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W Fu

Publications and source records attributed to W Fu.

At least 73 records · Page 4Linked to original sources
PubMed1998

Catecholamines potentiate amyloid beta-peptide neurotoxicity: involvement of oxidative stress, mitochondrial dysfunction, and perturbed calcium homeostasis.

Oxidative stress and mitochondrial dysfunction are implicated in the neuronal cell death that occurs in physiological settings and in neurodegenerative disorders. In Alzheimer's disease (AD) degenerating neurons are associated with deposits of amyloid beta-peptide (A beta), and there is evidence for increased membrane lipid peroxidation and protein oxidation in the degenerating neurons. Cell culture studies have shown that A beta can disrupt calcium homeostasis and induce apoptosis in neurons by a mechanism involving oxidative stress. We now report that catecholamines (norepinephrine, epinephrine, and dopamine) increase the vulnerability of cultured hippocampal neurons to A beta toxicity. The catecholamines were effective in potentiating A beta toxicity at concentrations of 10-200 microM, with the higher concentrations (100-200 microM) themselves inducing cell death. Serotonin and acetylcholine were not neurotoxic and did not modify A beta toxicity. Levels of membrane lipid peroxidation, and cytoplasmic and mitochondrial reactive oxygen species, were increased following exposure to neurons to A beta, and catecholamines exacerbated the oxidative stress. Subtoxic concentrations of catecholamines exacerbated decreases in mitochondrial energy charge and transmembrane potential caused by A beta, and higher concentrations of catecholamines alone induced mitochondrial dysfunction. Antioxidants (vitamin E, glutathione, and propyl gallate) protected neurons against the damaging effects of A beta and catecholamines, whereas the beta-adrenergic receptor antagonist propanolol and the dopamine (D1) receptor antagonist SCH23390 were ineffective. Measurements of intracellular free Ca2+ ([Ca2+]i) showed that A beta induced a slow elevation of [Ca2+]i which was greatly enhanced in cultures cotreated with catecholamines. Collectively, these data indicate a role for catecholamines in exacerbating A beta-mediated neuronal degeneration in AD and, when taken together with previous findings, suggest roles for oxidative stress induced by catecholamines in several different neurodegenerative conditions.

Amyloid beta-Peptides↗
PubMed1998

Gentisate 1,2-dioxygenase from Haloferax sp. D1227.

Gentisate 1,2-dioxygenase from the extreme halophile Haloferax sp. D1227 (Hf. D1227) was purified using a three-step procedure. The enzyme was found to be a homotetramer of 42,000 +/- 1,000 Da subunits, with a native molecular weight of 174,000 +/- 6,000 Da. The optimal salt concentration, temperature, and pH for enzyme activity were 2 M KCl or NaCl, 45 degrees C, and pH 7.2, respectively. The gene encoding Hf. D1227 gentisate 1,2-dioxygenase was cloned, sequenced, and expressed in Haloferax volcanii. The deduced amino acid sequence exhibited a 9.2% excess acidic over basic amino acids typical of halophilic enzymes. Four novel histidine clusters and a possible extradiol dioxygenase fingerprint region were identified.

Amino Acid Sequence↗
PubMed1998

Degradation of pinene by Bacillus pallidus BR425.

An aerobic thermophile has been isolated from an alpha-pinene enrichment culture. The isolate, which was designated BR425, has been tentatively identified as Bacillus pallidus using 16S ribosomal RNA gene sequencing and organism morphology. Monophasic and biphasic incubations of BR425 cells with alpha-pinene, beta-pinene, and limonene yielded a number of oxidized monoterpene metabolites with carveol as a common metabolite. A pinene degradation pathway with carveol and carvone as central metabolic intermediates is suggested.

Bacillus↗
PubMed1998

Par-4 is a mediator of neuronal degeneration associated with the pathogenesis of Alzheimer disease.

Prostate apoptosis response-4 (Par-4) is a protein containing both a leucine zipper and a death domain that was isolated by differential screening for genes upregulated in prostate cancer cells undergoing apoptosis. Par-4 is expressed in the nervous system, where its function is unknown. In Alzheimer disease (AD), neurons may die by apoptosis, and amyloid beta-protein (A beta) may play a role in this. We report here that Par-4 expression is increased in vulnerable neurons in AD brain and is induced in cultured neurons undergoing apoptosis. Blockade of Par-4 expression or function prevented neuronal apoptosis induced by Ab and trophic factor withdrawal. Par-4 expression was enhanced, and mitochondrial dysfunction and apoptosis exacerbated, in cells expressing presenilin-1 mutations associated with early-onset inherited AD.

Alzheimer Disease↗
PubMed1998

Bcl-2 protects isolated plasma and mitochondrial membranes against lipid peroxidation induced by hydrogen peroxide and amyloid beta-peptide.

The bcl-2 protooncogene product possesses antiapoptotic properties in neuronal and nonneuronal cells. Recent data suggest that Bcl-2's potency as a survival factor hinges on its ability to suppress oxidative stress, but neither the subcellular site(s) nor the mechanism of its action is known. In this report electron paramagnetic resonance (EPR) spectroscopy analyses were used to investigate the local effects of Bcl-2 on membrane lipid peroxidation. Using hydrogen peroxide (H2O2) and amyloid beta-peptide (A beta) as lipoperoxidation initiators, we determined the loss of EPR-detectable paramagnetism of nitroxyl stearate (NS) spin labels 5-NS and 12-NS. In intact cell preparations and postnuclear membrane fractions, A beta and H2O2 induced significant loss of 5-NS and 12-NS signal amplitude in control PC12 cells, but not PC12 cells expressing Bcl-2. Cells were subjected to differential subcellular fractionation, yielding preparations of plasma membrane and mitochondria. In preparations derived from Bcl-2-expressing cells, both fractions contained Bcl-2 protein. 5-NS and 12-NS signals were significantly decreased following A beta and H2O2 exposure in control PC12 mitochondrial membranes, and Bcl-2 largely prevented these effects. Plasma membrane preparations containing Bcl-2 were also resistant to radical-induced loss of spin label. Collectively, our data suggest that Bcl-2 is localized to mitochondrial and plasma membranes where it can act locally to suppress oxidative damage induced by A beta and H2O2, further highlighting the important role of lipid peroxidation in apoptosis.

Amyloid beta-Peptides↗
PubMed1998

Is oral clonidine effective in modifying the acute hemodynamic response during electroconvulsive therapy?

UNLABELLED: Clonidine decreases the stress-induced sympathoadrenal responses to painful stimuli and improves hemodynamic stability during general anesthesia. Because acute hypertensive responses are often observed immediately after electroconvulsive therapy (ECT), we designed a prospective, randomized, placebo-controlled, cross-over study to assess the effects of four different oral doses of clonidine (0.05-0.3 mg per os) on the acute hemodynamic response to ECT. Anesthesia was induced with methohexital 1 mg/kg followed by succinylcholine, 1.3 mg/kg i.v. A total of 110 treatments were evaluated in 22 patients. Noninvasive mean arterial pressure (MAP) and heart rate (HR) values, duration of motor and electroencephalographic (EEG) seizure activity, and recovery times were recorded. Clonidine produced a dose-related decrease in MAP before and after ECT. Although clonidine 0.2-0.3 mg per os decreased the peak MAP value after ECT, the changes in MAP from the prestimulation values were similar in all treatment groups. Clonidine produced no significant changes in HR, duration of motor and EEG seizure activity, or recovery times after anesthesia. These data suggest that clonidine decreases the peak MAP value after ECT by decreasing MAP immediately before the ECT stimulus. IMPLICATIONS: Oral clonidine (0.2-0.3 mg) decreases the acute hypertensive response after electroconvulsive therapy; however, this antihypertensive effect was achieved by decreasing the blood pressure before the electrical stimulus.

Administration, Oral↗
PubMed1998

shaven and sparkling are mutations in separate enhancers of the Drosophila Pax2 homolog.

We have previously shown that the sparkling gene, which like mammalian Pax2 plays an important role in eye development, is encoded by the Drosophila homolog of Pax2. Here we demonstrate that D-Pax2 also encodes the shaven function, which is crucial during bristle development. Both sv and spa alleles, previously thought to represent different genes, are mutations in two widely separated enhancers of D-Pax2. The sv function of D-Pax2 acts in at least two distinct steps of mechanosensory bristle development: the specification of the alternative fate of shaft as opposed to socket cell, and later the differentiation of the shaft cell.

Alleles↗
PubMed1998

The effect of environmental conditions and glucose feeding in shaking flask on glutathione (GSH) production.

The effects of pH, broth volume, initial sugar concentration, ratio of carbon to nitrogen and phosphorus, and the glucose feeding method on GSH production in a shaking flask were investigated. The results showed that the proper pH and broth content for GSH production were 6.0 and 60 ml broth per 500 ml flask, respectively. The initial glucose concentration distinctly affected the GSH production; the intracellular GSH content of yeast would decrease when the initial glucose concentration was beyond 12 g/L. A glucose feeding strategy with the purpose of controlling the specific growth rate at an expected value was developed and applied to a 12 hour fermentation with the total glucose concentration 26.2 g/L; the final cell concentration (DCW) and the intracellular GSH content could reach 8.78 g/L and 13.6 mg/g, respectively, while the total GSH in the broth was 119.4 mg/L and the yield of cell to glucose was 0.335 g/g.

Carbon↗
PubMed1998

Selective superior mesentery arteriography and guide wire as an intraoperative locating mark in small intestine resection for arteriovenous malformations.

OBJECTIVE: To investigate the effectiveness of selective superior mesentery arteriography and a guide wire as an intraoperative locating mark on diagnosing, locating the bleeding sites in the small intestines caused by arteriovenous malformations (AVMs). METHODS: The selective superior mesentery arteriography was done in seven patients with AVMs of the intestines, and a segment of guide wire was placed simultaneously as a locating mark. RESULTS: All the resected intestines were marked by sutures for pathological examination and confirmed as AVMs of the small intestines. The patients were followed up for an average of 25 months (17-35 months). During this period, all patients had no recurrence of hemorrhage. CONCLUSION: The selective superior mesentery arteriography and placement of a guide wire as an intraoperative locating mark in AVMs of the intestines can help surgeons successfully in finding and resecting the lesions without complications. It is a new method and has a perspective to be widely spread.

Adult↗
PubMed1998

Is there any relation between ischemic cerebrovascular disease and extracranial internal carotid stenosis?

OBJECTIVES: To confirm the existence of plaque or stenosis in the extracranial carotid arteries of patients with transient ischemia attack (TIA) or stroke, and to analyze the prevalence of extracranial carotid atherosclerotic stenosis, as well as the relation between the hemispheric symptoms and the degree of stenosis. METHODS: From January 1995 to March 1996, 188 patients underwent routine carotid artery duplex scan at Zhongshan Hospital, Shanghai. Of the 188 patients, 134 had TIA or stroke in the carotid territory during the previous 12 months, 54 were with peripheral arterial occlusive disease (PAOD). All patients were divided into three groups, that is, stroke/TIA group (Group 1, n = 128), PAOD group (Group 2, n = 36), and stroke/TIA + PAOD group (Group 3, n = 24). The classification of degree of stenosis in our study was as same as that applied by North American Symptomatic Carotid Endarterectomy Trial (NASCET) and European Carotid Surgery Trial (ECST). RESULTS: A total of 376 internal carotid arteries were examined by duplex scanning in this study. The prevalence of severe stenosis in the three groups was 12.5%, 8.3% and 37.5% separately. The severity of stenosis had a close relation with patients' symptoms (P < 0.01). CONCLUSIONS: Patients with stroke or TIA have atherosclerotic plaques in the carotid arteries. The prevalence of extracranial carotid stenosis is comparable to that reported in the literature. PAOD may be helpful to identify patients at high risk for severe carotid stenosis. Carotid duplex scanning should be performed as a routine examination for patients with stroke, TIA, and PAOD.

Aged↗
PubMed1998

[Experience in 237 patients undergoing infrarenal abdominal aortic aneurysm operations].

OBJECTIVE: To improve the safety of infrarenal abdominal aortic aneurysm (AAA) repair. METHODS: 237 patients underwent infrarenal abdominal aorta aneurysm operations from January 1, 1960 to December 1996. Retroperitoneal approach was for AAA operation. The new methods for control of the "neck" of aneurysm, aneurysmectomy and "parachute" of proximal aorta anastomosis were applied. RESULTS: The danger of AAA repair obviously decreased and operation time shortened to 2-3 hours. The perioperative mortality was 3.8% and the five-year survival 74.4%. CONCLUSION: The improvement of surgical and anesthetic techniques made AAA resection rapid and safe.

Adolescent↗
PubMed1998

[Reoperative treatment of recurrent retroperitoneal tumor].

OBJECTIVE: To improve the resection rate and survival rate for recurrent retroperitoneal tumor (RRT). METHOD: We analysed 34 patients with RRT who were treated in our hospital from 1987 to 1995. One patient had benign tumor, the others malignant. Because 7 patients were operated on over one time, we performed 53 operations including complete resection in 42 patients, palliative resection 8 and biopsy 3. RESULT: The 1-and 2-year survival rates for complete resection cases were 71.2% and 65.3%. The patients who received palliative resection and biopsy died within one year. CONCLUSION: The diagnosis, preoperative preparation and intraoperative management of RRT are important to operative safety and survival rate. We emphasize the importance of reoperation and complete resection for RRT.

Adolescent↗
PubMed1998

[Extra-anatomy axillary-femoral or femoro-femoral bypass grafting for the treatment of aorta-iliac occlusive disease].

OBJECTIVE: To study the result of extra-anatomy axillary-femoral or femoro-femoral bypass grafting which was performed to treat aorta-iliac arterial occlusive disease. METHOD: From 1978 through 1997, 32 patients with aorta-iliac occlusive disease underwent extra-anatomy axillary-femoral or femoro-femoral bypass grafting at our hospital. Eighteen patients with aorta or bilateral iliac artery occlusive lesion underwent axillary-femoral artery bypass, including axillary-bifemoral artery bypass (2 patients). Fourteen patients with one side iliac arterial occlusive lesion received femoro-femoral bypass grafting. In who had had axillary-femoral artery bypass 18 patients, 8 received, pure silk prosthesis, and 10 Gore-Tex prosthesis. In femoro-femoral arterial bypass, pure silk prosthesis was given to 8 patients, saphenous vein to one, and Gore-Tex prosthesis to 7. RESULT: Follow-up for 5 years, a patency rate of 78% was achieved in femoro-femoral artery bypass, in which no different patency rate was found between pure silk prosthesis and Gore-Tex prosthesis. In axillary-femoral bypass, eight pure silk prostheses were occluded after 5-year follow-up. One of 10 Gore-Tex prostheses was occluded, and false aneurysm in groin was found in another patient. CONCLUSION: This operation is easy and safe, it has less damage and no abdominal complication. The recovery of the patient is quick. Pure silk prostheses are only used in short segment femoro-femoral bypass grafting.

Adult↗
PubMed1998

[Detection of rotavirus RNA using DIG labelled probe prepared by polymerase chain reaction].

The digoxigenin (DIG) labelled cDNA probe of rotavirus was directly prepared by polymerase chain reaction (PCR). The results of cDNA-RNA hybridization showed that the DIG-cDNA probe exhibits rotavirus specificity and can detect as tiny as 10 pg rotavirus RNA. 120 fecal samples of diarrhea from infants and young children were tested by dot-blot hybridization. It was shown that the positive rate of dot-blot hybridization(65.0%) was significantly higher than that of PAGE(49.1%). This study indicated that direct preparation of DIG-labelled rotavirus-cDNA probe by PCR is much faster and simpler than common method of labeling.

Adult↗
PubMed1997

The actin-severing protein gelsolin modulates calcium channel and NMDA receptor activities and vulnerability to excitotoxicity in hippocampal neurons.

Calcium influx through NMDA receptors and voltage-dependent calcium channels (VDCC) mediates an array of physiological processes in neurons and may also contribute to neuronal degeneration and death in neurodegenerative conditions such as stroke and severe epileptic seizures. Gelsolin is a Ca2+-activated actin-severing protein that is expressed in neurons, wherein it may mediate motility responses to Ca2+ influx. Primary hippocampal neurons cultured from mice lacking gelsolin exhibited decreased actin filament depolymerization and enhanced Ca2+ influx after exposure to glutamate. Whole-cell patch-clamp analyses showed that currents through NMDA receptors and VDCC were enhanced in hippocampal neurons lacking gelsolin, as a result of decreased current rundown; kainate-induced currents were similar in neurons containing and lacking gelsolin. Vulnerability of cultured hippocampal neurons to glutamate toxicity was greater in cells lacking gelsolin. Seizure-induced damage to hippocampal pyramidal neurons was exacerbated in adult gelsolin-deficient mice. These findings identify novel roles for gelsolin in controlling actin-mediated feedback regulation of Ca2+ influx and in neuronal injury responses. The data further suggest roles for gelsolin and the actin cytoskeleton in both physiological and pathophysiological events that involve activation of NMDA receptors and VDCC.

Actins↗
PubMed1997

Activation of NF-kappaB protects hippocampal neurons against oxidative stress-induced apoptosis: evidence for induction of manganese superoxide dismutase and suppression of peroxynitrite production and protein tyrosine nitration.

The transcription factor NF-kappaB is expressed in neurons wherein it is activated in response to a variety of stress- and injury-related stimuli including exposure to cytokines such as tumor necrosis factor-alpha (TNFalpha), and excitotoxic and oxidative insults. NF-kappaB may play a role in the anti-death actions of TNFalpha in cultured hippocampal neurons exposed to metabolic and oxidative insults. We now report that pretreatment of hippocampal cell cultures with agents that activate NF-kappaB (TNFalpha and C2-ceramide) confers resistance of neurons to apoptosis induced by the oxidative insults FeSO4 and amyloid beta-peptide (Abeta25-35). The neuroprotective actions of TNFalpha and ceramide were abolished in cultures cotreated with kappaB decoy DNA demonstrating a requirement for NF-kappaB activation for prevention of cell death. Levels of manganese superoxide dismutase (Mn-SOD) in neurons were increased following exposure of cultures to TNFalpha and ceramide in control cultures, but not in cultures cotreated with kappaB decoy DNA. FeSO4 and Abeta25-35 induced accumulation of mitochondrial peroxynitrite, and membrane lipid peroxidation, in neurons. Peroxynitrite accumulation and lipid peroxidation were largely prevented in neurons pretreated with TNFalpha and ceramide prior to exposure to FeSO4 and Abeta25-35, an effect blocked by kappaB decoy DNA. Immunoreactivity of neurons with an anti-nitrotyrosine antibody was increased following exposure to FeSO4 and Abeta25-35; TNFalpha and C2-ceramide suppressed protein tyrosine nitration, and kappaB decoy DNA blocked the effects of TNFalpha and C2-ceramide. Finally, the peroxynitrite scavenger uric acid protected neurons against apoptosis induced by FeSO4 and Abeta, and suppressed peroxynitrite accumulation. We conclude that, by inducing production of Mn-SOD and suppressing peroxynitrite formation and membrane lipid peroxidation, NF-kappaB plays an anti-apoptotic role in neurodegenerative conditions that involve oxidative stress. The data further suggest important roles for peroxynitrite and NF-kappaB in the pathogenesis of neuronal degeneration in Alzheimer's disease.

Animals↗
PubMed1997

The Pax2 homolog sparkling is required for development of cone and pigment cells in the Drosophila eye.

A new Drosophila Pax gene, sparkling (spa), implicated in eye development, was isolated and shown to encode the homolog of the vertebrate Pax2, Pax5, and Pax8 proteins. It is expressed in the embryonic nervous system and in cone, primary pigment, and bristle cells of larval and pupal eye discs. In spa(pol) mutants, a deletion of an enhancer abolishes Spa expression in cone and primary pigment cells and results in a severely disturbed development of non-neuronal ommatidial cells. Spa expression is further required for activation of cut in cone cells and of the Bar locus in primary pigment cells. We suggest close functional analogies between Spa and Pax2 in the development of the insect and vertebrate eye.

Amino Acid Sequence↗