Synthese des 1-methyl-3-oxyflavons.

Thesis (doctoral)--

Ueber das 4-methyl-und 4-aethyl-anilopyrin.

Thesis (doctoral)--

Untersuchungen uber die [alpha]-Phenyl-p-Methylcinchoninsaure sowie [alpha]- Methyl-p-Methylcinghoninsaure und deren Derivate /

Thesis (doctoral)--Universitat Basel, 1898.

Ueber die Einwirkung von Natrium und Alkohol auf Antipyrin, Methylantipyrin und (1)Phenyl(3)methyl(4)dimethylpyrazolon /

Thesis (doctoral)--Universität Jena, 1896.

Uber basische Derivate von 1-Phenyl-3-methyl-4-azobenzol und 4-azobenzolsulfosaure-5-chlorpyrazol /

Thesis (doctoral)--Universitat Rostock, 1906.

Untersuchungen uber das Methyl-Benzimidazol /

Thesis (doctoral)--Universitat Marburg, 1898.

Zur kenntnis des 1-phenyl-3-methyl-4-dimethyl-5-pyrazolons.

Thesis (doctoral)--

Beitrage zur kenntniss des methyl-hexylenketons.

Thesis (doctoral)--

Uber (1)-phenyl-(3)-methyl-(4)-nitro-(5)-pyrazolon und (1)-phen...

Thesis (doctoral)--

Ueber das 3(5)-methyl- 4-athyl-pyrazol.

Thesis (doctoral)--

The absorption spectra of solutions of certain salts of cobalt, nickel, copper, iron, chromium, neodymium, praseodymium, and erbium in water, methyl alcohol, ethyl alcohol, and acetone, and in mixtures of water with the other solvents.

"A continuation of the work of Jones and Uhler on the absorption spectra of solutions (Carnegie publication no. 60)" cf. Pref.

Characterization and Degradation of Fatty Acid Methyl Esters and Biodiesel in Artificial Seawater Under UV Exposure Using Raman Spectroscopy

Thesis (Master's)--University of Washington, 2016-06

Morphine-3-glucuronide's neuro-excitatory effects are mediated via indirect activation of N-methyl-D-aspartic acid receptors: Mechanistic studies in embryonic cultured hippocampal neurones

Indirect evidence indicates that morphine-3-glucuronide (M3G) may contribute significantly to the neuro-excitatory side effects (myoclonus and allodynia) of large-dose systemic morphine. To gain insight into the mechanism underlying M3G' s excitatory behaviors, We used fluo-3 fluorescence digital imaging techniques to assess the acute effects of M3G (5-500 muM) on the cytosolic calcium concentration ([Ca2+](CYT)) in cultured embryonic hippocampal neurones. Acute (3 min) exposure of neurones to M3G evoked [Ca2+](CYT) transients that were typically either (a) transient oscillatory responses characterized by a rapid increase in [Ca2+](CYT) oscillation amplitude that was sustained for at least similar to30 s or (b) a sustained increase in [Ca2+](CYT) that slowly recovered to baseline. Naloxone-pretreatment decreased the proportion of M3G-responsive neurones by 10%-25%, implicating a predominantly non-opioidergic mechanism. Although the naloxone-insensitive M3G-induced increases in [Ca2+](CYT) were completely blocked by N-methyl-D-aspartic acid (NMDA) antagonists and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (alphaamino-3-hydroxy-5-methyl-4-isoxazolepropiordc acid/ kainate antagonist), CNQX did not block the large increase in [Ca2+](CYT) evoked by NMDA (as expected), confirming that N13G indirectly activates the NMDA receptor. Additionally, tetrodotoxin (Na+ channel blocker), baclofen (gamma-aminobutyric acid, agonist), MVIIC (P/Q-type calcium channel blocker), and nifedipine (L-type calcium channel blocker) all abolished M3G-induced increases in [Ca2+](CYT), suggesting that M3G may produce its neuro-excitatory effects by modulating neurotransmitter release. However, additional characterization is required.

Differential expression of N-methyl-D-aspartate receptor NR2 isoforms in Alzheimer's disease

We have previously shown that the expression of NMDA receptor NR1 subunit mRNA splice variants in Alzheimer's disease (AD) brain varies according to regional susceptibility to pathological damage. Here we investigated the expression of the modulatory NR2 subunits of the NMDA receptor using quantitative RT-PCR to assay all NR2 isoforms. Significantly lower expression of NR2A and NR2B transcripts was found in susceptible regions of AD brain, whereas expression of NR2C and NR2D transcripts did not differ from that in controls. Western blot analysis confirmed a lower expression of the NR2A and NR2B isoforms at the protein level. The results suggest that NR2 subunit composition may modulate NMDA receptor-mediated excitotoxicity. NMDA receptor dysfunction might give rise to the regionally selective pattern of neuronal loss that is characteristic of AD.

The preparation and characterization of tin(IV) complexes of 2-quinolinecarboxaldehyde Schiff bases of S-methyl- and S-benzyldithiocarbazates and the X-ray crystal and molecular structures of the 2-quinolinecarboxaldehyde Schiff base of S-benzyldithi

New tin(IV) complexes of empirical formula, Sn(NNS)I-3 (NNS = anionic forms of the 2-quinolinecarboxaldehyde Schiff bases of S-methyl- and S-benzyldithiocarbazate) have been prepared and characterized by a variety of physico-chemical techniques. In the solid state, the Schiff bases exist as the thione tautomer but in solution and in the presence of tin(IV) iodide they convert to the thiol tautomer and coordinate to the tin atom in their deprotonated thiolate forms. The structures of the free ligand, Hqaldsbz and its triiodotin(IV) complex, [Sn(qaldsbz)I-3] have been determined by X-ray diffraction. The complex, [Sn(qaldsbz)I-3] has a distorted octahedral structure with the Schiff base coordinated to the tin atom as a uninegatively charged tridentate chelating agent via the quinoline nitrogen atom, the azomethine nitrogen atom and the thiolate sulfur atom. The three iodo ligands are coordinated meridionally to the tin atom. The distortion from an ideal octahedral geometry of [Sn(qaldsbz)I-3] is attributed to the restricted bite size of the tridentate Schiff base ligand. (C) 2004 Elsevier Ltd. All rights reserved.