Search PubMed⌕ Search

Biomedical subjects

Y Guo

Publications and source records attributed to Y Guo.

At least 343 records · Page 19Linked to original sources
PubMed1998

The effects of electroendosmosis in agarose electrophoresis.

The effects of agarose gel strips without and with 0.03 m(r) electroendosmosis (EEO) on isoelectric focusing (IEF) were studied. It is shown that only agarose without EEO can be used for IEF. The effects of electrode buffer strips using agarose with different EEO of 0, 0.03, 0.08, 0.20 m(r) on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and native PAGE were also studied. It apparently did not affect SDS-PAGE, but affected native PAGE to a certain extent. The higher the EEO value was, the more water was present on the agarose gel strip during a separation. Agarose gel strips with an EEO of 0.2 m(r) are not suitable as electrode buffer strips for native PAGE.

Electrochemistry↗
PubMed1998

Subtyping of transferrin by isoelectric focusing in immobilized pH gradients.

Isoelectric focusing in immobilized pH gradients ranging from pH 5.05 to 5.60 was used to study the distribution of transferrin (Tf) subtypes and their gene frequencies from 188 unrelated healthy donors of the Han population in Beijing. Six phenotypes (TfC1, TfC2, TfC1C2, TfC1C3, TfC1Dchi and TfC2Dchi) were detected and Tf*C3 has never before been reported in the Han population. Gene frequencies were as follows: Tf*C1 = 0.7420, Tf*C2 = 0.2420, Tf*C3 =0.0027, Tf*Dchi = 0.0133. There is good agreement between the observed and expected values corresponding to the Hardy-Weinberg equilibrium (sum (chi2) = 0.9183, df = 2, 0.5 < P < 0.75). The allele frequencies for Tf*C1, Tf*C2 and Tf*Dchi agreed with those previously reported for the Chinese Han population.

Humans↗
PubMed1998

Treatment of hepatocellular carcinoma with the cellular tumor vaccines generated by in vitro modification of tumor cells with non gene transfer approaches.

Anti-tumor immune responses are mediated primarily by T cells. Down regulation of major histocompatibility complex (MHC) and the molecules that costimulate the immune responses is associated with defective signaling of tumor cells for T cell activation. In vitro fusion of autologous tumor cells with antigen presenting cells (APCs) or treatment of tumor cells with a combination of cytokines significantly increased the expression of MHC class I and adhesion molecules on tumor cell surfaces that costimulate host immune responses. The hybrid cells generated by fusion of tumor cells with APCs and the tumor cells treated in vitro with a combination of cytokines and pre-incubated with a bispecific monoclonal antibody (bi-Mab) cross-linking antigen on tumor cells to CD28 on T cells, become immunogenic and able to stimulate naive T cells with generation of tumor specific cytotoxic T cells both in vitro and in vivo. Immunization with the modified tumor cells elicits an immune response mediated by both CD4+ and CD8+ T cells. This response protected against a parental tumor cell challenge and cured established tumors. The approach was effective in both low immunogenic and non-immunogenic tumor systems. Modification of tumor cells with tumor:APC fusion or the two-step procedure may provide a strategy for development of tumor vaccines that is effective for cancer immunotherapy.

Animals↗
PubMed1998

Mouse glycosylphosphatidylinositol-specific phospholipase D (Gpld1) characterization.

Glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) is an 110-kDa monomeric protein found in the circulation that is capable of degrading the GPI anchor utilized by dozens of cell-surface proteins in the presence of detergent. This protein is relatively abundant (5-10 microgram/ml in human serum), yet its sites of synthesis, gene structure, and overall function are unclear. It is our purpose to use the mouse system to determine its putative roles in lipid transport, pathogen control, and diabetes. We have isolated murine full-length cDNA for GPI-PLD from a pancreatic alpha cell library. The deduced amino acid sequence shows 74% homology to bovine and human GPI-PLD. There is a single structural gene (Gpld1) mapping to mouse Chromosome (Chr) 13, and among nine tissues, liver showed the greatest abundance of GPI-PLD mRNA. Genetic differences in serum GPI-PLD activity were seen among four mouse strains, and no correlation was seen between GPI-PLD activity and circulating levels of high density lipoproteins in these mice. This is the first report of map position and genetic regulation for Gpld1. This information will enable us to further study the expression and function of GPI-PLD in normal and pathological conditions.

Amino Acid Sequence↗
PubMed1998

The nitric oxide hypothesis of late preconditioning.

Ischemic preconditioning (PC) occurs in two phases: an early phase, which lasts 2-3 h, and a late phase, which begins 12-24 h later and lasts 3-4 days. The mechanism for the late phase of PC has been the focus of intense investigation. We have recently proposed the "NO hypothesis of late PC", which postulates that NO plays a prominent role both in initiating and in mediating this cardioprotective response. The purpose of this essay is to review the evidence supporting the NO hypothesis of late PC and to discuss its implications. We propose that, on day 1, a brief ischemic stress causes increased production of NO (probably via eNOS) and .O2-, which then react to form ONOO-, ONOO-, in turn, activates the epsilon isoform of protein kinase C (PKC), either directly or via its reactive byproducts such as .OH. Both NO and secondary species derived from .O2- could also stimulate PKC epsilon independently. PKC epsilon activation triggers a complex signaling cascade that involves tyrosine kinases (among which Src and Lck appear to be involved) and probably other kinases, the transcription factor NF-kappa B, and most likely other as yet unknown components, resulting in increased transcription of the iNOS gene and increased iNOS activity on day 2, which is responsible for the protection during the second ischemic challenge. Tyrosine kinases also appear to be involved on day 2, possibly by modulating iNOS activity. According to this paradigm, NO plays two completely different roles in late PC: on day 1, it initiates the development of this response, whereas on day 2, it protects against myocardial ischemia. We propose that two different NOS isoforms are sequentially involved in late PC, with eNOS generating the NO that initiates the development of the PC response on day 1 and iNOS then generating the NO that protects against recurrent ischemia on day 2. The NO hypothesis of late PC puts forth a comprehensive paradigm that can explain both the initiation and the mediation of this complex phenomenon. Besides its pathophysiological implications, this hypothesis has potential clinical reverberations, since NO donors (i.e., nitrates) are widely used clinically and could be used to protect the ischemic myocardium in patients.

Animals↗
PubMed1998

A comparative study of the ciliary area of the maxillary sinus mucosa and computed tomographic images.

The ciliary area of the maxillary sinus mucosa and coronal sinus computed tomographic (CT) scans were studied in 36 maxillary sinuses of 28 patients with chronic sinusitis. Tissue specimens allowed ciliary surfaces to be observed under scanning electron microscopy, allowing surfaces to be expressed in terms of ciliary area (CA) as the percentage of mucosal surface occupied by cilia. The opacity produced by mucosal swelling and secretion in the maxillary sinus on CT was assessed by two methods: Min's and modified van der Veken's methods. Both techniques indicated an inverse correlation between opacity of the maxillary sinus and CA. Our findings suggest that the opacity of maxillary sinus on CT could be a significant parameter for predicting the surface conditions of ciliated maxillary mucosa prior to sinus surgery.

Adult↗
PubMed1998

A rare variant translocation t(3;8)(q29;q22) without AML1/ETO fusion transcript in a case of oligoblastic leukemia.

A 43-year-old man with oligoblastic leukemia and t(3;8) variant translocation is reported. At first he was classified as refractory anemia with excess of blasts in transformation according to the FAB criteria for myelodysplastic syndrome. Remission was obtained after intensive chemotherapy. After 8 months, a relapse occurred as overt M2 AML. At presentation chromosome study of bone marrow cells using R- and G-bandings revealed 45,X, -Y,t(3;8)(q29;q22) in 35 of the 42 metaphases analyzed and 46,XY,t(3;8) in one metaphase in addition to normal karyotype in the other six metaphases. However, RT-PCR assay showed no AML1/ETO fusion transcript. At relapse, a karyotype of 46, XY,t(3;8), deletion(4)(p14), add(7)(q32) was observed in all abnormal cells indicating a clonal karyotypic evolution. We believed that this case should be diagnosed as an early form of M2 AML initially. It may be the first case of oligoblastic leukemia with t(3;8) variant translocation. Further study is needed to elucidate its molecular entity.

Adult↗
PubMed1998

Identification of conserved amino acids in murine B7-1IgV domain critical for CTLA4/CD28:B7 interaction by site-directed mutagenesis: a novel structural model of the binding site.

The B7: CD28/CTLA4 interaction plays a major role in T cell responses. Immune intervention targeted at this interaction has demonstrated a vast potential in enhancing tumor immunity and blocking autoimmunity and transplant rejection. However, the structural basis for this interaction is unclear. While we and others have performed site-directed mutagenesis to define amino acids involved in binding CD28 and CTLA4, these residues are localized in different regions, and it is unlikely for all of them to be directly involved. In addition, the effect of the mutations on the overall conformation of B7 has not been systematically evaluated. In this study, we have carried out site-directed mutagenesis to define the amino acids within B7-1 IgV-like domain which participate B7:CD28/CTLA4 interaction. Four anti-B7-1 mAbs that recognize three independent antigenic epitopes on B7-1 were used to monitor the effect of mutations on the overall conformation of B7-1. Of the five mutations in the IgV domain that we have produced, D113 > A appears to interfere with cell surface expression and/or overall conformation of B7-1. while four others do not significantly affect the overall conformation and cell surface expression of B7-1. Among them, G115 > A and Y91 > A eliminated B7-1 binding to both CD28Ig and CTLA4Ig; our previously reported mutants L109 > A and W88 > A selectively affect the B7-1 binding to either CD28Ig or CTLA4Ig. Structural modeling of B7-1 based on the structure of immunoglobulin revealed that these four and other previously identified critical amino acids in both IgV- and IgC-like domains can form a localized structure.

Abatacept↗
PubMed1998

A case of acute megakaryocytic leukemia presenting as peripheral acute leukemia with complex karyotypic abnormalities.

Peripheral acute leukemia (PAL) is extremely rare. We report on the first case of acute megakaryocytic leukemia presenting with PAL and complex chromosomal abnormalities. At diagnosis, the patient had 10.5-21% marrow blasts and 55-60% peripheral blasts which expressed CD42b and CD61. Two related clones with the karyotype of 48,X,-X,+3,+9,del(9)(q12q31) x 2,+17,i(17)(q10)/ 49,idem, +18 were revealed by conventional cytogenetics, but no AML-1/ETO fusion transcript was detected by RT-PCR assay. The significance of this case is discussed concisely.

Acute Disease↗
PubMed1998

(+)-Verussurine, a new steroidal alkaloid from the roots and rhizomes of veratrum nigrum var. ussuriense and structure revision of (+)-verabenzoamine1

Two minor steroidal alkaloids, 1 and 2, have been isolated from the roots and rhizomes of Veratrum nigrum var. ussuriense. Their structures have been determined by the use of spectral data as 7-O-acetyl-15-O-(2-methylbutyroyl)-3-O-veratroylgermine (1) and 15-O-(2-methylbutyroyl)-3-O-veratroylgermine (2). By spectral data comparison with verabenzoamine, the structure of the latter compound has been revised from the previously reported 7-O-acetyl-15-O-(2-methylbutyroyl)-3-O-veratroylgermine (1) to 15-O-(2-methylbutyroyl)-3-O-veratroylgermine (2). Accordingly, alkaloid 1 [7-O-acetyl-15-O-(2-methylbutyroyl)-3-O-veratroylgermine] must be new, and it was given the trivial name verussurine.

Journal Article↗
PubMed1998

Two new steroidal alkaloids, 20-isoveratramine and verapatuline, from the roots and rhizomes of veratrum patulum

Roots and rhizomes of Veratrum patulum L. (Liliaceae), used as a source of the Chinese crude drug "Li-lu", have yielded two new steroidal alkaloids, 20-isoveratramine (1) and verapatuline (2), along with three known alkaloids, veratramine (3), veratrosine (4), and jervine (5). Structures of new alkaloids 1 and 2 were determined to be a C-20 epimer of 3 and N-(methoxycarbonyl)jervine, respectively, by the use of spectral data including 2D NMR.

Journal Article↗
PubMed1998

A chemokine receptor CCR2 allele delays HIV-1 disease progression and is associated with a CCR5 promoter mutation.

Viral and host factors influence the rate of HIV-1 disease progression. For HIV-1 to fuse, a CD4+ cell must express a co-receptor that the virus can use. The chemokine receptors CCR5 and CXCR4 are used by R5 and X4 viruses, respectively. Most new infections involve transmission of R5 viruses, but variants can arise later that also use CXCR4 (R5-X4 or X4 viruses). This is associated with an increased rate of CD4+ T-cell loss and poor prognosis. The ability of host cells to support HIV-1 entry also influences progression. The absence of CCR5 in approximately 1% of the Caucasian population, due to homozygosity for a 32-nucleotide deletion in the coding region (delta32-CCR5 allele), very strongly protects against HIV-1 transmission. Heterozygosity for the delta32-CCR5 allele delays progression typically by 2 years. A recent study showed that a conservative substitution (V64I) in the coding region of CCR2 also has a significant impact on disease progression, but not on HIV-1 transmission. This was unexpected, since CCR2 is rarely used as a co-receptor in vitro and the V64I change is in a transmembrane region. Because a subsequent study did not confirm this effect on progression to disease, we analyzed CCR2-V64I using subjects in the Chicago MACS. We show that CCR2-V64I is indeed protective against disease progression and go on to show that the CCR2-V64I allele is in complete linkage disequilibrium with a point mutation in the CCR5 regulatory region.

Alleles↗
PubMed1998

The effect of magnesium on oxidative neuronal injury in vitro.

The effect of magnesium on the oxidative neuronal injury induced by hemoglobin was assessed in murine cortical cell cultures. Exposure to 5 microM hemoglobin in physiologic (1 mM) magnesium for 26 h resulted in the death of about one-half the neurons and a sixfold increase in malondialdehyde production; glia were not injured. Increasing medium magnesium to 3 mM reduced neuronal death by about one-half and malondialdehyde production by about two-thirds; neuronal death and lipid peroxidation were approximately doubled in 0.3 mM magnesium. Comparable results were observed in spinal cord cultures. The NMDA antagonist MK-801 weakly attenuated hemoglobin neurotoxicity in low-magnesium medium, but tended to potentiate injury in physiologic magnesium. Incubation in low-magnesium medium alone for 24 h reduced cellular glutathione by approximately 50% in mixed neuronal and glial cultures but by only 10% in pure glial cultures. The iron-dependent oxidation of phosphatidylethanolamine liposomes was attenuated in a concentration-dependent fashion by 2.5-10 mM magnesium; a similar effect was provided by 0.01-0.1 mM cobalt. However, oxidation was weakly enhanced by 0.5-1 mM magnesium. These results suggest that the vulnerability of neurons to iron-dependent oxidative injury is an inverse function of the extracellular magnesium concentration. At high concentrations, magnesium inhibits lipid peroxidation directly, perhaps by competing with iron for phospholipid binding sites. At low concentrations, enhancement of cell death may be due to the combined effect of increased NMDA receptor activity, glutathione depletion, and direct potentiation of lipid peroxidation.

Animals↗
PubMed1998

Toxic effect of hemoglobin on spinal cord neurons in culture.

The vulnerability of spinal cord neurons to hemoglobin was quantitatively assessed in primary cultures derived from fetal mice. Exposure to hemoglobin for 28 h in a serum-free medium resulted in concentration-dependent neuronal death, with an EC50 of 0.9 microM; glia were not injured. Neuronal death was decreased by the ferric iron chelator deferoxamine, the alpha-tocopherol analogue Trolox C, ascorbate, and exogenous catalase, but was potentiated by superoxide dismutase. Neuronal death was also increased by depletion of cellular glutathione with the gamma-glutamylcysteine synthetase inhibitor buthionine sulfoxamine; inhibition of endogenous catalase with 3-amino-1,2,4-triazole had no significant effect. These results suggest that hemoglobin is toxic to spinal neurons via an iron-dependent, oxidative mechanism involving a hydrogen peroxide intermediate, and support the hypothesis that hemoglobin release may contribute to neuronal loss after spinal cord trauma.

Analysis of Variance↗