SLES


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SLES

(SuSE Linux Enterprise Server) See SuSE Linux.
References in periodicals archive ?
Etiology of SLE includes many components such as genetic environmental hormonal drugs etc (Helen et al 1999).
During the last few years by using hundreds of thou-sands of single nucleotide polymorphism (SNP) mar-kers understanding of genes involved in the pathoge-nesis of SLE has increased (Bertsias et al 2008).
Through unknown mechanisms in women hormones contribute to the increased prevalence of SLE (Duarte et al 2011).
Environmental triggers of SLE include ultraviolet light demethylating drugs and infections.
Up to 10% of SLE patients may actually have drug in-duced lupus (DIL) and approximately 80 percent of drugs have been implicated in causing DIL.
Immune responses against endogenous nuclear anti- gens are characteristic of SLE. Auto-antigens released
The pathogenesis of SLE involves a multitude of cells and molecules that participate in apoptosis inn-ate and adaptive immune responses.
Diagnosis of SLE is based on classification criteria established by the American College of Rheumatology (ACR).
Assessing disease activity in SLE is crucial to the phy-sician as it forms the basis for treatment decisions.
SLE activity has three patterns: flare chronic and long quiescence.
Clinical presentation of SLE can be nonspecific e.g.
Ninety percent of SLE patients have joint inflammat ion such as arthralgia arthritis tendinitis or early morning stiffness that is generally in knees wrists and hands.