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Biomedical subjects

J K Carter

Publications and source records attributed to J K Carter.

12 recordsLinked to original sources
PubMed1990

Cell culture amplification of a defective Marek's disease virus.

A highly amplified 4-kb EcoRI fragment was present in DNA isolated from high cell culture passaged stocks (greater than 93 passages) of 281MI/1, a serotype 2 Marek's disease virus (MDV). The isolated 4-kb fragment is amplified in the presence of MDV, replicating as a high molecular weight, head-to-tail concatemer. When the 4-kb fragment was cloned into pUC18 and cotransfected with MDV DNA into chicken embryo fibroblast cells, the plasmid clone also replicated as a high molecular weight concatemer.

Cloning, Molecular↗
PubMed1985

Isolation and characterization of monoclonal antibodies directed against two subunits of rabbit poxvirus-associated, DNA-directed RNA polymerase.

A library of monoclonal antibodies directed against individual proteins of the rabbit poxvirus (RPV) virion within a complex immunogenic mixture has been generated through the use of in vivo and in vitro immunization regimens. The relative efficacies of the two procedures were compared. Based on immunoblot analysis, the in vitro immunization regimen led both to a wider variety of monoclonal antibodies to different proteins and to a larger number of antibodies directed against proteins of higher molecular weights. Each method, however, has advantages, and the two procedures appear to be complementary. A simple method to recognize antibodies directed against the virion DNA-directed RNA polymerase was developed. Monoclonal antibodies directed against two subunits (137 and 34 kilodaltons [kDa]) of the RNA polymerase were identified and used to study the biogenesis of the enzyme and to map the two corresponding genes within the viral genome by using an RPV DNA library cloned into the lambda gtll expression vector. Both proteins are synthesized late in the infectious cycle and are restricted totally to the cytoplasm. Preliminary mapping data place the genes encoding the 137-kDa protein within the HindIII H fragment, whereas the gene for the 34-kDa protein is located within the left most region of the HindIII A fragment.

Antibodies, Monoclonal↗
PubMed1984

Specificity of avian leukosis virus-induced hyperlipidemia.

Rous-associated virus 7 (RAV-7) is a subgroup C avian leukosis virus which does not transform cells in vitro or carry an oncogene. When injected into 1-day-old hatched chicks, RAV-7 causes a low incidence of lymphoid leukosis after a latent period of several months. In contrast, infection of 10-day-old chicken embryos with RAV-7 leads to a disease syndrome characterized by stunting, obesity, atrophy of the bursa and the thymus, high triglyceride and cholesterol levels, reduced thyroxine levels, and increased insulin levels (Carter et al., Infect. Immun. 39:410-422, 1983; J.K. Carter and R.E. Smith, Infect. Immun. 40:795-805, 1983). Histopathological examination of tissues from affected chicks revealed an accumulation of lipid in the liver and an extensive infiltration of the thyroid and pancreas by lymphoblastoid cells. In the present investigation, the subgroup specificity of this syndrome was investigated. Other subgroup C avian leukosis viruses (transformation-defective B77, transformation-defective Prague C strain of Rous sarcoma virus, and RAV-49) caused stunting, infiltration of the thyroid and pancreas, increased liver weights, decreased thyroxine levels, and increased insulin levels, but they did not cause a uniform, profound increase in triglyceride and cholesterol levels. Avian leukosis viruses of subgroup A [myeloblastosis-associated virus 1 causing osteopetrosis [MAV-1(O)] and RAV-1], subgroup B [MAV-2(O), MAV-2 causing nephroblastoma [MAV-2(N)], and RAV-2], subgroup D (RAV-50), and subgroup F (ring-necked pheasant virus and RAV-61) did not cause a syndrome identical to that induced by RAV-7. All of the viruses examined induced some stunting and a reduction in thyroxine levels which correlated with the stunting. The two subgroup F viruses caused an infiltration of the thyroid which may have been secondary to severe lung involvement. We conclude that the RAV-7 syndrome is unique, particularly in the induction of a hyperlipidemia.

Animals↗
PubMed1983

Rous-associated virus type 7 induces a syndrome in chickens characterized by stunting and obesity.

Infection of 10-day-old chicken embryos with an avian retrovirus. Rous-associated virus type 7, resulted in a disease characterized by stunting and hyperlipidemia. By 20 days after hatch, infected chickens were smaller than hatchmates and developed ataxia and obesity over the next 30 days. Histological examinations of livers from infected chickens revealed a diffuse panlobular fatty infiltrate involving an accumulation of fat in microdroplets. Electron microscopic examinations of livers from infected chickens revealed hepatocytes with swollen mitochondria that lacked cristae. The thyroid and pancreas were infiltrated with lymphoblastoid cells by 1 week after hatch. An examination of the blood revealed a mild anemia, a frank lipemia, and high levels of uric acid. This syndrome induced by Rous-associated virus type 7 in chickens may be useful for elucidating the nature of several diseases, including that found in the fatty liver and kidney syndrome of chickens and that observed in a strain of obese chickens.

Anemia↗
PubMed1983

Induction of angiosarcomas by ring-necked pheasant virus.

Ring-necked pheasant virus, an avian leukosis virus, when injected into 10-day old chick embryos, caused angiosarcomas in the lungs of infected chickens within a short time. Angiosarcomas appeared as localized foci of proliferating cells in the lungs as early as 2 weeks posthatch, and by 6 weeks, the lungs of the infected chickens were frequently filled with tumor cells. Between 3 and 10 weeks of age, 80% of infected chickens died of the angiosarcomas; the 20% which lived 8 weeks or longer had small lung lesions and also developed fibrosarcomas, osteopetrosis, nephroblastoma, and lymphoid leukosis. Chickens with lung tumors were cyanotic, had breathing difficulty, and had packed cell volumes in excess of 50%. Other changes not necessarily correlated with lung tumor mass were stunting, lymphoid organ involution, and profuse diarrhea. Ring-necked pheasant virus has a genome RNA of 8.2 kb. This observation, together with its replication and disease induction after repeated plaque purification, suggests that ring-necked pheasant virus is a replication-competent avian retrovirus. Therefore, our results suggest that ring-necked pheasant virus is an avian leukosis virus which causes angiosarcomas rapidly at high incidence and which, therefore, may induce this type of tumor by a mechanism different from the induction of sarcomas by avian sarcoma viruses.

Animals↗
PubMed1983

Rapid induction of hypothyroidism by an avian leukosis virus.

Infection of 10-day chicken embryos with an avian leukosis virus, RAV-7, resulted in hypothyroidism within 3 weeks posthatching. Histological examination of the thyroids from infected chickens showed an extensive infiltration of lymphoblastoid cells by 7 days posthatching. Areas resembling germinal centers were present in the thyroids of infected chickens by 3 weeks posthatching. Examination of circulating thyroid and pancreas hormones showed a significant reduction in T3 and T4 levels and a trend toward higher insulin levels after 16 days posthatching. T4 supplementation of RAV-7-infected chickens alleviated some aspects of the disease syndrome but did not abrogate all symptoms. Marked involution of both bursa and thymus glands was noted. RAV-7 had an RNA genome of 8.2 kilobases and a polypeptide composition characteristic of an avian leukosis virus. The hypothyroidism followed a dose response to RAV-7 infection.

Animals↗
PubMedDate not supplied

Differences in transitional needs of high school students with and without learning disabilities.

Studies investigating the post-high-school vocational status of individuals with disabilities have frequently found that these individuals are more likely to be unemployed, underemployed, or employed part-time, when compared to nondisabled peers. Transition programs are needed for adolescents with disabilities to facilitate their vocational success. The current study surveyed 80 high school students with learning disabilities (LD) and 80 nondisabled (NLD) peers to determine their transitional needs. Results indicated that (a) more students with LD than NLD students are involved in transition programs; (b) career goals were established by the majority of both groups; (c) parents provided most of the assistance in making career decisions; and (d) twice as many NLD students as students with LD wanted to go to college, while twice as many students with LD as NLD students wanted to enter the job market. More students with LD than NLD students were aware of vocational rehabilitation (VR) services, but the number was still below 50%. The majority of the information about VR services came from the school.

Adolescent↗
PubMedDate not supplied

Isolation of surface tubules of fowlpox virus.

Surface tubules of fowlpox virus were isolated using chemical and physical methods. Suspensions of lipid cytoplasmic inclusion bodies were obtained by treating infected chorioallantoic membranes with 1% trypsin. Inclusions were treated with ultrasonic sound, detergents, and enzymes and were examined by electron microscopy. Although lipase treatment altered the morphology of lipid inclusions, no viral surface tubules were recovered. Treatment with the detergent Nonidet-P40 followed by 2-mercaptoethanol disrupted virions without allowing surface tubules to be recovered. Disruption of lipid inclusions by ultrasonic sound or manual grinding of chorioallantoic membranes produced free virions but only small numbers of tubules. These results indicate that surface tubules can be recovered, but that the lipid nature of cytoplasmic inclusions interferes with procedures commonly used in tubule purification.

Animals↗
PubMedDate not supplied

Influence of diet on a retrovirus-induced obesity and stunting syndrome.

An avian retrovirus, RAV-7, causes a syndrome characterized by stunting, high mortality, and obesity. In this study, the influence of the lipid content of the diet on the RAV-7-induced syndrome was examined. Failure to gain weight, a measure of the stunting, was not influenced by fat content of the diet, but a slight increase in mortality was noted with a low-fat diet.

Animals↗