Biomedical subjects
Publications and source records attributed to A D Miller.
Electrical stimulation of the brainstem of 15 decerebrate cats produced stimulus-bound vomiting in only 4 animals. Vomiting was reproducible in only one cat. Effective stimulating sites were located in the solitary tract and reticular formation. Restricted localization of a 'vomiting center', stimulation of which evoked readily reproducible results, could not be obtained.
A cDNA corresponding to the human gene for hypoxanthine phosphoribosyltransferase (HPRT; IMP:pyrophosphate phosphoribosyltransferase, EC 2.4.2.8) has been ligated into murine retroviral vectors such that it is under the transcriptional control of viral long terminal repeats. Transfection of HPRT- cells followed by superinfection with various helper viruses has led to the rescue of chimeric virus capable of transmitting the HPRT+ phenotype to HPRT- rodent or human cells. These genetically transformed cells contain authentic human HPRT at levels similar to normal HPRT+ cells.
Vestibular stimulation, by means of sinusoidal electrical polarization of the labyrinths of decerebrate cats, can produce vomiting and related activity resembling that seen in motion sickness. The symptoms include panting, salivation, swallowing, and retching as well as vomiting. These symptoms can be produced in cats with lesions of the posterior cerebellar vermis. In contrast to a previous proposal by Wang and Chinn in 1956, we suggest that a transcerebellar pathway from the vestibular apparatus through the nodulus and uvula to the 'vomiting center' is not essential for vestibular-induced vomiting and, by analogy, for the occurrence of many symptoms of motion sickness.
The dynamics of neurons in the vestibular nuclei of canal-plugged, decerebrate cats were studied in response to lateral (roll) tilt. Forelimb and neck extensor reflexes recorded simultaneously develop a progressive phase lag above 0.1 Hz. Neurons which exhibited a muscle-like phase lag were excited during low frequency stimuli by ipsilateral side-up tilt (beta response). Neurons with alpha responses, excited during side-down tilt, exhibited a constant phase, without a high frequency lag. Vestibulospinal neurons were present in both of these response groups, as were units driven at monosynaptic latencies by electrical stimulation of the ipsilateral labyrinth. The phase-lagging beta responses are appropriate for contributing to the reflexes observed in the ipsilateral neck and contralateral forelimb.
The effects of lesions of the vestibulospinal tracts on vestibular reflexes evoked by roll tilt in forelimb and neck extensors were examined in decerebrate cats. Sectioning the medial longitudinal fasciculus, which contains the medial vestibulospinal tract, had no major effect on the phase of the reflex, although some gain was usually lost at high stimulus frequencies. Spinal lesions at C2-C3, both cord hemisections and more restrictive lesions which cut the lateral vestibulospinal tract, produced two major effects on the forelimb. Background EMG activity was usually abolished in the triceps ipsilateral to the lesion, with partial loss of activity in the opposite limb. The tilt reflex response in the ipsilateral limb appeared normal, although it was usually necessary to raise the background excitability of the preparation by administering L-Dopa in order to observe the reflex. In contrast, the response in the contralateral limb showed a phase reversal of 180 deg at low stimulus frequencies, implying that the reflex in intact cats receives a crossed otolith-spinal input. Responses in the neck extensors splenius and biventer, recorded from compartments caudal to the spinal lesion, were relatively unaffected.
Participation of the pathway from the cerebellum through "motor" thalamus to motor cortex in movement initiation was tested in three. Cebus monkeys. The animals performed a simple reaction time (RT) task involving prompt elbow flexion or extension in response to an audiovisual "GO!" signal. RTs were not changed by reversible cooling of the arm area of the contralateral ventral lateral (VL) thalamus, that includes rostral VPL. In contrast, cooling the cerebellar dentate nucleus ipsilateral to the operant arm prolonged RTs by about 80 ms, as tested in two of the same monkeys. The results confirm cerebellar participation in prompt generation of well-learned intended arm movements; but they also indicate that although the route through VL-thalamus may be important, it is not essential for initiation of the same movements.
During a 9-day period in August 1980 in a New Jersey hospital, three pairs of consecutively numbered blood cultures from different patients were identified as positive for the same organism (two pairs of Klebsiella pneumoniae and one pair of group A Streptococcus), for each pair, both cultures were positive in the same atmosphere, both organisms had the same sensitivities, and the second of each pair grew at least 2 days after the first and was the only positive blood culture obtained from the patient. When the hospital laboratory discontinued use of its radiometric culture analyzer for 15 days, no more consecutive pairs of positive cultures occurred. Subsequent use of the machine for 9 days with a new power unit but the original circuit boards resulted in one more similar consecutive pair (Staphylococcus epidermidis). After replacement of the entire power unit, there were no further such pairs. Examination of the machine by the manufacturer revealed a defective circuit board which resulted in inadequate needle sterilization. Laboratories which utilize radiometric analyzers should be aware of the potential for cross contamination. Recognition of such events requires alert microbiologists and infection control practitioners and a record system in the bacteriology laboratory designed to identify such clusters.
This study was conducted to determine which supraspinal structures, if any, are essential for generation of late (M2 and M3) EMG responses to perturbations. EMGs were recorded during active arm movements made by Cebus monkeys trained to resist perturbations applied to a handle and/or during passive movements imposed on sedated or anesthetized animals. EMGs were tested during active movements after ablation of the arm areas of the sensory and caudal motor cortices, during cooling part of the sensorimotor cortex along the central sulcus, and during cooling the arm area in the ventral lateral (VL) thalamus. EMG responses to passive movements were tested after decerebration and decerebellation, after lesions of the motor and/or sensory cortices, during surface cooling the same, and during cooling the VL arm area and the cerebellar dentate nucleus. M1, M2, and M3 were not abolished in any monkey. Decreases in the magnitudes of these responses occurred in some animals, but no reproducible changes in the sizes of M2 and M3 (in comparison to M1) were observed following any procedure. The effects of cortical lesions on M1, M2, and M3 responses to passive movements were found to depend on the level of arousal of the animal. These results demonstrate that M1, M2, and M3 can be produced in the primate spinal cord and brainstem and that the sensorimotor cortex can facilitate these responses.
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Prostaglandin (PG) E1 enhances formation of 3H-adenosine-3',5'-cyclic monophasphate (3H-cAMP) in platelets pulse-labeled with 3H-adenine. This response was assessed as an index of receptor sensitivity and of PG function. Prostagladin E1-stimulated 3H-cAMP accumulation in paltelets from schizophrenics was significantly reduced compared with control subjects. Platelet incorporation of 3H-adenine and basal 3H-cAMP accumulation. We discuss the results in terms of the possible role of PGs in the etiopathology of schizophrenia and derivative implications for treatment.
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The H-Y locus is on the short arm of the human Y chromosome in most individuals but on the long arm in at least one of 17 individuals with structural abnormalities of the Y.
A streaming potential experiment was conducted on in vitro bone to determine the effects polyvalent salts have on bone zeta potential. Polyvalent metal salts would be introduced into local physiological electrolytes by corrosion of a metal implant or dissolution of a ceramic implant. It was hypothesized that a change in zeta potential of mineralized tissue, resulting from the introduction of polyvalent salts, could be a cause of tissue instability at the implant interface. Zeta potentials measured in bone were on the order of a few millivolts. Strongly hydrolytic metal cations such as Al+3 and Fe+3 did not have sufficient activity in buffered neutral electrolytes to alter bone zeta potential. Results suggest that less hydrolytic cations of high valence, and large polarizable anions may affect bone zeta potential.
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