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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. [ABSTRACT FROM AUTHOR]

Isoflurane has either neuroprotective or neurotoxic effects. High-dose oxygen is frequently used throughout the perioperative period. We hypothesized that hyperoxia will affect cell viability of rat pheochromocytoma (PC12) cells that were exposed to isoflurane and reactive oxygen species (ROS) may be involved. PC12 cells were exposed to 1.2% or 2.4% isoflurane for 6 or 24 h respectively, and cell viability was evaluated. To investigate the effects of hyperoxia, PC12 cells were treated with 21%, 50%, or 95% oxygen and 2.4% isoflurane for 6 h, and cell viability, TUNEL staining, ROS production, and expression of B-cell lymphoma 2 (BCL-2), BCL2-associated X protein (BAX), caspase-3 and beta-site APP cleaving enzyme (BACE) were measured. ROS involvement was evaluated using the ROS scavenger 2-mercaptopropiopylglycine (MPG). The viability of cells exposed to 2.4% isoflurane was lower than that of cells exposed to 1.2% isoflurane. Prolonged exposure (6 h vs. 24 h) to 2.4% isoflurane resulted in a profound reduction in cell viability. Treatment with 95% (but not 50%) oxygen enhanced the decrease in cell viability induced by 2.4% isoflurane alone. Levels of ROS, Bax, caspase-3 and BACE were increased, whereas expression of Bcl-2 was decreased, in cells treated with 95% oxygen plus 2.4% isoflurane compared with the control and 2.4% isoflurane plus air groups. MPG attenuated the effects of oxygen and isoflurane. In conclusion, isoflurane affects cell viability in a dose- and time-dependent manner. This effect is augmented by hyperoxia and may involve ROS, the mitochondrial apoptotic signaling pathway, and β-amyloid protein. [ABSTRACT FROM AUTHOR]

In this work, Li 2 FeSiO 4 nanoparticles with two types of morphologies, spherical and rod-shaped, were prepared via a facile water/ethylene-glycol-based solvothermal method by using different kinds of iron sources and surfactants. When evaluated as a cathode material for lithium-ion batteries, carbon-coated Li 2 FeSiO 4 nanospheres exhibited good cycling stability and large Li storage capacities, delivering 150 and 200 mA h g −1 at room temperature and 55 °C, respectively. [ABSTRACT FROM AUTHOR]

Lee JJ, Kim GS, Kim JA, Kim S-J, Kang JG, Kim GH, Jung HH. Improvement of sleep-related breathing disorder in patients with end-stage renal disease after kidney transplantation. Clin Transplant 2011: 25: 126-130. © 2009 John Wiley & Sons A/S. 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. [ABSTRACT FROM AUTHOR]

Abstract: 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. [Copyright &y& Elsevier]

Abstract: 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 μg/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. [Copyright &y& Elsevier]

• Isoflurane preconditioning protects against ischemia in vivo and in vitro model. • Applying 2-MPG just before reperfusion abrogated isoflurane preconditioning in vivo. • ROS scavenging for 10 min at the onset of reperfusion blocked isoflurane preconditioning. • ROS after OGD in an isoflurane preconditioning group was lower than in an OGD group. • ROS after reperfusion were increased by scavenging ROS immediately after OGD. 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. [ABSTRACT FROM AUTHOR]

• The new allelic variant found in CsaV3_7G029170 (CsaYf) linked to yellow endocarp in the PI200815 (CS-C) line via high-throughput sequencing. • A missense mutation in CsaYf changed the original Aspartic acid (D) in the JEF, KWSA, and CS-A (MEJ) line to Asparagine (N) in the CS-C line. • Concordant phenotype and genotype results suggest a 3:1 ratio and denote a single recessive gene inheritance for the yellow fruit flesh trait. • Downregulation of the CsaYf gene is inversely correlated with ß-carotene accumulation in the CS-C line's meso and endo carp tissues, indicating a need for further investigation. Cucumber (Cucumis sativus) is a globally valued and widely cultivated vegetable crop. However, most commercially available cucumbers contain white or green fruit flesh color, which has very low ß-carotene and other carotenoids. Conversely, orange or yellow-fleshed cucumbers are rich in carotenoids and offer significant dietary and nutritional benefits. To generate cucumber varieties with carotenoid-enriched fruit flesh, we conducted high-throughput sequencing of a yellow-fleshed cucumber PI200815 (CS-C) and white-fleshed cucumbers JEF, and KWSA, to identify the genomic region responsible for yellow-fleshed fruit. Building on the previous report by Lu et al. (2015), we identified seven unique DNA variations in five genes specific to the CS-C line using HiSeq2000 and genomic mapping to 'Chinese-Long v3′. Further, based on the Sanger gene sequencing, among the five candidate genes, we found the CsaV3_7G029170 (encodes for an ATP-binding cassette (ABC) transporter C family member 4 [ CsaYf ]) gene with a single nucleotide polymorphism (SNP) variation in the third exon resulted in a missense mutation caused an amino acid change from Aspartic acid (Asp) to Aspargine (Asn) in the CS-C line. Accordingly, the gene segregation analysis based on the SNP variation revealed that the CsaYf gene confers the yellow endocarp trait in the CS-C line through recessive Mendelian single-gene inheritance. Notably, we observed a negative correlation between the downregulation of CsaYf gene expression and the accumulation of ß-carotene in meso and endo carp tissues in the CS-C line, suggesting a further investigation into the underlying molecular mechanism. This finding provides a novel genetic basis for breeding cucumbers with enriched carotenoid content to enhance their nutritional value. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Given the key role 4-1BB plays in the stimulation of T cells, humanization of agonistic anti-human 4-1BB monoclonal antibody (mAb) may have important clinical applications. In this paper, we present the humanization of agonistic anti-human 4-1BB mAb, BBK-4, using a phage display library. We first prepared the combinatorial library by incorporating murine and human alternative at positions representing buried residues that might affect the structural integrity of the antigen binding site. Six humanized single chain Fv (scFv) fragments were selected from the combinatorial library expressing phage-displayed humanized scFv. They were found to retain the epitope specificity of the original mAb but had affinities of lower than 1/10 of the original. In spite of the lower affinity, the humanized scFv coated on the surface expanded human peripheral blood mononuclear cells (PBMCs) in MLR similarly to the original mAb in the presence of anti-CD3 mAb. These results suggest that humanized anti-human 4-1BB scFvs can be used as a valuable reagent for clinical application. [Copyright &y& Elsevier]

Oxidative stress is a primary pathogenesis in the brain, which is particularly vulnerable to oxidative stress. Maintenance of astrocyte functions under oxidative stress is essential to prevent neuronal injuries and to recover neuronal functions in various pathologic conditions. Imidazoline drugs have affinities for imidazoline receptors, which are highly distributed in the brain, and have been shown to be neuroprotective. This study presented the protective effects of several imidazoline drugs against oxidative cytotoxicity, in primary cultures of astrocytes. Imidazoline drugs, such as idazoxan, guanabenz, guanfacine, BU224, and RS-45041-190, showed protective effects against naphthazarin-induced oxidative cytotoxicity, as evidenced by LDH release and Hoechst 33342/propidium iodide staining. The imidazoline drugs stabilized lysosomes and inhibited naphthazarin-induced lysosomal destabilization, as evidenced by acridine orange relocation. Guanabenz inhibited, the leakage of lysosomal cathepsin D to cytosol, the decreased mitochondrial potential, and the release of mitochondrial cytochrome c, which were induced by naphthazarin. The lysosomal destabilization by oxidative stress and other apoptotic signals and subsequent cathepsin D leakage to the cytosol can induce apoptotic changes of mitochondria and eventually cell death. Therefore, lysosomal stabilization by imidazoline drugs may be ascribed to their protective effects against oxidative cytotoxicity. [Copyright &y& Elsevier]

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. [ABSTRACT FROM AUTHOR]

Objective We evaluated the effect of partial neuromuscular blockade (NMB) and no NMB on successful intraoperative monitoring of the lateral spread response (LSR) during microvascular decompression (MVD) surgery. Methods Patients were randomly allocated into one of three groups: the TOF group, the NMB was targeted to maintain two counts of train-of-four (TOF); the T1 group, maintain the T1/Tc (T1: amplitude of first twitch, Tc: amplitude of baseline twitch) ratio at 50%; and the N group, no relaxants after tracheal intubation. Successful LSR monitoring was defined as effective baseline establishment and maintenance of the LSR until dural opening. Results The success rate of LSR monitoring was significantly lower in the TOF group. But, there was no significant difference between T1 and N. The detection rate of spontaneous free-run electromyography (EMG) activity was significantly higher in the N group compared with the TOF and T1 groups. Conclusions Partial NMB with a target of T1/Tc ratio at 50% allows good recording of LSR with same outcome as surgery without NMB, and reduced spontaneous EMG activity. Significance We suggested the availability of partial NMB for intraoperative LSR monitoring. [ABSTRACT FROM AUTHOR]

Strangles, caused by Streptococcus equi subspecies equi ( S. equi ) is one of the most frequently diagnosed infectious diseases of horses and there remains a significant need to develop new preventative vaccines. We generated a live vaccine strain of S. equi containing deletions in six genes: sagA , hasA , aroB , pyrC , seM and recA , which was administered to nine Welsh mountain ponies via the intramuscular route. Four vaccinated ponies developed adverse reactions following the first vaccination from which the live vaccine strain was isolated. Two of these ponies were withdrawn from the study and seven ponies received a second vaccination, one of which then developed an adverse reaction. Nine control ponies injected with culture media alone developed no adverse reactions. Following challenge with a virulent strain of S. equi , none of the seven vaccinated ponies had developed clinical signs of strangles eleven days post-challenge, compared to six of nine control ponies over the same period ( P = 0.0114). A lymph node abscess was identified in one of the seven vaccinated ponies at post-mortem examination, whilst all nine control ponies had at least one lymph node abscess ( P = 0.0009). Three of the six vaccinated ponies that were protected from strangles had not developed an adverse reaction following vaccination, suggesting that a better understanding of the pro-inflammatory responses to S. equi could lead to the development of a live attenuated vaccine against strangles that is safe for administration via intramuscular injection. [ABSTRACT FROM AUTHOR]

Abstract: 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-1β. 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-β (TGF-β) 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-1β (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-1β increased by 33% (P < 0.05), decreased by 15.2% (P < 0.05), and did not change the production of TGF-β 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. [Copyright &y& Elsevier]

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. [ABSTRACT FROM AUTHOR]

Abstract: Pathogenic bacteria employ a variety of mechanisms to resist a barrage of stresses they encounter during active growth in or outside the host as well as during growth stasis. An in silico screen of the Salmonella genome sequence revealed that Salmonella typhimurium LT2 possesses a homologue belonging to the universal stress protein A (UspA) family. We assessed the transcriptional profile of uspA in S. typhimurium C5 by constructing a lacZ fusion revealing that uspA is induced by metabolic, oxidative, and temperature stresses. The highest transcriptional levels occurred in cells entering stationary phase, an observation consistent with expression patterns in Escherichia coli. The protein was purified as a fusion with GST (UspAF) and antibodies raised against UspAF revealed elevated protein levels in stressed and growth-arrested cells. Inactivation of uspA in S. typhimurium C5, lead to increased susceptibility to stress conditions. Furthermore, UspA makes an important contribution to the in vivo virulence of Salmonella in mice thus highlighting the importance of stress resistance regulation in pathogenicity and survival within the host. [Copyright &y& Elsevier]