Publications by authors named "Dongliang Ma"

18 Publications

  • Page 1 of 1

The discrepancy of aromatase expression in epicardial adipose tissue between CHD and non-CHD patients.

Cardiovasc J Afr 2021 Jun 7;32:1-4. Epub 2021 Jun 7.

Department of Cardiovascular Surgery, Shanxi Cardiovascular Hospital, Taiyuan, PR of China. Email:

Objectives: Epicardial adipose tissue (EAT) aromatase converts androstenedione and other adrenal androgens into oestrogens. The locally produced oestradiol (E) may have cardiovascular protective effects. Little is known about the relationship between EAT aromatase level and coronary heart disease (CHD). Here, we compared EAT aromatase levels in CHD versus non-CHD patients and assessed the relationship between EAT aromatase levels and lesion degree in the coronary arteries.

Methods: EAT and blood specimens were obtained from patients undergoing thoracotomy prior to cardiopulmonary bypass. Serum E levels were obtained from our hospital laboratory. EAT aromatase expression was determined by RT-qPCR and ELISA assays. All patients underwent coronary angiography and the level of coronary lesions was evaluated with the SYNTAX score.

Results: Compared with non-CHD patients, CHD patients had lower EAT aromatase mRNA and protein levels. In the CHD patients, EAT aromatase and oestrogen levels negatively correlated with the severity of coronary artery disease.

Conclusions: Our data revealed that reduced EAT aromatase levels correlated with coronary atherosclerotic lesions. Reduced EAT aromatase protein levels may aggravate the severity of atherosclerosis. Future studies should investigate the mechanisms regulating aromatase expression in epicardial fat.
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http://dx.doi.org/10.5830/CVJA-2021-012DOI Listing
June 2021

Correction to: Rescue of Methyl-CpG Binding Protein 2 Dysfunction-induced Defects in Newborn Neurons by Pentobarbital.

Neurotherapeutics 2019 Oct;16(4):1391

Programme in Neuroscience and Behavioral Disorders, Duke-NUS Graduate Medical School, Singapore, Singapore.

C.-H. Yang's appeared incorrectly on the original publication of this article.
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http://dx.doi.org/10.1007/s13311-019-00738-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6985302PMC
October 2019

Choline Rescues Behavioural Deficits in a Mouse Model of Rett Syndrome by Modulating Neuronal Plasticity.

Mol Neurobiol 2019 Jun 15;56(6):3882-3896. Epub 2018 Sep 15.

Neuroscience Academic Clinical Programme, Duke-NUS Medical School, 20 College Road, Singapore, 169856, Singapore.

Rett syndrome (RTT) is a postnatal neurodevelopmental disorder that primarily affects girls, with 95% of RTT cases resulting from mutations in the methyl-CpG-binding protein 2 (MECP2) gene. Choline, a dietary micronutrient found in most foods, has been shown to be important for brain development and function. However, the exact effects and mechanisms are still unknown. We found that 13 mg/day (1.7 × required daily intake) of postnatal choline treatment to Mecp2-conditional knockout mice rescued not only deficits in motor coordination, but also their anxiety-like behaviour and reduced social preference. Cortical neurons in the brains of Mecp2-conditional knockout mice supplemented with choline showed enhanced neuronal morphology and increased density of dendritic spines. Modelling RTT in vitro by knocking down the expression of the MeCP2 protein with shRNA, we found that choline supplementation to MeCP2-knockdown neurons increased their soma sizes and the complexity of their dendritic arbors. Rescue of the morphological defects could lead to enhanced neurotransmission, as suggested by an observed trend of increased expression of synaptic proteins and restored miniature excitatory postsynaptic current frequency in choline-supplemented MeCP2-knockdown neurons. Through the use of specific inhibitors targeting each of the known physiological pathways of choline, synthesis of phosphatidylcholine from choline was found to be essential in bringing about the changes seen in the choline-supplemented MeCP2-knockdown neurons. Taken together, these data reveal a role of choline in modulating neuronal plasticity, possibly leading to behavioural changes, and hence, a potential for using choline to treat RTT.
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http://dx.doi.org/10.1007/s12035-018-1345-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6505515PMC
June 2019

Maternal methamphetamine exposure causes cognitive impairment and alteration of neurodevelopment-related genes in adult offspring mice.

Neuropharmacology 2018 09 24;140:25-34. Epub 2018 Jul 24.

College of Forensic Medicine, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China; Key Laboratory of Health Ministry for Forensic Science, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, PR China. Electronic address:

Prenatal drug exposure altered cognitive function in individuals, and may also impact their offspring's susceptibility to cognitive impairment. The high incidence of methamphetamine (METH) abuse among adolescents and women of childbearing age elevates the importance to determine the influence of maternal METH exposure on cognitive functions in the descendants. We hypothesized that maternal METH exposure affects cognitive behavior in offspring mice by disrupting gene expression associated with neural development. Here, female C57BL/6 mice were exposed to intermittent escalating doses of METH or saline from adolescence to adulthood, and then continued through pregnancy. Interestingly, male but not female offspring exhibited impaired short-term recognition memory and long-term spatial memory retention in novel object recognition and Morris water maze test respectively. Additionally, maternal METH exposure altered neurodevelopmental genes in both male and female offspring, and 12 differentially expressed genes between male and female were observed in the HPC and NAc regions. These differentially expressed genes are involved in neurogenesis, axon guidance, neuron migration and synapse of neural development circuits. Our observations suggest that maternal METH exposure induced differential expression patterns of neurodevelopment-related genes in the HPC and NAc of male and female mice, which may underlie the different cognitive behavior phenotypes in both genders.
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http://dx.doi.org/10.1016/j.neuropharm.2018.07.024DOI Listing
September 2018

Human Rett-derived neuronal progenitor cells in 3D graphene scaffold as an in vitro platform to study the effect of electrical stimulation on neuronal differentiation.

Biomed Mater 2018 03 21;13(3):034111. Epub 2018 Mar 21.

Mechanobiology Institute Singapore, National University of Singapore, T-Lab, #05-01, 5A Engineering Drive 1, 117411, Singapore. Neuroscience Academic Clinical Programme, Duke-NUS Medical School, 20 College Road, 169856, Singapore.

Studies of electrical stimulation therapies for the treatment of neurological disorders, such as deep brain stimulation, have almost exclusively been performed using animal-models. However, because animal-models can only approximate human brain disorders, these studies should be supplemented with an in vitro human cell-culture based model to substantiate the results of animal-based studies and further investigate therapeutic benefit in humans. This study presents a novel approach to analyze the effect of electrical stimulation on the neurogenesis of patient-induced pluripotent stem cell (iPSC) derived neural progenitor cell (NPC) lines, in vitro using a 3D graphene scaffold system. The iPSC-derived hNPCs used to demonstrate the system were collected from patients with Rett syndrome, a debilitating neurodevelopmental disorder. The graphene scaffold readily supported both the wild-type and Rett NPCs. Electrical stimulation parameters were optimized to accommodate both wild-type and Rett cells. Increased cell maturation and improvements in cell morphology of the Rett cells was observed after electrical stimulation. The results of the pilot study of electrical stimulation to enhance Rett NPCs neurogenesis were promising and support further investigation of the therapy. Overall, this system provides a valuable tool to study electrical stimulation as a potential therapy for neurological disorders using patient-specific cells.
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http://dx.doi.org/10.1088/1748-605X/aaaf2bDOI Listing
March 2018

HoxC5 and miR-615-3p target newly evolved genomic regions to repress hTERT and inhibit tumorigenesis.

Nat Commun 2018 01 8;9(1):100. Epub 2018 Jan 8.

Cancer and Stem Cell Biology Program, Duke-NUS Medical School, 8 College Road, Singapore, 169857, Singapore.

The repression of telomerase activity during cellular differentiation promotes replicative aging and functions as a physiological barrier for tumorigenesis in long-lived mammals, including humans. However, the underlying mechanisms remain largely unclear. Here we describe how miR-615-3p represses hTERT expression. mir-615-3p is located in an intron of the HOXC5 gene, a member of the highly conserved homeobox family of transcription factors controlling embryogenesis and development. Unexpectedly, we found that HoxC5 also represses hTERT expression by disrupting the long-range interaction between hTERT promoter and its distal enhancer. The 3'UTR of hTERT and its upstream enhancer region are well conserved in long-lived primates. Both mir-615-3p and HOXC5 are activated upon differentiation, which constitute a feed-forward loop that coordinates transcriptional and post-transcriptional repression of hTERT during cellular differentiation. Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.
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http://dx.doi.org/10.1038/s41467-017-02601-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5758779PMC
January 2018

A 3D neurovascular microfluidic model consisting of neurons, astrocytes and cerebral endothelial cells as a blood-brain barrier.

Lab Chip 2017 01;17(3):448-459

Department of Research, National Neuroscience Institute, 20 College Road, 169856 Singapore and Neuroscience Academic Clinical Programme, Duke-NUS Medical School, 169857 Singapore. and Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 117597 Singapore and KK Research Center, KK Women's and Children's Hospital, Singapore 229899, Singapore.

The neurovascular unit is a complex, interdependent system composed of neurons and neural supporting cells, such as astrocytes, as well as cells that comprise the vascular system including endothelial cells, pericytes, and smooth muscle cells. Each cell type in the neurovascular unit plays an essential role, either in transmitting and processing neural signals or in maintaining the appropriate microenvironmental conditions for healthy neural function. In vitro neurovascular models can be useful for understanding the different roles and functions of the cells composing the neurovascular unit, as well as for assessing the effects on neural function of therapeutic compounds after crossing the endothelial barrier. Here, we report a novel three-dimensional neurovascular microfluidic model consisting of primary rat astrocytes and neurons together with human cerebral microvascular endothelial cells. These three cell types in our neurovascular chip (NVC) show distinct cell type-specific morphological characteristics and functional properties. In particular, morphological and functional analysis of neurons enables quantitative assessment of neuronal responses, while human cerebral endothelial cells form monolayers with size-selective permeability similar to existing in vitro blood-brain barrier (BBB) models.
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http://dx.doi.org/10.1039/c6lc00638hDOI Listing
January 2017

mRNA changes in nucleus accumbens related to methamphetamine addiction in mice.

Sci Rep 2016 11 21;6:36993. Epub 2016 Nov 21.

College of Forensic Medicine, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China.

Methamphetamine (METH) is a highly addictive psychostimulant that elicits aberrant changes in the expression of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in the nucleus accumbens of mice, indicating a potential role of METH in post-transcriptional regulations. To decipher the potential consequences of these post-transcriptional regulations in response to METH, we performed strand-specific RNA sequencing (ssRNA-Seq) to identify alterations in mRNA expression and their alternative splicing in the nucleus accumbens of mice following exposure to METH. METH-mediated changes in mRNAs were analyzed and correlated with previously reported changes in non-coding RNAs (miRNAs and lncRNAs) to determine the potential functions of these mRNA changes observed here and how non-coding RNAs are involved. A total of 2171 mRNAs were differentially expressed in response to METH with functions involved in synaptic plasticity, mitochondrial energy metabolism and immune response. 309 and 589 of these mRNAs are potential targets of miRNAs and lncRNAs respectively. In addition, METH treatment decreases mRNA alternative splicing, and there are 818 METH-specific events not observed in saline-treated mice. Our results suggest that METH-mediated addiction could be attributed by changes in miRNAs and lncRNAs and consequently, changes in mRNA alternative splicing and expression. In conclusion, our study reported a methamphetamine-modified nucleus accumbens transcriptome and provided non-coding RNA-mRNA interaction networks possibly involved in METH addiction.
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http://dx.doi.org/10.1038/srep36993DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116666PMC
November 2016

Choline Ameliorates Disease Phenotypes in Human iPSC Models of Rett Syndrome.

Neuromolecular Med 2016 Sep 5;18(3):364-77. Epub 2016 Jul 5.

Neuroscience Academic Clinical Programme, Duke-NUS Medical School, 8 College Road, Singapore, 169857, Singapore.

Rett syndrome (RTT) is a postnatal neurodevelopmental disorder that primarily affects girls. Mutations in the methyl-CpG-binding protein 2 (MECP2) gene account for approximately 95 % of all RTT cases. To model RTT in vitro, we generated induced pluripotent stem cells (iPSCs) from fibroblasts of two RTT patients with different mutations (MECP2 (R306C) and MECP2 (1155Δ32)) in their MECP2 gene. We found that these iPSCs were capable of differentiating into functional neurons. Compared to control neurons, the RTT iPSC-derived cells had reduced soma size and a decreased amount of synaptic input, evident both as fewer Synapsin 1-positive puncta and a lower frequency of spontaneous excitatory postsynaptic currents. Supplementation of the culture media with choline rescued all of these defects. Choline supplementation may act through changes in the expression of choline acetyltransferase, an important enzyme in cholinergic signaling, and also through alterations in the lipid metabolite profiles of the RTT neurons. Our study elucidates the possible mechanistic pathways for the effect of choline on human RTT cell models, thereby illustrating the potential for using choline as a nutraceutical to treat RTT.
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http://dx.doi.org/10.1007/s12017-016-8421-yDOI Listing
September 2016

Lentiviral silencing of GSK-3β in adult dentate gyrus impairs contextual fear memory and synaptic plasticity.

Front Behav Neurosci 2015 23;9:158. Epub 2015 Jun 23.

Program in Neuroscience and Behavioral Disorders, Duke-NUS Graduate Medical School Singapore, Singapore ; Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore Singapore, Singapore ; KK Research Center, KK Women's and Children's Hospital Singapore, Singapore.

Attempts have been made to use glycogen synthase kinase-3 beta (GSK3β) inhibitors for prophylactic treatment of neurocognitive conditions. However the use of lithium, a non-specific inhibitor of GSK3β results in mild cognitive impairment in humans. The effects of global GSK3β inhibition or knockout on learning and memory in healthy adult mice are also inconclusive. Our study aims to better understand the role of GSK3β in learning and memory through a more regionally, targeted approach, specifically performing lentiviral-mediated knockdown of GSK3β within the dentate gyrus (DG). DG-GSK3β-silenced mice showed impaired contextual fear memory retrieval. However, cue fear memory, spatial memory, locomotor activity and anxiety levels were similar to control. These GSK3β-silenced mice also showed increased induction and maintenance of DG long-term potentiation (DG-LTP) compared to control animals. Thus, this region-specific, targeted knockdown of GSK3β in the DG provides better understanding on the role of GSK3β in learning and memory.
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http://dx.doi.org/10.3389/fnbeh.2015.00158DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477161PMC
July 2015

The methyl-CpG-binding domain (MBD) is crucial for MeCP2's dysfunction-induced defects in adult newborn neurons.

Front Cell Neurosci 2015 24;9:158. Epub 2015 Apr 24.

Programme in Neuroscience and Behavioral Disorder, Duke-NUS Graduate Medical School Singapore, Singapore ; Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore Singapore, Singapore ; KK Research Center, KK Women's and Children's Hospital Singapore, Singapore.

Mutations in the human X-linked gene MECP2 are responsible for most Rett syndrome (RTT) cases, predominantly within its methyl-CpG-binding domain (MBD). To examine the role of MBD in the pathogenesis of RTT, we generated two MeCP2 mutant constructs, one with a deletion of MBD (MeCP2-ΔMBD), another mimicking a mutation of threonine 158 within the MBD (MeCP2-T158M) found in RTT patients. MeCP2 knockdown resulted in a decrease in total dendrite length, branching, synapse number, as well as altered spontaneous Ca(2+) oscillations in vitro, which could be reversed by expression of full length human MeCP2 (hMeCP2-FL). However, the expression of hMeCP2-ΔMBD in MeCP2-silenced neurons did not rescue the changes in neuronal morphology and spontaneous Ca(2+) oscillations, while expression of hMeCP2-T158M in these neurons could only rescue the decrease in dendrite length and branch number. In vivo over expression of hMeCP2-FL but not hMeCP2-ΔMBD in adult newborn neurons of the dentate gyrus also rescued the cell autonomous effect caused by MeCP2 deficiency in dendrites length and branching. Our results demonstrate that an intact and functional MBD is crucial for MeCP2 functions in cultured hippocampal neurons and adult newborn neurons.
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http://dx.doi.org/10.3389/fncel.2015.00158DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4408855PMC
May 2015

Rescue of Methyl-CpG Binding Protein 2 Dysfunction-induced Defects in Newborn Neurons by Pentobarbital.

Neurotherapeutics 2015 Apr;12(2):477-90

Programme in Neuroscience and Behavioral Disorders, Duke-NUS Graduate Medical School, Singapore, Singapore.

Rett syndrome is a neurodevelopmental disorder that usually arises from mutations or deletions in methyl-CpG binding protein 2 (MeCP2), a transcriptional regulator that affects neuronal development and maturation without causing cell loss. Here, we show that silencing of MeCP2 decreased neurite arborization and synaptogenesis in cultured hippocampal neurons from rat fetal brains. These structural defects were associated with alterations in synaptic transmission and neural network activity. Similar retardation of dendritic growth was also observed in MeCP2-deficient newborn granule cells in the dentate gyrus of adult mouse brains in vivo, demonstrating direct and cell-autonomous effects on individual neurons. These defects, caused by MeCP2 deficiency, were reversed by treatment with the US Food and Drug Administration-approved drug, pentobarbital, in vitro and in vivo, possibly caused by modulation of γ-aminobutyric acid signaling. The results indicate that drugs modulating γ-aminobutyric acid signaling are potential therapeutics for Rett syndrome.
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http://dx.doi.org/10.1007/s13311-015-0343-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404443PMC
April 2015

Enhanced differentiation of neural progenitor cells into neurons of the mesencephalic dopaminergic subtype on topographical patterns.

Biomaterials 2015 Mar 23;43:32-43. Epub 2014 Dec 23.

Mechanobiology Institute Singapore, National University of Singapore, T-Lab, #05-01, 5A Engineering Drive 1, Singapore 117411, Singapore; Department of Biomedical Engineering, National University of Singapore, EA-03-12, 9 Engineering Drive 1, Singapore 117575, Singapore; Department of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, NUHS Tower Block, 1E Kent Ridge Road, Singapore 119228, Singapore. Electronic address:

Parkinson's disease (PD) is a neurodegenerative disease attributed to the loss of midbrain dopaminergic (DA) neurons. The current lack of predictive models for this disease has been hampered by the acquirement of robust cells, posing a major barrier to drug development. Differentiation of stem cells into subtype specific cells may be guided by appropriate topographical cues but the role of topography has hitherto not been well understood. We used a Multi-Architecture (MARC) chip with various topographical structures and identified three topographies, which generate DA neurons from murine hippocampal neural progenitor cells with the highest percentage of neuronal (β-III-tubulin positive) and dopaminergic (tyrosine hydroxylase positive) populations. Analysis on single pattern structures showed that 2 μm gratings with 2 μm spacing and 2 μm height (2 μm gratings) and 2 μm gratings with hierarchical structure produced cells with the highest gene expression of TH and PITX3, with the longest neurite and highest percentage of alignment. Quantitative image analysis showed the 2 μm gratings produced cells with the highest expression of pituitary homeobox 3 (PITX3), LIM homeobox transcription factor 1 alpha (LMX1a), aldehyde dehydrogenase 1 family member A1 (ALDH1a1) and microtubule associated protein 2 (MAP2), as compared to nano-gratings and unpatterned controls. These patterns also enhance DA neuron differentiation on different substrate rigidities, as seen on both poly-dimethylsiloxane (PDMS) and tissue culture polystyrene (TCPS) substrates. These results show the use of topographical influence for neuronal subtype specification, which could be translated into a wide range of clinical applications for PD.
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http://dx.doi.org/10.1016/j.biomaterials.2014.11.036DOI Listing
March 2015

Mfsd2a is a transporter for the essential omega-3 fatty acid docosahexaenoic acid.

Nature 2014 May 14;509(7501):503-6. Epub 2014 May 14.

Signature Research Program in Cardiovascular and Metabolic Disorders, Duke-NUS Graduate Medical School Singapore, 8 College Road, 169857 Singapore.

Docosahexaenoic acid (DHA) is an omega-3 fatty acid that is essential for normal brain growth and cognitive function. Consistent with its importance in the brain, DHA is highly enriched in brain phospholipids. Despite being an abundant fatty acid in brain phospholipids, DHA cannot be de novo synthesized in brain and must be imported across the blood-brain barrier, but mechanisms for DHA uptake in brain have remained enigmatic. Here we identify a member of the major facilitator superfamily--Mfsd2a (previously an orphan transporter)--as the major transporter for DHA uptake into brain. Mfsd2a is found to be expressed exclusively in endothelium of the blood-brain barrier of micro-vessels. Lipidomic analysis indicates that Mfsd2a-deficient (Mfsd2a-knockout) mice show markedly reduced levels of DHA in brain accompanied by neuronal cell loss in hippocampus and cerebellum, as well as cognitive deficits and severe anxiety, and microcephaly. Unexpectedly, cell-based studies indicate that Mfsd2a transports DHA in the form of lysophosphatidylcholine (LPC), but not unesterified fatty acid, in a sodium-dependent manner. Notably, Mfsd2a transports common plasma LPCs carrying long-chain fatty acids such LPC oleate and LPC palmitate, but not LPCs with less than a 14-carbon acyl chain. Moreover, we determine that the phosphor-zwitterionic headgroup of LPC is critical for transport. Importantly, Mfsd2a-knockout mice have markedly reduced uptake of labelled LPC DHA, and other LPCs, from plasma into brain, demonstrating that Mfsd2a is required for brain uptake of DHA. Our findings reveal an unexpected essential physiological role of plasma-derived LPCs in brain growth and function.
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http://dx.doi.org/10.1038/nature13241DOI Listing
May 2014

Production and spectral properties of lattice defects in natural fibrous gypsum colored electrolytically at near room temperature using a pointed anode.

Spectrochim Acta A Mol Biomol Spectrosc 2013 Jul 10;111:188-91. Epub 2013 Apr 10.

Department of Physics, Tianjin University, Tianjin 300072, PR China.

Natural fibrous gypsum is colored electrolytically at near room temperatures and under various voltages using a pointed anode and a flat cathode. The SO4(-), SO3(-), SO2(-) and O(-) lattice defects are produced in the colored natural fibrous gypsum. No visible characteristic absorption band in the ultraviolet and visible wavelength regions is observed in the optical absorption spectrum of the natural fibrous gypsum before the electrolytic coloration. The characteristic absorption bands of the SO4(-), SO3(-), SO2(-) and O(-) lattice defects are observed in the optical absorption spectra of the colored natural fibrous gypsum. The production of the lattice defects is explained. Current-time curve for the electrolytic coloration of the natural fibrous gypsum and its relationship with the electrolytic coloration processes are given.
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http://dx.doi.org/10.1016/j.saa.2013.04.003DOI Listing
July 2013

Electrolytic coloration and spectral properties of natural fluorite crystals containing oxygen impurities.

Spectrochim Acta A Mol Biomol Spectrosc 2011 Nov 23;82(1):327-31. Epub 2011 Jul 23.

Department of Physics, Tianjin University, Tianjin 300072, PR China.

Natural fluorite crystals containing oxygen impurities are colored electrolytically by using a pointed cathode and a flat anode at various temperatures and voltages. F and F(2) color centers are produced in colored fluorite crystals. O(2-)-V(a)(+), O(2-)-V(a)(+) aggregate, Yb(2+), Ce(3+) and Sm(2+) absorption bands are observed in absorption spectra of uncolored fluorite crystals. O(2-)-V(a)(+), O(2-)-V(a)(+) aggregate, Yb(2+), Ce(3+), Sm(2+), F, M (F(2)) absorption bands and group of four absorption bands are observed simultaneously in absorption spectra of colored fluorite crystals. Current-time curve for electrolytic coloration of natural fluorite crystal and its relationship with electrolytic coloration process are given. Production and conversion of color centers are explained.
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http://dx.doi.org/10.1016/j.saa.2011.07.056DOI Listing
November 2011

Recombinant AAV-mediated expression of human BDNF protects neurons against cell apoptosis in Abeta-induced neuronal damage model.

J Huazhong Univ Sci Technolog Med Sci 2007 Jun;27(3):233-6

Department of Anatomy and Histology-Embryology, School of Medicine, Key Laboratory of Environment and Genes Related to Disease, Ministry of Education, Xi'an Jiaotong University, Xi'an 710061, China.

The human brain-derived neurotrophic factor (hBDNF) gene was cloned by polymerase chain reaction and the recombinant adeno-associated viral vector inserted with hBDNF gene (AAV-hBDNF) was constructed. Cultured rat hippocampal neurons were treated with Abeta(25-35) and serued as the experimental Abeta-induced neuronal damage model (AD model), and the AD model was infected with AAV-hBDNF to explore neuroprotective effects of expression of BDNF. Cell viability was assayed by MTT. The expression of bcl-2 anti-apoptosis protein was detected by immunocytochemical staining. The change of intracellular free Ca ion ([Ca2+]i) was measured by laser scanning confocal microscopy. The results showed that BDNF had protective effects against A-induced neuronal damage. The expression of the bcl-2 anti-apoptosis protein was raised significantly and the balance of [Ca2+]i was maintained in the AAv-hBDNF treatment group as compared with AD model group. These data suggested that recombinant AAV mediated a stable expression of hBDNF in cultured hippocampal neurons and resulted in significant neuron protective effects in AD model. The BDNF may reduce neuron apoptosis through increasing the expression of the bcl-2 anti-apoptosis protein and inhibiting intracellular calcium overload. The viral vector-mediated gene expression of BDNF may pave the way of a novel therapeutic strategy for the treatment of neurodegenerative diseases such as Alzheimer's disease.
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http://dx.doi.org/10.1007/s11596-007-0304-xDOI Listing
June 2007

[A probe to the treatment of Madelung deformity].

Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi 2005 May;19(5):361-3

Department of Hand Surgery, The Third Hospital of Hebei Medical University, Shijiazhuang Hebei, 050051, PR China.

Objective: To explore a method of treating Madelung deformity.

Methods: Seven cases of Madelung deformity had been treated with the excision of ulnar carpi ulnaris segment and distal osteotomy of radius and tight constrict of extensor carpi ulnaris from Mar. 2000 to Nov. 2003. The angle of ulnar tilting was 37-70 degrees and the angle of volar tilting was over 16 degrees. A longitudinal incision on each side of the radius and ulnar was made, the ulna was excised about 2-3 cm segment. Then the fracture of ulna was fixed by double across vertical steel wire and the radius was fixed with medullary wire. Lastly the extensor carpi ulnaris was shortened and sutured after the wrist was located rest-position.

Results: After surgery, the deformity of wrist was improved and pain-free in the seven cases. The angle of ulnar tilting was reduced to 22-24 degrees. The angle of volar tilting was reduced to 15 degrees below. Follow-ups were conducted in the 7 patients for 2 years in average. The activity of wrist joint and the rotation of forearm recovered from those before operation. The wrist joint could stretch fully.

Conclusion: This method of treating Madelung proves to be effective in recovering deformity, releasing pain, improving function, and reducing traumatic osteoarthritics of the distal radioulnar joint.
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May 2005
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