GWAS Reveals a Novel Candidate Gene CmoAP2/ERF in Pumpkin (Cucurbita moschata) Involved in Resistance to Powdery Mildew.

Pumpkin (Cucurbita moschata Duchesne ex Poir.) is a multipurpose cash crop rich in antioxidants, minerals, and vitamins; the seeds are also a good source of quality oils. However, pumpkin is susceptible to the fungus Podosphaera xanthii, an obligate biotrophic pathogen, which usually causes powdery mildew (PM) on both sides of the leaves and reduces photosynthesis. The fruits of infected plants are often smaller than usual and unpalatable. This study identified a novel gene that involves PM resistance in pumpkins through a genome-wide association study (GWAS). The allelic variation identified in the CmoCh3G009850 gene encoding for AP2-like ethylene-responsive transcription factor (CmoAP2/ERF) was proven to be involved in PM resistance. Validation of the GWAS data revealed six single nucleotide polymorphism (SNP) variations in the CmoAP2/ERF coding sequence between the resistant (IT 274039 [PMR]) and the susceptible (IT 278592 [PMS]). A polymorphic marker (dCAPS) was developed based on the allelic diversity to differentiate these two haplotypes. Genetic analysis in the segregating population derived from PMS and PMR parents provided evidence for an incomplete dominant gene-mediated PM resistance. Further, the qRT-PCR assay validated the elevated expression of CmoAP2/ERF during PM infection in the PMR compared with PMS. These results highlighted the pivotal role of CmoAP2/ERF in conferring resistance to PM and identifies it as a valuable molecular entity for breeding resistant pumpkin cultivars.

Intraoperative dexmedetomidine attenuates norepinephrine levels in patients undergoing transsphenoidal surgery: a randomized, placebo-controlled trial.

BACKGROUND: Dexmedetomidine has sympatholytic effects. We investigated whether dexmedetomidine could attenuate stress responses in patients undergoing endoscopic transnasal transseptal transsphenoidal surgery. METHODS: Forty-six patients were randomized to receive a continuous infusion of 0.9% saline (n = 23) or dexmedetomidine (n = 23). Immediately after general anesthesia induction, the dexmedetomidine group received a loading dose of 1 mcg/kg dexmedetomidine over 10 min, followed by a maintenance dose of 0.2-0.7 mcg/kg/h and the control group received 0.9% saline at the same volume until 30 min before the end of surgery. Serum levels of epinephrine, norepinephrine, and glucose were assessed before surgery (T1) and the end of drug infusion (T2). The primary outcome was the change in norepinephrine levels between the two time points. RESULTS: Changes (T2-T1 values) in perioperative serum norepinephrine levels were significantly greater in the dexmedetomidine group than in the control group (median difference, 56.9 pg/dL; 95% confidence interval, 20.7 to 83.8 pg/dL; P = 0.002). However, epinephrine level changes did not show significant intergroup differences (P = 0.208). Significantly fewer patients in the dexmedetomidine group than in the control group required rescue analgesics at the recovery area (4.3% vs. 30.4%, P = 0.047). CONCLUSIONS: Intraoperative dexmedetomidine administration reduced norepinephrine release and rescue analgesic requirement. Dexmedetomidine might be used as an anesthetic adjuvant in patients undergoing transnasal transseptal transsphenoidal surgery. TRIAL REGISTRATION: Clinical Trial Registry of Korea, identifier: KCT0003366; registration date: 21/11/2018; presenting author: Ji Seon Jeong.

Effects of continuous positive airway pressure in patients at high risk of obstructive sleep apnea during propofol sedation after spinal anesthesia.

In patients with obstructive sleep apnea, short-term use of a continuous positive airway pressure mask improves oxygenation, decreases the apnea-hypopnea index, and reduces hemodynamic instability. In this study, we investigated the effects of use of a continuous positive airway pressure mask in patients at high risk of obstructive sleep apnea during propofol sedation after spinal anesthesia. Forty patients who underwent propofol sedation after spinal anesthesia for transurethral bladder or prostate resection with a STOP-Bang score of 3 or more were enrolled in this study. Patients were randomly divided into two groups: a simple oxygen mask group (n = 20) and a continuous positive airway pressure mask group (n = 20). After spinal anesthesia, propofol was injected at a target concentration of 1.3 mcg/ml via a target concentration control injector. ApneaLink™ was applied to all patients. Patients in the simple oxygen mask group were administered oxygen at a rate of 6 L/min through a simple facial mask. Patients in the CPAP mask group were connected to a pressurizer, and oxygen (6 L/min, 5-15 cm H2O) was administered. Blood pressure, heart rate, respiratory rate, and oxygen saturation were recorded preoperatively, after spinal anesthesia, and every 5 min after the injection of propofol to observe hemodynamic changes. Apnea-hypopnea index was estimated using ApneaLink™. There were no significant differences in hemodynamic changes between the two groups. Apnea-hypopnea index was significantly reduced in the continuous positive airway pressure mask group compared to the simple facial mask group. Application of a continuous positive airway pressure mask in a patient at high risk of obstructive sleep apnea can lower the incidence of obstructive sleep apnea during sedation without a significant effect on hemodynamic stability.

The effect of fluvastatin on cardiac fibrosis and angiotensin-converting enzyme-2 expression in glucose-controlled diabetic rat hearts.

Independently of the lipid-lowering effects, statin has been reported to attenuate the development of diabetic cardiomyopathy. However, the effect of statin in glucose-controlled diabetic condition has not been demonstrated. We evaluated the effect of fluvastatin on cardiac function, fibrosis, and angiotensin-converting enzyme-2 (ACE2) expression in glucose-controlled diabetic rats. Male Wistar rats were randomly divided into four groups: control (Group C), diabetes (Group D), diabetes with insulin (Group I), and diabetes with insulin and fluvastatin (Group I+F). Diabetes was induced by a single injection of streptozotocin (65 mg/kg). After 8 weeks, the hearts were extracted following echocardiographic evaluation. Cardiac fibrosis was analyzed using Masson's trichrome stain. Collagens I and III and ACE2 expressions were evaluated by immunohistochemistry and western blot. Group D showed reduced cardiac systolic function compared to the other groups (all P < 0.05). However, diastolic function estimated by E/A ratio was significantly decreased in groups D and I (median: 0.88 and 1.45, respectively) compared to groups C and I+F (2.97 and 2.15) (all P < 0.05). Cardiac fibrosis was more severe in groups D and I than in groups C and I+F (all P < 0.05) on Masson's trichrome stain. On immunohistochemistry, ACE2 expression was significantly decreased only in group D (all P < 0.05). However, collagen I and III showed higher expressions in group D compared to groups C and I+F while no significant difference was observed compared with group I (all P < 0.05). On western blot, collagen I and ACE2 expressions in group D (median: 1.78 and 0.35, respectively) were significantly different from groups C (references: 1) and I+F (0.76 and 1.21) (all P < 0.05), but not from group I (1.19 and 0.92). Our study suggested a combination of fluvastatin and insulin would be more effective than insulin alone in diabetic hearts. However, the exact mechanism remains to be elucidated.

Reactive oxygen species by isoflurane mediates inhibition of nuclear factor κB activation in lipopolysaccharide-induced acute inflammation of the lung.

BACKGROUND: Although anesthetic-induced inhibition of lipopolysaccharide (LPS)-induced lung injury has been recognized, the underlying mechanism is obscure. Some studies suggest that reactive oxygen species (ROS) by isoflurane play a crucial role for anesthetic-induced protective effects on the brain or the heart; however, it still remains controversial. In this study, we examined the role of isoflurane-derived ROS in isoflurane-induced inhibition of lung injury and nuclear factor κB (NFκB) activation in LPS-challenged rat lungs. METHODS: Male Sprague-Dawley rats were subjected to inhalation of 1.0 minimum alveolar concentration of isoflurane for 60 minutes, and intratracheal LPS 0.1 mg was administered 60 minutes later. In some cases, ROS scavenger, 2-mercaptopropinyl glycine or N-acetylcysteine was given 30 minutes before isoflurane. ROS generation was measured by fluorometer before LPS challenge and 4 hours after. Isoflurane's preconditioning effect was assessed by histologic examination, protein content, neutrophil recruitment, and determination of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6 levels in bronchoalveolar lavage fluid and lung tissue. Western blotting measured phosphorylation of inhibitory κB α (ser 32/36), NFκB p65, and inducible nitric oxide synthase (iNOS). TNF-α and IL-6 mRNA expression and immunofluorescence staining for iNOS were also assessed. RESULTS: Isoflurane preconditioning reduced inflammatory lung injury and TNF-α, IL-1ß, and IL-6 release in the lung. Isoflurane upregulated ROS generation before LPS but inhibited a ROS burst after LPS challenge. ROS scavenger administration before isoflurane abolished the isoflurane preconditioning effect as well as isoflurane-induced inhibition of phosphorylation of inhibitory κBα, NFκB p65, iNOS activation, and mRNA expression of TNF-α and IL-6 in acute LPS-challenged lungs. CONCLUSIONS: This study suggests a crucial role of upregulated ROS generation by isoflurane for modification of inflammatory pathways by isoflurane preconditioning in acute inflammation of the lung.

The Efficacy of Scalp Nerve Block in Postoperative Pain Management after Microvascular Decompression: A Randomized Clinical Trial.

The scalp nerve block, created by injecting local anesthetics around the scalp nerves, is reported to effectively reduce pain after surgery. In this study, we evaluated the efficacy of scalp nerve block in patients with hemifacial spasm (HFS) undergoing microvascular decompression (MVD). Seventy-four patients who underwent MVD for HFS were enrolled. The block group received scalp nerve block with 0.5% ropivacaine before surgery. The primary outcome was cumulative dose of rescue analgesics 24 h postoperatively. The secondary outcomes were included pain scores, postoperative antiemetic consumption, and Quality of Recovery-15 scale. The cumulative dose of rescue analgesics at 24 h postoperatively was not significantly different between the two groups (4.80 ± 3.64 mg vs. 5.92 ± 3.95 mg, p = 0.633). However, the pain score was significantly reduced in the block group at 6, 12, and 24 h postoperatively. Postoperative antiemetic consumption was lower in the block group than the control group at 12 h. There were no significant differences between the two groups for other secondary outcomes. In MVD for HFS, a preoperative scalp nerve block might reduce postoperative pain in the early postoperative period, but a larger study using a multimodal approach is needed to confirm the efficacy of a scalp block.

Comparison of pulmonary morbidity using sevoflurane or propofol-remifentanil anesthesia in an Ivor Lewis operation.

OBJECTIVE: An inhalation anesthetic-induced attenuation effect on the inflammatory reaction during one-lung ventilation (OLV) has been reported. Pulmonary inflammation is a substantive prognostic factor for Ivor Lewis operations. Blood inflammatory parameters and postoperative pulmonary complications between sevoflurane and propofol-remifentanil anesthesia in patients undergoing Ivor Lewis operations were compared. DESIGN: A prospective, randomized study. SETTING: A medical university. PARTICIPANTS: Forty-eight patients undergoing Ivor Lewis operation allocated randomly into 2 groups. INTERVENTIONS: Patients received sevoflurane or total intravenous anesthesia using propofol and remifentanil (n = 24 per group). MEASUREMENTS AND MAIN RESULTS: Blood interleukin-6 (IL-6), malondialdehyde (MDA), oxygenation, abnormalities on a chest radiograph (CXR), extubation, intensive care unit (ICU) stay, length of hospitalization, and postoperative complications were compared between the 2 anesthetic techniques. The level of IL-6 at the end of surgery was lower for sevoflurane (69.5 [35.9-121.0] pg/mL) than propofol-remifentanil (128.2 [92.8-163.8] pg/mL, p = 0.03), but this difference was not maintained 24 hours after surgery. Frequencies of abnormalities measured by a CXR, PaO(2)/F(I)O(2)<300, and PaCO(2) <50 mmHg until discharge, the postoperative highest C-reactive protein level, white blood cells, and MDA did not differ between the 2 anesthetics. No differences in the extubation time, ICU stay, discharge day, or the incidence of hospital complications between sevoflurane and propofol-remifentanil anesthesia techniques were observed. CONCLUSIONS: Sevoflurane anesthesia attenuated an increase in blood IL-6 at the end of surgery but did not provide any advantages over propofol remifentanil in terms of postoperative pulmonary complications in Ivor Lewis operations.

Improvement of sleep-related breathing disorder in patients with end-stage renal disease after kidney transplantation.

Sleep-related breathing disorder (SRBD) is a common symptom of end-stage renal disease (ESRD). The aim of this study was to determine whether kidney transplantation improves SRBD. Twenty-four patients with ESRD, who were admitted for kidney transplantation, underwent a sleep study using a portable ventilation effort recorder on the night before transplantation. Of these patients, 20 could repeat the overnight monitoring two wk after the transplantation. The median apnea-hypopnea index (AHI) of the 20 patients was 13.5 (range, 2-40), and significantly reduced to 4.5 (range, 0-20) after transplantation (p = 0.003). This reduction was most prominent in 12 patients with SRBD, for whom the median AHI fell from 22 (range, 10-40) to 6.5 (range, 1-20; p = 0.010). SRBD improvement, defined as an AHI equal to or >50% and/or reduced to <10/h, was observed in eight of the 12 apneic patients. These results suggest that kidney transplantation may immediately improve SRBD in patients with ESRD. However, conclusions from this study should be taken with caution because of the limitations of our method, specifically the use of a portable recorder and a small number of patients.

Downregulation of constitutive and cytokine-induced complement 3 expression by morphine in rat astrocytes.

BACKGROUND: The effect of opioids on inflammation and immune responses is an important subject of investigation because immunoregulatory cytokines are produced in the central nervous system and opioid receptors are widespread in these cells. OBJECTIVES: The aim of this study was to evaluate the immunomodulatory effect of morphine on the C3 expression (both constitutive and proinflammatory cytokine-induced C3 expression) in primary rat astrocytes. METHODS: Primary rat astrocytes were untreated or treated with morphine in different concentrations (10(-6) to 10(-2) M) before incubation without or with 5 U/mL tumor necrosis factor-α (TNF-α), and C3 protein and mRNA expressions were measured. Similarly, astrocytes were treated with 10(-3) M morphine and stimulated with other proinflammatory cytokines, including 10 ng/mL interleukin-8 (IL-8) and 5 U/mL IL-1ß. Astrocytes were exposed to 10(-5) M naloxone for 2 hours before adding morphine, and TNF-α and C3 protein was measured. Tumor growth factor-ß (TGF-ß) was measured from the supernatants of each proinflammatory cytokine. RESULTS: All results are expressed as mean percentages of C3 production by normalizing C3 without morphine or any cytokine treatment as 100%. Constitutive C3 protein production was decreased at morphine 10(-3) M (57.2%) and 10(-2) M (30.1%). Pretreatment with morphine suppressed induction of C3 expression at both the protein and mRNA levels in astrocytes stimulated with TNF-α, IL-8, and IL-1ß (P < 0.05) in a dose-dependent manner. The inhibition of C3 protein production by morphine (10(-3) M; 33%) was partially attenuated by naloxone (52.0%) (P < 0.05). The pretreatment of astrocytes with morphine (10(-3) M) before stimulation with TNF-α, IL-8, and IL-1ß increased by 33% (P < 0.05), decreased by 15.2% (P < 0.05), and did not change the production of TGF-ß protein, respectively. CONCLUSIONS: Morphine downregulated both constitutive and proinflammatory cytokine-induced C3 expression of astrocytes at the transcriptional level, but not in a cytokine-specific manner.

Role of reactive oxygen species at reperfusion stage in isoflurane preconditioning-induced neuroprotection.

In this in vivo and in vitro study, we aimed to investigate whether isoflurane preconditioning-induced neuronal protection is mediated by reactive oxygen species (ROS) signaling at the reperfusion stage. In the in vivo study, Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) and in the in vitro study, rat pheochromocytoma (PC12) cells were subjected to oxygen glucose deprivation (OGD). Isoflurane preconditioning was carried out prior to MCAO or OGD and the ROS scavenger, N-2-mercaptopropiopylglycine (2-MPG), was administered at the start of reperfusion. Infarct volume, neurological severity score, and TUNEL staining were analyzed in the in vivo study and cell viability, Bcl-2/Bax ratio, cleaved caspase 3/caspase 3 ratio, and ROS fluorescence intensity were measured in the in vitro study. In the in vivo study, infarct volume, neurological severity score, and TUNEL-positive cell count were significantly decreased with preconditioning but were abrogated by administration of 2-MPG. In the in vitro study, cell viability and Bcl-2/Bax ratio were significantly increased with preconditioning, and cleaved caspase-3/caspase-3 ratio and ROS fluorescence intensity were significantly decreased. Administration of 2-MPG for 10 min abrogated this preconditioning effect, but it did not abolish the protection when administered for 60 min of reperfusion. Isoflurane preconditioning-induced protection was abolished by ROS scavengers at the start of reperfusion, indicating that ROS signaling can mediate the isoflurane preconditioning effect, which suggests that the time window can be important.

Pre-administration of remifentanil in target-controlled propofol and remifentanil anesthesia prolongs anesthesia induction in neurosurgical patients: A double-blind randomized controlled trial.

BACKGROUND: Pre- and co-administration of remifentanil in target-controlled propofol and remifentanil anesthesia are the most common methods in clinical practice. However, anesthesia induction time by timing remifentanil administration was not identified. Therefore, we investigated the induction time of anesthesia based on type of remifentanil administration in target-controlled anesthesia. METHODS: A total of 60 patients were randomly assigned to 1 of 2 groups: Pre-administered with remifentanil before propofol infusion (Group R, n = 30) and co-administered with remifentanil with propofol (Group N, n = 30). The primary outcome was total induction time based on the order of remifentanil administration. Secondary outcomes were from start of the propofol infusion time to loss of consciousness (LOC), rocuronium onset time, time to Bispectral index (BIS) 60, and hemodynamic variables. RESULTS: The mean ±â€ŠSD of total induction time was 180.5 ±â€Š49.0 s in Group N and 246.3 ±â€Š64.7 s in Group R (mean difference: 65.8 seconds; 95% CI: 35.0-96.5 s, P < .01). Time to BIS 60 and rocuronium onset time were longer in the Group R (P < .01 and P < .01, respectively). The Δheart rate and Δcardiac output values were lower in the Group R (P = .02 and P = .04, respectively). Injection pain was reported by 11 of 28 (39%) in the Group N and in 2 of 28 (7%) in the Group R (difference in proportion: 32%, 95% CI: 10-51%, P = .01). CONCLUSION: Pre-administration of remifentanil in target-controlled propofol and remifentanil anesthesia prolongs total induction time about 35% compared to co-administration of remifentanil and propofol by decreased CO.

Postconditioning with isoflurane reduced ischemia-induced brain injury in rats.

BACKGROUND: Preexposure of brain to isoflurane, a commonly used anesthetic, induces ischemic tolerance. This phenomenon is called isoflurane preconditioning. However, it is not known whether isoflurane application after ischemia provides neuroprotection. METHODS: Corticostriatal slices (400 microm) freshly prepared from adult male Sprague-Dawley rats were subjected to a 15-min oxygen-glucose deprivation (OGD; to simulate ischemia in vitro). Isoflurane was applied after OGD. Brain slices were harvested 2 h after OGD for measuring 2,3,5-triphenyltetrazolium chloride (TTC) conversion to quantify cell injury. Adult male Sprague-Dawley rats were also subjected to middle cerebral arterial occlusion for 90 min and then treated with or without 2% isoflurane for 60 min started at the onset of reperfusion. The infarct volumes, neurologic deficit scores, and performance on rotarod were evaluated at 24 h after the onset of reperfusion. RESULTS: Isoflurane applied immediately after the 15-min OGD for 30 min dose-dependently reversed the OGD-induced decrease of TTC conversion. The TTC conversion was 34 +/- 16% and 58 +/- 28% of the control, respectively, for OGD alone and OGD plus 2% isoflurane (P < 0.05, n = 12). Application of 2% isoflurane for 30 min started at 10 min after the OGD also reduced the OGD-decreased TTC conversion. The presence of 0.3 microm glibenclamide, a general adenosine 5'-triphosphate-sensitive potassium channel blocker, or 500 microm 5-hydroxydecanoic acid, a mitochondrial adenosine 5'-triphosphate-sensitive potassium channel blocker, during the application of 2% isoflurane abolished the isoflurane preservation of TTC conversion. Application of isoflurane during reperfusion also improved neurologic outcome after brain ischemia. CONCLUSIONS: The results suggest that isoflurane administrated after OGD or brain ischemia provides neuroprotection. Mitochondrial adenosine 5'-triphosphate-sensitive potassium channels may be involved in this protection.

Inability of volatile anesthetics to inhibit oxygen-glucose deprivation-induced glutamate release via glutamate transporters and anion channels in rat corticostriatal slices.

Ischemia-induced extracellular glutamate accumulation and the subsequent excitotoxicity contribute significantly to ischemic brain injury. Volatile anesthetics have been shown to reduce ischemic brain injury. Here, we showed that oxygen-glucose deprivation (OGD, to simulate ischemia in vitro) increased extracellular glutamate accumulation in the corticostriatal slices of adult rats. This increased accumulation was reduced by dihydrokinate, a glutamate transporter type 2 inhibitor, and 4,4'-dinitrostilbene-2,2'-disulfonic acid, a blocker for volume-activated anion channels. The volatile anesthetics isoflurane, sevoflurane and desflurane at clinically relevant concentrations did not affect the OGD-induced extracellular glutamate accumulation from brain slices of adult rats. Isoflurane also did not change the OGD-induced extracellular glutamate accumulation from brain slices of newborn/young rats. These results suggest that the OGD-induced glutamate accumulation involves reversed transport of glutamate via glutamate transporters and volume-activated anion channels. Volatile anesthetics may not inhibit this extracellular glutamate accumulation.

Genetic detoxification of an aroA Salmonella enterica serovar Typhimurium vaccine strain does not compromise protection against virulent Salmonella and enhances the immune responses towards a protective malarial antigen.

Live Salmonella vaccines are limited in use by the inherent toxicity of the lipopolysaccharide. The waaN gene encodes a myristyl transferase required for the secondary acylation of lipid A in lipopolysaccharide. A waaN mutant exhibits reduced induction of the inflammatory cytokines associated with lipopolysaccharide toxicity. Here the characteristics of a Salmonella enterica serovar Typhimurium aroA waaN mutant (SK100) in vitro and in vivo compared with its parent aroA strain (SL3261) were described. Phenotypic analysis of purified lipopolysaccharide obtained from SK100 confirmed that the physical and biological activities of the lipopolysaccharide had been altered. Nevertheless both strains had similar patterns of colonization and persistence in mice and significantly the aroA waaN mutant was equally as effective as the parent at protecting against challenge with wild-type S. Typhimurium. Furthermore, a SK100 strain was constructed expressing both tetanus toxin fragment C and the circumsporozoite protein of a malaria parasite. In marked contrast to its isogenic parent, the new attenuated strain induces significantly enhanced immune responses against the circumsporozoite protein. The waaN mutation enhances the ability of this strain to elicit immune responses towards guest antigens. This study provides important insights into the development of safe and effective multivalent Salmonella vaccines.

Blocking noise but not music lowers bispectral index scores during sedation in noisy operating rooms.

STUDY OBJECTIVE: To determine whether playing music or blocking noise can reduce bispectral index (BIS) values during propofol sedation. DESIGN: Prospective, randomized, single-blinded study. SETTING: Operating room. PATIENTS: 63 ASA physical status I and II patients, aged 55 to 75 years, undergoing total knee replacement. INTERVENTIONS: Patients were divided into three groups: noise, silence, and music. After induction of combined spinal-epidural anesthesia, sedation was begun with 1.2 mug/mL of propofol in a target-controlled infusion. In the silence group, patients' ears were packed tightly to block ambient noise, whereas patient-selected music was applied to patients in the music group. Patients in the noise group were exposed to ambient operating room noise. MEASUREMENTS: Bispectral index measurement was recorded 7 times during operation. Ambient room noise was recorded at the same time sequence. MAIN RESULTS: Sound level was highest when the saw (T3, 80.25 dB) and the impact device (T4, 80.98 dB) were in use. Bispectral index scores in the silence group during those times (T3, 68.5 vs 76.9, P = 0.025, and T4, 67.6 vs 78, P = 0.005) were lower than in the noise group. However, BIS scores were similar in the noise and music groups. Preoperative anxiety level, postoperative comfort level, and pain scores were similar in all groups. CONCLUSION: Blocking noise is more effective than playing music in reducing BIS scores during propofol sedation in a noisy environment.

Hyperthermia associated with biliary obstruction during living donor liver transplantation.

Intraoperative hypothermia occurs frequently, but hyperthermia is relatively rare during general anesthesia. We experienced a case of hyperthermia during living donor liver transplantation that appeared to be significantly associated with biliary obstruction. A 65-year-old male patient was diagnosed with intrahepatic cholangiocarcinoma, and living donor liver transplantation was planned after confirmation of no metastasis via intraoperative frozen biopsy. Following resection of a segment of common bile duct for frozen biopsy, the surgeon clamped the common bile duct, and the patient's body temperature increased gradually to 39.5°C. As the congested bile was drained, the body temperature decreased to the normal range. This case report suggests that when a patient develops unexplained hyperthermia during hepatobiliary surgery or in a chance of biliary obstruction, clinicians should consider bile congestion as a possible reason for hyperthermia.

Risk factors for an intraoperative arrhythmia during esophagectomy.

PURPOSE: Arrhythmias after an esophagectomy (most commonly atrial fibrillation) are a significant contributing factor to patient morbidity. However, the significance of an intraoperative arrhythmia is not completely understood. The aim of this retrospective study was to determine the occurrence and risk factors for developing intraoperative arrhythmias in patients undergoing an esophagectomy. MATERIALS AND METHODS: We reviewed the records of 427 patients who underwent a transthoracic esophagectomy between 2001 and 2005. Variables such as age, sex, hypertension, diabetes, cardiac disease, preoperative pulmonary function test (PFT) results, cancer level, combined radiochemotherapy, intrathoracic cavity adhesions and anastomosis site, hemoglobin, central venous pressure (CVP), fluid balance, serum potassium level, dose of vasopressors, temperature, and combined general and epidural anesthesia were analyzed as risk factors for the occurrence of an arrhythmia. We defined this arrhythmia as one not originating from the sinus node. RESULTS: The incidence of intraoperative arrhythmia in this subset of patients was 17.1%, with a 37.2% reoccurrence rate during the first three postoperative days. Univariate and multivariate analysis revealed the presence of heart disease, poor PFTs, cervical anastomosis, elevated CVP, and higher ephedrine doses to be independent predictors of the development of an intraoperative arrhythmia. CONCLUSION: The incidence of intraoperative arrhythmia during esophagectomy was 17.1% with a 37.2% of reoccurrence rate.

Effects of 6% hydroxyethyl starch 130/0.4 on postoperative blood loss and kidney injury in off-pump coronary arterial bypass grafting: A retrospective study.

We retrospectively evaluated the effects of 6% hydroxyethyl starch (HES) 130/0.4 on postoperative blood loss and acute kidney injury (AKI) in patients undergoing off-pump coronary artery bypass grafting (OPCAB).Electronic medical records of 771 patients who underwent OPCAB in our hospital between July 2012 and July 2014 were reviewed, and 249 patients without intraoperative HES-exposure (group NoHES) were matched 1:N with intraoperative HES-exposed 413 patients (group HES) based on propensity score. The effects of intraoperative HES on postoperative cumulative blood loss within the first 24 hours, need for bleeding-related reoperation, and occurrence of postoperative AKI (determined by KDIGO and RIFLE criteria) were analyzed.In our propensity score matched cohort, there were no significant differences between groups for median postoperative 24 hours blood loss (525 mL in group HES vs. 540 mL in group NoHES, P = .203) or need for bleeding-related reoperation (OR, 2.44; 95% confidence interval [CI], 0.64-9.34, P = .19). However, postoperative AKI (assessed by 2 criteria) occurred more frequently in group HES than in group NoHES (by KDIGO criteria: 10.7% vs. 3.6%; OR 3.43 [95% CI, 1.67-7.04]; P < .001 and by RIFLE criteria: 9.6% vs. 2%; OR 3.32 [95% CI, 1.34-8.24]; P = .01). The median volume of infused HES per patient weight was 16 mL/kg in group HES.In the patients undergoing OPCAB, intraoperative 6% HES 130/0.4 did not increase postoperative bleeding. However, renal safety remains a concern. Intraoperative use of HES should be determined cautiously during OPCAB.

Comparison of intrathecal morphine and surgical-site infusion of ropivacaine as adjuncts to intravenous patient-controlled analgesia in living-donor kidney transplant recipients.

INTRODUCTION: This prospective observational study compared the postoperative analgesic effectiveness of intrathecal morphine (ITM) and surgical-site infusion (SSI) of ropivacaine as adjuncts to intravenous (IV) patient-controlled analgesia (PCA) (fentanyl) in living-donor kidney transplant recipients. METHODS: Patients undergoing living-donor kidney transplantation who received ITM or SSI in addition to IV PCA were included. Rescue analgesia was achieved with IV meperidine as required. The primary outcome, measured using the Numeric Pain Rating Scale (NRS), was pain at rest and when coughing. Patients were assessed for 48 hours after surgery. RESULTS: A total of 53 patients (32 ITM, 21 SSI) were included in the study. The ITM group showed significantly lower NRS scores, at rest and when coughing, for up to 12 and eight hours. NRS scores were comparable between the groups at other times. The ITM group had significantly less postoperative systemic opioid requirement in the first 24 hours, but there was no significant difference between the systemic opioid consumption of the groups on postoperative Day 2. In the ITM group, 3 (9.4%) patients presented with bradypnoea and 1 (3.1%) with excessive sedation in the first 12 postoperative hours. More patients in the ITM group developed pruritus requiring treatment during the first 24 hours. There were no differences between the groups in other outcomes (e.g. nausea/vomiting, change in pulmonary or kidney functions). CONCLUSION: Compared with SSI, ITM reduced immediate postoperative pain and IV opioid consumption on postoperative Day 1 after living-donor kidney transplantation, but at the cost of increased pruritus and respiratory depression.