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In Search of In Vivo MSC

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452354 Year: Pages: 102 DOI: 10.3389/978-2-88945-235-4 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Biology
Added to DOAB on : 2017-10-13 14:57:01
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Stem cells and progenitor cells in ischemic stroke - fashion or future?

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197248 Year: Pages: 156 DOI: 10.3389/978-2-88919-724-8 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Stroke remains one of the most devastating diseases in industrialized countries. Recanalization of the occluded arterial vessel using thrombolysis is the only causal therapy available. However, thrombolysis is limited due to severe side effects and a limited time window. As such, only a minority of patients receives this kind of therapy, showing a need for new and innovative treatment strategies. Although neuroprotective drugs have been shown to be beneficial in a variety of experimental stroke models, they ultimately failed in clinical trials. Consequently, recent scientific focus has been put on modulation of post-ischemic neuroregeneration, either via stimulation of endogenous neurogenesis or via application of exogenous stem cells or progenitor cells. Neurogenesis persists within the adult brain of both rodents and primates. As such, neural progenitor cells (NPCs) are found within distinct niches like the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone of the dentate gyrus. Cerebral ischemia stimulates these astrocyte-like progenitor cells, upon which NPCs proliferate and migrate towards the site of lesion. There, NPCs partly differentiate into mature neurons, without significantly being integrated into the residing neural network. Rather, the majority of new-born cells dies within the first weeks post-stroke, leaving post-ischemic neurogenesis a phenomenon of unknown biological significance. Since NPCs do not replace lost brain tissue, beneficial effects observed in some studies after either stimulated or protected neurogenesis are generally contributed to indirect effects of these new-born cells. The precise identification of appropriated cellular mediators, however, is still elusive. How do these mediators work? Are they soluble factors or maybe even vesicular structures emanating from NPCs? What are the cues that guide NPCs towards the ischemic lesion site? How can post-ischemic neurogenesis be stimulated? How can the poor survival of NPCs be increased? In order to support post-ischemic neurogenesis, a variety of research groups have focused on application of exogenous stem/progenitor cells from various tissue sources. Among these, cultivated NPCs from the SVZ and mesenchymal stem cells (MSCs) from the bone marrow are frequently administered after induction of stroke. Although neuroprotection after delivery of stem/progenitor cells has been shown in various experimental stroke models, transplanted cells are usually not integrated in the neural network. Again, the vast amount of grafted cells dies or does not reach its target despite profound neuroprotection, also suggesting indirect paracrine effects as the cause of neuroprotection. Yet, the factors being responsible for these observations are under debate and still have to be addressed. Is there any “optimal” cell type for transplantation? How can the resistance of grafted cells against a non-favorable extracellular milieu be increased? What are the molecules that are vital for interaction between grafted cells and endogenous NPCs? The present research topic seeks to answer - at least in part - some of the aforementioned questions. Although the research topic predominantly focuses on experimental studies (and reviews alike), a current outlook towards clinical relevance is given as well.

Stem Cell and Biologic Scaffold Engineering

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ISBN: 9783039214976 9783039214983 Year: Pages: 110 DOI: 10.3390/books978-3-03921-498-3 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-12-09 11:49:15
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Tissue engineering and regenerative medicine is a rapidly evolving research field which effectively combines stem cells and biologic scaffolds in order to replace damaged tissues. Biologic scaffolds can be produced through the removal of resident cellular populations using several tissue engineering approaches, such as the decellularization method. Indeed, the decellularization method aims to develop a cell-free biologic scaffold while keeping the extracellular matrix (ECM) intact. Furthermore, biologic scaffolds have been investigated for their in vitro potential for whole organ development. Currently, clinical products composed of decellularized matrices, such as pericardium, urinary bladder, small intestine, heart valves, nerve conduits, trachea, and vessels, are being evaluated for use in human clinical trials. Tissue engineering strategies require the interaction of biologic scaffolds with cellular populations. Among them, stem cells are characterized by unlimited cell division, self-renewal, and differentiation potential, distinguishing themselves as a frontline source for the repopulation of decellularized matrices and scaffolds. Under this scheme, stem cells can be isolated from patients, expanded under good manufacturing practices (GMPs), used for the repopulation of biologic scaffolds and, finally, returned to the patient. The interaction between scaffolds and stem cells is thought to be crucial for their infiltration, adhesion, and differentiation into specific cell types. In addition, biomedical devices such as bioreactors contribute to the uniform repopulation of scaffolds. Until now, remarkable efforts have been made by the scientific society in order to establish the proper repopulation conditions of decellularized matrices and scaffolds. However, parameters such as stem cell number, in vitro cultivation conditions, and specific growth media composition need further evaluation. The ultimate goal is the development of “artificial” tissues similar to native ones, which is achieved by properly combining stem cells and biologic scaffolds and thus bringing them one step closer to personalized medicine. The original research articles and comprehensive reviews in this Special Issue deal with the use of stem cells and biologic scaffolds that utilize state-of-the-art tissue engineering and regenerative medicine approaches.

Biomaterials for Bone Tissue Engineering

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ISBN: 9783039289653 / 9783039289660 Year: Pages: 244 DOI: 10.3390/books978-3-03928-966-0 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Technology (General) --- General and Civil Engineering
Added to DOAB on : 2020-06-09 16:38:57
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Bone tissue engineering aims to develop artificial bone substitutes that partially or totally restore the natural regeneration capability of bone tissue lost under circumstances of injury, significant defects, or diseases such as osteoporosis. In this context, biomaterials are the keystone of the methodology. Biomaterials for bone tissue engineering have evolved from biocompatible materials that mimic the physical and chemical environment of bone tissue to a new generation of materials that actively interacts with the physiological environment, accelerating bone tissue growth. Mathematical modelling and simulation are important tools in the overall methodology. This book presents an overview of the current investigations and recent contributions in the field of bone tissue engineering. It includes several successful examples of multidisciplinary collaboration in this transversal area of research. The book is intended for students, researchers, and professionals of a number of disciplines, such as engineering, mathematics, physics, chemistry, biomedicine, biology, and veterinary. The book is composed of an editorial section and 16 original research papers authored by leading researchers of this discipline from different laboratories across the world

Keywords

Pelvis --- Bone tumor --- 3D-printed implant --- Fixation design --- von Mises stress --- dental implants --- osseointegration --- resonance frequency analysis --- biomaterials --- titanium --- powder metallurgy --- loose sintering --- finite element method --- mechanical behaviour --- bone tissue regeneration --- computed tomography --- Xenografts --- stem cell --- cartilage --- finite element --- finite-element simulation --- electric stimulation --- bone regeneration --- computational modelling --- electrically active implants --- bioelectromagnetism --- critical size defect --- maxillofacial --- minipig --- oxygen delivery --- optimization --- mass transfer --- transport --- bone tissue engineering --- computational fluid dynamics --- Lattice Boltzmann method --- scaffold design --- culturing protocol --- Lagrangian scalar tracking --- cortical bone --- damage --- finite elements --- numerical results --- adipogenesis --- bone marrow --- MSCs --- prediction marker --- bone tissue --- elastoplasticity --- finite element method --- fracture risk --- osteoporosis --- trabeculae --- trabecular bone score --- vertebra --- biomechanics --- finite element modelling --- pelvis --- bone adaptation --- musculoskeletal modelling --- bone tissue engineering --- biomaterials --- computational mechanobiology --- numerical methods in bioengineering --- Ti6Al4V scaffolds --- triply periodic minimal surfaces --- selective laser melting --- additive manufacturing --- biomaterial applications --- finite element analysis --- spark plasma sintering --- wollastonite --- human dental pulp stem cells --- substrate-mediated electrical stimulation --- direct current electric field --- osteo-differentiation --- bone morphogenesis proteins --- cortical bone --- digital image correlation --- multiscale analysis --- micromechanics --- computational mechanics --- cone beam computed tomography --- automatic segmentation --- sliding window --- 3D virtual surgical plan --- Otsu’s method --- n/a

Kidney Inflammation, Injury and Regeneration

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ISBN: 9783039285389 / 9783039285396 Year: Pages: 496 DOI: 10.3390/books978-3-03928-539-6 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Internal medicine
Added to DOAB on : 2020-06-09 16:38:57
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Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of subsequent chronic kidney disease. Although the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function is urgently needed. The Special Issue covers research articles that investigated the molecular mechanisms of inflammation and injury during different renal pathologies, renal regeneration, diagnostics using new biomarkers, and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models. The Special Issue contains important reviews that consider the current knowledge of cell death and regeneration, inflammation, and the molecular mechanisms of kidney diseases. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells or their derivates is summarized. This edition is complemented by reviews that deal with the current data situation on other specific topics like diabetes and diabetic nephropathy or new therapeutic targets.

Keywords

kidney injury --- alport syndrome --- modifier gene --- nephrin --- podocin --- glomerular basement membrane --- slit diaphragm --- focal segmental glomerulosclerosis --- inflammatory bowel disease (IBD) --- DSS-colitis --- glomerular filtration barrier (GFB) --- type IV collagen --- type I collagen --- type V collagen --- genotype --- IL-18 --- polymorphism --- renal cell carcinoma --- Taiwan --- mesenchymal stem cells --- acute and chronic kidney disease --- exosome --- natural products --- non-coding RNAs --- microRNAs --- long non-coding RNAs --- renal fibrosis --- biomarkers --- therapeutics targets --- rhabdomyolysis --- pigment nephropathy --- haem --- NLRP3 inflammasome --- acute kidney injury --- hypertension --- kidney --- molecular signaling --- hematuria --- inflammation --- oxidative stress --- tubular injury --- AKI --- chronic kidney disease (CKD) --- mesenchymal stromal cells --- extracellular vesicles --- acute kidney injury --- modified-MSCs --- microRNA --- mesenchymal stem cell --- mesodermal stem cell --- renal ischemia-reperfusion --- inflammation --- kidney transplantation --- microRNA --- extracellular vesicles --- exosomes --- B-cell attracting chemokine --- CXCL13 --- kidney transplantation --- allograft rejection --- T cell-mediated rejection --- diabetic nephropathy --- lysophosphatidic acid --- lysophosphatidic acid receptor --- chronic kidney injury --- kidney proximal tubule --- acute kidney failure --- signal transduction --- transcription --- CREB Regulated Transcriptional Coactivators (CRTC) --- cAMP Regulatory Element Binding Protein (CREB) --- Salt Inducible Kinase (SIK) --- Class IIa Histone Deacetylases (HDAC) --- lncRNA --- long non-coding RNA --- miRNA --- kidney --- glomerulus --- podocyte --- acute kidney injury --- AKI --- diabetic nephropathy --- diabetic kidney disease --- diabetic nephropathy --- inflammation --- signaling cascade --- ischemia-reperfusion --- acute kidney injury --- stem cell --- conditioned medium --- inflammation --- apoptosis --- necrosis --- regulated necrosis --- kidney injury --- tubular injury --- glomerular injury --- polyunsaturated fatty acids --- omega-3 fatty acid --- inflammatory maker --- C-reactive protein --- interleukin-6 --- LPS-binding protein --- fibrosis --- pericyte --- myofibroblast --- endotoxemia-induced oliguric kidney injury --- arachidonic acid --- cyclooxygenase --- lipoxygenase --- cytochrome P450 --- kidney inflammation --- therapeutic target --- obese kidney fibrosis --- endotoxemia --- ROS --- cPLA2 and COX-2 --- IgA nephropathy --- KIT assay --- KIT-IgA score --- noninvasive --- diagnostics --- prediction --- diabetic kidney diseases --- xanthine oxidase --- glomerular damage --- acute kidney injury --- chronic kidney disease --- renal progenitors --- polyploidization --- diabetic nephropathy --- diabetes mellitus --- GLP-1 receptor agonists --- SGLT2 inhibitors --- molecular mechanisms --- chemerin --- CmklR1 --- 2-kidney-1-clip --- 2k1c --- Thy1.1 nephritis --- renovascular hypertension --- renal inflammation --- renal injury --- renal fibrosis --- inflammation --- ischemia/reperfusion injury --- Farnesiferol B --- Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-?B) --- G-protein-coupled bile acid receptor (TGR5) --- renal stem cells --- differentiation --- scattered tubular cells --- papilla --- niches --- renal tubular cells --- epithelial cells --- proximal tubule --- cytotoxicity --- injury --- inflammation --- empagliflozin --- dapagliflozin --- kidney --- n/a

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