bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lichen and moss communities of Botany Bay, Granite Harbour, Ross Sea, Antarctica
Authors: Seppelt Rodney D. , Türk Roman , Green T.G. Allan , Moser Gerald , Pannewitz Stefan , Sancho Leo G. , Schroeter Burkhard 
Published: August 2010

AbstractBotany Bay is one of the richest sites for lichen and bryophyte biodiversity in continental Antarctica. A total of 29 lichen, nine moss and one liverwort species have been identified. The most extensive vegetation occurs on a sheltered raised beach terrace. Vegetation associations are described and compared to other continental Antarctic localities that also possess a rich vegetation cover. Ordination analysis clearly indicates the importance of the type of water supply, its regularity, the substrate type, and particularly in Botany Bay, the influence of nutrients derived from the local bird population in governing plant distribution and associations. A vegetation map has been produced and can be used as a baseline to assess vegetation changes over time.
Determining habitability: which exoEarths should we search for life?
Authors: Horner J. , Jones B.W. 
Published: August 2010

AbstractWithin the next few years, the first Earth-mass planets will be discovered around other stars. Some of those worlds will certainly lie within the classical ‘habitable zone’ of their parent stars, and we will quickly move from knowing of no exoEarths to knowing many. For the first time, we will be in a position to carry out a detailed search for the first evidence of life beyond our Solar System. However, such observations will be hugely taxing and time consuming to perform, and it is almost certain that far more potentially habitable worlds will be known than it is possible to study. It is therefore important to catalogue and consider the various effects that make a promising planet more or less suitable for the development of life. In this work, we review the various planetary, dynamical and stellar influences that could influence the habitability of exoEarths. The various influences must be taken in concert when we attempt to decide where to focus our first detailed search for life. While there is no guarantee that any given planet will be inhabited, it is vitally important to ensure that we focus our time and effort on those planets most likely to yield a positive result.
Effect of Nitric Oxide Synthase Inhibitors on Lipid Peroxide Formation in Liver Caused by Endotoxin Challenge
Authors: Sakaguchi Shuhei , Furusawa Shinobu , Yokota Katsushi , Sasaki Ken‐ichi , Takayanagi Motoaki , Takayanagi Yoshio 
Published: August 2010

Abstract:This study investigated the effect of nitric oxide on lipid peroxide formation during endotoxaemia. Nitric oxide synthase inhibitors NG‐monomethyl‐L‐arginine acetate (L‐NMMA, 20 mg/kg, intravenously), NG‐nitro‐L‐arginine‐methyl ester (L‐NAME, 10 mg/kg, intravenously), and NG‐nitro‐L‐arginine (L‐NA, 10 mg/kg, intravenously), and a relatively selective inducible nitric oxide synthase inhibitor aminoguanidine (10 mg/kg, intravenously), did not protect against endotoxin‐induced death of mice. Superoxide dismutase activity in liver 18 hr after administration of endotoxin (6 mg/kg, intraperitoneally) to L‐arginine analogues (L‐NMMA, L‐NAME, L‐NA)‐treated mice was lower than in mice treated with endotoxin alone, whereas the administration of L‐arginine analogues increased xanthine oxidase activity in the livers of endotoxin‐injected mice compared with mice treated with endotoxin alone. In mice treated with L‐arginine analogues and aminoguanidine, the levels of non‐protein sulfhydryl and lipid peroxide in liver 18 hr after endotoxin injection did not show significant differences from mice treated with endotoxin alone. L‐Arginine analogues and aminoguanidine had little effect on lipid peroxide formation in liver caused by endotoxin. Treatment with aminoguanidine (300 μM) significantly inhibited endotoxin‐induced intracellular peroxide in J774A.1 cells, however, aminoguanidine did not affect endotoxin‐induced cytotoxicity in J774A.1 cells. Our results clearly demonstrate that treatment with catalase (10 μg/ml), D‐mannitol (10 mM), or superoxide dismutase (100 U/ml), has little or no effect on nitric oxide production by endotoxin (1 μg/ml)‐activated J774A.1 cells. These findings suggest that nitric oxide is not crucial for lipid peroxide formation during endotoxaemia. Therefore, it is unlikely that nitric oxide plays a significant role in liver injury caused by free radical generation in endotoxaemia.
The Effect of Aminophylline on Right Heart Function in Young Pigs after Ligation of the Right Coronary Artery
Authors: Spalding Michael B. , Ala‐Kokko Tero I. , Kiviluoma Kai , Ruskoaho Heikki , Alahuhta Seppo 
Published: August 2010

Abstract:An experimental model of right heart failure was developed to determine the effects of fluid loading and aminophylline on right heart function. We hypothesised that aminophylline would specifically improve right heart function through a decrease in pulmonary vascular resistance and, possibly, an increase in cardiac contractility. Right heart infarct was induced in ten experimental pigs and seven control pigs by ligating branches of the right coronary artery. The effect of fluid loading with a colloid solution and subsequent bolus doses of aminophylline on haemodynamics was observed. Fluid loading improved haemodynamics as expected. Aminophylline transiently improved cardiac index and pulmonary vascular resistance, but simultaneously caused an increase in heart rate and a decrease in stroke volume. Although aminophylline may reduce right heart afterload, it did not improve overall cardiac function in this experimental model of right heart infarction.
Evaluation of Flutamide Genotoxicity in Rats and in Primary Human Hepatocytes
Authors: Martelli Antonietta , Brambilla Campart Giulia , Carrozzino Roberto , Ghia Marco , Mattioli Francesca , Mereto Eugenio , Orsi Patrizia , Porta Puglia Cristina 
Published: August 2010

Abstract:Flutamide, an effective competitive inhibitor of the androgen receptor used orally for palliative treatment of prostatic carcinoma and regulation of prostatic hyperplasia was evaluated for its genotoxic effects in the intact rat and in primary cultures of human hepatocytes. Negative responses were obtained in all the in vivo assays as well as in the in vitro assay. In rats given a single oral dose of 500 mg/kg flutamide, fragmentation and repair of liver DNA were absent, and no increase was observed in the frequency of micronucleated hepatocytes. In the liver of rats given flutamide as initiating agent at the dose of 500 mg/kg/week for 6 successive weeks, γ‐glutamyltraspeptidase‐positive foci were detected only in 3 of 10 rats. There was no evidence of a promoting effect on the development of aberrant crypt foci in rats given 100 mg/kg flutamide on alternate days for 8 successive weeks. In primary cultures of human hepatocytes from one male and one female donor DNA fragmentation as measured by the Comet assays, and DNA repair synthesis as revealed by quantitative autoradiography, were absent after a 20 hr exposure to flutamide concentrations ranging from 18 to 56 μM. Taken as a whole, our results seem to indicate that flutamide is a non‐genotoxic drug.
Nitric Oxide Protects Murine Embryonic Liver Cells (BNL CL.2) from Cytotoxicity Induced by Glucose Deprivation
Authors: Pae Hyun‐Ock , Kim Hong‐Gone , Paik Young‐Suk , Paik Sang‐Gi , Kim Young‐Myeong , Oh Gi‐Su , Chung Hun‐Taeg 
Published: August 2010

Abstract:We investigated the protective effects of nitric oxide on cell death of murine embryonic liver cells (BNL CL.2) after glucose deprivation. Endogenous nitric oxide production by BNL CL.2 cells was induced by 6 hr pretreatment with interferon‐gamma and lipopolysaccharide. We used sodium nitroprusside and S‐nitroso‐L‐glutathione as exogenous nitric oxide‐generating compounds. All agents were used at doses that did not show direct cytotoxicity as measured by crystal violet staining assay. In the BNL CL.2 cells, the viability dropped very steeply after 24 hr incubation with glucose‐free media. Endogenous nitric oxide produced by treatment of the cells with interferon‐gamma and lipopolysaccharide protected the cells from glucose deprivation‐induced cytotoxicity, but did not protect them in the presence of the nitric oxide synthesis inhibitor, NG‐monomethyl‐L‐arginine. Exogenous nitric oxide protected the cells from glucose deprivation‐induced cytotoxicity in a concentration‐dependent manner. Cytoprotection by nitric oxide donors was abolished by the use of nitric oxide scarvenger, 2‐phenyl‐4,4,5,5,‐tetramethylimidazole, but not by the soluble guanosine cyclase inhibitor, 1H‐[1,2,4]oxadiazole[4,3‐a]quinoxalin‐1‐one. In addition, cytoprotective effects comparable to endogenous or exogenous nitric oxide were not observed when the cells were incubated with dibutyl guanosine 3′,5′‐cyclic monophosphate. Based upon these results, we suggest that nitric oxide may enhance the cell survival of BNL CL.2 cells after glucose deprivation via a guanosine 3′,5′‐cyclic monophosphate‐independent pathway.
Ultrastructural Evidence of the Protective Effect of Na+/H+ Exchange Inhibition on the in vitro Damage Induced by Ischaemia Reperfusion in the Interventricular Septum of the Rabbit Heart
Authors: Salinas Pedro , Gil‐Loyzaga Pablo , Barrigon Santos 
Published: August 2010

Abstract:We investigated the effects of the Na+/H+ antiporter inhibitor, dimethylamiloride, on myocardial injury after 1 h global ischaemia and 30 min. reperfusion in the isolated arterially perfused interventricular septum of the rabbit heart. After ischaemia and reperfusion challenge, dimethylamiloride significantly increased the recovery of developed tension in a dose‐dependent manner, and significantly decreased the maximal increase in resting tension. Ultrastructural analysis of myocytes submitted to the experimental in vitro model supported functional maintenance of physiologically‐like conditions. Where myocardial portions were submitted to ischaemic conditions and reperfusion, myocyte cell damage reached usual characteristics of infarct‐like induced lesions. Intracellular oedema, severe disruption of myofibrils with loss of muscle striation and both swelling and fragmentation of mitochondria were the main characteristics observed. Dimethylamiloride treatment clearly modifies ultrastructural findings towards the normalization of cell shape and structure, only a slight‐middle intracellular oedema and contraction bands were found. On the basis of the present results, we suggest that the protective effects exhibited by dimethylamiloride on the ischaemic myocardium are compatible with its Na+/H+ antiporter inhibition properties, they diminish Na+ accumulation and then either Ca2+ overload or non‐exocytotic noradrenaline release during the ischaemia and reperfusion challenge.
Dose‐Dependent Protection by Lipoic Acid against Cisplatin‐Induced Nephrotoxicity in Rats: Antioxidant Defense System
Authors: Somani Satu M. , Husain Kazim , Whitworth Craig , Trammell Gary L. , Malafa Mokenge , Rybak Leonard P. 
Published: August 2010

Abstract:This study was designed to investigate the role of graded doses of lipoic acid pretreatment against cisplatin‐induced nephrotoxicity. Male Wistar rats were divided into six groups and treated as follows: 1) vehicle (saline) control; 2) cisplatin (16 mg/kg, intraperitoneally); 3) lipoic acid (100 mg/kg, intraperitoneally); 4) cisplatin plus lipoic acid (25 mg/kg); 5) cisplatin plus lipoic acid (50 mg/kg) and 6) cisplatin plus lipoic acid (100 mg/kg). Rats were sacrificed three days after treatment, and plasma as well as kidneys were isolated and analyzed. Plasma creatinine increased (677% of control) following cisplatin administration alone which was decreased by lipoic acid in a dose‐dependent manner. Cisplatin‐treated rats showed a depletion of renal glutathione (GSH), increased oxidized GSH and decreased GSH/GSH oxidized ratio (62%, 166% and 62% of control), respectively which were restored with lipoic acid pretreatment. Renal superoxide dismutase, catalase, glutathione peroxidase (GSH peroxidase) and glutathione reductase activities decreased (62%, 75%, 62% and 80% of control), respectively, and malondialdehyde content increased (204% of control) following cisplatin administration, which were restored with increasing doses of lipoic acid. The renal platinum concentration increased following cisplatin administration, which was possibly decreased by chelation with lipoic acid. The data suggest that the graded doses of lipoic acid effectively prevented a decrease in renal antioxidant defense system and prevented an increase in lipid peroxidation, platinum content and plasma creatinine concentrations in a dose‐dependent manner.
Age‐Dependent Induction of Aberrant Crypt Fociin Rat Colon by 2‐Amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine and Azoxymethane
Authors: Paulsen Jan Erik , Fulland Randi Cathrine , Alexander Jan 
Published: August 2010

Abstract:Pups and adult rats received seven oral exposures (three time weekly) of the food mutagen PhIP (50 mg/kg), or two subcutaneous exposures (once weekly) of the experimental carcinogen azoxymethane (3.75 mg/kg). Aberrant crypt foci (ACF) were scored 8 weeks after the first exposure. In addition, lactating dams with suckling pups were orally exposed to 50 mg/kg of PhIP, three times weekly for three weeks. Direct PhIP exposure of pups induced 2.2 times more ACF than similar exposure of adult rats (2.0±0.0 versus 0.9±0.8, P<0.05). The growth of ACF, expressed as crypt multiplicity AC/ACF, was 3.5 times larger in neonatally exposed rats than in rats exposed in adulthood (8.0±7.3 versus 2.3±1.6, P<0.05). PhIP exposure via breast milk induced ACF in 3 of 25 animals. However, the difference versus controls, which had no ACF, did not reach statistical significance. Contrary to PhIP, azoxymethane induced more ACF in adult rats than in pups (2.8±1.9 versus 4.8±1.7, P<0.05). Similarly to PhIP however, azoxymethane induced 3.2 times larger ACF (AC/ACF) in pups than in adult rats (11.9±8.4 versus 3.7±1.9, P<0.001). Whereas no PhIP‐induced ACF (0/15) were observed in the lymphoid follicles, approximately 60% of the azoxymethane‐induced ACF (32/56) were located in these structures. This difference was statistically significant (P<0.001). The density of azoxymethane‐induced ACF was 80 times larger in the lymphoid follicles than in the surrounding mucosa (P<0.01). Based on the assumption that the formation of ACF with high multiplicity is predicative for the tumour development we conclude that neonatal rats are more susceptible to PhIP and azoxymethane than adult rats.
Is the 5‐HT2C Receptor a Therapeutic Target in Cerebral Ischaemia?
Authors: Torup Lars , Diemer Nils Henrik 
Published: August 2010

Abstract:This study examines the effect of a 5‐HT2C agonist (RO 60–0175, (s)‐2‐(chloro‐5‐fluoro‐indol‐1‐yl)‐1‐methylethylamine) and a 5‐HT2C antagonist (RO 43–0440, benzofuran‐2‐carboxamidine) for neuroprotective activity in a rat model of global cerebral ischaemia. A mini‐osmotic pump implanted subcutaneously delivered 0.25 mg/kg/hr. Seven days after ischaemia the rats were sacrificed and the damage in the CA1 pyramidal cell layer in hippocampus was estimated and the treated groups were compared with vehicle groups. Pretreatment with the 5‐HT2C agonist RO 60–0175 significantly increased the damage, whereas the 5‐HT2C antagonist RO 43–0440 had no effect on the cell damage. Measurement of the core temperature in a RO 60–0175‐treated group of rats revealed no effect compared to a vehicle‐treated group. Thus the aggravation of damage in the RO 60–0175‐treated group cannot be explained by temperature effect. Our data do not indicate the 5‐HT2C receptor as a therapeutic target in cerebral ischaemia.
Evidence for a Trigger Function of Valproic Acid in Xenobiotic‐Induced Hepatotoxicity
Authors: Klee Sabine , Johanssen Sandra , Ungemach Fritz Rupert 
Published: August 2010

Abstract:The influence of the antiepileptic drug, valproic acid (2‐n‐propylpentanoic acid), on the hepatocellular capacity, to cope with an extrinsic oxidative stress was investigated. Freshly isolated rat hepatocytes exposed to therapeutic concentrations of valproic acid (0.25–1.0 mmol/l) were less resistant than controls, as evidenced by a significant cytotoxic response after challenge of the cells with a non‐toxic dose of allyl alcohol (2‐propen‐1‐ol). Valproic acid alone was not toxic to hepatocytes even at ten times higher concentrations (10 mmol/l), suggesting that cell damage was not a mere additive effect. Incubation with valproic acid plus allyl alcohol induced an irreversible depletion of hepatocellular glutathione, in contrast to allyl alcohol alone which induced a transient loss. Hepatocytes treated with valproic acid plus allyl alcohol were protected by N‐acetylcysteine, a precursor of glutathione. These findings indicate that valproic acid affects hepatocellular defence mechanisms and suggest that a predisposition of hepatocytes to oxidative stress may play a role in the fatal hepatotoxicity of valproic acid in epileptic patients.
Comparison of in vitro and in vivo Developmental Toxicity and Pharmacokinetics of Phenytoin in the Rat
Authors: Beekhuijzen Manon E. W. , Verhoef Aart , Klaassen Rob , Rompelberg Cathy J. M. , Piersma Aldert H. 
Published: August 2010

Abstract:The rat whole embryo culture was compared to an in vivo experiment with regard to embryotoxicity as well as exposure characteristics, using phenytoin as a model compound. Intra‐embryonic concentrations and their embryotoxic effects were determined on gestation day 11 after in vitro administration of 50–150 μg/ml or in vivo gavage of 500–1500 mg/kg body‐weight on gestation day 10. In addition, exposure kinetics were studied in vivo after a single oral dose on gestation day 10, and developmental defects on gestation day 21 were scored. The embryotoxic effects observed on gestation day 11 were more pronounced after in vitro exposure in comparison to in vivo exposure at similar intra‐embryonic concentrations. Exposure of phenytoin on gestation day 10 in vitro via the culture medium resulted in general embryotoxicity on gestation day 11, whereas in vivo effects as determined on gestation day 11 were minimal. Plasma concentrations of phenytoin increased and plateaued around 35 μg/ml during the 48 hr monitoring period. Plasma concentration curves and pharmacokinetic parameters did not show remarkable differences between the dose groups, indicating that absorption is the limiting factor at the dose range used. Although the developmental effects were minimal as observed in vivo on gestation day 11, specific malformations (defects encompassing the urogenital, craniofacial and skeletal systems) were observed on gestation day 21. These findings show that with similar intra‐embryonic concentrations of phenytoin the embryotoxicity in rat whole embryo culture was not comparable with the in vivo embryotoxicity as determined on gestation day 11. This discrepancy may at least partly be explained by differences in exposure characteristics.
Involvement of Iron (Ferric) Reduction in the Iron Absorption Mechanism of a Trivalent Iron‐Protein Complex (Iron Protein Succinylate
Authors: Raja Kishor B. , Jafri Shanaz E. , Dickson Dominic , Acebròn Alvaro , Cremonesi Piero , Fossati Gianluca , Simpson Robert J. 
Published: August 2010

Abstract:Iron protein succinylate is a non‐toxic therapeutic iron compound. We set out to characterise the structure of this compound and investigate the importance of digestion and intestinal reduction in determining absorption of the compound. The structure of the compound was investigated by variable temperature Mössbauer spectroscopy, molecular size determinations and kinetics of iron release by chelators. Intestinal uptake was determined with radioactive compound force fed to mice. Reduction of the compound was determined by in vitro incubation with intestinal fragments. The compound was found to contain only ferric iron, present as small particles including sizes below 10 nm. The iron was released rapidly to chelators. Digestion with trypsin reduced the molecular size of the compound. Intestinal absorption of the compound was inhibited by a ferrous chelator (ferrozine), indicating that reduction to ferrous iron may be important for absorption. The native compound was a poor substrate for duodenal reduction activity, but digestion with pepsin, followed by pancreatin, released soluble iron complexes with an increased reduction rate. We conclude that iron protein succinylate is absorbed by a mechanism involving digestion to release soluble, available ferric species which may be reduced at the mucosal surface to provide ferrous iron for membrane transport into enterocytes.
Effects of Neonatal Ganglioside GM1 Administration on Memory in Adult and Old Rats
Authors: Silva Regina H. , Bergamo Marcelo , Frussa‐Filho Roberto 
Published: August 2010

Abstract:Numerous investigations have been reporting the involvement of GM1 ganglioside in central nervous system development and memory formation. The effects of neonatal treatment with GM1 ganglioside on the performance of adult rats in a plus‐maze discriminative avoidance task and old rats in a step‐down passive avoidance task were investigated. Rats were injected subcutaneously from day 3 to 15 after birth with 10 mg/kg GM1 or saline. GM1 treatment did not modify indicative landmarks of physical and motor development. Behavioural tasks were carried out when the animals were 4 (discriminative avoidance) or 24 (passive avoidance) months old. Discriminative avoidance conditioning was performed in a modified elevated plus‐maze. During the training session, the animals received aversive stimulation (light and hot air blow) in one of the enclosed arms. Tests were performed 7, 14 and 21 days after conditioning (tests 1, 2 and 3), in the absence of the aversive stimulation. In all tests, GM1‐treated animals spent less time in the aversive arm than in the non‐aversive enclosed arm. Control animals, however, spent a shorter time in the aversive arm only in tests 1 and 2. Passive avoidance conditioning was performed in an acrylic box with a grid floor, that was partially covered by an inclined platform. Animals were placed on the platform and received a 0,5 mA foot shock when stepped down. A test was performed 48 hr later. Latency to step down presented by GM1‐treated animals was significantly higher in the test session, whereas no significant increase in latency to step down was found for control animals. The results suggest a possible action of GM1 on the maturation of the central nervous system that persists during adulthood and ageing.
2‐Phenylmelatonin: A Partial Agonist at Enteric Melatonin Receptors
Authors: Santagostino‐Barbone Maria Grazia , Masoero Elisabetta , Spelta Valeria , Lucchelli Adele 
Published: August 2010

Abstract:The effect of the melatonin receptor ligand, 2‐phenylmelatonin, has been assessed in isolated strips of the guinea‐pig proximal colon. 2‐Phenylmelatonin (0.01 nM‐1 μM) caused a concentration‐dependent contractile response. The potency value (−log EC50) was 9.3±1.0. The maximum effect was 25±4% of that elicited by the maximally effective concentration (0.3 μM) of 5‐HT and 43±3% of that by the maximally effective concentration (10 μM) of melatonin. When used as an antagonist, 2‐phenylmelatonin (0.01 nM and 0.1 nM) concentration‐dependently inhibited melatonin‐induced contractions with depression of the maximum response by 25% and 54%, respectively. Higher (1 nM) 2‐phenylmelatonin concentrations failed to antagonize melatonin‐induced response. Prazosin (0.3 μM), a selective antagonist of melatonin MT3 sites, antagonized melatonin‐induced contractions to an extent similar to that induced by 0.01 nM 2‐phenylmelatonin (with 30% reduction of the maximum effect to melatonin). The combination of 0.3 μM prazosin and 0.01 nM 2‐phenylmelatonin caused antagonism similar in extent to that caused by each individual antagonist. 2‐Phenylmelatonin at subnanomolar concentrations behaves as an antagonist of melatonin‐induced contractile responses while at nanomolar/micromolar concentrations it behaves as a weak contractile agonist.