Bertrambitsch4902

A group of six clinical isolates previously identified as Corynebacterium diphtheriae biovar Belfanti, isolated from human cutaneous or peritoneum infections and from one dog, were characterized by genomic sequencing, biochemical analysis and MALDI-TOF mass spectrometry. The six isolates were negative for the diphtheria toxin gene. Phylogenetic analyses showed that the six isolates (including FRC0190T) are clearly demarcated from C. diphtheriae, Corynebacterium belfantii, Corynebacterium ulcerans and Corynebacterium pseudotuberculosis. The average nucleotide identity of FRC0190T with C. diphtheriae NCTC11397T was 92.6%, and was 91.8% with C. belfantii FRC0043T. C. diphtheriae subsp. lausannense strain CHUV2995T appeared to be a later heterotypic synonym of C. belfantii (ANI, 99.3%). Phenotyping data revealed an atypical negative or heterogeneous intermediate maltose fermentation reaction for the six isolates. MALDI-TOF mass spectrometry differentiated the new group from the other Corynebacterium taxa by the presence of specific spectral peaks. rpoB sequences showed identity to atypical, maltose-negative C. diphtheriae biovar Belfanti isolates previously described from two cats in the USA. We propose the name Corynebacterium rouxii sp. nov. for the novel group, with FRC0190T (= CIP 111752T = DSM 110354T) as type strain. Listeria ivanovii is one of the two pathogenic species within the genus Listeria, the other being Listeria monocytogenes. In this study, we generated a stable pediocin resistant mutant Liv-r1 of a L. ivanovii strain, compared phenotypic differences between the wild-type and the mutant, localised the pediocin-induced mutations in the chromosome, and analysed the mechanisms behind the bacteriocin resistance. In addition to pediocin resistance, Liv-r1 was also less sensitive to nisin. The growth of Liv-r1 was significantly reduced with glucose and mannose, but less with cellobiose. The cells of Liv-r1 adsorbed less pediocin than the wild-type cells. Consequently, with less pediocin on the cell surface, the mutant was also less leaky, as shown as the release of intracellular lactate dehydrogenase to the supernatant. The surface of the mutant cells was more hydrophobic than that of the wild-type. Whole genome sequencing revealed numerous changes in the Liv-r1 chromosome. The mutations were found e.g., in genes encoding sigma-54-dependent transcription regulator and internalin B, as well as in genes involved in metabolism of carbohydrates such as glucose and cellobiose. Genetic differences observed in the mutant may be responsible for resistance to pediocin but no direct evidence is provided. CONTEXT Empathy is increasingly described as a learnable skill and is included in professionalism requirements for healthcare providers, yet there are few effective tools for developing and practicing empathy skills. INNOVATION An educational innovation intended to isolate and develop skills to respond to patients' emotions. The game-based tool was developed "on-the-job" during the authors' Hospice and Palliative Medicine fellowship year and was played with learners in various disciplines. OUTCOMES Feedback from learners was overwhelmingly positive, though a key factor in optimization of learning was the presence of a communication expert as facilitator. Learner responses were measured using a novel assessment tool, and findings suggest statistically significant expansion of language and intent to express empathy. Learners demonstrated immediate growth in naming emotions, reflecting understanding and respect of emotional expression, and supporting and exploring emotional content. COMMENT This innovative game-based learning tool is low cost and feasible to deploy. It could be easily incorporated into medical education curricula aimed at developing communication skills, especially the skill of responding to emotion with empathy. Future research is needed to assess the effects the innovation has on behavior, as well as its impact on patient-centered outcomes. Adolescence is a critical developmental period that is characterised by growth spurts and specific neurobiological, neuroimmune and behavioural changes. In tandem the gut microbiota, which is a key player in the regulation of health and disease, is shaped during this time period. Diet is one of the most important regulators of microbiota composition. Thus, we hypothesised that dietary disturbances of the microbiota during this critical time window result in long-lasting changes in immunity, brain and behaviour. C57BL/6 male mice were exposed to either high fat diet or cafeteria diet during the adolescent period from postnatal day 28 to 49 and were tested for anxiety-related and social behaviour in adulthood. Our results show long-lasting effects of dietary interventions during the adolescent period on microbiota composition and the expression of genes related to neuroinflammation or neurotransmission. Interestingly, changes in myelination-related gene expression in the prefrontal cortex following high fat diet exposure were also observed. However, these effects did not translate into overt behavioural changes in adulthood. Taken together, these data highlight the importance of diet-microbiota interactions during the adolescent period in shaping specific outputs of the microbiota-gut-brain axis in later life. BMS-986165 Cardiometabolic disease is a leading cause of adult morbidity and mortality globally. There is considerable evidence that childhood adversity is associated with markers of cardiometabolic disease risk in childhood, including obesity, blood pressure trajectories, and chronic inflammation. Experiences of racial discrimination may be an important, yet under explored, form of childhood adversity influencing childhood cardiometabolic risk. This study aimed to examine associations between self-reported racial discrimination and cardiometabolic risk markers among children. A total of 124 children (73 female) aged 11.4 years (SD 0.71) participated in the study. Most children (n = 79) identified as being from an Indigenous or an ethnic minority background. Markers of cardiometabolic risk were BMI, waist circumference, weight height ratio, systolic and diastolic blood pressure, and five inflammatory markers (C-reactive protein (CRP), Interleukin (IL)-1β, IL-6, IL-8, and TNF-α). Results showed that two or more reported experiences of racial discrimination were associated with increased BMI z-score (Beta 0.