Constructed wetlands with free water surface for treatment of aquaculture effluents

The aim of the study was to determine the reduction of the overall environmental load (in terms of organic and nutrient load) in effluents of a flow‐through trout farm. Effluents of a flow‐through system for rainbow trout (Oncorhynchus mykiss) production passed through constructed wetlands with free water surface. Removal of nutrients was determined in three wetlands of 350 m² each at hydraulic residence times (HRTs) of 3.5, 5.5 and 11 h. The areal load of total suspended solids (TSS), chemical oxygen demand (COD), total phosphorus (TP), and total nitrogen (TN) varied in terms of HRTs from 12.3–36.8 g m^?2 day^?1, 21.7–65.2 g m^?2 day^?1, 0.23–0.70 g m^?2 day^?1, and 1.46–4.37 g m^?2 day^?1. Values for reduction of suspended solids, COD, TP, and TN were 67–72%, 30–31%, 41–53% ,and 19–30%, respectively. Significantly lower nutrient concentrations in the effluent among the wetlands were only found for nitrogen parameters: TN and ammonia concentrations were lower in the wetlands with a HRT of 5.5 h (0.89 mg L^?1, 0.11 mg L^?1) and 11 h (0.81 mg L^?1, 0.11 mg L^?1) compared with the one with 3.5 h (0.96 mg L^?1, 0.16 mg L^?1).     

Dynamic compression counteracts IL-1β induced inducible nitric oxide synthase and cyclo-oxygenase-2 expression in chondrocyte/agarose constructs

Background  

Nitric oxide and prostaglandin E₂ (PGE₂play pivotal roles in both the pathogenesis of osteoarthritis and catabolic processes in articular cartilage. These mediators are influenced by both IL-1β and mechanical loading, and involve alterations in the inducible nitric oxide synthase (iNOS) and cyclo-oxygenase (COX)-2 enzymes. To identify the specific interactions that are activated by both types of stimuli, we examined the effects of dynamic compression on levels of expression of iNOS and COX-2 and involvement of the p38 mitogen-activated protein kinase (MAPK) pathway.     

Reinstatement of Phyllanthus retroflexus Brade (Phyllanthaceae)

Phyllanthus retroflexus Brade is reinstated. It and the very similar P. subemarginatus Müll. Arg. are described, illustrated, and their relationships are discussed, based on a morphological analysis of herbarium specimens. © 2008 The Linnean Society of London, Botanical Journal of the Linnean Society, 2008, 158 , 78–81.     

Elimination of colonic patches with lymphotoxin beta receptor-Ig prevents Th2 cell-type colitis

Past studies have shown that colonic patches, which are the gut-associated lymphoreticular tissues (GALT) in the colon, become much more pronounced in hapten-induced murine colitis, and this was associated with Th2-type T cell responses. To address the role of GALT in colonic inflammation, experimental colitis was induced in mice either lacking organized GALT or with altered GALT structures. Trinitrobenzene sulfonic acid was used to induce colitis in mice given lymphotoxin-beta receptor-Ig fusion protein (LTbetaR-Ig) in utero, a treatment that blocked the formation of both Peyer's and colonic patches. Mice deficient in colonic patches developed focal acute ulcers with Th1-type responses, whereas lesions in normal mice were of a diffuse mucosal type with both Th1- and Th2-type cytokine production. We next determined whether LTbetaR-Ig could be used to treat colitis in normal or Th2-dominant, IFN-gamma gene knockout (IFN-gamma(-/-)) mice. Four weekly treatments with LTbetaR-Ig resulted in deletion of Peyer's and colonic patches with significant decreases in numbers of dendritic cells. This pretreatment protected IFN-gamma(-/-) mice from trinitrobenzene sulfonic acid-induced colitis; however, in normal mice this weekly treatment was less protective. In these mice hypertrophy of colonic patches was seen after induction of colitis. We conclude that Th2-type colitis is dependent upon the presence of colonic patches. The effect of LTbetaR-Ig was mediated through prevention of colonic patch hypertrophy in the absence of IFN-gamma. Thus, LTbetaR-Ig may offer a possible treatment for the Th2-dominant form of colitis.