Abstract Objective: In this article, the author aims to discuss and review the relationship between gut microbiota and Tourette syndrome, and whether the change in gut microbiota can affect the severity of Tourette syndrome. Sources: Literature from PubMed, Google Scholar, and China National Knowledge Infrastructure was mainly reviewed. Both original studies and review articles were discussed. The articles were required to be published as of May 2022. Summary of the findings: Current studies on the gut microbiome have found that the gut microbiome and brain seem to interact. It is named the brain-gut-axis. The relationship between the brain-gut axis and neurological and psychiatric disorders has been a topic of intense interest. Tourette syndrome is a chronic neurological disease that seriously affects the quality of life of children, and there appears to be an increase in Ruminococcaceae and Bacteroides in the gut of patients with Tourette syndrome. After clinical observation and animal experiments, there appear to be particular gut microbiota changes in Tourette syndrome. It provides a new possible idea for the treatment of Tourette syndrome. Probiotics and fecal microbial transplantation have been tried to treat Tourette syndrome, especially Tourette syndrome which is not sensitive to drugs, and some results have been achieved. Conclusions: The relationship between gut microbiota and Tourette syndrome and how to alleviate Tourette syndrome by improving gut microbiota are new topics, more in-depth and larger sample size research is still needed.

Humans and guinea pigs are species which are unable to synthesize ascorbic acid (vitamin C) because, unlike rodents, they lack the enzyme L-gulonolactone oxidase (Gulo). Although the phenotype of lacking vitamin C in humans, named scurvy, has long been well known, information on the impact of lacking Gulo on the gene expression profiles of different tissues is still missing. This knowledge could improve our understanding of molecular pathways in which Gulo may be involved. Recently, we discovered a deletion that includes all 12 exons in the gene for Gulo in the sfx mouse, characterized by spontaneous bone fractures. We report here the initial analysis of the impact of the Gulo gene deletion on the murine gene expression profiles in the liver, femur and kidney.

Population size and phenotypic measurement are two key factors determining the detection power of quantitative trait loci (QTL) mapping. We evaluated how these two controllable factors quantitatively affect the detection of QTL and their localization using a large F2 murine mapping population and found that three main points emerged from this study. One finding was that the sensitivity of QTL detection significantly decreased as the population size decreased. The decrease in the percentage logarithm of the odd score (LOD score, which is a statistical measure of the likelihood of two loci being lied near each other on a chromosome) can be estimated using the formula 1 - n/N, where n is the smaller and N the larger population size. This empirical formula has several practical implications in QTL mapping. We also found that a population size of 300 seems to be a threshold for the detection of QTL and their localization, which challenges the small population sizes commonly-used in published studies, in excess of 60% of which cite population sizes <300. In addition, it seems that the precision of phenotypic measurement has a limited capacity to affect detection power, which means that quantitative traits that cannot be measured precisely can also be used in QTL mapping for the detection of major QTL.