PubMed Health⌕ Search

Biomedical subjects

Y P Wu

Publications and source records attributed to Y P Wu.

At least 19 recordsLinked to original sources
PubMed2006

Dietary factors and smoking as risk factors for PD in a rural population in China: a nested case-control study.

BACKGROUND: Dietary factors and history of smoking remain elusive in the pathogenesis of Parkinson's disease (PD). OBJECTIVE: We investigated the association of environmental factors with PD in a rural population in China. METHODS: Subjects were participants of a past nutritional intervention trial. Information on their characteristics was collected during the baseline interview of the trial. Control subjects were randomly selected from the same cohort and frequency matched for sex, age and residential area. RESULTS AND CONCLUSION: Among 16,488 subjects surveyed, we diagnosed 464 subjects with PD. Then, four sex- and age-matched controls were paired with each definite PD case. A total of 85 cases and 340 controls were analyzed. Meat consumption and the body mass index (BMI) were inversely associated with PD. The PD risk declined with the increment of BMI. A history of gastric ulcer was associated with an increased risk of PD. As to smoking, there seemed an increased risk of PD among individuals who smoked regularly, non-significantly. However, a significantly increased risk of PD was found among those who smoked more than 30 pack-years.

Adult↗
PubMed2004

Mineralization of polyethylene glycol in aqueous solution by hydrogen peroxide with basic oxygen furnace slag.

This study evaluated the dissolution behavior of basic oxygen furnace slag (BOF slag) and the performance of H2O2 with BOF slag denoted as H2O2/BOF slag process to degrade polyethylene glycol (PEG) in the aqueous solution. The concentration of total organic carbon (TOC) was chosen as a mineralization index of the degradation of PEG by the H2O2/BOF slag process. A first-order kinetic model with respect to TOC was adopted to represent the mineralization of PEG by H2O2/BOF slag process. The experimental results in this study suggested that dosages with 3.98 x 10(-4) mole min(-1) l(-1) H2O2 and 15 g l(-1) BOF slag loading in the solution at pH 2 provided the optimal operation conditions for the mineralization of PEG yielding a 75.5% treatment efficiency at 100 min reaction time. The H2O2/Fe2+ ratio was then determined to be 13.5:1.

Carbon↗
PubMed2003

Involvement of LEU13 in interferon-induced refractoriness of human RSa cells to cell killing by X rays.

Culture of human cells with human interferon alpha and beta (IFNA and IFNB) results in increased resistance of the cells to cell killing by X rays. To identify candidate genes responsible for the IFN-induced X-ray resistance, we searched for genes whose expression levels are increased in human RSa cells treated with IFNA, using an mRNA differential display method and Northern blotting analysis. RSa cells, which showed increased survival (assayed by colony formation) after X irradiation when they were treated with IFNA prior to irradiation, showed increased expression levels of LEU13 (IFITM1) mRNA after IFNA treatment alone. In contrast, IF(r) and F-IF(r) cells, both of which are derived from RSa cells, showed increased X-ray resistance and high constitutive LEU13 mRNA expression levels compared to the parental RSa cells. Furthermore, the IFNA-induced resistance of RSa cells to killing by X rays was suppressed by antisense oligonucleotides for LEU13 mRNA. LEU13, a leukocyte surface protein, was previously reported to mediate the actions of IFN such as inhibition of cell proliferation. The present results suggest a novel role of LEU13 different from that in the inhibition of cell proliferation, involved in IFNA-induced refractoriness of RSa cells to X rays.

Antigens, Differentiation↗
PubMed2001

Stent coating with titanium-nitride-oxide for reduction of neointimal hyperplasia.

BACKGROUND: Coronary stents prevent constrictive arterial remodeling but stimulate neointimal hyperplasia. Stainless steel induces a metallic foreign body reaction, which is absent for titanium. The hypothesis of the present study was that titanium renders the stent surface biologically inert, with reduced platelet and fibrinogen binding. METHODS AND RESULTS: Twelve pigs were instrumented with a stainless steel and 2 titanium-nitride-oxide-coated stents (TiNOX 1, ceramic; TiNOX 2, metallic). Animals were restudied after 6 weeks. Histological specimens of stented segments were analyzed by digital morphometry. Platelet adhesion and fibrinogen binding studies were performed in the perfusion chamber. Under in vitro conditions, TiNOX 1 showed reduced platelet adhesion (65+/-3%) compared with TiNOX 2 (72+/-5%; P<0.05) and stainless steel (71+/-4%; P<0.05). Platelet adhesion 48 hours after incubation with human plasma, however, was not different between TiNOX 1 (17+/-3%) and 2 (15+/-3%) but was significantly higher with stainless steel (23+/-2%; P<0.05). Fibrinogen binding was significantly reduced with TiNOX 2 (54+/-3%) compared with TiNOX 1 (82+/-4%, P<0.05) or stainless steel (100%, P<0.05). Histomorphometry revealed a significantly larger neointimal area in stainless steel (2.61+/-1.12 mm(2)) than in TiNOX 1-coated (1.47+/-0.84 mm(2), P<0.02) or TiNOX 2-coated (1.39+/-0.93 mm(2), P<0.02) stents. The reductions were 44% and 47%, respectively. CONCLUSIONS: TiNOX coating significantly reduces neointimal hyperplasia in stainless steel stents. The antiproliferative effect was similar for both TiNOX coatings, suggesting that the electrochemical properties are more important for attenuation of neointimal proliferation than the observed differences in platelet adhesion and fibrinogen binding.

Alloys↗
PubMed2001

Car accidents on a single-lane highway.

We study the occurrence of car accidents in the Nagel-Schreckenberg model. Both the effects of stochastic braking and speed limit are analyzed. An approximate scaling relation is observed with the varying of speed limit. The stochastic noise will enhance the probability for accidents in the low density region and suppress that in the high density region. The probability for car accidents to occur becomes a broadened distribution over a wide range of density.

Journal Article↗
PubMed2001

Expression of immune-related molecules is downregulated in twitcher mice following bone marrow transplantation.

Twitcher (twi/twi) is a murine model of a human genetic demyelinating disease, globoid cell leukodystrophy (Krabbe disease). The affected mice usually die before reaching age 45 days, having demyelination associated with extensive glial activation. The twi/twi mice that receive wild-type bone marrow transplantation (BMT) survive up to 3 times longer with improved pathology. We hypothesize that immune-related molecules such as cytokines and chemokines are partly responsible for the demyelination in twi/twi, and that the decrease in the expression of such molecules following BMT contributes to clinico-pathological improvement. Cells expressing TNF-alpha, MCP-1, and MIP-1beta were conspicuous in the twi/twi CNS accompanied by infiltration of Ia+ and CD8+/CD3- hematogenous cells. These cells decreased gradually after BMT TNF-alpha mRNA and mRNA of C-C chemokine families, including MCP-1, IP-10, MIP-1alpha, MIP-1beta, and RANTES, were upregulated in the twi/twi CNS but downregulated gradually following BMT. In twi/twi that survived to 20 wk of age, cells expressing TNF-alpha, MCP-1, MIP-1beta, Ia, or CD8 were hardly detected and pathology was clearly improved. These results are consistent with the hypothesis that cytokine expression in glial cells contributes (to some extent) to the pathogenesis of demyelinating lesions in the twi/twi mice.

Animals↗
PubMed2001

Absence of fibrinogen in afibrinogenemia results in large but loosely packed thrombi under flow conditions.

We studied the role of fibrinogen in platelet thrombus formation under flow on adhesive proteins using afibrinogenemic blood (LMWH anticoagulated) in a perfusion system. Perfusions with afibrinogenemic blood showed strong increased surface coverage and thrombus volume that normalized upon addition of fibrinogen. Similar studies using citrate anticoagulated blood showed that this was due to fibrinogen and not fibrin. Morphological analysis showed that afibrinogenemic thrombi were loosely packed and consisted mainly of dendritic platelets that contacted one another through filopodia. However, in the presence of fibrinogen, platelets formed lamellipodia and spread out on top of one another. Studies with radiolabeled platelets showed similar numbers of platelets in both conditions demonstrating that the difference is one of packing and the larger size is due to absence of lamellipodia formation and spreading. The found increased thrombus size and loosely packed platelets might help to understand thrombotic complications sometimes seen in afibrinogenemia patients.

Adult↗
PubMed2000

Prospective study of serum selenium levels and incident esophageal and gastric cancers.

BACKGROUND: From March 1986 through May 1991, we conducted a randomized nutritional intervention trial, the General Population Trial, in Linxian, China, a region with epidemic rates of squamous esophageal and adenomatous gastric cardia cancers. We found that participants who received selenium, beta-carotene, and vitamin E had significantly lower cancer mortality rates than those who did not. In the current study, we examined the relationship between selenium levels measured in pretrial (1985) sera from participants and the subsequent risk of developing squamous esophageal, gastric cardia, and gastric non-cardia cancers during the trial. METHODS: This study was designed and analyzed in accord with a stratified case-cohort sampling scheme, with the six strata defined by sex and three age categories. We measured serum selenium levels in 590 case subjects with esophageal cancer, 402 with gastric cardia cancers, and 87 with gastric non-cardia cancers as well as in 1062 control subjects. Relative risks (RRs), absolute risks, and population attributable risk for cancers were estimated on the basis of the Cox proportional hazards models. All statistical tests are two-sided. RESULTS: We found highly significant inverse associations of serum selenium levels with the incidence of esophageal (P: for trend <10(-4)) and gastric cardia (P: for trend <10(-6)) cancers. The RR and 95% confidence interval (CI) for comparison of highest to lowest quartile of serum selenium was 0.56 (95% CI = 0.44-0.71) for esophageal cancer and 0.47 (95% CI = 0.33-0.65) for gastric cardia cancer. The population proportion of these cancers that is attributable to low selenium levels was 26.4% (95% CI = 14.45-38.36). We found no evidence for a gradient of serum selenium associated with incidence of gastric non-cardia cancer (P: for trend =.96), with an RR of 1.07 (95% CI = 0.55-2.08) for the highest to lowest quartile of serum selenium. CONCLUSIONS: Our study supports findings from previous prospective studies and randomized trials that variations in selenium levels affect the incidence of certain cancers. In the United States, where intervention trials of selenium are in the planning stages, consideration should be given to including populations at high risk for squamous esophageal and gastric cardia cancers.

Adult↗
PubMed2000

Platelet adhesion to collagen in healthy volunteers is influenced by variation of both alpha(2)beta(1) density and von Willebrand factor.

Platelet thrombus formation on collagen is initiated by platelet GPIb interaction with von Willebrand factor (vWF) bound to collagen, followed by firm attachment of the platelet to collagen by the integrin alpha(2)beta(1). Platelet and plasma vWF levels and alpha(2)beta(1) density on the platelet surface are highly variable among normal subjects; however, little is known about the consequences of this variability on platelet adhesion to collagen. A population of 32 normal subjects was studied to evaluate the relation between genetic and phenotypic variations of alpha(2)beta(1) density on the platelet surface, plasma vWF levels, platelet vWF levels, and adenosine diphosphate and adenosine triphosphate concentrations on the one hand and platelet adhesion to collagen under flow on the other hand. Platelet adhesion to collagen types I and III under flow was correlated with plasma levels of vWF (r(2) = 0.45 and 0.42, respectively) and alpha(2)beta(1) density on the platelet surface (r(2) = 0.35 and 0.17, not significant). Platelet adhesion to collagen type IV under flow was significantly correlated with platelet vWF levels (r(2) = 0.34) and alpha(2)beta(1) density on the platelet surface (r(2) = 0.42). Platelet adhesion to collagen types I and III depends on both plasma levels of vWF and alpha(2)beta(1) density on the platelet surface, whereas platelet adhesion to collagen type IV is mediated by both platelet vWF levels and alpha(2)beta(1) density on the platelet surface. (Blood. 2000;96:1433-1437)

Adult↗
PubMed2000

Search for UV-responsive genes in human cells by differential mRNA display: involvement of human ras-related GTP-binding protein, Rheb, in UV susceptibility.

The search for genes responsible for the sensitivity of human cells to cell-killing effects of UV is an important area of biological research. To identify candidate genes responsible for UV sensitization, levels of mRNA expression were compared between UV-sensitive RSa cells and UV-resistant variant UV(r)-1 cells, using a differential display method and Northern blot analysis. Messenger RNA expression levels of human Ras homologue enriched in brain (Rheb) and/or a Rheb-like gene were up-regulated and slightly decreased in UV-irradiated RSa and UV(r)-1 cells, compared to in mock-irradiated cells, respectively. RSa and UV(r)-1 cells, both of which were treated with antisense oligonucleotides for Rheb RNA, exhibited an increased resistance to UV cell-killing. It remains unclear why UV(r)-1 cells are resistant to UV yet express Rheb mRNA at high levels. However, the results of antisense experiments together with the up-regulation in UV-irradiated RSa cells, suggest that Rheb is involved in the UV sensitization of both cells to UV cell-killing.

Cell Death↗
PubMed2000

Alleviation of neuronal ganglioside storage does not improve the clinical course of the Niemann-Pick C disease mouse.

Niemann-Pick disease Type C (NP-C) is a progressive neurodegenerative disorder caused by mutations in the NPC1 gene and characterized by intracellular accumulation of cholesterol and sphingo-lipids. The major neuronal storage material in NP-C consists of gangliosides and other glycolipids, raising the possibility that the accumulation of these lipids may participate in the neurodegenerative process. To determine if ganglioside accumulation is a crucial factor in neuropathogenesis, we bred NP-C model mice with mice carrying a targeted mutation in GalNAcT, the gene encoding the beta-1-4GalNAc transferase responsible for the synthesis of GM2 and complex gangliosides. Unlike the NP-C model mice, these double mutant mice did not exhibit central nervous system (CNS) accumulation of gangliosides GM2 or of glycolipids GA1 and GA2. Histological analysis revealed that the characteristic neuronal storage pathology of NP-C disease was substantially reduced in the double mutant mice. By contrast, visceral pathology was similar in the NP-C and double mutant mice. Most notably, the clinical phenotype of the double mutant mice, in the absence of CNS ganglioside accumulation and associated neuronal pathology, did not improve. The results demonstrate that complex ganglioside storage, while responsible for much of the neuronal pathology, does not significantly influence the clinical phenotype of the NP-C model.

Animals↗
PubMed2000

The tissue plasminogen activator (tPA)/plasmin extracellular proteolytic system regulates seizure-induced hippocampal mossy fiber outgrowth through a proteoglycan substrate.

Short seizure episodes are associated with remodeling of neuronal connections. One region where such reorganization occurs is the hippocampus, and in particular, the mossy fiber pathway. Using genetic and pharmacological approaches, we show here a critical role in vivo for tissue plasminogen activator (tPA), an extracellular protease that converts plasminogen to plasmin, to induce mossy fiber sprouting. We identify DSD-1-PG/phosphacan, an extracellular matrix component associated with neurite reorganization, as a physiological target of plasmin. Mice lacking tPA displayed decreased mossy fiber outgrowth and an aberrant band at the border of the supragranular region of the dentate gyrus that coincides with the deposition of unprocessed DSD-1-PG/phosphacan and excessive Timm-positive, mossy fiber termini. Plasminogen-deficient mice also exhibit the laminar band and DSD- 1-PG/phosphacan deposition, but mossy fiber outgrowth through the supragranular region is normal. These results demonstrate that tPA functions acutely, both through and independently of plasmin, to mediate mossy fiber reorganization.

Amygdala↗
PubMed2000

Distribution and characterization of GFP(+) donor hematogenous cells in Twitcher mice after bone marrow transplantation.

The twitcher mouse is a murine model of globoid cell leukodystropy, a genetic demyelinating disease caused by a mutation of the galactosylceramidase gene. Demyelination of the central nervous system commences around 20 postnatal days. Using GFP-transgenic mice as donors, the distribution of hematogenous cells after bone marrow transplantation was investigated in the twitcher mice. Bone marrow transplantation was carried out at 8 postnatal days. In twitcher chimeric mice examined before 30 postnatal days, numerous GFP(+) cells were detected in spleen and peripheral nerve but only a few were detected in the liver, lung, and spinal white matter. In contrast, at 35 to 40 postnatal days when demyelination is evident, many GFP(+) cells with ameboid form were detected in the white matter of the spinal cord, brainstem, and cerebrum. Approximately half of these GFP(+) cells were co-labeled with Mac-1. In twitcher chimeric mice examined after 100 postnatal days, the majority of GFP/Mac-1 double-positive cells displayed the morphological features of ramified microglia with fine delicate processes and was distributed diffusely in both gray and white matter. These results suggest that a significant number of donor hematogenous cells are able to infiltrate into the brain parenchyma, repositioning themselves into areas previously occupied by microglia, and to ameliorate lethality.

Animals↗
PubMed2000

Infiltration of hematogenous lineage cells into the demyelinating central nervous system of twitcher mice.

Infiltration of hematogenous lineage cells into the central nervous system (CNS) was investigated in the twitcher mouse, a murine model of globoid cell leukodystrophy in human. The hematogenous cells were selectively labeled following intraperitoneal injection of rhodamine isothiocyanate (RhIc). The frequency of detecting Rhlc-labeled cells (Rhlc+ cells) in the twitcher CNS varied with age. RhIc+ cells were hardly detected when injection was made prior to the postnatal day (PND) 30. The number of Rhlc' cells increased thereafter peaked at PND 35-38 and declined drastically at PND 40-45. The majority of RhIc+ cells were distributed in white matter of the CNS that correlated well with the areas of demyelination and of increased microglia/macrophage population described in our earlier studies. Almost all Rhlc+ cells were double-labeled with antibody for Mac-1 and also with MHC class II. Some small cells double-labeled with RhIc and antibodies for CD4, CD8, or IL-2R were also identified. By RT-PCR, the expression of monocyte chemoattractant protein- (MCP-1) mRNA increased drastically at PND 30, peaked at PND 35, and decreased gradually after PND 40. This pattern of mRNA changes correlated well with the dynamic pattern of the infiltration of hematogenous cells into the CNS, suggesting a role of chemokine(s) in the cellular infiltration in the twitcher brain. The expression of IL-10 mRNA also increased gradually. IL-10 is a cytokine inhibitory factor and a major regulator in suppressing the inflammatory response. Thus, our results indicated that hematogenous lineage cells infiltrated in the CNS of twitcher mice, and that MCP-1 and IL-10 may play an important role in regulating the cellular recruitment.

Animals↗
PubMed2000

Platelet thrombus formation on collagen at high shear rates is mediated by von Willebrand factor-glycoprotein Ib interaction and inhibited by von Willebrand factor-glycoprotein IIb/IIIa interaction.

We studied the role of von Willebrand Factor (vWF) in platelet thrombus formation in flowing blood by using a perfusion system and mutant forms of vWF lacking either interaction with glycoprotein Ib (GpIb) or with glycoprotein IIb/IIIa (alphaIIb-beta3). These mutants were added to the blood of patients with severe von Willebrand's disease (vWD) or to normal blood reconstituted with a human albumin solution instead of plasma. This blood was then perfused over collagen type III spray-coated on a glass surface and preincubated for 2 hours with 20 microg/mL plasma vWF. In this way, the adhesion step was mediated by the preincubated plasma vWF bound to collagen type III, whereas thrombus formation was mediated by mutant vWF added to the perfusate. Thrombus formation was absent at all 3 shear rates studied (300, 800, and 2600 s(-1)) when DeltaA1-vWF, lacking interaction with GpIb, was added to the perfusate, indicating the importance of GpIb-vWF interaction for thrombus formation. The interaction of vWF and GpIb is currently thought to be possible under physiological conditions in which the conformation of vWF has been changed by adsorption to a surface. Our results regarding the role of GpIb-vWF interaction in thrombus formation suggest that a second mechanism may operate by which a change may occur in GpIb on the surface of adhered platelets either by activation of the molecule or as a consequence of shear stress. Increased thrombus formation was observed when the Arg-Gly-Gly-Ser-vWF, which does not interact with alphaIIb-beta3, was added to vWD blood and perfused at 2600 s(-1). This increase was not observed in vWD blood at lower shear rates or after addition of Arg-Gly-Gly-Ser-vWF to reconstituted normal blood. Thrombus formation at a high shear rate was largest when either vWF or fibrinogen was present as a single ligand for alphaIIb-beta3 at a high shear rate. When both were present, thrombus formation was decreased. We postulate that thrombus formation is less efficient because of incomplete bridge formation when vWF and fibrinogen are both present as ligands for alphaIIb-beta3.

Antibodies↗
PubMed2000

[The expression patterns of genes in different biotypes by genome addition].

The patterns of SOD, EST and haemoglobin genes expression among the different combinations conducted with genome addition were investigated. The erythrocyte expression of these isozymes and protein were visualized by histochemical staining after polyacrylamide gradient gel electrophoresis. The results of our electrophoresis analysis have revealed that biochemical polymorphism exists in the combinations, and these genetic variance have resulted from the contribution of different genomes. This study provides additional evidence that gene dosages can be interpreted from the enzyme patterns and electrophoretic staining intensities existed in different ploidies, which suggests that subunit interactions for SOD are co-operative and additive. This would indicate that each allele could be differentially regulated so that even one-third genome can be expressed in triploid individuals. These genetic data could be used to construct genome specific varieties, and would not only help to maximize efficiency in the use of different biotypes identification, but also help to maximize studying the relationship between gene dosage, expression and regulation.

Animals↗
PubMed2000

Preparation of monoclonal antibody against human m3 receptor.

AIM: To raise monoclonal antibody against human m3 receptor. METHODS: The m3 receptor selective peptide segments deduced from its gene were chemically synthesized, coupled to keyhole limpet hemocyanin carrier protein, and injected to Balb/c mice to raise monoclonal antibody. Antibody was purified by a combination of two-step precipitation methods and ion-exchange chromatography. The specificity of monoclonal antibody was tested by enzyme-linked immunosorbent assay, immunohistochemistry, and radioligand binding assay of receptors. RESULTS: The monoclonal antibody specifically bound to the protein of rat salivary gland and m3 peptide, but not m4 peptide. In radioligand binding assay of receptors, monoclonal antibody inhibited the binding of 3H-QNB to muscarinic receptor in rat salivary gland, but not in rat heart, and could not inhibit the binding of 3H-PZ to rat brain cerebral cortex membrane protein. Immunohistochemical study showed that the human salivary cell surface was strongly stained, whereas the human heart cell surface was not. CONCLUSION: Highly purified (96.3%) monoclonal antibody against the m3 receptor peptide recognized the m3 receptor.

Animals↗