Vasoactive intestinal peptide receptor regulation of cAMP accumulation and glycogen hydrolysis in the human Ewing's sarcoma cell line WE-68.

This study describes functional characteristics of receptors for vasoactive intestinal peptide (VIP) on human Ewing's sarcoma WE-68 cells. These characteristics include 125I-VIP binding capacity, cellular cAMP generation, glycogen hydrolysis, and pharmacological specificity. Binding studies with 125I-VIP showed specific, saturable, binding sites for VIP in WE-68 cells. Scatchard analysis revealed the presence of a single class of high-affinity binding sites that exhibited a dissociation constant (Kd) of 90 pM and a maximal binding capacity (Bmax) of 24 fmol/mg of protein. VIP and VIP-related peptides competed for 125I-VIP binding in the following order of potency: human (h) VIP greater than human peptide with N-terminal histidine and C-terminal methionine (PHM) greater than chicken secretin much greater than porcine secretin. Glucagon and the C-terminal fragments VIP[10-28] and VIP[16-28] and the VIP analogue (D-Phe2)VIP did not inhibit 125I-VIP binding. Addition of hVIP to WE-68 cells provoked marked stimulation of cAMP accumulation, hVIP stimulated increases in cAMP content were rapid, concentration-dependent, and potentiated by 3-isobutyl-l-methylxanthine (IBMX). Half-maximal stimulation (EC50) occurred at 150 nM hVIP. The ability of hVIP and analogues to stimulate cAMP generation paralleled their potencies in displacing 125I-VIP binding. (D-Phe2)VIP, VIP[10-28], VIP[16-28], and (p-Cl-D-Phe6, Leu17)VIP, a putative VIP receptor antagonist, affected neither basal cAMP levels nor hVIP-induced cAMP accumulation. WE-68 cell responses to hVIP were desensitized by prior exposure to hVIP. Desensitization to hVIP did not modify the cAMP response to beta-adrenergic stimulation, and beta-adrenergic agonist desensitization did not modify responses to hVIP. hVIP also induced a time- and concentration-dependent hydrolysis of 3H-glycogen newly formed from 3H-glucose in WE-68 cultures. hVIP maximally decreased 3H-glycogen content by 36% with an EC50 value of about 8 nM. The order of potency of structurally related peptides of hVIP for stimulation of glycogenolysis correlated with their order of potency for inhibition of 125I-VIP binding. IBMX potentiated the glycogenolytic action of hVIP and PHM. The simultaneous presence of the calcium channel antagonist verapamil or the calcium ionophore A 23187 did not influence the glycogenolytic and cAMP stimulatory effects of hVIP. Collectively, these data indicate that Ewing's sarcoma (WE-68) cells are endowed with genuine VIP receptors which are coupled to the formation of cAMP that probably serves a second messenger role in stimulating glycogen hydrolysis in these cells in response to VIP.(ABSTRACT TRUNCATED AT 400 WORDS)

Estrone and estradiol in patients with cirrhosis of the liver: effects of ACTH and dexamethasone.

To study the influence of the adrenal gland on plasma estrogen levels in male patients with hepatic cirrhosis, estrone and estradiol were measured under a variety of experimental conditions. Compared to controls, estradiol levels were moderately elevated by 26% (P is less than 0.05) in patients with hepatic cirrhosis (28.5 +/- 5.4 vs. 36.0 +/- 4.7 pg/ml plasma; n: 12), whereas estrone levels exhibited a two- to threefold increase under basal conditions (32.5 +/- 5.6 vs. 67.8 +/- 20.8 pg/ml; P is less than 0.01). ACTH application resulted in a striking increase in plasma estrone levels in both patients with hepatic cirrhosis and in normal subjects (61.8 +/- 27.5 vs. 27.3 +/- 7.8 pg/ml). During stimulation with ACTH, estradiol levels showed no significant changes. After suppression of the adrenal gland by dexamethasone administered for 5 days, plasma concentrations of estrone and estradiol were found to be reduced. The absolute decrease of estrone was significantly greater in patients with hepatic cirrhosis than in healthy male subjects (35.5 +/- 12.6 vs. 21.3 +/- 6.0 pg/ml; P is less than 0.05; n: 8). Estrogen values, however, were still high in patients with hepatic cirrhosis after 5 days of dexamethasone administration (37.1 +/- 17.6 pg estrone/ml and 23.9 +/- 3.6 pg estradiol/ml plasma). It is suggested that elevated plasma values of estrogens in this disorder may be derived predominantly from adrenal production. Peripheral conversion of androgens to estrone rather than to estradiol appears to be more effective in sustaining plasma levels of estrogens in patients with hepatic cirrhosis.

The defect of intestinal calcium transport in hyperthyroidism and its response to therapy.

Skeletal demineralization occurs in thyrotoxicosis. Fecal calcium excretion may be enhanced, and calcium balance tends to be negative. We investigated intestinal calcium transport in 12 hyperthyroid patients. Absorption was measured by segmental perfusion in the proximal jejunum at calcium concentrations commensurate with those in the fasting and postprandial states. At low luminal concentrations, under conditions where calcium is transported predominantly by active processes, the calcium absorption rate was reduced though not abolished in hyperthyroid patients (16 +/- 4 (SE) mumol/h . 30 cm segment) as compared to normal subjects (71 +/- 8 mumol/h; P less than 0.001). When perfusate calcium was raised to 5 mmol/liter there was little increment of the net absorption rate in the hyperthyroid group (45 +/- 11 mumol/h), whereas that in the normal subjects rose to 183 +/- 17 mumol/h. Likewise, the unidirectional calcium flux out of the lumen was low in hyperthyroidism (43 +/- 7 mumol/h), suggesting that low net absorption rates were not due to transmucosal calcium loss. D-Xylose permeation was similar in all study groups. Treatment of the thyroid disease led to a marked increase in calcium absorption rates from 33 +/- 10 to 124 +/- 20 mumol/h (at 2 mmol/liter P less than 0.001; n = 5) into the range of values in normal subjects (124 +/- 9 mumol/h). Circulating levels of 1,25-dihydroxyvitamin D were low in hyperthyroid patients (38 +/- 11 pg/ml) and increased during treatment to 63 +/- 11 pg/ml (P less than 0.025; n = 9), whereas 25-hydroxyvitamin D was normal and remained unchanged. We conclude that intestinal calcium transport, particularly its active component, is reversibly decreased in hyperthyroidism. The association with low plasma levels of the active vitamin D metabolite suggests that the decrease in calcium absorption may be related to calcium-regulating mechanisms as a consequence of the net calcium efflux from bone in this disease.

Multiple pre- and postreceptor defects in pseudohypoparathyroidism (a multicenter study with twenty four patients).

Three different pathophysiological mechanisms are probably responsible for hereditary pseudohypoparathyroidism: 1) a defect at the prereceptor-level, 2) a defective membrane N-protein accounting for diminished second messenger production, and 3) a defect in the cytosolic response to the hormone. In a cooperative, study 24 patients (mean age, 13 yr; range, 3-23 yr, 8 girls, 16 boys) receiving vitamin D metabolites (5,000-80,000 U/day) were examined and compared to a control group of 36 normal children. Immunoreactive N-terminal PTH (N-PTH), mid-C-regional PTH (mid-C-PTH), intact PTH and bio-PTH, vitamin D metabolites, and serum calcium and phosphate, alkaline phosphatase activity, and the N-protein activity of erythrocyte membranes were measured in each subject. By clinical and biochemical criteria three groups were differentiated. Eight patients had the completely expressed features of Albright's Hereditary Osteodystrophy (AHO+), including brachydactyly and/or sc calcifications, and increased N-PTH, mid-C-PTH, and alkaline phosphatase activity. Bio-PTH, intact PTH, and N-protein were normal. Nine additional patients with complete (AHO+) had elevated levels of bio-PTH, N-PTH, and mid-C PTH, normal hydroxylation of vitamin D, but decreased N-protein activity. Seven patients with pseudohypoparathyroidism had no features of AHO (AHO-), no increase of urinary cAMP excretion after exogenous PTH, normal PTH peptide levels and N-protein activity, but elevated 25-hydroxyvitamin D and decreased 1,25-dihydroxyvitamin D concentrations. In conclusion, we identified three subpopulations of PsHP: group a had a dissociation of N-PTH and bio-PTH suggesting a defective N-PTH causing renal resistance, whereas their bones respond to PTH. Group b had defective N-protein causing generalized PTH resistance. Group c was characterized by high 25-hydroxyvitamin D and relatively low 1,25-dihydroxyvitamin D levels, thus providing evidence for a defect in the cytosolic interaction of the two different second messengers for PTH, cAMP, and calcium.

Functional characteristics of calcitonin gene-related peptide receptors in human Ewing's sarcoma WE-68 cells.

Calcitonin gene-related peptide (CGRP) receptor activity was studied in WE-68 human Ewing's sarcoma cells. 125I-human CGRP bound in a time-dependent, reversible and saturable manner. Scatchard plots were compatible with the presence of a homogenous population of CGRP receptors with high affinity (Kd = 15 pM, and Bmax = 1.9 fmol/mg protein). The potency order of unlabeled peptides in the presence of radioligand, was: human CGRP-II greater than human CGRP = chick CGRP greater than rat CGRP = rat [Tyr0]CGRP greater than human [Tyr0] CGRP much greater than salmon calcitonin (CT) greater than rat [Tyr0]CGRP-(28-37). Each peptide except CT and [Tyr0]CGRP-(28-37) stimulated cyclic AMP generation in a concentration-dependent manner, and the relative potencies paralleled their relative ability in inhibiting 125I-human CGRP binding. We conclude that WE-68 Ewing's sarcoma cells express genuine CGRP receptors which upon activation lead to stimulation of cyclic AMP formation

Neuropeptide Y inhibits vasoactive intestinal peptide- and dopamine-induced cyclic AMP formation in human Ewing's sarcoma WE-68 cells.

Neuropeptide Y (NPY) regulation of intracellular cyclic AMP accumulation was studied in human Ewing's sarcoma cell line, WE-68. NPY inhibited vasoactive intestinal peptide (VIP)- and dopamine-stimulated but not basal cyclic AMP formation. The peptide effect was rapid (less than 2 min), concentration-dependent with a half-maximal effective concentration (EC50) of 8 nM NPY, and maximal inhibition reaching 60-70% with 100 nM NPY. Prior exposure of WE-68 cells to pertussis toxin completely abolished the inhibitory action of NPY. It is concluded that NPY attenuates agonist-stimulated cyclic AMP formation in Ewing's sarcoma WE-68 cells, and may do so via the inhibitory guanine nucleotide regulatory protein of adenylate cyclase.

Forskolin inhibition of glucose transport in bone cell cultures through a cAMP-independent mechanism.

Studies are presented demonstrating inhibition of glucose transport by forskolin in human MG-63 osteosarcoma cells as well as osteoblast-like cells derived from normal human trabecular bone and chick calvaria. The cAMP-stimulators parathyroid hormone, prostaglandin E2, and isoproterenol did not influence glucose transport. Benzyl alcohol, a membrane lipid fluidity modulator, also provoked inhibition of the glucose uptake rate. Effects of forskolin and benzyl alcohol were not additive. It is suggested that cAMP is not a mediator of glucose transport in bone cells, and that forskolin inhibits glucose transport via a cAMP-independent mechanism.

Induction of glycogenolysis in cultured Ewing's sarcoma cells by dopamine and beta-adrenergic agonists.

This study describes hormonal regulation of glycogen metabolism in Ewing's sarcoma cells. 3H-Glycogen synthesized in cultured Ewing's sarcoma WE-68 cells from 3H-glucose was hydrolyzed in a concentration-dependent manner by various catecholamines. The order of potency for the glycogenolytic effects of catecholamines was isoproterenol greater than or equal to dopamine greater than norepinephrine greater than epinephrine. The concentrations giving half-maximal effectiveness (EC50) were about 2 x 10(-8) M, 3 x 10(-8) M, 8 x 10(-8) M, and 5 x 10(-7) M for isoproterenol, dopamine, norepinephrine, and epinephrine, respectively. Higher concentrations of each of the catecholamines were necessary to elicit EC50 stimulation of cyclic AMP production in Ewing's sarcoma cells. Glycogenolysis induced by dopamine was blocked by chlorpromazine, a dopamine D1-receptor antagonist, but not by haloperidol, a dopamine D2-receptor antagonist. The glycogenolytic action of norepinephrine was markedly reduced by propranolol, a beta-adrenoreceptor antagonist, and was not affected by yohimbine, an alpha-adrenoreceptor antagonist. In addition, chlorpromazine also antagonized the glycogenolytic response to norepinephrine. Dibutyryl cyclic AMP, 3-isobutyl-1-methylxanthine, and the diterpene forskolin were also found to induce 3H-glycogen hydrolysis. Our data indicate that catecholamines exert their glycogenolytic effects in Ewing's sarcoma cells by stimulation of cyclic AMP formation via beta-adrenergic receptors and dopamine D1-receptors.

cAMP-synthesis in a medullary thyroid carcinoma cell line: response to adrenergic agents and prostaglandines.

Calcitonin secretion by C-cells is mediated through intracellular 3'5'-cyclic adenosine monophosphate (cAMP) and calcium signaling. Calcitonin release stimulation tests may take advantage of both signaling cascades in screening for medullary thyroid carcinomas (MTC). To elucidate the regulation of the adenylyl cyclase system we have determined cAMP levels of a calcitonin-expressing MTC cell line (RG) after exposure to adrenergic agents and prostaglandines. In early passages (20-30) cAMP concentrations were significantly elevated in RG cells after exposure to beta-adrenergic agents and prostaglandines E1 and E2. In advanced passages (60-80) the beta-adrenergic response was no longer detectable and adrenergic receptors were uncoupled from the adenylyl cyclase complex; while the effect of prostaglandines E1 and E2 remained unaffected. Preincubation with dexamethasone, in a process requiring protein new synthesis, re-established the adrenergic response in later passages, indicating that RG cells dedifferentiated in culture over time. Our in vitro findings suggest that MTC cell dedifferentiation may be accompanied by adrenergic receptor-uncoupling from the adenylate cyclase system and that this process may be reversed by dexamethasone incubation.

Up to 9 years of follow-up after anatomic correction of simple transposition of the great arteries.

For a continued assessment of the two-stage anatomic correction, we have evaluated the postoperative results in terms of clinical status, ECG, ventricular function, aortic root size and stiffness for up to 9 years in all 18 survivors. Weight and height were normal, the ECG was normal except for complete (n = 3) and incomplete (n = 11) right bundle branch block and supraventricular tachyarrhythmias post Blalock-Hanlon septectomy (n = 1) and p-wave abnormalities (n = 6). The pressures and ejection fraction of the left and right ventricles were within normal limits. The end-diastolic and endsystolic left ventricular volume and the muscle volume index were elevated. Six of 17 patients were outside the normal range of the left ventricular ejection fraction-endsystolic stress relationship. The diameter of the aortic root was larger than normal in all patients. There was a relation between the size of the patients at banding and the stiffness of the aortic root after anatomic correction. Patients with simple transposition of the great arteries up to 9 years after anatomic correction develop normally without atrio-ventricular conduction delay, arrhythmias or signs of coronary and myocardial insufficiency. The stiff and enlarged aortic roots do not seem to dilate. The reasons for the elevated left ventricular volumes and muscle volume indices are not clear at present. Primary anatomic correction may prevent these abnormalities.

[Chronic occlusion of a renal artery with aneurysms in the para-aortic collateral circulation and multiple aneurysms in both kidneys (author's transl)]. / Chronisch-zentraler Nierenarterienverschluss mit Aneurysmen in der paraaortalen Kollateralarterie und multiplen Aneurysmen beider Nieren.

Chronic occlusion of the main renal artery may be followed by the development of a collateral circulation through ureteric and para-aortic arteries, and through lumbar and suprarenal arteries. A patient with occlusion of the left main renal artery is described, who developed a collateral circulation between the common iliac artery and the distal portion of the renal artery. The para-aortic collateral vessel developed one large and several small aneurysms, and there were aneurysms in both kidneys.

Undifferentiated arthritis and spondylarthropathy as a challenge for prospective follow-up.

Diagnosis of arthritis with recent onset is still an unresolved problem. In 1984 we started an outpatient clinic for patients with early arthritis of less than one year duration. Of a total of 226 patients seen 149 (66%) had definite (n = 76; 34%) or probable (n = 73; 32%) inflammatory rheumatic disease, and 77 (34%) had degenerative or extraarticular rheumatic disease. Thirtynine patients were classified as undifferentiated arthritis. This undefined arthritis was often monoarticular (12%) and oligoarticuler (44%). One patient met 5 ARA-criteria for rheumatoid arthritis, 14 (36%) met 3-4 ARA-criteria and 25 (64%) only 1-2 ARA-criteria. ESR was elevated in only 23 (59%) patients, rheumatoid factor was positive in 7 (19%) patients and HLA-B27 was positive in 9 (23%) patients. Seventeen (44%) patients had a history of recent infections preceding the beginning of joint symptoms. Thus undifferentiated arthritis represents a heterogeneous group of diseases. Despite diagnostic progresses in recent years a high proportion of early arthritis cannot be diagnosed definitely.

Evaluation of left ventricular contractile performance from baseline stress-shortening data in humans: comparison with pharmacological afterload challenge.

The purpose of this study was to evaluate whether the baseline stress-shortening data reflect the contractile state adequately and give results comparable to the evaluation of the end-systolic stress-shortening relationships using pharmacological manipulation of afterload. Five groups were studied (total 152 patients): a control group of 30 healthy volunteers, 32 patients after surgical correction of infantile tetralogy of Fallot, 50 patients treated for childhood malignancies with doxorubicin, 17 patients with left ventricular hypertrophy due to systemic hypertension, and 23 patients with congestive cardiomyopathy. In all patients except those with congestive cardiomyopathy, afterload was altered pharmacologically to evaluate the individual stress-shortening relationship. In all patients the baseline stress-shortening data were evaluated, as well as their relative positions to two predefined normal ranges for the relationship between end-systolic stress and shortening. Additionally, a slope value was calculated from the baseline data of the five groups studied and compared with the data obtained by pharmacological afterload increment. Our data show that the comparison of individual baseline data of end-systolic wall stress and fractional shortening with predefined normal ranges for the relationship between end-systolic stress and shortening is inadequate. The appropriate normal range to compare with is the 95% confidence interval of baseline stress-shortening data in normal subjects. Also the calculation of a slope value from the baseline stress-shortening data of a group of patients seems to be inappropriate.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic findings during exercise on a bicycle ergometer following balloon valvuloplasty of pulmonary stenosis in children and adolescents.

Eleven patients (4 female, 7 male), age range 3.3 to 24.8 years (mean 11.10 years) treated for isolated pulmonary stenosis underwent cardiac catheterization and percutaneous transluminal balloon valvuloplasty (PTVP). The right ventricular systolic pressure (RVSP) before valvuloplasty ranged from 31 to 127 mmHg (mean 79 mmHg) decreasing to 28 to 62 mmHg (mean 42 mmHg) immediately after the dilatation. The peak systolic gradient of the pulmonary valve (delta p RV-PA) before valvuloplasty ranged from 22 to 107 mmHg (mean 61 mmHg) and decreased to a range of 14 and 45 mmHg (mean 23 mmHg) immediately after the dilatation. Balloon valvuloplasty was performed using balloons of 13 to 31 mm in diameter. On 11 patients cardiac catheterization and Doppler echocardiography were repeated between 11 months and 5.3 years (mean 3.11 years) after the balloon valvuloplasty showed a further significant fall in the gradient of pressure. The right ventricular systolic pressure ranged from 20 to 51 mmHg (mean 31.7 mmHg) while the transpulmonary gradient varied from 3 to 24 mmHg (mean 11.6 mmHg). At the time of follow-up examination the patients were aged between 7.2 and 25.7 years (mean 15.9 years). On average the second catheterization was performed 3.11 years following the first hemodynamic study. The follow-up examination encompassed clinical examination, electrocardiogram, Doppler echocardiography, and right heart cardiac catheterization. During right heart cardiac catheterization the children exercised on a bicycle ergometer for three min at 50 or 100 W depending on their body surface area. During this exertion, pressures of the right ventricle and the pulmonary artery as well as heart rate and oxygen saturation were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Improved neurological outcome following early anatomical correction of transposition of the great arteries.

The incidence of neurological residuals following anatomical correction of transposition of the great arteries (d-TGA) has not been described so far. Clinical examination, EEG recordings, and computed tomography (CT) scans were carried out in a consecutive series of 38 children with d-TGA surviving anatomic corrective surgery. The patients were classified into one of three groups according to the type of operation: 15 patients after two-stage approach (TSA) (Stage 1: pulmonary artery banding+aortopulmonary shunt; Stage 2: anatomic correction); 12 patients with primary anatomic correction within the first 2 weeks of life (early switch, ES); 11 patients with primary anatomic correction later in infancy (later switch, LS). In 26 patients (68%) we found no abnormalities on neurologic examination, CT scan, or EEG. Four patients suffered from spastic hemiplegia, 3 of these had cortical brain damage visible on CT scan, and 3 had focal epilepsy as well. In 2 otherwise clinical normal patients cortical infarction could be seen on a CT scan. Thus, in 5 cases (13% of 38 patients) cerebral infarcts were diagnosed by CT scan. The cortical vascular infarction was seen in 4 patients after TSA and in 1 after LS. In 6 patients we found other neurological abnormalities. Early anatomic correction in patients with d-TGA reduces the risk of cortical vascular infarction.

Pitfalls in the diagnosis of tricuspid atresia: report of a new angiocardiographic sign.

Two patients with the classical clinical, angiographic, and echocardiographic signs of tricuspid atresia are reported, where the correct diagnoses were made at operation; one child had cor triatriatum dexter, the other child total anomalous systemic venous drainage to the left atrium. The literature on cor triatriatum dexter and total anomalous systemic venous drainage is discussed and a new angiographic sign for the differentiation from tricuspid atresia is reported: nonopacification of the right atrial appendage with right atrial angiocardiography.

Assessment of vitamin B2 status in performance athletes of various types of sports.

To determine the vitamin B2 supply, 62 athletes in various types of sports and 16 non-athletes were examined, using a weighed food record (7-day), alpha-EGR determination, microbiological blood, and HPLC urinary measurements. If the guidelines of 1.5 or 1.7 mg/day vitamin B2 or 0.6 mg/4,184 kJ (GRDA) are defined for adequate status, all sports groups (M +/- SEM) are above this level. The vitamin B2 blood concentrations show a range (mean) from 303-372 nmol/liter, which indicates that more than 90% of the athletes are above the reference value of 327 nmol/liter (mean). There is a correlation of r = 0.49 between the vitamin B2 intake (mean over 7 days) and the vitamin B2 blood level. Determination of vitamin B2 blood concentration is characterized by good precision (C.V. +/- 3.2%) and recovery (95.7%). The enzyme activation measurement (alpha-EGR) shows that all of the athletes are below the alpha-EGR reference value of < 1.50 (good supply). No significant correlations could be determined between alpha-EGR and vitamin B2 intake, blood concentrations, and urinary excretion. The measurement also shows high precision (C.V. 1.7%). The Vitamin B2 excretion in urine (mumol/g Cr.) was higher than the reference values for non-athletes in more than 90% of the athletes. There is a correlation of r = 0.89 between the vitamin B2 intake on the last day (Day 7) of the food record and the riboflavin excretion, and between vitamin B2 in blood and urinary excretion of r = 0.52. The C.V. of vitamin B2 urinary measurement using HPLC is 2.5%, with recovery of 98.2%. Combined measurement of vitamin B2 intake, blood concentration, and urine excretion appears to be a suitable procedure for determining the vitamin B2 status. Most of the performance athletes were sufficiently supplied with vitamin B2, compared to the reference values for non-athletes.

Clinical chemical methods for the routine assessment of the vitamin status in human populations. Part III: The apoenzyme stimulation tests for vitamin B1, B2 and B6 adapted to the Cobas-Bio analyzer.

The programming of the Cobas-Bio centrifugal analyzer for kinetic tests of transketolase, glutathione reductase and aspartate amino-transferase is described. The results obtained in a population of 200 healthy people of both sexes are reported.

[Differences in the psychological status of hysterectomy and non-hysterectomy women]. / Unterschiede in der psychischen Befindlichkeit zwischen hysterektomierten und nicht-hysterektomierten Frauen.

PURPOSE OF THE STUDY: Despite numerous investigations on the well-being of hysterectomized women, this issue is still discussed controversially. The aim of the present study was to reveal differences between a group of hysterectomized women with a fairly long follow-up period (7.9 years) and a group of non-hysterectomized women with respect to their psychological well-being. RESEARCH METHOD AND MATERIAL: In a questionnaire study we compared a group of 216 women who underwent hysterectomy with a group of 90 non-hysterectomized women. Dependent variables were: body complaints, psychological well-being, dysphoria, socio-sexual assertiveness, and gender-role orientation. RESULTS AND CONCLUSIONS: The group of hysterectomized women showed significantly higher levels of body complaints, depression, and unassertiveness in sexual situations, as well as decreased psychological well-being, and a more traditional gender-role orientation. Within the group of hysterectomized women, duration since hysterectomy, surgical techniques, and hormone substitution therapy seem to be unrelated to the psychological variables. The group differences cannot be causally attributed to the hysterectomy, since they may already have existed premorbidly. Nevertheless, the results suggest that a more thorough psychological examination prior to hysterectomy, as well as provision of support for the coping process after intervention is advantageous.