SYNOPSIS Placentae were examined from 120 women whose pregnancy and delivery was normal, from 264 women whose pregnancy or delivery was complicated, and from 98 women who were Rh-negative without antibodies and 35 women Rh-negative with antibodies. The presence of Kline's haemorrhages, intervillous thrombi, infarcts, and retroplacental haemorrhages was positively correlated with the presence of foetal cells in the maternal circulation. When there were no maternal antibodies transplacental haemorrhages occurred occasionally in the absence of such placental lesions but more frequently when these lesions were present. Moreover, the greater the number of lesions in a placenta the greater the size of the transplacental haemorrhage. In Rh-negative women with antibodies the observed incidence of transplacental haemorrhage was significantly less despite an appreciable increase in placental lesions.There is no direct anatomical communication between the maternal and foetal blood vessels in the placenta. Nevertheless, the not infrequent occurrence of transplacental foeto-maternal haemorrhage indicates that such communication must take place from time to time. The nature and mechanism of this leak is not understood. The object of the present investigation was to determine what relation, if any,

Increasing evidence suggests that a new birnavirus, named chicken proventricular necrosis virus (CPNV), is the aetiological agent of transmissible viral proventriculitis (TVP). The present work aimed to explore the possible presence of both TVP and CPNV in the UK. Forty-four chickens showing TVP-compatible gross lesions were classified into three groups based on the histological lesions: (i) TVP-affected chickens: lymphocytic infiltration and glandular necrosis (n = 15); (ii) lymphocytic proventriculitis (LP)-affected chickens: lymphocytic infiltration without necrosis (n = 18); and (iii) without proventriculitis (WP): no lymphocytic infiltration or necrosis (n = 11). Nine proventriculi (seven out of 15 corresponding to TVP, and two out of 11 corresponding to LP) were positive for CPNV by reverse transcriptase polymerase chain reaction (RT-PCR). These results support the previously suggested idea of CPNV as causative agent of TVP. Moreover, these data show that CPNV can also be detected in a number of cases with LP, which do not fulfil the histological TVP criteria. Phylogenetic analysis of partial sequences of gene VP1 showed that British CPNV sequences were closer to other European CPNV sequences and might constitute a different lineage from the American CPNV. TVP cases with negative CPNV PCR results may be due to chronic stages of the disease or to the reduced PCR sensitivity on formalin-fixed paraffin-embedded tissues. However, involvement of other agents in some of the cases cannot totally be ruled out. As far as the authors are aware, this is the first peer-reviewed report of TVP as well as of CPNV in the UK, and the first exploratory CPNV phylogenetic study.

No abstract

No abstract

Summary Haematological values in cord venous blood were studied in 458 newborn infants born at term. The severity of hypoxia in these babies was determined by measuring the pH in cord venous blood, and in cord arterial blood. Hypoxia was associated with increases in haemoglobin, in the red cell count, in the white cell count and in the haematocrit. Furthermore, the increase in the mean corpuscular volume, and decrease in mean corpuscular haemoglobin concentration could have been due to a net influx of less mature red cells into the circulation. It is suggested that fetal erythropoiesis is stimulated by intrapartum hypoxia.