bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reducing DUI among US college students: results of an environmental prevention trial
Authors: Clapp John D. , Johnson Mark , Voas Robert B. , Lange James E. , Shillington Audrey , Russell Cristel 
Published: February 2005

ABSTRACTAims  Driving under the influence (DUI) of alcohol is among the most common and serious alcohol‐related problems experienced by US college students. Community‐based prevention trials using environmental approaches to DUI prevention have been effective in reducing DUI. Such interventions remain untested in college settings. This study is the first to test the efficacy of an environmental prevention campaign to reduce DUI among college students.Design  We used a quasi‐experimental non‐equivalent comparison group design to test the efficacy of the DUI prevention intervention. Students at the experimental university were exposed to a DUI prevention intervention that included a social marketing campaign, a media advocacy campaign and increased law enforcement (DUI checkpoints and roving DUI patrols).Setting  Students from two large public universities located along the US/Mexico border participated in the seven‐semester study.Participants  In total, 4832 college students took part.Measures  Using telephone interviews of randomly selected students, we took pre‐ and postintervention measures of self‐reported DUI.Findings  Self‐reported DUI (past year) decreased significantly from pre‐test to post‐test (odds ratio = 0.55) at the intervention school, whereas rates at the comparison campus remained stable. The campus–intervention interaction was statistically significant (P < 0.05), suggesting that the campaign led to the observed change in DUI.Conclusions  Environmental DUI campaigns similar to those validated in community prevention trials can be effective in college settings. Further research, however, is needed to determine the robustness of the changes associated with such campaigns.
The role of the therapeutic alliance in the treatment of substance misuse: a critical review of the literature
Authors: Meier Petra S. , Barrowclough Christine , Donmall Michael C. 
Published: February 2005

ABSTRACTBackground  In the past two decades, a number of studies investigating the role of the therapeutic alliance in drug treatment have been published and it is timely that their findings are brought together in a comprehensive review.Aims  This paper has two principal aims: (1) to assess the degree to which the relationship between drug user and counsellor predicts treatment outcome and (2) to examine critically the evidence on determinants of the quality of the alliance.Methods  Peer‐reviewed research located through the literature databases Medline, PsycInfo and Ovid Full Text Mental Health Journals using predefined search‐terms and published in the past 20 years is considered. Further papers were identified from the bibliographies of relevant publications.Findings  A key finding is that the early therapeutic alliance appears to be a consistent predictor of engagement and retention in drug treatment. With regard to other treatment outcomes, the early alliance appears to influence early improvements during treatment, but it is an inconsistent predictor of post‐treatment outcomes. There is relatively little research on the determinants of the alliance. In studies that are available, clients’ demographic or diagnostic pre‐treatment characteristics did not appear to predict the therapeutic alliance, whereas modest but consistent relationships were reported for motivation, treatment readiness and positive previous treatment experiences.Conclusions  The therapeutic alliance plays an important role in predicting drug treatment process outcomes, but too little is known about what determines the quality of the relationship between drug users and counsellors.
High‐dose glucose‐insulin‐potassium treatment reduces myocardial apoptosis in patients with acute myocardial infarction
Authors: Zhang L. , Zhang L. , Li Y. H. , Zhang H. Y. , Chen M. L. , Gao M.‐M. , Hu A. H. , Yang H. S. , Yang H. S. 
Published: February 2005

AbstractBackground  Several clinical trials have suggested that a metabolic cocktail of glucose‐insulin‐potassium (GIK) decreases mortality rates in patients with acute myocardial infarction (AMI). It has also been reported that Fas‐mediated apoptosis plays an important role in ischaemic/reperfusion injury in the rat model. This study was designed to evaluate the interaction of ischaemic/reperfusion and reperfusion therapy coadministered with high‐dose GIK treatment on soluble Fas/APO‐1 (sFas) and Fas ligand (sFasL) plasma concentration in patients with AMI.Materials and methods  Seventy‐four patients presenting with AMI who underwent reperfusion therapy were randomized into a GIK group (n = 35) receiving high‐dose GIK for 24 h or a vehicle group (n = 39). Thirty‐four control subjects were also enrolled in the present study. Strepavidin‐biotin ELISA was used to determine the soluble sFas and sFasL plasma concentration at baseline, 24 h (h), 3 day (d), 7 d and 14 d.Results  Soluble Fas and sFas‐L serum concentrations ([sFas] and [sFas‐L]) of patients with AMI were significantly elevated at baseline as compared with normal controls (NCs; P < 0·01 vs. NC). The sFas in the GIK and vehicle groups markedly decreased 24 h after the GIK infusion (10·7→5·9 ng mL−1 and 9·7→6·5 ng mL−1; P < 0·01 vs. baseline) and then increased during the 3–7‐d period (5·9→12·1 ng mL−1 and 6·5→11·1 ng mL−1; P < 0·01 vs. 24 h). The GIK group demonstrated reduced sFas (12·1→5·9 ng mL−1) at 14 d (P < 0·01 vs. 7 d), with no concomitant changes in the vehicle group. The sFas‐L in the GIK and vehicle groups was not significant different during the 14‐d period.Conclusions  These results indicate that the sFas and sFasL in patients with AMI increased significantly compared with NC. Owing to the cardioprotective effects reported here and by others, a high‐dose GIK infusion co‐administered with the timely re‐establishment of nutritive perfusion should be strongly considered as a treatment of choice for AMI. Additionally, sFas may be a valuable marker of the physiological response to ischaemic/reperfusion injury and reperfusion associated with high‐dose GIK treatment.
Tissue‐specific regulation of lipoprotein lipase in humans: effects of fasting
Authors: Ruge T. , Svensson M. , Eriksson J. W. , Olivecrona G. 
Published: February 2005

AbstractBackground  We have previously reported that the activity of lipoprotein lipase (LPL) measured in postheparin plasma from humans fasted for 30 h is increased relative to the fed state. This is in contrast to laboratory animals, where the strong down‐regulation of LPL in their adipose tissue on fasting is reflected in decreased levels of LPL activity in postheparin plasma.Materials and methods  To search for the tissue source of the increase in LPL activity on fasting of humans, young, healthy subjects were fasted for 10, 20 or 30 h, and LPL was measured in plasma (pre‐ and postheparin) and in biopsies from subcutaneous adipose tissue (abdominal) and from a skeletal muscle (tibialis anterior). Both LPL activity and LPL protein mass were measured in the tissue homogenates. Values after fasting were compared with values from postprandial samples obtained 2 h after a meal.Results  Fasting for up to 30 h did not alter LPL activity in basal plasma (preheparin). LPL activity in postheparin plasma remained unchanged after 10 and 20 h of fasting, but was increased by 50% after 30 h (P < 0·05). Ten hours of fasting caused a 25% (P < 0·05) decrease in LPL activity in subcutaneous adipose tissue, while LPL activity in skeletal muscle remained unchanged. After 30 h of fasting, both LPL activity and mass had decreased by approximately 50% (P < 0·05) in adipose tissue, but had increased by approximately 100% (P < 0·05) in muscle.Conclusions  The increase in postheparin plasma LPL activity after 30 h of total food deprivation of healthy human subjects seemed to reflect an increased activity and mass of LPL in skeletal muscle.
Molecular mechanisms activating muscle protein degradation in chronic kidney disease and other catabolic conditions
Authors: Du J. , Hu Z. , Mitch W. E. 
Published: February 2005

AbstractMuscle atrophy is a prominent feature of chronic kidney disease (CKD) and is frequent in other catabolic conditions. Results from animal models of these conditions as well as patients indicate that atrophy is mainly owing to accelerated muscle proteolysis in the ubiquitin‐proteasome (Ub‐P'some) proteolytic system. The Ub‐P'some system, however, rapidly degrades actin or myosin but cannot breakdown actomyosin or myofibrils. Consequently, another protease must initially cleave the complex structure of muscle. We identified caspase‐3 as an initial and potentially rate‐limiting proteolytic step that cleaves actomyosin/myofibrils to produce substrates degraded by the Ub‐P'some system. In rodent models of CKD and other catabolic conditions, we find that caspase‐3 is activated and cleaves actomyosin to actin, myosin and their fragments. This initial proteolytic step in muscle leaves a characteristic footprint, a 14‐kDa actin band, providing a potential diagnostic tool to detect muscle catabolism. We also found that stimulation of caspase‐3 activity depends on inhibition of IRS‐1‐associated phosphatidylinositol 3‐kinase (PI3K) activity; inhibiting PI3K in muscle cells also leads to expression of a critical E3‐ubiquitin‐conjugating enzyme involved in muscle protein breakdown: atrogin‐1/MAFbx. Thus, protein breakdown by caspase‐3 and the ubiquitin‐proteasome system in muscle are stimulated by the same signal: a low PI3K activity. These responses could yield therapeutic strategies to block muscle atrophy.
Improvement of portal hypertension and hepatic blood flow in cirrhotic rats by oestrogen
Authors: Sakamoto M. , Ueno T. , Nakamura T. , Sakata R. , Hasimoto O. , Torimura T. , Sata M. 
Published: February 2005

AbstractBackground  In this study, we investigated the effects of oestrogen on nitric oxide synthase activity and nitric oxide production using the cirrhotic rat liver.Material and methods  Cirrhosis was induced by dimethylnitrosamine. Estradiol valerate was subcutaneously injected twice at week 4 after dimethylnitrosamine treatment. Furthermore, subcutaneous injection of an oestrogen receptor antagonist, ICI‐182·780, was performed 2 days before administration of estradiol valerate. Portal pressure and hepatic blood flow were measured. Nitric oxide synthase activity was assessed by l‐citrulline generation. Sinusoidal endothelial cells were isolated from the cirrhotic rat liver and cultured. The cells were incubated with estradiol and/or ICI‐182·780 for 24 h. Images for nitric oxide in sinusoidal endothelial cells were obtained using diaminofluorescein‐2 diacetate.Results  Cirrhotic rats treated with estradiol valerate showed a significant decrease in portal pressure and a significant increase in hepatic blood flow compared with those of control cirrhosis rats. However, in cirrhotic rats treated with ICI‐182·780, the reduction of portal pressure and elevation of hepatic blood flow were completely inhibited. In cirrhotic rats treated with estradiol valerate, nitric oxide synthase activity was increased compared with that in control cirrhotic rats. The fluorescent level of intracellular nitric oxide in estradiol‐stimulated, cultured, sinusoidal endothelial cells was higher than that in nontreated sinusoidal endothelial cells.Conclusions  The present study indicated that oestrogen plays an important role in the enhancement of nitric oxide production in sinusoidal endothelial cells of cirrhotic liver and reduces the portal pressure in cirrhotic rats.
Correlations between Ontogenetic Change in Color Pattern and Antipredator Behavior in the Racer, Coluber constrictor
Authors: Creer Douglas A. 
Published: February 2005

AbstractDifferences in snake color pattern have been demonstrated to affect behaviors involved in antipredator defense. Snakes with blotched or banded color patterns are concealed when not moving, and tend to rely on concealment and aggression for defense. In contrast, snakes with uniform or striped color patterns are easily seen when stationary, but their speed and direction are difficult to track when moving. They tend to rely on flight for protection. Some snake taxa exhibit ontogenetic change in color pattern, but the behavioral consequences of this change have not been investigated. I present results of a behavioral study in the racer, Coluber constrictor, which has a blotched juvenile color pattern but is uniformly colored as an adult. Hatchling racers were significantly more likely than adults to show aggressive behavior when confronted with a model predator, whereas adults were more likely to flee. This supports the hypothesis that changes in behavior and color pattern are correlated in this species to provide effective antipredator defense at different stages of life history. I also examined sprint speed, which may be an important factor in antipredator defense. Juvenile and adult racers showed a similar relationship between length and speed, a pattern also seen in other species that lack color change. This result suggests that sprint speed is not a causal factor in the evolution of ontogenetic color change.
Regulation and Non‐Toxicity of the Spit from the Pale Spitting Spider Scytodes Pallida (Araneae: Scytodidae)
Authors: Clements Reuben , Li Daiqin 
Published: February 2005

AbstractThe pale spitting spider Scytodes pallida (Aranae: Scytodidae) has a unique habit of spitting a glue‐like and possibly toxic substance at its prey to render them immobile prior to envenomation. Quantitative behavioural studies involving the spit, a first for S. pallida, demonstrate that the spider regulates its spit expenditure when offered prey of variable sizes and struggling intensities. This behaviour interestingly mirrors the regulation of venom expenditure according to prey sizes and difficulties exhibited in other non‐spitting spiders. The spit, however, did not appear to have any toxic effects on different prey types exposed to the spit, opposing the long‐standing belief that the spit from scytodids can poison prey.
Delay of myelin formation in arylsulphatase A‐deficient mice
Authors: Yaghootfam Afshin , Gieselmann Volkmar , Eckhardt Matthias 
Published: February 2005

AbstractMetachromatic leukodystrophy (MLD) is a lysosomal storage disorder caused by the deficiency of arylsulphatase A (ASA). This leads to the accumulation of the sphingolipid 3‐O‐sulphogalactosylceramide (sulphatide) and progressive demyelination in the nervous system of MLD patients. The mechanisms and development of pathology in the disease are still largely unknown. In this study we investigate how the inability to degrade sulphatide affects the formation of myelin in ASA‐deficient (ASA–/–) mice. In mice at 2 weeks of age there was a substantial reduction in myelin basic protein (MBP) mRNA and protein. This was confirmed by an immunohistochemical analysis. MBP mRNA and protein, however, reach normal levels at 3 weeks of age. Proteolipid protein (PLP) and MAL mRNA were also reduced in ASA–/– mice at 2 weeks of age; whereas the level of PLP mRNA was normal at 26 weeks of age, MAL mRNA expression remained reduced up to this age. In situ hybridization revealed no significant changes in the number of myelinating oligodendrocytes or oligodendrocyte precursor cells in ASA–/– mice. These results suggest that oligodendrocyte differentiation was normal in ASA–/– mice. No differences were found in the expression of the sulphatide synthesizing enzymes cerebroside sulphotransferase and UDP‐galactose : ceramide galactosyltransferase. Our data demonstrate a delay in myelin formation in ASA–/– mice. This raises the possibility that similar alterations in MLD patients may contribute to the pathology of the disease.
Novel transcription factor Satb2 interacts with matrix attachment region DNA elements in a tissue‐specific manner and demonstrates cell‐type‐dependent expression in the developing mouse CNS
Authors: Britanova Olga , Akopov Sergey , Lukyanov Sergey , Gruss Peter , Tarabykin Victor 
Published: February 2005

AbstractSatb1 is a first cell‐type‐specific transcription factor of a novel type that functions as a regulator of the transcription of large chromatin domains. We identified a close homologue of Satb1, Satb2, in a cDNA subtraction screening in a search for genes controlling neural differentiation. Satb2 showed 61% amino‐acid homology to Satb1. Satb2 and Satb1 expression was detected in different cell subpopulations of developing mouse CNS in a mutually exclusive manner. In the electrophoretic mobility shift assay we demonstrate that nuclear extracts from the embryonic day 18.5 mouse developing neocortex, in contrast to basal ganglia, contain a protein complex interacting with matrix attachment region DNA elements (MARs) with high affinity. Endogenous Satb2 protein is a part of this complex. In the developing neocortex Satb2 was detected largely in the superficial layers. In the developing spinal cord Satb2 expression marks a subpopulation of Lbx1‐positive neurons dorsally and a subgroup of Isl1‐positive neurons ventrally. In the Lbx1 mutants Satb2 expression is greatly reduced. We suggest that Satb2 may regulate differentiation of subsets of neurons at the level of higher order chromatin structure via binding to MARs.
Low doses of bromo‐ and iododeoxyuridine produce near‐saturation labeling of adult proliferative populations in the dentate gyrus
Authors: Burns Kevin A. , Kuan Chia‐Yi 
Published: February 2005

AbstractCell proliferation can be detected by the incorporation of tritiated thymidine (3H‐dT) or halopyrimidines during DNA synthesis in progenitor cells. Administration of two thymidine analogues at different times can further determine the cell‐cycle kinetics of proliferating cells. Traditionally, this was done by combining bromodeoxyuridine (BrdU) immunocytochemistry and 3H‐dT autoradiography, or by BrdU and iododeoxyuridine (IdU) double‐labeling using two mouse antibodies. However, these methods either require lengthy exposure time or involve complicated histological procedures for differentiating between two antibodies of the same species. Here we report a simple and reliable method of distinguishing BrdU‐ and IdU‐labeled cells by immunofluorescence. This method uses a mouse monoclonal antibody that recognizes both BrdU and IdU and a rat anti‐BrdU antibody that has no cross‐reactivity with IdU. When combined with species‐specific secondary antibodies that are conjugated to different fluorophores, this method identifies BrdU‐ and IdU‐incorporation as doubly and singly labeled cells, respectively. This method has broad applications. First, we demonstrate that this method can distinguish mouse cortical neurons generated on different embryonic days. Second, by administering IdU and BrdU at varying intervals, we used this method to calculate that the length of S‐phase of neural progenitor cells in the adult mouse dentate gyrus is approximately 6 h. Finally, we show that a six‐fold higher concentration of IdU detects only 10% more cells than the standard dose of BrdU (50 mg/kg) using the double‐labeling method. These results suggest that the standard dose of BrdU is sufficient to label the majority of proliferative populations in the S‐phase in pulse labeling experiments.
Neuromedin‐U is regulated by the circadian clock in the SCN of the mouse
Authors: Graham E. Scott , Littlewood Pauline , Turnbull Yvonne , Mercer Julian G. , Morgan Peter J. , Barrett Perry 
Published: February 2005

AbstractNeuromedin‐U (NMU) has been reported to drive several physiological or behavioural responses following i.c.v. injection of the peptide into the third ventricle of rodent brains. Many of these responses are mediated through a change in corticotrophin‐releasing factor (CRF) output from the paraventricular nucleus (PVN). A number of the physiological or behavioural responses are regulated in a circadian manner, e.g. feeding. We have previously reported NMU gene expression in the suprachiasmatci nucleus (SCN) and NMU‐2 receptor expression in the PVN, dorsal medial hypothalamus (DMH) and other regions of the mouse brain. We therefore hypothesized that NMU would be regulated by the circadian clock and may consequently drive a circadian rhythm of CRF expression in the PVN. Here we report that NMU is regulated in a circadian manner with peak expression during the light phase of a light–dark cycle. In C3H mice held in constant darkness, the NMU rhythm free runs with a period predicted by the free running period of locomotor activity in this mouse. The NMU mRNA transcript colocalizes with cells expressing AVP in the SCN and shows a coincident rhythm of expression with AVP. On the other hand, CRF did not express a circadian rhythm of expression in a light–dark cycle, although a rhythm was evident in constant darkness with a peak of expression prior to the rise of NMU in the same conditions. This would suggest that the circadian rhythm in NMU expression in the SCN does not drive a circadian rhythm in CRF in the PVN to be translated into physiological and behavioural responses mediated by NMU.
Ecosystem consequences of diversity depend on food chain length in estuarine vegetation
Authors: Emmett Duffy J. , Paul Richardson J. , France Kristin E. 
Published: February 2005

AbstractBiodiversity and food chain length each can strongly influence ecosystem functioning, yet their interactions rarely have been tested. We manipulated grazer diversity in seagrass mesocosms with and without a generalist predator and monitored community development. Changing food chain length altered biodiversity effects: higher grazer diversity enhanced secondary production, epiphyte grazing, and seagrass biomass only with predators present. Conversely, changing diversity altered top‐down control: predator impacts on grazer and seagrass biomass were weaker in mixed‐grazer assemblages. These interactions resulted in part from among‐species trade‐offs between predation resistance and competitive ability. Despite weak impact on grazer abundance at high diversity, predators nevertheless enhanced algal biomass through a behaviourally mediated trophic cascade. Moreover, predators influenced every measured variable except total plant biomass, suggesting that the latter is an insensitive metric of ecosystem functioning. Thus, biodiversity and trophic structure interactively influence ecosystem functioning, and neither factor's impact is predictable in isolation.
Introduced species as evolutionary traps
Authors: Schlaepfer Martin A. , Sherman Paul W. , Blossey Bernd , Runge Michael C. 
Published: February 2005

AbstractInvasive species can alter environments in such a way that normal behavioural decision‐making rules of native species are no longer adaptive. The evolutionary trap concept provides a useful framework for predicting and managing the impact of harmful invasive species. We discuss how native species can respond to changes in their selective regime via evolution or learning. We also propose novel management strategies to promote the long‐term co‐existence of native and introduced species in cases where the eradication of the latter is either economically or biologically unrealistic.