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Biomedical subjects

L Liao

Publications and source records attributed to L Liao.

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

[Determination and significance of nitric oxide and tumor necrosis factor-alpha induced by peripheral blood monocyte in vitro in patients with malignant bone tumors].

Peripheral blood monocytes from 15 cases of malignant bone tumors and 12 cases of health volunteers were seperated and induced by lipopolysaccharide(LPS) for 48-hour culture. The supernatant was collected for determining the content of nitrite and tumor necrosis factor-alpha(TNF-alpha) (by Griess and ELISA methods, respectively). The results were as follows: The content of nitrite and TNF-alpha in patients with malignant bone tumors was significantly higher than that in normal control; the content of nitrite and TNF-alpha in the malignant bone tumor group presented the positive correlation (r = 0.8909, P < 0.01). The results suggest that NO and TNF-alpha produced by activated macrophages may be related to the pathogenesis of malignant bone tumors.

Adolescent↗
PubMed1998

[Application of stress urethral pressure profile for diagnosis and treatment of stress incontinence].

OBJECTIVE: To apply the stress urethral pressure profile (SUPP) to diagnose the genuine stress incontinence (GSI) and to evaluate the results of treatment. METHOD: 22 patients with GSI underwent SUPP and rest urethral pressure profile (RUPP) using Dantec Menuet. RESULT: The results showed that the pressure transmission ratio (PTR) was 0.68 +/- 0.06, and urethral close pressure (UCP) was -0.62 +/- 0.22 kPa in 22 patients. PTR and UCP raised significantly after operation in 5 patients, P < 0.01. The results of SUPP were compared with those RUPP. CONCLUSION: SUPP is important in both diagnosis and evaluation of GSI, although some limitation exists. To improve the level of diagnosis, it should be combined with other method in clinical use.

Adult↗
PubMed1998

[Comparative observation on experimental infection with Echinococcus multilocularis in Cricetulus Migratorius and Meriones meridianus].

AIM: To search for an animal model with higher susceptibility to Echinococcus multilocularis and shorter experimental period. METHODS: Cricetulus migratorius, Meriones meridianus and NIH mice were experimentally infected with protoscolices of E. multilocularis and were autopsed at different times after their infection. The development of E. multilocularis in these three species of rodents was observed and compared. RESULTS: The average wet cyst weight and the ratio of cyst weight to body weight on the 91st day after infection were 15.0 +/- 2.1 g and 32.3% for C. migratorius, 3.3 +/- 1.1 g and 6.9% for M. meridianus, 0.6 +/- 0.6 g and 2.4% for NIH mice; and the corresponding figures on the 188th day after infection were 11.8 +/- 2.7 g and 21.7% for C. migratorius, 8.1 +/- 5.1 g and 15.4% for M. meridianus and 8.4 +/- 8.3 g and 26.7% for NIH mice, respectively. On the 91st day, matured protoscolices were found in C. migratorius and M. meridianus, whereas NIH mice had matured protoscolices on the 188th day after infection. CONCLUSION: C. migratorius has higher sensitivity to E. multilocularis infection than the other two species of animals as manifested by high infection rate, well-developed vesicles and rapid growth speed. C. migratorius proved to be an ideal experimental animal for E. multilocularis.

Animals↗
PubMed1997

Lysophosphatidylcholine regulates cationic amino acid transport and metabolism in vascular smooth muscle cells. Role in polyamine biosynthesis.

Lysophosphatidylcholine (lyso-PC) is a major component of atherogenic lipids that stimulate vascular smooth muscle cell (SMC) proliferation. Because cationic amino acids are metabolized to growth-stimulatory polyamines, we examined whether lyso-PC regulates the transcellular transport and metabolism of cationic amino acids by vascular SMC. Treatment of SMC with lyso-PC initially (0-2 h) decreased cationic amino acid uptake, whereas longer exposures (6-24 h) progressively increased transport. Kinetic studies indicated that lyso-PC-induced inhibition was associated with a decrease in affinity for cationic amino acids, but the stimulation was mediated by an increase in transport capacity. Lyso-PC strongly induced the expression of cationic amino acid transporter-2 mRNA while modestly elevating the level of cationic amino acid transporter-1 mRNA. In addition, lyso-PC stimulated intracellular cationic amino acid metabolism by inducing ornithine decarboxylase activity and mRNA expression and also by inducing arginase activity in vascular SMC. In contrast, lyso-PC inhibited the catabolism of L-arginine to nitric oxide by blocking inducible nitric oxide synthase expression. Lyso-PC increased markedly the capacity of SMC to generate putrescine, a polyamine, from extracellular L-ornithine and L-arginine. The lyso-PC-mediated increase in the production of putrescine was reversed by NG-methyl-L-arginine, a competitive inhibitor of cationic amino acid transport, or by alpha-difluoromethylornithine, an ornithine decarboxylase inhibitor. The formation of putrescine from L-arginine was also prevented by arginase inhibitor NG-hydroxy-L-arginine. These results demonstrate that lyso-PC stimulates polyamine synthesis in vascular SMC by inducing the expression of the genes that regulate both the transport and metabolism of cationic amino acids. The actions of lyso-PC in stimulating cationic amino acid uptake and directing their metabolism to growth-stimulatory polyamines while simultaneously inhibiting the synthesis of antiproliferative NO, may contribute to lyso-PC-induced SMC proliferation and atherosclerotic lesion formation.

Amino Acid Transport Systems, Basic↗
PubMed1997

Use of an alternate splice donor site in the human GAP gene is responsible for synthesis of the p100 isoform.

GAP (GTPase-activating protein), a negative regulator of the receptor tyrosine kinase signal transduction pathway, exists as two isoforms: a ubiquitous, p120 form and a primate placenta-specific p100 form lacking the N-terminal hydrophobic domain. The cDNA species encoding p120 and p100 GAP are identical except that p100 GAP cDNA contains a 65-bp insert not present in p120 cDNA. The purpose of this study was to locate the 65-bp insert in the genomic GAP sequence, thereby determining the mechanism by which alternate splicing produces the two mRNA species. It was found that the 65-bp insert is located just 3' to the sequence encoding the hydrophobic domain, indicating that the p100 form of GAP results from utilization of an alternate splice donor site. In addition, the sequence encoding the hydrophobic domain was found to be contained within a single large exon. The intron separating this exon from the exon encoding the 5'-portion of the SH2-N domain was determined to be at least 40 kb in length. Finally, it was found that the sequence encoding the SH2-N domain contains an intron 1006 bp long, and the sequence of this intron has been deduced. It is anticipated that the data presented in this paper will provide the basis for elucidating RNA processing mechanisms responsible for preferential expression of p100 GAP in the human placenta.

Alternative Splicing↗
PubMed1997

Molecular determinants of oxidized low-density lipoprotein-induced leukocyte adhesion and microvascular dysfunction.

Oxidized low-density lipoproteins (oxLDL) have been implicated in the leukocyte recruitment and microvascular dysfunction associated with atherosclerosis. The objectives of this study were to define the adhesion molecules that mediate oxLDL-induced leukocyte-endothelial cell adhesion and to determine whether leukocyte-endothelial cell adhesion contributes to the endothelial barrier dysfunction elicited by oxLDL. Leukocyte-endothelial cell adhesion and emigration, albumin extravasation, and mast cell degranulation were monitored in rat mesentery in response to native LDL (nLDL) or copper-oxidized LDL (oxLDL). Intra-arterial infusion of oxLDL but not nLDL elicited increases in leukocyte adherence and emigration, mast cell degranulation, and albumin leakage. The oxLDL-induced leukocyte adherence/emigration was attenuated by pretreatment with monoclonal antibodies directed against CD11/CD18, intercellular adhesion molecule-1, P-selectin, and L-selectin but not by pretreatment with a nonbinding monoclonal antibody. The albumin leakage and mast cell degranulation responses were attenuated by all of the same monoclonal antibodies except L-selectin. In addition, a peptide previously shown to inhibit leukocyte-endothelial cell adhesion in vitro also attenuated leukocyte adherence and mast cell degranulation in this model. These findings implicate CD11/ CD18, L-selectin, intercellular adhesion molecule-1, and P-selectin in the leukocyte recruitment elicited by oxLDL and invoke a role for adherent leukocytes in the accompanying increase in mast cell degranulation and albumin leakage.

Animals↗
PubMed1997

[Conventional and ambulatory urodynamic study on patients with chronic prostatitis syndrome].

To study the urodynamic findings of chronic prostatitis syndrome (CPS), 58 patients with chronic prostatitis and prostatodynia were subjected to the urodynamic investigation that included conventional medium filling urodynamic (CMG) tests (urethral pressure profile, filling cystometry, voiding pressure-flow study) and ambulatory urodynamic monitoring (AM) by using Dantec Menuet and Urodec 500 AM system. 55 BPH patients and 20 normal men were taken as control groups. CPS patients had function bladder outflow obstruction (FBOO). FBOO resulted in the detrusor instable (DIS, 12.1%), detrusor-sphincter dysnergia (DSD, 100%) and detrusor dysconstractility (DDC, 6.9%), and resulted in clinical symptoms. FBOO resulted from the urethal sphincter spasm and DSD.

Adolescent↗
PubMed1997

[Qualitative grading of detrusor contractility in benign prostatic hyperplasia patients].

To grade qualitatively detrusor contractility in benign prostatic hyperplasia (BPH), we studied 120 BPH patients aged from 58 to 89 years. The pressure-flow studies were performed. The passive urethral resistance relation (PURR) and Schäfer diagram were used to analyse the results. The detrusor contractility was divided into 4 classes: very weak (VW), weak (W), normal (N), and strong (ST). The types of pressure-flow were high pressure--low flow (HP-LF), high pressure--high flow (HP-HF), low pressure--low flow (LP-LF) and low pressure--high flow (LP-HF) type. The results showed that the incidence of VW, W, N and ST class was 12.5%, 26.7%, 47.5% and 13.3% respectively; the incidence of HP-LF, HP-HF and LP-LF type was 55%, 1.7% and 43.3% respectively. The weak detrusor strength could become powerful by the surgery treatment of bladder outflow obstruction (BOO) and the function training of detrusor. The detrusor strength class of a BPH patient was improved from W before surgery to N after surgery in our studies. The principles of the fluid dynamics and urodynamic and the clinical application of the qualitative grading of detrusor contractility were discussed.

Aged↗
PubMed1996

Compensatory modulation of GAP activity in response to oncogenic stimulation.

GAP is a key negative regulator of the receptor tyrosine kinase (RTK) signal transduction pathway. The purpose of this study was to determine if expression or activity of GAP is modulated by hyperstimulation of the RTK pathway. It was found that cells forced to express wild-type Ha-ras, viral Ha-ras, or v-src exhibit increased GAP activity as compared to control cells. In addition, a novel GAP isoform appears in all ras-expressing NIH3T3 cell clones. These data indicate that there is compensatory regulation of GAP in response to an increase in RTK pathway activity.

3T3 Cells↗
PubMed1996

TCR binding differs for a bacterial superantigen (SEE) and a viral superantigen (Mtv-9).

Both superantigens (SAG) and many anti-TCR monoclonal antibodies (mAb) have specificity for the V beta region of the TCR encoded by TCRBV genes. For instance the bacterial SAG staphylococcal enterotoxin E (SEE), the retroviral SAG MTV-9 and the mAb OT145 each react with human T cells expressing BV6S7. This BV gene encodes two common alleles. We found that SEE and the mAb preferentially activate T cells expressing BV6S7*1 as opposed to BV6S7*2, but Mtv-9 activates T cells expressing either allele. Thus binding to the TCR differs between the two SAGs. A mutation in the TCR HVR-4 region of BV6S7*1 (G72E), where the two BV6S7 alleles differ, indicated that HVR-4 is a component of the binding site for SEE and for the mAb OT145. BV6S7*2 has a charged E72 which may result in electrostatic repulsion of SEE, as SEE contains a similarly acidic aspartic acid residue at a TCR interaction site (204D).

Alleles↗
PubMed1996

Platelet-derived growth factor regulates vascular smooth muscle cell proliferation by inducing cationic amino acid transporter gene expression.

Since recent studies demonstrated that platelet-derived growth factor (PDGF) induces vascular smooth muscle cell (SMC) proliferation by stimulating polyamine synthesis, we examined whether the transcellular transport of L-ornithine, the cationic amino acid precursor of polyamines, could regulate the mitogenic response of PDGF. Treatment of SMC with PDGF stimulated DNA and putrescine synthesis, and this was enhanced further by increasing the extracellular concentration of L-ornithine. The potentiating effect of L-ornithine was reversed by the competitive inhibitor of cationic amino acid transport, methyl-L-arginine, or by preventing putrescine formation with alpha-difluoromethylornithine. Cationic amino acid uptake by SMC was Na+-independent and was mediated by both a high and low affinity carrier system. Treatment of SMC with PDGF initially (0-2 h) decreased basic amino acid transport, while longer exposures (6-24 h) progressively increased uptake. Kinetic studies indicated that PDGF-induced inhibition was associated with a decrease in affinity for cationic amino acids, while the stimulation was mediated by an increase in transport capacity. Endogenous PDGF released by collagen-activated platelets likewise up-regulated cationic amino acid transport in SMC. Reverse transcriptase-polymerase chain reaction detected the presence of mRNA encoding two distinct cationic amino acid transporter (CAT) proteins, CAT-1 and CAT-2B. Treatment of SMC with PDGF strongly induced the expression CAT-2B mRNA and modestly elevated the level of CAT-1 mRNA. These results demonstrate that PDGF-induced polyamine synthesis and SMC mitogenesis are dependent on the transcellular transport of L-ornithine. The capacity of PDGF to up-regulate the transport of L-ornithine by inducing the expression of the genes for CAT-1 and CAT-2B may modulate its mitogenic effect by providing SMC with the necessary intracellular precursor for polyamine biosynthesis.

Amino Acid Sequence↗
PubMed1996

Impact of an interactive video on decision making of patients with ischemic heart disease.

An experimental pilot study using repeated measures to examine the impact of an interactive video program on the decision making of patients with ischemic heart disease was carried on at a tertiary care center and a Veterans Affairs hospital. The patients (n = 80, mean age 61.1 years, 77% male, 75% white, 26.7% with acute myocardial infarction), who had undergone diagnostic cardiac catheterization and were found to have significant coronary artery disease (> or = 75% stenosis in at least one vessel), watched the Shared Decision-Making Program (SDP) for Ischemic Heart Disease (IHD), a novel interactive video system designed to provide information necessary for patients to participate actively in decision making. This program compares medical therapy, angioplasty, and bypass surgery through a physician narrator, patient testimonials, and empirically-based, patient-specific outcome estimates of short-time complications and long-term survival. Before and after viewing the SDP, patients completed surveys containing multiple choice questions and Likert scales. They rated the program as more helpful than all other decision aids except the physician, and after viewing the SDP they expressed increased confidence in their treatment choice and decreased confidence in alternative options (p = .0001). The greatest effects appeared to be concentrated in those patients with less education (p = .04), and the program appeared to increase anxiety in nonwhite patients compared with white patients (p = 0.07).

Decision Making↗
PubMed1996

Isolation and characterization of a gene encoding a chymotrypsin-like serine protease from Streptomyces lividans 66.

A gene encoding a Streptomyces lividans homologue of the chymotrypsin-like serine protease (SAM-P20) of Streptomyces albogriseolus was isolated using the Streptomyces griseus prtB gene as a hybridization probe. Nucleotide sequence analysis of a representative clone uncovered the possible presence of a sequence of 900 nucleotides encoding 300 amino acids, including a putative "prepro" region of 115 amino acids. Alignment of the predicted amino acid sequence of this putative gene with other members of the family of Streptomyces extracellular chymotrypsin-like proteases indicated a high degree of homology in all cases, especially with the SAM-P20 protease. This gene product has been identified as the second member of a potentially larger family of SAL (SAM-P20-like) proteases in S. lividans 66.

Amino Acid Sequence↗
PubMed1996

Role of mast cells in oxidized low-density lipoprotein-induced microvascular dysfunction.

Previous studies demonstrated that human low-density lipoprotein (LDL) oxidized with Cu2+ promotes leukocyte-endothelial cell adhesion, mast cell degranulation, and albumin extravasation in rat mesentery. The objective of this study was to determine whether the mast cell degranulation elicited by oxidized LDL accounts for the accompanying microvascular responses. Leukocyte rolling, adherence, and emigration, fluorescein isothiocyanate-albumin leakage, and mast cell degranulation were monitored in rat mesentery before and during local intra-arterial infusion of either normal LDL (nLDL) or copper-oxidized LDL (CuLDL). Infusion of CuLDL, but not nLDL, elicited significant increases in leukocyte rolling, adherence and emigration, albumin leakage, and mast cell degranulation. Pretreatment with the mast cell-stabilizing agent ketotifen or superfusion of the mesenteric microcirculation with iodoxamide significantly reduced CuLDL-induced mast cell degranulation. The mast cell stabilization was accompanied by attenuated leukocyte-endothelial cell adhesion and albumin leakage responses to CuLDL. The results of this study indicate that 1) CuLDL-induced microvascular dysfunction (albumin leakage) involves the activation of mast cells, and 2) the protective action of mast cell stabilizers may be related to their ability to blunt CuLDL-induced leukocyte-endothelial cell interactions in postcapillary venules.

Animals↗
PubMed1996

Oxidized low-density lipoproteins and microvascular responses to ischemia-reperfusion.

The objective of this study was to determine whether ischemia and reperfusion (I/R) and/or chronic arterial hypertension potentiates the leukocyte-endothelial cell adhesion (LECA) and microvascular dysfunction elicited by oxidized low-density lipoproteins (ox-LDL). Mast cell degranulation, leukocyte adherence and emigration, and albumin leakage were monitored in postcapillary venules of rat mesentery. Intra-arterial infusion of copper-oxidized LDL (Cu-LDL), at a concentration that does not directly affect the microvasculature, significantly enhanced the I/R-induced recruitment of adherent and emigrated leukocytes but does not affect the increased albumin leakage and mast cell degranulation responses normally observed after I/R. Infusion of a higher concentration of Cu-LDL in nonischemic mesentery of either normotensive Wistar-Kyoto or spontaneously hypertensive rats elicited significant yet similar increases in LECA, mast cell degranulation, and albumin leakage. These findings indicate that 1) ox-LDL act synergistically with I/R to promote leukocyte recruitment in postcapillary venules but without an accompanying exacerbation of albumin leakage, and 2) ox-LDL do not elicit a more intense inflammatory response in the microvasculature of hypertensive versus normotensive animals.

Animals↗
PubMed1996

Differential regulation of L-arginine transport and nitric oxide production by vascular smooth muscle and endothelium.

Since NO production is dependent on the availability of L-arginie, we examined whether L-arginine transport and NO synthesis are coregulated by vascular smooth muscle cells and endothelial cells cultured from the same vessel wall source. L-Arginine transport by both bovine aortic smooth muscle cells (BASMCs) and endothelial cells (BAECs) was primarily Na+ independent (approximately 70%) and was mediated by both a high- and low-affinity transport system. Treatment of BASMCs with tumor necrosis factor-alpha (TNF-alpha) or interleukin-1 beta (IL-1 beta) resulted in a significant increase in L-arginine transport (approximately 20%) and in the induction of NO release. Exposure of BASMCs to interferon gamma (IFN-gamma) or lipopolysaccharide (LPS) also stimulated NO release but did not affect L-arginine transport. In contrast, incubation of BAECs with TNF-alpha or LPS strikingly enhanced L-arginine uptake (2.5-fold), whereas IL-1 beta and IFN-gamma had no effect. Treatment of BAECs with any of the inflammatory mediators did not stimulate NO production. These results demonstrate that L-arginine uptake and NO synthesis by these cells are differentially regulated. In BASMCs, the coinduction of L-arginine transport and NO formation may function to provide increased levels of substrate to the cell during activation of the NO synthase enzyme. In contrast, the selective stimulation of L-arginine uptake in BAECs indicates that L-arginine transport is dissociated from NO generation in these cells.

Animals↗