bluuebunny/crossref_metadata_2025_split huggingface dataset:
Down‐regulation of dopamine transporter by iron chelationin vitrois mediated by altered trafficking, not synthesis
Authors: Wiesinger Jason A. , Buwen James P. , Cifelli Christopher J. , Unger Erica L. , Jones Byron C. , Beard John L. 
Published: November 2006

AbstractNeurological development and functioning of dopamine (DA) neurotransmission is adversely affected by iron deficiency in early life. Iron‐deficient rats demonstrate significant elevations in extracellular DA and a reduction in dopamine transporter (DAT) densities in the caudate putamen and nucleus accumbens. To explore possible mechanisms by which cellular iron concentrations control DAT functioning, endogenous DAT‐expressing PC12 cells were used to determine the effect of iron chelation on DAT protein and mRNA expression patterns. In addition, we used human DAT (hDAT)‐transfected Neuro2a (N2A) cells to examine DAT degradation and trafficking patterns. A 50 µmtreatment for 24 h with the iron chelator, desferrioxamine (DFO), significantly decreased dopamine uptake in a dose‐dependent manner, with no apparent change inKm, in both PC12 and N2A cells. Reduced DA uptake was accompanied by concentration‐ and time‐dependent reductions in total DAT protein levels in both cell lines. Exposure to increasing concentrations of DFO did not significantly alter DAT mRNA in either PC12 or N2A cells. However, DAT degradation rates increased three–fivefold in both cell types exposed to 50 µmDFO for 24 h. Biotinylation studies in N2A cells indicate a more dramatic loss of DAT in the membrane fraction, while OptiPrep fractionation experiments revealed an increase in lysosomal DAT with iron chelation. Inhibition of protein kinase C activation with staurosporin prevented the effect of iron chelation on DAT function, suggesting thatin vitroiron chelation affects DAT primarily through the effects on trafficking rather than on synthesis.
Adriamycin‐mediated nitration of manganese superoxide dismutase in the central nervous system: insight into the mechanism of chemobrain
Authors: Tangpong Jitbanjong , Cole Marsha P. , Sultana Rukhsana , Estus Steven , Vore Mary , St. Clair William , Ratanachaiyavong Suvina , St. Clair Daret K. , Butterfield D. Allan 
Published: November 2006

AbstractAdriamycin (ADR), a potent anti‐tumor agent, produces reactive oxygen species (ROS) in cardiac tissue. Treatment with ADR is dose‐limited by cardiotoxicity. However, the effect of ADR in the other tissues, including the brain, is unclear because ADR does not pass the blood–brain barrier. Some cancer patients receiving ADR treatment develop a transient memory loss, inability to handle complex tasks etc., often referred to by patients as chemobrain. We previously demonstrated that ADR causes CNS toxicity, in part, via systemic release of cytokines and subsequent generation of reactive oxygen and nitrogen species (RONS) in the brain. Here, we demonstrate that treatment with ADR led to an increased circulating level of tumor necrosis factor‐alpha in wild‐type mice and in mice deficient in the inducible form of nitric oxide (iNOSKO). However, the decline in mitochondrial respiration and mitochondrial protein nitration after ADR treatment was observed only in wild‐type mice, not in the iNOSKO mice. Importantly, the activity of a major mitochondrial antioxidant enzyme, manganese superoxide dismutase (MnSOD), was reduced and the protein was nitrated. Together, these results suggest that NO is an important mediator, coupling the effect of ADR with cytokine production and subsequent activation of iNOS expression. We also identified the mitochondrion as an important target of ADR‐induced NO‐mediated CNS injury.
Agmatine transport into spinal nerve terminals is modulated by polyamine analogs
Authors: Goracke‐Postle Cory J. , Overland Aaron C. , Stone Laura S. , Fairbanks Carolyn A. 
Published: November 2006

AbstractAgmatine (decarboxylated arginine) is an endogenous amine found in the CNS that antagonizes NMDA receptors and inhibits nitric oxide synthase. Intrathecally administered agmatine inhibits hyperalgesia evoked by inflammation, nerve injury and intrathecally administered NMDA. These actions suggest an antiglutamatergic neuromodulatory role for agmatine in the spinal cord. Such a function would require a mechanism of regulated clearance of agmatine such as neuronal or glial uptake. Consistent with this concept, radiolabeled agmatine has been shown to accumulate in synaptosomes, but the mechanism of this transport has not been fully characterized. The present study describes an agmatine uptake system in spinal synaptosomes that appears driven by a polyamine transporter. [3H]Agmatine uptake was Ca2+, energy and temperature dependent. [3H]Agmatine transport was not moderated byl‐arginine,l‐glutamate, glycine, GABA, norepinephrine or serotonin. In contrast, [3H]agmatine uptake was concentration dependently inhibited by unlabeled putrescine and by unlabeled spermidine (at significantly higher concentrations). Similarly, [3H]putrescine uptake was inhibited in a concentration‐dependent manner by unlabeled agmatine and spermidine. The polyamine analogs paraquat and methylglyoxal bis (guanylhydrazone) inhibited, whereas the polyamine transport enhancer difluoromethylornithine increased, [3H]agmatine transport. Taken together, these results suggest that agmatine transport into spinal synaptosomes may be governed by a polyamine transport mechanism.
Emerging concepts: novel integration of in vivo approaches to localize the function of nicotinic receptors
Authors: Maskos Uwe 
Published: November 2006

AbstractNicotinic acetylcholine receptors (nAChRs) are important targets of the neuromodulator acetylcholine (ACh) and the drug nicotine. The role of their different subunits has been analysed for a decade by the creation of knock‐out (KO) mice using homologous recombination. This technique shows that a given subunit is necessary for a given function. However, for ubiquitously expressed genes, it cannot demonstrate the localization for a given subunit in which its expression is sufficient, especially for behavioural phenotypes. Sufficient in this context means that the brain region requiring the expression of the gene product has been localized. Novel strategies have therefore been developed to re‐express, region specifically, nAChR subunits on a KO background using lentiviral vectors. Localized regeneration of fully functional high‐affinity nAChRs in defined brain regions has proven that these receptors are sufficient to restore a variety of functions: nicotine‐induced dopamine release, nicotine self‐administration in mice, dopamine neuron firing patterns, and exploratory and locomotor behaviours in a sequential locomotor task testing executive function were thus defined as depending exclusively on the ‘knock‐back’ of β2*‐nAChRs into the ventral tegmental area. These analyses highlight the important role of endogenous cholinergic regulation of a variety of functions. The novel integrated use of restricted re‐expressed nAChR subunits with in vivo electrophysiology and automated quantitative behavioural analysis enables the further analysis of defined neuronal circuits in nicotine addiction and higher cognitive function.
Changes in the serotonergic system in the main olfactory bulb of rats unilaterally deprived from birth to adulthood
Authors: Gómez C. , Briñón J. G. , Orio L. , Colado M. I. , Lawrence A. J. , Zhou F. C. , Vidal M. , Barbado M. V. , Alonso J. R. 
Published: November 2006

AbstractThe serotonergic system plays a key role in the modulation of olfactory processing. The present study examined the plastic response of this centrifugal system after unilateral naris occlusion, analysing both serotonergic afferents and receptors in the main olfactory bulb. After 60 days of sensory deprivation, the serotonergic system exhibited adaptive changes. Olfactory deprivation caused a general increase in the number of fibres immunopositive for serotonin but not of those immunopositive for the serotonin transporter. HPLC data revealed an increase in serotonin levels but not in those of its major metabolite, 5‐hydroxyindole acetic acid, resulting in a decrease in the 5‐hydroxyindole acetic acid/serotonin ratio. These changes were observed not only in the deprived but also in the contralateral olfactory bulb. Double serotonin–tyrosine hydroxylase immunolabelling revealed that the glomerular regions of the deprived olfactory bulb with a high serotonergic fibre density showed a strong reduction in tyrosine hydroxylase. Finally, the serotonin2A receptor distribution density and the number of juxtaglomerular cells immunopositive for serotonin2A receptor remained unaltered after olfactory deprivation. Environmental stimulation modulated the serotonergic afferents to the olfactory bulb. Our results indicate the presence of a bilateral accumulation of serotonin in the serotonergic axon network, with no changes in serotonin2A receptor density after unilateral olfactory deprivation.
Induction of haem oxygenase‐1 causes cortical non‐haem iron increase in experimental pneumococcal meningitis: evidence that concomitant ferritin up‐regulation prevents iron‐induced oxidative damage
Authors: Ren Hao , Leib Stephen L. , Ferriero Donna M. , Täuber Martin G. , Christen Stephan 
Published: November 2006

AbstractDesferrioxamine inhibits cortical necrosis in neonatal rats with experimental pneumococcal meningitis, suggesting that iron‐induced oxidative damage might be responsible for neuronal damage. We therefore examined the spatial and temporal profile of changes in cortical iron and iron homeostatic proteins during pneumococcal meningitis. Infection was associated with a steady and global increase of non‐haem iron in the cortex, particularly in neuronal cell bodies of layer II and V, and in capillary endothelial cells. The non‐haem iron increase was associated with induction of haem oxygenase (HO)‐1 in neurones, microglia and capillary endothelial cells, whereas HO‐2 levels remained unchanged, suggesting that the non‐haem iron increase might be the result of HO‐1‐mediated haem degradation. Indeed, treatment with the haem oxygenase inhibitor tin protoporphyrin (which completely blocked the accumulation of bilirubin detected in HO‐1‐positive cells) completely prevented the infection‐associated non‐haem iron increase. The same cells also displayed markedly increased ferritin staining, the increase of which occurred independently of HO activity. At the same time, no increase in DNA/RNA oxidation was observed in infected animals (as assessed by in situ detection of 8‐hydroxy[deoxy]guanosine), strongly suggesting that ferritin up‐regulation protected the brain from iron‐induced oxidative damage. Thus, although pneumococcal meningitis leads to an increase of cortical non‐haem iron, protective mechanisms up‐regulated in parallel prevent iron‐induced oxidative damage. Cortical damage does not appear to be a direct consequence of increased iron, therefore.
Multiple sclerosis: a battle between destruction and repair
Authors: McQualter Jonathan L. , Bernard Claude C. A. 
Published: November 2006

AbstractMultiple sclerosis (MS) is a chronic neurodegenerative disease of the CNS in which an unrelenting attack from the innate and adaptive arms of the immune system results in extensive demyelination, loss of oligodendrocytes and axonal degeneration. This review summarizes advances in the understanding of the cellular and molecular pathways involved in neurodegeneration following autoimmune‐mediated inflammation in the CNS. The mechanisms underlying myelin and axonal destruction and the equally important interaction between degenerative and repair mechanisms are discussed. Recent studies have revealed that the failure of CNS regeneration may be in part a result of the presence of myelin‐associated growth inhibitory molecules in MS lesions. Successful therapeutic intervention in MS is likely to require suppression of the inflammatory response, in concert with blockade of growth inhibitory molecules and possibly the mobilization or transplantation of stem cells for regeneration.
Acyl peptide hydrolase, a serine proteinase isolated from conditioned medium of neuroblastoma cells, degrades the amyloid‐β peptide
Authors: Yamin Rina , Bagchi Sandipan , Hildebrant Rick , Scaloni Andrea , Widom Russell L. , Abraham Carmela R. 
Published: November 2006

AbstractConsiderable evidence indicates that the amyloid‐β (Aβ) peptide, a proteolytic fragment of the amyloid precursor protein, is the pathogenic agent in Alzheimer's disease (AD). A number of proteases have been reported as capable of degrading Aβ, among them: neprilysin, insulin‐degrading enzyme, endothelin‐converting enzyme‐1 and ‐2, angiotensin‐converting enzyme and plasmin. These proteases, originating from a variety of cell types, degrade Aβ of various conformational states and in different cellular locations. We report here the isolation of a serine protease from serum‐free conditioned medium of human neuroblastoma cells. Tandem mass spectrometry (MS/MS)‐based sequencing of the isolated protein identified acyl peptide hydrolase (APH; EC3.4.19.1) as the active peptidase. APH is one of four members of the prolyl oligopeptidase family of serine proteases expressed in a variety of cells and tissues, including erythrocytes, liver and brain, but its precise biological activity is unknown. Here, we describe the identification of APH as an Aβ‐degrading enzyme, and we show that the degradation of Aβ by APH isolated from transfected cells is inhibited by APH‐specific inhibitors, as well as by synthetic Aβ peptide. In addition, we cloned APH from human brain and from neuroblastoma cells. Most importantly, our results indicate that APH expression in AD brain is lower than in age‐matched controls.
Body size, rarity, and phylogenetic community structure: insights from diving beetle assemblages of Alberta
Authors: Vamosi Jana C. , Vamosi Steven M. 
Published: November 2006

ABSTRACTAlthough it is implicit that interactions between species depend on their traits, studies on the probability of finding related species in a community are in their infancy. Community composition and species richness of predaceous diving beetles (Dytiscidae: Coleoptera) have been used as indicators of freshwater ecosystem function yet no incorporation of phylogenetic relationships of coexisting dytiscids has been attempted to date. Improved knowledge of phylogenetic relationships and phylogenetic community structure analysis methods may provide additional insight into the relationships between community composition and species richness, thus impacting our interpretation of aquatic indicator species metrics. Here, we use museum records of dytiscid beetles in 53 lakes of Alberta, Canada to: (1) compile a supertree of dytiscid beetles that live in the province, (2) examine whether coexisting dytiscids tend to be more or less related than expected by chance, and (3) examine whether phylogenetic structuring depends on species richness or mean size of coexisting species. We find that, although the majority of dytiscid assemblages exhibited phylogenetic clustering, the extent to which this occurred depended on the mean size of dytiscids. We discuss the potential mechanisms and implications of the observed patterns in phylogenetic clustering, along with data that would further improve our understanding of community dynamics in dytiscid beetles.
Risk Analysis in Developing Countries1
Authors: Pe Benito Claudio Corazon 
Published: November 2006

SUMMARY AND CONCLUSIONSIn summary, risk analysis is not yet well practiced in developing countries, although there are numerous, diverse environmental and other risk‐related issues and concerns that need attention. A few initiatives have been taken, but, so far, they have created only relatively small impact in a few areas. Many risk issues may not be addressed, partly as a result of lack of resources and inadequate knowledge by policy makers.Risk analysis is an essential tool for the planning and implementation of development projects. To enhance its use, however, risk analysis approaches and methods must be adapted to developing countries, and this requires research. Unfortunately, funds for research, in general, are hard to find. There are other problems in the implementation of risk analysis. Trained professionals on risk analysis are few. Existing institutions that are tasked with resolving environmental and other risk issues are overburdened. Risk‐related data are sorely lacking. Resources are very limited for addressing numerous natural and technological hazards.In most developing countries, political and economic stability is still threatened by both internal and external forces, hence, that is what receives priority attention. Activities like risk analysis, which generally lead to long‐term results and benefits, do not get enough interest. In addition, there is still little public awareness of risks even among those who have passed the stage of survival; thus, there is little public concern about them.We cannot afford this lack of concern for long. In the Philippines, the government was the first to recognize after our peaceful revolution in 1986 that “the environmental issues can add fuel to the insurgency; they can also hamper efforts towards national recovery”.(4) To this point, I have added that risk management (including risk assessment and risk communication), like attainment of peace and freedom, is a social imperative because risk issues affect our health, safety, and both our physical and economic well‐being.(7) Many of such issues in developing countries have not only local, but also global origin and impacts. They thus deserve the interest of each of us.
Nondigestible Oligo‐ and Polysaccharides (Dietary Fiber): Their Physiology and Role in Human Health and Food
Authors: Tungland B.C. , Meyer D. 
Published: November 2006

ABSTRACTNondigestible polysaccharides (NDP) and nondigestible oligosaccharides (NDO) occur naturally in many foods. The physicochemical and biological properties of these compounds, as they relate to dietary fiber, are associated with physiological actions in the small and large intestine, having important implications in human health. These properties include water dispersibility and solubility, viscosity effects, bulk, absorption and fermentability, and binding of other compounds. These features may lead to various physiological actions such as reducing cholesterol and attenuating blood glucose, maintaining gastrointestinal health, and positively affecting calcium bioavailability and immune function. Moreover, based on their physiochemical properties, many of the new oligosaccharides can help improve the organoleptic properties and nutritional value of foods.
Biofilm Formation and Control in Food Processing Facilities
Authors: Chmielewski R.A.N. , Frank J.F. 
Published: November 2006

ABSTRACTMicroorganisms on wet surfaces have the ability to aggregate, grow into microcolonies, and produce biofilm. Growth of biofilms in food processing environments leads to increased opportunity for microbial contamination of the processed product. These biofilms may contain spoilage and pathogenic microorganisms. Microorganisms within biofilms are protected from sanitizers increasing the likelihood of survival and subsequent contamination of food. This increases the risk of reduced shelf life and disease transmission. Extracellular polymeric substances associated with biofilm that are not removed by cleaning provide attachment sites for microorganisms newly arrived to the cleaned system. Biofilm formation can also cause the impairment of heat transfer and corrosion to metal surfaces. Some of the methods used to control biofilm formation include mechanical and manual cleaning, chemical cleaning and sanitation, and application of hot water.
Food Process Engineering: The Last 25 Years and Challenges Ahead
Authors: Bruin S. , Jongen Th.R.G. 
Published: November 2006

ABSTRACTIn the first part of this contribution, an overview is given of some of the main developments in food process engineering in the last 25 years of the 20th century. This overview is, of course, colored by the personal experience of the authors, but a sincere effort was made to maintain a general perspective. Topics that will be briefly discussed are: progress in understanding how to control food microstructure formation during processing, separation processes, conversion processes and stabilization processes, progress in flavor technology and understanding of flavor retention during processing and release. In the 2nd part, in our view, the most exiting future developments are briefly discussed. The major items here are: processing requirements for functional foods, integrated process design approaches, application of novel‘fields’in food processes,‘precision’processing, supply chain approaches to food manufacturing, and more.
Sporeformers as Human Probiotics: Bacillus, Sporolactobacillus, and Brevibacillus
Authors: Sanders M.E. , Morelli L. , Tompkins T.A. 
Published: November 2006

ABSTRACTThe value of exogenously supplied live bacteria for the maintenance of health in humans has been recognized both scientifically in the published literature and commercially in the availability of probiotic products. Although many bacteria characterized as probiotics are strains of Lactobacillus or Bifidobacterium, sporeforming bacteria, primarily of the genus Bacillus and related genera, have also been studied and commercialized as probiotics. This article reviews the characterization, efficacy, and safety of sporeformers used as probiotics.
Nucleation and Expansion During Extrusion and Microwave Heating of Cereal Foods
Authors: Moraru C.I. , Kokini J.L. 
Published: November 2006

ABSTRACTExpansion of biopolymer matrices is the basis for the production of a wide variety of cereal foods. A limited number of manufacturing processes provide practical solutions for the development of an impressive variety of expanded products, just by changing process variables. It is therefore essential that the mechanisms involved in expansion are well known and controlled. This paper summarizes the knowledge of nucleation and expansion in extruded and microwaved products available to date. The effect of processing conditions and properties of the biopolymeric matrix on nucleation and expansion are discussed. Moisture content enables the glassy polymeric matrix to turn into rubbery state at process temperatures, which allows superheated steam bubbles to form at nuclei and then expand, expansion being governed by the biaxial extensional viscosity of the matrix. Nucleation and expansion theories are presented along with quantitative data that support them.