- Chinese︱Feedback︱Save this page
Get RSS feed
Check out RSS, or use RSS reader to subscribe this item 
Confirmation
Authentication email has already been sent, please check your email box: and activate it as soon as possible.
You can login to My Profile and manage your email alerts.
If you haven’t received the email, please:
- Login︱Register
|
|
|
 |
|
||
| There are 181 papers published in subject: since this site started. | |||
| Select Subject |
| Select/Unselect all | For Selected Papers |
Saved Papers
Please enter a name for this paper to be shown in your personalized Saved Papers list
|
 |
| 1. Discussion on the Calculation of Absolute Bioavailability | |||
| Jiang Wei,Yang Juan-juan,Cao Lei,Shi Xiao-lian,Cao Yong-xiao* | |||
Basic Medicine 18 April 2015
|
|||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:The absolute bioavailability (F) is defined as the ratio of drug amounts between being absorbed and the total amount of drug being administrated one after extravascular administration. It is calculated as the ratio of area under plasma drug concentration-time curve (AUC) between the extravascular administration and the intravenous injection. However, the distribution of a drug after intravenous administration does not reach balance in the body when the plasma drug concentration declines sharp at the distribution phase. Therefore, at this phase plasma drug concentration can't reflect the total drug amount in body. The goal of the present investigation was to analyze its insufficient and give a modification. The literatures about absolute bioavailability were searched by the keyword "absolute bioavailability" in "Pubmed" from 1983 to 2014. The data on plasma drug concentration were obtained from literatures directly or recovered from the concentration-time curve by Microsoft Paint. The plasma drug concentrations were calculated at each time point at the distribution phase according to the plasma drug concentration-time relationship at elimination phase, which represent the drug amount in body. The AUC basing on the drug concentrations in distribution balance after intravenous injection was 75%±11% of the one basing on actual measured drug concentrations in literatures. The absolute bioavailability from the literatures was 76%±12% of the actual one basing on the AUC from distribution balanced drug concentrations. Therefore, the present method underestimating absolute bioavailability should be corrected. | |||
| TO cite this article:Jiang Wei,Yang Juan-juan,Cao Lei, et al. Discussion on the Calculation of Absolute Bioavailability[OL].[18 April 2015] http://en.paper.edu.cn/en_releasepaper/content/4638715 | |||
| 2. Low SNR signal automatic quantification in magnetic resonance spectroscopy data | |||
| LI Yao | |||
| Basic Medicine 28 January 2015
|
|||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:The quantification of magnetic resonance spectroscopy (MRS) signals remains challenging due to the low signal-to-noise ratio (SNR) of data. Time-domain quantification methods highly require user interactions, which reduce the reproducibility of the data quantification results. The goal of our work is to design a systematic methodology for automated quantification of MRS signals with low SNRs. We used Hankel singular value decomposition (HSVD) algorithm in our signal estimation step, along with extraction and reduction filter (ER-filter) as a frequency selective technique in the preprocessing step in order to avoid the interferences from nuisance peaks. In the automatic model order selection problem of HSVD, we implemented three strategies based on reconstruction residue measurement or information theoretic criteria. The performances were evaluated in terms of detection rate and relative root mean squared error (RRMSE). The simulations were run on both synthesized and semi-synthesized data. We tested the strategies in two cases, i.e., without and with an interfering signal nearby the signal of interest. It is shown that the minimum description length with condition (MDLcon) based methodology we proposed performs the best and can obtain reliable estimation performance (RRMSE<40%) when signal SNR is larger than -18dB, with a detection rate above 72.44%. The performance is consistent when the interfering signal is 0.08ppm separated. Overall, the MDLcon based automated MRS signal quantification methodology provides an effective way for low SNR MRS signal estimation and detection. Our work may shed light on automatic MRS signal quantification in clinical applications when the corresponding metabolite concentration is low. | |||
| TO cite this article:LI Yao. Low SNR signal automatic quantification in magnetic resonance spectroscopy data[OL].[28 January 2015] http://en.paper.edu.cn/en_releasepaper/content/4631195 | |||
| 3. Brain Activation Study during Stroke Recovery Using BOLD-fMRI | |||
| LI Yao | |||
| Basic Medicine 28 January 2015 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Stroke recovery involves a battery of plastic changes in the brain. Blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI) technology provides brain activation information with exquisite spatial resolution as a powerful tool for investigating changes in brain plasticity. In this paper, we performed a longitudinal study examining plasticity of functional activation as exhibited by BOLD-fMRI following stroke. Data were collected from 11 patients with corticospinal tract (CST) damage at three stages of recovery, i.e., acute stage (<2wks), early stage (1mon-3mons) and chronic stage (>3mons) post stroke. The evolution of cortical activations for both affected and unaffected hand motion tasks were studied. Quantitative activation measurements including the effective size and sum of t values were calculated and the correlations of these values with patient Fugl-Meyer index were analyzed across all stages. Stroke patients showed a shift from bilateral activation in acute and early stage to the ipsilesional activation in chronic stage when performing a movement task with the affected hand, which suggests a compensation effect from the contralesional hemisphere during the recovery process. The correlation analysis showed a significantly negative correlation with cingulate cortex activity at early stage from both quantitative activation measurements, implying the important role of cingulate cortex in stroke recovery. Further investigations are in need to improve the understanding of functional recovery in stroke patients. | |||
| TO cite this article:LI Yao. Brain Activation Study during Stroke Recovery Using BOLD-fMRI[OL].[28 January 2015] http://en.paper.edu.cn/en_releasepaper/content/4631071 | |||
| 4. Inhibition of GSK-3β activity decreases photoreceptor cell death in rat retina | |||
| Wang Baoying,Hu Chenghu,Feng Yan,Li Hongbo,Du Fangying,Zhu Chunhui,Yu Xiaorui | |||
| Basic Medicine 27 January 2015 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Photoreceptor cell death leading to retinal degeneration could be induced by physical or chemical treatments. However, the progress of photoreceptor cell death and underlying cellular and molecular mechanisms remain largely unexplored. Our previous studies have shown that Phosphatidylinositol-3-kinase (PI3K) signaling could mediate the effect of 17β-Estradiol (βE2) which protects photoreceptor cells from death. In present study, we report a novel finding that phosphorylation of glycogen synthase kinase-3β (GSK-3β) controlled by PI3K/Akt signaling is a potent mediator in photoreceptor cell death. In two different animal models of retinal degeneration, light-damaged or N-Methyl-N-nitrosourea (MNU)-induced, GSK-3β phosphorylation was inhibited. Furthermore, phosphorylating Ser9 of GSK-3β with Lithium chloride (LiCl) was able to protect photoreceptor cells, whereas inhibition of the PI3K/Akt with LY294002 which decreases GSK-3β phosphorylation could not protect retinal cells from death. Our results suggest GSK-3β activity is closely related to photoreceptor cell death, and the application of GSK-3β inhibitor LiCl can reduce photoreceptor cell death in retinal degeneration. | |||
| TO cite this article:Wang Baoying,Hu Chenghu,Feng Yan, et al. Inhibition of GSK-3β activity decreases photoreceptor cell death in rat retina[OL].[27 January 2015] http://en.paper.edu.cn/en_releasepaper/content/4630222 | |||
| 5. Evaluation of Scutellaria barbata D.Don ethanol extract and its components on antitumor effects of low dose 5-fluorouracil against hepatocellular carcinoma cells | |||
| XU Huanli,DU Guanhua | |||
Basic Medicine 30 December 2014
|
|||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Background: Some compounds derived from Chinese medicine have demonstrated prospective roles in sensitization to chemotherapy. Aim: This study aimed to investigate Scutellaria barbata D.Don ethanol extract (SBEE) and its components on antitumor effects of low dose 5-fluorouracil against hepatocellular carcinoma cells. Methods: The antitumor effects of SBEE and its components, and their combinations with 5-FU were detected by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium/phenazine methosulfate assay, and the effects of drug combinations were evaluated using Jin's formula. Results:SBEE and luteolin could inhibit tumor growth in time and dose dependent manners. Drug combination study showed that SBEE and luteolin could synergize the antitumor effects of 5-fluorouracil at different dose ratios against HepG2 and Bel-7402 cells.Conclusion: SBEE and luteolin showed synergistic antitumor effects when combined with low dose 5-FU, and the mechanism of the synergistic effect remains to be to be studied. | |||
| TO cite this article:XU Huanli,DU Guanhua. Evaluation of Scutellaria barbata D.Don ethanol extract and its components on antitumor effects of low dose 5-fluorouracil against hepatocellular carcinoma cells[OL].[30 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4625638 | |||
| 6. Autophagy-mediated HMGB1 release promotes survival of gastric cancer cells via the activation of ERK1/2 MAPK kinases | |||
| ZHANG Qiuyu,WU Linqing,HAN Yangfei,XU weiqun,ZHANG Tao | |||
| Basic Medicine 25 December 2014 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:OBJECT: To investigate the effect of extracellular high-mobility group box 1（HMGB1）on cell proliferation and signaling pathway in human gastric cancer cell. Methods: Immunohistochemistry and immunocytochemistry localized HMGB1 in gastric cancer tissues and gastric carcinoma cell lines. The protein level of microtubule light chain 3（LC3-I, LC3-II）and the formation of autophagic vesicles in gefitinib -induced BGC-823 cells were assessed by western blotting and confocal microscopy respectively. Western blot and ELISA were used to assess the effects of gefitinib, an epidermal growth factor receptor inhibitor, on autophagy and HMGB1 release in BGC-823 cells. MTT and Western blot assessed the effects of extracellular HMGB1 on cell proliferation and signaling transduction. Results: Released HMGB1 promoted proliferation through activation of ERK1/2 MAPK. HMGB1 expression in gastric cancer tissue and serum was significantly increased compared to control and healthy serum. Gastric carcinoma cells showed elevated HMGB1 in nuclei and cytoplasm, whereas GES-1 cells exhibited lower HMGB1 with nuclear localization. Gefitinib increased autophagy and cytoplasmic HMGB1 release from BGC-823 cells. Extracellular HMGB1 in autophagic cell supernatant promoted proliferation that was abolished by glycyrrhizic acid, an HMGB1 inhibitor. BGC-823 cells incubated with HMGB1 increased ERK1/2 phosphorylation, but did not affect JNK, p38 or AKT. Blocking RAGE-HMGB1 interaction with antibody or siRNA suppressed ERK1/2 activation and gastric cancer cell growth, indicating RAGE-mediated ERK1/2 signaling was necessary for tumor progression. Conclusions: Extracellular HMGB1 promoted growth through RAGE-dependent activation of ERK1/2 in gastric cancer. | |||
| TO cite this article:ZHANG Qiuyu,WU Linqing,HAN Yangfei, et al. Autophagy-mediated HMGB1 release promotes survival of gastric cancer cells via the activation of ERK1/2 MAPK kinases[OL].[25 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4624561 | |||
| 7. Arginine functionalized of hydroxyapatite nanoparticles and its bioactivity for Gene Delivery | |||
| Zhao Yanzhong,Wang Guohui,Tan Juan,Zhu Shaihong,Zhou Kechao | |||
| Basic Medicine 18 December 2014 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Hydroxyapatite nanoparticles is a kind of extremely development prospect of gene carrier material. In order to further improve its transfection efficiency, arginine functionalized hydroxyapatite (HAP/Arg) nanoparticles was synthesized by hydrothermal synthesis. The morphology, structure, crystallite size and Zeta potential of the HAP/Arg and its complex with DNA were characterized by transmission electron microscopy (TEM), Atomic Force Microscopy (AFM) and Zeta potential analyzer. The loading and protecting properties of HAP/Arg to DNA were tested by electrophoresis experiment. The cell viability and cytotoxicity of HAP/Arg were also performed in Hela cells and HAEC cells by MTT and LDH, and its transfection efficiency was examined by the fluorescence microscope and flow cytometry. The results reveal that the HAP/Arg is short rod and nano single crystal particles, the mean diameter of the nanoparticles is 50-90 nm and its Zeta potential is about 35.8 mV at pH of 7.4. HAP/Arg-DNA complexes can be formed by electrostatic self-assembly. The formed complex is compact with size approximately 101nm and slight positive surface charge (around +9.0 mV). What's more, it can protect DNA against degradation in DNase I and have high transfection efficiency in Hela cells with no cytotoxicity. These results suggest that the HAP/Arg nanoparticles can be a promising alternative as a novel gene delivery system. | |||
| TO cite this article:Zhao Yanzhong,Wang Guohui,Tan Juan, et al. Arginine functionalized of hydroxyapatite nanoparticles and its bioactivity for Gene Delivery[OL].[18 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4624395 | |||
| 8. Decreased carboxylesterases expression and hydrolytic activity in type 2 diabetic mice through Akt/mTOR/HIF-1α/ Stra13 pathway | |||
| Chen Ruini,Wang Yuwen,Ning Rui,Liu Wei,Xiong Jing,Yang Jian | |||
| Basic Medicine 05 December 2014 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Carboxylesterases constitute a class of enzymes that hydrolyze drugs containing such functional groups as esters, amides, thioesters and carbamates. Ljver has abundant carboxylesterases expression, however, the alteration of carboxylesterases in type 2 diabetes remains to be elucidated. In this study, type 2 diabetic (T2D) mice were prepared by combination of high-fat diet and streptozocin (STZ) injection. We found that the carboxylesterase 1d (Ces1d, CES1) and carboxylesterase 1e (Ces1e, CES2) expression and the capacity of hydrolytic activity of liver and intestine decreased, whereas the Akt/mTOR/HIF-1α/ Stra13 (DEC1) signaling was activated in T2D mice. Consistently, high insulin could come out the same results in high glucose DMEM condition, which mimicked T2D, in primary mouse hepatocytes. Perifosine or rapamycin almost abolished the decreases of Ces1d and Ces1e expression and hydrolytic activity induced by insulin in the primary mouse hepatocytes. Moreover, the responsiveness of human hepatoma (HepG2) cells to high insulin in high glucose condition was similar to the primary mouse hepatocytes in terms of altered expression of carboxylesterases. Knockdown of HIF-1α or DEC1 with shRNA construct abrogated the decreases of CES1 and CES2 expression induced by insulin. The data suggest that the decreased carboxylesterases expression and hydrolytic activity in T2D mice are through Akt/mTOR/HIF-1α/Stra13 (DEC1) pathway. The findings will contribute to guide rational use of drugs in type 2 diabetic patients. | |||
| TO cite this article:Chen Ruini,Wang Yuwen,Ning Rui, et al. Decreased carboxylesterases expression and hydrolytic activity in type 2 diabetic mice through Akt/mTOR/HIF-1α/ Stra13 pathway[OL].[ 5 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4620177 | |||
| 9. Xylocarpin H, a component of Xylocarpus granatum, produces antidepressant-like activities in mice | |||
| YIN Xi,LI Xin,HAO Yaoguang,ZHAO Yiwen,ZHOU Jinghong,SHI Haishui | |||
Basic Medicine 26 November 2014
|
|||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Major depression is a common psychiatric disorder worldwide that imposes a substantial health burden on society. Currently available antidepressants do not meet the clinical needs. Here, we report that Xylocarpin H, an active component of Xylocarpus granatum, has antidepressant-like effects in mouse models of depression. In mouse forced swimming- and tail suspension tests, two validated models of depression, oral administration of Xylocarpin H resulted in a dose-dependent decreased immobility duration within the dose range of 15-50 mg/kg. In addition, Xylocarpin H dose-dependently increased the time in the central zone at doses of 5-50 mg/kg in the locomotion activity test. The antidepressant-like activities of Xylocarpin H were associated with its inhibitory effects on hypothalamic-pituitary-adrenal (HPA) axis' hyperactivity in response to acute stress. Interestingly, these effective doses of Xylocarpin H did not affect locomotor- and HPA axis activities in the absence of stress. In summary, the present study, for the first time, demonstrated that Xylocarpin H exerts antidepressant-like effects in mouse behavioral models of depression, likely by inhibiting HPA axis systems. These data provide a strong basis for developing Xylocarpin H as a novel antidepressant agent for the treatment of major depression disorders. | |||
| TO cite this article:YIN Xi,LI Xin,HAO Yaoguang, et al. Xylocarpin H, a component of Xylocarpus granatum, produces antidepressant-like activities in mice[OL].[26 November 2014] http://en.paper.edu.cn/en_releasepaper/content/4620567 | |||
| 10. Inhibition of the mevalonate pathway ameliorates anoxia-induced down-regulation of FKBP12.6 and intracellular calcium handling dysfunction in H9c2 cells | |||
| YANG Ying,LV Xue,Rong Xiqing,LAI Dongwu,FU Guosheng | |||
| Basic Medicine 16 November 2014
|
|||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Statins have beneficial pleiotropic effects beyond lipid lowering on the cardiovascular system. These cardio-protective effects are mediated through inhibition of the intracellular mevalonate pathway, by decreasing isoprenoid intermediates synthesis and the subsequent post-translational modification of small GTPases, such as Ras, Rho, and Rac. Impaired intracellular calcium handling is considered an important physiopathologic mechanism responsible for cardiac dysfunction. Our study aimed at investigating the influence of mevalonate pathway, including its downstream small GTPases (Ras, RhoA, and Rac1) on anoxia-mediated alterations of calcium handling in H9c2 cardiomyocytes. Cultured H9c2 cardiomyocytes were exposed to acute anoxia after pretreatment with different drugs that specifically antagonize five key components in the mevalonate pathway, including 3-hydroxy-3-methylgutaryl-CoA reductase, farnesyl pyrophosphate synthase, Rho-kinase, Rac1 and Ras farnesyltransferase. Thereafter, we evaluated the effects of t?he mevalonate pathway on anoxia-induced cell death, expression of the sarcoplasmic reticulum calcium release channel (ryanodine receptor 2) and its regulator FK506-binding protein 12.6. Our experiments confirmed the role of prenylated proteins in regulating cardiomyocyte dysfunction, especially via RhoA- and Ras-related signaling pathways. Furthermore, our data demonstrated that inhibition of the mevalonate pathway could ameliorate anoxia-mediated calcium handling dysfunction with the up-regulated expression of FK506-binding protein 12.6 and consequently provided evidence for FK506-binding protein 12.6 as a "stabilizer" of ryanodine receptor 2. | |||
| TO cite this article:YANG Ying,LV Xue,Rong Xiqing, et al. Inhibition of the mevalonate pathway ameliorates anoxia-induced down-regulation of FKBP12.6 and intracellular calcium handling dysfunction in H9c2 cells[OL].[16 November 2014] http://en.paper.edu.cn/en_releasepaper/content/4618949 | |||
| Select/Unselect all | For Selected Papers |
Saved Papers
Please enter a name for this paper to be shown in your personalized Saved Papers list
|
|
 |
|
||||||||||||||
About Sciencepaper Online |
Privacy Policy |
Terms & Conditions |
Contact Us
Technology Partner - CERNET