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Kelp detritus fuels coastal food webs and may play an important role as a source of organic matter for natural carbon sequestration. Here, we conducted ex situ and in situ manipulations to evaluate the role of temperature and light availability in the breakdown of detrital material. We examined degradation rates of two North Atlantic species with contrasting thermal affinities: the 'warm water' kelp Laminaria ochroleuca and the 'cool water' Laminaria hyperborea. Detrital fragments were exposed to different temperatures in controlled conditions and across an in situ gradient of depth, corresponding to light availability. Overall, degradation rates (i.e. changes in F v /F m and biomass) were faster under lower light conditions and at higher temperatures, although responses were highly variable between plants and fragments. Crucially, as L. ochroleuca degraded faster than L. hyperborea under some conditions, a climate-driven substitution of the 'cool' for the 'warm' kelp, which has been observed at some locations, will likely increase detritus turnover rates and alter detrital pathways in certain environments. More importantly, ocean warming combined with decreased coastal water quality will likely accelerate kelp detritus decomposition, with potential implications for coastal food webs and carbon cycles., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Differences in the structure and functioning of intensively urbanized vs. less human-affected systems are reported, but such evidence is available for a much larger extent in terrestrial than in marine systems. We examined the hypotheses that (i) urbanization was associated to different patterns of variation of intertidal assemblages between urban and extra-urban environments; (ii) such patterns were consistent across mainland and insular systems, spatial scales from 10scm to 100skm, and a three months period. Several trends emerged: (i) a more homogeneous distribution of most algal groups in the urban compared to the extra-urban condition and the opposite pattern of most invertebrates; (ii) smaller/larger variances of most organisms where these were, respectively, less/more abundant; (iii) largest variability of most response variables at small scale; (iv) no facilitation of invasive species by urbanization and larger cover of canopy-forming algae in the insular extra-urban condition. Present findings confirm the acknowledged notion that future management strategies will require to include representative assemblages and their relevant scales of variation associated to urbanization gradients on both the mainland and the islands., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Understanding the mechanisms underlying biological invasions is essential to separate their actual ecological effects from those of other human disturbances. This study examined experimentally whether the non-native red seaweed Grateloupia turuturu is an opportunistic species taking advantage of degraded local conditions (passenger model), or the primary driver of changes in the structure of benthic assemblages (driver model). In a first experiment, traits of G. turuturu likely associated to its invasion success were compared between unmanipulated controls and treatments subjected to the removal of canopy-forming macroalgae to test for the passenger model. In a second experiment, rock pool assemblages where G. turuturu was selectively removed were compared with initially similar control (unmanipulated) assemblages to test for the driver model. Over a period of four months, G. turuturu showed larger cover, higher number of individuals and longer fronds in the canopy-removed compared to the control pools, while no significant differences were detected between assemblages where G. turuturu was continuously removed and those where invasion was allowed to occur. Present findings suggest that G. turuturu would rely on disturbances removing potential native competitors to spread into the recipient habitat, rather than being the main driver of ecological alterations., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

The zoonotic nematode Trichinella britovi has been documented in animals and/or humans of the Mediterranean islands of Corsica and Sardinia since 2004. From 2005 to 2007 in the Sardinia island, several surveys had shown that T. britovi was circulating among backyard and free-ranging pigs reared in the Orgosolo municipality but all attempts had failed to detect this parasite in wild susceptible animals. The aim of the present work was to investigate the circulation of T. britovi in pigs and wildlife of the Orgosolo municipality, and of surrounding municipalities and provinces in the 2010-2014 slaughtering/hunting seasons. The results show that the T. britovi circulation was still restricted to the Orgosolo municipality with a prevalence of 2.6% in free-ranging pigs and 0.2% in backyard pigs but, for the first time, this parasite was detected also in 0.4% of wild boar, and 27.6% of red foxes. No infection was detected in backyard pigs, wild boar, and red foxes of the other municipalities and provinces. Since 1978, African swine fever is endemic in Sardinia and foci of this virus are still active in the investigated areas favoring cannibalism and, consequently, the T. britovi transmission, due to the high mortality rate caused by this virus. This is the first documented report on the transmission of T. britovi between the domestic and the sylvatic cycle. The health authority of the island must provide a service to dispose animal carcasses and offal, stamping out illegal free-ranging pigs, and train hunters and pig owners to manage waste and by-products according to the EU regulations., (Copyright © 2015 Elsevier B.V. All rights reserved.)

The residue levels of fludioxonil (FLU) were determined in pear cultivars Precoce di Fiorano, Coscia, and Spadona estiva after a 2-min dip in an aqueous mixture of FLU containing 300 or 100 mg/liter of active ingredient at 20 or 50 degrees C and after 12 days at 17 degrees C and 80% relative humidity (simulated shelf life conditions). The accumulation trend of FLU residues was determined in 'Precoce di Fiorano' pears after treatments with 25, 50, 100, or 200 mg/liter of active ingredient at 20 or 50 degrees C for 2 min or at 60 degrees C for 1 min. The efficacy of heat treatments with water and FLU was investigated on artificially inoculated 'Precoce di Fiorano', 'Coscia', and 'Spadona estiva' pears for the control of postharvest blue mold and gray mold caused by Penicillium expansum and Botrytis cinerea, respectively. Treatment with 300 mg/liter FLU at 20 degrees C resulted in residue levels similar to those from treatment with 100 mg/liter FLU at 50 degrees C in 'Coscia' fruit but in significantly lower residues in 'Precoce di Fiorano' and 'Spadona estiva' pears. Post-shelf life residues decreased in all cultivars, especially in 'Spadona estiva' pears treated with 300 mg/liter FLU at 20 degrees C. Residue levels of FLU in 'Precoce di Fiorano' pears treated at 20, 50, or 60 degrees C were correlated with fungicide dosage. When an equal rate was used, treatment at 50 degrees C resulted in a higher and a notably higher FLU deposition than that found under treatment at 60 and 20 degrees C, respectively. The in vitro tests showed that both pathogens were very sensitive to FLU, with MICs averaging 0.05 and 0.1 mg/liter for B. cinerea and P. expansum isolates, respectively. The 50% effective concentration ranged between 0.01 and 0.05 mg/liter for B. cinerea and between 0.05 and 0.1 mg/liter for P. expansum. In the in vivo trials, hot water treatment effectively reduced the incidence of both diseases during the first 4 to 8 days, depending on cultivar, dip temperature, and type of inoculum. However, as the incubation time proceeded, decay reduction was generally lower and the benefit of heat treatments was notably reduced or almost lost. In contrast, all treatments with FLU had a long-lasting effect. Treatments with heated FLU were more effective than those with unheated FLU; reduced concentrations of active ingredient were required to achieve a comparable control of blue and gray mold decay in these pears.

Objectives: a positive correlation between cholesterol esterification, acyl-CoA:cholesterol acyltransferase (ACAT), multidrug resistance (MDR1) gene expression and atherosclerotic lesions has been shown in human arteries. The objective of this study was to map the expression of MDR1, ACAT genes and the cholesteryl ester content in normal, atherosclerotic and varicose human vessels., Materials: vascular segments were obtained from seven cadaveric donors, 27 patients undergoing vascular surgery for severe atherosclerotic disease and 11 patients with saphenous vein varicosities., Methods: lipid analysis and RT-PCR of MDR1 and ACAT mRNAs were performed., Results: an increase in cholesteryl ester content and in ACAT and MDR1 expression was demonstrated in relation to the age in the arteries prone to atherosclerosis; this expression was maximal in arteries from symptomatic patients. In resistant arteries and in veins cholesteryl ester accumulation was rare and light, while ACAT and MDR1 expression was not related to the age of the subjects., Conclusions: the results showed that an increase in MDR1 and ACAT expression may be responsible for the accumulation of cholesteryl esters as well as for cell growth rate acceleration in vessel sites prone to atherosclerosis., (Copyright 2001 Harcourt Publishers Limited.)

The ascites hepatoma Yoshida AH130 causes in the host a rapid and progressive body weight loss, associated with reduced food intake, and protein and lipid hypercatabolism. Because insulin regulates glucose as well as lipid and protein metabolism, we suggest that the observed alterations are at least in part secondary to hypoinsulinemia and/or to the increase of counterregulatory hormones in AH130-bearing rats. To verify this hypothesis, controls with free access to food (n = 4), controls with free access to food plus insulin (107 micromol. kg body wt-1. d-1) (n = 4), controls pair-fed to the tumor-bearing rats (n = 4), pair-fed controls treated with insulin (n= 4), tumor hosts (n = 9), and tumor hosts treated with insulin (n = 6) were used. The Yoshida ascites hepatoma cells ( approximately 10(8) cells/rat) were inoculated intraperitoneally. Daily food intake and body weight were measured; insulin was injected starting the day of tumor implantation for 6 d. The metabolism of both cholesterol and lipids was investigated in tumor cells, and ascitic fluid and blood serum were investigated at the end of treatment. Insulin prevented the reduction of food intake (19 +/- 0.6 vs. 13 +/- 0.4 g/d, P < 0.01; AH130 hosts treated and not treated with insulin, respectively), the loss of body weight (202 +/- 12 vs. 135 +/- 9 g, P < 0.01), lowered the circulating triglycerides (48.3 +/- 4.9 vs. 84.5 +/- 7.1 mmol/L, P < 0.01), and free fatty acids (561 +/- 47 vs. 989 +/- 54 mmol/L (P < 0.01), while corrected the decrease of adipose lipoprotein lipase activity (1,240 +/- vs. 300 +/- pmol FA, P < 0.01) observed in AH130 hosts. Moreover, insulin prevented the decrease in HDL cholesterol (13.2 +/- 0.8 vs. 9.3. +/- 0.7 mmol/L, P < 0.01) and significantly increased hepatic cholesterol synthesis as evaluated by 14C-acetate incorporation into cholesterol, in both liver (3,337 +/- 245 vs. 830 +/- 115 Bq/g, P < 0.01) and AH130 cells (11,676 +/- 1,693 vs. 4,196 +/- 527 Bq/10(6) cells, P < 0.01). Thus insulin treatment ameliorated many metabolic derangements, with a lengthening of rats survival time (7 +/- 1 vs. 11 +/- 1 d, P < 0.05) without significantly stimulating tumor growth. These data, together with our previous observations on the effectiveness of insulin on protein turnover perturbations, suggest that many metabolic alterations occurring during cancer cachexia can be avoided by the administration of this hormone.

We have examined the anticonvulsant properties of propofol in high doses in two experimental models of status epilepticus: generalized pentylenetetrazol (PTZ)-induced seizures and partial, cortically applied penicillin G-induced seizures. Propofol was administered either as a single bolus injection or as a bolus injection followed by an infusion for 1 h. When administered as a single bolus injection, propofol 12 mg kg-1 suppressed electrical and clinical seizures in PTZ generalized epileptic status, and an infusion of 50 mg kg-1 h-1 prevented the reappearance of electrical and clinical signs. In focal epileptic status, the single dose stopped paroxysmal activity and the associated clonic jerks for a few seconds. When the bolus dose was followed by an infusion, the firing bursts were replaced by isolated spikes, and contralateral jerks became sporadic and feeble. The greater efficacy of propofol against PTZ convulsions may be a reflection of the opposite action of the two drugs on neural membrane conductance: PTZ induces paroxysmal neural discharge by enhancing membrane conductance while propofol appears to decrease membrane conductance, thus suppressing paroxysmal discharge. There was no close relationship between blood concentration of the anaesthetic and its clinical effects, at least after a short-term infusion, as used in the present experiments. We suggest that propofol may be a potentially useful drug in status epilepticus in patients in whom benzodiazepines, barbiturates and phenytoin have failed.

The ontogeny of muscarinic cholinergic receptors has been studied in different regions of the human fetal brain. For a comparison, the same study has been carried out on newborn and premature brain. Regarding on the areas examined (frontal cortex, cerebellum, hippocampus, thalamus and basal ganglia) either an increase or a decrease of receptor density during gestation was observed. Thus, the ontogeny of the receptors follows a different pattern in areas which differ in function, cholinergic innervation and embryological origin. However, in all the regions the affinity of the binding site for the ligand [3H]quinuclidinyl benzilate [3H]QNB was very similar to that reported for muscarinic receptors from adult mammalian brain. Data obtained from agonist binding (acetylcholine and carbachol) revealed the presence of a high (H)- and a low-affinity binding site (L) from 10 weeks of gestation. The selective antagonist pirenzepine (PZ) also distinguished two different muscarinic receptor subtypes, which however had higher affinity than that seen in adult brain. In conclusion, during ontogeny, the muscarinic acetylcholine receptor shares some but not all of the pharmacological properties shown in the adult brain.

Long-term (20 days) treatment with methyl mercury (MeHg) increases the total number of benzodiazepine binding sites and decreases essentially the content of cyclic GMP in the cerebellar cortex. In contrast, this treatment fails to modify the content of GABA and cyclic AMP, GAD activity and GABA binding sites in the same brain area. The changes in cyclic GMP and benzodiazepine binding sites in the cerebellar cortex are discussed in relation to the motor disturbances associated with MeHg intoxication.