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Biomedical subjects

E Coen

Publications and source records attributed to E Coen.

At least 37 records · Page 2Linked to original sources
PubMed1995

Control of flower development and phyllotaxy by meristem identity genes in antirrhinum.

The flower meristem identity genes floricaula (flo) and squamosa (squa) promote a change in phyllotaxy from spiral to whorled in Antirrhinum. To determine how this might be achieved, we have performed a combination of morphological, genetic, and expression analyses. Comparison of the phenotypes and RNA expression patterns of single and double mutants with the wild type showed that flo and squa act together to promote flower development but that flo is epistatic to squa with respect to early effects on phyllotaxy. We propose that a common process underlies the phyllotaxy of wildtype, flo, and squa meristem development but that the relative timing of primordium initiation or growth is altered. This process depends on two separable events: setting aside zones for potential primordium initiation and partitioning these zones into discrete primordia. Failure of the second event can lead to the formation of continuous double spirals, which are occasionally seen in flo mutants.

Base Sequence↗
PubMed1995

Obstructive sleep hypopnea syndrome in a patient with Marfan syndrome treated with oxygen therapy.

A patient with Marfan's syndrome and obstructive sleep hypopnea syndrome is reported. She had complained about insomnia, tiredness and hypersomnolence lasting 2 years. A complete nightly polysomnography revealed 94 obstructive hypopneas (the hypopnea index was 12.85) and no obstructive apneas. Presumably an increased laxity of the pharyngeal wall was responsible for the phenomenon. A therapy with CPAP was started, but was not tolerated by the patient. Oxygen therapy on the other hand turned out to be effective and well tolerated.

Adult↗
PubMed1995

Sleep related breathing disorders: the respiratory control system and its instability during sleep.

Respiratory control and instability in the breathing pattern during sleep. Unstable breathing during sleep plays an important role in the development of sleep related breathing disorders (SRBD). Periodic breathing, as a hallmark of this instability, is a common initiator of these disorders. In addition, structure and function of the upper airway are prone to intrinsic and extrinsic, congenital and acquired abnormalities which are as well responsible for the pathogenesis of SRBD.

Body Mass Index↗
PubMed1994

Fimbriata controls flower development by mediating between meristem and organ identity genes.

Two major classes of genes directing flower development have so far been described: early activated genes regulating meristem identity and later acting genes controlling organ identity. Here, we show that the fimbriata (fim) gene acts between these two classes in a sequence of gene activation. The fim gene, originally described in 1930, was cloned by transposon tagging from Antirrhinum majus and encodes a product with no detectable homology to other proteins. Mutations in fim result in partial homeotic transformations of floral organs and in reduced determinacy of the meristem. Expression and function of fim depends on the activity of meristem identity genes, and fim in turn controls the spatial and temporal expression of organ identity genes. The pattern of fim expression defines a new domain of the floral meristem that changes with time in a complementary manner to those of the meristem identity gene floricaula and the organ identity gene plena.

Amino Acid Sequence↗
PubMed1993

Complementary floral homeotic phenotypes result from opposite orientations of a transposon at the plena locus of Antirrhinum.

Recessive mutations at the plena (ple) locus result in a homeotic conversion of sex organs to sterile perianth organs in flowers of Antirrhinum majus. A complementary phenotype, in which sex organs replace sterile organs, is conferred by semidominant ovulata mutations. The ple locus was identified and isolated using a homologous gene, agamous from Arabidopsis, as a probe. The expression of ple is normally restricted to the inner two whorls of the flower, where sex organs develop. However, in ovulata mutants, ple is expressed ectopically in the outer two whorls of the flower and in vegetative organs. These mutants correspond to gain-of-function alleles of ple, suggesting that ple is sufficient for promoting sex organ development within the context of the flower. The plena and ovulata phenotypes result from opposite orientations of the transposon Tam3 inserted in the large intron of ple.

Alleles↗
PubMed1986

Evidence for the presence of D2 but not D1 dopamine receptors in rat hypothalamic perifornical area.

Behavioural studies have shown that the perifornical hypothalamus (PFH) plays a fundamental role in mediating dopamine-induced anorexia. In the present report, we provide biochemical evidence for the occurrence of dopamine receptors in the PFH, but not in the paraventricular nucleus of the hypothalamus. Dopamine as well as bromocriptine, a D2 dopamine receptor agonist, strongly reduced the adenylate cyclase activity in the PFH. This inhibitory effect was reversed by haloperidol and by (-)-sulpiride, but not by (+)-sulpiride. On the contrary, the selective D1 dopamine agonist SKF 82526 was completely inactive in affecting adenylate cyclase activity. Our conclusion asserts the existence of dopamine D2 but not D1 receptors in the PFH, which therefore can be conceived as the only region in the brain where a single class of dopamine receptors is present.

Adenylyl Cyclases↗
PubMed1984

Involvement of arachidonic acid metabolites in beta-adrenoceptor desensitization: functional and biochemical studies.

The prolonged in vitro perfusion of rat lung with isoproterenol (Iso) induced a desensitization of beta-adrenoceptors which was dose- and time-dependent. The decrease in functional responsiveness of rat lung parenchyma to the beta-agonist correlated well with the loss of [3H]dihydroalprenolol ([3H]DHA) binding sites and adenylate cyclase activity after the beta-adrenoceptor desensitization procedure. The cyclooxygenase inhibitor indomethacin prevented the beta-adrenoceptor desensitization as was shown by the restored isoproterenol-induced relaxation in rat lung parenchyma strips and adenylate cyclase activity after the milder desensitization procedure. Inhibition of the arachidonic acid cascade at different levels with different compounds such as BW 755C and betamethasone prevented the desensitization of beta-adrenoceptors. These findings suggest a role for arachidonic acid metabolites in beta-adrenoceptor desensitization. The possible sites of action of arachidonic acid metabolites are also discussed in relation to the inability of indomethacin to prevent the desensitization of beta-adrenoceptors that was induced by the higher Iso concentration used.

Adenylyl Cyclases↗
PubMed1984

Methylazoxymethanol microencephaly in rats: neurochemical characterization and behavioral studies with the nootropic oxiracetam.

The administration of methylazoxymethanol (MAM) to pregnant rats induced a marked reduction in the weight of the offspring's brain. This reduction was due to aplasia of the cortex and hippocampus, whose thicknesses were 50% of those of control animals. A significant reduction was also observed in the striatum. This aplasia could be ascribed to the antimitotic effect of MAM, which, when given at gestational day 15, prevented the development of neurons in the three brain areas mentioned. Indeed, we infer here that the total number of GABA-receptor complexes, as measured by [3H]muscimol and [3H]flunitrazepam binding, was reduced to the same degree as was the weight of the cortex. Similarly, total [3H]haloperidol binding sites were reduced in the striatum. From the behavioral point of view, offspring of MAM-treated rats (MAM rats) showed impaired acquisition in the water-maze and pole-climbing tests, indicating that this brain aplasia had disrupted cognitive processes. In contrast, these animals showed normal growth, and grossly their behavior appeared normal. Oxiracetam, a new compound that belongs to the recently described class of nootropic drugs, was able to restore acquisition processes in MAM rats. We propose therefore that MAM rats might become an interesting and quite simple animal model for evaluation of new acquisition-enhancing drugs. Moreover, this model could also be useful to study the neurochemical correlates of cognitive processes.

Abnormalities, Drug-Induced↗
PubMed1983

Beta-adrenoceptor desensitization in rat lung: functional and biochemical aspects.

Rat lung parenchymal strips were used to study beta-adrenoceptor desensitization from both a functional and a biochemical point of view. Prolonged "in vitro' exposure of rat lung to the beta-agonist isoproterenol (10(-6) M for 20 min) markedly reduced the antagonistic activity of isoproterenol on carbachol-induced contractions. The loss of responsiveness to isoproterenol was associated with a 33% decrease of the beta-receptor number with concomitant reduction of isoproterenol-stimulated adenylate cyclase activity, whereas the enzyme response to NaF was identical in control and in desensitized rat lung. On the basis of these results obtained by comparing the functional and biochemical aspects of the desensitization process, we suggest that the marked reduction of pharmacological activity of isoproterenol after desensitization was primarily due to the decrease in the number of binding sites. The possible molecular mechanisms underlying desensitization are also discussed.

Adenylyl Cyclases↗
PubMed1983

Behavioural and biochemical effects in the adult rat after prolonged postnatal administration of clozapine.

Rats were administered 10 mg/kg SC of clozapine (C) or vehicle solution (S) daily from day 1 after birth until 20 days of age. At 60 days of age (40 days after the postnatal treatment with C or S was interrupted) the stereotyped behaviour and the effects on locomotor activity elicited by apomorphine in S- and C-pretreated rats were investigated. The intensity of stereotyped behaviour as well as the decrement in locomotion induced by apomorphine (0.5--1 mg/kg SC) were not influenced by chronic C administration during development. Finally, at 80 days of age (60 days after the postnatal treatment with C or S was interrupted) rats were subjected to a differential reinforcement of low rates schedule (DRL15s). The results indicate that the acquisition of the DRL task performance criterion (Rs/Rf less than or equal to 2.5) was significantly more rapid in S-pretreated rats than in C-pretreated ones. In parallel biochemical experiments, homovanillic acid (HVA) content was measured in striatum in rats at 60 days of age (40 days after the postnatal treatment with C or S was interrupted). The results indicate that even if an acute challenge dose of 10 mg/kg C shows a certain degree of tolerance a single dose of 20 mg/kg C is still able to increase striatal HVA concentration in chronic C-pretreated animals. These data indicate that early postnatal administration of a non-cataleptogenic neuroleptic, like C, induces, in the adult rat, behavioural and biochemical changes which significantly differ from those elicited by a cataleptogenic neuroleptic, like haloperidol.

Animals↗
PubMed1983

Early postnatal chlordiazepoxide administration: permanent behavioural effects in the mature rat and possible involvement of the GABA-benzodiazepine system.

The long term behavioural and biochemical effects of chronic chlordiazepoxide treatment during the period of neuronal maturation in the rat have been investigated. The administration to lactating mothers of chlordiazepoxide at very low doses (0.22 and 2.6 mg/kg) in their drinking water affects both behavioural and biochemical parameters in offspring at 60 days of age and undrugged since weaning. A deficit in the acquisition of the conditioned avoidance response in treated rats was observed, although no significant difference in spontaneous locomotor activity between control and treated rats was found. 3H-Flunitrazepam binding sites in cerebral cortex and hippocampus were decreased by the treatment, whereas no change was detected in cerebellum. Moreover, 3H-muscimol binding sites increased in hippocampus with no changes in cerebral cortex and cerebellum. According to the different regional distribution of benzodiazepine type 1 and type 2 receptors, we suggest that type 2 receptors are selectively affected by the treatment, and that the GABAergic receptor system is also permanently altered by administration of chlordiazepoxide during early postnatal life.

Animals↗
PubMed1983

Effects of buflomedil on the responsiveness of canine vascular smooth muscle.

Experiments were designed to determine the effect of buflomedil on vascular responsiveness. Rings of canine arteries and veins were suspended for isometric tension recording at 37 degrees C. Buflomedil caused concentration-dependent inhibition of the contractile responses to norepinephrine, methoxamine, phenylephrine, clonidine, xylazine and sympathetic nerve activation, but not of the responses to potassium, prostaglandin F2 alpha, acetylcholine or 5-hydroxytryptamine. The inhibitory effect of buflomedil was not affected by endothelium removal but was reduced by chemical sympathectomy with 6-hydroxydopamine and by inhibitors of neuronal uptake. Strips of canine saphenous veins were superfused after incubation with [3H]norepinephrine. Buflomedil augmented the efflux of [3H]norepinephrine, 3,4-[3H]dihydroxyphenylglyol, 3,4-[3H]dihydroxymandelic acid and [3H]-3-methoxy-4-hydroxyphenylglycol under basal conditions and the overflow of [3H]norepinephrine, 3,4-[3H]dihydroxymandelic acid and 3,4-[3H] dihydroxyphenylglycol during sympathetic nerve activation. The augmentation by buflomedil of the release of [3H]norepinephrine evoked by electrical stimulation was prevented by phentolamine. In the perfused gracilis muscle of the anesthetized dog, buflomedil depressed the vasoconstrictor response to norepinephrine more than that evoked by angiotensin II. These experiments suggest that buflomedial blocks alpha adrenoceptors, but is not selective for either the alpha-1 or alpha-2 adrenoceptor subtype. The presence of adrenergic nerve endings appear to augment the postjunctional inhibitory effects of buflomedil.

Adrenergic alpha-Antagonists↗