Bal Krishna Chaube

Scopus Publications

Impaired glycosylation promotes rapid transition to hepatocellular carcinoma in model of diet-induced steatotic liver disease
Abhishek K. Singh, Balkrishna Chaube, Kathryn M. Citrin, Joseph W.M. Fowler, Sungwoon Lee, Jonatas Catarino, James Knight, Sarah C. Lowery, Sonal Shree, Keira E. Mahoney, Nabil E. Boutagy, Inmaculada Ruz-Maldonado, Kathy Harry, Marya Shanabrough, Trenton T. Ross, Stacy A. Malaker, Yajaira Suárez, Carlos Fernández-Hernando, Kariona A. Grabińska, William C. Sessa
Journal of Clinical Investigation, 2026
Obesity-linked steatosis is a significant risk factor for hepatocellular carcinoma (HCC); however, the molecular mechanisms underlying the transition from metabolic dysfunction-associated steatotic liver disease (MASLD) to HCC remain unclear. Here, we explored the role of the ER-associated protein NgBR, an essential component of the cis-prenyltransferase (cis-PTase) enzyme, in chronic liver disease. Hepatocyte-specific NgBR deletion in mice (N-LKO) intensified triacylglycerol (TAG) accumulation, inflammatory responses, ER/oxidative stress, and fibrosis, ultimately resulting in HCC development with 100% penetrance after 4 months on a high-fat diet. Similarly, liver-specific knockout of DHDDS, NgBR's cis-PTase partner, and a knockin model carrying a human NgBR mutation that impairs cis-PTase activity developed HCC under high-fat diet conditions, although with lower penetrance. A single-cell transcriptomic atlas from affected livers provides a detailed molecular analysis of the transition from liver pathophysiology to HCC development. Mechanistically, NgBR deficiency promoted excessive hepatic TAG accumulation by enhancing lipid uptake and impairing VLDL secretion. Importantly, pharmacological inhibition of diacylglycerol acyltransferase-2 (DGAT2), a key enzyme in TAG synthesis, abrogated diet-induced liver damage and HCC burden in N-LKO mice. Overall, our findings establish cis-PTase as a critical suppressor of MASLD-HCC conversion and suggest DGAT2 inhibition may serve as a promising therapeutic approach to delay HCC formation in advanced metabolic dysfunction-associated steatohepatitis.
MRPL47 deficiency drives mitochondrial dysfunction via ROS-p38-p21 signaling in non-small cell lung cancer
Nikita Bhandari, Yengkhom Ghanapriya Devi, Disha Acharya, Vinita Bhat, Annesha Chatterjee, Shweta Yalshetti, Sharathchandra Arandkar, Bal Krishna Chaube, Sudhanshu Shukla
Journal of Biological Chemistry, 2026
Mitoribosomes are pivotal for cellular energy metabolism through the synthesis of proteins essential for the oxidative phosphorylation system. Although mitoribosomal dysregulation has been implicated in cancer, the genomic landscape of mitoribosomal proteins (MRPs) in nonsmall cell lung cancer (NSCLC) remains largely uncharacterized. In this study, we conducted a comprehensive analysis of expression, copy number variations, and mutations of MRPs using data from TCGA-NSCLC patients. This screen identified MRPL47 as a significantly amplified and overexpressed mitoribosomal gene in NSCLC. Validation across three independent datasets (n = 1513) confirmed MRPL47 as a robust and independent prognostic marker for poor survival. Functionally, MRPL47 inhibition significantly reduced NSCLC cell proliferation and migration. Intriguingly, MRPL47 depletion selectively impaired the translation of a subset of mitochondrial proteins, rather than causing a global defect, leading to impaired assembly of electron transport chain Complexes I and III. This resulted in a defective oxidative phosphorylation system, characterized by decreased ATP synthesis and elevated mitochondrial reactive oxygen species (ROS) levels. Transcriptomic analysis revealed a significant downregulation of E2F pathway activity in MRPL47-knockdown cells, with MRPL47 expression correlating with E2F target gene expression at both RNA and protein levels. Mechanistically, MRPL47 knockdown induced ROS accumulation, which promoted p38 phosphorylation and subsequent upregulation of p21. Increased p21, in turn, led to Rb hypophosphorylation, thereby inhibiting E2F activity and inducing G1 cell cycle arrest and senescence. Altogether, these findings establish that MRPL47 is amplified and overexpressed in NSCLC, functions as a strong prognostic predictor, and critically promotes tumor progression by modulating mitochondrial function and the ROS-p38-p21-Rb-E2F signaling axis.
Intracellular endothelial cell metabolism in vascular function and dysfunction
Kathryn M. Citrin, Balkrishna Chaube, Carlos Fernández-Hernando, Yajaira Suárez
Trends in Endocrinology and Metabolism, 2025
Endothelial cells (ECs) form the inner lining of blood vessels that is crucial for vascular function and homeostasis. They regulate vascular tone, oxidative stress, and permeability. Dysfunction leads to increased permeability, leukocyte adhesion, and thrombosis. ECs undergo metabolic changes in conditions such as wound healing, cancer, atherosclerosis, and diabetes, and can influence disease progression. We discuss recent research that has revealed diverse intracellular metabolic pathways in ECs that are tailored to their functional needs, including lipid handling, glycolysis, and fatty acid oxidation (FAO). Understanding EC metabolic signatures in health and disease will be crucial not only for basic biology but can also be exploited when designing new therapies to target EC-related functions in different vascular diseases.
Inflamed endothelial cells express S1PR1 inhibitor CD69 to induce vascular leak
Michel V. Levesque, Andreane Cartier, Yueh-Chien Lin, Raj Kumar Sah, Hanming Zhang, Balkhrisa Chaube, Mantu Bhaumik, Jakob Körbelin, Yajaira Suárez, Carlos Fernández-Hernando, Timothy Hla
Journal of Biological Chemistry, 2025
Inflammation disrupts endothelial barrier function and causes vascular leak into the tissue parenchyma. Sphingosine 1-phosphate receptor-1 (S1PR1) in endothelial cells (ECs) is a key inducer of endothelial junctions and barrier function. We report here that ECs activation by the cytokine TNFα and TLR3 agonist polyinosine/polycytosine (pI:C) induces the lymphocyte activation molecule CD69 via the canonical NFκB pathway. EC CD69 stimulates endocytosis of S1PR1, inhibits its downstream intracellular signaling events and barrier function. Administration of TLR4 or TLR3 agonists or intranasal infection of mouse-adapted influenza virus (H1N1) or coronavirus (MHV-A59) induced CD69 in lung ECs. Adeno-associated virus-mediated overexpression of CD69 in lung EC leads to decreased cell-surface expression of S1PR1 and tight junction protein claudin-5, concomitantly with increased vascular permeability in the lungs. Furthermore, lung vascular leak at the peak of H1N1 infection is attenuated in a genetic mouse model which lacks CD69 in the endothelium. These data suggest that endothelial activation during inflammation and viral host-defense induces CD69 which downregulates S1PR1 to induce vascular leakage. CD69 induction during endothelial dysfunction may drive exaggerated inflammation by antagonizing the endothelial protective S1PR1 pathway.
Editorial: Metabolic crosstalk between cancer cells and immune cells in the tumor microenvironment: cellular and molecular insights, and their therapeutic implications
Parmanand Malvi, Shivendra Vikram Singh, Balkrishna Chaube
Frontiers in Oncology, 2025
Cancer is fundamentally considered as an evolutionary disease characterized by mutation-driven clonal selection, shaped by microenvironmental and therapeutic pressures, leading to heterogeneity, malignant/metastatic progression, and therapy resistance (1)(2)(3). Cancer evolution is accompanied by heritable variation (such as point mutations, copy number variation, structural variants, epigenetic changes), selection (e.g., clonal expansion of cells with fitness-enhancing mutations), competition (for example, nutrient/oxygen competition, immune evasion and metabolic competition) and adaptation (such as drug resistance, metastasis and immune escape).As a part of cancer evolution, metabolic reprogramming is now widely recognized as one of the hallmarks of cancer (4)-not merely as a means by which tumor cells sustain proliferation, but as a central axis by which malignant cells shape their microenvironment and evade immune control (5). Simultaneously, immune cells themselves operate within the metabolic constraints of the tumor microenvironment (TME), adapting-or failing to adapt-to nutrient scarcity, metabolite accumulation, hypoxia, and altered redox states (6). This complex interplay between tumor-cell and immune-cell metabolism forms a dynamic and critical interface-one that presents both mechanistic insight and therapeutic opportunity (5,6).The Research Topic "Metabolic Crosstalk between Cancer Cells and Immune Cells in the Tumor Microenvironment: Cellular and Molecular Insights, and their Therapeutic Implications" encompasses 14 contributions-nine original research papers, four review articles, and one perspective article-collectively illuminating how metabolic pathways in tumor and immune cells converge, compete, and cooperate-and how these interactions could be harnessed in the clinic.The contributions to this Research Topic explore how metabolic programs in cancer and immune cells interact in the TME, and how those interactions can be exploited therapeutically. The collection emphasizes lipid, amino-acid and micronutrient metabolism, ferroptosis and redox biology, metabolic biomarkers and gene signatures, and strategies to improve immunotherapy by modulating metabolism. Thus, the collection maps a cross-cutting picture: metabolic programs in tumors are not cell-autonomousthey rewire local and systemic immunity, create metabolic barriers to effective antitumor responses, and offer multiple points for therapeutic intervention (from small-molecule metabolic inhibitors to combination of metabolic and immunotherapy strategies. These works advance our understanding of how metabolism modulates immunity and uncover new therapeutic opportunities for targeting metabolic vulnerabilities.Cancer cells exploit metabolic plasticity to adapt to nutrient-deprived environments and sustain proliferation (7). A key theme emerging across the original research articles is that metabolic reprogramming in tumor cells has dual purpose: supporting the malignant phenotype and actively modulating the immune microenvironment. Several studies in this collection dissect these intertwined processes at multiple biological aspects. Collectively, these investigations strengthen the concept that tumor and immune cell metabolisms are not separate trajectories but entwined circuits. Tumor cells not only compete for nutrients (such as glucose, amino acids, lipids) but release signaling intermediates/metabolites (e.g., lactate) that actively suppress or reprogram immune effectors. Conversely, immune cell metabolic fitness-and its underlying mitochondrial, lipid and amino-acid metabolism-determines whether immune responses succeed or falter in the TME.The accompanying articles in this collection also underscore the translational potential of mechanistic insights in oncology. By delineating the molecular and metabolic pathways that drive tumor progression and modulate immune responses, these studies pinpoint actionable vulnerabilities within cancer cells and the tumor microenvironment. Such insights provide a foundation for the rational development of targeted therapies and combination strategies, bridging fundamental biology and clinical implications.Elevated lactate levels within the TME play a critical role in modulating immune cell function in cancer (10) While the collective findings in this Research Topic provide a powerful snapshot of current progress, they also reveal critical gaps and future challenges. First, the metabolic heterogeneity of tumors remains a major barrier. Spatial and temporal variations in nutrient availability, oxygen tension, and metabolite gradients create complex immunometabolic niches. Advances in single-cell multi-omics and spatial metabolomics will be key to dissecting these interactions in situ. Second, metabolic targeting must efforts that integrate metabolic imaging, metabolite profiling, immune phenotyping, clinical oncology, and computational biology will accelerate the translation of immunometabolic discoveries into therapeutic advances. This integrated approach may allow stratification of patients likely to benefit from metabolic-immunotherapy combinations.The contributions assembled in this Research Topic collectively feature the importance of metabolism as a language of communication within the tumor microenvironment. From amino acids and lipids to lactate and kynurenine, these metabolites shape the immune landscape, influencing whether tumors thrive or regress.As the boundaries between cancer cell metabolism and immune regulation blur, it becomes increasingly clear that therapeutic success will depend on decoding-and ultimately rewriting-this metabolic dialogue. The studies presented here provide not only mechanistic insights but also translational pathways to exploit metabolic vulnerabilities for clinical gain.In summary, this collection reflects the vibrant and rapidly evolving field of cancer immunometabolism. It is our hope that this collection will stimulate deeper crossdisciplinary collaboration among metabolism researchers, immunologists and clinicians.It reaffirms that metabolic crosstalk is not merely a consequence of tumor growth but a driving force of tumor-immune dynamics. Continued integration of metabolic research with immunotherapy promises to unlock new frontiers in precision oncology.
Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice
Nabil E. Boutagy, Ana Gamez-Mendez, Joseph W.M. Fowler, Hanming Zhang, Bal K. Chaube, Enric Esplugues, Andrew Kuo, Sungwoon Lee, Daiki Horikami, Jiasheng Zhang, Kathryn M. Citrin, Abhishek K. Singh, Brian G. Coon, Monica Y. Lee, Yajaira Suarez, Carlos Fernandez-Hernando, William C. Sessa
Journal of Clinical Investigation, 2024
Blood vessels are continually exposed to circulating lipids, and elevation of ApoB-containing lipoproteins causes atherosclerosis. Lipoprotein metabolism is highly regulated by lipolysis, largely at the level of the capillary endothelium lining metabolically active tissues. How large blood vessels, the site of atherosclerotic vascular disease, regulate the flux of fatty acids (FAs) into triglyceride-rich (TG-rich) lipid droplets (LDs) is not known. In this study, we showed that deletion of the enzyme adipose TG lipase (ATGL) in the endothelium led to neutral lipid accumulation in vessels and impaired endothelial-dependent vascular tone and nitric oxide synthesis to promote endothelial dysfunction. Mechanistically, the loss of ATGL led to endoplasmic reticulum stress–induced inflammation in the endothelium. Consistent with this mechanism, deletion of endothelial ATGL markedly increased lesion size in a model of atherosclerosis. Together, these data demonstrate that the dynamics of FA flux through LD affects endothelial cell homeostasis and consequently large vessel function during normal physiology and in a chronic disease state.
Suppression of angiopoietin-like 4 reprograms endothelial cell metabolism and inhibits angiogenesis
Balkrishna Chaube, Kathryn M. Citrin, Mahnaz Sahraei, Abhishek K. Singh, Diego Saenz de Urturi, Wen Ding, Richard W. Pierce, Raaisa Raaisa, Rebecca Cardone, Richard Kibbey, Carlos Fernández-Hernando, Yajaira Suárez
Nature Communications, 2023
Angiopoietin-like 4 (ANGPTL4) is known to regulate various cellular and systemic functions. However, its cell-specific role in endothelial cells (ECs) function and metabolic homeostasis remains to be elucidated. Here, using endothelial-specific Angptl4 knock-out mice (Angptl4iΔEC), and transcriptomics and metabolic flux analysis, we demonstrate that ANGPTL4 is required for maintaining EC metabolic function vital for vascular permeability and angiogenesis. Knockdown of ANGPTL4 in ECs promotes lipase-mediated lipoprotein lipolysis, which results in increased fatty acid (FA) uptake and oxidation. This is also paralleled by a decrease in proper glucose utilization for angiogenic activation of ECs. Mice with endothelial-specific deletion of Angptl4 showed decreased pathological neovascularization with stable vessel structures characterized by increased pericyte coverage and reduced permeability. Together, our study denotes the role of endothelial-ANGPTL4 in regulating cellular metabolism and angiogenic functions of EC.
Editorial: Cancer metabolism: molecular insights, metabolic crosstalk in the tumor microenvironment, and implications for therapy
Balkrishna Chaube, Parmanand Malvi
Frontiers in Oncology, 2023
COPYRIGHT © 2023 Chaube and Malvi. This is an openaccess article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. TYPE Editorial PUBLISHED 18 September 2023 DOI 10.3389/fonc.2023.1289397
TCF7L2 transcriptionally regulates Fgf15 to maintain bile acid and lipid homeostasis through gut-liver crosstalk
Neha Bhat, Fatemehsadat Esteghamat, Bal Krishna Chaube, Kushan Gunawardhana, Mitra Mani, Clay Thames, Dhanpat Jain, Henry N. Ginsberg, Carlos Fernandes‐Hernando, Arya Mani
FASEB Journal, 2022
FGF19/FGF15 is an endocrine regulator of hepatic bile salt and lipid metabolism, which has shown promising effects in the treatment of NASH in clinical trials. FGF19/15 is transcribed and released from enterocytes of the small intestine into enterohepatic circulation in response to bile‐induced FXR activation. Previously, the TSS of FGF19 was identified to bind Wnt‐regulated TCF7L2/encoded transcription factor TCF4 in colorectal cancer cells. Impaired Wnt signaling and specifical loss of function of its coreceptor LRP6 have been associated with NASH. We, therefore, examined if TCF7L2/TCF4 upregulates Fgf19 in the small intestine and restrains NASH through gut‐liver crosstalk. We examined the mice globally overexpressing, haploinsufficient, and conditional knockout models of TCF7L2 in the intestinal epithelium. The TCF7L2+/− mice exhibited increased plasma bile salts and lipids and developed diet‐induced fatty liver disease while mice globally overexpressing TCF7L2 were protected against these traits. Comprehensive in vivo analysis revealed that TCF7L2 transcriptionally upregulates FGF15 in the gut, leading to reduced bile synthesis and diminished intestinal lipid uptake. Accordingly, VilinCreert2; Tcf7L2fl/fl mice showed reduced Fgf19 in the ileum, and increased plasma bile. The global overexpression of TCF7L2 in mice with metabolic syndrome‐linked LRP6R611C substitution rescued the fatty liver and fibrosis in the latter. Strikingly, the hepatic levels of TCF4 were reduced and CYP7a1 was increased in human NASH, indicating the relevance of TCF4‐dependent regulation of bile synthesis to human disease. These studies identify the critical role of TCF4 as an upstream regulator of the FGF15‐mediated gut‐liver crosstalk that maintains bile and liver triglyceride homeostasis.
MMAB promotes negative feedback control of cholesterol homeostasis
Leigh Goedeke, Alberto Canfrán-Duque, Noemi Rotllan, Balkrishna Chaube, Bonne M. Thompson, Richard G. Lee, Gary W. Cline, Jeffrey G. McDonald, Gerald I. Shulman, Miguel A. Lasunción, Yajaira Suárez, Carlos Fernández-Hernando
Nature Communications, 2021
Intricate regulatory networks govern the net balance of cholesterol biosynthesis, uptake and efflux; however, the mechanisms surrounding cholesterol homeostasis remain incompletely understood. Here, we develop an integrative genomic strategy to detect regulators of LDLR activity and identify 250 genes whose knockdown affects LDL-cholesterol uptake and whose expression is modulated by intracellular cholesterol levels in human hepatic cells. From these hits, we focus on MMAB, an enzyme which catalyzes the conversion of vitamin B12 to adenosylcobalamin, and whose expression has previously been linked with altered levels of circulating cholesterol in humans. We demonstrate that hepatic levels of MMAB are modulated by dietary and cellular cholesterol levels through SREBP2, the master transcriptional regulator of cholesterol homeostasis. Knockdown of MMAB decreases intracellular cholesterol levels and augments SREBP2-mediated gene expression and LDL-cholesterol uptake in human and mouse hepatic cell lines. Reductions in total sterol content were attributed to increased intracellular levels of propionic and methylmalonic acid and subsequent inhibition of HMGCR activity and cholesterol biosynthesis. Moreover, mice treated with antisense inhibitors of MMAB display a significant reduction in hepatic HMGCR activity, hepatic sterol content and increased expression of SREBP2-mediated genes. Collectively, these findings reveal an unexpected role for the adenosylcobalamin pathway in regulating LDLR expression and identify MMAB as an additional control point by which cholesterol biosynthesis is regulated by its end product.
Hepatocyte-specific suppression of ANGPTL4 improves obesity-associated diabetes and mitigates atherosclerosis in mice
Abhishek K. Singh, Balkrishna Chaube, Xinbo Zhang, Jonathan Sun, Kathryn M. Citrin, Alberto Canfrán-Duque, Binod Aryal, Noemi Rotllan, Luis Varela, Richard G. Lee, Tamas L. Horvath, Nathan L. Price, Yajaira Suárez, Carlos Fernández-Hernando
Journal of Clinical Investigation, 2021
Metformin induced lactic acidosis impaired response of cancer cells towards paclitaxel and doxorubicin: Role of monocarboxylate transporter
Shivendra Vikram Singh, Balkrishna Chaube, Shyamananda Singh Mayengbam, Abhijeet Singh, Parmanand Malvi, Naoshad Mohammad, Ankita Deb, Manoj Kumar Bhat
Biochimica Et Biophysica Acta Molecular Basis of Disease, 2021
Suppressing miR-21 activity in tumor-associated macrophages promotes an antitumor immune response
Mahnaz Sahraei, Balkrishna Chaube, Yuting Liu, Jonathan Sun, Alanna Kaplan, Nathan L. Price, Wen Ding, Stanley Oyaghire, Rolando García-Milian, Sameet Mehta, Yana K. Reshetnyak, Raman Bahal, Paolo Fiorina, Peter M. Glazer, David L. Rimm, Carlos Fernández-Hernando, Yajaira Suárez
Journal of Clinical Investigation, 2019
Brown adipose tissue derived ANGPTL4 controls glucose and lipid metabolism and regulates thermogenesis
Abhishek K. Singh, Binod Aryal, Balkrishna Chaube, Noemi Rotllan, Luis Varela, Tamas L. Horvath, Yajaira Suárez, Carlos Fernández-Hernando
Molecular Metabolism, 2018
Absence of ANGPTL4 in adipose tissue improves glucose tolerance and attenuates atherogenesis
Binod Aryal, Abhishek K. Singh, Xinbo Zhang, Luis Varela, Noemi Rotllan, Leigh Goedeke, Balkrishna Chaube, Joao-Paulo Camporez, Daniel F. Vatner, Tamas L. Horvath, Gerald I. Shulman, Yajaira Suárez, Carlos Fernández-Hernando
Jci Insight, 2018
AMPK, a key regulator of metabolic/energy homeostasis and mitochondrial biogenesis in cancer cells
B Chaube, M K Bhat
Cell Death and Disease, 2016
AMPK maintains energy homeostasis and survival in cancer cells via regulating p38/PGC-1α-mediated mitochondrial biogenesis
B Chaube, P Malvi, S V Singh, N Mohammad, B Viollet, M K Bhat
Cell Death Discovery, 2015
Proteasomal inhibition sensitizes cervical cancer cells to mitomycin C-induced bystander effect: the role of tumor microenvironment
S V Singh, A K Ajay, N Mohammad, P Malvi, B Chaube, A S Meena, M K Bhat
Cell Death and Disease, 2015
Strategy to enhance efficacy of doxorubicin in solid tumor cells by methyl-β-cyclodextrin: Involvement of p53 and Fas receptor ligand complex
Naoshad Mohammad, Shivendra Vikram Singh, Parmanand Malvi, Balkrishna Chaube, Dipti Athavale, Muralidharan Vanuopadath, Sudarslal Sadasivan Nair, Bipin Nair, Manoj Kumar Bhat
Scientific Reports, 2015
Obesity induced rapid melanoma progression is reversed by orlistat treatment and dietary intervention: Role of adipokines
Parmanand Malvi, Balkrishna Chaube, Vimal Pandey, Maleppillil Vavachan Vijayakumar, Purushotham Reddy Boreddy, Naoshad Mohammad, Shivendra Vikram Singh, Manoj Kumar Bhat
Molecular Oncology, 2015
Targeting metabolic flexibility by simultaneously inhibiting respiratory complex I and lactate generation retards melanoma progression
Balkrishna Chaube, Parmanand Malvi, Shivendra Vikram Singh, Naoshad Mohammad, Avtar Singh Meena, Manoj Kumar Bhat
Oncotarget, 2015
High fat diet promotes achievement of peak bone mass in young rats
Parmanand Malvi, Vikrant Piprode, Balkrishna Chaube, Satish T. Pote, Monika Mittal, Naibedya Chattopadhyay, Mohan R. Wani, Manoj Kumar Bhat
Biochemical and Biophysical Research Communications, 2014
Cholesterol depletion by methyl-β-cyclodextrin augments tamoxifen induced cell death by enhancing its uptake in melanoma
Naoshad Mohammad, Parmanand Malvi, Avtar Singh Meena, Shivendra Vikram Singh, Balkrishna Chaube, Garikapati Vannuruswamy, Mahesh J Kulkarni, Manoj Kumar Bhat
Molecular Cancer, 2014
Hyperglycemia regulates MDR-1, drug accumulation and ROS levels causing increased toxicity of carboplatin and 5-fluorouracil in MCF-7 cells
Vimal Pandey, Balkrishna Chaube, Manoj Kumar Bhat
Journal of Cellular Biochemistry, 2011

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