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  • Atomic and molecular structure and dynamics  (3)
  • Translational Highlights from ENDO, TRANSLATIONAL RESEARCH IN ENDOCRINOLOGY AND METABOLISM  (2)
  • ACE/Angiotension receptors, Other etiology  (1)
  • 2020-2023
  • 2010-2014  (6)
  • 1
    Publication Date: 2011-03-26
    Description: Author(s): L. M. Wang, Z.-C. Yan, H. X. Qiao, and G. W. F. Drake We present improved calculations of variational energy eigenvalues for the 1s^{2} 2s ^{2} S, 1s^{2} 3s ^{2} S, and 1s^{2} 2p ^{2} P states of lithium using basis sets with up to 30 224 terms in Hylleraas coordinates. The nonrelativistic energies for infinite nuclear mass are -7.478 060 32... [Phys. Rev. A 83, 034503] Published Fri Mar 25, 2011
    Keywords: Atomic and molecular structure and dynamics
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 2
    Publication Date: 2013-04-30
    Description: Author(s): Yin Tang, Liming Wang, Xuanyu Song, Xiaofeng Wang, Z.-C. Yan, and Haoxue Qiao The variational method in Hylleraas coordinates is applied to calculate the 1 s 2 2 s 0 , 1 s 2 2 p −1 , and 1 s 2 3 d −2 states of the lithium atom in magnetic fields with field strength up to 2×10 9 G. The computational method is based on multiple basis sets that are optimized for all nonlinear parameters for a giv... [Phys. Rev. A 87, 042518] Published Mon Apr 29, 2013
    Keywords: Atomic and molecular structure and dynamics
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 3
    Publication Date: 2012-11-28
    Description: Melanin-concentrating hormone (MCH) is a peptide produced in the hypothalamus and the zona incerta that acts on one receptor, MCH receptor 1 (MCH1R), in rodents. The MCH system has been implicated in the regulation of several centrally directed physiological responses, including the hypothalamus-pituitary-thyroid axis. Yet a possible direct effect of the MCH system on thyroid function has not been explored in detail. We now show that MCH1R mRNA is expressed in thyroid follicular cells and that mice lacking MCH1R [ MCH1R -knockout (KO)] exhibit reduced circulating iodothyronine (T 4 , free T 4 , T 3 , and rT 3 ) levels and high TRH and TSH when compared with wild-type (WT) mice. Because the TSH of MCH1R -KO mice displays a normal bioactivity, we hypothesize that their hypothyroidism may be caused by defective thyroid function. Yet expression levels of the genes important for thyroid hormones synthesis or secretion are not different between the MCH1R -KO and WT mice. However, the average thyroid follicle size of the MCH1R -KO mice is larger than that of WT mice and contained more free and total T 4 and T 3 than the WT glands, suggesting that they are sequestered in the glands. Indeed, when challenged with TSH, the thyroids of MCH1R -KO mice secrete lower amounts of T 4 . Similarly, secretion of iodothyronines in the plasma upon 125 I administration is significantly reduced in MCH1R -KO mice. Therefore, the absence of MCH1R affects thyroid function by disrupting thyroid hormone secretion. To our knowledge, this study is the first to link the activity of the MCH system to the thyroid function.
    Keywords: Translational Highlights from ENDO, TRANSLATIONAL RESEARCH IN ENDOCRINOLOGY AND METABOLISM
    Print ISSN: 0013-7227
    Topics: Medicine
    Published by Oxford University Press on behalf of The Endocrine Society.
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  • 4
    Publication Date: 2012-05-25
    Description: Author(s): L. M. Wang, Z.-C. Yan, H. X. Qiao, and G. W. F. Drake Nonrelativistic energies for the low-lying states of lithium are calculated using the variational method in Hylleraas coordinates. Variational eigenvalues for the infinite nuclear mass case with up to 34 020 terms are −7.478 060 323 910 147(1) a.u. for 1 s 2 2 s   2   S , −7.354 098 421 444 37(1) a.u. for 1 s ... [Phys. Rev. A 85, 052513] Published Thu May 24, 2012
    Keywords: Atomic and molecular structure and dynamics
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 5
    Publication Date: 2014-12-11
    Description: The dopaminergic and renin–angiotensin systems interact to regulate blood pressure. Disruption of the D 4 dopamine receptor gene in mice produces hypertension that is associated with increased renal angiotensin type 1 (AT 1 ) receptor expression. We hypothesize that the D 4 receptor can inhibit AT 1 receptor expression and function in renal proximal tubule cells from Wistar–Kyoto (WKY) rats, but the D 4 receptor regulation of AT 1 receptor is aberrant in renal proximal tubule cells from spontaneously hypertensive rats (SHRs). The D 4 receptor agonist, PD168077, decreased AT 1 receptor protein expression in a time- and concentration-dependent manner in WKY cells. By contrast, in SHR cells, PD168077 increased AT 1 receptor protein expression. The inhibitory effect of D 4 receptor on AT 1 receptor expression in WKY cells was blocked by a calcium channel blocker, nicardipine, or calcium-free medium, indicating that calcium is involved in the D 4 receptor–mediated signaling pathway. Angiotensin II increased Na + -K + ATPase activity in WKY cells. Pretreatment with PD168077 decreased the stimulatory effect of angiotensin II on Na + -K + ATPase activity in WKY cells. In SHR cells, the inhibitory effect of D 4 receptor on angiotensin II–mediated stimulation of Na + -K + ATPase activity was aberrant; pretreatment with PD168077 augmented the stimulatory effect of AT 1 receptor on Na + -K + ATPase activity in SHR cells. This was confirmed in vivo; pretreatment with PD128077 for 1 week augmented the antihypertensive and natriuretic effect of losartan in SHRs but not in WKY rats. We suggest that an aberrant interaction between D 4 and AT 1 receptors may play a role in the abnormal regulation of sodium excretion in hypertension.
    Keywords: ACE/Angiotension receptors, Other etiology
    Print ISSN: 0194-911X
    Topics: Medicine
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  • 6
    Publication Date: 2013-05-18
    Description: Antiestrogens such as tamoxifen (TAM) provided a successful treatment for estrogen receptor (ER)-positive breast cancer for the past four decades. However, most breast tumors are eventually resistant to TAM therapy. The molecular mechanisms underlying TAM resistance have not been well established. Recently, we reported that breast cancer patients with tumors expressing high concentrations of ER-α36, a variant of ER-α, benefited less from TAM therapy than those with low concentrations of ER-α36, suggesting that increased ER-α36 concentration is one of the underlying mechanisms of TAM resistance. Here, we investigated the function and underlying mechanism of ER-α36 in TAM resistance. We found that TAM increased ER-α36 concentrations, and TAM-resistant MCF7 cells expressed high concentrations of ER-α36. In addition, MCF7 cells with forced expression of recombinant ER-α36 and H3396 cells expressing high concentrations of endogenous ER-α36 were resistant to TAM. ER-α36 down-regulation in TAM-resistant cells with the short hairpinRNA method restored TAM sensitivity. We also found that TAM acted as a potent agonist by activating phosphorylation of the AKT kinase in ER-α36-expressing cells. Finally, we found that cells with high concentration of ER-α36 protein were hypersensitive to estrogen, activating ERK phosphorylation at picomolar range. Our results thus demonstrated that elevated ER-α36 concentration is one of the mechanisms by which ER-positive breast cancer cells escape TAM therapy and provided a rational to develop novel therapeutic approaches for TAM-resistant patients by targeting ER-α36.
    Keywords: Translational Highlights from ENDO, TRANSLATIONAL RESEARCH IN ENDOCRINOLOGY AND METABOLISM
    Print ISSN: 0013-7227
    Topics: Medicine
    Published by Oxford University Press on behalf of The Endocrine Society.
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