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A From

Publications and source records attributed to A From.

At least 19 recordsLinked to original sources
PubMed1999

Characterization of the mouse Rh blood group gene.

The Rh blood group system is of clinical importance in blood transfusion and as the cause of hemolytic disease of the newborn. Other than their role as carriers of Rh antigens, very little is known about the function of the Rh polypeptides. As a first step to generate an animal model system in which to study the structure and function of Rh, and to extend the phylogenetic analysis of RH genes, the Rh homologue from Mus musculus was characterized. Comparison of RH from humans and mice revealed 71 and 58% sequence identity at the nucleotide and amino acid levels, respectively. Mouse Rh mRNA encodes a protein which is 1 amino acid longer (418 aa) than that of human (417 aa). Rh protein was detected in mouse erythrocyte membranes and was comparable in size to human Rh. Mouse erythrocytes do not show serologic reactivity with human Rh antibodies, probably because the greatest divergence between the mouse and the human genes was seen in the predicted extracellular loops, while the transmembrane regions were more conserved. The mouse RH locus consists of only one gene, which is important for future genetic manipulation and which also indicates that the RH gene duplication seen in humans has occurred since the mammalian radiation.

Amino Acid Sequence↗
PubMed1999

Impedance stroke volume compared with dye and electromagnetic flowmeter values during drug-induced inotropic and vascular changes in dogs.

Stroke volumes measured by impedance were compared with values obtained by dye dilution and an electromagnetic flowmeter (EMF) on 14 dogs during drug-induced changes in cardiac contraction strength and peripheral resistance changes. Grouping all data for a total of 305 points showed correlations between dye and EMF, dye and impedance, and EMF and impedance of 0.89, 0.68, and 0.72, respectively. Correlations for individual dogs between dye and EMF, dye and impedance, and EMF and impedance ranged from 0.60 to 0.99, -0.39 to 0.96, and -0.26 to 0.89, respectively. These data suggest that the use of impedance cardiac output measurements to make treatment decisions about individual patients could result in serious error.

Animals↗
PubMed1991

Auranofin treatment in early rheumatoid arthritis may postpone early retirement. Results from a 2-year double blind trial.

The effect of early vs delayed initiation of slow acting antirheumatic drug (SAARD) therapy on the ability to maintain regular work, was evaluated in 83 patients with early rheumatoid arthritis (RA) in a placebo controlled, double blind 24-month study. The estimated probability to maintain working ability was higher in the early treatment group, especially during the second study year. Predicting factors were age, type of work, degree of disability and number of swollen joints. Despite the difficulties in interpreting the results due to the complexity of the underlying socioeconomical and labor market situation, the study supports early treatment in RA with regard to the maintenance of normal life.

Arthritis, Rheumatoid↗
PubMed1983

Acetylcholine and norepinephrine: compared actions thyroid metabolism.

Acetylcholine (ACh; 5 X 10(-4) M), like norepinephrine (NE; 6 X 10(-6) M), as shown previously, stimulated iodide organification by mouse thyroids in vitro, while at the same time it inhibited TSH- or (Bu)2cAMP-induced T4 release. However, thyroid cAMP was not changed by ACh, suggesting that ACh, like NE, exerted its effects at a step beyond cAMP production. Also, while ACh increased cGMP concentrations, (Bu)2cGMP and 8-bromo-cGMP were not effective on thyroid function in this system. Neurotransmitters, then, presumably do not exert their action through cyclic nucleotide stimulation ACh-induced stimulation of organification and inhibition of release was reversed by 10(-5) M atropine (ATR) but not by 10(-5) M d-tubocurarine, indicating that muscarinic receptors were involved. ATR also reversed inhibition of T4 release induced by NE, suggesting that the presynaptic cholinergic pathway may be responsible for stimulation of postsynaptic cholinergic and adrenergic neurotransmitters in the thyroid gland.

Acetylcholine↗
PubMed1981

Calcium depletion stimulates thyroxine release from the thyroid.

Excised mouse thyroids incubated in Ca++-free medium were stimulated to release increased amounts of stable thyroxine. This stimulation of thyroxine release by incubated thyroid tissue was not additive with TSH or (Bu)2cAMP. It was reversed by norepinephrine through an alpha adrenergic receptor, similar to TSH or (Bu)2cAMP stimulation. Depletion of Ca++ did not result, however, in an increase in the concentration of cAMP in incubated thyroid glands, suggesting that its locus of action was subsequent to TSH stimulation or cAMP production.

Animals↗
PubMed1981

Norepinephrine and thyrotropin effects on the thyroid in vitro: simultaneous stimulation of iodide organification and antagonism of thyroxine release.

Norepinephrine (NE), which has previously been shown to inhibit TSH-induced T4 release by mouse thyroids in vitro, was found to stimulate iodide organification. The concentration of NE (6 X 10(-7) M) necessary to stimulate organification of iodide was 10 times less than the concentration (6 X 10(-6) M) required for inhibition of TSH-induced T4 release. Both actions of NE were exerted through an alpha-adrenergic receptor, since they were inhibited by phentolamine but not by l-propranolol. One milliunit of TSH maximally stimulated T4 release only, but larger amounts (100 mU) also stimulated organification. TSH stimulation of T4 release and organification was not affected by adrenergic antagonists and therefore was not mediated by adrenergic receptors. N6, O2-Dibutyryl cAMP and isobutylmethylxanthine, like TSH, stimulated T4 release. Their actions were inhibited by NE. However, both compounds, unlike TSH, failed to enhance organification in mouse thyroids. The effects of TSH and NE on the cAMP content of incubated mouse thyroids were also studied. TSH induced a prolonged increase in thyroidal cAMP during the 90-min incubation; this increase was unaffected by alpha- or beta-adrenergic antagonists. In contrast, NE (6 X 10(-5) M) produced a transient but significant increase in cAMP only within the first 5 min. Unlike the action of NE on organification, this short term stimulatory effect on cAMP production was mediated by a beta-adrenergic receptor, since it was blocked by l-propranolol but not by phentolamine. The following conclusions were reached: 1) stimulation of iodide organification and thyroid hormone release involves different sensitivity thresholds for TSH and NE; 2) TSH stimulation of iodide organification, hormone release, and cAMP formation is not exerted through adrenergic receptors; 3) NE stimulates organification and inhibits TSH-stimulated T4 release through alpha-adrenergic receptors, but stimulates cAMP production through beta-receptors; and 4) cAMP may not be the mediator of all TSH actions on the thyroid.

1-Methyl-3-isobutylxanthine↗
PubMed1979

Action of gold thioglucose on pericapillary structures in the ventromedial hypothalamus.

The administration of GTG to mice leads to death of all structures in a circumscribed area of the VMH as a result of loss of blood circulation. The loss of circulation is due to damage by GTG of neural processes adjacent to some of the capillaries in this area; damage to these processes leads to abnormal capillary permeability. Pericapillary damage occurs under conditions where capillary damage and consequent necrosis are prevented. Abnormal capillary permeability appears to follow release of a vasoactive substance from the damaged neural processes. Damage to the pericapillary neural processes by GTG is insulin-dependent and is counteracted by glucocorticoids.

Animals↗
PubMed1979

Mediation by serotonin of gold thioglucose-induced necrosis of the ventromedial hypothalamus.

Agents that lower serotonin levels or inhibit serotonin action prevent GTG-indurea and that such damage leads to abnormally increased capillary permeability. Since the VMH is rich in serotonin and since serotonin is a potent oedema-producing agent mice, these findings indicate that the production of necrosis by GTG is mediated by release of serotonin from the damaged pericapillary processes.

Animals↗
PubMed1977

Inhibition of thyrotropin- and dibutyryl cyclic AMP-induced secretion of thyroxine and triiodothyronine by catecholamines.

Thyrotropin (TSH), 1 MU/ml and N6, O2'-dibutyryl adenosine 3',5-cyclic monophosphoric acid (dbcAMP) greatly enhanced the release of thyroxine (T4) and triiodothyronine (T3) from mouse thyroids incubated in vitro. L-Epinephrine (E) and L-norepinephrine (NE) strongly inhibited the TSH and dbcAMP-stimulated release of thyroid hormones; L-isoproterenol (IPNE) exerted a relatively weak inhibition. The inhibition by catecholamines was prevented by the alpha-adrenergic blocker, phentolamine; L-propranolol, a beta-adrenergic blocker, had no effect on the inhibition. The TSH-induced release of thyroid hormones was not affected by adrenergic blockers. Epinephrine did not affect the increase in thyroidal cAMP content induced by TSH. These results indicate that catecholamines act by way of an alpha-adrenergic receptor to suppress TSH-stimulated release of thyroid hormones at a point beyond cAMP formation.

Animals↗
PubMed1976

Morphological changes in liver biopsies from patients with rheumatoid arthritis.

Oxphenisatin is known to induce liver damage and is suspected to cause or perpetuate chronic liver disease. In order to evaluate the hepatotoxic effect of long-term therapy with oxyphenisatin 26 consecutive patients with rheumatoid arthritis were investigated for the presence of liver disease. In all cases, liver biopsy, biochemical liver function tests and determination of Hepatitis-B antigen were performed. Ten patients showed no pathological changes in the liver biopsy and a further 2 had only non-specific changes. Seven patients had fatty liver, 5 passive congestion, one haemosiderosis and only one had cirrhosis of the liver. No correlation was found between the activity of rheumatoid arthritis, and duration of the disease, the drug therapy given, and the liver damage.

Adolescent↗
PubMed1975

A double-blind trial with baclofen (Lioresal) and diazepam in spasticity due to multiple sclerosis.

In 17 in-patients suffering from spasticity due to multiple sclerosis, the effect and tolerability periods were 4 weeks each. As to efficacy, the variables: spasticity, clonus, flexor spasms, gait and bladder function were evaluated clinically. No significant difference was found between the two drugs. As far as side-effects are concerned, sedation was specifically inquired about. Apart from that, spontaneoulsy reported side-effects were recorded. Sedation was more often seen during treatment with diazepam, while the side-effects during baclofen treatment were more varied. The total number and severity of side-effects were equal in the two treatment groups. A preference for one of the two treatment periods was stated by the investigator before the code was broken. A significant difference (p less than 0.001) in favor of Lioresal was found. This is discussed in the light of the fact that no significant difference was found for the individual symptoms or side-effects.

Adult↗