bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interregional variation in the floristic recovery of post‐agricultural forests
Authors: De Frenne Pieter , Baeten Lander , Graae Bente J. , Brunet Jörg , Wulf Monika , Orczewska Anna , Kolb Annette , Jansen Ivy , Jamoneau Aurélien , Jacquemyn Hans , Hermy Martin , Diekmann Martin , De Schrijver An , De Sanctis Michele , Decocq Guillaume , Cousins Sara A. O. , Verheyen Kris 
Published: December 2010

Summary 1. Worldwide, the floristic composition of temperate forests bears the imprint of past land use for decades to centuries as forests regrow on agricultural land. Many species, however, display significant interregional variation in their ability to (re)colonize post‐agricultural forests. This variation in colonization across regions and the underlying factors remain largely unexplored. 2. We compiled data on 90 species and 812 species × study combinations from 18 studies across Europe that determined species’ distribution patterns in ancient (i.e. continuously forested since the first available land use maps) and post‐agricultural forests. The recovery rate (RR) of species in each landscape was quantified as the log‐response ratio of the percentage occurrence in post‐agricultural over ancient forest and related to the species‐specific life‐history traits and local (soil characteristics and light availability) and regional factors (landscape properties as habitat availability, time available for colonization, and climate). 3. For the herb species, we demonstrate a strong (interactive) effect of species’ life‐history traits and forest habitat availability on the RR of post‐agricultural forest. In graminoids, however, none of the investigated variables were significantly related to the RR. 4. The better colonizing species that mainly belonged to the short‐lived herbs group showed the largest interregional variability. Their recovery significantly increased with the amount of forest habitat within the landscape, whereas, surprisingly, the time available for colonization, climate, soil characteristics and light availability had no effect. 5. Synthesis. By analysing 18 independent studies across Europe, we clearly showed for the first time on a continental scale that the recovery of short‐lived forest herbs increased with the forest habitat availability in the landscape. Small perennial forest herbs, however, were generally unsuccessful in colonizing post‐agricultural forest – even in relatively densely forested landscapes. Hence, our results stress the need to avoid ancient forest clearance to preserve the typical woodland flora.
Neuroadaptation of GABAergic transmission in the central amygdala during chronic morphine treatment
Authors: Bajo Michal , Roberto Marisa , Madamba Samuel G. , Siggins George Robert 
Published: December 2010

ABSTRACTWe investigated possible alterations of pharmacologically‐isolated, evoked GABAAinhibitory postsynaptic potentials (eIPSPs) and miniature GABAAinhibitory postsynaptic currents (mIPSCs) in the rat central amygdala (CeA) elicited by acute application of µ‐opioid receptor (MOR) agonists (DAMGO and morphine; 1 µM) and by chronic morphine treatment with morphine pellets. The acute activation of MORs decreased the amplitudes of eIPSPs, increased paired‐pulse facilitation (PPF) of eIPSPs and decreased the frequency (but not the amplitude) of mIPSCs in a majority of CeA neurons, suggesting that acute MOR‐dependent modulation of this GABAergic transmission is mediated predominantly via presynaptic inhibition of GABA release. We observed no significant changes in the membrane properties, eIPSPs, PPF or mIPSCs of CeA neurons during chronic morphine treatment compared to CeA of naïve or sham rats. Superfusion of the MOR antagonist CTOP (1 µM) increased the mean amplitude of eIPSPs in a majority of CeA neurons to the same degree in both naïve/sham and morphine‐treated rats, suggesting a tonic activation of MORs in both conditions. Superfusion of DAMGO decreased eIPSP amplitudes and the frequency of mIPSCs equally in both naïve/sham and morphine‐treated rats but decreased the amplitude of mIPSCs only in morphine treated rats, an apparent postsynaptic action. Our combined findings suggest the development of tolerance of the CeA GABAergic system to inhibitory effects of acute activation of MORs on presynaptic GABA release and possible alteration of MOR‐dependent postsynaptic mechanisms that may represent important neuroadaptations of the GABAergic and MOR systems during chronic morphine treatment.
Effect of methamphetamine dependence on heart rate variability
Authors: Henry Brook L. , Minassian Arpi , Perry William 
Published: December 2010

ABSTRACTMethamphetamine (METH) is an increasing popular and highly addictive stimulant associated with autonomic nervous system (ANS) dysfunction, cardiovascular pathology and neurotoxicity. Heart rate variability (HRV) has been used to assess autonomic function and predict mortality in cardiac disorders and drug intoxication, but has not been characterized in METH use. We recorded HRV in a sample of currently abstinent individuals with a history of METH dependence compared to age‐ and gender‐matched drug‐free comparison subjects. HRV was assessed using time domain, frequency domain, and non‐linear entropic analyses in 17 previously METH‐dependent and 21 drug‐free comparison individuals during a 5 minute rest period. The METH‐dependent group demonstrated significant reduction in HRV, reduced parasympathetic activity, and diminished heartbeat complexity relative to comparison participants. More recent METH use was associated with increased sympathetic tone. Chronic METH exposure may be associated with decreased HRV, impaired vagal function, and reduction in heart rate complexity as assessed by multiple methods of analysis. We discuss and review evidence that impaired HRV may be related to the cardiotoxic or neurotoxic effects of prolonged METH use.
The endocannabinoid system modulates the valence of the emotion associated to food ingestion
Authors: Méndez‐Díaz Mónica , Rueda‐Orozco Pavel Ernesto , Ruiz‐Contreras Alejandra Evelyn , Prospéro‐García Oscar 
Published: December 2010

ABSTRACTEndocannabinoids (eCBs) are mediators of the homeostatic and hedonic systems that modulate food ingestion. Hence, eCBs, by regulating the hedonic system, may be modulating the valence of the emotion associated to food ingestion (positive: pleasant or negative: unpleasant). Our first goal was to demonstrate that palatable food induces conditioned place preference (CPP), hence a positive‐valence emotion. Additionally, we analyzed if this CPP is blocked by AM251, inducing a negative valence emotion, meaning avoiding the otherwise pursued compartment. The second goal was to demonstrate that CPP induced by regular food would be strengthened by the simultaneous administration of anandamide or oleamide, and if such, CPP is blocked by AM251. Finally, we tested the capacity of eCBs (without food) to induce CPP. Our results indicate that rats readily developed CPP to palatable food, which was blocked by AM251. The CPP induced by regular food was strengthened by eCBs and blocked by AM251. Finally, oleamide, unlike anandamide, induced CPP. These results showed that eCBs mediate the positive valence (CPP) of the emotion associated to food ingestion. It was also observed that the blockade of the CB1 receptor causes a loss of correlation between food and CPP (negative valence: avoidance). These data further support the role of eCBs as regulators of the hedonic value of food.
Repeated exposure to moderate doses of ethanol augments hippocampal glutamate neurotransmission by increasing release
Authors: Chefer Vladimir , Meis Jennifer , Wang Grace , Kuzmin Alexander , Bakalkin Georgy , Shippenberg Toni 
Published: December 2010

ABSTRACTThe present study used conventional and quantitative microdialysis to assess glutamatergic and GABAergic neurotransmission in the hippocampal CA3 area of the rat following a moderate‐dose ethanol treatment regimen. Male Wistar rats received 3.4 g/kg of ethanol or water for 6 days via gastric gavage. Microdialysis experiments commenced 2 days later. Basal and depolarization‐induced glutamate overflow were significantly elevated in ethanol‐treated animals. Basal and depolarization‐induced gamma‐aminobutyric acid (GABA) overflow were unaltered. Quantitative no‐net‐flux microdialysis was used to determine if changes in dialysate glutamate levels following ethanol administration are due to an increase in release or a decrease in uptake. To confirm the validity of this method for quantifying basal glutamate dynamics, extracellular concentrations of glutamate and the extraction fraction, which reflects changes in analyte clearance, were quantified in response to retro‐dialysis of the glutamate uptake blocker trans‐pyrrolidine‐2,4‐dicarboxylic acid (tPDC). tPDC significantly decreased the extraction fraction for glutamate, resulting in augmented extracellular glutamate concentrations. Repeated ethanol administration did not alter the glutamate extraction fraction. However, extracellular glutamate concentrations were significantly elevated, indicating that glutamate release is increased as a consequence of repeated ethanol administration. These data demonstrate that repeated bouts of moderate ethanol consumption alter basal glutamate dynamics in the CA3 region of the dorsal hippocampus. Basal glutamate release is augmented, whereas glutamate uptake is unchanged. Furthermore, they suggest that dysregulation of glutamate transmission in this region may contribute to the previously documented deficits in cognitive function associated with moderate dose ethanol use.
Brain reactivity to emotional, neutral and cigarette‐related stimuli in smokers
Authors: Versace Francesco , Minnix Jennifer A. , Robinson Jason D. , Lam Cho Y. , Brown Victoria L. , Cinciripini Paul M. 
Published: December 2010

ABSTRACTAddiction has been described as the pathological usurpation of the neural mechanisms normally involved in emotional processing. Event‐related potentials (ERPs) can provide a non‐invasive index of neural responses associated with the processing of emotionally relevant stimuli and serve as a tool for examining temporal and spatial commonalities between the processing of intrinsically motivating stimuli and drug cues. Before beginning a smoking cessation program, 116 smokers participated in a laboratory session in which dense‐array ERPs (129 sensors) were recorded during the presentation of pictures with emotional (pleasant and unpleasant), neutral and cigarette‐related content. ERP differences among categories were analyzed with use of randomization tests on time regions of interest identified by temporal principal component analysis. Both emotional and cigarette‐related pictures prompted significantly more positivity than did neutral pictures over central, parietal, and frontal sites in the 452–508 ms time window. During the 212–316 ms time window, both pleasant and cigarette‐related pictures prompted less positivity than neutral images did. Cigarette‐related pictures enhanced the amplitude of the P1 component (136–144 ms) above the levels measured in the emotional and neutral conditions. These results support the hypothesis that for smokers, cigarette‐related cues are motivationally relevant stimuli that capture attentional resources early during visual processing and engage brain circuits normally involved in the processing of intrinsically emotional stimuli.
The role of amygdaloid brain‐derived neurotrophic factor, activity‐regulated cytoskeleton‐associated protein and dendritic spines in anxiety and alcoholism
Authors: Moonat Sachin , Sakharkar Amul J. , Zhang Huaibo , Pandey Subhash C. 
Published: December 2010

ABSTRACTInnate anxiety appears to be a robust factor in the promotion of alcohol intake, possibly due to the anxiolytic effects of self‐medication with alcohol. Brain‐derived neurotrophic factor (BDNF) and its downstream target, activity‐regulated cytoskeleton‐associated (Arc) protein, play a role in the regulation of synaptic function and structure. In order to examine the role of the BDNF‐Arc system and associated dendritic spines in the anxiolytic effects of ethanol, we investigated the effects of acute ethanol exposure on anxiety‐like behaviors of alcohol‐preferring (P) and ‐nonpreferring (NP) rats. We also examined changes in the expression of BDNF and Arc, and dendritic spine density (DSD), in amygdaloid brain regions of P and NP rats with or without ethanol exposure. It was found that in comparison with NP rats, P rats displayed innate anxiety‐like behaviors, and had lower mRNA and protein levels of both BDNF and Arc, and also had lower DSD in the central amygdala (CeA) and medial amygdala (MeA), but not in the basolateral amygdala (BLA). Acute ethanol treatment had an anxiolytic effect in P, but not in NP rats, and was associated with an increase in mRNA and protein levels of BDNF and Arc, and in DSD in the CeA and MeA, but not BLA. These results suggest that innate deficits in BDNF‐Arc levels, and DSD, in the CeA and MeA may be involved in the anxiety‐like and excessive alcohol‐drinking behaviors of P rats, as ethanol increased these amygdaloid synaptic markers and produced anxiolytic effects in P rats, but not NP rats.
Single nucleotide polymorphism at exon 7 splice acceptor site of OAS1 gene determines response of hepatitis C virus patients to interferon therapy
Authors: El Awady Mostafa K , Anany Mohamed A , Esmat Gamal , Zayed Naglaa , Tabll Ashraf A , Helmy Amr , El Zayady Abdel Rahman , Abdalla Mohga S , Sharada Hayat M , El Raziky Maissa , El Akel Wafaa , Abdalla Shadia , Bader El Din Noha G 
Published: December 2010

AbstractBackground and Aim:  Response to interferon therapy and disease progression in hepatitis C virus (HCV) infected patients differs among individuals, suggesting a possibility of a contribution of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS1), an important component of the innate immune system with a proven antiviral function, may therefore have a relationship with the response to interferon therapy and clinical course of HCV disease. Our aim was to determine the frequency of single nucleotide polymorphism (SNP) at exon 7 splice acceptor site (SAS) of the OAS1 gene in relation to the interferon response and status of HCV infection.Methods:  A 203 bp fragment containing exon 7 SAS was amplified in 70 HCV chronic patients and 50 healthy controls. SNP was examined using restriction fragment length polymorphism (RFLP) genotyping method. Correlations of SNP genotypes with response to interferon and clinical status of patients were statistically analyzed.Results:  There was an increasing trend of response from AA to AG to GG genotypes (P = 0.007). Genotype AA was associated with non‐response to interferon and higher degree of liver fibrosis (P = 0.05). Multivariate analysis showed this SNP as independent and a significant determinant of the outcome of interferon therapy (odds ratio 4.913 [95% confidence interval 1.365–8.2], P = 0.006).Conclusions:  This is the first study to show a significant association between the functional SNP at exon 7 SAS of OAS1 gene and the viral response to interferon in chronic HCV patients. Patients with AA genotype were associated with progressive HCV disease and viral resistance to interferon therapy. This OAS SNP is a potential bio‐marker to predict IFN response in chronic hepatitis C patients.
Association genetics of complex traits in plants
Authors: Ingvarsson Pär K. , Street Nathaniel R. 
Published: December 2010

SummaryAssociation mapping is rapidly becoming the main method for dissecting the genetic architecture of complex traits in plants. Currently most association mapping studies in plants are preformed using sets of genes selected to be putative candidates for the trait of interest, but rapid developments in genomics will allow for genome‐wide mapping in virtually any plant species in the near future. As the costs for genotyping are decreasing, the focus has shifted towards phenotyping. In plants, clonal replication and/or inbred lines allows for replicated phenotyping under many different environmental conditions. Reduced sequencing costs will increase the number of studies that use RNA sequencing data to perform expression quantitative trait locus (eQTL) mapping, which will increase our knowledge of how gene expression variation contributes to phenotypic variation. Current population sizes used in association mapping studies are modest in size and need to be greatly increased if mutations explaining less than a few per cent of the phenotypic variation are to be detected. Association mapping has started to yield insights into the genetic architecture of complex traits in plants, and future studies with greater genome coverage will help to elucidate how plants have managed to adapt to a wide variety of environmental conditions.

Contents

Summary
909

I.
Introduction
910

II.
Genotyping
910

III.
Phenotyping
911

IV.
Study designs
912

V.
The genetics of the ‘omics’
912

VI.
Missing heritability: the dark matter of the genome
913

VII.
Gene interactions
914

VIII.
Many rare alleles
914

IX.
Looking in the wrong place
914

X.
Looking but not seeing
915

XI.
Needles in a haystack
915

XII.
Confounding effects
916

XIII.
Replicating and verifying associations
916

XIV.
The genetic architecture of quantitative traits in plants
917

XV.
Outlook
918

Acknowledgements
919

References
919
Inhibition of cPLA2 activation by Ginkgo biloba extract protects spinal cord neurons from glutamate excitotoxicity and oxidative stress‐induced cell death
Authors: Zhao Zhen , Liu Naikui , Huang Jingya , Lu Pei‐Hua , Xu Xiao‐Ming 
Published: December 2010

J. Neurochem. (2011) 116, 1057–1065.Abstract Ginkgo biloba extract (EGb761) has been shown to be neuroprotective; however, the mechanism by which EGb761 mediates neuroprotection remains unclear. We hypothesized that the neuroprotective effect of EGb761 is mediated by inhibition of cytosolic phospholipase A2 (cPLA2), an enzyme that is known to play a key role in mediating secondary pathogenesis after acute spinal cord injury (SCI). To determine whether EGb761 neuroprotection involves the cPLA2 pathway, we first investigated the effect of glutamate and hydrogen peroxide on cPLA2 activation. Results showed that both insults induced an increase in the expression of phosphorylated cPLA2 (p‐cPLA2), a marker of cPLA2 activation, and neuronal death in vitro. Such effects were significantly reversed by EGb761 administration. Additionally, EGb761 significantly decreased prostaglandin E2 (PGE2) release, a downstream metabolite of cPLA2. Moreover, inhibition of cPLA2 activity with arachidonyl trifluromethyl ketone improved neuroprotection against glutamate and hydrogen peroxide‐induced neuronal death, and reversed Bcl‐2/Bax ratio; notably, EGb761 produced greater effects than arachidonyl trifluromethyl ketone. Finally, we showed that the extracellular signal‐regulated kinase 1/2 signaling pathway is involved in EGb761’s modulation of cPLA2 phosphorylation. These results collectively suggest that the protective effect of EGb761 is mediated, at least in part, through inhibition of cPLA2 activation, and that the extracellular signal‐regulated kinase 1/2 signaling pathway may play an important role in mediating the EGb761’s effect.
Region‐specific regulation of 5‐HT1A receptor expression by Pet‐1‐dependent mechanismsin vivo
Authors: Jacobsen Kirsten X. , Czesak Margaret , Deria Mariam , Le François Brice , Albert Paul R. 
Published: December 2010

J. Neurochem.(2011)116, 1066–1076.AbstractSerotonin (5‐hydroxytryptamine, 5‐HT) neurotransmission is negatively regulated by 5‐HT1A autoreceptors on raphe neurons, and is implicated in mood disorders. Pet‐1/FEV is an ETS transcription factor expressed exclusively in serotonergic neurons and is essential for serotonergic differentiation, although its regulation of 5‐HT receptors has not yet been studied. Here, we show by electrophoretic mobility shift assay that recombinant human Pet‐1/FEV binds directly to multiple Pet‐1 elements of the human 5‐HT1A receptor promoter to enhance its transcriptional activity. In luciferase reporter assays, mutational analysis indicated that while several sites contribute, the Pet‐1 site at ‐1406 bp had the greatest effect on 5‐HT1A promoter activity. To address the effect of Pet‐1 on 5‐HT1A receptor regulationin vivo, we compared the expression of 5‐HT1A receptor RNA and protein in Pet‐1 null and wild‐type littermate mice. In the raphe nuclei of Pet‐1−/− mice tryptophan hydroxylase 2 (TPH2) RNA, and 5‐HT and TPH immunostaining were greatly reduced, indicating a deficit in 5‐HT production. Raphe 5‐HT1A RNA and protein levels were also reduced in Pet‐1‐deficient mice, consistent with an absence of Pet‐1‐mediated transcriptional enhancement of 5‐HT1A autoreceptors in serotonergic neurons. Interestingly, 5‐HT1A receptor expression was up‐regulated in the hippocampus, but down‐regulated in the striatum and cortex. These data indicate that, in addition to transcriptional regulation by Pet‐1 in raphe neurons, 5‐HT1A receptor expression is regulated indirectly by alterations in 5‐HT neurotransmission in a region‐specific manner that together may contribute to the aggressive/anxiety phenotype observed in Pet‐1 null mice.
Effect of transdermal opioids in experimentally induced superficial, deep and hyperalgesic pain
Authors: Andresen T , Staahl C , Oksche A , Mansikka H , Arendt‐Nielsen L , Drewes AM 
Published: December 2010

BACKGROUND AND PURPOSEChronic pain and hyperalgesia can be difficult to treat with classical opioids acting predominately at the µ‐opioid receptor. Buprenorphine and its active metabolite are believed to act through µ‐, κ‐ and δ‐receptors and may therefore possess different analgesic and anti‐hyperalgesic effects compared with pure µ‐receptor agonists, for example, fentanyl. Here, we have compared the analgesic and anti‐hyperalgesic effects of buprenorphine and fentanyl.EXPERIMENTAL APPROACHTwenty‐two healthy volunteers were randomized to treatment with transdermal buprenorphine (20 µg·h−1, 144 h), fentanyl (25 µg·h−1, 72 h) or placebo patches in a double‐blind, cross‐over experimental pain study. The experimental pain tests (phasic pain, sensitization) involved pressure at the tibial bone, cutaneous electrical and thermal stimulation, intramuscular nerve growth factor, UVB light burn injury model and intradermal capsaicin‐induced hyperalgesia. Pain testing was carried out at baseline, 24, 48, 72 and 144 h after application of the drugs.KEY RESULTSCompared with placebo, buprenorphine, but not fentanyl, significantly attenuated pressure at the tibial bone as well as pressure pain in the primary hyperalgesic area induced by UVB light The two drugs were equipotent and better than placebo against cutaneous thermal pain stimulation), but failed to show significant analgesic effect to cutaneous electrical stimulation, nerve growth factor‐induced muscle soreness and to capsaicin‐induced hyperalgesia.CONCLUSIONS AND IMPLICATIONSBuprenorphine, but not fentanyl, showed analgesic effects against experimentally induced, bone‐associated pain and primary hyperalgesia compared with placebo. These tissue‐ and modality‐differentiated properties may reflect the variable effects of opioid drugs observed in individual patients.