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Biomedical subjects

N Yang

Publications and source records attributed to N Yang.

At least 55 records · Page 3Linked to original sources
PubMed2000

[3-D motion detection system of human hand].

This paper presents a 3-D motion detection system of human hand, which is based on ordinary video cameras. It includes two pickup cameras, calibration frame and landmark identification system. The DLT algorithm is used to reconstruct the 3-D motion trajectory of human hand. The paper also presents the principle of the system and some detection experiments, and the results showed the good performance of the system. It offers a useful tool for the human hand motion quality analysis and evaluation.

Adult↗
PubMed2000

[Diagnosis and management of gestational trophoblastic tumor with liver metastases].

OBJECTIVE: To evaluate management options and clinical prognosis for women presenting gestational trophoblastic tumor (GTT) with liver metastases. METHODS: We retrospectively analyzed sixteen GTT patients with liver metastases treated in the Peking Union Medical College (PUMC) hospital from 1985 to 1998. All were treated with 5-FU combined chemotherapy or EMA/CO regimen. Eight of them received hepatic artery infusion chemotherapy. Treatment outcome was measured by beta subunit human chorionic gonadotropin assay (beta-hCG) and by imaging studies which included ultrasound and computerized tomography. RESULTS: Of 16 cases, 4 achieved complete remission; biochemical remission was obtained in 2 patients who were alive with residual tumor; 10 patients died of the disease. The overall survival rate was 37.5% (6/16). CONCLUSIONS: The outcome for women presenting with liver metastases from GTT is poor. Early diagnosis and prompt initiation with vigorous multi-agent chemotherapy given through multi-routes are emphasized for improving the treatment outcome.

Adult↗
PubMed1999

The N-terminal LIM domain negatively regulates the kinase activity of LIM-kinase 1.

LIM-kinase 1 (LIMK1, where LIM is an acronym of the three gene products Lin-11, Isl-1 and Mec-3) is a serine/threonine kinase that phosphorylates cofilin and regulates actin cytoskeletal reorganization. LIMK1 contains two LIM domains and a PDZ (an acronym of the three proteins PSD-95, Dlg and ZO-1) domain in the N-terminal half and a kinase domain in the C-terminal half. In this study we examined the role of the extra-catalytic region in the regulation of kinase activity of LIMK1. Limited proteolysis of LIMK1 resulted in the production of the 35-40-kDa kinase core fragments with 3.5-5. 5-fold increased kinase activity. The LIMK1 mutants with deleted LIM domains (DeltaLIM) or conserved cysteines in the two LIM domains replaced with glycines (dmLIMK1) had 3-7-fold higher kinase activities in vitro, compared with the wild-type LIMK1. The C-terminal kinase fragment of LIMK1 bound to the LIM domain but not to the PDZ domain. Furthermore, the LIM fragment dose-dependently inhibited the kinase catalytic activity of the kinase core fragment of LIMK1. Taken together, these results suggest that the N-terminal LIM domain negatively regulates the kinase activity of LIMK1 by direct interaction with the C-terminal kinase domain. In addition, expression of the DeltaLIM mutant in cultured cells induced punctate accumulation of actin filaments, an event distinct from the pattern of actin organization induced by expression of the wild-type LIMK1, suggesting that the LIM domain plays a role in the function of LIMK1 in vivo.

Actins↗
PubMed1999

Nuclear export of LIM-kinase 1, mediated by two leucine-rich nuclear-export signals within the PDZ domain.

LIM-kinase 1 (LIMK1) is a serine/threonine kinase that phosphorylates cofilin and regulates actin-filament dynamics. LIMK1, which contains two LIM domains and a single PDZ domain, localizes predominantly in the cytoplasm, but its mutant, deleted with the PDZ domain, localizes mainly in the nucleus, thereby indicating that the PDZ domain plays a role in the cytoplasmic localization of LIMK1. Here we provide evidence that the PDZ domain of LIMK1 contains two functional leucine-rich nuclear-export signals (NESs). The PDZ domain of LIMK1 fused with glutathione S-transferase (GST-PDZ), when injected into the nucleus, was rapidly excluded from the nucleus, but its mutant with replacements of conserved hydrophobic residues in two putative NESs by alanines remained in the nucleus. The nuclear export of GST-PDZ was sensitive to leptomycin B (LMB), a specific inhibitor of nuclear export mediated by leucine-rich NESs. Malfunctional mutation of two NESs or LMB treatment prevented the nuclear export of full-length LIMK1 and induced its nuclear accumulation. These results suggest that the predominant localization of LIMK1 in the cytoplasm is supported by two NESs within the PDZ domain and that LIMK1 normally shuttles between the cytoplasm and the nucleus. We also provide evidence that a short basic cluster sequence within the protein-kinase domain is involved in the nuclear import of LIMK1.

Amino Acid Sequence↗
PubMed1999

P53 gene mutations in non-Hodgkin's lymphoma.

To understand P53 gene change of non-Hodgkin's lymphoma (NHL) and human malignant lymphoma cell lines, the exons 5-7 of 29 patients with NHL and 9 kinds of human malignant lymphoma cell lines were studied by silver staining PCR-SSCP technique. Three cases of P53 gene point mutation was found in 29 cases of NHL. Mutation developed in exon 5 in 2 cases, and in exon 6 in 1 case. They were all diffuse lymphoma. In mutation cases, B-cell lymphoma accounted for 2 cases and the other one was T-cell lymphoma. There was no P53 gene mutation in low-grade follicular lymphoma. Seven strains out of 9 kinds of lymphoma cell lines had P53 gene point mutation. One strain had the mutation in exon 5; 5 strains in exon 6 and 1 strain in exons 5, 6, 7. There was a high mutation rate in lymphoma cell lines and low mutation rate in NHL patients. P53 gene plays an important role in lymphoma cell line establishment, cell regeneration and disease evolution.

Exons↗
PubMed1999

IL-1 up-regulates osteopontin expression in experimental crescentic glomerulonephritis in the rat.

Osteopontin (OPN) is a macrophage chemotactic and adhesion molecule that acts to promote macrophage infiltration in rat anti-glomerular basement membrane (GBM) glomerulonephritis. The present study investigated the role of interleukin-1 (IL-1) in the up-regulation of renal OPN expression in this disease model. Accelerated anti-GBM glomerulonephritis was induced in groups of six rats. Animals were treated by a constant infusion of the IL-1 receptor antagonist or saline (control) over days -1 to 14 (induction phase) or days 7 to 21 (established disease). In normal rat kidney, OPN was expressed in a few tubules (<5%) and absent from glomeruli. During the development of rat anti-GBM disease (days 7 to 21), there was substantial up-regulation of OPN mRNA and protein expression in glomeruli (>5 cells per glomerular cross-section) and tubular epithelial cells (50-75% OPN-positive). Up-regulation of OPN expression was associated with macrophage accumulation within the kidney, severe proteinuria, loss of renal function, and severe histological damage including glomerular crescentic formation and tubulointerstitial fibrosis. In contrast, IL-1 receptor antagonist treatment of either the induction phase of disease or established disease significantly reduced OPN mRNA and protein expression in glomeruli (/75-85%, P < 0.001) and tubules (/45-60%, P < 0.001). The reduction in OPN expression was associated with significant inhibition of macrophage accumulation and progressive renal injury. In vitro, the addition of IL-1 to the normal rat tubular epithelial cell line NRK52E up-regulated OPN mRNA and protein levels, an effect that was dose-dependent and inhibited by the addition of IL-1 receptor antagonist, thus demonstrating that IL-1 can act directly to up-regulate renal OPN expression. In conclusion, this study provides in vivo and in vitro evidence that IL-1 up-regulates OPN expression in experimental kidney disease and support for the argument that inhibition of OPN expression is one mechanism by which IL-1 receptor antagonist treatment suppresses macrophage-mediated renal injury.

Animals↗
PubMed1999

Kinetics of antibody responses in hens from chicken lines divergently selected for response to sheep red blood cells.

Changes in antibody titers to SRBC were monitored for 180 d after inoculation in hens from two lines divergently selected for 24 generations for high (HAS) or low (LAS) antibody response to SRBC. The HAS hens not only had a higher peak of antibody response (12.9 vs 9.4), but also showed greater persistence in maintaining antibody levels than LAS hens. As a result, HAS hens exhibited higher antibody titers for the 180-d assay period than LAS hens. Antibodies to SRBC were detected in all day-old chicks hatched from HAS eggs collected 10 to 14 d after inoculation as well as 92 to 119 d after inoculation. Only a portion (20 to 75%) of progeny for LAS hens had detectable levels of antibody during the same periods. Among responders, antibody titers were higher for HAS than for LAS progeny. There was a positive correlation among antibody titers taken at different times after the inoculation with SRBC.

Animal Husbandry↗
PubMed1999

Heterosis following long-term bidirectional selection for mating frequency in male Japanese quail.

Reciprocal crosses (sire line shown first and dam line second) among high (H) and low (L) selected lines and the randombred control line (C), which was the base population for the selected lines, were made after 40 generations of bidirectional selection for mating frequency of male Japanese quail. Significant heterosis for the selected trait was found only in crosses between Lines C and L, being 62 and 92% for LC and CL, respectively. Heterosis for percentage of maters was present in all crosses, ranging from 8% for HC and CH to 46% for HL. Three (HC, LH, and CL) of the six crosses had significant heterosis for both 4- and 8-wk BW. Heterosis for 4- and 8-wk BW was also significant for the HL and CH crosses, respectively. For area of the cloacal gland, heterosis was significant in five crosses. Although crosses tended to exhibit higher relative aggressiveness than their respective midparent means, heterosis for this trait was not significant. Reciprocal effects, although not important for most traits, were present for BW in crosses between Lines C and L and Lines H and C. In general, long-term selection for mating frequency of males changed the genetic basis of selected and correlated traits with considerable nonadditive genetic effects observed for most traits in specific crosses.

Animals↗
PubMed1999

Platelet-derived growth factor inhibits alpha1D-adrenergic receptor expression in vascular smooth muscle cells in vitro and ex vivo.

Indirect evidence suggests that stimulation of alpha1-adrenergic receptors (ARs) increases smooth muscle cell (SMC) growth in the growing and adult artery and worsens atherosclerosis and restenosis after balloon injury. In support of a direct adrenergic effect, we have previously shown that alpha1D-AR stimulation induces SMC hypertrophy in cell and vessel organ culture. Because interactions between alpha1-ARs and peptide growth factors may be important in normal and pathological SMC growth, herein we examined regulation of alpha1D-AR expression by growth factors. Platelet-derived growth factor (PDGF)-BB dose- and time-dependently lowered alpha1D mRNA in cultured quiescent SMCs (e.g., 58% inhibition at 20 ng/ml, 24 h, p <.05), whereas other alpha1-AR transcripts were unaffected. This same selective effect was seen in the medial layer of aorta in ex vivo organ culture. However, PDGF-AA, insulin-like growth factor-1, insulin, epidermal growth factor, endothelin, histamine, and serotonin had no effect, whereas thrombin induced a modest (1.8-fold) increase. PDGF-BB inhibition of alpha1D-AR mRNA was accompanied by a 42% reduction in total alpha1-AR density (p <.05) and a functional decrease in norepinephrine-mediated protein synthesis. alpha1D mRNA half-life was not significantly affected by PDGF-BB (3.8 versus 3.2 h). However, transcriptional activity of the alpha1D promoter was inhibited. Reduction in alpha1D-AR mRNA depended partly on new protein synthesis, and was abolished by protein kinase C inhibition, whereas phosphatidylinositol 3 kinase and mitogen-activated protein kinase kinase inhibition had no effect. These data demonstrate that PDGF-beta receptor stimulation (because PDGF-AA had no effect) induces a selective inhibition of alpha1D-AR expression and hence norepinephrine-mediated SMC growth. This down-regulation may lessen additive or synergistic growth effects of catecholamines with other growth factors in vascular hypertrophic diseases.

Adrenergic alpha-Agonists↗
PubMed1999

Platelet-derived growth factor-BB inhibits rat alpha1D-adrenergic receptor gene expression in vascular smooth muscle cells by inducing AP-2-like protein binding to alpha1D proximal promoter region.

We have previously found that, in addition to mediating contraction of vascular smooth muscle, activation of alpha1D-adrenergic receptors (AR) induces smooth muscle cell (SMC) hypertrophy. Despite their importance, little is known about how alpha1D-AR expression is regulated. Recently, we demonstrated that platelet-derived growth factor (PDGF)-beta receptor stimulation, but not various other growth factors, inhibits transcription of alpha1D-, but not alpha1A- or alpha1B-ARs, resulting in reduced norepinephrine-mediated SMC growth. To investigate this inhibitory mechanism, herein we cloned and characterized 1.6 kb of the 5'-flanking region of the rat alpha1D-AR gene. Reporter gene transfection assays in rat aorta and vena cava SMCs showed that this 5'-flanking region, which lacks a TATA-box, possesses strong promoter activity. Two transcription initiation sites and their flanking promotor regions were identified, wherein the proximal promotor mediated PDGF-BB inhibition of transcription. Gel mobility shift assays suggested that Sp1 binds constitutively at two consensus sites within the -399 base pair (bp)/-349-bp region of the proximal promotor. This constitutive binding was unaffected by PDGF-BB. In contrast, a flanking motif (-384 bp/-349 bp), possessing putative Sp1/activator protein-2 (AP-2) overlapping binding sites and located upstream of the proximal transcription initiation site, was required for PDGF-BB inhibition of alpha1D transcription. PDGF-BB increased AP-2 binding to the distal AP-2 site in this region in the context of SMCs. Furthermore, overexpression of AP-2 protein, by transgene transfection, dose-dependently inhibited alpha1D-AR activity driven by this motif. Thus, PDGF-BB may increase AP-2 binding within the proximal promoter to cause down-regulation of alpha1D-AR expression in SMCs when PDGF is elevated, such as in the postnatal growing vascular wall and in vascular hypertrophic diseases.

Animals↗
PubMed1999

[Primary sarcoma of pulmonary artery: a case report].

OBJECTIVE: To call attention to the rare involvement of pulmonary artery by sarcoma. METHODS: To summarize the clinical, radiological and pathologic features of a case of pulmonary artery sarcoma. RESULTS: Pulmonary artery sarcoma has similar clinical manifestations as other pulmonary artery obstructive diseases (including pulmonary thromboembolism). The diagnosis should be considered in the patient with clinical presentations suggested pulmonary embolism. The radiological findings included unilateral hilar enlargement, contiguously soft tissue-filled pulmonary artery and pulmonary nodules and clinically deterioration was found after anticoagulant therapy. CONCLUSION: Pulmonary artery sarcoma is usually misdiagnosed as other pulmonary artery obstructive diseases. More attention should be paid to it.

Adult↗
PubMed1999

[Human motion analysis system based on common video-camera].

A new human motion analysis system based on common video-camera is introduced in this paper. The image processing technique is used to recognize and track anatomic landmarks, which makes data processing more quickly and accurately. The system is cost-effective and can be easily operated because the common video-cameras instead of special instruments are used. Furthermore, the system can also be used for detection and analysis of other low-speed moving objects.

Algorithms↗
PubMed1999

[Fractal dimension analysis of the surface EMG].

Fractal analysis is a new method for biomedical signal processing. Present research on surface EMG and its parameterization method were introduced in this paper. Experiments were performed on three conditions: (1) different muscle contraction degree, (2) different static load, (3) different motion pattern. Problems and prospects in engineering application were also discussed here.

Adult↗
PubMed1998

Macrophage migration inhibitory factor expression in human renal allograft rejection.

BACKGROUND: Macrophage migration inhibitory factor (MIF) plays a pivotal role in immune-mediated diseases. Despite the long-standing association of MIF with the delayed-type hypersensitivity response, the potential role of MIF in allograft rejection is unknown. METHODS: MIF expression was assessed by in situ hybridization and immunohistochemistry staining in 62 biopsies of human renal allograft rejection and in normal human kidney. RESULTS: MIF mRNA and protein is constitutively expressed in normal kidney, being largely restricted to tubular epithelial cells, some glomerular epithelial cells, and vascular smooth muscle cells. In both acute and chronic renal allograft rejection, there was marked up-regulation of MIF mRNA and protein expression by intrinsic kidney cells such as tubular epithelial cells and vascular endothelial and smooth muscle cells. There was also MIF expression by infiltrating macrophages and T cells. Of note, macrophage and T cell infiltrates were largely restricted to areas with marked up-regulation of MIF expression, potentially contributing to the development of severe tubulitis and intimal or transmural arteritis. Quantitative analysis found that increased MIF expression in allograft rejection gave a highly significant correlation with macrophage and T cell accumulation in both the glomerulus and interstitium (P<0.001). In addition, the number of MIF+ tubules and interstitial MIF+ cells correlated significantly with the severity of allograft rejection (P<0.01), and the loss of renal function (P<0.01). In contrast, no up-regulation of renal MIF expression and no leukocyte accumulation was seen in allograft biopsies without evidence of rejection. CONCLUSIONS: This is the first study to demonstrate that local MIF expression is up-regulated during allograft rejection. The association between up-regulation of MIF expression, macrophage and T cell infiltration and the severity of renal allograft rejection suggests that MIF may be an important mediator in the process of allograft rejection.

Acute Disease↗
PubMed1998

Cofilin phosphorylation by LIM-kinase 1 and its role in Rac-mediated actin reorganization.

Rac is a small GTPase of the Rho family that mediates stimulus-induced actin cytoskeletal reorganization to generate lamellipodia. Little is known about the signalling pathways that link Rac activation to changes in actin filament dynamics. Cofilin is known to be a potent regulator of actin filament dynamics, and its ability to bind and depolymerize actin is abolished by phosphorylation of serine residue at 3; however, the kinases responsible for this phosphorylation have not been identified. Here we show that LIM-kinase 1 (LIMK-1), a serine/threonine kinase containing LIM and PDZ domains, phosphorylates cofilin at Ser 3, both in vitro and in vivo. When expressed in cultured cells, LIMK-1 induces actin reorganization and reverses cofilin-induced actin depolymerization. Expression of an inactive form of LIMK-1 suppresses lamellipodium formation induced by Rac or insulin. Furthermore, insulin and an active form of Rac increase the activity of LIMK-1. Taken together, our results indicate that LIMK-1 participates in Rac-mediated actin cytoskeletal reorganization, probably by phosphorylating cofilin.

Actin Depolymerizing Factors↗
PubMed1998

Cytoplasmic localization of LIM-kinase 1 is directed by a short sequence within the PDZ domain.

LIM-containing protein kinase 1 (LIMK1) is a serine/threonine kinase with a structure composed of two LIM domains, a PDZ domain, and a protein kinase domain. We examined the subcellular localization of LIMK1 and its variously deleted mutants in HeLa cells by transfection with these cDNAs. Immunofluorescence analysis revealed that the full-length LIMK1 and its mutants deleted with LIM domain or protein kinase domain preferentially localized in the cytoplasm, while the mutants deleted with the PDZ domain or a 52 amino acid region (B region) within the PDZ domain localized mainly in the nucleus. When the normally nuclear cyclin A was fused with the PDZ domain or the B region of LIMK1, it was localized in the cytoplasm of transfected cells. The corresponding region of the PDZ domain of postsynaptic density protein (PSD)-95 had no such function. Additionally, the PDZ domain of LIMK1 had no potential to bind to the C-terminal S/TXV peptides, to which the PSD-95 PDZ domain can bind. Taken together these results suggest that the PDZ domain, particularly the B region, of LIMK1 has a specific function to localize the protein in the cytoplasm. When glutathione S-transferase (GST) fused with the PDZ domain of LIMK1 (GST-PDZ) or GST-PDZ deleted with the B region (GST-PDZ delta B) was microinjected into the nucleus of COS cells, GST-PDZ was almost completely excluded from the nucleus within 30 min, whereas GST-PDZ delta B remained in the nucleus. These findings suggest that the B region of LIMK1 probably has nuclear export signal activity.

Amino Acid Sequence↗
PubMed1998

Dihydropteridine reductase deficiency: physical structure of the QDPR gene, identification of two new mutations and genotype-phenotype correlations.

Dihydropteridine reductase (DHPR) is an enzyme involved in recycling of tetrahydrobiopterin (BH4), the cofactor of the aromatic amino acid hydroxylases. Its deficiency is characterized by hyperphenylalaninemia due to the secondary defect of phenylalanine hydroxylase and depletion of the neurotransmitters dopamine and serotonin, whose syntheses are controlled by tryptophan and tyrosine hydroxylases. The DHPR cDNA has been cloned and mapped on 4p15.3. In the present study we report the genomic structure of the DHPR gene (QDPR). This gene includes seven exons within a range of 84-564 bp; the corresponding introns are flanked by canonic splice junctions. We also present a panel of PCR primers complementary to intronic sequences that greatly facilitates amplification of the gene and provides a genomic DNA approach for mutation detection. We have used this approach to study six patients with DHPR deficiency. Four known mutations (G23D, H158Y, IVS5G+ 1A, R221X) and two new mutations (Y150C and G218ins9bp) were found. The Y150C mutation was found in compound heterozygosity with G23D, a mutation always associated with a severe phenotype in homozygous patients. This patient has an intermediate phenotype (good response to monotherapy with BH4). The mutant enzyme for Y150C was expressed in an E. coli system. Comparison of its kinetic parameters with those of the G23D mutant enzyme showed that it is not as effective as the wild-type enzyme, but is more active than the G23D mutant. This patient's intermediate phenotype is thus due to the mild DHPR mutation Y150C. Correlations between genotypes and phenotypes were also found for the other mutations.

Alleles↗