热分析方法对几种不同产地山药的鉴别

目的：考察热分析方法对不同种质、地域山药鉴别的可行性。方法：对5个产地的山药分别在氮气与空气气氛下的DTA和DTG曲线进行分析，根据其图谱的特征差异进行鉴别。结果：不同种山药的DTA，DTG图谱，不同种、不同地域山药的DTG图谱均有差异。结论：此方法可用于不同种、不同地域山药的鉴别。     

Effects of low and high doses of selective sigma ligands: further evidence suggesting the existence of different subtypes of sigma receptors

Several high affinity sigma (σ) ligands, such as DTG, JO-1784, (+)-pentazocine, BD-737 and L-687,384, administered at low doses act as agonists by potentiating N-methyl-D-aspartate (NMDA)-induced activation of pyramidal neurons in the CA₃ region of the rat dorsal hippocampus. This potentiation is dose-dependent at doses between 1 and 1000 μg/kg, IV but bell-shaped dose-response curves are obtained. Other σ ligands like haloperidol, BMY-14802, (+)3-PPP and NE-100 administered at low doses act as σ antagonists, since they do not modify the NMDA response but suppress the potentiation of the NMDA response induced by σ agonists. Because high doses of the σ agonists do not potentiate the NMDA response, the present experiments were undertaken to assess if, at high doses, these σ ligands could also act as σ antagonists and suppress the potentiation induced by low doses of σ agonists. High doses of DTG, JO-1784, BD-737, and L-687,384, administered acutely, had an effect similar to that of low doses of haloperidol, by suppressing and preventing the potentiation induced by low doses of DTG, JO-1784, BD-737, L-687,384 and (+)-pentazocine. High doses of (+)-pentazocine suppressed the effect of a low dose of (+)-pentazocine but did not affect the potentiation induced by a low dose of the other σ agonists. The potentiation induced by a low dose of a σ₁ agonist was not further increased by the subsequent administration of another low dose of a σ₁ agonist. All together, these results strongly suggest that more than two subtypes of σ receptors exist in the CNS. Received: 1 April 1996 / Final version: 14 August 1996     

The cytochromes P-450 are not involved in the modulation of the N-methyl-D-aspartate response by sigma ligands in the rat CA3 dorsal hippocampus

Recent in vitro radioligand binding studies have shown that several cytochrome P-450 inhibitors can displace [³H] sigma ligands, suggesting that these ligands might bind to the cytochrome P-450 superfamily of enzymes. Using an in vivo electrophysiological model of extracellular recordings performed in the CA₃ region of the rat dorsal hippocampus, we have previously shown that intravenous administration of low doses of several sigma ligands, such as 1, 3-di(2-tolyl) guanidine (DTG), JO-1784, and (+)pentazocine potentiate the neuronal response induced by microiontophoretic applications of N-methyl-D-aspartate (NMDA) without affecting those induced by quisqualate and kainate, suggesting that they act as sigma agonists. Conversely, the sigma ligands haloperidol, (+)3-PPP, and BMY-14802, which have no effect by themselves on the NMDA response, prevent and suppress the potentiating effect of sigma agonists on the NMDA response, suggesting that they act as sigma antagonists. The present studies were undertaken to determine if cytochromes P-450 could be involved in the modulation of the NMDA response by sigma ligands. For this purpose, two cytochrome P-450 inhibitors, proadifen (SKF-525A) and piperonyl butoxide (PB), have been tested in our model. Unlike sigma agonists, at low doses, neither SKF-525A nor PB affected the NMDA response of CA₃ dorsal hippocampus pyramidal neurons. Unlike sigma antagonists, neither of these drugs reversed or prevented the DTG-induced potentiation of the NMDA response. In addition, following high doses of SKF-525A or PB, sufficient to induce a complete inactivation of cytochromes P-450, DTG still potentiated the NMDA response. The present data suggest that cytochrome P-450 inhibitors do not modulate the NMDA response like sigma agonists or antagonists do in this brain region. Furthermore, they rule out the involvement of cytochromes P-450 in the modulation of the NMDA response by sigma ligands. © 1993 Wiley-Liss, Inc.     

Experimental and spectroscopic studies of charge transfer reaction between sulfasalazine antibiotic drug with different types of acceptors

The charge-transfer (CT) interactions between the electron donor sulfasalazine (SS) and the acceptors 2,3-dichloro-5,6-dicyano-1,4-benzoquinone (DDQ), p-chloranil (CHL), picric acid (PA) and iodine have been studied spectrophotometrically in CHCl(3) or CH(3) OH solutions. The formed solid CT complexes were also isolated and characterized through infrared, (1) H-NMR, mass spectra as well as elemental and thermal analysis. The CT complexes were discussed in terms of formation constant (K(CT) ), molar extinction coefficient (ε(CT) ), standard free energy (ΔG°), oscillator strength (f), transition dipole moment (μ), resonance energy (R(N) ) and ionization potential (I(D) ). The stoichiometry of these complexes was found to be 1:1 molar ratio and having the formulae [(SS)(DDQ)], [(SS)(CHL)], [(SS)(PA)] and [(SS)(2) I](+) · I(3) (-) , respectively. The charge transfer interaction was successfully applied to the determination of SS drug using mentioned σ and π-acceptors also, the results obtained herein are satisfactory for estimation of SS compound in the pharmaceutical form.     

DTG thermal analyses and viscosity measurements of three commercial agar impression materials

Three commercial agar impression materials, two for clinical uses and one for dental laboratory, were examined for their thermal properties by differential thermogravimetric (DTG) thermal analyses and viscosity measurements. On DTG profiles, an endothermic peak along with weight loss at around 100 degrees C was observed on all three agar impression materials as a result of water evaporation. Two clinical agar impression materials were more susceptible to this trend than the remaining one dental laboratory agar impression material. The viscosity of three agar impression materials could be expressed in the exponential function of temperature. Viscosity at 46 degrees C of one dental laboratory agar impression material far exceeded those of two clinical agar impression materials. Monitoring the viscosity could facilitate the detailed analysis of setting process of agar impression materials upon cooling, and might be useful for future development of agar-based dental impression materials.     

Use of Bacteria to Activate Ground-Granulated Blast-Furnace Slag (GGBFS) as Cementless Binder

Ground-granulated blast-furnace slag (GGBFS) can be used as a cementless binder after activation. Recent approaches to activate GGBFS have focused on chemical methods that use NaOH, KOH, and CaO. This study introduces the use of bacteria to activate GGBFS as a biological approach. The presence of bacteria (volumetric ratio), curing temperature (23 °C and 60 °C), and number of curing days (3, 7, and 28 d) are investigated. The use of urea is considered owing to the possibility of calcium carbonate formation. The activated GGBFS is evaluated in the form of a cube (5 cm × 5 cm × 5 cm) for its strength, mineral identification, and pore size distribution. A brick (19 cm × 9 cm × 5.7 cm) is prefabricated to see the feasibility of commercializing bacteria-activated GGBFS based on water absorption and strength measurements. All results are compared with those of water-activated GGBFS. The results indicate that the use of urea inhibits the strength improvement of bacteria-activated GGBFS. Bacterial suspension enhances the GGBFS strength at a curing temperature of 60 °C. Mineral identification tests show that the strength increase is primarily due to the formation of calcite. The compressive strength satisfies the commercial standard of concrete bricks; however, the water absorption rate must be resolved.     

Haloperidol treatment differentially regulates [H]DTG and [H](+)-3-PPP labeled σ binding sites

The effect of repeated haloperidol administration on σ binding sites in brain membranes was assessed using [³H](+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine ((+)-3-PPP) and [³H]1,3-di-o-tolylguanidine (DTG). Administration of haloperidol (1 mg/kg, i.p.) to guinea pigs for 14 consecutive days followed by a 4 day drug-free period prior to sacrifice resulted in 75% and 6% decreases in the specific binding of [³H](+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine and [³H]1,3-di-o-tolylguanidine, respectively, when measured using a single concentration (2 nM) of radioligand. Scatchard analysis revealed a reduction in both the maximum number of [³H](+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine binding sites and the affinity of these sites for the radioligand; the potency of 1,3-di-o-tolylguanidine to inhibit [³H](+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine binding was also reduced. In parallel studies, the potency of 1,3-di-o-tolylguanidine to inhibit [³H]1,3-di-o-tolylguanidine binding was unaffected by haloperidol treatment, but the potency of (+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine against [³H]1,3-di-o-tolylguanidine was reduced 3-fold. Phenytoin, which increased (10-fold) the potency of dextromethorphan to inhibit [³H]1,3-di-o-tolylguanidine binding in control membranes, had no effect in membranes obtained from haloperidol-treated animals. The reduction in [³H](+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine binding was dependent upon the duration of the drug-free period and amounted to 73% and 25% in brain membranes prepared from animals sacrificed 14 days and 28 days, respectively, following cessation of drug treatment. Repeated administration of other antipsychotic and σ agents including DTG, dextromethorphan, spiperone, chlorpromazine and clozapine had no effect on [³H](+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine or [³H]1,3-di-o-tolylguanidine binding. These findings suggest that repeated haloperidol administration selectively regulates [³H](+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine binding in guinea pig brain membranes. However, the observations that repeated drug treatment resulted in (1) reduced affinity of (+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine for [³H]1,3-di-o-tolylguanidine binding sites, and (2) a loss of the ability of phenytoin to increase dextromethorphan's potency against [³H]1,3-di-o-tolylguanidine, suggest that [³H](+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine and [³H]1,3-di-o-tolylguanidine binding sites are distinct but functionally coupled.     

Repeated administration of Sigma ligands alters the population activity of rat midbrain dopaminergic neurons

Acute and repeated administration of antipsychotic drugs produce distinctive profiles of electrophysiological effects on the population activity of midbrain dopaminergic (DA) neurons which correlate with their clinical effects. Sigma receptors have been hypothesized to be involved in psychosis and in the efficacy of antipsychotic drugs, but little is known about the effects of repeated treatment with sigma ligands on the activity of midbrain DA neuronal populations. In the present study, the cells-pertrack cell-sampling method was used to evaluate the effects of 3 sigma ligands on the numbers of spontaneously active A9 and A10 DA neurons in chloral hydrate-anesthetized rats. One-hour pretreatment with either (+)-pentazocine (10 mg/kg, i.p.), DTG (2 mg/kg, i.p.), or JO 1784 (1 or 10 mg/kg, s.c.) did not alter the number of spontaneously active DA neurons encountered per electrode track. Repeated treatment (21 daily injections) with (+)-pentazocine (1 or 10 mg/kg) or DTG (0.2 or 2 mg/kg) increased the number of A10 DA cells per track; JO 1784 (10 mg/kg but not 1 mg/kg) moderately decreased the number of active A9 DA cells and increased the firing rate of A10 DA neurons. The effect of JO 1784 on A9 DA neurons was not due to depolarization inactivation. The effects of all 3 sigma ligands differ from those of antipsychotic drugs, all of which inactivate A10 DA neurons after repeated treatment. Clinical studies are necessary to determine if selective sigma ligands will provide a novel alternative to DA antagonists in the treatment of psychosis. © 1993 Wiley-Liss, Inc.     

Microinjection of sigma ligands into cranial nerve nuclei produces vacuous chewing in rats

Many typical neuroleptics carry a high risk for producing motor side effects in humans, and have significant affinities for sigma (σ) receptors. Sigma receptors are densely concentrated in cranial nerve nuclei that comprise the final common pathways for lingual, facial and masticatory movements; thus, they may serve as important substrates for some of the unwanted movements that can accompany neuroleptic treatment. Therefore, the purpose of this study was to evaluate whether microinjection of σ ligands into the facial nucleus or spinal trigeminal nucleus, oralis would cause orofacial dyskinesias, and whether these effects could be attenuated with σ receptor antagonists. Microinjection of the high affinity σ ligands, di-o-tolylguanidine or haloperidol (0–10 nmol/0.5 μl), produced a marked increase in vacuous chewing and facial tremors in rats, while coadministration of the functional σ antagonists, BD1047 or BD1063 (5 nmol), greatly attenuated these drug-induced movements. Sulpiride and clozapine (10 nmol/0.5 μl), σ inactive/ dopamine active atypical antipsychotic drugs with a much reduced risk for producing motor side effects in humans, were unable to elicit orofacial dyskinesias when microinjected into the facial or spinal trigeminal nucleus, oralis. These studies indicate that σ receptors may contribute to some forms of motor side effects resulting from antipsychotic drug treatment. Received: 23 July 1997/Final version: 22 October 1997