PubMed Health⌕ Search

Biomedical subjects

Y M Lu

Publications and source records attributed to Y M Lu.

At least 37 records · Page 2Linked to original sources
PubMed1999

Evaluation of the quality of surgical gloves among four different manufactures.

A randomized trial was conducted to evaluate the quality of four different brands of surgical gloves in terms of the perforation rate, ventilation, fitness, allergic reaction, elasticity, thickness, powder, and satisfaction. Gloves of four different manufactures which were used by various medical centres were distributed to participants according to a computer-generated randomization table. A structured questionnaire was self-administered by volunteers immediately after the surgical procedure to gather the information from participants, including the demographic data, allergy history, length of use, and variables of quality measures. Two brands, A and D, were significantly inferior to the best manufacture among the four, B, in terms of the ventilation, elasticity, and thickness, odds ratios ranging from 6 to 24, p < 0.05. For the amount of corn starch powder and satisfaction, all three other brands were inferior to brand B, odds ratios ranging from 6 to 44, p < 0.05. Gloves worn longer than 2 hours had a slightly higher perforation rate post procedures (11.5% vs. 2.1%, p = 0.048). The rate of latex allergic reaction was not significantly different between surgeons (8.3%) and the others (6.7%). No difference of the allergic reaction rate was found between subjects with allergy history (7.7%) and those without the history (7.5%). The quality of surgical gloves differs from brand to brand. The government and institutions should take the responsibility of monitoring the quality of surgical gloves in order to provide a safer and more comfortable environment for the surgical personnel and patients.

Adult↗
PubMed1998

Autoradiographic identification of a gastrin receptor on the human parietal cell.

Gastrin plays an important role in regulating gastric acid secretion and gastrointestinal mucosal growth but its cellular sites of action in man have not been determined. Using cryostat sections of gastric mucosal tissue we have identified (125I-gastrin binding followed by fixation-wet emulsion autoradiography) and characterized (125I-gastrin binding followed by counting) a gastrin receptor binding site in the human stomach. This site displayed binding characteristics similar to those observed in isolated cell systems: specifically, 125I-gastrin binding was rapid (t1/2 approximately 10 min at 37 degrees C), temperature-dependent (3.5 fold more radioligand bound at 22 degrees C than at 4 degrees C) and saturable. The binding of the radioligand was also tissue specific and was five-fold greater in the gastric body than in the gastric antrum and duodenum. In the autoradiographs, silver grains were localized only to parietal cells and not to other epithelial cell types. In the presence of 40 nM gastrin grains were no longer present over parietal cells demonstrating that these sites were both saturable and of high affinity. These data provide the first demonstration of gastrin binding sites (putative receptors) on parietal cells in the human stomach and suggest that gastrin acts directly on these cells to help regulate gastric acid secretion and/or mucosal growth.

Adult↗
PubMed1998

Src activation in the induction of long-term potentiation in CA1 hippocampal neurons.

Long-term potentiation (LTP) is an activity-dependent strengthening of synaptic efficacy that is considered to be a model of learning and memory. Protein tyrosine phosphorylation is necessary to induce LTP. Here, induction of LTP in CA1 pyramidal cells of rats was prevented by blocking the tyrosine kinase Src, and Src activity was increased by stimulation producing LTP. Directly activating Src in the postsynaptic neuron enhanced excitatory synaptic responses, occluding LTP. Src-induced enhancement of alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) receptor-mediated synaptic responses required raised intracellular Ca2+ and N-methyl-D-aspartate (NMDA) receptors. Thus, Src activation is necessary and sufficient for inducing LTP and may function by up-regulating NMDA receptors.

Amino Acid Sequence↗
PubMed1998

The effect of fluid loss on the viscoelastic behavior of the lumbar intervertebral disc in compression.

A viscoelastic finite element model of a L2-L3 motion segment was constructed and used to study: (1) the behavior of the intervertebral disc with different amounts of nucleus fluid loss; and (2) the effect of different rates of fluid loss on the viscoelastic behavior of the disc. The results indicate that: (1) The viscoelastic behavior of the intervertebral disc depends to a large extent on the rate of fluid loss from the disc; the intrinsic properties of disc tissue play a role only at the early stage of compressive loading; (2) the axial strain increases, whereas the intradiscal pressure and the posterior radial disc bulge decrease with increasing fluid loss; (3) a decreasing fluid loss rate with a total fluid loss of 10 to 20 percent (from the nucleus) during the first hour of compressive loading best predicts the overall viscoelastic behavior of a disc.

Biomechanical Phenomena↗
PubMed1998

Ankle arthrography and chronic lateral ankle instability.

Sixty-five ankle arthrograms of the patients who underwent surgical reconstruction for their chronic ankle instability from 1987 to 1995 were studied retrospectively by comparing their operative findings. There were 15 cases (23.1%) with definite positive arthrographic findings. In the remaining 50 cases (76.9%), the arthrograms showed a "tear-drop" extravasation of dye beneath the fibular tip which we called "suspectable positive". Of these all but one, which had normal ligament, proved to correspond to the operative finding. As there was only one false positive finding among our surgical cases with both the "definite" and "suspectable" positive arthrograms, we concluded that ankle arthrography is relatively reliable and may be worth doing even in chronic cases if only for reference. Even when other diagnostic methods are negative, arthrography might help surgeons make surgical decisions in clinical symptomatic cases.

Adolescent↗
PubMed1997

Mice lacking metabotropic glutamate receptor 5 show impaired learning and reduced CA1 long-term potentiation (LTP) but normal CA3 LTP.

Class I metabotropic glutamate receptors (mGluRs) have been postulated to play a role in synaptic plasticity. To test the involvement of one member of this class, we have recently generated mutant mice that express no mGluR5 but normal levels of other glutamate receptors. The CNS revealed normal development of gross anatomical features. To examine synaptic functions we measured evoked field EPSPs in the hippocampal slice. Measures of presynaptic function, such as paired pulse facilitation in mutant CA1 neurons, were normal. The response of mutant CA1 neurons to low concentrations of (1S,3R)-1-amino-cyclopentane-1,3-dicarboxylic acid (ACPD) was missing, which suggests that mGluR5 may be the primary high affinity ACPD receptor in these neurons. Long-term potentiation (LTP) in mGluR5 mutants was significantly reduced in the NMDA receptor (NMDAR)-dependent pathways such as the CA1 region and dentate gyrus of the hippocampus, whereas LTP remained intact in the mossy fiber synapses on the CA3 region, an NMDAR-independent pathway. Some of the difference in CA1 LTP could lie at the level of expression, because the reduction of LTP in the mutants was no longer observed 20 min after tetanus in the presence of 2-amino-5-phosphonopentanoate. We propose that mGluR5 plays a key regulatory role in NMDAR-dependent LTP. These mutant mice were also impaired in the acquisition and use of spatial information in both the Morris water maze and contextual information in the fear-conditioning test. This is consistent with the hypothesis that LTP in the CA1 region may underlie spatial learning and memory.

Animals↗
PubMed1996

Do bending, twisting, and diurnal fluid changes in the disc affect the propensity to prolapse? A viscoelastic finite element model.

STUDY DESIGN: A finite element model of a lumbar motion segment was constructed. OBJECTIVES: The model was directed toward understanding the effect of compression, bending and twisting, and diurnal fluid changes in the disc on the propensity to disc prolapse. Tensile stresses in the anulus fibers were computed and used to determine the successive steps required to create a fissure in the disc. SUMMARY OF BACKGROUND DATA: Disc prolapse is more likely under combined loading involving compression and bending and twisting. Changes in fluid content in the disc also affect the mechanical behavior of the disc. METHODS: The three-dimensional model accounted for the viscoelastic material properties of the anulus fibers and ligaments. Diurnal fluid exchange was simulated by changing the fluid content in the nucleus of the disc. Combined with bending and twisting, a compressive load was applied at different loading rates. RESULTS: The maximum tensile stress in the anulus fibers always occurred in the fibers at the inner posterior anulus at the junction of the disc and the endplate. Of the three models tested, the "weakest" (or the first to fail) was the saturated disc subjected to compression and bending and twisting. As the loading rate increased, anulus fiber failure was initiated at a lower value of compressive load. An increasing compressive load applied to a flexed, twisted, and saturated disc resulted in progressive failure, or fissure propagation, starting at the posterior inner anulus at the junction of the disc and the endplate. CONCLUSIONS: The results from this study suggest that there are several key factors involved in the initiation and propagation of anulus failure: axial compressive load, bending and twisting, and disc saturation. If one of these is lacking, anulus failure is harder to achieve.

Elasticity↗
PubMed1996

Can variations in intervertebral disc height affect the mechanical function of the disc?

STUDY DESIGN: The finite element method was used to investigate the effect of variations in disc height on the mechanical behavior of the intervertebral disc. OBJECTIVES: The effect of disc height on the mechanical behavior of a human lumbar spine segment in terms of axial displacement, intradiscal pressure, posterolateral disc bulge, tensile stress in the peripheral anulus fibers, and longitudinal stress distribution at the end plate-vertebra interface was evaluated. SUMMARY OF BACKGROUND DATA: Disc height varies with individuals, disc level, abnormal conditions, and clinical management. METHODS: A three-dimensional finite element model of L2-L3 disc body unit was developed. Parametric studies were undertaken by studying discs of three different heights: 8 mm, 10 mm, and 12 mm, whereas disc cross sectional area, finite element mesh density, and all other parameters were kept constant. The model accounted for geometric nonlinearity but assumed that the material properties were linear. RESULTS: Variations in disc height had a significant influence on the axial displacement, the posterolateral disc bulge, and the tensile stress in the peripheral anulus fibers, but the effect on the intradiscal pressure and the longitudinal stress distribution at the endplate vertebra interface was minimal. CONCLUSIONS: Variations in disc height may compromise the general conclusions reached from experimental work and analytic studies in which geometric parameters (especially disc height and disc cross-sectional area) are not taken into consideration.

Biomechanical Phenomena↗
PubMed1996

Ca(2+)-permeable AMPA/kainate and NMDA channels: high rate of Ca2+ influx underlies potent induction of injury.

Neurodegeneration may occur secondary to glutamate-triggered Ca2+ influx through any of three routes: NMDA channels, voltage-sensitive Ca2+ channels (VSCC), and Ca(2+)-permeable AMPA/kainate channels (Ca-A/K). This study aims to examine Ca2+ ion dynamics in the generation of excitotoxic injury by correlating the relative amounts of 45Ca2+ that flow into cortical neurons through each of these routes over a 10 min epoch ("10 min Ca2+ loads;" a measure of influx rate), with resultant levels of intracellular free Ca2+ ([Ca2+]) and subsequent injury. Neurons possessing Ca-A/K make up a small subset (approximately 13%) of cortical neurons in culture, which can be identified by a histochemical stain based on kainate-stimulated Co2+ uptake (Co2+ (+) neurons) and which are unusually vulnerable to AMPA/kainate receptor-mediated injury. Initial studies using brief kainate exposures (to selectively destroy Co2+ (+) neurons) along with kainate-triggered 45Ca2+ influx measurements suggested that kainate causes rapid Ca2+ influx into Co2+ (+) neurons (comparable to that caused by NMDA). Influx through both Ca-A/K and NMDA channels increased proportionately with extracellular Ca2+, suggesting that these channels have high Ca2+ permeability. When cultures were subjected to exposures that gave similar 10 min Ca2+ loads through different routes, comparable levels of injury were observed, suggesting that net intracellular Ca2+ accumulation is a critical determinant of injury. However, the relationship between [Ca2+]i and influx was less direct: although exposures that gave the lowest or highest 10 min Ca2+ loads showed correspondingly lower or higher mean [Ca2+]i responses, there appears to be a wide range of exposures over which individual neuronal differences and sequestration/buffering mechanisms obscure [Ca2+]i as a reflection of influx rate.

Animals↗
PubMed1995

Ca2+ permeable AMPA/kainate channels permit rapid injurious Ca2+ entry.

Small subsets of central neurons possessing Ca2+ permeable AMPA/kainate channels can be identified by a histochemical stain based on kainate-stimulated Co2+ uptake (Co2+(+)neurons) and are unusually vulnerable to AMPA/kainate receptor-mediated injury. Using brief kainate exposures (which selectively destroy Co2+(+) neurons) along with kainate triggered 45Ca2+ influx measurements, we estimate kainate to cause an unusually high rate of Ca2+ influx into Co2+(+) neurons. Also, while fura-2 Ca2+ imaging revealed low (10 microM) kainate exposures to preferentially induce intracellular free Ca2+ ([Ca2+]i) elevations in Co2+(+) neurons, intense (100 microM) kainate exposures used in the 45Ca2+ influx studies triggered comparable [Ca2+]i rises in all neurons. These findings suggest that the exceptional vulnerability of Co2+(+) neurons to AMPA/kainate receptor-mediated injury reflects a high rate of agonist triggered Ca2+ influx, and that [Ca2+]i rises may only poorly reflect influx rate.

Animals↗
PubMed1995

[Single channel analysis of aconitine blockade of calcium channels in rat myocardiocytes].

Ventricular myocardiocytes from neonatal Wistar rats were isolated and cultured. Aconitine, Ca2+ channel blocker verapamil or Ca2+ channel activator BAY K8644 were added to the bath solution separately. Using the cell-attached configuration of the patch clamp technique, the single channel activities of L type Ca2+ channel were recorded before and after addition of all three drugs. The results showed the blocking effect of aconitine (50 micrograms.ml-1) on L type Ca2+ channels. Its mechanism may be relevant to the decrease in both open state probability and the mean open time of Ca2+ channel. The difference was statistically significant compared with control group (P < 0.01). The amplitude of Ba2+ currents, which flow through open L type Ca2+ channel was unchanged.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Arthroscopic debridement for osteoarthritis of the knee: a seven years follow-up study.

We reviewed 32 knees with osteoarthritis of the knee treated by either arthroscopic debridement in association with drilling the subchondral bone or arthroscopic debridement alone and followed for 2.5 to 11 years. Eighteen knees had arthroscopic debridement and drilling the subchondral bone, and 14 knees had arthroscopic debridement alone. In the group treated with arthroscopic debridement and drilling the subchondral bone, 55.6% had good to excellent results, 22.2% had fair results, and 22.2% had poor results. In the group that had arthroscopic debridement alone, 57.2% had good to excellent results, 35.7% had fair results, and 7.1% had poor results. There was better relief of pain in the group with arthroscopic debridement alone.

Adult↗
PubMed1994

P-type calcium channels are blocked by the alkaloid daurisoline.

IN looking for a structurally defined non-peptide P-channel blocker we have tested the alkaloid daurisoline which has been isolated from traditional Chinese medicinal herb (Menispermum dauricum) used for the treatment of epilepsy, hypertension and asthma. We have found that daurisoline is an inhibitor of omega-Aga-IVA sensitive barium currents in cerebellar Purkinje cells and of excitatory postsynaptic potentials evoked in Purkinje cells by stimulating parallel fibres in acutely prepared cerebellar slices. Daurisoline did not significantly affect omega-Aga-IVA-insensitive barium currents recorded from granule cells freshly isolated from rat cerebellum. Daurisoline passes the blood-brain barrier and will, therefore, facilitate the functional characterization of brain calcium channels as well as the exploration of P-type calcium channels as possible drug targets.

Alkaloids↗
PubMed1993

Alterations of G-protein coupling function in phosphoinositide signalling pathways of rat hippocampus by ischaemic brain injury.

The activation of membrane-associated phospholipase C is rapidly and transiently induced in the central nervous system by a variety of stimuli. Ischaemic brain injury is one of the situations that leads to a dramatic increase in polyphosphoinositide (PPI) turnover. In this study, stimulation of PPI hydrolysis by glutamate (500 microM) was measured in hippocampal slices from rats up to 21 days after an ischaemic insult of 30 min. Ischaemia was induced using the four-vessel occlusion method. PPI hydrolysis elicited by glutamate was significantly increased in the slices prepared from ischaemic rats 24 h after reperfusion, the accumulation of inositol phosphates (InsPs) and inositol 1,4,5-trisphosphate (Insp3) was 614 +/- 74% (n = 8) and 182 +/- 11% (n = 9) of the basal level respectively. This potentiation was also observed 21 days after ischaemia. Hyper-responsiveness to glutamate was also accompanied by an increase in AIF4(-)-stimulated formation of [3H]inositol phosphates. In addition, global ischaemia did not change either high-affinity [3H]glutamate binding in hippocampal membranes or the stimulation of PPI hydrolysis by carbachol or noradrenaline in hippocampal slices. The present results suggest that the increased responsiveness to glutamate is the result, at least in part, of functional changes at the G-protein level, and may contribute to the pathophysiology of ischaemic brain injury or to the regenerative phenomena that accompany ischaemic damage.

Aluminum Compounds↗
PubMed1993

Accumulation of glutamate is regulated by calcium and protein kinase C in rat hippocampal slices exposed to ischemic states.

There is now convincing evidence that excessive accumulation of the excitatory amino acid glutamate (Glu) in the extracellular space is toxic to neurons. However, the regulation of the release and uptake of Glu in producing this toxic concentration has not been adequately ascertained. The authors report that in hippocampal slices, the output of Glu significantly increased under in vitro ischemic states. Glu in the extracellular space increased fivefold. Since daurisoline, a drug that blocks N-type Ca2+ channels, or Ca(2+)-free solution potently and effectively lowered this stimulated output, it was hypothesized that the Glu output is mediated by Ca2+ influx in nerve terminals. When the slices were incubated for 30 minutes under ischemic state, daurisoline caused only small alterations in the postischemic accumulation of Glu. However, Glu accumulation was markedly attenuated by H-7, but not by calmidazolium, facilitated by PDB whereas 8-bromo-cAMP was without effect. It appears therefore that during a 30-minute ischemic insult, protein kinase C (PKC) was involved in the Glu accumulation of supernatant. A direct demonstration of this concept was obtained by showing significant increases in PKC activation in presynaptic nerve terminals (from 1.34 +/- 0.1 to 9.34 +/- 0.89 U) following 30 minutes of ischemia. DNQX, a non-NMDA receptor antagonist, potently reduced PKC activities and decreased extra Glu accumulation. Also observed was the inhibition of 1-[3H]-Glu uptake into synaptosomes by PDB. These results provide direct evidence that Ca2+ influx enhances Glu release, which in turn leads to inhibition of its reuptake, and is coupled with PKC activities in presynaptic nerve terminals.

Alkaloids↗
PubMed1991

Effects of Ca2+ antagonists on glutamate release and Ca2+ influx in the hippocampus with in vivo intracerebral microdialysis.

1. The extracellular glutamate content and Ca2+ level in vivo in rat hippocampus were measured by brain microdialysis following administration of two depolarizing agents (veratridine, KCl) and quinolinic acid (Quin). 2. The two depolarizing agents increased the extracellular glutamate level (to between 280 and 320% basal) and decreased the extracellular Ca2+ content (to 48% of basal). However, Quin did not change the glutamate level but decreased the Ca2+ content. 3. The effects of Ca2+ antagonists on the changes of glutamate and Ca2+ level were evaluated in this experimental model. At a dose of 0.5 mg kg-1, i.v., nimodipine (L-type channel blocker) did not produce significant changes in the stimulated-glutamate release. A statistically significant inhibition of Ca2+ influx was observed at a dose of 0.05 mg kg-1. In contrast, in those animals receiving the N-type Ca2+ antagonist, daurisoline (0.1, 1 or 5 mg kg-1, i.v.), a potent attenuation of both glutamate release and Ca2+ influx was found. 4. We propose that the pharmacological properties of Ca2+ influx and of neurotransmitter release differ and that nimodipine-sensitive L-type channels may not be very common in nerve terminals but are localized in cell soma. Daurisoline-sensitive N-type channels in nerve terminals have a much greater influence on excitatory amino acid release.

Alkaloids↗
PubMed1991

Effects of nimodipine on l-glutamate-induced seizures and Ca2+ influx in hippocampus in freely moving rats.

Seizure (EEG) was studied in rats unilaterally injected in the dorsal hippocampus with l-glutamate (Glu). Extracellular Ca2+ content [(Ca2+)e] in the injected area was assessed by brain microdialysis coupled to automatic atomic absorption spectrophotometry. In this experimental epileptic model, an inhibition of Glu-stimulated epileptic activity and a fall in (Ca2+)e by nimodipine (Nim, 100 micrograms.kg-1) were seen. The spike- and wave-burst frequency was reduced from 30 to 5 bursts.min-1 (P less than 0.01, n = 8). Nim 25 and 50 micrograms.kg-1, without anticonvulsant activity, did not prevent the drop in (Ca2+)e. These results indicate that Nim exerts an antiepileptic effect on Glu-induced epilepsy. The mechanisms may be involved in blocking Ca2+ influx into neurons.

Animals↗