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Biomedical subjects

J L Walker

Publications and source records attributed to J L Walker.

At least 145 records · Page 8Linked to original sources
PubMed1971

Serologic evidence that a herpes-type virus is the etiologic agent of heterophile-positive infectious mononucleosis.

The antibody activity against herpes-type virus (HTV) of heterophile-positive infectious mononucleosis sera and "normal" sera from humans was determined with immunoferritin. The antiviral activity of the mononucleosis sera was associated with the IgM antibodies, while the antiviral activity of the "normal" human sera was associated with the IgG antibodies. It was concluded from these findings that the appearance of antibodies to herpes-type virus in heterophile-positive sera represents a primary immunogenic exposure to this virus, or to a serologically related virus. This conclusion, in turn, suggests that herpes-type virus or a serologically related virus is the etiologic agent of heterophile-positive mononucleosis.

Adolescent↗
PubMed1970

Unified account of the variable effects of carbon dioxide on nerve cells.

When the abdominal ganglion of Aplysia californica is exposed to 5 percent carbon dioxide, certain neurons are depolarized, others hyperpolarized, and some are unaffected. The effect of increased carbon dioxide is due solely to the concomitant fall in extracellular pH, which causes an increase in membrane chloride conductance of responsive cells. The directional change of the membrane potential in different neurons is determined by the relative values of the chloride equilibrium and the resting potentials. The chloride equilibrium potentials are calculated after direct measurement of the intracellular chloride activity with a chloride microelectrode.

Animals↗
PubMed1970

Increased chloride conductance as the proximate cause of hydrogen ion concentration effects in Aplysia neurons.

A fall in extracellular pH increased membrane conductance of the giant cell in the abdominal ganglion of Aplysia californica. Chloride conductance was trebled whereas potassium conductance was increased by 50%. Half the giant cells were hyperpolarized (2-8 mv) and half were depolarized (3-10 mv) by lowering the pH. The hyperpolarizing response always became a depolarizing response in half-chloride solutions. When internal chloride was increased electrophoretically, the hyperpolarization was either decreased or changed to depolarization. The depolarizing response was reduced or became a hyperpolarizing response after soaking the cell in 10.0 mM chloride, artificial seawater solution for 1 hr. Depolarization was unaffected when either external sodium, calcium, or magnesium was omitted. A glass micropipette having an organic liquid chloride ion exchanger in its tip was used to measure intracellular chloride activity in 14 giant cells; 7 had values of 27.7 +/- 1.8 mM (SEM) and 7 others 40.7 +/- 1.5 mM. Three of the first group were hyperpolarized when pH was lowered and three of the second group were depolarized. In all six cells, these changes of membrane potential were in the direction of the chloride equilibrium potential. Intracellular potassium activity was measured by means of a potassium ion exchanger microelectrode.

Animals↗
PubMed1970

Oxotremorine-induced hypertension in the anaesthetized rat.

1. Oxotremorine exerts an action on peripheral cholinoceptors in the anaesthetized rat. After the blockade of peripheral cholinoceptors with the quaternary atropine derivative, atropine methylbromide, oxotremorine produced a rise in arterial blood pressure and tachycardia.2. The rise in arterial pressure and tachycardia was absent in rats that had been pithed or had undergone high spinal cord transection.3. A non-quaternary atropine derivative antagonized these cardiovascular effects.4. Drugs which inhibit activity of the sympathetic nervous system antagonized the oxotremorine-induced hypertension and tachycardia.5. It is concluded that the rise in arterial pressure and tachycardia seen in the anaesthetized rat treated with a quaternary derivative of atropine is due to an action of oxotremorine on the central nervous system at a supraspinal level, resulting in an increase in activity of the efferent sympathetic nervous system.

Adrenal Glands↗