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Biomedical subjects

L Yao

Publications and source records attributed to L Yao.

At least 109 records · Page 6Linked to original sources
PubMed1997

Saccadic eye movements to visual and auditory targets.

Recent neurophysiological studies of the saccadic ocular motor system have lent support to the hypothesis that this system uses a motor error signal in retinotopic coordinates to direct saccades to both visual and auditory targets. With visual targets, the coordinates of the sensory and motor error signals will be identical unless the eyes move between the time of target presentation and the time of saccade onset. However, targets from other modalities must undergo different sensory-motor transformations to access the same motor error map. Because auditory targets are initially localized in head-centered coordinates, analyzing the metrics of saccades from different starting positions allows a determination of whether the coordinates of the motor signals are those of the sensory system. We studied six human subjects who made saccades to visual or auditory targets from a central fixation point or from one at 10 degrees to the right or left of the midline of the head. Although the latencies of saccades to visual targets increased as stimulus eccentricity increased, the latencies of saccades to auditory targets decreased as stimulus eccentricity increased. The longest auditory latencies were for the smallest values of motor error (the difference between target position and fixation eye position) or desired saccade size, regardless of the position of the auditory target relative to the head or the amplitude of the executed saccade. Similarly, differences in initial eye position did not affect the accuracy of saccades of the same desired size. When saccadic error was plotted as a function of motor error, the curves obtained at the different fixation positions overlapped completely. Thus, saccadic programs in the central nervous system compensated for eye position regardless of the modality of the saccade target, supporting the hypothesis that the saccadic ocular motor system uses motor error signals to direct saccades to auditory targets.

Acoustic Stimulation↗
PubMed1997

Differential regulation of substance P by all members of the nerve growth factor family of neurotrophins in avian dorsal root ganglia throughout development.

This study examined the effects of nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4/5 on substance P levels in dorsal root ganglia of the quail shortly after ganglia formation (stage 26, embryonic day 4.5), during the middle of development (stage 33, embryonic day 7.5) and during late development (stage 44, embryonic day 14). It has already been shown that nerve growth factor increases levels of substance P during the middle and late stages of development, and that messenger RNA for the neurotrophin receptors, trkA, trkB and trkC is present at all of these stages. Dorsal root ganglia were isolated, rinsed with defined medium to dilute endogenous neurotrophins and exposed to one of the neurotrophins for either 4 or 20 h. Substance P levels were quantitated using enzyme immunoassay. None of the neurotrophins had any effect on substance P levels in dorsal root ganglia obtained at stage 26 after either a 4 or 20 h exposure time. Nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4/5 all significantly increased levels of substance P after either a 4 h or 20 h incubation in ganglia obtained at stages 33 and 44. The effects of nerve growth factor and neurotrophin-3 were specific: increases in substance P were completely blocked by simultaneous exposure to antibodies against either nerve growth factor or neurotrophin-3. The absence of any effect of neurotrophins on substance P expression during early development was unexpected, since dorsal root ganglia exhibit substantial levels of substance P and receptors for the neurotrophins are present and are apparently functional. It was also surprising that brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4/5 induced increases in substance P levels during the middle and late stages of development, since substance P was thought to be exclusively localized to small TrkA neurons in dorsal root ganglia. However, immunocytochemical examination of dorsal root ganglia at stages 33 and 44 revealed substance P-like immunoreactivity in larger neurons as well as in small neurons. The results of this study have shown that different cellular responses to neurotrophins, such as effects on survival and/or peptide expression, may be acquired with differing temporal patterns not strictly related to expression of their receptors. Further, the regulation of neuropeptide synthesis in dorsal root ganglia is not due to any one neurotrophic factor. and the factors that regulate expression during early development are still unknown.

Animals↗
PubMed1997

Reactivity of mesenteric arteries from fructose hypertensive rats to endothelin-1.

We previously demonstrated that mesenteric arteries from hyperinsulinemic, insulin resistant fructose hypertensive (FH) rats contain a higher absolute amount of ET-1 and exhibit defective endothelium-dependent vasodilation. Furthermore, chronic ET receptor blockade with bosentan completely prevented the rise in blood pressure in these rats. The present study was undertaken to examine 1) whether the reactivity of mesenteric arteries to ET-1 is altered in FH rats, and 2) whether chronic bosentan treatment has any effect on ET-1 responsiveness and endothelium-dependent vasodilation. Male Sprague Dawley rats were divided into four groups: control (C), control bosentan-treated (CB), fructose (F) and fructose bosentan-treated (FB). Chronic oral bosentan treatment (100 mg/kg/day) was initiated in the CB and FB groups 1 week prior to initiating the fructose diet. At week 16, the F group was hyperinsulinemic and hypertensive when compared to the C group (plasma insulin: 5.8 +/- 0.3 v C 3.2 +/- 0.5 ng/mL, P < .001; systolic BP: 157 +/- 5 v C 130 +/- 4 mm Hg, P < .001). Treatment of the F group with bosentan prevented the rise in BP (FB: 133 +/- 3 mm Hg; P < .001 v F). Analysis of the pressurized mesenteric resistance arterioles demonstrated that the wall thickness as expressed as percentage of internal diameter did not differ between arteries from C and F rats, when measured over a range of transmural pressures. Constrictor responses of resistance arterioles to NE were similar for C and F rats when studied at transmural pressures of either 120 mm Hg or 160 mm Hg, respectively. The maximum contractile response and the sensitivity of superior mesenteric arteries to NE did not differ between the groups, either with or without the endothelium. However, the maximum contractile response to ET-1 was depressed in the F group both with (+) and without (-) the endothelium [(+): 1.50 +/- 0.11 v C 1.88 +/- 0.1 g/mm3, P < .05, (-): 1.68 +/- 0.11 v C 2.05 +/- 0.1 g/mm3, P < .05.]. Furthermore, the endothelium intact F arteries exhibited a decreased sensitivity to ET-1 (pD2 values F 8.36 +/- 0.11 v C 8.83 +/- 0.07). Chronic bosentan treatment of the F group restored the maximum tension responses of arteries to ET-1 [(+) in the FB group: 1.88 +/- 0.12 g/mm3 v C, P > .05, (-): 1.95 +/- 0.05 g/mm3 v C, P > .05] but had no effect on the responses of the CB group. In arteries with intact endothelium, bosentan treatment restored the sensitivity of the F arteries to ET-1 (pD2 values FB 8.82 +/- 0.05 v C, P < .05). Endothelium-dependent relaxation responses were diminished in the F group, which were unaffected by bosentan treatment. These data suggest that mesenteric arteries from FH demonstrate a specific alteration towards the reactivity to ET-1, which is restored by long-term bosentan treatment.

Animals↗
PubMed1997

Saline versus gadolinium-enhanced magnetic resonance arthrography of porcine cartilage.

RATIONALE AND OBJECTIVES: The authors compared saline and dilute gadopentetate dimeglumine as injectants for magnetic resonance (MR) arthrography. METHODS: Sixty-three lesions were created on the joint surfaces of six pig patellas. MR arthrography (1.5 T) was performed with the specimens in saline and then in 2 mmol gadopentetate dimeglumine by using fat-saturated two-dimensional (2D) and three-dimensional (3D) sequences. Two musculoskeletal radiologists independently interpreted the images. RESULTS: At 2D MR arthrography, reader 1 performed equally well with saline and gadolinium solutes, whereas reader 2 had better sensitivity with the saline solute (P < .05); interobserver agreement was equivalent for saline and gadolinium solutes. With 3D MR arthrography, reader 2 performed equally well with saline and gadolinium solutes, whereas reader 1 had better sensitivity (P < .0001) but poorer specificity (P < .001) with the gadolinium solute; interobserver agreement was significantly better for saline than for gadopentetate dimeglumine (P < .05). CONCLUSION: In this initial evaluation, there was no clear advantage to using gadolinium-enhanced MR arthrography over saline MR arthrography for detecting lesions in porcine hyaline cartilage.

Animals↗
PubMed1997

Ethanol alters the subcellular localization of delta- and epsilon protein kinase C in NG108-15 cells.

Protein kinase C (PKC) has been shown to regulate the ethanol sensitivity of membrane-bound receptors and transporters, but little is known about the molecular mechanisms underlying this regulation. PKC is a family of isozymes that translocate to new intracellular sites on activation. Here we present immunochemical data showing that ethanol causes translocation of delta- and epsilon-PKC to new intracellular sites. Ethanol causes translocation of delta-PKC from the Golgi to the perinucleus; this translocation is similar to that induced by activation of PKC with phorbol esters. In contrast, epsilon-PKC translocation caused by ethanol is different from that induced by phorbol esters; ethanol causes translocation of epsilon-PKC from the perinucleus to the cytoplasm, whereas phorbol ester activation causes translocation of epsilon-PKC to the nucleus. Because the substrate specificity of these kinases is determined by their site of localization, ethanol-induced translocation of delta- and epsilon-PKC to new intracellular sites may explain some of the pleiotropic effects of ethanol on cellular functions.

Biological Transport↗
PubMed1997

Correlation of histopathologic and bacteriologic changes with cytokine expression in an experimental murine model of bacteremic Staphylococcus aureus infection.

Staphylococcus aureus infections are often life threatening. Relatively little is known about the host response to these infections, in particular, the role played by cytokines. We established a mouse model of bacteremic S. aureus infection to correlate bacteriologic findings and pathologic changes with cytokine gene expression. Bacterial density in blood and tissue was highest at 1 h and minimal by 48 h. Despite the rapid clearance of bacteria, pathologic abnormalities and inflammatory cytokines were detected after clearance of the bacteria. The number of infiltrating inflammatory cells, as well as the size of inflammatory foci, increased with time. Interstitial accumulation of inflammatory cells and tissue damage, such as microabscesses, edema, and necrosis progressed following clearance of bacteria from the tissues. Levels of tumor necrosis factor and interleukin-1 protein in serum were detectable at 1 h and peaked at 4 h. Interleukin-6 protein expression showed different kinetics, with low levels detected at 1 h and increasing levels at 72 h postinfection. Tumor necrosis factor and the interleukins were expressed in inflammatory and noninflammatory cells in lung, liver, and heart tissues. Leukocytes in the infected tissues were highly reactive with antibodies to the three cytokines, suggesting that activated leukocytes are a major source of inflammatory cytokines after staphylococcal infection. Expression of interleukin-1 and interleukin-6 in tissue-specific cells and endothelial cells was also detected in infected tissues, indicating that cells other than leukocytes contribute to the elevated cytokine levels in this model. Once initiated, expression of inflammatory cytokines contributes to the pathogenesis of S. aureus disease.

Animals↗
PubMed1997

Dopamine D1A receptors and renin release in rat juxtaglomerular cells.

Two dopamine D1-like receptors have been cloned from mammals, the D1 and D5 receptors, also known as D1A and D1B receptors, respectively, in rodents. Although D1-like receptors are known to stimulate renin release, the receptor subtype mediating this action has not been determined. We investigated D1 receptor subtype expression in rat juxtaglomerular cells obtained after enzymatic dispersion of kidney cortex and differential centrifugation. Juxtaglomerular cells in primary culture were immunocytochemically 85% to 95% renin positive. These cells expressed the D1A but not the D1B receptor (mRNA and protein). D1-like receptor function was demonstrated by a concentration-dependent stimulation of cAMP production by dopamine (n = 5-9 per group). Fenoldopam, a D1-like receptor agonist, also caused a concentration-dependent increase in cAMP production and renin secretion that was blocked by the selective D1-like receptor antagonist SCH23390 (n = 4-13 per group). Although the D1 ligands do not distinguish between the cloned D1-like receptors, the actions of fenoldopam were due to occupancy of the D1A receptor: (1) the D1B receptor, the only other mammalian D1-like receptor, is not expressed in juxtaglomerular cells; (2) antisense but not sense D1A oligonucleotides completely blocked the stimulatory effect of fenoldopam on cAMP production and renin secretion. We conclude that there is selective dopamine receptor gene expression in juxtaglomerular cells; the dopamine receptor subtype linked to the stimulation of cAMP and renin secretion in juxtaglomerular cells is the D1A subtype.

Animals↗
PubMed1997

[Clinical application of biological bone carrier in repair of long bone defect of femur].

It is difficult to repair long defect of bone. Biological bone carrier (BBC) was one of the artifical bone substitutes. It was obtained from human or swine bone after a series of biochemical treatment. It had good histocompatibility. It had the same components and structure of bone, and its biological strength was samiliar to bone. In clinic, BBC was applied to repair of long defect of bone in two cases. The lengths of defect were 13 cm and 11 cm, respectively. After followed up for 2 to 3 years, it was found that the implanted BBC had been combined with the femur with new bone. It had the same metabolism and density as that of the normal bone.

Adolescent↗
PubMed1996

Pre- and peristroke treatment with the adenosine kinase inhibitor, 5'-deoxyiodotubercidin, significantly reduces infarct volume after temporary occlusion of the middle cerebral artery in rats.

The adenosine kinase inhibitor, 5'-deoxyiodotubercidin (5dITU), was examined in a rat focal stoke model with temporary (105 min) middle cerebral artery occlusion (MCAO) followed by a 24 h recovery period. Inhibition of this adenosine metabolizing enzyme indirectly enhances the actions of endogenous adenosine without inducing cardiovascular side effects. Such effects could limit the potential clinical application of any approach targeting adenosine receptor activation. MCAO was accomplished with a transluminal 4-0 nylon suture inserted through the common carotid artery to block blood flow at the origin of the MCA. Treatment with 5dITU 30 min prior to and 5 h after MCAO resulted in a dose dependent (0.1-0.5 mg/kg, i.p.) reduction in infarct volume. A significant (P = 0.02) 44% reduction (control, 265 +/- 35 mm3; treated, 149 +/- 30 mm3) was observed at 0.5 mg/kg. However, at the highest dose examined (1.0 mg/kg) infarct volume was unaffected. To assess the potential for acute (i.e. post-occlusion) treatment, 5dITU was administered (0.33 mg/kg, i.v.) successively at each of 0.5, 1.75 and 3.5 h after MCAO. Post-occlusion treatment resulted in a significant (P = 0.037) 32% reduction in infarct volume (control, 314 +/- 34 mm3; treated, 212 +/- 28 mm3). At this dose there were no apparent changes in a number of physiological parameters monitored over the period of MCAO. The present study shows that intervention with an adenosine kinase inhibitor in an ischemic brain injury model is neuroprotective whether treatment is begun prior to or just after MCAO.

Adenosine Kinase↗
PubMed1996

The role of protein kinase C in cellular tolerance to ethanol.

We have shown that ethanol inhibits uptake of adenosine by a specific nucleoside transporter in NG108-15 neuroblastoma x glioma cells and that cAMP-dependent protein kinase (PKA) activity is required for this inhibition. After chronic exposure to ethanol, adenosine uptake is no longer inhibited on rechallenge with ethanol, i.e. transport has become tolerant to ethanol. Here we show that protein kinase C (PKC) contributes to ethanol-induced tolerance of adenosine transport. Activation of PKC by phorbol esters in control cells results in an ethanol-tolerant phenotype, similar to that produced by chronic ethanol exposure. In addition, chronic exposure to ethanol increases the amounts of alpha, delta, and epsilon PKC. However, reducing PKC activity by inhibition with chelerythrine during chronic exposure to ethanol or down-regulation by phorbol esters prevents the development of ethanol-induced tolerance of adenosine transport. By contrast, the inhibition of PKA activity produces tolerance to ethanol inhibition of adenosine uptake. When protein phosphatase inhibitors are present, inhibiting PKA activity has no effect on ethanol sensitivity of adenosine uptake, suggesting a role for protein phosphatases in the regulation of ethanol sensitivity of uptake. Taken together, our results suggest that PKA and PKC have opposing effects on the ethanol sensitivity of adenosine transport; PKA activity is required for ethanol sensitivity, and PKC activation produces tolerance. Based on these data, we propose that chronic ethanol exposure increases PKC activity, leading to the activation of a protein phosphatase (1 or 2A). This phosphatase then dephosphorylates a PKA-phosphorylated site, which is required for ethanol to inhibit adenosine uptake. Therefore, the sensitivity of adenosine transport to ethanol appears to be maintained by a balance of PKA and protein phosphatase activities, and PKC may regulate phosphatase activity.

Adenosine↗
PubMed1996

Interleukin 4 or oncostatin M induces a prolonged increase in P-selectin mRNA and protein in human endothelial cells.

During acute inflammation, P-selectin is transiently mobilized from Weibel-Palade bodies to the surface of histamine-activated endothelial cells, where it mediates rolling adhesion of neutrophils under hydrodynamic flow. During chronic or allergic inflammation, sustained expression of P-selectin on the endothelial cell surface has been observed. We found that the cytokines interleukin 4 (IL-4) or oncostatin M (OSM) induced a five- to ninefold increase in P-selectin messenger RNA (mRNA) in human umbilical vein endothelial cells (HUVEC) that persisted as long as 72 h. IL-4 elevated P-selectin mRNA by increasing its transcription rate rather than by prolonging its already long half-life. Stimulation of P-selectin transcription by IL-4 or OSM required new protein synthesis and tyrosine phosphorylation of cellular proteins. Tumor necrosis factor alpha, IL-1 beta, lipopolysaccharide, or IL-3 did not increase P-selectin mRNA in HUVEC, and did not augment the IL-4-induced increase in P-selectin transcripts. IL-4 or OSM increased P-selectin protein on the cell surface as well as in Weibel-Palade bodies. Under flow conditions, neutrophils rolled on P-selectin expressed by IL-4-treated HUVEC, and even more neutrophils rolled on P-selectin after IL-4-treated HUVEC were stimulated with histamine. These data demonstrate that IL-4 or OSM stimulates endothelial cells to synthesize more P-selectin over prolonged periods. The increased expression of P-selectin may facilitate the emigration of leukocytes into sites of chronic or allergic inflammation.

Animals↗
PubMed1996

Expression of neurotrophin trk and p75 receptors in quail embryos undergoing gastrulation and neurulation.

We have previously demonstrated the presence of mRNA for the full-length neurotrophin receptors trkA, trkB and trkC in quail embryos from stages 1 through 6 using reverse transcription followed by the polymerase chain reaction (RT-PCR; Yao et al. [1994] Dev. Biol. 165: 727-730). Furthermore, we showed that mRNA for the neurotrophins brain-derived neurotrophic factor and neurotrophin-3 was present from stage 1 onward, while nerve growth factor mRNA began to be expressed at stage 5. In the present study, wholemount in situ hybridization was used to localize full-length trk mRNA in embryos from stages 3 through 10. Structures expressing trkC mRNA included the primitive streak and Hensen's node, the neural plate or notochord, somites and the rostral neural tube. trkA and trkB mRNA were expressed at much lower levels than trkC mRNA; however, staining was detected on the primitive streak and Hensen's node. In addition to trk mRNA, we have also demonstrated the presence of full-length Trk protein in embryos from stages 3 through 11, suggesting that the trk mRNA detected at these early stages is translated into functional cell surface receptors. To support this hypothesis, we have shown that neurotrophins can induce phosphorylation of Trk on tyrosine residues, at least at stage 11. We also detected mRNA and protein for the nontyrosine kinase neurotrophin receptor, p75, at similar stages. The presence of neurotrophin receptors, as well as neurotrophin mRNA, in embryos undergoing gastrulation and neurulation leads to speculation that neurotrophins may be playing a role in these processes.

Animals↗
PubMed1996

2D locally focused MRI: applications to dynamic and spectroscopic imaging.

Conventional magnetic resonance images have uniform spatial resolution across the entire field of view. A method of creating MR images with user-specified spatial resolution along one dimension of the field of view was described recently by the authors. This paper presents the 2D generalization of this technique, which allows the user to specify arbitrary spatial resolution in arbitrary 2D regions. These images are reconstructed from signals that sparsely sample the k-space representation of the image. Therefore, locally focused images can be acquired in less time than that required by Fourier imaging with uniformaly high resolution. In this paper the authors show how to increase the temporal resolution of dynamic imaging (e.g., interventional imaging) by using high resolution in areas of expected change and lower resolution elsewhere. Alternatively, by matching the local spatial resolution to the expected edge content of the image, it is possible to avoid the localized truncation artifacts that mark Fourier images reconstructed from the same number of signals. For example, the authors show how proton spectroscopic images of the head may be improved by using high resolution in the neighborhood of scalp lipids that might otherwise cause truncation artifacts.

Brain↗
PubMed1996

Defective endothelium-dependent relaxation in fructose-hypertensive rats.

The present study examined the endothelium-dependent and -independent responses of isolated mesenteric arteries to acetylcholine and the endothelium-independent vasodilator sodium nitroprusside in mesenteric arteries from fructose-induced hypertensive rats. Fructose feeding resulted in hyperinsulinemia and elevated blood pressure when compared to controls (plasma insulin, 5.9 +/- 0.4 v control 3.6 +/- 0.4 ng/mL, P < .05; systolic blood pressure, 154 +/- 5 v control 127 +/- 7 mm Hg, P < .05). The maximum contractile response of mesenteric arteries to norepinephrine did not differ between the control and fructose groups, either with or without the endothelium. In arteries with intact endothelia, precontracted with the approximate ED50 of norepinephrine, the percent maximum relaxation produced by acetylcholine in hypertensive rats was lower than the control arteries (62 +/- 7 v control 95 +/- 5, P < .05) without any change in sensitivity. In arteries precontracted with norepinephrine, the endothelium-independent vasodilator sodium nitroprusside produced a dose-dependent relaxation in arteries obtained from control and fructose groups, both with and without the endothelium. The maximum relaxation produced by sodium nitroprusside did not differ between control and fructose arteries, either with or without the endothelium; however, removal of the endothelium caused an increase in sensitivity of this agonist. These data suggest that in the insulin resistant and hyperinsulinemic fructose-hypertensive rats, there is a defective endothelium-dependent yet preserved endothelium-independent relaxation.

Acetylcholine↗
PubMed1996

Lateral down-sloping of the acromion: a useful MR sign?

OBJECTIVE: The anterior acromion may appear to slope downward in a lateral direction on coronal-oblique magnetic resonance (MR) images of the shoulder. We sought to determine the significance of this finding as a marker of rotator cuff impingement. PATIENTS AND METHODS: MR studies of 58 subjects (26 with impingement, 32 with glenohumeral instability) were retrospectively analysed. Subjective down-sloping of the acromion was compared to standardized acromial measurements made on MR (acromial axis, width of the anterior acromion, and distance of the acromioclavicular joint from the superior glenoid) and clinical diagnosis. RESULTS: Interobserver variance for lateral down-sloping was fair (kappa = 0.5). One reader's assessment of lateral down-sloping of the acromion correlated with standardized MR measurements. Subjective lateral down-sloping of the acromion did not, however, correlate with impingement. CONCLUSION: The subjective finding of a laterally down-sloping acromion on coronal-oblique MR images, while partially validated by standardized measurements, is not predictive of impingement syndrome.

Acromion↗
PubMed1996

Tec family protein-tyrosine kinases and pleckstrin homology domains in mast cells.

Tec family protein-tyrosine kinases (PTKs) have been recognized as a distinct subfamily for only a few years. Two of them, Btk and Emt, are tyrosine-phosphorylated and enzymatically activated upon cross-linking of the high-affinity IgE receptor (Fc epsilonRI), suggesting their involvement in mast cell activation. Since Lyn and other Src family PTKs phosphorylate Btk at Tyr-551 and activate the latter kinase, the receptor-associated Lyn seems to activate Btk in mast cells. The Btk kinase activity, on the other hand, is regulated negatively by phosphorylation by protein kinase C (PKC) that is associated with Btk via Btk's pleckstrin homology (PH) domain. PH domains also bind to phospholipids and the beta subunit of heterotrimeric GTP-binding proteins. Therefore, it has been hypothesized that PH domains play roles in membrane localization.

Binding Sites↗