Statistical methods for analyses of incomplete clinical service records: concurrent use of longitudinal and cross-sectional data.

Statistical procedures that have become routine in other social sciences were used to analyze data from clinical service records. Despite the absence of control groups, nonrandom assignment of clients to treatment conditions, and incomplete records, effective analyses of psychotherapeutic processes were possible. Multivariate regression models, with variables that were transformed to significantly improve skewness and regression linearity, were controlled for heteroskedasticity and for end-point censoring of dependent variables. They were also used to measure the effects of a categorical variable (gender) and a scalable variable (intake distress) on a reactive outcome measure (of acute distress) and on an unreactive one (of long-term life satisfaction). Graphical methods for summarizing large data sets helped identify intake variables that could control for attrition-related sampling biases. These longitudinal covariates and corrections to adjust degrees of freedom for cases with repeated measures were then used to construct statistical models that were equivalents of pure cross-sectional designs.

Effects of stimulus color, pattern, and practice on sex differences in mental rotations task performance.

Redundant color information improved performance for both sexes on the Shepard Mental Rotations Task (MRT; Shepard & Metzler, 1971). Absolute score gains for women were larger than those for men; therefore, relative improvement was greater. Substantial practice effects, also favoring women, were apparent in both studies. Study 1 showed that redundant color improved performance by 0.25 SD. Study 2 demonstrated that redundant black-and-white pattern information did not have any effect; a second visuospatial channel, redundant color, was a critical factor in improving scores of men and women on difficult mental rotations tasks.

Oxazepam induced mouse killing by rats.

Oxazepam (2.5-80 mg/kg) induced significant mouse killing among large samples (N = 100/dose) of Holtzman strain albino rats. Meprobamate (2.5-80 mg/kg) and Chlorpromazine (0.5-4 mg/kg) did not induce killing. Despite its lesser tendency to induce aggression in humans, Oxazepam is as potent as Chlordiazepoxide for inducing killing by rats. Induction of mouse killing by rats appears to the predict clinical potency rather than the aggressive side-effects of anxiolytic benzodiazepines.

Pilocarpine, food deprivation, and induction of mouse killing by cats.

Effects of three treatments that induce mouse killing by rats were examined with cats. Food deprivation induced about 50% killing after 24 hr and almost 100% killing by 27 hr. Pilocarpine (at doses of 1.0 mg/kg that produced marked side-effects, and whether or not methyl atropine pretreatment blocked those side-effects) and chlordiazepoxide (at doses of 1.0--2.0 mg/kg) did not induce any killing. Pilocarpine produced a dose-related inhibition of spontaneous mouse killing (as it does in rats), but this was antagonised by methyl atropine. The side-effects of pilocarpine and chlordiazepoxide did not seem to account for their failure to induce killing. In contrast with food deprivation, the mechanisms by which pilocarpine and chloridazepoxide induce killing in rats may not have homologs in cats.

Despite various drugs, cats continue to kill mice.

Amphetamines (d- at 0.5--4 mg/kg; 1- at 2--4 mg/kg) inhibited spontaneous mouse killing by some, but not all cats. Various other drugs (drugs and maximum tested doses were: imipramine, 64 mg/kg; amitriptyline, 32 mg/kg; tranylcypromine, 2 mg/kg; tripelennamine, 4 mg/kg; scopolamine, 1 mg/kg; methyl scopolamine 1 mg/kg; chlordiazepoxide 16 mg/kg; diazepam 4 mg/kg; meprobamate, 80 mg/kg; pentobarbital, 16 mg/kg; chlorpromazine, 8 mg/kg; and haloperidol, 0.5 mg/kg) did not reliably inhibit such killing. In contrast with rats, mouse killing by cats was not consistently blocked by antidepressants or amphetamines. When individual cats were inhibited, their reduction of killing seemed related to anorexia rather than to affective arousal.

Drinking induced by parenteral injections of pilocarpine.

Parenteral (IP) injections of pilocarpine, in doses from 3.75 - 30 mg/kg, reliably produced drinking in water-satiated rats. This effect was not diminished by pretreatment with either centrally active (scopolaime, atropine) or peripherally active (methyl scopolamine, methyl atropine) cholinergic blocking agents, suggesting that pilocarpine does not induce drinking via a cholingergic meachnism. Repated injections of low doses, but not high doses, of pilocarpine augments drinking over trials.

Chlordiazepoxide and diazepam induced mouse killing by rats.

Chlordiazepoxide HCl, at dose levels from 2.5 mg/kg to 80 mg/kg, significantly increased the low base rates of mouse killing (3-9%) observed in large samples (N = 100/dose) of Holtzman strain albino male rats. Maximal killing rates were obtained at doses from 7.5 mg/kg to 20 mg/kg. Diazepam was equally effective, and several times more potent than chlordiazepoxide. Pentobarbital did not increase killing. Killing induced by chlordiazepoxide was blocked by d-amphetamine SO4, but not by l-amphetamine, at dose levels similar to those that block undrugged killing in this strain (ED50 = 1.5 mg/kg). Unlike pilocarpine-induced killing, the effects of chlordiazepoxide were not increased or decreased significantly by either peripherally or centrally active anticholinergic drugs, over wide dose ranges of these agents; nor were the effects of chlordiazepoxide increased by repeated daily administration.

Inhibitory effects of pre- and posttest drugs on mouse-killing by rats.

Mouse-killing in rats was gradually inhibited by repeated posttest injections of d-amphetamine (1.5 mg/kg), l-amphetamine (1.5 mg/kg) or pilocarpine (7.5 mg/kg), but not by control substances. Of these drugs, only d-amphetamine inhibited killing when given prior to a mouse-killing test. Further experiments suggested that anorexia per se did not contribute to drug-induced inhibitory effects, but that changes in internal state were important to the development of inhibition. Pretest injections appear to inhibit predatory killing by a direct pharmacological action on some target site or sites, while posttest injections produce a learned aversion to predatory killing.

The aversive control of excessive alcohol consumption by chronic alcoholics in the laboratory setting.

The efficacy of several methods of aversive control of excessive alcoholic drinking was investigated in a semi-naturalistic setting that permitted objective measurement of the drinking behavior of chronic alcoholics. Studies 1A and 1B compared an excape-conditioning precedure with a control procedure in which aversive electrical shocks were administered before drinking. Neither procedure effectively decreased subjects' pretreatment, baseline alcoholic drinking behavior. In Study 2, aversive response-contingent shocks effectively suppressed alcoholic drinking, but drinking subsequently returned to its former levels after withdrawal of punishment. Self-administered shock appeared to be as effective as experimenter-administered punishment for controlling drinking, even when the punishment contingency was faded out over time. Study 3 replicated the suppressant effect of punishment, and demonstrated that contingent shock was significantly more effective than yoked, noncontingent shock. A direct comparison of self-versus experimenter-administered punishment suggested a possible slight advantage for the latter.