Replicate separation from dead dwarf cells of Stentor coeruleus.

INTRODUCTION: The present studies initially show the induction of dwarf forms from the disrupted cells of the large unicellular organism, Stentor coeruleus. The dwarf cells placed in a toxic solution showed evidence of cell death. Within minutes a morphological replicate of the cell separates and subsequently fades. METHODS: Dehydration of the commercially available Stentor media in deep well slides (n = 9) caused disruption of the large cells. Rehydration with sterile media allowed formation of mobile dwarf forms. The latter (n = 9) placed in a toxic solution lost mobility and showed evidence of cell death, i.e., apoptosis. Deep well slides (n = 9) containing sterile Stentor media were used as controls. RESULTS: In the slides following dehydration/ rehydration of the living Stentor media, 7of 9 showed mobile dwarf cells compared to 0 of 9 with the sterile media alone, p < 0.05). Within 8-12 min, the stationary dwarf cell progressively released a morphological replicate of the dead cell which contained entrapped bacteria. Subsequent fading of the replicate allowed dispersion of the bacteria. CONCLUSION: These findings provide evidence that cell death indicated by apopotosis (blebbing) is followed by a sequence consisting of the progressive separation of a replicate image which is initially visible then becoming a progressively non-visible, faded image.

Magnetism and cardiac arrhythmias.

Low-level electromagnetic fields (EMFs) have been used to treat various neurologic disorders. In the present study, we applied micro Gauss (microG) levels of EMFs either to the vagosympathetic nerve trunks, dissected in the neck, or across the chest in anesthetized dogs. Based on theoretical and empiric grounds, we compared EMFs (2.87 microG at 0.043 Hz) delivered to the vagosympathetic trunks in an experimental set (n = 5) with a sham control group (n = 6). Over a period of 2 to 3 hours, heart rate decreased after an initial 5-minute EMF exposure. The maximal heart rate changes in the experimental versus control groups was 29% versus 12% (P = 0.03). The voltage applied to the autonomic nerves required to induce atrioventricular (AV) conduction block decreased by 60% in the experimental group versus a 5% increase in the control group (P = 0.005). This effect also lasted 2 to 3 hours. Another EMF setting (amplitude 0.34 microG, frequency 2 kHz) applied for 5 minutes to the vagosympathetic trunks was associated with a significant increase in the occurrence of atrial premature depolarizations (APDs), atrial tachycardia (AT), and atrial fibrillation (AF) in response to autonomic nerve stimulation compared with control states before EMF exposure. No atrial arrhythmias could be induced after propranolol and atropine, even at the highest voltage used to stimulate the autonomic nervous input to the heart (n = 11). Only 2 dogs showed no response to this EMF application. In 3 dogs in whom atrial pacing (cycle length = 250 ms) and autonomic nerve stimulation induced AF, an EMF (2.87 microG at 0.043 Hz) delivered for 35 minutes across the chest suppressed AF for up to 3 to 4 hours, after which the same protocol again induced AF. We conclude that in these preliminary experiments, specific low-level EMFs alter heart rate, AV conduction, and heart rhythm. These effects were mediated through the autonomic nervous system inputs to the heart based on adjunctive effect of autonomic nerve stimulation and the inhibitory action of autonomic blockers.