Human responses to catastrophe.
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Biomedical subjects
Publications and source records attributed to S A Murphy.
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This paper describes the development and pilot testing of an empirically and theoretically based preventive intervention program for bereaved parents whose adolescent and young adult children died suddenly following an accident. The parents were assigned to either an early (2-6 months postloss) or a later (7-13 months postloss) transition group (N = 15) in which they received two-dimensional preventive intervention: informational support and emotional support. A comparison group (N = 19) received no intervention. Weekly and summative evaluations completed by bereaved parents and group leaders showed the therapeutic benefits of the preventive intervention for both treated groups. However, the two groups responded differently to the interventions, suggesting that timing and type of support might both be important factors to consider.
In the lacrimal gland, cholinergic agonists stimulate protein and electrolyte/water secretion by producing inositol trisphosphate (IP3) from phosphatidylinositol bisphosphate. To determine which IP3 isomers were produced and whether inositol tetrakisphosphate (IP4) was produced during activation of secretion, rat exorbital gland acini were [3H]inositol-labeled and stimulated by the cholinergic agonist carbachol. Water-soluble inositol phosphates were separated by anion-exchange chromatography using Dowex columns or high-performance liquid chromatography. Intracellular Ca2+ concentration ([Ca2+]i) was measured by fluorescence using the Ca2+ dye fura-2. Carbachol (10(-3) M) produced a time-dependent increase in 1,4,5-IP3, 1,3,4-IP3, and 1,3,4,5-IP4 levels during 0-60 s of stimulation. The 1,4,5-IP3 level increased rapidly and was followed by a slower rise in 1,3,4-IP3 and 1,3,4,5-IP4 levels. A 3-s carbachol (10(-8) to 10(-2) M) stimulation caused a concentration-dependent rise in the 1,4,5-IP3 level. Carbachol (10(-9) to 10(-2) M) increased [Ca2+]i in a concentration-dependent manner. Carbachol (10(-3) M) increased [Ca2+]i to a maximum level by 10 s; by 60 s [Ca2+]i decreased by 38%. The maximum increase in 1,4,5-IP3 levels occurred at a higher carbachol concentration than the increase in [Ca2+]i or protein secretion. We concluded that cholinergic stimulation of the lacrimal gland rapidly increased 1,4,5-IP3 levels, which was responsible for the initial increase in [Ca2+]i and initial rapid phase of protein and fluid secretion. Cholinergic stimulation also increased 1,3,4-IP3 and 1,3,4,5-IP4, but more slowly; either acting alone or with 1,4,5-IP3, they could account for the slower phase of secretion.
The development and testing of an explanatory model of recovery from disaster loss are described. The sample consisted of 155 persons at Time1-1981, 101 persons at Time2-1983, and represented five magnitudes of disaster loss: bereaved of disaster victims presumed dead; bereaved of disaster victims confirmed dead; persons whose permanent homes were destroyed; persons whose recreational property was destroyed; and a no disaster-loss comparison group. Data tested in the model were collected 1 and 3 years following the volcanic eruption of Mt. St. Helens in 1980 on eight variables: magnitude of loss, mass media coverage, negative rating of change, change in income, self-efficacy, social support, satisfaction with financial settlement, and mental distress. Path analysis was selected to estimate the magnitude of hypothesized direct and indirect linkages between variables presumed as causes of variables treated as effects. Results showed an improvement of goodness of fit by testing the model with the 1981 data, respecifying the model, and testing it again with the 1983 data. The greatest explanatory effects on mental distress 3 years postdisaster were mental distress reported 1 year postdisaster and negative ratings of change associated with disaster loss.
The abuse of alcohol and drugs has become a major health and social problem in the United States. Nurses comprise the largest segment of health-care professionals, yet report their educational experiences offer little to prepare them to develop substance abuse prevention and intervention programs. This article identifies factors that contribute to this educational gap, discusses challenges in planning and implementing substance abuse curricula, and offers specific guidelines for improving educational experiences.
This paper illustrates the usefulness of solvent control trials and presents a statistical analysis for mouse L5178Y lymphoma data. Examination of solvent control trials establishes that the natural logarithm of mutant frequency is approximately normally distributed and that both the mean and variance of mutant frequency vary by trial. There is little evidence of downturns at higher doses in the dose-response curves studied; therefore, a trend test is proposed for the detection of an increasing dose-response curve. A Monte Carlo investigation confirms that the proposed trend test is better able to detect an increasing dose-response than 4 alternate methods of analysis.
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Addition of a cholinergic agonist carbachol and vasoactive intestinal peptide (VIP) to dispersed rat exorbital lacrimal gland acini produces protein secretion, measured by secretion of the enzyme peroxidase, that was statistically significantly greater than additive (potentiated). To determine where in stimulus-secretion coupling these secretagogues interact to potentiate secretion, rat exorbital gland acini were incubated simultaneously with cyclic AMP- and Ca2+-dependent agonists and protein secretion, cyclic AMP level, or Ca2+ concentration measured. As a measure of protein secretion, the supernatant obtained after centrifugation of acini was analyzed for peroxidase, a protein secreted by rat lacrimal glands. Interaction did not occur at the receptor level, because peroxidase secretion also was potentiated by simultaneous addition of carbachol and forskolin, which activates the catalytic subunit of adenyl cyclase. A potentiated increase in the cyclic AMP level did not potentiate protein secretion, because the level was the same with VIP as with carbachol and VIP added together at concentrations that potentiated peroxidase secretion. A potentiated increase in free intracellular [Ca2+] did not potentiate protein secretion, because [Ca2+] was greater with carbachol than with carbachol and VIP added together at concentrations that potentiated peroxidase secretion. We conclude that cholinergic- and VIP-dependent pathways interact to potentiate lacrimal gland protein secretion after the rise of intracellular cyclic AMP or Ca2+.
To identify a role for protein kinase C in lacrimal gland protein secretion, we incubated rat exorbital lacrimal gland acini in the ester 4-beta-phorbol 12, 13 dibutyrate (beta-phorbol dibutyrate), its inactive isomer 4-alpha-phorbol 12, 13 dibutyrate (alpha-phorbol dibutyrate), and the diacylglycerol analog 1,2-oleoyl acetylglycerol (OAG). We determined protein secretion by measuring the activity of peroxidase, a protein secreted by lacrimal gland acini. beta-phorbol dibutyrate, but not alpha-phorbol dibutyrate, stimulated peroxidase secretion in a concentration-dependent manner with 3 X 10(-8) M producing maximal secretion. OAG (10(-6) M) also stimulated peroxidase secretion. To determine whether muscarinic and alpha 1-adrenergic agonists activate protein kinase C, we added beta-phorbol dibutyrate (10(-7) M) simultaneously with carbachol (10(-5) M) or phenylephrine (10(-4) M); under both conditions, secretion was less than additive. Protein secretion in the presence of beta-phorbol dibutyrate (10(-7) M) and vasoactive intestinal peptide (VIP) (10(-8) M), the latter that acts through cAMP, was additive, and when the beta-phorbol dibutyrate but not the VIP concentration was decreased to 10(-8) M, secretion was potentiated. We conclude that muscarinic and alpha 1-adrenergic agonists, but not VIP, stimulated lacrimal gland protein secretion by activating protein kinase C.
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Bereaved, property loss, and control groups (N = 155) studied 11 months following the 1980 volcanic eruption of Mt. St. Helens were recontacted 35 months postdisaster to test the hypotheses that the greater the loss experienced, the higher the stress, and the poorer the health. In general, the hypotheses were supported. Even though mental distress decreased between the two data collection periods, the mental health of the bereaved group remained poorer than both the property loss and control groups. At 3 years postdisaster, only 4% of the study participants reported complete recovery from disaster loss. Findings are compared with those of other recent disasters and clinical and theoretical implications are discussed.
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Bereaved, property loss, and control groups (N = 155) were compared 11 months after the volcanic eruption of Mt. St. Helens using standardized instruments and structured interviews. It was hypothesized that the greater the loss the greater the stress and the poorer the health. Bereaved subjects reported significantly higher levels of stress and lower levels of mental health, but not physical health. Persons who lost their permanent homes reported high rates of stress, but did not report significantly higher levels of depression, somatization, or poorer physical health. Conceptual and methodological implications are discussed.
Serial bronchoalveolar lavage (BAL) was performed prospectively on 10 normal control subjects, 20 Respiratory Distress Syndrome (RDS), and 11 Bronchopulmonary Dysplasia (BPD) newborn infants to evaluate the role of pulmonary inflammation in neonatal lung disease. Minimal inflammation was found in BAL at less than 24 h of life in all groups, but significant pulmonary polymorphonuclear leukocyte (PMN) influxes were noted at 96 h in RDS and BPD compared with control subjects. By 1 wk of life, BAL PMN counts returned to normal in RDS, but counts remained significantly elevated through 5 wk in BPD. Alveolar macrophage (AM) counts were significantly elevated at 96 h in RDS (p less than 0.05), but were significantly depressed in BPD at 4 and 5 wk (p less than 0.05). The BAL elastase/alpha 1-proteinase inhibitor (alpha 1Pi) ratios in RDS did not differ from those of normal control subjects; however, these ratios were significantly elevated from 1 through 4 wk of life in BPD, placing these infants at risk for proteolytic lung damage. Lavage elastase levels were elevated in both RDS and BPD, associated with a parallel increase in BAL alpha 1Pi in RDS and depressed BAL alpha 1Pi in BPD. These findings suggest that pulmonary inflammation, associated with a prolonged PMN influx and an imbalance between elastase and alpha 1Pi, may contribute to the development of the neonatal chronic lung disease, BPD.