188,189 In addition to the above, Seth et al. also identified novel molecules (plasminogen, annexinA2, p11, osteopontin) that regulate activation of plasmin and fibrinolysis

in human ALD, in vivo and in vitro cell culture models of alcohol.83,101,186 In the latter models, a moderate dose of alcohol (10 mM; 2 g/kg) caused steatosis with overexpression of pro-fibrinolytic R788 nmr annexin A2, p11, tPA and plasminogen, associated with plasmin activation and enhanced fibrinolysis. Contrary to this, a high dose of alcohol (100 mM; 6 g/kg) inhibited expression of pro-fibrinolytic genes but sustained an increase in anti-fibrinolytic PAI-1 in vitro and in vivo.186 It is intriguing that a single high dose of alcohol alters the fibrinolytic balance towards the anti-fibrinolytic profile prior to histopathological evidence of cellular injury in this model. These data and other reports187 suggest a role for PAI-1 in the progression of ALD. Indirect evidence of a genetic predisposition to ALD was

addressed earlier. In the past, genetic studies in ALD have focused on genes involved in alcohol metabolism (ADH, ALDH, CYP2E1), oxidative stress (GST, superoxide dismutase [SOD] ), endotoxin (TNF-α, CD14, TLR4), cytokines (IL-10), immune (cytotoxic T-lymphocyte antigen-4) and fibrosis (collagen, MMPs, osteopontin, TGF-β) and are extensively reviewed.190 Due to the differences in the capacity to metabolize alcohol to acetaldehyde, individuals with find more more active ADH1B*2 and ADH1C*1 alleles are considered to be at Tanespimycin ic50 increased risk of higher acetaldehyde exposure and development of alcoholic liver injury.191 But results from several studies are inconsistent due to ethnic variability

in the populations studied, with ADH1B*2 being a rare allele in Caucasians. The only large study with a sufficient number of cases and controls failed to detect a significant association between ADH1C variants and alcoholic cirrhosis.192 Further, a meta-analysis of all available studies also failed to show any evidence of an association between ADH or ALDH genotypes and ALD.193 In contrast to ADH and ALDH, CYP2E1 is an inducible enzyme and its activity can increase up to 20-fold following continuous alcohol consumption. There are several polymorphic loci within the human CYP2E1 gene194 with two mutations in linkage disequilibrium giving rise to c1 and c2 alleles. The CYP2E1*5 (c2) allele is associated with approximately 10-fold higher mRNA and protein levels as well as enzyme activity than c1 allele; it could therefore cause a higher exposure of the liver to acetaldehyde and ROS.195 Several studies have looked for an association between a promoter region polymorphism of CYP2E1 and ALD, but no consistent results have emerged in any population. Manganese-dependent superoxide dismutase (SOD2) is a key player in ALD pathogenesis since it is involved in the body’s antioxidant defenses and protects mitochondria from peroxidative damage.

A comprehensive questionnaire including family history, demographics, ethnicity, environmental exposures (alcohol and smoking), medications and relevant medical history was administered. Patients were referred for genetic counselling +/- genetic testing after which EUS was performed. A follow up adverse effects phone call was done

at one week. Cancer risk perception, quality of life and screening specific anxiety was determined pre and post EUS. Results: Forty two individuals completed their first screening program [FPC 33, BRCA2+ 9; M 12, F30; mean age 54 (range 39–78); smokers 4]. Seven individuals had a previous cancer (breast 5, brain 1, prostate 1). EUS results: 14 (33%) had an identifiable focal lesion (12 cysts, 2 hypoechoic areas) and 16 (38%) had “chronic http://www.selleckchem.com/products/dabrafenib-gsk2118436.html pancreatitis”-like parenchymal changes. The cysts had morphological features compatible with BD-IPMN (mean size 5 mm; range 3–14 mm) and were located predominantly in the body and tail. EUS-guided FNA was done in 1 patient only. No pancreatic malignancy was identified and no patient was referred for surgery. Several incidental extrapancreatic lesions were found: multifocal hepatoma 1, duodenal GIST 1, coeliac disease 1, splenic cyst. There were no significant adverse events post EUS. Thirty seven (87%) of the cohort found genetic counselling

useful. Prior to screening the majority of the cohort were moderately to severely worried about developing PC but following Birinapant EUS, 36 (86%) reported reduced anxiety regarding their future cancer risk. Conclusion: HRI have a higher rate of cystic lesions (BD-IPMN) compared

to the general population (33% vs 2.6%1), findings similar to other reported screening programs2. EUS changes of “chronic pancreatitis”, found in 38% of our cohort, are thought to represent imaging correlates of lobular atrophy which is associated with precursor lesions (PanIN, IPMN)3–5.. Genetic counseling was found to be very useful by participants and involvement in a screening program reduced anxiety regarding future cancer risk. However, this website the natural history of precursor lesions remains unclear and it is uncertain if surveillance programs will ultimately reduce cancer incidence. 1 Lafan T, Horton K Prevalence of unsuspected pancreatic cysts by MDCT, American Journal of Roentgenology.2008;191:802–807. 2 Canto MI, Hruban RH, Fishman EK, et al. Frequent Detection of Pancreatic Lesions in Asymptomatic High-Risk Individuals. Gastroenterology 2012. 3 Brune K, Hruban R Multifocal neoplastic precursor lesions associated with lobular atrophy of the pancreas in patients having a strong family history of pancreatic cancer. Am J Surg Pathol. 2006 Sep;30(9):1067–1076.

Total FAs (and SFAs and MUFAs) in all species showed Angiogenesis inhibitor significant negative correlations with N cell quota (QN) under N deficiency, but PUFAs had species-specific correlations with

QN. The results show that characteristic FA profiles of algal genus or species (representing particular algal classes) underlie fluctuations according to culture conditions. The significant correlation between FAs and QN under N deficiency suggests that elemental and biochemical limitation of phytoplankton should be considered mutually as determinants of food quality for zooplankton in marine ecosystems. The transfer of energy and matter across the plant–herbivore interface is of critical importance in aquatic food webs (Lindeman 1942, Brett and Müller-Navarra 1997). The factors regulating the trophic transfer efficiency have been widely studied. Of all limiting factors, elemental and biochemical limitation of phytoplankton have been suggested as major determinants of food quality for herbivorous zooplankton (Gulati and DeMott 1997, Sterner and Schulz 1998, Anderson et al. 2004, Müller-Navarra 2008). Elemental (especially Belnacasan datasheet phosphorus; P) versus biochemical (especially FAs) limitation of food quality for zooplankton is a well-known controversy, which has attracted more attention in limnology than in marine ecology (Lampert 2009).

To date, studies have considered these two limiting factors as mutually nonexclusive mechanisms in freshwater environments (Gulati and DeMott 1997, Lynn et al. 2000, Boersma et al. 2001, Gladyshev et al. 2007); however, there is no information on the relationship between elemental and biochemical limitation of phytoplankton in marine ecosystems. Nitrogen (N):P concentrations and supply ratios reveal a strong spatiotemporal variability in coastal seas and some oceanic areas (Karl et al. 1993, Cavender-Bares et al. 2001, Twomey and Thompson

2001, Ford et al. 2008, Lam and Kuypers 2011). Under a large variation in N and P supplies, nonhomeostasis of phytoplankton N:P stoichiometry was observed in several classic this website chemostat experiments (Rhee 1978, Goldman et al. 1979, Ahlgren 1985), as well as in our previous study (Bi et al. 2012), which analyzed how the intracellular concentrations (cell quota) of N and P (QN and QP) varied in dependence of N:P supply ratios and μ. The results in our previous study show that the relationship between QN (and QP) and μ can be interpreted from biochemical considerations (Bi et al. 2012). FAs are key biochemicals in the regulation of trophic interactions (Müller-Navarra 2008). FAs as basic constituents of lipids play an important role in cellular membrane functions, energy storage, and metabolic processes (Mourente et al. 1990, Roessler 1990, Guschina and Harwood 2009).

Designed to overcome these shortcomings

and treatment limitations imposed by gastrointestinal signs and symptoms, the NP101 patch avoids the need for oral administration, does not depend upon gastrointestinal absorption, and provides more consistent, predictable plasma concentrations than oral and intranasal formulations of sumatriptan and a lower maximum plasma concentration than sumatriptan injection. Methods.— Patients diagnosed with migraine who had participated in a randomized, double-blind, Phase III study of the NP101 patch were given the option to use NP101 to treat migraine episodes with moderate or severe headache pain for up to 12 months in this open-label trial. Tyrosine Kinase Inhibitor Library chemical structure Results.— One hundred eighty-three patients applied 2089 study patches. The most common adverse events involved the patch application site (45% of patients). The only non-application-site adverse events reported in >2% of patients were nausea (n = 6, 3.3%), upper respiratory tract infection (n = 6, 3.3%), and nasopharyngitis (n = 4, 2.2%). FGFR inhibitor The incidence of triptan-associated adverse events was 1.6%. Across all visits for investigator assessments, the majority of patients (ranging from 74.7% at Month 1 to 92.2%

at Month 9) were scored as having no erythema at patch application sites. For patient assessments, the percentage of patch placement sites scored as having no or minimal redness was 38.2% at the time of patch removal and 65.4% 24 hours after patch activation. Two hours

after patch activation across all patch treatments over the 12-month study, 23.8% of initial acute migraine episodes were scored as being free from headache pain, 58.2% as having headache selleck chemicals llc pain relief,78.9% as nausea free, 60.1% as phonophobia free, 53.4% as photophobia free, and 20.7% as migraine free. No evidence of waning tolerability or efficacy was observed over the 12-month study period. Conclusion.— NP101, a transdermal sumatriptan formulation in development for the acute treatment of migraine, demonstrated tolerability and efficacy with successive uses over 12 months in this clinical trial. “
“(Headache 2011;51:295-299) “
“Migraine is a prevalent and disabling episodic brain state with protean symptoms dominated by headache. When migraine attacks are frequent or severe over a sustained period, use of daily preventive medications are indicated to significantly reduce disability and improve quality of life. Recently issued evidence-based guidelines outline an array of pharmaceutical and complementary treatment choices with data establishing them as effective or probably effective for prevention of episodic or menstrually associated migraine. OnabotulinutoxinA is the only Food and Drug Administration-approved medication for the prevention of chronic migraine. “
“(Headache 2011;51:1191-1201) Background.

Designed to overcome these shortcomings

and treatment limitations imposed by gastrointestinal signs and symptoms, the NP101 patch avoids the need for oral administration, does not depend upon gastrointestinal absorption, and provides more consistent, predictable plasma concentrations than oral and intranasal formulations of sumatriptan and a lower maximum plasma concentration than sumatriptan injection. Methods.— Patients diagnosed with migraine who had participated in a randomized, double-blind, Phase III study of the NP101 patch were given the option to use NP101 to treat migraine episodes with moderate or severe headache pain for up to 12 months in this open-label trial. Sorafenib in vivo Results.— One hundred eighty-three patients applied 2089 study patches. The most common adverse events involved the patch application site (45% of patients). The only non-application-site adverse events reported in >2% of patients were nausea (n = 6, 3.3%), upper respiratory tract infection (n = 6, 3.3%), and nasopharyngitis (n = 4, 2.2%). Target Selective Inhibitor Library The incidence of triptan-associated adverse events was 1.6%. Across all visits for investigator assessments, the majority of patients (ranging from 74.7% at Month 1 to 92.2%

at Month 9) were scored as having no erythema at patch application sites. For patient assessments, the percentage of patch placement sites scored as having no or minimal redness was 38.2% at the time of patch removal and 65.4% 24 hours after patch activation. Two hours

after patch activation across all patch treatments over the 12-month study, 23.8% of initial acute migraine episodes were scored as being free from headache pain, 58.2% as having headache selleck compound pain relief,78.9% as nausea free, 60.1% as phonophobia free, 53.4% as photophobia free, and 20.7% as migraine free. No evidence of waning tolerability or efficacy was observed over the 12-month study period. Conclusion.— NP101, a transdermal sumatriptan formulation in development for the acute treatment of migraine, demonstrated tolerability and efficacy with successive uses over 12 months in this clinical trial. “
“(Headache 2011;51:295-299) “
“Migraine is a prevalent and disabling episodic brain state with protean symptoms dominated by headache. When migraine attacks are frequent or severe over a sustained period, use of daily preventive medications are indicated to significantly reduce disability and improve quality of life. Recently issued evidence-based guidelines outline an array of pharmaceutical and complementary treatment choices with data establishing them as effective or probably effective for prevention of episodic or menstrually associated migraine. OnabotulinutoxinA is the only Food and Drug Administration-approved medication for the prevention of chronic migraine. “
“(Headache 2011;51:1191-1201) Background.

Coordinators who did not initially respond were contacted up to three additional times. Areas were asked to report data from the most recently available 12-month continuous period prior to August 2008. Across all areas, this resulted

in data collected from refugees who entered the United States between 2006 and 2008. We pooled information BGJ398 supplier from across jurisdictions about refugees from the same country of origin. Using these data, we estimated the prevalence of HBsAg among refugees from each country of origin by dividing the number of HBsAg-positive refugees by the total number tested. We also pooled data and estimated prevalence by continent. Several jurisdictions provided numerical count data regarding the total number of refugees screened combined with proportional data about the countries of origin and the HBsAg prevalence observed among refugees from each country of origin. For these jurisdictions, we estimated the number of refugees tested and the number of HBsAg-positive refugees from each country by multiplying the total number of refugees screened by the proportion screened from each country, then multiplied that number by the proportion screened from that country Z-VAD-FMK in vitro of origin who were HBsAg-positive. We present our results for countries

from which we estimate that 30 or more refugees were tested. We calculated 95% confidence intervals (CIs) for each prevalence rate using the Wilson procedure with a correction for continuity.6 Of the 47 jurisdictions we attempted to contact, 31 responded with at least some information and 16 states did not respond, for a 66% response rate. Of the 31 areas that responded, 28 reported that they systematically screened at least some groups of refugees for hepatitis B, whereas three areas reported that hepatitis B testing was not part of the refugee health screening process. Of these 28, 20 were able to provide a count of the total number of refugees selleck screening library screened, and 13 were able to provide an estimate of the overall prevalence among all refugees

screened; of these 13, nine areas were able to provide data by country of origin. The 20 areas that provided data on the number of refugees screened screened a total of 42,303 refugees in the preceding 12 months, which is approximately 55% of the total number of refugees arriving in the United States in 2008. The nine areas that provided data by country of origin screened 31,980 refugees, or approximately 42% of refugees arriving in the United States in 2008. Screened refugees with country of origin data originated from 44 countries and 11 continental subregions across four continents. Of the 31,980 refugees with complete country of origin data, 891 (2.8%; 95% CI 2.6%–3.0%) tested positive for HBsAg. This rate varied by continent, continental region, and country of origin (Table 1).

6, 95% confidence interval [CI] = 8.4-65.8, P = 5.1 × 10−7). This was principally due to the p.Q1236H substitution which compromised polγ function in yeast. Therapeutic doses of VPA inhibited human cellular proliferation and high doses caused nonapoptotic cell death, which was not mediated through mitochondrial DNA depletion, mutation, or a defect of fatty acid metabolism. Conclusion: These findings implicate impaired liver regeneration in VPA toxicity and show that prospective genetic testing of POLG will identify individuals at high risk of this potentially

fatal consequence of treatment. (HEPATOLOGY 2010;52:1791-1796) Over 1 in 37,000 subjects exposed to sodium valproate (valproic

acid, VPA) develop idiosyncratic liver toxicity, with the risk reaching ≈1 in 500 in young children selleck on polytherapy.1 Increased awareness has contributed to a decline in fatal VPA-induced liver failure,2 but the worldwide use of VPA continues to increase through its use in other clinical contexts. In addition to its use as a first-line anticonvulsant, VPA is now in regular use for migraine, bipolar disorder, chronic headache, and as adjuvant chemotherapy. The prompt recognition of early symptoms and immediate discontinuation of the drug can prevent fulminant liver failure,2 but initial clinical clues are often mild and nonspecific, making it difficult to identify individuals before significant liver damage occurs. BGJ398 Liver biopsy characteristically reveals

microvesicular steatosis, and occasionally severe hepatocellular necrosis.3 Fever, rash, lymphadenopathy, and/or peripheral eosinophilia are rarely present during VPA hepatotoxicity, consistent with a direct toxic effect of the drug, rather than an immune-mediated hypersensitivity reaction typical of other antiepileptic drugs.4 The recent description of mutations in mitochondrial DNA (mtDNA) polymerase γ (POLG) as a major cause of Alpers-Huttenlocher syndrome (AHS)5 provides selleck compound a clue to the underlying mechanism of VPA hepatotoxicity. AHS is a rare childhood encephalopathy characterized by developmental delay and intractable epilepsy and liver disease.6, 7 Most cases have homozygous or compound heterozygote mutations in POLG,5 and ≈1/3 of AHS patients develop liver failure within 3 months of exposure to VPA.8, 9 This raises the possibility that a common genetic variation in POLG predisposes individuals to VPA-induced liver failure in the absence of a recognizable AHS-phenotype. AHS, Alpers-Huttenlocher syndrome; ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate amino transferase; COX, cytochrome c oxidase; DILIN, Drug Induced Liver Injury Network; EtBr, ethidium bromide; POLG, polymerase γ; ULN, upper limit of normal; VPA, sodium valproate.

Results: There were sixty-five www.selleckchem.com/products/LBH-589.html subjects with constipation (34 women and 31 men; mean age 49.1 years) and thirty healthy control subjects (14 males and 16 females; mean age 47.3 years). According to the manometric results during simulated evacuation, 65 patients were divided into normal group and 4 constipation types (type I, type II, type III and type IV). In constipation group, average anal resting pressure was 96.5 ± 29.3 mmHg,

maximum squeeze pressure was 217.7 ± 73.3 mmHg, anal squeeze duration was 16.1 ± 5.1 s and anal HPZ length was 3.3 ± 0.6 cm. Conclusion: A solid state 3-D HRM anorectal recording system with circumferential sensors could provide a highly integrated, dynamic representation of pressures within the anorectum. And this is the first reports on solid-state 3-D HRM using ManoScan software to assess anorectal physiology. Key Word(s): 1. Constipation; 2. manometry; 3. anal sphincter; Presenting Author: ARNALDOJOSE Luminespib GANC Additional Authors: RICARDOLEITE GANC, ALBERTO FRISOLI JR, JACYR PASTERNAK Corresponding Author: ARNALDOJOSE GANC Affiliations: IGED; Albert Einstein Jewish

hospital; Albert Einstein Jewish Hospital. Objective: The concept of fecal transplantation (FT) in order to treat Pseudomembranous colitis (PC) has emerged as an alternative treatment to antibiotics. The usual choice for oral administration of fecal microbiota (OAFM) is through a nasoduodenal tube. Nonetheless, besides being an unappealing method, duodenal-gastro-esophageal reflux (DGER) has been described, leading to eventual belching. To our knowledge there has been no description of per-oral FT with the use

of a pediatric colonoscope. Methods: Ten consecutive patients with PC due to resistant Clostridium difficile were treated with FT. After collection and preparation of fresh stools learn more from two donors, an upper GI endoscopy was performed with a pediatric colonoscope inserted into the proximal jejunum. Five hundred mL of the solution were slowly infused, taking care to avoid DGER. No bowel preparation or extra administration of antibiotics was performed. The patients were followed for 4 weeks, when a new test for C. Difficile was done. Results: Diarrhea ceased in all patients. The average response time was 3 days (1–5 d). Most patients had diarrhea after the procedure, but it was considered related to their underlying disease. No patients had belching, vomits or bacteremia, nonetheless one of the patients presented with fever 2 hours after the procedure. Three patients had transient cramping. One patient received a new cycle of antibiotics due to urinary tract infection and even though he had no diarrhea, he tested positive for C. Difficile and was considered a failure.

We found no effect of liposomal clodronate on HSC viability, thereby excluding the possibility that liposomal clodronate directly induces HSC apoptosis in fibrotic livers (Fig. 2I). We also observed reduced IL-1β and TNF-α mRNA in fibrotic livers from clodronate-treated mice (Fig. 4C). To test the in vivo relevance of this pathway, we first investigated how deficiency of IL-1β, the predominant activator of NF-κB in our coculture experiments, affects liver fibrosis. In contrast to previously published studies, we found no statistically significant difference in BDL-induced liver fibrosis between IL-1R1 knockout and wild-type mice, and further confirmed

this data in the learn more CCl4 and thioacetamide models of liver fibrosis (Supporting Fig. 6). If IL-1 signaling promoted

liver fibrosis by increasing NF-κB–dependent HSC survival rather than direct HSC activation, it would be likely that TNF-α, the other major NF-κB–activating cytokine produced by macrophages, could still achieve NF-κB activation in HSCs and thus compensate for the loss of IL-1 signaling in this model. Based on the hypothesis that absence of both IL-1 and TNF signaling would be required to reduce HSC survival and liver fibrosis, we performed BDL in TNFR1/IL1R1 double knockout mice (dko) and wild-type control mice. Compared with wild-type mice, dko mice showed significantly reduced hepatic fibrosis after 5 or 15 days of BDL (Fig. 5A-B) and a five-fold increase in apoptotic TUNEL and desmin double-positive HSCs without significant differences in hepatic injury (Fig. 5B), supporting Bafilomycin A1 our hypothesis that suppression selleck kinase inhibitor of both IL-1 and TNF signaling are required to affect HSC survival and liver fibrosis. Moreover, we found a significant reduction of NF-κB–dependent genes—including Il6, Cxcl5, Saa3, Serpinb2, and Timp1—in ultrapure unplated HSCs from dko mice, thus confirming that NF-κB activation in HSCs was mediated by TNF

and IL-1 (Fig. 5C). Our microarray analysis revealed an up-regulation of two Trail decoy receptors, murine Trail decoy receptor 1 (Tntrsf23) and murine Trail decoy receptor 2 (Tnfrs22), in HSCs cocultured with HMs and in HSCs from BDL and CCl4 livers (Fig. 5D and Supporting Table 2). Notably, Trail-mediated apoptosis is a major contributor to HSC cell death induced by hepatic natural killer cells in vitro and in vivo.[11, 25] Neutralization of TNF or IL-1 prevented the up-regulation of Tnfrsf22 and Tnfrsf23 mRNA by HMs in coculture experiments (Supporting Fig. 7A). Moreover, depletion of HMs by liposomal clodronate or dko of TNFR1 and IL1R1 reduced Tnfrsf22 and Tnfrsf23 expression in vivo (Supporting Fig. 7B). Liposomal clodronate does not affect HSC number[13] or biology (Fig. 2H,I), but may deplete DCs, a highly endocytotic cell population, as demonstrated by our FACS analysis (Fig. 6A).

On the basis of the above mentioned results, three studies in adults directly

Saracatinib research buy assessed the effect of the administration of probiotics on H. pylori gastritis by the histological examination of gastric biopsies showing that L. johnsonii La1 [42,49] and L. acidophilus La5 and B. lactis Bb12 contained in the yogurt [50] resulted effective in both reducing the density of H. pylori colonization, and the gastric mucosal inflammation. No study has been performed in children to explore this issue. In most adult studies, the effect of probiotic treatment on the level of H. pylori infection has been estimated indirectly by the 13C-urea breath test (13C-UBT) delta over baseline value, a well known semi quantitative measurement of the bacterial load [51]. In detail subjects treated either with L. johnsonii La1 [25,52], L. brevis CD2 lyophilized bacteria [53], yogurts containing L. acidophilus La5 and B. lactis Bb12 [50], L. gasseri OLL 2716 [54], a milk containing B. bifidum BF-1 [55], a drink consisting of equal doses of L. rhamnosus GG, L. rhamnosus LC705, P. freudenreichii JS and B. lactis Bb12 [45], or with L. reuteri ATCC 55730 [56] showed a significant decrease in 13C-UBT values. In children, two studies have

been performed (by the same investigators) to evaluate the ability of probiotics to interfere with the intragastric bacterial load (seeTable 1). First, CP-690550 purchase Cruchet et al. performed a randomized, double blind, controlled study on 326 asymptomatic children screened for H. pylori by the 13C-UBT [57]; H. pylori -colonized see more subjects were distributed into five groups to receive a product containing live L. johnsonii La1 or L. paracasei ST11, heat-killed La1 or L. paracasei ST11, or just vehicle everyday for 4 weeks. A second 13C-UBT was carried out at the end of this period. The authors detected a moderate but significant difference in 13C-UBT values in children receiving live La1 (−7.64 per thousand; 95% CI: −14.23

to −1.03), whereas no differences were observed in the other groups. Subsequently, in a randomized open trial, Gotteland et al. [58] randomized 182 asymptomatic H. pylori -positive children to receive either 7-day triple therapy, or Saccharomyces boulardii as a symbiotic simultaneously with inulin or L. acidophilus LB daily for 8 weeks. An additional 81 asymptomatic H. pylori -positive children were followed for 8 weeks without any treatment. A significant decrease in 13C-UBT values (repeated after 8 weeks) was observed in the antibiotic group (−26.6%; 95% CI: −33.9 to −19.3%) and in the S. boulardii group (−6.31; 95% CI: −11.84 to −0.79) but not in the L. acidophilus LB group (+0.70; 95% CI: −5.84 to +7.24). No changes in 13C-UBT values were observed in untreated children. These results suggest that anti-H. pylori activity is species and strain specific, with some probiotics, such as S. boulardii and L. johnsonii La1, interfering with H. pylori in vivo more actively than others (L. acidophilus LB, L. paracasei ST11).