bluuebunny/crossref_metadata_2025_split huggingface dataset:
Remembering kauri on the ‘Kauri Coast’
Authors: Boswijk Gretel 
Published: July 2010

AbstractThis paper explores how the recent history of kauri is remembered and commemorated on the Kauri Coast, western Northland, focusing on three specific heritage sites: The Kauri Museum at Matakohe, Trounson Kauri Park, and Waipoua Forest Sanctuary. Each site was established to preserve elements of the past before they were lost or irrevocably altered. The museum commemorates the pioneers and the kauri timber and gum industries, while Trounson Kauri Park and Waipoua Forest were intended to represent primeval forest and stand as monuments to people who advocated their protection.
Performing a new regional geography
Authors: Winder Gordon , Lewis Nick 
Published: July 2010

AbstractIn this introduction to the Special Issue ‘Practising a New Regional Geography in Northland’, we call for a new regional geography. We use the experience of a field course to reflect upon the opportunities and challenges associated with doing ‘regional geography’ in the regions, a subdiscipline that has in recent decades been pushed into the backwaters of the discipline. We reinterpret the maxim ‘geography is what geographers do’ in a new way that emphasises pedagogy and research practice. The case of Northland and helping our students to learn experientially about community and environment under the rubric of sustainability allows us to argue the case for a reinterpretation of regional geography in these terms. We position the contributions in this Special Issue in terms of our call.
Effects of exercise training on adipogenesis of stromal‐vascular fraction cells in rat epididymal white adipose tissue
Authors: Sakurai T. , Endo S. , Hatano D. , Ogasawara J. , Kizaki T. , Oh‐ishi S. , Izawa T. , Ishida H. , Ohno H. 
Published: July 2010

AbstractAim:  Previous studies have shown that exercise training reduced white adipose tissue (WAT) mass compared to that in sedentary controls, and that the smaller mass contained fewer adipocytes. However, the effect of exercise training on adipogenesis is not completely clear. Therefore, we re‐examined the effect of exercise training on adipocyte numbers in WAT and, if such an effect was found tested the adipogenic responses of stromal‐vascular fraction (SVF) cells containing adipose tissue‐derived stem cells (ADSC) in epididymal WAT from exercise‐trained (TR) rats.Methods:  Wistar male rats were divided into two groups: control (C) and TR. The TR rats were subjected to exercise on a treadmill for 9 weeks. SVF cells containing ADSC were separated from epididymal WAT by centrifugation. Expression of adipocyte differentiation‐related genes and adipogenesis of SVF cells were examined.Results:  In SVF cells of TR rats, the expression of peroxisome proliferator‐activated receptor γ (PPARγ) and that of PPARγ target lipogenic genes was dramatically downregulated, whereas that of preadipocyte factor‐1 gene was significantly upregulated. Lipid accumulation in SVF cells of TR rats after the induction of adipocyte differentiation was significantly suppressed in comparison with that of C rats. Moreover, increased expression of hypoxia‐inducible factor‐1α (HIF‐1α) protein was observed in SVF cells of TR rats. Pre‐treatment of YC‐1, a potent HIF‐1α inhibitor, in SVF cells of TR rats restored adipogenesis.Conclusion:  These results suggest that exercise training suppresses the ability of SVF cells to differentiate into adipocytes, and that underlying mechanisms involve the upregulation of HIF‐1α expression.
First record of Blastopsylla occidentalis Taylor, 1985 (Hemiptera: Psyllidae), a Eucalyptus psyllid in Cameroon, Central Africa
Authors: TAMESSE Joseph Lebel , LAURENTINE Soufo , WENCESLAS Yana , JOLY Dzokou Victor 
Published: July 2010

AbstractIn order to investigate the biodiversity of psyllids in Cameroon, we collected a psyllid on Eucalyptus spp. (Myrtaceae) for the first time. Morphometric and morphological studies of this psyllid enable us to identify it as Blastopsylla occidentalis Taylor (Hemiptera: Psylloidea). Blastopsylla occidentalis lives on four Eucalyptus species (Eucalyptus globulus, E. saligna, E. deglupta, E. camaldulensis) in the Western and Central regions of the country. A description and illustration of the different developmental stages of B. occidentalis will allow the identification of this pest of Eucalyptus.
Taxonomic study of Korean Eriborus Förster (Hymenoptera: Ichneumonidae: Campopleginae) new to Korea
Authors: CHOI Jin‐Kyung , LEE Jong‐Wook 
Published: July 2010

AbstractWe report one species, Eriborus vulgaris (Morley, 1913), new to Korea. A revised key to the species of Korean Eriborus Förster, redescriptions and photographs of diagnostic characters are provided.
Apoptosis: A Two‐edged Sword in Aging
Authors: WARNER HUBER R. 
Published: July 2010

ABSTRACTHere we summarize briefly what is known about both the positive and negative impacts of apoptosis during aging in mammalian systems and also update an earlier review. It is important to understand both of these impacts to devise useful interventions. Such interventions include both physiological and molecular approaches, including transgenic interventions. The critical roles of the mitochondria in both generating reactive oxygen species, and in initiating apoptosis are recognized, suggesting that maintaining mitochondrial function could be an important therapeutic goal, especially in post‐mitotic tissues. In contrast, the ability to eliminate unwanted, damaged and dysfunctional cells through apoptosis has anti‐aging implications in mitotic tissues.
Neither Caspase‐3 nor DNA Fragmentation Factor Is Required for High Molecular Weight DNA Degradation in Apoptosis
Authors: WALKER P. ROY , LEBLANC JULIE , CARSON CHRISTINE , RIBECCO MARIA , SIKORSKA MARIANNA 
Published: July 2010

ABSTRACTIn this paper, we show that there is a two‐step process of DNA fragmentation in apoptosis; DNA is first cleaved to large fragments of 50–300 kb that are subsequently cleaved to smaller oligonucleosomes in some, but not all cells. Significantly, only the first stage is considered essential for cell death since some cells, for example human MCF7 breast carcinoma cells and human NT2 neuronal cells, do not show this behavior but still display normal nuclear morphological apoptotic changes. In cells that usually produce small fragments blocking the second (internucleosomal) stage of DNA fragmentation prevents neither nuclear condensation nor apoptosis. We are beginning to understand why the extent of DNA fragmentation during apoptosis varies enormously and why it appears to be a function of the cell type not the inducer. Presumably, this reflects the content of not only endonuclease activit(ies) but also on the ability of the cells to activate caspases, particularly caspase‐3, and other proteases that may be involved in endonuclease activation. Since NT2 cells activate caspase‐3, but do not correctly process DFF45, b other factors must also impinge on the inevitability of that process.
Regulation of Transglutaminases by Nitric Oxide
Authors: BERNASSOLA FRANCESCA , ROSSI ANTONELLO , MELINO GERRY 
Published: July 2010

ABSTRACTNitric oxide (NO) is an inorganic diffusible molecular messenger that plays several central roles in pathophysiology. NO can affect the biological activity of proteins through the direct or indirect (via intermeidate S‐nitrosothiols) S‐nitrosylation of protein thiol groups. Transglutaminases (TGases), CA++‐dependent enzymes that modify proteins by cross‐linking reactions, require a cysteine residue in the active site as a prerequisite for their catalytic activity. Therefore, NO may regulate enzymatic activity of TGases and their biological effects, via S‐nitrosylation of their crucial thiol groups. We here review the effects of NO on coagulation factor XIII (fXIII, or plasma TGase) and Tgase 2 (or tissue transglutaminase). NO has an inhibitory effect on fXIII, thus suppressing the γ‐chain cross‐linking in fibrin gels, and subsequent clot formation. Tissue transglutaminase, an apoptotic effector molecule, also represents a molecular target for NO. Accordingly, the inhibition of tissue transglutaminase enzymatic activity by NO is able to prevent the induction of apoptosis.
Bone Morphogenetic Proteins Regulate Interdigital Cell Death in the Avian Embryo
Authors: MERINO RAMÓN , GAÑÁN YOLANDA , MACIAS DOMINGO , RODRÍGUEZ‐LEÓN JOAQUÍN , HURLE JUAN M. 
Published: July 2010

ABSTRACTThe embryonic limb bud provides an excellent model for analyzing the mechanisms that regulate programmed cell death during development. At the time of digit formation in the developing autopod, the undifferentiated distal mesodermal cells may undergo or chondrogenic differentiation or apoptosis depending whether they are incorporated into the future digital rays or into the interdigital spaces. Both chondrogenesis or apoptosis are induced by local BMPS. However, whereas the chondrogenic‐promoting activity of BMPs appears to be regulated through the BMPR‐ 1b receptor, the mechanism by which the BMPs execute the death program remains unknown. The BMP proapoptotic activity requires the expression of members of the msx family of closely related homeobox‐containing genes and is finally mediated by caspase activation, but the nature of the caspase(s) directly responsible for the cell death is also unknown. Finally, other growth factors present in the developing autopod at the stages of digit formation such as members of the FGF and TGFβ families modulate the ability of BMPs to induce cell death or chondrogenesis.
The Immune Response to Apoptotic Cells
Authors: MEVORACH DROR 
Published: July 2010

ABSTRACTProgrammed cell death (PCD) can be divided into two distinct but linked sequential processes, killing of the cells and removal of the dead cells, which may be a neighboring cell or a professional phagocyte. Following internalization of the apoptotic cell, the phagocyte typically triggers neither the development of a pro‐inflammatory response not the production of autoantibodies directed against apoptotic self antigens. Since apoptotic cells are characterized by translocation of autoantigens such as nucleosomes to the surface of the cell, we tested the hypothesis that excess or abnormally processed apoptotic cells can generate autoantibodies. We have found that syngeneic apoptotic load can induce transient hypergammaglobulinemia, anti‐DNA, anticardiolipin, and glomerular depositions in normal mice. Furthermore, we also found that one of the important mechanisms of uptake of apoptotic cells involves opsonization by the complement system, suggesting that deficient states could lead to aberrant handling of apoptotic cells. Therefore, conditions in which apoptotic cells become immunogenic may explain antigen selection in inflammatory and autoimmune conditions, such as in systemic lupus erythematosus (SLE).
Studies of Amphetamine or Methamphetamine Psychosis in Japan: Relation of Methamphetamine Psychosis to Schizophrenia
Authors: YUI KUNIO , IKEMOTO SHIGENORI , ISHIGURO TAKEO , GOTO KIMIHIKO 
Published: July 2010

AbstractThere exist clinical characteristics of methamphetamine (MAP) psychosis in the Japanese population. MAP psychosis involves paranoid‐hallucinatory states indistinguishable from paranoid schizophrenia, with residual volitional disturbances (e.g., loss of spontaneity and idleness). Paranoid‐hallucinatory states persist after the pharmacological effects of MAP have worn off and readily reappear upon a reinjection of MAP. Individuals with a history of MAP psychosis further undergo spontaneous recurrence of their paranoid‐hallucinatory states in response to stress. The development of MAP psychosis might therefore be related to persisting brain damage or changes in brain metabolism induced by repeated MAP use, and thus studies of the clinical course and neurological basis of MAP psychosis could provide insights into the pathophysiology of schizophrenia. Accordingly, psychiatrists have studied the clinical characteristics of MAP psychosis and examined the neurobiological basis of MAP‐induced behavioral sensitization, using animals. MAP‐induced behavioral sensitization might well be related to dopamine supersensitivity; however, the contribution of presynaptic autoreceptors remains controversial, and other hypotheses should be considered. Recently, the process that triggers spontaneous recurrence of MAP psychosis (flashbacks) and corresponding peripheral neurotransmitter functions has been studied. Stress sensitization associated with noradrenergic hyperactivity, involving increased dopamine release, appears to be crucial in the development of flashbacks. Overall, MAP‐induced susceptibility to paranoid‐hallucinatory states and to abnormal behavior (e.g., stereotyped behavior) in animals is examined as a model for predicting relapses of paranoid schizophrenia. Further extensive studies on the neurobiological and molecular mechanisms of this susceptibility are required.
Activation of an Effector Immediate‐early Genearcby Methampetamine
Authors: YAMAGATA KANATO , SUZUKI KYOKO , SUGIURA HIROKO , KAWASHIMA NAOYA , OKUYAMA SHIGERU 
Published: July 2010

AbstractAs immediate‐early genes (IEGs) are thought to play a critical role in mediating stimulus‐induced neural plasticity, IEG response induced by methamphetamine (METH) has been characterized to define the changes in gene expression that may underlie its long‐lasting behavioral effects. Although activation of several transcription factor IEGs has been described, little is known about effector IEGs. Here, we have examined whether METH administration affects expression of an effector IEGarc(activity‐regulated, cytoskeleton‐associated) that encodes a protein with homology to spectrin. Usingin situhybridization, we observed that METH caused a rapid and transient dose‐dependent increase inarcmRNA level in the striatum and cortex that was abolished by pretreatment with the specific dopamine D1 receptor antagonist SCH‐23390 but not by an atypical neuroleptic clozapine. METH inducedarcmRNA in layers IV and VI of the cortex which dopamine receptor are localized to. These results suggest that D1 receptors are coupled to activation ofarcgene, which may be involved in functional or structural alterations underlying neural plasticity triggered by METH.
Neuroprotective Role of Estrogen upon Methamphetamine and Related Neurotoxins within the Nigrostriatal Dopaminergic System
Authors: DLUZEN DEAN E. , McDERMOTT JANET L. 
Published: July 2010

AbstractIn this report we describe some of the data on the capacity for estrogen to function as a neuroprotectant of the nigrostriatal dopaminergic (NSDA) system. The data show that estrogen (E) can alter two different response characteristics to NSDA neurotoxins. The first being that striatal DA concentrations of ovariectomized rodents treated with E are consistently greater than non‐E‐treated animals in response to neurotoxins which produce degeneration of the NSDA system. The second being that E significantly reduces the amount of DA output upon initial exposure to the NSDA neurotoxin, 1‐methyl‐4‐phenylpyridium ion (MPP+). At present, it is not known whether these two response characteristics are related. An intriguing possibility is that the E‐dependent changes in initial DA output are related to the resultant neurotoxicity (attenuations in DA concentration reductions). So far our incipient findings do not seem to support this eventuality. However, additional testing on this topic is required. The present data suggest that one of the mechanisms by which E can exert these effects is through inhibition of DAT activity. This conclusion results from data which show that E produces: 1) an inhibition of [3H]DA uptake, 2) a reduction in DA clearance rates, and 3) an effect upon DA recovery that is similar to that observed to the putative DA uptake blocker, nomifensine. The capacity and significance for steroid hormones to modulate neurotransmitter transporters has been recently reviewed.
Effect ofd‐Amphetamine and Sydnocarb on the Extracellular Level of Dopamine, 3,4‐Dihydroxyphenylacetic Acid, and Hydroxyl Radicals Generation in Rat Striatum
Authors: ANDERZHAONOVA E. A. , AFANAS'EV I. I. , KUDRIN V. S. , RAYEVSKY K. S. 
Published: July 2010

Abstractd‐AMPH and its congeners are able to produce several neurotoxic effects, including behavioral evidences of dopaminergic dysfunction, enhanced generation of reactive oxygen species, and depletion of endogenous DA. As has been shown, Sydnocarb produces a slow and gradual increase of the parameters of dopaminergic dysfunction. Present investigations report that Sydnocarb, the original Russian psychostimulant, at a dose of 23.8 mg/kg (equimolar to 5 mg/kgd‐AMPH) elicited a moderate increase in the extracellular level of DA. We found that Sydnocarb increased OH generation in less degree than that byd‐AMPH. Sydnocarb was also able to elicit stereotyped behavior, but to a less extent thand‐AMPH. Differences between the mode of action of this drug were previously observed. In our study, the DOPAC extracellular level was significantly decreased after the fourth injection of Sydnocarb, unlike withd‐AMPH treatment. Taken together, this finding probably reflects less neurotoxic potential of the novel, original psychostimulant Sydnocarb with good clinical efficaciousness in comparison to the amphetamine.
Prevention of Dopaminergic Neurotoxicity by Targeting Nitric Oxide and Peroxynitrite: Implications for the Prevention of Methamphetamine‐induced Neurotoxic Damage
Authors: IMAM SYED Z. , ISLAM FAKHRUL , ITZHAK YOSSEF , SLIKKER WILLIAM , ALI SYED F. 
Published: July 2010

AbstractMethamphetamine (METH) is a neurotoxic psychostimulant that produces catecholaminergic brain damage by producing oxidative stress and free radical generation. The role of oxygen and nitrogen radicals is well documented as a cause of METH‐induced neurotoxic damage. In this study, we have obtained evidence that METH‐induced neurotoxicity is the resultant of interaction between oxygen and nitrogen radicals, and it is mediated by the production of peroxynitrite. We have also assessed the effects of inhibitors of neuronal nitric oxide synthase (nNOS) as well as scavenger of nitric oxide and a peroxynitrite decomposition catalyst. Significant protective effects were observed with the inhibitor of nNOS, 7‐nitroindazole (7‐NI), as well as by the selective peroxynitrite scavenger or decomposition catalyst, 5,10,15,20‐tetrakis(2,4,6‐trimethyl‐3,5‐sulfonatophenyl)porphyrinato iron III (FeTPPS). However, the use of a nitric oxide scavenger, 2‐phenyl‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl‐3‐oxide (c‐PTIO), did not provide any significant protection against METH‐induced hyperthermia or peroxynitrite generation and the resulting dopaminergic neurotoxicity. In particular, treatment with FeTPPS completely prevented METH‐induced hyperthermia, peroxynitrite production, and METH‐induced dopaminergic depletion. Together, these data demonstrate that METH‐induced dopaminergic neurotoxicity is mediated by the generation of peroxynitrite, which can be selectively protected by nNOS inhibitors or peroxynitrite scavenger or decomposition catalysts.
Dopamine Uptake Blockers Nullify Methamphetamine‐induced Decrease in Dopamine Uptake and Plasma Membrane Potential in Rat Striatal Synaptosomes
Authors: WESTPHALEN R. I. , STADLIN A. 
Published: July 2010

AbstractRat striatal synaptosomes showed a reduced capacity to generate a membrane potential after being exposed to methamphetamine (METH) for 1 h. As a consequence, the dopamine (DA) synaptosomes were impeded in their electrogenic‐dependent reuptake of dopamine. The capacity for METH‐exposed nerve terminals to generate a membrane potential may contribute to the ability of METH to destroy dopaminergic neurons. DA uptake inhibitors (DAUIs) were found to counteract the METH‐induced decrease in synaptosomal [3H]DA Vmax by stablizing METH‐induced reductions in PMP. Because DAUIs showed the same effects as a Na+‐channel blocker, DAUIs may prevent METH‐induced destruction of dopaminergic neurons by raising plasma membrane potential.
Age as a Susceptibility Factor in the Striatal Dopaminergic Neurotoxicity Observed in the Mouse following Substituted Amphetamine Exposure
Authors: MILLER DIANE B. , O'CALLAGHAN JAMES P. , ALI SYED F. 
Published: July 2010

AbstractA number of substituted amphetamines, including methamphetamine (METH) are considered dopaminergic neurotoxicants. METH causes long‐term depletions of striatal dopamine (DA) and its metabolites (DOPAC and HVA) that are accompanied by other changes indicative of nerve terminal degeneration. These include argyrophilia as detected by silver degeneration stains and an elevation in glial fibrillary acidic protein (GFAP), a marker of reactive gliosis in response to injury, as well as a long‐term decrease in tyrosine hydroxylase (TH) protein levels. The susceptibility to the dopaminergic neurotoxicity of METH and the other amphetamines can be affected by a number of factors including age, gender, stress, and environment. Many of these susceptibility factors have been extensively investigated in the rat but less so in the mouse. As the availability of genetically altered mice continues to expand, this species is increasingly selected for study. Thus, in previous work we determined that stress, gender, and the environment can significantly impact the neurotoxicity of the amphetamines. Here we determined how age affects the striatal DA depletion and GFAP elevation induced byd‐METH in C57BL/6 mice. Age was a significant determinant of the ability of a known neurotoxic regimen ofd‐METH (10 mg/kg × 4) to produce striatal DA depletion with one‐month‐old C57BL/6 mice displaying minimal and nonpersistent depletion of DA or its metabolites while mice 12 months of age displayed large and persistent depletions of DA (87%), DOPAC (71%), and HVA (94%). Large elevations in striatal GFAP were induced in mice 2‐23 months of age byd‐METH, with lower dosages ofd‐METH being effective in the older mice. In contrast, the usual neurotoxic regimen ofd‐METH was minimally effective in inducing GFAP elevations (49% over control) in one‐month‐old mice, despite elevations in body temperature equivalent to those observed in older mice. Although increasing the dosage ofd‐METH (20 to 80 mg/kg) did increase the GFAP response (100% over control), it was still well below that usually exhibited at the usual neurotoxic dosage (300‐400% over control) in fully mature mice. These data suggest maturity of striatal dopamine systems may be an essential element in the striatal damage induced by the neurotoxic amphetamines.