Trophic consequences of an invasive, small-bodied non-native fish, sunbleak Leucaspius delineatus, for native pond fishes

Assessments of the trophic consequences of invasive fishes are important for quantifying their ecological impacts on native species more generally. A small-bodied cyprinid fish native to continental Europe and introduced in the 1970s to the U.K, the sunbleak Leuciscus delineatus, has been shown previously to establish closer social associations with native species of similar size than do native species amongst themselves. To assess the potential detrimental trophic consequences of native species associations with L. delineatus, a field-based experiment was undertaken in summer 2015 in six outdoor, artificial ponds containing three native cyprinid species (rudd Scardinius erthrophthalamus, gudgeon Gobio gobio, tench Tinca tinca). Three ponds were controls (no L. delineatus) and three were treatments (L. delineatus present). The results of stable isotope analysis (SIA) of fish tissue samples provided strong evidence that the isotopic niches of both native benthic fishes were reduced in the presence of L. delineatus, although there were no significant effects on the trophic position, body size or condition of two of the three native fish species. Introduced L. delineatus maintained a core isotopic niche that was distinct from the two native benthic fishes, with no overlap detected between native and non-native fishes when including 40 % and 95% of the data. These results indicate that the response of the native fishes to the introduction of L. delineatus was niche constriction via trophic specialisation, with this response sufficient to maintain their growth rates and condition. This result is similar to studies on a range of small-bodied invasive fishes, suggesting the trophic impacts of these invaders are relatively consistent across species and systems

The structure and function of Alzheimer's gamma secretase enzyme complex

The production and accumulation of the beta amyloid protein (Aβ) is a key event in the cascade of oxidative and inflammatory processes that characterizes Alzheimer’s disease (AD). A multi-subunit enzyme complex, referred to as gamma (γ) secretase, plays a pivotal role in the generation of Aβ from its parent molecule, the amyloid precursor protein (APP). Four core components (presenilin, nicastrin, aph-1, and pen-2) interact in a high-molecular-weight complex to perform intramembrane proteolysis on a number of membrane-bound proteins, including APP and Notch. Inhibitors and modulators of this enzyme have been assessed for their therapeutic benefit in AD. However, although these agents reduce Aβ levels, the majority have been shown to have severe side effects in pre-clinical animal studies, most likely due to the enzymes role in processing other proteins involved in normal cellular function. Current research is directed at understanding this enzyme and, in particular, at elucidating the roles that each of the core proteins plays in its function. In addition, a number of interacting proteins that are not components of γ-secretase also appear to play important roles in modulating enzyme activity. This review will discuss the structural and functional complexity of the γ-secretase enzyme and the effects of inhibiting its activity

Hepatic morphological alterations, glycogen content and cytochrome P450 activities in rats treated chronically with N-omega-nitro-L-arginine methyl ester (L-NAME)

Chronic treatment of rats with N-omega stop-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) biosynthesis, results in hypertension mediated partly by enhanced angiotensin-I-converting enzyme (ACE) activity. We examined the influence of L-NAME on rat liver morphology, on hepatic glycogen, cholesterol, and triglyceride content, and on the activities of the cytochrome P450 isoforms CYP1A1/2, CYP2B1/2, CYP2C11, and CYP2E1. Male Wistar rats were treated with L-NAME (20 mg/rat per day via drinking water) for 2, 4, and 8 weeks, and their livers were then removed for analysis. Enzymatic induction was produced by treating rats with phenobarbital (to induce CYP2B1/2), beta-naphthoflavone (to induce CYP1A1/2), or pyrazole (to induce CYP2E1). L-NAME significantly elevated blood pressure; this was reversed by concomitant treatment with enalapril (ACE inhibitor) or losartan (angiotensin II AT(1) receptor antagonist). L-NAME caused vascular hypertrophy in hepatic arteries, with perivascular and interstitial fibrosis involving collagen deposition. Hepatic glycogen content also significantly increased. L-NAME did not affect fasting glucose levels but significantly reduced insulin levels and increased the insulin sensitivity of rats, based on an intraperitoneal glucose tolerance test. Immunoblotting experiments indicated enhanced phosphorylation of protein kinase B and of glycogen synthase kinase 3. All these changes were reversed by concomitant treatment with enalapril or losartan. L-NAME had no effect on hepatic cholesterol or triglyceride content or on the basal or drug-induced activities and protein expression of the cytochrome P450 isoforms. Thus, the chronic inhibition of NO biosynthesis produced hepatic morphological alterations and changes in glycogen metabolism mediated by the renin-angiotensin system. The increase in hepatic glycogen content probably resulted from enhanced glycogen synthase activity following the inhibition of glycogen synthase kinase 3 by phosphorylation.3291455

Neutralization of the pharmacological effects of bothropstoxin-I from Bothrops jararacussu (jararacucu) venom by crotoxin antiserum and heparin

Bothropstoxin-I (BthTX-1), the principal myotoxin of Bothrops jararacussu venom, is devoid of phospholipase A(2) (PLA(2)) activity but capable of blocking neuromuscular transmission in mouse nerve-muscle preparations. In this study, the ability of crotoxin antiserum and heparin in preventing the neurotoxic and myotoxic effects of BthTX-I was investigated. Phrenic nerve-diaphragm preparations (PND) stimulated indirectly with supramaximal stimuli (0.2 ms, 0.1 Hz) were incubated with BthTX-I (20 mug/ml) alone or with BthTX-I preincubated with antiserum or heparin for 30 min at 37 degreesC prior to testing. Control preparations were incubated with Tyrode solution, antiserum or heparin alone. BthTX-I (20 mug/ml) produced 50% neuromuscular blockade in the PND preparations in 31 +/- 4 min, with complete blockade occurring in 120 min. The antiserum and heparin significantly prevented the neuromuscular blockade caused by BthTX-I (84 +/- 4% and 100% protection, respectively). Light microscopy examination of the muscles at the end of the 120 min incubation showed that BthTX-I damaged 48 +/- 6% of the fibers. Preincubating the toxin with antivenom significantly reduced the extent of this damage (only 15 +/- 4% of fibers affected, corresponding to 69% protection, P < 0.01) whereas heparin offered no protection (34 +/- 7% of fibers affected, not significantly different from that seen with toxin alone). These results show that the antivenom was more effective in neutralizing the myotoxic effects of BthTX-I than was heparin. (C) 2001 Elsevier Science Ltd. All rights reserved.39101477148