Incision-less frontalis suspension.
Explore the source record for details and available documents.
Blepharoplasty↗
Biomedical subjects
T L Cook
Publications and source records attributed to T L Cook.
Gene activation during early stages of lens induction in Xenopus.
Several stages in the lens determination process have been defined, though it is not known which gene products control these events. At mid-gastrula stages in Xenopus, ectoderm is transiently competent to respond to lens-inducing signals. Between late gastrula and neural tube stages, the presumptive lens ectoderm acquires a lens-forming bias, becomes specified to form lens and begins differentiation. Several genes have been identified, either by expression pattern, mutant phenotype or involvement in crystallin gene regulation, that may play a role in lens bias and specification, and we focus on these roles here. Fate mapping shows that the transcriptional regulators Otx-2, Pax-6 and Sox-3 are expressed in the presumptive lens ectoderm prior to lens differentiation. Otx-2 appears first, followed by Pax-6, during the stages of lens bias (late neural plate stages); expression of Sox-3 follows neural tube closure and lens specification. We also demonstrate the expression of these genes in competent ectoderm transplanted to the lens-forming region. Expression of these genes is maintained or activated preferentially in ectoderm in response to the anterior head environment. Finally, we examined activation of these genes in response to early and late lens-inducing signals. Activation of Otx-2, Pax-6 and Sox-3 in competent ectoderm occurs in response to the early inducing tissue, the anterior neural plate. Since Sox-3 is activated following neural tube closure, we tested its dependence on the later inducing tissue, the optic vesicle, which contacts lens ectoderm at this stage. Sox-3 is not expressed in lens ectoderm, nor does a lens form, when the optic vesicle anlage is removed at late neural plate stages. Expression of these genes demarcates patterning events preceding differentiation and is tightly coupled to particular phases of lens induction.
Animals↗
Anteroposterior neural tissue specification by activin-induced mesoderm.
The transforming growth factor beta superfamily member, activin, is able to induce mesodermal tissues in animal cap explants from Xenopus laevis blastula stage embryos. Activin can act like a morphogen of the dorsoventral axis in that lower doses induce more ventral, and higher doses more dorsal, tissue types. Activin has also previously been reported to induce neural tissues in animal caps. From cell mixing experiments it was inferred that this might be an indirect effect of induced mesoderm signaling to uninduced ectoderm. Here we demonstrate directly that neural tissues do indeed arise by the action of induced mesoderm on uninduced ectoderm. Dorsal mesoderm is itself subdivided into posterior and anterior domains in vivo, but this had not been demonstrated for induced mesoderm. We therefore tested whether different concentrations of activin recreate these different anteroposterior properties as well. We show that the anteroposterior positional value of induced mesoderm, including its neuroinductive properties, depends on the dose of activin applied to the mesoderm, with lower doses inducing more posterior and higher doses giving more anterior markers. We discuss the implications of these results for patterning signals and the relationship between anteroposterior and dorsoventral axes.
Activins↗
Defining intermediate stages in cell determination: acquisition of a lens-forming bias in head ectoderm during lens determination.
Cell determination in vertebrates requires integration of many events, although the mechanisms controlling the different stages in this process are poorly understood. While studies of lens determination have helped define some of these stages, we know very little about the intermediate steps involved in the commitment of ectoderm to lens formation. Lens determination begins during gastrulation when ectoderm is briefly competent to respond to lens-inducing signals and progresses to a point, at the neural tube stage, when the presumptive lens ectoderm is specified. Between these two stages important regulatory genes are activated in the presumptive lens ectoderm, including the transcription factor Pax-6, and transplantation experiments presented here suggest that the presumptive lens ectoderm is becoming "biased" toward lens formation. We show that competent ectoderm from Xenopus laevis embryos forms well-differentiated lenses in most cases when transplanted to the presumptive lens area of neural plate stage hosts, where the lens-inductive environment is strong. When placed into later, neural tube stage hosts, optimally competent ectoderm does form small lenses in about half the cases, but the overall response is much weaker. Even in this weakly inducing environment, however, lens ectoderm that is part way through the inductive process (at the neural plate stage) is shown to have a lens-forming bias, since it forms well differentiated lenses in nearly all cases. While we find that ectoderm surrounding the lens-forming area at neural plate stages does not have a lens-forming bias, non-lens head ectoderm at the neural tube stage does, suggesting that a large region of head ectoderm is biased during neurulation. Using Rana palustris embryos, a species used in the earliest lens induction studies, we were also able to show that the optic vesicle can induce lenses in non-lens head ectoderm at neural tube stages. These results lead us to refine the definition of lens cell determination and provide a context that should allow clarification of determination mechanisms.
Animals↗
Iatrogenic creation of a monoamniotic twin gestation in severe twin-twin transfusion syndrome.
Explore the source record for details and available documents.
Adult↗
Lens induction in axolotls: comparison with inductive signaling mechanisms in Xenopus laevis.
Amphibian lens induction is an embryonic process whose broad outlines are conserved between anurans and urodeles; however, it has been argued that some aspects of this process differ significantly between even closely related species. Classical embryologists concluded that in some species direct contact between the optic vesicle and ectoderm was both necessary and sufficient to induce the ectoderm to form a lens, while in other species tissues other than the optic vesicle induce lens formation. Recent studies of lens induction in Xenopus have argued that lens induction may be more conserved evolutionarily than was previously thought and that the different conclusions reached in the classical literature may be due more to experimental methodology than to actual differences in the process of lens induction. We have tested this hypothesis by examining the timing of lens induction in the axolotl and the ability of various tissues to induce lenses in explant cultures. We find that, despite the evolutionary divergence between Xenopus and Ambystoma, the mechanism of lens specification is substantially similar in the two species. These results support the hypothesis that the mechanism of lens induction is evolutionarily conserved among amphibians.
Ambystoma↗
Timing of coincidence anticipation by NCAA division I softball athletes.
After visual screening, 44 NCAA Division I softball athletes qualified to participate in this study conducted at the 1993 National Invitational Championship Tournament to assess anticipation of coincidence of these athletes. A full-swing batting motion was used to intercept a stimulus apparently moving at 45 or 70 mph, using the Bassin Anticipation Timer. Scores were recorded as early or late after each subject swung a standardized bat which interrupted a photoelectric beam when each of 20 randomly administered slow or fast simulated pitches was presented. Analyses of variance of AE, CE, and VE showed athletes swung significantly early on the 45-mph and late on the 70-mph simulated pitch speed. More specifically, less AE and CE error was recorded at the slow speed; athletes were more consistent (VE) in response to the fast speed. Results supported prior findings in which simulated-pitch speeds were similar to the present ones. Runway length, simulated-pitch speed, and the degree of swing simulation were suggested as variables to consider in similar investigations.
Acceleration↗
Behavioral effects of trace and subanesthetic halothane and nitrous oxide in man.
Using tests of complex reaction time and of immediate recall (digit span), the authors could not demonstrate that trace concentrations of halothane (to 0.02 per cent, or 200 parts per million) or halothane plus nitrous oxide (0.002 per cent plus 0.05 per cent, respectively) or nitrous oxide alone (0.4 per cent) affected mental function of male volunteers. However, subanesthetic concentrations of both nitrous oxide (20 to 30 per cent) and halothane (0.2 per cent) did impair mental function.
Adult↗
Tension pneumothorax following internal jugular cannulation and general anesthesia.
Explore the source record for details and available documents.
Anesthesia, General↗
[Renal effects and metabolism of sevoflurane in Fisher 3444 rats: an in-vivo and in-vitro comparison with methoxyflurane].
Sevoflurane, 1.4 per cent (MAC), was administered to groups of Fischer 344 rats for 10 hours, 4 hours, or 1 hour; additional rats received 0.5 per cent methoxyflurane for 3 hours or 1 hour. Urinary inorganic fluoride excretion of sevoflurane in vivo was a third to a fourth that of methoxyflurane. However, using hepatic microsomes, sevoflurane and methoxyflurane were defluorinated in vitro at essentially the same rate. The discrepancy between defluorination of sevoflurane and methoxyflurane in vivo and in vitro was probably due to differences in tissue solubility between the drugs. There were no renal functional or morphologic defects following sevoflurane administration. An unexplained adverse effect was significant weight loss, which occurred following all exposures to sevoflurane.
Anesthesia, Inhalation↗
A comparison of renal effects and metabolism of sevoflurane and methoxyflurane in enzyme-induced rats.
Twenty-five 5-month-old male Fischer-344 rats were randomly divided into 5 groups: Group I, no anesthesia; Group II, 1.4 precent sevoflurane for 2 hours; Group III, 0.1 percent phenobarbital, ad lib, in drinking water for 7 days; followed by 1.4 percent sevoflurane for 2 hours; Group IV, 0.25 percent methoxyflurane, 1 hour; Group V, phenobarbital in water as in Group III, followed by methoxyflurane as in group IV. Pre- and postanesthetic serum and urinary osmolality, Na+, K+, urea nitrogen (BUN), inorganic fluoride (F-) levels, and 24-hour urine volume were measured. Kidney tissue was obtained for examination by light and electron microscopy. Sevoflurane was metabolized to F- to a lesser extent than was methoxyflurane; treatment with phenobarbital-sevoflurane doubled urinary F- excretion, resulting in a value similar to that seen after methoxyflurane alone. There was no functional or morphologic evidence of renal abnormalities in either group of rats anesthetized with sevoflurane. Methoxyflurane dosage was sufficiently low that renal abnormalities did not occur except in rats treated also with phenobarbital; these animals developed polyuria and the morphologic lesion typically associated with F--induced nephrotoxicity.
Anesthetics↗
Thermoregulatory defect in rats during anesthesia.
Male rats of the Fischer 344, Sprague-Dawley, Brattleboro, and Wistar strains, balb/C mice, and Hartley guinea pigs were divided into 2 treatment groups. One group drank tap water while the other group drank water containing 1 mg/ml of phenobarbital. Animals were exposed to sevoflurane, enflurane, methoxyflurane, isoflurane, or halothane in a closed chamber. In some of the experiments, soda lime was included and in other the chamber was heated to 39 degrees C with a water blanket. Eighty-six percent (43/50) of Fischer 344 rats treated with phenobarbital and esposed to either sevoflurane or enflurane, in the presence of either soda lime or exogenous heat, died within a few hours after exposure. Fischer 344 rats and rats of other strains drinking phenobarbital water and exposed to methoxyflurane were affected, but to a lesser degree. Rats drinking ordinary tap water and phenobarbital-treated rats not exposed to either soda lime or exogenous heat were unaffected. Guinea pigs and mice also were unaffected. We postulate that the toxic response represents a species-specific thermoregulatory defect, precipitated by heat and occurring in rats treated with phenobarbital in combination with sevoflurane, endlurane, or methoxyflurane.
Anesthesia, General↗
Is your vaporizer off?
We found that both variable bypass (Tec-type) and measured flow (Kettle type) vaporizers that nominally are turned off may permit anesthetic to leak into the bypass or the diluent stream. The contamination ranges from 1 to 3,300 parts per million of halothane (0.0001 to 0.33 percent). It appears to result either from diffusion of agent from the liquid reservoir into the bypass or diluent stream or from a reservoir in the piping connecting vaporizer to the diluent stream.
Anesthesia, Inhalation↗
Effect of subanesthetic concentration of enflurane and halothane on human behavior.
Ten male volunteers performed 3 tasks before, during, and following administration of 3 levels of alveolar halothane (0.05, 0.1, and 0.2%) for one-half hour each and (on a separate occasion) enflurane (0.15, 0.3, and 0.4%) for one-half hour each. The concentrations of halothane tested representing 7, 13, and 27% of MAC values, respectively; those of enflurane were 9, 18, and 24% of MAC. The tasks were a choice-reaction time test, a digit span test, and a Purdue Pegboard Assembly test. Volunteers also were tested for amnesia with word pairs and a picture. No effects or only slight effects on mental function could be detected at the lowest concentrations of either agent. At higher concentrations both agents impaired function, as indicated by an increase in reaction time, decreased ability to remember numbers, and decreased ability to assemble a simple structural array. Amnesia for word pairs but not pictures occurred at 27% of MAC for halothane and 18% of MAC for enflurane. All test scores reverted to control levels within one-half hour after discontinuing the anesthetic. Our results indicate that subanesthetic but not trace levels of enflurane or halothane can impair mental performance and manual dexterity and produce amnesia. The levels of anesthetic required far exceed those experienced by operating room personnel. However, such levels might be found for several hours in patients following prolonged anesthesia.
Adult↗