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Effects of intra-abdominal drainages on adhesion formation and prevention by phospholipids in a rat model. Drainages and adhesion formation.

BACKGROUND AND AIMS: The study was designed to asses the adhesiogenic capacity of silicone drainages and the protective effect of phospholipids (PL). MATERIALS AND METHODS: A total of 75 Wistar rats were randomly assigned to the different groups. In a preliminary trial (pt; n = 15), all rats underwent midline laparotomy. The control group (C(pt); n = 5) received no further treatment. In the other animals, either an 'easy flow' drainage (EF(pt); n = 5) or an 'Aachen' drainage (AC(pt); n = 5) was placed into the abdominal cavity. In the final study (fs; n = 60), rats underwent laparotomy and colonic anastomosis. The control groups (C(fs)) received no drainages. In the other groups either one of the two types of drainages (EF(fs), AC(fs)) were introduced. In 50% of the rats, 75 mg/kg of PL were administered intraperitoneally (C(fs)+PL, EF(fs)+PL, AC(fs)+PL). The other rats received no additional treatment (C(fs)ØPL, EF(fs)ØPL, AC(fs)ØPL). All animals were sacrificed 10 days after surgery. Areas of adhesions and anastomotic bursting pressures were measured (mean +/- SD). RESULTS: In the preliminary trial, analysis of variance (ANOVA) revealed no differences between the groups after application of drainages (values are given in mean +/- SD): C(pt) mean 23.3 +/- 29.4 mm(2), EF(pt) 829.7 +/- 679.3 mm(2), AC(pt) 609.9 +/- 219.4 mm(2). In the final study, 2-factorial ANOVA showed a significant effect (p < 0.001) for the use of drainages but not for the application of PL (C(fs)ØPL 140.6 +/- 124.2 mm(2), C(fs)+PL 67.7 +/- 60.4 mm(2), EF(fs)ØPL 1,217.0 +/- 458.3 mm(2), EF(fs)+PL 1,266.8 +/- 368.3 mm(2), AC(fs)ØPL 861.7 +/- 274.8 mm(2), AC(fs)+PL 544.2 +/- 193.8 mm(2)). Post hoc test for pairwise comparisons adjusted to Bonferroni showed significant differences (p < 0.001) between all of the three pairs (C(fs) 104.1 +/- 92.3 mm(2) vs. EF(fs) 1,241.9 mm(2) +/- 413.3 mm(2); C(fs) vs. AC(fs) 702.9 mm +/- 234.3 mm(2); EF(fs) vs. AC(fs)). DISCUSSION: The final study demonstrates the adhesiogenic capacity of silicone drainage tubes in combination with anastomoses. Any protective effect of PL alone or in combination with drainages could not be shown. CONCLUSIONS: Indication for the use of drainages in standard surgical procedures should be reconsidered within the scope of their potential to cause adhesions and subsequent complications.

Abdomen↗

Precedence of cell-zona adhesion over cell-cell adhesion during marsupial blastocyst formation prohibits morula formation and ensures that both the pluriblast and trophoblast are superficial.

This study, based on 38 samples taken between the 16-cell stage on day 2.5 of gestation and the expanded 1.0-mm-diameter unilaminar blastocyst on day 6, describes the ultrastructural changes that occur in the conceptus of the marsupial Sminthopsis macroura in relation to cell-zonal adhesion initiated at the zygote stage and cell-cell adhesion initiated at the 16-cell stage, lineage allocation, extracellular matrix (ECM) secretion and embryo coat changes. In S. macroura, rather flattened pluriblast and rounded trophoblast cells appear as different cell types during the fourth division when nucleolar reticulation suggests activation of the zygotic genome in both cell types. The differences disappear nearly completely in blastocysts of 0.6-0.8 mm in diameter, but the two cell types then reappear as two distinct populations. The ECM varies depending on its location within the conceptus up to the stage of the expanding blastocyst. It is of rather granular appearance between the cell lining and zona pellucida and consists of patches of homogeneous material embedded in an electron-lucent substance in the cleavage cavity. Homogeneous ECM coats trophoblast but not pluriblast cells on blastocoelic surfaces. Transient structures such as 'myosin-like' fibrillar arrays, probably associated with exocytosis of ECM, and pearl string-like whorls are still present, but both disappear during further expansion of the 0.6- to 0.8-mm blastocyst. During blastocyst expansion, the patchy homogeneous ECM in the blastocoel changes structure and appears flocculent, while the continuous ECM coating trophoblast cells disappears. Pluriblast cells and yolk mass identify the embryonic pole and hemisphere, and the opposite hemisphere becomes abembryonic and is eventually fully lined by trophoblast cells. An increase in endocytotic, mainly coated vesicles at the apical, zona-orientated surface of both cell types is noticed and is probably responsible for uptake of the mucoid coat. In 1-mm blastocysts, numerous vesicles contain rod-shaped crystalline inclusions.

Animals↗

Mechanism of bilirubin diglucuronide formation in intact rats: bilirubin diglucuronide formation in vivo.

Although it is well established that bilirubin monoglucuronide is formed in the liver from bilirubin by a microsomal bilirubin uridine diphosphate (UDP)-glucuronosyltransferase, the subcellular site of conversion of monoglucuronide to diglucuronide and the molecular mechanism involved in diglucuronide synthesis have not been identified. Based on in vitro studies, it has been proposed that two fundamentally different enzyme systems may be involved in diglucuronide synthesis in rat liver: (a) a microsomal UDP-glucuronosyltransferase system requiring UDP-glucuronic acid as sugar donor or (b) a transglucuronidation mechanism that involves transfer of a glucuronosyl residue from one monoglucuronide molecule to another, catalyzed by a liver plasma membrane enzyme. To clarify the mechanism by which bilirubin monoglucuronide is converted in vivo to diglucuronide, three different experimental approaches were used. First, normal rats were injected with either equal amounts of bilirubin-IIIalpha [(14)C]monoglucuronide and unlabeled bilirubin-XIIIalpha monoglucuronide, or bilirubin-XIIIalpha [(14)C]monoglucuronide and unlabeled bilirubin-IIIalpha monoglucuronide. Analysis of radiolabeled diglucuronide excreted in bile showed that [(14)C]glucuronosyl residues were not transferred between monoglucuronide molecules. Second, in normal rats infused intravenously with dual-labeled [(3)H]bilirubin [(14)C]monoglucuronide, no transfer or exchange of the [(14)C]glucuronosyl group between injected and endogenously produced bilirubin monoglucuronide could be detected in the excreted bilirubin diglucuronide. Third, in homozygous Gunn rats, injected (14)C-labeled or unlabeled bilirubin mono- or diglucuronides were excreted in bile unchanged (except that diglucuronide was hydrolyzed to a minor degree). This indicates that Gunn rats, which lack bilirubin UDP-glucuronosyltransferase activity, are unable to convert injected monoglucuronide to diglucuronide. Collectively, these findings establish that a transglucuronidation mechanism is not operational in vivo and support the concept that bilirubin diglucuronide is formed by a microsomal UDP-glucuronosyltransferase system.

Animals↗

The Drosophila proneural gene amos promotes olfactory sensillum formation and suppresses bristle formation.

Proneural genes encode basic-helix-loop-helix (bHLH) transcription factors required for neural precursor specification. Recently amos was identified as a new candidate Drosophila proneural gene related to atonal. Having isolated the first specific amos loss-of-function mutations, we show definitively that amos is required to specify the precursors of two classes of olfactory sensilla. Unlike other known proneural mutations, a novel characteristic of amos loss of function is the appearance of ectopic sensory bristles in addition to loss of olfactory sensilla, owing to the inappropriate function of scute. This supports a model of inhibitory interactions between proneural genes, whereby ato-like genes (amos and ato) must suppress sensory bristle fate as well as promote alternative sense organ subtypes.

Animals↗