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Biomedical subjects

Q Chen

Publications and source records attributed to Q Chen.

At least 307 records · Page 17Linked to original sources
PubMed1999

Resolution enhancement in single-shot imaging using simultaneous acquisition of spatial harmonics (SMASH).

Spatial resolution in single-shot imaging is limited by signal attenuation due to relaxation of transverse magnetization. This effect can be reduced by minimizing acquisition times through the use of short interecho spacings. However, the minimum interecho spacing is constrained by limits on gradient switching rates, radiofrequency (RF) power deposition and RF pulse length. Recently, simultaneous acquisition of spatial harmonics (SMASH) has been introduced as a method to acquire magnetic resonance images at increased speeds using a reduced number of phase-encoding gradient steps by extracting spatial information contained in an RF coil array. In this study, it is shown that SMASH can be used to reduce the effects of relaxation, resulting in single-shot images with increased spatial resolution without increasing imaging time. After a brief theoretical discussion, two strategies to reduce signal attenuation and increase spatial resolution in single-shot imaging are introduced and their performance is evaluated in phantom studies. In vivo single-shot echoplanar imaging (EPI), BURST, and half-Fourier single-shot turbo spin-echo (HASTE) images are then presented demonstrating the practical implementation of these resolution enhancement strategies. Images acquired with SMASH show increased spatial resolution and improved image quality when compared with images obtained with the conventional acquisitions. The general principles presented for imaging with SMASH can also be applied to other partially parallel imaging techniques.

Computer Simulation↗
PubMed1999

Quantitative assessment of pulmonary perfusion with dynamic contrast-enhanced MRI.

The feasibility of qualitative assessment of pulmonary perfusion using dynamic contrast enhanced MRI with ultra-short TE has recently been demonstrated. In the current study, quantitative analysis was attempted based on the indicator dilution principle using a pig model of pulmonary embolism. The results were compared with the absolute pulmonary perfusion obtained with colored microspheres. The inverse of apparent mean transit time (1/tau(app)), distribution volume (V), and V/tau(app) were correlated well with the absolute lung perfusion. This study demonstrates that MR has the potential to evaluate pulmonary perfusion quantitatively. Magn Reson Med 42:1033-1038, 1999.

Adult↗
PubMed1999

Functional MRI of basal ganglia responsiveness to levodopa in parkinsonian rhesus monkeys.

Functional MRI (fMRI) was used to study striatal sensitivity to levodopa in hemiparkinsonian rhesus monkeys. Responses consistent with increased neuronal activity were seen in areas whose normal dopaminergic input from the substantia nigra pars compacta had been ablated by MPTP. Sites of increased activity following levodopa included the lateral putamen, the ventral region of the caudate head, septal areas, and midlateral amygdala in the MPTP-lesioned hemisphere. Increased activity was also observed in the same areas in the nonlesioned hemisphere, but was less pronounced in spatial extent and magnitude, suggesting either subclinical contralateral damage and/or functional adaptations in the contralateral dopamine systems. The increases in neuronal activity following levodopa treatment were temporally correlated with increases in striatal dopamine levels. Chronic levodopa treatment reduced behavioral responsiveness to levodopa and abolished the fMRI response. These results suggest that fMRI can detect changes in dopamine receptor-mediated neuronal sensitivity to dopaminergic agents.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1999

NMDA and non-NMDA receptor-mediated excitotoxicity are potentiated in cultured striatal neurons by prior chronic depolarization.

The excitatory input from cortex and/or thalamus to striatum appears to promote the maturation of glutamate receptors on striatal neurons, but the mechanisms by which it does so have been uncertain. To explore the possibility that the excitatory input to striatum might influence glutamate receptor maturation on striatal neurons, at least in part, by its depolarizing effect on striatal neurons, we examined the influence of chronic KCl depolarization on the development of glutamate receptor-mediated excitotoxic vulnerability and glutamate receptors in cultured striatal neurons. Dissociated striatal neurons from E17 rat embryos were cultured for 2 weeks in Barrett's medium containing either low (3 mM) or high (25 mM) KCl. The vulnerability of these neurons to NMDA receptor agonists (NMDA and quinolinic acid), non-NMDA receptor agonists (AMPA and KA), and a metabotropic glutamate receptor agonist (trans-ACPD) was examined by monitoring cell loss 24 h after a 1-h agonist exposure. We found that high-KCl rearing potentiated the cell loss observed with 500 microM NMDA or 250 microM KA and yielded cell loss with 250 microM AMPA that was not evident under low KCl rearing. In contrast, neither QA up to 5 mM nor trans-ACPD had a significant toxic effect in either KCl group. ELISA revealed that chronic high KCl doubled the abundance of NMDA NR2A/B, AMPA GluR2/3, and KA GluR5-7 receptor subunits on cultured striatal neurons and more than doubled AMPA GluR1 and GluR4 subunits, but had no effect on NMDA NR1 subunit levels. These receptor changes may contribute to the potentiation of NMDA and non-NMDA receptor-mediated excitotoxicity shown by these neurons following chronic high-KCl rearing. Our studies suggest that membrane depolarization produced by corticostriatal and/or thalamostriatal innervation may be required for maturation of glutamate receptors on striatal neurons, and such maturation may be important for expression of NMDA and non-NMDA receptor-mediated excitotoxicity by striatal neurons. Striatal cultures raised under chronically depolarized conditions may, thus, provide a more appropriate culture model to study the role of NMDA or non-NMDA receptor subtypes in excitotoxicity in striatum.

Animals↗
PubMed1999

Excitotoxic cell death dependent on inhibitory receptor activation.

Although excitotoxic cell death is usually considered a Ca(2+)-dependent process, in certain neuronal systems there is strong evidence that excitotoxic cell death is independent of Ca2+ and is instead remarkably dependent on extracellular Cl-. We have shown (in isolated chick embryo retina) that at least some of the lethal Cl- entry is through GABA and glycine receptors. Here we show that when all the GABA and glycine receptors are blocked by using an appropriate cocktail of inhibitors, agonist-induced excitotoxic cell death can be completely prevented. To determine if ligand-gated Cl- channels contribute to excitotoxic cell death in other neurons, we examined KA-induced cell death in cultured rat cerebellar granule cells. GABA receptor blockade with either a competitive or noncompetitive antagonist provides complete neuroprotection. KA stimulates Cl- uptake by the granule cells, and this is blocked by the GABA antagonists. Granule cell cultures take up [3H]GABA and release it in response to KA treatment. A subpopulation of neurons in the cultures is shown to have GAD and high concentrations of GABA, and this presumably is the source of the GABA that leads to receptor activation and lethal Cl- entry. Finally, we show that retinal cell death due to 1 h of simulated ischemia (combined oxygen and glucose deprivation) is completely prevented by blocking the inhibitory receptors. These results indicate that, paradoxically, excitotoxic cell death is completely dependent on activation of inhibitory receptors, in at least some neuronal systems, and this pathological process may contribute to disease.

Action Potentials↗
PubMed1999

Regulation of the biosynthesis of 22:5n-6 and 22:6n-3: a complex intracellular process.

Both 22:4n-6 and 22:5n-3 are synthesized from n-6 and n-3 fatty acid precursors in the endoplasmic reticulum. The synthesis of both 22:5n-6 and 22:6n-3 requires that 22:4n-6 and 22:5n-3 are metabolized, respectively, to 24:5n-6 and 24:6n-3 in the endoplasmic reticulum. These two 24-carbon acids must then move to peroxisomes for partial degradation followed by the movement of 22:5n-6 and 22:6n-3 back to the endoplasmic reticulum for use as substrates in membrane lipid biosynthesis. Clearly an understanding of the control of intracellular fatty acid movement as well as of the reactions carried out by microsomes, peroxisomes, and mitochondria are all required in order to understand not only what regulates the biosynthesis of 22:5n-6 and 22:6n-3 but also why most tissue lipids selectively accumulate 22:6n-3.

Animals↗
PubMed1999

Measurement of serum circulating intercellular adhesion molecule-1 and its clinical significance in hepatocellular carcinoma: preliminary report.

Serum circulating intercellular adhesion molecule-1 (cICAM-1) was measured in 50 patients with hepatocellular carcinoma (HCC). The mean cICAM-1 level in the 50 patients was 2220 ng/ml and 43 patients (86%) had a high level of cICAM-1 - more than 1000 ng/ml. Comparative analysis of cICAM-1 and alpha-fetoprotein (AFP) levels in the HCC patients showed that serum AFP level was negative (<20 ng/ml) in five patients or "questionable positive" (20-90 ng/ml) in ten patients, while the levels of cICAM-1 in these patients were 1810 and 1710 ng/ml, respectively. Seven patients who underwent hepatectomy had tumor recurrences during a follow-up period of 6-18 months. Their serum AFP levels were lower than 200 ng/ml (mean value, 27 ng/ml), but their mean cICAM-1 level was 1956 ng/ml at the time tumor recurrence was diagnosed. We suggest that the measurement of serum cICAM-1 is not only useful for prediction of the progression and prognosis of HCC, but that it may also be an important marker for the early diagnosis of the disease, and for monitoring postoperative recurrence, particularly in patients with low levels of serum AFP.

Adolescent↗
PubMed1999

Mechanisms of gallbladder hypomotility in pregnant guinea pigs.

BACKGROUND & AIMS: Gallbladder muscle contraction becomes impaired during pregnancy. This study was designed to investigate the mechanisms of gallbladder hypomotility induced by pregnancy in guinea pigs. METHODS: Gallbladder muscle cells were obtained by enzymatic digestion. Cell contraction was expressed as percent shortening of initial control cell length. RESULTS: Contraction induced by cholecystokinin (CCK)-8 or guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS) was reduced in muscle cells from pregnant guinea pigs. The response to KCl or D-myo-inositol 1,4, 5-trisphosphate was not different between controls and pregnant animals. These findings suggest that impaired contraction in pregnancy might be caused by defective G protein activation. The function and content of G proteins were examined by using [35S]GTPgammaS binding and G protein subunit quantitation. In female controls, CCK-8 at 1 micromol/L caused increased [35S]GTPgammaS binding to Galphai3 but not to Galphaq/11, Galphai1-2, or Galphas. GTPgammaS binding to Galphai3 induced by CCK-8 was reduced in gallbladder muscle from pregnant guinea pigs. Measurements of basal G proteins showed that the content of Galphai3 was significantly lower and the Galphas content was higher in muscles from pregnant guinea pigs than in controls. CONCLUSIONS: Pregnancy may cause down-regulation of contractile G proteins such as Galphai3 and up-regulation of Galphas that mediates relaxation, resulting in impaired gallbladder muscle contraction.

Animals↗
PubMed1999

Excess membrane cholesterol alters human gallbladder muscle contractility and membrane fluidity.

BACKGROUND & AIMS: The relationship between muscle contractility, plasma membrane cholesterol, and fluidity was investigated in human gallbladders with gallstones. METHODS: Isolated gallbladder muscle cells were used to measure contraction. Plasma membranes of gallbladder muscle were purified in a sucrose gradient and measured for cholesterol content and cholesterol/phospholipid mole ratio. Membrane fluidity was determined by using fluorescence polarization and was expressed as the reciprocal of anisotropy. RESULTS: The maximal contraction induced by cholecystokinin octapeptide was significantly less in gallbladders with cholesterol stones than in those with pigment stones. The membrane cholesterol content and cholesterol/phospholipid mole ratio were significantly higher in gallbladders with cholesterol stones than in those with pigment stones. Membrane anisotropy was also higher than in gallbladders with pigment stones, reflecting lower membrane fluidity in gallbladders with cholesterol stones. After muscle cells from cholesterol stone gallbladders were incubated with cholesterol-free liposomes for 4 hours, cholecystokinin octapeptide-induced contraction, membrane cholesterol content and cholesterol/phospholipid ratio, and membrane fluidity returned to normal levels. CONCLUSIONS: Gallbladder muscle from patients with cholesterol stones has increased membrane cholesterol/phospholipid mole ratio and decreased membrane fluidity resulting in impaired muscle contractility. These abnormalities are corrected by removing the excess cholesterol from the plasma membranes.

Cell Membrane↗
PubMed1999

Intramural mechanics of the human tongue in association with physiological deformations.

Contraction of the tongue musculature during speech and swallowing is associated with characteristic patterns of tissue deformation. In order to quantify local deformation (strain) in the human tongue, we used a non-invasive NMR tagging technique that represents tissue as discrete deforming elements. Subjects were studied with a fast gradient echo pulse sequence (TR,TE 2.3/0.8 ms, slice thickness 10 mm, and effective spatial resolution 1.3x1.3 mm). Individual elements were defined by selectively supersaturating bands of magnetic spills in resting tongue tissue along the antero-posterior and superior inferior directions of the mid-sagittal plane, resulting in a rectilinear square grid. Axial and shear strains relative to the rest condition were determined for each clement and represented by two-dimensional surface strain maps. During forward protrusion, the anterior tongue underwent positive antero posterior strain (elongation) (maximum 200%) and symmetrical negative medial lateral and superior inferior strain (contraction). During sagittal curl directed to the hard palate, the tongue exhibited positive asymmetrical antero posterior strain (maximum 160%) that increased radially as a function of distance from the center of curvature (r = 0.9216, p<0.0005), and commensurate negative strain in the medial lateral direction. Similarly, the magnitude of anterior posterior strain during left-directed tongue curl was proportional to the distance from the curved inner surface (r = O.8978, p<0.0005). We conclude that the regulation of tongue position for the motions studied was related to regional activation of the intrinsic lingual musculature.

Biomechanical Phenomena↗
PubMed1999

Apatite formation on PDMS-modified CaO-SiO2-TiO2 hybrids prepared by sol-gel process.

Dense and homogeneous monolithics of polydimethylsiloxane (PDMS)-modified CaO-SiO2-TiO2 hybrids were successfully synthesized by sol-gel process. They were assumed to be composed of a silica and titania network incorporated with PDMS and the calcium ion ionically bonded to the network. Among them, the hybrids containing relatively larger amounts of the calcium in their surfaces formed an apatite on their surfaces within only 1 or 0.5 day in a simulated body fluid with ion concentrations nearly equal to those of human flood plasma. This indicates that they are highly bioactive. Organic-inorganic hybrids synthesized by a sol-gel process usually exhibit high ductility, low elastic modulus and high mechanical strength. The present hybrids are, therefore, expected to be useful as a new kind of bone-repairing material, because of their high bioactivity and unique mechanical properties.

Apatites↗
PubMed1999

Magnetic resonance imaging of the thorax. Past, present, and future.

Magnetic resonance is a valuable modality of extreme flexibility for specific problem-solving capability in the thorax. This article reviews MR applications in the imaging of great vessels, which are currently the most important applications in the thorax; other established applications in the thorax; and pulmonary functional MR imaging.

Aortic Diseases↗
PubMed1999

Fast magnetic resonance imaging techniques.

This article reviews fast magnetic resonance (MR) techniques currently used for body imaging. Improvements in gradient performance have made very short repetition and echo times on clinical scanners feasible, thus enabling subsecond image acquisition. The article provides a fundamental overview of the technical aspects from the concept of k-space and k-space segmentation technique, fast MR imaging techniques including fast spin echo, fast gradient echo with or without magnetization preparation to echo planar and hybrid techniques. The article also addresses the use of different fat suppression techniques in MR imaging of the body and improvements in coil technology to obtain faster images and higher signal-to-noise.

Echo-Planar Imaging↗
PubMed1999

Fast magnetic resonance imaging of the lung.

The impact of fast MR techniques developed for MR imaging of the lung will soon be recognized as equivalent to the high-resolution technique in chest CT imaging. In this article, the difficulties in MR imaging posed by lung morphology and its physiological motion are briefly introduced. Then, fast MR imaging techniques to overcome the problems of lung imaging and recent applications of the fast MR techniques including pulmonary perfusion and ventilation imaging are discussed. Fast MR imaging opens a new exciting window to multi-functional MR imaging of the lung. We believe that fast MR functional imaging will play an important role in the assessment of pulmonary function and disease process.

Humans↗
PubMed1999

Magnetic resonance T2* measurements of the normal human lung in vivo with ultra-short echo times.

The objective of this study was to measure T2* values of the normal human lung in vivo during breathhold using a rapid gradient-echo sequence with ultra-short echo times (TE). A sagittal slice of the right lung was imaged in six volunteers with various TE ranging from 0.5 ms to 5 ms using a clinical 1.5 Tesla MR scanner. T2* values were calculated in a region of interest in the dependent and non-dependent lung. In the dependent lung, T2* values of 1.1 ms+/-0.15 ms were measured, and in the non-dependent lung, 0.86 ms+/-0.11 (p < 0.01). T2* measurements of the normal human lung during breathhold are feasible with a clinical MR unit. The short T2* values require the use of very short TE times (< 2.5 ms) in gradient-echo sequences to obtain adequate signal intensity from lung tissue.

Adult↗
PubMed1999

Presence of aldehydic epitopes on a minor low-density lipoprotein fraction.

A more negatively charged low-density lipoprotein (LDL), named minor LDL (mi-LDL), was separated by ionic exchange chromatography and further characterized. This mi-LDL contained lower amounts of polyunsaturated fatty acids, alpha- or gamma- tocopherol, but higher amounts of lipid hydroperoxides than the major LDL fraction (ma-LDL). We show here for the first time that apoB of mi-LDL is modified by lipid peroxidation products, such as 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA). Using polyclonal antibodies, generated against 4-HNE- or MDA-LDL and apoB, the ratio of 4-HNE- or MDA-derived epitopes to apoB of mi-LDL and ma-LDL was estimated by means of a solid phase fluorescence immunoassay. The ratio of 4-HNE-derived epitopes to apoB on mi-LDL was fourfold higher, while the ratio of MDA-derived epitopes to apoB was twofold higher, compared with the ratios obtained with ma-LDL. In a competition assay with mi- and ma-LDL, only mi-LDL was an effective competitor to inhibit the immunoreaction of anti-4-HNE-LDL with 4-HNE-LDL (by 24%) and of anti-MDA-LDL with MDA-LDL (by 10%).

Aldehydes↗
PubMed1999

Up-regulation of Fas ligand and down-regulation of Fas expression in oral carcinogenesis.

An important molecule involved in delivering the death signal that initiates apoptosis is called Fas, or Apo-1, which sits on the cell surface. When another molecule called the Fas ligand (FasL) binds to it, Fas triggers a series of events inside the cell that leads to apoptosis. In order to investigate the mechanism of immune escape and the expression of Fas and FasL in oral premalignant lesions (OPLs) and oral squamous cell carcinomas (OSCCs), a total of 64 samples were evaluated by an immunohistochemical method using a labelled streptavidin-biotin assay. These samples comprised nine hyperkeratotic and 24 oral premalignant lesions (nine of mild, moderate, and six of severe dysplastic lesions), and 24 OSCCs, together with seven healthy controls. The results demonstrated that the majority of invasive OSCCs showed down-regulation of Fas expression but up-regulation of FasL expression. These phenomena were also detected in OPLs. The results indicate that the expression of Fas and FasL is involved in oral carcinogenesis and this may be a mechanism by which the cancer cells evade the host immune assault. Perhaps, in future, Fas/FasL system may be used as a prognostic biomarker in predicting the behavior of oral premalignant lesions.

Apoptosis↗