Evidence for McKusick''s hypothesis of deficient collagen cross-linking in patients with homocystinuria

Fractionation of the venom of the spider Phoneutria nigriventer revealed that it was a mixture of several neurotoxic peptides. The peptides so far characterized either inhibited or induced neurotransmitter release. These effects were mediated by Ca2+ channels or increasing Na+ permeability through voltage sensitive Na(+)-channels, respectively. The pooled toxic components (fraction P4) showed stimulatory effects on acetylcholine release from brain cortical slices. In addition, a component of the observed effects resembling that of alpha-latrotoxin was identified, which was characterized by the ability to provoke release of acetylcholine (ACh) at low temperature and in a manner independent of extracellular Ca2+ and of voltage sensitive Na(+)-channels.     

Structural units and the redintegrative power of picture fragments

We suppose that line drawings are perceived and represented in memory as a hierarchy of related parts and subparts, as dictated by Gestalt laws like common direction and spatial proximity. Therefore, a figure fragment comprising a natural part of an orginally studied pattern should serve as a strong retrieval cue for redintegrating memory for the pattern, whereas an equally large fragment suggesting either no units of misleading units should lead to poorer recall. This was confirmed in an experiment in which subjects studied 33 nonsense line drawings; recall of each was tested with good, mediocre, or bad (misleading) fragments of the original patterns. Good cues had about five time more redintegrative power than bad cues. A second experiment testing multiple-choice recognition memory showed that subjects confused an originally studied pattern about four times as often with a structurally similar distractor as with a structurally dissimilar distractor (which had an equal-sized change). Thus, memory cuing by fragments and memory confusions with slightly altered distractors indicate the significant constitutents of a figure.     

Choroidal neovascular membrane in Best's vitelliform macular dystrophy

The right eye of a 9-year-old white boy with Best's vitelliform macular dystrophy had an intact egg-yolk lesion and a retinal pigment epithelial defect superiorly, suggesting an early pseudohypopyon stage. The disruptive phase of the left eye showed subretinal hemorrhages, a "signet ring," and a subretinal neovascular membrane.     

Role of pelvic nerves in the postcopulatory abbreviation of behavioral estrus in female rats

The role of the pelvic nerves in the postmating abbreviation of behavioral estrus in domestic female rats was investigated. Mating during a period of 40 min at the beginning of hormonally induced estrus in spayed female rats resulted in a rapid decrease in receptivity as measured hourly by the lordosis response. Moreover, the length of the receptive period was significantly shortened by mating at the start of the period. Bilateral pelvic nerve transection completely abolished these effects of mating. Continuous exposure to sexually active males throughout the period of receptivity resulted in a more pronounced decline in receptivity but again was without effect in pelvectomized females. Apparently genital stimuli mediated by the pelvic nerves are responsible for the postcopulatory decrease in receptive behavior in the female rat.     

Induction of the cortical reaction in hamster eggs by membrane-active agents

Fusion of capacitated spermatozoa with the vitelline membrane, but not actual penetration, appears to initiate the cortical reaction in hamster eggs. The reaction can be artificially induced by the application of positively charged particles to the vitelline surface, a situation which may normally be prevented by the zona pellucida. Exposure of hamster eggs to neuraminidase, to lectins (concanavalin A and phytohaemagglutinin-P), to a monovalent ionophore (boromycin) and to 1,3-bis(4-chlorocinnamylideneamino)guanidine elicits a cortical granule discharge resulting in a block to fertilization. These agents all appear to act by inducing depolarization of the vitelline membrane.     

A delayed suppression of the renin-aldosterone axis following saline infusion in human hypertension

The purpose of this study was to compare the acute suppressibility of the renin-angiotensin-aldosterone (RAA) axis in normotensive (n = 23) and essential hypertensive (n = 62) subjects. Only those hypertensive subjects with normal plasma renin activity (PRA) levels (sodium restricted, upright) were included in the study. Acute suppression of the RAA axis was determined by measuring PRA, plasma angiotensin II (A II), and plasma aldosterone (PA) at frequent intervals during the infusion of isotonic saline (500 ml/hour for 6 hours). Although all parameters fell significantly from control levels by 20-30 minutes in the normotensive subjects, we found that 60% of the hypertensive subjects showed no significant decline in PRA or PA until 120-240 minutes after beginning the infusion. The other hypertensive subjects showed normal RAA suppression. In addition, while there were no significant differences between the three groups in control PRA or PA levels, we found that the PA levels from 30 to 240 minutes during the saline were significantly higher (P less than 0.01) in the hypertensive subjects with delayed suppression. That there were two distinct populations in the hypertensive group was suggested by the bimodality of the frequency response curve, with peaks occurring at 30 and 240 minutes. These studies indicate an abnormality in the acute suppression of the RAA axis in a substantial proportion of subjects with normal renin essential hypertension. Since previous studies in normal subjects have reported that the early phase of response to saline infusion is related to the sodium ion per se and not to intravascular volume expansion, we have come to the conclusion that the present data are consistent with the hypothesis that the delayed suppression hypertensive group has a diminished ability to respond to the sodium ion.