Invited review: Genetic contributions underlying the development of preimplantation bovine embryos.

In recent years, it has become evident that genetic selection to improve milk production has resulted in a decline in dairy cattle fertility. Growing evidence suggests that the greatest loss occurs early in pregnancy around the time of embryo implantation. As a means to make genetic improvements and to assist in reproductive performance, use of artificial reproductive technologies such as artificial insemination and in vitro production of embryos have been widely used. Both of these technologies rely on the competence and quality of gametes for successful development of embryos. Often, selection of animals is based on the genetic merit of the animal, although specific fertility markers are relatively underdeveloped compared with markers for production traits. Similarly, current in vitro fertilization systems could benefit from a uniform method for selection of the best quality embryos to transfer into recipients for successful implantation and delivery of healthy offspring. As genetics underlie biological processes such as fertility, the need exists to further identify and characterize genes that affect fertility and development within both the parental gametes and the embryo. Furthermore, the magnitude of the contribution of each parental genome to the success of embryo development and pregnancy is not clear. As such, the objective of this review is to provide an overview of studies relating to genetic markers at the DNA level, parental and embryonic gene expression, and the effects of epigenetics on embryonic development. Future studies should exploit advances in molecular technologies to identify and classify genes underlying fertility and development to establish biomarkers and predictors for improved genetic selection.

Comparison of endocrine and cellular mechanisms regulating the corpus luteum of primates and ruminants.

The corpus luteum (CL) is a transient endocrine organ that is essential for maintenance of pregnancy in both ruminants and primates. The cellular and endocrine mechanisms that regulate the CL in these species have commonalities and some distinct and intriguing differences. Both species have similar cellular content with large luteal cells derived from the granulosa cells of the follicle, small luteal cells from follicular thecal cells, and large numbers of capillary endothelial cells that form the vasculature that has an essential role in optimal CL function. Intriguingly, the large luteal cells in ruminants grow larger than in primates and acquire a capacity for high constitutive progesterone (P4) production that is independent of stimulation from LH. In contrast, the primate CL and the granulosa lutein cells from primates continue to require stimulation by LH/CG throughout the luteal phase. Although the preovulatory follicle of women and cows had similar size and steroidogenic output (10 to 20 mg/h), the bovine CL had about ten-fold greater P4 output compared to the human CL (17.4 vs. 1.4 mg/h), possibly due to the development of high constitutive P4 output by the bovine large luteal cells. The continued dependence of the primate CL on LH/CG/cAMP also seems to underlie luteolysis, as there seems to be a requirement for greater luteotropic support in the older primate CL than is provided by the endogenous LH pulses. Conversely, regression of the ruminant CL is initiated by PGF from the nonpregnant uterus. Consequently, the short luteal phase in ruminants is primarily due to premature secretion of PGF by the nonpregnant uterus and early CL regression, whereas CL insufficiency in primates is related to inadequate luteotropic support and premature CL regression. Thus, the key functions of the CL, pregnancy maintenance and CL regression in the absence of pregnancy, are produced by common cellular and enzymatic pathways regulated by very distinct luteotropic and luteolytic mechanisms in the CL of primates and ruminants.

Endoscopic sclerotherapy for bleeding oesophageal varices: experience in Sudan.

INTRODUCTION: Bleeding due to oesophageal varices is the commonest cause of upper gastrointestinal tract haemorrhage in Sudan. Endoscopic injection sclerotherapy (EST) is a valuable therapeutic modality for the management of variceal bleeding. Other options for treatment such as variceal banding are either expensive or unavailable. STUDY AIMS: A retrospective study to evaluate the outcome of EST in the management of bleeding oesophageal varices due to portal hypertension in a developing country (Sudan). PATIENTS AND METHODS: A total of 1070 patients over a period of 10 years (1986-1996) were studied. Inclusion criteria was bleeding oesophageal varices consequent to portal hypertension. EST was performed using a standard technique. Ethanolamine oleate 5% was the sclerosing agent utilized. The procedure was done on a day- case basis. RESULTS: There were 904 males (84.5%) and 166 females (15.5%). The cause of portal hypertension was schistosomal periportal fibrosis (PPF) in 999 (93.3%) patients, liver cirrhosis 59 (5.5%), mixed PPF and cirrhosis 5 (0.46%), portal vein thrombosis 6 (0.64%) and congenital hepatic fibrosis was present in 1 patient. A total of 100 (9.4%) patients presented with bleeding which occurred after surgery. Full obliteration of varices required a mean of 4 sessions with a range of 2-6. 462 (43.2%) have been followed up until complete sclerosis of varices. CONCLUSION: This study provides evidence that endoscopic injection sclerotherapy is an essential component in the management of bleeding oesophageal varices caused by portal hypertension. It is a feasible and a cost-effective therapeutic strategy in developing countries.

Radiation damage in electron microscopy of organic materials: effect of low temperatures.

As measured by the life-time of their electron diffraction patterns, the radiation sensitivity of anthracene and coronene at 500 kV is reduced by a factor of three to four at liquid helium temperature in comparison to room temperature, For l-valine the ratio is about 1-8 but there is a wide variation in the results, possibly due to differences in crystal thickness. The end-dose at 20 degrees K for valine is equivalent to 13 electrons/A2; for anthracene and coronene it is about 600 electrons/A2 at room temperature. The variation of end-dose with temperature shows that at least two mechanisms must be involved in damage to such compounds, possibly concerning the breaking of intermolecular and intramolecular bonds, respectively.