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Y Xu

Publications and source records attributed to Y Xu.

At least 1,171 records · Page 65Linked to original sources

Enhancement of cellular immune function during cold adaptation of BALB/c inbred mice.

The cell-mediated immune function of cold-adapted BALB/c inbred mice was studied in experiments of splenic lymphocyte blastogenesis, indicated by tritium-labeled deoxythymidine incorporation and SDS-PAGE autoradiography of synthetic proteins in lymphocytes. Male BALB/c inbred mice were randomly divided into two groups: control (living at 25 degrees C) and cold-exposed (living at 2 degrees C). Results are as follows: in contrast with the control group, there was an obvious fluctuation of cell-mediated immune function in the cold-exposed group at initial cold exposure because of transient stress to cold; then cell-mediated immune function gradually recovered to control level. From Day 15, the cell-mediated immune function of the cold-exposed group was remarkably enhanced. On Day 15, the lymphocyte blastogenesis rate was increased by 20.66% (P less than 0.05), which implies the onset of cold adaptation; on Days 21 and 31, the rates increased by 80.15% (P less than 0.05) and 40.36% (P less than 0.05), respectively. Two to six months later, with continuing cold exposure, the murine lymphocyte blastogenesis rate in the cold-exposed group remained higher than that in the control group. The lymphocyte protein synthesis of the cold-exposed group, indicated by tritium-labeled leucine incorporation, apparently increased on Day 15 and the stimulated rate was 101.47% (P less than 0.05). SDS-PAGE autoradiography of synthetic proteins in lymphocytes demonstrated that after 2 weeks of cold exposure, protein bands were enriched in both quantity and quality. These results are identical to the results obtained from lymphocyte blastogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

Genetic and physical maps of human chromosome 4 based on dinucleotide repeats.

Characterization of inherited variations within tandem arrays of dinucleotide repeats has substantially advanced the construction of genetic maps using linkage approaches over the last several years. Using a backbone of 10 newly identified microsatellite repeats on human chromosome 4 and 6 previously identified short tandem repeat element polymorphisms, we have constructed several genetic maps and a physical map of human chromosome 4. The genetic and physical maps are in complete concordance with each other. The genetic maps include a 15-locus microsatellite-based linkage map, a framework map of high support incorporating a total of 39 independent loci, a 25-locus high-heterozygosity, easily used index map, and a gene-based comprehensive map that provides the best genetic location for 35 genes mapped to chromosome 4. The 16 microsatellite markers are each localized to one of nine regions of chromosome 4, delineated by a panel of somatic cell hybrids. These results demonstrate the utility of PCR-based repeat elements for the construction of genetic maps and provide a valuable resource for continued high-resolution mapping of chromosome 4 and of genetic disorders to this chromosome.

Base Sequence↗

Increased 8-oxodeoxyguanosine levels in lung DNA of A/J mice and F344 rats treated with the tobacco-specific nitrosamine 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone.

Evidence for the involvement of free radicals in nitrosamine carcinogenesis comes mainly from increased lipid peroxidation as a result of nitrosamine treatment. More direct evidence for nitrosamine-induced oxidative DNA damage has been lacking. In this study we examined the levels of 8-oxodeoxyguanosine or 8-hydroxydeoxyguanosine (8-OH-dG) in tissue DNA of mice and rats treated with the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Multiple doses of NNK (0.25 or 0.50 mg/mouse, 3 times weekly for 3 weeks) administered by gavage resulted in a significant elevation of 8-OH-dG in lung DNA, from 2.1 to 3.8 adducts/10(5) dG for the lower dose or to 6.6 adducts/10(5) dG for the higher dose, 2 h after the last NNK administration. A single dose treatment of NNK by gavage (4 mg/mouse) also resulted in an increase of this lesion in the lung DNA, however, the increase was not statistically significant. In liver, however, the increase was only significant by multiple doses at the higher dose, from 2.3 to 3.4 adducts/10(5) dG. This lesion appeared to be repaired efficiently. At 4 and 24 h after NNK treatment, the 8-OH-dG levels declined to the basal levels in both liver and lung. A single dose of NNK (20 mg/rat) also caused a significant increase of 8-OH-dG from 3.0 to 5.1 adducts/10(5) dG in rat lung DNA. An increase of 8-OH-dG in liver DNA was also seen, however, it was not statistically significant. Unlike the liver and the lung, the 8-OH-dG levels in rat kidney, a non-target tissue, were inert to NNK treatment. These results provide for the first time direct evidence supporting the role of oxidative DNA damage in NNK lung tumorigenesis.

8-Hydroxy-2'-Deoxyguanosine↗

Removal of Qa-2 antigen alters the Ped gene phenotype of preimplantation mouse embryos.

Embryo survival is influenced by both genetic and environmental factors. Previous research in our laboratory has identified one gene associated with embryonic survival, the Ped gene, a gene that is linked to the major histocompatibility complex (MHC) of the mouse. The Ped gene has been shown to influence the rate of preimplantation embryonic cleavage division, as well as litter size, birth weight, and weaning weight. Genetic mapping of the Ped gene has located it in the Q region of the MHC and has suggested that possible Q region genes encoding the Ped gene are Q3, Q5, Q6, Q7, Q8, and/or Q9. Whereas the protein products of the Q3 and Q5 genes are unknown, the protein product of the very similar Q6, Q7, Q8, and Q9 genes is the Qa-2 antigen. Two forms of membrane-bound Qa-2 antigen are known: glycosylphosphatidylinositol (GPI)-linked and transmembrane bound. Only the GPI-linked form is sensitive to cleavage by phosphatidylinositol phospholipase C (PI-PLC). The first purpose of the present study was to determine the nature of the linkage of the Qa-2 antigen to the cell surface of preimplantation mouse embryos. It was found that all detectable Qa-2 antigen on the embryonic cell surface is sensitive to cleavage by PI-PLC and is therefore bound to the cell membrane by a GPI linkage. Furthermore, removal of Qa-2 antigen from the embryonic cell surface slows down the rate of development of preimplantation mouse embryos. These results suggest the likelihood that the Qa-2 antigen is the Ped gene product.

Animals↗

Human recombinant transforming growth factor-beta 1 modulation of biochemical and cellular events in healing of ulcer wounds.

The effects of recombinant human transforming growth factor beta 1 (rhTGF-beta 1) on wound healing were examined in a rabbit ear ulcer model in which rhTGF-beta 1 was applied to full-thickness biopsy ulcers on the ears. The influence of perichondrium on healing was studied by comparing ulcers with and without perichondrium on 1) formation of total healing wound area (HWA, the newly formed connective and granulation tissues within the ulcer) over time and 2) the amount of collagen synthesized by the wound tissue at day 5. The HWA of ulcers with intact perichondrium increased sharply with time and reached a plateau at day 7, whereas a slower healing occurred in the perichondrium-free model where maximal HWA appeared at day 14. Topical application of 100 ng of rhTGF-beta 1 per wound accelerated healing by increasing HWA in both models. The enhancement of healing by rhTGF-beta 1 was associated with increased collagen synthesis. The percent collagen synthesis in the rhTGF-beta 1 was doubled in the perichondrium-intact ulcers and increased 40% in the perichondrium-free ulcers. DNA synthesis in the perichondrium-intact ulcers was not altered by rhTGF-beta 1 when measured at day 5 by in vitro labeling with [3H]thymidine ([3H]TdR). Autoradiography indicated that the primary cells labeled in the wound tissue were epithelial cells and rhTGF-beta 1 enhanced the migration of these cells from the wound margin towards the center. To evaluate the effects of rhTGF-beta 1 on fibroblasts derived from the granulation tissue of the wound, cells were treated with increasing concentrations of rhTGF-beta 1 and DNA and collagen synthesis were determined. rhTGF-beta 1 elicited a biphasic change in percent collagen synthesis with a maximal increase of 50% at 20 pM followed by a decline. A twofold increase in [3H]TdR incorporation that plateaued at 1 nM was also observed. Our results indicate that the cellular responses to rhTGF-beta 1 differ in vivo and in vitro. The perichondrium-intact ulcers contain more wound tissue and have larger responses to rhTGF-beta 1 stimulation, which allows better examination of biochemical and cellular events. The in vivo mechanisms are multi-factorial, which may involve cell migration and recruitment as results of numerous cell/cell and cell/matrix interactions.

Animals↗

Expression and modulation of the vitronectin receptor on human dermal microvascular endothelial cells.

Microvascular endothelial cells express a variety of cell-surface integrins in vivo and in vitro with varying affinities for matrix proteins. The vitronectin receptor (VnR), a complex of the alpha v and beta 3 integrin chains, is capable of binding to a variety of matrix proteins that are deposited in injured tissues, including vitronectin, fibrinogen, and thrombin. Staining of frozen sections of human skin with antibodies recognizing the VnR and examination by immunofluorescence microscopy demonstrates staining in a vascular pattern suggesting in vivo expression of the vitronectin receptor on endothelial cells. Examination of pure cultures of human dermal microvascular endothelial cells (HDMEC) by flow-cytometric analysis and enzyme-linked immunosorbent assay confirmed that HDMEC also express cell surface VnR complex in vitro. Stimulation of human dermal microvascular endothelial cells in vitro with agents that stimulate protein kinase C resulted in dose- and time-dependent increases in expression of alpha v and beta 3 integrin chains. Additionally, stimulation with basic fibroblast growth factor induced similar increases, but stimulation with transforming growth factor-beta or interleukin-1 alpha failed to increase VnR expression. Increases in cell-surface VnR expression also correlated with an increased ability of microvascular endothelial cells to bind to vitronectin, but not fibronectin-coated surfaces. Although increases in cell-surface expression of beta 3 paralleled increases in expression of cell-surface alpha v, regulation of mRNA expression was distinct for each chain. These data suggests that microvascular endothelial cells express the VnR complex in vivo, that the cell-surface expression of this integrin on dermal microvascular endothelial cells can be regulated, and that this regulation may be important in cell adherence, cell migration, and wound healing.

Blotting, Northern↗

Role of thapsigargin-sensitive intracellular Ca2+ pools in secretion induced by muscarinic agonists in porcine adrenal chromaffin cells.

The role of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]-sensitive Ca2+ pools in secretion, induced by muscarinic agonists in porcine adrenal chromaffin cells, was studied. Activation of muscarinic receptors, as in other species, was found to increase inositol phosphate production including that of Ins(1,4,5)P3. Treatment of cells with thapsigargin, which is known to deplete Ins(1,4,5)P3-sensitive Ca2+ pools, eliminated the initial transient component of increases in the cytosolic free Ca2+ concentration ([Ca2+]in) induced by the muscarinic agonist, methacholine, in both the presence and the absence of extracellular Ca2+. Thapsigargin treatment also decreased methacholine-induced secretion by about 30% in the presence of extracellular Ca2+ and essentially eliminated secretion that occurred independently of extracellular Ca2+ (which was about 30% of the secretory response that occurred in the presence of extracellular Ca2+). Thapsigargin itself had no effect on inositol phosphate production. These results indicate that about 30% of muscarinic agonist-induced secretion is mediated by the release of Ca2+ from Ins(1,4,5)P3- and thapsigargin-sensitive intracellular Ca2+ pools. These results also suggest that Ca2+ influx activated by muscarinic agonists is not due to depletion of intracellular Ca2+ pools, as prior depletion of these pools had no effect on the portion of the methacholine-induced secretory response and [Ca2+]in signal that was dependent on extracellular Ca2+.

Animals↗

Occurrence of fumonisin in forage grass in new zealand.

Fumonisin B(1) (FB(1)) was isolated from samples of forage grass originating in paddocks associated with an idiopathic disease of Canadian wapiti and wapiti-red deer hybrids characterized by "ill thrift" and liver dysfunction. Four of 40 samples contained 1, 3, 6, and 9 ppm (micrograms per gram) of FB(1) and 4, 0.5, 2, and 0.5 ppm, respectively, of the methyl ester of FB(1). Analyses were done by ion spray mass spectrometry and confirmed by both fast atom bombardment (solids probe) and mass spectral analysis by electron impact ionization of the trifluoroacetate derivative of the base hydrolyzed product (pentolamine) of FB(1). This article contains the first report of the presence of fumonisin B(1) in grass.

Journal Article↗

Information for Mandarin tones in the amplitude contour and in brief segments.

While the tones of Mandarin are conveyed mainly by the F0 contour, they also differ consistently in duration and in amplitude contour. The contribution of these factors was examined by using signal-correlated noise stimuli, in which natural speech is manipulated so that it has no F0 or formant structure but retains its original amplitude contour and duration. Tones 2, 3 and 4 were perceptible from just the amplitude contour, even when duration was not also a cue. In two further experiments, the location of the critical information for the tones during the course of the syllable was examined by extracting small segments from each part of the original syllable. Tones 2 and 3 were often confused with each other, and segments which did not have much F0 change were most often heard as Tone 1. There were, though, also cases in which a low, unchanging pitch was heard as Tone 3, indicating a partial effect of register even in Mandarin. F0 was positively correlated with amplitude, even when both were computed on a pitch period basis. Taken together, the results show that Mandarin tones are realized in more than just the F0 pattern, that amplitude contours can be used by listeners as cues for tone identification, and that not every portion of the F0 pattern unambiguously indicates the original tone.

Adult↗

The role of cytokines in the pathogenesis of hepatic granulomatous disease in Schistosoma mansoni infected mice.

Cytokines are important in the cell-mediated response to Schistosoma mansoni eggs. We have found that Th2 cytokine responses (e.g. IL-4 and IL-5) are augmented after egg laying begins while Th1 responses (IL-2 and IFN-gamma) are down regulated in S. mansoni infected mice. Treatment of mice with anti-IL-5 monoclonal antibodies (Mab) suppressed the eosinophil response almost completely but did not affect granuloma size and slightly increased hepatic fibrosis. Anti-IL-4 treatment abolished IgE responses in infected mice and decreased hepatic fibrosis slightly. Anti-IFN-gamma treatment had no effect on hepatic pathology. Anti-IL-2 treatment decreased granuloma size significantly and decreased hepatic fibrosis markedly. Anti-IL-2 treatment dramatically decreased IL-5 secretion by splenic cells in vitro and decreased peripheral blood and tissue eosinophilia. In contrast IL-4 secretion was unaffected and serum IgE was normal or increased. IL-2 and IFN-gamma secretion by splenic cells of treated mice were slightly but not significantly increased suggesting that anti-IL-2 treatment is affecting Th2 rather than Th1 responses.

Animals↗

Changes of fibronectin in the right and left ventricles of rats exposed to chronic normobaric hypoxia.

Changes of fibronectin (FN) in the right and left ventricles of adult rats exposed to chronic normobaric hypoxia were observed by a peroxidase immunohistochemical stain technique and analyzed quantitatively by a point counting method. Fifty-six rats were randomly divided into control groups of day 0 (immediately prior to the experiment), day 5, day 15, and day 30 and hypoxia groups of day 5, day 15, and day 30. Rats of the hypoxia groups were put into a normobaric hypoxia chamber with oxygen concentration adjusted to 10 percent. The rats of the control groups breathed room air. From day 5 on, the ratio of the weight of the right ventricle (RV) to that of the left ventricle (LV) plus interventricular septum (SP), RV/(LV+SP), and the ratio of the weight of the right ventricle (RV) to the body weight (BW), RV/BW, in the hypoxia groups increased significantly as compared with those of the control groups. The amount of immunoreactive FN in the right ventricle increased significantly in the hypoxia groups after exposure to hypoxia environment for 15 days (10.31% +/- 2.15%, mean +/- S.D.) and for 30 days (9.55% +/- 1.65%) as compared with those in the day 0 control group (3.05% +/- 1.15%, p < 0.01), the day 15 control group (3.26% +/- 0.83%, p < 0.01), and the day 30 control group (3.19% +/- 0.51%, p < 0.01). However, there were no significant changes in the amount of immunoreactive FN in the left ventricle of the hypoxia groups as compared with the control groups. These results suggest that chronic hypoxia may lead to an increase of FN in the hypertrophied right ventricle but not in the left ventricle, which indicates that pulmonary hypertension induced by chronic hypoxia rather than chronic hypoxia itself is a major cause for the increase of FN in the myocardium. The increased FN in the right ventricle may accelerate the accumulation of collagen and, in turn, contribute to the increase of the myocardial stiffness and eventually to the diastolic dysfunction of the hypertrophied right ventricle induced by chronic hypoxia.

Animals↗

The stress distribution of the lumbar spine and disc degeneration.

A three-dimensional finite element model of the lumbar motion segment was developed to study the effect of disc degeneration upon stress distribution in the lumbar spine. The results showed that after degeneration of the intervertebral disc, the stress distribution and load transmission of the lumbar spine are significantly changed. It is concluded that these changes provide a biomechanical basis for understanding the etiology of spinal canal stenosis and nerve root entrapment.

Biomechanical Phenomena↗

[Investigation of maternal peripheral plasma concentration of PG in induction of labor by nutrition food inductive drug].

The used nutrition food inductive drug to induce labor in 33 pregnant women, 22 of 33 succeeded and 11 failed. The PGs level in maternal peripheral blood was measured twice. One before taking and the second sample was drawn blood during second stage of labor. Another 13 pregnant women of spontaneous labor were measured as control group. The 6-keto-PGF1 alpha level was significantly increased in the succeeding group than in the tailed induced group, the PGE concentration seems no significant change in these three groups. The data suggested that the nutritional food inductive drug may accelerate the synthesis of prostaglandin in the succeeding group.

6-Ketoprostaglandin F1 alpha↗

[The correlation between the maturation of rbcL transcripts and its flanking sequence in a prokaryotic system].

There is a 15bp large reverse repeated sequence proceeded by a 7bp small one in the 3'flanking region of rbcL of Nicotiana tabacum. A 383 bp of XbaI fragment containing these tandemly repeats was inserted into the plasmid p lambda S delta, at the position between the lambda p and the cat gene. Then these two repeats were separated and deleted systematically to obtain various deletions. The deletion pRT65, pRT74 and pRT83 was sequenced to determine the deleted base pairs exactly. S1 mapping analysis was adopted to investigate the transcripts of these deletions in E. coli JM83. The results showed us that the stability of mature 306bp mRNA relied on the large repeat and a short sequence downstream. The small one was not efficient. The regulation level of the rbcL termination was also investigated. The XbaI-EcoRI fragments from pRT65, pRT74 and pRT83 were transferred into pSP-TT* at the position between the spinach promoter and threonine terminator to construct pRT65, pRT74 and pRT83 respectively. The results from S1 mapping analysis showed that the E. coli RNA polymerase read through the 3' flanking region of rboL gene and terminated at the stop site of threonine terminator. These results suggested that mature rbcL mRNA might be the product precisely processed from a precursor mRNA and the 3' flanking sequence might be the signal for precursor mRNA to be processed to the correct position.

Base Sequence↗

[Papillary adenoma of the lung-two cases report].

Two rare cases of papillary adenoma of the lung were reported. Histologically, the tumor cells had noninfiltrating papillary growth, cuboidal to columnar with eosinophilc granular cytoplasm and without nuclear atypia. Ultrastructurally, the tumor cells had cytoplasmic osmiophilic lamellar bodies. This benign papillary adenoma of the lung has morphologic characteristics consistent with aveolar type II pneumocyte differentiation.

Adult↗

[3,4-Diaminopyridine-evoked norepinephrine release from hippocampal in the absence of extracellular calcium].

Slices of rat hippocampus, preincubated with [3H]norepinephrine ([3H]NE), were superfused and stimulated by addition of 3,4-diaminopyridine (3,4-DAP) for 10 min to the superfusion medium. 3,4-DAP-evoked [3H]NE release both in the absence and presence of extracellular Ca2+. 3,4-DAP-evoked Ca(2+)-independent release of [3H]NE was highly sensitive to sodium channel blocker, tetrodotoxin (TTX, 100% inhibition), suggesting that Na+ per se entered into nerve terminals but not depolarization of membrane followed by Ca2+ channel opening is necessary for 3,4-DAP-evoked Ca(2+)-independent release of [3H]NE. Phorbol ester PDB increased by 480% of control and polymyxin B (PMB) decreased 3,4-DAP-evoked [3H]NE release by 94% of control in the absence of extracellular Ca2+ indicating that the alterations of voltage-dependent Ca(2+)-currents into the cells are not involved in the mechanism of the modulation of 3,4-DAP-evoked [3H]NE release by protein kinase C.

4-Aminopyridine↗