Clustered binary logistic regression in teratology data using a finite mixture distribution.

The beta-binomial distribution introduced by Skellam has been applied in many teratology problems for modelling the litter effect. Recently, Morel and Nagaraj proposed a new distribution for modelling cluster multinomial data when the clustering is believed to be caused by clumped sampling. It turns out that the distribution is a mixture of two binomial distributions and accommodates the estimation of an additional parameter to account for intra-litter effect.

Effect of a 14-day hindlimb suspension on cytosolic Ca2+ concentration in rat portal vein myocytes.

Effects of a 14-day hindlimb suspension were examined on increases in cytosolic Ca2+ concentration ([Ca2+]i) evoked by vasoactive compounds and on Ca2+ channels in rat portal vein myocytes. The maximal increases in [Ca2+]i elicited by caffeine, norepinephrine, and angiotensin II were reduced by 30-50% in suspended rats, and complete recovery was obtained 4 days after suspension removal. In contrast, voltage-gated Ca2+ channels were unaffected by hindlimb suspension.

A betagamma dimer derived from G13 transduces the angiotensin AT1 receptor signal to stimulation of Ca2+ channels in rat portal vein myocytes.

A G protein composed of alpha13, beta1, and gamma3 subunits selectively couples the angiotensin AT1A receptors to increase cytoplasmic Ca2+ concentration ([Ca2+]i) in rat portal vein myocytes (Macrez-Leprêtre, N., Kalkbrenner, F., Morel, J.

Long-term therapy with trimetazidine in cardiomyopathic Syrian hamster BIO 14:6.

The cardiomyopathic Syrian hamster (CMH) of the strain BIO 14:6 is a model for both cardiac and skeletal muscle abnormalities. It has reduced longevity and noticeable hypertrophy of the heart and liver. At 220 days, CMHs display a total Ca2+ overload, 1.

Purification of a new dimeric protein from Cliona vastifica sponge, which specifically blocks a non-L-type calcium channel in mouse duodenal myocytes.

Marine sponges are synthesizing a wide variety of peptidic and organic molecules with biological activities. Multiple-step purification of Cliona vastifica extract led to a new dimeric peptide (mapacalcine; M(r) = 19,064) that is composed of two homologous chains, each containing nine cysteins. This protein has been found to selectively block a new calcium conductance characterized in mouse duodenal myocytes with an IC50 value of approximately 0.

Specific Gq protein involvement in muscarinic M3 receptor-induced phosphatidylinositol hydrolysis and Ca2+ release in mouse duodenal myocytes.

1. Cytosolic Ca2+ concentration ([Ca2+]i) during exposure to acetylcholine or caffeine was measured in mouse duodenal myocytes loaded with fura-2. Acetylcholine evoked a transient increase in [Ca2+]i followed by a sustained rise which was rapidly terminated after drug removal.

G protein heterotrimer Galpha13beta1gamma3 couples the angiotensin AT1A receptor to increases in cytoplasmic Ca2+ in rat portal vein myocytes.

The subunit composition of angiotensin AT1 receptor-activated G protein was identified by using antisense oligonucleotide injection into the nucleus of rat portal vein myocytes. In these cells, we have previously shown that increases in the cytoplasmic calcium concentration ([Ca2+]i) induced by activation of angiotensin AT1 receptors were dependent on extracellular Ca2+ entry by L-type Ca2+ channels and subsequent Ca2+-induced Ca2+ release from the intracellular stores. The angiotensin AT1 receptor-activated increases in [Ca2+]i were selectively inhibited by injection of antisense oligonucleotides directed against the mRNAs coding for the alpha13, beta1, and gamma3 subunits.

Shape and length of myosin heads and radial compressive forces in muscle.

Irrespective of the exact shape and length of myosin heads, it is shown that radial compressive forces occur in contracting muscle, which tend to bring the myofilaments closer to each other. This is in contradiction with common observation: a muscle that shortens swells laterally. The presence of these forces is model-dependent and they appear only in the case of the traditional concepts of force generation.

Algebraically structured colored Petri nets to model sequential processes.

Sequential processes can hardly be modeled with Colored Petri Nets (CPN). Their standard functions (such as "Succ" and "Prec") can only describe simple cases whereas modeling a complex sequence requires the definition of a function via a cumbersome and static table. In order to overcome these limitations, we first introduce a mixed structure based upon CPN and FIFO queues; then, we define an isomorphism between the set of colors and a finite field Z/pZ enabling symbolic calculation using polynomials associated with arcs instead of linear functions mapping sets into sets.

The expression of the tobacco Tnt1 retrotransposon is linked to plant defense responses.

Activation of retrotransposons by stresses and external changes is common in all eukaryotic systems, including plants. The transcription of the tobacco Tnt1 retrotransposon was studied in its natural host as well as in Arabidopsis and tomato. It is activated by factors of microbial origin, by external stresses, and by viral, bacterial, and fungal attacks.

The promoter of the tobacco Tnt1 retrotransposon is induced by wounding and by abiotic stress.

The transcription of the tobacco Tnt1 retrotransposon was previously shown to be induced, in tobacco and in heterologous species, by microbial elicitors and by pathogen infections. We report here that the expression of the Tnt1 promoter is also activated in heterologous species such as tomato and Arabidopsis by wounding, freezing and by other abiotic factors known to induce the plant defence response, such as salicylic acid, CuCl2, or oxidative stress. A similar regulation is observed in tobacco for most treatments.

Influence of a methanogenic flora on the breath H2 and symptom response to ingestion of sorbitol or oat fiber.

Background And Objectives: We investigated the possibility that a variant of the normal colonic flora, a high concentration of methanogens, influences the host's response to ingestion of nonabsorbable, fermentable materials.

Methods: To better evaluate symptomatic and breath H2 and methane (CH4) responses, subjects were placed on a basal diet (primarily rice and hamburger) that contained minimal amounts of nonabsorbable, fermentable substrate. A breath CH4/H2 ratio of greater or less than 1 on the second day of the basal diet was used to categorize subjects as high (N = 9) or low (N = 25) CH4 producers.

Angiotensin II-mediated activation of L-type calcium channels involves phosphatidylinositol hydrolysis-independent activation of protein kinase C in rat portal vein myocytes.

The action of angiotensin II (ANG II) was studied in single myocytes from rat portal vein, in which the cytoplasmic Ca++ concentration was estimated by emission from fluorescent dyes and the Ca++ channel current was measured with the whole-cell mode of the patch-clamp technique. ANG II stimulated Ca++ channel current through L-type Ca++ channels and initiated a slow and small increase in the cytoplasmic Ca++ concentration in cells in which intracellular Ca++ stores had been depleted by pretreatment with ryanodine and caffeine. Both Ca++ channel current stimulation and Ca++ responses were selectively inhibited by losartan, indicating activation of angiotensin AT1 receptors.

Angiotensin II-activated Ca2+ entry-induced release of Ca2+ from intracellular stores in rat portal vein myocytes.

1. The action of angiotensin II (AII) was studied in single myocytes from rat portal vein in which the cytoplasmic Ca2+ concentration was estimated by emission from dyes Fura-2 or Indo-1 and the Ca2+ channel current was measured with the whole-cell mode of the patch-clamp technique. 2.

Effects of phospholipase C inhibitors on Ca2+ channel stimulation and Ca2+ release from intracellular stores evoked by alpha 1A- and alpha 2A-adrenoceptors in rat portal vein myocytes.

The ability of phospholipase C inhibitors to inhibit Ca2+ channel stimulation and Ca2+ release from intracellular stores evoked by norepinephrine in single rat portal vein myocytes was investigated in the aim of identifying the type of phospholipase C involved in the transduction pathways activated by alpha 1A- and alpha 2A-adrenoceptors. U73122 (an inhibitor of phosphatidylinositol-phospholipase C) inhibited in a concentration-dependent manner the release of Ca2+ from the intracellular stores induced by activation of alpha 1A-adrenoceptors and related to inositol phosphate production whereas U73343 was ineffective. Both compounds had no effect on the release of Ca2+ induced by caffeine.

Nitric oxide synthesis inhibition attenuates behavioral actions of neuropeptide FF.

Neuropeptide FF (NPFF) has certain antiopiate actions and may play a role in opiate tolerance and dependence. Third ventricle injection of 10 micrograms NPFF induces a quasimorphine abstinence syndrome in opiate-naive rats. Nitric oxide synthesis may also contribute to opiate tolerance and dependence.

Phenytoin embryopathy: effect of epoxide hydrolase inhibitor on phenytoin exposure in utero in C57BL/6J mice.

Previous animal research has suggested that the phenytoin arene oxide metabolite is teratogenic in acute studies and that the fetal effects were increased after injecting an inhibitor of microsomal epoxide hydrolase (mEH) (Martz et al., Pharmacol Exp Ther 203:231-239, 1977, Barcellona et al., Teratog Carcinog Mutagen 7:159-168, 1987).

Subcutaneous injection of an analog of neuropeptide FF prevents naloxone-precipitated morphine abstinence syndrome.

There is evidence that neuropeptide FF (NPFF) has antiopiate activity and may play a role in opiate dependence and subsequent abstinence syndrome. A fragment of NPFF was modified at the C-terminal in an effort to convert it to an NPFF antagonist. It was also dansylated at the N-terminal in an effort to render it more lipophilic and increase its penetration of the blood-brain barrier.

A Gi1-2-protein is required for alpha 2A-adrenoceptor-induced stimulation of voltage-dependent Ca2+ channels in rat portal vein myocytes.

In rat portal vein myocytes, alpha 2A-adrenoceptors activate voltage-dependent Ca2+ channels via a transduction pathway requiring protein kinase C activation mediated by a pertussis-toxin-sensitive G-protein. As revealed by the use of antibodies directed against the different alpha-subunits expressed in portal vein myocytes, we show that the clonidine-induced stimulation of voltage-dependent Ca2+ channels is mainly mediated by a Gi1-2-protein.

F-actin-myosin-subfragment-1 (S1) interactions. Identification of the refractory state of S1 with the S1 dimer.

Several conflicting experiments have been carried out concerning the existence of a refractory state for myosin subfragment 1 (S1; i.e. unable to bind to F-actin), in the presence of Mg-nucleotide compounds, at low temperature.

Both alpha 1A- and alpha 2A-adrenoreceptor subtypes stimulate voltage-operated L-type calcium channels in rat portal vein myocytes. Evidence for two distinct transduction pathways.

Previously, we have shown that myocytes from rat portal vein express alpha 1A-adrenoreceptors that couple with a Gq/G11-protein to stimulate phosphoinositide turnover and release of calcium from intracellular stores. The purpose of this study was to investigate the contribution of both alpha 1- and alpha 2-adrenoreceptor subtypes in inducing stimulation of voltage-operated calcium channels. Norepinephrine (a nonselective alpha-adrenoreceptor agonist), phenylephrine (an alpha 1-adrenoreceptor agonist), clonidine, and oxymetazoline (alpha 2-adrenoreceptor agonists) stimulated the calcium channel current by a similar extent.