Ueber die Bestimmung des Gerbstoffs in Gerbstoffmaterialien

Ohne Zusammenfassung     

Surfaces with Harmonic Inverse Mean Curvature and Painlevé Equations

In this paper we study surfaces immersed in R³ such that the mean curvature function H satisfies the equation (1/H) = 0, where is the Laplace operator of the induced metric. We call them HIMC surfaces. All HIMC surfaces of revolution are classified in terms of the third Painlevé transcendent. In the general class of HIMC surfaces we distinguish a subclass of -isothermic surfaces, which is a generalization of the isothermic HIMC surfaces, and classify all the -isothermic HIMC surfaces in terms of the solutions of the fifth and sixth Painlevé transcendents.     

Rate and Equilibrium Constants for Reactions Transferring a Dimethylcarbamoyl Group between Pyridines

We have studied 18 reactions, including four identity reactions, involving transfer of a dimethylcarbamoyl group with N-acylpyridinium bonds to pyridine and its 4-substituted derivatives in acetonitrile solutions at 298 K. The rate constants k _ij varied within the range 0.4 to 10^–6 L/mol·s; the equilibrium constants K _ij varied from 10⁷ to 10^–5. The rate and equilibrium for exchange of carbamoyl groups are described satisfactorily by the Brönsted equation. We have shown that all the reactions occur according to a forced concerted S _N2 mechanism. The structure of the transition state and its position on the reaction coordinate for identity transfer are considered using a More O'Ferrall-Jencks diagram.     

Rate and Equilibrium Constants of Dimethylcarbamoyl Transfer between Pyridine N-Oxides

Dimethylcarbamoyl transfer from N-acyloxypyridinium salts to pyridine N-oxides in acetonitrile occurs in one stage by the forced concerted S_N2 mechanism. The rate and equilibrium of the reaction are fairly described by the Brönsted equation. The Marcus equation provides a much higher quality of reactivity predictions.     

The IL-10 gene is not involved in the predisposition to inflammatory bowel disease

Although genetic predisposition for inflammatory bowel disease (IBD) is well established, little is known about the accountable genes. The pathogenesis of IBD is characterized by an imbalanced activation of Th1- and Th2-lymphocytes. IL-10 represents an anti-inflammatory cytokine which downregulates the production of Th1-derived cytokines. To evaluate the role of the IL-10 gene in IBD, two polymorphisms in the promoter region (G/A at position -1082 and C/A at position -592) were genotyped in 142 patients with Crohn's disease (CD), 104 patients with ulcerative colitis (UC), and 400 healthy controls. Significant differences were not apparent, neither in the allele frequencies of either polymorphism, nor in the haplotype frequencies. Screening of the coding region of the IL-10 gene by polymerase chain reaction--single strand conformation polymorphism (PCR-SSCP) analysis revealed a rare sequence variation in exon 1 leading to an amino acid exchange (G-->A; G15R) in two patients with CD and five healthy controls. Therefore, polymorphisms of the IL-10 gene are not demonstrably involved in the predisposition of IBD in our cohorts of patients.     

The abundances of fragment ions formed via skeletal rearrangements from 2,5-disubstituted-1,3,4-oxadiazoles and their theoretical calculated stabilities

Protonated molecules of 2,5-di-R1,R2-substituted-1,3,4-oxadiazoles lose isocyanic acid (loss of mass 43) via skeletal rearrangement. This was observed in low-energy CID mass spectra recorded by using electrospray ionisation (ESI). On electron ionisation induced decomposition these compounds also reveal complex skeletal rearrangement, consisting on N2 and CO elimination, leading to the formation of fluorene or indene type ions. It was found that abundances of fragment ions formed in these processes are in good agreement with their theoretically calculated stabilities. In the case of ESI use the fragment ion abundances were calculated in relation to [M+H]+ ion abundances and for EI use, where extensive fragmentations proceed, the sums of the abundances of [M-N2-CO]+. ions and abundances of fragment ions derived from them, were expressed as a percentage of total-ion current.     

Three dimensional model of severe acute respiratory syndrome coronavirus helicase ATPase catalytic domain and molecular design of severe acute respiratory syndrome coronavirus helicase inhibitors

The modeling of the severe acute respiratory syndrome coronavirus helicase ATPase catalytic domain was performed using the protein structure prediction Meta Server and the 3D Jury method for model selection, which resulted in the identification of 1JPR, 1UAA and 1W36 PDB structures as suitable templates for creating a full atom 3D model. This model was further utilized to design small molecules that are expected to block an ATPase catalytic pocket thus inhibit the enzymatic activity. Binding sites for various functional groups were identified in a series of molecular dynamics calculation. Their positions in the catalytic pocket were used as constraints in the Cambridge structural database search for molecules having the pharmacophores that interacted most strongly with the enzyme in a desired position. The subsequent MD simulations followed by calculations of binding energies of the designed molecules were compared to ATP identifying the most successful candidates, for likely inhibitors—molecules possessing two phosphonic acid moieties at distal ends of the molecule.