Improving weekend handover between junior doctors on medical and surgical wards.

Poor weekend handover has been implicated as one of the causes of observed higher mortality rates at weekends in UK hospitals. In a large teaching hospital we, a group of junior doctors, set about improving the quality and effectiveness of weekend handover. We used the Model for Improvement to implement a weekend handover sticker through an iterative process using multiple Plan/Do/Study/Act (PDSA) cycles. Over the 16 week study period the number of completed weekend tasks increased by 30% and the number of patients with a documented weekend handover increased by nearly 50%. Junior doctors are well positioned to notice the quality and safety shortcomings within hospitals, and by using effective improvement methods they can improve these systems at little or no cost.

Actions of veratridine on tetrodotoxin-sensitive voltage-gated Na currents, Na1.6, in murine vas deferens myocytes.

BACKGROUND AND PURPOSE: The effects of veratridine, an alkaloid found in Liliaceae plants, on tetrodotoxin (TTX)-sensitive voltage-gated Na(+) channels were investigated in mouse vas deferens. EXPERIMENTAL APPROACH: Effects of veratridine on TTX-sensitive Na(+) currents (I(Na)) in vas deferens myocytes dispersed from BALB/c mice, homozygous mice with a null allele of Na(V)1.6 (Na(V)1.6(-/-)) and wild-type mice (Na(V)1.6(+/+)) were studied using patch-clamp techniques. Tension measurements were also performed to compare the effects of veratridine on phasic contractions in intact tissues. KEY RESULTS: In whole-cell configuration, veratridine had a concentration-dependent dual action on the peak amplitude of I(Na): I(Na) was enhanced by veratridine (1-10 microM), while higher concentrations (> or =30 microM) inhibited I(Na). Additionally, two membrane current components were evoked by veratridine, namely a sustained inward current during the duration of the depolarizing rectangular pulse and a tail current at the repolarization. Although veratridine caused little shift of the voltage dependence of the steady-state inactivation curve and the activation curve for I(Na), veratridine enhanced a non-inactivating component of I(Na). Veratridine caused no detectable contractions in vas deferens from Na(V)1.6(-/-) mice, although in tissues from Na(V)1.6(+/+) mice, veratridine (> or =3 microM) induced TTX-sensitive contractions. Similarly, no detectable inward currents were evoked by veratridine in Na(V)1.6(-/-) vas deferens myocytes, while veratridine elicited both the sustained and tail currents in cells taken from Na(V)1.6(+/+) mice. CONCLUSIONS AND IMPLICATIONS: These results suggest that veratridine possesses a dual action on I(Na) and that the veratridine-induced activation of contraction is induced by the activation of Na(V)1.6 channels.

Actions of kurtoxin on tetrodotoxin-sensitive voltage-gated Na+ currents, NaV1.6, in murine vas deferens myocytes.

Kurtoxin is described as a selective inhibitor of Ca(V)3.1. Using patch-clamp techniques, the modulatory effects of kurtoxin on tetrodotoxin-sensitive voltage-gated Na(+) currents (I(Na)) recorded from mouse vas deferens myocytes were investigated. Kurtoxin increased the peak amplitude of I(Na) between -40 and -30 mV, whilst inhibited the peak amplitude at more positive potentials than -10 mV, thereby demonstrating a dual action on the peak amplitude of I(Na). The time to reach the peak amplitude of I(Na) became significantly longer in the presence of kurtoxin in comparison with that of the controls. Kurtoxin also slowed the deactivation of I(Na) at more positive membrane potentials than -30 mV. Kurtoxin enhanced the total amount of electrical charge of I(Na) in a concentration-dependent manner. These results suggest that kurtoxin is a modulator of Na(V)1.6 in native freshly dispersed smooth muscle cells from mouse vas deferens as well as its action on Ca(V)3.1.

Molecular and biophysical properties of voltage-gated Na+ channels in murine vas deferens.

The biological and molecular properties of tetrodotoxin (TTX)-sensitive voltage-gated Na(+) currents (I(Na)) in murine vas deferens myocytes were investigated using patch-clamp techniques and molecular biological analyses. In whole-cell configuration, a fast, transient inward current was evoked in the presence of Cd(2+), and was abolished by TTX (K(d) = 11.2 nM), mibefradil (K(d) = 3.3 microM), and external replacement of Na(+) with monovalent cations (TEA(+), Tris(+), and NMDG(+)). The fast transient inward current was enhanced by veratridine, an activator of voltage-gated Na(+) channels, suggesting that the fast transient inward current was a TTX-sensitive I(Na). The values for half-maximal (V(half)) inactivation and activation of I(Na) were -46.3 mV and -26.0 mV, respectively. RT-PCR analysis revealed the expression of Scn1a, 2a, and 8a transcripts. The Scn8a transcript and the alpha-subunit protein of Na(V)1.6 were detected in smooth muscle layers. Using Na(V)1.6-null mice (Na(V)1.6(-/-)) lacking the expression of the Na(+) channel gene, Scn8a, I(Na) were not detected in dispersed smooth muscle cells from the vas deferens, while TTX-sensitive I(Na) were recorded in their wild-type (Na(V)1.6(+/+)) littermates. This study demonstrates that the molecular identity of the voltage-gated Na(+) channels responsible for the TTX-sensitive I(Na) in murine vas deferens myocytes is primarily Na(V)1.6.