Dietary bioactive lipid compounds rich in menthol alter Interactions among members of ruminal microbiota in sheep

This study aimed to investigate the effects of two practically relevant doses of menthol-rich plant bioactive lipid compounds (PBLC) on fermentation, microbial community composition, and their interactions in sheep rumen. Twenty-four growing Suffolk sheep were divided into three treatments and were fed hay ad libitum plus 600 g/d of concentrate containing no PBLC (Control) or PBLC at low dose (80 mg/d; PBLC-L) or high dose (160 mg/d; PBLC-H). After 4 weeks on the diets, samples of ruminal digesta were collected and analyzed for short-chain fatty acid (SCFA), ammonia, and microbiota; microbiota being analyzed in the solid and the liquid digesta fractions separately. Ruminal SCFA and ammonia concentrations were not affected by the PBLC treatments. The microbiota in the solid fraction was more diverse than that in the liquid fraction, and the relative abundance of most taxa differed between these two fractions. In the solid fraction, phylogenetic diversity increased linearly with increased PBLC doses, whereas evenness (lowest in PBLC-L) and Simpson diversity index (greatest in PBLC-H) changed quadratically. In the liquid fraction, however, the PBLC supplementation did not affect any of the microbial diversity measurements. Among phyla, Chloroflexi (highest in PBLC-L) and unclassified_bacteria (lowest in PBLC-L) were altered quadratically by PBLC. Lachnospiraceae, Bacteroidaceae (increased linearly), BS11 (increased in PBLC-L), Christensenellaceae (decreased in PBLC treatments), and Porphyromonadaceae (increased in PBLC treatments) were affected at the family level. Among genera, Butyrivibrio increased linearly in the solid fraction, YRC22 increased linearly in the liquid fraction, whereas Paludibacter increased and BF311 increased linearly with increasing doses of PBLC in both fractions. The PBLC treatments also lowered methanogens within the classes Thermoplasmata and Euryarchaeota. Correlation network analysis revealed positive and negative correlations among many microbial taxa. Differential network analysis showed that PBLC supplementation changed the correlation between some microbial taxa and SCFA. The majority of the predicted functional features were different between the solid and the liquid digesta fractions, whereas the PBLC treatments altered few of the predicted functional gene categories. Overall, dietary PBLC treatments had little influence on the ruminal fermentation and microbiota but affected the associations among some microbial taxa and SCFA

The Pathological Roles of Ganglioside Metabolism in Alzheimer's Disease: Effects of Gangliosides on Neurogenesis

Conversion of the soluble, nontoxic amyloid β-protein (Aβ) into an aggregated, toxic form rich in β-sheets is a key step in the onset of Alzheimer's disease (AD). It has been suggested that Aβ induces changes in neuronal membrane fluidity as a result of its interactions with membrane components such as cholesterol, phospholipids, and gangliosides. Gangliosides are known to bind Aβ. A complex of GM1 and Aβ, termed “GAβ”, has been identified in AD brains. Abnormal ganglioside metabolism also may occur in AD brains. We have reported an increase of Chol-1α antigens, GQ1bα and GT1aα, in the brain of transgenic mouse AD model. GQ1bα and GT1aα exhibit high affinities to Aβs. The presence of Chol-1α gangliosides represents evidence for genesis of cholinergic neurons in AD brains. We evaluated the effects of GM1 and Aβ1–40 on mouse neuroepithelial cells. Treatment of these cells simultaneously with GM1 and Aβ1–40 caused a significant reduction of cell number, suggesting that Aβ1–40 and GM1 cooperatively exert a cytotoxic effect on neuroepithelial cells. An understanding of the mechanism on the interaction of GM1 and Aβs in AD may contribute to the development of new neuroregenerative therapies for this disorder

Arp 302: Non-starburst Luminous Infrared Galaxies

Arp 302, a luminous infrared source (L_{IR} = 4.2x10^{11} Lsun), consisting of two spiral galaxies (VV340A and VV340B) with nuclear separation of 40'', has the highest CO luminosity known. Observations with the BIMA array at 5'' X 7'' resolution reveal that the CO emission is extended over 23.0 kpc in the edge-on spiral galaxy, VV340A, corresponding to 6.7x10^{10} Msun of H_2. In the companion face-on galaxy, VV340B, the CO emission is extended over ~10.0 kpc, with 1.1x10^{10} Msun of H_2. The large CO extent is in strong contrast to starburst systems, such as Arp 220, in which the CO extent is typically $\le$ 1 kpc. Furthermore, $L_{IR}/M$(H_2) is found to be $\le$ 6.0 Lsun/Msun throughout both galaxies. Thus the high IR luminosity of Arp 302 is apparently not due to starbursts in the nuclear regions, but is due to its unusually large amount of molecular gas forming stars at a rate similar to giant molecular clouds in the Milky Way disk. Arp 302 consists of a pair of very gas-rich spiral galaxies that may be interacting and in a phase before a likely onset of starbursts.Comment: AAS Latex plus two postscript figures. ApJ Letters (accepted

Distorted HI Gas in the Widely Separated LIRG Arp 256

We present new interferometric HI and CO (1-0) observations of the luminous infrared source, Arp 256. Arp 256 consists of two spiral galaxies in an early stage of merging, with a projected nuclear separation of 29 kpc (54") and an infrared luminosity of 2.0E11 L_sun. Despite the large separation of the galaxies' nuclei and mildly disrupted stellar components, the HI disks are found to be strongly disrupted, and the southern galaxy in Arp 256 shows an elevated star formation efficiency, which is consistent with a nuclear starburst. Both of these results run contrary to expectations, posing interesting questions on the physical mechanisms involved in stimulating star formation during an interaction.Comment: 19 pages, 7 figures. Accepted for publication in AJ. Author added. Full resolution figures available at http://astro.uchicago.edu/home/web/jchen/arp25

Cytotoxic effects of GM1 ganglioside and amyloid β-peptide on mouse embryonic neural stem cells

AD (Alzheimer’s disease) is a neurodegenerative disease and the most common form of dementia. One of the pathological hallmarks of AD is the aggregation of extracellular Aβs (amyloid β-peptides) in senile plaques in the brain. The process could be initiated by seeding provided by an interaction between GM1 ganglioside and Aβs. Several reports have documented the bifunctional roles of Aβs in NSCs (neural stem cells), but the precise effects of GM1 and Aβ on NSCs have not yet been clarified. We evaluated the effect of GM1 and Aβ-(1–40) on mouse NECs (neuroepithelial cells), which are known to be rich in NSCs. No change of cell number was detected in NECs cultured in the presence of either GM1 or Aβ-(1–40). On the contrary, a decreased number of NECs were cultured in the presence of a combination of GM1 and Aβ-(1–40). The exogenously added GM1 and Aβ-(1–40) were confirmed to incorporate into NECs. The Ras–MAPK (mitogen-activated protein kinase) pathway, important for cell proliferation, was intact in NECs simultaneously treated with GM1 and Aβ-(1–40), but caspase 3 was activated. NECs treated with GM1 and Aβ-(1–40) were positive in the TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) assay, an indicator of cell death. It was found that GM1 and Aβ-(1–40) interacted in the presence of cholesterol and sphingomyelin, components of cell surface microdomains. The cytotoxic effect was found also in NSCs prepared via neurospheres. These results indicate that Aβ-(1–40) and GM1 co-operatively exert a cytotoxic effect on NSCs, likely via incorporation into NEC membranes, where they form a complex for the activation of cell death signalling

Mid-Infrared Images of Luminous Infrared Galaxies in a Merging Sequence

We report mid-infrared observations of several luminous infrared galaxies (LIGs) carried out with the Infrared Space Observatory. Our sample was chosen to represent different phases of a merger sequence of galaxy-galaxy interaction with special emphasis on early/intermediate stages of merging. The mid-infrared emission of these LIGs shows extended structures for the early and intermediate mergers, indicating that most of the mid-infrared luminosities are not from a central active galactic nucleus (AGN). Both the infrared hardness (indicated by the IRAS 12, 25, and 60 \micron flux density ratios) and the peak-to-total flux density ratios of these LIGs increase as projected separation of these interacting galaxies become smaller, consistent with increasing star formation activities that are concentrated to a smaller area as the merging process advances. These observations provide among the first observational constraint of largely theoretically based scenarios.Comment: 10 pages, 3 figures, please refer to ApJ Letters for the final versio

Loss of α-Synuclein Does Not Affect Mitochondrial Bioenergetics in Rodent Neurons.

Increased α-synuclein (αsyn) and mitochondrial dysfunction play central roles in the pathogenesis of Parkinson's disease (PD), and lowering αsyn is under intensive investigation as a therapeutic strategy for PD. Increased αsyn levels disrupt mitochondria and impair respiration, while reduced αsyn protects against mitochondrial toxins, suggesting that interactions between αsyn and mitochondria influences the pathologic and physiologic functions of αsyn. However, we do not know if αsyn affects normal mitochondrial function or if lowering αsyn levels impacts bioenergetic function, especially at the nerve terminal where αsyn is enriched. To determine if αsyn is required for normal mitochondrial function in neurons, we comprehensively evaluated how lowering αsyn affects mitochondrial function. We found that αsyn knockout (KO) does not affect the respiration of cultured hippocampal neurons or cortical and dopaminergic synaptosomes, and that neither loss of αsyn nor all three (α, β and γ) syn isoforms decreased mitochondria-derived ATP levels at the synapse. Similarly, neither αsyn KO nor knockdown altered the capacity of synaptic mitochondria to meet the energy requirements of synaptic vesicle cycling or influenced the localization of mitochondria to dopamine (DA) synapses in vivo. Finally, αsyn KO did not affect overall energy metabolism in mice assessed with a Comprehensive Lab Animal Monitoring System. These studies suggest either that αsyn has little or no significant physiological effect on mitochondrial bioenergetic function, or that any such functions are fully compensated for when lost. These results implicate that αsyn levels can be reduced in neurons without impairing (or improving) mitochondrial bioenergetics or distribution