Failed endotracheal intubation and adverse outcomes among extremely low birth weight infants.

OBJECTIVE: To quantify the importance of successful endotracheal intubation on the first attempt among extremely low birth weight (ELBW) infants who require resuscitation after delivery. STUDY DESIGN: A retrospective chart review was conducted for all ELBW infants ⩽1000 g born between January 2007 and May 2014 at a level IV neonatal intensive care unit. Infants were included if intubation was attempted during the first 5 min of life or if intubation was attempted during the first 10 min of life with heart rate <100. The primary outcome was death or neurodevelopmental impairment. The association between successful intubation on the first attempt and the primary outcome was assessed using multivariable logistic regression with adjustment for birth weight, gestational age, gender and antenatal steroids. RESULTS: The study sample included 88 ELBW infants. Forty percent were intubated on the first attempt and 60% required multiple intubation attempts. Death or neurodevelopmental impairment occurred in 29% of infants intubated on the first attempt, compared with 53% of infants that required multiple attempts, adjusted odds ratio 0.4 (95% confidence interval 0.1 to 1.0), P<0.05. CONCLUSION: Successful intubation on the first attempt is associated with improved neurodevelopmental outcomes among ELBW infants. This study confirms the importance of rapid establishment of a stable airway in ELBW infants requiring resuscitation after birth and has implications for personnel selection and role assignment in the delivery room.

Pharmacodynamic comparison of LY3023703, a novel microsomal prostaglandin e synthase 1 inhibitor, with celecoxib.

To assess the safety, tolerability, and pharmacology of LY3023703, a microsomal prostaglandin E synthase 1 (mPGES1) inhibitor, a multiple ascending dose study was conducted. Forty-eight subjects received LY3023703, celecoxib (400 mg), or placebo once daily for 28 days. Compared with placebo, LY3023703 inhibited ex vivo lipopolysaccharide-stimulated prostaglandin E2 (PGE2 ) synthesis 91% and 97% on days 1 and 28, respectively, after 30-mg dosing, comparable to celecoxib's effect (82% inhibition compared to placebo). Unlike celecoxib, which also inhibited prostacyclin synthesis by 44%, LY3023703 demonstrated a maximal increase in prostacyclin synthesis of 115%. Transient elevations of serum aminotransferase were observed in one subject after 30-mg LY3023703 dosing (10× upper limit of normal (ULN)), and one subject after 15-mg dosing (about 1.5× ULN). Results from this study suggest that mPGES1 inhibits inducible PGE synthesis without suppressing prostacyclin generation and presents a novel target for inflammatory pain.

Serotonergic modulation of startle-escape plasticity in an African cichlid fish: a single-cell molecular and physiological analysis of a vital neural circuit.

Social life affects brain function at all levels, including gene expression, neurochemical balance, and neural circuits. We have previously shown that in the cichlid fish Astatotilapia burtoni brightly colored, socially dominant (DOM) males face a trade-off between reproductive opportunities and increased predation risk. Compared with camouflaged subordinate (SUB) males, DOMs exposed to a loud sound pip display higher startle responsiveness and increased excitability of the Mauthner cell (M-cell) circuit that governs this behavior. Using behavioral tests, intracellular recordings, and single-cell molecular analysis, we show here that serotonin (5-HT) modulates this socially regulated plasticity via the 5-HT receptor subtype 2 (5-HTR(2)). Specifically, SUBs display increased sensitivity to pharmacological manipulation of 5-HTR(2) compared with DOMs in both startle-escape behavior and electrophysiological properties of the M-cell. Immunohistochemistry showed serotonergic varicosities around the M-cells, further suggesting that 5-HT impinges directly onto the startle-escape circuitry. To determine whether the effects of 5-HTR(2) are pre- or postsynaptic, and whether other 5-HTR subtypes are involved, we harvested the mRNA from single M-cells via cytoplasmic aspiration and found that 5-HTR subtypes 5A and 6 are expressed in the M-cell. 5-HTR(2), however, was absent, suggesting that it affects M-cell excitability through a presynaptic mechanism. These results are consistent with a role for 5-HT in modulating startle plasticity and increase our understanding of the neural and molecular basis of a trade-off between reproduction and predation.

Increased susceptibility of the lungs of hyperthyroid rats to oxidant injury: specificity of effects.

Results from previous studies indicate that hyperthyroidism increases the risk of ozone-induced lung toxicity. This observation raised the possibility that pulmonary damage from other oxidant substances might be greater in a hyperthyroid state. To address this hypothesis, pulmonary responses to crystalline silica, a particulate with oxidant properties, were evaluated in normal or hyperthyroid adult male rats. To induce a hyperthyroid condition, time-release pellets containing thyroxine were implanted subcutaneously; control rats received placebo pellets. After 7 days, the animals were exposed to saline or silica (0.1mg/100g BW or 1.0mg/100g BW) by intratracheal instillation. Following silica treatment, there was a dose-related increase in bronchoalveolar lavage (BAL) albumin levels and neutrophil numbers. However, the effects of silica were similar in both normal and hyperthyroid rats. These findings were confirmed and contrasted with those regarding ozone (1ppm, 4h inhalation) in a subsequent experiment. The results indicated that, although exposure to either ozone or silica resulted in increases in BAL albumin levels and neutrophil numbers, only responses to ozone were enhanced in hyperthyroid rats. These findings suggest that specificity exists in regards to the modulation of oxidant-induced lung damage and inflammation by thyroid hormones.

Increased susceptibility of hyperthyroid rats to ozone: early events and mechanisms.

Previous studies demonstrated that ozone-induced lung damage and inflammation are much greater in hyperthyroid rats, compared to normal rats, at 18 h postexposure. The purpose of the present investigation was to study early events and mechanisms underlying the increased sensitivity to ozone in a hyperthyroid state. Specifically, the degree of lung epithelial cell barrier disruption, the antioxidant status of the extracellular lining fluid, and the release of inflammatory mediators were examined. To induce a hyperthyroid state, mature male Sprague-Dawley rats were implanted with time-release pellets containing thyroxine; control rats received placebo pellets. After 7 d, the animals were exposed to air or ozone (2 ppm, 3 h). Immediately following the end of the exposure, bronchoalveolar lavage (BAL) fluid and cells were harvested. BAL fluid albumin levels and total antioxidant status were examined. In addition, levels of prostaglandin E2 (PGE2), macrophage inflammatory protein (MIP)-2, MCP-1, and tumor necrosis factor (TNF)-alpha were determined in BAL fluid and in media samples following ex vivo culture of BAL cells harvested after in vivo inhalation exposures. The results of this study are consistent with the following hypotheses: (1) A marked increase in the permeability of the alveolar-capillary barrier is an early event following ozone exposure in a hyperthyroid state; however this does not appear to be due to overall changes in BAL fluid antioxidant potential. (2) Early increases in MIP-2, but not PGE2, are involved in the enhanced lung response to ozone in a hyperthyroid state. (3) Inflammatory mediator production (i.e., PGE2, MIP-2, MCP-1, and TNF-alpha) by alveolar macrophages plays a minimal role in the initial responses to ozone in a hyperthyroid state.

Enhanced pulmonary inflammatory response to inhaled endotoxin in pregnant rats.

Evidence suggests that pregnant animals are more sensitive than nonpregnant animals to the systemic administration of endotoxin. Studies were undertaken to assess whether an enhanced sensitivity of the pulmonary system to aerosolized endotoxin might exist during pregnancy. Pregnant Sprague-Dawley female rats (17 d of gestation) or age-matched virgin female rats were exposed to air or endotoxin (lipopolysaccharide) by inhalation for 3 h. At 18 h following exposure to endotoxin, lactate dehydrogenase activity levels in bronchoalveolar lavage (BAL) fluid samples from pregnant rats were 1.5-fold greater than those from endotoxin-exposed virgin rats. BAL polymorphonuclear leukocyte (PMN) numbers were also approximately twofold greater in pregnant rats than in virgins following the inhalation of endotoxin. The increases in BAL PMNs in pregnant rats following endotoxin exposure were observed just following exposure to endotoxin as well as at 18 h following exposure. These results indicate that an increased pulmonary inflammatory response to inhaled endotoxin occurs during pregnancy in rats. Additional findings suggest that these pregnancy-linked pulmonary responses to endotoxin cannot be explained by the following potential mechanisms: changes in the inhaled dose of endotoxin, or alterations in the responsiveness of alveolar macrophages to endotoxin. To our knowledge this is the first study that has evaluated pulmonary responses to inhaled endotoxin during pregnancy. Our finding that pregnancy is associated with an increased lung inflammatory response to aerosolized endotoxin raises the possibility that there may be a generalized enhancement of pulmonary responses to inhaled toxic agents during pregnancy.

Nitric oxide production by rat bronchoalveolar macrophages or polymorphonuclear leukocytes following intratracheal instillation of lipopolysaccharide or silica.

Exposure of the lung to lipopolysaccharide (LPS) or silica results in an activation of alveolar macrophages (AMs), recruitment of polymorphonuclear leukocytes (PMNs) into bronchoalveolar spaces, and the production of free radicals. Nitric oxide (NO) is one of the free radicals generated by bronchoalveolar lavage (BAL) cell populations following either LPS or silica exposure. The purpose of the present study was to assess the relative contributions of AMs and PMNs to the amounts of NO produced by BAL cells following intratracheal (IT) instillation of either LPS or silica. Male Sprague Dawley rats (265-340 g body wt.) were given LPS (10 mg/100 g body wt.) or silica (5 mg/100 g body wt.). BAL cells were harvested 18-24 h post-IT and enriched for AMs or PMNs using density gradient centrifugation. Media levels of nitrate and nitrite (NOx; the stable decomposition products of NO) were then measured 18 h after ex vivo culture of these cells. Following IT exposure to either LPS or silica, BAL cell populations were approximately 20% AMs and approximately 80% PMNs. After density gradient centrifugation of BAL cells from LPS- or silica-treated rats, cell fractions were obtained which were relatively enriched for AMs (approximately 60%) or PMNs (approximately 90%). The amounts of NOx produced by the AM-enriched fractions from LPS- or silica-treated rats were approximately 2-4-fold greater than that produced by the PMN-enriched fractions. Estimations of the relative contribution of AMs or PMNs to the NOx produced indicated that: (i) following LPS treatment, 75%-89% of the NOx was derived from AMs and 11%-25% from PMNs; and (ii) following silica treatment, 76%-100% of the NOx was derived from AMs and 0-24% from PMNs. Immunohistochemistry for inducible NO synthase on lung tissue sections supported these findings. We conclude that AMs are the major source of the NO produced by BAL cells during acute pulmonary inflammatory responses to LPS or silica.

Influence of hyperthyroidism on rat lung cytokine production and nuclear factor-kappaB activation following ozone exposure.

Results from previous studies indicate that hyperthyroidism increases the risk of ozone-induced lung toxicity. To better understand the processes that might contribute to the increased pulmonary inflammatory response to ozone in hyperthyroidism, we evaluated bronchoalveolar lavage fluid levels of selected cytokines in control and hyperthyroid rats after exposure to air or ozone. In addition, we assessed whether there is a relative increase in nuclear factor-kappa B (NF-kappaB) binding activity in cells harvested by bronchoalveolar lavage from hyperthyroid rats following the inhalation of ozone. A hyperthyroid condition was induced by the administration of thyroxine (0.5 mg/kg body weight) for 7 days. Control rats received vehicle injections. The animals were then exposed by inhalation to air or ozone (2 ppm for 3 h) and studied 18 h following the exposure. Bronchoalveolar lavage levels of MIP-2 and MCP-1 were increased in both control and hyperthyroid rats by ozone exposure. However, the increases in hyperthyroid rats were much greater, MIP-2 1.5-fold and MCP-1 11-fold, when compared to levels in controls following ozone. These changes appeared to be relatively specific; bronchoalveolar lavage fluid levels of interleukin (IL)-6, IL-4, and IL-10 were generally low or nondetectable across all of the studied groups at the 18-h postexposure time point. We also found that NF-kappaB binding activity was increased at both 4 and 18 h following ozone exposure in bronchoalveolar lavage cell extracts from hyperthyroid rats relative to the activity in control samples. Collectively, these results suggest that mechanisms contributing to the enhanced pulmonary inflammatory response to ozone in a hyperthyroid state include an increase in NF-kappaB activation and an upregulation of chemokine production.

Family environment and cognitive abilities in girls with fragile-X syndrome.

BACKGROUND: There remains some variance in cognitive ability that is unexplained in children with fragile-X syndrome (FXS). Studies in typically developing children suggest that family environment might be one contributor to this unexplained variance. However, the effect of family environment in relation to cognition in atypical children with FXS has been relatively unexplored to date. METHODS: The present authors examined the putative genetic and environmental factors associated with cognition in a group of age-matched children consisting of 26 females with FXS and 31 typically developing children. All subjects were administered the Wechsler Intelligence Scale for Children-Revised; and the subjects' parents were administered the Wechsler Adult Intelligence Scale-Revised, and completed the Hollingshead Index of Social Status and the Moos & Moos Family Environment Scale. RESULTS: Using a multiple regression analytic strategy, the present authors found that family environment contributed significantly to cognitive abilities in typically developing girls, but did not have a unique contribution to cognitive abilities in girls with FXS. There was a suggestion that, for girls with FXS, socio-economic status, a measure of sociocultural environment, was correlated with IQ. CONCLUSIONS: The present study provides a basis for future research on the environmental contributions to cognitive abilities, particularly work related to verbal cognition.

Identifying characteristics of older and younger females with attention-deficit hyperactivity disorder.

This study examines the manifestation of attention-deficit hyperactivity disorder (ADHD) among females of varying ages by testing the utility of particular tests to discriminate older from younger females with ADHD. A retrospective clinical chart review was conducted at a community outpatient mental health center for 75 girls from 4 to 19 years of age with a diagnosis of ADHD or subthreshold symptoms of ADHD. Signal detection methods were used to identify which variables best differentiate older (mean age = 12.06, SD = 2.61) from younger (mean age = 7.11, SD = 1.08) girls with ADHD. Girls with comorbid diagnoses of a depressive disorder and higher verbal IQ scores were more likely to be older. Overall, the findings suggest that approaches to diagnosing ADHD among females may need to be modified to include appropriate age-based criteria.

Poor adolescent expectant mothers: can we assess their potential for child abuse?

PURPOSE: To explore the correlates of high scores on the Child Abuse Potential Inventory in adolescent expectant mothers. METHODS: Child Abuse Potential scores and data on demographics, pregnancy desire, history of maltreatment, psychological functioning, and perceived social support were obtained by self-report and semi-structured interview. The sample consisted of 50 poor single adolescents recruited from prenatal clinics during the second half of the pregnancy. The relationships among the variables were assessed using Pearson product-moment correlation and multiple regression strategies. RESULTS: Higher Child Abuse Potential scores were associated with higher maternal psychological distress, maternal history of psychiatric diagnosis, and lack of perceived support by the father of the baby. Older pregnant teenagers were more likely to report childhood history of maltreatment, higher psychological distress, and perceived and expected less support by the maternal mother. Expectant mothers who were raised by a single parent were more likely to have a history of childhood maltreatment, less likely to live with the father of the baby during their pregnancy and to expect less support from him. CONCLUSIONS: Child Abuse Potential scores, obtained during pregnancy in a sample of poor single adolescents provide a marker of maternal prenatal functioning and perceived social support. Further studies are warranted to validate prenatal use of the Child Abuse Potential Inventory (CAPI), which may help identify populations at particularly high risk for child abuse during pregnancy and inform strategies for early preventive interventions. Adolescent education on family planning, child rearing, and social support programs should address the importance of the fathers' role.

Cytokine and nitric oxide release by J774A.1 macrophages is not regulated by estradiol.

Estradiol is able to regulate the release of inflammatory mediators by macrophages; however, the presence, extent, and direction of this modulation varies with species, tissue of origin, and cell culture conditions. This study examines the effects of 17-beta-estradiol (E2) on the release of inflammatory mediators by the J774A.1 mouse macrophage cell line. For experiments, cells were plated in phenol red-free DMEM containing 5% charcoal-dextran stripped calf serum. Western analysis showed that J774A.1 cells contain the estrogen receptor alpha (ER alpha) protein. We found that physiological and pharmacological levels of E2 (10(-12) M-10(-6) M) have no effect on the release of nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), or monocyte chemoattractant protein-1 (MCP-1). This suggests that J774A.1 cells grown under these culture conditions would be useful for the investigation of non-estrogen-dependent mechanisms by which certain endocrine disruptors may affect their targets in macrophages.

Hyperthyroidism increases the risk of ozone-induced lung toxicity in rats.

The risk of lung injury from ozone exposure has been well documented. It is also known that various factors may significantly influence the susceptibility of animals to the toxic effects of ozone. In the present study, we investigated the possibility that hyperthyroidism might be associated with increases in ozone-induced pulmonary toxicity. To create a hyperthyroid condition, mature male Sprague--Dawley rats were given injections of thyroxine (dose range: 0.1 to 1 mg/kg body wt daily for 7 days). Control rats received vehicle injections. The animals were then exposed to air or ozone (dose range: 0.5 to 3 ppm for 3 h). At 18 h postexposure, bronchoalveolar lavage fluid and cells were harvested. In hyperthyroid animals, ozone exposure was associated with three- to sixfold increases in bronchoalveolar lavage fluid lactate dehydrogenase activities and albumin levels as well as the number of polymorphonuclear leukocytes harvested by bronchoalveolar lavage above levels observed in ozone-exposed control rats. Additional results from the present study suggest that these thyroid hormone-linked effects cannot be fully explained by differences in whole-body metabolic rate or changes in the inhaled dose of ozone. These findings indicate that the risk of ozone-induced lung toxicity is substantially increased in a hyperthyroid state and suggest that the susceptibility of the lung to damage from ozone exposure may be significantly influenced by individual thyroid hormone status.

The Child Abuse Potential Inventory and pregnancy outcome in expectant adolescent mothers.

OBJECTIVE: The study explores the prenatal Child Abuse Potential (pCAP) scores derived from the Child Abuse Potential Inventory administered to expectant adolescent mothers. The aim of the study was to assess the association of the pCAP scores with maternal negative prenatal behaviors, and evaluate the contribution of the pCAP scores to neonatal morbidity. METHOD: The pCAP scores, demographic data, and self-report on prenatal behaviors were obtained during the second half of the pregnancy in a sample of 45 poor single adolescent mothers. A pediatrician blind to the prenatal data reviewed the neonatal records to assess neonatal morbidity. Maternal prenatal records were reviewed for obstetric risk assessment by an obstetrician who was blind to the rest of the data. The relations among the pCAP scores, prenatal behaviors, and neonatal morbidity were analyzed. RESULTS: In the prenatal period, the pCAP scores were positively correlated with self-reported prenatal smoking and substance use. The multiple linear regression analysis showed that the pCAP scores significantly contributed to neonatal morbidity independently of obstetric risk factors. CONCLUSIONS: The Child Abuse Potential scores obtained during pregnancy in poor single adolescent mothers reflect domains of maternal functioning that are associated with negative prenatal behaviors and appear to be important for predicting neonatal morbidity. Further studies are warranted to validate the prenatal use of the Child Abuse Potential Inventory.

Lung responses to hypothyroidism, hyperthyroidism, and lipopolysaccharide challenge in rats.

The objectives of this investigation were to study the effects of hypo- and hyperthyroidism on some factors involved in lung injury under basal conditions (air exposure) and during an inflammatory response induced by inhalation exposure to lipopolysaccharide (LPS; 100 microg/ml; 3 h) in adult rats. Thyroid status was altered by thyroidectomy or thyroxine injections for 15 d. Hyperthyroidism alone caused a greater degree of lung cell damage, an increase in the permeability of the alveolar-capillary barrier, a rise in the total number of phagocytic cells obtained by bronchoalveolar lavage (BAL), and enhanced nitric oxide (NO) release by phagocytic cells relative to that in euthyroid control animals. Hypothyroidism alone was associated with opposite effects. Exposure of animals to LPS produced inflammatory responses, which included significant increases in lung cell damage, permeability of the alveolar-capillary barrier, number of phagocytic cells obtained by BAL, and NO production by the phagocytic cells. In general, hyperthyroidism enhanced the effects of LPS, while hypothyroidism reduced LPS-induced responses. These results suggest that thyroid status alone can affect some of the factors involved in lung injury and also modulate some of the inflammatory effects of LPS. Hyperthyroidism tends to enhance lung injury, while hypothyroidism seems to reduce lung injury.

Cortisol and social stressors in children with fragile X: a pilot study.

Evidence of neuroendocrine dysfunction, behavioral features of social anxiety and avoidance, and neuroanatomical abnormalities suggest that abnormal hypothalamic-pituitary-adrenal (HPA) function may be a component of the fragile X (fra X) syndrome. In this preliminary study, salivary cortisol levels of males (n = 8, mean age = 13.5 yr) and females (n = 7, mean age = 13.9 yr) with the fra X full mutation were studied for 3 days. Day 1 was an experimental day, during which subjects experienced a Social Stressor task midmorning. Days 2 and 3 were routine days, during which the subjects were engaged in their typical activities. Saliva samples were collected before breakfast, lunch, dinner, and bedtime. On the experimental day, the prelunch sample collection occurred 30 and 90 minutes after the Social Stressor task. Compared with children's norms, the combined group of males and females with fra X had significantly higher cortisol levels in the prelunch and the prebedtime samples for the routine days. Comparisons between the two fra X groups for the experimental day revealed similar diurnal patterns for cortisol level. However, compared with females with fra X, males with fra X had significantly higher cortisol levels at two points during the day: 30 minutes after the social stressor and at bedtime. These preliminary data suggest that individuals with fra X have abnormal HPA function. Understanding the relations among HPA dysfunction, abnormalities in brain structure and/or function, and maladaptive behavior and cognition in fra X could inform the design of early interventions using pharmacological or environmental measures designed to normalize neuroendocrine function.

Prescribing books for immigrant children: a pilot study to promote emergent literacy among the children of Hispanic immigrants.

OBJECTIVES: To assess book-sharing activities within first-generation Hispanic immigrant families, and to assess the effect of pediatricians giving books to their patients. DESIGN: Survey. PARTICIPANTS: Convenience sample of 122 predominantly Hispanic immigrant parents of children aged 2 months to 5 years. Of these parents, 56 had received children's books from the pediatrician, and 66 had not. SETTING: House staff continuity clinic at a university children's hospital. MAIN OUTCOME MEASURE: Frequent Book Sharing (FBS) was defined as a parent's reporting more than 3 days per week of sharing books with the child. Main independent variables included the following: (1) exposure to the Reach Out and Read program, defined as having received a children's book from the pediatrician; (2) socioeconomics, as measured by parents' years of education and Medicaid enrollment; (3) acculturation, as defined by 4 questions relating to parents' proficiency with the English language; (4) parent's country of origin; (5) parent literacy, as measured by a parent's reporting more than 3 days per week of reading alone; (6) parent's age; (7) marital status; (8) household size; (9) child's age; (10) child's sex. RESULTS: Ninety percent of the parents were born outside of the United States (71% in Mexico), 85% spoke Spanish in the home, and 63% had completed less than a high-school education. Seventy-five percent of children's medical insurance was provided by Medi-Cal (Medicaid), and 9% of children were uninsured. Sixty-seven percent spoke exclusively Spanish at home, and 84% of parents want their children to learn to read in both English and Spanish. High FBS was reported among parents whose children had received books from the physician when compared with parents whose children had received no books. The odds ratio (OR) was 3.62 (95% confidence interval [CI], 1.40-9.37; P<.05). Also associated with FBS were parents reading frequently to themselves (OR = 9.52; 95% CI, 2.09-43.27; P<.05) and national origin outside Mexico (OR = 5.54; 95% CI, 1.59-19.27; P<.05). These findings were independent of parent's educational level, parent's employment, parent's age, acculturation, and family size. CONCLUSIONS: Pediatricians can promote literacy development among Hispanic immigrant children through the provision of free books at well-child visits. Our findings also suggest the independent effects of adult literacy and child age. Further research is needed to understand the effect of pediatric literacy programs on Hispanic immigrant children, their bilingual environments, and their readiness for school entry. Arch Pediatr Adolesc Med. 2000;154:771-777

Mothers' and fathers' perceptions of three year olds' attachment behavior.

This investigation reports on the antecedents and cross-sectional predictors of young children's attachment security based on Q-sort methodology, with particular consideration of the convergence of parental reports. Mothers' and fathers' ratings of child temperament and child behavior problems, as well as each parent's construction of the marital relationship and his/her affective state, were examined in relation to Q-sort assessments of mother-child and father-child attachment security. Generally, a moderate degree of convergence between maternal and paternal perceptions of attachment security was found; this association was stronger than the correlations reported based on studies using the Strange Situation procedure at 12 to 18 months of age. Antecedent relationships between ratings of parental affective symptoms, as well as ratings of marital quality and security of attachment, were stronger for fathers than for mothers. These findings may suggest closer links for fathers than for mothers between parental nurturing responses and psychological state, or they may reveal a stronger subjective bias for fathers inherent in the Q-sort method.