Methods: (ABCD stratification) Anti-HP antibody levels and the serum PG I / PG II were measured. HP infection was defined as positive when the anti-HP antibody titer was 10 U/ml or more. The PG status was defined as positive when Ferroptosis targets the criteria of both PG I ≦ 70 ng/mL and PG I /

PG II ≦ 3.0 were simultaneously fulfilled. We divided the subjects into 4 groups according to their serological status. The 4 groups were group A for HP(−)/PG(−), group B for HP(+)/PG(−), group C for HP(+)/PG(+) and group D for HP(−)/PG(+). (Grading of AG) Endoscopists who were not informed the result of ABCD stratification performed UE. The grade of AG was endoscopically graded according to the Kimura–Takemoto classification. (Endpoint) Primary endpoint was detection rate of GC according to grades of ABCD stratification and the Kimura–Takemoto classification. Secondary endpoint was Raf inhibition investigation of GC found

in group A. Results: 40 GCs were detected. According to ABCD stratification, detection rates of GC in A, B, C and D group were 0.1% (7/7246), 0.7% (12/1930), 0.8% (17/2161) and 1% (4/346), respectively. According to the Kimura–Takemoto classification, detection rates of GC in without AG group, C-I, C-II, C-III, O-I, O-II, and O-III were 0% (0/4865), 0.09% (1/1124), 0.15% (2/1310), 0.27% (2/754), 0.6% (11/1695), 1.1% (15/1510), and 2.1% (9/425), respectively. No GC was detected in without AG group. 上海皓元 Detection rates increased with progression of AG. 7 GCs were found in group A. The ratio of male was 71% and the mean age was 75 (48–82). All of them had AG (C-II 1, C-III 1, O-I 1, O-II 2, and O-III 2) and 43% had a history of HP eradication. Histological types were 4 well / 2 moderately and 1 poorly differentiated adenocarcinoma. Conclusion: 7 of 40 (18%) with GC belonged to group A, while no GC was detected in without AG group. Endoscopic grade of AG is more

effective to predict the risk of GC than ABCD stratification. Key Word(s): 1. ABCD stratification; 2. atrophic gastritis; 3. Helicobacter pylori; 4. pepsinogen; Presenting Author: WEN-MING WANG Additional Authors: GUEI-FEN CHIU, YANG-PEI CHANG, HUANG-MING HU, CHAO-HUNG KUO, MING-TSANG WU, FU-CHEN KUO, DENG-CHYANG WU Corresponding Author: DENG-CHYANG WU Affiliations: Kaohsiung Municipal Ta-Tung Hospital; Kaohsiung Medical University Hospital; E-Da Hospital, I-Shou University; Kaohsiung Municipal Hsiao-Kang Hospital Objective: Helicobacter pylori (H pylori) is a risk factor for Alzheimer’s disease. We investigated whether H pylori eradication is associated with Alzheimer’s disease risk in patients with peptic ulcer diseases. Methods: This nationwide cohort study was based on the Taiwan National Health Insurance Database (NHID), which provided data on 30142 patients who were the Alzheimer’s disease patients between 1997 and 2008 with a primary diagnosis of peptic ulcer diseases and.

These changes lead to in an impaired matrix integrity as measured by a diminished glycosaminoglycan content of the tissue [2]. Even after a follow-up period of 10 weeks matrix synthesis is still inhibited [3]. The in vitro experiments mimic the natural joint haemorrhage, as 4 days is considered to be the natural evacuation time in humans. These effects were confirmed

by canine in vivo experiments. Injections of autologous blood decreased matrix synthesis and content, and enhanced release of matrix components. The effects persisted for a prolonged period of time despite an apparently ineffective repair activity [4]. However, finally repair activity prevailed and cartilage damage vanished [3]. Preliminary results of recent studies demonstrated that sufficient repeated joint bleeds finally lead to persisting

cartilage damage (ongoing work of van Meegeren). Clearly the effects in dogs were less severe than in vitro. Compound Library molecular weight It was demonstrated that blood was cleared from the canine joint this website much quicker than generally observed in humans. After injection of a maximum amount of blood in the canine knee joint, the volume of blood decreased to less than 5% within 48 hours [5]. In vitro it was found that exposure to a concentration of at least 10% for more than 2 days was needed to maintain the irreversible adverse effects [6]. Disturbance of matrix turnover in the long-term is considered to be caused by apoptosis of the chondrocyte. Inhibition of caspases, involved in the apoptotic process, results in normalization of matrix synthesis [7]. Since the low proliferating chondrocyte is the only cell type of cartilage and is responsible for production and maintenance of the extracellular matrix, apoptosis of chondrocytes will result in a long-lasting, if not permanent, impaired matrix turnover. In that condition, cartilage will be unable to handle normal loading

resulting in further damage of the tissue, as supported by canine in vivo studies [8]. In 上海皓元医药股份有限公司 vitro studies revealed that the combination of mononuclear cells (MNC) and red blood cells (RBC) present in whole blood can have the same effect on their own as whole blood. A possible explanation for the irreversible damage by this combination is the conversion of hydrogen peroxide, produced by IL-1 activated monocytes/macrophages, and a catalyst in the form of iron supplied by RBC, into hydroxyl radicals. Scavenging these hydroxyl radicals with e.g. dimethylsulphoxide (DMSO) diminishes inhibition of matrix synthesis [9]. Apoptosis of chondrocytes can be inhibited by addition of IL-10 [10]. Most recently it appeared that IL-4 has even more protective effects on blood-induced cartilage damage than IL-10 (manuscript in preparation). It has been reported that IL-4 and IL-10 alone and in combination are able to inhibit inflammation in arthritic conditions [11]. This merges the direct degenerative activity of blood on cartilage with the inflammation driven activity of repeated joint bleeds.

Conclusion: These data suggest that blocking hepatic CB1R improves both carbohydrate and lipid metabolism and confirm that peripheral CB1R should be considered as a promising target to reduce cardiometabolic risk in obesity. (HEPATOLOGY 2011) It is well established that activation of the central endocannabinoid system (ECS) through cannabinoid receptor 1 (CB1R) promotes food intake and weight gain.1-3 Accordingly, pharmacological strategies have been developed PF 2341066 to antagonize CB1R. Rimonabant (SR141716) was the first CB1R antagonist to be marketed and

prescribed as an antiobesity agent. Its efficiency for weight reduction was supported by a series of major reports.4, 5 CB1R antagonism has also been shown to improve several pathological features associated with obesity, including insulin resistance, hyperglycemia, dyslipidemia, and liver steatosis in rodents6-8 and humans.9, 10 Nevertheless, development and sales check details of rimonabant was suspended after clinical studies provided compelling evidence that it was associated with the development of severe adverse psychiatric events.11 Both side effects and body-weight loss (and associated beneficial metabolic effects) induced by CB1R antagonism appeared to be related to the blockade of central CB1R. However, several data collected from animal and human studies

indicate that peripheral CB1R may also directly control lipid metabolism,12-15 promoting the emerging concept that selective targeting of peripheral CB1R may constitute a novel therapeutic MCE approach. The dominant role played by the liver in mediating the efficacy of CB1R blockage has been highlighted in recent studies using transgenic mice.16, 17 This notion has been particularly well evidenced in a mouse model presenting a hepatocyte-selective deletion of

CB1R, because these animals developed neither liver steatosis nor changes in cardiovascular risk factors when maintained on a high-fat diet, whereas their degree of obesity was similar to that of wild-type mice.16 In this study, the investigators demonstrated that activation of hepatic CB1R increases de novo lipogenesis and provided supportive evidence that it also inhibits fatty acid (FA) oxidation. Nevertheless, the mechanisms by which the selective activation or blockade of hepatic CB1R influence liver metabolism remain difficult to explore in vivo because of the biochemical cross-talk between organs. To precisely determine the metabolic changes induced by the blockade of hepatic CB1R on liver lipid and carbohydrate metabolism, we sought to test the direct effect of the specific CB1R antagonist, SR141716, in an in vitro model, in which neural pathways and peripheral influences were excluded. For this, we adapted a model of cultured explants from precision-cut liver slices retaining intact cell structure and respecting the biological organization of the organ.

Complete obstruction of the bile duct is managed by further surgery, usually an hepaticojejunostomy. Bile duct leaks are usually managed by endoscopic therapy but there has been debate about the relative merits of endoscopic and operative management for bile duct strictures. Although endoscopic dilatation and endoscopic stents are of Ibrutinib chemical structure temporary

benefit, many of these patients have developed recurrent strictures and on-going symptoms. Because of this, surgical management has been recommended for most patients, usually a choledochojejunostomy or hepaticojejunostomy. However, additional endoscopic options include the use of multiple stents over a prolonged period of time or covered metallic stents that can be left in situ for several months and then removed. Unfortunately, these options have not

been tested in randomized controlled trials. In the Rucaparib in vitro patient illustrated below, a good long-term outcome was achieved with multiple plastic stents. A 48-year-old woman was investigated because of the development of upper abdominal pain and fever, 1 month after laparoscopic cholecystectomy. Liver function tests were abnormal and an abdominal ultrasound study showed mild dilatation of the common hepatic duct and intrahepatic ducts. Endoscopic retrograde cholangiopancreatography showed a stricture, 2 cm in length, in the mid-bile duct (Figure 1). Over a 7 month period, a total of eight plastic stents were sequentially inserted to achieve continuous and progressive 上海皓元 dilatation of the stricture. Eight stents have a diameter of approximately

77 F (2.6 cm). The stents were left in situ for 15 months to allow for complete remodelling of the area. There was no apparent stricture after removal of the stents and a repeat ERCP after 10 years showed a normal bile duct (Figure 2). The patient remains asymptomatic. The use of multiple stents for 12-24 months is an option for patients with post-operative biliary strictures and appears to be associated with lower recurrence rates than stenting for shorter periods with one or two stents. Contributed by “
“Live donor liver transplantation (LDLT) is a viable alternative to the liver graft supply shortage when both donor and recipient are carefully chosen and when the surgery and donor evaluation are performed at a transplant center with expertise in this procedure. Over 6000 LDLT have been performed worldwide. In the USA, LDLT makes up less than 5% of the total number of liver transplants performed annually. Advantages of LDLT over deceased-donor transplantation include elective surgical performance, excellent liver graft and the chance of rescuing the recipient from mortality on the waiting list. However, not all recipients are candidates for LDLT. The sizes of both recipient and donor helps predict the amount of liver mass needed for donation.

Among a collection of 1,049 miRNA loci (miRBase-Release 1631), we identified one or more E-boxes in the promoters, first exons, or first introns in 834 cases (Supporting Fig. 4A and Supporting Table 3). We then determined whether these E-boxes are located in CpG islands, because Myc-binding E-boxes are usually located within such contexts. As shown in Supporting Fig. 4A and Supporting Table 3, 94 of the 834 loci resided within CpG islands. Further analyses showed 21 of these loci

to be conserved between humans and mice (Supporting Fig. 4A and Supporting Table 3). Interestingly, miRNAs from 10 of these loci have been reported to be regulated by Myc and to mediate a variety of Myc functions32, 33(Table 1 and Supporting Fig. 4B,C). Therefore, miRNAs from the other 11 loci may also be regulated by Myc HDAC inhibitor and have important roles in mediating Myc learn more function. To address whether Myc regulates expression of miRNAs

from the remaining 11 loci, we tested the effects of Myc inhibition or Myc induction on the expression of these miRNAs. As shown in Fig. 1A and Supporting Table 2, induction of MycER activation in HL7702 cells resulted in the down-regulation of several of the miRNAs, including miR-148a-5p and miR-363-3p, whereas inhibition of Myc in HepG2 and BEL-7402 cells resulted in up-regulation of other miRNAs, including miR-148a-5p and miR-363-3p. Taken together, Myc differentially regulates these miRNAs in a cell context–dependent manner. Stem-loop quantitative RT-PCR results in all three cell lines indicated miR-363-3p to be the most significantly regulated miRNA in response to Myc activation or inhibition (Supporting Table 2). In addition, prediction of miRNA targets showed the 3′-UTR of Myc to contain one highly conserved miR-148a-5p-binding site 上海皓元 from human to dog. Based on these findings, we selected miR-363-3p and miR-148a-5p for additional analyses. To address whether Myc directly binds the promoter regions of miR-148a and miR-363,

we conducted a chromatin IP assay in HepG2 and BEL-7402 cells. This revealed that Myc binds both miR-148a and miR-363 promoter regions containing the highly conserved E-box regions in CpG islands (Fig. 1B-D and Supporting Fig. 5). These results provided strong evidence that both miRNAs are directly regulated by Myc. In addition, our unpublished data show that inhibition of both miRNAs by Myc is accompanied by a prominent decrease in active histone marks around the transcription start sites of both miRNAs. To examine the consequences of relieving the suppression of miR-148a-5p and miR-363-3p in hepatocarcinoma, we tested whether ectopic expression of these miRNAs affected the biology of liver cells. As shown in Fig. 2A-C and Supporting Fig.

Semi-structured interviews addressed participants’ internet use and thoughts about a website for AWH. The interviews were audio-recorded and transcribed verbatim. Three independent reviewers coded the data to determine descriptive categories and grouped them into themes. Eleven of 12 subjects approached consented to interviews. Data saturation was achieved. Most participants had used the internet to find haemophilia information, although none could recall specific websites they had visited for information. Some felt more comfortable using the internet than asking health care providers. Others liked the 24/7 availability of the internet if questions arose. Overall, they felt a website

for AWH would help them to learn about haemophilia

and explain it to others. Online social networking with an older GSI-IX peer mentor with haemophilia, as well as with others of their age was cited as a potentially valuable source of support. AWH are interested in a haemophilia website and have identified a variety of features this website which they believe may help to support them during transition to adult care and beyond. Website development is ongoing. “
“Antibody eradication is the ultimate goal of inhibitor management. The only clinically proven strategy for achieving antigen-specific tolerance to factor VIII and IX is immune tolerance induction (ITI). Knowledge MCE about ITI in hemophilia A and B was originally derived from small cohort studies and ITI registries. Practise has been further influenced by prospective cohorts, and the results of a single prospective randomized ITI trial. There have been few comparable data to inform an evidence-based approach to factor IX inhibitors. This is problematic given the morbidity associated with unique allergic reactions that herald factor IX antibody development and preclude effective eradication.

This chapter discusses current understanding of immune tolerance outcome and outcome predictors for hemophilia A and B; reviews the current practise recommendations for ITI; and summarizes the immunology of antibody formation and tolerance. It will suggest how emerging knowledge could inform future investigative priorities. “
“Summary.  Annual reporting of inhibitors to factors (FVIII) and IX (FIX) to the Canadian Haemophilia Registry has suggested a lower prevalence than that published in the literature. We performed a prospective study to determine the prevalence of patients with inhibitors directed against either FVIII or FIX. Patients with inhibitors were classified as: (i) inhibitor test positive; (ii) inhibitor test negative but on immune tolerance induction (ITI); (iii) inhibitor test negative but bypass treatment recommended; or (iv) inhibitor resolved. One year later, the cohort was re-classified. The prevalence of inhibitors on 1 May, 2007 was 3.

[28, 31, 32] In this model, spontaneous and chronic ileitis that closely resembles human CD develops in the absence of chemical, immunological, or genetic manipulation.[31] We have reported previously that the blockade of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) or P-selectin glycoprotein ligand-1 attenuates T lymphocyte or monocyte recruitment in the intestinal mucosa and ameliorates ileitis in this model.[33, 34] We fed SAMP1/Yit mice with omega-3 PUFA for 16 weeks. Fat-feeding treatment was performed from 14 weeks (when ileitis began to occur) to 30 weeks (when ileitis

Doxorubicin was completely established). We chose fish oil (containing 25–30% EPA and DHA) or perilla oil (containing 55–60% A-LA) as omega-3 PUFA. The amount of fat is the same (8% w/w) with the diet that were used in chronic DSS-induced colitis model.[35] Both diet rich in fish oil and diet rich in perilla oil diet MAPK inhibitor ameliorated ileitis significantly as assessed by histologically and macroscopically.[36] In both the omega-3 PUFA-rich diet groups, the number of infiltrating monocytes/macrophages and beta7-integrin positive lymphocytes were decreased significantly compared with those in the control diet group. Degree of expression of MAdCAM-1, which is a key adhesion molecule to

be involved in CD, was decreased significantly by both treatments of diet. Degree of improvement was higher by perilla oil diet than by fish oil diet. From these observations, the mechanisms that omega-3 PUFA have beneficial role on ileitis is at least explained by its effect on leukocyte recruitment. In contrast with the effect of omega-3 PUFA-rich on colitis, omega-3 PUFA-rich diet have beneficial role even in a higher concentration. Although CD can affect any part of gastrointestinal tract, efficacy of treatment differs among the location of the disease, suggesting that pathophysiology

of this disease differs among the location of disease. For example, antibiotics therapy is effective in colonic type CD but not in isolated small intestinal CD, suggesting that role of microbiota is involved more in colonic inflammation.[37, 38] The microbiota is critical for maintaining intestinal homeostasis through activation of innate 上海皓元医药股份有限公司 immune Toll-like receptors.[39] Dysbiotic microbiota is able to induce colitis in mice, and it is also observed in CD patients with the reduction in microbial diversity.[40] Recently, emerging evidence has also identified that nutrients including dietary lipid intake can cause dysbiosis. It is plausible explanation that effect of dietary fat intake is at least in part due to change of microbiota. In mice fed a diet high in fat, there are many key gut population changes, such as the absence of gut barrier-protecting Bifidobacteria spp.[41] Fish oil enhances recovery of intestinal microbiota and epithelial integrity in chronic rejection of intestinal transplant.

The good-response genotype (C/C Dorsomorphin purchase rs12979860 or T/T rs8099917) was strongly

associated with an increased rate of sustained virological response despite the addition of a directly acting antiviral agent. This suggests that patient IL-28B genotype will remain relevant in the dawning era of specifically targeted antiviral therapy for hepatitis C virus because a combination with peg-IFN and RBV is required to restrict the development of antiviral resistance. It will, therefore, be important to consider IL-28B genotype in clinical development programs; because of the population frequency of the good-response IL-28B variant and its association with rapid viral decline during peg-IFN therapy,2 it is possible for small early-phase efficacy trials www.selleckchem.com/products/Adriamycin.html to be confounded by an imbalance in the IL-28B genotype across treatment arms. We statistically modeled the probability of an imbalance in the good-response IL-28B variant (C/C rs12979860) between treatment arms for three hypothetical situations: a phase

1 trial (n = 60), a phase 2a trial (n = 120), and a phase 2b trial (n = 240). Each involved three randomized arms (Fig. 1). The probability of an imbalance in one treatment arm of ±10% (<23% or >43% when the C/C genotype frequency was assumed to be 33%2) was 31%, 18%, and 6% for the phase 1, 2a, and 2b trials, respectively, and the probability of an imbalance in one treatment arm of ±20% was 10%, 0.4%, and <0.01% for the phase 1, 2a, and 2b trials, respectively. We assumed a Caucasian population for this analysis; the inclusion of other ethnic groups would be expected to increase the risk of sampling error.2 We then modeled

the implications of such an imbalance for the primary outcome of viral load MCE reduction at week 4 in studies combining a direct antiviral agent with peg-IFN and RBV (Table 1). An imbalance in the IL-28B genotype of 10% to 20% could lead to differences in HCVRNA reduction of 0.2- to 0.5-log10 IU/mL between treatment arms due to peg-IFN alone. This has great relevance for dose-finding studies in which the dose-related antiviral potency must be weighed against toxicity. In the setting of more extreme mismatching (e.g., in a mixed-ethnicity cohort), confounding by IL-28B genotype might even affect the decision to advance a compound from proof of concept to the next stage of clinical development. Indeed, Anadys Pharmaceuticals recently reported an imbalance in the frequency of the C/C genotype that confounded the week 12 results of a phase 2 trial (the C/C genotype frequency was 21% in the active treatment arms and 56% in the control arm).

The feces from these patients were collected using the stool collection devices, and were stored at −20°C. All the subjects provided their written informed consent, and the use of fecal samples and isolated H. pylori strains for this study was approved by the ethics committee of Hirosaki University. The following laboratory bacterial strains were used: Sorafenib solubility dmso H. pylori ATCC 43504, H. hepaticus ATCC 51448, H. felis ATCC 49179, H. mustelae ATCC 43772, H. cinaedi ATCC 35683, Campylobacter jejuni ATCC 29428, Escherichia coli ATCC 25922, Bacteroides vulgatus IFO 14921, Bifidobacterium breve JCM 1192, and Bifidobacterium infantis JCM 1222. H. pylori strains isolated

from 1344 Japanese patients who underwent gastro-duodenoscopy at Hyogo College of Medicine Hospital were also tested. Culturing and whole-cell disruption of all of the bacterial strains was carried out as described previously.8 The standard H. pylori cellular antigen was prepared from H. pylori ATCC 43504 and cultured on Difco Brain Heart Infusion Agar (Becton, Dickinson and Company, Franklin Lakes, NJ, USA) plates containing 5% horse blood in a microaerophilic environment (Anaero Pack Helico System; Mitsubishi Gas Chemical Co. Inc., Tokyo, Japan).

The culture plate was incubated for 7 days in an anaerobic environment (Anaero Pack Anaero System; Mitsubishi Gas Chemical Co. Inc.). Bacterial cells Venetoclax molecular weight were harvested, washed with PBS, suspended in PBS containing 0.5% formalin, and then incubated at 4°C for overnight. The bacterial cells were washed three times with PBS and disrupted by sonication (Biom’c Model 7250, Seiko Instruments & Electronics, Ltd, Tokyo, Japan). H. pylori ATCC 43504 antigen was obtained from the supernatant upon centrifugation of the sonicated suspension and was stored at −30°C until use. The protein concentration of antigens from the clinical strains was adjusted to 5 µg/mL with the diluent buffer. The protein concentration of the laboratory strains was adjusted to 40 000, 8000, 1600, 320, and 64 ng/mL for TPAg EIA test,

and adjusted to 10 µg/mL for Rapid TPAg test. Catalase activity of the bacterial MCE antigen prepared from 127 H. pylori clinical strains was determined at 25°C by spectrophotometry15 using a molar absorption coefficient of 43.48 L/mol/cm at 240 nm.16 The protein concentration was determined with a bicinchoninic acid protein assay reagent (PIERCE., Rockford, IL, USA) with bovine serum albumin as the standard. TPAg EIA and Rapid TPAg were stored at 30°C for 12 months. The diagnostic performances of the TPAg EIA and Rapid TPAg were examined using the H. pylori ATCC 43504 antigen and five clinical fecal samples. Three of the fecal samples were from H. pylori-positive patients, and two samples were from H. pylori-negative patients. Correlation between catalase activity and the absorbance value of TPAg EIA was calculated by Pearson’s correlation coefficient.

Dara de Las Heras, Dr. Tim Shallcross; NHS Isle of Wight: Dr. Christopher Sheen; NHS Lanarkshire: Dr. Stuart Campbell, Dr. Richard Crofton, Dr. Andrzej Prach, Dr. Elaine Robertson; NHS Lothian: Dr. Andrew Bathgate, Dr. Kel Palmer;

NHS Tayside: Dr. Alan Shepherd; Norfolk and Norwich University Hospitals NHS Foundation Trust: Dr. Hugh Kennedy, Dr. Simon Rushbrook; North Bristol NHS Trust: Dr. Robert Przemioslo, Dr. Ashish Sinha; North Cumbria University Hospitals NHS Trust: Dr. Babur Javaid, Dr. Chris McDonald; North Tees and Hartlepool NHS Foundation Trust: Dr. Basant Chaudhury, Dr. Jane Metcalf; North Wales NHS Trust: Dr. Thiriloganathan Mathialahan, Dr. David Ramanaden; North Erlotinib manufacturer West London Hospitals NHS Trust: Dr. Maxton Pitcher; North West Wales NHS Trust: Dr. Richard Evans, Dr. Jaber Gasem; Northampton General Hospital NHS Trust: Dr. Udi Shmueli; Northern Devon Healthcare NHS Trust: Dr. Andrew Davis; Northern Lincolnshire and Goole Hospitals NHS Trust: Dr. Asifabbas Naqvi; Northumbria Healthcare NHS Trust:

Dr. Mark Welfare; selleck Nottingham University Hospitals NHS Trust: Dr. Steve Ryder; Oxford Radcliffe Hospitals NHS Trust: Dr. Roger Chapman, Dr. Jane Collier; Pennine Acute Hospitals NHS Trust: Dr. Howard Klass; Peterborough and Stamford Hospitals NHS Foundation Trust: Dr. Mary Ninkovic; Plymouth Hospitals NHS Trust: Dr. Matthew Cramp; Portsmouth Hospitals NHS Trust: Dr. Patrick Goggin; Princess Alexandra Hospital NHS Trust: Dr. David Preston; Queen Elizabeth Hospital King’s Lynn NHS Trust: Dr. Andrew Douds; Rotherham NHS Foundation Trust: Dr. Barbara Hoeroldt; Royal Berkshire NHS Foundation Trust: Dr. Jonathan Booth; Royal Bolton Hospital NHS Foundation Trust: Dr. George Lipscomb; Royal Bournemouth and Christchurch Hospitals NHS Foundation Trust: Dr.

Earl Williams; Royal Cornwall Hospitals NHS Trust: Dr. Hyder Hussaini; Royal Devon and Exeter NHS Foundation Trust: Dr. Reuben Ayres; Royal Free Hampstead NHS Trust: Professor Andrew Burroughs, Dr. this website Giacomo Germani, Dr. Jesica Makanyanga; Royal Liverpool and Broadgreen University Hospitals NHS Trust: Professor Martin Lombard, Dr. Paul Richardson; Royal United Hospital Bath NHS Trust: Dr. Mark Farrant, Dr. Duncan Robertson; Royal Wolverhampton Hospitals NHS Trust: Dr. Matthew Brookes; Salisbury NHS Foundation Trust: Dr. Andrew Tanner; Sandwell and West Birmingham Hospitals NHS Trust: Dr. Saket Singhal; Scarborough and North East Yorkshire Health Care NHS Trust: Dr. Sathish Babu; Sheffield Teaching Hospitals NHS Foundation Trust: Dr. Dermot Gleeson; Shrewsbury and Telford Hospital NHS Trust: Dr. Jeff Butterworth; South Devon Healthcare NHS Trust: Dr. Keith George; South London Healthcare NHS Trust: Dr. Howard Curtis, Dr. Alastair McNair, Dr. Ikram Nasr; South Tees Hospitals NHS Trust: Dr. Andrew Douglas; South Tyneside NHS Foundation Trust: Dr. Simon Panter; South Warwickshire General Hospitals NHS Trust: Dr.