You will be shown an abstract from a biomedical research paper. Given this abstract, your task is to extract all unique entities of the following types: ["HealthCareActivity", "InjuryOrPoisoning", "BodySubstance", "IntellectualProduct", "AnatomicalStructure", "SpatialConcept", "Chemical", "Bacterium", "MedicalDevice", "Organization", "BiomedicalOccupationOrDiscipline", "Finding", "BiologicFunction", "Virus", "ResearchActivity", "ClinicalAttribute", "PopulationGroup", "Eukaryote", "BodySystem", "Food", "ProfessionalOrOccupationalGroup"].

Please return the output as a JSON object of the format: {"Virus": ["HIV", ...], "Bacterium": ["MRSA", ...], "AnatomicalStructure": ["Lung", ...], "BodySystem": ["CNS", ...], "BodySubstance": ["Serum", ...], "Finding": ["Headache", ...], "InjuryOrPoisoning": ["Fracture", ...], "BiologicFunction": ["Death", ...], "HealthCareActivity": ["Biopsy", ...], "ResearchActivity": ["Clinical trial", ...], "MedicalDevice": ["Lenses", ...], "SpatialConcept": ["Camps", ...], "BiomedicalOccupationOrDiscipline": ["Forensic medicine", ...], "Organization": ["WHO", ...], "ProfessionalOrOccupationalGroup": ["Provider", ...], "PopulationGroup": ["Swimmers", ...], "Chemical": ["Gold", ...], "Food": ["Rice", ...], "IntellectualProduct": ["RPAM", ...], "ClinicalAttribute": ["Biomarker", ...], "Eukaryote": ["Dogs", ...]}. The keys should be entity types and values should be lists of extracted entities belonging to the corresponding type. If you cannot find entities belonging to a specific type, the value should be [].

Only output the JSON object and do not include any additional text.

Abstract:

Vascular smooth muscle cell peroxisome proliferator-activated receptor γ protects against endothelin-1 - induced oxidative stress and inflammation Peroxisome proliferator-activated receptor γ (PPARγ) agonists reduce blood pressure and vascular injury in hypertensive rodents. Pparγ inactivation in vascular smooth muscle cells (VSMC) enhances vascular injury. Transgenic mice overexpressing endothelin (ET)-1 selectively in the endothelium (eET-1) exhibit endothelial dysfunction, increased oxidative stress and inflammation. We hypothesized that inactivation of the Pparγ gene in VSMC (smPparγ) would exaggerate ET-1 - induced vascular injury. eET-1, smPparγ and eET-1 / smPparγ mice were treated with tamoxifen for 5 days and studied 4 weeks later. SBP was higher in eET-1 and unaffected by smPparγ inactivation. Mesenteric artery vasodilatory responses to acetylcholine were impaired only in smPparγ. N-Nitro-L-arginine methyl ester abrogated relaxation responses, and the Ednra / Ednrb mRNA ratio was decreased in eET-1 / smPparγ, which could indicate that nitric oxide production was enhanced by ET-1 stimulation of endothelin type B receptors. Mesenteric artery media / lumen was greater only in eET-1 / smPparγ. Mesenteric artery reactive oxygen species increased in smPparγ and were further enhanced in eET-1 / smPparγ. Perivascular fat monocyte / macrophage infiltration was higher in eET-1 and smPparγ and increased further in eET-1 / smPparγ. Spleen CD11b cells were increased in smPparγ and further enhance d in eET-1 / smPparγ, whereas Ly-6C monocytes increased in eET-1 and smPparγ but not in eET-1 / smPparγ. Spleen T regulatory lymphocytes increased in smPparγ and decreased in eET-1, and decreased further in eET-1 / smPparγ. VSMC Pparγ inactivation exaggerates ET-1 - induced vascular injury, supporting a protective role for PPARγ in hypertension through modulation of pro-oxidant and proinflammatory pathways. Paradoxically, ET-1 overexpression preserved endothelial function in smPparγ mice, presumably by enhancing nitric oxide through stimulation of endothelin type B receptors.
{"AnatomicalStructure": ["Ednra", "Ly-6C monocytes", "smPpar\u03b3", "fat monocyte", "vascular smooth muscle cells", "Ppar\u03b3 gene", "endothelial", "macrophage", "T regulatory lymphocytes", "endothelium", "Ednrb", "Spleen", "Mesenteric artery", "VSMC", "Vascular smooth muscle cell"], "Bacterium": [], "BiologicFunction": ["blood pressure", "inactivation", "inflammation", "vasodilatory", "overexpression", "endothelial dysfunction", "infiltration", "overexpressing", "hypertension", "pathways", "oxidative stress"], "BiomedicalOccupationOrDiscipline": [], "BodySubstance": [], "BodySystem": [], "Chemical": ["reactive oxygen species", "smPpar\u03b3", "pro-oxidant", "acetylcholine", "peroxisome proliferator-activated receptor \u03b3", "eET-1", "endothelin type B receptors", "tamoxifen", "endothelin-1", "Ppar\u03b3", "(eET-1)", "agonists", "Peroxisome proliferator-activated receptor \u03b3", "endothelin (ET)-1", "mRNA", "PPAR\u03b3", "N-Nitro-L-arginine methyl ester", "ET-1", "nitric oxide"], "ClinicalAttribute": ["SBP"], "Eukaryote": ["mice", "rodents", "Transgenic mice"], "Finding": ["treated", "hypertensive"], "Food": [], "HealthCareActivity": [], "InjuryOrPoisoning": ["vascular injury"], "IntellectualProduct": [], "MedicalDevice": [], "Organization": [], "PopulationGroup": [], "ProfessionalOrOccupationalGroup": [], "ResearchActivity": ["studied"], "SpatialConcept": ["modulation", "Perivascular"], "Virus": []}