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Matt Damon Says He Missed Out On $250M In Royalties By Turning Down Avatar
By Joseph Gibson on October 14, 2019 in Articles › Celebrity News
Most of us have some manner of regret in our lives, particularly when we reflect on "what could have been." Matt Damon is no different, as a recent GQ interview with the actor reveals. During the chat, Damon revealed the fascinating tidbit that when director James Cameron was casting his monster hit Avatar, he asked Damon to take on the leading role. And that by turning it down, Damon missed out on some $250 million in Avatar profits.
As Damon tells it, it went like this:
"Jim Cameron offered me Avatar. And when he offered it to me, he goes, 'Now, listen. I don't need anybody. I don't need a name for this, a named actor. If you don't take this, I'm going to find an unknown actor and give it to him, because the movie doesn't really need you. But if you take the part, I'll give you ten per cent of…[the profits]."
As it turns out, Cameron was right about not needing a known movie star for Avatar, since with then-unknown Sam Worthington the film went on to become the highest-grossing box office hit of all time, a record that stood until Avengers: Endgame this year. It pulled in some $2.79 billion worldwide, which would have earned Damon more than $250 million under Cameron's proposed deal.
Angela Weiss/Getty Images
Of course, even though Damon knows the sting of missed opportunity, he acknowledges that he's still doing pretty well in his chosen field, even without Avatar:
"So, yeah. I've left more money on the table than any actor actually… So that sucked and that's still brutal. But my kids are all eating. I'm doing OK."
As for why Damon decided to pass on Avatar, he says it was due to scheduling conflicts with The Bourne Ultimatum, which he prioritized due to his strong relationship with director Paul Greengrass and the rest of the Bourne franchise cast and crew. It was only afterward, he says, that he realized that Cameron's sporadic-at-best directing habits meant that he would likely never get the chance to star in one of the master filmmaker's movies ever again – but with several Avatar sequels reportedly on the way, it's possible that he's mistaken.
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Posts Tagged 'IL1b'
The Role of Exosomes in Metabolic Regulation
Posted in Biological Networks, Chemical Biology and its relations to Metabolic Disease, Exosomes: Natural Carriers for siRNA Delivery, Microfuidics, RNA Biology, tagged alix, annexins, autoimmunity, body fluids, cancer genomics and therapy, caspase-1, cellular immunity, DNA, ESCRT, Exosomes, extracellular vesicles (EVs), flotillin, heat shock proteins, Hsp60, Hsp70, Hsp90, IL18, IL1b, immune cells, immune resistance, Inflammasome, intercellular communication, interleukins, intraluminal vessicles, LRR, metabolic diseases, MicroRNA, microvessicles, miRNA, multiple vesicle bodies (MVBs), myocardial hypertrophy, neurodegenerative diseases, NLRP3, platelets, RNA, Schwann cells, siRNA, tetraspanin on October 8, 2017| Leave a Comment »
Author: Larry H. Bernstein, MD, FCAP
On 9/25/2017, Aviva Lev-Ari, PhD, RN commissioned Dr. Larry H. Bernstein to write a short article on the following topic reported on 9/22/2017 in sciencemission.com
Exosomes are the missing link to insulin resistance in diabetes
We are publishing, below the new article created by Larry H. Bernstein, MD, FCAP.
During the period between 9/2015 and 6/2017 the Team at Leaders in Pharmaceutical Business Intelligence (LPBI) has launched an R&D effort lead by Aviva Lev-Ari, PhD, RN in conjunction with SBH Sciences, Inc. headed by Dr. Raphael Nir.
This effort, also known as, "DrugDiscovery @LPBI Group" has yielded several publications on EXOSOMES on this Open Access Online Scientific Journal. Among them are included the following:
QIAGEN – International Leader in NGS and RNA Sequencing, 10/08/2017
cell-free DNA (cfDNA) tests could become the ultimate "Molecular Stethoscope" that opens up a whole new way of practicing Medicine, 09/08/2017
Detecting Multiple Types of Cancer With a Single Blood Test (Human Exomes Galore), 07/02/2017
Reporter and Curator: Irina Robu, PhD
Exosomes: Natural Carriers for siRNA Delivery, 04/24/2017
One blood sample can be tested for a comprehensive array of cancer cell biomarkers: R&D at WPI, 01/05/2017
Curator: Marzan Khan, B.Sc
SBI's Exosome Research Technologies, 12/29/2016
A novel 5-gene pancreatic adenocarcinoma classifier: Meta-analysis of transcriptome data – Clinical Genomics Research @BIDMC, 12/28/2016
Curator: Tilda Barliya, PhD
Liquid Biopsy Chip detects an array of metastatic cancer cell markers in blood – R&D @Worcester Polytechnic Institute, Micro and Nanotechnology Lab, 12/28/2016
Reporters: Tilda Barliya, PhD and Aviva Lev-Ari, PhD, RN
Exosomes – History and Promise, 04/28/2016
Exosomes, 11/17/2015
Curator: Larry H. Bernstein, MD, FCAP
Liquid Biopsy Assay May Predict Drug Resistance, 11/16/2015
Glypican-1 identifies cancer exosomes, 10/31/2015
Circulating Biomarkers World Congress, March 23-24, 2015, Boston: Exosomes, Microvesicles, Circulating DNA, Circulating RNA, Circulating Tumor Cells, Sample Preparation, 03/24/2015
Cambridge Healthtech Institute's Second Annual Exosomes and Microvesicles as Biomarkers and Diagnostics Conference, March 16-17, 2015 in Cambridge, MA, 03/17, 2015
The newly created think-piece on the relationship between regulatory functions of Exosomes and Metabolic processes is developed conceptually, below.
We have had more than a half century of research into the genetic code and transcription leading to abundant work on RNA and proteomics. However, more recent work in the last two decades has identified RNA interference in siRNA. These molecules may be found in the circulation, but it has been a challenge to find their use in therapeutics. Exosomes were first discovered in the 1980s, but only recently there has been a huge amount of research into their origin, structure and function. Exosomes are 30–120 nm endocytic membrane-bound extracellular vesicles (EVs)(1-23) , and more specifically multiple vesicle bodies (MVBs) by a budding process from invagination of the outer cell membrane that carry microRNA (miRNA), and have structures composed of protein and lipids (1,23-27 ). EVs are the membrane vesicles secreted by eukaryotic cells for intracellular communication by transferring the proteins, lipids, and RNA under various physiologic conditions as well as during the disease stage. EVs also act as a signalosomes in many biological processes. Inward budding of the plasma membrane forms small vesicles that fuse. Intraluminal vesicles (ILVs) are formed by invagination of the limiting endosomal membrane during the maturation process of early endosome.
EVs are the MVBs secreted that serve in intracellular communication by transferring a cargo consisting of proteins, lipids, and RNA under various physiologic conditions (4, 23). Exosome-mediated miRNA transfer between cells is considered to be necessary for intercellular signaling and exosome-associated miRNAs in biofluids (23). Exosomes carry various molecular constituents of their cell of origin, including proteins, lipids, mRNAs, and microRNAs (miRNAs) (. They are released from many cell types, such as dendritic cells (DCs), lymphocytes, platelets, mast cells, epithelial cells, endothelial cells, and neurons, and can be found in most bodily fluids including blood, urine, saliva, amniotic fluid, breast milk, hydrothoracic fluid, and ascitic fluid, as well as in culture medium of most cell types.Exosomes have also been shown to be involved in noncoding RNA surveillance machinery in generating antibody diversity (24). There are also a vast number of long non-coding RNAs (lncRNAs) and enhancer RNAs (eRNAs) that accumulate R-loop structures upon RNA exosome ablation, thereby, resolving deleterious DNA/RNA hybrids arising from active enhancers and distal divergent eRNA-expressing elements (lncRNA-CSR) engaged in long-range DNA interactions (25). RNA exosomes are large multimeric 3′-5′ exo- and endonucleases representing the central RNA 3′-end processing factor and are implicated in processing, quality control, and turnover of both coding and noncoding RNAs. They are large macromolecular cages that channel RNA to the ribonuclease sites (29). A major interest has been developed to characterize of exosomal cargo, which includes numerous non-randomly packed proteins and nucleic acids (1). Moreover, exosomes play an active role in tumorigenesis, metastasis, and response to therapy through the transfer of oncogenes and onco-miRNAs between cancer cells and the tumor stroma. Blood cells and the vascular endothelium is also exosomal shedding, which has significance for cardiovascular, neurologicological disorders, stroke, and antiphospholipid syndrome (1). Dysregulation of microRNAs and the affected pathways is seen in numerous pathologies their expression can reflect molecular processes of tumor onset and progression qualifying microRNAs as potential diagnostic and prognostic biomarkers (30).
Exosomes are secreted by many cells like B lymphocytes and dendritic cells of hematopoietic and non-hematopoietic origin viz. platelets, Schwann cells, neurons, mast cells, cytotoxic T cells, oligodendrocytes, intestinal epithelial cells were also found to be releasing exosomes (4). They are engaged in complex functions like persuading immune response as the exosomes secreted by antigen presenting cells activate T cells (4). They all have a common set of proteins e.g. Rab family of GTPases, Alix and ESCRT (required for transport) protein and they maintain their cytoskeleton dynamics and participate in membrane fusion. However, they are involved in retrovirus disease pathology as a result of recruitment of the host`s endosomal compartments in order to generate viral vesicles, and they can either spread or limit an infection based on the type of pathogen and its target cells (5).
Upon further consideration, it is understandable how this growing biological work on exosomes has enormous significance for laboratory diagnostics (1, 3, 5, 6, 11, 14, 15, 17-20, 23,30-41) . They are released from many cell types, such as dendritic cells (DCs), lymphocytes, platelets, mast cells, epithelial cells, endothelial cells, and neurons, and can be found in most bodily fluids including blood, urine, saliva, amniotic fluid, breast milk, thoracic and abdominal effusions, and ascitic fluid (1). The involvement of exosomes in disease is broad, and includes: cancer, autoimmune and infectious disease, hematologic disorders, neurodegenerative diseases, and cardiovascular disease. Proteins frequently identified in exosomes include membrane transporters and fusion proteins (e.g., GTPases, annexins, and flotillin), heat shock proteins (e.g., HSC70), tetraspanins (e.g., CD9, CD63, and CD81), MVB biogenesis proteins (e.g., alix and TSG101), and lipid-related proteins and phospholipases. The exosomal lipid composition has been thoroughly analyzed in exosomes secreted from several cell types including DCs and mast cells, reticulocytes, and B-lymphocytes (1). Dysregulation of microRNAs of pathways observed in numerous pathologies (5, 10, 12, 21, 27, 35, 37) including cancers (30), particularly, colon, pancreas, breast, liver, brain, lung (2, 6, 17-20, 30, 33-36, 38, 39). Following these considerations, it is important that we characterize the content of exosomal cargo to gain clues to their biogenesis, targeting, and cellular effects which may lead to identification of biomarkers for disease diagnosis, prognosis and response to treatment (42).
We might continue in pursuit of a particular noteworthy exosome, the NLRP3 inflammasome, which is activated by a variety of external or host-derived stimuli, thereby, initiating an inflammatory response through caspase-1 activation, resulting in inflammatory cytokine IL-1b maturation and secretion (43).
Inflammasomes are multi-protein signaling complexes that activate the inflammatory caspases and the maturation of interleukin-1b. The NLRP3 inflammasome is linked with human autoinflammatory and autoimmune diseases (44). This makes the NLRP3 inflammasome a promising target for anti-inflammatory therapies. The NLRP3 inflammasome is activated in response to a variety of signals that indicate tissue damage, metabolic stress, and infection (45). Upon activation, the NLRP3 inflammasome serves as a platform for activation of the cysteine protease caspase-1, which leads to the processing and secretion of the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18. Heritable and acquired inflammatory diseases are both characterized by dysregulation of NLRP3 inflammasome activation (45).
Receptors of innate immunity recognize conserved moieties associated with either cellular damage [danger-associated molecular patterns (DAMPs)] or invading organisms [pathogen-associated molecular patterns (PAMPs)](45). Either chronic stimulation or overwhelming tissue damage is injurious and responsible for the pathology seen in a number of autoinflammatory and autoimmune disorders, such as arthritis and diabetes. The nucleotide-binding domain leucine-rich repeat (LRR)-containing receptors (NLRs) are PRRs are found intracellularly and they share a unique domain architecture. It consists of a central nucleotide binding and oligomerization domain called the NACHT domain that is located between an N-terminal effector domain and a C-terminal LRR domain (45). The NLR family members NLRP1, NLRP3, and NLRC4 are capable of forming multiprotein complexes called inflammasomes when activated.
The (NLRP3) inflammasome is important in chronic airway diseases such as asthma and chronic obstructive pulmonary disease because the activation results, in pro-IL-1β processing and the secretion of the proinflammatory cytokine IL-1β (46). It has been proposed that Activation of the NLRP3 inflammasome by invading pathogens may prove cell type-specific in exacerbations of airway inflammation in asthma (46). First, NLRP3 interacts with the adaptor protein ASC by sensing microbial pathogens and self-danger signals. Then pro-caspase-1 is recruited and the large protein complex called the NLRP3 inflammasome is formed. This is followed by autocleavage and activation of caspase-1, after which pro-IL-1β and pro-IL-18 are converted into their mature forms. Ion fluxes disrupt membrane integrity, and also mitochondrial damage both play key roles in NLRP3 inflammasome activation (47). Depletion of mitochondria as well as inhibitors that block mitochondrial respiration and ROS production prevented NLRP3 inflammasome activation. Futhermore, genetic ablation of VDAC channels (namely VDAC1 and VDAC3) that are located on the mitochondrial outer membrane and that are responsible for exchanging ions and metabolites with the cytoplasm, leads to diminished mitochondrial (mt) ROS production and inhibition of NLRP3 inflammasome activation (47). Inflammasome activation not only occurs in immune cells, primarily macrophages and dendritic cells, but also in kidney cells, specifically the renal tubular epithelium. The NLRP3 inflammasome is probably involved in the pathogenesis of acute kidney injury, chronic kidney disease, diabetic nephropathy and crystal-related nephropathy (48). The inflammasome also plays a role in autoimmune kidney disease. IL-1 blockade and two recently identified specific NLRP3 inflammasome blockers, MCC950 and β-hydroxybutyrate, may prove to have value in the treatment of inflammasome-mediated conditions.
Autophagosomes derived from tumor cells are referred to as defective ribosomal products in blebs (DRibbles). DRibbles mediate tumor regression by stimulating potent T-cell responses and, thus, have been used as therapeutic cancer vaccines in multiple preclinical cancer models (49). It has been found that DRibbles could induce a rapid differentiation of monocytes and DC precursor (pre-DC) cells into functional APCs (49). Consequently, DRibbles could potentially induce strong innate immune responses via multiple pattern recognition receptors. This explains why DRibbles might be excellent antigen carriers to induce adaptive immune responses to both tumor cells and viruses. This suggests that isolated autophagosomes (DRibbles) from antigen donor cells activate inflammasomes by providing the necessary signals required for IL-1β production.
The Hsp90 system is characterized by a cohort of co-chaperones that bind to Hsp90 and affect its function (50). The co-chaperones enable Hsp90 to chaperone structurally and functionally diverse client proteins. Sahasrabudhe et al. (50) show that the nature of the client protein dictates the contribution of a co-chaperone to its maturation. The study reveals the general importance of the cochaperone Sgt1 (50). In addition to Hsp90, we have to consider Hsp60. Adult cardiac myocytes release heat shock protein (HSP)60 in exosomes. Extracellular HSP60, when not in exosomes, causes cardiac myocyte apoptosis via the activation of Toll-like receptor 4. the protein content of cardiac exosomes differed significantly from other types of exosomes in the literature and contained cytosolic, sarcomeric, and mitochondrial proteins (21).
A new Protein Organic Solvent Precipitation (PROSPR) method efficiently isolates the EV repertoire from human biological samples. Proteomic profiling of PROSPR-enriched CNS EVs indicated that > 75 % of the proteins identified matched previously reported exosomal and microvesicle cargoes. In addition lipidomic characterization of enriched CNS vesicles identified previously reported EV-specific lipid families and novel lipid isoforms not previously detected in human EVs. The characterization of these structures from central nervous system (CNS) tissues is relevant to current neuroscience, especially to advance the understanding of neurodegeneration in amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD) and Alzheimer's disease (AD)(15). In addition, study of EVs in brain will enable characterization of the degenerative posttranslational modifications (DPMs) occurring in those proteins.
Neurodegenerative disease is characterized by dysregulation because of NLRP3 inflammasome activation. Alzheimer's disease (AD) and Parkinson's disease (PD), both neurodegenerative diseases are associated with the NLRP3 inflammasome. PD is characterized by accumulation of Lewy bodies (LB) formed by a-synuclein (aSyn) aggregation. A recent study revealed that aSyn induces synthesis of pro-IL-1b by an interaction with TLR2 and activates NLRP3 inflammasome resulting in caspase-1 activation and IL-1b maturation in human primary monocytes (43). In addition mitophagy downregulates NLRP3 inflammasome activation by eliminating damaged mitochondria, blocking NLRP3 inflammasome activating signals. It is notable that in this aberrant activation mitophagy downregulates NLRP3 inflammasome activation by eliminating damaged mitochondria, blocking NLRP3 inflammasome activating signals (43).
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redpajama_set_name: RedPajamaCommonCrawl


As I write this, I am busy getting ready for my Art and Faith exhibit opening November 4th at Inspiration Studios. I am very excited and nervous and thrilled and…. I really hope ya'll come and just hang out. Have a snack. Enjoy some art.
In case you missed it, CBS Milwaukee did a really sweet video segment on Inspiration Studios. This place has a lot going on! It has a black box theater and of course, art gallery. Each event supports the other. And Erico Ortiz, the owner and founder of Inspiration Studios, is one of those people I wanted to hug as soon as I met him. He celebrates creativity and I love everything he is doing to support the arts in Milwaukee. He is really an inpsiration, so I'm especially grateful to have this exhibit at this place that has been created with such joy and positive energy.
So please, check out the segment about Inspiration Studios and if you get to the 4:49 (ish) point of the video, you'll see a mention of me and my exhibit. It's quick! But how cool that they included me.
I've also created a video for the exhibit which is available on my YouTube channel. Please feel free to share it!
Thanks for your support. It means so much to me.


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Jun 14, 2018, 7:14 PM by Eric M. Zeman @zeman_e
AT&T today said it has completed its purchase of Time Warner, a deal originally valued at $85.4 billion when it was announced in October 2016. Earlier this week, a U.S. judge sided with AT&T after the Justice Department sued the company to block the deal. After losing the case, the Justice Department made no further recommendations against the deal and AT&T wrapped up the legal paperwork quickly. Time Warner — and now AT&T — owns Warner Bros., HBO, and Turner, which in turn owns CNN and other media properties. "Combine [Warner's content] with AT&T's strengths in direct-to-consumer distribution, and we offer customers a differentiated, high-quality, mobile-first entertainment experience," said Randall Stephenson, chairman and CEO of AT&T in a prepared statement. "We're going to bring a fresh approach to how the media and entertainment industry works for consumers, content creators, distributors and advertisers." Many fear the deal will lead to less choice and higher prices for consumers. Moving forward, AT&T will consist of four core businesses: AT&T Communications (mobile, broadband), AT&T media (Turner, HBO), AT&T International (mobile in Mexico), and AT&T's advertising and analytics. AT&T says it will create a formal name for this last business unit later in the year. John Donovan will serve as CEO of AT&T Communications, John Stankey will serve as CEO of AT&T's media business, Lori Lee will serve as CEO of AT&T International, and Brian Lesser will serve as CEO of AT&T's ad and analytics business. All four will report to Randall Stephenson, who remains chairman and CEO of AT&T Inc.
Justice Dept. Gives AT&T-Time Warner Judge a Way Out
The Justice Department, during closing arguments of its case against the AT&T-Time Warner merger, suddenly suggested the judge weigh "alternative" remedies should he choose not to block the deal. The Justice Department has fought against the merger from the start, saying AT&T would use Time Warner's content as a weapon against consumers, raising prices and limiting competition.
Justice Department Pushes Courts for Action On AT&T Appeal
The Justice Department has asked the D.C. Circuit Court of Appeals to prioritize its appeal against last month's decision regarding AT&T's acquisition of Time Warner.
Judge Says AT&T Can Buy Time Warner
AT&T today was given permission to buy Time Warmer with no conditions and no divestitures. The ruling was handed down by U.S.
DOJ Sues to Halt AT&T/Time Warner Merger
The U.S. Department of Justice has sued to stop the proposed merger between AT&T and Time Warner.
Justice Dept. Probing Sprint/T-Mobile Merger Effect on MVNOs
The U.S. Department of Justice is exploring what impact the proposed merger of Sprint and T-Mobile will have on smaller carriers and MVNOs.
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So the new Company will be called?
What will the new company be called TW-ATT?
Mark_S
This is how they compete with Verizon.
Like primates at the zoo.
Throwing feces at each other.
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College: Penn State
17 @Ravens L 10 - 28
16 @Jets L 10 - 16
2018 Pittsburgh Steelers 2 0 2 1 1 0 0 0
2019 Pittsburgh Steelers 1 0
Drafted by the Steelers with the first of their two fifth round selections (148th overall) in the 2018 NFL Draft... saw action in two games during the 2018 season.... made his NFL debut Dec. 2 against the Chargers.
PRO (2-0/0-0): Drafted by the Steelers with the first of their two fifth round selections (148th overall) in the 2018 NFL Draft.
2018 (2-0/0-0): Saw action in two games during the regular season.
12/2 vs. L.A. Chargers: Made his NFL debut.
COLLEGE: Totaled 321 tackles at Penn State, ranking fifth in school history in career tackles and becoming the sixth player in program history to record at least 300 stops in a career…earned first-team All-Big Ten accolades from the coaches and second-team honors from the media in 2017 after starting all 13 games and recording 72 tackles (46 solo) with one interception and forcing two fumbles…selected as a team captain in 2017…tabbed All-Big Ten third-team by the coaches and honorable mention by the media panel in 2016…named Big Ten Co-Defensive Player of the Week after a 22-tackle game vs. Minnesota in 2016…started all 14 games, notching 10 tackles or more in three games, en route to recording a career-best 110 tackles in 2016 to become the first safety to lead Penn State in tackles since 2002…honorable mention All-Big Ten by the coaches and media in 2015, finishing second on the defense with 81 tackles…started seven of 13 games played in 2014, tying for third on the squad with 58 tackles…majored/graduated in broadcast journalism.
PERSONAL: Attended Dr. Henry Wise HS (Upper Marlboro, Md.)…posted 15 tackles and two fumble recoveries in three games as a senior before suffering an ankle injury…helped the Pumas advance to a perfect 14-0 record and the Maryland 4A State Championship as a junior, producing 70 tackles, three interceptions and 10 pass breakups…was invited to participate in the Big 33 Classic and Maryland Crab Bowl following his senior year…son of Shawn and Latonya Allen...is the godson of Pro Football Hall of Fame running back Curtis Martin.


Basic techniques and procedures for making systematic observations in a wide variety of psychological situations, both laboratory and field. Psychological methods demonstrated through topics of current research and application, and through demonstration-lab projects.
Prerequisites: PSYC 2010 or equivalent.