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Article ; Online: Recent advances of cannabidiol studies in medicinal chemistry, pharmacology and therapeutics.

Thakkar, Karishma / Ruan, Cheng-Huai / Ruan, Ke-He

Future medicinal chemistry

2021 Volume 13, Issue 22, Page(s) 1935–1937

MeSH term(s)	Animals ; Anti-Inflammatory Agents/chemistry ; Anti-Inflammatory Agents/isolation & purification ; Anti-Inflammatory Agents/pharmacology ; Antineoplastic Agents, Phytogenic/chemistry ; Antineoplastic Agents, Phytogenic/isolation & purification ; Antineoplastic Agents, Phytogenic/pharmacology ; Antioxidants/chemistry ; Antioxidants/isolation & purification ; Antioxidants/pharmacology ; Brain Diseases/drug therapy ; Cannabidiol/chemistry ; Cannabidiol/isolation & purification ; Cannabidiol/pharmacology ; Cannabis/chemistry ; Chemistry, Pharmaceutical ; Humans ; Neoplasms/drug therapy ; Oxidative Stress/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Antineoplastic Agents, Phytogenic ; Antioxidants ; Cannabidiol (19GBJ60SN5)
Language	English
Publishing date	2021-09-29
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Review
ISSN	1756-8927
ISSN (online)	1756-8927
DOI	10.4155/fmc-2021-0125
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Instantly Converting Atrial Fibrillation into Sinus Rhythm by a Digital Rectal Exam on a 29-year-Old Male.

Ruan, Cheng-Huai

Clinical medicine insights. Case reports

2010 Volume 3, Page(s) 51–54

Abstract: Vagal maneuvers cause increase in vagal tone, which has been shown to slow many types supraventricular tachycardia, such as atrial fibrillation (AF). However, the conversion of AF to sinus rhythm is usually not associated with vagal manuvers. Thus, AF is ...

Abstract	Vagal maneuvers cause increase in vagal tone, which has been shown to slow many types supraventricular tachycardia, such as atrial fibrillation (AF). However, the conversion of AF to sinus rhythm is usually not associated with vagal manuvers. Thus, AF is classically treated with medication and electrical cardioversion. Here, we present a 29-year-old male with no cardiovascular history and a low atherosclerotic risk profile who developed AF which converted into sinus rhythm immediately after a digital rectal exam. The patient remained asymptomatic after a 3-month follow-up. This implies that the digital rectal exam can be considered as an additional attempt to convert AF to sinus rhythm in AF patients.
Language	English
Publishing date	2010-08-13
Publishing country	United States
Document type	Case Reports
ZDB-ID	2580498-4
ISSN	1179-5476 ; 1179-5476
ISSN (online)	1179-5476
ISSN	1179-5476
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Article ; Online: Instantly Converting Atrial Fibrillation into Sinus Rhythm by a Digital Rectal Exam on a 29-year-Old Male

Cheng-Huai Ruan

Clinical Medicine Insights: Case Reports, Vol

2010 Volume 3

Abstract	Vagal maneuvers cause increase in vagal tone, which has been shown to slow many types supraventricular tachycardia, such as atrial fibrillation (AF). However, the conversion of AF to sinus rhythm is usually not associated with vagal manuvers. Thus, AF is classically treated with medication and electrical cardioversion. Here, we present a 29-year-old male with no cardiovascular history and a low atherosclerotic risk profile who developed AF which converted into sinus rhythm immediately after a digital rectal exam. The patient remained asymptomatic after a 3-month follow-up. This implies that the digital rectal exam can be considered as an additional attempt to convert AF to sinus rhythm in AF patients.
Keywords	Medicine (General) ; R5-920
Language	English
Publishing date	2010-01-01T00:00:00Z
Publisher	SAGE Publishing
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Establishing novel prostacyclin-synthesizing cells with therapeutic potential against heart diseases.

Ruan, Ke-He / Mohite, Anita / So, Shui-Ping / Ruan, Cheng-Huai

International journal of cardiology

2013 Volume 163, Issue 2, Page(s) 163–169

Abstract: Background: For decades, there have been many ongoing attempts to use prostaglandin I(2) (PGI(2)) to treat heart diseases, such as pulmonary arterial hypertension. However, the short half life of PGI(2) has limited the therapeutic impact potential.: ... ...

Abstract	Background: For decades, there have been many ongoing attempts to use prostaglandin I(2) (PGI(2)) to treat heart diseases, such as pulmonary arterial hypertension. However, the short half life of PGI(2) has limited the therapeutic impact potential. Methods: Here, we have engineered a novel adipose tissue-derived cell that constantly produces PGI(2,) through transfecting of an engineered cDNA of a hybrid enzyme (human COX-1-10-aa-PGIS) which has superior triple catalytic functions in directly converting arachidonic acid into PGI(2). Results: The gene-transfected cells were further converted into a stable cell line, in which cells constantly express the hybrid enzyme and are capable of producing large-amounts of PGI(2). In a comparison between un-transfected- and gene-transfected cells, it was determined that the majority of the endogenous AA metabolism shifted from that of unwanted PGE(2) (in un-transfected cells) to that of the preferred PGI(2) (in gene-transfected cells) with a PGI(2)/PGE(2) ratio change from 0.03 to 25. The PGI(2)-producing cell line not only exhibited an approximate 50-fold increase in PGI(2) biosynthesis, but also demonstrated superior anti-platelet aggregation in vitro, and increased reperfusion in the mouse ischemic hindlimb model in vivo. Conclusions: The cells, which have an ability to increase the biosynthesis of the vascular protector, PGI(2), while reducing that of the vascular inflammatory mediator, PGE(2), provide a dual effect on vascular protection, which is not available through any existing drug treatments. Thus, the current finding has potential to be an experimental intervention for PGI(2)-deficient heart diseases, such as pulmonary arterial hypertension.
MeSH term(s)	Animals ; Cells, Cultured/metabolism ; Cyclooxygenase 1/biosynthesis ; Epoprostenol/biosynthesis ; Heart Diseases/drug therapy ; Humans ; Mice ; Transfection
Chemical Substances	Epoprostenol (DCR9Z582X0) ; Cyclooxygenase 1 (EC 1.14.99.1)
Language	English
Publishing date	2013-02-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	779519-1
ISSN	1874-1754 ; 0167-5273
ISSN (online)	1874-1754
ISSN	0167-5273
DOI	10.1016/j.ijcard.2011.06.007
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Article ; Online: Inducible COX-2 dominates over COX-1 in prostacyclin biosynthesis: mechanisms of COX-2 inhibitor risk to heart disease.

Ruan, Cheng-Huai / So, Shui-Ping / Ruan, Ke-He

Life sciences

2010 Volume 88, Issue 1-2, Page(s) 24–30

Abstract: Aim: Our aim is to understand the molecular mechanisms of the selective nonsteroidal anti-inflammatory drugs (NSAID), cyclooxygenase-2 (COX-2) inhibitors', higher "priority" to reduce synthesis of the vascular protector, prostacyclin (PGI2), compared to ...

Abstract	Aim: Our aim is to understand the molecular mechanisms of the selective nonsteroidal anti-inflammatory drugs (NSAID), cyclooxygenase-2 (COX-2) inhibitors', higher "priority" to reduce synthesis of the vascular protector, prostacyclin (PGI2), compared to that of nonselective NSAIDs. Main methods: COX-1 or COX-2 was co-expressed with PGI2 synthase (PGIS) in COS-7 cells. The Km and initial velocity (½t Vmax) of the coupling reaction between COX-1 and COX-2 to PGIS were established. The experiment was further confirmed by a kinetics study using hybrid enzymes linking COX-1 or COX-2 to PGIS. Finally, COX-1 or COX-2 and PGIS were respectively fused to red (RFP) and cyanic (CFP) fluorescence proteins, and co-expressed in cells. The distances between COXs and PGIS were compared by FRET. Key findings: The Km for converting arachidonic acid (AA) to PGI2 by COX-2 coupled to PGIS is ~2.0μM; however, it was 3-fold more (~6.0μM) for COX-1 coupled to PGIS. The Km and ½t Vmax for COX-2 linked to PGIS were ~2.0μM and 20s, respectively, which were 2-5 folds faster than that of COX-1 linked to PGIS. The FRET study found that the distance between COX-2-RFP and PGIS-CFP is shorter than that between COX-1-RFP and PGIS-CFP. Significance: The study provided strong evidence suggesting that the low Km, faster ½t Vmax, and closer distance are the basis for COX-2 dominance over COX-1 (coupled to PGIS) in PGI2 synthesis, and further demonstrated the mechanisms of selective COX-2 inhibitors with higher potential to reduce synthesis of the vascular protector, PGI2.
MeSH term(s)	Animals ; Arachidonic Acid/metabolism ; Blotting, Western ; COS Cells ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/physiopathology ; Chlorocebus aethiops ; Chromatography, High Pressure Liquid ; Cyclooxygenase 1/metabolism ; Cyclooxygenase 1/physiology ; Cyclooxygenase 2/metabolism ; Cyclooxygenase 2/physiology ; Cyclooxygenase 2 Inhibitors/pharmacology ; Electrophoresis, Polyacrylamide Gel ; Epoprostenol/biosynthesis ; Microscopy, Fluorescence
Chemical Substances	Cyclooxygenase 2 Inhibitors ; Arachidonic Acid (27YG812J1I) ; Epoprostenol (DCR9Z582X0) ; Cyclooxygenase 1 (EC 1.14.99.1) ; Cyclooxygenase 2 (EC 1.14.99.1)
Language	English
Publishing date	2010-10-28
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2010.10.017
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Article ; Online: A strategy using NMR peptide structures of thromboxane A2 receptor as templates to construct ligand-recognition pocket of prostacyclin receptor

Ruan Ke-He / Wu Jaixin / Ruan Cheng-Huai

BMC Biochemistry, Vol 6, Iss 1, p

2005 Volume 23

Abstract: Abstract Background: Prostacyclin receptor (IP) and thromboxane A2 receptor (TP) belong to rhodopsin-type G protein-coupling receptors and respectively bind to prostacyclin and thromboxane A2 derived from arachidonic acid. Recently, we have determined ... ...

Abstract	Abstract Background: Prostacyclin receptor (IP) and thromboxane A2 receptor (TP) belong to rhodopsin-type G protein-coupling receptors and respectively bind to prostacyclin and thromboxane A2 derived from arachidonic acid. Recently, we have determined the extracellular loop (eLP) structures of the human TP receptor by 2-D 1H NMR spectroscopy using constrained peptides mimicking the individual eLP segments. The studies have identified the segment along with several residues in the eLP domains important to ligand recognition, as well as proposed a ligand recognition pocket for the TP receptor. Results: The IP receptor shares a similar primary structure in the eLPs with those of the TP receptor. Forty percent residues in the second eLPs of the receptors are identical, which is the major region involved in forming the ligand recognition pocket in the TP receptor. Based on the high homology score, the eLP domains of the IP receptor were constructed by the homology modeling approach using the NMR structures of the TP eLPs as templates, and then configured to the seven transmembrane (TM) domains model constructed using the crystal structure of the bovine rhodopsin as a template. A NMR structure of iloprost was docked into the modeled IP ligand recognition pocket. After dynamic studies, the segments and residues involved in the IP ligand recognition were proposed. A key residue, Arg173 involved in the ligand recognition for the IP receptor, as predicted from the modeling, was confirmed by site-directed mutagenesis. Conclusion: A 3-D model of the human IP receptor was constructed by homology modeling using the crystal structure of bovine rhodopsin TM domains and the NMR structures of the synthetic constrained peptides of the eLP domains of the TP receptor as templates. This strategy can be applied to molecular modeling and the prediction of ligand recognition pockets for other prostanoid receptors.
Keywords	G protein-coupled receptor ; GPCR ; prostacyclin (prostaglandin I 2 (PGI 2 ) receptor ; protein modeling ; thromboxane A 2 receptor ; NMR structure ; synthetic peptide. ; Biochemistry ; QD415-436 ; Organic chemistry ; QD241-441 ; Chemistry ; QD1-999 ; Science ; Q ; DOAJ:Biochemistry ; DOAJ:Life Sciences ; DOAJ:Biology and Life Sciences
Subject code	540
Language	English
Publishing date	2005-11-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Inducible COX-2 dominates over COX-1 in prostacyclin biosynthesis: Mechanisms of COX-2 inhibitor risk to heart disease

Ruan, Cheng-Huai / So, Shui-Ping / Ruan, Ke-He

Life sciences. 2011 Jan. 3, v. 88, no. 1-2

2011

Abstract: AIM: Our aim is to understand the molecular mechanisms of the selective nonsteroidal anti-inflammatory drugs (NSAID), cyclooxygenase-2 (COX-2) inhibitors', higher “priority” to reduce synthesis of the vascular protector, prostacyclin (PGI2), compared to ... ...

Abstract	AIM: Our aim is to understand the molecular mechanisms of the selective nonsteroidal anti-inflammatory drugs (NSAID), cyclooxygenase-2 (COX-2) inhibitors', higher “priority” to reduce synthesis of the vascular protector, prostacyclin (PGI2), compared to that of nonselective NSAIDs. MAIN METHODS: COX-1 or COX-2 was co-expressed with PGI2 synthase (PGIS) in COS-7 cells. The Km and initial velocity (½t Vmax) of the coupling reaction between COX-1 and COX-2 to PGIS were established. The experiment was further confirmed by a kinetics study using hybrid enzymes linking COX-1 or COX-2 to PGIS. Finally, COX-1 or COX-2 and PGIS were respectively fused to red (RFP) and cyanic (CFP) fluorescence proteins, and co-expressed in cells. The distances between COXs and PGIS were compared by FRET. KEY FINDINGS: The Km for converting arachidonic acid (AA) to PGI2 by COX-2 coupled to PGIS is ~2.0μM; however, it was 3-fold more (~6.0μM) for COX-1 coupled to PGIS. The Km and ½t Vmax for COX-2 linked to PGIS were ~2.0μM and 20s, respectively, which were 2–5 folds faster than that of COX-1 linked to PGIS. The FRET study found that the distance between COX-2-RFP and PGIS–CFP is shorter than that between COX-1-RFP and PGIS–CFP. SIGNIFICANCE: The study provided strong evidence suggesting that the low Km, faster ½t Vmax, and closer distance are the basis for COX-2 dominance over COX-1 (coupled to PGIS) in PGI2 synthesis, and further demonstrated the mechanisms of selective COX-2 inhibitors with higher potential to reduce synthesis of the vascular protector, PGI2.
Keywords	arachidonic acid ; biosynthesis ; fluorescent proteins ; heart diseases ; nonsteroidal anti-inflammatory agents ; prostacyclin ; prostaglandin synthase ; prostaglandin-I synthase ; risk
Language	English
Dates of publication	2011-0103
Size	p. 24-30.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2010.10.017
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A profile of NSAID-targeted arachidonic acid metabolisms in human embryonic stem cells (hESCs): implication of the negative effects of NSAIDs on heart tissue regeneration.

Chillar, Annirudha / So, Shui-Ping / Ruan, Cheng-Huai / Shelat, Harnath / Geng, Yong-Jian / Ruan, Ke-He

International journal of cardiology

2011 Volume 150, Issue 3, Page(s) 253–259

Abstract: Introduction: An emerging technology using human embryonic stem cells (hESCs) to regenerate infarcted heart tissue has been underdeveloped. However, because non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, are taken during the infarction, ...

Abstract	Introduction: An emerging technology using human embryonic stem cells (hESCs) to regenerate infarcted heart tissue has been underdeveloped. However, because non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, are taken during the infarction, it becomes critical to know whether the NSAIDs have negative impacts on heart tissue regeneration when using hESCs. Methods: Mass spectrometry (LC/MS/MS) and high performance liquid chromatography (HPLC) analyses were used to analyze the functional presence of the elaborate prostanoids' biosynthesis and signaling systems in hESCs. The detected endogenous arachidonic acid (AA) released in the hESC membranes reflects the activity of phospholipase which directly controls the biosyntheses of the prostanoids. Results: The complete inhibition of the endogenous prostaglandin E(2) (PGE(2)) biosynthesis by the cyclooxygenase-2 (COX-2) inhibitor, NS398, confirmed that the major prostanoids synthesized in the hESCs are mediated by the COX-2 enzyme. We also found that PGE(2) and the prostacyclin (PGI(2)) metabolite, 6-keto-PGF(1α), are present in the undifferentiated hESCs. Conclusion: This indicated different cyclooxygenase (COX)-downstream synthases and metabolizing enzymes are involved in the AA products' signaling through the COX-1 and COX-2 pathways. The presence of many enzymes' and receptors' [(COX-1, COX-2, microsomal prostaglandin E synthase (mPGES), cytosolic prostaglandin E synthase (cPGES), prostaglandin I synthase (PGIS), the PGE(2) subtype receptors (EP(1), EP(2), and EP(4)) and the prostacyclin receptor (IP)] involvement in the prostanoid biosynthesis and activity was confirmed by western blot. The studies implied the negative effects of NSAIDs, such as aspirin and COX-2 inhibitors, which suppress prostanoid production during tissue regeneration for infarcted heart when using hESCs.
MeSH term(s)	Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Arachidonic Acid/antagonists & inhibitors ; Arachidonic Acid/metabolism ; Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cells, Cultured ; Drug Delivery Systems/methods ; Embryonic Stem Cells/drug effects ; Embryonic Stem Cells/metabolism ; Feeder Cells/drug effects ; Feeder Cells/metabolism ; Growth Inhibitors/adverse effects ; Heart/drug effects ; Heart/physiology ; Humans ; Prostaglandins/biosynthesis ; Regeneration/drug effects ; Regeneration/physiology
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Growth Inhibitors ; Prostaglandins ; Arachidonic Acid (27YG812J1I)
Language	English
Publishing date	2011-08-04
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	779519-1
ISSN	1874-1754 ; 0167-5273
ISSN (online)	1874-1754
ISSN	0167-5273
DOI	10.1016/j.ijcard.2010.04.015
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Article ; Online: A strategy using NMR peptide structures of thromboxane A2 receptor as templates to construct ligand-recognition pocket of prostacyclin receptor.

Ruan, Cheng-Huai / Wu, Jaixin / Ruan, Ke-He

BMC biochemistry

2005 Volume 6, Page(s) 23

Abstract: Background: Prostacyclin receptor (IP) and thromboxane A2 receptor (TP) belong to rhodopsin-type G protein-coupling receptors and respectively bind to prostacyclin and thromboxane A2 derived from arachidonic acid. Recently, we have determined the ... ...

Abstract	Background: Prostacyclin receptor (IP) and thromboxane A2 receptor (TP) belong to rhodopsin-type G protein-coupling receptors and respectively bind to prostacyclin and thromboxane A2 derived from arachidonic acid. Recently, we have determined the extracellular loop (eLP) structures of the human TP receptor by 2-D 1H NMR spectroscopy using constrained peptides mimicking the individual eLP segments. The studies have identified the segment along with several residues in the eLP domains important to ligand recognition, as well as proposed a ligand recognition pocket for the TP receptor. Results: The IP receptor shares a similar primary structure in the eLPs with those of the TP receptor. Forty percent residues in the second eLPs of the receptors are identical, which is the major region involved in forming the ligand recognition pocket in the TP receptor. Based on the high homology score, the eLP domains of the IP receptor were constructed by the homology modeling approach using the NMR structures of the TP eLPs as templates, and then configured to the seven transmembrane (TM) domains model constructed using the crystal structure of the bovine rhodopsin as a template. A NMR structure of iloprost was docked into the modeled IP ligand recognition pocket. After dynamic studies, the segments and residues involved in the IP ligand recognition were proposed. A key residue, Arg173 involved in the ligand recognition for the IP receptor, as predicted from the modeling, was confirmed by site-directed mutagenesis. Conclusion: A 3-D model of the human IP receptor was constructed by homology modeling using the crystal structure of bovine rhodopsin TM domains and the NMR structures of the synthetic constrained peptides of the eLP domains of the TP receptor as templates. This strategy can be applied to molecular modeling and the prediction of ligand recognition pockets for other prostanoid receptors.
MeSH term(s)	Amino Acid Sequence ; Animals ; Binding Sites/physiology ; COS Cells ; Cattle ; Cercopithecus aethiops ; Humans ; Ligands ; Models, Molecular ; Molecular Sequence Data ; Nuclear Magnetic Resonance, Biomolecular/methods ; Receptors, Epoprostenol/chemistry ; Receptors, Epoprostenol/genetics ; Receptors, Epoprostenol/metabolism ; Receptors, Thromboxane A2, Prostaglandin H2/chemistry ; Receptors, Thromboxane A2, Prostaglandin H2/genetics ; Receptors, Thromboxane A2, Prostaglandin H2/metabolism ; Sequence Analysis, Protein/methods ; Templates, Genetic
Chemical Substances	Ligands ; Receptors, Epoprostenol ; Receptors, Thromboxane A2, Prostaglandin H2
Language	English
Publishing date	2005-11-04
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2041216-2
ISSN	1471-2091 ; 1471-2091
ISSN (online)	1471-2091
ISSN	1471-2091
DOI	10.1186/1471-2091-6-23
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Article ; Online: Prostacyclin therapy for pulmonary arterial hypertension.

Ruan, Cheng-Huai / Dixon, Richard A F / Willerson, James T / Ruan, Ke-He

Texas Heart Institute journal

2010 Volume 37, Issue 4, Page(s) 391–399

Abstract: In pulmonary arterial hypertension, the blood vessels that carry blood between the heart and lungs are constricted, making it difficult for the heart to pump blood through the lungs. Prostacyclin, a prostanoid metabolized from endogenous arachidonic acid ...

Abstract	In pulmonary arterial hypertension, the blood vessels that carry blood between the heart and lungs are constricted, making it difficult for the heart to pump blood through the lungs. Prostacyclin, a prostanoid metabolized from endogenous arachidonic acid through the cyclooxygenase (COX) pathway, is a potent vasodilator that has been identified as one of the most effective drugs for the treatment of pulmonary arterial hypertension. Currently, prostacyclin and its analogues are widely used in the clinical management of pulmonary arterial hypertension patients. However, the mortality rate associated with pulmonary arterial hypertension has not been significantly reduced within the past 5 years. More powerful therapeutic approaches are needed. This article briefly reviews the current management of pulmonary arterial hypertension to identify the problems associated with present therapies; then it focuses on the emerging technology of prostacyclin synthase gene therapy and cell-based therapy using native stem cells and engineered stem cells with enhanced prostacyclin production capacity. By using the recent advances in technology and the molecular understanding of prostacyclin synthesis, researchers are prepared to make significant advances in the treatment of pulmonary arterial hypertension.
MeSH term(s)	Antihypertensive Agents/adverse effects ; Antihypertensive Agents/therapeutic use ; Blood Pressure/drug effects ; Cytochrome P-450 Enzyme System/genetics ; Cytochrome P-450 Enzyme System/metabolism ; Epoprostenol/adverse effects ; Epoprostenol/metabolism ; Epoprostenol/therapeutic use ; Genetic Therapy/methods ; Humans ; Hypertension, Pulmonary/diagnosis ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/physiopathology ; Hypertension, Pulmonary/therapy ; Intramolecular Oxidoreductases/genetics ; Intramolecular Oxidoreductases/metabolism ; Pulmonary Artery/drug effects ; Pulmonary Artery/physiopathology ; Stem Cell Transplantation ; Stem Cells/metabolism ; Treatment Outcome ; Vasodilator Agents/adverse effects ; Vasodilator Agents/therapeutic use
Chemical Substances	Antihypertensive Agents ; Vasodilator Agents ; Cytochrome P-450 Enzyme System (9035-51-2) ; Epoprostenol (DCR9Z582X0) ; Intramolecular Oxidoreductases (EC 5.3.-) ; prostacyclin synthetase (EC 5.3.99.4)
Language	English
Publishing date	2010-09-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604761-0
ISSN	1526-6702 ; 0730-2347
ISSN (online)	1526-6702
ISSN	0730-2347
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