bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diurnal fluctuations of dissolved nitrous oxide (N2O) concentrations and estimates of N2O emissions from a spring‐fed river: implications for IPCC methodology
Authors: CLOUGH TIM J. , BUCKTHOUGHT LAURA E. , KELLIHER FRANCIS M. , SHERLOCK ROBERT R. 
Published: April 2007

AbstractThere is uncertainty in the estimates of indirect nitrous oxide (N2O) emissions as defined by the Intergovernmental Panel on Climate Change (IPCC). The uncertainty is due to the challenge and dearth of in situ measurements. Recent work in a subtropical stream system has shown the potential for diurnal variability to influence the downstream N transfer, N form, and estimates of in‐stream N2O production. Studies in temperate stream systems have also shown diurnal changes in stream chemistry.The objectives of this study were to measure N2O fluxes and dissolved N2O concentrations from a spring‐fed temperate river to determine if diurnal cycles were occurring. The study was performed during a 72 h period, over a 180 m reach, using headspace chamber methodology. Significant diurnal cycles were observed in radiation, river temperature and chemistry including dissolved N2O‐N concentrations. These data were used to further assess the IPCC methodology and experimental methodology used. River NO3‐N and N2O‐N concentrations averaged 3.0 mg L−1 and 1.6 μg L−1, respectively, with N2O saturation reaching a maximum of 664%. The N2O‐N fluxes, measured using chamber methodology, ranged from 52 to 140 μg m−2 h−1 while fluxes predicted using the dissolved N2O concentration ranged from 13 to 25 μg m−2 h−1. The headspace chamber methodology may have enhanced the measured N2O flux and this is discussed. Diurnal cycles in N2O% saturation were not large enough to influence downstream N transfer or N form with variability in measured N2O fluxes greater and more significant than diurnal variability in N2O% saturation. The measured N2O fluxes, extrapolated over the study reach area, represented only 6 × 10−4% of the NO3‐N that passed through the study reach over a 72 h period. This is only 0.1% of the IPCC calculated flux.
Programming of the stress response: a fundamental mechanism underlying the long‐term effects of the fetal environment?
Authors: Phillips D. I. W. 
Published: April 2007

Abstract.There is a large body of evidence which suggests that an adverse fetal environment results in a heightened biobehavioural response to stress, with increased activity of the classical mediators of the stress response, including the hypothalamic‐pituitary adrenal axis and autonomic nervous system. Although this has been amply demonstrated in animal experiments, several recent studies suggest that the same processes operate in human populations and may have important consequences for health. The evidence suggests that an adverse early environment or markers of an adverse environment such as low birth weight are linked with long‐term alterations in these neuroendocrine systems. However, these studies also demonstrate that there is a considerable degree of heterogeneity in the responses observed which appear to depend on a variety of factors such as the nature or timing of the adverse exposure as well as the gender of the offspring. The mediators of these classical neuroendocrine responses such as cortisol and catecholamines are biologically potent and may directly influence disease susceptibility by means of their effects on metabolism and the vasculature. However, lifelong changes in the set point of these neuroendocrine systems in response to the early environment may also direct the course of development during fetal life, infancy and childhood towards the generation of a phenotype adapted for the adult environment predicted by the clues available during fetal life. This has biological advantages if the actual adult environment turns out to be appropriate for the phenotype. However, ill health may occur if the phenotype is not well matched to the actual environment encountered in adult life.
Decline and recovery in otter Lutra lutra populations in Italy
Authors: PRIGIONI CLAUDIO , BALESTRIERI ALESSANDRO , REMONTI LUIGI 
Published: April 2007

ABSTRACT

Changes in otter Lutra lutra distribution in Italy were examined by analysing geographical, historical and survey data.
As in other European countries, otters declined sharply in Italy during the late 1970s and throughout the 1980s. Between 1985 and 2004 the species became extinct, except for some reintroductions, in northern and most of central Italy while the species appears to have substantially recovered in its southern range. This recovery of the otter population is apparently not due to increased research effort, but reflects a real expansion of range.
Differences in the degree of range reduction during the second half of the 20th century and in the availability of suitable habitats are probably the major factors that have determined the two opposite trends shown by otter populations in the last 20 years.
Better knowledge of otter status and distribution is needed for effective conservation management. We suggest that a national survey of the Italian otter population that employs genetic approaches should represent a first step of the national action plan for otter conservation.
Glial cell loss, proliferation and replacement in the contused murine spinal cord
Authors: Lytle Judith M. , Wrathall Jean R. 
Published: April 2007

AbstractStudies in the rat have shown that contusive spinal cord injury (SCI) results in devastating pathology, including significant loss of mature oligodendrocytes and astrocytes even in spared white matter. Subsequently, there is increased proliferation of endogenous NG2+ cells, postulated to contribute to replacement of mature glia chronically, which is important for functional recovery. Studies of mechanisms that stimulate endogenous progenitor cells would be facilitated by using mouse models with naturally occurring and genetically engineered mutations. To determine whether the murine response is similar to that in the rat, we performed contusive SCI on adult female C57Bl/6 mice at the T8–9 level. Animals received bromodeoxyuridine injections in the first week following injury and were killed at 1, 3, 4, 7 or 28 days postinjury (DPI). The overall loss of macroglia and the temporal–spatial response of NG2+ cells after SCI in the (C57Bl/6) mouse was very similar to that in the (Sprague–Dawley) rat. By 24 h after SCI nearly half of the macroglia in spared ventral white matter had been lost. Cell proliferation was increased at 1–7 DPI, peaking at 3–4 DPI. Dividing cells included NG2+ cells and Cd11b+ macrophages and microglia. Furthermore, cells dividing in the first week expressed markers of mature glia at 28 DPI. The similarities in endogenous progenitor cell response to SCI in the mouse and rat suggest that this is a fundamental injury response, and that transgenic mouse models may be used to further probe how this cellular response to SCI might be enhanced to improve recovery after SCI.
Chronic intracerebral prolactin attenuates neuronal stress circuitries in virgin rats
Authors: Donner Nina , Bredewold Remco , Maloumby Rodrigue , Neumann Inga D. 
Published: April 2007

AbstractProlactin (PRL) has been shown to promote maternal behaviour, and to regulate neuroendocrine and emotional stress responses. These effects appear more important in the peripartum period, when the brain PRL system is highly activated. Here, we studied the mechanisms that underlie the anti‐stress effects of PRL. Ovariectomized, estradiol‐substituted Wistar rats were implanted with an intracerebroventricular cannula and treated with ovine PRL (0.01, 0.1 or 1 µg/h; 5 days via osmotic minipumps) or vehicle, and their responses to acute restraint stress was assessed. Chronic PRL treatment exerted an anxiolytic effect on the elevated plus‐maze, and attenuated the acute restraint‐induced rise in plasma adrenocorticotropin, corticosterone and noradrenaline. At the neuronal level, in situ hybridization revealed PRL effects on the expression patterns of the immediate‐early gene c‐fos and corticotropin‐releasing factor (CRF). Under basal conditions, PRL significantly reduced c‐fos mRNA expression within the central amygdala. In response to restraint, the expression of both c‐fos mRNA and protein and of CRF mRNA was decreased in the parvocellular part of the paraventricular nucleus (PVN) of PRL‐treated compared with vehicle‐treated animals. In conclusion, our data demonstrate that chronic elevation of PRL levels within the brain results in reduced neuronal activation within the hypothalamus, specifically within the PVN, in response to an acute stressor. Thus, PRL acting at various relevant brain regions exerts profound anxiolytic and anti‐stress effects, and is likely to contribute to the attenuated stress responsiveness found in the peripartum period, when brain PRL levels are physiologically upregulated.
Brain‐derived neurotrophic factor modulates cell excitability in the mouse medial nucleus of the trapezoid body
Authors: Youssoufian M. , Walmsley B. 
Published: April 2007

AbstractNeurotrophins are a large class of trophic factors located throughout the central nervous system. While the role of neurotrophins in neuronal survival and axon guidance is well known, their secondary role in modulating synaptic transmission and cell firing properties is largely unexplored. In this study we examined the expression of neurotrophins in the mouse medial nucleus of the trapezoid body (MNTB) and investigated the effect of exogenous brain‐derived neurotrophic factor (BDNF) application on the firing properties of MNTB principal cells. The expression levels of nerve growth factor, BDNF, neurotrophin‐3, neurotrophin‐4/5 and major receptor tyrosine kinase B was found to be moderate to high at postnatal day 12, indicating that the neurotrophins may have a role following synaptogenesis. A 2‐h exposure to exogenous BDNF (100 ng/mL) had a significant effect on principal cell firing properties and voltage‐gated potassium currents. Importantly, preincubation in BDNF increased the incidence of multifiring and rebounding cells, and significantly increased the number of action potentials fired in response to a single depolarizing step. BDNF exposure also significantly decreased underlying voltage‐gated potassium currents, including both the low‐ and high‐voltage‐activated components. Our data show that the neurotrophins, specifically BDNF, may have a novel role in modulating cell excitability in the auditory brainstem.
Development of non‐phosphorylated neurofilament protein expression in neurones of the New World monkey dorsolateral frontal cortex
Authors: Burman Kathleen J. , Lui Leo L. , Rosa Marcello G. P. , Bourne James A. 
Published: April 2007

AbstractWe studied developmental changes in the expression of non‐phosphorylated neurofilament protein (NNF) (a marker of the structural maturation of pyramidal neurones) in the dorsolateral frontal cortex of marmoset monkeys, between embryonic day 130 and adulthood. Our focus was on cortical fields that send strong projections to extrastriate cortex, including the dorsal and ventral subdivisions of area 8A, area 46 and area 6d. For comparison, we also investigated the maturation of prefrontal area 9, which has few or no connections with visual areas. The timing of expression of NNF immunostaining in early life can be described as the result of the interaction of two developmental gradients. First, there is an anteroposterior gradient of maturation in the frontal lobe, whereby neurones in caudal areas express NNF earlier than those in rostral areas. Second, there is a laminar gradient, whereby the first NNF‐immunoreactive neurones emerge in layer V, followed by those in progressively more superficial parts of layer III. Following a peak in density of NNF‐immunopositive cell numbers in layer V at 2–3 months of age, there is a gradual decline towards adulthood. In contrast, the density of immunopositive cells in layer III continues to increase throughout the first postnatal year in area 6d and until late adolescence (> 1.5 years of age) in prefrontal areas. The present results support the view that the maturation of visual cognitive functions involves relatively late processes linked to structural changes in frontal cortical areas.
Investor Attention and Time‐varying Comovements
Authors: Peng Lin , Xiong Wei , Bollerslev Tim 
Published: April 2007

Abstract This paper analyses the effect of an increase in market‐wide uncertainty on information flow and asset price comovements. We use the daily realised volatility of the 30‐year treasury bond futures to assess macroeconomic shocks that affect market‐wide uncertainty. We use the ratio of a stock's idiosyncratic realised volatility with respect to the S&P500 futures relative to its total realised volatility to capture the asset price comovement with the market. We find that market volatility and the comovement of individual stocks with the market increase contemporaneously with the arrival of market‐wide macroeconomic shocks, but decrease significantly in the following five trading days. This pattern supports the hypothesis that investors shift their (limited) attention to processing market‐level information following an increase in market‐wide uncertainty and then subsequently divert their attention back to asset‐specific information.
Inhibition of the myosin light chain kinase prevents hypoxia‐induced blood–brain barrier disruption
Authors: Kuhlmann Christoph R.W. , Tamaki Ryo , Gamerdinger Martin , Lessmann Volkmar , Behl Christian , Kempski Oliver S. , Luhmann Heiko J. 
Published: April 2007

AbstractIncreased mortality after stroke is associated with development of brain edema. The aim of the present study was to examine the contribution of endothelial myosin light chain (MLC) phosphorylation to hypoxia‐induced blood–brain barrier (BBB) opening. Measurements of trans‐endothelial electrical resistance (TEER) were performed to analyse BBB integrity in an in vitro co‐culture model (bovine brain microvascular endothelial cells (BEC) and rat astrocytes). Brain fluid content was analysed in rats after stroke induction using a two‐vein occlusion model. Dihydroethidium was used to monitor intracellular generation of reactive oxygen species (ROS) in BEC. MLC phosphorylation was detected using immunohistochemistry and immunoblot analysis. Hypoxia caused a decrease of TEER values by more than 40%, which was prevented by inhibition of the MLC‐kinase (ML‐7, 10 μmol/L). In addition, ML‐7 significantly reduced the brain fluid content in vivo after stroke. The NAD(P)H‐oxidase inhibitor apocynin (500 μmol/L) prevented the hypoxia‐induced TEER decrease. Hypoxia‐dependent ROS generation was completely abolished by apocynin. Furthermore, ML‐7 and apocynin blocked hypoxia‐dependent phosphorylation of MLC. Our data demonstrate that hypoxia causes a breakdown of the BBB in vitro and in vivo involving ROS and the contractile machinery.
Major Cdk5‐dependent phosphorylation sites of amphiphysin 1 are implicated in the regulation of the membrane binding and endocytosis
Authors: Liang Shuang , Wei Fan‐Yan , Wu Yu‐Mei , Tanabe Kenji , Abe Tadashi , Oda Yoshiya , Yoshida Yumi , Yamada Hiroshi , Matsui Hideki , Tomizawa Kazuhito , Takei Kohji 
Published: April 2007

AbstractAmphiphysin 1 (amph 1) is an endocytic protein enriched in the nerve terminals that functions in the clathrin‐mediated endocytosis. It acts as membrane curvature sensor, a linker of clathrin coat proteins, and an enhancer of dynamin Guanosine Triphosphatase (GTPase) activity. Amph 1 undergoes phosphorylation by cyclin‐dependent kinase 5 (Cdk5), at five phosphorylation sites, serine 262, 272, 276, 285, and threonine 310, as determined by mass spectrometry (MS). We show here that Cdk5‐dependent phosphorylation of amph 1 is enhanced in the presence of lipid membranes. Analysis by tandem liquid chromatograph MS revealed that the phosphorylation occurs at two phosphorylation sites. The phosphorylation was markedly decreased by mutation either Ser276 or Ser285 of amph 1 to alanine (S276A and S285A). Furthermore, mutation of both sites (S276, 285A) completely eliminated the phosphorylation. Functional studies indicated that binding of amph 1 to lipid membrane was attenuated by Cdk5‐dependent phosphorylation of wild type amph 1, but not of the S276, 285A form. Interestingly, endocytosis was increased in rat pheochromocytoma cells expressing amph 1 S276, 285A in comparison with wild type. These results suggest that Ser276 and Ser285 are regulatory Cdk5 phosphorylation sites of amph 1 in the lipid‐bound state. Phosphorylation at these sites alters binding of amph 1 to lipid membranes, and may be an important regulatory aspect in the regulation of synaptic vesicle endocytosis.
Rapid regulation of dopamine transporters by tyrosine kinases in rat neuronal preparations
Authors: Hoover B. R. , Everett C. V. , Sorkin A. , Zahniser N. R. 
Published: April 2007

AbstractTermination of dopamine neurotransmission is primarily controlled by the plasma membrane‐localized dopamine transporter. In this study, we investigated how this transporter is regulated by tyrosine kinases in neuronal preparations. In rat dorsal striatal synaptosomes, inhibition of tyrosine kinases by genistein or tyrphostin 23 resulted in a rapid (5–15 min), concentration‐dependent decrease in [3H]dopamine uptake because of a reduction in maximal [3H]dopamine uptake velocity and dopamine transporter cell surface expression. The reduced transporter activity was associated with a decrease in phosphorylated p44/p42 mitogen‐activated protein kinases. In primary rat mesencephalic neuronal cultures, the tyrosine kinase inhibitors similarly reduced [3H]dopamine uptake. When cultures were serum‐deprived, acute activation of tyrosine kinase‐coupled TrkB receptors by 100 ng/mL brain‐derived neurotrophic factor significantly increased [3H]dopamine uptake; the effects were complex with increased maximal velocity but reduced affinity. The facilitatory effect of brain‐derived neurotrophic factor on dopamine transporter activity depended on both the mitogen‐activated protein kinase and phosphatidylinositol 3‐kinase pathways. Taken together, our results suggest that striatal dopamine transporter function and cell surface expression is constitutively up‐regulated by tyrosine kinase activation and that brain‐derived neurotrophic factor can mediate this type of rapid regulation.
Loss of hippocampal neuronal nitric oxide synthase contributes to the stress‐related deficit in learning and memory
Authors: Palumbo María Laura , Fosser Nicolás Sebastián , Rios Hugo , Zubilete María Aurelia Zorrilla , Guelman Laura Ruth , Cremaschi Graciela Alicia , Genaro Ana María 
Published: April 2007

AbstractNitric oxide (NO) has been involved in many pathophysiological brain processes. However, the exact role of NO in the cognitive deficit associated to chronic stress exposure has not been elucidated. In this study, we investigated the participation of hippocampal NO production and their regulation by protein kinase C (PKC) in the memory impairment induced in mice subjected to chronic mild stress model (CMS). CMS mice showed a poor learning performance in both open field and passive avoidance inhibitory task respect to control mice. Histological studies showed a morphological alteration in the hippocampus of CMS mice. On the other hand, chronic stress induced a diminished NO production by neuronal nitric oxide synthase (nNOS) correlated with an increment in gamma and zeta PKC isoenzymes. Partial restoration of nNOS activity was obtained after PKC activity blockade. NO production by inducible nictric oxide synthase isoform was not detected. The magnitude of oxidative stress, evaluated by reactive oxygen species production, after excitotoxic levels of NMDA was increased in hippocampus of CMS mice. Moreover, ROS formation was higher in the presence of nNOS inhibitor in both control and CMS mice. Finally, treatment of mice with nNOS inhibitors results in behavioural alterations similar to those observed in CMS animals. These findings suggest a novel role for nNOS showing protective activity against insults that trigger tissue toxicity leading to memory impairments.
Establishment and characterization of a novel imatinib‐sensitive chronic myeloid leukemia cell line MYL, and an imatinib‐resistant subline MYL‐R showing overexpression of Lyn
Authors: Ito Takuo , Tanaka Hideo , Kimura Akiro 
Published: April 2007

AbstractIn chronic myeloid leukemia (CML), resistance to imatinib is diverse. In addition to BCR‐ABL‐dependent mechanisms, BCR‐ABL‐independent mechanisms have been proposed. Here we established and characterized novel CML cell lines, an imatinib‐sensitive cell line, MYL, and an imatinib‐resistant subline, MYL‐R. Treatment with imatinib inhibited phosphorylation of BCR‐ABL and CrkL in both MYL and MYL‐R, even though imatinib‐induced apoptosis was preferentially observed in MYL than MYL‐R, indicating that the resistance is based on a BCR‐ABL‐independent mechanism. MYL‐R showed elevated expressions of Lyn mRNA, Lyn protein, phosphorylated Lyn, and phosphorylated STAT5. Silencing of Lyn by short‐interfering RNA (siRNA) in MYL‐R, but not in MYL, induced significant growth‐inhibition, increased caspase‐3 activity, and induced partial recovery from imatinib‐resistance. Expression of Bcl‐2, previously reported to be associated with Lyn‐mediated resistance, was not elevated in MYL‐R. Expression of Bim, which plays an important role in imatinib‐induced cell‐killing, was not suppressed in MYL‐R. These results imply that diverse mechanisms of resistance exist among cell types. Treatment of MYL‐R cells with various reagents known to have anti‐leukemic activity revealed that zoledronic acid and the farnesyl transferase inhibitor (SCH 66336) showed strong synergism with imatinib; interferon α, PP2, CGP76030, and FK228 (depsipeptide) showed synergism; whereas soluble TRAIL and As2O3 showed additivity or antagonism, and 17‐AAG and radicicol showed antagonism. Treatment with either PP2 or zoledronic acid induced greater growth‐reduction in MYL‐R than MYL. Taken together, Lyn may play an important role in imatinib‐resistance in MYL‐R. Some novel reagents, including siRNA targeting Lyn, may have good potential to overcome this resistance.
Psychosis as presenting symptom in adult-onset Hallervorden-Spatz syndrome
Authors: Panas Marios , Spengos Konstantinos , Koutsis Georgios , Tsivgoulis Georgios , Sfagos Konstantinos , Kalfakis Nikolaos , Vassilopoulos Dimitris 
Published: April 2007

Background:Hallervorden-Spatz syndrome is characterized by pyramidal and extrapyramidal signs, and dysarthria and dementia. Psychiatric symptomatology can emerge in the course of the disorder. Mutations in the pantothenate kinase 2 gene have been found in many cases. We report a case with psychosis as sole presenting symptom.Case:A 41-year-old man presented with change in behavior and paranoid delusional ideation. Six months later, spasticity, extrapyramidal rigidity and dysarthria were added to the picture. Eventually, the patient became mute and wheel-chair bound. The brain magnetic resonance imaging (MRI) was consistent with iron depositions in the globus pallidus and substantia nigra.Conclusions:In this case, the combination of clinical and MRI findings was consistent with Hallervorden-Spatz syndrome. The combination of psychiatric and MRI findings should lead to further neurological investigation.