Superb microvascular imaging: Added value and novel applications

Suheil Artul, William Nseir, Zaher Armaly, Michalle Soudack

Journal of Clinical Imaging Science 2017 7(1):45-45

Determining the presence and characteristics of vascular flow is an essential part of sonography interrogation. However, small vessels and low velocities are not always possible to depict with conventional color and power Doppler ultrasound. This can be frustrating, especially when the diagnosis depends mainly on the existence of vascular flow, the sonographic examination will be inconclusive, further imaging examinations will be required and diagnosis delayed. Superb microvascular imaging (SMI) is a novel vascular imaging mode, which provides visualization of low velocity and microvascular flow. SMI uses a clutter suppression algorithm to extract flow signals and depicts this information as a color overlay image or as a monochrome or color map of flow. By using SMI, high frame rates and high-resolution images remain maintained. With SMI, it is possible to visualize small vessels including their branches that, until now, it is possible to demonstrate only using contrast-enhanced ultrasound. Availability of this additional technology on all ultrasound machines may make some of the computed tomography scans unnecessary. In our paper, we describe six patients, aged 16–73 years, in which final diagnosis was achieved only with SMI and where conventional color and power Doppler failed. All these examinations were performed using Aplio 500 Platinum ultrasound unit (Toshiba Medical Systems, Tokyo, Japan).

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Masseter muscle thickness in unilateral partial edentulism: An ultrasonographic study

S Sathasivasubramanian, PM Venkatasai, CV Divyambika, Rupesh Mandava, R Jeffrey, N A Nathera Jabeen, S Shankar Kumar

Journal of Clinical Imaging Science 2017 7(1):44-44

Introduction: Teeth and facial muscles play a very important role in occlusal equilibrium and function. Occlusal derangement, seen in unilateral partially edentulous individuals, has an effect on masseter muscle anatomy and function. The present study aims to evaluate masseter muscle thickness in unilateral partial edentulism. Patients and Methods: Institutional ethics committee approval was obtained before the commencement of the study. The study involved patients who routinely visited the Department of Oral Medicine and Radiology, Sri Ramachandra University. The study sample included 27 unilateral edentulous patients (Group E) and 30 controls (Group C). The masseter muscle thickness was evaluated using high-resolution ultrasound real-time scanner (linear transducer − 7.5–10 MHz) at both relaxed and contracted states. Statistical Analysis Used: The results were analyzed using paired t-test and independent t-test. Duration of edentulism and muscle thickness was assessed using Pearson's correlation coefficient. Results: The study patients' age ranged between 25 and 48 years (mean – 36 years). The comparative evaluation of masseter muscle thickness between the dentulous and edentulous sides of experimental group was statistically significant (P < 0.05). However, no statistically significant difference in masseter muscle thickness was found between the dentulous side of control and experimental groups. The correlation between the duration of partial edentulism and muscle thickness was statistically insignificant. Conclusion: The study proves masseter atrophy in the edentulous side. However, since the difference is found to be marginal with the present sample, a greater sample is necessary to establish and prove the present findings as well as to correlate with the duration of edentulism. Further studies are aimed to assess the muscle morphology after prosthetic rehabilitation.

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High resolution 3D microscopy study of cardiomyocytes on polymer scaffold nanofibers reveals formation of unusual sheathed structure

Publication date: Available online 27 December 2017
Source:Acta Biomaterialia
Author(s): Victor Balashov, Anton Efimov, Olga Agapova, Alexander Pogorelov, Igor Agapov, Konstantin Agladze
Building functional and robust scaffolds for engineered biological tissue requires a nanoscale mechanistic understanding of how cells use the scaffold for their growth and development. A vast majority of the scaffolds used for cardiac tissue engineering are based on polymer materials, the matrices of nanofibers. Attempts to load the polymer fibers of the scaffold with additional sophisticated features, such as electrical conductivity and controlled release of the growth factors or other biologically active molecules, as well as trying to match the mechanical features of the scaffold to those of the extracellular matrix, cannot be efficient without a detailed knowledge of how the cells are attached and strategically positioned with respect to the scaffold nanofibers at micro and nanolevel. Studying single cell – single fiber interactions with the aid of confocal laser scanning microscopy (CLSM), scanning probe nanotomography (SPNT), and transmission electron microscopy (TEM), we found that cardiac cells actively interact with substrate nanofibers, but in different ways. While cardiomyocytes often create a remarkable "sheath" structure, enveloping fiber and, thus, substantially increasing contact zone, fibroblasts interact with nanofibers in the locations of focal adhesion clusters mainly without wrapping the fiber.Statements of SignificanceWe found that cardiomyocytes grown on electrospun polymer nanofibers often create a striking "sheath" structure, enveloping fiber with the formation of a very narrow (∼22 nm) membrane gap leading from the fiber to the extracellular space. This wrapping makes the entire fiber surface available for cell attachment. This finding gives a new prospective view on how scaffold nanofibers may interact with growing cells. It may play a significant role in effective design of novel nanofiber scaffolds for tissue engineering concerning mechanical and electrical properties of scaffolds as well as controlled drug release from "smart" biomaterials.

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Copper-containing mesoporous bioactive glass promotes angiogenesis in an in vivo zebrafish model

Publication date: Available online 27 December 2017
Source:Acta Biomaterialia
Author(s): Lilian B. Romero-Sánchez, Manuel Marí-Beffa, Paloma Carrillo, Miguel Ángel Medina, Aránzazu Díaz-Cuenca
The osteogenic and angiogenic responses of organisms to the ionic products of degradation of bioactive glasses (BGs) are being intensively investigated. The promotion of angiogenesis by copper (Cu) has been known for more than three decades. This element can be incorporated to delivery carriers, such as BGs, and the materials used in biological assays. In this work, Cu-containing mesoporous bioactive glass (MBG) in the SiO2-CaO-P2O5 compositional system was prepared incorporating 5% mol Cu (MBG-5Cu) by replacement of the corresponding amount of Ca. The biological effects of the ionic products of MBG biodegradation were evaluated on a well-known endothelial cell line, the bovine aorta endothelial cells (BAEC), as well as in an in vivo zebrafish (Danio rerio) embryo assay. The results suggest that ionic products of both MBG (Cu free) and MBG-5Cu materials promote angiogenesis. In vitro cell cultures show that the ionic dissolution products of these materials are not toxic and promote BAEC viability and migration. In addition, the in vivo assay indicates that both exposition and microinjection of zebrafish embryos with Cu free MBG material increase vessel number and thickness of the subintestinal venous plexus (SIVP), whereas assays using MBG-5Cu enhance this effect.Statement of SignificanceMesoporous bioactive glasses (MBGs) with high specific surface area, well-ordered pores, large pore volumes and controllable amount of ions are interesting to develop controlled drug delivery systems for bone tissue regeneration. Copper (Cu) incorporation to the basic SiO2-CaO-P2O5 composition has attracted high interest due to its multifunctional biological properties. Promotion of angiogenesis is one of these properties, which can be integrated to the biomaterial with lower cost and higher stability when compared with growth factors.This work reports the synthesis and characterization of Cu-containing MBG evaluating its angiogenic properties in the subintestinal vessel zebrafish assay. This transgenic in vivo assay is merging as an alternative model providing short-time consuming protocols and facilities during pro-angiogenic drug screenings. The report shows that the ionic products of this MBG material delivered to the zebrafish incubation media significantly enhance angiogenesis in comparison with control groups. Besides, results indicate Cu ions may exhibit a synergic effect with Si, Ca, and P ions in angiogenesis stimulation both in vitro and in vivo. To our knowledge, this is the first time that zebrafish in vivo assays are used to evaluate angiogenic activity of ionic dissolution products from MBG materials.

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Disturbance of redox homeostasis in Down Syndrome: Role of iron dysmetabolism

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Eugenio Barone, Andrea Arena, Elizabeth Head, D. Allan Butterfield, Marzia Perluigi
Down Syndrome (DS) is the most common genetic form of intellectual disability that leads in the majority of cases to development of early-onset Alzheimer-like dementia (AD). The neuropathology of DS has several common features with AD including alteration of redox homeostasis, mitochondrial deficits, and inflammation among others. Interestingly, some of the genes encoded by chromosome 21 are responsible of increased oxidative stress (OS) conditions that are further exacerbated by decreased antioxidant defense. Previous studies from our groups showed that accumulation of oxidative damage is an early event in DS neurodegeneration and that oxidative modifications of selected proteins affects the integrity of the protein degradative systems, antioxidant response, neuronal integrity and energy metabolism.In particular, the current review elaborates recent findings demonstrating the accumulation of oxidative damage in DS and we focus attention on specific deregulation of iron metabolism, which affects both the central nervous system and the periphery. Iron dysmetabolism is a well-recognized factor that contributes to neurodegeneration; thus we opine that better understanding how and to what extent the concerted loss of iron dyshomeostasis and increased OS occur in DS could provide novel insights for the development of therapeutic strategies for the treatment of Alzheimer-like dementia.

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Clinical aspects and biomarkers of Alzheimer's disease in Down syndrome

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Panagiotis Zis, Andre Strydom
Alzheimer's disease (AD) may affect in excess of 90% of individuals with Down syndrome (DS) after age 60, due to duplication of the APP gene in trisomy of chromosome 21, with neuropathology that is comparable to Sporadic AD and Familial AD (FAD). Previous literature suggested some unique features in clinical presentation of dementia in DS (DSd), which might be due to diagnostic difficulties, or represent a real difference compared to SAD or FAD. We review current knowledge on clinical diagnosis and presentation of dementia in DS in comparison with FAD due to APP mutations and APP duplication. We suggest that the clinical presentation in DS (prominent memory decline and behavioral symptoms, and early development of myoclonus and seizures) are similar to the clinical features associated with APP mutations that is known to have an increased Aβ42/ Aβ40 ratio, and highlight the relative lack of vascular complications associated with cerebral amyloid angiopathy in DS in comparison with those rare individuals with FAD due to duplication APP. We consider the biomarker evidence associated with DS and DSd with reference to Aβ peptide levels and oxidative stress, and suggest future directions for research to explore the potential mechanisms associated with the clinical presentation of DSd.

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Dysfunction of autophagy and endosomal-lysosomal pathways: Roles in pathogenesis of Down syndrome and Alzheimer's Disease

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Daniel J. Colacurcio, Anna Pensalfini, Ying Jiang, Ralph A. Nixon
Individuals with Down syndrome (DS) have an increased risk of early-onset Alzheimer's Disease (AD), largely owing to a triplication of the APP gene, located on chromosome 21. In DS and AD, defects in endocytosis and lysosomal function appear at the earliest stages of disease development and progress to widespread failure of intraneuronal waste clearance, neuritic dystrophy and neuronal cell death. The same genetic factors that cause or increase AD risk are also direct causes of endosomal-lysosomal dysfunction, underscoring the essential partnership between this dysfunction and APP metabolites in AD pathogenesis. The appearance of APP-dependent endosome anomalies in DS beginning in infancy and evolving into the full range of AD-related endosomal-lysosomal deficits provides a unique opportunity to characterize the earliest pathobiology of AD preceding the classical neuropathological hallmarks. Facilitating this characterization is the authentic recapitulation of this endosomal pathobiology in peripheral cells from people with DS and in trisomy mouse models. Here, we review current research on endocytic-lysosomal dysfunction in DS and AD, the emerging importance of APP/βCTF in initiating this dysfunction, and the potential roles of additional trisomy 21 genes in accelerating endosomal-lysosomal impairment in DS. Collectively, these studies underscore the growing value of investigating DS to probe the biological origins of AD as well as to understand and ameliorate the developmental disability of DS.

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Editorial Board

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114





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Neurogenesis impairment: An early developmental defect in Down syndrome

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Fiorenza Stagni, Andrea Giacomini, Marco Emili, Sandra Guidi, Renata Bartesaghi
Down syndrome (DS) is characterized by brain hypotrophy and intellectual disability starting from early life stages. Accumulating evidence shows that the phenotypic features of the DS brain can be traced back to the fetal period since the DS brain exhibits proliferation potency reduction starting from the critical time window of fetal neurogenesis. This defect is worsened by the fact that neural progenitor cells exhibit reduced acquisition of a neuronal phenotype and an increase in the acquisition of an astrocytic phenotype. Consequently, the DS brain has fewer neurons in comparison with the typical brain. Although apoptotic cell death may be increased in DS, this does not seem to be the major cause of brain hypocellularity. Evidence obtained in brains of individuals with DS, DS-derived induced pluripotent stem cells (iPSCs), and DS mouse models has provided some insight into the mechanisms underlying the developmental defects due to the trisomic condition. Although many triplicated genes may be involved, in the light of the studies reviewed here, DYRK1A, APP, RCAN1 and OLIG1/2 appear to be particularly important determinants of many neurodevelopmental alterations that characterize DS because their triplication affects both the proliferation and fate of neural precursor cells as well as apoptotic cell death. Based on the evidence reviewed here, pathways downstream to these genes may represent strategic targets, for the design of possible interventions.

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Epidemiology of estrogen and dementia in women with Down syndrome

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Nicole Schupf, Joseph H. Lee, Deborah Pang, Warren B. Zigman, Benjamin Tycko, Sharon Krinsky-McHale, Wayne Silverman
Several lines of investigation have shown a protective role for estrogen in Alzheimer's disease through a number of biological actions. This review examines studies of the role of estrogen-related factors in age at onset and risk for Alzheimer's disease in women with Down syndrome, a population at high risk for early onset of dementia. The studies are consistent in showing that early age at menopause and that low levels of endogenous bioavailable estradiol in postmenopausal women with Down syndrome are associated with earlier age at onset and overall risk for dementia. Polymorphisms in genes associated with estrogen receptor activity and in genes for estrogen biosynthesis affecting endogenous estrogen are related to age at onset and cumulative incidence of dementia, and may serve as biomarkers of risk. To date, no clinical trials of estrogen or hormone replacement therapy (ERT/HRT) have been published for women with Down syndrome. While findings from clinical trials of ERT or HRT for dementia have generally been negative among women in the neurotypical population, the short interval between menopause and onset of cognitive decline, together with a more positive balance between potential benefits and risks, suggests an opportunity to evaluate the efficacy of ERT/HRT for delaying or preventing dementia in this high risk population, although questions concerning the optimal formulation and timing of the hormone therapy are not yet resolved.

Graphical abstract

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Down syndrome, beta-amyloid and neuroimaging

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Elizabeth Head, Alex M. Helman, David Powell, Frederick A. Schmitt
This review focuses on the role of Aβ in AD pathogenesis in Down syndrome and current approaches for imaging Aβ in vivo. We will describe how Aβ deposits with age, the posttranslational modifications that can occur, and detection in biofluids. Three unique case studies describing partial trisomy 21 cases without APP triplication, and the occurrences of low level mosaic trisomy 21 in an early onset AD patient are presented. Brain imaging for Aβ includes those by positron emission tomography and ligands (Pittsburgh Compound B, Florbetapir, and FDDNP) that bind Aβ have been published and are summarized here. In combination, we have learned a great deal about Aβ in DS in terms of characterizing age of onset of this pathology and it is exciting to note that there is a clinical trial in DS targeting Aβ that may lead to clinical benefits.

Graphical abstract

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Down syndrome: From development to adult life to Alzheimer disease

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): D. Allan Butterfield, Marzia Perluigi




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Dendritic spine pathology and thrombospondin-1 deficits in Down syndrome

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Maria D. Torres, Octavio Garcia, Cindy Tang, Jorge Busciglio
Abnormal dendritic spine structure and function is one of the most prominent features associated with neurodevelopmental disorders including Down syndrome (DS). Defects in both spine morphology and spine density may underlie alterations in neuronal and synaptic plasticity, ultimately affecting cognitive ability. Here we briefly examine the role of astrocytes in spine alterations and more specifically the involvement of astrocyte-secreted thrombospondin 1 (TSP-1) deficits in spine and synaptic pathology in DS.

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GABAergic over-inhibition, a promising hypothesis for cognitive deficits in Down syndrome

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Javier Zorrilla de San Martin, Jean-Maurice Delabar, Alberto Bacci, Marie-Claude Potier
Down syndrome (DS), also known as trisomy 21, is the most common genetic cause of intellectual disability. It is also a model human disease for exploring consequences of gene dosage imbalance on complex phenotypes. Learning and memory impairments linked to intellectual disabilities in DS could result from synaptic plasticity deficits and excitatory-inhibitory alterations leading to changes in neuronal circuitry in the brain of affected individuals. Increasing number of studies in mouse and cellular models converge towards the assumption that excitatory-inhibitory imbalance occurs in DS, likely early during development. Thus increased inhibition appears to be a common trend that could explain synaptic and circuit disorganization. Interestingly using several potent pharmacological tools, preclinical studies strongly demonstrated that cognitive deficits could be restored in mouse models of DS. Clinical trials have not yet provided robust data for therapeutic application and additional studies are needed. Here we review the literature and our own published work emphasizing the over-inhibition hypothesis in DS and their links with gene dosage imbalance paving the way for future basic and clinical research.

Graphical abstract

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Dysregulation of neurotrophin signaling in the pathogenesis of Alzheimer disease and of Alzheimer disease in Down syndrome

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Xu-Qiao Chen, Mariko Sawa, William C. Mobley
Neurotrophic factors, including the members of the neurotrophin family, play important roles in the development and maintenance of the nervous system. Trophic factor signals must be transmitted over long distances from axons and dendrites to the cell bodies of neurons. A mode of signaling well suited to the challenge of robust long distance signaling is the signaling endosome. We review the biology of signaling endosomes and the "signaling endosome hypothesis". Evidence for disruption of signaling endosome function in disorders of the nervous system is also reviewed. Changes in endosome structure in Alzheimer disease (AD) and Down syndrome (DS) are present early in these disorders. Data for the APP products responsible are reviewed and the consequent changes in signaling from endosomes discussed. We conclude by pointing to the need for additional studies to explore the biology of signaling endosomes in normal neurons and to elucidate their role in the pathogenesis of neurodegeneration.

Graphical abstract

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Mitochondria as pharmacological targets in Down syndrome

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Daniela Valenti, Nady Braidy, Domenico De Rasmo, Anna Signorile, Leonardo Rossi, A.G. Atanasov, Mariateresa Volpicella, Alexandra Henrion-Caude, S.M. Nabavi, R.A. Vacca
Mitochondria play a pivotal role in cellular energy-generating processes and are considered master regulators of cell life and death fate. Mitochondrial function integrates signalling networks in several metabolic pathways controlling neurogenesis and neuroplasticity. Indeed, dysfunctional mitochondria and mitochondrial-dependent activation of intracellular stress cascades are critical initiating events in many human neurodegenerative or neurodevelopmental diseases including Down syndrome (DS). It is well established that trisomy of human chromosome 21 can cause DS. DS is associated with neurodevelopmental delay, intellectual disability and early neurodegeneration. Recently, molecular mechanisms responsible for mitochondrial damage and energy deficits have been identified and characterized in several DS-derived human cells and animal models of DS. Therefore, therapeutic strategies targeting mitochondria could have great potential for new treatment regimens in DS. The purpose of this review is to highlight recent studies concerning mitochondrial impairment in DS, focusing on alterations of the molecular pathways controlling mitochondrial function. We will also discuss the effects and molecular mechanisms of naturally occurring and chemically synthetized drugs that exert neuroprotective effects through modulation of mitochondrial function and attenuation of oxidative stress. These compounds might represent novel therapeutic tools for the modulation of energy deficits in DS.

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mTOR in Down syndrome: Role in Aß and tau neuropathology and transition to Alzheimer disease-like dementia

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Fabio Di Domenico, Antonella Tramutola, Cesira Foppoli, Elizabeth Head, Marzia Perluigi, D. Allan Butterfield
The mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase involved in the regulation of protein synthesis and degradation, longevity and cytoskeletal formation. The mTOR pathway represents a key growth and survival pathway involved in several diseases such as cancer, obesity, cardiovascular disease and neurodegenerative diseases. Numerous studies linked the alterations of mTOR pathway to age-dependent cognitive decline, pathogenesis of Alzheimer disease (AD) and AD-like dementia in Down syndrome (DS). DS is the most frequent chromosomal abnormality that causes intellectual disability. The neuropathology of AD in DS is complex and involves impaired mitochondrial function, defects in neurogenesis, increased oxidative stress, altered proteostasis and autophagy networks as a result of triplication of chromosome 21(chr 21). The chr21 gene products are considered a principal neuropathogenic moiety in DS. Several genes involved respectively in the formation of senile plaques and neurofibrillary tangles (NFT), two main pathological hallmarks of AD, are mapped on chr21. Further, in subjects with DS the activation of mTOR signaling contributes to Aβ generation and the formation of NFT. This review discusses recent research highlighting the complex role of mTOR associated with the presence of two hallmarks of AD pathology, senile plaques (composed mostly of fibrillar Aß peptides), and NFT (composed mostly of hyperphosphorylated tau protein). Oxidative stress, associated with chr21-related Aβ and mitochondrial alterations, may significantly contribute to this linkage of mTOR to AD-like neuropathology in DS.

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Exosomal biomarkers in Down syndrome and Alzheimer's disease

Publication date: January 2018
Source:Free Radical Biology and Medicine, Volume 114
Author(s): Eric D. Hamlett, Aurélie Ledreux, Huntington Potter, Heidi J. Chial, David Patterson, Joaquin M. Espinosa, Brianne M. Bettcher, Ann-Charlotte Granholm
Every person with Down syndrome (DS) has the characteristic features of Alzheimer's disease (AD) neuropathology in their brain by the age of forty, and most go on to develop AD dementia. Since people with DS show highly variable levels of baseline function, it is often difficult to identify early signs of dementia in this population. The discovery of blood biomarkers predictive of dementia onset and/or progression in DS is critical for developing effective clinical diagnostics. Our recent studies show that neuron-derived exosomes, which are small extracellular vesicles secreted by most cells in the body, contain elevated levels of amyloid-beta peptides and phosphorylated-Tau that could indicate a preclinical AD phase in people with DS starting in childhood. We also found that the relative levels of these biomarkers were altered following dementia onset. Exosome release and signaling are dependent on cellular redox homeostasis as well as on inflammatory processes, and exosomes may be involved in the immune response, suggesting a dual role as both triggers of inflammation in the brain and propagators of inflammatory signals between brain regions. Based on recently reported connections between inflammatory processes and exosome release, the elevated neuroinflammatory state observed in people with DS may affect exosomal AD biomarkers. Herein, we discuss findings from studies of people with DS, people with DS and AD (DS-AD), and mouse models of DS showing new connections between neuroinflammatory pathways, oxidative stress, exosomes, and exosome-mediated signaling, which may inform future AD diagnostics, preventions, and treatments in the DS population as well as in the general population.

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Daily stock index return for the Canadian, UK, and US equity markets, compiled by Morgan Stanley Capital International, obtained from Datastream

Publication date: February 2018
Source:Data in Brief, Volume 16
Author(s): Leon Li
The data presented in this article are related to the research article entitled "Testing and comparing the performance of dynamic variance and correlation models in value-at-risk estimation. North American Journal of Economics and Finance, 40, 116–135. doi:10.1016/j.najef.2017.02.006 (Li, 2017) [1]. Data on daily stock index return for the Canadian, UK, and US equity markets, as compiled by Morgan Stanley Capital International, are provided in this paper. The country indices comprise at least 80% of the stock market capitalization of each country. The data cover the period from January 1, 1990, through September 8, 2016, and include 6963 observations. All stock prices are stated in dollars.



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Astrocytes as therapeutic targets in brain diseases

Publication date: January 2018
Source:Neuroscience Research, Volume 126
Author(s): Hajime Hirase, Schuichi Koizumi




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