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Chemical Compound Review

Decaject     (8S,9S,10S,11S,13S,14S,16R,17R )-9-fluoro...

Synonyms: Decameth, Dexasone, Hexadrol, Oradexon, Decaspray, ...
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Disease relevance of Dectancyl


Psychiatry related information on Dectancyl

  • CONCLUSIONS: The dex/CRH test is abnormal in both remitted and non-remitted patients with bipolar disorder [6].
  • In a first series of studies a refined neuroendocrine test to probe the integrity of HPA system status--the combined dexamethasone suppression/CRH challenge (DEX/CRH) test--was developed and the differential effects of aging and depressed psychopathology on DEX/CRH test outcome were described [7].

High impact information on Dectancyl


Chemical compound and disease context of Dectancyl


Biological context of Dectancyl

  • Together, these data support the hypothesis that resistance to Dxm-induced apoptosis in NOD immature thymocytes is controlled by a genetic factor within the region that also contributes to type 1 diabetes pathogenesis [15].
  • Herein, we refine this phenotype using a time-course experiment of apoptosis induction upon Dxm treatment [15].
  • RESULTS: NIM had no effect on the number of GR binding sites, in contrast to NAP and DEX [1].
  • Extent of the expression of neuron-associated properties in several cell clones after the addition of dexamethazone (DEX) seems to correlate well with the levels of the v-Ha-ras gene expression [16].
  • The inhibition of cellular proliferation which occurs at 48 h after release in the dex-treated CEM-C7 cells was preceded by an inhibition of acetate incorporation into cholesterol, first evident at 24 h, inhibition of protein synthesis at 30 h, and the development of a cell cycle block in G1 at 36 h [4].

Anatomical context of Dectancyl

  • In nontransfected wild-type NIH 3T3 cells, DEX did not induce DDP resistance nor did it decrease DDP accumulation [10].
  • After the induction of v-Ha-ras expression with DEX in these cell lines, sustained elevation of the levels of cAMP as well as of phosphatidylinositol (PtdIns) metabolites, inositol trisphosphate, and diacylglycerol, is observed [16].
  • DEX treatment increased adrenal gland cholesteryl ester and oil red O staining in z. fasciculata cells in which the apoE mRNA concentration was increased as well as in other cortical cells in which apoE mRNA was unchanged [17].
  • These cells accumulate lipids and differentiate into adipocytes when treated with insulin, triiodothyronine and dexamethazone [18].
  • 3H-RU 486 binds with high affinity (KDeq approximately 0.4 nM) to the same high affinity receptor-binding sites as dex (KD approximately 0.5 nM) in the cell cytosol, as indicated by Scatchard plot, gradient-ultracentrifugation and competition studies [19].

Associations of Dectancyl with other chemical compounds

  • Despite no difference in basal pituitary-adrenal activity or in their ACTH and cortisol responses to CRH, LBW men had significantly lower pituitary-adrenal responses in the DEX/CRH test [20].
  • When HeLa cells were treated with both estradiol and Dex, the steroids counteracted each other's transcriptional effects [21].
  • When administered in combination with RU486, dex partially reversed the increased uterine intraluminal fluid retention at 0900 h estrus, but did not modify the inhibitory effect of RU486 on the primary gonadotropin surges or the secondary surge of FSH [22].
  • Moreover, the simultaneous injection of DEX and progesterone yielded an additive effect on the relative rates of ovalbumin and conalbumin gene transcription [23].
  • The CRH part of the DEX/CRH-test outcome might indicate the loss of endogenous CRH-Arginine-Vasopressin (AVP) synergism of the HPA system of these patients [24].

Gene context of Dectancyl


Analytical, diagnostic and therapeutic context of Dectancyl

  • In frozen sections, the GR immunoreactivity in cell nuclei was weak in the absence and very strong in the presence of Dex, while no GR-specific cytoplasmic staining was observed [28].
  • Northern blot analysis showed marked blunting of mRNA expression in RMC treated with DX, in concordance with functional studies [29].
  • Quantitative Western blot analysis and immunocytochemistry indicated that ACTH and 17alpha-E2 treatment greatly increased SR-BI expression in the adrenal (especially in the microvillar compartment of adrenocortical cells), whereas DEX treatment led to a decrease of SR-BI by all measurements [30].
  • The inhibitory effect of DX was confirmed using a reporter cell bioassay, whereas cGMP was measured as a reflection of bioactive NO [29].
  • Male Sprague-Dawley rats (3 or 24 mo old) were divided into seven groups: three groups received 1.5 mg/kg of DEX once a day by intraperitoneal injection for 3, 5, or 7 days; three groups were pair fed to the three treated groups, respectively; and one control group of healthy rats was fed ad libitum [31].


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