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Biomedical subjects

D Xu

Publications and source records attributed to D Xu.

At least 145 records · Page 8Linked to original sources
PubMed2000

[Separation of thoracopagus conjoined twins].

OBJECTIVE: To sam up the experience in diagnosis and separation of a thoracopagus conjoined twins. METHODS: Thoracopagus twin boys were admitted for evaluating possible separation and repair at age of 21 days. X-rays, CT, MRI, and ultrasound scan of torso showed separate and normal gastrointestinal and biliary tracts, little shared vasculature, but shared pericardium, diaphragm and liver parenchyma. The chest junctions were at the sternums and the most inferior two pairs of the ribs. One twin (twin A) had a protruding heart with VSD and ASD. RESULTS: The infants were separated successfully at age of 45 days. The chest defect of twin A was closed with aid of a polyester pericardial patch graft and a silicon supporter. Managing anesthesia met some difficulty in understanding of the anatomical and physiological consequences of the complex anomaly. They are had brain edema and multiple system organ failures after separation, and were cured under intensive care. They are alive and well 6 months after surgery. CONCLUSIONS: Careful preoperative evaluation proper anesthesia and surgical technique, and postoperative care are essential to the successful separation of the conjoined twins.

Anesthesia↗
PubMed2000

[Distribution of HIV resistance CCR5-delta 32, CCR2-64 I and SDF1-3'A alleles and their polymorphisms in the Han population in China].

OBJECTIVE: To study the frequency and polymorphism of three mutations (CCR5(Delta)32, CCR2-64I and SDF1-3'A alleles) conferring resistance to determined HIV-1/AIDS in the indigenous Han population in China. METHODS: The study population included 1,267 subjects, of which consisted 98.7% (1,251/1,267) Han people. The genotypes of the three mutations were respectively, detected by polymerase chain reaction (PCR) for CCR5(Delta)32 mutation, or by PCR/RFLP (restriction fragment length polymorphism) assay with the digestion of restriction endonuclease Bsa BI and Msp I for CCR2-64I and SDF1-3'A mutations. DNA sequencing was employed to confirm the accuracy of PCR or PCR/RFLP products. RESULTS: The frequency of the mutant alleles were: 0.00119 for CCR5(Delta)32; 0.20023 for CCR2-64I, and 0.28723 for SDF1-3'A. The three heterozygous CCR5-wt/Delta32 mutants were identified and no homozygotes were detected in indigenous Han population. The frequencies of CCR2-64I and SDF1-3'A alleles in China were higher than those of Caucasians descents in the USA and Europe. CONCLUSION: Our data was the first findings on the frequency and polymorphism of CCR5(Delta)32, CCR2-64I and SDF1-3'A alleles in indigenous Han population in China which implied that the indigenous Han people might have a higher genetic susceptibility to the infection of sexually transmitted HIV-1 (R-5) strain. Further study is needed to clarify the significance of higher frequency of CCR2-64I and SDF1-3'A alleles in Han population.

Alleles↗
PubMed2000

[Study on development history of Taoist medicine in Wudang].

This accomplishment of textual research on the development of Wudang Taoist medicine covers the history from the record on Wudang priests practicing medicine in early period, herb pills and internal alchemy in Song - Yuan period to Taoist medicine when at its peak and the strive of doctors of Taoist priests made a vitalize Taoism after its period of declination.

China↗
PubMed2000

[The effects of starfish sterol on platelet aggregation].

Through the internal and external experiments of platelet aggregation on rats and rabbits, we study the effects of starfish sterol (No. A1998) on the formation of experimental thrombus in vitro and the effects of platelet aggregation induced by arachidonic acid (AA), ADP, CaCl2. Starfish sterol A 1998 can inhibit the formation of experimental thrombus in vitro of rats on the rates of 10.0%, 20.1%, 25.9% (P < 0.01), p.o. starfish sterol 4.5, 13.5, 40.5 mg/kg. A 1998 can inhibit platelet aggregation induced by AA, ADP, CaCl2 in the same time. It can be concluded that starfish sterol has inhibitory effects on platelet aggregation.

Adenosine Diphosphate↗
PubMed2000

[Improving memory effects of eel oil capsule on memory obstruction of mice hurt by anisodine].

The effects of eel oil capsule on memory obstruction of mice were observed in step-down test, step-through test, Y-maze test and Japanese labyrinth test. The results indicated that the eel oil capsule treating group with dosages of 0.234, 0.702 and 2.106 g/kg markedly enhance the acquirement, strengthing and reappearance of memory, having the functions of improving brain memory hurt by Anisodine.

Animals↗
PubMed2000

[Orientation of H-bonds revealed by cryogenic FTIR spectroscopy].

We propose a new way to reveal structural arrangement of hydrogen bond network using FTIR spectroscopy. When KBr pellet and fluorolube mull methods are used to prepare samples for IR measurements, the resultant spectra sometimes show significant differences, sometimes not. The reason is unknown. We use cryogenic FTIR spectra to prove pressure effect accounts for spectral variation in different sampling process. The sensitivity of the FTIR spectra to external pressure is related to the three-dimensional arrangement of hydrogen bonding network in the sample. When hydrogen bonds are in one plane, they can not resist external pressure applied perpendicular to that plane. Consequently, large differences appear between the spectra obtained using KBr pellet and fluorolube mull methods. On the other hand, when hydrogen bonds orientate towards various directions, the hydrogen bonding system can resist pressure from any directions. Thus, the FTIR spectra exhibit little variation using different sampling methods. We propose that the spectral variation obtained using above methods is a criterion to judge whether the hyrogen bonds orientate toward various directions in three-dimensional space or not.

Cholesterol↗
PubMed1999

Genetic evidence of an accessory activity required specifically for cubilin brush-border expression and intrinsic factor-cobalamin absorption.

Cubilin is a high molecular weight multiligand receptor that mediates intestinal absorption of intrinsic factor-cobalamin and selective protein reabsorption in renal tubules. The genetic basis of selective intestinal cobalamin malabsorption with proteinuria was investigated in a canine model closely resembling human Imerslund-Gräsbeck syndrome caused by cubilin mutations. Canine CUBN cDNA was cloned and sequenced, showing high identity with human and rat CUBN cDNAs. An intragenic CUBN marker was identified in the canine family and used to test the hypothesis of genetic linkage of the disease and CUBN loci. Linkage was rejected, indicating that the canine disorder resembling Imerslund-Gräsbeck syndrome is caused by defect of a gene product other than cubilin. These results imply that there may be locus heterogeneity among human kindreds with selective intestinal cobalamin malabsorption and proteinuria and that normal brush-border expression of cubilin requires the activity of an accessory protein.

Amino Acid Sequence↗
PubMed1999

Phase I trial of a humanized, Fc receptor nonbinding OKT3 antibody, huOKT3gamma1(Ala-Ala) in the treatment of acute renal allograft rejection.

BACKGROUND: HuOKT3gamma1(Ala-Ala) is a genetically-engineered derivative of the parental murine OKT3 monoclonal antibody, in which the six complementarity-determining regions have been grafted within a human IgG1 mAb, and whose C(H)2 region has been altered by site-directed mutagenesis to alter FcR-binding activity, thereby eliminating T cell activation properties. This report describes the results of a phase I trial of huOKT3gamma1(Ala-Ala) treatment of acute renal allograft rejection. METHODS: Acute renal allograft rejection in kidney and kidney-pancreas transplant recipients was treated with huOKT3gamma1(Ala-Ala). huOKT3gamma1(Ala-Ala) dosing consisted of daily 5- or 10-mg doses adjusted initially to achieve target levels of 1000 ng/ml. RESULTS: A total of seven patients, five kidney transplant and two kidney-pancreas transplant recipients, were treated with the monoclonal antibody for first rejection episodes. Corticosteroids (500 mg i.v. Solumedrol) were given 2 hr before the first huOKT3gamma1(Ala-Ala) dose only. Banff classification of treated rejections were the following: grade I, 1 patient, grade IIA, 1 patient, grade IIB, 4 patients, and grade III, 1 patient. Median time from transplant to rejection was 15 days, and median follow up 12 months (range 10-17 months). HuOKT3gamma1(Ala-Ala) therapy was given for 10.1+/-2.5 days, and mean total dose was 76+/-27 mg. Rejection was reversed in five of seven patients, and recurrent rejection was observed in one patient. Serum creatinine values peaked on day 1 of huOKT3gamma1(Ala-Ala) therapy, and thereafter demonstrated a progressive decline. Rejection reversal (return of creatinine to baseline) occurred at a median of 4 days and a mean of 4.1+/-2 days. Renal allograft biopsies obtained during huOKT3gamma1(Ala-Ala) therapy provided evidence of rapid rejection reversal. Patient and graft survival were both 100%. First dose reactions were minimal, and anti-OKT3 antibodies were not detected. Elevations in serum IL-10, but not IL-2 levels were observed after the first huOKT3gamma1(Ala-Ala) dose. Marked reductions in circulating CD2+, CD4+, and CD8+ T cells were observed after the first huOKT3gamma1(Ala-Ala) dose, followed by a slow progressive return of cell counts toward pretreatment values. Pharmacokinetic analysis revealed a half-life of 142+/-32 hr. CONCLUSIONS: HuOKT3gamma1(Ala-Ala) possesses the ability to reverse vigorous rejection episodes in kidney and kidney-pancreas transplant recipients, and in comparison to murine OKT3, possesses minimal first dose reactions and does not seem to induce antibodies that bind the OKT3 idiotype. These results support the conduct of additional clinical trials with the huOKT3gamma1(Ala-Ala) antibody.

Acute Disease↗
PubMed1999

Protective immune responses induced by vaccination with an expression genomic library of Leishmania major.

To develop an effective vaccine against the intracellular protozoan parasite Leishmania spp., we investigated the feasibility of expression library immunization (ELI) in the mouse. Genomic expression libraries of L. major were constructed and used to immunize mice. One of the three libraries (L1, with 10(5) clones) induced a significant protective immune response and delayed the onset of lesion development in highly susceptible BALB/c mice after i.m. immunization, compared with control mice immunized with the empty vector (EV). L1 was then divided into five sublibraries of approximately 2 x 10(4) clones each. Mice immunized with one of the sublibraries (SL1A) developed an even stronger protective effect than that induced by L1. SL1A was further divided into 20 sublibraries (SL2) of approximately 10(3) clones each. One of the SL2 libraries (SL2G) induced a strong protective effect against L. major infection. In direct comparative studies, the protective effect of the sublibraries was in the order of SL2G > SL1A > L1. Lymphoid cells from mice vaccinated with SL2G produced more IFN-gamma and NO, compared with cells from control mice injected with EV. Serum from the vaccinated mice also contained more parasite-specific IgG2a Ab, compared with controls. Therefore, these data demonstrate that ELI is feasible against this complex intracellular parasitic infection, by preferentially inducing the development of Th1 responses. Furthermore, by sequential division of the libraries, this approach may be used to enrich and identify protective genes for effective gene vaccination against other parasitic infections.

Animals↗
PubMed1999

A requirement for K+-channel activity in growth factor-mediated extracellular signal-regulated kinase activation in human myeloblastic leukemia ML-1 cells.

Voltage-gated K+ channels have been shown to be required for proliferation of various types of cells. Much evidence indicates that K+-channel activity is required for G1 progression of the cell cycle in different cell backgrounds, suggesting that K+-channel activity is required for early-stage cell proliferation in these cells. However, little is known about the molecular mechanisms that underlie this phenomenon. We have shown in human myeloblastic leukemia ML-1 cells that K+ channels are activated by epidermal growth factor (EGF), whereas serum starvation deprivation suppressed their activity. In addition, voltage-gated K+ channels are required for G1/S-phase transition of the cell cycle. We report here that suppression of K+ channels prevented the activation of extracellular signal-regulated protein kinase 2 (ERK-2) in response to EGF and serum. However, blockade of K+ channels did not prevent ERK-2 activation induced by 12-O-tetradecanoyl-phorbol 13-acetate (TPA). Elimination of extracellular Ca2+ did not alter either ERK-2 activation or the effect of K+-channel blockade on ERK-2 activation. Our data demonstrate that the K+ channel is a part of the EGF-mediated mitogenic signal-transduction process and is required for initiation of the EGF-mediated mitogen-activated protein kinase (MAPK) pathways. Our findings may thus explain why an increase in K+-channel activity is associated with cell proliferation in many types of cells, including ML-1 cells.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1999

Attenuation of ischemia-induced cellular and behavioral deficits by X chromosome-linked inhibitor of apoptosis protein overexpression in the rat hippocampus.

Transient forebrain ischemia produced by four-vessel occlusion (4-VO) triggers the delayed death of CA1 neurons in the hippocampus, resulting in behavioral deficits of spatial learning performance. We demonstrate that CA1 neuronal loss induced by 4-VO (12 min) is preceded by a selective and marked elevation of catalytically active caspase-3 in these neurons, indicative of apoptosis. Virally mediated overexpression of the anti-apoptotic gene X chromosome-linked inhibitor of apoptosis protein (XIAP) prevented both the production of catalytically active caspase-3 and degeneration of CA1 neurons after transient forebrain ischemia. CA1 neurons protected in this manner appeared to function normally, as assessed by immunohistochemical detection of the neuronal activity marker nerve growth factor inducible-A and by spatial learning performance in the Morris water maze. These findings indicate that caspase-3 activation is a key event in ischemic neuronal death and that blockade of this event by XIAP overexpression permits CA1 neurons to survive and operate properly after an ischemic insult.

Animals↗
PubMed1999

Involvement of caspases in proteolytic cleavage of Alzheimer's amyloid-beta precursor protein and amyloidogenic A beta peptide formation.

The amyloid-beta precursor protein (APP) is directly and efficiently cleaved by caspases during apoptosis, resulting in elevated amyloid-beta (A beta) peptide formation. The predominant site of caspase-mediated proteolysis is within the cytoplasmic tail of APP, and cleavage at this site occurs in hippocampal neurons in vivo following acute excitotoxic or ischemic brain injury. Caspase-3 is the predominant caspase involved in APP cleavage, consistent with its marked elevation in dying neurons of Alzheimer's disease brains and colocalization of its APP cleavage product with A beta in senile plaques. Caspases thus appear to play a dual role in proteolytic processing of APP and the resulting propensity for A beta peptide formation, as well as in the ultimate apoptotic death of neurons in Alzheimer's disease.

Acute Disease↗
PubMed1999

The role of threonine 37 in flavin reactivity of the old yellow enzyme.

Threonine 37 is conserved among all the members of the old yellow enzyme (OYE) family. The hydroxyl group of this residue forms a hydrogen bond with the C-4 oxygen atom of the FMN reaction center of the enzyme [Fox, K. M. & Karplus, P. A. (1994) Structure 2, 1089-1105]. The position of Thr-37 and its interaction with flavin allow for speculations about its role in enzyme activity. This residue was mutated to alanine and the mutant enzyme was studied and compared with the wild-type OYE1 to evaluate its mechanistic function. The mutation has different effects on the two separate half-reactions of the enzyme. The mutant enzyme has enhanced activity in the oxidative half-reaction but the reductive half-reaction is slowed down by more than one order of magnitude. The peaks of the absorption spectra for enzyme bound with phenolic compounds are shifted toward shorter wavelengths than those of wild-type OYE1, consistent with its lower redox potential. It is suggested that Thr-37 in the wild-type OYE1 increases the redox potential of the enzyme by stabilizing the negative charge of the reduced flavin through hydrogen bonding with it.

Amino Acid Substitution↗
PubMed1999

Stable transduction of quiescent CD34(+)CD38(-) human hematopoietic cells by HIV-1-based lentiviral vectors.

We compared the efficiency of transduction by an HIV-1-based lentiviral vector to that by a Moloney murine leukemia virus (MLV) retroviral vector, using stringent in vitro assays of primitive, quiescent human hematopoietic progenitor cells. Each construct contained the enhanced green fluorescent protein (GFP) as a reporter gene. The lentiviral vector, but not the MLV vector, expressed GFP in nondivided CD34(+) cells (45.5% GFP+) and in CD34(+)CD38(-) cells in G0 (12.4% GFP+), 48 hr after transduction. However, GFP could also be detected short-term in CD34(+) cells transduced with a lentiviral vector that contained a mutated integrase gene. The level of stable transduction from integrated vector was determined after extended long-term bone marrow culture. Both MLV vectors and lentiviral vectors efficiently transduced cytokine-stimulated CD34(+) cells. The MLV vector did not transduce more primitive, quiescent CD34(+)CD38(-) cells (n = 8). In contrast, stable transduction of CD34(+)CD38(-) cells by the lentiviral vector was seen for over 15 weeks of extended long-term culture (9.2 +/- 5.2%, n = 7). GFP expression in clones from single CD34(+)CD38(-) cells confirmed efficient, stable lentiviral transduction in 29% of early and late-proliferating cells. In the absence of growth factors during transduction, only the lentiviral vector was able to transduce CD34(+) and CD34(+)CD38(-) cells (13.5 +/- 2.5%, n = 11 and 12.2 +/- 9.7%, n = 4, respectively). The lentiviral vector is clearly superior to the MLV vector for transduction of quiescent, primitive human hematopoietic progenitor cells and may provide therapeutically useful levels of gene transfer into human hematopoietic stem cells.

ADP-ribosyl Cyclase↗
PubMed1999

Evidence for the existence of an unfolding intermediate state for aminoacylase during denaturation in guanidine solutions.

The equilibrium unfolding of pig kidney aminoacylase in guanidinium chloride (GdmCl) solutions was studied by following the fluorescence and circular dichroism (CD). At low concentrations of GdmCl, less than 1.0 M, the fluorescence intensity decreased with a slight red shift of the emission maximum (from 335 to 340 nm). An unfolding intermediate was observed in low concentrations of denaturant (between 1.2 and 1.6 M GdmCl). This intermediate was characterized by a decreased fluorescence emission intensity, a red-shifted emission maximum, and increased binding of the fluorescence probe 1-anilino-8-naphthalenesulfonate. No significant changes of the secondary structure were indicated by CD measurement. This conformation state is similar to a molten globule state which may exist in the pathway of protein folding. Further changes in the fluorescence properties occurred at higher concentrations of GdmCl, more than 1.6 M, with a decrease in emission intensity and a significant red shift of the emission maximum from 340 to 354 nm. In this stage, the secondary structure was completely broken. A study of apo-enzyme (Zn2+-free enzyme) produced similar results. However, comparison of the changes of the fluorescence emission spectra of native (Holo-) enzyme with Zn2+-free (Apo-) enzyme at low GdmCl concentrations showed that the structure of the Holo-enzyme was more stable than that of the Apo-enzyme.

Amidohydrolases↗
PubMed1999

An ultraviolet-activated K+ channel mediates apoptosis of myeloblastic leukemia cells.

Exposure of mammalian cells to UV light causes initial changes in the cell membrane, induces phosphorylation and clustering of growth factor/cytokine receptors, and activates the Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) signaling pathway leading to programmed cell death (apoptosis). In this study, we found that an early event in the cell membrane of myeloblastic leukemia (ML-1) cells was the vigorous activation of the voltage-gated K+ channel by UV irradiation. The strong enhancement by UV irradiation of K+ channel activity in the cell membrane subsequently activated the JNK/SAPK signaling pathway and resulted in myeloblastic leukemia cell apoptosis. Suppression of UV-induced K+ channel activation with specific channel blockers prevented UV-induced apoptosis through inhibition of UV-induced activation of the proteins SEK (SPAK kinase) and JNK. However, suppression of K+ channel activity could not protect cells from etoposide-induced apoptosis, which bypasses the membrane event. Elimination of extracellular Ca2+ had no effect on the UV-induced and K+ channel-mediated JNK/SAPK activation. Thus, we have identified a novel mechanism in which activation of K+ channels by UV-irradiation upstream of SEK and SAPK/JNK mediates UV-induced myeloblastic cell apoptosis.

Apoptosis↗
PubMed1999

Catalytic activity of carboxypeptidase B and of carboxypeptidase Y with anisylazoformyl substrates.

Anisylazoformyllysine (CH3OC6H4-N = N-CO-Lys-OH) is rapidly hydrolyzed at the acyl-lysine linkage by the zinc-enzyme porcine carboxypeptidase B. The catalytic reaction is readily monitored spectrophotometrically by disappearance of the intense absorption (348.5 nm, epsilon 18400) of the azo chromophore, which chemically fragments after substrate cleavage. Carboxypeptidase Y has no activity toward this type of substrate.

Animals↗