PubMed Health⌕ Search

Biomedical subjects

L H Billups

Publications and source records attributed to L H Billups.

8 recordsLinked to original sources
PubMed1981

Lung cancer model system using 3-methylcholanthrene in inbred strains of mice.

A model system has been established for studying lung carcinogenesis using intratracheal instillation of 3-methylcholanthrene in C3H/AnfCum and C57BL/Cum X C3H/AnfCum F1 (hereafter called BC3F1/Cum) mice. The animals in these studies were screened for adventitious agents and were free throughout their lifetime of two important lung viruses, Sendai virus and pneumonia virus of mice. Under these conditions, the occurrence of spontaneous and chemically indiced lung cancers was determined over the lifetime of the animals. Data were analyzed by the actuarial method for lung tumor probability. Probability was found to be dose and time dependent. Over 95% of the 3-methylcholanthrene-treated BC3F1/Cum and over 88% of the C3H/AnfCum mice were found at death to have pulmonary carcinomas. Tumors observed in animals which died up to 40 weeks on test were almost always squamous cell carcinomas (approximately 85%), while tumors which were observed in animals which died after 50 weeks were mainly alveolar adenocarcinomas (approximately 80%). Both tumors types metastasized widely. Spontaneous lung cancers (only alveolar adenocarcinomas were observed) occurred in these two strains at low frequency and were expressed late in life. Thus, the system described affords a suitable model to study the induction, expression, and progression of lung tumors under conditions where a vast majority of animals develop neoplasia.

Animals↗
PubMed1980

Correlation of inducibility of aryl hydrocarbon hydroxylase with susceptibility to 3-methylcholanthrene-induced lung cancers.

C57BL/6Cum, DBA/2Cum, first filia (F1), and backcross progeny from these 2 parental strains of mice were evaluated for their susceptibility to 3-methylcholanthrene-induced lung cancers. In the crosses among these mice, aryl hydrocarbon hydroxylase (AHH) responsiveness segregated as a single autosomal dominant gene (the Ah locus). AHH responsive mice (Ahb allele) expressed 40-60 units AHH activity/g wet wt liver following intraperitoneal treatment with 3-methylcholanthrene (MCA) compared to AHH non-responsive mice (Ahd allele) which expressed 7-11 units AHH activity/g wet wt liver after MCA treatment. Intratracheal administration of 500 microgram MCA for a total of 4 times at weekly intervals yielded a variety of pulmonary cancers, including squamous cell carcinomas, alveolar adenocarcinomas, and adeno-squamous cell carcinomas among mice that survived 1 year after the carcinogen treatment. The AHH responsive C57BL/6Cum, F1, and C57BL/6Cum X F1 animals were much more susceptible to MCA-induced lung cancers than the AHH non-responsive DBA/2Cum mice. The lung cancers were also not randomly distributed in DBA/2Cum X F1 backcross progeny since significantly more lung cancers were found in AHH-responsive progeny than in AHH non-responsive mice. Data support genetic linkage between susceptibility to MCA-induced lung carcinomas and the Ahb allele.

Animals↗
PubMed1978

Hepatic jaundice in a colony of nude mice.

A colony of nude mice was maintained under controlled standards of care for 12 months, at which time a rapidly escalating liver disease developed in the animals, characterized by jaundice, emaciation, and rapid death. Histologically, the livers had swollen, vacuolated hepatic cells and increased numbers of enlarged Kupffer cells. Mouse hepatitis virus was not isolated from the livers of sick mice. Although the nature of the lesions suggested toxicity, efforts to reproduce the lesions by increased exposure to chemical compounds used for colony husbandry were unsuccessful. A definitive determination of the causative agent was not made.

Animals↗
PubMed1977

Characterization and responsiveness of the Madison 109 lung carcinoma to various antitumor agents.

The Madison 109 (M109) tumor was discovered in 1964 in the lung of a BALB/c mouse. This experimental carcinoma is maintained in vivo by sc passage in the right axillary region. When implanted im (5 X 10(5) cells) into the right hind leg of BALB/c mice for testing, the primary progresses with metastases to the lung, spleen, and liver. The metastases to the lung are visible within 3 weeks and result in the death of the host in about 35 days after tumor implant. Implantation of a lung nodule is tumorigenic and lethal. Pyran polymer therapy delayed the appearance of lung metastases, inhibited the growth of the primary tumor, and significantly increased the lifespan of BALB/c mice inoculated with the M109 tumor. No spontaneous regression has been observed and very few "no takes" have occurred in untreated BALB/c mice inoculated with at least 500 M109 cells. Of the 82 agents tested so far, the M109 model has selected active agents such as actinomycin D, adriamycin, daunorubicin, DNA, procarbazine, and pyran polymer. It has not shown sensitivity as tested to several standard therapeutic agents including cytosine arabinoside, BCNU, hydroxyurea, mechlorethamine, melphalan, triethylenemelamine, and vincristine.

Animals↗
PubMed1975

Pathophysiologic features of Q fever-infected guinea pigs.

Guinea pigs infected with 9-mile phase I strain of Coxiella burnetii had increased blood glucose concentrations; alkaline phosphatase (ALP), glutamic-oxalacetic transaminase (GOT), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH), and creatine phosphokinase (CPK) activities; and bilirubin value. Hypocalcemia and hypophosphatemia were evident in the latter days of infection. At necropsy of the guinea pigs, necrotic foci were in liver, spleen, and heart. Seemingly, the major pathophysiologic changes in infected guinea pigs were the direct result of lesions in liver, spleen, and heart in which rickettsial bodies were readily observable with histologic staining procedures. The guinea pig may serve as an animal disease model for Q fever.

Alkaline Phosphatase↗