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Several Neurological (several + neurological)
Terms modified by Several Neurological Selected AbstractsTransgenic expression of Cre recombinase from the tyrosine hydroxylase locusGENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 2 2004Jonas Lindeberg Abstract Catecholaminergic neurons are affected in several neurological and psychiatric diseases. Tyrosine hydroxylase (TH) is the first, rate-limiting enzyme in catecholamine synthesis. We report a knockin mouse expressing Cre-recombinase from the 3,-untranslated region of the endogenous Th gene by means of an internal ribosomal entry sequence (IRES). The resulting Cre expression matches the normal pattern of TH expression, while the pattern and level of TH are not altered in the knockin mouse. Crossings with two different LacZ reporter mice demonstrated Cre-mediated genomic recombination in TH expressing tissues. In addition, LacZ was found in some unexpected cell populations (including oocytes), indicating recombination due to transient developmental TH expression. Our novel knockin mouse can be used for generation of tissue-specific or general knockouts (depending on scheme of crossing) in mice carrying genes flanked by loxP sites. This knockin mouse can also be used for tracing cell lineages expressing TH during development. genesis 40:67,73, 2004. © 2004 Wiley-Liss, Inc. [source] AIDS dementia complex and Hashimoto encephalopathy in a senescent womanINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 12 2007Robert Waltereit Abstract AIDS dementia complex is one of the specific infectious dementias, which is rarely seen in senescent (>75 years of age) subjects. Hashimoto encephalopathy has been described as the cause of several neurological and psychiatric syndromes including dementia. The proposed pathophysiological mechanism is an autoimmune reaction to shared, thyroid gland and CNS epitopes with subsequent cerebral dysfunction. We report here the first case of a patient who fulfils both, the criteria for AIDS dementia complex and Hashimoto encephalopathy, yet being unresponsive to steroid therapy. Diagnostic and therapeutic implications are discussed. Copyright © 2007 John Wiley & Sons, Ltd. [source] Synthesis of [18F]3-[1-(3-fluoropropyl)-(S)-pyrrolidin-2-ylmethoxy]pyridine ([18F]NicFP): a potential ,4,2 nicotinic acetylcholine receptor radioligand for PETJOURNAL OF LABELLED COMPOUNDS AND RADIOPHARMACEUTICALS, Issue 14 2003Filip Dumont Abstract Nicotinic acetylcholine receptors are widely distributed throughout the human brain and are believed to play a role in several neurological and psychiatric disorders. In order to identify an effective PET radioligand for in vivo assessment of the ,4,2 subtype of nicotinic receptor, we synthesized [18F]3-[1-(3-fluoropropyl)-(S)-pyrrolidin-2-ylmethoxy]pyridine (NicFP). The in vitro KD of NicFP was determined to be 1.1 nM, and the log P value obtained by HPLC analysis of the unlabelled standard was found to be 2.2. The radiosynthesis of [18F]NicFP was carried out by a nucleophilic substitution reaction of anhydrous [18F]fluoride and the corresponding mesylate precursor. After purification by HPLC, the radiochemical yield was determined to be 11.3±2.1% and the specific activity was 0.47±0.18 Ci/,mol (EOS, n = 3). The time of synthesis and purification was 99±2 min. The final product was prepared as a sterile saline solution suitable for in vivo use. Copyright © 2003 John Wiley & Sons, Ltd. [source] Transgenic mouse models of dopamine deficiencyANNALS OF NEUROLOGY, Issue S6 2003Linan Chen PhD The dopamine system is implicated in several neurological and psychiatric disorders. Genetic mutations or variations that affect dopamine system functions either directly cause or contribute to these disorders, even though other genetic and environmental factors may contribute significantly to some of these disorders as well. Transgenic mice increasingly become important tools in revealing functions of genes that are essential components of the dopamine system as well as in modeling human genetic disorders. We have reviewed a comprehensive list of those genes and compared genetic mutations/variations in humans and transgenic mouse models. The significance and limitations of these animal models as well as future directions are discussed. Ann Neurol 2003;54 (suppl 6):S91,S102 [source] |