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A randomized clinical trial and meta-analysis of early surgery vs. initial conservative treatment in patients with spontaneous lobar intracerebral hemorrhage.

miR-513a-5p and mRNA transcribed from the susceptibility allele (A allele) of rs4148941 was enhanced in vitro compared with transcripts from other alleles. Additionally, expression of CHST3 mRNA was significantly reduced in the intervertebral disc cells of human subjects carrying the A allele of rs4148941. In theory, it makes sense that CHST3 should be implicated in the pathogenesis of LDD. CHST3 is known to play a key role in proper hydration and function of cartilaginous tissues. The proteoglycan aggrecan is concentrated in disc matrix and chondroitin sulphate glycosaminoglycan side chains are abundant. Appropriate sulfation of glycosaminoglycan side chains is important for water retention to maintain proper osmotic pressure to resist compressive forces within the nucleous pulposus. It seems to follow that activity of CHST3, an enzyme that catalyzes proteoglycan sulfation, would be important for intervertebral disc function, and that mutations of the gene could result in accelerated disc degeneration. Overall, their data suggest an interplay between genetic risk factors and miRNA, and provide new insights into the etiology of LDD. While these results are fascinating, their translation into clinical practice is limited at this time. But, in an effort to one day modify the risk factors of developing LDD, we must first come a long way in understanding the etiology behind the disease. In that sense, the work of Song et al brings us one step closer to that goal, opening up new targets for therapeutic intervention in the future.