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Biomedical subjects

A Marino

Publications and source records attributed to A Marino.

At least 19 recordsLinked to original sources
PubMed1992

Electrical states in the rabbit brain can be altered by light and electromagnetic fields.

The effect of low-frequency magnetic fields on the rabbit electroencephalograph (EEG) was studied using a quantitative procedure that permitted statistical evaluation of the response of individual animals. The field conditions used were those predicted by various theories to result in field-animal interactions; light and sham exposure were employed as positive and negative controls, respectively. Sixty-seven percent of the rabbits exhibited changes in the EEG power spectra when light was presented in 2-s epochs; none of the animals responded to sham exposure. When 1 Gauss, 5 Hz, was presented in 2-s epochs, 100% of the animals tested responded to the presence of the field. The rabbits did not respond when the magnetic-field frequency was higher than the physiological range (1-20 Hz) or when it was tuned for resonance of K+. The results showed that an electrical state function may be operationally defined for the rabbit brain, and used to assess the occurrence of an interaction between an animal and external magnetic fields.

Animals↗
PubMed1992

Characterization by photoaffinity labeling of a steroid binding protein in rat liver plasma membrane.

The mechanism of steroid uptake by the cell remains controversial. [3H]R5020 was utilized to characterize by photoaffinity labeling the steroid binding site in plasma membrane. This binding was saturable, reversible and had one type of binding site (Kd = 33 +/- 4 nM, Bmax = 32 +/- 2 pmol/mg). [3H]R5020 could be prevented from binding by a variety of steroids (cortisol, progesterone, deoxycorticosterone, and levonorgestrel); estradiol did not have affinity for this binding site. The kinetics of R5020 photoactivation was time dependent and saturable. SDS-PAGE showed a specific band which corresponded to a 53-kDa peptide. The sucrose density gradient analysis has revealed the existence of a protein with a sedimentation coefficient of 3.6 +/- 0.2 S. This polypeptide shows different characteristics than cytosolic steroid receptor or serum steroid binding proteins. This binding protein could correspond to the steroid binding site previously found in the plasma membrane.

Affinity Labels↗
PubMed1992

Intracellular Ca2+ mobilization and not calcium influx promotes phorbol ester-stimulated thromboxane A2 synthesis in human platelets.

Phorbol esters, potent activators of protein kinase C (PKC), greatly enhance the release of arachidonic acid and its metabolites (TXA2, HETES, HHT) by Ca2+ ionophores in human platelets. In this paper, we report the relationship between intracellular Ca2+ mobilization and external calcium influx into platelets and the ability of PMA plus A23187 to promote thromboxane A2 (TXA2) synthesis. The enhanced levels of TXA2 due to the synergistic stimulation of the platelets with A23187 and phorbol esters are not affected significantly by the presence of external Ca2+ or the calcium-chelator EGTA. PKC inhibitors, staurosporine and sphingosine, abolished phorbol myristate acetate (PMA) potentiation of TXA2 production which strongly supports the role of PKC in the synergism. Platelet aggregation is more sensitive to PMA and external calcium than TXA2 formation. PMA increased TXA2 production as much as 4-fold at low ionophore concentrations. The A23187-induced rise in [Ca2+]i was reduced by pretreatment of human platelets with phorbol esters, both in the presence and absence of EGTA, and staurosporine reversed this inhibitory effect. These results indicate that the synergistic stimulation of TXA2 production by A23187 and phorbol esters is promoted by intracellular Ca2+ mobilization and not by external calcium influx. Our data also suggest that PKC is involved in the regulation of Ca2+ mobilization from some specific intracellular stores and that PKC may also stimulate the Ca(2+)-dependent phospholipase A2 at suboptimal Ca2+i concentrations.

Alkaloids↗
PubMed1992

Molecular mechanisms mediating the effects of L-alpha-glycerylphosphorylcholine, a new cognition-enhancing drug, on behavioral and biochemical parameters in young and aged rats.

The behavioral effects of the acute and subchronic administration of L-alpha-glycerylphosphorylcholine (alpha-GPC) on passive and active avoidance behavioral tasks were investigated. When administered IP after training together with scopolamine 2 h before retest, alpha-GPC reverses the scopolamine-induced amnesia in the passive avoidance conditioning in young and old rats. Furthermore, the subchronic treatment with alpha-GPC positively and significantly influences the performance of both young and old animals in the active avoidance test. Moreover, in in vitro/ex vivo experiments alpha-GPC potentiates receptor-stimulated phosphatidylinositol hydrolysis in cortical synaptoneurosomes derived from young and old animals. In young but not old animals, alpha-GPC significantly potentiates potassium (40 mM)-stimulated intrasynaptosomal calcium oscillations in purified synaptosomes derived from the hippocampus. These results show that alpha-GPC improves the performance of animals in both active and passive conditioning tasks. Furthermore, subchronic treatment with the compound enhances in young and restores in aged animals the transduction of the signal, namely, the receptor-mediated production of inositol phosphate and the potassium-induced calcium mobilization. These modifications may represent at least part of the molecular mechanism of action of the compound.

Adenylyl Cyclases↗
PubMed1992

Modulation by GTP of basal and agonist-stimulated striatal adenylate cyclase activity following chronic blockade of D1 and D2 dopamine receptors: involvement of G proteins in the development of receptor supersensitivity.

Rats receiving injections of specific antagonists of dopamine receptors (SCH 23390 for D1, haloperidol for D2, and haloperidol+SCH 23390) once daily for 21 days develop a selective supersensitivity of the blocked receptors. To study the molecular correlates of these adaptive changes, we evaluated the involvement of GTP-binding proteins in the development of supersensitivity of dopamine receptors. By means of adenylate cyclase studies, we tested whether any of the treatments modified the functional response to GTP in striata dissected from control and treated rats. Our data show that the chronic blockade of D1 and/or D2 receptors potentiates both basal and dopamine receptor-stimulated adenylate cyclase activity in response to GTP. D1 receptor up-regulation correlates with an increased adenylate cyclase response to GTP, whereas D2 receptor up-regulation is accompanied by an enhanced GTP-induced inhibition of enzyme activity, in both basal and receptor-activated conditions. This potentiation does not seem to match the changes in mRNA content of Gs and Gi alpha subunits. Unexpectedly, however, a significant increase in Gi alpha subunit mRNA was found after the chronic blockade of D1 receptors; this result could be explained by cross-regulation between GTP-binding protein-mediated pathways. This cross-regulation could serve as a protective mechanism whereby cells exposing up-regulated receptors protect themselves from a condition of hyperactivity of the adenylate cyclase enzyme.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1992

[Update on benzodiazepines].

The Authors shortly review the benzodiazepine (BDZ) pharmacology and therapeutic. They start from the supposed mechanism of action, then the main indications, counterindications and side effects are reported. Finally, the pharmacokinetic and general classification of the drugs are examined.

Adult↗
PubMed1992

[Multiorgan damage in exertion heatstroke].

The paper reports a fatal case of exertion heat stroke. The etiopathogenetic, clinical and therapeutic aspects of the case are described; although rarely observed, this pathology must be taken into account by the intensive care unit in order to ensure rapid aid and treatment in an attempt to modify the severe prognosis due to multiorgan damage which increases with the intensity and duration of hyperthermia.

Adult↗
PubMed1991

General and selective isolation procedure for high-performance liquid chromatographic determination of anabolic steroids in tissues.

A multi-residue method has been developed for the determination of anabolic steroids in animal tissue. The analytes are extracted from tissue with methanol and the extract is subjected to two solid-phase extractions, one using a non-specific adsorbing material, such as graphitized carbon black (Carbopack B), and the other Amberlite CG-400 I in the OH form. This procedure allowed the neutral anabolics (testosterone, trenbolone and progesterone) to be isolated and separated from the acidic type (phenolic group), such as diethylstilbestrol, oestradiol, zeranol/zearalenone and their respective metabolites. The determination was effected using high-performance liquid chromatography with different detectors (ultraviolet, fluorimetric and electrochemical). Several analytical parameters were studied: chromatographic conditions, recoveries, evaporation step, solvent flow-rate, cartridges reusability, interference of plastic cartridges. For all the anabolics investigated the recoveries were greater than 83.6%.

Adsorption↗
PubMed1991

[The role of atrial natriuretic factor in cardiovascular physiopathology].

In this review, the authors examine the biochemical mechanism involved in synthesis and release of ANF and its physiological effects concerning kidney and cardiovascular system. In addition, the authors underline the possible interactions of ANF with other hormones, particularly with the renin-angiotensin-aldosterone system and with vasopressin. Finally, the authors consider the possible physiopathological implications of ANF in the genesis of hypertension and hydrosaline retention.

Animals↗
PubMed1991

Steroid hormone specifically binds to rat kidney plasma membrane.

A high-affinity and low-capacity corticosterone specific binding was detected in the purified plasma membrane preparation from rat kidney using an in vitro steroid hormone binding assay. The specific-bound hormone was efficiently distinguished from the irreversible-bound hormone with 10 microM corticosterone. Under standardized conditions of pH 7.4 at 2 degrees C and 30 min incubation time, the binding was saturable and showed Kd = 13 +/- 3 nM and Bmax = 616 +/- 34 fmol/mg of protein. Competitive binding studies with analogue steroids indicated that corticosterone binding to kidney plasma membrane is hormone-specific. Results indicated that the possible nongenomic effects of steroids could be mediated by their interaction with plasma membrane.

Animals↗
PubMed1991

Specific binding sites for corticosterone in isolated cells and plasma membrane from rat liver.

The specific binding of [3H]corticosterone to hepatocytes is a nonsaturable, reversible and temperature-dependent process. The binding to liver purified plasma membrane fraction is also specific, reversible and temperature dependent but it is saturable. Two types of independent and equivalent binding sites have been determined from hepatocytes. One of them has high affinity and low binding capacity (KD = 8.8 nM and Bmax = 1477 fmol/mg protein) and the other one has low affinity and high binding capacity (KD = 91 nM and Bmax = 9015 fmol/mg). In plasma membrane only one type of binding site has been characterized (KD = 11.2 nM and Bmax = 1982 fmol/mg). As it can be deduced from displacement data obtained in hepatocytes and plasma membrane the high affinity binding sites are different from the glucocorticoid, progesterone nuclear receptors and the Na+,K(+)-ATPase digitalis receptor. Probably it is of the same nature that the one determinate of [3H]cortisol and [3H]corticosterone in mouse liver plasma membrane. Beta- and alpha-adrenergic antagonists as propranolol and phentolamine did not affect [3H]corticosterone binding to hepatocytes and plasma membranes; therefore, these binding sites are independent of adrenergic receptors. The binding sites in hepatocytes and plasma membranes are not exclusive for corticosterone but other steroids are also bound with very different affinities.

Animals↗
PubMed1991

Dual effects of ATP on phosphatidylinositol breakdown in rat hepatocyte membranes.

The mechanisms whereby adenosine-5'-triphosphate (ATP) regulates the inositol phospholipid-signalling system were studied in rat hepatocytes. Intact hepatocytes respond to extracellular ATP, adenosine-5'-O-(3-thiotriphosphate) (ATP gamma S), ADP and weakly to guanosine-5'-triphosphate (GTP), but not to other purine nucleotides (GDP or AMP). This is consistent with the idea that a P2 purinergic receptor is coupled to the phosphatidylinositol metabolism in these cells. Partially purified plasma membranes prepared from myo-[3H]inositol prelabelled hepatocytes exhibit a phosphatidylinositol-4,5-bisphosphate phospholipase C activity sensitive to ATP, ATP gamma S and guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S). Moreover the GTP gamma S effect is greatly enhanced by ATP and ATP gamma S. These potentiating effects differ according to the adenylnucleotide considered. ATP produces (1) an increase in the GTP gamma S-PLC sensitivity, (2) a potentiation of the phospholipase C (PLC) response induced by maximal dose of GTP gamma S, and (3) an increase in the inositol lipids pools. At variance, ATP gamma S, a nonhydrolysable analogue of ATP, only increases the PLC-sensitivity towards GTP gamma S. These results may signify that ATP stimulates inositol phosphate accumulation via at least two distinct mechanisms (i) a direct activation of a P2 purinergic receptor coupled to a PLC via a GTP binding protein and (ii) a stimulation of the phosphatidylinositol (PI) and phosphatidylinositol-4-phosphate (PIP) kinases which increased the pool of phospholipase C substrates.

Adenosine Triphosphate↗
PubMed1991

The effect of electrical stimulation on bone formation around hydroxyapatite implants placed on the rabbit mandible.

Nonresorbable, nonporous, particulate hydroxyapatite (HA) was implanted on the mandible in rabbits and stimulated electrically, 4 hours per day, during the first postoperative week. Stimulated and control implant sites were recovered 8 weeks postoperatively and examined histologically. The HA migrated into the mandible in the electrically treated specimens, and was routinely found in intimate association with preexisting mandibular bone. In the controls, the HA remained superior to the mandibular surface. In further studies (without electrical stimulation) in which the implant site was recovered 26 weeks postoperatively, HA was observed in the mandible; some HA particles migrated completely through the mandible and were found in the adjacent soft tissue. It was concluded that, under the conditions studied, electrical stimulation does not promote bone growth into HA, but rather produces the opposite result--it promotes more rapid movement of HA particles into the mandibular bone. The HA particle migration into the mandible observed (longer postoperative times) in the absence of electrical stimulation suggests that migration is a general property of HA particles when placed over bone under muscle.

Animals↗
PubMed1991

Effects of sodium naproxen eye drops on rabbit ocular inflammation induced by sodium arachidonate.

Sodium naproxen, a reversible competitive inhibitor of cyclooxygenase, is widely used as an anti-inflammatory agent in clinical practice. The purpose of this study was to determine whether eye drops containing 0.5% (w/v) sodium naproxen reduce a number of inflammatory responses produced by sodium arachidonate in the rabbit's eye. Sodium naproxen eye drops successfully reduced the primary signs of ocular inflammation elicited by 0.5% sodium arachidonate on conjunctiva and iris. However, the drug was less effective in reducing conjunctival inflammation induced by 1% sodium arachidonate. Sodium naproxen treatment significantly reduced the levels of prostaglandin E2 (PGE2), polymorphonuclear leukocytes and protein concentration in aqueous humor samples obtained from the eyes of rabbits treated with 0.5% sodium arachidonate whereas aqueous humor levels of leukotriene B4(LTB4) were not found significantly different from control rabbits. Interestingly, PGE2 as well as LTB 4 "de novo" production by corneas and lenses obtained from rabbits sacrificed 2 h after arachidonate and incubation "in vitro" for 20 min were significantly higher in samples taken from controls than in tissues obtained from the eyes treated with sodium naproxen eye drops. Finally, this drug treatment significantly antagonized the rise in intraocular pressure induced by 0.5% sodium arachidonate. Present data suggest that sodium naproxen may be employed topically to prevent ocular inflammatory reactions where the arachidonic acid cascade is activated.

Animals↗
PubMed1991

Adenylate cyclase activity in crude liver membranes during chemical hepatocarcinogenesis.

Crude plasma membranes were prepared from the liver of control rats or of rats submitted to an initiation by diethyl-nitrosamine and selection with 2-acetylaminofluorene and carbon tetrachloride (group IS) or of rats submitted to an initiation-selection protocol followed by a promotion with phenobarbital (group IS PB). In control rats, the diterpene forskolin and glucagon stimulated the activity of adenylate cyclase 6- to 7-fold. Guanosine-5'-O-(2-thiodiphosphate) (GDP beta S) inhibited the stimulation by both agents and the non-hydrolyzable GTP analog, guanyl-5'-yl-imidodiphosphate [Gpp(NH)p], potentiated the stimulatory effect of glucagon. In rats of the IS group, no modification of the activity of the liver cyclase was found, except for an increased response to forskolin and glucagon. In the IS PB group, for the rats without tumor, the only effect of adding phenobarbital was to increase the sensitivity of the cyclase to forskolin. In tumoral tissue, the response to Gpp(NH)p, glucagon and forskolin were increased when compared to the surrounding tissue. In contrast to the surrounding tissue, GDP beta S potentiated the stimulatory effect of forskolin. When the affinity of the glucagon receptors for the hormone was measured in binding experiments, no difference was observed among the rats of the various groups, except for a higher affinity in tumoral tissue. Similarly, GTP inhibited the binding of glucagon with the same potency in each group. It is concluded that during hepatocarcinogenesis, the sensitivity of the adenylate cyclase towards glucagon increases secondarily to a better binding of the hormone to its receptor and to an impairment of the inhibitory regulatory site.

Adenylyl Cyclases↗