Methods to quickly measure organic matter degradation have been well developed for terrestrial and freshwater ecosystems. However, these methods have not been adapted to marine environments. Current methods of assessing organic matter degradation in marine ecosystems are costly, difficult to relate across spatial scales and rarely include sediment depth components to account for redox effects and subsurface macrofaunal activity. We developed a method which is cost effective and time efficient to directly measure rates of organic matter degradation across vertical and horizontal spatial scales in marine sediments. This rapid organic matter assay (ROMA), utilizes a simple design consisting of an acrylic plate with a series of machined wells (0.9 ml) filled with carbon rich substrate. Substrate can be easily adapted to any carbon source by simply modifying the recipe. The plates are deployed with minimal disturbance to the sediment surface and subsurface stratification. Once collected, the resulting change in carbon substrate volume is equated to organic matter degradation. Rapid organic matter assay was shown to be a useful tool in comparing organic matter degradation across sediment redox potentials, habitats within an estuary, and similar habitats across different estuaries. Here, we demonstrate its utility, versatility, and ease of use across a variety of habitats and environments. Rapid organic matter assay is an effective assay for in situ, whole community (micro, meio and macrofauna) organic matter degradation across a myriad of habitats. This supports intensive spatial and temporal analysis that are costly and logistically difficult with current methods. Because it is simple, cost effective, and adaptable, it is an ideal candidate for a standard method to measure organic matter degradation rates in estuaries globally.
Summary A seasonal variation in the month of initial detection of breast cancer has been previously observed in pre-menopausal women, and it has been proposed that this may be due to
Hormones such as melatonin whose serum concentrations vary seasonally have been previously implicated in the growth of breast cancer. The present study was undertaken to identify possible seasonal variation in a range of mammotrophic hormones which could exert a chronobiologic influence in women with breast tumours. Fifteen premenopausal women with a history of previous breast cancer (BC subjects) and 10 control women underwent 2-hourly serum sampling for 24 h at both summer and winter solstice for measurement of melatonin, growth hormone (GH), insulin-like growth factor-I (IGF-I), cortisol, prolactin and thyrotrophin (TSH). Hormone secretion at the different seasons was compared by measuring the area under the 24 h serum hormone concentration x time curves and by time series analysis of summer-to-winter differences in hormone concentration. Control women had significantly higher GH and IGF-I levels in summer compared to winter and significantly higher cortisol secretion in winter than summer. In contrast, BC women had no significant seasonal difference in IGF-I concentrations and had a reversal of the normal seasonal pattern of melatonin secretion, although seasonal changes in GH production were similar to controls. Prolactin and TSH showed no significant summer/winter variation in either group. Thus, seasonal variations in hormone secretion seen in normal women were, with exception of GH, absent or reversed in women with a previous history of breast cancer. As a result these individuals may be exposed to an asynchronous hormonal stimulus which could influence tumour growth. These changes could reflect a constitutional abnormality in BC women or may have been induced by the previous breast tumour.
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