Hypnosis in a primary care practice: developing skills for the "new morbidities".

Training in hypnotherapy provides the primary care practitioner with skills needed to address increasingly common, significant sources of childhood morbidity: stressful life events, psychophysiological symptoms, chronic disease, and behavioral problems. Although there are many reports on the utility of hypnosis in these areas, there are few on its use within primary care. This paper describes the integration of hypnotherapeutic methods into the continuum of pediatric encounters in a solo general pediatric practice. Specific techniques for approaching and examining young patients and their problems are illustrated. Preliminary data are presented from a prospective chart review of those children and adolescents within the practice who use hypnosis. Guidelines for the application of hypnosis in pediatric primary care are summarized. Emphasis is placed on the necessity and opportunity for research on the efficacy of these methods in the primary care setting.

Normalization of plasma arginine vasopressin concentrations when children with meningitis are given maintenance plus replacement fluid therapy.

We hypothesized that plasma arginine vasopressin (AVP) concentrations in children with meningitis are appropriate for the children's degree of hypovolemia, even though the concentrations were higher than expected for the serum osmolality. A randomized study was conducted to compare the effect on plasma AVP concentrations of giving maintenance fluid requirements plus replacement of any deficit versus restricting fluids to two thirds of maintenance requirements for 24 hours. Plasma AVP concentrations and serum osmolality were measured before fluid therapy was begun and again after 24 hours. Nineteen children, 2 months to 17 years of age, were studied; 13 had bacterial meningitis (12 with Haemophilus influenzae type b). Ten children (seven with bacterial meningitis) received a mean of 1.42 times the calculated maintenance fluid requirements, and nine (six with bacterial meningitis) were restricted to a mean of 0.65 times maintenance. Children in the maintenance group also received significantly more sodium (mean = 6.3 mEq/kg/24 hr) than children in the fluid-restricted group (mean = 2.0 mEq/kg/24 hr). The two groups were comparable for plasma AVP concentration and serum osmolality before fluid therapy was begun. The plasma AVP concentration was significantly lower after 24 hours of maintenance plus replacement fluids than after fluid restriction (p = 0.005), and the change in AVP concentration correlated with the amount of sodium given (p less than 0.02). This study supports the hypothesis that serum AVP concentrations are elevated in patients with meningitis because of hypovolemia and become normal when sufficient sodium is given to facilitate reabsorption of water by the proximal tubule of the kidney. Patients with meningitis can be given maintenance plus replacement fluids but should be monitored for the development of the syndrome of inappropriate secretion of antidiuretic hormone.

Cell-free mercury(II)-reducing activity in a plasmid-bearing strain of Escherichia coli.

The ability to reduce Hg(II) to Hg(0), which is determined by a plasmid-borne gene in Escherichia coli, is conferred by a Hg(II)-inducible activity which is located in the cytoplasm rather than in the periplasmic space of the cell. This Hg(II)-reducing activity can be isolated from the supernatant of a 160,000 x g centrifugation after French Press disruption of the cells. The activity is dependent on glucose-6-phosphate, glucose-6-phosphate dehydrogenase, and 2-mercaptoethanol, but is not enhanced by added nicotinamide adenine dinucleotide phosphate. Treatment of the active fraction with N-ethylmaleimide causes irreversible loss of the Hg(II)-reducing activity. Unlike the Hg(II)-reducing activity found in intact cells, the cell-free activity is not inhibited by toluene, potassium cyanide, or m-chlorocarbonylcyanide-phenylhydrazone; however, it is inhibited by Ag(I) and phenylmercuric acetate to the same extent as the activity in intact cells. Neither phenylmercuric acetate nor methylmercuric chloride is reduced to Hg(0) by the cell-free activity. Au(III), however, is a substrate for the cell-free activity; it is reduced to metallic colloidal Au(0).