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Biomedical subjects

L Chevrette

Publications and source records attributed to L Chevrette.

14 recordsLinked to original sources

Sequence analysis and homology modeling suggest that primary congenital glaucoma on 2p21 results from mutations disrupting either the hinge region or the conserved core structures of cytochrome P4501B1.

We recently reported three truncating mutations of the cytochrome P4501B1 gene (CYP1B1) in five families with primary congenital glaucoma (PCG) linked to the GLC3A locus on chromosome 2p21. This could be the first direct evidence supporting the hypothesis that members of the cytochrome P450 superfamily may control the processes of growth and differentiation. We present a comprehensive sequence analysis of the translated regions of the CYP1B1 gene in 22 PCG families and 100 randomly selected normal individuals. Sixteen mutations and six polymorphisms were identified, illustrating an extensive allelic heterogeneity. The positions affected by these changes were evaluated by building a three-dimensional homology model of the conserved C-terminal half of CYP1B1. These mutations may interfere with heme incorporation, by affecting the hinge region and/or the conserved core structures (CCS) that determine the proper folding and heme-binding ability of P450 molecules. In contrast, all polymorphic sites were poorly conserved and located outside the CCS. Northern hybridization analysis showed strong expression of CYP1B1 in the anterior uveal tract, which is involved in secretion of the aqueous humor and in regulation of outflow facility, processes that could contribute to the elevated intraocular pressure characteristic of PCG.

Amino Acid Sequence↗

Novel TIGR/MYOC mutations in families with juvenile onset primary open angle glaucoma.

Mutations in the trabecular meshwork induced glucocorticoid response protein (TIGR) or myocilin (MYOC) has recently been shown to cause juvenile onset primary open angle glaucoma (JOAG). In this study, we identified two new mutations (Asp380Ala and Ser502Pro) in two British families and another (Pro370Leu) in a French-Canadian family. These mutations were not present in a total of 106 normal chromosomes. In another Turkish family with JOAG, we also detected a sequence variant that was proven to be an amino acid polymorphism (Arg76Lys). No other sequence changes were found in the entire coding region and splice junctions of the TIGR/MYOC gene in this family. However, it is still possible that mutations either in the TIGR promoter or in another neighbouring gene could cause glaucoma in this JOAG family. Our results confirm the role of the TIGR/MYOC gene in the aetiology of the JOAG phenotype.

Adolescent↗

Pattern electroretinogram and spatial contrast sensitivity in primary congenital glaucoma.

OBJECTIVE: The authors investigated the temporal and spatial characteristics of pattern electroretinogram (PERG) and spatial contrast sensitivity (CS) in primary congenital glaucoma (PCG) to determine whether the PERG and CS could be useful tools in the diagnosis of childhood glaucoma, especially PCG. PARTICIPANTS: The PERGs were evaluated in eyes from ten patients with PCG and nine age-matched visually normal subjects. INTERVENTION: All patients received complete ophthalmologic evaluations including visual field testing. MAIN OUTCOME MEASURES: The PERGs were recorded using phase-alternating (2, 4, and 16 reversals per second [rps]) checkerboard patterns (30' and 60' checks). RESULTS: The patients with PCG exhibited decreased CS when compared with that of control subjects. Significant PERG deficits also were detected in these patients. However, PERG amplitude in patients with PCG almost reached control subject levels at high (16 rps) temporal frequency. This was true for both 30' and 60' checks. Taken together, these observations on PERG amplitude suggest a more important deficiency of the neural response of the retinal cells at lower temporal frequency (rps) in patients with PCG. This is unlike primary open-angle glaucoma (POAG) in which significant PERG deficits are observed at high temporal frequencies. CONCLUSIONS: The PERG amplitude is reduced in patients with PCG, and this is consistent with a loss of CS and visual field changes in these patients. However, the spatiotemporal characteristics of the PERG deficits in PCG differ from those of POAG. This could suggest a difference in the mechanisms mediating retinal ganglion cell dysfunction in the two types of glaucoma.

Adolescent↗

A second locus (GLC3B) for primary congenital glaucoma (Buphthalmos) maps to the 1p36 region.

Primary congenital glaucoma (gene symbol: GLC3) is an ocular disorder that occurs for 0.01-0.04% of blind people. In the majority of familial cases reported so far, this condition is inherited as an autosomal recessive trait. We have recently used a group of 17 GLC3 families with a minimum of two affected offspring and consanguinity in most of the parental generation and mapped the first GLC3 locus (GLC3A) to the 2p21 region. Six families did not show any linkage to the GLC3A locus and thus provided evidence for genetic heterogeneity of this disorder. A total of eight families unlinked to the 2p21 region were used to search for the chromosomal location of the second GLC3 locus. Herein, we describe mapping of a new locus (designated GLC3B) for primary congenital glaucoma to the short arm of chromosome 1 (1p36.2-36.1) that is situated centromeric to the neuroblastoma and Charcot-Marie-Tooth type 2A (CMT2A) loci. A total of 17 DNA markers were genotyped from this region of chromosome 1. Four families showed no recombination with the two markers D1S2834 and D1S402 with a maximum lod score of 4.510 and 4.157 respectively. Pairwise and multipoint linkage analysis and inspection of the haplotypes revealed that the remaining four families are not linked to this part of chromosome 1, thus providing further evidence that at least one more locus for the autosomal recessive form of GLC3 must exist in the genome. Based on the recombination events, the overall linkage map of this region is: tel-D1S1192-D1S1635-D1S1193 - (D1S1597/-D1S489/D1S228)- [GLC3B/D1S2834/D1S402] - (D1S1176/D1S507/D1S407) - D1S2728-(MFAP2/D1S170) - D1S1368 - D1S436-D1S1592-cen.

Chromosome Mapping↗

Assignment of a locus (GLC3A) for primary congenital glaucoma (Buphthalmos) to 2p21 and evidence for genetic heterogeneity.

Primary congenital glaucoma (GLC3) is an inherited eye disorder that accounts for 0.01-0.04% of total blindness. Although a large number of chromosomal abnormalities have already been reported in patients with congenital glaucoma, the precise location and pathogenesis of this condition remain elusive. By using a group of 17 GLC3 families and a combination of both candidate regional and general positional mapping strategies, we have mapped a locus for GLC3 to the short arm of chromosome 2. Eleven families showed no recombination with 3 tightly linked markers of D2S177 (Z = 9.40), D2S1346 (Z = 8.83), and D2S1348 (Z = 8.90) with a combined haplotype lod score of 11.50. Haplotype and multipoint linkage analyses of 14 DNA markers from 2p indicated that the disease gene is located in the 2p21 region and is flanked by DNA markers D2S1788/D2S1325 (theta = 0.03; Z = 5.42) and D2S1356 (theta = 0.05; Z = 4.69). Inspection of haplotype and heterogeneity analysis confirmed that 6 families are not linked to the 2p21 region, thus providing the first proof of genetic heterogeneity for this phenotype. We therefore designated the locus on 2p21 GLC3A and positioned it in the overall linkage map of Tel-D2S405-D2S367-(D2S1788/D2S1325)-[(GLC3A++ +, D2S177)/(D2S1346/D2S1348)]-D2S1356-D2S119- D2S1761-D2S1248-D2S1352-D2S406- D2S441-Cen. Of the seven genes mapping to the 2p21 region, CAD, CALM2, and LHCGR are centromeric to D2S119 and can be excluded as a candidate for GLC3A, but mutations in PRKR, TIK, SOS1, or SPTBN1 may still be accountable for this phenotype. As human 2p21 shows homology with mouse chromosomes 11 and 17, the homolog of GLC3A is expected to reside on one of these two chromosomes.

Animals↗

Clinical evaluation of aminocaproic acid for managing traumatic hyphema in children.

PURPOSE: The purpose of this study is to determine the incidence of secondary hemorrhage after traumatic hyphema in children and to evaluate the efficacy of epsilon aminocaproic acid in reducing this incidence. METHODS: In a prospective, randomized, double-blind study performed between November 1987 and February 1994, 94 children admitted for traumatic hyphema were assigned to receive either aminocaproic acid (n = 48) (100 mg/kg every 4 hours; maximum, 30 g daily) or placebo (n = 46) for 5 days. Patients who had ingested aspirin in the week preceding admission were excluded from the study. RESULTS: Mean age of the patients was 9.4 years. Black patients comprised 4% of the study population. Secondary hemorrhage occurred in only three patients (3.2%), two from the placebo group and one from the aminocaproic acid group, none of whom had any complications. The duration of hospital stay and the clot resorption times were increased significantly in the aminocaproic acid group (P < 0.001). CONCLUSIONS: The authors report a very low incidence of secondary hemorrhage compared with most previous studies. This difference is likely related to the small proportion of black patients in our study and to the exclusion of patients having ingested aspirin, two factors that seem to be associated with higher rates of rebleeding. The efficacy of aminocaproic acid could not be determined due to the low incidence of hemorrhage. The results of this study, however, suggest that the incidence of secondary hemorrhage in white patients without prior ingestion of aspirin is insufficient to justify routine use of aminocaproic acid in managing traumatic hyphema. Rather, an individualized decision based on the risk factors of each patient would seem more appropriate to avoid a slower clot resorption time and possible side effects of this medication.

Administration, Oral↗

Incidence and prognosis of childhood glaucoma. A study of 63 cases.

Sixty-three consecutive cases (95 eyes) of glaucoma in children were studied. Glaucoma associated with congenital anomalies (group II) formed the largest group in this study. This accounted for 46% of the cases compared to primary congenital glaucoma (group I) that accounted for 22.2%. Secondary glaucoma (group III) occurred in 31.8%. The presenting signs and symptoms in group I were tearing and corneal edema. In 50% of the cases in groups II and III, diagnosis was made on a routine ophthalmologic examination. Surgery was performed in 95.8% of eyes in group I, 53.2% in group II, and 54.2% in group III. The best visual prognosis occurred in group I where 77.3% of affected eyes had visual acuity equal to or better than 20/50 with good pressure control in all. This was followed by group II where 41.5% had vision equal to or better than 20/50 and 41.4% had 20/200 vision or less. Intraocular pressure remained uncontrolled in 19.1% of this group. The worst prognosis and morbidity was found in group III where 30.5% of eyes had 20/50 vision or better and 47.8% had 20/200 vision or less. In group III, 33.3% had uncontrolled intraocular pressure.

Child, Preschool↗

[Orbital apex syndrome in a child with Wegener's granulomatosis].

The authors report the case of a 10 year-old child presenting with orbital apex syndrome as the initial manifestation of Wegener's granulomatosis. Orbital apex syndrome is characterized by complete or partial paralysis of the third, fourth and sixth cranial nerves with involvement of the trigeminal nerve's ophthalmic branch. The different mechanisms responsible for ocular complications in Wegener's granulomatosis and the usefulness of computer assisted tomography in this clinical situation are discussed.

Child↗

On- and off-responses in the photopic electroretinogram in complete-type congenital stationary night blindness.

We examined the on- and off-responses of the photopic electroretinogram in patients with complete congenital stationary night blindness. Standard flash electroretinograms as well as those produced in a ganzfeld modified for long-duration light stimuli (500 msec) permitted the separation of on- and off-responses in four patients and four normal subjects. The amplitude and latency of the elctroretinogram on-response (a- and b-waves) and off-response (d-wave) in addition to the oscillatory potentials of the off-response in normal subjects and patients were compared. The abnormal on-response was demonstrated in all the patients, and the off-response with its oscillatory potentials were preserved. We showed that the second portion of the off-response (of inner retinal origin) is normal. If congenital stationary night blindness is a defect of depolarizing bipolar cells, these results preclude input of the depolarizing bipolar cells and support the hyperpolarizing bipolar cells as the cellular origin of the off-response electroretinogram.

Adolescent↗