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Author (up) Fisher, J.O.; Birch, L.L. file  url
  Title Restricting access to foods and children's eating Type Journal Article
  Year 1999 Publication Appetite Abbreviated Journal Appetite  
  Volume 32 Issue 3 Pages 405-419  
  Keywords Child Behavior/*psychology; Child, Preschool; Feeding Behavior/*psychology; Female; Food Preferences; Humans; Male; *Mother-Child Relations; Nutritional Requirements; Obesity/psychology; Sex Factors  
  Abstract This study evaluated maternal restriction of children's access to snack foods as a predictor of children's intake of those foods when they were made freely available. In addition, child and parent eating-related “risk” factors were used to predict maternal reports of restricting access. Participants were 71, 3-to-5-year-old children (36 boys, 35 girls) and their parents. Children's snack food intake was measured immediately following a meal, in a setting offering free access to palatable snack foods. Child and maternal reports of restricting children's access to those snack foods were obtained. In addition, information on child and parent adiposity as well as parents' restrained and disinhibited eating was used to examine “risk” factors for restricting access. For girls only, child and maternal reports of restricting access predicted girls' snack food intake, with higher levels of restriction predicting higher levels of snack food intake. Maternal restriction, in turn, was predicted by children's adiposity. Additionally, parents' own restrained eating style predicted maternal restriction of girls' access to snack foods.  
  Call Number Serial 1690  
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Author (up) Fisher, M.C.; Henk, D.A.; Briggs, C.J.; Brownstein, J.S.; Madoff, L.C.; McCraw, S.L.; Gurr, S.J. file  url
  Title Emerging fungal threats to animal, plant and ecosystem health Type Journal Article
  Year 2012 Publication Nature Abbreviated Journal Nature  
  Volume 484 Issue 7393 Pages 186-194  
  Keywords Animals; Communicable Diseases, Emerging/epidemiology/*microbiology/veterinary; *Ecosystem; Extinction, Biological; Food Supply; Fungi/classification/genetics/isolation & purification/*pathogenicity; Humans; Mycoses/*epidemiology/microbiology/*veterinary; Plants/*microbiology; Virulence/genetics  
  Abstract The past two decades have seen an increasing number of virulent infectious diseases in natural populations and managed landscapes. In both animals and plants, an unprecedented number of fungal and fungal-like diseases have recently caused some of the most severe die-offs and extinctions ever witnessed in wild species, and are jeopardizing food security. Human activity is intensifying fungal disease dispersal by modifying natural environments and thus creating new opportunities for evolution. We argue that nascent fungal infections will cause increasing attrition of biodiversity, with wider implications for human and ecosystem health, unless steps are taken to tighten biosecurity worldwide.  
  Call Number Serial 2168  
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Author (up) Fisone, G.; Borgkvist, A.; Usiello, A. file  url
doi  openurl
  Title Caffeine as a psychomotor stimulant: mechanism of action Type Journal Article
  Year 2004 Publication Cellular and Molecular Life Sciences : CMLS Abbreviated Journal Cell Mol Life Sci  
  Volume 61 Issue 7-8 Pages 857-872  
  Keywords *Adenosine A1 Receptor Antagonists; *Adenosine A2 Receptor Antagonists; Animals; Basal Ganglia/cytology/metabolism; Caffeine/*metabolism/*pharmacology; Central Nervous System Stimulants/*metabolism; Dopamine/metabolism; Dopamine and cAMP-Regulated Phosphoprotein 32; Enzyme Inhibitors/metabolism; Humans; Motor Activity/*drug effects; *Nerve Tissue Proteins; Neurons/metabolism; Neuroprotective Agents/metabolism; Parkinson Disease/metabolism; Phosphoproteins/metabolism; Receptor, Adenosine A1/metabolism; Receptor, Adenosine A2A/metabolism; Receptors, Dopamine D2/metabolism; Signal Transduction; Synaptic Transmission/physiology  
  Abstract The popularity of caffeine as a psychoactive drug is due to its stimulant properties, which depend on its ability to reduce adenosine transmission in the brain. Adenosine A(1) and A(2A) receptors are expressed in the basal ganglia, a group of structures involved in various aspects of motor control. Caffeine acts as an antagonist to both types of receptors. Increasing evidence indicates that the psychomotor stimulant effect of caffeine is generated by affecting a particular group of projection neurons located in the striatum, the main receiving area of the basal ganglia. These cells express high levels of adenosine A(2A) receptors, which are involved in various intracellular processes, including the expression of immediate early genes and regulation of the dopamine- and cyclic AMP-regulated 32-kDa phosphoprotein DARPP-32. The present review focuses on the effects of caffeine on striatal signal transduction and on their involvement in caffeine-mediated motor stimulation.  
  Call Number Serial 215  
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Author (up) Flinn, M.V.; Ponzi, D.; Muehlenbein, M.P. file  url
  Title Hormonal mechanisms for regulation of aggression in human coalitions Type Journal Article
  Year 2012 Publication Human Nature (Hawthorne, N.Y.) Abbreviated Journal Hum Nat  
  Volume 23 Issue 1 Pages 68-88  
  Keywords Adolescent; Adult; Aggression--physiology; Animals; Biological Evolution; Child; Competitive Behavior--physiology; Cooperative Behavior; Cultural Evolution; Dominica; Family; Female; Friends; Hominidae--psychology; Humans; Hydrocortisone--metabolism; Interpersonal Relations; Male; Middle Aged; Models, Psychological; Neurosecretory Systems--physiology; Pair Bond; Pan troglodytes--psychology; Rural Population; Saliva--chemistry; Sports; Testosterone--metabolism, physiology; Young Adult  
  Abstract Coalitions and alliances are core aspects of human behavior. All societies recognize alliances among communities, usually based in part on kinship and marriage. Aggression between groups is ubiquitous, often deadly, fueled by revenge, and can have devastating effects on general human welfare. Given its significance, it is surprising how little we know about the neurobiological and hormonal mechanisms that underpin human coalitionary behavior. Here we first briefly review a model of human coalitionary behavior based on a process of runaway social selection. We then present several exploratory analyses of neuroendocrine responses to coalitionary social events in a rural Dominican community, with the objective of understanding differences between in-group and out-group competition in adult and adolescent males. Our analyses indicate: (1) adult and adolescent males do not elevate testosterone when they defeat their friends, but they do elevate testosterone when they defeat outsiders; (2) pre-competition testosterone and cortisol levels are negatively associated with strength of coalitionary ties; and (3) adult males usually elevate testosterone when interacting with adult women who are potential mates, but in a striking reversal, they have lower testosterone if the woman is a conjugal partner of a close friend. These naturalistic studies hint that reciprocity, dampening of aggression, and competition among friends and allies may be biologically embedded in unique ways among humans.  
  Call Number Serial 125  
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Author (up) Flores-Mireles, A.L.; Walker, J.N.; Caparon, M.; Hultgren, S.J. file  url
doi  openurl
  Title Urinary tract infections: epidemiology, mechanisms of infection and treatment options Type Journal Article
  Year 2015 Publication Nature Reviews. Microbiology Abbreviated Journal Nat Rev Microbiol  
  Volume 13 Issue 5 Pages 269-284  
  Keywords Anti-Bacterial Agents/therapeutic use; Bacterial Infections/*drug therapy/economics/*epidemiology/microbiology; Humans; Risk Factors; Urinary Tract Infections/*drug therapy/economics/*epidemiology/microbiology  
  Abstract Urinary tract infections (UTIs) are a severe public health problem and are caused by a range of pathogens, but most commonly by Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Enterococcus faecalis and Staphylococcus saprophyticus. High recurrence rates and increasing antimicrobial resistance among uropathogens threaten to greatly increase the economic burden of these infections. In this Review, we discuss how basic science studies are elucidating the molecular details of the crosstalk that occurs at the host-pathogen interface, as well as the consequences of these interactions for the pathophysiology of UTIs. We also describe current efforts to translate this knowledge into new clinical treatments for UTIs.  
  Call Number Serial 1181  
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Author (up) Foltz, D.R.; Jansen, L.E.T.; Black, B.E.; Bailey, A.O.; Yates, J.R. 3rd; Cleveland, D.W. url  doi
  Title The human CENP-A centromeric nucleosome-associated complex Type Journal Article
  Year 2006 Publication Nature Cell Biology Abbreviated Journal Nat Cell Biol  
  Volume 8 Issue 5 Pages 458-469  
  Keywords Amino Acid Sequence; Autoantigens--chemistry, isolation & purification; metabolism; Centromere--metabolism; Chromatin Assembly Factor-1; Chromatin Assembly and Disassembly--genetics; Chromosomal Proteins, Non-Histone--chemistry, isolation & purification, metabolism; Chromosomes, Human genetics; DNA-Binding Proteins--metabolism; HeLa Cells; Histones--chemistry; Humans; Mitosis--genetics; Molecular Sequence Data; Nucleosomes--metabolism; Protein Binding; Signal Transduction  
  Abstract The basic element for chromosome inheritance, the centromere, is epigenetically determined in mammals. The prime candidate for specifying centromere identity is the array of nucleosomes assembled with CENP-A, the centromere-specific histone H3 variant. Here, we show that CENP-A nucleosomes directly recruit a proximal CENP-A nucleosome associated complex (NAC) comprised of three new human centromere proteins (CENP-M, CENP-N and CENP-T), along with CENP-U(50), CENP-C and CENP-H. Assembly of the CENP-A NAC at centromeres is dependent on CENP-M, CENP-N and CENP-T. Facilitates chromatin transcription (FACT) and nucleophosmin-1 (previously implicated in transcriptional chromatin remodelling and as a multifunctional nuclear chaperone, respectively) are absent from histone H3-containing nucleosomes, but are stably recruited to CENP-A nucleosomes independent of CENP-A NAC. Seven new CENP-A-nucleosome distal (CAD) centromere components (CENP-K, CENP-L, CENP-O, CENP-P, CENP-Q, CENP-R and CENP-S) are identified as assembling on the CENP-A NAC. The CENP-A NAC is essential, as disruption of the complex causes errors of chromosome alignment and segregation that preclude cell survival despite continued centromere-derived mitotic checkpoint signalling.  
  Call Number Serial 13  
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Author (up) Foote, H.W.; Hamer, J.D.; Roland, M.M.; Landy, S.R.; Smitherman, T.A. file  url
  Title Psychological flexibility in migraine: A study of pain acceptance and values-based action Type Journal Article
  Year 2016 Publication Cephalalgia : an International Journal of Headache Abbreviated Journal Cephalalgia  
  Volume 36 Issue 4 Pages 317-324  
  Keywords *Adaptation, Psychological; Adult; Chronic Pain/psychology; Cross-Sectional Studies; Female; Humans; Male; Migraine Disorders/*psychology; Surveys and Questionnaires; Migraine; acceptance; acceptance and commitment therapy; disability; headache; psychological flexibility  
  Abstract BACKGROUND: Studies of musculoskeletal pain patients confirm that acceptance of pain and values-based action are strong predictors of pain-related disability and that interventions fostering “psychological flexibility” confer positive outcomes. However, data on these processes in migraine remain limited. This cross-sectional study examined relations between components of psychological flexibility and headache among treatment-seeking migraineurs. METHODS: A total of 103 adults (M age = 41.5 (11.9) years; 88.2% female) with ICHD-confirmed migraine (71.8% episodic, 28.2% chronic) across three clinics completed measures of psychological flexibility and headache-related disability. Hierarchical regressions quantified relations between acceptance/values-based action and headache variables after first controlling for pain severity and gender. RESULTS: Acceptance of pain and values-based action accounted for 10% of unique variance in headache severity (DeltaR(2) p = 0.006) and up to 20% in headache-related disability (DeltaR(2) ps = 0.02 and < 0.001) but were weakly related to headache frequency. Psychological flexibility was more strongly associated with MIDAS-measured disability than was headache severity or headache frequency. Significant effects were typically of medium-to-large size and driven primarily by values-based action. CONCLUSIONS: Paralleling results from the broader chronic pain literature, pain acceptance and values-based action play significant roles in headache pain and disability. Further study of interventions targeting these processes may enhance existing treatments.  
  Call Number Serial 2062  
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Author (up) Forehand, R.; Biggar, H.; Kotchick, B.A. file  url
  Title Cumulative risk across family stressors: short- and long-term effects for adolescents Type Journal Article
  Year 1998 Publication Journal of Abnormal Child Psychology Abbreviated Journal J Abnorm Child Psychol  
  Volume 26 Issue 2 Pages 119-128  
  Keywords Achievement; Adaptation, Psychological; Adjustment Disorders/diagnosis/*epidemiology; Adolescent; *Adolescent Psychology; Adult; Affective Symptoms/diagnosis/epidemiology; Analysis of Variance; Child; Conduct Disorder/diagnosis/epidemiology; Depressive Disorder/diagnosis/epidemiology; Educational Measurement; Educational Status; *Family Relations; Female; Humans; Juvenile Delinquency/statistics & numerical data; Male; Parent-Child Relations; Personality Inventory/statistics & numerical data; Risk Factors; Social Adjustment  
  Abstract This study examined the relationship between number of family risk factors during adolescence and three areas of psychosocial adjustment (internalizing problems, externalizing problems, and academic achievement) in adolescence and 6 years later in young adulthood. Risk factors examined included parental divorce, interparental conflict, maternal physical health problems, maternal depressive mood, and mother-adolescent relationship difficulties. The findings indicated both concurrent and long-term associations between number of family risk factors and psychosocial adjustment; however, the results differed based on area of adjustment examined and whether concurrent or longitudinal data were considered. Furthermore, a steep increase in adjustment difficulties occurred when number of risk factors increased from three to four. The results are discussed in the framework of four hypotheses which were tested, and clinical implications are delineated.  
  Call Number Serial 289  
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Author (up) Forstermann, U.; Kleinert, H.; Gath, I.; Schwarz, P.; Closs, E.I.; Dun, N.J. file  url
  Title Expression and expressional control of nitric oxide synthases in various cell types Type Journal Article
  Year 1995 Publication Advances in Pharmacology (San Diego, Calif.) Abbreviated Journal Adv Pharmacol  
  Volume 34 Issue Pages 171-186  
  Keywords Animals; Cells/*enzymology; Gene Expression Regulation, Enzymologic/*physiology; Humans; Isoenzymes/*biosynthesis/genetics; Nitric Oxide Synthase/*biosynthesis/genetics  
  Abstract Three isozymes of nitric oxide synthase (NOS) have been identified. Their cDNA- and protein structures as well as their genomic DNA structures have been described. NOS I (ncNOS, originally discovered in neurons) and NOS III (ecNOS, originally discovered in endothelial cells) are low output, Ca2+-activated enzymes whose physiological function is signal transduction. NOS II (iNOS, originally discovered in cytokine-induced macrophages) is a high output enzyme which produces toxic amounts of NO that represent an important component of the antimicrobial, antiparasitic and antineoplasic activity of these cells. Depending on the species, NOS II activity is largely (human) or completely (mouse and rat) Ca2+-independent. In the human species, the NOS isoforms I, II and III are encoded by three different genes located on chromosomes 12, 17 and 7, respectively. The amino acid sequences of the three human isozymes (deduced from the cloned cDNAs) show less than 59% identity. Across species, amino acid sequences are more than 90% conserved for NOS I and III, and greater 80% identical for NOS II. All NOS produce NO by oxidizing a guanidino nitrogen of L-arginine utilizing molecular oxygen and NADPH as co-substrates. All isoforms contain FAD, FMN and heme iron as prosthetic groups and require the cofactor BH4. NOS I and III are constitutively expressed in various cells. Nevertheless, expression of these isoforms is subject to regulation. Expression is enhanced by e.g. estrogens (for NOS I and III), shear stress, TGF-&#946;1, and (in certain endothelial cells) high glucose (for NOS III). TNF-&#945; reduces the expression of NOS III by a post-trancriptional mechanism destabilizing the mRNA. The regulation of the NOS I expression seems to be very complex as reflected by at least 8 different promoters transcribing 8 different exon 1 sequences which are expressed differently in different cell types. Expression of NOS II is mainly regulated at the transcriptional level and can be induced in many cell types with suitable agents such as LPS, cytokines, and other compounds. Whether some cells can express NOS II constitutively is still under debate. Pathways resulting in the induction of the NOS II promoter may vary in different cells. Activation of transcription factor NF-&#954;B seems to be an essential step for NOS II induction in most cells. The induction of NOS II can be inhibited by a wide variety of immunomodulatory compounds acting at the transcriptional levels and/or post-transcriptionally.  
  Call Number Serial 134  
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Author (up) Fox, D.J.; Tharp, D.F.; Fox, L.C. file  url
  Title Neurofeedback: an alternative and efficacious treatment for Attention Deficit Hyperactivity Disorder Type Journal Article
  Year 2005 Publication Applied Psychophysiology and Biofeedback Abbreviated Journal Appl Psychophysiol Biofeedback  
  Volume 30 Issue 4 Pages 365-373  
  Keywords Attention Deficit Disorder with Hyperactivity/drug therapy/*therapy; *Biofeedback, Psychology; Central Nervous System Stimulants/adverse effects/therapeutic use; Child; Humans  
  Abstract Current research has shown that neurofeedback, or EEG biofeedback as it is sometimes called, is a viable alternative treatment for Attention Deficit Hyperactivity Disorder (ADHD). The aim of this article is to illustrate current treatment modalities(s), compare them to neurofeedback, and present the benefits of utilizing this method of treatment to control and potentially alleviate the symptoms of ADHD. In addition, this article examines the prevalence rates and possible etiology of ADHD, the factors associated with ADHD and brain dysfunction, the current pharmacological treatments of ADHD, Ritalin, and the potential risks and side effects. Behavior modification and cognitive behavioral treatment for ADHD is discussed as well. Lastly, a brief history of the study of neurofeedback, treatment successes and clinical benefits, comparisons to medication, and limitations are presented.  
  Call Number Serial 1726  
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