Age, personality, and the Holtzman Inkblot Technique

Recent longitudinal studies using personality questionnaires and ratings have shown remarkable stability across the adult years. In an investigation of age changes and differences in personality as measured by the Holtzman Inkblot Technique (HIT), ninety-three men and women aged twenty-five to ninety were administered Form A of the HIT; forty-four of these were retested one to three years later. Stability coefficients ranged from .07 for Form Appropriateness to .73 for Form Definiteness, with most variables showing significant but moderate stability. Repeated measures analyses of variance showed increases in six variables and decreases in two others, but only one of these changes was paralleled by cross-sectional age differences. Correlations with self-report measures of the broad personality domains of neuroticism, extraversion, and openness to experience failed to show hypothesized relations, and the associations seen were attributable to chance. It was concluded that the HIT measures perceptual-cognitive variables that are moderately stable in adulthood.     

Interaction of short chain aliphatic alcohols with muscarinic receptor-stimulated phosphoinositide metabolism in cerebral cortex from neonatal and adult rats.

Muscarinic receptor-stimulated phosphoinositide metabolism has been recently suggested as a possible target for the neurotoxic effects of ethanol during brain development. Since two other alcohols, tertiary butanol and n-propanol, have been shown to cause microencephaly in the rat when administered during the brain growth spurt, in the present study we investigated the in vitro effects of five short chain aliphatic alcohols on muscarinic receptor-stimulated phosphoinositide metabolism in cerebral cortical slices from 7 day-old rats. In neonatal animals all alcohols tested inhibited carbachol (1 mM)-stimulated [3H]inositol phosphates accumulation in a dose- and time-dependent manner. The order of potency was t-butanol greater than n-propanol greater than or equal to iso-propanol greater than ethanol greater than methanol. After 90 min of incubation, ethanol, n-propanol and t-butanol caused a significant inhibition of muscarinic receptor-stimulated inositol metabolism at doses as low as 15 - 50 mM, comparable to the blood concentrations reached after in vivo administration of doses able to induce developmental neurotoxicity. The inhibitory effect of ethanol was additive to that of iso-propanol or t-butanol. Differently from these effects in 7 day-old rats, in cortical slices from adult animals methanol and ethanol had no effect on carbachol-stimulated phosphoinositide metabolism, while the two propanol isomers and t-butanol were less effective than in neonatal animals. These results suggest that muscarinic receptor-coupled phosphoinositide metabolism might be a common neurochemical target for the developmental neurotoxicity of short chain aliphatic alcohols.     

Delayed increase of Ca2+ influx elicited by glutamate: role in neuronal death

The mechanism of delayed neurotoxicity, triggered by glutamate, was studied in 7-8-day-old primary cultures of rat cerebellar granule cells. Treatment of cultures for 15 min with 50 microM glutamate in Mg2+ -free medium, followed by removal of the excitoxin, resulted in neuronal death, which started to appear 2-3 hr after the termination of glutamate treatment. The number of dead neurons increased gradually in the next few hours and 80-85% of neurons were found dead 24 hr later. Antagonists of N-methyl-D-aspartate-sensitive glutamate receptors (phencyclidine) or 1.2 mM MgCl2, but not the antagonist of N-methyl-D-asparatate-insensitive glutamate receptors (6-cyano-7-nitroquinoxaline-2,3-dione), abolished the neurotoxic effect of kainate. Development of glutamate-induced neuronal death depends strongly on Ca2+. Removal of extracellular Ca2+ (with 1mM ethyleneglycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid) immediately after the termination of glutamate exposure and before the appearance of the early signs of neuronal death (post-glutamate period) dramatically reduced neuronal degeneration. Neurotoxic concentrations of glutamate induced sustained increase of 45Ca2+ uptake in the post-glutamate period. The delayed increase of 45Ca2+ uptake, as well as the delayed neurotoxicity, were not affected by post-glutamate treatment with phencyclidine, dibenzocyclohepteneimine; DL-2-amino-5-phosphonovalerate, or MgCl2 or with voltage-dependent Ca2+ channel blockers (nitrendipine, verapamil, diltiazem). Neurotoxic concentrations of glutamate also induced a delayed sustained increase of [3H]phorbol-12,13-dibutyrate binding, reflecting an increased translocation of protein kinase C (PKC) from cytosol to the cell membrane during the post-glutamate period. Pretreatment of neurons with the ganglioside GT1b (trisialosylgangliotetraglycosylceramide), followed by removal of free GT1b from the incubation medium, prevented PKC translocation, the sustained increase of 45Ca2+ uptake in the post-glutamate period, and the delayed neuronal death. We suggest that the sustained activation and translocation of PKC primed by glutamate receptor stimulation may be the triggering event causing the protracted increase of neuronal Ca2+ influx. This influx is insensitive to voltage-dependent Ca2+ channel blockers and glutamate receptor antagonists. It appears that this delayed increase of Ca2+ influx may be important in causing neuronal death.     

Efficacy of adjunctive carbamazepine in the treatment of chronic schizophrenia

Six treatment-resistant schizophrenic patients were given a ten-week single-blind trial of carbamazepine. Treatment resistance was determined on the basis of documented failure to respond to treatment with at least three neuroleptic drugs from two different chemical classes. The adjunctive use of carbamazepine resulted in a significant improvement of the negative symptoms of schizophrenia. These symptoms are often poorly responsive to conventional antipsychotic drugs. Therefore, controlled studies should be performed to further assess the possible efficacy of carbamazepine in schizophrenia.     

Systemic necrotizing vasculitis associated with childhood sarcoidosis

Childhood sarcoidosis is a rare disorder with protean manifestations. The case of a child with prolonged fever, hepatosplenomegaly, pancytopenia, and systemic necrotizing vasculitis manifesting as fever, rash and skin infarctions, digital pregangrene, and foot drop is reported. This is the first case of systemic necrotizing vasculitis reported in sarcoidosis. The fulminant course of the disease required treatment with intravenous pulsed cyclophosphamide and high doses of corticosteroids. The spectrum of vasculitis in childhood and adult sarcoidosis is reviewed.     

Detection of subclinical ascorbate deficiency in early Parkinson''s disease

From mid-October 1989 to mid-July 1990 all newly admitted residents to Bury Local Authority Residential Homes were comprehensively medically screened. In a series of 100 residents eight had early Parkinson's disease (six of them hitherto undiagnosed). Seven showed evidence of Vitamin C deficiency. Of the seven showing evidence of deficiency, four suffered from early Parkinson's disease. Of the 93 without evidence of Vitamin C deficiency only four had Parkinson's disease. This indicates a significantly higher prevalence of Parkinson's disease in the group with Vitamin C deficiency (P less than 0.001 using Fisher's exact).     

Atypical complication of surgery for otospongiosis: the formation of cholesteatoma

Presenting a clinical case, the authors reveal the possible cholesteatoma complications arising from otospongious surgery. He notice that there are very few literature about similar cases. Underlining the rarity of this complication, the authors will put forward concisely the principal etiological mechanisms occurring in this kind of pathology. Since the reoperation must often be carried out on fragile inner ears, the authors stress on the necessity to respect the elementary rules of prevention in order to avoid the formation of precholesteatoma states.     

Intravenous Phenylephrine Preconditioning of Cardiac Grafts From Non–Heart-Beating Donors

Background. Hypoxia and warm ischemia produce severe injury to cardiac grafts harvested from non–heart-beating donors. To potentially improve recovery of such grafts, we studied the effects of intravenous phenylephrine preconditioning.Methods. Thirty-seven blood-perfused rabbit hearts were studied. Three groups of non–heart-beating donors underwent intravenous treatment with phenylephrine at 12.5 (n = 8), 25 (n = 7), or 50 μg/kg (n = 7) before initiation of apnea. Non–heart-beating controls (n = 8) received saline vehicle. Hypoxic cardiac arrest occurred after 6 to 12 minutes of apnea, followed by 20 minutes of warm in vivo ischemia. A 45-minute period of ex vivo reperfusion ensued. Nonischemic controls (n = 7) were perfused without antecedent hypoxia or ischemia.Results. Phenylephrine 25 μg/kg significantly delayed the onset of hypoxic cardiac arrest compared with saline controls (9.6 ± 0.5 versus 7.7 ± 0.4 minutes; p = 0.00001), yet improved recovery of left ventricular developed pressure compared with saline controls (57.1 ± 5.3 versus 41.0 ± 3.4 mm Hg; p = 0.04). Phenylephrine 25 μg/kg also yielded a trend toward less myocardial edema than saline vehicle (p = 0.09).Conclusions. Functional recovery of nonbeating cardiac grafts is improved by preconditioning. We provide evidence that the myocardium can be preconditioned with phenylephrine against hypoxic cardiac arrest.(Ann Thorac Surg 1997;63:1664–8)