Discussion Only a few studies have reported increased serum BNP levels in patients with head AZD0156 cost trauma [7–10].

Costa et al. reported that serum BNP levels did not increase in patients with head injury and it had no correlation with cerebral salt-wasting syndrome [12]. Kavalci et al. reported that serum BNP might be useful in evaluation of head trauma [13]. Cevik et al. demonstrated that BNP levels exceeding 10 pg/ml were associated with an intracranial abnormality in patients with head injury [7]. Sviri et al. showed that serum BNP levels increased selleck inhibitor immediately following head injury [8]. Similarly, Lu et al. reported that BNP levels increased in patients with head trauma [9]. Cevik et al. showed that serum BNP levels significantly differed between patients with and without head trauma [7]. In contrast, we did not detect any significant difference between the 2 groups. We believe that this resulted from a low patient number in Group 2. We suggest that further studies with larger sample size may establish a relationship between serum BNP and head trauma. Neither, Çevik et al. nor Kavalci et al. showed a significant correlation between trauma mechanism and serum BNP. We also found a similar result. BNP appears to be released https://www.selleckchem.com/products/bay80-6946.html into bloodstream in all kinds of head trauma. Çevik et al. reported a significant relevance between delay in admission and

BNP levels. They showed that a positive correlation exists between admission time and BNP levels [7]. Kavalci et al. showed that there was no significant correlation between the serum BNP levels and admission time [13]. Our results are support to Kavalci et al. GCS is commonly used for assessment of neurological status of head trauma patients. There is a general agreement on the predictive power of GCS in patients with mild and serious head trauma, although there are various approach considerations with respect to radiological evaluation of minor head trauma cases. Thus, studies aiming to establish the indications

of CT scanning of the head region or criteria for hospital admission by using some biochemical markers and clinical features [3–5]. Some reports suggested that the severity of head trauma and serum BNP levels are not significantly correlated [7, 10, 13]. Wu et al., in contrast, reported that serum BNP levels increased to a greater Thiamine-diphosphate kinase extent in patients with more severe head trauma [11]. We found no significant correlation between head trauma severity and serum BNP levels. However, all of our patients with minor head trauma group. This subject should be further clarified with adequate studies. In a study by Çevik et al. serum BNP levels were significantly higher in patients with an intracranial lesion compared to those who did not. Cevik et al. proposed that serum BNP levels can be used as a surrogate marker of head trauma [7]. In contrast, Stewart et al. and Kavalci et al. suggested that this biomarker has no any appreciable value for this indication [10].

KCTC 11604BP. Significant differences in the regulation observed between these two strains obviously have a profound influence on the process development efforts at the industrial scale. Finally, we have demonstrated a potential for FK506 yield increase in engineered strains of S. tsukubaensis by simple overexpression of fkbN and fkbR, which could see more result in rapid and straightforward improvement of FK506 yield in the industrial fermentation process. Acknowledgements We thank the Government of Slovenia, Ministry of Higher Education, Science and Technology (Slovenian Research Agency, ARRS) for the award of Grant No. J4-9331 and No. L4-2188 to Hrvoje Petković. We also thank

the Ministry of the Economy, the JAPTI Selleck Akt inhibitor Agency and the European Social Fund for the funds awarded for employment of Gregor Kosec (contract No. 102/2008). This work was also supported by a Grant of the European Union ERA-IB project EU2008-0333656

to Juan F. Martin. C. Barreiro was supported by the European Union program ERA-IB [BioProChemBB project (EIB.08.008)]. M. Martínez-Castro received a PFU fellowship of the Ministry of Education and Science. We would like to thank Dr. Paul Herron and Prof. Lain Hunter for providing us the ermE* promoter with Streptomyces RBS. Electronic supplementary material Additional file 1: Table containing primers for PCR amplifications of the target putative regulatory genes (The file presents primers and their corresponding sequences, that have been used for PCR amplification of whole genes or homologous regions and promoter regions). (PDF 41 KB) Additional file 2: Schematic representation of FkbR and FkbN protein domains and deleted regions (This file illustrates FkbR and FkbN proteins and their organization before Etomidate and after inactivation). (PDF 13 KB)

Additional file 3: Primers used for RT-PCR analysis (This file presents a list of primers and their corresponding sequences, that have been used for RT-PCR experiments). (PDF 42 KB) References 1. Thomson AW: FK-506 enters the clinic. Immunol Today 1990,11(2):35–36.PubMedCrossRef 2. Wallemacq PE, Reding R: FK506 (tacrolimus), a novel immunosuppressant in organ transplantation: clinical, biomedical, and analytical aspects. Clin Chem 1993,39(11 Pt 1):2219–2228.PubMed 3. Meingassner JG, Stutz A: Immunosuppressive macrolides of the type FK 506: a novel class of topical agents for treatment of skin diseases? J Invest Dermatol 1992,98(6):851–855.PubMedCrossRef 4. Easton JB, Houghton PJ: Therapeutic potential of target of rapamycin inhibitors. Expert Opin Ther Targets 2004,8(6):551–564.PubMedCrossRef 5. Graziani EI: Recent advances in the chemistry, biosynthesis and pharmacology of rapamycin analogs. Nat Prod Rep 2009,26(5):602–609.PubMedCrossRef 6. McDaniel R, Welch M, Nec-1s datasheet Hutchinson CR: Genetic approaches to polyketide antibiotics. 1. Chem Rev 2005,105(2):543–558.PubMedCrossRef 7.

Another 24 patients who were recruited into a prospective randomized controlled trial were also excluded. Finally, the data obtained from 141 patients were analyzed to elucidate the renal outcome. The patients were followed

up until April 2012 or the last day of serum creatinine measurement before April 2012. The cohort study was conducted in accordance with the Declaration of Helsinki, and approved by the selleck chemicals llc Medical Ethics Committee of Jikei University School of Medicine. Definitions The endpoint was defined as a 50 % increase in serum creatinine from baseline. Disappeared proteinuria or hematuria was defined as a urinary protein excretion (UPE) <0.3 g/day or having urinary sediment of red blood cells (U-RBC) <5/high power field (hpf). Clinical remission was defined as the disappearance of both proteinuria and hematuria. The estimated glomerular filtration rate (eGFR) was calculated by the Japanese eGFR equation based on age, sex and serum creatinine [13]. Uncontrolled hypertension was defined as arterial blood AG-881 concentration pressure (BP) ≥130/80 mmHg [14]. Smoking status was defined according

to a report by Yamamoto et al. [15]. Treatment The 6-month steroid therapy was previously reported by Pozzi et al. [11, 12], and was modified for Japanese patients as follows: the patients received 0.5 g of methylprednisolone intravenously for three consecutive days at the beginning of the steroid course and again 2 and 4 months later; they were also given

oral prednisolone at a dose of 0.5 mg/kg every other day for 6 months. Some patients received a tonsillectomy for chronic tonsillitis complicated with IgAN just before the 6 months of steroid therapy. The patients were administered angiotensin-converting BCKDHA enzyme inhibitors or angiotensin receptor blockers (RAAS inhibitors) and antiplatelet agents as needed. Histology To examine the impact of pathological changes on renal survival, renal biopsy data were obtained if a biopsy was performed within 1 year before corticosteroid therapy. All renal biopsy specimens were processed 3-Methyladenine cell line routinely for light microscopy. Sections were stained with hematoxylin and eosin and periodic acid–Schiff, together with silver methenamine and Masson’s trichrome. Pathological variables were evaluated according to the Oxford classification [16]. “Histological grade (HG)” recently reported from the Special Study Group on Progressive Glomerular Disease in Japan was also adopted in this study [17]. Briefly, four histological grades, HG 1, HG 2, HG 3 and HG 4, were established corresponding to <25, 25–49, 50–74 and ≥75 % of glomeruli exhibiting cellular or fibrocellular crescents, global sclerosis, segmental sclerosis or fibrous crescents. Statistical analyses Normally distributed variables were expressed as the mean ± standard deviation (SD) and compared using the t test or one-way ANOVA.

This last finding is in contrast with the recent results reported by Ho and colleagues LY2606368 price [23] who analyzed the role of YodA (ZinT) in the E. coli O157:H7 strain EDL933, observing that the zin T mutant strain exhibits a dramatic reduction in its ability to adhere to HeLa cells and to colonize the infant rabbit intestine [23]. Furthermore, they observed a reduction in growth

of the zin T mutant also in LB medium. In principle, divergences between these two studies could due to genotypic differences between the strains employed or to differences in the E. coli ability to interact with different eukaryotic cell lines. However, it is worth nothing that the reduction in growth of the zinT mutant in LB medium observed by Ho et al. is unexpected on the basis of the presumed role of ZinT in zinc import and that, in line with the here reported results, zin T mutants of S. enterica [18] and E.

coli K12 [24, 25] grow as well as the wild type parental strains in zinc replete media. Moreover, Ho and colleagues identified ZinT even in the culture supernatants of E. coli O157:H7 strain and suggested that it is a substrate of the type 2 secretion CYT387 system (T2SS) [23]. We have confirmed that a fraction of ZinT is actually exported selectively (ZnuA is not secreted) in the culture medium (Figure 7), but we failed to validate the suggestion that the secretion of this protein is facilitated by T2SS. In fact, ZinT is exported with comparable efficiency by the click here wild type strain or by mutant strains lacking etp C or etp D genes which encode for two different components of the T2SS gene cluster [33]. Moreover, we observed that ZinT is secreted also in E. coli K12 and B strains. This observation strongly

argues against the involvement of T2SS in the export of ZinT because the genes encoding for the T2SS system are not expressed in E. coli K12 due to the repression by the histone-like nucleoid-structuring protein H-NS [34, 35]. We hypothesize that pheromone the different result obtained by Ho et al. could be explained by their choice to analyze the secretion of ZinT in a strain overexpressing a V5-tagged ZinT. The T2SS might be involved in the recognition of this specific tag or in the secretion of proteins when overexpressed [37]. In any case, the T2SS system seems not to participate in the secretion of chromosomally encoded ZinT. We have demonstrated that ZinT can be exported in the extracellular environment only in the metal free form. In fact, when ZinT is constitutively expressed in bacteria grown in media containing cadmium or zinc, it can not be identified in the culture supernatants, despite it is present in the periplasmic space (Figure 7). The release of metal-free ZinT in the extracellular environment may influence properties of the bacterial or host cells.

100 μL from each well were plated onto TS agar and incubated overnight at 37°C. For the invasion assay, the monolayer Barasertib clinical trial was washed three times with DPBS. Two millilitres of cell culture medium supplemented with 1% antibiotic/antimycotic solution and 100 μg/mL gentamicin (Gibco) were added to each well. The 6-well

plates were incubated for another 2 h at 37°C and 5% CO2 to kill extracellular and surface-adherent bacteria. Afterwards, the monolayers were washed three times with DPBS and bacteria were quantified as described for the adherence assay. Assays were performed in duplicate and repeated twice. For comparative reasons, isolate 21702 was used as an internal assay control in every assay. Antibiotic efficacy Ro 61-8048 mw of the invasion assay was tested for all strains with concentrations of 107 CFU/mL in pure cell culture medium, confirming that no viable bacteria were present after 2 h incubation (data not shown). Mechanical stretch Cultures of EA.hy926 were subjected

to cyclic tension using a FlexCell vacuum system (FlexCell, Dunn Laboratories, Hillsborough, USA). Cells were cultured on BioFlex culture plates (FlexCell) coated with collagen I in a humidified atmosphere with 5% CO2 at 37°C for 72 h. Afterwards cultures were stretched by 10% with a frequency of 1 Hz in a square wave pattern for another 24 h. EA.hy926 from the same preparation and cultured without mechanical Exoribonuclease stretch were used as controls. Stretched cells and controls were infected immediately after completion of mechanical stretch as described above. Biofilm assay The biofilm assay used in this study was performed as described previously [30] with the following modifications: absorbance was measured using the GENios Plate Reader (Tecan Deutschland GmbH, Crailsheim, Germany) at 450 nm (total bacterial growth) and 550 nm (crystal violet (CV), biofilm formation). Each strain was assayed in quintuplicate. ECM assay

96 well microtiter plates were coated with 10 μg/mL fibrinogen (human plasma, Sigma). Microtiter plates precoated with collagen I, collagen II, collagen IV, fibronectin, laminin, tenascin and vitronectin were purchased from Chemicon (Millipore, Schwalbach, Germany). Wells coated with BSA were used as negative controls and values were subtracted. Late-log-phase cultures of bacteria were inoculated into 100 μL BHI medium (Oxoid) and incubated on pre-coated wells without agitation for 2 h at 37°C. Subsequently, wells were washed twice with DPBS and dried for 20 min at 60°C. In parallel, bacteria were plated onto BHI agar and incubated overnight at 37°C. Attached bacteria were stained with 100 μL of 0.4% CV at room temperature for 45 min. Wells were rinsed five times with PBS and air dried. CV was solubilized in 100 μL ethanol (99%), and the absorbance was measured at 550 nm. Each strain was assayed in Cilengitide cell line quadruplicate for the different ECM proteins.

We have thought this system as two parallel ‘wires’ connected to the same reservoirs, whether the the leads are made of graphene or another material. This consideration allows us to study the transport of a hypothetical circuit made of graphene ‘wires’ in different scenarios. A schematic view of a considered system is shown

in Figure 1. We have focused our analysis on the electronic transport modulations due to the geometric confinement www.selleckchem.com/products/go-6983.html and the presence of an external magnetic field. In this sense, we have studied the transport response due to variations of the length and widths of the central ribbons, considering symmetric and asymmetric configurations. We have obtained interference effects at low energies due to the extra spatial confinement, which is manifested by the apparition of resonant states at this energy range, and find more consequently, a resonant tunneling behaviour in the conductance curves. On the other hand, we have considered the interaction of electrons

with a uniform external magnetic field applied perpendicular to the heterostructure. We have observed periodic modulations of the transport properties as function of the external field, obtaining metal-semiconductor transitions as function of the magnetic flux. Figure 1 Schematic view of the conductor. Two finite armchair graphene ribbons (red lines). The length L of the conductor is measured in unitary cell units. Methods All considered systems have been described using a single Π-band tight binding Hamiltonian, taking AZD4547 research buy into account only the nearest neighbour interactions selleck compound with a hopping γ 0 = 2.75eV[24]. We have described the heterostructures using surface Green’s function formalism within a renormalization scheme [16, 17, 25]. In the linear response approach, the conductance is calculated using the Landauer formula. In terms of the conductor Green’s function, it can be written as [26]: (1) where , is the transmission function of an electron crossing the conductor region,

is the coupling between the conductor and the respective lead, given in terms of the self-energy of each lead: Σ L/R  = V C,L/R g L/R V L/R,C . Here, V C,L/R are the coupling matrix elements and g L/R is the surface Green’s function of the corresponding lead [16]. The retarded (advanced) conductor Green’s function is determined by [26]: , where H C is the hamiltonian of the conductor. Finally, the magnetic field is included by the Peierls phase approximation [27–31]. In this scheme, the magnetic field changes the unperturbed hopping integral to , where the phase factor is determined by a line integral of the vector potential A by: (2) Using the vectors exhibited in Figure 1, R 1 = (1, 0)a, and , where a = |R n,m | = 1.

01% CO2, Scott Medical Products, USA). Respiratory data were averaged at 30 s intervals to determine VO2max taken as the highest average value. The ventilatory threshold (VT) and the respiratory compensation point (RCP) were measured by three independent

reviewers according to methods described by Wasserman selleck inhibitor et al. [21]. In addition, heart rate was continuously recorded using a portable heart rate monitor (Polar RS800 SD, Finland). Heart rate data were averaged at 10 s intervals and the maximum heart rate was defined as the heart rate achieved at the point of exhaustion. Nutritional data After the test all the athletes received nutritional guidelines and were encouraged to follow a high carbohydrate diet during the three days prior to the competition in order to optimize their glycogen replenishment. However, during the competition, there were no constraints and the nutritional pattern was programmed by the cyclists themselves. Furthermore, they received no Selleck 17-AAG direct instructions from the investigators during the event. Seven trained investigators were divided among the boxes weighing and recording all the food and fluid ingested by each participant

during the recovery periods. To weigh all the food, we used two digital scales (Soehnle 8020, Spain) with a precision of 1 g increments up to 1 kg and 2 g between 1 and 2 kg. During the race, it was forbidden to provide to the athletes food and fluids in any point of the circuit with the exception of the box. All the food and fluids that cyclists consumed before NU7441 every relay were weighed and recorded by the researchers. Immediately after every relay, food and fluids were weighed and recorded by the researchers again. The difference in weight was considered as the amount of food and fluids ingested by the cyclists during exercise. The type of food and fluids of sport products such as energy Etoposide price bars and gels ingested by the cyclists were described and recorded using the labels of the products. Information derived from prepared foods such as pasta, rice or sandwich

was provided asking the form of preparation, directly, to the cyclists. The nutritional data was analyzed for nutrient composition using nutritional software. To guarantee a more accurate conversion of energy and nutrient intakes, we used a database of food from the country where the study was carried out (CESNID 1.0, Barcelona University, Spain). Information about the nutritional content of food not available in the computer program was obtained from the manufacturer. We divided the ingestion of energy derived from solid and fluid food (i.e. classified as products that did not need mastication). Each subject was weighed 30 minutes prior to the race, after every cycle session and immediately after finishing the competition. The subjects were always weighed in clothing, shoes and bicycle helmets in order to facilitate the collection of the research data during the event. Weights were measured on calibrated scales placed on a hard level surface.

SMH also drafted the manuscript. YW carried

out the Western blot analysis and drafted the manuscript. J-PZ, LW and FH participated in the survival analysis. G-DG conceived of the study, and participated in its design and coordination. All authors read and approved the final manuscript.”
“Background Various weight loss supplements are commercially TSA HDAC molecular weight available and are composed of a wide variety of ingredients. Combined with a low calorie diet, some dietary supplements could possibly lead to changes in metabolism and/or suppression of appetite that could lead to improved body composition. The purpose of this study was to investigate the effects of ingesting a commercially available find more dietary supplement and its effects on body composition, resting energy expenditure Emricasan mw (REE), hunger, and various blood markers in free-living, overweight individuals. Methods Fifty-four male and female (40.7 ± 8.28 yrs, 90.82 ± 15.62 kg, 34.02 ± 7.42 %BF) subjects completed both acute (2.5 hours) and sub-acute (8 days) testing in a double-blind and placebo controlled design. Participants were divided into three groups: placebo (PL), high dose (EXP1), and standard dose (EXP2) in a matched-pair, randomized manner based on %BF. Baseline measurements included body composition

via DEXA, blood collection, hunger scale, hemodynamics, and REE. Participants consumed the supplement and repeated testing at various time points for a period of 2 hours while resting in a supine position. Participants consumed the supplement (proprietary blend of: L-arginine, L-carnitine, L-ornithine, EGCG, saffron extract, black cohosh) for 7 days (daily dose per group: EXP1: 3032 mg; EXP2: 1516 mg) and repeated all testing. Dependent variables were analyzed as means and delta (Δ) responses from baseline using a 2-way (group X time) ANOVA with repeated measures (p

< 0.05). Results Significant main effect for time was seen for Δfat mass (p = 0.002), Δbody mass (p = 0.029), and Δ%BF (p = 0.006). A trend for significance (p = 0.08) was observed for %BF, indicating a possible benefit for a reduction heptaminol in body fat in the standard dose group (EXP2). Change in %BF from baseline was greatest in EXP2 (PL: -0.167 ± 1.17, EXP1: -0.23 ± 0.93, EXP2: -1.01 ± 1.49 Δ%BF). Significant main effect for time (p = 0.000) and a group x time interaction for acute free fatty acid (FFA) appearance (T1: p = 0.000; T2: p = 0.014) were observed. Post-hoc testing indicated FFA levels rose significantly at 90 and 120 mins in EXP2, while PL significantly decreased over the same time period. Despite mean increases in REE, no differences for time or group were observed. No negative effects on blood (complete metabolic panel/CBC) or hemodynamic (SBP, DBP, RHR) safety variables were observed.

The lysing solution causes protein Crenigacestat clinical trial denaturation, so theoretically, the sensitivity-resistance assay is adequate to investigate sensitivity to fluoroquinolones at the relevant doses. CIP-mediated DSBs are natively unconstrained and are considered irreversible and lethal. In the case of first-generation quinolones such as nalidixic acid, the technique would artificially unconstrain DSBs that are naturally confined in the cleaved complex. If so, both reversible non-lethal DSBs and later lethal unconstrained DSBs should be detected Ralimetinib supplier without but cannot be differentiated in the

assay. Addition of the chelating agent EDTA seems to reverse the cleaved complex formation by quinolones [7], possibly because incubation with EDTA before lysis allows the resealing of the reversible DNA breaks so that only the irreversible DSBs would be detected. CIP-induced DSBs were not totally irreversible, and a progressive repair activity with time was evident in TG1. The magnitude of DNA repair was inversely related to dose and was noticeable after a dose of 0.1 μg/ml but scarce after a dose of 10 μg/ml. This repair was evident when the antibiotic was removed after the 40 min incubation and when TG1 was exposed continuously to the low dose (0.1 μg/ml) without CIP removal. The progressive selleckchem spontaneous CIP degradation or inactivation with time in

culture cannot be discounted, and the effect of CIP could be smaller despite being long lasting, especially if added at a low dose. E. coli may repair DSBs by RecA-dependent homologous recombination (HR) [24]. CIP-induced DSBs could be processed to single-stranded DNA, a target for RecA, which promotes recombinatorial repair and induction of the SOS response through activation of the autocleavage of the LexA repressor [25, 26]. Rapid lethality is increased by the lexA Tau-protein kinase Ind-allele, and recombination-deficient E. coli strains are hypersensitive

to quinolones [27]. The RecBCD nuclease/helicase also seems to be required for SOS induction by quinolones, as demonstrated with nalidixic acid [28]. Interestingly, DSBs may also be repaired by a non-homologous end joining (NHEJ) mechanism that comprises break recognition, end processing, and ligation activities. Although E. coli lacks a NHEJ pathway, its presence has been demonstrated in mycobacteria and bacillus [29]. Nevertheless, NHEJ deficiency caused by the loss of Ku and ligD has no effect on the sensitivity to quinolones of Mycobacterium smegmatis [30]. Repair of quinolone-induced DSBs probably needs more complex processing because both 5′ ends of cleaved DNA are linked covalently via phosphotyrosine bonds to a topoisomerase subunit. These DNA-protein crosslinks (DPCs) could be eliminated in coordination with the nucleotide excision repair (NER) mechanism. The urvABC nuclease, which initiates the NER pathway in E.

The decreased operative space requires a more experienced surgeon and increases the learning curve. This exposure level was not sufficient for morbidly obese patients, men with very strong abdominal muscles, or those without good anesthesia. Abdominal respiration, which is not eliminated by EPA, produces a “tidal” up and down motion in the surgical field in some patients. To avoid injury to the small check details intestine, some procedures must be performed during the ebb. Furthermore,

gasless exposure is generally limited to a specific quadrant of the abdomen, which restricts exploration of the epigastric zone. It would be BVD-523 cost befitting to acknowledge the limitations of our study. First, our follow up was limited to 1 month postoperatively. Our aim was to look for early postoperative complications postdischarge. Second, the treatment allocation and clinical outcome assessment were not blinded. Third, fentanyl consumption may not be representative because PCA was only administered XAV939 to those patients who asked to use it. Conclusions In our study, GLA and LA had comparable operative durations, complications, and total hospital stay lengths. However, GLA significantly reduced

the hospital cost. The demand for postoperative analgesics may also decrease following GLA. In conclusion, GLA is a safe and feasible procedure in selected patients. Future studies should assess GLA in elderly patients with chronic obstructive pulmonary disease.

It has been demonstrated that laparoscopic surgery is associated with a lower systemic stress response than open surgery, but intraperitoneal carbon dioxide insufflation attenuates peritoneal immunity [29]. Ultrastructural, filipin metabolic, and immune alterations are observed at the peritoneal surface in response to a pneumoperitoneum [30]. Therefore, gasless laparoscopy may preserve peritoneal immunity theoretically. But this also requires confirmation in future studies. Acknowledgement The project is supported by the National Natural Science Foundation of China (Grant No. 81100324) and The Department of Health of Shanghai (Grant No. 2010Y085). References 1. Semm K: Endoscopic appendectomy. Endoscopy 1983, 15:59–64.PubMedCrossRef 2. Nguyen NT, Zainabadi K, Mavandadi S, Paya M, Stevens CM, Root J, Wilson SE: Trends in utilization and outcomes of laparoscopic versus open appendectomy. Am J Surg 2004, 188:813–820.PubMedCrossRef 3. Laine S, Rantala A, Gullichsen R, Ovaska J: Laparoscopic appendectomy-is it worthwhile? A prospective, randomized study in young women. Surg Endosc 1997, 11:95–97.PubMedCrossRef 4. Egawa H, Morita M, Yamaguchi S, Nagao M, Iwasaki T, Hamaguchi S, Kitajima T, Minami J: Comparison between intraperitoneal CO2 insufflation and abdominal wall lift on QT dispersion and rate-corrected QT dispersion during laparoscopic cholecystectomy. Surg Laparosc Endosc Percutan Tech 2006, 16:78–81.PubMedCrossRef 5.