Aconite contains four highly toxic diester-diterpene alkaloids (DDAs): aconitine, mesaconitine, hypaconitine, and jesaconitine. The efficacy of charcoal hemoperfusion (CHP) in treating aconite poisoning has recently been reported in several East Asian cases. This study evaluated the potential efficacy of CHP using two simulation experiments and one clinical case. One simulation examined the saturated adsorption capacity of activated charcoal for aconitine, whereas the other assessed the time course of perfusate aconitine concentrations at the inlet and outlet of an activated-charcoal column. The clinical case involved a 61-year-old female with stage V chronic kidney disease who underwent CHP for an electrical storm due to aconite poisoning. Her initial plasma DDA concentration was markedly higher than those reported in previous cases. This elevated concentration raises the possibility of substantial ingestion, although the exact amount cannot be determined. CHP was initiated 2 hr after ingestion and continued for 7 hr. In the simulations, activated charcoal showed a saturated adsorption capacity of 110 mg of aconitine per gram, and the column removed most aconitine in a single pass. In the clinical case, plasma DDA concentrations rapidly decreased after 7 hr of CHP, with a clearance rate of approximately 70 mL/min at a blood-flow rate of 100 mL/min. The terminal elimination half-life of plasma DDAs was 109.5 hr, likely reflecting the patient's underlying kidney disease. Taken together, these findings suggest that CHP may contribute to DDA elimination under severe renal impairment, although its broader clinical relevance remains uncertain.

Background:Labor epidural analgesia is recognized worldwide as the gold standard for maternal pain relief during delivery and has been increasingly used in Japan. However, studies on labor analgesia in Japan are scarce, and evaluation of neonatal outcomes associated with this procedure remains limited. Among the key aspects in the safety evaluation of labor epidural analgesia are the potential effects on neonatal umbilical arterial blood pH (UmA-pH) and Apgar score. Therefore, we determined whether labor epidural analgesia during vaginal delivery is associated with neonatal UmA-pH and Apgar score among women delivering in Japan. Methods:In this birth cohort study, we prospectively analyzed data collected from the Japan Environment and Children's Study (JECS). We included Japanese pregnant women who had singleton vaginal deliveries. The primary exposure was labor epidural analgesia, and the primary outcomes were UmA-pH and Apgar score at 1 and 5 min following birth. Multivariate logistic regression was employed to examine the associations between labor epidural analgesia and neonatal outcomes, with adjustment for potential confounders. Adjusted odds ratios (aOR) and 95% confidence intervals (CIs) were reported. Furthermore, a sensitivity analysis using stabilized inverse probability of treatment weighting (IPTW) was conducted. Results:Of the 96,443 women who had singleton deliveries in the JECS, 55,227 were included in the final analysis, 1,311 (2.4%) of whom received labor epidural analgesia. In the multivariate logistic regression analysis, a statistically significant association was observed between labor epidural analgesia and a 1-min Apgar score < 7 (aOR: 1.54; 95% CI: 1.03-2.29). However, only one neonate in the labor epidural analgesia group had a 5-min Apgar score < 7. Moreover, no significant association was observed between labor epidural analgesia and UmA-pH < 7.2 (aOR: 0.94; 95% CI: 0.76-1.17). In the IPTW-based sensitivity analysis, the effect estimates were consistent in direction with the primary analysis, supporting the robustness of the main findings. Conclusion:In this large cohort of singleton vaginal births in Japan, the use of labor epidural analgesia had little to no clinically meaningful effect on neonatal outcomes, including UmA-pH < 7.2 and Apgar score < 7. These findings support informed decision-making for pregnant women in Japan who are considering labor epidural analgesia.

Massive intraoperative hemorrhage is a time-critical event requiring simultaneous hemodynamic resuscitation, bleeding source control, transfusion support, equipment preparation, and escalation to multidisciplinary support. This technical report provides, to our knowledge, the first English-language description of the Systematic Urgent Team Response in the Operating Room (SUTO) protocol for intraoperative massive hemorrhage. The protocol was previously developed and reported in Japanese as an institution-specific response system. This English-language report was prepared with permission from the original journal and describes the protocol for an international readership, with additional emphasis on simulation-based preparation and clinical deployment during an actual episode of intraoperative massive hemorrhage. The SUTO protocol was designed to convert the general principles of hemorrhage management into a locally executable, role-based workflow, with predefined procedures for emergency activation, command assignment, task allocation, transfusion support, equipment mobilization, and escalation to cardiovascular surgery and interventional radiology support. The protocol was posted at the entrance of each operating room as an environmental cognitive aid and linked to a dedicated massive hemorrhage cart. Multidisciplinary in situ simulation was conducted using actual operating room equipment to rehearse emergency activation, parallel task execution, transfusion preparation, and escalation pathways. Clinical deployment is illustrated by an unexpected massive hemorrhage caused by splenic artery injury during surgery for esophagogastric junction cancer. Emergency activation, commander declaration, transfusion preparation, equipment mobilization, and consultation with cardiovascular, hepatopancreatobiliary, and interventional radiology teams proceeded in parallel. Definitive hemostasis was achieved by proximal and distal ligation of the injured splenic artery, and the patient was discharged on postoperative day 17. Although causality cannot be inferred from a single clinical deployment, this report suggests that the SUTO protocol may provide a shared operational framework for rapid multidisciplinary coordination during high-acuity operating room crises. Regular simulation and feedback-driven revision are required to maintain organizational readiness as staff and workflows change.

Chronic postsurgical pain (CPSP) is being increasingly recognized as an important clinical problem. The purpose of this prospective multicenter study was to evaluate the prevalence and risk factors of CPSP at 3 months after surgery in a Japanese population. Adult patients who underwent lung cancer surgery (L) or knee arthroplasty (K) at university hospitals in Japan and provided informed consent were included. Perioperative demographic, clinical, and psychological data were collected. Postsurgical pain scores were assessed via face-to-face interviews at each time point. We also investigated analgesic use at each time point in patients with CPSP. A total of 494 (L) and 194 (K) patients completed our interviews at all visits up to 3 months after surgery. The prevalence of clinically relevant CPSP was 10

Aconite contains four highly toxic diester-diterpene alkaloids, including aconitine, mesaconitine, hypaconitine, and jesaconitine, in all plant parts. Aconite has been used as for suicide, murder, and as an arrow poison since ancient Greek and Roman times. Ventricular tachyarrhythmias are the most common cause of death in aconite poisoning, and antiarrhythmic drugs and cardioversion are ineffective. A 61-year-old woman ingested the crushed raw roots of a single aconite plant. An ambulance brought her to the Tottori University Hospital 30 min after ingestion. She had a history of chronic stage 5 kidney disease but was not on dialysis. Her heart rate (HR) was 120 bpm upon arrival. The patient developed sustained supraventricular tachycardia (SVT) at an HR of 165 bpm with frequent premature ventricular contractions (PVCs) 15 min after arrival. She then developed sustained monomorphic ventricular tachycardia (VT) at an HR of 200 bpm 20 min after arrival, which progressed to pulseless polymorphic VT. Cardioversion was unsuccessful. External cardiac massage restored spontaneous circulation; however, her underlying rhythm remained sustained SVT with frequent PVCs. These arrhythmias repeatedly led to circulatory arrest. She was administered six intravenous boluses of 2 g of MgSO4 in the emergency department, which prevented her from going into sustained pulseless VT. Hemoperfusion (HP) with activated charcoal was performed 1.5 h after arrival. The aconitine, mesaconitine, and hypaconitine plasma concentrations were high at 8.9, 23.5, and 5.5 ng/mL, respectively, before the start of HP but decreased to 1.7, 4.0, and 2.7 ng/mL, respectively, after 7 h of HP. She returned to sinus rhythm on the second day of hospitalization; however, the patient required maintenance hemodialysis. We concluded that high-dose IV MgSO4 is an effective treatment for fatal tachyarrhythmias due to aconite poisoning, and that in cases of renal failure, HP may be required to remove aconite toxins from the body.

It remains to be elucidated whether Ca2+ antagonists induce pharmacological preconditioning to protect the heart against ischemia/reperfusion injury. The aim of this study was to determine whether and how pretreatment with a Ca2+ antagonist, azelnidipine, could protect cardiomyocytes against hypoxia/reoxygenation (H/R) injury in vitro. Using HL-1 cardiomyocytes, we studied effects of azelnidipine on NO synthase (NOS) expression, NO production, cell death and apoptosis during H/R. Action potential durations (APDs) were determined by the whole-cell patch-clamp technique. Azelnidipine enhanced endothelial NOS phosphorylation and NO production in HL-1 cells under normoxia, which was abolished by a heat shock protein 90 inhibitor, geldanamycin, and an antioxidant, N-acetylcysteine. Pretreatment with azelnidipine reduced cell death and shortened APDs during H/R. These effects of azelnidipine were diminished by a NOS inhibitor, L-NAME, but were influenced by neither a T-type Ca2+ channel inhibitor, NiCl2, nor a N-type Ca2+ channel inhibitor, ω-conotoxin. The azelnidipine-induced reduction in cell death was not significantly enhanced by either additional azelnidipine treatment during H/R or increasing extracellular Ca2+ concentrations. RNA sequence (RNA-seq) data indicated that azelnidipine-induced attenuation of cell death, which depended on enhanced NO production, did not involve any significant modifications of gene expression responsible for the NO/cGMP/PKG pathway. We conclude that pretreatment with azelnidipine protects HL-1 cardiomyocytes against H/R injury via NO-dependent APD shortening and L-type Ca2+ channel blockade independently of effects on gene expression.

Aconite contains four highly toxic diester-diterpene alkaloids, including aconitine, mesaconitine, hypaconitine, and jesaconitine, in all plant parts. Aconite has been used as for suicide, murder, and as an arrow poison since ancient Greek and Roman times. Ventricular tachyarrhythmias are the most common cause of death in aconite poisoning, and antiarrhythmic drugs and cardioversion are ineffective. A 61-year-old woman ingested the crushed raw roots of a single aconite plant. An ambulance brought her to the Tottori University Hospital 30 min after ingestion. She had a history of chronic stage 5 kidney disease but was not on dialysis. Her heart rate (HR) was 120 bpm upon arrival. The patient developed sustained supraventricular tachycardia (SVT) at an HR of 165 bpm with frequent premature ventricular contractions (PVCs) 15 min after arrival. She then developed sustained monomorphic ventricular tachycardia (VT) at an HR of 200 bpm 20 min after arrival, which progressed to pulseless polymorphic VT. Cardioversion was unsuccessful. External cardiac massage restored spontaneous circulation; however, her underlying rhythm remained sustained SVT with frequent PVCs. These arrhythmias repeatedly led to circulatory arrest. She was administered six intravenous boluses of 2 g of MgSO4 4 in the emergency department, which prevented her from going into sustained pulseless VT. Hemoperfusion (HP) with activated charcoal was performed 1.5 h after arrival. The aconitine, mesaconitine, and hypaconitine plasma concentrations were high at 8.9, 23.5, and 5.5 ng/mL, respectively, before the start of HP but decreased to 1.7, 4.0, and 2.7 ng/mL, respectively, after 7 h of HP. She returned to sinus rhythm on the second day of hospitalization; however, the patient required maintenance hemodialysis. We concluded that high-dose IV MgSO4 4 is an effective treatment for fatal tachyarrhythmias due to aconite poisoning, and that in cases of renal failure, HP may be required to remove aconite toxins from the body.

当院では近年の手術件数急増などにより麻酔科医の業務負担が深刻化し，麻酔科術後回診は不十分であった．2018年度より麻酔科医の補助業務を担う周麻酔期看護師が専従で配置され，麻酔科医と麻酔科管理の全症例を対象に術後回診を開始した．周麻酔期看護師は手術翌日の患者状態を電子カルテで把握した後，麻酔科医とともに術後回診を行った．この方法により麻酔科医の負担が軽減し，平日の勤務時間内の術後回診実施率の向上と病院の利益増収につながった．今後は，周麻酔期看護師が麻酔科医と各診療科の医師や病棟看護師間のコンサルタントとしての役割を担い，患者が適切な術後鎮痛や早期回復を享受できる環境を構築することが目標となる．

Coenzyme Q10 (CoQ10) promotes wound healing in vitro and in vivo. However, the molecular mechanisms underlying the promoting effects of CoQ10 on wound repair remain unknown. In the present study, we investigated the molecular mechanisms through which CoQ10 induces wound repair using a cellular wound-healing model. CoQ10 promoted wound closure in a dose-dependent manner and wound-mediated cell polarization after wounding in HaCaT cells. A comparison with other CoQ homologs, benzoquinone derivatives, and polyisoprenyl compounds suggested that the whole structure of CoQ10 is required for potent wound repair. The phosphorylation of Akt after wounding and the plasma membrane translocation of Akt were elevated in CoQ10-treated cells. The promoting effect of CoQ10 on wound repair was abrogated by co-treatment with a phosphatidylinositol 3-kinase (PI3K) inhibitor. Immuno-histochemical and biochemical analyses showed that CoQ10 increased the localization of caveolin-1 (Cav-1) to the apical membrane domains of the cells and the Cav-1 content in the membrane-rich fractions. Depletion of Cav-1 suppressed CoQ10-mediated wound repair and PI3K/Akt signaling activation in HaCaT cells. These results indicated that CoQ10 increases the translocation of Cav-1 to the plasma membranes, activating the downstream PI3K/Akt signaling pathway, and resulting in wound closure in HaCaT cells.

Case reports from as early as the 1970s have shown that intravenous injection of even a small dose of volatile anesthetics result in fatal lung injury. Direct contact between volatile anesthetics and pulmonary vasculature triggers chemical damage in the vessel walls. A wide variety of factors are involved in lung ischemia-reperfusion injury (LIRI), such as pulmonary endothelial cells, alveolar epithelial cells, alveolar macrophages, neutrophils, mast cells, platelets, proinflammatory cytokines, and surfactant. With a constellation of factors involved, the assessment of the protective effect of volatile anesthetics in LIRI is difficult. Multiple animal studies have reported that with regards to LIRI, sevoflurane demonstrates an anti-inflammatory effect in immunocompetent cells and an anti-apoptotic effect on lung tissue. Scattered studies have dismissed a protective effect of desflurane against LIRI. While a single-center randomized controlled trial (RCT) found that volatile anesthetics including desflurane demonstrated a lung-protective effect in thoracic surgery, a multicenter RCT did not demonstrate a lung-protective effect of desflurane. LIRI is common in lung transplantation. One study, although limited due to its small sample size, found that the use of volatile anesthetics in organ procurement surgery involving "death by neurologic criteria" donors did not improve lung graft survival. Future studies on the protective effect of volatile anesthetics against LIRI must examine not only the mechanism of the protective effect but also differences in the effects of different types of volatile anesthetics, their optimal dosage, and the appropriateness of their use in the event of marked alveolar capillary barrier damage.

Ventilation in the prone position improves the prognosis of patients with severe acute respiratory distress syndrome (ARDS). Contraindications to ventilation in this position include unstable systemic circulation. Only a few reports exist on the effects of prone ventilation in respiratory failure on systemic circulation. This animal study compared systemic hemodynamic changes between supine and prone positions in anesthetized rabbits under acute systemic hypoxia (breathing 15% O-2). Cardiac output and the systemic O-2 extraction ratio increased under the hypoxia, but only in the supine group. Besides, the rate pressure product was higher in the prone group than in the supine group. This study showed that prone ventilation increases myocardial O-2 consumption and suppresses compensatory mechanisms to maintain aerobic metabolism during systemic hypoxia. First of all, it will be necessary to examine the effect of prone ventilation on the O-2 supply-demand balance in the ARDS model.

Pain during intravenous propofol injection occurs in 60% to 70% of patients.1Jalota L Kalira V George E et al.Prevention of pain on injection of propofol: Systematic review and meta-analysis.BMJ. 2011; 342: d1110Crossref PubMed Scopus (155) Google Scholar Anterior chest wall pain secondary to propofol injection previously has not been reported. A 54-year-old man with a history of hemodialysis for chronic renal failure presented for arteriovenous graft revision under general anesthesia. Because the left and right forearms, antecubital fossae, and upper arms previously had been used for vascular access, the left thigh was selected for a new arteriovenous graft. Computed tomography revealed collateral circulation between the subcutaneous veins in the anterior chest and the veins in the upper extremities on each side (Fig 1). A 22-gauge intravenous catheter was inserted into the dorsum of the left hand. Immediately after injection of 200 µg of fentanyl, a target-controlled infusion device (TE-371; Terumo, Tokyo, Japan) was used to administer propofol (1% Diprivan Injection Kit; Aspen Japan, Tokyo, Japan) with a target plasma concentration of 4.0 µg/mL. The patient complained of superficial left anterior chest pain within 30 seconds of propofol administration until he lost consciousness approximately 90 seconds later. Electrocardiography revealed no ischemic or hemodynamic changes, and we ascribed his pain to the propofol injection. Our patient most likely had chronically impaired venous return involving the axillary and subclavian veins in both upper limbs. Collateral circulation between the bilateral upper limb veins and the subcutaneous veins of the anterior chest wall most likely developed in compensation.2Koratala A Bhattacharya D Chamarthi G. Blood finds its own way: Axillary vein thrombosis with extensive chest-wall collaterals.Clin Case Rep. 2018; 6: 1917-1918Crossref PubMed Scopus (1) Google Scholar It is believed that venous blood from the upper limbs returns to the brachiocephalic vein from the subcutaneous veins of the anterior chest wall via the internal thoracic vein.3Drake RL Vogl W Mitchell AW. Gray's anatomy for students. Churchill Livingstone Elsevier, Philadelphia, PA2010Google Scholar During the equilibrium phase of the dynamic computed tomography scan, stagnation of the contrast medium was observed bilaterally in the subcutaneous veins of the chest wall (Fig 1, B). Therefore, the left anterior chest pain most likely originated in the left upper limb during the intravenous injection of propofol. The authors thank Editage (www.editage.com) for English language editing. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Myocardial ischemia/reperfusion injury worsens in the absence of nitric oxide synthase (NOS). Cilnidipine, a Ca2+ channel blocker, has been reported to activate endothelial NOS (eNOS) and increases nitric oxide (NO) in vascular endothelial cells. We examined whether pretreatment with cilnidipine could attenuate cardiac cell deaths including apoptosis caused by hypoxia/reoxygenation (H/R) injury. HL-1 mouse atrial myocytes as well as H9c2 rat ventricular cells were exposed to H/R, and cell viability was evaluated by an autoanalyzer and flow cytometry; eNOS expression, NO production, and electrophysiological properties were also evaluated by western blotting, colorimetry, and patch clamping, respectively, in the absence and presence of cilnidipine. Cilnidipine enhanced phosphorylation of eNOS and NO production in a concentration-dependent manner, which was abolished by siRNAs against eNOS or an Hsp90 inhibitor, geldanamycin. Pretreatment with cilnidipine attenuated cell deaths including apoptosis during H/R; this effect was reproduced by an NO donor and a xanthine oxidase inhibitor. The NOS inhibitor L-NAME abolished the protective action of cilnidipine. Pretreatment with cilnidipine also attenuated H9c2 cell death during H/R. Additional cilnidipine treatment during H/R did not significantly enhance its protective action. There was no significant difference in the protective effect of cilnidipine under normal and high Ca2+ conditions. Action potential duration (APD) of HL-1 cells was shortened by cilnidipine, with this shortening augmented after H/R. L-NAME attenuated the APD shortening caused by cilnidipine. These findings indicate that cilnidipine enhances NO production, shortens APD in part by L-type Ca2+ channel block, and thereby prevents HL-1 cell deaths during H/R.

Background Breathing during a marathon is often empirically conducted in a so-called "2:2 breathing rhythm," which is based on a four-phase cycle, consisting of the 1st and 2nd inspiratory and the 1st and 2nd expiratory phases. We developed a prototype ventilator that can perform intermittent positive pressure ventilation, mimicking the breathing cycle of the 2:2 breathing rhythm. This mode of ventilation was named the marathoners' breathing rhythm ventilation (MBV). We hypothesized that MBV may have a lung protective effect. Methods We examined the effects of the MBV on the pulmonary pre-edema model in isolated perfused rabbit lungs. The pulmonary pre-edema state was induced using bloodless perfusate with low colloid osmotic pressure. The 14 isolated rabbit lung preparations were randomly divided into the conventional mechanical ventilation (CMV) group and MBV group, (both had an inspiratory/expiratory ratio of 1/1). In the CMV group, seven rabbit lungs were ventilated using the Harvard Ventilator 683 with a tidal volume (TV) of 8 mL/kg, a respiratory rate (RR) of 30 cycles/min, and a positive end-expiratory pressure (PEEP) of 2 cmH(2)O for 60 min. In the MBV group, seven rabbit lungs were ventilated using the prototype ventilator with a TV of 6 mL/kg, an RR of 30 cycles/min, and a PEEP of 4 cmH(2)O (first step) and 2 cmH(2)O (second step) for 60 min. The time allocation of the MBV for one cycle was 0.3 s for each of the 1st and 2nd inspiratory and expiratory phases with 0.2 s of intermittent resting between each phase. Results Peak airway pressure and lung wet-to-dry ratio after 60 min of ventilation were lower in the MBV group than in the CMV group. Conclusion MBV was considered to have a lung-protective effect compared to CMV.

Rationale: Coronary angiography (CAG) findings of acute myocardial infarction (AMI) in pregnant women are characterized by a high incidence of normal coronary arteries. This is the first report of AMI with normal coronary arteries during pregnancy, showing coronary spasm and pregnancy-related acquired protein S (PS) deficiency. Patient concerns: A 30-year-old Japanese woman was admitted to an emergency department. One hour before admission, she developed sudden onset of precordial discomfort, back pain, and dyspnea. She was a primigravida at 39 weeks' gestation and had no abnormality in the pregnancy thus far. She had no history of heart disease, diabetes, hypertension, dyslipidemia, deep vein thrombosis (DVT), smoking, or oral contraceptive use and no family history of ischemic heart disease, hemostasis disorder, or DVT. She did not take any medication. Diagnosis: Electrocardiography showed ST-segment elevations in leads II, III, aVF, and V2-V6. Heart-type fatty acid-binding protein was positive. Echocardiography showed hypokinesis of the anterior interventricular septum and inferior wall. Continuous intravenous infusion of isosorbide dinitrate was initiated. Coronary computed tomography angiography revealed diffuse narrowing of the apical segment of the left anterior descending coronary artery. Three hours after admission, troponin T became positive, and the following enzymes reached their peak levels: creatine kinase (CK), 1,886U/L; CK-muscle/brain, 130U/L. She was diagnosed with transmural AMI due to severe coronary spasm and administered benidipine hydrochloride. Five hours after admission, premature membrane rupture occurred. Interventions: Emergency cesarean section was performed. There were no anesthetic or obstetrical complications during the operation. On postpartum day 1, the free PS antigen level was low (29%). On postpartum day 18, she was discharged with no reduction in physical performance. Outcomes: Four months after the infarction, CAG showed normal coronary arteries. Acetylcholine provocation test showed diffuse vasospasm in the coronary artery. She was advised that her next pregnancy should be carefully planned. Two years after delivery, free PS antigen level was within normal range, at 86%. She had not experienced recurrence of angina during the 2-year period. Her child was also developing normally. Lessons: In addition to coronary spasm, pregnancy-related acquired PS deficiency may be involved in AMI etiology.

Small gauze is used in laparoscopy; therefore, retention of gauze can occur. We experienced a case of retention of a radiopaque thread that ruptured from a piece of gauze and moved into the peritoneum during a scheduled laparoscopy. The patient was a 65-year-old woman who underwent laparoscopic-assisted transverse colon resection for transverse colon cancer. A commercial gauze commonly used for laparoscopy was used during the surgery. To more easily identify the gauze during surgery, radiopaque threads extending up to 3.0 cm from the two diagonal corners of the gauze body were attached. After wound closure, radiography showed a radiopaque thread-like substance in the abdomen. Minor laparotomy was performed, and part of the radiopaque thread was discovered. On postoperative day 22, the patient was in remission and discharged.

Post-septic neurological and psychiatric illness (PSNPI) including dementia and depression may be observed after sepsis. However, the etiology of PSNPI and therapeutic treatment of PSNPI are unclear. We show that glutamate produced from microglia through the activity of system xc− plays a role in PSNPI. We established a mouse model of PSNPI by lipopolysaccharide (LPS) treatment that shows a disturbance of short/working memory and depression-like hypoactivity. Glutamate receptor antagonists (MK801 and DNQX) reduced these phenotypes, and isolated microglia from LPS-treated mice released abundant glutamate. We identified system xc− as a source of the extracellular glutamate. xCT, a component of system xc−, was induced and expressed in microglia after LPS treatment. In xCT knockout mice, PSNPI were decreased compared to those in wildtype mice. Moreover, TNF-α and IL-1β expression in wildtype mice was increased after LPS treatment, but inhibited in xCT knockout mice. Thus, system xc− in microglia may be a therapeutic target for PSNPI. The administration of sulfasalazine, an inhibitor of xCT, in symptomatic and post-symptomatic mice improved PSNPI. Our results suggest that glutamate released from microglia through system xc− plays a critical role in the manifestations of PSNPI and that system xc− may be a therapeutic target for PSNPI.

We performed a multicenter observational study to assess the prevalence and risk factors of persistent pain after lung cancer surgery and total knee arthroplasty (TKA) in the Japanese population. After receiving Ethics Committee approval, a retrospective chart review was performed for patients who underwent surgery at seven university hospitals in Japan in 2013. A total of 511 patients who underwent lung cancer surgery and 298 patients who underwent TKA were included. The prevalence of chronic postsurgical pain (CPSP) at 3 and 6 months was 18 and 12% after lung surgery and 49 and 33% after TKA, respectively. The prevalence of analgesic use at 3 and 6 months was 16 and 9% after lung surgery and 34 and 22% after TKA, respectively. In both groups, preoperative analgesic use was associated with CPSP. Anesthetic methods or techniques during both types of surgery did not significantly affect the prevalence of CPSP. This is the first study in which the prevalence of CPSP after lung surgery and TKA in Japanese population was extensively evaluated in a multicenter trial. Further prospective studies are needed to confirm the prevalence of CPSP in the Japanese population and to identify risk factors and prevention methods.

We investigated the expansion of stacking faults (SFs) under a high current pulse stress in detail. In situ observations showed bar-shaped SFs and two types of triangle SFs with different nucleation sites. The calculated partial dislocation velocity of the bar-shaped SFs was four times faster than that of the triangle SFs. The temperature dependence of the partial dislocation velocity was used to estimate activation energies of 0.23±0.02 eV for bar-shaped SFs and 0.27±0.05 eV for triangle SFs. We also compared the electrical characteristics before and after the stress. The forward voltage drop slightly increased by 0.05 V, and the leakage current did not increase.