Free perforation of the small bowel due to regional enteritis.
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Biomedical subjects
Publications and source records attributed to I L Craft.
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Extracts of fresh tissue from the feto-placental unit and myometrium were tested for their ability to inhibit ADP-induced platelet aggregation and to degrade ADP. Placental extracts caused rapid reversal of aggregation and degraded ADP, both effects being mimicked by HPAP. However, whereas the latter was inhibited by L-phenylalanine but not by heating to 65 degrees C for 5 minutes, the reverse was true for crude placental extracts. Umbilical cord vessels and myometrium totally inhibited platelet aggregation in a similar way to pure PGI2. Both tissues also exhibited ADP-ase activity but were much less potent in this respect than placenta. In the system used, little or no anti-aggregatory activity was detected in extracts of non-vascular cord tissue, fetal membranes or amniotic fluid, although the two latter tissues had a weak ADP-degrading effect. Thus, it appears that in contrast to myometrium and umbilical cord vessels, the major inhibitor of platelet aggregation in placenta is an ADP-ase and not PGI2. While part of the inhibitory effect of placenta may be due to HPAP, other ADP-degrading enzymes also seem to contribute to the overall anti-aggregatory property of this organ.
Corticosteroid conversion by early (7 to 10 weeks) and late (36 to 42 weeks) human placenta, fetal membranes and decidua was studied. Tritiated cortisol, cortisone, corticosterone, 11-dehydrocorticosterone (DHC) and 11-deoxycorticosterone (DOC) were incubated in vitro with homogenates of these tissues and extracts chromatographed on Sephadex LH20 columns. 11 beta-hydroxysteroid dehydrogenase activity (11 beta-HSD; EC 1.1.1.146) was present in all these tissues from as early as the seventh week of pregnancy. In the fetal membranes the enzyme activity was present in the chorion, the amnion showing no activity. Only the decidua could convert cortisone and DHC to the biologically more active cortisol and corticosterone, respectively. DOC was not transformed by any of the tissues. No 11 beta-HSD activity was found in amniotic fluid, retroplacental serum, umbilical cord plasma or cord tissue.
We have previously demonstrated that the human placenta possesses potent platelet anti-aggregatory activity. This activity was exhibited only when aggregation was induced by adenosine diphosphate (ADP), but not when induced by adrenaline, ristocetin or collagen. We have also shown that placental extracts degrade ADP. We therefore concluded that the placenta's anti-aggregatory activity, in vitro, was not due to prostacyclin (PGI2) but to an 'ADPase'. In view of some reports claiming that the human placenta produces PGI2, we carried out a series of experiments to establish whether human placental tissue can convert [14C]-arachidonic acid [( 14C]-AA) to 6-oxo-PGF1 alpha, the stable metabolite of PGI2. Tissue from placenta and the membranes did not show any appreciable conversion of [14C]-AA into 6-oxo-PGF1 alpha. This finding was confirmed by radioimmunoassay techniques where the placenta was shown to produce spontaneously only minimal amounts of 6-oxo-PGF1 alpha. We conclude that placental tissue and the fetal membranes do not synthesize a significant amount of PGI2, certainly not enough to account for the potent platelet anti-aggregatory activity of the placenta in vitro. Placental platelet anti-aggregatory activity in vitro, is probably due entirely to ADPase activity.
Four distinct studies were carried out using two data sets of percutaneous epididymal sperm aspiration (PESA) and intracytoplasmic sperm injection (ICSI) procedures performed from March 1993 to January 1997. In study A, an analysis of 181 ICSI treatment cycles following PESA revealed a successful epididymal sperm retrieval rate of 83%. It confirmed that PESA is an effective sperm retrieval method and the associated ICSI pregnancy rate (35% per embryo transfer) compared favourably with that of other sperm retrieval methods. In study B, the relevance of a prior diagnostic PESA procedure was ascertained by comparing the sperm retrieval rates in two groups of patients having their first ICSI treatment cycle with spermatozoa retrieved through PESA. Group B1 (n = 50) had diagnostic PESA prior to the ICSI treatment cycle PESA procedure, unlike patients in group B2 (n = 64) who did not. The sperm retrieval rate in the treatment cycle procedure was not different at 90 and 82.8% for groups B1 and B2 respectively. However, the discontinuation of diagnostic PESA is fraught with problems including liability to medico-legal sanctions. In study C, analysis of 177 treatment cycles involving PESA and ICSI revealed a successful sperm retrieval rate by PESA of 82% in the first cycle, 93% in the second, 96% in the third and 100% in the fourth cycle. The same trend was evident when sperm retrieval was examined in relation to each of the epididymides. Retrieved spermatozoa were found to be motile in 67-100% of cases and the frequency of samples containing motile spermatozoa did not decrease with increase in the number of PESA attempts. These results show that PESA does not jeopardize future epididymal sperm retrieval. In study D, the outcome of treatment with ICSI using ejaculated spermatozoa (305 cycles) (group D1) was compared with that of ICSI using spermatozoa obtained through PESA (54 cycles) (group D2). The median age of women in the two groups of couples was similar (34 years). In group D1, 70% of metaphase II oocytes were fertilized compared with 61% in group D2 (P < 0.01). The cleavage rate and the median numbers of transferred and cryopreserved embryos were similar in both groups. There was no significant difference between the clinical pregnancy rates (33 and 42% in groups D1 and D2 respectively). Our results show that the outcome of PESA-ICSI treatment compares favourably with that of ICSI using ejaculated spermatozoa.
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