Smaller fetal thymuses in pre-eclampsia: a prospective cross-sectional study.

OBJECTIVE: To determine whether the thymus is smaller in fetuses of pre-eclamptic mothers than in those of normal controls. METHODS: This was a cross-sectional, prospective, comparative study of sonographically determined fetal thymus measurements in 39 pregnancies with pre-eclampsia and 70 healthy pregnancies. RESULTS: Both the diameter and the perimeter of the fetal thymus were smaller in pregnancies with pre-eclampsia than in healthy controls. The means of the thymus diameters were 28.6 ± 5.9 and 32.9 ± 4.5 mm and of thymus perimeters 80.9 ± 16.5 and 93.1 ± 16.6 mm for pre-eclamptic and healthy pregnancies, respectively (P < 0.001). General linear models showed that smaller fetal thymuses in pre-eclampsia were independent of gestational age, estimated fetal weight, small for gestational age status and antenatal steroid use. CONCLUSIONS: Pre-eclampsia is associated with smaller fetal thymuses.

Smoking in help-seeking veterans with PTSD returning from Afghanistan and Iraq.

Past research has shown that veterans and individuals with posttraumatic stress disorder (PTSD) have increased rates of smoking. However, the rates of smoking in younger help-seeking veterans returning from Afghanistan and Iraq, and possible correlates of smoking among this population are unknown. In this study, we evaluated the rate of lifetime and current smoking among a sample of 90 returning male veterans diagnosed with PTSD. Fifty-nine percent reported a lifetime history of smoking including 32% that were current smokers. Current smokers were significantly younger than non-smokers. Current smokers (mean age=31) reported a mean age of smoking onset as 15.86 with a pack year history of 8.89. These smokers reported on average five previous quit attempts. According to a stages of change model, one-half of the smokers were in the contemplation phase of stopping smoking (50%), 29% were in the pre-contemplation phase and 21% were in the preparation phase. The results are placed in the context of non-psychiatric and psychiatric smokers.

Pulmonary dendritic cells and alveolar macrophages are regulated by gammadelta T cells during the resolution of S. pneumoniae-induced inflammation.

gammadelta T cells commonly associate with mucosal and epithelial sites, fulfilling a variety of immunoregulatory functions. While lung gammadelta T cells have well-characterized pro-inflammatory activity, their potential role in the resolution of lung inflammation has yet to be explored in any detail. Indeed, given the importance of minimizing inflammation, the cellular mechanisms driving the resolution of lung inflammation are poorly understood. Using a murine model of acute Streptococcus pneumoniae-mediated lung inflammation, we now show that resolution of inflammation following bacterial clearance is associated with a > 30-fold increase in gammadelta T-cell number. Although inflammation eventually resolves in TCR delta(-/-) mice, elevated numbers of alveolar macrophages and pulmonary dendritic cells, and the appearance of well-formed granulomas in lungs of TCR delta(-/-) mice, together indicated a role for gammadelta T cells in regulating mononuclear phagocyte number. Ex vivo, both alveolar macrophages and pulmonary dendritic cells were susceptible to lung gammadelta T cell-mediated cytotoxicity, the first demonstration of such activity against a dendritic cell population. These findings support a model whereby expansion of gammadelta T cells helps restore mononuclear phagocyte numbers to homeostatic levels, protecting the lung from the consequences of inappropriate inflammation.

Dietary n-3 and n-6 fatty acids alter avian glucose metabolism.

(1) This investigation studied the effects of dietary saturated and polyunsaturated fatty acids (PUFAs) from the n-3 and n-6 series on insulin action and glucose uptake in broiler chickens. (2) One-day-old male chicks were fed on a commercial starter diet for 3 weeks, randomly divided into three groups (n = 6) and fed ad libitum on isonitrogenous experimental diets of equal energy density for a further 6 weeks. The diets contained 20.8 g/100 g protein and 80 g/kg of either edible tallow, fish oil or sunflower oil, giving diets high in saturated fatty acids, n-S PUFAs or n-6 PUFAs, respectively. (3) Jugular catheterisation was performed under general anaesthesia during week 4 of the dietary treatments and the birds given 7 d post-surgery to recover. To estimate insulin action, a bolus glucose infusion (1 g/kg) was given to each chicken and sequential blood samples taken over a one-hour period. To estimate the disappearance rate of glucose from the plasma and its incorporation into tissues, 2-deoxy-D-3H glucose (2DG-3H glucose) was infused into each chicken (50 microCi) 2 d later. (4) Although there were no significant differences in glucose clearance rate following the glucose infusion, the maximal insulin release in response to the glucose infusion was higher in the tallow group than in either the n-3 or n-6 PUFA dietary groups. There were no significant differences in the clearance rate of 2DG-3H glucose. Labelled glucose incorporation into the breast muscle was greater in birds given fish oil than in birds given tallow and significantly greater than in birds given sunflower oil. (5) The data suggest that the type of dietary fat can influence glucose metabolism and that this change in glucose utilisation may alter the energy metabolism of the broiler.

Dietary n-3 and n-6 fatty acids alter avian pituitary sensitivity.

The effects of dietary saturated and polyunsaturated fatty acids (PUFAs) of the n-3 and n-6 series on avian pituitary sensitivity were investigated by infusing human growth hormone (GH) releasing hormone--fragment 1-29--and chicken luteinising hormone releasing hormone (LHRH) into catheterized broiler chickens. At 3 weeks of age three groups (n = 18; six birds per group) were fed for 6 weeks isonitrogenous and isoenergetic experimental diets containing 80 g/kg of edible tallow (saturated fatty acids), fish oil (n-3 PUFAs) or sunflower oil (n-6 PUFAs). Jugular catheterisation was performed under general anaesthesia during week four of the dietary treatments and the birds allowed 7 days post surgery to recover. A bolus of LHRH (20 microg/bird) and a GH releasing hormone (12.5 microg/kg) infusion was given on different days to each chicken and serial blood samples taken over a 1 h period. Plasma luteinising hormone and GH concentrations were measured by radioimmunoassay. Pre-infusion GH concentrations were similar for the tallow, fish and sunflower oil dietary groups (5.2 +/- 3.9, 5.2 +/- 1.0 and 6.1 +/- 3.1 ng/ml, respectively), however, GH concentration in response to the GH releasing hormone infusion was elevated in the sunflower oil group (44.7 +/- 5.7 ng/ml) when compared to chicken fed tallow (33.7 +/- 9.7ng/ml) or fish oil (21.3 +/- 5.0 ng/ml). There was a significant decrease (P < 0.05) in the clearance rate of plasma GH for the birds fed the fish oil compared with those fed sunflower oil with an intermediate value being observed in the tallow fed group. Pre-infusion plasma luteinising hormone concentrations for the birds fed tallow (3.2 +/- 0.7 ng/ml) were significantly elevated (P < 0.05) when compared to birds fed either the sunflower oil (0.84 +/- 0.25 ng.ml) or fish oil (0.93 +/- 0.22 ng/ml) diets. There were no significant differences between the dietary groups in either the maximal plasma luteinising concentration or its disappearance rate following the LHRH infusion. The data demonstrate that dietary fatty acids alter avian pituitary sensitivity and this modulation is determined by the nature of the dietary fat rather than the degree of saturation per se. In addition, this study also shows that dietary fats have a differential effect on pituitary cell activity and are specific to certain pituitary cell types.

Doppler sonographic measurements of arterial blood flow and their repeatability in the equine foot during weight bearing and non-weight bearing.

In six normal adult horses, pulsed-wave Doppler sonographic inspections were made of the left and right lateral palmar proper digital artery (LPPDA) of each thoracic limb. Using a two-period, crossover design with repeated measures, each LPPDA was inspected on four occasions throughout the day over a 7 hour period and, on each occasion, with the limb weight bearing and non-weight bearing. In comparison with the observations made during weight bearing, there were significant increases (P<0.001) in blood-flow velocities when the limb was non-weight bearing. There was no relationship between blood velocities and the time of day, the order in which the inspections were made, resting heart rate, age of the horse, or hoof angle. In both weight bearing and nonweight bearing, the Doppler waveform demonstrated a systolic peak followed by at least two diastolic peaks and an end diastolic plateau. Horses that moved least during sonographic inspections had the lowest co-efficients variation.

Postprandial arterial vasodilation in the equine distal thoracic limb.

The effects of feeding on blood flow to the equine foot are poorly understood. In a temperature-controlled room, duplex Doppler ultrasonographic observations were made pre- and postprandially of the lateral proper palmar digital artery of 5 horses, randomly assigned to twice and 4 times daily feeding in an unbalanced 2 period crossover design. Arterial diameter and blood velocity were measured over 4 h and additional observations made of heart rate, blood pressure, total plasma protein, packed cell volume, plasma glucose and insulin. There was no effect of the feeding regimen on any variable. Postprandially, there were significant increases in arterial diameter, blood velocity, total plasma protein, plasma glucose and insulin; the other variables were unchanged. It appeared that the normal postprandial response was an increase in blood flow to the foot. The value of ultrasonography for noninvasive investigation of the peripheral vasculature of the conscious horse was established; and in the future it may have a role in the diagnosis of vascular diseases of the foot.

Differential involvement of dendritic cell subsets during acute Salmonella infection.

Within murine CD11c(+) dendritic cells (DC), CD8alpha+, CD8alpha-CD4+, and CD8alpha-CD4- subsets are defined. This study characterized the localization, number, and function of these subsets during acute Salmonella typhimurium infection. Immunohistochemical and flow cytometric analyses of spleens from mice orally infected with virulent S. typhimurium revealed that in situ redistribution and alteration in the absolute number and function of DC occurred in a subset-specific manner during infection. CD8alpha-CD4+ DC present at B cell follicle borders in the spleen of naive mice were absent 5 days post-Salmonella infection, despite no overall change in the absolute number of CD8alpha-CD4+ splenic DC. CD8alpha+ and CD8alpha-CD4- DC were prominently associated with the red pulp, and the frequency of these cells increased strikingly 5 days post-Salmonella infection. Significant quantitative increases in both CD8alpha+ and CD8alpha-CD4- subsets were associated with the in situ redistribution. Examination of Salmonella-infected TAP1(-/-)/beta(2)-microglobulin(-/-) mice, which lack CD8alpha+ T cells, confirmed the differential subset-specific modulations in the DC populations both in situ and quantitatively. Ex vivo intracellular cytokine analysis showed significantly increased frequencies of CD8alpha(+) DC producing TNF-alpha at days 2 and 5 postinfection. In contrast, CD4+ DC producing TNF-alpha were transiently increased followed by a significant reduction. No significant increase in IL-12p40 or IL-10 production by splenic DC was detected during the first 5 days post-S. typhimurium infection. Together these data reveal differential modulation of splenic DC subsets with regard to organization, number, and cytokine production during the course of acute Salmonella infection.

Drug use and validity of substance use self-reports in veterans seeking help for posttraumatic stress disorder.

The present study assessed drug use and the validity of self-reports of substance use among help-seeking veterans referred to a specialty clinic for the assessment of posttraumatic stress disorder (PTSD). Patients (n = 341) were asked to provide a urine sample for use in drug screening as part of an evaluation of PTSD. Self-reports of substance use were compared with same-day supervised urine samples for 317 patients who volunteered to participate in a drug screening. Results suggested that self-reports were generally quite valid. Only 8% of the cases involved patients not reporting substance use detected by urine screens. A total of 42% of the participants were identified as using drugs of abuse (excluding alcohol) through self-report and urine drug screens. Among participants using drugs, PTSD diagnosis was significantly associated with greater marijuana and depressant use as compared with stimulant (cocaine and amphetamines) use.

Soluble and cell-associated forms of the adhesion molecule LFA-3 (CD58) are differentially regulated by inflammatory cytokines.

The adhesion molecule lymphocyte function-associated antigen 3 (LFA-3) (CD58) is an important regulator of immune cell function which occurs as both surface-associated and 'soluble' forms. This study has investigated the inter-relationship and the effects of cytokines on the expression of LFA-3 isoforms. The surface antigen was found to be relatively unaffected by cytokines, but the release of soluble LFA-3 (sLFA-3) was highly responsive to interleukin 1beta (IL-1beta), interferon gamma (IFN-gamma) and tumour necrosis factor alpha (TNF-alpha). This modulation was cell-specific, particularly with regard to IFN-gamma, which up-regulated sLFA-3 release by A431 cells but down-regulated the release of the soluble form from HEp2 and HepG2 cells. We further demonstrated that LFA-3 is also present in a cytoplasmic 'pool' in each of the cells and, moreover, that cleavage of LFA-3 from the cell surface by phospholipase C resulted in an increase in the levels of the intracellular LFA-3 and replacement of the membrane-associated antigen. These observations suggest that the expression of the surface, soluble and intracellular forms of LFA-3 may be linked by regulatory mechanisms which are likely to exert an important influence on inflammatory interactions.

Feigning combat-related posttraumatic stress disorder on the personality assessment inventory.

This study examined whether individuals who were instructed on the Diagnostic and Statistical Manual of Mental Disorders (4th ed. [DSM-IV]; American Psychiatric Association, 1994) criteria for posttraumatic stress disorder (PTSD) could feign PTSD on the Personality Assessment Inventory (PAI; Morey, 1991). The study also investigated whether PAI indexes of symptom exaggeration, the Negative Impression Management (NIM) scale and the Malingering index, could identify individuals feigning PTSD. The diagnostic rule for PTSD (Morey, 1991, 1996) was applied to the profiles of a group of 23 veterans with combat-related PTSD and 23 male undergraduates instructed to malinger PTSD. Seventy percent of the student malingerers produced profiles that received diagnostic consideration for PTSD. The NIM cutting score (> or = 8) was highly effective in detecting simulation of PTSD but resulted in the misclassification of a large number of true PTSD cases. There were no significant differences in the overall efficiency of the test with various validity criteria. We discuss the implications of these findings for the use of the PAI in the diagnosis of combat-related PTSD.

Regulation of LFA-3 (CD58) by dexamethasone and retinoic acids in vitro.

INTRODUCTION: The oral form of lichen planus (OLP) is a chronic inflammatory disease characterized by the accumulation of T cells below the basal layer of the buccal mucosa. We have previously shown that the adhesion molecule lymphocyte function-associated antigen-3 (LFA-3; CD58) is up-regulated in lesional tissue and may play an important part in the molecular pathology of this disease. OLP is often treated with glucocorticoids, and glucocorticoid-resistant cases with retinoid drugs. However, it is not yet known whether the pharmacological action of these drugs is mediated directly or indirectly via LFA-3. METHODS: In the present experiments we have used the technique of flow cytometry (FCM) to accurately measure the effects of the glucocorticoid dexamethasone (DEX), all-trans retinoic acid (ATRA) and 13-cis retinoic acid (13RA) on LFA-3 expression by three main cell types found in OLP lesions--an oral epithelial cell line (KB cells), a T lymphocyte cell line (Jurkat cells) and an antigen presenting myelomonocytic cell line (U937 cells). The relative levels of the specific receptors for the drugs were also determined in these cell lines using FCM. RESULTS: ATRA and 13RA were found to have a more pronounced inhibitory effect on LFA-3 expression than did DEX, the U937 cells being the most sensitive and the KB cells the least affected. The KB cells also expressed the lowest relative levels of drug receptors. DISCUSSION: The results showed that the three drugs differentially down-regulated LFA-3 expression by each of the cell lines. Moreover, the relative inhibitory effects of the drugs appeared to be related to the relative expression of the specific drug receptors by each of the cells. Our findings suggest that the down-regulation of LFA-3 in vitro might explain at least partly the efficacy of glucocorticoids and retinoids in the treatment of inflammatory diseases in vivo.

Pravastatin therapy and the risk of stroke.

BACKGROUND: Several epidemiologic studies have concluded that there is no relation between total cholesterol levels and the risk of stroke. In some studies that classified strokes according to cause, there was an association between increasing cholesterol levels and the risk of ischemic stroke and a possible association between low cholesterol levels and the risk of hemorrhagic stroke. Recent reviews of trials of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors have suggested that these agents may reduce the risk of stroke. METHODS: In a double-blind trial (the Long-Term Intervention with Pravastatin in Ischaemic Disease study), we compared the effects of pravastatin on mortality due to coronary heart disease (the primary end point) with the effects of placebo among 9014 patients with a history of myocardial infarction or unstable angina and a total cholesterol level of 155 to 271 mg per deciliter (4.0 to 7.0 mmol per liter). Our goal in the present study was to assess effects on stroke from any cause and nonhemorrhagic stroke, which were secondary end points. RESULTS: There were 419 strokes among 373 patients over a follow-up period of six years. A total of 309 strokes were classified as ischemic, 31 as hemorrhagic, and 79 as of unknown type. Among the patients given placebo, the risk of stroke was 4.5 percent, as compared with 3.7 percent among those given pravastatin (relative reduction in risk, 19 percent; 95 percent confidence interval, 0 to 34 percent; P=0.05). Non-hemorrhagic stroke occurred in 4.4 percent of the patients given placebo, as compared with 3.4 percent of those given pravastatin (reduction in risk, 23 percent; 95 percent confidence interval, 5 to 38 percent; P=0.02). Pravastatin had no effect on hemorrhagic stroke (incidence, 0.2 percent in the placebo group vs. 0.4 percent in the pravastatin group; P=0.28). CONCLUSIONS: Pravastatin has a moderate effect in reducing the risk of stroke from any cause and the risk of nonhemorrhagic stroke in patients with previous myocardial infarction or unstable angina.

Echocardiographic measurements in greyhounds, whippets and Italian greyhounds--dogs with a similar conformation but different size.

OBJECTIVE: To determine the effect of body size on various echocardiographic measurements in dogs of widely differing size, but identical body conformation. DESIGN: A randomised echocardiographic study of healthy sighthounds. ANIMALS: 60 dogs comprising an equal number (20) of racing Greyhounds, Whippets and Italian Greyhounds. PROCEDURE: Following sedation with acepromazine and morphine, and acclimatization, a thorough echocardiographic examination was performed on each dog using standard methods. RESULTS: Dimensions measured echocardiographically were highly correlated with body size. These data were subsequently examined using analyses of variance and regression. Body surface area was the best overall predictor of dimensional measurements. In comparison to previous studies using dogs of differing size and conformation, the spread of values for measurements plotted against body surface area showed substantially narrower ranges. Thus, the relationship between echocardiographic measurements and body surface area was much closer for dogs with an identical somatotype than for dogs of differing size and conformation. Commonly used ejection phase indices (fractional shortening, ejection fraction and velocity of circumferential fibre shortening) were negatively correlated with body size. In contrast, the thickening fraction of the left ventricular posterior wall, another ejection phase index, was independent of body weight and body surface area for all three breeds and when the data were pooled. CONCLUSION: Taken in consideration with previous work, this study demonstrates that body conformation and body size both influence canine echocardiographic measurements. Commonly used ejection phase indices are significantly affected by body size, with larger sighthounds having lower values. A more appropriate method of quantitating left ventricular function may be the determination of the thickening fraction of the left ventricular posterior wall.

Localized adhesion molecule expression and circulating LFA-3 levels in adult and early onset forms of periodontitis.

Because of their importance in mediating cellular interactions in chronic inflammatory diseases, this study has examined the expression of a number of adhesion molecules in adult (n=11), generalized early onset (n=5) and localized early onset (n=2) forms of periodontitis. In comparison with immunostaining profiles of cryostat sections of healthy gingival tissue (n=7), the beta 1 integrins VLA-1, VLA-2 and VLA-4 were found to be up-regulated in periodontitis, with VLA-6 being markedly elevated. Although only small differences were observed in ICAM-1 and LFA-3 expression in the gingival epithelium, there was particularly notable up-regulation of these adhesion molecules within the inflammatory infiltrates of the diseased tissues. However, there were no statistically significant differences between the serum levels of a soluble form of LFA-3 in periodontitis patients (n=47) compared with healthy control subjects (n=40), although the generalized early onset and adult periodontitis groups exhibited wider ranges of circulating LFA-3. These findings show that there is localized modulation of adhesion molecule expression in the chronic inflammatory periodontal diseases studied, but that the levels of LFA-3 in the circulation nevertheless remain unaffected.

LFA-3 (CD58) mediates T-lymphocyte adhesion in chronic inflammatory infiltrates.

Previous studies have suggested that LFA-3 has an important role in a number of chronic inflammatory pathologies, although an active role for LFA-3 within in vivo inflammatory reactions has not previously been directly observed in humans. To assess the importance of LFA-3 in this process, this study used an adaptation of the Stamper-Woodruff lymphocyte adhesion assay to measure the binding of exogenous activated lymphocytes to the T-cell-dominated chronic inflammatory infiltrate of oral lichen planus. Antibody blockade experiments showed that anti-LFA-3 monoclonal antibody reduced lymphocyte adhesion by approximately 29%, while anti-ICAM-1 produced a reduction of 26%. These results thus suggest that both LFA-3 and ICAM-1 are likely to mediate cell-cell interactions within lesional tissues in vivo. Moreover, these findings are also the first to directly demonstrate that LFA-3-mediated adhesion, like that of ICAM-1, is functionally important in the molecular pathology of inflammatory mucosal disease.

Atrocities exposure in Vietnam combat veterans with chronic posttraumatic stress disorder: relationship to combat exposure, symptom severity, guilt, and interpersonal violence.

Vietnam combat veterans (N = 151) with chronic posttraumatic stress disorder (PTSD) completed measures of atrocities exposure, combat exposure, PTSD symptom severity, guilt and interpersonal violence. PTSD symptom severity, guilt and interpersonal violence rates were similar to previously reported studies that examined treatment seeking combat veterans with PTSD. Controlling for combat exposure, endorsement of atrocities exposure was related to PTSD symptom severity, PTSD B (reexperiencing) symptoms, Global Guilt, Guilt Cognitions, and cognitive subscales of Hindsight-Bias/Responsibility and Wrongdoing. These results are discussed in the context of previous research conducted regarding atrocities exposure and PTSD.

Health status, somatization, and severity of posttraumatic stress disorder in Vietnam combat veterans with posttraumatic stress disorder.

OBJECTIVE: A two-part study was conducted to examine the health status of Vietnam veterans with posttraumatic stress disorder (PTSD). In part 1, veterans with and without PTSD were compared on health behaviors and on self-reported and physician-rated health problems. Consistency of self-report with physician rating for health problems across the two groups was compared. In part 2, the association between health status and PTSD symptom severity, depression, somatization, and health behaviors in PTSD patients was evaluated. METHOD: In part 1, 276 combat veterans (225 with PTSD and 51 without PTSD) provided health status information, and medical records were reviewed. In part 2, 225 PTSD patients completed standardized PTSD severity, somatization, and depression measures. RESULTS: When analyses controlled for age, socioeconomic status, minority status, combat exposure, alcohol use, and pack-year history, veterans with PTSD reported and were rated as having a greater number of health problems than veterans without PTSD. Agreement between self-report and physician ratings for both groups ranged from low to moderate. Level of agreement between patient and physician was similar across groups. In the analysis of veterans with PTSD, somatization and PTSD symptom severity were significantly related to self-report of health problems, whereas only PTSD symptom severity was related to physician-rated health. Pack-year history was significantly related to self-reported health status in both groups. CONCLUSIONS: The presence and severity of PTSD in veterans were associated with greater physical health problems and conditions. Psychological variables (e.g., PTSD status, PTSD severity, somatization) and a behavioral variable (pack-year history) were related to health status.

Immunohistochemical and serological comparison of idiopathic and hepatitis C virus-associated forms of oral lichen planus.

The oral form of the inflammatory disease lichen planus occurs spontaneously due to unknown aetiological factors. However, it has recently been observed to occur with increased frequency in patients infected with the hepatitis C virus. Because of the prominent role of adhesion molecules in immune cell interactions, we have compared the expression of these antigens in the hepatitis C virus-associated and idiopathic forms of the disease. The results show similar patterns of expression of very late activation antigen-4, lymphocyte function-associated antigen-3 and intercellular adhesion molecule-1, but relatively elevated levels of these antigens in oral lichen planus patients with no hepatitis C virus infection. In addition to differences in Langerhans cell distribution, serum levels of "soluble" intercellular adhesion molecule-1 as well as immunoglobulin G were significantly increased in the hepatitis C virus-associated group. These findings show that there are some differences in the lesional and systemic immune reactivities of the two types of oral lichen planus which may be related to possibly distinct pathogenic mechanisms.

Interpersonal violence and its correlates in Vietnam veterans with chronic posttraumatic stress disorder.

Two studies were conducted to investigate interpersonal violence in Vietnam veterans with posttraumatic stress disorder (PTSD). In study one, combat veterans with PTSD reported significantly greater occurrence of violent behaviors over the past year (22 acts) versus combat veterans without PTSD (.2 acts). Combat exposure had an independent positive association with interpersonal violence. In study two, variables related to current interpersonal violent behavior in 118 PTSD combat veterans were evaluated. In rank order of importance, lower socioeconomic status, increased aggressive responding and increased PTSD severity were related to interpersonal violence. These results suggest that combat veterans with PTSD exhibit greater interpersonal violence than combat veterans without PTSD, and that there are multiple factors in this population which determine violent behavior.