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3. The assessment of public perception towards chronic kidney disease in Jordan: a cross-sectional study

Author

Abass M. Al-Momany, Ensaf Y. Almomani, Laila Al-Omari, Ahmad M. Qablan, and Huda Y. Almomani

Subjects
Chronic kidney disease (CKD), public perception, public health, Medicine
Abstract

Objectives Kidney diseases are considered silent killers due to the lack of well-defined symptoms. Public knowledge about chronic kidney disease (CKD) management has been shown to decrease the risk of CKD onset and progression to end-stage renal disease and renal failure. The main objective of this study was to assess the knowledge of kidney function, CKD symptoms, etiology, prevention and treatment in the general population.Methods A cross-sectional study using a validated questionnaire was conducted in Jordan to assess public knowledge of CKD. Public knowledge of CKD was assessed using a questionnaire consisting of 32 knowledge questions, including risk factors, symptoms, treatment, protective measures and kidney function. The knowledge level was classified according to the total score: poor (0–50%), intermediate (51–70%) and good/high (71–100%). Multiple regression analysis was performed to compare knowledge scores (KS) and predict associations with the participants’ baseline characteristics.Results The level of knowledge about CKD among the 2181 participants was intermediate. The KS was significantly higher among participants with health issues such as hypertension, diabetes and heart problems, first-degree relatives working in the medical field, majors relevant to health, married, employed, highly educated, high-income and smokers. The main sources of knowledge about CKD were health professionals, TV shows, books and magazines. Multiple regression analysis showed an association between KS and age, sex, functional status, educational level and field, income, smoking status, having a family member/spouse work in the medical field, and knowledge source.Conclusions The public level of knowledge about CKD management is greatly influenced by participants’ health and social factors. Thus, improving public knowledge and perception through education and the media will significantly reduce CKD prevalence and incidence.

Published
2024
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5. Team-Based Learning and Lecture-Based Learning: Comparison of Sudanese Medical Students’ Performance

Author

Salih KEMA, El-Samani EFZ, Bilal JA, Hamid EK, Elfaki OA, Idris MEA, Elsiddig HA, Salim MM, Missawi H, Abass M, and Elfakey W

Subjects
team-based learning, lecture-based curriculum, medical education, curriculum, assessment, Special aspects of education, LC8-6691, Medicine (General), R5-920
Abstract

Karim Eldin M A Salih,1– 3 El-Fatih Z El-Samani4 ,† Jalal Ali Bilal,5 Emtinan K Hamid,6 Omer Abdelgadir Elfaki,7 Muawia EA Idris,1 Hind A Elsiddig,8 Maha M Salim,8 Hashim Missawi,9 Mohammed Abass,10 Walyeldin Elfakey1 1Department of Pediatrics, Faculty of Medicine, University of Bahri, Khartoum, Sudan; 2Department of Pediatrics, College of Medicine, University of Bisha, Bisha, Saudi Arabia; 3Department of Medical Education, College of Medicine, University of Bisha, Bisha, Saudi Arabia; 4Department of Community Medicine, School of Medicine, Ahfad University for Women, Khartoum, Sudan; 5Department of Pediatrics, College of Medicine, Shaqra University, Shaqra, Saudi Arabia; 6Department of Community Medicine, Faculty of Medicine, University of Khartoum, Khartoum, Sudan; 7Department of Internal Medicine and Medical Education Unit, Al-Rayan Medical Colleges, Medina Munawara, Saudi Arabia; 8Department of Pathology, Faculty of Medicine, University of Bahri, Khartoum, Sudan; 9Department of Pathology, Maternity and Children Hospital, Medina Munawara, Saudi Arabia; 10Department of Pediatrics, College of Medicine, Arabian Gulf University, Manama, Bahrain†El-Fatih Z. El-Samani passed away on 23.12.2020Correspondence: Walyeldin ElfakeyDepartment of Pediatrics, Faculty of Medicine, University of Bahri, Po Box: 1660, Khartoum, SudanTel +249912364272Fax +249 155 888 406Email Walyeldina@aol.co.ukAim: Students’ performance in TBL compared to LBL needs to be evaluated. This study aimed to compare students’ performance in team-based learning and traditional lectures.Methods: A total of 176 class 4 and 202 class 6 medical students from University of Bahri, Khartoum, Sudan, participated in the study during 2018. Experienced staff were selected to conduct the teaching and assessment of the two groups, using the standard team-based learning procedure (iRAT, gRAT and AppT) in the first topic and the lecture-based learning procedure in the second, within the same time limit for the two methods.Results: The two classes overall mean score has a significant 5.1 points difference (p< 0.001; 95% CI: 3.5, 6.0). Separate analysis showed consistency of superiority of TBL to LBL in either gender. A remarkable difference was observed when we compared the two methods in class 6 separately from class 4. Class 6 mean score was high for both TBL and LBL (77.2 and 70.2, respectively), with a significant mean difference of 7.0 (p< 0.001; 95% CI: 5.1, 8.9). In class 4, the score was lower for both methods (mean of 62.8 for TBL and 59.9 for LBL). The mean difference of 2.95 points was still significant (p< 0.05; 95% CI: 0.46, 5.43). Separate multivariate linear regression for TBL and LBL showed no significant difference in performance of males and females in either method. Controlling for gender in TBL, class 4 had a mean of − 14.26 points, (p< 0.001; 95% CI: − 12.54, − 15.98) less than class 6. Similarly, in LBL, class 4 had a mean of − 10.18 points (p< 0.001, 95% CI: − 7.02, − 13.35), less than class 6.Conclusion: Students’ performance using team-based learning was superior to lecture-based learning, irrespective of students’ gender, noticeable among senior students.Keywords: team-based learning, lecture-based curriculum, medical education, curriculum, assessment

Published
2021

10. A Validated Model for the Imaging Diagnosis of Cystic Lung Disease

Author

Wallace T. Miller, Karen C. Patterson, Shweta Sood, James E. Schmitt, Arshad A. Wani, Robert Borden, Maya Galperin-Aisenberg, Mary K. Porteus, Michelle L. Hershman, Michael Hewitt, Jennifer Levy, Victor D. Babatunde, Tetiana Glushko, Timothy J. Niesen, Sergey Leshchinskiy, Karine Sahakyan, Keyur Desai, Jennifer A. Gillman, Sandeep Reddy, Michael Shriver, Nathaniel B. Linna, Abass M. Noor, Aysenur Buz, Matthew E. Biron, and Scott Simpson

Subjects
General Medicine
Published
2023
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11. Worldwide Disparities in Recovery of Cardiac Testing 1 Year Into COVID-19

Author

Einstein, A, Hirschfeld, C, Williams, M, Vitola, J, Better, N, Villines, T, Cerci, R, Shaw, L, Choi, A, Dorbala, S, Karthikeyan, G, Lu, B, Sinitsyn, V, Ansheles, A, Kudo, T, Bucciarelli-Ducci, C, Norgaard, B, Maurovich-Horvat, P, Campisi, R, Milan, E, Louw, L, Allam, A, Bhatia, M, Sewanan, L, Malkovskiy, E, Cohen, Y, Randazzo, M, Narula, J, Morozova, O, Pascual, T, Pynda, Y, Dondi, M, Paez, D, Hinterleitner, G, Lu, Y, Xu, Z, Erinne, I, Shetty, M, Lopez-Mattei, J, Parwani, P, Goda, A, Shirka, E, Bouyoucef, S, Chelghoum, L, Mansouri, F, Medjahedi, A, Naili, Q, Ridouh, M, Alasia, D, Alberghina, L, Aramayo, N, Buchara, D, Busso, F, Bustos Rivadero, J, Camilletti, J, Campanelli, H, Castro, R, Daicz, M, del Riego, H, Dragonetti, L, Echazarreta, D, Erriest, J, Faccio, F, Facello, A, Gallegos, H, Geronazzo, R, Glait, H, Hasbani, V, Jager, V, Lewkowicz, J, Lotti, J, Maciel, N, Masoli, O, Mastrovito, E, Medus, M, Merani, M, Molteni, S, Montecinos, M, Parisi, G, Sueldo, C, Perez de Arenaza, D, Quintana, L, Radzinschi, A, Redruello, M, Rodriguez, M, Rojas, H, Acuna, A, Schere, D, Traverso, S, Vazquez, G, Zeffiro, S, Sakanyan, M, Beuzeville, S, Boktor, R, Crowley, M, Downie, D, Dwivedi, G, Elison, B, Farouque, O, Jasper, K, Joshi, S, Lee, J, Lee, K, Lui, E, Mcconachie, P, Meaker, J, Nandurkar, D, Neill, J, O'Rourke, E, O'Sullivan, P, Pandos, G, Premaratne, M, Prior, D, Rutherford, N, Saunders, C, Taubman, K, Tauro, A, Taylor, A, Theuerle, J, Thomas, P, Tow, J, Upton, A, Vamadevan, S, Wayne, V, Wegner, E, Wong, D, Younger, J, Beitzke, D, Feuchtner, G, Sommer, O, Weiss, K, Maroz-Vadalazhskaya, N, Tserakhau, U, Homans, F, Van De Heyning, C, Araujo, R, Soldat-Stankovic, V, Stankovic, S, Almeida, A, Anselmi, C, Azevedo, G, Bittencourt, M, Pianta, D, Cabeda, E, Carreira, L, Coelho, I, de Amorim Fernandes, F, de Lorenzo, A, Delgado, R, Erthal, F, Fernandes, F, Fernandes, J, Ferreira de Souza, T, Foppa, M, Matos Alves, W, Gontijo, C, Gottlieb, I, Grossman, G, Albernaz Siqueira, M, Nomura, C, Koga, K, Lima, R, Lopes, R, Marcal Filho, H, Masiero, P, Mastrocola, L, Menezes de Siqueira, M, Mesquita, C, Naves, D, Penna, F, Pinto, I, Rocha, T, Rocha, J, Rodrigues, A, Salioni, L, Sanches, A, Santos, M, Da Silva, L, Schvartzman, P, Matushita, C, Senra, T, Silva, M, Soares, C, Spiro, B, Suaide Silva, C, Torres, R, Monte, G, Vilela, A, Villa, A, Voss, T, Waltrick, R, Zapparoli, M, Naseer, H, Garcheva-Tsacheva, M, Ouattara, T, Thou, S, Varoeun, S, Abikhzer, G, Beanlands, R, Chetrit, M, Dabreo, D, Dennie, C, Friedrich, M, Hafez, M, Hanneman, K, Miller, R, Oikonomou, A, Roifman, I, Small, G, Tandon, V, Trivedi, A, White, J, Zukotynski, K, Alay, R, Concha, C, Massardo, T, Abad, P, Anzola, K, Arturo, H, Benitez, L, Cadena, A, Zamudio, C, Calderon, A, Gutierrez Villamil, C, Jaimes, C, Londono, J, Lopez, N, Merlano-Gaitan, S, Murgieitio-Cabrera, R, Valencia, M, Vergel, D, Santamaria, A, Solis, F, Batinic, T, Franceschi, M, Paar, M, Prpic, M, Felipe Batista, C, Cabrera, L, Peix, A, Pena, Y, Rochela Vazquez, L, Ntalas, I, Kaminek, M, Kincl, V, Lang, O, Abdulla, J, Bottcher, M, Busk, M, Geisler, U, Gormsen, L, Hansson, N, Hess, S, Hove, J, Jensen, L, Jensen, M, Kragholm, K, Ovrehus, K, Rasmussen, J, Ronnow Sand, N, Sondergaard, H, Zaremba, T, Speckter, H, Amores, N, Velez, M, Alrahman, T, Elsamad, S, Abdelfattah, A, Elkaffas, S, Hassan, M, Hussein, E, Ibrahim, A, Kandeel, A, Ali, M, Shaaban, M, Flores, C, Gomez Leiva, V, Liiver, A, Larikka, M, Uusitalo, V, Agostini, D, Berger, C, Dietz, M, Hyafil, F, Ohana, M, Prigent, K, Regaieg, H, Sarda-Mantel, L, H-Ici, D, Ayetey, H, Angelidis, G, Fragkaki, C, Fragkiadaki, C, Georgoulias, P, Koutelou, M, Kyrozi, E, Lama, N, Prassopoulos, V, Spartalis, M, Zaglavara, T, Gonzalez, C, Gutierrez, G, Maldonado, A, Martinez, Y, Kovacs, A, Szilveszter, B, Banthia, N, Bhat, V, Choudhury, P, Chowdekar, V, Christopher, J, Garg, T, Goyal, N, Gupta, R, Gupta, A, Hephzibah, J, Jain, S, Krupa, J, Kumar, P, Kumar, S, Lalchandani, A, Mishra, A, Mishra, V, Mohan, P, Ozair, A, Pandey, S, Parameswaran, R, Patel, C, Patel, T, Patel, S, Vimala, L, Kumar Sarangi, D, Sengupta, S, Sethi, A, Sharma, A, Sharma, P, Shrigiriwar, A, Singh, S, Singh, H, Sood, A, Verma, A, Vyas, A, Soeriadi, E, Bun, E, Hutomo, F, Syawaluddin, H, Yudistiro, R, Albadr, A, Assadi, M, Emami, F, Emami-Ardekani, A, Farzanehfar, S, Jafari, R, Manafi-Farid, R, Tajik, M, Arnson, Y, Fuchs, S, Goldkorn, R, Kennedy, J, Leitman, M, Shalev, A, Acampa, W, Albano, D, Alongi, P, Arnone, G, Assante, R, Baritussio, A, Bauckneht, M, Bianco, F, Bonfiglioli, R, Bovenzi, F, Bruno, I, Bruno, A, Busnardo, E, Califaretti, E, Casoni, R, Censullo, V, Chierichetti, F, Chiocchi, M, Cittanti, C, Clemente, A, Cuocolo, A, De Rimini, M, De Vincentis, G, Della Tommasina, V, Dellegrottaglie, S, Erba, P, Evangelista, L, Faggi, L, Faragasso, E, Florimonte, L, Frantellizzi, V, Gatti, M, Gaudiano, A, Gelardi, F, Gerali, A, Gimelli, A, Guglielmo, M, Leccisotti, L, Liga, R, Liguori, C, Longo, G, Maffione, M, Marcassa, C, Matassa, G, Mele, D, Mircoli, L, Paccagnella, A, Pacella, S, Padovano, F, Pellegrini, D, Pergola, V, Pugliese, L, Quartuccio, N, Rampin, L, Ricci, F, Rubini, G, Russo, V, Sambuceti, G, Scatteia, A, Sciagra, R, Spidalieri, G, Stefanelli, A, Tedeschi, C, Ventroni, G, Baugh, D, Madu, E, Aikawa, T, Asano, H, Fujimoto, S, Fujise, K, Fukushima, Y, Fukuyama, K, Ichikawa, Y, Ideguchi, R, Iguchi, N, Imai, M, Ishimura, H, Isobe, S, Ito, K, Izawa, Y, Kadokami, T, Kasai, T, Kato, T, Kawamoto, T, Kiryu, S, Kumita, S, Manabe, O, Maruno, H, Matsumoto, N, Miyagawa, M, Moroi, M, Nagamachi, S, Nakajima, K, Nakazato, R, Nanasato, M, Naya, M, Norikane, T, Ohta, Y, Otomi, Y, Otsuka, H, Oyama-Manabe, N, Saito, M, Sarai, M, Sato, J, Sato, D, Shiraishi, S, Takanami, K, Takehana, K, Taniguchi, Y, Teragawa, H, Tomizawa, N, Umeji, K, Wakabayashi, Y, Yamada, S, Yamazaki, S, Yoneyama, T, Rawashdeh, M, Dautov, T, Makhdomi, K, Abass, M, Garashi, M, Siraj, Q, Kalnina, M, Haidar, M, Komiagiene, R, Kviecinskiene, G, Vajauskas, D, Karim, N, Doucoure, M, Reichmuth, L, Samuel, A, Dieng, M, Naojee, A, Hernandez, E, Alducin Tellez, C, Alexanderson-Rosas, E, Barragan, E, Cabada, M, Calderon, D, Carvajal-Juarez, I, Esparza, J, Gama-Moreno, M, Quinto, V, Gonzalez, N, Herrera-Zarza, M, Meave, A, Medina Verdugo, J, Melendez, G, Morales Murguia, R, Navarro Quiroz, C, Ornelas, M, Preciado-Anaya, A, Preciado-Gutierrez, O, Puente, A, Salazar, A, Rosales Uvera, S, Rosales-Uvera, S, Serna Macias, J, Sierra-Galan, L, Tirado Alderete, J, Vallejo, E, Faraggi, M, Sereegotov, E, Ben Rais, N, Alaoui, N, Kyiphyu, T, Oo, S, Win, S, Zar, H, Ghimire, R, Neupane, M, Glaudemans, A, Slart, R, Verschure, D, Allen, B, Edmond, J, Mckenzie, C, Tie, S, Van Pelt, N, Worthington, K, Young, C, Soli, I, Kana, S, Onubogu, U, Sani, M, Braten, A, Jorgensen, A, Vassbotn, H, Al Dhuhli, H, Jawa, Z, Tag, N, Fatima, S, Imran, M, Younis, M, Saadullah, M, Malo, Y, Lenturut-Katal, D, Castillo, M, Ortellado, J, Akhter, A, Cader, F, Hussain, R, Khan, S, Mandal, T, Nasreen, F, An, Y, Cao, D, Gong, L, Hou, Y, Jia, C, Li, T, Li, C, Liu, H, Liu, W, Liu, J, Ng, M, Shi, H, Tang, C, Wang, X, Wang, Z, Wang, Y, Wu, J, Yi, Y, Yuan, L, Zhang, T, Zhang, L, Chavez, E, Cruz, C, Llontop, C, Morales, R, Abrihan, P, Bustos-Barroso, A, Duldulao-Ogbac, M, Eduarte, C, Obaldo, J, Quinon, A, San Juan, B, San Juan, C, Sauler-Gomez, M, Uy, M, Kostkiewicz, M, Kunikowska, J, Teresinska, A, Urbanik, T, Bettencourt, N, Fontes-Carvalho, R, Gavina, C, Goncalves, L, Macedo, F, Moreno, N, Sousa, C, Timoteo, A, Vidigal, M, Al Heidous, M, Ramanathan, S, Arnous, S, Aytani, S, Byrne, A, Gleeson, T, Kerins, D, O'Brien, J, Bang, J, Bom, H, Cheon, M, Cheon, G, Cho, S, Hong, C, Jeong, Y, Kang, W, Kang, Y, Kim, J, Oh, S, So, Y, Song, H, Won, K, Yoo, S, Mitevska, I, Vavlukis, M, Salobir, B, Stalc, M, Benedek, T, Pop, M, Stan, C, Dariy, O, Gagarina, N, Itskovich, I, Karalkin, A, Kokov, A, Marina, G, Migunova, E, Pospelov, V, Ryzhkova, D, Sayfullina, G, Sergienko, V, Shurupova, I, Vakhromeeva, M, Valiullina, N, Zavadovsky, K, Zhuravlev, K, Abazid, R, Al Garni, T, Alasnag, M, Aljizeeri, A, Amer, H, Amro, A, Hamdy, H, Smettei, O, Saranovic, D, Vlajkovic, M, Keng, F, See, J, Berecova, Z, Mistinova, J, Evbuomwan, O, Govender, N, Hack, J, Hadebe, B, Hlongwa, K, Kaplan, M, Lakhi, H, Milos, K, Modiselle, M, More, S, Muambadzi, N, Scholtz, L, Barreiro-Perez, M, Blanco, I, Broncano, J, Camarero, A, Casans-Tormo, I, De Haro, J, Flotats, A, Garcia, E, Mendiguchia, C, Jimenez-Heffernan, A, Leta, R, Diaz, J, Vega, L, Manovel-Sanchez, A, Monzonis, A, Patrut, B, Pubul, V, Perez, R, Zeidan, N, Nanayakkara, D, Suliman, A, Engblom, H, Murtadha, M, Ostenfeld, E, Simonsson, M, Alkadhi, H, Buechel, R, Burger, P, Grani, C, Kamani, C, Kawel-Bohm, N, Klaeser, B, Manka, R, Prior, J, Kaewchur, T, Khiewvan, B, Kositwattanarerk, A, Namwongprom, S, Thientunyakit, T, Sayman, H, Yuksel, M, Sebikali, M, Okello, E, Korol, P, Noverko, I, Satyr, M, Ahmad, T, Alfakih, K, Andrade, I, Buckingham, S, Bularga, A, Carpenter, J, Cole, G, Cusack, D, David, S, Davis, P, Fairbairn, T, Ghosh, A, Ramkumar, P, Hamilton, M, Haque, F, Hudson, B, Johnstone, A, Karthikeyan, V, Kay, M, Khan, M, Kitt, J, Low, C, Mcalindon, E, Mccreavy, D, Morrissey, B, Motwani, M, Na, D, Nicol, E, Patel, D, Rodrigues, J, Rofe, C, Schofield, R, Semple, T, Sheikh, A, Sinha, A, Subedi, D, Topping, W, Tweed, K, Underwood, S, Weir-Mccall, J, Zuhairy, H, Abbasi, T, Abohashem, S, Abramson, S, Al-Mallah, M, Kumar, M, Balmer-Swain, M, Berman, D, Bernheim, A, Bhatti, S, Biederman, R, Bieging, E, Bingham, S, Bloom, S, Blue, S, Borges, A, Branch, K, Bravo, P, Buddhe, S, Budoff, M, Bullock-Palmer, R, Cahill, M, Candela, C, Cao, J, Chatterjee, S, Chatzizisis, Y, Chaudhuri, N, Cheezum, M, Chelliah, A, Chen, T, Chen, M, Chen, L, Chokshi, A, Chung, J, Danciu, S, Desisto, W, Dilorenzo, M, Doukky, R, Duvall, W, Ferencik, M, Foster, C, Fuisz, A, Gannon, M, German, D, Gerson, M, Geske, J, Hage, F, Haider, A, Haider, S, Hamirani, Y, Hassen, K, Hendel, R, Henkel, J, Horgan, S, Hyun, M, Janardhanan, R, Jerome, S, Kalra, D, Kassop, D, Kinkhabwala, M, Kinzfogl, G, Koch, B, Koweek, L, Krepp, J, Kwon, Y, Layer, J, Lesser, J, Leung, S, Lisske, B, Magurany, K, Markowitz, J, Mccullough, B, Moalemi, A, Moffitt, C, Montanez, J, Moore, W, Morayati, S, Mossa-Basha, M, Mrsic, Z, Murthy, V, Nagpal, P, Nelson, K, Nijjar, P, O'Quinn, R, Passen, E, Patil, P, Pursnani, A, Quachang, N, Rabbat, M, Ranjan, P, Lozano, P, Schemmer, M, Seifried, R, Shah, N, Shah, A, Shanbhag, S, Sharma, G, Skotnicki, R, Sobczak, M, Soman, P, Sorrell, V, Srichai, M, Streeter, J, Strickland, L, Suliman, S, Tebyanian, N, Thomas, D, Thompson, R, Uretsky, S, Vallurupalli, S, Vandyck-Acquah, M, Verma, V, Weinstein, J, Wolinsky, D, Zareba, K, Zgaljardic, M, Beretta, M, Ferrando, R, Kapitan, M, Mut, F, Djuraev, O, Rozikhodjaeva, G, Vera, L, Duc, B, Nguyen, X, Hiep Nguyen, P, Einstein A. J., Hirschfeld C., Williams M. C., Vitola J. V., Better N., Villines T. C., Cerci R., Shaw L. J., Choi A. D., Dorbala S., Karthikeyan G., Lu B., Sinitsyn V., Ansheles A. A., Kudo T., Bucciarelli-Ducci C., Norgaard B. L., Maurovich-Horvat P., Campisi R., Milan E., Louw L., Allam A. H., Bhatia M., Sewanan L., Malkovskiy E., Cohen Y., Randazzo M., Narula J., Morozova O., Pascual T. N. B., Pynda Y., Dondi M., Paez D., Hinterleitner G., Lu Y., Xu Z., Hirschfeld C. B., Erinne I., Shetty M., Choi A., Lopez-Mattei J., Parwani P., Goda A., Shirka E., Bouyoucef S., Chelghoum L., Mansouri F., Medjahedi A., Naili Q., Ridouh M., Alasia D., Alberghina L., Aramayo N., Buchara D., Busso F. G., Bustos Rivadero J. J., Camilletti J., Campanelli H., Castro R. B., Daicz M., del Riego H., Dragonetti L., Echazarreta D., Erriest J., Faccio F., Facello A., Gallegos H., Geronazzo R., Glait H., Hasbani V., Jager V., Lewkowicz J. M., Lotti J., Maciel N., Masoli O., Mastrovito E., Medus M., Merani M. F., Molteni S., Montecinos M., Parisi G., Sueldo C. P., Perez de Arenaza D., Quintana L., Radzinschi A., Redruello M., Rodriguez M., Rojas H., Acuna A. R., Schere D., Traverso S., Vazquez G., Zeffiro S., Sakanyan M., Beuzeville S., Boktor R., Crowley M., Downie D. A., Dwivedi G., Elison B., Farouque O., Jasper K., Joshi S., Lee J., Lee K., Lui E., Mcconachie P., Meaker J., Nandurkar D., Neill J., O'Rourke E., O'Sullivan P., Pandos G., Premaratne M., Prior D., Rutherford N., Saunders C., Taubman K., Tauro A., Taylor A., Theuerle J., Thomas P., Tow J., Upton A., Vamadevan S., Wayne V., Wegner E. A., Wong D., Younger J., Beitzke D., Feuchtner G., Sommer O., Weiss K., Maroz-Vadalazhskaya N., Tserakhau U., Homans F., Van De Heyning C. M., Araujo R., Soldat-Stankovic V., Stankovic S., Almeida A., Anselmi C., Azevedo G. S. A., Bittencourt M. S., Pianta D. B., Cabeda E., Carreira L., Coelho I., de Amorim Fernandes F., de Lorenzo A., Delgado R., Erthal F., Fernandes F., Fernandes J., Ferreira de Souza T., Foppa M., Matos Alves W. F., Gontijo C., Gottlieb I., Grossman G., Albernaz Siqueira M. H., Nomura C. H., Koga K. H., Lima R., Lopes R., Marcal Filho H. H., Masiero P., Mastrocola L., Menezes de Siqueira M. E., Mesquita C., Naves D., Penna F., Pinto I., Rocha T., Rocha J. L., Rodrigues A., Salioni L., Sanches A., Santos M., Da Silva L. S., Schvartzman P., Matushita C. S., Senra T., Silva M., Soares C. E., Spiro B., Suaide Silva C. E., Torres R., Monte G. U., Vilela A., Villa A. V., Vitola J., Voss T., Waltrick R., Zapparoli M., Naseer H., Garcheva-Tsacheva M., Ouattara T. F., Thou S., Varoeun S., Abikhzer G., Beanlands R., Chetrit M., Dabreo D., Dennie C., Friedrich M., Hafez M. 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A., Balmer-Swain M., Berman D., Bernheim A., Bhatti S., Biederman R., Bieging E., Bingham S., Bloom S., Blue S., Borges A., Branch K., Bravo P., Buddhe S., Budoff M., Bullock-Palmer R., Cahill M., Candela C., Cao J., Chatterjee S., Chatzizisis Y., Chaudhuri N. R., Cheezum M., Chelliah A., Chen T., Chen M., Chen L., Chokshi A., Chung J., Danciu S., DeSisto W., Dilorenzo M., Doukky R., Duvall W., Ferencik M., Foster C., Fuisz A., Gannon M., German D., Gerson M., Geske J., Hage F., Haider A., Haider S., Hamirani Y., Hassen K., Hendel R., Henkel J., Horgan S., Hyun M., Janardhanan R., Jerome S., Kalra D., Kassop D., Kinkhabwala M., Kinzfogl G., Koch B., Koweek L., Krepp J., Kwon Y., Layer J., Lesser J., Leung S., Lisske B., Magurany K., Markowitz J., Mccullough B., Moalemi A., Moffitt C., Montanez J., Moore W., Morayati S., Mossa-Basha M., Mrsic Z., Murthy V., Nagpal P., Nelson K., Nijjar P., O'Quinn R., Passen E., Patil P., Pursnani A., Quachang N., Rabbat M., Ranjan P., Lozano P. R., Schemmer M., Seifried R., Shah N., Shah A., Shanbhag S., Sharma G., Skotnicki R., Sobczak M., Soman P., Sorrell V., Srichai M., Streeter J., Strickland L., Suliman S., Tebyanian N., Thomas D., Thompson R., Uretsky S., Vallurupalli S., Vandyck-Acquah M., Verma V., Villines T., Weinstein J., Wolinsky D., Zareba K., Zgaljardic M., Beretta M., Ferrando R., Kapitan M., Mut F., Djuraev O., Rozikhodjaeva G., Vera L., Duc B. D., Nguyen X. C., and Hiep Nguyen P. M.

Abstract

Background: The extent to which health care systems have adapted to the COVID-19 pandemic to provide necessary cardiac diagnostic services is unknown. Objectives: The aim of this study was to determine the impact of the pandemic on cardiac testing practices, volumes and types of diagnostic services, and perceived psychological stress to health care providers worldwide. Methods: The International Atomic Energy Agency conducted a worldwide survey assessing alterations from baseline in cardiovascular diagnostic care at the pandemic's onset and 1 year later. Multivariable regression was used to determine factors associated with procedure volume recovery. Results: Surveys were submitted from 669 centers in 107 countries. Worldwide reduction in cardiac procedure volumes of 64% from March 2019 to April 2020 recovered by April 2021 in high- and upper middle-income countries (recovery rates of 108% and 99%) but remained depressed in lower middle- and low-income countries (46% and 30% recovery). Although stress testing was used 12% less frequently in 2021 than in 2019, coronary computed tomographic angiography was used 14% more, a trend also seen for other advanced cardiac imaging modalities (positron emission tomography and magnetic resonance; 22%-25% increases). Pandemic-related psychological stress was estimated to have affected nearly 40% of staff, impacting patient care at 78% of sites. In multivariable regression, only lower-income status and physicians’ psychological stress were significant in predicting recovery of cardiac testing. Conclusions: Cardiac diagnostic testing has yet to recover to prepandemic levels in lower-income countries. Worldwide, the decrease in standard stress testing is offset by greater use of advanced cardiac imaging modalities. Pandemic-related psychological stress among providers is widespread and associated with poor recovery of cardiac testing.

Published
2022

16. LES COMPLICATIONS ASSOCIEES AU VOLVULUS DE LINTESTIN GRELE CHEZ LES GRANDS PREMATURES : A PROPOS DE CINQ CAS

Author

A.M. Abass, M. Ait Idir, Y. Mohamed Sghair, and S. Khat And V. Biran

Subjects
Volvulus Grands Prematures Complications
Abstract

Le volvulus de lintestin grele est une urgence chirurgicale neonatale. La presentation atypique chez les nouveau-nes prematures, impose une intervention chirurgicale sans delai, en raison du risque de necrose etendue de lintestin grele, dont la consequence digestive est connue par le syndrome du grele court. Le but de cette etude (soutenu publiquement le 15/10/2018 pour lobtention dun diplome de formation medicale specialisee) est de presenter les cas de volvulus de lintestin grele prouves chirurgicalement chez les grands prematures dans le service de reanimation neonatale de lhopital Robert Debre et danalyser leur evolution nutritionnelle et les complications associees a leur prise en charge.Une revue retrospective des cas de volvulus complet de lintestin grele chez les grands prematures (moins de 32 semaines dâge gestationnel) a ete realisee de mai a septembre 2017 dans le Service de reanimation neonatale, Hopital Robert Debre, Paris, France. Cinq très grands prematures avaient un diagnostic de volvulus dans notre centre sur une periode de 4 mois (de mai 2017 a septembre 2017). Lâge gestationnel median a la naissance etait de 29 semaines (26-32 semaines), avec un poids median a la naissance de 1130g (870-1600g). Le debut des symptomes variait entre le 6èmeet le 58èmejour de vie (mediane : 24 jours), avec un âge gestationnel median de 33 + 2 semaines (27 + 1 – 35 + 3 semaines). Ils ont tous eu une resection intestinale etendue, laissant une longueur intestinale mediane de 26 cm (24-40 cm). Trois prematures (60%) sont decedes 1 a 21 jours après la première intervention chirurgicale. Les deux prematures qui ont survecu ont ete operes avec un retard de 72 heures après les premiers signes abdominaux. Chez ces deux enfants, la nutrition parenterale prolongee etait le seul moyen dassurer des besoins necessaires a leur croissance compte tenu de la longueur de lintestin grele restante, actuellement en cours a domicile a 1 an et 1an et demi avec nutrition orale et une croissance staturoponderale satisfaisante. Ils ont presente 2 infections sur catheter central, une cholestase transitoire. Le suivi neurosensoriel est normal a 12 et 18 mois.Le volvulus chez les grands prematures est souvent diagnostique avec retard en raison de la presentation non specifique faisant evoquer une ECUN initialement, ce qui conduit a une intervention chirurgicale retardee. Les sequelles digestives, ainsi que la prematurite associee imposent une prise en charge multidisciplinaire prolongee. &nbsp

Published
2022
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17. Resistant Hypertension and Its Correlated Disease

Author

Abass M. Ahmed and Abdirizak S Daror

Subjects
hypertension, resistant hypertension, obstructive sleep apnea
Abstract

Resistant hypertension is defined as blood pressure above the patient’s goal despite the use of 3 or more antihypertensive agents from different classes at optimal doses, one of which should ideally be a diuretic .Evaluating patients with resistive hypertension should first confirm that they have genuine resistant hypertension through elimination or correction of pseude resistence factors such as white coat hypertension, suboptimal blood pressure measurement technique, poor medication compliance, inappropriate antihypertensive dosage or combinaison, and white coat effects and clinical inertia.Resistant hypertension therapy includes improved compliance with the use of drugs, secondary hypertension detection and treatment, use of lifestyle measures and treatment of obesity, and other comorbidities. switching to a long-acting diuretic type of thiazide like chlorthalidone could improve the BP from the patients taking hydrochlorothiazide. However, clinical trials of OSAHS have heterogeneous outcomes, surrogate outcomes, subjective outcomes, composite outcomes, and a lack of endpoints or patient perspectives. The diagnosis is confirmed by a sleep study. The main treatment for OSAS is the use of continuous positive airway pressure (CPAP) at night via a nasal or oronasal mask, which usually results in rapid improvement of symptoms. Patients who cannot tolerate CPAP therapy can be successfully treated with a mandibular advancement device. Supportive measures include regular and sufficiently long sleep periods, refraining from smoking and alcohol consumption in the evening, and weight reduction in overweight patients. Keywords: hypertension, resistant hypertension . obstructive sleep apnea. Title: Resistant Hypertension and Its Correlated Disease Author: Abass M. Ahmed, Abdirizak s Daror International Journal of Recent Research in Life Sciences (IJRRLS) ISSN 2349-7823 Vol. 9, Issue 3, July 2022 - September 2022 Page No: 14-18 Paper Publications Website: www.paperpublications.org Published Date: 16-August-2022 DOI: https://doi.org/10.5281/zenodo.6997949 Paper Download Link (Source) https://www.paperpublications.org/upload/book/Resistant%20Hypertension-16082022-4.pdf, International Journal of Recent Research in Life Sciences (IJRRLS), ISSN 2349-7823, Paper Publications, Website: www.paperpublications.org, {"references":["[1]\tGBD 2016 Risk Factor Collaborators. Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2016: a systematic analysis for the global burden of disease study 2016. Lancet 390, 1345–1422 (2017).","[2]\tPersell, S. D. Prevalence of resistant hypertension in the United States, 2003–2008. Hypertension 57, 1076–1080 (2011).","[3]\tSarafidis, P. A., Georgianos, P. & Bakris, G. L.Resistant hypertension- its identification andepidemiology. Nat. Rev. Nephrol. 9, 51–58 (2013).","[4]\tMancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Böhm M, Christiaens T, Cifkova R, De Backer G, Dominiczak A, Galderisi M, Grobbee DE, Jaarsma T, Kirchhof P, Kjeldsen SE,","[5]\tLaurent S, Manolis AJ, Nilsson PM, Ruilope LM, Schmieder RE, Sirnes PA, Sleight P, Viigimaa M,Waeber B, Zannad F. 2013 ESH/ ESC practice guidelines for the management of arterial hypertension.","[6]\tTask Force for the Management of Arterial Hypertension of the European Society of Hypertension and the European Society of Cardiology. Blood Press. 2014;23(1):3–16.",[7],"[8]\tPark, J.G., K. Ramar, and E.J. Olson. Updates on definition, consequences, and management of obstructive sleep apnea. in Mayo Clinic Proceedings. 2011. Elsevier.","[9]\tCrummy, F., A. Piper, and M.T. Naughton, Obesity and the lung: 2· Obesity and sleep-disordered breathing. Thorax, 2008. 63(8): p. 738-746.","[10]\tPeppard, P.E., et al., Prospective study of the association between sleep-disordered breathing and hypertension. New England Journal of Medicine, 2000. 342(19): p. 1378-1384.","[11]\tPeker, Y., J. Carlson, and J. Hedner, Increased incidence of coronary artery disease in sleep apnoea: a long-term follow-up. European Respiratory Journal, 2006. 28(3): p. 596-602.","[12]\tDesalu, O., et al., Prevalence, awareness and reporting of symptoms of obstructive sleep apnoea among hospitalized adult patients in Nigeria: a multicenter study. Ethiopian Journal of Health Sciences, 2016. 26(4): p. 321-330.","[13]\tMarin, J.M., et al., Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. The Lancet, 2005. 365(9464): p. 1046-1053.","[14]\tPunjabi, N.M., The epidemiology of adult obstructive sleep apnea. Proceedings of the American Thoracic Society, 2008. 5(2): p. 136-143.","[15]\tTanner RM, Calhoun DA, Bell EK, Bowling CB, Gutierrez OM, Irvin MR, Lackland DT, Oparil S, Warnock D, Muntner P. Prevalence of apparent treatment-resistant hypertension among individuals with CKD. Clin JAm Soc Nephrol. 2013;8:1583–1590. doi: 10.2215/CJN.00550113.","[16]\tThomas G, Xie D, Chen HY, Anderson AH, Appel LJ, Bodana S, Brecklin CS, Drawz P, Flack JM, Miller ER 3rd, Steigerwalt SP, Townsend RR, Weir MR, Wright JT Jr, Rahman M; CRIC Study Investigators. Prevalence and prognostic significance of apparent treatment resistant","[17]\thypertension in chronic kidney disease: report from the Chronic Renal Insufficiency Cohort Study. Hypertension. 2016;67:387–396. doi:10.1161/HYPERTENSIONAHA.115.06487.","[18]\tMuntner P, Davis BR, Cushman WC, Bangalore S, Calhoun DA, Pressel SL, Black HR, Kostis JB, Probstfield JL, Whelton PK, Rahman M; for the ALLHAT Collaborative Research Group. Treatment-resistant hypertension and the incidence of cardiovascular disease and end-stage renaldisease: results from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart AttacTrial Hypertension. 2014;64:1012–1021 doi: 10.1161/HYPERTENSIONAHA.114. 03850.","[19]\tPimenta E, Calhoun DA. Resistant hypertension: incidence, prevalence, and prognosis. Circulation. 2012;125:1594–1596. doi: 10.1161/ CIRCULATIONAHA.112.097345.","[20]\tKirkham, J.J., et al., Outcome measures in rheumatoid arthritis randomised trials over the last 50 years. Trials, 2013. 14(1): p. 1-8."]}

Published
2022
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18. The Impact of IT on Insurance of the Technological Industry.

Author

Ali Albasheir, Kawther Abass M.

Subjects
INSURANCE companies, INFORMATION technology, DIGITAL technology, DATA privacy, INSURANCE, EMAIL security, TECHNOLOGY convergence
Abstract

The insurance industry has undergone significant transformations due to the rapid advancement of information technology (IT); This paper explores the multifaceted impact of IT on the insurance sector, covering various aspects such as customer experience, operational efficiency, risk assessment, and data security. Through a comprehensive review of existing literature and industry trends, this paper highlights the ways in which IT has revolutionized insurance processes and business models. " Additionally, this paper delves into the paradigm shift brought about by Insurtech startups, which leverage the convergence of IT and insurance to offer innovative solutions like peer-to-peer insurance and usage-based coverage. These startups are reshaping industry dynamics and compelling traditional insurers to adopt digital innovations to remain competitive. Furthermore, the regulatory landscape and compliance considerations arising from technological disruption are explored. The challenges of navigating data privacy compliance and the collaborative efforts between regulators and industry players in shaping technological policies are discussed. Ethical considerations related to IT-driven insurance are also examined, emphasizing the importance of maintaining transparency, fairness, and accountability in decision-making. Ultimately, this research paper underscores the pivotal role of IT in shaping the insurance industry's future, As technology continues to evolve, insurers that strategically integrate IT tools are better positioned to provide innovative, customer-centric solutions while enhancing operational efficiency, risk assessment accuracy, and data security, By embracing IT-driven transformations, insurers can navigate challenges, tap into opportunities, and maintain a competitive edge in the dynamic and rapidly evolving landscape of the insurance sector. [ABSTRACT FROM AUTHOR]

Published
2023

19. Evaluation of Gelling Agent Alternatives during in Vitro Multiplication of Yucca elephantipes L.

Author

Abass, M. M. M., Thabet, R. S., Abdelfattah, M. F. G., and Fahmy, Asmaa A.

Subjects
GELATION, PLANT micropropagation, CORNSTARCH, STARCH, POTATOES, PLANT propagation, MULTIPLICATION
Abstract

Copyright of Journal of Plant Production is the property of Egyptian National Agricultural Library (ENAL) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2023
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23. 293-OR: IFN-a Evokes a Heterogeneous, Rapid ROS Response from a Subset of Human Islet Beta Cells in Situ

Author

Matthew Arvin, Charanya Muralidharan, Kara S. Orr, Abass M. Conteh, Michelle M. Martinez Irizarry, Amelia K. Linnemann, and Kenneth W. Dunn

Subjects
geography, education.field_of_study, geography.geographical_feature_category, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Population, Human leukocyte antigen, Biology, Islet, medicine.disease, medicine.disease_cause, Autoimmunity, Cytokine, Immune system, Immunology, Internal Medicine, Unfolded protein response, medicine, education, Insulitis
Abstract

A large body of evidence reveals a web of complex, multifaceted genetic, and environmental factors that influences incidence of T1D. Among these, viral infection has been discussed as a factor implicated in onset. Production of type 1 interferons (IFN) is the archetypal immune response to viral infection. Indeed, at-risk children exhibit IFN-associated transcriptional profiles and IFN-stimulated genes are elevated in new onset T1D patients. IFN-α induces ER stress, substantial overexpression of HLA class 1, and insulitis in the islet. β-cells are known to be sensitive to reactive oxygen species (ROS) accumulation which may contribute to autoimmunogenicity in the IFN response. In order to detect the in vivo effects of IFN-α on the physiology of human islets, we conducted intravital microscopy studies of human islets transplanted in the mouse kidney - following transduction with a ratiometric fluorescent redox biosensor. These studies revealed that intravenous IFN-α elicited a mild overall accumulation of ROS in human islets, but rapid and pronounced accumulation of ROS in a subset of islet β-cells - a population of cells we termed, “ROSponders." Interestingly, the percentage of β-cells categorized as ROSponders was variable between donors (ranging from ~1% to 6% of all β-cells). Recent observations have drawn attention to the importance of β-cell expression and functional heterogeneity within the islet. Furthermore, recent work suggests that blockade of IFN-α signaling prior to clinical T1D manifestation may intercept autoimmunity and abort onset. Altogether, this work identifies novel heterogeneity of response to an inflammatory cytokine implicated in T1D onset and may inform future approaches to the treatment of T1D. Disclosure M. Arvin: None. C. Muralidharan: None. A. M. Conteh: None. M. M. Martinez irizarry: None. K. Orr: None. K. W. Dunn: None. A. K. Linnemann: None. Funding Human Islet Research Network (RRID:SCR_014393; UC4 DK104162); National Institutes of Health (3T32DK064466-18S1)

Published
2021
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24. Pancreatic Beta Cell Autophagy is Impaired in Type 1 Diabetes

Author

Michelle Marasco, Pascal de Boer, Charanya Muralidharan, Jeroen Kuipers, Justin J. Crowder, Ben N G Giepmans, Abass M. Conteh, and Amelia K. Linnemann

Subjects
Autophagosome, medicine.medical_specialty, Type 1 diabetes, Chemistry, Autophagy, Nod, medicine.disease, Endocrinology, medicine.anatomical_structure, Lysosome, Internal medicine, medicine, Beta cell, Proinsulin, NOD mice
Abstract

Aims/hypothesisPancreatic beta cells are highly metabolic secretory cells that are subjected to exogenous damaging factors such as proinflammatory cytokines or excess glucose that can cause accumulation of damage-inducing reactive oxygen species (ROS) during the pathogenesis of diabetes. We and others have shown that beta cell autophagy can reduce ROS to protect against apoptosis both in vitro and in vivo. While impaired islet autophagy has been demonstrated in human type 2 diabetes, it is unknown if islet autophagy is perturbed in the pathogenesis of type 1 diabetes. We hypothesized that beta cell autophagy is dysfunctional in type 1 diabetes, and that there is a progressive loss during early diabetes development.MethodsMouse pancreata were collected from chloroquine injected and non-injected NOR, nondiabetic NOD, and diabetic NOD mice. Age and BMI-matched pancreas tissue sections from human organ donors (n=34) were obtained from the Network for Pancreatic Organ Donors with Diabetes (nPOD). To assess autophagic flux, we injected the mice with chloroquine to inhibit the final stages of autophagy. We analyzed tissues for markers of autophagy via immunofluorescence analysis. Tissue sections were stained with antibodies against proinsulin or insulin (beta cell markers), LC3A/B (autophagosome marker), Lamp1 (lysosome marker), and p62 (autophagy adaptor protein and marker for autophagic flux). Images were collected on a scanning laser confocal microscope then analyzed with CellProfiler and ImageJ. Secondary lysosomes and telolysosomes (formerly called lipofuscin bodies, residual bodies or tertiary lysosomes) were analyzed in electron micrographs of pancreatic tissue sections from human organ donors (nPOD; n=12) deposited in www.nanotomy.org/OA/nPOD. Energy Dispersive X-ray (EDX) analysis was also performed on these tissues to analyze distribution of elements such as nitrogen, phosphorus, and osmium in secondary lysosomes and telolysosomes of nondiabetic and autoantibody positive donor tissues (n=5).ResultsWe observed increased autophagosome numbers in islets of diabetic NOD mice (p=0.0077) and increased p62 in islets of both nondiabetic and diabetic NOD mice (pConclusions/interpretationCollectively, we provide evidence of impairment in the final degradation stages of islet macroautophagy and crinophagy in human type 1 diabetes. We also document an accumulation of telolysosomes with nitrogen accumulation at their periphery in the beta cells of autoantibody positive donors. This demonstrates clear differences in the lysosome contents of autoantibody positive donors that may be associated with lysosome dysfunction prior to clinical hyperglycemia. We observe similar impairments in macroautophagy in the diabetic NOD mouse, a model of type 1 diabetes, suggesting that this mouse model can be appropriately used to study the pathogenesis of autophagy/crinophagy loss and how it relates to disease initiation and progression. Considering these data in the context of what is known regarding the cell-protective effects of islet autophagy, we suggest targeting beta cell autophagy pathways as an approach to reduce apoptosis in individuals at risk for type 1 diabetes development.Research in contextWhat is already known about this subject?Autophagy confers a cytoprotective role in the beta cell.Autophagy is reduced in type 2 diabetes.Autophagy in the context of type 1 diabetes is unexplored.What is the key question?Is autophagy reduced during the pathogenesis of human type 1 diabetes?What are the new findings?We provide evidence of reduced autophagy and crinophagy in human type 1 diabetes.These data are supported by observations of reduced autophagy in a mouse model of autoimmune diabetes.How might this impact on clinical practice in the foreseeable future?This study provides evidence that autophagy is impaired in human type 1 diabetes. Prior studies have shown that loss of autophagy in the islet is associated with increased beta cell apoptosis, therefore we propose that therapeutic targeting of autophagy pathways may reduce beta cell death in type 1 diabetes development.

Published
2020
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25. 2115-P: Beta-Cell Autophagy Is Reduced in Type 1 Diabetes

Author

Abass M. Conteh, Michelle Marasco, Charanya Muralidharan, Justin J. Crowder, and Amelia K. Linnemann

Subjects
Autophagosome, Type 1 diabetes, medicine.medical_specialty, business.industry, Endocrinology, Diabetes and Metabolism, Insulin, medicine.medical_treatment, Autophagy, Type 2 diabetes, medicine.disease, Endocrinology, Internal medicine, Internal Medicine, medicine, Beta cell, business, NOD mice, Proinsulin
Abstract

Autophagy is a dynamic recycling mechanism that maintains beta cell homeostasis, whereas the related process of crinophagy also plays a specific role in insulin granule regulation. Impairment of autophagy and crinophagy have been implicated in beta cell death and dysfunction in the context of type 2 diabetes; however, there is currently no literature describing beta cell autophagy in type 1 diabetes pathogenesis. Therefore, we set out to determine if beta cell autophagy and crinophagy are impaired in the context of type 1 diabetes. We utilized immunofluorescent staining of LC3 (autophagosome marker), Lamp1 (lysosome marker), and proinsulin to analyze pancreatic islet autophagy and crinophagy in the NOD (non-obese diabetic) mouse model of type 1 diabetes as well as in human pancreas tissue obtained from the network for Pancreatic Organ donors with Diabetes (nPOD). We observed evidence of reduced macroautophagy in the residual proinsulin-positive islet cells of human donors with type 1 diabetescompared to controls, as measured by significantly reduced autophagosome:lysosome colocalization (p=0.034). Similarly, there was a trend towards reduced autophagosome:lysosome colocalization in islets of diabetic NOD mice compared to nondiabetic NOR mice (p=0.08). We also observed significantly reduced colocalization of proinsulin with lysosomes in the proinsulin positive cells from human donors with type 1 diabetes in comparison to both controls without diabetes (p=0.0014) and autoantibody positive donors (p= 0.0278), as well as in diabetic NOD vs. nondiabetic NOR mice (p=0.0121), suggesting that crinophagy is also reduced as a function of type 1 diabetes. Collectively, we provide evidence that macroautophagy and crinophagy are reduced in the context of type 1 diabetes. Considering these data in the context of what is known regarding the cell-protective effects of islet autophagy, we suggest targeting beta cell autophagy pathways as an approach to reduce apoptosis in individuals at risk for type 1 diabetes development. Disclosure C. Muralidharan: None. M. Marasco: Employee; Spouse/Partner; Eli Lilly and Company. J. Crowder: Employee; Spouse/Partner; Eli Lilly and Company. A.M. Conteh: None. A.K. Linnemann: None.

Published
2020
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26. Illegal harvesting threatens fruit production and seedling recruitment of Balanites aegyptiaca in Dinder Biosphere Reserve, Sudan

Author

Mohammed, Elmugheira M., Hamed, Abass M. E., Ndakidemi, Patrick A., Treydte, Anna C., Mohammed, Elmugheira M., Hamed, Abass M. E., Ndakidemi, Patrick A., and Treydte, Anna C.

Abstract

Illegal harvesting negatively affects the forest tree populations, particularly in sub-Saharan Africa, but little is known how fruit production and seedling recruitment are impacted. We assessed recruitment parameters of Balanites aegyptiaca trees in the Dinder Biosphere Reserve (DBR) across 100 sample plots of 25 m x 40 m in both human-impacted (disturbed) and undisturbed sites. We found that the average number of fruiting branches of B. aegyptiaca in the undisturbed sites were three times as high as those in the disturbed sites (F1,98 = 139, P < 0.001). Further, fruiting branches were positively correlated with crown width (R2 = 0.71, beta = 7.1, P = 0.01) across both sites. The height and crown width of B. aegyptiaca in the undisturbed sites were double that of the disturbed sites (F1,196 = 80, P < 0.001; F1,196 = 94.8, P < 0.001). Saplings and seedlings at the undisturbed sites were three times and twice that of the disturbed sites, respectively (F1,196 = 94.5, P < 0.001; F1,196 = 100.8, P < 0.001), with a positive correlation to the average number of fruiting branches (R2 = 0.74, beta = 0.45, P < 0.001). The soil nitrogen and phosphorus contents beneath trees in the undisturbed sites were almost double that of those in the disturbed sites (F1, 196 = 68.1, P < 0.001; F1, 196 = 97.9, P < 0.001) while sodium and electrical conductivity were by about 50% lower (F1, 196 = 535.8, P < 0.001; F1, 196 = 16.1, P < 0.001). We conclude that illegal harvesting in DBR severely reduced tree structure and recruitment parameters of B. aegyptiaca, which might also have impacted soil fertility. We urge for intensive monitoring and awarenessraising programs to conserve this vulnerable tree species.

Published
2021
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27. Interleukin-6 Reduces β-Cell Oxidative Stress by Linking Autophagy With the Antioxidant Response

Author

John E. Cupit, Raghavendra G. Mirmira, Abass M. Conteh, Amelia K. Linnemann, Michelle Marasco, Evan M. Appleman, and Christopher A. Reissaus

Subjects
0301 basic medicine, Programmed cell death, Endocrinology, Diabetes and Metabolism, Mice, Transgenic, Tissue Banks, Mitochondrion, medicine.disease_cause, Streptozocin, Diabetes Mellitus, Experimental, Tissue Culture Techniques, 03 medical and health sciences, Random Allocation, Cell Line, Tumor, Insulin-Secreting Cells, Mitophagy, Alloxan, Internal Medicine, medicine, Autophagy, Animals, Humans, Interleukin 6, chemistry.chemical_classification, Mice, Knockout, Reactive oxygen species, biology, Interleukin-6, Streptozotocin, Receptors, Interleukin-6, Recombinant Proteins, 3. Good health, Cell biology, Rats, Mice, Inbred C57BL, Oxidative Stress, 030104 developmental biology, chemistry, Islet Studies, biology.protein, Reactive Oxygen Species, Oxidative stress, Biomarkers, medicine.drug, Signal Transduction
Abstract

Production of reactive oxygen species (ROS) is a key instigator of β-cell dysfunction in diabetes. The pleiotropic cytokine interleukin 6 (IL-6) has previously been linked to β-cell autophagy but has not been studied in the context of β-cell antioxidant response. We used a combination of animal models of diabetes and analysis of cultured human islets and rodent β-cells to study how IL-6 influences antioxidant response. We show that IL-6 couples autophagy to antioxidant response and thereby reduces ROS in β-cells and human islets. β-Cell-specific loss of IL-6 signaling in vivo renders mice more susceptible to oxidative damage and cell death through the selective β-cell toxins streptozotocin and alloxan. IL-6-driven ROS reduction is associated with an increase in the master antioxidant factor NRF2, which rapidly translocates to the mitochondria to decrease mitochondrial activity and stimulate mitophagy. IL-6 also initiates a robust transient decrease in cellular cAMP levels, likely contributing to the stimulation of mitophagy to mitigate ROS. Our findings suggest that coupling autophagy to antioxidant response in β-cells leads to stress adaptation that can reduce cellular apoptosis. These findings have implications for β-cell survival under diabetogenic conditions and present novel targets for therapeutic intervention.

Published
2018

30. Inhibition of 12/15-Lipoxygenase Protects Against β-Cell Oxidative Stress and Glycemic Deterioration in Mouse Models of Type 1 Diabetes

Author

Ryan M. Anderson, Gaurav Chopra, Chanelle Benjamin, Jonathan Fine, Jerry L. Nadler, Raghavendra G. Mirmira, Abass M. Conteh, Sarah A. Tersey, David J. Maloney, Marimar Hernandez-Perez, Jennifer B. Nelson, Kara S. Benninger, and Amelia K. Linnemann

Subjects
0301 basic medicine, Blood Glucose, medicine.medical_specialty, Programmed cell death, endocrine system diseases, Endocrinology, Diabetes and Metabolism, Thiophenes, Biology, Naphthalenes, medicine.disease_cause, Arachidonate 12-Lipoxygenase, Proinflammatory cytokine, 03 medical and health sciences, Mice, Mice, Inbred NOD, Diabetes mellitus, Internal medicine, Insulin-Secreting Cells, Internal Medicine, medicine, Animals, Arachidonate 15-Lipoxygenase, Humans, Computer Simulation, Lipoxygenase Inhibitors, Cells, Cultured, chemistry.chemical_classification, Reactive oxygen species, geography, Type 1 diabetes, geography.geographical_feature_category, Molecular Structure, Isoxazoles, medicine.disease, Islet, Pharmacology and Therapeutics, 3. Good health, Oxidative Stress, 030104 developmental biology, Endocrinology, Diabetes Mellitus, Type 1, chemistry, Hydroxyquinolines, Female, Insulitis, Oxidative stress, Software, Protein Binding
Abstract

Islet β-cell dysfunction and aggressive macrophage activity are early features in the pathogenesis of type 1 diabetes (T1D). 12/15-Lipoxygenase (12/15-LOX) is induced in β-cells and macrophages during T1D and produces proinflammatory lipids and lipid peroxides that exacerbate β-cell dysfunction and macrophage activity. Inhibition of 12/15-LOX provides a potential therapeutic approach to prevent glycemic deterioration in T1D. Two inhibitors recently identified by our groups through screening efforts, ML127 and ML351, have been shown to selectively target 12/15-LOX with high potency. Only ML351 exhibited no apparent toxicity across a range of concentrations in mouse islets, and molecular modeling has suggested reduced promiscuity of ML351 compared with ML127. In mouse islets, incubation with ML351 improved glucose-stimulated insulin secretion in the presence of proinflammatory cytokines and triggered gene expression pathways responsive to oxidative stress and cell death. Consistent with a role for 12/15-LOX in promoting oxidative stress, its chemical inhibition reduced production of reactive oxygen species in both mouse and human islets in vitro. In a streptozotocin-induced model of T1D in mice, ML351 prevented the development of diabetes, with coincident enhancement of nuclear Nrf2 in islet cells, reduced β-cell oxidative stress, and preservation of β-cell mass. In the nonobese diabetic mouse model of T1D, administration of ML351 during the prediabetic phase prevented dysglycemia, reduced β-cell oxidative stress, and increased the proportion of anti-inflammatory macrophages in insulitis. The data provide the first evidence to date that small molecules that target 12/15-LOX can prevent progression of β-cell dysfunction and glycemic deterioration in models of T1D.

Published
2017

31. Glucagon-Like Peptide 1 Receptor Activation Augments Cardiac Output and Improves Cardiac Efficiency in Obese Swine After Myocardial Infarction

Author

Daniel J. Sassoon, Abass M. Conteh, Joshua T. Sturek, Johnathan D. Tune, Adam G. Goodwill, Mackenzie A. Eagleson, Kieren J. Mather, and Jillian N. Noblet

Subjects
medicine.medical_specialty, Cardiac output, Swine, Endocrinology, Diabetes and Metabolism, Diastole, Myocardial Infarction, 030209 endocrinology & metabolism, 030204 cardiovascular system & hematology, Pathophysiology, Glucagon-Like Peptide-1 Receptor, Ventricular Function, Left, Contractility, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Internal Medicine, Medicine, Animals, Hypoglycemic Agents, Myocardial infarction, Obesity, Cardiac Output, Sympathomimetics, business.industry, Liraglutide, Heart, medicine.disease, Treatment Outcome, Coronary occlusion, Anesthesia, Ventricular pressure, Cardiology, Dobutamine, Receptors, Adrenergic, beta-1, business, medicine.drug
Abstract

This study tested the hypothesis that glucagon-like peptide 1 (GLP-1) therapies improve cardiac contractile function at rest and in response to adrenergic stimulation in obese swine after myocardial infarction. Obese Ossabaw swine were subjected to gradually developing regional coronary occlusion using an ameroid occluder placed around the left anterior descending coronary artery. Animals received subcutaneous injections of saline or liraglutide (0.005–0.015 mg/kg/day) for 30 days after ameroid placement. Cardiac performance was assessed at rest and in response to sympathomimetic challenge (dobutamine 0.3–10 μg/kg/min) using a left ventricular pressure/volume catheter. Liraglutide increased diastolic relaxation (dP/dt; Tau 1/2; Tau 1/e) during dobutamine stimulation (P < 0.01) despite having no influence on the magnitude of myocardial infarction. The slope of the end-systolic pressure volume relationship (i.e., contractility) increased with dobutamine after liraglutide (P < 0.001) but not saline administration (P = 0.63). Liraglutide enhanced the slope of the relationship between cardiac power and pressure volume area (i.e., cardiac efficiency) with dobutamine (P = 0.017). Hearts from animals treated with liraglutide demonstrated decreased β1-adrenoreceptor expression. These data support that GLP-1 agonism augments cardiac efficiency via attenuation of maladaptive sympathetic signaling in the setting of obesity and myocardial infarction.

Published
2017

32. 197-OR: IL-6 Protects Pancreatic ß Cells from Oxidative Stress via NRF2 Mitochondrial Translocation and Mitophagy

Author

Michelle Marasco, Charanya Muralidharan, Elizabeth Pfeifer, Abass M. Conteh, and Amelia K. Linnemann

Subjects
Chemistry, Endocrinology, Diabetes and Metabolism, Autophagy, Cellular homeostasis, Chromosomal translocation, respiratory system, Mitochondrion, environment and public health, KEAP1, Cell biology, Apoptosis, Mitophagy, Internal Medicine, Phosphorylation
Abstract

Glucose-stimulated insulin secretion by pancreatic β-cells results in a high level of metabolic activity and ROS production. Excess ROS can cause cellular damage leading to apoptosis. We recently reported that the cytokine interleukin 6 (IL-6) stimulates autophagy and protects β-cells from ROS-induced damage and apoptosis via the autophagic degradation of an antioxidant response repressor, KEAP1. This results in increased protein levels of the master antioxidant factor, NRF2. IL-6 also stimulates early markers of mitophagy in a NRF2-dependent manner. Interestingly, these effects are associated with noncanonical translocation of NRF2 to the mitochondria. Here, we set out to validate these findings and determine how NRF2 mitochondrial translocation is regulated. Using fluorescence imaging of mt-keima, we demonstrate that IL-6 stimulates mitophagy. This occurs without effects on mitochondrial function as measured by the Seahorse MitoStress Test. We also find that IL-6 rapidly stimulates NRF2 mitochondrial translocation, an effect that does not occur in response to treatment with hydrogen peroxide or a chemical inhibitor of KEAP1. These data indicate that liberating NRF2 from KEAP1 alone does not lead to NRF2 mitochondrial translocation, suggesting that IL-6 regulates NRF2 localization by additional mechanisms. NRF2 has extensive post-translational modifications, some of which are associated with nuclear localization. Therefore, we hypothesized that IL-6 induces specific NRF2 post-translational modifications that promote mitochondrial translocation. Indeed, we found that IL-6 stimulates serine phosphorylation on NRF2. Based on our findings described here, we propose that selective modification of NRF2 regulates its distinct subcellular localization and that selective translocation determines the mechanism of NRF2-mediated antioxidant response that functions to reduce ROS and restore cellular homeostasis in pancreatic β-cells. Disclosure M. Marasco: Employee; Spouse/Partner; Eli Lilly and Company. A.M. Conteh: None. C. Muralidharan: None. E. Pfeifer: None. A.K. Linnemann: None. Funding National Institutes of Health (K01DK102492), (R03DK115990 to A.K.L.)

Published
2019
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33. Combined targeting of TGF-β, EGFR and HER2 suppresses lymphangiogenesis and metastasis in a pancreatic cancer model

Author

Murray Korc, Monica Cheng, Imade E. Imasuen-Williams, Kelly E. Craven, Abass M. Conteh, and Jesse Gore

Subjects
Male, 0301 basic medicine, Cancer Research, endocrine system diseases, Receptor, ErbB-2, Angiogenesis, Receptor, Transforming Growth Factor-beta Type I, Angiogenesis Inhibitors, Apoptosis, medicine.disease_cause, Metastasis, 0302 clinical medicine, Cell Movement, Transforming Growth Factor beta, Antineoplastic Combined Chemotherapy Protocols, Molecular Targeted Therapy, Genes, Retinoblastoma, Lymphangiogenesis, Neovascularization, Pathologic, ErbB Receptors, Phenotype, Oncology, 030220 oncology & carcinogenesis, Quinolines, Female, KRAS, Carcinoma, Pancreatic Ductal, Signal Transduction, Mice, Transgenic, Protein Serine-Threonine Kinases, Biology, Article, Proto-Oncogene Proteins p21(ras), 03 medical and health sciences, Amphiregulin, Pancreatic cancer, Genetic model, medicine, Animals, Humans, Genetic Predisposition to Disease, Neoplasm Invasiveness, Cyclin-Dependent Kinase Inhibitor p16, Gene Expression Profiling, Lapatinib, Gene signature, medicine.disease, digestive system diseases, Pancreatic Neoplasms, 030104 developmental biology, Mutation, Quinazolines, Cancer research, Pyrazoles, Receptors, Transforming Growth Factor beta
Abstract

Pancreatic ductal adenocarcinomas (PDACs) are aggressive with frequent lymphatic spread. By analysis of data from The Cancer Genome Atlas, we determined that ~35% of PDACs have a pro-angiogenic gene signature. We now show that the same PDACs exhibit increased expression of lymphangiogenic genes and lymphatic endothelial cell (LEC) markers, and that LEC abundance in human PDACs correlates with endothelial cell microvessel density. Lymphangiogenic genes and LECs are also elevated in murine PDACs arising in the KRC (mutated Kras; deleted RB) and KIC (mutated Kras; deleted INK4a) genetic models. Moreover, pancreatic cancer cells (PCCs) derived from KRC tumors express and secrete high levels of lymphangiogenic factors, including the EGF receptor ligand, amphiregulin. Importantly, TGF-β1 increases lymphangiogenic genes and amphiregulin expression in KRC PCCs but not in murine PCCs that lack SMAD4, and combinatorial targeting of the TGF-β type I receptor (TβRI) with LY2157299 and EGFR/HER2 with lapatinib suppresses tumor growth and metastasis in a syngeneic orthotopic model, and attenuates tumor lymphangiogenesis and angiogenesis while reducing lymphangiogenic genes and amphiregulin and enhancing apoptosis. Therefore, this combination could be beneficial in PDACs with lymphangiogenic or angiogenic gene signatures.

Published
2016
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34. Longitudinal Intravital Imaging of Biosensor-labeled In Situ Islet Beta Cells

Author

Richard O. Day, Kenneth W. Dunn, Amelia K. Linnemann, Malgorzata M. Kamocka, Sarah A. Tersey, Raghavendra G. Mirmira, Abass M. Conteh, Michelle Martinez, Kara S. Orr, Ashley N. Twigg, and Christopher A. Reissaus

Subjects
chemistry.chemical_classification, geography, Reactive oxygen species, geography.geographical_feature_category, Transgene, Islet, Streptozotocin, Cell biology, Green fluorescent protein, chemistry, Apoptosis, In vivo, medicine, Intravital microscopy, medicine.drug
Abstract

Impaired function and apoptosis of insulin-secreting islet β-cells is central to disease progression in both type 1 and type 2 diabetes. Oxidative damage resulting from excess reactive oxygen species (ROS) is a central factor in β-cell dysfunction and death, but the dynamic nature of ROS accumulation and its depletion pose a problem for mechanistic studies in vivo. Biosensors, including the redox-sensitive GFP (roGFPs), coupled with intravital microscopy provide a sensitive and dynamic solution to this problem. Here, we utilize a virally-delivered roGFP2-containing human glutaredoxin-1 (Grx1-roGFP2) to selectively monitor β-cell ROS dynamics in vivo in response to toxic glucose analogs. We paired viral biosensor delivery with implanted abdominal imaging windows over the pancreas, thus allowing longitudinal measurements of β-cell ROS and islet area during and after streptozotocin (STZ) exposure. The studies presented here represent a robust experimental platform that could be readily adapted to various transgenic or physiological mouse models in conjunction with any number of available biosensors, and thus opens a vast realm of potential for discovery in islet biology in vivo.

Published
2019
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35. An In Vivo Zebrafish Model for Interrogating ROS-Mediated Pancreatic β-Cell Injury, Response, and Prevention

Author

Abhishek Kulkarni, Ryan M. Anderson, Sarah A. Tersey, Anjali Mirmira, Amelia K. Linnemann, Cody A. Sorrell, Raghavendra G. Mirmira, and Abass M. Conteh

Subjects
0301 basic medicine, Aging, Article Subject, Transgene, medicine.medical_treatment, Caspase 3, Biochemistry, 03 medical and health sciences, 0302 clinical medicine, In vivo, Genetic predisposition, medicine, lcsh:QH573-671, Zebrafish, chemistry.chemical_classification, Reactive oxygen species, geography, geography.geographical_feature_category, biology, lcsh:Cytology, Insulin, Cell Biology, General Medicine, biology.organism_classification, Islet, Cell biology, 030104 developmental biology, chemistry, 030217 neurology & neurosurgery
Abstract

It is well known that a chronic state of elevated reactive oxygen species (ROS) in pancreaticβ-cells impairs their ability to release insulin in response to elevated plasma glucose. Moreover, at its extreme, unmitigated ROS drives regulated cell death. This dysfunctional state of ROS buildup can result both from genetic predisposition and environmental factors such as obesity and overnutrition. Importantly, excessive ROS buildup may underlie metabolic pathologies such as type 2 diabetes mellitus. The ability to monitor ROS dynamics inβ-cells in situ and to manipulate it via genetic, pharmacological, and environmental means would accelerate the development of novel therapeutics that could abate this pathology. Currently, there is a lack of models with these attributes that are available to the field. In this study, we use a zebrafish model to demonstrate that ROS can be generated in aβ-cell-specific manner using a hybrid chemical genetic approach. Using a transgenic nitroreductase-expressing zebrafish line,Tg(ins:Flag-NTR)s950, treated with the prodrug metronidazole (MTZ), we found that ROS is rapidly and explicitly generated inβ-cells. Furthermore, the level of ROS generated was proportional to the dosage of prodrug added to the system. At high doses of MTZ, caspase 3 was rapidly cleaved,β-cells underwent regulated cell death, and macrophages were recruited to the islet to phagocytose the debris. Based on our findings, we propose a model for the mechanism of NTR/MTZ action in transgenic eukaryotic cells and demonstrate the robust utility of this system to model ROS-related disease pathology.

Published
2018

36. An

Author

Abhishek A, Kulkarni, Abass M, Conteh, Cody A, Sorrell, Anjali, Mirmira, Sarah A, Tersey, Raghavendra G, Mirmira, Amelia K, Linnemann, and Ryan M, Anderson

Subjects
Disease Models, Animal, Insulin-Secreting Cells, Animals, Reactive Oxygen Species, Zebrafish, Research Article
Abstract

It is well known that a chronic state of elevated reactive oxygen species (ROS) in pancreatic β-cells impairs their ability to release insulin in response to elevated plasma glucose. Moreover, at its extreme, unmitigated ROS drives regulated cell death. This dysfunctional state of ROS buildup can result both from genetic predisposition and environmental factors such as obesity and overnutrition. Importantly, excessive ROS buildup may underlie metabolic pathologies such as type 2 diabetes mellitus. The ability to monitor ROS dynamics in β-cells in situ and to manipulate it via genetic, pharmacological, and environmental means would accelerate the development of novel therapeutics that could abate this pathology. Currently, there is a lack of models with these attributes that are available to the field. In this study, we use a zebrafish model to demonstrate that ROS can be generated in a β-cell-specific manner using a hybrid chemical genetic approach. Using a transgenic nitroreductase-expressing zebrafish line, Tg(ins:Flag-NTR)s950, treated with the prodrug metronidazole (MTZ), we found that ROS is rapidly and explicitly generated in β-cells. Furthermore, the level of ROS generated was proportional to the dosage of prodrug added to the system. At high doses of MTZ, caspase 3 was rapidly cleaved, β-cells underwent regulated cell death, and macrophages were recruited to the islet to phagocytose the debris. Based on our findings, we propose a model for the mechanism of NTR/MTZ action in transgenic eukaryotic cells and demonstrate the robust utility of this system to model ROS-related disease pathology.

Published
2017

37. Perivascular Adipose Tissue and Coronary Vascular Disease

Author

Adam G. Goodwill, Jillian N. Noblet, Abass M. Conteh, Daniel J. Sassoon, Johnathan D. Tune, and Meredith K. Owen

Subjects
medicine.medical_specialty, Adipose tissue, Adipokine, Inflammation, Coronary Artery Disease, Article, Coronary artery disease, Vascular health, Internal medicine, Paracrine Communication, medicine, Animals, Humans, business.industry, medicine.disease, Coronary Vessels, Coronary vascular disease, Coronary arteries, Phenotype, medicine.anatomical_structure, Adipose Tissue, Gene Expression Regulation, Cardiology, medicine.symptom, Cardiology and Cardiovascular Medicine, Vascular function, business, Signal Transduction
Abstract

Coronary perivascular adipose tissue is a naturally occurring adipose tissue depot that normally surrounds the major coronary arteries on the surface of the heart. Although originally thought to promote vascular health and integrity, there is a growing body of evidence to support that coronary perivascular adipose tissue displays a distinct phenotype relative to other adipose depots and is capable of producing local factors with the potential to augment coronary vascular tone, inflammation, and the initiation and progression of coronary artery disease. The purpose of the present review is to outline previous findings about the cardiovascular effects of coronary perivascular adipose tissue and the potential mechanisms by which adipose-derived factors may influence coronary vascular function and the progression of atherogenesis.

Published
2014
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38. Privacy Enforcement on Subscribers Data in Cloud Computing.

Author

Akinboro, S. A., Asanga, U. J., and Abass, M. O.

Subjects
CLOUD computing, SYMMETRIC-key algorithms, ADVANCED Encryption Standard, DATA encryption, SECURE Sockets Layer (Computer network protocol)
Abstract

Data stored in the cloud are susceptible to an array of threats from hackers. This is because threats, hackers and unauthorized access are not supported by the cloud service providers as implied. This study improves user privacy in the cloud system, using privacy with non-trusted provider (PNTP) on software and platform as a service model. The subscribers encrypt the data using user's personal Advanced Encryption Standard (AES) symmetric key algorithm and send the encrypted data to the storage pool of the Cloud Service Provider (CSP) via a secure socket layer. The AES performs a second encryption on the data sent to the cloud and generates for the subscriber a key that will be used for decryption of previously stored data. The encryption and decryption keys are managed by the key server and have been hardcoded into the PNTP system. The model was simulated using the Stanford University multimedia dataset and benchmarked with a Privacy with Trusted cloud Provider (PTP) model using encryption time, decryption time and efficiency (brute force hacking) as parameters. Results showed that it took a longer time to access the user files in PNTP than in the PTP system. The brute force hacking took a longer time (almost double) to access data stored on the PNTP system. This will give subscribers a high level of control over their data and increase the adoption of cloud computing by businesses and organizations with highly sensitive information. [ABSTRACT FROM AUTHOR]

Published
2021
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39. CO2 laser spot welding of thin sheets AISI 321 austenitic stainless steel.

Author

Shehab, A. A., Nawi, S. A., Al-Rubaiy, A. AAG, Hammoudi, Z., Hafedh, S. A., Abass, M. H., Alali, M. S., and Ali, S. D.

Subjects
SPOT welding, AUSTENITIC stainless steel, FINITE element method, CARBON dioxide analysis, WELDING
Abstract

Purpose: The present work aims to investigate the influence of CO2 laser spot welding (LSW) parameters on welding profile and mechanical properties of lap joint of AISI 321 thin sheet metals, and analyze the welding profile numerically by finite element (FE) method. Design/methodology/approach: The weld carried out using 150 W CO2 continues wave laser system. The impact of exposure time and laser power on the welding profile was investigated using an optical microscope. Microhardness and tensile strength tests were used to evaluate the mechanical properties of the joint. Ansys software was utilized to simulate the welding profile numerically. Findings: The results revealed that 2 s exposure time and 50 W power have led to uniform welding profile and highest shear force (340 N), lower hardness gradient across the heat affected zone (HAZ) and fusion zone (FZ). Finite element (FE) analysis of the welding profile showed good agreement with experimental analysis. Research limitations/implications: The selection of laser spot welding parameters for thin sheet metal was critical due to the probability of metal vaporisation with extra heat input during welding. Practical implications: Laser welding of AISI 321 steel is used in multiple industrial sectors such as power plants, petroleum refinement stations, pharmaceutical industry, and households. Thus, selecting the best welding parameters ensures high-quality joint. Originality/value: The use of CO2 laser in continuous wave (CW) mode instead of pulse mode for spot welding of thin sheet metal of AISI 321 austenitic stainless steel consider a real challenge because of the difficulty of control the heat input via proper selection of the welding parameters in order to not burn the processed target. Besides, the maintenance is easier and operation cost is lower in continuous CO2 than pulse mode. [ABSTRACT FROM AUTHOR]

Published
2020
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41. Obesity alters molecular and functional cardiac responses to ischemia/reperfusion and glucagon-like peptide-1 receptor agonism

Author

Jeanette N. McClintick, Adam G. Goodwill, Kieren J. Mather, B. Paul Herring, Johnathan D. Tune, Abass M. Conteh, Jillian N. Noblet, and Daniel J. Sassoon

Subjects
Proteomics, 0301 basic medicine, Cardiac function curve, medicine.medical_specialty, Swine, Physiology, Ischemia, Myocardial Reperfusion Injury, 030204 cardiovascular system & hematology, Glucagon, Article, Glucagon-Like Peptide-1 Receptor, 03 medical and health sciences, 0302 clinical medicine, Glucagon-Like Peptide 1, Physiology (medical), Internal medicine, medicine, Hyperinsulinemia, Animals, Obesity, Oligonucleotide Array Sequence Analysis, biology, business.industry, Gene Expression Profiling, Stroke volume, medicine.disease, Troponin, Disease Models, Animal, 030104 developmental biology, Blood pressure, Endocrinology, Coronary occlusion, biology.protein, Transcriptome, Cardiology and Cardiovascular Medicine, business
Abstract

This study tested the hypothesis that obesity alters the cardiac response to ischemia/reperfusion and/or glucagon like peptide-1 (GLP-1) receptor activation, and that these differences are associated with alterations in the obese cardiac proteome and microRNA (miRNA) transcriptome. Ossabaw swine were fed normal chow or obesogenic diet for 6 months. Cardiac function was assessed at baseline, during a 30-minutes coronary occlusion, and during 2 hours of reperfusion in anesthetized swine treated with saline or exendin-4 for 24 hours. Cardiac biopsies were obtained from normal and ischemia/reperfusion territories. Fat-fed animals were heavier, and exhibited hyperinsulinemia, hyperglycemia, and hypertriglyceridemia. Plasma troponin-I concentration (index of myocardial injury) was increased following ischemia/reperfusion and decreased by exendin-4 treatment in both groups. Ischemia/reperfusion produced reductions in systolic pressure and stroke volume in lean swine. These indices were higher in obese hearts at baseline and relatively maintained throughout ischemia/reperfusion. Exendin-4 administration increased systolic pressure in lean swine but did not affect the blood pressure in obese swine. End-diastolic volume was reduced by exendin-4 following ischemia/reperfusion in obese swine. These divergent physiologic responses were associated with obesity-related differences in proteins related to myocardial structure/function (e.g. titin) and calcium handling (e.g. SERCA2a, histidine-rich Ca(2+) binding protein). Alterations in expression of cardiac miRs in obese hearts included miR-15, miR-27, miR-130, miR-181, and let-7. Taken together, these observations validate this discovery approach and reveal novel associations that suggest previously undiscovered mechanisms contributing to the effects of obesity on the heart and contributing to the actions of GLP-1 following ischemia/reperfusion.

Published
2016
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43. Inhibition of 12/15-Lipoxygenase Protects Against β-Cell Oxidative Stress and Glycemic Deterioration in Mouse Models of Type 1 Diabetes

Author

Hernandez-Perez, Marimar, primary, Chopra, Gaurav, additional, Fine, Jonathan, additional, Conteh, Abass M., additional, Anderson, Ryan M., additional, Linnemann, Amelia K., additional, Benjamin, Chanelle, additional, Nelson, Jennifer B., additional, Benninger, Kara S., additional, Nadler, Jerry L., additional, Maloney, David J., additional, Tersey, Sarah A., additional, and Mirmira, Raghavendra G., additional

Published
2017
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45. Effects of Liraglutide on Cardiac Function and Myocardial Infarct Size in the Setting of Obesity

Author

Adam G. Goodwill, Daniel J. Sassoon, Abass M. Conteh, Kieren J. Mather, Johnathan D. Tune, and Jillian N. Noblet

Subjects
Cardiac function curve, medicine.medical_specialty, business.industry, Liraglutide, medicine.disease, Biochemistry, Obesity, Internal medicine, Genetics, medicine, Cardiology, Myocardial infarction, business, Molecular Biology, Biotechnology, medicine.drug
Published
2015
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47. The effect of annealing and anisotropic behaviour on tensile and fatigue properties of AA 8090.

Author

Abass, M. H., Mahmud, F., Alali, M. S., and Abood, A. N.

Subjects
TENSILE strength, MATERIAL fatigue, ANNEALING of crystals, ANISOTROPY, MICROSTRUCTURE, MECHANICAL behavior of materials
Abstract

Purpose: This paper aims to assess microstructures and mechanical properties of annealed and un-annealed Al-Li alloys (AA8090) and provide valid information regarding influence of anisotropy on tensile properties, fatigue lives. Design/methodology/approach: The methodology included investigating the influence of annealing on grain size, tensile strength and fatigue lives of AA8090. Optical microscope, scanning electron microscope and X-ray diffraction were utilized to analyse the crystallographic texture. Findings: The results showed that the un-annealed alloy exhibited much finer grain structure in three directions, namely longitudinal (L) rolling direction, L-45° and Long transverse (LT) combined with stronger crystallographic texture. Regarding to mechanical properties, un-annealed alloy presented superior tensile strength with strong anisotropic behaviour. L and LT grains direction showed highest tensile strength value of 550 MPa and L-45° showed lowest tensile strength value of 420 MPa. Results of fatigue test revealed that annealed Al-Li alloy has lower fatigue lives with high influence of test direction on fatigue properties. Higher variation in fatigue life to failure links with un-annealed alloy over annealed alloy. Examination of fractured surface showed that the morphology of fractured surface is a mixture of ductile and brittle fractures in both annealed and un-annealed alloys with more brittle behaviour in un-annealed alloy. Research limitations/implications: The main challenge of this work is the determination of the test direction (test angle in respect to rolling direction), which is necessary to provide correct information regarding mechanical properties. Further study of low cycle fatigue can be done in future, which will be an excellent indication to mechanical properties of this alloy since it provides more understanding to the behaviour of the material and better comprehend crack propagation and strain stress concentration. Practical implications: AA8090 alloy is an important candidate for aerospace and aircraft industries. Influence of annealing heat treatment and rolling direction on mechanical properties of AA8090 alloy provides more accurate information to the manufacturers who deal with this alloy. Originality/value: This study is affording a significant information regarding the effect of annealing and anisotropic behaviour on mechanical properties of AA8090. To our knowledge, there are few reports that study this combination of factors on AA8090 alloy. [ABSTRACT FROM AUTHOR]

Published
2019
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48. OPTICAL AND PHOTOCONDUCTIVE PROPERTIES OF CHEMICALLY DEPOSITED NANOCRYSTALLINE PbS THIN FILMS.

Author

NASIR, E. M. and ABASS, M. M.

Subjects
*THIN films, *OPTICAL properties, *OPTICAL measurements, *CHEMICAL solution deposition, *ATOMIC force microscopes, *METALLIC thin films
Abstract

A nanocrystalline thin films of PbS with both thickness (400 and 600)nm have been prepared successfully by chemical bath deposition technique on glass and Si substrates. The structure and morphology of these films were studied by X-ray diffraction and atomic force microscope. It shows that the structure is polycrystalline and the average crystallite size has been measured. The optical parameters of the prepared films as absorption, transmittance, reflectance, optical energy gap, and absorption coefficient were found as affected by varying the thickness. The optical measurement showed that (PbS) films have an allowed direct energy gap (Eg) and that decreases with thickness increasing. The photoconductive measurement gives the positive photoconductive for PbS thin films. [ABSTRACT FROM AUTHOR]

Published
2019

49. CARDIOVASCULAR AND HEMODYNAMIC EFFECTS OF GLUCAGON-LIKE PEPTIDE-1

Author

Abass M. Conteh, Adam G. Goodwill, Kieren J. Mather, Johnathan D. Tune, Daniel J. Sassoon, and Jillian N. Noblet

Subjects
endocrine system, business.industry, Endocrinology, Diabetes and Metabolism, digestive, oral, and skin physiology, Hemodynamics, Incretin, Disease, Pharmacology, Bioinformatics, medicine.disease, Glucagon-like peptide-1, Cardiovascular System, Article, Endocrinology, Blood pressure, Glucagon-Like Peptide 1, Diabetes mellitus, Heart rate, medicine, Animals, Humans, business, Hemodynamic effects, hormones, hormone substitutes, and hormone antagonists
Abstract

Glucagon-like peptide-1 (GLP-1) is an incretin hormone that has been shown to have hemodynamic and cardioprotective capacity in addition to its better characterized glucoregulatory actions. Because of this, emerging research has focused on the ability of GLP-1 based therapies to drive myocardial substrate selection, enhance cardiac performance and regulate heart rate, blood pressure and vascular tone. These studies have produced consistent and reproducible results amongst numerous laboratories. However, there are obvious disparities in findings obtained in small animal models versus those of higher mammals. This species dependent discrepancy calls to question, the translational value of individual findings. Moreover, few studies of GLP-1 mediated cardiovascular action have been performed in the presence of a pre-existing comorbidities (e.g. obesity/diabetes) which limits interpretation of the effectiveness of incretin-based therapies in the setting of disease. This review addresses cardiovascular and hemodynamic potential of GLP-1 based therapies with attention to species specific effects as well as the interaction between therapies and disease.

Published
2014

50. Glucagon-like peptide-1 (7–36) but not (9–36) augments cardiac output during myocardial ischemia via a Frank–Starling mechanism

Author

Daniel J. Sassoon, Adam G. Goodwill, Abass M. Conteh, Johnathan D. Tune, Eli D. Casalini, Kieren J. Mather, and Jillian N. Noblet

Subjects
Cardiac function curve, medicine.medical_specialty, Cardiac output, Swine, Physiology, Myocardial Ischemia, Ischemia, Inferior vena cava, Article, Contractility, Glucagon-Like Peptide 1, Physiology (medical), Internal medicine, medicine, Animals, Cardiac Output, Frank–Starling law of the heart, business.industry, medicine.disease, Peptide Fragments, Disease Models, Animal, Preload, Blood pressure, medicine.vein, Anesthesia, Cardiology, Peptides, Cardiology and Cardiovascular Medicine, business
Abstract

This study examined the cardiovascular effects of GLP-1 (7-36) or (9-36) on myocardial oxygen consumption, function and systemic hemodynamics in vivo during normal perfusion and during acute, regional myocardial ischemia. Lean Ossabaw swine received systemic infusions of saline vehicle or GLP-1 (7-36 or 9-36) at 1.5, 3.0, and 10.0 pmol/kg/min in sequence for 30 min at each dose, followed by ligation of the left circumflex artery during continued infusion at 10.0 pmol/kg/min. Systemic GLP-1 (9-36) had no effect on coronary flow, blood pressure, heart rate or indices of cardiac function before or during regional myocardial ischemia. Systemic GLP-1 (7-36) exerted no cardiometabolic or hemodynamic effects prior to ischemia. During ischemia, GLP-1 (7-36) increased cardiac output by approximately 2 L/min relative to vehicle-controls (p = 0.003). This response was not diminished by treatment with the non-depolarizing ganglionic blocker hexamethonium. Left ventricular pressure-volume loops measured during steady-state conditions with graded occlusion of the inferior vena cava to assess load-independent contractility revealed that GLP-1 (7-36) produced marked increases in end-diastolic volume (74 ± 1 to 92 ± 5 ml; p = 0.03) and volume axis intercept (8 ± 2 to 26 ± 8; p = 0.05), without any change in the slope of the end-systolic pressure-volume relationship vs. vehicle during regional ischemia. GLP-1 (9-36) produced no changes in any of these parameters compared to vehicle. These findings indicate that short-term systemic treatment with GLP-1 (7-36) but not GLP-1 (9-36) significantly augments cardiac output during regional myocardial ischemia, via increases in ventricular preload without changes in cardiac inotropy.

Published
2014
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