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Biomedical subjects

Y Fu

Publications and source records attributed to Y Fu.

At least 145 records · Page 8Linked to original sources
PubMed1999

Prophylactic effects of tetramethyl pyrazine on mice with endotoxemia and its relationship with platelet-activating factor.

AIM: To study the prophylactic effects of tetramethyl pyrazine (TMP) on mice with endotoxemia and its relationship with platelet-activating factor (PAF). METHODS: LD80 of lipopolysaccharides (LPS, 15 mg.kg-1) was injected into mice (i.v.) pretreated with TMP (i.p.). The survival rate and the level of serum PAF were observed. The PAF induced by LPS in vivo and in vitro, and the activities of PLA2 and acetyl-CoA: lyso-PAF acetyltransferase were determined. RESULTS: TMP (10, 30, 90 mg.kg-1) obviously lowered the mortality of mice and also dose-dependently decreased the level of serum PAF [(25.5 +/- 1.7), (13.4 +/- 3.2), (9.6 +/- 2.1) micrograms.L-1, vs control (29.3 +/- 2.1) micrograms.L-1, P < 0.01]. TMP (0.05, 0.5, 5, 50 mumol.L-1) dose-dependently decreased the release of PAF [(12.7 +/- 1.6), (8.9 +/- 1.2), (6.9 +/- 0.8), (5.5 +/- 1.0) micrograms.L-1 vs control (11.9 +/- 1.8) micrograms.L-1, P < 0.01] from PMO cultured with LPS (5 mg.L-1), reduced the PLA2 activity [(149.9 +/- 2.8), (117.5 +/- 2.0), (89.6 +/- 2.0), (75.0 +/- 2.8) U vs control (170.8 +/- 3.9) U, P < 0.01] and acetyl-CoA: lyso-PAF acetyltransferase activity [PAF (9.5 +/- 0.7), (5.2 +/- 0.7), (2.9 +/- 0.3), (2.5 +/- 0.3) micrograms.g-1 (protein).min-1 vs control (11.0 +/- 0.7) micrograms.g-1 (protein).min-1, P < 0.01] of PMO lysate. CONCLUSION: TMP protected the mice with endotoxemia from the death by decreasing the biosynthesis of PAF through the inhibition of the activities of PLA2 and acetyl-CoA: lyso-PAF acetyl-transferase.

Acetyltransferases↗
PubMed1999

Action sites of rotation and unit firing induced by l-stepholidine and DA agonists in basal ganglia of 6-OHDA-lesioned rats.

AIM: To elucidate the action sites of l-stepholidine (SPD) in the basal ganglia. METHODS: Counting the rotations after intra-nucleus microinjection and recording the neuron firing by microiontophoresis of SPD and DA agonists in the basal ganglia of 6-hydroxydopamine (6-OHDA)-lesioned rats. RESULTS: The DA immunoreactive substance was markedly reduced in the 6-OHDA-lesioned rats. The intra-neostriatum microinjection of apomorphine (Apo, D1/D2), SK&F 38393 (D1), and SPD elicited remarkable rotation, and the characteristics of SK&F 38393-produced rotation were of long latency and long duration. The intra-substantia nigra pars reticulata (SNR) injection of Apo, SK&F 38393, and SPD induced the rotation response, while the selective D2 agonist quinpirole hydrochloride (Ly171555) did not because of scarce D2 receptors in the SNR. The intraglobus pallidus (GP) injection of DA agonists and SPD failed to evoke rotation, but the GP nucleus still had the contribution to rotation elicited by i.p. injection of DA agonists and SPD in the 6-OHDA-lesioned rats with successive kainic acid (KA) lesion. Besides, the successive lesion of entopeduncular nucleus (EP) on rotation was less important than that of GP nucleus. The microiontophoresis of Apo and SPD into the SNR could evoke the neuron firing, but failed to activate the GP neurons, which were activated by sodium glutamate (Glu) and inhibited by gamma-aminobutyric acid (GABA). CONCLUSION: The action sites of SPD-induced rotation and neuron firing via the D1 receptors are in the neostriatum and SNR instead of GP. The direct neurocircuit through SNR is the most important for rotation of 6-OHDA-lesioned rats.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1999

[Relevance of Fc gamma R polymorphism to the susceptibility of early-onset periodontitis].

OBJECTIVE: To investigate the polymorphism of the Fc gamma R genotype and its association with the susceptibility of early-onset periodontitis (EOP). METHODS: DNA of the white blood cells from 33 subjects with EOP and 27 healthy controls was extracted. Genotypes of the Fc gamma RIIA and Fc gamma RIIIB were determined by PCR followed by BstUI restriction endonuclease digestion and DNA sequencing, respectively. Then compared the differences in distribution of each genotype. RESULTS: No statistical difference in distribution of Fc gamma RIIA was observed between patients and controls. However, a significant over-representation of the Fc gamma RIIIB NA1/NA1 was found in EOP. CONCLUSION: These results suggest that the Fc gamma RIIIB NA1/NA1 may be a risk indicator for the susceptibility of the EOP.

Adolescent↗
PubMed1999

[The value of combined use of bone marrow smear and section in lymphoma for diagnosis and staging].

OBJECTIVE: To explore the value of combined use of bone marrow smear and section in lymphoma for diagnosis and staging. METHODS: Smears of peripheral blood and bone marrow from 114 cases of lymphoma were stained according to Wright. Plastic embedded sections of the 114 cases were stained according to HE, HGF and Gomori. RESULTS: None of the 7 patients with Hodgkin's lymphoma (HD) presented bone marrow involvement, while 32 (29.9%) of the 107 patients with Non-Hodgkin's lymphoma (NHL) presented bone marrow involvement, 13 (40.6%) of the 32 cases in stage I, II, III were promoted to stage IV after bone marrow examination. In 5 of the 32 patients without lymphadenopathy the diagnosis of lymphoma was established through bone marrow study. Lymphoma cells in bone marrow and peripheral blood varied in morphology. Bone marrow involvement might be focal (81.3%) or diffused (18.7%). There were mainly five type: (1) Small lymphocyte type. (2) blast-like lymphocyte type. (3) multimorphology type. (4) lymphoplasmacytoid cell type. (5) granuloma type. CONCLUSION: Bone marrow examination is of importance in patients with known or suspected lymphomas and it may be diagnostic in patients without lymphadenopathy or in cases with no conclusive histological evidence from other sites.

Adolescent↗
PubMed1999

[Analysis and prevention of reoperation on congenital choledochal cyst].

OBJECTIVE: To investigate the reasons and prevention of reoperation on congenital choledochal cyst (CCC). METHODS: The sex, age, cyst type, timing and method of operation were analyzed 22 reoperated (CCC) patients who underwent reoperation. RESULTS: The reoperation rate was 24.4% (22/90). The gender age and cyst type were not related to reoperation rate (P > 0.05). Reoperation rate was correlated with the timing the modality and the manoeuvre of the surgery. The previous emergent surgery incurred higher reoperation rate than that of selective operation (P < 0.01). The reoperation rate was 88.9% in patients previously undergoing CCC extracorporeal drainage, it was 52.4% in group of internal drainage and 5.0% in group previously undergoing CCC resection (P < 0.01). CONCLUSIONS: Congenital choledochal cyst should be treated by surgery in its early stage. Pradent policy should be adopted on the use of PTC and ERCP. Outer drainage was used as the first-aid measure; internal drainage should be abandoned; resection of the cyst with Roux-Y hepaticojejunostomy should be the therapy of choice.

Adult↗
PubMed1999

[The relationship between surgical staging, pathologic grading, operative type and postoperative recurrence in giant cell tumor of bone].

Sixty-eight surgical procedures of 58 patients with Giant Cell Tumor of Bone(GCT) were followed up over two years. The recurrence rate of GCT was Stage 1: 0 in 5, Stage 2: 15.4% in 39 and Stage 3: 37.5% in 24. It was significantly higher in Stage 3 than in Stage 2 (P < 0.05). The recurrence rate of GCT in Stage 2 was 30.8% in 13 intralesional curettage, and 0 in 17 wide or radical resection(P < 0.05). We conclude that the surgical staging of GCT has important value in predicting postoperative recurrence, in accurately evaluating the operative efforts and in guiding treatment, and that the operative type is a significant factor effecting on the recurrence of GCT.

Adolescent↗
PubMed1999

[The relationship between nasopharynx surface-active agents and otitis media effusion].

This experiment was done with a view to exploring the etiologic mechanism and new therapy of otitis media effusion (OME). The amount of lecithin, which is representative of the surfactants in the nasopharynx irrigation wash liquid, was determined by photometry in 40 cases OME and 40 normal controls. The results showed the surfactant of otitis media effusion (8.637 +/- 2.730 mg/L) was significantly lower than that of normal (39.212 +/- 2.437 mg/L) in the nasopharynx irrigation wash liquid (P < 0.01). The surfactant of child group of OME (8.062 +/- 2.925 mg/L) significantly lower than that of normal control(39.787 +/- 2.557 mg/L, P < 0.01). The surfactant of otitis media effusion in the nasopharynx irrigation wash liquid was not associated with the course of OME. These data suggest that the surfactant reduction in the nasopharynx could indirectly reflect the level of the surfactant in the eustachian tube and the middle ear and influence the eustachian tube function. Surfactant reduction may be one of the etiologic mechanisms of OME. Increasing the surfactant in the nasopharynx and eustachian tube could be beneficial to reducing the persistent otitis media effusion.

Adolescent↗
PubMed1998

Acute coronary syndromes in the GUSTO-IIb trial: prognostic insights and impact of recurrent ischemia. The GUSTO-IIb Investigators.

BACKGROUND: Recurrent ischemia after an acute coronary syndrome portends an unfavorable outcome and has major resource-use implications. This issue has not been studied systematically among the spectrum of patients with acute coronary presentations, encompassing those with and without ST-segment elevation. METHODS AND RESULTS: We assessed the 1-year prognosis of the 12 142 patients enrolled in the GUSTO-IIb trial by the presence (n=4125) or absence (n=8001) of ST-segment elevation. This latter group was further categorized into those with baseline myocardial infarction (n=3513) or unstable angina (n=4488). We also assessed the incidence of recurrent ischemia and its impact on outcomes. Recurrent ischemia was significantly rarer in those with ST-segment elevation (23%) than in those without (35%; P<0.001). Mortality at 30 days was greater among patients with ST-segment elevation (6.1% versus 3.8%; P<0.001) but less so at 6 months; by 1 year, mortality did not differ significantly (9.6% versus 8.8%). Patients with non-ST-segment-elevation infarction had higher rates of reinfarction at 6 months (9.8% versus 6.2%) and higher 6-month (8.8% versus 5.0%) and 1-year mortality rates (11.1% versus 7.0%) than such patients who had unstable angina. CONCLUSIONS: Refractory ischemia was associated with an approximate doubling of mortality among patients with ST-segment elevation and a near tripling of risk among those without ST elevation. This study highlights not only the substantial increase in late mortality and reinfarction with non-ST-segment-elevation infarction but also the opportunities for better triage and application of therapeutic strategies for patients with recurrent ischemia.

Acute Disease↗
PubMed1998

Formation of the human fibrinogen subclass fib420: disulfide bonds and glycosylation in its unique (alphaE chain) domains.

COS cell transfection has been used to monitor the assembly and secretion of fibrinogen molecules, both those of the subclass containing the novel alphaE chain and those of the more abundant subclass whose alpha chains lack alphaE's globular C-terminus. That region, referred to as the alphaEC domain, is closely related to the ends of beta and gamma chains of fibrinogen (betaC and gammaC). Transfection of COS cells with alphaE, beta, and gamma cDNAs alone results in secretion of the symmetrical molecule (alphaEbetagamma)2, also known as Fib420. Cotransfection with cDNA for the shorter alpha chain yielded secretion of both (alphabetagamma)2 and (alphaEbetagamma)2 but no mixed molecules of the structure alphaalphaE(betagamma)2. Exploiting the COS cells' fidelity with regard to Fib420 production, identification was made of the highly conserved Asn667 as the sole site of N-linked glycosylation in the alphaE chain. No evidence from Cys --> Ser replacements was found for interchain disulfide bridges involving the four cysteines of the alphaEC domain. However, for fibrinogen secretion, the alphaE, beta, and gamma subunits do exhibit different requirements for integrity of the two intradomain disulfide bridges located at homologous positions in their respective C-termini, indicating dissimilar structural roles in the process of fibrinogen assembly.

Animals↗
PubMed1998

[The microsatellite instability and loss of heterozygosity in chromosome translocation breakpoint in leukemia].

OBJECTIVE: To investigate the microsatellite instability (MSI) and loss of heterozygosity (LOH) near the chromosome translocation breakpoints of various types of leukemia. METHODS: PCR amplification of 11 microsatellite loci closely linked to chromosome translocation breakpoints in 30 leukemia patients. RESULTS: Twenty one in 30 cases of leukemia had MSI in from 1 to 14 microsatellite loci. Eleven in 15 cases of acute leukemia had microsatellite instability (MSI) in more than 1 locus; among them 4 cases had MSI in from 7 to 11 loci. In order of MSI presence rate were D22S315>D9S179>D16S515>D8S559>D12S89. In six cases of chronic myeloid leukemia, 4 cases had MSI in more than 3 loci. Thirteen (2/15) percent of acute leukemia patients had loss of heterozygosity (LOH); the rate was higher than that in other leukemia types. CONCLUSION: The results of MSI and LOH in many cases indicate that there are a lot of allelic alterations in leukemia patients, but those changes have no special relationship with chromosome translocation breakpoints in various leukemia types.

Chromosome Breakage↗
PubMed1998

Cloning and disruption of caPLB1, a phospholipase B gene involved in the pathogenicity of Candida albicans.

The Candida albicans PLB1 gene was cloned using a polymerase chain reaction-based approach relying on degenerate oligonucleotide primers designed according to the amino acid sequences of two peptide fragments obtained from a purified candidal enzyme displaying phospholipase activity (Mirbod, F., Banno, Y., Ghannoum, M. A., Ibrahim, A. S., Nakashima, S., Yasuo, K., Cole, G. T., and Nozawa, Y. (1995) Biochim. Biophys. Acta 1257, 181-188). Sequence analysis of a 6.7-kilobase pair EcoRI-ClaI genomic clone revealed a single open reading frame of 1818 base pairs that predicts for a pre-protein of 605 residues. Comparison of the putative candidal phospholipase with those of other proteins in data base revealed significant homology to known fungal phospholipase Bs from Saccharomyces cerevisiae (45%), Penicillium notatum (42%), Torulaspora delbrueckii (48%), and Schizosaccharomyces pombe (38%). Thus, we have cloned the gene encoding a C. albicans phospholipase B homolog. This gene, designated caPLB1, was mapped to chromosome 6. Disruption experiments revealed that the caplb1 null mutant is viable and displays no obvious phenotype. However, the virulence of strains deleted for caPLB1, as assessed in a murine model for hematogenously disseminated candidiasis, was significantly attenuated compared with the isogenic wild-type parental strain. Although deletion of caPLB1 did not produce any detectable effects on candidal adherence to human endothelial or epithelial cells, the ability of the caplb1 null mutant to penetrate host cells was dramatically reduced. Thus, phospholipase B may well contribute to the pathogenicity of C. albicans by abetting the fungus in damaging and traversing host cell membranes, processes which likely increase the rapidity of disseminated infection.

Amino Acid Sequence↗
PubMed1998

Mechanism of reductive activation of potato tuber ADP-glucose pyrophosphorylase.

The potato tuber (Solanum tuberosum L.) ADP-glucose pyrophosphorylase activity is activated by a incubation with ADP-glucose and dithiothreitol or by ATP, glucose- 1-phosphate, Ca2+, and dithiothreitol. The activation was accompanied by the appearance of new sulfhydryl groups as determined with 5, 5'-dithiobis(2-nitrobenzoic acid). By analyzing the activated and nonactivated enzymes on SDS-polyacrylamide gel electrophoresis under nonreducing conditions, it was found that an intermolecular disulfide bridge between the small subunits of the potato tuber enzyme was reduced during the activation. Further experiments showed that the activation was mediated via a slow reduction and subsequent rapid conformational change induced by ADP-glucose. The activation process could be reversed by oxidation with 5, 5'-dithiobis(2-nitrobenzoic acid). Incubation with ADP-glucose and dithiothreitol could reactivate the oxidized enzyme. Chemical modification experiments with [14C]iodoacetic acid and 4-vinylpyridine determined that the intermolecular disulfide bridge was located between Cys12 of the small subunits of the potato tuber enzyme. Mutation of Cys12 in the small subunit into either Ala or Ser eliminated the requirement of DTT on the activation and prevented the formation of the intermolecular disulfide of the potato tuber enzyme. The mutants had instantaneous activation rates as the wild-type in the reduced state. A two-step activation model is proposed.

Adenosine Triphosphate↗
PubMed1998

Characterization and chromosomal localization of PTP-NP-2, a new isoform of protein tyrosine phosphatase-like receptor, expressed on synaptic boutons.

Recently, there have been several reports describing the cloning and characterization of the novel family of protein tyrosine phosphatase-like receptor molecules (known as IA-2 and PTP-NP/PTP-IAR/IA-2beta/phogrin), which may act as autoantigens in diabetes. Here, we report the molecular characterization and chromosomal localization of a new isoform of this family in brain termed PTP-NP-2 (for PTP-NP tyrosine phosphatase isoform), and its function in rat primary hippocampal neurons. PTP-NP-2 has 48% identity to IA-2. The principal difference between PTP-NP-2 and PTP-NP is a 17-amino-acid insert near the N-terminus of PTP-NP that is absent in PTP-NP-2. Genomic DNA analysis indicates that the 17-amino-acid insert is coded by a separate exon, suggesting that both IA-2beta and PTP-NP-2 are isoforms arising by alternate splicing of the same gene. Reverse transcriptase-PCR revealed that both isoforms are present in human SH-SY5Y neuroblastoma cells. PTP-NP-2 mRNA expression is highly restricted, with a 5.5-kb specific transcript in human fetal and adult brain and 5.5 and 3. 8 kb in human adult pancreas. SH-SY5Y neuroblastoma and U87-MG glioblastoma cells showed specific transcripts of 5.5 and 3.8 kb, respectively, indicating the existence of several isoforms of this molecule in the nervous system. The human gene encoding PTP-NP-2 was assigned to human chromosome 7q22-qter using Southern blot analysis of genomic DNAs from rodent/human somatic hybrid cell lines. Confocal microscopy analyses of rat primary hippocampal neurons revealed that PTP-NP-2 is abundantly expressed on synaptic boutons in primary neurons. Wild-type PTP-NP-2 showed no measurable tyrosine phosphatase activity using an in-vitro pNPP assay. Examination of the PTP-NP-2 catalytic consensus sequence revealed that this sequence differed from the typical tyrosine phosphatase-domain consensus sequence by an alanine to aspartate change (amino acid 930). Mutation of aspartate 930 to alanine produced a catalytically active enzyme, suggesting that native PTP-NP and its isoform PTP-NP-2 are catalytically inactive receptor protein tyrosine phosphatase homologues. Taken together, these results indicate that the tyrosine phosphatase PTP-NP-2 is a new isoform of PTP-NP tyrosine phosphatase, is expressed on synaptic boutons and may participate in the regulation of synaptic bouton endocytosis.

Adult↗
PubMed1998

Delivery of epitopes by the Salmonella type III secretion system for vaccine development.

Avirulent strains of Salmonella typhimurium are being considered as antigen delivery vectors. During its intracellular stage in the host, S. typhimurium resides within a membrane-bound compartment and is not an efficient inducer of class I-restricted immune responses. Viral epitopes were successfully delivered to the host-cell cytosol by using the type III protein secretion system of S. typhimurium. This resulted in class I-restricted immune responses that protected vaccinated animals against lethal infection. This approach may allow the efficient use of S. typhimurium as an antigen delivery system to control infections by pathogens that require this type of immune response for protection.

Animals↗
PubMed1998

Identification of novel susceptibility loci for inflammatory bowel disease on chromosomes 1p, 3q, and 4q: evidence for epistasis between 1p and IBD1.

The idiopathic inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis (UC), are chronic, frequently disabling diseases of the intestines. Segregation analyses, twin concordance, and ethnic differences in familial risks have established that CD and UC are complex, non-Mendelian, related genetic disorders. We performed a genome-wide screen using 377 autosomal markers, on 297 CD, UC, or mixed relative pairs from 174 families, 37% Ashkenazim. We observed evidence for linkage at 3q for all families (multipoint logarithm of the odds score (MLod) = 2.29, P = 5.7 x 10(-4)), with greatest significance for non-Ashkenazim Caucasians (MLod = 3.39, P = 3.92 x 10(-5)), and at chromosome 1p (MLod = 2.65, P = 2.4 x 10(-4)) for all families. In a limited subset of mixed families (containing one member with CD and another with UC), evidence for linkage was observed on chromosome 4q (MLod = 2.76, P = 1.9 x 10(-4)), especially among Ashkenazim. There was confirmatory evidence for a CD locus, overlapping IBD1, in the pericentromeric region of chromosome 16 (MLod = 1.69, P = 2.6 x 10(-3)), particularly among Ashkenazim (MLod = 1.51, P = 7.8 x 10(-3)); however, positive MLod scores were observed over a very broad region of chromosome 16. Furthermore, evidence for epistasis between IBD1 and chromosome 1p was observed. Thirteen additional loci demonstrated nominal (MLod > 1.0, P < 0.016) evidence for linkage. This screen provides strong evidence that there are several major susceptibility loci contributing to the genetic risk for CD and UC.

Chromosome Mapping↗
PubMed1998

Antigen processing and autoimmunity. Evaluation of mRNA abundance and function of HLA-linked genes.

Quantitative defects in the density of conformationally correct human lymphocyte antigen (HLA) class I complexes on the surface of lymphocytes are apparent in patients with diverse HLA-linked autoimmune diseases, including Type I diabetes and Sjögren's syndrome. First, HLA class I expression was investigated in individuals with two rare and genetically divergent polyglandular autoimmune diseases. Polyglandular failure patients whose disease showed HLA linkage, but not those whose disease was not HLA linked, exhibited decreased HLA class I expression on the surface of their lymphocytes as well as a reduced abundance of transcripts of the HLA-linked genes Tap1 and Tap2, both of which encode proteins that contribute to HLA class I processing. Second, lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM), Sjögren's syndrome, Graves' disease, and Hashimoto's disease showed varying degrees of decreased abundance of mRNAs that encode Tap1, Tap2, Lmp2, or Lmp7 (the latter two proteins also contribute to HLA class I processing). Third, in twins discordant for IDDM, reduced transcript abundance was preferential to diabetic subjects. Fourth, functional assays of isolated diabetic proteasomes, the peptide cutting complex containing LMP2 and LMP7 proteins, revealed altered peptidase activity. These data suggest that defective transcription of HLA class I-processing genes could contribute to the quantitative defect in cell-surface expression in autoimmune lymphocytes of HLA-controlled disease.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Desensitization and resensitization of norepinephrine release in the rat hippocampus with repeated nicotine administration.

Desensitization of norepinephrine release was investigated with repeated intravenous (i.v.) infusions of nicotine and in vivo microdialysis of the hippocampus. At 100 min intervals, rats received three infusions of one of the following doses of nicotine: 0.045, 0.09 or 0.135 mg/kg. Doses of 0.09 mg/kg or higher increased norepinephrine release (F= 2.41, P < 0.05). However, the norepinephrine response to the second or third infusion was significantly reduced, compared to the first. The extent of desensitization and rate of resensitization was investigated further by administering consecutive infusions of nicotine (0.135 mg/kg) 40, 60, 100 or 200 min apart. Less norepinephrine was released after a second nicotine infusion given 40 to 100 min later, but this was not reduced further by a third infusion. Norepinephrine release was unchanged with a 200 min inter-infusion interval. Therefore, in the hippocampus, maximal desensitization of nicotine-stimulated norepinephrine release occurs as early as 40 min and persists for at least 100 min; thereafter, resensitization becomes the dominant process.

Animals↗