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https://www.readbyqxmd.com/read/28918516/valve-sparing-aortic-root-surgery-con-remodeling
#1
Takashi Kunihara
The two major valve-sparing root replacement procedures, aortic valve reimplantation (reimplantation) and aortic root remodeling (remodeling), have advantages and disadvantages, which are reviewed herein. The main advantage of reimplantation is the resulting annular support, and the disadvantages are the unfavorable hemodynamics and relatively long procedure time. The main advantages of remodeling are the physiological hemodynamics and decreased procedure time, and the disadvantage is the lack of annular support...
September 16, 2017: General Thoracic and Cardiovascular Surgery
https://www.readbyqxmd.com/read/28918442/the-role-of-periostin-in-lung-fibrosis-and-airway-remodeling
#2
REVIEW
David N O'Dwyer, Bethany B Moore
Periostin is a protein that plays a key role in development and repair within the biological matrix of the lung. As a matricellular protein that does not contribute to extracellular matrix structure, periostin interacts with other extracellular matrix proteins to regulate the composition of the matrix in the lung and other organs. In this review, we discuss the studies exploring the role of periostin to date in chronic respiratory diseases, namely asthma and idiopathic pulmonary fibrosis. Asthma is a major health problem globally affecting millions of people worldwide with significant associated morbidity and mortality...
September 16, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28918418/new-aspects-in-the-pathomechanism-of-diseases-of-civilization-particularly-psychosomatic-disorders-part-1-theoretical-background-of-a-hypothesis
#3
Andras Sikter, Zoltan Rihmer, Roberto de Guevara
The stress defence-cascade is mostly not biphasic as Cannon thought, the sympathicotonic stress response is preceded by a vagotonic phase called freeze response. Alteration of the carbon dioxide level plays an important role during defence-cascade as its changes interfere with stress hormones, e.g. with catecholamines, thus affecting the degree of arousal. In case of humans, learned behaviour dominates instead of instinctive, so the fight-or-flight often lags; the consequence can be persistent hypocapnia or hypercapnia...
June 2017: Neuropsychopharmacologia Hungarica
https://www.readbyqxmd.com/read/28918227/bone-remodeling-of-the-distal-femur-after-uncemented-total-knee-arthroplasty-a-2-year-prospective-dxa-study
#4
Mikkel Rathsach Andersen, Nikolaj S Winther, Thomas Lind, Henrik M Schrøder, Michael Mørk Petersen
Loss of bone stock as a response to the bone trauma, immobilization, and stress shielding related to joint replacement surgery increases the risk of fracture of the distal femur after total knee arthroplasty. Previous studies of uncemented femoral components have reported very high levels of bone loss in the distal femur. This study investigates the adaptive bone remodeling of the distal femur after uncemented total knee arthroplasty. We performed a 2-year follow-up of 53 patients (mean age 61.5 [38-70] years, F/M = 27/26, body mass index 29...
September 13, 2017: Journal of Clinical Densitometry
https://www.readbyqxmd.com/read/28918046/microrna-as-therapeutic-targets-for-chronic-wound-healing
#5
REVIEW
Eoghan J Mulholland, Nicholas Dunne, Helen O McCarthy
Wound healing is a highly complex biological process composed of three overlapping phases: inflammation, proliferation, and remodeling. Impairments at any one or more of these stages can lead to compromised healing. MicroRNAs (miRs) are non-coding RNAs that act as post-transcriptional regulators of multiple proteins and associated pathways. Thus, identification of the appropriate miR involved in the different phases of wound healing could reveal an effective third-generation genetic therapy in chronic wound care...
September 15, 2017: Molecular Therapy. Nucleic Acids
https://www.readbyqxmd.com/read/28918000/nitric-oxide-prevents-aft1-activation-and-metabolic-remodeling-in-frataxin-deficient-yeast
#6
David Alsina, Joaquim Ros, Jordi Tamarit
Yeast frataxin homolog (Yfh1) is the orthologue of human frataxin, a mitochondrial protein whose deficiency causes Friedreich Ataxia. Yfh1 deficiency activates Aft1, a transcription factor governing iron homeostasis in yeast cells. Although the mechanisms causing this activation are not completely understood, it is assumed that it may be caused by iron-sulfur deficiency. However, several evidences indicate that activation of Aft1 occurs in the absence of iron-sulfur deficiency. Besides, Yfh1 deficiency also leads to metabolic remodeling (mainly consisting in a shift from respiratory to fermentative metabolism) and to induction of Yhb1, a nitric oxide (NO) detoxifying enzyme...
September 6, 2017: Redox Biology
https://www.readbyqxmd.com/read/28917940/natural-and-synthetic-polymers-bioceramics-bioactive-compounds-mediated-cell-signaling-in-bone-tissue-engineering
#7
REVIEW
S Harsha Rao, B Harini, R Pranav Kumar Shadamarshan, K Balagangadharan, N Selvamurugan
Bone is a highly integrative and dynamic tissue of the human body. It is continually remodeled by bone cells such as osteoblasts, osteoclasts. When a fraction of a bone is damaged or deformed, stem cells and bone cells under the influence of several signaling pathways regulate bone regeneration at the particular locale. Effective therapies for bone defects can be met via bone tissue engineering which employs drug delivery systems with biomaterials to enhance cellular functions by acting on signaling pathways such as Wnt, BMP, TGF-β, and Notch...
September 13, 2017: International Journal of Biological Macromolecules
https://www.readbyqxmd.com/read/28917705/long-term-retention-of-ecm-hydrogel-after-implantation-into-a-sub-acute-stroke-cavity-reduces-lesion-volume
#8
Harmanvir Ghuman, Madeline Gerwig, Francesca J Nicholls, Jessie Liu, Julia Donnelly, Stephen F Badylak, Michel Modo
Salvaging or functional replacement of damaged tissue caused by stroke in the brain remains a major therapeutic challenge. In situ gelation and retention of a hydrogel bioscaffold composed of 8 mg/mL extracellular matrix (ECM) can induce a robust invasion of cells within 24 hours and potentially promote a structural remodeling to replace lost tissue. Herein, we demonstrate a long-term retention of ECM hydrogel within the lesion cavity. A decrease of approximately 32% of ECM volume is observed over 12 weeks...
September 13, 2017: Acta Biomaterialia
https://www.readbyqxmd.com/read/28916993/periostin-in-the-pathogenesis-of-skin-diseases
#9
REVIEW
Hiroyuki Murota, Yang Lingli, Ichiro Katayama
Skin is an organ that is susceptible to damage by external injury, chronic inflammation, and autoimmunity. Tissue damage causes alterations in both the configuration and type of cells in lesional skin. This phenomenon, called tissue remodeling, is a universal biological response elicited by programmed cell death, inflammation, immune disorders, and tumorigenic, tumor proliferative, and cytoreductive activity. In this process, changes in the components of the extracellular matrix are required to provide an environment that facilitates tissue remodeling...
September 15, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28916968/hmgb-proteins-and-arthritis
#10
REVIEW
Noboru Taniguchi, Yasuhiko Kawakami, Ikuro Maruyama, Martin Lotz
The high-mobility group box (HMGB) family includes four members: HMGB1, 2, 3 and 4. HMGB proteins have two functions. In the nucleus, HMGB proteins bind to DNA in a DNA structure-dependent but nucleotide sequence-independent manner to function in chromatin remodeling. Extracellularly, HMGB proteins function as alarmins, which are endogenous molecules released upon tissue damage to activate the immune system. HMGB1 acts as a late mediator of inflammation and contributes to prolonged and sustained systemic inflammation in subjects with rheumatoid arthritis...
September 15, 2017: Human Cell
https://www.readbyqxmd.com/read/28916915/inflammatory-diseases-and-bone-fragility
#11
REVIEW
K Briot, P Geusens, I Em Bultink, W F Lems, C Roux
Systemic osteoporosis and increased fracture rates have been described in chronic inflammatory diseases such as rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, inflammatory bowel diseases, and chronic obstructive pulmonary disease. Most of these patients receive glucocorticoids, which have their own deleterious effects on bone. However, the other main determinant of bone fragility is the inflammation itself, as shown by the interactions between the inflammatory mediators, the actors of the immune system, and the bone remodelling...
September 15, 2017: Osteoporosis International
https://www.readbyqxmd.com/read/28916766/stimulatory-secretions-of-airway-epithelial-cells-accelerate-early-repair-of-tracheal-epithelium
#12
Egi Kardia, Rafeezul Mohamed, Badrul Hisham Yahaya
Airway stem/progenitor epithelial cells (AECs) are notable for their differentiation capacities in response to lung injury. Our previous finding highlighted the regenerative capacity of AECs following transplantation in repairing tracheal injury and reducing the severity of alveolar damage associated acute lung injury in a rabbit model. The goal of this study is to further investigate the potential of AECs to re-populate the tracheal epithelium and to study their stimulatory effect on inhibiting pro-inflammatory cytokines, epithelial cell migration and proliferation, and epithelial-to-mesenchymal transition (EMT) process following tracheal injury...
September 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28916764/rapid-and-reversible-epigenome-editing-by-endogenous-chromatin-regulators
#13
Simon M G Braun, Jacob G Kirkland, Emma J Chory, Dylan Husmann, Joseph P Calarco, Gerald R Crabtree
Understanding the causal link between epigenetic marks and gene regulation remains a central question in chromatin biology. To edit the epigenome we developed the FIRE-Cas9 system for rapid and reversible recruitment of endogenous chromatin regulators to specific genomic loci. We enhanced the dCas9-MS2 anchor for genome targeting with Fkbp/Frb dimerizing fusion proteins to allow chemical-induced proximity of a desired chromatin regulator. We find that mSWI/SNF (BAF) complex recruitment is sufficient to oppose Polycomb within minutes, leading to activation of bivalent gene transcription in mouse embryonic stem cells...
September 15, 2017: Nature Communications
https://www.readbyqxmd.com/read/28916763/maternal-diabetes-causes-developmental-delay-and-death-in-early-somite-mouse-embryos
#14
Jing Zhao, Theodorus B M Hakvoort, Jan M Ruijter, Aldo Jongejan, Jan Koster, Sigrid M A Swagemakers, Aleksandar Sokolovic, Wouter H Lamers
Maternal diabetes causes congenital malformations and delays embryonic growth in the offspring. We investigated effects of maternal diabetes on mouse embryos during gastrulation and early organogenesis (ED7.5-11.5). Female mice were made diabetic with streptozotocin, treated with controlled-release insulin implants, and mated. Maternal blood glucose concentrations increased up to embryonic day (ED) 8.5. Maternal hyperglycemia induced severe growth retardation (approx.1 day) in 53% of the embryos on ED8.5, death in most of these embryos on ED9...
September 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28916721/loss-of-cardiac-carnitine-palmitoyltransferase-2-results-in-rapamycin-resistant-acetylation-independent-hypertrophy
#15
Andrea S Pereyra, Like Y Hasek, Kate L Harris, Alycia G Berman, Frederick W Damen, Craig J Goergen, Jessica M Ellis
Cardiac hypertrophy is closely linked to impaired fatty acid oxidation, but the molecular basis of this link is unclear. Here, we investigated the loss of an obligate enzyme in mitochondrial long-chain fatty acid oxidation, carnitine palmitoyltransferase 2 (CPT2), on muscle and heart structure, function, and molecular signatures in a muscle- and heart-specific CPT2-deficient mouse (Cpt2M-/-) model. CPT2 loss in heart and muscle reduced complete oxidation of long-chain fatty acids by 87% and 69%, respectively, without altering body weight, energy expenditure, respiratory quotient, or adiposity...
September 15, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28916646/serac1-deficiency-causes-complicated-hsp-evidence-from-a-novel-splice-mutation-in-a-large-family
#16
Benjamin Roeben, Rebecca Schüle, Susanne Ruf, Benjamin Bender, Bader Alhaddad, Tanja Benkert, Thomas Meitinger, Selina Reich, Judith Böhringer, Claus-Dieter Langhans, Frédéric M Vaz, Saskia B Wortmann-Hagemann, Thorsten Marquardt, Tobias B Haack, Ingeborg Krägeloh-Mann, Ludger Schöls, Matthis Synofzik
OBJECTIVE: To demonstrate that mutations in the phosphatidylglycerol remodelling enzyme SERAC1 can cause juvenile-onset complicated hereditary spastic paraplegia (cHSP) clusters, thus adding SERAC1 to the increasing number of complex lipid cHSP genes. METHODS: Combined genomic and functional validation studies (whole-exome sequencing, mRNA, cDNA and protein), biomarker investigations (3-methyl-glutaconic acid, filipin staining and phosphatidylglycerols PG34:1/PG36:1), and clinical and imaging phenotyping were performed in six affected subjects from two different branches of a large consanguineous family...
September 15, 2017: Journal of Medical Genetics
https://www.readbyqxmd.com/read/28916541/a-proteomic-atlas-of-insulin-signalling-reveals-tissue-specific-mechanisms-of-longevity-assurance
#17
Luke S Tain, Robert Sehlke, Chirag Jain, Manopriya Chokkalingam, Nagarjuna Nagaraj, Paul Essers, Mark Rassner, Sebastian Grönke, Jenny Froelich, Christoph Dieterich, Matthias Mann, Nazif Alic, Andreas Beyer, Linda Partridge
Lowered activity of the insulin/IGF signalling (IIS) network can ameliorate the effects of ageing in laboratory animals and, possibly, humans. Although transcriptome remodelling in long-lived IIS mutants has been extensively documented, the causal mechanisms contributing to extended lifespan, particularly in specific tissues, remain unclear. We have characterized the proteomes of four key insulin-sensitive tissues in a long-lived Drosophila IIS mutant and control, and detected 44% of the predicted proteome (6,085 proteins)...
September 15, 2017: Molecular Systems Biology
https://www.readbyqxmd.com/read/28916263/autophagy-dependent-generation-of-free-fatty-acids-is-critical-for-normal-neutrophil-differentiation
#18
Thomas Riffelmacher, Alexander Clarke, Felix C Richter, Amanda Stranks, Sumeet Pandey, Sara Danielli, Philip Hublitz, Zhanru Yu, Errin Johnson, Tobias Schwerd, James McCullagh, Holm Uhlig, Sten Eirik W Jacobsen, Anna Katharina Simon
Neutrophils are critical and short-lived mediators of innate immunity that require constant replenishment. Their differentiation in the bone marrow requires extensive cytoplasmic and nuclear remodeling, but the processes governing these energy-consuming changes are unknown. While previous studies show that autophagy is required for differentiation of other blood cell lineages, its function during granulopoiesis has remained elusive. Here, we have shown that metabolism and autophagy are developmentally programmed and essential for neutrophil differentiation in vivo...
September 1, 2017: Immunity
https://www.readbyqxmd.com/read/28916169/the-large-and-small-spen-family-proteins-stimulate-axon-outgrowth-during-neurosecretory-cell-remodeling-in-drosophila
#19
Tingting Gu, Tao Zhao, Uday Kohli, Randall S Hewes
Split ends (SPEN) is the founding member of a well conserved family of nuclear proteins with critical functions in transcriptional regulation and the post-transcriptional processing and nuclear export of transcripts. In animals, the SPEN proteins fall into two size classes that perform either complementary or antagonistic functions in different cellular contexts. Here, we show that the two Drosophila representatives of this family, SPEN and Spenito (NITO), regulate metamorphic remodeling of the CCAP/bursicon neurosecretory cells...
September 12, 2017: Developmental Biology
https://www.readbyqxmd.com/read/28916165/muc1-deficiency-exacerbates-pulmonary-fibrosis-in-a-mouse-model-of-silicosis
#20
Kosuke Kato, Marina A Zemskova, Alec D Hanss, Marianne M Kim, Sandra J Gendler, Ross Summer, Kwang Chul Kim
BACKGROUND: MUC1 (MUC in human and Muc in animals) is a membrane-tethered mucin expressed on the apical surface of lung epithelial cells. However, in the lungs of patients with interstitial lung disease, MUC1 is aberrantly expressed in hyperplastic alveolar type II epithelial (ATII) cells and alveolar macrophages (AM), and elevated levels of extracellular MUC1 are found in bronchoalveolar lavage (BAL) fluid and the serum of these patients. While pro-fibrotic effects of extracellular MUC1 have recently been described in cultured fibroblasts, the contribution of MUC1 to the pathobiology of pulmonary fibrosis is unknown...
September 12, 2017: Biochemical and Biophysical Research Communications
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