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2. Characterization of three sialidases from Danio rerio

Author

Forcella, M, Manzoni, M, Benaglia, G, Bonanomi, M, Giacopuzzi, E, Papini, N, Bresciani, R, Fusi, P, Borsani, G, Monti, E, Forcella M., Manzoni M., Benaglia G., Bonanomi M., Giacopuzzi E., Papini N., Bresciani R., Fusi P., Borsani G., Monti E., Forcella, M, Manzoni, M, Benaglia, G, Bonanomi, M, Giacopuzzi, E, Papini, N, Bresciani, R, Fusi, P, Borsani, G, Monti, E, Forcella M., Manzoni M., Benaglia G., Bonanomi M., Giacopuzzi E., Papini N., Bresciani R., Fusi P., Borsani G., and Monti E.

Abstract

Zebrafish encodes several sialidases belonging to the NEU3 group, the plasma membrane-associated member of the family with high specificity toward ganglioside substrates. Neu3.1, Neu3.2 and Neu 3.3 have been expressed in E. coli and purified using the pGEX-2T expression system. Although all the enzymes are expressed by bacterial cells, Neu3.1 formed insoluble aggregates that hampered its purification. Neu3.2 and Neu3.3 formed oligomers as demonstrated by gel filtration chromatography experiments. Actually, the first formed a trimer whereas the second a pentamer. Intriguingly, despite relevant degree of sequence identity and similarity, the two enzymes showed peculiar substrate specificities toward gangliosides other than GM3, two glycoproteins and two forms of sialyllactose. Using molecular modelling and the crystal structure of the human cytosolic sialidase NEU2 as a template, the 3D models of the sialidases from zebrafish have been generated. As expected, the 3D models showed the typical six blade beta-propeller typical of sialidases, with an overall highly conserved active site architecture. The differences among the three zebrafish enzymes and human NEU2 are mainly located in the loops connecting the antiparallel beta strands of the propeller core. These portions of the proteins are probably responsible for the differences observed in substrate specificities, as well as in the different subcellular localization and aggregation features observed in solution. Finally, the in silico analysis of RNA-Seq data evidenced a peculiar expression profile of the three genes during embryogenesis, suggesting different roles of these sialidases during development.

Published
2021

4. Duration of ruptured membranes and vertical transmission of HIV-1: a meta-analysis from 15 prospective cohort studies

Author

Bulterys, M. B., Fowler, M. G., Hanson, I. C., Lemay, M., Mayaux, M. J., Mofenson, L., Newell, M. -L., Peavy, H., Peckham, C., Read, J. S., Rother, C., Simpson, B. J., Van Dyke, R. B., Harris, D. R., Peavy, H. H., Easley, K., Khammy, A., Nugent, R. P., Mitchell, R., Owen, W., Van Dyke, R., Widmayer, S., Bardeguez, A., Hanson, C., Wiznia, A., Luzuriaga, K., Viscarello, R., Ho, D., Koup, R., Chen, I., Krogstad, P., Mullins, J., Wolinsky, S., Korber, B., Walker, B., Ammann, A., Clapp, S., Mcdonald, D., Lapointe, N., Boucher, M., Fauvel, M., Hankins, C., Samson, J., Newell, M. L., Peckham, C. S., Thorne, C. N., Giaquinto, C., Ruga, E., De Rossi, A., Truscia, D., Grosch-Worner, I., Schafer, A., Mok, J., Johnstone, F., Jiminez, J., de Alba, C., Garcia Rodriguez, M. C., Bates, I., de Josee, I., Hawkins, F., Martinez Zapico, R., Pena, J. M., Gonzalez Garcia, J., Arribas Lopez, J. R., Asensi-Botet, F., Otero, M. C., Peerez-Tamarit, D., Moya, A., Galbis, M. J., Scherpbier, H., Boer, K., Bohlin, A. B., Lindgren, S., Anzen, B., Belfrage, E., Lidin-Jansson, G., Levy, J., Barlow, P., Hainaut, M., Peltier, A., Ferrazin, A., De Maria, A., Gotta, C., Mur, A., Vinolas, M., Paya, A., Loepez-Vilchez, M. A., Coll, O., Fortuny, C., Boguna, J., Casellas Caro, M., Canet, Y., Pardi, G., Ravizza, M., Semprini, E., Castagna, C., Fiore, S., Guerra, B., Lanari, M., Bianchi, S., Bovicelli, L., Prati, E., Zanelli, S., Duse, M., Soresina, A., Scaravelli, G., Stegagno, M., De Santis, M., Muggiasca, M. L., Vigano, A., Spinillo, A., Ravagni Probizer, F., Bucceri, A., Rancilio, L., Taylor, G. P., Lyall, H., Penn, Z., Blott, M., Valerius, N. H., Martinelli, P., Buffolano, W., Tibaldi, C., Ziarati, N., Semprini, A., Della Torre, M., Parazzini, F., Dallacasa, P., Bianchi, U., Pachi, A., Mancuso, S., Villa, P., Conti, M., Principi, N., Muggiasca, M., Marchisio, P., Zara, C., Ravagni, F., Vignali, M., Rossi, G., Selvaggi, L., Greco, P., Vimercati, A., Massi, G., Innocenti, T., Fiscella, A., Sansone, M., Benedetto, C., Tadrist, B., Thevenieau, D., Gondry, J., Paulard, B., Alisy, C., Brault, D., Tordjeman, N., Mamou, J., Rozan, M., Colombani, D., Pincemaille, O., Salvetti, A., Chabanier, C., Hernandorena, X., Leroy, J., Schaal, J., Balde, P., Faucher, P., Lachassinne, E., Benoit, S., Douard, D., Hocke, C., Barjot, P., Brouard, J., Delattre, P., Stien, L., Audibert, F., Labrune, P., Vial, M., Mazy, F., Sitbon, D., Crenn-Hebert, C., Floch-Tudal, C., Akakpo, R., Daveau, C., Leblanc, A., Cesbron, P., Duval-Arnould, M., Huraux-Rendu, C., Lemerle, S., Touboul, C., Guerin, M., Maingueneau, C., Reynaud, I., Rousseau, T., Ercoil, V., Lanza, M., Denavit, M., Garnier, J., Lahsinat, K., Pia, P., Allouche, C., Nardou, M., Grall, F., May, A., Dallot, M., Lhuillier, P., Cecile, W., Mezin, R., Bech, A., Lobut, J., Algava, G., Chalvon Dermesay, A., Busuttil, R., Jacquemot, M., Bader-Meunier, B., Fridman, S., Codaccioni, X., Maxingue, F., Thomas, D., Alain, J., De Lumley, L., Tabaste, J., Bailly Salin, P., Seaume, H., Guichard, A., Kebaill, K., Roussouly, C., Botto, C., De Lanete, A., Wipff, P., Cravello, L., De Boisse, P., Leclaire, M., Michel, G., Crumiere, C., Lefevre, V., Le Lorier, B., Pauly, I., Robichez, B., Seguy, D., Delhinger, M., Rideau, F., Talon, P., Benos, P., Huret, C., Nicolas, J., Heller-Roussin, B., Saint-Leger, S., Delaporte, M., Hubert, C., De Sarcus, B., Karoubi, P., Mechinaud, F., Bertcrottiere, D., Bongain, A., Monpoux, F., De Gennes, C., Devianne, F., Nisand, I., Rousset, M., Mouchnino, G., Muray, J., Munzer, M., Quereux, C., Brossard, V., Clavier, B., Allemon, M., Rotten, D., Stephan, J., Varlet, M., Guyot, B., Narcy, P., Bardinet, F., De Caunes, F., Jeny, R., Robin, M., Raison Boulley, A., Savey, L., Berrebi, A., Tricoire, J., Borderon, J., Fignon, A., Guillot, F., Maria, B., Broyard, A., Chitrit, Y., Firtion, G., Mandelbrot, L., Lafay Pillet, M., Parat, S., Boissinot, C., Garec, N., Levine, M., Ottenwalter, A., Schaller, F., Vilmer, E., Courpotin, C., Brunner, C., Ciraru-Vigneron, N., Hatem-Gantzer, G., Fritel, X., Wallet, A., Bouille, J., Milliez, J., Bensaid Mrejen, D., Dermer, E., Noseda, G., Bardou, D., Cressaty, J., Francoual, C., Carlus Moncomble, C., Cohen, H., Blanche, S., Bastion, H., Benifla, J., Benkhatar, F., Berkane, N., Hervee, F., Ronzier, M., Mayaux, Mj., de Martino, M., Tovo, P. -A., Galli, L., Gabiano, C., Ferraris, G., Garetto, S., Palomba, E., Riva, C., Vierucci, A., de Luca, M., Farina, S., Fundaro, C., Genovese, O., Mereu, G., Forni, G. L., Casadei, A., Zuccotti, G. V., Riva, E., Cellini, M., Baraldi, C., Consolini, R., Palla, G., Ruggeri, M., Ciccimarra, F., Guarino, A., Osimani, P., Benaglia, G., Romano, A., De Mattia, D., Caselli, D., Boni, S., Dell'Erba, G., Bassanetti, F., Sticca, M., Timpano, C., Magnani, C., Salvatore, C., Lipreri, R., Tornaghi, R., Pinzani, R., Cecchi, M. T., Bezzi, T., Battisti, L., Bresciani, E., Castelli Gattinara, G., Nasi, C., Pellegatta, A., Mazza, A., Baldi, F., Altobelli, R., Deiana, M., Colnaghi, C., Tarallo, L., Tondo, U., Anastasio, E., Chiriaco, P. G., Ruggeri, C., Scott, G., Hutto, C., O'Sullivan, M., Malmsberry, A., Willoughby, A., Burns, D., Goedert, J., Landesman, S., Minkoff, H., Mendez, H., Holman, S., Rubinstein, A., Durako, S., Muenz, L., Goodwin, S., Bryson, Y., Dillon, M., Nielsen, K., Boyer, P., Liao, D., Keller, M., Deveikis, A., Nesheim, S., Lindsay, M., Lee, F., Nahmias, A., Sawyer, M., Vink, P., Farley, J., Alger, L., Abrams, E., Bamji, M., Lambert, G., Schoenbaum, E., Thomas, P., Weedon, J., Palumbo, P., Denny, T., Oleske, J., Bulterys, M., Simonds, R., Ethier-Ives, J., Rogers, M., Schluchter, M., Kutner, M., Kaplan, S., Kattan, M., Lipshultz, S., Mellins, R., Shearer, W., Sopko, G., Sloand, E., Wu, M., Kind, C., Nadal, D., Rudin, C., Siegrist, C. -A., Wyler, C. -A., Cheseaux, J. -J., Aebi, C., Gnehm, H., Schubiger, G., Klingler, J., Hunziker, U., Kuchler, H., Gianinazzi, M., Buhlmann, U., Biedermann, K., Lauper, U., Irion, O., Brunelli, A., Spoletini, G., Schreyer, A., Hosli, I., Saurenmann, E., Drack, G., Isenschmid, M., Poorbeik, M., Schupbach, J., Perrin, L., Erb, P., Joller, H., Kovacs, A., Stek, A., Chan, L., Khoury, M., Diaz, C., Pacheco-Acosta, E., Tuomala, R., Cooper, E., Mesthene, D., Pitt, J., Higgins, A., Moroso, G., Rich, K., Turpin, D., Cooper, N., Davenny, K., Thompson, B., Andiman, W., Simpson, J., THE INTERNATIONAL PERINATAL HIV, Group, Martinelli, Pasquale, Bulterys M.B., Fowler M.G., Hanson I.C., Lemay M., Mayaux M.J., Mofenson L., Newell M.-L., Peavy H., Peckham C., Read J.S., Rother C., Simpson B.J., Van Dyke R.B., Harris D.R., Peavy H.H., Easley K., Khammy A., Nugent R.P., Mitchell R., Owen W., Van Dyke R., Widmayer S., Bardeguez A., Hanson C., Wiznia A., Luzuriaga K., Viscarello R., Ho D., Koup R., Chen I., Krogstad P., Mullins J., Wolinsky S., Korber B., Walker B., Ammann A., Clapp S., McDonald D., Lapointe N., Boucher M., Fauvel M., Hankins C., Samson J., Newell M.L., Peckham C.S., Thorne C.N., Giaquinto C., Ruga E., De Rossi A., Truscia D., Grosch-Worner I., Schafer A., Mok J., Johnstone F., Jiminez J., de Alba C., Garcia Rodriguez M.C., Bates I., de Josee I., Hawkins F., Martinez Zapico R., Pena J.M., Gonzalez Garcia J., Arribas Lopez J.R., Asensi-Botet F., Otero M.C., Peerez-Tamarit D., Moya A., Galbis M.J., Scherpbier H., Boer K., Bohlin A.B., Lindgren S., Anzen B., Belfrage E., Lidin-Jansson G., Levy J., Barlow P., Hainaut M., Peltier A., Ferrazin A., De Maria A., Gotta C., Mur A., Vinolas M., Paya A., Loepez-Vilchez M.A., Coll O., Fortuny C., Boguna J., Casellas Caro M., Canet Y., Pardi G., Ravizza M., Semprini E., Castagna C., Fiore S., Guerra B., Lanari M., Bianchi S., Bovicelli L., Prati E., Zanelli S., Duse M., Soresina A., Scaravelli G., Stegagno M., De Santis M., Muggiasca M.L., Vigano A., Spinillo A., Ravagni Probizer F., Bucceri A., Rancilio L., Taylor G.P., Lyall H., Penn Z., Blott M., Valerius N.H., Martinelli P., Buffolano W., Tibaldi C., Ziarati N., Semprini A., Della Torre M., Parazzini F., Dallacasa P., Bianchi U., Pachi A., Mancuso S., Villa P., Conti M., Principi N., Muggiasca M., Marchisio P., Zara C., Ravagni F., Vignali M., Rossi G., Selvaggi L., Greco P., Vimercati A., Massi G., Innocenti T., Fiscella A., Sansone M., Benedetto C., Tadrist B., Thevenieau D., Gondry J., Paulard B., Alisy C., Brault D., Tordjeman N., Mamou J., Rozan M., Colombani D., Pincemaille O., Salvetti A., Chabanier C., Hernandorena X., Leroy J., Schaal J., Balde P., Faucher P., Lachassinne E., Benoit S., Douard D., Hocke C., Barjot P., Brouard J., Delattre P., Stien L., Audibert F., Labrune P., Vial M., Mazy F., Sitbon D., Crenn-Hebert C., Floch-Tudal C., Akakpo R., Daveau C., Leblanc A., Cesbron P., Duval-Arnould M., Huraux-Rendu C., Lemerle S., Touboul C., Guerin M., Maingueneau C., Reynaud I., Rousseau T., Ercoil V., Lanza M., Denavit M., Garnier J., Lahsinat K., Pia P., Allouche C., Nardou M., Grall F., May A., Dallot M., Lhuillier P., Cecile W., Mezin R., Bech A., Lobut J., Algava G., Chalvon Dermesay A., Busuttil R., Jacquemot M., Bader-Meunier B., Fridman S., Codaccioni X., Maxingue F., Thomas D., Alain J., De Lumley L., Tabaste J., Bailly Salin P., Seaume H., Guichard A., Kebaill K., Roussouly C., Botto C., De Lanete A., Wipff P., Cravello L., De Boisse P., Leclaire M., Michel G., Crumiere C., Lefevre V., Le Lorier B., Pauly I., Robichez B., Seguy D., Delhinger M., Rideau F., Talon P., Benos P., Huret C., Nicolas J., Heller-Roussin B., Saint-Leger S., Delaporte M., Hubert C., De Sarcus B., Karoubi P., Mechinaud F., Bertcrottiere D., Bongain A., Monpoux F., De Gennes C., Devianne F., Nisand I., Rousset M., Mouchnino G., Muray J., Munzer M., Quereux C., Brossard V., Clavier B., Allemon M., Rotten D., Stephan J., Varlet M., Guyot B., Narcy P., Bardinet F., De Caunes F., Jeny R., Robin M., Raison Boulley A., Savey L., Berrebi A., Tricoire J., Borderon J., Fignon A., Guillot F., Maria B., Broyard A., Chitrit Y., Firtion G., Mandelbrot L., Lafay Pillet M., Parat S., Boissinot C., Garec N., Levine M., Ottenwalter A., Schaller F., Vilmer E., Courpotin C., Brunner C., Ciraru-Vigneron N., Hatem-Gantzer G., Fritel X., Wallet A., Bouille J., Milliez J., Bensaid Mrejen D., Dermer E., Noseda G., Bardou D., Cressaty J., Francoual C., Carlus Moncomble C., Cohen H., Blanche S., Bastion H., Benifla J., Benkhatar F., Berkane N., Hervee F., Ronzier M., Mayaux MJ., de Martino M., Tovo P.-A., Galli L., Gabiano C., Ferraris G., Garetto S., Palomba E., Riva C., Vierucci A., de Luca M., Farina S., Fundaro C., Genovese O., Mereu G., Forni G.L., Casadei A., Zuccotti G.V., Riva E., Cellini M., Baraldi C., Consolini R., Palla G., Ruggeri M., Ciccimarra F., Guarino A., Osimani P., Benaglia G., Romano A., De Mattia D., Caselli D., Boni S., Dell'Erba G., Bassanetti F., Sticca M., Timpano C., Magnani C., Salvatore C., Lipreri R., Tornaghi R., Pinzani R., Cecchi M.T., Bezzi T., Battisti L., Bresciani E., Castelli Gattinara G., Nasi C., Pellegatta A., Mazza A., Baldi F., Altobelli R., Deiana M., Colnaghi C., Tarallo L., Tondo U., Anastasio E., Chiriaco P.G., Ruggeri C., Scott G., Hutto C., O'Sullivan M., Malmsberry A., Willoughby A., Burns D., Goedert J., Landesman S., Minkoff H., Mendez H., Holman S., Rubinstein A., Durako S., Muenz L., Goodwin S., Bryson Y., Dillon M., Nielsen K., Boyer P., Liao D., Keller M., Deveikis A., Nesheim S., Lindsay M., Lee F., Nahmias A., Sawyer M., Vink P., Farley J., Alger L., Abrams E., Bamji M., Lambert G., Schoenbaum E., Thomas P., Weedon J., Palumbo P., Denny T., Oleske J., Bulterys M., Simonds R., Ethier-Ives J., Rogers M., Schluchter M., Kutner M., Kaplan S., Kattan M., Lipshultz S., Mellins R., Shearer W., Sopko G., Sloand E., Wu M., Kind C., Nadal D., Rudin C., Siegrist C.-A., Wyler C.-A., Cheseaux J.-J., Aebi C., Gnehm H., Schubiger G., Klingler J., Hunziker U., Kuchler H., Gianinazzi M., Buhlmann U., Biedermann K., Lauper U., Irion O., Brunelli A., Spoletini G., Schreyer A., Hosli I., Saurenmann E., Drack G., Isenschmid M., Poorbeik M., Schupbach J., Perrin L., Erb P., Joller H., Kovacs A., Stek A., Chan L., Khoury M., Diaz C., Pacheco-Acosta E., Tuomala R., Cooper E., Mesthene D., Pitt J., Higgins A., Moroso G., Rich K., Turpin D., Cooper N., Davenny K., Thompson B., Andiman W., and Simpson J.

Subjects
Time Factors, Epidemiology, Infectious Disease Transmission, Prevention of perinatal transmission, Extraembryonic Membranes, Human immunodeficiency virus (HIV), HIV Infections, medicine.disease_cause, Cohort Studies, Pregnancy, Risk Factors, INFECTION, Vertical, Immunology and Allergy, HIV Infection, MOTHER-TO-CHILD, Pregnancy Complications, Infectious, Prospective cohort study, prevention of perinatal transmission, vertical transmission, obstetrics/gynaecology, epidemiology, Obstetrics, Transmission (medicine), Infectious, HUMAN-IMMUNODEFICIENCY-VIRUS, MOTHER-TO-CHILD, ZIDOVUDINE PROPHYLAXIS, RISK-FACTORS, TYPE-1, PREGNANCY, INFECTION, TRIAL, PREVENTION, Breast Feeding, Infectious Diseases, Meta-analysis, HUMAN-IMMUNODEFICIENCY-VIRUS, Vertical transmission, Regression Analysis, TRIAL, Female, Delivery, Obstetrics gynaecology, Human, medicine.medical_specialty, Time Factor, Ruptured membranes, Immunology, Regression Analysi, NO, ZIDOVUDINE PROPHYLAXIS, Extraembryonic Membrane, medicine, Humans, TYPE-1, business.industry, Risk Factor, Infant, Newborn, Infant, Obstetric, Delivery, Obstetric, Newborn, PREVENTION, Infectious Disease Transmission, Vertical, Pregnancy Complications, Obstetrics/gynaecology, RISK-FACTORS, Cohort Studie, business
Abstract

Objective: To test the a priori hypothesis that longer duration of ruptured membranes is associated with increased risk of vertical transmission of HIV. Design: The relationship between duration of ruptured membranes and vertical transmission of HIV was evaluated in an individual patient data meta-analysis. Methods: Eligible studies were prospective cohort studies including at least 100 mother-child pairs, from regions where HIV-infected women are counselled not to breastfeed. Analyses were restricted to vaginal deliveries and non-elective Cesarean sections; elective Cesarean section deliveries (those performed before onset of labour and before rupture of membranes) were excluded. Results: The primary analysis included 4721 deliveries with duration of ruptured membranes ≤ 24 h. After adjusting for other factors known to be associated with vertical transmission using logistic regression analysis to assess the strength of the relationship, the risk of vertical HIV transmission increased approximately 2% with an increase of 1 h in the duration of ruptured membranes [adjusted odds ratio, 1.02; 95% confidence interval, 1.01-1.04; for each 1 h increment]. There were no significant interactions of duration of ruptured membranes with study cohort or with any of the covariates, except maternal AIDS. Among women diagnosed with AIDS, the estimated probability of transmission increased from 8% to 31% with duration of ruptured membranes of 2 h and 24 h respectively (P < 0.01). Conclusions: These results support the importance of duration of ruptured membranes as a risk factor for vertical transmission of HIV and suggest that a diagnosis of AIDS in the mother at the time of delivery may potentiate the effect of duration of ruptured membranes. © 2001 Lippincott Williams & Wilkins.

Published
2001
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5. Puberty in perinatal HIV-1 infection: a multicentre longitudinal study of 212 children

Author

de Martino M, Tovo PA, Galli L, Gabiano C, Chiarelli F, Zappa M, Gattinara GC, Bassetti D, Giacomet V, Chiappini E, Duse M, Garetto S, Caselli D, Italian Register for HIV infection in Children ( Catania S, FundaroÁ C, Cellini M, Lipreri R, Zuccotti GV, Cecchi MT, Mazza A, Masi M, Consolini R, Bezzi MT, Benaglia G, Ganau A., GUARINO, ALFREDO, de Martino, M, Tovo, Pa, Galli, L, Gabiano, C, Chiarelli, F, Zappa, M, Gattinara, Gc, Bassetti, D, Giacomet, V, Chiappini, E, Duse, M, Garetto, S, Caselli, D, Italian Register for HIV infection in Children, ( Catania S, Fundaroá, C, Cellini, M, Lipreri, R, Zuccotti, Gv, Cecchi, Mt, Guarino, Alfredo, Mazza, A, Masi, M, Consolini, R, Bezzi, Mt, Benaglia, G, and Ganau, A.

Subjects
Male, Percentile, Pediatrics, medicine.medical_specialty, Longitudinal study, adolescence, HIV-1, perinatal infection, puberty, Tanner stage, Adolescent, Anti-HIV Agents, Immunology, HIV Infections, Age Distribution, Acquired immunodeficiency syndrome (AIDS), Immunopathology, medicine, Immunology and Allergy, Humans, Longitudinal Studies, Child, Rank correlation, business.industry, Puberty, Infant, Newborn, medicine.disease, Confidence interval, Log-rank test, Fetal Diseases, Infectious Diseases, El Niño, Female, business
Abstract

OBJECTIVE: To define age at entry into Tanner stages in children with perinatal HIV-1 infection. DESIGN: Multicentre longitudinal study including 212 perinatally HIV-1-infected children (107 girls and 105 boys) followed-up during puberty (from 8 and 9 years onwards in girls and boys, respectively). Healthy children (843 girls and 821 boys) provided reference percentiles. P2 or B2 stages in girls and P2 or G2 stages in boys defined onset of puberty. METHODS: The cumulative probability [95% confidence limit (CI)] of entry into each stage at different ages was estimated by the Kaplan-Meier product-limit method; differences were evaluated by log rank test. Relationships were tested using the Spearman's rank correlation coefficient. RESULTS: Ages of girls [years (95%CI)] at P2 [12.9 (12.6-13.2)], P3 [13.4 (13.0-13.8)], P4 [14.6 (14.0-15.2)], B2 [12.7 (12.2-13.2)], B3 [13.3 (12.8-14.0)] and B4 [14.6 (14.0-15.2)] stages were > 97th percentile (> or = 21 month delay) of controls. Ages of boys [years (95%CI)] at P2 [12.6 (12.1-13.1)], P3 [13.9 (13.4-14.4)], P4 [14.9 (14.2-15.6)], G2 [12.1 (11.5-12.7)], G3 [13.6 (13.1-14.1)] and G4 [14.9 (14.1-15.7)] stages were at the 75-97th percentiles (< or = 15 month delay). Age at onset of puberty was not related to clinical and immunological condition, antiretroviral treatment, weigh for height and age at onset of severe disease or immune suppression. CONCLUSION: Perinatal HIV-1 infection interferes with sexual maturation. The mechanisms by which this occurs should be elucidated and intervention strategies designed. Intervention could save much psychological distress, since associated linear growth failure can exacerbate adolescents' feelings of being different and unwell.

Published
2001

6. HIV-1 transmission through breast-milk

Author

De Martino, M., Tovo, P. A., Tozzi, A. E., Pezzotti, P., Galli, L., Liviadotti, S., Caselli, D., Marchisio, P., Giaquinto, G., Fioredda, F., Plebani, A., Gabiano, C., Zuccotti, V. G., Conte, A., Rizzi, M., Mazzoni, P. L., Ibba, P., Ferrarris, G., Benaglia, G., Stegagno, M., Masi, M., Dallacasa, P., Duse, Marzia, Rossi, G., Sciotto, A., Barbanera, M., De Mattia, D., Zaniboni, M., Bezzi, T., Campelli, A., Ciccimarra, F., Bassanetti, F., Consolini, R., Mazza, A., Tarallo, L., Altobelli, R., Castaldo, A., and Fundarò, C.

Subjects
medicine.medical_specialty, Multivariate analysis, business.industry, Immunology, Gestational age, Odds ratio, Logistic regression, medicine.disease, Confidence interval, Surgery, Infectious Diseases, Acquired immunodeficiency syndrome (AIDS), Immunology and Allergy, Medicine, Risk factor, business, Breast feeding, Demography
Abstract

Objectives To estimate the risk of HIV-1 transmission through breast-milk in children born to infected mothers, and to determine the relationship between duration of breast-feeding and risk. Design and methods The study population included 168 breast-fed and 793 bottle-fed children born to seropositive mothers. All subjects were enrolled and followed-up in the Italian Register for HIV Infection in Children; HIV sero-status was defined in all children. Multivariate analysis was performed using a logistic regression model. Independent variables included biological factors (duration of breast-feeding, gestational age, clinical condition of mother at delivery, mode of delivery, birth-weight and sex). Year of birth and age when HIV infection was diagnosed were also considered in the analysis attempting to control for possible selection biases. Results Breast-feeding increased the risk of HIV-1 transmission. The estimated adjusted odds ratio for 1 day of breast- versus bottle-feeding was 1.19 (95% confidence interval, 1.10-1.28). The infection odds ratio of breast- versus bottle-feeding increased with the natural logarithm of the duration of practice. Conclusions These results are the first to provide an appraisal of the additional risk of HIV-1 transmission associated with a seropositive mother breast-feeding her child. Biological significance of this route of transmission was supported by demonstration of a relationship between duration of breast-feeding and risk of HIV-1 transmission.

Published
1992
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8. Mother to child transmission of Hepatitis C Virus in a province of Northern Italy

Author

Veronesi, Licia, Verrotti Di Pianella, C, Benassi, L, Benaglia, G, Affanni, Paola, Tanzi, Elisabetta, Veronesi, Licia, Verrotti Di Pianella, C, Benassi, L, Benaglia, G, Affanni, Paola, and Tanzi, Elisabetta

Abstract

NTRODUCTION: Study reports of mother to child transmission of hepatitis C virus (HCV) have shown transmission rates ranging from 3 to 37%, according to maternal viremia and HIV-1 coinfection. The present study evaluated the prevalence of the HCV infection in the general population and the incidence of vertical transmission, from women who delivered in the Obstetric Clinic of the Hospital of Parma from January 1st 1996 to 31st 2001 December. METHODS: Mothers and children were tested for the presence of HCV-RNA within one week after delivery. Children were considered to be infected when they were found positive at least twice for viral RNA or antibodies were still detectable at the end of the follow-up period (18 months) in blood. RESULTS: Out of 13,025 women, 110 (0.8%) were found positive for anti-HCV antibodies; 72 of them (65.4%) were HCV-RNA positive. All 110 children were positive for anti-HCV antibodies in the first blood sample (time 0); 8 of them were HCV-RNA positive. Three children were still viremic at the end of the follow-up whereas 5 showed a clearance. No significant differences were found between viremic and nonviremic children with respect to gestational week, maternal alanine aminotransferase (ALT) levels and newborns weight at birth. CONCLUSION: This investigation shows that vertical transmission may occur in a general obstetric population despite a low prevalence of HCV-positive subjects.

Published
2007

10. Fallout from Chernobyl Thyroid cancer in children increased dramatically in Belarus

Author

Williams, E D, primary, Abelin, T, additional, Egger, M, additional, Ruchti, C, additional, Petridou, E, additional, Kampmann, B, additional, Sperling, K, additional, Pelz, J, additional, Wegner, R D, additional, Dorries, A, additional, Gruters, A, additional, Mikkelsen, M, additional, Butturini, A, additional, Izzi, G, additional, Benaglia, G, additional, Lloyd, D, additional, Pass, B, additional, Gale, R P, additional, Boice, J, additional, Linet, M, additional, Ambach, W, additional, Rehwald, W, additional, Auvinen, A, additional, Arvela, H, additional, Rahola, T, additional, Suomela, M, additional, Rytomaa, T, additional, Hakama, M, additional, Hakulinen, T, additional, and Soderman, B, additional

Published
1994
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11. EPIDEMIOLOGY, CLINICAL FEATURES, AND PROGNOSTIC FACTORS OF PAEDIATRIC HIV INFECTION

Author

Tovo, P. A., de Martino, M., Caramia), G., Armenio, L., Schettini, F., De Mattia, D., Chiodo, F., Masi, M., Trombacco, M. G., Zaniboni, M. G., Duse, Marzia, Vertua, G., Quarta, G., Cao, A., Dessi', C., Di Gregorio, F., Bezzi, T., Cocchi, P., Calabri, G., Vierucci, A., Galli, L., Boeri, E., Jannuzzi, C., Terragna, A., De Maria, A., Sanpietro, F., Barbanera, M., Bardare, M., Plebani, A., Giovannini, M., Magni, L. A., Marchisio, P., Tornaghi, R., Rossi, A., Esposito, L., Guarino, A., Romano, G., Viggiano, D., Zacchello, F., Giaquinto, C., Chieco Bianchi, L., Benaglia, G., Bertolini, P., Arico', M., Caselli, D., Bassanetti, F., Consolini, R., Antonellini, A., Magnani, C., Calvani, M., Falconieri, P., Segni, G., Fundaro', C., Gabiano, C., Palomba, E., Perugini, L., and Negro, F.

Subjects
Hepatitis, Pediatrics, medicine.medical_specialty, Pregnancy, business.industry, Vaginal delivery, Mortality rate, Secondary infection, General Medicine, medicine.disease, Substance abuse, Epidemiology, medicine, Lymphoid interstitial pneumonia, business
Abstract

486 children born to HIV-positive mothers, 57 children infected by blood products, and 1 child for whom the personal history was not available were studied. Perinatal infection had a more varied clinical picture and a worse outcome compared with infection acquired later in childhood. Severe secondary infections, neurological disorders, and hepatitis (but not lymphoid interstitial pneumonia) were linked to a high mortality rate in perinatally infected children, in whom an early onset of symptoms was also a bad prognostic factor. Perinatal HIV infection occurred in 32·6% of children born to seropositive mothers, with a higher transmission rate in children born by vaginal delivery and then breast-fed. Preterm delivery and low birthweight seemed to be related to drug abuse during pregnancy, not to intrauterine HIV infection. Girls had a higher rate of perinatal infection and, of those infected, had an increased mortality.

Published
1988
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15. Characterization of three sialidases from Danio rerio

Author

Matilde Forcella, Eugenio Monti, Roberto Bresciani, Giuseppe Borsani, Nadia Papini, Paola Fusi, Giuliana Benaglia, Edoardo Giacopuzzi, Marta Manzoni, Marcella Bonanomi, Forcella, M, Manzoni, M, Benaglia, G, Bonanomi, M, Giacopuzzi, E, Papini, N, Bresciani, R, Fusi, P, Borsani, G, and Monti, E

Subjects
0301 basic medicine, Aggregation in solution, In silico gene expression, Molecular modelling, Recombinant sialidases, Substrate specificities, Animals, Humans, Neuraminidase, Protein Domains, Recombinant Proteins, Zebrafish Proteins, Protein Multimerization, Zebrafish, Pentamer, In silico, Beta sheet, Sialidase, Antiparallel (biochemistry), Biochemistry, NEU2, 03 medical and health sciences, 030102 biochemistry & molecular biology, biology, Chemistry, Recombinant sialidase, Active site, General Medicine, biology.organism_classification, 030104 developmental biology, biology.protein, Substrate specificitie
Abstract

Zebrafish encodes several sialidases belonging to the NEU3 group, the plasma membrane-associated member of the family with high specificity toward ganglioside substrates. Neu3.1, Neu3.2 and Neu 3.3 have been expressed in E. coli and purified using the pGEX-2T expression system. Although all the enzymes are expressed by bacterial cells, Neu3.1 formed insoluble aggregates that hampered its purification. Neu3.2 and Neu3.3 formed oligomers as demonstrated by gel filtration chromatography experiments. Actually, the first formed a trimer whereas the second a pentamer. Intriguingly, despite relevant degree of sequence identity and similarity, the two enzymes showed peculiar substrate specificities toward gangliosides other than GM3, two glycoproteins and two forms of sialyllactose. Using molecular modelling and the crystal structure of the human cytosolic sialidase NEU2 as a template, the 3D models of the sialidases from zebrafish have been generated. As expected, the 3D models showed the typical six blade beta-propeller typical of sialidases, with an overall highly conserved active site architecture. The differences among the three zebrafish enzymes and human NEU2 are mainly located in the loops connecting the antiparallel beta strands of the propeller core. These portions of the proteins are probably responsible for the differences observed in substrate specificities, as well as in the different subcellular localization and aggregation features observed in solution. Finally, the in silico analysis of RNA-Seq data evidenced a peculiar expression profile of the three genes during embryogenesis, suggesting different roles of these sialidases during development.

Published
2021

16. Metabolic correction in oligodendrocytes derived from metachromatic leukodystrophy mouse model by using encapsulated recombinant myoblasts

Author

Sergio Marchesini, Massimo Conese, Nicole Déglon, Antonella Consiglio, Claudio Bordignon, Sabata Martino, Patrick Aebischer, Lawrence Wrabetz, Gabriella Cusella, Giuliana Benaglia, Giovanni Maria Severini, D. Dolcetta, Aldo Orlacchio, Consiglio, A., Martino, S., Dolcetta, D., Cusella, G., Conese, M., Marchesini, S., Benaglia, G., Wrabetz, L., Orlacchio, A., Déglon, N., Aebischer, P., Severini, G. M., and Bordignon, Claudio

Subjects
Capsules/therapeutic use, Arylsulfatase A, Polymers, Myoblasts, Genetic Vectors/*genetics, Mice, Transduction, Genetic, Myoblasts/enzymology/*transplantation, Transgenes, Arylsulfatases, Mice, Knockout, Cell Survival/physiology, Oligodendrocytes, Genetic/*methods, Graft Survival, Metachromatic/enzymology/genetics/*therapy, Cell encapsulation, Graft Survival/physiology, Up-Regulation, Cell biology, Oligodendroglia, Treatment Outcome, medicine.anatomical_structure, Neurology, Biochemistry, Neuroglia, MLD mouse model, C2C12, Nerve Regeneration/genetics, Gene therapy, Cell Survival, Transgenes/genetics, Knockout, Genetic Vectors, Transplantation, Heterologous, Capsules, Biology, Cell Line, Viral vector, Up-Regulation/genetics, Transduction, medicine, Animals, Humans, Viability assay, Polymers/therapeutic use, Transplantation, Sulfoglycosphingolipids, Animal, Leukodystrophy, Leukodystrophy, Metachromatic, medicine.disease, Heterologous/methods, Nerve Regeneration, Metachromatic leukodystrophy, Disease Models, Animal, Oligodendroglia/*enzymology, Sulfoglycosphingolipids/metabolism, Cell culture, Disease Models, Arylsulfatases/genetics/metabolism/secretion, Neurology (clinical)
Abstract

In an effort to develop an encapsulated cell-based system to deliver arylsulfatase A (ARSA) to the central nervous system of metachromatic leukodystrophy (MLD) patients, we engineered C2C12 mouse myoblasts with a retroviral vector containing a full-length human ARSA cDNA and evaluated the efficacy of the recombinant secreted enzyme to revert the MLD phenotype in oligodendrocytes (OL) of the As2-/- mouse model. After transduction, C2C12 cells showed a fifteen-fold increase in intracellular ARSA activity and five-fold increase in ARSA secretion. The secreted hARSA collected from transduced cells encapsulated in polyether-sulfone polymer, was taken up by enzyme-deficient OL derived from MLD mice and normally sorted to the lysosomal compartment, where transferred enzyme reached 80% of physiological levels, restoring the metabolism of sulfatide. To evaluate whether secreted enzyme could restore metabolic function in the brain, encapsulated cells and secreted ARSA were shown to be stable in CSF in vitro. Further, to test cell viability and enzyme release in vivo, encapsulated cells were implanted subcutaneously on the dorsal flank of DBA/2J mice. One month later, all retrieved implants released hARSA at rates similar to unencapsulated cells and contained well preserved myoblasts, demonstrating that encapsulation maintains differentiation of C2C12 cells, stable transgene expression and long-term cell viability in vivo. Thus, these results show the promising potential of developing an ARSA delivery system to the CNS based on the use of a polymer-encapsulated transduced xenogenic cell line for gene therapy of MLD.

Published
2007
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17. In vivo gene therapy of metachromatic leukodystrophy by lentiviral vectors: correction of neuropathology and protection against learning impairments in affected mice

Author

Antonella Consiglio, D. Dolcetta, Jean Charles Bensadoun, Claudio Bordignon, Sabata Martino, Luigi Naldini, Alberto Oliverio, Angelo Quattrini, Giuliana Benaglia, Alessandra Trojani, Sergio Marchesini, Vincenzo Cestari, Consiglio, A., Quattrini, A, Martino, S., Bensadoun, J. C., Dolcetta, D., Trojani, A., Benaglia, G., Marchesini, S., Cestari, V., Oliviero, A, Bordignon, Claudio, and Naldini, Luigi

Subjects
Arylsulfatase A, Genetic enhancement, Central nervous system, Genetic Vectors, lysosomal enzymes, Neuropathology, Biology, Cerebroside-Sulfatase/genetics/metabolism, arylsulfatase A activity, General Biochemistry, Genetics and Molecular Biology, Brain/enzymology/metabolism/pathology, Mice, In vivo, medicine, Animals, Humans, Metachromatic/complications/pathology/*therapy, Gene, Cerebroside-Sulfatase, lipid metabolic restoration, Learning Disabilities, Leukodystrophy, Lentivirus, Brain, General Medicine, Lentivirus/*genetics, Genetic Therapy, Leukodystrophy, Metachromatic, medicine.disease, Lipid Metabolism, gene therapy, Metachromatic leukodystrophy, medicine.anatomical_structure, Immunology, Cancer research, Learning Disorders/etiology/*prevention & control
Abstract

Metachromatic leukodystrophy (MLD) is a lipidosis caused by deficiency of arylsulfatase A (ARSA). Although the genetics of MLD are known, its pathophysiology is not understood. The disease leads to progressive demyelination and early death and no effective treatment is available. We used lentiviral vectors to deliver a functional ARSA gene (human ARSA) into the brain of adult mice with germ-line inactivation of the mouse gene encoding ARSA, As2. We report sustained expression of active enzyme throughout a large portion of the brain, with long-term protection from development of neuropathology and hippocampal-related learning impairments. We show that selective degeneration of hippocampal neurons is a central step in disease pathogenesis, and provide evidence that in vivo transfer of ARSA by lentiviral vectors reverts the disease phenotype in all investigated areas. Therefore, in vivo gene therapy offers a unique option for MLD and other storage diseases affecting the central nervous system.

Published
2001

18. Downregulation of Zebrafish Cytosolic Sialidase Neu3.2 Affects Skeletal Muscle Development.

Author

Zizioli D, Codenotti S, Benaglia G, Manzoni M, Massardi E, Fanzani A, Borsani G, and Monti E

Subjects
Animals, Down-Regulation, Muscle, Skeletal, Muscle Development genetics, Neuraminidase genetics, Zebrafish, Zebrafish Proteins genetics
Abstract

Sialidases remove terminal sialic acids residues from the non-reducing ends of glycoconjugates. They have been recognized as catabolic enzymes that work within different subcellular compartments and can ensure the proper turn-over of glycoconjugates. Four mammalian sialidases (NEU1-4) exist, with different subcellular localization, pH optimum and substrate specificity. In zebrafish, seven different sialidases, with high homology to mammalian counterparts, have been identified. Zebrafish Neu3.2 is similar to the human cytosolic sialidase NEU2, which is involved in skeletal muscle differentiation and exhibits a broad substrate specificity toward gangliosides and glycoproteins. In zebrafish neu3.2 , mRNA is expressed during somite development, and its enzymatic activity has been detected in the skeletal muscle and heart of adult animals. In this paper, 1-4-cell-stage embryos injected with neu3.2 splice-blocking morpholino showed severe embryonic defects, mainly in somites, heart and anterior-posterior axis formation. Myog and myod1 expressions were altered in morphants, and impaired musculature formation was associated with a defective locomotor behavior. Finally, the co-injection of Neu2 mouse mRNA in morphants rescued the phenotype. These data are consistent with the involvement of cytosolic sialidase in pathologies related to muscle formation and support the validity of the model to investigate the pathogenesis of the diseases.

Published
2023
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19. Human sialic acid acetyl esterase: Towards a better understanding of a puzzling enzyme.

Author

Orizio F, Damiati E, Giacopuzzi E, Benaglia G, Pianta S, Schauer R, Schwartz-Albiez R, Borsani G, Bresciani R, and Monti E

Subjects
Acetylesterase chemistry, Acetylesterase genetics, Amino Acid Sequence, Animals, COS Cells, Chlorocebus aethiops, Humans, Molecular Sequence Data, Phylogeny, Protein Isoforms chemistry, Protein Isoforms genetics, Protein Isoforms metabolism, Protein Structure, Tertiary, Protein Transport, Acetylesterase metabolism
Abstract

Sialic acid acetyl esterase (SIAE) removes acetyl moieties from the hydroxyl groups in position 9 and 4 of sialic acid. Recently, a dispute has been opened on its association to autoimmunity. In order to get new insights on human SIAE biology and to clarify its seemingly contradictory molecular properties, we combined in silico characterization, phylogenetic analysis and homology modeling with cellular studies in COS7 cells. Genomic and phylogenetic analysis revealed that in most tissues only the "long" isoform, originally referred to lysosomal sialic acid esterase, is detected. Using the homology modeling approach, we predicted a model of SIAE 3D structure, which fulfills the topological features of SGNH-hydrolase family. In addition, the model and site-directed mutagenesis experiments allowed the definition of the residues involved in catalysis. SIAE transient expression revealed that the protein is glycosylated and is active in vitro as an esterase with a pH optimum corresponding to 8.4-8.5. Moreover, glycosylation influences the biological activity of the enzyme and is essential for release of SIAE into the culture medium. According to these findings, co-localization experiments demonstrated the presence of SIAE in membranous structures corresponding to endoplasmic reticulum and Golgi complex. Thus, at least in COS7 cells, SIAE behaves as a typical secreted enzyme, subjected to glycosylation and located along the classical secretory route or in the extracellular space. In these environments, the enzyme could act on 9-O-acetylated sialic acid residues, contributing to the fine-tuning of the various functions played by this acidic sugar., (© The Author 2015. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Published
2015
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20. In vivo gene therapy of metachromatic leukodystrophy by lentiviral vectors: correction of neuropathology and protection against learning impairments in affected mice.

Author

Consiglio A, Quattrini A, Martino S, Bensadoun JC, Dolcetta D, Trojani A, Benaglia G, Marchesini S, Cestari V, Oliverio A, Bordignon C, and Naldini L

Subjects
Animals, Brain enzymology, Brain metabolism, Brain pathology, Cerebroside-Sulfatase genetics, Cerebroside-Sulfatase metabolism, Humans, Learning Disabilities etiology, Leukodystrophy, Metachromatic complications, Leukodystrophy, Metachromatic pathology, Lipid Metabolism, Mice, Genetic Therapy, Genetic Vectors, Learning Disabilities prevention & control, Lentivirus genetics, Leukodystrophy, Metachromatic therapy
Abstract

Metachromatic leukodystrophy (MLD) is a lipidosis caused by deficiency of arylsulfatase A (ARSA). Although the genetics of MLD are known, its pathophysiology is not understood. The disease leads to progressive demyelination and early death and no effective treatment is available. We used lentiviral vectors to deliver a functional ARSA gene (human ARSA) into the brain of adult mice with germ-line inactivation of the mouse gene encoding ARSA, As2. We report sustained expression of active enzyme throughout a large portion of the brain, with long-term protection from development of neuropathology and hippocampal-related learning impairments. We show that selective degeneration of hippocampal neurons is a central step in disease pathogenesis, and provide evidence that in vivo transfer of ARSA by lentiviral vectors reverts the disease phenotype in all investigated areas. Therefore, in vivo gene therapy offers a unique option for MLD and other storage diseases affecting the central nervous system.

Published
2001
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