Until

recently, a salient exception appeared to be the stegosaurs, whose low diversity was anomalous to this general model. However, new discoveries of stegosaurs have increased our knowledge of their diversity: Carpenter selleck chemical (2001) estimates that at least five stegosaur species are now known from the Morrison Formation of the western United States (although Galton & Upchurch (2004b) recognize only three). This would appear to simplify the problem, but there is an additional caveat: the species are not all contemporaneous (K. Carpenter, pers. comm., 2004), and there may be geographic differentiation as well within the Morrison. The lack of contemporaneity could have several explanations, including insufficient stratigraphic sampling to establish that more of these species lived at the same time than it now appears. However, another approach is phylogenetic. If these five species turned www.selleckchem.com/products/pf-562271.html out to be morphotypes of a single anagenetic lineage, there would indeed be no evidence for contemporaneity. Would the hypothesis of species recognition thereby be weakened (Fig. 7, left)? In fact, such a result would weaken a hypothesis of anti-hybridization, but it would not

weaken or test the hypothesis of positive assortative mating (Paterson, 1993). However, if phylogenetic analysis revealed that these species indeed represented different lineages, and their ‘ghost ranges’ indicated that they must have diverged from others

at an earlier time, then at one time the test of contemporaneous species would have been passed (Fig. 7, right). Sorafenib mouse It is not impossible that such a pattern could also indicate other processes than species recognition, such as sexual or social selection, but in concert with non-directional evolutionary change the indication would be rather more strongly in favor of species recognition. Phylogenetic analysis and further biostratigraphic sampling can test this hypothesis. Finally, we return to the test of the Mate Recognition Hypothesis that Sampson (1999) proposed. We found that in every criterion, mostly related to higher rates of speciation and habitat shifts, the concept of ‘species recognition’ could be substituted for the terms related to sexual selection without any apparent difference in results. The exception was his fourth criterion (speciation will often be correlated with vicariance events rather than the formation of peripheral isolates), which we suggest is untestable in the fossil record, and in any case would not discriminate between sexual selection and species recognition as a cause.

Until

recently, a salient exception appeared to be the stegosaurs, whose low diversity was anomalous to this general model. However, new discoveries of stegosaurs have increased our knowledge of their diversity: Carpenter check details (2001) estimates that at least five stegosaur species are now known from the Morrison Formation of the western United States (although Galton & Upchurch (2004b) recognize only three). This would appear to simplify the problem, but there is an additional caveat: the species are not all contemporaneous (K. Carpenter, pers. comm., 2004), and there may be geographic differentiation as well within the Morrison. The lack of contemporaneity could have several explanations, including insufficient stratigraphic sampling to establish that more of these species lived at the same time than it now appears. However, another approach is phylogenetic. If these five species turned GSK-3 inhibitor out to be morphotypes of a single anagenetic lineage, there would indeed be no evidence for contemporaneity. Would the hypothesis of species recognition thereby be weakened (Fig. 7, left)? In fact, such a result would weaken a hypothesis of anti-hybridization, but it would not

weaken or test the hypothesis of positive assortative mating (Paterson, 1993). However, if phylogenetic analysis revealed that these species indeed represented different lineages, and their ‘ghost ranges’ indicated that they must have diverged from others

at an earlier time, then at one time the test of contemporaneous species would have been passed (Fig. 7, right). filipin It is not impossible that such a pattern could also indicate other processes than species recognition, such as sexual or social selection, but in concert with non-directional evolutionary change the indication would be rather more strongly in favor of species recognition. Phylogenetic analysis and further biostratigraphic sampling can test this hypothesis. Finally, we return to the test of the Mate Recognition Hypothesis that Sampson (1999) proposed. We found that in every criterion, mostly related to higher rates of speciation and habitat shifts, the concept of ‘species recognition’ could be substituted for the terms related to sexual selection without any apparent difference in results. The exception was his fourth criterion (speciation will often be correlated with vicariance events rather than the formation of peripheral isolates), which we suggest is untestable in the fossil record, and in any case would not discriminate between sexual selection and species recognition as a cause.

The most common primary tumors are lung in men and breast in women; oral metastases from colorectal primary are exceedingly rare. In fact, gingival metastasis is a very rare and late presentation VX770 of colorectal carcinoma, and the consequent survival is just a few weeks or months. The gross appearance of gingival metastasis may be indistinguishable from other benign buccal lesions, such as pyogenic granuloma and giant cell granuloma. Histological examination with immunohistochemical

techniques is thus essential to confirm the diagnosis. Gingival metastasis can cause progressive discomfort, such as pain or bleeding, as illustrated in our case. Therefore, even in cases with advanced or disseminated disease, palliative treatment such as radiotherapy is necessary to improve the quality of life of patients. In selected cases with solitary oral metastasis, surgical resection can be considered. Contributed by “
“We read with interest the letter by Kershenobich et al. in Hepatology regarding the meta-analysis of randomized trials comparing Lumacaftor cost pegylated interferon (PEG-IFN) alpha-2a and alpha-2b in the treatment of chronic hepatitis C (CHC) by Awad et al.1, 2 We agree regarding the importance of a uniform study population

in treatment-naïve patients with CHC. This is especially true for the study by Laguno et al., which included patients coinfected with human immunodeficiency virus (HIV).3 We performed a meta-analysis of four available studies comparing PEG-IFN alpha-2a and peginterferon alpha-2b in the treatment of patients with

CHC who have concomitant HIV coinfection: one randomized,3 one prospective–retrospective,4 and two prospective studies5, 6 with one of them reported Cyclooxygenase (COX) as an abstract.6 A total of 1009 patients (581 treated with PEG-IFN alpha-2a; sample size, 63-557; mean age, 41 years; 69%-75% males) were treated in the four studies.3-6 Pooled analysis of the data showed that the odds of achieving rapid virologic response (RVR), early virologic response (EVR), and sustained virologic response (SVR) were similar with PEG-IFN alpha-2a and PEG-IFN alpha-2b (Table 1). Similarly, the odds of treatment discontinuation due to serious adverse effects were similar with PEG-IFN alpha-2a and PEG-IFN alpha-2b (Table 1). The data were homogeneous for all the analyses. There was no evidence to indicate any publication bias. After excluding the study reported as an abstract, the results with the two PEG-IFN compounds were still similar. The SVR rates were 36% and 35% with PEG-IFN alpha-2a and PEG-IFN alpha-2b, respectively. Subgroup analyses of the SVR based on the genotype status (genotype 1 or 4 and genotype 2 or 3) and viral load showed similar efficacy and safety data for the two types of PEG-IFN. The data were homogeneous without any suggestion of publication bias in all the analyses.

8, mean cell volume of 62, and a ferritin value of 3. BCS, Budd-Chiari syndrome; CAT, computerized axial tomography; IR, interventional radiology; IVC, inferior vena cava; PH, portal hypertension; US, ultrasound. On physical exam, her temperature was 97.9°F, pulse was 82, respiratory rate was 17, and blood pressure was 94/70. She was found to have hepatomegaly and moderate

ascites on abdominal BVD-523 concentration exam and was heme negative on rectal exam. An esophagogastroduodenoscopy and colonoscopy were unremarkable for a source of blood loss, and small bowel biopsies were not consistent with celiac sprue. A right upper quadrant ultrasound (US) revealed moderate ascites and hepatosplenomegaly. The liver had a lobular contour to it with increased echogenicity. A subsequent computerized axial tomography (CAT) scan illustrated a “nutmeg liver” and ascites (Fig. 1). A repeat US with Doppler showed patent hepatic and portal veins with normal direction of flow. Her liver function studies were all within normal limits, along with hepatitis serologies, antinuclear antibody, and Epstein-Barr virus titers. The ascites was sampled, revealing a serum ascites albumin gradient of >1.1 and a protein level of <2.5, consistent with portal hypertension (PH). Hepatic venous pressures were attempted by interventional radiology (IR). The pressure AZD2281 in the intrahepatic portion of

the inferior vena cava (IVC) was elevated to 14 mmHg, and the right heart pressure was normal at 4 mmHg, yielding a 10-mmHg venous pressure gradient between the supra- and intrahepatic portion of the IVC. Attempts were made to cannulate the hepatic veins MRIP to obtain free hepatic pressures; however, these were unsuccessful because of a narrowing in the intrahepatic portion of the IVC. This prompted a third US in IR, demonstrating a web and turbulent flow at the origin of the hepatic vein from the IVC. IR performed a transhepatic venogram, and the web was found at the confluence of the middle hepatic vein and the IVC. The initial pressure gradient between the middle

hepatic vein and the right atrium was significantly elevated at 20 mmHg. IR executed a successful angioplasty of the web with a 12 mm × 4 cm balloon, and the pressure gradient dropped to 4 mmHg (Fig. 2). The patient recovered nicely, with resolution of her ascites and symptoms. A 1-month follow-up US illustrated no residual stenosis (Fig. 3). A CAT scan 5 months later showed a dramatic improvement in the appearance of her liver (Fig. 4). As for her anemia, it was believed to be secondary to her menses and corrected nicely with iron supplementation. Budd-Chiari syndrome (BCS) occurs as a result of PH from hepatic venous outflow obstruction, usually from a hepatic vein thrombosis. Membranous webs can also rarely form in the hepatic venous system, eliciting the same organic response. Venous thrombosis can require pharmacologic thrombolysis and even liver transplantation.

MHCC97-L and MHCC97-H cells demonstrate a mesenchymal phenotype with decreased expression of E-cadherin and increased expression of c-Met, fibronectin, and Zeb2 compared with Huh7 and Hep3B cells, which have an epithelial phenotype. PHA665752 treatment blocked phosphorylation of c-Met and downstream phosphoinositide 3-kinase/Akt and mitogen-activated protein kinase/Erk pathways, inhibited cell proliferation, and induced apoptosis in

c-Met–positive MHCC97-L and MHCC97-H cells. In xenograft models, administration of PHA665752 significantly inhibited c-Met–positive MHCC97-L and MHCC97-H tumor growth, and PHA665752-treated tumors U0126 demonstrated marked reduction of both c-Met phosphorylation and cell proliferation. c-Met–negative Huh7 and Hep3B cells were not affected by c-Met inhibitor treatment in vitro or in vivo. In addition, c-Met–positive MHCC97-L and MHCC97-H cells demonstrated cancer stem cell–like characteristics, such as resistance

to chemotherapy, tumor sphere formation, and increased expression of CD44 and ABCG2, and PHA665752 treatment suppressed tumor sphere formation and inhibited CD44 expression. Conclusion: c-Met represents a potential target of personalized treatment for HCC with an active HGF/c-Met pathway. (HEPATOLOGY 2011;) Hepatocellular carcinoma (HCC) represents the third leading cause of cancer-related death worldwide and is the only carcinoma Pembrolizumab with increasing mortality in the United States during the last decade.1 Although surgical resection and transplantation have significantly improved MK-8669 survival in patients with small tumors and no evidence of invasion or metastasis, the prognosis of HCC for late stage diseases remains very poor.2 In addition, recurrent and metastatic disease remain the most important factors for survival in HCC transplantation patients.3 In addition to tumor number, size, and vascular invasion observed on imaging studies, c-Met expression is a molecular characteristic that appears to

predict poor survival in HCC (Supporting Table 1).4-7 Hepatocyte growth factor (HGF) is an autocrine and paracrine factor that is produced by stromal cells. HGF acts on c-Met, a high-affinity tyrosine kinase receptor.8 During development, homozygous deletion of HGF or c-Met is embryonic-lethal.9, 10 Although HGF/c-Met signaling does not play a role in liver homeostasis during normal physiologic conditions, many studies have demonstrated the important role of HGF in liver regeneration, hepatocyte survival, and tissue remodeling after acute injury.11, 12 After c-Met phosphorylation and activation, multiple signaling pathways are involved as downstream targets, such as the phosphoinositide 3-kinase (PI3K)/Akt and mitogen-activated protein kinase (MAPK)/Erk pathways.

To explore the functions of LIN28B, two specific siRNAs against LIN28B mRNA were synthesized. As shown in Fig. 6A, both siRNAs remarkably reduced the expression of LIN28B protein. Cell proliferation assays showed that both si-LIN28B-1 and si-LIN28B-2 significantly inhibited the proliferation of Huh-7 cells (Fig. 6B). Furthermore, we investigated the effect of si-LIN28B on cell cycle progression by way of fluorescence-activated

cell sorting analysis. The results showed that both si-LIN28B-1 and si-LIN28B-2 blocked G1/S transition and retained Huh-7 cells at G1 phase (P = 0.0476 and 0.0221, respectively) (Fig. 6C). The suppression of proliferation and blockade of cell cycle progression by si-LIN28B-1 and si-LIN28B-2 mimicked the phenotype induced by enforced expression of miR-125b in HCC cells. We next CP690550 investigated the effect of si-LIN28B on the migration and invasion of Huh-7 cells. Remarkably, transwell assay without matrigel coating showed that si-LIN28B-1 elicited an inhibitory effect on Huh-7 cell migration

compared with the control group (Fig. 6D). Si-LIN28B-2 showed a greater inhibitory effect than si-LIN28B-1, because si-LIN28B-2 had a better knockdown of the LIN28B protein level. Transwell assay with matrigel coating showed that si-LIN28B-1 and si-LIN28B-2 significantly reduced the invasion LY2109761 price ability of HCC cells (Fig. 6E). Together, our results indicate that reduction of LIN28B through siRNA interference has similar effects on the HCC cells to those induced by miR-125b, suggesting that LIN28B may act as a downstream functional mediator for miR-125b. If LIN28B

indeed acts as a functional target of miR-125b, reintroduction of LIN28B into miR-125b–expressing cells Myosin should be able to antagonize the effects of miR-125b. To test the hypothesis, we first constructed a lentiviral expression vector of LIN28B without the 3′-UTR and infected miR-125b–expressing cells. As shown in Supporting Fig. 7A, the expression of LIN28B was recovered after LIN28B lentivirus infection. Interestingly, cell proliferation assay demonstrated that reintroduction of LIN28B enhanced the proliferation of miR-125b–expressing cells (Fig. 7A). Moreover, the inhibition of miR-125b on the colony formation was also antagonized by enforced expression of LIN28B (Supporting Fig. 7B). Furthermore, enforced expression of LIN28B significantly counteracted the G1 arrest induced by miR-125b (Fig. 7B). In addition, in vitro migration and invasion assays showed that enforced expression of LIN28B rescued the migration and invasion suppression induced by miR-125b (Fig. 7C,D). It is noteworthy that the LIN28B overexpressing cells displayed a phenotype of faster growth and increased aggressiveness compared with the other cells due to higher expression of LIN28B in these cells.

1D), we focused further study on these two subsets. Percentages of CD11b/Gr1mid and CD11b/Gr1low cells Sorafenib supplier in bone marrow, blood, and liver of tumor-bearing mice were analyzed at various time points during metastatic growth. Levels of CD11b/Gr1mid cells in bone marrow peaked at day 5, and decreased thereafter, which coincided with increasing levels in blood and liver.

Circulating and hepatic CD11b/Gr1mid cell numbers continued to rise by day 14 (Fig. 2B). In contrast, bone marrow and circulating CD11b/Gr1low cell numbers remained constant with time while increasing in the liver abruptly from day 12 (Fig. 2C). These results suggest that the CD11b/Gr1mid subset is recruited from bone marrow during development of liver metastasis, whereas the CD11b/Gr1low population

likely derived from expansion or differentiation of resident cells after metastases had established. To confirm the bone marrow origin of the CD11b/Gr1mid subset, GFP+ cells isolated from bone marrow of GFP transgenic mice were transferred intravenously into C57BL/6 mice 11 days after MC38 or PBS inoculation. Significantly more GFP+ bone marrow cells were found in MC38-inoculated tumor-bearing livers compared with PBS-inoculated controls (Fig. 2D). These GFP+ cells were in the peritumoral Fulvestrant supplier regions of liver metastases (Fig. 2E), and were CD11b+, CCR2+, and F4/80+ (Fig. 2F), markers expressed only by the CD11b/Gr1mid population. To investigate whether similar CD11b/Gr1mid and CD11b/Gr1low subsets are associated with liver metastasis of other cancer cell lines, we inoculated B16F1GFP+ and LLCGFP+ cells into C57BL/6 mice. Metastases were observed in the liver at day 14 when myeloid infiltrates were assessed. Formation of LLCGFP+ tumor colonies resulted

in a significant increase in the Tau-protein kinase CD11b/Gr1mid population, similar in extent to MC38GFP+ inoculation. In contrast, CD11b/Gr1mid cell numbers were not significantly altered after B16F1GFP+ colonization (Fig. 3A). LLCGFP+ inoculation also led to a substantial increase in CD11b/Gr1low cell numbers, whereas moderate increases were observed after B16F1GFP+ and MC38GFP+ inoculation (Supporting Fig. 3C). Thus, LLCGFP+ colonization was analogous to that of MC38GFP+ in recruiting CD11b/Gr1mid cells, whereas this recruitment was dispensable for B16F1GFP+ cells. To identify factors involved in recruitment of bone marrow-derived CD11b/Gr1mid cells to liver metastases, we compared the cytokine expression profile of MC38, B16F1, and LLC cells. MC38 cells expressed high levels of CCL2 and moderate levels of CXCL1, CXCL10, and tissue inhibitor of metalloproteinase 1 (TIMP-1). Moderate levels of CCL2, CXCL1, and TIMP-1 were also detected in culture medium of LLC cells. B16F1 cells produced moderate levels of CXCL10 and CCL5 but CCL2 was not detected (Fig. 3B). Additionally, we tested another B16 melanoma variant cell line, B16F10, and found it to have a similar cytokine expression profile as B16F1 (Supporting Fig.

, 2007). Negative frequency-dependent selection (NFDS), in which a rare morph has a fitness advantage over common morphs, can account for the existence of different morphs at stable frequencies in a population (Clarke & O’Donald, 1964; Ayala & Campbell, 1974), and has been proposed to explain

polymorphisms in a number of contexts (Hori, 1993; Fincke, 2004; Sinervo & Calsbeek, 2006; McKillup & McKillup, 2008; Hampton, Hughes & Houde, 2009; Koskella & Lively, 2009). Evidence of NFDS has been observed both in laboratory (Kojima & Tobari, AP24534 clinical trial 1969; Maskell, Parkin & Verspoor, 1977; Anderson & Brown, 1984; Gigord, Macnair & Smithson, 2001; Fitzpatrick et al., 2007; Koskella & Lively, 2009) Talazoparib supplier and natural conditions (Reid, 1987; Hori, 1993; Svensson, Abbott & Hardling, 2005; Olendorf et al., 2006; Bleay, Comendant & Sinervo, 2007; McKillup & McKillup, 2008; Takahashi & Watanabe, 2010). Nevertheless, considerable uncertainty exists about the relative importance of this and other mechanisms in the maintenance of genetic and

phenotypic diversity in real populations. There are some genetic polymorphisms that do not affect phenotypic traits. They occur in non-coding areas of the genome, and have been used as markers for studies in population genetics, evolution and medicine (Hacia et al., 1999; Jorde et al., 2000; Syvänen, 2001; Williamson et al., 2007). Polymorphisms that do affect phenotypic traits are not always apparent to the observer, such as some of those involving why behaviour and resistance to parasites or diseases (Thornhill, 1979; Field & Keller, 1993; Kirkup & Riley, 2004; Duncan & Little, 2007; Laine & Tellier, 2008). In contrast, conspicuous polymorphisms, particularly those involving colouration, are easy to score, and their study has been central in attempts to understand the mechanisms that could be maintaining genetic and phenotypic variation in populations. Colouration is known to serve an adaptive function in processes such as thermoregulation (Quartau & Borges, 1997; Phifer-Rixey

et al., 2008), attraction of mates (Nielsen & Watt, 2000), avoidance of predators (Hoese et al., 2006) and attraction of prey (Hauber, 2002; Heiling et al., 2005; Bush, Yu & Herberstein, 2008). This strongly suggests that the maintenance of conspicuous colour polymorphisms is influenced by selection, and NFDS in particular has often been assumed to play a key role. Many species of insect, mollusc, arachnid and crustacean display conspicuous and easily measured polymorphic colour traits. Such invertebrates are typically easier to manipulate than vertebrates, both in the field and in the laboratory, and it is relatively easy to get large sample sizes. As a result, many of the most detailed case studies of the potential influence of NFDS on traits come from the study of colour-polymorphic invertebrates.

, 2007). Negative frequency-dependent selection (NFDS), in which a rare morph has a fitness advantage over common morphs, can account for the existence of different morphs at stable frequencies in a population (Clarke & O’Donald, 1964; Ayala & Campbell, 1974), and has been proposed to explain

polymorphisms in a number of contexts (Hori, 1993; Fincke, 2004; Sinervo & Calsbeek, 2006; McKillup & McKillup, 2008; Hampton, Hughes & Houde, 2009; Koskella & Lively, 2009). Evidence of NFDS has been observed both in laboratory (Kojima & Tobari, PS-341 manufacturer 1969; Maskell, Parkin & Verspoor, 1977; Anderson & Brown, 1984; Gigord, Macnair & Smithson, 2001; Fitzpatrick et al., 2007; Koskella & Lively, 2009) AZD8055 research buy and natural conditions (Reid, 1987; Hori, 1993; Svensson, Abbott & Hardling, 2005; Olendorf et al., 2006; Bleay, Comendant & Sinervo, 2007; McKillup & McKillup, 2008; Takahashi & Watanabe, 2010). Nevertheless, considerable uncertainty exists about the relative importance of this and other mechanisms in the maintenance of genetic and

phenotypic diversity in real populations. There are some genetic polymorphisms that do not affect phenotypic traits. They occur in non-coding areas of the genome, and have been used as markers for studies in population genetics, evolution and medicine (Hacia et al., 1999; Jorde et al., 2000; Syvänen, 2001; Williamson et al., 2007). Polymorphisms that do affect phenotypic traits are not always apparent to the observer, such as some of those involving Avelestat (AZD9668) behaviour and resistance to parasites or diseases (Thornhill, 1979; Field & Keller, 1993; Kirkup & Riley, 2004; Duncan & Little, 2007; Laine & Tellier, 2008). In contrast, conspicuous polymorphisms, particularly those involving colouration, are easy to score, and their study has been central in attempts to understand the mechanisms that could be maintaining genetic and phenotypic variation in populations. Colouration is known to serve an adaptive function in processes such as thermoregulation (Quartau & Borges, 1997; Phifer-Rixey

et al., 2008), attraction of mates (Nielsen & Watt, 2000), avoidance of predators (Hoese et al., 2006) and attraction of prey (Hauber, 2002; Heiling et al., 2005; Bush, Yu & Herberstein, 2008). This strongly suggests that the maintenance of conspicuous colour polymorphisms is influenced by selection, and NFDS in particular has often been assumed to play a key role. Many species of insect, mollusc, arachnid and crustacean display conspicuous and easily measured polymorphic colour traits. Such invertebrates are typically easier to manipulate than vertebrates, both in the field and in the laboratory, and it is relatively easy to get large sample sizes. As a result, many of the most detailed case studies of the potential influence of NFDS on traits come from the study of colour-polymorphic invertebrates.

“
“Summary.  Currently, patients with severe haemophilia can expect

to lead a relatively normal life including prevention of disabling arthropathy as a result of the development of factor replacement therapy and advances in the understanding of the use of such therapy given prophylactically. Unfortunately, a subset of patients develops neutralizing antibodies termed inhibitors rendering such therapy ineffective. These patients frequently develop recurrent joint bleeding resulting in arthropathy. Until recently, prophylactic GDC-0449 cell line therapy was not considered for patients with inhibitors because of the perceived lack of an effective therapeutic agent. However, an accumulation of case reports and a recent prospective study have suggested that prophylaxis with the currently

available bypassing agents could be effective and appears to be safe in selected cases. This report will review the current data on prophylaxis with bypassing agents and suggest specific situations in which prophylaxis in inhibitor patients could be considered. “
“Summary.  For patients with haemophilia, gastrointestinal (GI) bleeding is a life-threatening complication and can be caused by the Helicobacter pylori infection. Among children with haemophilia who had visited with GI bleeding, the prevalence of H. pylori infection and the recurrence rate after H. pylori eradication was investigated. Seven children with haemophilia A with hematemesis (age: 5.3–17.0 years) were evaluated for the causes C59 wnt price of GI bleeding and the detection of H. pylori. Gastroendoscopy was done to find the bleeding focus and for further evaluation including rapid

urease test and mucosal biopsy. Four patients had dyspepsia and abdominal pain for several weeks or months prior to hematemesis. Three patients see more did not show any symptoms of bleeding. From gastroendoscopy, four patients were diagnosed as duodenal ulcer, one as H. pylori associated chronic gastritis and one as haemorrhagic gastritis. One patient showing a normal finding was diagnosed with adenoid haemorrhage after nasopharyngoscopy. Helicobacter pylori infection was found in four of six patients with GI bleeding (3, duodenal ulcer; 1, H. pylori associated chronic gastritis). The patients with H. pylori infection had an eradication treatment of triple therapy and no recurrence happened. In children with haemophilia, H. pylori should also be considered as an important cause of GI bleeding. The recurrence of the infection and GI bleeding can be prevented with eradication of H. pylori. Screening test for H. pylori would be needed in children with haemophilia in endemic area. “
“Effective healthcare delivery necessitates evaluation of the effect of interventions in the form of outcome assessment.