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Amyotrophic lateral sclerosis (ALS) is a rapidly progressive, devastating and fatal disease characterized by selective loss of upper and lower motor neurons of the cerebral cortex, brainstem, spinal cord and muscle atrophy. In spite of many years of research, the pathogenesis of ALS is still not well understood. ALS is a multifaceted genetic disease, in which genetic susceptibility to motor neuron death interacts with environmental factors and there is still no cure for this deleterious disease. At present, there is only one FDA approved drug, Riluzole which according to past studies only modestly slows the progression of the disease, and improves survival by up to three months. The suffering of the ALS patients, and their families is enormous and the economic burden is colossal. There is therefore a pressing need for new therapies. Different molecular pathways and pathological mechanisms have been implicated in ALS. According to past studies, altered calcium homeostasis, abnormal mitochondrial function, protein misfolding, axonal transport defects, excessive production of extracellular superoxide radicals, glutamate-mediated excitotoxicity, inflammatory events, and activation of oxidative stress pathways within the mitochondria and endoplasmic reticulum can act as major contributor that eventually leads to loss of connection between muscle and nerve ultimately resulting to ALS. However, the detailed molecular and cellular pathophysiological mechanisms and origin and temporal progression of the disease still remained elusive. Ongoing research and future advances will likely advance our improve understanding about various involved pathological mechanism ultimately leading to discoveries of new therapeutic cures. Importantly, clinical biomarkers of disease onset and progression are thus also urgently needed to support the development of the new therapeutic agents and novel preventive and curative strategies. Effective translation from pre-clinical to clinical studies will further require extensive knowledge regarding drug activity, bioavailability and efficacy in both the pre-clinical and clinical setting, and proof of biological activity in the target tissue. During the last decades, the development of new therapeutic molecules, advance neuroimaging tools, patient derived induced stem cells and new precision medicine approaches to study ALS has significantly improved our understanding of disease. In particular, new genetic tools, neuroimaging methods, cellular probes, biomarker study and molecular techniques that achieve high spatiotemporal resolution have revealed new details about the disease onset and its progression. In our effort to provide the interested reader, clinician and researchers a comprehensive summaries and new findings in this field of ALS research, hereby we have created this electronic book which comprises of twenty seven chapters having various reviews, perspective and original research articles. All these chapters and articles in this book not only summarize the cutting-edge techniques, approaches, cell and animal models to study ALS but also provide unprecedented coverage of the current developments and new hypothesis emerging in ALS research. Some examples are novel genetic and cell culture based models, mitochondria-mediated therapy, oxidative stress and ROS mechanism, development of stem cells and mechanism-based therapies as well as novel biomarkers for designing and testing effective therapeutic strategies that can benefit ALS patients who are at the earlier stages in the disease. I am extremely grateful to all the contributors to this book and want to thank them for their phenomenal efforts. Amyotrophic lateral sclerosis (ALS) is a rapidly progressive, devastating and fatal disease characterized by selective loss of upper and lower motor neurons of the cerebral cortex, brainstem, spinal cord and muscle atrophy. In spite of many years of research, the pathogenesis of ALS is still not well understood. ALS is a multifaceted genetic disease, in which genetic susceptibility to motor neuron death interacts with environmental factors and there is still no cure for this deleterious disease. At present, there is only one FDA approved drug, Riluzole which according to past studies only modestly slows the progression of the disease, and improves survival by up to three months. The suffering of the ALS patients, and their families is enormous and the economic burden is colossal. There is therefore a pressing need for new therapies. Different molecular pathways and pathological mechanisms have been implicated in ALS. According to past studies, altered calcium homeostasis, abnormal mitochondrial function, protein misfolding, axonal transport defects, excessive production of extracellular superoxide radicals, glutamate-mediated excitotoxicity, inflammatory events, and activation of oxidative stress pathways within the mitochondria and endoplasmic reticulum can act as major contributor that eventually leads to loss of connection between muscle and nerve ultimately resulting to ALS. However, the detailed molecular and cellular pathophysiological mechanisms and origin and temporal progression of the disease still remained elusive. Ongoing research and future advances will likely advance our improve understanding about various involved pathological mechanism ultimately leading to discoveries of new therapeutic cures. Importantly, clinical biomarkers of disease onset and progression are thus also urgently needed to support the development of the new therapeutic agents and novel preventive and curative strategies. Effective translation from pre-clinical to clinical studies will further require extensive knowledge regarding drug activity, bioavailability and efficacy in both the pre-clinical and clinical setting, and proof of biological activity in the target tissue. During the last decades, the development of new therapeutic molecules, advance neuroimaging tools, patient derived induced stem cells and new precision medicine approaches to study ALS has significantly improved our understanding of disease. In particular, new genetic tools, neuroimaging methods, cellular probes, biomarker study and molecular techniques that achieve high spatiotemporal resolution have revealed new details about the disease onset and its progression. In our effort to provide the interested reader, clinician and researchers a comprehensive summaries and new findings in this field of ALS research, hereby we have created this electronic book which comprises of twenty seven chapters having various reviews, perspective and original research articles. All these chapters and articles in this book not only summarize the cutting-edge techniques, approaches, cell and animal models to study ALS but also provide unprecedented coverage of the current developments and new hypothesis emerging in ALS research. Some examples are novel genetic and cell culture based models, mitochondria-mediated therapy, oxidative stress and ROS mechanism, development of stem cells and mechanism-based therapies as well as novel biomarkers for designing and testing effective therapeutic strategies that can benefit ALS patients who are at the earlier stages in the disease. I am extremely grateful to all the contributors to this book and want to thank them for their phenomenal efforts.

Mitochondria --- neurodegenerative disease --- Ca2+ signaling --- multidrug therapy --- Amyotrophic lateral sclerosis (ALS) --- Superoxide dismutase 1 (SOD1) --- Motor neuron disease (MND) --- excitotoxicity --- Riluzole --- multifactorial disease

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This Special Issue is a collection of research articles focused on the production and role of nitric oxide in plants. Nitric oxide is a crucial molecule used in the orchestration of cellular events in animals and plants. With a mixture of primary research papers and review articles written by some of the top researchers in the field, this work encompasses many aspects of this important and growing area of biochemistry.

catalase --- monodehydroascorbate reductase --- tyrosine nitration --- nitric oxide --- peroxisome --- reactive oxygen species --- S-nitrosation --- superoxide dismutase --- antioxidants --- hydrogen gas --- hydrogen peroxide --- hydrogen sulfide --- S-nitrosothiols --- S-nitrosoglutathione reductase --- S-(hydroxymethyl)glutathione --- nitrate reductase --- NOFNiR --- nitrogen metabolism --- NIA1 --- NIA2 --- nitrite --- nitrate --- methyl viologen --- benzyl viologen --- NO analyzer --- molybdenum cofactor --- Arabidopsis thaliana --- nitro-fatty acids --- nitroalkenes --- nitroalkylation --- electrophile --- nucleophile --- signaling mechanism --- post-translational modification --- reactive lipid species --- nitro-lipid-protein adducts --- Trebouxia --- microalgae --- lipid peroxidation --- diaphorase activity --- lichens --- nitric oxide synthase --- nitrogen dioxide --- plant growth --- cell enlargement --- cell proliferation --- early flowering --- PsbO --- nitric oxide homeostasis --- cue1/nox1 --- reactive nitrogen species --- germination --- root development --- stress responses --- sugar metabolism --- nitration --- S-nitrosylation --- SNO-reductase --- thiol modification

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Jonathan Scragg documents his work on a very promising material suitable for use in solar cells. Copper Zinc Tin Sulfide (CZTS) is a low cost, earth-abundant material suitable for large scale deployment in photovoltaics. Jonathan pioneered and optimized a low cost route to this material involving electroplating of the three metals concerned, followed by rapid thermal processing (RTP) in sulfur vapour. His beautifully detailed RTP studies – combined with techniques such as XRD, EDX and Raman – reveal the complex relationships between composition, processing and photovoltaic performance. This exceptional thesis contributes to the development of clean, sustainable and alternative sources of energy.

Scots pine -- Physiology. --- Superoxide dismutase. --- Physics --- Chemistry --- Physical Sciences & Mathematics --- Atomic Physics --- Physical & Theoretical Chemistry --- Photovoltaic power generation. --- Solar cells. --- Thin films. --- Metal sulfides. --- Metal sulphides --- Metallic sulfides --- Films, Thin --- Solid film --- Cells, Solar --- Photovoltaic energy conversion --- Photovoltaics --- Chemistry. --- Renewable energy resources. --- Electrochemistry. --- Surfaces (Physics). --- Interfaces (Physical sciences). --- Renewable energy sources. --- Alternate energy sources. --- Green energy industries. --- Metals. --- Metallic Materials. --- Renewable and Green Energy. --- Surface and Interface Science, Thin Films. --- Solid state electronics --- Solids --- Surfaces (Technology) --- Coatings --- Thick films --- Sulfides --- Direct energy conversion --- Photovoltaic cells --- Solar batteries --- Solar energy --- Materials. --- Alternate energy sources --- Alternative energy sources --- Energy sources, Renewable --- Sustainable energy sources --- Power resources --- Renewable natural resources --- Agriculture and energy --- Engineering --- Engineering materials --- Industrial materials --- Engineering design --- Manufacturing processes --- Physical sciences --- Materials --- Surface chemistry --- Surfaces (Physics) --- Metallic elements --- Chemical elements --- Ores --- Metallurgy --- Chemistry, Physical and theoretical

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The first national conference with international participation, “Fundamental aspects of atherosclerosis: scientific research for improving the technologies of personalized medicine”, was held in Novosibirsk on 15 October, 2021. The purpose of this conference was to disseminate the latest basic and clinical findings in the fields of etiology, clinical characteristics, and modern diagnostics and treatments of atherosclerosis among various relevant specialists. The conference was intended for practicing cardiologists, primary care physicians, medical geneticists, and physician–scientists. The conference included plenary sessions, specialty sessions, satellite symposia, an open competition for young scientists.

metalloproteinases --- calcification --- atherosclerosis --- multiplex assay --- coronary heart disease --- aspirin --- resistance --- non-sensitivity --- antiplatelet --- light transmission aggregometry --- Plateletworks® --- familial hypercholesterolemia --- targeted sequencing technologies --- multiplex ligation-dependent probe amplification --- LDLR --- APOB --- ABCG5 --- APOC3 --- LPL --- SREBF1 --- rare variants --- coronary atherosclerosis --- ischemic heart disease --- saturated fatty acids --- monounsaturated fatty acids --- polyunsaturated fatty acids --- oxidative stress --- superoxide dismutase --- catalase --- glutathione peroxidase --- cumulative LDL-C level --- prognosis --- DNA methylation --- epigenetic age --- myocardial infarction --- acute coronary syndrome --- population --- nested case-control --- HAPIEE project --- HAPIEE study --- atrial fibrillation --- arterial hypertension --- obesity --- diabetes mellitus --- aging --- determinants --- prevalence --- Russian population cohort --- Cox regression analysis --- adiponectin --- leptin --- interleukin-6 --- epicardial adipose tissue --- perivascular adipose tissue --- circulating biochemical markers --- coronary atherosclerosis presence and severity --- integrated biomarker (i-BIO) --- validation --- visual markers --- lipoprotein(a) --- immune cells blood count --- n/a

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The combination of an increasing prevalence of diabetes and the aging of populations enables the appearance of a greater number of associated complications such as diabetic retinopathy. Diabetic retinopathy is the leading cause of preventable vision loss in working-age adults. The objective of this Special Issue is to highlight the existing evidence regarding the relationship between oxidative stress and low-grade chronic inflammation induced by hyperglycemia with the development and progression of diabetic retinopathy, with an emphasis on the importance of early diagnosis and the use of antioxidant and anti-inflammatory approaches to prevent or delay the harmful effects of diabetes on retinal tissue.

eicosanoids --- oxidative stress --- diabetic retinopathy --- cyclooxygenase --- lipoxygenase --- Cytochrome P450 --- HDAC6 --- tubastatin A --- retinal endothelial cells --- retinal endothelial cell senescence --- db/db mice --- Cinnamomi Ramulus --- Paeoniae Radix --- CPA4-1 --- blood-retinal barrier --- occludin --- human retina --- epiretinal membrane --- internal limiting membrane --- vitreoretinal surgery --- macular hole --- proliferative diabetic retinopathy --- antioxidants --- diabetes mellitus --- free radicals --- high-mobility group box 1 (HMGB1) --- inflammatory pathways --- novel therapies --- diabetic retinopathy (DR) --- inflammation --- angiogenesis --- extracellular vesicles --- miRNA --- biomarkers --- apoptosis --- fenofibrate --- thioredoxin --- hyperglycemia --- astaxanthin --- carotenoid --- reactive oxygen species --- photoreceptor cells --- PI3K --- Nrf2 --- eicosapentaenoic acid (EPA) --- docosahexaenoic acid (DHA) --- retinal pigment epithelium --- antioxidant --- ascorbic acid --- retinal disease --- vitamin D --- GLP-1 --- superoxide dismutase --- biomarkers of diabetic retinopathy --- metabolic memory --- tear film --- aqueous humor --- vitreous humor --- mitochondria --- redox --- photoreceptor --- glycation --- aging --- glyoxalase --- n/a