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In the space available for this essay I can provide only a cursory review of the many methodological contributions of R. B. Cattell. I have chosen to look at these from the vantage point of contemporary issues in structural equation modeling. Cattell's factor analytic approach is compared With current modeling practices. A critical evaluation is offered which finds much of Cattell's work still innovative, still technically advanced, and still of great value to contemporary model builders.

The resting membrane potential (RMP) of denervated mammalian muscle fibers increases when reinnervation occurs. This recovery of RMP is temporally associated with the return of a ouabain-sensitive fraction of the RMP. The data suggest that the activity of an electrogenic pump within the sarcolemma is, either directly or indirectly, under neurotrophic regulation.

The triangularis sterni muscle (TS) of the mouse is a thin trapezoidal sheet of fibres in which individual neuromuscular junctions are easily observed with Nomarski optics. Thus, microelectrodes are readily positioned to accurately record various synaptic phenomena. For example, miniature end-plate currents were easily recorded with a focally positioned extracellular electrode and the end-plate sensitivity to acetylcholine averaged 2062 mV/nC. In addition, the intercostal nerves segmentally innervate the TS. Electrophysiologic and histologic analysis showed that each nerve innervates a sharply defined territory of the muscle surface. These preliminary observations suggest that the TS may be ideal for studies of synaptic function and the processes underlying synapse stabilization in the mammal.

Cinnamedrine is an active ingredient in preparations used to relieve dysmenorrhea. It has been reported to have local anesthetic properties in nerve. This property prompted us to evaluate the effects of cinnamedrine on the cardiac action potential. Cinnamedrine (10-35 microM) significantly reduced the overshoot and maximum rate of rise, and also prolonged the duration of action potentials recorded from rat and guinea pig ventricular tissues. The action of cinnamedrine to depress upstroke velocity in guinea pig papillary muscle was dependent on the rate of stimulation. In addition, the refractory period of rat ventricular muscle was prolonged markedly. Finally, cinnamedrine (10 microM) significantly reduced, or totally abolished, epinephrine-induced automatic activity in both dog and rat myocardium in vitro. Prolongation of action potential duration and refractory period, and depression of upstroke velocity are characteristics which cinnamedrine shares with antiarrhythmic drugs.

Some reports in the medical literature have mentioned the occurrence of psychotic reactions in response to the use of certain ergot alkaloids in therapeutic doses. Prompted by these observations, we undertook a search for cases of "pure" puerperal psychosis (ie, typical manifestations 3-14 days postpartum) in order to evaluate the clinical background of this phenomenon. Special attention was paid to the medications that the patients had received peripartum. In the last 10 years, out of eight perinatal centers, we found only three cases that fulfilled the criteria of the quoted entity. In all instances, the manifestations of puerperal psychosis had been preceded by the administration of ergot derivatives. Based on the presented data, we hypothesize that typical postpartum psychosis may represent an idiosyncratic reaction to potent vasoactive drugs including ergot derivatives. The similarities between the clinical manifestations of ergotism and puerperal psychosis, and some of the epidemiologic features of the latter condition, appear to implicate ergot alkaloids as potential causative agents. Although the validity of the suggested interpretation requires further evaluation, we believe that the currently available data warrant caution with regard to the administration of ergot derivatives postpartum. These drugs should not be used in the absence of clear indication or in unnecessarily high doses. We suggest that ergotism be included in the differential diagnosis in cases of pure puerperal psychosis.

Miniature end plate potential (mepp) frequency in innervated extensor muscle is significantly higher than in soleus muscle. 9 days after nerve crush mepps of low amplitude and prolonged duration reappeared at a frequency of 2% of control and were similar to normal muscles after 35 days. Membrane potential began to increase 9-10 days after nerve crush and at 30 days was similar to controls. The region most sensitive to ACh in denervated and reinnervated muscles was the end plate. Caffeine (20 mM, 23 degrees C) induced contracture in innervated soleus but not in extensor muscles. After denervation the extensor became sensitive to caffeine while the soleus muscles decreased in sensitivity to the drug; 4-5 days after reinnervation the effect of caffeine on these muscles was similar to control. The events during reinnervation are: (a) reappearance of mepps at the same time as end plate potential and muscle twitch; (b) partial restoration of the membrane potential; (c) return of caffeine-induced contracture to normal levels in the soleus and its absence in the extensor muscles; (d) return of membrane resistance to normal values in both muscles at about 25 days; and (e) return of ACh-sensitivity to control levels at about 30 days in both muscles. Although these results suggest that the membrane potential and sarcoplasmic reticulum are under neural influence, it remains to be established whether or not separate neurotrophic factors are involved.