There is considerable and ongoing debate surrounding the teaching of anatomy to medical students, and the anatomical knowledge of those medical students once they graduate. Few attempts have been made to gather the opinions of clinicians on this subject. A questionnaire was sent to 362 senior clinicians in hospitals affiliated to the University of Aberdeen. A total of 162 replies were received, with this sample being representative of the population of hospital consultants. Our results indicate that the majority of clinicians feel that the current anatomical education of medical students is inadequate, and below the minimum necessary for safe medical practice. There is widespread support among clinicians for more vertical integration of anatomy teaching throughout the undergraduate curriculum.

The clear morphological differences between the granulated metrial gland (GMG) cells which develop in the uteri of rats and mice have been used to assess the origin of GMG cells in radiation chimaeras. Lethally irradiated mice were reconstituted with either rat or mouse bone marrow cells. Control mice were ovariectomised. A schedule of steroid injections was carried out allowing deciduoma formation to be induced in the irradiated and control animals. Deciduoma formation was impaired, and there were few GMG cells in the irradiated, bone marrow-reconstituted mice in comparison with the ovariectomised controls. However, it was possible to identify, by their distinctive morphology, 1) rat GMG cells in the mice reconstituted with rat bone marrow cells, and 2) mouse GMG cells in the mice reconstituted with mouse bone marrow cells. Conversely, no typical mouse or rat GMG cells were identified in mice reconstituted, respectively, with rat or mouse bone marrow cells. The observations indicate that GMG cells differentiate from a precursor derived from bone marrow.

A study has been made of the distribution of, and synthesis of DNA by, granulated metrial gland cells at implantation sites in the pregnant mouse uterus. Granulated cells were found in small numbers randomly distributed throughout the endometrium on day 4 1/2 of pregnancy. Subsequently cells of this type were lost from the antimesometrial and lateral decidua but increased dramatically in number in the developing decidua basalis. From day 7 1/2 granulated cells populated the mesometrial triangle to form the metrial gland. A high proportion of granulated cells was found to incorporate tritiated thymidine and the distribution of such cells is described. However, no granulated cells were found to incorporate tritiated thymidine at or after day 12 of pregnancy. In addition the loss of granulated metrial gland cells from the implantation site is described and is accounted for by degeneration in situ and also by migration via vascular channels. It is suggested that this latter route could be of functional significance.

Pathogens may impair reproduction in association or not with congenital infections. We have investigated the effect of acute infection with Trypanosoma cruzi, the protozoan agent of Chagas' disease in Latin America, on reproduction of mice. Although mating of infected mice occurred at a normal rate, 80% of them did not become gravid. In the few gravid infected mice, implantation numbers were as in uninfected control mice, but 28% of fetuses resorbed. Such infertility and early fetal losses were significantly associated with high maternal parasitemia. The remaining fetuses presented with reduced weights and all died later in gestation or within 48 hours after birth. Several organs of these fetuses were infiltrated by polynuclear cells and presented ischemic necrosis but did not harbor T. cruzi parasites, discarding congenital infection as the cause of mortality. However, surprisingly, the deciduas were massively invaded by T. cruzi parasites, harboring 125-fold more amastigotes than the maternal heart or other placental tissues. Parasites were significantly more numerous in the placentas of dead fetuses. In addition, placentas contained inflammatory infiltrates and displayed ischemic necrosis, fibrin deposits, and vascular thromboses. These results show that acute T. cruzi infection totally impairs reproduction in mice through inducing infertility or fetal-neonatal losses in association with placental parasite invasion and ischemic necrosis. Besides direct effects of infection on placentas and fetuses, poor pregnancy outcome might arise from disturbances in the complex biological processes tightly regulated by hormones and cytokines involved in mammal reproduction.3-5 Indeed, proinflammatory/type 1 cytokines such as tumor necrosis factor-␣ and interferon-␥, produced at high levels in response to some pathogens, have been shown to be harmful for pregnancy. 6,7 Information on the effect of infection with T. cruzi (the protozoa agent of Latin American Chagas' disease) on pregnancy is scarce though, and according to the endemic area, such infection affects 3 to 51% of pregnant women from which 2 to 10% congenitally transmit the parasite. 8,9 Some studies suggest that Chagas' disease might cause abortion or prematurity, whereas others fail to show such a relation.9 -11 Studies in experimental infection might reinforce our knowledge of maternofetal interactions in T. cruzi infection. Infertility and fetal growth retardation, associated or not with congenital infection, have been reported in chronic infection of mice. 12,13 In acute experimental infection, placental infection has been reported without congenital transmission, 14 despite the high circulating level of parasites, known to release proinflammatory molecules 15,16 and the systemic production of cytokines potentially deleterious for pregnancy. 17,18 The aim of the present work was to gain more insight into the relation between acute T. cruzi infection and gestation in mice, by studying the reproductive capacity, the pregnancy outcome, and the histopathology of...