We are perhaps most familiar with this story because it is also the story used to market new technologies to us as consumers, although it is also quite prevalent in academic and journalistic commentaries on technology. The idea that a new medium is closer to reality and more immersive and interactive than its predecessor is based on this story—whether the new medium in question is the Orthophonic Victrola, compact discs, high-definition tv, virtual reality, or 3D cinema. This idea can be projected backward to the earliest cave paintings and musical instruments, but it generally references the rise of mechanical, electric, and electronic media. Of course, claims about increased definition or the pleasures of immersion are in many cases true, but they are not the whole story.”
Questions: Who is the author and what is the name of the text? What does this theorist mean by “the dream of verisimilitude” and how is that different from “increased definition?” How does this relate to the idea of the “format?” What does it mean to claim that the standards imposed by formats are also standardizing? Choose a format and provide a short analysis of how it institutes norms. Compare this theorist’s position with one other theorist we have encountered in the course.
This page of the exposition has 1239 words. Download the full form above. Tight intersections (TJs) are impeding intersections which go about as boundaries that control paracellular penetrability and manage trans-epithelial water and solute development. The structures are made out of vital transmembrane proteins that connection neighboring cells, with an impact on cell-cell bond and epithelial porousness. It additionally fills in as a limit between the apical and basolateral plasma film areas to make the polarization of endothelial and epithelial cells. These intersections are contained arrangements of ceaseless systems administration strands in the ostensibly confronting cytoplasmic pamphlet, with correlative depressions in the internally confronting extra cytoplasmic flyer. Figure 1: Tight intersection area between the epithelial cells and paracellular transport. (Singh, Sharma, and Dhawan, 2010) Claudins Claudin in ovarian malignant growth Claudin proteins comprises of 24 transmembrane proteins displaying particular tissue and are the principle segment of tight intersections that capacity as specific obstructions. Claudins are communicated in both epithelial and endothelial cells in which they structure a complex with impeding (Leech A.O et al 2015). Clauidns assume significant jobs in shaping and capacity of the tight intersection in ordinary epithelial and endothelial cells. Claudins structure the foundation of TJs and interrelate with one another in homotypic and heterotypic style. There are two transmembrane areas N-ends and C-ends with the two parts of the bargains situated in the cytoplasm. This planning brings about the development of two extracellular parts. The C-terminal locale contains a PDZ-space restricting theme that can collaborate with PDZ-area containing proteins, for example, ZO proteins (Morin, 2007). Figure 2: The structure of claudin proteins and the extracellular circles. The C-terminal is PDZ restricting space. (Morin, 2007) Ovarian Cancer Ovarian malignant growth is a kind of disease that starts in tissues of ovaries. The ovaries are the female regenerative organs which produce eggs (ova) just as female hormones estrogen and progesterone. Ovarian malignant growth is the fourth driving reason for disease among ladies in Europe and United States, there are a greater number of passings than in some other malignant growth because of troubles in determination and treatment. In UK ovarian malignant growth is the fifth most normal disease in ladies, around 7000 cases were recorded in 2012. As indicated by (Globocan 2012) around 239000 ladies were to have been determined to have ovarian malignant growth in 2012, and is the eighth most normal reason for disease passing in ladies around the world. The ovaries are comprised of three primary sorts of cells and each kind of cell can form into an alternate sort of tumor, the three sorts of ovarian diseases (tumors); epithelial ovarian malignancy, Germ cell ovarian malignancy and stromal ovarian disease. • Epithelial ovarian malignant growth is the most regular type of ovarian disease it is gotten from cells on the outside of the ovary. • Germ cell ovarian malignant growth are considerably less normal and influences youngsters or high school young ladies. It is gotten from the egg creating cells inside the body of the ovary. • Stromal cell ovarian malignant growth begins in the cells that hold the ovaries together and produce female hormones. Page 2: Molecular instrument of Ovarian Cancer Major Ovarian malignancy flagging pathways are associated with ovarian disease cell improvement. The harmful instruments and change of ovary cells to epithelial ovarian disease are a way to recognize specific ovarian malignancy biomarkers. A large portion of these qualities are connected to cell flagging pathways in which they assume a fundamental job in disease cell development, intrusion, endurance and metastasis. The flagging pathways which are related with ovarian malignant growth are; • Nuclear factor kappa enacted B cells (NF-kB) • Activator of interpretation 3 (Jak-STAT 3) • Mitogen initiated protein kinase (MAPK) • Proto oncogene tyrosine protein kinase Src • ErbB initiation, the lysophosphatidic corrosive (LPA) • Phosphatidylinositol 3 kinase (PI3K) • Vascular Endothelial Growth Factor (VEGF) • Epidermal Growth Factor Receptor (EGFR) (Longuespée et al., 2012). The majority of the above flagging pathways happen in atomic system of ovarian malignant growth and associate with one another anyway EGFR transformations are uncommon and not fundamentally overexpressed. EGFR is an individual from ErbB group of receptor tyrosine kinase which incorporates HER 2, Erb3 and Erb4. – Epidermal development factor flagging has been shown to adjust the declaration of the claudins in different cell types. In ongoing examination system of the TJ protein guideline in ovarian malignancies was investigated by treating both ovarian mucinous and serous cystadenocarcinoma cell lines with EGF. – It's enacted by different ligands, for example, EGF and TGF and assumes job in upgrading and restraining tumor endurance. – Following authoritative of its ligand EGFR is initiated and EGFR tyrosine movement phosphorylates tyrosine deposits on the EGFR and different proteins causing their actuation and causing a succession of downstream effectors which lead to expanded cell development. – This than prompts initiation of different intercellular flagging pathways, for example, (MAPK) and (PI3K) AKT pathways, which are engaged with endurance and cell multiplication (Dutta et al., 2010). – EGF found to downregulate claudin 3 in mucinous ovarian carcinoma cell lines and claudin 4 in ovarian serous cystadenocarinoma by inciting the debasement of these proteins with likewise changes in the structure and capacity of tight intersection through the MEK/ERK or P13K/AKT flagging pathway (Ogawa et al., 2012). Claudin overexpression of claudin proteins in ovarian malignant growth gives off an impression of being the most conspicuous in epithelial tumors because of the sex line and stromal tumors which don't express the proteins at noteworthy levels. In ongoing investigation demonstrated that the crucial atomic systems engaged with ovarian disease, a two pathway model for ovarian tumorigenesis with Type 1 pathway associated with the advancement of poor quality tumors and type 2 pathways in the age of genuine high evaluation tumors (Li et al., 2009). The watched atomic highlights in ovarian malignancy, frequently overexpress of a few individuals from the claudin group of tight intersection proteins. It has been recommended that claudin 3 and claudin 4 are regularly raised in ovarian malignancy. In different tumors certain caludins to have been as prognostic markers and in ovarian malignant growth claudin 3 and 7, levels are conversely interrelated with endurance (Li et al., 2009). The system of the expanded Claudin 3 and Claudin4 articulation in ovarian disease is believed to be the consequence of epigenetic alterations of the Claudin advertiser areas in the malignancy cells which in coming about expanded cell endurance, attack and motility (English and Santin, 2013). In the investigation microarray examination have been utilized so as to recognize the sub-atomic changes that happen in claudin 4 overexpressing cells, as cell communicating claudin 4 display raised angiogenesis properties as estimated by both in vitro and vivo measures. Claudin quality CLDN16 an individual from the claudin family, CLDN16 has been recommended to be raised in ovarian malignant growth. It has significant impact in the upkeep of cell extremity, cell course of action, bond, paracellular transport and ionic porousness of different epithelial. (English and Santin, 2013) Table 1: Claudin articulation in gynaecologic malignant growth Step by step instructions to distinguish Claudin in ovarian malignant growth Looks into on claudin in ovarian disease has been included both on a fundamental and clinical level. In fundamental research including cell line or creature examinations, for example, – Detection of articulation numerous claudins – Exploring the system of quality articulation Sequential investigation of Gene Expression (SAGE) is strategies used to break down ovarian malignancy quality articulation and CLDN3/CLDN4 discovered for the most part up managed in the ovarian disease. In a few examinations CLDN7 have been seen that overexpress in ovarian malignant growth anyway this change is less reliable than what is recognized for CLDN3 and CLDN4. (Morin, 2007) Because of the overexpression designs in ovarian malignant growth claudin proteins may speak to valuable ovarian disease markers to recognize, analyze or treatment at a beginning time (Morin, 2007). In End Claudin 3, 4 and 7 are particularly communicated in ovarian malignant growth, understanding the careful job of these proteins in ovarian remain inadequately characterized just as other human tumors. (Morin, 2007)>GET ANSWER