Search results: Found 2

Listing 1 - 2 of 2
Sort by
Putting the "why" back into bone "archytecture"

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193110 Year: Pages: 82 DOI: 10.3389/978-2-88919-311-0 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Medicine (General)
Added to DOAB on : 2017-02-03 17:04:57
License:

Loading...
Export citation

Choose an application

Abstract

A large literature exists on trabecular and cortical bone morphology. The engineering performance of bone, implied from its 3d architecture, is often the endpoint of bone biology experiments, being clinically relevant to bone fracture. How and why does bone travel along its complex spatio-temporal trajectory to acquire its architecture? The question "why" can have two meanings. The first, "teleological - why is an architecture advantageous?" – is the domain of substantial biomechanical research to date. The second, "etiological – how did an architecture come about?" – has received far less attention. This Frontiers Bone Research Topic invited contributions addressing this "etiological why" – what mechanisms can coordinate the activity of bone forming and resorbing cells to produce the observed complex and efficient bone architectures? One mechanism is proposed – chaotic nonlinear pattern formation (NPF) which underlies – in a unifying way – natural structures as disparate as trabecular bone, swarms of birds flying or shoaling fish, island formation, fluid turbulence and others. At the heart of NPF is the fact that simple rules operating between interacting elements multiplied and repeated many times, lead to complex and structured patterns. This paradigm of growth and form leads to a profound link between bone regulation and its architecture: in bone "the architecture is the regulation". The former is the emergent consequence of the latter. Whatever mechanism does determine bone's developing architecture has to operate at the level of individual sites of formation and resorption and coupling between the two. This has implications as to how we understand the effect on bone of agents such as gene products or drugs. It may be for instance that the "tuning" of coupling between formation and resorption might be as important as the achievement of enhanced bone volume. The ten articles that were contributed to this Topic were just what we hoped for – a snapshot of leading edge bone biology research which addresses the question of how bone gets its shape. We hope that you find these papers thought-provoking, and that they might stimulate new ideas in the research into bone architecture, growth and adaptation, and how to preserve healthy bone from gestation and childhood until old age.

Links between Fibrogenesis and Cancer: Mechanistic and Therapeutic Challenges: Mechanistic and Therapeutic Challenges

Author:
ISBN: 9783039217069 / 9783039217076 Year: Pages: 348 DOI: 10.3390/books978-3-03921-707-6 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Internal medicine
Added to DOAB on : 2019-12-09 11:49:16
License:

Loading...
Export citation

Choose an application

Abstract

Tissue fibrosis may occur for unknown causes or be the consequence of many pathological conditions including chronic inflammatory or infectious diseases, autoimmune disorders, graft rejection, or malignancy. On the other hand, malignant tumors have been identified in fibrotic tissues decades ago, and now accumulating evidence suggests that fibrotic lesions enhance the risk of cancer in several organs such as liver, lungs, and breast. Disruption of an organ parenchymal cells and of its normal structural scaffold during tissue fibrogenesis appears to induce loss of cell polarity, promoting uncontrolled cell proliferation that may eventually lead to cancer development. Many cellular and molecular abnormalities including aberrant expression of microRNAs, genetic and epigenetic alterations, evasion or delayed apoptosis, unregulated intracellular signal pathways, and dysregulation or defective intercellular communications have been proposed to explain this link between fibrogenesis and carcinogenesis. However, the precise mechanisms of this fibrosis-to-cancer transition remain unclear. This book presents a collection of reviews and original articles summarizing recent advances in understanding the molecular mechanisms of cancer development in fibrotic organs.

Keywords

lung cancer --- renal injury --- fibrosis --- crizotinib --- anaplastic lymphoma kinase --- cystic formation --- pulmonary fibrosis --- butylidenephthalide --- SOX2 --- type I collagen --- bleomycin --- YAP --- TAZ --- Hippo pathway --- fibrosis --- cancer --- mechanotransduction --- TGF-? --- Wnt --- uterine fibroid --- leiomyoma --- tumor --- tumor necrosis factor ? --- cytokine --- growth factor --- inflammation --- clinical symptoms --- pathophysiology --- therapy --- hepatocellular carcinoma --- cirrhosis --- regeneration --- inflammation --- cytokines --- genetic instability --- reactive oxygen species --- idiopathic pulmonary fibrosis (IPF) --- lung cancer (LC) --- non-small cell lung cancer (NSCLC) --- acute lung injury --- protein S --- apoptosis --- signal pathway --- Erk1/2 --- lipopolysaccharide --- uterine fibroid --- leiomyoma --- smooth muscle tumor of uncertain malignant potential --- leiomyosarcoma --- myometrium --- immunohistochemistry --- marker --- pathology --- tumor --- diagnosis --- cancer-associated fibroblasts --- tumor microenvironment --- nanoparticles --- breast cancer --- antitumor efficacy --- cirrhosis --- HBV --- HCV --- hepatocellular carcinoma --- idiopathic pulmonary fibrosis --- lung cancer --- pathogenesis --- common pathways --- hepatocellular carcinoma (HCC) --- fibrosis --- cancer-associated fibroblasts (CAFs) --- hepatic stellate cells (HSCs) --- tumor microenvironment --- hepatocellular carcinoma --- non-alcoholic steatohepatitis --- fibrosis --- hepatic stellate cells --- extracellular matrix --- carcinogenesis --- angiogenesis --- cancer-associated fibroblasts --- extracellular matrix --- fibrosis --- heterogeneity --- interstitial fluid pressure --- metabolic reprogramming --- transforming growth factor-? --- tumor stiffness --- GPR40 --- GPR120 --- DHA --- omega-3 fatty acid --- SREBP-1 --- hepatocytes --- EMT --- lncRNA --- metastasis --- miRNA --- SMAD --- TGF-? --- targeted therapy --- tumor microenvironment --- n/a

Listing 1 - 2 of 2
Sort by
Narrow your search
-->