Biomedical subjects

S J Liu

Publications and source records attributed to S J Liu.

At least 55 records · Page 3Linked to original sources

PubMed1998

Stimulation of different phospholipase A2 isoforms by TNF-alpha and IL-1beta in adult rat ventricular myocytes.

We previously showed that in adult rat ventricular myocytes interleukin (IL)-1beta activates a membrane-associated, Ca2+-independent phospholipase A2 (iPLA2). In this study, we examined the possible existence of different PLA2 isoforms and effects of tumor necrosis factor (TNF)-alpha on iPLA2 activities. Western blot analysis identified iPLA2 in both membrane (approximately 82 kDa) and cytosolic (approximately 40 kDa) fractions and identified Ca2+-dependent PLA2 (cPLA2) only in cytosolic fractions. With plasmenylcholine or alkylacyl glycerophosphorylcholine as substrate, TNF-alpha elicited a twofold transient increase in cytosolic iPLA2 activity accompanied by an increase in arachidonic acid release and decreased membrane-associated iPLA2 activity with plasmenylcholine. With phosphatidylcholine as substrate, TNF-alpha decreased both cytosolic and membrane-associated iPLA2 activities. TNF-alpha-induced increases in cytosolic iPLA2 activity and arachidonic acid release were completely blocked by methyl arachidonyl fluorophosphonate (MAFP) but not by bromoenol lactone (BEL). TNF-alpha and IL-1beta together enhanced synergistically cytosolic and membrane PLA2 activities and arachidonic acid release that were blocked differentially by MAFP and BEL, respectively, and inhibited completely by MAFP plus BEL. These results suggest that TNF-alpha and IL-1beta act on different PLA2 isoforms in ventricular myocytes.

Animals↗

PubMed1997

Immunohistochemical study of calpain-mediated breakdown products to alpha-spectrin following controlled cortical impact injury in the rat.

This study examined the effect of unilateral controlled cortical impact on the appearance of calpain-mediated alpha-spectrin breakdown products (BDPs) in the rat cortex and hippocampus at various times following injury. Coronal sections were taken from animals at 15 min, 1 h, 3 h, 6 h, and 24 h after injury and immunolabeled with an antibody that recognizes calpain-mediated BDPs to alpha-spectrin (Roberts-Lewis et al., 1994). Sections from a separate group of rats were also taken at the same times and stained with hematoxylin and eosin. Analyses of early time points (15 min, 1 h, 3 h, and 6 h following injury) revealed alpha-spectrin BDPs in structurally intact neuronal soma and dendrites in cortex ipsilateral to site of injury that was not present in tissue from sham-injured control rats. By 24 h after injury labeling was not restricted to clearly defined neuronal structures in ipsilateral cortex, although there was an increased extent of diffuse labeling. BDPs to alpha-spectrin in axons were not detected until 24 h after injury, in contrast to the more rapid accumulation of BDPs observed in neuronal soma and dendrites. The presence of BDPs to alpha-spectrin in the cortex at the site of impact, and in the rostral and contralateral cortex, coincided with morphopathology detected by hematoxylin and eosin. alpha-Spectrin BDPs were also observed in the hippocampus ipsilateral to the injury in the absence of overt cell death. This investigation provides further evidence that calpain is activated after controlled cortical impact and could contribute to necrosis at the site of injury. The appearance of calpain-mediated BDPs at sites distal to the contusion site and in the hippocampus also suggests that calpain activation may precede and/or occur in the absence of extensive morphopathological changes.

Animals↗

PubMed1996

Increased expression of brain-derived neurotrophic factor but not neurotrophin-3 mRNA in rat brain after cortical impact injury.

Levels of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) mRNA expression were measured in a rodent model of traumatic brain injury (TBI) following unilateral injury to the cerebral cortex. To obtain reliable data on the co-expression of neurotrophin genes, adjacent coronal sections from the same rat brains were hybridized in situ with BDNF and NT3 cRNA probes. BDNF mRNA increased at 1,3, and 5 hr after unilateral cortical injury in the cortex ipsilateral to the injury site and bilaterally in the dorsal hippocampus. NT3 mRNA did not change significantly following injury. Our results suggest that TBI produces rapid increases in BDNF mRNA expression in rat brain without changes in NT3 mRNA expression, a finding which differs from studies of ischemia and seizures. It is possible that increased levels of BDNF mRNA rather than NT3 are important components of pathophysiological responses to TBI.

Analysis of Variance↗

PubMed1996

Characterization of an experimental spinal cord injury model using waveform and morphometric analysis.

STUDY DESIGN: A weight-drop device based on a displacement transducer and feedback detection circuitry was designed to produce consistent experimental spinal cord injuries in a rat model. The device was characterized and evaluated based on biomechanical parameters, quantitative histology, and neurologic behavior. OBJECTIVE: To develop, characterize, and evaluate a spinal cord injury device for use in animal models. SUMMARY OF BACKGROUND DATA: The biomechanical parameters of spinal cord injury, including compression, velocity, force, energy, impulse-momentum, and power, can be derived from the displacement waveform. It has been shown that the magnitude and variability of certain of these injury parameters are correlated with lesion size and neurologic deficit. METHODS: Two groups of six male Sprague-Dawley rats were injured using the device and their injury displacement waveforms digitally recorded on a personal computer equipped with a data acquisition board. Group 1 animals were sacrificed immediately after injury, whereas Group 2 animals were sacrificed 14 days after injury. Quantitative morphometric and numerical analyses were performed on histologic specimens and injury waveforms, respectively. Biomechanical injury parameters were compared with histologic and behavioral measures of injury. RESULTS: All kinetic injury parameters were reproducible to within standard deviations of less than +/- 22%, whereas spinal cord displacement variability was +/- 29%. Motor scores for animals on day 14 animals were 4.3 +/- 0.4, whereas lesion sizes were much more variable, exhibiting percent volumes of 5.5 +/- 2.5 immediately after injury, and 11.9 +/- 7.1 on day 14. CONCLUSION: This device should benefit studies of experimental spinal cord injury in animals by reducing interanimal variations in injury severity, especially in the acute phase of injury.

Animals↗

PubMed1996

Time dependence of N-acetyl-aspartate, lactate, and pyruvate concentrations following spinal cord injury.

The time dependence of N-acetyl-aspartate (NAA) concentrations relative to lactate and pyruvate in the injured rat spinal cord was investigated. Segments of spinal cord from regions rostral, caudal, and at the epicenter of the injury were analyzed. NAA concentrations were determined by gas chromatography-mass spectrometry and lactate and pyruvate concentrations were determined by UV spectroscopy at 20 min, 60 min, 2 h, 8 h, 24 h, 3 days, and 1 week after injury. NAA levels fell most significantly at the epicenter of the injury, reaching 30% of basal levels within 24 h. In all segments, lactate levels increased significantly shortly after injury, peaking at two to five times normal basal levels between 20 and 60 min after injury. Rostral and caudal to the injury site, lactate elevations and NAA reductions were less dramatic. Pyruvate concentrations were not significantly altered in any of the sections after injury. The temporal and spatial relationships of NAA and lactate changes indicated that ischemic conditions due to injury in the upper thoracic rat spinal cord were distributed asymmetrically. Acute ischemia was more severely caudal to the injury site, and NAA concentrations were more severely impaired in the rostral direction. The results suggest that the extent of neuronal degeneration due to spinal cord injury does not correlate directly with acute ischemic severity as measured by the lactate/pyruvate ratio, and may be more closely related to secondary changes in the neuronal environment.

Animals↗

PubMed1996

mu-calpain activation and calpain-mediated cytoskeletal proteolysis following traumatic brain injury.

Increasing evidence suggests that excessive activation of the calcium-activated neutral protease mu-calpain could play a major role in calcium-mediated neuronal degeneration after acute brain injuries. To further investigate the changes of the in vivo activity of mu-calpain after unilateral cortical impact injury in vivo, the ratio of the 76-kDa activated isoform of mu-calpain to its 80-kDa precursor was measured by western blotting. This mu-calpain activation ratio increased to threefold in the pellet of cortical samples ipsilateral to the injury site at 15 min, 1 h, 3 h, and 6 h after injury and returned to control levels at 24-48 h after injury. We also investigated the effect of mu-calpain activation on proteolysis of the neuronal cytoskeletal protein alpha-spectrin. Immunoreactivity for alpha-spectrin breakdown products was detectable within 15 min after injury in cortical samples ipsilateral to the injury site. The levels of alpha-spectrin breakdown products increased in a biphasic manner, with a large increase between 15 min and 6 h after injury, followed by a smaller increase between 6 and 24 h after the insult. No further accumulation of alpha-spectrin breakdown products was observed between 24 and 48 h after injury. Histopathological examinations using hematoxylin and eosin staining demonstrated dark, shrunken neurons within 15 min after traumatic brain injury. No evidence of mu-calpain autolysis, calpain-mediated alpha-spectrin degradation, or hematoxylin and eosin neuronal pathology was detected in the contralateral cortex. Although mu-calpain autolysis and cytoskeletal proteolysis occurred concurrently with early morphological alterations, evidence of calpain-mediated proteolysis preceded the full expression of evolutionary histopathological changes. Our results indicate that rapid and persistent mu-calpain activation plays an important role in cortical neuronal degeneration after traumatic brain injury. Our data also suggest that specific inhibitors of calpain could be potential therapeutic agents for the treatment of traumatic brain injury in vivo.

Analysis of Variance↗

PubMed1996

Cytoskeletal derangements of cortical neuronal processes three hours after traumatic brain injury in rats: an immunofluorescence study.

Semiquantitative Western blot analyses have shown that traumatic brain injury (TBI) can produce significant loss of cytoskeletal proteins (neurofilament 68 [NF68], neurofilament 200 [NF200] and microtubule associated protein 2 [MAP2]) possibly by calpain-mediated proteolysis. Thus, we employed immunofluorescence (light and confocal microscopy) to study the histopathological correlates of acute neurofilament and MAP2 protein decreases observed 3 hours following unilateral cortical injury in rats. TBI induced dramatic alterations in NF68, NF200, and MAP2 immunolabeling in dendrites within and beyond contusion sites ipsilateral and contralateral to the injury site. Marked changes in immunolabeling were associated with but not exclusively restricted to regions of dark shrunken neurons labeled by hematoxylin and eosin staining, a morphopathological response to injury suggesting impending cell death. Light microscopic studies of NF200 immunofluorescence revealed a prominent fragmented appearance of apical dendrites of pyramidal neurons within layers 3 and 5, as well as a loss of fine dendritic arborization within layer 1. Confocal microscopy detected varying degrees of NF200 disassembly associated with these areas of neurofilament fragmentation. Light microscopic studies of NF68 immunofluorescence detected subtle and less severe structural changes including smaller breaks and focal vacuolization of apical dendrites. Light microscopic immunofluorescence of MAP2 revealed changes similar to those seen for NF200. Acute axonal alterations detected with NF68 were minimal compared to immunofluorescence changes seen in dendritic regions. Therefore, preferential dendritic cytoskeletal derangements may be an early morphological feature of experimental traumatic brain injury in vivo. In addition, these cytoskeletal derangements may not be exclusively restricted to sites of contusion and cell death.

Animals↗

PubMed1996

[Clinical study on treatment of chemo- or radiotherapy induced leukopenia with fuzheng compound].

The therapeutic effect of Fuzhen Compound, a Chinese herbal medicine, on leukocyte count in 59 patients with cancer of advanced stage after chemo-or radiotherapy were observed. Among 41 cases with leukopenia before treatment, leukocyte of 37 cases were normalized after treatment, the count pre-and post-treatment were (2.8 +/- 0.6) x 10(9)/L and (5.9 +/- 1.4) x 10(9)/L respectively (P < 0.01). In 18 patients with normal leukocyte count before treatment, the counts of 17 cases were still kept in normal after treatment. The time for leukcoyte recovering was 8.0 days in average, while that of 23 patients did not take Fuzhen Compound was 20.6 +/- 1.8 days. The results indicated that the Fuzhen Compound could alleviate the inhibition of chemo-or radiotherapy on hemopoietic function of bone marrow and has leukocytogenic effect.

Adult↗

PubMed1995

Autonomic and central nervous system effects of lead in female glass workers in China.

To clarify the effects of lead on autonomic and central nervous system functions, electrocardiographic R-R interval variability (CVRR) as well as visual and brainstem auditory evoked potentials (VEP and BAEP) were measured in 36 female workers exposed to lead (exposed group) and in 15 female textile workers (unexposed group). The C-CVLF, C-CVHF (two component CVs of the CVRR reflecting sympathetic and parasympathetic activities, respectively), and LF/HF ratio (indicator of sympatho-vagal balance) were also computed from component spectral powers by means of autoregressive spectral and component analyses. The exposed group had engaged in glass work for 2-17 (mean 7.8) years. Blood lead (BPb) concentrations were 25.8-79.3 (mean 55.6) micrograms/dl in the exposed group and 4.7-8.6 (mean 6.3) micrograms/dl in the unexposed group. The CVRR, C-CVLF, C-CVHF, and LF/HF ratio in the exposed group were significantly lower than those in the unexposed group. Also, the exposed group had more complaints of subjective symptoms and signs than did the unexposed group. On the other hand, no significant differences in either VEP or BAEP latencies were found between the two groups. It is suggested that autonomic nervous function is more susceptible to lead than visual and auditory nervous functions; lead affects sympathetic activity more strongly than parasympathetic activity.

Adult↗

PubMed1995

Microcomputer-based pulse stimulator.

A low-cost PC-based 2-channel stimulator was designed. This device can generate regular current pulses for many neuroscience experiments. It can also generate irregular pulses for nerve stimulation, thus could possibly avoid the problem of sensitization or habituation in the central nervous system. The stimulation frequency (can be < 0.0005 Hz) and pulse duration (5 microseconds to 65 ms) of this device can be programmed by an interactive user interface. Furthermore, the output current (0-10 mA) can be continuously varied and was optically isolated to minimize stimulus artifact. Moreover, features such as low-power consumption (0.2 mA of a 9 V battery) and high-compliance output (> 120 V) could accommodate the stimulator for widespread applications. A trial of nerve stimulation was illustrated besides the electrical specifications of the stimulator.

Electric Stimulation↗

PubMed1995

Time course of increased vulnerability of cholinergic neurotransmission following traumatic brain injury in the rat.

We have previously shown that spatial memory changes following experimental traumatic brain injury (TBI) include long-term changes that are (1) 'overt': detected by routine behavioral assessments, or (2) 'covert': undetected in the absence of a secondary pharmacological challenge, such as by the cholinergic antagonist, scopolamine. Our objective in this study was to extend this finding by characterizing the time course of recovery of overt and covert spatial memory performance following two magnitudes of experimental TBI. The Morris water maze was used to assess cognitive performance. Rats received either moderate magnitude (6 m/s, 1.77 mm deformation) or low magnitude (6 m/s, 1 mm deformation) impacts through a lateral craniectomy under isoflurane anesthesia. Sham rats underwent identical surgical procedures but were not injured. To avoid motor deficits, water maze testing started two weeks post-injury. Rats were given four trials per day for seven consecutive days. For each trial, latency to find a hidden platform was timed. On the sixth, rats were injected (i.p.) with scopolamine (1 mg/kg) 15 min prior to maze testing. The next day, rats were retested. This testing regimen was repeated, beginning 4, 6, and 10 weeks post-TBI. Results showed that, while the low-magnitude injury produced no overt spatial memory deficits, the moderate-magnitude group exhibited overt deficits during the first test regimen. Also, while both injury magnitudes produced an enhanced sensitivity to spatial memory impairment by scopolamine at two weeks post-TBI, this covert deficit persisted only in the severe group at 4, 6, and 10 weeks post-TBI. Qualitative light microscopy showed that both injury groups had graded cortical necrosis. However, underlying subcortical structures such as the hippocampus appeared intact, with no overt cellular or parenchymal damage to the neuropil. These data suggest three distinct stages of functional recovery: (1) the initial period when overt deficits are present, (2) a period following recovery from overt deficits within which covert deficits can be reinstated by a pharmacological challenge, and (3) a period following recovery from both overt and covert deficits. Covert deficits can persist long after the recovery of overt deficits and, like other neurological deficits, the rate of recovery is dependent on the magnitude of TBI. Finally, spatial memory deficits can occur in the absence of light microscopic evidence of cell death in the hippocampus.

Acetylcholine↗

PubMed1995

Intracellular mediators regulate CD2 lateral diffusion and cytoplasmic Ca2+ mobilization upon CD2-mediated T cell activation.

CD2 is a T cell surface glycoprotein that participates in T cell adhesion and activation. These processes are dynamically interrelated, in that T cell activation regulates the strength of CD2-mediated T cell adhesion. The lateral redistribution of CD2 and its ligand CD58 (LFA-3) in T cell and target membranes, respectively, has also been shown to affect cellular adhesion strength. We have used the fluorescence photobleaching recovery technique to measure the lateral mobility of CD2 in plasma membranes of resting and activated Jurkat T leukemia cells. CD2-mediated T cell activation caused lateral immobilization of 90% of cell surface CD2 molecules. Depleting cells of cytoplasmic Ca2+, loading cells with dibutyric cAMP, and disrupting cellular microfilaments each partially reversed the effect of CD2-mediated activation on the lateral mobility of CD2. These intracellular mediators apparently influence the same signal transduction pathways, because the effects of the mediators on CD2 lateral mobility were not additive. In separate experiments, activation-associated cytoplasmic Ca2+ mobilization was found to require microfilament integrity and to be negatively regulated by cAMP. By directly or indirectly controlling CD2 lateral diffusion and cell surface distribution, cytoplasmic Ca2+ mobilization may have an important regulatory role in CD2 mediated T cell adhesion.

Actin Cytoskeleton↗

PubMed1994

Quantitative MRI of spinal cord injury in a rat model.

Sequential in vivo MRI studies of experimental spinal cord injuries (SCI) were performed using a three-dimensional implementation of the FATE (Fast low-Angle spin echo sequence with short TE) sequence. MRI-observed pathology was quantified using a multispectral segmentation algorithm. Neurological analysis was performed on the same animals concurrently, in addition to end-point histology, for comparison with quantitative MRI results. These studies suggest that it is possible to use MRI to detect the onset of secondary injury in the spinal cord. The data also indicate that early detection of MRI-visible pathology may provide the necessary markers for predicting the long-term level of neurologic deficit.

Algorithms↗

PubMed1994

Exposure of workers to a mixture of toluene and xylenes. II. Effects.

The health effects of exposure to a mixture of toluene and xylene isomers was studied on the fourth or fifth days of a working week in factories in China. The study population comprised 233 subjects (122 men and 111 women), who were exposed to the time weighted geometric mean (maximum) concentrations of toluene (3 (203) ppm) and xylenes (4 (103) ppm). For comparison, 241 non-exposed controls (116 men and 125 women) were recruited from the same regions. The prevalence of some subjective symptoms significantly increased in the exposed population, and the symptom profiles were similar to those found after exposure to toluene or xylenes alone. Haematology and serum biochemistry did not show notable changes. It seems reasonable to conclude that the effects of the toxicities of toluene and xylenes in combination are additive.

Adult↗

PubMed1994

[Studies on generation and inhibition of active oxygen in alveolar macrophage by chrysolite and aluminum citrate].

Chrysolite-induced generation and aluminum citrate-induced inhibition of active oxygen in alveolar macrophage were studied with ESR spin-trapping technique, cytochrome C reduction and phenol red oxidation assays. Results showed, under certain conditions, Mangya and Laiyuan chrysolite fiber could stimulate macrophage to generate OH., O2-. and H2O2 in a dose-dependent manner. But such an induced-generation of active oxygen would be inhibited by the treatment of chrysolite with aluminum citrate solution at room temperature for one hour.

Animals↗

PubMed1994

[Effects of chrysotile on the conformation of membrane protein and the antagonistic action of aluminum citrate].

Effects of Mangai and Laiyuan chrysotile on the conformation of membrane protein and the antagonistic action of aluminum citrate to them were studied with circular dichroism. Results showed that these two kinds of chrysotile could significantly reduce the amount of alpha-helix in membrane protein of human erythrocytes in 20 minutes with a dose-dependent manner. Effect of Mangai chrysotile was stronger than that of Laiyuan one. It suggested the changes in the conformation of membrane protein were the key link in chrysotile-caused hemolysis. After treatment with aluminum citrate, these effects weakened. It provided important information for elucidating the mechanism of aluminum citrate in antagonism to cytotoxicity of chrysotile.

Asbestos, Serpentine↗

PubMed1994

[Changes of cellular hydroxyl proline and some other parameters of rats in early bronchoalveolar lavage treated with quartz dust].

The changes of cellular hydroxyl proline (Hyp) and some other parameters in bronchoalveolar lavage (BAL) induced by different doses of quartz dust (5, 10, 20, or 40mg/per rat) were studied. Quartz dust was administered intratracheally and the rats were killed two weeks after quartz administration. The results showed that the differential count of polymorphonuclear leukocytes (PMN) in BAL, the concentrations of Hyp and total lipids in BAL cells, and the levels of total lipids, total protein, lactic dehydrogenase (LDH) and ceruloplasmin in BAL supernatant all changed significantly in quartz treated groups compared with the control group. Further investigation revealed that the cellular Hyp correlated best with total lung collagen (r = 0.834). This indicated that Hyp might be a specific and important parameter reflecting early increase of total lung collagen after quartz dust administration.

Animals↗

PubMed1994

Fibula osteoseptocutaneous flap for reconstruction of composite mandibular defects.

The fibula osteoseptocutaneous flap is a versatile method for reconstruction of composite-tissue defects of the mandible. The vascularized fibula can be osteotomized to permit contouring of any mandibular defect. The skin flap is reliable and can be used to resurface intraoral, extraoral, or both intraoral and extraoral defects. Twenty-seven fibula osteoseptocutaneous flaps were used for composite mandibular reconstructions in 25 patients. All the defects were reconstructed primarily following resection of oral cancers (23), excision of radiation-induced osteonecrotic lesions (2), excision of a chronic osteomyelitic lesion (1), or postinfective mandibular hypoplasia (1). The mandibular defects were between 6 and 14 cm in length. The number of fibular osteotomy sites ranged from one to three. All patients had associated soft-tissue losses. Six of the reconstructions had only oral lining defects, and 1 had only an external facial defect, while 18 had both lining and skin defects. Five patients used the skin portion of the fibula osteoseptocutaneous flaps for both oral lining and external facial reconstruction, while 13 patients required a second simultaneous free skin or musculocutaneous flap because of the size of the defects. Four of these flaps used the distal runoff of the peroneal pedicles as the recipient vessels. There was one total flap failure (96.3 percent success). There were no instances of isolated partial or complete skin necrosis. All osteotomy sites healed primarily. The contour of the mandibles was good to excellent.

Adult↗