Conservative spine care: opportunities to improve the quality and value of care.

Low back pain (LBP) has received considerable attention from researchers and health care systems because of its substantial personal, social, work-related, and economic consequences. A narrative review was conducted summarizing data about the epidemiology, care seeking, and utilization patterns for LBP in the adult US population. Recommendations from a consensus of clinical practice guidelines were compared to findings about the current state of clinical practice for LBP.

A targeted approach to reducing overutilization: use of percutaneous coronary intervention in stable coronary artery disease.

Overutilization, defined as use of unnecessary care when alternatives may produce similar outcomes, results in higher cost without increased value. Overutilization can be understood by focusing on settings where overuse is obvious. One example is percutaneous coronary intervention (PCI) in chronic stable angina.

Analysis of SRrp86-regulated alternative splicing: control of c-Jun and IκBβ activity.

Previous work led to the hypothesis that SRrp86, a related member of the SR protein superfamily, can interact with and modulate the activity of other SR proteins. Here, we sought to test this hypothesis by examining the effect of changing SRrp86 concentrations on overall alternative splicing patterns. SpliceArrays were used to examine 9,854 splicing events in wild-type cells, cells overexpressing SRrp86, and cells treated with siRNAs to knockdown SRrp86.

Growth hormone deficiency and splicing fidelity: two serine/arginine-rich proteins, ASF/SF2 and SC35, act antagonistically.

The majority of mutations that cause isolated growth hormone deficiency type II are the result of aberrant splicing of transcripts encoding human growth hormone. Such mutations increase skipping of exon 3 and encode a 17.5-kDa protein that acts as a dominant negative to block secretion of full-length protein produced from unaffected alleles.

Splicing fidelity, enhancers, and disease.

Eukaryotic pre-mRNA splicing allows for a large, diverse proteome to be coded by a relatively small genome. Alternative splicing events are well regulated, but when mutations disrupt the splice sites or regulatory elements, disease can occur. Similarly, mutations can cause disease through aberrant transcript production.