Disease relevance of Sart1

• Mechanism of hyperalgesia in SART stressed (repeated cold stress) mice: antinociceptive effect of neurotropin [1].
• In order to hematologically characterize SART-stressed (repeated cold-stressed) animals, which are regarded as model animals of clinical dysautonomia, general hematological analyses were performed in mice subjected to various types of stress [2].
• Changes of both gastric and dermal blood flow in SART-stressed mice were dose-dependently prevented and maintained within normal limits by the treatment with Neurotropin, a sedative analgesic which is an extract isolated from vaccinia virus-inoculated and inflamed skin of rabbits [3].
• Splenectomy failed to inhibit the SART stress-induced thrombocytopenia [2].

Psychiatry related information on Sart1

• Decrease in pain threshold in SART stressed mice [4].

High impact information on Sart1

• Intron loss in the SART1 genes of Fugu rubripes and Tetraodon nigroviridis [5].
• We have examined the genomic structure and cDNA sequence of the SART1 gene in the compact genomes of the pufferfish Fugu rubripes and Tetraodon nigroviridis [5].
• The entire coding regions of both the Fugu and Tetraodon SART1 genes are contained within single exons [5].
• The behavior of SART-stressed mice in the plus-maze would thus appear to arise from anxiety, to which benzodiazepine and serotonin receptors are related, but the diazepam binding inhibitor, an endogenous anxiogenic protein, is not [6].
• Shortening of immobility time in SART-stressed mice was inhibited by diazepam and repeated imipramine but not by lithium carbonate [7].

Biological context of Sart1

• Among the above changes, the decreased platelet count was particularly characteristic of SART-stressed mice [2].
• The bleeding time of SART-stressed mice was more than double that of normal mice [2].
• Active oxygens would thus appear to be, at least partially, involved in the development of abnormal hemostasis induced by SART stress [8].
• SART-stressed mice showed significant increases in erythrocyte count, hemoglobin, hematocrit and specific gravity of whole blood, no change in leukocyte count and a marked decrease in platelet count [2].

Anatomical context of Sart1

• From the present results, it is suggested that SART-stressed mice may be characterized by thrombocytopenia, which is not attributable to enhanced function of the spleen or suppressed platelet production in the bone marrow [2].
• Consecutive administrations of Neurotropin, a sedative analgesic, completely blocked the alterations in platelet count, megakaryocyte count and bleeding time in SART-stressed mice without producing any effect in unstressed mice [2].
• The pre-administration of psychotropic drugs showed marked suppression on the enhancement of response of the duodenum of the RWIS animal, though there was a quantitative difference between the RWIS and SART animals [9].
• The relationship of hyperalgesia in SART (repeated cold)-stressed animals to the autonomic nervous system [10].
• 4. Lesion of ventromedial (VMH), anterior (AH) or posterior hypothalamus (PH) prevented decrease in the nociceptive threshold of rats by SART stress, but lesion of the lateral hypothalamus (LH) had no such effect [10].

Associations of Sart1 with chemical compounds

• In contrast, neither single nor repeated administrations of lithium carbonate had effect on the immobility time of SART-stressed mice [11].
• Subsensitivity to substance P in SART-stressed mice [12].
• Mild DIC-like phenomena develop in rodents exposed to environmental stress, induced by prolonged fluctuation in ambient temperature, known as SART (specific alternation of rhythm in temperature) stress, the symptoms being essentially similar to those produced by endotoxin [13].
• 2) Haloperidol, phenoxybenzamine, reserpine, bicuculline, scopolamine, physostigmine and naloxone alone did not influence the nociceptive threshold in SART stressed mice [1].
• 1) Neurotropin, 5-hydroxytryptophan and L-dihydroxyphenylalanine significantly normalized the decrease in nociceptive threshold, and muscimol tended to inhibit it in nociceptive threshold in SART stressed mice [1].

Analytical, diagnostic and therapeutic context of Sart1

• Sequence analysis of genes encoding rodent homologues of the human tumor-rejection antigen SART-1 [14].
• These rodent genes should be a novel tool for studies on the biological roles of the SART-1 gene, and also in the construction of animal models of specific immunotherapy using SART-1 gene products [14].
• Southern blot hybridisation of Fugu genomic DNA confirmed the SART1 gene to be single copy [5].
• When mice were loaded with SART stress after left-cervical vagotomy, SART stress failed to elicit any decrease in gastric blood flow [3].
• Both immobility time in the forced swimming test and time spent in open arms in the elevated plus-maze test in unstressed and SART-stressed mice were unaffected by adrenalectomy [15].

References