Kim, Dong-Hwan;Hwang, Jong-Seob;Lee, Min-Hee;Ok, Gon
Proceedings of the Korean Environmental Sciences Society Conference
/
2003.11a
/
pp.85-88
/
2003
Polycyclic aromatic hydrocarbons (PARs) are an important group of organic contaminants present in sewage sludge, due to their persistence, toxic, bioaccumulative and long range transfer. These characters make themselves as Persistent Organic Pollutants(POPs) in Long Range Transboundary Air Pollutions convention(LRT AP) of Europe. A method of the gas chromatographic-mass spectrometric (GC-MS) determination of PARs present in sewage sludge was developed and applied to analyzed samples from five sewerage treatment plants (SWTPs), having different treatment types. PARs were extracted from freeze-dried samples by toluene 16 hours in a soxhlet extraction system. The sludge extracts were cleaned-up by an activated silica gel column chromatography. The sum of the 16 US Environmental Protection Agency PARs sewage sludge samples varied from 2.44 to 4.82 ${\mu}g$/g. Concentration of emission carcinogen PARs(PARcarc), such as Benzo(a)anthracene, Benzo(b)fluoranthene, Benzo(k)fluoranthene, Benzo(a)pyrene, Dibenzo(a, h)anthracene and Indeno(1, 2, 3-cd)pyrene ranged from 0.62 to 1.03 ${\mu}g$/g. The total amount of PAHs emission from sewage sludge in Korea was calculated as a top-down approach. PARs and $\sum$PAHcarc from sewage treatment plants had several pathway each by-products. In the ocean dumping, PAHs and $\sum$PAHcarc emissions were 1155.95 kg/year and 5040.32 kg/year. In recycle, PAHs and $\sum$PAHcarc emissions were 98.36 kg/year and 428.87 kg/year. In the landfill, PAHs and $\sum$PAHcarc emissions were 190.40 kg/year and 830.21 kg/year. In the incineration, PAHs and $\sum$PAHcarc emission were 33.10 kg/year and 830.21 kg/year. (In case of incineration, the whole provisions of PARs and $\sum$PAHcarc contained to flowed in sludge was supposed to be exhausted to environment through exhaust after incineration.)
The aim of the study was to evaluate the effect of sodium nitrate consumption on egg quality and quantity, and some blood parameters of native breeder hens of West Azerbaijan province. One hundred native hens were used from wk 25 to 32 of age. These birds were divided into two groups. One group was fed the control diet (CD) but the other fed the same diet supplemented with 4.2 g/kg sodium nitrate (ND). After 2 wks of adaptation, eggs were collected daily and egg mass and egg production were measured weekly for five weeks. To assess the egg quality parameters, two eggs from each replicate pen were collected for three consecutive days each week. At the end of experimental period (wk 32 of age), blood samples of 5 birds per replicate were collected from the wing vein into anticoagulant tubes. Dietary sodium nitrate didn't affect the egg production, shell stiffness, shell thickness and Haugh unit (p>0.05) but it decreased the both egg production and egg mass during the last three weeks (wks 30, 31 and 32) (p<0.05). Furthermore, a treatment effect was observed for yolk colour (p<0.05). Both the egg production and egg mass were increased over time (p<0.05). No significant treatment${\times}$time interaction was observed for egg weight, egg production and egg mass (p>0.05). No effect of time or treatment${\times}$time were observed for shell stiffness (p>0.05). Over time, shell thickness was decreased while Haugh unit increased (p<0.05). None of the blood TP and TG or the activity of ALT, AST and LDH enzymes were affected by dietary consumption of sodium nitrate at wk 32 of age (p>0.05). Sodium nitrite decreased both the TAC and TC at wk 32 of age (p<0.001). It was concluded that the lower body antioxidant capacity of nitrate fed birds resulted in the lower performance (egg weight, egg production and egg mass).
The isoform 1 of cyclodextrin glycosyltransferase (CGTase, EC 2.4.1.19) from Paenibacillus sp. A11 was purified by a preparative gel electrophoresis. The importance of histidine, tryptophan, tyrosine, and carboxylic amino acids for isoform 1 activity is suggested by the modification of the isoform 1 with various group-specific reagents. Activity loss, when incubated with diethylpyrocarbonate (DEP), a histidine modifying reagent, could be protected by adding 25 mM methyl-$\beta$-cyclodextrin substrate prior to the modification. Inactivation kinetics of isoform 1 with DEP resulted in second-order rate constants ($k_{inactivation}$) of $29.5\;M^{-1}s^{-1}$. The specificity of the DEP-modified reaction for the histidine residue was shown by the correlation between the loss of isoform activity and the increase in the absorbance at 246 nm of N-carbethoxyhistidine. The number of histidines that were modified by DEP in the absence and presence of a protective substrate was estimated from the increase in the absorbance using a specific extinction coefficient of N-carbethoxyhistidine of $3,200\;M^{-1}cm^{-1}$. It was discovered that methyl-$\beta$-CD protected per mole of isoform 1, two histidine residues from the modification by DEP. To localize essential histidines, the native, the DEP-modified, and the protected forms of isoform 1 were digested by trypsin. The resulting peptides were separated by HPLC. The peptides of interest were those with $R_t$ 11.34 and 40.93 min. The molecular masses of the two peptides were 5,732 and 2,540 daltons, respectively. When the data from the peptide analysis were checked with the sequence of CGTase, then His-140 and His-327 were identified as essential histidines in the active site of isoform 1.
The hemolytic uremic syndrome (HUS) is a rare disease of microangiopathic hemolytic anemia, low platelet count and renal impairment. HUS usually occurs in young children after hemorrhagic colitis by shigatoxin-producing enterohemorrhagic E. coli (D+HUS). HUS is the most common cause of acute renal failure in infants and young children, and is a substantial cause of acute mortality and morbidity; however, renal function recovers in most of them. About 10% of children with HUS do not reveal preceding diarrheal illness, and is referred to as D- HUS or atypical HUS. Atypical HUS comprises a heterogeneous group of thrombomicroangiopathy (TMA) triggered by non-enteric infection, virus, drug, malignancies, transplantation, and other underlying medical condition. Emerging data indicate dysregulation of alternative complement pathway in atypical HUS, and genetic analyses have identified mutations of several regulatory genes; i.e. the fluid phase complement regulator Factor H (CFH), the integral membrane regulator membrane cofactor protein (MCP; CD46) and the serine protease Factor I (IF). The uncontrolled activation of the complement alternative pathway results in the excessive consumption of C3. Plasma exchange or plasma infusion is recommended for treatment of, and has dropped the mortality rate. However, overall prognosis is poor, and many patients succumb to end-stage renal disease. Clinical presentations, response to plasma therapy, and outcome after renal transplantation are influenced by the genotype of the complement regulators. Thrombotic thrombocytopenic purpura (TTP), another type of TMA, occurs mainly in adults as an acquired disease accompanied by fever, neurologic deficits and renal abnormalities. However, less frequent cases of congenital or hereditary TTP associated with ADAMTS-13 (a disintegrin and metalloprotease, with thrombospondin 1-like domains 13) gene mutations have been reported, also. Recent advances in molecular genetics better allow various HUS to be distinguished on the basis of their pathogenesis. The genetic analysis of HUS is important in defining the underlying etiology, predicting the genotype-related outcome and optimizing the management of the patients.
Park, Si-Deok;Lee, Geum-Hong;Lee, Young-Sun;Kwon, Young-Kyu;Park, Jong-Hyun;Choi, Sun-Mi;Shin, Sang-Woo
Journal of Physiology & Pathology in Korean Medicine
/
v.21
no.2
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pp.414-424
/
2007
Adenophorae Radix (AR), Liriopis Tuber (LT), Dendrobii Monile (DM), Polygonati Officinalis (PO), Polygonati Rhizoma (PR) have been used to treated a variety condition/diseases in traditional oriental medicine. The present study was conducted to investigate the immunmodulatory effects of the water-extracted AR, LT, DH, PO and PR. In spleen cell proliferation assay, DH was significantly enhanced mitogenic activity compared with control group. In RT-PCR, DH ad PO induced IL-2 and IFNr cytokine gene expression in mouse spleen cells. Methotrexate(MTX), immune supression agent, was significantly inhibited mouse spleen cell proliferation(1600 mg/ml). In spite of MTX treatement, DH and PO sustained the spleen cell proliferation, In the flow cytometry analysis, DH stimulated mouse spleen cells showed an increase in B-cell phenotype (CD45R/B220). The water-extracted DH and PO inhibited NO production and iNOS expression in LPS-stimulated RAW 264.7 macrophage cell. DH induced IL-2 and IFNg gene expression in human peripheral mononuclear cells. The GC-MS analysis show that the main component of water-extracted DH was b-Nitroethyl alcohol. The main components of water-extracted PO were Dipirartril-tropico, Methyl sulfoxide and Demsodrox. These data suggest that among these extracts, DH has a protective effcet of immune suppression caused by MTX. DH may be enhance cellular and humoral immune response by the regulation of cytokine gene expression, NO production and B cell production.
Objectives: We performed an immunohistochemical study to examine the place of neovascularization in the tumorigenic process of follicular thyroid carcinoma and to determine whether tumor angiogenic activity in follicular carcinoma plays a role in tumor aggression. Materials & Methods: We studied 63 follicular thyroid carcinomas and compared with 22 follicular adenomas. The areas of capsular invasion, vascular invasion and cellular atypism of the tumor were confimed on H & E stains. The paraffin embedded tissues were stained by the use of monoclonal antibodies against Ag CD34. Microvesseles were counted in the area of highest vascular density at 200 times magnification. The microvessel densities(MVD) were analized in relation to histologic type and location of the tumors. Results: There were 59 minimal invasive types and 4 widely invasive types of carcinoma. In the histologic specimens of carcinomas, capsular invasion was identified in all the cases, vascular invasion in 46 and cellular atypism in 24. Mean values of the MVDs of the minimal invasive carcinomas, the widely invasive carcinomas and the adenomas were $263.8{\pm}69.2,\;256.l{\pm}49.3\;and\;241.5{\pm}159.4$, respectively and there was no significant difference between each group. In follicular carcinomas, there was a regional difference of the MVDs. The areas of tumor showing cellular atypism and adjacent to or penetrating the capsule, in which represents the tumorigenic process of carcinoma, had a higher rate of vascularization, than other areas of the tumor(p<0.05). However, these features were not noted in the follicular adenomas. Conclusion: Although there was no significant difference of the MVD between follicular carcinomas and adenomas, there was a regional difference of the MVD within the carcinomas and the values were significantly higher in the more malignant areas, as indicated by cellular atypism and capsular invasion. Therefore, tumor angiogenic activity measured by MVD may play a role in tumor aggression in follicular thyroid carcinoma.
This study evaluated the protective effects of ginseng leaf extract (GLE) against high fat-diet-induced hyperglycemia and hyperlipidemia, and explored the potential mechanism underlying these effects in C57BL/6J mice. The mice were randomly divided into four groups: normal control, high fat diet control (HFD), GLE-treated at 250 mg/kg, and GLE-treated at 500 mg/kg. To induce hyperglycemic and hyperlipidemic states, mice were fed a high fat diet for 6 weeks and then administered GLE once daily for 8 weeks. At the end of the treatment, we examined the effects of GLE on plasma glucose, lipid levels, and the expression of genes related to lipogenesis, lipolysis, and gluconeogenesis. Both GLE groups lowered levels of plasma glucose, insulin, triglycerides, total cholesterol, and non-esterified fatty acids when compared to those in HFD group. Histological analysis revealed significantly fewer lipid droplets in the livers of GLE-treated mice compared with HFD mice. To elucidate the mechanism, Western blots and RT-PCR were performed using liver tissue. Compared with HFD mice, GLE-treated mice showed higher levels of phosphorylation of AMP-activated protein kinase (AMPK) and its substrate, acetyl-CoA carboxylase, but no differences in the expression of lipogenic genes such as sterol regulatory element-binding protein 1a, fatty acid synthase, sterol-CoA desaturase 1 and glycerol-3-phosphate acyltransferase. However, the expression levels of lipolysis and fatty acid uptake genes such as peroxisome proliferator-activated receptor-$\alpha$ and CD36 were increased. In addition, phosphoenolpyruvate carboxykinase gene expression was decreased. These results suggest that GLE ameliorates hyperglycemia and hyperlipidemia by inhibiting gluconeogenesis and stimulating lipolysis, respectively, via AMPK activation.
Using a cantilever type nanoprobe having a 100㎚m aperture at the apex of the pyramidal tip of a near-field scanning optical microscope (NSOM), nanopatterning of polymer films are conducted. Two different types of polymer, namely a positive photoresist (DPR-i5500) and an azopolymer (Poly disperse orange-3), spincoated on a silicon wafer are used as the substrate. A He-Cd laser with a wavelength of 442㎚ is employed as the illumination source. The optical near-field produced at the tip of the nanoprobe induces a photochemical reaction on the irradiated region, leading to the fabrication of nanostructures below the diffraction limit of the laser light. By controlling the process parameters properly, nanopatterns as small as 100㎚ are produced on both the photoresist and azopolymer samples. The shape and size variations of the nanopatterns are examined with respect to the key process parameters such as laser beam power, irradiation time or scanning speed of the probe, operation modes of the NSOM (DC and AC modes), etc. The characteristic features during the fabrication of ordered structures such as dot or line arrays using NSOM lithography are investigated. Not only the direct writing of nano array structures on the polymer films but also the fabrication of NSOM-written patterns on the silicon substrate were investigated by introducing a passivation layer over the silicon surface. Possible application of thereby developed NSOM lithography technology to the fabrication of data storage is discussed.
Park, Dae-Rim;Chung, Yong-Chae;Choi, Kyung-Ho;Kim, Hyung-Jin
Journal of the Korean Chemical Society
/
v.51
no.6
/
pp.526-535
/
2007
Ru(II)-terpyridine complexes (8, 9, 11) linked with adamantyl or β-cyclodextrin moieties were synthesized and characterized based on their 1H and 13C NMR spectra as well as MS spectra. Ru(II)-terpyridine complexes (8, 11) linked with adamantyl moiety were readily dissolved in aqueous solution via encapsulation by β-cyclodextrin when they were mixed with an equimolar amount of β-cyclodextrin. In the similar way, the adamantane guest of the Ru(II)-terpyridine complexes (8, 11) were encapsulated by β-cyclodextrin moiety of the ruthenium complex 9 to afford supramolecular assemblies in aqueous environment. Formation of assemblies was corroborated by 1H NMR spectroscopy.
The stable anchorage of pyridoxal 5'-phosphate (PLP) in the active site of D-amino acid transaminase (D-AT) is crucial for the enzyme catalysis. The three-dimensional structure of D-AT revealed that Glu32 is one of the active site groups that may playa role in PLP binding. To prove the role of Glu32 in PLP stability, we firstly checked the rate of the potential rate-limiting step. The kinetic analysis showed that the rate of the ${\alpha}$-deprotonation step reduced to 26-folds in E32A mutant enzyme. Spectral analyses of the reaction of D-AT with D-serine revealed that the E32A mutant enzyme failed to stabilize the key enzyme-substrate intermediate, namely a quinonoid intermediate (E-Q). Finally, analysis of circular dichroism (CD) on the wild-type and E32A mutant enzymes showed that the optical activity of PLP in the enzyme active site was lost by the removal of the carboxylic group, proving that Glu32 is indeed involved in the cofactor anchorage. The results suggested that the electrostatic interaction network through the groups from PLP, Glu32, His47, and Arg50, which was observed from the three-dimensional structure of the enzyme, plays a crucial role in the stable anchorage of the cofactor to give necessary torsion to the plane of the cofactor-substrate complex.
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