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Best strategy of Moving Averages\nMauzo: Best strategy of Moving Averages\n06-22-2017, 04:40 AM #1\n214 posts pe 354 martaba thanks\nAssalam-O-Alaikum! Dosto main aaj ap ka sath Moving Averages ki ak strategy share karny ja rah hon jo main kud use karta hon main nay ak picture upload ki jas main main nay Moving Average ko show kyia hy jas main ap ko sell potion nazar aa rahi ho gi agher Moving Average as potion pay ati hy to as potion pay sell kar sakty hy ya chart H1 time frame ka hy as time frame pay takprofit 40 pip kar sakty hy as ki setting main nay kud ki hoi hy aur main ya strategy 4 saal sy use kar rah hon agher ya hi potion H4 py banti hy to ap as ka tak profit 60 pip kar sakty hy aur agher ya hi potion D1 py banti hy to ap as ka tak profit 120 pip kar sakty hy Dosto main nay aaj tak as strategy sy loss ni kya ap apny capital ka hasab sy trade opne kar sakty hy aur ascha profit earn kar sakty hy.\nLast edited by IFX786; 06-22-2017 at 03:50 PM.\nThe Following 6 Users Say Thank You to IFX786 For This Useful Post:\nBabarkhan8384 (07-26-2017),forexsignal (03-20-2020),lawa786 (01-13-2019),pakravian (07-18-2017),sidra anjum (07-28-2017),zs22 (08-09-2019)\n07-13-2017, 09:03 PM #2\n2,891 posts pe 7,005 martaba thanks\nBro boht thanks but main to rsi indicator use kerta hoon our moving average ka 8 our 21 ka combination ker k use kerna humery leay best hay us main hum cross over strategy pay buy our sell ker sagty hain but rsi simple oir best indicator hay jes say mujhey achy results mily hain us k sath investment ache honi chahy\n01-13-2019, 04:21 PM #3\n856 posts pe 2,019 martaba thanks\nIc men koi shak nai moving average aik achi stragty ha aur agr iska sahe istamal krna a jaye to bahut had tak hum ic say profit hasil kr sktay hain. Ap nay jo explain kea ha thora mazid agr guide kr dain to aur bhi acha ho ga aur sath yeh bta dain k moving average k combination ko kis tarha say use krtay hain.\nThe Following 0 Users Say Thank You to lawa786 For This Useful Post:\n03-31-2019, 03:58 PM #4\nRe: Best strategy of Moving Averages\nMoving Average k leye jo bhout zaida zarori hai woh ap ki values hai or time frame hai jab tak ap yeh nahi set kar skain gy tu ap ko moving average ho ya koi dosra indicator ho best result nahi mily ga. ager ap moving average ko MCAD k sath use karty hian tu ap ko bhout he acha result mily ga.\n08-09-2019, 05:34 AM #5\nSir aapne bilkul theek kaha hai moving average indicator best indicator hai aur aapne iske bare mein bahut acchi information share ki hai is tarah aap ne bataya Hai ismein scalping karke bhi bahut accha profithasil Kiya ja sakta hai aur kam waqt mein jyada profit hotel Kiya ja sakta hai kyunki aisi movement mein scalping Hi best hai\nraja77 (08-23-2019),Zain640 (08-21-2019)\n03-01-2020, 08:44 PM #6\nMoving average ko alag se use karain gay tu confirm ap ko strategy es ki sahi samaj nahi aye gi es kay sath ap koi oscillator add kar lain or dunu ko mila kar use karain gay tu ap ko acha result rahy ga. alag se use na karain nahi tu es se khas resul nahi mily ga. time to time apni strategy ko updaet karty rahain tu ap kamyab hain.\n03-20-2020, 07:52 PM #7\nW.salam Bhai ap ki stretgy bht achi hai magr main short term k liye almost stochastic use krta hun aur just ek he pair pr trdae krta hun magr kafi waqt sy market k halat kuch sahi nhi hai aur yeh kissi bhi waqt kabhi up to kabhi down mar deti hai, i hope so k bht jald market apny level pr aa jaegi, IN SHA ALLAH.\nThe Following 0 Users Say Thank You to forexsignal For This Useful Post:\n05-03-2020, 08:08 AM #8\nAssalamualaikum dear ap ny bhot hi achi information share ki mn pehly es k bara mn ni janata tha jaisy k ap ny btia k hm scalping kr k kisi acha pairs pr trdae laga sakty hn or es sy hmin kafi acha profit mil sakta hy to ap log bhi scalping ko use kr k trade laga sakty hn


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Assalamu Alaykum, mufti sahb (i asked you a que. no.4184), mufti sahb sarkaar huzur mufti e azam duniya se parda kiye uss ko 30 saal bhi nahi hue. to kya mike wala jo fatwa he woh zamaane ke hissan se badal jata he. aur rahi baat duniya kii to duniya aur insaan HAMARE MAZHAB K mohtaj he. ISLAAM KABHI BHI KISI KA MOHTAJ NAHI. TO KYA ZAMAANE JAISE HI CHANGE HO JAYE USS TARAH SHARIYAT KII PABANDIYA KHATAM HO JAYENGI.....; BESHAK, HUZUR SALLALLAHO ALAYHE WASALLAM KE JO KAUL HE WOH TO AAYENGE HI...., MERA SAWAAL YEHI HE KII KYA AULIYA E KIRAM AUR BUZURGON KE DUNIYA ME PARDA KERNE SE UNKE FATWE UNKE batayee hui shariyat kii pabandiya khatam ho jayengi.... ? aap ke behtareen jawab ka talbgaar.\nMuhtarami wa Mukrami mera aap se sawal hai keh. Mein-ne aik nazar mani thee keh agar mera baita paida howa tu mein apne buzarg/pir murshed keliye pagrhi, chadar aur jothi (Yani 2000 ropay ka) kharcha karonga. Lekin Allah Taala Rabbi Kareem ne mujhe baiti atta farmai (Sawal No. 1: Kia Nazar Pora karna Lazmi hai ya Nahi). Lekan Pher be mein 2000 ropay lekar mein apni masjid ki muhtaram ustad ke paas pohancha aur us se kaha barai mehrabani in ropo se buzarg/pir murshed keliye pagrhi, chadar aur jothi kharide likan us ne koch dino ki baad mujhe batha diya keh kia is ko dosri jhaga istimaal karli mein-ne kaha thek hai karle. (Sawal No. 2: Kia Mujhe jawab dena tha ke nahi pagri, chadar aur jothi khareden ya thek jo chahi. Matlab nazar mein banda ikhtyar raktha hai keh jins tabdil kare yani zurorat ki mutabik istimaal kari).\nassalamualaikum,maine ek dost se suna hai ke jab bacha paida hota hai to wo maa ke kauk se pehle baap ke reed ki haddi me ande[egg] ke shakal me rehta hai.kya ye sahi hai?\nsalam agar koi muslim khud kushi kartha hai tho un ka janaza para jai ga aur un ke marne ke ba\_\_\_'d us ki maghfrat ho sakte hai 2 kya ye sach hai ke hazoor Ghous Azam (radi allah anhu)ne qawali ki ijaazat di hai aur peer mehar ali shah hud qawali par\_\_\_'the thay? 3 kya ye sach he ke qawali me music nahi hotha tha\nAslam-o-alikum, mujhe information chahye jis se wahabi aur sunni ka diff mil sake aur wahabiyon ko galat sabat kar sakin.give me some books name plz. Jazak ALLAH\nAslam-o-alikum, app plz quran o hades se ye wazie karin k ALLAH sirf arsh pe nai balke har taraf hain?ya mujhe koi book ka name with aouther bata dain jis main quran o hades se ye baat wazea ho. jazak ALLAH khair\nAssalam o alykum kia farmate hain ulamae deen va muftiyan-e-shara-e-mateen is masla ke bare main ke zed apne maan baap ke judai(talaq) ke baad 18 saal ke baad apni walida se mila. jab zed ke maan ne apne doosre shohar (zed ke sotele baap) ko bataya ke mugh se zed aa kar mila hay to us ne sakht narazgi ka izhar kiya aur ainda sakhti se na milne ka kaha. daryaft talb amar ye hay ke kia zed apni maan se chori shupe apne sotele baap ke adam maujudgi main us ke ghar ja kar mil sakta hay? milne ke soorat main kia maan shohar ke nafarmani ke murtaqib to na ho ge? neez zed ko kia karna chahiye?\nmufti sahab aslamoalakum mai nay app say pehlay b question kea tha hooro kay baray mai app nay kaha tha jannat mai hasad aur bugaz nai hota wives mai b hasad aur bugaz nai hoo ga magar mufti sahib admi aur aurat dono duneya ki taqleef berdasht kertay hai apnay ALLAH ki abadat kertay hain dono ko apna apna rutba milta hai jannat mai tu kea mufti sahib aurat yee duwa ya khowaish mang sakti Hai ALLAH say kay us ka shoher 1 wife rakhay mere friends say baat howi thi hooroo per tu unhoo nay kaha tha kaY jo wife duneya ki hoo gi serf wohi jannat mai hoo gi\nassalam alaykum janab mera sawal yeh hai ki madi aur mani me kya farq hai aur kya yeh pak hai ya napak. aalae khas se ek pani jesi ratubat jo chiknai jesi hoti he kya ye hi madi he aur ye akasar nikalti rehti he iska kya hukum ha kya isse ghusal toot jata hai aur agar ye kapde par gili aur sukhi halat me lagi ho to kya hukum hai kya isse namaz ho jayegi aur baitul khula me pakhane karte waqt bhi kuchh chiknai jesi ratubat peshab ke raste nikalti hai yeh kya he mani ya madi kya isse bhi ghusal jata raha aur musht zani ke bare mai batlaye ham log dubai me rahte hai bivi bachho se door to kabhi kabhi mushtzani karte hai kya ye sahi hai jazakallah\nAssal Alikum aap sa ya poochna hai kay marnay kay bad maa,bap,mian, biwi, aulad ka rishta hamasa kay liya katam hojata hay ya kayamat kay bad sab ek dusaray sa mil sakay gay ya nahi kas kar mian aur biwi kya marnay ka bad bhi ek dusaray sa mil sakay ga ya nahi. Agar marnay ka bad mian aur biwi may say ek jannati aur dusara dozaqi ho tu kay per bhi wo ek dosaray say mil sakay gay ya nahi. dosara sawal ya hai kay Dajjal kay finay say kon log mutasir hoon gay jo dunia may zinda hoongay ya jo dunia say ja chukay hai wo bhi mutasir hoon gay. Thanxs\nmera 1 dost factory main kam karta hai vehan per aik badmazhab imamat krvata hai aor sabit hai k vo gustakhi rasool bhi hai agar mera dost akaila namaz perta hai to log shikayat krtay hain k ya shar phalata hai.Kisee sunee alam sey pooch kr ab vo asu k peechay namaz per kr baad main duhra laita hai.Aap say poochna hai k kia ausay bajamaat niamz ka savab milay ga aor kia vo 72 madni inamat main \_"yes\_" kar sakta hai mazeed kia aus k peechay nimaz pertay hoo ai jab vo chup rhay kuch peray ga naheen to kiya vo chup rehnay ki bajay Durood Shareef per sakta hai. Allah hafiz Ikram (sardarabad)\nAssalam o alaikum Hazrat main aik naikis ul aqal insan hu mujhay main kush karnay ki himmat to nahi per bus jo karna chahta hu usko apni sooch tak hi mehdood rakh kay apnay ulma e ahl e sunnat ko sunata hu..pahlay to main aik kush khabri sunai ga kay mujhay kal raat ameer e ahl e sunnat ki ziyarat huye or mainay ye daikha kay ameer e ahl e sunnat HAZRAT MUHAMMAD ILYAS QARDI SAHAB meray ghar main 3 din say kiyam farmaye huye hia..or unkay sath aik or buzurg bhi hia..or AMEER E AHL E SUNNAT nay white shalwar kameez or sabz emama or emama k uper white colour ka jali wala kapra lapaita huwa hia..subhanAllah...Mashallah... Ab main kuch kahna chahta hu k...sunnay main aya hia kay ulma e ahl e sunnat k apas main bhi booht say ikhtilafat hai jis ki waja say AHL E SUNNAT WAL JAMAT ka jo mission thaa wo apni jaga per hi ruk gaya hia. balkay ahl e sunnat wal jamat aik khamosh kitab ki tarha rah gaye hia..bad aqeeda loog apni kitabo k zariye logo ko gumrah kiye ja rahay hia..khass toor pay SHIA..pahlay to sunni shia debate hote the logo ko nazar ata tha kay shia kis kadar jhoot baktya hia or jhootya makkar hia..ab wo sub bhi daikhnay main nahi ata..hamaray BUZURGO k mazarat pay wo loog matam kartya hia..koi roknay ala nahi hia..hamaray peeran e peer roshan zameer huzoor e GHOUS E PAK k mazar shareef bhi unhi k hatho main hia..jub kay hum GHOUS E PAK ko apna hajat rawa kahtya hia..or hum khamoosh baithay hia..ulm e ahl e sunnat main akhir aisay kon say ikhtelafat hia jo hal nahi kiye ja saktya or kub tak hal nahi hogay k ab wo waqt hia k jis kay pas power hia usi ki jeet hia to hum to Alhamdulillah haq per hia..hamare jamat aik kaseeer tadad per mushtamil hia..phir hum log aik ho kar koshish kyu nahi kartya...hamain ab her us jaga ko bad kirdar logo say khali karwana hoga jis jaga ka taluq AHL E SUNNAT say hia..main ap say ye guzarish hia kay ap aik letter banaye jis main mare is baat ko madday nazar rakhay or tamam ulma e ahl e sunnat ko bhehay ..main apni masjid say inshallah iskam ka agaz karooga..or phir inshallah hum her mazar her us masjid jo sunnio ki the or un per kabza karliya gaya sub ko azad karwaye gay...laiken is main sub say pahlay tamam ulma e ahl e sunnat ko aik hona paray ga...chahye wo QADRI SISILAY KA HO YA NAQSBANDI SOHARWARDI YA CHISTI...PEER HO YA FAKEER..ab sub ko aik hona hia..ab HAZOOR E GHOUS E PAK k kaisay mureed hia kay unkay mazar ko aye din shaheed kiar diya jata hia or hum bus apni masjido main hi usko bura tasawar karkay thanday hojatay hia,,,baraye mehar bani ab aik letter banaye or mujhay meray postal address pay send karain main uski copies karwa kay inshallah tamam ulma e ahl e sunnat ko bhejo ga..or sooye huye sunnio ko phir say jagaonga..inshallah.. aik baat or ye kay ab jis tarha logo ko sawalat ka jawab daytya hai..is tarha is website main aik postion banaye jo sirf o sirf shia hazrat k liye ho or shuru say lay kay akhir tak jo baray baray ikhtilafat hia un ka sawal or jawab ko audio main save karay mujh say jitna ho sakaty ga main us audio ko shio tak mail karoonga..mainay pahlay bhi likha tha kay is wweb main shia ka bhi aik alag section banaya jaye takay uskay link ko logo tak bheja jaye kabhi na kabhi koi to shia usko parhay ga ... ASSALAM O ALIKUM


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Date: 6th Muharram 1438 Hijri / 8th Oct 2016 Speaker: Hujjat Ul Islam Maulana Akhtar Abbas Jaun Topic: Ashaab e Imam Hussain [as] ki wilayat Pazeeri Venue: Jama Masjid, Tahseen Ganj, Lucknow - India. Date: 6th Muharram 1438 Hijri / 8th Oct 2016 Speaker: Hujjat Ul Islam Maulana Akhtar Abbas Jaun Topic: Ashaab e Imam Hussain [as] ki wilayat Pazeeri Venue: Jama Masjid, Tahseen Ganj, Lucknow - India. Show Less >>


Shabby Chic | S.H.E. Event Planning - S.H.E. strives to create special moments to be remembered...


The latest Online film of Bahar\nA complete list of 119 Online films of Bahar\n(Urdu - Color - Tuesday, 19 January, 1999)\n(Punjabi - Color - Friday, 9 November, 2001)\n(Double version Punjabi/Urdu - Color - Friday, 6 September, 1991)\n(Punjabi - Color - Friday, 30 May, 1980)\nBahar: Filmography of 322 released films\n(81 Urdu, 216 Punjabi and 7 Pashto films)\n(Urdu - Friday, 11 August, 1961)\nActors: Bahar, Sultan, Kemal, Husna\nActors: Anjuman, Ghulam Mohayuddin, Bahar, Iqbal Hassan\n(Double version Punjabi/Urdu - Friday, 24 April, 1992)\nActors: Madiha Shah, Shaan, Anmol, Rustam, Bahar\nActors: Nadia, Izhar Qazi, Sonia, Yasir, Rustam, Bahar, Shafqat\nActors: Reema, Babar Ali, Saud, Babar Ali, Saood, Rambo, Nargis, Bahar, Momar Rana\n(Urdu - Friday, 31 July, 1998)\nActors: Reema, Shaan, Saud, Saima, Rambo, Izhar Qazi, Bahar\n(Urdu - Friday, 15 October, 1999)\nActors: Reema, Saud, Saima, Rambo, Khushboo, Arbaz, Bahar\nKahan Hay Qanoon\n(Urdu - Friday, 8 September, 2000)\nActors: Saima, Shaan, Resham, Saud, Nirma, Bahar, Shafqat\nActors: Saima, Shaan, Moamar Rana, Meera, Bahar, Shafqat\n(Punjabi - Friday, 5 October, 2001)\nActors: Saima, Shaan, Nawaz, Shaishta, Bahar, Shafqat\n(Punjabi - Friday, 12 October, 2001)\nActors: Sana, Shaan, Babar Ali, Nargis, Bahar, Raheel, Cheema\n(Punjabi - Friday, 9 November, 2001)\nActors: Reema, Saud, Sana, Babar Ali, Khushbu, Bahar, Shafqat\nActors: Saima, Shaan, Reema, Moamer Rana, Rambo, Nargis, Bahar\n(Punjabi - Friday, 29 March, 2002)\nActors: Moamar Rana, Babar, Resham, Malik Heera, Noor, Bahar\nDirector: Amjad Malik\nMusic: Rafiq Mehdi\nActors: Zahid Ali, Dua Qureshi, Bahar, Agha Majid, Amjad Rana, Shazib Mirza, Barkha\nBahar: Filmography as a supporting/guest artist\n(Total 64 released films, 12 Urdu, 39 Punjabi films)\nBahar: Unreleased films\nThe latest Online film songs of Bahar\nSinger(s): Zubaida Khanum & Co., Music: Rasheed Attray, Poet: Tufail Hoshiarpuri\nBahar: Main playback singers\nBahar: Songography of 12 film songs - 0 Online Songs\n(3 Urdu and 9 Punjabi songs - incomplete figures!)\n2. Bunday Chandi day, Sonay di Nath lay kay, aa ja ho..\nFilm: Chann Mahi (Punjabi - 1956)\nSinger(s): Zubaida Khanum & Co. - Music: Rasheed Attray - Poet: Tufail Hoshiarpuri - Actor(s): Bahar\n3. Bura maan kay kahan Chal diye, Adab Arz hay..\nFilm: Shararat (Urdu - 1963)\nSinger(s): Masood Rana, Irene Parveen - Music: Deebo - Poet: Masroor Anwar - Actor(s): Mohammad Ali, Bahar\n4. Dil Harya, Teray Tun Warya, Shakkan Deya Marya..\nSinger(s): Naheed Niazi - Music: G.A. Chishti - Poet: ? - Actor(s): Bahar\n5. Dil Toren Tay Mitti Nu Joren, Way Murtan Banan Waleya..\n6. Dillan dian Mailian nay Chann jeyan Surtan..\n7. Gali Gali Main Dil bechun, Naam Mera Dildar..\n8. Mahi Mout da Sunehra ditta Gall way..\nSinger(s): Zubaida Khanum - Music: Rasheed Attray - Poet: Tufail Hoshiarpuri - Actor(s): Bahar\n9. Meray 2 Anmol Lal..\n10. Ni Chithiye Sajna diy, Teinu Ghutt Ghutt Japhian pawan..\n11. Pher Leyan Chann Mahi Akhian..\n12. Saday Ang Ang wich Pyar nay Peenga payan nay..\nSinger(s): Zubaida Khanum, Saleem Raza - Music: Rasheed Attray - Poet: Tufail Hoshiarpuri - Actor(s): Bahar


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Results 1-25 (1502424)\n1. Both the Caspase CSP-1 and a Caspase-Independent Pathway Promote Programmed Cell Death in Parallel to the Canonical Pathway for Apoptosis in Caenorhabditis elegans Denning, Daniel P. | Hatch, Victoria | Horvitz, H. Robert\n2. Caspase-2 Maintains Bone Homeostasis by Inducing Apoptosis of Oxidatively-Damaged Osteoclasts Sharma, Ramaswamy | Callaway, Danielle | Vanegas, Difernando | Bendele, Michelle | Lopez-Cruzan, Marisa | Horn, Diane | Guda, Teja | Fajardo, Roberto | Abboud-Werner, Sherry | Herman, Brian\n3. Abstracts from the 3rd International Genomic Medicine Conference (3rd IGMC 2015) Shay, Jerry W. | Homma, Noriko | Zhou, Ruyun | Naseer, Muhammad Imran | Chaudhary, Adeel G. | Al-Qahtani, Mohammed | Hirokawa, Nobutaka | Goudarzi, Maryam | Fornace, Albert J. | Baeesa, Saleh | Hussain, Deema | Bangash, Mohammed | Alghamdi, Fahad | Schulten, Hans-Juergen | Carracedo, Angel | Khan, Ishaq | Qashqari, Hanadi | Madkhali, Nawal | Saka, Mohamad | Saini, Kulvinder S. | Jamal, Awatif | Al-Maghrabi, Jaudah | Abuzenadah, Adel | Chaudhary, Adeel | Al Qahtani, Mohammed | Damanhouri, Ghazi | Alkhatabi, Heba | Goodeve, Anne | Crookes, Laura | Niksic, Nikolas | Beauchamp, Nicholas | Abuzenadah, Adel M. | Vaught, Jim | Budowle, Bruce | Assidi, Mourad | Buhmeida, Abdelbaset | Al-Maghrabi, Jaudah | Buhmeida, Abdelbaset | Assidi, Mourad | Merdad, Leena | Kumar, Sudhir | Miura, Sayaka | Gomez, Karen | Carracedo, Angel | Rasool, Mahmood | Rebai, Ahmed | Karim, Sajjad | Eldin, Hend F. Nour | Abusamra, Heba | Alhathli, Elham M. | Salem, Nada | Al-Qahtani, Mohammed H. | Kumar, Sudhir | Faheem, Hossam | Agarwa, Ashok | Nieschlag, Eberhard | Wistuba, Joachim | Damm, Oliver S. | Beg, Mohd A. | Abdel-Meguid, Taha A. | Mosli, Hisham A. | Bajouh, Osama S. | Abuzenadah, Adel M. | Al-Qahtani, Mohammed H. | Coskun, Serdar | Abu-Elmagd, Muhammad | Buhmeida, Abdelbaset | Dallol, Ashraf | Al-Maghrabi, Jaudah | Hakamy, Sahar | Al-Qahtani, Wejdan | Al-Harbi, Asia | Hussain, Shireen | Assidi, Mourad | Al-Qahtani, Mohammed | Abuzenadah, Adel | Ozkosem, Burak | DuBois, Rick | Messaoudi, Safia S. | Dandana, Maryam T. | Mahjoub, Touhami | Almawi, Wassim Y. | Abdalla, S. | Al-Aama, M. Nabil | Elzawahry, Asmaa | Takahashi, Tsuyoshi | Mimaki, Sachiyo | Furukawa, Eisaku | Nakatsuka, Rie | Kurosaka, Isao | Nishigaki, Takahiko | Nakamura, Hiromi | Serada, Satoshi | Naka, Tetsuji | Hirota, Seiichi | Shibata, Tatsuhiro | Tsuchihara, Katsuya | Nishida, Toshirou | Kato, Mamoru | Mehmood, Sajid | Ashraf, Naeem Mahmood | Asif, Awais | Bilal, Muhammad | Mehmood, Malik Siddique | Hussain, Aadil | Jamal, Qazi Mohammad Sajid | Siddiqui, Mughees Uddin | Alzohairy, Mohammad A. | Al Karaawi, Mohammad A. | Nedjadi, Taoufik | Al-Maghrabi, Jaudah | Assidi, Mourad | Al-Khattabi, Heba | Al-Ammari, Adel | Al-Sayyad, Ahmed | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Zitouni, Hédia | Raguema, Nozha | Ali, Marwa Ben | Malah, Wided | Lfalah, Raja | Almawi, Wassim | Mahjoub, Touhami | Elanbari, Mohammed | Ptitsyn, Andrey | Mahjoub, Sana | El Ghali, Rabeb | Achour, Bechir | Amor, Nidhal Ben | Assidi, Mourad | N’siri, Brahim | Morjani, Hamid | Nedjadi, Taoufik | Al-Ammari, Adel | Al-Sayyad, Ahmed | Salem, Nada | Azhar, Esam | Al-Maghrabi, Jaudah | Chayeb, Vera | Dendena, Maryam | Zitouni, Hedia | Zouari-Limayem, Khedija | Mahjoub, Touhami | Refaat, Bassem | Ashshi, Ahmed M. | Batwa, Sarah A. | Ramadan, Hazem | Awad, Amal | Ateya, Ahmed | El-Shemi, Adel Galal Ahmed | Ashshi, Ahmad | Basalamah, Mohammed | Na, Youjin | Yun, Chae-Ok | El-Shemi, Adel Galal Ahmed | Ashshi, Ahmad | Basalamah, Mohammed | Na, Youjin | Yun, Chae-Ok | El-Shemi, Adel Galal | Refaat, Bassem | Kensara, Osama | Abdelfattah, Amr | Dheeb, Batol Imran | Al-Halbosiy, Mohammed M. F. | Al lihabi, Rghad Kadhim | Khashman, Basim Mohammed | Laiche, Djouhri | Adeel, Chaudhary | Taoufik, Nedjadi | Al-Afghani, Hani | Łastowska, Maria | Al-Balool, Haya H. | Sheth, Harsh | Mercer, Emma | Coxhead, Jonathan M. | Redfern, Chris P. F. | Peters, Heiko | Burt, Alastair D. | Santibanez-Koref, Mauro | Bacon, Chris M. | Chesler, Louis | Rust, Alistair G. | Adams, David J. | Williamson, Daniel | Clifford, Steven C. | Jackson, Michael S. | Singh, Mala | Mansuri, Mohmmad Shoab | Jadeja, Shahnawaz D. | Patel, Hima | Marfatia, Yogesh S. | Begum, Rasheedunnisa | Mohamed, Amal M. | Kamel, Alaa K. | Helmy, Nivin A. | Hammad, Sayda A. | Kayed, Hesham F. | Shehab, Marwa I. | El Gerzawy, Assad | Ead, Maha M. | Ead, Ola M. | Mekkawy, Mona | Mazen, Innas | El-Ruby, Mona | Shahid, S. M. A. | Jamal, Qazi Mohammad Sajid | Arif, J. M. | Lohani, Mohtashim | Imen, Moumni | Leila, Chaouch | Houyem, Ouragini | Kais, Douzi | Fethi, Chaouachi Dorra Mellouli | Mohamed, Bejaoui | Salem, Abbes | Faggad, Areeg | Gebreslasie, Amanuel T. | Zaki, Hani Y. | Abdalla, Badreldin E. | AlShammari, Maha S. | Al-Ali, Rhaya | Al-Balawi, Nader | Al-Enazi, Mansour | Al-Muraikhi, Ali | Busaleh, Fadi | Al-Sahwan, Ali | Borgio, Francis | Sayyed, Abdulazeez | Al-Ali, Amein | Acharya, Sadananda | Zaki, Maha S. | El-Bassyouni, Hala T. | Shehab, Marwa I. | Elshal, Mohammed F. | M., Kaleemuddin | Aldahlawi, Alia M. | Saadah, Omar | McCoy, J. Philip | El-Tarras, Adel E. | Awad, Nabil S. | Alharthi, Abdulla A. | Ibrahim, Mohamed M. M. | Alsehli, Haneen S. | Dallol, Ashraf | Gari, Abdullah M. | Abbas, Mohammed M. | Kadam, Roaa A. | Gari, Mazen M. | Alkaff, Mohmmed H. | Abuzenadah, Adel M. | Gari, Mamdooh A. | Abusamra, Heba | Karim, Sajjad | eldin, Hend F. Nour | Alhathli, Elham M. | Salem, Nada | Kumar, Sudhir | Al-Qahtani, Mohammed H. | Moradi, Fatima A. | Rashidi, Omran M. | Awan, Zuhier A. | Kaya, Ibrahim Hamza | Al-Harazi, Olfat | Colak, Dilek | Alkousi, Nabila A. | Athanasopoulos, Takis | Bahmaid, Afnan O. | Alhwait, Etimad A. | Gari, Mamdooh A. | Alsehli, Haneen S. | Abbas, Mohammed M. | Alkaf, Mohammed H. | Kadam, Roaa | Dallol, Ashraf | Kalamegam, Gauthaman | Eldin, Hend F. Nour | Karim, Sajjad | Abusamra, Heba | Alhathli, Elham | Salem, Nada | Al-Qahtani, Mohammed H. | Kumar, Sudhir | Alsayed, Salma N. | Aljohani, Fawziah H. | Habeeb, Samaher M. | Almashali, Rawan A. | Basit, Sulman | Ahmed, Samia M. | Sharma, Rakesh | Agarwal, Ashok | Durairajanayagam, Damayanthi | Samanta, Luna | Abu-Elmagd, Muhammad | Abuzenadah, Adel M. | Sabanegh, Edmund S. | Assidi, Mourad | Al-Qahtani, Mohammed | Agarwal, Ashok | Sharma, Rakesh | Samanta, Luna | Durairajanayagam, Damayanthi | Assidi, Mourad | Abu-Elmagd, Muhammad | Al-Qahtani, Mohammed | Abuzenadah, Adel M. | Sabanegh, Edmund S. | Samanta, Luna | Agarwal, Ashok | Sharma, Rakesh | Cui, Zhihong | Assidi, Mourad | Abuzenadah, Adel M. | Abu-Elmagd, Muhammad | Al-Qahtani, Mohammed | Alboogmi, Alaa A. | Alansari, Nuha A. | Al-Quaiti, Maha M. | Ashgan, Fai T. | Bandah, Afnan | Jamal, Hasan S. | Rozi, Abdullraheem | Mirza, Zeenat | Abuzenadah, Adel M. | Karim, Sajjad | Al-Qahtani, Mohammed H. | Karim, Sajjad | Schulten, Hans-Juergen | Al Sayyad, Ahmad J. | Farsi, Hasan M. A. | Al-Maghrabi, Jaudah A. | Mirza, Zeenat | Alotibi, Reem | Al-Ahmadi, Alaa | Alansari, Nuha A. | Albogmi, Alaa A. | Al-Quaiti, Maha M. | Ashgan, Fai T. | Bandah, Afnan | Al-Qahtani, Mohammed H. | Ebiya, Rasha A. | Darwish, Samia M. | Montaser, Metwally M. | Abusamra, Heba | Bajic, Vladimir B. | Al-Maghrabi, Jaudah | Gomaa, Wafaey | Hanbazazh, Mehenaz | Al-Ahwal, Mahmoud | Al-Harbi, Asia | Al-Qahtani, Wejdan | Hakamy, Saher | Baba, Ghali | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Al-Maghrabi, Jaudah | Al-Harbi, Abdullah | Al-Ahwal, Mahmoud | Al-Harbi, Asia | Al-Qahtani, Wejdan | Hakamy, Sahar | Baba, Ghalia | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Alhathli, Elham M. | Karim, Sajjad | Salem, Nada | Eldin, Hend Nour | Abusamra, Heba | Kumar, Sudhir | Al-Qahtani, Mohammed H. | Alyamani, Aisha A. | Kalamegam, Gauthaman | Alhwait, Etimad A. | Gari, Mamdooh A. | Abbas, Mohammed M. | Alkaf, Mohammed H. | Alsehli, Haneen S. | Kadam, Roaa A. | Al-Qahtani, Mohammed | Gadi, Rawan | Buhmeida, Abdelbaset | Assidi, Mourad | Chaudhary, Adeel | Merdad, Leena | Alfakeeh, Saadiah M. | Alhwait, Etimad A. | Gari, Mamdooh A. | Abbas, Mohammed M. | Alkaf, Mohammed H. | Alsehli, Haneen S. | Kadam, Roaa | Kalamegam, Gauthaman | Ghazala, Rubi | Mathew, Shilu | Hamed, M. Haroon | Assidi, Mourad | Al-Qahtani, Mohammed | Qadri, Ishtiaq | Mathew, Shilu | Mira, Lobna | Shaabad, Manal | Hussain, Shireen | Assidi, Mourad | Abu-Elmagd, Muhammad | Al-Qahtani, Mohammed | Mathew, Shilu | Shaabad, Manal | Mira, Lobna | Hussain, Shireen | Assidi, Mourad | Abu-Elmagd, Muhammad | Al-Qahtani, Mohammed | Rebai, Ahmed | Assidi, Mourad | Buhmeida, Abdelbaset | Abu-Elmagd, Muhammad | Dallol, Ashraf | Shay, Jerry W. | Almutairi, Mikhlid H. | Ambers, Angie | Churchill, Jennifer | King, Jonathan | Stoljarova, Monika | Gill-King, Harrell | Assidi, Mourad | Abu-Elmagd, Muhammad | Buhmeida, Abdelbaset | Al-Qatani, Muhammad | Budowle, Bruce | Abu-Elmagd, Muhammad | Ahmed, Farid | Dallol, Ashraf | Assidi, Mourad | Almagd, Taha Abo | Hakamy, Sahar | Agarwal, Ashok | Al-Qahtani, Muhammad | Abuzenadah, Adel | Karim, Sajjad | Schulten, Hans-Juergen | Al Sayyad, Ahmad J. | Farsi, Hasan M. A. | Al-Maghrabi, Jaudah A. | Buhmaida, Abdelbaset | Mirza, Zeenat | Alotibi, Reem | Al-Ahmadi, Alaa | Alansari, Nuha A. | Albogmi, Alaa A. | Al-Quaiti, Maha M. | Ashgan, Fai T. | Bandah, Afnan | Al-Qahtani, Mohammed H. | Satar, Rukhsana | Rasool, Mahmood | Ahmad, Waseem | Nazam, Nazia | Lone, Mohamad I. | Naseer, Muhammad I. | Jamal, Mohammad S. | Zaidi, Syed K. | Pushparaj, Peter N. | Jafri, Mohammad A. | Ansari, Shakeel A. | Alqahtani, Mohammed H. | Bashier, Hanan | Al Qahtani, Abrar | Mathew, Shilu | Nour, Amal M. | Alkhatabi, Heba | Zenadah, Adel M. Abu | Buhmeida, Abdelbaset | Assidi, Mourad | Al Qahtani, Muhammed | Faheem, Muhammad | Mathew, Shilu | Mathew, Shiny | Pushparaj, Peter Natesan | Al-Qahtani, Mohammad H. | Alhadrami, Hani A. | Dallol, Ashraf | Abuzenadah, Adel | Hussein, Ibtessam R. | Chaudhary, Adeel G. | Bader, Rima S. | Bassiouni, Randa | Alquaiti, Maha | Ashgan, Fai | Schulten, Hans | Alama, Mohamed Nabil | Al Qahtani, Mohammad H. | Lone, Mohammad I. | Nizam, Nazia | Ahmad, Waseem | Jafri, Mohammad A. | Rasool, Mahmood | Ansari, Shakeel A. | Al-Qahtani, Muhammed H. | Alshihri, Eradah | Abu-Elmagd, Muhammad | Alharbi, Lina | Assidi, Mourad | Al-Qahtani, Mohammed | Mathew, Shilu | Natesan, Peter Pushparaj | Al Qahtani, Muhammed | Kalamegam, Gauthaman | Pushparaj, Peter Natesan | Khan, Fazal | Kadam, Roaa | Ahmed, Farid | Assidi, Mourad | Sait, Khalid Hussain Wali | Anfinan, Nisreen | Al Qahtani, Mohammed | Naseer, Muhammad I. | Chaudhary, Adeel G. | Jamal, Mohammad S. | Mathew, Shilu | Mira, Lobna S. | Pushparaj, Peter N. | Ansari, Shakeel A. | Rasool, Mahmood | AlQahtani, Mohammed H. | Naseer, Muhammad I. | Chaudhary, Adeel G. | Mathew, Shilu | Mira, Lobna S. | Jamal, Mohammad S. | Sogaty, Sameera | Bassiouni, Randa I. | Rasool, Mahmood | AlQahtani, Mohammed H. | Rasool, Mahmood | Ansari, Shakeel A. | Jamal, Mohammad S. | Pushparaj, Peter N. | Sibiani, Abdulrahman M. S. | Ahmad, Waseem | Buhmeida, Abdelbaset | Jafri, Mohammad A. | Warsi, Mohiuddin K. | Naseer, Muhammad I. | Al-Qahtani, Mohammed H. | Rubi | Kumar, Kundan | Naqvi, Ahmad A. T. | Ahmad, Faizan | Hassan, Md I. | Jamal, Mohammad S. | Rasool, Mahmood | AlQahtani, Mohammed H. | Ali, Ashraf | Jarullah, Jummanah | Rasool, Mahmood | Buhmeida, Abdelbasit | Khan, Shahida | Abdussami, Ghufrana | Mahfooz, Maryam | Kamal, Mohammad A. | Damanhouri, Ghazi A. | Jamal, Mohammad S. | Jarullah, Bushra | Jarullah, Jummanah | Jarullah, Mohammad S. S. | Ali, Ashraf | Rasool, Mahmood | Jamal, Mohammad S. | Assidi, Mourad | Abu-Elmagd, Muhammad | Bajouh, Osama | Pushparaj, Peter Natesan | Al-Qahtani, Mohammed | Abuzenadah, Adel | Jamal, Mohammad S. | Jarullah, Jummanah | Mathkoor, Abdulah E. A. | Alsalmi, Hashim M. A. | Oun, Anas M. M. | Damanhauri, Ghazi A. | Rasool, Mahmood | AlQahtani, Mohammed H. | Naseer, Muhammad I. | Rasool, Mahmood | Sogaty, Sameera | Chudhary, Adeel G. | Abutalib, Yousif A. | Merico, Daniele | Walker, Susan | Marshall, Christian R. | Zarrei, Mehdi | Scherer, Stephen W. | Al-Qahtani, Mohammad H. | Naseer, Muhammad I. | Faheem, Muhammad | Chaudhary, Adeel G. | Rasool, Mahmood | Kalamegam, Gauthaman | Ashgan, Fai Talal | Assidi, Mourad | Ahmed, Farid | Zaidi, Syed Kashif | Jan, Mohammed M. | Al-Qahtani, Mohammad H. | Al-Zahrani, Maryam | Lary, Sahira | Hakamy, Sahar | Dallol, Ashraf | Al-Ahwal, Mahmoud | Al-Maghrabi, Jaudah | Dermitzakis, Emmanuel | Abuzenadah, Adel | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Al-refai, Abeer A. | Saleh, Mona | Yassien, Rehab I. | Kamel, Mahmmoud | Habeb, Rabab M. | Filimban, Najlaa | Dallol, Ashraf | Ghannam, Nadia | Al-Qahtani, Mohammed | Abuzenadah, Adel Mohammed | Bibi, Fehmida | Akhtar, Sana | Azhar, Esam I. | Yasir, Muhammad | Nasser, Muhammad I. | Jiman-Fatani, Asif A. | Sawan, Ali | Lahzah, Ruaa A. | Ali, Asho | Hassan, Syed A. | Hasnain, Seyed E. | Tayubi, Iftikhar A. | Abujabal, Hamza A. | Magrabi, Alaa O. | Khan, Fazal | Kalamegam, Gauthaman | Pushparaj, Peter Natesan | Abuzenada, Adel | Kumosani, Taha Abduallah | Barbour, Elie | Al-Qahtani, Mohammed | Shabaad, Manal | Mathew, Shilu | Dallol, Ashraf | Merdad, Adnan | Buhmeida, Abdelbaset | Al-Qahtani, Mohammed | Assidi, Mourad | Abu-Elmagd, Muhammad | Gauthaman, Kalamegam | Gari, Mamdooh | Chaudhary, Adeel | Abuzenadah, Adel | Pushparaj, Peter Natesan | Al-Qahtani, Mohammed | Hassan, Syed A. | Tayubi, Iftikhar A. | Aljahdali, Hani M. A. | Al Nono, Reham | Gari, Mamdooh | Alsehli, Haneen | Ahmed, Farid | Abbas, Mohammed | Kalamegam, Gauthaman | Al-Qahtani, Mohammed | Mathew, Shilu | Khan, Fazal | Rasool, Mahmood | Jamal, Mohammed Sarwar | Naseer, Muhammad Imran | Mirza, Zeenat | Karim, Sajjad | Ansari, Shakeel | Assidi, Mourad | Kalamegam, Gauthaman | Gari, Mamdooh | Chaudhary, Adeel | Abuzenadah, Adel | Pushparaj, Peter Natesan | Al-Qahtani, Mohammed | Abu-Elmagd, Muhammad | Kalamegam, Gauthaman | Kadam, Roaa | Alghamdi, Mansour A. | Shamy, Magdy | Costa, Max | Khoder, Mamdouh I. | Assidi, Mourad | Pushparaj, Peter Natesan | Gari, Mamdooh | Al-Qahtani, Mohammed | Kharrat, Najla | Belmabrouk, Sabrine | Abdelhedi, Rania | Benmarzoug, Riadh | Assidi, Mourad | Al Qahtani, Mohammed H. | Rebai, Ahmed | Dhamanhouri, Ghazi | Pushparaj, Peter Natesan | Noorwali, Abdelwahab | Alwasiyah, Mohammad Khalid | Bahamaid, Afnan | Alfakeeh, Saadiah | Alyamani, Aisha | Alsehli, Haneen | Abbas, Mohammed | Gari, Mamdooh | Mobasheri, Ali | Kalamegam, Gauthaman | Al-Qahtani, Mohammed | Faheem, Muhammad | Mathew, Shilu | Pushparaj, Peter Natesan | Al-Qahtani, Mohammad H. | Mathew, Shilu | Faheem, Muhammad | Mathew, Shiny | Pushparaj, Peter Natesan | Al-Qahtani, Mohammad H. | Jamal, Mohammad Sarwar | Zaidi, Syed Kashif | Khan, Raziuddin | Bhatia, Kanchan | Al-Qahtani, Mohammed H. | Ahmad, Saif | AslamTayubi, Iftikhar | Tripathi, Manish | Hassan, Syed Asif | Shrivastava, Rahul | Tayubi, Iftikhar A. | Hassan, Syed | Abujabal, Hamza A. S. | Shah, Ishani | Jarullah, Bushra | Jamal, Mohammad S. | Jarullah, Jummanah | Sheikh, Ishfaq A. | Ahmad, Ejaz | Jamal, Mohammad S. | Rehan, Mohd | Abu-Elmagd, Muhammad | Tayubi, Iftikhar A. | AlBasri, Samera F. | Bajouh, Osama S. | Turki, Rola F. | Abuzenadah, Adel M. | Damanhouri, Ghazi A. | Beg, Mohd A. | Al-Qahtani, Mohammed | Hammoudah, Sahar A. F. | AlHarbi, Khalid M. | El-Attar, Lama M. | Darwish, Ahmed M. Z. | Ibrahim, Sara M. | Dallol, Ashraf | Choudhry, Hani | Abuzenadah, Adel | Awlia, Jalaludden | Chaudhary, Adeel | Ahmed, Farid | Al-Qahtani, Mohammed | Jafri, Mohammad A. | Abu-Elmagd, Muhammad | Assidi, Mourad | Al-Qahtani, Mohammed | khan, Imran | Yasir, Muhammad | Azhar, Esam I. | Al-basri, Sameera | Barbour, Elie | Kumosani, Taha | Khan, Fazal | Kalamegam, Gauthaman | Pushparaj, Peter Natesan | Abuzenada, Adel | Kumosani, Taha Abduallah | Barbour, Elie | EL Sayed, Heba M. | Hafez, Eman A. | Schulten, Hans-Juergen | Elaimi, Aisha Hassan | Hussein, Ibtessam R. | Bassiouni, Randa Ibrahim | Alwasiyah, Mohammad Khalid | Wintle, Richard F. | Chaudhary, Adeel | Scherer, Stephen W. | Al-Qahtani, Mohammed | Mirza, Zeenat | Pillai, Vikram Gopalakrishna | Karim, Sajjad | Sharma, Sujata | Kaur, Punit | Srinivasan, Alagiri | Singh, Tej P. | Al-Qahtani, Mohammed | Alotibi, Reem | Al-Ahmadi, Alaa | Al-Adwani, Fatima | Hussein, Deema | Karim, Sajjad | Al-Sharif, Mona | Jamal, Awatif | Al-Ghamdi, Fahad | Al-Maghrabi, Jaudah | Baeesa, Saleh S. | Bangash, Mohammed | Chaudhary, Adeel | Schulten, Hans-Juergen | Al-Qahtani, Mohammed | Faheem, Muhammad | Pushparaj, Peter Natesan | Mathew, Shilu | Kumosani, Taha Abdullah | Kalamegam, Gauthaman | Al-Qahtani, Mohammed | Al-Allaf, Faisal A. | Abduljaleel, Zainularifeen | Alashwal, Abdullah | Taher, Mohiuddin M. | Bouazzaoui, Abdellatif | Abalkhail, Halah | Ba-Hammam, Faisal A. | Athar, Mohammad | Kalamegam, Gauthaman | Pushparaj, Peter Natesan | Abu-Elmagd, Muhammad | Ahmed, Farid | Sait, Khalid HussainWali | Anfinan, Nisreen | Gari, Mamdooh | Chaudhary, Adeel | Abuzenadah, Adel | Assidi, Mourad | Al-Qahtani, Mohammed | Mami, Naira Ben | Haffani, Yosr Z. | Medhioub, Mouna | Hamzaoui, Lamine | Cherif, Ameur | Azouz, Msadok | Kalamegam, Gauthaman | Khan, Fazal | Mathew, Shilu | Nasser, Mohammed Imran | Rasool, Mahmood | Ahmed, Farid | Pushparaj, Peter Natesan | Al-Qahtani, Mohammed | Turkistany, Shereen A. | Al-harbi, Lina M. | Dallol, Ashraf | Sabir, Jamal | Chaudhary, Adeel | Abuzenadah, Adel | Al-Madoudi, Basmah | Al-Aslani, Bayan | Al-Harbi, Khulud | Al-Jahdali, Rwan | Qudaih, Hanadi | Al Hamzy, Emad | Assidi, Mourad | Al Qahtani, Mohammed | Ilyas, Asad M. | Ahmed, Youssri | Gari, Mamdooh | Ahmed, Farid | Alqahtani, Mohammed | Salem, Nada | Karim, Sajjad | Alhathli, Elham M. | Abusamra, Heba | Eldin, Hend F. Nour | Al-Qahtani, Mohammed H. | Kumar, Sudhir | Al-Adwani, Fatima | Hussein, Deema | Al-Sharif, Mona | Jamal, Awatif | Al-Ghamdi, Fahad | Al-Maghrabi, Jaudah | Baeesa, Saleh S. | Bangash, Mohammed | Chaudhary, Adeel | Al-Qahtani, Mohammed | Schulten, Hans-Juergen | Alamandi, Alaa | Alotibi, Reem | Hussein, Deema | Karim, Sajjad | Al-Maghrabi, Jaudah | Al-Ghamdi, Fahad | Jamal, Awatif | Baeesa, Saleh S. | Bangash, Mohammed | Chaudhary, Adeel | Schulten, Hans-Juergen | Al-Qahtani, Mohammed | Subhi, Ohoud | Bagatian, Nadia | Karim, Sajjad | Al-Johari, Adel | Al-Hamour, Osman Abdel | Al-Aradati, Hosam | Al-Mutawa, Abdulmonem | Al-Mashat, Faisal | Al-Maghrabi, Jaudah | Schulten, Hans-Juergen | Al-Qahtani, Mohammad | Bagatian, Nadia | Subhi, Ohoud | Karim, Sajjad | Al-Johari, Adel | Al-Hamour, Osman Abdel | Al-Mutawa, Abdulmonem | Al-Aradati, Hosam | Al-Mashat, Faisal | Al-Qahtani, Mohammad | Schulten, Hans-Juergen | Al-Maghrabi, Jaudah | shah, Muhammad W. | Yasir, Muhammad | Azhar, Esam I | Al-Masoodi, Saad | Haffani, Yosr Z. | Azouz, Msadok | Khamla, Emna | Jlassi, Chaima | Masmoudi, Ahmed S. | Cherif, Ameur | Belbahri, Lassaad | Al-Khayyat, Shadi | Attas, Roba | Abu-Sanad, Atlal | Abuzinadah, Mohammed | Merdad, Adnan | Dallol, Ashraf | Chaudhary, Adeel | Al-Qahtani, Mohammed | Abuzenadah, Adel | Bouazzi, Habib | Trujillo, Carlos | Alwasiyah, Mohammad Khalid | Al-Qahtani, Mohammed | Alotaibi, Maha | Nassir, Rami | Sheikh, Ishfaq A. | Kamal, Mohammad A. | Jiffri, Essam H. | Ashraf, Ghulam M. | Beg, Mohd A. | Aziz, Mohammad A. | Ali, Rizwan | Rasool, Mahmood | Jamal, Mohammad S. | Samman, Nusaibah | Abdussami, Ghufrana | Periyasamy, Sathish | Warsi, Mohiuddin K. | Aldress, Mohammed | Al Otaibi, Majed | Al Yousef, Zeyad | Boudjelal, Mohamed | Buhmeida, Abdelbasit | Al-Qahtani, Mohammed H. | AlAbdulkarim, Ibrahim | Ghazala, Rubi | Mathew, Shilu | Hamed, M. Haroon | Assidi, Mourad | Al-Qahtani, Mohammed | Qadri, Ishtiaq | Sheikh, Ishfaq A. | Abu-Elmagd, Muhammad | Turki, Rola F. | Damanhouri, Ghazi A. | Beg, Mohd A. | Suhail, Mohd | Qureshi, Abid | Jamal, Adil | Pushparaj, Peter Natesan | Al-Qahtani, Mohammad | Qadri, Ishtiaq | El-Readi, Mahmoud Z. | Eid, Safaa Y. | Wink, Michael | Isa, Ahmed M. | Alnuaim, Lulu | Almutawa, Johara | Abu-Rafae, Basim | Alasiri, Saleh | Binsaleh, Saleh | Nazam, Nazia | Lone, Mohamad I. | Ahmad, Waseem | Ansari, Shakeel A. | Alqahtani, Mohamed H.\n4. Inflammatory arthritis in caspase-1 gene deficient mice: Contribution of proteinase 3 for caspase-1-independent production of bioactive IL-1β Joosten, Leo A.B. | Netea, Mihai G. | Fantuzzi, Giamila | Koenders, Marije I. | Helsen, Monique M.A. | Sparrer, Helmut | Pham, Christine T. | van der Meer, Jos W.M. | Dinarello, Charles A. | van den Berg, Wim B.\nArthritis and rheumatism 2009;60(12):3651-3662.\nCaspase-1 is a known cysteine proteases and is a critical component of the inflammasome. Caspase-1 and neutrophil serine proteases, such as proteinase 3 (PR3) can process pro-IL-1β a crucial cytokine linked to the pathogenesis of rheumatoid arthritis, but their relative importance is unknown.\nTo this end we induced acute and chronic arthritis in caspase-1−/− mice and investigated the lack of caspase-1 on joint swelling, cartilage metabolism and joint pathology. In addition, caspase-1 activity was inhibited in mice lacking active cysteine proteases and evaluated the effect of dual blockade of caspase-1 and serine proteinase on arthritis severity and joint pathology.\nSurprisingly, caspase-1−/− mice developed joint swelling similar to wild-type mice in models of neutrophil-dominated arthritis. Joint fluid concentrations of bioactive IL-1β were comparable in caspase-1−/− mice and controls. In contrast, induction of chronic arthritis with minimal numbers of neutrophils in caspase-1−/− mice lead to reduced joint inflammation and cartilage damage, implying caspase-1 dependence. In mice lacking neutrophil serine PR3, inhibition caspase-1 activity results in decreased bioactive IL-1β concentrations in synovial tissue and less suppression of chondrocyte anabolic function. In addition, dual blockade of both PR-3 and caspase-1 lead to protection against cartilage and bone destruction.\nWe conclude that caspase-1 deficiency does not affect neutrophil-dominated joint inflammation, whereas in chronic arthritis the lack of caspase-1 results in reduced joint pathology. This study implies that caspase-1 inhibitors are not able to interfere with the whole spectrum of IL-1β production and hence may be of therapeutic value only in inflammatory conditions where limited numbers of neutrophils are present.\n5. Reduced Lipoapoptosis, Hedgehog Pathway Activation, and Fibrosis in Caspase-2 deficient Mice with Nonalcoholic Steatohepatitis Machado, MV | Michelotti, GA | Pereira de Almeida, T | Boursier, J | Kruger, L | Swiderska-Syn, M | Karaca, G | Xie, G | Guy, CD | Bohnic, B | Lindblom, KR | Johnson, E | Kornbluth, S | Diehl, AM\nCaspase-2 is an initiator caspase involved in multiple apoptotic pathways, particularly in response to specific intracellular stressors (eg. DNA damage, ER stress). We recently reported that caspase-2 was pivotal for the induction of cell death triggered by excessive intracellular accumulation of long chain fatty acids, a response known as lipoapoptosis. The liver is particularly susceptible to lipid-induced damage, explaining the pandemic status of non-alcoholic fatty liver disease (NAFLD). Progression from NAFLD to non-alcoholic steatohepatitis (NASH) results, in part, from hepatocyte apoptosis and consequential paracrine-mediated fibrogenesis. We evaluated the hypothesis that caspase-2 promotes NASH-related cirrhosis.\nCaspase-2 was localized in liver biopsies from NASH patients. Its expression was evaluated in different mouse models of NASH, and outcomes of diet-induced NASH were compared in wild type (WT) and caspase-2 deficient mice. Lipotoxicity was modeled in vitro using hepatocytes derived from WT and caspase-2 deficient mice.\nWe showed that caspase-2 is integral to the pathogenesis of NASH-related cirrhosis. Caspase-2 is localized in injured hepatocytes and its expression was markedly up-regulated in patients and animal models of NASH. During lipotoxic stress, caspase-2 deficiency reduced apoptosis, inhibited induction of pro-fibrogenic Hedgehog target genes in mice, and blocked production of Hedgehog ligands in cultured hepatocytes.\nThese data point to a critical role for caspase-2 in lipid-induced hepatocyte apoptosis in vivo, for the production of apoptosis-associated fibrogenic factors and in the progression of lipid-induced liver fibrosis. This raises the intriguing possibility that caspase-2 may be a promising therapeutic target to prevent progression to NASH.\nnonalcoholic steatohepatitis; caspase-2; apoptosis; fibrosis\n6. The Enigmatic Roles of Caspases in Tumor Development Jäger, Richard | Zwacka, Ralf M.\ncaspase; cancer; apoptosis; tumor suppressor; non-apoptotic functions; mutations; LOH\n7. Comparison of activated caspase detection methods in the gentamicin-treated chick cochlea Kaiser, Christina L. | Chapman, Brittany J. | Guidi, Jessica L. | Terry, Caitlin E. | Mangiardi, Dominic A. | Cotanche, Douglas A.\nHearing research 2008;240(1-2):1-11.\nAminoglycoside antibiotics induce caspase-dependent apoptotic death in cochlear hair cells. Apoptosis, a regulated form of cell death, can be induced by many stressors, which activate signaling pathways that result in the controlled dismantling of the affected cell. The caspase family of proteases is activated in the apoptotic signaling pathway and is responsible for cellular destruction. The initiator caspase-9 and the effector caspase-3 are both activated in chick cochlear hair cells following aminoglycoside exposure. We have analyzed caspase activation in the avian cochlea during gentamicin-induced hair cell death to compare two different methods of caspase detection: caspase antibodies and CaspaTag kits. Caspase antibodies bind to the cleaved activated form of caspase-9 or caspase-3 in specific locations in fixed tissue. CaspaTag is a fluorescent inhibitor that binds to a reactive cysteine residue on the large subunit of the caspase heterodimer in unfixed tissue.\nTo induce cochlear hair cell loss, 1-2 week-old chickens received a single injection of gentamicin (300 mg/kg). Chicks were sacrificed 24, 30, 42, 48, 72, or 96 h after injection. Cochleae were dissected and labeled for activated caspase-9 or caspase-3 using either caspase-directed antibodies or CaspaTag kits. Ears were co-labeled with either phalloidin or myosin VI to visualize hair cells and to determine the progression of cochlear damage. The timing of caspase activation was similar for both assays; however, caspase-9 and caspase-3 antibodies labeled only those cells currently undergoing apoptotic cell death. Conversely, CaspaTag-labeled all the cells that have undergone apoptotic cell death and ejection from the sensory epithelium, in addition to those that are currently in the cell death process. This makes CaspaTag ideal for showing an overall pattern or level of cell death over a period of time, while caspase antibodies provide a snapshot of cell death at a specific time point.\nApoptosis; Caspase; Avian; Aminoglycoside; Cochlea; Gentamicin; Hair cells\n8. Genetic ablation of caspase-7 promotes solar-simulated light-induced mouse skin carcinogenesis: the involvement of keratin-17 Lee, Mee-Hyun | Lim, Do Young | Kim, Myoung Ok | Lee, Sung-Young | Shin, Seung Ho | Kim, Jae Young | Kim, Sung-Hyun | Kim, Dong Joon | Jung, Sung Keun | Yao, Ke | Kundu, Joydeb Kumar | Lee, Hye Suk | Lee, Cheol-Jung | Dickinson, Sally E. | Alberts, David | Bowden, G.Timothy | Stratton, Steven | Curiel, Clara | Einspahr, Janine | Bode, Ann M. | Surh, Young-Joon | Cho, Yong-Yeon | Dong, Zigang\nThe increased incidence and multiplicity of solar simulated light-induced skin papillomas and elevated expression of keratin-17 in casapse-7 knock-out mice reflects a novel insight into the role of caspase-7-mediated cleavage of keratin-17 and subsequent induction of apoptosis in preventing skin photocarcinogenesis.\nSolar ultraviolet irradiation is an environmental carcinogen that causes skin cancer. Caspase-7 is reportedly expressed at reduced levels in many cancers. The present study was designed to examine the role of caspase-7 in solar-simulated light (SSL)-induced skin cancer and to elucidate its underlying molecular mechanisms. Our study revealed that mice with genetic deficiency of caspase-7 are highly susceptible to SSL-induced skin carcinogenesis. Epidermal hyperplasia, tumor volume and the average number of tumors were significantly increased in caspase-7 knockout (KO) mice compared with SKH1 wild-type mice irradiated with SSL. The expression of cell proliferation markers, such as survivin and Ki-67, was elevated in SSL-irradiated skin of caspase-7 KO mice compared with those observed in SSL-exposed wild-type SKH1 mouse skin. Moreover, SSL-induced apoptosis was abolished in skin from caspase-7 KO mice. Two-dimensional gel electrophoresis, followed by matrix-assisted laser desorption/ionization-time-of-flight analysis of skin tissue lysates from SSL-irradiated SKH1 wild-type and caspase-7 KO mice revealed an aberrant induction of keratin-17 in caspase-7 KO mice. Immunohistochemical analysis of skin tumors also showed an increase of keratin-17 expression in caspase-7 KO mice compared with SKH1 wild-type mice. The expression of keratin-17 was also elevated in SSL-irradiated caspase-7 KO keratinocytes as well as in human basal cell carcinomas. The in vitro caspase activity assay showed keratin-17 as a substrate of caspase-7, but not caspase-3. Overall, our study demonstrates that genetic loss of caspase-7 promotes SSL-induced skin carcinogenesis by blocking caspase-7-mediated cleavage of keratin-17.\n9. Caspase-1-Dependent and -Independent Cell Death Pathways in Burkholderia pseudomallei Infection of Macrophages Bast, Antje | Krause, Kathrin | Schmidt, Imke H. E. | Pudla, Matsayapan | Brakopp, Stefanie | Hopf, Verena | Breitbach, Katrin | Steinmetz, Ivo\nPLoS Pathogens 2014;10(3):e1003986.\nThe cytosolic pathogen Burkholderia pseudomallei and causative agent of melioidosis has been shown to regulate IL-1β and IL-18 production through NOD-like receptor NLRP3 and pyroptosis via NLRC4. Downstream signalling pathways of those receptors and other cell death mechanisms induced during B. pseudomallei infection have not been addressed so far in detail. Furthermore, the role of B. pseudomallei factors in inflammasome activation is still ill defined. In the present study we show that caspase-1 processing and pyroptosis is exclusively dependent on NLRC4, but not on NLRP3 in the early phase of macrophage infection, whereas at later time points caspase-1 activation and cell death is NLRC4- independent. In the early phase we identified an activation pathway involving caspases-9, -7 and PARP downstream of NLRC4 and caspase-1. Analyses of caspase-1/11-deficient infected macrophages revealed a strong induction of apoptosis, which is dependent on activation of apoptotic initiator and effector caspases. The early activation pathway of caspase-1 in macrophages was markedly reduced or completely abolished after infection with a B. pseudomallei flagellin FliC or a T3SS3 BsaU mutant. Studies using cells transfected with the wild-type and mutated T3SS3 effector protein BopE indicated also a role of this protein in caspase-1 processing. A T3SS3 inner rod protein BsaK mutant failed to activate caspase-1, revealed higher intracellular counts, reduced cell death and IL-1β secretion during early but not during late macrophage infection compared to the wild-type. Intranasal infection of BALB/c mice with the BsaK mutant displayed a strongly decreased mortality, lower bacterial loads in organs, and reduced levels of IL-1β, myeloperoxidase and neutrophils in bronchoalveolar lavage fluid. In conclusion, our results indicate a major role for a functional T3SS3 in early NLRC4-mediated caspase-1 activation and pyroptosis and a contribution of late caspase-1-dependent and -independent cell death mechanisms in the pathogenesis of B. pseudomallei infection.\n10. Glutamate-induced apoptosis in primary cortical neurons is inhibited by equine estrogens via down-regulation of caspase-3 and prevention of mitochondrial cytochrome c release Zhang, YueMei | Bhavnani, Bhagu R\nBMC Neuroscience 2005;6:13.\n11. The Inflammasome-Mediated Caspase-1 Activation Controls Adipocyte Differentiation and Insulin Sensitivity Stienstra, Rinke | Joosten, Leo A.B. | Koenen, Tim | van Tits, Berry | van Diepen, Janna A. | van den Berg, Sjoerd A.A. | Rensen, Patrick C.N. | Voshol, Peter J. | Fantuzzi, Giamilla | Hijmans, Anneke | Kersten, Sander | Müller, Michael | van den Berg, Wim B. | van Rooijen, Nico | Wabitsch, Martin | Kullberg, Bart-Jan | van der Meer, Jos W.M. | Kanneganti, Thirumala | Tack, Cees J. | Netea, Mihai G.\n12. DECREASED EXPRESSION LEVEL OF APOPTOSIS-RELATED GENES AND/OR PROTEINS IN SKELETAL MUSCLES, BUT NOT IN HEARTS, OF GROWTH HORMONE RECEPTOR KNOCKOUT MICE Gesing, Adam | Masternak, Michal M. | Wang, Feiya | Lewinski, Andrzej | Karbownik-Lewinska, Malgorzata | Bartke, Andrzej\n13. Caspase-2 impacts lung tumorigenesis and chemotherapy response in vivo Terry, M R | Arya, R | Mukhopadhyay, A | Berrett, K C | Clair, P M | Witt, B | Salama, M E | Bhutkar, A | Oliver, T G\nCell Death and Differentiation 2014;22(5):719-730.\n14. Leptin attenuates cardiac apoptosis after chronic ischaemic injury McGaffin, Kenneth R. | Zou, Baobo | McTiernan, Charles F. | O’Donnell, Christopher P.\n15. Caspase-8 tyrosine-380 phosphorylation inhibits CD95 DISC function by preventing procaspase-8 maturation and cycling within the complex Powley, I R | Hughes, M A | Cain, K | MacFarlane, M\nCaspase-8 is a key initiator of apoptotic cell death where it functions as the apical protease in death receptor-mediated apoptosis triggered via the death-inducing signalling complex (DISC). However, the observation that caspase-8 is upregulated in many common tumour types led to the discovery of alternative non-apoptotic, pro-survival functions, many of which are contingent on phosphorylation of a tyrosine residue (Y380) found in the linker region between the two catalytic domains of the enzyme. Furthermore, Src-mediated Y380 phosphorylation leads to increased resistance to CD95-induced apoptosis; however, the mechanism underlying this impaired response to extrinsic apoptotic stimuli has not been identified. Consequently, we have employed a number of model systems to further dissect this protective mechanism. First, using an in vitro DISC model together with recombinant procaspase-8 variants, we show that Y380 phosphorylation inhibits procaspase-8 activation at the CD95 DISC, thereby preventing downstream activation of the caspase cascade. Second, we validated this finding in a cellular context using transfected neuroblastoma cell lines deficient in caspase-8. Reconstitution of these lines with phosphomimetic-caspase-8 results in increased resistance to CD95-mediated apoptosis and enhanced cell migration. When the in vitro DISC is assembled in the presence of cell lysate, caspase-8 Y380 phosphorylation attenuates DISC activity by inhibiting procaspase-8 autoproteolytic activity but not recruitment or homodimerization of caspase-8 within the complex. Once incorporated into the DISC, phosphorylated caspase-8 is unable to be released from the complex; this inhibits further cycling and release of active catalytic subunits into the cytoplasm, thus resulting in increased apoptotic resistance. Taken together, our novel findings expand our understanding of the key mechanisms underlying the anti-apoptotic functions of caspase-8 which may act as a critical block to existing antitumour therapies. Importantly, reversal or inhibition of caspase-8 phosphorylation may prove a valuable avenue to explore for sensitization of resistant tumours to extrinsic apoptotic stimuli.\n16. Prostaglandin F2alpha- and FAS-activating antibody-induced regression of the corpus luteum involves caspase-8 and is defective in caspase-3 deficient mice Carambula, Silvia F | Pru, James K | Lynch, Maureen P | Matikainen, Tiina | Gonçalves, Paulo Bayard D | Flavell, Richard A | Tilly, Jonathan L | Rueda, Bo R\nReproductive biology and endocrinology : RB&E 2003;1:15.\nWe recently demonstrated that caspase-3 is important for apoptosis during spontaneous involution of the corpus luteum (CL). These studies tested if prostaglandin F2α (PGF2α) or FAS regulated luteal regression, utilize a caspase-3 dependent pathway to execute luteal cell apoptosis, and if the two receptors work via independent or potentially shared intracellular signaling components/pathways to activate caspase-3. Wild-type (WT) or caspase-3 deficient female mice, 25–26 days old, were given 10 IU equine chorionic gonadotropin (eCG) intraperitoneally (IP) followed by 10 IU human chorionic gonadotropin (hCG) IP 46 h later to synchronize ovulation. The animals were then injected with IgG (2 micrograms, i.v.), the FAS-activating antibody Jo2 (2 micrograms, i.v.), or PGF2α (10 micrograms, i.p.) at 24 or 48 h post-ovulation. Ovaries from each group were collected 8 h later for assessment of active caspase-3 enzyme and apoptosis (measured by the TUNEL assay) in the CL. Regardless of genotype or treatment, CL in ovaries collected from mice injected 24 h after ovulation showed no evidence of active caspase-3 or apoptosis. However, PGF2α or Jo2 at 48 h post-ovulation and collected 8 h later induced caspase-3 activation in 13.2 ± 1.8% and 13.7 ± 2.2 % of the cells, respectively and resulted in 16.35 ± 0.7% (PGF2α) and 14.3 ± 2.5% TUNEL-positive cells when compared to 1.48 ± 0.8% of cells CL in IgG treated controls. In contrast, CL in ovaries collected from caspase-3 deficient mice whether treated with PGF2α , Jo2, or control IgG at 48 h post-ovulation showed little evidence of active caspase-3 or apoptosis. CL of WT mice treated with Jo2 at 48 h post-ovulation had an 8-fold increase in the activity of caspase-8, an activator of caspase-3 that is coupled to the FAS death receptor. Somewhat unexpectedly, however, treatment of WT mice with PGF2α at 48 h post-ovulation resulted in a 22-fold increase in caspase-8 activity in the CL, despite the fact that the receptor for PGF2α has not been shown to be directly coupled to caspase-8 recruitment and activation. We hypothesize that PGF2α initiates luteolysis in vivo, at least in part, by increasing the bioactivity or bioavailability of cytokines, such as FasL and that multiple endocrine factors work in concert to activate caspase-3-driven apoptosis during luteolysis.\n17. Recql5 protects against lipopolysaccharide/D-galactosamine-induced liver injury in mice Liao, Wan-Qin | Qi, Ya-Lei | Wang, Lin | Dong, Xiao-Ming | Xu, Tao | Ding, Chao-Dong | Liu, Rui | Liang, Wei-Cheng | Lu, Li-Ting | Li, He | Li, Wen-Feng | Luo, Guang-Bin | Lu, Xin-Cheng\n18. The Pro-Apoptotic BH3-only, Bcl-2 Family Member Puma Is Critical for Acute Ethanol-Induced Neuronal Apoptosis Ghosh, Arindam P. | Walls, Ken C. | Klocke, Barbara J. | Toms, Rune | Strasser, Andreas | Roth, Kevin A.\nJournal of neuropathology and experimental neurology 2009;68(7):747-756.\nSynaptogenesis in humans occurs in the last trimester of gestation and in the first few years of life whereas it occurs in the postnatal period in rodents. A single exposure of neonatal rodents to ethanol during this period evokes extensive neuronal apoptosis. Previous studies indicate that ethanol triggers the intrinsic apoptotic pathway in neurons and that this requires the multi-BH domain, pro-apoptotic Bcl-2 family member Bax. To define the upstream regulators of this apoptotic pathway, we examined the possible roles of p53 and a subclass of pro-apoptotic Bcl-2 family members (i.e. the BH3 domain-only proteins) in neonatal wild-type and gene-targeted mice that lack these cell death inducers. Acute ethanol exposure produced greater caspase-3 activation and neuronal apoptosis in wild type mice than in saline-treated littermate controls. Loss of Puma resulted in marked protection from ethanol-induced caspase-3 activation and apoptosis. Although Puma expression has been reported to be regulated by p53, p53-deficient mice exhibited a similar extent of ethanol-induced caspase-3 activation and neuronal apoptosis as wild-type mice. Mice deficient in other pro-apoptotic BH3-only proteins, including Noxa, Bim or Hrk, showed no significant protection from ethanol-induced neuronal apoptosis. Collectively, these studies indicate a p53-independent, Bax- and Puma-dependent mechanism of neuronal apoptosis and identify Puma as a possible molecular target for inhibiting the effects of intrauterine ethanol exposure in humans.\nApoptosis; Bax; BH3-only; Caspase-3; Ethanol; Noxa; p53; Puma\n19. Lyapunov exponents and phase diagrams reveal multi-factorial control over TRAIL-induced apoptosis Aldridge, Bree B | Gaudet, Suzanne | Lauffenburger, Douglas A | Sorger, Peter K\n20. Non-apoptotic functions of caspase-7 during osteogenesis Svandova, E | Lesot, H | Vanden Berghe, T | Tucker, A S | Sharpe, P T | Vandenabeele, P | Matalova, E\nCell Death & Disease 2014;5(8):e1366-.\nCaspase-3 and -7 are generally known for their central role in the execution of apoptosis. However, their function is not limited to apoptosis and under specific conditions activation has been linked to proliferation or differentiation of specialised cell types. In the present study, we followed the localisation of the activated form of caspase-7 during intramembranous (alveolar and mandibular bones) and endochondral (long bones of limbs) ossification in mice. In both bone types, the activated form of caspase-7 was detected from the beginning of ossification during embryonic development and persisted postnatally. The bone status was investigated by microCT in both wild-type and caspase-7-deficient adult mice. Intramembranous bone in mutant mice displayed a statistically significant decrease in volume while the mineral density was not altered. Conversely, endochondral bone showed constant volume but a significant decrease in mineral density in caspase-7 knock-out mice. Cleaved caspase-7 was present in a number of cells that did not show signs of apoptosis. PCR array analysis of the mandibular bone of caspase-7-deficient versus wild-type mice pointed to a significant decrease in mRNA levels for Msx1 and Smad1 in early bone formation. These observations might explain the decrease in the alveolar bone volume of adult knock-out mice. In conclusion, this study is the first to report a non-apoptotic function of caspase-7 in osteogenesis and also demonstrates further specificities in endochondral versus intramembranous ossification.\n21. Listeria monocytogenes Infection in Caspase-11-Deficient Mice Mueller, Nicolas J. | Wilkinson, Robert A. | Fishman, Jay A.\nInfection and Immunity 2002;70(5):2657-2664.\nCaspase-11 (Cas11) is a cysteine protease involved in programmed cell death and cytokine maturation. Through activation of Cas1 (interleukin-1β [IL-1β]-converting enzyme), Cas11 is directly involved in the maturation of IL-1β and IL-18. Apoptosis is mediated through Cas3. Given the role of apoptosis and cytokine signaling during the innate immune response in intracellular infection, we examined Cas11-deficient (Cas11−/−) mice during infection with Listeria monocytogenes. Cas11−/− and wild-type C57BL/6 mice were equally susceptible to intravenous infection with L. monocytogenes, resulting in similar bacterial burdens in tissue and similar survival rates. By contrast, enhanced susceptibility was observed in control mice on a mixed genetic 129/C57BL/DBA2 background. Cas11−/− and wild-type mice infected with Listeria had similar hepatic microabscess formation in terms of histologic appearance, size, and number. Apoptosis of L. monocytogenes-infected hepatocytes in vivo and in vitro in primary culture was not altered by the absence of Cas11. Serum IL-18 and IL-1β levels were similar in Cas11−/− mice and controls. Endotoxin (lipopolysaccharide [LPS])-challenged Cas11−/− mice were deficient in the production of gamma interferon. IL-1β responses in Cas11−/− were normal with intravenous administration of LPS but decreased with intraperitoneal administration. Our findings suggest that Cas11 deficiency does not impair the immune response to infection with L. monocytogenes. Apoptosis and maturation of IL-18 and IL-1β were normal despite Cas11 deficiency. LPS-induced proinflammatory pathways are altered by the absence of Cas11. While Cas11-mediated Cas1 and Cas3 activation is crucial for cytokine maturation and apoptosis during inflammation, alternative pathways allow normal inflammatory and apoptotic responses during infection with L. monocytogenes.\n22. Retina Is Protected by Neuroserpin from Ischemic/Reperfusion-Induced Injury Independent of Tissue-Type Plasminogen Activator Gu, R. P. | Fu, L. L. | Jiang, C. H. | Xu, Y. F. | Wang, X. | Yu, J.\nPLoS ONE 2015;10(7):e0130440.\nThe purpose of the present study was to investigate the potential neuroprotective effect of neuroserpin (NSP) on acute retinal ischemic/reperfusion-induced (IR) injury. An IR injury model was established by elevating intraocular pressure (IOP) for 60 minutes in wild type and tPA-deficient (tPA-/-) mice. Prior to IR injury, 1 μL of 20 μmol/L NSP or an equal volume of bovine serum albumin (BSA) was intravitreally administered. Retinal function was evaluated by electroretinograph (ERG) and the number of apoptotic neurons was determined via TUNEL labeling. Caspase-3, -8, -9,poly (ADP-ribose) polymerase (PARP)and their cleaved forms were subsequently analyzed. It was found that IR injury significantly damaged retinal function, inducing apoptosis in the retina, while NSP attenuated the loss of retinal function and significantly reduced the number of apoptotic neurons in both wild type and tPA-/- mice. The levels of cleaved caspase-3, cleaved PARP (the substrate of caspase-3) and caspase-9 (the modulator of the caspase-3), which had increased following IR injury, were significantly inhibited by NSP in both wild type and tPA-/- mice. NSP increased ischemic tolerance in the retina at least partially by inhibiting the intrinsic cell death signaling pathway of caspase-3. It was therefore concluded that the protective effect of neuroserpin maybe independent from its canonical interaction with a tissue-type plasminogen activator.\n23. Caspase-Dependent Inhibition of Mousepox Replication by gzmB Pardo, Julián | Gálvez, Eva Ma | Koskinen, Aulikki | Simon, Markus M. | Lobigs, Mario | Regner, Matthias | Müllbacher, Arno\nPLoS ONE 2009;4(10):e7512.\nHere we analysed the physiological relevance of those pro-apoptotic pathways in ectromelia infection, by incubating ectromelia-immune ex vivo Tc cells from granzyme A deficient (GzmB+ Tc cells) or granzyme A and granzyme B deficient (GzmA×B−/− Tc cell) mice with ectromelia-infected target cells. We found that gzmB-induced apoptosis was totally blocked in ectromelia infected or peptide pulsed cells lacking caspases-3/-7. However ectromelia inhibited only partially apoptosis in cells deficient for Bid/Bak/Bax and not at all when both pathways were operative suggesting that the virus is able to interfere with apoptosis induced by gzmB in case not all pathways are activated. Importantly, inhibition of viral replication in vitro, as seen with wild type cells, was not affected by the lack of Bid/Bak/Bax but was significantly reduced in caspase-3/-7-deficient cells. Both caspase dependent processes were strictly dependent on gzmB, since Tc cells, lacking both gzms, neither induced apoptosis nor reduced viral titers.\nOut findings present the first evidence on the biological importance of the independent gzmB-inducible pro-apoptotic pathways in a physiological relevant virus infection model.\n24. Sex-specific alterations in glucose homeostasis and metabolic parameters during ageing of caspase-2-deficient mice Wilson, C H | Nikolic, A | Kentish, S J | Shalini, S | Hatzinikolas, G | Page, A J | Dorstyn, L | Kumar, S\nCell Death Discovery 2016;2:16009-.\n25. Caspase-7: a protease involved in apoptosis and inflammation Lamkanfi, Mohamed | Kanneganti, Thirumala-Devi\nThe international journal of biochemistry & cell biology 2009;42(1):21-24.\ncaspase-7; caspase-3; apoptosis; inflammation


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