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T A Carter

Publications and source records attributed to T A Carter.

17 recordsLinked to original sources
PubMed2006

Laboratory observation of a nonlinear interaction between shear Alfvén waves.

An experimental investigation of nonlinear interactions between shear Alfvén waves in a laboratory plasma is presented. Two Alfvén waves, generated by a resonant cavity, are observed to beat together, driving a pseudomode at the beat frequency. The pseudomode then scatters the Alfvén waves, generating a series of sidebands. The observed interaction is very strong, with the normalized amplitude of the driven pseudomode comparable to the normalized magnetic field amplitude (deltaB/B) of the interacting Alfvén waves.

Journal Article↗
PubMed2006

Use of a litter material made from cotton waste, gypsum, and old newsprint for rearing broiler chickens.

Three experiments, which included 4 broiler flocks, were conducted to examine the usefulness of a novel bedding material for rearing broilers. The control bedding was pine shavings. The novel bedding, aGroChips (AC), was a chopped material made from cotton lint waste, gypsum, and old newsprint using a proprietary paper manufacturing process (Novovita, Inc., Raleigh, NC). All birds were fed the same feeding program: starter from 0 to 3 wk, grower from 3 to 5 or 6 wk, and finisher during the last week. Birds were marketed at either 6 or 7 wk of age. Feed consumption by pen and individual bird BW were measured at 3 and 6 or 7 wk. Mean BW and feed conversion, adjusted to include weight of mortality, were calculated. A sample of birds (n = 10) from each pen was evaluated for hock and foot pad condition. Each pen was evaluated at the end of the trial for litter cake index in 3 of the 4 flocks. Litter cake index scores were generally higher for birds reared on AC litters. There were no other differences in bird performance for any of the flocks. In conclusion, broilers reared on AC bedding perform as well as those reared on pine shavings.

Animal Husbandry↗
PubMed2004

From disease genes to cellular pathways: a progress report.

Mutations in a large number of retinal and retinal pigment epithelium (RPE) expressed genes can lead to the degeneration of photoreceptors and consequently the loss of vision. The genetic and phenotypic heterogeneity of retinal dystrophies poses a complex problem with respect to rational development of therapeutic strategies. Delineation of physiological functions of disease genes and identification of pathways that lead to disease pathogenesis represent essential goals towards developing a systematic and global approach to gene-based treatments. We are interested in identifying cellular pathways that are involved in photoreceptor differentiation, function and degeneration. We are, therefore, generating comprehensive gene expression profiles of retina and RPE of humans and mice using both cDNA- and oligonucleotide-based (Affymetrix) microarrays. Because of the under-representation of retinal/RPE genes in the public databases, we have constructed several unamplified cDNA libraries and produced almost twenty thousand expressed sequence tags (ESTs) that are being printed onto glass slides ('I-Gene' microarrays). In this presentation, we will report the microarray analysis of the rodless (and cone-enhanced) retina from the Nrl-knockout mouse as a paradigm to initiate the identification of cellular pathways involved in photoreceptor differentiation and function.

DNA-Binding Proteins↗
PubMed2001

Measurement of lower-hybrid drift turbulence in a reconnecting current sheet.

We present a detailed study of fluctuations in a laboratory current sheet undergoing magnetic reconnection. The measurements reveal the presence of lower-hybrid-frequency-range fluctuations on the edge of current sheets produced in the magnetic reconnection experiment (MRX). The measured fluctuation characteristics are consistent with theoretical predictions for the lower-hybrid drift instability (LHDI). Our observations suggest that the LHDI turbulence alone cannot explain the observed fast reconnection rate in MRX.

Journal Article↗
PubMed2001

Ataxia telangiectasia mutated is essential during adult neurogenesis.

Ataxia telangiectasia (A-T) is an autosomal recessive disease characterized by normal brain development followed by progressive neurodegeneration. The gene mutated in A-T (ATM) is a serine protein kinase implicated in cell cycle regulation and DNA repair. The role of ATM in the brain and the consequences of its loss on neuronal survival remain unclear. We studied the role of ATM in adult neural progenitor cells in vivo and in vitro to define the role of ATM in dividing and postmitotic neural cells from Atm-deficient (Atm(-/-)) mice in a physiologic context. We demonstrate that ATM is an abundant protein in dividing neural progenitor cells but is markedly down-regulated as cells differentiate. In the absence of ATM, neural progenitor cells of the dentate gyrus show abnormally high rates of proliferation and genomic instability. Atm(-/-) cells in vivo, and in cell culture, show a blunted response to environmental stimuli that promote neural progenitor cell proliferation, survival, and differentiation along a neuronal lineage. This study defines a role for ATM during the process of neurogenesis, demonstrates that ATM is required for normal cell fate determination and neuronal survival both in vitro and in vivo, and points to a mechanism for neuronal cell loss in progressive neurodegenerative diseases.

Animals↗
PubMed2001

Chipping away at complex behavior: transcriptome/phenotype correlations in the mouse brain.

Highly parallel gene expression profiling has the potential to provide new insight into the molecular mechanisms of complex brain diseases and behavioral traits. We review how gene expression profiling in various brain regions of inbred mouse strains has been used to identify genes that may contribute to strain-specific phenotypes. New data, which demonstrate the use of gene expression profiling in combination with behavioral testing to identify candidate genes involved in mediating variation in running wheel activity, are also presented. These and other studies suggest that a combination of gene expression profiling and more traditional genetic approaches, such as quantitative trait locus analysis, can be used to identify genes responsible for specific neurobehavioral phenotypes.

Animals↗
PubMed2000

Mice with a targeted mutation in the thyroid hormone beta receptor gene exhibit impaired growth and resistance to thyroid hormone.

Patients with mutations in the thyroid hormone receptor beta (TRbeta) gene manifest resistance to thyroid hormone (RTH), resulting in a constellation of variable phenotypic abnormalities. To understand the molecular basis underlying the action of mutant TRbeta in vivo, we generated mice with a targeted mutation in the TRbeta gene (TRbetaPV; PV, mutant thyroid hormone receptor kindred PV) by using homologous recombination and the Cre/loxP system. Mice expressing a single PV allele showed the typical abnormalities of thyroid function found in heterozygous humans with RTH. Homozygous PV mice exhibit severe dysfunction of the pituitary-thyroid axis, impaired weight gains, and abnormal bone development. This phenotype is distinct from that seen in mice with a null mutation in the TRbeta gene. Importantly, we identified abnormal expression patterns of several genes in tissues of TRbetaPV mice, demonstrating the interference of the mutant TR with the gene regulatory functions of the wild-type TR in vivo. These results show that the actions of mutant and wild-type TRbeta in vivo are distinct. This model allows further study of the molecular action of mutant TR in vivo, which could lead to better treatment for RTH patients.

Alleles↗
PubMed2000

Regional and strain-specific gene expression mapping in the adult mouse brain.

To determine the genetic causes and molecular mechanisms responsible for neurobehavioral differences in mice, we used highly parallel gene expression profiling to detect genes that are differentially expressed between the 129SvEv and C57BL/6 mouse strains at baseline and in response to seizure. In addition, we identified genes that are differentially expressed in specific brain regions. We found that approximately 1% of expressed genes are differentially expressed between strains in at least one region of the brain and that the gene expression response to seizure is significantly different between the two inbred strains. The results lead to the identification of differences in gene expression that may account for distinct phenotypes in inbred strains and the unique functions of specific brain regions.

Animals↗
PubMed1997

Extensive DNA deletion associated with severe disease alleles on spinal muscular atrophy homologues.

Spinal muscular atrophy (SMA) is a motor neuron disease presenting with a wide spectrum of phenotypic variations. The primary cause of most, if not all, forms of childhood-onset spinal muscular atrophy appears to be the homozygous loss of the telomeric copy of the survival motor neuron (SMNT) gene. It is interesting that approximately half of all affected patients are likewise homozygous nulls for the neuronal apoptosis inhibitory protein (NAIP) gene and a somewhat lesser fraction for the basal transcription factor, p44 subunit (BTF2p44) gene. It has been proposed that homozygous loss of SMNT is the primary cause of spinal muscular atrophy while the loss of NAIP and perhaps other genes primarily affects the severity of disease manifestation. We explored this hypothesis by evaluating the extent of gene deletions in three multigenerational families with spinal muscular atrophy exhibiting dramatic intrafamilial phenotypic variation. Using somatic cell hybrid lines to sequester individual spinal muscular atrophy homologues, we show that homologues missing several contiguous genes correlate with "severe" disease alleles and homologues missing only SMNT correlate with "mild" disease alleles. These observations support the hypothesis that phenotypic severity among the childhood-onset spinal muscular atrophies is directly correlated with the extent of disease-specific deletions.

Adult↗
PubMed1997

A multicopy transcription-repair gene, BTF2p44, maps to the SMA region and demonstrates SMA associated deletions.

The childhood-onset spinal muscular atrophies are a clinically heterogeneous group of autosomal recessive disorders characterized by selective degeneration of the anterior horn cells with subsequent weakness and atrophy of limb muscles. The disease locus has been mapped to a region of chromosome 5q13 characterized by genetic instability and DNA duplication. Among the duplicated genes in this region, SMNT (telomeric copy; survival motor neuron) is thought to be the major disease determining gene since it is missing in the majority of SMA patients and since small, intragenic mutations in the gene have been associated with the disorder. Approximately half of the severely affected SMA I patients are also missing both homologues of a neighboring gene, the neuronal apoptosis inhibitory protein (NAIP). These data indicate that loss of NAIP may affect disease severity and further, that the molecular events underlying the childhood-onset SMAs are complex, possibly involving multiple genes. We report a third multicopy gene in the SMA region, encoding the p44 subunit of basal transcription factor II (BTF2p44). One copy of this transcription-repair gene is deleted in at least 15% of all SMA cases.

Chromosome Mapping↗
PubMed1996

Characterization of survival motor neuron (SMNT) gene deletions in asymptomatic carriers of spinal muscular atrophy.

Previous reports have established that the telomeric copy of the survival motor neuron (SMNT) gene and the intact copy of the neuronal apoptosis inhibitory protein (NAIP) gene are preferentially deleted in patients with spinal muscular atrophy (SMA). Although deletions or mutations in the SMNT gene are most highly correlated with SMA, it is not clear to what extent NAIP or other genes influence the SMA phenotype, or whether a small fraction of SMA patients actually have functional copies of both SMNT and NAIP. To evaluate further the part of SMNT in the development of SMA, we analyzed 280 asymptomatic SMA family members for the presence or absence of SMNT exons 7 and 8. We report the following observations: (i) 4% of the sample harbored a polymorphic variant of SMNT exon 7 that looks like a homozygous deletion; (ii) approximately 1% of the parents are homozygously deleted for both exons 7 and 8; (iii) one asymptomatic parent lacking both copies of SMNT exons 7 and 8 displays a 'subclinical phenotype' characterized by mild neurogenic pathology; (iv) another asymptomatic parent lacking both SMNT exons showed no signs of motor neuron disorder by clinical and neurodiagnostic analyses. The demonstration of polymorphic variants of exon 7 that masquerade as homozygous nulls, and the identification of SMA parents who harbor two disease alleles, serve as a caution to those conducting prenatal tests with these markers.

Adolescent↗
PubMed1995

Refinement of the spinal muscular atrophy locus by genetic and physical mapping.

We report the mapping and characterization of 12 microsatellite markers including 11 novel markers. All markers were generated from overlapping YAC clones that span the spinal muscular atrophy (SMA) locus. PCR amplification of 32 overlapping YAC clones shows that 9 of the new markers (those set in italics) map to the interval between the two previous closest flanking markers (D5S629 and D5S557): cen-D5S6-D5S125-D5S435-D5S1407- D5S629-D5S1410-D5S1411/D5S1412-D5S1413- D5S1414-D5Z8-D5Z9-CATT1-D5Z10/D5Z6- D5S557-D5S1408-D5S1409-D5S637-D5S351-MA P1B-tel. Four of these new markers detect multiple loci in and out of the SMA gene region. Genetic analysis of recombinant SMA families indicates that D5S1413 is a new proximal flanking locus for the SMA gene. Interestingly, among the 40 physically mapped loci, the 14 multilocus markers map contiguously to a genomic region that overlaps, and perhaps helps define, the minimum genetic region encompassing the SMA gene(s).

Base Sequence↗
PubMed1984

Effect of the insect growth regulator CGA-72662 (Larvadex) on broiler breeder production, hatchability, and subsequent chick performance.

Broiler breeders were fed CGA -72662 ( Larvadex ) at dosages of 0, 30, 300, and 3000 mg/kg (ppm) diet in a standard breeder diet from 25 to 65 weeks of age. The 3000 ppm level was reduced stepwise to 1000 ppm from 25 to 27 weeks due to a significant increase in male and female mortality. Feed consumption did not differ significantly due to treatment. However, birds fed 300 ppm exhibited significantly improved feed conversion and increased egg production on a hen-day basis compared to those fed 0 and 30 ppm with the 1000 ppm level intermediate. On an egg per hen-housed basis, birds fed 300 ppm produced significantly more eggs than those fed 0 ppm with 30 ppm intermediate. Hens fed 1000 ppm produced significantly fewer eggs than all other treatments due to higher initial mortality. Body weight gains for males and females among treatments were similar. Mortality was significantly greater at 1000 ppm than for all other treatments. Egg specific gravity at 50 and 60 weeks was not affected significantly by any treatment. Egg weight, when compared to the 0 ppm level, was decreased significantly at the 1000 ppm level at 50 weeks and by both 300 and 1000 ppm levels at 60 weeks. Egg shell weight was not affected significantly at 50 weeks, but was decreased significantly by both 300 and 1000 ppm Larvadex at 60 weeks. There were no significant effects due to treatment level on fertility, early deads , pipped eggs, hatchability of fertile eggs, or hatchability of eggs set.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Relationship of dietary calcium level during the prelay phase of an induced molt to postmolt performance.

Leghorn laying hens were induced to molt by a combination of photoperiod reduction and fasting for 14 days, during which time the hens lost 31.5% of their initial body weight. The hens were then assigned to one of four diets containing 1.0, 1.75, 2.5, or 3.5% calcium until egg production resumed. The 3.5% calcium diet was fed to all treatments from the resumption of 5% egg production. Postmolt egg production and feed conversion were not affected significantly. Egg weight, shell weight, and egg specific gravity were not affected consistently. It was concluded that high dietary calcium levels immediately postfast have no adverse effect on postmolt performance.

Animals↗
PubMedDate not supplied

Pituitary gigantism in a 31 month old girl: endocrine studies and successful response to hypophysectomy.

A case of pituitary gigantism occurring in a 31 month old female child is reported. Growth records indicate that the disorder began early in the second yr of life. Apart from her size and history of excessive sweating, there were no characteristic clinical features of endocrinopathy. Elevated and autonomous secretion of GH (60-109 microgram/l) and prolactin were corrected by the removal of an eosinophilic pituitary adenoma. In the subsequent 6 yr, despite the presence of immunoreactive GH (4.6-17.3 microgram/l), plasma somatomedin was subnormal and the patient showed growth failure which responded normally to exogenous GH therapy. This case, which appears to be the youngest example of verified pituitary gigantism on record, illustrates that a successful outcome can be achieved by surgical ablative therapy.

Adenoma, Acidophil↗