Combined effects of probucol and cholestyramine in familial type II hyperlipoproteinaemia.
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Biomedical subjects
Publications and source records attributed to M Parenti.
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A dopamine-activated adenylate cyclase has been identified in a membrane fraction of rat spinal cord. The concentration of dopamine producing half-maximal activation is about 5 microM and the activation is blocked by haloperidol. Apomorphine also activates the cyclase. Following transection of the cord, adenylate cyclase becomes about 5-10 times more sensitive to dopamine below the transection. The presence of dopamine-activated adenylate cyclase in the cord is consistent with reports of dopamine-containing tracts in spinal cord. This neuronal system may play an essential role in normal spinal mechanisms, in disease associated with dopaminergic neurons, as well as in the side-effects of neuroleptic drugs.
The new preparation Broncaspin (guacetisal) has been experimented in the form of 1.2 g suppositories and 5% suspension, in 40 patients suffering from chronic bronchopneumopathy at acute phase. The drug exerted a marked therapeutic action in objective and subjective symptomatology in 87.5% of cases. The action was manifold in relation to the typical expectorant fluidifying, bronchiole disobstructing and anti-inflammatory characteristics of the drug. Tolerance was always excellent.
A simple rapid method for the determination of 5-hydroxytryptophan, serotonin (5-hydroxytryptamine), and 5-hydroxyindoleacetic acid in brain is presented. Brain proteins are precipitated with Zn(OH)2. The indoles in the supernatant are separated by HPLC in less than than 8 min on a reverse phase column and detected electrochemically. As little as 38 fmol of hydroxyindole compound can be detected and quantitated. Because the method is rapid and uncomplicated many samples can be processed in a day.
A simple fluorometric method for the determination of cAMP is presented. The fluorescent derivative is 1,N6-etheno cyclic 3,5-monophosphate (etheno-cAMP). Maximal formation of this derivative occurs after reacting cAMP with chloroacetaldehyde for 15 minutes at 100 degrees C. Fluorescent derivatives are also produced from compounds which contain a 6-amino purine. The specificity of the method resides in the use of a reverse phase/HPLC system. The derivatization as well as the fluorescent response of etheno-cAMP is linear between 2.5 and 700 picomoles of cAMP. Studies of brain adenylate cyclase by the fluorometric/HPLC method indicated that this method is comparable to the established radioenzymatic method. Thus, the present method provides a simple rapid nonradioactive means for the determination of adenylate cyclase activity.
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A group of patients with athero-arteriosclerotic vascular disease (coronary heart disease and atherosclerosis of the extremities) have been subjected to platelet antiaggregating-antidyslipidaemic treatment with a chlofibrate-dipyridamol association; a control series was treated with chlofibrate alone. Frequency of angina pectoris, pain intensity and trinitrine consumption ware evaluated in patients with coronary heart disease, claudicometry, oscillometry and thermometry in patients with atherosclerosis of the extremities. The following laboratory parameters were also analysed: cholesterolaemia, triglyceridaemia, prothrombin activity, fibrinogenaemia, uricaemia and tolerance of oral glucose loading. Analysis of the results has shown that the association improved the parameters considered in statistically significant fashion; chlofibrate alone led to significant modifications of coronaropathic group parameters (with the exception of pain intensity) whereas it did not lead to significant changes in parameters evaluated for atherosclerosis of the extremities. All laboratory parameters were modified favourably by the association to a statistically greater extent than by chlofibrate alone. Both the association and chlofibrate were well tolerated.
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Camazepam, 5 mg/kg iv, was injected in rats and mice to study its distribution in the blood and brain. Peak blood levels were about 0.9 microgram/ml in rats and 0.6 microgram/ml in mice. Peak brain levels were about 1.5 microgram/g in rats and 0.8 microgram/g in mice. The apparent blood half-life of camazepam was 9 min in mice and 20 min in rats.
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