Perception of transitional care quality associated with functional outcomes among patients with fractures and stroke in Taiwan.

This study aimed to examine the relationship between self-perceived quality of transitional care and functional outcome among patients with stroke and fractures. The Care Transition Measure (CTM-15) was used to survey patient's self-perceived transitional care quality before discharge. General estimating equations were used to investigate the influences of transitional care quality on patient's functional outcomes at before, 1 week after, and 1 or 3 months after discharge. Among stroke patients, higher CTM-15 scores were positively associated with greater outcome in Instrumental Activities of Daily Living (IADL) following discharge. Higher scores for "reader-friendly written care plan," "consideration of patient's preferences," and "understanding of health management" had significantly positive effects on functional recovery in IADL among both patient groups following discharge. These findings suggest that heterogeneity in transitional care needs between medical and surgical patients shall not be overlooked. A one-size-fits-all strategy may be insufficient for ensuring patient care continuity following discharge.

Myotonia congenita mutation enhances the degradation of human CLC-1 chloride channels.

Myotonia congenita is a hereditary muscle disorder caused by mutations in the human voltage-gated chloride (Cl(-)) channel CLC-1. Myotonia congenita can be inherited in an autosomal recessive (Becker type) or dominant (Thomsen type) fashion. One hypothesis for myotonia congenita is that the inheritance pattern of the disease is determined by the functional consequence of the mutation on the gating of CLC-1 channels. Several disease-related mutations, however, have been shown to yield functional CLC-1 channels with no detectable gating defects. In this study, we have functionally and biochemically characterized a myotonia mutant: A531V. Despite a gating property similar to that of wild-type (WT) channels, the mutant CLC-1 channel displayed a diminished whole-cell current density and a reduction in the total protein expression level. Our biochemical analyses further demonstrated that the reduced expression of A531V can be largely attributed to an enhanced proteasomal degradation as well as a defect in protein trafficking to surface membranes. Moreover, the A531V mutant protein also appeared to be associated with excessive endosomal-lysosomal degradation. Neither the reduced protein expression nor the diminished current density was rescued by incubating A531V-expressing cells at 27°C. These results demonstrate that the molecular pathophysiology of A531V does not involve anomalous channel gating, but rather a disruption of the balance between the synthesis and degradation of the CLC-1 channel protein.