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Biomedical subjects

Yue Wang

Publications and source records attributed to Yue Wang.

At least 91 records · Page 5Linked to original sources
PubMed2005

A focused microarray to assess dopaminergic and glial cell differentiation from fetal tissue or embryonic stem cells.

We designed oligonucleotide gene-specific probes to develop a focused array that can be used to discriminate between neural phenotypes, identify biomarkers, and provide an overview of the process of dopaminergic neuron and glial differentiation. We have arrayed approximately 100 genes expressed in dopaminergic neurons, oligodendrocytes, and astrocytes, an additional 200 known cytokines, chemokines, and their respective receptors, as well as markers for pluripotent and progenitor cells. The gene-specific 60-mer 3' biased oligonucleotides for these 281 genes were arrayed in a 25 x 12 format based on function. Using human adult brain substantia nigra, human embryonic stem cells (ESCs), and the differentiated progeny of pluripotent cells, we showed that this array was capable of distinguishing dopaminergic neurons, glial cells, and pluripotent cells by their gene expression profiles in a concentration-dependent manner. Using linear correlation coefficients of input RNA with output intensity, we identified a list of genes that can serve as reporting genes for detecting dopaminergic neurons, glial cells, and contaminating ESCs and progenitors. Finally, we monitored NTera2 differentiation toward dopaminergic neurons and have shown the ability of this array to distinguish stages of differentiation and provide important clues to factors regulating differentiation, the degree of contaminating populations, and stage of cell maturity. We suggest that this focused array will serve as a useful complement to other large-scale arrays in routine assessment of cell properties prior to their therapeutic use.

Base Sequence↗
PubMed2005

Selective butyrylcholinesterase inhibition elevates brain acetylcholine, augments learning and lowers Alzheimer beta-amyloid peptide in rodent.

Like acetylcholinesterase, butyrylcholinesterase (BChE) inactivates the neurotransmitter acetylcholine (ACh) and is hence a viable therapeutic target in Alzheimer's disease, which is characterized by a cholinergic deficit. Potent, reversible, and brain-targeted BChE inhibitors (cymserine analogs) were developed based on binding domain structures to help elucidate the role of this enzyme in the central nervous system. In rats, cymserine analogs caused long-term inhibition of brain BChE and elevated extracellular ACh levels, without inhibitory effects on acetylcholinesterase. In rat brain slices, selective BChE inhibition augmented long-term potentiation. These compounds also improved the cognitive performance (maze navigation) of aged rats. In cultured human SK-N-SH neuroblastoma cells, intra- and extracellular beta-amyloid precursor protein, and secreted beta-amyloid peptide levels were reduced without affecting cell viability. Treatment of transgenic mice that overexpressed human mutant amyloid precursor protein also resulted in lower beta-amyloid peptide brain levels than controls. Selective, reversible inhibition of brain BChE may represent a treatment for Alzheimer's disease, improving cognition and modulating neuropathological markers of the disease.

Acetylcholine↗
PubMed2005

Retrospective analysis on Chinese patients diagnosed with acute renal failure hospitalized during the last decade (1994-2003).

OBJECTIVES: To investigate the epidemiology, diagnosis and prognosis of acute renal failure (ARF) in hospitalized Chinese during the last decade. METHODS: The diagnosis of patients with ARF in Peking University Third Hospital from January 1994 to December 2003 was reconfirmed and the data of epidemiology, etiology and prognosis were analyzed. RESULTS: Only 209 discharged cases were diagnosed with ARF and all were reconfirmed. Two peak occurrences were found at ages of 35-45 and 60-80 with a male predominance of approximately 59.7%. Patients diagnosed with ARF accounted for 1.19 per thousand of the admissions in the same period and increased significantly in the last 5 years (p = 0.038). The creatinine level at diagnosis was 345.8 +/- 122.6 micromol/l and had no significant change (p > 0.05). The percent of hospital-acquired ARF (HA-ARF) demonstrated a significant increase in 1999-2003 compared to 1994-1998 (p = 0.008). Intrarenal ARF accounted for 73.69% and was multifactorial, with drugs, infections and operations as leading causes. Renal biopsy was performed in 37.32% (78/209) with 53.84% (42/78) having acute interstitial nephritis. Maintenance dialysis was discontinued in 46.41% because their renal function completely or partially recovered. The overall mortality was 37.91% without improvement over time. The mortality was 6.25% for patients in nephrology department, but 65.51% in ICU (p < 0.001), and was 21.6% for patients in community-acquired ARF (CA-ARF), but 63.1% in HA-ARF (p < 0.001). CONCLUSIONS: During the past 10 years, the number of patients diagnosed with ARF has been rising in hospitalized Chinese. HA-ARF was the major source, and infections, drugs and operations were the leading causes. The diagnosis and prognosis of acute renal failure did not improve much in this population over the decade studied.

Acute Kidney Injury↗
PubMed2005

CD4+ T-cell-dependent immune damage of liver parenchymal cells is mediated by alloantibody.

BACKGROUND: Allogeneic hepatocytes initiate both CD4- and CD8-dependent rejection responses. The current studies address the hypothesis that acute damage of allogeneic liver parenchymal cells by the CD4-dependent pathway is alloantibody-mediated and examines immune conditions which promote activation of this pathway. METHODS: The role of alloantibody in CD4-dependent hepatocyte rejection was evaluated by assessing hepatocyte (FVB/N, H-2q) survival in CD8-depleted B-cell knockout (KO) (H-2b) recipients and by monitoring hepatocyte survival in C57BL/6.SCID (H-2b) recipients transfused with donor-reactive alloantibody. The development of donor-reactive alloantibody in C57BL/6 (H-2b), CD8-depleted C57BL/6, CD8 KO (H-2b), IFN-gamma KO (H-2b), perforin KO (H-2b), and FasL mutant gld/gld (H-2b) hepatocyte recipients was assessed. RESULTS: Hepatocyte rejection in B-cell KO mice was significantly delayed by CD8+ T-cell depletion (median survival time [MST], 35 days) when compared to untreated (MST, 8 days) and CD4-depleted (MST, 10 days) recipient mice. Transfusion of donor-reactive alloantibody into SCID recipients with functional hepatocellular allografts was sufficient to precipitate rejection in a dose-dependent fashion. Donor-reactive alloantibody was minimal in the serum of C57BL/6 hepatocyte recipients, but was produced in significant quantities in hepatocyte recipients genetically deficient in or depleted of CD8+ T cells and in recipients with impaired cytotoxic effector mechanisms. In addition, recipients with defects in Th1 immunity, such as IFN-gamma KO recipients, also produced readily detectable alloantibody. CONCLUSIONS: Collectively, these data support the hypothesis that acute immune damage of allogeneic hepatocytes by the CD4-dependent pathway is mediated by alloantibody and that this pathway is favored when Th1- or cell-mediated cytotoxic effector immune mechanisms are impaired.

Animals↗
PubMed2005

Sensory neurons from Nf1 haploinsufficient mice exhibit increased excitability.

Neurofibromatosis type 1 (NF1) is a common genetic disorder characterized by tumor formation. People with NF1 also can experience more intense painful responses to stimuli, such as minor trauma, than normal. NF1 results from a heterozygous mutation of the NF1 gene, leading to decreased levels of neurofibromin, the protein product of the NF1 gene. Neurofibromin is a guanosine triphosphatase activating protein (GAP) for Ras and accelerates the conversion of active Ras-GTP to inactive Ras-GDP; therefore mutation of the NF1 gene frequently results in an increase in activity of the Ras transduction cascade. Using patch-clamp electrophysiological techniques, we examined the excitability of capsaicin-sensitive sensory neurons isolated from the dorsal root ganglia of adult mice with a heterozygous mutation of the Nf1 gene (Nf1+/-), analogous to the human mutation, in comparison to wildtype sensory neurons. Sensory neurons from adult Nf1+/- mice generated a more than twofold higher number of action potentials in response to a ramp of depolarizing current as wild-type neurons. Consistent with the greater number of action potentials, Nf1+/- neurons had lower firing thresholds, lower rheobase currents, and shorter firing latencies than wild-type neurons. Interestingly, nerve growth factor augmented the excitability of wild-type neurons in a concentration-related manner but did not further alter the excitability of the Nf1+/- sensory neurons. These data clearly suggest that GAPs, such as neurofibromin, can play a key role in the excitability of nociceptive sensory neurons. This increased excitability may explain the painful conditions experienced by people with NF1.

Action Potentials↗
PubMed2005

STM study on quinacridone derivative assemblies: modulation of the two-dimensional structure by coadsorption with dicarboxylic acids.

We describe the two-dimensional (2D) assemblies of N,N'-dialkyl-substituted quinacridone derivatives on highly orientated pyrolytic graphite observed by scanning tunneling microscopy, and focus our discussion on whether the supramolecular organization can be modulated by the coadsorption of dicarboxylic acids. Our experiments have demonstrated that the quinacridone derivatives can form different 2D nanostructures when coadsorbed with dicarboxylic acids of different length at the liquid/graphite interface. Interestingly, N,N'-dihexadecyl-substituted quinacridone derivative alternately takes two different conformations in two columns for its coadsorption with pentadecanedioic acid and form a gridlike structure. It is shown that a cooperative effect of different interactions can be modulated by introducing guest molecule, leading to formation of different self-assembled nanostructures.

Journal Article↗
PubMed2005

Identification and functional characterization of a novel Candida albicans gene CaMNN5 that suppresses the iron-dependent growth defect of Saccharomyces cerevisiae aft1Delta mutant.

In Saccharomyces cerevisiae, the transcription factor Aft1p plays a central role in regulating many genes involved in iron acquisition and utilization. An aft1Delta mutant exhibits severely retarded growth under iron starvation. To identify the functional counterpart of AFT1 in Candida albicans, we transformed a C. albicans genomic DNA library into aft1Delta to isolate genes that could allow the mutant to grow under iron-limiting conditions. In the present paper, we describe the unexpected discovery in this screen of CaMNN5. CaMnn5p is an alpha-1,2-mannosyltransferease, but its growth-promoting function in iron-limiting conditions does not require this enzymatic activity. Its function is also independent of the high-affinity iron transport systems that are mediated by Ftr1p and Fth1p. We obtained evidence suggesting that CaMnn5p may function along the endocytic pathway, because it cannot promote the growth of end4Delta and vps4Delta mutants, where the endocytic pathway is blocked at an early and late step respectively. Neither can it promote the growth of a fth1Delta smf3Delta mutant, where the vacuole-cytosol iron transport is blocked. Expression of CaMNN5 in S. cerevisiae specifically enhances an endocytosis-dependent mechanism of iron uptake without increasing the uptake of Lucifer Yellow, a marker for fluid-phase endocytosis. CaMnn5p contains three putative Lys-Glu-Xaa-Xaa-Glu iron-binding sites and co-immunoprecipitates with 55Fe. We propose that CaMnn5p promotes iron uptake and usage along the endocytosis pathway under iron-limiting conditions, a novel function that might have evolved in C. albicans.

Amino Acid Motifs↗
PubMed2005

Hepatitis C virus core protein and hepatitis activity are associated through transactivation of interleukin-8.

BACKGROUND: We evaluated the association between variations in hepatitis C virus (HCV) core protein and hepatitis severity in patients with chronic HCV infection who achieved remission without viral eradication and had a biochemical response to interferon (IFN) therapy, to evaluate the effect of HCV core sequence in the absence of the influence of host factors. METHODS. Using serum from 10 patients with a biochemical response and 10 patients with no response, we measured serum levels of interleukin (IL)-1 beta , IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IFN- gamma , and tumor necrosis factor- alpha before and after IFN therapy. Expression vectors with the core region were transfected into Huh7 cells, and cytokine induction was evaluated by reporter assay. RESULTS: In biochemical responders, only IL-8 levels decreased after IFN therapy (P=.04). Changes in the C-terminal hydrophobic region were observed more frequently in biochemical responders. Activation of the IL-8 promoter by HCV core protein was significantly decreased in biochemical responders after IFN therapy (P=.04). When 69 C-terminal amino acids from before IFN therapy were replaced with those from after IFN therapy in 3 biochemical responders, their ability to transactivate IL-8 decreased. CONCLUSIONS: Differences in amino acids in the HCV core protein correlates with hepatitis activity through the modulation of IL-8 induction in HCV-infected patients.

Adult↗
PubMed2005

The formin family protein CaBni1p has a role in cell polarity control during both yeast and hyphal growth in Candida albicans.

Formins are conserved eukaryotic proteins playing key roles in regulating cell polarity. We have characterized the roles of a formin CaBni1p in the polymorphic fungus Candida albicans. CaBni1p localized persistently to hyphal tips during hyphal growth but to distinct growth sites at different cell cycle stages during yeast growth. Cabni1Delta yeast cells exhibited several morphological defects, such as round and enlarged cells, widened bud necks and a random budding pattern. Although Cabni1Delta cells could still undergo yeast-hypha growth switch, the hyphae were markedly swollen. Cabni1Delta also showed defects in spindle and cytoplasmic microtubule orientation and positioning. Coincidentally, the spindle orientation protein CaKar9p in Cabni1Delta yeast cells appeared as multiple random cortical spots, in contrast to the single spot at the bud tip of many wild-type cells. Interestingly, several defects manifested in Cabni1Delta yeast cells were partially corrected during hyphal growth. We found that the second formin CaBnr1p was recruited to hyphal tips, while it localized only to the bud neck during yeast growth. This behavior of CaBnr1p may play a key role in correcting Cabni1Delta defects during hyphal growth. Cabni1Delta exhibited reduced virulence in mice. These results indicate that the formins play an important role in Candida albicans polarized growth and CaBni1p's function is required for virulence.

Actins↗
PubMed2005

(2,2'-Biquinoline-kappa(2)N,N')dichloropalladium(II), -copper(II) and -zinc(II).

In the three title complexes, namely (2,2'-biquinoline-kappa(2)N,N')dichloropalladium(II), [PdCl2(C18H12N2)], (I), and the corresponding copper(II), [CuCl2(C18H12N2)], (II), and zinc(II) complexes, [ZnCl2(C18H12N2)], (III), each metal atom is four-coordinate and bonded by two N atoms of a 2,2'-biquinoline molecule and two Cl atoms. The Pd(II) atom has a distorted cis-square-planar coordination geometry, whereas the Cu(II) and Zn(II) atoms both have a distorted tetrahedral geometry. The dihedral angles between the N-M-N and Cl-M-Cl planes are 14.53 (13), 65.42 (15) and 85.19 (9) degrees for (I), (II) and (III), respectively. The structure of (II) has twofold imposed symmetry.

Models, Molecular↗
PubMed2005

Tetrakis(mu(2)-1,8-naphthyridine)-1:2kappa(4)N:N';3:4kappa(4)N:N'-bis(mu(2)-salicylato)-1:4kappa(2)O:O';2:3kappa(2)O:O'-tetrakis(salicylic acid)-1kappaO,2kappaO,3kappaO,4kappaO-tetrasilver(I)(4 Ag-Ag).

The title complex, [Ag4(C7H5O3)2(C8H6N2)4(C7H6O3)4], lies about an inversion centre and has a unique tetranuclear structure consisting of four Ag(I) atoms bridged by four N atoms from two 1,8-naphthyridine (napy) ligands to form an N:N'-bridge and four O atoms from two salicylate (SA) ligands to form an O:O'-bridge. The Ag atoms have distorted octahedral coordination geometry. The centrosymmetric Ag4 ring has Ag-Ag separations of 2.772 (2) and 3.127 (2) A, and Ag-Ag-Ag angles of 107.70 (4) and 72.30 (4) degrees . All SA hydroxy groups take part in intramolecular O-H...O hydrogen bonding. In the crystal packing, the napy rings are oriented parallel and overlap one another. These pi-pi interactions, together with weak intermolecular C-H...O contacts, stabilize the crystal structure.

Journal Article↗
PubMed2005

Corticotropin-releasing hormone contributes to the peripheral inflammatory response in experimental autoimmune encephalomyelitis.

Peripheral corticotropin-releasing hormone (CRH) is thought to have proinflammatory effects. We used the model of experimental autoimmune encephalomyelitis (EAE) to study the role of CRH in an immune-mediated disease. We showed that CRH-deficient mice are resistant to EAE, with a decrease in clinical score as well as decreased cellular infiltration in the CNS. Furthermore, Ag-specific responses of primed T cells as well as anti-CD3/anti-CD28 TCR costimulation were decreased in crh(-/-) mice with decreased production of Th1 cytokines and increased production of Th2 cytokines. Wild-type mice treated in vivo with a CRH antagonist showed a decrease in IFN-gamma production by primed T cells in vitro. This effect of CRH is independent of its ability to increase corticosterone production, because adrenalectomized wild-type mice had similar disease course and severity as control mice. We found that IkappaBalpha phosphorylation induced by TCR cross-linking was decreased in crh(-/-) T cells. We conclude that peripheral CRH exerts a proinflammatory effect in EAE with a selective increase in Th1-type responses. These findings have implications for the treatment of Th1-mediated diseases such as multiple sclerosis.

Animals↗
PubMed2005

Mycobacteria inhibition of IFN-gamma induced HLA-DR gene expression by up-regulating histone deacetylation at the promoter region in human THP-1 monocytic cells.

Infection of macrophages with mycobacteria has been shown to inhibit the macrophage response to IFN-gamma. In the current study, we examined the effect of Mycobacteria avium, Mycobacteria tuberculosis, and TLR2 stimulation on IFN-gamma-induced gene expression in human PMA-differentiated THP-1 monocytic cells. Mycobacterial infection inhibited IFN-gamma-induced expression of HLA-DRalpha and HLA-DRbeta mRNA and partially inhibited CIITA expression but did not affect expression of IFN regulatory factor-1 mRNA. To determine whether inhibition of histone deacetylase (HDAC) activity could rescue HLA-DR gene expression, butyric acid and MS-275, inhibitors of HDAC activity, were added at the time of M. avium or M. tuberculosis infection or TLR2 stimulation. HDAC inhibition restored the ability of these cells to express HLA-DRalpha and HLA-DRbeta mRNA in response to IFN-gamma. Histone acetylation induced by IFN-gamma at the HLA-DRalpha promoter was repressed upon mycobacteria infection or TLR2 stimulation. HDAC gene expression was not affected by mycobacterial infection. However, mycobacterial infection or TLR2 stimulation up-regulated expression of mammalian Sin3A, a corepressor that is required for MHC class II repression by HDAC. Furthermore, we show that the mammalian Sin3A corepressor is associated with the HLA-DRalpha promoter in M. avium-infected THP-1 cells stimulated with IFN-gamma. Thus, mycobacterial infection of human THP-1 cells specifically inhibits HLA-DR gene expression by a novel pathway that involves HDAC complex formation at the HLA-DR promoter, resulting in histone deacetylation and gene silencing.

Acetylation↗
PubMed2005

[Protective immunity of the recombinant Schistosoma japonicum specific very low density lipoprotein binding protein as a vaccine candidate].

OBJECTIVE: To investigate the protective immunity against Schistosoma japonicum in mice immunized with recombinant specific very low density lipoprotein binding protein (SVLBP) and its potential as vaccine candidate. METHODS: Recombinant SVLBP antigen was over-expressed under IPTG induction and purified by Ni-NTA affinity chromatography. C57BL/6 mice were immunized three times with purified reSVLBP complexed with Freund's adjuvant, at biweekly intervals. Then 35+/-1 cercariae of S. japonicum were given to each mouse by abdominal skin 10 days after the 3rd immunization. 45 days later, all mice were sacrificed to collect adult worms and count liver eggs. serum samples were collected before immunization and after challenge respectively, and were probed the antigen-specific antibodies using a panel of ELISAs. RESULTS: The worm burden and the egg deposition in liver tissue were reduced by 33.4% and 47.6% respectively in the immunized group, in comparison with the adjuvant control group (P<0.05). Higher titer (>1:6 400) of total IgG was observed after challenge infection. The vaccinated mice developed significantly higher levels of IgG2a, IgG2b, IgG1 than those of control mice. CONCLUSION: The recombinant tegumental SVLBP antigen could induce partial protection against S. japonicum infection. These data demonstrate the potential of SVLBP as a schistosome vaccine candidate.

Animals↗
PubMed2005

Supramolecular structures and assembly and luminescent properties of quinacridone derivatives.

The synthesis and single-crystal X-ray structures of two quinacridone derivatives, N,N'-di(n-butyl)quinacridone (1) and N,N'-di(n-butyl)-1,3,8,10-tetramethylquinacridone (2), are reported, and the 1H NMR, absorption, photoluminescent (PL), and electroluminescent (EL) characteristics are presented. Both these crystal structures are characterized by intermolecular pi...pi and hydrogen bonding interactions. The intermolecular pi...pi interactions lead to the formation of molecular columns in the solids of 1 and 2, and the interplanar contact distances between two adjacent molecules are 3.48 and 3.55 angstroms, respectively. Crystals of 1 display shorter intermolecular pi...pi contacts and higher density than 2. These results suggest that tighter intermolecular interactions exist in 1. The 1H NMR, absorption, and PL spectra of 1 and 2 in solutions exhibit concentration-dependent properties. The PL quantum yields of 1 in solutions decrease more quickly with the increase of concentration compared to that of 2 in solutions. For solid thin films of Alq3:1 (Alq3 = tris(8-hydroxyquinolinato)aluminum), emission intensities dramatically decrease and obvious red shifts are observed when the dopant concentration is above 4.2%, while for films of Alq3:2, a similar phenomenon occurs when the concentration is above 6.7%. EL devices with Alq3:1 as emitting layer only show high efficiencies (20.3-14.5 cd/A) within the narrow dopant concentration range of 0.5-1.0%. In contrast, high efficiencies (21.5-12.0 cd/A) are achieved for a wider dopant concentration range of 0.5-5.0% when Alq3:2 films are employed as emitting layer. The different PL and EL concentration-dependent properties of the solid thin films Alq3:1 and Alq3:2 are attributed to their different molecular packing characteristics in the solid state.

Journal Article↗
PubMed2005

Vitamin K2 binds 17beta-hydroxysteroid dehydrogenase 4 and modulates estrogen metabolism.

Vitamin K is a cofactor for gamma-glutamyl carboxylase, an enzyme that is important for blood coagulation. Recent studies have shown that vitamin K has other roles, in addition to post-transcriptional modification, such as bone metabolism and antitumoral actions; these findings have indicated that there might be unknown intracellular binding proteins that are specific for vitamin K. In this study, vitamin K-binding proteins were characterized by pull-down experiment using a chemically synthesized biotynylated vitamin K followed by mass spectrometric identification of the pull-downed components. The results indicated that 17beta hydroxy steroid dehydrogenase 4, apolipoportein E, and 40S ribosomal proteins S7 and S13 might be the candidates of the vitamin K-binding proteins. Subsequent experiments showed that vitamin K2 binds 17beta hydroxysteroid dehydrogenase 4 and decreases the intracellular estradiol:estrone ratio, which resulted in the inhibition of the amount of estrogen receptor alpha-binding to its target DNA. These results suggest a possible novel role for vitamin K in modulating estrogen function.

17-Hydroxysteroid Dehydrogenases↗
PubMed2005

(Di-2-pyridylamine-kappa2N,N')(naphthalene-2,3-diolato-kappa2O,O')palladium(II) monohydrate and (di-2-pyridylamine-kappa2N,N')(3-oxidonaphthalene-2-carboxylato-kappa2O,O')palladium(II).

In the title complexes, [Pd(C10H6O2)(C10H9N3)].H2O, (I), and [Pd(C11H6O3)(C10H9N3)], (II), the Pd(II) centers have a distorted cis-square-planar geometry. In (I), the Pd(II) atom is coordinated to two N atoms of the di-2-pyridylamine (DPA) ligand and two O atoms of the naphthalene-2,3-diolate (ND) dianion. In (II), the Pd(II) atom is coordinated to two N atoms of the DPA ligand, one carboxylate O atom and one oxide O atom from the 3-oxidonaphthalene-2-carboxylate (NC) ligand. The dihedral angle between the planes of the two pyridine rings of DPA in (I) is 16.20 (12) degrees and that in (II) is 29.45 (10) degrees . In (I), the molecules are linked by N-H...O and O-H...O hydrogen bonds to generate centrosymmetric dimers. In (II), molecules are linked by N-H...O and C-H...O hydrogen bonds to generate spirals.

Amines↗