LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 7 of total 7

Search options

  1. Article: Mechanisms of acid and base secretion by the airway epithelium.

    Fischer, Horst / Widdicombe, Jonathan H

    The Journal of membrane biology

    2006  Volume 211, Issue 3, Page(s) 139–150

    Abstract: ... focused on the mechanisms responsible for acid and base secretion into the ASL. Advances resulted ... of acid and base transporters and their potential roles in airway mucosal pH regulation is reviewed here. ... One of the main functions of the airway epithelium is to inactivate and remove infectious particles ...

    Abstract One of the main functions of the airway epithelium is to inactivate and remove infectious particles from inhaled air and thereby prevent infection of the distal lung. This function is achieved by mucociliary and cough clearance and by antimicrobial factors present in the airway surface liquid (ASL). There are indications that airway defenses are affected by the pH of the ASL and historically, acidification of the airway surfaces has been suggested as a measure of airway disease. However, even in health, the ASL is slightly acidic, and this acidity might be part of normal airway defense. Only recently research has focused on the mechanisms responsible for acid and base secretion into the ASL. Advances resulted from research into the airway disease associated with cystic fibrosis (CF) after it was found that the CFTR Cl(-) channel conducts HCO (3) (-) and, therefore, may contribute to ASL pH. However, the acidity of the ASL indicated parallel mechanisms for H(+) secretion. Recent investigations identified several H(+) transporters in the apical membrane of the airway epithelium. These include H(+) channels and ATP-driven H(+) pumps, including a non-gastric isoform of the H(+)-K(+) ATPase and a vacuolar-type H(+) ATPase. Current knowledge of acid and base transporters and their potential roles in airway mucosal pH regulation is reviewed here.
    MeSH term(s) Acid-Base Equilibrium/physiology ; Acids/metabolism ; Animals ; Biological Transport/physiology ; Bronchoalveolar Lavage Fluid/chemistry ; Humans ; Hydrogen-Ion Concentration ; Models, Biological ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/physiology
    Chemical Substances Acids
    Language English
    Publishing date 2006
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 3082-x
    ISSN 1432-1424 ; 0022-2631
    ISSN (online) 1432-1424
    ISSN 0022-2631
    DOI 10.1007/s00232-006-0861-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 613: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article: Mechanisms of Acid and Base Secretion by the Airway Epithelium

    Fischer, Horst / Widdicombe, Jonathan H

    Journal of membrane biology. 2006 May, v. 211, no. 3

    2006  

    Abstract: ... focused on the mechanisms responsible for acid and base secretion into the ASL. Advances resulted ... One of the main functions of the airway epithelium is to inactivate and remove infectious particles ... in the apical membrane of the airway epithelium. These include H⁺ channels and ATP-driven H⁺ pumps, including ...

    Abstract One of the main functions of the airway epithelium is to inactivate and remove infectious particles from inhaled air and thereby prevent infection of the distal lung. This function is achieved by mucociliary and cough clearance and by antimicrobial factors present in the airway surface liquid (ASL). There are indications that airway defenses are affected by the pH of the ASL and historically, acidification of the airway surfaces has been suggested as a measure of airway disease. However, even in health, the ASL is slightly acidic, and this acidity might be part of normal airway defense. Only recently research has focused on the mechanisms responsible for acid and base secretion into the ASL. Advances resulted from research into the airway disease associated with cystic fibrosis (CF) after it was found that the CFTR Cl- channel conducts HCO ₃ - and, therefore, may contribute to ASL pH. However, the acidity of the ASL indicated parallel mechanisms for H⁺ secretion. Recent investigations identified several H⁺ transporters in the apical membrane of the airway epithelium. These include H⁺ channels and ATP-driven H⁺ pumps, including a non-gastric isoform of the H⁺-K⁺ ATPase and a vacuolar-type H⁺ ATPase. Current knowledge of acid and base transporters and their potential roles in airway mucosal pH regulation is reviewed here.
    Language English
    Dates of publication 2006-05
    Size p. 139-150.
    Publisher Springer-Verlag
    Publishing place New York
    Document type Article
    ZDB-ID 3082-x
    ISSN 1432-1424 ; 0022-2631
    ISSN (online) 1432-1424
    ISSN 0022-2631
    DOI 10.1007/s00232-006-0861-0
    Database NAL-Catalogue (AGRICOLA)

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 613: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article: Dual mechanisms for Na-K-Cl cotransport regulation in airway epithelial cells.

    Haas, M / McBrayer, D G / Yankaskas, J R

    The American journal of physiology

    1993  Volume 264, Issue 1 Pt 1, Page(s) C189–200

    Abstract: ... ATP and UTP, which stimulate apical Cl channels and Cl secretion in normal and CF airway cells ... of ATP and UTP on binding are inhibited by apical addition of a Cl channel blocker, the indanyloxyacetic acid ... in airway epithelia, we determined saturable basolateral [3H]bumetanide binding, a measure of functioning ...

    Abstract To investigate cellular mechanisms involved in the regulation of basolateral Na-K-Cl cotransport in airway epithelia, we determined saturable basolateral [3H]bumetanide binding, a measure of functioning cotransporters, in primary cultures of canine tracheal and human nasal epithelial cells, including cells from patients with cystic fibrosis (CF). As we previously reported [M. Haas, L. G. Johnson, and R. C. Boucher. Am. J. Physiol. 259 (Cell Physiol. 28): C557-C569, 1990], isoproterenol and hypertonic cell shrinkage produce an equivalent stimulation of [3H]bumetanide binding to dog tracheal cells. We now find that apical ATP and UTP, which stimulate apical Cl channels and Cl secretion in normal and CF airway cells by an adenosine 3',5'-cyclic monophosphate (cAMP)-independent mechanism (S. J. Mason, A. M. Paradiso, and R. C. Boucher. Br. J. Pharmacol. 103: 1649-1656, 1991), increase basolateral [3H]bumetanide binding to dog tracheal cells to the same extent as do isoproterenol and hypertonic shrinkage. The stimulatory effects of ATP and UTP on binding are inhibited by apical addition of a Cl channel blocker, the indanyloxyacetic acid derivative IAA-94 (0.2 mM), or by raising basolateral K concentration ([K]b) from 3.3 to 40 mM, suggesting these effects are secondary to apical Cl efflux via channels. Apical IAA-94 and increased [K]b also inhibit stimulation of binding by isoproterenol by approximately 50%, suggesting that part (but not all) of the effect of the beta-agonist on basolateral cotransport is secondary to apical Cl efflux, with an additional component of direct stimulation of cotransport via cAMP. In support of this interpretation, we find that isoproterenol and a membrane-permeable cAMP analogue increase [3H]bumetanide binding to primary cultures of CF nasal epithelial cells, in which significant cAMP-mediated stimulation of apical Cl efflux does not occur. [3H]bumetanide binding to CF nasal cells is also stimulated by apical ATP, and levels of saturable [3H]bumetanide binding to CF cells are 1.3-1.5 times those in non-CF nasal cells under both basal and stimulated conditions. The results suggest that basolateral Na-K-Cl cotransport in airway cells may be upregulated in two distinct ways: 1) directly via a cAMP-dependent cascade, and 2) as a secondary response to apical Cl channel activation. Both of these mechanisms appear to be intact in CF.
    MeSH term(s) Adenosine Triphosphate/pharmacology ; Animals ; Bumetanide/metabolism ; Carrier Proteins/metabolism ; Cells, Cultured ; Cystic Fibrosis/metabolism ; Cystic Fibrosis/pathology ; Dogs ; Epithelial Cells ; Epithelium/metabolism ; Glycolates/pharmacology ; Humans ; Isoproterenol/pharmacology ; Nasal Mucosa/metabolism ; Nasal Mucosa/pathology ; Potassium/metabolism ; Sodium-Potassium-Chloride Symporters ; Trachea/cytology ; Trachea/metabolism ; Uridine Triphosphate/pharmacology
    Chemical Substances Carrier Proteins ; Glycolates ; Sodium-Potassium-Chloride Symporters ; Bumetanide (0Y2S3XUQ5H) ; MK 473 (54197-05-6) ; Adenosine Triphosphate (8L70Q75FXE) ; Isoproterenol (L628TT009W) ; Potassium (RWP5GA015D) ; Uridine Triphosphate (UT0S826Z60)
    Language English
    Publishing date 1993-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2948-8
    ISSN 0002-9513
    ISSN 0002-9513
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MA 19: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article: Mechanisms of airway goblet cell mucin release: studies with cultured tracheal surface epithelial cells.

    Kim, K C / Nassiri, J / Brody, J S

    American journal of respiratory cell and molecular biology

    1989  Volume 1, Issue 2, Page(s) 137–143

    Abstract: ... mechanisms. Each of these mechanisms may play a role in epithelial mucin secretion associated with airway ... with secretory cells that synthesize and release mucins. Using this cell culture system, we investigated possible ... Both acidic (pH less than 4) and basic (pH greater than 9) media caused significant increases in mucin release ...

    Abstract Confluent hamster tracheal surface epithelial (HTSE) cells in primary culture are enriched with secretory cells that synthesize and release mucins. Using this cell culture system, we investigated possible mechanisms of goblet cell mucin release by altering the media bathing the apical surface of HTSE cells: medium hyperosmolarity decreased mucin release, whereas hypo-osmolarity increased release without causing a cytoplasmic leak due to plasma membrane damage. A Ca2+ ionophore, A23187, did not influence mucin release. Both acidic (pH less than 4) and basic (pH greater than 9) media caused significant increases in mucin release secondary to cell membrane damage. Physiologic concentrations of chemical mediators such as prostaglandins (PGE2 and PGF2 alpha) and leukotrienes (LTC4 and LTD4) did not influence mucin release. Both elastase and cathepsin G derived from human neutrophils caused marked increases in release, whereas trypsin from the porcine pancreas produced a small increase only at a high concentration. We conclude that mucin release by cultured airway goblet cells can be enhanced by: (1) irritant gases, (2) luminal fluid osmolarity, (3) pharmacologic concentrations of LTC4 and LTD4, and (4) cationic proteases, each presumably acting by different mechanisms. Each of these mechanisms may play a role in epithelial mucin secretion associated with airway inflammation.
    MeSH term(s) Animals ; Calcium/physiology ; Cell Membrane/metabolism ; Cell Membrane/pathology ; Cells, Cultured ; Cricetinae ; Epithelium/secretion ; Humans ; Hydrogen-Ion Concentration ; Leukotrienes/physiology ; Mesocricetus ; Mucins/isolation & purification ; Mucins/secretion ; Osmolar Concentration ; Peptide Hydrolases/physiology ; Prostaglandins/physiology ; Trachea/cytology ; Trachea/secretion
    Chemical Substances Leukotrienes ; Mucins ; Prostaglandins ; Peptide Hydrolases (EC 3.4.-) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 1989-08
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/ajrcmb/1.2.137
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: LL-37 secreted by epithelium promotes fibroblast collagen production: a potential mechanism of small airway remodeling in chronic obstructive pulmonary disease.

    Sun, Congcong / Zhu, Maoxiang / Yang, Zhihua / Pan, Xiujie / Zhang, Yuke / Wang, Qin / Xiao, Wei

    Laboratory investigation; a journal of technical methods and pathology

    2014  Volume 94, Issue 9, Page(s) 991–1002

    Abstract: ... expression in epithelium and the structural changes of small airway remodeling was analyzed. In vitro ... thickness and collagen deposition. In vitro, CSE-induced epithelial secretion of LL-37 promoted fibroblast ... is highly expressed in small airway epithelium from COPD patients. However, it is unknown ...

    Abstract Emerging evidence suggests that the process of small airway remodeling is mediated by profibrotic growth factors produced by epithelium, which are capable of activating the underlying mesenchymal cells with excessive collagen production. It has been demonstrated that human cathelicidin antimicrobial protein LL-37 is highly expressed in small airway epithelium from COPD patients. However, it is unknown whether the increased levels of LL-37 in epithelium are involved in the pathogenesis of small airway remodeling in COPD. In this study, we examined the expression of LL-37 in small airways from smokers with COPD and controls (non-smokers and smokers without COPD) by immunohistochemistry, and then the association between LL-37 expression in epithelium and the structural changes of small airway remodeling was analyzed. In vitro, the effect of CSE-induced epithelial secretion of LL-37 on collagen production in human lung fibroblasts (HFL-1 cell line) was studied in a co-culture system. Finally, the signaling pathways involved in the effect of LL-37 on fibroblast collagen production were evaluated. The results showed that LL-37 immunoreactivity in airway epithelium was significantly elevated in smokers with COPD compared with controls. In addition, the magnitude of LL-37 expression in epithelium was positively correlated with airway wall thickness and collagen deposition. In vitro, CSE-induced epithelial secretion of LL-37 promoted fibroblast collagen production. Finally, we showed that formyl peptide receptor-like 1 (FPRL1)-dependent extracellular signal-regulated kinase (ERK) signaling pathway was essential for LL-37-induced collagen production in HFL-1 cells. These results suggest that after cigarette smoke exposure, the increased levels of LL-37 in airway epithelium could stimulate collagen production in the underlying lung fibroblasts and may contribute to small airway remodeling in COPD.
    MeSH term(s) Adult ; Airway Remodeling ; Amino Acid Sequence ; Antimicrobial Cationic Peptides/chemistry ; Antimicrobial Cationic Peptides/metabolism ; Antimicrobial Cationic Peptides/physiology ; Base Sequence ; Case-Control Studies ; Cell Line ; Collagen/biosynthesis ; DNA Primers ; Female ; Fibroblasts/metabolism ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Smoking ; Cathelicidins
    Chemical Substances Antimicrobial Cationic Peptides ; DNA Primers ; Collagen (9007-34-5) ; Cathelicidins
    Language English
    Publishing date 2014-06-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80178-1
    ISSN 1530-0307 ; 0023-6837
    ISSN (online) 1530-0307
    ISSN 0023-6837
    DOI 10.1038/labinvest.2014.86
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.164: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: Proprotein convertase inhibition promotes ciliated cell differentiation - a potential mechanism for the inhibition of Notch1 signalling by decanoyl-RVKR-chloromethylketone.

    Lee, Sang-Nam / Choi, In-Suk / Kim, Hyun Jun / Yang, Eun Jin / Min, Hyun Jin / Yoon, Joo-Heon

    Journal of tissue engineering and regenerative medicine

    2016  Volume 11, Issue 9, Page(s) 2667–2680

    Abstract: ... regulator of basal cell differentiation toward secretory cell lineages in the airway epithelium, and down ... Chronic repetitive rounds of injury and repair in the airway lead to airway remodelling, including ... ciliated cell loss and mucous cell hyperplasia. Airway remodelling is mediated by many growth and ...

    Abstract Chronic repetitive rounds of injury and repair in the airway lead to airway remodelling, including ciliated cell loss and mucous cell hyperplasia. Airway remodelling is mediated by many growth and differentiation factors including Notch1, which are proteolytically processed by proprotein convertases (PCs). The present study evaluated a novel approach for controlling basal cell-type determination based on the inhibition of PCs. It was found that decanoyl-RVKR-chloromethylketone (CMK), a PC inhibitor, promotes ciliated cell differentiation and has no effect on the ciliary beat frequency in air-liquid interface (ALI) cultures of human nasal epithelial cells (HNECs). Comparative microarray analysis revealed that CMK considerably increases ciliogenesis-related gene expression. Use of cell-permeable and cell-impermeable PC inhibitors suggests that intracellular PCs regulate basal cell-type determination in ALI culture. Furthermore, CMK effect on ciliated cell differentiation was reversed by a Notch inhibitor N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT). CMK inhibited the processing of Notch1, a key regulator of basal cell differentiation toward secretory cell lineages in the airway epithelium, and down-regulated the expression of Notch1 target genes together with furin, a PC. Specific lentiviral shRNA-mediated knockdown of furin resulted in reduced Notch1 processing and increased numbers of ciliated cells in HNECs. Moreover, CMK inhibited Notch1 processing and promoted regeneration and ciliogenesis of the mouse nasal respiratory epithelium after ZnSO
    MeSH term(s) Amino Acid Chloromethyl Ketones/pharmacology ; Cell Differentiation/drug effects ; Cilia/metabolism ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Furin/metabolism ; Humans ; Nasal Mucosa/cytology ; Nasal Mucosa/metabolism ; Proprotein Convertases/antagonists & inhibitors ; Proprotein Convertases/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Receptor, Notch1/metabolism
    Chemical Substances Amino Acid Chloromethyl Ketones ; NOTCH1 protein, human ; Protein Synthesis Inhibitors ; Receptor, Notch1 ; Proprotein Convertases (EC 3.4.21.-) ; FURIN protein, human (EC 3.4.21.75) ; Furin (EC 3.4.21.75)
    Language English
    Publishing date 2016-11-22
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-7005
    ISSN (online) 1932-7005
    DOI 10.1002/term.2240
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  7. Article: Platelet-activating factor provokes release of mucin-like glycoproteins from guinea pig respiratory epithelial cells via a lipoxygenase-dependent mechanism.

    Adler, K B / Akley, N J / Glasgow, W C

    American journal of respiratory cell and molecular biology

    1992  Volume 6, Issue 5, Page(s) 550–556

    Abstract: ... of arachidonic acid to HETEs within the epithelium, and stimulation of secretion by these epithelial-derived HETEs via ... secretion stimulated by PAF, but nordihydroguiaretic acid (NDGA), a mixed cyclooxygenase and ... suggest that PAF stimulates release of MLG by guinea pig airway epithelium in vitro by a mechanism ...

    Abstract Primary cultures of guinea pig tracheal epithelial cells maintained in an air/liquid interface system that maintains differentiated characteristics were grown to near confluence and exposed for 1 h to platelet-activating factor (PAF) on both apical and basal sides. PAF provoked release of high-molecular-weight mucin-like glycoproteins (MLG) from the cells, with maximal stimulation occurring at 10(-8) and 10(-9) M. The inactive form of PAF, lyso-PAF, was without effect. Indomethacin, the cyclooxygenase inhibitor, did not affect secretion stimulated by PAF, but nordihydroguiaretic acid (NDGA), a mixed cyclooxygenase and lipoxygenase inhibitor, attenuated secretion stimulated by PAF in a concentration-dependent manner. High performance liquid chromatography assay of the culture medium after addition of PAF revealed increased production of 15-, 12-, and 5-hydroxyeicosatetraenoic acids (15-, 12-, and 5-HETEs). The stimulatory effect of PAF on both mucin secretion and formation of HETEs was inhibited by the PAF receptor antagonists, CV-3988 and Ro 19 3704, with Ro 19 3704 acting at a concentration 10-fold lower than CV-3988 in inhibiting both effects. When added exogenously to the cell cultures, the combination of 5-, 12-, and 15-HETEs stimulated MLG release in a concentration-dependent manner. The results suggest that PAF stimulates release of MLG by guinea pig airway epithelium in vitro by a mechanism involving binding of PAF to receptors on epithelial cell surfaces, stimulation of lipoxygenase metabolism of arachidonic acid to HETEs within the epithelium, and stimulation of secretion by these epithelial-derived HETEs via an autocrine or paracrine mechanism.
    MeSH term(s) Animals ; Cells, Cultured ; Chromatography, High Pressure Liquid ; Cyclooxygenase Inhibitors/pharmacology ; Epithelium/metabolism ; Glyceryl Ethers/pharmacology ; Guinea Pigs ; Hydroxyeicosatetraenoic Acids/metabolism ; In Vitro Techniques ; Indomethacin/pharmacology ; Lipoxygenase/physiology ; Lipoxygenase Inhibitors/pharmacology ; Masoprocol/pharmacology ; Mucins/metabolism ; Phospholipid Ethers/pharmacology ; Platelet Activating Factor/pharmacology ; Platelet Membrane Glycoproteins ; Receptors, Cell Surface/antagonists & inhibitors ; Receptors, G-Protein-Coupled ; Thiazoles/pharmacology ; Trachea/metabolism
    Chemical Substances Cyclooxygenase Inhibitors ; Glyceryl Ethers ; Hydroxyeicosatetraenoic Acids ; Lipoxygenase Inhibitors ; Mucins ; Phospholipid Ethers ; Platelet Activating Factor ; Platelet Membrane Glycoproteins ; Receptors, Cell Surface ; Receptors, G-Protein-Coupled ; Thiazoles ; platelet activating factor receptor ; Ro 19-3704 (106556-34-7) ; Masoprocol (7BO8G1BYQU) ; CV 3988 (85703-73-7) ; Lipoxygenase (EC 1.13.11.12) ; Indomethacin (XXE1CET956)
    Language English
    Publishing date 1992-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/ajrcmb/6.5.550
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top