Visual field defects after selective amygdalohippocampectomy and standard temporal lobectomy.

BACKGROUND: Selective amygdalohippocampectomy (SelAH) is increasingly performed in patients with mesial temporal lobe epilepsy and hippocampal sclerosis. To determine whether visual field defects are less pronounced after SelAH than after standard temporal lobectomy (StTL), we retrospectively analyzed postoperative quantitative visual fields after the 2 procedures. METHODS: Humphrey visual field analysis was obtained postoperatively in 18 patients who had undergone SelAH and in 33 patients who had undergone StTL. The SelAH was performed via a transcortical approach through the middle temporal gyrus and included the amygdala, 3 cm of the hippocampus, and the parahippocampal gyrus. The visual field pattern deviation was used for analysis. We considered a defect clinically significant if there were 3 contiguous coordinates affected at the 5% level or 2 at the 1% level. RESULTS: All but 2 of 18 patients who had undergone SelAH had homonymous superior quadrantic visual field defects contralateral to the side of the surgery. One patient had no defects by our criteria, and one had a mild defect that reached significance only in the ipsilateral eye. The averaged defect affected mostly coordinates close to the vertical meridian with relative sparing of points close to the horizontal meridian. All but 3 of the 33 patients who had undergone StTL had homonymous superior quadrantic visual field defects. One patient had no defects; 2 had defects that reached significance in only one eye. The averaged defect involved all points in the affected quadrant, but was also greater near the vertical meridian. Of 13 tested visual field coordinates, 4 were significantly less affected by SelAH in the ipsilateral eye and 3 in the contralateral eye. The coordinates close to the horizontal meridian were significantly spared by SelAH. CONCLUSIONS: Visual field defects are very common after SelAH but are significantly less pronounced than after StTL. In particular, the visual field close to the horizontal meridian is relatively spared in SelAH.

The GlideScope Video Laryngoscope: randomized clinical trial in 200 patients.

BACKGROUND: The GlideScope Video Laryngoscope is a new intubating device. It was designed to provide a view of the glottis without alignment of the oral, pharyngeal and tracheal axes. The aim of the study was to describe the use of the GlideScope in comparison with direct laryngoscopy for elective surgical patients requiring tracheal intubation. METHODS: Two hundred patients were randomly assigned to intubation by direct laryngoscopy using a Macintosh size 3 blade (DL, n=100) or intubation using the GlideScope (GS, n=100). Prior to intubation all patients were given a Cormack and Lehane (C&L) grade by a separate anaesthetist using a Macintosh size 3 blade. The patient was then intubated, using direct laryngoscopy or the GlideScope, by a different anaesthetist during which the larynx was inspected and given a laryngoscopy score. Time to intubate was measured. RESULTS: In the GS group, laryngoscopy grade was improved in the majority (28/41) of patients with C&L grade >1 and in all but one of patients who were grade 3 laryngoscopy (P<0.001). The overall mean time to intubate was 30 (95% CI 28-33) s in the DL group and 46 (95% CI 43-49) s in the GS group. The time to intubate for C&L grade 3 was similar in both groups, being 47 s for the DL group and 50 s for the GS group respectively. CONCLUSION: In most patients, the GlideScope provided a laryngoscopic view equal to or better than that of direct laryngoscopy, but it took an additional 16 s (average) for tracheal intubation. It has potential advantages over standard direct laryngoscopy for difficult intubations.

Glutamate injury-induced epileptogenesis in hippocampal neurons: an in vitro model of stroke-induced "epilepsy".

BACKGROUND AND PURPOSE: Stroke is the major cause of acquired epilepsy. The mechanisms of ischemia-induced epileptogenesis are not understood, but glutamate is associated with both ischemia-induced injury and epileptogenesis in several models. The objective of this study was to develop an in vitro model of epileptogenesis induced by glutamate injury in hippocampal neurons as observed during stroke. METHODS: Primary hippocampal cultures were exposed to 5 micromol/L glutamate for various durations. Whole-cell current clamp electrophysiology was used to monitor the acute effects of glutamate on neurons and chronic alterations in neuronal excitability up to 8 days after glutamate exposure. RESULTS: A single, 30-minute, 5-micromol/L glutamate exposure produced a subset of neurons that died and a larger population of injured neurons that survived. Neuronal injury was characterized by prolonged reversible membrane depolarization, loss of synaptic activity, and neuronal swelling. Surviving neurons manifested spontaneous, recurrent, epileptiform discharges in neural networks characterized by paroxysmal depolarizing shifts and high-frequency spike firing that persisted for the life of the culture. CONCLUSIONS: This study demonstrates that glutamate injury produced a permanent epileptiform phenotype expressed as spontaneous, recurrent epileptiform discharges for the life of the hippocampal neuronal culture. These results suggest a novel in vitro model of glutamate injury-induced epileptogenesis that may help elucidate some of the mechanisms that underlie stroke-induced epilepsy.

Microbial and reducing agents catalyze the rearrangement of taxanes.

5alpha, 7beta, 9alpha, 10beta, 13alpha-Pentahydroxy-4(20),11(12)-taxadiene derivative 1 was converted to two unprecedented 1(15-->11)abeo-taxanes and a taxane derivative with a C10-C11 double bond by Absidia coerula ATCC 10738a. A similar compound was obtained from treatment with zinc of a triacetoxy-4(20),11(12)-taxadiene derivative.

Biotransformation of a 4(20),11(12)-taxadiene derivative.

A 4(20),11(12)-taxadiene derivative was converted to hydroxylated derivatives by Cunninghamella elegans AS3.2033 and Cunninghamella elegans var chibaensis ATCC 20230. Both microorganisms led to C-1 hydroxylations and conversion to a C-15-hydroxylated abeo-taxane. Additional products from the two fungi differed: a C-14 oxidation and a trans-cis isomerization of the cinnamoyl for one and an unprecedented hydroxylation at C-17 for the other.

A new 7,8-euphadien-type triterpenoid from Brackenridgea nitida and Bleasdalea bleasdalei that inhibits DNA polymerase beta.

Bioassay-guided fractionation of extracts prepared from Brackenridgea nitida and Bleasdalea bleasdalei, using an assay to detect DNA polymerase beta inhibition, resulted in the isolation of the inhibitory principle, (24E)-3beta-hydroxy-7,24-euphadien-26-oic acid (1), a new euphane triterpenoid. The structure of 1 was established on the basis of HRMS and 1D and 2D NMR spectroscopic methods and was confirmed further by X-ray crystallographic analysis. Compound 1 inhibited rat DNA polymerase beta with an IC(50) value of 23 microM in the presence of bovine serum albumin (BSA) and 9.7 microM in the absence of BSA, consistent with the possibility that 1 may be of utility in vivo. This possibility was further supported by the finding that 1 potentiated the inhibitory action of the anticancer drug bleomycin in cultured P-388D(1) cells, reducing the number of viable cells by 48% when employed at a concentration of 25 microM in the presence of an otherwise nontoxic (75 nM) concentration of bleomycin. Compound 1 is the first euphane-type triterpenoid found to inhibit DNA polymerase beta.

DNA polymerase beta inhibitors from Sandoricum koetjape.

Bioassay-guided fractionation of Sandoricum koetjape using an assay sensitive to DNA polymerase beta inhibition led to the isolation of three active compounds (1-3) having IC(50) values from 20 to 36 microM. Derivatives 5-14 were prepared from compounds 1 and 2; derivatives 11, 12, and 13 showed activity against DNA polymerase beta with IC(50) values ranging from 16 to 36 microM.