Rapid suppression of the superconducting gap in overdoped Bi2Sr2CaCu2O8+ delta.
Explore the source record for details and available documents.
Journal Article↗
Biomedical subjects
Z Shen
Publications and source records attributed to Z Shen.
Observation of Spin-Charge Separation in One-Dimensional SrCuO2.
Explore the source record for details and available documents.
Journal Article↗
Self-association of human RAD52 protein.
The yeast RAD52 protein is required for both homologous DNA recombination and repair of DNA double-strand breaks. RAD52 can bind to the yeast RAD51 protein, which shares a functional similarity with the bacterial RecA protein. The gene encoding the human homolog of the yeast RAD52 protein shares significant N-terminus amino acid homology with the yeast RAD52 protein. Using a yeast two hybrid system and purified GST-RAD52 fusion protein, we demonstrate that the human RAD52 protein self-associates both in vivo and in vitro. The region of RAD52 required for its self-interaction, mapped here as amino acid residues 65-165, has significant homology with the yeast RAD52 (52% identity, and 89% similarity), suggesting the importance of self-association for RAD52's function.
Binding Sites↗
Associations of UBE2I with RAD52, UBL1, p53, and RAD51 proteins in a yeast two-hybrid system.
The yeast RAD52-dependent pathway is involved in DNA recombination and double-strand break repair. Yeast ubiquitin-conjugating enzyme UBC9 participates in S- and M-phase cyclin degradation and mitotic control. Using the human RAD52 protein as the "bait" in a yeast two-hybrid system, we have identified a human homolog of yeast UBC9, designated UBE2I, that interacts with RAD52, RAD51, p53, and a ubiquitin-like protein UBL1. These interactions are UBE2I-specific, since another DNA repair-related ubiquitin-conjugating enzyme, RAD6 (UBC2), does not interact with these proteins. The interaction of UBE2I with RAD52 is mediated by RAD52's self-association region. These results suggest that the RAD52-dependent processes, cell cycle control, p53-mediated pathway(s), and ubiquitination interact through human UBE2I.
Carrier Proteins↗
UBL1, a human ubiquitin-like protein associating with human RAD51/RAD52 proteins.
The RAD51/RAD52-dependent DNA repair pathway is involved in DNA recombination and DNA double-strand break repair in yeast. Although many proteins in the RAD51/RAD52-dependent DNA repair pathway have been identified in yeast, a novel protein(s) that functions with RAD51/RAD52 may also exist in humans. Using a yeast two-hybrid system, we have identified a 12-kDa protein that associates with the human RAD51 and RAD52 proteins. This protein shares significant amino acid homology with the yeast protein SMT3, which functionally associates with the yeast mitosis fidelity protein MIF2. It also shares moderate homology with ubiquitin and several other proteins, including the N-terminus of the RAD23 protein and a ubiquitin cross reacting protein. Therefore, the gene is tentatively designated UBL1 for ubiquitin-like 1. The UBL1 mRNA is expressed in many human tissues, most highly in testis. The UBL1 gene is mapped to chromosome 2q32.2-q33, and a related sequence may be located on chromosome 1q23-q25.
Amino Acid Sequence↗
Excitation Gap in the Normal State of Underdoped Bi2Sr2CaCu2O8+delta
Angle-resolved photoemission experiments reveal evidence of an energy gap in the normal state excitation spectrum of the cuprate superconductor Bi2Sr2CaCu2O8+delta. This gap exists only in underdoped samples and closes around the doping level at which the superconducting transition temperature Tc is a maximum. The momentum dependence and magnitude of the gap closely resemble those of the dx2-y2 gap observed in the superconducting state. This observation is consistent with results from several other experimental techniques, which also indicate the presence of a gap in the normal state. Some possible theoretical explanations for this effect are reviewed.
Journal Article↗
Unconventional electronic structure evolution with hole doping in Bi2Sr2CaCu2O8+ delta : Angle-resolved photoemission results.
Explore the source record for details and available documents.
Journal Article↗
Electronic structure and the metal-insulator transition in NiS2-xSex.
Explore the source record for details and available documents.
Journal Article↗
Specific interactions between the human RAD51 and RAD52 proteins.
Processing of DNA damage by the DNA double-strand break repair pathway in mammalian cells is accomplished by multiprotein complexes. However, the nature of these complexes and details of the molecular interactions are not fully understood. Interaction of the yeast RAD51 and RAD52 proteins plays a crucial role in yeast DNA homologous recombination and DNA double-strand break repair. Here, specific interactions between human RAD51 and RAD52 proteins are demonstrated both in vivo, using the yeast two-hybrid system and immunoprecipitation of insect cells co-infected with RAD51 and RAD52 recombinant viruses, and in vitro, using affinity chromatography with purified recombinant proteins. These results suggest that RAD52 may modulate the catalytic activities of RAD51 protein such as homologous pairing and strand exchange through a direct physical interaction. In addition, the domain in RAD52 that mediates this interaction was determined in vitro and in vivo. The RAD51-interacting region (amino acids 291-330) of the human RAD52 protein shows no homology with the yeast RAD52 protein, indicating that the interaction between RAD51 and RAD52 is species-specific.
Base Sequence↗
Tolerance to cardiac allografts requires a time lag between intrathymic treatment and transplantation.
Permanent tolerance to an experimental heterotopic cardiac allograft can be achieved by pretreatment with antilymphocyte serum (ALS) and intrathymic inoculation of donor cells. Most successful experimental protocols have employed a time lag of 2 to 3 weeks between intrathymic pretreatment and transplantation, which makes this treatment strategy impractical for clinical heart transplantation. In these experiments we modified the standard protocol by giving ALS 24 hr prior to both intrathymic injection of donor cells and heterotopic transplantation. Seven Lewis rats had intraperitoneal injection of 1 ml of ALS and 24 hr later underwent intrathymic injection of 5 X 10(7) donor Lewis-Brown Norway (LBN) splenocytes and heterotopic cardiac transplantation using an LBN donor. Mean graft survival was 24.4 days, significantly longer than the 7.8-day graft survival observed in untreated Lewis recipients (n = 5) (P < 0.02). However, graft survival was not different from that observed in Lewis rats pretreated with ALS alone (n = 5) (25.8 days, P = NS). Permanent graft survival was produced in two rats receiving only A-LS and in one rat receiving both ALS and intrathymic inoculation. In these experiments it appears that prolongation of graft survival may have been due to the effect of A-LS alone. These results suggest that there is a critical time period between intrathymic inoculation and transplantation that is needed for permanent tolerance to be induced consistently. This may be due to the kinetics of the effects of ALS on alloreactive T-lymphocytes or to a time-dependent requirement for antigen processing in the thymus.
Animals↗
Fetal inoculation with donor cells in cardiac xenotransplantation.
BACKGROUND: In utero fetal inoculation with allogeneic cells has produced subsequent tolerance to experimental cardiac allografts. We attempted to extend this observation to a model of xenogeneic cardiac transplantation. METHODS: Lewis rat fetuses were inoculated with Golden Syrian hamster thymocytes (n = 5) or whole spleen cells (n = 5) on the tenth day of intrauterine life. Six weeks after the birth of pretreated fetuses, heterotopic cardiac transplantation using a hamster donor was performed. Three to 4 weeks after parturition, we performed heterotopic cardiac transplantation using hamster donors in the female Lewis rats whose fetuses had been treated in utero. RESULTS: Animals treated in utero with either thymocytes or whole spleen cells had graft survival of 3 days, not different from that in untreated Lewis rats (n = 5) (p = not significant). Maternal Lewis rats whose fetuses were treated with thymocytes (n = 5) or whole spleen cells (in = 4) had markedly reduced survival of xenogeneic cardiac grafts (range, 3 to 20 hours; mean, 15 hours; p < 0.01; and range, 5 to 15 minutes; mean, 10 minutes; p < 0.01, respectively). Female Lewis rats without intrauterine inoculation (n = 5) had expected xenograft survival time (3 days) (p = not significant). Immunohistochemical staining of hyperacutely rejected grafts showed deposits of immunoglobulin M as well as immunoglobulin G and complement. In normally rejected xenografts, no immunoglobulin M was detected. CONCLUSIONS: These studies reveal the surprising observation that fetal exposure to xenogeneic cells sensitizes the maternal rat without tolerizing the fetal rat as observed in an allograft model. In addition, whole spleen cells produce a more vigorous hyperacute rejection than thymocytes, suggesting that B cells or macrophages may be the sensitizing agents. The accelerated rejection observed has the characteristics of an immunoglobulin M antibody-mediated hyperacute rejection response with deposition of complement.
Animals↗
K(+)-induced stimulation of K+ secretion involves activation of the IsK channel in vestibular dark cells.
Vestibular dark cells in the inner ear secrete K+ from perilymph containing 4 mM K+ to endolymph containing 145 mM K+. Sensory transduction causes K+ to flow from endolymph to perilymph, thus threatening the homeostasis of the perilymphatic K+ concentration which is crucial for maintaining sensory transduction since the basolateral membranes of the sensory cells and adjacent neuronal elements need to be protected from K(+)-induced depolarization. The present study addresses the questions (1) whether increases in the perilymphatic K+ concentration by as little as 1 mM are sufficient to stimulate KCl uptake across the basolateral membrane of vestibular dark cells, (2) whether K(+)-induced stimulation of KCl uptake causes stimulation of the IsK channel in the apical membrane, and (3) whether the rate of transepithelial K+ secretion depends on the perilymphatic (basolateral) K+ concentration when the apical side of the epithelium is bathed with a solution containing 145 mM K+, as in vivo. Uptake of KCl was monitored by measuring cell height as an indicator for cell volume. The current (IIsK), conductance (gIsK) and inactivation time constant (tau IsK) of the IsK channel as well as the apparent reversal potential of the apical membrane (Vr) were obtained with the cell-attached macro-patch technique. Vr was corrected for the membrane voltage previously measured with microelectrodes. The rate of transepithelial K+ secretion JK was obtained as equivalent short circuit current from measurements of the transepithelial voltage (Vt) and resistance (Rt) measured in the micro-Ussing chamber. Cell height of vestibular dark cells was 7.2 microns (average). Elevations of the extracellular K+ concentration from 3.5 to 4.5 mM caused cell swelling with an initial rate of cell height change of 11 nm/s. With 3.6 mM K+ in the pipette IIsK was outwardly directed and elevation of the extracellular K+ concentration from 3.6 to 25 mM caused an increase of IIsK from 12 to 65 pA, gIsK from 152 to 950 pS and tau IsK from 278 to 583 ms as well as a hyperpolarization of Vr from -50 to -60 mV. With 150 mM K+ in the pipette IIsK was inwardly directed and the elevation of the extracellular K+ concentration caused an increase of IIsK from -1 to -143 pA, gIsK from 141 to 1833 pS and tau IsK from 248 to 729 ms. Vr remained within +/- 10 mV from zero. JK was 4.8 nmol x cm-2 x s-1 when the both the apical side and the basolateral side of the epithelium were perfused with a solution containing 3.5 mM K+. Elevation of the basolateral K+ concentration by 1 mM caused JK to increase by 1.1 nmol x cm-2 x s-1 or 23%. When the basolateral side of the epithelium was perfused with a solution containing 3.5 mM K+ and the apical side with a solution containing 145 mM K+, as in vivo, JK was 0.8 nmol x cm-2 x s-1 and elevation of the basolateral K+ concentration by 1 mM caused JK to increase by 0.8 nmol x cm-2 x s-1 or 100%. These data suggest that physiologically relevant increases in the perilymphatic K+ concentration increase JK by increasing KCl uptake across the basolateral membrane and activation of K+ release via the IsK channel in the apical membrane. Thus, the data demonstrate that vestibular dark cells adjust the rate of K+ secretion into endolymph according to the perilymphatic K+ concentration.
Animals↗
Induction of tolerance to an experimental cardiac allograft through intrathymic inoculation of class II major histocompatibility complex disparate antigens.
Indefinite donor-specific tolerance to a cardiac allograft can be induced through pretransplantation intrathymic injection of donor spleen cells and a single intraperitoneal injection of antilymphocyte serum. This study was designed to determine whether this phenomenon was reproducible with grafts differing in either class I major histocompatibility complex only or class II MHC only. Donors of cells and hearts in all experiments were RP rats. Class I MHC disparate grafts were performed by placing an RP heart into a Lewis recipient, and class II disparate grafts were performed with RP donors and Wistar Furth recipients. Lewis (n = 10) and Wistar Furth (n = 10) recipients underwent intraperitoneal injection of 1 ml antilympocyte serum and intrathymic injection of 5 x 10(7) RP spleen cells. Three weeks later, heterotopic cardiac transplantation was done with a heart from an RP rat. Control rats had no pretreatment or received antilympocyte serum alone. Without pretreatment, RP hearts survived 7 to 9 days (mean 8 days) in Lewis recipients (n = 5) and 9 to 14 days (mean 12 days) in Wistar Furth recipients (n = 5). Antilymphocyte serum alone produced slight prolongation of graft survival. Lewis rats pretreated with class I disparate RP splenocytes and antilympocyte serum had graft survivals of 8 to 27 days (mean 14 days), not significantly different from the results with antilympocyte serum alone. Class II disparate RP grafts placed in pretreated Wistar Furth rats had significant prolongation of graft survival, with four of five grafts surviving longer than 60 days (p < 0.01 vs antilympocyte serum alone). These results suggest that a disparity at the class II locus of the major histocompatibility complex is critical for the induction of cardiac allograft tolerance after intrathymic inoculation of allogeneic cells.
Animals↗
T-cell receptor expression in C57BL/6 mice that reject or are rendered tolerant to bm1 cardiac grafts.
To study the molecular immunologic features of allograft rejection and tolerance induction by intrathymic pretreatment we developed a murine model of cardiac transplantation. In this model the transplant recipient was the C57BL/6 mouse with its major histocompatibility phenotype H-2b. Donors of cells for intrathymic pretreatment and of hearts for grafting were mice of the bm1 mutation. The bm1 mutation involves substitution of three amino acids in one of the alpha helixes of the class I H-2Kb molecule. Because of the discrete molecular configuration of the transplant antigen we hypothesized that there would be limited heterogeneity of receptor expression on C57BL/6 T cells responding to bm1 cardiac grafts and that intrathymic pretreatment would alter the T-cell repertoire of graft recipients by causing elimination of T cells responsible for graft rejection. Mice were given 0.3 ml of antilymphocyte serum intraperitoneally and had intrathymic injection of 25 x 10(6) bm1 splenocytes 12 to 21 days before transplantation with a bm1 cardiac graft. Flow cytometric analysis of lymph node and spleen cells was used to study the V beta T-cell repertoire of graft recipients. Cells were stained with monoclonal antibodies to CD3 and 13 V beta regions (n = 5, each group) of T cells in naive, sensitized, and tolerant animals. Untreated C57BL/6 mice (n = 9) rejected bm1 cardiac grafts a mean of 20.4 days after transplantation. Twelve mice pretreated with antilymphocyte serum and intrathymic bm1 cells had permanent graft survival (> 100 days, p < 0.0001). Animals treated with antilymphocyte serum alone (n = 5) or pretreated animals undergoing third-party BALB/c grafts (n = 4) rejected grafts in the normal time frame. There was significant alteration of percentage receptor expression of V beta 5.1, 7, 12, 13, and 17a in sensitized and tolerant mice. Of interest, V beta 7 expression was increased in the sensitized mice (3.8% to 8.3%,p = 0.005) and was virtually eliminated in tolerant mice (p = 0.005). In conclusion, these data suggest that V beta 7 is a critical receptor in the C57BL/6 response to subcutaneous bm1 cardiac grafts. Pretreatment of graft recipients with one dose of antilymphocyte serum and intrathymic bm1 cells appears to produce permanent tolerance to bm1 grafts with elimination of T cells expressing receptor chain V beta 7.
Animals↗
Durability of donor-specific and organ-specific heart transplant tolerance induced by intrathymic pretreatment with allogeneic spleen cells.
Permanent acceptance of an experimental cardiac allograft can be achieved in the rat by pretreating the recipient with antilymphocyte serum and intrathymic donor lymphocytes. We investigated the durability and specificity of the tolerance produced by this pretreatment in a rat model of heterotopic heart transplantation with Lewis-Brown Norway donors and Lewis recipients. Pretreated Lewis rats received 1 ml antilymphocyte serum intraperitoneally and 5 x 10(7) Lewis-Brown Norway splenocytes intrathymically, followed 21 days later by Lewis-Brown Norway cardiac transplantation. The first Lewis-Brown Norway cardiac allograft survived long term (mean 140 days) in pretreated recipients who were given no subsequent immunosuppression. After 60 days with a beating Lewis-Brown Norway allograft, tolerant Lewis recipients underwent a second cardiac allograft with either a Lewis-Brown Norway heart or a third-party Wistar-Furth heart. The second Lewis-Brown Norway cardiac allograft was not rejected (mean survival 76 days), but that from the third-party Wistar-Furth donor was rejected in a normal fashion (mean survival 10.4 days). The presence of second grafts did not affect survival of first grafts. Tolerant Lewis recipients of two Lewis-Brown Norway heart grafts underwent subsequent transplantation with Lewis-Brown Norway skin. Skin allograft survival in this group (mean 8.4 days) was not different from that in Lewis recipients without pretreatment. Rejection of skin grafts had no effect on the heart grafts. These data suggest that tolerance to cardiac allografts produced by intrathymic pretreatment is durable and extends to a second heart graft from a genetically identical donor. Tolerant rats reject third-party hearts and primary donor skin grafts normally, and tolerance to previously placed heart grafts is not abrogated by this rejection. Non-major histocompatibility complex skin antigens not present on cardiac cells may account for the tissue specificity of the tolerance produced by intrathymic treatment in this model.
Animals↗
Local immune response in Helicobacter pylori-infected cats and identification of H. pylori in saliva, gastric fluid and faeces.
Helicobacter pylori-infected cats were screened by culture and polymerase chain reaction (PCR) for the presence of H. pylori in salivary secretions, gastric juice, gastric tissue and faeces. H. pylori was cultured from salivary secretions in six of 12 (50%) cats and from gastric fluid samples in 11 of 12 (91%) cats. A 298 base pair polymerase chain reactions (PCR) product specific for an H. pylori 26000 MW surface protein was amplified from dental plaque samples from five of 12 (42%) cats and from the faeces of four of five (80%) cats studied. Analyses of serum and mucosal secretions by enzyme-linked immunosorbent assay (ELISA) revealed an H. pylori-specific immunoglobulin G (IgG) response, and elevated IgA anti-H. pylori antibody levels in salivary and local gastric secretions. Immunohistochemical analyses of gastric tissue revealed the presence of IgM+ B cells assembled into multiple lymphoid follicles surrounded by clusters of CD4+ and CD8+ T cells. The lamina propria also contained single cells or aggregates of IgA+ and IgM+ B cells. These observations show that H. pylori can be identified in feline mucosal secretions, and that a localized IgA immune response develops in gastric tissue of H. pylori-infected cats. The findings suggest a zoonotic risk from exposure to personnel handling H. pylori-infected cats in vivaria.
Animals↗
Use of PCR and culture to detect Helicobacter pylori in naturally infected cats following triple antimicrobial therapy.
Helicobacter pylori causes gastritis and peptic ulcers and is linked to gastric cancer. Domestic cats from a commercial source were found to be naturally infected with H. pylori, and studies were undertaken to eradicate H. pylori from infected cats by using triple antimicrobial therapy. Eight cats infected with H. pylori were used in the study. Six cats received a 21-day course of oral amoxicillin, metronidazole, and omeprazole, and two cats served as controls. Two weeks and 4 weeks posttreatment (p.t.), all six treated cats were negative at several sites (saliva, gastric juice, and gastric mucosa) for H. pylori by culture. However, as determined by PCR with primers specific for the 26-kDa product, the majority of cats at 2 and 4 weeks p.t. had gastric fluid samples which were positive for H. pylori and three of three cats at 2 weeks p.t. had dental plaque which was positive for H. pylori. At 6 weeks p.t., all six cats had H. pylori-negative cultures for samples from several gastric sites taken at necropsy, and only one cat had H. pylori cultured from gastric juice. PCR analysis revealed that five of six cats had H. pylori DNA amplification products from plaque, saliva, and/or gastric fluid samples. Negative bacterial cultures for cats for which there was demonstrable PCR amplification of H. pylori DNA may reflect the inability of in vitro culture techniques to isolate small numbers of H. pylori organisms, focal colonization at sites not cultured, or a failure of the antibiotics to successfully eradicate H. pylori from extragastric sites which allowed subsequent recolonization of the stomach after cessation of therapy. Alternatively, the treatment strategy may have induced in vivo viable but nonculturable coccoid forms of H. pylori. The H. pylori cat model should allow further studies to test these hypotheses as well as the efficacies of other combined therapeutic regimens. Also, because 100% of these cats were naturally infected with H.pylori, this model should prove useful in exploring mechanisms whereby human populations in underdeveloped countries, which have H. pylori infection rates approaching 100%, have a high rate of recurrence of H. pylori infection after use of prescribed antibiotic therapies that successfully eradicate H. pylori in individuals in developed countries.
Amoxicillin↗
Isolation of Vibrio harveyi acyl carrier protein and the fabG, acpP, and fabF genes involved in fatty acid biosynthesis.
We report the isolation of Vibrio harveyi acyl carrier protein (ACP) and cloning of a 3,973-bp region containing the fabG (encoding 3-ketoacyl-ACP reductase, 25.5 kDa), acpP (encoding ACP, 8.7 kDa), fabF (encoding 3-ketoacyl-ACP synthase II, 43.1 kDa), and pabC (encoding aminodeoxychorismate lyase, 29.9 kDa) genes. Predicted amino acid sequences were, respectively, 78, 86, 76, and 35% identical to those of the corresponding Escherichia coli proteins. Five of the 11 sequence differences between V. harveyi and E. coli ACP were nonconservative amino acid differences concentrated in a loop region between helices I and II.
3-Oxoacyl-(Acyl-Carrier-Protein) Reductase↗