Search

Awake fibreoptic intubation is often considered the technique of choice when a difficult airway is anticipated. However, videolaryngoscopes are being used more commonly. We searched the current literature and performed a meta-analysis to compare the use of videolaryngoscopy and fibreoptic bronchoscopy for awake tracheal intubation. Our primary outcome was the time needed to intubate the patient's trachea. Secondary outcomes included: failed intubation; the rate of successful intubation at the first attempt; patient-reported satisfaction with the technique; and any complications resulting from intubation. Eight studies examining 429 patients were included in this review. The intubation time was shorter when videolaryngoscopy was used instead of fibreoptic bronchoscopy (seven trials, 408 participants, mean difference (95%CI) -45.7 (-66.0 to -25.4) s, p < 0.0001, low-quality evidence). There was no significant difference between the two techniques in the failure rate (six studies, 355 participants, risk ratio (95%CI) 1.01 (0.24-4.35), p = 0.99, low-quality evidence) or the first-attempt success rate (six studies, 391 participants, risk ratio (95%CI) 1.01 (0.95-1.06), p = 0.8, moderate quality evidence). The level of patient satisfaction was similar between both groups. No difference was found in two reported adverse events: hoarseness/sore throat (three studies, 167 participants, risk ratio (95%CI) 1.07 (0.62-1.85), p = 0.81, low-quality evidence), and low oxygen saturation (five studies, 337 participants, risk ratio (95%CI) 0.49 (0.22-1.12), p = 0.09, low-quality evidence). In summary, videolaryngoscopy for awake tracheal intubation is associated with a shorter intubation time. It also seems to have a success rate and safety profile comparable to fibreoptic bronchoscopy. [ABSTRACT FROM AUTHOR]

Glutamate carboxypeptidase II (GCPII, EC 3.14.17.21) is a membrane-bound enzyme found on the extracellular face of glia. The gene for this enzyme is designated FOLH1 in humans and Folh1 in mice. This enzyme has been proposed to be responsible for inactivation of the neurotransmitter N-acetylaspartylglutamate (NAAG) following synaptic release. Mice harboring a disruption of the gene for GCPII/Folh1 were generated by inserting into the genome a targeting cassette in which the intron-exon boundary sequences of exons 1 and 2 were removed and stop codons were inserted in exons 1 and 2. Messenger RNA for GCPII was not detected by northern blotting or RT-PCR analysis of RNA from the brains of -/mutant mice nor was GCPII protein detected on western blots of this tissue. These GCPII null mutant mice developed normally to adulthood and exhibited a normal range of neurologic responses and behaviors including mating, open field activity and retention of position in rotorod tests. No significant differences were observed among responses of wild type, heterozygous mutant and homozygous mutant mice on tail flick and hot plate latency tests. Glutamate, NAAG and mRNA for metabotropic glutamate receptor type 3 levels were not significantly altered in response to the deletion of glutamate carboxypeptidase II. A novel membrane-bound NAAG peptidase activity was discovered in brain, spinal cord and kidney of the GCPII knock out mice. The kinetic values for brain NAAG peptidase activity in the wild type and GCPII null mutant were V[sub max] = 45 and 3 pmol/mg/min and K[sub m] = 2650 nM and 2494 nM, respectively. With the exception of magnesium and copper, this novel peptidase activity had a similar requirement for metal ions as GCPII. Two potent inhibitors of GCPII, 4,4'phosphinicobis-(butane-1,3 dicarboxilic acid) (FN6) and 2-(phosphonomethyl)pentanedioic acid (2-PMPA) inhibited the residual activity. The IC[sub 50] value for 2-PMPA was about 1 nM for wild-type brain membrane NAAG... [ABSTRACT FROM AUTHOR]

Abstract Objective Rectourethral fistula is a rare complication of prostatic surgery and other pelvic procedures. We report our experience of surgical repair of using a rectal advancement flap. Patients Three patients with rectourethral fistula following prostatic surgery were treated. Two patients had an anterior partial thickness of rectal flap advancement via a trans-anal approach without urinary or faecal diversion. In one patient a rectal flap repair was performed through a posterior transsphincteric approach following urinary and faecal diversion. Results No significant postoperative complications occured. Healing was successful in each patient and faecal and urinary continence was normal. Conclusion Transanal rectal advancement flap is a simple and effective technique for the treatment of a rectourethral fistula with no need for urinary or faecal diversion. [ABSTRACT FROM AUTHOR]

The peptide neurotransmitter, N-acetylaspartylglutamate (NAAG), is a selective agonist at the type 3 metabotropic glutamate receptor (mGluR3) where it acts to decrease cAMP levels. Rat cortical interneurons express both NAAG and glutamic acid decarboxylase, as well as mGluR3 mRNA. In the presence of ionotropic glutamate receptor antagonists, both NAAG and the group II metabotropic glutamate receptor agonist, DCG-IV, reduced the calcium-dependent, KCl-induced [(3)H]-GABA release from rat cortical neurons by 35%. This release process was unaffected by tetrodotoxin. The group II antagonist, ethyl glutamate, reversed the effects of DCG-IV and NAAG. The mGluR3-selective antagonist, beta-N-acetylaspartylglutamate, reversed the effect of NAAG. While pretreatment of cortical neurons with forskolin alone did not significantly affect KCl-stimulated [(3)H]-GABA-release, forskolin abolished the inhibition of release produced by NAAG. The protein kinase A inhibitor, H-89, decreased [(3)H]-GABA release while NAAG produced no additional inhibition in the presence of H-89. In contrast, the protein kinase C inhibitor, Ro 31--8220, had no effect on KCl-stimulated release, nor did it affect the inhibition of release produced by NAAG. The L-type calcium channel blocker, nifedipine, also inhibited the release of [(3)H]-GABA and coapplication with NAAG resulted in no significant additional inhibition of release. These data support the hypothesis that the inhibition of KCl-stimulated [(3)H]-GABA release by NAAG is mediated via presynaptic mGluR3 on GABAergic cortical neurons and that this effect is obtained by decreasing cAMP with a consequent decrease in protein kinase A activity and L-type calcium channel conductance.