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AIMS: To identify whether brief cognitive-behavioural interventions are feasible among regular users of amphetamine, to assess the effectiveness of intervention overall and to pilot two- and four-session interventions. DESIGN: Subjects were assigned randomly to individually receive a cognitive-behavioural intervention (n = 32) of either two or four sessions' duration or a self-help booklet (control condition; n = 32). SETTING: Subjects were volunteers recruited from needle exchange schemes and treatment centres in Newcastle, Australia. PARTICIPANTS: Regular (at least monthly) users of amphetamine were recruited. INTERVENTION: Either four sessions of cognitive-behaviour therapy, consisting of a motivational interview and skills training in avoidance of high-risk situations, coping with craving and relapse prevention, or two sessions consisting of a motivational interview and discussion of skills. MEASUREMENTS: The Opiate Treatment Index was the main measure at pre-treatment and 6-month follow-up. FINDINGS: There was a significant reduction in amphetamine use among the sample as a whole, with inconclusive differences between intervention subgroups. There was a moderate overall intervention effect, with the intervention group reporting over twice the reduction in daily amphetamine use as the control group. Significantly more people in the cognitive-behavioural intervention condition abstained from amphetamine at 6-month follow-up compared to the control condition. CONCLUSION: Brief cognitive-behavioural interventions appear feasible among regular users of amphetamine. A larger randomised controlled trial of the effectiveness of such interventions appears warranted.

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This report describes expression of heritable reticuloendotheliosis virus (REV) vector ME111 in 20 independent lines of transgenic chickens. The results are strikingly different from studies of Moloney virus in transgenic mice, where restricted expression of inherited proviruses has led to their use primarily as insertional mutagens rather than general agents for gene transfer. In contrast, the REV ME111 provirus is actively transcribed in a variety of tissues from transgenic chickens, is expressed from transcriptional control elements present in the long terminal repeat of the provirus, and codes for active neomycin phosphotransferase II. The REV vector system as applied to the chicken represents a departure from the long-established paradigm of retroviral transgenes in mice and provides a new approach to the study of avian biology.

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Injection of infectious non-replicating REV vector directly beneath the chicken blastoderm leads to infection of embryonic stem cells. Vector sequences are present in a variety of specialized tissues of embryos and mature birds derived from infected blastoderms. Breeding studies show that replication-defective REV vectors can transfer heritable, non-viral genetic information into the chicken germ line.

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Replication-defective vectors derived from reticuloendotheliosis virus were used to transduce exogenous genes into early somatic stem cells of the chicken embryo. One of these vectors transduced and expressed the chicken growth hormone coding sequence. The helper cell line, C3, was used to generate stocks of vector containing about 10(4) transducing units per ml. Injection of 5- to 20-microliters volumes of vector directly beneath the blastoderm of unincubated chicken embryos led to infection of somatic stem cells. Infected embryos and adults contained unrearranged integrated proviral DNAs. Embryos expressed the transduced chicken growth hormone gene and contained high levels of serum growth hormone. Blood, brain, muscle, testis, and semen contained from individuals injected as embryos contained vector DNA. Replication-defective vectors of the reticuloendotheliosis virus transduced exogenous genes into chicken embryonic stem cells in vivo.

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Difficulties associated with in vitro manipulation and culture of the early chicken embryo have restricted generation of transgenic chickens to approaches that use replication-competent retroviruses. The need to produce transgenic chickens in the absence of replicating virus prompted development of a new method of gene transfer into the chicken. Microinjection of the replication-defective reticuloendotheliosis virus (REV) vector ME111 beneath unincubated chicken embryo blastoderms results in infection of germline stem cells. This vector contains genetic information exogenous to the chicken genome, including both the herpes simplex virus type 1 thymidine kinase gene and the Tn5 neomycin phosphotransferase gene. About 8 percent of male birds hatched from injected embryos contained vector DNA in their semen. All four positive males tested passed vector sequences onto their progeny. Analysis of G1 offspring showed that gonads of G0 male birds were mosaic with respect to insertion of vector provirus. Thus, primordial germ cells present in the unincubated chicken embryo blastoderm are susceptible to infection by defective REV vectors.

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The effect of high-dosage E treatment (Rx) initiated at the stage of 3-plus active disease (target serum E levels, 5-6 mg/dl) was evaluated by a standardized scoring system of visual morbidity at the one to two year eye exam among infants cared for in the University of Pennsylvania Neonatal Complex (1976-1978). The incidence of legal blindness in both eyes or worse was decreased from 71 to 40% in E Rx (n = 10) as compared to non-E Rx (n = 14) infants, and the number of infants with minimal visual morbidity was increased. Pilot studies (1972-76; target serum E level, 1.5 and 3.0 mg/dl) of the prophylactic effect of E Rx from birth on showed a decrease in mean severity of acute stage disease and a decrease in sequelae at one to two years. A strikingly difference in visual morbidity following resolved low-grade ROP was seen when prestudy infants (1968-72) who were fed early iron supplements and given formulas with low E:PUFA ratios were compared to non-E Rx as well as to E Rx 1972-76 infants. Vitamin E seems to exert a beneficial effect at all stages of ROP, perhaps because of its broadly based regulatory role.

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A refined classification of the stages of the retinopathy of prematurity (RLF) based on the experience of over 7500 examinations during the past decade is presented. We have been using the basic elements of this classification since 1972 in order to evaluate the influence of vitamin E on retrolental fibroplasia (RLF). It is our impression that it provides a more accurate clinical method of following the course of the retinopathy and a tool for assessing the factors other than prematurity and hyperoxia that may play a subtle role in the development of RLF.

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Diminished total plasma cortisol levels have been demonstrated in postmature neonates, suggesting that fetal glucocorticoids may be involved in the cause of postmaturity. This hypothesis was tested by adrenocortical stimulation in 32 newborns: 12 were postmature; 12 were postterm, but not postmature; and 8 were normal term neonates. The mean pre- and poststimulation total plasma cortisol levels were 3.9 and 50.9 microgram/100 ml, respectively, for the postmature newborns, 9.7 and 44.0 microgram/100 ml for the postterm, but nonpostmature newborns, and 9.8 and 37.1 microgram/100 ml for the normal term newborns. The differences in the poststimulation rise in plasma cortisol between the postmature and merely postterm infants or between the postterm and normal term infants were not statistically significant. The mean poststimulation cortisol rise in the postmature group exceeded that of the normal term group (P less than 0.05). The adequacy and promptness of response to adrenocortical stimulation eliminate the likelihood of adrenal insufficiency in postmature infants.

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Neurologic and developmental performance during the first year of life was correlated with maximum neonatal serum bilirubin levels for 27,000 infants in the Collaborative Perinatal Project. The infants were grouped by race and by five birth weight/gestational age categories to control for the effect of these factors on hyperbilirubinemia and developmental outcome. Low mean eight-month motor scores and delayed one-year motor development were associated with serum bilirubin levels in the range of 10 to 14 mg/dl and above. This relationship was strongest for low-birth-weight/short-gestational-period infants. A persistent association of developmental outcome with hyperbilirubinemia was found over and above the variation of maturity within the birth weight/gestational age categories.

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A full-term male infant delivered by caesarean section following a prolonged rupture of the amniotic membranes of 30 hours' duration manifested peculiar skin lesions at the time of birth consistent with the healing phase of bullous impetigo. He was colonized with beta-hemolytic Streptococcus group B that was also cultured from the mother's cervix. It is possible this infant became infected in utero since the healing stage of the lesions suggest that they were present sometime before birth.

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Total plasma cortisol in cord and neonatal blood was measured by a radioassay method in neonates resulting from (1) term vaginal delivery following uncomplicated labor (control group), (2) term vaginal delivery following fetal distress during labor, (3) postterm, postmature vaginal delivery following fetal distress during labor, and (4) postterm, postmature emergency cesarean section performed because of signs of severe fetal distress during labor. Comparison of the mean peripheral plasma cortisol values showed that whereas the mean level (plus or minus S.E.) of the distressed term neonates (22.2 plus or minus 5.3 mug per 100 ml.) use 180 per cent of that of the control group (12.3 plus or minus 1.1 mug per 100 ml.; P smaller than 0.01) the mean level for the vaginally delivered postmature group (7.5 plus or minus 1.8 mug per 100 ml.) was only 61 per cent of that of the control group (P smaller than 0.05). Furthermore, in the postmature group with sufficient intrapartum distress to warrant emergency cesarean section the mean level (4.6 plus or minus 1.5 mug per 100 ml.) was found to be only 37 per cent of that of the control group. No differences were observed among the cord plasma cortisol values. These results are strongly suggestive of a relative adrenocortical insufficiency in postmature neonates. Such insufficiency could result from a defect in any portion of the adrenal-pituitary-hypothalamic axis. Effort is under way to further define such a defect.

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Plasma cortisol levels were studied in the cord blood and neonatal blood of the following vaginally delivered groups: (A) postmature; (B) postterm (but not postmature); and (C) term neonates. Significantly lower levels of 8 A.M. neonatal plama cortisol were found in postmature neonates when compared with term neonates (P LESS THAN 0.02) or merely postterm neonates (P LESS THAN 0.02). No difference was found in the cord blood cortisol levels in all three groups. Contrary to the traditional belief that postmaturity results from placental aging, our findings appear to indicate that postmaturity represents a specific fetal disorder. Fetal adrenal insufficiency may be a characteristic of this disorder. Prolonged pregnancy in these cases may be reflected inability of the affected fetus to initiate labor.

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Three cases of early neonatal pneumoperitoneum as a result of progressive massive tension pneumomediastinum are described. The important roentgenographic features include massive pneumomediastinum located both above and behind the heart, absence of free peritoneal fluid, pneumothorax, and air in the stomach. Laparotomy should be avoided in this condition.

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