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51.
Y.R. Song B. Wu Y.T. Yang J. Chen L.J. Zhang Z.W. Zhang H.Y. Shi C.L. Huang J.X. Pan P. Xie 《Brazilian journal of medical and biological research》2015,48(11):973-982
Bipolar disorder (BD) is a common psychiatric mood disorder affecting more than 1-2%
of the general population of different European countries. Unfortunately, there is no
objective laboratory-based test to aid BD diagnosis or monitor its progression, and
little is known about the molecular basis of BD. Here, we performed a comparative
proteomic study to identify differentially expressed plasma proteins in various BD
mood states (depressed BD, manic BD, and euthymic BD) relative to healthy controls. A
total of 10 euthymic BD, 20 depressed BD, 15 manic BD, and 20 demographically matched
healthy control subjects were recruited. Seven high-abundance proteins were
immunodepleted in plasma samples from the 4 experimental groups, which were then
subjected to proteome-wide expression profiling by two-dimensional electrophoresis
and matrix-assisted laser desorption/ionization-time-of-flight/time-of-flight tandem
mass spectrometry. Proteomic results were validated by immunoblotting and
bioinformatically analyzed using MetaCore. From a total of 32 proteins identified
with 1.5-fold changes in expression compared with healthy controls, 16 proteins were
perturbed in BD independent of mood state, while 16 proteins were specifically
associated with particular BD mood states. Two mood-independent differential
proteins, apolipoprotein (Apo) A1 and Apo L1, suggest that BD pathophysiology may be
associated with early perturbations in lipid metabolism. Moreover, down-regulation of
one mood-dependent protein, carbonic anhydrase 1 (CA-1), suggests it may be involved
in the pathophysiology of depressive episodes in BD. Thus, BD pathophysiology may be
associated with early perturbations in lipid metabolism that are independent of mood
state, while CA-1 may be involved in the pathophysiology of depressive episodes. 相似文献
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Imaging chemical exchange saturation transfer (CEST) effects following tumor‐selective acidification using lonidamine 下载免费PDF全文
Increased lactate production through glycolysis in aerobic conditions is a hallmark of cancer. Some anticancer drugs have been designed to exploit elevated glycolysis in cancer cells. For example, lonidamine (LND) inhibits lactate transport, leading to intracellular acidification in cancer cells. Chemical exchange saturation transfer (CEST) is a novel MRI contrast mechanism that is dependent on intracellular pH. Amine and amide concentration‐independent detection (AACID) and apparent amide proton transfer (APT*) represent two recently developed CEST contrast parameters that are sensitive to pH. The goal of this study was to compare the sensitivity of AACID and APT* for the detection of tumor‐selective acidification after LND injection. Using a 9.4‐T MRI scanner, CEST data were acquired in mice approximately 14 days after the implantation of 105 U87 human glioblastoma multiforme (GBM) cells in the brain, before and after the administration of LND (dose, 50 or 100 mg/kg). Significant dose‐dependent LND‐induced changes in the measured CEST parameters were detected in brain regions spatially correlated with implanted tumors. Importantly, no changes were observed in T1‐ and T2‐weighted images acquired before and after LND treatment. The AACID and APT* contrast measured before and after LND injection exhibited similar pH sensitivity. Interestingly, LND‐induced contrast maps showed increased heterogeneity compared with pre‐injection CEST maps. These results demonstrate that CEST contrast changes after the administration of LND could help to localize brain cancer and monitor tumor response to chemotherapy within 1 h of treatment. The LND CEST experiment uses an anticancer drug to induce a metabolic change detectable by endogenous MRI contrast, and therefore represents a unique cancer detection paradigm which differs from other current molecular imaging techniques that require the injection of an imaging contrast agent or tracer. Copyright © 2015 John Wiley & Sons, Ltd. 相似文献
55.
J. C. Sun M. Xu J. L. Lu Y. F. Bi Y. M. Mu J. J. Zhao C. Liu L. L. Chen L. X. Shi Q. Li T. Yang L. Yan Q. Wan S. L. Wu Y. Liu G. X. Wang Z. J. Luo X. L. Tang G. Chen Y. N. Huo Z. N. Gao Q. Su Z. Ye Y. M. Wang G. J. Qin H. C. Deng X. F. Yu F. X. Shen L. Chen L. B. Zhao T. G. Wang S. H. Lai D. H. Li W. Q. Wang G. Ning 《Diabetic medicine》2015,32(7):935-943
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