Biomedical subjects

S J Liu

Publications and source records attributed to S J Liu.

At least 19 recordsLinked to original sources

PubMed1999

Does loss of gray- and white-matter contrast in injured spinal cord signify secondary injury? In vivo longitudinal MRI studies.

Longitudinal in vivo magnetic resonance imaging (MRI) of moderately injured rat spinal cord was performed to investigate the transient loss in gray matter (GM) and white matter (WM) contrast. In addition, neurobehavioral scores (based on open field walking, inclined plane test, and grid walking) and tissue cholesterol concentrations at pre-determined time points were measured. On MRI, a loss in contrast between GM and WM in sections 2-4 mm caudal to the site of injury was consistently observed 2 days after injury. A substantial recovery in the contrast was observed within 1 week after injury. A strong correlation between the loss of GM-WM contrast and the cholesterol concentration was also observed. The neurobehavioral scores improved with the return of the GM-WM contrast. These serial MRI studies indicate that the loss of contrast in the cord is mainly due to edema accumulated in the WM. The resolution of edema seems to occur around the same time as the restoration of cholesterol in the cord tissue. It is speculated that the compromised membrane stability due to the loss of cholesterol may be one of the factors leading to the accumulation of edema in WM.

Animals↗

PubMed1999

Bone healing of tibial lengthening is delayed by cigarette smoking: study of bone mineral density and torsional strength on rabbits.

OBJECTIVE: We investigated the effect of intermittent cigarette smoke inhalation on the bone healing of tibial lengthening in rabbits. METHODS: Twelve male rabbits were divided into two groups of six animals each. The first group underwent intermittent cigarette smoke inhalation, and the second group did not undergo intermittent cigarette smoke inhalation. Each animal's right tibia was lengthened 5 mm by using an uniplanar lengthening device. Bone mineral density (BMD) study was performed for all of the animals 1 day before operation and 3, 4, 5, and 6 weeks after operation. All of the animals were killed 6 weeks postoperatively for biomechanical testing. RESULTS: By using the preoperative BMD as an internal control, we found that the BMD of the smoke-inhalation group was decreased significantly compared with the non-smoke-inhalation group. The mean %BMD at 3, 4, 5, and 6 weeks were 49.9%, 61.2%, 65.9%, and 71.0%, respectively, in the smoke-inhalation group, whereas the mean %BMD were 54.9%, 71.8%, 76.4%, and 82.0%, respectively, in the non-smoke-inhalation group (two-tailed t test, p > 0.05, p < 0.01, p < 0.01 and p < 0.01 at 3, 4, 5, and 6 weeks, respectively). By using the contralateral nonoperated tibia as internal control, we found that torsional strength of the smoke-inhalation group was decreased significantly compared with the non-smoke-inhalation group. The mean percentage of maximal torque was 63.8% in the smoke-inhalation group, whereas the mean percentage of maximal torque was 77.1% in the non-smoke-inhalation group (two tailed t test, p < 0.01). CONCLUSION: This study suggests that cigarette smoking delays the mineralization during the bone healing process of distraction osteogenesis and, thus, decreases the mechanical strength of the regenerating bone.

Absorptiometry, Photon↗

PubMed1999

Purification, characterization, crystallization and preliminary X-ray diffraction of acuthrombin-B, a thrombin-like enzyme from Agkistrodon acutus venom.

Acuthrombin-B, a thrombin-like enzyme from Agkistrodon acutus venom, has been isolated and purified to homogeneity by ion-exchange chromatography on DEAE-Sepharose, gel filtration on Sephacryl S-100 and fast performance liquid chromatography on DEAE-8HR. The protease is an acid protein (pI 6.0) consisting of two non-identical polypeptide chains (14.4 and 16 kDa) and there is no disulfide bond between the subunits. Its molecular weight is 27 kDa as estimated by gel filtration on Sephacryl S-100. The protease has arginine-esterase activity and hydrolyzes synthetic substrates such as p-toluenesulfonyl arginine methyl ester and alpha-N-benzoyl-L-arginine amide ethyl ester, and shows clotting activity with human fibrinogen, rabbit citrated plasma and human citrated plasma in vitro. The specific activity with human fibrinogen was estimated to be 230 NIH units mg-1. The protease is considered as a serine-type protease and contains metal ion(s) to some extent, as indicated by the fact that its clotting and arginine-esterase activities could be completely inhibited by PMSF and partially inhibited by the chelating agent EDTA, while the thrombin inhibitor heparin had no effect on its clotting activity towards rabbit citrated plasma. Acuthrombin-B crystals with a resolution limit of 2.06 A were obtained by conventional hanging-drop vapour diffusion. The crystals belong to space group P21 with unit-cell parameters a = 34.97, b = 53.58, c = 67.88 A, beta = 98.89 degrees and contain one molecule per asymmetric unit.

Agkistrodon↗

PubMed1999

Suppression of beta-adrenergic responsiveness of L-type Ca2+ current by IL-1beta in rat ventricular myocytes.

The possible mechanism by which interleukin-1beta (IL-1beta) affects beta-adrenergic responsiveness of L-type Ca2+ current (ICa,L) was examined in adult rat ventricular myocytes by use of whole cell patch-clamp techniques. In the presence of isoproterenol (Iso), exposure for 3 min to IL-1beta suppressed the Iso-activated ICa,L. In the presence of IL-1beta, the response of ICa,L to Iso was decreased, and the EC50 for Iso stimulation was increased. However, IL-1beta had no effect on [3H]CGP-12177 binding, displacement of [3H]CGP-12177 binding by Iso, or on basal and Iso-enhanced cAMP content. When ICa,L was activated by extracellular application of forskolin or 8-(4-chlorophenylthio)-cAMP, a membrane-permeable cAMP analog, or by intracellular dialysis with cAMP, IL-1beta had little effect on ICa,L. In contrast, in the presence of cAMP, IL-1beta still suppressed the Iso-enhanced ICa,L. These results show that the IL-1beta-induced decrease in beta-adrenergic responsiveness of ICa,L does not result from inhibition of beta-adrenoceptor binding, adenylyl cyclase activity, or cAMP-mediated pathways, suggesting a cAMP-independent mechanism.

Animals↗

PubMed1999

Biological effects of man-made mineral fibers (I)--Reactive oxygen species production and calcium homeostasis in alveolar macrophages.

10 types of standard mineral fiber samples (JFM fibers) were tested for their cytotoxicity in alveolar macrophages (AM) in vitro experiments, in which UICC chrysotile B was used as a positive control. The cytotoxicity included the production of superoxide anion radical and hydrogen peroxide, depletion of glutathione (GSH) and increase of intracellular free calcium. The results showed that chrysotile and most of the 10 mineral fibers could increase the production of superoxide anion and hydrogen peroxide, deplete the concentration of GSH and increase the level of free intracellular Ca2+ in AM. But all the effects of JFM fibers were lower than that induced by UICC chrysotile B. Although the cytotoxicity of JFM fibers were lower than that of asbestos, these mineral fibers should be used with highly care for workers in industries.

Animals↗

PubMed1999

Development of a biodegradable antibiotic delivery system.

Antibiotic beads have been used as a drug delivery system for the treatment of various surgical infections. In this study, the copolymer 50:50 poly(DL-lactide):co-glycolide was mixed with vancomycin powder and hot compressing molded at 55 degrees C to form five types of biodegradable antibiotic beads. The beads were placed in 1 mL of phosphate buffered saline and incubated at 37 degrees C. The phosphate buffered saline was changed daily, and the removed buffer solutions were stored at -70 degrees C until the antibiotic concentration in each sample was determined by high performance liquid chromatography system assay. The concentration of vancomycin in each sample was well above the breakpoint sensitivity concentration (the antibiotic concentration at the transition point between bacterial killing and resistance to the antibiotic) for more than 32 days. The release was most marked during the first 48 hours. All copolymer 50:50 poly(DI lactide):co-glycolide biodegradable beads released high concentrations of the antibiotics in vitro for the time needed to treat bone infections (4 to 6 weeks). The diameter of the sample inhibition zone ranged from 6.5 mm to 10 mm, and the relative activity of vancomycin ranged from 12.5% to 100%. Copolymers with low heat of formation temperatures are required for making a controlled release system to prevent antibiotic decomposition, which occurs when using the hot compressing molded method. The rate and duration of release from the antibiotic beads can be adjusted by varying the diameter of the beads. This offers a convenient method to adjust the release rate to meet the specific antibiotic requirements for different patients.

Absorbable Implants↗

PubMed1998

Treatment of B-cell lymphoma with chimeric IgG and single-chain Fv antibody-interleukin-2 fusion proteins.

Anti-idiotype (Id) antibodies (Abs) have been shown to be effective in treatment of B-cell lymphoma in animal models and in clinical trials. The combination of interleukin-2 (IL-2) can augment the therapeutic effect of anti-Id Abs. To further improve the power of the combined therapy, a monoclonal anti-Id Ab, S5A8, specifically recognizing a murine B-cell lymphoma 38C13, was genetically modified to contain the IL-2 domain and thus use the unique targeting ability of Abs to direct IL-2 to the tumor site. Two forms of the anti-Id-IL-2 fusion proteins were constructed: one configuration consisting of mouse-human chimeric IgG (chS5A8-IL-2) and the other containing only the variable light (VL) and variable heavy (VH) Ab domains covalently connected by a peptide linker (scFvS5A8-IL-2). Both forms of the anti-Id-IL-2 fusion proteins retained IL-2 biological activities and were equivalent in potentiating tumor cell lysis in vitro. In contrast, the antigen-binding ability of scFvS5A8-IL-2 was 30- to 40-fold lower than that of the bivalent chS5A8-IL-2. Pharmacokinetic analysis showed that scFvS5A8-IL-2 was eliminated about 20 times faster than chS5A8-IL-2. Finally, it was shown that chS5A8-IL-2 was very proficient in inhibiting 38C13 tumor growth in vivo, more effectively than a combined therapy with anti-Id Abs and IL-2, whereas scFvS5A8-IL-2 did not show any therapeutic effect. These results demonstrate that the anti-Id-IL-2 fusion protein represents a potent reagent for treatment for B-cell lymphoma and that the intact IgG fusion protein is far more effective than its single-chain counterpart.

Adjuvants, Immunologic↗

PubMed1998

The expression of two splice variants of the Kv3.1 potassium channel gene is regulated by different signaling pathways.

The Kv3.1 potassium channel gene gives rise to two different channel proteins, Kv3.1a and Kv3.1b, by alternative splicing of nuclear RNA. During development the levels of Kv3.1b mRNA (but not Kv3.1a) substantially increase in rat cerebellum after postnatal day 8. The molecular mechanism underlying the differential regulation of the two transcripts is not known. Using in vitro slices of cerebellum, we have found that basic fibroblast growth factor (bFGF) upregulates both Kv3.1a and Kv3.1b at this developmental stage, but that depolarization by elevated potassium concentrations is without effect. Combined treatment with bFGF and depolarization, however, prevents the increase in Kv3.1a transcripts and selectively increases Kv3.1b mRNA levels. A protein kinase C (PKC) inhibitor blocks the increase in Kv3.1a mRNA levels induced by bFGF alone but does not affect the increase in Kv3.1b mRNA. Measurement of nuclear protein kinase C activity shows that bFGF activates this enzyme and that depolarization blocks this activation. In contrast to these findings at postnatal day 8, bFGF fails to alter Kv3.1 transcripts in slices from adult animals, and PKC activity is enhanced rather than suppressed by depolarization. Our results indicate that different signaling pathways regulate Kv3.1a and Kv3.1b expression and suggest that Kv3.1a mRNA levels may be modulated by neuronal activity.

Alternative Splicing↗

PubMed1998

Duplication of ATR inhibits MyoD, induces aneuploidy and eliminates radiation-induced G1 arrest.

Chromosome 3q alterations occur frequently in many types of tumours. In a genetic screen for loci present in rhabdomyosarcomas, we identified an isochromosome 3q [i(3q)], which inhibits muscle differentiation when transferred into myoblasts. The i(3q) inhibits MyoD function, resulting in a non-differentiating phenotype. Furthermore, the i(3q) induces a 'cut' phenotype, abnormal centrosome amplification, aneuploidy and loss of G1 arrest following gamma-irradiation. Testing candidate genes within this region reveals that forced expression of ataxia-telangiectasia and rad3-related (ATR) results in a phenocopy of the i(3q). Thus, genetic alteration of ATR leads to loss of differentiation as well as cell-cycle abnormalities.

Aneuploidy↗

PubMed1998

Subcellular localization and duration of mu-calpain and m-calpain activity after traumatic brain injury in the rat: a casein zymography study.

Casein zymographic assays were performed to identify changes in mu-calpain and m-calpain activity in naive, sham-injured, and injured rat cortex at 15 minutes, 3 hours, 6 hours, and 24 hours after unilateral cortical impact brain injury. Cortical samples ipsilateral and contralateral to the site of injury were separated into cytosolic and total membrane fractions. Marked increases in mu-calpain activity in cytosolic fractions in the ipsilateral cortex occurred as early as 15 minutes, became maximal at 6 hours, and decreased at 24 hours to levels observed at 15 minutes after injury. A similar temporal profile of cytosolic mu-calpain activity in the contralateral cortex was observed, although the increases in the contralateral cortex were substantially lower than those in the ipsilateral cortex. Differences were also noted between cytosolic and total membrane fractions. The detection of a shift in mu-calpain activity to the total membrane fraction first occurred at 3 hours after traumatic brain injury and became maximal at 24 hours after traumatic brain injury. This shift in mu-calpain activity between the two fractions could be due to the redistribution of mu-calpain from the cytosol to the membrane. m-Calpain activity was detected only in cytosolic fractions. m-Calpain activity in cytosolic fractions did not differ significantly between ipsilateral and contralateral cortices, and increased in both cortices from 15 minutes to 6 hours after injury. Relative magnitudes of m-calpain versus mu-calpain activity in cytosolic fractions differed at different time points after injury. These studies suggest that traumatic brain injury can activate both calpain isoforms and that calpain activity is not restricted to sites of focal contusion and cell death at the site of impact injury but may represent a more global response to injury.

Animals↗

PubMed1998

Bone healing of tibial lengthening is enhanced by hyperbaric oxygen therapy: a study of bone mineral density and torsional strength on rabbits.

We investigated the effect of intermittent hyperbaric oxygen (HBO) therapy on the bone healing of tibial lengthening in rabbits. Twelve male rabbits were divided into two groups of six animals each. The first group went through 2.5 atmospheres absolute of hyperbaric oxygenation for 2 hours daily, and the second group did not go through hyperbaric oxygenation. Each animal's right tibia was lengthened 5 mm using an uniplanar lengthening device. Bone mineral density (BMD) study was performed for all of the animals at 1 day before operation and at 3, 4, 5, and 6 weeks after operation. All of the animals were killed at 6 weeks postoperatively for biomechanical testing. Using the preoperative BMD as an internal control, we found that the BMD of the HBO group was increased significantly compared with the non HBO group. The mean %BMD at 3, 4, 5, and 6 weeks were 69.5%, 80.1%, 87.8%, and 96.9%, respectively, in HBO group, whereas the mean %BMD were 51.6%, 67.7%, 70.5%, and 79.2%, respectively, in non-HBO group (two tailed t test, p < 0.01, p < 0.01, p < 0.01, and p < 0.01 at 3, 4, 5, and 6 weeks, respectively). Using the contralateral nonoperated tibia as an internal control, we found that torsional strength of lengthened tibia of the HBO group was increased significantly compared with the non-HBO group. The mean percent of maximal torque was 88.6% in HBO group at 6 weeks, whereas the mean percent of maximal torque was 76.0% in non-HBO group (two-tailed t test, p < 0.01). The results of this study suggest that the bone healing of tibial lengthening is enhanced by intermittent hyperbaric oxygen therapy.

Absorptiometry, Photon↗

PubMed1998

Calcium-inhibitable current in cultured embryonic chick cardiac myocytes: possibly via a novel chloride channel.

The role of extracellular Ca2+ (Ca(2+)o) in the modulation of cardiac Cl- currents (I(Cl)) such as those activated by cAMP or swelling is uncertain. The effects of Ca(2+)o and extracellular cadmium (Cd(2+)o) on Cl- currents in cultured chick cardiac myocytes were investigated in Na+- and K+-free internal and external solutions using the whole-cell patch-clamp technique. In the absence of Na+ and K+ internally and externally, the whole-cell current was predominantly I(Cl). In the absence of cAMP, removal of Ca(2+)o (+ 1 mM EGTA) resulted in an increase in the current that was suppressed by reduction of Cl(o)- with a rightward shift of the zero-current potential towards the CI- reversal potential. We designated this current as a Ca2+-inhibitable I(Cl). Addition of 0.5 mM Cd(2+)o with or without removal of Ca(2+)o also resulted in a 1.5- to 2.0-fold increase in I(Cl) that was attenuated by 1 mM DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid). Under similar conditions, I(Cl) activated by Cd(2+)o (in 1 mM Ca(2+)o solution) was not further increased by subsequent removal of Ca(2+)o, suggesting that addition of Cd(2+)o and removal of Ca(2+)o activated the same I(Cl). In contrast, exposure to 1 microM forskolin further enhanced I(Cl) in the presence of Cd(2+)o. With 10 microM cAMP in the pipette solution, Ca2+-inhibitable I(Cl) could be activated in myocytes that do not possess cAMP-activated Cl- channels, indicating that activation of Ca2+-inhibitable I(Cl) does not require cAMP. In the presence of cAMP, in cells that display the cAMP-activated I(Cl), removal of Ca(2+)o resulted in a further increase in I(Cl) comparable to the Ca2+-inhibitable I(Cl). The Ca2+-inhibitable I(Cl) was minimized when pipette solutions contained 1.5 microM Ca2+. These results suggest that removal of Ca(2+)o or application of Cd(2+)o activates a Ca2+-inhibitable I(Cl) that is distinct from the cAMP-activated I(Cl).

Animals↗

PubMed1998

alpha1-Adrenergic activation of L-type Ca current in rat ventricular myocytes: perforated patch-clamp recordings.

alpha1-Adrenergic stimulation has little effect on L-type Ca2+ channel current (ICa,L) in adult cardiac myocytes measured using conventional whole cell voltage-clamp techniques. In this study using perforated-patch techniques, we reevaluated the effect of alpha1-adrenergic stimulation on ICa,L in adult rat ventricular myocytes. Action potentials and ICa,L were examined in the presence of 1 microM nadolol, a beta-adrenergic antagonist, in myocytes internally dialyzed with Na+- and K+-free solutions (Cs+ and tetraethylammonium as substitutes). Phenylephrine (PE; 30 microM) increased the action potential duration measured at 25 and 70% of repolarization by 104 and 86%, respectively. In the perforated-patch configuration, PE elicited a transient decrease followed by a approximately 60% increase in ICa,L, whereas only the transient decrease in ICa,L was observed in myocytes when the conventional whole cell configuration was used. The PE-induced increase in ICa,L was reversibly blocked by 1 microM prazosin, an alpha1-adrenergic antagonist. These results suggest that alpha1-adrenergic stimulation enhances cardiac ICa,L and that obligatory intracellular mediators for this action are lost during whole cell recordings.

Action Potentials↗

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↗