Automatic speech analysis to early detect functional cognitive decline in elderly population

This study aimed at evaluating whether people with a normal cognitive function can be discriminated from subjects with a mild impairment of cognitive function based on a set of acoustic features derived from spontaneous speech. Voice recordings from 90 Italian subjects (age >65 years; group 1: 47 subjects with MMSE>26; group 2: 43 subjects with 20≤ MMSE ≤26) were collected. Voice samples were processed using a MATLAB-based custom software to derive a broad set of known acoustic features. Linear mixed model analyses were performed to select the features able to significantly distinguish between groups. The selected features (% of unvoiced segments, duration of unvoiced segments, % of voice breaks, speech rate, and duration of syllables), alone or in addition to age and years of education, were used to build a learning-based classifier. The leave-one-out cross validation was used for testing and the classifier accuracy was computed. When the voice features were used alone, an overall classification accuracy of 0.73 was achieved. When age and years of education were additionally used, the overall accuracy increased up to 0.80. These performances were lower than the accuracy of 0.86 found in a recent study. However, in that study the classification was based on several tasks, including more cognitive demanding tasks. Our results are encouraging because acoustic features, derived for the first time only from an ecologic continuous speech task, were able to discriminate people with a normal cognitive function from people with a mild cognitive decline. This study poses the basis for the development of a mobile application performing automatic voice analysis on-the-fly during phone calls, which might potentially support the detection of early signs of functional cognitive decline

Campi Flegrei active seismic experiments waveforms compilation

A new experiment called SERAPIS (SEismic Reflection/Refraction Acquisition Project for Imaging complex volcanic Structures) has been planned and carried out, based on off-shore seismic energization and data acquisition on land and on sea-bottom. The experiment was performed in September, 2001 during which the vessel NADIR of IFREMER (equipped with 12, 16-liters airgun) produced more than 5000 air gun shots recorded at a sea-bottom seismograph array of 72 OBS and 62 stations installed on-land. Active seismic refraction DSS (Deep Seismic Soundings) acquired during the surveys conducted in 1980 and 1985 were recovered jointly with seismic data acquired in the Campi Flegrei area in the framework of the MareVes97 (an experiment devoted to the definition of the structure of the Somma-Vesuvio complex) offshore survey. The data set acquired during the SERAPIS experiment has been successfully used to infer 3D images of the volcanic structures of Campi Flegrei and Neapolitan bay. Active seismic waveforms and related P-picks (more than 90000 data) from the SERAPIS experiment are also available in the project data server

TLR4 and NKT Cell Synergy in Immunotherapy against Visceral Leishmaniasis

NKT cells play an important role in autoimmune diseases, tumor surveillance, and infectious diseases, providing in most cases protection against infection. NKT cells are reactive to CD1d presented glycolipid antigens. They can modulate immune responses by promoting the secretion of type 1, type 2, or immune regulatory cytokines. Pathogen-derived signals to dendritic cells mediated via Toll like Receptors (TLR) can be modulated by activated invariant Natural Killer T (iNKT) cells. The terminal β-(1–4)-galactose residues of glycans can modulate host responsiveness in a T helper type-1 direction via IFN-γ and TLRs. We have attempted to develop a defined immunotherapeutic, based on the cooperative action of a TLR ligand and iNKT cell using a mouse model of visceral leishmaniasis. We evaluated the anti-Leishmania immune responses and the protective efficacy of the β-(1–4)-galactose terminal NKT cell ligand glycosphingophospholipid (GSPL) antigen of L. donovani parasites. Our results suggest that TLR4 can function as an upstream sensor for GSPL and provoke intracellular inflammatory signaling necessary for parasite killing. Treatment with GSPL was able to induce a strong effective T cell response that contributed to effective control of acute parasite burden and led to undetectable parasite persistence in the infected animals. These studies for the first time demonstrate the interactions between a TLR ligand and iNKT cell activation in visceral leishmaniasis immunotherapeutic

The making of a mammalian peroxisome, version 2.0: mitochondria get into the mix

This is the author accepted manuscript. The final version is available from Nature Publishing Group via the DOI in this record.A recent report from the laboratory of Heidi McBride (McGill University) presents a role for mitochondria in the de novo biogenesis of peroxisomes in mammalian cells (1). Peroxisomes are essential organelles responsible for a wide variety of biochemical functions, from the generation of bile, to plasmalogen synthesis, reduction of peroxides, and the oxidation of very long chain fatty acids (2). Like mitochondria, peroxisomes proliferate primarily through growth and division of pre-existing peroxisomes (3-6). However, unlike mitochondria, peroxisomes do not fuse (5,7); further, and perhaps most importantly, they can also be born de novo, a process thought to occur through the generation of pre-peroxisomal vesicles that originate from the endoplasmic reticulum (reviewed in (8,9). De novo peroxisome biogenesis has been extensively studies in yeast, with a major focus on the role of the ER in this process. Comprehensive studies in mammalian cells are, however, scarce (5,10-12). By exploiting patient cells lacking mature peroxisomes, Sugiura et al. (1) now assign a role to ER and mitochondria in de novo mammalian peroxisome biogenesis by showing that the formation of immature preperoxisomes occurs through the fusion of Pex3- / Pex14-containing mitochondriaderived vesicles with Pex16-containing ER-derived vesicles

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

Regulation of human erythrocyte glyceraldehyde-3-phosphate dehydrogenase by ferriprotoporphyrin IX

Erythrocyte glyceraldehyde-3-phosphate dehydrogenase (G3PD) is a glycolytic enzyme containing critical thiol groups and whose activity is reversibly inhibited by binding to the cell membrane. Here, we demonstrate that the insertion of ferriprotoporphyrin IX (FP) into the red cell membranes exerts two opposite effects on membrane bound G3PD. First, the enzyme is partially inactivated through oxidation of critical thiols. Dithiothreitol restores part of the activity, but some critical thiols are irreversibly oxidized or crosslinked to products of FP-induced lipid peroxidation. Second, G3PD binding to the membrane is modified and the enzyme is activated through displacement into the cytosol and/or release from its binding site