Traumatic brain injury (TBI) is a major neurological disorder without FDA-approved therapies. In this study, we have examined the concept that TBI might trigger global brain proteolysis in the acute post-injury phase. Thus, we conducted a systemic proteolytic peptidomics analysis using acute cerebrospinal fluid (CSF) samples from TBI patients and normal control samples. We employed ultrafiltration-based low molecular weight (LMW; < 10 kDa) peptide enrichment, coupled with nano-reversed-phase liquid chromatography/tandem mass spectrometry analysis, followed with orthogonal quantitative immunoblotting-based protein degradation analysis. We indeed identified novel patterns of injury-dependent proteolytic peptides derived from neuronal components (pre-and post-synaptic terminal, dendrites, axons), extracellular matrix, oligodendrocytes, microglial cells, and astrocytes. Among these, post-synaptic protein neurogranin was identified for the first time converted to neurogranin peptides including neurogranin peptide (aa 16-64) that is phosphorylated at Ser-36/48 (P-NG-fragment) in acute human TBI CSF samples vs. normal control with a receiver operating characteristic area under the curve of 0.957. We also identified detailed processing of astroglia protein (vimentin) and oligodendrocyte protein (MBP and Golli-MBP) to protein breakdown products (BDPs) and/or LMW proteolytic peptides after TBI. In addition, using MS/ MS selected reaction monitoring method, two C-terminally released MBP peptides TQDENPVVHFF and TQDENPVVHF were found to be elevated in acute and subacute TBI CSF samples as compared to their normal control counterparts. These findings imply that future therapeutic strategies might be placed on the suppression of brain proteolysis as a target. The endogenous proteolytic peptides discovered in human TBI biofluid could represent useful diagnostic and monitoring tools for TBI.

A series of pyridoxal aroylhydrazones has been synthesized and their UV, IF? and 'H NMR spectra studied. In neutral methanol these hydrazones exist in the enolimine form, while in aqueous solution (pH ca 7.0) they exist predominantly in the zwitterionic form in which the phenolic proton is transferred to the pyridine nitrogen. Their aqueous acid-base equilibria show three successive steps for which protonation constants have been determined. The different acidity constants are correlated with Hammett substituent constants. The acid hydrolysis reactions of these hydrazones have also been investigated and the attack of a water molecule on the protonated azomethine seems t o be the rate-controlling step. The hydrolysis reactions of N-salicylidene-and Nbenzylidenebenzoylhydrazines have been studied for comparison.Paper 1 /02437J

In present study the experimental data of solids Cu(II)-Br-pyrimidine-2-carboxylate (1) (orthorhombic Pmc21) and Cu(II)-pyrimidine-4,6-dicarboxylate (2) (triclinic P1 -) were used to calculate their crystal parameters (a,b,c,α,β,γ) and the J exchange coupling constants of Cu-Cu interactions. The calculations were done employing the DFT method, using several density functionals for comparison. Keywords: DFT method, Spin exchange coupling, Crystal parameters.Asian Journal of Chemistry; Vol. 29, No. 12 (2017), 2739-2742 example of a uniform S = 1/2 antiferromagnetic Heisenberg chain with exchange parameter J = -12.5 cm -1

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In a spectrophotometric study of the substitution reactions of the title complexes (I) with the amines (II) two successive steps (III) and (IV) are observed.