Biomedical subjects

P Dai

Publications and source records attributed to P Dai.

At least 19 recordsLinked to original sources

PubMed2003

In-plane thermal conductivity of Nd2CuO4: evidence for magnon heat transport.

We report the temperature and magnetic field dependence of the in-plane thermal conductivity (kappa(ab)) of high-quality monocrystalline Nd2CuO4. Isothermal measurements of the field dependence of kappa(ab) at low temperatures (2 K<or=T<or=5 K) show no change in kappa(ab) below a critical magnetic field H(c) (H(c) approximately 4.5 T for H parallel [100]) and H(c) approximately 2.5 T for H approximately parallel [110]). Above H(c), kappa(ab) more than doubles as H is increased to 9 T. At H(c), there is a transition from a noncollinear to a collinear arrangement of the Nd and Cu spins and a collapse of the gap, Delta, in an acoustic magnon branch at k=0. Closure of this gap appears to allow the conduction of substantial amounts of heat by acoustic magnons.

Journal Article↗

PubMed2003

Somatic instability of the DNA sequences encoding the polymorphic polyglutamine tract of the AIB1 gene.

BACKGROUND: AIB1 contains a polymorphic polyglutamine tract (poly Q) that is encoded by a trinucleotide CAG repeat. Previously there have been conflicting results regarding the effect of the poly Q tract length on breast cancer. Since poly Q is not encoded by a perfect CAG repeat, the heterozygous polymorphic alleles need to be resolved, to understand the exact DNA sequences encoding poly Q. METHODS: Poly Q encoding sequences of AIB1 from 107 DNA samples, including breast cancer cell lines, sporadic primary breast tumours, and blood samples from BRCA1/BRCA2 mutation carriers and the general population, were resolved by PCR/cloning followed by sequencing of each individual clone. RESULTS: 25 distinct poly Q encoding sequence patterns were found. More than two distinct sequence patterns were found in a significantly higher proportion of tumours and cell lines than that of the general population, suggesting somatic instability. A significantly higher proportion of cancer cell lines or primary breast tumours than that of the general population contained rare sequence patterns. The proportion of sporadic breast tumours having at least one allele < or =27 repeats is significantly higher than that in the blood of BRCA1/BRCA2 mutation carrier breast cancer patients or the general population. CONCLUSION: The poly Q encoding DNA sequences are somatically unstable in tumour tissues and cell lines. A missense mutation and a very short glutamine repeat in primary tumours suggests that AIB1 activity may be modulated through poly Q, which in turn plays a role in the cotransactivation of gene expressions in breast cancers.

Adult↗

PubMed2001

Novel SNP at the common primer site of exon IIIa of FGFR2 gene causes error in molecular diagnosis of craniosynostosis syndrome.

Most mutations in Crouzon, Pfeiffer, and Apert syndromes are in the extracellular, third immunoglobulin-like domain and adjacent linker regions (exons IIIa and IIIc) of the fibroblast growth factor receptor 2 (FGFR2) gene. Using the published primers for PCR, a patient with Crouzon syndrome was found to be homozygous for a mutation that results in a Q289P amino acid substitution in FGFR2. Two additional patients; one with Apert syndrome and P253R mutation, the other with Pfeiffer syndrome and S267P mutation, also appeared to be homozygous. Using a new primer located 146 bp 5' of exon IIIa for PCR followed by sequencing revealed an A to G polymorphism at -62 [corrected] position of exon IIIa. All three patients were heterozygous for both the mutation and the polymorphism. These results indicate that the polymorphism and the mutation are not on the same chromosome. The single nucleotide polymorphism is located at the second to the last base of the 3' end of the published primer. This primer mismatch caused the failure of amplification of the normal chromosome and thus, the apparent homozygosity. The frequency of this novel polymorphism was determined to be 0.03 by studying 326 chromosomes from the general population. We propose that a new primer should be used for mutational analysis of exon IIIa of FGFR2 to avoid misdiagnosis caused by primer mismatch.

Base Sequence↗

PubMed2001

Severe lactic acidosis caused by a novel frame-shift mutation in mitochondrial-encoded cytochrome c oxidase subunit II.

We report the first frame-shift truncation mutation in a mitochondrial DNA (mtDNA)-encoded subunit II of cytochrome c oxidase (COXII). The mutation was identified by temporal temperature gradient gel electrophoresis (TTGE) followed by direct DNA sequencing in an infant who died at 12 days of age following a course of apnea, bradycardia, and severe lactic acidosis. The patient had a twin brother who died at two days of age of similar course. The mutation, 8042delAT, produced a truncated protein that was 72 amino acids shorter than the wild type protein. The mutant protein, missing one third of the amino acid residues at the C-terminal essential for hydrophilic interaction with cytochrome c, ligand binding to CuA and Mg, and the formation of proton and water channels, apparently has devastating effects on mitochondrial respiratory function.

Acidosis, Lactic↗

PubMed2001

Jahn-Teller phonon anomaly and dynamic phase fluctuations in La0.7Ca0.3MnO3.

Inelastic neutron scattering was used to study the temperature (T) dependence of the lattice excitations in La 0.7Ca 0.3MnO (3). An optical Jahn-Teller phonon exhibits continuous but anomalous damping with increasing temperature in the ferromagnetic-metallic phase and collapses above the Curie temperature T(C) (240 K). We attribute this anomaly to the growing dynamic phase segregation as T-->T(C), thus providing evidence of local fluctuations associated with the short-range polaron or charge/orbital ordering in the ferromagnetic-metallic state.

Journal Article↗

PubMed2001

Molecular genetics of glycogen-storage disease type 1a in Chinese patients of Taiwan.

The mutation spectrum of the glucose 6-phosphatase (G6Pase) gene in Chinese patients with type 1a glycogen-storage disease of Taiwan was studied by PCR/RFLP, temporal temperature gradient gel electrophoresis, and direct DNA sequencing methods. In addition to the two most prevalent mutations, 727G --> T (44.4%) and R83H (36.1%), that were detected by RFLP analysis, five other mutations, 341delG, 933insAA, Q104X, I341N, and H119L were identified. The frameshift mutations (341delG and 933insAA) and the nonsense mutation (Q104X) that produce truncated proteins are predicted to be disease-causing. The missense mutation, I341N, occurring in the last transmembrane domain of the ER-bound enzyme, retains a small amount of residual activity of approximately 10%. Except for R83H, the mutations have been described only in Asians. H119L, however, is of particular interest because of the essential role of the catalytic histidine of phosphohydrolase. This amino acid is believed to be involved in the formation of the phosphoryl-enzyme intermediate during catalysis. The patient who was compound heterozygous for 727G --> T and H119L mutations had essentially no G6Pase activity in her liver biopsy. This observation is consistent with the importance of H119L in catalysis.

Base Sequence↗

PubMed2001

A family of depsi-peptide fungal metabolites, as selective and competitive human tachykinin receptor (NK2) antagonists: fermentation, isolation, physico-chemical properties, and biological activity.

Four tachykinin (NK2) receptor inhibitors, SCH 378161 (1), SCH 217048 (2), SCH 378199 (3), and SCH 378167 (4) were isolated from the fermentation broth of a taxonomically unidentified fungus. These compounds were separated from the fermentation broth by ethyl acetate extraction. Purification and separation of the individual compounds were achieved by NK2 assay-guided fractionation using gel filtration, reverse phase chromatography and HPLC. They were identified to be a family of depsipeptides by spectroscopic and degradation studies. Compounds 1 and 3 contain proline and differ as an amide and acid whereas 2 and 4 contain pipecolic acid and differ in being an amide and acid. All of these compounds contain an identical hydroxy acid. They are selective NK2 inhibitors with Ki values ranging from 27-982 nM and demonstrate no activity at 10 microM in the NK1 and NK3 assays. In addition, compounds 1 and 2 inhibited NKA-induced increases in the concentration of intracellular Ca2+, [Ca2+]i, in a CHO cell expressing the human NK2 receptor; this inhibition was competitive in nature with pA2 values of 7.2 and 7.5, respectively. These data demonstrate that these natural products are selective and competitive receptor antagonists of the human NK2 receptor.

Animals↗

PubMed2001

[Rat hearing loss and hearing organs mitochondrial DNA4834 deletions associated with hypercholesteremia].

OBJECTIVE: To determine whether or not the rat hypercholesteremia contributes to hearing organs mtDNA4834 deletion and involves in the development of hearing loss. METHODS: The rat hypercholesteremia model (n = 38) was established by feeding with high cholesterol diet and the control group (n = 22) with common diet for 6 months. The rats were tested for auditory sensitivity using auditory brainstem response (ABR). Twenty-one left cochleae and 27 left cochlear nuclei from experimental group and 10 left cochleae and 13 left cochlear nuclei from control group were harvested. The total DNA of them was extracted. mtDNA was amplified by nest PCR to examine the presence of mtDNA4834 deletion. RESULTS: Our result showed: (1) There is a significant increase in serum cholesterol level and ABR threshold in the experimental group. (2) The mitochondrially-encoded tRNA and ND1 segments were amplified from all samples, as well as mtDNA4834 deletions. (3) The incidence of mtDNA4834 deletions in hearing organs of hypercholesteremia rats was significantly higher than that of the control group (P < 0.05). CONCLUSION: Extended hypercholesteremia can induce hearing loss, and mtDNA4834 deletion in hearing organs may be one of the pathogenic mechanisms.

Animals↗

PubMed2000

Short-range polaron correlations in the ferromagnetic La1-xCaxMnO3

We use neutron scattering to demonstrate the presence of lattice polarons and their short-range correlations for several samples of La1-xCaxMnO3 in the Ca doping range 0.15</=x</=0.3. We establish the doping dependence of the orientation, commensuration, and coherence length of the polaron correlations and show that the populations of correlated and uncorrelated polarons are intimately related to the transport properties of the materials.

Journal Article↗

PubMed2000

Resonance as a measure of pairing correlations in the high-Tc superconductor YBa2Cu3O6.6

One of the most striking properties of the high-transition-temperature (high-Tc) superconductors is that they are all derived from insulating antiferromagnetic parent compounds. The intimate relationship between magnetism and superconductivity in these copper oxide materials has intrigued researchers from the outset, because it does not exist in conventional superconductors. Evidence for this link comes from neutron-scattering experiments that show the unambiguous presence of short-range antiferromagnetic correlations (excitations) in the high-Tc superconductors. Even so, the role of such excitations in the pairing mechanism for superconductivity is still a subject of controversy. For YBa2Cu3O(6+x), where x controls the hole-doping level, the most prominent feature in the magnetic excitation spectrum is a sharp resonance (refs 6-11). Here we show that for underdoped YBa2Cu3O6.6, where x and Tc are below their optimal values, modest magnetic fields suppress the resonance significantly, much more so for fields approximately perpendicular to the CuO2 planes than for parallel fields. Our results indicate that the resonance measures pairing and phase coherence, suggesting that magnetism plays an important role in high-Tc superconductivity. The persistence of a field effect above Tc favours mechanisms in which the superconducting electron pairs are pre-formed in the normal state of underdoped copper oxide superconductors, awaiting transition to the superconducting state.

Journal Article↗

PubMed2000

Commensurate dynamic magnetic correlations in La2Cu0.9Li0.1O4

When sufficient numbers of holes are introduced into the two-dimensional CuO2 square lattice, dynamic magnetic correlations become incommensurate with underlying lattice in all previously investigated La(2-x)A(x)Cu(1-z)B(z)O(4+y) ( A = Sr or Nd, B = Zn) including high T(c) superconductors and insulators, and in bilayered superconducting YBa2Cu3O6.6 and Bi2Sr2CaCu2O8. Magnetic correlations also become incommensurate in structurally related La2NiO4 when doped with Sr or O. We report an exception to this so-far well-established experimental "rule" in La(2)Cu(1-z)Li(z)O4 in which magnetic correlations remain commensurate.

Journal Article↗

PubMed2000

One-dimensional nature of the magnetic fluctuations in YBa2Cu3O6.6

There is increasing evidence that inhomogeneous distributions of charge and spin--so-called 'striped phases'--play an important role in determining the properties of the high-temperature superconductors. For example, recent neutron-scattering measurements on the YBa2Cu3O(7-x) family of materials show both spin and charge fluctuations that are consistent with the striped-phase picture. But the fluctuations associated with a striped phase are expected to be one-dimensional, whereas the magnetic fluctuations observed to date appear to display two-dimensional symmetry. We show here that this apparent two-dimensionality results from measurements on twinned crystals, and that similar measurements on substantially detwinned crystals of YBa2Cu3O6.6 reveal the one-dimensional character of the magnetic fluctuations, thus greatly strengthening the striped-phase interpretation. Moreover, our results also suggest that superconductivity originates in charge stripes that extend along the b crystal axis, where the superfluid density is found to be substantially larger than for the a direction.

Journal Article↗

PubMed2000

Inhibitory interaction of c-Myb and GATA-1 via transcriptional co-activator CBP.

Gene targeting experiments have revealed that transcription factors such as c-Myb and GATA-1 play crucial roles during hematopoietic differentiation. c-Myb is necessary in the immature cells of almost every hematopoietic lineage and GATA-1 is essential for the development of the erythroid lineage. In addition, CREB-binding protein (CBP) acts as a transcriptional adapter for various transcription factors, including c-Myb and GATA-1. In this paper, we show that the transcription factors c-Myb and GATA-1 each inhibit the transcriptional activity of the other and that any possible bipartite complexes c-Myb, GATA-1, and CBP could be formed, but the tripartite complex was hardly formed. The exclusive binding of GATA-1 and c-Myb to CBP is probably the molecular basis for the mutual inhibition of their transcriptional activity. Our data suggest that cross-talk between these three factors might be important for hematopoietic differentiation and that CBP functions as a key molecule during the process.

Animals↗

PubMed2000

[Cochlear hypoxia and mtDNA deletion: possible correlated factors to cause presbycusis].

OBJECTIVE: To find the relationship among the most common mitochondrial DNA (mtDNA) 4,977 bp deletion, aging and deterioration of acoustic organ and determine the pathologic factors causing mtDNA 4,977 bp deletion. METHODS: Sixty-seven temporal bones from a presbycusis group, an age-matched control group and a young control group were evaluated. The nested PCR and tri-nested PCR techniques were used to test the presence of mtDNA 4,977 deletion. Computer imaging processing was used to measure the parameters of blood vessels in the internal acoustic meatus. RESULTS: Temporal bones from patients aged 50 years or over frequently showed mtDNA 4,977 deletions. In presbycusis patients, 17 of 34 ears showed mtDNA 4,977 deletion, whereas only 4 of 19 ears from the age-matched control group showed mtDNA 4,977 deletions. mtDNA 4,977 deletions were often seen in the spiral ganglion and vestibular ganglion neurons. In the presbycusis group, the lumen of the vasa nervosum of the internal auditory meatus showed a more severe reduction in patients with mtDNA 4,977 deletion than in those without deletion. CONCLUSION: There is a strong correlation between presbycusis and mtDNA 4,977 deletion. We hypothesize that cochlear hypoxia may cause mtDNA 4,977 deletions and other mtDNA mutants which in turn may cause a reduction of mitochondrial oxidative phosphorylation and decreased auditory nerve function. The symptoms of neural presbycusis, however, may appear only after mtDNA metabolism decreases below a specific threshold.

Aged↗

PubMed2000

Computer-aided 3-D reconstruction and measurement of the optic canal and intracanalicular structures.

OBJECTIVE: To reconstruct the human optic canal and its inner structures, and to provide detailed knowledge of this region for optic nerve decompression for further understanding on the pathologic mechanisms of indirect optic nerve injury. METHODS: Six optic canals and their inner structures were reconstructed using a computer-aided 3-dimensional reconstruction system. Quantitative measurement of the canal wall thickness, bony canal transverse area, optic nerve transverse area, dural sheath transverse area, subarachnoid space transverse area, and subarachnoid space volume were done by means of the computer morphometric analysis system. The detailed spatial relationship among intracanalicular structures were also carefully identified on the 3-D models. RESULTS: The thinnest portion of the canal was the middle part of the medial wall (0.45 +/- 0.35 mm) and the narrowest space was in the middle part of the optic canal (the transverse area was 18.21 +/- 2.50 mm2). The volume of subarachnoid space which can be considered the compensatory space for distention incurred by the hemorrhage, optic nerve edema, or hematoma was 21.16 +/- 4.31 mm3. At the cranial opening, the middle part and orbital opening, its transverse area was 4.45 +/- 1.12 mm2, 2.68 +/- 1.32 mm2 and 1.23 +/- 0.83 mm2, respectively. CONCLUSIONS: Since the compensatory space was limited, even a tiny amount of blood or swelling of the nerve may cause optic nerve compression. Because the narrowest space was in the middle part of the optic canal and the compensatory space for distention gradually decreases from cranial end to orbital end, the middle part and the anterior part of the optic canal and dural sheath are critical in optic nerve decompression.

Eye↗

PubMed2000

[A comprehensive evaluation on psychological quality among automobile drivers].

OBJECTIVE: To study the comprehensive evaluation on the indexes of psychological quality on automobile drivers. METHODS: A index system, consisted of seven psychological indexes (including relevant physiological indexes), was developed through Delphi method and mathematical statistics. Basic data of the seven psychological and physiological indexes including mean, standard deviation and percentile, were taken from more than 8,000 occupational licensed automobile drivers and more than 6,000 trainees who were randomly sampled from 5 cities across China. The weight coefficients of indexes were determined by analytical hierarchy process (AHP). RESULTS: Comprehensive evaluation equations of the occupational automobile drivers and the trainees were established respectively. The critical values of evaluation were divided into grades by the percentiles of evaluated values. Verified results showed that there was significant difference of the values under evaluation between drivers who had accidents and who did not (t = 14.68, P < 0.01; H = 73.61, P < 0.001). The test of consistence showed that the consistence was quite good (rate of consistence = 92.99%; kappa = 0.85). CONCLUSION: Results showed that the comprehensive equations for evaluation were reasonable and feasible for detecting the potential accident-proneness drivers.

Accident Proneness↗

PubMed1999

The magnetic excitation spectrum and thermodynamics of high-Tc superconductors

Inelastic neutron scattering was used to study the wave vector- and frequency-dependent magnetic fluctuations in single crystals of superconducting YBa2Cu3O6+x. The spectra contain several important features, including a gap in the superconducting state, a pseudogap in the normal state, and the much-discussed resonance peak. The appearance of the pseudogap determined from transport and nuclear resonance coincides with formation of the resonance in the magnetic excitations. The exchange energy associated with the resonance has the temperature and doping dependences as well as the magnitude to describe approximately the electronic specific heat near the superconducting transition temperature (Tc).

Journal Article↗

PubMed1999

Sonic Hedgehog-induced activation of the Gli1 promoter is mediated by GLI3.

Drosophila transcription factor cubitus interruptus (Ci) and its co-activator CRE (cAMP response element)-binding protein (CBP) activate a group of target genes on the anterior-posterior border in response to hedgehog protein (Hh) signaling. In the anterior region, in contrast, the carboxyl-truncated form of Ci generated by protein processing represses Hh expression. In vertebrates, three Ci-related transcription factors (glioblastoma gene products (GLIs) 1, 2, and 3) were identified, but their functional difference in Hh signal transduction is unknown. Here, we report distinct roles for GLI1 and GLI3 in Sonic hedgehog (Shh) signaling. GLI3 containing both repression and activation domains acts both as an activator and a repressor, as does Ci, whereas GLI1 contains only the activation domain. Consistent with this, GLI3, but not GLI1, is processed to generate the repressor form. Transcriptional co-activator CBP binds to GLI3, but not to GLI1. The trans-activating capacity of GLI3 is positively and negatively regulated by Shh and cAMP-dependent protein kinase, respectively, through a specific region of GLI3, which contains the CBP-binding domain and the phosphorylation sites of cAMP-dependent protein kinase. GLI3 directly binds to the Gli1 promoter and induces Gli1 transcription in response to Shh. Thus, GLI3 may act as a mediator of Shh signaling in the activation of the target gene Gli1.

3T3 Cells↗