• Asian-Australasian Journal of Animal Sciences
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• v.18 no.8
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• pp.1130-1134
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• 2005

An experiment was performed using 20 calves of about one-month old to investigate the effect of chelation therapy with calcium disodium ethylenediaminetetraacetate ($CaNa_2$EDTA) alone or along with antioxidant $\alpha$-tocopherol in lead loaded calves on blood trace minerals, erythrocytic sulfahydryl groups and some haematobiochemical parameters. Fifteen calves were given lead orally at a daily dose of 7.5 mg of 99% pure lead acetate/kg body weight for 28 days. Then the lead was withdrawn on day 28 and the calves were randomly divided into three groups. Each group of five animals was either treated with $CaNa_2$EDTA alone at the dose rate of 110 mg/kg body weight in two divided doses for 4 days or along with $\alpha$-tocopherol at the dose rate of 100 mg/kg body weight orally daily for 7 days, keeping the remaining five calves as lead-exposed untreated controls. Blood samples were collected at the end of the lead exposure (day 0) and thereafter on day 2, 4, 7 and 10 from the start of the chelation treatment. The treatment with EDTA alone led to slow but non-significant improvement in blood copper level, but incorporation of antioxidant $\alpha$-tocopherol in chelation therapy resulted in its significant decline, as recorded on day 7-post treatment. Withdrawal of lead or treatment with $CaNa_2$EDTA alone or along with $\alpha$-tocopherol enhanced the erythrocytic thiol contents and the levels of T-SH and P-SH became statistically (p<0.05) comparable to those of lead-exposed controls by day 7 and 4, respectively. There was no significant (p>0.05) change in serum urea, creatinine, total protein and albumin levels between the treatment groups. It is concluded from the present investigation that treatment with $CaNa_2$EDTA at the present dose rate is safe to be used for chelation in lead loaded calves.

• Bulletin of the Korean Chemical Society
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• v.28 no.10
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• pp.1645-1650
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• 2007

This paper describes a racemic and stereoselective synthetic route for a novel cyclohexenyl carbocyclic adenine analogue. The required stereochemistry of the target compound was controlled using a stereoselective glycolate Claisen rearrangement followed by α-chelated carbonyl addition. The introduction of 6-chloropurine was achieved using Mitsunobu conditions, and further modifications of the corresponding heterocycle gave the target cyclohexenyl nucleoside.

• Korean Journal of Clinical Laboratory Science
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• v.49 no.4
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• pp.495-497
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• 2017

Thalassemia major is a genetic disorder with a defective synthesis of either the alpha or the beta chain of hemoglobin A. Blood transfusion is crucial for the survival in these patients. Unfortunately, endocrine dysfunction is a very common complication in these patients and is principally due to excessive iron overload as a result of frequent blood transfusions. Although regular blood transfusion may increase life expectancy, disturbances in growth and pubertal development, abnormal gonadal functions, impaired thyroid, parathyroid and adrenal functions, diabetes, and disorderly bone growth are common side effects. We hereby present a case of a 23-year-old, unmarried woman with beta thalassemia major presenting with primary amenorrhea, poor development of secondary sexual character, and short stature. Thorough history, clinical examination, and laboratory investigation, including dynamic function test (insulin tolerance test) were conducted. These tests confirmed that she had multiple endocrinopathies, including hypogonadotropic hypogonadism, growth hormone deficiency, and subclinical adrenal insufficiency, which were caused by iron overload. She required hormone replacement therapy. Early recognition of possible deficiencies in hypothalamo-pituitary-end organ hormones caused by iron overload in thalassemia patients that undergo frequent blood transfusion procedures is essential. Appropriate treatments, including transfusion regimen and chelation therapy, as well as specific treatment of each complication are the crucial for the successful management and improvement of quality of life these patients.

• Bulletin of the Korean Chemical Society
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• v.23 no.6
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• pp.851-856
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• 2002

The Reaction of S-methyl-S-cysteine(L-Smc) with racemic $s-cis-[Co(demba)Cl_2]-1$ (Hydmedba = $NN'-dimethylethylenediamine-NN'-di-\alpha-butyric$, acid) yields ${\Delta}$-s-cis-[Co(dmedba)(L-Smc)] 2 with N, O-chelation. Oxidation of sulfur of 2 with $H_2O_2$ in a 1 : 1 mole ratio gives ${\Delta}$-s-cis[Co(dmedba)(L-S(O)mc)] 3 having an uncoordinated sulfenate group. Oxidation of sulfur of L-Sm with $H_2O_2in$ a 1: 1 mole ratio produces S-methyl-L-cysteinesulfenate (L-S(O)me) 5. Direct reaction of 1 with 5 in basic medium gives an N.O-chelated ${\Delta}$s-cis[Co(dmedba)(L-S(O)mc)-N.O], which turmed out be same as obtained by oxidation of 2, while an N, S-chelated ${\Delta}$-s-cis-[Co(dmedba)(S-S(O)mc)-N,O] complex 4 is obtained in acidic medium from the reaction of 1 with 5. This is one of the rare $[$Co^{III}$(N_2O_2-type$ ligand)(amino acid)] type complex preparations, where the reaction conditions determine which mode of N, O and N, S caelation modes is favored.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.425-431
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• 1996

Human neutrophil elastases (HNElastase, EC 3.4.21.37), a causative factor of inflammatory diseases, are regulated by plasma proteinase inhibitors, alpha-proteinase inhibitor and ${\alpha}_2-macroglobulin$. Under certain pathological conditions, however, released enzymes or abnormal function of inhibitors may cause various inflammatory disease. NSAIDs have been clinically applied for treatment of inflammatory diseases. Inhibition of cyclooxygenase is a known mechanism of action of NSAIDs in the treatment of inflammatory disease. In in vitro experiments, HNElastase was inhibited by naproxen, phenylbutazone, and oxyphenbutazone, but ibuprofen, ketoprofen, aspirin, salicylic acid, and tolmetin did not inhibit elastase. HNElastase was also inhibited by chelating agents, EDTA & EGTA, and tetracyclines. Removal of divalent metal ions by EDTA caused inhibition of elastase, and reconstitution of the metal ions recovered the enzyme activity to a certain level. Frequencies and contours in the Raman spectra of various conditions of human neutrophil elastase undergo drastic changes upon partial removal and/or reconstitution of calcium and zinc ions. The metal ion content dependent activities and change of the contour of the Raman spectrogram suggest us that the mechanism of action of a chelator or chelator-like agents on neutrophil elastase may be related to the conformational change at/or near the active site, especially -C=O radical or -COOH radical.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.3
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• pp.195-200
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• 2009

Zinc released from excited glutamatergic neurons accelerates amyloid ${\beta}$ (A ${\beta}$) aggregation, underscoring the therapeutic potential of zinc chelation for the treatment of Alzheimer's disease (AD). Zinc can also alter A ${\beta}$ concentration by affecting its degradation. In order to elucidate the possible role of zinc influx in secretase-processed A ${\beta}$ production, SH-SY5Y cells stably expressing amyloid precursor protein (APP) were treated with pyrrolidine dithiocarbamate (PDTC), a zinc ionophore, and the resultant changes in APP processing were examined. PDTC decreased A ${\beta}$ 40 and A ${\beta}$ 42 concentrations in culture media bathing APP-expressing SH-SY5Y cells. Measuring the levels of a series of C-terminal APP fragments generated by enzymatic cutting at different APP-cleavage sites showed that both ${\beta}$-and ${\alpha}$-cleavage of APP were inhibited by zinc influx. PDTC also interfered with the maturation of APP. PDTC, however, paradoxically increased the intracellular levels of A ${\beta}$ 40. These results indicate that inhibition of secretase-mediated APP cleavage accounts -at least in part- for zinc inhibition of A ${\beta}$ secretion.