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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Excessive production of reactive oxygen species in the vasculature contributes to cardiovascular pathogenesis. Among biologically relevant and abundant reactive oxygen species, superoxide (O2*-) and hydrogen peroxide (H2O2) appear most important in redox signaling. Whereas O2*- predominantly induces endothelial dysfunction by rapidly inactivating nitric oxide (NO*), H2O2 influences different aspects of endothelial cell function via complex mechanisms. This review discusses recent advances establishing a critical role of H2O2 in the development of vascular disease, in particular, atherosclerosis, and mechanisms whereby vascular NAD(P)H oxidase-derived H2O2 amplifies its own production. Recent studies have shown that H2O2 stimulates reactive oxygen species production via enhanced intracellular iron uptake, mitochondrial damage, and sources of vascular NAD(P)H oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS). This self-propagating phenomenon likely prolongs H2O2-dependent pathological signaling in vascular cells, thus contributing to vascular disease development. The latest progress on Nox functions in vascular cells is also discussed [Nox for NAD(P)H oxidases, representing a family of novel NAD(P)H oxidases].
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PMID:NAD(P)H oxidase-dependent self-propagation of hydrogen peroxide and vascular disease. 1586 Jul 62

The reduced antioxidant defense in apolipoprotein E epsilon4/epsilon4 carriers may contribute to beta-amyloidosis. Previously we found that Fe(2+)-induced oxidative stress caused greater protein oxidation in epsilon4/epsilon4 than in epsilon3/epsilon3 human brain vascular smooth muscle cells. Moreover, Fe(2+) induced lysosomal accumulation of endogenous Abeta and APOE in cultured cells, and Abeta deposition in vascular tunica media in organotypic cultures of brain vessels. Here we demonstrated that Fe(2+) enhanced an uptake of exogenous Abeta 1-40 and its deposition together with APOE in lysosomes in myocytes. Abeta deposits were associated with lipid-peroxidation and protein ubiquitination, and were more abundant and stable in epsilon4/epsilon4 than in epsilon3/epsilon3 cells. In organotypic cultures of brain vessels Fe(2+) induced deposition of non-fibrillar and fibrillar Abeta 1-40 in vascular tunica media. We hypothesize that locally increased concentrations of iron induce accumulation of exogenous and endogenous Abeta in SMCs, triggering beta-amyloid angiopathy. The greater susceptibility of epsilon4 carriers to Fe(2+) ions may result in an increased risk of beta-amyloidosis.
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PMID:Induction of vascular amyloidosis-beta by oxidative stress depends on APOE genotype. 1599 87

Brazilian purpuric fever is a severe vascular disease caused by an invasive clone of Haemophilus influenzae biogroup aegyptius, which normally causes self-limiting eye infections. A previous genome subtraction procedure resulted in the isolation of a DNA fragment, which encodes a putative IgA1 protease, specific to the F3031 Brazilian purpuric fever type strain. Cloning and sequencing of the entire F3031 iga1 gene showed that the subtracted DNA fragment encompasses the iga1 region encoding the active site and the cleavage specificity determinant of the protein, which are different from the cognate regions of the proteases produced by other H. influenzae strains. Western and IgA cleavage assays together with clustering analysis showed that the F3031 IgA1 protease is most similar to the type 2 proteases produced by H. influenzae type c and e strains. Analysis of the promoter region of the F3031 iga1 gene revealed the presence of Fur binding sites. However, real-time PCR analysis and transcriptional fusion assays showed that the expression of iga1 is not regulated by iron or hemin under the conditions tested.
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PMID:Characterization of the IgA1 protease from the Brazilian purpuric fever strain F3031 of Haemophilus influenzae biogroup aegyptius. 1608 69

Imaging of endothelial-specific markers is critically important in non-invasive detection of early signs of vascular pathologies (eg inflammation, atherosclerosis and angiogenesis). A model of adoptive human endothelial cell (HUVEC) transfer was used to test-specific imaging probes for human vascular disease consisting of cross-linked iron oxide (CLIO) nanoparticles conjugated to anti-human E-selectin (CLIO-F(ab')(2)). To perform in vivo imaging of E-selectin expression in functional blood vessels, human vascular endothelium cells (HUVECs) were implanted in athymic mice in Matrigel solution, which served as a temporary neovascularization scaffold after the solidification. The formation of HUVEC-containing vessels was established by histology and microscopy. CLIO-F(ab')(2) probes were administered via an i.v. injection following the induction of E-selectin expression by IL-1beta. High-resolution MR images were obtained before and after the administration of CLIO-F(ab')(2), which showed specific hypointensity only if treated with IL-1beta. A three-times higher CLIO-induced MR signal decrease on T2(*) images was measured in HUVEC implants in response to IL-1beta treatment. Image signal intensity did not change in control animals that: (1) harbored Matrigel alone, (2) in the absence of IL-1beta treatment or (3) in animals injected with CLIO linked to the idiotype-matched control F(ab')(2). Experiments in an adoptive transfer model demonstrated that HUVEC-containing neovessels are perfused and that IL-1beta inducible E-selectin expression in these vessels is detectable with non-invasive imaging by using targeted nanoparticles.
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PMID:Targeted imaging of human endothelial-specific marker in a model of adoptive cell transfer. 1660 78

Vascular diseases are characterized by impairment of endothelial-derived nitric oxide (NO) bioactivity and increased vascular levels of hydrogen peroxide (H(2)O(2)). Here we examined the implications of H(2)O(2) for agonist-stimulated endothelial NO bioactivity in rabbit aortic rings and cultured porcine aortic endothelial cells (PAEC). Vessels pre-treated with H(2)O(2) exhibited impaired endothelial-dependent relaxation induced by acetylcholine or calcium ionophore. In contrast, H(2)O(2) had no effect on endothelium-independent relaxation induced by a NO donor, indicating a defect in endothelium-derived NO. This defect was not related to eNOS catalytic activity; treatment of PAEC with H(2)O(2) enhanced agonist-stimulated eNOS activity indicated by increased eNOS phosphorylation at Ser-1177 and de-phosphorylation at Thr-495 and enhanced conversion of [(3)H]-L-arginine to [(3)H]-L-citrulline that was prevented by inhibitors of Src and phosphatidylinositol-3 kinases. Despite activating eNOS, H(2)O(2) impaired endothelial NO bioactivity indicated by attenuation of the increase in intracellular cGMP in PAEC stimulated with calcium ionophore or NO. The decrease in cGMP was not due to impaired guanylyl cyclase as H(2)O(2) treatment increased cGMP accumulation in response to BAY 41-2272, a NO-independent activator of soluble guanylyl cyclase. At concentrations that impaired endothelial NO bioactivity H(2)O(2) increased intracellular oxidative stress and size of the labile iron pool in PAEC. The increase in oxidative stress was prevented by the free radical scavenger's tempol or tiron and the iron chelator desferrioxamine and these antioxidants reversed the H(2)O(2)-induced impairment of NO bioactivity in PAEC. This study shows that despite promoting eNOS activity, H(2)O(2) impairs endothelial NO bioactivity by promoting oxidative inactivation of synthesized NO. The study highlights another way in which oxidative stress may impair NO bioactivity during vascular disease.
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PMID:Hydrogen peroxide restrains endothelium-derived nitric oxide bioactivity -- role for iron-dependent oxidative stress. 1686 1

Recently, a number of medications approved for nondermatologic use have proved useful against dermatologic diseases. This article reviews the dermatologic uses and effects of deferasirox, bortezomib, dasatinib, and cyclosporine eye drops. Deferasirox--an oral iron chelator--could be an effective treatment against porphyria cutanea tarda, hemochromatosis, and pathogens such as mucor that thrive in iron rich environments. Bortezomib, a proteasome inhibitor and multiple myeloma treatment, may be effective against nodular amyloid and has been effectively used against squamous cell carcinoma; although trials demonstrate it is ineffective against metastatic melanoma. Bortezomib has many cutaneous side effects including erythematous plaques or nodules, a generalized morbilliform erythema with ulcerations and fever, purpuric eruptions, leukocytoclastic vasculitis, Sweet's syndrome, and folliculitis. Dasatinib is a multi-targeted tyrosine kinase inhibitor active in vitro against most cell lines containing BCR-ABL mutations that confer resistance to imatinib. Dasatinib is likely to be effective against dermatofibroma sarcoma protuberans and cutaneous acute lymphoblastic leukemia, and has caused panniculitis. Cyclosporine 0.05% ocular emulsion (eye drops) are approved to treat dry eyes including dry eyes caused by collagen vascular disease. Cyclosporine eye drops might also have utility in treating eye pathology of ocular rosacea, atopic keratoconjunctivitis, graft versus host disease, herpes keratitis, chronic sarcoidosis of the conjunctiva, conjunctival manifestations of actinic prurigo, keratitis of keratitis-ichthyosis deafness (KID) syndrome, and lichen planus-related kerato-conjunctivitis. This article speculates that cyclosporine eye drops would also be useful for any disease causing ectropion or eclabion of the eye as well as toxic epidermal necrolysis-related eye pathology (in particular corneal scarring).
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PMID:A review of deferasirox, bortezomib, dasatinib, and cyclosporine eye drops: possible uses and known side effects in cutaneous medicine. 1737 1

This article reviews the changes in bronchoalveolar lavage (BAL) cytology and cell differentials in some of the rarer interstitial lung diseases. In a few of these diseases BAL has a diagnostic value and can replace lung biopsy. In pulmonary Langerhans cell histiocytosis the characteristic diagnostic finding is an increase in CD1 + Langerhans cells greater than 4% of total cells. The sensitivity of this cutoff value is low because only approximately 50% of patients show this elevation. In pulmonary alveolar proteinosis, the sensitivity of a diagnostic BAL is almost 100%, and the characteristic finding of milky and turbid fluid on gross examination and the characteristic findings with acellular globules that stain pink with PAS (periodic-acid-Schiff), along with abnormal foamy macrophages and a characteristic dirty background obviates the need for lung biopsy. In diffuse alveolar hemorrhage, BAL is the method of choice to diagnose the alveolar bleeding by showing free red blood cells and hemosiderin-laden, iron-positive macrophages. The underlying disorder has to be identified by history and clinical and laboratory tests. In eosinophilic lung disease, the diagnosis can be made if the BAL cell differentials show 25% or more eosinophils. In collagen vascular disease-associated lung fibrosis, the precise role of BAL in assessment and monitoring disease remains unclear. In drug-induced interstitial lung disease BAL may support a certain clinical/pathological pattern of lung involvement and is helpful for exclusion of other diseases, such as malignancies with pulmonary metastasis, heart disease with pulmonary congestion, or infections. The same is true for radiation-induced lung injury.
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PMID:Bronchoalveolar lavage in other interstitial lung diseases. 1797 79

Great attention has been placed on the protective role of heme oxygenase-1 (HO-1) for several vascular diseases such as atherosclerosis. HO-1, by exerting anti-inflammatory, antiproliferative, anti-apoptotic and anti-oxidant effects on the vasculature, protects against atherosclerosis. The precise underlying mechanisms for HO-1-based protection are not yet completely understood, but appear to involve the protective effects of HO-1 by-products, carbon monoxide (CO), biliverdin/bilirubin and free iron. Among the HO-1 by-products, CO has been shown to mimic some protective actions of HO-1, specifically, in vascular system. There is evidence supporting that HO-1-derived CO also interacts with other gaseous molecules, such as nitric oxide (NO) and hydrogen sulfide (H2S) that may relate to either vascular protection or injury. CO, NO and H2S not only exert comparable biological actions but also compete with and are antagonists with each other for maintaining vascular homeostasis. This review will highlight the protective roles of HO-1/CO in vascular injury/disease, and emphasize the potential roles of CO in possible interplay among three gaseous molecules, which may be important to explore the overall protective roles of HO-1/CO system in the pathogenesis of human vascular disease.
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PMID:Role of heme oxygenase-1 in vascular disease. 1828 69

The content of total flavone in carthmus tinctorius L in Xinjiang was determined by ultraviolet spectrophotometry with scan from 200 to 400 nm where the maximum absorption wavelength was 267.00 nm. The contents of ten trace elements and constant elements in carthmus tinctorius L including potassium, sodium, calcium, magnesium, iron, chromium, nickel, manganese, copper and zinc were determined by flame atomic absorption spectrophotometry. The results showed that there were comparatively rich trace elements and high total flavone, among which are comparatively high calcium, magnesium, chromium, copper and zinc in carthmus tinctorius L. It provided useful data for discussing the relationship between the content of total flavone and the trace elements in carthmus tinctorius L, and for studing the relationship between the trace elements in carthmus tinctorius L and the cure for cardio-cerebral vascular disease.
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PMID:[Analysis and study of total flavone and trace element in carthmus tinctorius L]. 1842 59

Magnetic resonance imaging (MRI) plays an important role in differentiating idiopathic Parkinson's disease (PD) from its atypical forms. Causes like chronic vascular disease and normal-pressure hydrocephalus are easily visualized. Furthermore, specific atrophy patterns can be found with multi-system atrophies, corticobasal degeneration and progressive supranuclear palsy. In addition the review also deals with specific imaging criteria of other neurodegenerative disorders, such as Wilson's disease, neurodegeneration with iron accumulation in the brain and Huntington's chorea. MRI is of minor importance for differentiating Alzheimer's disease from frontotemporal dementia or dementia with Lewy bodies. However, specific patterns are found in cerebral amyloid angiopathy and prion diseases..
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PMID:[Morphological magnetic resonance imaging: its value for the diagnosis of neurodegenerative diseases]. 1843 37


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