Pulmonary mechanics in guinea pigs: repeated measurements using a nonsurgical computerized method.
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Biomedical subjects
Publications and source records attributed to R J Jaeger.
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Two children and 29 of 31 crew members aboard a grain freighter became acutely ill after inhaling the toxic fumigant phosphine; one child died. Predominant symptoms were headache, fatigue, nausea, vomiting, cough, and shortness of breath. Abnormal physical findings included jaundice, paresthesias, ataxia, intention tremor, and diplopia. Focal myocardial infiltration with necrosis, pulmonary edema, and widespread small-vessel injury were found at postmortem examination of the dead child. The surviving child showed ECG and echocardiographic evidence of myocardial injury and transient elevation of the MB fraction of serum creatinine phosphokinase. Illness was significantly associated with living or working amidships or on the forward deck areas of the vessel. Phosphine gas was found to have escaped from the holds through a cable housing located near the midships ventilation intake and around hatch covers on the forward deck. The outbreak illustrates the hazards associated with shipboard fumigation.
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The sources of innervation of the internal structures of the eye in monkey and rabbit were investigated by injecting horseradish peroxidase (HRP) intraocularly and monitoring its retrograde transport. HRP-labeled cells were found in the ciliary ganglia and in the midbrain throughout the dorsoventral extent of the midline of the oculomotor complex. The results suggest that a direct pathway exists from the midbrain, and it is argued that this pathway is for the control of accomodation. Either this pathway is direct, with no synapse interposed, or the postsynaptic neurons are near or in the intrinsic musculature. A third but not so likely possibility is that retrograde transsynaptic transport of HRP occurred across electrotonic synapses in the ciliary ganglion. These findings may challenge the commoly held view that the entire pathway for the control of the intrinsic musculature synapses in the ciliary ganglion. On the other hand, it may be that this direct path is a sensory system much like the mesencephalic nucleus of the trigeminal nerve.
Exposure of fasted rats to 200 ppm 1,1-dichloroethylene (1,1-DCE) for 1-4 hours resulted in striking aberrations in hepatic Na, K, Ca, and GSH levels which preceded and/or accompanied catastrophic histologic alterations of the liver. Na levels began to rise during the first hour, and preceded the morphologically apparent injury. Ca levels increased markedly and K levels declined between the second and fourth hour of exposure, and accompanied the catastrophic morphologic alterations. GSH levels were rapidly depleted but began to recover before the end of the exposure to 1,1-DCE. Functions of components of the mixed-function oxidase system of the liver endoplasmic reticulum were not appreciably affected early in the course of 1,1-DCE exposure; but after injury became massive, cytochrome P-450 and oxidative N-demethylase were deactivated. Thus effects on the functional components of the endoplasmic reticulum mixed-function oxidase system do not appear to be primary events in 1,1-DCE cytotoxicity. In contrast, there were progressive declines in mitochondrial K and marked imbalances in mitochondrial Na, Zn, and Mg preceding the massive influx of Ca into the cell, indicating that mitochondria are involved early in he evolution of injurious molecular events elicited by this potent hepatotoxin.
The toxicity of the mixture NIAX-ESN which contains 95% dimethylaminopropionitrile was evaluated in male rats. Large doses (2.0 ml/kg ip) rapidly produced CNS excitation followed by depression and death. The mixture (given orally as two doses of 0.31 or 0.62 ml/kg respectively) induced acute urinary bladder lesions in 3 days. The changes consisted of massive transmural edema, acute ulcers and inflammation and, occassionally hemorrhagic necrosis of the bladder wall.
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Many studies have shown that subjects can correct their own errors of movement more quickly than they can react to external stimuli. In the control of movements, three general categories of feedback have been defined as follows: (a) knowledge of results, primarily visually mediated, (b) proprioceptive or kinesthetic, such as from muscle spindles and joint receptors, and (c) corollary discharge or efference copy within the central nervous system. Experiments were conducted on eight normal human subjects to study the effects of these feedbacks on simple RT, choice RT, and error correction time. The movement used was plantarflexion and dorsiflexion of the ankle joint. The feedback loops were modified (a) by inverting the visual display to alter the subject's perception of results and (b) by applying a 100-Hz vibration simultaneously to both flexor and extensor muscles of the ankle joint. Central processing was altered by giving the subjects moderated doses of alcohol (blood-alcohol concentration levels of up to.10%). Vibration and alcohol increased both simple and choice RT but not the error correction time. These data reinforce the concept that there is a central pathway which can mediate error correcting responses.
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