Superradiance can trigger the formation of an ultralight boson cloud around a spinning black hole. Once formed, the boson cloud is expected to emit a nearly periodic, long-duration, ...gravitational-wave signal. For boson masses in the range (10−13–10−11) eV, and stellar mass black holes, such signals are potentially detectable by gravitational-wave detectors, like Advanced LIGO and Virgo. In this Letter, we present full band upper limits for a generic all-sky search for periodic gravitational waves in LIGO O2 data, and use them to derive-for the first time-direct constraints on the ultralight scalar boson field mass.
Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and PARK2/Parkin mutations cause autosomal recessive forms of Parkinson's disease. Upon a loss of mitochondrial membrane ...potential ( $\Delta \Psi _m$ ) in human cells, cytosolic Parkin has been reported to be recruited to mitochondria, which is followed by a stimulation of mitochondrial autophagy. Here, we show that the relocation of Parkin to mitochondria induced by a collapse of $\Delta \Psi _m$ relies on PINK1 expression and that overexpression of WT but not of mutated PINK1 causes Parkin translocation to mitochondria, even in cells with normal $\Delta \Psi _m$ We also show that once at the mitochondria. Parkin is in close proximity to PINK1, but we find no evidence that Parkin catalyzes PINK1 ubiquitinationorthatPINKI phosphorylates Parkin. However, co-overexpression of Parkin and PINK1 collapses the normal tubular mitochondrial network into mitochondrial aggregates and/or large perinuclear clusters, many of which are surrounded by autophagic vacuoles. Our results suggest that Parkin, together with PINK1, modulates mitochondrial trafficking, especially to the perinuclear region, a subcellular area associated with autophagy. Thus by impairing this process, mutations in either Parkin or PINK1 may alter mitochondrial turnover which, in turn, may cause the accumulation of defective mitochondria and, ultimately, neurodegeneration in Parkinson's disease.
Dietary fiber and phenolic compounds are two recognized dietary factors responsible for potential effects on human health; therefore, they have been widely used to increase functionality of some ...foods. This paper focuses on showing the use of both substances as functional ingredients for enriching foods, and at the same time, describes the use of a single material that combines the properties of the two types of substances. The last part of the work describes some facts related to the interaction between dietary fiber and phenolic compounds, which could affect the bioaccessibility and absorption of phenolics in the gut. In this sense, the purpose of the present review is to compile and analyze evidence relating to the use of dietary fiber and phenolic compounds to enhance technological and nutritional properties of foods and hypothesize some of the possible effects in the gut after their ingestion.
Fungi and mycotoxins in silage: an overview Alonso, V.A.; Pereyra, C.M.; Keller, L.A.M. ...
Journal of applied microbiology,
September 2013, Letnik:
115, Številka:
3
Journal Article
Recenzirano
Odprti dostop
Summary
The present revision shows the early and current knowledge in the field of silage fungi and mycotoxins explaining the relevance of fungi and mycotoxins in silage. The problem does not end in ...animal disease or production losses as mycotoxins in feed can lead to the presence of their metabolic products in dairy products, which will be eventually affecting human health, mainly infants. Silage is green forage preserved by lactic fermentation under anaerobic conditions. This ecosystem maintains its quality and nutritional value depending on interactions among physical, chemical and biological agents. Forages used for ensilage are naturally in contact with yeasts and filamentous fungi, and the contamination often occurs in the field and can also occur during harvesting, transport, storage. Moreover, postharvest poor management can lead to a rapid spoilage. Studies on fungal contamination of dairy cattle feed have shown how corn silage influences the contamination degree of feed supplied to livestock. Increasing knowledge in this area will help elucidate the influence that this microbiota exerts on production and/or degradation of mycotoxins present in silage. Some of these fungi, although opportunist pathogens, are relevant epidemiologically and represent a high risk of contamination to farm workers who handle them improperly.
Autophagy has emerged as a key cellular process for organellar quality control, yet this pathway apparently fails to eliminate mitochondria containing pathogenic mutations in mitochondrial DNA ...(mtDNA) in patients with a variety of human diseases. In order to explore how mtDNA-mediated mitochondrial dysfunction interacts with endogenous autophagic pathways, we examined autophagic status in a panel of human cytoplasmic hybrid (cybrid) cell lines carrying a variety of pathogenic mtDNA mutations. We found that both genetic- and chemically induced loss of mitochondrial transmembrane potential (Δψ
m) caused recruitment of the pro-mitophagic factor Parkin to mitochondria. Strikingly, however, the loss of Δψ
m alone was insufficient to prompt delivery of mitochondria to the autophagosome (mitophagy). We found that mitophagy could be induced following treatment with the mTORC1 inhibitor rapamycin in cybrids carrying either large-scale partial deletions of mtDNA or complete depletion of mtDNA. Further, we found that the level of endogenous Parkin is a crucial determinant of mitophagy. These results suggest a two-hit model, in which the synergistic induction of both (i) mitochondrial recruitment of Parkin following the loss of Δψ
m and (ii) mTORC1-controlled general macroautophagy is required for mitophagy. It appears that mitophagy can be accomplished by the endogenous autophagic machinery, but requires the full engagement of both of these pathways.
Directly detecting thermal emission from young extrasolar planets allows measurement of their atmospheric compositions and luminosities, which are influenced by their formation mechanisms. Using the ...Gemini Planet Imager, we discovered a planet orbiting the ∼20-million-year-old star 51 Eridani at a projected separation of 13 astronomical units. Near-infrared observations show a spectrum with strong methane and water-vapor absorption. Modeling of the spectra and photometry yields a luminosity (normalized by the luminosity of the Sun) of 1.6 to 4.0 × 10–6 and an effective temperature of 600 to 750 kelvin. For this age and luminosity, "hot-start" formation models indicate a mass twice that of Jupiter. This planet also has a sufficiently low luminosity to be consistent with the "cold-start" core-accretion process that may have formed Jupiter.
It has been observed that the optimal speed (OPT) of human walking is independent of load on level surfaces because of the unaltered trajectory of the center of mass and consequent conservation of ...the pendular mechanism. However, the role of the inverted pendulum mechanism that combines speed, load, and gradient during walking remains unknown. In the present study, 10 subjects walked on a treadmill, with and without loading (25% of the body mass), at different speeds and slopes (0%, +7%, and +15%). The three‐dimensional motion and VO2 were simultaneously registered. The mechanical external and internal work and the cost of transport (C) changed with the speed and gradient, but the load only affected C. OPT decreased with increasing gradient, and the pendular mechanics (R) was modified mainly as a result of changes in speed and gradient. OPT and R were independent of the load in these gradients. Remarkably, R increased with increasing speed and decreased (to 30%) with an increasing gradient; moreover, R was independent of load. Therefore, the energy‐saving strategy by the pendular mechanism persists, although at a diminished level, in loaded walking on gradients and partially explains the OPT in this condition.
The early evolution of metazoans has been reconstructed by studies on exceptionally preserved molds in siliciclastic rocks from the Ediacaran Period. However, there remains considerable controversy ...regarding the formation mechanisms of this unusual 'Ediacaran-style' preservation. Proposed hypotheses usually include early authigenesis of minerals, but evidence for this is scarce. In a recently discovered deposit of Ediacaran biota in Brazil, we show that the classic moldic preservation is related to clay mineral authigenesis. Specifically, these clays originated from the alteration of original pyroclastic sediments, likely enhanced by microbial activity, leading to early illitization and morphological templating of the fossiliferous surfaces at a micrometric scale. Such high-fidelity preservation was made possible by rapid burial during volcanic events and the in-situ templating of tissue by clays via microbially-mediated mineralization. This newly described Lagerstätte demonstrates that a number of minerals can facilitate preservation, and that perhaps 'Ediacaran-style' preservation result from different processes leading to the same broad style of preservation.
PINK1 is a mitochondrial kinase proposed to have a role in the pathogenesis of Parkinson's disease through the regulation of mitophagy. Here, we show that the PINK1 main cleavage product, PINK152, ...after being generated inside mitochondria, can exit these organelles and localize to the cytosol, where it is not only destined for degradation by the proteasome but binds to Parkin. The interaction of cytosolic PINK1 with Parkin represses Parkin translocation to the mitochondria and subsequent mitophagy. Our work therefore highlights the existence of two cellular pools of PINK1 that have different effects on Parkin translocation and mitophagy.
Synopsis
The kinase PINK1, mutants of which are associated with Parkinson disease development, is thought to function in mitochondria. Here, PINK1 is shown to participate in maintaining a healthy pool of mitochondria also by functioning in the cytosol, where it interacts with Parkin.
Cleaved PINK152 is retrotranslocated from mitochondria into the cytosol.
PINK152 directly interacts with Parkin in the cytosol and prevents Parkin mitochondrial translocation.
Cytosolic PINK152 attenuates valinomycin‐induced mitophagy.
PINK1, mutants of which are associated with Parkinson, is thought to function in mitochondria. Here, PINK1 is shown to be exported into the cytosol after cleavage, where it binds Parkin, inhibiting its mitochondrial recruitment and preventing mitophagy.
In some 5% of patients with facioscapulohumeral muscular dystrophy (FSHD), no D4Z4 repeat contraction on chromosome 4q35 is observed. Such patients, termed patients with FSHD2, show loss of DNA ...methylation and heterochromatin markers at the D4Z4 repeat that are similar to patients with D4Z4 contractions (FSHD1). This commonality suggests that a change in D4Z4 chromatin structure unifies FSHD1 and FSHD2. The aim of our study was to critically evaluate the clinical features in patients with FSHD2 in order to establish whether these patients are phenotypically identical to FSHD1 and to establish the effects of the (epi-) genotype on the phenotype.
This cross-sectional study studied 33 patients with FSHD2 from 27 families, the largest cohort described to date. All patients were clinically assessed using a standardized clinical evaluation form. Genotype analysis was performed by pulsed field gel electrophoresis and PCR; D4Z4 methylation was studied by methylation-sensitive Southern blot analysis.
FSHD2 is identical to FSHD1 in its clinical presentation. Notable differences include a higher incidence (67%) of sporadic cases and the absence of gender differences in disease severity in FSHD2. Overall, average disease severity in FSHD2 was similar to that reported in FSHD1 and was not influenced by D4Z4 repeat size. In FSHD2, a small effect of the degree of hypomethylation on disease severity was observed.
Clinically, patients with FSHD2 are indistinguishable from patients with FSHD1. The present data suggest that FSHD1 and FSHD2 are the result of the same pathophysiologic process.
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