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Journal articles on the topic 'Complement 5'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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1

Justice, Monica J., and Vernon C. Bode. "Three ENU-induced alleles of the murine quaking locus are recessive embryonic lethal mutations." Genetical Research 51, no. 2 (April 1988): 95–102. http://dx.doi.org/10.1017/s0016672300024101.

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SummaryThe quaking (qk) locus on mouse chromosome 17 has been defined by a single viable quaking allele. Three new alleles of quaking were selected after ENU mutagenesis by their failure to complement the quaking phenotype. The qkk2 allele was induced on wild-type chromatin and the qkkt1 and qkkt4 alleles were induced on t-chromatin. Each is a recessive embryonic lethal mutation. They fail to complement each other and are not complemented by the deletion, TtOrl. Homozygotes and hemizygotes die at 8–9·5 days gestation, but not at a single precise time. Because the classical quaking mutation complements the lethality of these new alleles, but they fail to complement its quaking phenotype (myelination defect), we conclude that the quaking+ function is required for embryonic survival as well as for myelination.

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2

Boylston, A. W., and Fiona Lancaster. "Complement." Immunology Today 9, no. 12 (December 1988): 401. http://dx.doi.org/10.1016/0167-5699(88)91245-5.

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3

Andersen, Gregers Rom, Nick Laursen, Folmer Fredslund, and Lars Sottrup-Jensen. "Structure of human complement component 5." Acta Crystallographica Section A Foundations of Crystallography 65, a1 (August 16, 2009): s14. http://dx.doi.org/10.1107/s0108767309099784.

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4

Liem, Vo Thanh, and Gerard A. Venema. "On the Asphericity of Knot Complements." Canadian Journal of Mathematics 45, no. 2 (April 1, 1993): 340–56. http://dx.doi.org/10.4153/cjm-1993-016-5.

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AbstractTwo examples of topological embeddings of S2 in S4 are constructed. The first has the unusual property that the fundamental group of the complement is isomorphic to the integers while the second homotopy group of the complement is nontrivial. The second example is a non-locally flat embedding whose complement exhibits this property locally.Two theorems are proved. The first answers the question of just when good π1 implies the vanishing of the higher homotopy groups for knot complements in S4. The second theorem characterizes local flatness for 2-spheres in S4 in terms of a local π1 condition.

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5

Davies, Kevin A. "7 Complement." Baillière's Clinical Haematology 4, no. 4 (December 1991): 927–55. http://dx.doi.org/10.1016/s0950-3536(06)80037-5.

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6

Kimura, Yuko, Mayur Madhavan, Mindy K. Call, William Santiago, Panagiotis A. Tsonis, John D. Lambris, and Katia Del Rio-Tsonis. "Expression of Complement 3 and Complement 5 in Newt Limb and Lens Regeneration." Journal of Immunology 170, no. 5 (March 1, 2003): 2331–39. http://dx.doi.org/10.4049/jimmunol.170.5.2331.

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7

Fredslund, Folmer, Nick S. Laursen, Pietro Roversi, Lasse Jenner, Cristiano L. P. Oliveira, Jan S. Pedersen, Miles A. Nunn, et al. "Structure of and influence of a tick complement inhibitor on human complement component 5." Nature Immunology 9, no. 7 (June 8, 2008): 753–60. http://dx.doi.org/10.1038/ni.1625.

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8

Lachmann, P. J., and M. J. Hobart. "Genetics of complement." Trends in Genetics 1 (January 1985): 145–50. http://dx.doi.org/10.1016/0168-9525(85)90057-5.

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9

Reid, Kenneth. "The complement system." Immunology Today 10, no. 2 (February 1989): 67–68. http://dx.doi.org/10.1016/0167-5699(89)90312-5.

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10

Orren, A., T. Owen, P. C. Potter, F. Leisegang, B. P. Morgan, and R. Wurzner. "Complement component 5 deficiency (C5D) in South Africa." Molecular Immunology 48, no. 14 (August 2011): 1683. http://dx.doi.org/10.1016/j.molimm.2011.06.273.

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11

Pipattanajinda, Nirutt, and Yangkok Kim. "TREES WITH DIAMETER 5 AND NON-SINGULAR COMPLEMENT." Advances and Applications in Discrete Mathematics 16, no. 2 (November 2, 2015): 111–24. http://dx.doi.org/10.17654/aadmoct2015_111_124.

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12

Chen, Qian, Melanie Manzke, Andrea Hartmann, Maike Büttner, Kerstin Amann, Diana Pauly, Michael Wiesener, Christine Skerka, and Peter F. Zipfel. "Complement Factor H-Related 5-Hybrid Proteins Anchor Properdin and Activate Complement at Self-Surfaces." Journal of the American Society of Nephrology 27, no. 5 (October 2, 2015): 1413–25. http://dx.doi.org/10.1681/asn.2015020212.

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13

Fredslund, Folmer, Nick S. Laursen, Pietro Roversi, Lasse Jenner, Cristiano L. P. Oliveira, Jan S. Pedersen, Miles A. Nunn, et al. "Erratum: Structure of and influence of a tick complement inhibitor on human complement component 5." Nature Immunology 9, no. 8 (August 2008): 945. http://dx.doi.org/10.1038/ni0808-945.

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14

Smith, G. "Membrane-targeted complement inhibitors." Molecular Immunology 38, no. 2-3 (August 2001): 249–55. http://dx.doi.org/10.1016/s0161-5890(01)00047-5.

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15

Schifferli, J. A. "Complement and immune complexes." Research in Immunology 147, no. 2 (January 1996): 109–10. http://dx.doi.org/10.1016/0923-2494(96)87183-5.

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16

Mattacks, Christine A., and Caroline M. Pond. "The effects of dietary restriction and exercise on the volume of adipocytes in two intra-orbital depots in the guinea-pig." British Journal of Nutrition 53, no. 2 (March 1985): 207–13. http://dx.doi.org/10.1079/bjn19850028.

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1. The volume of adipocytes in two intra-orbital sites and fourteen superficial and intra-abdominal sites, and the total adipocyte complement have been measured in virgin and reproductive guinea-pigs maintained on several different regimens of diet and exercise.2. The adipocytes around the ocular muscles at the back of the orbit (peripheral fat) are always larger than those just behind the eyeball (orbital fat).3. The adipocytes in both the intra-orbital sites are significantly larger in guinea-pigs whose total adipocyte complement is smaller than one standard deviation from the mean, than in those which have a normal-size or large adipocyte complement.4. The volume of intra-orbital adipocytes correlates very significantly with the volume of adipocytes in superficial and intra-abdominal sites in guinea-pigs which have large adipocyte complements, correlates weakly in those with normal adipocyte complements and not at all in those with small adipocyte complements.5. It is suggested that there may be fewer intra-orbital adipocytes in animals which have small adipocyte complements, and that, because the intra-orbital adipose tissue occupies a constant volume, the adipocytes in these sites become larger when they are less numerous.

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17

Rasool, Dr Khetam Habeeb. "Evaluation of Immunoglobulins, Complement and Interleukine-6 in Serum of Iraqi Sepsis Neonates." Indian Journal of Applied Research 4, no. 7 (October 1, 2011): 16–18. http://dx.doi.org/10.15373/2249555x/july2014/5.

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18

Chai, L., Y. Q. Song, K. Y. Zee, and W. K. Leung. "Single nucleotide polymorphisms of complement component 5 and periodontitis." Journal of Periodontal Research 45, no. 3 (June 2010): 301–8. http://dx.doi.org/10.1111/j.1600-0765.2009.01234.x.

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19

Wilk, C. Matthias. "Coronaviruses hijack the complement system." Nature Reviews Immunology 20, no. 6 (April 14, 2020): 350. http://dx.doi.org/10.1038/s41577-020-0314-5.

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20

Tincani, Angela, Ilaria Cavazzana, Tamara Ziglioli, Andrea Lojacono, Valentina De Angelis, and Pierluigi Meroni. "Complement Activation and Pregnancy Failure." Clinical Reviews in Allergy & Immunology 39, no. 3 (November 11, 2009): 153–59. http://dx.doi.org/10.1007/s12016-009-8183-5.

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21

Villiers, C. L., L. A. Perrin-Cocon, S. Chesne, and P. N. Marche. "Antigen targeting by complement receptors." Immunopharmacology 49, no. 1-2 (August 2000): 48. http://dx.doi.org/10.1016/s0162-3109(00)80143-5.

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22

Seifert, Paul S., and Michel D. Kazatchkine. "The complement system in atherosclerosis." Atherosclerosis 73, no. 2-3 (October 1988): 91–104. http://dx.doi.org/10.1016/0021-9150(88)90030-5.

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23

Kavanagh, David, and Tim Goodship. "Genetics and complement in atypical HUS." Pediatric Nephrology 25, no. 12 (June 6, 2010): 2431–42. http://dx.doi.org/10.1007/s00467-010-1555-5.

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24

Mironova, Anna A., and Lydia A. Shenshina. "Private and public transfers: substitute or complement?" Population and Economics 5, no. 2 (June 30, 2021): 1–15. http://dx.doi.org/10.3897/popecon.5.e60293.

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The paper analyzes the relationship between private and public social transfers in Russia. The research relies on the data from the Russian Longitudinal Monitoring Survey (RLMS-HSE) carried out by the Higher School of Economics in 1994–2018. The household is the unit of the analysis, the method of logistic regression is applied. The study has shown that when a household receives public social transfers, it is less likely to receive private transfers. So, the findings appear to bear out the hypothesis that public transfers crowd out private transfers in Russia.

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25

Baas, Dominique C., Lintje Ho, Sarah Ennis, Joanna E. Merriam, Michael W. T. Tanck, André G. Uitterlinden, Paulus T. V. M. de Jong, et al. "The Complement Component 5 Gene and Age-Related Macular Degeneration." Ophthalmology 117, no. 3 (March 2010): 500–511. http://dx.doi.org/10.1016/j.ophtha.2009.08.032.

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26

Gervacio, Severino V. "Trees with diameter less than 5 and non-singular complement." Discrete Mathematics 151, no. 1-3 (May 1996): 91–97. http://dx.doi.org/10.1016/0012-365x(94)00086-x.

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27

Rogne, Sissel, Ola Myklebost, Keith Stanley, and Ad Geurts van Kessel. "The gene for human complement C9 is on chromosome 5." Genomics 5, no. 1 (July 1989): 149–52. http://dx.doi.org/10.1016/0888-7543(89)90100-6.

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28

Nielsen, K., and J. R. Duncan. "Bovine IgM: Does it fix guinea pig complement in the absence of bovine complement components?" Veterinary Immunology and Immunopathology 14, no. 4 (April 1987): 335–43. http://dx.doi.org/10.1016/0165-2427(87)90036-5.

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29

Takematou, Hideaki, and Hachiro Tagami. "Assessment of complement activation in psoriasis by use of complement fragment C4d and Bb measurement." Journal of Dermatological Science 1, no. 2 (March 1990): 114. http://dx.doi.org/10.1016/0923-1811(90)90234-5.

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30

Carlsson, Hanna, Kerstin Sandholm, Haben Woldu Haddish, Lars Brudin, Kristina Nilsson Ekdahl, and Ivar Tjernberg. "Complement activation in individuals with previous subclinical Lyme borreliosis and patients with previous Lyme neuroborreliosis." European Journal of Clinical Microbiology & Infectious Diseases 39, no. 5 (December 31, 2019): 855–62. http://dx.doi.org/10.1007/s10096-019-03807-5.

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AbstractLyme borreliosis (LB) is caused by Borrelia burgdorferi and infection may lead to not only a large variety of clinical manifestations but also a subclinical outcome. The aim of the present study was to investigate if there is a constitutional difference in complement activation between individuals with previous subclinical Lyme borreliosis (SB) and patients previously diagnosed with Lyme neuroborreliosis (LNB).Lepirudin plasma for activation studies was collected from 60 SB individuals and from 22 patients pre-diagnosed with LNB. The plasma was incubated with live Borrelia spirochetes of two strains (complement sensitive B. garinii Lu59 and complement resistant B. afzelii ACA1).Complement factor C3 was measured in non-activated lepirudin plasma with immune-nephelometry and C3a and sC5b-9 generated during complement activation were measured by enzyme-linked immunosorbent assay.We found that the complement sensitive Lu59 induced higher complement activation than the complement resistant ACA1 when measuring activation products C3a and sC5b-9 in SB and LNB patients, p < 0.0001. No significant difference was found between SB and LNB patients in systemic levels of C3. Furthermore, SB individuals generated a higher activation of C3 cleavage to C3a (C3a/C3 ratio) than LNB patients after activation with ACA1, p < 0.001, but no significant differences were found in response to Lu59. In conclusion, Lu59 induced higher complement activation than ACA1 and individuals with previous SB showed increased generation of C3a compared with patients with previous LNB. In our study population, this mechanism could lead to less elimination of spirochetes in LNB patients and thereby be a factor contributing to the clinical outcome.

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31

Bahia El Idrissi, Nawal, Pranab K. Das, Kees Fluiter, Patricia S. Rosa, Jeroen Vreijling, Dirk Troost, B. Paul Morgan, Frank Baas, and Valeria Ramaglia. "M. leprae components induce nerve damage by complement activation: identification of lipoarabinomannan as the dominant complement activator." Acta Neuropathologica 129, no. 5 (March 15, 2015): 653–67. http://dx.doi.org/10.1007/s00401-015-1404-5.

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32

Xu, Lantao, and Yanyan Wu. "Pathways of Complement Activation Following Intestinal Ischemia-Reperfusion in Macaque." Journal of Medical Biochemistry 31, no. 3 (July 1, 2012): 228–33. http://dx.doi.org/10.2478/v10011-012-0004-3.

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Pathways of Complement Activation Following Intestinal Ischemia-Reperfusion in MacaqueComplement activation is a key component in the inflammation cascade. In the present study, intestinal ischemia-reperfusion (IIR) was introduced to macaques, and the pathways of complement activation in the multiple organ dysfunction syndrome (MODS) following IIR were investigated, which may provide evidence on the mechanisms underlying the endogenous protection in systemic inflammatory response. IIR was performed by clamping superior mesenteric artery and releasing clamp in 5 macaques. Immunization rate nephelometry and CH50 total complement detection were employed to measure the serum concentration of C3, C4, C-reactive protein (CRP) and total complements. Immunocytochemistry was carried out to detect the contents of IL-1 and NF-κB in polymorphonuclear cells (PMN). Flow cytometry was done to measure the apoptosis rate of PMN. At 24 h after IIR, the amount of total complement (106.6±18.07 U/mL) was reduced to 62.1±9.52 U/mL (p<0.05). In addition, the C3 was reduced by 30% (p<0.05) but C4 remained unchanged after IIR (0.1342±0.07 vs 0.1420±0.06, P>0.05). The apoptosis rate (15.4%±1.14%) of PMN was markedly reduced (3.5%±0.53%) following IIR (p<0.05) accompanied by increased contents of IL-1 and NF-κB. Moreover, CRP was also significantly elevated after IIR (4.33±1.13 mg/L vs 17.73±0.86 mg/L; p<0.01). Following IIR, complements are activated through the alternative pathway. Complement activation fragments can inhibit the apoptosis of PMN and elevate the expressions of acute phase inflammatory proteins including CRP and IL-1, which promotes the inflammation cascade and facilitates the occurrence of MODS.

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33

Johnson, John B., Ken Grant, and Griffith D. Parks. "The Paramyxoviruses Simian Virus 5 and Mumps Virus Recruit Host Cell CD46 To Evade Complement-Mediated Neutralization." Journal of Virology 83, no. 15 (May 20, 2009): 7602–11. http://dx.doi.org/10.1128/jvi.00713-09.

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ABSTRACT The complement system is a critical component of the innate immune response that all animal viruses must face during natural infections. Our previous results have shown that treatment of the paramyxovirus simian virus 5 (SV5) with human serum results in deposition of complement C3-derived polypeptides on virion particles. Here, we show that the virion-associated C3 component includes the inactive form iC3b, suggesting that SV5 may have mechanisms to evade the host complement system. Electron microscopy, gradient centrifugation, and Western blot analysis indicated that purified SV5 virions derived from human A549 cells contained CD46, a plasma membrane-expressed regulator of complement that acts as a cofactor for cleavage and inactivation of C3b into iC3b. In vitro cleavage assays with purified complement components showed that SV5 virions had C3b cofactor activity, resulting in specific factor I-mediated cleavage of C3b into inactive iC3b. SV5 particles generated in CHO cells, which do not express CD46, did not have cofactor activity. Conversely, virions derived from a CHO cell line that was engineered to overexpress human CD46 contained elevated levels of virion-associated CD46 and displayed enhanced C3b cofactor activity. In comparison with C3b, purified SV5 virions had very low cofactor activity against C4b, consistent with the known preference of CD46 for C3b versus C4b. Similar results were obtained for the closely related mumps virus (MuV), except that MuV particles derived from CHO-CD46 cells had higher C4b cofactor activity than SV5 virions. In neutralization assays with human serum, SV5 and MuV containing CD46 showed slower kinetics and more resistance to neutralization than SV5 and MuV that lacked CD46. Our results support a model in which the rubulaviruses SV5 and MuV incorporate cell surface complement inhibitors into progeny virions as a mechanism to limit complement-mediated neutralization.

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34

Bova, G., A. L. Pasqui, M. Saletti, and A. Auteri. "P41 Complement system in myocardial infarction." Atherosclerosis 145 (July 1999): S21. http://dx.doi.org/10.1016/s0021-9150(99)90185-5.

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35

Tedesco, F., F. Fischetti, M. Pausa, A. Dobrina, R. B. Sim, and M. R. Daha. "Complement-endothelial cell interactions: pathophysiological implications." Molecular Immunology 37, no. 1-2 (January 2000): 91. http://dx.doi.org/10.1016/s0161-5890(00)00036-5.

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36

Veerhuis, R., I. Janssen, S. S. Zahn, and P. Eikelenboom. "Complement components in Alzheimer's disease brain." Journal of Neuroimmunology 54, no. 1-2 (October 1994): 203. http://dx.doi.org/10.1016/0165-5728(94)90566-5.

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37

Fishelson, Zvi. "Cell triggering by activated complement components." Immunology Letters 11, no. 5-6 (January 1985): 261–76. http://dx.doi.org/10.1016/0165-2478(85)90107-5.

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38

Vatandoost, Ebrahim, and Yasser Golkhandypour. "Domination in Commuting Graph and its Complement." Iranian Journal of Science and Technology, Transactions A: Science 41, no. 2 (June 13, 2016): 383–91. http://dx.doi.org/10.1007/s40995-016-0028-5.

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39

Li, Yujia, and Griffith Parks. "Relative Contribution of Cellular Complement Inhibitors CD59, CD46, and CD55 to Parainfluenza Virus 5 Inhibition of Complement-Mediated Neutralization." Viruses 10, no. 5 (April 25, 2018): 219. http://dx.doi.org/10.3390/v10050219.

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40

Jo, Dong Hyun, Jin Hyoung Kim, Wonjun Yang, Hyori Kim, Shinjae Chang, Dongjo Kim, Minseok Chang, Kihwang Lee, Junho Chung, and Jeong Hun Kim. "Anti-complement component 5 antibody targeting MG4 domain inhibits choroidal neovascularization." Oncotarget 8, no. 28 (April 19, 2017): 45506–16. http://dx.doi.org/10.18632/oncotarget.17221.

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41

Gyapon-Quast, Frederick, Elena Goicoechea de Jorge, Talat Malik, Nian Wu, Jin Yu, Wengang Chai, Ten Feizi, Yan Liu, and Matthew C. Pickering. "Defining the Glycosaminoglycan Interactions of Complement Factor H–Related Protein 5." Journal of Immunology 207, no. 2 (June 30, 2021): 534–41. http://dx.doi.org/10.4049/jimmunol.2000072.

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42

Chang, Te Jen, Ping Sheng Huang, Shan Jen Cheng, Ching Yin Chen, and I. Hui Pan. "Low-Complexity Multiplication Using Complement and Signed-Digit Recoding Methods." Applied Mechanics and Materials 619 (August 2014): 342–46. http://dx.doi.org/10.4028/www.scientific.net/amm.619.342.

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In this paper, a fast multiplication computing method utilizing the complement representation method and canonical recoding technique is proposed. By performing complements and canonical recoding technique, the number of partial products can be reduced. Based on these techniques, we propose algorithm provides an efficient multiplication method. On average, our proposed algorithm to reduce the number of k-bit additions from (0.25k+logk/k+2.5) to (k/6 +logk/k+2.5), where k is the bit-length of the multiplicand A and multiplier B. We can therefore efficiently speed up the overall performance of the multiplication. Moreover, if we use the new proposes to compute common-multiplicand multiplication, the computational complexity can be reduced from (0.5 k+2 logk/k+5) to (k/3+2 logk/k+5) k-bit additions.

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43

Sapozhnikov, Valeriy, Vladimir Sapozhnikov, Dmitriy Efanov, and Dmitriy Pyvovarov. "Application of constant-weight code "1-out-if-5" for the organization of combinational circuits check." Proceedings of Petersburg Transport University, no. 2 (June 20, 2017): 307–19. http://dx.doi.org/10.20295/1815-588x-2017-2-307-319.

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Objective: To study specificities of “1-out of-5”equilibrium code application in the process of concurrent error detection of combinational logic circuits organization. Methods: Information and coding theories, as well as technical diagnostics of discrete systems were applied. Results: It was suggested to apply a “1-out of-5”equilibrium code in organizing of combinational circuits control by means of Boolean complement method, the tester of which has a simple structure and needs five testing patterns for its full check. The calculation method of Boolean complement functions was given; the former makes it possible to provide testability of a Boolean complement block and a tester within a checking circuit. The advantages of a “1-out of-5”equilibrium code application were presented, compared to the usage of other equilibrium codes with a shorter length of a code word for organization of combinational circuits’ check. Practical importance: The application of a “1-out of-5”equilibrium code for organization of combinational circuits’ check is promising for self-checking discrete automatic and calculating machines.

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44

Cunnion, K. M., H. M. Zhang, and M. M. Frank. "Availability of Complement Bound to Staphylococcus aureus To Interact with Membrane Complement Receptors Influences Efficiency of Phagocytosis." Infection and Immunity 71, no. 2 (February 2003): 656–62. http://dx.doi.org/10.1128/iai.71.2.656-662.2003.

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ABSTRACT Complement-mediated opsonization of encapsulated Staphylococcus aureus (CP+) of the predominant capsule types, 5 and 8, remains poorly understood. Our previous work showed that complement is important for mouse survival of CP+ type 5 bacteremia and that the type 5 capsule inhibits the binding of opsonic C3 fragments to the organism. The importance of complement-mediated opsonization of CP+ was tested by neutrophil phagocytosis assays. Complement-mediated opsonization of CP+ increased phagocytosis by 57% compared to opsonization in complement-inhibited serum. Agar-grown CP+, enhancing capsule expression, was phagocytosed only one-tenth as well as the capsule-negative organisms (CP−), supporting the belief that staphylococcal polysaccharide capsules impair phagocytosis. Despite relatively poor phagocytosis of CP+ compared to CP−, complement activation increased the phagocytosis of CP+ by 103%. Thus, complement in normal human serum may have an important role in opsonizing CP+, even when capsule expression is strong. The ability of bound C3 fragments to interact with complement receptor 1 (CD35) on the membrane of human erythrocytes was tested in an immune adherence assay. S. aureus capsule was able to mask C3 fragments on the organism from binding to complement receptor 1. The inhibition of C3 binding to CP+ and the masking of deposited C3 fragments caused by the presence of capsule was associated with markedly decreased phagocytosis. The addition of anti-capsule antibodies to normal human serum was found to markedly improve the recognition of deposited C3 fragments by complement receptor 1 even when the absolute number of C3 molecules bound to S. aureus was not increased.

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45

Yap, Kai Lee, Michael J. Hafez, Tsui-Lien Mao, Robert J. Kurman, Kathleen M. Murphy, and Ie-Ming Shih. "Lack of a Y-Chromosomal Complement in the Majority of Gestational Trophoblastic Neoplasms." Journal of Oncology 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/364508.

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Gestational trophoblastic neoplasms (GTNs) are a rare group of neoplastic diseases composed of choriocarcinomas, placental site trophoblastic tumors (PSTTs) and epithelioid trophoblastic tumors (ETTs). Since these tumors are derivatives of fetal trophoblastic tissue, approximately 50% of GTN cases are expected to originate from a male conceptus and carry a Y-chromosomal complement according to a balanced sex ratio. To investigate this hypothesis, we carried out a comprehensive analysis by genotyping a relatively large sample size of 51 GTN cases using three independent sex chromosome genetic markers; Amelogenin, Protein Kinase and Zinc Finger have X and Y homologues that are distinguishable by their PCR product size. We found that all cases contained the X-chromosomal complement while only five (10%) of 51 tumors harbored the Y-chromosomal complement. Specifically, Y-chromosomal signals were detected in one (5%) of 19 choriocarcinomas, one (7%) of 15 PSTTs and three (18%) of 17 ETTs. The histopathological features of those with a Y-chromosome were similar to those without. Our results demonstrate the presence of a Y-chromosomal complement in GTNs, albeit a low 10% of cases. This shortfall of Y-chromosomal complements in GTNs may reinforce the notion that the majority of GTNs are derived from previous molar gestations.

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46

Doszpoly, Andor, Fernando de la Cuesta, Estrella Lopez-Gordo, Cécile Bénézech, Stuart A. Nicklin, and Andrew H. Baker. "Human Adenovirus Serotype 5 Is Sensitive to IgM-Independent Neutralization In Vitro and In Vivo." Viruses 11, no. 7 (July 5, 2019): 616. http://dx.doi.org/10.3390/v11070616.

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Human adenovirus 5 (HAdV-5) is used as a vector in gene therapy clinical trials, hence its interactions with the host immune system have been widely studied. Previous studies have demonstrated that HAdV-5 binds specifically to murine coagulation factor X (mFX), inhibiting IgM and complement-mediated neutralization. Here, we examined the physical binding of immune components to HAdV-5 by nanoparticle tracking analysis, neutralization assays, mass spectrometry analysis and in vivo experiments. We observed that purified mouse Immunoglobulin M (IgM) antibodies bound to HAdV-5 only in the presence of complement components. Active serum components were demonstrated to bind to HAdV-5 in the presence or absence of mFX, indicating that immune molecules and mFX might bind to different sites. Since binding of mFX to HAdV-5 blocks the neutralization cascade, these findings suggested that not all complement-binding sites may be involved in virion neutralization. Furthermore, the data obtained from serum neutralization experiments suggested that immune molecules other than IgM and IgG may trigger activation of the complement cascade in vitro. In vivo experiments were conducted in immunocompetent C57BL/6 or immuno-deficient Rag2-/- mice. HAdV-5T* (a mutant HAdV-5 unable to bind to human or mFX) was neutralized to some extent in both mouse models, suggesting that murine immunoglobulins were not required for neutralization of HAdV-5 in vivo. Liquid Chromatography-Mass Spectrometry (LC-MS/MS) analysis of HAdV-5 and HAdV-5T* after exposure to murine sera showed stable binding of C3 and C4b in the absence of mFX. In summary, these results suggest that HAdV-5 neutralization can be mediated by both the classical and alternative pathways and that, in the absence of immunoglobulins, the complement cascade can be activated by direct binding of C3 to the virion.

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47

Weitz, Ilene Ceil. "Complement the hemostatic system: an intimate relationship." Thrombosis Research 133 (May 2014): S117—S121. http://dx.doi.org/10.1016/s0049-3848(14)50020-5.

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Sibileau, E., F. Paisant-Thouveny, A. Bouvier, C. Nedelcu, S. Delépine, W. Abi Khalil, A. Furber, S. Willoteaux, and C. Aube. "Indications du coroscanner en complement d’une coronarographie." Journal de Radiologie 90, no. 10 (October 2009): 1327. http://dx.doi.org/10.1016/s0221-0363(09)75279-5.

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49

Devine, Dana V. "The Regulation of Complement on Cell Surfaces." Transfusion Medicine Reviews 5, no. 2 (April 1991): 123–31. http://dx.doi.org/10.1016/s0887-7963(91)70199-5.

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Ratnoff, William D. "INHERITED DEFICIENCIES OF COMPLEMENT IN RHEUMATIC DISEASES." Rheumatic Disease Clinics of North America 22, no. 1 (February 1996): 75–94. http://dx.doi.org/10.1016/s0889-857x(05)70263-5.

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