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1. Impact of Geographical Location on the Gut Microbiota Profile in Egyptian Children with Type 1 Diabetes Mellitus: A Pilot Study

Author: Elsherbiny NM, Ramadan M, Abu Faddan NH, Hassan EA, Ali ME, Abd El-Rehim ASE, Abbas WA, Abozaid MAA, Hassanin E, Mohamed GA, Hetta HF, and Salah M
Subjects: gut microbiota, dysbiosis, type1 diabetes mellitus, children, Medicine (General), R5-920
Abstract: Nahla M Elsherbiny,1 Mohammed Ramadan,2 Nagla H Abu Faddan,3 Elham Ahmed Hassan,4 Mohamed E Ali,2 Abeer Sharaf El-Din Abd El-Rehim,4 Wael A Abbas,5 Mohamed AA Abozaid,5 Ebtisam Hassanin,6 Ghada A Mohamed,7 Helal F Hetta,1 Mohammed Salah8 1Department of Medical Microbiology and Immunology, Faculty of Medicine, Assiut University, Assiut, Egypt; 2Department of Microbiology and Immunology, Faculty of Pharmacy, Al-Azhar University, Assiut Branch, Assiut, Egypt; 3Department of Pediatrics, Faculty of Medicine, Assiut University, Assiut, Egypt; 4Department of Gastroenterology and Tropical Medicine, Faculty of Medicine, Assiut University, Assiut, Egypt; 5Department of Internal Medicine, Gastroenterology and Hepatology Unit, Faculty of Medicine, Assiut University, Assiut, Egypt; 6Clinical Pathology, Ministry of Health, Assiut, Egypt; 7Department of Internal Medicine, Endocrine Unit, Faculty of Medicine, Assiut University, Assiut, Egypt; 8Department of Microbiology and Immunology, Faculty of pharmacy, Port Said University, Port Said, EgyptCorrespondence: Elham Ahmed Hassan, Department of Gastroenterology and Tropical Medicine, Faculty of Medicine, Assiut University, Assiut, 71515, Egypt, Tel +20 882410285, Fax +20 882333327, Email mam_elham75@yahoo.com; elham.abdelhalem@med.aun.edu.egPurpose: To investigate the compositional and functional characteristics of T1DM-associated gut microbiota in two Egyptian cities and to study the geographical locality effects.Patients and Methods: This case-control study included 32 children with controlled T1DM and 16 controls, selected from two different regions of Egypt. The gut microbiota of both diabetic and control children was analyzed through 16S rRNA gene sequencing; this was done using the Illumina MiSeq platform.Results: Consistent findings among the diabetic children included significantly lower alpha diversity than the control children, as well as a lower mean Firmicutes/Bacteroidetes (F/B) ratio, and reduced proportions of Firmicutes and the genera Prevotella and Ruminococcus. In the diabetic children, there were also significantly enriched representations of Actinobacteria, Bacteroidetes, and Proteobacteria and the genera Lactobacilli, Bacteroides, and Faecalibacterium. When comparing the two diabetic groups, the Ismailia group (IsDM) was found to have a significantly higher F/B ratio and diversity indices, with resultant differences at the functional level.Conclusion: There are a number of consistent changes in the microbiota profile characterizing the diabetic groups irrespective of the geographical location including significantly lower alpha diversity, mean Firmicutes/ Bacteroidetes (F/B) ratio, and reduced proportions of Firmicutes and genera Prevotella and Ruminococcus. There are also significantly enriched representations of Actinobacteria, Bacteroidetes, and Proteobacteria and genera Lactobacilli, Bacteroides, and Faecalibacterium pointing to the greater driving power of the disease.Keywords: gut microbiota, dysbiosis, type 1 diabetes mellitus, children
Published: 2022

2. Correction: Epidemiology and outcomes of early-onset AKI in COVID-19-related ARDS in comparison with non-COVID-19-related ARDS: insights from two prospective global cohort studies (Critical Care, (2023), 27, 1, (3), 10.1186/s13054-022-04294-5)

Author: McNicholas B. A., Mcnicholas, B, Rezoagli, E, Simpkin, A, Khanna, S, Suen, J, Yeung, P, Brodie, D, Bassi, G, Pham, T, Bellani, G, Fraser, J, Laffey, J, Al-Dabbous, T, Alfoudri, H, Shamsah, M, Alhadad, Q, Hanan, M, Elapavaluru, S, Berg, A, Horn, C, Abdelhalim, A, Amer, A, Elnaggar, C, Hassan, A, Abdelaziz, A, Abdelhalim, M, Orabi, Y, Alaraji, Z, Muhaisen, M, Almasri, L, Mustafa, D, Hamdan, S, Al-Saba'a, Y, Dalloul, Z, Alkahlout, M, Jaber, H, Aldabbourosama, O, Hussein, A, Emad, Z, Khaled, S, Mohamed, N, Hassanin, E, Hamdi, A, Ragab, A, Azizeldin, M, Mayasi, Y, Schroll, S, Meyer, D, Velazco, J, Ploskanych, L, Fikes, W, Bagewadi, R, Dao, M, White, H, Laviena, A, Ehlers, A, Shalabi-McGuire, M, Witt, T, Grazioli, L, Lorini, L, Grandin, E, Nunez, J, Reyes, T, O'Briain, D, Hunter, S, Ramanan, M, Affleck, J, Veerendra, H, Rai, S, Russell-Brown, J, Nourse, M, Joseph, M, Mitchell, B, Tenzer, M, Abe, R, Cho, H, Jeong, I, Rahman, N, Kakar, V, Sun, H, Hanley, A, Brozzi, N, Mehkri, O, Krishnan, S, Duggal, A, Houltham, S, Graf, J, Diaz, R, Orrego, R, Delgado, C, Gonzalez, J, Sanchez, M, Piagnerelli, M, Sarrazin, J, Zabert, G, Espinosa, L, Delgado, P, Delgado, V, Rincon, D, Yanten, A, Duque, M, Abouelmagd, K, Elhazmi, A, Al-Hudaib, A, Javidfar, J, Callahan, M, Dong, A, D'Orleans, C, Taufik, M, Wardoyo, E, Gunawan, M, Trisnaningrum, N, Irawany, V, Rayhan, M, Panigada, M, Pesenti, A, Zanella, A, Grasselli, G, Colombo, S, Martinet, C, Florio, G, Antonelli, M, Carelli, S, Grieco, D, Asaki, M, Hoshino, K, Salazar, L, Monsalve, M, Cosgrave, D, Atif, M, Qutishat, F, Laffey, C, Van Der Walt, M, Mccaffrey, J, Bone, A, Hakeem, Y, Winearls, J, Tallott, M, Thomson, D, Joubert, I, Arnold-Day, C, Piercy, J, van Zyl Smit, R, Miller, M, Seymour, L, van Heyningen, F, Teyangesikayi, G, Fredericks, D, Hssain, A, Aliudin, J, Alqahtani, A, Mohamed, K, Mohamed, A, Tan, D, Villanueva, J, Zaqout, A, Kurtzman, E, Ademi, A, Dobrita, A, El Aoudi, K, Segura, J, Giwangkancana, G, Ohshimo, S, Osatnik, J, Joosten, A, Torres, A, Yang, M, Motos, A, Luna, C, Arancibia, F, Williams, V, Noel, A, Luque, N, Fantini, M, Garcia, R, Alvarez, E, Greti, A, Ceccato, A, Sanchez, A, Vazquez, A, Roche-Campo, F, Franch-Llasat, D, Tuazon, D, Amato, M, Cassimiro, L, Pola, F, Ribeiro, F, Fonseca, G, Dalton, H, Desai, M, Osborn, E, Deeb, H, Arcadipane, A, Martucci, G, Panarello, G, Vitiello, S, Bianco, C, Occhipinti, G, Rossetti, M, Cuffaro, R, Cho, S, Whitman, G, El Sayed, M, Mokhtar, W, El-Shenawy, E, Shimizu, H, Moriyama, N, Kim, J, Kitamura, N, Gebauer, J, Yokoyama, T, Al-Fares, A, Buabbas, S, Alamad, E, Alawadhi, F, Alawadi, K, Khalefa, M, Al Ajeel, N, Aly, M, Al-Saleh, A, Naanouh, A, Elshourbgy, A, Gad, M, Elrazaz, R, Khadadah, I, Almumin, A, Altarakma, H, Albannay, H, Alsaleh, M, Radwan, M, Saadallah, I, Tanaka, H, Hashimoto, S, Yamazaki, M, Oh, T, Epler, M, Forney, C, Kruse, L, Feister, J, Williamson, J, Grobengieser, K, Gnall, E, Golden, S, Caroline, M, Shapiro, T, Karaj, C, Thome, L, Sher, L, Vanderland, M, Welch, M, Mcdermott, S, Brain, M, Mineall, S, Unwin, M, Chen, L, Trezise, T, Mckeon, L, Kimura, D, Brazzi, L, Sales, G, Montrucchio, G, Ogston, T, Nagpal, D, Fischer, K, Lorusso, R, van Bussell, B, De Piero, M, Mariani, S, Rangappa, R, Shetty, R, Rai, P, Ganesan, A, Esperatti, M, Fuentes, N, Gonzalez, M, Carton, E, Sen, A, Palacios, A, Rainey, D, Samoukoviv, G, Campisi, J, Durham, L, Neumann, E, Seefeldt, C, Falcucci, O, Emmrich, A, Guy, J, Johns, C, Potzner, K, Zimmermann, C, Espinal, A, Buchtele, N, Schwameis, M, Korhnfehl, A, Brock, R, Staudinger, T, Stecher, S, Barnikel, M, Anton, S, Pawlikowski, A, Zaaqoq, A, Galloway, L, Merley, C, Nichol, A, Csete, M, Quesada, L, Saba, I, Kasugai, D, Hiraiwa, H, Tanaka, T, Marwali, E, Purnama, Y, Dewayanti, S, Ardiyan, Juzar, D, Siagian, D, Chen, Y, Ogino, M, Nasa, P, Matthew, C, Majeed, N, Ratsep, I, Post, A, Sillaots, P, Krund, A, Lehiste, M, Lepik, T, Manetta, F, Mihelis, E, Sarmiento, I, Narasimhan, M, Varrone, M, Komats, M, Garcia-Diaz, J, Harmon, C, Satyapriya, S, Bhatt, A, Mokadam, N, Uribe, A, Gonzalez, A, Shi, H, Mckeown, J, Pasek, J, Fiorda, J, Echeverria, M, Moreno, R, Zakhary, B, Cavana, M, Cucino, A, Foti, G, Giani, M, Fumagalli, B, Chiumello, D, Castagna, V, Dell'Amore, A, Navalesi, P, Shum, H, Vuysteke, A, Usman, A, Acker, A, Smood, B, Mergler, B, Sertic, F, Subramanian, M, Sperry, A, Rizer, N, Burhan, E, Rasmin, M, Akmal, E, Sitompul, F, Lolong, N, Naivedh, B, Erickson, S, Barrett, P, Dean, D, Daugherty, J, Loforte, A, Khan, I, Quraishi, M, Desantis, O, So, D, Kandamby, D, Mandei, J, Natanael, H, Yudhalantang, E, Lantang, A, Wijaya, S, Jung, A, Ng, G, Ng, W, Ng, P, Fang, S, Tabah, A, Ratcliffe, M, Duroux, M, Alajeeli, A, Tarhabat, A, Adachi, S, Nakao, S, Blanco, P, Prieto, A, Sanchez, J, Nicholson, M, Butt, W, Serratore, A, Delzoppo, C, Janin, P, Yarad, E, Totaro, R, Coles, J, Pujo, B, Balk, R, Vissing, A, Kapania, E, Hays, J, Fox, S, Yantosh, G, Mishin, P, Yuliarto, S, Santoso, K, Djajalaksana, S, Fatoni, A, Fukuda, M, Liu, K, Pelosi, P, Battaglini, D, Jimenez, J, Bastos, D, Gaiao, S, Rusmawatiningtyas, D, Cho, Y, Lee, S, Kawasaki, T, Munshi, L, Sakiyalak, P, Nitayavardhana, P, Elagili, M, Salem, T, Seitz, T, Arora, R, Kent, D, Marino, D, Parwar, S, Cheng, A, Miller, J, Fujitani, S, Shimizu, N, Madhok, J, Owyang, C, Buscher, H, Reynolds, C, Maasikas, O, Aleksanbeljantsev, Mihnovits, V, Akimoto, T, Aizawa, M, Horibe, K, Onodera, R, Hodgson, C, Burrell, A, Young, M, George, T, Shekar, K, Mcguinness, N, Irvine, L, Flynn, B, Endo, T, Sugiyama, K, Shimizu, K, Fan, E, Exconde, K, Ichiba, S, Binnawara, M, Lussier, L, Lotz, G, Malfertheiner, M, Maier, L, Dreier, E, Kusumastuti, N, Mccloskey, C, Dabaliz, A, Elshazly, T, Smith, J, Szuldrzynski, K, Bielanski, P, Wille, K, Murthy, S, Parhar, K, Fiest, K, Codan, C, Shahid, A, Fayed, M, Evans, T, Gutierrez, A, Song, T, Rose, R, Bennett, S, Richardson, D, Peek, G, Arora, L, Rappapport, K, Rudolph, K, Sibenaller, Z, Stout, L, Walter, A, Herr, D, Vedadi, N, Bartlett, R, Thompson, S, Hoffman, J, Ying, X, Williams, B, Sanchez, E, Akwani, C, Kennedy, R, Elhadi, M, Griffee, M, Mone, M, Ciullo, A, Kida, Y, Roca, R, Riera, J, Contreras, S, Alegre, C, Kay, C, Fischer, I, Renner, E, Taniguci, H, Lee, J, Plotkin, D, Citarella, B, Merson, L, Hartley, E, Lubis, B, Ikeyama, T, Alhamad, A, Fathi, M, Hadhoud, M, Alhouri, H, Mechi, A, Alyasiri, M, Elsaid, M, Shahla, H, Bhaskar, B, Jung, J, Mcguinness, S, Eastwood, G, Marta, S, Guarracino, F, Gerle, S, Coxon, E, Claro, B, Eleisawy, M, Osama, H, Loverde, D, Patil, N, Parrini, V, Mcbride, A, Negaard, K, Ratsch, A, Uribe, J, Peris, A, Sanders, M, Emerson, D, Kamal, M, Faida, H, Povoa, P, Francis, R, Cherif, A, Joseph, S, Di Nardo, M, Heard, M, Kyle, K, Blackwell, R, Ouyahia, A, Biston, P, Jeong, H, Smith, R, Prawira, Y, Garcia, A, Salterain, N, Meyns, B, Elnasser, M, Moreno, M, Walia, R, Mehta, A, Schweda, A, Williams, M, Emadamkhatirah, Kim, K, Assad, A, Giraldo, E, Karolak, W, Balik, M, Pocock, E, Gajkowski, E, Masafumi, K, Barrett, N, Takeyama, Y, Park, S, Amin, F, Andriyani, F, Sudakevych, S, Schnur, J, Vera, M, Cornejo, R, Schwarz, P, Mardini, A, de Paula, T, Neto, A, Villoldo, A, Colafranceschi, A, Iglesias, A, Granjean, J, Melro, L, Romualdo, G, Gaia, D, Souza, H, Galas, F, Mendiluce, R, Sosa, A, Martinez, I, Kurosawa, H, Almoshantaf, M, Salgado, J, Hugi-Mayr, B, Charbonneau, E, Barzilai, V, Monteiro, V, de Souza, R, Harper, M, Siddig, N, Suzuki, H, Adams, C, Brieva, J, Khamees, A, Graige, F, Supriatna, M, Nyale, G, Eltatar, F, Fatani, J, Baeissa, H, Masri, A, Rabie, A, Hui, M, Yamane, M, Jung, H, Margaret, A, Nacpil, N, Ruck, K, Bakken, R, Jara, C, Felton, T, Tharwat, S, Berra, L, Shah, B, Chakraborty, A, Cardona, M, Capatos, G, Akkanti, B, Orija, A, Jain, H, Ito, A, Muftah, M, Housni, B, Aldhalia, A, Low, S, Iihara, K, Chavez, J, Ramanathan, K, Naidoo, K, Seppelt, I, Vandyk, M, Macdonald, S, Hafez, W, Mcgregor, R, Siebenaler, T, Flynn, H, Lofton, K, Aokage, T, Kvirkvelia, B, Shigemitsu, K, Moscatelli, A, Fiorentino, G, Baumgaertel, M, Mba, S, Assy, J, Hutahaean, A, Roush, H, Sichting, K, Alessandri, F, Burns, D, Alkhubouli, T, Nasrallah, A, Salt, G, Garabedian, C, Millar, J, Sim, M, Mattke, A, Mcauley, D, Tadili, J, Frenzel, T, Bar-Lavie, Y, Ortiz, A, Stone, J, Attokaran, A, Farquharson, M, Patel, B, Gunning, D, Baillie, K, Adem, S, Watson, P, Tamai, K, Sajinadiyasa, G, Kanyawati, D, Salgado, M, Sassine, A, Yudo, B, Mccaul, S, Lee, B, Afek, A, Iwashita, Y, Fadlalmola, H, Semedi, B, Mansour, N, Metiva, J, Van Belle, N, Martin-Loeches, I, Al-Sadawi, M, Kirakli, C, Shimaa, A, Abdurraouf, A, Ivatt, L, Moharam, S, Woon, C, Kang, H, Smith, T, James, E, Al-Rawas, N, Almjersah, A, Iwasaki, Y, Ashour, H, Embarek, H, King-Chung, K, Gudzenko, V, Taccone, F, Perdhana, F, Lamarche, Y, Ribeiro, J, Bradic, N, Van den Bossche, K, Lansink, O, Singh, G, Debeuckelaere, G, Stelfox, H, Yi, C, Elia, J, Tribble, T, Shankar, S, Padmanabhan, R, Hallinan, B, Paoletti, L, Leyva, Y, Fykuda, T, Badulak, J, Koch, J, Janowaik, L, Hackman, A, Hernandez, D, Osofsky, J, Donadello, K, Lawang, A, Fine, J, Davidson, B, Abdehaleem, I, McNicholas B. A., Rezoagli E., Simpkin A. J., Khanna S., Suen J. Y., Yeung P., Brodie D., Bassi G. L., Pham T., Bellani G., Fraser J. F., Laffey J., Al-Dabbous T., Alfoudri H., Shamsah M., Alhadad Q., Hanan M., Elapavaluru S., Berg A., Horn C., Abdelhalim A. R. M. E., Amer A. E., Elnaggar C. O. R., Hassan A. A., Abdelaziz A., Abdelhalim M., Orabi Y. S. S. A., Alaraji Z. A., Muhaisen M. R., Almasri L., Mustafa D., Hamdan S., Al-Saba'a Y., Dalloul Z., Alkahlout M., Jaber H., Aldabbourosama O., Hussein A. A. R. M., Emad Z. K., Khaled S., Mohamed N., Hassanin E., Hamdi A., Ragab A., Azizeldin M. G., Mayasi Y., Schroll S., Meyer D., Velazco J., Ploskanych L., Fikes W., Bagewadi R., Dao M., White H., Laviena A. B., Ehlers A., Shalabi-McGuire M., Witt T., Grazioli L., Lorini L., Grandin E. W., Nunez J., Reyes T., O'Briain D., Hunter S., Ramanan M., Affleck J., Veerendra H. H., Rai S., Russell-Brown J., Nourse M., Joseph M., Mitchell B., Tenzer M., Abe R., Cho H. J., Jeong I. S., Rahman N., Kakar V., Sun H., Hanley A., Brozzi N., Mehkri O., Krishnan S., Duggal A., Houltham S., Graf J., Diaz R., Orrego R., Delgado C., Gonzalez J., Sanchez M. S., Piagnerelli M., Sarrazin J. V., Zabert G., Espinosa L., Delgado P., Delgado V., Rincon D. F. B., Yanten A. M. M., Duque M. B., Abouelmagd K., Elhazmi A., Al-Hudaib A., Javidfar J., Callahan M., Dong A., D'Orleans C. C., Taufik M. A., Wardoyo E. Y., Gunawan M., Trisnaningrum N. S., Irawany V., Rayhan M., Panigada M., Pesenti A., Zanella A., Grasselli G., Colombo S., Martinet C., Florio G., Antonelli M., Carelli S., Grieco D. L., Asaki M., Hoshino K., Salazar L., Monsalve M. A. M., McNicholas B., Cosgrave D., Atif M., Qutishat F., Laffey C., Van Der Walt M., McCaffrey J., Bone A., Hakeem Y., Winearls J., Tallott M., Thomson D., Joubert I., Arnold-Day C., Piercy J., van Zyl Smit R., Miller M., Seymour L., van Heyningen F., Teyangesikayi G., Fredericks D., Hssain A. A., Aliudin J., Alqahtani A. -R., Mohamed K., Mohamed A., Tan D., Villanueva J., Zaqout A., Kurtzman E., Ademi A., Dobrita A., El Aoudi K., Segura J., Giwangkancana G., Ohshimo S., Osatnik J., Joosten A., Torres A., Yang M., Motos A., Luna C., Arancibia F., Williams V., Noel A., Luque N., Fantini M., Garcia R. N. J., Alvarez E. C., Greti A., Ceccato A., Sanchez A., Vazquez A. L., Roche-Campo F., Franch-Llasat D., Tuazon D., Amato M., Cassimiro L., Pola F., Ribeiro F., Fonseca G., Dalton H., Desai M., Osborn E., Deeb H., Arcadipane A., Martucci G., Panarello G., Vitiello S., Bianco C., Occhipinti G., Rossetti M., Cuffaro R., Cho S. -M., Whitman G., El Sayed M., Mokhtar W., El-Shenawy E., Shimizu H., Moriyama N., Kim J. -B., Kitamura N., Gebauer J., Yokoyama T., Al-Fares A., Buabbas S., Alamad E., Alawadhi F., Alawadi K., Khalefa M. A., Al Ajeel N. A. A., Aly M. F., Al-Saleh A., Naanouh A., Elshourbgy A. M., Gad M. Y., ElRazaz R. M., Khadadah I., Almumin A. M., Altarakma H., Albannay H., Alsaleh M. K., Radwan M. S. A., Saadallah I. A., Tanaka H., Hashimoto S., Yamazaki M., Oh T. -H., Epler M., Forney C., Kruse L., Feister J., Williamson J., Grobengieser K., Gnall E., Golden S., Caroline M., Shapiro T., Karaj C., Thome L., Sher L., Vanderland M., Welch M., McDermott S., Brain M., Mineall S., Unwin M., Chen L., Trezise T., McKeon L., Kimura D., Brazzi L., Sales G., Montrucchio G., Ogston T., Nagpal D., Fischer K., Lorusso R., van Bussell B., De Piero M. E., Mariani S., Rangappa R., Shetty R. M., Rai P. S., Ganesan A., Esperatti M., Fuentes N. A., Gonzalez M. E., Carton E. G., Sen A., Palacios A., Rainey D., Samoukoviv G., Campisi J., Durham L., Neumann E., Seefeldt C., Falcucci O., Emmrich A., Guy J., Johns C., Potzner K., Zimmermann C., Espinal A., Buchtele N., Schwameis M., Korhnfehl A., Brock R., Staudinger T., Stecher S. -S., Barnikel M., Anton S., Pawlikowski A., Zaaqoq A., Galloway L. A., Merley C., Nichol A., Csete M., Quesada L., Saba I., Kasugai D., Hiraiwa H., Tanaka T., Marwali E., Purnama Y., Dewayanti S. R., Juzar D. A., Siagian D., Chen Y. -S., Ogino M., Nasa P., Matthew C., Majeed N. A., Ratsep I., Post A. -M., Sillaots P., Krund A., Lehiste M. -H., Lepik T., Manetta F., Mihelis E., Sarmiento I. C., Narasimhan M., Varrone M., Komats M., Garcia-Diaz J., Harmon C., Satyapriya S. V., Bhatt A., Mokadam N. A., Uribe A., Gonzalez A., Shi H., McKeown J., Pasek J., Fiorda J., Echeverria M., Moreno R., Zakhary B., Cavana M., Cucino A., Foti G., Giani M., Fumagalli B., Chiumello D., Castagna V., Dell'Amore A., Navalesi P., Shum H. -P., Vuysteke A., Usman A., Acker A., Smood B., Mergler B., Sertic F., Subramanian M., Sperry A., Rizer N., Burhan E., Rasmin M., Akmal E., Sitompul F., Lolong N., Naivedh B., Erickson S., Barrett P., Dean D., Daugherty J., Loforte A., Khan I., Quraishi M. A., DeSantis O., So D., Kandamby D., Mandei J. M., Natanael H., YudhaLantang E., Lantang A., Wijaya S. O., Jung A., Ng G., Ng W. Y., Ng P. Y., Fang S., Tabah A., Ratcliffe M., Duroux M., Alajeeli A., Tarhabat A., Adachi S., Nakao S., Blanco P., Prieto A., Sanchez J., Nicholson M., Butt W., Serratore A., Delzoppo C., Janin P., Yarad E., Totaro R., Coles J., Pujo B., Balk R., Vissing A., Kapania E., Hays J., Fox S., Yantosh G., Mishin P., Yuliarto S., Santoso K. H., Djajalaksana S., Fatoni A. Z., Fukuda M., Liu K., Pelosi P., Battaglini D., Jimenez J. F. M., Bastos D., Gaiao S., Rusmawatiningtyas D., Cho Y. -J., Lee S. H., Kawasaki T., Munshi L., Sakiyalak P., Nitayavardhana P., Elagili M. B., Salem T. A. A., Seitz T., Arora R., Kent D., Marino D., Parwar S., Cheng A., Miller J., Fujitani S., Shimizu N., Madhok J., Owyang C., Buscher H., Reynolds C., Maasikas O., AleksanBeljantsev, Mihnovits V., Akimoto T., Aizawa M., Horibe K., Onodera R., Hodgson C., Burrell A., Young M., George T., Shekar K., McGuinness N., Irvine L., Flynn B., Endo T., Sugiyama K., Shimizu K., Fan E., Exconde K., Ichiba S., Binnawara M., Lussier L., Lotz G., Malfertheiner M., Maier L., Dreier E., Kusumastuti N. P., McCloskey C., Dabaliz A. -A., Elshazly T. B., Smith J., Szuldrzynski K. S., Bielanski P., Wille K., Murthy S., Parhar K. K. S., Fiest K. M., Codan C., Shahid A., Fayed M., Evans T., Garcia R., Gutierrez A., Song T., Rose R., Bennett S., Richardson D., Peek G., Arora L., Rappapport K., Rudolph K., Sibenaller Z., Stout L., Walter A., Herr D., Vedadi N., Bartlett R., Thompson S., Hoffman J., Ying X., Williams B., Sanchez E., Akwani C., Kennedy R., Elhadi M., Griffee M., Mone M., Ciullo A., Kida Y., Roca R. F., Riera J. I., Contreras S., Alegre C., Kay C., Fischer I., Renner E., Taniguci H., Lee J., Plotkin D., Citarella B. W., Merson L., Hartley E., Lubis B., Ikeyama T., Alhamad A., Fathi M., Hadhoud M. M., Alhouri H., Mechi A., Alyasiri M. S., Elsaid M. Z. A., Shahla H., Bhaskar B., Jung J. -S., McGuinness S., Eastwood G., Marta S. R., Guarracino F., Gerle S., Coxon E., Claro B., Eleisawy M., Osama H., Loverde D., Patil N., Parrini V., McBride A., Negaard K., Ratsch A., Uribe J. D., Peris A., Sanders M., Emerson D., Kamal M., Faida H., Povoa P., Francis R., Cherif A., Joseph S., Di Nardo M., Heard M., Kyle K., Blackwell R. A., Ouyahia A., Biston P., Jeong H. W., Smith R., Prawira Y., Garcia A. H., Salterain N., Meyns B., Elnasser M., Moreno M., Walia R., Mehta A., Schweda A., Williams M., EmadAmkhatirah, Kim K. H., Assad A., Giraldo E., Karolak W., Balik M., Pocock E., Gajkowski E., Masafumi K., Barrett N., Takeyama Y., Park S., Amin F., Andriyani F. M., Sudakevych S., Schnur J., Vera M., Cornejo R., Schwarz P., Mardini A. C., de Paula T., Neto A. S., Villoldo A., Colafranceschi A. S., Iglesias A. U., Granjean J., Melro L. M. G., Romualdo G. F., Gaia D., Souza H., Galas F., Mendiluce R. M., Sosa A., Martinez I., Kurosawa H., Almoshantaf M. B., Salgado J., Hugi-Mayr B., Charbonneau E., Barzilai V. S., Monteiro V., de Souza R. R., Harper M., Siddig N., Suzuki H., Adams C., Brieva J., Khamees A., Graige F., Supriatna M., Nyale G., Eltatar F. S., Fatani J., Baeissa H., Masri A. A. L., Rabie A., Hui M. Y., Yamane M., Jung H., Margaret A. M., Nacpil N., Ruck K., Bakken R., Jara C., Felton T., Tharwat S., Berra L., Shah B., Chakraborty A., Cardona M., Capatos G., Akkanti B., Orija A., Jain H., Ito A., Muftah M., Housni B., Aldhalia A., Low S., Iihara K., Chavez J., Ramanathan K., Naidoo K., Seppelt I., VanDyk M., MacDonald S., Hafez W., McGregor R., Siebenaler T., Flynn H., Lofton K., Aokage T., Kvirkvelia B., Shigemitsu K., Moscatelli A., Fiorentino G., Baumgaertel M., Mba S. E., Assy J., Hutahaean A., Roush H., Sichting K. A., Alessandri F., Burns D., Alkhubouli T. H., Nasrallah A., Salt G., Garabedian C. P., Millar J., Sim M., Mattke A., McAuley D., Tadili J., Frenzel T., Bar-Lavie Y., Ortiz A. B., Stone J., Attokaran A., Farquharson M., Patel B., Gunning D., Baillie K., Adem S., Watson P., Tamai K., Sajinadiyasa G. K., Kanyawati D., Salgado M., Sassine A., Yudo B., McCaul S., Lee B., Lee S. M., Afek A., Iwashita Y., Fadlalmola H., Semedi B. P., Mansour N. M., Metiva J., Van Belle N., Martin-Loeches I., Al-Sadawi M., Kirakli C., Shimaa A. -T., Abdurraouf A., Ivatt L., Moharam S., Woon C. Y., Kang H. M., Smith T., James E., Al-Rawas N., Almjersah A., Iwasaki Y., Ashour H., Embarek H., King-Chung K. C., Gudzenko V., Taccone F., Perdhana F., Lamarche Y., Ribeiro J. M., Bradic N., Van den Bossche K., Lansink O., Singh G., Debeuckelaere G., Stelfox H. T., Yi C., Elia J., Tribble T., Shankar S., Padmanabhan R., Hallinan B., Paoletti L., Leyva Y., Fykuda T., Badulak J., Koch J., Janowaik L., Hackman A., Hernandez D., Osofsky J., Donadello K., Lawang A., Fine J., Davidson B., Vazquez A. O. R., Abdehaleem I., McNicholas B. 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S., Rahman N., Kakar V., Sun H., Hanley A., Brozzi N., Mehkri O., Krishnan S., Duggal A., Houltham S., Graf J., Diaz R., Orrego R., Delgado C., Gonzalez J., Sanchez M. S., Piagnerelli M., Sarrazin J. V., Zabert G., Espinosa L., Delgado P., Delgado V., Rincon D. F. B., Yanten A. M. M., Duque M. B., Abouelmagd K., Elhazmi A., Al-Hudaib A., Javidfar J., Callahan M., Dong A., D'Orleans C. C., Taufik M. A., Wardoyo E. Y., Gunawan M., Trisnaningrum N. S., Irawany V., Rayhan M., Panigada M., Pesenti A., Zanella A., Grasselli G., Colombo S., Martinet C., Florio G., Antonelli M., Carelli S., Grieco D. L., Asaki M., Hoshino K., Salazar L., Monsalve M. A. M., McNicholas B., Cosgrave D., Atif M., Qutishat F., Laffey C., Van Der Walt M., McCaffrey J., Bone A., Hakeem Y., Winearls J., Tallott M., Thomson D., Joubert I., Arnold-Day C., Piercy J., van Zyl Smit R., Miller M., Seymour L., van Heyningen F., Teyangesikayi G., Fredericks D., Hssain A. A., Aliudin J., Alqahtani A. -R., Mohamed K., Mohamed A., Tan D., Villanueva J., Zaqout A., Kurtzman E., Ademi A., Dobrita A., El Aoudi K., Segura J., Giwangkancana G., Ohshimo S., Osatnik J., Joosten A., Torres A., Yang M., Motos A., Luna C., Arancibia F., Williams V., Noel A., Luque N., Fantini M., Garcia R. N. J., Alvarez E. C., Greti A., Ceccato A., Sanchez A., Vazquez A. L., Roche-Campo F., Franch-Llasat D., Tuazon D., Amato M., Cassimiro L., Pola F., Ribeiro F., Fonseca G., Dalton H., Desai M., Osborn E., Deeb H., Arcadipane A., Martucci G., Panarello G., Vitiello S., Bianco C., Occhipinti G., Rossetti M., Cuffaro R., Cho S. -M., Whitman G., El Sayed M., Mokhtar W., El-Shenawy E., Shimizu H., Moriyama N., Kim J. -B., Kitamura N., Gebauer J., Yokoyama T., Al-Fares A., Buabbas S., Alamad E., Alawadhi F., Alawadi K., Khalefa M. A., Al Ajeel N. A. A., Aly M. F., Al-Saleh A., Naanouh A., Elshourbgy A. M., Gad M. Y., ElRazaz R. M., Khadadah I., Almumin A. M., Altarakma H., Albannay H., Alsaleh M. K., Radwan M. S. A., Saadallah I. A., Tanaka H., Hashimoto S., Yamazaki M., Oh T. -H., Epler M., Forney C., Kruse L., Feister J., Williamson J., Grobengieser K., Gnall E., Golden S., Caroline M., Shapiro T., Karaj C., Thome L., Sher L., Vanderland M., Welch M., McDermott S., Brain M., Mineall S., Unwin M., Chen L., Trezise T., McKeon L., Kimura D., Brazzi L., Sales G., Montrucchio G., Ogston T., Nagpal D., Fischer K., Lorusso R., van Bussell B., De Piero M. E., Mariani S., Rangappa R., Shetty R. M., Rai P. S., Ganesan A., Esperatti M., Fuentes N. A., Gonzalez M. E., Carton E. G., Sen A., Palacios A., Rainey D., Samoukoviv G., Campisi J., Durham L., Neumann E., Seefeldt C., Falcucci O., Emmrich A., Guy J., Johns C., Potzner K., Zimmermann C., Espinal A., Buchtele N., Schwameis M., Korhnfehl A., Brock R., Staudinger T., Stecher S. -S., Barnikel M., Anton S., Pawlikowski A., Zaaqoq A., Galloway L. A., Merley C., Nichol A., Csete M., Quesada L., Saba I., Kasugai D., Hiraiwa H., Tanaka T., Marwali E., Purnama Y., Dewayanti S. R., Juzar D. A., Siagian D., Chen Y. -S., Ogino M., Nasa P., Matthew C., Majeed N. A., Ratsep I., Post A. -M., Sillaots P., Krund A., Lehiste M. -H., Lepik T., Manetta F., Mihelis E., Sarmiento I. C., Narasimhan M., Varrone M., Komats M., Garcia-Diaz J., Harmon C., Satyapriya S. V., Bhatt A., Mokadam N. A., Uribe A., Gonzalez A., Shi H., McKeown J., Pasek J., Fiorda J., Echeverria M., Moreno R., Zakhary B., Cavana M., Cucino A., Foti G., Giani M., Fumagalli B., Chiumello D., Castagna V., Dell'Amore A., Navalesi P., Shum H. -P., Vuysteke A., Usman A., Acker A., Smood B., Mergler B., Sertic F., Subramanian M., Sperry A., Rizer N., Burhan E., Rasmin M., Akmal E., Sitompul F., Lolong N., Naivedh B., Erickson S., Barrett P., Dean D., Daugherty J., Loforte A., Khan I., Quraishi M. A., DeSantis O., So D., Kandamby D., Mandei J. M., Natanael H., YudhaLantang E., Lantang A., Wijaya S. O., Jung A., Ng G., Ng W. Y., Ng P. Y., Fang S., Tabah A., Ratcliffe M., Duroux M., Alajeeli A., Tarhabat A., Adachi S., Nakao S., Blanco P., Prieto A., Sanchez J., Nicholson M., Butt W., Serratore A., Delzoppo C., Janin P., Yarad E., Totaro R., Coles J., Pujo B., Balk R., Vissing A., Kapania E., Hays J., Fox S., Yantosh G., Mishin P., Yuliarto S., Santoso K. H., Djajalaksana S., Fatoni A. Z., Fukuda M., Liu K., Pelosi P., Battaglini D., Jimenez J. F. M., Bastos D., Gaiao S., Rusmawatiningtyas D., Cho Y. -J., Lee S. H., Kawasaki T., Munshi L., Sakiyalak P., Nitayavardhana P., Elagili M. B., Salem T. A. A., Seitz T., Arora R., Kent D., Marino D., Parwar S., Cheng A., Miller J., Fujitani S., Shimizu N., Madhok J., Owyang C., Buscher H., Reynolds C., Maasikas O., AleksanBeljantsev, Mihnovits V., Akimoto T., Aizawa M., Horibe K., Onodera R., Hodgson C., Burrell A., Young M., George T., Shekar K., McGuinness N., Irvine L., Flynn B., Endo T., Sugiyama K., Shimizu K., Fan E., Exconde K., Ichiba S., Binnawara M., Lussier L., Lotz G., Malfertheiner M., Maier L., Dreier E., Kusumastuti N. P., McCloskey C., Dabaliz A. -A., Elshazly T. B., Smith J., Szuldrzynski K. S., Bielanski P., Wille K., Murthy S., Parhar K. K. S., Fiest K. M., Codan C., Shahid A., Fayed M., Evans T., Garcia R., Gutierrez A., Song T., Rose R., Bennett S., Richardson D., Peek G., Arora L., Rappapport K., Rudolph K., Sibenaller Z., Stout L., Walter A., Herr D., Vedadi N., Bartlett R., Thompson S., Hoffman J., Ying X., Williams B., Sanchez E., Akwani C., Kennedy R., Elhadi M., Griffee M., Mone M., Ciullo A., Kida Y., Roca R. F., Riera J. I., Contreras S., Alegre C., Kay C., Fischer I., Renner E., Taniguci H., Lee J., Plotkin D., Citarella B. W., Merson L., Hartley E., Lubis B., Ikeyama T., Alhamad A., Fathi M., Hadhoud M. M., Alhouri H., Mechi A., Alyasiri M. S., Elsaid M. Z. A., Shahla H., Bhaskar B., Jung J. -S., McGuinness S., Eastwood G., Marta S. R., Guarracino F., Gerle S., Coxon E., Claro B., Eleisawy M., Osama H., Loverde D., Patil N., Parrini V., McBride A., Negaard K., Ratsch A., Uribe J. D., Peris A., Sanders M., Emerson D., Kamal M., Faida H., Povoa P., Francis R., Cherif A., Joseph S., Di Nardo M., Heard M., Kyle K., Blackwell R. A., Ouyahia A., Biston P., Jeong H. W., Smith R., Prawira Y., Garcia A. H., Salterain N., Meyns B., Elnasser M., Moreno M., Walia R., Mehta A., Schweda A., Williams M., EmadAmkhatirah, Kim K. H., Assad A., Giraldo E., Karolak W., Balik M., Pocock E., Gajkowski E., Masafumi K., Barrett N., Takeyama Y., Park S., Amin F., Andriyani F. M., Sudakevych S., Schnur J., Vera M., Cornejo R., Schwarz P., Mardini A. C., de Paula T., Neto A. S., Villoldo A., Colafranceschi A. S., Iglesias A. U., Granjean J., Melro L. M. G., Romualdo G. F., Gaia D., Souza H., Galas F., Mendiluce R. M., Sosa A., Martinez I., Kurosawa H., Almoshantaf M. B., Salgado J., Hugi-Mayr B., Charbonneau E., Barzilai V. S., Monteiro V., de Souza R. R., Harper M., Siddig N., Suzuki H., Adams C., Brieva J., Khamees A., Graige F., Supriatna M., Nyale G., Eltatar F. S., Fatani J., Baeissa H., Masri A. A. L., Rabie A., Hui M. Y., Yamane M., Jung H., Margaret A. M., Nacpil N., Ruck K., Bakken R., Jara C., Felton T., Tharwat S., Berra L., Shah B., Chakraborty A., Cardona M., Capatos G., Akkanti B., Orija A., Jain H., Ito A., Muftah M., Housni B., Aldhalia A., Low S., Iihara K., Chavez J., Ramanathan K., Naidoo K., Seppelt I., VanDyk M., MacDonald S., Hafez W., McGregor R., Siebenaler T., Flynn H., Lofton K., Aokage T., Kvirkvelia B., Shigemitsu K., Moscatelli A., Fiorentino G., Baumgaertel M., Mba S. E., Assy J., Hutahaean A., Roush H., Sichting K. A., Alessandri F., Burns D., Alkhubouli T. H., Nasrallah A., Salt G., Garabedian C. P., Millar J., Sim M., Mattke A., McAuley D., Tadili J., Frenzel T., Bar-Lavie Y., Ortiz A. B., Stone J., Attokaran A., Farquharson M., Patel B., Gunning D., Baillie K., Adem S., Watson P., Tamai K., Sajinadiyasa G. K., Kanyawati D., Salgado M., Sassine A., Yudo B., McCaul S., Lee B., Lee S. M., Afek A., Iwashita Y., Fadlalmola H., Semedi B. P., Mansour N. M., Metiva J., Van Belle N., Martin-Loeches I., Al-Sadawi M., Kirakli C., Shimaa A. -T., Abdurraouf A., Ivatt L., Moharam S., Woon C. Y., Kang H. M., Smith T., James E., Al-Rawas N., Almjersah A., Iwasaki Y., Ashour H., Embarek H., King-Chung K. C., Gudzenko V., Taccone F., Perdhana F., Lamarche Y., Ribeiro J. M., Bradic N., Van den Bossche K., Lansink O., Singh G., Debeuckelaere G., Stelfox H. T., Yi C., Elia J., Tribble T., Shankar S., Padmanabhan R., Hallinan B., Paoletti L., Leyva Y., Fykuda T., Badulak J., Koch J., Janowaik L., Hackman A., Hernandez D., Osofsky J., Donadello K., Lawang A., Fine J., Davidson B., Vazquez A. O. R., and Abdehaleem I.
Abstract: Following publication of the original article [1], the authors identified that the collaborating authors part of the collaborating author group CCCC Consortium was missing. The collaborating author group is available and included as Additional file 1 in this article.
Published: 2023

3. An Unusual Case of Chronic Cough: Cladosporium Pneumonia

Author: Hassanin, E.-H., primary, Weyer, A., additional, Duarte, A., additional, and Nannaka, V.B., additional
Published: 2023
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4. An Unusual Cause of Miliary Radiographic Findings

Author: Duarte, A., primary, Hassanin, E.-H., additional, Weyer, A., additional, and Nannaka, V.B., additional
Published: 2023
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5. An Unexpected Cause of Shortness of Breath

Author: Weyer, A., primary, Hassanin, E.-H., additional, Duarte, A., additional, and Nannaka, V.B., additional
Published: 2023
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6. Dissecting the genetic heterogeneity of gastric cancer

Author: Hess, T., Maj, C., Gehlen, J., Borisov, O., Haas, S. L., Gockel, I., Vieth, M., Piessen, G., Alakus, H., Vashist, Y., Pereira, C., Knapp, M., Schuller, V., Quaas, A., Grabsch, H. I., Trautmann, J., Malecka-Wojciesko, E., Mokrowiecka, A., Speller, J., Mayr, A., Schroder, J., Hillmer, A. M., Heider, D., Lordick, F., Perez-Aisa, A., Campo, R., Espinel, J., Geijo, F., Thomson, C., Bujanda, L., Sopena, F., Lanas, A., Pellise, M., Pauligk, C., Goetze, T. O., Zelck, C., Reingruber, J., Hassanin, E., Elbe, P., Alsabeah, S., Lindblad, M., Nilsson, M., Kreuser, N., Thieme, R., Tavano, F., Pastorino, Roberta, Arzani, D., Persiani, Roberto, Jung, J. -O., Nienhuser, H., Ott, K., Schumann, R. R., Kumpf, O., Burock, S., Arndt, V., Jakubowska, A., Lawniczak, M., Moreno, V., Martin, V., Kogevinas, M., Pollan, M., Dabrowska, J., Salas, A., Cussenot, O., Boland-Auge, A., Daian, D., Deleuze, J. -F., Salvi, E., Teder-Laving, M., Tomasello, G., Ratti, M., Senti, C., De Re, V., Steffan, A., Holscher, A. H., Messerle, K., Bruns, C. J., Sivins, A., Bogdanova, I., Skieceviciene, J., Arstikyte, J., Moehler, M., Lang, H., Grimminger, P. P., Kruschewski, M., Vassos, N., Schildberg, C., Lingohr, P., Ridwelski, K., Lippert, H., Fricker, N., Krawitz, P., Hoffmann, Christian Pieter, Nothen, M. M., Veits, L., Izbicki, J. R., Mostowska, A., Martinon-Torres, F., Cusi, D., Adolfsson, R., Cancel-Tassin, G., Hoblinger, A., Rodermann, E., Ludwig, M., Keller, G., Metspalu, A., Brenner, H., Heller, J., Neef, M., Schepke, M., Dumoulin, F. L., Hamann, L., Cannizzaro, Rino, Ghidini, Maria Candida, Plassmann, D., Geppert, M., Malfertheiner, P., Gehlen, O., Skoczylas, T., Majewski, M., Lubinski, J., Palmieri, O., Boccia, Stefania, Latiano, A., Aragones, N., Schmidt, T., Dinis-Ribeiro, M., Medeiros, R., Al-Batran, S. -E., Leja, M., Kupcinskas, J., Garcia-Gonzalez, M. A., Venerito, M., Schumacher, J., Pastorino R. (ORCID:0000-0001-5013-0733), Persiani R. (ORCID:0000-0002-1537-5097), Hoffmann P., Cannizzaro R., Ghidini M., Boccia S. (ORCID:0000-0002-1864-749X), Hess, T., Maj, C., Gehlen, J., Borisov, O., Haas, S. L., Gockel, I., Vieth, M., Piessen, G., Alakus, H., Vashist, Y., Pereira, C., Knapp, M., Schuller, V., Quaas, A., Grabsch, H. I., Trautmann, J., Malecka-Wojciesko, E., Mokrowiecka, A., Speller, J., Mayr, A., Schroder, J., Hillmer, A. M., Heider, D., Lordick, F., Perez-Aisa, A., Campo, R., Espinel, J., Geijo, F., Thomson, C., Bujanda, L., Sopena, F., Lanas, A., Pellise, M., Pauligk, C., Goetze, T. O., Zelck, C., Reingruber, J., Hassanin, E., Elbe, P., Alsabeah, S., Lindblad, M., Nilsson, M., Kreuser, N., Thieme, R., Tavano, F., Pastorino, Roberta, Arzani, D., Persiani, Roberto, Jung, J. -O., Nienhuser, H., Ott, K., Schumann, R. R., Kumpf, O., Burock, S., Arndt, V., Jakubowska, A., Lawniczak, M., Moreno, V., Martin, V., Kogevinas, M., Pollan, M., Dabrowska, J., Salas, A., Cussenot, O., Boland-Auge, A., Daian, D., Deleuze, J. -F., Salvi, E., Teder-Laving, M., Tomasello, G., Ratti, M., Senti, C., De Re, V., Steffan, A., Holscher, A. H., Messerle, K., Bruns, C. J., Sivins, A., Bogdanova, I., Skieceviciene, J., Arstikyte, J., Moehler, M., Lang, H., Grimminger, P. P., Kruschewski, M., Vassos, N., Schildberg, C., Lingohr, P., Ridwelski, K., Lippert, H., Fricker, N., Krawitz, P., Hoffmann, Christian Pieter, Nothen, M. M., Veits, L., Izbicki, J. R., Mostowska, A., Martinon-Torres, F., Cusi, D., Adolfsson, R., Cancel-Tassin, G., Hoblinger, A., Rodermann, E., Ludwig, M., Keller, G., Metspalu, A., Brenner, H., Heller, J., Neef, M., Schepke, M., Dumoulin, F. L., Hamann, L., Cannizzaro, Rino, Ghidini, Maria Candida, Plassmann, D., Geppert, M., Malfertheiner, P., Gehlen, O., Skoczylas, T., Majewski, M., Lubinski, J., Palmieri, O., Boccia, Stefania, Latiano, A., Aragones, N., Schmidt, T., Dinis-Ribeiro, M., Medeiros, R., Al-Batran, S. -E., Leja, M., Kupcinskas, J., Garcia-Gonzalez, M. A., Venerito, M., Schumacher, J., Pastorino R. (ORCID:0000-0001-5013-0733), Persiani R. (ORCID:0000-0002-1537-5097), Hoffmann P., Cannizzaro R., Ghidini M., and Boccia S. (ORCID:0000-0002-1864-749X)
Abstract: Background: Gastric cancer (GC) is clinically heterogenous according to location (cardia/non-cardia) and histopathology (diffuse/intestinal). We aimed to characterize the genetic risk architecture of GC according to its subtypes. Another aim was to examine whether cardia GC and oesophageal adenocarcinoma (OAC) and its precursor lesion Barrett's oesophagus (BO), which are all located at the gastro-oesophageal junction (GOJ), share polygenic risk architecture. Methods: We did a meta-analysis of ten European genome-wide association studies (GWAS) of GC and its subtypes. All patients had a histopathologically confirmed diagnosis of gastric adenocarcinoma. For the identification of risk genes among GWAS loci we did a transcriptome-wide association study (TWAS) and expression quantitative trait locus (eQTL) study from gastric corpus and antrum mucosa. To test whether cardia GC and OAC/BO share genetic aetiology we also used a European GWAS sample with OAC/BO. Findings: Our GWAS consisting of 5816 patients and 10,999 controls highlights the genetic heterogeneity of GC according to its subtypes. We newly identified two and replicated five GC risk loci, all of them with subtype-specific association. The gastric transcriptome data consisting of 361 corpus and 342 antrum mucosa samples revealed that an upregulated expression of MUC1, ANKRD50, PTGER4, and PSCA are plausible GC-pathomechanisms at four GWAS loci. At another risk locus, we found that the blood-group 0 exerts protective effects for non-cardia and diffuse GC, while blood-group A increases risk for both GC subtypes. Furthermore, our GWAS on cardia GC and OAC/BO (10,279 patients, 16,527 controls) showed that both cancer entities share genetic aetiology at the polygenic level and identified two new risk loci on the single-marker level. Interpretation: Our findings show that the pathophysiology of GC is genetically heterogenous according to location and histopathology. Moreover, our findings point to common molecular me
Published: 2023

7. Heated, humidified high flow therapy at home setting in children with respiratory failure- Single centre experience

Author: Hassanin, E, primary, Gopalakaje, S, additional, and Edwards, C, additional
Published: 2022
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8. Probable Creutzfeldt-Jakob Disease in the Context of a Recent COVID-19 Infection

Author: Hassanin, E.-H., primary, Sexe, J., additional, Upendran, I., additional, Almas, M.S., additional, and Russell, D., additional
Published: 2022
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9. Where Did the Platelets Go- Covid Vaccine Induced Bone Marrow Suppression

Author: Randhawa, N.K., primary, Hassanin, E.-H., additional, and Randhawa, S., additional
Published: 2022
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10. Can Sex Kill?: Sexual Intercourse and Aortic Dissection

Author: Hassanin, E.-H., primary and Iskander, S., additional
Published: 2022
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11. The Use of Bruton Tyrosine Kinase Inhibitors in Severe Covid-19 Patients

Author: Hassanin, E.-H., primary, Terada, R., additional, Alvarado, C., additional, Wadle, C., additional, Swindall, R., additional, Cook, A., additional, Devine, M.S., additional, and Philley, J., additional
Published: 2022
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12. Breast and prostate cancer risk: the interplay of polygenic risk, high-impact monogenic variants, and family history

Author: Peter Krawitz, Andreas J. Forstner, Hassanin E, Isabel Spier, Aldisi R, Stefan Aretz, Patrick May, Carlo Maj, Markus M. Nöthen, and Dheeraj Reddy Bobbili
Subjects: Oncology, medicine.medical_specialty, Proportional hazards model, business.industry, Incidence (epidemiology), Cancer, Odds ratio, Logistic regression, medicine.disease, Prostate cancer, Internal medicine, medicine, Cumulative incidence, Family history, business
Abstract: PurposeInvestigate to which extent polygenic risk scores (PRS), high-impact monogenic variants, and family history affect breast and prostate cancer risk by assessing cancer prevalence and cancer cumulative lifetime incidence.Methods200,643 individuals from the UK Biobank were stratified as follows: 1. carriers or non-carriers of high impact constitutive, monogenic variants in cancer susceptibility genes, 2. high or non-high PRS (90th percentile threshold), 3. with or without a family history of cancer.Multivariable logistic regression was used to compare the odds ratio (OR) across the different groups while Cox proportional hazards models were used to compute the cumulative incidence through life.ResultsBreast and prostate cancer cumulative incidence by age 70 is 7% and 5% for non-carriers with non-high PRS and reaches 37% and 32% among carriers of high-impact variants in cancer susceptibility genes with high PRS.The additional presence of family history is associated with a further increase of the risk of developing cancer reaching an OR of 14 and 21 for breast and prostate cancer, respectively.ConclusionHigh PRS confers a cancer risk comparable to high-impact monogenic variants. Family history, monogenic variants, and PRS contribute additively to breast and prostate cancer risk.
Published: 2021

13. Assessing the role of polygenic background on the penetrance of monogenic forms in Parkinson’s disease

Author: Carlo Maj, Peter Krawitz, Patrick May, Hassanin E, Dheeraj Reddy Bobbili, and Aldisi R
Subjects: Oncology, medicine.medical_specialty, Parkinson's disease, business.industry, Single-nucleotide polymorphism, Genome-wide association study, Disease, Odds ratio, medicine.disease, Penetrance, Internal medicine, medicine, Family history, business, Exome
Abstract: BackgroundSeveral rare and common variants are associated with Parkinson’s disease. However, there is still an incomplete penetrance in the carriers of rare variants associated with Parkinson’s disease. To address this issue, we investigated whether a PRS calculated from significant GWAS SNPs affects the penetrance of Parkinson’s disease among carriers of rare monogenic variants in known Parkinson’s disease genes and those with a family history.MethodsWe calculated the PRS based on common variants and selected the carriers of rare monogenic variants by using the exome data from UK Biobank. Individuals were divided into three risk categories based on PRS: low (90%) risk groups. We then compared how PRS affects Parkinson’s disease risk among carriers of rare monogenic variants and those with family-history.ResultsWe observed a two-fold higher odds ratio for a carrier of a monogenic variant that had a high PRS (OR 4.07,95% CI, 1.72-8.08) compared to carriers with a low PRS (OR 1.91, 95% CI, 0.31-6.05). In the same line, carriers with a first-degree family history and with >90% PRS have even a higher risk of developing PD (OR 23.53, 95%CI 5.39-71.54) compared to those with ConclusionsOur results show that PRS, carrier status, and family history contribute independently and additively to the Parkinson’s disease risk.
Published: 2021

14. Evaluation of Sex hormones in male and female Egyptian population naturally exposed to Dibutyl phthalate: a cross-sectional study

Author: Donia, Radwa, primary, Abdel-Ghaffar, Abdel-Rahman, additional, Sultan, E., additional, Hassanin, E., additional, and Borai, Ibrahim, additional
Published: 2021
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15. EFFECT OF CROP ROTATION ON THE CONTROL OF WILD OAT IN WHEAT IN UPPER EGYPT

Author: AL-MARSAFY, HAFEZ T., primary and HASSANEIN, EL-HASSANIN E., additional
Published: 1998
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16. Large-scale application of ClinGen-InSiGHT APC-specific ACMG/AMP variant classification criteria leads to substantial reduction in VUS.

Author: Yin X, Richardson M, Laner A, Shi X, Ognedal E, Vasta V, Hansen TVO, Pineda M, Ritter D, de Dunnen J, Hassanin E, Lin WL, Borras E, Krahn K, Nordling M, Martins A, Mahmood K, Nadeau E, Beshay V, Tops C, Genuardi M, Pesaran T, Frayling IM, Capellá G, Latchford A, Tavtigian SV, Maj C, Plon SE, Greenblatt MS, Macrae FA, Spier I, and Aretz S
Abstract: Pathogenic constitutional APC variants underlie familial adenomatous polyposis, the most common hereditary gastrointestinal polyposis syndrome. To improve variant classification and resolve the interpretative challenges of variants of uncertain significance (VUSs), APC-specific variant classification criteria were developed by the ClinGen-InSiGHT Hereditary Colorectal Cancer/Polyposis Variant Curation Expert Panel (VCEP) based on the criteria of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology (ACMG/AMP). A streamlined algorithm using the APC-specific criteria was developed and applied to assess all APC variants in ClinVar and the International Society for Gastrointestinal Hereditary Tumours (InSiGHT) international reference APC Leiden Open Variation Database (LOVD) variant database, which included a total of 10,228 unique APC variants. Among the ClinVar and LOVD variants with an initial classification of (likely) benign or (likely) pathogenic, 94% and 96% remained in their original categories, respectively. In contrast, 41% ClinVar and 61% LOVD VUSs were reclassified into clinically meaningful classes, the vast majority as (likely) benign. The total number of VUSs was reduced by 37%. In 24 out of 37 (65%) promising APC variants that remained VUS despite evidence for pathogenicity, a data-mining-driven work-up allowed their reclassification as (likely) pathogenic. These results demonstrated that the application of APC-specific criteria substantially reduced the number of VUSs in ClinVar and LOVD. The study also demonstrated the feasibility of a systematic approach to variant classification in large datasets, which might serve as a generalizable model for other gene- or disease-specific variant interpretation initiatives. It also allowed for the prioritization of VUSs that will benefit from in-depth evidence collection. This subset of APC variants was approved by the VCEP and made publicly available through ClinVar and LOVD for widespread clinical use., Competing Interests: Declaration of interests S.E.P. is a member of the scientific advisory panel of Baylor Genetics Laboratories., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
Published: 2024
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17. Genome-wide association study of copy number variations in Parkinson's disease.

Author: Landoulsi Z, Sreelatha AAK, Schulte C, Bobbili DR, Montanucci L, Leu C, Niestroj LM, Hassanin E, Domenighetti C, Pavelka L, Sugier PE, Radivojkov-Blagojevic M, Lichtner P, Portugal B, Edsall C, Kru Ger J, Hernandez DG, Blauwendraat C, Mellick GD, Zimprich A, Pirker W, Tan M, Rogaeva E, Lang AE, Koks S, Taba P, Lesage S, Brice A, Corvol JC, Chartier-Harlin MC, Mutez E, Brockmann K, Deutschländer AB, Hadjigeorgiou GM, Dardiotis E, Stefanis L, Simitsi AM, Valente EM, Petrucci S, Straniero L, Zecchinelli A, Pezzoli G, Brighina L, Ferrarese C, Annesi G, Quattrone A, Gagliardi M, Burbulla LF, Matsuo H, Nakayama A, Hattori N, Nishioka K, Chung SJ, Kim YJ, Kolber P, van de Warrenburg BP, Bloem BR, Singleton AB, Toft M, Pihlstrom L, Guedes LC, Ferreira JJ, Bardien S, Carr J, Tolosa E, Ezquerra M, Pastor P, Wirdefeldt K, Pedersen NL, Ran C, Belin AC, Puschmann A, Clarke CE, Morrison KE, Krainc D, Farrer MJ, Lal D, Elbaz A, Gasser T, Krüger R, Sharma M, and May P
Abstract: Objective: Our study investigates the impact of copy number variations (CNVs) on Parkinson's disease (PD) pathogenesis using genome-wide data, aiming to uncover novel genetic mechanisms and improve the understanding of the role of CNVs in sporadic PD., Methods: We applied a sliding window approach to perform CNV-GWAS and conducted genome-wide burden analyses on CNV data from 11,035 PD patients (including 2,731 early-onset PD (EOPD)) and 8,901 controls from the COURAGE-PD consortium., Results: We identified 14 genome-wide significant CNV loci associated with PD, including one deletion and 13 duplications. Among these, duplications in 7q22.1, 11q12.3 and 7q33 displayed the highest effect. Two significant duplications overlapped with PD-related genes SNCA and VPS13C , but none overlapped with recent significant SNP-based GWAS findings. Five duplications included genes associated with neurological disease, and four overlapping genes were dosage-sensitive and intolerant to loss-of-function variants. Enriched pathways included neurodegeneration, steroid hormone biosynthesis, and lipid metabolism. In early-onset cases, four loci were significantly associated with EOPD, including three known duplications and one novel deletion in PRKN . CNV burden analysis showed a higher prevalence of CNVs in PD-related genes in patients compared to controls (OR=1.56 [1.18-2.09], p=0.0013), with PRKN showing the highest burden (OR=1.47 [1.10-1.98], p=0.026). Patients with CNVs in PRKN had an earlier disease onset. Burden analysis with controls and EOPD patients showed similar results., Interpretation: This is the largest CNV-based GWAS in PD identifying novel CNV regions and confirming the significant CNV burden in EOPD, primarily driven by the PRKN gene, warranting further investigation.
Published: 2024
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18. Systematic large-scale application of ClinGen InSiGHT APC -specific ACMG/AMP variant classification criteria substantially alleviates the burden of variants of uncertain significance in ClinVar and LOVD databases.

Author: Yin X, Richardson M, Laner A, Shi X, Ognedal E, Vasta V, Hansen TVO, Pineda M, Ritter D, den Dunnen JT, Hassanin E, Lyman Lin W, Borras E, Krahn K, Nordling M, Martins A, Mahmood K, Nadeau EAW, Beshay V, Tops C, Genuardi M, Pesaran T, Frayling IM, Capellá G, Latchford A, Tavtigian SV, Maj C, Plon SE, Greenblatt MS, Macrae FA, Spier I, and Aretz S
Abstract: Background: Pathogenic constitutional APC variants underlie familial adenomatous polyposis, the most common hereditary gastrointestinal polyposis syndrome. To improve variant classification and resolve the interpretative challenges of variants of uncertain significance (VUS), APC-specific ACMG/AMP variant classification criteria were developed by the ClinGen-InSiGHT Hereditary Colorectal Cancer/Polyposis Variant Curation Expert Panel (VCEP)., Methods: A streamlined algorithm using the APC -specific criteria was developed and applied to assess all APC variants in ClinVar and the InSiGHT international reference APC LOVD variant database., Results: A total of 10,228 unique APC variants were analysed. Among the ClinVar and LOVD variants with an initial classification of (Likely) Benign or (Likely) Pathogenic, 94% and 96% remained in their original categories, respectively. In contrast, 41% ClinVar and 61% LOVD VUS were reclassified into clinically actionable classes, the vast majority as (Likely) Benign. The total number of VUS was reduced by 37%. In 21 out of 36 (58%) promising APC variants that remained VUS despite evidence for pathogenicity, a data mining-driven work-up allowed their reclassification as (Likely) Pathogenic., Conclusions: The application of APC -specific criteria substantially reduced the number of VUS in ClinVar and LOVD. The study also demonstrated the feasibility of a systematic approach to variant classification in large datasets, which might serve as a generalisable model for other gene-/disease-specific variant interpretation initiatives. It also allowed for the prioritization of VUS that will benefit from in-depth evidence collection. This subset of APC variants was approved by the VCEP and made publicly available through ClinVar and LOVD for widespread clinical use.
Published: 2024
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19. Trans-ancestry polygenic models for the prediction of LDL blood levels: an analysis of the United Kingdom Biobank and Taiwan Biobank.

Author: Hassanin E, Lee KH, Hsieh TC, Aldisi R, Lee YL, Bobbili D, Krawitz P, May P, Chen CY, and Maj C
Abstract: Polygenic risk score (PRS) predictions often show bias toward the population of available genome-wide association studies (GWASs), which is typically of European ancestry. This study aimed to assess the performance differences of ancestry-specific PRS and test the implementation of multi-ancestry PRS to enhance the generalizability of low-density lipoprotein (LDL) cholesterol predictions in the East Asian (EAS) population. In this study, we computed ancestry-specific and multi-ancestry PRSs for LDL using data obtained from the Global Lipid Genetics Consortium, while accounting for population-specific linkage disequilibrium patterns using the PRS-CSx method in the United Kingdom Biobank dataset (UKB, n = 423,596) and Taiwan Biobank dataset (TWB, n = 68,978). Population-specific PRSs were able to predict LDL levels better within the target population, whereas multi-ancestry PRSs were more generalizable. In the TWB dataset, covariate-adjusted R 2 values were 9.3% for ancestry-specific PRS, 6.7% for multi-ancestry PRS, and 4.5% for European-specific PRS. Similar trends (8.6%, 7.8%, and 6.2%) were observed in the smaller EAS population of the UKB (n = 1,480). Consistent with R 2 values, PRS stratification in EAS regions (TWB) effectively captured a heterogenous variability in LDL blood cholesterol levels across PRS strata. The mean difference in LDL levels between the lowest and highest EAS-specific PRS (EAS_PRS) deciles was 0.82, compared to 0.59 for European-specific PRS (EUR_PRS) and 0.76 for multi-ancestry PRS. Notably, the mean LDL values in the top decile of multi-ancestry PRS were comparable to those of EAS_PRS (3.543 vs. 3.541, p = 0.86). Our analysis of the PRS prediction model for LDL cholesterol further supports the issue of PRS generalizability across populations. Our targeted analysis of the EAS population revealed that integrating non-European genotyping data with a powerful European-based GWAS can enhance the generalizability of LDL PRS., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Hassanin, Lee, Hsieh, Aldisi, Lee, Bobbili, Krawitz, May, Chen and Maj.)
Published: 2023
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20. Ability of a polygenic risk score to refine colorectal cancer risk in Lynch syndrome.

Author: Dueñas N, Klinkhammer H, Bonifaci N, Spier I, Mayr A, Hassanin E, Diez-Villanueva A, Moreno V, Pineda M, Maj C, Capellà G, Aretz S, and Brunet J
Abstract: Background: Polygenic risk scores (PRSs) have been used to stratify colorectal cancer (CRC) risk in the general population, whereas its role in Lynch syndrome (LS), the most common type of hereditary CRC, is still conflicting. We aimed to assess the ability of PRS to refine CRC risk prediction in European-descendant individuals with LS., Methods: 1465 individuals with LS (557 MLH1 , 517 MSH2/EPCAM , 299 MSH6 and 92 PMS2 ) and 5656 CRC-free population-based controls from two independent cohorts were included. A 91-SNP PRS was applied. A Cox proportional hazard regression model with 'family' as a random effect and a logistic regression analysis, followed by a meta-analysis combining both cohorts were conducted., Results: Overall, we did not observe a statistically significant association between PRS and CRC risk in the entire cohort. Nevertheless, PRS was significantly associated with a slightly increased risk of CRC or advanced adenoma (AA), in those with CRC diagnosed <50 years and in individuals with multiple CRCs or AAs diagnosed <60 years., Conclusion: The PRS may slightly influence CRC risk in individuals with LS in particular in more extreme phenotypes such as early-onset disease. However, the study design and recruitment strategy strongly influence the results of PRS studies. A separate analysis by genes and its combination with other genetic and non-genetic risk factors will help refine its role as a risk modifier in LS., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.)
Published: 2023
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21. Gene-based burden scores identify rare variant associations for 28 blood biomarkers.

Author: Aldisi R, Hassanin E, Sivalingam S, Buness A, Klinkhammer H, Mayr A, Fröhlich H, Krawitz P, and Maj C
Subjects: Humans, Biomarkers, Phenotype, Multifactorial Inheritance genetics, Genetic Predisposition to Disease genetics, Exome
Abstract: Background: A relevant part of the genetic architecture of complex traits is still unknown; despite the discovery of many disease-associated common variants. Polygenic risk score (PRS) models are based on the evaluation of the additive effects attributable to common variants and have been successfully implemented to assess the genetic susceptibility for many phenotypes. In contrast, burden tests are often used to identify an enrichment of rare deleterious variants in specific genes. Both kinds of genetic contributions are typically analyzed independently. Many studies suggest that complex phenotypes are influenced by both low effect common variants and high effect rare deleterious variants. The aim of this paper is to integrate the effect of both common and rare functional variants for a more comprehensive genetic risk modeling., Methods: We developed a framework combining gene-based scores based on the enrichment of rare functionally relevant variants with genome-wide PRS based on common variants for association analysis and prediction models. We applied our framework on UK Biobank dataset with genotyping and exome data and considered 28 blood biomarkers levels as target phenotypes. For each biomarker, an association analysis was performed on full cohort using gene-based scores (GBS). The cohort was then split into 3 subsets for PRS construction and feature selection, predictive model training, and independent evaluation, respectively. Prediction models were generated including either PRS, GBS or both (combined)., Results: Association analyses of the cohort were able to detect significant genes that were previously known to be associated with different biomarkers. Interestingly, the analyses also revealed heterogeneous effect sizes and directionality highlighting the complexity of the blood biomarkers regulation. However, the combined models for many biomarkers show little or no improvement in prediction accuracy compared to the PRS models., Conclusion: This study shows that rare variants play an important role in the genetic architecture of complex multifactorial traits such as blood biomarkers. However, while rare deleterious variants play a strong role at an individual level, our results indicate that classical common variant based PRS might be more informative to predict the genetic susceptibility at the population level., (© 2023. BioMed Central Ltd., part of Springer Nature.)
Published: 2023
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22. Corrigendum to "Dissecting the genetic heterogeneity of gastric cancer".

Author: Hess T, Maj C, Gehlen J, Borisov O, Haas SL, Gockel I, Vieth M, Piessen G, Alakus H, Vashist Y, Pereira C, Knapp M, Schüller V, Quaas A, Grabsch HI, Trautmann J, Malecka-Wojciesko E, Mokrowiecka A, Speller J, Mayr A, Schröder J, Hillmer AM, Heider D, Lordick F, Pérez-Aísa Á, Campo R, Espinel J, Geijo F, Thomson C, Bujanda L, Sopeña F, Lanas Á, Pellisé M, Pauligk C, Goetze TO, Zelck C, Reingruber J, Hassanin E, Elbe P, Alsabeah S, Lindblad M, Nilsson M, Kreuser N, Thieme R, Tavano F, Pastorino R, Arzani D, Persiani R, Jung JO, Nienhüser H, Ott K, Schumann RR, Kumpf O, Burock S, Arndt V, Jakubowska A, Ławniczak M, Moreno V, Martín V, Kogevinas M, Pollán M, Dąbrowska J, Salas A, Cussenot O, Boland-Auge A, Daian D, Deleuze JF, Salvi E, Teder-Laving M, Tomasello G, Ratti M, Senti C, De Re V, Steffan A, Hölscher AH, Messerle K, Bruns CJ, Sīviņš A, Bogdanova I, Skieceviciene J, Arstikyte J, Moehler M, Lang H, Grimminger PP, Kruschewski M, Vassos N, Schildberg C, Lingohr P, Ridwelski K, Lippert H, Fricker N, Krawitz P, Hoffmann P, Nöthen MM, Veits L, Izbicki JR, Mostowska A, Martinón-Torres F, Cusi D, Adolfsson R, Cancel-Tassin G, Höblinger A, Rodermann E, Ludwig M, Keller G, Metspalu A, Brenner H, Heller J, Neef M, Schepke M, Dumoulin FL, Hamann L, Cannizzaro R, Ghidini M, Plaßmann D, Geppert M, Malfertheiner P, Glehen O, Skoczylas T, Majewski M, Lubiński J, Palmieri O, Boccia S, Latiano A, Aragones N, Schmidt T, Dinis-Ribeiro M, Medeiros R, Al-Batran SE, Leja M, Kupcinskas J, García-González MA, Venerito M, and Schumacher J
Published: 2023
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23. Assessing the performance of European-derived cardiometabolic polygenic risk scores in South-Asians and their interplay with family history.

Author: Hassanin E, Maj C, Klinkhammer H, Krawitz P, May P, and Bobbili DR
Subjects: Humans, Obesity genetics, Risk Factors, United Kingdom, Asian People, Multifactorial Inheritance, Coronary Artery Disease genetics, Diabetes Mellitus, Type 2 genetics, Obesity, Morbid
Abstract: Background & Aims: We aimed to assess the performance of European-derived polygenic risk scores (PRSs) for common metabolic diseases such as coronary artery disease (CAD), obesity, and type 2 diabetes (T2D) in the South Asian (SAS) individuals in the UK Biobank. Additionally, we studied the interaction between PRS and family history (FH) in the same population., Methods: To calculate the PRS, we used a previously published model derived from the EUR population and applied it to the individuals of SAS ancestry from the UKB study. Each PRS was adjusted according to an individual's genotype location in the principal components (PC) space to derive an ancestry adjusted PRS (aPRS). We calculated the percentiles based on aPRS and stratified individuals into three aPRS categories: low, intermediate, and high. Considering the intermediate-aPRS percentile as a reference, we compared the low and high aPRS categories and generated the odds ratio (OR) estimates. Further, we measured the combined role of aPRS and first-degree family history (FH) in the SAS population., Results: The risk of developing severe obesity for SAS individuals was almost twofold higher for individuals with high aPRS than for those with intermediate aPRS, with an OR of 1.95 (95% CI = 1.71-2.23, P < 0.01). At the same time, the risk of severe obesity was lower in the low-aPRS group (OR = 0.60, CI = 0.53-0.67, P < 0.01). Results in the same direction were found in the EUR data, where the low-PRS group had an OR of 0.53 (95% CI = 0.51-0.56, P < 0.01) and the high-PRS group had an OR of 2.06 (95% CI = 2.00-2.12, P < 0.01). We observed similar results for CAD and T2D. Further, we show that SAS individuals with a familial history of CAD and T2D with high-aPRS are associated with a higher risk of these diseases, implying a greater genetic predisposition., Conclusion: Our findings suggest that CAD, obesity, and T2D GWAS summary statistics generated predominantly from the EUR population can be potentially used to derive aPRS in SAS individuals for risk stratification. With future GWAS recruiting more SAS participants and tailoring the PRSs towards SAS ancestry, the predictive power of PRS is likely to improve further., (© 2023. The Author(s).)
Published: 2023
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24. Dissecting the genetic heterogeneity of gastric cancer.

Author: Hess T, Maj C, Gehlen J, Borisov O, Haas SL, Gockel I, Vieth M, Piessen G, Alakus H, Vashist Y, Pereira C, Knapp M, Schüller V, Quaas A, Grabsch HI, Trautmann J, Malecka-Wojciesko E, Mokrowiecka A, Speller J, Mayr A, Schröder J, Hillmer AM, Heider D, Lordick F, Pérez-Aísa Á, Campo R, Espinel J, Geijo F, Thomson C, Bujanda L, Sopeña F, Lanas Á, Pellisé M, Pauligk C, Goetze TO, Zelck C, Reingruber J, Hassanin E, Elbe P, Alsabeah S, Lindblad M, Nilsson M, Kreuser N, Thieme R, Tavano F, Pastorino R, Arzani D, Persiani R, Jung JO, Nienhüser H, Ott K, Schumann RR, Kumpf O, Burock S, Arndt V, Jakubowska A, Ławniczak M, Moreno V, Martín V, Kogevinas M, Pollán M, Dąbrowska J, Salas A, Cussenot O, Boland-Auge A, Daian D, Deleuze JF, Salvi E, Teder-Laving M, Tomasello G, Ratti M, Senti C, De Re V, Steffan A, Hölscher AH, Messerle K, Bruns CJ, Sīviņš A, Bogdanova I, Skieceviciene J, Arstikyte J, Moehler M, Lang H, Grimminger PP, Kruschewski M, Vassos N, Schildberg C, Lingohr P, Ridwelski K, Lippert H, Fricker N, Krawitz P, Hoffmann P, Nöthen MM, Veits L, Izbicki JR, Mostowska A, Martinón-Torres F, Cusi D, Adolfsson R, Cancel-Tassin G, Höblinger A, Rodermann E, Ludwig M, Keller G, Metspalu A, Brenner H, Heller J, Neef M, Schepke M, Dumoulin FL, Hamann L, Cannizzaro R, Ghidini M, Plaßmann D, Geppert M, Malfertheiner P, Gehlen O, Skoczylas T, Majewski M, Lubiński J, Palmieri O, Boccia S, Latiano A, Aragones N, Schmidt T, Dinis-Ribeiro M, Medeiros R, Al-Batran SE, Leja M, Kupcinskas J, García-González MA, Venerito M, and Schumacher J
Subjects: Humans, Genome-Wide Association Study, Genetic Heterogeneity, Risk Factors, Stomach Neoplasms genetics, Barrett Esophagus genetics, Adenocarcinoma pathology, Esophageal Neoplasms genetics
Abstract: Background: Gastric cancer (GC) is clinically heterogenous according to location (cardia/non-cardia) and histopathology (diffuse/intestinal). We aimed to characterize the genetic risk architecture of GC according to its subtypes. Another aim was to examine whether cardia GC and oesophageal adenocarcinoma (OAC) and its precursor lesion Barrett's oesophagus (BO), which are all located at the gastro-oesophageal junction (GOJ), share polygenic risk architecture., Methods: We did a meta-analysis of ten European genome-wide association studies (GWAS) of GC and its subtypes. All patients had a histopathologically confirmed diagnosis of gastric adenocarcinoma. For the identification of risk genes among GWAS loci we did a transcriptome-wide association study (TWAS) and expression quantitative trait locus (eQTL) study from gastric corpus and antrum mucosa. To test whether cardia GC and OAC/BO share genetic aetiology we also used a European GWAS sample with OAC/BO., Findings: Our GWAS consisting of 5816 patients and 10,999 controls highlights the genetic heterogeneity of GC according to its subtypes. We newly identified two and replicated five GC risk loci, all of them with subtype-specific association. The gastric transcriptome data consisting of 361 corpus and 342 antrum mucosa samples revealed that an upregulated expression of MUC1, ANKRD50, PTGER4, and PSCA are plausible GC-pathomechanisms at four GWAS loci. At another risk locus, we found that the blood-group 0 exerts protective effects for non-cardia and diffuse GC, while blood-group A increases risk for both GC subtypes. Furthermore, our GWAS on cardia GC and OAC/BO (10,279 patients, 16,527 controls) showed that both cancer entities share genetic aetiology at the polygenic level and identified two new risk loci on the single-marker level., Interpretation: Our findings show that the pathophysiology of GC is genetically heterogenous according to location and histopathology. Moreover, our findings point to common molecular mechanisms underlying cardia GC and OAC/BO., Funding: German Research Foundation (DFG)., Competing Interests: Declaration of interests MDR reports consulting fees from Roche Diagnostics and Medtronic; leadership or fiduciary role in the European Society of Gastrointestinal Endoscopy (ESGE) and World Endoscopy Organization (WEO). All other authors report no conflict of interest., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)
Published: 2023
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25. Effectiveness and Safety of Inactivated SARS-CoV-2 Vaccine (BBIBP-CorV) among Healthcare Workers: A Seven-Month Follow-Up Study at Fifteen Central Hospitals.

Author: Ashmawy R, Kamal E, Amin W, Sharaf S, Kabeel S, Albiheyri R, El-Maradny YA, Hassanin E, Elsaka N, Fahmy O, Awd A, Aboeldahab H, Nayle M, Afifi M, Ibrahim M, Rafaat R, Aly S, and Redwan EM
Abstract: Background: During a pandemic, healthcare workers are at high risk of contracting COVID-19. To protect these important individuals, it is highly recommended that they receive the COVID-19 vaccine. Our study focused on evaluating the safety and efficacy of Egypt's first approved vaccine, the Sinopharm vaccine (BBIBP-CorV), and comparing these findings with other vaccines., Methods: An observational study was conducted in fifteen triage and isolation hospitals, from the 1st of March until the end of September 2021. The study included fully vaccinated and unvaccinated participants, and we measured vaccine effectiveness (using 1-aHR), the incidence rate of severely to critically ill hospitalized cases, COVID-19-related work absenteeism, and the safety of the vaccine as outcomes., Results: Of the 1364 healthcare workers who were interviewed, 1228 agreed to participate. After taking the hazard ratio into account, the vaccine effectiveness was found to be 67% (95% CI, 80-43%) for symptomatic PCR-confirmed cases. The incidence rate ratio for hospitalization was 0.45 (95% CI, 0.15-1.31) in the vaccinated group compared to the unvaccinated group, and there was a significant reduction in absenteeism among the vaccinated group ( p < 0.007). Most adverse events were mild and well tolerated. Vaccinated pregnant and lactating mothers did not experience any sentinel adverse events., Conclusion: Our study found that the BBIBP-CorV vaccine was effective in protecting healthcare workers from COVID-19.
Published: 2023
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26. Clinically relevant combined effect of polygenic background, rare pathogenic germline variants, and family history on colorectal cancer incidence.

Author: Hassanin E, Spier I, Bobbili DR, Aldisi R, Klinkhammer H, David F, Dueñas N, Hüneburg R, Perne C, Brunet J, Capella G, Nöthen MM, Forstner AJ, Mayr A, Krawitz P, May P, Aretz S, and Maj C
Subjects: Humans, Incidence, Risk Factors, Germ Cells, Germ-Line Mutation, Colorectal Neoplasms
Abstract: Background and Aims: Summarised in polygenic risk scores (PRS), the effect of common, low penetrant genetic variants associated with colorectal cancer (CRC), can be used for risk stratification., Methods: To assess the combined impact of the PRS and other main factors on CRC risk, 163,516 individuals from the UK Biobank were stratified as follows: 1. carriers status for germline pathogenic variants (PV) in CRC susceptibility genes (APC, MLH1, MSH2, MSH6, PMS2), 2. low (< 20%), intermediate (20-80%), or high PRS (> 80%), and 3. family history (FH) of CRC. Multivariable logistic regression and Cox proportional hazards models were applied to compare odds ratios and to compute the lifetime incidence, respectively., Results: Depending on the PRS, the CRC lifetime incidence for non-carriers ranges between 6 and 22%, compared to 40% and 74% for carriers. A suspicious FH is associated with a further increase of the cumulative incidence reaching 26% for non-carriers and 98% for carriers. In non-carriers without FH, but high PRS, the CRC risk is doubled, whereas a low PRS even in the context of a FH results in a decreased risk. The full model including PRS, carrier status, and FH improved the area under the curve in risk prediction (0.704)., Conclusion: The findings demonstrate that CRC risks are strongly influenced by the PRS for both a sporadic and monogenic background. FH, PV, and common variants complementary contribute to CRC risk. The implementation of PRS in routine care will likely improve personalized risk stratification, which will in turn guide tailored preventive surveillance strategies in high, intermediate, and low risk groups., (© 2023. The Author(s).)
Published: 2023
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27. Voluntary deep inspiration breath-hold with volumetric modulated arc therapy in pediatric patients with mediastinal Hodgkin lymphoma.

Author: Shaheen H, Zaghloul MS, Ammar H, Aly B, Hassanin E, Mohsen SA, and Ahmed S
Subjects: Cone-Beam Computed Tomography, Humans, Male, Female, Child, Adolescent, Hodgkin Disease diagnostic imaging, Hodgkin Disease radiotherapy, Mediastinal Neoplasms diagnostic imaging, Mediastinal Neoplasms radiotherapy, Breath Holding, Inhalation, Radiotherapy, Intensity-Modulated
Abstract: Background: Deep inspiration breath-hold (DIBH) has been established to decrease normal tissue radiation dose in breast cancer. Methods: Forty-nine patients had two CT scans during DIBH or free breathing. Chest-wall position, setup verification and breath-hold monitoring were performed. Cone-beam CT and a surface image system were used for verification. Results: A total of 1617 breath-holds were analyzed in 401 fractions. The mean time bit was 6.01 min. The mean breaths-holds per fraction was 4.96. The median for intra-breath hold variability was 3 mm. No patient stopped treatment for intolerance. Clinical target volume margins were calculated as 0.36, 0.36 and 0.32 for the three translational positions. The mean saved volume was 26.3%. Conclusion: Voluntary DIBH is feasible, tolerable and easy to apply for children with Hodgkin lymphoma involving the mediastinum.
Published: 2023
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28. GenRisk: a tool for comprehensive genetic risk modeling.

Author: Aldisi R, Hassanin E, Sivalingam S, Buness A, Klinkhammer H, Mayr A, Fröhlich H, Krawitz P, and Maj C
Subjects: Phenotype, Open Reading Frames, Risk Factors, Software, Multifactorial Inheritance
Abstract: Summary: The genetic architecture of complex traits can be influenced by both many common regulatory variants with small effect sizes and rare deleterious variants in coding regions with larger effect sizes. However, the two kinds of genetic contributions are typically analyzed independently. Here, we present GenRisk, a python package for the computation and the integration of gene scores based on the burden of rare deleterious variants and common-variants-based polygenic risk scores. The derived scores can be analyzed within GenRisk to perform association tests or to derive phenotype prediction models by testing multiple classification and regression approaches. GenRisk is compatible with VCF input file formats., Availability and Implementation: GenRisk is an open source publicly available python package that can be downloaded or installed from Github (https://github.com/AldisiRana/GenRisk)., Supplementary Information: Supplementary data are available at Bioinformatics online., (© The Author(s) 2022. Published by Oxford University Press.)
Published: 2022
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29. Breast and prostate cancer risk: The interplay of polygenic risk, rare pathogenic germline variants, and family history.

Author: Hassanin E, May P, Aldisi R, Spier I, Forstner AJ, Nöthen MM, Aretz S, Krawitz P, Bobbili DR, and Maj C
Subjects: Aged, Genetic Predisposition to Disease, Germ Cells, Humans, Male, Multifactorial Inheritance genetics, Risk Factors, Breast Neoplasms epidemiology, Breast Neoplasms genetics, Prostatic Neoplasms epidemiology, Prostatic Neoplasms genetics
Abstract: Purpose: We aimed to investigate to what extent polygenic risk scores (PRS), rare pathogenic germline variants (PVs), and family history jointly influence breast cancer and prostate cancer risk., Methods: A total of 200,643 individuals from the UK Biobank were categorized as follows: (1) heterozygotes or nonheterozygotes for PVs in moderate to high-risk cancer genes, (2) PRS strata, and (3) with or without a family history of cancer. Multivariable logistic regression and Cox proportional hazards models were used to compute the odds ratio across groups and the cumulative incidence through life., Results: Cumulative incidence by age 70 years among the nonheterozygotes across PRS strata ranged from 9% to 32% and from 9% to 35% for breast cancer and prostate cancer, respectively. Among the PV heterozygotes it ranged from 20% to 48% in moderate-risk genes and from 51% to 74% in high-risk genes for breast cancer, and it ranged from 30% to 59% in prostate cancer risk genes. Family history was always associated with an increased cancer odds ratio., Conclusion: PRS alone provides a meaningful risk gradient leading to a cancer risk stratification comparable to PVs in moderate risk genes, whereas acts as a risk modifier when considering high-risk genes. Including family history along with PV and PRS further improves cancer risk stratification., Competing Interests: Conflict of Interest The authors declare no conflicts of interest., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)
Published: 2022
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30. Autoimmune Hepatitis: Shifts in Gut Microbiota and Metabolic Pathways among Egyptian Patients.

Author: Elsherbiny NM, Rammadan M, Hassan EA, Ali ME, El-Rehim ASA, Abbas WA, Abozaid MAA, Hassanin E, and Hetta HF
Abstract: Autoimmune hepatitis (AIH) is a chronic inflammatory disorder with complex immunopathogenesis. Dysbiosis has been linked to many autoimmune diseases, but its detailed role in autoimmune hepatitis (AIH) still needs rigorous evaluation, especially in Egypt. We aimed to identify the shift in the gut microbiota profile and resultant metabolic pathways in AIH Egyptian patients compared to healthy individuals. Stool samples were collected from 15 AIH-naive patients and from 10 healthy individuals. The V3-V4 hyper-variable regions in16S rRNA gene was amplified and sequenced using Illumina MiSeq platform. Significantly lower bacterial diversity in AIH patients was found compared to the controls. A phylum-level analysis showed the overrepresentation of Firmicutes, Bacteroides, and Proteobacteria. At the genus level, AIH-associated enrichment of Faecalibacterium , Blautia , Streptococcus , Haemophilus, Bacteroides , Veillonella , Eubacterium , Lachnospiraceae and Butyricicoccus was reported in contrast to Prevotella , Parabacteroides and Dilaster , which were significantly retracted in such patients. Overall, the predicted metabolic pathways associated with dysbiosis in AIH patients could orchestrate the potential pathogenic roles of gut microbiota in autoimmune disease, though not in a disease-specific manner, calling for future large-scale studies.
Published: 2020
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31. Immediate discontinuation of intravenous fluids after common surgical procedures.

Author: Al-Awad NI, Wosomu L, Al Hassanin EA, Al-Mulhim AA, Adu-Gyamfi Y, Shawan SM, and Abdulhadi MS
Abstract: Background: Intravenous (IV) fluids and nasogastric (MG) intubation can be discarded safely in some abdominal operations, but this practice seems rare in our community., Setting: A University teaching hospital in Eastern Saudi Arabia., Aims: To determine the feasibility of the practice in our setting and increase clinicians' awareness of it and encourage its general adoption., Method: A prospective verification study in consecutive ASA Classes I and II adult patients scheduled for four commonly performed operations., End Points: The practice was considered successful if the patient accepted early oral fluids and did not require re-insertion of IV line., Results: The operations studied were appendicectomy (44), laparoscopic cholecystectomy (35), herniorrhaphy (19) and diagnostic laparoscopy (2). The patients' mean age was 34.1 years (range 14 to 68); 60% were males. The overall success rate was 98%. Thus postoperative IV fluids proved to be unnecessary in these patients; cost savings were achieved and treating teams were freed to focus on other patients who truly required IV fluids., Conclusions: In our setting also, routine IV fluids are unnecessary and can be discarded safely after appendecectomy, cholecystectomy and herniorrhaphy in adults.
Published: 2000

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31 results on '"Hassanin E"'

1. Impact of Geographical Location on the Gut Microbiota Profile in Egyptian Children with Type 1 Diabetes Mellitus: A Pilot Study

2. Correction: Epidemiology and outcomes of early-onset AKI in COVID-19-related ARDS in comparison with non-COVID-19-related ARDS: insights from two prospective global cohort studies (Critical Care, (2023), 27, 1, (3), 10.1186/s13054-022-04294-5)

3. An Unusual Case of Chronic Cough: Cladosporium Pneumonia

4. An Unusual Cause of Miliary Radiographic Findings

5. An Unexpected Cause of Shortness of Breath

6. Dissecting the genetic heterogeneity of gastric cancer

7. Heated, humidified high flow therapy at home setting in children with respiratory failure- Single centre experience

8. Probable Creutzfeldt-Jakob Disease in the Context of a Recent COVID-19 Infection

9. Where Did the Platelets Go- Covid Vaccine Induced Bone Marrow Suppression

10. Can Sex Kill?: Sexual Intercourse and Aortic Dissection

11. The Use of Bruton Tyrosine Kinase Inhibitors in Severe Covid-19 Patients

12. Breast and prostate cancer risk: the interplay of polygenic risk, high-impact monogenic variants, and family history

13. Assessing the role of polygenic background on the penetrance of monogenic forms in Parkinson’s disease

14. Evaluation of Sex hormones in male and female Egyptian population naturally exposed to Dibutyl phthalate: a cross-sectional study

15. EFFECT OF CROP ROTATION ON THE CONTROL OF WILD OAT IN WHEAT IN UPPER EGYPT

16. Large-scale application of ClinGen-InSiGHT APC-specific ACMG/AMP variant classification criteria leads to substantial reduction in VUS.

17. Genome-wide association study of copy number variations in Parkinson's disease.

18. Systematic large-scale application of ClinGen InSiGHT APC -specific ACMG/AMP variant classification criteria substantially alleviates the burden of variants of uncertain significance in ClinVar and LOVD databases.

19. Trans-ancestry polygenic models for the prediction of LDL blood levels: an analysis of the United Kingdom Biobank and Taiwan Biobank.

20. Ability of a polygenic risk score to refine colorectal cancer risk in Lynch syndrome.

21. Gene-based burden scores identify rare variant associations for 28 blood biomarkers.

22. Corrigendum to "Dissecting the genetic heterogeneity of gastric cancer".

23. Assessing the performance of European-derived cardiometabolic polygenic risk scores in South-Asians and their interplay with family history.

24. Dissecting the genetic heterogeneity of gastric cancer.

25. Effectiveness and Safety of Inactivated SARS-CoV-2 Vaccine (BBIBP-CorV) among Healthcare Workers: A Seven-Month Follow-Up Study at Fifteen Central Hospitals.

26. Clinically relevant combined effect of polygenic background, rare pathogenic germline variants, and family history on colorectal cancer incidence.

27. Voluntary deep inspiration breath-hold with volumetric modulated arc therapy in pediatric patients with mediastinal Hodgkin lymphoma.

28. GenRisk: a tool for comprehensive genetic risk modeling.

29. Breast and prostate cancer risk: The interplay of polygenic risk, rare pathogenic germline variants, and family history.

30. Autoimmune Hepatitis: Shifts in Gut Microbiota and Metabolic Pathways among Egyptian Patients.

31. Immediate discontinuation of intravenous fluids after common surgical procedures.

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