For quantitative PCR, NK cells were purified from PBMCs using the NK-Cell Isolation Kit (Miltenyi Biotec GmbH, Bergisch Gladbach, Germany). RNA was extracted from purified NK cells (NucleoSpin RNAII, Macherey-Nagel) and reverse transcribed by High Capacity cDNA Reverse Transcription Kit (Applied Biosystems, Foster City, CA, USA) according to manufacturer’s

protocol. The real-time PCRs were performed by Applied Biosystems 7500 Real-Time PCR System in 10 μL reaction mixture volumes containing 1× Power SYBR Green I Master Mix (Applied Biosystems, Warrington, UK), 0.3 μM of KIR-specific primers [25] or 0.3 μM housekeeping gene (GAPDH) (Forward: 5′-GAC CCC TTC ATT GAC CTC AAC TAC A-3′, Reverse: 5′-CTA AGC AGT TGG TGG TGC AGG-3′) and 1 μL of postreverse-transcription mixture. PCR

cycling conditions were set to 2 min at 50°C and 10 min at 95°C followed by 50 CH5424802 cycles of 15 s at 95°C selleck screening library and 1 min at 60°C. The melting curve stage was added to the program in order to control samples’ quality. Resting KIR repertoire expression was compared between CMV-seropositive and -seronegative donors by unpaired t-test. KIR expression after CMV co-culture was compared by paired t-test in samples exposed to CMV versus cells from the same donor cultured in the absence of CMV. All p-values presented are two-sided and were considered significant if < 0.05. This study was supported by grants from the Swiss National Science Foundation (grant PPOOP3_128461 / 1 to M.S.) and from the “Stiftung Forschung Infektionskrankheiten”. The authors would like to express their gratitude to Beatrice Hess (Institute of Microbiology, Basel University) for help in setting up the CMV co-culture. The authors declare no financial or commercial conflict of interest. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support issues arising from supporting information

(other than missing files) should be addressed to the authors. Figure S1. NK cell KIR and NKG2A expression in CMVseropositive and seronegative donors PBMCs from CMV-seropositive (CMV+) Urease or CMV-seronegative (CMV-) donors were stained for cell surface expression of the inhibitory receptors (A) KIR2DL1, (B) KIR2DL2/3, (C) KIR2DL5, (D) KIR3DL1 and of the activating receptors (E) KIR2DS1, (H) KIR2DS4, and (J) KIR3DS1 after gating on CD56+/CD3- NK cells. mRNA quantity was compared for the activating receptors KIR2DS2, KIR2DS3, and KIR2DS5 in immunomagnetically sorted NK cells by qRT-PCR. Data represent 6 experiments performed in 54 donors. Expression of each KIR is shown only in donors that carry the respective KIR gene. Horizontal lines represent means. Comparison between groups was made by Student’s T-test. Figure S2.

The mean survival time of group D was longer than that of group C (P = 0·0039, Fig. 4c). The score of aGVHD in group D was lower than that in group C (P = 0·0422). We detected donor spleen Ferroptosis inhibition cell chimerism (H-2b) in the long-term surviving mice of group D by FACS. The donor mouse chimerism rate was 3·15 ± 1·59%, which is higher than that of normal BALB/C spleen cells (0·61 ± 0·32%) (P = 0·0062, Fig. 5b). Although the chimerism rate was much lower, we could

detected the chimerism by PCR again (Fig. 5a). The liver and small bowel of dead mice and the long-term surviving mice of group D following the observation period were taken for GVHD histological examination. The aGVHD histological manifestations in the long-term surviving group D mice were slight, such as the damage to sinus hepaticus endothelial cells and anabrosis of the mucous membrane Selleckchem Saracatinib of the small intestine (Fig. 6c and d). However, the histological manifestations

in those mice which died of aGVHD were serious, showing diffuse cellular swelling, degeneration of hepatic parenchymal cells and complete damage of the mucous membrane gland of the small intestine (Fig. 6e,f). IL-2 is the first T cell growth factor to be cloned molecularly and remains the cytokine of choice for the propagation of T cells in culture [37]. Because IL-2 can induce T cell expansion potently in vitro, it has been assumed for many years that IL-2 played an analogous role in amplifying T cell responses in vivo. This assumption led to the development of therapeutic strategies aimed at modulating IL-2 signal strength for clinical efficacy. On one hand, IL-2 itself is infused in patients with cancer or acquired immune deficiency syndrome (AIDS) to enhance T cell numbers and function [38,39]. On the other hand, antibodies to the IL-2R are used to inhibit IL-2 signalling to suppress rejection of the transplanted

organs [40]. These agents show clinical efficacy Dipeptidyl peptidase in some cases, lending support to the notion that IL-2 serves as an important T cell growth factor and can promote immunity in vivo. However, this notion is now being challenged. IL-2 is critical for the development and peripheral expansion of CD4+CD25+ regulatory T cells, which promote self-tolerance by suppressing T cell responses in vivo (for a review, see [41]). A short course of high-dose IL-2 [42], begun on the day of bone marrow transplantation, protects against GVHD. This inhibitory effect is directed against donor CD4+ cells, even though the mechanism has not yet been elucidated. In this study, our results showed that IL-2 can inhibit T lymphocyte immunity. The up-regulation of SOCS-3 mRNA induced by IL-2 played a critical role during this course.

05) (data not shown). Host genetic factors are

proposed to be governing the pathology of HCV disease progression or regression along with the viral and environmental factors. Interplay of HLA-restricted T lymphocytes, antibody-secreting B lymphocytes, natural killer cells and cytokines conditions the immune response to viral infections. Effective presentation of viral antigens to CD4+ T cells and CD8+ T cells by HLA Class II and Class I molecules, respectively, is the key regulation of optimum immune response against viral infection and further KPT 330 dictates viral clearance or persistence [20]. The results of the present study demonstrated that HLA-A11 is the only HLA click here Class I antigens that show statistical significant association with chronic HCV infection (P = 0.001, Pc = 0.021), suggesting that HLA-A11 antigen may be a susceptibility antigen for viral persistence and chronic liver disease in Egyptian patients infected with HCV. Although HLA-B12, HLA-B13, HLA-B17 and HLA-B40 were more frequent in patients (P = 0.02, P = 0.04, P = 0.04, P = 0.02, respectively) and HLA-A32 (P = 0.03) and HLA-B14 (P = 0.015) were more frequent in controls, the significance was lost after correction for multiple testing and no other HLA Class I antigens were

associated with chronic HCV infection in this

study. The associations between HLA Class I antigens and the outcome of HCV infection are extensively investigated in different ethnic populations such as Caucasian Americans and populations from Korea, Italy, Russia, Spain, Ireland, Saudi Arabia, Western India, Japan and Germany [21–37]. The earlier reported associations showed ethnic and geographical differences sometimes with contradictory results. While HLA-A11 is associated with HCV persistence in Ireland [14, 25] in agreement with the results of the present study, Tau-protein kinase HLA-A*1101 showed stronger association with viral clearance both in Caucasians and African Americans [29]. HLA-A32 in populations from Western India [27] and HLA-B14 in Italy [22] are associated with HCV infection in contrast to our findings. On other hand, several studies failed to demonstrate an association between the outcome of HCV infection and HLA Class I antigens [34–36]. In Egyptian, association was reported between HLA-A28, HLA-A29, HLA-B14 and HCV infection, and HLA-B50(21) with viral clearance in two cases of the studied sera [17]. HLA-A28 and HLA-29 were not detected in patients with HCV infection of the present study; in the same time, HLA-B14 shows a trend with protection (OR = 0.1) and not susceptibility.

Studies in animals demonstrate the basis for an excitatory urethra to bladder reflex. Urethral stimulation by prostaglandin E2 induces an excitatory effect on micturition reflex by activation of C-fiber afferent nerves. α1A-adrenoceptor blocker has an inhibitory effect on the micturition EGFR inhibitor reflex, suggesting excitatory urethra to bladder reflex is mediated by α1A-adrenoceptor. Even if there is no obstruction, increase in urethral sensory due to BPE may induce the development of the detrusor overactivity. “
“Objectives: We investigated the time

course of the stromal cell-derived factor 1α (SDF1α) expression and behavior of intravenously administered bone marrow-derived stromal (BMS) cells in the urinary bladder of partial bladder outlet obstruction (PBOO) rats. Methods: Study 1: Recombinant SDF1α or saline was directly injected into the bladder wall of female rats followed by intravenous administration of BMS cells isolated from green fluorescent protein (GFP) transgenic

rats. The bladder was examined with immunohistochemistry to determine whether SDF1α would enhance migration of BMS cells to the bladder. Study 2: Following surgery of PBOO or sham in female rats, bladders were removed on days 1–14, and expression of hypoxia inducible factor 1α (HIF1α) and SDF1α were examined with real-time polymerase chain reaction (PCR) to determine if PBOO preferentially increased their expression. Study 3: Female rats underwent PBOO or sham surgery followed by intravenous administration learn more of GFP-positive BMS cells. Bladders were examined with immunohistochemistry on days 1–14 to determine whether Metalloexopeptidase BMS cells preferentially accumulated in the bladder. Results: BMS cells were accumulated in the injection site of SDF1α but not saline in the bladder. SDF1α and HIF1α increased at day 1 after PBOO compared to sham. More BMS cells accumulated in the bladder of PBOO on day 1, and some BMS cells expressed smooth muscle phenotypes by day 14. Conclusion: SDF1α induced with ischemia/hypoxia due to PBOO is implicated in the accumulation

of BMS cells in the bladder and regeneration of the bladder for PBOO. “
“Objectives: Ketamine abuse can damage the urinary tract and cause lower urinary tract symptoms (LUTS). This report presents our observations and management on urinary tract damage caused by ketamine abuse. Methods: From November 2006 to February 2009, 20 patients visited Taipei Veterans General Hospital due to ketamine-related lower urinary tract symptoms. We analyzed the clinical presentations, daily ketamine dose, interval between ketamine usage to develop LUTS, urodynamic studies, radiological image findings, cystoscopic and ureterorenoscopic findings, histological findings, urinary ketamine levels and treatment responses.

The precise Epacadostat mechanisms relating RNASEH2, SAMHD1 and ADAR1 dysfunction to the AGS phenotype remain to be clarified. Of particular note, unlike the other AGS-related proteins, the RNASEH2 complex is not induced by interferon, and the RNaseH2B knock-out

mouse does not demonstrate an obvious up-regulation of innate immune signaling [28]. However, clinical and biochemical (see below) overlap observed in human studies across the six disease-associated genotypes leads us to predict that the pathogenesis of all forms of AGS relates to inappropriate stimulation of the innate immune system by nucleic acids. Because of already-accrued neurological damage, and also because of recognized intrafamilial variability, it will be difficult to monitor treatment efficacy using only clinical/radiological

criteria in the context of early, proof-of-principle clinical trials. Rather, it would be ideal to assess the effects of therapy by assaying a reactive biomarker. As discussed above, AGS is associated with increased levels of interferon alpha in the CSF and serum. Interferon alpha levels and white cell counts in the CSF of AGS patients have been reported to fall during the first few years of life, perhaps corresponding with the apparent ‘burning-out’ of the encephalopathic period already described [29]. However, due Z-VAD-FMK cost to the obvious difficulties of repeat CSF sampling, very few serial data are available

(i.e. systematic interferon alpha profiling beyond infancy has not been undertaken). Of significance, in currently unpublished data we have observed that >90% of AGS patients, of any genotype, sampled at any age, demonstrate a so-called ‘interferon signature’, i.e. increased expression of multiple type I interferon-stimulated genes (ISGs), in whole blood. Beyond the interesting biological questions that our findings raise, most particularly why we observe a persistent interferon signature when the disease is, apparently, ‘clinically quiescent’ (see earlier), we propose that the level of ISGs measured in blood samples from patients with AGS might Thiamine-diphosphate kinase be used as a biomarker of disease activity, and potentially of treatment efficacy. Other cytokines and chemokines are also increased in the CSF and serum of AGS subjects and may, similarly, be considered as possible biomarkers for the future assessment of therapeutic effect. Of note, for some patients/families, chilblains are a major disease-associated problem (e.g. precluding the use of splinting for the prevention of contractures). Because of their visibility, chilblain status could possibly also serve as an indicator of treatment efficacy. It is clear that AGS is a disorder of inappropriate immune activation, demonstrating some characteristics of both autoinflammatory and autoimmune disease.

This risk was also more pronounced in females compared with males, which appears to be the first significant gender-by-treatment interaction identified. For patients under 50 years, a significantly lower mortality rate was found when treated with PD versus HD. Limitations: This is a large study with significant power, making it quite easy to identify statistically www.selleckchem.com/products/Romidepsin-FK228.html significant population differences. When applied in the clinical context, these statistical differences may not be clinically relevant. The study

was not adjusted for differences in comorbidity, disease severity, dialysis adequacy or patient nutritional status. This registry data study by Heaf et al.12 retrieved records from 4921 patients commencing dialysis between 1990 and 1999. The authors adjusted for age, sex and primary renal disease. The results described a substantial advantage of PD over HD during the first 1–2 years of dialysis, after which results are approximately similar. The difference was less marked for older patients and those with diabetes, but this study found no subgroup where treatment with PD had a statistically significant detrimental effect. Limitations: Due to the use of observational registry data, one cannot exclude a modality selection bias. This study was carried out by Liem et al.4 and looked

at registry data from the Dutch End-Stage Renal Disease Registry (RENINE). A total of 16 643 patients were enrolled from 1 January 1987 to 31 December 2002 and adjusted GS-1101 nmr for age, gender, primary renal disease, centre of dialysis and year of start. The results demonstrated an initial survival advantage for PD therapy compared with Tyrosine-protein kinase BLK HD therapy. However, over time with increasing age and

the presence of diabetes as the cause of renal failure, the survival advantage diminished. Limitations: The RENINE registry does not include data on patient comorbidity. The data were not adjusted for ethnicity, nutritional status or dialysis adequacy. Lombardy Dialysis and Transplant Registry data analysis by Locatelli et al.13 included 4191 patients commencing dialysis between 1 January 1994 and 31 December 1997. The Italian group wanted to look at both mortality depending on modality choice and the risk of developing de novo CVD. Relevant endpoints for this study included death, the development of ischaemic heart disease or chronic heart failure. CVD was defined by either of the following conditions: coronary artery disease The results, when adjusted for age, gender and established CVD, did not show any survival differences between PD and HD. There was also no difference in the number of patients in either modality group who developed de novo CVD. Limitations: This study was only a 3-year follow up, which may be too early to see cardiovascular changes. It is also observational, as all registry data are, meaning that there may be some modality selection bias.

All patients had experienced symptoms for a prolonged time period (mean time of disease 10±14 years) and presented with mucosal lesions involving the nasal cavity (100%), pharynx (35%) and/or larynx (11%). All tissue specimens were obtained before treatment; afterwards, patients received N-methylglucamine antimoniate (20 mg/Sb/kg/d) for 30 days. Nasal mucosal biopsy was performed under BTK signaling inhibitors local anaesthesia with Lidocaine® spray (10%). Normal mucosal samples were obtained from turbinectomy nasal

surgery. Tissue fragments were cryopreserved or conserved in 10% formalin. This study was approved by the Gonçalo Moniz Research Center (CPqGM/FIOCRUZ-Bahia) Institutional Review Board, and informed consent was obtained from all patients before enrolment. Frozen sections (5 μm thick) were obtained and immunohistochemistry was performed as described previously 2. The following primary antibodies were used: rabbit anti-IL-17 (4 μg/mL) or anti-TGF-β (2 μg/mL) (both Santa Cruz Biotechnology, Santa Cruz, CA, USA), goat anti-IL-23 (0.01 μg/mL), mouse anti-IL-6 (25 μg/mL), mouse anti-IL-1β (10 μg/mL) learn more or goat anti-MMP-9 (4 μg/mL) (all R&D Systems,

Abingdon, UK), goat anti-MPO (4 μg/mL; US Biological, Swampscott, MA, USA) and goat anti-NE (12 μg/mL; Santa Cruz Biotechnology). Biotin-labelled anti-rabbit, anti-mouse or anti-goat IgG (Vector Laboratories, Peterborough, Tideglusib England) was used as a secondary antibody. Isotype control antibodies (R&D Systems) were used as negative controls. Positive-control sections consisted of frozen mucosal tonsillar tissue and frozen nasal polyps. Digital images of tissue sections were captured using a Nikon E600 light microscope and a Q-Color 1 Olympus digital camera. Quantification of stained areas was performed using Image Pro-Plus software (Media Cybernetics). Double immunofluorescence staining was performed for IL-17 and CD4, CD8, CD14 or

CCR6 markers. The following primary antibodies were used: mouse anti-CD4 (BD Biosciences, San Jose, CA, USA), mouse anti-CD8 (BD Biosciences), mouse anti-CCR6 (R&D Systems) and rabbit anti-IL-17 (8 μg/mL, Santa Cruz Biotechnology). Secondary antibodies were biotin anti-mouse IgG (Vector Laboratories) or anti-rabbit Alexa 488 (Molecular Probes, Eugene, OR, USA). Streptavidin Cy3 (Sigma, Buchs, Switzerland) was used after biotin antibodies. Multiple images representing positive staining and negative controls were acquired using a confocal microscope (Leica TCS SP2 SE and SP5 AOB5). Image Pro Plus was used for image processing. The extraction of total RNA from mucosal tissues was performed following the protocol recommended by the manufacturer (Life Technologies, Rockville, MD, USA). cDNA was synthesised using 1 μg of RNA through a reverse transcription reaction (M-MLV reverse transcriptase, Promega, Madison, WI, USA).

Three independent cultures have been performed for each time point. Differences in the quantified proliferation rates of JEG-3 cells were statistically assessed by Student’s t-test and considered significant find protocol when P < 0.05. JEG-3 cells were stimulated up to 24 hr with 10 ng/mL LIF, and the expression of miRNAs was assessed at five different time points by real-time PCR. LIF stimulation significantly reduces the expression of miR-141 after 4 and 6 hr compared with the respective basal expression levels. MiR-93 increases at all time points (significantly after 2 and 24 hr of LIF stimulation up to 9.2-fold), and miR-21 increases significantly after 1, 6, and 24 hr with a maximum

Decitabine cost of 19.8-fold. After 4 hr of LIF stimulation, miR-21 expression is significantly reduced compared with that at the aforementioned time points. This

strong reduction has been obvious in each individual experiment. All other changes, including the 2.3-fold increase in let-7g expression at 2 hr LIF stimulation, were not significant (Fig. 1). Because we have observed the most stable LIF-induced changes in miR-141, we decided to analyze its impact on proliferation by silencing and over-expression in JEG-3 cells. Transfection of JEG-3 cells with control substances reduces proliferation at all analyzed time points. Only silencing of miR-141 leads to a block of proliferation, when compared with its respective control, and is, after 48 hr, approximately 50% lower than in cells transfected with a non-genomic control sequence. In all other settings, proliferation is time-dependent. Over-expression of miR-141 does not lead to a further increase in proliferation (Fig. 2). We have observed a significant influence of LIF on the expression of the miRNAs miR-21, miR-93 (upregulation), and miR-141 (downregulation). The strongest effects were observable 4 and 6 hr after stimulation with LIF

when miR-141 was downregulated by far more than 50%. A surprising result was the downregulation of miR-21 after 4 hr of LIF stimulation compared with the earlier and later analyses. Silencing of miR-141 inhibits proliferation of JEG-3 cells, while over-expression does not further induce proliferation. To the best of our knowledge, P-type ATPase thus far, no studies have been published on LIF-induced miRNA in any cell type, but several STAT3-induced miRNAs have been described. LIF is well known to phosphorylate and activate STAT3 in a variety of cells including trophoblastic cells, where it induces invasiveness.3 In our experiments, LIF stimulation of JEG-3 cells significantly increased miR-21 expression. This is compatible with previous reports that in head and neck carcinoma, osteosarcoma, ovarian carcinomas, and others, miR-21 promotes proliferation, migration, and invasion.

Herein, we compare the overall outcomes between hemodialysis (HD) and peritoneal dialysis (PD) to address this issue. Methods: Data on 7925 patients aged ≥70 years were obtained from the Korean Health Insurance database, all of whom started HD (n = 6715) or PD (n = 1210) between 2005 and 2008. To compare the risks of cardiovascular morbidity and all-cause mortality between HD and PD, Cox proportional hazard ratio (HR) analysis was used after adjusting multiple variables. Results: The risks of cardiovascular events such as

acute myocardial infarction, percutaneous coronary intervention, or hemorrhagic stroke were similar between both dialysis modalities. Composite risks considering cardiac and cerebral events together were also similar between Vincristine dialysis modalities. However, the risk of ischemic stroke was lower in the PD group: HR, 0.67 (0.43–0.99). For all-cause mortality, patients undergoing PD were at greater risk: HR, 1.30 (1.21–1.39) [Figure]. When limiting analyses into the patients without diabetes or cardiovascular comorbidities (n = 2330), patients undergoing PD had a slightly

greater risk of mortality than HD patients: HR, 1.16 (0.99–1.33). Conclusion: Overall cardiovascular risks are similar between dialysis modalities in the elderly patients with end-stage renal disease. However, the mortality risk is greater in the elderly patients undergoing PD. MORINAGA HIROSHI1, SUGIYAMA HITOSHI1, ITO YASUHIKO2, TSURUYA KAZUHIKO3, YOSHIDA HISAKO3, MARUYAMA HIROKI4, GOTO SHIN4, NISHINO TOMOYA5, TERAWAKI HIROYUKI6, Saracatinib ic50 NAKAYAMA MASAAKI6, NAKAMOTO HIDETOMO7, MATSUO SEIICHI2, MAKINO HIROFUMI1 1Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences; 2Nagoya University Graduate School of Medicine; 3Graduate School of Medical Sciences, Kyushu University; 4Niigata University Graduate School of Medical and Dental Sciences; 5Nagasaki University School of Medicine; 6Fukushima Medical University; 7Saitama

Medical School Introduction: Beta-2 microglobulin Chloroambucil (B2M) is an 11,800-molecular-weight polypeptide that is generated at a constant rate and eliminated by the kidneys. An elevated serum level of B2M is a potential risk factor predicting mortality in predialysis patients. However, it remains unknown whether B2M has an impact on the outcomes of patients on peritoneal dialysis (PD). Methods: A prospective multicenter observational study of Japanese PD patients, called the PDR-CS, began enrolling patients in December 2009. The data including demography, comorbidities, laboratory data at the baseline, cardiovascular complications, onset of EPS, and prognosis are collected using a web-based case report form. Five university hospitals participated in the PDR-CS and 227 PD patients were enrolled in the study, as of December 2012 (mean age, 59.1 years; male, 67.4%; diabetic nephropathy, 26.0%). Results: The serum B2M level increased with PD duration.

Drawbacks to screening include the risks of radiation (if imaging is performed) and those associated with endoscopy. Screening is unlikely to be cost-effective in low-risk populations [20], and is only of value if it detects risk factors that can be modified or early-stage disease that can be treated effectively [21].

The question for CVID patients is whether a higher risk of gastric cancer can be defined in particular groups. H. pylori is a Gram-negative bacterium and is implicated in the development of chronic gastritis, peptic ulceration, gastric carcinoma and MALT lymphoma. In 1994 the World Health Organization (WHO) classified H. pylori as a class I (or definite) carcinogen [22]. A multi-step model for the pathogenesis of LY294002 manufacturer gastric carcinoma has been proposed from epidemiological and pathological studies [23,24]. Chronic gastritis and gastric atrophy result from infection with H. pylori, and a higher gastric pH appears to permit the proliferation of nitrate-reducing anaerobic bacteria, resulting in the production of N-nitroso compounds [25], promoting carcinogenesis through intestinal metaplasia and

dysplasia to carcinoma [26]. This suggests that gastric pathology such as gastritis, gastric atrophy, metaplasia or dysplasia might be regarded as precancerous NVP-AUY922 lesions. Data from prospective studies suggest that in the general population H. pylori infection confers a two- to ninefold increased risk of gastric cancer. A meta-analysis of three prospective studies Edoxaban into the risk of gastric cancer attributable to H. pylori demonstrated a relative risk of 9 in subjects followed for up to 25 years [27], while a systematic review of nested case–control studies, which included 800 gastric cancer cases, found only a two- to threefold increased risk (95% CI 1·9–3·4) of gastric cancer in patients chronically infected with H.

pylori[28]. More recently, an analysis of 12 case–control studies nested within prospective cohorts, which examined H. pylori serology before gastric cancer diagnosis in 1228 non-cardia gastric cancer cases, found that the relative risk of non-cardia cancers associated with prior H. pylori infection was 5·9 (95% CI 3·4–10·3); however, there was no increased risk of cancers of the gastric cardia [29]. This means that H. pylori infection should be taken into account in any surveillance programme. Pernicious anaemia is a chronic autoimmune disease in which atrophic gastritis, typically sparing the antrum, results in a lack of intrinsic factor and vitamin B12 malabsorption with megaloblastic anaemia.