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Biomedical subjects

P Sun

Publications and source records attributed to P Sun.

At least 37 records · Page 2Linked to original sources
PubMed2001

Adolescent smoking in Wuhan, China: baseline data from the Wuhan Smoking Prevention Trial.

BACKGROUND: This study reports the prevalence of adolescent smoking in the urban and rural areas of Wuhan, China, the capital of Hubei Province, on the Yangtze River in central China. METHODS: Smoking behavior was examined by age, gender, and urbanicity as part of the Wuhan Smoking Prevention Trial. Subjects included 6994 seventh- to ninth-grade students attending 22 randomly selected schools in urban and rural districts. Outcome measures included lifetime smoking, past-30-day smoking, established smoking (>100 cigarettes in lifetime), and susceptibility to smoking (absence of a firm commitment not to smoke). RESULTS: Lifetime smoking prevalence was 47% among boys and 18% among girls. Past-30-day smoking prevalence was 16% among boys and 4% among girls. Established smoking prevalence was 2% among boys and 0% among girls. The prevalence of susceptibility to smoking was 31% among boys and 10% among girls. Smoking increased significantly with age (p<.0005). Susceptibility was more prevalent in rural areas than in urban areas (p<.05), but there were no urban-rural differences in lifetime, past 30-day smoking, or established smoking. Trend analyses revealed that smoking increased with age more rapidly among boys than among girls (p<.05). Smoking was more prevalent among rural boys than among urban boys, but it was more prevalent among urban girls than among rural girls (p<.05). CONCLUSIONS: Adolescent smoking is a significant public health problem in China. Boys are at particularly high risk, as are girls living in urban areas. Effective smoking prevention programs for adolescents, as well as restrictions on tobacco industry marketing and youth access to tobacco, are needed to prevent tobacco-related morbidity and mortality in China.

Adolescent↗
PubMed2001

Ganglioside modulates ligand binding to the epidermal growth factor receptor.

Whereas previous investigations have shown that pharmacologic addition of gangliosides inhibits keratinocyte proliferation by downregulating epidermal growth factor receptor phosphorylation, the underlying biochemical basis and physiologic relevance are unknown. Using Scatchard and displacement plots, we have shown that supplemental purified gangliosides decrease the binding of (125)I-labeled epidermal growth factor to keratinocyte-derived SCC12 cells. Conversely, SCC12 cells transfected with sialidase and thus depleted of gangliosides show increased ligand binding to the epidermal growth factor receptor, which is consistent with their increased proliferation in response to epidermal growth factor and transforming growth factor-alpha, and increased phosphorylation of the epidermal growth factor receptor, and downstream signal transduction pathway components. The mechanism of the altered binding appears to involve primarily decreased numbers of available receptors within the intact membrane, but not altered receptor protein expression. These studies provide evidence that the effect of gangliosides on keratinocyte proliferation results, at least in part, from the direct binding of ganglioside to the receptor and disruption of the receptor-ligand interaction. Manipulation of membrane ganglioside content may be a powerful new means to alter epidermal growth factor receptor-dependent cell proliferation.

DNA, Complementary↗
PubMed2001

Epidermal growth factor receptor glycosylation is required for ganglioside GM3 binding and GM3-mediated suppression [correction of suppresion] of activation.

Gangliosides are able to bind to the epidermal growth factor receptor and inhibit its activation, but the mechanism of this inhibition is unknown. To address the role of receptor carbohydrates in facilitating interaction with gangliosides, we examined the ability of GM3 to bind the deglycosylated receptor and inhibit its autophosphorylation. Flow cytometry studies demonstrated that deglycosylation of the receptor did not affect its ability to be transported to the cell membrane. In contrast with the native (fully glycosylated) receptor, GM3 did not coimmunoprecipitate with the deglycosylated receptor. Using a novel colorimetric bead binding assay, GM3 was shown to bind well to the immunoprecipitated native receptor but not at all to the deglycosylated receptor. Finally, the addition of GM3 to cells with deglycosylated epidermal growth factor receptors did not result in significant further inhibition of autophosphorylation of the receptor, despite a 10-fold decrease in phosphorylation of the native epidermal growth factor receptor by 200 microM GM3. These studies suggest that ganglioside affects epidermal growth factor receptor activity through a direct interaction that requires receptor glycosylation, and contribute to our understanding of the role of gangliosides in cell membrane function.

Cell Line↗
PubMed2001

Fetal neurosurgery.

SURGERY BEFORE BIRTH has been performed for lethal conditions for several years. The techniques that have been developed are being applied to nonlethal conditions such as meningomyelocele. It is possible that fetal surgery might find a place in the management of certain forms of hydrocephalus as well. The challenge is to define which patients might benefit from such radical procedures before these techniques are accepted as standard care.

Animals↗
PubMed2000

Carbohydrate-carbohydrate binding of ganglioside to integrin alpha(5) modulates alpha(5)beta(1) function.

Gangliosides GT1b and GD3, components of keratinocyte membranes, inhibit keratinocyte adhesion to fibronectin. Although ganglioside sialylation is known to be important, the mechanism of inhibition is unknown. Using purified insect recombinant alpha(5) and beta(1) proteins and alpha(5)beta(1) integrin from lysed keratinocyte-derived SCC12 cells, we have shown that GT1b and GD3 inhibit the binding of alpha(5)beta(1) to fibronectin. Co-immunoprecipitation of GT1b and alpha(5)beta(1) from SCC12 cells and direct binding of GT1b and GD3 to affinity-purified alpha(5)beta(1) from SCC12 cells and insect recombinant alpha(5)beta(1), particularly the alpha(5) subunit, further suggest interaction between ganglioside and alpha(5)beta(1). The carbohydrate moieties of integrin appear to be critical since gangliosides are unable to bind deglycosylated forms of alpha(5)beta(1) from SCC12 and insect cells or poorly glycosylated recombinant alpha(5)beta(1) from Escherichia coli cells. The GT1b-alpha(5)beta(1) interaction is inhibited by concanavalin A, suggesting that GT1b binds to mannose structures in alpha(5)beta(1). The preferential binding of GT1b to high mannose rather than reduced mannose ovalbumin further implicates the binding of GT1b to mannose structures. These data provide evidence that highly sialylated gangliosides regulate alpha(5)beta(1)-mediated adhesion of epithelial cells to fibronectin through carbohydrate-carbohydrate interactions between GT1b and the alpha(5) subunit of alpha(5)beta(1) integrin.

Cell Adhesion↗
PubMed2000

Periodic NADH oxidase activity associated with an endoplasmic reticulum fraction from pig liver. Response to micromolar concentrations of retinol.

An endoplasmic reticulum fraction from pig liver enriched in transitional endoplasmic reticulum vesicles capable of forming 50-60 nm buds in the presence of ATP and retinol was assayed for retinol-responsive oxidation of NADH and cleavage of a dithiodipyridine (DTDP) protein disulfide-thiol interchange substrate. Maxima for the two activities alternated giving rise to a 24 min period. The NADH oxidase activity was inhibited by micromolar and submicromolar concentrations of retinol. Retinol at 0.1 mM stimulated the activity. The inhibition was confined to two activity maxima separated in time by about 5 min. In contrast, with the DTDP substrate, the activity was stimulated by retinol and the stimulations were in the part of the oscillatory pattern where retinol inhibition of NADH oxidation was observed. The findings support an earlier proposed mechanism whereby retinol exerted opposing effects on NADH oxidation and protein disulfide reductions.

Animals↗
PubMed2000

CoQ10 fails to protect brain against focal and global ischemia in rats.

OBJECTIVE: Release of oxygen free radicals occurs following cerebral ischemia. Studies show that oxygen free radicals mediate ischemic brain injury. CoQ10 is a potent free radical scavenger and may offset brain injury associated with reperfusion. We tested exogeneous CoQ10 as a neuroprotectant in rats following both global and focal ischemic insults. METHODS: Rats were subjected to either 4-vessel occlusion ischemia (4-VO, 10 min occlusion, 7-day survival) or middle cerebral artery occlusion (MCAO, 120 min-occlusion, 22.5 h survival). Regional cerebral blood flows (rCBF) and physiological variables such as blood pressure, pO2, pCO2, plasma glucose and hematocrit were monitored and measured in focal ischemia. The animals were randomized to receive treatments of either phosphate buffered saline (PBS) vehicle or CoQ10 following global or focal ischemia. Injection times were at the end of ischemia and 3 h later for both models of ischemia. Histological outcomes are expressed as a percentage of hippocampal CA(1) cell injury in global ischemia or percentage of cortical infarct over that of non-ischemic hemisphere in focal ischemia. RESULTS: In global ischemia, animals treated with PBS vehicle and CoQ10 had 86+/-5% (n=8) and 83+/-10% (n=8), respectively, of hippocampal CA(1) cell injury (P>0.05). The percentage of infarct volumes in animals following focal ischemia were 23+/-9% (control, n=10) and 25+/-9% (CoQ10, n=10). There were no temperature or physiological differences between the two treatment groups. CONCLUSION: Acute treatment with CoQ10 via intraperitoneal injection does not prevent neuronal injuries following global and focal ischemia.

Animals↗
PubMed2000

Dynamic behaviors of the Ricker population model under a set of randomized perturbations.

We studied the dynamics of the Ricker population model under perturbations by the discrete random variable epsilon which follows distribution P¿epsilon=a(i)¿=p(i),i=1,ellipsis,n,0 /=1. Under the perturbations, n+1 blurred orbits appeared in the bifurcation diagram. Each of the n+1 blurred orbits consisted of n sub-orbits. The asymptotes of the n sub-orbits in one of the n+1 blurred orbits were N(t)=a(i) for i=1,ellipsis,n. For other n blurred orbits, the asymptotes of the n sub-orbits were N(t)=a(i)exp[r(1-a(i))]+a(j),j=1,2,ellipsis,n, for i=1,ellipsis,n, respectively. The effects of variances of the random variable epsilon on the bifurcation diagrams were examined. As the variance value increased, the bifurcation diagram became more blurred. Perturbation effects of the approximate continuous uniform random variable and random error were compared. The effects of the two perturbations on dynamics of the Ricker model were similar, but with differences. Under different perturbations, the attracting equilibrium points and two-cycle periods in the Ricker model were relatively stable. However, some dynamic properties, such as the periodic windows and the n-cycle periods (4), could not be observed even when the variance of a perturbation variable was very small. The process of reversal of the period-doubling, an important feature of the Ricker and other population models observed under constant perturbations, was relatively unstable under random perturbations.

Animals↗
PubMed2000

The role of intrahepatic lymphocytes in mediating protective immunity induced by attenuated Plasmodium berghei sporozoites.

Exposure to irradiated Plasmodium sporozoites (gamma-spz) results in protection against malaria. Like infectious spz, gamma-spz colonize hepatocytes to undergo maturation. Disruption of liver stage development prevents the generation of protection, which appears, therefore, to depend on liver stage antigens. Although some mechanisms of protection have been identified, they do not include a role for intrahepatic mononuclear cells (IHMC). We demonstrated that P. berghei gamma-spz-immune murine IHMC adoptively transfer protection to naive recipients. Characterization of intrahepatic CD4+ T cells revealed an immediate, albeit transient, response to gamma-spz, while the response of CD8+ T cells is delayed until acquisition of protection. It is presumed that activated CD8+ T cells home to the liver to die; gamma-spz-induced CD8+CD45RB(lo)CD44(hi) T cells, however, persist in the liver, but not the spleen, during protracted protection. The association between CD8+CD45RB(lo)CD44(hi) T cells and protection has been verified using MHC class I and CD1 knockout mice and mice with disrupted liver stage parasites. Based on kinetic studies, we propose that interferon-gamma, presumably released by intrahepatic effector CD8+ T cells, mediates protection; the persistence of CD8+ T cells is, in turn, linked to Plasmodium antigen depots and cytokines released by CD4+ T cells and/or NK T cells.

Adoptive Transfer↗
PubMed2000

CHOP Infant Coma Scale ("Infant Face Scale"): a novel coma scale for children less than two years of age.

The Glasgow Coma Scale (GCS) is the most frequently used tool worldwide for assessing the severity of neurologic injury after brain trauma, although applying this scale to infants and younger children can be problematic. The CHOP Infant Coma Scale, or Infant Face Scale (IFS), is a novel scale for children under 2 years of age which differs from other pediatric coma scales in the following ways: (1) it relies on objective behavioral observations; (2) it assesses cortical as well as brainstem function; (3) it parallels the GCS in scoring but is based on infant-appropriate behaviors; and (4) it can be applied to intubated patients. We report the results of a prospective study designed to compare interrater reliability between the IFS and GCS in children less than 2 years of age. Seventy-five hospitalized children less than 2 years of age were assessed simultaneously by a pair of observers, representing a spectrum of health care professionals, who scored the children using both the IFS and GCS. Interrater reliability for each pair of observers for each scale was assessed using the kappa statistic. A second series of 10 infants in the intensive care unit with specific diagnoses of acute traumatic or hypoxic/ischemic brain injury were similarly assessed. In the 75 hospitalized infants with a variety of diagnoses, interrater reliability for the GCS was in the "almost perfect," "slight," and "fair" range for the eye-opening, motor, and verbal subtests, respectively. In contrast, the IFS showed interrater reliability in the "almost perfect," "substantial," and "almost perfect" ranges for the three subtests. When applied to infants in an intensive care unit with acute traumatic brain injury or hypoxia/ischemia, the GCS interrater reliability scores were in the "fair" range, while the IFS scores were in the "almost perfect" range. The IFS demonstrates improved interrater reliability in direct comparison to the GCS, particularly in the "verbal/face" component where most pediatric coma scales are deficient. The IFS may prove to be a simple and practical bedside index of brain injury severity in children less than two years of age.

Brain Injuries↗
PubMed2000

Blood pressure, LDL cholesterol, and intima-media thickness: a test of the "response to injury" hypothesis of atherosclerosis.

The "response to injury" hypothesis is a plausible model of the development of atherosclerosis supported by observations from animal models. The present study uses epidemiological data to investigate the hypothesis that wall damage due to hypertension is a precursor of low density lipoprotein cholesterol (LDL-C)-mediated atherosclerosis. The Los Angeles Atherosclerosis Study is following a cohort of 576 participants who were aged 40 to 60 years and were free of symptomatic cardiovascular disease at recruitment. Common carotid artery intima-media thickness (IMT) was assessed by B-mode ultrasonography. After exclusion for nonfasting blood draw and other missing data, 511 subjects were available for analysis. IMT was regressed on LDL-C within tertiles of systolic blood pressure (SBP): low (93 to 122 mm Hg), middle (123 to 132 mm Hg), and high (133 to 175 mm Hg). Covariates were age, sex, body height, body mass index, ethnicity, smoking status, diabetes, and pharmacological treatment for hypertension or hypercholesterolemia. IMT was significantly related to LDL-C in the high SBP group (beta=0.025+/-0.008, where beta values are IMT [mm]/LDL-C [mmol/L]; P=0.002) but not in the middle (beta=-0.006+/-0.008, P=0.39) or low (beta=-0.004+/-0.009, P=0.64) SBP group. The slope in the high SBP group was significantly greater than in the middle (P=0.004) or low (P=0.014) SBP group. Results were similar for women and men, and after the exclusion of diabetics and persons using antihypertensive or lipid-lowering medications. Elevated LDL-C was associated with increased IMT in the upper tertile of SBP but not in the lower tertiles. These findings are consistent with the hypothesis that wall injury due to elevated SBP increases the susceptibility of the artery wall to LDL-C-mediated atherogenesis.

Adult↗
PubMed2000

Caspase inhibitors reduce neuronal injury after focal but not global cerebral ischemia in rats.

BACKGROUND AND PURPOSE: Studies show that blocking the activation of caspases by the caspase inhibitors z-VAD.FMK and z-DEVD.FMK can reduce ischemic neuronal injury after cerebral ischemia. Because the severity of ischemia was mild in some studies, we tested the efficacy of these caspase inhibitors on moderately severe but transient forebrain and focal ischemic insults in the rat. METHODS: Various regimens of z-VAD, z-DEVD, and control DMSO were given to rats subjected to either 4-vessel occlusion ischemia (4-VO, 10-minute occlusion, 7-day survival) or distal middle cerebral artery occlusion (MCAo, 90-minute occlusion, 22.5-hour survival). In global ischemia, treatments were given immediately after ischemia (experiment 1) or as preischemic and postischemic treatments (experiment 2). Three focal ischemia experiments were done. Injection times were 60 minutes into ischemia (experiment 1) and 60 minutes into ischemia plus 30 and 120 minutes after ischemia (experiment 2). Experiment 3 was identical to experiment 2 except that a 30-minute preischemia treatment was instituted. Core normothermia was maintained in all experiments during ischemia. However, in the last focal and global experiments, core and brain temperatures, respectively, were also measured after ischemia with telemetry probes. Because hyperthermia accompanied z-DEVD treatment, an extra z-DEVD-treated group (MCAo) was included with temperature clamped at normothermia. RESULTS: Neither z-VAD nor z-DEVD significantly reduced CA1 injury after global ischemia. In focal ischemia, both drugs significantly reduced infarction, but only in the third experiment, and the prevention of hyperthermia that accompanied z-DEVD treatment did not alter this. CONCLUSIONS: These results suggest a detrimental role of caspases in moderately severe focal but not global cerebral ischemia.

Amino Acid Chloromethyl Ketones↗
PubMed2000

[Foundational study of subcritical water chromatography].

AIM: To study the subcritical water chromatographic discipline of compounds with medium and high polarity on the capillary and packed column. METHODS: A packed and capillary subcritical water chromatography-FID detection system was built up. Six alcohols were well separated on a C18 column and the influence of temperature on chromatographic behavior of alcohols with different polarity was studied. The influence of temperature and pressure on chromatographic behavior of benzoic acid and gensenoside Rg1 on a SE-54 capillary column were also studied. RESULTS: Increasing temperature resulted in the decreasing polarity of mobile phase, shortened retention times of components separated, narrowed peak shape and improved tailing as well. CONCLUSION: Temperature programming could be used successfully to separate compounds with various polarity selectively. Thermostable capillary column could enlarge the range of temperature even more.

Chromatography, Liquid↗
PubMed2000

[Cloning and expression of the gene encoding maltoologosyl trehalose synthase from Sulfolobus shibatae in E. coli].

2.2 kb DNA fragment encoding a novel enzyme, maltooligosyl trehalose synthase (MTSase) was amplified from Sulfolobus shibatae by using PCR technique. The amplified 2.2 kb DNA fragment was inserted into an expression vector, pBV220, to yield the recombinant plasmid pSBGT1. MTSase gene in pBSGT1 was expressed in E. coli. The molecular weight of expressed MTSase detected by SDS-PAGE was about 74 kD, which is conformed with that deduced from nucleotide sequence. The expressed MTSase protein accounted for about 4.4% of the total cell protein. The MTSase from transformants containing pBSGT1 is capable of decreasing DE value, forming non-reducing or less-reducing saccharides when allowed to act on reducing partial starch hydrolysates.

Cloning, Molecular↗
PubMed1999

Identification of benzo[a]pyrene metabolites in cervical mucus and DNA adducts in cervical tissues in humans by gas chromatography-mass spectrometry.

Epidemiological studies indicate that cigarette smoking increases the risk of cervical cancer. To address questions regarding possible mechanisms of tobacco-related cervical carcinogenesis, in a pilot study, using supercritical fluid extraction and a gas chromatographic-mass spectrometric (GC-MS) technique, we detected and characterized benzo[a]pyrene and its metabolites, namely B[a]P-dihydrodiols, phenols and tetraols in cervical mucus samples from eight smokers and non-smokers. Twenty-eight epithelial and stromal cervical tissue samples from seventeen patients undergoing surgery for non-malignant disease were quantitatively analyzed for BPDE-DNA adducts by a GC-MS technique. BPDE-DNA adducts were found in 25 samples. The mean level of BPDE-DNA adducts in epithelial cervical tissues of smokers was nearly two-fold greater than that in self-reported non-smokers; P = 0.02. The mean number of BPDE-adducts (+/- SD) in epithelial cervical tissues of smokers was 3.5 +/- 1.06 adducts/10(8) nucleotides while that in non-smokers was 1.8 +/- 0.96 adducts/10(8) nucleotides. The mean number of BPDE-DNA adducts in stromal cervical tissues of the same subjects was 1.8 +/- 0.96 adducts/10(8) nucleotides in smokers and that in the stromal tissues of non-smokers was 1.4 +/- 1.1 adducts/10(8). These results suggest that polynuclear aromatic hydrocarbons (PAHs) from tobacco smoke and other environmental sources can be transported to the cervix where they are metabolized in the cervical epithelium to ultimate carcinogenic agents, although transport of ultimate carcinogenic metabolites from other organs to the cervix cannot be ruled out. Exposure of cervical epithelia to PAHs and their carcinogenic metabolites suggests a potential role of such carcinogens in the pathogenesis of cervical cancer in humans.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1999

Identification of a novel zinc finger gene, zf5-3, as a potential mediator of neuroblastoma differentiation.

We established a unique parental neuroblastoma cell line, NUB-7, which mimics the bipotentiality of neuroblastoma in vivo along neuronal and Schwann cell lineages following dibutyryl cAMP and retinoic acid treatments, respectively. Differential display identified a putative novel zinc finger gene as a potential differentiation-responsive gene coincident with retinoic acid treatment of NUB-7. This cDNA clone, now designated zf5-3, was mapped to chromosome 19 using somatic cell hybrids, and a larger cDNA clone further localized this gene to band 13.1-13.2 by fluorescent in situ hybridization. zf5-3 possesses 4 characteristic zinc finger DNA-binding motifs as determined by its nucleic acid and proposed amino acid sequence. Expression of zf5-3 is restricted to fetal neuronal, hepatic and renal tissues and their tumor-derived cell lines, including 8/9 neuroblastomas and 2/2 malignant rhabdoid tumors of kidney. The restricted expression in the kidney of zf5-3 to collecting tubules and ureter epithelium is suggestive of an ectodermal histogenesis of malignant rhabdoid tumors of kidney. During development of the fetal human brain, high levels of zf5-3 mRNA are restricted to the mitotically active, undifferentiated neuroblasts. Morphological evidence of overt differentiation was generally accompanied by a marked loss in zf5-3 expression. Therefore, the neuronal tissue expression profile and the down-regulation coincident with retinoic acid-induced neuroblastoma maturation implicate zf5-3 as a potential mediator of their differentiation.

Amino Acid Sequence↗
PubMed1999

Tissue plasminogen activator does not increase neuronal damage in rat models of global and focal ischemia.

BACKGROUND: Intravenous tissue plasminogen activator (tPA) is the only approved treatment for acute ischemic stroke. Recent results from both in vitro and in vivo animal model experiments suggest the possibility that tPA is neurotoxic. METHODS: The authors evaluated the putative neurotoxicity of tPA in both global and focal animal models of ischemic stroke. Global ischemia was induced in male Wistar rats using a modified four-vessel occlusion technique, with percentage neuronal injury assessed at 7 days through necrotic and normal cell count in the CA1 region. Transient focal ischemia was induced in male spontaneously hypertensive rats subjected to middle cerebral artery clipping, with measurement of cortical infarct volume at 24 hours. tPA was administered in 1, 5, or 10 mg/kg doses given intravenously as a 10% bolus, 90% over the following hour, analogous to current human treatment protocols. RESULTS: In the global model, percent hippocampal injury was 60%+/-23%, 66%+/-26%, 55%+/-26%, and 52%+/-12% in the saline control, 1, 5, and 10 mg/kg tPA groups, respectively. In the focal model, after 120 minutes of ischemia, the control infarct size was 151+/-39 mm3, and for the group given 10 mg/kg of tPA, it was 158+/-28 mm3. CONCLUSIONS: Despite sublethal insults, with moderate injury induced by ischemia, there was no evidence that increasing doses of tPA exacerbated ischemic injury.

Animals↗