Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As early as in 1948 a woman with severe rheumatoid arthritis (RA) was successfully treated with glucocorticoids. However, not until recently has the role of GCs in the treatment of RA been clarified and supported by scientific evidence in a limited number of randomised studies. The present article reviews four reports from the BARFOT (Better Anti-Rheumatic FarmacOTherapy) low-dose prednisolone study based on 250 patients with early RA. These patients were randomised to have either DMARDs only or DMARDs plus prednisolone 7.5 mg daily for two years. It was shown that low-dose prednisolone in addition to a DMARD was superior to DMARDs alone in the ability to inhibit joint damage and induce clinical remission. A follow-up study demonstrated that remission after 2 years with low-dose prednisolone was associated with reduced joint destruction also after 4 years. Prednisolone had no or minor effects on bone density and the frequency of adverse effects was small. A third article measuring markers of bone synthesis and resorption demonstrated that the suppressive effect on bone synthesis exerted by prednisolone was counteracted by the ability of prednisolone to hamper the inflammatory mediated increase in bone resorption. In a fourth article assessing intima-media thickness and endothelial function, no influence of prednisolone 7.5 mg daily on atherosclerosis was observed. Altogether, these four studies provide evidence for recommending low-dose prednisolone treatment in combination with DMARDs for at least two years to patients with recent onset RA.
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PMID:Effects on joint destruction and remission, bone turnover and lack of influence on atherogenesis: a review of the BARFOT low-dose prednisolone studies on patients with early RA. 2201 86

Inflammation is a protective response to stimuli trauma, which can also lead to severe tissue injury. The existing anti-inflammatory drugs, such as corticosteroids and glucocorticoids, generally exhibit side effects and poor accumulation in inflammatory tissue. Hence, a theranostic nanoplatform with serial reactive oxygen species (ROS) responsiveness and two-photon AIE bioimaging has been constructed for dimensional diagnosis and accurate therapy of inflammation. Prednisolone (Pred) is bridged to a two-photon fluorophore (TP) developed by us via a ROS sensitive bond to form a diagnosis-therapy compound TPP, which is then loaded by the amphipathic polymer PMPC-PMEMA (PMM) through self-assembling into the core-shell structured micelles (TPP@PMM). With a particle size of 57.5 nm, TPP@PMM can realize the accumulation in the inflammatory site via the oedematous tissue and the accurate release of anti-inflammatory drug Pred through the serial response to the local overexpressed ROS. The micellar structure is first interrupted by the ROS triggered hydrophobic-to-hydrophilic conversion of PMEMA, which allows the release of TPP. Then the ROS responsive bond in TPP is subsequently broken, resulting in the accurate delivery of Pred and the inflammation therapy. Furthermore, TPP@PMM can be traced in vivo with a distinct two-photon imaging due to the AIE active fluorophore TP. The theranostic TPP@PMM reveals high-resolution inflammation diagnosis and efficient anti-inflammatory activity owing to the two-photon fluorophore and the serial ROS responsiveness and has been proven to achieve the efficient treatment of acute lung injury, arthritis, and atherosclerosis. Therefore, TPP@PMM holds considerable promise as a potential strategy for acute and chronic inflammation theranostics.
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PMID:Reactive Oxygen Species Responsive Theranostic Nanoplatform for Two-Photon Aggregation-Induced Emission Imaging and Therapy of Acute and Chronic Inflammation. 3237 16