8 results on '"Yildirim AD"'
Search Results
2. A comprehensive health effects assessment of the use of sanitizers and disinfectants during COVID-19 pandemic: a global survey.
- Author
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Hashemi F, Hoepner L, Hamidinejad FS, Haluza D, Afrashteh S, Abbasi A, Omeragić E, Imamović B, Rasheed NA, Taher TMJ, Kurniasari F, Wazqar DY, Apalı ÖC, Yildirim AD, Zhao B, Kalikyan Z, Guo C, Valbuena AC, Mititelu M, Pando CM, Saridi M, Toska A, Cuba ML, Kwadzokpui PK, Tadele N, Nasibova T, Harsch S, Munkh-Erdene L, Menawi W, Evangelou E, Dimova A, Marinov D, Dimitrova T, Shalimova A, Fouly H, Suraya A, da Silva Faquim JP, Oumayma B, Annunziato MA, Lalo R, Papastavrou E, Ade AD, Caminada S, Stojkov S, Narvaez CG, Mudau LS, Rassas I, Michel D, Kaynar NS, Iqbal S, Elshwekh H, Hossain I, Al-Fayyadh S, Sydorchuk A, Alnusairat DMH, Abdullahi AM, Iqbal N, Pandey A, Gómez-Gómez B, Akyildiz AG, Morosan E, Dwarica D, Dorj G, Hasan SY, Al-Shdayfat NM, Knezevic B, Valladares W, Severi C, Fuentes SC, Augusto S, Sidorova E, Moelyaningrum AD, Alawad T, Khalid A, Elehamer NMK, Mihaylova A, Tsigengagel O, Menouni A, Wojtecka A, Hod R, Idayat YB, Othman K, Harfouch RM, Paunov T, Omar M, Benderli NC, Nurika G, Amjad S, Elnoamany S, Elesrigy F, Shaban MM, Acevedo-López D, Kartashova M, Khalaf A, Jaafar SA, Kadhim TA, Hweissa NA, Teng Y, Mohammed FE, Sasikumar T, Hikaambo CN, Kharat A, Lyamtseva U, Aldeeb MA, Pawlas N, Khorolsuren L, Koonjul RP, Maïnassara HB, Chahal P, Wangeci RW, Kumar AB, Zamora-Corrales I, Gracy S, Mahamat M, Adamczyk J, Rahman HA, Matiashova L, Elsherif OE, Alkhateeb NE, Aleaga Y, Bahrami S, Al-Salihy SR, Cabrera-Galeana P, Lalic-Popovic M, Brown-Myrie E, Bhandari D, Mayaboti CA, Stanišić S, Pestic SK, Bektay MY, Al Sabbah H, Hashemi S, Assia B, Merritt AS, Ramzi Z, Baboolal H, Isstaif J, Shami R, Saad R, Nyirongo T, and Hoseini M
- Subjects
- Humans, Sodium Hypochlorite chemistry, Pandemics prevention & control, Chlorine, Cross-Sectional Studies, Chlorides chemistry, Formaldehyde, Alcohols, Surveys and Questionnaires, Disinfectants chemistry, COVID-19
- Abstract
COVID-19 has affected all aspects of human life so far. From the outset of the pandemic, preventing the spread of COVID-19 through the observance of health protocols, especially the use of sanitizers and disinfectants was given more attention. Despite the effectiveness of disinfection chemicals in controlling and preventing COVID-19, there are critical concerns about their adverse effects on human health. This study aims to assess the health effects of sanitizers and disinfectants on a global scale. A total of 91,056 participants from 154 countries participated in this cross-sectional study. Information on the use of sanitizers and disinfectants and health was collected using an electronic questionnaire, which was translated into 26 languages via web-based platforms. The findings of this study suggest that detergents, alcohol-based substances, and chlorinated compounds emerged as the most prevalent chemical agents compared to other sanitizers and disinfectants examined. Most frequently reported health issues include skin effects and respiratory effects. The Chi-square test showed a significant association between chlorinated compounds (sodium hypochlorite and per-chlorine) with all possible health effects under investigation (p-value <0.001). Examination of risk factors based on multivariate logistic regression analysis showed that alcohols and alcohols-based materials were associated with skin effects (OR, 1.98; 95%CI, 1.87-2.09), per-chlorine was associated with eye effects (OR, 1.83; 95%CI, 1.74-1.93), and highly likely with itching and throat irritation (OR, 2.00; 95%CI, 1.90-2.11). Furthermore, formaldehyde was associated with a higher prevalence of neurological effects (OR, 2.17; 95%CI, 1.92-2.44). Furthermore, formaldehyde was associated with a higher prevalence of neurological effects (OR, 2.17; 95%CI, 1.92-2.44). The use of sodium hypochlorite and per-chlorine also had a high chance of having respiratory effects. The findings of the current study suggest that health authorities need to implement more awareness programs about the side effects of using sanitizers and disinfectants during viral epidemics especially when they are used or overused., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
- Published
- 2023
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3. ER Stress-Induced Sphingosine-1-Phosphate Lyase Phosphorylation Potentiates the Mitochondrial Unfolded Protein Response.
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Yildirim AD, Citir M, Dogan AE, Veli Z, Yildirim Z, Tufanli O, Traynor-Kaplan A, Schultz C, and Erbay E
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- Animals, Phosphorylation, Endoribonucleases genetics, Endoplasmic Reticulum Stress, Protein Serine-Threonine Kinases genetics, Aldehyde-Lyases metabolism, Ribonucleases metabolism, Inositol, Mammals metabolism, RNA, Double-Stranded, Unfolded Protein Response
- Abstract
The unfolded protein response (UPR) is an elaborate signaling network that evolved to maintain proteostasis in the endoplasmic reticulum (ER) and mitochondria (mt). These organelles are functionally and physically associated, and consequently, their stress responses are often intertwined. It is unclear how these two adaptive stress responses are coordinated during ER stress. The inositol-requiring enzyme-1 (IRE1), a central ER stress sensor and proximal regulator of the UPR
ER , harbors dual kinase and endoribonuclease (RNase) activities. IRE1 RNase activity initiates the transcriptional layer of the UPRER , but IRE1's kinase substrate(s) and their functions are largely unknown. Here, we discovered that sphingosine 1-phosphate (S1P) lyase (SPL), the enzyme that degrades S1P, is a substrate for the mammalian IRE1 kinase. Our data show that IRE1-dependent SPL phosphorylation inhibits SPL's enzymatic activity, resulting in increased intracellular S1P levels. S1P has previously been shown to induce the activation of mitochondrial UPR (UPRmt ) in nematodes. We determined that IRE1 kinase-dependent S1P induction during ER stress potentiates UPRmt signaling in mammalian cells. Phosphorylation of eukaryotic translation initiation factor 2α (eif2α) is recognized as a critical molecular event for UPRmt activation in mammalian cells. Our data further demonstrate that inhibition of the IRE1-SPL axis abrogates the activation of two eif2α kinases, namely double-stranded RNA-activated protein kinase (PKR) and PKR-like ER kinase upon ER stress. These findings show that the IRE1-SPL axis plays a central role in coordinating the adaptive responses of ER and mitochondria to ER stress in mammalian cells., Competing Interests: Conflict of Interest The authors declare that they have no conflicts of interest with the contents of this article., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2022
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4. PACT establishes a posttranscriptional brake on mitochondrial biogenesis by promoting the maturation of miR-181c.
- Author
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Dogan AE, Hamid SM, Yildirim AD, Yildirim Z, Sen G, Riera CE, Gottlieb RA, and Erbay E
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- Animals, Electron Transport Complex I metabolism, Mice, RNA-Induced Silencing Complex metabolism, Adipose Tissue, Brown metabolism, MicroRNAs genetics, Mitochondria, Organelle Biogenesis, RNA-Binding Proteins genetics, RNA-Binding Proteins metabolism
- Abstract
The double-stranded RNA-dependent protein kinase activating protein (PACT), an RNA-binding protein that is part of the RNA-induced silencing complex, plays a key role in miR-mediated translational repression. Previous studies showed that PACT regulates the expression of various miRs, selects the miR strand to be loaded onto RNA-induced silencing complex, and determines proper miR length. Apart from PACT's role in mediating the antiviral response in immune cells, what PACT does in other cell types is unknown. Strikingly, it has also been shown that cold exposure leads to marked downregulation of PACT protein in mouse brown adipose tissue (BAT), where mitochondrial biogenesis and metabolism play a central role. Here, we show that PACT establishes a posttranscriptional brake on mitochondrial biogenesis (mitobiogenesis) by promoting the maturation of miR-181c, a key suppressor of mitobiogenesis that has been shown to target mitochondrial complex IV subunit I (Mtco1) and sirtuin 1 (Sirt1). Consistently, we found that a partial reduction in PACT expression is sufficient to enhance mitobiogenesis in brown adipocytes in culture as well as during BAT activation in mice. In conclusion, we demonstrate an unexpected role for PACT in the regulation of mitochondrial biogenesis and energetics in cells and BAT., Competing Interests: Conflict of interest The authors declare that they have no competing interests., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2022
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5. Targeting IRE1 endoribonuclease activity alleviates cardiovascular lesions in a murine model of Kawasaki disease vasculitis.
- Author
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Marek-Iannucci S, Yildirim AD, Hamid SM, Ozdemir AB, Gomez AC, Kocatürk B, Porritt RA, Fishbein MC, Iwawaki T, Noval Rivas M, Erbay E, and Arditi M
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- Animals, Disease Models, Animal, Endoribonucleases genetics, Humans, Mice, Mice, Inbred C57BL, NLR Family, Pyrin Domain-Containing 3 Protein genetics, Protein Serine-Threonine Kinases genetics, Ribonucleases, Lacticaseibacillus casei, Mucocutaneous Lymph Node Syndrome drug therapy, Mucocutaneous Lymph Node Syndrome pathology, Vasculitis
- Abstract
Kawasaki disease (KD) is the leading cause of noncongenital heart disease in children. Studies in mice and humans propound the NLRP3/IL-1β pathway as the principal driver of KD pathophysiology. Endoplasmic reticulum (ER) stress can activate the NLRP3 inflammasome, but the potential implication of ER stress in KD pathophysiology has not been investigated to our knowledge. We used human patient data and the Lactobacillus casei cell wall extract (LCWE) murine model of KD vasculitis to characterize the impact of ER stress on the development of cardiovascular lesions. KD patient transcriptomics and single-cell RNA sequencing of the abdominal aorta from LCWE-injected mice revealed changes in the expression of ER stress genes. Alleviating ER stress genetically, by conditional deletion of inositol-requiring enzyme 1 (IRE1) in myeloid cells, or pharmacologically, by inhibition of IRE1 endoribonuclease (RNase) activity, led to significant reduction of LCWE-induced cardiovascular lesion formation as well as reduced caspase-1 activity and IL-1β secretion. These results demonstrate the causal relationship of ER stress to KD pathogenesis and highlight IRE1 RNase activity as a potential new therapeutic target.
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- 2022
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6. Double bond configuration of palmitoleate is critical for atheroprotection.
- Author
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Cimen I, Yildirim Z, Dogan AE, Yildirim AD, Tufanli O, Onat UI, Nguyen U, Watkins SM, Weber C, and Erbay E
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- Animals, Atherosclerosis metabolism, Atherosclerosis pathology, Cells, Cultured, Male, Mice, Mice, Knockout, Atherosclerosis prevention & control, Fatty Acids, Monounsaturated chemistry, Fatty Acids, Monounsaturated pharmacology
- Abstract
Objective: Saturated and trans fat consumption is associated with increased cardiovascular disease (CVD) risk. Current dietary guidelines recommend low fat and significantly reduced trans fat intake. Full fat dairy can worsen dyslipidemia, but recent epidemiological studies show full-fat dairy consumption may reduce diabetes and CVD risk. This dairy paradox prompted a reassessment of the dietary guidelines. The beneficial metabolic effects in dairy have been claimed for a ruminant-derived, trans fatty acid, trans-C16:1n-7 or trans-palmitoleate (trans-PAO). A close relative, cis-PAO, is produced by de novo lipogenesis and mediates inter-organ crosstalk, improving insulin-sensitivity and alleviating atherosclerosis in mice. These findings suggest trans-PAO may be a useful substitute for full fat dairy, but a metabolic function for trans-PAO has not been shown to date., Methods: Using lipidomics, we directly investigated trans-PAO's impact on plasma and tissue lipid profiles in a hypercholesterolemic atherosclerosis mouse model. Furthermore, we investigated trans-PAO's impact on hyperlipidemia-induced inflammation and atherosclerosis progression in these mice., Results: Oral trans-PAO supplementation led to significant incorporation of trans-PAO into major lipid species in plasma and tissues. Unlike cis-PAO, however, trans-PAO did not prevent organelle stress and inflammation in macrophages or atherosclerosis progression in mice., Conclusions: A significant, inverse correlation between circulating trans-PAO levels and diabetes incidence and cardiovascular mortality has been reported. Our findings show that trans-PAO can incorporate efficiently into the same pools that its cis counterpart is known to incorporate into. However, we found trans-PAO's anti-inflammatory and anti-atherosclerotic effects are muted due to its different structure from cis-PAO., (Copyright © 2019 The Authors. Published by Elsevier GmbH.. All rights reserved.)
- Published
- 2019
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7. Intercepting the Lipid-Induced Integrated Stress Response Reduces Atherosclerosis.
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Onat UI, Yildirim AD, Tufanli Ö, Çimen I, Kocatürk B, Veli Z, Hamid SM, Shimada K, Chen S, Sin J, Shah PK, Gottlieb RA, Arditi M, and Erbay E
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- Animals, Endoplasmic Reticulum immunology, Humans, Inflammation Mediators metabolism, Mice, Mitochondria metabolism, Oxidative Stress, Phosphorylation, Signal Transduction, Atherosclerosis immunology, Dietary Fats metabolism, Eukaryotic Initiation Factor-2 metabolism, Inflammasomes metabolism, Interleukin-1beta metabolism, Stress, Physiological immunology
- Abstract
Background: Eukaryotic cells can respond to diverse stimuli by converging at serine-51 phosphorylation on eukaryotic initiation factor 2 alpha (eIF2α) and activate the integrated stress response (ISR). This is a key step in translational control and must be tightly regulated; however, persistent eIF2α phosphorylation is observed in mouse and human atheroma., Objectives: Potent ISR inhibitors that modulate neurodegenerative disorders have been identified. Here, the authors evaluated the potential benefits of intercepting ISR in a chronic metabolic and inflammatory disease, atherosclerosis., Methods: The authors investigated ISR's role in lipid-induced inflammasome activation and atherogenesis by taking advantage of 3 different small molecules and the ATP-analog sensitive kinase allele technology to intercept ISR at multiple molecular nodes., Results: The results show lipid-activated eIF2α signaling induces a mitochondrial protease, Lon protease 1 (LONP1), that degrades phosphatase and tensin-induced putative kinase 1 and blocks Parkin-mediated mitophagy, resulting in greater mitochondrial oxidative stress, inflammasome activation, and interleukin-1β secretion in macrophages. Furthermore, ISR inhibitors suppress hyperlipidemia-induced inflammasome activation and inflammation, and reduce atherosclerosis., Conclusions: These results reveal endoplasmic reticulum controls mitochondrial clearance by activating eIF2α-LONP1 signaling, contributing to an amplified oxidative stress response that triggers robust inflammasome activation and interleukin-1β secretion by dietary fats. These findings underscore the intricate exchange of information and coordination of both organelles' responses to lipids is important for metabolic health. Modulation of ISR to alleviate organelle stress can prevent inflammasome activation by dietary fats and may be a strategy to reduce lipid-induced inflammation and atherosclerosis., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)
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- 2019
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8. Suppression of intragenic transcription requires the MOT1 and NC2 regulators of TATA-binding protein.
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Koster MJ, Yildirim AD, Weil PA, Holstege FC, and Timmers HT
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- Adenosine Triphosphatases genetics, Alleles, Chromatin metabolism, DNA-Binding Proteins metabolism, Nuclear Proteins biosynthesis, Nuclear Proteins genetics, Phosphoproteins genetics, Promoter Regions, Genetic, Repressor Proteins metabolism, Saccharomyces cerevisiae genetics, Saccharomyces cerevisiae metabolism, Saccharomyces cerevisiae Proteins biosynthesis, Saccharomyces cerevisiae Proteins genetics, Saccharomyces cerevisiae Proteins metabolism, TATA-Binding Protein Associated Factors genetics, Trans-Activators biosynthesis, Trans-Activators genetics, Trans-Activators metabolism, Transcription Factors genetics, Adenosine Triphosphatases physiology, Gene Expression Regulation, Fungal, Phosphoproteins physiology, Saccharomyces cerevisiae Proteins physiology, TATA-Binding Protein Associated Factors physiology, TATA-Box Binding Protein metabolism, Transcription Factors physiology, Transcription, Genetic
- Abstract
Chromatin structure in transcribed regions poses a barrier for intragenic transcription. In a comprehensive study of the yeast chromatin remodelers and the Mot1p-NC2 regulators of TATA-binding protein (TBP), we detected synthetic genetic interactions indicative of suppression of intragenic transcription. Conditional depletion of Mot1p or NC2 in absence of the ISW1 remodeler, but not in the absence of other chromatin remodelers, activated the cryptic FLO8 promoter. Likewise, conditional depletion of Mot1p or NC2 in deletion backgrounds of the H3K36 methyltransferase Set2p or the Asf1p-Rtt106p histone H3-H4 chaperones, important factors involved in maintaining a repressive chromatin environment, resulted in increased intragenic FLO8 transcripts. Activity of the cryptic FLO8 promoter is associated with reduced H3 levels, increased TBP binding and tri-methylation of H3K4 and is independent of Spt-Ada-Gcn5-acetyltransferase function. These data reveal cooperation of negative regulation of TBP with specific chromatin regulators to inhibit intragenic transcription.
- Published
- 2014
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