Collinsella urealyticum sp. nov., a urease-positive bacterial strain isolated from swine faeces.

A novel actinobacterial strain, designated AGMB00827T, was isolated from swine faeces. Strain AGMB00827T was obligately anaerobic, Gram-stain-positive, non-motile, non-spore-forming and rod-shaped bacterium. Comparative analyses based on the 16S rRNA gene and whole genome sequence revealed that strain AGMB00827T was affiliated to the genus Collinsella, and was most closely related to Collinsella vaginalis Marseille-P2666T (= KCTC 25056T). Biochemical analysis showed strain AGMB00827T was negative for catalase and oxidase. Interestingly, strain AGMB00827T possessed urease activity, which was determined by traditional methods (API test and Christensen's urea medium), unlike related strains. Furthermore, the major cellular fatty acids (> 10%) of the isolate were C18:1 ω9c, C16:0, C16:0 DMA and C18:2 ω9,12c DMA. Based on the whole genome sequence analysis, the DNA G + C content of strain AGMB00827T was 52.3%, and the genome size and numbers of rRNA and tRNA genes were 1,945,251 bp, 3 and 46, respectively. The average nucleotide identity and digital DNA-DNA hybridization values between strain AGMB00827T and C. vaginalis KCTC 25056 T were 71.0 and 23.2%, respectively. Additionally, the genome analysis revealed that strain AGMB00827T possesses urease gene cluster including ureABC and ureDEFG while the related strains do not have those genes, which is consistent with the urease activity. On the basis of polyphasic taxonomic approach, strain AGMB00827T represents a novel species within the genus Collinsella, for which the name Collinsella urealyticum sp. nov. is proposed. The type strain is AGMB00827T (= KCTC 25287T = GDMCC 1.2724T).

Combination Assessment of Clinical Complete Response of Patients With Rectal Cancer Following Chemoradiotherapy With Endoscopy and Magnetic Resonance Imaging.

PURPOSE: The response to neoadjuvant chemoradiotherapy (CRT) for rectal cancer can be assessed using digital rectal examination, endoscopy and magnetic resonance imaging (MRI). Precise assessment of clinical complete response (CR) after CRT is essential when deciding between optimizing surgery or organ-preserving treatment. The objectives of this study were to correlate the CR finding in endoscopy and MRI with pathologic CR and to determine the appropriate approach for combining endoscopy and MRI to predict the pathologic CR in patients with rectal cancer after neoadjuvant CRT. METHODS: This retrospective cohort study included 102 patients with rectal cancer who underwent endoscopy and MRI at 2-4 weeks after CRT. We assigned a confidence level (1-4) for the endoscopic and MRI assessments. Accuracy, sensitivity, and specificity were analyzed based on the endoscopy, MRI, and combination method findings. Diagnostic modalities were compared using the likelihood ratios. RESULTS: Of 102 patients, 17 (16.7%) had a CR. The accuracy, sensitivity, and specificity for the prediction CR of endoscopy with biopsy were 85.3%, 52.9%, and 91.8%, while those of MRI were 91.2%, 70.6%, and 95.3%, and those of combined endoscopy and MRI were 89.2%, 52.9%, and 96.5%, respectively. No significant differences were noted in the sensitivity and specificity of any each modality. The prediction rate for CR of the combination method was 92.6% after the posttest probability test. CONCLUSION: Our study demonstrated that combining the interpretation of endoscopy with biopsy and MRI could provide a good prediction rate for CR in patients with rectal cancer after CRT.

p53 deficiency and defective mitotic checkpoint in proliferating T lymphocytes increase chromosomal instability through aberrant exit from mitotic arrest.

During the proliferation of T cells for successful immune responses against pathogens, the fine regulation of cell cycle is important to the maintenance of T cell homeostasis and the prevention of lymphoproliferative disorders. However, it remains to be elucidated how the cell cycle is controlled at the mitotic phase in proliferating T cells. Here, we show that during the proliferation of primary T cells, the disruption of the mitotic spindle leads to cell-cycle arrest at mitosis and that prolonged mitotic arrest results in not only apoptosis but also the form of chromosomal instability observed in human cancers. It is interesting that in response to spindle damage, the phosphorylation of BubR1, a mitotic checkpoint kinase, was significantly induced in proliferating T cells, and the expression of the dominant-negative mutant of BubR1 compromised mitotic arrest and subsequent apoptosis and thus led to the augmentation of polyploidy formation. We also show that in response to prolonged spindle damage, the expression of p53 but not of p73 was significantly induced. In addition, following sustained mitotic arrest, p53-deficient T cells were found to be more susceptible to polyploidy formation than the wild type. These results suggest that during flourishing immune response, mitotic checkpoint and p53 play important roles in the prevention of chromosomal instability and in the maintenance of the genomic integrity of proliferating T cells.