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Biomedical subjects

A Brambilla

Publications and source records attributed to A Brambilla.

At least 37 records · Page 2Linked to original sources
PubMed1998

1,25-Dihydroxyvitamin D3 upregulates functional CXCR4 human immunodeficiency virus type 1 coreceptors in U937 minus clones: NF-kappaB-independent enhancement of viral replication.

U937 cell clones which sustain efficient or poor replication of human immunodeficiency virus type 1 (HIV-1) (referred to herein as plus clones and minus clones, respectively) have been previously described. 1,25-Dihydroxyvitamin D3 (vitamin D3) potently induced HIV-1 replication and proviral DNA accumulation in minus clones but not in plus clones. Vitamin D3 did not induce NF-kappaB activation but selectively upregulated CXCR4 expression in minus clones. The CXCR4 ligand stromal-cell derived factor-1 induced Ca2+ fluxes and inhibited both constitutive and vitamin D3-enhanced HIV replication in minus clones.

Base Sequence↗
PubMed1997

A simple signal element mediates transcription termination and mRNA 3' end formation in the DEG1 gene of Saccharomyces cerevisiae.

DEG1 is a weakly transcribed gene of Saccharomyces cerevisiae, closely associated with CEN6. We mapped its major poly(A) site only 24 nucleotides (nt) downstream of the stop codon, and only 26 nt upstream of the CDEI centromere element. The deletion of this 50 nt stretch completely abolishes formation of the mRNA 3' end. A shorter deletion of a 16 nt sequence in the 3'-untranslated region has the same effect on transcription termination and 3'-maturation function. A TATATA sequence within this 16 nt region is essential for both functions, while a TGTATA sequence has a weak compensating activity in 3' end maturation if the TATATA stretch is deleted. We assume that the 3' end formation signals of the DEG1 gene have this simple structure: a single essential element (TATATA, whether alone or with the few surrounding nucleotides), probably, but not necessarily, cooperating with the sequence at the poly(A) site. This simple structure differs from the emerging model for 3' end-processing signals in that (i) it is shorter: 24 nt long at the most, while the model suggests 39 nt; (ii) there is no element located downstream of the TATATA signal to position the poly(A) site; and (iii) unlike the other naturally occurring signals studied, no cooperation among multiple TATATA-like elements is observed. We found that the same TATATA sequence also directs transcription termination, irrespective of promoter strength, and presumably without the cooperation of a downstream polymerase II pausing site. Taken together, these findings support the hypothesis that the DEG1 3' end-forming signals are more condensed than in other yeast genes, probably because of their proximity to CEN6.

Base Sequence↗
PubMed1996

Pharmacological characterization of AMPA-induced biting behaviour in mice.

The spinal cord dorsal horn contains neural mechanisms which can greatly facilitate pain. It is well established that excitatory amino acids, aspartate and glutamate, are involved in the spinal transmission of nociceptive information and in the development of hyperalgesia. In the present study, intrathecal (i.t.) administration of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA), a structural analog of L-glutamate, produced a dose-dependent behavioural syndrome characterized by caudally directed biting in mice. We demonstrated that peripheral pre-administration of the AMPA receptor antagonists 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(F)quinoxaline (NBQX, 10-100 mg/kg s.c.) and 1-(4-aminophenyl)-3-methylcarbamoyl-4-methyl-3,4-dihydro-7, 8-methylene-dioxy-5H-2,3-benzo-diazepine-HCl (GYKI 53655, 3-10 mg/kg s.c.), and also of the NMDA receptor antagonist 5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5, 10-imine maleate (MK 801, 0.3-1 mg/kg s.c.) reversed this effect. These findings suggest that the hyperalgesia induced by the i.t. injection of AMPA in mice involves the activation of both NMDA and non-NMDA excitatory amino acid receptor sites.

Animals↗
PubMed1996

Disruption of the GTP-cyclohydrolase I gene in Saccharomyces cerevisiae.

GTP-cyclohydrolase I is the first enzyme in the biosynthetic pathway leading to folic acid and tetrahydrobiopterin. We determined the complete sequence of the GTP-cyclohydrolase I gene from the yeast Saccharomyces cerevisiae. The gene, which is located in the subtelomeric region of the right arm of chromosome VII, gives a major transcript of about 1000 nt and encodes a protein of 243 amino acids, which is highly homologous to the GTP-cyclohydrolase I from bacteria to man. We obtained by gene replacement a knock-out mutant that shows a recessive conditional lethality due to folinic acid auxotrophy, and lacks any detectable specific enzymatic activity. The gene was identified as FOL2, previously genetically mapped in the same region (J. Game, personal communication).

Amino Acid Sequence↗
PubMed1996

[Characteristics of a new controlled release formulation of ursodesoxycholic acid].

Ursodeoxycholic acid, like all weak acids, has to be formulated so as his release and absorption depend as little as possible by the pH of gastrointestinal tract. To obtain this result a controlled release formulation of UDCA was developed, based on bioadhesive technique. This allowed a longer residence and absorption time of the active ingredient both at gastric (due to gastrosoluble rate) and duodenal-jejunum level (gastroresistant rate). Thus, all the absorption windows for bile acids are utilized, to ameliorate the total bioavailability of the drug.

Biological Availability↗
PubMed1994

Cerebral ischemia in a patient with protein S deficiency and carotid stenosis.

Congenital protein S deficiency is an important risk factor for venous and, more rarely, arterial thrombosis. Here, we describe the case of a 35-year old patient with cerebral ischemia, protein S deficiency and carotid stenosis. Other members of the family were found to have the same protein S deficit and a history of venous thrombotic manifestations.

Adult↗
PubMed1994

Effect of DAU 6215, a novel 5-HT3 receptor antagonist, on scopolamine-induced amnesia in the rat in a spatial learning task.

The effects of different doses (1, 10, 30, and 100 micrograms/kg, IP) of a new 5-hydroxytryptamine3 (5-HT3) receptor antagonist, 3-alpha-tropanyl)1H-benzimidazolone-3-carboxamide chloride (DAU 6215), on memory and performance deficits induced by SC 0.2 mg/kg scopolamine were assessed in the Morris water maze task. No effect was observed on the performance of rats treated with DAU 6215 alone. The doses of 10 and 30 micrograms/kg DAU 6215 attenuated these scopolamine-induced behavioral deficits.

Amnesia↗
PubMed1993

DAU 6215, a novel 5-HT3-receptor antagonist, selectively antagonizes scopolamine-induced deficit in a passive-avoidance task, but not scopolamine-induced hypermotility in rats.

This study examined the effects of DAU 6215, a selective 5-HT3-receptor antagonist, on either impairment of a passive-avoidance task or hypermotility, both caused by scopolamine in rats. In the first experiment, scopolamine (0.75 mg kg-1, i.p.) disrupted acquisition of a one-trial 'step through' passive-avoidance response. Pretreatment with DAU 6215 (1, 10, 30 and 100 micrograms kg-1, i.p.) antagonized this deficit induced by scopolamine, with a bell-shaped dose-response curve. Scopolamine (0.75 mg kg-1, i.p.) produced a significant increase in locomotor activity which was unaffected by pretreatment with DAU 6215 (10 and 30 micrograms kg-1, i.p.). The present results further support the suggestion that 5-HT3-receptor antagonists may prevent the memory disturbance caused by a reduction in central cholinergic function in the rat. The inefficacy shown by DAU 6215 on hyperactivity induced by scopolamine appears to rule out the possibility of a pharmacokinetic interference between DAU 6215 and scopolamine.

Animals↗
PubMed1992

[A new inclusion complex of silibinin and beta-cyclodextrins: in vitro dissolution kinetics and in vivo absorption in comparison with traditional formulations].

The very low bioavailability of silybinin, the main constituent of silymarin, so far prevented the development of an oral pharmaceutical specialty based on this active ingredient. To overcome this difficulty, an inclusion complex between Silybinin and beta-Cyclodextrin was prepared. The new complex was compared in vitro tests (dissolution rate) and in a in vivo test (rat bile elimination) with silybinin, silymarin and one traditional formulation based on silybinin. The results show a dramatic increase in the dissolution rate of the complex (> 90% within 5 min) respect to the silybinin that confirm to be practically insoluble (< 5%). The in vivo results agree with the dissolution rates; after administration of the silybinin complex p.o., the silybinin concentration in the rat bile was near 20 times more than after administration of silybinin as is or in a traditional formulation. In the last two cases, the silybinin concentration was even 6 times less than after administration of the same amount of silymarin. These data show that the beta-CD complex solved the problem of the bioavailability of silybinin which, in the traditional formulation utilised as reference, proved to be not bioavailable.

Absorption↗
PubMed1991

Muscarinic M3 receptors mediate secretion from sweat glands in the rat.

We investigated a series of muscarinic antagonists for their ability to inhibit muscarinic-mediated secretions from salivary and sweat glands in the rat. Their potency in blocking saliva secretion was compatible with the inhibition of M3 receptors. A highly significant correlation was found between their potency in blocking secretion from both salivary and sweat glands. These results indicate that salivary and sweat glands possess the same muscarinic receptors which conform to the M3 subtype.

Animals↗
PubMed1991

The effects of L-sulpiride on reflux oesophagitis.

Prokinetic drugs are commonly used for treatment of reflux oesophagitis. Although much data has been collected in clinical trials, their therapeutic effects are still uncertain. In this study the effects of L-sulpiride, if any, were examined when used to treat reflux oesophagitis in thirty patients. The patients were divided into two groups: a control group and a group given 25 mg t.i.v./day, p.o. of L-sulpiride for 30 days. They were treated as outpatients and had endoscopic, histological and ultrastructural examinations on the 30th and 60th days of treatment. It was found that the symptoms of patients with reflux oesophagitis were alleviated and the endoscopic and ultrastructural lesions of patients with minor oesophagitis were also decreased. In other patients, symptoms improved without resolution of the lesions. The authors conclude, therefore, that L-sulpiride would be appropriate treatment for Grade I cases.

Double-Blind Method↗
PubMed1990

Synthesis and biological evaluation of new antimuscarinic compounds with amidine basic centers. A useful bioisosteric replacement of classical cationic heads.

Amidines (guanidine, formamidine, and acetamidine) were introduced as substitutes for the cationic heads present in atropine, scopolamine, and corresponding quaternary derivatives. Amidine systems are intermediate in structure between tertiary amines and quaternary compounds, at least as regards ionization and electronic properties, but differ from the latter in shape (planar not tetrahedral). They have additional binding opportunities on account of their hydrogen-bond-forming capacity. The effect of the introduction of these cationic heads on the affinity for different muscarinic acetyl choline receptor (m-AcChR) subtypes was investigated in vitro, in binding displacement studies, and in functional tests on isolated organs. All new compounds (3a,b-5a,b) showed high affinity for the m-AcChR considered, comparable or slightly inferior to that of the parent drugs (1a-e). The new amidine derivatives proved effective as spasmolytic agents, with little tendency to cause central effects. However, no separation was achieved of spasmolytic and other untoward effects, like inhibition of salivation. Thus, amidine moieties are effective bioisosteric substitutes for conventional cationic heads present in antimuscarinic agents. Their unusual physical-chemical properties make them useful tools when modulation of pharmacokinetic or pharmacodynamic effects is required.

Amidines↗
PubMed1988

Atypical features and prognosis of Wallenberg syndrome: longitudinal study.

The lessons of a retrospective study of 24 consecutive cases of Wallenberg syndrome observed during a 6-year span are described: the high frequency of signs and symptoms not considered typical, such as headache, diplopia, supranuclear homolateral facial paresis and homolateral brachiocrural hemiparesis; the unfavorable short term course in a high percentage of cases, and the risk of sudden respiratory arrest.

Aged↗
PubMed1987

WEB 2086. A potent PAF antagonist exerts protective effect toward PAF-induced gastric damage.

Single intravenous administration of platelet activating factor (PAF; 4 micrograms/kg) induced reproducible gastric damage in the conscious rat which was prevented by WEB 2086, a potent and specific PAF-antagonist. Intravenous and oral ED50s in protecting rats from gastric damage were 61 and 633 micrograms/kg, respectively. Because of the reported association between septic shock and gastrointestinal ulceration, the therapeutic potential of PAF-antagonists might be broader than previously thought.

Animals↗
PubMed1987

Effect of mifentidine on mepirizole-induced duodenal ulcer in the rat.

The H2-receptor antagonists mifentidine, famotidine, cimetidine and ranitidine were examined for their ability to prevent the duodenal ulcer caused by mepirizole (250 mg/kg p.o.), a non-steroidal anti-inflammatory agent, in the conscious rat. All the compounds exerted a dose-related protective effect and on the basis of their ED50s, the following rank order of potency was found: mifentidine = famotidine greater than ranitidine greater than cimetidine. The antiulcer activity displayed by the H2-receptor antagonists evaluated in this model reflects their potency in inhibiting basal and stimulated gastric acid secretion in rat. The results of these studies indicate mifentidine as a potent anti-ulcer agent.

Animals↗
PubMed1986

Effect of pirenzepine and PGE2 on taurocholic acid-induced gastric lesions.

Cytoprotective activity of Pirenzepine (PZ) and Prostaglandin E2 (PGE2) was investigated in the gastric damage induced by taurocholic acid (TA) in the rat. Gastric mucosal potential difference (PD) and gross mucosal erosions were measured. Intravenous PZ (18 mg/kg) and PGE2 (5 micrograms/kg) prevented both the sharp decrease of PD and the gastric lesions caused by intragastric TA (40 mM). When TA administration preceeded drug treatment, both compounds reversed the PD fall but only PZ was able to restore gross mucosal integrity. It is thought that TA causes gastric damage by producing back-diffusion of H+ ions across the mucosal layer. It is speculated that antimuscarinic, such as PZ, might reduce gastric damage either by preventing, at the submucosal level, the spreading of cytolesive process triggered by H+ retro-diffusion and/or by inhibition of acid secretion in the depth of the gastric glands.

Animals↗