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Brain Injury as a Neurodegenerative Disorder

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199013 Year: Pages: 102 DOI: 10.3389/978-2-88919-901-3 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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It has been long assumed that following the resolution of acute injuries, traumatic brain injury represents a stable neural entity. However, there is growing evidence that a single moderate-severe brain injury may instead trigger an ongoing deteriorative process that commences sub-acutely, and occurs regardless of age. For scientists and clinicians, it is critical to examine this body of evidence and to explore its implications. Do the findings represent a neurodegenerative process or can they be alternatively explained? What are the neural, behavioural and functional characteristics of this progressive deterioration? Such information is needed to develop treatments to prevent or mitigate decline, and to inform the clinical care of brain injured patients. Research and clinical practice are influenced by the assumption that moderate-severe TBI is non-progressive, with few studies exploring treatments to prevent progression, and rehabilitation typically concentrated in the early stages of injury. Brain injuries can never be fully prevented. However, understanding that such progressive deterioration occurs opens a novel area of research - prevention of secondary decline - offering new possibilities for the improvement of long-term outcomes in people with traumatic brain injury.

The enigma of Balint's syndrome: complexity of neural substrates and cognitive deficits

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195992 Year: Pages: 130 DOI: 10.3389/978-2-88919-599-2 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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Bálint’s syndrome is named after the Hungarian physician who first reported a remarkable case of a man with complex visuospatial deficits following bilateral lesions within parietal and occipital cortex (Bálint, 1909). The syndrome has three primary symptoms: simultanagnosia (impaired spatial awareness of more than one object at time), optic ataxia (misreaching to visual targets) and ocular apraxia (described by Bálint as “psychic paralysis of gaze”). Balint’s patients not only cannot perceive more than one object at time and therefore show poor comprehension of multi-object visual scenes i.e. poor detection of all the objects present and difficulty in grasping the relationship between them; in addition they typically fail to reach towards location of the single object, which they can perceive. The deficit of the allocation of spatial attention in Balint’s syndrome has been linked to a problem in feature binding which results in illusory conjunctions. Patients with Balint’s syndrome also show deficits in global processing i.e. when integration of multiple local elements into global compound shapes is required. Consequently, Balint’s syndrome provides a unique opportunity to study the nature and neuroanatomy of human visuospatial processing, in particular multi-level object representation, spatial awareness and the distribution of visual attention. The studies collected here cover both the anatomical and the cognitive mechanisms of the different symptoms associated with the syndrome. Furthermore, the dissociations between the components of Bálints’ syndrome, in particular simultanagnosia and optic ataxia, can also co-occur with visual neglect and extinction and the different combinations of reported lesions raises a question about the status of the syndrome and whether it should be merely treated as a historical compilation of symptoms which may or may not coexist cohesively. This interesting argument is raised here.

Mitochondria in Skeletal Muscle Health, Aging and Diseases

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450732 Year: Pages: 142 DOI: 10.3389/978-2-88945-073-2 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2017-07-06 13:27:36
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Skeletal muscle is the most abudant tissue of the human body, making up to 40 to 50% of the human body mass. While the importance of optimal muscle function is well recognized in the athletic field, its significance for general health is often underappreciated. In fact, the evidence that muscle mass, strength and metabolism are essential for our overall health is overwhelming. As the largest protein reservoir in the human body, muscles are essential in the acute response to critical illness such as sepsis, advanced cancer, and traumatic injury. Loss of skeletal muscle mass has also been associated with weakness, fatigue, insulin resistance, falls, fractures, frailty, disability, several chronic diseases and death. As a consequence, maintaining skeletal muscle mass, strength and metabolism throughout the lifespan is critical to the maintenance of whole body health. Mitochondria are fascinating organelles regulating many critical cellular processes for skeletal muscle physiology, including for instance energy supply, reactive oxygen species production, calcium homeostasis and the regulation of apoptosis. It is therefore not surprising that mitochondrial dysfunction has been implicated in a large number of adverse events/conditions and pathologies affecting skeletal muscle health. While the importance of normal mitochondrial function is well recognized for muscle physiology, there are important aspects of mitochondrial biology that are still poorly understood. These include mitochondrial dynamics (fusion and fission processes), morphology and processes involved in mitochondrial quality control (mitophagy). Defining the mechanisms regulating these different aspects of mitochondrial biology, their importance for muscle physiology, as well as the interrelations will be critical for expanding understanding of the role played by mitochondria in skeletal muscle physiology and health. The present research topic provides readers with novel experimental approaches, knowledge, hypotheses and findings related to all aspects of mitochondrial biology in healthy and diseased muscle cells.Skeletal muscle is the most abudant tissue of the human body, making up to 40 to 50% of the human body mass. While the importance of optimal muscle function is well recognized in the athletic field, its significance for general health is often underappreciated. In fact, the evidence that muscle mass, strength and metabolism are essential for our overall health is overwhelming. As the largest protein reservoir in the human body, muscles are essential in the acute response to critical illness such as sepsis, advanced cancer, and traumatic injury. Loss of skeletal muscle mass has also been associated with weakness, fatigue, insulin resistance, falls, fractures, frailty, disability, several chronic diseases and death. As a consequence, maintaining skeletal muscle mass, strength and metabolism throughout the lifespan is critical to the maintenance of whole body health. Mitochondria are fascinating organelles regulating many critical cellular processes for skeletal muscle physiology, including for instance energy supply, reactive oxygen species production, calcium homeostasis and the regulation of apoptosis. It is therefore not surprising that mitochondrial dysfunction has been implicated in a large number of adverse events/conditions and pathologies affecting skeletal muscle health. While the importance of normal mitochondrial function is well recognized for muscle physiology, there are important aspects of mitochondrial biology that are still poorly understood. These include mitochondrial dynamics (fusion and fission processes), morphology and processes involved in mitochondrial quality control (mitophagy). Defining the mechanisms regulating these different aspects of mitochondrial biology, their importance for muscle physiology, as well as the interrelations will be critical for expanding understanding of the role played by mitochondria in skeletal muscle physiology and health. The present research topic provides readers with novel experimental approaches, knowledge, hypotheses and findings related to all aspects of mitochondrial biology in healthy and diseased muscle cells.

AMP-Activated Protein Kinase Signalling

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ISBN: 9783038976622 Year: Pages: 452 DOI: 10.3390/books978-3-03897-663-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-03-21 14:08:22
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Starting from a kinase of interest, AMP-activated protein kinase (AMPK) has gone far beyond an average biomolecule. Being expressed in all mammalian cell types and probably having a counterpart in every eukaryotic cell, AMPK has attracted interest in virtually all areas of biological research. Structural and biophysical insights have greatly contributed to a molecular understanding of this kinase. From good old protein biochemistry to modern approaches, such as systems biology and advanced microscopy, all disciplines have provided important information. Thus, multiple links to cellular events and subcellular localizations have been established. Moreover, the crucial involvement of AMPK in human health and disease has been evidenced. AMPK accordingly has moved from an interesting enzyme to a pharmacological target. However, despite our extensive current knowledge about AMPK, the growing community is busier than ever. This book provides a snapshot of recent and current AMPK research with an emphasis on work providing molecular insight, including but not limited to novel physiological and pathological functions, or regulatory mechanisms. Up-to-date reviews and research articles are included.

Keywords

exercise --- glucose uptake --- AMP-activated protein kinase --- TBC1D4 --- AS160 --- AMP-activated protein kinase --- developmental origins of health and disease (DOHaD) --- hypertension --- kidney disease --- nutrient-sensing signals --- oxidative stress --- renin-angiotensin system --- AMPK --- autophagy --- co-expression --- microarrays --- 3T3-L1 --- adipocyte --- differentiation --- AMPK --- tight junctions --- epithelial cells --- ZO-1 --- par complex --- MDCK --- nectin-afadin --- adherent junctions --- TAK1 --- AMPK --- phosphorylation --- AMPK kinase --- endothelial nitric-oxide synthase --- vasodilation --- phenylephrine --- vasoconstriction --- endothelial cells --- ionomycin --- AMPK --- liver --- lipid metabolism --- fatty acid oxidation --- indirect calorimetry --- atrophy --- regrowth --- sirtuin 1 (SIRT1) --- peroxisome proliferator-activated receptor gamma coactivator 1-? (PGC1?) --- heat shock protein --- fiber-type --- AMPK --- monocytes --- macrophages --- differentiation --- autophagy --- AML --- MDS --- CML --- CMML --- pregnancy --- catechol-O-methyltransferase --- 2-methoxyestradiol --- preeclampsia --- gestational diabetes mellitus --- AMPK --- IL-1? --- NLRP3 --- nutrition --- dietary fatty acids --- metabolic-inflammation --- nutrigenomics --- AMPK --- LKB1 --- autophagy --- proteasome --- hypertrophy --- atrophy --- skeletal muscle --- AICAR --- mTOR --- protein synthesis --- AMPK --- epigenetics --- chromatin remodeling --- histone modification --- DNA methylation --- medulloblastoma --- sonic hedgehog --- AMPK --- AMP-activated protein kinase (AMPK) --- spermatozoa --- motility --- mitochondria --- membranes --- signaling --- stress --- assisted reproduction techniques --- AMP-activated protein kinase --- epigenetics --- protein acetylation --- KATs --- HDACs --- acetyl-CoA --- NAD+ --- AMP-activated protein kinase --- glycogen --- exercise --- metabolism --- cellular energy sensing --- energy utilization --- liver --- skeletal muscle --- metabolic disease --- glycogen storage disease --- resveratrol --- AMPK --- hepatocyte --- liver --- steatosis --- transporter --- carrier --- pump --- membrane --- energy deficiency --- AMPK --- infection --- mycobacteria --- host defense --- energy metabolism --- AMPK --- activation loop --- AID --- ?-linker --- ?-linker --- CBS --- LKB1 --- CaMKK2 --- ?RIM --- hypothalamus --- adenosine monophosphate-activated protein kinase --- adipose tissue --- food intake --- adaptive thermogenesis --- beiging --- AMPK --- HDAC4/5 --- p70S6K --- MyHC I(?), motor endplate remodeling --- soleus muscle --- mechanical unloading --- hindlimb suspension --- AMPK --- synaptic activation --- PKA --- CREB --- soluble Adenylyl cyclase --- Immediate early genes --- transcription --- AMPK --- autophagy --- metabolism --- mTOR --- ULK --- AMP-activated protein kinase --- protein kinase B --- Akt --- insulin signalling --- A769662 --- endothelial function --- n/a

Gluten-Free Diet

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ISBN: 9783038977360 9783038977377 Year: Pages: 318 DOI: 10.3390/books978-3-03897-737-7 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Internal medicine
Added to DOAB on : 2019-04-25 16:37:17
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In the last few years, an increasing number of individuals have adopted a gluten free diet (GFD). A significant proportion of that includes patients affected by celiac disease (CD), who have to follow a strict GFD for medical purposes. However, a high number of individuals are currently following a GFD without medical counseling and without a specific diagnosis needing a gluten withdrawal from the diet. This is due to the frequently incorrect information diffused on the Internet and mass media on the topic of GFD. For these reasons, research on the GFD and its clinical use and biological effects is urgently needed.

Keywords

Celiac Disease --- depression --- gluten-free diet --- dietary adherence --- gluten --- gastric emptying --- cholecyst --- celiac disease --- non celiac gluten sensitivity --- gluten-free diet --- gastrointestinal symptoms --- quality of life --- Brazilian CD-QoL --- quality of life --- celiac disease --- questionnaire --- coeliac disease --- celiac disease --- gluten --- gluten-free diet --- fortification --- micronutrient --- cost --- celiac disease --- diagnosis --- gliadin --- gluten --- glutenin --- non-celiac gluten sensitivity --- oral food challenge --- pepsin --- wheat allergy --- celiac disease (CD) --- quality of life (QoL) --- gluten-free diet --- disease duration --- place of residence --- educational level --- economic status --- body mass index (BMI) --- celiac disease --- gluten-free diet --- gut microbiota --- gluten-free diet --- celiac disease --- children --- teenagers --- gluten-related disorders --- celiac disease --- gut microbiota --- gluten-free diet --- Pseudomonas --- gluten-free diet --- mineral --- deficiency --- calcium --- iron --- magnesium --- zinc --- celiac disease --- non-celiac gluten sensitivity --- gut motility --- gluten-free diet --- gluten-related disorders --- gluten-free diet --- coeliac disease --- non-coeliac gluten sensitivity --- irritable bowel syndrome --- mood disorders --- affective disorders --- depression --- major depressive disorder --- mental health --- nutrition --- celiac disease --- gluten-free diet --- diary recommended intake --- food habit --- body composition --- non-coeliac gluten sensitivity --- gluten --- wheat --- low FODMAP diet --- irritable bowel syndrome --- beta cell --- beta-cell stress --- celiac disease --- gluten-free diet --- high-fat diet-induced obesity --- intestinal permeability --- islet of Langerhans --- NOD mouse --- type 1 diabetes --- type 2 diabetes --- FODMAP intake --- celiac disease --- irritable bowel syndrome --- gluten-free diet --- gastrointestinal symptoms --- celiac disease --- gluten-free diet --- effectiveness --- adherence --- nutritionists --- clinic --- serology --- duodenal biopsies --- structured questionnaires --- peptides derived from gluten in faeces and urine --- gluten --- adherence --- serology --- villous atrophy --- mucosal recovery --- threshold --- celiac disease --- body composition --- gluten free diet --- children --- celiac disease --- gluten --- gluten-free diet --- screening --- outcome --- gluten sensitivity --- osteoporosis --- non-celiac gluten sensitivity --- gluten re-introduction --- gluten-free diet --- gastrointestinal symptoms --- celiac disease --- ?-gliadin --- 33-mer --- DQ2.5-glia-?1 --- DQ2.5-glia-?2 --- DQ2.5-glia-?3 epitopes --- wheat species --- n/a --- gluten --- gluten-free diet --- coeliac disease --- non-celiac gluten sensitivity --- non-coeliac wheat sensitivity --- gliadin --- microbiota

Extraintestinal Manifestations of Coeliac Disease

Authors: ---
ISBN: 9783038977988 9783038977995 Year: Pages: 270 DOI: 10.3390/books978-3-03897-799-5 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology --- Nutrition and Food Sciences
Added to DOAB on : 2019-04-25 16:37:17
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Coeliac Disease (CD) affects at least 1% of the population. “Classical” CD refers to gastrointestinal presentations with anaemia and gastrointestinal symptoms. CD can, however, present with extraintestinal manifestations, the commonest of which are dermatitis herpetiformis and neurological presentations (e.g., ataxia, neuropathy, encephalopathy). Recognition and research into the pathophysiology of such manifestations is likely to enhance our understanding of this complex autoimmune disorder.

Keywords

dermatitis herpetiformis --- coeliac disease --- fracture --- bone health --- quality of life --- Gilles de la Tourette syndrome (GTS) --- children and adults --- motor and vocal/phonic tics --- obsessive-compulsive disorder (OCD) --- non-coeliac gluten sensitivity (NCGS) --- gluten-free diet --- one-year adherence --- dermatitis herpetiformis --- coeliac disease --- prevalence --- epidermal transglutaminase --- gluten-free diet --- long-term prognosis --- dermatitis herpetiformis --- coeliac disease --- gluten-free diet --- small bowel --- villous atrophy --- prognosis --- gluten neuropathy --- coeliac disease --- gluten free diet --- quality of life --- male --- extra-intestinal --- gastrointestinal --- celiac disease --- celiac disease --- dermatitis herpetiformis --- urticaria --- atopic dermatitis --- psoriasis --- recurrent aphtous ulceration --- rosacea --- alopecia areata --- cutaneous vasculitis --- gluten-free diet --- celiac disease --- glandular autoimmunity --- autoimmune thyroid disease --- type 1 diabetes --- polyglandular autoimmune syndrome --- coeliac disease --- osteoporosis --- fractures --- celiac disease --- non-celiac gluten sensitivity --- psychiatric disorders --- depression --- anxiety disorders --- eating disorders --- ADHD --- autism --- psychosis --- autoimmunity --- celiac hepatitis --- gut–liver axis --- liver immunity --- non-alcoholic fatty liver disease --- tolerance --- intestinal barrier --- celiac disease --- extraintestinal --- recognition --- diagnosis --- clinical presentation --- gluten-free diet --- prognosis --- movement disorders --- coeliac disease --- gluten --- gluten free diet --- celiac disease --- gluten --- gliadin --- autoantibody --- B cell --- T cell --- transglutaminase --- synapsin --- ganglioside --- gluten sensitivity --- gastrointestinal symptoms --- molecular mimicry --- intermolecular help --- biomarker --- autoimmune pancreatitis --- coeliac disease --- pancreatic disorders --- screening --- Gluten ataxia --- antigliadin antibodies --- coeliac disease --- MR spectroscopy --- gluten sensitive enteropathy --- antigliadin antibody titre --- gluten sensitivity --- coeliac disease --- gluten free diet --- migraine --- headache --- fatigue --- energy --- celiac disease --- extra-intestinal manifestations --- gluten --- latent celiac disease --- potential celiac disease --- extra-intestinal manifestations --- mild enteropathy --- early developing celiac disease --- genetic gluten intolerance --- natural history --- celiac trait --- celiac disease --- gluten neuropathy --- gluten ataxia --- prevalence --- incidence --- gluten-free diet

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