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Biomedical subjects

R J Brown

Publications and source records attributed to R J Brown.

At least 109 records · Page 6Linked to original sources

Fibrous osteodystrophy in a wild dolphin.

Skeletal lesions observed during necropsy of a wild mature male dolphin (Delphinus delphis) were consistent with fibrous osteodystrophy when examined microscopically. The lesions were pronounced in the ribs, scapulae, and pelvis, with no apparent skull or vertebral involvement. Whether the cause was nutritional or nonnutritional was not determined.

Animal Population Groups↗

Neuroblastoma of the head and neck.

We reviewed 105 cases of neuroblastoma, which were seen at the Buffalo Children's Hospital between 1936 and 1976. We describe seven patients with primary neuroblastoma of the head and neck. The results of postmortem examination in two of these patients proved without any doubt that the tumor was primarily in the head and neck region. Although metastasis of neuroblastomas to the head and neck from more common primary sites in the abdomen, pelvis, or thorax is common, to our knowledge, well-documented primary head and neck lesions are quite rare. The prognosis of invasive neuroblastoma of the head and neck is poor, with rapid and widespread metastasis being the rule. However, some success has been reported with early and massive therapy that involves surgery, chemotherapy, and radiation therapy.

Child↗

Mutagenicity testing of certified food colors and related azo, xanthene and triphenylmethane dyes with the Salmonella/microsome system.

Thirty-seven azo, xanthene and triphenylmethane dyes including FD and C colors currently approved for use in the U.S.A. and a number of delisted food colors, were tested in the Salmonella/microsome system. In addition to direct plate tests with five tester strains (TA1535, TA100, TA1537, TA1538, TA98), the azo dyes were also assayed after chemical reduction to their component amines. Also, a selected group of azo dyes was subjected to liquid tests (both aerobic with microsomes and anaerobic) and to plate tests involving initial 16 h anaerobic incubations to facilitate microbial reduction of the azo bond. None of the presently listed FD and C colors was mutagenic in any of the test modifications. Among formerly listed colors only Butter Yellow (p-dimethylaminoazobenzene), a recognized animal carcinogen, was mutagenic in the aerobic liquid test. Several other azo dyes were either directly mutagenic, viz. Acid Alizarin Yellow R and Alizarin Yellow GG; required microsomal activation, viz. Acid Alizarin Red B and Methyl Red; or required chemical reduction and microsomal activation, viz. Acid Alizarin Violet N and Sudan IV. Of the non-azo dyes tested only two xanthene dyes appeared to be mutagenic, viz. 9-(2-sulfophenyl)-6-hydroxy-3-isoxanthenone and its 2,4,5,7-tetrabromo derivative.

Azo Compounds↗

Naturally-occurring leptospirosis in northern fur seals (Callorhinus ursinus).

A 4-year study of Northern fur seal (Callorhinus ursinus) leptospirosis in the Bering Sea has shown that in newborn pups Leptospira pomona is associated with a multiple hemorrhage syndrome. Adults may develop an interstitial nephritis and shed organisms in the urine. The hed prevalence, based on microscopic slide agglutination tests, ranged between 7.0% and 15.4% for adult females and 3-4 year old bachelor bulls, whereas nursing pups averaging 4 months of age had a prevalence of 2%. These results are used to conclude that leptospirosis is not acquired primarily on the breeding rookeries but rather is more frequently acquired subsequent to the purps leaving the rookeries, presumably through the food chain during their first pelagic cycle.

Animals↗

Accidental methyl methacrylate inhalation toxicity in a rhesus monkey (Macaca mulatta).

A rhesus monkey (Macaca mulatta), accidentally exposed to vapors of methyl methacrylate for 22 hours was found in a comatose condition. Attempts to revive the animal were unsuccessful. Necropsy revealed a diffusely mottled liver, pulmonary edema, and atelectasis. The thoracic cavities each contained 30 ml of clear yellow fluid. Histopathologic review of the tissues showed central lobular liver necrosis, pulmonary edema, pulmonary emphysema, and atelectasis. Analysis of a blood sample obtained from the monkey 1.5 hours prior to death showed a normal hemogram, but elevated values for serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, lactate dehydrogenase, phosphohexose isomerase, blood urea nitrogen, and serum sodium. The pathologic findings, laboratory results, and clinical history suggested a diagnosis of methyl methacrylate poisoning.

Animals↗

Vasoactive properties of prostaglandin compounds on the in vitro human basilar artery.

The action of six prostaglandins A1, E1, (A2, E2, F1 alpha, F2 alpha) on in vitro human basilar artery circumferential strips was evaluated to assess relative vasoreactivity. Degree of contraction was compared with 5-hydroxytryptamine (5-HT), hitherto the most active in this laboratory. The three most vasoactive prostaglandins were E1, E2, and F2, alpha. The three PGs giving highest magnitude of response were F1 alpha, F2 alpha, and E2. Most were more active when compared to 5-HT. Vasodilation did not occur. Because of their vasoconstrictive qualities, prostaglandins may participate in arterial vasospasm. It is postulated that prolonged vasoconstriction may lead to vasospasm and that the latter may result from one or more autacoids acting along or synergistically.

Basilar Artery↗

Mutagenesis by 9,10-anthraquinone derivatives and related compounds in Salmonella typhimurium.

Ninety 9,10-anthraquinone (AQ) derivatives and related anthracene derivatives were screened for mutagenicity with five Salmonella typhimurium tester strains with and without mammalian microsomal activation. About 35% of the compounds tested are considered to be mutagenic. Three patterns of mutagenesis were apparent. (1)Direct frameshift mutagenesis by certain AQ compounds bearing free hydroxyl groups. The most potent were anthragallol (1,2,3-trihydroxy-AQ), purpurin (1,2,4-trihydroxy-AQ) and anthraufin (1,5-dihydroxy-AQ). Some hydroxy-AQ compounds exhibited activation by mammalian microsomal preparations, particularly at lower concentrations, and the majority of mutagenic hydroxy-AQs appeared to revert strain TA1537 (his 3076) specifically.(2)Frameshift mutagenesis by certain AQ compounds with primary amino and, in a few cases, with secondary amino groups. Mammalian microsomes invariably potentiated frameshift mutagenesis, and activity with strain TA100 (sensitive to base pair substitution) is seen in a few cases, e.g. 1,2-diamino-AQ. (3)AQ compounds with one or more nitro groups. These derivatives exhibit the least specificity with regard to tester strain reverted and to microsomal activation. All seven nitro-AQ's tested were mutagenic. In those compounds with mixed "mutagenic" functional groups, the type of mutagenesis observed is usually N02 greater than 0H greater than NH2. AQs bearing halogens, sulfonate or alkyl groups were non-mutagenic, as were AQs substituted solely with secondary amines.

Anthraquinones↗