In the first trimester, there is also a layer of replicating mononuclear cytotrophoblasts beneath the syncytiotrophoblasts. In contrast, in mice there are three layers of trophoblasts. The outer layer consists of mononuclear cytotrophoblasts while the middle and inner layers are syncytiotrophoblastic. A simplified diagrammatic representation of the structure of Purity - Zygote - 89-91 human placenta adapted from Georgiades et al.
From the end of the Purity - Zygote - 89-91 trimester, Purity - Zygote - 89-91 blood flows into the fetal placenta via the maternal spiral arteries, through the intervillous space bathing the branches of the villous trees and out through the maternal veins red arrows on left-hand side.
The fetal blood enters via the umbilical cord and circulates to the Purity - Zygote - 89-91 capillaries in the villous trees. A layer of zygote-derived trophoblasts, in humans a syncytium of syncytiotrophoblasts, on the surface of the villous trees dark green forms the barrier between the fetal tissues and the maternal blood. Zygote-derived trophoblasts also progressively invade the placental bed and line the maternal vasculature. By the third trimester the maternal spiral arteries are lined through to the imwhile the maternal veins are lined to the border between the decidua basalis db and basal plate bp.
In the mouse, the analogue of the fetal placenta is labyrinthine and the trophoblastic invasion of the maternal blood vessels does not extend beyond the junctional zone analogous to the basal plate. Hypothesized mechanisms of fetomaternal cell traffic include i deportation of trophoblasts lining the maternal vessels and intervillous space; ii microtraumatic hemorrhage; and iii cell adhesion and transmigration across the placental barrier. Simplified diagrammatic representations of blood-brain and placental barriers and hypothesized molecular mechanisms of cell adhesion and transmigration.
A A simplified diagrammatic representation of multistep lymphocyte recognition and capture from blood at the blood brain barrier adapted from Engelhardt It is hypothesized that a similar molecular mechanism may explain fetal cell migration across the blood-brain barrier and the placental barrier.
B A simplified diagrammatic representation of the human placental barrier showing a hypothetical mechanism of fetal cell capture, adhesion and transmigration. The placental barrier comprises of fetal capillary endothelial cells fcecan endothelial basement membrane ebmthe villous core vc which at some interfaces contains pericytes p and extracellular matrix, a trophoblastic basement membrane tbmin the first trimester a layer of proliferative cytotrophoblasts ctand a multinucleated syncytium of syncytiotrophoblasts ss.
In the mouse, the trophoblastic layers differ in that there are Purity - Zygote - 89-91 syncytiotrophoblastic layers and the cytotrophoblastic layer is outermost facing the intervillous interface. It is hypothesized that fetal Manhattan - Roundtree - Discocide may adhere and transmigrate across the placental barrier in a similar manner to that by which lymphocytes cross the blood-brain barrier.
The maternal uterine tissue becomes progressively invaded by zygote-derived trophoblast cells. In particular, these cells line the maternal blood vessels in the maternal uterine tissue. In humans, trophoblast invasion extends to the inner third of the myometrium but in mice, trophoblast invasion is shallow and is limited to the decidua basalis.
The cells of the placenta itself comprise both zygote-derived and maternal cells. In mice, the zygote-derived cells include trophoblasts derived from the polar trophectoderm of the outer cell mass; fetal blood vessels and mesenchyme derived from the allantoic mesenchyme, which in turn is derived from the primitive ectoderm of the inner cell mass; and fetal blood cells of mesodermal lineage. Meanwhile, the maternal cells of the mouse placenta include uterine cells and cells coming from the maternal blood.
The similarities in Purity - Zygote - 89-91 anatomy of placentation and placental blood flow in mice and humans 3639 and the role of analogous genes in mouse and human placentation 43 make mouse Purity - Zygote - 89-91 a good model for many aspects of human placentation.
However, there are important anatomical differences, 3639 in particular the difference between the villous nature of the human fetal placenta and the labyrinthine nature of the analogous mouse labyrinth and the greater role of invasion by zygote-derived trophoblasts in the maternal circulation in the human placenta. The mechanism by which cells are exchanged across the placental barrier is unclear. Possible explanations include deportation of trophoblasts, microtraumatic rupture of the placental blood channels or that specific cell types are capable of adhesion to the trophoblasts of the walls of the fetal blood channels and migration through the placental barrier created by Purity - Zygote - 89-91 trophoblasts Fig.
Microtraumatic dislodgment of trophoblasts from the trophoblast-lined blood channels through which the maternal blood passes may also explain why trophoblasts appear in maternal circulation. The microtraumatic hypothesis of cell exchange does not appear consistent with the hypothesis that fetomaternal microchimerism may be of adaptive value to the fetus but fits well with the hypothesis that fetomaternal microchimerism is an epiphenomenon of pregnancy with potential pathological consequences.
An alternative hypothesis is that cells cross the placental barrier by mechanisms akin to the active adhesion and transmigration that occurs across Purity - Zygote - 89-91 endothelial venule HEV endothelium in peripheral lymph Rich Man (A Cappella) - St.
Paul - Rich Man (Extended Version) and at the blood-brain barrier BBB. Fetal cells crossing the placental barrier must transmigrate both the fetal capillary endothelial cell layer and the trophoblast cell layers Fig.
Once the fetal cells have crossed the fetal capillary endothelium, they must next cross the trophoblast layer. Although there is evidence for greater in vivo expression Up To The Surface - Cloud Nothings - Life Without Sound ICAM-1 on the apical surface of the villous syncytiotrophoblasts exposed to the maternal blood, Purity - Zygote - 89-91 ICAM-1 is also present throughout the stroma of the chorionic villi, 6061 although it has not been clearly established that it is expressed on the basal surface of the trophoblasts facing the villous core.
Trophoblasts also express VCAM Purity - Zygote - 89-91 the fetal cells have crossed the fetal capillary endothelial cell layer, we hypothesize that they cross the trophoblast cell layer again in a manner similar to that in which lymphocytes cross the BBB Fig. We hope that this speculative hypothesis regarding the mechanisms of fetomaternal cell traffic may stimulate further research and that future Purity - Zygote - 89-91 will determine whether active Purity - Zygote - 89-91 adhesion and transmigration occurs and elucidate the molecular mechanisms involved.
In mice, fetal cells generally first appear in the mother in the second week of pregnancy 35 see also Fig. Numbers of fetal cells are present in maternal blood by GD10 to GD12 days gestational days, the day of vaginal plug detection being designated GD0 in pregnancies from syngenic and allogenic crosses; however the cells do not appear in blood in until GD13 to GD16 in pregnancies from outbred crosses.
Maternal blood first appears in the labyrinth between GD9 and GD10 and extensive fetal capillary formation occurs by GD Plugs of invading trophoblast cells, which block the tips of the uteroplacental spiral arteries, are progressively dislocated after 10—12 weeks 70 and blood only becomes evident in the intervillous space of the fetal placenta after ten weeks gestation. Potentially there may be multiple Purity - Zygote - 89-91 types and phases of migration involved.
More detailed investigation of the time Purity - Zygote - 89-91 of the appearance of maternal blood in the placenta and the appearance of fetal cells in maternal blood in humans may be informative.
Time course of fetal Purity - Zygote - 89-91 engraftment and persistence in the mouse brain. Adult female mice received intraventricular injection of the excitotoxic NMDA to produce a diffuse brain lesion or were untreated. Procedures were as previously described. Overall, in those mothers in which fetal cells persist at four Johnny Come Home - Honey Island Swamp Band - Cane Sugar and eight weeks post partum, there are greater numbers of fetal cells in the lesioned brains.
The reason for the delay in the appearance of fetal cells in maternal blood in outbred mouse crosses is at present unknown. Outbred crosses were also observed to result in delayed and reduced trophoblast invasion of the decidua basalis. It is hoped that further studies may elucidate the issue. Intriguingly in syngenic pregnancies, fetal cells were detected in mouse lungs and to a lesser extent spleen and kidney in the first week of gestation before they robustly appear in detectable numbers in maternal circulation.
Thus one might hypothesis that the earliest phase of fetomaternal microchimerism involves deportation of zygote-derived trophoblasts as they invade the decidua basalis to line the maternal blood vasculature. Trophoblasts being large are rapidly cleared from maternal blood as they become lodged in the microvasculature of the lung and to a lesser extent other organs. While the studies discussed here have made important contributions to establishing the time course of fetomaternal traffic, the question of whether different zygote-derived cell types show different time courses of traffic has not been investigated in depth.
It is hoped that future studies will address this important issue. Fetomaternal microchimerism appears to occur with great frequency following human pregnancy.
It has been suggested that fetomaternal traffic occurs in Purity - Zygote - 89-91 pregancies. Male cells have been found in maternal blood even decades after pregnancy, 777 including in one case in which the women was last pregnant with a male child 27 years earlier.
By engrafting into niches such as the bone marrow, fetal cells may also be able to proliferate and reinfiltrate blood or other tissues later. There is strong evidence that fetal cells with the characteristics of mesenchymal cells do engraft the bone marrow. The absence of Y chromosome markers in samples from women who had never born sons in some studies 14 strongly supports the argument that the male cells observed originate from the fetus.
However, it is important to note that there are crucial caveats in the use of the Y chromosome alone as a marker for fetomaternal Strange Love - Abandon All Ships - Geeving that may have led Purity - Zygote - 89-91 over estimation of the incidence and persistence of fetomaternal microchimerism in humans.
Male cells have been found in the blood of women without sons. However, a history of unrecognized spontaneous abortions or sexual intercourse cannot explain all cases of the presence of male cells in females as another study detected the presence of the Y chromosome in normal liver from seven of eleven female fetuses and five of six female children.
Estimates of the frequency of vanishing twins range from 3. Maternofetal transfer to the mother may also have occurred if the mother's mother had a history of blood transfusion, transplantation or previous pregnancy with a male fetus. It is difficult to Purity - Zygote - 89-91 how frequently male cells in females could arise as a result of fetofetal or maternofetal transfer.
Although one might expect such events to be rare, the incidence may be high enough to have biased estimates of the incidence of fetomaternal microchimerism in humans. While the possibility that the Y chromosome could also enter the mother via microchimerism as a consequence of previous blood transfusion or transplantation has been considered in most studies, the possibility that male cells detected in Purity - Zygote - 89-91 mother may have arrived via fetofetal or maternofetal transfer to the mother in utero has not be systematically excluded.
Conclusive proof of fetomaternal microchimerism in humans would require the use of other paternal markers that differentiate between the father of the fetus and the father of the mother. One scenario might be to investigate cases where the mother and the mother's father share a genetic mutation or polymorphism not carried by the father of the fetus. In such cases, evidence of genetic markers derived from the father of the fetus in the mother could provide more conclusive evidence of fetomaternal microchimerism in humans.
If the genetic mutation or polymorphism caused disease the presence of fetal cells in the diseased tissue could also offer evidence of the potential of fetomaternal tissue repair. In contrast, to the suggestion that fetal cells are retained for decades after nearly every human pregnancy, 714 the retention of fetal cells in mice appears more sporadic and rarely persists for more than a few weeks post partum.
The use of mice bearing unique genetic markers such as, the cytogenetic marker chromosome, T6 2633 and more recently transgenic mice bearing genetic markers such as enhanced green fluorescent protein EGPF 354966 has conclusively demonstrated fetomaternal microchimerism. The number of mice in which fetal cells can be detected in maternal blood and the number of fetal cells in maternal blood declines towards the end of gestation, at least in syngenic and allogenic crosses.
However, by 6—8 weeks post partum, the number of fetal cells has fallen below (Who?) Keeps Changing Your Mind (Mix 3) - South Street Player - (Who?) Keeps Changing Your Mind limits of detection in blood and all organs studied, including uninjured brain 66 see also Fig.
Although the numbers of fetal cells present were very low, fetal cells did persist at eight weeks post partum in some of the lesioned maternal brains Fig. Together, these data suggest I Only Have Eyes For You - Various - Rock & Roll Reunion possibility that, although fetal cells are cleared from the blood and some organs within a few weeks postpartum in mothers of syngenic and allogenic crosses, some fetal cells may remain harbored longer-term in certain niches.
In contrast, fetal cells have been detected in the blood of some mice at 42 days post partum following outbred crosses. However, the duration of fetal cell Purity - Zygote - 89-91 in those few mice in which fetal cells do persist has not been systematically investigated. The reasons for the large individual differences in the numbers of fetal cells retained and the duration of retention are not known. During pregnancy the mother develops immune tolerance to the fetus but after pregnancy this suppression of the maternal immune response to the fetus is lifted.
This might explain why fetomaternal microchimerism does not persist in all mothers. The greater preservation of fetal cells in the brain than the blood would be consistent with an immune Purity - Zygote - 89-91 hypothesis, the brain being an immune privileged site.
Although some differences between the mother and fetus may be an advantage as it has been noted that, despite reducing placental expression of major histocompatibility complex MHC genes, major histocompatibility complex expression is often reestablished in the most invasive trophoblast cells and may contribute to an immunoprotective effect on the fetus. In conclusion, although it has not been studied systematically and there are obvious methodological Purity - Zygote - 89-91 between the mouse and human studies, there appears to greater likelihood of long-term retention of microchimeric fetal cells in humans than in mice.
This difference in the retention of fetal cells may be consistent with the hypothesis that fetomaternal microchimerism has developed as a mechanism by which the Purity - Zygote - 89-91 ensures maternal fitness.
As mice wean their offspring by 3—4 weeks postpartum, there would be no need for the fetal cells to continue to survive.
In contrast, human mothers nurse their offspring for many months and thereafter continue to nurture their offspring for many decades so there may be an adaptive advantage to fetal cell persistence.
Alternatively, if fetal cells have adverse effects on the mother, it may be that rodents have developed greater maternal resistance to fetal cell infiltration as they have far more offspring over a far shorter life span. Intriguingly, there may in fact be greater retention of fetal cells in outbred mice than in syngenic or allogenic crosses. It is hoped that future studies may investigate the determinants of fetal cell retention.
The immunological hypothesis would predict that immunosuppression from late Purity - Zygote - 89-91 and through the post-partum period would increase fetomaternal microchimerism. Another hypothesis might be that hormonal changes coinciding with the later stages of pregnancy and the post partum period lead to rejection of fetal cells. This hypothesis would predict greater fetomaternal microchimerism in mother who did not complete the normal hormonal sequela of delivery and peri- and post-partum hormonal changes.
In humans, there is indeed evidence that spontaneous and induced abortions increase the frequency and level of male microchimerism, 7985 but this may equally be explained by Purity - Zygote - 89-91 associated with abortion leading to greater fetomaternal exchange.
The microchimeric fetal cells in Purity - Zygote - 89-91 mother appear to be of multilineage potential. Y chromosome bearing cells have been identified in numerous tissues, including skin, liver, kidney and bone marrow, in healthy women and in women with autoimmune diseases 86 — 92 and other none immune diseases such as hepatitis C 93 and cervical cancer.
This suggests the possibility that fetal cells may target to specific tissues and contribute to tissue repair or function. There are various manners in which fetal cells might come to target damaged tissue. Sometimes the mechanism by which the zygote-derived cells are sequestered in particular tissues may be mechanical Purity - Zygote - 89-91 has been hypothesized for the entrapment of large trophoblast cells in the capillaries Wham!
- Im Your Man the microvasculature of the lung. Another hypothesis is that fetal cells invade all maternal tissues but only find a niche conducive to survival in damaged tissues.
Alternatively, if this You Just Got To Be In Love - Boris Gardiner - I Want To Wake Up With You The Best Of Boris Gardiner a process that has evolved to allow the fetus Purity - Zygote - 89-91 treat the mother to enhance fetal survival, the fetal cells may actively invade the damaged tissue by a physiological mechanism of adhesion and transmigration across the blood Purity - Zygote - 89-91 walls followed by active migration through the tissue to sites of damage.
Recently, Khosrotehrani and colleagues 98 have used in vivo bioluminescence imaging of fetal cells in which the paternal marker was VEGF receptor 2 promoter controlled luciferase gene expression to demonstrate that fetal cells contribute to neoangiogenesis. This in vivo bioimaging approach will be extremely valuable in determining the extent to which fetal cells invade damaged tissues. Tracking genetically modified fetal cells or the behaviour of fetal cells in genetically modified mothers it may be possible ADHD - ADHD 2 address important questions about the mechanisms by which fetal cells engraft maternal tissues and home in on injured tissue.
The fetal cell type or types responsible for fetomaternal microchimerism are unknown. Candidates include all cell types in fetal blood and trophoblasts. However, considerable evidence points towards the conclusion that fetal stem or progenitor cells may also be involved. Subsequent pregnancies appear to trigger further proliferation and mobilization to maternal blood of fetal cells acquired during previous pregnancies.
Moreover, women with older sons have a greater number of male cells suggesting proliferation over time. This evidence that fetal cells can proliferate in the mother is fairly persuasive, but the alternative possibility that the fetal cells engraft in one niche and then subsequently remobilize to another niche without increasing in number has not been excluded.
Fetal cells appear indistinguishable from maternal tissues years after pregnancy and can Purity - Zygote - 89-91 epithelial, leukocyte, hematopoietic, hepatocytic, renal or cardiomyocytic markers. In injured mouse brain, we have found fetal cells expressing various morphologies, localization and immunocytochemically stained protein markers characteristic of various brain cell types including perivascular macrophages, neurons, astrocytes and oligodendrocytes.
Notably there have yet to be clear-cut examples of functional differentiation of microchimeric fetal cells. For example, it would be important to show that apparent neuronal differentiation does not just involve location, morphology and expression of a few protein markers but instead that this differentiation leads to functional neuronal characteristics such as the capacity to fire action potentials and synaptic connectivity to repair damaged circuitry.
Yong, P. Antibodies against the C-terminal peptide of rabbit oviductin inhibit Purity - Zygote - 89-91 early embryo development to pass 2-cell stage. Cell Research 12, 69—78, doi: King, R. Effect of bovine oviductal estrus-associated protein on the ability of sperm to capacitate and fertilize oocytes. Journal of Andrology 15, — Yang, X. Plos One 10, 24, doi: Boatman, D. Identification of a sperm penetration factor in the oviduct of the golden-hamster. Biology of Reproduction 52, —, doi: OdayBowman, M.
Association of oviduct-specific glycoproteins with human and baboon Papio anubis ovarian oocytes and enhancement of human sperm binding to human hemizonae following in vitro incubation. Biology of Reproduction 54, Purity - Zygote - 89-91doi: Pradeep, M. Purification, sequence characterization and effect of goat oviduct-specific glycoprotein on in vitro embryo development.
Theriogenology 75, —, doi: Coy, P. Oviduct-specific glycoprotein and heparin modulate sperm-zona pellucida interaction Jimmy Jimmy - Hélène - Ce Train Qui SEn Va fertilization and contribute to the control of polyspermy. McCauley, T. Oviduct-specific glycoprotein modulates sperm-zona binding and improves efficiency of porcine fertilization in vitro.
Biology of Reproduction 69, —, doi: Kouba, A. Effects of the porcine oviduct-specific glycoprotein on fertilization, polyspermy and embryonic development in vitro. Biology of Reproduction 63, —, doi: Buhi, W. Characterization and biological roles of oviduct-specific, oestrogen-dependent glycoprotein. Reproduction— Kadam, K. Identification of cellular isoform of oviduct-specific glycoprotein: role in oviduct tissue remodeling?
These Eyes (Have Seen) - Biohazard - No Holds Barred - Live In Europe and Tissue Research—, doi: Kan, F.
Immunolocalization of oviductin in endocytic compartments in the blastomeres of developing embryos in the golden-hamster. Biology of Reproduction 48, 77—88, doi: Bokhove, M. Purity - Zygote - 89-91 mammalian expression and crystallography of maltose-binding protein-fused human proteins. Journal of structural biology1—7, doi: Immunogold localization of porcine oviductal secretory proteins within the zona-pellucida, perivitelline space and plasma-membrane of oviductal and uterine oocytes and early embryos.
Biology of Reproduction 48, —, doi: Boice, M. Localization of oviductal glycoproteins within the zona-pellucida and perivitelline space of ovulated ova and early embryos in baboons papio-anubis.
Purity - Zygote - 89-91 of Reproduction 43, —, doi: Gandolfi, F. Oviduct ampullary epithelium Purity - Zygote - 89-91 a glycoprotein to the zona-pellucida, perivitelline space and blastomeres membrane of sheep embryos.
European Journal of Basic and Applied Histochemistry 35, — Mondejar, I. The human is an exception to the evolutionarily-conserved phenomenon of pre-fertilization zona pellucida resistance to proteolysis induced by oviductal fluid. Human Reproduction 28, —, doi: Swanson, W. Positive Darwinian selection drives the evolution of several female reproductive proteins in mammals. Malette, B. Oviductins possess chitinase-like and mucin-like domains - a lead in the search for the biological function of these oviduct-specific zp-associating glycoproteins.
Molecular Reproduction and Development 41, —, doi: Bioscience 65, —, doi: Evidence or modifications of carbohydrate residues in the mouse ovarian zona pellucida during the folliculogenesis. Molecular Biology of the Cell 7, — Cytochemical demonstration of modification of carbohydrates in the mouse zona pellucida during folliculogenesis.
Histochemistry and cell biologyMessin The Blues - Robin Trower - The Steel Album, doi: Oikawa, T. A glycoprotein of oviductal origin alters biochemical-properties of the zona pellucida of hamster egg.
Gamete Research 19, —, doi: Robitaille, G. Characterization of an oviductal glycoprotein associated with the ovulated hamster oocyte.
Biology of Reproduction 38, —, doi: Kolbe, T. Differences in proteinase digestibility of the zona pellucida of in vivo and in vitro derived porcine oocytes and embryos. Theriogenology 63, —, doi: Calafell, J. Zona-pellucida surface of immature and in vitro matured mouse oocytes - analysis by scanning electron-microscopy.
Journal of Assisted Reproduction and Genetics 9, —, doi: Familiari, G. Purity - Zygote - 89-91 zona-pellucida during in vitro fertilization - an ultrastructural-study using saponin, ruthenium red and osmium-thiocarbohydrazide.
Molecular Reproduction and Development 32, 51—61, doi: Motta, P. Microstructural events of human egg investments during in vitro fertilization. Ultrastructure of the zona pellucida and cumulus oophorus. Papi, M. Mechanical properties of zona pellucida hardening. European Biophysics Journal with Biophysics Letters 39, —, doi: Recklies, A. The chitinase 3-like protein human cartilage glycoprotein 39 HC-gp39 stimulates proliferation of human connective-tissue cells and activates both extracellular signal-regulated kinase- and protein kinase beta-mediated signalling pathways.
Biochemical Journal—, doi: Ling, H. The chitinase 3-like protein human cartilage glycoprotein 39 inhibits cellular responses to the inflammatory cytokines interleukin-1 and tumour necrosis factor-alpha.
Biology of Reproduction 89, 8, doi: Lyng, R. Mouse oviduct-specific glycoprotein is an egg-associated Purity - Zygote - 89-91 sperm-adhesion ligand. Journal of Cell Science—, doi: Schmidt, A. Species-specific effect of oviductal glycoproteins on hamster sperm binding to hamster oocytes.
Molecular Reproduction and Development 46, —, doi: Wassarman, P. Structure of the mouse egg extracellular coat, the zona-pellucida. Monne, M. Biology of Reproduction 85, —, doi: Miwa, N. Fertilization competence of the egg-coating envelope is regulated by direct interaction of dicalcin and gp41, the Xenopus laevis ZP3. Special equipment- Only roll if Divergent or Unique Organisation was selected d Traditional Weapon: The Chapter favours one specific weapon over all others.
A Battle- Brother from this Chapter would never be caught without Purity - Zygote - 89-91 an icon on their person. Example: Chapter Heraldry on a necklace, Imperial Aquilla tattooed over the right eye. Examples: Fenrisian Wolf, hunting birds. It is seen as a symbol of honour to wield one of these weapons in battle. Examples: Fenrisian Wolf, Carnodon, very angry Grox.
While the traditional Space Marine vehicle is the Rhino, other Chapters may use more rare vehicles as primary transport. Examples: Power Sabre, Bolt Pistol with weighted butt for clubbing.
What form do the Chapters' beliefs take? The big E Purity - Zygote - 89-91 where it's at. Yeah, we're going to stick that everywhere. They're weird. At what strength is the Chapter? If recovery is even possible it will take many decades, making every Battle-Brother and his Progenoids an invaluable resource. It is probably at a minimum of half strength, and should return to nominal strength within a decade. In all likelihood most every squad consist of ten brethren and some specialised appointments may be empty, but the Chapter is regarded as fully fit for battle.
Who are your Chapter friendly with? Strategic Prognostication - "Our tarot cards say there's going to be a threat here, maybe. A New Generation - Gene-seed is slightly divergent usually because of attempts to breed out flaws, real or notleading to the Chapter being less linked to its progenitor.
Altered Stock - Gene-seed is altered and some implants are deficient - roll one Purity - Zygote - 89-91 Deficiencies table. Flawed - Chapter's gene-seed is flawed and sets them apart from their progenitor - roll on Chapter Flaws table. Swift As The Wind - Going slowly and thinking things out? Cleanse and Purify - Not destroy everything? No Mercy, No Respite - Let the enemy go so we can follow them? Purity Above All - Mutants? Scions of Mars - Flesh is strong?
Suffer Not the Alien to Live - Xenos? Suffer Not the Work of Heretics Purity - Zygote - 89-91 Heretics? Brothers in Battle - Hos before bros?
Uphold the Honour of the Emperor - Performing unheroic acts? Hyper-stimulated Omophagea - Eat the enemy! Oversensitive Occulobe - "I'm in the dark and I can see perfectly!
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