Response of intraocular pressure to retrobulbar and peribulbar anesthesia

BACKGROUND AND OBJECTIVE: To evaluate the response of intraocular pressure (IOP) to retrobulbar and peribulbar anesthesia. PATIENTS AND METHODS: Patients were prospectively masked and randomized to receive either 4 cc of retrobulbar anesthesia (X = 29) or 6 cc of peribulbar anesthesia (X = 30), each consisting of a 50:50 mixture of 2% xylocaine and 0.75% bupivacaine with 150 units of hyaluronidase. IOPs were measured pre-anesthesia and 1, 2, and 5 minutes post-anesthesia in nonglaucoma patients undergoing cataract extraction and intraocular lens implantation. RESULTS: Mean IOPs in the retrobulbar group as determined with a tonometer were 18.24, 18.66, 19.14, and 17.86 mm Hg pre-anesthesia and 1, 2, and 5 minutes post-anesthesia, respectively. In the peribulbar group, the mean IOPs were 18.53, 21.20, 20.40, and 19.20 mm Hg, respectively. The 1-minute pressures in the two groups were statistically different (P = .023). Within the peribulbar group, the 1- and 2-minute pressures were statistically different from the pre-anesthesia IOP (P = .001 and P = .018, respectively). CONCLUSION: Peribulbar anesthesia, with its higher volume of anesthetic (6 vs 4 cc), results in a higher initial IOP. This difference was slight and short lived, and occurred in the absence of any external ocular compression. This study may have application in avoiding elevation of IOP in select patients undergoing a local procedure.     

Escherichia coli associated cellulitis in broilers: correlation with systemic infection and microscopic visceral lesions, and evaluation for skin trimming

In Alberta, cellulitis condemnations average 0.5% and are among the highest in Canada. Presently, all cellulitis-affected birds are condemned for fear of systemic infections and public health implications. In a slaughterhouse sample of 102 birds condemned with cellulitis, Escherichia coli was isolated from 83.3% of the lesions. All hearts were cultured and from 11.2% E. coli was recovered. Gross lesions of perihepatitis, infected oviducts, and arthritis were found in 11.2%, 6.7%, and 2.9% of the birds, respectively. Serotyping suggested that visceral infection occurs independent of cellulitis in at least half of the cases. There was no correlation between microscopic visceral lesions and positive bacterial cultures. Two E. coli isolates of serogroup 0157 produced no toxin and neither isolate produced CS31A, F107, or F1845 fimbriae. Cellulitis lesions ranged from 0.55 to 218.9 cm2. All lesions under 16 cm2 and 64% of lesions up to 48 cm2 were considered suitable for trimming.     

Opposing actions of CSW and RasGAP modulate the strength of Torso RTK signaling in the Drosophila terminal pathway

The NMDA receptor antagonistic effects of budipine were assessed using concentration- and patch-clamp techniques on cultured striatal, hippocampal, cortical and superior colliculus neurones. Inward current responses of striatal neurones to NMDA (200 microM) at -70 mV were antagonized by budipine in a concentration-dependent manner (50% inhibitory concentration (IC50) 59.4 +/- 10.7 microM, n = 17) with 24 times lower potency than memantine but similar potency to amantadine. In striatal neurones, budipine blocked outward currents at +70 mV with an IC50 of 827 microM, suggesting that the binding site is less deep in the channel (delta = 0.45) than for memantine. However, more detailed analysis of the fractional block by budipine 300 microM in hippocampal neurones gave a delta-value of 0.90, but revealed that 28% block is mediated at a voltage-independent site. This voltage-insensitive site was accessible in the absence of agonist. Budipine exhibited concentration-dependent open channel blocking kinetics (kappa(on) = 0.71 x 10(4) M(-1) s(-1)) whereas the fast offset rate was concentration-independent (kappa(off) = 0.63 s(-1)). Calculation of the ratio kappa(off)/kappa(on) revealed an apparent Kd value of 88.7 microM. Budipine, memantine and amantadine had similar effects against NMDA-induced currents in cultured hippocampal, cortical and superior colliculus neurones, although amantadine was somewhat more potent in cultured striatal neurones. The relevance of NMDA receptor antagonism to the anti-Parkinsonian effects of budipine remains to be established.     

Do resources bolster coping and does coping buffer stress? An organizational study with longitudinal aspect and control for negative affectivity

Psychiatric workers facing redeployment completed questionnaire measures of stressors, resources (locus of control and perceived social support), coping, well-being, and negative affectivity, at baseline (N = 109) and 1 year later (loss of 7 participants). Regression analyses of the baseline data suggested that as stressors increased, so did avoidance coping, but less so for those high in internality or perceived social support. Problem-focused coping was bolstered by internality and emotion-focused coping by perceived social support. Other regression analyses, with a longitudinal aspect, suggested that stressors had a deleterious effect on well-being. Problem- and emotion-focused coping had beneficial effects, whereas avoidance coping had a (delayed) deleterious effect. These effects of coping were predominantly main and not buffering effects.     

Identification of residues in the cysteine-rich domain of Raf-1 that control Ras binding and Raf-1 activity

We have identified mutations in Raf-1 that increase binding to Ras. The mutations were identified making use of three mutant forms of Ras that have reduced Raf-1 binding (Winkler, D. G., Johnson, J. C., Cooper, J. A., and Vojtek, A. B. (1997) J. Biol. Chem. 272, 24402-24409). One mutation in Raf-1, N64L, suppresses the Ras mutant R41Q but not other Ras mutants, suggesting that this mutation structurally complements the Ras R41Q mutation. Missense substitutions of residues 143 and 144 in the Raf-1 cysteine-rich domain were isolated multiple times. These Raf-1 mutants, R143Q, R143W, and K144E, were general suppressors of three different Ras mutants and had increased interaction with non-mutant Ras. Each was slightly activated relative to wild-type Raf-1 in a transformation assay. In addition, two mutants, R143W and K144E, were active when tested for induction of germinal vesicle breakdown in Xenopus oocytes. Interestingly, all three cysteine-rich domain mutations reduced the ability of the Raf-1 N-terminal regulatory region to inhibit Xenopus oocyte germinal vesicle breakdown induced by the C-terminal catalytic region of Raf-1. We propose that a direct or indirect regulatory interaction between the N- and C-terminal regions of Raf-1 is reduced by the R143W, R143Q, and K144E mutations, thereby increasing access to the Ras-binding regions of Raf-1 and increasing Raf-1 activity.     

Differential regulation by estrogens of growth and prolactin synthesis in pituitary cells suggests that only a small pool of estrogen receptors is required for growth

PR1 cells are a prolactin (PRL)-secreting cell line derived from a pituitary lactotroph tumor found in 17beta-estradiol-treated Fischer 344 rats. We examined the effect of estrogen on cell proliferation and PRL synthesis under various culture conditions. Estrogen, at extremely low concentrations, induces cell proliferation in this cell line, whereas antiestrogen inhibits proliferation. Interestingly, the proliferation response is much more sensitive than the PRL response because 0.01 pM estradiol or diethylstilbestrol induces half-maximal growth induction [ approximately 0.1% estrogen receptor (ER) occupancy is required], whereas 0.01 nM concentration is required for half-maximal PRL induction ( approximately 50% ER occupancy is required). The proliferation response is not as sensitive to antiestrogen as the PRL response, because 10 nM concentration of the pure antiestrogen ICI 182,780 could not inhibit 1 nM estradiol- or diethylstilbestrol-induced proliferation. The same concentration of ICI 182,780 decreased PRL secretion to 1% of estradiol- or diethylstilbestrol-induced prolactin secretion suggesting a possible dichotomy of ER control of proliferation and PRL synthesis. The Kd of ER binding in these cells is about 3 x 10(-11) M. These results with the PR1 cells extend previous studies in other estrogen- regulated systems and suggest that only a small pool of ER is required for cell proliferation in contrast with the regulation of expression of specific genes. They also raise questions as to how a dimeric receptor functions when only one ligand site is occupied or when both an estrogen and an antiestrogen occupy one dimer.     

On the design of feedback control for relative stability

A basic theorem on relative stability is generalized and carefully interpreted. Two new theorems are then presented which simplify the calculation of feedback gains to achieve a prescribed damping ratio.