Secondary techniques for increasing fault coverage of fault detection test sequences for asynchronous sequential networks

The generation of fault detection sequences for asynchronous sequential networks is considered here. Several techniques exist for the generation of fault detection sequences on combinational and clocked sequential networks. Although these techniques provide closed solutions for combinational and clocked networks, they meet with much less success when used as strategies on asynchronous networks. It is presently assumed that the general asynchronous problem defies closed solution. For this reason, a secondary procedure is presented here to facilitate increased fault coverage by a given fault detection test sequence. This procedure is successful on all types of logic networks but is, perhaps, most useful in the asynchronous case since this is the problem on which other techniques fail. The secondary procedure has been designed to improve the fault coverage accomplished by any fault detection sequence regardless of the origin of the sequence. The increased coverage is accomplished by a minimum amount of additional internal hardware and/or a minimum of additional package outputs. The procedure presented here will function as part of an overall digital fault detection system, which will be composed of: 1) a compatible digital logic simulator, 2) a set of fault detection sequence generators, 3) secondary procedures for increasing fault coverage, 4) procedures to allow for diagnosis to a variable level. This research is directed at presenting a complete solution to the problems involved with developing secondary procedures for increasing the fault coverage of fault detection sequences --Abstract, pages ii-iii

Axotomy-Induced Loss of m2 Muscarinic Receptor mRNA in the Rat Facial Motor Nucleus Precedes a Decrease in Concentration of Muscarinic Receptors

The abundance of muscarinic receptors and m2 muscarinic receptor mRNA. in the facial nuclei of rats was evaluated by autoradiographic procedures at various times up to 14 days after transection of the right facial nerve. Receptors were labelled by in vitro incubation of brain sections with L-[3Hlquinuclidinyl benzilate, while in situ hybridization with a 35S-labelled oligonucleotide was used to identify m2 muscarinic receptor mRNA in neighbouring sections. The right and left facial nuclei of non-operated control rats appeared equivalent in abundance of muscarinic receptors (359 ± 8 versus 376 ± 9 fmol per mg tissue, n = 5) and the presence of m2 mRNA. Axotomy had no effect on the concentration of receptors in the contralateral facial nucleus but caused a gradual loss of receptors from the ipsilateral side. No change was detected at 1 day after nerve transection, but a 23% decrease relative to the contralateral facial nucleus had occurred by 3 days. A maximum decrease of 51% was achieved by 1 week after nerve transection. By comparison, m2 mRNA was nearly eliminated from the ipsilateral facial nucleus at 1 day post-taxonomy and remained depleted for the duration of study. Previous work has established that no significant loss of motoneurons occurs within this period. Accordingly, it is postulated that axonal injury inhibits transcription of the m2 muscarinic receptor gene, resulting in a later decrease in muscarinic receptor protein expression