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Query: UMLS:C0004153 (
atherosclerosis
)
77,401
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The aims in this study were designed to clarify the contents of calcium (Ca), phosphorus (P) and
aluminum
(Al) in central nervous system (CNS), liver and kidney of rabbits with
atherosclerosis
experimentally induced by cholesterol-rich diet, and investigate scavenger effect of 14-ethoxycarbonyl-(3 alpha, 16 alpha-ethyl)-14,15-eburnamenine (vinpocetine) on the deposition of these elements in CNS and soft tissues of experimental
atherosclerosis
. Sixteen male rabbits were divided into 4 groups. Each group was fed with standard diet (Group A), standard diet containing 1.5% cholesterol (Group B), standard diet containing 1.5% cholesterol plus oral administration of 3 mg/kg/day vinpocetine (Group C), and standard diet containing 1.5% cholesterol plus administration of 10 mg/kg/day vinpocetine (Group D). After 3 months' feeding, experimental
atherosclerosis
was produced with a modified method of Kritchevsky et al in rabbits of Groups B, C and D. Blood was collected by cardiocentesis under the anesthesia of ether and then rabbits sacrificed to remove CNS and other tissues. The blood was stood for 1 hour at room temperature and separated by centrifugation at 3000 rpm for 10 min to determine serum total cholesterol, phospholipids, HDL-cholesterol, peroxide lipid, NEFA and calcium levels. Ca, P and Al contents in the frontal lobe, pons, cerebellum, spinal cord, liver and kidney were determined by neutron activation analysis. Ca contents of CNS, liver and kidney in Group B significantly increased than those of Group A (p less than 0.01), and significantly decreased in Groups C and D compared with those of Group B (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Contents of calcium, phosphorus and aluminum in central nervous system, liver and kidney of rabbits with experimental atherosclerosis--scavenger effects of vinpocetine on the deposition of elements]. 239 Mar 64
Magnesium--
aluminum
(Mg--Al) alloy wire was surgically implanted in the abdominal aorta and carotid and renal arteries of virgin (no arterial disease) and breeder (testicular and ovarian arterial lesions) spontaneously hypertensive rats (SHR). The Mg--Al implants promptly dissolved causing increased adrenal glandular weight, thymic involution, depression of the abnormally elevated blood pressure, and poor growth. Serum enzymes (CPK, SGOT, SGPT and LDH) were elevated, circulating levels of triglycerides and cholesterol were reduced, corticosterone and deoxycorticosterone secretion increased. Histologically, fibrocellular, intimal lesions, rich in ground substance, developed about the Mg-Al implants. Occlusive thromboses with cholesterol-positive clefts appeared in the Mg-Al-implanted carotid arteries of breeder SHR with preexisting arterial (limited to gonadal arterioles) disease. It is suggested that adrenocortical and gonadal hormonal factors may condition the responsiveness of the arterial wall of SHR to injury and repair.
Atherosclerosis
1980 Aug
PMID:Pathophysiologic responses of spontaneously hypertensive rats to arterial magnesium--aluminum wire implants. 741 74
A novel in vitro radiographic technique using saline/iodine displacement, which can be used to study the bone-equivalent and soft-tissue-equivalent thicknesses within vessel walls, was applied to imaging of arterial specimens. Results concerning the accuracy and precision of the bone-equivalent and soft-tissue-equivalent thickness measurements obtained with this technique are reported and discussed. Planar radiographs of a phantom were obtained under two different conditions: (1) when it is immersed in an isotonic saline solution using a 45-kVp spectrum with no added filtration, and (2) when it is immersed in a concentrated iodine solution using a 100-kVp spectrum with 12.5-mm
aluminum
-added filtration. Calibration step wedges made out of bone-mimicking and soft-tissue-mimicking materials are imaged simultaneously to generate calibration curves that are used to convert the radiographs into bone-equivalent and total-thickness images. A soft-tissue-thickness image is obtained from the subtraction of the bone-equivalent image from the total-thickness image. Thickness measurements obtained from these images yielded average accuracies of +/- 110 microns for both the bone-equivalent and the soft-tissue-equivalent images. The precision (one standard deviation) of the thickness measurements was +/- 60 and +/- 90 microns for the bone-equivalent and the soft-tissue-equivalent images, respectively. In conclusion, since calcified plaque can become as thick as 3-4 mm, the saline/iodine displacement technique has the potential to be a very useful technique for ex vivo studies of the progression of
atherosclerosis
because of its high accuracy and precision.
...
PMID:X-ray imaging technique for in vitro tissue composition measurements using saline/iodine displacement: experimental verification. 908 86
We performed photodynamic therapy (PDT) using the Yttrium
Aluminium
Garnet-Optical Parametric Oscillated (YAG-OPO) laser in cases of
atherosclerosis
, and examined its efficacy in vivo. We also performed PDT using an Argon-dye (Ar-dye) laser with the same output, and compared the efficacies. Following balloon denudation injury of the thoracoabdominal aorta, rabbits were raised on a cholesterol diet for 16 weeks, producing atheroma in that region. At 24 h following the administration of Photofrin 5 mg/kg, PDT was performed, and animals were sacrificed at 1 day, 1 week, and 2 weeks following the procedure to examine its efficacy. This was compared with the efficacy of PDT using the Ar-dye laser. Following PDT using a YAG-OPO laser, an increase in the vessel lumen was seen due to reduction of the hypertrophic intima and media, without the appearance of inflammatory cells. This result was seen more strongly in PDT using the pulse wave YAG-OPO laser than with the continuous wave Ar-dye laser, affecting not just the intima but also the media. These data demonstrated that PDT can effectively regress atherosclerotic lesions.
...
PMID:Photodynamic therapy of atherosclerosis using YAG-OPO laser and Porfimer sodium, and comparison with using argon-dye laser. 1047 77
Elastin, an abundant structural protein present in the arterial wall, is prone to calcification in a number of disease processes including porcine bioprosthetic heart valve calcification and
atherosclerosis
. The mechanisms of elastin calcification are not completely elucidated. In the present work, we demonstrated calcification of purified elastin in rat subdermal implants (Ca(2+) = 89.73 +/- 9.84 microgram/mg after 21 days versus control, unimplanted Ca(2+) = 0.16 +/- 0.04 microgram/mg). X-ray diffraction analysis along with resolution enhanced FTIR spectroscopy demonstrated the mineral phase to be a poorly crystalline hydroxyapatite. We investigated the time course of calcification, the effect of glutaraldehyde crosslinking on calcification, and mechanisms of inhibition of elastin calcification by pretreatment with
aluminum
chloride (AlCl(3)). Glutaraldehyde pretreatment did not affect calcification (Ca(2+) = 89.06 +/- 17.93 microgram/mg for glutaraldehyde crosslinked elastin versus Ca(2+) = 89.73 +/- 9.84 microgram/mg for uncrosslinked elastin). This may be explained by radioactive ((3)H) glutaraldehyde studies showing very low reactivity between glutaraldehyde and elastin. Our results further demonstrated that AlCl(3) pretreatment of elastin led to complete inhibition of elastin calcification using 21-day rat subdermal implants, irrespective of glutaraldehyde crosslinking (Ca(2+) = 0.73-2.15 microgram/mg for AlCl(3) pretreated elastin versus 89.73 +/- 9.84 for untreated elastin). The AlCl(3) pretreatment caused irreversible binding of
aluminum
ions to elastin, as assessed by atomic emission spectroscopy. Moreover,
aluminum
ion binding altered the spatial configuration of elastin as shown by circular dichroism (CD), Fourier transform infrared (FTIR), and (13)C nuclear magnetic resonance (NMR) spectroscopy studies, suggesting a net structural change including a reduction in the extent of beta sheet structures and an increase in coil-turn conformations. Thus, it is concluded that purified elastin calcifies in rat subdermal implants, and that the AlCl(3)-pretreated elastin completely resists calcification due to irreversible
aluminum
ion binding and subsequent structural alterations caused by AlCl(3).
...
PMID:Elastin calcification and its prevention with aluminum chloride pretreatment. 1048 55
The effects of the administration of coenzyme Q10 (3 mg/kg per day) (group A, n=10) and placebo (
aluminum
hydroxide, 3 mg/kg per day) (group B, n=10) were compared over 24 weeks in a randomized, single-blind, controlled trial. There were two groups of rabbits receiving a trans fatty acid (TFA)-rich diet (5-8 g/day) for 36 weeks. Oxidized rabbit chow with vitamin C plus ferric chloride was administered for 4 weeks in all rabbits. Intervention with coenzyme Q10 after feeding of TFA-rich diet was associated with a significant decline in thiobarbituric acid reactive substances (TBARS), diene conjugates and malondialdehyde, and an increase in plasma levels of vitamin E in the coenzyme Q group compared to placebo group. These changes, which were indicators of a decrease in oxidative damage, were independent of lipid lowering. The aortic and coronary artery plaque sizes, coronary
atherosclerosis
index, aortic and coronary
atherosclerosis
scores were significantly lower in the coenzyme Q group than placebo group. Aortic and coronary plaque frequencies, as well as frequencies of ulceration, thrombosis or hemorrhage, and cracks and fissures, were also significantly lower in the coenzyme Q group, indicating a better quality of atheroma compared to those in the control group. Aortic cholesterol, triglycerides and sudanophilia were significantly lower and vitamin E significantly higher in the coenzyme Q group in comparison to the placebo group indicating that coenzyme Q10 can have beneficial effect on the chemical composition of atheroma. The findings suggest that antioxidant therapy with coenzyme Q10 may be used as an adjunct to lipid lowering for additional beneficial effects related to chemical composition and quality of atheroma independent of hypolipidemic agents.
Atherosclerosis
2000 Feb
PMID:Effect of coenzyme Q10 on experimental atherosclerosis and chemical composition and quality of atheroma in rabbits. 1065 62
Calcification of elastin occurs in many pathological cardiovascular diseases including
atherosclerosis
. We have previously shown that purified elastin when subdermally implanted in rats undergoes severe calcification and
aluminum
chloride (AlCl(3)) pretreatment of elastin inhibits calcification. In the present study we investigated whether matrix metalloproteinase (MMP) binding to elastin and elastin degradation is prevented by AlCl(3) pretreatment. Subdermal implantation of AlCl(3)-pretreated elastin showed significantly lower MMP-9 and MMP-2 activity surrounding the implant as compared to the control implants. AlCl(3) pretreatment also significantly inhibited elastin implant calcification at the seven-day implant period (AlCl(3)-pretreated 4.07 +/- 1.27, control 23.82 +/- 2.24 microg/mg; p<0.0001). Moreover, elastin gel zymography studies showed that gel pretreatment with AlCl(3) inhibited elastolysis by MMP-9. We also demonstrate significant suppression of MMP-2 activity in aortic wall segments of AlCl(3)-pretreated porcine bioprosthetic heart valve implants as compared to control valve implants in sheep mitral valve replacement studies. AlCl(3) pretreatment also significantly inhibited calcification of elastin in this model. Thus, we conclude that
aluminum
ion binding to elastin prevents MMP-mediated elastolysis and thus prevents elastin calcification.
...
PMID:Aluminum chloride pretreatment of elastin inhibits elastolysis by matrix metalloproteinases and leads to inhibition of elastin-oriented calcification. 1173 47
Universally, the general population is exposed to a variety of "toxic" substances. Some of these are from manufactured goods and some from air and water pollution. Toxins are also normally found in many foods; however, unless the exposure is overwhelming, we are many times (even unknowingly) protected by the foods we eat. A judicious choice of food will counteract noxious agents. Therefore, the diet can be a major factor in determining who does and who does not show toxic symptoms following exposure. This review will cover three aspects. The first will be on protectors against metal toxicity. For example, whereas humans can consume fish that have absorbed mercury from contaminated bay water, selenium can act as a natural antagonist for mercury poisoning. (Naturally, too much selenium itself can be detrimental!) Some vegetables can accumulate cadmium from contaminated soil, and zinc from a variety of nuts is an antagonist of cadmium toxicity. Nitrites in preserved meats can be converted into nitroamines by saliva or mild stomach acid. Vitamin C found in oranges and bell peppers can inhibit that conversion. In addition, calcium antagonizes both lead and
aluminum
toxicity. The second aspect is on oxidants and antioxidants. Oxidative stress can lead to some cancers,
atherosclerosis
, and adverse effects of aging. Antioxidants are the best protectors of the damage caused by reactive oxygen species (ROS). The most effective antioxidants are found in highly colored fruits and vegetables such as carrots, tomatoes, and berries, called carotenoids. Flavonoids (polyphenols), another class of effective antioxidants that negate ROS, may or may not be colored. The third aspect is on gaps in current knowledge. Many foods naturally contain chemicals that are, in larger concentrations, quite toxic or carcinogenic. Biotransformations (detoxification mechanisms) involving type I and type II enzymes are known. Some foods do modify these enzymes either positively or negatively. Grapefruit contains a substance that inhibits an isoform of P450, making some cardiac drugs, as substrates, more toxic. There is inadequate information on what specific components are in a variety of foods that are associated with cancer prevention. The experimental carcinogenic compound (and suspected as a human carcinogen) found in overcooked, burnt, and fried meats and fish, namely IQ (2-amino-3-methyl-3H-imidazo[4,5f]quinoline, will be used as a prototype for what needs to be known about foods that will affect toxins.
...
PMID:Can nutrition affect chemical toxicity? 1239 88
A 72-year-old male painter, who complained of his "lungs burning" for 2 weeks, died suddenly. Autopsy examination revealed severe coronary
atherosclerosis
with plaque rupture as the cause of death. Examination of the lungs revealed emphysema, interstitial fibrosis, and multinucleated giant cells with intra- and extracellular brown-black, crystalline, polarizable foreign material. Energy-dispersive X-ray microanalysis showed the material to contain titanium,
aluminum
, silicon, and iron. An increased incidence of respiratory disease has been reported in professional painters. Titanium is widely used as a pigment in the manufacturing of commercial paints. Cases of pneumoconiosis and alveolar proteinosis have been described in painters in which analysis of lung tissue revealed increased levels of titanium. This case is presented as an example of a rarely reported phenomenon, which may have clinical implications for evaluation and management of lung disease in painters.
...
PMID:Titanium particles identified by energy-dispersive X-ray microanalysis within the lungs of a painter at autopsy. 1274 5
Elastin degeneration and calcification occur in many cardiovascular diseases, including medial arterial elastocalcinosis,
atherosclerosis
, and bioprosthetic heart valve mineralization. In the present study, we tested the hypothesis that the onset and progression of elastin-oriented calcification is associated with matrix remodeling and elastin degradation events. We studied whether
aluminum
ions inhibit elastin calcification by reducing elastin degradation and altering remodeling events. Subdermal implantation of pure elastin in juvenile rats resulted in a time-dependent calcification of elastin, reaching high levels 21 days after implantation. In situ hybridization showed that elastin calcification was associated with an up-regulation of matrix metalloproteinase (MMP) mRNA expression, specifically MMP-9 and MMP-2. Gelatin zymography demonstrated increased MMP-9 and MMP-2 enzyme activities in early stages of elastin calcification. Calcified elastin displayed a time-dependent pattern of tenascin-C (TN-C) and alkaline phosphatase (AP) expression. Pretreatment of pure elastin with
aluminum
ions prior to implantation resulted in complete inhibition of elastin calcification.
Aluminum
ion binding to elastin was found to protect elastin against MMP-mediated degradation in vitro. Noncalcified, explanted
aluminum
-pretreated elastin exhibited reduced activities of MMPs. TN-C expression in elastin implants exhibited a time-dependent pattern that was also affected by pretreatment of elastin with
aluminum
ions. In conclusion, elastin calcification is accompanied by matrix remodeling events, and the efficacy of
aluminum
pretreatment in inhibiting elastin calcification may be related in part to its effects on elastin remodeling.
...
PMID:Involvement of matrix metalloproteinases and tenascin-C in elastin calcification. 1508 71
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