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Sökning: WFRF:(Archer Trevor 1949 ) > Medicin och hälsovetenskap

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1.
  • Archer, Trevor, 1949, et al. (författare)
  • Influence of noradrenaline denervation on MPTP-induced deficits in mice
  • 2006
  • Ingår i: Journal of neural transmission. - : Springer Science and Business Media LLC. - 0300-9564 .- 1435-1463. ; 113:9, s. 1119-1129
  • Tidskriftsartikel (refereegranskat)abstract
    • C57/BL6 mice were administered either DSP4 (50 mg/kg, s.c., 30 min after injection of zimeldine, 20 Cemg/kg, s.c.) or vehicle (saline) at 63 days of age. Three weeks later, one group (n = 10) of DSP4-treated and one group of vehicle-treated mice were administered MPTP (2 x 40 mg/kg, s.c., 24 hours between injections; the High dose groups), one group (n = 10) of DSP4-treated and one group of vehicle-treated mice were administered MPTP (2 x 20 mg/kg, s.c., 24 hours between injections; the Low dose groups), and one group (n = 10) of DSP4-treated and one group of vehicle-treated mice were administered vehicle. Three weeks later, all six groups were tested in motor activity test chambers, followed by injections of L-Dopa (20 mg/kg, s.c.), and then tested over a further 360 min in the activity test chambers. It was found that pretreatment with the selective NA neurotoxin, DSP4, deteriorated markedly the dose-dependent motor activity deficits observed in the vehicle pretreated MPTP treated mice. These 'ultra-deficits' in the spontaneous motor behaviour of MPTP-treated mice were observed over all three parameters: locomotion, rearing and total activity, and were restricted to the 1(st) and 2(nd) 20-min periods. Administration of L-Dopa (20 mg/kg) following the 60-min testing of spontaneous behaviour restored the motor activity of Vehicle + MPTP treated mice (neither the Vehicle + MPTP-Low nor the Vehicle + MPTP-High groups differed from the Vehicle-Vehicle group, here) but failed to do so in the DSP4 pretreated mice. Here, a dose-dependent deficit of L-Dopa-induced motor activity (over all three parameters) was obtained thereby offering further evidence of an 'ultra-deficit' of function due to previous denervation of the NA terminals. The present findings support the notion that severe damage to the locus coeruleus noradrenergic system, through systemic DSP4, disrupts the facilitatory influence on the nigrostriatal DA system, and interferes with the ability of the nigrostriatal pathway to compensate for or recover from marked injury, MPTP treatment.
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4.
  • Archer, Trevor, 1949, et al. (författare)
  • Physical Exercise Improves Cognition and Health in ADHD
  • 2014
  • Ingår i: Journal of Novel Physiotherapies. - : OMICS Publishing Group. - 2165-7025. ; 4:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Attention-Deficit Hyperactive Disorder (ADHD) disrupts normal functioning and health parameters in children and adults with the additional burden of continuing on into adulthood thereby implying marked disadvantages over the individual’s life-span. In this paper we review interventions that incorporate physical exercise programs, independent of specific type of activity or the proportions or endurance/resistence ingredients. These interventions have been found invariably to improve and alleviate symptom profiles, sometimes replacing the traditional treatments. In many cases, the presence of accompanying behavioral disruptions may be alleviated through exercise regimes.
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5.
  • Archer, Trevor, 1949, et al. (författare)
  • Attention-Deficit/Hyperactivity Disorder: Focus upon Aberrant N-Methyl-D-Aspartate Receptors Systems
  • 2016
  • Ingår i: R. M. Kostrzewa & T. Archert (Eds.), Neurotoxin Modeling of Brain Disorders – Life-long Outcomes in Behavioral Teratology, Volume 29 of the series Current Topics in Behavioral Neurosciences.. - Amsterdam : Springer. - 9783319341347 ; , s. 295-311
  • Bokkapitel (refereegranskat)abstract
    • Attention-deficit/hyperactivity disorder (ADHD) pathophysiology persists in an obscure manner with complex interactions between symptoms, staging, interventions, genes, and environments. Only on the basis of increasing incidence of the disorder, the need for understanding is greater than ever. The notion of an imbalance between central inhibitory/excitatory neurotransmitters is considered to exert an essential role. In this chapter, we first review how the default mode network functions and dysfunction in individuals diagnosed with ADHD. We also present and briefly review some of the animal models used to examine the neurobiological aspects of ADHD. There is much evidence indicating that compounds/interventions that antagonize/block glutamic acid receptors and/or block the glutamate signal during the "brain growth spurt" or in the adult animal may induce functional and biomarker deficits. Additionally, we present evidence suggesting that animals treated with glutamate blockers at the period of the "brain growth spurt" fail to perform the exploratory activity, observed invariably with control mice, that is associated with introduction to a novel environment (the test cages). Later, when the control animals show less locomotor and rearing activity, i.e., interest in the test cages, the MK-801, ketamine and ethanol treated mice showed successively greater levels of locomotion and rearing (interest), i.e., they fail to "habituate" effectively, implying a cognitive dysfunction. These disturbances of glutamate signaling during a critical period of brain development may contribute to the ADHD pathophysiology. As a final addition, we have briefly identified new research venues in the interaction between ADHD, molecular studies, and personality research.
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6.
  • Archer, Trevor, 1949, et al. (författare)
  • Epigenetic Influences on Anxious and Depressive Behaviors: BDNF Links
  • 2016
  • Ingår i: JSM Anxiety and Depression. - 2475-9139. ; 1:3
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • The identification of genetic biomarkers facilitates the staging of brain disorders, their prognosis, choice of treatments and interventions, prediction of response, and prognosis of outcomes over a wide spectrum of symptoms associated with affective states, possibly optimizing clinical practice treatments and procedures. In this regard, epigenetic mechanisms mediate the effects of the environment on human-animal neurodevelopment of behavioral repertoires and imply also that employing the sensitivity of laboratory animals to environmental cues may be applied usefully for the consideration of long-term health and welfare of individuals.
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7.
  • Archer, Trevor, 1949, et al. (författare)
  • Exercise and Dietary Restriction for Promotion of Neurohealth Benefits
  • 2015
  • Ingår i: Health. - : Scientific Research Publishing, Inc.. - 1949-4998 .- 1949-5005. ; 7:1, s. 136-152
  • Tidskriftsartikel (refereegranskat)abstract
    • Physical exercise, whether of aerobic, endurance or resistance types, plays a central role in estab-lishing and maintaining the integrity of the brain and central nervous system (CNS). When exer-cise is adhered to in conjunction with selective food/drink intake and dietary restriction it pro-motes neurohealth. In this article, we review the interactions of age and gender, as well as insulin and diabetes, with exercise, individuals’ cognitive-affective status and its interactions with exer-cise propensity. All of which modulate the eventual outcomes of the influence of exercise upon parameters of neurohealth. The combination of exercise with dietary restriction provides nu-merous factors pertaining to psychological, neurochemical and anti-pathological manifestations of neurophysiological resilience even through aging. The challenge evoked by the exercise-diet com-bination in the body mobilizes a multitude of adaptive cellular stress-response signaling pathways in neurons involving neurotrophic factors, anti-inflammatory cytokines, DNA-repair proteins, macroautophagy, and mitochondrial biogenesis.
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8.
  • Archer, Trevor, 1949, et al. (författare)
  • Exercise Influences upon Stress-Resilience and Resilient Health
  • 2016
  • Ingår i: Journal of Neuropsychology & Stress Management. ; 1:1: 100101
  • Tidskriftsartikel (refereegranskat)abstract
    • Regular physical exercise prevents tissue and cellular senescence with active individuals at lower risk for malignancies such as cancer of the colon and prostate, osteoporosis, depression and anxiety, diabetes and pre- diabetic individuals, and neurodegenerative disorders.
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9.
  • Archer, Trevor, 1949, et al. (författare)
  • Physical Exercise Improves Cognition in Brain Disorders: Alzheimer's Disease
  • 2015
  • Ingår i: Farooqui, T., & Farooqui, A. A. (2015). Diet and Exercise in Cognitive Function and Neurological Diseases. - New Jersey : John Wiley & Sons, Inc.. - 9781118840559 ; , s. 175-181
  • Bokkapitel (refereegranskat)abstract
    • Physical exercise impacts upon several aspects of psychological and somatic health, cognitive performance, emotional regulation, brain structure and function, and the integrity of a wide range of biomarkers linked to molecular systems important for maintaining neural function and plasticity. Manifestations of the essential beneficial influence upon neurological and neuropsychiatric disorders have been described, as well as in conditions of brain damage and neurodevelopmental disruption. Several studies have addressed the influence of exercise upon expressions of disorders associated with epilepsy and conditions linked to neuroimmune functioning. Evidence from several perspectives has reinforced the notion that exercise intervention ought to be integrated with conventional therapies for the improvement of brain function and resistance to neurodegenerative and neuropsychiatric disorders in addition to offering a complementary non-pharmacological, noninvasive alternative.
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10.
  • Daria, Cipollone, et al. (författare)
  • Biological Therapeutics and Pharmacovigilance in Italy
  • 2014
  • Ingår i: International Journal of Autoimmune Disorders & Therapies. ; :1:102
  • Tidskriftsartikel (refereegranskat)abstract
    • Biological therapeutics (BTs) presents a novel frontier for the treatment of autoimmune diseases, such as rheumatoid arthritis, psoriasis, Crohn's disease and several other conditions. BTs constitute highly selective compounds targeted upon specific structures that may be proteins, receptors, or DNA sequences. In the case of autoimmune diseases, the use of BTs is directed against pro-inflammatory cytokines that exert a central role in the inflammatory machinery. In the present review, attention is focused upon BTs that inhibit pro-inflammatory cytokines thereby blocking the inflammation, such as monoclonal antibodies (e.g. infliximab and adalimumab) and soluble receptors (e.g. etanercept). The interleukin-1 and interleukin-6 antagonists, anakinra and tocilizumab, rituximab, which decrease the number of circulating B-lymphocytes and abatacept, thereby counteracting T-lymphocyte activation, are described also. Despite the utility of BTs for patients presenting autoimmune diseases, they have been linked to opportunistic viral, bacterial, mycotic infections and to tumor cases. The occurrence of these pathologies is due to their immunosuppressive functions thereby requiring the meticulous monitoring by pharmacovigilance and drug safety techniques to assess risk analysis. Whether or not adverse drug events (ADEs) occur more frequently in patients administered BTs, compared to traditional drugs, is currently an essential topic of investigation.
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