Search

Your search keyword '"Moosavi, Mohammad Amin"' showing total 34 results
Start Over Author "Moosavi, Mohammad Amin" Search Limiters Full Text
34 results on '"Moosavi, Mohammad Amin"'

3. a systematic analysis for the Global Burden of Disease Study 2019

Author

Tran, Khanh Bao, Lang, Justin J, Compton, Kelly, Xu, Rixing, Acheson, Alistair R, Henrikson, Hannah Jacqueline, Kocarnik, Jonathan M, Penberthy, Louise, Aali, Amirali, Abbas, Qamar, Abbasi, Behzad, Abbasi-kangevari, Mohsen, Abbasi-kangevari, Zeinab, Abbastabar, Hedayat, Abdelmasseh, Michael, Abd-elsalam, Sherief, Abdelwahab, Ahmed Abdelwahab, Abdoli, Gholamreza, Abdulkadir, Hanan Abdulkadir, Abedi, Aidin, Abegaz, Kedir Hussein, Abidi, Hassan, Aboagye, Richard Gyan, Abolhassani, Hassan, Absalan, Abdorrahim, Abtew, Yonas Derso, Abubaker Ali, Hiwa, Abu-gharbieh, Eman, Achappa, Basavaprabhu, Acuna, Juan Manuel, Addison, Daniel, Addo, Isaac Yeboah, Adegboye, Oyelola A, Adesina, Miracle Ayomikun, Adnan, Mohammad, Adnani, Qorinah Estiningtyas Sakilah, Advani, Shailesh M, Afrin, Sumia, Afzal, Muhammad Sohail, Aggarwal, Manik, Ahinkorah, Bright Opoku, Ahmad, Araz Ramazan, Ahmad, Rizwan, Ahmad, Sajjad, Ahmad, Sohail, Ahmadi, Sepideh, Ahmed, Haroon, Ahmed, Luai A, Ahmed, Muktar Beshir, Ahmed Rashid, Tarik, Aiman, Wajeeha, Ajami, Marjan, Akalu, Gizachew Taddesse, Akbarzadeh-khiavi, Mostafa, Aklilu, Addis, Akonde, Maxwell, Akunna, Chisom Joyqueenet, Al Hamad, Hanadi, Alahdab, Fares, Alanezi, Fahad Mashhour, Alanzi, Turki M, Alessy, Saleh Ali, Algammal, Abdelazeem M, Al-hanawi, Mohammed Khaled, Alhassan, Robert Kaba, Ali, Beriwan Abdulqadir, Ali, Liaqat, Ali, Syed Shujait, Alimohamadi, Yousef, Alipour, Vahid, Aljunid, Syed Mohamed, Alkhayyat, Motasem, Al-maweri, Sadeq Ali Ali, Almustanyir, Sami, Alonso, Nivaldo, Alqalyoobi, Shehabaldin, Al-raddadi, Rajaa M, Al-rifai, Rami H Hani, Al-sabah, Salman Khalifah, Al-tammemi, Ala'a B, Altawalah, Haya, Alvis-guzman, Nelson, Amare, Firehiwot, Ameyaw, Edward Kwabena, Aminian Dehkordi, Javad Javad, Amirzade-iranaq, Mohammad Hosein, Amu, Hubert, Amusa, Ganiyu Adeniyi, Ancuceanu, Robert, Anderson, Jason A, Animut, Yaregal Animut, Anoushiravani, Amir, Anoushirvani, Ali Arash, Ansari-moghaddam, Alireza, Ansha, Mustafa Geleto, Antony, Benny, Antwi, Maxwell Hubert, Anwar, Sumadi Lukman, Anwer, Razique, Anyasodor, Anayochukwu Edward, Arabloo, Jalal, Arab-zozani, Morteza, Aremu, Olatunde, Argaw, Ayele Mamo, Ariffin, Hany, Aripov, Timur, Arshad, Muhammad, Artaman, Al, Arulappan, Judie, Aruleba, Raphael Taiwo, Aryannejad, Armin, Asaad, Malke, Asemahagn, Mulusew A, Asemi, Zatollah, Asghari-jafarabadi, Mohammad, Ashraf, Tahira, Assadi, Reza, Athar, Mohammad, Athari, Seyyed Shamsadin, Atout, Maha Moh'd Wahbi, Attia, Sameh, Aujayeb, Avinash, Ausloos, Marcel, Avila-burgos, Leticia, Awedew, Atalel Fentahun, Awoke, Mamaru Ayenew, Awoke, Tewachew, Ayala Quintanilla, Beatriz Paulina, Ayana, Tegegn Mulatu, Ayen, Solomon Shitu, Azadi, Davood, Azadnajafabad, Sina, Azami-aghdash, Saber, Azanaw, Melkalem Mamuye, Azangou-khyavy, Mohammadreza, Azari Jafari, Amirhossein, Azizi, Hosein, Azzam, Ahmed Y Y, Babajani, Amirhesam, Badar, Muhammad, Badiye, Ashish D, Baghcheghi, Nayereh, Bagheri, Nader, Bagherieh, Sara, Bahadory, Saeed, Baig, Atif Amin, Baker, Jennifer L, Bakhtiari, Ahad, Bakshi, Ravleen Kaur, Banach, Maciej, Banerjee, Indrajit, Bardhan, Mainak, Barone-adesi, Francesco, Barra, Fabio, Barrow, Amadou, Bashir, Nasir Z, Bashiri, Azadeh, Basu, Saurav, Batiha, Abdul-monim Mohammad, Begum, Aeysha, Bekele, Alehegn Bekele, Belay, Alemayehu Sayih, Belete, Melaku Ashagrie, Belgaumi, Uzma Iqbal, Bell, Arielle Wilder, Belo, Luis, Benzian, Habib, Berhie, Alemshet Yirga, Bermudez, Amiel Nazer C, Bernabe, Eduardo, Bhagavathula, Akshaya Srikanth, Bhala, Neeraj, Bhandari, Bharti Bhandari, Bhardwaj, Nikha, Bhardwaj, Pankaj, Bhattacharyya, Krittika, Bhojaraja, Vijayalakshmi S, Bhuyan, Soumitra S, Bibi, Sadia, Bilchut, Awraris Hailu, Bintoro, Bagas Suryo, Biondi, Antonio, Birega, Mesfin Geremaw Birega, Birhan, Habitu Eshetu, Bjørge, Tone, Blyuss, Oleg, Bodicha, Belay Boda Abule, Bolla, Srinivasa Rao, Boloor, Archith, Bosetti, Cristina, Braithwaite, Dejana, Brauer, Michael, Brenner, Hermann, Briko, Andrey Nikolaevich, Briko, Nikolay Ivanovich, Buchanan, Christina Maree, Bulamu, Norma B, Bustamante-teixeira, Maria Teresa, Butt, Muhammad Hammad, Butt, Nadeem Shafique, Butt, Zahid A, Caetano Dos Santos, Florentino Luciano, Cámera, Luis Alberto, Cao, Chao, Cao, Yin, Carreras, Giulia, Carvalho, Márcia, Cembranel, Francieli, Cerin, Ester, Chakraborty, Promit Ananyo, Charalampous, Periklis, Chattu, Vijay Kumar, Chimed-ochir, Odgerel, Chirinos-caceres, Jesus Lorenzo, Cho, Daniel Youngwhan, Cho, William C S, Christopher, Devasahayam J, Chu, Dinh-toi, Chukwu, Isaac Sunday, Cohen, Aaron J, Conde, Joao, Cortés, Sandra, Costa, Vera Marisa, Cruz-martins, Natália, Culbreth, Garland T, Dadras, Omid, Dagnaw, Fentaw Teshome, Dahlawi, Saad M A, Dai, Xiaochen, Dandona, Lalit, Dandona, Rakhi, Daneshpajouhnejad, Parnaz, Danielewicz, Anna, Dao, An Thi Minh, Darvishi Cheshmeh Soltani, Reza, Darwesh, Aso Mohammad, Das, Saswati, Davitoiu, Dragos Virgil, Davtalab Esmaeili, Elham, De La Hoz, Fernando Pio, Debela, Sisay Abebe, Dehghan, Azizallah, Demisse, Biniyam, Demisse, Fitsum Wolde, Denova-gutiérrez, Edgar, Derakhshani, Afshin, Derbew Molla, Meseret, Dereje, Diriba, Deribe, Kalkidan Solomon, Desai, Rupak, Desalegn, Markos Desalegn, Dessalegn, Fikadu Nugusu, Dessalegni, Samuel Abebe A, Dessie, Gashaw, Desta, Abebaw Alemayehu, Dewan, Syed Masudur Rahman, Dharmaratne, Samath Dhamminda, Dhimal, Meghnath, Dianatinasab, Mostafa, Diao, Nancy, Diaz, Daniel, Digesa, Lankamo Ena, Dixit, Shilpi Gupta, Doaei, Saeid, Doan, Linh Phuong, Doku, Paul Narh, Dongarwar, Deepa, Dos Santos, Wendel Mombaque, Driscoll, Tim Robert, Dsouza, Haneil Larson, Durojaiye, Oyewole Christopher, Edalati, Sareh, Eghbalian, Fatemeh, Ehsani-chimeh, Elham, Eini, Ebrahim, Ekholuenetale, Michael, Ekundayo, Temitope Cyrus, Ekwueme, Donatus U, El Tantawi, Maha, Elbahnasawy, Mostafa Ahmed, Elbarazi, Iffat, Elghazaly, Hesham, Elhadi, Muhammed, El-huneidi, Waseem, Emamian, Mohammad Hassan, Engelbert Bain, Luchuo, Enyew, Daniel Berhanie, Erkhembayar, Ryenchindorj, Eshetu, Tegegne, Eshrati, Babak, Eskandarieh, Sharareh, Espinosa-montero, Juan, Etaee, Farshid, Etemadimanesh, Azin, Eyayu, Tahir, Ezeonwumelu, Ifeanyi Jude, Ezzikouri, Sayeh, Fagbamigbe, Adeniyi Francis, Fahimi, Saman, Fakhradiyev, Ildar Ravisovich, Faraon, Emerito Jose A, Fares, Jawad, Farmany, Abbas, Farooque, Umar, Farrokhpour, Hossein, Fasanmi, Abidemi Omolara, Fatehizadeh, Ali, Fatima, Wafa, Fattahi, Hamed, Fekadu, Ginenus, Feleke, Berhanu Elfu, Ferrari, Allegra Allegra, Ferrero, Simone, Ferro Desideri, Lorenzo, Filip, Irina, Fischer, Florian, Foroumadi, Roham, Foroutan, Masoud, Fukumoto, Takeshi, Gaal, Peter Andras, Gad, Mohamed M, Gadanya, Muktar A, Gaipov, Abduzhappar, Galehdar, Nasrin, Gallus, Silvano, Garg, Tushar, Gaspar Fonseca, Mariana, Gebremariam, Yosef Haile, Gebremeskel, Teferi Gebru, Gebremichael, Mathewos Alemu, Geda, Yohannes Fikadu, Gela, Yibeltal Yismaw, Gemeda, Belete Negese Belete, Getachew, Melaku, Getachew, Motuma Erena, Ghaffari, Kazem, Ghafourifard, Mansour, Ghamari, Seyyed-hadi, Ghasemi Nour, Mohammad, Ghassemi, Fariba, Ghimire, Ajnish, Ghith, Nermin, Gholamalizadeh, Maryam, Gholizadeh Navashenaq, Jamshid, Ghozy, Sherief, Gilani, Syed Amir, Gill, Paramjit Singh, Ginindza, Themba G, Gizaw, Abraham Tamirat T, Glasbey, James C, Godos, Justyna, Goel, Amit, Golechha, Mahaveer, Goleij, Pouya, Golinelli, Davide, Golitaleb, Mohamad, Gorini, Giuseppe, Goulart, Bárbara Niegia Garcia, Grosso, Giuseppe, Guadie, Habtamu Alganeh, Gubari, Mohammed Ibrahim Mohialdeen, Gudayu, Temesgen Worku, Guerra, Maximiliano Ribeiro, Gunawardane, Damitha Asanga, Gupta, Bhawna, Gupta, Sapna, Gupta, Veer Bala, Gupta, Vivek Kumar, Gurara, Mekdes Kondale, Guta, Alemu, Habibzadeh, Parham, Haddadi Avval, Atlas, Hafezi-nejad, Nima, Hajj Ali, Adel, Haj-mirzaian, Arvin, Halboub, Esam S, Halimi, Aram, Halwani, Rabih, Hamadeh, Randah R, Hameed, Sajid, Hamidi, Samer, Hanif, Asif, Hariri, Sanam, Harlianto, Netanja I, Haro, Josep Maria, Hartono, Risky Kusuma, Hasaballah, Ahmed I, Hasan, S M Mahmudul, Hasani, Hamidreza, Hashemi, Seyedeh Melika, Hassan, Abbas M, Hassanipour, Soheil, Hayat, Khezar, Heidari, Golnaz, Heidari, Mohammad, Heidarymeybodi, Zahra, Herrera-serna, Brenda Yuliana, Herteliu, Claudiu, Hezam, Kamal, Hiraike, Yuta, Hlongwa, Mbuzeleni Mbuzeleni, Holla, Ramesh, Holm, Marianne, Horita, Nobuyuki, Hoseini, Mohammad, Hossain, Md Mahbub, Hossain, Mohammad Bellal Hossain, Hosseini, Mohammad-salar, Hosseinzadeh, Ali, Hosseinzadeh, Mehdi, Hostiuc, Mihaela, Hostiuc, Sorin, Househ, Mowafa, Huang, Junjie, Hugo, Fernando N, Humayun, Ayesha, Hussain, Salman, Hussein, Nawfal R, Hwang, Bing-fang, Ibitoye, Segun Emmanuel, Iftikhar, Pulwasha Maria, Ikuta, Kevin S, Ilesanmi, Olayinka Stephen, Ilic, Irena M, Ilic, Milena D, Immurana, Mustapha, Innos, Kaire, Iranpour, Pooya, Irham, Lalu Muhammad, Islam, Md Shariful, Islam, Rakibul M, Islami, Farhad, Ismail, Nahlah Elkudssiah, Isola, Gaetano, Iwagami, Masao, J, Linda Merin, Jaiswal, Abhishek, Jakovljevic, Mihajlo, Jalili, Mahsa, Jalilian, Shahram, Jamshidi, Elham, Jang, Sung-in, Jani, Chinmay T, Javaheri, Tahereh, Jayarajah, Umesh Umesh, Jayaram, Shubha, Jazayeri, Seyed Behzad, Jebai, Rime, Jemal, Bedru, Jeong, Wonjeong, Jha, Ravi Prakash, Jindal, Har Ashish, John-akinola, Yetunde O, Jonas, Jost B, Joo, Tamas, Joseph, Nitin, Joukar, Farahnaz, Jozwiak, Jacek Jerzy, Jürisson, Mikk, Kabir, Ali, Kacimi, Salah Eddine Oussama, Kadashetti, Vidya, Kahe, Farima, Kakodkar, Pradnya Vishal, Kalankesh, Laleh R, Kalankesh, Leila R, Kalhor, Rohollah, Kamal, Vineet Kumar, Kamangar, Farin, Kamath, Ashwin, Kanchan, Tanuj, Kandaswamy, Eswar, Kandel, Himal, Kang, Hyejung, Kanno, Girum Gebremeskel, Kapoor, Neeti, Kar, Sitanshu Sekhar, Karanth, Shama D, Karaye, Ibraheem M, Karch, André, Karimi, Amirali, Kassa, Bekalu Getnet, Katoto, Patrick Dmc, Kauppila, Joonas H, Kaur, Harkiran, Kebede, Abinet Gebremickael, Keikavoosi-arani, Leila, Kejela, Gemechu Gemechu, Kemp Bohan, Phillip M, Keramati, Maryam, Keykhaei, Mohammad, Khajuria, Himanshu, Khan, Abbas, Khan, Abdul Aziz Khan, Khan, Ejaz Ahmad, Khan, Gulfaraz, Khan, Md Nuruzzaman, Khan, Moien Ab, Khanali, Javad, Khatab, Khaled, Khatatbeh, Moawiah Mohammad, Khatib, Mahalaqua Nazli, Khayamzadeh, Maryam, Khayat Kashani, Hamid Reza, Khazeei Tabari, Mohammad Amin, Khezeli, Mehdi, Khodadost, Mahmoud, Kim, Min Seo, Kim, Yun Jin, Kisa, Adnan, Kisa, Sezer, Klugar, Miloslav, Klugarová, Jitka, Kolahi, Ali-asghar, Kolkhir, Pavel, Kompani, Farzad, Koul, Parvaiz A, Koulmane Laxminarayana, Sindhura Lakshmi, Koyanagi, Ai, Krishan, Kewal, Krishnamoorthy, Yuvaraj, Kucuk Bicer, Burcu, Kugbey, Nuworza, Kulimbet, Mukhtar, Kumar, Akshay, Kumar, G Anil, Kumar, Narinder, Kurmi, Om P, Kuttikkattu, Ambily, La Vecchia, Carlo, Lahiri, Arista, Lal, Dharmesh Kumar, Lám, Judit, Lan, Qing, Landires, Iván, Larijani, Bagher, Lasrado, Savita, Lau, Jerrald, Lauriola, Paolo, Ledda, Caterina, Lee, Sang-woong, Lee, Shaun Wen Huey, Lee, Wei-chen, Lee, Yeong Yeh, Lee, Yo Han, Legesse, Samson Mideksa, Leigh, James, Leong, Elvynna, Li, Ming-chieh, Lim, Stephen S, Liu, Gang, Liu, Jue, Lo, Chun-han, Lohiya, Ayush, Lopukhov, Platon D, Lorenzovici, László, Lotfi, Mojgan, Loureiro, Joana A, Lunevicius, Raimundas, Madadizadeh, Farzan, Mafi, Ahmad R, Magdeldin, Sameh, Mahjoub, Soleiman, Mahmoodpoor, Ata, Mahmoudi, Morteza, Mahmoudimanesh, Marzieh, Mahumud, Rashidul Alam, Majeed, Azeem, Majidpoor, Jamal, Makki, Alaa, Makris, Konstantinos Christos, Malakan Rad, Elaheh, Malekpour, Mohammad-reza, Malekzadeh, Reza, Malik, Ahmad Azam, Mallhi, Tauqeer Hussain, Mallya, Sneha Deepak, Mamun, Mohammed A, Manda, Ana Laura, Mansour-ghanaei, Fariborz, Mansouri, Borhan, Mansournia, Mohammad Ali, Mantovani, Lorenzo Giovanni, Martini, Santi, Martorell, Miquel, Masoudi, Sahar, Masoumi, Seyedeh Zahra, Matei, Clara N, Mathews, Elezebeth, Mathur, Manu Raj, Mathur, Vasundhara, Mckee, Martin, Meena, Jitendra Kumar, Mehmood, Khalid, Mehrabi Nasab, Entezar, Mehrotra, Ravi, Melese, Addisu, Mendoza, Walter, Menezes, Ritesh G, Mengesha, Sisay Derso, Mensah, Laverne G, Mentis, Alexios-fotios A, Mera-mamián, Andry Yasmid Mera, Meretoja, Tuomo J, Merid, Mehari Woldemariam, Mersha, Amanual Getnet, Meselu, Belsity Temesgen, Meshkat, Mahboobeh, Mestrovic, Tomislav, Miao Jonasson, Junmei, Miazgowski, Tomasz, Michalek, Irmina Maria, Mijena, Gelana Fekadu Worku, Miller, Ted R, Mir, Shabir Ahmad, Mirinezhad, Seyed Kazem, Mirmoeeni, Seyyedmohammadsadeq, Mirza-aghazadeh-attari, Mohammad, Mirzaei, Hamed, Mirzaei, Hamid Reza, Misganaw, Abay Sisay, Misra, Sanjeev, Mohammad, Karzan Abdulmuhsin, Mohammadi, Esmaeil, Mohammadi, Mokhtar, Mohammadian-hafshejani, Abdollah, Mohammadpourhodki, Reza, Mohammed, Arif, Mohammed, Shafiu, Mohan, Syam, Mohseni, Mohammad, Moka, Nagabhishek, Mokdad, Ali H, Molassiotis, Alex, Molokhia, Mariam, Momenzadeh, Kaveh, Momtazmanesh, Sara, Monasta, Lorenzo, Mons, Ute, Montasir, Ahmed Al, Montazeri, Fateme, Montero, Arnulfo, Moosavi, Mohammad Amin, Moradi, Abdolvahab, Moradi, Yousef, Moradi Sarabi, Mostafa, Moraga, Paula, Morawska, Lidia, Morrison, Shane Douglas, Morze, Jakub, Mosapour, Abbas, Mostafavi, Ebrahim, Mousavi, Seyyed Meysam, Mousavi Isfahani, Haleh, Mousavi Khaneghah, Amin, Mpundu-kaambwa, Christine, Mubarik, Sumaira, Mulita, Francesk, Munblit, Daniel, Munro, Sandra B, Murillo-zamora, Efrén, Musa, Jonah, Nabhan, Ashraf F, Nagarajan, Ahamarshan Jayaraman, Nagaraju, Shankar Prasad, Nagel, Gabriele, Naghipour, Mohammadreza, Naimzada, Mukhammad David, Nair, Tapas Sadasivan, Naqvi, Atta Abbas, Narasimha Swamy, Sreenivas, Narayana, Aparna Ichalangod, Nassereldine, Hasan, Natto, Zuhair S, Nayak, Biswa Prakash, Ndejjo, Rawlance, Nduaguba, Sabina Onyinye, Negash, Wogene Wogene, Nejadghaderi, Seyed Aria, Nejati, Kazem, Neupane Kandel, Sandhya, Nguyen, Huy Van Nguyen, Niazi, Robina Khan, Noor, Nurulamin M, Noori, Maryam, Noroozi, Nafise, Nouraei, Hasti, Nowroozi, Ali, Nuñez-samudio, Virginia, Nzoputam, Chimezie Igwegbe, Nzoputam, Ogochukwu Janet, Oancea, Bogdan, Odukoya, Oluwakemi Ololade, Oghenetega, Onome Bright, Ogunsakin, Ropo Ebenezer, Oguntade, Ayodipupo Sikiru, Oh, In-hwan, Okati-aliabad, Hassan, Okekunle, Akinkunmi Paul, Olagunju, Andrew T, Olagunju, Tinuke O, Olakunde, Babayemi Oluwaseun, Olufadewa, Isaac Iyinoluwa, Omer, Emad, Omonisi, Abidemi E Emmanuel, Ong, Sokking, Onwujekwe, Obinna E, Orru, Hans, Otstavnov, Stanislav S, Oulhaj, Abderrahim, Oumer, Bilcha, Owopetu, Oluwatomi Funbi, Oyinloye, Babatunji Emmanuel, P A, Mahesh, Padron-monedero, Alicia, Padubidri, Jagadish Rao, Pakbin, Babak, Pakshir, Keyvan, Pakzad, Reza, Palicz, Tamás, Pana, Adrian, Pandey, Anamika, Pandey, Ashok, Pant, Suman, Pardhan, Shahina, Park, Eun-cheol, Park, Eun-kee, Park, Seoyeon, Patel, Jay, Pati, Siddhartha, Paudel, Rajan, Paudel, Uttam, Paun, Mihaela, Pazoki Toroudi, Hamidreza, Peng, Minjin, Pereira, Jeevan, Pereira, Renato B, Perna, Simone, Perumalsamy, Navaraj, Pestell, Richard G, Pezzani, Raffaele, Piccinelli, Cristiano, Pillay, Julian David, Piracha, Zahra Zahid, Pischon, Tobias, Postma, Maarten J, Pourabhari Langroudi, Ashkan, Pourshams, Akram, Pourtaheri, Naeimeh, Prashant, Akila, Qadir, Mirza Muhammad Fahd, Quazi Syed, Zahiruddin, Rabiee, Mohammad, Rabiee, Navid, Radfar, Amir, Radhakrishnan, Raghu Anekal, Radhakrishnan, Venkatraman, Raeisi, Mojtaba, Rafiee, Ata, Rafiei, Alireza, Raheem, Nasiru, Rahim, Fakher, Rahman, Md Obaidur, Rahman, Mosiur, Rahman, Muhammad Aziz, Rahmani, Amir Masoud, Rahmani, Shayan, Rahmanian, Vahid, Rajai, Nazanin, Rajesh, Aashish, Ram, Pradhum, Ramezanzadeh, Kiana, Rana, Juwel, Ranabhat, Kamal, Ranasinghe, Priyanga, Rao, Chythra R, Rao, Sowmya J, Rashedi, Sina, Rashidi, Amirfarzan, Rashidi, Mahsa, Rashidi, Mohammad-mahdi, Ratan, Zubair Ahmed, Rawaf, David Laith, Rawaf, Salman, Rawal, Lal, Rawassizadeh, Reza, Razeghinia, Mohammad Sadegh, Rehman, Ashfaq Ur, Rehman, Inayat Ur, Reitsma, Marissa B, Renzaho, Andre M N, Rezaei, Maryam, Rezaei, Nazila, Rezaei, Negar, Rezaei, Nima, Rezaei, Saeid, Rezaeian, Mohsen, Rezapour, Aziz, Riad, Abanoub, Rikhtegar, Reza, Rios-blancas, Maria, Roberts, Thomas J, Rohloff, Peter, Romero-rodríguez, Esperanza, Roshandel, Gholamreza, Rwegerera, Godfrey M, S, Manjula, Saber-ayad, Maha Mohamed, Saberzadeh-ardestani, Bahar, Sabour, Siamak, Saddik, Basema, Sadeghi, Erfan, Saeb, Mohammad Reza, Saeed, Umar, Safaei, Mohsen, Safary, Azam, Sahebazzamani, Maryam, Sahebkar, Amirhossein, Sahoo, Harihar, Sajid, Mirza Rizwan, Salari, Hedayat, Salehi, Sana, Salem, Marwa Rashad, Salimzadeh, Hamideh, Samodra, Yoseph Leonardo, Samy, Abdallah M, Sanabria, Juan, Sankararaman, Senthilkumar, Sanmarchi, Francesco, Santric-milicevic, Milena M, Saqib, Muhammad Arif Nadeem, Sarveazad, Arash, Sarvi, Fatemeh, Sathian, Brijesh, Satpathy, Maheswar, Sayegh, Nicolas, Schneider, Ione Jayce Ceola, Schwarzinger, Michaël, Šekerija, Mario, Senthilkumaran, Subramanian, Sepanlou, Sadaf G, Seylani, Allen, Seyoum, Kenbon, Sha, Feng, Shafaat, Omid, Shah, Pritik A, Shahabi, Saeed, Shahid, Izza, Shahrbaf, Mohammad Amin, Shahsavari, Hamid R, Shaikh, Masood Ali, Shaka, Mohammed Feyisso, Shaker, Elaheh, Shannawaz, Mohammed, Sharew, Mequannent Melaku Sharew, Sharifi, Azam, Sharifi-rad, Javad, Sharma, Purva, Shashamo, Bereket Beyene, Sheikh, Aziz, Sheikh, Mahdi, Sheikhbahaei, Sara, Sheikhi, Rahim Ali, Sheikhy, Ali, Shepherd, Peter Robin, Shetty, Adithi, Shetty, Jeevan K, Shetty, Ranjitha S, Shibuya, Kenji, Shirkoohi, Reza, Shirzad-aski, Hesamaddin, Shivakumar, K M, Shivalli, Siddharudha, Shivarov, Velizar, Shobeiri, Parnian, Shokri Varniab, Zahra, Shorofi, Seyed Afshin, Shrestha, Sunil, Sibhat, Migbar Mekonnen, Siddappa Malleshappa, Sudeep K, Sidemo, Negussie Boti, Silva, Diego Augusto Santos, Silva, Luís Manuel Lopes Rodrigues, Silva Julian, Guilherme, Silvestris, Nicola, Simegn, Wudneh, Singh, Achintya Dinesh, Singh, Ambrish, Singh, Garima, Singh, Harpreet, Singh, Jasvinder A, Singh, Jitendra Kumar, Singh, Paramdeep, Singh, Surjit, Sinha, Dhirendra Narain, Sinke, Abiy H, Siraj, Md Shahjahan, Sitas, Freddy, Siwal, Samarjeet Singh, Skryabin, Valentin Yurievich, Skryabina, Anna Aleksandrovna, Socea, Bogdan, Soeberg, Matthew J, Sofi-mahmudi, Ahmad, Solomon, Yonatan, Soltani-zangbar, Mohammad Sadegh, Song, Suhang, Song, Yimeng, Sorensen, Reed J D, Soshnikov, Sergey, Sotoudeh, Houman, Sowe, Alieu, Sufiyan, Mu'awiyyah Babale, Suk, Ryan, Suleman, Muhammad, Suliankatchi Abdulkader, Rizwan, Sultana, Saima, Sur, Daniel, Szócska, Miklós, Tabaeian, Seidamir Pasha, Tabarés-seisdedos, Rafael, Tabatabaei, Seyyed Mohammad, Tabuchi, Takahiro, Tadbiri, Hooman, Taheri, Ensiyeh, Taheri, Majid, Taheri Soodejani, Moslem, Takahashi, Ken, Talaat, Iman M, Tampa, Mircea, Tan, Ker-kan, Tat, Nathan Y, Tat, Vivian Y, Tavakoli, Ahmad, Tavakoli, Arash, Tehrani-banihashemi, Arash, Tekalegn, Yohannes, Tesfay, Fisaha Haile, Thapar, Rekha, Thavamani, Aravind, Thoguluva Chandrasekar, Viveksandeep, Thomas, Nihal, Thomas, Nikhil Kenny, Ticoalu, Jansje Henny Vera, Tiyuri, Amir, Tollosa, Daniel Nigusse, Topor-madry, Roman, Touvier, Mathilde, Tovani-palone, Marcos Roberto, Traini, Eugenio, Tran, Mai Thi Ngoc, Tripathy, Jaya Prasad, Ukke, Gebresilasea Gendisha, Ullah, Irfan, Ullah, Saif, Ullah, Sana, Unnikrishnan, Bhaskaran, Vacante, Marco, Vaezi, Maryam, Valadan Tahbaz, Sahel, Valdez, Pascual R, Vardavas, Constantine, Varthya, Shoban Babu, Vaziri, Siavash, Velazquez, Diana Zuleika, Veroux, Massimiliano, Villeneuve, Paul J, Violante, Francesco S, Vladimirov, Sergey Konstantinovitch, Vlassov, Vasily, Vo, Bay, Vu, Linh Gia, Wadood, Abdul Wadood, Waheed, Yasir, Walde, Mandaras Tariku, Wamai, Richard G, Wang, Cong, Wang, Fang, Wang, Ning, Wang, Yu, Ward, Paul, Waris, Abdul, Westerman, Ronny, Wickramasinghe, Nuwan Darshana, Woldemariam, Melat, Woldu, Berhanu, Xiao, Hong, Xu, Suowen, Xu, Xiaoyue, Yadav, Lalit, Yahyazadeh Jabbari, Seyed Hossein, Yang, Lin, Yazdanpanah, Fereshteh, Yeshaw, Yigizie, Yismaw, Yazachew, Yonemoto, Naohiro, Younis, Mustafa Z, Yousefi, Zabihollah, Yousefian, Fatemeh, Yu, Chuanhua, Yu, Yong, Yunusa, Ismaeel, Zahir, Mazyar, Zaki, Nazar, Zaman, Burhan Abdullah, Zangiabadian, Moein, Zare, Fariba, Zare, Iman, Zareshahrabadi, Zahra, Zarrintan, Armin, Zastrozhin, Mikhail Sergeevich, Zeineddine, Mohammad A, Zhang, Dongyu, Zhang, Jianrong, Zhang, Yunquan, Zhang, Zhi-jiang, Zhou, Linghui, Zodpey, Sanjay, Zoladl, Mohammad, Vos, Theo, Hay, Simon I, Force, Lisa M, Murray, Christopher J L, NOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM), and DCM - Departamento de Ciência dos Materiais

Subjects
SDG 3 - Good Health and Well-being
Abstract

Funding: J A Loureiro reports support for the present manuscript from Scientific Employment Stimulus (FCT; CEECINST/00049/2018) as support to their salary and from UIDB/00511/2020 of the LEPABE, funded by national funds through the FCT/MCTES (PIDDAC) as research support. BACKGROUND: Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally. METHODS: The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk-outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented. FINDINGS: Globally, in 2019, the risk factors included in this analysis accounted for 4·45 million (95% uncertainty interval 4·01-4·94) deaths and 105 million (95·0-116) DALYs for both sexes combined, representing 44·4% (41·3-48·4) of all cancer deaths and 42·0% (39·1-45·6) of all DALYs. There were 2·88 million (2·60-3·18) risk-attributable cancer deaths in males (50·6% [47·8-54·1] of all male cancer deaths) and 1·58 million (1·36-1·84) risk-attributable cancer deaths in females (36·3% [32·5-41·3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20·4% (12·6-28·4) and DALYs by 16·8% (8·8-25·0), with the greatest percentage increase in metabolic risks (34·7% [27·9-42·8] and 33·3% [25·8-42·0]). INTERPRETATION: The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden. FUNDING: Bill & Melinda Gates Foundation. publishersversion published

Published
2022

7. Computer-aided peptide-based drug design for inositol-requiring enzyme 1.

Author

Ghanbari, Alireza, Norouzy, Amir, Balmeh, Negar, Fard, Najaf Allahyari, and Moosavi, Mohammad Amin

Subjects
COMPUTER-assisted drug design, PROTEIN kinases, MOLECULAR structure, NILOTINIB, GLUCOSE-regulated proteins, ENZYMES, COMPUTATIONAL chemistry, PROSTATE cancer
Published
2022

8. Exploring the role of non-coding RNAs in autophagy.

Author

Ghafouri-Fard, Soudeh, Shoorei, Hamed, Mohaqiq, Mahdi, Majidpoor, Jamal, Moosavi, Mohammad Amin, and Taheri, Mohammad

Subjects
NON-coding RNA, LINCRNA, AUTOPHAGY, MYOCARDIAL infarction, VENOUS thrombosis, HOMEOSTASIS
Abstract

As a self-degradative mechanism, macroautophagy/autophagy has a role in the maintenance of energy homeostasis during critical periods in the development of cells. It also controls cellular damage through the eradication of damaged proteins and organelles. This process is accomplished by tens of ATG (autophagy-related) proteins. Recent studies have shown the involvement of non-coding RNAs in the regulation of autophagy. These transcripts mostly modulate the expression of ATG genes. Both long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been shown to modulate the autophagy mechanism. Levels of several lncRNAs and miRNAs are altered in this process. In the present review, we discuss the role of lncRNAs and miRNAs in the regulation of autophagy in diverse contexts such as cancer, deep vein thrombosis, spinal cord injury, diabetes and its complications, acute myocardial infarction, osteoarthritis, pre-eclampsia and epilepsy. Abbreviations: AMI: acute myocardial infarction; ATG: autophagy-related; lncRNA: long non-coding RNA; miRNA: microRNA. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

10. Evaluation of squamous cell carcinoma antigen 1 expression in oral squamous cell carcinoma (tumor cells and peritumoral T-lymphocytes) and verrucous carcinoma and comparison with normal oral mucosa

Author

Derakhshan, Samira, primary, Poosti, Arvin, additional, Razavi, Amirnader Emami, additional, Moosavi, Mohammad Amin, additional, Mahdavi, Nazanin, additional, Naieni, Fereshteh Baghaei, additional, Hesari, Kambiz Kamyab, additional, and Rahpeima, Amirsina, additional

Published
2021
Full Text
View/download PDF

12. Resveratrol, a popular dietary supplement for human and animal health: Quantitative research literature analysis - a review

Author

Yeung, Andy Wai Kan, Aggarwal, Bharat Bhushan, Orhan, Ilkay Erdogan, Barreca, Davide, Battino, Maurizio, Belwal, Tarun, Bishayee, Anupam, Daglia, Maria, Devkota, Hari Prasad, Echeverria, Javier, El-Demerdashl, Amr, Balacheva, Aneliya, Georgieva, Maya, Godfrey, Keith, Gupta, Vijai Kumar, Horbanczuk, Jaroslaw Olav, Huminiecki, Lukasz, Artur Jóźwik, Strzalkowska, Nina, Mocan, Andrei, Mozos, Ioana, Nabavi, Seyed Mohammad, Pajpanova, Tamara, Pittala, Valeria, Feder-Kubis, Joanna, Sampino, Silvestre, Silva, Ana Sanches, Sheridan, Helen, Sureda, Antoni, Tewari, Devesh, Wang, Dongdong, Weissig, Volkmar, Yang, Yang, Zengin, Goekhan, Shanker, Karuna, Moosavi, Mohammad Amin, Shah, Muhammad Ajmal, Kozuharova, Ekaterina, Al-Rimawi, Fuad, Durazzo, Alessandra, Lucarini, Massimo, Souto, Eliana B., Santini, Antonello, Malainer, Clemens, Djilianov, Dimitar, Tancheva, Lyubka P., Li, Hua-Bin, Gan, Ren-You, Tzvetkov, Nikolay T., and Atanasov, Atanas G.

Subjects
bibliometrics, biological activities, cancer, citation analysis, pharmacology, resveratrol, Web of Science, VOSviewer, food and beverages
Abstract

Resveratrol is a stilbene-type bioactive molecule with a broad spectrum of reported biological effects. In this sense, the current work provides a comprehensive literature analysis on resveratrol, representing a highly-researched commercially available dietary ingredient. Bibliometric data were identified by means of the search string TOPIC=("resveratrol*") and analyzed with the VOSviewer software, which yielded 17,561 publications extracted from the Web of Science Core Collection electronic database. 'I'he ratio of original articles to reviews was 9.5:1. More than half of the overall manuscripts have been published since 2013. Major contributing countries were USA, China, Italy, South Korea, and Spain. Most of the publications appeared in journals specialized in biochemistry and molecular biology, pharmacology and pharmacy, food science technology, cell biology, or oncology. The phytochemicals or phytochemical classes that were frequently mentioned in the keywords of analyzed publications included, in descending order: resveratrol, trans-resveratrol, polyphenols, flavonoids, quercetin, stilbenes, curcumin, piceatannol, cis-resveratrol, and anthocyanins.

Published
2019

16. New frontiers in the treatment of colorectal cancer: Autophagy and the unfolded protein response as promising targets

Author

Mokarram, Pooneh, primary, Albokashy, Mohammed, additional, Zarghooni, Maryam, additional, Moosavi, Mohammad Amin, additional, Sepehri, Zahra, additional, Chen, Qi Min, additional, Hudecki, Andrzej, additional, Sargazi, Aliyeh, additional, Alizadeh, Javad, additional, Moghadam, Adel Rezaei, additional, Hashemi, Mohammad, additional, Movassagh, Hesam, additional, Klonisch, Thomas, additional, Owji, Ali Akbar, additional, Łos, Marek J., additional, and Ghavami, Saeid, additional

Published
2017
Full Text
View/download PDF

20. Health Concerns of Various Nanoparticles: A Review of Their in Vitro and in Vivo Toxicity.

Author

Ajdary, Marziyeh, Moosavi, Mohammad Amin, Rahmati, Marveh, Falahati, Mojtaba, Mahboubi, Mohammad, Mandegary, Ali, Jangjoo, Saranaz, Mohammadinejad, Reza, and Varma, Rajender S.

Subjects
*NANOPARTICLE toxicity, *NANOPARTICLES, *BIOCOMPATIBILITY, *THERAPEUTICS
Abstract

Nanoparticles (NPs) are currently used in diagnosis and treatment of many human diseases, including autoimmune diseases and cancer. However, cytotoxic effects of NPs on normal cells and living organs is a severe limiting factor that hinders their use in clinic. In addition, diversity of NPs and their physico-chemical properties, including particle size, shape, surface area, dispersity and protein corona effects are considered as key factors that have a crucial impact on their safe or toxicological behaviors. Current studies on toxic effects of NPs are aimed to identify the targets and mechanisms of their side effects, with a focus on elucidating the patterns of NP transport, accumulation, degradation, and elimination, in both in vitro and in vitro models. NPs can enter the body through inhalation, skin and digestive routes. Consequently, there is a need for reliable information about effects of NPs on various organs in order to reveal their efficacy and impact on health. This review covers the existing knowledge base on the subject that hopefully prepares us better to address these challenges. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

21. Nucleostemin Depletion Induces Post-G1 Arrest Apoptosis in Chronic Myelogenous Leukemia K562 Cells

Author

Seyed-Gogani, Negin, Rahmati, Marveh, Zarghami, Nosratollah, Asvadi-Kermani, Iraj, Hoseinpour-Feyzi, Mohammad Ali, and Moosavi, Mohammad Amin

Subjects
RNA interference, lcsh:Therapeutics. Pharmacology, hemic and lymphatic diseases, lcsh:RM1-950, Apoptosis, Nucleostemin, 610 Medical sciences, Medicine, Cell cycle, K562, Research Article
Abstract

Purpose: Despite significant improvements in treatment of chronic myelogenous leukemia (CML), the emergence of leukemic stem cell (LSC) concept questioned efficacy of current therapeutical protocols. Remaining issue on CML includes finding and targeting of the key genes responsible for self-renewal and proliferation of LSCs. Nucleostemin (NS) is a new protein localized in the nucleolus of most stem cells and tumor cells which regulates their self-renewal and cell cycle progression. The aim of this study was to investigate effects of NS knocking down in K562 cell line as an in vitro model of CML. Methods: NS gene silencing was performed using a specific small interfering RNA (NS-siRNA). The gene expression level of NS was evaluated by RT-PCR. The viability and growth rate of K562 cells were determined by trypan blue exclusion test. Cell cycle distribution of the cells was analyzed by flow cytometry. Results: Our results showed that NS knocking down inhibited proliferation and viability of K562 cells in a time-dependent manner. Cell cycle studies revealed that NS depletion resulted in G1 cell cycle arrest at short times of transfection (24 h) followed with apoptosis at longer times (48 and 72 h), suggest that post-G1 arrest apoptosis is occurred in K562 cells. Conclusion: Overall, these results point to essential role of NS in K562 cells, thus, this gene might be considered as a promising target for treatment of CML., Advanced Pharmaceutical Bulletin; eISSN 2251-7308

Published
2013

22. Endoplasmic Reticulum Stress as a Therapeutic Target in Cancer: A mini review.

Author

Rahmati, Marveh, Amanpour, Saeid, Kharman-Biz, Amirhossein, and Moosavi, Mohammad Amin

Subjects
ENDOPLASMIC reticulum, CANCER treatment, PROTEIN folding, HOMEOSTASIS, IMMUNE response
Abstract

Perturbation of endoplasmic reticulum (ER) homeostasis leads to a stress condition described as "ER stress" which can induce the well-regulated program termed as unfolded protein response (UPR). The principal purpose of UPR is to reestablish the ER homeostasis. Some of the physiological and pathological situations that disrupt the homeostasis include hypoxia, glucose limitations, nutrient deprivation, low pH, genomic instability, and some cytotoxic compounds are frequently observed during the core formation and progression of tumors. These stressful microenvironments around the tumors affect the innate and adaptive immune responses. In addition, different immunoregulatory myeloid populations, like dendritic cells, myeloid-derived suppressor cells (MDSCs) and macrophages, accumulate in the tumor milieu and act as barriers to cancer immunotherapy. In these stressful situations, ER stress is usually induced to activate the UPR. Although the UPR mechanism is primarily a pro-survival process, preserved and/or prolonged excessive stress may induce cell apoptosis. Cancer and sustained ER stress may have modifications in ER stress mediated cell apoptosis and facilitate chronic inflammation and immune suppression within tumors. In this mini review, at first, we highlight the the role of UPR and its mediators in cancerous cells fate and then discuss their potential opportunities in cancer therapy. [ABSTRACT FROM AUTHOR]

Published
2017

24. TRAIL Triggers CRAC-Dependent Calcium Influx and Apoptosis through the Recruitment of Autophagy Proteins to Death-Inducing Signaling Complex.

Author

Airiau, Kelly, Vacher, Pierre, Micheau, Olivier, Prouzet-Mauleon, Valerie, Kroemer, Guido, Moosavi, Mohammad Amin, and Djavaheri-Mergny, Mojgan

Subjects
CELL death, ACUTE promyelocytic leukemia, TRAIL protein, GENE expression profiling, AUTOPHAGY, APOPTOSIS
Abstract

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively kills various cancer cell types, but also leads to the activation of signaling pathways that favor resistance to cell death. Here, we investigated the as yet unknown roles of calcium signaling and autophagy regulatory proteins during TRAIL-induced cell death in leukemia cells. Taking advantage of the Gene Expression Profiling Interactive Analysis (GEPIA) project, we first found that leukemia patients present a unique TRAIL receptor gene expression pattern that may reflect their resistance to TRAIL. The exposure of NB4 acute promyelocytic leukemia cells to TRAIL induces intracellular Ca2+ influx through a calcium release-activated channel (CRAC)-dependent mechanism, leading to an anti-apoptotic response. Mechanistically, we showed that upon TRAIL treatment, two autophagy proteins, ATG7 and p62/SQSTM1, are recruited to the death-inducing signaling complex (DISC) and are essential for TRAIL-induced Ca2+ influx and cell death. Importantly, the treatment of NB4 cells with all-trans retinoic acid (ATRA) led to the upregulation of p62/SQSTM1 and caspase-8 and, when added prior to TRAIL stimulation, significantly enhanced DISC formation and the apoptosis induced by TRAIL. In addition to uncovering new pleiotropic roles for autophagy proteins in controlling the calcium response and apoptosis triggered by TRAIL, our results point to novel therapeutic strategies for sensitizing leukemia cells to TRAIL. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

25. Induction of Differentiation and Apoptosis in Three Human Leukemia Cell Lines by a New Compound from Dendrostellera lessertii.

Author

Yazdanparast, Razieh, Mahdavi, Majid, and Moosavi, Mohammad Amin

Subjects
APOPTOSIS, LEUKEMIA, CELL lines, THYMELAEACEAE, PLANT extracts, CELL proliferation
Abstract

It has previously been shown that Dendrostellera lessertii (Thymelaeaceae) has strong anticancer activity. In this study, the antileukemic activity of another new compound from the same plant extract is reported. Promyelocytic (NB4 and HL-60) and erythroleukemia (K562) cells were cultured in the presence of various concentrations of the new compound (0.5–3.0 μg/ml) for 3 d. The cell numbers were then determined by trypan blue exclusion test. The new compound inhibited growth and proliferation of NB4, HL-60 and K562 with IC50 values of 1.5, 2.0 and 2.5 μg/ml, respectively. We also found that the new compound inhibited cell proliferation in a dose- and time-dependent manner. At low concentrations and after 48 h of treatment, approximately 50%–70% of NB4 and HL-60 cells were differentiated to monocyte/ macrophage lineage and approximately 30%–40% of the treated K562 cells were differentiated in the mega-karyocytic lineage, as evidenced by morphological changes and nitro blue tetrazolium reduction assays. Results of Hoechst 33258 staining also indicated that the new compound induced NB4 and HL-60 cell apoptosis at their respective IC50 values after 72 h of treatment. Based on the present data, the new compound seems a good candidate for further evaluation as an effective chemotherapeutic agent acting through induction of differentiation and apoptosis. [ABSTRACT FROM AUTHOR]

Published
2006
Full Text
View/download PDF

26. Berberine, a popular dietary supplement for human and animal health: Quantitative research literature analysis – a review

Author

Yeung, Andy Wai Kan, Orhan, Ilkay Erdogan, Aggarwal, Bharat Bhushan, Battino, Maurizio, Belwal, Tarun, Bishayee, Anupam, Daglia, Maria, Devkota, Hari Prasad, Amr El-Demerdash, Balacheva, Aneliya A., Georgieva, Maya G., Gupta, Vijai Kumar, Horbanczuk, Jaroslaw Olav, Jozwik, Artur, Mozos, Ioana, Nabavi, Seyed Mohammad, Pittal, Valeria, Feder-Kubis, Joanna, Silva, Ana Sanches, Sheridan, Helen, Sureda, Antoni, Wang, Dongdong, Weissig, Volkmar, Yang, Yang, Zengin, Gokhan, Shanker, Karuna, Moosavi, Mohammad Amin, Shah, Muhammad Ajmal, Al-Rimawi, Fuad, Durazzo, Alessandra, Lucarini, Massimo, Souto, Eliana B., Santini, Antonello, Djilianov, Dimitar, Das, Niranjan, Skotti, Efstathia P., Wieczorek, Anna, Lysek-Gladysinska, Malgorzata, Michalczuk, Monika, Sieron, Dominik, Horbanczuk, Olaf K., Tzvetkov, Nikolay T., Atanasov, Atanas G., and Universidade do Minho

Subjects
Alzheimers disease, Science & Technology, Berberine, Citation analysis, Bibliometrics, VOSviewer, Alkaloid, Diabetes, Web of Science, Obesity, Alzheimer’s disease
Abstract

Berberine is an alkaloid with a wide range of reported beneficial health effects. The current work provides an extensive literature analysis on berberine. Bibliometric data were identified by means of the search string TOPIC=(berberin* OR umbellatine*), which yielded 5,547 publications indexed in the Web of Science Core Collection electronic database. The VOSviewer software generated bubble maps to visualize semantic terms with citation results. The ratio of original articles to reviews was 13.6:1. The literature has been growing more quickly since the 2010s. Major contributing countries were China, the United States, India, Japan, and South Korea. Most of the publications appeared in journals specialized in pharmacology pharmacy, biochemistry molecular biology, chemistry, and plant science. Some of the frequently mentioned chemicals/chemical classes were alkaloid, palmatine, jatrorrhizine, coptisine, isoquinoline, and sanguinarine. The prevalent medical conditions under investigation included Alzheimers disease, cancer, diabetes, and obesity., Acknowledge the support by the Polish KNOW (LeadingNational Research Centre) Scientific Consortium “Healthy Animal-Safe Food,” decision of Ministry of Science and Higher Education No. 05-1/KNOW2/2015 and the European Union under the European Regional Development Fund (Homing/2017-4/41). Antoni Sureda has been supported by the Institute of Health Carlos III (Project CIBEROBN CB12/03/30038). Joanna Feder-Kubis was financed by the Polish Ministry of Science and Higher Education for the Faculty of Chemistry of Wrocław University of Science and Technology., info:eu-repo/semantics/publishedVersion

27. Expression and Clinical Significance of IRE1-XBP1s, p62, and Caspase-3 in Colorectal Cancer Patients.

Author

Zarafshani, Mohammadkian, Mahmoodzadeh, Habibollah, Soleimani, Vahid, Moosavi, Mohammad Amin, and Rahmati, Marveh

Subjects
*PROTEIN metabolism, *ACADEMIC medical centers, *AUTOPHAGY, *IMMUNOHISTOCHEMISTRY, *RETROSPECTIVE studies, *APOPTOSIS, *CELL physiology, *COLORECTAL cancer, *TRANSFERASES, *GENE expression profiling, *RESEARCH funding, *TUMOR markers, *DATA analysis software, *CARRIER proteins, *MEDICAL logic
Abstract

Background: Three main cell signaling pathways including the endoplasmic reticulum stress (ERS) response, autophagy, and apoptosis play critical roles in both cell survival and death. They were found to crosstalk with one another during tumorigenesis and cancer progression. This study aimed to investigate the expression of the spliced form of X-box binding protein 1 (XBP1s), p62, and caspase-3, as the essential biomarkers of ERS, autophagy, and apoptosis in patients with colorectal cancer (CRC), as well as the correlation between their expression and clinicopathological data. Methods: This retrospective study was conducted on formalinfixed paraffin-embedded (FFPE) blocks, which were collected from patients and their tumor margins, from the tumor bank of Imam Khomeini Hospital (Tehran, Iran) from 2017 to 2019. Tissue microarray (TMA) was used to measure the XBP1s, p62, and caspase-3 biomarkers. Data were analyzed using SPSS software version 20, and P≤0.05 was considered statistically significant. Results: Evaluating the total of 91 patients, a significant relationship was found between XBP1s expression and TNM stage (P=0.003), primary tumor (pT) (P=0.054), and the degree of differentiation (P=0.006); and between caspase-3 with pT (P=0.004), and lymphovascular invasion (P=0.02). However, no significant correlation was found between p62 and clinicopathological data. Furthermore, a positive relationship between XBP1s and p62 was confirmed (correlation coefficient: 22.2% and P=0.05). Conclusion: Our findings indicated that XBP1s could be considered as a target for therapy in personalized medicine. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

30. The International Natural Product Sciences Taskforce (INPST) and the power of Twitter networking exemplified through #INPST hashtag analysis.

Author

Singla RK, De R, Efferth T, Mezzetti B, Sahab Uddin M, Sanusi, Ntie-Kang F, Wang D, Schultz F, Kharat KR, Devkota HP, Battino M, Sur D, Lordan R, Patnaik SS, Tsagkaris C, Sai CS, Tripathi SK, Găman MA, Ahmed MEO, González-Burgos E, Babiaka SB, Paswan SK, Odimegwu JI, Akram F, Simal-Gandara J, Urquiza MS, Tikhonov A, Mondal H, Singla S, Lonardo SD, Mulholland EJ, Cenanovic M, Maigoro AY, Giampieri F, Lee S, Tzvetkov NT, Louka AM, Verma P, Chopra H, Olea SP, Khan J, Alvarez Suarez JM, Zheng X, Tomczyk M, Sabnani MK, Medina CDV, Khalid GM, Boyina HK, Georgiev MI, Supuran CT, Sobarzo-Sánchez E, Fan TP, Pittala V, Sureda A, Braidy N, Russo GL, Vacca RA, Banach M, Lizard G, Zarrouk A, Hammami S, Orhan IE, Aggarwal BB, Perry G, Miller MJ, Heinrich M, Bishayee A, Kijjoa A, Arkells N, Bredt D, Wink M, Fiebich BL, Kiran G, Yeung AWK, Gupta GK, Santini A, Lucarini M, Durazzo A, El-Demerdash A, Dinkova-Kostova AT, Cifuentes A, Souto EB, Zubair MAM, Badhe P, Echeverría J, Horbańczuk JO, Horbanczuk OK, Sheridan H, Sheshe SM, Witkowska AM, Abu-Reidah IM, Riaz M, Ullah H, Oladipupo AR, Lopez V, Sethiya NK, Shrestha BG, Ravanan P, Gupta SC, Alzahrani QE, Dama Sreedhar P, Xiao J, Moosavi MA, Subramani PA, Singh AK, Chettupalli AK, Patra JK, Singh G, Karpiński TM, Al-Rimawi F, Abiri R, Ahmed AF, Barreca D, Vats S, Amrani S, Fimognari C, Mocan A, Hritcu L, Semwal P, Shiblur Rahaman M, Emerald M, Akinrinde AS, Singh A, Joshi A, Joshi T, Khan SY, Balla GOA, Lu A, Pai SR, Ghzaiel I, Acar N, Es-Safi NE, Zengin G, Kureshi AA, Sharma AK, Baral B, Rani N, Jeandet P, Gulati M, Kapoor B, Mohanta YK, Emam-Djomeh Z, Onuku R, Depew JR, Atrooz OM, Goh BH, Andrade JC, Konwar B, Shine VJ, Ferreira JMLD, Ahmad J, Chaturvedi VK, Skalicka-Woźniak K, Sharma R, Gautam RK, Granica S, Parisi S, Kumar R, Atanasov AG, and Shen B

Subjects
Humans, Social Media, Biological Products
Abstract

Background: The development of digital technologies and the evolution of open innovation approaches have enabled the creation of diverse virtual organizations and enterprises coordinating their activities primarily online. The open innovation platform titled "International Natural Product Sciences Taskforce" (INPST) was established in 2018, to bring together in collaborative environment individuals and organizations interested in natural product scientific research, and to empower their interactions by using digital communication tools., Methods: In this work, we present a general overview of INPST activities and showcase the specific use of Twitter as a powerful networking tool that was used to host a one-week "2021 INPST Twitter Networking Event" (spanning from 31st May 2021 to 6th June 2021) based on the application of the Twitter hashtag #INPST., Results and Conclusion: The use of this hashtag during the networking event period was analyzed with Symplur Signals (https://www.symplur.com/), revealing a total of 6,036 tweets, shared by 686 users, which generated a total of 65,004,773 impressions (views of the respective tweets). This networking event's achieved high visibility and participation rate showcases a convincing example of how this social media platform can be used as a highly effective tool to host virtual Twitter-based international biomedical research events., Competing Interests: Conflict of Interest Authors Dr. Rajeev K. Singla and Shailja Singla have an honorary-based associations with the iGlobal Research and Publishing Foundation (iGRPF), New Delhi, India. Dr. Bernd Fiebich is associated with VivaCell Biotechnology GmbH. RKS, SS and BF along with the remaining authors, declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Given their role as Editor/Associate Editor/ Editorial board members, “Prof. Thomas Efferth”, “Ilkay Erdogan Orhan”, “Milen Georgiev”, “Davide Barreca”, “Maurizio Battino”, “Anupam Bishayee”, “Michael Heinrich”,and“Jianbo Xiao”had no involvement in the peer-review of this article and has no access to information regarding its peer-review., (Copyright © 2022 The Author(s). Published by Elsevier GmbH.. All rights reserved.)

Published
2023
Full Text
View/download PDF

31. Anti-oxidant and Selective Anti-proliferative Effects of the Total Cornicabra Olive Polyphenols on Human Gastric MKN45 Cells.

Author

Nowdijeh AA, Moosavi MA, Hosseinzadeh S, Soleimani M, Sabouni F, and Hosseini-Mazinani M

Abstract

Background: According to the epidemiological studies, consuming olive products can decrease the incidence of the different types of cancers mostly due to the high anti-oxidant properties of their polyphenolic compounds., Objectives: To evaluate the anti-oxidant and anti-proliferative potentials of the olive fruits total polyphenols on the gastric adenocarcinoma MKN45 cells in comparison to the normal Hu02 cells., Materials and Methods: The total phenolic content of the olive fruits and radical scavenging activity were determined by Folin and 2,2-diphenyl-1-picrylhydrazyl (DPPH) tests respectively. MTT assay was performed for the evaluation of the cell viability. Intracellular reactive oxygen species (ROS) level was measured using DCFH-DA. Statistical analysis was performed using SPSS 16 statistical software., Results: Treatment of the MKN45 cells with the phenolic compounds extracted from olive fruits decreased growth and viability of the cells in a dose- and time-dependent manner. In addition, treatment of the MKN45 cells with a combination of the phenolic compounds extracts and cytarabine further decreased cell compared to monotherapy of the cells with each compound alone. Mechanistically, we showed that the anti-cancer effects of the olive polyphenols in the MKN45 cells are mediated through depletion of ROS. Similarly, polyphenolic extracts were found to decrease ROS level in the normal cells at the concentrations of 500 and 1000 μg.mL -1 and short treatment times (6 h), but the viability of these cells did not significantly change. At high concentrations (2000 μg.mL -1 ) of the phenolic extracts or at longer times of incubation (12 h), however, both ROS levels and the viability of the cells were significantly decreased in the normal cells., Conclusions: The olive fruits polyphenolic extract modulates ROS levels and selectively targets cancerous cells at low concentrations. Also, the effects of cytarabine could be potentiated by the olive fruits polyphenols. Thus, for a combined protocol of cancer cell therapy, olive fruit polyphenolic compound could be proposed as a proper candidate.

Published
2019
Full Text
View/download PDF

32. Photodynamic N-TiO 2 Nanoparticle Treatment Induces Controlled ROS-mediated Autophagy and Terminal Differentiation of Leukemia Cells.

Author

Moosavi MA, Sharifi M, Ghafary SM, Mohammadalipour Z, Khataee A, Rahmati M, Hajjaran S, Łos MJ, Klonisch T, and Ghavami S

Subjects
Humans, K562 Cells, Leukemia metabolism, Leukemia pathology, Autophagy drug effects, Cell Differentiation drug effects, Leukemia drug therapy, Nanoparticles chemistry, Nanoparticles therapeutic use, Nitrogen chemistry, Nitrogen pharmacology, Photochemotherapy methods, Reactive Oxygen Species metabolism, Titanium chemistry, Titanium pharmacology
Abstract

In this study, we used nitrogen-doped titanium dioxide (N-TiO 2 ) NPs in conjugation with visible light, and show that both reactive oxygen species (ROS) and autophagy are induced by this novel NP-based photodynamic therapy (PDT) system. While well-dispersed N-TiO 2 NPs (≤100 μg/ml) were inert, their photo-activation with visible light led to ROS-mediated autophagy in leukemia K562 cells and normal peripheral lymphocytes, and this increased in parallel with increasing NP concentrations and light doses. At a constant light energy (12 J/cm 2 ), increasing N-TiO 2 NP concentrations increased ROS levels to trigger autophagy-dependent megakaryocytic terminal differentiation in K562 cells. By contrast, an ROS challenge induced by high N-TiO 2 NP concentrations led to autophagy-associated apoptotic cell death. Using chemical autophagy inhibitors (3-methyladenine and Bafilomycin A1), we confirmed that autophagy is required for both terminal differentiation and apoptosis induced by photo-activated N-TiO 2 . Pre-incubation of leukemic cells with ROS scavengers muted the effect of N-TiO 2 NP-based PDT on cell fate, highlighting the upstream role of ROS in our system. In summary, PDT using N-TiO 2 NPs provides an effective method of priming autophagy by ROS induction. The capability of photo-activated N-TiO 2 NPs in obtaining desirable cellular outcomes represents a novel therapeutic strategy of cancer cells.

Published
2016
Full Text
View/download PDF

33. Modeling and structural analysis of human Guanine nucleotide-binding protein-like 3,nucleostemin.

Author

Nazmi F, Moosavi MA, Rahmati M, and Hoessinpour-Feizi MA

Abstract

Human GNL3 (nucleostemin) is a recently discovered nucleolar protein with pivotal functions in maintaining genomic integrity and determining cell fates of various normal and cancerous stem cells. Recent reports suggest that targeting this GTP-binding protein may have therapeutic value in cancer. Although, sequence analyzing revealed that nucleostemin (NS) comprises 5 permuted GTP-binding motifs, a crystal structure for this protein is missing at Protein Data Bank (PDB). Obviously, any attempt for predicting of NS structure can further our knowledge on its functional sites and subsequently designing molecular inhibitors. Herein, we used bioinformatics tools and could model 262 amino acids of NS (132-393 aa). Initial models were built by MODELLER, refined with Scwrl4 program, and validated with ProsA and Jcsc databases as well as PSVS software. Then, the best quality model was chosen for motif and domain analyzing by Pfam, PROSITE and PRINTS. The final model was visualized by vmd program. This predicted model may pave the way for next studies regarding ligand binding states and interaction sites as well as screening of databases for potential inhibitors.

Published
2015
Full Text
View/download PDF

34. Nucleostemin depletion induces post-g1 arrest apoptosis in chronic myelogenous leukemia k562 cells.

Author

Seyed-Gogani N, Rahmati M, Zarghami N, Asvadi-Kermani I, Hoseinpour-Feyzi MA, and Moosavi MA

Abstract

Purpose: Despite significant improvements in treatment of chronic myelogenous leukemia (CML), the emergence of leukemic stem cell (LSC) concept questioned efficacy of current therapeutical protocols. Remaining issue on CML includes finding and targeting of the key genes responsible for self-renewal and proliferation of LSCs. Nucleostemin (NS) is a new protein localized in the nucleolus of most stem cells and tumor cells which regulates their self-renewal and cell cycle progression. The aim of this study was to investigate effects of NS knocking down in K562 cell line as an in vitro model of CML., Methods: NS gene silencing was performed using a specific small interfering RNA (NS-siRNA). The gene expression level of NS was evaluated by RT-PCR. The viability and growth rate of K562 cells were determined by trypan blue exclusion test. Cell cycle distribution of the cells was analyzed by flow cytometry., Results: Our results showed that NS knocking down inhibited proliferation and viability of K562 cells in a time-dependent manner. Cell cycle studies revealed that NS depletion resulted in G(1) cell cycle arrest at short times of transfection (24 h) followed with apoptosis at longer times (48 and 72 h), suggest that post-G1 arrest apoptosis is occurred in K562 cells., Conclusion: Overall, these results point to essential role of NS in K562 cells, thus, this gene might be considered as a promising target for treatment of CML.

Published
2014
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results