Mood Matters: Negative Mood Induction Activates Dysfunctional Attitudes in Women Vulnerable to Depression

Cognitive theory holds that dysfunctionalattitudes are important risk factors for depression.Critics have questioned this view, noting that, althoughdysfunctional attitudes are elevated in depression, they are not evident in vulnerable individualswho are asymptomatic. To deal with this criticism,Miranda and Persons (1988) have advanced the mood-statedependent hypothesis, which suggests that cognitive vulnerability factors are indeed present invulnerable individuals, but remain dormant untilactivated by negative mood. To test this hypothesis, 33women with and 67 women without histories of depression reported dysfunctional attitudes before andafter a film negative mood induction. As predicted,vulnerable subjects who reported increased negative moodreported increased dysfunctional attitudes.Unexpectedly, nonvulnerable subjects who reported increasednegative mood reported decreased dysfunctionalattitudes. These findings support the mood-statedependent hypothesis, and suggest that a deficit in theability to regulate negative emotions may be animportant feature of vulnerability todepression.     

Stereoselective disposition of flecainide in relation to the sparteine/debrisoquine metaboliser phenotype.

1. The disposition of the enantiomers of the antiarrhythmic drug flecainide has been studied in five extensive (EM) and five poor (PM) metabolisers of sparteine/debrisoquine after administration of 50 mg of racemic flecainide acetate under conditions of high urinary flow rate and acidic urinary pH. 2. In the EM subjects there were no significant differences in the oral clearance, half-life or urinary excretion of (+)-S- and (-)-R-flecainide. 3. In the PM subjects differences in the pharmacokinetics of S- and R-flecainide were observed. The oral clearance of R-flecainide (467 +/- 109 ml min-1) was less (P less than 0.03) than that of the S-enantiomer (620 +/- 172 ml min-1). The half-life of R-flecainide (12.9 h) was longer (P less than 0.03) than that of S-flecainide (9.8 h). The renal clearance of the two enantiomers was, however, comparable and similar to that observed in the EM subjects. The urinary recovery of R-flecainide (15.6 +/- 3.7 mg) was greater (P less than 0.03) than that of the S-enantiomer (12.0 +/- 3.7 mg). The enantioselective disposition observed in PMs is therefore due to greater impairment in the metabolism of R- than S-flecainide. 4. The urinary recoveries of two major metabolites of flecainide, meta-O-dealkylated flecainide (MODF) and the meta-O-dealkylated lactam of flecainide (MODLF) were lower (P less than 0.05) in PMs, 12.0% +/- 3.1% and 8.2% +/- 3.2% of the dose administered, respectively, than in EMs of 17.7% +/- 3.3% and 16.5% +/- 3.3%, respectively. 5. One PM subject had a greatly diminished flecainide metabolic capacity and a rare genotype, as assigned by Xbal RFLP analysis.     

An A2-purinoceptor agonist, NECA, potentiates acetylcholine-induced glucagon secretion.

The effect of a stable structural analogue of adenosine, 5'-N-ethylcarboxamidoadenosine (NECA), was studied on glucagon secretion induced by acetylcholine (ACh) in the isolated perfused pancreas of the newborn dog. The perfusion solution contained a physiological concentration of glucose (4.2 mM). In the first set of experiments, ACh (0.5 microM) infused alone for 10 min induced a significant rise of glucagon secretion (370 +/- 98%, 4 min after the beginning of infusion). In the second set, NECA (2.2 nM) infused 10 min before ACh administration, had no effect per se, but considerably increased the response to ACh (929 +/- 262% of basal value within 3 min). So, the more specific A2 purinoceptor agonist, NECA, potentiated glucagon secretion induced by the cholinoceptor agonist, ACh.     

Paracrine renal endothelin system in rats with liver cirrhosis.

1. Liver cirrhosis was induced in rats by CCl4 administration. We analysed the expression of endothelin receptor subtypes in the renal cortex and medulla using Scatchard analysis and receptor autoradiography, and measured plasma as well as renal-tissue endothelin-1 concentrations using a specific radioimmunoassay. Furthermore, we analysed the effects of the non-selective (A/B) endothelin receptor antagonist, bosentan (6 and 100 mg kg-1 day-1) on mean arterial blood pressure, water and sodium excretion and glomerular filtration rate. 2. Our study revealed an overexpression of the endothelin B receptor (ETB) in the renal medulla of rats with liver cirrhosis (Cir: 2775 +/- 299 fmol mg-1; Con: 1695 +/- 255 fmol mg-1; n = 8; means +/- s.d., P < 0.01), whereas the density of ETB in the cortex and the endothelin A receptor (ETA) in the cortex and medulla were similar in both cirrhotic and control rats. Receptor autoradiography showed that the upregulation of medullary ETB in cirrhotic rats was due to an upregulation of ETB in the inner medullary collecting duct cells. 3. The tissue endothelin-1 concentrations were increased in the renal medulla of cirrhotic rats (Cir: 271 +/- 68 pg g-1wet wt.; Con: 153 +/- 36 pg g-1 wet wt., n = 8; means +/- s.d., P < 0.01). 4. The glomerular filtration rate was slightly decreased in cirrhotic rats but not altered after bosentan treatment in either cirrhotic or control rats. Bosentan decreased sodium excretion to a similar extent in both cirrhotic and control rats, whereas water excretion was significantly reduced by both dosages of bosentan in cirrhotic rats only (Cir + vehicle: 12.5 +/- 0.62 m day-1, Cir + 6 mg kg-1 day-1 bosentan: 8.6 +/- 1.0 ml day-1; Cir + 100 mg kg-1 day-1 bosentan: 7.4 +/- 0.6 ml day-1; n = 10; means +/- s.e.mean). 5. We therefore suggest that the upregulation of the medullary ETB in cirrhotic rats is involved in the regulation of water excretion in rats with CCl4-induced liver cirrhosis.     

What Motivates Participation and Dropout Among Low‐Income Urban Families of Color in a Prevention Intervention?*

Low‐income urban parents of color enrolled in a parent training study were interviewed to understand what motivated their participation and what led 30% of them to subsequently drop out. Most enrolled because they wanted to be better parents. Most dropped out because of time and schedule constraints. Retention was higher when parents' motivations for participation matched program goals. Program location and qualities of the recruiter were cited most often as important; financial compensation was cited least often as important.     

Neonatal rectal colonization with Malassezia furfur

Malassezia furfur and Candida albicans are fungal pathogens which have been recognized with increasing frequency as agents of mortality and serious morbidity in neonatal intensive care unit patients. A longitudinal study of oral, rectal and umbilical colonization by these organisms of newborns admitted to a neonatal intensive care unit within 24 h of birth was undertaken. Of 71 infants followed for a minimum of 10 days, 24 were colonized with M furfur and 12 with C albicans during the first 10 days of life. The lower gastrointestinal tract was found to be the most common colonization site for both organisms. Statistically significant (P<0.05) inverse associations were demonstrated between gestational age and risk of colonization with either organism at any site, and between birthweight or gestational age and risk of rectal colonization with either organism. Antibiotics were associated with a relative risk colonization of 4.06 (P=0.06) with either organism at any site. It is concluded that M furfur and C albicans are common colonizing organisms in a neonatal intensive care unit setting and are most frequently harboured in the lower gastrointestinal tract. M furfur, recently implicated as a systemic pathogen in this population, has not been previously recognized as a gastrointestinal commensal organism. The relationship between colonization and invasive fungal disease, and potential roles for preventive strategies, remain to be elucidated.     

Head injury mortality in two centers with different emergency medical services and intensive care

The authors report data collected prospectively on 551 cases of head injury in New Delhi, India, and 822 cases in Charlottesville, Virginia. The mortality rate, adjusted for initial severity of injury, was 11.0% in New Delhi versus 7.2% in Charlottesville (p less than 0.02). There was a striking similarity in mortality rates at both centers when comparing patients with the least severe head injuries and those with the most severe injuries according to the motor score of the Glasgow Coma Scale (GCS M). However, in the group with an abnormal but purposeful motor response (GCS M = 5), the mortality rate was 12.5% in New Delhi versus 4.8% in Charlottesville (p less than 0.01). The relative absence of prehospital emergency care and the delay in admission after head injury in New Delhi are cited as two possible causes for the differences in mortality rates in this subgroup of patients with "moderate" head injuries.