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Biomedical subjects

C Yan

Publications and source records attributed to C Yan.

At least 19 recordsLinked to original sources
PubMed2007

End-grafted low-molecular-weight PNIPAM does not collapse above the LCST.

The interfacial properties of end-grafted temperature-responsive poly(N-isopropylacryamide) (PNIPAM) were quantified by direct force measurements both above and below the lower critical solution temperature (LCST) of 32 degrees C. The forces were measured between identical, opposing PNIPAM films and between a PNIPAM film and a lipid membrane. At the grafting densities and molecular weights investigated, the polymer extension did not change significantly above the LCST, and the polymers did not adhere. Below the LCST, the force-distance profiles suggest a vertical phase separation, which results in a diluter outer layer and a dense surface proximal layer. At large separations, the force profiles agree qualitatively with simple polymer theory but deviate at small separations. Importantly, at these low grafting densities and molecular weights, the end-grafted PNIPAM does not collapse above the LCST. This finding has direct implications for triggering liposomal drug release with end-grafted PNIPAM, but it increases the temperature range where these short PNIPAM chains function as steric stabilizers.

Acrylic Resins↗
PubMed2006

Electrooxidation of methanol on upd-Ru and upd-Sn modified Pt electrodes.

The electrochemical oxidation of methanol has been investigated on underpotentially deposited-ruthenium-modified platinum electrode (upd-Ru/Pt) and on underpotentially deposited-tin-modified platinum electrode (upd-Sn/Pt). The submonolayers of upd-Ru and upd-Sn on a Pt electrode increased the rate of methanol electrooxidation several times as large as that on a pure Pt electrode. The best performance for methanol electrooxidation was obtained on a ternary platinum based catalyst modified by upd-Ru and upd-Sn simultaneously. The influence of the submonolayers of upd-Ru adatoms and upd-Sn adatoms on the oxidation of methanol in acid has been investigated. The effect of Ru on methanol electrooxidation lies on the distribution of Ru adatoms on a Pt surface. It has been shown that as long as the amount of upd-Ru deposits were controlled in a proper range, upd-Ru deposits would enhance the methanol oxidation obtained on a Pt electrode at whichever deposition potential the upd-Ru deposits were obtained. The effects of tin are sensible to the potential range. The enhancement effect of upd-Sn adatoms for the oxidation of methanol will disappear as the electrode potential is beyond a certain value. It is speculated that there exists a synergetic effect on the Pt electrode as adatoms Ru and Sn participate simultaneously in the methanol oxidation.

Journal Article↗
PubMed2006

Identification of an histone H3 acetylated/K4-methylated-bound intragenic enhancer regulatory for urokinase receptor expression.

The transcriptionally regulated urokinase-type plasminogen activator receptor (u-PAR) contributes to cancer progression. Although previous studies have identified multiple 5' regulatory elements, these cis motifs cannot fully account for u-PAR expression prompting a search for hitherto uncharacterized regulatory elements. DNase I hypersensitivity and chromatin immunoprecipitation assays using u-PAR-expressing colon cancer cells indicated a hypersensitive region (+665/+2068) in intron 1 enriched with acetylated histone 3 (H3) and H3 methylated at lysine 4, markers of regulatory regions. The +665/+2068 region increased transcription from a u-PAR-promoter in an orientation- and distance-independent manner fulfilling the criteria of an enhancer. Optimal stimulation of the u-PAR promoter by phorbol ester required this enhancer. Systematic truncations combined with DNase I footprinting revealed two protected regions (+1060/+1099 and +1123/+1134) with deletion of the latter practically abolishing enhancer activity. The +1123/+1134 region harbored non-consensus activator protein-1 and Ets1 binding sites bound with c-Jun (and/or the related JunD/JunB) and c-Fos (and/or the related FosB/Fra-1/Fra-2) as revealed with chromatin immunoprecipitation. Further, nuclear extract from resected colon cancers showed elevated protein binding to a +1123/+1134-spanning probe coordinate with elevated u-PAR protein. Thus, we have defined a novel intragenic enhancer in the u-PAR gene required for constitutive and inducible expression.

Acetylation↗
PubMed2006

Transcatheter closure of patent ductus arteriosus with severe pulmonary arterial hypertension in adults.

BACKGROUND: Surgical closure of patent ductus arteriosus (PDA) with severe pulmonary arterial hypertension in adults carries higher risk than in children. OBJECTIVES: To investigate the application of self-expandable occluders for transcatheter closure of PDA associated with severe pulmonary arterial hypertension in adults, and the assessment of immediate and short-term results. METHODS: 29 adult patients (6 men, 23 women) underwent attempted transcatheter closure of PDA at a mean (standard deviation (SD)) age of 31.1 (11.4) years (range 18-58 years) and a mean (SD) weight of 54.1 (7.1) kg (range 42-71 kg). On the basis of haemodynamic and clinical data obtained before and after trial occlusion, the final duct occlusion was determined and carried out. Radiographs of the chest, electrocardiograms and echocardiograms were used for follow-up evaluation of the treatment within 1 day, 1 month and 3-6 months after successful closure. RESULTS: 20 of the 29 patients had successful occlusion (group 1), and 9 patients failed (named group 2). In group 1, in which occlusion was successful, mean (SD) pulmonary arterial pressures decreased markedly after trial occlusion: 78 (19.3) mm Hg (range 50-125 mm Hg) before occlusion and 41 (13.8) mm Hg (range 23-77 mm Hg) after occlusion. Systemic arterial oxygen saturation was found to be >90% in 19 patients and <90% in the remaining patient before inhalation of oxygen, and >95% during inhalation of oxygen or after occlusion in all 20 patients. In group 2, the occlusion was not successful, because in two patients the device was not available; another two patients showed worsening of symptoms. The other five patients showed increased pulmonary arterial pressures after trial closure; their mean (SD) pulmonary arterial pressures increased by 10.3 (6) mm Hg (4-16 mm Hg) after trial occlusion, and systemic arterial oxygen saturation was 85.5% (2.6%) (range 82.6-88%) before inhalation of oxygen and 94.7% (1.7%) (range 90.7-99.1%) during inhalation of oxygen. In group 1, the dimensions of the left atrium, left ventricle and pulmonary artery increased considerably in 3-6-months of follow-up compared with those of preocclusion. CONCLUSIONS: Transcatheter closure is an effective treatment for adults with PDA associated with reversible severe pulmonary arterial hypertension. Further research is needed for the evaluation of long-term results.

Adolescent↗
PubMed2006

Inhibition of growth and increase of alkaline phosphatase activity in cultured human oral cancer cells by all-trans retinoic acid.

In this study, the effects of all-trans retinoic acid (ATRA) on human oral cancer cells with regard to cell growth, the cell cycle, and alkaline phosphatase (ALP) activity were evaluated. Human oral cancer KB cells were treated with various concentrations of ATRA, and cell growth was then determined using the MTT viability assay. The cell-cycle distribution and ALP activity were analysed using a flow cytometer and chemical analyser, respectively. The KB cells were inhibited by ATRA at concentrations of 1-16 microM (1 microM, P<0.05; 2 microM, P<0.01; 4, 8 and 16 microM, P<0.001) in a dose-dependent manner. ATRA arrested KB cells in the G0/G1 phase. The ALP activity in KB cells was increased by ATRA. This is one of the first studies to focus on the expression of ALP in human head-and-neck carcinoma cells treated with retinoids. These findings suggest that the anti-tumour effects of ATRA on human oral cancer are associated with G0/G1 phase arrest and an increase in ALP activity.

Alkaline Phosphatase↗
PubMed2005

A new congenital form of X-linked autophagic vacuolar myopathy.

In a new family with X-linked congenital autophagic vacuolar myopathy (AVM), seven affected boys presented with congenital hypotonia, dyspnea, and dysphagia with delayed motor milestones. Muscle pathology revealed autophagic vacuoles with sarcolemmal features, multilayered basal lamina with marked sarcolemmal deposition of C5-9 membrane attack complex and calcium, histologically indistinguishable from childhood-onset X-linked myopathy with excessive autophagy (XMEA). Haplotype analysis suggests that this new AVM and XMEA may be allelic despite different clinical presentations.

Antigens, Protozoan↗
PubMed2005

Cyclooxygenase-2 expression is associated with VEGF-C and lymph node metastases in gastric cancer patients.

Previous studies have suggested that cyclooxygenase-2 (COX-2) over-expression is associated with angiogenesis in gastric cancer. However, the relationship between COX-2 and lymphangiogenesis is still unclear. The aim of this study was to determine the relationship between COX-2 expression and lymphangiogenic factor, vascular endothelial growth factor-C (VEGF-C), in human gastric cancer, as well as to correlate with clinicopathological parameters. Sixty-three gastric cancer patients underwent radical gastrectomy (D2 or D3) were enrolled in this study. The expression of COX-2 and VEGF-C were detected by immunohistochemistry, and the small lymphatic vessels were immunohistochemically stained by LYVE-1 antibody. The association between COX-2 and VEGF-C expressions and clinicopathological parameters (such as gender, tumor location, lymph node status and Lauren classification) were determined. VEGF-C over-expression was observed in 33 of 63 patients (52%), while COX-2 over-expression occurred in 42 of 63 tumor samples (67%). Presence of microlymphatic vessels with LYVE-1 staining was found in 35 cases. COX-2 over-expression was highly correlated with VEGF-C over-expression (P = 0.032), microlymphatic vessels (P = 0.002) as well as presence of metastatic lymph nodes (P = 0.007). However, no significant correlation was found between COX-2 expression and other clinicopathological parameters. Our data suggest that COX-2 expression is associated with lymphangiogenesis and lymph node metastasis in human gastric carcinoma. This raises the possibility that COX-2-mediated VEGF-C over-expression might promote lymph node metastasis via lymphangiogenesis pathway in patients with gastric cancer.

Aged↗
PubMed2005

Inhaled fluticasone in bronchiectasis: a 12 month study.

BACKGROUND: The clinical efficacy of inhaled corticosteroid (ICS) treatment has not been evaluated in bronchiectasis, despite the presence of chronic airway inflammation. METHODS: After three consecutive weekly visits, 86 patients were randomised to receive either fluticasone 500 mug twice daily (n = 43, 23F, mean (SD) age 57.7 (14.4) years) or matched placebo (n = 43, 34F, 59.2 (14.2) years) and reviewed regularly for 52 weeks in a double blind fashion. RESULTS: 35 and 38 patients in the fluticasone and placebo groups completed the study. Significantly more patients on ICS than on placebo showed improvement in 24 hour sputum volume (OR 2.5, 95% CI 1.1 to 6.0, p = 0.03) but not in exacerbation frequency, forced expiratory volume in 1 second, forced vital capacity, or sputum purulence score. Significantly more patients with Pseudomonas aeruginosa infection receiving fluticasone showed improvement in 24 hour sputum volume (OR 13.5, 95% CI 1.8 to 100.2, p = 0.03) and exacerbation frequency (OR 13.3, 95% CI 1.8 to 100.2, p = 0.01) than those given placebo. Logistic regression models revealed a significantly better response in sputum volume with fluticasone treatment than with placebo among subgroups of patients with 24 hour sputum volume <30 ml (p = 0.04), exacerbation frequency </=2/year (p = 0.04), and sputum purulence score >5 (p = 0.03). CONCLUSIONS: ICS treatment is beneficial to patients with bronchiectasis, particularly those with P. aerurginosa infection.

Administration, Inhalation↗
PubMed2005

A prediction rule for clinical diagnosis of severe acute respiratory syndrome.

A prospective study was undertaken to identify clinical, radiographical, haematological and biochemical profiles of severe acute respiratory syndrome (SARS) patients. A prediction rule, which demarcates low from high risk patients for SARS in an outbreak situation was developed. A total of 295 patients with unexplained respiratory illnesses, admitted to Queen Mary Hospital, Hong Kong SAR, China, in March to July 2003, were evaluated for clinical, radiological, haematological and alanine transaminase (ALT) data daily for 3 days after hospitalisation. In total, 44 cases were subsequently confirmed to have SARS by RT-PCR (68.2%) and serology (100%). The scoring system of attributing 11, 10, 3, 3 and 3 points to the presence of independent risk factors, namely: epidemiological link, radiographical deterioration, myalgia, lymphopenia and elevated ALT respectively, generated high and low-risk (total score 11-30 and 0-10, respectively) groups for SARS. The sensitivity and specificity of this prediction rule in positively identifying a SARS patient were 97.7 and 81.3%, respectively. The positive and negative predictive values were 47.8 and 99.5%, respectively. The prediction rule appears to be helpful in assessing suspected patients with severe acute respiratory syndrome at the bedside, and should be further validated in other severe acute respiratory syndrome cohorts.

Adult↗
PubMed2004

Angular distributions for (3,4)(Lambda)H bound states in the (3,4)He(e,e(')K+) reaction.

The (3,4)(Lambda)H and (4)(Lambda)H hypernuclear bound states have been observed for the first time in kaon electroproduction on (3,4)He targets. The production cross sections have been determined at Q(2)=0.35 GeV2 and W=1.91 GeV. For either hypernucleus the nuclear form factor is determined by comparing the angular distribution of the (3,4)He(e,e(')K+)(3,4)(Lambda)H processes to the elementary cross section 1H(e,e K+)Lambda on the free proton, measured during the same experiment.

Journal Article↗
PubMed2003

High resolution spectroscopy of the 12Lambda B hypernucleus produced by the (e,e'K+) reaction.

High-energy, cw electron beams at new accelerator facilities allow electromagnetic production and precision study of hypernuclear structure, and we report here on the first experiment demonstrating the potential of the (e,e'K+) reaction for hypernuclear spectroscopy. This experiment is also the first to take advantage of the enhanced virtual photon flux available when electrons are scattered at approximately zero degrees. The observed energy resolution was found to be approximately 900 keV for the (12)(Lambda)B spectrum, and is substantially better than any previous hypernuclear experiment using magnetic spectrometers. The positions of the major excitations are found to be in agreement with a theoretical prediction and with a previous binding energy measurement, but additional structure is also observed in the core excited region, underlining the future promise of this technique.

Journal Article↗
PubMed2003

Early events in Bcl-2-enhanced apoptosis.

Transfection of PC12 pheochromocytoma cells with bcl-2 potentiates apoptosis induced by the antimitotic agent, neocarzinostatin (NCS). The mechanism of potentiation involves caspase 3-dependent cleavage of Bcl-2 to its pro-apoptotic counterpart, but the cellular events proximal to caspase 3 activation in this system are not known. Two min after initiation of NCS treatment, Bax begins to translocate from cytosol to the mitochondria; the mitochondrial localization of Bax persists for 30 min after NCS treatment. At the same time, cytochrome C is released from the mitochondria to cytosol. The mitochondrial membrane potential exhibits differential change in mock- and bcl-2 -transfected PC12 cells. In mock-transfected PC12 cells, the mitochondrial membrane potential increases immediately, peaks at 15 min following initiation of NCS treatment, and drops thereafter. In contrast, in bcl-2 -transfected PC12 cells, the membrane potential drops immediately following NCS treatment. Caspase 9 is activated and peaks at 10 min in both mock- and bcl-2 transfected PC12 cells, however, the peak activity of caspase 9 is higher and caspase 9 activation lasts longer (30 min) after the treatment in bcl-2 transfectants. Not until 30 min after initiation of a 1 h treatment with NCS is Bcl-2 protein cleaved in bcl-2 -transfected cells. Thus, in bcl-2 -transfected cells, the mitochondrial membrane potential drops and cytochrome C is released from the mitochondria despite the presence of large amounts of intact mitochondrial Bcl-2. This makes it unlikely that cleavage of Bcl-2 is the only factor involved in potentiation of NCS-induced apoptosis by Bcl-2.

Animals↗
PubMed2003

Down-regulation of aquaporin 3 in bronchiectatic airways in vivo.

Bronchiectasis is characterized pathologically by permanent abnormal bronchial dilation, and clinically by chronic sputum production. Aquaporin 3 (AQP3), a recently described water channel that is also found in large airway cell membrane, could play a role in the pathogenesis and particularly that of bronchorrhea in bronchiectasis. However, little is known of its in vivo distribution and physiological role in human airways. We have, therefore, performed this quantitative immunohistochemistry study on endobronchial biopsies to evaluate the expression and clinical relevance of AQP3 in patients with idiopathic bronchiectasis (n = 25, 15 F, 64.3 +/- 11.5 years) and control subjects (n = 14, 5 F, 57.5 +/- 12.0 years). Quantitative image analysis was performed to evaluate the expression of AQP3 in the bronchial epithelial cells. Our results show that AQP3 was predominantly expressed in the basal cells of the epithelial layer in both groups. Expression of AQP3 was significantly reduced in the basal, but not columnar, epithelial cells in bronchiectasis compared with control airways (p = 0.02, 0.35). Only bronchiectatic patients with regular sputum production, but not their counterparts, had significant downregulation of epithelial AQP3 expression compared with control airways (p = 0.004, 0.24). Our findings suggest that AQP3 could have an important role in the pathogenesis of increased mucus production in bronchiectasis.

Aquaporin 3↗
PubMed2003

Coriolus versicolor polysaccharide peptide slows progression of advanced non-small cell lung cancer.

BACKGROUND: Non-small cell lung cancer (NSCLC) is a leading cause of cancer deaths, and over 60% of patients present with advanced stages. Although polysaccharide peptides (PSP), isolated from the fungus Coriolus versicolor, have been reported to have anti-tumor effects, its clinical efficacy has not been properly evaluated. METHODS: Double-blind placebo-controlled randomized study to evaluate the effects of 28-day administration of PSP (Windsor Pharmaceutical, Hong Kong) on patients, who had completed conventional treatment for advanced NSCLC. RESULTS: Thirty-four patients, with no significant difference in their baseline demographic, clinical or tumor characteristics, or previous treatment regimes (P>0.05) were recruited into each of the PSP and control arms. After 28-day treatment, there was a significant improvement in blood leukocyte and neutrophil counts, serum IgG and IgM, and percent of body fat among the PSP, but not the control, patients (P<0.05). Although the evaluable PSP patients did not improve in NSCLC-related symptoms, there were significantly less PSP patients withdrawn due to disease progression, than their control counterparts (5.9 and 23.5%, respectively; P=0.04; OR 4.00). There was no reported adverse reaction attributable to the trial medications. CONCLUSION: PSP treatment appears to be associated with slower deterioration in patients with advanced NSCLC.

Adult↗
PubMed2002

An inhibitor of c-jun aminoterminal kinase (SP600125) represses c-Jun activation, DNA-binding and PMA-inducible 92-kDa type IV collagenase expression.

The 92-kDa type IV collagenase (MMP-9) contributes to tumor invasion and metastases and strategies to down-regulate its expression could ultimately be of clinical utility. Although the expression of this collagenase is regulated by numerous growth factors, the signaling pathways that transduce these signals are fewer in number and therefore represent pharmacological targets. In this regard, we previously reported that MMP-9 expression was regulated by the c-jun amino terminal kinase (JNK) signaling cascade. Therefore, we undertook a study to determine the efficacy of a novel compound (SP600125), which binds to the ATP binding site of all known JNKs, in repressing MMP-9 expression. In OVCAR-3 cells, SP600125 inhibited the PMA-dependent secretion of MMP-9 in a time-dependent manner and over a dose range that blocked c-Jun phosphorylation and AP-1 binding. SP600125 repressed the activity of a PMA-stimulated MMP-9 promoter-driven luciferase reporter, suggesting that diminished secretion of this collagenase reflected reduced transcription. Further, the activity of a GAL4-driven reporter in PMA-treated cells, co-transfected with an expression construct encoding the trans-activation domain of c-Jun fused to the DNA binding domain of GAL4, was repressed by SP600125. These findings indicate the efficacy of SP600125 in inhibiting c-Jun activation, DNA-binding and the PMA-dependent induction of MMP-9 expression.

Anthracenes↗
PubMed2002

Overexpression of matrix metalloproteinase-8 and -9 in bronchiectatic airways in vivo.

The progressive bronchial dilatation in bronchiectasis is likely to be the result of continued airway matrix destruction, although little is known about the role of neutrophil matrix metalloproteinases (MMPs) in this process. Immunohistochemistry has been used to investigate the expression and cellular localisation of MMP-8 and MMP-9 in bronchiectatic airways in vivo. Endobronchial biopsies were taken from 25 bronchiectatic patients, and from the right lower lobe in 14 control subjects. MMP-8, MMP-9, neutrophils and macrophages were stained with monoclonal antibodies and quantified as positive cell x mm(-2) of the lamina propria by using an image analysis system. There were significantly higher densities of MMP-8 and MMP-9 positive cells in the lamina propria of bronchiectatic than control airways. In bronchiectatic airways, the densities of MMP-8 and MMP-9 positive cells correlated with each other and with neutrophil density, but not with macrophage density. In control airways, a significant correlation was found between MMP-8 with neutrophil and MMP-9 with macrophage densities. An overexpression of neutrophil matrix metalloproteinases in bronchiectatic airways could help explain the continuation of airway destruction in bronchiectasis. In view of the clinical availability of matrix metalloproteinase antagonists, the results presented here could have a significant impact on the development of novel therapies of this untreatable disease.

Aged↗
PubMed2001

Upregulation of phosphodiesterase 1A1 expression is associated with the development of nitrate tolerance.

BACKGROUND: The efficacy of nitroglycerin (NTG) as a vasodilator is limited by tolerance, which develops shortly after treatment begins. In vascular smooth muscle cells (VSMCs), NTG is denitrated to form nitric oxide (NO), which activates guanylyl cyclase and generates cGMP. cGMP plays a key role in nitrate-induced vasodilation by reducing intracellular Ca(2+) concentration. Therefore, one possible mechanism for development of nitrate tolerance would be increased activity of the cGMP phosphodiesterase (PDE), which decreases cGMP levels. METHODS AND RESULTS: To test this hypothesis, rats were made tolerant by continuous infusion of NTG for 3 days (10 microgram kg(-1). min(-1) SC) with an osmotic pump. Analysis of PDE activities showed an increased function of Ca(2+)/calmodulin (CaM)-stimulated PDE (PDE1A1), which preferentially hydrolyzes cGMP after NTG treatment. Western blot analysis for the Ca(2+)/CaM-stimulated PDE revealed that PDE1A1 was increased 2.3-fold in NTG-tolerant rat aortas. Increased PDE1A1 was due to mRNA upregulation as measured by relative quantitative reverse transcription-polymerase chain reaction. The PDE1-specific inhibitor vinpocetine partially restored the sensitivity of the tolerant vasculature to subsequent NTG exposure. In cultured rat aortic VSMCs, angiotensin II (Ang II) increased PDE1A1 activity, and vinpocetine blocked the effect of Ang II on decrease in cGMP accumulation. CONCLUSIONS: Induction of PDE1A1 in nitrate-tolerant vessels may be one mechanism by which NO/cGMP-mediated vasodilation is desensitized and Ca(2+)-mediated vasoconstriction is supersensitized. Inhibiting PDE1A1 expression and/or activity could be a novel therapeutic approach to limit nitrate tolerance.

3',5'-Cyclic-GMP Phosphodiesterases↗