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1.
EJB-Egyptian Journal of Biochemistry and Molecular Biology [The]. 2011; 29 (2): 343-360
em Inglês | IMEMR | ID: emr-117199

RESUMO

It was relevant to assess the impact of a HPV-16 [human papillomavirus-16] which is a high-risk genotype on head and neck cancers and its relation to CIAP-2 expression [Cellular Inhibitor of apoptosis-2]. Tissue samples were taken from patients diagnosed as head and neck cancer. All samples were subjected to qualitative polymerase chain reaction [PCR] analysis for HPV, qualitative and semi-quantitative reverse transcription polymerase chain reaction [RT-PCR] of CIAP-2. There was a significant association between HPV-16 and CIAP2 positivity and head and neck tumors. CIAP-2 expression in malignant tissues was highly associated with HPV-16 infection at sensitivity 73.9% and absolute specificity


Assuntos
Humanos , Papillomavirus Humano 16/genética , Reação em Cadeia da Polimerase/métodos , Sensibilidade e Especificidade
2.
EJB-Egyptian Journal of Biochemistry and Molecular Biology [The]. 2004; 22 (2): 41-54
em Inglês | IMEMR | ID: emr-205514

RESUMO

The imbalance in the cytokine production by the hepatitis C viral [HCV] infection might contribute to the chronicity of liver inflammation with subsequent progression to hepatocellular carcinoma [HCC]. The current study was performed to evaluate the immunomodulatory effects of HCV infection of normal donor peripheral blood mononuclear cells [PBMC] as well as in patients with chronic HCV infection and patients. The study included 363 subjects [group 1] with chronic liver disease and 40 healthy control subjects [group 2]. Of group 1, three hundred and thirty seven patients were HCV Ab positive as was measured by HCV enzyme immunoassay [EIA] version 3.0. Only 250 patients had HCV RNA in their sera as evidenced by polymerase chain reaction [PCR]. Of the PCR positive patients, sixty-eight patients were further as a representative subgroup, 68 HCV RNA positive patients were subjected to HCV subjected to quantitative branched DNA assay, 12 patients had high viremia, 33 had moderate viremia and 23 had low viremia. All patients were subjected to lL-4, IL-1Beta, and TNF-alpha estimation by ELISA viremia. All subjects were subjected to IL-4, lL-1Beta, and TNF-alpha estimation by EIA. Group 1 showed a significant increase in serum levels of TNF-alpha, lL-4 and ALT, and lowered levels of IL-1Beta and albumin compared to Group 2. Within group 1, HCV RNA positive patients demonstrated increased levels of lL-4 and ALT, and decreased levels of IL-1Beta and albumin compared to Nov RNA negative patients. TNF-alpha levels showed insignificant change among between both subgroups. Treatment of phytohaemaggiutinin [PHA]-stimulated normal donor-PBMC with pelleted virus led to decrease in their rate of proliferation [as determined by H3. Thymidine uptake] in a dose response manner. This response was partaliy reversed after addition of HCV RNA positive patients’ sera. To conclude, HCV infection leads to imbalance of cytokine release with predominance of Th2 cytokines over Th1, which was evident from the increased levels of IL-4, and the decreased levels of lL-1beta in patients' sera infected with HCV

3.
Eduan Wilkinson; Marta Giovanetti; Houriiyah Tegally; James E San; Richard Lessels; Diego Cuadros; Darren P Martin; Abdel-Rahman N Zekri; Abdoul Sangare; Abdoul Salam Ouedraogo; Abdul K Sesay; Adnene Hammami; Adrienne A Amuri; Ahmad Sayed; Ahmed Rebai; Aida Elargoubi; Alpha K Keita; Amadou A Sall; Amadou Kone; Amal Souissi; Ana V Gutierrez; Andrew Page; Arnold Lambisia; Arash Iranzadeh; Augustina Sylverken; Azeddine Ibrahimi; Bourema Kouriba; Bronwyn Kleinhans; Beatrice Dhaala; Cara Brook; Carolyn Williamson; Catherine B Pratt; Chantal G Akoua-Koffi; Charles Agoti; Collins M Moranga; James D Nokes; Daniel J Bridges; Daniel L Bugembe; Deelan Doolabh; Deogratius Ssemwanga; Derek Tshabuila; Diarra Bassirou; Dominic S.Y. Amuzu; Dominique Goedhals; Dorcas Maruapula; Edith N Ngabana; Eddy Lusamaki; Edidah Moraa; Elmostafa El Fahime; Emerald Jacob; Emmanuel Lokilo; Enatha Mukantwari; Essia Belarbi; Etienne Simon-Loriere; Etile A Anoh; Fabian Leendertz; Faida Ajili; Fares Wasfi; Faustinos T Takawira; Fawzi Derrar; Feriel Bouzid; Francisca M Muyembe; Frank Tanser; Gabriel Mbunsu; Gaetan Thilliez; Gert van Zyl; Grit Schubert; George Githinji; Gordon A Awandare; Haruka Abe; Hela H Karray; Hellen Nansumba; Hesham A Elgahzaly; Hlanai Gumbo; Ibtihel Smeti; Ikhlass B Ayed; Imed Gaaloul; Ilhem B.B. Boubaker; Inbal Gazy; Isaac Ssewanyana; Jean B Lekana-Douk; Jean-Claude C Makangara; Jean-Jacques M Tamfum; Jean M Heraud; Jeffrey G Shaffer; Jennifer Giandhari; Jingjing Li; Jiro Yasuda; Joana Q Mends; Jocelyn Kiconco; Jonathan A Edwards; John Morobe; John N Nkengasong; John Gyapong; John T Kayiwa; Jones Gyamfi; Jouali Farah; Joyce M Ngoi; Joyce Namulondo; Julia C Andeko; Julius J Lutwama; Justin O Grady; Kefenstse A Tumedi; Khadija Said; Kim Hae-Young; Kwabena O Duedu; Lahcen Belyamani; Lavanya Singh; Leonardo de O. Martins; Madisa Mine; Mahmoud el Hefnawi; Mahjoub Aouni; Maha Mastouri; Maitshwarelo I Matsheka; Malebogo Kebabonye; Manel Turki; Martin Nyaga; Matoke Damaris; Matthew Cotten; Maureen W Mburu; Maximillian Mpina; Michael R Wiley; Mohamed A Ali; Mohamed K Khalifa; Mohamed G Seadawy; Mouna Ouadghiri; Mulenga Mwenda; Mushal Allam; My V.T. Phan; Nabil Abid; Nadia Touil; Najla Kharrat; Nalia Ismael; Nedio Mabunda; Nei-yuan Hsiao; Nelson Silochi; Ngonda Saasa; Nicola Mulder; Patrice Combe; Patrick Semanda; Paul E Oluniyi; Paulo Arnaldo; Peter K Quashie; Reuben Ayivor-Djanie; Philip A Bester; Philippe Dussart; Placide K Mbala; Pontiano Kaleebu; Richard Njouom; Richmond Gorman; Robert A Kingsley; Rosina A.A. Carr; Saba Gargouri; Saber Masmoudi; Samar Kassim; Sameh Trabelsi; Sami Kammoun; Sanaa Lemriss; Sara H Agwa; Sebastien Calvignac-Spencer; Seydou Doumbia; Sheila M Madinda; Sherihane Aryeetey; Shymaa S Ahmed; Sikhulile Moyo; Simani Gaseitsiwe; Edgar Simulundu; Sonia Lekana-Douki; Soumeya Ouangraoua; Steve A Mundeke; Sumir Panji; Sureshnee Pillay; Susan Engelbrecht; Susan Nabadda; Sylvie Behillil; Sylvie van der Werf; Tarik Aanniz; Tapfumanei Mashe; Thabo Mohale; Thanh Le-Viet; Tobias Schindler; Upasana Ramphal; Magalutcheemee Ramuth; Vagner Fonseca; Vincent Enouf; Wael H Roshdy; William Ampofo; Wolfgang Preiser; Wonderful T Choga; Yaw Bediako; Yenew K. Tebeje; Yeshnee Naidoo; Zaydah de Laurent; Sofonias K Tessema; Tulio de Oliveira.
Preprint em Inglês | PREPRINT-MEDRXIV | ID: ppmedrxiv-21257080

RESUMO

The progression of the SARS-CoV-2 pandemic in Africa has so far been heterogeneous and the full impact is not yet well understood. Here, we describe the genomic epidemiology using a dataset of 8746 genomes from 33 African countries and two overseas territories. We show that the epidemics in most countries were initiated by importations, predominantly from Europe, which diminished following the early introduction of international travel restrictions. As the pandemic progressed, ongoing transmission in many countries and increasing mobility led to the emergence and spread within the continent of many variants of concern and interest, such as B.1.351, B.1.525, A.23.1 and C.1.1. Although distorted by low sampling numbers and blind-spots, the findings highlight that Africa must not be left behind in the global pandemic response, otherwise it could become a breeding ground for new variants.

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