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Biomedical subjects

P Ferrari

Publications and source records attributed to P Ferrari.

At least 325 records · Page 18Linked to original sources
PubMed1988

Serotonin metabolism and other biochemical parameters in infantile autism. A controlled study of 22 autistic children.

The serotonin metabolism was extensively studied in 22 couples of autistic children and age- and sex-matched controls. Histamine, calcium, and uric acid were also measured in urine and whole blood or plasma. Autistics and controls did not differ in histamine, and only minor changes were noticed in calcium content. According to previous reports, serotonin levels were often, but not always, elevated in the blood of autistic children. Based on data including urinary serotonin and 5-hydroxyindoleacetic acid, platelet serotonin uptake and efflux, platelet monoamine oxidase and glutathione peroxidase activities, and uric acid and plasma tryptophan, the origin(s) of such hyperserotonemia in autism appear(s) to be of metabolic origin, i.e., a decreased catabolism and/or an increased biosynthesis of serotonin.

Adolescent↗
PubMed1988

Gonadotropin-releasing hormone (GnRH) analog suppression renders polycystic ovarian disease patients more susceptible to ovulation induction with pulsatile GnRH.

Pulsatile GnRH administration consistently restores normal reproductive hormone levels and ovulation in women with hypogonadotropic hypogonadism, but is less effective in those with polycystic ovarian disease (PCOD). We pharmacologically created a hypogonadotropic condition with a GnRH analog (GnRH-A) in six women with PCOD to investigate the role of deranged gonadotropin secretion in PCOD and to improve the response to pulsatile GnRH ovulation induction. Before GnRH and GnRH-A treatment the women with PCOD had increased LH pulse frequency [one pulse every 55 +/- 2 (+/- SE) min; P less than 0.05] and LH pulse amplitude (10.9 +/- 1.4 U/L; P less than 0.05) compared to normal women in the follicular phase of their menstrual cycle. Each PCOD woman completed one cycle of pulsatile GnRH administration for ovulation induction before (pre-A cycles; n = 6) and one or two cycles after (post-A cycles; n = 9) GnRH-A administration [D-Ser(tBu)6-Des,Gly10-GnRH; 300 micrograms, sc, twice daily for 8 weeks]. Pulsatile GnRH (5 micrograms/bolus) was given at 60-min intervals using a Zyklomat pump. Daily blood samples were drawn during the pulsatile GnRH ovulation induction cycles for the determination of serum LH, FSH, estradiol (E2), progesterone, and testosterone, and pelvic ultrasonography was done at 1- to 4-day intervals. Mean (+/- SE) serum LH levels were elevated during the pre-A cycle (49.2 +/- 3.1 IU/L) and decreased to normal levels during the post-A cycles (19.6 +/- 1.4 IU/L; P less than 0.0001). Mean testosterone concentrations were lower during the post-A cycles [88 +/- 2 ng/dL (3.1 +/- 0.1 nmol/L)] than during the pre-A cycles [122 +/- 3 ng/dL (4.2 +/- 0.1 nmol/L); P less than 0.0001]. In the follicular phase of the post-A cycles E2 levels were significantly lower [81 +/- 5 pg/mL (300 +/- 20 pmol/L) vs. 133 +/- 14 pg/mL (490 +/- 50 pmol/L); P less than 0.0001], preovulatory ovarian volume was smaller (24.6 +/- 2.0 vs. 31.4 +/- 2.4 cm3; P less than 0.01), and the FSH to LH ratio was higher (0.56 +/- 0.03 vs. 0.16 +/- 0.01) than in the pre-A cycle, suggesting more appropriate function of the pituitary-gonadal axis. Excessive LH and E2 responses to pulsatile GnRH administration in the early follicular phase of the pre-A cycle were abolished in the post-A cycles.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

A40926 aglycone and pseudoaglycones: preparation and biological activity.

A40926 antibiotics are new glycopeptides which are much more active than other members of this class against Neisseria gonorrhoeae. Their activity against Gram-positive bacteria, including coagulase-negative Staphylococci, is similar to that of other glycopeptides. An A40926 preparation containing factors A and B ("A40926 A + B complex") was hydrolyzed to the aglycone and to the mannosyl and N-acylaminoglucuronyl aglycones. The mannosyl aglycone and the aglycone were less active than A40926 A + B complex against Streptococci and Gram-positive anaerobes and lost the anti-gonorrheal activity. In contrast, the N-acylaminoglucuronyl aglycones were as active as the parent complex against these Gram-positive bacteria and were moderately active against N. gonorrhoeae. The aglycone and, even more so, the N-acylaminoglucuronyl aglycones, had better activity than the parent complex against coagulase-negative Staphylococci. In experimental septicemia in the mouse, A40926 A + B complex and its derivatives had activity proportional to their MIC for the test organism.

Animals↗
PubMed1988

Renal abnormalities at the prehypertensive stage of essential hypertension.

An approach to evaluating the genetic components of essential hypertension using an animal model, the Milan hypertensive strain (MHS) of rats, and studies in human families with positive and negative histories for high blood pressure are described and discussed. Differences at renal and cellular levels between MHS and its normotensive control strain, MNS, show many similarities to those between offspring from hyper- and normotensive families in humans. These include, with respect to the former group of each species, lower erythrocyte volume and Na content, higher Na-K cotransport across red blood cell (RBC) membranes higher Na excretion after load, and greater pressor effect in transplanted kidneys. A novel protein found in rat RBC cytoskeleton appears to have a function in Na-K cotransport and it may, eventually, be possible to demonstrate in man.

Animals↗
PubMed1988

[Sodium transport and renal hemodynamics in arterial hypertension of genetic origin: primary or secondary changes?].

Essential hypertension develops from the interaction of genetic and environmental factors. In the Milan hypertensive strain (MHS) rat before the development of hypertension, there is a genetically inherited increase of tubular reabsorption which is the cause of the following increase of blood pressure. Also in young normotensive humans, predisposed to develop essential hypertension later in life, there is an abnormal pattern of renal function that may be explained by increase of tubular reabsorption. The studies of the erythrocyte membrane transport support these data and suggest that at least a subset of essential hypertensive humans may develop a form of hypertension that has pathogenetic mechanisms similar to the ones of MHS rats.

Animals↗
PubMed1987

Catecholamines metabolism in infantile autism: a controlled study of 22 autistic children.

In a group of 22 autistic children aged 5 to 16 years and a group of normal controls matched for age and sex, catecholamines metabolism was investigated in plasma, platelets, and urine. This investigation was part of a research project in which several biological parameters (including serotonin) were explored simultaneously in the same children. In the autistic group, epinephrine and norepinephrine were significantly elevated in plasma, while epinephrin, norepinephrine, and dopamine were significantly lower in isolated platelets. No significant difference was found between the two groups for the urinary excretion of epinephrine, norepinephrine, dopamine, DOPAC, and MHPG. Other differences between the two groups in the statistical correlations of several biochemical parameters also suggest abnormalities of bioamine metabolism in the platelets of autistic children.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Relationship between erythrocyte volume and sodium transport in the Milan hypertensive rat and age-dependent changes.

The relationship between differences in red blood cell (RBC) volume and ion transport across the erythrocyte cell membrane were investigated in the Milan Hypertensive (MHS) and Milan Normotensive (MNS) rat strains, under different experimental conditions and during ageing. The results obtained indicate that: the difference in Na+/K+ cotransport between MHS and MNS disappear when the RBC volume of the two strains becomes equal under hypotonic swelling; MHS RBCs are osmotically more fragile than those of MNS, probably because of a different membrane structure rather than a different amount of membrane surface, and the smaller volume and the lower Na+ content of MHS RBCs are maintained throughout the life span, while Na+/K+ pump activity and Na+/K+ cotransport undergo age-dependent changes, related to the development of hypertension. All these findings suggest that a primary abnormality of the cell membrane structure of MHS, probably located in the cytoskeleton, is responsible for the cell functional alterations that we previously demonstrated to be genetically associated with MHS hypertension.

Animals↗
PubMed1987

A40926, a new glycopeptide antibiotic with anti-Neisseria activity.

In the course of a search for glycopeptide antibiotics having novel biological properties, we isolated A40926. Produced by an actinomycete of the genus Actinomadura, A40926 is a complex of four main factors which contain a fatty acid as part of a glycolipid attached to the peptide backbone. Its activity was, in most respects, similar to that of other glycopeptides, such as vancomycin and teicoplanin. However, in addition to inhibiting gram-positive bacteria, A40926 was very active against Neisseria gonorrhoeae. A40926 was rapidly bactericidal for N. gonorrhoeae clinical isolates at concentrations equal to or slightly higher than the MIC. In mice, levels in serum were higher and more prolonged than those of an equivalent subcutaneous dose of teicoplanin. These properties suggest that A40926 may have potential in the therapy of gonorrhea.

Anti-Bacterial Agents↗
PubMed1987

Selective modification of renal alpha 2-adrenergic receptors in Milan hypertensive rat strain.

Cerebral and renal alpha-adrenergic receptors play an important role in the control of blood pressure. We studied alpha-adrenergic receptors in the cerebral and renal cortex of Milan hypertensive strain (MHS) and normotensive strain (MNS) rats, a genetic model of spontaneous hypertension linked to a kidney abnormality. Binding of the selective alpha 1-adrenergic antagonist [3H]prazosin and the alpha 2-adrenergic antagonist [3H]rauwolscine was used for receptor studies in tissues of prehypertensive (24-day-old) and hypertensive (60-day-old) rats. In the cerebral cortex, no between-strain differences in alpha 1-adrenergic and alpha 2-adrenergic receptor density and affinity were observed in prehypertensive and hypertensive periods. The density of these receptors increased similarly with age in MHS and MNS rats. In the renal cortex, the differences between MHS and MNS rats concerned alpha 2-adrenergic receptors only. Compared with their age-matched normotensive controls, MHS rats showed 1) a lower affinity for the antagonist (p less than 0.05) in the prehypertensive period, 2) absence of the normal age-related increase in receptor density, and 3) a lower density of [3H]rauwolscine binding sites (p less than 0.001) in the hypertensive period. In this period, studies of competitive inhibition of [3H]rauwolscine binding showed that l-epinephrine bound to one class of sites in MHS rats (pseudo-Hill plot, 0.90) and to two classes in MNS rats (pseudo-Hill plot, 0.68). In addition, the lack of any guanylylimidodiphosphate effect on the l-epinephrine competition curve observed in MHS rats suggests the uncoupling of these receptors from the guanosine 5'-triphosphate binding protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1987

The Milan hypertensive rat as a model for studying cation transport abnormality in genetic hypertension.

Environmental factors, genetic polymorphisms, and different experimental designs have been the main impediments to evaluating a genetic association between cell membrane cation transport abnormalities and human essential or genetic hypertension. We review the results obtained in the Milan hypertensive strain of rats (MHS) and in its appropriate control normotensive strain (MNS) to illustrate our approach to defining the role of cation transport abnormality in a type of genetic hypertension. Before the development of a difference in blood pressure between the two strains, the comparison of kidney and erythrocyte functions showed that MHS had an increased glomerular filtration rate and urinary output, and lower plasma renin and urine osmolality. Kidney cross-transplantation between the strains showed that hypertension is transplanted with the kidney. Proximal tubular cell volume and sodium content were lower in MHS while sodium transport across the brush border membrane vesicles of MHS was faster. Erythrocytes in MHS were smaller and had lower sodium concentration, and Na+-K+ cotransport and passive permeability were faster. The differences in volume, sodium content, and Na+-K+ cotransport between erythrocytes of the two strains persisted after transplantation of bone marrow to irradiated F1 (MHS X MNS) hybrids. Moreover, in normal segregating F2 hybrid populations there was a positive correlation between blood pressure and Na+-K+ cotransport. These results suggest a genetic and functional link in MHS between cell membrane cation transport abnormalities and hypertension. Thus erythrocyte cell membrane may be used for approaching the problem of defining the genetically determined molecular mechanism underlying the development of a type of essential hypertension.

Animals↗
PubMed1987

Cytochemically assayable Na+,K+-ATPase inhibition by Milan hypertensive rat plasma.

The ability of plasma from 3- and 9-week-old Milan hypertensive rats and their normotensive controls to inhibit Na+,K+-adenosine triphosphatase (ATPase) was studied using cytochemical bioassay techniques in fresh tissue. With a validated cytochemical bioassay that measures the capacity of biological samples to stimulate glucose-6-phosphate dehydrogenase activity in guinea pig proximal tubules as an indication of their capacity to inhibit Na+,K+-ATPase, the mean glucose-6-phosphate dehydrogenase-stimulating ability of the plasma of the 9-week-old Milan hypertensive rats and their normotensive controls was 586.0 +/- 88 and 23.4 +/- 8.3 U/ml (n = 7; p less than 0.001), while that of the 3-week-old Milan hypertensive rats (before the main rise in arterial pressure) and their normotensive controls was 99.9 +/- 27.4 and 7.8 +/- 1.8 U/ml (n = 7; p less than 0.001). With the use of a semiquantitative cytochemical assay that measures Na+,K+-ATPase activity directly, plasma from the adult hypertensive rats had a much greater capacity to inhibit Na+,K+-ATPase than the plasma of the control rats. The significantly raised levels found in the young hypertensive rats before the main rise in arterial pressure are consistent with the hypothesis that the rise in the ability of plasma to inhibit Na+,K+-ATPase is due to an inherited renal difficulty in excreting sodium.

Animals↗
PubMed1987

Cholinergic mediation of growth hormone secretion induced by thyrotropin-releasing hormone in cirrhotic patients.

In order to evaluate the possible involvement of muscarinic cholinergic receptors in the GH response to TRH in patients with liver cirrhosis, 8 males with post-hepatitic cirrhosis and 11 males with post-alcoholic cirrhosis were primed with the anticholinergic agent pirenzepine and tested with TRH. In addition, 10 male patients affected by piecemeal necrosis were tested in a similar manner. High basal concentrations of GH were found in all groups. None of the patients with piecemeal necrosis responded to TRH, whereas in patients with post-hepatitic and in post-alcoholic cirrhosis, TRH induced a significant rise in GH levels. The priming with pirenzepine (40 mg given iv 10 min before TRH) completely blocked the TRH-induced GH increase, but did not affect the TRH-induced TSH release. These data suggest that a muscarinic cholinergic pathway is involved in the anomalous response of GH to TRH in patients with liver cirrhosis. The lack of effect of pirenzepine on the TRH-stimulated TSH release suggests that the muscarinic cholinergic mediation is peculiar for the effect of TRH on GH secretion.

Adult↗
PubMed1987

Metabolic oxidation of the pyrrole ring: structure and origin of some urinary metabolites of the anti-hypertensive pyrrolylpyridazinamine, mopidralazine. III: Studies with the 13C-labelled drug.

The metabolism of the anti-hypertensive drug, mopidralazine, N-(2',5'-dimethyl-1H-pyrrol-1-yl)-6-(4"-morpholinyl)-3-pyridazinamine, was reinvestigated in rats using the [2'(5')-13CH3]-labelled drug to determine the significance of the pharmacologically active intermediate 3-hydrazino-6-(4-morpholinyl)pyridazine. The previously proposed mesonic structure of the major metabolite I, i.e., 5'-hydroxy-3',6'-dimethyl-1'-[6-(4"-morpholinyl)-3-pyridazinyl]pyrida zinium hydroxide inner salt, was confirmed by chemical synthesis, X-ray diffraction analysis and 1H n.m.r. of the [3',6'-13CH3]-labelled metabolite I. Metabolite II, 3-methyl-6-(4-morpholinyl)-triazolo [4,3-6 b]pyridazine and metabolite VII, 3-methyl-7-(4-morpholinyl)-3H-pyridazino[1,6-c]pyridazine, were shown to retain the 13CH3 labelling of mopidralazine, whereas metabolite X, 3-acetyl-hydrazino-6-(4-morpholinyl)-pyridazine, loses the labelling, indicating that their formation involves two different pathways. It is hypothesized that the oxidation of the pyrrole leads to ring opening followed by a chemical rearrangement giving rise directly to metabolites II and VII or, with the intermediacy of the pharmacologically active 3-hydrazino-6-(4-morpholinyl) derivative and an enzymic acetylation or conjugation with pyruvic acid, to metabolites X, II and VII.

Animals↗
PubMed1987

Synthesis and biological activity of some esters of the N-acetylglucosaminyl aglycone and of the aglycone of teicoplanin.

A series of ester derivatives of teicoplanin-N-acetylglucosaminyl aglycone (T-A3-2) and deglucoteicoplanin was prepared starting from teicoplanin and from the corresponding deglycosylation compounds. The modification of the ionic and lipophilic character of the parent antibiotic strongly influences the spectrum of antibacterial activity in vitro.

Anti-Bacterial Agents↗