Urological manifestations of obstructive sleep apnoea and their clinical utility in screening.

BACKGROUND: The cardiovascular outcomes of obstructive sleep apnoea (OSA) are well understood. The effects of OSA on the urological system are emerging and they have the potential to impact quality of life and patient outcomes. OBJECTIVE: This article aims to strengthen the connection between OSA and urological complaints, summarise their response to CPAP treatment and discuss their clinical utility in OSA. DISCUSSION: Common urological complaints associated with OSA are nocturnal polyuria, overactive bladder symptoms and erectile dysfunction. Urinary symptoms are thought to be related to recurrent hypoxic episodes and have a significant impact on quality of life. Multiple studies report that urological symptoms and quality of life improve with CPAP treatment. However, current OSA screening questionnaires rely heavily on cardiorespiratory symptoms and specific risk factors that are not present in all OSA population subgroups. We review data that support clinicians incorporating urological symptoms when screening for OSA.

An inhibitor of chondroitin sulfate proteoglycan synthesis promotes central nervous system remyelination.

Remyelination is the generation of new myelin sheaths after injury facilitated by processes of differentiating oligodendrocyte precursor cells (OPCs). Although this repair phenomenon occurs in lesions of multiple sclerosis patients, many lesions fail to completely remyelinate. A number of factors have been identified that contribute to remyelination failure, including the upregulated chondroitin sulfate proteoglycans (CSPGs) that comprise part of the astrogliotic scar. We show that in vitro, OPCs have dramatically reduced process outgrowth in the presence of CSPGs, and a medication library that includes a number of recently reported OPC differentiation drugs failed to rescue this inhibitory phenotype on CSPGs. We introduce a novel CSPG synthesis inhibitor to reduce CSPG content and find rescued process outgrowth from OPCs in vitro and accelerated remyelination following focal demyelination in mice. Preventing CSPG deposition into the lesion microenvironment may be a useful strategy to promote repair in multiple sclerosis and other neurological disorders.