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Estuaries have strong physicochemical gradients that lead to complex variability and often high rates of biogeochemical processes. The biogeochemistry of many estuaries is also increasingly impacted by human activities. Yet our understanding of estuarine biogeochemistry remains skewed towards temperate systems in the northern hemisphere, with far less research from tropical estuaries. This study examined seasonal and spatial variability in dissolved organic matter (DOM) and nutrient biogeochemistry along a partly eutrophic, mixed agricultural/urban estuary system in Southeast Asia, the Johor River and the East Johor Strait. Dissolved organic carbon (DOC) and chromophoric DOM (CDOM) properties showed non-conservative mixing, indicating significant DOM inputs along the estuary. The CDOM spectral slopes and CDOM:DOC ratios suggest that these inputs are dominated by terrigenous, soil-derived DOM along the Johor River, but that phytoplankton production and microbial recycling are more important DOM sources in the Johor Strait. Nitrate consistently showed conservative mixing, while nitrite concentrations peaked at intermediate salinities of 10–25. Ammonia decreased with salinity in the Johor River. In the Johor Strait, however, ammonia increased up to 50 µmol l-1, often dominating the dissolved inorganic nitrogen (DIN) pool. Phosphate was low (<0.5 µmol l-1) throughout the Johor River, but increased in the Johor Strait, where DIN:phosphate ratios were typically at or above 16:1. This suggests that phytoplankton in the Johor Strait may sometimes experience phosphorus limitation. Moreover, internal recycling is likely important for maintaining high nutrient concentrations in the Johor Strait. [ABSTRACT FROM AUTHOR]

During K(+)-induced depolarization of isolated rat brain nerve terminals (synaptosomes), 1 mM Ba2+ could substitute for 1 mM Ca2+ in evoking the release of endogenous glutamate. In addition, Ba2+ was found to evoke glutamate release in the absence of K(+)-induced depolarization. Ba2+ (1-10 mM) depolarized synaptosomes, as measured by voltage-sensitive dye fluorescence and [3H]-tetraphenylphosphonium cation distribution. Ba2+ partially inhibited the increase in synaptosomal K+ efflux produced by depolarization, as reflected by the redistribution of radiolabeled 86Rb+. The release evoked by Ba2+ was inhibited by tetrodotoxin (TTX). Using the divalent cation indicator fura-2, cytosolic [Ca2+] increased during stimulation by approximately 200 nM, but cytosolic [Ba2+] increased by more than 1 microM. Taken together, our results indicate that Ba2+ initially depolarizes synaptosomes most likely by blocking a K+ channel, which then activates TTX-sensitive Na+ channels, causing further depolarization, and finally enters synaptosomes through voltage-sensitive Ca2+ channels to evoke neurotransmitter release directly. Though Ba(2+)-evoked glutamate release was comparable in level to that obtained with K(+)-induced depolarization in the presence of Ca2+, the apparent intrasynaptosomal level of Ba2+ required for a given amount of glutamate release was found to be several-fold higher than that required of Ca2+.

The apparent rate of evolution of resistance of weeds to herbicides has increased substantially over the past decade. Data suggests phenotypic expression is affected by the mechanism of action of the herbicide, the taxonomy of the weed, the extent and frequency of selection and the agronomic context of herbicide use that contribute to the development of herbicide resistance. The opportunities for herbicide resistance are maximized in weeds that produce prolific seed, have relatively short half-life in the seedbank, and are obligate outcrossers; for herbicides that have a single target site that is not conserved or have multiple non-target resistance mechanisms; and in management, those management systems that do not use a diverse set of weed management tools and rely only on herbicides for weed control. The ability to identify weed and herbicide combinations that are most likely to develop herbicide resistance can aid in education and management systems to delay herbicide resistance.

Nonalcoholic fatty liver disease (NAFLD) is a major worldwide health problem. Recent studies suggest that the gut microbiota influences NAFLD pathogenesis. Here, a murine model of high-fat diet-induced (HFD-induced) NAFLD was used, and the effects of alterations in the gut microbiota on NAFLD were determined. Mice treated with antibiotics or tempol exhibited altered bile acid composition, with a notable increase in conjugated bile acid metabolites that inhibited intestinal farnesoid X receptor (FXR) signaling. Compared with control mice, animals with intestine-specific Fxr disruption had reduced hepatic triglyceride accumulation in response to a HFD. The decrease in hepatic triglyceride accumulation was mainly due to fewer circulating ceramides, which was in part the result of lower expression of ceramide synthesis genes. The reduction of ceramide levels in the ileum and serum in tempol--or antibiotic-treated mice fed a HFD resulted in downregulation of hepatic SREBP1C and decreased de novo lipogenesis. Administration of C16:0 ceramide to antibiotic-treated mice fed a HFD reversed hepatic steatosis. These studies demonstrate that inhibition of an intestinal FXR/ceramide axis mediates gut microbiota- associated NAFLD development, linking the microbiome, nuclear receptor signaling, and NAFLD. This work suggests that inhibition of intestinal FXR is a potential therapeutic target for NAFLD treatment., Introduction Nonalcoholic fatty liver disease (NAFLD) is characterized by massive ectopic triglyceride accumulation in the liver in the absence of other liver disease or significant alcohol consumption (1). NAFLD is [...]