Specific strains of lactic acid bacteria possessing antimutagenic properties are suggested to remove mutagenic contaminants of foods through binding and an investigation of their substrate specificity is required. The ability of Lactobacillus rhamnosus strains GG and LC-705 in viable and non-viable (heat- and acidtreated) forms to remove both dietary mutagens and other aromatic dietary substrates from solution was studied using HPLC. Overall, removal increased in the order: caffeine = vitamin B₁₂ = folic acid < ochratoxin A < aflatoxin B₁ = PhIP (2-amino-1-methyl-6-phenylimidazo[4,5- b]pyridine) < Trp-P-1 (3-amino-1, 4-dimethyl-5 H -pyrido[4,3- b]indole) (p < 0.05). Aflatoxin B₁, Trp-P-1 and PhIP were removed in high amounts (77–95%) and ochratoxin A was removed in moderate amounts (36–76%). By contrast, only minimal amounts of caffeine, vitamin B₁₂ and folic acid were removed (9–28%). The significant removal of selected mutagens, but not other substrates, suggests these strains may be useful for dietary detoxification. Since exposure to multiple mutagens is likely, the removal of aflatoxin B₁ and Trp-P-1 from a mixture of these substrates was also investigated. Removal of AFB₁ significantly increased (p < 0.05) in the presence of Trp-P-1, while removal of Trp-P-1 significantly decreased (p < 0.05) in the presence of AFB₁. Overall, no significant differences in removal were found between bacterial strains or between viable, heat- and acid-treated bacteria.

Oligodendrocytes are responsible for producing and maintaining myelin throughout the CNS. One of the pathological features observed following traumatic brain injury (TBI) is the progressive demyelination and degeneration of axons within white matter tracts. While the effect of TBI on axonal health has been well documented, there is limited information regarding the response of oligodendrocytes within these areas. The aim of this study was to characterize the response of both mature oligodendrocytes and immature proliferative oligodendrocyte lineage cells across a 3 month timecourse following TBI. A computer-controlled cortical impact model was used to produce a focal lesion in the left motor cortex of adult mice. Immunohistochemical analyses were performed at 48 hours, 7 days, 2 weeks, 5 weeks and 3 months following injury to assess the prevalence of mature CC-1⁺ oligodendrocyte cell death, immature Olig2⁺ cell proliferation and longer term survival in the corpus callosum and external capsule. Decreased CC-1 immunoreactivity was observed in white matter adjacent to the site of injury from 2 days to 2 weeks post TBI, with ongoing mature oligodendrocyte apoptosis after this time. Conversely, proliferation of Olig2⁺ cells was observed as early as 48 hours post TBI and significant numbers of these cells and their progeny survived and remained in the external capsule within the injured hemisphere until at least 3 months post injury. These findings demonstrate that immature oligodendrocyte lineage cells respond to TBI by replacing oligodendrocytes lost due to damage and that this process occurs for months after injury.

Nanodiamonds (NDs) containing silicon vacancy (SiV) defects were evaluated as a potential biomarker for the labeling and fluorescent imaging of neural precursor cells (NPCs). SiV-containing NDs were synthesized using chemical vapor deposition and silicon ion implantation. Spectrally, SiV-containing NDs exhibited extremely stable fluorescence and narrow bandwidth emission with an excellent signal to noise ratio exceeding that of NDs containing nitrogen-vacancy centers. NPCs labeled with NDs exhibited normal cell viability and proliferative properties consistent with biocompatibility. We conclude that SiV-containing NDs are a promising biomedical research tool for cellular labeling and optical imaging in stem cell research.

Adult neural precursor cells (NPCs) respond to injury or disease of the CNS by migrating to the site of damage or differentiating locally to replace lost cells. Factors that mediate this injury induced NPC response include chemokines and pro-inflammatory cytokines, such as tumor necrosis factor-α (TNFα) and interferon-γ (IFNγ), which we have shown previously promotes neuronal differentiation. RT-PCR was used to compare expression of chemokines and their receptors in normal adult mouse brain and in cultured NPCs in response to IFNγ and TNFα. Basal expression of many chemokines and their receptors was found in adult brain, predominantly in neurogenic regions, with OB≫SVZ>hippocampus and little or no expression in non-neurogenic regions, such as cortex. Treatment of SVZ-derived NPCs with IFNγ and TNFα (alone and in combination) resulted in significant upregulation of expression of specific chemokines, with CXCL1, CXCL9 and CCL2 most highly upregulated and CCL19 downregulated. Unlike IFNγ, chemokine treatment of NPCs in vitro had little or no effect on survival, proliferation or migration. Neuronal differentiation was promoted by CXCL9, CCL2 and CCL21, while astrocyte and total oligodendrocyte differentiation was not affected. However, IFNγ, CXCL1, CXCL9 and CCL2 promoted oligodendrocyte maturation. Therefore, not only do NPCs express chemokine receptors, they also produce several chemokines, particularly in response to inflammatory mediators. This suggests that autocrine or paracrine production of specific chemokines by NPCs in response to inflammatory mediators may regulate differentiation into mature neural cell types and may alter NPC responsiveness to CNS injury or disease.

Adult neural precursor cells (NPCs) in the subventricular zone (SVZ) normally migrate via the rostral migratory stream (RMS) to the olfactory bulb (OB). Following neural injury, they also migrate to the site of damage. This study investigated the role of Rho-dependent kinase (ROCK) on the migration of NPCs in vitro and in vivo. In vitro, using neurospheres or SVZ explants, inhibition of ROCK using Y27632 promoted cell body elongation, process protrusion, and migration, while inhibiting NPC chain formation. It had no effect on proliferation, apoptosis, or differentiation. Both isoforms of ROCK were involved. Using siRNA, knockdown of both ROCK1 and ROCK2 was required to promote NPC migration and morphological changes; knockdown of ROCK2 alone was partially effective, with little/no effect of knockdown of ROCK1 alone. In vivo, infusion of Y27632 plus Bromodeoxyuridine (BrdU) into the lateral ventricle for 1 week reduced the number of BrdU-labeled NPCs in the OB compared with BrdU infusion alone. However, ROCK inhibition did not affect the tangential-to-radial switch of NPC migration, as labeled cells were present in all OB layers. The decrease in NPC number at the OB was not attributed to a decrease in NPCs at the SVZ. However, ROCK inhibition decreased the density of BrdU-labeled cells in the RMS and increased the distribution of these cells to ectopic brain regions, such as the accessory olfactory nucleus, where the majority differentiated into neurons. These findings suggest that ROCK signaling regulates NPC migration via regulation of cell-cell contact and chain migration.

A procedure has been developed for the isolation of cell walls from the hyphae of the causal agent for barley leaf scald, Rhynchosporium secalis (Oudem) J.J. Davis. Based primarily on monosaccharide linkage analysis, but also on the limited use of linkage‐specific glucan hydrolases and solvent fractionation, the walls consist predominantly of (1,3/1,6)‐β‐d‐glucans, (1,3;1,4)‐β‐d‐glucans, galactomannans of (1,2;1,6)‐Manp residues and (1,5)‐galactofuranosyl [(1,5)‐Galf] side chains, rhamnomannans of (1,6)‐Manp residues and rhamnopyranosyl [(1,2)‐Rhap] side chains, and chitin; the walls also contain ≈23% (w/w) protein. Electron microscopy shows the presence of distinct inner and outer wall layers. Treatment of wall preparations with guanidine hydrochloride dissolves the outer layer and enables separate analysis of the inner and outer walls. The insoluble, inner wall layer is composed of (1,3/1,6)‐β‐d‐glucans, galacto‐ and rhamnomannans, (1,3;1,4)‐β‐d‐glucans and chitin, whereas the soluble outer wall material contains a high proportion of rhamnomannan, and smaller proportions of galactomannan, (1,3;1,4)‐β‐d‐glucan and (1,3/1,6)‐β‐d‐glucan with only trace levels of chitin. It was confirmed by immunochemical and enzymatic analysis that at least a portion of the (1,3;1,4)‐β‐d‐glucan component of the inner wall exists as a (1,3;1,4)‐β‐d‐glucan. The analyses not only provide information that is important for a complete understanding of the interactions between R. secalis and barley, but they also identify potential targets for the development of fungicides or resistant transgenic barley varieties.