Cirrhosis Open Access Articles

Open access to the scientific literature means the removal of barriers (including price barriers) from accessing scholarly work. There are two parallel roads towards open access: Open Access articles and self-archiving. Open Access articles are immediately, freely available on their Web site, a model mostly funded by charges paid by the author (usually through a research grant). The alternative for a researcher is “self-archiving” (i.e., to publish in a traditional journal, where only subscribers have immediate access, but to make the article available on their personal and/or institutional Web sites (including so-called repositories or archives)), which is a practice allowed by many scholarly journals. Open Access raises practical and policy questions for scholars, publishers, funders, and policymakers alike, including what the return on investment is when paying an article processing fee to publish in an Open Access articles, or whether investments into institutional repositories should be made and whether self-archiving should be made mandatory, as contemplated by some funders. Cirrhosis is a disease related to the liver which is characterized by loss of liver cells which is replaced by fibrosis. The major causes of cirrhosis are alcohol and viral hepatitis B and C. It can be diagnosed by liver biopsy. The slowly progressing disease in which healthy liver tissue is replaced with scar tissue, eventually preventing the liver from functioning properly is termed as liver cirrhosis. The scar tissue blocks the flow of blood through the liver and slows the processing of nutrients, hormones, drugs, and naturally produced toxins. It also slows the production of proteins and other substances made by the liver. The relationship between liver and blood plays a vital role in maintain bodys various functions. However, in cirrhosis this relation between blood and liver gets affected further leading to many other complications.

• Share this page
• 
• 
• 
• 
• 
• 

Last date updated on April, 2024