Long non-coding RNA UCA1 promotes gallbladder cancer progression by epigenetically repressing p21 and E-cadherin expression.

"Lupus nephritis", a serious complication of systemic lupus erythematosus (SLE), is an entity of recent vintage. The term "lupus", derived from Latin for wolf, was introduced in the Middle Ages to denote nondescript erosive skin lesions which resembled wolf bites that were known theretofore by their Greek name of "herpes esthiomenos", used in the Hippocratic Corpus for the spread of the lesions like a crawling snake. The specific dermatologic features of lupus were characterized as an "erythematous" butterfly rash in 1828 and dubbed "lupus erythematosus" in 1850. Their association with systemic manifestations was described in 1872 and termed "disseminated lupus erythematosus" by the close of the century. A preference for "systemic" rather than "disseminated" was suggested in 1904 but would not prevail until the 1960s. The generic term "nephritis", denoting "inflammation of the kidnies" dating to the 1580s, was first used to describe the renal lesions of SLE in 1902. Although albuminuria and abnormal urine sediment were often noted in SLE patients, the early study of their renal changes was limited to postmortem studies. Refinements in their identification came in the late 1950s after the introduction of kidney needle biopsies and refined thereafter by immunofluorescent and electron microscopic studies. Subsequent lupus nephritis studies paralleled the emerging discipline of immunology that identified autoimmunity as the cause of SLE. The varied lesions observed were classified by glomerular changes in 1975 and refined in 2003. Advances in genetic and molecular profiling have enriched the management of lupus nephritis based on kidney biopsies.