3B). Interestingly, RANKL treatment had no effect on the recruitment of neutrophils to the liver, as measured by liver MPO content, in either moderate or severe I/R injury (Fig. 3). These biochemical findings were confirmed by histological examination (Fig. 3). After an 8-hour reperfusion, the control group showed significant congestion

Fulvestrant mouse and hepatocellular necrosis, whereas the RANKL treatment group showed less congestion and smaller areas of necrosis compared to the control group. These effects were observed in both moderate (Fig. 3A) and severe (Fig. 3B) models of I/R. In order to determine if the protective effects of RANKL were a result of altered expression of cytokines, we assessed the expression

of a panel of cytokines known to be involved in I/R injury. RANKL treatment had no effect on the expression of TNF-α, MIP-2, or KC (Table 2). RANK-RANKL interactions result in the activation of NF-κB.24 Our Alvelestat research buy previous studies show that NF-κB activation in hepatocytes is cytoprotective during I/R.12, 25 Given that we found strong RANK expression on hepatocytes and very limited expression on Kupffer cells, we next assessed the activation of NF-κB in the liver after I/R. Treatment with recombinant RANKL significantly increased liver NF-κB activation after 8 hours of reperfusion in both moderate and severe models of I/R (Fig. 4A). We then examined the effect of RANKL on Bcl-2 expression. Bcl-2 is an antiapoptotic gene regulated by NF-κB that is known to have hepatoprotective effects in I/R injury.26-28 Treatment with recombinant RANKL significantly upregulated Bcl-2 protein expression after 8 hours reperfusion in both moderate and severe I/R models in a manner similar to NF-κB induction (Fig. 4B). Because we found that RANKL increases hepatic NF-κB activation in vivo, we sought to determine whether RANKL induces

Oxalosuccinic acid NF-κB activation in hepatocytes. The murine hepatocyte cell line, AML-12, was used to assess the effects of RANKL on NF-κB activation. In these cells, treatment with 10 or 100 ng/mL recombinant RANKL resulted in robust activation of NF-κB within 1 hour (Fig. 5A). These results were validated in primary hepatocytes, where 10 ng/mL recombinant RANKL significantly induced NF-κB activation within 30 minutes and its activation was maintained for at least 3 hours (Fig. 5B). Finally, we assessed whether RANKL has direct effects on hepatocytes to limit cell death. Primary mouse hepatocytes were isolated and treated with recombinant RANKL prior to inducing cell injury with 200 μM H2O2 and 50 ng/mL TNF-α. Treatment with RANKL significantly reduced hepatocyte cell death by approximately 40% (Fig. 5C). Thus far, our data suggest that recombinant RANKL is protective against hepatic I/R injury when administered prior to injury.

Notably, basal respiration was decreased in cells harboring HCV

proteins, yet oxygen consumption could still be stimulated by FCCP, suggesting that HCV protein expression affected ATP synthesis. This result is consistent with our recent report showing a significant inhibition of the FoF1 ATP-ase activity in HCV protein-expressing cells.23 Consistently, CypD was found to affect synthesis and hydrolysis of ATP by binding ATP synthase with CsA modulating this binding and, thereby, the activity of the ATP synthase.25 This could contribute to the observed rescue of resting respiration by alisporivir. A major trigger Obeticholic Acid purchase of MPTP opening is mitochondrial calcium overload.15 By using the calcium probe Rhod-1, which specifically detects intramitochondrial calcium (mtCa2+), we previously found that HCV protein expression Small molecule library solubility dmso for 48 hours resulted in a significant increase of mtCa2+.19 Inhibitors of the mitochondrial calcium uniporter

or of the endoplasmic reticulum (ER) calcium channel efficiently prevented mitochondrial calcium overload.19, 20 Importantly, alisporivir prevented mtCa2+ accumulation in a dose-dependent fashion. As shown in Fig. 3, maximal protective effect was already observed at a concentration of 0.125 μM. Mounting evidence from experimental and clinical observations indicates that HCV infection is causally linked with alterations of the intracellular redox state and that these may be involved in the pathogenesis of hepatitis C.20 Notably, oxidative stress proved to be a condition favoring MPTP opening.26, 27 As reported previously,19 HCV protein expression resulted in a marked increase of cellular ROS

production, as assessed by the hydrogen peroxide-sensitive fluorescent probe dichlorofluorescein (Fig. 4A). Closer analyses by LSCM revealed a bright fluorescence signal in intracellular compartments corresponding to the mitochondrial network. Alisporivir prevented ROS production as a result of HCV protein expression at a concentration as low as 0.125 μM (Fig. 4B). The results above clearly demonstrate that alisporivir prevents HCV protein-mediated mitochondrial Nintedanib (BIBF 1120) dysfunction. Next, we asked whether alisporivir may also revert already established mitochondrial dysfunction. To this end, treatment with alisporivir at a concentration of 0.125 μM was initiated 36 hours after the induction of HCV protein expression. As shown in Fig. 5A-C, alisporivir reverted within 12 hours HCV protein-mediated collapse of the mtΔΨ, production of ROS and mitochondrial calcium overload of mtCa2+. Thus, alisporivir cannot only prevent but also revert already established mitochondrial dysfunction in this experimental setting. Opening of the MPTP elicits redistribution of small proapoptotic proteins located in the mitochondrial intermembrane space, such as cytochrome c, to the extramitochondrial compartment.12 As shown in Fig. 6A, inducible expression of the HCV polyprotein resulted in a marked change of the cytochrome c–related immunofluorescence detection.

05). Ta screws had a statistically higher preload loss percent than WC/CTa learn more screws

in all three implant connections (p < 0.05), indicating that WC/CTa screws were superior in maintaining the preload than Ta screws. Conclusions: Within the limits of present study, the following conclusions were made: (1) WC/CTa screws provided higher preload than noncoated Ta screws in all three implant connection systems. (2) The initial removal torque for Ta screws required higher force than WC/CTa screws, whereas postload removal torque for Ta screws was lower than WC/CTa screws. Calculated Ta screw preload loss percent was higher than for WC/CTa screws, suggesting that WC/CTa screws were more effective in maintaining the preload than Ta screws. (3) Internal conical connections were more effective in maintaining the screw preload in cyclic loads than external-hex butt joint connections. "
“Purpose: The purpose of this prospective clinical study was to determine the success rate of single-unit this website posterior fixed dental prostheses (FDPs) with zirconia copings generated with two CAD/CAM systems, compared to porcelain-fused-to-metal (PFM) single-unit posterior FDPs after 5 years of function. Materials

and Methods: From 2005 to 2006, 60 patients who needed a single-unit FDP on a first molar in the mandibular jaw (left or right) in a private office setting were included in this study. The 60 first mandibular molars were randomly divided into three groups (n = 20): in the control group (group C), 20 PFM FDPs were included. In the other two groups CAD/CAM technology was used for the fabrication of the zirconium-oxide copings: 20 single-unit posterior FDPs with zirconia copings were generated with the Procera system (group P, Nobel Biocare); 20 single-unit Interleukin-2 receptor posterior FDPs with zirconia copings were generated with the Lava system (group L, 3M ESPE).

For the ANOVA follow-up data, the clinical life table method was applied. The statistical analysis was performed using two nonparametric tests, the log-rank test for k-groups and the Fisher exact test. Results: No statistically significant difference in the clinical outcome of zirconia–ceramic FDPs of both groups (P and L) evaluated together and metal–ceramic posterior single FDPs was found at 5 years of function; however, clinical data showed that technical problems, such as extended fracture of the veneering ceramic, tended to occur more frequently in the zirconia–ceramic FDP groups. The difference in the frequency of failure was statistically significant only in the comparison of groups C and P.

Q-RT-PCR was performed to detect ISGs 6 hours posttreatment. HepG2 cells transfected with pEco63-1.3 (HBV 1.3x expression plasmid constructed using HBV sequence from pEco63) were treated with cTCR-L/IFNα ± 10 μg/mL HBc18-27 peptide, Roferon, or Peg-IFNα (Pegasys). After 72 hours the viral supernatant was collected and S-antigen was quantified using an HBsAg chemiluminescence Z-VAD-FMK immunoassay kit. HBV-specific CD8 T cells were cocultured with HBV peptide-pulsed or not pulsed HepG2 cells

with TCR-L/IFNα, fixed, and stained for IFNγ-PE. HepG2 were incubated with HBV-specific CD8 T cells alone or with TCR-L/IFNα overnight. Supernatants were collected after 18 hours and concentrations of CXCL-9 and CXCL-10 were measured using the Cytometric Bead Array System (BD Biosciences, San Jose, CA). In selected experiments, intracellular cytokine staining using fluorescent-conjugated anti-CXCL-10 antibodies was used. We recently reported the production and characterization click here of a murine IgG1 antibody specific for the surface HBs183-91/A*02:01 complex (sTCR-L).11 A second antibody specific for core HBc18-27/A*02:01 complex, a dominant HLA-A201 HBV-epitope, was produced using the same method. Figure 1 shows the specificity data of both cTCR-L (specific for HBc18-27/A*02:01) and sTCR-L (specific for HBs183-91/A*02:01). Both TCR-Ls selectively recognize

HLA-A*02:01+ targets pulsed with the respective specific peptides (Fig. 1A). In addition,

both TCR-Ls bound to HBV-producing HepG2 cells, but did not bind to HepG2 cells that had not been transfected with HBV (Supporting Fig. 1) or cells pulsed with other A*02:01 these binding peptides. The specific recognition of HBc18-27 pulsed cells or HBV-producing cells by cTCR-L antibodies was not influenced by the presence of serum from CHB patients (data not shown), as demonstrated for sTCR-L.11 The two antibodies were tested for their ability to recognize naturally infected cells by immunohistochemistry on frozen liver biopsies from patients with CHB (Fig. 1B) or by staining of isolated hepatocytes purified from CHB patients biopsies (Fig. 1C). Both antibodies specifically recognized, with variable frequencies, the hepatocytes of HLA-A*02:01+ patients with CHB, but they did not bind to hepatocytes purified from HLA-A*02:01-negative subjects (Fig. 1B,C). The possible broadness of applicability of both cTCR-L and sTCR-L in patients of different ethnicities infected by different HBV genotypes was studied by analyzing the TCR-Ls ability to recognize the peptides of the respective HBc18-27 and HBs183-91 epitopes of HBV genotypes A, B, C, D, E, and F presented by different HLA-A*02 allotypes. Amino acid sequences of the corresponding peptides are shown in Fig. 1D with a description of the HLA-A02* subtypes present in distinct human populations listed in Fig. 1D.

Q-RT-PCR was performed to detect ISGs 6 hours posttreatment. HepG2 cells transfected with pEco63-1.3 (HBV 1.3x expression plasmid constructed using HBV sequence from pEco63) were treated with cTCR-L/IFNα ± 10 μg/mL HBc18-27 peptide, Roferon, or Peg-IFNα (Pegasys). After 72 hours the viral supernatant was collected and S-antigen was quantified using an HBsAg chemiluminescence Fludarabine datasheet immunoassay kit. HBV-specific CD8 T cells were cocultured with HBV peptide-pulsed or not pulsed HepG2 cells

with TCR-L/IFNα, fixed, and stained for IFNγ-PE. HepG2 were incubated with HBV-specific CD8 T cells alone or with TCR-L/IFNα overnight. Supernatants were collected after 18 hours and concentrations of CXCL-9 and CXCL-10 were measured using the Cytometric Bead Array System (BD Biosciences, San Jose, CA). In selected experiments, intracellular cytokine staining using fluorescent-conjugated anti-CXCL-10 antibodies was used. We recently reported the production and characterization SAHA HDAC of a murine IgG1 antibody specific for the surface HBs183-91/A*02:01 complex (sTCR-L).11 A second antibody specific for core HBc18-27/A*02:01 complex, a dominant HLA-A201 HBV-epitope, was produced using the same method. Figure 1 shows the specificity data of both cTCR-L (specific for HBc18-27/A*02:01) and sTCR-L (specific for HBs183-91/A*02:01). Both TCR-Ls selectively recognize

HLA-A*02:01+ targets pulsed with the respective specific peptides (Fig. 1A). In addition,

both TCR-Ls bound to HBV-producing HepG2 cells, but did not bind to HepG2 cells that had not been transfected with HBV (Supporting Fig. 1) or cells pulsed with other A*02:01 Amylase binding peptides. The specific recognition of HBc18-27 pulsed cells or HBV-producing cells by cTCR-L antibodies was not influenced by the presence of serum from CHB patients (data not shown), as demonstrated for sTCR-L.11 The two antibodies were tested for their ability to recognize naturally infected cells by immunohistochemistry on frozen liver biopsies from patients with CHB (Fig. 1B) or by staining of isolated hepatocytes purified from CHB patients biopsies (Fig. 1C). Both antibodies specifically recognized, with variable frequencies, the hepatocytes of HLA-A*02:01+ patients with CHB, but they did not bind to hepatocytes purified from HLA-A*02:01-negative subjects (Fig. 1B,C). The possible broadness of applicability of both cTCR-L and sTCR-L in patients of different ethnicities infected by different HBV genotypes was studied by analyzing the TCR-Ls ability to recognize the peptides of the respective HBc18-27 and HBs183-91 epitopes of HBV genotypes A, B, C, D, E, and F presented by different HLA-A*02 allotypes. Amino acid sequences of the corresponding peptides are shown in Fig. 1D with a description of the HLA-A02* subtypes present in distinct human populations listed in Fig. 1D.

Data regarding therapy for CHC patients with occult HBV are limited and based on small case numbers. However, the available information does not support occult HBV alone as a major factor that influences rates of SVR. Therefore, universal screening of HBV DNA by PCR for CHC patients before the initiation of antiviral therapy is not recommended but should be considered in selected cases. “
“Aim: 

This study investigated the correlation between remnant spleen volume after splenectomy (SPX) and the degree of hepatic steatosis and/or inflammation. Methods:  Male Sprague–Dawley rats selleck inhibitor were fed HF food and divided into three groups: sham-operation (Sham) group, a hemisplenectomy (H-SPX) group, and a total-splenectomy (T-SPX) group. Serum was collected and livers removed 12 weeks after surgery. We measured serum lipid markers and evaluated liver changes by comparing the three groups. Additionally, we examined liver changes 24 weeks after SPX. Results:  Serum triglyceride and free fatty acid levels after SPX were higher than those of sham controls,

and a significant difference was found between T-SPX and the other groups (P < 0.05 for each). Increased intrahepatic fat accumulation was shown in SPX rats along with lower residual spleen volume; this fat accumulation after SPX was accelerated in rats at 24 weeks. Additionally, liver inflammatory changes, including an increase in the Kupffer cell population and pro-inflammatory cytokine production, as well as a high level of oxidative stress, were observed in the liver sections from SPX rats, which correlated significantly with less volume Barasertib of the residual spleen. Also, an increase in pro-inflammatory cytokine content and a decrease in anti-inflammatory cytokine content were shown in the residual spleen from H-SPX rats, as compared to those of sham controls (P < 0.05 for each). Conclusion:  These results indicate the importance of preserving splenic tissue. This residual spleen may play an Nutlin-3 purchase important role in preventing the progression from diet-induced hepatic steatosis to steatohepatitis. “
“Hepatic

steatosis is an important parameter to assess in chronic liver disease patients. The controlled attenuation parameter (CAP) assesses liver steatosis using transient elastography. To determine the accuracy of CAP for evaluation of hepatic steatosis in chronic hepatitis B virus (CHBV)-infected, chronic hepatitis C virus (CHCV)-infected, and non-alcoholic fatty liver disease (NAFLD) patients and to determine the influence of etiology on the diagnostic accuracy of CAP. One hundred forty-six CHBV patients, 108 CHCV-infected patients and 63 patients with NAFLD, who underwent both liver biopsy and successful CAP measurements within the study period, were assessed. Area under the receiver operating characteristics was used to evaluate performance of CAP for diagnosing steatosis compared with biopsy.

Future studies should consider PCR product size when designing pyrosequencing assays for plasma DNA. Using ≥5% methylation as the cutoff for positivity, the frequency of positive plasma DNA samples ranged from

37% to 63%. When any one gene positive was used to define a positive case, 87% were positive. These results, in conjunction with our previous study of plasma from controls,22 suggest that analysis of plasma DNA is feasible and may be useful for the diagnosis of HCC. However, the quality of the bisulfite-treated plasma DNA will be a key component of a successful screening assay. Among the strengths of our study is that it is the largest sample-size methylation-array study of HCC to date. Among the limitations is the lack of information on AFB1-DNA in adjacent nontumor tissue, for some cases. In addition, data on alcohol consumption and cigarette smoking were missing Roscovitine supplier for approximately 20% of the cases. These missing data limited our ability to investigate relationships between methylation profiles and these factors. In addition, almost all our cases were infected with either HBV or HCV or both. Thus, we could not investigate the role of viral infection on methylation. FG4592 Another limitation was the lack of healthy tissue from unaffected controls as a comparison group for

our array studies. Our tumor adjacent tissues were primarily cirrhotic. Thus, we identified genes whose methylation was increased in progression from cirrhosis to HCC. Because our aim was to identify genes whose methylation is associated

with HCC but not cirrhosis, this comparison is appropriate, but tells us nothing about progression from normal tissue. A limitation of our plasma DNA analysis is that only samples from cases were available. Thus, whereas the frequency of methylation was high, we have no data on controls. In our previous prospective study of plasma DNA analyzing three genes using methylation-specific PCR, we found 2 of 50 (4%) controls with CDKN2A methylation and comparable many cases positive (44% versus 48%).22 In summary, we used genome-wide methylation arrays to identify genes methylated in HCC from primarily HBV-infected Taiwanese cases. Pyrosequencing of candidate genes validated the array data, and analysis of plasma DNA suggests that these genes may be appropriate to apply as biomarkers of early HCC diagnosis. We are in the process of testing custom arrays for analyzing larger numbers of CpG sites followed by pyrosequencing that can be applied to small amounts of plasma DNA. We will then use this methodology in our prospective study that includes HCC cases and controls, as required, to further determine the utility of this approach. The authors thank Dr. Abby Siegel for careful reading of the manuscript for this article. Additional Supporting Information may be found in the online version of this article.

Identification of the cell(s) of origin and the signaling pathways involved are challenging issues in liver cancers with pivotal implications in the clinicopathological and therapeutic perspectives. VINCENZO CARDINALE, M.D.1 “
“A 17-year-old girl presented with a history of elevated alkaline phosphatase and gamma-glutamyl transpeptidase selleck chemicals llc (γGT) levels for several years. She was asymptomatic and did not have jaundice, pruritus, abdominal pain, nausea, vomiting, weight loss, rashes,

or diarrhea. Viral hepatitis serologies, autoimmune serologies, and thyroid studies were all normal. γGT, gamma-glutamyl transpeptidase; MRCP, magnetic resonance cholangiopancreatography. She had a past medical history of anxiety, which was treated with Celexa. Otherwise, she was healthy and had no major childhood illnesses or history of substance abuse. She had traveled extensively with her family during her childhood, notably to Northern and Eastern Africa and Southeast Asia. Her physical examination was unremarkable. An abdominal

ultrasound examination was performed, and the findings were normal. Magnetic resonance cholangiopancreatography (MRCP) showed mild beading of the intrahepatic ducts this website consistent with the diagnosis of primary sclerosing cholangitis involving the small ducts. The patient was started on ursodiol (300 mg three times per day), and her alkaline phosphatase and γGT levels promptly normalized. Subsequently, colonoscopy was performed to

rule out concomitant inflammatory bowel disease. The mucosa appeared normal on endoscopic examination, but random biopsy samples were taken to rule out quiescent colitis. The pathology specimens revealed schistosoma eggs, and stool studies were positive for Schistosomamansoni. Percutaneous liver biopsy was then performed to evaluate hepatic involvement. There were portal intravenular Baf-A1 chemical structure granulomas in two triads with a schistosoma egg with otherwise minimal lobular fibrosis There was no evidence of mucopolysaccharide production or hyperplasia of the ductular epithelium (Fig. 1). An endoscopic examination was negative for esophageal varices. She was treated with praziquantel, and ursodiol was continued. One year later, repeat MRCP showed minimal changes with resolution of duct dilation in segment 6. Schistosomiasis, which is also known as bilharzia, affects more than 207 million people worldwide, with 1 of every 30 people infected with the trematode. Free cercariae penetrate the skin, travel to the pulmonary vessels, and then eventually lodge in the liver; there, they mature, mate, and migrate distally against the venous flow in the portal system. Eggs pass through the intestinal wall into the bowel lumen. Chronic disease results from the ongoing host response to accumulating tissue-trapped eggs.

“
“Tibetiella pulchra Y. L. Li, D. M. Williams et Metzeltin is described from River Nujiang. Its main features are heteropolar valves, which are linear with capitate ends; narrow sternum, expanding at its center; 2–5 rimoportulae at each apex; uniseriate striae; two short projections arising on the surface above each apical pore plate; and an ocellulimbus, extending from the edge of the valve margin to the edge of the valve surface. Of these characters, it is defined by the 2–5 rimoportulae at each apex. T. pulchra Crizotinib was common to abundant on rocks in the samples examined herein. “
“Polyadenylation is best known for occurring to mRNA of eukaryotes transcribed

by RNA polymerase II to stabilize mRNA molecules and promote their translation. rRNAs transcribed by RNA polymerase I or III are typically believed not to be polyadenylated. However, there is increasing evidence that polyadenylation occurs to nucleus-encoded rRNAs as part of the RNA degradation pathway. To examine whether the same polyadenylation-assisted degradation pathway occurs in algae, we surveyed representative species of algae including diatoms, chlorophytes, dinoflagellates and pelagophytes using oligo (dT)-primed reversed transcription PCR (RT-PCR). In all the algal species examined, truncated 18S rRNA or its precursor molecules with homo- or hetero-polymeric poly(A) tails were detected. Mining existing algal expressed sequence tag (EST) data revealed

polyadenylated www.selleckchem.com/products/Paclitaxel(Taxol).html truncated 18S rRNA in four additional phyla of algae. rRNA polyadenylation occurred at various internal positions along the 18S rRNA and its precursor sequences. Moreover, putative homologs of noncanonical poly(A) polymerase (ncPAP) Trf4p, which is responsible for polyadenylating nuclear-encoded RNA and targeting it for degradation, were detected from the genomes and transcriptomes

of five phyla of algae. Our results suggest that polyadenylation-assisted RNA degradation mechanism widely exists in algae, particularly for the nucleus-encoded rRNA and its precursors. “
“The subfamily Crucigenioideae was traditionally classified within the well-characterized family Scenedesmaceae (Chlorophyceae). Several morpho-logical revisions and questionable taxonomic changes hampered the correct classification of crucigenoid species resulting in a high number click here of synonymous genera. We used a molecular approach to determine the phylogenetic position of several Tetrastrum and Crucigenia species. The molecular results were correlated with morphological and ontogenetic characters. Phylogenetic analyses of the SSU rDNA gene resolved the position of Tetrastrum heteracanthum and T. staurogeniaeforme as a
age within the Oocystis clade of the Trebouxiophyceae. Crucigenia tetrapedia, T. triangulare, T. punctatum, and T. komarekii were shown to be closely related to Botryococcus (Trebouxiophyceae) and were transferred to Lemmer-mannia.

Methods: 33 morbidly obese subjects (17 M:16 F; age: 59.4 ± 9.6 yrs; BMI: 41.0 ± 6.3 kg/m2), of which 8 had co-existing OSA, underwent colonoscopy with inhaled Penthrox® as a method of discomfort relief during colonoscopy. Patients with renal and liver diseases were excluded. Details on the degree of discomfort and anxiety before, during and after the colonoscopy were assessed using the visual analogue scale (VAS) pain score and State-Trait Anxiety Inventory Form Y-1 (STAI Y-1) score. Details on the performance of the colonoscopy as well

as the occurrence of adverse events were also documented. Vital signs and oxygen saturation during selleck compound the procedure were monitored every 3 minutes. Data were compared to 25 obese and/or OSA patients (12M:13F; age: 55.4 ± 17.5 yrs; BMI: 34.0 ± 6.8 kg/m2), who underwent anaesthesia assisted colonoscopy. Results: Colonoscopy was successfully and safely completed in all (100%) subjects who received Penthrox®, with no adverse effects such as respiratory depression, arrhythmia or hypotension. Inhaled Penthrox® did not affect the performance of colonoscopy with caecal arrival time of 8 ± 1 min, withdrawal time of 8 ± 1 min and polyp detection rate of 63% (21/33). The total procedural time in FK228 datasheet patients with Penthrox® was significantly shorter than that of anaesthesia-assisted colonoscopy (24 ± 1 vs. 35 ± 1 min, P < 0.0001). Compared to anaesthesia-assisted

colonoscopy, Penthrox® had significantly lower incidence of hypotension (2/33 vs. 17/25, P < 0.001) and no episodes of de-saturation (0/33 vs. 9/25, P < 0.001). The mean VAS pain score during the procedure was 3.6 ± 1.1 (0–10 scale). The overall satisfaction score was 98 ± 5 (0–100 scale) with 24/25 subjects willing to use Penthrox® for colonoscopy again. All subjects with Penthrox®

were alert during and at the completion of the colonoscopy, 6-phosphogluconolactonase and were discharged much earlier than patients who had anaesthesia-assisted colonoscopy (27 ± 2 vs. 101 ± 4 min, P < 0.0001). Conclusions: In patients with morbid obesity and/or OSA, inhaled Penthrox® for colonoscopy is feasible, safe and 100% successful without influencing the procedural time and polyp detection rate. Without sedative and adverse effects of anaesthesia, colonoscopy with Penthrox® analgesia in these high-risk subjects allows earlier discharge, which facilitates work-flow and improves cost effectiveness of busy endoscopy units. H THOMPSON, A VANDELEUR, A AGARWAL, R HODGSON, M APPLEYARD, ENDOSCOPY NURSES COLLABORATIVE (ENC), TM RAHMAN Department of Gastroenterology & Hepatology, The Prince Charles Hospital, Rode Road, Chermside, Brisbane, Queensland, Australia 4053 Introduction: Hypothermia is associated with increased morbidity and mortality in day case surgery. Complications include haemodynamic instability, haemhorrage and prolonged patient recovery.