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Biomedical subjects

X Z Yu

Publications and source records attributed to X Z Yu.

At least 19 recordsLinked to original sources
PubMed2006

Interactions of rice (Oryza sativa L.) and PAH-degrading bacteria (Acinetobacter sp.) on enhanced dissipation of spiked phenanthrene and pyrene in waterlogged soil.

The effects of cultivation of rice (Oryza sativa L.) and PAH-degrading bacteria (Acinetobacter sp.) separately, and in combination, on the dissipation of spiked phenanthrene and pyrene (0, 50+50, 100+100, 200+200 mg kg(-1)) in waterlogged soil were studied using pot trials. The population of introduced PAH-degrading bacteria remained at 10(5) CFU g(-1) dry soil after 20 days of treatment with Acinetobacter sp. only, but increased to 10(6) when planted with rice simultaneously. Shoot and root biomass of rice when grown alone was adversely affected by spiked PAHs, but significantly increased by 2-55% and 8-409%, respectively, when inoculated with Acinetobacter sp.. Phenanthrene and pyrene concentrations in roots ranged from 1-27 and 20-98 mg kg(-1), respectively, while their concentrations in shoots were generally lower than 0.2 mg kg(-1). The dissipation of phenanthrene was mainly due to abiotic loss as 70-78% phenanthrene was lost from the control soil at the end of 80 days, while removal of 86-87% phenanthrene had been achieved after 40 days in the treatment co-cultivated with Acinetobacter sp. and rice. Compared with the control where only 6-15% of pyrene was removed from soil, a much higher dissipation of pyrene (43-62%) was attained for the treatments co-cultivated with Acinetobacter sp. and rice at the end of 80 days. The results demonstrated that co-cultivation of rice and PAH-degrading bacteria may have a great potential to accelerate the bioremediation process of PAH-contaminated soil under waterlogged conditions.

Acinetobacter↗
PubMed2006

Distribution of polycyclic aromatic hydrocarbons in soils at Guiyu area of China, affected by recycling of electronic waste using primitive technologies.

The concentration, distribution, profile and possible source of polycyclic aromatic hydrocarbons (PAHs) in soil were studied in Guiyu, an electronic waste (E-waste) recycling center, using primitive technologies in Southeast China. Sixteen USEPA priority PAHs were analyzed in 49 soil samples (0-10 cm layer) in terms of individual and total concentrations, together with soil organic matter (SOM) concentrations. The concentrations of a sum of 16 PAHs ranged from 44.8 to 3206 microgkg(-1) (dry weight basis), in the descending order of E-waste open burning sites (2065 microgkg(-1))>areas near burning sites (851microgkg(-1))>rice fields (354 microgkg(-1))>reservoir areas (125microgkg(-1)). The dominant PAHs were naphthalene, phenanthrene and fluoranthene, which were mainly derived from incomplete combustion of E-waste (e.g. wire insulations and PVC materials), and partly from coal combustion and motorcycle exhausts. All individual and total PAH concentrations were significantly correlated with SOM except for naphthalene and acenaphthylene. Principal component analysis was performed, which indicated that PAHs were mainly distributed into three groups in accordance with their ring numbers and biological and anthropogenic source. In conclusion, PAH concentrations in the Guiyu soil were affected by the primitive E-waste recycling activities.

China↗
PubMed2005

Observation of magnetic ripple and nanowidth domains in a layered ferromagnet.

We investigated ferromagnetic domain structures on nanometer to micrometer scale for single crystals of a layered ferromagnet, La(2-2x)Sr(1+2x)Mn2O7 (0.32 < or = x < or = 0.40), as functions of x and temperature by means of Lorentz electron microscopy. We have succeeded in observing the evolution of magnetic ripple structure, dynamically, related to a spin reorientation transition where the magnetization direction switches between parallel and perpendicular to the layers. Our high-resolution magnetic domain imaging revealed that the ripple state is characterized by the evolution of magnetic nanowidth domains.

Journal Article↗
PubMed2004

Metallic ferromagnet with square-lattice CoO2 sheets.

A single-crystalline film of Sr2CoO4 with square-lattice CoO2 sheets (K2NiF4-type structure) was synthesized, and its electronic properties were characterized. The compound exhibited both ferromagnetic and metallic behaviors, with a fairly high Curie temperature T(C) of approximately 250 K, in contrast to the superconductivity recently found in a triangular-lattice CoO2-sheet compound. The film's large magnetoresistance with current perpendicular to the CoO2 plane showed field-hysteretic behavior analogous to tunneling magnetoresistance. The electronic structure of Sr2CoO4 was also investigated to characterize the quasi-two-dimensional ferromagnetic metal state in terms of optical spectroscopy and first-principles calculation.

Journal Article↗
PubMed2004

X-ray directional dichroism of a polar ferrimagnet.

In a polar ferrimagnet GaFeO3, we have found a novel magneto-optical effect, termed x-ray nonreciprocal directional dichroism (XNDD), that the x-ray absorption at around the K edge of an Fe ion depends on whether the x-ray propagation vector is parallel or antiparallel to the outer product of the magnetization and electric-polarization vectors. The XNDD spectroscopy as demonstrated here can be a useful tool to probe the local magnetism in noncentrosymmetric systems such as magnetic interfaces and nanostructures.

Journal Article↗
PubMed2004

Magnetization-induced second harmonic generation in a polar ferromagnet.

Second harmonic generation (SHG) induced by spontaneous magnetization has been investigated for a polar ferromagnetic crystal of GaFeO3. The Kerr rotation of the second harmonic light becomes gigantic with decreasing temperature below the magnetic transition temperature (approximately =205 K), e.g., as large as 73 degrees at 100 K. The magnetic domains can be visualized by using that large nonlinear Kerr rotation. The spectrum of the magnetization-induced SHG as measured indicates the two-photon resonant electronic process on a Fe3+ ion in the crystal.

Journal Article↗
PubMed2001

Anti-CD3 epsilon F(ab')2 prevents graft-versus-host disease by selectively depleting donor T cells activated by recipient alloantigens.

Transplantation tolerance is facilitated by activation-induced apoptosis of peripheral T cells triggered by specific AG: Abs specific for the nonpolymorphic CD3 component of the TCR complex bind to APCs through Fc-FcR interactions, mimic MHC-peptide, and activate polyclonal T cells. In contrast, F(ab')(2) of anti-CD3epsilon Abs do not activate naive T cells but induce apoptosis of Ag-activated, cycling T cells. Here, we report that treatment with anti-CD3epsilon F(ab')(2) can selectively induce apoptosis of donor T cells that recognize a recipient alloantigen, thereby preventing graft-vs-host disease initiated by a TCR-transgenic T cell population. The selective elimination of Ag-activated T cells by non-FcR-binding anti-CD3epsilon Abs could serve as an ideal strategy to prevent graft-vs-host disease and allograft rejection or to treat autoimmune disorders.

Animals↗
PubMed2001

Prevalence and analysis of risk factors for infections caused by resistant Escherichia coli strains in Anhui, China.

BACKGROUND: This study analyzes the prevalence of hospital and community-acquired infections caused by Escherichia coli. PATIENTS AND METHODS: The antibiotic resistance pattern was used to characterize the isolates, and a retrospective observational study was performed to assess the relationship between antimicrobial use and bacterial resistance. The study was conducted during a 1-year and 7-month period in a 1,500-bed tertiary care hospital in Anhui, China. RESULTS: An E. coli infection was diagnosed in 1.4% of patients (519/36,179) admitted to the hospital between March 1, 1999 and August 31, 2000. Of the 519 isolates, 489 (94.2%) were resistant to at least one antimicrobial; 86% were resistant to ampicillin, 85% to cephalothin, 83% to piperacillin, 77% to ampicillin/sulbactam, 72% to trimethoprim/sulfamethoxazole (TMP-SMZ), 70% to ciprofloxacin, 61% to cefoperazone, 58% to tobramycin, 56% to gentamicin, 48% to ticarcillin-clavulanate, 44% to cefazolin, 43% to cefuroxime, 36% to cefoxitin, 32% to cefepime, 29% to aztreonam, cefetaxime and ceftriaxone, 28% to ceftazidime, 19% to piperacillin/tazobactam, 10% to amikacin, while all strains tested were susceptible to imipenem. CONCLUSION: Prior receipt of amtimicrobial therapy was significantly associated with infection caused by a resistant organism.

Adolescent↗
PubMed2000

Non-Fc receptor-binding humanized anti-CD3 antibodies induce apoptosis of activated human T cells.

Human trials in organ allografts have demonstrated that murine anti-CD3 mAbs are immunosuppressive. By mimicking Ag, anti-CD3 can produce T cell activation, anergy, or death. Activation of resting T cells in vivo results in dose-limiting cytokine release and is caused by Ab-mediated cross-linking of T cells and Fcgamma receptor (FcR)-bearing cells. With the goal of minimizing cytokine-induced toxicity, anti-CD3 have been engineered to lower Fc binding avidity. Preclinical murine studies have indicated that non-FcR-binding anti-CD3 can induce apoptosis of Ag-activated T cells. Since induction of T cell apoptosis may be an important mechanism of immunosuppression by anti-CD3, we tested whether Fc mutations affect the ability of anti-human CD3 to induce apoptosis of activated T cells. We compared wild-type murine anti-CD3, M291, and OKT3 and their humanized, FcR- and non-FcR-binding structural variants in quantitative assays of T cell apoptosis. Non-FcR-binding variants produced more sustainable phosphorylation of extracellular signal-regulated kinase-2, greater release of IFN-gamma, and more effectively caused activation-dependent T cell apoptosis. Non-FcR-binding variants dissociated more quickly from the T cell surface and caused less internalization of the TCR, which then remained available in greater abundance on the cell surface for signaling. Cross-linking of non-FcR-binding variants by antiglobulin enhanced TCR internalization and minimized induction of T cell apoptosis. We conclude that non-FcR-binding, humanized anti-CD3 have improved ability to induce apoptosis of activated T cells, presumably by allowing durable expression of the TCR and sustained signaling.

Adult↗
PubMed2000

CD28-specific antibody prevents graft-versus-host disease in mice.

The costimulatory molecules B7-1 and B7-2 regulate T cell activation by delivering activation signals through CD28 and inhibitory signals through CTLA4. Graft-vs-host disease (GVHD) is caused by activated donor T cells. Previously, we showed that CD28-deficient donor T cells induced less-severe GVHD than wild-type donor T cells, suggesting that CD28 signals exacerbate GVHD. In this paper we demonstrate that CTLA4 signals attenuate the severity of GVHD. Targeting the CD28 receptor with a specific mAb modulates the receptor in vivo, inhibits donor T cell expansion, and prevents GVHD. CTLA4 signaling was necessary for this effect because treatment with a soluble ligand that blocks binding of B7 to both CD28 and CTLA4 did not prevent GVHD as effectively as anti-CD28 mAb. These results support the current model of T cell costimulation in which CD28 signals amplify GVHD while CTLA4 signals inhibit GVHD, providing evidence that selective targeting of CD28 might be a better therapeutic strategy for inducing immunological tolerance than blocking the ligands for both CD28 and CTLA4.

Abatacept↗
PubMed2000

Enhancement of susceptibility to Fas-mediated apoptosis of TH1 cells by nonmitogenic anti-CD3epsilon F(ab')2.

BACKGROUND: Anti-CD3epsilon F(ab')2 are nonmitogenic for naive T cells but can induce apoptosis of antigen-activated T cells in vitro and in vivo. We studied the mechanisms by which nonmitogenic anti-CD3epsilon F(ab')2 antibodies induce T cell death. METHODS: OVA-responsive T cell lines were generated by immunization in vivo and restimulation in vitro. Fas or Fas ligand (FasL) expression was tested by surface staining with specific mAbs. The apoptotic DNA and cell cycle phase were tested by staining DNA with propidium iodide. Interferon-gamma was measured by ELISA, whereas interleukin (IL)-2 and IL-4 were detected by bioassays. RESULTS: Restimulation with anti-CD3epsilon F(ab')2 induced apoptosis of antigen-activated wild-type T cells, but not Fas or FasL-defective T cells. Anti-CD3epsilon F(ab')2 induced death of cells expressing high levels of Fas and FasL, and preferentially deleted T helper (Th)1 cells but spared Th2 cells. Soluble anti-CD3epsilon F(ab')2 did not regulate Fas or induce FasL expression, indicating that the ability of anti-CD3epsilon F(ab')2 to induce T cell apoptosis depends on a distinct mechanism. T cells in S/G2 were found relatively resistant to Fas-mediated apoptosis, but anti-CD3epsilon F(ab')2 rendered those T cells exquisitely sensitive to Fas-mediated apoptosis. CONCLUSIONS: Anti-CD3epsilon F(ab')2 induces apoptosis of cycling CD4+ T cells through activation of the Fas/FasL pathway. Anti-CD3epsilon F(ab')2 does not regulate Fas or FasL expression but induces susceptibility to Fas-mediated apoptosis of cycling T cells. Anti-CD3epsilon F(ab')2 can induce death of polarized Th1 cells, but not Th2 cells, thus potentially skewing the repertoire of antigen-activated T cells toward the Th2 phenotype. These features predict that nonmitogenic anti-CD3epsilon F(ab')2-like antibodies can be useful to prevent or reverse pathogenic immune responses mediated by Th1 cells.

Animals↗
PubMed1999

Visualization, fate, and pathogenicity of antigen-specific CD8+ T cells in the graft-versus-host reaction.

To follow the fate of alloreactive T cell effectors in graft-vs-host disease, Ld-specific CD8+ T cells from C57BL/6 2C TCR-transgenic donors were transplanted into sublethally irradiated (750 cGy) Ld+ or Ld- recipients. In Ld- C57BL/6 or (BALB/c-dm2 x C57BL/6)F1 recipients, naive 2C T cells engrafted and survived long term, but did not acquire effector function. In Ld+ (BALB/c x C57BL/6)F1 recipients, 2C T cells engrafted, expanded, became cytolytic, destroyed host B cells and double-positive thymocytes, and later disappeared. Despite marked damage to lymphoid and hemopoietic cells by 2C T cells, no significant pathology was detected in other organs, and recipients survived. Ld+ (BALB/c x C57BL/6)F1 recipients died when LPS/endotoxin was administered on day 7 after cell transfer, while Ld- (BALB/c-dm2 x C57BL/6)F1 recipients survived. Our findings show that under certain conditions, a CD8+ T cell population recognizing an extremely limited repertoire of Ags can initiate graft-vs-host disease.

Animals↗
PubMed1999

Flow cytometric analysis of the toxicity of nitrofen in cultured keratinocytes.

Lactate dehydrogenase (LDH) release test, 3H-thymidine (3H-TdR) and 3H-leucine (3H-Leu) incorporation tests and flow cytometric analysis (FCM) of cell cycle were employed to elucidate cellular and molecular mechanism of nitrofen-induced toxicity in cultured keratinocytes. The results showed that cell morphologic damages were observed after exposure to 1.0 mmol/L and 10.0 mmol/L nitrofen. LDH release increased in a dose- and time-dependent manner. Depressions in 3H-TdR and 3H-Leu incorporation were found even at 0.01 mmol/L, and increased with the exposure dose. Cell cycle was analyzed from the DNA- histogram with propidium iodide stain. The results showed that there was no pronounced alteration in cell cycle after cells exposed to 0.01 and 0.1 mmol/L nitrofen. At dose of 1.0 mmol/L, S phase cells increased 2 times of that of control. With the increase of dose, G2/M phase cells became to increase about 5 times of that of the control. At 1.0 mmol/L, time course of cell cycle after exposure was observed. At the beginning of exposure, cells in S phase and G2/M phase were about 8.7% and 11%. Following 24 h incubation with nitrofen, cells in S phase increased to 18.0% with almost no change in G2/M. 72 h after exposure, G2/M phase cells increased to 63.3%. The above results demonstrated that S phase and G2/M phase blockage in cultured keratinocytes after exposed to nitrofen seems of importance in the mechanism of nitrofen-induced toxicity.

Animals↗
PubMed1998

Role of CD28 in acute graft-versus-host disease.

Because CD28-mediated T-cell costimulation has a pivotal role in the initiation and maintenance of T-cell responses, we tested the hypothesis that CD28 is critical for the development of graft-versus-host disease (GVHD). We compared the in vivo effects of CD28(-/-) T cells transplanted from B6 donor with the CD28 gene deleted by homologous recombination with those of CD28(+/+) T cells transplanted from wild-type C57BL/6 (B6) donor. Fifty million CD28(-/-) or CD28(+/+) splenocytes from B6 mice were transplanted into unirradiated (B6 x DBA/2)F1 (BDF1) recipients. Unlike CD28(+/+), CD28(-/-) T cells from B6 mice had lower levels of proliferation and interleukin-2 production, had a limited ability to generate cytotoxic T lymphocytes against the recipient, and did not induce immune deficiency, despite survival in the recipient for at least 28 days. The ability to prevent rejection was reduced by the absence of CD28, because as many as 1.0 x 10(7) CD28(-/-) CD8(+) cells were needed to prevent rejection of major histocompatibility complex (MHC) class-I incompatible marrow in sublethally irradiated (550 cGy) bm1 recipients, whereas 8.0 x 10(5) CD28(+/+) CD8(+) T cells were sufficient to produce a similar effect, indicating that CD28 on donor CD8(+) cells helps to eliminate host immunity. Two million CD4(+) CD28(-/-) or CD28(+/+) T cells were transplanted into sublethally irradiated (750 cGy), MHC class-II incompatible (B6 x bm12)F1 recipients. With CD28(-/-) cells, 44% of the recipients died at a median of 20 days compared with 94% at a median of 15 days with CD28(+/+) cells (P < .001). Two million CD8(+) CD28(-/-) or CD28(+/+) T cells were transplanted into sublethally irradiated (750 cGy), MHC class-I incompatible (B6 x bm1) F1 recipients. With CD28(-/-) cells, 25% of the recipients died at a median of 41 days compared with 100% at a median of 15 days with CD28(+/+) cells (P < . 001). (B6 x bm12)F1 and (B6 x bm1)F1 mice surviving after transplantation of CD28(-/-) cells recovered thymocytes, T cells, and B cells in numbers and function comparable with that of irradiation-control F1 mice. We conclude that CD28 contributes to the pathogenesis and the severity of GVHD. Our results suggest that the severity of GVHD could be decreased by the administration of agents that block CD28 function in T lymphocytes.

Acute Disease↗
PubMed1996

Induction of apoptosis by anti-CD3 epsilon F(ab')2 in antigen receptor transgenic murine T cells activated by specific peptide.

Peripheral T cell tolerance can be achieved through deletion of mature CD4+ cells activated by high dose Ag. We tested whether apoptosis of peripheral CD4+ cells could be induced by a stimulatory dose of Ag plus a soluble ligand to the nonpolymorphic epsilon-chain of the TCR-associated CD3 complex. CD4+ T cells from the DO10 mouse express a transgenic TCR-alphabeta specific for OVA peptide 323-339 presented by I-A(d). OVA alone induced clonal activation and expansion of peripheral CD4+/TCR transgene+ cells. Simultaneous exposure to specific Ag plus soluble anti-CD3 Fos, a nonmitogenic anti-CD3epsilon genetically engineered F(ab')2-like Ab, blocked expansion and induced death of CD4+/TCR transgene+ cells, but not CD4+/TCR transgene- T cells. In contrast, a mitogenic anti-CD3epsilon Ab induced polyclonal activation and nonselective T cell death. Sequential stimulation by Ag followed by anti-CD3 Fos also induced death of TCR transgene+ cells, whereas stimulation by anti-CD3 Fos followed by Ag did not affect cell viability or function. Anti-CD3 Fos-induced death was associated with DNA fragmentation characteristic of apoptosis, was facilitated by IL-2, and was initiated by stimulation during the S-G2 phases of the cell cycle. Anti-CD3 Fos could induce deletion of Ag-activated T cells by apoptosis in vivo. Thus, a soluble, non-Fc-binding anti-CD3 Ab can induce programmed cell death of Ag-activated peripheral CD4+ T cells by CD3epsilon cross-linking during S or G2. Peripheral T cell deletion by activation-driven apoptosis is under cell cycle control and can be exploited to achieve selective immunosuppression by nonmitogenic anti-CD3epsilon Abs.

Amino Acid Sequence↗
PubMed1996

A long-term culture system for the expansion of hematopoietic stem cells from embryonic yolk sac with the capacity to seed erythroid and lymphoid development in vitro and to reconstitute the lymphoid compartment in severe combined immunodeficient mice.

We have established a long-term culture system under which hematopoietic stem cells derived from the embryonic yolk sac may be maintained for long periods. Evidence for the persistence of stem cells in this culture is provided by three experimental observations. First, erythroid progenitors, as evidenced by morphological, functional, and phenotypical analysis, may be generated from these yolk sac cultures after more than 7 months in culture. The yolk sac derived erythroid progenitors are distinct from those of bone marrow derived cells both qualitatively and quantitatively. This is evidenced by the high colony plating efficiency, large colony size, different growth factor requirements, increased sensitivity to Epo and other cytokines, as well as significant and prolonged expansion capability, suggesting that the yolk sac derived progenitors are both more proliferative and more primitive than their bone marrow derived analogs. Second, under different conditions, lymphoid progenitors may also be derived from these long term yolk sac cultures in the presence of the appropriate cytokines. Third, preliminary data suggest the engraftment of these yolk sac cells and reconstitution of at least some compartments of the hematopoietic system of host animals. This long-term culture system will provide a useful model for the study of early embryonic hematopoiesis, and the cells derived from this culture system may also have the potential of serving as donor cells for hematopoietic cell transplantation.

Animals↗