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PubMed2006

Cigarette smoking, fish consumption, omega-3 fatty acid intake, and associations with age-related macular degeneration: the US Twin Study of Age-Related Macular Degeneration.

OBJECTIVE: To evaluate modifiable risk and protective factors for age-related macular degeneration (AMD) among elderly twins. METHODS: The US Twin Study of Age-Related Macular Degeneration comprises elderly male twins from the National Academy of Sciences-National Research Council World War II Veteran Twin Registry. To determine genetic and environmental risk factors for AMD, twins were surveyed for a prior diagnosis of AMD and underwent an eye examination, fundus photography, and food frequency and risk factor questionnaires. This environmental component of the study includes 681 twins: 222 twins with AMD (intermediate or late stages) and 459 twins with no maculopathy or early signs. Risk for AMD according to cigarette smoking and dietary fat intake was estimated using logistic regression analyses. RESULTS: Current smokers had a 1.9-fold increased risk (95% confidence interval, 0.99-3.68, P = .06) of AMD while past smokers had about a 1.7-fold increased risk (95% confidence interval, 1.2-2.6, P = .009). Increased intake of fish reduced risk of AMD, particularly for 2 or more servings per week (P trend = .04). Dietary omega-3 fatty intake was inversely associated with AMD (odds ratio, 0.55; 95% confidence interval, 0.32-0.95) comparing the highest vs lowest quartile. Reduction in risk of AMD with higher intake of omega-3 fatty acids was seen primarily among subjects with low levels (below median) of linoleic acid intake, an omega-6 fatty acid (P trend<.001). The attributable risk percentage was 32% for smoking and the preventive fraction was 22% for higher omega-3 intake. CONCLUSIONS: This study of twins provides further evidence that cigarette smoking increases risk while fish consumption and omega-3 fatty acid intake reduce risk of AMD.

Aged↗
PubMed1987

Retinal degeneration with nanophthalmos, cystic macular degeneration, and angle closure glaucoma. A new recessive syndrome.

Seven related patients had a progressive pigmentary retinal degeneration, characterized by nyctalopia, visual field restriction, and cystic macular degeneration in younger patients and a macula of nonspecific atrophic appearance in older patients. In addition, each patient had high hyperopia (+9.50 to +16.00) and nanophthalmos (axial lengths, less than 20 mm), with diffuse choroidal thickening on ultrasound. Younger patients had slitlike anterior chamber angles; older patients developed progressive synechial angle closure and eventual glaucoma. Chromosomes were normal. On electroretinographic testing, younger patients had absent rod signals, with normal cone wave form and near-normal b-wave amplitudes but markedly delayed cone b-wave implicit times; older patients had severely diminished or extinguished electroretinograms. This family appears to represent a newly recognized autosomal-recessive syndrome.

Adult↗
PubMed1997

Interferon alfa-2a is ineffective for patients with choroidal neovascularization secondary to age-related macular degeneration. Results of a prospective randomized placebo-controlled clinical trial. Pharmacological Therapy for Macular Degeneration Study Group.

BACKGROUND: Interferon alfa-2a has been shown to be effective as an antiangiogenic agent for several systemic human angiogenic disorders and has shown antiangiogenic activity in the laboratory. OBJECTIVE: To evaluate the safety and efficacy of interferon alfa-2a for the treatment of choroidal neovascularization secondary to age-related macular degeneration. METHODS: A randomized, placebo-controlled, parallel, multicenter double-blind trial was performed at 45 ophthalmic centers worldwide. Four hundred eighty-one patients were randomly assigned to 4 treatment groups: placebo or interferon alfa-2a (Roferon-A), 1.5, 3.0, or 6.0 million international units (MIU). Visual acuity testing, clinical examination, fluorescein angiography, and indocyanine green angiography were evaluated, with the primary end point being a comparison of the number of patients who experienced a loss of 3 lines or more of vision at 1 year. RESULTS: At 52 weeks, 40 (38%; 95% confidence interval, 29%-48%) of 105 placebo-treated patients had lost at least 3 lines of vision (with 12% unavailable for follow-up), compared with 142 (50%; 95% confidence interval, 44%-55%) of 286 in the 3 active treatment groups combined. The difference in proportions was not statistically significant. However, a pairwise comparison of these proportions for the placebo group vs the group that received interferon alfa-2a, 6 MIU (with 26% unavailable for follow-up), showed a statistically significant difference in favor of the placebo group (P = .02) and a nearly significant difference for the placebo vs the 1.5-MIU group (P = .05) (with 16% unavailable for follow-up), again favoring the placebo group. The 3-MIU group (with 22% unavailable for follow-up) did not show a statistically significant difference in pairwise comparison (P = .48), suggesting that a dose-response relationship was not evident. CONCLUSION: Interferon alfa-2a provides no benefit as a treatment for choroidal neovascularization secondary to age-related macular degeneration and may be associated with a poorer visual outcome when given at a dose of 6 MIU. However, the absence of a clear dose-response relationship raises the possibility that the observed differences result from chance.

Aged↗
PubMed1999

A novel retinal degeneration locus identified by linkage and comparative mapping of canine early retinal degeneration.

Early retinal degeneration (erd) is an early onset progressive retinal atrophy, a hereditary canine retinal disease phenotypically similar to human retinitis pigmentosa (RP). In previous efforts to identify the erd locus, canine homologs of genes causally associated with RP in humans, such as opsin (RHO), the beta-subunit gene for cyclic GMP phosphodiesterase (PDE6B), and RDS/peripherin, were excluded. A genome-wide screen was undertaken on canine families segregating the erd disease. Analysis of over 150 canine-specific markers has localized erd to a single linkage group comprising two previously identified canine linkage groups, 20 and 26, corresponding to canine radiation hybrid groups RH.34-a and RH.40-a. Multipoint analysis places erd in the interval between marker FH2289 (distance 23.6 cM) and FH2407 (5.9 cM) with a lod score of 12.23. Although the erd linkage group has not been assigned to an identified canine chromosome, conserved synteny of this linkage group with human 12p13-q13 suggests several candidates for erd and identifies a novel retinal degeneration locus. The rapid progress now occurring in canine genetics will expedite identification of the genes and molecular mechanisms underlying the inherited traits and diseases that make the dog a unique asset for study of mammalian traits.

Animals↗
PubMed2004

Frontotemporal lobar degeneration with motor neuron disease-type inclusions predominates in 76 cases of frontotemporal degeneration.

This report presents the largest series of consecutive, neuropathologically confirmed cases of frontotemporal degeneration (FTD). Prior studies have found dementia lacking distinctive histology (DLDH) to be the most common pathology underlying the clinical diagnosis of FTD. In this series of 76 cases, 29 (38%) were found to have frontotemporal lobar degeneration with motor neuron disease-type inclusions (FTLD-MND-type) or FTLD-MND (with ALS), the most common neuropathological classification in our series. Only eight (11%) were classified as Pick's disease. Several cases originally designated as DLDH could be reclassified as FTLD-MND-type based on current recommendations for classification of FTD.

Dementia↗
PubMed2003

Visual acuity and contrast sensitivity in patients with neovascular age-related macular degeneration. Results from the Radiation Therapy for Age-Related Macular Degeneration (RAD-) Study.

BACKGROUND: Patients with advanced age-related macular degeneration (AMD) suffer not only from impairment in central visual acuity (VA), but also from reduction in contrast sensitivity (CS). We examined VA and CS changes over time in patients with subfoveal choroidal neovascularizations (CNV) as well as the correlation between the two parameters. METHODS: VA was determined according to a standardized protocol with the Early Treatment Diabetic Retinopathy (ETDRS) chart. CS was measured with Pelli-Robson charts. The angiographic characteristics of CNV and the presence of CNV in the fellow eye as well as gender and age were evaluated as possible prognostic factors of VA and CS progression. Two hundred and five patients with neovascular AMD were recruited within the Radiation Therapy for Age-Related Macular Degeneration (RAD) Study and were reviewed over 2 years. The treatment and control groups showed no significant difference for VA or for CS ( P>0.05), and both groups were considered together. RESULTS: At baseline, mean VA was 55.6+/-14.5 SD letters (EDTRS chart), and mean CS was 22.8+/-6.9 letters (Pelli-Robson chart). Spearman Correlation Coefficient ( r(s)) between VA and CS was r(s)=0.60, P=0.0001. Over 2 years the mean VA loss was 23.6+/-21.4 letters and mean CS reduction was 9.0+/-9.7 letters. Agreement between change of VA and change of CS was moderate ( r(s)=0.65, P=0.0001; kappa coefficient (grouped into VA loss < or =15, >15, >30 letters; CS loss < or =6, >6, >15 letters) kappa=0.43, 95% CI [0.32;0.54]). Proportional hazard models did not show any apparent influence of type of CNV, or CNV in the fellow eye, on change in VA and CS. CONCLUSION: The results indicate that VA and CS do not always show the same progression in visual function loss although they show a moderate correlation in eyes with neovascular AMD. Both parameters provide important information about visual disability and should be evaluated as outcome in interventional studies.

Aged↗
PubMed1995

Degeneration of rat cholinergic basal forebrain neurons and reactive changes in nerve growth factor expression after chronic neurotoxic injury--I. Degeneration and plastic response of basal forebrain neurons.

The process of degeneration and dendritic reorganization of cholinergic neurons was investigated in the rat basal forebrain under the conditions of chronic neurotoxic injury induced by long-term consumption of ethanol. After 28 weeks of ethanol treatment (20% v/v), both the number of choline acetyltransferase-immunoreactive basal forebrain neurons and levels of biochemical measures of cholinergic neurons, such as the activity of choline acetyltransferase and the synthesis and content of acetylcholine, were decreased by about 60-80%. The number of cholinergic neurons showing a positive hybridization signal to choline acetyltransferase messenger RNA was decreased to a similar extent. On the contrary, the reduction in the number of neurons immunoreactive for nerve growth factor receptor p75, which in control brains is highly co-localized with the expression of choline acetyltransferase, was much less pronounced and reached only 20-30%. The loss of choline acetyltransferase expression was associated with a cellular hypertrophy. Neurons which had survived the neurotoxic damage, furthermore, showed a remodelling of the dendritic organization which was quantitatively investigated after Golgi impregnation. This process of dendritic reorganization was mainly characterized by an increase in number and length of terminal dendritic segments. The results indicate that under the conditions of the present paradigm of chronic neurodegeneration, a certain number of cholinergic neurons persists in a form where they lost their ability to express detectable amounts of choline acetyltransferase messenger RNA and the enzyme protein. Persisting neurons, however, show both expression of nerve growth factor receptor p75 and signs of perikaryal and dendritic growth. It might, therefore, be hypothesized that chronic degeneration of cholinergic basal forebrain neurons triggers reactive attempts of repair which involve the action of trophic factors such as nerve growth factor.

Alcohol Drinking↗
PubMed1992

Complete rescue of photoreceptor dysplasia and degeneration in transgenic retinal degeneration slow (rds) mice.

retinal degeneration slow (rds) is a semidominant mutation of mice with the phenotype of abnormal development of rod and cone photoreceptors, followed by their slow degeneration. The rds gene has been putatively cloned and its novel protein product initially characterized biochemically. In the present study we undertook to correct in vivo the retinal phenotype of mice with the rds mutation. We assembled a transgene containing a regulatory segment of the opsin gene positioned upstream of the wild-type rds coding region. Mice from three transgenic lines, homozygous for the rds mutation, were analyzed for expression of the transgene and for their retinal phenotypes. In two high expressing lines, we observed complete reversion to wild-type retinal morphology. In a third, low expressing line, we observed a retinal phenotype intermediate between wild type and rds/rds, suggesting partial rescue of the mutation. These results constitute formal proof that we have cloned the rds gene.

Animals↗
PubMed2000

Dominant late-onset retinal degeneration with regional variation of sub-retinal pigment epithelium deposits, retinal function, and photoreceptor degeneration.

PURPOSE: To clarify the pathogenesis of late-onset retinal degeneration (L-ORD), an autosomal dominant disorder characterized by thick deposits of lipid-rich material between the retinal pigment epithelium (RPE) and Bruch's membrane. STUDY DESIGN: Comparative clinicopathologic case report and case series. TISSUES: Eyes of an 82-year-old L-ORD eye donor and an age-matched control. SUBJECTS: Five descendants of the eye donor and his affected sister. METHODS: The eyes were processed for histopathologic examination, including electron microscopy and immunohistochemistry. Family members were examined clinically and with retinal function tests. RESULTS: The L-ORD eye had sub-RPE deposits that were positive for lipid, including esterified and unesterified cholesterol. The deposits were thinnest in the macula, which retained the highest percentage of photoreceptors. In the periphery, RPE thinning and photoreceptor loss correlated with thickness of the sub-RPE deposits. The eye donor was asymptomatic until his late 50s, when he developed problems with adapting to darkness. At age 68, the eye donor had normal acuity but a midperipheral scotoma and subnormal electroretinograms (ERGs); visual loss was progressive. The five descendants (at the time of examination ages 44-58) of the eye donor and his affected sister, who were at 50/50 risk of inheriting L-ORD, had normal ERGs, but four showed defects in dark adaptation. The dark adaptation abnormalities had a distribution similar to the thickness of the sub-RPE deposits in the eye donor, with slow kinetics in the midperiphery and normal kinetics centrally. CONCLUSIONS: The L-ORD donor eye differed from a previous case in the regional distribution of sub-RPE deposits and photoreceptors. In the next generation of this L-ORD family, the first expression of disease, abnormal dark adaptation, mirrored the regional distribution of the deposits in the donor eye. The fine structure and staining characteristics of the sub-RPE deposits in L-ORD resemble those in age-related macular degeneration and Sorsby fundus dystrophy.

Adult↗
PubMed1997

In vivo evidence for free radical involvement in the degeneration of rat brain 5-HT following administration of MDMA ('ecstasy') and p-chloroamphetamine but not the degeneration following fenfluramine.

1. Administration of 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') to several species results in a long lasting neurotoxic degeneration of 5-hydroxytryptaminergic neurones in several regions of the brain. We have now investigated whether this degeneration is likely to be the result of free radical-induced damage. 2. Free radical formation can be assessed by measuring the formation of 2,3- and 2,5-dihydroxybenzoic acid (2,3-DHBA and 2,5-DHBA) from salicylic acid. An existing method involving implantation of a probe into the hippocampus and in vivo microdialysis was modified and validated. 3. Administration of MDMA (15 mg kg-1, i.p.) to Dark Agouti (DA) rats increased the formation of 2,3-DHBA (but not 2,5-DHBA) for at least 6 h. Seven days after this dose of MDMA, the concentration of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) was reduced by over 50% in hippocampus, cortex and striatum, reflecting neurotoxic damage. There was no change in the concentration of dopamine or 3,4-dihydroxyphenylacetic acid (DOPAC) in the striatum. 4. p-Chloroamphetamine (PCA), another compound which produces a neurotoxic loss of cerebral 5-HT content, when given at a dose of 5 mg kg-1 also significantly increased the formation of 2.3-DHBA (but not 2,5-DHBA) in the dialysate for over 4.5 h. post-injection starting 2 h after treatment. 5. In contrast, fenfluramine administration (15 mg kg-1, i.p.) failed to increase the 2,3-DHBA or 2,5-DHBA concentration in the dialysate. A single fenfluramine injection nevertheless also markedly decreased the concentration of 5-HT and 5-HIAA in the hippocampus, cortex and striatum seven days later. 6. When rats pretreated with fenfluramine (15 mg kg-1, i.p.) seven days earlier were given MDMA (15 mg kg-1, i.p.) no increase in 2,3-DHBA was seen in the dialysate from the hippocampal probe. This indicates that the increase in free radical formation following MDMA is occurring in 5-HT neurones which have been damaged by the prior fenfluramine injection. 7. Administration of the free radical scavenging agent alpha-phenyl-N-tert-butyl nitrone (PBN; 120 mg kg-1, i.p.) 10 min before and 120 min after an MDMA (15 mg kg-1, i.p.) injection prevented the acute rise in the 2,3-DHBA concentration in the dialysate and attenuated by 30% the long term damage to hippocampal 5-HT neurones (as indicated by a smaller MDMA-induced decrease in both the concentration of 5-HT and 5-HIAA and also the binding of [3H]-paroxetine). 8. These data indicate that a major mechanism by which MDMA and PCA induce damage to 5-hydroxytryptaminergic neurones in rat brain is by increasing the formation of free radicals. These probably result from the degradation of catechol and quinone metabolites of these substituted amphetamines. In contrast, fenfluramine induces damage by another mechanism not involving free radicals; a proposal supported by some of our earlier indirect studies. 9. We suggest that these different modes of action render untenable the recent suggestion that MDMA will not be neurotoxic in humans because fenfluramine appears safe at clinical doses.

Animals↗
PubMed2006

From basic to clinical research: a journey with the retina, the retinal pigment epithelium, the cornea, age-related macular degeneration and hereditary degenerations, as seen in the rear view mirror.

PURPOSE: This Acta Ophthalmologica Award and Gold Medal Honorary Lecture (the Lundsgaard Gold Medal Honorary Lecture) reviews some of the work I have carried out with my mentors and many of my wonderful collaborators and research students over more than 40 years, also including related work by other groups. It concentrates on the basic electrophysiology and ultrastructure of the retina and the retinal pigment epithelium (RPE), as well as covering basic and clinical aspects of the cornea, contact lenses, age-related macular degeneration (AMD) and hereditary diseases. METHODS: The review describes research performed using light and electron microscopy, basic and clinical electrophysiology, genetics and biochemistry in animal experiments and in research on patients. It also outlines clinically used techniques, such as laser and photodynamic treatment and scanning laser ophthalmoscopy. RESULTS: The paper reports on the following subjects: the mechanisms behind some of the electrical potentials originating in the retina and the RPE and the use of these potentials in hereditary diseases; corneal receptors for lectins and presumably for bacteria; the turnover of the photoreceptor outer segment and the formation of lipofuscin, including the relation of these processes to AMD; certain treatments for AMD, and hereditary degenerations in animal models, such as the RPE65 gene mutation in Briard dogs, which makes them a model of Leber's congenital amaurosis. The dogs are now treated successfully with gene therapy in the USA, and a clinical trial is in preparation. CONCLUSIONS: During the last 40 years we have had the good fortune to experience a dramatic growth in knowledge and understanding within ophthalmic science of basic mechanisms. Huge progress has been made in diagnostics and clinical ophthalmological treatments, much to the benefit of our patients. Even a small contribution made by my group to these developments has been well worth the effort, particularly as scientific work is not just deeply satisfying: it is also fun!

Awards and Prizes↗
PubMed1987

Ultrastructure of the retina of Drosophila melanogaster: the mutant ora (outer rhabdomeres absent) and its inhibition of degeneration in rdgB (retinal degeneration-B).

The Drosophila mutant ora lacks rhodopsin in the R1-6 set of photoreceptors and has a diminution of the photopigment containing rhabdomeres of R1-6. Newly emerged flies have rhabdomeres, albeit small, which extend from the distal rhabdomere cap to the proximal basement membrane. As the fly ages, these are reduced until only distal remnants remain. Carotenoid deprivation does not protect ora flies from rhabdomere loss. When first characterized, ora was designated as a non-formation mutant rather than a degeneration mutant. The truth lies between, since rhabdomeres diminish with age but cells do not die. The plasmalemma of R1-6 have unusual dense striated areas like the "zippers" described earlier for the Drosophila mutant norpA. Similar membranes are also present within the receptor somata, especially in young flies. The latter probably become internalized from the plasmalemma. They are likely not related to the diminished rhabdomeres as claimed earlier. R7 and R8 have normal rhabdomeres, and in particular, they have normal coated vesicles and multivesicular bodies (MVB's), early steps in the degradation phase of normal rhabdomere maintenance. No MVB's are seen in the R1-6 somata, indicating that the routes for rhabdomere degradation differ from those of normal receptors. However, some MVB-like structures are seen in the intraommatidial cavity. The compound mutant rdgB;ora has a phenotype just like that of ora. This means that ora protects rdgB from the light induced degeneration of R1-6 which characterizes rdgB.

Animals↗
PubMed1982

Choroidal neovascular membranes and senile macular choroidal degeneration: their association in disciform macular degeneration.

Senile macular choroidal degeneration (SMCD) is responsible for the majority of cases of new central vision loss in the over-fifty population. It is also the single largest cause of legal blindness in the United States. Choroidal neovascular membranes are frequently associated with SMCD and initiate a disciform process that may lead to profound central vision loss. Clinically, it is very difficult to visualize actual new vessel membranes without the aid of rapid sequence fluorescein angiography; various clinical signs, however, are indicative of their presence. Recognition of choroidal neovascular membranes is important; certain membranes lend themselves to photocoagulation by the retinal specialist. This treatment may be successful in preventing further severe and permanent visual loss in some individuals. The purpose of this paper is to discuss the mechanisms of disciform macular degeneration, as well as the clinical signs important to the recognition of choroidal neovascular membranes.

Choroid↗
PubMed1978

Systems-matching by degeneration. II. Interpretation of the generation and degeneration of retinal ganglion cells in the chicken by a mathematical model.

Quantitative data on generation and degeneration of retinal ganglion cells during development (Rager and Rager, 1978) are interpreted in terms of a mathematical model which consists of a system of differential equations. By these equations we attempt to describe the formation of retinal ganglion cells and their termination domains in the tectum. Since ganglion cells seem not to degenerate before their axons have arrived at their termination site and start branching, from the arrival time on they may become competent either to continue to mature or to die. Therefore, to find the actual number of competent cells the extension of the fiber pathway between the retina and the optic tectum had also to be measured and computed. The differential equations are united by the principle that at any given time cells in excess of the number of termination domains have to die. By this model the mathematical function was determined. Several parameter values of this function were optimized with the Gauss-Newton method by which the curve was fitted to the measured values. The high correlation obtained by this method allows to conclude that, to a first approximation, the model may be satisfactory. The evidence of competition for termination sites and of systems-matching by cell death is discussed.

Age Factors↗
PubMed1975

[An autopsy case of olivocerebellar and thalamic degeneration, diffuse sclerosis and hypertrophic neuropathy: infantile system degeneration? (author's transl)].

The brain of a 21-year-old man with imbecility and spastic tetraplegia since early childhood showed a diffuse sclerosis of the cerebral white matter and symmetrical degeneration of the thalamus and olivocerebellar system. The spinal nerve roots as well as proximal branches of the spinal nerves were hypertrophic and there was seen a marked fibrosis with some onion-bulb formations of Schwann cells. In spite of a possible relation to an unknown infection at the age of 3 months this case could preferably be regarded as a peculiar form of the combined system degeneration in the early childhood, including the cerebral white matter and peripheral nerves. An uncle of the patient had died of a similar nervous disease at the age of 20 years.

Adult↗
PubMed2000

Degeneration of the cerebellar dentate nucleus in corticobasal degeneration: neuropathological and morphometric investigations.

To resolve the controversy regarding the involvement of the dentate nucleus in corticobasal degeneration (CBD), an entire profile of the dentate nucleus was exposed in a sagittal plane and divided into four fields, and the number of neurons in each filed was counted separately using a computer-assisted analyzer in five cases of CBD and compared to those from seven age-matched controls. The size of the nucleus and the number of neurons were significantly reduced in all five cases of CBD. The neuronal loss had a definite regional predilection, more severe in the caudolateral neodentatum than in the rostromedial palaeodentatum, and was accompanied by grumose degeneration and astrogliosis which paralleled the severity of the neuronal loss. Thus, the dentate nucleus appears to be a cardinal target in CBD.

Aged↗
PubMed1982

Mitral cell degeneration and sensory function in the neurological mutant mouse Purkinje cell degeneration (PCD).

Selective degeneration of mitral cells, the principal relay neuron in the central olfactory pathway, is described in the mutant mouse Purkinje cell degeneration (PCD). Concomitant effects are described in adjacent layers of the olfactory bulb which suggest a reorganization of local neuronal circuits. The 2-deoxyglucose technique produced results which suggested that the topographical distribution of sensory afferent input to the bulb was not affected.

Animals↗
PubMed1992

Degenerate oligonucleotide-primed PCR: general amplification of target DNA by a single degenerate primer.

A version of the polymerase chain reaction (PCR), termed degenerate oligonucleotide-primed PCR (DOP-PCR), which employs oligonucleotides of partially degenerate sequence, has been developed for genome mapping studies. This degeneracy, together with a PCR protocol utilizing a low initial annealing temperature, ensures priming from multiple (e.g., approximately 10(6) in human) evenly dispersed sites within a given genome. Furthermore, as efficient amplification is achieved from the genomes of all species tested using the same primer, the method appears to be species-independent. Thus, for the general amplification of target DNA, DOP-PCR has advantages over interspersed repetitive sequence PCR (IRS-PCR), which relies on the appropriate positioning of species-specific repeat elements. In conjunction with chromosome flow sorting, DOP-PCR has been applied to the characterization of abnormal chromosomes and also to the cloning of new markers for specific chromosome regions. DOP-PCR therefore represents a rapid, efficient, and species-independent technique for general DNA amplification.

Animals↗