Evaluation of four elastomeric interocclusal recording materials

Background: The fabrication of dental prosthesis requires the transfer of interocclusal records from patient's mouth to semiadjustable articulators using different kinds of recording media. Any inaccuracy in these interocclusal records leads to occlusal errors in the final prosthesis. This study was conducted to evaluate the dimensional changes occurring in the interocclusal recording material over a given period of time and the material's resistance to compression during the cast mounting on the articulator.     

The effects of baclofen and pertussis toxin on epileptiform activity induced in the hippocampal slice by magnesium depletion

Bathing hippocampal slices in artificial cerebrospinal fluid without magnesium elicits repetitive, long ictal-like discharges termed ictaform events. The ictaform events are separated by interictal periods that are initially silent with no interictal bursts. Interictal bursts appear in the later part of the interictal periods and intensify just before the next ictaform event. The GABAB agonist, baclofen, entirely suppressed interictal bursts during the interictal periods and produced a dose-dependent prolongation of the interictal period. Conversely, in slices pretreated with pertussis toxin to reduce the GABAB neurotransmission, interictal bursts were greatly increased, often occupying the entire interictal period, although the total duration of the interictal periods was not affected. Pertussis toxin pretreatment also lengthened the ictaform events. These opposing effects of baclofen and pertussis toxin suggest that GABAB neuro-transmission is important in regulating both the occurrence of interictal bursts in the interictal period, as well as the duration of ictaform events in the low magnesium model of epileptiform activity.     

7β-(6-取代-2-喹诺酮-3-乙酰氨基)头孢菌素的合成

以6-取代-2-喹诺酮-3-乙酸为侧链,用CDI法和潘化酯法与7-ADCA,7-ACA,7-ACT,和7-ACD缩合,合成了16个新的7β-(6-取代-2-喹诺酮-3-乙酰氨基)头孢菌素类化合物,通过溶媒转提,葡聚糖凝胶(Sephadex LH-20)柱层析及离心薄层层析分离精制,得到纯品。初步体外抑菌试验表明:新化合物对革兰氏阳性及某些阴性菌具有高度敏感性。大多数化合物对所试试验菌的抗菌活性与头孢唑啉和青霉素G钠相当,有些比它们还强。     

亮氨酸脑啡肽的电子结构及构效关系研究

对亮氨酸脑啡肽进行了量子化学(INDO)计算,研究其电子结构特征,讨论其活性部位、作用机理及构效关系。同吗啡和R31833进行了活性部位的电子结构与空间结构比较,推断它们的活性药效结构具有共同特点,与阿片受体相互作用时作用方式相同,作用部位有对应关系,因而具有相同的药理性质。     

The NMDA receptor antagonist 2-amino-5-phosphonovalerate blocks stimulus train-induced epileptogenesis but not epileptiform bursting in the rat hippocampal slice

The role of N-methyl-D-aspartate (NMDA) receptors in producing stimulus train-induced bursting (STIB) was examined in area CA3 of the rat hippocampus. Extracellular recordings were made from the CA3 pyramidal cell layer. Bursting was induced by trains of electrical stimuli delivered to the stratum radiatum of CA3, or by bath application of NMDA. The specific NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV) was then bath applied to test its ability to block STIB and NMDA activated bursting. A dose-response relation for NMDA activation indicated that bath application of 1 and 5 microM NMDA had little or no effect on the response to a paired stimulus pulse (triggered response) and did not induce spontaneous bursting. Ten micromolar NMDA induced strong triggered and spontaneous bursting during the application of NMDA in 72% of the slices. Fifty to one hundred micromolar NMDA caused the abolition of the excitatory postsynaptic potential (EPSP) and orthodromic population spike and the decrease or abolition of the antidromic population spike. In the normal medium wash following 10 microM NMDA, those slices that produced triggered and spontaneous bursting in 10 microM NMDA underwent an early phase of decreased excitability in which spontaneous bursting occurred in only 6% of the slices that were bursting in NMDA. Later in the wash spontaneous bursting began occurring in half of the slices that were bursting in NMDA, and the excitability of the triggered bursts increased slightly. The ability of the NMDA receptor antagonist APV to block NMDA-activated bursting was tested. Bath application of 100 or 200 microM APV alone caused little change in the normal triggered response. When 10 microM NMDA was added to the APV solution, there was little or no change in the triggered response, and no spontaneous bursting occurred. However, when 100 or 500 APV was added to the NMDA solution after NMDA burst activation had occurred, triggered bursting was reduced, but not blocked, although spontaneous bursting was blocked. In those slices that continued bursting after the washout of NMDA, bath application of 100 or 500 microM APV reduced, but did not block, triggered bursting. Spontaneous bursting continued in all slices. The ability of APV to block the induction of bursting by trains of electrical stimuli was then tested.(ABSTRACT TRUNCATED AT 400 WORDS)