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Biomedical subjects

Y Chen

Publications and source records attributed to Y Chen.

At least 37 records · Page 2Linked to original sources
PubMed2006

Forward neutral pion production in p + p and d + Au collisions at square root sNN=200 GeV.

Measurements of the production of forward pi0 mesons from p + p and d + Au collisions at square root sNN=200 GeV are reported. The p + p yield generally agrees with next-to-leading order perturbative QCD calculations. The d + Au yield per binary collision is suppressed as eta increases, decreasing to approximately 30% of the p + p yield at eta =4.00, well below shadowing expectations. Exploratory measurements of azimuthal correlations of the forward pi0 with charged hadrons at eta approximately 0 show a recoil peak in p + p that is suppressed in d + Au at low pion energy. These observations are qualitatively consistent with a saturation picture of the low-x gluon structure of heavy nuclei.

Journal Article↗
PubMed2006

Vaccination against nicotine does not prevent nicotine-induced changes in fetal nicotinic receptor binding and c-fos mRNA expression in rats.

Gestational exposure of rats to nicotine produces long-lasting alterations in brain development. Vaccination of adult female rats against nicotine reduces the distribution of maternally administered nicotine to fetal brain, suggesting that vaccination might protect against these effects. In the current study, the effects of vaccination on nicotine-induced changes in fetal (3)H-epibatidine binding and c-fos mRNA expression were evaluated using tissue from a previous pharmacokinetic study of vaccination. An intermittent nicotine dosing regimen designed to resemble nicotine intake in a smoker was administered from GD1-20. Peak nicotine levels in fetal brain were reduced by vaccination, whereas the chronic accumulation of nicotine in fetal brain was not. Gestational nicotine exposure produced significant increases in (125)I-epibatidine binding to brain and spinal cord on GD20, and decreased c-fos mRNA expression in fetal striatum, adrenal and lung. Vaccination did not significantly alter these effects. These data suggest that nicotine dosing, using a clinically relevant intermittent bolus dose regimen, produces substantial changes in fetal nicotinic receptor and c-fos mRNA expression. The decrease in c-fos mRNA expression contrasts with previously reported increases, and suggests that the nicotine dosing regimen used may influence its effects. The lack of effect of vaccination suggests that the cumulative exposure of fetal tissues to nicotine may influence the measured parameters to a greater extent than peak exposure levels.

Analysis of Variance↗
PubMed2006

Abnormal changes of plasma acute phase proteins in schizophrenia and the relation between schizophrenia and haptoglobin (Hp) gene.

In this study we focused on detecting schizophrenia related changes of plasma proteins using proteomic technology and examining the relation between schizophrenia and haptoglobin (Hp) genotype. We investigated plasma proteins from schizophrenic subjects (n = 42) and healthy controls (n = 46) by two-dimensional gel electrophoresis (2-DE) in combination with mass spectrometry. To further reveal the genetic relationship between acute phase proteins (APPs) and schizophrenia disease, we tested Hp alpha1/Hp alpha2 (Hp 1/2) polymorphism and two single nucleotide polymorphisms (SNPs) of Hp, rs2070937 and rs5473, for associations with schizophrenia in the Chinese Han population. With the relatively high number of samples for 2-DE work, we found that four proteins in the family of positive APPs were all up-regulated in patients. In genetic association study, we found significant associations existing between schizophrenia and Hp polymorphisms, Hp 1/2 and rs2070937 variants. Schizophrenia is accompanied by both an altered expression of Hp protein and a different genotype distribution of Hp gene, demonstrating that Hp is associated with schizophrenia. The results from proteomic and genomic aspects both indicate that acute phase reaction is likely to be an aetiological agent in the pathophysiology of schizophrenia, but not just an accompanying symptom. The positive APPs are schizophrenic related proteins, with the highly concordant results on four positive APPs.

Acute-Phase Proteins↗
PubMed2006

Soluble factors from LPS- and PHA-activated PBMC induce MAPK, Stat1 and Stat3 phosphorylation in primary cultures of human term placental trophoblasts: implications for infection and prematurity.

Infection of the maternal vaginal tract is one of the single most important antecedents of premature labor. We have hypothesized that the abundant local synthesis of pro-inflammatory cytokines that occurs during infection may disrupt the delicate "immunological cross-talk" that must occur between maternal and fetal tissues in order to carry pregnancy to term. These experiments were undertaken as part of a larger study directed at testing that hypothesis. We prepared primary cultures of human trophoblasts from term placentas. Cell cultures were stimulated with conditioned medium from resting, PHA or LPS-activated peripheral blood mononuclear cells (PBMC). Medium with LPS or PHA at the same concentration as that used to stimulate the PBMC was used as an additional control. Lysates were subjected to western blotting for activated forms of the mitogen-activated protein kinases (MAPK), Stat1, and Stat3. Western blotting showed phosphorylation of the Jun kinase (JNK), p38, and Erk1/Erk2 MAPK in trophoblasts incubated with conditioned medium from LPS or PHA-activated PBMC but not from medium from resting PBMC, or with PHA or LPS alone. Phosphorylation could be detected as early as 5 min and was still observable by 10 min, the latest time point tested. Similarly, Stat1 and Stat3 phosphorylation was observed within 10 min of exposure to conditioned medium and was still observable 10 min after exposure. Immunohistochemistry also demonstrated nuclear translocation of both Stat1 and Stat3 after stimulation of trophoblasts with medium from activated PBMC. These findings are compatible with the hypothesis that immunologic balance at the maternal-fetal interface is maintained by ongoing "cross-talk" between the fetus (and fetally-derived tissues) and the maternal immune system. Infection of the maternal vaginal tract may disrupt this delicate immunologic balance, initiating inflammatory events that ultimately result in preterm labor.

Enzyme Activation↗
PubMed2006

Mitochondrial factors with dual roles in death and survival.

At least in mammals, we have some understanding of how caspases facilitate mitochondria-mediated cell death, but the biochemical mechanisms by which other factors promote or inhibit programmed cell death are not understood. Moreover, most of these factors are only studied after treating cells with a death stimulus. A growing body of new evidence suggests that cell death regulators also have 'day jobs' in healthy cells. Even caspases, mitochondrial fission proteins and pro-death Bcl-2 family proteins appear to have normal cellular functions that promote cell survival. Here, we review some of the supporting evidence and stretch beyond the evidence to seek an understanding of the remaining questions.

Animals↗
PubMed2006

Association between diabetes and depression: Sex and age differences.

OBJECTIVE: To examine the association between diabetes and the prevalence of depression in different sex and age groups by analysing the cross-sectional data from the National Population Health Survey, conducted in Canada in 1996-1997. STUDY DESIGN: A total of 53072 people aged 20-64 years were included in the analysis. Depression was defined as depression scale 5, based on the Composite International Diagnostic Interview Short-Form (CIDI-SF). Respondents who answered the following question affirmatively were considered to have diabetes: 'do you have diabetes diagnosed by a health professional?'. METHODS: A multiple logistic regression model was used to adjust for potential confounding effects, and a bootstrap procedure was used to take sampling weights and design effects into account. RESULTS: The prevalence of diabetes was much higher in people aged 40-64 years than in people aged 20-39 years (men: 4.7% vs. 0.5%; women: 3.5% vs. 0.8%, respectively). In contrast, people aged 20-39 years had a slightly higher prevalence of depression than those aged 40-64 years (men: 3.1% vs. 2.9%; women: 6.6% vs. 5.4%, respectively). Diabetes was significantly associated with depression in women aged 20-39 years (odds ratio [OR]=2.52, 95% confidence interval [CI]=1.19, 5.32), but not in women aged 40-64 years (OR=1.62, and 95% CI=0.65, 4.06). The association was not significant in both age groups in men, but it tended to be stronger in the younger age group. CONCLUSIONS: The data suggest that diabetes is significantly associated with depression, particularly in young adults.

Adult↗
PubMed2006

Coupling mitochondrial respiratory chain to cell death: an essential role of mitochondrial complex I in the interferon-beta and retinoic acid-induced cancer cell death.

Combination of retinoic acids (RAs) and interferons (IFNs) has synergistic apoptotic effects and is used in cancer treatment. However, the underlying mechanisms remain unknown. Here, we demonstrate that mitochondrial respiratory chain (MRC) plays an essential role in the IFN-beta/RA-induced cancer cell death. We found that IFN-beta/RA upregulates the expression of MRC complex subunits. Mitochondrial-nuclear translocation of these subunits was not observed, but overproduction of reactive oxygen species (ROS), which causes loss of mitochondrial function, was detected upon IFN-beta/RA treatment. Knockdown of GRIM-19 (gene associated with retinoid-interferon-induced mortality-19) and NDUFS3 (NADH dehydrogenase (ubiquinone) Fe-S protein 3), two subunits of MRC complex I, by siRNA in two cancer cell lines conferred resistance to IFN-beta/RA-induced apoptosis and reduced ROS production. In parallel, expression of late genes induced by IFN-beta/RA that are directly involved in growth inhibition and cell death was also repressed in the knockdown cells. Our data suggest that the MRC regulates IFN-beta/RA-induced cell death by modulating ROS production and late gene expression.

Apoptosis Regulatory Proteins↗
PubMed2006

Single-walled carbon nanotubes-mediated in vivo and in vitro delivery of siRNA into antigen-presenting cells.

Antigen-presenting cells such as dendritic cells (DCs) play a critical role in inducing and regulating immune responses. One effective strategy for DC-based immunotherapy is to regulate maturation and function of DC. In this study, we apply single-walled carbon nanotubes (SWNTs) to carry small interfering RNA (siRNA) to reach, enter and genetically modify DCs in vivo. We prepared positively charged SWNTs (SWNTs+) using 1,6-diaminohexane which was demonstrated by transmission electron microscopy equipped with energy-dispersive X-ray spectroscopy and atomic force microscope. The functionalized SWNTs+ could absorb siRNA to form complexes of siRNA with SWNTs. These siRNA:SWNT+ complexes were preferentially taken up by splenic CD11c+ DCs, CD11b+ cells and also Gr-1+CD11b+ cells comprising DCs, macrophages and other myeloid cells to silence the targeting gene. Suppressor of cytokine signaling 1 (SOCS1) restricts the ability of DCs to break self-tolerance and induce antitumor immunity. Infusion of SWNTs+ carrying SOCS1siRNA reduced SOCS1 expression and retarded the growth of established B16 tumor in mice, indicating the possibility of in vivo immunotherapeutics using SWNTs-based siRNA transfer system.

Animals↗
PubMed2006

Work-induced changes in skeletal muscle IGF-1 and myostatin gene expression in uremia.

Resistance to growth hormone (GH)-induced insulin-like growth factor-1 (IGF-1) gene expression contributes to uremic muscle wasting. Since exercise stimulates muscle IGF-1 expression independent of GH, we tested whether work overload (WO) could increase skeletal muscle IGF-1 expression in uremia and thus bypass the defective GH action. Furthermore, to provide insight into the mechanism of uremic wasting and the response to exercise we examined myostatin expression. Unilateral plantaris muscle WO was initiated in uremic and pairfed (PF) normal rats by ablation of a gastrocnemius tendon and adjoining part of this muscle with the contralateral plantaris as a control. Some rats were GH treated for 7 days. WO led to similar gains in plantaris weight in both groups and corrected the uremic muscle atrophy. GH increased plantaris IGF-1 mRNA >twofold in PF rats but the response in uremia was severely attenuated. WO increased the IGF-1 mRNA levels significantly in both uremic and PF groups, albeit less brisk in uremia; however, after 7 days IGF-1 mRNA levels were elevated similarly, >2-fold, in both groups. In the atrophied uremic plantaris muscle basal myostatin mRNA levels were increased significantly and normalized after an increase in WO suggesting a myostatin role in the wasting process. In the hypertrophied uremic left ventricle the basal myostatin mRNA levels were reduced and likely favor the cardiac hypertrophy. Together the findings provide insight into the mechanisms of skeletal muscle wasting in uremia and the hypertrophic response to exercise, and suggest that alterations in the balance between IGF-1 and myostatin play an important role in these processes.

Animals↗
PubMed2006

Cellular and molecular mechanisms of hippocampal activation by acute stress are age-dependent.

The effects of stress, including their putative contribution to pathological psychiatric conditions, are crucially governed by the age at which the stress takes place. However, the cellular and molecular foundations for the impact of stress on neuronal function, and their change with age, are unknown. For example, it is not known whether 'psychological' stress signals are perceived by similar neuronal populations at different ages, and whether they activate similar or age-specific signaling pathways that might then mediate the spectrum of stress-evoked neuronal changes. We employed restraint and restraint/noise stress to address these issues in juvenile (postnatal day 18, [P18]) and adult rats, and used phosphorylation of the transcription factor CREB (pCREB) and induction of c-fos as markers of hippocampal neuronal responses. Stress-activated neuronal populations were identified both anatomically and biochemically, and selective blockers of the stress-activated hippocampal peptide, corticotropin-releasing hormone (CRH) were used to probe the role of this molecule in stress-induced hippocampal cell activation. Stress evoked strikingly different neuronal response patterns in immature vs adult hippocampus. Expression of pCREB appeared within minutes in hippocampal CA3 pyramidal cells of P18 rats, followed by delayed induction of Fos protein in the same cell population. In contrast, basal pCREB levels were high in adult hippocampus and were not altered at 10-120 min by stress. Whereas Fos induction was elicited by stress in the adult, it was essentially confined to area CA1, with little induction in CA3. At both age groups, central pretreatment with either a nonselective blocker of CRH receptors (alpha-helical CRH [9-41]) or the CRF1-selective antagonist, NBI 30775, abolished stress-evoked neuronal activation. In conclusion, hippocampal neuronal responses to psychological stress are generally more rapid and robust in juvenile rats, compared to fully mature adults, and at both ages, CRH plays a key role in this process. Enhanced hippocampal response to stress during development, and particularly the activation of the transcription factor CREB, may contribute to the enduring effects of stress during this period on hippocampal function.

Age Factors↗
PubMed2006

Incidence by occupation and industry of work-related skin diseases in the United Kingdom, 1996-2001.

BACKGROUND: Work-related skin disease is common but few cases are documented in statutory reports or disability systems. Voluntary reporting by specialist physicians provides more complete information. AIMS: To summarize incidence rates of work-related skin diseases reported by consultant dermatologists and occupational physicians, with emphasis on contact and allergic dermatitis by occupation and industry. METHODS: Cases reported in 1996-2001 to the EPIDERM and OPRA national surveillance schemes were analysed by causal agent, occupation and industry, with incidence rates calculated against appropriate denominators. RESULTS: Average annual incidence rates based on data from dermatologists were 97 per million overall, 74 for contact dermatitis and 14 for neoplasia. The corresponding rates for occupational physicians were 623 overall, 510 and 2, respectively. For infective disease, the rates for occupational physicians were 28 compared to 2 for dermatologists. Contact dermatitis was most frequently attributed to rubber chemicals, soaps and cleaners, wet work, nickel and acrylics; most cases of contact urticaria were attributed to rubber chemicals or foods and flour. The pattern of incidence rates by occupation and industry was complex, but correlated with the probable type of exposure. Rates of contact dermatitis were highest among skilled workers in the petrochemical and rubber and plastic manufacturing industries, with machine operators and technical workers in metal and automotive industries also at increased risk. High proportions of cases attributed to rubber chemicals were in nurses and technicians in the health and social services. CONCLUSIONS: These findings identify jobs and types of work where contact with causal agents is common and potentially preventable.

Adult↗
PubMed2006

A traveling wave ultrasonic motor of high torque.

A traveling wave ultrasonic motor of high torque with a new configuration is proposed in this paper. In the new design, a part of the motor serves as the stator. The rotor is the vibrator consisting of a toothed metal ring with piezoelectric ceramic bonded, which generates ultrasonic vibration. The rotor is in contact with the shell of motor and is driven by the friction between the rotor and the stator. This configuration not only removes the rotor in a conventional type of traveling wave ultrasonic motor but also changes the interaction between the rotor and the stator of the motor so that it improves the output performance of the motor. Although an electric brush is added to the ultrasonic motor, it is easy to be fabricated because of the low speed of motor. The finite element method was used to compute the vibration modes of an ultrasonic motor with a diameter of 100mm to optimize the design of the motor. A 9th mode was chosen as the operation mode with a resonance frequency about 25 kHz. According to the design, a prototype was fabricated. Its performance was measured. The rotation speed-torque curves for various frequencies were obtained. The result shows that its stall torque is greater than 4 Nm within a range of 400 Hz. This ultrasonic motor was used to drive the window glass of a mobile car and the result was satisfactory. In the further the research on the friction material between the stator and the rotor is under way to improve the efficiency of the ultrasonic motor.

Journal Article↗
PubMed2006

Hec1 sequentially recruits Zwint-1 and ZW10 to kinetochores for faithful chromosome segregation and spindle checkpoint control.

Faithful chromosome segregation is essential for maintaining the genomic integrity, which requires coordination among chromosomes, kinetochores, centrosomes and spindles during mitosis. Previously, we discovered a novel coiled-coil protein, highly expressed in cancer 1 (Hec1), which is indispensable for this process. However, the precise underlying mechanism remains unclear. Here, we show that Hec1 directly interacts with human ZW10 interacting protein (Zwint-1), a binding partner of Zeste White 10 (ZW10) that is required for chromosome motility and spindle checkpoint control. In mitotic cells, Hec1 transiently forms complexes with Zwint-1 and ZW10 in a temporal and spatial manner. Although the three proteins have variable cell cycle-dependent expression profiles, they can only be co-immunoprecipitated during M phase. Immunofluorescent study showed that Hec1 and Zwint-1 co-localize at kinetochores beginning at prophase and that ZW10 joins them later at prometaphase. Depletion of Hec1 impairs the recruitment of both Zwint-1 and ZW10 to kinetochores, while depletion of Zwint-1 abrogates the kinetochore localization of ZW10 but not Hec1. The results suggest that the localization of Hec1 at kinetochores is required for the sequential recruitment of Zwint-1 and ZW10. Disrupting this recruitment by inhibiting the expression of Hec1 or Zwint-1 causes chromosome missegregation, spindle checkpoint failure, and eventually cell death upon cytokinesis. Taken together, these results, at least in part, provide a molecular basis to explain how Hec1 plays a crucial role for spindle checkpoint control and faithful chromosome segregation.

Cell Cycle Proteins↗
PubMed2006

Synthesis, DNA binding and cytotoxicity of new pyrazole emodin derivatives.

A series of new anthrapyrazoles were derived from emodin by attaching various cationic alkyl amino side chains onto a pyrazole ring which had been incorporated into the anthraquinone chromophore. Compared with emodin, the derivatives had significantly higher DNA binding affinity based on interaction with calf thymus DNA, and much more potent cytotoxicity against different tumor cells. The derivatives with a mono-cationic alkyl side chain exhibited the highest DNA binding affinity and cytotoxicity.

Animals↗
PubMed2006

Laparoscopic blockage of uterine artery and myomectomy: a new method of treating symptomatic uterine leiomyomas.

BACKGROUND: The goal of this study was to evaluate the effects of laparoscopic coagulation or blockage of the uterine arteries and myomectomy in treating symptomatic myomas. METHODS: A total of 142 women with symptomatic fibroids warranting surgical treatment and wanting to retain their uteri were treated by laparoscopic coagulation or blocking of the uterine arteries and myomectomy. RESULTS: Most of the 142 patients had multi-myomas of the uterus, as intramural myomas (54), subserous myomas (65), and submucosal myomas (25). The number of myomas in each patient varied from 1 to 4. The size of the myomas in all patients ranged from 2 to 12 cm. In 86 cases (60.4%) the uterine wall was sutured in one layer. Average operating time was 124.2 +/- 33.1 min, and average blood loss was 117.8 +/- 48.6 ml. Mean postoperative hospital stay was 4.8 +/- 1.2 days. All patients underwent technically successful laparoscopic coagulation or blocking of uterine arteries and myomectomy without intraoperative complications. The mean follow-up time was 16.2 months (16-26). Symptomatic improvement was achieved in all patients. Five patients experienced recurrence of myomas. CONCLUSIONS: Laparoscopic coagulation or block of the uterine arteries and myomectomy appears to be a safe, effective, and promising new method for treating symptomatic uterine myomas.

Adult↗
PubMed2006

Distribution and ultrastructural localization of GEC1 in the rat CNS.

We have previously demonstrated that GEC1 interacts with the kappa opioid receptor and GEC1 expression enhances cell surface expression of the receptor in Chinese hamster ovary cells. In this study, we generated an antiserum (PA629) directed against GEC1 in rabbits, characterized its specificity, and investigated distribution of GEC1 in tissues and in brain regions and spinal cord and its subcellular localization in hypothalamic neurons in the rat. Immunofluorescence staining demonstrated that PA629 recognized HA-GEC1 transfected into Chinese hamster ovary cells, but not HA-GABARAP or HA-GATE-16, although the three share high homology. Pre-incubation of PA629 with GST-GEC1, but not GST, abolished the staining. In immunoblotting, affinity-purified PA629 (PA629p) recognized GEC1, GABARAP and GATE-16. GEC1 migrated slower than GABARAP and GATE-16, with a M(r) of 16 kDa for GEC1 and M(r) of 14 kDa for GABARAP and GATE-16. Immunoblotting results showed that GEC1 level was higher in liver and brain than in lung and heart, and very low in kidney and skeletal muscle. GEC1 was present in all rat brain regions examined and spinal cord. Immunohistochemistry demonstrated that GEC1 immunoreactivity was distributed ubiquitously in the rat CNS with highly intense immunoreactivity in various brain nuclei and motor neurons of the spinal cord. Ultrastructural examination of neurons in the paraventricular nucleus of the hypothalamus showed that GEC1 was associated with endoplasmic reticulum and Golgi apparatus and distributed along plasma membranes and in cytosol. Coupled with our previous observation that GEC1 interacts with N-ethylmaleimide-sensitive factor, these findings strongly suggest that GEC1 functions in intracellular trafficking in the biosynthesis pathway and perhaps also the endocytic pathway. The widespread distribution of GEC1 suggests that GEC1 may be associated with many proteins, in addition to the kappa opioid receptor.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Cited2 modulates TGF-beta-mediated upregulation of MMP9.

Cited (CBP/p300-interacting transactivators with glutamic acid (E)/aspartic acid (D)-rich C-terminal domain) 2, which is a CBP/p300-binding transcription co-activator without typical DNA-binding domains, has been implicated in control of cell growth and malignant transformation in Rat1 cells. In this report, we provide evidence that Cited2 is an important regulator of transforming growth factor (TGF)-beta signaling. Overexpression of Cited2 enhanced TGF-beta-mediated transcription of a Smad-Binding Element-containing luciferase reporter construct, SBE4-Luc. This may occur through a direct physical association of Cited2 with Smads 2 and 3, as supported by co-immunoprecipitation, mammalian two-hybrid and glutathione S-transferase-pull down assays. The transcription factor p300, which binds to Smad3, was shown to further enhance the interaction between Cited2 and Smad3, and the transcriptional responses of Smad3 by Cited2 in reporter assays. Cited2 enhances TGF-beta-mediated upregulation of matrix metalloproteinase 9 (MMP9) in Cited2 inducible mouse embryo fibroblasts. Overexpression of Cited2 enhanced TGF-beta-mediated MMP9 promoter reporter activity. Moreover, knockdown of Cited2 in MDA-MB-231 cells attenuated TGF-beta-mediated upregulation of MMP9 and TGF-beta-mediated cell invasion. Chromatin immunoprecipitation showed that Cited2 and Smad3 were recruited to MMP9 promoter upon TGF-beta stimulation. This is the first demonstration that Cited2 functions as a Smad3/p300-interacting transcriptional co-activator in modulating the expression of MMP9, which could affect tumor cell invasion mediated by TGF-beta.

Animals↗