reported that T cell deficiency reduced infarct sizes after transient middle cerebral artery (MCA) suture occlusion in mice. However, how reperfusion and different models affect the detrimental effects of T cells have not been studied. We investigated the effects of T cell deficiency in nude rats using two stroke models and compared their infarct sizes with those in WT rats. In the distal MCA occlusion (MCAo) model, the distal MCA was permanently occluded and the bilateral common carotid arteries (CCAs) were transiently occluded for 60min. In the suture MCAo model, the MCA was transiently occluded for 100min by the insertion of a monofilament suture. Our results showed that T cell deficiency resulted in about a 50% reduction in infarct size in the suture MCAo model, whereas it had no effect in the distal MCAo model, suggesting the protective effects of T cell deficiency are dependent on the ischemic model used. We further found more total T cells, CD4 T cells and CD8 T cells in the ischemic brains of WT rats in the suture MCAo model than in the distal MCAo model. In addition, we detected more CD68-expressing macrophages in the ischemic brains of WT rats than in nude rats in the suture MCAo but not the distal MCAo model. Lymphocyte reconstitution in nude rats resulted in larger infarct sizes in the suture MCAo, but not in the distal MCAo stroke model. The results of regional CBF measurement indicated a total reperfusion in the MCAo model but only a partial reperfusion in the distal MCAo model. In conclusion, the protective effects of T cell deficiency on brain injury are dependent on the ischemic model used; likely associated with different degrees of reperfusion. [Copyright &y& Elsevier]