Objective Radiation proctitis (RP) is a complication of pelvic radiotherapy which affects both the host and microbiota. Herein we assessed the radiation effect on microbiota and its relationship to tissue damage using a rectal radiation mouse model. Design We evaluated luminal and mucosa-associated dysbiosis in irradiated and control mice at two postradiation time points and correlated it with clinical and immunological parameters. Epithelial cytokine response was evaluated using bacterial-epithelial co-cultures. Subsequently, germ-free (GF) mice were colonised with postradiation microbiota and controls and exposed to radiation, or dextran sulfate-sodium (DSS). Interleukin (IL)-1β correlated with tissue damage and was induced by dysbiosis. Therefore, we tested its direct role in radiation-induced damage by IL-1 receptor antagonist administration to irradiated mice. Results A postradiation shift in microbiota was observed. A unique microbial signature correlated with histopathology.

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A composite genetic melon map was generated based on two recombinant inbred line (RI) populations. By analyzing the segregation of 346 AFLPs, 113 IMAs and phenotypic characters on a RI population of 163 individuals derived from the cross Védrantais x PI 161375, a first map was constructed. About 20% of the molecular markers were skewed, and the residual heterozygosity was estimated at 4.43% which was not significantly different from the theoretical value of 4.2%. The genome distribution of molecular markers among the 12 linkage groups was not different from a random distribution with the exception of linkage group XII which was found significantly less populated. The genome distributions of IMAs and AFLPs were complementary. AFLPs were found mainly in the middle of each linkage group and sometimes clustered, whereas IMAs were found mainly at the end. A total of 318 molecular markers, mainly AFLP and IMA markers, were mapped on 63 RIs of the second population, Védrantais x PI 414723. Comparison of the maps enables one to conclude that AFLPs and IMAs of like molecular size, amplified with the same primer combination, correspond to the same genetic locus. Both maps were joined through 116 common markers comprising 106 comigrating AFLPs/IMAs, plus five SSRs and five phenotypic markers. The integrated melon map contained 668 loci issuing from the segregation of 1,093 molecular markers in the two RI populations. The composite map spanned 1,654 cM on 12 linkage groups which is the haploid number of chromosomes in melon. Thirty two known-function probes, i.e. known-function genes (9) and morphological traits (23), were included in this map. In addition, the composite map was anchored to previously published maps through SSRs, RFLPs and phenotypic characters.

Random amplified polymorphic DNA (RAPD) and simple sequence repeat (SSR) markers were used to characterize genetic relationships among 46 accessions in two C. melo L. subsp. melo (Cantalupensis, Inodorus) and subsp. agrestis (Conomon and Flexuosus) groups. Genetic distance (GD) estimates were made among and between accessions in four melon market classes [Galia, Ogen, Charentais, and Shipper (European and U.S. types)] of Cantalupensis, one market class of Inodorus (Cassaba and Honey Dew), one accession of Conomon, and one accession of Flexuosus by employing three GD estimators; simple matching coefficient, Jaccard's coefficient, and Nei's distance-D. Differences detected among 135 RAPD bands and 54 SSR bands (products of 17 SSR primers) were used to calculate GD. Band polymorphisms observed with 21 RAPD primers and 7 SSR primers was important in the detection of genetic differences. Estimators of GD were highly correlated (P > 0.0001; rs = 0.64 to 0.99) when comparisons were made between estimation methods within a particular marker system. Lower correlations (P > 0.001; rs = 0.17 to 0.40) were detected between marker systems using any one estimator. The GD of the Conomon and Flexuosus accessions was significantly different from the mean GD of all the market classes examined, and market classes were distinguishable from each other. Although lower coefficients of variation can be attained in the estimation of GD when using RAPDs compared to SSRs, the genetic relationships identified using these markers were generally similar. Results of RAPD marker analysis suggest that 80 marker bands were adequate for assessing the genetic variation present in the accessions examined.

Vibrio cholerae is the etiological agent of cholera. Its natural reservoir is the aquatic environment. To date, practical typing of V. cholerae is mainly serological and requires about 200 antisera. Simple sequence repeats (SSR), also termed VNTR (for variable number of tandem repeats), provide a source of high genomic polymorphism used in bacterial typing. Here we describe an SSR-based typing method that combines the variation in highly mutable SSR loci, with that of shorter, relatively more stable mononucleotide repeat (MNR) loci, for accurate and rapid typing of V. cholerae. Vibrio cholerae, a gram-negative bacterium, is the causal agent of the severe diarrheal disease cholera. Its natural reservoir is the aquatic environment (49, 84). Cholera pandemics are caused by specific serogroups of V. cholerae that are pathogenic only to humans (35,84). Since 1817, V. cholerae has caused a number of pandemics. The first seven were presumed to be caused by O1 serogroup of V. cholerae (68). In October 1992, a new serogroup, defined O139, caused a severe outbreak of cholera in southeast India. Within 10 months, the O139 serogroup was disseminated all over the Indian subcontinent and soon thereafter spread to 11 neighboring countries, temporarily displacing the O1 serogroups (64). Since then both serogroups coexist and are responsible for large outbreaks. Genomic studies indicated that O139 epidemic strain arose by horizontal acquisition of unique DNA (15, 47).Traditionally, V. cholerae classification is serological and requires about 200 antisera based on the somatic O antigen (72). Isolates of V. cholerae are divided into three major subgroups: O1, O139, and non-O1/non-O139, of which only the O1 and O139 serogroups are associated with cholera pandemics and epidemics. Non-O1, non-O139 serogroups are recognized as causative agents of sporadic and localized outbreaks (73). Pathogenic V. cholerae isolates carry virulence genes, such as the toxins genes ctxAB (25,65,68). The environmental V. cholerae strains from non-O1, non-O139 serogroups are a possible natural reservoir of potentially new emerging epidemic strains (67,73). This assumption is supported by the finding that some of these environmental strains harbor virulence genes (23) and thus are likely to evolve into novel pathogenic strains by horizontal gene transfer (24,25). The emergence of new pathogenic V. cholerae strains requires not only an efficient, rapid, and accurate identification tool but also a means for determining genetic relationships among environmental and clinical isolates.Genome-based bacterial identification and typing is essential for several disciplines, including taxonomy, epidemiology, determining phylogenetic relationships, and the study of evolutionary mechanisms. It allows distinguishing among strains within a species to monitor epidemics and routes of contamination. Recent advances in biotechnology have resulted in the development of numerous methods for microorganism typing that differ in their sensitivity, rapidity, complexity, discrimin...