The Fate Of The FuriousMovie 2017
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The Fate of the Furious (alternatively known as F8 and titled on-screen as Fast & Furious 8 internationally) is a 2017 American action film directed by F. Gary Gray and written by Chris Morgan. It is the sequel to Furious 7 (2015) and the eighth installment in the Fast & Furious franchise. The film stars Vin Diesel as Dominic Toretto, alongside Dwayne Johnson, Jason Statham, Michelle Rodriguez, Tyrese Gibson, Chris \"Ludacris\" Bridges, Scott Eastwood, Nathalie Emmanuel, Elsa Pataky, Kurt Russell, Charlize Theron and Kristofer Hivju. In the film, Dom has settled down with his wife Letty Ortiz, until cyberterrorist Cipher (Theron) coerces him into working for her and turns him against his team, forcing them to find Dom and take down Cipher.
The Fate of the Furious premiered in Berlin on April 4, 2017, and was theatrically released in conventional and IMAX theatres in the United States on April 14, by Universal Pictures. It received mixed to positive reviews from critics. It got praised for the performances of the cast and action sequences but criticised the storyline. The film was a box office success, grossing over $1.2 billion worldwide, making it the nineteenth film (and the second in the franchise, after Furious 7) to gross over $1 billion, the third-highest-grossing film of 2017, and the eleventh highest-grossing film of all time at the time. It also grossed $541.9 million worldwide during its opening weekend, which made it the highest-grossing worldwide opening of all time until the release of Avengers: Infinity War (2018). The sequel, F9, was released in June 2021.
Brian Tyler, who scored the third, fourth, fifth, and seventh installments, was tapped to compose the film score for the eighth picture.[52] A soundtrack album by Atlantic Records was released on April 14, 2017, coinciding with the film's US theatrical release.[53] The film's score album was released on April 28, by Back Lot Music.[54]
The Fate of the Furious had its world premiere in Berlin on April 4, 2017.[55] The film was theatrically released in the United States on April 14.[22][23] The film was released in 1,074 IMAX screens around the world, making it the widest opening in IMAX history.[56]
Tattoos and permanent make-up work by depositing insoluble pigments into the dermal skin layer (Fig. 1). In conjunction with tattoos, pigmented and enlarged lymph nodes have been noticed in tattooed individuals for decades7. After the traumatic insertion of inks during the tattooing procedure, the body will excrete as many components as possible via the damaged epidermis. Other ways to clean the site of entrance are through active transport to lymph nodes by phagocytizing cells, or passively along the lymphatic vessels8,9,10,11. In addition to observations in humans, an in vivo study in mice revealed colored lymph nodes after tattooing with an azo pigment12. Even though this leaves little doubt that the pigment originates from corresponding tattoos, the origin and fate of pigments in human lymph nodes have never been analytically investigated so far. Lately, the only study analyzing human lymph nodes in tattooed individuals assessed its contents on carcinogenic polycyclic aromatic hydrocarbons deriving from carbon black particles13.
The Fate of the Furious[2] (also known as Furious 8, Fast 8 and Fast & Furious 8)[note 1][3] is an 2017 American action film directed by F. Gary Gray. The eighth feature length film in Universal Pictures's The Fast and the Furious franchise, The Fate of the Furious was officially announced by Vin Diesel and Universal Pictures on April 23, 2015 at CinemaCon. The film premiered in Berlin on April 4, 2017, and was released on April 14, 2017 in North America, with major international releases for IMAX 3D, 3D and 4DX showings.[1]
April 23, Vin Diesel appeared at the 2015 CinemaCon and officially announced that The Fate of the Furious would be released April 14, 2017.[1][10] Diesel's announcement was confirmed by an official press release from Universal Pictures, detailing the rescheduling of several major upcoming films under their distribution, including Warcraft and the the sequel to Guillermo del Toro's Pacific Rim. Also announced were two sequels to Fifty Shades of Grey.[11]
February 5, 2016, a minute long TV Spot for The Fate of the Furious was aired during the the 51st Super Bowl event.[59][60] At the time of the TV Spot's release during the Super Bowl, it was the most viewed trailer online with a record number of 42.27M views.[61] March 31, the trailer for the 2017 adaptation of Stephen King's 1986 novel It became the most viewed trailer across various social media platforms within 24 hours with 197 million views, beating the established record set by The Fate of the Furious during the Super Bowl.[62]
April 2, 2017, pre-sale tickets for The Fate of the Furious ticket began in China. Prior to the film's release on April 14, the Hollywood Reporter reported that The Fate of the Furious broke ticket sales records, earning $18.1 million (RMB 125 million) in advanced ticketing sales, breaking the pre-sale records set by Journey to the West: The Demons Strike Back (which originally earned RMB 101 million, or $14.6 million).[65] The Fate of the Furious also earned $2.4 million (RMB 16.5 million) in advanced IMAX ticket sales, breaking the record set by Captain America: Civil War when it earned RMB 10 million ($1.4 million at current rates) last year.[65]
The Various Artists soundtrack, The Fate of the Furious: The Album was released April 14, 2017 in conjunction with the film. The soundtrack features predominantly Pop and Hip-Hop artists. Lil Uzi Vert, Travis Scott, and Quavo performed the theme of the film, \"Go Off\"; Pitbull, J Balvin and Camila Cabello recorded a Spanish and English language single \"Hey Ma\" to promote the film internationally. G-Eazy and Kehlani performed the soundtrack's third single, \"Good Life\"; Wiz Khalifa]] and 2 Chainz, who were previously featured on the soundtrack for Fast & Furious 6 and Furious 7, collaborated with Young Thug for the soundtrack's fourth single \"Gang Up\".
This chronological acquisition of deuterium by circulating monocyte subsets is most likely to be explained by a sequential ontogeny scenario in which deuterium is incorporated into precursors that differentiate into classical monocytes in bone marrow; these classical monocytes are released into the circulation, where they undergo one of two fates: they either differentiate into intermediate monocytes or disappear by death or migration. Similarly, intermediate monocytes either leave the blood (by death or migration) or differentiate into nonclassical monocytes. The likelihood of each onward differentiation step (classical to intermediate and then intermediate to nonclassical) was denoted by the rate αr for each subpopulation, resulting in a corresponding rate of loss from the circulating pool (by death or migration) of (1-α)r. This model is summarized in Fig. 1 e. The alternative parallel ontogeny scenario was also considered; in this model, the three subsets arise from separate linages, each with its own distinct postmitotic kinetics. This model could certainly be made to fit the data mathematically, as it has so many free parameters, but was deemed unlikely on biological grounds. First, it predicts the presence of intermediate and nonclassical monocytes in the bone marrow, contrary to our observations where only classical monocytes were detected following bone marrow biopsy (Fig. 1 f; blood monocyte contamination could be detected in bone marrow aspirate), and second, because it would be inconsistent with information from studies in rodents (Sunderkötter et al., 2004; Yrlid et al., 2006; Varol et al., 2007; Yona et al., 2013; Gamrekelashvili et al., 2016). In the sequential model used here (Fig. 1 e) proliferation is restricted to the bone marrow; we excluded models in which circulating subsets proliferate in the blood on the basis of (1) the absence of any deuterium enrichment in such cells 24 h after labeling (Fig. 1 d) and (2) the absence of markers of cell cycling (Fig. S1 b).
Given the sequential maturation of monocyte subsets during healthy homeostasis and, reappearance of monocytes following endotoxin challenge, we investigated the developmental relationship between human monocytes subsets in a humanized animal model. To this end, we analyzed the fate of classical human monocytes isolated from healthy volunteers and grafted into MISTRG mice (Fig. 3). The MISTRG mouse is a novel humanized mouse containing human versions of five genes encoding the cytokines thrombopoietin, IL-3, CSF2 (GM-CSF), SIRPα, and CSF1 (M-CSF) that help maintain human mononuclear phagocyte development (Rongvaux et al., 2014; Deng et al., 2015). Recipient mice were sacrificed at various time points following transfer, and peripheral blood was subjected to flow cytometry analysis. 10 min after transfer engraftment, (human) CD45+ cells detected in recipient blood displayed a classical monocyte phenotype; by 24 h, the grafted cells had transitioned to intermediate monocytes, and by 96 h, all grafted cells were nonclassical monocytes (Fig. 3 c). Collectively, this establishes for the first time that human classical monocytes have the potential to become intermediate monocytes before finally differentiating into nonclassical monocytes in vivo. These studies are reminiscent of previous rodent experiments, where classical Ly6Chi monocytes were shown to convert into nonclassical cells over time (Varol et al., 2007; Yona et al., 2013; Gamrekelashvili et al., 2016). Although the conversion times differed from those seen in the in vivo deuterium-labeling studies, this is most likely due to grafted cells already being mature classical monocytes. A recent murine study has demonstrated Notch2 signaling is required for classical Ly6C+ monocytes to convert to nonclassical monocytes (Gamrekelashvili et al., 2016). Due to the challenging nature of ex vivo monocyte culture, this has not been demonstrated in human cells, but hopefully, future advances in cell culture will enable us to fully comprehend the mechanisms involved in human monocyte conversion. 59ce067264
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