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Biomedical subjects

G Wu

Publications and source records attributed to G Wu.

At least 433 records · Page 24Linked to original sources

GM1 ganglioside modulates prostaglandin E1 stimulated adenylyl cyclase in neuro-2A cells.

This study demonstrates modulation by GM1 ganglioside of prostaglandin E1 (PGE1)-induced cAMP formation in Neuro-2a neuroblastoma cells. Pretreatment of the cells with neuraminidase, an enzyme that increases cell surface GM1, resulted in significant elevation of PGE1-induced cAMP formation, as did preincubation of the cells with nmolar concentrations of GM1. Pretreatment with brain ganglioside mixture lacking GM1 had no effect. Cholera toxin B subunit, a specific GM1-binding ligand, inhibited adenylyl cyclase. When the concentration of exogenous GM1 in which the cells were preincubated was increased from nmolar to mu molar levels there was a dose-responsive fall off in cAMP elevation, attributed to progressive inhibition of adenylyl cyclase by increasing GM1. These results are interpreted as indicating modulation of this PGE1 receptor in Neuro-2a cells by plasma membrane-localized GM1 in a structure-specific manner.

Adenylyl Cyclases↗

Defects of TGF-beta receptor signaling in mammary cell tumorigenesis.

Transforming growth factor beta (TGF-beta) receptor expression and signal transduction in human breast cancer are reviewed as a function of estrogen receptor (ER) expression. ER+ breast cancer cells are generally resistant to the inhibitory effects of TGF-beta. The only known exception appears to be MCF-7 early passage cells which are initially sensitive to TGF-beta, but gain resistance after long-term passage in tissue culture. A number of studies have shown that loss of sensitivity is due to inadequate TGF-beta type II (TGFRII) receptor expression. Stable transfection of TGFRII into ER+ breast cancer cell lines results in the acquisition of TGF-beta sensitivity and reversion of malignancy. Although there are exceptions, ER- breast cancer cells usually express TGFRII, but nevertheless show a low level of sensitivity to TGF-beta. Thus resistance in these cells implies a postreceptor mechanism. Given the frequency with which loss of TGF-beta sensitivity has been associated with loss of TGFRII, the ER- breast cancer cell lines may represent valuable models for identifying postreceptor mechanisms of resistance.

Animals↗

Limitations of quasi-static estimation of human joint loading during locomotion.

The forces and moments at the ankle, knee and hip joints of the human lower limbs are divided into static and inertial components. They are calculated for various activities ranging from slow walking to running. The relative roles of these two components in the 'total' joint loads are studied, and the limitations of using a quasi-static analysis approach for joint load approximation are discussed. The results indicate that the static loads only reflect the gravitational and external reactions between the body and the environment, whereas the inertial loads provide dynamic information on each body segment involved. The effect of the inertial forces and moments becomes more important as the speed of locomotion increases; where the more proximal joints in the human lower extremity are concerned; and where the shear components of the force and moment are of interest. On the other hand, it seems that most of the joint moments in the lower extremity during walking and even running could reasonably be approximated by static components.

Biomechanical Phenomena↗

Steroidal glycosides from Tribulus terrestris.

In addition to hecogenin 3-O-beta-D-glucopyranosyl(1--> 4)-beta-D-galactopyranoside, two new steroidal saponins were isolated from the aerial parts of Tribulus terrestris L. On the basis of chemical and spectroscopic evidence, especially 2D NMR spectroscopic techniques, the structures of the new saponins were established as 26-O-beta-D-glucopyranosyl-3-O-[-beta-D-xylopyranosyl(1--> 3)--beta-D-galactopyranosyl(1-->2)--beta-D-glucopyranosyl (1--> 4)-beta-D-glucopyranosyl]-5 alpha-furost-20(22)-en-12-one-3 beta,26-diol and 26-O-beta-D-glucopyranosyl-3-O-[{beta-D-xylopyranosyl (1-->3)--beta-D-galactopyranosyl(1-->2)--beta-D-glucopyranosyl(1 -->4)-beta-D-glucopyranosyl]-5 alpha-furostan-12-one-3 beta,22,26-triol.

Carbohydrate Conformation↗

Hepatocyte culture on carbohydrate-modified star polyethylene oxide hydrogels.

We describe the synthesis and in vitro biological characterization of a new class of carbohydrate-modified hydrogels based on radiation-cross-linked star polyethylene oxide (PEO). Hydrogels were synthesized from either of two types of PEO star molecules in order to vary the terminal hydroxyl content of the gels while keeping other gel properties such as molecular weight between cross-links and water content constant. The resulting gels were covalently modified with monosaccharide ligands and the behaviour of primary rat hepatocytes on the modified gels was evaluated under culture conditions. Hepatocytes exhibited a sugar-specific adhesion to the modified gels, adhering to gels bearing galactose but not glucose. Cell spreading was observed on both types of galactose-modified PEO star gels; moreover, the gels supported long-term (6 d) culture and differentiated function of primary hepatocytes. Further, on comparing the cell spreading behaviour observed on the PEO star gels with that reported previously for galactose-modified polyacrylamide, we find that our gels elicit spreading at ligand concentrations lower by an order of magnitude. A simple mechanistic analysis indicates that this enhanced ability of PEO star gels to support spreading of primary hepatocytes on low concentrations of immobilized galactose derives from freedom of the immobilized ligands to come within sufficiently close proximity to mimic a high-affinity branched oligosaccharide.

Animals↗

Prostaglandin E1 (PGE1) reduces cardiac-derived TXA2 release in ischaemic arrest in isolated working rat heart.

To determine whether PGE1 plays a beneficial role in crystalloid cardioplegia in the isolated working rat heart, twenty isolated rat hearts were studied. The hearts were subjected to 90 min cardioplegic arrest under hypothermia (25 degrees C) and 30 min reperfusion. Prior to ischaemic arrest, the amount of TXA2 in coronary effluent, left ventricular developed pressure (LVDP), left ventricular end diastolic pressure (LVEDP), coronary flow (CF), aortic flow (AF) and cardiac output (CO) did not differ between the control and PGE1 treated rats (28 nmol/l). However, at 30 min reperfusion, the recovery of LVDP, LVEDP, CF, AF, CO and SV in hearts from PGE1 treated rats was more than in control hearts. TXA2 levels from coronary effluent were increased during reperfusion in control rats. On the other hand, PGE1 (28 nmol/l) inhibited the release of TXA2 at reperfusion. The present studies confirm that the cardiac-derived TXA2 are increased after ischaemia/reperfusion. Infusion of cardioplegia solution containing PGE1 results in the inhibition of release of cardiac-derived TXA2 and in a better preservation of cardiac function after ischaemic arrest.

Alprostadil↗

Effects of concanavalin A and phorbol myristate acetate on glutamine metabolism and proliferation of porcine intestinal intraepithelial lymphocytes.

This study was designed to determine the effects of concanavalin A (ConA) (a T-cell mitogen) and phorbol myristate acetate (PMA) (an activator of protein kinase C) plus ionomycin (Iono) on glutamine metabolism and proliferation of porcine intestinal intraepithelial lymphocytes (IEL). IEL were prepared from jejunum of 29-day-old pigs weaned at 21 days of age. Cells were cultured at 37 degrees C for 48 hr in RPMI-1640 medium containing 10 mM D-glucose, 0 to 4 mM L-glutamine, 0 to 5 micrograms/ml ConA, or 20 ng/ml PMA + 375 ng/ml Iono. The medium was also supplemented with 0 or 0.1 mM adenosine, guanosine, inosine, uridine or cytosine to study the effect of nucleosides or bases on IEL proliferation. IEL proliferation was assessed by pulsing with 3H-thymidine for 18 hr. Glutamine metabolism was studied in incubated IEL in the presence of Krebs-Henseleit bicarbonate buffer containing 5 mM D-glucose and 1 mM L-[U-14C]glutamine. PMA+Iono markedly stimulated 3H-thymidine incorporation and glutamine metabolism to ammonia, glutamate, aspartate and CO2. When stimulated by PMA+Iono, rates of 3H-thymidine incorporation and glutamine metabolism were much lower in IEL than in mesenteric lymph node lymphocytes. Glutamine was required for IEL proliferation, and it could not be replaced by adenosine, guanosine, inosine, uridine or cytosine, suggesting that porcine IEL cannot interconvert purine and pyrimidine nucleotides. Porcine IEL poorly or not at all responded to ConA stimulation, in contrast to lymph node lymphocytes, in terms of both [3H]thymidine uptake and glutamine metabolism.

Acetates↗

Chronic continuous infusion of (-)nicotine reduces basic fibroblast growth factor messenger RNA levels in the ventral midbrain of the intact but not of the 6-hydroxydopamine-lesioned rat.

A negative correlation has been found between smoking and Parkinson's disease. There is evidence to suggest that this correlation appears to be associated with a neuroprotective role of nicotine for dopamine neurons at least in relation to mechanical injury. However, 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine (MPTP) neurotoxicity to dopamine neurons is enhanced by chronic continuous (-)nicotine. More recently, basic fibroblast growth factor has been found to possess neurotrophic activities for many nerve cells including the dopamine cells in vivo and in vitro. Therefore, it is of interest to explore a possible effect of nicotine on basic fibroblast growth factor expression in the ventral midbrain of intact and 6-hydroxydopamine-lesioned rats and how treatment with nicotine can alter the 6-hydroxydopamine-induced injury of the nigral dopamine nerve cells as evaluated by dopamine biochemistry. In the present paper, an analysis of the effects of chronic continuous infusion of (-)nicotine via minipumps was carried out on basic fibroblast growth factor expression in the vental midbrain of the intact male rat and of the 6-hydroxydopamine lesioned rat. A quantitative messenger RNA protection assay analysis was used as well as an immunocytochemical analysis in the substantia nigra. Our findings give evidence that a two-week continuous infusion with (-)nicotine in the intact rat leads to substantial and dose-related (0.03-0.3 mg/kg per h) reductions of basic fibroblast growth factor messenger RNA levels in the ventral midbrain. These changes are not associated with changes in neuronal and glial basic fibroblast growth factor immunoreactivity in this region with the antibodies used. However, a one-week continuous infusion with (-)nicotine (0.125 mg/kg per h) failed to significantly alter the basic fibroblast growth factor messenger RNA levels in the ventral midbrain of solvent and 6-hydroxydopamine-injected rats and thus also the 6-hydroxydopamine-induced increase of basic fibroblast growth factor messenger RNA levels in the ventral midbrain of the lesioned side observed at this time-interval and known to be of astroglial origin [Chadi G. et al. (1994) Neuroscience 61, 891-910]. In agreement, the 6-hydroxydopamine-induced depletion of dopamine in the neostriatum was unaltered by the nicotine treatment (0.125 mg/kg per h). Thus, chronic continuous (-)nicotine treatment may lead to a reduced basic fibroblast growth factor trophic tone in the ventral midbrain of the intact but not of the 6-hydroxydopamine-lesioned rat neither on the lesioned nor on the unlesioned side of the ventral midbrain. It seems possible that chronic nicotine treatment mainly reduces basic fibroblast growth factor messenger RNA levels of neuronal origin, since the astroglial messenger RNA levels dominate after the 6-hydroxydopamine-induced lesions.

Animals↗

The affinities of procolipase and colipase for interfaces are regulated by lipids.

It has been suggested that at physiological pH, the trypsin-catalyzed activation of the lipase cofactor, procolipase, to colipase has no consequence for intestinal lipolysis and serves primarily to release the N-terminal pentapeptide, enterostatin, a satiety factor (Larsson, A., and C. Erlanson-Albertsson 1991. The effect of pancreatic procolipase and colipase on pancreatic lipase activation. Biochim. Biophys. Acta 1083:283-288). This hypothesis was tested by measuring the adsorption of [14C]colipase to monolayers of 1-stearoyl-2-oleoyl-sn-3-glycerophosphocholine and 13, 16-cis, cis-docosadienoic acid in the presence and absence of procolipase. With saturating [14C]colipase in the subphase, the surface excess of [14C]colipase is 29% higher than that of procolipase, indicating that colipase packs more tightly in the interface. With [14C]colipase-procolipase mixtures, the proteins compete equally for occupancy of the argon-buffer interface. However, if a monolayer of either or both lipids is present, [14C]colipase dominates the adsorption process, even if bile salt is present in the subphase. If [14C]colipase and procolipase are premixed for > 12 h at pH approximately 8, this dominance is partial. If they are not premixed, procolipase is essentially excluded from the interface, even if procolipase is added before [14C]colipase. These results suggest that the tryptic cleavage of the N-terminal pentapeptide of procolipase may be of physiological consequence in the intestine.

Adsorption↗

delta Opioid extends hypothermic preservation time of the lung.

To test the hypothesis that a delta opioid, DADLE ([D-Ala2, D-Leu5]-enkephalin), could protect tissue from ischemic damage during hypothermic lung preservation, we studied three groups of rats. In group 1 (n = 8), lung function was studied immediately after harvesting. In group 2 (n = 8), the lung was flushed with 4 degrees C Euro-Collins solution and preserved for 24 hours. In group 3 (n = 8), the lung was flushed with 4 degrees C Euro-Collins solution plus DADLE (1 mg/kg) and preserved for 24 hours. Lung function was studied by using a living rat perfusion model. Venous blood from the host rat perfused the pulmonary artery of the isolated lung. Blood from the isolated lung was returned to the carotid artery of the host rat with a roller pump. Severe pulmonary edema, hemorrhage, and occlusive pulmonary artery resistance occurred in group 2 within 30 minutes of perfusion. Perfusion studies were carried out for more than 60 minutes in groups 1 and 3. Pulmonary blood flow was lower in group 2 than in either group 1 or group 3. Pulmonary vascular resistance was much higher in group 2 than in groups 1 and 3 (p < 0.05). Airway pressure and airway resistance were much higher in group 2 than in groups 1 and 3 (p < 0.05). Airway resistance was also higher in group 3 than in group 1 after 20 minutes of perfusion (p < 0.05). Oxygen tensions from the pulmonary vein of the isolated lung in group 2 were lower than those in groups 1 and 3 (p < 0.05). Alveolar-arterial oxygen difference was much higher in group 2 than in groups 1 and 3 (p < 0.05). Lung tissue wet/dry weight ratio after perfusion was much higher in group 2 than in groups 1 and 3. The results clearly show, for the first time, that DADLE can effectively enhance hypothermic lung preservation in rats.

Airway Resistance↗

Calcitonin receptor mRNA expression in the human prostate.

OBJECTIVES: A subpopulation of prostate neuroendocrine (NE) cells contain calcitonin (CT). It has been postulated that CT-producing cells in the prostate account for the high CT level in the semen, and may be involved in the regulation of other epithelial cells via a paracrine mechanism. The presence of CT binding sites in the plasma membrane fraction of prostate tissue has been demonstrated by radioligand binding assay. In the present study, we investigated the CT receptor gene expression in the human prostate, a key component of the autocrine/paracrine loop in the CT functional pathway. METHODS: Reverse transcription polymerase chain reaction (RT-PCR) was carried out to evaluate the CT receptor mRNA expression in normal prostate tissue. Subsequent DNA sequencing was used to verify RT-PCR amplified products and to determine the isoform of the receptor. To define the location of the CT receptor expression, nonradioactive in situ hybridization was performed with a digoxigenin-labeled probe complementary to the coding region of the CT receptor mRNA. A polyclonal antibody against CT was used to reveal the CT-secreting cells in the prostate. RESULTS: CT receptor MRNA expression was detected in the prostate tissue. Further analysis of the DNA sequence showed that CT receptor expressed in the prostate was the isoform without a 16-amino acid insert in the first intracellular domain. In situ hybridization revealed that CT receptor was present in the prostate NE cells. Immunocytochemical staining of mirror image sections showed that some CT-secreting cells also expressed CT receptor. CONCLUSIONS: CT receptor expression in the prostate, a key component in the CT functional pathway, is located in subsets of dispersed NE cells (CT secreting and CT nonsecreting), which indicates that prostate CT may play an important role in the autocrine/paracrine regulation of the prostate NE system.

Base Sequence↗

Beneficial effects of iloprost cardioplegia in ischemic arrest in isolated working rat heart.

To determine whether the prostacyclin analog iloprost plays a beneficial role in crystalloid cardioplegia in isolated working rat hearts, 20 isolated rat hearts were studied after sustaining 90 min of cardioplegic arrest under hypothermia (20 degrees C). The findings indicated that thromboxane A2 (TXA2) levels in coronary effluent were increased during reperfusion. Iloprost (12 nm/l) inhibited the release of TXA2 and improved the recovery of cardiac hemodynamics after ischemia. These data demonstrated that cardiac-derived TXA2 appeared to mediate reperfusion injury after prolonged aortic clamp or cardiac transplantation and iloprost cardioplegic infusion resulted in the inhibition of release of cardiac-derived TXA2 and in a better preservation of cardiac function after ischemic arrest.

Animals↗

Phenotype, genotype and clonality of Reed-Sternberg cells in nodular sclerosis Hodgkin's disease: results of a single-cell study.

The genotype and clonality of Reed-Sternberg (RS) cells in Hodgkin's disease (HD) has remained a controversial issue, largely due to the scarcity of RS cells in tissues and the limitations of the techniques used to resolve this issue. Southern hybridization and polymerase chain reaction (PCR) assays using DNA extracted from tissues can only document clonal gene rearrangements, but do not indicate which cellular population is responsible for such rearrangements. To overcome the limitations of these previous techniques for studying the genotype and clonality of RS cells, we analysed single RS cells with a single-cell PCR assay to detect immunoglobulin heavy chain gene (IgH) rearrangements and X-chromosome inactivation. Six cases of nodular sclerosis (NS) HD were studied. The RS cells displayed a B-cell phenotype in three cases and a null-cell phenotype in the other three cases. IgH rearrangements were detected in the RS cells of the three cases with a B-cell phenotype, but not in the other cases. In these three cases the IgH rearrangements in the RS cells were polyclonal, although a subpopulation of clonal RS cells was documented in one case. The finding that the RS cells with IgH rearrangements were not monoclonal was supported in one case by studying the pattern of X-chromosome inactivation in single RS cells by a single-cell human androgen receptor gene (HUMARA) PCR assay. Our results indicate that NSHD begins as a polyclonal process in which a clonal RS cell population may arise; and that the RS cells in a subset of NSHD show evidence of B-lineage differentiation.

Base Sequence↗

Pretreatment with tetramethylpyrazine increases the release of PGI2 and decreases TXA2 release in isolated rat heart.

We investigated the release of PGI2 and TXA2 by measuring their stable metabolites of 6-keto-PGF1a and TXB2 in the perfusate in the isolated rat heart after pretreatment with tetramethylpyrazine (TMP). Pretreatment with TMP (12 mg/kg, i.p.) 7 days before preparation produced a significant elevation of 6-keto-PGF1a from 2.30 +/- 0.65 ng/min/g of untreated controls to 3.8 +/- 0.77 ng/mir/g (p < 0.05). Pretreatment with TMP also decreased TXB2 release (p < 0.05 versus control).

6-Ketoprostaglandin F1 alpha↗

Unusual abundance of arginine and ornithine in porcine allantoic fluid.

The concentrations of free arginine, ornithine, and glutamine in porcine allantoic and amniotic fluids were determined on Days 30,35, 40, and 45 of gestation. Arginine and ornithine were the most abundant amino acids in allantoic fluid on Days 35-40 and 45 of gestation, respectively. Arginine and ornithine nitrogen accounted for 40%, 50%, and 55% of the total free alpha-amino acid nitrogen in allantoic fluid on Days 35, 40, and 45 of gestation, respectively. Glutamine was the most abundant amino acid in amniotic fluid during early gestation and was also abundant in allantoic fluid. On Day 45 of gestation, glutamine nitrogen accounted for 41% of the total free alpha-amino acid nitrogen in amniotic fluid. The unusual abundance of arginine (2.5-4.1 mM) and ornithine (1.08-2.52 mM) in allantoic fluid on Days 35-40 of gestation has not been reported for any other biological fluid. These results are novel and interesting with respect to the role of these two basic amino acids in fetal-placental nutrition and metabolism.

Allantoin↗

Lck dependence of signaling pathways activated by gamma-irradiation and CD3 epsilon engagement in RAG-1(-/-)-immature thymocytes.

The src family tyrosine kinase, Lck, transduces signals from the pre-TCR complex which regulate the development and expansion of CD4/CD8 double-positive (DP) thymocytes from CD25(+) CD4/CD8 double-negative progenitors. We and others have recently shown that sublethal gamma-irradiation bypasses the need for TCRbeta expression to promote the development and expansion of DP thymocytes in scid or recombinase-activating gene (RAG)-deficient mice. Here we demonstrate that gamma-irradiation activates an Lck-dependent signaling process in immature thymocytes similar to that initiated physiologically by the pre-TCR complex.

Animals↗

Dietary glutamine supplementation prevents jejunal atrophy in weaned pigs.

The early-weaned pig develops intestinal atrophy and provides a readily accessible animal model for determining the role of dietary supplementation of glutamine (Gln, a major fuel for enterocytes) in preventing intestinal damage. Three experiments were conducted to determine the stability of dietary Gln in the acidic part of the gastrointestinal tract using pigs surgically fitted with a T-cannula in mid-duodenum (Exp. 1), and the effects of dietary Gln supplementation on the villus height and lamina propria depth of duodenum and jejunum (Exp. 2) as well as growth performance (Exp. 3) of pigs weaned at 21 d of age. Postweaning pigs were fed for 14 d corn- and soybean meal-based diets supplemented with 0.0, 0.2, 0.6 or 1.0% free L-Gln. Dietary Gln was not subject to measurable acid hydrolysis in the stomach and upper part of duodenum and was substantially available for the small intestine for metabolic utilization. Glutamine supplementation (1.0%) prevented jejunal atrophy (as indicated by villus height) during the first week postweaning and increased the gain:feed ratio (an indicator of growth performance) by 25% during the second week postweaning. Glutamine supplementation (1.0%) increased plasma concentrations of aspartate, glutamate and alanine and reduced the extent to which plasma taurine concentration fell in postweaning pigs. These results provide an experimental basis for enteral use of Gln in swine production and clinical nutrition to prevent intestinal epithelial damage.

Alanine↗

Lymphomatous polyposis. A neoplasm of either follicular mantle or germinal center cell origin.

Lymphomatous polyposis (LP) is generally thought to be an expression of non-Hodgkin's lymphoma (NHL) of follicular mantle cell (MC) origin. We report nine patients with LP from more than 3,500 cases of NHL studied by the Nebraska Lymphoma Study Group. Our patients differed from those reported previously in that LP represented a follicular center cell (FCC) NHL in two of the nine cases, with the remainder consisting of MC NHL. Three patients developed LP during a relapse of previously diagnosed and treated extraintestinal MC NHL (parotid gland, tonsil, and inguinal lymph node, respectively), whereas the other six patients presented with primary LP. In seven of the nine LP cases, a large mass predominated among a myriad of small polyps. The FCC cases were confined to the small intestine, whereas the MC cases were either pan-intestinal or colonic on their localization. Two MC cases studied by Southern blotting exhibited rearrangement of the bcl-1 locus. Bcl-2 rearrangement was not detected in any of the nine cases when studied by either a polymerase chain reaction-based assay (seven cases) or by Southern blotting (two cases). To date, four patients (three MC, one FCC) have experienced recurrent NHL in gastrointestinal sites. With follow-up ranging from 13 to 147 months, the entire group had a median survival of 41 months (primary MC LP:13, 13, 41, and 77 months; primary FCC LP:45 and 147 months; secondary MC LP:17, 41 and 76 months), and only one patient has died. We conclude that LP is a rare manifestation of NHL of either follicular MC or germinal center cell origin.

Adult↗