Search PubMed⌕ Search

Biomedical subjects

T Wu

Publications and source records attributed to T Wu.

At least 163 records · Page 9Linked to original sources
PubMed1997

Cross-Polarized Magic-Angle Spinning (sup13)C Nuclear Magnetic Resonance Spectroscopic Characterization of Soil Organic Matter Relative to Culturable Bacterial Species Composition and Sustained Biological Control of Pythium Root Rot.

We report the use of a model system that examines the dynamics of biological energy availability in organic matter in a sphagnum peat potting mix critical to sustenance of microorganism-mediated biological control of pythium root rot, a soilborne plant disease caused by Pythium ultimum. The concentration of readily degradable carbohydrate in the peat, mostly present as cellulose, was characterized by cross-polarized magic-angle spinning (sup13)C nuclear magnetic resonance spectroscopy. A decrease in the carbohydrate concentration in the mix was observed during the initial 10 weeks after potting as the rate of hydrolysis of fluorescein diacetate declined below a critical threshold level required for biological control of pythium root rot. Throughout this period, total microbial biomass and activity, based on rates of [(sup14)C]acetate incorporation into phospholipids, did not change but shifts in culturable bacterial species composition occurred. Species capable of inducing biocontrol were succeeded by pleomorphic gram-positive genera and putative oligotrophs not or less effective in control. We conclude that sustained efficacy of naturally occurring biocontrol agents was limited by energy availability to this microflora within the organic matter contained in the potting mix. We propose that this critical role of organic matter may be a key factor explaining the variability in efficacy typically encountered in the control of pythium root rot with biocontrol agents.

Journal Article↗
PubMed1997

Antisense inhibition of 85-kDa cPLA2 blocks arachidonic acid release from airway epithelial cells.

Inflammatory cytokines play a critical role in the initiation and perpetuation of inflammation. Several cytokines are known to increase the production of arachidonic acid (AA) metabolites, which may mediate cytokine-induced acute and chronic inflammation. Although cytokines upregulate phospholipase A2 (PLA2) in several target cells, the contribution of individual PLA2 to cytokine-induced AA release and eicosanoid production remains unclear because of the existence of various forms of cellular PLA2. To examine the role of 85-kDa cytosolic PLA2 (cPLA2) in cytokine-induced AA release, a system was developed to inhibit the expression of cPLA2 in a human bronchial epithelial cell line (BEAS-2B cells) by antisense RNA. Cells stably expressing antisense cPLA2 exhibited decreased cPLA2 protein levels as well as decreased cPLA2 activity assayed in vitro. The effects of cytokines interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 alpha (IL-1 alpha) on the release of prelabeled [3H]AA were then tested in cells stably transfected with vector alone as well as cells transfected with cPLA2 antisense plasmid. IFN-gamma (300 U/ml), TNF-alpha (20 ng/ml), and IL-1 alpha (20 ng/ml) all induced a significantly increased release of prelabeled [3H]AA after 15 min to 2 h of treatment in control cells, and their effects were significantly reduced in cells transfected with cPLA2 antisense vector. These results demonstrate a critical role of cPLA2 in inflammatory cytokine-induced AA metabolism.

Antisense Elements (Genetics)↗
PubMed1997

[Effects of fructus cnidii coumarins compared with nilestriol on osteoporosis in ovariectomized rats].

AIM: To compare the total coumarins from dried fruits of Cnidium monnieri (TCCM) and nilestriol (Nil) against osteoporosis. METHODS: SD rats (40, female, 3-month-old) were randomly divided into basal control, age control, ovariectomized (Ova), Ova + TCCM 67 mg.kg-1, Ova + TCCM 200 mg.kg-1, 6 times a week, and Ova + Nil 1 mg.kg-1, i.g. once a week. After 12 wk, sections (20 microns) of proximal tibiae were examined histologically. RESULTS: Ova reduced markedly the trabecular bone mass due to bone resorption excessed bone formation (% Tb. Ar -59%). Treatment with TCCM 67 mg.kg-1 partly suppressed bone turnover, but did not inhibit bone loss in Ova rats (% Tb.Ar -43%). Treatment with TCCM 200 mg.kg-1 and Nil 1 mg.kg-1 increased the trabecular area (% Tb. Ar +100% and +274%). CONCLUSION: Nil was more potent than TCCM in protecting against osteoporosis in Ova rats via supression of bone turnover.

Animals↗
PubMed1997

Effects of total coumarins of Cnidium monnieri on bone density and biomechanics of glucocorticoids-induced osteoporosis in rats.

AIM: To evaluate the effects of total coumarins from dried fruits of Cnidium monnieri (TCCM) on glucocorticoids (GC)-induced osteoporosis (OP) in rats. METHODS: Single photon absorptiometric and biomechanical character measurements of femurs were used. RESULTS: The bone density (BD) indices in proximal, middle, and distal segments in GC group were decreased by 12% (P < 0.05), 14% (P < 0.05), and 12% (P < 0.05), respectively vs control group. The BD on proximal, middle, and distal segments in GC-TCCM group were increased by 26% (P < 0.01), 34% (P < 0.01), and 31% (P < 0.01), respectively vs GC group. The biomechanical competence in femoral middle segments in GC group tended to decrease vs control group. In GC-TCCM group, the torsional strength, energy, maximal torsional angle, and rigidity were increased by 15% (P < 0.05), 32% (P < 0.05), 14% (P > 0.05), and 13% (P > 0.05), respectively vs the GC group. CONCLUSION: TCCM not only prevented glucocorticoids-induced osteoporosis but also increased the torsional strength of femurs in rats.

Animals↗
PubMed1997

[Recurrent acoustic neuroma: report of 11 cases].

To improve the therapeutic effect of acoustic neuroma, 158 patients with acoustic neuroma treated in our hospital were retrospectively reviewed. Among them, 11 recurrent acoustic neuroma were found. The clinical analysis demonstrated that the recurrence of acoustic neuroma had close relationship with the size of the tumor, operative approach and extent of excision. All recurrent acoustic neuroma was large-sized when first operated. The more the tumor was excised, the lower the recurrent rate was. The recurrent rates were 19.4% for partial resection, 13.2% for near-total resection, 0% for total resection respectively. Retrolabyrinthine approach was more likely to recur than other approaches. The key to decrease recurrent rate was to excise as much tumor as possible. According to growth rate and double time of acoustic neuroma measured in this study, regular follow-up with CT or MRI at interval of 6 months was emphasized. X-knife was effective for early-diagnosed recurrent acoustic neuroma.

Adult↗
PubMed1997

[Preventive effect of gubao on hydrocortisone-induced osteoporosis in rats].

The antagonistic effect of Gubao (consisting of Herba Epimedii, Radix Astragali, etc.) on hydrocortisone-induced osteoporosis in rats was observed in quantitative bone histomorphometry study with stereological method. The results of experiment show that Gubao helps to reduce trbecular bone resorption and increase bone formation in ratsuith hydrocortisone-induced osteoporosis. It is suggested that Gubao is useful in preventing glucocorticoid-induced osteoporosis.

Animals↗
PubMed1996

The excitatory effect of cholecystokinin on rat neostriatal neurons: ionic and molecular mechanisms.

Whole-cell patch-clamp recordings were performed to study ionic and molecular mechanisms by which cholecystokinin (CCK) peptides modulate the membrane excitability of acutely dissociated rat neostriatal neurons. Immunohistochemical staining studies indicated that about 95% of acutely isolated neostriatal neurons were GABA(gamma-aminobutyric acid)ergic medium-sized cells. During current-clamp recordings, sulfated cholecystokinin octapeptide (CCK-8) depolarized neostriatal neurons and evoked action potentials. During voltage-clamp recordings, CCK-8 induced inward currents at negative membrane potentials by increasing the voltage-insensitive and non-selective cationic conductance. Cholecystokinin tetrapeptide (CCK-4), a selective CCKB receptor agonist, also evoked cationic currents. The CCK-8-induced cation currents were antagonized by PD135,158 (4-{[2-[[3-(1H-indol-3yl)-2-mehtyl-1-oxo-2-[[[1.7.7.-trimeth yl-bicyclo [2.2.1]hept-2-yl)oxy]carbonyl]amino]propyl]amino]-1-phenylethyl]amino-4- oxo- [1S-1 alpha, 2 beta [S*(S*)]4 alpha]}-butanoate N-methyl-D-glucamine), a highly specific and potent CCKB receptor antagonist. The CCK-8-evoked inward currents were blocked by the internal perfusion of 1 mM GDP-beta-S. In neostriatal neurons dialyzed with 0.5 mM GTP-gamma-S, the cationic currents produced by CCK-8 became irreversible. Pretreating neostriatal neurons with 500 ng/ml pertussis toxin did not prevent CCK-8 from evoking cationic currents. Internal administration of heparin (2 mg/ml), an inositol 1,4,5-trisphosphate (IP3) receptor antagonist, and buffering of intracellular calcium with the Ca(2+)-chelator, BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, 10 mM), suppressed CCK-8-evoked cationic currents. These findings suggest that, by activating CCKB receptors, CCK-8 excites rat neostriatal neurons through enhancing a non-selective cationic conductance and that pertussis toxin-insensitive G-proteins mediate CCK-8 enhancement of the cationic conductance. The coupling mechanism via G-proteins is likely to involve the production of IP3, and the subsequent IP3-evoked Ca2+ release leads to the opening of non-selective cation channels.

Action Potentials↗
PubMed1996

Characterization of terminal sialic acid linkages on human thymocytes. Correlation between lectin-binding phenotype and sialyltransferase expression.

T cell surface sialylation changes during maturation in the thymus. We have previously demonstrated increased expression of mRNA encoding the Gal beta 1, 3GalNAc alpha 2,3-sialyltransferase in mature medullary human thymocytes, compared with immature cortical thymocytes. For this enzyme, increased expression of transferase mRNA correlated with increased sialylation of O-glycans. We have now examined the pattern of expression in the human thymus of two additional sialyltransferases, the Gal beta 1,4GlcNAc alpha 2,6-sialyltransferase (ST6N) and the Gal beta 1,3/4GlcNAc alpha 2,3-sialyltransferase (ST3N). The patterns of mRNA expression were compared with the pattern of binding of two sialic acid-specific plant lectins, Sambucus nigra agglutinin and Maackia amurensis agglutinin, which preferentially recognize alpha 2,6- and alpha 2,3-linked sialic acids, respectively, on N-glycans. By in situ hybridization, mRNA encoding ST3N was detected uniformly throughout the thymus. All thymocytes bound M. amurensis agglutinin, demonstrating a direct correlation between the level of ST3N mRNA expression and cell-surface glycosylation. In contrast, mRNA encoding ST6N was also expressed uniformly throughout the thymus; however, only mature (CD3hi) medullary thymocytes bound S. nigra agglutinin. On mature thymocytes, S. nigra agglutinin appeared to bind primarily to the cell-surface glycoprotein CD45; since only the mature thymocytes expressed the CD45RA isoform, while both mature and immature populations expressed the CD45R0 isoform, CD45RA may be a preferred substrate for ST6N. These results demonstrate that glycoprotein sialylation is tightly regulated during T cell development and that the developmentally regulated expression of specific oligosaccharide structures on the cell surface may be influenced by expression of both the relevant glycosyltransferase and specific acceptor substrates.

Cells, Cultured↗
PubMed1996

Tumor necrosis factor-alpha induces the 85-kDa cytosolic phospholipase A2 gene expression in human bronchial epithelial cells.

Phospholipase A2 (PLA2) activity has been suggested to mediate some of the tumor necrosis factor (TNF) induced cellular responses including cytotoxicity. We evaluated the induction of both the 85-kDa cytosolic phospholipase A2 (cPLA2) and non-pancreatic group II PLA2 gene expression by TNF-alpha in a human bronchial epithelial cell line (BEAS 2B cell). TNF-alpha (20 ng/ml) induced a significantly increased release of prelabeled [3H]arachidonic acid (AA) following 4-24 h incubation. Calcium ionophore A23187 (10(-5) M) further increased the [3H]AA release from the TNF-alpha-treated cells. In vitro activity assay revealed that TNF-alpha increased the dithiothreitol (DTT)-resistant PLA2 activity which was blocked by the cPLA2 inhibitor AACOCF3. Treatment with TNF-alpha for 4-24 h increased the cPLA2 protein and mRNA levels which were blocked by the broad inhibitor of protein kinases staurosporine, the protein kinase C (PKC) inhibitor calphostin C, and to a lesser extent the calcium/calmodulin-dependent protein kinase inhibitor W-7. Reverse transcription and polymerase chain reaction amplification of the group II PLA2 mRNA showed that it is expressed in human lung but not in the bronchial epithelial cell line. TNF-alpha failed to induce the expression of group II PLA2 in the BEAS 2B cells. These results demonstrate that the cPLA2 gene expression is up-regulated by TNF-alpha and this effect may contribute to the TNF-alpha stimulated AA release in airway epithelial cells.

Arachidonic Acid↗
PubMed1996

Hypoxia-induced paracrine regulation of vascular endothelial growth factor receptor expression.

Vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF), an endothelial cell (EC)-specific mitogen, stimulates angiogenesis in vivo, particularly in ischemic regions. VEGF/VPF expression by cells of hypoxic tissues coincides with expression of its two receptors, KDR and flt-1, by ECs in the same tissues. We investigated whether hypoxia or hypoxia-dependent conditions operate in coordinating this phenomenon. Human umbilical vein and microvascular ECs were exposed to direct hypoxia or to medium conditioned (CM) by myoblasts maintained in hypoxia for 4 d. Control ECs were maintained in normoxia or normoxia-CM. Binding of 125I-VEGF to ECs was then evaluated. Hypoxic treatment of ECs had no effect on 125I-VEGF binding. However, treatment of ECs with hypoxia-CM produced a threefold increase in 125I-VEGF binding, with peak at 24 h (P < 0.001, ANOVA). Scatchard analysis disclosed that increased binding was due to a 13-fold increase in KDR receptors/cell, with no change in KDR affinity (Kd = 260 +/- 51 pM, normoxia-CM versus Kd = 281 +/- 94 pM, hypoxia-CM) and no change in EC number (35.6 +/- 5.9 x 10(3) ECs/cm2, normoxia-CM versus 33.5 +/- 5.5 x 10(3) ECs/cm2, hypoxia-CM). Similar results were obtained using CM from hypoxic smooth muscle cells. KDR upregulation was not prevented by addition to the hypoxia-CM of neutralizing antibodies against VEGF, tumor necrosis factor-alpha, transforming growth factor beta 1 or basic fibroblast growth factor. Similarly, addition of VEGF or lactic acid to the normoxia-CM had no effect on VEGF binding. We conclude that mechanism(s) initiated by hypoxia can induce KDR receptor upregulation in ECs. Hypoxic cells, normal or neoplastic, not only can produce VEGF/VPF, but can also modulate its effects via paracrine induction of VEGF/VPF receptors in ECs.

Animals↗
PubMed1996

Comparison of muscle force, muscle endurance, and electromyogram activity during an expedition at high altitude.

Handgrip force (HF), maximal pinch force (MF), muscle endurance (ME), and the median power frequency (MdPF) of the activity shown in the electromyogram (EMG) were studied at various altitudes in eight normal healthy subjects. MF and ME were measured between the index finger and thumb, and all measurements were obtained at altitudes ranging from 610 to 4860 m during an expedition in the Qinghai Plateau in China. With the change in altitude HF, ME, and MF showed no significant change. Compared to the MdPF at 2260 m on ascent, the MdPF at other altitudes showed a significant decrease (P < 0.01). Thus, we conclude that muscle performance (HF, MF, and ME) was not affected by the environment at high altitude. However, MdPF was affected and the mean MdPF at 610 m after the expedition did not recover to initial values of MdPF. We suggest these results may have been affected by fatigue and chronic exposure to the hypobaric hypoxic environment, since the members of the expedition party expressed feelings of sluggishness and fatigue after the expedition.

Acclimatization↗
PubMed1996

A novel intact circular dsDNA supercoil.

A novel intact circular dsDNA supercoil is proposed as an alternative to the conventional DNA supercoil, so that the two complementary strands of ssDNA circles are separable without any covalent bond breakage. This new structure can be visualized by using two tubings: one black and one clear. Twist the black tubing a number of times and connect its two ends. Do the same for the clear tubing. Then wrap the two tubings together. This forms the separable or novel supercoil. On the other hand, the conventional supercoil can be modeled by twisting the black and clear tubings together and then connect their respective ends, so that the two tubings are not separable unless one of them is cut. Experimentally, in the absence of any enzyme, many intact plasmid dsDNA circles give two bands on agarose gel electrophoresis under a certain given condition, while the same plasmid molecules after cutting once by a restriction enzyme give only one band under the same condition. In the case of intact pUC19 plasmids, these two bands can then be recovered and sequenced separately, using two primers in opposite directions. Each band gives mostly one sequence which is complementary to that of the other band. The combination of the above theoretical model and experimental results strongly suggests that there is an alternative structure of DNA which does not have the usual difficulty of unwinding, rewinding and requiring numerous covalent bond breakages and ligations during semiconservative.

Base Sequence↗
PubMed1996

G alpha q/11 mediates neurotensin excitation of substantia nigra dopaminergic neurons.

Using acutely dissociated substantia nigra pars compacta (SNC) dopaminergic (DA) neurons, our previous studies indicated that neurotensin (NT) excites SNC DA neurons by increasing the cationic conductance and reducing the inwardly rectifying K+ conductance. Further investigation also revealed that pertussis toxin (PTX)- insensitive G-proteins mediate neurotensin modulation of cation and potassium channels. G alpha q and G alpha 11 are widely distributed in various tissues including the brain and likely to mediate PTX-insensitive signal transductions in the nervous system. In this study, two different experiments were conducted to test the hypothesis that G alpha q/11 mediates neurotensin regulation of the cationic and K+ conductances. First, we investigated the expression of G alpha q and G alpha 11 mRNAs in NT-responsive SNC DA neurons by combining whole-cell patch-clamp recordings with single-cell reverse transcriptase-polymerase chain reaction (RT-PCR) assay. After recording NT-evoked membrane currents, the cellular content was harvested from single neurons and used as the template for the subsequent RT-PCR analysis. Both G alpha q and G alpha 11 mRNAs were present in all SNC DA neurons that responded to neurotensin. SNC DA neurons were also internally dialyzed with an antibody directed against the common C-terminus of G alpha q and G alpha 11 during whole-cell recordings. In DA neurons perfused with the anti-G alpha q/11 antiserum, neurotensin failed to evoke inward currents resulting from the opening of cation channels and the closure of inward rectifier K+ channels. It is concluded that NT modulation of cation and inward rectifier K+ channels in SNC DA neurons is transduced by G alpha q and/or G alpha 11.

Animals↗
PubMed1996

Fluctuating hemiparesis caused by a quadrigeminal arachnoid cyst: case report.

A 42-year-old woman presented with intermittent hemiparesis mimicking a reversible ischemic neurologic deficit. Magnetic resonance imaging (MRI) demonstrated a compression of the left side of the midbrain by a quadrigeminal arachnoid cyst without hydrocephalus. After the cystic wall was widely excised under operating microscope, the patient made a good recovery and remained well at a follow-up of 18 months. The absence of hydrocephalus in a symptomatic patient with a quadrigeminal cyst was exceptional, which might result from the early diagnosis with MRI. The use of microsurgical technique made it possible to excise the cystic wall widely and omit a shunting procedure.

Adult↗
PubMed1996

G alpha q/11 mediates cholecystokinin activation of the cationic conductance in rat substantia nigra dopaminergic neurons.

Using acutely isolated rat substantia nigra neurons, our previous studies indicated that sulfated cholecystokinin octapeptide (CCK-8) excites substantia nigra dopaminergic neurons by increasing the cationic conductance and that pertussis toxin-insensitive G proteins mediate CCK-8 induction of cationic currents. G alpha q and G alpha 11 are expressed in various tissues, including the brain, and likely to mediate pertussis toxin-insensitive neural signal transductions. In the present study, two different experiments were performed to test the hypothesis that G alpha q/11 mediates CCK-8 enhancement of the cationic conductance. First, we investigated the expression of G alpha q and G alpha 11 mRNAs in CCK-8-responsive substantia nigra dopaminergic neurons by combining whole-cell patch-clamp recordings with a single-cell reverse transcriptase-polymerase chain reaction assay. After CCK-8-evoked cationic currents were recorded, cellular RNA was harvested from single neurons and used as a template for the subsequent reverse transcriptase-polymerase chain reaction analysis. G alpha q and G alpha 11 mRNAs were present in all substantia nigra dopaminergic neurons that responded to CCK-8. Substantia nigra dopaminergic neurons were also internally perfused with the antibody raised against the common C-terminus of G alpha q and G alpha 11 during whole-cell recordings. CCK-8 failed to induce cationic currents after dopaminergic neurons were dialyzed with the anti-G alpha q/11 antibody. Our studies suggest that CCK-8 activation of the cationic conductance in substantia nigra dopaminergic neurons is transduced by G alpha q and/or G alpha 11.

Animals↗
PubMed1996

In-vitro proteinase production by oral Candida albicans isolates from individuals with and without HIV infection and its attenuation by antimycotic agents.

In-vitro proteinase production by oral Candida albicans isolates from patients with and without HIV infection (18 isolates from each group) was assessed by image analysis of a plate assay, with bovine serum albumin (BSA) as a substrate. The effect of sub-minimal inhibitory concentrations (sub-MICs) of nystatin, amphotericin B, clotrimazole and miconazole on in-vitro proteinase production by these yeast isolates was also investigated. Proteinase production by C. albicans isolates from patients with HIV infection was significantly greater than production by those from individuals without infection. All 18 isolates from HIV-infected individuals produced proteinase, in comparison to 56% of isolates from uninfected individuals. Pre-exposure of C. albicans isolates (seven proteinase producers from each group) to 1/4 and 1/16 MICs of nystatin, amphotericin B, clotrimazole and miconazole resulted in decreased proteinase production in all isolates tested. However, after exposure to the four antimycotic agents, proteinase production was decreased to a significantly greater extent in isolates from uninfected individuals than in those with HIV disease. Furthermore, when the relative concentration effect of antimycotic agents on proteinase production was compared, C. albicans isolates from the HIV-free group demonstrated a salient dose-response relationship compared with the HIV-infected group. These results indicate that C. albicans from patients with HIV infection are significantly more proteolytic than those from individuals without the infection, and that polyenes and imidazoles curtail the proteolytic activity of all C. albicans isolates, albeit to a lesser extent in those from HIV-infected patients. It appears that HIV disease favours oral colonisation by more proteolytic C. albicans isolates, with resilient proteolytic activity.

AIDS-Related Opportunistic Infections↗
PubMed1996

Adenovirus type 5 early region 4 is responsible for E1A-induced p53-independent apoptosis.

In the absence of E1B, the 289- and 243-residue E1A products of human adenovirus type 5 induce p53-dependent apoptosis. However, our group has shown recently that the 289-residue E1A protein is also able to induce apoptosis by a p53-independent mechanism (J. G. Teodoro, G. C. Shore, and P. E. Branton, Oncogene 11:467-474, 1995). Preliminary results suggested that p53-independent cell death required expression of one or more additional adenovirus early gene products. Here we show that both the E1B 19-kDa protein and cellular Bcl-2 inhibit or significantly delay p53-independent apoptosis. Neither early region E2 or E3 appeared to be necessary for such cell death. Analysis of a series of E1A mutants indicated that mutations in the transactivation domain and other regions of E1A correlated with E1A-mediated transactivation of E4 gene expression. Furthermore, p53-deficient human SAOS-2 cells infected with a mutant which expresses E1B but none of the E4 gene products remained viable for considerably longer times than those infected with wild-type adenovirus type 5. In addition, an adenovirus vector lacking both E1 and E4 was unable to induce DNA degradation and cell killing in E1A-expressing cell lines. These data showed that an E4 product is essential for E1A-induced p53-independent apoptosis.

3T3 Cells↗