Three strategies for changing attributions about severe mental illness.

The effects of three strategies for changing stigmatizing attitudes--education (which replaces myths about mental illness with accurate conceptions), contact (which challenges public attitudes about mental illness through direct interactions with persons who have these disorders), and protest (which seeks to suppress stigmatizing attitudes about mental illness)--were examined on attributions about schizophrenia and other severe mental illnesses. One hundred and fifty-two students at a community college were randomly assigned to one of the three strategies or a control condition. They completed a questionnaire about attributions toward six groups--depression, psychosis, cocaine addiction, mental retardation, cancer, and AIDS--prior to and after completing the assigned condition. As expected, results showed that education had no effect on attributions about physical disabilities but led to improved attributions in all four psychiatric groups. Contact produced positive changes that exceeded education effects in attributions about targeted psychiatric disabilities: depression and psychosis. Protest yielded no significant changes in attributions about any group. This study also examined the effects of these strategies on processing information about mental illness.

Use of the drop volume of amniotic fluid in predicting fetal lung maturity. Clinical experience.

Respiratory distress syndrome (RDS), resulting from inadequate amounts of alveolar surfactant, is a leading cause of neonatal mortality. This study analyzed the drop volume for predicting the risk of neonatal RDS by evaluating the surface tension of amniotic fluid. The drop-volume method quantifies the surface tension of amniotic fluid using the fact that the volume of a falling drop of liquid is proportional to the quantity of surface-active substances (surfactant) in the solution. Distilled water is used as a reference solution. The test is simple to perform and requires only two minutes and 2 mL of amniotic fluid. Amniotic fluid was obtained by amniocentesis from 120 pregnancies, ranging from 24 to 42 weeks of gestation, within four days of delivery. Specimens contaminated with meconium or hemolyzed blood or from patients with clinical chorioamnionitis were not used. The lecithin:sphingomyelin ratio and phosphatidylglycerol tests were also determined for 54 of the study cases. A mature drop-volume test result was associated with a healthy infant with no RDS 95% of the time (negative predictive value). Fifty-two percent of the healthy infants in the study were predicted by an arbitrary unit of time (S) value of less than or equal to 85.0 (specificity). Thirteen of the 16 infants who developed RDS (81%) were predicted by an S value of greater than or equal to 85.1 (sensitivity). Of those infants with an S value of greater than or equal to 85.1, 21% developed RDS (positive predictive value).

The 1995 Lindberg Award. Nonthermally mediated muscle injury and necrosis in electrical trauma.

Joule heating has long been considered the principal component of tissue damage in electrical injury. Recent studies suggest electroporation, a nonthermally mediated mechanism of cell membrane damage, is also a factor. We investigated whether electroporation-mediated muscle necrosis can occur in vivo without significant Joule heating. Pulsed electric fields approximately 150 V/cm were produced in the hind limbs of anesthetized rats. In shocked limbs core muscle temperature rose less than 1.8 degrees C, yet significant damage occurred as determined by technetium-99m pyrophosphate uptake, elevated serum creatine phosphokinase, and prominent hypercontraction band degeneration of myofibers on histopathologic examination. This study is significant because it directly addresses whether nonthermal mechanisms of cell damage can cause tissue necrosis. These results indicate that electroporation effects can mediate skeletal muscle necrosis without visible thermal changes. Thus the phenomenon of "progressive recognition" may be characteristically largely explained by the occurrence of nonthermally mediated tissue damage.

Comparison of associated high-risk factors and perinatal outcome between symmetric and asymmetric fetal intrauterine growth retardation.

This study compares associated high-risk factors and perinatal outcome between 273 symmetric and 445 asymmetric infants with intrauterine growth retardation. No differences were seen in 17 obstetric, medical, and environmental-behavioral high-risk factors between symmetric and asymmetric intrauterine growth retardation. In preeclampsia, the incidence of symmetric intrauterine growth retardation is higher than that of asymmetric intrauterine growth retardation. The timing of the interaction between the high-risk factor and the stage of gestation is more important than the specific high-risk factor in determining whether symmetric or asymmetric intrauterine growth retardation is produced. On comparison of perinatal outcome between the two groups, we concluded: (1) that the onset of symmetric intrauterine growth retardation occurs much earlier in the course of pregnancy than does asymmetric intrauterine growth retardation, (2) that more symmetric than asymmetric pregnancies with intrauterine growth retardation result in preterm delivery, (3) that the neonatal morbidity rate for symmetric intrauterine growth retardation is higher than that for asymmetric intrauterine growth retardation, and (4) that term symmetric infants with intrauterine growth retardation tend to have a lower mean birth weight and a higher incidence of small placentas than term infants with asymmetric intrauterine growth retardation.

Dihydrotestosterone decreases beta-adrenergic receptor binding in the fetal rabbit lung.

Tritium-labeled dihydroalprenolol was used to quantify the beta-adrenergic receptor sites in day 30 fetal rabbit lung tissue. Each of the fetuses of New Zealand White rabbits on day 28 of gestation was injected with dihydrotestosterone (2.0 micrograms) in one horn of the uterus and 10% ethanol in normal saline (the solvent) in the contralateral one. The animals were sacrificed 48 hours later and the fetal lung tissue was assayed. Dihydrotestosterone decreased the beta-adrenergic receptor site number in the treatment group compared with the control group (86 versus 111 fmol/mg protein, p less than 0.05 by paired t-test). In the presence of dihydrotestosterone, beta-adrenergic receptor binding is inhibited in the preterm fetal rabbit. This effect may be implicated in the beta-adrenergic mediation of phospholipid synthesis and/or release by fetal alveolar cells.

The effect of estrogen and progesterone on beta-adrenergic receptor activity in rabbit lung tissue.

Study of the effect of sex steroids on the development of beta-adrenergic receptors may be essential to an understanding of the mechanisms of both lung maturation and the initiation of labor. (3H)Dihydroalprenolol (DHA) was used to quantify beta-adrenergic receptor sites in mature and immature rabbit lung tissue. DHA binding was rapid, saturable, of high affinity (dissociation constant = 2 nM), and of low capacity (246 to 576 fmoles/mg of protein), and a adrenergic competitors demonstrated both stereoselectivity ([-]isomer much greater than [+]isomer) and a rank order of potency (isoproterenol much greater than norepinephrine greater than epinephrine) characteristic of the beta-adrenergic receptor. beta-Adrenergic receptors in the lung tissue of both mature and immature female New Zealand White rabbits were investigated under various sex steroid situations. Estrogen (diethylstilbestrol, 5 micrograms/day for 10 days) increased the beta-adrenergic receptor site number in immature rabbits compared to matched controls (435 versus 339 fmoles/mg of protein, p less than 0.02 by paired t test). Addition of progesterone (diethylstilbestrol, 5 micrograms/day for 10 days, plus progesterone, 5 mg/day for 3 days) returned the beta-adrenergic receptor site number to control values (321 fmoles/mg of protein, p less than 0.01). In mature rabbits, treatment with progesterone alone (10 mg/day for 4 days) caused a significant reduction in beta-adrenergic receptor site numbers compared to untreated, matched controls (357 versus 493 fmoles/mg of protein, p less than 0.05 by paired t test). in the presence of estrogen, beta-adrenergic receptor activity is enhanced in both mature and immature rabbit lung tissue. Addition of progesterone restores this activity to control values.

Estrogen increases beta-adrenergic binding in the preterm fetal rabbit lung.

Tritium-labeled dihydroalprenolol was used to quantify beta-adrenergic-receptor sites in day 28 fetal rabbit lung tissue. Each of the amniotic sacs of pregnant New Zealand White rabbits on day 26 of gestation was injected in vivo with estrogen (estradiol phosphate, 1.6 micrograms) in one horn and normal saline solution in the contralateral one. The animals were put to death 48 hours later and the fetal lung tissues were assayed. Estrogen increased the number of beta-adrenergic-receptor sites in the treatment group compared to the control group (216 versus 163 fmol/mg of protein, p less than 0.02 by paired t test). In the presence of estrogen, beta-adrenergic-receptor activity is enhanced in the preterm fetal rabbit. This effect may be implicated in the beta-adrenergic mediation of phospholipid synthesis and release in fetal alveolar cells.

Surfactant-induced sealing of electropermeabilized skeletal muscle membranes in vivo.

Victims of major electrical trauma frequently suffer extensive skeletal muscle and nerve damage, which is postulated to be principally mediated by electroporation and/or thermally driven cell membrane permeabilization. We have investigated the efficacy of two blood-compatible chemical surfactants for sealing electroporated muscle membranes. In studies using cultured skeletal muscle cells, poloxamer 188 (P188; an 8.4-kDa nonionic surfactant) blocks, and neutral dextran (10.1 kDa) substantially retards, carboxyfluorescein release from electropermeabilized cell membranes. To test whether P188 administered intravenously could have the same therapeutic effect in vivo, the rat biceps femoris muscle flap attached by its arteriovenous pedicle was electropermeabilized until its electrical resistivity dropped to 50% of the initial value. P188 (460 mg/kg) administered intravenously 20 min postshock restored the resistivity to 77% of the initial value. When P188 was administered intravenously 5 min before shock, a dose-dependent impedance recovery rate was observed. Neither neutral dextran (460 mg/kg) nor sterile saline was effective. Histopathologic studies indicated that postshock poloxamer administration reduced tissue inflammation and damage in comparison with dextran-treated or control tissues. Electrophysiologic evidence of membrane damage was not observed in flaps of animals pretreated with poloxamer. These results suggest that it may be possible to seal in vivo tissue membranes injured by electrical, thermal, or other membrane-damaging forces.