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Biomedical subjects

R J Adams

Publications and source records attributed to R J Adams.

At least 181 records · Page 10Linked to original sources
PubMed1979

Hereditary canine spinal muscular atrophy.

Hereditary canine spinal muscular atrophy is a newly recognized motor neuron disease occurring in Brittany Spaniels. The clinical manifestations, pattern of inheritance, electrodiagnostic findings, and muscle biopsies have features in common with human spinal muscular atrophy. Neuropathological examination discloses some loss of motor neurons in the spinal cord and brainstem. Many of the surviving motor neurons have neurofibrillary swellings in proximal axons, an abnormality similar to that which occurs early in the course of human amyotrophic lateral sclerosis. These axonal swellings are filled with maloriented skeins of neurofilaments. Since the proteins comprising neurofilaments are carried by slow axonal transport, their accumulation within axons suggest that the swellings may result from impaired slow transport, a hypothesis that can be tested in affected Brittany Spaniels. Hereditary canine spinal muscular atrophy is a new genetic, clinical, and pathological entity, and, at present, it appears to be the best currently available animal model of motor neuron disease.

Animals↗
PubMed1979

Magnification radiography of the temporomandibular joint: technical considerations.

The design, application, and advantages of a temporomandibular joint (TMJ) positioning unit adapted to the RSI microfocus manigification system are described. The reasons for improved TMJ images with this system are discussed and the rationale for film-screen choice presented. The issue of patient radiation exposure is also considered. This system provided superior TMJ images at acceptable levels of exposure.

Humans↗
PubMed1979

Chronic active hepatitis in dogs associated with leptospires.

Chronic active hepatitis was diagnosed in five American Foxhounds from one kennel. Spirochetes were demonstrated in the liver in four of the dogs. A rising titer to Leptospira interrogans serovar grippotyphosa was found in the fifth dog, although spirochetes were not demonstrated in tissues. A serologic survey at the kennel revealed evidence of exposure of 6 of 13 dogs to grippotyphosa. This is the first report of an association between chronic active hepatitis leptospiral infection in any species.

Animals↗
PubMed1978

The cerebrospinal fluid in visna, a slow viral disease of sheep.

The temporal development of the CSF abnormalities was examined in visna, a chronic neurological disease caused by a persistent viral infection of sheep. Two types of changes were observed. During the first 30 to 40 days there was an intense mononuclear pleocytosis associated with high protein and proportionately elevated IgG. Later, there was a persistent slight pleocytosis associated with mildly elevated protein which had an increased proportion of IgG and antivisna antibody. These later cellular and protein changes are similar to those found in a number of chronic neurological diseases of man.

Animals↗
PubMed1978

Bioassay of TSH using dog thyroid cells in monolayer culture.

The cAMP response to TSH stimulation in dog thyroid cells in monolayer culture was adapted as a means to assay TSH bioactivity. Of a variety of polypeptide hormones examined, only TSH and LH stimulated thyroid cell cAMP generation, but stimulation by LH probably represented contamination with TSH. Serum was found to be a potent, noncompetitive inhibitor of the thyroid cell cAMP response to TSH stimulation. The inhibitor(s) present in serum was nondialyzable and, on Sephadex G-200 gel filtration, eluted over a wide range between the void volume and the albumin peak. Because of this inhibitory effect of serum, partial purification of TSH from serum was necessary, and was achieved using Sephacryl S-200 gel filtration. Columns were calibrated with human TSH as measured by radioimmunoassay and bovine TSH as measured by bioassay. Intraassay variation of the thyroid cell cAMP response to a 100 microU/ml TSH standard was 9.2%. TSH standards were added to human serum following which the TSH was extracted by gel filtration and assayed for bioactivity. With TSH standards of 100 microU/ml intra-assay variation was 19.9%; and with TSH standards of 25 microU/ml, interassay variation was 34.5%. TSH bioactivity was demonstrable in serum from 21 of 25 patients with primary hypothyroidism, 4 of 14 normal subjects and none of 3 patients on exogenous thyroxine replacement. Although a positive correlation was observed between serum TSH bioactivity and immunoactivity, numerous individual samples displayed a dichotomy between the two measurements. This study provides new evidence that immunoassayable TSH in the serum of patients with primary hypothyroidism is not necessarily synonymous with TSH bioactivity.

Animals↗
PubMed1977

Cultured thyroid cell adenosine 3',5'-cyclic monophosphate response to thyrotropin: loss and restoration of sensitivity to iodide inhibition.

Unlike in all other thyroid preparations, exposure of dog thyroid cells in long-term monolayer culture to iodide (10(-7) to 10(-3) M for up to 19 h did not blunt the subsequent adenosine 3', 5'-cyclic monophosphate (cAMP) response to thyrotropin (TSH) stimulation. This lack of effect of iodide was observed even when confluent thyroid cells were "follicularized" by the action of TSH in the culture medium. Preincubation of these cells in thyroxine (T4) and triiodothyronine (T3) was similarly without effect on the subsequent cAMP response to TSH. Study of thyroid cells during the early phase of primary culture demonstrated that inhibition by iodide (10(-4) M) of the cAMP response to TSH occurred after 7 h but was lost after 48 h of cell culture. This inhibitory effect of iodide was prevented by the inclusion of methimazole in the preincubation medium. As with iodide-insensitive cells, T4 and T3 were without effect on the cAMP response to TSH in iodide-sensitive thyroid cells. Exposure of iodide-insensitive thyroid cells to iodide-containing medium obtained after 2 h of incubation with dog thyroid slices, as well as to medium enriched with the 100,000 g supernatant fraction of homogenates prepared from these thyroid slices, did not restore the inhibitory action of iodide. However, iodide-sensitivity of the cAMP response to TSH was restored by preincubation of iodide-insensitive cells in 10(-4) M iodide plus an H2O2-generating system (glucose-glucose oxidase). These data suggest that T4 and T3 are not organic iodine inhibitors of the thyroid cAMP response to TSH. In addition, they provide evidence against the existence of a soluble, freely diffusible, organic iodine inhibitor of thyroid adenylate cyclase. The loss of sensitivity to iodide inhibition of adenylate cyclase that occurs in thyroid cells shortly after initiation of primary culture appears to be related to a defect in the cellular organification mechanism, possibly the H2O2-generating system.

Adenylyl Cyclases↗
PubMed1976

Induction of refractoriness to thyrotropin stimulation in cultured thyroid cells. Dependence on new protein synthesis.

Cultured dog thyroid cells were used to investigate the mechanism by which previous exposure to thyrotropin (TSH) induces refractoriness to further TSH stimulation of cellular adenosine 3'-5'-monophosphate (cAMP). Refractoriness of the cAMP response to TSH could not be overcome by exposure of the cells to supramaximal stimulatory concentrations of TSH. Although an unknown factor present in human and fetal calf serum was found to inhibit the thyroid cell cAMP response to TSH, this factor could not account for refractoriness because refractoriness could be induced in the absence of serum. Induction of thyroid refractoriness did not appear to be related to cellular concentrations of cyclic AMP, because equal refractoriness was produced by TSH alone or TSH plus the phosphodiesterase inhibitor, 3-isobutyl-1-methyl xanthine. In addition, preincubation of thyroid cells in 10(-4) M cAMP did not result in subsequent refractoriness. Recovery from the refractory process required almost 24 h. Short term (15 min) stimulation with TSH did not produce thyroid cell refractoriness, and reversal of the stimulation was obtained by thorough washing of the cells. Long term TSH stimulation (16 h), however, resulted in both supramaximal cAMP response to TSH, and inclusion of TSH together with cycloheximide did not produce refractoriness. Cyclic AMP phosphodiesterase activity in thyroid cell homogenate was unaltered by TSH or dibutyryl cyclic AMP pretreatment of the cells for up to 24 h, or cycloheximide for up to 4 h. In contrast, TSH-stimulated, but not F--stimulated, adenylate cyclase activity was reduced in thyroid cell homogenates after preincubation of the cells in TSH. Refractoriness to TSH stimulation was not associated with an alteration in the binding of 125I-TSH to cultured thyroid cells. These studies suggest that the thyroid cAMP response to TSH is modulated by an inhibitory mechanism dependent upon new protein synthesis. TSH stimulation itself increases the degree of this inhibition through a mechanism not involving cAMP.

Animals↗
PubMed1976

An analysis of the mechanisms of egg transport in the ampulla of the rabbit oviduct.

Ampullary transport of supravitally stained cumulus egg masses was studied in intact oviducts of anesthetized rabbits whose abdomens had been opened for observation. Following observations of normal transport, muscular activity of the ampulla was inhibited pharmacologically with Acepromazine, a preanesthetic tranquilizer. With muscle contractions blocked, egg transport continued but in a dramatically altered fashion; in the final two thirds of the ampulla the motion changed from rapid to-and-fro movements to a slow uniform prouterine movement which was attributed to ciliary activity. However, the net velocity of transport did not change when the smooth muscle was inhibited indicating that muscle contractions are at least unnecessary and perhaps ineffective for ampullary egg transport in the rabbit.

Acepromazine↗
PubMedDate not supplied

Rapid transport of foreign particles microinjected into crab axons.

The rapid transport of optically detectable organelles in axons has been well documented, although its molecular mechanism remains unknown. Here we report that synthetic particles microinjected into the giant axons of the shore crab, Carcinus maenas, are also transported, moving as though they were endogenous organelles. Polystyrene beads, polyacrolein beads, paraffin droplets and glass fragments, of sizes up to 0.5 micron in diameter, have been tested. Many of these foreign particles move rapidly and for long distances along the axon in the anterograde direction, travelling in a saltatory fashion, within a well defined velocity range. In many respects the movements are indistinguishable from those of anterogradely moving endogenous organelles seen by phase-contrast in these axons. Our results indicate that there is a transport system in axons capable of carrying almost any particle of suitable physical properties in an anterograde direction.

Acrolein↗