bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adaptive Support Ventilation Prevents Ventilator-induced Diaphragmatic Dysfunction in Piglet
Authors: Jung Boris , Constantin Jean-Michel , Rossel Nans , Le Goff Charlotte , Sebbane Mustapha , Coisel Yannael , Chanques Gerald , Futier Emmanuel , Hugon Gerald , Capdevila Xavier , Petrof Basil , Matecki Stefan , Jaber Samir 
Published: May 2010

Background
Contrary to adaptive support ventilation (ASV), prolonged totally controlled mechanical ventilation (CMV) results in the absence of diaphragm activity and causes ventilator-induced diaphragmatic dysfunction. Because maintaining respiratory muscles at rest is likely a major cause of ventilator-induced diaphragmatic dysfunction, ASV may prevent its occurrence in comparison with CMV. The aim of our study was to compare the effects of ASV with those of CMV on both in vivo and in vitro diaphragmatic properties.

Methods
Two groups of six anesthetized piglets were ventilated during a 72-h period. Piglets in the CMV group (n = 6) were ventilated without spontaneous ventilation, and piglets in the ASV group (n = 6) were ventilated with spontaneous breaths. Transdiaphragmatic pressure was measured after bilateral, supramaximal transjugular stimulation of the two phrenic nerves. A pressure-frequency curve was drawn after stimulation from 20 to 120 Hz of the phrenic nerves. Diaphragm fiber proportions and mean sectional area were evaluated.

Results
After 72 h of ventilation, transdiaphragmatic pressure decreased by 30% of its baseline value in the CMV group, whereas it did not decrease in the ASV group. Although CMV was associated with an atrophy of the diaphragm (evaluated by mean cross-sectional area of both the slow and fast myosin chains), atrophy was not detected in the ASV group.

Conclusion
Maintaining diaphragmatic contractile activity by using the ASV mode may protect the diaphragm against the deleterious effect of prolonged CMV, as demonstrated both in vitro and in vivo, in healthy piglets.
Anesthetic Sevoflurane Causes Neurotoxicity Differently in Neonatal Naïve and Alzheimer Disease Transgenic Mice
Authors: Lu Yan , Wu Xu , Dong Yuanlin , Xu Zhipeng , Zhang Yiying , Xie Zhongcong 
Published: May 2010

Background
Recent studies have suggested that children undergoing surgery under anesthesia could be at an increased risk for the development of learning disabilities, but whether anesthetics contribute to this learning disability is unclear. Therefore, the authors set out to assess the effects of sevoflurane, the most commonly used inhalation anesthetic, on caspase activation, apoptosis, beta-amyloid protein levels, and neuroinflammation in the brain tissues of neonatal naïve and Alzheimer disease (AD) transgenic mice.

Methods
Six-day-old naïve and AD transgenic (B6.Cg-Tg[amyloid precursor protein swe, PSEN1dE9]85Dbo/J) mice were treated with sevoflurane. The mice were killed at the end of the anesthesia, and the brain tissues were harvested and then subjected to Western blot, immunocytochemistry, enzyme-linked immunosorbent assay, and real-time polymerase chain reaction.

Results
Herein, the authors show for the first time that sevoflurane anesthesia induced caspase activation and apoptosis, altered amyloid precursor protein processing, and increased beta-amyloid protein levels in the brain tissues of neonatal mice. Furthermore, sevoflurane anesthesia led to a greater degree of neurotoxicity in the brain tissues of the AD transgenic mice when compared with naïve mice and increased tumor necrosis factor-alpha levels in the brain tissues of only the AD transgenic mice. Finally, inositol 1,4,5-trisphosphate receptor antagonist 2-aminoethoxydiphenyl borate attenuated sevoflurane-induced caspase-3 activation and beta-amyloid protein accumulation in vivo.

Conclusion
These results suggest that sevoflurane may induce neurotoxicity in neonatal mice. AD transgenic mice could be more vulnerable to such neurotoxicity. These findings should promote more studies to determine the potential neurotoxicity of anesthesia in animals and humans, especially in children.
Pharmacokinetics of Lidocaine, Bupivacaine, and Levobupivacaine in Plasma and Brain in Awake Rats
Authors: Ikeda Yuko , Oda Yutaka , Nakamura Taketo , Takahashi Ryota , Miyake Wakako , Hase Ichiro , Asada Akira 
Published: May 2010

Background
We have compared the pharmacokinetics and brain distribution of lidocaine, racemic bupivacaine (bupivacaine), and levobupivacaine in awake, spontaneously breathing rats.

Methods
Lidocaine (0.5 mg x kg x min), bupivacaine (0.1 mg x kg x min), or levobupivacaine (0.1 mg x kg x min) was continuously administered to rats for 2 h (n = 12, each anesthetic). Blood samples and cerebral dialysate were collected during infusion and for 2 h after termination of infusion. Concentrations of anesthetics in the cerebral extracellular fluid were measured by microdialysis using the retrodialysis calibration method. Tissue-to-plasma partition coefficients calculated from the total (protein-bound and unbound) and unbound concentrations in plasma and brain as well as pharmacokinetic parameters in plasma and cerebral extracellular fluid were compared among the three anesthetics.

Results
There were no differences in plasma total or unbound concentrations between bupivacaine and levobupivacaine. Concentrations of bupivacaine in the cerebral extracellular fluid were significantly higher than levobupivacaine (P < 0.001). Despite no differences in the ratio of total brain concentration to total plasma concentration among the three anesthetics, the ratio of cerebral extracellular fluid concentration to plasma unbound fraction of bupivacaine was significantly higher than lidocaine and levobupivacaine (0.58 +/- 0.09, 0.47 +/- 0.18, and 0.40 +/- 0.09, respectively; P = 0.03 and 0.003, respectively).

Conclusions
Although the ratio of total brain concentration to total plasma concentrations of lidocaine, bupivacaine, and levobupivacaine was similar, concentration ratio of bupivacaine in the cerebral extracellular fluid to plasma unbound fraction was significantly higher than lidocaine and levobupivacaine.
Effect of PSD-95/SAP90 and/or PSD-93/Chapsyn-110 Deficiency on the Minimum Alveolar Anesthetic Concentration of Halothane in Mice
Authors: Tao Feng , Skinner John , Yang Ya , Johns Roger A. 
Published: May 2010

Background
The authors have previously shown that the clinically relevant concentrations of inhalational anesthetics dose-dependently inhibit the postsynaptic density protein (PSD)-95, Dlg, and ZO-1 domain-mediated protein interactions between N-methyl-d-aspartate receptors and PSD-95/synaptic-associated protein (SAP) 90 or PSD-93/Chapsyn-110 and that the knockdown of spinal PSD-95/SAP90 significantly reduces the minimum alveolar concentration (MAC) for isoflurane in rats.

Methods
The authors designed antisense oligodeoxynucleotides based on the mouse PSD-95/SAP90 and PSD-93/Chapsyn-110 messenger RNAs that correspond to their PSD-95, Dlg, and ZO-1 domain nucleotides and can specifically knock down the respective proteins. The authors intrathecally injected antisense oligodeoxynucleotides into wild-type and PSD-93/Chapsyn-110 knockout mice to investigate the effect of PSD-95/SAP90 and/or PSD-93/Chapsyn-110 deficiency on halothane anesthesia.

Results
Both PSD-95/SAP90 and PSD-93/Chapsyn-110 antisense oligodeoxynucleotides caused a dose-dependent and significant reduction in the MAC of halothane in wild-type mice. The intrathecal injection of PSD-95/SAP90 antisense oligodeoxynucleotide at different doses (25 and 50 microg) reduced halothane MAC by 40 and 55%, respectively, and intrathecal injection of PSD-93/Chapsyn-110 antisense oligodeoxynucleotide at different doses (12 and 24 microg) reduced halothane MAC by 25 and 53%, respectively. The PSD-95/SAP90 antisense oligodeoxynucleotide showed similar effect on halothane MAC in wild-type and PSD-93/Chapsyn-110 knockout mice, suggesting that the combination of PSD-95/SAP90 knockdown with PSD-93/Chapsyn-110 deletion did not have an additive effect on halothane anesthesia.

Conclusions
The current results indicate that PSD-95/SAP90 and PSD-93/Chapsyn-110 are involved in the molecular mechanisms of halothane anesthesia and that the functional role of PSD-95/SAP90 in halothane anesthesia is not enhanced after PSD-93/Chapsyn-110 deletion.
A Prominent Role of the Flagellin Receptor FLAGELLIN-SENSING2 in Mediating Stomatal Response to Pseudomonas syringae pv tomato DC3000 in Arabidopsis
Authors: Zeng Weiqing , He Sheng Yang 
Published: May 2010

Abstract
The FLAGELLIN-SENSING2 (FLS2) receptor kinase recognizes bacterial flagellin and initiates a battery of downstream defense responses to reduce bacterial invasion through stomata in the epidermis and bacterial multiplication in the apoplast of infected plants. Recent studies have shown that during Pseudomonas syringae pv tomato (Pst) DC3000 infection of Arabidopsis (Arabidopsis thaliana), FLS2-mediated immunity is actively suppressed by effector proteins (such as AvrPto and AvrPtoB) secreted through the bacterial type III secretion system (T3SS). We provide evidence here that T3SS effector-based suppression does not appear to be sufficient to overcome FLS2-based immunity during Pst DC3000 infection, but that the phytotoxin coronatine (COR) produced by Pst DC3000 also plays a critical role. COR-deficient mutants of Pst DC3000 are severely reduced in virulence when inoculated onto the leaf surface of wild-type Columbia-0 plants, but this defect was rescued almost fully in fls2 mutant plants. Although bacteria are thought to carry multiple microbe-associated molecular patterns, stomata of fls2 plants are completely unresponsive to COR-deficient mutant Pst DC3000 bacteria. The responses of fls2 plants were similar to those of the Arabidopsis G-protein alpha subunit1-3 mutant, which is defective in abscisic acid-regulated stomatal closure, but were distinct from those of the Arabidopsis non-expressor of PR genes1 mutant, which is defective in salicylic acid-dependent stomatal closure and apoplast defense. Epistasis analyses show that salicylic acid signaling acts upstream of abscisic acid signaling in bacterium-triggered stomatal closure. Taken together, these results suggest a particularly important role of FLS2-mediated resistance to COR-deficient mutant Pst DC3000 bacteria, and nonredundant roles of COR and T3SS effector proteins in the suppression of FLS2-mediated resistance in the Arabidopsis-Pst DC3000 interaction.
The Acidic A-Domain of Arabidopsis Toc159 Occurs as a Hyperphosphorylated Protein
Authors: Agne Birgit , Andrès Charles , Montandon Cyril , Christ Bastien , Ertan Anouk , Jung Friederike , Infanger Sibylle , Bischof Sylvain , Baginsky Sacha , Kessler Felix 
Published: May 2010

Abstract
The translocon at the outer membrane of the chloroplast assists the import of a large class of preproteins with amino-terminal transit sequences. The preprotein receptors Toc159 and Toc33 in Arabidopsis (Arabidopsis thaliana) are specific for the accumulation of abundant photosynthetic proteins. The receptors are homologous GTPases known to be regulated by phosphorylation within their GTP-binding domains. In addition to the central GTP-binding domain, Toc159 has an acidic N-terminal domain (A-domain) and a C-terminal membrane-anchoring domain (M-domain). The A-domain of Toc159 is dispensable for its in vivo activity in Arabidopsis and prone to degradation in pea (Pisum sativum). Therefore, it has been suggested to have a regulatory function. Here, we show that in Arabidopsis, the A-domain is not simply degraded but that it accumulates as a soluble, phosphorylated protein separated from Toc159. However, the physiological relevance of this process is unclear. The data show that the A-domain of Toc159 as well as those of its homologs Toc132 and Toc120 are targets of a casein kinase 2-like activity.
Smoking cessation in severe mental illness: what works?
Authors: Banham Lindsay , Gilbody Simon 
Published: May 2010

ABSTRACTAims  The physical health of people with severe mental illness (SMI) is poor. Smoking‐related illnesses are a major contributor to excess mortality and morbidity. An up‐to‐date review of the evidence for smoking cessation interventions in SMI is needed to inform clinical guidelines.Methods  We searched bibliographic databases for relevant studies and independently extracted data. Included studies were randomized controlled trials (RCTs) of smoking cessation or reduction conducted in adult smokers with SMI. Interventions were compared to usual care or placebo. The primary outcome was smoking cessation and secondary outcomes were smoking reduction, change in weight, change in psychiatric symptoms and adverse events.Results  We included eight RCTs of pharmacological and/or psychological interventions. Most cessation interventions showed moderate positive results, some reaching statistical significance. One study compared behavioural support and nicotine replacement therapy (NRT) to usual care and showed a risk ratio (RR) of 2.74 (95% CI 1.10–6.81) for short‐term smoking cessation, which was not significant at longer follow‐up. We pooled five trials that effectively compared bupropion to placebo giving an RR of 2.77 (95% CI 1.48–5.16), which was comparable to Hughes et al.'s 2009 figures for general population data; RR = 1.69 (95% CI 1.53–1.85). Smoking reduction data were too heterogeneous for meta‐analysis, but results were generally positive. Trials suggest few adverse events. All trials recorded psychiatric symptoms and the most significant changes favoured the intervention groups over the control groups.Conclusions  Treating tobacco dependence is effective in patients with SMI. Treatments that work in the general population work for those with severe mental illness and appear approximately equally effective. Treating tobacco dependence in patients with stable psychiatric conditions does not worsen mental state.
Factors that affect the diagnostic accuracy of liver fibrosis measurement by Fibroscan in patients with chronic hepatitis B
Authors: Kim S. U. , Seo Y. S. , Cheong J. Y. , Kim M. Y. , Kim J. K. , Um S. H. , Cho S. W. , Paik S. K. , Lee K. S. , Han K.‐H. , Ahn S. H. 
Published: May 2010

Aliment Pharmacol Ther 2010; 32: 498–505SummaryBackground  Interquartile range/median value (IQR/M) of liver stiffness measurement (LSM) is a factor in chronic hepatitis C (CHC) leading to over estimation of fibrosis by Fibroscan.Aim  To investigate factors that affect the accuracy of LSM in chronic hepatitis B (CHB).Methods  One hundred and ninety‐nine patients were enrolled. Only procedures yielding ≥10 valid measurements were considered reliable. Liver fibrosis was evaluated using the Batts and Ludwig system. Liver biopsy (LB) specimens <15 mm were considered ineligible.Results  The mean age (142 men and 57 women) was 40.1 years. A significant discordance (discordance of at least two stages between LB and LSM) was identified in 38 (19.1%) and 47 (23.6%) patients respectively, according to Marcellin et al. and Chan et al.’s cutoff values. In multivariate analyses, BMI and fibrosis stage (F0–2 vs. F3–4) were identified as independent predictors for significant discordance (P = 0.040; hazard ratio [HR], 1.126; 95% confidence interval [CI], 1.005–1.261 and P = 0.036; HR, 0.450; 95% CI, 0.213–0.949 respectively) with Marcellin et al.’s cutoffs, whereas fibrosis stage was the only independent predictor (P = 0.004; HR, 0.300; 95% CI, 0.131–0.685) with Chan’s cutoffs.Conclusions  Success rate and IQR/M were not predictive factors of the accuracy for diagnosing liver fibrosis by Fibroscan in CHB. Fibrosis stage (F0‐2) was the only factor to predict significant discordance between LB and LSM.
Effect‐site concentration of propofol for reduction of remifentanil‐induced cough
Authors: Kim J. Y. , Lee S. Y. , Kim D. H. , Park S. K. , Min S. K. 
Published: May 2010

SummaryThis study examined the effectiveness of different propofol infusion target concentrations on cough suppression, during a target‐controlled remifentanil infusion. Four hundred patients were randomly assigned to receive propofol target effect‐site concentrations of 0, 3.0, 4.5, or 6.0 μg.ml−1. When the propofol effect‐site concentration reached the target, remifentanil was administered at a target effect‐site concentration of 4.0 ng.ml−1. Episodes of cough were recorded over a 2‐min period after remifentanil commencement, and graded as mild (1–2), moderate (3–4), or severe (5 or more). The overall incidence of cough was significantly decreased in by propofol 6.0 μg.ml−1 compared with 0 or 3.0 μg.ml−1 propofol (p < 0.001). The incidence of severe cough was significantly lower with propofol 6.0 μg.ml−1 compared with 3.0 μg.ml−1 (p = 0.03). A propofol target effect‐site concentration of 6.0 μg.ml−1 effectively suppressed remifentanil‐induced cough when remifentanil was administrated at a target effect‐site concentration of 4.0 ng.ml−1.
Trans‐Atlantic, trans‐Pacific and trans‐Indian Ocean dispersal in the small Gondwanan Laurales family Hernandiaceae
Authors: Michalak Ingo , Zhang Li‐Bing , Renner Susanne S. 
Published: May 2010

AbstractAim  To investigate the historical biogeography of the pantropical flowering plant family Hernandiaceae (Laurales), which today comprises 62 species in five genera.Location  Hernandiaceae occur in Africa (9 species), Madagascar (4), the Neotropics (25), Australia (3), southern China, Indochina, Malesia, and on numerous Pacific Islands (32). These numbers include two widespread species, Hernandia nymphaeifolia, which ranges from East Africa to the Ogasawara Islands and New Caledonia, and Gyrocarpus americanus, thought to have a pantropical range.Methods  We sampled 37 species from all genera, the widespread ones with multiple accessions, for a chloroplast DNA matrix of 2210 aligned nucleotides, and used maximum likelihood to infer species relationships. Divergence time estimation relied on an uncorrelated‐rates relaxed molecular clock calibrated with outgroup fossils of Lauraceae and Monimiaceae.Results  The deepest split in the family is between a predominantly African–Madagascan–Malesian lineage comprising Hazomalania, Hernandia and Illigera, and an African–Neotropical lineage comprising Gyrocarpus and Sparattanthelium; this split may be 122 (110–134) Myr old. The stem lineages of the five genera date back at least to the Palaeocene, but six splits associated with transoceanic range disjunctions date only to the Oligocene and Miocene, implying long‐distance dispersal. It is inferred that Hernandia beninensis reached the West African islands of São Tomé and Bioko from the West Indies or the Guianas; Hernandia dispersed across the Pacific; and Illigera madagascariensis reached Madagascar from across the Indian Ocean.Main conclusions  The disjunct ranges and divergence times of sister clades in the Hernandiaceae are partly congruent with the break‐up of West Gondwana, but mostly with later transoceanic dispersal. An exceptional ability to establish following prolonged oceanic dispersal may be largely responsible for the evolutionary persistence of this small clade.
Biogeography of the Monimiaceae (Laurales): a role for East Gondwana and long‐distance dispersal, but not West Gondwana
Authors: Renner Susanne S. , Strijk Joeri S. , Strasberg Dominique , Thébaud Christophe 
Published: May 2010

AbstractAim  The biogeography of the tropical plant family Monimiaceae has long been thought to reflect the break‐up of West and East Gondwana, followed by limited transoceanic dispersal.Location  Southern Hemisphere, with fossils in East and West Gondwana.Methods  We use phylogenetic analysis of DNA sequences from 67 of the c. 200 species, representing 26 of the 28 genera of Monimiaceae, and a Bayesian relaxed clock model with fossil prior constraints to estimate species relationships and divergence times. Likelihood optimization is used to infer switches between biogeographical regions on the highest likelihood tree.Results  Peumus from Chile, Monimia from the Mascarenes and Palmeria from eastern Australia/New Guinea form a clade that is sister to all other Monimiaceae. The next‐deepest split is between the Sri Lankan Hortonia and the remaining genera. The African Monimiaceae, Xymalos monospora, then forms the sister clade to a polytomy of five clades: (I) Mollinedia and allies from South America; (II) Tambourissa and allies from Madagascar and the Mascarenes; (III) Hedycarya, Kibariopsis and Leviera from New Zealand, New Caledonia and Australia; (IV) Wilkiea, Kibara, Kairoa; and (V) Steganthera and allies, all from tropical Australasia.Main conclusions  Tree topology, fossils, inferred divergence times and ances‐tral area reconstruction fit with the break‐up of East Gondwana having left a still discernible signature consisting of sister clades in Chile and Australia. There is no support for previous hypotheses that the break‐up of West Gondwana (Africa/South America) explains disjunctions in the Monimiaceae. The South American Mollinedia clade is only 28–16 Myr old, and appears to have arrived via trans‐Pacific dispersal from Australasia. The clade apparently spread in southern South America prior to the Andean orogeny, fitting with its first‐diverging lineage (Hennecartia) having a southern‐temperate range. The crown ages of the other major clades (II–V) range from 20 to 29 Ma, implying over‐water dispersal between Australia, New Caledonia, New Zealand, and across the Indian Ocean to Madagascar and the Mascarenes. The endemic genus Monimia on the Mascarenes provides an interesting example of an island lineage being much older than the islands on which it presently occurs.
Alexithymia and eating behaviour in severely obese patients
Authors: Noli G. , Cornicelli M. , Marinari G. M. , Carlini F. , Scopinaro N. , Adami G. F. 
Published: May 2010

AbstractBackground:  Alexithymia is the inability to express feelings with words and comprises a psychological construct frequently found in obese individuals. In eating disordered patients who show a tendency to lose control over food intake, personality traits with alexithymic characteristics have been demonstrated. The present cross‐sectional study investigated the relationships between alexithymia and eating behaviour in severely obese patients.Methods:  This study analysed 150 obese patients undergoing bariatric surgery and 132 subjects at more than 1 year after biliopancreatic diversion (BPD), when body weight has steadily normalised and any preoccupation with weight, food and diet has been completely abandoned. Obese and operated subjects completed the Toronto Alexithymia Scale (TAS), and eating behaviour was assessed via a semi‐structured interview exploring binge eating disorder (BED), night eating and emotional eating, as well as by utilisation of the Three Factor Eating Questionnaire (TFEQ).Results:  Although alexithymic patients showed deranged eating behaviour, as evaluated by the TFEQ scores, the frequency of BED, night eating and emotional eating was similar in alexithymic (TAS > 60) and non‐alexithymic patients. However, the prevalence of alexithymia was similar in obese and BPD subjects, whereas, in the operated subjects, TFEQ scores were lower (P < 0.005) than those in obese patients.Conclusions:  These data suggest that, in severely obese patients, alexithymia does not influence eating behaviour; in severely obese patients, the tendency to lose control over food intake apparently represents a psychological construct that is substantially independent from alexithymia.