Video-Assisted Versus Conventional Tracheal Intubation in Morbidly Obese Patients

Background  We compared tracheal intubation characteristics and arterial oxygenation quality during airway management of morbidly obese patients whose trachea was intubated under video assistance with the LMA CTrach™ (SEBAC, Pantin, France) or the Airtraq™ laryngoscope (VYGON, écouen, France) with that of the conventional Macintosh laryngoscope. Methods  After standardized induction of anesthesia, 318 morbidly obese patients scheduled for elective morbid obesity surgery received tracheal intubation with the LMA CTrach™, the Airtraq™ laryngoscope, or the conventional Macintosh laryngoscope. Duration of apnea, time to tracheal intubation, and oxygenation quality during airway management were compared between the LMA CTrach™ and the laryngoscope groups. Results  Patients’ characteristics were similar in the three groups. The success rate for tracheal intubation was 100% with the LMA CTrach™ and the Airtraq™ laryngoscope. One patient of the Macintosh laryngoscope group received LMA CTrach™ intubation because of early arterial oxygen desaturation associated with unstable facemask ventilation. The duration of apnea was shorter with the LMA CTrach™ than that of the Airtraq™ laryngoscope and the Macintosh laryngoscope. The duration tracheal intubation was shorter with the Airtraq™ laryngoscope than with the Macintosh laryngoscopes and the LMA CTrach™. During airway management, arterial oxygenation was of better quality with the LMA CTrach™ and the Airtraq™ laryngoscope than that of the Macintosh laryngoscope. Conclusion  Because LMA CTrach™ promoted short apnea time and the Airtraq™ laryngoscope allowed early definitive airway, both video-assisted tracheal intubation devices prevented most serious arterial oxygenation desaturation evidenced during tracheal intubation of morbidly obese patients with the conventional Macintosh laryngoscope. Support was provided solely from department sources. LMA and PRODOL Companies promoted material support for the airways.     

Open-label, randomized comparison trial of long-term outcomes of levofloxacin versus standard antibiotic therapy in acute exacerbations of chronic obstructive pulmonary disease

BACKGROUND AND OBJECTIVE: This study investigated whether treating acute exacerbations of COPD (AE-COPD) with levofloxacin modifies the long-term outcome of COPD patients in comparison with standard antibiotic regimens. METHODS: A 6-month open-label clinical trial of AE-COPD patients compared the outcomes of treating with levofloxacin versus standard therapy (clarithromycin, cefuroxime, or amoxicillin/clavulanate) at recommended doses for 10 days. Several variables were analysed: pulse oximetry, FEV1, health-related quality of life, infection-free interval, number of exacerbations, hospitalizations due to an exacerbation and mortality. RESULTS: Of the 116 patients initially enrolled, completion or withdrawal information was available for 50 patients in the levofloxacin arm and 52 in the standard therapy arm. At the end of the study, there were no differences in mortality (17.8% vs. 22.9%, P = 0.53), number of exacerbations (33 vs. 41, P = 0.40), pulse oximetry (median 91.71% vs. 92.46%, P = 0.18), FEV1 (median 51.31% vs. 47.14%, P = 0.30), health-related quality of life (median 8.63 vs. 10.75, P = 0.94) and infection-free interval (median 112 vs. 101 days, P = 0.72), for the levofloxacin and standard therapy, respectively. However, 12 out of 33 (33.6%) exacerbations treated with levofloxacin required in-hospital management versus 27 out of 41 (65.8%) treated with standard therapy (P = 0.02). CONCLUSION: This preliminary study suggests that 10-day treatment of AE-COPD with levofloxacin is associated with a reduction in hospitalizations compared with standard antibiotics despite there being no significant benefit in other outcome variables.     

The Swiss Childhood Cancer Registry: rationale, organisation and results for the years 2001-2005

QUESTIONS UNDER STUDY: Childhood cancer is a rare but severe disease. Therefore central registration of all cases is essential for surveillance and management. This paper describes the methodology and basic results of the Swiss Childhood Cancer Registry (SCCR). METHODS: The SCCR was established in 1976, originally as a national hospital-based registry of childhood malignancies. All 9 paediatric oncology-haematology clinics in Switzerland provide baseline and follow-up information on all children diagnosed with cancer. These data are registered centrally and diagnoses are coded according to the International Classification of Childhood Cancer. RESULTS: From 2001-2005, 887 cases of childhood cancer in Swiss residents under the age of 15 years were registered in the SCCR. Of these, 281 (31.7%) were leukaemias, 223 (24.0%) were CNS tumours, and 116 (13.1%) were lymphomas. The age-standardised annual incidence per 1 Million person-years (age below 15 years; world standardisation) was 154.0 (95% CI 143.7-164.3; N = 887). The incidence was higher for boys (170.2, 155.0-185.4; N = 501) than for girls (136.9, 123.0-150.8; N = 386). CONCLUSION: The close collaboration between all paediatric oncologists-haematologists in Switzerland and a university department allowed the creation of a national population-based cancer registry with detailed clinical information. The SCCR produces cancer type specific incidence and survival estimates and allows the development of nested research projects on childhood cancer aetiology, management and outcome, both on a national and on an international level.     

Prognostic value of hyperintense vessel signals on fluid-attenuated inversion recovery sequences in acute cerebral ischemia

BACKGROUND: Fluid-attenuated inversion recovery (FLAIR) sequences may reveal hyperintense vessel signals (HVS) at the acute stage of cerebral ischemia. The aim of this study was to test the hypothesis that HVS are associated with a worse outcome. METHODS: We included 30 consecutive patients admitted within 12 h after onset of hemispheric cerebral ischemia. The outcome was assessed with the modified Rankin Scale at month 1. RESULTS: Proximal HVS were present in 9 patients and distal HVS in 16. All patients with proximal occlusions on time-of-flight sequences had distal HVS on FLAIR. Patients with poor outcome at month 1 (modified Rankin Scale 3-6) more frequently had had HVS on MRI (12/13 vs. 4/17; p< 0.001). CONCLUSION: Distal HVS found on FLAIR sequences within 12 h of acute cerebral ischemia are associated with a worse 1-month outcome.     

BH3-only proteins Bid and Bim(EL) are differentially involved in neuronal dysfunction in mouse models of Huntington's disease

Apoptosis, a cell death mechanism regulated by Bcl-2 family members, has been proposed as one of the mechanisms leading to neuronal loss in Huntington's disease (HD). Here we examined the regulation of Bcl-2 family proteins in three different mouse models of HD with exon 1 mutant huntingtin: the R6/1, the R6/1:BDNF+/-, and the Tet/HD94 in which the huntingtin transgene is controlled by the tetracycline-inducible system. Our results disclosed an increase in the levels of the BH3-only proteins Bid and Bim(EL) in the striatum of HD mouse models that was different depending on the stage of the disease. At 16 weeks of age, Bid was similarly enhanced in the striatum of R6/1 and R6/1:BDNF+/- mice, whereas Bim(EL) protein levels were enhanced only in R6/1:BDNF+/- mice. In contrast, at later stages of the disease, both genotypes displayed increased levels of Bid and Bim(EL) proteins. Furthermore, Bax, Bak, Bad, Bcl-2, and Bcl-x(L) proteins were not modified in any of the points analyzed. We next explored the potential reversibility of this phenomenon by analyzing conditional Tet/HD94 mice. Constitutive expression of the transgene resulted in increased levels of Bid and Bim(EL) proteins, and only the Bid protein returned to wild-type levels 5 months after mutant huntingtin shutdown. In conclusion, our results show that enhanced Bid protein levels represent an early mechanism linked to the continuous expression of mutant huntingtin that, together with enhanced Bim(EL), may be a reporter of the progress and severity of neuronal dysfunction.     

Contribution of hand motor circuits to counting

The finding that number processing activates a cortical network partly overlapping that recruited for hand movements has renewed interest in the relationship between number and finger representations. Further evidence about a possible link between fingers and numbers comes from developmental studies showing that finger movements play a crucial role in learning counting. However, increased activity in hand motor circuits during counting may unveil unspecific processes, such as shifting attention, reciting number names, or matching items with a number name. To address this issue, we used transcranial magnetic stimulation to measure changes in corticospinal (CS) excitability during a counting task performed silently and using either numbers or letters of the alphabet to enumerate items. We found an increased CS excitability of hand muscles during the counting task, irrespective of the use of numbers or letters, whereas it was unchanged in arm and foot muscles. Control tasks allowed us to rule out a possible influence of attention allocation or covert speech on CS excitability increase of hand muscles during counting. The present results support a specific involvement of hand motor circuits in counting because no CS changes were found in arm and foot muscles during the same task. However, the contribution of hand motor areas is not exclusively related to number processing because an increase in CS excitability was also found when letters were used to enumerate items. This finding suggests that hand motor circuits are involved whenever items have to be put in correspondence with the elements of any ordered series.     

Structural basis for the high all-trans-retinaldehyde reductase activity of the tumor marker AKR1B10

AKR1B10 is a human aldo-keto reductase (AKR) found to be elevated in several cancer types and in precancerous lesions. In vitro, AKR1B10 exhibits a much higher retinaldehyde reductase activity than any other human AKR, including AKR1B1 (aldose reductase). We here demonstrate that AKR1B10 also acts as a retinaldehyde reductase in vivo. This activity may be relevant in controlling the first step of retinoic acid synthesis. Up-regulation of AKR1B10, resulting in retinoic acid depletion, may lead to cellular proliferation. Both in vitro and in vivo activities of AKR1B10 were inhibited by tolrestat, an AKR1B1 inhibitor developed for diabetes treatment. The crystal structure of the ternary complex AKR1B10–NADP⁺–tolrestat was determined at 1.25-Å resolution. Molecular dynamics models of AKR1B10 and AKR1B1 with retinaldehyde isomers and site-directed mutagenesis show that subtle differences at the entrance of the retinoid-binding site, especially at position 125, are determinant for the all-trans-retinaldehyde specificity of AKR1B10. Substitutions in the retinaldehyde cyclohexene ring also influence the specificity. These structural features should facilitate the design of specific inhibitors, with potential use in cancer and diabetes treatments.