bluuebunny/crossref_metadata_2025_split huggingface dataset:
Uncoupling protein‐2 promotes nigrostriatal dopamine neuronal function
Authors: Andrews Zane B. , Rivera Alicia , Elsworth John D. , Roth Robert H. , Agnati Luigi , Gago Belen , Abizaid Alfonso , Schwartz Michael , Fuxe Kjell , Horvath Tamas L. 
Published: July 2006

AbstractUncoupling protein 2 (UCP2) is known to promote neuroprotection in many forms of neurological pathologies including Parkinson's disease. Here, we examined the hypothesis that UCP2 also mediates aspects of normal nigrostriatal dopamine (DA) function. Mice lacking UCP2 exhibited reduced dopamine turnover in the striatum as measured by the 3,4‐dihydoxyphenylacetic acid/dopamine (DOPAC/DA) ratio, reduced tyrosine hydroxylase immunoreactivity (TH IR) in the substantia nigra pars compacta (SNc) and reticulata, striatum and nucleus accumbens. UCP2‐knockout (KO) mice also had reduced dopamine transporter immunoreactivity (DAT IR) in the SNc but not other brain regions examined. In order to determine if these biochemical deficits are transcribed into behavioural deficits, we examined locomotor function in UCP2‐KO mice compared to wild‐type (WT) controls. UCP2‐KO mice exhibited significantly reduced total movement distance, movement velocity and increased rest time compared to wild‐type controls. These results suggest that UCP2 is an important mitochondrial protein that helps to maintain normal nigrostriatal dopamine neuronal function and a reduction in UCP2 levels may predispose individuals to environmental causes of Parkinson's disease.
Extinction is not a sufficient condition to prevent fear memories from undergoing reconsolidation in the basolateral amygdala
Authors: Duvarci Sevil , Mamou Cyrinne ben , Nader Karim 
Published: July 2006

AbstractConsolidated memories when reactivated may return to a state that requires protein synthesis in order to be restabilized (reconsolidation). It has been shown in a variety of systems that if reactivation induces significant extinction then extinction is the protein synthesis dependent memory state, rather than reconsolidation. Thus, extinction consolidation may prevent the memory from undergoing reconsolidation. We investigated whether such an interaction also exists between extinction and reconsolidation of fear memories within the amygdala, by using a within subjects experimental design. We found that inhibition of protein synthesis in the basolateral amygdala (BLA) impaired reconsolidation for both the briefly reactivated and extinguished fear memories suggesting that extinction is not a sufficient condition to prevent induction of reconsolidation in the amygdala. These findings demonstrate that extinction consolidation does not always interact with reconsolidation. Therefore, under these conditions, extinction is not a boundary condition on reconsolidation of fear memories in the basolateral amygdala.
Coselection for microbial resistance to metals and antibiotics in freshwater microcosms
Authors: Stepanauskas Ramunas , Glenn Travis C. , Jagoe Charles H. , Tuckfield R. Cary , Lindell Angela H. , King Catherine J. , McArthur J. V. 
Published: July 2006

SummaryBacterial resistances to diverse metals and antibiotics are often genetically linked, suggesting that exposure to toxic metals may select for strains resistant to antibiotics and vice versa. To test the hypothesis that resistances to metals and antibiotics are coselected for in environmental microbial assemblages, we investigated the frequency of diverse resistances in freshwater microcosms amended with Cd, Ni, ampicillin or tetracycline. We found that all four toxicants significantly increased the frequency of bacterioplankton resistance to multiple, chemically unrelated metals and antibiotics. An ampicillin‐resistant strain of the opportunistic human pathogen Ralstonia mannitolilytica was enriched in microcosms amended with Cd. Frequencies of antibiotic resistance were elevated in microcosms with metal concentrations representative of industry and mining‐impacted environments (0.01–1 mM). Metal but not antibiotic amendments decreased microbial diversity, and a weeklong exposure to high concentrations of ampicillin (0.01–10 mg l−1) and tetracycline (0.03–30 mg l−1) decreased microbial abundance only slightly, implying a large reservoir of antibiotic resistance in the studied environment. Our results provide first experimental evidence that the exposure of freshwater environments to individual metals and antibiotics selects for multiresistant microorganisms, including opportunistic human pathogens.
Multi‐agency collaboration, multiple levels of meaning: social constructionism and the CMM model as tools to further our understanding
Authors: Salmon Gill , Faris Jeff 
Published: July 2006

This study explores the discourse emerging when professionals from a child and adolescent mental health service meet with professionals from other agencies to discuss cases. The study is timely, given the current political contextual forces pushing agencies to work together which run alongside an expanding literature acknowledging the obstacles to achieving this.A thematic analysis identified nine themes, defined according to their discourse type, including single agency discourse, case complexity discourse and multi‐agency discourse. In this paper, the usefulness of the coordinated management of meaning model (CMM) is examined as an additional tool which may be used in data analysis to help understand the discourse within multi‐agency meetings. The two approaches to data analysis are complementary to each other, with both allowing for different layers of context and complexity to emerge from the data.
GROWTH POLICY IN THE SPIRIT OF STEINDL AND KALECKI
Authors: Guger Alois , Marterbauer Markus , Walterskirchen Ewald 
Published: July 2006

ABSTRACTThere are large differences between Steindl’s ideas on growth policies and the Brussels/Paris consensus. Steindl called for innovation and education policies, whereas the mainstream today rather favours deregulation and privatization. Steindl stressed the positive demand‐side effects of the public sector and the contribution of lower household savings and anticyclical policies to growth. The economic mainstream praises the efficiency effects of a declining public sector, the importance of high savings for investment and warns of active anticyclical policies being an impediment to budget consolidation. Steindl and the Keynesians regarded the labour market situation as a consequence of economic growth. Today many economists see low growth as a result of labour market rigidities.
DISTRIBUTIVE AND DEMAND CYCLES IN THE US ECONOMY—A STRUCTURALIST GOODWIN MODEL
Authors: Barbosa‐Filho Nelson H. , Taylor Lance 
Published: July 2006

ABSTRACTThere are regular counterclockwise cycles involving capacity utilization u (horizontal axis) and the labor share ψ (vertical axis) in the US economy since 1929. As in Goodwin’s cyclical growth model, ψ can be interpreted as a Lotka–Volterra predator variable and u as prey. In a phase diagram, dynamics around the u̇=0 schedule respond to effective demand that econometric estimation (1948–2002) shows to be profit‐led. Distributive dynamics around the =0 curve demonstrate a long‐term profit squeeze. Across cycles, the real wage and labor productivity grow at 0.57 per cent per quarter, holding the labor share broadly stable. Modeling the cycle in the (u, ψ) plane provides a parsimonious description of demand and distributive dynamics, consistent with the macroeconomics embedded in the work of Kalecki, Steindl, Goodwin and many subsequent authors.
Influence of density dependence on the detection of trends in unobserved life‐history stages
Authors: Shea K. , Wolf N. , Mangel M. 
Published: July 2006

AbstractIn many species, certain life‐history stages are difficult or impossible to observe directly, hampering management. Often more easily observed stages are monitored instead, but the extent to which various forms of uncertainty cloud our ability to discern trends in one critical life‐history stage by observing another is poorly studied. We develop a stochastic simulation model for threatened California coho salmonOncorhynchus kisutchto examine how well trends in one stage can be detected from observations of another. In particular, we use the model to examine the effect density dependence has on our ability to detect trends. We present a structural form for the transition between life‐history stages that encompasses the common functional forms: density independence, Beverton–Holt compensatory density dependence and Ricker‐type over‐compensation. In small populations, such density dependence is often ignored. However, it may in fact be extremely important, for example if population decline was caused by a decrease in carrying capacity. Our results show that density dependence in any life‐history transition significantly reduces the ability to detect trends in abundance; critical but inaccessible stages cannot generally be studied by monitoring more easily observed stages, especially if density dependence is present for any life‐cycle transition.
Toxicity mediated by soluble oligomers of β‐amyloid(1–42) on cholinergic SN56.B5.G4 cells
Authors: Heinitz Katrin , Beck Martin , Schliebs Reinhard , Perez‐Polo J. Regino 
Published: July 2006

AbstractAlzheimer's disease (AD) is characterized by cholinergic dysfunction and progressive basal forebrain cell loss which has been assumed to be as a result of the extensive accumulation of β‐amyloid (Aβ). In addition to Aβ fibrillar assemblies, there are pre‐fibrillar forms that have been shown to be neurotoxic, although their role in cholinergic degeneration is still not known. Using the cholinergic cell line SN56.B5.G4, we investigated the effect of different Aβ(1–42) aggregates on cell viability. In our model, only soluble oligomeric but not fibrillar Aβ(1–42) forms induced toxicity in cholinergic cells. To determine whether the neurotoxicity of oligomeric Aβ(1–42) was caused by its oxidative potential, we performed microarray analysis of SN56.B5.G4 cells treated either with oligomeric Aβ(1–42) or H2O2. We showed that genes affected by Aβ(1–42) differed from those affected by non‐specific oxidative stress. Many of the genes affected by Aβ(1–42) were present in the endoplasmic reticulum (ER), Golgi apparatus and/or otherwise involved in protein modification and degradation (chaperones, ATF6), indicating a possible role for ER‐mediated stress in Aβ‐mediated toxicity. Moreover, a number of genes, which are known to be involved in AD (clusterin, Slc18a3), were identified. This study provides important leads for the understanding of oligomeric Aβ(1–42) toxicity in cholinergic cells, which may account in part for cholinergic degeneration in AD.
Akt inhibits MLK3/JNK3 signaling by inactivating Rac1: a protective mechanism against ischemic brain injury
Authors: Zhang Quan‐Guang , Wang Xiao‐Tian , Han Dong , Yin Xiao‐Hui , Zhang Guang‐Yi , Xu Tian‐Le 
Published: July 2006

AbstractThe overall goal of this study was to determine the molecular basis by which mixed‐lineage kinase 3 (MLK3) kinase and its signaling pathways are negatively regulated by the pro‐survival Akt pathway in cerebral ischemia. We demonstrated that tyrosine phosphorylation of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) underlies the increased Akt‐Ser473 phosphorylation by orthovanadate. Co‐immunoprecipitation analysis revealed that endogenous Akt physically interacts with Rac1 in the hippocampal CA1 region, and this interaction is promoted on tyrosine phosphatase inhibition. The elevated Akt activation can deactivate MLK3 by phosphorylation at the Ser71 residue of Rac1, a small Rho family of guanidine triphosphatases required for MLK3 autophosphorylation. Subsequently, inhibition of c‐Jun N‐terminal kinase 3 (JNK3) results in decreased serine phosphorylation of 14‐3‐3, a cytoplasmic anchor of Bax, and prevents ischemia‐induced mitochondrial translocation of Bax, release of cytochrome c and activation of caspase 3. At the same time, the expression of Fas‐ligand decreases in the CA1 region after inhibition of c‐Jun activation. The neuroprotective effect of Akt activation is significant in the CA1 region after global cerebral ischemia. Our results suggest that the activation of the pro‐apoptotic MLK3/JNK3 cascade induced by ischemic stress can be suppressed through activation of the anti‐apoptotic phosphatidylinositol 3‐kinase/Akt pathway, which provides a direct link between Akt and the family of stress‐activated kinases.
Hepatoma‐derived growth factor, a new trophic factor for motor neurons, is up‐regulated in the spinal cord of PQBP‐1 transgenic mice before onset of degeneration
Authors: Marubuchi Shigeki , Okuda Tomohiro , Tagawa Kazuhiko , Enokido Yasushi , Horiuchi Daisuke , Shimokawa Reiko , Tamura Takuya , Qi Mei‐Ling , Eishi Yoshinobu , Watabe Kazuhiko , Shibata Masao , Nakagawa Masaya , Okazawa Hitoshi 
Published: July 2006

AbstractHepatoma‐derived growth factor (HDGF) is a nuclear protein homologous to the high‐mobility group B1 family of proteins. It is known to be released from cells and to act as a trophic factor for dividing cells. In this study HDGF was increased in spinal motor neurons of a mouse model of motor neuron degeneration, polyglutamine‐tract‐binding protein‐1 (PQBP‐1) transgenic mice, before onset of degeneration. HDGF promoted neurite extension and survival of spinal motor neurons in primary culture. HDGF repressed cell death of motor neurons after facial nerve section in newborn rats in vivo. We also found a significant increase in p53 in spinal motor neurons of the transgenic mice. p53 bound to a sequence in the upstream of the HDGF gene in a gel mobility shift assay, and promoted gene expression through the cis‐element in chloramphenicol acetyl transfer (CAT) assay. Finally, we found that HDGF was increased in CSF of PQBP‐1 transgenic mice. Collectively, our results show that HDGF is a novel trophic factor for motor neurons and suggest that it might play a protective role against motor neuron degeneration in PQBP‐1 transgenic mice.
Lymphedematous HIV‐associated Kaposi's sarcoma
Authors: Ramdial Pratistadevi K. , Chetty Runjan , Singh Bhugwan , Singh Rajendrakumar , Aboobaker Jamila 
Published: July 2006

Background:  Advanced Kaposi's sarcoma is frequently associated with chronic lymphedema (cLO). The histopathological features of lymphedematous HIV‐associated KS (KS) are poorly documented and the co‐existence of fibroma‐like nodules in lymphedematous KS is under‐recognized. The aims of this study were to assess the clinicopathological spectrum and diagnostic difficulties associated with lymphedematous KS and to highlight the clinicopathological profile of fibroma‐like nodules. In addition, the pathogenesis of fibroma‐like nodules and cLO is revisited.Materials and methods:  Prospective 17‐month clinicopathological study of all biopsies from patients with lymphedematous KS.Results:  Seventy‐four biopsies, the majority from the lower limbs, from 41 patients were evaluated. Nineteen, 14, five and three patients had one, two, three or four biopsies each, respectively. In 14 biopsies, there was poor clinicopathological correlation of KS stage. Exclusive lesional KS (patch, plaque, nodule or lymphangioma‐like) was identified in 29 biopsies; 23 and eight biopsies demonstrated KS or fibroma‐like morphology and the adjacent dermis demonstrated cLO. There was variable intratumoral and peritumoral venous compression and lymphatic dilatation. Fourteen biopsies demonstrated cLO exclusively. Smaller fibroma‐like nodules lacked KS spindle cells, whereas >5 mm nodules demonstrated focal KS spindle cell proliferation and aggregation on extensive sectioning. The subcutis of 42 biopsies demonstrated variable fibrosis, hemosiderin deposits, lymphocytes, plasma cells, KS, interstitial granular material and pools of lymph fluid. Subcutaneous abscesses were identified in six biopsies. All biopsies had variable epidermal features of cLO.Conclusions:  cLO influences clinicopathological correlation of KS stage and may also mask the presence of KS and the co‐existence of subcutaneous abscesses. Smaller fibroma‐like nodules are hypothesized to be a manifestation of cLO that have the potential to acquire the characteristics of KS. Lymphatic and venous obstruction, protein‐rich interstitial fluid, tissue hemosiderin and subcutaneous infection are hypothesized to play a combined role in the evolution and perpetuation of cLO.
Cutaneous marginal zone B‐cell lymphoma in the setting of fluoxetine therapy: a hypothesis regarding pathogenesis based on in vitro suppression of T‐cell‐proliferative response
Authors: Breza Thomas S. , Zheng Pan , Porcu Pierluigi , Magro Cynthia M. 
Published: July 2006

Introduction:  Drugs may be an important cause of atypical lymphocytic infiltration. Oftentimes, these infiltrates are in the context of pseudolymphomata. We report a patient who developed lymphocytoma cutis temporally associated with initiation of fluoxetine therapy that later went on to develop cutaneous marginal zone B‐cell lymphoma. The response of peripheral blood lymphocytes to fluoxetine and other drugs was examined in an attempt to ascertain the potential role for drugs in the propagation of these infiltrates.Materials and Methods:  Routine light microscopic analysis and phenotypic studies were performed on tissue obtained from a skin biopsy. Lymphocyte mitogenic studies were carried out using increasing concentrations of fluoxetine, bupropion, and two anticonvulsants.Results:  An initial biopsy was consistent with lymphocytoma cutis. The patient stopped fluoxetine associated with lesional regression. The lesions recurred despite being off fluoxetine; a repeat biopsy was compatible with marginal zone lymphoma. Lymphocyte proliferation assays revealed a suppressive effect on T‐lymphocyte proliferation at physiologic concentrations. Other tested drugs did not have a similar suppressive effect.Conclusion:  Fluoxetine may be associated with pseudolymphomata and marginal zone lymphoma. The inhibitory effects on T‐lymphocyte function and more specifically T‐suppressor function may lead to excessive antigen‐driven B‐cell proliferation.
Atypical nevi of the scalp in adolescents
Authors: Fabrizi Giujeppe , Pagliarello Calogero , Parente Paola , Massi Guido 
Published: July 2006

Background:  A few reports in the literature point out that in special areas of the body, nevi can have peculiar pseudomelanomatous features. In our routine work, we have met few examples of atypical nevi with peculiar features on the scalp of teenagers. To evaluate the frequency and the biological behaviour of these lesions, we have conducted a complete survey on melanocytic lesions on the scalp in a significant group of patients.Materials and methods:  Thirty‐nine nevi of the scalp were from adolescents (12–18 years), 160 from adults, and 30 from children below the age of 12 years.Results:  About 10% of the melanocytic nevi of the scalp of adolescents have atypical cytological and architectural aspects that are different from those seen in Clark’s dysplastic nevus. The most striking features were the presence of large bizarrely shaped nests scattered disorderly along the junction with follicular involvement. Other findings were pagetoid spread of cells above the junction and the discohesive pattern of the melanocytes in the nests. Mild cytological atypia was present but less significant. Such distinctive aspects are not found in nevi of the same site in adults or younger children. The general pattern of these atypical nevi of the scalp of adolescents closely recalls that of the so‐called atypical nevi on special sites, i.e. nevi on mammary line, genitalia and body’s folds. Despite the architectural and cytological atypia, clinical follow‐up does not show any tendency to recur or proclivity to malignant behaviour.Conclusions:  Despite their similarities with melanoma, the nevi with atypical features of the scalp of adolescents are probably an entirely benign entity, at least at the moment of their excision. However, although benign, the relationship of this peculiar group of nevi with melanomas developed in adulthood remains entirely unknown, and the complete excision with conservative margins seems a recommendable procedure.
Systemic vaccination prevents the total destruction of mucosal CD4 T cells during acute SIV challenge
Authors: Mattapallil Joseph J. , Hill Brenna , Douek Daniel C. , Roederer Mario 
Published: July 2006

AbstractBackground  Acute human immunodeficiency virus (HIV)/simian immunodeficiency virus (SIV) infections are accompanied by a systemic loss of memory CD4 T cells, with mucosal sites serving as a major site for viral replication, dissemination and CD4 T cell depletion. Protecting the mucosal CD4 T cell compartment thus is critical to contain HIV, and preserve the integrity of the mucosal immune system. The primary objective of this study was to determine if systemic vaccination with DNA/rAd‐5 encoding SIV‐mac239‐env, gag and pol could prevent the destruction of CD4 T cells in mucosal tissues.Methods  Rhesus macaques were immunized with DNA/r‐Ad‐5 encoding SIV genes and compared with those immunized with sham vectors following high dose intravenous challenge with SIVmac251. SIV specific CD4 and CD8 T cell responses, cell associated viral loads and mucosal CD4 T cell dynamics were evaluated.Results  Strong SIV specific immune responses were induced in mucosal tissues of vaccinated animals as compared with sham controls. These responses expanded rapidly following challenge suggesting a strong anamnestic response. Immune responses were associated with a decrease in cell associated viral loads, and a loss of fewer mucosal CD4 T cells. Approximately 25% of mucosal CD4 T cells were preserved in vaccinated animals as compared with <5% in sham controls. These results demonstrate that systemic immunization strategies can induce immune responses in mucosal tissues that can protect mucosal CD4 T cells from complete destruction following challenge.Conclusions  Preservation of mucosal CD4 T cells can contribute to maintaining immune competence in mucosal tissues and provide a substantial immune benefit to the vaccinees.
Morphometric and hormonal changes during the Chimpanzee menstrual cycle
Authors: Machatschke Ivo H. , Dittami John , Wallner Bernard 
Published: July 2006

AbstractBackground  Sex steroids affect many peripheral tissue sites in female mammals. Receptors for these hormones have been found in skin, fat, and bone. In women, these tissues can show morphological changes during the menstrual cycle that may be directly related to steroid secretion.Methods The present study was done on chimpanzees to document morphometric markers associated with these tissues (anogenital swelling volume, skin fold thickness as indicator of subcutaneous fat, bony diameters of mandible, wrist, and elbow) and to compare them with cyclic patterns of estradiol, progesterone, testosterone, gonadotropins, and prolactin.Results  Swelling volume changed significantly over the menstrual cycle. All other morphometric parameters showed variation without statistical significance. Skin folds were thickest during the luteal phase. Bony diameters displayed similar but less distinctive changes. Testosterone correlated positively with diameter sites, inversely with subcutaneous fat. No relationships with either estradiol or progesterone were found. We assume that subcutaneous fat and morphometric bone parameters exhibit cycle‐dependent changes that may be caused by changes in steroid secretion.