bluuebunny/crossref_metadata_2025_split huggingface dataset:
Marmosets as a next‐generation model of comparative cognition
Authors: YAMAZAKI YUMIKO , WATANABE SHIGERU 
Published: September 2009

AbstractCommon marmosets have traditionally been used in fields such as comparative psychology, cognitive neuroscience, and ethology, and as animal models of human disease research because of their relatively small body size, high reproductive rate, similar breeding system characteristics to those of humans, high dependency on vocal communication, and behavioral effects from drug administration that resemble those of humans. Although the animal has proved to be quite advantageous in animal model research in comparison to rodents, and has specific ecological and evolutionary characteristics that are worthy of exploration, few attempts have been made until recently to combine both types of approach. Thus, supported by neuroscientific methodologies that have recently been developed using this species, the authors suggest that the evolutionary origins of cognitive and social functions common to or differentiated in primates, could be uncovered through research that explores the behavioral and neural bases of cognition in the marmosets.
Valproic acid induces functional heat‐shock protein 70 via Class I histone deacetylase inhibition in cortical neurons: a potential role of Sp1 acetylation
Authors: Marinova Zoya , Ren Ming , Wendland Jens R. , Leng Yan , Liang Min‐Huei , Yasuda Shigeru , Leeds Peter , Chuang De‐Maw 
Published: September 2009

AbstractNeuroprotective properties of the mood stabilizer valproic acid (VPA) are implicated in its therapeutic efficacy. Heat‐shock protein 70 (HSP70) is a molecular chaperone, neuroprotective and anti‐inflammatory agent. This study aimed to investigate underlying mechanisms and functional significance of HSP70 induction by VPA in rat cortical neurons. VPA treatment markedly up‐regulated HSP70 protein levels, and this was accompanied by increased HSP70 mRNA levels and promoter hyperacetylation and activity. Other HDAC inhibitors – sodium butyrate, trichostatin A, and Class I HDAC‐specific inhibitors MS‐275 and apicidin, – all mimicked the ability of VPA to induce HSP70. Pre‐treatment with phosphatidylinositol 3‐kinase inhibitors or an Akt inhibitor attenuated HSP70 induction by VPA and other HDAC inhibitors. VPA treatment increased Sp1 acetylation, and a Sp1 inhibitor, mithramycin, abolished the induction of HSP70 by HDAC inhibitors. Moreover, VPA promoted the association of Sp1 with the histone acetyltransferases p300 and recruitment of p300 to the HSP70 promoter. Further, VPA‐induced neuroprotection against glutamate excitotoxicity was prevented by blocking HSP70 induction. Taken together, the data suggest that the phosphatidylinositol 3‐kinase/Akt pathway and Sp1 are likely involved in HSP70 induction by HDAC inhibitors, and induction of HSP70 by VPA in cortical neurons may contribute to its neuroprotective and therapeutic effects.
Immunoreactivity of the phosphorylated axonal neurofilament H subunit (pNF‐H) in blood of ALS model rodents and ALS patients: evaluation of blood pNF‐H as a potential ALS biomarker
Authors: Boylan Kevin , Yang Cui , Crook Julia , Overstreet Karen , Heckman Michael , Wang Yong , Borchelt David , Shaw Gerry 
Published: September 2009

AbstractLevels of neurofilament subunits, potential biomarkers of motor axon breakdown, are increased in amyotrophic lateral sclerosis (ALS) patient’s CSF but data on blood are not available. We measured blood levels of the phosphorylated axonal form of neurofilament H (pNF‐H) by ELISA in transgenic rodent models of superoxide dismutase 1 (SOD1) ALS, and in 20 ALS patients and 20 similar aged controls monthly for 4 months. All symptomatic rodent ALS models showed robust levels of blood pNF‐H, while control rodents or mice transgenic for unmutated SOD1 showed no detectable blood pNF‐H. Average pNF‐H levels in the G93A SOD1 mouse progressively increased from day 74 through death (day ∼130). Median blood pNF‐H level in ALS patients was 2.8‐fold higher than controls (p < 0.001). Median ALSFRS‐R declined a median of 0.8 pt/month (p < 0.001); higher baseline pNF‐H level appeared to be associated with faster ALSFRS‐R decline over 4 months (p = 0.087). The median rate of decline in ALSFRS‐R was 1.9 pt/month in patients with baseline pNF‐H levels above the median pNF‐H value of 0.53 ng/mL; ALSFRS‐R declined at a median of 0.6 pt/month in patients below this level. The pNF‐H levels were relatively stable month to month in individual patients, raising questions regarding the molecular pathogenesis of ALS. Baseline control human pNF‐H levels were higher in men than women and increased minimally over time. These data suggest that blood pNF‐H can be used to monitor axonal degeneration in ALS model rodents and support further study of this protein as a potential biomarker of disease prognosis in ALS patients.
Neuro‐inflammation induced in the hippocampus of ‘binge drinking’ rats may be mediated by elevated extracellular glutamate content
Authors: Ward Roberta J. , Colivicchi Maria Alessandra , Allen Rachel , Schol François , Lallemand Frédéric , De Witte Philippe , Ballini Chiara , Corte Laura Della , Dexter David 
Published: September 2009

AbstractThe neuropathological and immune changes induced in the brain by ‘binge drinking’ have been investigated in a rat model. Evidence of neuro‐inflammation was identified in the ‘binge drinking’ rat model of alcohol abuse after 3 weeks of administration of 2 or 3 g/kg ethanol (EtOH), three times per day for two consecutive days, followed by 5 days of abstinence: Firstly, alveolar macrophages, isolated from these animals, showed significant increases in inducible nitric oxide synthase, as assayed by nitrite release, both before and after lipopolysaccaharide stimulation. Secondly, significant numbers of activated microglia were present in the dentate gyrus region of the hippocampus of the ‘binge drinking’ model, after major histocompatibility complex class II staining, by comparison with the control. Microdialysis studies in the ventral hippocampus identified a significant increase in the basal extracellular concentration of glutamate, in both the 2 and 3 g/kg administered ‘binge drinking’ rats. In contrast, no changes in the hippocampal extracellular concentrations, of GABA and taurine, or the dopamine and serotonin metabolites were observed under basal conditions. A further dose of EtOH induced a significant decrease in the concentrations of both 3,4‐dihydroxyphenylacetic acid and 5‐hydroxyindoleacetic acid, whereas glutamate, taurine and GABA levels were unaffected. There was no evidence that EtOH preference was initiated by the ‘binge drinking’ regimen. Our results suggest that the possible toxicity associated with ‘binge drinking’ maybe directed by the elevated glutamate levels, which in turn, activate phagocytic cells to release their inflammatory cytokines and chemokines, ultimately leading to neuro‐inflammation.
Retracted: Broad DNA repair responses in neural injury are associated with activation of the IL‐6 pathway in cholesterol‐fed rabbits
Authors: Wu Min , Audet Aaron , Cusic Jenna , Seeger Drew , Cochran Richard , Ghribi Othman 
Published: September 2009

AbstractThe importance of DNA repair in the pathogenic mechanism of Alzheimer’s Disease (AD) is still poorly understood. Here, we report that a broad range of responses by DNA repair proteins plays a critical role in the regulation of inflammatory response in rabbits fed with cholesterol‐rich diet, a model system for AD. We found accumulation of oxodG DNA adduct in the brain of rabbits fed with cholesterol‐enriched diets compared to control diets, which subsequently induced a broad range of DNA repair protein activities. Also, the hippocampus was identified as the primary site of oxidative DNA damage and elevated OGG1 activity. In addition, a physical interaction between XPB and OGG1 may account for a potential mechanism involving these DNA repair responses. DNA repair proteins also impact activation of various signaling cascades, including Src in response to cholesterol oxidation. Furthermore, OGG1 deficient mice showed no IL‐6 activation as seen in wt mice but a drastic increase of TNF‐α, a pro‐inflammatory cytokine. Thus, OGG1 may be associated with cytokine production induced by high cholesterol levels, impacting neurodegeneration. Together, our studies suggest that critical DNA repair proteins are associated with development of AD, and may serve as potential targets for the treatment of AD.
Capsaicin affects brain function in a model of hepatic encephalopathy associated with fulminant hepatic failure in mice
Authors: Avraham Y , Grigoriadis NC , Magen I , Poutahidis T , Vorobiav L , Zolotarev O , Ilan Y , Mechoulam R , Berry EM 
Published: September 2009

Background and purpose:  Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver failure. In view of the effects of cannabinoids in a thioacetamide‐induced model of hepatic encephalopathy and liver disease and the beneficial effect of capsaicin (a TRPV1 agonist) in liver disease, we assumed that capsaicin may also affect hepatic encephalopathy.Experimental approach:  Fulminant hepatic failure was induced in mice by thioacetamide and 24 h later, the animals were injected with one of the following compound(s): 2‐arachidonoylglycerol (CB1, CB2 and TRPV1 receptor agonist); HU308 (CB2 receptor agonist), SR141716A (CB1 receptor antagonist); SR141716A+2‐arachidonoylglycerol; SR144528 (CB2 receptor antagonist); capsaicin; and capsazepine (TRPV1 receptor agonist and antagonist respectively). Their neurological effects were evaluated on the basis of activity in the open field, cognitive function in an eight‐arm maze and a neurological severity score. The mice were killed 3 or 14 days after thioacetamide administration. 2‐arachidonoylglycerol and 5‐hydroxytryptamine (5‐HT) levels were determined by gas chromatography‐mass spectrometry and high‐performance liquid chromatography with electrochemical detection, respectively.Results:  Capsaicin had a neuroprotective effect in this animal model as shown by the neurological score, activity and cognitive function. The effect of capsaicin was blocked by capsazepine. Thioacetamide induced astrogliosis in the hippocampus and the cerebellum and raised brain 5‐hydroxytryptamine levels, which were decreased by capsaicin, SR141716A and HU‐308. Thioacetamide lowered brain 2‐arachidonoylglycerol levels, an effect reversed by capsaicin.Conclusions:  Capsaicin improved both liver and brain dysfunction caused by thioacetamide, suggesting that both the endocannabinoid and the vanilloid systems play important roles in hepatic encephalopathy. Modulation of these systems may have therapeutic value.
Landscape Features and Panthers in Florida
Authors: MAEHR DAVID S. , COX JAMES A. 
Published: September 2009

Abstract: We used a geographic information system (GIS) to document spatial associations of Florida panthers, land cover, and other geographical features. Panther radio locations (n = 14,548) occurred in hardwood hammock, mixed hardwood swamp, and cypress swamp in greater proportion than in randomly positioned points (n = 8500). Panther radio locations occurred less frequently in agricultural, barren, and shrub and brush land cover. Panther home ranges consisted of a combination of preferred and avoided cover types, including freshwater marsh, cypress swamp, hardwood swamp, and agricultural land. These cover types accounted for 62% of the area in panther home ranges. We used correlation and discriminant function analyses to assess the potential importance of 20 landscape features. These panther locations were effectively distinguished from random points using four landscape variables: (1) the size of a contiguous patch of preferred land cover; (2) the proximity to preferred land cover; (3) the diversity of three preferred cover types within a window 120 × 120 m, and (4) the matrix within which preferred cover types occurred. Eighty‐three percent of the panther locations and 81.9% of the random points were correctly classified based on a linear model constructed using these four variables. Large, contiguous areas of preferred land‐cover types were especially important because 96% of all panther locations occurred within 90 m of preferred land cover. The average preferred forest patch size that was used by these panthers was 20,816 ha, and a regression equation suggests that patches larger than 500 ha are important. Maps of panther habitat suitability were developed using coefficients derived from discriminant analysis. Large areas of suitable land cover that are heavily used by panthers occur on private ranches covering 3606 km2. Conservation of preferred habitat on these private lands is essential to maintaining a free‐ranging population of panthers in southwest Florida.Características del paisaje y las panteras en Florida
Priming Deficiency in Male Subjects at Risk for Alcoholism: The N4 During a Lexical Decision Task
Authors: Roopesh Bangalore N. , Rangaswamy Madhavi , Kamarajan Chella , Chorlian David B. , Stimus Arthur , Bauer Lance O. , Rohrbaugh John , O’Connor Sean J. , Kuperman Samuel , Schuckit Marc , Porjesz Bernice 
Published: September 2009

Background:  While there is extensive literature on the relationship between the P3 component of event‐related potentials (ERPs) and risk for alcoholism, there are few published studies regarding other potentially important ERP components. One important candidate is the N4(00) component in the context of semantic processing, as abnormalities in this component have been reported for adult alcoholics.Method:  A semantic priming task was administered to nonalcohol dependent male offspring (18 to 25 years) of alcoholic fathers [high risk (HR) n = 23] and nonalcoholic fathers [low risk (LR) n = 28] to study whether the 2 groups differ in terms of the N4 component. Subjects were presented with 150 words and 150 nonwords. Among the words, 50 words (primed) were preceded by their antonyms (prime, n = 50), whereas the remaining 50 words were unprimed. For the analysis, N4 amplitude and latency as well as behavioral measures for the primed and unprimed words were considered.Results:  A significant interaction effect was observed between semantic condition and group, where HR subjects did not show N4 attenuation for primed stimuli.Conclusion:  The lack of N4 attenuation to primed stimuli and/or inability to differentiate between primed and unprimed stimuli, without latency and reaction time being affected, suggest deficits in semantic priming, especially in semantic expectancy and/or postlexical semantic processing in HR male offspring. Further, it indicates that it might be an electrophysiological endophenotype that reflects genetic vulnerability to develop alcoholism.
Bone marrow derived cells in the tumour microenvironment contain cells with primitive haematopoietic phenotype
Authors: Deak Erika , Göttig Stephan , Rüster Brigitte , Paunescu Virgil , Seifried Erhard , Gille Jens , Henschler Reinhard 
Published: September 2009

AbstractInfiltration of bone marrow derived cells is part of the angiogenic switch required for uncontrolled tumour growth. However, the nature of the tumour‐infiltrating cells from bone marrow has not been fully elucidated. To investigate the phenotype of bone marrow derived cells within a tumour, we employed the Lewis lung carcinoma (LLC) murine tumour model. We followed bone marrow derivation of tumour‐infiltrating cells through transplantation of CD45.2 bone marrow cells into pre‐irradiated CD45.1 mice. We found robust CD45.2 donor type chimerism in bone marrow and blood of CD45.1 recipient tumour‐bearing mice. Flow cytometric analysis of LLC tumours showed, in addition to previously described pro‐angiogenic CD45+VEGFR2+‘endothelial progenitor cells’ (EPC), or CD45+Tie2+‘Tie2‐expressing monocytes’ (TEM), incorporation of donor type lineage marker negative (Lin−) and Lin−Sca1+ undifferentiated haematopoietic cell types. Immunohistochemical analysis confirmed the extravasal location of the primitive haematopoietic cells. Flow‐cytometric sorting of bone marrow cells and subsequent analysis in haematopoietic colony‐forming assays revealed that cells with a Lin−Sca1+ phenotype, which were initially negative for VEGFR2 and Tie2, gave rise to VEGFR2+ and/or Tie2+ cells. Moreover, Lin− bone marrow cells pre‐labelled with the membrane dye PKH26 (a red fluorochrome) and transplanted i.v. into tumour‐bearing mice were found to extravasate and incorporate into LLC tumours within 24 hrs. Thus, primitive haematopoietic precursors which are thought to be precursors of EPC and TEMs, constitute a part of the tumour microenvironment. This makes them an attractive target cell population for tumour‐directed cellular therapies.
Anti‐CD44 induces apoptosis in T lymphoma via mitochondrial depolarization
Authors: Rajasagi Mohini , von Au Anja , Singh Rahul , Hartmann Natalie , Zöller Margot , Marhaba Rachid 
Published: September 2009

AbstractA blockade of CD44 can interfere with haematopoietic and leukemic stem cell homing, the latter being considered as a therapeutic option in haematological malignancies. We here aimed to explore the molecular mechanism underlying the therapeutic efficacy of anti‐CD44. We noted that in irradiated mice reconstituted with a bone marrow cell transplant, anti‐CD44 exerts a stronger effect on haematopoietic reconstitution than on T lymphoma (EL4) growth. Nonetheless, in the non‐reconstituted mouse anti‐CD44 suffices for a prolonged survival of EL4‐bearing mice, where anti‐CD44‐prohibited homing actively drives EL4 cells into apoptosis. In vitro, a CD44 occupancy results in a 2–4‐fold increase in apoptotic EL4 cells. Death receptor expression (CD95, TRAIL, TNFRI) remains unaltered and CD95 cross‐linking‐mediated apoptosis is not affected. Instead, CD44 ligation promotes mitochondrial depolarization that is accompanied by caspase‐9 cleavage and is inhibited in the presence of a caspase‐9 inhibitor. Apoptosis becomes initiated by activation of CD44‐associated phosphatase 2A (PP2A) and proceeds via ERK1/2 dephosphorylation without ERK1/2 degradation. Accordingly, CD44‐induced apoptosis could be mimicked by ERK1/2 inhibition, that also promotes EL4 cell apoptosis through the mitochondrial pathway. Thus, during haematopoietic stem cell reconstitution care should be taken not to interfere by a blockade of CD44 with haematopoiesis, which could be circumvented by selectively targeting leukemic CD44 isoforms. Beyond homing/settlement in the bone marrow niche, anti‐CD44 drives leukemic T cells into apoptosis via the mitochondrial death pathway by CD44 associating with PP2A. Uncovering this new pathway of CD44‐induced leukemic cell death provides new options of therapeutic interference.
Altered interaction between cardiac vagal influence and delta sleep EEG suggests an altered neuroplasticity in patients suffering from major depressive disorder
Authors: Jurysta F. , Kempenaers C. , Lancini J. , Lanquart J.‐P. , Van De Borne P. , Linkowski P. 
Published: September 2009

Jurysta F, Kempenaers C, Lancini J, Lanquart J‐P, van de Borne P, Linkowski P. Altered interaction between cardiac vagal influence and delta sleep EEG suggests an altered neuroplasticity in patients suffering from major depressive disorder.Objective:  Major depressive disorder (MDD), which is associated with altered neuroplasticity and increased relative cardiac sympathic activity, enhances the risk of cardiovascular pathologies. Interaction between cardiac sympatho‐vagal indexes and delta sleep power is probably altered in MDD.Method:  Sleep characteristics and cardiac sympatho‐vagal indexes of 10 depressive patients were compared to 10 control men across the first three non‐rapid eye movement (NREM)–REM cycles. Interaction between normalized high frequency (HF) and delta power bands was studied using coherence analysis.Results:  Patients showed increased sleep latency, stage 1 and wake durations. No differences in heart rate variabilities were observed: Total power, HF and RR‐interval decreased from NREM to REM sleep and wakefulness in both groups. Gain value was lower in patients while coherence and phase shift were similar between groups. Modifications in HF appear 8 min before modifications in delta.Conclusion:  Major depressive disorder is related to an altered link between cardiac vagal influence and delta sleep, suggesting disorders in cardiovascular controls and an altered neuroplasticity.
The relationship between childhood trauma history and the psychotic subtype of major depression
Authors: Gaudiano B. A. , Zimmerman M. 
Published: September 2009

Gaudiano BA, Zimmerman M. The relationship between childhood trauma history and the psychotic subtype of major depression.Objective:  Increasing evidence exists linking childhood trauma and primary psychotic disorders, but there is little research on patients with primary affective disorders with psychotic features.Method:  The sample consisted of adult out‐patients diagnosed with major depressive disorder (MDD) at clinic intake using a structured clinical interview. Patients with MDD with (n = 32) vs. without psychotic features (n = 591) were compared as to their rates of different types of childhood trauma.Results:  Psychotic MDD patients were significantly more likely to report histories of physical (OR = 2.81) or sexual abuse (OR = 2.75) compared with non‐psychotic MDD patients. These relationships remained after controlling for baseline differences. Within the subsample with comorbid post‐traumatic stress disorder, patients with psychotic MDD were significantly more likely to report childhood physical abuse (OR = 3.20).Conclusion:  Results support and extend previous research by demonstrating that the relationship between childhood trauma and psychosis is found across diagnostic groups.
Prenatal and postnatal parental smoking and acute otitis media in early childhood
Authors: Håberg SE , Bentdal YE , London SJ , Kværner KJ , Nystad W , Nafstad P 
Published: September 2009

AbstractAim:  To explore the associations between acute otitis media in early childhood and prenatal and postnatal tobacco smoke exposure.Methods:  Subjects were 32 077 children born between 2000 and 2005 in the Norwegian Mother and Child Study with questionnaire data on tobacco smoke exposure and acute otitis media up to 18 months of age. Multivariate regression models were used to obtain adjusted relative risks for acute otitis media.Results:  Acute otitis media was slightly more common in children exposed to parental smoking. The incidence from 0 to 6 months was 4.7% in unexposed children and 6.0% in children exposed both prenatally and postnatally. After adjusting for postnatal exposure and covariates, the relative risk for acute otitis media 0–6 months when exposed to maternal smoking in pregnancy was 1.34, 95% confidence interval: 1.06–1.69. Maternal smoking in pregnancy was associated with acute otitis media up to 12 months of age. Compared with non‐exposed children, there was a slightly increased risk of recurrent acute otitis media for children exposed both prenatally and postnatally with a relative risk of 1.24, 95% confidence interval: 1.01–1.52.Conclusion:  Even in a cohort with relatively low exposure levels of parental smoking, maternal smoking in pregnancy was associated with an increased risk of acute otitis media in early childhood.