Human Genetics And Molecular Medicine - Research Publications
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Item Wild-type p53 suppresses formin-binding protein-17 (FBP17) to reduce invasion(Oxford University Press, 2022-01-28T00:00:00) Suman, Prabhat; Mehta, Vikrant; Craig, Andrew W. B.; Chander, HarishInvading tumor cells develop membrane protruding structures called invadopodia to invade and metastasize. Previously, we have reported the role of formin-binding protein-17 (FBP17) in extracellular matrix degradation and invadopodia formation in breast cancer cells. Here, we report a novel axis between tumor-suppressor p53 and FBP17. We observed that cell lines with mutant p53 express FBP17 to a higher level. The expression of FBP17 was reduced upon stabilizing wild-type p53. Furthermore, the immunohistochemistry analysis of breast cancer tissue microarrays demonstrated the correlation between the accumulation of p53 and enhanced FBP17 staining in invasive ductal carcinomas. The double knockdown of p53 and FBP17 showed the contribution of FBP17 in the invasion of cancer cells where p53 lost the regulatory control over FBP17. Taken together, these studies indicate that FBP17 may be a marker to understand the invasion propensity of breast cancer. � 2022 The Author(s). Published by Oxford University Press. All rights reserved.Item Global, regional, and national burden of diabetes from 1990 to 2021, with projections of prevalence to 2050: a systematic analysis for the Global Burden of Disease Study 2021(Elsevier B.V., 2023-06-23T00:00:00) Ong, Kanyin Liane; Stafford, Lauryn K.; McLaughlin, Susan A.; Boyko, Edward J.; Vollset, Stein Emil; Smith, Amanda E.; Dalton, Bronte E.; Duprey, Joe; Cruz, Jessica A.; Hagins, Hailey; Lindstedt, Paulina A.; Aali, Amirali; Abate, Yohannes Habtegiorgis; Abate, Melsew Dagne; Abbasian, Mohammadreza; Abbasi-Kangevari, Zeinab; Abbasi-Kangevari, Mohsen; ElHafeez, Samar Abd; Abd-Rabu, Rami; Abdulah, Deldar Morad; Abdullah, Abu Yousuf Md; Abedi, Vida; Abidi, Hassan; Aboagye, Richard Gyan; Abolhassani, Hassan; Abu-Gharbieh, Eman; Abu-Zaid, Ahmed; Adane, Tigist Demssew; Adane, Denberu Eshetie; Addo, Isaac Yeboah; Adegboye, Oyelola A.; Adekanmbi, Victor; Adepoju, Abiola Victor; Adnani, Qorinah Estiningtyas Sakilah; Afolabi, Rotimi Felix; Agarwal, Gina; Aghdam, Zahra Babaei; Agudelo-Botero, Marcela; Arriagada, Constanza Elizabeth Aguilera; Agyemang-Duah, Williams; Ahinkorah, Bright Opoku; Ahmad, Danish; Ahmad, Rizwan; Ahmad, Sajjad; Ahmad, Aqeel; Ahmadi, Ali; Ahmadi, Keivan; Ahmed, Ayman; Ahmed, Ali; Ahmed, Luai A.; Ahmed, Syed Anees; Ajami, Marjan; Akinyemi, Rufus Olusola; Al Hamad, Hanadi; Al Hasan, Syed Mahfuz; AL-Ahdal, Tareq Mohammed Ali; Alalwan, Tariq A.; Al-Aly, Ziyad; AlBataineh, Mohammad T.; Alcalde-Rabanal, Jacqueline Elizabeth; Alemi, Sharifullah; Ali, Hassam; Alinia, Tahereh; Aljunid, Syed Mohamed; Almustanyir, Sami; Al-Raddadi, Rajaa M.; Alvis-Guzman, Nelson; Amare, Firehiwot; Ameyaw, Edward Kwabena; Amiri, Sohrab; Amusa, Ganiyu Adeniyi; Andrei, Catalina Liliana; Anjana, Ranjit Mohan; Ansar, Adnan; Ansari, Golnoosh; Ansari-Moghaddam, Alireza; Anyasodor, Anayochukwu Edward; Arabloo, Jalal; Aravkin, Aleksandr Y.; Areda, Demelash; Arifin, Hidayat; Arkew, Mesay; Armocida, Benedetta; Arnlov, Johan; Artamonov, Anton A.; Arulappan, Judie; Aruleba, Raphael Taiwo; Arumugam, Ashokan; Aryan, Zahra; Asemu, Mulu Tiruneh; Asghari-Jafarabadi, Mohammad; Askari, Elaheh; Asmelash, Daniel; Astell-Burt, Thomas; Athar, Mohammad; Athari, Seyyed Shamsadin; Atout, Maha Moh'd Wahbi; Avila-Burgos, Leticia; Awaisu, Ahmed; Azadnajafabad, Sina; Darshan, B.B.; Babamohamadi, Hassan; Badar, Muhammad; Badawi, Alaa; Badiye, Ashish D.; Baghcheghi, Nayereh; Bagheri, Nasser; Bagherieh, Sara; Bah, Sulaiman; Bahadory, Saeed; Bai, Ruhai; Baig, Atif Amin; Baltatu, Ovidiu Constantin; Baradaran, Hamid Reza; Barchitta, Martina; Bardhan, Mainak; Barengo, Noel C.; Barnighausen, Till Winfried; Barone, Mark Thomaz Ugliara; Barone-Adesi, Francesco; Barrow, Amadou; Bashiri, Hamideh; Basiru, Afisu; Basu, Sanjay; Basu, Saurav; Batiha, Abdul-Monim Mohammad; Batra, Kavita; Bayih, Mulat Tirfie; Bayileyegn, Nebiyou Simegnew; Behnoush, Amir Hossein; Bekele, Alehegn Bekele; Belete, Melaku Ashagrie; Belgaumi, Uzma Iqbal; Belo, Luis; Bennett, Derrick A.; Bensenor, Isabela M.; Berhe, Kidanemaryam; Berhie, Alemshet Yirga; Bhaskar, Sonu; Bhat, Ajay Nagesh; Bhatti, Jasvinder Singh; Bikbov, Boris; Bilal, Faiq; Bintoro, Bagas Suryo; Bitaraf, Saeid; Bitra, Veera R.; Bjegovic-Mikanovic, Vesna; Bodolica, Virginia; Boloor, Archith; Brauer, Michael; Brazo-Sayavera, Javier; Brenner, Hermann; Butt, Zahid A.; Calina, Daniela; Campos, Luciana Aparecida; Campos-Nonato, Ismael R.; Cao, Yin; Cao, Chao; Car, Josip; Carvalho, Marcia; Castaneda-Orjuela, Carlos A.; Catala-Lopez, Ferran; Cerin, Ester; Chadwick, Joshua; Chandrasekar, Eeshwar K.; Chanie, Gashaw Sisay; Charan, Jaykaran; Chattu, Vijay Kumar; Chauhan, Kirti; Cheema, Huzaifa Ahmad; Abebe, Endeshaw Chekol; Chen, Simiao; Cherbuin, Nicolas; Chichagi, Fatemeh; Chidambaram, Saravana Babu; Cho, William C. S.; Choudhari, Sonali Gajanan; Chowdhury, Rajiv; Chowdhury, Enayet Karim; Chu, Dinh-Toi; Chukwu, Isaac Sunday; Chung, Sheng-Chia; Coberly, Kaleb; Columbus, Alyssa; Contreras, Daniela; Cousin, Ewerton; Criqui, Michael H.; Cruz-Martins, Natalia; Cuschieri, Sarah; Dabo, Bashir; Dadras, Omid; Dai, Xiaochen; Damasceno, Albertino Antonio Moura; Dandona, Rakhi; Dandona, Lalit; Das, Saswati; Dascalu, Ana Maria; Dash, Nihar Ranjan; Dashti, Mohsen; Davila-Cervantes, Claudio Alberto; De la Cruz-Gongora, Vanessa; Debele, Gebiso Roba; Delpasand, Kourosh; Demisse, Fitsum Wolde; Demissie, Getu Debalkie; Deng, Xinlei; Denova-Gutierrez, Edgar; Deo, Salil V.; Dervi�evi?, Emina; Desai, Hardik Dineshbhai; Desale, Aragaw Tesfaw; Dessie, Anteneh Mengist; Desta, Fikreab; Dewan, Syed Masudur Rahman; Dey, Sourav; Dhama, Kuldeep; Dhimal, Meghnath; Diao, Nancy; Diaz, Daniel; Dinu, Monica; Diress, Mengistie; Djalalinia, Shirin; Doan, Linh Phuong; Dongarwar, Deepa; dos Santos Figueiredo, Francisco Winter; Duncan, Bruce B.; Dutta, Siddhartha; Dziedzic, Arkadiusz Marian; Edinur, Hisham Atan; Ekholuenetale, Michael; Ekundayo, Temitope Cyrus; Elgendy, Islam Y.; Elhadi, Muhammed; El-Huneidi, Waseem; Elmeligy, Omar Abdelsadek Abdou; Elmonem, Mohamed A.; Endeshaw, Destaw; Esayas, Hawi Leul; Eshetu, Habitu Birhan; Etaee, Farshid; Fadhil, Ibtihal; Fagbamigbe, Adeniyi Francis; Fahim, Ayesha; Falahi, Shahab; Faris, MoezAlIslam Ezzat Mahmoud; Farrokhpour, Hossein; Farzadfar, Farshad; Fatehizadeh, Ali; Fazli, Ghazal; Feng, Xiaoqi; Ferede, Tomas Y.; Fischer, Florian; Flood, David; Forouhari, Ali; Foroumadi, Roham; Koudehi, Masoumeh Foroutan; Gaidhane, Abhay Motiramji; Gaihre, Santosh; Gaipov, Abduzhappar; Galali, Yaseen; Ganesan, Balasankar; Garcia-Gordillo, M.A.; Gautam, Rupesh K.; Gebrehiwot, Mesfin; Gebrekidan, Kahsu Gebrekirstos; Gebremeskel, Teferi Gebru; Getacher, Lemma; Ghadirian, Fataneh; Ghamari, Seyyed-Hadi; Nour, Mohammad Ghasemi; Ghassemi, Fariba; Golechha, Mahaveer; Goleij, Pouya; Golinelli, Davide; Gopalani, Sameer Vali; Guadie, Habtamu Alganeh; Guan, Shi-Yang; Gudayu, Temesgen Worku; Guimaraes, Rafael Alves; Guled, Rashid Abdi; Gupta, Rajeev; Gupta, Kartik; Gupta, Veer Bala; Gupta, Vivek Kumar; Gyawali, Bishal; Haddadi, Rasool; Hadi, Najah R.; Haile, Teklehaimanot Gereziher; Hajibeygi, Ramtin; Haj-Mirzaian, Arvin; Halwani, Rabih; Hamidi, Samer; Hankey, Graeme J.; Hannan, Md Abdul; Haque, Shafiul; Harandi, Hamid; Harlianto, Netanja I.; Mahmudul Hasan, S.M.; Hasan, Syed Shahzad; Hasani, Hamidreza; Hassanipour, Soheil; Hassen, Mohammed Bheser; Haubold, Johannes; Hayat, Khezar; Heidari, Golnaz; Heidari, Mohammad; Hessami, Kamran; Hiraike, Yuta; Holla, Ramesh; Hossain, Sahadat; Hossain, Md Shakhaoat; Hosseini, Mohammad-Salar; Hosseinzadeh, Mehdi; Hosseinzadeh, Hassan; Huang, Junjie; Huda, Md Nazmul; Hussain, Salman; Huynh, Hong-Han; Hwang, Bing-Fang; Ibitoye, Segun Emmanuel; Ikeda, Nayu; Ilic, Irena M.; Ilic, Milena D.; Inbaraj, Leeberk Raja; Iqbal, Afrin; Islam, Sheikh Mohammed Shariful; Islam, Rakibul M.; Ismail, Nahlah Elkudssiah; Iso, Hiroyasu; Isola, Gaetano; Itumalla, Ramaiah; Iwagami, Masao; Iwu, Chidozie C. D.; Iyamu, Ihoghosa Osamuyi; Iyasu, Assefa N.; Jacob, Louis; Jafarzadeh, Abdollah; Jahrami, Haitham; Jain, Rajesh; Jaja, Chinwe; Jamalpoor, Zahra; Jamshidi, Elham; Janakiraman, Balamurugan; Jayanna, Krishnamurthy; Jayapal, Sathish Kumar; Jayaram, Shubha; Jayawardena, Ranil; Jebai, Rime; Jeong, Wonjeong; Jin, Yinzi; Jokar, Mohammad; Jonas, Jost B.; Joseph, Nitin; Joseph, Abel; Joshua, Charity Ehimwenma; Joukar, Farahnaz; Jozwiak, Jacek Jerzy; Kaambwa, Billingsley; Kabir, Ali; Kabthymer, Robel Hussen; Kadashetti, Vidya; Kahe, Farima; Kalhor, Rohollah; Kandel, Himal; Karanth, Shama D.; Karaye, Ibraheem M.; Karkhah, Samad; Katoto, Patrick D. M. C.; Kaur, Navjot; Kazemian, Sina; Kebede, Sewnet Adem; Khader, Yousef Saleh; Khajuria, Himanshu; Khalaji, Amirmohammad; Khan, Moien A. B.; Khan, Maseer; Khan, Ajmal; Khanal, Saval; Khatatbeh, Moawiah Mohammad; Khater, Amir M.; Khateri, Sorour; Khorashadizadeh, Fatemeh; Khubchandani, Jagdish; Kibret, Biruk Getahun; Kim, Min Seo; Kimokoti, Ruth W.; Kisa, Adnan; Kivimaki, Mika; Kolahi, Ali-Asghar; Komaki, Somayeh; Kompani, Farzad; Koohestani, Hamid Reza; Korzh, Oleksii; Kostev, Karel; Kothari, Nikhil; Koyanagi, Ai; Krishan, Kewal; Krishnamoorthy, Yuvaraj; Defo, Barthelemy Kuate; Kuddus, Mohammed; Kuddus, Md Abdul; Kumar, Rakesh; Kumar, Harish; Kundu, Satyajit; Kurniasari, Maria Dyah; Kuttikkattu, Ambily; Vecchia, Carlo La; Lallukka, Tea; Larijani, Bagher; Larsson, Anders O.; Latief, Kamaluddin; Lawal, Basira Kankia; Le, Thao Thi Thu; Le, Trang Thi Bich; Lee, Shaun Wen Huey; Lee, Munjae; Lee, Wei-Chen; Lee, Paul H.; Lee, Sang-Woong; Lee, Seung Won; Legesse, Samson Mideksa; Lenzi, Jacopo; Li, Yongze; Li, Ming-Chieh; Lim, Stephen S.; Lim, Lee-Ling; Liu, Xuefeng; Liu, Chaojie; Lo, Chun-Han; Lopes, Graciliana; Lorkowski, Stefan; Lozano, Rafael; Lucchetti, Giancarlo; Maghazachi, Azzam A.; Mahasha, Phetole Walter; Mahjoub, Soleiman; Mahmoud, Mansour Adam; Mahmoudi, Razzagh; Mahmoudimanesh, Marzieh; Mai, Anh Tuan; Majeed, Azeem; Sanaye, Pantea Majma; Makris, Konstantinos Christos; Malhotra, Kashish; Malik, Ahmad Azam; Malik, Iram; Mallhi, Tauqeer Hussain; Malta, Deborah Carvalho; Mamun, Abdullah A.; Mansouri, Borhan; Marateb, Hamid Reza; Mardi, Parham; Martini, Santi; Martorell, Miquel; Marzo, Roy Rillera; Masoudi, Reza; Masoudi, Sahar; Mathews, Elezebeth; Maugeri, Andrea; Mazzaglia, Giampiero; Mekonnen, Teferi; Meshkat, Mahboobeh; Mestrovic, Tomislav; Jonasson, Junmei Miao; Miazgowski, Tomasz; Michalek, Irmina Maria; Minh, Le Huu Nhat; Mini, G.K.; Miranda, J. Jaime; Mirfakhraie, Reza; Mirrakhimov, Erkin M.; Mirza-Aghazadeh-Attari, Mohammad; Misganaw, Awoke; Misgina, Kebede Haile; Mishra, Manish; Moazen, Babak; Mohamed, Nouh Saad; Mohammadi, Esmaeil; Mohammadi, Mohsen; Mohammadian-Hafshejani, Abdollah; Mohammadshahi, Marita; Mohseni, Alireza; Mojiri-Forushani, Hoda; Mokdad, Ali H.; Momtazmanesh, Sara; Monasta, Lorenzo; Moniruzzaman, Md; Mons, Ute; Montazeri, Fateme; Ghalibaf, AmirAli Moodi; Moradi, Yousef; Moradi, Maryam; Sarabi, Mostafa Moradi; Morovatdar, Negar; Morrison, Shane Douglas; Morze, Jakub; Mossialos, Elias; Mostafavi, Ebrahim; Mueller, Ulrich Otto; Mulita, Francesk; Mulita, Admir; Murillo-Zamora, Efren; Musa, Kamarul Imran; Mwita, Julius C.; Nagaraju, Shankar Prasad; Naghavi, Mohsen; Nainu, Firzan; Nair, Tapas Sadasivan; Najmuldeen, Hastyar Hama Rashid; Nangia, Vinay; Nargus, Shumaila; Naser, Abdallah Y.; Nassereldine, Hasan; Natto, Zuhair S.; Nauman, Javaid; Nayak, Biswa Prakash; Ndejjo, Rawlance; Negash, Hadush; Negoi, Ruxandra Irina; Nguyen, Hau Thi Hien; Nguyen, Dang H.; Nguyen, Phat Tuan; Nguyen, Van Thanh; Nguyen, Hien Quang; Niazi, Robina Khan; Nigatu, Yeshambel T.; Ningrum, Dina Nur Anggraini; Nizam, Muhammad A.; Nnyanzi, Lawrence Achilles; Noreen, Mamoona; Noubiap, Jean Jacques; Nzoputam, Ogochukwu Janet; Nzoputam, Chimezie Igwegbe; Oancea, Bogdan; Odogwu, Nkechi Martina; Odukoya, Oluwakemi Ololade; Ojha, Vivek Anand; Okati-Aliabad, Hassan; Okekunle, Akinkunmi Paul; Okonji, Osaretin Christabel; Okwute, Patrick Godwin; Olufadewa, Isaac Iyinoluwa; Onwujekwe, Obinna E.; Ordak, Michal; Ortiz, Alberto; Osuagwu, Uchechukwu Levi; Oulhaj, Abderrahim; Owolabi, Mayowa O.; Padron-Monedero, Alicia; Padubidri, Jagadish Rao; Palladino, Raffaele; Panagiotakos, Demosthenes; Panda-Jonas, Songhomitra; Pandey, Ashok; Pandey, Anamika; Pandi-Perumal, Seithikurippu R.; Stoian, Anca Mihaela Pantea; Pardhan, Shahina; Parekh, Tarang; Parekh, Utsav; Pasovic, Maja; Patel, Jay; Patel, Jenil R.; Paudel, Uttam; Pepito, Veincent Christian Filipino; Pereira, Marcos; Perico, Norberto; Perna, Simone; Petcu, Ionela-Roxana; Petermann-Rocha, Fanny Emily; Podder, Vivek; Postma, Maarten J.; Pourali, Ghazaleh; Pourtaheri, Naeimeh; Prates, Elton Junio Sady; Qadir, Mirza Muhammad Fahd; Qattea, Ibrahim; Raee, Pourya; Rafique, Ibrar; Rahimi, Mehran; Rahimifard, Mahban; Rahimi-Movaghar, Vafa; Rahman, Md Obaidur; Rahman, Muhammad Aziz; Rahman, Mohammad Hifz Ur; Rahman, Mosiur; Rahman, Md Mosfequr; Rahmani, Mohamed; Rahmani, Shayan; Rahmanian, Vahid; Rahmawaty, Setyaningrum; Rahnavard, Niloufar; Rajbhandari, Bibek; Ram, Pradhum; Ramazanu, Sheena; Rana, Juwel; Rancic, Nemanja; Ranjha, Muhammad Modassar Ali Nawaz; Rao, Chythra R.; Rapaka, Deepthi; Rasali, Drona Prakash; Rashedi, Sina; Rashedi, Vahid; Rashid, Ahmed Mustafa; Rashidi, Mohammad-Mahdi; Ratan, Zubair Ahmed; Rawaf, Salman; Rawal, Lal; Redwan, Elrashdy Moustafa Mohamed; Remuzzi, Giuseppe; Rengasamy, Kannan R. R.; Renzaho, Andre M. N.; Reyes, Luis Felipe; Rezaei, Nima; Rezaei, Nazila; Rezaeian, Mohsen; Rezazadeh, Hossein; Riahi, Seyed Mohammad; Rias, Yohanes Andy; Riaz, Muhammad; Ribeiro, Daniela; Rodrigues, Monica; Rodriguez, Jefferson Antonio Buendia; Roever, Leonardo; Rohloff, Peter; Roshandel, Gholamreza; Roustazadeh, Abazar; Rwegerera, Godfrey M.; Saad, Aly M. A.; Saber-Ayad, Maha Mohamed; Sabour, Siamak; Sabzmakan, Leila; Saddik, Basema; Sadeghi, Erfan; Saeed, Umar; Moghaddam, Sahar Saeedi; Safi, Sare; Safi, Sher Zaman; Saghazadeh, Amene; Sharif-Askari, Narjes Saheb; Sharif-Askari, Fatemeh Saheb; Sahebkar, Amirhossein; Sahoo, Soumya Swaroop; Sahoo, Harihar; Saif-Ur-Rahman, K.M.; Sajid, Mirza Rizwan; Salahi, Sarvenaz; Salahi, Saina; Saleh, Mohamed A.; Salehi, Mohammad Amin; Salomon, Joshua A.; Sanabria, Juan; Sanjeev, Rama Krishna; Sanmarchi, Francesco; Santric-Milicevic, Milena M.; Sarasmita, Made Ary; Sargazi, Saman; Sathian, Brijesh; Sathish, Thirunavukkarasu; Sawhney, Monika; Schlaich, Markus P.; Schmidt, Maria Ines; Schuermans, Art; Seidu, Abdul-Aziz; Kumar, Nachimuthu Senthil; Sepanlou, Sadaf G.; Sethi, Yashendra; Seylani, Allen; Shabany, Maryam; Shafaghat, Tahereh; Shafeghat, Melika; Shafie, Mahan; Shah, Nilay S.; Shahid, Samiah; Shaikh, Masood Ali; Shanawaz, Mohd; Shannawaz, Mohammed; Sharfaei, Sadaf; Shashamo, Bereket Beyene; Shiri, Rahman; Shittu, Aminu; Shivakumar, K.M.; Shivalli, Siddharudha; Shobeiri, Parnian; Shokri, Fereshteh; Shuval, Kerem; Sibhat, Migbar Mekonnen; Silva, Luis Manuel Lopes Rodrigues; Simpson, Colin R.; Singh, Jasvinder A.; Singh, Paramdeep; Singh, Surjit; Siraj, Md Shahjahan; Skryabina, Anna Aleksandrovna; Sohag, Abdullah Al Mamun; Soleimani, Hamidreza; Solikhah, Solikhah; Soltani-Zangbar, Mohammad Sadegh; Somayaji, Ranjani; Sorensen, Reed J. D.; Starodubova, Antonina V.; Sujata, Sujata; Suleman, Muhammad; Sun, Jing; Sundstr�m, Johan; Tabar�s-Seisdedos, Rafael; Tabatabaei, Seyyed Mohammad; Tabatabaeizadeh, Seyed-Amir; Tabish, Mohammad; Taheri, Majid; Taheri, Ensiyeh; Taki, Elahe; Tamuzi, Jacques J. L. Lukenze; Tan, Ker-Kan; Tat, Nathan Y.; Taye, Birhan Tsegaw; Temesgen, Worku Animaw; Temsah, Mohamad-Hani; Tesler, Riki; Thangaraju, Pugazhenthan; Thankappan, Kavumpurathu Raman; Thapa, Rajshree; Tharwat, Samar; Thomas, Nihal; Ticoalu, Jansje Henny Vera; Tiyuri, Amir; Tonelli, Marcello; Tovani-Palone, Marcos Roberto; Trico, Domenico; Trihandini, Indang; Tripathy, Jaya Prasad; Tromans, Samuel Joseph; Tsegay, Guesh Mebrahtom; Tualeka, Abdul Rohim; Tufa, Derara Girma; Tyrovolas, Stefanos; Ullah, Sana; Upadhyay, Era; Vahabi, Seyed Mohammad; Vaithinathan, Asokan Govindaraj; Valizadeh, Rohollah; van Daalen, Kim Robin; Vart, Priya; Varthya, Shoban Babu; Vasankari, Tommi Juhani; Vaziri, Siavash; Verma, Madhur Verma; Verras, Georgios-Ioannis; Vo, Danh Cao; Wagaye, Birhanu; Waheed, Yasir; Wang, Ziyue; Wang, Yanqing; Wang, Cong; Wang, Fang; Wassie, Gizachew Tadesse; Wei, Melissa Y. Wei; Weldemariam, Abrha Hailay; Westerman, Ronny; Wickramasinghe, Nuwan Darshana; Wu, YiFan; Wulandari, Ratna D. W. I.; Xia, Juan; Xiao, Hong; Xu, Suowen; Xu, Xiaoyue; Yada, Dereje Y.; Yang, Lin; Yatsuya, Hiroshi; Yesiltepe, Metin; Yi, Siyan; Yohannis, Hunachew Kibret; Yonemoto, Naohiro; You, Yuyi; Zaman, Sojib Bin; Zamora, Nelson; Zare, Iman; Zarea, Kourosh; Zarrintan, Armin; Zastrozhin, Mikhail Sergeevich; Zeru, Naod Gebrekrstos; Zhang, Zhi-Jiang; Zhong, Chenwen; Zhou, Jingjing; Zieli?ska, Magdalena; Zikarg, Yossef Teshome; Zodpey, Sanjay; Zoladl, Mohammad; Zou, Zhiyong; Zumla, Alimuddin; Zuniga, Yves Miel H.; Magliano, Dianna J.; Murray, Christopher J. L.; Hay, Simon I.; Vos, TheoBackground: Diabetes is one of the leading causes of death and disability worldwide, and affects people regardless of country, age group, or sex. Using the most recent evidentiary and analytical framework from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD), we produced location-specific, age-specific, and sex-specific estimates of diabetes prevalence and burden from 1990 to 2021, the proportion of type 1 and type 2 diabetes in 2021, the proportion of the type 2 diabetes burden attributable to selected risk factors, and projections of diabetes prevalence through 2050. Methods: Estimates of diabetes prevalence and burden were computed in 204 countries and territories, across 25 age groups, for males and females separately and combined; these estimates comprised lost years of healthy life, measured in disability-adjusted life-years (DALYs; defined as the sum of years of life lost [YLLs] and years lived with disability [YLDs]). We used the Cause of Death Ensemble model (CODEm) approach to estimate deaths due to diabetes, incorporating 25 666 location-years of data from vital registration and verbal autopsy reports in separate total (including both type 1 and type 2 diabetes) and type-specific models. Other forms of diabetes, including gestational and monogenic diabetes, were not explicitly modelled. Total and type 1 diabetes prevalence was estimated by use of a Bayesian meta-regression modelling tool, DisMod-MR 2.1, to analyse 1527 location-years of data from the scientific literature, survey microdata, and insurance claims; type 2 diabetes estimates were computed by subtracting type 1 diabetes from total estimates. Mortality and prevalence estimates, along with standard life expectancy and disability weights, were used to calculate YLLs, YLDs, and DALYs. When appropriate, we extrapolated estimates to a hypothetical population with a standardised age structure to allow comparison in populations with different age structures. We used the comparative risk assessment framework to estimate the risk-attributable type 2 diabetes burden for 16 risk factors falling under risk categories including environmental and occupational factors, tobacco use, high alcohol use, high body-mass index (BMI), dietary factors, and low physical activity. Using a regression framework, we forecast type 1 and type 2 diabetes prevalence through 2050 with Socio-demographic Index (SDI) and high BMI as predictors, respectively. Findings: In 2021, there were 529 million (95% uncertainty interval [UI] 500�564) people living with diabetes worldwide, and the global age-standardised total diabetes prevalence was 6�1% (5�8�6�5). At the super-region level, the highest age-standardised rates were observed in north Africa and the Middle East (9�3% [8�7�9�9]) and, at the regional level, in Oceania (12�3% [11�5�13�0]). Nationally, Qatar had the world's highest age-specific prevalence of diabetes, at 76�1% (73�1�79�5) in individuals aged 75�79 years. Total diabetes prevalence�especially among older adults�primarily reflects type 2 diabetes, which in 2021 accounted for 96�0% (95�1�96�8) of diabetes cases and 95�4% (94�9�95�9) of diabetes DALYs worldwide. In 2021, 52�2% (25�5�71�8) of global type 2 diabetes DALYs were attributable to high BMI. The contribution of high BMI to type 2 diabetes DALYs rose by 24�3% (18�5�30�4) worldwide between 1990 and 2021. By 2050, more than 1�31 billion (1�22�1�39) people are projected to have diabetes, with expected age-standardised total diabetes prevalence rates greater than 10% in two super-regions: 16�8% (16�1�17�6) in north Africa and the Middle East and 11�3% (10�8�11�9) in Latin America and Caribbean. By 2050, 89 (43�6%) of 204 countries and territories will have an age-standardised rate greater than 10%. Interpretation: Diabetes remains a substantial public health issue. Type 2 diabetes, which makes up the bulk of diabetes cases, is largely preventable and, in some cases, potentially reversible if identified and managed early in the disease course. However, all evidence indicates that diabetes prevalence is increasing worldwide, primarily due to a rise in obesity caused by multiple factors. Preventing and controlling type 2 diabetes remains an ongoing challenge. It is essential to better understand disparities in risk factor profiles and diabetes burden across populations, to inform strategies to successfully control diabetes risk factors within the context of multiple and complex drivers. Funding: Bill & Melinda Gates Foundation. � 2023 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licenseItem Variants in KCNQ1 increase type II diabetes susceptibility in South Asians: A study of 3,310 subjects from India and the US(2011) Been, L.F.; Ralhan, S.; Wander, G.S.; Mehra, N.K.; Singh, J.; Mulvihill, J.J.; Aston, C.E.; Sanghera, D.K.Background: Polymorphisms in intron 15 of potassium voltage-gated channel, KQT-like subfamily member 1 (KCNQ1) gene have been associated with type II diabetes (T2D) in Japanese genome-wide association studies (GWAS). More recently a meta-analysis of European GWAS has detected a new independent signal associated with T2D in intron 11 of the KCNQ1 gene. The purpose of this investigation is to examine the role of these variants with T2D in populations of Asian Indian descent from India and the US.Methods: We examined the association between four variants in the KCNQ1 gene with T2D and related quantitative traits in a total of 3,310 Asian Indian participants from two different cohorts comprising 2,431 individuals of the Punjabi case-control cohort from the Sikh Diabetes Study and 879 migrant Asian Indians living in the US.Results: Our data confirmed the association of a new signal at the KCNQ1 locus (rs231362) with T2D showing an allelic odds ratio (OR) of 1.24 95%CI [1.08-1.43], p = 0.002 in the Punjabi cohort. A moderate association with T2D was also seen for rs2237895 in the Punjabi (OR 1.14; p = 0.036) and combined cohorts (meta-analysis OR 1.14; p = 0.018). Three-site haplotype analysis of rs231362, rs2237892, rs2237895 exhibited considerably stronger evidence of association of the GCC haplotype with T2D showing OR of 1.24 95%CI [1.00-1.53], p = 0.001, permutation p = 8 ? 10-4in combined cohorts. The 'C' risk allele carriers of rs2237895 had significantly reduced measures of HOMA-B in the US cohort (p = 0.008) as well as in combined cohort in meta-analysis (p = 0.009).Conclusions: Our investigation has confirmed that the variation within the KCNQ1 locus confers a significant risk to T2D among Asian Indians. Haplotype analysis further suggested that the T2D risk associated with KCNQ1 SNPs may be derived from 'G' allele of rs231362 and 'C' allele of rs2237895 and this appears to be mediated through ? cell function. ? 2011 Been et al; licensee BioMed Central Ltd.Item Shared and unique common genetic determinants between pediatric and adult celiac disease(BioMed Central Ltd., 2016) Senapati, S.; Sood, A.; Midha, V.; Sood, N.; Sharma, S.; Kumar, L.; Thelma, B.K.Background: Based on age of presentation, celiac disease (CD) is categorised as pediatric CD and adult CD. It however remains unclear if these are genetically and/or phenotypically distinct disorders or just different spectrum of the same disease. We therefore explored the common genetic components underlying pediatric and adult CD in a well characterized north Indian cohort. Methods: A retrospective analysis of children (n = 531) and adult (n = 871) patients with CD between January 2001 and December 2010 was done. The database included basic demographic characteristics, clinical presentations, associated diseases and complications, if any. The genotype dataset was acquired for children (n = 217) and adult CD patients (n = 340) and controls (n = 736) using Immunochip. Association analysis was performed using logistic regression model to identify susceptibility genetic variants. Results: The predominant form of CD was classical CD in both pediatric and adult CD groups. There was remarkable similarity between pediatric and adult CD except for quantitative differences between the two groups such as female preponderance, non-classical presentation, co-occurrence of other autoimmune diseases being more common amongst adult CD. Notably, same HLA-DQ2 and -DQ8 haplotypes were established as the major risk factors in both types of CD. In addition, a few suggestively associated (p < 5 ? 10-4) non-HLA markers were identified of which only ANK3 (rs4948256-A; rs10994257-T) was found to be shared and explain risk for ?45 % of CD patients with HLA allele. Discussion: Overall phenotypic similarity between pediatric and adult CD groups can be explained by contribution of same HLA risk alleles. Different non-HLA genes/loci with minor risk seem to play crucial role in disease onset and extra intestinal manifestation of CD. None of the non-HLA risk variants reached genome-wide significance, however most of them were shown to have functional implication to disease pathogenesis. Functional relevance of our findings needs to be investigated to address clinical heterogeneity of CD. Conclusions: This present study is the first comparative study based on common genetic markers to suggest that CD in pediatric age group and in adults are the spectrum of the same disease with novel and shared genetic risk determinants. Follow-up fine mapping studies with larger study cohorts are warranted for further genetic investigation. ? 2016 The Author(s).Item Role of TLR4 (C1196T) and CD14 (C-260T) Polymorphisms in Development of Ischemic Stroke, Its Subtypes and Hemorrhagic Stroke(Springer New York LLC, 2017) Das, Satrupa; Kaul, & Subhash; Jyothy, Akka; Munshi, AnjanaIn the present study, we evaluated the association of TLR4 and CD14 polymorphisms, i.e. C1196T and C-260T, respectively, with ischemic stroke (n?=?700), its subtypes and hemorrhagic stroke (n?=?300) in a South Indian population from Telangana. The genotypes were determined using PCR?RFLP, and the strength of association between genotypes and stroke was determined by odds ratio with 95% confidence interval (CI) and chi-square analysis. The results revealed a lack of association for TLR4 variant with ischemic stroke and hemorrhagic stroke, although a significant association was observed with the subtypes extracranial large artery (p?=?0.008), other determined aetiology (p?=?0.03) and undetermined aetiology (p?=?0.01). Investigations on the variant of CD14 gene revealed negative association among ischemic stroke patients; however, a significant association was observed for hemorrhagic stroke following dominant and recessive genotypic model (p?=?0.05, p?=?0.02). Among ischemic stroke subtype, a significant association was observed with intracranial large artery, extracranial large artery, other determined aetiology and undetermined aetiology form of stroke (p?Item PPARG and ADIPOQ gene polymorphisms increase type 2 diabetes mellitus risk in Asian Indian Sikhs: Pro12Ala still remains as the strongest predictor(2010) Sanghera, D.K.; Demirci, F.Y.; Been, L.; Ortega, L.; Ralhan, S.; Wander, G.S.; Mehra, N.K.; Singh, J.; Aston, C.E.; Mulvihill, J.J.; Kamboh, I.M.We have examined the association of 14 tagging single nucleotide polymorphisms (tagSNPs) in peroxisome proliferator activated receptor-? transcripts 1 and 2 (PPARG1 and 2) and 5 tagSNPs in adiponectin (ADIPOQ) genes for their effect on type 2 diabetes mellitus (T2D) risk in Asian Indian Sikhs. A total of 554 T2D cases and 527 normoglycemic controls were examined for association with T2D and other subphenotypes of T2D. With the exception of a strong association of PPARG2/Pro12Ala with T2D (odds ratio, 0.13; 95% confidence interval, 0.03-0.56; P = .0007), no other tagSNP in the PPARG locus revealed any significant association with T2D in this population. Similarly, none of the tagSNPs in the ADIPOQ gene was associated with T2D susceptibility in single-site analysis. However, haplotype analysis provided strong evidence of association of these loci with T2D. Three-site haplotype analysis in the PPARG locus using the 2 marginally associated SNPs (P/rs11715073 and P/rs3892175) in combination with Pro12 Ala (P/rs1801282) revealed a strong association of 1 "risk" (CGC) (P = .003, permutation P = .015) and 1 "protective" (CAC) (P = .001, permutation P = .005) haplotype associated with T2D. However, the major effect still appears to be driven by Pro12Ala, as the association of these haplotypes did not remain significant when analyzed conditional upon Pro12Ala (P = .262). In addition, 2-site haplotype analysis in the ADIPOQ locus using only 2 marginally associated SNPs (AD/rs182052 and AD/rs7649121) revealed a significant protective association of the GA haplotype with T2D (P = .009, permutation P = .026). Multiple linear regression analysis also revealed significant association of an ADIPOQ variant (AD/rs12495941) with total body weight (P = .010), waist (P = .024), and hip (P = .021), although these associations were not significant after adjusting for multiple testing. Our new findings strongly suggest that the genetic variation in PPARG and ADIPOQ loci could contribute to the risk for the development of T2D in Indian Sikhs. Identification of causal SNPs in these important biological and positional candidate genes would help determine the true physiologic significance of these loci in T2D and obesity. ? 2010 Elsevier Inc. All rights reserved.Item Oxidative stress in the development of genetic generalised epilepsy: An observational study in southern Indian population(Journal of Clinical and Diagnostic Research, 2017) Prasad, D.K.V.; Satyanarayana, U.; Shaheen, U.; Surya Prabha, T.; Munshi, A.Introduction: Oxidative stress resulting from excessive generation of Reactive Oxygen Species (ROS) plays a significant role in neurodegeneration associated with seizures/epilepsy. Aim: To evaluate oxidative stress markers and antioxidant enzymes in Genetic Generalised Epilepsy (GGE) and to know the extent of oxidative stress induced by Anti-Epileptic Drugs (AEDs) with the time duration of treatment. Materials and Methods: In this case-control study, 310 GGE patients (male:female=203:107), who were on AED treatment (n=235) and 75 untreated patients (male:female=49:26) along with 310 age and sex matched healthy controls were recruited. Oxidative stress markers such as Nitric Oxide (NO), Malondialdehyde (MDA) and antioxidant enzyme activities namely Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx) and Catalase (CAT) were measured spectrophotometrically. Results: Significantly higher levels of serum NO, MDA and low levels of plasma Total Antioxidant Capacity (TAC) were found in patients as compared to controls (p<0.001) whereas erythrocyte SOD, CAT and GPx activities were found to be significantly low in patients when compared to the control group (p<0.001). Statistically significant higher levels of NO, MDA and lower levels of SOD, CAT and TAC were observed in patients subgroup, who were on AEDs for more than >5 years compared to other groups (? 1 year and 1-? 5 years) (p=0.02, p=0.01, p=0.001, p=0.01 and p=0.05 respectively). Further, significant increase in the levels of NO, MDA and decreased activities of SOD, CAT were found in treated patients compared to untreated patients (p<0.05) denoting that additional oxidative stress induced by AEDs which results in seizure recurrence and drug intractability. Conclusion: Our study demonstrated that GGE patients have additional oxidative stress due to AEDs and decreased antioxidant enzyme activities causing an imbalance between oxidant and antioxidant status, which might contribute to the pathogenesis of GGE. ? 2017, Journal of Clinical and Diagnostic Research. All rights reserved.Item Interleukin 1ß (+3954, -511 and -31) polymorphism in chronic periodontitis patients from North India(Informa Healthcare, 2015) Amirisetty, Ramesh; Patel, Ritu Prabha; Das, Satrupa; Saraf, Jitendra; Jyothy, Akka; Munshi, AnjanaObjective. Several studies have implicated the role of interleukin-1 in various chronic diseases including periodontitis. The present study was carried out with an aim to evaluate the role of interleukin 1? polymorphisms, namely +3954C/T, -511C/T and -31T/C, in the development of chronic periodontitis. Materials and methods. Twenty-nine chronic periodontitis patients and 31 healthy controls of North Indian origin from Chhattisgarh were recruited for the study. The genotypes for the three variants were determined using the PCR-RFLP technique and the strength of association between genotypes and periodontitis was determined by odds ratio with 95% confidence interval (CI) and chi-square analysis. Results. Analysis for the +3954 allelic and genotypic frequencies of the polymorphism revealed a significant difference in the CT genotype between periodontitits patients and controls (p = 0.03). A significant difference was also observed in the allelic frequencies between the two groups (p = 0.02). For the -511 site, TT genotype revealed a significant association with the disease (p = 0.01). A significant association was also found following the co-dominant model (p = 0.007). However, the -31 polymorphism revealed no significant difference between patients and controls. Conclusions. In conclusion, the present study suggests a strong association of the TT genotype of -511 and CT genotype of +3954 variant of interleukin 1? with chronic periodontitis. However, the -31 variant did not show a significant association with the disease. ? Informa Healthcare.Item Genome-wide association study identifies a novel locus contributing to type 2 diabetes susceptibility in Sikhs of Punjabi origin from India(American Diabetes Association Inc., 2013) Saxena, R.; Saleheen, D.; Been, L.F.; Garavito, M.L.; Braun, T.; Bjonnes, A.; Young, R.; Ho, W.K.; Rasheed, A.; Frossard, P.; Sim, X.; Hassanali, N.; Radha, V.; Chidambaram, M.; Liju, S.; Rees, S.D.; Ng, D.P.-K.; Wong, T.-Y.; Yamauchi, T.; Hara, K.; Tanaka, Y.; Hirose, H.; McCarthy, M.I.; Morris, A.P.; Basit, A.; Barnett, A.H.; Katulanda, P.; Matthews, D.; Mohan, V.; Wander, G.S.; Singh, J.R.; Mehra, N.K.; Ralhan, S.; Kamboh, M.I.; Mulvihill, J.J.; Maegawa, H.; Tobe, K.; Maeda, S.; Cho, Y.S.; TaWe performed a genome-wide association study (GWAS) and a multistage meta-analysis of type 2 diabetes (T2D) in Punjabi Sikhs from India. Our discovery GWAS in 1,616 individuals (842 case subjects) was followed by in silico replication of the top 513 independent single nucleotide polymorphisms (SNPs) (P < 10-3) in Punjabi Sikhs (n = 2,819; 801 case subjects). We further replicated 66 SNPs (P < 10-4) through genotyping in a Punjabi Sikh sample (n = 2,894; 1,711 case subjects). On combined meta-analysis in Sikh populations (n = 7,329; 3,354 case subjects), we identified a novel locus in association with T2D at 13q12 represented by a directly genotyped intronic SNP (rs9552911, P = 1.82 ? 10-8) in the SGCG gene. Next, we undertook in silico replication (stage 2b) of the top 513 signals (P < 10-3) in 29,157 non-Sikh South Asians (10,971 case subjects) and de novo genotyping of up to 31 top signals (P < 10-4) in 10,817 South Asians (5,157 case subjects) (stage 3b). In combined South Asian meta-analysis, we observed six suggestive associations (P < 10-5 to < 10-7), including SNPs at HMG1L1/CTCFL, PLXNA4, SCAP, and chr5p11. Further evaluation of 31 top SNPs in 33,707 East Asians (16,746 case subjects) (stage 3c) and 47,117 Europeans (8,130 case subjects) (stage 3d), and joint meta-analysis of 128,127 individuals (44,358 case subjects) from 27 multiethnic studies, did not reveal any additional loci nor was there any evidence of replication for the new variant. Our findings provide new evidence on the presence of a population-specific signal in relation to T2D, which may provide additional insights into T2D pathogenesis. ? 2013 by the American Diabetes Association.Item Association of GABRA6 1519 T>C (rs3219151) and Synapsin II (rs37733634) gene polymorphisms with the development of idiopathic generalized epilepsy(Elsevier, 2014) Prasad, D.K.V.; Shaheen, U.; Satyanarayana, U.; Prabha, T.S.; Jyothy, A.; Munshi, A.The idiopathic generalized epilepsy (IGE) is a neurological disorder which accounts for approximately 30% of all epilepsy cases. Patients identified with IGE syndromes have pharmacoresponsive epilepsies without abnormal neurological symptoms, structural brain lesions and are of unknown origin. A genetic etiology to IGEs has been proposed. Gamma amino butyric acid (GABA), a major inhibitory neurotransmitter acts by binding to transmembrane GABAA and GABAB receptors of both pre- and postsynaptic neurons. Synapsin II (SynII), a neuron specific phosphoprotein plays a major role in synaptogenesis and neurotransmitter release. The present study was carried out with an aim to evaluate the association of GABRA6 (rs3219151) T>C and Syn II (rs37733634) A>G gene polymorphisms with IGE. Molecular analysis revealed that the frequency of 'CC' genotype and 'C'allele of GABRA6 (rs3219151) T>C gene polymorphism was significantly higher in IGE patients compared to healthy controls [CC vs. TT, ?2=26; p<0.001; Odds ratio=3.6 (95% CI; 2.1-5.9); C vs T, ?2=24.7; p<0.001; Odds ratio=1.78 (95% CI; 1.4-2.2)]. The frequency of 'GG' genotype and 'G' allele of the intronic polymorphism A>G in Syn II gene was also found to be significantly associated with the disease when compared to controls [GG vs AA, ?2=64.52; p<0.001; Odds ratio=7.37 (95% CI; 4.4-12.3); G vs. A, ?2=65.78; p<0.001; Odds ratio=2.57 (95% CI; 2.0-3.2)]. The generalized multifactor dimensionality reduction method was employed to detect gene-gene interactions. The gene-gene interaction at two loci involving GABRA6 and Syn II revealed a significant association [?2=36.6, p<0.001, Odds ratio=3.17 (95% CI; 2.2-4.6)] with IGE. Therefore, the present study clearly indicates that both GABRA6 (rs3219151) T>C and Syn II (rs37733634) A>G polymorphisms are important risk factors for the development of IGE in the South Indian population from Andhra Pradesh. The gene-gene interaction studies demonstrated significant interactive effects of these two loci in the development of the disease. ? 2014 Elsevier B.V.