302 research outputs found
UHF-Dielectrophoresis Crossover Frequency as a New Marker for Discrimination of Glioblastoma Undifferentiated Cells
BiCMOS microfluidic sensor for single cell label-free monitoring through microwave intermodulation
Inspiring a Self-Reliant Learning Culture while Brewing the Next Silicon Valley in North Wales
Sulfur Metabolism and Sulfur-Containing Amino Acids: I- Molecular Effectors
The biology of the macro-element sulfur (S) is attracting an ever growing attention concerning cell physiology and
human health. Sulfur metabolism works at the interplay between genetics and epigenetic as well as in the maintain
of cell redox homeostasis. Indeed, unbalanced levels of S compounds in the body are actually under investigation as
vulnerability factors and/or indicators of impaired cell oxidation state in a variety of human diseases. The purpose of this
article is to overview some main S metabolic pathways in humans and their relevance in cell physiology and pathology.
Since S is an essential nutrient for life, we first present its distribution and significance in the biosphere, focusing then
on S metabolic fluxes which encompass S-containing amino acids (S-AAs), as well as sulfoconjugation, the synthesis
and release of H2S together the formation of iron-sulfur cluster proteins. Despite the vastness of the topic, we would like
to emphasize herein that the study of S networks in human pathology, especially in complex, multi-factorial disorders,
deserves greater impulsion and deepening
Sulfur Metabolism and Sulfur-Containing Amino Acids Derivatives â II: Autism Spectrum Disorders, Schizophrenia and Fibromyalgia
The metabolism of sulfur (S) compounds concurs to the maintain of cell homeostasis and tissue integrity in the
human body. Sulfur chemical species act in all cells as anti-oxidant/scavenging agents or regulators of membrane
stability/excitability. At the same time, they also exert tissue-dependent functions behaving as protective molecules of
the liver and cardiovascular system, as modulators of the immune response, gut activity and CNS neurotransmitter
signaling. The involvement of S compounds in human complex, chronic, disabling diseases at multifaceted pathogenesis
is actually under investigation: altered levels of S metabolites could be in fact bio-indicators of impaired oxidation state in
the body and their unbalance could be risk factors for disease onset. By the present review, we will discuss data from the
literature which unearth an altered S biochemistry in human complex illnesses, taking as an example highly invalidating
neuropsychiatry and pain perception diseases as autism spectrum disorders (ASD), schizophrenia and fibromyalgia.
As well, we will depict herein the utility at applying to this area of the clinical research high resolving -omics strategies
in combination with methodological tools which specifically explore S metabolism in patients. The perspectives of these
kind of analyses would be the adoption of more valuable, personalized therapeutics protocols and, possibly, an improved
bio-monitoring of patients, also including their response to treatments
Parkinsonâs Disease and Alpha-Synucleinopathies: from Arising Pathways to Therapeutic Challenge
Parkinsonâs Disease (PD) and alpha synucleinopathies are multifactorial disorders, which
manifest through motor symptoms and non-motor symptoms involving the Central Nervous System
(CNS), the Peripheral Nervous System (PNS) and, recently, also the Enteric Nervous System (ENS).
The typical hallmarks of alpha synucleinopathies are proteinaceous inclusions of alpha synuclein (αS).
In PD they are known as Lewy Bodies (LBs) and Lewy Neurites (LNs), discovered in dopaminergic
neurons of substantia nigra (pars compacta) as well as in other regions of the central and peripheral
nervous systems. Despite the clear causes which lead to LBs/LNs are still unknown, according to
Braakâs theory, these inclusions appear first in PNS to spread, following neuronal innervation, towards the CNS in a spatio-
temporal dissemination described in a staging procedure. In line with these observations, several animal models have
been used with the purpose to reproduce PD as well as to propose new therapeutic approaches. Different pathways can
cooperate to neurodegeneration in PD such as genetic mutations of αS gene, mitochondrial dysfunctions, neuroinflammation.
The present review highlights αS as the key-word for PD pathology and alpha synucleinopathies and a main target in
PD research. Several therapeutic approaches can be proposed, however all of them are addressed in advanced stages of the
pathology. Our focus will be the alteration of αS physiological pathway, which allows to address therapy in early stages at
intracellular or extracellular level, such as the use of anti ER-stress compounds and innovative immunotherapy, which
could be promising tools to reduce neuronal degeneration and to halt PD progression
Tryptophan Biochemistry: Structural, Nutritional, Metabolic, and Medical Aspects in Humans
L-Tryptophan is the unique protein amino acid (AA) bearing an indole ring: its biotransformation in living organisms contributes either to keeping this chemical group in cells and tissues or to breaking it, by generating in both cases a variety of bioactivemolecules. Investigations on the biology of Trp highlight the pleiotropic effects of its small derivatives on homeostasis processes. In addition to protein turn-over, in humans the pathways of Trp indole derivatives cover the synthesis of the neurotransmitter/hormone serotonin (5-HT), the pineal gland melatonin (MLT), and the trace amine tryptamine. The breakdown of the Trp indole ring defines instead the âkynurenine shuntâ which produces cell-response adapters as L-kynurenine, kynurenic and quinolinic acids, or the coenzyme nicotinamide adenine dinucleotide (NAD+). This reviewaims therefore at tracing a âmapâ of themainmolecular effectors in human tryptophan (Trp) research, starting from the chemistry of this AA, dealing then with its biosphere distribution and nutritional value for humans, also focusing on some proteins responsible for its tissue-dependent uptake and biotransformation.We will thus underscore the role of Trp biochemistry in the pathogenesis of human complex diseases/syndromes primarily involving the gut, neuroimmunoendocrine/stress responses, and the CNS, supporting the use of -Omics approaches in this field
Recent Approaches to Design and Analysis of Electrical Impedance Systems for Single Cells using Machine Learning
Super-Resolution Imaging by Dielectric Superlenses: TiO2 Metamaterial Superlens versus BaTiO3 Superlens
All-dielectric superlens made from micro and nano particles has emerged as a simple yet effective solution to label-free, super-resolution imaging. High-index BaTiO3 Glass (BTG) microspheres are among the most widely used dielectric superlenses today but could potentially be replaced by a new class of TiO2 metamaterial (meta-TiO2) superlens made of TiO2 nanoparticles. In this work, we designed and fabricated TiO2 metamaterial superlens in full-sphere shape for the first time, which resembles BTG microsphere in terms of the physical shape, size, and effective refractive index. Super-resolution imaging performances were compared using the same sample, lighting, and imaging settings. The results show that TiO2 meta-superlens performs consistently better over BTG superlens in terms of imaging contrast, clarity, field of view, and resolution, which was further supported by theoretical simulation. This opens new possibilities in developing more powerful, robust, and reliable super-resolution lens and imaging systems
Hydroxyindole-O-methyltransferase (HIOMT) activity in the retina of melatonin-proficient mice
Numerous pieces of evidence support the expression by the mammalian retina of Hydroxyindole-O-methyltransferase (HIOMT, EC 2.1.1.4), the enzyme directly responsible for the biosynthesis of the pineal chronobiotic hormone melatonin (MLT). However, conflicting results obtained so far by enzyme-kinetic and immune-detection techniques still make HIOMT presence and relevance in the eye a matter of debate. This work aimed at evaluating unambiguously HIOMT activity in the mouse retina, a valuable model for studying the effects of MLT variations on ocular pathophysiology. Since laboratory mouse strains can bear genetic polymorphisms yielding defective enzymes of MLT biosynthesis, retinas and control pineal glands used in this study were obtained in a MLT-proficient crossing of A/J mice, the A/J/C57BL/10 strain. To improve the radiochemical reference assay, we tested different homogenization procedures coupled with HPLC detection. Concomitantly, we quantified MLT, and its precursor N-acetyl-serotonin (NAS) by HPLC coupled to electrochemical detection in retinas isolated from either light- or dark-adapted mice. Results showed that the standard radio-chemical assay was successful for pineal HIOMT only, whereas specific homogenization buffers and HPLC were required to detect retinal activity, presumably due to interfering methyl-transferases inhibited by NAS. Under present conditions, retinal HIOMT Vmax accounted for by â 40 fmol/h/mg protein, 2.6-hundreds-fold lower than the pineal counterpart, displaying equivalent KMs (â10 ÎŒM). Moreover, NAS and MLT rapidly decreased in light-exposed isolated retinas, corroborating light-sensitive in-situ MLT formation. Conclusively, we measured mouse retinal HIOMT kinetics under basal conditions, a useful result to elucidate the regulatory patterns, the possible impact on eye health, and therapeutic approaches related to this enzyme
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