The aim of the study was to compare histological and endocrinological indices of ovarian follicle health in cattle with monitoring of follicle growth and regression by ultrasound imaging in vivo. Ultrasound scanning was performed daily. Follicles were obtained at ovariectomy; follicular fluid was collected for assay, and the degree of atresia was assessed histologically. Histological atresia was correlated with growth patterns when anovulatory growing and regressing follicles were compared (P < 0.05), but was not different between growing and static follicles. Oestradiol concentrations were lower in static than in growing follicles, although the difference was not significant (35 +/- 7 versus 260 +/- 120 ng ml-1; P < 0.08), and were significantly lower in regressing follicles (7 +/- 5 ng ml-1; P < 0.05). Oestradiol concentrations were significantly lower in histologically atretic than in nonatretic follicles (16 +/- 8 versus 282 +/- 132 ng ml-1; P < 0.05), but were not different between nonatretic and early atretic follicles (P > 0.05). There was a significant negative correlation between oestradiol concentration and the number of days the follicle was visible by ultrasound (r = -0.71; P < 0.001). Concentrations of progesterone in follicular fluid were correlated with the number of days the follicles were detected (r = 0.61; P < 0.01) and were higher in regressing than in growing follicles (122 +/- 71 versus 48 +/- 13 ng ml-1; P < 0.05) but not significantly higher in atretic compared with nonatretic follicles (129 +/- 102 versus 53 +/- 15 ng ml-1).(ABSTRACT TRUNCATED AT 250 WORDS)

HighlightsMicrobiota disturbances promote tumor growth in several breast cancer models Increased tumor volume positively correlates with stromal mast cell density Supplementation with a commensal restores tumor growth to normal

BackgroundStem cells are thought to play a critical role in minimizing the accumulation of mutations, but it is not clear which strategies they follow to fulfill that performance objective. Slow cycling of stem cells provides a simple strategy that can minimize cell pedigree depth and thereby minimize the accumulation of replication-dependent mutations. Although the power of this strategy was recognized early on, a quantitative assessment of whether and how it is employed by biological systems is missing.ResultsHere we address this problem using a simple self-renewing organ – the C. elegans gonad – whose overall organization is shared with many self-renewing organs. Computational simulations of mutation accumulation characterize a tradeoff between fast development and low mutation accumulation, and show that slow-cycling stem cells allow for an advantageous compromise to be reached. This compromise is such that worm germ-line stem cells should cycle more slowly than their differentiating counterparts, but only by a modest amount. Experimental measurements of cell cycle lengths derived using a new, quantitative technique are consistent with these predictions.ConclusionsOur findings shed light both on design principles that underlie the role of stem cells in delaying aging and on evolutionary forces that shape stem-cell gene regulatory networks.Electronic supplementary materialThe online version of this article (doi:10.1186/s12915-015-0148-y) contains supplementary material, which is available to authorized users.

There is emerging evidence that resident microbiota communities, that is, the microbiota, play a key role in cancer outcomes and anticancer responses. Although this has been relatively well studied in colorectal cancer and melanoma, other cancers, such as breast cancer (BrCa), have been largely overlooked to date. Importantly, many of the environmental factors associated with BrCa incidence and progression are also known to impact the microbiota, for example, diet and antibiotics. Here, we explore BrCa risk factors from large epidemiology studies and microbiota associations, and more recent studies that have directly profiled BrCa patients' gut microbiotas. We also discuss how in vivo studies have begun to unravel the immune mechanisms whereby the microbiota may influence BrCa responses, and finally we examine how diet and specific nutrients are also linked to BrCa outcomes. We also consider future research avenues and important considerations with respect to study design and implementation, and we highlight some of the important unresolved questions, which currently limit our overall understanding of the mechanisms underpinning microbiota-BrCa responses.