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Biomedical subjects

E Molinari

Publications and source records attributed to E Molinari.

At least 91 records · Page 5Linked to original sources
PubMed1992

Aspirin abolishes the decreased low-density lipoprotein (LDL) entry into the rabbit arterial wall induced by the calcium channel blocker isradipine.

After deendothelialization and experimentally induced hypercholesterolemia in rabbits, an increased LDL entry into the vascular wall can be monitored using radiolabelled LDL. In male rabbits aged 6 months the abdominal aortic endothelium was removed by a Fogarty catheter. The animals fed a 1% cholesterol supplemented diet were treated either with isradipine (0.3 mg/kg/daily) (n = 36) alone or in combination with aspirin (5 mg/kg/daily) (n = 36) for four weeks. Thirty-six animals served as controls. 1, 3, 6, 12, 24 and 48 hours prior to sacrificing, 10 microCi 125I-LDL was administered intravenously to six rabbits in each group. The LDL entry was quantified in the abdominal aorta according to morphologically assessed type of surface lining. Aortic cholesterol content was assessed by Sudan-III staining and quantitative determination. Endothelialized segments exhibited a significantly (p less than 0.05 - p less than 0.001) lower LDL uptake as compared to re- or deendothelialized segments. The LDL entry was significantly lower with isradipine treatment than in controls. In parallel the cholesterol content decreased and the Sudan-III-positive areas were smaller in size. This beneficial effect as well as that on aortic lipid content was abolished by a pretreatment with aspirin. While in the isradipine-treated animals PGI2 synthesis was significantly (p less than 0.01) enhanced, it was almost completely blocked by aspirin. These findings indicate that the benefit of reduced LDL entry caused by isradipine may be mediated by an increased endogenous PGI2 synthesis.

Animals↗
PubMed1991

Comparison of different methods for LDL isolation and radioiodination on liver LDL receptor binding in vitro.

Lipoproteins were isolated either by immunoaffinity chromatography (LDL and VLDL) or ultracentrifugation (LDL). Purified lipoproteins were labeled with 123I using either Iodogen or iodine-monochloride (IC1) each followed by purification with gel-chromatography or dialysis (total of 4 combinations). Lipoprotein-concentrations of 0.1-6 micrograms protein/mL were used for direct binding assays investigating the specific binding of labeled lipoproteins (in the presence of a 50-fold excess of unlabeled lipoproteins) to human liver apo-B, E-receptors. In separate experiments displacement of bound 123I-lipoproteins (labeled by the methods mentioned) by unlabeled ones was studied. The binding capacities estimated by Scatchard analysis were similar to each other (141-163 ng protein bound/mg liver plasma membrane protein) independent from the method used for isolation and labeling. Also the affinity constants were very similar and ranged from 0.9 to 1.7 micrograms protein/L. It is concluded that immunoaffinity chromatography or ultracentrifugation for isolation of lipoproteins and the Iodogen or IC1-method for radiolabeling can be recommended to be equally good for in vitro receptor investigation.

Adult↗
PubMed1991

Isradipine, a calcium-entry blocker, decreases vascular [125-I]low-density lipoprotein entry in hypercholesterolemic rabbits.

In 72 male rabbits aged 6 months, the endothelium of the abdominal aorta was abraded by a Fogarthy catheter. The animals were then fed a 1% cholesterol-supplemented diet for 4 weeks. In addition, half of the animals were treated for the entire period with isradipine (0.3 mg/kg daily), a dihydropyridine calcium antagonist; the other 36 animals served as controls. One hour and 3, 6, 12, 24, and 48 hours before the animals were killed, [125-I]low-density lipoprotein (LDL 10 microCi) was administered intravenously (i.v.) to six animals in each group. The [125-I]LDL entry was quantified in the abdominal aorta according to the type and presence of endothelial lining. Isradipine significantly reduced the [125-I]LDL entry at most time intervals. In parallel, an increase in vascular prostaglandin (PGI2) synthesis was noted, which might be the underlying mechanism for the decreased LDL entry.

Animals↗
PubMed1991

Prostaglandin E1 decreases the low-density-lipoprotein entry into rabbit arterial wall.

1. In 72 male rabbits fed a 1% cholesterol supplemented diet the effect of a 4 weeks daily infusion of prostaglandin E1 (PGE1, 20 micrograms kg-1 min-1 over 2 h) on [125I]-low density lipoprotein (LDL) accumulation (10 microCi; 0.5 mg protein ml-1) was examined versus sham-treatment after removal of the endothelium of the abdominal aorta by a Fogarthy catheter. 2. The uptake of [125I]-LDL was significantly (P less than 0.01) higher in endothelium-free aortic segments (showing the highest peak maximum at around 12 h after 125I-injection) as compared to aortic segments with endothelium intact (showing the lowest uptake of [125I]-LDL with the peak maximum at 48 h, last control time). Segments with the endothelium restored showed a similar LDL-retention curve to segments with endothelium however, being again significantly (P less than 0.01) higher. 3. PGE1-treatment caused reduction in LDL-accumulation, being significantly (P less than 0.001) pronounced in segments without endothelium and in segments with endothelium restored. 4. The findings indicate a beneficial effect of PGE1 in lipid metabolism by decreasing the LDL-influx into the arterial wall in-vivo.

Alprostadil↗
PubMed1991

Parental perceptions of childhood illness.

This article takes parental perception as the starting point of an analysis of the relationship between ill children, their families, and their doctors in the handling of a child's illness. A modified version of Creer, Marion, and Creer's Asthma Problem Behavior Checklist, adapted to suit Italian conditions, was used. The questionnaire was given to a sample of 460 parents of 230 preadolescent children. The sample was divided into two groups: The first sample was comprised of 84 parents of 42 preadolescent children with atopic symptoms (asthma, bronchitis, or hay fever), and the second sample was comprised of 376 parents of 188 preadolescents who had never had either atopic disturbances or any other serious disease. The results showed that both groups of parents felt their children were capable of autonomously managing their disease, and that they see medical facilities as their primary resource. Children were not perceived as being altered by their illness, although their illness undoubtedly affected family relationships; this was particularly true in the case of families with members who experience atopic problems. The factors causing the greatest difficulties were: disagreements over treatment, anxiety caused by the disease, and the sacrifices made by family members as a result of illness.

Adolescent↗
PubMed1990

Immunochemical determination of lipoprotein Lp(a): comparison of Laurell electrophoresis and ELISA.

The lipoprotein Lp(a) concentrations in serum from 520 persons (317 men and 203 women) were measured by two different Laurell electrophoresis assays (one in house and one commercial) and by an ELISA technique, using polyclonal antibodies from two different animal species. The following results were obtained. 1. The two Laurell techniques gave similar results. The mean values of all three methods were comparable, whereas median values obtained by ELISA were markedly lower (0.85, 0.97 and 0.057 g/l for the two Laurell assays and the ELISA, respectively). 2. All three methods correlated very well with a correlation coefficient of greater than 0.95. 3. Women had significantly higher values than men (p less than 0.01). It was concluded that Lp(a) serum concentrations in the 'pathological range' could be measured with high enough precision by Laurell electrophoresis and by ELISA using polyclonal antibodies from different animal species.

Electrophoresis↗
PubMed1990

International study on the comparability of Apo A-1 and Apo B methods.

Apo A-1 and Apo B levels have become increasingly important as a mean of assessing risk and susceptibility to cardiovascular diseases. These proteins are measured routinely in numerous clinical and research laboratories due primarily to the ability to mechanise the immunological assay method and to the ready availability of commercially produced antisera and standards which are often sold in kit form. However, if these variables are to be used to assess the clinical risk of disease reliably, the test methods should have a low degree of imprecision and inaccuracy, to reduce false positive and negative results. The 'normal' and 'pathological' ranges for both proteins also need to be clearly defined. In order to be able to define clinical ranges and establish quality control limits on both a national and international level the inaccuracy and imprecision of the different methods used to assay the parameters need to be established. Since the technical expertise and the equipment and reagents used vary between laboratories, and because there is no internationally recognized calibration material, a survey conducted to establish imprecision and inaccuracy must include many laboratories to take these variations into account. At the WHO Collaborating Lipid Reference Centre, The Institute for Clinical and Experimental Medicine in Prague, Czechoslovakia, we have been involved in the external quality control programme for cholesterol, triglyceride, HDL-cholesterol and thiocyanate methods for more than 15 yr. Although the Centre was originally created as a European Reference Centre, laboratories participating in our quality control scheme now come from Asia, the USA and New Zealand as well as Europe due to their involvement in the large scale population studies like 'MONICA', 'ERICA' and 'CINDI'. In addition we also cooperate with some laboratories expected to join WHO projects and with others running either national or their own research programmes. Due to the increasing need to learn more about the methods used for Apo A-1 and Apo B assays in both research and preventive schemes for cardiovascular diseases, we decided, following the combined IUIS and NHLBI-CDC Apolipoprotein standardization surveys, to arrange for an international survey to determine the precision and relative accuracy of EIA, ELISA, INA, TURB and RID methods. Our survey originally intended to include only European laboratories but the number of participants increased (Table I) and we believe it supplies complementary information to the IUIS-NHLBI-CDC surveys because both research and routine clinical laboratories were included in our survey.

Apolipoprotein A-I↗