High taxonomic level fingerprint of the human intestinal microbiota by Ligase Detection Reaction - Universal Array approach

<p>Abstract</p> <p>Background</p> <p>Affecting the core functional microbiome, peculiar high level taxonomic unbalances of the human intestinal microbiota have been recently associated with specific diseases, such as obesity, inflammatory bowel diseases, and intestinal inflammation.</p> <p>Results</p> <p>In order to specifically monitor microbiota unbalances that impact human physiology, here we develop and validate an original DNA-microarray (HTF-Microbi.Array) for the high taxonomic level fingerprint of the human intestinal microbiota. Based on the Ligase Detection Reaction-Universal Array (LDR-UA) approach, the HTF-Microbi.Array enables specific detection and approximate relative quantification of 16S rRNAs from 30 phylogenetically related groups of the human intestinal microbiota. The HTF-Microbi.Array was used in a pilot study of the faecal microbiota of eight young adults. Cluster analysis revealed the good reproducibility of the high level taxonomic microbiota fingerprint obtained for each of the subject.</p> <p>Conclusion</p> <p>The HTF-Microbi.Array is a fast and sensitive tool for the high taxonomic level fingerprint of the human intestinal microbiota in terms of presence/absence of the principal groups. Moreover, analysis of the relative fluorescence intensity for each probe pair of our LDR-UA platform can provide estimation of the relative abundance of the microbial target groups within each samples. Focusing the phylogenetic resolution at division, order and cluster levels, the HTF-Microbi.Array is blind with respect to the inter-individual variability at the species level.</p

Gas structure inside dust cavities of transition disks: Ophiuchus IRS 48 observed by ALMA

List of DEGs between hypothalamus and ovary. Positive value in the LogFC column refers to genes over-expressed in the vary; negative values indicates genes over-expressed in hypothalamus. (XLSX 1257 kb

I resti archeobotanici: analisi botaniche e chimiche

Il contributo presenta le analisi archeobotaniche e chimiche applicate a due contesti dello scavo del Tempio romano di Nora (2008-2014), ossia ad un forno da pane (tannur) che conservava le ultime tracce di combustione e ad un apprestamento all'interno di un'anfora segata, probabilmente riferibile ad attivit\ue0 di produzione o conservazione di pece in et\ue0 fenicia

Resveratrol protects neuronal-like cells expressing mutant Huntingtin from dopamine toxicity by rescuing ATG4-mediated autophagosome formation.

Parkinsonian-like motor deficits in Huntington's Disease (HD) patients are associated with abnormal dopamine neurotransmission in the striatum. Dopamine metabolism leads to the formation of oxidized dopamine quinones that exacerbates mitochondrial dysfunction with production of reactive oxygen species (ROS) that eventually lead to neuronal cell death. We have previously shown that dopamine-induced oxidative stress triggers apoptotic cell death in dopaminergic neuroblastoma SH-SY5Y cells hyper-expressing the mutant polyQ Huntingtin (polyQ-Htt) protein. Dopamine toxicity was paralleled by impaired autophagy clearance of the polyQ-Htt aggregates. In this study, we found that Dopamine affects the stability and function of ATG4, a redox-sensitive cysteine-protein involved in the processing of LC3, a key step in the formation of autophagosomes. Resveratrol, a dietary polyphenol with anti-oxidant and pro-autophagic properties, has shown neuroprotective potential in HD. Yet the molecular mechanism through which Resveratrol can protect HD cells against DA is not known. Here, we show that Resveratrol prevents the generation of ROS, restores the level of ATG4, allows the lipidation of LC3, facilitates the degradation of polyQ-Htt aggregates and protects the cells from Dopamine toxicity. The present findings provide a mechanistic explanation of the neuroprotective activity of Resveratrol and support its inclusion in a therapeutic regimen to slow down HD progression

Dopamine exacerbates mutant Huntingtin toxicity via oxidative-mediated inhibition of autophagy in SH-SY5Y neuroblastoma cells: Beneficial effects of anti-oxidant therapeutics

Neuronal cell death in Huntington's Disease (HD) is associated with the abnormal expansions of a polyglutamine (polyQ) tract in the huntingtin protein (Htt) at the N-terminus that causes the misfolding and aggregation of the mutated protein (mHtt). Autophagy-lysosomal degradation of Htt aggregates may protect the neurons in HD. HD patients eventually manifest parkinsonian-like symptoms, which underlie defects in the dopaminergic system. We hypothesized that dopamine (DA) exacerbates the toxicity in affected neurons by over-inducing an oxidative stress that negatively impinges on the autophagy clearance of mHtt and thus precipitating neuronal cell death. Here we show that the hyper-expression of mutant (>113/150) polyQ Htt is per se toxic to dopaminergic human neuroblastoma SH-SY5Y cells, and that DA exacerbates this toxicity leading to apoptosis and secondary necrosis. DA toxicity is mediated by ROS production (mainly anion superoxide) that elicits a block in the formation of autophagosomes. We found that the pre-incubation with N-Acetyl-l-Cysteine (a quinone reductase inducer) or Deferoxamine (an iron chelator) prevents the generation of ROS, restores the autophagy degradation of mHtt and preserves the cell viability in SH-SY5Y cells expressing the polyQ Htt and exposed to DA. The present findings suggest that DA-induced impairment of autophagy underlies the parkinsonism in HD patients. Our data provide a mechanistic explanation of the DA toxicity in dopaminergic neurons expressing the mHtt and support the use of anti-oxidative stress therapeutics to restore protective autophagy in order to slow down the neurodegeneration in HD patients

Nuovi dati sulla conservazione e sulla cottura di alimenti da due contesti fenicio-punici di Nora (Sardegna, Italia)

Nell\u2019ambito delle ricerche condotte dall\u2019Universit\ue0 degli Studi di Padova presso l\u2019area del cd. Tempio romano di Nora, \ue8 stato possibile indagare due contesti di et\ue0 fenicia e punica di notevole rilevanza per lo studio dell\u2019alimentazione fenicia e punica in Sardegna: un impianto produttivo costituito da un\u2019anfora segata e reimpiegata per la lavorazione o lo stoccaggio della pece (prima met\ue0 del VI sec. a.C.) e un forno tannur in straordinario stato di conservazione (II-I sec. a.C.). Le analisi archeobotaniche condotte dal laboratorio di Archeobiologia dei Musei Civici di Como hanno permesso di identificare i combustibili impiegati e tracce dei resti alimentari di origine vegetale e animale, combusti negli ultimi episodi di cottura documentati in situ. Le analisi radiometriche hanno confermato le dazioni crono-tipologiche dei contenitori, mentre lo studio degli impasti dell\u2019anfora e del tannur ha messo in luce la presenza diffusa di degrassanti vegetali, in particolare resti di tegumento riferibile ad orzo vestito, che si conferma cos\uec uno dei cereali diffusamente coltivati in Sardegna sin dall\u2019et\ue0 fenicia

Limits of permutation-based entropies in assessing complexity of short heart period variability

The study compares permutation-based and coarse-grained entropy approaches for the assessment of complexity of short heart period (HP) variability recordings. Shannon permutation entropy (SPE) and conditional permutation entropy (CPE) are computed as examples of permutation-based entropies, while the k-nearest neighbor conditional entropy (KNNCE) is calculated as an example of coarse-grained conditional entropy. SPE, CPE and KNNCE were applied to ad-hoc simulated autoregressive processes corrupted by increasing amounts of broad band noise and to real HP variability series recorded after complete vagal blockade obtained via administration of a high dose of atropine (AT) in nine healthy volunteers and during orthostatic challenge induced by 90\ub0 head-up tilt (T90) in 15 healthy individuals. Over the simulated series the performances of SPE and CPE degraded more rapidly with the amplitude of the superimposed broad band noise than those of KNNCE. Over real data KNNCE identified the expected decrease of the HP variability complexity both after AT and during T90. Conversely SPE and CPE detected the decrease of HP variability complexity solely during T90 as a likely result of the more favorable signal-to-noise ratio during T90 than after AT. Results derived from both simulations and real data indicated that permutation-based entropies had a larger susceptibility to broad band noise than KNNCE. We recommend caution in applying permutation-based entropies in presence of short HP variability series characterized by a low signal-to-noise ratio

Equisetum arvense standardized dried extract hinders age-related osteosarcopenia

: Age-associated osteosarcopenia is an unresolved syndrome characterized by the concomitant loss of bone (osteopenia) and skeletal muscle (sarcopenia) tissues increasing falls, immobility, morbidity, and mortality. Unbalanced resorption of bone in the remodeling process and excessive protein breakdown, especially fast type II myosin heavy chain (MyHC-II) isoform and myofiber metabolic shift, are the leading causes of bone and muscle deterioration in the elderly, respectively. Equisetum arvense (EQ) is a plant traditionally recommended for many pathological conditions due to its anti-inflammatory properties. Thus, considering that a chronic low-grade inflammatory state predisposes to both osteoporosis and sarcopenia, we tested a standardized hydroalcoholic extract of EQ in in vitro models of muscle atrophy [C2C12 myotubes treated with proinflammatory cytokines (TNFα/IFNγ), excess glucocorticoids (dexamethasone), or the osteokine, receptor activator of nuclear factor kappa-B ligand (RANKL)] and osteoclastogenesis (RAW 264.7 cells treated with RANKL). We found that EQ counteracted myotube atrophy, blunting the activity of several pathways depending on the applied stimulus, and reduced osteoclast formation and activity. By in silico target fishing, IKKB-dependent nuclear factor kappa-B (NF-κB) inhibition emerges as a potential common mechanism underlying EQ's anti-atrophic effects. Consumption of EQ (500 mg/kg/day) by pre-geriatric C57BL/6 mice for 3 months translated into: i) maintenance of muscle mass and performance; ii) restrained myofiber oxidative shift; iii) slowed down age-related modifications in osteoporotic bone, significantly preserving trabecular connectivity density; iv) reduced muscle- and spleen-related inflammation. EQ can preserve muscle functionality and bone remodeling during aging, potentially valuable as a natural treatment for osteosarcopenia