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porphyrin/infarction
Krækjan er vistuð á klemmuspjaldið
Bls 1 frá 31 niðurstöður
Urinary excretion of porphyrin precursors in myocardial infarction.
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Non-invasive Macrophage Tracking Using Novel Porphysome Nanoparticles in the Post-myocardial Infarction Murine Heart.
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We generated a folate-conjugated porphyrin nanoparticle (porphysome) suitable for multimodal non-invasive active macrophage tracking post-myocardial infarction (MI).
Macrophage uptake of folate-conjugated porphysomes was selective. Folate-porphysome cardiac macrophage tracking was detected in vivo
[The mechanisms of the porphyrin conformation of normal blood hemoglobin and in pathology].
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The spectra of resonance Raman scattering of blood in norm and under pathology (myocardial infarction and sepsis), as well after artificial hemotransfusion or UV photomodification have been studied. It has been shown that under heart pathology the structure of hemoglobin porphyrin macrocycle of
Fe Porphyrin-Based SOD Mimic and Redox-Active Compound, (OH)FeTnHex-2-PyP 4+, in a Rodent Ischemic Stroke (MCAO) Model: Efficacy and Pharmacokinetics as Compared to Its Mn Analogue, (H 2 O)MnTnHex-2-PyP 5
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Mn(III) meso-tetrakis(N-n-hexylpyridinium-2-yl)porphyrin, (H2O)MnTnHex-2-PyP5+ (MnHex) carrying long hexyl chains, is a lipophilic mimic of superoxide dismutase (SOD) and a redox-active drug candidate. MnHex crosses the blood-brain barrier, and improved neurologic outcome and
[Long-term effects of heme oxygenase 1 overexpression on post-infarction heart function in diabetic rats].
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OBJECTIVE
To clarify the impact of increased heme oxygenase-1 (HO-1) expression on cardiac function of diabetic rats with myocardial infarction and its mechanism.
METHODS
Sixty adult male Wistar rats were randomly divided into five groups (n = 12): sham operation group (sham), diabetes + sham
Targeting and modulating infarct macrophages with hemin formulated in designed lipid-based particles improves cardiac remodeling and function.
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Uncontrolled activation of pro-inflammatory macrophages after myocardial infarction (MI) accelerates adverse left ventricular (LV) remodeling and dysfunction. Hemin, an iron-containing porphyrin, activates heme oxygenase-1 (HO-1), an enzyme with anti-inflammatory and cytoprotective properties. We
Circulating microparticles from patients with myocardial infarction cause endothelial dysfunction.
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BACKGROUND
Shed membrane microparticles circulate in the peripheral blood of nonischemic (NI) patients and patients with myocardial infarction (MI). We investigated whether or not these microparticles would affect endothelium-dependent responses.
RESULTS
Rat aortic rings with endothelium were
Metallothionein Protects the Heart Against Myocardial Infarction via the mTORC2/FoxO3a/Bim Pathway.
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Aims: Cardiac-specific overexpression of metallothionein (MT) has been shown to be beneficial in ischemic heart disease, but the detailed mechanisms through which MT protects against myocardial infarction (MI) remain unknown. This study assessed the involvement of the mTORC2/FoxO3a/Bim
Rescue of neurons from ischemic injury by peroxisome proliferator-activated receptor-gamma requires a novel essential cofactor LMO4.
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Activation of peroxisome proliferator-activated receptor-gamma (PPARgamma) signaling after stroke may reduce brain injury, but this effect will depend on the levels of receptor and cofactors. Here, we showed that the direct effect of PPARgamma signaling to protect neurons from ischemic injury
Peroxynitrite induces HMGB1 release by cardiac cells in vitro and HMGB1 upregulation in the infarcted myocardium in vivo.
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OBJECTIVE
High-mobility group box 1 (HMGB1) is a nuclear protein actively secreted by immune cells and passively released by necrotic cells that initiates pro-inflammatory signalling through binding to the receptor for advance glycation end-products. HMGB1 has been established as a key inflammatory
Induction of hemeoxygenase-1 expression after inhibition of hemeoxygenase activity promotes inflammation and worsens ischemic brain damage in mice.
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Hemeoxygenase (HO) is an enzymatic system that degrades heme. HO-1 is an inducible isoform whereas HO-2 is constitutive. Stroke strongly induces HO-1 expression but the underlying mechanisms are not fully elucidated. Cytokines that are up-regulated after ischemia, like interleukin (IL)-10, can
Hematuria in rabbits.
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A nine year retrospective study of hematuria in 14 New Zealand White rabbits was conducted to classify possible etiologies of this clinical finding. Physical examination, laboratory tests, radiography and postmortem examination were utilized in most cases to verify the presence of hematuria and to
The new airborne disease. Community air pollution.
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Community air pollution is the new airborne disease of our generation's communities. It is caused by the increasing use of fuel, associated with both affluence and careless waste. Photochemical air pollution of the California type involves newly defined atmospheric reactions, is due mostly to motor
Ischemic preconditioning alters real-time measure of O2 radicals in intact hearts with ischemia and reperfusion.
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Reactive oxygen species (ROS) are believed to be involved in triggering cardiac ischemic preconditioning (IPC). Decreased formation of ROS on reperfusion after prolonged ischemia may in part underlie protection by IPC. In heart models, these contentions have been based either on the effect of ROS
Macrocycles and Supramolecules as Antioxidants: Excellent Scaffolds for Development of Potential Therapeutic Agents
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Oxidative stress due to the high levels of reactive oxygen species (ROS) that damage biomolecules (lipids, proteins, DNA) results in acute inflammation. However, without proper intervention, acute inflammation progresses to chronic inflammation and then to several chronic diseases, including cancer,
Heillasta gagnagrunnur lækningajurtanna sem studdur er af vísindum
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Sláðu inn einkenni eða sjúkdóm og lestu um jurtir sem gætu hjálpað, sláðu jurt og sjáðu sjúkdóma og einkenni sem hún er notuð við.
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