Journal articles: 'Endō'

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Liu, Chiu-Ping, Tsung-I. Tsai, Ting Cheng, Vidya S. Shivatare, Chung-Yi Wu, Chung-Yi Wu, and Chi-Huey Wong. "Glycoengineering of antibody (Herceptin) through yeast expression and in vitro enzymatic glycosylation." Proceedings of the National Academy of Sciences 115, no. 4 (January 8, 2018): 720–25. http://dx.doi.org/10.1073/pnas.1718172115.

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Monoclonal antibodies (mAbs) have been developed as therapeutics, especially for the treatment of cancer, inflammation, and infectious diseases. Because the glycosylation of mAbs in the Fc region influences their interaction with effector cells that kill antibody-targeted cells, and the current method of antibody production is relatively expensive, efforts have been directed toward the development of alternative expressing systems capable of large-scale production of mAbs with desirable glycoforms. In this study, we demonstrate that the mAb trastuzumab expressed in glycoengineered P. pastoris can be remodeled through deglycosylation by endoglycosidases identified from the Carbohydrate Active Enzymes database and through transglycosylation using glycans with a stable leaving group to generate a homogeneous antibody designed to optimize the effector functions. The 10 newly identified recombinant bacterial endoglycosidases are complementary to existing endoglycosidases (EndoA, EndoH, EndoS), two of which can even accept sialylated tri- and tetraantennary glycans as substrates.

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Abellón-Ruiz, Javier, Sonoko Ishino, Yoshizumi Ishino, and Bernard A. Connolly. "Archaeal DNA Polymerase-B as a DNA Template Guardian: Links between Polymerases and Base/Alternative Excision Repair Enzymes in Handling the Deaminated Bases Uracil and Hypoxanthine." Archaea 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/1510938.

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In Archaea repair of uracil and hypoxanthine, which arise by deamination of cytosine and adenine, respectively, is initiated by three enzymes: Uracil-DNA-glycosylase (UDG, which recognises uracil); Endonuclease V (EndoV, which recognises hypoxanthine); and Endonuclease Q (EndoQ), (which recognises both uracil and hypoxanthine). Two archaeal DNA polymerases, Pol-B and Pol-D, are inhibited by deaminated bases in template strands, a feature unique to this domain. Thus the three repair enzymes and the two polymerases show overlapping specificity for uracil and hypoxanthine. Here it is demonstrated that binding of Pol-D to primer-templates containing deaminated bases inhibits the activity of UDG, EndoV, and EndoQ. Similarly Pol-B almost completely turns off EndoQ, extending earlier work that demonstrated that Pol-B reduces catalysis by UDG and EndoV. Pol-B was observed to be a more potent inhibitor of the enzymes compared to Pol-D. Although Pol-D is directly inhibited by template strand uracil, the presence of Pol-B further suppresses any residual activity of Pol-D, to near-zero levels. The results are compatible with Pol-D acting as the replicative polymerase and Pol-B functioning primarily as a guardian preventing deaminated base-induced DNA mutations.

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Kollenz, Gert, Ralf Smounig, Ferdinand Belaj, David Kvaskoff, and Curt Wentrup. "Molecular cleft or tweezer compounds derived from trioxabicyclo[3.3.1]nonadiene diisocyanate and diacid dichloride." Beilstein Journal of Organic Chemistry 11 (January 2, 2015): 1–8. http://dx.doi.org/10.3762/bjoc.11.1.

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The structures of two derivatives of the bisdioxine diisocyanate 1, the bisurea 4 and the biscarbamate 5, are established by X-ray crystallography and DFT calculations. These compounds possess endo,endo structures, in the case of the bisurea 4 with two nearly parallel pendant chains. The X-ray structures are reproduced very well by DFT calculations. Similar endo,endo conformations are calculated for the bisamide crown ether derivatives 7, where two proximate and nearly parallel crown ether units endow the molecules with a claw-like molecular cleft or tweezer structure as evidenced by an enhanced ability to extract some alkali, alkaline earth and rare earth metal ions.

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Malinky, John M. "Early and Middle Cambrian Hyolitha (Mollusca) from northeastern China." Journal of Paleontology 64, no. 2 (March 1990): 228–40. http://dx.doi.org/10.1017/s0022336000018394.

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The hyolithid species Hyolithes crebescens Resser and Endo, Hyolithes cybele Walcott, and Hyolithes delphus Resser and Endo from the Middle Cambrian of China are assigned respectively to the genera Nevadotheca Malinky, Novakotheca n. gen., family Hyolithidae, and Crestjahitus Syssoiev, family uncertain, all in the order Hyolithida. Recognition of Nevadotheca extends its geographic range from North America to China, and the occurrence of Crestjahitus in the Middle Cambrian of China increases its geographic and stratigraphic distribution from the Early Cambrian of the Soviet Union.Poor preservation of the type specimens of Hyolithes? aliger Resser and Endo, H.? aplatus Resser and Endo, H.? cariniferus Resser and Endo, H.? daphnis Walcott, H.? delia Walcott, H.? endoi Howell (as H. ornatus Resser and Endo), H.? mantouensis Resser and Endo, and H.? tenuis Resser and Endo renders their generic identification uncertain. Hyolithes (Orthotheca) glabrus Resser and Endo is here transferred to the hyolith order Orthothecida Marek and referred with question to Decoritheca Syssoiev, family Novitatidae.Morphology of the types of “Hyolithes” fuchouensis Resser and Endo, “H.” kuantungensis Resser and Endo, “H.” sondai Resser and Endo, “Orthotheca” daulis Walcott, and “O.” doris Walcott does not support assignment to the Hyolitha for these species; their phylogenetic affinity is uncertain.

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Krishnan, Devika R., Nicky Haridas, VP Prabath Singh, and Biju Balakrishnan. "Effective Management of a Perio-endo Lesion associated with Palatoradicular Groove." Conservative Dentistry and Endodontic Journal 2, no. 1 (2017): 16–23. http://dx.doi.org/10.5005/jp-journals-10048-0019.

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ABSTRACT This case report highlights the effective management of a maxillary lateral incisor with perio-endo lesion precipitated and complicated by the presence of a deep palatoradicular groove extending up to the root apex. Despite an apparently poor prognosis, the tooth was successfully managed by a collaborative endodontic and surgical periodontal therapy. The periodontal ligament attachment and periradicular healing were appreciated both clinically and radiographically at 3-month follow-up. How to cite this article Krishnan DR, Haridas N, Singh VPP, Balakrishnan B. Effective Management of a Perio-endo Lesion associated with Palatoradicular Groove. Cons Dent Endod J 2017;2(1):16-23.

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Camacho, Alejandro D., and John H. Borden. "RESPONSE OF THE WESTERN BALSAM BARK BEETLE, DRYOCOETES CONFUSUS SWAINE (COLEOPTERA: SCOLYTIDAE), TO HOST TREES BAITED WITH ENANTIOSPECIFIC BLENDS OF EXO- AND ENDO-BREVICOMIN." Canadian Entomologist 126, no. 1 (February 1994): 43–48. http://dx.doi.org/10.4039/ent12643-1.

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AbstractThe response of the western balsam bark beetle, Dryocoetes confusus Swaine, to subalpine firs, Abies lasiocarpa (Hook.) Nutt., baited with (±)-exo-brevicomin (EXOB) or 9:1 blends of EXOB and endo-brevicomin (ENDOB), in two chiral combinations: (+):(±) and (+):(+), was assessed in a heavily infested stand in British Columbia. Unbaited control trees were not attacked, and the proportion of mass-attacked baited trees was similar for all other treatments. However, trees baited with the (+):(+) blend had the highest number of attacks per square metre, and they were also surrounded by the most attacked trees. The (+):(±) blend was intermediate in attractancy, and (±)EXOB was the least attractive bait. Pheromone-based management of D. confusus infestations may be more effective with the 9:1 blend of (+)EXOB:(+)ENDOB than with the previously used (±)EXOB baits.

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Rico, Eva, Cristina Oliva, Kilian Jesús Gutierrez, Juan Fernando Alzate, Carlos Mario Genes, David Moreno, Elena Casanova, et al. "Leishmania infantum EndoG Is an Endo/Exo-Nuclease Essential for Parasite Survival." PLoS ONE 9, no. 2 (February 26, 2014): e89526. http://dx.doi.org/10.1371/journal.pone.0089526.

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Ishino, Sonoko, Naruto Makita, Miyako Shiraishi, Takeshi Yamagami, and Yoshizumi Ishino. "EndoQ and EndoV work individually for damaged DNA base repair in Pyrococcus furiosus." Biochimie 118 (November 2015): 264–69. http://dx.doi.org/10.1016/j.biochi.2015.06.015.

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Kulesh, D. A., and R. G. Oshima. "Cloning of the human keratin 18 gene and its expression in nonepithelial mouse cells." Molecular and Cellular Biology 8, no. 4 (April 1988): 1540–50. http://dx.doi.org/10.1128/mcb.8.4.1540-1550.1988.

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Human keratin 18 (K18) and the homologous mouse protein, Endo B, are intermediate filament subunits of the type I keratin class. Both are expressed in many simple epithelial cell types including trophoblasts, the first differentiated cell type to appear during mouse embryogenesis. The K18 gene was identified and cloned from among the 15 to 20 similar sequences identified within the human genome. The identity of the cloned gene was confirmed by comparing the sequence of the first two exons to the K18 cDNA sequence and transfecting the gene into various murine cell lines and verifying the encoded protein as K18 by immunoprecipitation and partial peptide mapping. The transfected K18 gene was expressed in mouse HR9 parietal endodermal cells and mouse fibroblasts even though the fibroblasts fail to express endogenous Endo B. S1 nuclease protection analysis indicated that mRNA synthesized from the transfected K18 gene is initiated at the same position as authentic K18 mRNA found in both BeWo trophoblastoma cells and HeLa cells. Pulse-chase experiments indicated that the human K18 protein is stable in murine parietal endodermal cells (HR9) which express EndoA, a complementary mouse type II keratin. Surprisingly, however, K18 was degraded when synthesized in cells which lack a type II keratin. This turnover of K18 may be an important mechanism by which epithelial cells maintain equal molar amounts of both type I and II keratins. In addition, the levels of the endogenous type I Endo B in parietal endodermal cells were compensatingly down regulated in the presence of the K18 protein, while the levels of the endogenous type II Endo A were not affected in any of the transfected cell lines.

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Kulesh, D. A., and R. G. Oshima. "Cloning of the human keratin 18 gene and its expression in nonepithelial mouse cells." Molecular and Cellular Biology 8, no. 4 (April 1988): 1540–50. http://dx.doi.org/10.1128/mcb.8.4.1540.

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Human keratin 18 (K18) and the homologous mouse protein, Endo B, are intermediate filament subunits of the type I keratin class. Both are expressed in many simple epithelial cell types including trophoblasts, the first differentiated cell type to appear during mouse embryogenesis. The K18 gene was identified and cloned from among the 15 to 20 similar sequences identified within the human genome. The identity of the cloned gene was confirmed by comparing the sequence of the first two exons to the K18 cDNA sequence and transfecting the gene into various murine cell lines and verifying the encoded protein as K18 by immunoprecipitation and partial peptide mapping. The transfected K18 gene was expressed in mouse HR9 parietal endodermal cells and mouse fibroblasts even though the fibroblasts fail to express endogenous Endo B. S1 nuclease protection analysis indicated that mRNA synthesized from the transfected K18 gene is initiated at the same position as authentic K18 mRNA found in both BeWo trophoblastoma cells and HeLa cells. Pulse-chase experiments indicated that the human K18 protein is stable in murine parietal endodermal cells (HR9) which express EndoA, a complementary mouse type II keratin. Surprisingly, however, K18 was degraded when synthesized in cells which lack a type II keratin. This turnover of K18 may be an important mechanism by which epithelial cells maintain equal molar amounts of both type I and II keratins. In addition, the levels of the endogenous type I Endo B in parietal endodermal cells were compensatingly down regulated in the presence of the K18 protein, while the levels of the endogenous type II Endo A were not affected in any of the transfected cell lines.

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Blatherwick, Donald, and Amy Larkin. "ODP568 Success of CME at Improving Knowledge, Competence and Confidence Related to Diagnosing and Treating Hypophosphetemic Bone Disease." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A184. http://dx.doi.org/10.1210/jendso/bvac150.380.

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Abstract Introduction We sought to determine if an online continuing medical education (CME) activity could improve knowledge and competence of endocrinologists (endos) and rheumatologists (rheums) related to diagnosis and treatment of patients with hypophosphatemic bone disease. Methods The effect of an online, 30-minute, CME-certified roundtable discussion among 3 faculty was analyzed to determine efficacy. The activity posted November 4, 2020, and data were collected through February 4, 2021. Results Overall, 33% of endo learners and 48% of rheum learners improved their knowledge/competence. Conclusions This study demonstrates the success of an online 30-minute roundtable discussion on improving knowledge, competence, and confidence regarding diagnosis and treatment of hypophosphatemic bone disease, with gaps identified for future education. Presentation: No date and time listed

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Carothers, Ann, Amy Larkin, and John Maeglin. "ODP567 Success of CME at Improving Knowledge and Confidence Related to Hyperglycemia Associated with Cushing Disease and Acromegaly." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A341. http://dx.doi.org/10.1210/jendso/bvac150.710.

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Abstract Introduction We sought to determine if an online continuing medical education (CME) activity could improve knowledge and confidence of primary care physicians (PCPs) and endocrinologists (endos) related to hyperglycemia associated with cushing disease (CD) and acromegaly. Methods The effect of an online, 30-minute, CME-certified roundtable discussion among 3 faculty was analyzed to determine efficacy. The activity posted April 29, 2021, and data were collected through July 7, 2021. Results Overall, 51% of PCP learners and 55% of endo learners improved their knowledge. Conclusions This study demonstrates the success of an online, 30-minute roundtable discussion on improving knowledge and confidence regarding hyperglycemia associated with CD or acromegaly, with gaps identified for future education. Presentation: No date and time listed

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Larkin, Amy, and John Maeglin. "ODP603 Impact of CME at Improving Knowledge, Competence and Confidence Related to Management of Cushing Disease." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A520. http://dx.doi.org/10.1210/jendso/bvac150.1082.

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Abstract Introduction We sought to determine if an online continuing medical education (CME) activity could improve knowledge, competence and confidence of primary care physicians (PCPs) and endocrinologists (endos) related to management of patients with Cushing disease (CD). Methods Educational design included a "test, then teach" approach to elicit cognitive dissonance, with evidence-based feedback provided following each learner response. A repeated pairs pre-/post-assessment study design was used and McNemar's test (5% significance level, P .8 large). The activity posted June 22, 2021, and data were collected through August 27, 2021. Results Overall, 74% of PCP learners (N=468, Cohen's d=.96) and 75% of endo learners (N=81, Cohen's d=1.14) improved their knowledge/competence(both P Presentation: No date and time listed

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Carothers, Ann, Amy Larkin, and John Maeglin. "ODP566 Success of CME at Improving Knowledge, Competence and Confidence Related to Guideline-Based Diagnosis and Management of Acromegaly." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A184. http://dx.doi.org/10.1210/jendso/bvac150.379.

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Abstract Introduction We sought to determine if a series of online continuing medical education (CME) activities could improve knowledge, competence and confidence of primary care physicians (PCPs) and endocrinologists (endos) related to guideline-based diagnosis and management of patients with acromegaly. Methods The effect of two (2) separate online, 30-minute, CME-certified roundtable discussions among 3 faculty were analyzed to determine efficacy. The activities posted December 16, 2020, and May 19, 2021, and data were collected for 3 months for each activity. Results Overall, 42% and 30% of PCP learners and 20% and 43% of endo learners improved their knowledge/competence. Conclusions This study demonstrates the success of 2 online, 30-minute roundtable discussions on improving knowledge, competence, and confidence of both PCPs, and endocrinologists regarding guideline-based diagnosis and management of acromegaly, with gaps identified for future education. Presentation: No date and time listed

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Gonçalves, Gabriela Sumie Yaguinuma, Tayna Natsumi Takakura, Anderson Catelan, Rosalinda Tanuri Zaninotto Venturim, Carolina dos Santos Santinoni, and Christine Men Martins. "Tratar ou extrair? Tratamento de lesão endoperiodontal, um relato de caso clínico." ARCHIVES OF HEALTH INVESTIGATION 9, no. 6 (April 20, 2020): 535–40. http://dx.doi.org/10.21270/archi.v9i6.4814.

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Introdução: Lesões endoperiodontais são lesões originadas de produtos inflamatórios encontrados tanto em periodonto quanto em polpa. Tais lesões podem se originar devido a uma infecção pulpar ou periodontal. Visando o prognóstico favorável, é imprescindível o conhecimento da etiologia, realização do correto diagnóstico e elaboração do plano de tratamento que envolve o tratamento endodôntico precedido do tratamento periodontal. Objetivo: O propósito do presente trabalho foi de relatar um caso clínico de lesão endoperiodontal e o tratamento realizado. Relato de caso clínico: Paciente gênero feminino, 51 anos, compareceu à clínica com uma fístula na região do dente 46, procedeu-se com exame radiográfico, rastreamento de fístula, testes endodônticos e avaliação periodontal. Foi diagnosticada lesão endoperiodontal. Executou-se, então, o tratamento endodôntico em sessões múltiplas, utilizando hidróxido de cálcio como medicação intracanal e o tratamento periodontal concomitante; finalizou-se endodontia obturando-se os canais radiculares. Conclusão: Observou-se, no controle, que a associação de tratamentos foi eficaz e houve melhora significativa do quadro, constatando-se silêncio clínico e sucesso do tratamento. Realizar o tratamento conservador a despeito da exodontia foi a melhor escolha para a paciente. Descritores: Endodontia; Periodontia; Polpa Dentária; Periodonto. Referências Sunitha VR, Emmadi P, Namasivayam A, Thyegarajan R, Rajaraman V. The periodontal - endodontic continuum A review. J Conserv Dent. 2008;11(2):54-62. Betancourt P, Elgueta R, Fuentes R. Treatment of endo-periodontal lesion using leukocyte-platelet-rich fibrin - a case report. Colomb Med. 2017;48(4):204-7. Lopes HP, Siqueira JF. Endodontia: Biologia e Técnica. Rio de Janeiro: Medsi-Guanabara Koogan; 2015. Lindhe J, Karring T, Lang NP. Tratado de periodontia clínica e implantologia oral. Rio de Janeiro: Guanabara Koogan; 2010. Anand V, Govila V, Gulati M. Endo-perio lesion part II (the treatment) - a review. 2012;3(1):10-6. Rotstein I, Simon JH. Diagnosis, prognosis and decision-making in the treatment of combined periodontal-endodontic lesions. J Periodontol. 2004;34:165-203. Parolia A, Gait TC, Porto ICCM, Mala K. Endo-perio lesion: a dilemma from 19th until 21st century. J Interdisp Dent. 2013;3(1):2-11. Kim E, Song JS, Jung IY, Lee SJ, Kim S. Prospective clinical study evaluating endodontic microsurgery outcomes for cases with lesions of endodontic origin compared with cases with lesions of combined periodontal-endodontic origin. J Endod. 2008;34(5):546-51. Heasman PA. An endodontic conundrum: the association between pulpal infection and periodontal disease. Br Dent J. 2014;216(6):275-9. Schmidt JC, Walter C, Amato M, Weiger R. Treatment of periodontal-endodontic lesions--a systematic review. J Clin Periodontol. 2014; 41(8):779-90. Jivoinovici R, Suciu I, Dimitriu B, Perlea P, Bartok R, Malita M, Ionescu C. Endo-periodontal lesion--endodontic approach. J Med Life. 2014;7(4):542-44. Estrela C. Endodontia laboratorial e clínica, Série Abeno: Odontologia Essencial - Parte Clínica. São Paulo: Artes Médicas; 2013. Vera J, Siqueira JF Jr, Ricucci D, Loghin S, Fernández N, Flores B et al. One-versus two-visit endodontic treatment of teeth with apical periodontitis: a histobacteriologic study. J Endod. 2012;38(8):1040-52. Mohammadi Z, Dummer PMH. Properties and applications of calcium hydroxide in endodontics and dental traumatology. Inter Endod J. 2011;44(8):697-730. Batista VES, Olian DA, Mori GG. Diffusion of hydroxyl ions from calcium hydroxide and aloe vera pastes. Braz Dent J. 2014;25(3):212-16. Pereira TC, da Silva Munhoz Vasconcelos LR, Graeff MSZ, Ribeiro MCM, Duarte MAH, de Andrade FB. Intratubular decontamination ability and physicochemical properties of calcium hydroxidepastes. Clin Oral Investig. 2019;23(3):1253-62. Andolfatto C, da Silva GF, Cornélio AL, Guerreiro-Tanomaru JM, Tanomaru-Filho M, Faria G, Bonetti-Filho I, Cerri PS. Biocompatibility of intracanal medications based on calcium hydroxide. ISRN Dent. 2012;2012:904963. Duque TM, Prado M, Herrera DR, Gomes BPFA. Periodontal and endodontic infectious/inflammatory profile in primary periodontal lesions with secondary endodontic involvement after a calcium hydroxide-based intracanal medication. Clin Oral Investig. 2019;23(1):53-63. Kim D, Kim E. Antimicrobial effect of calcium hydroxide as an intracanal medicament in root canal treatment: a literature review - Part I. In vitro studies. Restor Dent Endod. 2014; 39(4):241-52. Adl A, Motamedifar M, Shams MS, Mirzaie A. Clinical investigation of the effect of calcium hydroxide intracanal dressing on bacterial lipopolysaccharide reduction from infected root canals. Aust Endod J. 2015;41(1):12-6. Hilton TJ, Ferracane JL, Mancl L; Northwest Practice-based Research Collaborative in Evidence-based Dentistry (NWP). Comparison of CaOH with MTA for direct pulp capping: a PBRN randomized clinical trial. J Dent Res. 2013;92(7 Suppl):16S-22S. Labban N, Yassen GH, Windsor LJ, Platt JA. The direct cytotoxic effects of medicaments used in endodontic regeneration on human dental pulp cells. Dent Traumatol. 2014;30(6):429-34. McIntyre PW, Wu JL, Kolte R, Zhang R, Gregory RL, Bruzzaniti A, Yassen GH. The antimicrobial properties, cytotoxicity, and differentiation potential of double antibiotic intracanal medicaments loaded into hydrogel system. Clin Oral Investig. 2019;23(3):1051-59. Bergenholtz, G., Hasselgren, G. Endodontics and periodontics. In: Lindhe, K., Karring, T., Lang, N. Clinical periodontology and implant dentistry. Copenhagen:Munksgaard; 2015. Harrington GW, Steiner DR, Ammons WF. The periodontal-endodontic controversy. Periodontol 2000. 2002;30:123-30. Fernandes LA, Martins TM, Almeida JM, Nagata MJ, Theodoro LH, Garcia VG, Bosco AF. Experimental periodontal disease treatment by subgingival irrigation with tetracycline hydrochloride in rats. J Appl Oral Sci. 2010;18(6):635-40. Storrer CM, Bordin GM, Pereira TT. How to diagnose and treat periodontal endodontic lesions? 2012;9(4):427-33. Verma PK, Srivastava R, Gupta KK, Srivastava A. Combined endodontic periodontal lesions: A clinical dilema. J Interdiscip Dent. 2011;1(2):119-24. Oh SL, Fouad AF, Park SH. Treatment strategy for guided tissue regeneration in combined endodontic-periodontal lesions: case report and review. J Endod. 2009;35(10):1331-36. Malli R, Lele P, Vishakha. Guided tissue regeneration in communicating periodontal and endodontic lesions - a hope for the hopeless. J Indian Soc Periodontol. 2011;15(4):410-13. Ghezzi C, Virzì M, Schupbach P, Broccaioli A, Simion M. Treatment of combined endodontic-periodontic lesions using guided tissue regeneration: clinical case and histology. Int J Periodontics Restorative Dent. 2012;32(4):433-9. Sun J, Liu Q. [Bio-Oss collagen bone grafting in the treatment of endodontic-periodontic lesion]. Nan Fang Yi Ke Da Xue Xue Bao. 2009;29(9):1905-6. Sharma R, Hegde V, Siddharth M, Hegde R, Manchanda G, Agarwal P. Endodontic-periodontal microsurgery for combined endodontic-periodontal lesions: An overview. J Conserv Dent. 2014;17(6):510-16. Li Y, Wang X, Xu J, Zhou X, Xie K. [The clinical study on the use of diode laser irradiation in the treatment of periodontal-endodontic combined lesions]. Hua Xi Kou Qiang Yi Xue Za Zhi. 2012;30(2):161-64, 168. Narang S, Narang A, Gupta R. A sequential approach in treatment of perio-endo lesion. J Indian Soc Periodontol. 2011;15(2):177-80. Pereira AL, Orzechowski PR, Filho SB, Cortelli JR. Subepithelial connective tissue graft: an alternative application for treating endoperiodontal lesions. Gen Dent. 2013;61(2):50-3. Yoneda M, Motooka N, Naito T, Maeda K, Hirofuji T. Resolution of furcation bone loss after non-surgical root canal treatment: application of a peptidase-detection kit for treatment of type I endoperiodontal lesion. J Oral Sci. 2005; 47(3):143-47. Shenoy N, Shenoy A. Endo-perio lesions: diagnosis and clinical considerations. Indian J Dent Res. 2010;21(4):579-85. Gerritsen AE, Allen PF, Witter DJ, Bronkhorst EM, Creugers NH. Tooth loss and oral health-related quality of life: a systematic review and meta-analysis. Health Qual Life Outcomes. 2010;8:126.

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Iliescu, Alexandru Andrei, Paula Perlea, Sînziana Adina Scărlătescu, and Irina Maria Gheorghiu. "Endo-antral syndrome in aspergillosis." Romanian Journal of Stomatology 63, no. 4 (December 31, 2017): 169–73. http://dx.doi.org/10.37897/rjs.2017.4.4.

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While initiating an endo-antral syndrome, inside the endodontic system and the chronic apical lesions of upper teeth anatomicaly related to the maxillary sinus floor, may be found both endopathogenic bacteria and filamentous fungi. Similarly the improper root canal treatments may facilitate an emerging aspergillosis of maxillary sinus. By phenotype and genotype analysis in 10% of chronic apical periodontitis were disclosed filamentous fungi of Aspergillus genus (A. fumigatus, A. versicolor and A. niger). Accordingly might be also taken into consideration the hypothesis of mutual pathogenical relationship between pulpal and sinusal pathology, since at its turn the aspergillosis of maxillarx sinus can also promote the contamination of already filled or still untreated necrotic root canals with filamentous fungi.

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Shoba, K., R. Abhilash, Jithin Balan, and MR Sreelakshmi. "External Inflammatory Root Resorption: Management of a Tooth with hopeless Prognosis." Conservative Dentistry and Endodontic Journal 2, no. 1 (2017): 24–27. http://dx.doi.org/10.5005/jp-journals-10048-0020.

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ABSTRACT The treatment of external root resorption and associated periodontal defect can be challenging to the most ingenious clinician. A correct diagnosis and an understanding of the etiology and dynamics of root resorption, which is the progressive loss of dentin and cementum through action of osteoclastic cells, are critical for effective management. The article describes the management of an external root resorption in maxillary central incisor where a combined endo-perio management strategy was implemented. Cone beam computed tomography was used as an adjunctive diagnostic aid. A combined approach using biodentine for root surface repair, bone graft, collagen membrane, and platelet-rich fibrin to address the associated osseous lesion appears to be viable modality in treatment of the same. After a follow-up period of 12 months, the patient was found to be asymptomatic. Postoperative radiographs also demonstrated satisfactory bone fill and arrest of the resorptive lesion. How to cite this article Abhilash R, Balan J, Shoba K, Sreelakshmi MR. External Inflammatory Root Resorption: Management of a Tooth with hopeless Prognosis. Cons Dent Endod J 2017;2(1):24-27.

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La Noue, George. "Colleges: To Endow or Not to Endow?" Academic Questions 35, no. 1 (March 18, 2022): 41–47. http://dx.doi.org/10.51845/35.1.7.

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As colleges and universities undergo rapid institutional change and ideological capture, George R. La Noue believes it is imperative that donors ask three questions before entering into endowment agreements.

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Fox, Peter, Bo Gao, Bavanthi Balakrishnar, Alexander M. Menzies, Shang Heng Yeap, Sayed Sahanawaz Ali, Val Gebski, et al. "Factors predicting endoxifen levels in breast cancer patients taking standard-dose tamoxifen and following dose escalation." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 543. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.543.

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543 Background: Tamoxifen (TAM) is transformed via CYP2D6 to its major active metabolite endoxifen (Endox). Recent data suggest that 15nM Endox may be a therapeutic threshold for breast cancer . This study identified predictors of achieving specified Endox target levels (15nM and 30nM) on standard dose TAM, and following dose escalation. Methods: Baseline Endox was measured in 122 breast cancer pts on TAM 20mg pd. Pts with baseline Endox <30nM underwent incremental dose escalation to a maximum of 60mg pd until Endox reached 30nM or dose limiting toxicity. Clinical data were collected and CYP2D6 genotype was used to specify extensive, intermediate or poor metabolizer categories (EM, IM, PM). Multiple regression analyses examined associations between Endox and potential predictive factors. Results: Baseline Endox ranged from 3.1-72.2nM (mean 27.6nM). In 19% (n=23), baseline Endox was below 15nM and 62% (n=76) were below 30nM. Low baseline Endox was associated with CYP2D6 genotype (IM or PM, p<0.001) and younger age (p=0.02). Following dose escalation, 96% (n=117) attained an Endox level of 15nM and 76% (n=93) reached 30nM. Baseline Endox level was the only variable independently associated with achieving both targets (p=0.02, p<0.001 respectively). CYP2D6 genotype did not independently predict attainment of Endox targets following dose escalation (p>0.4). The ratio of Endox to its precursor N-desmethylTAM, an indicator of CYP2D6 activity, was stable with dose escalation, suggesting that CYP2D6 was not saturated. Conclusions: Although IM/PM predict for low Endox on 20mg TAM, only low baseline Endox predicted failure to achieve both 15nM and 30nM targets following dose escalation. These results suggest a role for Endox level monitoring to determine optimal TAM dose. Clinical trial information: NCT01075802. [Table: see text]

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Barés, Gisel, Aida Beà, Luís Hernández, Raul Navaridas, Isidre Felip, Cristina Megino, Natividad Blasco, et al. "ENDOG Impacts on Tumor Cell Proliferation and Tumor Prognosis in the Context of PI3K/PTEN Pathway Status." Cancers 13, no. 15 (July 28, 2021): 3803. http://dx.doi.org/10.3390/cancers13153803.

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EndoG influences mitochondrial DNA replication and is involved in somatic cell proliferation. Here, we investigated the effect of ENDOG/Endog expression on proliferation in different tumor models. Noteworthy, ENDOG deficiency reduced proliferation of endometrial tumor cells expressing low PTEN/high p-AKT levels, and Endog deletion blunted the growth of PTEN-deficient 3D endometrial cultures. Furthermore, ENDOG silencing reduced proliferation of follicular thyroid carcinoma and glioblastoma cell lines with high p-AKT expression. High ENDOG expression was associated with a short time to treatment in a cohort of patients with chronic lymphocytic leukemia (CLL), a B-cell lymphoid neoplasm with activation of PI3K/AKT. This clinical impact was observed in the less aggressive CLL subtype with mutated IGHV in which high ENDOG and low PTEN levels were associated with worse outcome. In summary, our results show that reducing ENDOG expression hinders growth of some tumors characterized by low PTEN activity and high p-AKT expression and that ENDOG has prognostic value for some cancer types.

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Andrade, Evilazio da Silva, Ricardo José Nunes, and Marina Uieara. "Synthesis and Characterization of Exo‐endo and Endo‐endo Benzenesulfonylaziridines." Synthetic Communications 34, no. 17 (January 2004): 3073–81. http://dx.doi.org/10.1081/scc-200028524.

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Watt, F. M. "Sharyn Endow." Journal of Cell Science 117, no. 5 (March 1, 2004): 655–56. http://dx.doi.org/10.1242/jcs.00985.

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Wicker, Tom. "Endof anAffair." Change: The Magazine of Higher Learning 26, no. 3 (June 1994): 27–29. http://dx.doi.org/10.1080/00091383.1994.9940633.

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Bruggemann, W., and J. R. Niklas. "Stochastic ENDOR." Journal of Magnetic Resonance, Series A 108, no. 1 (May 1994): 25–29. http://dx.doi.org/10.1006/jmra.1994.1084.

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Lubitz, Wolfgang, and Gerald T. Babcock. "ENDOR spectroscopy." Trends in Biochemical Sciences 12 (January 1987): 96–100. http://dx.doi.org/10.1016/0968-0004(87)90045-4.

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Mallya, Dr Laxmeesh, Dr Shashirashmi Acharya, Dr Nandita Shenoy, and Dr Kanchana Kamath. "The Pathway of Endo Perio Relationship." Global Journal For Research Analysis 3, no. 5 (June 15, 2012): 107–9. http://dx.doi.org/10.15373/22778160/may2014/40.

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Yang, Jinghua, Yuan Zhou, Luxia Zhang, Nehal Shah, Cheng Jin, Robert J. Palmer, and John O. Cisar. "Cell Surface Glycoside Hydrolases of Streptococcus gordonii Promote Growth in Saliva." Applied and Environmental Microbiology 82, no. 17 (June 17, 2016): 5278–86. http://dx.doi.org/10.1128/aem.01291-16.

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ABSTRACTThe growth of the oral commensalStreptococcus gordoniiin saliva may depend on a number of glycoside hydrolases (GHs), including three cell wall-anchored proteins that are homologs of pneumococcal β-galactosidase (BgaA), β-N-acetylglucosaminidase (StrH), and endo-β-N-acetylglucosaminidase D (EndoD). In the present study, we introduced unmarked in-frame deletions into the corresponding genes ofS. gordoniiDL1, verified the presence (or absence) of the encoded proteins on the resulting mutant strains, and compared these strains with wild-type strain DL1 for growth and glycan foraging in saliva. The overnight growth of wild-type DL1 was reduced 3- to 10-fold by the deletion of any one or two genes and approximately 20-fold by the deletion of all three genes. The only notable change in the salivary proteome associated with this reduction of growth was a downward shift in the apparent molecular masses of basic proline-rich glycoproteins (PRG), which was accompanied by the loss of lectin binding sites for galactose-specificErythrina cristagalliagglutinin (ECA) and mannose-specificGalanthus nivalisagglutinin (GNA). The binding of ECA to PRG was also abolished in saliva cultures of mutants that expressed cell surface BgaA alone or together with either StrH or EndoD. However, the subsequent loss of GNA binding was seen only in saliva cocultures of different mutants that together expressed all three cell surface GHs. The findings indicate that the growth ofS. gordoniiDL1 in saliva depends to a significant extent on the sequential actions of first BgaA and then StrH and EndoD on N-linked glycans of PRG.IMPORTANCEThe ability of oral bacteria to grow on salivary glycoproteins is critical for dental plaque biofilm development. Little is known, however, about how specific salivary components are attacked and utilized by different members of the biofilm community, such asStreptococcus gordonii. Streptococcus gordoniiDL1 has three cell wall-anchored glycoside hydrolases that are predicted to act on host glycans. In the present study, we introduced unmarked in-frame deletions in the corresponding genes, verified the presence (or absence) of encoded proteins on the resulting mutant strains, and compared these strains with wild-type DL1 for growth and glycan foraging in saliva. The results indicate that the growth ofS. gordoniiDL1 depends to a significant extent on sequential action of these cell surface GHs on N-linked glycans of basic proline-rich salivary glycoproteins, which appears to be an essential first step in salivary glycan foraging.

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Brown, Betsy. "Endo." College English 50, no. 6 (October 1988): 638. http://dx.doi.org/10.2307/377735.

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Ülkü, Dinçer, Cengiz Arıcı, Osman Çakmak, and Metin Balcı. "endo,endo,endo-9,9,10,11,12-Pentabromotricyclo[6.2.2.02,7]dodeca-2(7),3,5-triene." Acta Crystallographica Section E Structure Reports Online 58, no. 4 (March 8, 2002): o382—o384. http://dx.doi.org/10.1107/s1600536802004257.

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Griffin, Cora, Eddie C. Y. Wang, Brian P. McSharry, Carole Rickards, Helena Browne, Gavin W. G. Wilkinson, and Peter Tomasec. "Characterization of a highly glycosylated form of the human cytomegalovirus HLA class I homologue gpUL18." Journal of General Virology 86, no. 11 (November 1, 2005): 2999–3008. http://dx.doi.org/10.1099/vir.0.81126-0.

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Human cytomegalovirus (HCMV) gpUL18 is a HLA class I (HLA-I) homologue with high affinity for the inhibitory receptor LIR-1/ILT2. The previously described 67 kDa form of gpUL18 is shown here to be sensitive to endoglycosidase-H (EndoH). A novel form of gpUL18 with a molecular mass of ∼160 kDa and resistance to EndoH was identified in cells infected with HCMV strain AD169 or the low passage HCMV isolates Merlin and Toledo. The 67 kDa EndoH-sensitive gpUL18 glycoform was detected earlier in a productive infection (from 24 h post-infection) than the slower-migrating EndoH-resistant glycoform (from 72 h post-infection). Deletion of the US2–US11 region from the HCMV genome was associated with a substantial up-regulation of endogenous HLA-I in infected cells, but had no obvious effect on the gpUL18 expression pattern. Vaccinia virus and adenovirus vectors were used to further analyse gpUL18 expression. Depending on the delivery vector system, differences in the electrophoretic motility of the EndoH-resistant >105 kDa form of gpUL18, but not the EndoH-sensitive 67 kDa form, were observed; post-translational modification of the higher molecular mass glycoform appears to be influenced by active virus infection and vector delivery. The EndoH-sensitive 67 kDa gpUL18 had a rapid turnover, while the maturation to the EndoH-resistant >105 kDa form was relatively slow and inefficient. However, synthesis of the EndoH-resistant >105 kDa form was enhanced with elevated levels of β 2-microglobulin. When expressed by using an adenovirus vector, both the EndoH-sensitive 67 kDa and the EndoH-resistant >105 kDa gpUL18 forms could be detected on the cell surface.

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Morigaki, Kazuo. "Light-induced defect creation processes and light-induced defects in hydrogenated amorphous silicon." European Physical Journal Applied Physics 90, no. 2 (May 2020): 20101. http://dx.doi.org/10.1051/epjap/2020190257.

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We have proposed a model of light-induced defect creation processes and light-induced defects. Recently, important results using pulsed electron-nuclear double resonance (ENDOR) by Fehr et al. [M. Fehr, A. Schnegg, C. Teutloff, R. Bittl, O. Astakhov, F. Finger, B. Rech, K. Lips, Phys. Status Solidi A 207, 552 (2010)] have been reported, so that these results are interpreted on the basis of our model. Fehr et al. have observed ENDOR signals due to hydrogen nuclei distributed around a dangling bond. The ENDOR spectra due to hydrogen nuclei being located with distance of r from the dangling bond have been calculated, taking into accounts the dipolar interaction, and also the Fermi-type contact hyperfine interaction for the H-related dangling bond (HDB) that is a dangling bond having hydrogen at a nearby site. The typical features of the observed ENDOR spectra are that the spectrum has a shoulder at the low frequency side from the natural NMR frequency of hydrogen and it has a dip in the central part. The calculated ENDOR spectrum of HDB exhibits such a shoulder. This is consistent with our model of light-induced defects such as HDB. The ENDOR spectra with various values of r are calculated. In this paper, we also deal with the distant ENDOR precisely, using the theory of distant ENDOR by Lambe et al. [J. Lambe, N. Laurance, K.C. McIrvine, R.W. Terhune, Phys. Rev. 122, 1161 (1961)]. The calculated distant ENDOR spectrum shows a dip in the central part. Concerning the dip, Fehr et al. attribute the dip to be due to the suppression of the matrix ENDOR line (this is called the artifact). Thus, it is not obvious whether the dip is due to such an artifact or the central part of the distant ENDOR spectrum.

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Zhdanov, D. D., N. S. Novachly, M. V. Pokrovskaya, S. S. Aleksandrova, T. A. Kabardokov, and N. N. Sokolov. "Identification of genes whose mRNAs are subjected to alternative splicing by endonuclease EndoG action in human and murine CD4+ T lymphocytes." Biomedical Chemistry: Research and Methods 3, no. 2 (2020): e00128. http://dx.doi.org/10.18097/bmcrm00128.

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The aim of this work was to identify genes whose mRNAs were subjected to alternative splicing by apoptotic endonuclease EndoG in CD4+ T lymphocytes from healthy humans, mice, and rats. In order to induce EndoG, lymphocytes were transfected with an EndoG-containing plasmid, or a control pGFP plasmid, or were incubated with cisplatin. Efficiency of transfection, number of cells with DNA damages and the level of EndoG expression have been monitored. Total cell mRNA has been sequenced and the changes in proportion of splice variants of genes were analyzed. The changes in the proportion of 28 mRNA splice variants have been identified in human and murine lymphocytes in both transfected with EndoG gene or incubated with cisplatin. Thus, EndoG can be considered as a potent modulator of alternative splicing of mRNA of identified genes.

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Trimble, R. B., and A. L. Tarentino. "Identification of distinct endoglycosidase (endo) activities in Flavobacterium meningosepticum: endo F1, endo F2, and endo F3. Endo F1 and endo H hydrolyze only high mannose and hybrid glycans." Journal of Biological Chemistry 266, no. 3 (January 1991): 1646–51. http://dx.doi.org/10.1016/s0021-9258(18)52343-7.

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Kong, Xiang Yi, Erik Sebastian Vik, Meh Sameen Nawaz, Natalia Berges, Tuva Børresdatter Dahl, Cathrine Vågbø, Rajikala Suganthan, et al. "Deletion of Endonuclease V suppresses chemically induced hepatocellular carcinoma." Nucleic Acids Research 48, no. 8 (February 21, 2020): 4463–79. http://dx.doi.org/10.1093/nar/gkaa115.

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Abstract Endonuclease V (EndoV) is a conserved inosine-specific ribonuclease with unknown biological function. Here, we present the first mouse model lacking EndoV, which is viable without visible abnormalities. We show that endogenous murine EndoV cleaves inosine-containing RNA in vitro, nevertheless a series of experiments fails to link an in vivo function to processing of such transcripts. As inosine levels and adenosine-to-inosine editing often are dysregulated in hepatocellular carcinoma (HCC), we chemically induced HCC in mice. All mice developed liver cancer, however, EndoV−/− tumors were significantly fewer and smaller than wild type tumors. Opposed to human HCC, adenosine deaminase mRNA expression and site-specific editing were unaltered in our model. Loss of EndoV did not affect editing levels in liver tumors, however mRNA expression of a selection of cancer related genes were reduced. Inosines are also found in certain tRNAs and tRNAs are cleaved during stress to produce signaling entities. tRNA fragmentation was dysregulated in EndoV−/− livers and apparently, inosine-independent. We speculate that the inosine-ribonuclease activity of EndoV is disabled in vivo, but RNA binding allowed to promote stabilization of transcripts or recruitment of proteins to fine-tune gene expression. The EndoV−/− tumor suppressive phenotype calls for related studies in human HCC.

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Patiño-Márquez, Isabel A., Juan F. Alzate, and Edwin Patiño-González. "Cristalización de la endonucleasa EndoG recombinante de <i>Leishmania (Viannia) panamensis</i>." Actualidades Biológicas 37, no. 102 (October 2, 2017): 27–32. http://dx.doi.org/10.17533/udea.acbi.329004.

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Antecedentes y objetivos: La endonucleasa G (EndoG) es una enzima que escinde específicamente en las posiciones dG y dC del ADN de cadena doble y se ha demostrado que participa en la degradación de la cromatina durante el proceso de apoptosis en Leishmania. El objetivo principal de este trabajo fue la purificación y cristalización de EndoG como preámbulo para los estudios estructurales futuros que permitan entender detalladamente el funcionamiento de esta enzima. Materiales y métodos: La proteína EndoG fue purificada en condiciones desnaturalizantes usando cromatografía de Ni, luego fue renaturalizada in vitro y cristalizada por el método de difusión de vapor por gota colgante. Resultados y conclusión: La proteína EndoG de Leishmania (viannia) panamensis fue sobreexpresada, renaturalizada, purificada y demostró estar enzimáticamente activa. Aquí, se registra la primera cristalización exitosa de la proteína EndoG de este grupo de parásitos protozoarios. La proteína fue cristalizada por el método de difusión de vapor por gota colgante. Se obtuvieron cristales de alta calidad de EndoG que posiblemente nos permitirán determinar la estructura tridimensional de EndoG usando difracción de rayos-X.

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Hong, Patrick W. P., Karen B. Flummerfelt, Aymeric de Parseval, Kevin Gurney, John H. Elder, and Benhur Lee. "Human Immunodeficiency Virus Envelope (gp120) Binding to DC-SIGN and Primary Dendritic Cells Is Carbohydrate Dependent but Does Not Involve 2G12 or Cyanovirin Binding Sites: Implications for Structural Analyses of gp120-DC-SIGN Binding." Journal of Virology 76, no. 24 (December 15, 2002): 12855–65. http://dx.doi.org/10.1128/jvi.76.24.12855-12865.2002.

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ABSTRACT The calcium-dependent lectin, DC-SIGN, binds to human immunodeficiency virus (HIV) (and simian immunodeficiency virus) gp120 and mediates the binding and transfer of HIV from monocyte-derived dendritic cells (MDDCs) to permissive T cells. However, it has been recently reported that DC-SIGN binding to HIV gp120 may be carbohydrate independent. Here, we formally demonstrate that gp120 binding to DC-SIGN and MDDCs is largely if not wholly carbohydrate dependent. Endo-β-N-glucosaminidase H (EndoH) treatment of gp120-Fc under conditions that maintained wild-type CD4 binding—and the full complement of complex glycans—significantly decreased (>90%) binding to DC-SIGN expressing cell lines, as well as to MDDCs. Any residual binding of EndoH-treated gp120-Fc to DC-SIGN was completely competed off with mannan. Mutational analysis indicated that no single glycosylation site affected the ability of gp120-Fc to bind DC-SIGN. To further guide our efforts in mapping the DC-SIGN binding sites on gp120, we used two well-characterized HIV inhibitory agents (2G12 monoclonal antibody and cyanovirin) that bind to high-mannose sugars on gp120. We showed that 2G12 and DC-SIGN bound to nonoverlapping sites in gp120 because (i) 2G12 did not block soluble gp120 or virion binding to DC-SIGN, (ii) 2G12 bound to gp120-Fc that was prebound to cell surface DC-SIGN, and (iii) gp120-Fc mutants that lack glycosylation sites involved in 2G12's epitope were also fully capable of binding DC-SIGN. These data were substantiated by the inability of cyanovirin to block gp120-Fc binding to DC-SIGN. Cyanovirin has been shown to effectively compete for 2G12 binding to gp120. Indeed, high concentrations of cyanovirin dramatically enhanced gp120-Fc binding to cell surfaces in the presence or absence of DC-SIGN. We provide evidence that this enhancement may be due to cyanovirin's ability to bridge gp120 to mannosylated cell surface proteins. These results have implications for antiviral therapeutics and for ongoing efforts to finely map the glycan structures on gp120 responsible for DC-SIGN binding.

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Bhan, Chandur, Chenyu Sun, Nimarta Bheesham, Fnu Shakuntulla, Zain I. Siddiqui, John Pocholo W. Tuason, Arpana Paudel, et al. "ENDOV upregulation and outcomes in females with colorectal adenocarcinoma." Journal of Clinical Oncology 40, no. 4_suppl (February 1, 2022): 175. http://dx.doi.org/10.1200/jco.2022.40.4_suppl.175.

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175 Background: Colorectal adenocarcinoma (COAD) is a common cancer in gastrointestinal tract. Endonuclease V (ENDOV), an enzyme with specificity for deaminated adenosine (inosine) in nucleic acids, was found to be involved in the development of certain cancers. Thus, this study was performed to explore the effects of ENDOV on the prognosis of COAD. Methods: RNA-sequencing FPKM data and corresponding clinical information of 41 normal tissues and 480 tumor tissues of COAD were acquired from The Cancer Genome Atlas (TCGA). Then ENDOV expression differences between the normal and cancer tissues were compared with Wilcoxon rank-sum test via ‘limma’ package. Overall survival (OS) and disease specific survival (DSS) analyses were conducted by Kaplan–Meier (K–M) method via ‘survminer’ package. Subgroup analyses of different genders were also performed. Results: The expression of ENDOV was downregulated in tumors compared with normal tissues (p < 0.001). However, higher expression of ENDOV is associated with worse OS (HR: 1.83, 95%CI: 1.23-2.73, P = 0.003) and DSS (HR: 1.75, 95%CI 1.06-2.91, P = 0.03). Subgroup analysis found that higher expression of ENDOV was associated with worse OS (HR: 2.17, 95%CI 1.18-3.98, P = 0.012) in females, but not in males (HR: 1.48, 95%CI 0.86-2.53, P = 0.158). As for DSS, higher expression of ENDOV was also correlated with worse outcome (HR: 2.36, 95%CI 1.07-5.19, P = 0.033) in females, but not in males (HR: 1.45, 95%CI 0.73-2.86, P = 0.287). Conclusions: ENDOV is overall downregulated in COAD tumor samples. However, higher expression of ENDOV in certain COAD patients is associated worse OS and DSS in females but not in males. This indicates the potential role of ENDOV in predicating the prognosis of COAD in female patients.

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Apostolov, Eugene O., Debarti Ray, Wilson M. Alobuia, Marina V. Mikhailova, Xiaoying Wang, Alexei G. Basnakian, and Sudhir V. Shah. "Endonuclease G mediates endothelial cell death induced by carbamylated LDL." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 6 (June 2011): H1997—H2004. http://dx.doi.org/10.1152/ajpheart.01311.2010.

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End-stage kidney disease is a terminal stage of chronic kidney disease, which is associated with a high incidence of cardiovascular disease. Cardiovascular disease frequently results from endothelial injury caused by carbamylated LDL (cLDL), the product of LDL modification by urea-derived cyanate. Our previous data suggested that cLDL induces mitogen-activated protein kinase-dependent mitotic DNA fragmentation and cell death. However, the mechanism of this pathway is unknown. The current study demonstrated that cLDL-induced endothelial mitotic cell death is independent of caspase-3. The expression of endonuclease G (EndoG), the nuclease implicated in caspase-independent DNA fragmentation, was significantly increased in response to cLDL exposure to the cells. The inhibition of EndoG by RNAi protected cLDL-induced DNA fragmentation, whereas the overexpression of EndoG induced more DNA fragmentation in endothelial cells. Ex vivo experiments with primary endothelial cells isolated from wild-type (WT) and EndoG knockout (KO) mice demonstrated that EndoG KO cells are partially protected against cLDL toxicity compared with WT cells. To determine cLDL toxicity in vivo, we administered cLDL or native LDL (nLDL) intravenously to the WT and EndoG KO mice and then measured floating endothelial cells in blood using flow cytometry. The results showed an increased number of floating endothelial cells after cLDL versus nLDL injection in WT mice but not in EndoG KO mice. Finally, the inhibitors of MEK-ERK1/2 and JNK-c-jun pathways decreased cLDL-induced EndoG overexpression and DNA fragmentation. In summary, our data suggest that cLDL-induced endothelial toxicity is caspase independent and results from EndoG-dependent DNA fragmentation.

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Călugăreanu, Grigore, Andrey R. Chekhlov, and Piotr A. Krylov. "Subgroups generated by images of endomorphisms of Abelian groups and duality." Journal of Group Theory 21, no. 5 (September 1, 2018): 885–900. http://dx.doi.org/10.1515/jgth-2018-0013.

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Abstract A subgroup H of a group G is called endo-generated if it is generated by endo-images, i.e. images of endomorphisms of G. In this paper we determine the following classes of Abelian groups: (a) the endo-groups, i.e. the groups all of whose subgroups are endo-generated; (b) the endo-image simple groups, i.e. the groups such that no proper subgroup is an endo-image; (c) the pure-image simple, i.e. the groups such that no proper pure subgroup is an endo-image; (d) the groups all of whose endo-images are pure subgroups; (e) the ker-gen groups, i.e. the groups all of whose kernels are endo-generated. Some dual notions are also determined.

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Wijayanti, Indah Emilia. "Endo-prime submodules in endo-multiplication modules." International Mathematical Forum 9 (2014): 1321–32. http://dx.doi.org/10.12988/imf.2014.47139.

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Karimi Beiranvand, Parvin, and Reza Beyranvand. "On endo-semiprime and endo-cosemiprime modules." Algebraic structures and their applications 5, no. 1 (April 1, 2018): 69–80. http://dx.doi.org/10.29252/asta.5.1.69.

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Nasca, Alessia, Andrea Legati, Megi Meneri, Melisa Emel Ermert, Chiara Frascarelli, Nadia Zanetti, Manuela Garbellini, et al. "Biallelic Variants in ENDOG Associated with Mitochondrial Myopathy and Multiple mtDNA Deletions." Cells 11, no. 6 (March 12, 2022): 974. http://dx.doi.org/10.3390/cells11060974.

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Endonuclease G (ENDOG) is a nuclear-encoded mitochondrial-localized nuclease. Although its precise biological function remains unclear, its proximity to mitochondrial DNA (mtDNA) makes it an excellent candidate to participate in mtDNA replication, metabolism and maintenance. Indeed, several roles for ENDOG have been hypothesized, including maturation of RNA primers during mtDNA replication, splicing of polycistronic transcripts and mtDNA repair. To date, ENDOG has been deemed as a determinant of cardiac hypertrophy, but no pathogenic variants or genetically defined patients linked to this gene have been described. Here, we report biallelic ENDOG variants identified by NGS in a patient with progressive external ophthalmoplegia, mitochondrial myopathy and multiple mtDNA deletions in muscle. The absence of the ENDOG protein in the patient’s muscle and fibroblasts indicates that the identified variants are pathogenic. The presence of multiple mtDNA deletions supports the role of ENDOG in mtDNA maintenance; moreover, the patient’s clinical presentation is very similar to mitochondrial diseases caused by mutations in other genes involved in mtDNA homeostasis. Although the patient’s fibroblasts did not present multiple mtDNA deletions or delay in the replication process, interestingly, we detected an accumulation of low-level heteroplasmy mtDNA point mutations compared with age-matched controls. This may indicate a possible role of ENDOG in mtDNA replication or repair. Our report provides evidence of the association of ENDOG variants with mitochondrial myopathy.

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Allhorn, Maria, Juana G. Briceño, Lucie Baudino, Christian Lood, Martin L. Olsson, Shozo Izui, and Mattias Collin. "The IgG-specific endoglycosidase EndoS inhibits both cellular and complement-mediated autoimmune hemolysis." Blood 115, no. 24 (June 17, 2010): 5080–88. http://dx.doi.org/10.1182/blood-2009-08-239020.

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Abstract EndoS from Streptococcus pyogenes is an immunomodulating enzyme that specifically hydrolyzes glycans from human immunoglobulin G and thereby affects antibody effector functions. Autoimmune hemolytic anemia is caused by antibody-mediated red blood cell (RBC) destruction and often resists treatment with corticosteroids that also cause frequent adverse effects. We show here that anti-RhD (anti-D) and rabbit anti–human-RBC antibodies (anti-RBC) mediated destruction of RBC, ie, phagocytosis, complement activation, and hemolysis in vitro and in vivo was inhibited by EndoS. Phagocytosis by monocytes in vitro was inhibited by pretreatment of anti-D with EndoS before sensitization of RBCs and abrogated by direct addition of EndoS to blood containing sensitized RBCs. The toxic effects of monocytes stimulated with anti-D–sensitized RBCs, as measured by interleukin-8 secretion and oxygen metabolite production, was restrained by EndoS. Agglutination of RBCs and complement-mediated hemolysis in vitro in whole human blood caused by rabbit anti-RBCs was inhibited by EndoS. Development of anemia in mice caused by a murine anti-RBC immunoglobulin G2a monoclonal autoantibody and complement activation and erythrophagocytosis by Kupffer cells in the liver were reduced by EndoS. Our data indicate that EndoS is a potential therapeutic agent that might be evaluated as an alternative to current treatment regimens against antibody-mediated destruction of RBCs.

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Takashima, Shou, Masaki Kurogochi, Kenji Osumi, Shu-ichi Sugawara, Mamoru Mizuno, Yoshio Takada, Junko Amano, and Akio Matsuda. "Novel endo-β-N-acetylglucosaminidases from Tannerella species hydrolyze multibranched complex-type N-glycans with different specificities." Glycobiology 30, no. 11 (April 27, 2020): 923–34. http://dx.doi.org/10.1093/glycob/cwaa037.

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Abstract Endo-β-N-acetylglucosaminidases are enzymes that hydrolyze the N,N′-diacetylchitobiose unit of N-glycans. Many endo-β-N-acetylglucosaminidases also exhibit transglycosylation activity, which corresponds to the reverse of the hydrolysis reaction. Because of these activities, some of these enzymes have recently been used as powerful tools for glycan remodeling of glycoproteins. Although many endo-β-N-acetylglucosaminidases have been identified and characterized to date, there are few enzymes that exhibit hydrolysis activity toward multibranched (tetra-antennary or more) complex-type N-glycans on glycoproteins. Therefore, we searched for novel endo-β-N-acetylglucosaminidases that exhibit hydrolysis activity toward multibranched complex-type N-glycans in this study. From database searches, we selected three candidate enzymes from Tannerella species—Endo-Tsp1006, Endo-Tsp1263 and Endo-Tsp1457—and prepared them as recombinant proteins. We analyzed the hydrolysis activity of these enzymes toward N-glycans on glycoproteins and found that Endo-Tsp1006 and Endo-Tsp1263 exhibited hydrolysis activity toward complex-type N-glycans, including multibranched N-glycans, preferentially, whereas Endo-Tsp1457 exhibited hydrolysis activity toward high-mannose-type N-glycans exclusively. We further analyzed substrate specificities of Endo-Tsp1006 and Endo-Tsp1263 using 18 defined glycopeptides as substrates, each having a different N-glycan structure. We found that Endo-Tsp1006 preferred N-glycans with galactose or α2,6-linked sialic acid residues in their nonreducing ends as substrates, whereas Endo-Tsp1263 preferred N-glycans with N-acetylglucosamine residues in their nonreducing ends as substrates.

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45

Oh, Soram, Bong-Ki Jeon, and Seok Woo Chang. "Mechanical Properties and Torque/Force Generation of XP-Endo Shaper, Trunatomy, Spring Endo File, and Spring Endo Heated Finish File, Part 1." Applied Sciences 12, no. 20 (October 15, 2022): 10393. http://dx.doi.org/10.3390/app122010393.

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We evaluated the mechanical properties and torque/force generated during canal shaping by four NiTi files with innovative designs. Each of the 52 TruNatomy Prime, XP-endo Shaper, Spring Endo files with unheated finish (Spring Endo), and Spring Endo files with heated finish (Spring H) were subjected to bending, buckling, cyclic fatigue, and torsional resistance tests (n = 10 per NiTi file type). Canal shaping was simulated with J-shaped resin blocks (n = 10). Phase transformation behavior was investigated using differential scanning calorimetry (n = 2). Statistical analysis was performed by one-way ANOVA and the Games–Howell test. Spring Endo and Spring H files showed higher bending and buckling resistances, ultimate torsional strength, and elastic modulus than TruNatomy and XP-endo Shaper (p < 0.05). XP-endo Shaper demonstrated the highest cyclic fatigue resistance and angle of rotation to fracture (p < 0.05). The elastic modulus increased in the order of XP-endo Shaper, TruNatomy Prime, Spring H, and Spring Endo. During simulated canal shaping, XP-endo Shaper generated greater clockwise torque and less screw-in force compared to Spring Endo files, with superior cutting ability. TruNatomy Prime generated the least clockwise torque and screw-in force. At room temperature, TruNatomy and XP-endo Shaper files consisted of mixed phases of austenite, martensite, and R-phase; Spring H files consisted of martensite; and Spring Endo files consisted of austenite.

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46

Alhallak, Iad, Garrett L. Graham, Charles M. Quick, and Rosalia C. M. Simmen. "Co-Morbidity of Type 1 Diabetes Promotes Endometriosis Status-A Pilot Study." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A433. http://dx.doi.org/10.1210/jendso/bvab048.883.

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Abstract Diabetes (DM) is a disease with significant morbidity and mortality and is a major public health problem worldwide. Endometriosis (ENDO) is a chronic estrogen-dependent gynecological condition that affects ~10% of reproductive-age women, causes debilitating pain and infertility, and carries an increased risk for ovarian cancer. Little is known about the co-morbidity of endometriosis and diabetes (Type 1, T1DM; Type 2, T2DM), despite both conditions sharing similar pathophysiology including chronic inflammation triggered by overactivation of the immune response. To evaluate if ENDO is promoted in women diagnosed with DM, we analyzed the expression of key molecular ENDO markers in endometriosis with no associated ovarian lesions collected from non-diabetic and diabetic patients at ENDO surgery. Formalin-fixed, paraffin-embedded sections, identified from analyses of TRINETX data set and retrieved from the Pathology Department, represented women with ENDO alone (n=10; mean age of 42 yo), ENDO/T1DM (n=6; mean age of 28 yo), and ENDO/T2DM (n=7, mean age of 42 yo). Body mass indices (kg/m2) were comparable for women with T1DM (mean of 44.8) and T2DM (mean of 42.5) and higher than for ENDO alone women (mean of 30.8). Endometriotic lesions were analyzed by immunohistochemistry for markers of cellular proliferation (Ki67, PTEN, NICD1) and steroid hormone receptor expression (ESR1, ESR2, PGR-Total, PGR-B) in the epithelial and stromal compartments. We found that immunoreactive ESR1 in lesion epithelial glands (cytoplasm and nuclei) were higher in ENDO/T1DM and ENDO/T2DM than in ENDO alone (P<0.05). ENDO/T1DM lesions also showed higher immunoreactivity for ESR2 (epithelial cytoplasm and nuclei; P<0.05) and Ki67 (epithelial and stromal nuclei; P<0.05) than for ENDO alone and ENDO/T2DM. The nuclear levels of immunoreactive NICD1, the intracellular signaling component of NOTCH1, and of tumor suppressor PTEN tended to be higher and were lower (P<0.05), respectively in lesion stroma of ENDO/T1DM than of the other groups. The nuclear levels of immunoreactive PGR-T in lesion stroma were highly attenuated in ENDO/T1DM compared to ENDO alone and ENDO/T2DM (P<0.05). There were no differences noted in nuclear PGR-B levels among the groups. Limitations to the current study include the small size of patient cohorts, and the diagnosis of DM at, or close to, the time of ENDO surgery. Given the significant changes in key ENDO markers (lower PGR-T and PTEN; higher ESR1, ESR2, Ki67 and NICD1) associated with co-morbid T1DM in ectopic lesions, our findings suggest that women with T1DM show more significant ENDO progression than women without DM and with T2DM. Our results support synergistic co-morbidity of ENDO and T1DM, which while currently underdiagnosed, may have significant implications in ENDO disease management.

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47

Hubbell, Larry. "Waiting to Endow." Public Voices 3, no. 3 (April 11, 2017): 45. http://dx.doi.org/10.22140/pv.353.

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Among the many responsibilities of today's academic department head is manager and fundraiser. This is the story of how Jerry O'Neill, and academic department head, deals with two difficult management problems. On the one hand, he must deal with a potential donor given to making embarrassing statement and on the other hand handle a non-perfurming academic.

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48

Herrmann, B. "To Endow Trust." Science 338, no. 6104 (October 11, 2012): 195. http://dx.doi.org/10.1126/science.1224363.

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49

Hoffman, Brian M. "ENDOR of Metalloenzymes." Accounts of Chemical Research 36, no. 7 (July 2003): 522–29. http://dx.doi.org/10.1021/ar0202565.

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50

Bühlmann, C., A. Schweiger, and R. R. Ernst. "Hyperfine-selective ENDOR." Chemical Physics Letters 154, no. 4 (January 1989): 285–91. http://dx.doi.org/10.1016/0009-2614(89)85357-6.

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Journal articles on the topic 'Endō'

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