Search results for "P.O.S"
showing 10 items of 5765 documents
Neurodegenerative changes are prevented by Erythropoietin in the pmn model of motoneuron degeneration
2014
Motoneuron diseases are fatal neurodegenerative disorders characterized by a progressive loss of motoneurons, muscle weakness and premature death. The progressive motor neuronopathy (pmn) mutant mouse has been considered a good model for the autosomal recessive childhood form of spinal muscular atrophy (SMA). Here, we investigated the therapeutic potential of Erythropoietin (Epo) on this mutant mouse. Symptomatic or pre-symptomatic treatment with Epo significantly prolongs lifespan by 84.6% or 87.2% respectively. Epo preserves muscle strength and significantly attenuates behavioural motor deficits of mutant pmn mice. Histological and metabolic changes in the spinal cord evaluated by immunoh…
Coronary microvascular dysfunction
2020
Patients with coronary microvascular dysfunction (CMVD) represent a widespread population and despite the good prognosis, many of them have a poor quality of life with strong limitations in their daily activities because of the angina symptoms. This article summarizes the most frequent clinical presentation pictures like stable and unstable microvascular angina. Main risk factors are discussed, followed by the latest updates on the subject about different pathogenic hypotheses, diagnosis and treatment. Not very well understood microvascular alterations, like slow flow phenomenon and no reflow are discussed and both prognosis and the impact of the disease in the quality of life are analyzed.
Mechanisms of C-reactive protein-induced blood-brain barrier disruption.
2009
Background and Purpose— Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood–brain barrier stability and to analyze the underlying signaling pathways. Methods— We used a cell coculture model of the blood–brain barrier and the guinea pig isolated whole brain preparation. Results— We could show that CRP at clinically relevant concentrations (10 to 20 μg/mL) causes a disruption of the blood–brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fcγ receptors CD16/32 fo…
Beta-adrenoceptor stimulation enhances transmitter output from the rat phrenic nerve.
1988
Abstract 1. Neurally-evoked output of newly synthesized [3H]-acetylcholine from the rat phrenic nerve was measured in the absence of cholinesterase inhibitors. 2. Noradrenaline and isoprenaline enhanced neurally-evoked transmitter output markedly. Moreover, immediately after the application of noradrenaline the basal tritium efflux increased significantly. 3. Pretreatment with propranolol (0.1 mumol l-1) or atenolol (0.3 mumol l-1) completely prevented the stimulatory effect of noradrenaline and isoprenaline on evoked transmitter output. 4. The facilitatory effect of isoprenaline declined, when the exposure time was increased. This observation supports the assumption that beta-adrenoceptors…
Acupressure therapy for insomnia in adolescents: a polysomnographic study
2013
Marco Carotenuto,1 Beatrice Gallai,2 Lucia Parisi,3 Michele Roccella,3 Maria Esposito11Sleep Clinic for Developmental Age, Clinic of Child and Adolescent Neuropsychiatry, Second University of Naples, Naples, 2Unit of Child and Adolescent Neuropsychiatry, University of Perugia, Perugia, 3Child Neuropsychiatry, Department of Psychology, University of Palermo, Palermo, ItalyBackground: The purpose of this study was to assess the efficacy of acupressure therapy in a sample of adolescents with insomnia using a standard polysomnographic evaluation.Methods: For this study, 25 adolescents affected by psychophysiological insomnia (mean age 15.04 ± 1.18 years, 12 boys) were enrolled. A dev…
Towards a framework for treatment effectiveness in schizophrenia
2014
Georg Juckel,1 Andrea de Bartolomeis,2 Philip Gorwood,3 Sergey Mosolov,4 Luca Pani,5 Alessandro Rossi,6 Julio Sanjuan7 1Department of Psychiatry, LWL-University Hospital, Ruhr-University Bochum, Bochum, Germany; 2Laboratory of Molecular Psychiatry and Unit of Treatment Resistant Psychosis, University School of Medicine of Naples Federico II, Napoli, Italy; 3Groupe Hospitalier Sainte-Anne (CMME), Paris-Descartes University, Paris, France; 4Moscow Research Institute of Psychiatry, Moscow, Russia; 5Institute of Translational Pharmacology, Italian National Research Council, Rome, Italy; 6Università de L’Aquila, L’Aquila, Italy; 7Clinic Hospital, Spanish Mental Hea…
Presence of muscarinic inhibitory and absence of nicotinic excitatory receptors at the terminal sympathetic nerves of chicken hearts.
1976
Nicotine (2 X 10(-4) M) or acetylcholine (5.5 X 10(-4) M) in the presence of 3 X 10(-6) M atropine did not increase the rate or amplitude of contraction in isolated atria or ventricular strips of the chicken heart; both drugs also did not cause an output of noradrenaline or adrenaline and did not evoke antidromic discharges in the right sympathetic nerves of isolated perfused chicken hearts. In contrast, "high K+-solutions" evoked an output of noradrenaline and adrenaline and caused a burst of antidromic discharges. Dimethylphenylpiperazine (DMPP; 3.1 X 10(-4) M), by a tyramine-like action, elicited a small output of noradrenaline and increased rate and amplitude of contraction" but did not…
Differential blockade by nifedipine and ω-conotoxin GVIA of α1- and β1-adrenoceptor-controlled calcium channels on motor nerve terminals of the rat
1990
Electrically evoked release of [3H]acetylcholine ([3H]ACh) from the rat phrenic nerve and its facilitation by stimulation of presynaptic alpha 1- and beta 1-adrenoceptors were investigated in the absence and presence of nifedipine and omega-conotoxin GVIA. Both calcium channel antagonists did not modify electrically evoked [3H]ACh release, but selectively blocked the effect triggered by both facilitatory adrenergic receptors. The increase in [3H]ACh release mediated via beta 1-adrenoceptor activation was abolished by low concentrations (1 nM) of omega-conotoxin GVIA, whereas nifedipine (100 nM) abolished the facilitatory effect mediated via alpha 1-adrenoceptor stimulation. Therefore, the b…
Effect of cocaine and related drugs on the uptake of noradrenaline by heart and spleen
1961
Noradrenaline uptake by heart and spleen after intravenous infusion of noradrenaline was measured in the pithed rat. Cocaine, given before the infusion, inhibited the noradrenaline uptake in relation (a) to the dose administered and (b) to the amount of noradrenaline infused. There was an association between increase in the pressor response to a test dose of noradrenaline and inhibition of the uptake by the heart. Drugs related chemically to cocaine, such as alpha-cocaine, amethocaine, and atropine, did not alter the noradrenaline uptake or potentiate the blood pressure response to noradrenaline. The noradrenaline uptake by the heart was unchanged after dibenamine, but blocked by the dichlo…
Lack of binding of gestodene to estrogen receptor in human breast cancer tissue
1990
Competition studies with progesterone and estradiol receptors of human myometrial tissue as well as of mammary cancer tissue showed that gestodene bound with high affinity to the progesterone receptor, as did other synthetic and natural progestogens. However, gestodene did not bind to the estradiol receptor. The relative binding affinities of all tested synthetic and natural ligands showed no organ-specific differences and no differences between neoplastically transformed and normal tissues.