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26 results on '"Fakhraldeen, Saja A."'

2. Shotgun metagenomics reveals the interplay between microbiome diversity and environmental gradients in the first marine protected area in the northern Arabian Gulf.

Author

Fakhraldeen, Saja A., Madhusoodhanan, Rakhesh, Habibi, Nazima, Al-Haddad, Sakinah, Alagarsamy, Surendraraj, Habeebullah, Sabeena F. K., Al-Zakri, Walid M., Thuslim, Fathima, Fernandes, Loreta, Al-Yamani, Faiza, and Al-Said, Turki

Subjects
MARINE parks & reserves, ECOLOGICAL resilience, COASTAL development, MICROBIAL communities, MARINE ecology
Abstract

Introduction: The northwest Arabian Gulf encounters significant anthropogenic pressures, including nutrient enrichment from coastal development and effluent discharge. Methods: This study presents the first shotgun metagenomics-based characterization of microbial communities in Kuwaiti waters of the northwest Arabian Gulf, focusing on Kuwait's first Marine Protected Area (MPA) in Sulaibikhat Bay, a vital nursery ground for commercially important fish. Results: Analysis revealed significantly higher microbial diversity within the MPA compared to adjacent waters, with Rhodobacteraceae (27.8%) and Flavobacteriaceae (15.3%) being dominant. Elevated inorganic phosphorus, nitrogen, and salinity were key factors driving this diversity. Multivariate analysis highlighted phosphate as a critical component affecting the MPA microbial community structure, particularly for the families Microbacteriaceae, Flavobacteriaceae, and Rhodobacteraceae. Discussion: This study underscores the ecological importance of MPAs and highlights the impact of nutrient enrichment and other environmental stressors on microbial diversity, emphasizing the need to reduce nutrient influx to mitigate eutrophication and enhance marine ecosystem resilience in stressed environments. [ABSTRACT FROM AUTHOR]

Published
2025
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5. The First Marine Protected Area in the Northern Arabian Gulf Contains Unique Communities of Microbes that are Significantly Affected by Phosphate Levels

Author

Fakhraldeen, Saja A., primary, Madhusoodhanan, Rakhesh, additional, Habibi, Nazima, additional, Al-Haddad, Sakinah, additional, Alagarsamy, Surendraraj, additional, Habeebullah, Sabeena F. K., additional, Al-Zakri, Walid M., additional, Thuslim, Fathima, additional, Fernandes, Loreta, additional, Al-Yamani, Faiza Y., additional, and Al-Said, Turki, additional

Published
2024
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12. Genomic analysis of sewage from 101 countries reveals global landscape of antimicrobial resistance

Author

Munk, Patrick, Brinch, Christian, Møller, Frederik Duus, Petersen, Thomas N., Hendriksen, Rene S., Seyfarth, Anne Mette, Kjeldgaard, Jette S., Svendsen, Christina Aaby, van Bunnik, Bram, Berglund, Fanny, Bego, Artan, Power, Pablo, Rees, Catherine, Lambrinidis, Dionisia, Neilson, Elizabeth Heather Jakobsen, Gibb, Karen, Coventry, Kris, Collignon, Peter, Cassar, Susan, Allerberger, Franz, Begum, Anowara, Hossain, Zenat Zebin, Worrell, Carlon, Vandenberg, Olivier, Pieters, Ilse, Victorien, Dougnon Tamègnon, Gutierrez, Angela Daniela Salazar, Soria, Freddy, Grujić, Vesna Rudić, Mazalica, Nataša, Rahube, Teddie O., Tagliati, Carlos Alberto, Rodrigues, Dalia, Oliveira, Guilherme, de Souza, Larissa Camila Ribeiro, Ivanov, Ivan, Juste, Bonkoungou Isidore, Oumar, Traoré, Sopheak, Thet, Vuthy, Yith, Ngandijo, Antoinette, Nzouankeu, Ariane, Olivier, Ziem A. Abah Jacques, Yost, Christopher K., Kumar, Pratik, Brar, Satinder Kaur, Tabo, Djim-Adjim, Adell, Aiko D., Paredes-Osses, Esteban, Martinez, Maria Cristina, Cuadros-Orellana, Sara, Ke, Changwen, Zheng, Huanying, Baisheng, Li, Lau, Lok Ting, Chung, Teresa, Jiao, Xiaoyang, Yu, Yongjie, JiaYong, Zhao, Morales, Johan F. Bernal, Valencia, Maria Fernanda, Donado-Godoy, Pilar, Coulibaly, Kalpy Julien, Hrenovic, Jasna, Jergović, Matijana, Karpíšková, Renáta, Deogratias, Zozo Nyarukweba, Elsborg, Bodil, Hansen, Lisbeth Truelstrup, Jensen, Pernille Erland, Abouelnaga, Mohamed, Salem, Mohamed Fathy, Koolmeister, Marliin, Legesse, Mengistu, Eguale, Tadesse, Heikinheimo, Annamari, Le Guyader, Soizick, Schaeffer, Julien, Villacis, Jose Eduardo, Sanneh, Bakary, Malania, Lile, Nitsche, Andreas, Brinkmann, Annika, Schubert, Sara, Hesse, Sina, Berendonk, Thomas U., Saba, Courage Kosi Setsoafia, Mohammed, Jibril, Feglo, Patrick Kwame, Banu, Regina Ama, Kotzamanidis, Charalampos, Lytras, Efthymios, Lickes, Sergio A., Kocsis, Bela, Solymosi, Norbert, Thorsteinsdottir, Thorunn R., Hatha, Abdulla Mohamed, Ballal, Mamatha, Bangera, Sohan Rodney, Fani, Fereshteh, Alebouyeh, Masoud, Morris, Dearbhaile, O’Connor, Louise, Cormican, Martin, Moran-Gilad, Jacob, Battisti, Antonio, Diaconu, Elena Lavinia, Corno, Gianluca, Di Cesare, Andrea, Alba, Patricia, Hisatsune, Junzo, Yu, Liansheng, Kuroda, Makoto, Sugai, Motoyuki, Kayama, Shizuo, Shakenova, Zeinegul, Kiiyukia, Ciira, Ng’eno, Eric, Raka, Lul, Jamil, Kazi, Fakhraldeen, Saja Adel, Alaati, Tareq, Bērziņš, Aivars, Avsejenko, Jeļena, Kokina, Kristina, Streikisa, Madara, Bartkevics, Vadims, Matar, Ghassan M., Daoud, Ziad, Pereckienė, Asta, Butrimaite-Ambrozeviciene, Ceslova, Penny, Christian, Bastaraud, Alexandra, Rasolofoarison, Tiavina, Collard, Jean-Marc, Samison, Luc Hervé, Andrianarivelo, Mala Rakoto, Banda, Daniel Lawadi, Amin, Arshana, Rajandas, Heraa, Parimannan, Sivachandran, Spiteri, David, Haber, Malcolm Vella, Santchurn, Sunita J., Vujacic, Aleksandar, Djurovic, Dijana, Bouchrif, Brahim, Karraouan, Bouchra, Vubil, Delfino Carlos, Pal, Pushkar, Schmitt, Heike, van Passel, Mark, Jeunen, Gert-Jan, Gemmell, Neil, Chambers, Stephen T., Mendoza, Fania Perez, Huete-Pιrez, Jorge, Vilchez, Samuel, Ahmed, Akeem Olayiwola, Adisa, Ibrahim Raufu, Odetokun, Ismail Ayoade, Fashae, Kayode, Sørgaard, Anne-Marie, Wester, Astrid Louise, Ryrfors, Pia, Holmstad, Rune, Mohsin, Mashkoor, Hasan, Rumina, Shakoor, Sadia, Gustafson, Natalie Weiler, Schill, Claudia Huber, Rojas, Maria Luz Zamudio, Velasquez, Jorge Echevarria, Magtibay, Bonifacio B., Catangcatang, Kris, Sibulo, Ruby, Yauce, Felipe Campos, Wasyl, Dariusz, Manaia, Celia, Rocha, Jaqueline, Martins, Jose, Álvaro, Pedro, Di Yoong Wen, Doris, Shin, Hanseob, Hur, Hor-Gil, Yoon, Sukhwan, Bosevska, Golubinka, Kochubovski, Mihail, Cojocaru, Radu, Burduniuc, Olga, Hong, Pei-Ying, Perry, Meghan Rose, Gassama, Amy, Radosavljevic, Vladimir, Tay, Moon Y. F., Zuniga-Montanez, Rogelio, Wuertz, Stefan, Gavačová, Dagmar, Pastuchová, Katarína, Truska, Peter, Trkov, Marija, Keddy, Karen, Esterhuyse, Kerneels, Song, Min Joon, Quintela-Baluja, Marcos, Lopez, Mariano Gomez, Cerdà-Cuéllar, Marta, Perera, R.R.D.P., Bandara, N.K.B.K.R.G.W., Premasiri, H.I., Pathirage, Sujatha, Charlemagne, Kareem, Rutgersson, Carolin, Norrgren, Leif, Örn, Stefan, Boss, Renate, Van der Heijden, Tanja, Hong, Yu-Ping, Kumburu, Happiness Houka, Mdegela, Robinson Hammerthon, Hounmanou, Yaovi Mahuton Gildas, Chonsin, Kaknokrat, Suthienkul, Orasa, Thamlikitkul, Visanu, de Roda Husman, Ana Maria, Bidjada, Bawimodom, Njanpop-Lafourcade, Berthe-Marie, Nikiema-Pessinaba, Somtinda Christelle, Levent, Belkis, Kurekci, Cemil, Ejobi, Francis, Kalule, John Bosco, Thomsen, Jens, Obaidi, Ouidiane, Jassim, Laila Mohamed, Moore, Andrew, Leonard, Anne, Graham, David W., Bunce, Joshua T., Zhang, Lihong, Gaze, William H., Lefor, Brett, Capone, Drew, Sozzi, Emanuele, Brown, Joe, Meschke, John Scott, Sobsey, Mark D., Davis, Michael, Beck, Nicola Koren, Sukapanpatharam, Pardi, Truong, Phuong, Lilienthal, Ronald, Kang, Sanghoon, Wittum, Thomas E., Rigamonti, Natalia, Baklayan, Patricia, Van, Chinh Dang, Tran, Doan Minh Nguyen, Do Phuc, Nguyen, Kwenda, Geoffrey, Larsson, D. G. Joakim, Koopmans, Marion, Woolhouse, Mark, Aarestrup, Frank M., Virology, Producció Animal, and Sanitat Animal

Subjects
genomic analysis, sewage, antimicrobial resistance, Multidisciplinary, Sewage, Drug Resistance, Bacterial, Metagenome, General Physics and Astronomy, Drug Resistance, Bacterial/genetics, Genomics, General Chemistry, General Biochemistry, Genetics and Molecular Biology, Anti-Bacterial Agents/pharmacology, Anti-Bacterial Agents
Abstract

Antimicrobial resistance (AMR) is a major threat to global health. Understanding the emergence, evolution, and transmission of individual antibiotic resistance genes (ARGs) is essential to develop sustainable strategies combatting this threat. Here, we use metagenomic sequencing to analyse ARGs in 757 sewage samples from 243 cities in 101 countries, collected from 2016 to 2019. We find regional patterns in resistomes, and these differ between subsets corresponding to drug classes and are partly driven by taxonomic variation. The genetic environments of 49 common ARGs are highly diverse, with most common ARGs carried by multiple distinct genomic contexts globally and sometimes on plasmids. Analysis of flanking sequence revealed ARG-specific patterns of dispersal limitation and global transmission. Our data furthermore suggest certain geographies are more prone to transmission events and should receive additional attention. Antimicrobial resistance (AMR) is a major threat to global health. Understanding the emergence, evolution, and transmission of individual antibiotic resistance genes (ARGs) is essential to develop sustainable strategies combatting this threat. Here, we use metagenomic sequencing to analyse ARGs in 757 sewage samples from 243 cities in 101 countries, collected from 2016 to 2019. We find regional patterns in resistomes, and these differ between subsets corresponding to drug classes and are partly driven by taxonomic variation. The genetic environments of 49 common ARGs are highly diverse, with most common ARGs carried by multiple distinct genomic contexts globally and sometimes on plasmids. Analysis of flanking sequence revealed ARG-specific patterns of dispersal limitation and global transmission. Our data furthermore suggest certain geographies are more prone to transmission events and should receive additional attention.

Published
2022
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24. p53 null Fluorescent Yellow Direct Repeat (FYDR) mice have normal levels of homologous recombination

Author

Massachusetts Institute of Technology. Department of Biological Engineering, Wiktor-Brown, Dominika M., Sukup-Jackson, Michelle R., Fakhraldeen, Saja A., Hendricks, Carrie A., Engelward, Bevin P., Massachusetts Institute of Technology. Department of Biological Engineering, Wiktor-Brown, Dominika M., Sukup-Jackson, Michelle R., Fakhraldeen, Saja A., Hendricks, Carrie A., and Engelward, Bevin P.

Abstract

The tumor suppressor p53 is a transcription factor whose function is critical for maintaining genomic stability in mammalian cells. In response to DNA damage, p53 initiates a signaling cascade that results in cell cycle arrest, DNA repair or, if the damage is severe, programmed cell death. In addition, p53 interacts with repair proteins involved in homologous recombination. Mitotic homologous recombination (HR) plays an essential role in the repair of double-strand breaks (DSBs) and broken replication forks. Loss of function of either p53 or HR leads to an increased risk of cancer. Given the importance of both p53 and HR in maintaining genomic integrity, we analyzed the effect of p53 on HR in vivo using Fluorescent Yellow Direct Repeat (FYDR) mice as well as with the sister chromatid exchange (SCE) assay. FYDR mice carry a direct repeat substrate in which an HR event can yield a fluorescent phenotype. Here, we show that p53 status does not significantly affect spontaneous HR in adult pancreatic cells in vivo or in primary fibroblasts in vitro when assessed using the FYDR substrate and SCEs. In addition, primary fibroblasts from p53 null mice do not show increased susceptibility to DNA damage-induced HR when challenged with mitomycin C. Taken together, the FYDR assay and SCE analysis indicate that, for some tissues and cell types, p53 status does not greatly impact HR., National Institute of Environmental Health Sciences (ES02109), National Cancer Institute (U.S.) (R33CA112151), National Cancer Institute (U.S.) (R01CA79827), United States. Dept. of Energy (DE-FG01-04ER04-21), National Institute of Environmental Health Sciences (T32 ES007020, NIEHS Training Grant in Environmental Toxicology), National Science Foundation (U.S.) (Fellowship)

Published
2014

25. Antiestrogen Therapy Increases Plasticity and Cancer Stemness of Prolactin-Induced ERα + Mammary Carcinomas.

Author

Shea MP, O'Leary KA, Fakhraldeen SA, Goffin V, Friedl A, Wisinski KB, Alexander CM, and Schuler LA

Subjects
Adenocarcinoma chemically induced, Adenocarcinoma pathology, Animals, Antineoplastic Agents, Hormonal therapeutic use, Breast Neoplasms pathology, Cell Proliferation drug effects, Epithelial-Mesenchymal Transition drug effects, Estrogen Receptor alpha metabolism, Female, Fulvestrant therapeutic use, Humans, Mammary Neoplasms, Animal chemically induced, Mammary Neoplasms, Animal pathology, Mice, Prolactin adverse effects, Tumor Cells, Cultured, Wnt Signaling Pathway physiology, Adenocarcinoma drug therapy, Breast Neoplasms drug therapy, Cell Plasticity drug effects, Estrogen Receptor Antagonists therapeutic use, Estrogen Receptor alpha antagonists & inhibitors, Mammary Neoplasms, Animal drug therapy, Neoplastic Stem Cells pathology
Abstract

Although antiestrogen therapies are successful in many patients with estrogen receptor alpha-positive (ERα + ) breast cancer, 25% to 40% fail to respond. Although multiple mechanisms underlie evasion of these treatments, including tumor heterogeneity and drug-resistant cancer stem cells (CSC), further investigations have been limited by the paucity of preclinical ERα + tumor models. Here, we examined a mouse model of prolactin-induced aggressive ERα + breast cancer, which mimics the epidemiologic link between prolactin exposure and increased risk for metastatic ERα + tumors. Like a subset of ERα + patient cancers, the prolactin-induced adenocarcinomas contained two major tumor subpopulations that expressed markers of normal luminal and basal epithelial cells. CSC activity was distributed equally across these two tumor subpopulations. Treatment with the selective estrogen receptor downregulator (SERD), ICI 182,780 (ICI), did not slow tumor growth, but induced adaptive responses in CSC activity, increased markers of plasticity including target gene reporters of Wnt/Notch signaling and epithelial-mesenchymal transition, and increased double-positive (K8/K5) cells. In primary tumorsphere cultures, ICI stimulated CSC self-renewal and was able to overcome the dependence of self-renewal upon Wnt or Notch signaling individually, but not together. Our findings demonstrate that treatment of aggressive mixed lineage ERα + breast cancers with a SERD does not inhibit growth, but rather evokes tumor cell plasticity and regenerative CSC activity, predicting likely negative impacts on patient tumors with these characteristics. Significance: This study suggests that treatment of a subset of ERα + breast cancers with antiestrogen therapies may not only fail to slow growth but also promote aggressive behavior by evoking tumor cell plasticity and regenerative CSC activity. Cancer Res; 78(7); 1672-84. ©2018 AACR ., (©2018 American Association for Cancer Research.)

Published
2018
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26. Wnt signaling in mammary glands: plastic cell fates and combinatorial signaling.

Author

Alexander CM, Goel S, Fakhraldeen SA, and Kim S

Subjects
Animals, Breast Neoplasms metabolism, Cell Differentiation, Cell Lineage, Epithelial Cells cytology, Epithelial Cells metabolism, Female, Humans, Mammary Neoplasms, Experimental genetics, Mammary Neoplasms, Experimental metabolism, Mice, Models, Biological, Mammary Glands, Animal metabolism, Wnt Signaling Pathway physiology
Abstract

The mouse mammary gland is an outstanding developmental model that exemplifies the activities of many of the effector pathways known to organize mammalian morphogenesis; furthermore, there are well-characterized methods for the specific genetic manipulation of various mammary epithelial cell components. Among these signaling pathways, Wnt signaling has been shown to generate plasticity of fate determination, expanding the genetic programs available to cells in the mammary lineage. It is responsible first for the appearance of the mammary fate in embryonic ectoderm and then for maintaining bi-potential basal stem cells in adult mammary ductal trees. Recent technical developments have led to the separate analysis of various mammary epithelial cell subpopulations, spurring the investigation of Wnt-dependent interactions. Although Wnt signaling was shown to be oncogenic for mouse mammary epithelium even before being identified as the principle oncogenic driver for gut epithelium, conclusive data implicating this pathway as a tumor driver for breast cancer lag behind, and we examine potential reasons.

Published
2012
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