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Articles by B. h Tan
Total Records ( 2 ) for B. h Tan
  E. H. C Liu , R. W. L Goy , B. H Tan and T. Asai
  Background

The GlideScope® (Verathon Inc., Bothell, WA, USA) and Airway Scope® (Hoya Corp., Tokyo, Japan) have both been used for difficult airway management, including in patients with cervical spine pathology. The Airway Scope®'s disposable blade has a tube channel to guide tracheal tube insertion through the glottis. Our hypothesis is that this tube guidance system improves the ease of tracheal intubation compared with the GlideScope®, which does not have a tube guiding system. We tested this hypothesis in a randomized comparison of the two videolaryngoscopes in patients whose cervical spines were immobilized.

Methods

Seventy consenting patients were randomized to have tracheal intubation with the GlideScope® (n=35) or the Airway Scope® (n=35). In all patients, we applied manual in-line stabilization of the cervical spine throughout airway management. All the airway procedures were carried out by two anaesthetists experienced in the use of both videolaryngoscopes.

Results

The tracheal intubation time was 34.2 (sd 25.1) s with the Airway Scope® compared with 71.9 (47.9) s with the GlideScope® (P<0.001). Tracheal intubation was successful with the Airway Scope® in 35 (100%) patients compared with 31 (88.6%) patients with the GlideScope® (P=0.114). Tracheal intubation was successful within 60 s in 33 (94.3%) patients with the Airway Scope® and 22 (62.9%) patients with the GlideScope® (P=0.003).

Conclusions

These results suggest that the Airway Scope®'s tube guide system enables more rapid tracheal intubation compared with the GlideScope® in patients with cervical spine immobilization.

  J Cheng , D. W Van Norstrand , A Medeiros Domingo , C Valdivia , B. h Tan , B Ye , S Kroboth , M Vatta , D. J Tester , C. T January , J. C Makielski and M. J. Ackerman
 

Background— Sudden infant death syndrome (SIDS) is a leading cause of death during the first 6 months after birth. About 5% to 10% of SIDS may stem from cardiac channelopathies such as long-QT syndrome. We recently implicated mutations in 1-syntrophin (SNTA1) as a novel cause of long-QT syndrome, whereby mutant SNTA1 released inhibition of associated neuronal nitric oxide synthase by the plasma membrane Ca-ATPase PMCA4b, causing increased peak and late sodium current (INa) via S-nitrosylation of the cardiac sodium channel. This study determined the prevalence and functional properties of SIDS-associated SNTA1 mutations.

Methods and Results— Using polymerase chain reaction, denaturing high-performance liquid chromatography, and DNA sequencing of SNTA1’s open reading frame, 6 rare (absent in 800 reference alleles) missense mutations (G54R, P56S, T262P, S287R, T372M, and G460S) were identified in 8 (3%) of 292 SIDS cases. These mutations were engineered using polymerase chain reaction–based overlap extension and were coexpressed heterologously with SCN5A, neuronal nitric oxide synthase, and PMCA4b in HEK293 cells. INa was recorded using the whole-cell method. A significant 1.4- to 1.5-fold increase in peak INa and 2.3- to 2.7-fold increase in late INa compared with controls was evident for S287R-, T372M-, and G460S-SNTA1 and was reversed by a neuronal nitric oxide synthase inhibitor. These 3 mutations also caused a significant depolarizing shift in channel inactivation, thereby increasing the overlap of the activation and inactivation curves to increase window current.

Conclusions— Abnormal biophysical phenotypes implicate mutations in SNTA1 as a novel pathogenic mechanism for the subset of channelopathic SIDS. Functional studies are essential to distinguish pathogenic perturbations in channel interacting proteins such as 1-syntrophin from similarly rare but innocuous ones.

 
 
 
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