Helicobacter pylori ( H. pylori ) infection is highly prevalent in the human population and may lead to severe gastrointestinal pathology including gastric and duodenal ulcers, mucosa associated tissue lymphoma and gastric adenocarcinoma. In recent years, an alarming increase in antimicrobial resistance and subsequently failing empiric H. pylori eradication therapies have been noted worldwide, also in many European countries. Therefore, rapid and accurate determination of H. pylori ’s antibiotic susceptibility prior to the administration of eradication regimens becomes ever more important. Traditionally, detection of H.pylori and its antimicrobial resistance is done by culture and phenotypic drug susceptibility testing that are cumbersome with a long turn-around-time. Recent advances in diagnostics provide new tools, like real-time polymerase chain reaction (PCR) and line probe assays, to diagnose H. pylori infection and antimicrobial resistance to certain antibiotics, directly from clinical specimens. Moreover, high-throughput whole genome sequencing technologies allow the rapid analysis of the pathogen’s genome, thereby allowing identification of resistance mutations and associated antibiotic resistance. In the first part of this review, we will give an overview on currently available diagnostic methods for detection of H. pylori and its drug resistance and their implementation in H. pylori management. The second part of the review focusses on the use of next generation sequencing technology in H. pylori research. To this end, we conducted a literature search for original research articles in English using the terms “ Helicobacter ”, “transcriptomic”, “transcriptome”, “next generation sequencing” and “whole genome sequencing”. This review is aimed to bridge the gap between current diagnostic practice (histology, rapid urease test, H. pylori culture, PCR and line probe assays) and new sequencing technologies and their potential implementation in diagnostic laboratory settings in order to complement the currently recommended H. pylori management guidelines and subsequently improve public health.

An adequate mineral supply to preterm infants is essential for normal growth and development. This study aimed to compare the mineral contents of human milk (HM) from healthy mothers of preterm (28–32 weeks) and full term (>37 weeks) infants. Samples were collected weekly for eight weeks for the term group (n = 34) and, biweekly up to 16 weeks for the preterm group (n = 27). Iron, zinc, selenium, copper, iodine, calcium, magnesium, phosphorus, potassium, and sodium were quantitatively analyzed by Inductively Coupled Plasma-Mass Spectrometry. The mineral contents of both HM showed parallel compositional changes over the period of lactation, with occasional significant differences when compared at the same postpartum age. However, when the comparisons were performed at an equivalent postmenstrual age, preterm HM contained less zinc and copper from week 39 to 48 (p < 0.002) and less selenium from week 39 to 44 (p < 0.002) than term HM. This translates into ranges of differences (min–max) of 53% to 78%, 30% to 72%, and 11% to 33% lower for zinc, copper, and selenium, respectively. These data provide comprehensive information on the temporal changes of ten minerals in preterm HM and may help to increase the accuracy of the mineral fortification of milk for preterm consumption.

Background Glucose induces the release of gastrointestinal (GI) satiation hormones, such as glucagon-like peptide-1 (GLP-1), and peptide tyrosine tyrosine (PYY) in part via the activation of the gut sweet taste receptor (T1R2/T1R3). Objectives The primary objective was to investigate the importance of T1R2/T1R3 for the release of cholecystokinin (CCK), GLP-1 and PYY in response to D-allulose and erythritol by assessing the effect of the T1R2/T1R3 antagonist lactisole on these responses and as secondary objectives to study the effect of the T1R2/T1R3 blockade on gastric emptying, appetite-related sensations and GI symptoms. Methods In this randomized, controlled, double-blind, cross-over study, 18 participants (five men, mean ± SD BMI: 21.9 ± 1.7 kg/m2, age: 24 ± 4 y) received an intragastric administration of 25 g D-allulose, 50 g erythritol, or tap water, with or without 450 parts per million (ppm) lactisole, respectively, in six different sessions. 13C-sodium acetate was added to all solutions to determine gastric emptying. At fixed time intervals, blood and breath samples were collected, and appetite-related sensations and GI symptoms were assessed. Data were analyzed with linear mixed model analysis. Results D-allulose and erythritol induced a significant release of CCK, GLP-1 and PYY compared to tap water (all PHolm &lt; 0.0001, dz &gt; 1). Lactisole did not affect the D-allulose- and erythritol-induced release of CCK, GLP-1, and PYY (all PHolm &gt; 0.1). Erythritol significantly delayed gastric emptying, increased fullness and decreased prospective food consumption compared to tap water (PHolm = 0.0002, dz = –1.05, PHolm = 0.0190, dz = 0.69 and PHolm = 0.0442, dz = -0.62, respectively). Conclusions D-allulose and erythritol stimulate the secretion of GI satiation hormones in humans. Lactisole had no effect on CCK, GLP-1, and PYY release, indicating that D-allulose- and erythritol-induced GI satiation hormone release is not mediated via T1R2/T1R3 in the gut. Clinical Trial Registry number and website: Number: NCT04027283, Website: https://clinicaltrials.gov/ct2/show/NCT04027283?term=NCT04027283&draw=2&rank=1.

Background Whether decreased physical functioning of patients with mitochondrial disease (MD) is related to altered body composition or low protein intake needs clarification at the background of the nutrition state. Methods In this 2‐site cross‐sectional study, MD patients were age‐, body mass index (BMI)–, and gender‐matched to controls. Body composition was assessed by dual‐energy x‐ray absorptiometry. Physical functioning was measured by handgrip strength, 6‐minute walking test, 30‐second sit‐to‐stand test (30SCT), and 6‐minute mastication test. Total daily protein intake was calculated by 3‐day food records. Malnutrition was assessed by Patient‐Generated Subjective Global Assessment and the Global Leadership Initiative on Malnutrition (GLIM) criteria and sarcopenia by the 2018 consensus. Data were analyzed using independent samples t‐tests, Fisher exact test, and Spearman and Pearson correlation coefficients. Results Thirty‐seven MD patients (42 ± 12 years, BMI: 23 ± 4 kg/m2, 59% females) and 37 matched controls were included. Handgrip strength was moderate, inversely related to fat mass index in both MD patients and controls, whereas it correlated with fat‐free mass index in controls solely. Protein intake was associated with muscle strength (handgrip strength and 30SCT) in MD patients but not in controls. Twenty‐seven MD patients (73%) were malnourished, and 5 (14%) were classified as sarcopenic. Conclusions Muscle strength is related to body composition and protein intake in MD patients. This, in combination with the high incidence of both malnutrition and sarcopenia, warrants individual nutrition assessment in MD patients.