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Biomedical subjects

B Becker

Publications and source records attributed to B Becker.

At least 145 records · Page 8Linked to original sources

Microtubular reaction in human fibroblasts infected by cytomegalovirus. Brief report.

By the use of indirect immunofluorescence it is shown that "early" functions of human cytomegalovirus induce a loss of microtubuli in human foreskin fibroblasts within 12 hours postinfection (p.i.) which persists until about 60 hours p.i. At later times p.i. microtubular structures are eventually reestablished. Following depression during the initial 48 hours p.i. tubulin synthesis in infected cells is significantly enhanced during the initial 48 hours p.i. tubulin synthesis in infected cells is significantly enhanced during the late phase of the infectious cycle suggesting that the mechanisms regulating tubulin synthesis are not impaired.

Cytomegalovirus↗

Long-term results of valve implants in filtering surgery for eyes with neovascular glaucoma.

Filtration surgery was performed with a pressure-sensitive, unidirectional valve implant in 79 eyes with neovascular glaucoma. The device consisted of an open Supramid tube (outside diameter 0.58 mm) sealed to a Silastic tube with a slit valve. The Supramid tube was inserted at the corneoscleral limbus 1 to 4 mm into the anterior chamber. The Silastic portion was located under a scleral flap. Of the 79 eyes, 53 had postoperative intraocular pressures less than or equal to 24 mm Hg after a mean follow-up period of 23.7 +/- 10.9 months. Bleb revision for external scarring was required in ten of these 53 eyes and postoperative medical therapy was required in 26. The valve implant failed to control intraocular pressure in 26 of the 79 eyes. Failure was secondary to scarring of the external bleb in 18 eyes and to closure of the internal Supramid tube in five eyes. Mortality during the follow-up period was high: 12 of the 53 successfully treated patients and five of the unsuccessfully treated patients died.

Adolescent↗

Lack of correlation between ocular hypertensive response to topical corticosteroids and progression of retinopathy in insulin-dependent diabetes mellitus.

We studied the relationship of intraocular pressure responsiveness to topical corticosteroids and the development of retinopathy in 86 patients with insulin-dependent juvenile-onset diabetes available for long-term follow-up and examination during 1982. Eleven patients had background retinopathy at the initial examinations. High (GG) and intermediate (NG) corticosteroid responsiveness was more common in these 86 patients (13 high responders and 39 intermediate responders) than in previously reported volunteer series. Background diabetic retinopathy was present at the end of the study in 75 of the 86 patients and proliferative retinopathy was present in 29. The proportions of patients developing either type of retinopathy were similar among the low (NN), intermediate, and high response groups. The rate of diabetic retinopathy development was related to the duration of the disease and not to the intraocular pressure response to topical corticosteroids.

Administration, Topical↗

Influence of beta-receptor-agonists and glucocorticoids on alpha- and beta-adrenoceptors of isolated blood cells from asthmatic children.

The most attractive "adrenergic theory" has proposed that in asthmatic patients the bronchial hyperreactivity might be caused by a decreased beta-receptor and an increased alpha-receptor responsiveness. Based upon the assumption that an abnormality of adrenergic receptors might be a general phenomenon, we have performed receptor-binding studies on lymphocytes and thrombocytes from asthmatic children who had and had not undergone treatment with beta-receptor agonists and/or glucocorticoids. Iodo-cyano-pindolol and tritium-labeled yohimbine were used as beta- and alpha-receptor ligands. The following results have been obtained: 1) The number and affinity of alpha- and beta-adrenoceptors on thrombocytes and lymphocytes showed no significant differences in asthmatic children and their age-matched controls. 2) In vivo treatment of asthmatic children with beta-receptor agonists immediately reduced the number of beta-receptors ("down regulation"). A reversal of the number of beta-receptors occurred within 1 day after cessation of the therapy. Although it appeared that some asthmatics with severe asthma have a reduced number of beta-receptors, in vivo treatment with beta-receptor agonists thus might mimic a beta-receptor blockade. 3) High-dose treatment with glucocorticoids increased the number of beta-receptors but left the alpha-receptors unaffected.

Adolescent↗

Pharmacokinetics of dexamethasone in children.

A pharmacokinetic data analysis of plasma level data for dexamethasone obtained from children with various diseases and healthy adults was performed. A total of 33 subjects participated in the study. The results show: The pharmacokinetics of dexamethasone can be described satisfactorily within the frame of classic linear pharmacokinetic theory. The variance of important pharmacokinetic parameters is large. Therefore, if a close relationship between drug levels and therapeutic and adverse effects exists, which still has to be proved, optimal individual dosage regimens have to be calculated, guided by drug-level monitoring. When treating newborns, one should be aware that high drug levels are likely to occur, possibly necessitating a dose reduction.

Adolescent↗

Fluorometric studies on the blood-retinal barrier in experimental animals.

Fluorophotometry was used to evaluate the blood-ocular barrier in rats following streptozocin-induced diabetes, experimental systemic hypertension, sodium iodate treatment, diet-induced galactosemia, and aldose reductase inhibitors. After administration of intravenous (IV) fluorescein sodium, diabetes, hypertension, or sodium iodate treatment resulted in an increased vitreous accumulation of IV fluorescein. Accumulation of dextran-labeled fluorescein (3,000 and 19,000 molecular weight [mol wt]) was not increased in diabetic or sodium iodate-treated animals. However, 3,000-mol wt dextran-labeled dye accumulated in the vitreous of hypertensive rats. The disappearance of fluorescein injected into the vitreous was significantly delayed in diabetic and sodium iodate-treated rats, whereas this rate was normal in hypertension animals. Galactosemia did not alter vitreous fluorophotometric measurements. Pretreatment for systemic effects with aldose reductase inhibitors did not correct the vitreous fluorophotometric measurements of diabetic rats.

Aldehyde Reductase↗

Timolol and epinephrine: long-term evaluation of concurrent administration.

Thirty-two ocular hypertensive subjects were treated for 90 days with either 0.5% timolol maleate or 2% epinephrine hydrochloride twice daily to one eye and both drugs to the fellow eye. The ocular hypotensive effects of timolol and epinephrine were partially additive throughout the course of this study. On the 91st day, eyes treated with epinephrine had a 25.8% mean reduction of intraocular pressure from baseline, whereas their fellow eyes treated with epinephrine and timolol had a 33.9% reduction. Eyes treated with timolol had a 27.2% mean reduction of IOP, whereas fellow eyes treated with timolol and epinephrine had a 29% reduction. These results suggest that the majority of patients being treated with either drug are unlikely to have a substantial long-term reduction in IOP when the other drug is added to their therapeutic regimen.

Administration, Topical↗

Timolol and acetazolamide. A study of concurrent administration.

A five-week clinical trial of the concurrent administration of topical timolol maleate and oral acetazolamide was conducted to determine the additivity of the ocular hypotensive effects of the two drugs. One drop of 0.5% timolol maleate, every 12 hours, produced a mean reduction in outflow pressure from baseline of 36.0%. When added to an eye pretreated with oral acetazolamide, timolol caused an additional mean decrease in outflow pressure of 27.6%. Acetazolamide, 500 mg orally every 12 hours, produced a mean reduction in outflow pressure from baseline of 48.6%. When added to an eye receiving topical timolol, oral acetazolamide caused an additional mean decrease in outflow pressure of 43.2%. Concurrent administration of oral acetazolamide and topical timolol reduced outflow pressure only slightly less than the predicted reduction assuming full additivity of the drugs. This study supported the clinical usefulness of concurrent administration of acetazolamide and timolol to lower intraocular pressure.

Acetazolamide↗

Q-T prolongation and polymorphous ("torsade de pointes") ventricular arrhythmias associated with organophosphorus insecticide poisoning.

It is not generally appreciated in the Western world that organophosphorus poisoning may be associated with a serious and often fatal cardiac complication: Q-T interval prolongation with malignant ventricular arrhythmias of the "torsade de pointes" type. This insidious complication may lead to delayed, sudden death after the patients appears to be well on the way to recovery from the other, more dramatic respiratory and neurologic symptoms. In this study 15 patients with organophosphorus poisoning are described. Q-T prolongation was observed in 14 and malignant tachyarrhythmias in 6. In view of the dismal prognosis of these patients, ventricular pacing, previously used with success in other conditions associated with this syndrome, was tried in four patients and successfully shortened the Q-T interval and eliminated the arrhythmias. Isoproterenol did the same in a fifth patient. Awareness of this lethal, but preventable complication of organophosphorus poisoning is called for. Careful electrocardiographic monitoring is necessary until the Q-T interval returns to normal. Electrical pacing appears to be the treatment of choice for the tachyarrhythmias.

Adolescent↗

Central corneal endothelial cell density and central corneal thickness in ocular hypertension and primary open-angle glaucoma.

In order to assess the effect of increased intraocular pressure on the corneal endothelium, we classified 254 patients into four groups: Group 1, those with normal intraocular pressures; Group 2, those with untreated ocular hypertension; Group 3, those with treated ocular hypertension; and Group 4, those with primary open-angle glaucoma. One eye of each patient underwent specular microscopy and pachymetry. The eyes in the four groups did not differ significantly as to central corneal endothelial cell density or central corneal thickness. These measurements were not related to sex, race, or intraocular pressure (P greater than .12 in all cases). Increasing age was associated with a decrease in central corneal endothelial cell density (P = .0001), but was not associated with a change in central corneal thickness (P = .22). There was no significant relationship between the use of topical ocular hypotensive medications and central corneal endothelial cell density (P = .38) or central corneal thickness (P = .07) in patients with ocular hypertension or primary open-angle glaucoma. Neither uncomplicated peripheral iridectomy nor trabeculectomy produced significant changes when preoperative measurements were compared to measurements made 12 weeks postoperatively (P greater than .30 in all cases). Two eyes with flat anterior chambers following trabeculectomy had substantial decreases in central corneal endothelial cell density.

Adult↗

The onset and evolution of glaucomatous visual field defects.

Long-term follow-up was recorded on the visual fields of 251 patients with chronic open-angle glaucoma and 826 patients with ocular hypertension. Observation periods exceeded ten years for 73 patients with manifest glaucoma. Initial glaucomatous defects appeared in 98 eyes of 72 patients while under continuous observation. Initial defects were characteristically shallow and were located most commonly in the superior Bjerrum region adjacent to the blind spot. Three-dimensional (contiguous area) static perimetry provided superior resolution in detecting and characterizing the full extent of such shallow defects. The chronologic course of initial defects defects was marked in 22 of the 98 eyes by a phenomenon of a transiently appearing defect. Disappearance and reappearance of transient defects did not occur synchronously with short-term fluctuations in intraocular pressure. Ten-year follow-up of 63 eyes with manifest glaucomatous defects showed a high incidence (73%) of progression to dense involvement of the originally affected altitudinal hemifield. All eyes were treated continuously, but visual field loss occurred in spite of only marginally elevated levels of intraocular pressure.

Female↗