The Relationship of Locus of Control Dimensions to Reported Hostility and Aggression

Sadowski, Cyril J.; Wenzel, D

doi:10.1080/00223980.1982.9915378

Cited by 12 publications

(2 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Brissett and Nowicki (1973) found similar results. Sadowski and Wenzel (1982) asked college students to complete a scale of locus of control with sub-scales of fatalism and social system control, and a hostility-aggression inven-tory. The total scale was significantly positively correlated with the hostility dimension, but only the fatalism sub-scale was significantly positively correlated with the aggression dimension.…”

Section: Person Variablesmentioning

confidence: 99%

Organizational Frustration and Aggressive Behaviors

Heacox¹,

Sorenson²

2007

Journal of Emotional Abuse

View full text Add to dashboard Cite

This study, conducted in a large public agency and a large private transportation company in the U.S., found strong relationships between organizational characteristics and frustration. Role ambiguity, role conflict, work constraints, and warmth and support predicted the level of frustration experienced by employees. In turn, frustration predicted supervisor-and self-reported aggression. Frustration also predicted self-reported criterion behaviors such as withdrawal, aggression turned inward, and abandonment of goal. Frustration mediated the relationships between organizational characteristics and the criteria. In the study we developed two scales: (1) a self-report scale of behavioral reactions to frustration, and (2) the Workplace Aggressive Behaviors Scale, a guideline to increase supervisors' ability to judge the seriousness of aggressive behaviors in the work environment.

show abstract

Section: Person Variablesmentioning

confidence: 99%

Organizational Frustration and Aggressive Behaviors

Heacox¹,

Sorenson²

2007

Journal of Emotional Abuse

View full text Add to dashboard Cite

show abstract

“…They were administered the Brown Adult ADHD Scale,132 the N.E.O. Five Factor Personality Test—Revised,183,184 the Cloninger Temperament Character Inventory,185,186 the SCL‐90,187 the Locus of Control test,188–190 the Buss‐Durkee hostility scale,191 and the Defense Style Questionnaire 192,193. Among the ATU subjects, there was a significant correlation at p ≤ 0.001 between the subscores of 41 of 57 (71.9%) in these tests and a significant correlation at p ≤ 0.05 between 89.5% of the subscores.…”

Section: Assessment Of Adult Addmentioning

confidence: 99%

Clinical and Molecular Genetics of ADHD and Tourette Syndrome

Comings

2001

Annals of the New York Academy of Sciences

134

View full text Add to dashboard Cite

ADHD is a polygenic disorder due to the additive effect of genes affecting dopamine, norepinephrine, serotonin, GABA, and other neurotransmitters. Some of the specific loci involved are dopamine genes—DRD2, DRD4, DRD5, and the dopamine transporter; norepinephrine (NE) and epinephrine (EPI) genes—dopamine b‐hydroxylase, ADRA2A, ADRA2C, PNMT, norepinephrine transporter, MAOA, COMT; serotonin genes—TDO2, HTR1A, HTR1DA, serotonin transporter; GABA genes—GABRB3; androgen receptor and other genes. This model is consistent with all of the present knowledge about ADHD including (a) the increased frequency of ADHD in the relatives of ADHD probands, (b) the presence of a wide spectrum of comorbid behaviors (depression, anxiety, learning, conduct, oppositional‐defiant, conduct and substance abuse disorders) in ADHD probands and their relatives on both parental sides, (c) the close relationship to Tourette syndrome (TS), (d) the failure to find the genes for TS using linkage analysis, (e) the brain imaging studies showing hypometabolism of the frontal lobes, (f) the relationship between dopamine D2 receptor density and regional blood flow, (g) the correlation between tics and dopamine D2 receptor density in TS, (h) the motor hyperactivity of dopamine transporter and dopamine D3 receptor gene knockout mice, (i) the LeMoal and Shaywitz dopamine deficiency animal models of ADHD, (j) the NE models of ADHD, (k) the failure to explain ADHD on the basis of any single neurotransmitter defect, (l) the response of ADHD to dopamine and a2‐adrenergic agonists, (m) the small percentage of the variance of specific behaviors accounted for by each gene, and numerous other aspects of ADHD. The implications of the polygenic model for the understanding, diagnosis and treatment of ADHD and TS, as well as other psychiatric disorders, are reviewed.

show abstract