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M Amyot

Publications and source records attributed to M Amyot.

17 recordsLinked to original sources
PubMed2006

Gross photoreduction kinetics of mercury in temperate freshwater lakes and rivers: application to a general model of DGM dynamics.

Previous published measurements of mercury photoreduction are for net-photoreduction, since photooxidation processes occur simultaneously. In this research we combine continuous dissolved-gaseous mercury (DGM) analysis with a photoreactor and a quartz sparger in order to derive mercury gross photoreduction rate constants for UVB and UVA irradiations. The DGM concentration in each filter-sterilized freshwater was measured at 5 min intervals over a period of 23 h. Photoreduction proceeded for the initial 200 min, after which, reducible mercury was depleted in the sample. Substantial losses in DOC fluorescence were observed during the incubations for UVA radiation but not for UVB; therefore, UVB photoreduction dynamics are not linked to a loss in DOC fluorescence. Pseudo first-order reaction kinetics fit the data well (r2 > 0.87). The rate constants appear divided between lakes and rivers with the mean lake UVB rate constant (kUVB = 8.91 x 10(-5) s(-1)), significantly less than the mean rate constant (kUVB = 1.81 x 10(-4) s(-1)) for the river samples. However, while there were differences for the UVB rates between lakes and rivers, the mean and median rate constants for UVA in lakes (kUVA = 7.76 x 10(-5) s(-1)) did not differ significantly from the mean rate constant forthe river sites (kUVA = 1.78 x 10(-4) s(-1)). Here, we propose a model for mercury photoredox dynamics for both temperate lake and river systems. The lake model was validated using principal axis analysis to compare observed and predicted DGM data (n=279) from a variety of lake sites in Nova Scotia and Central Quebec. Principal axis analysis found a linear fit (correlation = 0.81; slope = 2.13) between predicted and observed environmental DGM values when log-normalized. The constant bias on the predicted values was attributed to estimates of available reducible mercury and the effect of DGM volatilization on observed data.

Fresh Water↗
PubMed2001

Photooxidation of Hg(0) in artificial and natural waters.

The oxidation of volatile aqueous Hg(0) in aquatic systems may be important in reducing fluxes of Hg out of aquatic systems. Here we report the results of laboratory and field experiments designed to identify the parameters that control the photooxidation of Hg(0)(aq) and to assess the possible importance of this process in aquatic systems. The concentrations of elemental and total Hg were measured as a function of time in both artificial and natural waters irradiated with a UV-B lamp. No change in Hg speciation was observed in dark controls, while a significant decrease in Hg(0) was observed in UV-B irradiated artificial solutions containing both chloride ions and benzoquinone. Significant photooxidation rates were also measured in natural samples spiked with Hg(0)(aq); the photooxidation of Hg(0) then follows pseudo first-order kinetics (k = 0.6 h(-1)). These results indicate that the previously observed Hg(II) photoreduction rates in natural waters could represent a net balance between Hg(0) photoreduction and Hg(0) photooxidation. As calculated from Hg(0) photooxidation rates, the dominant Hg(0) sink is likely to be photooxidation rather than volatilization from the water column during summer days.

Air Pollutants↗
PubMed2001

Clear lens extraction with intraocular lens followed by photorefractive keratectomy or laser in situ keratomileusis.

OBJECTIVE: To study photorefractive keratectomy (PRK) or laser in situ keratomileusis (LASIK) after clear lens extraction (CLE) with intraocular lens (IOL) implantation for hyperopia or astigmatism. DESIGN: Retrospective, noncomparative interventional case series. PARTICIPANTS: Sixty-five eyes (55 subjects) had CLE with posterior chamber IOL implants for hyperopia up to 12.25 diopters (D); 31 eyes were retreated with PRK, and 34 eyes were retreated with LASIK for residual ametropias. INTERVENTION: For PRK and LASIK, the refractive surgery was performed with the slit-scanning excimer laser Nidek EC-5000, Nidek Co., Tokyo, Japan. MAIN OUTCOME MEASURES: Manifest refraction, best-spectacle and uncorrected Snellen visual acuity, haze, and halos were evaluated before surgery and at 1, 3, 6, and 12 months postoperative. RESULTS: Forty-seven eyes were evaluated at the 12-month postoperative examination: 96% of these eyes had spherical equivalents (SE) within +/-2 D of emmetropia, 79% of eyes had SE within +/-1 D of emmetropia and 51% of eyes had SE within +/-0.50 D of emmetropia. Eighty-five percent of the eyes at 12 months postoperative had uncorrected visual acuity of 20/40 or better, and 46% of eyes had uncorrected visual acuity of 20/20 or better. Eighty-seven percent of the eyes at 12 months postoperative had uncorrected visual acuity within 1 Snellen line of their initial best spectacle-corrected visual acuity (BSCVA) before all treatment. No eye lost 2 Snellen lines of BSCVA at 3, 6, or 12 months after PRK or after LASIK. CONCLUSIONS: IOL implantation for CLE, although an invasive technique, resulted in better refractive outcomes without laser-related clinical complications after PRK or LASIK adjustment.

Adult↗
PubMed2000

Dorzolamide and corneal recovery from edema in patients with glaucoma or ocular hypertension.

PURPOSE: To investigate whether dorzolamide alters corneal hydration control in patients with glaucoma or ocular hypertension. METHODS: Pachymetry, tonometry, and endothelial cell density were measured by a masked observer in 19 subjects with bilateral glaucoma or ocular hypertension. They were treated with 2% dorzolamide in one eye, and with saline in the other, before wearing contact lenses under patched eyes. Corneal thickness, measured each 30 minutes up to 4.5 hours after contact lens removal, enabled estimation of percentage recovery per hour and time for 95% of corneal thickness recovery for both eyes. Seven patients repeated this test after 1 year of dorzolamide use, and their results were compared with those of the preceding year. RESULTS: After induction of hypoxic corneal edema, there was no significant difference between paired corneas in swelling levels (60.0+/-11.8 and 59.8+/-12.9 microm) (P = .94), time to 95% recovery (440.6+/-255.8 and 445.4+/-186.7 minutes) (P = .93), and percentage recovery per hour (38.1%+/-10.9% and 36.1%+/-9.6%) (P = .40). Subjects followed up after 1 year of dorzolamide use did not differ significantly in values of endothelial cell density, percentage recovery per hour, or time to 95% recovery from those obtained a year before. One subject developed persistent corneal edema after his stress test in the eye treated with dorzolamide. CONCLUSION: There is no significant difference in the recovery from induced corneal edema after either a short-term or 1-year use of dorzolamide in patients with glaucoma or ocular hypertension with a normal corneal endothelium. One patient had persistent corneal edema after the stress test was performed on the dorzolamide-treated eye.

Aged↗
PubMed1997

Corneal endothelial cell density in glaucoma.

PURPOSE: We studied corneal endothelial cell density in patients with glaucoma. METHODS: One hundred two patients with glaucoma were compared with 52 patients without glaucoma of the same age group. Exclusion criteria included history of either corneal disease, ocular inflammation, trauma, or surgery other than peripheral iridectomy. The following data were extracted from the patient files: glaucoma type and duration, laser treatments, glaucoma medications, and documented intraocular pressure (IOP) measurements. Specular microscopies were performed on central corneas, endothelial images were analyzed by computerized planimetry, and cell counts were calculated. RESULTS: Corneal endothelial cell counts were significantly lower in patients with glaucoma (2,154 +/- 419 cells/mm2) than in controls (2,560 +/- 360 cells/mm2; t test, p < 0.0001). In the glaucoma group, cell counts were inversely proportional to the means of IOPs. Patients receiving three or four glaucoma medications had lower cell counts than those receiving one or two medications. Cell counts were significantly lower both in primary angle-closure glaucoma and in primary open-angle glaucoma. CONCLUSION: This study suggests that patients with glaucoma may have lower corneal endothelial cell density than those without glaucoma of the same age group. The proposed mechanisms are direct damage from IOP, congenital alteration of the corneal endothelium in patients with glaucoma, glaucoma medication toxicity, or a combination of these.

Aged↗
PubMed1995

Motion perception deficits in glaucomatous optic neuropathy.

The mechanisms mediating impaired motion perception in glaucoma were investigated. Direction discrimination thresholds for low (4.2 deg/sec) and high (12.5 deg/sec) velocity random-dot kinematograms were measured in controls and patients with glaucoma or ocular hypertension. Thresholds were elevated significantly in glaucoma patients and individual ocular hypertensives. Threshold elevations were not due to blur or pupil size. After compensating for motion reversals, high but not low velocity thresholds remained elevated. Only high velocity thresholds correlated with differential luminance sensitivity. A hypothesis that different mechanisms mediate glaucoma-induced deficits at high and low velocities is presented.

Adult↗
PubMed1995

A common gene for juvenile and adult-onset primary open-angle glaucomas confined on chromosome 1q.

Primary open-angle glaucoma (POAG), which causes progressive loss of the visual fields, was subdivided into two groups according to age at onset: (1) chronic open-angle glaucoma (COAG) diagnosed after age 40 years and (2) juvenile open-angle glaucoma (JOAG) diagnosed between 3 years of age and early adulthood. A JOAG gene (GLC1A) was recently mapped to chromosome 1q. We studied 142 members of a huge multigenerational French Canadian family affected with autosomal dominant POAG. Either JOAG or COAG was diagnosed in 40 patients. Six subjects were also diagnosed with ocular hypertension (OHT), which may lead to POAG. To localize a common disease gene that might be responsible for both glaucoma subsets, we performed linkage analysis considering JOAG and COAG under the same phenotypic category. JOAG/COAG was tightly linked to seven microsatellite markers on chromosome 1q23-q25; a maximum lod score of 6.62 was obtained with AF-M278ye5. To refine the disease locus, we exploited a recombination mapping strategy based on a unique founder effect. The same characteristic haplotype, composed of 14 markers spanning 12 cM between loci D1S196 and D1S212, was recognized in all persons affected by JOAG, COAG, or OHT, but it did not occur in unaffected spouses and in normal family members > 35 years of age, except for three obligatory carriers. Key recombination events confined the disease region within a 9-cM interval between loci D1S445 and D1S416/D1S480. These observations demonstrate that the GLC1A gene is responsible for both adult-onset and juvenile glaucomas and suggest that the JOAG and COAG categories within this family may be part of a clinical continuum artificially divided at age 40 years.

Adolescent↗
PubMed1979

[Timolol maleate. Pharmacology and review of the literature].

The sympathetic system is composed of alpha and beta receptors. Beta blockers block the beta effect competitively. They slow the heart and decrease its contractile strength. They block bronchodilatation and the vasodillation of muscular arteries. Timolol is a non specific beta blocker. It decreases intraocular pressure by reducing aqueous humor formation. It does not change outflow facility. Its action starts twenty minutes after a topical drop, is maximum two to four hours later and lasts 24 hours and more. Timolol o.50% seems equivalent to pilocarpine 4% while Timolol 0.25% seems equivalent to epinephrine 2%. There is a further drop in pressure when added to pilocarpine, diamox as maximum medical treatment. Tables show its advantages, drawback, adverse reactions, and precautions to be taken.

Acetazolamide↗
PubMed1970

[Rieger's syndrome].

Explore the source record for details and available documents.

Abnormalities, Multiple↗
PubMedDate not supplied

Estimation of the misclassification rate of self-reported visual disability.

PURPOSE: To estimate the misclassification rate of self-reported visual disabilities in a hospital-based population with known visual impairment. METHODS: Subjects (N=570) were recruited among patients aged 50 years and more and classified to three categories of visual impairment level. The questionnaire was administered to consenting patients through a telephone interview. Data collected from questionnaires and medical records were compared regarding severity of visual impairment. Sensitivity and specificity were determined for each question. Predictive ability and misclassification rates were computed for various prevalences. RESULTS: Questions related to near and far distance visual acuity with glasses have both a good sensitivity (82.6% and 81.8%) and a good specificity (85.6% and 88.9%) for the presence of severe visual impairment. CONCLUSION: The findings allow the determination of the misclassification rate and predictive ability. This could be useful to estimate the prevalence of visual impairment from health surveys.

Aged↗