High technology for low vision.
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Humans↗
Biomedical subjects
J Fishbaugh
Publications and source records attributed to J Fishbaugh.
Subconjunctival hemorrhage--something more you should know.
Subconjunctival hemorrhage is a common disorder that can occur in all subspecialty areas. An area of sudden and painless bright red blood appears, often during sleep (Berson, 1993), under the clear conjunctiva when a subconjunctival blood vessel breaks.
Conjunctival Diseases↗
Negotiating the nurse research coordinator role.
Ophthalmic nurses may be asked to be part of a research team. This article suggests ways the nurse can prepare for the research coordinator role and negotiate added compensation. Without preparation, the nurse's workload may not be adjusted to accommodate additional tasks and there may be a lack of remuneration. At worst, the nurse may fail to meet the expectations of the investigator and sponsor. Nurse research coordinators can learn new marketable skills, increase income, create opportunities for publications and speaking engagements, and widen their professional network. Sources of additional information about the research coordinator role are provided.
Humans↗
Look who's driving now--visual standards for driver licensing in the United States.
The current visual standards for driver licensing of the general population in all 50 states and the District of Columbia are described. Minimum visual acuity standards range from 20/40 (73%) to vision less than 20/200 (Washington). The majority of states (92%) offer some type of restricted license which provide an opportunity for low vision drivers to keep their independence while at the same time affording society a high level of safety in the driving system. Tips for the ophthalmic nurse are provided.
Automobile Driving↗
Nursing care of the patient with cornea graft rejection.
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Corneal Transplantation↗
Lessons on dilation.
Mydriatics cause pupil dilation by blocking the responses to the sphincter muscle of the iris from cholinergic stimulation. Cycloplegics paralyze the action of the ciliary muscles thereby prohibiting accommodation of the lens.
Humans↗
Overview and new technology in cyclodestructive procedures.
When all medical and surgical measures have failed to lower intraocular pressure (IOP) in patients with severe and uncontrolled glaucoma, ophthalmologists must turn to cyclodestructive procedures to decrease aqueous production. Several months ago, the FDA (Food and Drug Administration) came through with an approval for a new technology in cyclophotocoagulation therapy. The IRIS Medical G-Probe used in conjunction with a semiconductor diode laser may be the superior alternative to previously available cyclodestructive techniques for which ophthalmologists have been searching.
Glaucoma↗
Retina: indocyanine green (ICG) angiography.
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Fluorescein Angiography↗
Cornea: confocal microscopy.
The confocal microscope opens a whole new window in early diagnosis of ocular conditions. Previously, details at the cellular level could only be viewed with conventional microscopes in a laboratory setting. By using confocal microscopy, results can now be obtained instantaneously in the living human eye. This non-invasive high magnification technique provides real-time images of cornea morphology.
Cornea↗
Visual acuity, residual astigmatism, and graft clarity following penetrating keratoplasty for keratoconus.
In summary, these finding show us several things. First, we know that with surgery keratoconus patients can be rehabilitated to achieve excellent vision. A postoperative average visual acuity of 20/20 after an average preoperative visual acuity of 20/500 is a most positive outcome. Secondly, the average amount of postoperative astigmatism of 3.5 diopters shows that even after totally removing a corneal button and replacing it with 360 degrees of sutures we can still achieve a relatively small amount of residual astigmatism and a relatively spherical cornea. Thirdly, with the exception of one primary donor failure, a total of one hundred percent clear grafts, even after the occurrence of two graft rejection episodes, indicated an extremely high success rate of keratoplasty in keratoconus.
Astigmatism↗
Ethanol induced growth inhibition and growth adaptation in vitro. Cell cycle delay in late G1.
We have characterized the growth responses of HTC rat hepatoma sublines after exposure to clinically relevant concentrations of ethanol. These experiments demonstrate growth inhibition by ethanol, and both adaptive and non-adaptive growth responses after chronic exposure. Examination of the cell cycle compartmentation of HTC lines shows that a rapid accumulation of G0/G1 cells is induced by ethanol. Estimates of cellular G1 RNA content by flow cytometry reveal increases in mean G1 RNA and in late G1 cells in the line which growth adapts, and decreases in these parameters in a line which does not adapt to ethanol. Both the growth responses and the timing of cell cycle restriction by ethanol in the adapting line suggest parallels with the reported data for regenerating rat liver. Ethanol induced late G1 restriction appears to be of significant interest in the study of cellular mechanisms which are disturbed by ethanol in proliferating tissues.
Animals↗
Nurses endorsing transplantation.
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Humans↗
Induction of HL-60 monocytic cell differentiation promoted by a perturbation of DNA synthesis: hydroxyurea promotes action of TPA.
Control of terminal cell differentiation was studied using the human promyelocytic leukemia cell line, HL-60. HL-60 cells are known to undergo terminal monocytic differentiation when continuously exposed to 1.6 nM tetradecanoylphorbol acetate (TPA). The dose-response relationship between TPA concentration and induced differentiation is relatively steep. TPA (1.1 nM) induces little G1/0 specific growth inhibition or phenotypic differentiation. In contrast, pretreating the cells with a pulse exposure to hydroxyurea promotes their capability to terminally differentiate in response to TPA. Initially exponentially proliferating cells exposed for 20 h, approximately one doubling time, to 0.3 mM hydroxyurea, a subcytotoxic dose, underwent rapid G1/0 specific growth arrest and cell differentiation in response to subsequent exposure to 1.1 nM TPA. The extent of terminal differentiation was comparable to that induced by 1.6 nM TPA. The results support the hypothesis that early events in induction of terminal HL-60 cell differentiation depend on an S phase-specific process which may involve gene amplification.
Cell Differentiation↗
We believe--in organ transplantation.
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Corneal Transplantation↗
Control of HL-60 cell differentiation lineage specificity, a late event occurring after precommitment.
Terminal cell differentiation of HL-60 promyelocytic leukemia cells results when they are continuously exposed to retinoic acid. This process involves an intermediate regulatory state, the precommitment memory state, which occurs before onset of differentiation or growth arrest in G0. The cellular processes occurring prior to onset of terminal differentiation can be resolved into early events anteceding development of the precommitment memory state and late events subsequent to it. While it has been suggested that retinoic acid induced early events regulate G1/0 specific growth arrest associated with terminal differentiation, the significance of induced late events is not known. Exploiting the capability of HL-60 cells to undergo either myeloid or monocytic differentiation in response to different inducers, the present studies examine the response of HL-60 cells to the sequential application of myeloid and monocytic inducers prior to onset of terminal differentiation. The results indicate that the precommitment state induced by retinoic acid is not differentiation lineage specific. Sequential application first of retinoic acid, a myeloid inducer, and then of 1,25-dihydroxyvitamin D3, a monocytic inducer, and vice versa, show that cellular choice of a specific differentiation lineage is regulated by late inducer driven events. The data support a two-step model for induction of terminal differentiation where early events anteceding precommitment regulate growth arrest and late events subsequent to precommitment regulate choice of a specific differentiation lineage. The results are of potential significance to the use of differentiation-inducing agents in chemotherapy. The potential toxicity of prolonged exposure to a single inducer might thus be mitigated by sequential brief exposures to different inducers.
Calcitriol↗
Precommitment states induced during HL-60 myeloid differentiation: possible similarities of retinoic acid- and DMSO-induced early events.
The possible relationship of the pathways by which two inducers, retinoic acid and DMSO, cause myeloid differentiation of HL-60 promyelocytic leukemia cells was studied. HL-60 cells were first exposed to retinoic acid and then washed free of it. As reported previously, this brief exposure results in no subsequent G0 growth arrest or phenotypic differentiation. When these cells were subsequently exposed to DMSO, onset of G1/0 growth arrest but not phenotypic differentiation occurred within 24 h. Since in these cells retinoic acid or DMSO normally requires 48 h of continuous exposure for onset of significant G0 growth arrest and phenotypic differentiation, it appears that retinoic acid and DMSO induce similar early cellular events needed for subsequent G0 growth arrest but not for phenotypic differentiation. While onset of growth arrest and differentiation occur together when the cells are exposed for 48 h to retinoic acid, the present results indicate that their occurrence can be uncoupled by this split dosage to inducers. The results are discussed in terms of a previously hypothesized model of cellular response to the inducers.
Cell Cycle↗
Control of HL-60 monocytic differentiation. Different pathways and uncoupled expression of differentiation markers.
Control of expression of the terminally differentiated phenotype was studied using the human promyelocytic leukemia cell line HL-60. Three known inducers of HL-60 monocytic differentiation were compared: 1,25-dihydroxy vitamin D3, tetradecanoylphorbol acetate (TPA), and sodium butyrate. At concentrations where all three inducers resulted in similar courses of G1/0-specific growth arrest, the kinetics of appearance of certain differentiation markers typically characteristic of mature monocytic cells was determined. The markers were inducible oxidative metabolism, non-specific esterase activity, and the cell surface determinants Mo1, My4, and Mo2. The results indicate that: Regulation of the expression of these markers during induced monocytic differentiation is not controlled in common. The three monocytic inducers do not induce the same metabolic cascade leading to differentiation. Similar states of differentiation could thus be reached by different pathways apparently due to the fact that control of expression of different differentiation markers was not tightly coupled.
Antigens, Surface↗
Hydroxyurea indices precommitment during retinoic induced HL-60 terminal myeloid differentiation: possible involvement of gene amplification.
Control of terminal cell differentiation was studied in the HL-60 human promyeloctyic leukemia cell line. Retinoic acid is known to induce myeloid differentiation associated with GO arrest in these cells. In this case, onset of terminal differentiation occurs after an exposure period corresponding to two division cycles. This is preceded by acquisition of a precommitment memory state occurring by one division cycle. Cells in precommitment undergo accelerated onset of terminal differentiation upon reexposure to inducer. The present report shows that the precommitment state can be induced by a pulse exposure to hydroxyurea. While the hydroxyurea exposure does not itself induce terminal differentiation, the treated cells undergo accelerated onset of phenotypic differentiation and GO arrest upon exposure to retinoic acid. Thus a perturbation of S-phase specific cellular metabolism induces the early precommitment regulatory state in the course of induced HL-60 terminal myeloid differentiation. The results support a model in which initiation of a cellular program of terminal differentiation depends on an S-phase specific event associated with replication of cellular DNA and possibly involving gene amplification. Significantly, the results indicate that a conventional chemotherapeutic agent such as hydroxyurea can synergistically interact with a differentiation inducing agent such as retinoic acid. This indicates the significance of investigating the interaction between conventional S-phase specific chemotherapeutic agents and differentiation inducing agents as a potential treatment modality.
Cell Differentiation↗