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Biomedical subjects

X Hong

Publications and source records attributed to X Hong.

At least 55 records · Page 3Linked to original sources
PubMed1998

Dual-orthogonal radial basis function networks for nonlinear time series prediction.

A new structure of Radial Basis Function (RBF) neural network called the Dual-orthogonal RBF Network (DRBF) is introduced for nonlinear time series prediction. The hidden nodes of a conventional RBF network compare the Euclidean distance between the network input vector and the centres, and the node responses are radially symmetrical. But in time series prediction where the system input vectors are lagged system outputs, which are usually highly correlated, the Euclidean distance measure may not be appropriate. The DRBF network modifies the distance metric by introducing a classification function which is based on the estimation data set. Training the DRBF networks consists of two stages. Learning the classification related basis functions and the important input nodes, followed by selecting the regressors and learning the weights of the hidden nodes. In both cases, a forward Orthogonal Least Squares (OLS) selection procedure is applied, initially to select the important input nodes and then to select the important centres. Simulation results of single-step and multi-step ahead predictions over a test data set are included to demonstrate the effectiveness of the new approach.

Journal Article↗
PubMed1998

Modulation of alloimmunity to major histocompatibility complex class I by cotransfer of cytokine genes in vivo.

Major histocompatibility complex (MHC) class I antigen is a potent stimulus for alloimmune responses and is the principal immunologic target mediating acute cellular rejection of allografts. Using a method of direct in vivo gene transfer of cDNA encoding donor type MHC class I, we showed in a rat model that recipient muscle could express the transferred MHC class I cDNA, resulting in alloimmunization of the recipient. This was most graphically demonstrated by accelerated rejection of cardiac allografts expressing the same MHC class I as encoded by the immunizing cDNA. We now report the use of the particle-mediated gene transfer via a gene gun (Geneva, Middleton, WI, USA) to transfer MHC class I, as well as cytokine gene expression vectors, into rat skin. Compared to intramuscular injection, gene gun transfer to skin resulted in more efficient immunization. Donor-specific cytotoxic T lymphocyte (CTL) responsiveness and antibody levels increased. Furthermore, coexpression of certain cytokine genes with the MHC class I cDNA modulated the immune response. Specifically, coimmunization with IL-10 cDNA abrogated immunity to allo-MHC class I, while coimmunization with GM-CSF cDNA enhanced it. The influence of expression of these genes in skin was demonstrated by alteration of donor cardiac allograft survival. This model is useful for induction and modulation of alloimmune responses and may be used to develop gene therapy strategies to modify them.

Animals↗
PubMed1998

Role of enhanced ceramide generation in DNA damage and cell death in chemical hypoxic injury to LLC-PK1 cells.

BACKGROUND: Ceramide has been implicated to be a second messenger in the cell signaling pathway involved in cell growth, proliferation, and apoptotic cell death. However, there is little information of a role of ceramide in DNA damage and cell death in hypoxic injury known to induce necrotic cell death. METHODS: Ceramide generation was measured in LLC-PK1 cells exposed to chemical hypoxia with a mitochondrial electron transport inhibitor, antimycin A and glucose deprivation. The effect of inhibition of ceramide generation on chemical hypoxia-induced DNA damage and cell death and the effect of exogenous ceramide on cellular injury were also determined. RESULTS: Chemical hypoxia resulted in a rapid increase in ceramide production prior to any evidence of DNA damage and cell death in LLC-PK1 cells. The inhibitor of ceramide synthase, fumonisin B1, provided a marked protection against chemical hypoxia-induced DNA strand breaks, DNA fragmentation and cell death. Fumonisin B1 did not affect adenosine triphosphate (ATP) depletion induced by antimycin A, suggesting that fumonisin B1 does not alter cellular uptake of antimycin A. We confirmed the ability of ceramide synthase inhibitor, fumonisin B1, to suppress chemical hypoxia-induced ceramide generation. Exposure of LLC-PK1 cells to synthetic ceramide, C2- and C6-ceramide, but not C2-dihydroceramide, the structural analog of C2-ceramide, resulted in DNA strand breaks, DNA fragmentation and cell death in a dose- and time-dependent manner similar to the effect of chemical hypoxia. CONCLUSIONS: Our data indicate that ceramide is a key modulator for DNA damage and cell death in chemical hypoxia to renal tubular epithelial cells.

Animals↗
PubMed1998

[Evaluation of the intubating conditions and maintenance doses of rocuronium].

OBJECTIVE: To assess intubating conditions after administration of rocuronium 0.6 mg/kg at 60 or 90 s and neuromuscular blocking effects of rocuronium. METHODS: Thirty-two patients were randomly designated to two groups: 60 s group and 90 s group. Anesthesia consisted of thiopentone, fentanyl, N2O/O2 and enflurane. After a 2 x ED95 dose the trachea was intubated at 60 or 90 s and the intubating conditions were recorded. After intubation was finished, patients were allocated randomly to receive either intravenous infusion or bolus injection of rocuronium to maintain surgical relaxation. RESULTS: Intubating conditions were not different between the two groups and were found to be clinically acceptable (good or excellent) in all patients. The maintenance of surgical relaxation was satisfactory either with repeated bolus and infusion of rocuronium. CONCLUSION: Intubation can be performed under good to excellent conditions within 60-90 seconds after a bolus dose of 0.6 mg/kg rocuronium. This indicates that rocuronium may be a suitable alternative to succinycholine during rapid-sequence induction of anesthesia.

Adjuvants, Anesthesia↗
PubMed1998

Primate renal transplants using immunotoxin.

BACKGROUND: T-lymphocyte depletion 7 days before transplantation with immunotoxin FN 18-CRM9 has resulted in tolerance to subsequent renal allografts. We tested the effect of giving immunotoxin on the day of the transplantation and evaluated its effect on rhesus monkey and allograft survival, on antibody production, and on T-cell recovery. METHODS: Major histocompatibility complex mismatched renal allografts were performed in rhesus monkeys. Immunotoxin was given starting on the day of transplantation, with and without prednisone and mycophenolate mofetil for 3 days. T-cell subsets and alloantibody levels were measured by flow cytometry. The ability of treated monkeys to develop antibody to tetanus, diphtheria, and xenoantibody was measured. Histology of renal transplants was read in a blinded manner. RESULTS: Immunotoxin started on the day of transplantation resulted in prolonged allograft survival in all treatment groups. Graft loss between days 50 and 135 was most often due to interstitial nephritis. Later graft loss was due to chronic rejection. Monkeys had intact antibody responses to alloantigen, tetanus, diphtheria, and xenoantibody. Their CD4 cells recovered gradually over 6 months. CONCLUSIONS: Immunotoxin reliably prolongs renal allograft survival when started on the day of transplantation, but interstitial nephritis and chronic rejection limit the development of long-term tolerance. T-cell-dependent B-cell responses remain intact after treatment.

Animals↗
PubMed1997

CTLA4-Ig and anti-CD40 ligand prevent renal allograft rejection in primates.

Selective inhibition of T cell costimulation using the B7-specific fusion protein CTLA4-Ig has been shown to induce long-term allograft survival in rodents. Antibodies preventing the interaction between CD40 and its T cell-based ligand CD154 (CD40L) have been shown in rodents to act synergistically with CTLA4-Ig. It has thus been hypothesized that these agents might be capable of inducing long-term acceptance of allografted tissues in primates. To test this hypothesis in a relevant preclinical model, CTLA4-Ig and the CD40L-specific monoclonal antibody 5C8 were tested in rhesus monkeys. Both agents effectively inhibited rhesus mixed lymphocyte reactions, but the combination was 100 times more effective than either drug alone. Renal allografts were transplanted into nephectomized rhesus monkeys shown to be disparate at major histocompatibility complex class I and class II loci. Control animals rejected in 5-8 days. Brief induction doses of CTLA4-Ig or 5C8 alone significantly prolonged rejection-free survival (20-98 days). Two of four animals treated with both agents experienced extended (>150 days) rejection-free allograft survival. Two animals treated with 5C8 alone and one animal treated with both 5C8 and CTLA4-Ig experienced late, biopsy-proven rejection, but a repeat course of their induction regimen successfully restored normal graft function. Neither drug affected peripheral T cell or B cell counts. There were no clinically evident side effects or rejections during treatment. We conclude that CTLA4-Ig and 5C8 can both prevent and reverse acute allograft rejection, significantly prolonging the survival of major histocompatibility complex-mismatched renal allografts in primates without the need for chronic immunosuppression.

Abatacept↗
PubMed1997

Direct MHC class I complementary DNA transfer to thymus induces donor-specific unresponsiveness, which involves multiple immunologic mechanisms.

Our purposes were 1) to determine whether direct transfer of cDNA encoding allogeneic MHC class I Ag to the rat thymus would be capable of inducing donor-specific unresponsiveness and 2) to study the immunologic mechanism of this effect. Plasmid DNA encoding donor strain (ACI-RT1.Aa) MHC class I Ag was directly injected into Lewis (RT1(l)) rat recipient thymus 7 to 10 days before ACI liver transplantation. A single dose of anti-lymphocyte serum was given i.p. on the day of thymic injection. Rats injected intrathymically with plasmid DNA and treated with anti-lymphocyte serum demonstrated prolonged survival in 9 of 13 rats (>100 days). PCR was used to demonstrate that RT1.Aa cDNA was expressed in thymus transiently and later appeared in spleen. CTL limiting dilution assays showed that CTL precursor frequency was decreased in tolerant liver recipients. To test the hypothesis of clonal deletion vs anergy, CTL limiting dilution assays cultures were restimulated with donor cells and IL-2 to reverse anergy. Restimulation caused CTL precursor frequency to return to near normal in only one of five tolerant rats, suggesting clonal deletion or a dense anergic state. Passive transfer of splenocytes from tolerant rats to naive recipients prolonged cardiac allograft survival, suggesting that suppressor-type cells may also contribute to thymic tolerance in our model. In summary, our data suggest that donor MHC class I Ag expressed in thymus by direct DNA injection, followed by liver allografting, results in donor-specific unresponsiveness. The mechanism of this effect is complex, involving multiple immunologic mechanisms.

Adoptive Transfer↗
PubMed1997

[Effect of dynorphin A1-13 on hypoxia-ischemic brain injury in neonatal rats].

OBJECTIVES: To study the secondary pathological changes in the central nervous system after injury and the role of dynorphin A1-13 in hypoxi-ischemic brain injury in neonatal rats. METHODS: Changes of concentrations of dynorphin A1-13 immunoreactives in some brain areas at different times after brain injury and the effect of injecting 8 microliters dynorphin A1-13 anti-serum into the medulla pool on pathological process of brain injury were observed in perinatal cerebral hypoxia ischemic rat models prepared by permanent ligation of right common carotid artery combined with a temporary systematic hypoxia at 37 degrees C in 7 day old Wistar rats. RESULTS: Concentrations of dynorphin A1-13 in cortex, hypothalamus and hippocampus increased significantly after the injury. Microinjection of anti-dynorphin A1-13 serum into the medulla pool 1 h preinjury might markedly reduce brain edema and improve the physiological condition. CONCLUSIONS: Dynorphin A1-13 plays a role in the pathophysiological process of brain hypoxia-ischemia and excessive amount of dynorphin A1-13 had some detrimental effect on the process.

Animals↗
PubMed1996

Activation of stable DNA replication in rapidly growing Escherichia coli at the time of entry to stationary phase.

The conditions are described in which DNA replication can occur, in the absence of protein synthesis, in wild-type Escherichia coli cells. Chromosome replication, which is normally inhibited by addition of chloramphenicol, becomes resistant to this drug after nutritional shiftup, e.g. from minimal medium to Luria broth. This replication activity appears transiently when nutritionally upshifted cells enter stationary phase. The activity strictly requires recA+, but it is independent of recB+ and dnaA+. It can occur in the absence of concomitant transcription. Activation of the replication does not result from induction of the SOS response. As the characteristics of this DNA replication resemble those of the previously characterized stable DNA replication, it is termed nutritional shiftup-activatable stable DNA replication, nSDR. Possible mechanisms of the activation of nSDR in rapidly growing cells at the time of entry to stationary phase are discussed.

Bacterial Proteins↗
PubMed1996

[Comparison between kinetics of positive inotropism of ibopamine and ouabain].

AIM: To compare the kinetics of positive inotropism between ibopamine (Ibo) and ouabain (Oua). METHODS: The isolated right papillary muscle of cat was used to assess the positive inotropic effects by cummulative concentrations of Ibo and Oua. The maximal effects was recognized as the contraction just before the appearance of spontaneous contraction. A Hill equation was developed by using lg [E/(Emax-E)] vs lg C. RESULTS: The S value of Ibo was smaller than that of Oua, causing C95/C5 (ratio of concentrations producing 95%/5% of Emax) of Ibo (264) elevenfold as large as Oua (22.9). Comparing with Oua, concentrations of Ibo initiating effects were lower, the slope was smaller, and higher concentrations were required for producing maximal effect. During drug concentration declining, the effect-concentration curve of Ibo showed a counter-hysteresis loop, more remarkable than Oua. CONCLUSION: The changes in positive inotropism of Ibo against drug concentrations were less than those of Oua.

Animals↗
PubMed1996

[Receptor mechanism of dynorphin A in rat secondary spinal cord injuries].

OBJECTIVE: To clarify the effects of dynorphin A on secondary spinal cord injuries. METHODS: Spinal cord injured rat model made according to modified Allen's method was used by comparing the effect of intrathecal dynorphin A antiserum and that of its receptor antagonist nor-BNI. RESULTS: The recovery of the muscle tension and motor function of the hindlimb in dynorphin antiserum group was markedly faster than that in both control and nor-BNI groups. Also, the recovery of motor function in the nor-BNI group was favorable at the early stage of injury, compared to the control group. Pathological observation showed that the residual area of the spinal cord in dynorphin A1-13 antiserum group was larger than that in both control and nor-BNI groups. The residual area of the spinal cord in the nor-BNI group was also larger than that in the control group. CONCLUSION: These observations support the hypothesis that dynorphin contributes to certain pathophysiological changes following traumatic SCI through both opiate-receptor mediated and nonopioid mechanisms.

Animals↗