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Biomedical subjects

H J Chen

Publications and source records attributed to H J Chen.

At least 19 recordsLinked to original sources
PubMed2004

Aerobic biotransformation of octylphenol polyethoxylate surfactant in soil microcosms.

The biotransformation of octylphenol polyethoxylate surfactant (Triton X-100) and bacterial communities in soil microcosms was investigated. The soil microcosms were designed to simulate real sites of bioremediation. The soil used in this study was contaminated with pesticides and alkylphenol polyethoxylate surfactants over a long period of time. The nitrogen source, (NH4)2SO4 and the mineral salt basal solution were added to the microcosm and the water content was adjusted to 50% with distilled water. The microcosms were aerated using an aeration system with an air flow rate of 0.3 l min(-1). The exogenous bacterial strain Pseudomonas sp. SH4 was added to the microcosms to increase the rate of biotransformation of the Triton X-100. The number of microorganisms and the theoretical extent of formation of carbon dioxide were estimated to evaluate the biotransformation of Triton X-100 in the microcosms. The analytical results revealed that the exogenous bacteria could increase the rate of transformation of Triton X-100 by approximately 50%. Aeration of the microcosm increased the biotransformation of Triton X-100 by 45%. Bacterial count of 6.8x10(10) MPN g(-1) of soil was achieved in the M5 microcosm. Analysis of the bacterial community by 16S rDNA sequences revealed that Pseudomonas sp. SH4 could dominate all the microcosms to which it was added as an exogenous bacteria. The quantity of the indigenous bacterial strains Stenotrophomonas maltophilia, Stenotrophomonas sp. and clone 4-70 were also enhanced in the microcosms by the aeration, and the addition of carbon and nitrogen source.

Bacteria, Aerobic↗
PubMed2003

Combined dorsal root entry zone lesions and neural reconstruction for early rehabilitation of brachial plexus avulsion injury.

Brachial plexus avulsion injury is one of the major complications after traffic, especially motorcycle accidents. During the past 12 years, we have encountered more than 40 brachial plexus avulsion injuries. The neurological deficits included pain and paralysis of the damaged limb. Dorsal root entry zone lesions made by thermocoagulation were performed for intractable pain in 34 cases. The pain relief rate was good in about 75%. Combined neural reconstruction was performed in 15 cases. The reconstruction included neurolysis, nerve graft, nerve transfer, and functioning muscle/tendon transfer etc. There were 13 male and 2 female patients. Age distribution was from 21 to 61 years with a mean age of 41.8 years. Eleven patients were found to have whole brachial plexus injury and 4 with upper brachial plexus injury. Twelve patients had good pain relief. Six patients showed good functional result after reconstruction. Three had no improvement. Combined pain control and reconstruction offer an early rehabilitation for brachial plexus avulsion injury.

Adult↗
PubMed2003

Integrating entrapped mixed microbial cell (EMMC) process for biological removal of carbon and nitrogen from dilute swine wastewater.

An entrapped mixed microbial cells (EMMC) process was used to investigate the simultaneous removal of carbon and nitrogen from dilute swine wastewater. Cellulose triacetate was used as the matrix for entrapping the mixed microbial cells. The EMMC process was tested with various oxygen supply conditions (ratios of aeration to non-aeration times) and two types of carrier sizes (large and medium). Also, various pre-treatments with chemical coagulation, screen separation and ammonium crystallization prior to the EMMC process, and post-treatment after the EMMC process were investigated. It was found that at a hydraulic retention time of 30 h and one hour of aeration and one hour of non-aeration, the EMMC process packed with medium carriers after the pretreatment of ammonium crystallization, exhibited the best total nitrogen removal efficiency of 95.1 +/- 1.0% when compared to the other two pre-treatment methods. The total chemical oxygen demand (TCOD) and soluble chemical oxygen demand removal efficiencies were 83.5 +/- 2.2% and 84.1 +/- 1.1%, respectively. Lime post-treatment provided TCOD and total phosphorus removal efficiencies of 59.6 +/- 2.7% and 98.0 +/- 0.5%, respectively. Thus, a cost analysis for ammonium crystallization pre-treatment, EMMC process, and post-treatment with lime was conducted. The unit cost for a 2000 pig operation is approximately dollars 4.91/pig/year. For the application of the EMMC process with the proposed pre- and post-treatments, a suitable farm size needs to be greater than a 2000 pig operation. Because of the high efficiency and the simple operation of simultaneous carbon and nitrogen removal, the EMMC process has the potential for treatment of dilute swine wastewater in a land-limited area and can be manufactured as pre-fabricated wastewater treatment units.

Animals↗
PubMed2002

Protection of myocytes from hypoxia-reoxygenation injury by nitric oxide is mediated by modulation of transforming growth factor-beta1.

BACKGROUND: Reoxygenation injury is a result of several complex events, including release of reactive oxygen species, protein kinase C (PKC) activation, and altered expression of transforming growth factor-beta1 (TGF-beta(1)). Nitric oxide (NO) generally protects tissues from reperfusion injury. METHODS AND RESULTS: We examined the modulation of TGF-beta1 expression and activity and PKC activation in cultured rat heart myocytes exposed to a brief period of hypoxia-reoxygenation (H-R) by NO donor 3-morpholino-sydnonimine (SIN-1). H-R resulted in an increased expression of total TGF-beta1 (mRNA and protein) but a decrease in the release of active TGF-beta1. Myocyte PKC-alpha protein level was not altered by H-R, but its phosphorylation was augmented. Pretreatment of myocytes with SIN-1 diminished myocyte injury quantified as lactate dehydrogenase release. Simultaneously, release of active TGF-beta1 increased and total TGF-beta1 expression decreased (all P<0.05 versus H-R alone). PKC-alpha phosphorylation increased further in cells treated with SIN-1. The effects of SIN-1 were blocked by the NO scavenger phenyl-tetramethyl-imidazoline-oxyl-oxide as well as by the PKC inhibitor staurosporine. To examine if another NO donor would have a similar effect, cardiomyocytes were treated with nitroglycerin before H-R. With nitroglycerin treatment, similar to SIN-1 treatment, myocyte injury was diminished, TGF-beta1 release increased, and total TGF-beta1 expression decreased. CONCLUSIONS: These observations suggest modulation of TGF-beta1 expression as a novel mechanism of salutary effect of NO donors. PKC-alpha activation may play an important role in the protective effect of NO against H-R injury.

Animals↗
PubMed2002

Oxidized low-density lipoprotein receptor LOX-1 and apoptosis in human atherosclerotic lesions.

BACKGROUND: Lectin-like oxidized LDL receptor-1 (LOX-1), a novel receptor for oxidized low-density lipoprotein, mediates oxidized low-density lipoprotein-induced apoptosis of endothelial cells, monocyte adhesion to endothelium, and phagocytosis of aged cells. The present study examined the role of LOX-1 and apoptosis in human atherosclerotic lesions. METHODS AND RESULTS: Grafted vein (n = 8), human carotid artery endarterectomy (n = 11), and normal human internal mammary artery (n = 8) specimens were used to study the expression of LOX-1 and apoptosis. LOX-1 expression was determined by reverse transcriptase-polymerase chain reaction, Western analysis, and immunostaining. Presence of apoptosis was determined by fluorescent in situ nick end-labeling staining and by the presence of poly (ADP-ribose) polymerase protein (an apoptotic marker). Expression of LOX-1 was significantly increased in atherosclerotic grafted vein and carotid artery specimens compared with that in normal arteries. LOX-1 was expressed in endothelial cells, macrophages, and smooth muscle cells. LOX-1 was extensively expressed in the new blood vessels in the core of advanced atherosclerotic lesions. Double immunostaining showed LOX-1 expression to be colocalized with apoptotic cells. Fluorescent in situ nick end-labeling staining showed that the apoptotic cells were present mostly in the rupture-prone regions of the atherosclerotic plaque. CONCLUSION: These observations indicate that LOX-1 is extensively expressed in the proliferated intima of grafted veins and in advanced atherosclerotic carotid arteries. Further, LOX-1 is colocalized with apoptotic cells. These observations may relate to the phenomenon of plaque rupture, and provide targets for developing new therapies.

Aged↗
PubMed2001

Inhibition of LOX-1 by statins may relate to upregulation of eNOS.

LOX-1, a receptor for oxidized low-density lipoprotein (ox-LDL), plays a critical role in endothelial dysfunction and atherosclerosis; both of these conditions are associated with diminished expression of constitutive endothelial nitric oxide synthase (eNOS). Recent studies show that HMG CoA reductase inhibitors (statins) exert cardioprotective effect. We examined the role of LOX-1 in eNOS expression and modulation of this relationship by two different statins, simvastatin and atorvastatin in human coronary artery endothelial cells (HCAECs). Ox-LDL (40 microg/ml) upregulated the expression of LOX-1; simultaneously, there was a reduction in eNOS expression. Pretreatment of HCAECs with simvastatin or atorvastatin (1 and 10 microM) reduced ox-LDL-induced upregulation of LOX-1 and downregulation of eNOS (both P < 0.05). High concentration of statins (10 microM) was more potent than the low concentration (1 microM) (P < 0.05). Both statins also attenuated ox-LDL-mediated activation of MAP kinase. These observations indicate that statins attenuate the effect of ox-LDL on eNOS expression. Inhibitory effect on LOX-1 and subsequently MAP kinase activity provides a potential mechanism of beneficial effects of statins beyond lowering cholesterol.

Atorvastatin↗
PubMed2001

Poly[cadmium(II)-mu-4,4'-oxydianiline-N:N'-di-mu-thiocyanato-N:S].

The title polymeric complex, [Cd(SCN)(2)(C(12)H(12)N(2)O)], exhibits a three-dimensional framework in which each Cd(II) atom is bridged by two eta-1,3-(SCN)(-) groups, forming a double-stranded chain. The unique Cd(II) atom lies on an inversion centre and the coordination sphere is completed by two terminal N atoms from two different 4,4'-oxydianiline (4,4'-Oda) ligands, furnishing a CdS(2)N(4) octahedral geometry. Adjacent polymeric double-stranded chains are linked via the 4,4'-Oda ligands, which lie across twofold rotation axes.

Journal Article↗
PubMed2001

Molecular interactions between poly(ADP-ribose) polymerase (PARP I) and topoisomerase I (Topo I): identification of topology of binding.

The molecular interactions of poly(ADP-ribose) polymerase I (PARP I) and topoisomerase I (Topo I) have been determined by the analysis of physical binding of the two proteins and some of their polypeptide components and by the effect of PARP I on the enzymatic catalysis of Topo I. Direct association of Topo I and PARP I as well as the binding of two Topo I polypeptides to PARP I are demonstrated. The effect of PARP I on the 'global' Topo I reaction (scission and religation), and the activation of Topo I by the 36 kDa polypeptide of PARP I and catalytic modifications by poly(ADP-ribosyl)ation are also shown. The covalent binding of Topo I to circular DNA is activated by PARP I similar to the degree of activation of the 'global' Topo I reaction, whereas the religation of DNA is unaffected by PARP I. The geometry of PARP I-Topo I interaction compared to automodified PARP I was reconstructed from direct binding assays between glutathione S-transferase fusion polypeptides of Topo I and PARP I demonstrating highly selective binding, which was correlated with amino acid sequences and with the 'C clamp' model derived from X-ray crystallography.

Binding Sites↗
PubMed2001

Transthoracic endoscopic T-2, 3 sympathectomy for facial hyperhidrosis.

Twenty-five patients (20 men and 5 women) with the chief complaint of facial hyperhidrosis were treated by transthoracic endoscopic T-2, 3 sympathectomy. All patients were essentially in good health except the embarrassment of facial sweating. Fifteen of them also suffered from distressing palmar hyperhidrosis. The ages ranged from 18 to 40 years (mean age 25 years). All of them except two obtained a satisfactory improvement of facial hyperhidrosis after 3 months to 2 years of follow-up. One man demonstrated very mild ptosis in the right eye. Pre- and postoperative sympathetic skin response (SSR) revealed the absence rate from 20% to 72% with electrical stimulation (p < 0.05). This study shows that T-2, 3 sympathectomy is a choice of treatment for facial hyperhidrosis and sympathetic supply to the face may at least partly be from T-2, 3 level.

Adolescent↗
PubMed2001

Role for p27(Kip1) in Vascular Smooth Muscle Cell Migration.

BACKGROUND: Rapamycin is a potent inhibitor of smooth muscle cell (SMC) proliferation and migration. Rapamycin-mediated inhibition of SMC proliferation is associated with upregulation of the cyclin-dependent kinase inhibitor p27(Kip1). Previously, we showed that mixed embryonic fibroblasts obtained from p27(Kip1)(-/-) mice were relatively rapamycin-resistant, suggesting that p27(Kip1) plays an integral role in modulating the antiproliferative effects of rapamycin. We hypothesized that the antimigratory effect of rapamycin may also be mediated by p27(Kip1). METHODS AND RESULTS: Rapamycin (1 to 10 nmol/L) inhibited basic fibroblast growth factor-induced migration of wild-type (WT) but not p27(Kip1)(-/-) SMCs in a dose-dependent manner (P<0.05) in a modified Boyden chamber. The effects of rapamycin on aortic SMC explant migration were also studied with WT, p27(+/-), and p27(-/-) mice. Rapamycin 4 mg. kg(-1). d(-1) IP for 5 days inhibited SMC migration by 90% in the WT and p27(Kip1)(+/-) (P<0.05) but not p27(Kip1)(-/-) animals. CONCLUSIONS: Lack of p27(Kip1) reduces rapamycin-mediated inhibition of SMC migration. These novel findings suggest a role for p27(Kip1) in the signaling pathway(s) that regulates SMC migration.

ADP Ribose Transferases↗
PubMed2001

Attenuation of tissue P-selectin and MCP-1 expression and intimal proliferation by AT(1) receptor blockade in hyperlipidemic rabbits.

Angiotensin-II (Ang-II) participates in the development and progression of atherosclerosis by activating type 1 (AT(1)) receptors. In vitro studies show that inflammatory factors, such as P-selectin and MCP-1, which can be upregulated by Ang-II, play an important role in atherogenesis. We examined the effect of AT(1) receptor blockade with losartan on the expression of P-selectin and MCP-1 in hypercholesterolemic rabbits. Since AT(1) receptor blockade is associated with feedback upregulation of renin-angiotensin system (RAS), we also examined alterations in plasma Ang-II levels by losartan therapy. Male NZW rabbits were fed regular chow (high cholesterol diet or high cholesterol diet + losartan 25 mg/kg/day). As expected, there was a marked intimal proliferation in association with increase in serum cholesterol (P < 0.001). In addition, there was a modest increase in plasma Ang-II levels (P < 0.05), and a significant increase in the expression of AT(1) receptors, P-selectin and MCP-1 in aortas of high cholesterol diet rabbits. Concurrent administration of losartan with high cholesterol diet attenuated aortic intimal proliferation induced a fivefold increase in plasma Ang-II levels and caused a marked decrease in expression of P-selectin and MCP-1 without change in serum lipid levels and aortic AT(1) receptor expression. These observations in hypercholesterolemic animal models show that AT(1) receptor blockade is associated with modulation of P-selectin and MCP-1 expression concurrent with reduction in intimal proliferation. The rise in plasma Ang-II does not appear to limit the potential beneficial effect of losartan.

Angiotensin II↗
PubMed2001

Activity staining of isocitrate lyase after electrophoresis on either native or sodium dodecyl sulfate polyacrylamide gels.

Isocitrate was cleaved into succinate and glyoxylate by isocitrate lyase (ICL) in the glyoxylate cycle. We used lactate dehydrogenase as an ancillary enzyme to further metabolize the glyoxylate to glycolate in the presence of NADH. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and 2,6-dichlorophenol-indolphenol (DCPIP) were used in the coupling reactions for detecting ICL activity after electrophoresis on either native or sodium dodecyl sulfate (SDS) polyacrylamide gels. This fast and sensitive method can be used in the process of ICL enzyme purification and characterization.

Acrylic Resins↗
PubMed2001

Statins inhibit oxidized-LDL-mediated LOX-1 expression, uptake of oxidized-LDL and reduction in PKB phosphorylation.

OBJECTIVES: LOX-1, a lectin-like receptor on endothelial cells, facilitates the uptake of oxidized-LDL. Expression of LOX-1 is involved in the pathobiological effects of oxidized-LDL in endothelial cells, including apoptosis, suppression of cNOS activity and cell adhesion. Recent studies show that intracellular signal protein kinase B (PKB) is involved in the regulation of cNOS. Further, HMG CoA reductase inhibitors (statins) may affect LOX-1 expression. In this study, we examined the modulation of LOX-1 expression and PKB activity in response to oxidized-LDL by two different statins (simvastatin and atorvastatin). METHODS AND RESULTS: Cultured human coronary artery endothelial cells (HCAECs) were used in this study. Oxidized-LDL (40 microg/ml) was found to upregulate the expression of LOX-1 (mRNA and protein), enhance [125I]-ox-LDL uptake and to reduce the phosphorylation of PKB (p-PKB). Two different statins, simvastatin and atorvastatin (each 1 and 10 microM), upregulated the activity of PKB and decreased LOX-1 expression and [125I]-ox-LDL uptake. A high concentration of statins (10 microM) gave a more potent effect than the low concentration (1 microM). The effects of the two different statins were similar. CONCLUSIONS: These observations show that statins decrease LOX-1 expression, a novel oxidized-LDL endothelial receptor, and uptake of oxidized-LDL in HCAECs. The effect of statins on LOX-1 expression is associated with an increase in PKB activity in HCAECs.

Analysis of Variance↗