Example sentences for: prostaglandin

How can you use “prostaglandin” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • The marginal efficacy of prostaglandin isn't likely to keep the baby boomers from buying the urological spin.

  • Regular use of aspirin and other non-steroidal anti-inflammatory dugs (NSAIDs) has been consistently associated with reduced risk of colorectal cancer and adenoma [ 1 2 3 4 ] , possibly due to NSAID-related inhibition of prostaglandin synthesis, enhancement of cellular immune response, or induction of apoptosis [ 5 6 7 8 ] . A number of epidemiological studies have investigated the potential protective effect of NSAIDs with respect to other cancer sites.

  • Non-small cell lung cancer (NSCLC); Prostaglandin E-2 (PGE-2); Interleukin 10 (IL10); cytotoxic T cell (CTL)

  • COX-2 is an inducible enzyme upregulated in inflammatory states [ 20 21 ] . Notably, many NSCLC and what have been characterized as "premalignant" lung lesions have been shown to constitutively express the COX-2 enzyme and produce prostaglandin E-2 (PGE-2), the primary product of the COX-2 pathway [ 22 23 24 25 26 ] . Importantly, PGE-2 production by tumor cells has been linked to tumor-induced immunosuppression in NSCLC [ 2 3 4 5 ] . PGE-2 has been shown to directly suppress T cell mediated immunity, the primary effector against tumor cells, at a variety of levels [ 2 3 4 5 6 7 ] . Further, PGE-2 has been shown to induce the IL10 in mononuclear cells [ 4 5 ] . IL10 is a prominent immunosuppressive cytokine that may have a dominant role in preventing innate antitumor responses in the NSCLC environment [ 2 3 4 5 ] , [ 8 9 10 11 12 13 14 15 16 17 18 19 ] . Among myriad suppressive effects on T cells and antigen presenting cells, IL10 is known to inhibit IL12 production [ 14 15 16 17 18 ] . IL12 plays a key role in the initiation and potentiation of cellular immune responses and alteration of the IL12 producing function in circulating mononuclear phagocytes may be a critical factor in suppressed T cell immunity to NSCLC [ 27 28 ] .

  • In addition, IL-4 inhibits growth factor-induced RA synoviocyte proliferation, and expression of prostaglandin E and matrix metalloproteinase-3 in RA synovial fibroblast [ 14, 15, 16], and reduces bone resorption.


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