GFP-labeled pathogens have been used to study the systematic colonization and infection of Fusarium spp. in maize [20] and [21]. Red fluorescent protein (DsRed), discovered in radiating mushroom coral (Discosoma striata), has an emission spectrum in the far-red zone [22] and permits dual or multi-color labeling of many fungal species. The DsRed protein has been used effectively to label a number

of filamentous fungi, S3I-201 order such as Aspergillus, Trichoderma, and Oculimacular spp. [23], [24] and [25]. In a previous study, we generated F. verticillioides strains expressing red fluorescence by introducing the gene DsRed via Agrobacterium tumefaciens-mediated transformation (ATMT) [26]. Using a DsRed-labeled fungal strain, this study was initiated to investigate the differences

in colonization Neratinib in vitro and reaction of resistant and susceptible maize lines challenged with F. verticillioides. Wild type strain Fv-1 of F. verticillioides was isolated from Yayuan County, Jilin Province, China. Its identity was confirmed by morphological and interval transcribed spacer (ITS) sequence analyses. Susceptible maize inbred lines B73, P138 and Lu 9804, and the resistant lines Qi 319, Dan 340 and Zhongzi 01, were used in the study. The plasmid pCAMDsRed [27], which contains the gene DsRed driven by the promoter PgpdA, as well the selectable gene hpg for resistance to the antibiotic hygromycin, was used in ATMT of F. verticillioides as described previously [26] and [28]. Analyses of mitotic stability of DsRed protein expression,

growth rates of colonies, and metabolism of extracellular enzymes (i.e., protease, Resminostat cellulase, amylase, and pectase) in the transformants were performed to characterize the DsRed-labeled strain of F. verticillioides [26]. Seeds of the maize inbred lines were washed with running water, surface sterilized in 75% alcohol for 5 min and in 0.4% sodium hypochlorite for 15–20 min, and then rinsed with distilled water. The surface-sterilized seeds were sown in pots (10 L) filled with vermiculite in a greenhouse set at 25–30 °C for 16 h of light and at 16 °C for 8 h of darkness. When the second seedling leaves were unfolded, the top 12 cm of vermiculite was removed from pots, mixed with the suspensions of the DsRed-labeled fungus (108 conidia mL− 1) at a rate of 1:5 (V/W), and returned to the pots. In the untreated checks, soil similarly treated with distilled water was used as mock inoculation. Root cross sections were prepared using a Microtome (MTH-I, Tokyo, Japan) without fixation to ensure living root cells and real-time observation. Systemic colonization by F. verticillioides in root tissues was determined by observing the red fluorescence emitted by the DsRed-labeled fungus with an epifluorescent microscope (BX60, Olympus, Tokyo, Japan) under emission wavelengths of 515/560 nm. Light microscopy was performed with the same microscope without a filter. To determine the infection and colonization by F.

The average number of sequence reads that contained P. maxima diagnostic SNPs within this Olaparib other P. maxima database was 103 (± SE 9.15) and 62 (± SE 17.81) for the P. margaritifera SNPs within the P. margaritifera database. All putative biomineralisation genes (N = 7) were found to be expressed by the donor oyster (Fig. 2). Three of these genes N66, Perline and N44, were solely expressed by the donor with no expression from the host oyster. Here, the P. maxima diagnostic SNPs only detected expression of N66, Perline and N44 in the xenografts where P. maxima was the donor oyster

(Bs) and the P. margaritifera diagnostic SNPs only detected expression from the xenografts where P. margaritifera was the donor oyster (Sb) ( Fig. 2). For four of the seven biomineralisation genes (Linkine, Selleck BMS 907351 PfCHS1, MSI60 and Calreticulin), both donor and host oyster transcripts were detected within the xenografted pearl sacs (Bs, Sb; Fig. 2). Here, P. margaritifera SNPs detected expression of Linkine, PfCHS1, MSI60 and Calreticulin in the xenografts where P. margaritifera was the donor and host oyster (Sb, Bs) and P. maxima SNPs detected expression in the xenografts where P. maxima was the donor and host oyster (Bs, Sb), with the exception of Linkine ( Fig. 2). Gene transcripts from Calreticulin and MSI60, however, were detected in gonad

tissue samples from P. maxima and P. margaritifera. No specific amplification of Linkine and PfCHS1 transcripts was detected in the gonad samples. To further confirm the expression of biomineralisation genes from the host oyster and to validate the sequencing data (Illumina GAII), a highly informative region (40 bp in length) of Linkine was sequenced that contained five known species diagnostic single nucleotide polymorphisms (SNPs). Individuals from the allografted pearl sacs (Ss, N = 2; Bb, N = 2) were also sequenced to validate that the SNPs were species diagnostic, followed by sequencing of individuals from the xenografted pearl sacs (Sb, N = 5; Bs, N = 5) to determine whether the host or donor oyster species diagnostic SNPs were present ( Table 3). All P.

margaritifera allografted pearl sacs (Bb) showed an A nucleotide at a particular isothipendyl SNP site, whilst P. maxima allografted pearl sacs (Ss) had a T nucleotide at the SNP site. All five xenografted pearl sacs, where P. maxima was the donor oyster (Bs), had a P. maxima diagnostic SNP (T). Whilst four of the xenografts where P. margaritifera was the donor oyster (Sb) possessed the P. margaritifera SNP (A). However, one of these xenografted pearl sacs where P. margaritifera is the donor possessed the P. maxima diagnostic SNP (T), suggesting that the host was expressing Linkine in this individual ( Table 3). The other four diagnostic SNPs within the region sequenced for Linkine showed the same pattern as the above mentioned SNP site.

Three minutes at 93 °C were programmed as the initial step, followed by 35 cycles of 1 min at 93 °C, 1 min at 52 °C and 5 min at 74 °C. A final polymerization step of 5 min at 74 °C was added. The amplified gene was inserted in the plasmid pLW previously digested with the enzyme EcoR V. The recombinant plasmid was named pLW-hah5. In vitro culture of HEK-293 cell line (ATCC CRL-1573) was carried out in flasks of selleck kinase inhibitor 25 cm2 (Greiner Bio-One, Germany) using the culture medium Dulbecco’s

modified Eagle’s medium (DMEM) (Sigma, USA) supplemented with 10% of fetal calf serum (FCS) (PAA, Canada), 0,3 mg/mL of l-glutamine (Sigma, USA), 1 mM of sodium pyruvate (Sigma, USA) and an antibiotic–antimycotic solution 100× (GibcoBRL, USA) at a final concentration of 1×. Cells were incubated at 37 °C, 5% of CO2 and 95% of relative humidity. One hour before the transfection, the medium of the cell culture at 80% of confluence was changed for fresh medium without FCS. Transfection was performed using the polycation polyethylenimine 25 000 (PEI) (Sigma, USA) at 0,81 mg/mL, pH 7 and the plasmids pAEC-hah5 and pEGFP. The last plasmid was generated by including a transcription unit with the enhanced green fluorescent protein (EGFP) gene under the control of the CMV enhanced promoter into check details the

pMOS-Blue backbone. DNA was used at 0,72 μg/cm2. The ratio pAEC-hah5/pEGFP was 36:1 and the ratio PEI/DNA was 1 μL/1 μg. DNA and PEI were diluted in separate tubes using 5% of glucose until reaching 50 μL each. After samples were vigorously mixed during 10 s and allowed to stand for 5 min, PEI was added to DNA, which were vigorously mixed during 1 min and allowed to stand for 20 min. Subsequently, 900 μL of fresh DMEM was added to the PEI/DNA complex and the mixture of 1 mL was carefully added to the cell culture. Six hours later, FCS was added at a final concentration of 10%. Negative control was performed as above but with the plasmid pAEC-Spt. Transfection was verified after 72 h by observing the production

of the EGFP Niclosamide protein in transfected cells at the fluorescence microscope using a magnification of 400×. Transfection of the HEK-293FT cell line (Invitrogen, USA) with the plasmids pLP1, pLP2, pLP/VSVG (Invitrogen, USA), pEGFP and pLW-hah5 was carried out in 6 flasks of 175 cm2 (Greiner Bio-One, Germany) using PEI as explained above. In each flask, DNA was used at 0,411 μg/cm2. The ratio DNA/pEGFP was 36:1 and the ratio pLW-hah5/each helping plasmid (pLP1, pLP2 and pLP/VSVG) was 2:1. Negative control was performed in the same way but with the plasmid pLW. Six hours after adding the mixture of PEI/DNA to the cell culture, FCS was added until reaching 10%. After 48 h, the supernatant was centrifuged at 1000 × g, filtered using a pore size of 0,45 μm and ultracentrifuged at 25 000 × g for 1:30 h. The supernatant was removed and lentiviral particles were resuspended in fresh DMEM.

While this study has shown the rocky reef feature in the SAC is greater in scale than the actual visually observed reef, only

the rocky habitats benefit if management is feature based. Unfortunately, the full extent of a functional reef is often larger than its legal protection Selleckchem GSK126 (Rees et al., in press) and results here show that the full extent can only be visually recognised once recovery has started to take place. The presented results will hopefully inform discussions among managers and governmental authorities to include other substrata and associated species in order to appropriately maintain and restore the full extent of the functional reef (Rees et al., in press). Furthermore, based on our findings we recommend that reef features of conservation interest are protected at the scale of the MPA site (e.g. SAC boundary for EU Habitats Directive) at least until species have begun to recover and indicate where features extend to. Only then should detailed lines be drawn and buffer zones introduced (Halpern et al., 2010). No comparison is made here between the sessile RAS on sediment to sessile RAS on observable hard reef. However, even if they were considered substandard assemblages, this reef expansion, and increase in biogenic structure in these areas connecting rocky PD-1/PD-L1 inhibitor habitats would increase overall ecosystem health and

resilience of benthic systems to environmental change, such as ocean acidification, temperature rise, and invasive species (Carpenter et al., 2008, Hoegh-Guldberg et al., 2007, Stachowicz et al., 2002 and Veron et al., 2009). The Convention on Biological Diversity (CBD

tetracosactide COP 10 2011-2020) requests that by 2020 ecosystem based management approaches are applied in marine systems to avoid overfishing. This is in accordance with the site rather than feature based approach. A mosaic of habitat types is essential for the success of any marine ecosystem, as different life stages or foraging techniques often require different substratum types (Christensen et al., 2003). Functional boundaries should also consider not only extent of adult RAS but their entire benthic life history. Only considering adult stages limits our interpretation of functional habitat use by reef organisms. It has been documented that some reef organisms such as lobsters use neighbouring sediments for burying juvenile stages or foraging (Howard and Bennett, 1979), and this should be taken into account when proposing MPA boundaries. Differing life history traits demonstrate the importance of managers being able to employ adaptive management strategies that could result in the expansion of conservation features and recovery of benthic systems (Folke et al., 2004). This study highlights a fundamental management predicament known as shifting baselines.

137.0 mequiv./L; P = 0.001); P = no. No differences were observed with respect to age, race, aetiology of cirrhosis, diabetes, hypertension, hepatocellular carcinoma, prior upper gastrointestinal bleeding, spontaneous check details bacterial peritonitis, current use of diuretics, urea, haemoglobin, platelets, serum sodium, serum potassium, spot urine potassium, ALT, ALP, GGT, albumin, and INR when individual with poor urinary sodium excretion were compared to those with Nau24h ≥ 78 mequiv. There was a strong positive correlation between the

Na/Ku and Nau24h (r = 0. 857, P < 0.001) ( Fig. 1). A negative correlation between MELD score (r = −0.498; P = 0.025) and serum creatinine (r = −0.498; P = 0.025) was evidenced. There were no significant correlations between the Na/Ku ratio and age, platelet count, serum sodium, AST, ALT, direct bilirubin, GSK1120212 chemical structure albumin and INR. The AUROC for Na/Ku in the prediction of

Nau24h < 78 mequiv. was 0.948 ± 0.046, P = 0.001 ( Fig. 2). Table 3 shows in details the diagnostic performance of the Na/Ku ratio in predicting Nau24h < 78 mequiv. For the Na/Ku ratio, the classical cut-off (≤1.0) showed 70% positive predictive value (PPV) to diagnose Nau24h dosage < 78 mequiv. with negative predictive value (NPV) of 90%, accuracy of 80%, 88% sensitivity and specificity of 75%. Cirrhosis is the twelfth leading cause of death in the United States of America.17 Several authors evaluated patients with decompensated liver cirrhosis ascites. Usually, the studied population is predominantly composed by men, 59–74%, age ranging from 53.6 to 60 years.18, 19 and 20 In this study it has been observed that 70% of subjects were male; mean age was 56.1 years, which coincides with that described in literature. With regard to the aetiology of cirrhosis, it varies according to the prevalence of the diseases on the studied area,

with a higher prevalence of HBV (64.8%) in China, higher incidence of alcoholic cirrhosis (76.4%) in Germany (19) and Barcelona (44.7%).18 The present study demonstrated a higher prevalence of HCV as compared to Europe and Asia, the latter Abiraterone being an area of high prevalence of HBV21 and exhibits high prevalence of alcoholism as a cause of chronic liver disease. In cirrhosis, the development of ascites and diuretic response are determined by the renin–angiotensin–aldosterone and renal sodium handling.22 This study observed that patients presenting with more severe liver disease (MELD, creatinine, bilirubin, AST) are those who have lowest urinary sodium excretion. Likewise, Cholongitas et al. recently demonstrated that the factors independently associated with poor urinary sodium excretion in cirrhosis are albumin, creatinine and Na/Ku.11 The Na/Ku ratio emerged as an option to Nau24h in evaluating the ability of cirrhotic patients with ascites to excrete salt. During ascites treatment, absence of weight loss may be secondary to poor response to diuretics or a consequence of non-adherence to low sodium diet.

, 2004 and Cole et al., 2011). In other studies of marine debris, primarily from coastal assessments, 60–80% of marine debris is petroleum-based plastic (Derraik, 2002). Petroleum in any form entering the marine environment by anthropogenic means is a pollutant. A wide range of marine life, including marine mammals, reptiles and birds, is impacted by plastic pollution through entanglement or ingestion (Laist, 1987 and Van Franeker et al., 2011), and the persistent organic pollutants GABA receptor function that sorb onto plastic (Mato et al., 2001, Teuten et al., 2007, Teuten et al., 2009 and Rios et al., 2010). Plastic pollution also has the potential to transport non-native

species to other regions (Astudillo et al., 2009, Barnes and Fraser, Raf activity 2003, Bravo et al., 2011, Gregory, 2009 and Webb et al., 2009). The coastal margins of the South Pacific Ocean, and the Southern Ocean, are main contributors to plastic pollution in the SPSG (Lebreton et

al., 2012). In the western region of the SPSG plastic pollution is an emerging contaminant on island shorelines and adjacent coastal and oceanic waters, impacting fisheries, creating navigational hazards, and affecting tourism by its negative aesthetic appeal (Gregory, 1999a). In the southeastern South Pacific Ocean, surveys of plastic pollution near the coast, including fragments of foamed polystyrene, plastic bags, and food sacks from salmon farms identified aquaculture as the most significant contributor (Hinojosa and Thiel, 2009). Along the Chilean coast, large amounts of plastics also come directly from beach and shore activities (Thiel et al., old 2011). Other types of marine debris, including pumice and wood,

are injected into the ocean near Patagonian Fjords, with their abundance corresponding to river runoff after spring snowmelt (Hinojosa et al., 2011). Plastic pollution has also been detected in the surface waters of the Southern Ocean (Barnes and Milner, 2005). In a survey of waters near Antarctica, plastic pollution was the only type of marine debris found south of 63°S (Barnes et al., 2010). While large pieces of plastic pollution have been documented in the southern ocean and in the South Pacific, the presence and abundance of microplastics has not yet been confirmed. In particular, the area of the SPSG remains unstudied. Therefore, in this study we examined the abundance and composition of microplastics along a transect that crosses directly through the SPSG. To explore the presence and distribution of plastic pollution in the eastern South Pacific, an expedition on the sailing vessel Sea Dragon was organized and carried out by the 5 Gyres Institute. 8 The expedition started on March 23rd, 2011 from Valdivia, Chile and sailed to Pitcairn Island, which it reached on April 21, 2011.

9 ms and TR=23 ms) preceded by a 15° FE pulse, resulting in a 135-ms low-resolution acquisition window. The resolution was 4.8×4.8×3 mm at 261×261×24 mm field of view, reconstructed to 0.5×0.5×1.5 mm. Each high-resolution segment consisted of two interleaves of a 75-interleave 3D center-out spiral acquisition with eight through-plane phase encode steps. The first interleaf of each segment was acquired with a 45° WE pulse and the second with a 90° WE pulse. Each interleave consisted of 4096 points acquired over 10 ms (TE=3.4 ms and TR=1 RR interval). A spatial saturation pulse was applied to the chest wall immediately prior to the high-resolution imaging segment in order to minimize artifacts from structures not moving

with the coronary artery. The high-resolution data were temporally located in the subject-specific right coronary rest period. Where possible, the low-resolution BMS-754807 concentration data were also acquired during this period of minimal motion, but the timing of the high-resolution data was prioritized. As the low-resolution data are acquired in a reverse-centric kz phase order, the effect of any motion during the low-resolution acquisition is expected to be minimal. The total acquisition duration was 300 cardiac cycles (assuming 100% respiratory efficiency) or 5 min (with a heart rate of 60 beats/min). The acquired resolution was 0.7×0.7×3 mm over a 570×570×24

mm field of view which was reconstructed to a 0.7×0.7×1.5 mm pixel size. The high field of view was Ribose-5-phosphate isomerase used to bolster signal to noise ratio (SNR) in the images and to move any characteristic spiral artifacts Selleckchem Entinostat away from the anatomy of interest. The high-resolution acquisition window was 35 ms. All images were reconstructed and processed offline using in-house software written in MATLAB 2009a (The Mathworks, Natick, MA). Beat-to-beat 3D respiratory displacement of the right coronary artery was determined using a 3D local normalized subpixel cross-correlation of the low-resolution volumes acquired in each cardiac cycle. An end

expiratory volume was chosen as a reference using the diaphragmatic navigator information. A cuboid-shaped reference region around the coronary origin was defined on the reference volume, aided by a colored overlay of the fat image on the uncorrected high-resolution water image, as seen in Fig. 3. A search region was also defined on this volume and copied to the other low-resolution volumes for the subsequent beat-to-beat cross-correlation. In order to determine the appropriate dimensions for the search region, the cross-correlation was initially performed on a subset of 20 of the low-resolution volumes before performing the full procedure. The two high-resolution spiral interleaves acquired in each cardiac cycle were corrected [2] for respiratory motion using the 3D beat-to-beat translations obtained, and high-resolution images were reconstructed using a standard gridding [27] and fast Fourier transform technique.

Ethical and moral principles require that we search for new ways to engage these reluctant patients in shared decision making rather than abandoning the attempt. Shared decision making is not an inborn talent but consists of specific behaviors that can be taught. It is useful to describe the behaviors expected by both patients and clinicians, notably during a shared decision making encounter [35]. Using socio-cognitive theories, interventions that act on the determinants Compound C datasheet of shared decision making behaviors, such as decision

aids, can enable these specific behaviors. Decision aids are client-mediated interventions for changing clinicians’ practices [36]. A Cochrane systematic review of 115 studies on patient decision aids found that they reduce the proportion of people who remain passive or undecided in decision making and facilitate the adoption of shared decision making by providers. They have also been shown to reduce the overuse of options not clearly associated with benefits for all, while potentially enhancing the use of options clearly associated with benefits [17]. Also, according to two systematic reviews on interventions to improve the adoption of shared

decision selleck screening library making by healthcare providers [13] and [37], interventions targeting both patients and clinicians are more likely to increase shared decision making as reported by both patients and clinicians than those that solely focus on clients or solely on healthcare providers [38] and [39]. A recent study by Mendel and colleagues compared patients’ preferences for treatment before and after receiving their physician’s advice. They found that 48%

of a sample of patients receiving treatment for schizophrenia and 26% of a sample of patients receiving treatment for multiple sclerosis followed the advice of their doctor and chose a treatment Nabilone option that went against their initial preference [40]. In other words, the doctor proposing a course of action can lead patients to make decisions that do not match their fundamental values and preferences. Using socio-cognitive theories, we have conducted studies that explore how the doctor influences the patient’s desire to engage in shared decision making. We found that after controlling for other psychosocial variables at the patient level, the variable most significantly associated with the patient’s intention to engage in shared decision making was the physician’s attitude toward it [33]. This suggests that patients respond to the doctor’s enthusiasm, or lack of it, for sharing decisions, and that a significant number of patients may go against their treatment preference if they follow the clinician’s advice without participating in the decision making process. As mentioned previously, the role of patients in decision making represents a set of specific behaviors that are modifiable like any other health-related behaviors [41].

Although careful statements can be made about specific pathogen transport or survival under certain landscape alteration scenarios or given climatic factors, there is a notable lack of robust literature on the relationship between pathogen pollution and climate change. Trichostatin A solubility dmso This knowledge

gap illustrates the dire need for research to assist accurate model building efforts for predicting pathogen emergence and disease outbreaks given certain landscape and climate change scenarios. Efforts to address this gap will depend on successful transdisciplinary interactions that encourage collaborative research between disease experts such as veterinarians, physicians, and epidemiologists with physical scientists including hydrologists, oceanographers, and engineers. While this editorial is intended to draw attention to yet another harmful outcome of climate and landscape change, it is not intended to be all grim. Clearly defining problems and their associated variables

provide the building blocks for accurately predicting disease risk, and the power to implement practices aimed at reducing further coastal pathogen pollution. Human behavior, policy, and science must come together to implement solutions that will improve nearshore water quality and promote human and marine animal health. Reducing the carbon footprint is an obvious goal, though many readers of this editorial would agree that a

certain degree of change is inevitable, given present climate observations Bortezomib and lack of immediate international action. An adjunct and immediate goal that should also be targeted is to reduce our “fecal footprint”. Keeping pet cats indoors and picking up after dogs on a walk, incorporating vegetation buffers between livestock and waterways (Miller et al., 2008), and implementing Mirabegron “green” urban design practices that promote rainwater percolation and storm water treatment (Cook, 2007), are just a few examples. Our scientific community should take a leading role in educating policy makers and the public on the consequences of pathogen pollution, and in providing science-based guidance on monitoring coastal water quality and reducing further pollution. The health of our oceans and all the life they support depend on it. “
“Most marine protected areas are only partially protected in that they commonly permit fishing, a primary ecosystem-distorting activity. Many indeed are no more than ‘paper parks’. The creation of no-take MPAs lags well behind several national declarations of intent and certainly lags behind need. A letter calling for more of these no-take zones has been signed by 250 of the world’s leading scientists (http://www.globaloceanlegacy.org/).

[22] także analizowali skuteczność suplementacji L. reuteri w leczeniu ostrej biegunki. Badaniem z randomizacją objęli niemowlęta see more i małe dzieci hospitalizowane z powodu ostrej biegunki, w większości przypadków o etiologii rotawirusowej. Dzieciom podawano L. reuteri 1010-1011 CFU lub placebo codziennie przez cały okres hospitalizacji lub przez 5 dni, jeśli hospitalizacja trwała dłużej. Czas trwania biegunki był krótszy w

grupie otrzymującej probiotyk, choć różnica nie była znamienna statystycznie (p=0,07), natomiast w drugim dniu statystycznie istotnie mniej dzieci w grupie suplementowanej miało wodniste stolce, krótszy także u nich był czas występowania wymiotów (ustępowały po pierwszym dniu suplementacji probiotyku, a w grupie kontrolnej trwały do dnia szóstego). Shornikova i wsp. [23] opublikowali wyniki badań, w których dzieciom w wieku od 6 do 26 miesięcy, hospitalizowanym z powodu biegunki rotawirusowej, podawano losowo 1010 lub 107 CFU L. reuteri lub placebo do 5 dni. Podaż L. reuteri miała związek ze skróceniem czasu trwania wodnistej biegunki, efekt ten był znaczniejszy przy podaży większej dawki probiotyku. Znaczącym

problemem gastroenterologicznym, zarówno u dzieci, jak i dorosłych, jest zakażenie H. pylori. Jego eradykacja często bywa nieskuteczna, co wynikać może zarówno z narastającej antybiotykooporności bakterii, jak i efektów ubocznych standardowej terapii, która bywa ze względu na nie przerywana. Wykazano, że suplementacja L. reuteri poprawia tolerancję antybiotykoterapii poprzez zapobieganie dysbakteriozie przewodu pokarmowego w jej przebiegu. Ponadto ma Nintedanib solubility dmso właściwości hamujące namnażanie H. pylori. Lionetti i wsp. [24] przeprowadzili badania, których celem było sprawdzenie, czy L. reuteri może zapobiec lub zminimalizować skutki ubocznych efektów terapii GBA3 eradykacyjnej H. pylori ze strony przewodu pokarmowego. Do badania

tego włączono 40 dzieci zakażonych H. pylori (w wieku średnio 12,3 roku), które poddano 10-dniowemu standardowemu leczeniu eradykacyjnemu (dzieci przez 5 dni otrzymywały omeprazol i amoxycylinę, a następnie przez 5 dni omeprazol, klarytomycynę i tynidazol). Badanych podzielono na grupy, w których podawano placebo lub L. reuteri ATCC 55730 (108 CFU na dobę) przez 20 dni w 1 dawce dobowej 2 godziny po jedzeniu. Dzieci z pomocą rodziców wypełniały formularz dotyczący występowania objawów ze strony przewodu pokarmowego przed, w czasie (5. i 10. dzień) i po leczeniu (15. i 20. dzień). Zastosowano 15-punktową skalę oceny ciężkości i częstości występowania tych objawów. Po 8 tygodniach wykonywano kontrolny test oddechowy. Stwierdzono, że w grupie badanej podczas eradykacji i po niej występuje mniej objawów ze strony układu pokarmowego, a także mają one mniejsze nasilenie niż u dzieci z grupy porównawczej. Scaccianoce i wsp. [25] u pacjentów zakażonych H. pylori podawali standardową 7-dniową terapię trójlejkową z lub bez dodatkowej podaży L.