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Biomedical subjects

A Mortensen

Publications and source records attributed to A Mortensen.

At least 19 recordsLinked to original sources
PubMed2006

Observation of three-dimensional long-range order in small ion coulomb crystals in an rf trap.

Three-dimensional long-range ordered structures in smaller and near-spherically symmetric Coulomb crystals of (40)Ca(+) ions confined in a linear rf Paul trap have been observed when the number of ions exceeds approximately 1,000 ions. This result is unexpected from ground state molecular dynamics (MD) simulations, but found to be in agreement with MD simulations of metastable ion configurations. Previously, three-dimensional long-range ordered structures have only been reported in Penning traps in systems of approximately 50,000 ions or more.

Journal Article↗
PubMed2004

Nondestructive identification of cold and extremely localized single molecular ions.

We demonstrate a simple and nondestructive method for identification of a single molecular ion sympathetically cooled by a single laser cooled atomic ion in a linear Paul trap. The technique is based on a precise nondestructive determination of the molecular ion mass through a measurement of the eigenfrequency of a common motional mode of the two ions. The demonstrated mass resolution is sufficiently high that molecular ion mass doublets can potentially be distinguished from each other. The obtained results represent an important step towards single molecule gas phase chemical physics.

Journal Article↗
PubMed2003

Transmitted light microscopy of a fibre reinforced metal.

A method is presented for studying fibre damage in continuous fibre reinforced composites. It is based on contrasting the transmission of light through intact translucent fibres with the light through fractured or dead-ended fibres. The method is applied in order to detect processing-induced fibre fractures in aluminium reinforced with continuous alumina fibres.

Journal Article↗
PubMed2002

New animal model for the study of postmenopausal coronary and cerebral artery function: the Watanabe heritable hyperlipidemic rabbit fed on a diet avoiding phytoestrogens.

OBJECTIVE: To evaluate the effect of estrogen replacement therapy (ERT) on the functional characteristics of coronary and cerebral arteries in a new rabbit model for postmenopausal vascular function. METHODS: Female ovariectomized Watanabe heritable hyperlipidemic (WHHL) rabbits were randomized to treatment for 16 weeks with either 17 beta-estradiol or placebo. The chow used was semi-synthetic, thereby avoiding the influence of phytoestrogens. Ring segments of cerebral and coronary arteries were mounted for isometric tension recordings in myographs. The passive and active length-tension relationships for electromechanical (high potassium), pharmacomechanical (histamine) and combined electro- and pharmacomechanical (high potassium plus histamine) contraction were evaluated. RESULTS: Treatment with 17 beta-estradiol significantly changed the active length-tension relationship for the electromechanical response in the proximal coronary arteries. No changes were observed for the passive length-tension relationships. CONCLUSIONS: Long-term treatment with 17 beta-estradiol lowered the electromechanical tonus of atherosclerotic coronary arteries proximally, where the atherosclerosis is most developed. This could be one of the mechanisms behind the putative protective effect of hormone replacement therapy against ischemic heart disease. The study presents a promising new animal model for the investigation of postmenopausal coronary and cerebral artery function. The data correspond well with epidemiological observations in postmenopausal women.

Animal Nutritional Physiological Phenomena↗
PubMed2001

Scavenging of acetylperoxyl radicals and quenching of triplet diacetyl by beta-carotene: mechanisms and kinetics.

Beta-carotene scavenges triplet diacetyl generated by laser flash photolysis with a second-order rate constant of 9.1+/-0.9 x 10(9) M(-1) s(-1) in deaerated benzene at 20 degrees C. In the presence of oxygen diacetyl dissociates to generate acetylperoxyl radicals. It is demonstrated that diacetyl does not dissociate to any appreciable extent in the absence of oxygen. The acetylperoxyl radical is scavenged by beta-carotene with second-order rate constant 9.2+/-0.6 x 10(8) M(-1) s(-1) in aerated benzene at 20 degrees C to give an adduct between the acetylperoxyl radical and beta-carotene, whereas no evidence of oxidation of beta-carotene by the strongly oxidizing acetylperoxyl radical to give the beta-carotene radical cation is found. This adduct decays with first-order rate constant 1.35+/-0.16 x 10(3) s(-1) to give (presumably) a beta-carotene epoxide and the acetyloxyl radical.

Benzene↗
PubMed2001

The interaction of dietary carotenoids with radical species.

Dietary carotenoids react with a wide range of radicals such as CCl3O2*, RSO2*, NO2*, and various arylperoxyl radicals via electron transfer producing the radical cation of the carotenoid. Less strongly oxidizing radicals, such as alkylperoxyl radicals, can lead to hydrogen atom transfer generating the neutral carotene radical. Other processes can also arise such as adduct formation with sulphur-centered radicals. The oxidation potentials have been established, showing that, in Triton X-100 micelles, lycopene is the easiest carotenoid to oxidize to its radical cation and astaxanthin is the most difficult. The interaction of carotenoids and carotenoid radicals with other antioxidants is of importance with respect to anti- and possibly pro-oxidative reactions of carotenoids. In polar environments the vitamin E (alpha-tocopherol) radical cation is deprotonated (TOH*+ --> TO* + H+) and TO* does not react with carotenoids, whereas in nonpolar environments such as hexane, TOH*+ is converted to TOH by hydrocarbon carotenoids. However, the nature of the reaction between the tocopherol and various carotenoids shows a marked variation depending on the specific tocopherol homologue. The radical cations of the carotenoids all react with vitamin C so as to "repair" the carotenoid.

Adjuvants, Immunologic↗
PubMed2001

Heating of TEM specimens during ion milling.

Sample heating during preparation of electron-thin specimens for observation in transmission electron microscopy (TEM) can produce artefacts which invalidate observations. This is particularly true of two-phase materials such as metal matrix composites, for which sample cooling with liquid nitrogen cannot be used to preserve the substructure during milling. A series of experiments is conducted using an age-hardenable aluminium alloy which produces a trace of peak temperature attained by TEM specimens during ion milling. It is shown that peak temperatures of the order of 650 K can be attained using conventional milling parameters; the technique must therefore be used with caution with materials such as metal matrix composites. A simplified one-dimensional heat transfer analysis of the problem is conducted to show that the most critical parameter is heat transfer along the sample holder legs and across interfaces along the heat path. Temperature differentials within the TEM specimen are shown to be less significant, yet these alone are capable of reaching 60 K within a dimpled specimen under usual milling conditions.

Journal Article↗
PubMed2001

17beta-Estradiol but not the phytoestrogen naringenin attenuates aortic cholesterol accumulation in WHHL rabbits.

The effects of 17beta-estradiol (17beta-E(2)) or the phytoestrogen naringenin on spontaneous atherosclerosis were studied in 36 ovariectomized homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits receiving a semisynthetic control diet; this diet added 0.0040% 17beta-E(2;) or 0.20% naringenin, for 16 weeks. The uterine weight was increased (P < 0.001) and the concentration of estrogen receptor alpha was decreased (P < 0.001) in the 17beta-E(2) group compared with the controls. Total plasma cholesterol and triglycerides were not different from those in the controls. In lipoproteins, HDL cholesterol was increased (P < 0.01), and LDL triglyceride and IDL triglyceride were lowered (P < 0.05). The oxidation (as concentration of malondialdehyde) was increased in LDL (P < 0.05) but not in plasma. The cholesterol accumulation was decreased (P < 0.05) in the ascending aorta and in the total aorta but the ratio of intima to media and area of intima in ascending, thoracic, and abdominal aorta were not significantly different. In the naringenin group the only differences, compared with the control group, were increased HDL cholesterol (P < 0.001) and decreased activity of glutathione reductase (P < 0.05). In conclusion, 17beta-E(2), but not naringenin, attenuated aortic cholesterol accumulation independently of plasma and LDL cholesterol. Further, these results support previously suggested pro-oxidant ability of 17beta-E(2) toward LDL and a possible connection between the pro-oxidant nature of 17beta-E(2) and its antiatherogenic effect.

Animals↗
PubMed2000

Kinetics and mechanism of the primary steps of degradation of carotenoids by acid in homogeneous solution.

The kinetics of reaction between trifluoroacetic acid as an acid of medium strength and the carotenoids beta-carotene, zeaxanthin, canthaxanthin, and astaxanthin has been examined in detail including the effects of dioxygen, acid concentration, and carotenoid structure. Reaction between acid and carotenoid leads to species absorbing in the red and near-infrared (NIR) spectral regions, intermediates that subsequently disappear. ESR experiments clearly show that these species are not carotenoid radicals, although their NIR absorption is similar to the absorption of carotenoid radical cations. Under most reaction conditions, the disappearance of carotenoids follows pseudo-zero-order kinetics, whereas the reaction order is >1 with respect to acid, and the long-lived (hours) intermediates are suggested to be mono- (700 nm) and diprotonated carotenoid ( approximately 950 nm). Acid induces cis/trans-isomerization via the protonated intermediates, which also decay to nonradical species with shorter conjugated systems-most probably carotenoid esters. Slow protonization of the methine carbon is the primary step in the degradation, but dioxygen increases the rate as a result of formation of a charge-transfer complex with the carotenoids as indicated by a red-shift of the NIR absorption bands. Carotenoids with carbonyl groups (astaxanthin and canthaxanthin) have slower rates of degradation than beta-carotene and zeaxanthin, indicating preferential nondegradative protonation of the carbonyl groups.

Canthaxanthin↗
PubMed1999

Probucol selectively increases oxidation of atherogenic lipoproteins in cholesterol-fed mice and in Watanabe heritable hyperlipidemic rabbits.

The anti-atherogenic and cholesterol-lowering drug probucol (0.5-1%) or quercetin (1%), a natural antioxidant, was given to cholesterol-fed (1.5%) mice for a period of 6 weeks and to Watanabe heritable hyperlipidemic (WHHL) rabbits for a period of 8 weeks to investigate the oxidative changes in plasma and lipoproteins. Oxidation was measured as the total amount of malondialdehyde (nmol MDA/g protein) by a very specific MDA-HPLC method. A large and significant increase in MDA was seen in LDL from probucol treated WHHL rabbits (1778.7+/-585.5 nmol/g vs. 394.4+/-144.5 nmol/g, P < 0.001) and cholesterol-fed mice (579.7 + 47.3 nmol/g vs. 408.1+/-85.8 nmol/g, P < 0.05) as compared to controls while LDL cholesterol was lowered (WHHL rabbits: P < 0.05; mice: P < 0.01). In WHHL rabbits VLDL oxidation was determined additionally, and also revealed a large increase in the probucol group (2102.7+/-1156.1 nmol/g vs. 455.0+/-207.8 nmol/g, P< 0.01). In contrast, the oxidation of plasma and HDL from probucol treated animals was not statistically significantly increased, implying that probucol mediates a selective oxidation of atherogenic cholesterol-transporting lipoproteins. Quercetin treated animals did not show increased oxidation of LDL (and VLDL in rabbits) and cholesterol levels were not decreased. Furthermore, no protective antioxidant effect of quercetin was seen. In conclusion, the results suggest that a prooxidant mechanism rather than antioxidative effects influences lipoprotein metabolism in these animals. It is hypothesized that the oxidation of lipoproteins might be a physiological mechanism performed by macrophages or other cells for uptake and degradation (by macrophages and liver) of excessive amounts of LDL or VLDL and that probucol oxidizes atherogenic lipoproteins and thereby leads to a decrease in cholesterol levels.

Animals↗
PubMed1999

Type 2 diabetes: one disease, multiple cardiovascular risk factors.

Type 2 diabetes mellitus is a major independent risk factor for coronary artery disease. Atherosclerosis accounts for about 80% of all deaths from type 2 diabetes, of which roughly 75% are attributable to coronary artery disease and the remainder to cerebrovascular or peripheral vascular events [1]. The earlier onset and accelerated course of atherosclerosis in individuals with type 2 diabetes mellitus is multifactorial. Type 2 diabetes is associated with abnormalities in lipoprotein metabolism and increased propensity for oxidative damage. The hyperglycemia of patients with type 2 diabetes, in itself, may accelerate vascular damage. Type 2 diabetes is a hypercoagulable state attributable to enhanced coagulation and decreased fibrinolysis, as well as platelet hyperaggregability and endothelial dysfunction. Hypertension is common in individuals with type 2 diabetes and has a major impact in the accelerated atherosclerosis of this disease. This review provides an overview of selected aspects of these alterations.

Arteriosclerosis↗
PubMed1998

The effect of soy isoflavones on the development of intestinal neoplasia in ApcMin mouse.

Data from epidemiological studies suggest that isoflavones in soy may have a protective effect on the development of colon cancer in humans. Therefore, we have investigated whether soy isoflavones will inhibit intestinal tumour development in Apc(Min) mice. The mice were fed a Western-type high risk diet (high fat, low fibre and calcium) containing two different isolates of soy protein as a protein source. For the control and test groups this resulted in the administration of about 16 and 475 mg of total isoflavones per kg diet, respectively. As a positive control. a third group of mice was administered a low isoflavone diet supplemented with 300 ppm sulindac. No significant differences in the incidence, multiplicity, size and distribution of intestinal tumours were observed between Min mice fed low and high isoflavone-containing diets. However, a clear reduction in the number of small intestinal tumours was observed for the sulindac diet. Thus, in contrast to epidemiological studies, our results demonstrate that high amounts of soy isoflavones present in a Western-type high risk diet do not protect against intestinal tumour development in a relevant animal model such as the Min mice.

Animals↗
PubMed1998

Reactivity of beta-carotene towards peroxyl radicals studied by laser flash and steady-state photolysis.

Peroxyl radicals, as model for peroxyl radicals formed during autoxidation of lipids, have been generated in three solvent systems (cyclohexane, tetrahydrofuran and tert-butanol/water) by steady-state and laser flash photolysis, and their reaction with beta-carotene studied. Steady-state photolysis experiments showed that alkyl, alkoxyl and alkylperoxyl radicals all react with beta-carotene. However, laser flash photolysis experiments indicated that the reaction with peroxyl radicals (second-order rate constant estimated to be less than 10(6) M(-1) s(-1)) is slower than with alkyl and alkoxyl radicals, and that beta-carotene is hence a poor direct scavenger of peroxyl radicals. Scavenging of peroxyl radicals by beta-carotene is suggested not to proceed via electron transfer but rather by adduct formation and/or hydrogen abstraction. For different phenoxyl radicals, differences in reactivity towards beta-carotene seem to be correlated with standard reduction potential.

Cyclohexanes↗
PubMed1998

Effects of long-term feeding with 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in C57BL/ByA and E mu-pim-1 mice.

The heterocyclic amine PhIP, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, has been shown to be carcinogenic in rats producing colon and mammary carcinomas. There is, so far, only a single long-term study report on PhIP carcinogenicity in mice. However, this study focuses on the lymphoma induction only. Whether PhIP induces tumors in other organs in mice after long-term exposure is yet to be established. To contribute to the knowledge about the long-term effects of PhIP feeding the remaining animals from a 7 months feeding study (0.03% PhIP) were put on standard diet and followed up to 18 months. The results confirmed that PhIP is a potent mouse lymphomagen. In addition, treatment with 0.03% PhIP in the diet for the first 7 months of a life-time study (18 months) gave rise to very few and sporadic tumors in other tissues, indicating weak, if any, carcinogenicity of PhIP to organs other than the lymphatic system under the present study design.

Animals↗
PubMed1998

Innervation of the human middle meningeal artery: immunohistochemistry, ultrastructure, and role of endothelium for vasomotility.

The majority of nerve fibers in the middle meningeal artery and branching arterioles are sympathetic, storing norepinephrine and neuropeptide Y (NPY). A sparse supply of fibers contain acetylcholinesterase activity and immunoreactivity toward vasoactive intestinal peptide (VIP), peptidine histidine methionine (PHM), and calcitonin gene-related peptide (CGRP). Only few substance P and neuropeptide K immunoreactive fibers are noted. Electronmicroscopy shows axons and terminals at the adventitial medial border of the human middle meningeal artery, with a fairly large distance to the smooth muscle cells (>500 nM). Several axon profiles contain vesicles of different types, including putative sensory profiles. The perivascularly stored signal substances, norepinephrine and NPY induced vasoconstrictor. Relaxations were induced by acetylcholine and substance P, and these were significantly reduced in arteries without endothelium, while the responses to norepinephrine, NPY, VIP, PHM, and CGRP were not changed by endothelium removal. Blockade experiments showed that the vasomotor responses to norepinephrine were blocked by prazosin, to NPY by BIBP 3226, acetylcholine by atropin, substance P by RP 67580, and the human alpha-CGRP response by human alpha-CGRP(8-37).

Acetylcholine↗
PubMed1998

Comparison of the effects of fish oil and olive oil on blood lipids and aortic atherosclerosis in Watanabe heritable hyperlipidaemic rabbits.

To compare the effects of fish oil and olive oil on the development of atherosclerosis in Watanabe heritable hyperlipidaemic (WHHL) rabbits, 6-week-old animals were given a daily dose (1.5 ml/kg body weight) of fish oil (n 10) or olive oil (n 10) by oral administration for 16 weeks. Plasma cholesterol and triacylglycerols were measured once monthly, and their concentrations in lipoproteins, together with susceptibility of LDL to oxidation were measured in vitro at the termination of the experiment. Aortic atherosclerosis was quantified biochemically and microscopically. After 4 weeks of treatment, and throughout the study thereafter, blood lipids were significantly (P < 0.05) lower in the fish-oil group than in the olive-oil group (cholesterol: 17.0 v. 30.3 mmol/l, triacylglycerols 2.97 v. 6.25 mmol/l, at termination). In the fish-oil group cholesterol was significantly lower in intermediate-density lipoproteins (2.69 v. 6.76 mmol/l) and VLDL (3.36 v. 11.51 mmol/l). Triacylglycerol levels of intermediate-density lipoproteins and VLDL in the fish-oil group were also significantly lower when compared with the olive-oil group (0.54 v 1.36 mmol/l and 0.92 v. 2.87 mmol/l respectively). No group differences were recorded for LDL- and HDL-cholesterol or triacylglycerol levels. A significantly higher oxidation of LDL was recorded 1 h after exposure to CuSO4 in the fish-oil group when compared with the olive-oil group (0.465 v. 0.202, arbitrary units). The following indicators of atherosclerosis development were significantly lower in the fish-oil group than in the olive-oil group: the cholesterol content (mg/g tissue) in the ascending aorta (29.8 v. 48.9), the intima:media value (4.81 v. 18.24) and the area of intima (0.10 v. 0.57 mm2) in the thoracic aorta. It was concluded that fish-oil treatment decreased blood lipids and the development of aortic atherosclerosis in WHHL rabbits when compared with olive-oil treatment.

Animals↗
PubMed1998

Re-appraisal of the tocopheroxyl radical reaction with beta-carotene: evidence for oxidation of vitamin E by the beta-carotene radical cation.

Photobleached beta-carotene (Car) is regenerated in hexane on a microsecond timescale in the presence of alpha-tocopherol (TOH) but not when alpha-tocopherol is absent, as studied by laser flash photolysis. Beta-carotene radical cations (Car.+) likewise react with (excess) alpha-tocopherol: Car.+ + TOH-->Car + TO. + H+ (second-order rate constant of k = 1.7 +/- 0.1 x 10(7) M(-1) s(-1) in homogeneous di-tert-butylperoxide/benzene at 20 degrees C) rather than alpha-tocopheroxyl radicals (TO.) reacting with beta-carotene. In hexane, hexane radicals formed by pulse radiolysis react considerably faster with beta-carotene (k = 2.1 +/- 0.1 x 10(9) M(-1) s(-1)) than with alpha-tocopherol (k = 4.9 +/- 0.1 x 10(6) M(-1) s(-1)). No evidence was obtained for a slower rate of beta-carotene radical cation formation in beta-carotene/alpha-tocopherol mixtures resulting from alpha-tocopheroxyl radical oxidation of beta-carotene. Steady-state radiolysis experiments confirmed that alpha-tocopherol protects beta-carotene from oxidation by hexane radicals. In both solvent systems, beta-carotene is regenerated from the radical cation by alpha-tocopherol rather than alpha-tocopherol being regenerated by beta-carotene from the alpha-tocopheroxyl radical.

Cations↗