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J P Wu

Publications and source records attributed to J P Wu.

At least 19 recordsLinked to original sources
PubMed2006

Characterization of metallothioneins (MT-I and MT-II) in the yak.

The cDNA-encoding sequences for yak metallothionein isoforms I (MT-I) and II (MT-II) were amplified and cloned by reverse-transcription PCR to characterize the nucleotide sequence and protein structure of metallothionein in the yak. The cDNA sequences of MT-I and MT-II were subjected to BLAST searching at the National Center for Biotechnology Information, and the results indicated that the nucleotide sequences of yak MT-I and MT-II, when compared among different species of mammals, are highly conserved. The yak open reading frames have a length of 183 nucleotides, which encode for yak MT-I and MT-II proteins of 61 AA, respectively. Analysis of hydrophobicity, trans-membrane region, and signal peptides suggested that metallothioneins of the yak are nonsecretory proteins. There were several conserved tripeptide sequences, such as C-X-C, C-C-X-C-C, and C-X-X-C (X designates AA excluding cysteine in MT-I and MT-II), and they are highly conserved in their evolution. By homologous comparative modeling, we predicted the molecular spatial structures of yak MT-I and MT-II, which are composed of alpha- and beta-domains that are linked by the conserved tripeptide Lys(30)-Lys(31)-Ser(32) (KKS).

Amino Acid Sequence↗
PubMed2001

Expression of neural cell adhesion molecule in spinal cords following a complete transection.

Neural cell adhesion molecule (NCAM) regulates tissue organization during development and in the adult. NCAM upregulation occurs after an injury to brains and sciatic nerves. However, little is known about NCAM expression after spinal cord injury (SCI). By using a complete spinal cord transection with a 5 mm tissue removal, an increase in the NCAM level is detected in spinal cord stumps proximal and distal to the transection site at 1 d and 3 d post injury, while its expression at 8 d is declined to a lower level than that observed in sham-operated spinal cords. The strong NCAM expression is present in motor neurons at 3 d post transection whereas the intensive NCAM immunostaining is localized in dorsal sensory and corticospinal fiber tracts at 8 d following injury. Collectively, NCAM level is elevated and strongly expressed in dorsal fiber tracts after SCI, implying that the endogenous process for spinal cord regeneration may take place after SCI.

Animals↗
PubMed2000

Tumor necrosis factor-alpha modulates the proliferation of neural progenitors in the subventricular/ventricular zone of adult rat brain.

Little is known about the response of neural progenitors to inflammation following injuries of the central nervous system. In combination with bromodeoxyuridine (BrdU) intraperitoneally (i.p.) injected, tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine that increased ED1+ activated microglia/macrophage population at injured sites, was administrated into adult rat brains. No difference in the immunostaining for proliferating cell nuclear antigen (PCNA) was observed in the subventricular/ventricular zone (SVZ/VZ) between TNF-alpha injected sites and controls. However, BrdU+ cells were apparently observed in the SVZ/VZ proximal to TNF-alpha injected site, and the number of BrdU+ cells increased at 6 and 24 h post injection. Since cell apoptosis was rarely found in the SVZ/VZ after TNF-alpha injection, these observations suggest that the diffusible TNF-alpha may directly and/or indirectly modulate the proliferation of neural progenitors.

Animals↗
PubMed2000

Microstimulation-induced inhibition of neuronal firing in human globus pallidus.

Neurosurgical treatment of Parkinson's disease (PD) frequently employs chronic high-frequency deep brain stimulation (DBS) within the internal segment of globus pallidus (GPi) and can very effectively reduce L-dopa-induced dyskinesias and bradykinesia, but the mechanisms are unknown. The present study examined the effects of microstimulation in GPi on the activity of neurons close to the stimulation site. Recordings were made from GPi using two fixed or independently controlled microelectrodes, with the electrode tips usually approximately 250 or >600 micrometer apart in PD patients undergoing stereotactic exploration to localize the optimal site for placement of a lesion or DBS electrode. The spontaneous activity of nearly all of the cells (22/23) recorded in GPi in three patients was inhibited by microstimulation at currents typically <10 microA (0.15-ms pulses at 5 Hz). The inhibition had a duration of 10-25 ms at threshold. These findings suggest that microstimulation within GPi preferentially excites the axon terminals of striatal and/or external pallidal neurons causing release of GABA and inhibition of GPi neurons.

Action Potentials↗
PubMed2000

Tetrandrine inhibits inward rectifying potassium current in cultured bovine aortic endothelial cells.

AIM: To study the effect of tetrandrine (Tet) on inward rectifying potassium current in cultured bovine aortic endothelial cells. METHODS: Inward rectifying potassium current (IRK) was observed by the whole cell patch-clamp technique. RESULTS: IRK was inhibited by Tet in a concentration-dependent manner and recovered to normal after wash with drug-free external solution. IRK was reduced from (582 +/- 48) pA to (221 +/- 40) pA at a holding potential of -70 mV by Tet 30 mumol/L. IC50 was 2.8 mumol/L. CONCLUSION: Tet inhibited inward rectifying potassium current in cultured bovine aortic endothelial cells.

Alkaloids↗
PubMed1999

Responses of microglia and neural progenitors to mechanical brain injury.

Neural cells have distinct responses to CNS injury; however, neural progenitor response to CNS injury is not yet documented. Stab injury combined with injection of bromodeoxyuridine (BrdU), a thymidine analog, into adult rat cortex above the lateral ventricle for 10 min resulted in activated microglia/macrophage infiltration along with nuclear factor kappa B (NF kappa B)/p65 activation at the lesion site. Most NF kappa B/p65+ cells displayed a phagocytic morphology. Under these conditions, profound cell apoptosis took place in the injured corpus callosum, but not in the subventricular/ventricular zone (SVZ/VZ). The SVZ/VZ-derived neural progenitors in both injected and non-injected contralateral hemispheres showed strong BrdU immunostaining, indicating that SVZ/VZ-derived neural progenitors of both hemispheres may undergo DNA synthesis in response to unilateral brain injury.

Animals↗
PubMed1999

Brainstem projections to the ventromedial medulla in cat: retrograde transport horseradish peroxidase and immunohistochemical studies.

Stimulation of the nucleus magnocellularis (NMC) of the medulla produces changes in locomotion, muscle tone, heart rate, and blood pressure. Glutamatergic input has been found to modulate muscle tone, whereas cholinergic input has been found to mediate cardiovascular changes produced by stimulation of the NMC. The current study was designed to identify the brainstem afferents to NMC by using retrograde transport of wheat germ agglutinin and horseradish peroxidase (WGA-HRP) combined with glutamate and choline acetyltransferase (ChAT) immunohistochemical and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemical techniques. Fifty nanoliters of 2.5% WGA-HRP were microinjected into the NMC in the cat. A heavy density of WGA-HRP-labeled neurons was found in the ipsilateral mesencephalic reticular formation (MRF), periaqueductal gray, Kolliker-Fuse nucleus, and pontis centralis caudalis (PoC), in the contralateral pontis centralis oralis (PoO), and bilaterally in the nucleus paragigantocellularis lateralis. A moderate density of retrogradely labeled neurons was found in the ipsilateral side of the nuclei parvocellularis, retrorubral (RRN), PoO, and vestibular complex, in the contralateral PoC and nucleus gigantocellularis, and bilaterally in the inferior vestibular nucleus. Retrograde HRP/glutamate-positive cells could be found throughout the brainstem, with a high percentage in RRN, PoO, PoC, and MRF. Double-labeled WGA-HRP/ChAT neurons were found in the pedunculopontine nucleus. Double-labeled WGA-HRP/NADPH-d-positive neurons could be seen in many nuclei of the brainstem, although the number of labeled neurons was small. The dense glutamatergic projections to the NMC support the hypothesis that rostral brainstem glutamatergic mechanisms regulate muscle activity and locomotor coordination via the NMC, whereas the pontine cholinergic projections to the NMC participate in cardiovascular regulation.

Animals↗
PubMed1999

Neurotoxic N-methyl-D-aspartate lesion of the ventral midbrain and mesopontine junction alters sleep-wake organization.

The dorsal regions of the midbrain and pons have been found to participate in sleep regulation. However, the physiological role of the ventral brainstem in sleep regulation remains unclear. We used N-methyl-D-aspartate-induced lesions of the ventral midbrain and pons to address this question. Unlike dorsal mesencephalic reticular formation lesions, which produce somnolence and electroencephalogram synchronization, we found that ventral midbrain lesions produce insomnia and hyperactivity. Marked increases in waking and decreases in slow wave sleep stage 1 (S1), stage 2 (S2) and rapid eye movement sleep were found immediately after the lesion. Sleep gradually increased, but never returned to baseline levels (baseline/month 1 post-lesion: waking, 30.6 +/- 4.58%/62.3 +/- 10.1%; S1, 5.1 +/- 0.74/3.9 +/- 1.91%; S2, 46.2 +/- 4.74%/23.1 +/- 5.47%; rapid eye movement sleep, 14.1 +/- 3.15%/7.2 +/- 5.42%). These changes are comparable in magnitude to those seen after basal forebrain lesions. Neuronal degeneration was found in the ventral rostral pons and midbrain, including the substantia nigra, ventral tegmental area, retrorubral nucleus, and ventral mesencephalic and rostroventral pontine reticular formation. We conclude that nuclei within the ventral mesencephalon and rostroventral pons play an important role in sleep regulation.

Animals↗
PubMed1998

Ferrous ion diminished the antiarrhythmic effect of naloxone in myocardial ischemia of isolated rat hearts.

This investigation was to examine the effect of ferrous ion (a prooxidant) on the antiarrhythmic effect of naloxone (an endogenous opioid receptor antagonist) in isolated rat hearts. Isolated Sprague-Dawley rat hearts were perfused in the Langendorff mode and myocardial ischemia was performed by ligating the left descending coronary artery. Cardiac rhythm was recorded. Heart alpha-tocopherol concentrations were analyzed. Naloxone (1.2 micromol/heart) was effective in reducing the severity of arrhythmia (arrhythmia score; mean+/-S.E.M: 2.82+/-0.69 for naloxone vs. 5.18+/-0.38 for control, p<0.01). Fe2+ (100 nmol/heart) alone did not significantly affect the arrhythmia score (5.63+/-0.32) when compared with the control, however, Fe2+ administration did cause significant early onset of ventricular premature contraction and ventricular tachycardia. Additionally, Fe2+ administration diminished the naloxone's antiarrhythmic effect (arrhythmia score 4.12+/-0.40). Alpha-tocopherol, a major free radical scavenger that exerts protective functions on heart tissues during myocardial ischemia/reperfusion, was significantly higher in the naloxone-treated group (59.05+/-3.00 nmol/g wet wt) than in the control group (43.84+/-4.17 nmol/g wet wt, p<0.05). These results suggest that endogenous opioid peptides and reactive oxygen species might be related to ischemia-induced arrhythmia.

Analysis of Variance↗
PubMed1998

Quantitative study of Stewart-Holmes test.

Stewart-Homes test (SHT) is an ordinary neurological test performed for the diagnosis for cerebellar disease. We developed a quantitative method based on SHT carried out on the upper limb. Nineteen cerebellar patients and fifteen volunteer healthy subjects were tested. During the test, acceleration of forearm and two associated surface EMGs over biceps and triceps brachialis were recorded and analyzed. (1) Acceleration curve showed an oscillating pattern with flexion and extension over the elbow in both groups, but in cerebellar patient group, the acceleration oscillation wave was more pronounced and latencies of peak acceleration were significantly longer. (2) Correspondingly, the EMGs timing parameters were also different between the two groups: in patient group, ceasing isometric biceps contraction was delayed; rebound EMGs bursts over both biceps and triceps were prolonged. (3) Modelization of the oscillation of acceleration curve with dampened oscillation model showed that in patient group the oscillating amplitude attenuated much more slowly than in control group. A standard curve was established for detecting the acceleration profile abnormalities of SHT in cerebellar patients.

Adult↗
PubMed1997

Evaluation of extracellular lipid peroxidation in brain cortex of anaesthetized rats by microdialysis perfusion and high-performance liquid chromatography with fluorimetric detection.

A method for in vivo evaluation of lipid peroxidation in the extracellular space of anaesthetized rat brain cortex was developed. This method involved the use of microdialysis perfusion and high-performance liquid chromatography. The microdialysates, eluted from implanted probes, were reacted with thiobarbituric acid (TBA) prior to analysis by an HPLC system equipped with a fluorescence detector (excitation and emission wavelengths were 515 and 550 nm, respectively). Lipid peroxidation in the extracellular space was evaluated as the concentration of malondialdehyde, a lipid peroxidation end product which reacts with TBA to form a fluorescent conjugate. Significantly increased production of malondialdehyde following hydrogen peroxide perfusion (0.03%, 0.3% at a flow-rate of 1 microl/min) was observed in the brain cortex of anaesthetized rats.

Anesthesia↗
PubMed1996

In vivo, continuous and automatic monitoring of extracellular ascorbic acid by microdialysis and on-line liquid chromatography.

A system for in vivo, automatic, continuous monitoring of organ extracellular ascorbic acid in anesthetized rat is described. This system involves microdialysis perfusion and a LC system equipped with an electrochemical detector. Microdialysate, eluted from a microdialysis probe implanted in the brain cortex or in the left ventricular myocardium of anesthetized rats was collected in the sample loop of an on-line injector for direct injection onto the LC system. This automated method provides a shortened sample processing time. This system was utilized to investigate the effect of cerebral ischemia on cortex extracellular ascorbic acid and the effect of myocardial ischemia on left ventricular myocardium extracellular ascorbic acid in anesthetized rats. Basal ascorbic acid concentrations in the cortex and left ventricular myocardium ranged from 9.7 to 15.4 microM (mean +/- S.D., 12.7 +/- 2.5 microM from the results of eight rats) and from 9.3 to 36.0 microM (mean +/- S.D., 24.3 +/- 8.9 microM from the results of twelve rats), respectively. Cerebral ischemia significantly elevated ascorbic acid levels in the cortex extracellular space, while myocardial ischemia did not significantly alter ascorbic acid levels in the left ventricular myocardium extracellular space.

Animals↗
PubMed1994

[24-hour electroencephalography monitoring in children: analysis of 403 cases].

24-hour EEG monitoring was performed in 403 children with repeated seizure of various types. The positive rate was 82.7% for defined epilepsy. Epileptic discharges mainly occurred in NREM stage and focal discharges accounted for 69%. More than 70% of the children suspected of epilepsy were excluded from epileptic seizures. 24-hour EEG monitoring is of significant value in determining seizure characteristics, epilepsy types, the relations between epilepsy and sleep and between clinical seizures and EEGs.

Adolescent↗
PubMed1993

Opioids in myocardial ischaemia: potentiating effects of dynorphin on ischaemic arrhythmia, bradycardia and cardiogenic shock following coronary artery occlusion in the rat.

The endogenous opioid peptide (EOP) dynorphin and opioid receptors have been found in the heart. This opioid system plays important roles in cardiovascular regulation and is involved in the pathophysiology of shock, heart failure and myocardial ischaemia. The aim of this study was to evaluate whether the EOP dynorphin modulates or potentiates ischaemia-induced arrhythmias and whether its effects are prevented by the opiate antagonist naloxone. Following coronary artery occlusion, all rats in the control group developed ischaemia-induced arrhythmias, bradycardia and hypotension, which were significantly potentiated by pre-treatment with dynorphin and attenuated by treatment with naloxone. The results clearly indicate that EOPs may be released when myocardial ischaemia occurs, thus causing arrhythmias, bradycardia and hypotension. Dynorphin and naloxone, by virtue of their opioid agonistic and antagonistic actions, respectively, potentiate and attenuate these fatal complications secondary to myocardial ischaemia. This suggests that EOPs play an important part in ischaemic heart disease.

Animals↗
PubMed1993

Beneficial effects of the opiate antagonist naloxone on hemodynamics and ventricular function following coronary artery occlusion and reperfusion in the dog.

It has been shown that endogenous opioid peptides (EOP) subserve important roles in cardiovascular regulation and are involved in the pathophysiology of myocardial ischemia, contributing to the deleterious effects. The aim of this study was to evaluate the effects of the opiate antagonist naloxone on the hemodynamics and ventricular function following coronary artery occlusion and reperfusion in the dog, utilizing the technique of cardiac catheterization. During myocardial ischemia and reperfusion, it was found that in the control group, there was reduction in the aortic, left ventricular, right atrial, pulmonary arterial and wedge pressures, and in the left ventricular dP/dt. The reduction in the aortic, left ventricular and pulmonary arterial pressures, and left ventricular dP/dt were significantly attenuated by pretreatment with naloxone. The results indicate a regulatory role of EOP in the cardiovascular function and suggest a possible involvement of EOP in myocardial ischemia and reperfusion causing detrimental effects such as arrhythmias, bradycardia, hypotension and, as shown in this study, impaired hemodynamics and ventricular function. The beneficial effects of naloxone on circulatory dynamics may have clinical implications in the prevention and treatment of ischemic heart disease.

Animals↗