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Stroke is a leading cause of disability and mortality globally. In the first few hours after ischaemic stroke, the severity and irreversibility of brain injury increase as time passes. The primary goal of the emergent management of acute ischaemic stroke is stabilization and reperfusion of the ischaemic penumbra if eligibility criteria are met and contraindications are ruled out. The primary reperfusion strategies are administration of intravenous tissue plasminogen activator (IV tPA) and endovascular thrombectomy (EVT). Close monitoring is warranted prior to, during, and after these reperfusion procedures to detect early neurologic deterioration that may signify complications from treatment.

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REASONS FOR PERFORMING STUDY: Relatively few journals publish their annual acceptance rate, although this figure is of scientific and academic interest. OBJECTIVES: To determine the acceptance rate for manuscripts submitted to veterinary peer-reviewed journals during 2012 and to determine the proportions of submitted manuscripts that were accepted without revision, accepted after revision or rejected. STUDY DESIGN: Self-reporting email questionnaire METHODS: Editors of 118 peer-reviewed journals listed in the Web of Science in the subject category veterinary sciences were invited by email to submit data pertinent to manuscripts submitted to their journal in 2012. RESULTS: Data were received from 30 (26%) journals. Mean ± s.d. acceptance rate was 47 ± 15%. On average 3 ± 5% submitted manuscripts were accepted without revision, 44% ± 15% manuscripts were accepted after revision, 4 ± 4% manuscripts were withdrawn by authors, 46 ± 17% manuscripts were rejected and 3 ± 5% manuscripts were still pending at the end of the study period. CONCLUSIONS: With so few manuscripts accepted without revision, prospective authors must expect to expend time and effort revising and resubmitting their manuscripts for publication. Although authors are frequently able to correct manuscript flaws identified by reviewers, the knowledge that less than half submitted manuscripts are accepted might help stimulate prospective authors to try to submit better quality manuscripts.

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Carbon (C), nitrogen (N) and phosphorous (P) burial rates were determined within natural saltmarsh (NSM) and 'managed realignment' (MR) sediments of the Blackwater estuary, UK. Methane (CH(4)) and nitrous oxide (N(2)O) fluxes were measured along with their ability to offset a portion of the C burial to give net C sequestration. C and N densities (Cρ and Nρ) of NSM sediments (0.022 and 0.0019 g cm(-3)) are comparable to other UK NSM sediments. Less vegetationally developed MR sediments have lower Cρ and Nρ (0.012 and 0.0011 g cm(-3)) while the more vegetationally developed sites possess higher Cρ and Nρ (0.023 and 0.0030 g cm(-3)) than NSM. Both NSM and MR areas were small CH(4) (0.10-0.40 g m(-2)yr(-1)) and N(2)O (0.03-0.37 g m(-2) yr(-1)) sources. Due to their large Global Warming Potentials, even these relatively small greenhouse gas (GHG) fluxes reduced the net C sequestration within MR marshes by as much as 49%, but by only 2% from NSM. Potential MR areas within the Blackwater estuary (29.5 km(2) saltmarsh and 23.7 km(2) intertidal mudflat) could bury 5478 t C yr(-1) and 695.5 t N yr(-1), with a further 476t N yr(-1) denitrified. The saltmarsh MR would also sequester 139.4 t Pyr(-1). GHG fluxes would reduce the C burial benefit by 24% giving a C sequestration rate of 4174 t Cyr(-1). Similar areas within the Humber estuary (74.95 km(2)) could bury 3597 t Cyr(-1) and 180 t N yr(-1), with a further 442 t Nyr(-1) denitrified. GHG fluxes would reduce the C burial benefit by 31% giving a C sequestration rate of 2492 t C yr(-1). Overall, MR sites provide sustainable coastal defence options with significant biogeochemical value and, despite being net sources of CH(4) and N(2)O, can sequester C and reduce estuarine nutrient loads.

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The relationship between stool character and whole gut transit time (WGTT), which is the average time for the passage of material through the lumen of the alimentary tract from ingestion to defecation, was studied in eight control dogs and 12 dogs with non-specific dietary sensitivity. Dogs were fed four diets in a cross-over design, and faecal quality was assessed daily and WGTT determined using plastic pellets. Faecal quality was unaffected by diet in the control dogs. Dogs with dietary sensitivity produced looser faeces compared with the control dogs, and this was significant for two of the diets. There was no significant effect of diet on mean WGTT within or between groups. Minimum WGTT, which was the interval to the first appearance of markers in faeces, was shorter in sensitive dogs compared with controls, and this was significant for two of the four diets. There were significant, inverse relationships between minimum WGTT and both mean faeces score and percentage unacceptable defecations. These data suggest that rapid transit of certain dietary components may impact negatively on stool quality and contribute to loose faeces in dogs with non-specific dietary sensitivity.

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OBJECTIVE: Endothelial cell injury by polymorphonuclear neutrophil (neutrophil [PMN]) respiratory burst after trauma and hemorrhagic shock (T/HS) predisposes subjects to acute respiratory distress syndrome and multiple organ failure. T/HS mesenteric lymph injures endothelial cell and lymph duct ligation (LDL) before T/HS prevents pulmonary injury. We investigated the role of mesenteric lymph in PMN priming by T/HS. DESIGN: Prospective experiment in rats. SETTING: University hospital laboratory. SUBJECTS: Adult male rats. INTERVENTIONS: Mesenteric lymph was obtained from rats undergoing T/HS (30 mm Hg, 90 mins) or sham shock (T/SS). Plasma was harvested from uninstrumented control (UC), T/HS, T/SS, and T/HS+LDL rats. PMNs were isolated from UC, T/HS, and T/HS+LDL rats. MEASUREMENTS AND MAIN RESULTS: PMNs from UC rats were incubated in buffer, 1% T/HS lymph, and 1% T/SS lymph. PMNs from UC rats were incubated in UC, T/HS, T/SS, and T/HS+LDL plasma. PMN respiratory burst was initiated by using macrophage inflammatory protein (MIP)-2/platelet-aggregating factor (PAF) or phorbol myristate acetate. Cytosolic calcium ([Ca2+]i) responses to MIP-2/PAF were assayed in PMN from UC, T/HS, and T/HS+LDL rats. PMN preincubated in T/HS lymph showed significant elevations in MIP/PAF-elicited respiratory burst compared with T/HS lymph or buffer only (p <.05; analysis of variance/Tukey's test). T/HS lymph incubation also increased (p <.05) phorbol myristate acetate elicited respiratory burst compared with buffer or T/SS. Preincubation in T/HS plasma increased MIP-2/PAF-elicited respiratory burst (p <.05) compared with UC or T/SS plasma. LDL blocked T/HS priming of respiratory burst. Control PMN [Ca2+]i responses to MIP-2 and PAF were low. T/SS PMN were significantly more responsive, but the T/HS PMN showed still higher responses (p <.01). LDL reversed the priming of [Ca2+]i responses by T/HS (p <.01). CONCLUSIONS: PMNs are primed by T/HS lymph but not T/SS lymph and by T/HS plasma but not T/SS plasma. LDL before shock prevents T/HS plasma from priming PMN. The magnitude of respiratory burst found here paralleled the [Ca2+]i responses seen to receptor dependent initiating agonists. Mesenteric lymph is both necessary and sufficient to prime PMN after T/HS in the rat, and it primes PMN in part by enhancing [Ca2+]i responses to G-protein coupled chemoattractants. Mesenteric lymph mediates postshock PMN dysfunction.

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BACKGROUND: Previous studies have shown that mesenteric lymph duct interruption prevents lung injury and decreases lung neutrophil sequestration after hemorrhagic shock (HS). Since endothelial cells rapidly express P-selectin after ischemia/reperfusion injury and HS-induced lung injury appears to involve neutrophil-endothelial cell interactions, we tested the following two hypotheses. First, that HS increases endothelial cell P-selectin expression and that interruption of mesenteric lymph flow in vivo would diminish this expression. Second, that incubation of human umbilical vein endothelial cells with post-HS mesenteric lymph but not sham shock (SS) lymph or postshock portal vein plasma would up-regulate P-selectin expression. METHODS: Pulmonary microvascular P-selectin expression was measured in male rats subjected to 90 minutes of HS (30 mm Hg), SS, or HS with lymphatic ligation, with a dual radiolabeled monoclonal antibody technique. The lungs from these animals were subsequently harvested and P-selectin expression was expressed as mean +/- SEM nanograms of monoclonal antibody per gram of tissue. RESULTS: Pulmonary P-selectin expression was 2.0 +/- 0.4 after SS, 9.7 +/- 3.0 after HS, but decreased to 2.3 +/- 0.3 after HS with lymph interruption (p < 0.05 HS vs. SS or HS plus lymph ligation). Incubation of human umbilical vein endothelial cells with shock lymph collected 3 to 4 hours after shock resulted in a nearly fivefold increase in P-selectin expression (p < 0.001) as compared with SS lymph, lymph collected 6 hours after shock, or postshock portal vein plasma. CONCLUSION: These results support the concept that gut-derived lymph promotes HS-induced lung injury through up-regulation of microvascular adhesion molecules and that intestinal lymph duct interruption may prevent distant organ injury by blunting the expression of these molecules.

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Previously, we have documented that gut-derived lymph from rats subjected to trauma/hemorrhagic shock (T/HS) is injurious to human umbilical vein endothelial cells (HUVEC). To verify these findings in an all rat systems, the ability of T/HS lymph to increase rat pulmonary microvascular endothelial cell (RPMVEC) monolayer permeability and kill RPMVEC was compared with that observed with HUVECs. RPMVEcs isolated from male rats or HUVECs were grown in 24-well plates for the cytotoxicity assays or on permeable filters in a two-chamber system for permeability assays. Mesenteric lymph was collected from male rats subjected to trauma (laparotomy) plus hemorrhagic shock (T/HS group) or to a laparotomy plus sham-shock (T/SS group). The T/HS group had their mean arterial pressure decreased to 30 mmHg and kept there for 90 min. Lymph samples centrifuged to remove the cellular component were incubated with the RPMVECs or HUVECs at a 10% concentration. Neither T/SS lymph nor post-T/HS portal vein plasma was toxic to or increased the permeability of the RPMVECs or HUVECs. The pattern of cytotoxicity observed in the HUVECs incubated with T/HS mesenteric lymph was similar to that observed in the RPMVECs, as reflected by trypan blue dye exclusion, with more than 95% of the HUVECs and RPMVECs being killed after a 16-h incubation with T/HS mesenteric lymph. However, at earlier time points the amount of LDH released from the HUVEC cells incubated with T/HS lymph was greater than that observed with the PRMVEC, although trypan blue dye exclusion was similar. Similarly, incubation with 10% T/HS lymph increased the permeability of both HUVEC and RPMVEC monolayers more than 2-fold, even with an incubation period as short as 1 h. In conclusion, these results provide further evidence that T/HS lymph, but not T/SS lymph or post-T/HS portal vein plasma, is injurious to endothelial cells and that RPMVECs are as susceptible to injury as HUVECs. Additionally, these studies support the emerging concept that gut-induced distant organ injury is mediated by factors contained in mesenteric lymph.

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OBJECTIVE: To determine whether hemorrhagic shock-induced bone marrow failure is mediated by the gut through the production of toxic mesenteric lymph and whether shock-induced bone marrow failure could be prevented by division of the mesenteric lymphatics. DESIGN: Prospective, controlled study. SETTING: University surgical research laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Rats were divided into five groups: unmanipulated controls (n = 12), hemorrhagic shock with laparotomy (n = 8), hemorrhagic shock with mesenteric lymph duct ligation (n = 10), sham shock with laparotomy (n = 6), and sham shock with mesenteric lymph duct ligation (n = 7). At either 3 or 6 hrs after resuscitation, bone marrow was obtained for determination of early (cobblestone forming cells) and late (granulocyte-macrophage colony forming unit and erythroid burst forming unit) hematopoietic progenitor cell growth. Parallel cultures were plated with plasma (1% and 2% v/v) from all groups to determine the effect of lymphatic ligation on hematopoiesis. MEASUREMENTS AND MAIN RESULTS: Bone marrow cellularity, cobblestone forming cells, granulocyte-macrophage colony forming unit, and erythroid burst forming unit growth in rats subjected to hemorrhagic with lymph duct ligation were similar to those observed in sham-treated animals and significantly greater than in rats subjected to shock and laparotomy without lymphatic duct ligation. Plasma from rats subjected to shock without lymph ligation was inhibitory to hematopoietic progenitor cell growth. In contrast, this shock-induced inhibition was not observed with plasma obtained from shocked rats that underwent mesenteric lymph ligation. CONCLUSIONS: Hemorrhagic shock suppresses bone marrow hematopoiesis as measured by a decrease in early and late progenitor cell growth. This suppression appears mediated through mesenteric lymph as the effect is abrogated by mesenteric lymph duct ligation. These data clearly demonstrate a link between the gut and bone marrow failure after hemorrhagic shock

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G-protein coupled (GPC) chemoattractants are important neutrophil (PMN) activators in human shock and sepsis, acting in part by increasing cytosolic calcium ([Ca2+]i). Rats are widely used as laboratory models of shock and sepsis, but reports of [Ca2+]i flux in circulating rat PMN are rare. Moreover, the [Ca2+]i values reported often differ markedly from human systems. We developed study methods where basal [Ca2+]i values in circulating rat PMN were comparable to human PMN, but rat PMN still mobilized calcium poorly after stimulation. Trauma (laparotomy) did not change rat PMN basal [Ca2+]i, but induced brisk [Ca2+]i responses to chemokine and lipid mediators that approximated human PMN responses. This was associated with marked loading of microsomal calcium stores. Formyl peptides still mobilized calcium less well in rat than human PMN. Normal rat PMN appear to circulate in a less mature or primed form than human PMN. A very limited injury rapidly converts rat PMN to a more activated phenotype. PMN thus activated act quite similar to human PMN in terms of GPC receptor-mediated calcium mobilization. Trauma enhances rat PMN responses to GPC agonists at least in part by loading cell calcium stores.

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BACKGROUND: Post-shock mesenteric lymph kills and injures endothelial cells (ECs), but neither the mechanism nor the mediators of lymph's toxic effect are known. Thus, in these studies we investigated and characterized potential factors that may be involved in lymph's toxic effect on ECs. METHODS: Lymph was collected hourly from rats before shock, during the shock period, and for 6 hours post-shock and processed in several ways-including removal of cellular elements, freezing, heating, or separation by molecular weight-after which they were tested for toxicity (lactate dehydrogenase as a marker of cell injury and trypan blue as a marker of cell viability). RESULTS: Controls consisting of medium, pre-shock lymph, and post-shock portal vein plasma had no EC toxicity. Lymph collected 1 to 3 hours post-shock resulted in the death of 90% to 95% of ECs and caused an 8- to 10-fold increase in lactate dehydrogenase release; however, this toxic effect waned by 4 hours post-shock. Endotoxin neutralization and immune cell removal did not decrease lymph cytotoxicity but complement inactivation did. By fractionating the toxic lymph samples by size, it appears that the putative EC cytotoxic mediator(s) is larger than 100,000 d. CONCLUSIONS: Mesenteric lymph collected 1 to 3 hours after hemorrhagic shock is toxic to ECs, but this effect is lost by 4- to 5-hours post-shock and is not dependent on the presence of immune cells or endotoxin but does involve complement and other putative mediators of greater than 100,000 d.

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Recently we have shown that ligation of the main mesenteric lymph (MLN) duct prior to an episode of hemorrhagic shock (HS) prevents shock-induced lung injury. Yet, ligation or diversion of intestinal lymph immediately prior to injury is not clinically feasible. Diversion of intestinally derived lymph after injury to protect against secondary insults is possible, but it is not known how long the protective effects of lymph ligation would last. Thus, we tested whether ligation of the MLN duct seven days prior to HS would still be protective. Male Sprague-Dawley rats were subjected to laparotomy with or without MLN duct ligation. Seven days later, half of the sham and actual MLN duct ligated animals randomly were selected to undergo HS (30 mmHG for 90 min). The other half of the animals was subjected to sham shock. Lung permeability, pulmonary myeloperoxidase (MPO) activity, and bronchoalveolar fluid (BALF) protein content were used to determine lung injury. Lymphatic division 7 days prior to HS continued to prevent shock induced lung injury as assessed by a lower Evans Blue dye concentration, BALF protein and MPO activity. In addition, there was no evidence of Patent Blue dye in the previously ligated MLN duct. Since ligation of the main mesenteric lymphatic duct continues to protect against shock-induced lung injury 1 week after duct ligation, it is feasible that lymphatic ligation performed after an injury remains protective against certain secondary insults for at least 1 week.

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Recent studies have established gut-derived lymph rather than portal blood as the major source of toxic mediators after hemorrhagic shock that causes distant organ injury. Similarly, emerging data have identified sex as a major modifier of the response to injury and illness. Thus we tested the hypothesis that female rats would be more resistant to shock-induced lung injury than male rats because females are more resistant to shock-induced gut injury and produce mesenteric lymph that is less toxic to endothelial cells. Male and female rats were subjected to sham or hemorrhagic shock and lung permeability was quantitated by Evans blue dye and protein extravasation into the alveolar space. Next, mesenteric lymph collected from shocked and sham-shocked rats of both sexes was incubated with human umbilical vein endothelial cells (HUVECs) and assayed for toxicity. Trypan blue dye exclusion and the release of lactate dehydrogenase assessed HUVEC viability and injury respectively. Lastly, sections of the terminal ileum were histologically examined for evidence of shock-induced mucosal injury. Male rats but not female rats subjected to hemorrhagic shock had evidence of increased lung permeability and produced mesenteric lymph that was cytotoxic to HUVECs. Shock caused gut injury in the male rats whereas histological evidence of gut injury was not observed in the female rats. Hemorrhagic shock-induced lung injury depends on gut injury and mesenteric lymph appears to be the route by which gut-derived toxic factors exit the gut to cause lung injury. The resistance of female rats to shock-induced lung injury appears to be secondary to their resistance to shock-induced gut injury.

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Using broth conjugation, we found that 19 of 29 (66%) oxytetracycline (OT)-resistant isolates of Aeromonas salmonicida transferred the OT resistance phenotype to Escherichia coli. The OT resistance phenotype was encoded by high-molecular-weight R-plasmids that were capable of transferring OT resistance to both environmental and clinical isolates of Aeromonas spp. The molecular basis for antibiotic resistance in OT-resistant isolates of A. salmonicida was determined. The OT resistance determinant from one plasmid (pASOT) of A. salmonicida was cloned and used in Southern blotting and hybridization experiments as a probe. The determinant was identified on a 5.4-kb EcoRI fragment on R-plasmids from the 19 OT-resistant isolates of A. salmonicida. Hybridization with plasmids encoding the five classes (classes A to E) of OT resistance determinants demonstrated that the OT resistance plasmids of the 19 A. salmonicida isolates carried the class A resistance determinant. Analysis of data generated from restriction enzyme digests showed that the OT resistance plasmids were not identical; three profiles were characterized, two of which showed a high degree of homology.

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AIMS: The objectives of this study were to determine the effect of brain trauma on the multiple pathways of metabolism of valproate and to evaluate the use of the urinary 6beta-hydroxycortisol to cortisol ratio in predicting changes in hepatic metabolism induced by brain injury. METHODS: Fourteen patients with severe head injuries received a 15 mg kg(-1) loading dose and a maintenance dose of valproate to maintain therapeutic plasma concentrations. A minimum of one steady state trough blood sample and one dosage interval urine were collected during days 3-6 and during days 7-14 post-injury. Total and unbound valproate plasma concentrations were determined by gas chromatography-flame ionization detection (GC-FID) with and without ultrafiltration. Urinary valproate metabolites were measured by gas chromatography/mass spectrometry (GC-MS) (n = 10). Urinary 6beta-hydroxycortisol and cortisol concentrations were determined by high performance liquid chromatography (h.p.l.c.) (n = 14). Total intrinsic clearance (CL[int]) for valproate and individual formation clearances (CL[f]) to its major metabolites were calculated. Data obtained during baseline (days 3-6) were averaged for each patient and were compared with averaged data obtained from days 7 to 14 using a paired t-test. RESULTS: Statistically significant increases in the CL(int), CL(f) of VPA glucuronide, 2-ene-VPA, and 4-OH-VPA pathways and the 6beta-hydroxycortisol to cortisol ratio were found. The percent change in the 6beta-hydroxycortisol to cortisol ratio correlated significantly with the changes in the CL(int) of valproate. CONCLUSIONS: Brain trauma results in induction of multiple pathways of valproate metabolism and increases in the 6beta-hydroxycortisol to cortisol ratio, suggesting a non-specific enzyme induction in response to head injury.

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Oral and topical antibiotics play a major role in acne therapy. Physicians base treatment choices on personal perceptions of efficacy, cost-effectiveness or risk-benefit ratios and rarely take bacterial resistance into account. Propionibacterium acnes isolates resistant to one or more anti-acne antibiotics have been reported in Europe, the USA, Japan and New Zealand. Therapeutic failure on some but not all antibiotic regimens is an increasing management problem. In Leeds, UK, resistant strains are found in 60% of acne patients and 50% of close contacts. Recommendations for the use of antibiotics in acne therapy to help prevent the emergence of resistance in P. acnes include the implementation of antibiotic usage policies and the encouragement of improved prescribing habits. Strategies to reduce the resistant P. acnes population are necessary. This paper reports preliminary data demonstrating that oral isotretinoin (Roaccutane/Accutane) significantly reduces total numbers of resistant P. acnes on the skin of all patients.

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The complete sequence of a sunflower (Helianthus annuus) gene, HaG5, encoding a 2 S albumin storage protein was determined. The predicted unprocessed precursor has 295 amino acids, is rich in glutamine residues (24%) and contains a hydrophobic amino-terminus that is similar to the consensus signal peptide. Amino acid sequencing of the mature protein revealed extensive post-translational processing. Nuclease protection and primer extension analysis indicated a major transcriptional start 30 nucleotides 5' of the predicted ATG start codon. Additional sequence data, determined from a nearly full length cDNA recombinant, indicate that HaG5 is a member of a small gene family comprised of at least two divergent genes. Comparison of the predicted HaG5 gene product with sequences of other known plant proteins revealed distant but significant homology with the napins of Brassica and other heterogeneous seed proteins in the albumin superfamily.

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Phosphoenolpyruvate carboxylase (PEPCase; EC 4.1.1.31) from Flaveria trinervia Mohr (C4), F. floridana Johnston (C3-C4), and F. cronquistii Powell (C3) leaves were compared by electrotransfer blotting/enzyme-linked immunoassay (Western-blot analysis), mobility of the native enzyme in polyacrylamide gels and in isoelectric focusing (IEF) gels, peptide mapping, and in-vitro translation of RNA isolated from each plant. The PEPCases from the C3 and C3-C4 plants were very similar to each other in terms of electrophoretic mobilities on gels and isoenzyme patterns on IEF gels, and identical in peptide mapping. Quantitative differences were noted, however, in that the C3-C4 intermediate plant contained more PEPCase overall and that the relative activity of individual isoenzymes shifted between the C3 and C3-C4 intermediate PEPCases. The PEPCase from the C4 plant had a different isoenzyme pattern, a different peptide map, and was far more abundant than the other two enzymes. Western blot analysis demonstrated the cross-reactivity of PEPCases from all three Flaveria species with antibody raised against maize PEPCase. The results provide evidence, at the molecular level, that supports the view of C3-C4 intermediate species as C3-like plants with some C4-like photosynthetic characteristics, but there are differences from the C3 plant in the quantity and properties of the PEPCase from the C3-C4 intermediate plant.

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The developmental potential of inner cell mass (ICM) and trophectoderm (TE) derived from parthenogenetic or biparental gynogenetic embryos was examined in reconstituted blastocysts with normal TE or ICM, respectively. The results demonstrate that when a normal ICM was introduced inside a trophectoderm vesicle derived from parthenogenetic or gynogenetic blastocysts, postimplantation development was characterized by the almost complete failure of trophoblast proliferation and without compensating cellular contribution from the normal ICM to the outer trophoblast lineage. Consequently, the normal ICMs also failed to develop adequately and only a few retarded embryos were detected on day 11-12 of pregnancy. In most respects, development of these reconstituted blastocysts resembled that obtained with unoperated gynogenetic and a parthenogenetic blastocyst. By contrast, an ICM from a parthenogenetic or gynogenetic embryo introduced inside a normal trophectoderm vesicle induced substantial proliferation of the trophoblast but again without a detectable cellular contribution from the ICM to the outer trophoblast lineage. However, with the improved development of the trophoblast, both the parthenogenetic and gynogenetic ICMs developed substantially better and without a detectable cellular contribution from the TE to the embryo. Almost all the embryos developed at least up to the 25-somite stage and many of them reached the 30- to 40-somite stage. Some of the most advanced day-11 and -12 gynogenones and parthenogenones yet seen have now been obtained in this way. Nevertheless, all the embryos were still smaller than the equivalent control embryos and showed signs of some tissue degeneration. The yolk sac was also suboptimal with poor blood supply and may need to be improved to obtain further improvement in the development of the embryos. The combined results demonstrate that the trophoblast proliferates very poorly even in the presence of a normal ICM, if the TE tissue lacks a paternal genome. However, ICM tissues which lack a paternal genome can develop to an advanced embryonic stage if they are introduced inside a normal trophectoderm vesicle. The results give further insight into the differential roles of maternal and paternal genomes during development of the embryo and extraembryonic tissues in the mouse.

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