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

Tubular uptake of ferritin given intravenously was studied in the right and left kidneys of 74 Goldblatt-hypertensive rats. Previous observations pointed out the pathologically enhanced permeability of glomerular barrier as the cause of the phenomenon. It was assumed, that the extent of tubular areas taking up ferritin, refers to the number of damaged glomeruli. The process was characterized semiquantitatively by planimetric measurements and determination of the non-hemin iron concentration in the renal cortical tissue. A more frequent and extensive tubular ferritin-uptake (and glomerular damage) was bilaterally recorded in the kidneys of malignant hypertensive rats in comparison to the benign ones. The development of the phenomenon in the clamped kidneys, being defended from high blood pressure, suggests a humoral factor behind the enhanced glomerular permeability. Saline intake has a beneficial effect on the glomerular damage similar to the hypertensive angiopathy.
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PMID:Renal tubular ferritin-uptake, a consequence of the increased glomerular permeability, during the benign and malignant course of renal hypertension in rats. 42 54

Sera from two patients with granulocytopenia associated with collagen vascular disease caused the destruction of normal human granulocytes by autologous lymphocytes in vitro. Granulocyte cytotoxicity was measured by the release of 51Cr during incubation with test sera and lymphocytes in microtiter plates. Between 8% and 46% granulocytoxicity was produced in granulocytes from 8 normal donors by the sera from these two patients. Less than 6% granulocytotoxicity was seen with the sera from 14 normal subjects and 29 patient controls. Treatment of lymphocyte preparations with carbonyl iron and magnetic separation to remove phagocytic cells or treatment with complement-coated red cells followed by repeated gradient centrifugation to remove complement receptor-bearing lymphocytes did not reduce the granulocytotoxicity. There was a dose-response relationship between the concentration of positive sera and granulocytotoxicity. When these sera were fractionated by Sephadex G-200 gel filtration and by ion-exchange chromatography with DEAE-cellulose, the active component appeared in the IgG-containing fractions. Thus, IgG antibody-dependent, lymphocyte-mediated granulocyte cytotoxicity represents a means of detecting human granulocyte antibodies and is a possible mechanism of autoimmune neutropenia in these two patients.
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PMID:Antibody-dependent lymphocyte-mediated granulocyte cytotoxicity in man. 61 59

Electron probe microanalysis demonstrates the presence of aluminium, magnesium, iron, calcium, phosphorus in and around blood vessels in the pallidum (vascular siderosis) and in the putaminal parenchyma in five out of six cases of striatonigral degeneration, associated with orthostatic hypotension in two of these cases. These results suggest that striatonigral degeneration could be the result of a vascular disease, the result of an elemental intoxication of unknown cause.
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PMID:[Presence of aluminum and magnesium in the cerebral arteries and parenchyma of patients with striatonigral syndrome: study by Castaing's microprobe]. 82 52

Cerebral infarction in children is often caused by intracranial vascular disorder, cardiac disease, head injury, or infection, and is rarely induced by blood disease. In this paper, we describe an infantile case of cerebral infarction associated with thrombocytosis. A female infant of eight months of age developed left hemiparesis after a slight head injury. Her CT and MRI demonstrated a cerebral infarction located from the right internal capsule to the right corona radiata. Laboratory findings revealed iron-deficiency anemia and thrombocytosis with a platelet count 107.5 x 10(4)/mm3. Although she had no disorder that had caused iron deficiency, serum Fe value of the patient was low with a count of 18 micrograms/dl. Her bone marrow was normal except for a slight increase in the number of megakaryocytes. One month later, her anemia was improved by means of oral iron replacement. However, her platelet count remained at more than 100 x 10(4)/mm3 as it had been before. Her condition of left-sided hemiparesis gradually improved by a program of rehabilitation, and did not recur after aspirin administration. Although the main cause of her thrombocytosis that led to a transient cerebrovascular accident is obscure, it is postulated that her iron deficiency anemia induced secondary thrombocytosis, or else the patient had essential thrombocytosis.
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PMID:[An infantile case of cerebral infarction associated with thrombocytosis]. 159 Oct 25

In Alzheimer's dementia (AD) the Primum Movens is Amyloid (AM) production on precapillaries: Dyshoric Angiopathy, and capillaries: Senile Plaques (SP) producing Blood-Brain-Barrier (BBB) disturbances, entry in the brain of toxic metals which displace the zinc. Cerebral AM alone may be asymptomatic. Clinical symptoms (Amnesia, Instrumental Disorders) appear when AM induces Neighbouring neuritic alterations: Paired Hellical Filaments (PHF) and Distant neuronal body lesions: Neurofibrillary Tangles (NFT). The AM is coded by a locus on the chromosome 21 and a duplication of this locus should be the etiology of cerebral AM in AD. In AD cerebral zinc decreases particularly in the hippocampus. The zinc-enzyme Superoxyde-Dismutase (SOD) is coded by a locus also on the chromosome 21 near AM and the plasma level of SOD is high in AD. Zinc deposits observed in capillary AM-SP, result probably from the excess of plasmatic SOD. Other metals: Iron, aluminium are also observed in the AM-SP and their excess in the brain may be related to the decrease of zinc by metal to metal displacement. The decrease of functional zinc in the brain may interfere in the pathogenesis of PHF-NFT by metalotoxicity, neighbouring and distant to AM. Without AM, NFT are produced also by metalotoxicity and therefore brain zinc displacement. a) by lead: Encephalopathia saturnica b) by many metals: Guam Encephalopathy c) by aluminium d) by BBB disturbances leading probably to an abnormal entry of metals in the brain (Dementia Pugilistica, viral encephalitides). NFT may be produced by the deficiency of the following zinc enzymes: 1. Those of DNA metabolism, indicating abnormal DNA and therefore abnormal protein synthesis: PHF-NFT. 2. Those of neuronal detoxication: SOD, Carbonic Anhydrase, Lactate Dehydrogenase leading to neuronal toxicity particularly in the hippocampus normally rich in SOD. 3. Of Glutamate (GLU) Dehydrogenase (GDH) resulting in an excitotoxic increase of GLU. 4. Those of the metabolism of neurotransmitters (NT): neuropeptides, Histamine, GABA, Acetylcholine. Therapeutic proposition: a zinc complex crossing the BBB should be useful a) to prevent that the AM produces PHF-NFT by Neighbouring and Distant metalotoxicity and DNA changes; b) to regularise zinc-enzymes of neuronal detoxification and of neurotransmitters metabolisms. Preliminary trials by zinc Aspartate give yet promising results.
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PMID:[Alzheimer's dementia and zinc]. 170 60

Brain is a logical target of free radical damage, considering the large lipid content of myelin sheaths and the high rate of brain oxidative metabolism. Thus, the hypothesis that free radicals may be involved in the pathogenesis of certain CNS diseases has gained increasing popularity in recent years. In CNS ischemia-reperfusion injury, the role of free radicals appears to be well established, however, involvement of other factors, such as excitatory amino acids and prostaglandins, may also contribute to the production of neuronal necrosis following ischemia. Liberation of free iron appears to play a crucial role in the generation of reactive oxygen species in posttraumatic epilepsy. Although there is no direct evidence to indicate free radical involvement in the pathogenesis of Alzheimer's disease, brain trauma with release of iron, amyloid angiopathy and disturbances in blood-brain barrier function all appear to contribute to the development of ischemic episodes with free radical generation and neuronal degeneration. In Parkinson's disease, the substantia nigra appears to be under oxidative stress as evidenced by the findings of increased lipid peroxidation, reduced GSH levels, high concentration of iron and free radical generation via autocatalytic mechanisms within neuromelanin-containing catecholaminergic neurons. Regardless of the initial insult, a cascade of events involving both reactive oxygen radicals and mitochondrial metabolism is likely to contribute to cell injury.
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PMID:Oxygen, antioxidants and brain dysfunction. 837 80

This article reviews our current understanding of the mechanisms of low-density lipoprotein (LDL) oxidation and the potential role of oxidized lipoproteins in atherosclerosis. Studies in hypercholesterolemic animal models indicate that oxidation of LDL is likely to play an important role in atherogenesis. Epidemiological investigations further suggest that the dietary intake of antioxidants is inversely associated with the risk of vascular disease, suggesting that oxidized LDL may be important in human atherosclerosis. By activating inflammatory events, oxidized lipoproteins may contribute to all stages of the atherosclerotic process. Lipoprotein oxidation is promoted by several different systems in vitro, including free and protein-bound metal ions, thiols, reactive oxygen intermediates, lipoxygenase, peroxynitrite, and myeloperoxidase. Intracellular proteins that bind iron or regulate iron metabolism might also play an important role. The physiologically relevant pathways have yet to be identified, however. We assess recent findings on the effects of antioxidants in vivo and suggest potential strategies for inhibiting oxidation in the vessel wall.
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PMID:The role of oxidized lipoproteins in atherogenesis. 872 15

Polyvinylpyrrolidone (PVP), formerly a plasma expander, has continued to be inappropriately used in Taiwan for intravenous injection as a "blood tonic." Five cases of PVP storage disease with cutaneous involvement were studied. Two patients presented with cutaneous eruptions mimicking collagen vascular disease and chronic pigmented purpuric dermatosis. Two other cases were found incidentally: one was with a metastatic tumor and the other in a pemphigus lesion. The fifth case was seen in a blind skin biopsy specimen taken to exclude Niemann-Pick disease after hematologic examination of a bone marrow smear. The latter patient and the patient with a collagen vascularlike disease also had severe anemia and serious orthopedic and neurologic complications due to massive infiltration of PVP-containing cells in the bone marrow with destruction of the bone. Severe irreversible anemia due to PVP storage disease has not been reported before. Three patients admitted having a history of receiving intravenous injection of PVP. The samples obtained from two of them indeed contained 5% PVP as determined by chemical analysis. PVP storage disease can be diagnosed by its histopathologic features. The skin biopsy specimens all showed a variable number of characteristic blue-gray vacuolated cells around blood vessels and adnexal structures with positive tinctorial reactions to mucicarmine, colloidal iron, and alkaline Congo red and negative to periodic acid-Schiff (PAS) and alcian blue. The PVP storage cells were shown to be CD68+ macrophages. The presence of PVP in the skin induced little or no inflammatory reaction. Only the pelvic mass in one patient had a foreign body granuloma formation. Our study showed that systemic parenteral administration of PVP preparation could result in the accumulation of PVP storage cells in the skin, with or without clinical eruptions. The diagnosis of systemic PVP storage disease can be established by performing a skin biopsy for pathologic study. It is important for pathologists and clinicians to be aware of this iatrogenic storage disease to avoid misdiagnosis for hereditary storage disease, osteomyelitis, or signet-ring cell carcinoma. Serious hematologic and orthopedic complications can be caused by repeated massive intravenous injection of PVP. Therefore, PVP preparations should be strictly prohibited for systemic administration.
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PMID:Cutaneous involvement in polyvinylpyrrolidone storage disease: a clinicopathologic study of five patients, including two patients with severe anemia. 935 74

Background-Homozygosity for a relatively common Cys282Tyr mutation of the human hemochromatosis-associated (HFE) gene was recently found to account for most cases of hereditary hemochromatosis. Because excess iron has been postulated to enhance risk of vascular disease, we studied whether occurrence of this mutation was associated with increased risk of first acute myocardial infarction in healthy middle-aged men in a prospective cohort study. Methods and Results-Study subjects were the 1150 participants in the population-based Kuopio Ischemic Heart Disease Risk Factor Study (KIHD), aged 42, 48, 54, or 60 years at baseline, who had no coronary heart disease at baseline and for whom a DNA sample was available. Information about myocardial infarctions was collected prospectively by use of FINMONICA (FINnish MONItoring of trends and determinants in CArdiovascular disease study) and hospital data. Events were classified by MONICA (MONItoring of trends and determinants in CArdiovascular disease study) diagnostic criteria. The HFE Cys282Tyr mutation was assayed by a solid-phase minisequencing technique. One subject was homozygous and 76 individuals were heterozygous for the HFE Cys282Tyr mutation (6.7%). During a mean follow-up of 9 years, 8 (10.4%) of 77 carriers and 60 (5.6%) of 1073 noncarriers experienced an acute myocardial infarction. In a Cox proportional hazards model allowing for the other strongest risk factors, the carriers had a 2.3-fold (95% CI 1. 1 to 4.8; P=0.03) risk of acute myocardial infarction compared with noncarriers. Conclusions-Male carriers of the common hemochromatosis gene mutation are at 2-fold risk for first acute myocardial infarction compared with noncarriers.
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PMID:Increased risk of acute myocardial infarction in carriers of the hemochromatosis gene Cys282Tyr mutation : a prospective cohort study in men in eastern Finland. 1049 67

Free radical are highly reactive chemical species with an unpaired electron in an atomic or molecular orbital. In biological systems, the most important free radicals are superoxide anion and hydrogen peroxide; in the presence of transition metals such as iron, copper and manganese both these free radicals produce hydroxyl radicals. Free radicals attack proteins, nuclei acids and membranes containing large quantities of polyunsaturated fatty acids. Because of their toxicity, the organism has developed ways to deactivate them. The superoxide dismutase enzyme (SOD) catalyzes dismutation of the superoxide radical into hydrogen peroxide and oxygen hydrogen peroxide is in turn reduced to water and oxygen by peroxidase glutathione and catalase enzymes. The production of radicals in the brain is due to catecholamine metabolism such as dopamine and norepinephrine and is increased by the presence of transition metals and by a deficiency of antioxidant agents such as vitamin E. Two main groups of dementia exist in older age: the multi-infarctual dementias, caused by cerebrovascular disorders and the primary degenerative disorders such as Alzheimer, where no vascular disease is evident. Free radicals play an important role in Parkinson's disease, in Alzheimer's disease and in stroke. The value of SOD and CAT activity following the above mentioned degenerative diseases differ among the various studies carried out. In Alzheimer's disease, the value of SOD activity probably increases in the neuropathologically involved areas. In stroke, the SOD value does not vary either in the ischemic area or in the peri-infarctual one during the first 24 hrs after lesion, while the CAT value decreases.
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PMID:Free radicals: important cause of pathologies refer to ageing. 1070 16


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