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One-dimensional polar gases in deep optical lattices present a severely constrained dynamics due to the interplay between dipolar interactions, energy conservation, and finite bandwidth. The appearance of dynamically bound nearest-neighbor dimers enhances the role of the 1/r^{3} dipolar tail, resulting in the absence of external disorder, in quasi-localization via dimer clustering for very low densities and moderate dipole strengths. Furthermore, even weak dipoles allow for the formation of self-bound superfluid lattice droplets with a finite doping of mobile, but confined, holons. Our results, which can be extrapolated to other power-law interactions, are directly relevant for current and future lattice experiments with magnetic atoms and polar molecules.

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Pyridalyl is an insecticide of a novel chemical class (unclassified insecticides). Toxicity of pyridalyl to two insect pest species, Spodoptera litura and Frankliniella occidentalis, an insect predator, Orius stringicollis, and a pollinator, Bombus terrestris, was evaluated in the laboratory. The insecticidal activity of pyridalyl against S. litura was evaluated using the leaf-dipping method. The potency of pyridalyl was highly effective against all development stages (2nd to 6th instar larvae) of S. litura. This compound was also evaluated against F. occidentalis using the direct spray method. For F. occidentalis, toxicity of pyridalyl was almost similar to that of acrinathrin, but greater than acrinathrin for adults. Then the toxicity of this product to the natural enemies, Orius stringicollis and the pollinating insect Bombus terrestris, was evaluated using the body-dipping method or direct spray method. No acute toxicity of this product was observed on these non-target insects. Moreover, the influence of pyridalyl to the nest of Bombus terrestris was evaluated using the direct spray to the inside of the nest. No apparent influence of this compound was observed by 21 days after treatment. The cytotoxicity of pyridalyl to the Sf9 insect cell line and the CHO-K1 mammalian cell line was evaluated using the trypan-blue exclusion method. High toxicity to the insect cell line, but almost no toxicity to the mammalian cell line, was observed. Thus, pyridalyl exhibited high selectivity in cytotoxicity between the insect and mammalian cell line as well as in insecticidal activity among insect species. We infer pyridalyl may be useful for IPM programs of greenhouse cultivation system.

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This study was designed to clarify the relationship between the antihypertensive effects of the calcium antagonist nilvadipine, and circadian changes in blood pressure. Based on measurements using an ambulatory blood pressure monitoring system (ABPM), 17 outpatients with untreated essential hypertension were divided into two groups: a sustained hypertensive group (with a fall in blood pressure during sleep < 10%, n = 7) and a waking time hypertensive group (with a fall in blood pressure during sleep > or = 10%, n = 10). During treatment with nilvadipine (8 mg/day, > or = 2 weeks), patients were reexamined by ABPM. The antihypertensive effect of nilvadipine was significantly and negatively correlated with the night time fall in blood pressure: this effect was significantly greater in the sustained hypertensive group than in the waking time hypertensive group. These data suggest that the long acting calcium antagonist nilvadipine has more potent antihypertensive effects in patients with sustained hypertension ("nondippers") than in those whose hypertension lessens during sleep ("dippers").

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Lymphocytes are widely used as a model for the cardiovascular beta-adrenoceptor-adenylate cyclase system. We evaluated the role of this system in the pathogenesis of hypertension by studying lymphocytes obtained from patients with essential hypertension. Untreated hypertensive patients and normotensive control subjects were studied. The number and affinity of the beta-adrenoceptors were measured by a radioligand binding method with 125I-cyanopindolol. The responses of cyclic adenosine monophosphate (cAMP) to isoproterenol, cholera toxin, and forskolin were also determined. The concentration and affinity of beta-adrenoceptors did not differ significantly in the two groups, nor was a significant difference found in the basal level of cAMP. The effects of isoproterenol on the accumulation of cAMP were reduced in the lymphocytes from the hypertensive compared with the normotensive subjects. There was no significant difference in the effect of forskolin on cAMP accumulation in the two groups. These results indicate that the activity of the stimulatory nucleotide binding regulatory protein (Gs-protein) is reduced in lymphocytes from patients with essential hypertension. This defect of Gs-protein in the lymphocytes may represent a defect of Gs-protein in the cardiovascular system in such patients.

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A case of orthostatic and postexertional hypotension with ischemic electrocardiographic changes is reported. The etiology was considered to be the partial dysfunction of efferent sympathetic nerve endings. Peripheral adrenergic receptors (alpha and beta) were up-regulated, which might have caused pseudoischemic electrocardiographic changes and abnormal vasodilation after exercise.

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1. Systemic (s.c. or p.o.) administration of L-threo-3,4-dihydroxyphenylserine (droxidopa, L-threo-DOPS; L-DOPS), a noradrenaline precursor, at a dose-range of 100-800 mg kg-1, produced naloxone-resistant antinociception in a dose-dependent manner in the mouse, as assessed by the tail flick test, kaolin-induced writhing test and formalin-induced nociception test. 2. Antinociception elicited by L-DOPS (400 mg kg-1, s.c.) was not affected by s.c. injection of benserazide, a peripherally preferential L-aromatic amino acid decarboxylase inhibitor, but was suppressed by its intracerebroventricular (i.c.v.) injection. 3. I.c.v. or intrathecal (i.t.) administration of the non-selective alpha-blocker, phentolamine, significantly reduced L-DOPS-induced antinociception. 4. I.c.v. administration of the alpha 1-blocker, prazosin, but not the alpha 2-blocker, yohimbine, abolished the antinociceptive effects of L-DOPS. In contrast, both blockers, when administered i.t., exhibited significant inhibitory effects. 5. These results suggest that systemic L-DOPS produces opioid-independent antinociception, mediated by supraspinal alpha 1-adrenoceptors and by spinal alpha 1- and alpha 2-adrenoceptors and may predict additional therapeutic applications of L-DOPS as an analgesic.

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L-Tyrosine methyl ester (L-Tyr-OMe) produces naloxone-reversible antinociception in mice. This effect was characterized in the present study. L-Tyr-OMe administered s.c. at doses of 100-400 mg/kg elicited dose-dependent antinociception, which was antagonized by s.c. and i.c.v. naloxone at 1 mg/kg and 10 ng/mouse, respectively, but not by i.t. injection at 10 ng/mouse. The antinociceptive effect of systemic L-Tyr-OMe was also inhibited by naltrindole (0.1 mg/kg s.c.), a selective delta-opioid receptor antagonist, but was resistant to L-leucyl-L-arginine (3 micrograms/mouse i.c.v.), a kyotorphin (L-tyrosyl-L-arginine) receptor antagonist. This effect was reduced by i.t., but not by i.c.v., phentolamine at 0.1-1 microgram/mouse, while methysergide (10 microgram/mouse i.t.) and p-chlorophenylalanine (500 mg/kg s.c.) did not have such an inhibitory effect. L-Tyr-OMe, given i.c.v. and i.t. at 0.1-10 microgram/mouse, also produced dose-dependent antinociception, the latter effect being naloxone-reversible but resistant to i.t. phentolamine. These results suggest that L-Tyr-OMe (s.c.)-induced antinociception is mediated by central delta-opioid receptors and by the bulbo-spinal noradrenergic system, but not by the central 'kyotorphinergic' system, and that L-Tyr-OMe, when given i.t., produces antinociception via spinal opioidergic, but not noradrenergic systems.

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