3% [95% CI: 27, 40%]). Other commonly cited reasons related to access to care. Most migraineurs presenting to the ED have a PCP and health insurance. ED visits commonly result from an inability to access care elsewhere and because patients consider pain to be an emergency condition. Missed opportunities for diagnosis and treatment likely contribute to ED visits. “
“(Headache 2011;51:839-842) Significant sex differences exist in migraine and other headache disorders. Several hypotheses have been proposed to explain these differences, including fluctuations

in sex hormones AG-014699 chemical structure and receptor binding, genetic factors, differences in exposure to environmental stressors, as well as differences in response to stress and pain perception; but how valid are some of these findings and can we improve the quality of research in this field? It is notable that the preponderance of animal pain studies use male subjects to study a predominantly female disorder. Furthermore, with respect to headache and migraine sex differences, limited data have been derived from animal models. Additionally, although sex differences (based on the categorization of male vs female) may be more routinely evaluated in clinical headache research than in the basic science MK-8669 supplier research, greater attention to potential differences

across the life cycle of women (ie, premenopausal vs postmenopausal differences) and menstrual cycle is warranted. In this manuscript we define the differences between “sex” and “gender” and highlight the importance of their application and use in headache research. The enhanced recognition and implementation of attention to sex differences throughout the hormonal and life-cycle phase in both human and animal research will only help to strengthen and further our understanding of migraine and may help guide the direction of future headache research. “
“Objective.— To assess the frequency of opioid use for acute migraine treatment

and characterize use groups by sociodemographics, health-care resource utilization (HRU), comorbidities and probable dependence within a large, US population-based sample of persons with migraine. Background.— Opioids are used in the acute treatment of migraine. medchemexpress However, their use is controversial. Methods.— Data from the 2009 American Migraine Prevalence and Prevention (AMPP) study were used to categorize persons with migraine into 4 groups based on reported opioid use: nonusers (between 2005 and 2009), previous users (history of use between 2005 and 2008 but no-use in 2009), and current opioid users (those reporting use of opioids in the 3 months preceding the 2009 American Migraine Prevalence and Prevention survey). Current opioid users were divided into nondependent and probable dependence users according to criteria for dependence adapted for inclusion in the survey from the Diagnostic and Statistical Manual of Mental Disorders–4th edition.

Genotyping was performed with the Infinium HumanHap 550K chip. All SNPs were in Hardy-Weinberg equilibrium. Linear regression models were used to assess associations, adjusting for age, sex, steatosis, ALT, type

of elastography probe, HOMA-IR, spleen size, presence of viral hepatitis and alcohol intake, using additive genetic models. Results: In 1037 participants (age 74.1±5.6 years; 50.7% males) reliable LSM and genetic data were obtained. Median LSM was 5.1 kPa (IQR 4.2-6.4). NAFLD was detected in 331 participants (31.9%). Two SNPs in the IFNGR2 gene, rs9976971 and rs2284553, were associated with LSM in the total cohort (p=0.018 and 0.011 respectively). This relationship remained Caspase activity significant in a multivariable model (p=0.043 and 0.010 respectively). A third polymorphism in the IFNGR2 gene, rs9808753, showed a trend towards significance in a multivariable model (p=0.08). In participants with NAFLD all three IFNGR2 SNPs were significantly associated with LSM (p=0.046; 0.044 and 0.003 respectively). In a multivariable model this relationship remained significant for rs9808753 (p=0.010). rs738409, rs12980275 and rs8099917, in the PNPLA3 and near the IL28B gene, were not associated with LSM in the total cohort, nor in participants

with NAFLD (all p-values >0.17). Conclusions: Two IFNGR2 SNPs FDA-approved Drug Library cost were associated with liver stiffness in this large population based cohort. In a subgroup of participants with NAFLD all three tested IFNGR2 variants showed an association with LSM. PNPLA3 and IL28B variants were not related to liver stiffness in the total cohort, nor in participants with NAFLD. These results suggest that IFNGR2 variants could not only

上海皓元医药股份有限公司 play a role in liver fibrogenesis in risk populations, but in the general population as well. Disclosures: Harry L. Janssen – Consulting: Abbott, Bristol Myers Squibb, Debio, Gilead Sciences, Merck, Medtronic, Novartis, Roche, Santaris; Grant/Research Support: Anadys, Bristol Myers Squibb, Gilead Sciences, Innogenetics, Kirin, Merck, Medtronic, Novartis, Roche, Santaris The following people have nothing to disclose: Elisabeth P. Plompen, Jeoffrey Schouten, Daan W. Loth, Bettina E. Hansen, Albert Hofman, Andre G. Uitterlinden, Bruno H. Stricker, Frank W. Leebeek Background: The response to chronic liver injury in hepatitis C (HCV) is fibrogenesis, which is characterized by the accumulation and reorganization of extracellular matrix. This extensive remodeling generates protein fragments originating from fibro-genesis or fibrosis resolution. These fragments may reflect the degree of fibrosis and/or the turnover of fibrotic processes and potentially serve as biomarkers that carry diagnostic and prognostic information. Aims: We aimed to evaluate the diagnostic and prognostic performance of two different sub-pools of type III collagen: Pro-C3, a cleavage specific formation biomarker and C3M, a biomarker for a MMP generated fragment.

Genotyping was performed with the Infinium HumanHap 550K chip. All SNPs were in Hardy-Weinberg equilibrium. Linear regression models were used to assess associations, adjusting for age, sex, steatosis, ALT, type

of elastography probe, HOMA-IR, spleen size, presence of viral hepatitis and alcohol intake, using additive genetic models. Results: In 1037 participants (age 74.1±5.6 years; 50.7% males) reliable LSM and genetic data were obtained. Median LSM was 5.1 kPa (IQR 4.2-6.4). NAFLD was detected in 331 participants (31.9%). Two SNPs in the IFNGR2 gene, rs9976971 and rs2284553, were associated with LSM in the total cohort (p=0.018 and 0.011 respectively). This relationship remained selleck screening library significant in a multivariable model (p=0.043 and 0.010 respectively). A third polymorphism in the IFNGR2 gene, rs9808753, showed a trend towards significance in a multivariable model (p=0.08). In participants with NAFLD all three IFNGR2 SNPs were significantly associated with LSM (p=0.046; 0.044 and 0.003 respectively). In a multivariable model this relationship remained significant for rs9808753 (p=0.010). rs738409, rs12980275 and rs8099917, in the PNPLA3 and near the IL28B gene, were not associated with LSM in the total cohort, nor in participants

with NAFLD (all p-values >0.17). Conclusions: Two IFNGR2 SNPs AZD1208 mouse were associated with liver stiffness in this large population based cohort. In a subgroup of participants with NAFLD all three tested IFNGR2 variants showed an association with LSM. PNPLA3 and IL28B variants were not related to liver stiffness in the total cohort, nor in participants with NAFLD. These results suggest that IFNGR2 variants could not only

MCE play a role in liver fibrogenesis in risk populations, but in the general population as well. Disclosures: Harry L. Janssen – Consulting: Abbott, Bristol Myers Squibb, Debio, Gilead Sciences, Merck, Medtronic, Novartis, Roche, Santaris; Grant/Research Support: Anadys, Bristol Myers Squibb, Gilead Sciences, Innogenetics, Kirin, Merck, Medtronic, Novartis, Roche, Santaris The following people have nothing to disclose: Elisabeth P. Plompen, Jeoffrey Schouten, Daan W. Loth, Bettina E. Hansen, Albert Hofman, Andre G. Uitterlinden, Bruno H. Stricker, Frank W. Leebeek Background: The response to chronic liver injury in hepatitis C (HCV) is fibrogenesis, which is characterized by the accumulation and reorganization of extracellular matrix. This extensive remodeling generates protein fragments originating from fibro-genesis or fibrosis resolution. These fragments may reflect the degree of fibrosis and/or the turnover of fibrotic processes and potentially serve as biomarkers that carry diagnostic and prognostic information. Aims: We aimed to evaluate the diagnostic and prognostic performance of two different sub-pools of type III collagen: Pro-C3, a cleavage specific formation biomarker and C3M, a biomarker for a MMP generated fragment.

0007) significantly predicts low fibrinogen level. In non-cholestatic liver disease, K, R, AA and MA (p < 0.005) all significantly predict low fibrinogen level. None of the cholestatic liver disease this website patients developed thrombotic complications (0/13). 8.7% of non-cholestatic liver disease patients (9/103) developed pre- or post-transplant thrombosis (portal vein or other systemic thrombosis). The only significant predictor of thrombosis is low INR (p = 0.04). Conclusion: We found significant differences between coagulation profiles of cholestatic liver disease

versus non-cholestatic liver disease. In non-cholestatic liver disease, rising MELD predicts abnormal TEG scores (K, R, AA and MA) and decreasing fibrinogen level. In cholestatic liver disease, rising MELD only significantly correlates with rising INR and not with TEG or traditional coagulation tests (including fibrinogen level). When comparing TEG against traditional coagulation click here studies, we found in cholestatic liver disease, low MA predicts low fibrinogen level. Therefore in cholestatic liver disease, MA is a useful independent predictor of low fibrinogen level. We also found the only significant

predictor of thrombotic complication in non-cholestatic liver disease patients is a lower INR when compared with other cirrhotic patients (p = 0.04). RL VAN LEEST,1 AT DEV,1,2 F RUSLI,1 S PIANKO,1 W SIEVERT,1 S LEE,1 V KNIGHT,1 DT RATNAM1,2 Gastroenterology and Hepatology Unit, Monash Medical Centre1, Department of Medicine, Monash University2 Background and aim: Entecavir is now a 1st line therapeutic option for chronic Hepatitis B (CHB).

However, most of the evidence is reliant on controlled phase III trials or real world data in treatment naïve populations. This may not reflect its true efficacy in the treatment experienced population. This study aims to document the real MCE world experience of using ETV in an Australian cohort and compares nucleoside analogue naïve patients to those exposed to other agents. Methods: 175 CHB patients at a tertiary centre with annual viral loads treated with Entecavir for 6 months or more were identified retrospectively through pharmacy and clinic records. Baseline demographic data and progressive 6 monthly pathology, fibroscan and imaging reports in addition to clinic notes were reviewed. Treatment outcomes were defined as time to undetectable viral load, time to viral load under 360 IU, new advanced cirrhosis or HCC and time to eAg seroconversion. Interim results: HBeAg positive: 77 patients (70.1% male, 63.6% treatment naïve, 76.6% Asian ethnicity, average age 45.8 years). Median ALT 42.5 IU/L, 23% advanced fibrosis. HBeAg negative: 95 patients (74.7% male, 84.2% treatment naïve, 68.4% Asian ethnicity, median age 54.8 years). Median ALT 30.5 IU/L, 37.9% advanced fibrosis.

0007) significantly predicts low fibrinogen level. In non-cholestatic liver disease, K, R, AA and MA (p < 0.005) all significantly predict low fibrinogen level. None of the cholestatic liver disease Staurosporine order patients developed thrombotic complications (0/13). 8.7% of non-cholestatic liver disease patients (9/103) developed pre- or post-transplant thrombosis (portal vein or other systemic thrombosis). The only significant predictor of thrombosis is low INR (p = 0.04). Conclusion: We found significant differences between coagulation profiles of cholestatic liver disease

versus non-cholestatic liver disease. In non-cholestatic liver disease, rising MELD predicts abnormal TEG scores (K, R, AA and MA) and decreasing fibrinogen level. In cholestatic liver disease, rising MELD only significantly correlates with rising INR and not with TEG or traditional coagulation tests (including fibrinogen level). When comparing TEG against traditional coagulation PF-562271 studies, we found in cholestatic liver disease, low MA predicts low fibrinogen level. Therefore in cholestatic liver disease, MA is a useful independent predictor of low fibrinogen level. We also found the only significant

predictor of thrombotic complication in non-cholestatic liver disease patients is a lower INR when compared with other cirrhotic patients (p = 0.04). RL VAN LEEST,1 AT DEV,1,2 F RUSLI,1 S PIANKO,1 W SIEVERT,1 S LEE,1 V KNIGHT,1 DT RATNAM1,2 Gastroenterology and Hepatology Unit, Monash Medical Centre1, Department of Medicine, Monash University2 Background and aim: Entecavir is now a 1st line therapeutic option for chronic Hepatitis B (CHB).

However, most of the evidence is reliant on controlled phase III trials or real world data in treatment naïve populations. This may not reflect its true efficacy in the treatment experienced population. This study aims to document the real medchemexpress world experience of using ETV in an Australian cohort and compares nucleoside analogue naïve patients to those exposed to other agents. Methods: 175 CHB patients at a tertiary centre with annual viral loads treated with Entecavir for 6 months or more were identified retrospectively through pharmacy and clinic records. Baseline demographic data and progressive 6 monthly pathology, fibroscan and imaging reports in addition to clinic notes were reviewed. Treatment outcomes were defined as time to undetectable viral load, time to viral load under 360 IU, new advanced cirrhosis or HCC and time to eAg seroconversion. Interim results: HBeAg positive: 77 patients (70.1% male, 63.6% treatment naïve, 76.6% Asian ethnicity, average age 45.8 years). Median ALT 42.5 IU/L, 23% advanced fibrosis. HBeAg negative: 95 patients (74.7% male, 84.2% treatment naïve, 68.4% Asian ethnicity, median age 54.8 years). Median ALT 30.5 IU/L, 37.9% advanced fibrosis.

A case–control study was defined as a cross sectional study that included a number of patients with inhibitors (cases) and another group of (matched) patients without inhibitors (controls). Specified risk factors for inhibitor development were then analysed in both groups. Case series were defined as a longitudinal follow-up of a group of patients selected for certain risk factors to evaluate the outcome/inhibitor development at the end of the observation period. Extracted data were used to populate a standard form. Items included: study design; number of patients in the study; patient characteristics BMN 673 solubility dmso (severity of haemophilia, treatment status);

inhibitor testing (frequency, assay used and cut-off level); treatment characteristics (type of product); analysis of the risk factor [relative risk (RR), hazard ratio, odds ratio (OR) or otherwise, as stated by the authors]. If no RR or OR was given these measures were calculated whenever possible, using the available

data in the article. The EHTSB is an established group of internationally recognized European experts in the field of haemophilia and blood clotting disorders. Founded in 2003 by Baxter, the board currently represents 24 large European haemophilia centres in 15 countries, taking care of >4000 patients with severe congenital bleeding disorders from birth to adulthood. In conjunction with the literature review, a survey was undertaken to assess all members’ opinions of the importance of KU-57788 clinical trial risk factors on the development of inhibitors and how this influenced their clinical practice. medchemexpress In a subgroup of 14 EHTSB members, the potentially most important factors involved in inhibitor development were discussed and listed. Based on this risk factor selection, two questionnaires were prepared and administered to all 24 EHTSB members. In the first questionnaire, board members were asked to rank each risk factor on a scale of 0–5 (0 = not important or not influential; 5 = very important or very influential)

for importance of its potential role in inhibitor development. In the other questionnaire, the influence of the same single factors on their clinical practice was rated on a scale of 0–100. The consensus recommendations were formulated following a discussion held within the subgroup of 14 members during an EHTSB meeting in Brussels on 15–16 January, 2009 and reviewed after the literature update in 2010. Antenatal exposure to maternal FVIII, and breast feeding, has been considered potentially protective against inhibitor development [9]. Supporting this hypothesis is the fact that human breast milk affects normal gastrointestinal development and oral immune tolerance [10]. Moreover, the presence of fat globule proteins in breast milk that bear strong homology with FVIII might facilitate immune tolerance in the immature neonatal system, thus decreasing the likelihood of inhibitor formation [9,11]. Five studies were identified for review (Table 1) [12–16].

PHT is usually a result of advanced fibrosis, but the need for established

cirrhosis in every case remains contentious. Sampling error remains a significant issue for all biopsy procedures in any chronic liver disease with advanced fibrosis. On the basis of our findings, it is likely that the finding of Scheuer stage 2 or 3 fibrosis in patients with clinical PHT reflects a combination of both principles: established cirrhosis is not always required for the development of PHT, and some patients with established cirrhosis may have a biopsy sample interpreted as falling short of this staging. Thus, our conclusion that dual-pass liver biopsy improves the detection of significant fibrosis find more (F2-F4), with another 16% detected with two passes (P = 0.01), is an important observation from this study. It is not surprising that dual-pass biopsy improved the sensitivity of fibrosis detection. Sample size and focal histological lesions have commonly presented challenges in many liver diseases. Various techniques, including dual passes, rejection of sections with fewer than five portal tracts, and quantitative histochemistry (all portrayed here), help to overcome these limitations.19 In the current study, a single biopsy core might have

missed a diagnosis of fibrosis in 22% of the patients. Gaskin et al.21 reported discordance between percutaneous biopsy and open liver biopsy in 11 CFLD patients. Routinely buy CH5424802 obtaining two cores for the evaluation of suspected CFLD is therefore advised for clinical purposes because the second pass in our 上海皓元 study detected additional patients (12.5%) whose fibrosis was missed by the first pass. However, the agreement of fibrosis stages between the first and second passes was substantial (weighted κ = 0.61), and this suggests that one pass is better than no biopsy at all. Some of these concerns may be overcome by the application of alternative and more quantitative histological methods, such as confirmatory α-SMA immunoreactivity, as shown in this study. Certainly, dual biopsy would have even more relevance in research studies for which a gold-standard point of

reference is necessary (e.g., for the evaluation of noninvasive diagnostic modalities) or in therapeutic trials. These data, in conjunction with our earlier comparison of US with liver histology,8 suggest that caution is warranted in interpreting US findings in patients with suspected CFLD, particularly in the absence of liver nodularity and splenomegaly. This is contrary to the conclusions of Lenaerts et al.,6 who did not evaluate liver histology or clinically significant outcomes such as PHT. It is widely recognized that US poorly differentiates between liver steatosis and fibrosis; this is evidenced by the finding of heterogeneous echogenicity on scans in patients with steatosis but no fibrosis. However, US may value add to monitoring for PHT once the presence of hepatic fibrosis is confirmed by liver biopsy or novel noninvasive means.

We determined the thermoneutral zone of six young northern fur seals by measuring their metabolism in ambient air and controlled water temperatures (0°C–12°C) from ages 8 to 24 mo. We found that the ambient air temperatures within

our study (overall 1.5°C–23.9°C) did not affect resting metabolic rates. Calculated lower critical temperatures in water varied between 3.9°C and 8.0°C, while an upper A-769662 molecular weight critical temperature in water was only discernible during a single set of trials. These thermal responses provide insight into the possible physiological constraints on foraging ecology in young northern fur seals, as well as the potential energetic consequences of ocean climate change and altered prey distributions. “
“The route taken by northward migrating gray whales during spring between Vancouver Island and southeastern Alaska, a distance of about 575 km, has long been uncertain. It is generally selleck compound believed that the whales closely follow the western, outer coastline of Haida Gwaii (formerly the Queen Charlotte Islands), an archipelago lying between Vancouver Island and southeastern Alaska, consistent with their pattern of migrating close to shore over the majority of their northward migratory

corridor. By tracking satellite-tagged individuals and surveying whales from shore bases, we provide evidence that this is not the primary migratory corridor, but instead that most whales migrate through Hecate Strait and Dixon Entrance,

broad waterways that lie to the east and north MCE of Haida Gwaii. By using this route, northbound gray whales potentially face a wider range of industrial activities and developments than they would by migrating along the outer coast. “
“Previous studies of the odontocete forelimb have not considered flipper anatomy in an evolutionary context. This study of 39 cetacean species (1 extinct archaeocete, 31 extant and 3 extinct odontocetes, and 4 mysticetes), provides a detailed comparative analysis of the major bones and muscles of the odontocete flipper. Differences across families in the anatomy of the deltoid, supraspinatus, coracobrachialis, and subscapularis muscles correspond directly to size and shape of forelimb elements. Specialization of the different shoulder girdle muscles allows for more maneuverability of the flipper by independent control of muscular columns. Maximum likelihood analyses helped determine the correlation of characters studied by ancestral state reconstruction, and revealed independent evolution of osteological and external characters among various lineages. Comparative Analyses by Independent Contrast (CAIC), found several contrasts between flipper area and body length for several extant odontocetes and a linear relationship was inferred.

1A). SHP, CAR, and NCOA3 mRNA levels were increased in HCV-infected patients in comparison with normal controls. Hepatic RXRα, PPARα, and PPARβ mRNA levels were decreased in HCV-infected patients compared with normal controls. There was no change in the expression levels of other nuclear receptors including FXR (Supporting Fig. 1A). The expression of genes (Supporting Table 1) that play pivotal roles in regulating lipid homeostasis was studied. The mRNA level of

steroid MLN0128 manufacturer regulatory element-binding protein (SREBP)-1c was decreased in HCV-infected livers (Fig. 1B). The expression levels of SREBP-1c target genes (fatty acid synthase [FAS], acyl-CoA carboxylase [ACC], and fatty acyl-CoA elongase [FAE]) were modestly reduced in HCV-infected livers, but did not reach statistical significance (Supporting Fig. 1B). Genes responsible for fatty acid uptake (fatty acid transport protein 2 and 5 [FATP2 and FATP5]) and glucose uptake (facilitated glucose transporter 2 [GLUT2]) were up-regulated in HCV-infected livers (Fig. 1B). The expression of low-density lipoprotein receptor (LDLR), which plays a key role in viral entry to the hepatocyte,22 PD0325901 purchase was decreased by four-fold

in HCV-infected patients (Fig. 1B). In addition, the mRNA levels of microsomal triglyceride transfer protein (MTP), which is essential for very low-density lipoprotein (VLDL) and HCV secretion from the infected cells,23 was increased in HCV-infected livers (Fig. 1B). Cytochrome P450, family 7, subfamily A, polypeptide 1 (CYP7A1) catalyzes a rate-limiting step in cholesterol catabolism and bile acid biosynthesis. Na+/taurocholate cotransporter (NTCP) controls the uptake of bile acid. The expression levels

of both genes were increased in HCV-infected livers (Fig. 1C). The mRNA level of CYP7A1 increased more than 13-fold. CYP7A1 and NTCP are negatively regulated by SHP. However, HCV-infected patients have increased CYP7A1 and NTCP as well as SHP mRNA levels. Inflammatory pathway gene expression was altered in HCV-infected livers (Fig. 1D). HCV-infected patients had increased expression of tumor necrosis factor α (TNF; three-fold) and nitric oxide synthase 2 (NOS2; seven-fold). The expression of genes in the fatty 上海皓元 acid oxidation pathway and antioxidant system showed no significant difference (Supporting Fig. 1C,D). There is a sex difference in alcohol intake and alcoholic liver disease; female sex is a protective factor for drinking and yet female individuals are more susceptible than male individuals to the development of alcoholic liver disease.19 It is essential to use sex-matched populations to study biomarkers for alcohol use. Thus, we compared gene expression patterns between HCV-infected men with and without an alcohol drinking history.

A comparison of 29 commercial serological kits (17 ELISAs and 12 ICTs) was carried out in France.

Depending on the type of analysis performed, 2 to 4 of the ELISAs presented an excellent performance. In contrast, only one of the 12 ICTs had an accuracy >90% [32]. A line assay using 6 recombinant proteins corresponding to virulence factors (CagA, VacA, GroEL, gGT, HcpC, and UreA) was developed in Germany. It was validated on a group of 600 patients (42% H. pylori positive by histology) and showed 97.6% sensitivity and 96.2% specificity, that is, an improvement on currently available serological tests [33]. The same group in collaboration with researchers in Iran was able to identify a H. pylori protein, FliD, essential in the Adriamycin assembly of the flagella. The recombinant FliD protein was tested on a group of 618 patients (51.4% H. pylori positive) with 97.4% sensitivity and 99% specificity using a line assay, and 97 and 96% by ELISA, respectively [34]. Other attempts to select antigenic proteins of potential diagnostic value were made (CafI, ureG, ureB), but have not been evaluated yet [35]. Interestingly, using

Helicoblot 2.1 (Genelabs Diagnostics, Singapore), it was possible to identify a low molecular weight protein (35KDa) associated with a low risk of GC (OR = 0.4, 95% CI:0.1–0.9) and the VacA protein associated with a high risk of GC (OR = 2.7, 95 CI:1–7.1) among patients with GC (102) and dyspepsia (122) in Iran [36]. A review on ICTs was also produced last year [37]. Pepsinogen http://www.selleckchem.com/products/bgj398-nvp-bgj398.html I and II and their ratio as predictors of atrophy were evaluated this year in Iran [38], Turkey [39], and Italy [40], but they were found to be insensitive predictors of these 上海皓元医药股份有限公司 lesions. A toll-like receptor 4 was found helpful to differentiate between dysplasia and other precancerous lesions [39]. Both miR-106b and miR-21 were found as markers of increased risk for GC after H. pylori eradication [41]. The progress in imaging techniques allows now to have a more accurate approach of

the features associated to H. pylori infection. There are continuous attempts to improve the existing diagnostic methods or to evaluate their use in real life. Competing interest: The authors have no competing interests. “
“Background:  A remarkable variety of restriction-modification (R-M) systems is found in Helicobacter pylori. Since they encompass a large portion of the strain-specific H. pylori genes and therefore contribute to genetic variability, they are suggested to have an impact on disease outcome. Type I R-M systems comprise three different subunits and are the most complex of the three types of R-M systems. Aims:  We investigated the genetic diversity and distribution of type I R-M systems in clinical isolates of H. pylori. Material and methods:  Sixty-one H. pylori isolates from a Swedish hospital based case-control study and 6 H.