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Biomedical subjects

Bin He

Publications and source records attributed to Bin He.

102 records · Page 6Linked to original sources
PubMed2002

Identification of differentially expressed genes in human uterine leiomyomas using differential display.

UNLABELLED: In searching of differentially expressed genes in human uterine leiomyomas, differential display was used with twelve pairs of primers to compare human uterine leiomyomas with matched myometrium. False positives were eliminated by reverse Northern analysis. Positives were confirmed by Northern blot analysis. RESULTS: Four of 69 cDNA fragments (3 up-regulated named L1, L2 and L3 and 1 down-regulated named M1 in leiomyoma) were confirmed by Northern analysis. Sequence comparison and Northern analysis proved that L1 is exactly the human ribosomal protein S19. It was present ubiquitously in 13 tissues tested but in various levels and even in different size. L1 was highly expressed in parotidean cystadenocarcinoma, pancreatic cancer and breast cancer examined. No mutations have been found in human uterine leiomyomas (n=6). CONCLUSIONS: hRPS19 overexpression might be a universal signal in rapid cell growth tissues.

DNA, Complementary↗
PubMed2002

Spatial resolution of body surface potential and Laplacian pace mapping.

The spatial resolution (SR) of the body surface Laplacian map (BSLM) was assessed using a three-dimensional, realistically shaped, heart-torso model. The BSLMs were estimated from the body surface potential maps (BSPMs) generated by pacing different sites of the ventricle of a three-dimensional computer heart model using a novel three-dimensional spline Laplacian algorithm. Pacing was performed at a total of 88 myocardial units in five regions of the AV ring (anterior, left wall, posterior, right wall, and septum) and three regions adjacent to the AV ring in the middle anterior and posterior of the ventricles. The SR of the BSPMs and BSLMs were investigated by means of the correlation coefficient (CC) of maps. When 5 microV and 10 microV Gaussian white noises were added into the simulated BSPMs, the SR, at 36 ms after the onset of pacing, was about 5.0 +/- 1.2 mm and 5.4 +/- 1.3 mm for the BSPMs, and 3.3 +/- 0.8 mm and 4.0 +/- 0.9 mm for the BSLMs, respectively. The results of the present simulation study suggest that the BSLM has higher SR and may provide a more accurate means than the BSPMs for differentiating between the accessory pathways or the sites of other ectopic cardiac beats along the AV ring and in its neighboring regions.

Atrial Premature Complexes↗
PubMed2002

Estimation of noise level and signal to noise ratio of laplacian electrocardiogram during ventricular depolarization and repolarization.

Body surface Laplacian ECG (LECG) has demonstrated its enhanced capability to localize cardiac electrical sources closest to the recording site. The aim of the present study was to evaluate the noise level and signal to noise ratio (SNR) in the LECG as compared to the potential ECG (PECG). Such evaluation is important to determine the applicability of the LECG to localizing and imaging of cardiac electrical activity in an experimental setting. Experimental studies were conducted in six healthy men. A 150-channel PECG was recorded from the anterolateral chest and the LECG was estimated using the finite difference algorithm. The noise level in the PECG and LECG was evaluated using multiple estimation protocols. The signal level during ventricular depolarization and repolarization was also estimated, and the corresponding SNR was calculated. Different filtering techniques were examined to evaluate their effects on the noise level and SNR of the LECG and PECG. The experimental results indicate that with basic signal processing techniques (baseline adjustment, three-point moving average filter, and Wiener spatial filter), the SNR of the LECG is about 30-40% of that of the PECG. Furthermore, the SNR estimated during ventricular depolarization is about three times that obtained during ventricular repolarization for the PECG and LECG. The present study indicates that the LECG derived from the PECG using a local finite difference estimation procedure has satisfactory SNR during the periods of ventricular depolarization and repolarization, and suggests the feasibility of estimating the LECG from the recorded PECG in human subjects in an experimental setting.

Body Surface Potential Mapping↗
PubMed2002

A spline Laplacian ECG estimator in a realistic geometry volume conductor.

We have developed a spline-based Laplacian estimator over an arbitrarily shaped surface of a volume conductor and tested its applicability to Laplacian electrocardiogram (ECG) mapping. In the newly developed algorithm, estimation of the parameters associated with the spline Laplacian is formulated by seeking the general inverse of a transfer matrix. Only one spline-parameter needs to be determined through regularization in order to estimate the realistic geometry surface Laplacian from the body surface potentials. It has been demonstrated that the rich knowledge on regularization in the inverse problems can be directly applied to estimate the spline Laplacian ECG (LECG), such as the discrepancy principle. Computer simulations have been conducted to validate the new approach in a spherical volume conductor and test the feasibility of mapping cardiac electrical sources in a realistic geometry heart-torso model. The present results demonstrate that the realistic geometry spline LECG can be estimated conveniently from the body surface potentials, is more robust against measurement noise and has better performance than the conventional five-point local Laplacian estimator.

Algorithms↗
PubMed2002

An equivalent current source model and laplacian weighted minimum norm current estimates of brain electrical activity.

We have developed a method for estimating the three-dimensional distribution of equivalent current sources inside the brain from scalp potentials. Laplacian weighted minimum norm algorithm has been used in the present study to estimate the inverse solutions. A three-concentric-sphere inhomogeneous head model was used to represent the head volume conductor. A closed-form solution of the electrical potential over the scalp and inside the brain due to a point current source was developed for the three-concentric-sphere inhomogeneous head model. Computer simulation studies were conducted to validate the proposed equivalent current source imaging. Assuming source configurations as either multiple dipoles or point current sources/sinks, in computer simulations we used our method to reconstruct these sources, and compared with the equivalent dipole source imaging. Human experimental studies were also conducted and the equivalent current source imaging was performed on the visual evoked potential data. These results highlight the advantages of the equivalent current source imaging and suggest that it may become an alternative approach to imaging spatially distributed current sources-sinks in the brain and other organ systems.

Algorithms↗
PubMed2002

Signals that dictate nuclear, nucleolar, and cytoplasmic shuttling of the gamma(1)34.5 protein of herpes simplex virus type 1.

The gamma(1)34.5 protein of herpes simplex virus type 1 (HSV-1) is required for viral neurovirulence in vivo. In infected cells, this viral protein prevents the shutoff of protein synthesis mediated by double-stranded-RNA-dependent protein kinase PKR. This is accomplished by recruiting protein phosphatase 1 to dephosphorylate the alpha subunit of translation initiation factor eIF-2 (eIF-2 alpha). Moreover, the gamma(1)34.5 protein is implicated in viral egress and interacts with proliferating cell nuclear antigen. In this report, we show that the gamma(1)34.5 protein encoded by HSV-1(F) is distributed in the nucleus, nucleolus, and cytoplasm in transfected or superinfected cells. Deletion analysis revealed that the Arg-rich cluster from amino acids 1 to 16 in the gamma(1)34.5 protein functions as a nucleolar localization signal. The region from amino acids 208 to 236, containing a bipartite basic amino acid cluster, is able to mediate nuclear localization. R(215)A and R(216)A substitutions in the bipartite motif disrupt this activity. Intriguingly, leptomycin B, an inhibitor of nuclear export, blocks the cytoplasmic accumulation of the gamma(1)34.5 protein. L(134)A and L(136)A substitutions in the leucine-rich motif completely excluded the gamma(1)34.5 protein from the cytoplasm. These results suggest that the gamma(1)34.5 protein continuously shuttles between the nucleus, nucleolus, and cytoplasm, which may be a requirement for the different activities of the gamma(1)34.5 protein in virus-infected cells.

Amino Acid Sequence↗
PubMed2002

Parathyroid hormone is essential for normal fetal bone formation.

Parathyroid hormone (PTH) is a potent pharmacologic inducer of new bone formation, but no physiologic anabolic effect of PTH on adult bone has been described. We investigated the role of PTH in fetal skeletal development by comparing newborn mice lacking either PTH, PTH-related peptide (PTHrP), or both peptides. PTH-deficient mice were dysmorphic but viable, whereas mice lacking PTHrP died at birth with dyschondroplasia. PTH-deficient mice uniquely demonstrated diminished cartilage matrix mineralization, decreased neovascularization with reduced expression of angiopoietin-1, and reduced metaphyseal osteoblasts and trabecular bone. Compound mutants displayed the combined cartilaginous and osseous defects of both single mutants. These results indicate that coordinated action of both PTH and PTHrP are required to achieve normal fetal skeletal morphogenesis, and they demonstrate an essential function for PTH at the cartilage-bone interface. The effect of PTH on fetal osteoblasts may be relevant to its postnatal anabolic effects on trabecular bone.

Animals↗
PubMed2002

Domain interactions between coregulator ARA(70) and the androgen receptor (AR).

The coregulator function of AR-associated protein 70 (ARA(70)) was investigated to further characterize its interaction with the AR. Using a yeast two-hybrid assay, androgen-dependent binding of ARA(70) deletion mutants to the AR ligand-binding domain (LBD) was strongest with ARA(70) amino acids 321-441 of the 614 amino acid ARA(70) protein. Mutations adjacent to or within an FxxLF motif in this 120-amino acid region abolished androgen-dependent binding to the AR-LBD both in yeast and in glutathione-S-transferase affinity matrix assays. Yeast one-hybrid assays revealed an intrinsic ARA(70) transcriptional activation domain within amino acids 296-441. In yeast assays the ARA(70) domains for transcriptional activation and for binding to the AR-LBD were inhibited by the C-terminal region of ARA(70). Full-length ARA(70) increased androgen-dependent AR transactivation in transient cotransfection assays using a mouse mammary tumor virus-luciferase reporter in CV1 cells. ARA(70) also increased constitutive transcriptional activity of an AR NH(2)-terminal-DNA binding domain fragment and bound this region in glutathione-S-transferase affinity matrix assays. Binding was independent of the ARA(70) FxxLF motif. The results identify an ARA(70) motif required for androgen-dependent interaction with the AR-LBD and demonstrate that ARA(70) can interact with the NH(2)-terminal and carboxyl-terminal regions of AR.

Amino Acid Motifs↗
PubMed1998

Identification of the Subunits of C3P4 and Estimation of Their Molecular Weights by UV Cross-linking Assay.

The subunits and their molecular weights of an unknown DNA-binding protein C3P4 induced by androgen were studied by UV cross-linking assay. The results indicate that there are two subunits with molecular weights of about 110 kD and 27 kD in the C3P4 complex. Ferguson plot further shows the molecular weight of native C3P4 to be about 127 kD. It suggests that C3P4 very likely exists as heterodimer composed of one 110 kD subunit and one 27 kD subunit. The 110 kD subunit may play an important role in DNA-binding.

Journal Article↗
PubMedDate not supplied

Partial androgen insensitivity with phenotypic variation caused by androgen receptor mutations that disrupt activation function 2 and the NH(2)- and carboxyl-terminal interaction.

Partial androgen insensitivity with sex phenotype variation in two unrelated families was associated with missense mutations in the androgen receptor (AR) gene that disrupted the AR NH(2)-terminal/carboxy terminal interaction. Each mutation caused a single amino acid change within the region of the ligand-binding domain that forms activation function 2 (AF2). In one family, the mutation I737T was in alpha helix 4 and in the other F725L was between helices 3 and 4. Neither mutation altered androgen binding as determined by assays of mutant AR in the patient's cultured genital skin fibroblasts or of recombinant mutant receptors transfected into COS cells. In transient cotransfection assays in CV1 cells, transactivation with the AR mutants at low concentrations of DHT was reduced several fold compared with wild-type AR but increased at higher concentrations. Defects in NH(2)-terminal/carboxy terminal interactions were identified in mammalian two hybrid assays. In similar assays, there was reduced binding of the p160 coactivators TIF2/SRC2 and SRC1 to the mutant AR ligand binding domains (LBD). In the family with AR I737T, sex phenotype varied from severely defective masculinization in the proband to a maternal great uncle whose only manifestation of AIS was severe gynecomastia. He was fertile and passed the mutation to two daughters. The proband of the F725L family was also incompletely masculinized but was raised as a male while his half-sibling by a different father was affected more severely and reared as a female. These studies indicate that the function of an AR AF2 mutant in male development can vary greatly depending on the genetic background.

Amino Acid Substitution↗