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Biomedical subjects

W Liu

Publications and source records attributed to W Liu.

At least 325 records · Page 18Linked to original sources
PubMed2000

Pacing-induced heart failure causes a reduction of delayed rectifier potassium currents along with decreases in calcium and transient outward currents in rabbit ventricle.

OBJECTIVE: Heart failure in patients and in animal models is associated with action potential prolongation of the ventricular myocytes. Changes in several membrane currents have been already demonstrated to underlie this prolongation. However, information on the two components (I(Kr) and I(Ks)) of the delayed rectifier potassium current (I(K)) in rapid pacing induced heart failure is lacking. METHODS AND RESULTS: Action potentials and whole-cell currents, I(K), I(to1), I(K1), and I(Ca-L) were recorded in apical myocytes of left ventricle from 10 rabbits subjected to left ventricular pacing at 350-380 beats/min for 3-4 weeks and 10 controls with sham operation. Action potential duration at 90% repolarization (APD(90)) was prolonged in myocytes from failing hearts compared to controls at both cycle lengths of 333 and 1000 ms. Both E-4031-sensitive and -resistant components of I(K) (I(Kr), I(Ks)) in myocytes from failing hearts were significantly less than those of control hearts; tail current densities of I(Kr) and I(Ks) following depolarization to +50 mV were 0.62+/-0.05 vs. 0.96+/-0.12 pA/pF (P<0.05), and 0.27+/-0.08 vs. 0.52+/-0.08 pA/pF (P<0.05), respectively. There was no significant difference between control and failing myocytes in the voltage- and time-dependence of activation of total I(K), I(Kr) and I(Ks). The peak of L-type Ca(2+) current (I(Ca-L)) was significantly reduced in myocytes from failing hearts (at +10 mV, -9.29+/-0.52 vs. -12.28+/-1.63 pA/pF, P<0.05), as was the Ca(2+)-independent transient outward current (I(to1); at +40 mV, 4.8+/-0.9 vs. 9.6+/-1.3 pA/pF, P<0.05). Steady state I-V curve for I(K1) was similar in myocytes from failing and control hearts. CONCLUSIONS: Decrease of I(K) (both I(Kr) and I(Ks)) in addition to reduced I(to1), may underly action potential prolongation at physiological cycle length and thereby contribute to arrhythmogenesis in heart failure.

Action Potentials↗
PubMed2000

The effect of hamstring muscle compensation for anterior laxity in the ACL-deficient knee during gait.

The hamstring muscles have been recognized as an important element in compensating for the loss of stability in the ACL-deficient knee, but it is still not clear whether the hamstring muscle force can completely compensate for the loss of ACL, and the consequences of increased hamstring muscle force. A two-dimensional anatomical knee model in the sagittal plane was developed to examine the effect of various levels of hamstring muscle activation on restraining anterior tibial translation in the ACL-deficient knee during level walking. The model included the tibiofemoral and patellofemoral joints, four major ligaments, the medial capsule, and five muscle units surrounding the knee. Simulations were conducted to determine anterior tibial translation and internal joint loading at a single selected position when the knee was under a peak external flexion moment during early stance phase of gait. Incremental hamstring muscle forces were applied to the modeled normal and the ACL-deficient knees. Results of simulations showed that the ACL injury increased the anterior tibial translation by 11.8mm, while 56% of the maximal hamstring muscle force could reduce the anterior translation of the tibia to a normal level during the stance phase of gait. The consequences of increased hamstring muscle force included increased quadriceps muscle force and joint contact force.

Anterior Cruciate Ligament↗
PubMed2000

A mechanical model to determine the influence of masses and mass distribution on the impact force during running.

Simple spring-damper-mass models have been widely used to simulate human locomotion. However, most previous models have not accounted for the effect of non-rigid masses (wobbling masses) on impact forces. A simple mechanical model of the human body developed in this study included the upper and lower bodies with each part represented by a rigid and a wobbling mass. Spring-damper units connected different masses to represent the stiffness and damping between the upper and lower bodies, and between the rigid and wobbling masses. The simulated impact forces were comparable to experimentally measured impact forces. Trends in changes of the impact forces due to changes in touch-down velocity reported in previous studies could be reproduced with the model. Simulated results showed that the impact force peaks increased with increasing rigid or wobbling masses of the lower body. The ratio of mass distribution between the rigid and wobbling mass in the lower body was also shown to affect the impact force peak, for example, the impact force peak increased with increasing rigid contribution. The variation in the masses of upper body was shown to have a minimum effect on the impact force peak, but a great effect on the active force peak (the second peak in the ground reaction force). Future studies on the dynamics and neuro-muscular control of human running are required to take into consideration the influence of individual variation in lower body masses and mass distribution.

Biomechanical Phenomena↗
PubMed2000

Potentiation of ethanol-induced loss of the righting reflex by ascorbic acid in mice: interaction with dopamine antagonists.

The present investigation was carried out to determine the effect of ascorbic acid on ethanol-induced loss of the righting reflex (LORR) and the interactions between ascorbic acid and dopamine receptor antagonists in affecting this action of ethanol in mice. To test the effect of each drug on ethanol-induced LORR, ascorbic acid (31.25, 62.5, 125, 250, 500, 1000 mg/kg intraperitoneally [IP]) and dopamine receptor antagonists (haloperidol 0.5, 1.0 mg/kg; L-sulpiride 20, 40, 80 mg/kg; clozapine 0.625, 1.25, 2.5 mg/kg; SCH 23390 0.5, 1.0, 2.0 mg/kg subcutaneously [SC]) were administered, respectively, 30 min before ethanol (4.0 g/kg IP) administration. Ascorbic acid, at the dose of 1000 mg/kg, significantly potentiated ethanol-induced LORR in mice. Dopamine D(2) antagonists haloperidol (0.5, 1.0 mg/kg SC), and L-sulpiride (80 mg/kg SC) also significantly prolonged the duration of LORR induced by ethanol. Clozapine and SCH 23390, at the doses used, did not affect ethanol-induced LORR. In the interaction study, the synergistic effect of ascorbic acid (1000 mg/kg IP) on ethanol-induced LORR was significantly enhanced by dopamine D(2) antagonists haloperidol, L-sulpiride, and clozapine, and the highest dose of dopamine D(1) antagonist SCH 23390. These results suggest that ascorbic acid may potentiate ethanol-induced LORR partially via a mechanism mainly linked to blockade of dopamine D(2) receptors.

Animals↗
PubMed2000

Evaluation of the Effect of Radiation Therapy to Nasopharyngeal Carcinoma by Positron Emission Tomography with 2-

Purpose: This investigation evaluated the effectiveness of positron emission tomography with 2-[F-18]fluoro-2-deoxy-D-glucose (PET-FDG) in assessing residual tumor or tumor recurrence in postradiation nasopharyngeal carcinoma (NPC) patients.Procedures: Forty-six patients with histologically proven NPC who received radiotherapy were included. PET-FDG images were analyzed by a semiquantitative method, metabolic ratio (tumor to cerebellum ratio).Results: The overall sensitivity and specificity of PET-FDG to detect residual tumors and recurrent lesions in the postradiation patients were 80% (12/15) and 87% (27/31), respectively. In patients with PET-FDG 6 months after radiation therapy, the sensitivity and specificity raised to 92% (11/12) and 100% (20/20), respectively.Conclusions: PET-FDG is effective in the evaluation of NPC treated with radiation. The optimal timing in assessing residual tumor or tumor recurrence in postradiation patients should be 6 months or later.

Journal Article↗
PubMed2000

Investigation of TTV by in situ hybridization in patients with chronic hepatitis.

To clarify whether TT virus (TTV) was present in liver tissues, 12 liver tissue samples from patients with chronic hepatitis positive for TTV in their serum and 11 samples from serum-negative patients were obtained by needle biopsies and investigated using in situ hybridization. Positive staining was observed in nine (75%) of 12 cases positive for TTV (serum-positive group) and three (27.3%) of 11 cases negative for TTV (serum-negative group) (P=0.061). Three kinds of staining patterns were observed: nuclear, cytoplasmic and both. In 58.3% (7/12) of the patients positive for TTV staining, the stained areas were found in both the nucleus and cytoplasm. Only cytoplasmic staining was observed in three cases from the serum-positive group. Only nuclear staining was observed in two cases from the serum-negative group. No significant differences were found in the clinical background between the in situ hybridization-positive and -negative groups, and between the serum-positive and -negative groups. The present study shows that TTV exists in the liver tissue, especially in hepatocytes, of chronic hepatitis patients and that the localization of TTV in the cell is different from case to case, although why this is so remains to be clarified.

Journal Article↗
PubMed2000

Sorption and catalytic hydrolysis of diethatyl-ethyl on homoionic clays.

Sorption and catalytic hydrolysis of the herbicide diethatyl-ethyl [N-chloroacetyl-N-(2,6-diethylphenyl)glycine ethyl ester] on homoionic Na(+)-, K(+)-, Ca(2+)-, and Mg(2+)-montmorillonite clays were studied in aqueous media. The Freundlich sorption coefficient, K(f), measured from isotherms on clay followed the order of Na(+) approximately K(+) > Mg(2+) approximately Ca (2+). Analysis of FT-IR spectra of diethatyl-ethyl sorbed on clay suggests probable bonding at the carboxyl and amide carbonyl groups of the herbicide. The rate of herbicide hydrolysis in homoionic clay suspensions followed the same order as that for sorption, indicating that sorption may have preceded and thus caused hydrolysis. Preliminary product identification showed that hydrolysis occurred via nucleophilic substitution at the carboxyl carbon, causing cleavage of the ester bond and formation of diethatyl and its dechlorinated derivative, and at the amide carbon, yielding an ethyl ester derivative and its acid. These pathways also suggest that hydrolysis of diethatyl-ethyl was catalyzed by sorption on the clay surface.

Adsorption↗
PubMed2000

Structural influences in relative sorptivity of chloroacetanilide herbicides on soil.

Adsorption of the chloroacetanilide herbicides acetochlor, alachlor, metolachlor, and propachlor was determined on soils and soil components, and their structural differences were used to explain their sorptivity orders. On all soils and soil humic acids, adsorption decreased in the order: metolachlor > acetochlor > propachlor > alachlor. On Ca(2+)-saturated montmorillonite, the order changed to metolachlor > acetochlor > alachlor > propachlor. FT-IR differential spectra of herbicide-clay or herbicide-humic acid-clay showed possible formation of hydrogen bonds and charge-transfer bonds between herbicides and adsorbents. The different substitutions and their spatial arrangement in the herbicide molecule were found to affect the relative sorptivity of these herbicides by influencing the reactivity of functional groups participating in these bond interactions. It was further suggested that structural characteristics of pesticides from the same class could be used to improve prediction of pesticide adsorption on soil.

Acetamides↗
PubMed2000

Activated neutrophils impair gastric cytoprotection role of neutrophil elastase.

Neutrophil elastase decreases production of PGI2 by cultured endothelial cells. Thus, neutrophil elastase may play an important role in gastric mucosal injury by decreasing the tissue level of PGI2, an important gastric cytoprotective substance. We examined whether activated neutrophils inhibit gastric PGI2 production in rats subjected to water-immersion restraint stress. Gastric 6-keto-PGF1alpha levels were determined by enzyme immunoassay. Gastric mucosal blood flow was determined by laser-Doppler flowmeter. Gastric microvascular permeability was determined by Evans blue leakage. Gastric levels of 6-keto-PGF1alpha were transiently increased 0.5 hr after the stress, followed by a decrease to below baseline at 6 hr, when mucosal blood flow fell to 60% of baseline. Gastric levels of 6-keto-PGF1alpha were significantly higher in animals with nitrogen mustard-induced leukocytopenia than in controls 1 and 6 hr after the stress. In leukocytopenic animals, levels 6 hr after stress were not lower than those preceding stress. Leukocytopenia markedly limited both the decrease in mucosal blood flow and the increase in gastric microvascular permeability. The level of gastric mucosal injury observed 6 hr after the stress was markedly attenuated by leukocytopenia. Pretreatment with neutrophil elastase inhibitors (ONO-5046 and Eglin C) or an anti-P-selectin monoclonal antibody produced effects similar to leukocytopenia. Neutrophil elastase is involved in the stress-induced gastric mucosal injury by decreasing gastric production of PGI2. Thus, pharmacologic inhibition of neutrophil elastase should help to prevent stress-induced gastric mucosal injury.

6-Ketoprostaglandin F1 alpha↗
PubMed2000

Characterisation of two distinct HKT1-like potassium transporters from Eucalyptus camaldulensis.

Potassium is an essential macronutrient in higher plants. It plays an important physiological role in stoma movements, osmoregulation, enzyme activation and cell expansion. The demand for potassium can be substantial, especially when the plant concerned is a Eucalyptus tree in excess of 50 m tall. We have isolated two cDNAs, EcHKT1 and EcHKT2, from Eucalyptus camaldulensis (river red gum) which are expressed in leaves, stems and roots. These encode potassium transporter polypeptides with homology to the wheat K+-Na+ symporter, HKT1. EcHKT1 and EcHKT2 both complemented the K+-limited growth of an Escherichia coli K+-uptake-deficient triple mutant. EcHKT1 and EcHKT2 also mediated Na+ and K+ uptake when expressed in Xenopus oocytes. A comparison of the EcHKT1 and EcHKT2 sequences and their transport properties indicated that these cDNAs represent two K+ transporters with distinct functional characteristics. The functional and structural conservation between these two E. camaldulensis genes and the wheat HKT1 suggests that they play an important, albeit elusive, physiological role.

Amino Acid Sequence↗
PubMed2000

Endothelial cell survival and apoptosis in the tumor vasculature.

Angiogenesis is essential for the growth and metastasis of solid tumors. The balance of endothelial cell (EC) proliferation and apoptosis is a major determinant in tumor angiogenesis. Recently, several studies demonstrated that numerous angiogenic factors not only induce angiogenesis but also function as EC survival factors. Vascular endothelial growth factor (VEGF), a potent angiogenic factor, is also an EC survival factor in embryonic vasculogenesis and tumor angiogenesis. VEGF activates specific intracellular survival pathways in ECs including Bcl-2, A1, IAP, Akt, and Erk. Integrins may function as EC survival factors by preventing anoikis by enhancing binding to the extracellular matrix. In addition, integrins may function in concert with VEGF to promote EC survival. Angiopoietin-1 (Ang-1) has recently been shown to stabilize EC networks by binding to the EC-specific tyrosine kinase receptor Tie-2. Pericytes also function as EC survival factors, by cell-cell contact, secretion of survival factors, or both. Targeting any of the above mechanisms for EC survival may provide novel antineoplastic strategies.

Angiopoietin-1↗
PubMed2000

Role of the tumor microenvironment in mediating response to anti-angiogenic therapy.

Despite the development of innovative anti-angiogenic strategies, early clinical trials have not replicated the results observed from preclinical models. One reason for this apparent discrepancy is the fact that tumor endothelium is phenotypically distinct from normal tissue endothelium. Moreover, it has recently become apparent that each individual tumor may display a different angiogenic phenotype. The expression of angiogenic factors in tumors is controlled by both intrinsic factors in the tumor cell and the influence of the host microenvironment. The diversity of angiogenic factor expression in tumors growing at different sites, combined with the fact that endothelial cells in different organs and tumors are phenotypically distinct, constitutes a formidable challenge for the development of effective anti-angiogenic regimens. This review provides an overview of how the microenvironment regulates tumor angiogenesis and affects the efficacy of anti-angiogenic therapy.

Angiogenesis Inhibitors↗
PubMed2000

p53 accumulation due to down-regulation of ubiquitin: relevance for neuronal apoptosis.

The p53 tumor suppressor protein is a major regulator of cell growth arrest and apoptosis in response to DNA damage. Both p53 function and stability are tightly controlled by Mdm2, which binds to the p53 N-terminus and targets p53 for ubiquitin-mediated proteolysis. Previous studies suggest that adrenalectomy-induced neuronal apoptosis is p53-dependent. Here we demonstrate both nuclear accumulation and functional activation of p53 protein in apoptotic hippocampal neurons from adrenalectomized rats. Increased p53 expression occurred despite the accumulation of its negative regulator, Mdm2, and the formation of p53-Mdm2 complexes. The persistence of p53 expression was explained by a striking decrease in free ubiquitin in p53-positive neurons. The addition of exogenous ubiquitin to p53-Mdm2 complexes from apoptotic neurons restored p53 degradation. These findings demonstrate a novel mechanism of p53 stabilization mediated by decreased ubiquitin levels. Regulation of free ubiquitin may therefore be an effective way to modulate p53-dependent apoptosis in certain cell types.

Adrenalectomy↗
PubMed2000

Isolation and characterization of a new bacteriocin from Lactobacillus gasseri KT7.

A bacteriocin-producing Lactobacillus gasseri strain, KT7, was isolated from infant faeces. The supernatant fluid showed inhibitory activity not only against some lactic acid bacteria but also, against some pathogenic and food-spoilage species, including Clostridium, Listeria and Enterococcus. An antimicrobial peptide designated gassericin KT7 was isolated from Lactobacillus gasseri KT7. It was purified to homogeneity by a single four-step procedure: a crude supernatant fluid obtained from early stationary-phase culture in MRS medium was subjected to ammonium sulphate fractionation, CM-Sephadex cation-exchange chromatography, Phenyl-Sepharose hydrophobic chromatography and reverse-phase HPLC chromatography. Gassericin KT7 was sensitive to proteolytic enzymes, resistant to heat, active over a wide range of pH, and migrated as a 4.5-5.0 kDa peptide on SDS-PAGE. The bacteriocin was produced constitutively during exponential growth. It was bactericidal to sensitive cells and the bactericidal effect was not produced by cell lysis. The amino acid composition of the bacteriocin was determined and no modified amino acid was found among the residues identified.

Amino Acids↗
PubMed2000

Plasticity of the urothelial phenotype: effects of gastro-intestinal mesenchyme/stroma and implications for urinary tract reconstruction.

The present study tests the hypothesis that heterotypic stromal-epithelial interactions cause phenotypic changes in urothelium. The rational for the experimental design is to simulate heterotypic stromal-epithelial interactions that are created at the anastomotic site of intestinal-bladder augmentations and internal urinary diversions where the urothelium is in direct contact with the gastro-intestinal tract tissues. Tissue recombination experiments were performed by combining 14-day embryonic rat and mouse rectal mesenchyme with urothelium from embryonic, newborn, and adult mice or rats. All tissue recombinants were grown beneath the renal capsule of athymic mouse hosts for 6-16 weeks. Analyses were performed to detect expression of uroplakins, cytokeratin 7, 14, 19 and mucin secreting epithelial cells via Periodic Acid-Schiff (PAS). The phenotype of both mouse and rat urothelium was changed to a glandular morphology under the influence of rectal mesenchyme. Immunohistochemical staining revealed a loss of the urothelial specific uroplakins and cytokeratins 7, 14, and 19 (characteristic of urothelium). Histologic analysis revealed the presence of mucin secreting glandular structures which stained positive for PAS. The urothelial transdifferentiation into glandular epithelium was not a function of epithelial age and occurred in the embryonic, newborn and adult urothelium. Likewise, rectal mesenchyme from embryonic, neonatal, and adult animals was able to induce glandular differentiation in bladder epithelium. Urothelium exhibits the plasticity to change into an intestinal like epithelium as a result of mesenchymal/stromal stimulation from the gastro-intestinal tract. This experimental result is germane to heterotypic stromal-epithelial interactions that are created in patients with urinary tract reconstructions (intestinal augmentations, de-mucosalized urothelial lined bladder patches, and internal urinary diversion such as ureterosigmoidostomies). We propose that heterotypic stromal-epithelial interactions may play a role in determining histodifferentiation of urothelial cells at the anastomotic site between bowel and bladder tissue in patients with gastro-intestinal urothelial reconstructions.

Animals↗