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D Gordon

Publications and source records attributed to D Gordon.

At least 55 records · Page 3Linked to original sources
PubMed2000

The use of prophylactic Stamey bladder neck suspension to prevent post-operative stress urinary incontinence in clinically continent women undergoing genitourinary prolapse repair.

The present study was undertaken to evaluate the efficacy of Stamey bladder neck suspension in preventing post-perative stress urinary incontinence in clinically continent women undergoing surgery for genitourinary prolapse. Thirty clinically continent women with severe genitourinary prolapse were found to have a positive stress test with re-positioning of the prolapse. They all had significant urethrovesical junction hypermobility. In addition to the genitourinary prolapse repair, these patients underwent a prophylactic Stamey procedure to prevent the possible development of post-operative stress urinary incontinence. The mean duration of follow-up was 8+/-4.5 months (range, 3-19 months). Seven (23.30%) patients developed overt post-operative stress urinary incontinence that was confirmed urodynamically. Eleven (36.7%) other patients denied stress incontinence; however, post-operative urodynamics demonstrated sphincteric incontinence. Post-operative complications were uncommon and minor. In conclusion, continent patients with a positive stress test demonstrated on re-positioning of the prolapse during pre-operative urodynamic evaluation are considered to be at high risk of developing post-operative stress urinary incontinence. In these patients, an additional, effective anti-incontinence procedure should be considered during surgical correction of genitourinary prolapse. The Stamey procedure, although simple and safe, does not appear to be the optimal solution to this clinical problem.

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PubMed2000

Modulation of cloned skeletal muscle sodium channels by the scorpion toxins Lqh II, Lqh III, and Lqh alphaIT.

The scorpion alpha-toxins Lqh II, Lqh III, and Lqh alphaIT from Leiurus quinquestriatus hebraeus are representatives of typical alpha-toxins, specific for either mammals (Lqh II) or insects (Lqh alphaIT), and alpha-like toxins (Lqh III) which act on both mammals and insects. For a comparative study of the effects of these toxins on mammalian sodium channels we stably expressed rat skeletal muscle sodium channel alpha subunits (microI) in HEK 293 cells and measured Na+ currents in the whole-cell patch-clamp mode. The alpha- and alpha-like toxins strongly slowed down channel inactivation with a half-maximal effect at 1.4 nM (Lqh II), 5.4 nM (Lqh III), and 0.5 nM (Lqh alphaIT). The recovery from fast inactivation was accelerated by all toxins with the potency sequence: Lqh II>Lqh alphaIT>Lqh III. The voltage dependence of inactivation and recovery from inactivation were reduced while the threshold for activation was only slightly shifted by approximately equal to 10 mV without altering the slope factors, suggesting uncoupling of the impaired inactivation from the activation. The toxins induced an increase in peak inward current, which was accounted for by an increased maximal open-channel probability. Although all three toxins induced similar modifications of the channel properties, their kinetics of association and dissociation were very different. Between -140 and -80 mV toxin association was not voltage dependent. In 100 nM toxin the association time constants were: 1.3 s (Lqh II), 20 s (Lqh III), and 3.8 s (Lqh alphaIT). At positive voltages the toxin dissociated from the channel; at +100 mV the dissociation time constants were 30, 321, and 135 ms, respectively. In contrast to the association, dissociation was voltage dependent with a similar slope of about 12 mV per e-fold change for all three toxins. The strong differences in the association and dissociation kinetics of these toxins may identify them as members of different scorpion alpha-toxin subgroups.

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PubMed2000

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