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Biomedical subjects

S E Andrew

Publications and source records attributed to S E Andrew.

At least 19 recordsLinked to original sources
PubMed2006

Msh2 deficiency leads to chromosomal abnormalities, centrosome amplification, and telomere capping defect.

Msh2 is a key mammalian DNA mismatch repair (MMR) gene and mutations or deficiencies in mammalian Msh2 gene result in microsatellite instability (MSI+) and the development of cancer. Here, we report that primary mouse embryonic fibroblasts (MEFs) deficient in the murine MMR gene Msh2 (Msh2(-/-)) showed a significant increase in chromosome aneuploidy, centrosome amplification, and defective mitotic spindle organization and unequal chromosome segregation. Although Msh2(-/-) mouse tissues or primary MEFs had no apparent change in telomerase activity, telomere length, or recombination at telomeres, Msh2(-/-) MEFs showed an increase in chromosome end-to-end fusions or chromosome ends without detectable telomeric DNA. These data suggest that MSH2 helps to maintain genomic stability through the regulation of the centrosome and normal telomere capping in vivo and that defects in MMR can contribute to oncogenesis through multiple pathways.

Animals↗
PubMed2003

Connective tissue growth factor in tear film of the horse: detection, identification and origin.

BACKGROUND: Healing of corneal ulcers in horses is often associated with profound corneal stromal fibrosis and scar formation resulting in visual impairment. Connective tissue growth factor (CTGF) is a fibrogenic cytokine involved in wound healing and scarring. The purpose of this study was to determine whether CTGF was present in the tear fluid of normal horse eyes and the eyes of horses with corneal ulcers in order to evaluate the role of CTGF in corneal wound healing and corneal scar formation. METHODS: Tear fluid samples were collected from 65 eyes of 44 horses; 32 samples from normal eyes, 21 samples from eyes with corneal ulceration, and 12 samples from the unaffected contralateral eyes of horses with ulcers. CTGF levels in the tears were determined by enzyme immunoassay using goat IgG against human CTGF. Antigenetic similarity of human and horse CTGF was established in a bio-equivalence assay. The identity of horse CTGF was confirmed by western blot. Lacrimal and nictitating membrane glands were investigated by immunohistochemistry in the attempt to clarify the origin of tear fluid CTGF. RESULTS: CTGF was detected in tear film of 23 normal unaffected eyes (72%) and 8 normal contralateral eyes (67%), with the mean CTGF levels (+/- SEM) being 51.5+/-19.2 and 13.4+/-3.9 ng/ml respectively. CTGF was found in 8 eyes with corneal ulcers (38%) with the mean CTGF concentration of 26.3+/-14.8 ng/ml. Western blot identified the protein detected as CTGF. The identification of CTGF in lacrimal glands suggests a major role of these glands in the presence of CTGF in tears. CONCLUSIONS: CTGF is present in horse tear fluid and derives, at least partly, from the lacrimal gland. Equine CTGF has strong antigenic similarity with human CTGF. Corneal disease leads to a decrease of CTGF concentrations in tears. The possible role of CTGF in the healing process of ocular surface requires further investigation.

Animals↗
PubMed2003

Corneal thickness and endothelial cell density measured by non-contact specular microscopy and pachymetry in Rhesus macaques (Macaca mulatta) with laser-induced ocular hypertension.

PURPOSE: Sustained increase in intraocular pressure (IOP) in humans results in a loss of corneal endothelial cells and an increase of corneal thickness. The effects of chronically elevated IOP on the corneal endothelium of monkeys with laser-induced ocular hypertension, a commonly used animal model of human glaucoma have not been documented. This study examined the central corneal thickness (CCT), the corneal endothelial cell density (ECD), and the corneal endothelial cell size (ACS) in Rhesus monkeys with experimental ocular hypertension. Materials and methods. Ten male monkeys with argon laser-induced ocular hypertension in one eye for an average duration of 2.4+/-0.7 years, were sedated with ketamine hydrochloride, and the CCT, ECD, and ACS measured at the center of the cornea of both eyes with a Topcon SP-2000P non-contact specular microscope (Topcon America Corporation((R)), Paramus, NJ, USA). CCT was also measured using a DHG-500 Pachette ultrasonic pachymeter (DHG Technology Inc., Exton, PA, USA). Mean and standard deviation (S.D.) of CCT, ECD and ACS for each eye was calculated and statistically compared.Results. Mean CCT in the hypertensive and normal eyes measured by specular microscopy was 0.477+/-0.023mm and 0.468+/-0.020 mm, respectively. Mean ECD in the hypertensive and normal eyes was 2601.7+/-631.8 and 3990.2+/-402.9 cells mm(-2), respectively. The mean size of the endothelial cells was 252.4+/-23.9 micro m(2) in the normal eye and 408.7+/-115.0 microm m(2) in the hypertensive eye. No significant difference in the measurement of CCT was observed between the specular microscope and the pachymeter (p=0.46). No significant difference in the mean CCT was observed between the two eyes (p=0.4820), whereas the mean ECD was significantly lower in the hypertensive eye than in the normal eye (p<0.001). The ECD was inversely related to the length of IOP elevation (p<0.001). CONCLUSIONS: No difference in the corneal thickness measurement was observed between the specular microscopy and the pachymetry techniques. Chronic ocular hypertension did not significantly affect the CCT, but caused a significant loss of endothelial cells in the center of the cornea of the laser treated eyes compared to the normotensive eyes. The duration of elevated IOP was the most important factor affecting the ECD.

Animals↗
PubMed2003

Changes in antibiotic resistance in equine bacterial ulcerative keratitis (1991-2000): 65 horses.

OBJECTIVE: To document changes in antibiotic resistance of organisms in cases of equine bacterial ulcerative keratitis over a 10-year time period. DESIGN: A retrospective study. PARTICIPANTS: Medical records of equine patients with bacterial ulcerative keratitis seen at the University of Florida's VMTH for the years 1991-2000 were reviewed. MATERIALS AND METHODS: All cases of equine bacterial ulcerative keratitis for the above mentioned years were examined. Bacterial isolates were identified and subjected to Kirby-Bauer disc diffusion method sensitivity tests. Antibiotics used in the sensitivity tests included bacitracin, ampicillin, gentamicin, chloramphenicol, polymyxin B, trimethoprim-sulfa, neomycin, kanamycin, carbenicillin, tobramycin and enrofloxacin. RESULTS: A total of 65 bacterial isolates were subjected to sensitivity testing. Of these isolates, Pseudomonas aeruginosa accounted for 14 of the bacterial isolates (22%), Streptococcus equi subspecies zooepidemicus accounted for 13 of the bacterial isolates (20%), and Staphylococcus aureus accounted for four of the isolates (6%). A statistically significant increase in resistance of Pseudomonas aeruginosa isolates to the antibiotics gentamicin and tobramycin was found between the isolates from 1992 to 1998 and those from 1999 to 2000. An increase in resistance of Streptococcus equi subspecies zooepidemicus to gentamicin was found between the isolates from 1993 to 1997 and those from 1998 to 2000. CONCLUSIONS: Streptococcus equi subspecies zooepidemicus and Pseudomonas aeruginosa were the most common organisms isolated from cases of equine bacterial keratitis referred to the University of Florida's VMTH for the years 1991-2000. There appears to be an increase in resistance of Streptococcus equi subspecies zooepidemicus to gentamicin over the past 10 years. In addition, there is a significant increase in resistance of Pseudomonas aeruginosa to both gentamicin and tobramycin over the same time period.

Animals↗
PubMed2003

Effect of topical tropicamide on tear production as measured by Schirmer's tear test in normal dogs and cats.

OBJECTIVE: To evaluate the effect of a single dose of topical 1% tropicamide on tear production as measured by the Schirmer tear test (STT) in the normal dog and cat. MATERIAL AND METHODS: Twenty-eight dogs and 32 cats received 50 micro l : l of 1% tropicamide in one eye and the opposite eye served as the control. STTs were performed immediately before instillation of tropicamide and then at 1, 4, 8 and 24 h post drug instillation. STT results were compared between the control and treated eyes at the different times. RESULTS: Aqueous tear production in dogs, measured by STT, was not significantly reduced. The mean +/- SEM STTs for the baseline time for control and tropicamide-treated eyes were 19.9 +/- 0.8 and 20.3 +/- 0.8 mm wetting/min, respectively. For the control eyes, the subsequent mean +/- SEM STT levels were 20.3 +/- 0.9 (1 h), 21.1 +/- 0.8 (4 h), 20.1 +/- 0.9 (8 h), and 18.7 +/- 0.7 (24 h). For the tropicamide-treated eyes, the subsequent mean +/- SEM STT levels were 19.4 +/- 0.9 (1 h), 19.3 +/- 0.9 (4 h), 20.0 +/- 0.9 (8 h), and 18.4 +/- 0.8 (24 h). Aqueous tear production of both eyes was significantly reduced in cats at 1 h but returned to baseline by 4 h post tropicamide instillation. The mean +/- SEM STT levels for the baseline time in cats for control and tropicamide-treated eyes were 14.9 +/- 0.8 and 14.7 +/- 0.8 mm wetting/min, respectively. Subsequent mean +/- SEM STT levels for the control eyes were 6.4 +/- 1.1 (1 h), 11.9 +/- 1.0 (4 h), 13.9 +/- 0.8 (8 h), and 16.4 +/- 1.0 (24 h). For the tropicamide-treated eyes, the subsequent mean +/- SEM STT levels were 5.3 +/- 0.8 (1 h), 10.2 +/- 0.8 (4 h), 14.7 +/- 1.0 (8 h), and 16.6 +/- 1.0 (24 h). CONCLUSION: Single dose 1% tropicamide does not significantly lower tear production rates, as measured by the STT, in normal dogs. However, in normal cats single doses of 1% tropicamide in one eye cause significant reductions in tear production of both eyes at 1 h that recovered to baseline levels by 4 h.

Administration, Topical↗
PubMed2001

The "flap" endonuclease gene FEN1 is excluded as a candidate gene implicated in the CAG repeat expansion underlying Huntington disease.

At least 12 disorders including Huntington disease (HD) are associated with expansion of a trinucleotide repeat (TNR). Factors contributing to the risk of expansion of TNRs and the mechanism of expansion have not been elucidated. Data from Saccharomyces cerevisiae suggest that the flap endonuclease FEN1 plays a role in expansion of repetitive DNA tracts. It has been hypothesized that insufficiency of FEN1 or a mutant FEN1 might contribute to the occurrence of expansion events of long repetitive DNA tracts after polymerase slippage events during lagging strand synthesis. The expression pattern of FEN1 was determined, and ubiquitous tissue expression, including germ cells, suggested that FEN1 has the potential to be involved in HD. Fifteen HD parent/child pairs that demonstrated intergenerational increases in CAG length of greater than 10 repeats were examined for possible mutations or polymorphisms within the FEN1 gene that could underlie the saltatory repeat expansions seen in these individuals. No alterations were observed compared to 50 controls, excluding FEN1 as a trans-acting factor underlying TNR expansion. The identification of a candidate gene(s) in HD or other CAG-expansion disorders implicated in TNR instability will elucidate the mechanism of expansion for this growing family of neurological disorders.

Animals↗
PubMed2001

Corneoconjunctival transposition for the treatment of feline corneal sequestra: a retrospective study of 17 cases (1990-1998).

OBJECTIVE: To describe and evaluate the use of corneoconjunctival transposition as a surgical treatment for corneal sequestra in cats. ANIMALS STUDIED: Fifteen cats (17 eyes) of various breeds and ages with corneal sequestra treated surgically with corneoconjunctival transposition. PROCEDURE: Retrospective medical records study. RESULTS: Median age was 39 months. Eight patients were castrated males, five were spayed females, and two were intact females. The left eye was affected in eight cats, the right eye was affected in five cats, and both eyes were affected in two cats. Mean (+/- SD) sequestrum diameter was 4.4 +/- 2.4 mm (range 1-10 mm) and the sequestrum was located centrally in all cases. Sequestra occurred in the superficial stroma in 8/17 corneas, in the anterior one third of the stroma in 3/17 corneas, and in the middle one third of the stroma in 6/17 corneas. Median duration of clinical signs prior to presentation was 39 days (range 14-1095 days). Median time to healing, defined as the number of days from surgery to cessation of medical treatment, was 34 days (range 25-86 days). There were no recurrences and minimal scar formation. CONCLUSIONS: Corneoconjunctival transposition is a valid procedure for surgical treatment of corneal sequestra in cats. The procedure results in excellent cosmesis and functional vision with no recurrences.

Animals↗
PubMed2001

Enrofloxacin-associated retinal degeneration in cats.

OBJECTIVE: The objective of this study was to evaluate the possible relationship between the administration of parenteral and/or oral [corrected] enrofloxacin and the onset of acute retinal degeneration in cats. The animals studied included 17 cats that received systemic enrofloxacin and developed retinal degeneration soon thereafter. PROCEDURES: In this retrospective clinical study, cats that received parenteral and/or oral [corrected] enrofloxacin and developed acute blindness were identified. Parameters recorded included breed, age, sex, enrofloxacin dosage (daily dose and number of days administered), medical condition for which the antibiotic had been prescribed, ophthalmic signs, examination results, and the visual outcome. Fundus photographs were obtained in seven cats, and electroretinography was performed in five cats. Histopathology was performed on two eyes from one cat (case 1) that received enrofloxacin 5 months previously and developed retinal degeneration. RESULTS: All cats were the domestic shorthair breed; seven were females (one neutered) and ten were males (seven castrated). Ages ranged from 3 to 16 years old (mean +/- SD; 8.8 +/- 4.6 years). The medical disorders for which enrofloxacin was administered ranged from lymphoma and pancreatitis to otitis and dermatitis, and eight cats had urinary diseases. The daily and total dosage of enrofloxacin and number of days of administration were also highly variable. Presenting clinical signs were most often mydriasis and acute blindness. All cats had diffuse retinal degeneration as evidenced by increased tapetal reflectivity and retinal vascular attenuation. Absence of recordable electroretinographic responses suggested diffuse and extensive outer retinal disease. Vision returned in a few cats, but the retinal degeneration persisted or even progressed. Histopathology of two eyes revealed primarily outer retinal degeneration, with diffuse loss of the outer nuclear and photoreceptor layers, and hypertrophy and proliferation of the retinal pigment epithelium. CONCLUSION: Parenteral and/or oral [corrected] enrofloxacin is potentially retinotoxic in some cats, and may result in acute and diffuse retinal degeneration. Blindness often results, but some cats may regain vision. Practitioners should adhere closely to the manufacturer's current enrofloxacin dosage recommendation (5 mg/kg q 24 h), and continue clinical observations for this drug toxicity in cats.

Acute Disease↗
PubMed2001

Ocular manifestations of feline herpesvirus.

Feline herpesvirus-1 (FHV-1) infection is ubiquitous in the domestic cat population worldwide. The most common clinical ocular manifestations of infection with FHV-1 are conjunctivitis and keratitis. This paper reviews the pathogenesis of feline herpesvirus-1 and discusses the various clinical ocular manifestations, diagnostic techniques and treatment of FHV-1-induced diseases. Ocular manifestations include: conjunctivitis, keratitis, stromal keratitis, keratoconjunctivitis sicca, ophthalmia neonatorium, symblepharon, corneal sequestrum, eosinophilic keratitis and anterior uveitis. Diagnostic techniques discussed include: virus isolation, fluorescent antibody testing, serum neutralising titers, ELISA and polymerase chain reaction. Various therapies are also discussed.

Animals↗
PubMed2001

DNA instability and human disease.

It is now well established that non-Mendelian examples of DNA instability are associated with human disease. Most malignancies are associated with various chromosomal instabilities, such as aneuploidy, gene amplification, and chromosomal deletion. Furthermore, widespread microsatellite instability (MSI) is associated with a variety of tumors, and instability at specific dynamic repeat expansions underlies a family of neurologic disorders. Inactivation of DNA mismatch repair genes results in genomic instabilities affecting microsatellite regions. Mutations in genes involved in DNA polymerization or Okazaki fragment processing are also associated with MSI. Such instabilities convey a 'mutator' phenotype which is pathogenic. The mechanisms controlling trinucleotide repeat expansions are less well understood. Why this type of genomic instability is particularly pathogenic to neurons is also not clear. An understanding of what normally maintains stability is the first step towards preventing such loss of control and maintaining health.

Cell Transformation, Neoplastic↗
PubMed2001

Density of corneal endothelial cells and corneal thickness in eyes of euthanatized horses.

OBJECTIVE: To determine density of corneal endothelial cells and corneal thickness in eyes of euthanatized horses. SAMPLE POPULATION: 52 normal eyes from 26 horses. PROCEDURE: Eyes were enucleated after horses were euthanatized. Eyes were examined to determine that they did not have visible ocular defects. Noncontact specular microscopy was used to determine density of corneal endothelial cells. Corneal thickness was measured, using ultrasonic pachymetry or specular microscopy. RESULTS: Mean density of corneal endothelial cells was 3,155 cells/mm2. Cell density decreased with age, but sex did not affect cell density. Values did not differ significantly between right and left eyes from the same horse. Cell density of the ventral quadrant was significantly less than cell density of the medial and temporal quadrants. Mean corneal thickness was 893 microm. Sex or age did not affect corneal thickness. Dorsal and ventral quadrants were significantly thicker than the medial and temporal quadrants and central portion of the cornea. We did not detect a correlation between corneal thickness and density of endothelial cells in normal eyes of horses. CONCLUSIONS AND CLINICAL RELEVANCE: Density of corneal endothelial cells decreases with age, but corneal thickness is not affected by age or sex in normal eyes of horses. The technique described here may be useful for determining density of endothelial cells in the cornea of enucleated eyes. This is clinically relevant for analyzing corneal donor tissue prior to harvest and use for corneal transplantation.

Age Factors↗
PubMed2000

Development of glaucoma after cataract surgery in dogs: 220 cases (1987-1998).

OBJECTIVE: To examine postoperative ocular hypertension (POH) and other variables as predictors of the risk of developing glaucoma after cataract surgery in dogs. DESIGN: Retrospective study. ANIMALS: 220 dogs that had cataract surgery. PROCEDURE: Medical records of 220 dogs (346 eyes) that had extracapsular cataract removal or phacoemulsification of cataracts were reviewed. With respect to glaucoma development, 8 variables were analyzed, which included development of POH, breed, sex, age at time of surgery, eye (right vs left), phacoemulsification time, intraocular lens (IOL) placement (yes or no), and stage of cataract development. Eyes developed glaucoma within 6 or 12 months of surgery or did not have signs of glaucoma at least 6 or 12 months after cataract surgery. RESULTS: Of 346 eyes, 58 (16.8%) developed glaucoma after surgery. At 6 months, 32 of 206 (15.5%) eyes examined had glaucoma; at 12 months, 44 of 153 (28.8%) eyes examined had glaucoma. Median follow-up time was 5.8 months (range, 0.1 to 48 months). Mixed-breed dogs were at a significantly lower risk for glaucoma, compared with other breeds. Eyes with IOL placement were at a significantly lower risk for glaucoma, compared with eyes without IOL placement. Eyes with hypermature cataracts were at a significantly higher risk for glaucoma, compared with eyes with mature or immature cataracts. CONCLUSIONS AND CLINICAL RELEVANCE: Multiple factors appear to contribute to the onset of glaucoma in dogs after cataract surgery. Complications prohibiting IOL placement during cataract surgery may lead to a high risk of glaucoma development.

Animals↗
PubMed2000

Feline infectious peritonitis.

Feline infectious peritonitis is a noncurable viral disease affecting cats worldwide. Recent evidence suggests that the FIPV has evolved as a deletion mutation of FECV. Immune complex deposition and vasculitis with pyogranulomatous lesions are the hallmark of FIP. The only definitive antemortem diagnostic test for FIP is histopathologic examination of tissue. Ocular manifestations occur commonly with noneffusive FIP. The most common clinical sign is a bilateral granulomatous anterior uveitis often accompanied by chorioretinitis. Treatment of ocular FIP is symptomatic, and the mainstay of palliative therapy is topical or systemic corticosteroids or both.

Animals↗
PubMed2000

Candidate mutator genes in mismatch repair-deficient thymic lymphomas: no evidence of mutations in the DNA polymerase delta gene.

DNA mismatch repair (MMR) proteins recognize nucleotides that are incorrectly paired. Deficiencies in MMR lead to increased genomic instability reflected in an increased mutation frequency and predisposition to tumorigenesis. Mice lacking the MMR gene, Msh2, develop thymic lymphomas that exhibit much higher mutational frequencies than other Msh2(-/-) tumours and Msh2(-/-) normal thymic tissue, suggesting that an additional mutator may have been acquired in a tissue-specific manner. Clustered mutations observed exclusively in the thymic lymphomas suggests that a gene(s) associated with the replication machinery might have become altered during tumorigenesis. Based on mutation studies in Saccharomyces cerevisiae lacking Msh2 and DNA polymerase delta (DNA pol delta), we hypothesized that the acquisition of mutations in DNA pol delta could contribute to the hypermutator phenotype and tumorigenesis in Msh2(-/-) thymic tissue. Furthermore, previous reports have suggested that genes containing mononucleotide repeats are non-random mutational targets in the absence of MMR. Therefore, we sequenced all 26 exons of the DNA pol delta catalytic subunit, including the six exons containing mononucleotide repeats of >5 bp, from nine Msh2(-/-) thymic lymphomas and two wild-type controls. No DNA pol delta pathogenic mutations were found in the thymic lymphomas, although several DNA base differences compared with published DNA pol delta sequences were observed. We conclude, therefore, that inactivating mutations in DNA pol delta are not a contributing factor in the development of the hypermutator phenotype in MMR-deficient murine thymic lymphomas.

Animals↗
PubMed2000

Tumors arising in DNA mismatch repair-deficient mice show a wide variation in mutation frequency as assessed by a transgenic reporter gene.

We reported previously that thymic lymphomas arising in mice lacking the DNA mismatch repair (MMR) gene, Msh2(-/-), exhibited striking elevations in the mutation frequency of a transgenic lacI reporter gene when compared with normal Msh2(-/-) tissues. To investigate whether hypermutation was a feature of all tumors arising in MMR-deficient mice, lacI transgene mutation frequencies were obtained from several different mouse tumors deficient for PMS2 and/or MSH2. While lacI gene hypermutation was again clearly evident in Msh2 +/- ms2(-/-) and Msh2(-/-)Pms2(-/-) thymic lymphomas, three non-thymic MSH2-deficient tumors failed to show lacI gene mutation frequency elevations when compared with a normal tissue of MMR-deficient mice. The elevated mutation frequencies in the lymphoid tumors, and the finding of multiple clustered mutations in lacI genes rescued from these tumors, suggest that they are possibly generated by a lymphoma-specific hypermutational mechanism.

Animals↗
PubMed2000

Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts.

DNA mismatch repair (MMR) deficiency leads to an increased mutation frequency and a predisposition to neoplasia. 'Knockout' mice deficient in the MMR proteins Msh2 and Pms2 crossed with mutation detection reporter (supF, lacI and cII) transgenic mice have been used to facilitate a comparison of the changes in mutation frequency and spectra. We find that the mutation frequency was consistently higher in Msh2-deficient mice than Pms2-deficient mice. The lacI target gene, which is highly sensitive to point mutations, demonstrated that both Msh2- and Pms2-deficient mice accumulate transition mutations as the predominant mutation. However, when compared with Msh2(-/-) mice, lacI and cII mutants from Pms2-deficient mice revealed an increased proportion of +/-1 bp frameshift mutations and a corresponding decrease in transversion mutations. The supF target gene, which is sensitive to frameshift mutations, and the cII target gene revealed a strong tendency for -1 bp deletions over +1 bp insertions in Msh2(-/-) compared with Pms2(-/-) mice. These data indicate that Msh2 and Pms2 deficiency have subtle but differing effects on mutation avoidance which may contribute to the differences in tumor spectra observed in the two 'knockout' mouse models. These variances in mutation accumulation may also play a role, in part, in the differences seen in prevalence of MSH2 and PMS2 germline mutations in hereditary non-polyposis colorectal cancer patients.

Adenosine Triphosphatases↗
PubMed1999

Comparison of selectable and plaque assay systems to detect menadione- and UV-induced lacI mutations in mammalian cells.

We have compared the spontaneous mutation frequency and spectrum of lacI genes recovered from a rat embryonic fibroblast line transfected with a lambda-phage shuttle vector (Rat2lambdalacI) using both the traditional plaque assay as well as a positive selection assay. In addition, mutation frequencies and spectrum were determined after treatment of the cells with either the intracellular superoxide-generating compound, menadione, or UVC light. The differences in mutation frequency between the two systems suggested that the selectable assay was better at discerning relatively small mutation frequency increases, more rapidly and at lower cost, than the plaque assay method. Some novel lacI mutations were observed in mutants derived from the selectable assay. This indicates that the selectable assay system may be a useful tool for assessing the mutagenic potential of different agents.

Animals↗