A prospective combined study of consecutive patients with severe pregnancy anaemia (haemoglobin value less than 8 g. per 100 ml.) was performed in five countries to determine the relationship between maternal anaemia and placental weight. Data were recorded in 732 pregnancies and the important finding was that placental hypertrophy was associated with maternal anaemia in all centres. There was a positive correlation between maternal anaemia and placental weight which was statistically highly significant; Melbourne and Thailand, P = 0.01; India, P(0.025; Singapore and New Guinea, P

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Aqueous extracts of frozen human corpora lutea were tested for the presence of an inhibitor of luteinizing hormone-receptor site binding (LHRBI) and for the subsequent effect on the stimulatory response of luteinizing hormone (LH) on progesterone synthesis by sheep ovarian cells. In the presence of human corpus luteum extract of normal menstrual cycle (30,000-g supernatant), the binding of ¹²⁵I human chorionic gonadotrophin (hCG) to granulosa and luteal cells of sheep ovaries was markedly reduced, but the ability of rat testicular LH receptors to bind labelled hCG was less affected. However, extracts of corpora lutea of the first trimester of pregnancy appeared to be less inhibitory on the binding of LH/hCG to ovarian cells and had no effect on the binding of rat testicular cells compared to those of normal menstrual cycle. Addition of both extracts separately inhibited the LH-stimulated in vitro progesterone synthesis by granulosa cell cultures and by incubated sheep corpus luteum slices. These findings provide evidence for the presence of LHRBI in human corpus luteum.

Changes in the protein and steroid hormones of follicular fluid, aspirated from different follicles of sheep and human ovaries, have been measured and correlated with the size of the follicles. As the fluid contains a number of proteins, steroids have been measured directly and after ether extraction. The follicular fluid concentrations of progesterone and 17β-oestradiol measured directly in the fluid increased with the size of the follicles. The levels of free testosterone remained constant in all sizes of follicles, while those of bound hormone showed a 10- to 15-fold increase over the free testosterone concentrations in both the sheep and human follicular fluid. A decrease in the levels of bound testosterone in the fluid of large follicles (LFFL) coincided with the increase in bound 17β-oestradiol, suggesting the possible conversion of bound testosterone to oestrogen as the follicle attained maturity. The ratio of follicle-stimulating hormone (FSH) to luteinizing hormone (LH) varied in the fluid obtained from different size follicles, being 1:7 in small (SFFL), 1.3.5 in medium (MFFL) and 1:2.3 in large (LFFL) follicles of sheep ovaries. The LH content of follicular fluid of different size follicles appeared to be the same, with LFFL showing a minor increase over SFFL. In the human, the fluid from medium follicles contained very little LH compared to LFFL. These differences in the pattern of LH levels present in the fluid from different size follicles between human and sheep ovaries presumably reflect species variations in the entry of LH into the follicles.

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Summary: In a series of 31 consecutive patients with malignant trophoblastic disease there were 28 patients with choriocarcinomas and 3 with invasive moles. More than three‐quarters of the patients were less than 30 years of age. Of the patients with choriocarcinoma, 13 died in hospital, 6 died at home within 3 months, 1 survived, and 8 were lost to follow‐up.

Recent studies have shown that patients with aggressive histology non-hodgkins lymphoma (NHL) bearing translocations leading to aberrant expression of c-myc have a rapid clinical course and poor outcome, especially when accompanied by translocations involving BCL-2 such as t(14;18). We retrospectively reviewed patients with NHL in which abnormalities of the c-myc gene (rearrangement, extra copies, deletion) were found and correlated the cytogenetic abnormality with presenting characteristics and outcome. Methods: From May 2002 to June 2005, 138 samples were assessed for c-myc; 27 cases of NHL (excluding Burkitt [BL]and BL-like) with c-myc abnormalities were identified and included (25 tissue biopsies, 1 bone marrow, 1 CSF sample). Testing for c-myc abnormalities was initiated for: differential diagnosis of atypical BL or one or more of the following: high MIB-1 index (>70%) − 63%; aggressive morphological features − 81%; aggressive clinical course − 52%; suspected transformation of indolent lymphoma − 19%. Results: There were 12 males and 15 females included with an age range of 26–83 years; 67% had stage 3 or 4 disease and 38% had B-symptoms. The pathological diagnosis was follicular lymphoma (FL) in 3 cases, diffuse large B-cell lymphoma (DLBCL) in 22 cases [13 de novo, 5 transformed from FL, 4 recurrent/refractory] and 2 cases with both FL and DLBCL. FISH analysis for c-myc by the Vysis dual colour break-apart probe (8q24.1) revealed 12 cases with only extra copies (polyploidy) [group 1]; 13 with rearrangement (4 also had extra-copies) [group 2]; one with gene deletion and one with gene deletion and extra-copies. BCL-2 rearrangements were also detected in 22 cases (in group 1, 44%; group 2 69%). All patients were to receive multiagent anthracycline based chemotherapy; chemotherapy was initiated in 89% and one died before this could be given. Thus far, 41% of the patients have died and 19% are alive with refractory disease. The clinical course for group 1 after c-myc abnormality identified was as follows: refractory to chemotherapy - 6 cases, 5 in complete remission (CR), one spontaneous remission without treatment (FL). The median survival for group 1 was 5 months (range 1–21 months) and deaths occurred shortly after current diagnosis (range 1–7 months). The clinical course for group 2 was as follows: refractory to chemotherapy - 11 cases and 3 are currently in a CR. The median survival for group 2 was 9 months (follow-up 1–13 months) and again deaths occurred shortly after current diagnosis (range 1–9 months). Conclusions: Both c-myc gene rearrangement and extra copies of c-myc seem to confer poor prognosis in NHL. Not all patients with c-myc abnormalities have morphological features suggestive of Burkitt-like lymphoma, while some patients with only extra copies of c-myc did have Burkitt-like lymphoma features. Testing for c-myc abnormalities may be indicated not only in patients with aggressive histology but also in those with clinically aggressive patterns of disease, and prospective evaluation of a c-myc testing algorithm to evaluate impact on therapy is required.