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D Higgins

Publications and source records attributed to D Higgins.

31 records · Page 2Linked to original sources

Seroepidemiology of Q fever among cats in New Brunswick and Prince Edward Island.

The indirect microimmunofluorescence test was used to determine the presence of antibodies to phase I and phase II Coxiella burnetii antigens in New Brunswick and Prince Edward Island cats. Twenty of 104 (19.2%) New Brunswick cats tested had antibodies to phase II antigen; five of these (4.8%) also had antibodies to phase I antigen. Six of 97 (6.2%) Prince Edward Island cats tested had antibodies to phase I and phase II antigens. Our data suggest that cats may be important in the epidemiology of Q fever in these provinces.

Animals

Astrocytes induce dendritic development in cultured sympathetic neurons.

Sympathetic neurons in culture require the influence of Schwann cells in order to develop dendrites comparable to those seen in vivo. This study demonstrates that astrocytes induce dendritic development in greater than 90% of sympathetic neurons after two weeks of co-culture. We conclude that dendrite inducing factors are distributed on both central and peripheral glia.

Animals

Age-dependent changes in the capacity of rat sympathetic neurons to form dendrites in tissue culture.

We compared the ability of prenatal and postnatal rat sympathetic neurons to form dendrites in tissue culture. Dendrites were distinguished from axons by light microscopic criteria after intracellular dye injection and by differential immunostaining with antibodies to microtubule-associated protein-2 and to both non-phosphorylated and phosphorylated forms of the M and H neurofilament subunits. When maintained in the absence of serum and non-neuronal cells, most (72%) prenatal neurons were unipolar and had only an axon. In contrast, most (89%) neurons derived from postnatal ganglia were multipolar and extended both axons and dendrites. The dendritic morphology of postnatal neurons was usually simple with cells commonly having 2-5 short (50-200 microns), relatively unbranched dendrites. Thus, as the development of the dendritic arbor progresses in situ, sympathetic neurons acquire an enhanced ability to extend dendrites in tissue culture. To determine whether changes in the capacity to develop dendrites might occur with aging in vitro, ganglia were removed from prenatal rats and grown as explants for 3 weeks in the presence of non-neuronal cells; under these conditions, prenatal neurons within the explant became multipolar. When neurons derived from aged explants were subsequently maintained in dissociated cell culture, most formed dendrites. In cultures treated with an antimitotic agent, neurons typically had 1-4 unbranched dendrites; greater amounts of dendritic growth occurred in cultures in which ganglionic non-neuronal cells were allowed to proliferate. We conclude that: (1) the acquisition of the capacity to form dendrites in dissociated cell culture does not require either normal afferent input or physical contact with the target tissue; and (2) even after aging in vitro, sympathetic neurons remain responsive to the dendrite-promoting activity of ganglionic non-neuronal cells.

Adrenergic Fibers

Laminin and a basement membrane extract have different effects on axonal and dendritic outgrowth from embryonic rat sympathetic neurons in vitro.

We have characterized the effects of laminin and a basement membrane extract (BME) on the morphology of embryonic rat sympathetic neurons maintained in tissue culture in the absence of nonneuronal cells. Neurons were grown on polylysine-coated coverslips in the presence or absence of laminin or BME in serum-free medium. Axons were distinguished from dendrites using intracellular dye injections, immunocytochemistry, and [3H]uridine autoradiography. In short-term (less than or equal to 24 hr) culture, laminin had a potent neurite-promoting effect, causing increases in the number of processes, total neuritic length, and neuritic branching. In long-term (3-35 days) cultures chronically exposed to laminin, most (greater than 75%) neurons maintained supernumerary axons but failed to form dendrites. In contrast, most neurons (greater than 70%) grown in long-term culture on polylysine in the absence of laminin were unipolar, extending a single axon. BME caused sympathetic neurons to extend multiple (range, 1-15) dendrites. Morphometric measurements made after 1 month of exposure to BME indicated that the amount of dendritic growth that occurred in vitro was similar to that normally occurring during a comparable period in situ. BME did not cause changes in the number of axons per neuron or in the uptake of neurotransmitter. Preliminary characterization of the dendrite-promoting activity of BME suggests that it resides in extracellular matrix (ECM) molecules and not in low-molecular weight contaminants. These observations indicate that (1) axonal and dendritic growth may be differentially regulated by various constituents of the ECM, and (2) such process-specific interactions can significantly affect the morphological development of sympathetic neurons.

Animals

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Adult

Hypothalamic Na+ and Ca++ ions and temperature set-point: new mechanisms of action of a central or peripheral thermal challenge and intrahypothalamic 5-HT, NE, PGEi and pyrogen.

The effects of changes in ambient and central temperature, amines, PGEu and pyrogen were investigated with respect to the mechanism of Na+-Ca++ ratio in the posterior hypothalamus of the unrestrained cat. Guide tubes were implanted bilaterally above the posterior hypothalamic area of 23 cats so as to accommodate push-pull cannulae. After a Na+ or Ca++ sensitive site was identified by perfusion at 50 mul/min of an artificial CSF containing 10.4 mM excess Ca++ ions or 13.6 mM excess Na+ ions, several types of experiments were undertaken with the results summarized as follows: if the cat was exposed to a cold or warm environmental temperature as the posterior hypothalamus was perfused with excess cation, the typical hypothermia was produced by Ca++ and hyperthermia by Na+ ions. However, if the cat was exposed to peripheral cooling or warming 30 min prior to the perfusion, the fall or rise produced by Ca++ or Na+ was attenuated or prevented. In other experiments, 1.0 muCi 45Ca++ was injected in the ion sensitive site in the posterior hypothalamus to label stores of the cation. Raising of ambient temperature caused a retention of 45Ca++ in this hypothalmic area, whereas a cold environmental temperature enhanced the efflux of 45Ca++ at the same perfusion site. The magnitude of change in 45Ca++ efflux depended upon the intensity of the thermal challenge. Similarly, warming of the anterior hypothalmic, preoptic area by means of implanted thermodes caused an immediate diminution in 45Ca++ efflux in the posterior hypothalamus, whereas cooling of this anterior region augmented the extrusion of 45Ca++ ions from the posterior area. When substances which produce a temperature change were applied to the same thermosensitive zone, the direction of shift in 45Ca++ flux in the posterior area corresponded to the signal for heat production or heat loss. That is, the microinjection of 5-HT, PGE1 or Salmonella typhosa into the anterior hypothalamus enhanced the efflux of 45Ca++ in the posterior hypothalamus as hyperthermia developed, whereas a similar microinjection of norepinephrine reduced the 45Ca++ output from the same sites. Finally, locally anesthetizing the cells of the anterior hypothalamus by the nerve blocker, procaine, prevented the cold and heat-induced 45Ca++ eflux and retention, respectively. These results suggest that if the Na+-Ca++ ratio in the posterior hypothalamus establishes and maintains the set-point for body temperature of 37 degrees -38 degrees C, the mechanism of lability of Ca++ through changes in binding characteristics, transport, or metabolism of the cation serves two purposes: (1) the active defense of the set-point temperature through gradations in ion shifts; and (2) the upward or downward change in set-point value, pathological or normal, triggered by virtue of impulses relayed from the anterior hypothalamus.

Animals

Anxiety and endocrine responses to surgery: paradoxical effects of preoperative relaxation training.

It has been argued that surgery is a form of psychological stress, and that the response to it should therefore be modifiable by psychological means. To test this hypothesis, we assessed the effect of preoperative relaxation instructions on endocrine, cardiovascular, and subjective responses in 21 patients undergoing minor abdominal surgery. Controls (N = 19) received general procedural information. In the relaxation group only, there was a significant increase in cortisol and adrenaline concentration from immediately before induction of anesthesia to immediately after surgery. Noradrenaline values were unaffected by relaxation. In contrast, relaxation reduced state-anxiety on the preoperative day and the two postoperative days; maximal peroperative systolic and diastolic blood pressures were also reduced. The results are consistent with previous evidence that adrenaline and cortisol responses to surgery are greater in less anxious patients.

Adaptation, Psychological

Comparison of isocapnic hyperventilation and histamine or methacholine inhalation for the assessment of airway responsiveness.

Several stimuli have been used to evaluate the degree of airway hyperresponsiveness in asthma. Each of these has possible advantages and disadvantages when compared to the other methods. The most widely used involves the inhalation of chemical bronchoconstrictors, most commonly histamine or methacholine. This paper contrasts these inhalation tests with airway challenges using isocapnic hyperventilation of dry air. Isocapnic hyperventilation uses a naturally occurring stimulus to provoke bronchoconstriction rather than a chemical stimulus and can be administered in a dose-response fashion. Therefore, isocapnic hyperventilation may be particularly useful in epidemiologic surveys. The maximal dose administered, however, is determined by the level of a subject's maximal voluntary ventilation: also the equipment needed to administer the challenge is relatively complex when compared to other methods. By contrast, histamine and methacholine inhalation tests require simple, inexpensive equipment and can be inhaled at high concentrations, which means that airway responsiveness can be measured even in many nonasthmatic subjects. However, at high inhaled concentrations, histamine has many more systemic side effects than methacholine. Once the factors known to influence the measurements of airway responsiveness are controlled, the measurements made with one method correlate well with all other methods. Therefore, the method chosen will often depend on the requirements of the study or clinical laboratory.

Asthma