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  1. Article ; Online: An Outbreak of Beta-2 Adrenergic Toxicity from Adulterated Heroin.

    Ali, Moiez / Foster, Yevgeniya / Brooks, Megan / Roomiany, Pahresah

    The American journal of medicine

    2016  Volume 129, Issue 8, Page(s) e125–6

    MeSH term(s) Adrenergic Agents ; Adrenergic beta-Agonists/poisoning ; Adult ; Clenbuterol/poisoning ; Disease Outbreaks ; Drug Contamination ; Heroin ; Humans ; Male ; Poisoning/epidemiology
    Chemical Substances Adrenergic Agents ; Adrenergic beta-Agonists ; Heroin (70D95007SX) ; Clenbuterol (XTZ6AXU7KN)
    Language English
    Publishing date 2016-04-18
    Publishing country United States
    Document type Case Reports ; Letter
    ZDB-ID 80015-6
    ISSN 1555-7162 ; 1873-2178 ; 0002-9343 ; 1548-2766
    ISSN (online) 1555-7162 ; 1873-2178
    ISSN 0002-9343 ; 1548-2766
    DOI 10.1016/j.amjmed.2016.03.027
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Milk Production and Composition in Camel and Its Beneficial Uses

    Wajid Ali / Ethem Akyol / Ayhan Ceyhan / Sadia Dilawar / Asia Firdous / Muhammad Zia ul Qasim / Muhammad Moiez Ahmad

    Turkish Journal of Agriculture: Food Science and Technology, Vol 7, Iss 12, Pp 2142-

    A Review

    2019  Volume 2147

    Abstract: Globally, 16.9% of milk used by humans is taken from different species other than a cow. These species are sheep, horse, yak, ass, goat, camel and buffalo. The global camel (Camelus dromedarius) population is about 34 million head with sharing of almost ... ...

    Abstract Globally, 16.9% of milk used by humans is taken from different species other than a cow. These species are sheep, horse, yak, ass, goat, camel and buffalo. The global camel (Camelus dromedarius) population is about 34 million head with sharing of almost 0.4% of world’s non-cattle milk. Within the last 20 years, the curiosity of camel farming is amassed remarkably in different countries of the world including the Netherland, Italy and USA for camel milk production. The camel is considered as a goal animal of the 21st century because it produces high quality milk under extreme temperature, deficiency of pasture and dearth of water. The average milk production of camel fluctuates from 4 to 30 lt with lactation length ranges from 9 to18 months having peak yield in second to the third month of lactation. Camel’s milk is used globally because of its salty taste, high vitamin C concentration and its medicinal properties. Nevertheless, it gives many valuable benefits such as treatment of autism, control diabetes and allergy, prevention from liver cirrhosis and replacer of cow milk to avoid an infant’s allergic reaction. The camel milk is a natural treatment of diabetes as it has a substantial result in a decrease of mean blood glucose and conserves necessary insulin doses. Camel milk constitutes of protein (2.5-4.5%), fat (2.9-5.5%), solid not fat (8.9 -14.3%), ash (0.35-0.95%), lactose (2.9-5.8%) and water (86.3-88.5%) as mean specific gravity is 1.03. Due to its distinct properties, the consumption of camel milk is increasing day by day and a number of industries are working to promote camel milk production and processing. Therefore, the tenacity of this review article is to explicate the beneficial uses and production of camel milk over the globe.
    Keywords camel ; milk ; insulin ; composition of milk ; population ; Agriculture ; S ; Agriculture (General) ; S1-972
    Subject code 630
    Language English
    Publishing date 2019-12-01T00:00:00Z
    Publisher Turkish Science and Technology Publishing (TURSTEP)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Small-molecule targeted therapies induce dependence on DNA double-strand break repair in residual tumor cells.

    Ali, Moiez / Lu, Min / Ang, Hazel Xiaohui / Soderquist, Ryan S / Eyler, Christine E / Hutchinson, Haley M / Glass, Carolyn / Bassil, Christopher F / Lopez, Omar M / Kerr, D Lucas / Falcon, Christina J / Yu, Helena A / Hata, Aaron N / Blakely, Collin M / McCoach, Caroline E / Bivona, Trever G / Wood, Kris C

    Science translational medicine

    2022  Volume 14, Issue 638, Page(s) eabc7480

    Abstract: Residual cancer cells that survive drug treatments with targeted therapies act as a reservoir from which eventual resistant disease emerges. Although there is great interest in therapeutically targeting residual cells, efforts are hampered by our limited ...

    Abstract Residual cancer cells that survive drug treatments with targeted therapies act as a reservoir from which eventual resistant disease emerges. Although there is great interest in therapeutically targeting residual cells, efforts are hampered by our limited knowledge of the vulnerabilities existing in this cell state. Here, we report that diverse oncogene-targeted therapies, including inhibitors of epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), KRAS, and BRAF, induce DNA double-strand breaks and, consequently, ataxia-telangiectasia mutated (ATM)-dependent DNA repair in oncogene-matched residual tumor cells. This DNA damage response, observed in cell lines, mouse xenograft models, and human patients, is driven by a pathway involving the activation of caspases 3 and 7 and the downstream caspase-activated deoxyribonuclease (CAD). CAD is, in turn, activated through caspase-mediated degradation of its endogenous inhibitor, ICAD. In models of
    MeSH term(s) Animals ; Carcinoma, Non-Small-Cell Lung/drug therapy ; DNA ; DNA Repair ; Humans ; Lung Neoplasms/drug therapy ; Mice ; Neoplasm, Residual
    Chemical Substances DNA (9007-49-2)
    Language English
    Publishing date 2022-03-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abc7480
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6941: Show issues Location:
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  4. Article ; Online: Codon bias imposes a targetable limitation on KRAS-driven therapeutic resistance

    Moiez Ali / Erin Kaltenbrun / Grace R. Anderson / Sarah Jo Stephens / Sabrina Arena / Alberto Bardelli / Christopher M. Counter / Kris C. Wood

    Nature Communications, Vol 8, Iss 1, Pp 1-

    2017  Volume 11

    Abstract: KRAS mutations drive resistance to diverse targeted therapies. In this study, the authors show that the rare codons of KRAS, yielding low oncogene expression, can be overcome to drive resistance to anti-EGFR therapy in CRC through upregulation of global ... ...

    Abstract KRAS mutations drive resistance to diverse targeted therapies. In this study, the authors show that the rare codons of KRAS, yielding low oncogene expression, can be overcome to drive resistance to anti-EGFR therapy in CRC through upregulation of global translation or through selection of more potent KRASQ61mutations.
    Keywords Science ; Q
    Language English
    Publishing date 2017-06-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Dysregulation of mitochondrial dynamics proteins are a targetable feature of human tumors

    Grace R. Anderson / Suzanne E. Wardell / Merve Cakir / Catherine Yip / Yeong-ran Ahn / Moiez Ali / Alexander P. Yllanes / Christina A. Chao / Donald P. McDonnell / Kris C. Wood

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 13

    Abstract: Mitochondrial dynamics regulate critical processes. Here the authors show that genes regulating mitochondrial dynamics are frequently amplified in human cancers, and that these alterations are associated with changes in drug sensitivity including ... ...

    Abstract Mitochondrial dynamics regulate critical processes. Here the authors show that genes regulating mitochondrial dynamics are frequently amplified in human cancers, and that these alterations are associated with changes in drug sensitivity including increased sensitivity to the apoptosis-targeting Smac mimetics.
    Keywords Science ; Q
    Language English
    Publishing date 2018-04-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Dysregulation of mitochondrial dynamics proteins are a targetable feature of human tumors

    Grace R. Anderson / Suzanne E. Wardell / Merve Cakir / Catherine Yip / Yeong-ran Ahn / Moiez Ali / Alexander P. Yllanes / Christina A. Chao / Donald P. McDonnell / Kris C. Wood

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 13

    Abstract: Mitochondrial dynamics regulate critical processes. Here the authors show that genes regulating mitochondrial dynamics are frequently amplified in human cancers, and that these alterations are associated with changes in drug sensitivity including ... ...

    Abstract Mitochondrial dynamics regulate critical processes. Here the authors show that genes regulating mitochondrial dynamics are frequently amplified in human cancers, and that these alterations are associated with changes in drug sensitivity including increased sensitivity to the apoptosis-targeting Smac mimetics.
    Keywords Science ; Q
    Language English
    Publishing date 2018-04-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Codon bias imposes a targetable limitation on KRAS-driven therapeutic resistance.

    Ali, Moiez / Kaltenbrun, Erin / Anderson, Gray R / Stephens, Sarah Jo / Arena, Sabrina / Bardelli, Alberto / Counter, Christopher M / Wood, Kris C

    Nature communications

    2017  Volume 8, Page(s) 15617

    Abstract: KRAS mutations drive resistance to targeted therapies, including EGFR inhibitors in colorectal cancer (CRC). Through genetic screens, we unexpectedly find that mutant HRAS, which is rarely found in CRC, is a stronger driver of resistance than mutant KRAS. ...

    Abstract KRAS mutations drive resistance to targeted therapies, including EGFR inhibitors in colorectal cancer (CRC). Through genetic screens, we unexpectedly find that mutant HRAS, which is rarely found in CRC, is a stronger driver of resistance than mutant KRAS. This difference is ascribed to common codon bias in HRAS, which leads to much higher protein expression, and implies that the inherent poor expression of KRAS due to rare codons must be surmounted during drug resistance. In agreement, we demonstrate that primary resistance to cetuximab is dependent upon both KRAS mutational status and protein expression level, and acquired resistance is often associated with KRAS
    MeSH term(s) Antibodies, Monoclonal/pharmacology ; Antineoplastic Agents, Immunological/pharmacology ; Cell Line, Tumor ; Cell Proliferation ; Cetuximab/pharmacology ; Codon/genetics ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Drug Resistance, Neoplasm/genetics ; ErbB Receptors/antagonists & inhibitors ; ErbB Receptors/genetics ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Panitumumab ; Proto-Oncogene Proteins p21(ras)/genetics ; RNA Interference ; RNA, Small Interfering/genetics
    Chemical Substances Antibodies, Monoclonal ; Antineoplastic Agents, Immunological ; Codon ; KRAS protein, human ; RNA, Small Interfering ; Panitumumab (6A901E312A) ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; HRAS protein, human (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Cetuximab (PQX0D8J21J)
    Language English
    Publishing date 2017-06-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/ncomms15617
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: An extra copy of

    Moding, Everett J / Min, Hooney D / Castle, Katherine D / Ali, Moiez / Woodlief, Loretta / Williams, Nerissa / Ma, Yan / Kim, Yongbaek / Lee, Chang-Lung / Kirsch, David G

    JCI insight

    2016  Volume 1, Issue 10

    Abstract: The tumor suppressor p53 blocks tumor progression in multiple tumor types. Radiation-induced cancer following exposure to radiation therapy or space travel may also be regulated by p53 because p53 has been proposed to respond to DNA damage to suppress ... ...

    Abstract The tumor suppressor p53 blocks tumor progression in multiple tumor types. Radiation-induced cancer following exposure to radiation therapy or space travel may also be regulated by p53 because p53 has been proposed to respond to DNA damage to suppress tumorigenesis. Here, we investigate the role of p53 in lung carcinogenesis and lymphomagenesis in
    Language English
    Publishing date 2016-07-07
    Publishing country United States
    Document type Journal Article
    ISSN 2379-3708
    ISSN 2379-3708
    DOI 10.1172/jci.insight.86698
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Dysregulation of mitochondrial dynamics proteins are a targetable feature of human tumors.

    Anderson, Gray R / Wardell, Suzanne E / Cakir, Merve / Yip, Catherine / Ahn, Yeong-Ran / Ali, Moiez / Yllanes, Alexander P / Chao, Christina A / McDonnell, Donald P / Wood, Kris C

    Nature communications

    2018  Volume 9, Issue 1, Page(s) 1677

    Abstract: Altered mitochondrial dynamics can broadly impact tumor cell physiology. Using genetic and pharmacological profiling of cancer cell lines and human tumors, we here establish that perturbations to the mitochondrial dynamics network also result in specific ...

    Abstract Altered mitochondrial dynamics can broadly impact tumor cell physiology. Using genetic and pharmacological profiling of cancer cell lines and human tumors, we here establish that perturbations to the mitochondrial dynamics network also result in specific therapeutic vulnerabilities. In particular, through distinct mechanisms, tumors with increased mitochondrial fragmentation or connectivity are hypersensitive to SMAC mimetics, a class of compounds that induce apoptosis through inhibition of IAPs and for which robust sensitivity biomarkers remain to be identified. Further, because driver oncogenes exert dominant control over mitochondrial dynamics, oncogene-targeted therapies can be used to sensitize tumors to SMAC mimetics via their effects on fission/fusion dynamics. Collectively, these data demonstrate that perturbations to the mitochondrial dynamics network induce targetable vulnerabilities across diverse human tumors and, more broadly, suggest that the altered structures, activities, and trafficking of cellular organelles may facilitate additional cancer therapeutic opportunities.
    MeSH term(s) Animals ; Antineoplastic Agents/administration & dosage ; Cell Line, Tumor ; Female ; Humans ; Mice ; Mice, Nude ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Dynamics ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism
    Chemical Substances Antineoplastic Agents ; Mitochondrial Proteins
    Language English
    Publishing date 2018-04-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-018-04033-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Yeast Short-Lived Actin-Associated Protein Forms a Metastable Prion in Response to Thermal Stress.

    Chernova, Tatiana A / Kiktev, Denis A / Romanyuk, Andrey V / Shanks, John R / Laur, Oskar / Ali, Moiez / Ghosh, Abheek / Kim, Dami / Yang, Zhen / Mang, Maggie / Chernoff, Yury O / Wilkinson, Keith D

    Cell reports

    2017  Volume 18, Issue 3, Page(s) 751–761

    Abstract: Self-perpetuating ordered protein aggregates (amyloids and prions) are associated with a variety of neurodegenerative disorders. Although environmental agents have been linked to certain amyloid diseases, the molecular basis of their action remains ... ...

    Abstract Self-perpetuating ordered protein aggregates (amyloids and prions) are associated with a variety of neurodegenerative disorders. Although environmental agents have been linked to certain amyloid diseases, the molecular basis of their action remains unclear. We have employed endogenous yeast prions as a model system to study environmental control of amyloid formation. A short-lived actin-associated yeast protein Lsb2 can trigger prion formation by other proteins in a mode regulated by the cytoskeleton and ubiquitin-dependent processes. Here, we show that such a heterologous prion induction is due to the ability of Lsb2 to form a transient prion state, generated in response to thermal stress. Evolutionary acquisition of prion-inducing activity by Lsb2 is traced to a single amino acid change, coinciding with the acquisition of thermotolerance in the Saccharomyces yeast lineage. This raises the intriguing possibility that the transient prion formation could aid in functioning of Lsb2 at higher temperatures.
    Language English
    Publishing date 2017-01-17
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2016.12.082
    Database MEDical Literature Analysis and Retrieval System OnLINE

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