Publications by authors named "Hua-Dong Liu"

9 Publications

  • Page 1 of 1

Relationship Between Carbohydrate Antigen 125 and Coronary Artery Calcification in Patients without Known Coronary Artery Disease.

Med Sci Monit 2018 May 7;24:2873-2877. Epub 2018 May 7.

Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China (mainland).

BACKGROUND This study was designed to investigate the association between serum carbohydrate antigen 125 (CA125) and coronary artery calcification (CAC) score in patients without known coronary artery disease. MATERIAL AND METHODS The study groups included 348 consecutive subjects with chest pain but without known coronary artery disease, and who underwent an estimation of CAC score in our hospital. RESULTS The clinical and laboratory characteristics of all subjects are presented according to serum CA125 concentrations tertiles. The CAC score was found to be increased in the tertiles (31.6 ±82.10, 73.3±125.6, 122.9±135.9 U/mL, p<0.001). Serum CA125 concentrations are increased in calcium-positive patients compared with calcium-negative ones (9.3±4.79 vs. 11.2±7.36, p=0.003). A positive correlation between serum CA125 and CAC score was observed (r=0.319, p<0.001) in all participants. Similarly, the serum concentrations of CA125 were found to be positively correlated with CAC score in both women and men (r=0.328, p<0.001; r=0.265, p=0.001, respectively). Multiple linear regression analysis results indicated that serum CA125 concentrations are independently related to CAC score in the study population (beta=0.173, p=0.001), and age, sex, diabetes mellitus, and high-sensitivity C-reactive protein (hs-CRP) were also associated with CAC score in multiple linear regression analysis. CONCLUSIONS Serum CA125 concentrations are correlated with CAC score in the population without known coronary artery disease, and serum CA125 may be considered as a marker to estimate CAC in the study population.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.12659/MSM.907418DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5960219PMC
May 2018

Protective effects of Huanglian Wendan Decoction aganist cognitive deficits and neuronal damages in rats with diabetic encephalopathy by inhibiting the release of inflammatory cytokines and repairing insulin signaling pathway in hippocampus.

Chin J Nat Med 2016 Nov;14(11):813-822

Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, 210009, China. Electronic address:

Huanglian Wendan decoction (HLWDD) has been used for the treatment of symptom of "Re", one of major causes in diabetes and metabolic disorders, according to the theory of traditional Chinese medicine. The present study aimed at investigating the cerebral protective effects of HLWDD on diabetic encephalopathy (DE), one of the major diabetic complications. The effects of HLWDD and metformin were analyzed in the streptozocin (STZ) + high-glucose-fat (HGF) diet-induced DE rats by gastric intubation. In the present study, the effects of HLWDD on cognition deficits were investigated after 30-day intervention at two daily dose levels (3 and 6 g·kg). To explore the potential mechanisms underlying the effects of HLWDD, we detected the alterations of neuronal damages, inflammatory cytokines, and impaired insulin signaling pathway in hippocampus of the DE rats. Based on our results from the present study, we concluded that the protective effects of HLWDD against the cognitive deficits and neuronal damages through inhibiting the release of inflammatory cytokines and repairing insulin signaling pathway in hippocampus of the DE rats.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/S1875-5364(16)30098-XDOI Listing
November 2016

Responses of astrocyte to simultaneous glutamate and arachidonic acid treatment.

Neurochem Int 2009 Jul-Aug;55(1-3):143-50. Epub 2009 Mar 5.

Neuroscience Research Institute, Peking University, Beijing, China.

After cellular injury many endogenous toxins are released from injured cells and result in secondary injury. To elucidate mechanisms of such injury many of these toxins have been studied individually. However, the data obtained is only useful for reference and does not accurately represent the multifactorial situation under pathophysiological conditions. Primary astrocytic cultures were treated individually and simultaneously with two well-studied toxins, glutamate (Glu) and arachidonic acid (AA). Both are simultaneously released from neural cells during injury. Measurements of cellular protein content, intracellular water space, lactate dehydrogenase release, and malondialdehyde formation indicated that Glu and AA act through different mechanisms. Glu+AA applied together had a synergistic effect on the levels of Caspase-3 gene expression, and Bcl-2 and Hsp70 protein. Atomic force microscopy observed that Glu caused cell membrane roughness and nuclear swelling, while AA induced pores in the cell membrane and nuclear shrinkage. Glu+AA accelerated nuclear shrinkage and resulted in more serious cell damage. This study not only distinguishes the different responses of astrocytes to Glu and AA, but also provides a new view into the synergistic effect of these biochemicals; highlighting the need to be cautious in applying single factor experimental data to interpret complex physiological and pathological conditions in animals. Two or more factors may act not only on different targets but also on the same target synergistically.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.neuint.2009.02.016DOI Listing
July 2009

Ischemia activates JNK/c-Jun/AP-1 pathway to up-regulate 14-3-3gamma in astrocyte.

J Neurochem 2009 May;109 Suppl 1:182-8

Department of Neurobiology, School of Basic Medical Sciences, Neuroscience Research Institute, the Key Laboratory for Neuroscience (Ministry of Education), Peking University, Beijing, China.

Ischemia occurs in the brain as the result of stroke and other related injuries and few therapies are effective. If more is understood then potential treatments could be investigated. It was previously reported that 14-3-3gamma could be up-regulated by ischemia in astrocyte to protect cells from ischemia-induced apoptosis. In this study, we attempted to uncover the mechanism responsible for this 14-3-3gamma up-regulation in primary culture of astrocytes under ischemic-like conditions. It was found that in vitro ischemia may activate PI3K/Akt and MAPK signaling pathways. Astrocyte cultures were treated with LY294002 (PI3K inhibitor), U0126 (ERK inhibitor), SB203580 (p38 inhibitor) and SP600125 (JNK inhibitor). Only SP600125 could inhibit the ischemia-induced 14-3-3gamma up-regulation in astrocytes. At the same time, we observed an ischemia-induced nuclear translocation of p-c-Jun, a major downstream component of JNK. Inhibition of AP-1 with curcumin also inhibited 14-3-3gamma up-regulation indicating that ischemia-induced up-regulation of 14-3-3gamma in astrocyte involves activation of the JNK/p-c-Jun/AP-1 pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1471-4159.2009.05974.xDOI Listing
May 2009

[The effects of 40 mg atorvastatin on serum lipids, inflammatory markers and clinical events in ACS patients post PCI].

Zhonghua Xin Xue Guan Bing Za Zhi 2006 Apr;34(4):353-6

Department of Cardiology, The Second Clinical Hospital of Jinan University (Shenzhen People's Hospital), Shenzhen 518026, China.

Objective: To assess the safety and effects of 40 mg atorvastatin on serum lipids, inflammatory markers and clinical events in ACS patients post PCI.

Methods: A total of 92 patients with ACS post successful PCI were randomly divided into atorvastatin 10 mg/d (group A) and atorvastatin 40 mg/d (group B) on top of the standard medical therapy. Blood were taken at baseline, 4, 12 and 24 weeks for serum alanine aminotransferase (ALT), lipids, high-sensitive C-reactive protein (hs-CRP) and matrix metalloprotease-9 (MMP-9) measurements. The major adverse cardiac events (MACE) were also observed.

Results: There was no significant difference in medication withdrawn (2 vs. 3 cases) due to increased ALT (3 times higher than normal) and incidence of MACE (5 vs. 7 cases) between the groups. TC and LDL were significantly reduced in both groups 4 weeks and thereafter post medication compared to pre-treatment (P < 0.05) and the reduction was more significant in group B than that in group A at 24 weeks post medication (P < 0.05) while TG and HDL remained unchanged. hs-CRP was significantly reduced at 12 and 24 weeks in both groups compared to baseline and the reduction was more significant in group B than that in group A at 24 weeks. MMP-9 was significantly reduced in both groups 4 weeks and thereafter post medication compared to pre-treatment (P < 0.05) and the reduction was more significant in group B than that in group A at 12 weeks post medication (P < 0.05).

Conclusion: Both atorvastatin doses significantly reduced TC, LDL, hs-CRP and MMP-9 in ACS patients post PCI and the reduction was more significant in high dose atorvastatin group at 24 weeks while the MACE and drug withdraw rates were similar between the groups.
View Article and Find Full Text PDF

Download full-text PDF

Source
April 2006

Characterization of copper binding to the peptide amyloid-beta(1-16) associated with Alzheimer's disease.

Biopolymers 2006 Sep;83(1):20-31

Key Laboratory of Bioorganic Phosphorus Chemistry and Chemical Biology (Ministry of Education), Department of Chemistry, Tsinghua University, 100084 Beijing, China.

Amyloid-beta peptide (Abeta) is the principal constituent of plaques associated with Alzheimer's disease (AD) and is thought to be responsible for the neurotoxicity associated with the disease. Copper binding to Abeta has been hypothesized to play an important role in the neruotoxicity of Abeta and free radical damage, and Cu2+ chelators represent a possible therapy for AD. However, many properties of copper binding to Abeta have not been elucidated clearly, and the location of copper binding sites on Abeta is also in controversy. Here we have used a range of spectroscopic techniques to characterize the coordination of Cu2+ to Abeta(1-16) in solution. Electrospray ionization mass spectrometry shows that copper binds to Abeta(1-16) at pH 6.0 and 7.0. The mode of copper binding is highly pH dependent. Circular dichroism results indicate that copper chelation causes a structural transition of Abeta(1-16). UV-visible absorption spectra suggest that three nitrogen donor ligands and one oxygen donor ligand (3N1O) in Abeta(1-16) may form a type II square-planar coordination geometry with Cu2+. By means of fluorescence spectroscopy, competition studies with glycine and L-histidine show that copper binds to Abeta(1-16) with an affinity of Ka approximately 10(7) M(-1) at pH 7.8. Besides His6, His13, and His14, Tyr10 is also involved in the coordination of Abeta(1-16) with Cu2+, which is supported by 1H NMR and UV-visible absorption spectra. Evidence for the link between Cu2+ and AD is growing, and this work has made a significant contribution to understanding the mode of copper binding to Abeta(1-16) in solution.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/bip.20523DOI Listing
September 2006

Novel acetylation-aided migrating rearrangement of uridine-diphosphate-N-acetylglucosamine in electrospray ionization multistage tandem mass spectrometry.

J Mass Spectrom 2006 Feb;41(2):208-15

Key Laboratory of Bioorganic Phosphorus Chemistry and Chemical Biology (Ministry of Education), Department of Chemistry, Tsinghua University, Beijing 100084, PR China.

Uridine 5'-diphospho-N-acetylglucosamine (UDP-GlcNAc) is the final product of hexosamine biosynthetic pathway (HSP) and the donor substrate for the modification of nucleocytoplasmic proteins at serine and threonine residues with N-acetylglucosamine (GlcNAc) catalyzed by O-GlcNAc transferase (OGT). Many analogs of UDP-GlcNAc were designed to interfere with the process of protein O-glycosylation by blocking OGT. A novel rearrangement reaction was observed in which phosphate-N-acetylglucosamine moiety migrated to 3' terminus of ribose in ESI-MS(n) of UDP-GlcNAc. Results from tandem mass spectrometry, control experiments and calculation showed that the phosphate-N-acetylglucosamine migration might undergo a pentacoordinate phosphoric intermediate. Furthermore, the acetylation of glucosamine in UDP-GlcNAc was essential in the migration process.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jms.979DOI Listing
February 2006

Identification of a mouse synaptic glycoprotein gene in cultured neurons.

Neurochem Res 2005 Oct;30(10):1289-94

Neuroscience Research Institute, Peking University, Beijing, P.R. China.

Neuronal differentiation and aging are known to involve many genes, which may also be differentially expressed during these developmental processes. From primary cultured cerebral cortical neurons, we have previously identified various differentially expressed gene transcripts from cultured cortical neurons using the technique of arbitrarily primed PCR (RAP-PCR). Among these transcripts, clone 0-2 was found to have high homology to rat and human synaptic glycoprotein. By in silico analysis using an EST database and the FACTURA software, the full-length sequence of 0-2 was assembled and the clone was named as mouse synaptic glycoprotein homolog 2 (mSC2). DNA sequencing revealed transcript size of mSC2 being smaller than the human and rat homologs. RT-PCR indicated that mSC2 was expressed differentially at various culture days. The mSC2 gene was located in various tissues with higher expression in brain, lung, and liver. Functions of mSC2 in neurons and other tissues remain elusive and will require more investigation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11064-005-8800-5DOI Listing
October 2005

[A review of clinical studies on Chinese patent drugs in 20th century].

Zhongguo Zhong Yao Za Zhi 2003 Nov;28(11):1009-12

College of Basic Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu 210029

View Article and Find Full Text PDF

Download full-text PDF

Source
November 2003
-->