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Summary We determined the concentrations of immunoreactive epidermal growth factor in the urine (U-irEGF) of 97 adult patients with various malignancies, including carcinomas of the urinary bladder, kidney, stomach, colon, rectum, breast, endometrium, uterine cervix, ovary, vagina, prostate, pancreas and thyroid, liposarcoma and skin melanoma. The relative U-irEGF concentrations (ng m-1 creatinine) were higher (P=0.002) for the whole series of female patients than for healthy controls matched for sex and age. Such difference did not appear for male patients. The only specific group with a statistically supranormal U-irEGF concentration (P=0.0005) comprised women with endometrial carcinoma of the uterus.Epidermal growth factor (EGF) appears to be involved in the regulation of proliferation, differentiation and differentiated functions of a multitude of cell types (Gospodarowicz, 1981;Carpenter & Zendegui, 1986). In certain normal cells in vitro EGF elicits transformation-associated responses (Stoscheck et al., 1986). There is also a considerable body of evidence associating EGF receptor with oncogenesis. The EGF receptor is the product of the c-erbB proto-oncogene, which is closely related to the v-erb B (Downward et al., 1984). The receptor is present in enormous numbers on the cells of many human epidermoid and glial malignancies (Lin et al., 1984;Merlino et al., 1984;Libermann et al., 1984). Many malignant cells produce another EGF receptor agonist, transforming growth factor alpha (TGF-a) Roberts et al., 1980). TGF-cx is excreted in urine by patients with various malignancies (Sherwin et al., 1983), but not by healthy subjects (Twardzik et al., 1985). Uchihashi et al. (1983) and Kurobe et al. (1985) found urinary excretion of EGF to be higher in patients with cancer than in healthy persons. This has not been generally accepted. We have now measured urinary immunoreactive EGF (U-irEGF) levels in patients with a variety of malignancies before and after tumour removal. Materials and methodsSubjects and samples Spot urine samples were collected from 97 patients (49 men and 48 women, aged 28-88 years) with various malignancies before surgical removal (or any other treatment) of the tumour. In addition to those shown in Figure 1, six patients had carcinomas, I of the vagina, 2 of the pancreas, and 3 of the thyroid, and 1 patient had liposarcoma and 1 skin melanoma. The malignancies included both metastasized and in situ tumours. We also measured U-irEGF concentration in 24 patients daily during the first week after removal of the tumour, and in a further 7 patients on the sixth postoperative day. For comparison, urine samples were collected from age-and sex-matched healthy subjects (56 men and 62 women, aged 28-86 years).Assay procedures Human EGF, used both as standard and labelled tracer, and a rabbit antiserum against it (8C-217,3129) were donated by AMGen (Thousand Oaks, California). U-irEGF was measured by a specific homologous radioimmunoassay (Mattila et al., 1985) and creatinine by the kinetic method of Ja...

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Summary The placental and fetal response to the intra‐amniotic injection of prostaglandin F2α (PGF2α) for midtrimester abortions was evaluated. Maternal blood samples for radioimmunological determinations of serum progesterone, human placental lactogen (HPL) and alpha‐fetoprotein (AFP) were taken before and serially until 24 hours after the injection of 40 mg (nine patients) or 75 mg (seven patients) of PGF2α. Fetal heart action was monitored ultrasonically during the same period. The average induction‐abortion interval was 22.6 hours and was independent of the dose of PGF2α used. The mean progesterone and HPL levels showed a significant fall half an hour after PGF2α. The constant decreases began only at 5 hours and later. The mean AFP levels increased rapidly after 5 hours following injection of PGF2α. The fetal heart stopped at a mean of 10.4 hours (range 0.5 to 25 hours) after the injection of PGF2α. No relationship between the time of fetal death or rises in AFP and the induction‐abortion interval could be detected. The primary hormonal response of the placenta and the efficacy of exogenous PGF2α were not related, indicating the possibility that the abortifacient property of PGF2α is not related to its primary effect on placental hormone synthesis or release.

The plasma concentration of ACTH (by radioimmunoassay) was measured in 56 healthy parturients and their newborns. Umbilical cord and maternal venous blood were collected immediately after delivery. In addition one venous blood sample was taken from 50 newborns at the age of 15, 30, 60 min, 2, 6, 12, or 24 h. The maternal and cord plasma ACTH levels were higher than the levels in healthy nonpregnant women. There are no differences between the mean maternal (226 +/- 146 pg/ml) and cord (226 +/- 147 pg/ml) values of ACTH. The high ACTH levels of cord plasma remain unchanged for 30 min, decrease significantly during the 1-6 h after birth, because of the elimination process of the circulated foetal ACTH, and increase over the next 12-24 h and slightly thereafter indicating an initiation of neonatal pituitary ACTH secretion. The plasma ACTH level in the mothers with membranes ruptured for 1-5 h was significantly (P less than 0.05) higher compared with that in the mothers with membranes ruptured for less than 1 h. However, the duration of ruptured membranes appeared to have no effect on the cord blood ACTH level.

Summary Human placental lactogen (HPL) concentrations in maternal serum were measured by double antibody radioimmunoassay in 25 patients who were undergoing abortion by intra‐ and extra‐amniotic injection of prostaglandin F2α (PGF2α) and by extra‐amniotic injection of hypertonic saline in the first and second trimesters of pregnancy. The injection of 150 ml. of 20 per cent NaCl did not change the HPL level but the extra‐amniotic injection of 5 to 6 mg. of PGF2α and the intra‐amniotic injection of 20 to 25 mg. of PGF2α decreased the serum HPL level significantly (p<0.01) in the two hours after the injections. PGF2α administered by intrauterine routes appeared to have a direct effect on the placental synthesis and/or the secretion of HPL in early pregnancy.

SYNOPSIS To study the role of the proaggregatory, vasoconstrictory thromboxane A 2 (TxA 2 ) in migraine, the plasma levels of Thromboxane B 2 (TxB 2 ), the stabile metabolite of TxA 2 , were measured from 14 adults and 8 children with migraine during the attack‐free interval. In addition, the platelets' capacity to generate TxB 2 during spontaneous clotting was studied. The plasma TxB 2 concentrations were lowered in the adult migraine patients. Also the platelets' capacity to produce TxB 2 was reduced in migraine children and in adults with classic migraine. The decreased platelet TxA 2 synthesis in the attack‐free period of migraine patients may reflect a deficient pool of platelet arachidonic acid, the precursor of TxA 2 , perhaps as a result of increased consumption during migraine attacks.