ABSTRACT
The orientation of a CdSe/CdS nanocrystal attached at the end of a scanning near field optical microscope (SNOM) tip is analyzed by its coupling with a flat gold layer. The Purcell factors for a set of distances to the gold surface are measured after a NC is caught by a SNOM tip. These measurements are compared with the modeling of the emission of a 2D dipole on a gold layer taking into account the layer of polymer serving as a glue for the NC. The 2D dipole is perpendicular to the c-axis of the NC, which is the growth axis. The behavior of the Purcell factor as a function of the distance to the gold layer depends on the angle made by this axis and the surface. The adjustment of the experimental results and the modelization gives the orientation of the NC at the end of the SNOM tip. Different orientations of the c-axis are determined.
ABSTRACT
Human presenilin-1 (PS1) mutations are a major cause of autosomal dominant Alzheimer's disease. Forebrain cholinergic innervation was estimated in transgenic mice with the A246E mutation by measuring the activity of the non-specific catabolic enzyme, acetylcholinesterase (AChE). In the model, Abeta(42) concentrations increase without neuritic plaques or cell degeneration. PS1/A246E transgenic mice had altered AChE activity in several regions also vulnerable in Alzheimer pathology. In particular, AChE activity was upregulated in major cholinergic cell nuclei (medial septum, vertical diagonal band, substantia inominata) and in cortical and thalamic regions (eye field, posterior parietal and visual cortices, posterior thalamic and lateral geniculate nuclei) responsible for selective attention and visuomotor coordination, as well as limbic structures (hippocampal formation and amygdala) with related regions (midline, periventricular, reticular thalamic nuclei, and lateral prefrontal, agranular insular cortices) involved in cognition, arousal, emotion, and plasticity. As the murine model caused no apparent learning defects, cholinergic network changes in forebrain seem to be an early event caused by soluble Abeta peptides. PS1/A246E mice mimic to some extent pre-symptomatic Alzheimer's disease neuropathology, useful for studying early neurochemical changes often inaccessible in clinical studies.
Subject(s)
Acetylcholinesterase/metabolism , Alzheimer Disease/genetics , Brain/enzymology , Brain/pathology , Mutation , Presenilin-1/genetics , Alzheimer Disease/pathology , Amyloid beta-Peptides/metabolism , Analysis of Variance , Animals , Disease Models, Animal , Fluoresceins , Humans , Mice , Mice, Transgenic , Organic Chemicals , Peptide Fragments/metabolismABSTRACT
This title comes from the one given by Ibn Sina - Avicenna in the West - to volume V of his work Al-Qanun fil'tibb or The Canon of medicine. Ibn Sina's works constitute a very important legacy and this is confirmed by volumes II ans V of The canon in particular. Volume II deals with basic drugs: it details some 800 monographs covering the plant, the animal and the mineral kingdoms. Volume V, under the title of Aqrabadin (i.e. pharmacopoeia), deals with complex drugs; 434 formulae are recorded in its part 1 and 162 in part 2. In this volume Ibn Sina describes many galenics like theriacas, electuaries, hieras, syrups, suppositories and sublingual tablets, together with "diachylon" plasters. All these confections were tried by the author who also mentions the expiry date of drugs and recommends their sensible use.
Subject(s)
Pharmacopoeias as Topic/history , Antidotes , Arab World , History, MedievalABSTRACT
The article illustrates the history of pharmacology in the Arab world. The author analyzes the relations between medical and pharmaceutical sciences before the Xth century; he describes the first pharmacopoeias, the most important works in the Xth and XIth centuries, the organization of the pharmaceutical profession, and the history of Arabian pharmacology from the XIIth to the XVIIIth century, through the lives and books of the most important medical writers.
