The Friction of Structurally Modified Isotactic Polypropylene

The purpose of studies was to analyse an impact of heterogeneous nucleation of modified isotactic polypropylene (iPP) on its tribological properties. The iPP injection molded samples, produced by mold temperature of 20 and 70 °C, were modified with compositions of two nucleating agents (NA’s), DMDBS creating α-form and mixture of pimelic acid with calcium stearate (PACS) forming β–phase of iPP, with a total content 0.2 wt.% of NA’s. A polymorphic character of iPP, with both, monoclinic (α) and pseudo-hexagonal (β) crystalline structures, depending on the NA’s ratio, was verified. The morphology observation, DSC, hardness and tribological measurements as test in reciprocating motion with “pin on flat” method, were realized, followed by microscopic observation (confocal and SEM) of the friction patch track. It was found that Shore hardness rises along with DMBDS content, independent on mold temperature. The friction coefficient (COF) depends on NA’s content and forming temperature—for upper mold temperature (70 °C), its value is higher and more divergently related to NA’s composition, what is not the case by 20 °C mold temperature. The height of friction scratches and the width of patch tracks due to its plastic deformation, as detected by confocal microscopy, are related to heterogeneous nucleation modified structure of iPP.

Metabolomic changes in animal models of depression: a systematic analysis

Extensive research has been carried out on the metabolomic changes in animal models of depression; however, there is no general agreement about which metabolites exhibit constant changes. Therefore, the aim of this study was to identify consistently altered metabolites in large-scale metabolomics studies of depression models. We performed vote counting analyses to identify consistently upregulated or downregulated metabolites in the brain, blood, and urine of animal models of depression based on 3743 differential metabolites from 241 animal metabolomics studies. We found that serotonin, dopamine, gamma-aminobutyric acid, norepinephrine, N-acetyl-L-aspartic acid, anandamide, and tryptophan were downregulated in the brain, while kynurenine, myo-inositol, hydroxykynurenine, and the kynurenine to tryptophan ratio were upregulated. Regarding blood metabolites, tryptophan, leucine, tyrosine, valine, trimethylamine N-oxide, proline, oleamide, pyruvic acid, and serotonin were downregulated, while N-acetyl glycoprotein, corticosterone, and glutamine were upregulated. Moreover, citric acid, oxoglutaric acid, proline, tryptophan, creatine, betaine, L-dopa, palmitic acid, and pimelic acid were downregulated, and hippuric acid was upregulated in urine. We also identified consistently altered metabolites in the hippocampus, prefrontal cortex, serum, and plasma. These findings suggested that metabolomic changes in depression models are characterized by decreased neurotransmitter and increased kynurenine metabolite levels in the brain, decreased amino acid and increased corticosterone levels in blood, and imbalanced energy metabolism and microbial metabolites in urine. This study contributes to existing knowledge of metabolomic changes in depression and revealed that the reproducibility of candidate metabolites was inadequate in previous studies.

Use of additives to regulate solute aggregation and direct conformational polymorph nucleation of pimelic acid

Understanding the nucleation pathway and achieving regulation to produce the desired crystals are mutually beneficial. The authors previously proposed a nucleation pathway of conformational polymorphs in which solvation and solute self-assembly could affect the result of the conformational rearrangement and further nucleation outcomes. Based on this, herein α,ω-alkanedicarboxylic acids (DAn, where n represents the number of carbon atoms in the molecule, n = 2–6, 8–11) were designed as homologous additives to interfere with the self-assembly of pimelic acid (DA7) to further induce the form II compound, which differs from form I only in conformation. Interestingly, longer-chain additives (DA6–11) have a stronger form II-inducing ability than short-chain ones (DA2–4). In addition, an apparent gradient of the degree of interference with solute self-assembly, consistent with form II-inducing ability, was detected by infrared and nuclear magnetic resonance spectroscopy. The calculated molecular electrostatic potential charges also clearly indicate that additive–solute electrostatic interactions gradually increase with increasing carbon chain length of the additives, reaching a maximum value with DA6–11. This novel use of additives demonstrates a direct link between solute aggregation and conformational polymorph nucleation.

α-proteobacteria synthesize biotin precursor pimeloyl-ACP using BioZ 3-ketoacyl-ACP synthase and lysine catabolism

Pimelic acid, a seven carbon α,ω-dicarboxylic acid (heptanedioic acid), is known to provide seven of the ten biotin carbon atoms including all those of the valeryl side chain. Distinct pimelate synthesis pathways were recently elucidated in Escherichia coli and Bacillus subtilis where fatty acid synthesis plus dedicated biotin enzymes produce the pimelate moiety. In contrast, the α-proteobacteria which include important plant and mammalian pathogens plus plant symbionts, lack all of the known pimelate synthesis genes and instead encode bioZ genes. Here we report a pathway in which BioZ proteins catalyze a 3-ketoacyl-acyl carrier protein (ACP) synthase III-like reaction to produce pimeloyl-ACP with five of the seven pimelate carbon atoms being derived from glutaryl-CoA, an intermediate in lysine degradation. Agrobacterium tumefaciens strains either deleted for bioZ or which encode a BioZ active site mutant are biotin auxotrophs, as are strains defective in CaiB which catalyzes glutaryl-CoA synthesis from glutarate and succinyl-CoA.

The primary step of biotin synthesis in mycobacteria

Biotin plays an essential role in growth of mycobacteria. Synthesis of the cofactor is essential forMycobacterium tuberculosisto establish and maintain chronic infections in a murine model of tuberculosis. Although the late steps of mycobacterial biotin synthesis, assembly of the heterocyclic rings, are thought to follow the canonical pathway, the mechanism of synthesis of the pimelic acid moiety that contributes most of the biotin carbon atoms is unknown. We report that theMycobacterium smegmatisgene annotated as encoding Tam, anO-methyltransferase that monomethylates and detoxifiestrans-aconitate, instead encodes a protein having the activity of BioC, anO-methyltransferase that methylates the free carboxyl of malonyl-ACP. TheM. smegmatisTam functionally replacedEscherichia coliBioC both in vivo and in vitro. Moreover, deletion of theM. smegmatis tamgene resulted in biotin auxotrophy, and addition of biotin toM. smegmatiscultures repressedtamgene transcription. Although its pathogenicity precluded in vivo studies, theM. tuberculosisTam also replacedE. coliBioC both in vivo and in vitro and complemented biotin-independent growth of theM. smegmatis tamdeletion mutant strain. Based on these data, we propose that the highly conserved mycobacterial tamgenes be renamedbioC.M. tuberculosisBioC presents a target for antituberculosis drugs which thus far have been directed at late reactions in the pathway with some success.