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Biomedical subjects

G Bianchi

Publications and source records attributed to G Bianchi.

At least 343 records · Page 19Linked to original sources
PubMed1989

Nasal meningioma. Report of a case.

A case of intranasal meningioma is reported. The possible etiopathogenic hypotheses are discussed. A possible primary intracranial localisation has to be excluded. Therapy is also briefly discussed.

Aged↗
PubMed1988

Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria.

Idiopathic hypercalciuria is a common disorder whose inheritance suggests an enzyme abnormality in calcium transport. We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones. As compared with 41 healthy controls, the patients with hypercalciuria had increased erythrocyte-membrane calcium-magnesium-ATPase activity (64.2 +/- 2.19 vs. 51.6 +/- 1.91 nmol of ATP split per milligram per minute; P less than 0.01) and increased sodium-potassium pump activity (6866 +/- 233 vs. 6096 +/- 228 mumol of sodium per liter of red cells per hour; P less than 0.05). No significant difference between the two groups was found in erythrocyte sodium-potassium cotransport, sodium-lithium countertransport, or potassium content. In 66 patients with kidney stones (38 with hypercalciuria and 28 with normal calcium excretion), 24-hour urinary calcium excretion correlated with calcium-magnesium-ATPase activity (r = 0.46, P less than 0.001). Erythrocyte calcium-magnesium-ATPase activity remained unchanged in eight subjects studied after four months on a low-calcium diet. A study of 30 healthy families found significant correlations between mean values in parents and those in offspring for calcium-magnesium-ATPase (r = 0.68, P less than 0.001) and urinary calcium excretion (r = 0.45, P less than 0.02), with no significant correlations between parents with respect to these measures (r = 0.27 and r = 0.08, respectively). We conclude that abnormalities in erythrocyte calcium-magnesium-ATPase activity may represent an inherited defect in calcium transport related to the cause of idiopathic hypercalciuria.

Adult↗
PubMed1988

The alpha 2-adrenoceptor antagonist activity of ipsapirone and gepirone is mediated by their common metabolite 1-(2-pyrimidinyl)-piperazine (PmP).

Ipsapirone and gepirone, analogs of buspirone, a newly developed antianxiety agent, form 1-(2-pyrimidinyl)-piperazine (PmP) during their biotransformation in rats. After oral administration (10 mg/kg) of a parent drug, e.g. ipsapirone or gepirone, the metabolite appears in significant amounts in plasma, with maximal concentrations of 0.9 and 1.4 nmol/ml respectively. The metabolite half-life ranged from about 140 to 200 min. Ipsapirone is eliminated more slowly than gepirone, with a half-life of about 100 and 30 min, respectively. The metabolite to parent drug ratios for the areas under the plasma concentration-time curve (AUC) were 1 for ipsapirone and 14 for gepirone. PmP (0.5-2 mg/kg p.o), ipsapirone, gepirone and buspirone (5-20 mg/kg p.o.) dose dependently antagonized the slowing of gastrointestinal transit induced by clonidine 0.1 mg/kg s.c. The doses inhibiting the antitransit effect of clonidine by 50% were 0.8 mg/kg for PmP, 14 mg/kg for ipsapirone and 9 mg/kg for both gepirone and buspirone. Analysis of small intestinal longitudinal muscle of rats given the ED50 of PmP, ipsapirone, gepirone, buspirone showed that PmP concentrations in the longitudinal muscle (with attached myenteric plexus) fell within a relatively narrow range and were consistent with the appropriate transit scores. The plasma was also tested for anticlonidine activity. These data indicate that PmP formation is a pharmacologically significant metabolic process for the buspirone-related drugs, ipsapirone and gepirone, and that this metabolite is responsible for the alpha 2-adrenoceptor blocking activity exerted by these drugs in vivo in the rat.

Administration, Oral↗
PubMed1988

Calcium transport in basolateral plasma membranes from kidney cortex of Milan hypertensive rats.

Ca2+ transport was investigated in basolateral plasma membranes (BLM) isolated from kidney cortex of the Milan strain of genetically hypertensive rats (MHS) and their normotensive controls (MNS) during a pre-hypertensive stage (age 3-4 weeks). It was found that the Vmax of ATP-dependent Ca2+ transport (in the presence of calmodulin) was about 16% lower in MHS than in control rats. In membranes from MNS rats which had been isolated in the presence of EGTA, the ATP-dependent Ca2+ transport showed a hyperbolic Ca2+ concentration dependence, a high Km (Ca2+) and a low Vmax; upon addition of exogenous calmodulin, the kinetics became sigmoidal, the Km (Ca2+) was decreased and the Vmax was increased. In membranes from MHS rats, the Ca2+ concentration dependence of ATP-driven Ca2+ transport was sigmoidal and the Ca2+ affinity was high in the absence of added calmodulin. Addition of exogenous calmodulin to these membranes resulted in an increase in Vmax, but no change in other kinetic parameters. Low-affinity hyperbolic kinetics of Ca2+ transport could only be obtained in MHS rats if the membranes were extracted with hypotonic EDTA and hypertonic KCl. These data suggest that the plasma membrane Ca2+-ATPase, which catalyses the ATP-dependent Ca2+ transport, exists in BLM of pre-hypertensive MHS rats predominantly in an activated, high-affinity form.

Adenosine Triphosphate↗
PubMed1988

Blockade of alpha 2-adrenoceptors by 1-(2-pyrimidinyl)-piperazine (PmP) in vivo and its relation to the activity of buspirone.

The effect of 1-(2-pyrimidinyl)-piperazine (PmP) and the parent drug, buspirone in counteracting the behavioral and biochemical effects of clonidine were evaluated in the rat. Intraperitoneal or oral administration of PmP, buspirone and yohimbine, but not of prazosin, antagonized the slowing of gastrointestinal motility induced by subcutaneous clonidine (0.1 mg/kg). The doses that inhibited the effect of clonidine on the transit time by 50% were 0.5 mg/kg i.p. and 0.7 mg/kg p.o. for PmP, 7 mg/kg i.p. and 9 mg/kg p.o. for buspirone and 0.5 mg/kg i.p. for yohimbine. PmP (0.5 mg/kg) did not block the antitransit effect of clonidine when administered by intracerebroventricular injection. The antitransit effect of a low dose of morphine (0.05 mg/kg i.p.) was not blocked by PmP (2 mg/kg i.p.). The prolongation of the hexobarbital-induced loss of the righting reflex that occurs after clonidine (0.25 mg/kg i.p.) administration was inhibited by pretreatment with PmP (0.1-2 mg/kg p.o.) or yohimbine (1 mg/kg i.p.) but not by pretreatment with prazosin (2 mg/kg i.p.). Buspirone (1-20 mg/kg) also reduced the effect of clonidine after oral administration, with a maximal effect at 5 mg/kg, whereas the same dose administered i.v. had less effect. PmP (2 mg/kg) and buspirone (15 mg/kg) raised the levels of total 3-methoxy-4-hydroxyphenylgycol (MHPG) in rat cerebral cortex, and prevented the decrease in MHPG induced by clonidine. These findings show that buspirone, in doses at which it is active as an anxiolytic, suppresses the central and peripheral effects of clonidine. This action occurs through alpha 2-adrenoceptors and is mediated primarily by the metabolite, PmP.

Adrenergic alpha-Antagonists↗
PubMed1988

Oligoclonal IgG bands in cerebrospinal fluid and serum during asymptomatic human immunodeficiency virus infection.

Serum and cerebrospinal fluid (CSF) samples from asymptomatic patients seropositive for human immunodeficiency virus (HIV) showed frequent evidence of intrathecal IgG synthesis and oligoclonal IgG bands, with different isoelectric focusing patterns in serum and CSF; 2 of 7 had a CSF pleocytosis. The results suggest frequent, early, chronic central nervous system infection following HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1988

A hybrid FLEET model for emergency medical service system design.

Covering models have been used to locate emergency services such as ambulance and fire protection systems. As an example, in the late seventies, an analysis of the Baltimore, Maryland fire protection system was conducted with the development and use of a covering model called the Facility Location and Equipment Emplacement Technique (FLEET). The FLEET model combined the location of fire stations with the allocation of primary and special service equipment to the stations. Further, in a recent study of Austin, Texas the ambulance system was restructured based on the use of a covering model. Covering models have also been extended to handle some of the special circumstances involved in emergency service systems. One example is the maximal expected coverage problem (MEXCLP). This paper presents a new covering model which utilizes both the special coverage structure of the MEXCLP and the simultaneous station location and equipment allocation of the FLEET model. Optimal solutions are found using linear and integer programming. Results of the model applied to several planning data sets (including a form of the Austin, Texas planning problem) demonstrate that more concentrated ambulance allocation patterns exist which may lead to easier dispatching, reduced facility costs, and better crew load balancing with little or no loss of service coverage. Tradeoff curves are presented which show that significant reductions in the number of dispatching sites (keeping the number of ambulances constant) can be made without any major changes in service level.

Ambulances↗
PubMed1988

Sulfhydryl groups and peroxidase-like activity of albumin as scavenger of organic peroxides.

The concentration, the reactivity of sulfhydryl (SH) groups and the peroxidase-like activity (PLA) of bovine serum albumin (BSA) have been determined in vitro after treatment with peroxides. Tert-butylhydroperoxide (tBOOH), cumene hydroperoxide (CuOOH), benzoyl hydroperoxide (BOOH) and hydrogen peroxide reacted with BSA, decreasing the titratable SH group concentration and increasing the value of the ratio between the reaction rate and the concentration of albumin SH groups in the sulfhydryl-disulfide exchange reaction. This value was defined as reaction constant (Kr). PLA of albumin was independent of the presence of the SH group, as SH depleted BSA maintained the same activity as the control. From our findings it derives that albumin may have two possibilities of scavenging peroxides: PLA and the SH group. The plasma SH concentration, Kr and PLA of albumin were also determined in carrageenan paw edema and in experimental adjuvant-arthritis in rats. A decrease in SH concentration, an increase in Kr and PLA of rat plasma albumin were observed in both inflammatory processes.

Animals↗
PubMed1988

Antihypertensive effect of captopril, canrenoate potassium, and atenolol. Relations with red blood cell sodium transport and renin.

We compared the antihypertensive efficacy of atenolol (100 mg/d), canrenoate potassium (200 mg/d), and captopril (75 mg/d) in 30 essential hypertensives. The three drugs were administered in a randomized change-over sequence for four-months each. The main variables associated with blood pressure regulation were measured in the basal condition and at the end of each treatment period. The erythrocyte Na transport systems were measured only in the basal condition and at the end of the first treatment period. The average blood pressure reduction was similar for each drug. Mean blood pressure levels after captopril correlated positively with those after atenolol in the individual patients (P less than 0.0001); mean blood pressure levels after canrenoate potassium, on the contrary, did not correlate with those after the other two drugs. Captopril and canrenoate potassium treatment reduced intraerythrocyte Na content (P less than 0.02), canrenoate potassium increased Na-K pump (P0.05), atenolol did not change any erythrocyte membrane Na transport parameters. The ouabain-resistant Na transport systems were not modified by any drug. The patients were divided in three groups according to their antihypertensive response: nonresponders (six patients), canrenoate potassium responders (nine patients) and captopril-atenolol responders (15 patients, equally responsive to both drugs). Nonresponders had the lowest basal Na pump (P less than 0.02). Canrenoate potassium responders had higher basal Na-K cotransport than captopril-atenolol responders (P less than 0.02). Atenolol-captopril responders had the highest basal plasma renin activity (PRA, P less than 0.02). The blood pressure reduction after atenolol correlated with the induced fall in PRA (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Characterization of erythrocyte adducin from the Milan hypertensive strain of rats.

Previous studies showed that erythrocytes from the Milan hypertensive strain of rats (MHS) are smaller and have a faster Na-K cotransport when compared with their normotensive controls (MNS). These characteristics are determined within the stem cell, are genetically associated with hypertension and are similar to other renal tubular cell abnormalities more directly involved in the development of hypertension in MHS. The difference in volume is maintained in ghost membranes, while the difference in transport is abolished in inside-out vesicles. Ghosts and cytoskeletons contain a 105-kilodalton protein already characterized by immunoblotting. This protein has been identified with erythrocyte adducin by several criteria, including binding to calmodulin and protein kinase C, phosphorylation and full immunological cross-reactivity with human adducin. Since only MHS rats immunized with MNS erythrocyte cytoskeletons produce anti-adducin antibodies, we suggest an immunogenic structural difference in adducin from the two strains, and an involvement of this difference in the alteration of Na-K cotransport observed.

Animals↗
PubMed1988

Erythrocyte deficiency in calpain inhibitor activity in essential hypertension.

The calpain-calpain inhibitor system was evaluated in erythrocytes of patients with essential hypertension and normotensive controls, either with or without a family history of hypertension. Calpain levels were similar in the controls and hypertensive patients, whereas the inhibitor activity level was significantly reduced in the latter (301.8 +/- 26.4 vs 220 +/- 14 U/mg hemoglobin, p less than 0.001). Borderline hypertensive patients and a few controls with a history of hypertension showed low inhibitor activity. Similar results have recently been reported in genetically hypertensive rats of the Milan strain. A significant inverse correlation (r = -0.43, p less than 0.001) was found between mean arterial pressure and calpain inhibitor. Although the pathophysiological significance of these observations is not yet clear, they suggest a new area of investigation into the molecular mechanisms underlying essential hypertension and its complications.

Adult↗
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↗