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No. 13 (PC 13) Effects of alpha lipoic acid as an antioxidant in preventing renal mitochondrial oxidative damage in diabetic rats Noraihan Mat Harun, Rahajoe Imam Santosa Department of Basic Medical Sciences, Kulliyyah of Medicine, International Islamic University, Malaysia, Kuantan-Malaysia Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycemia due to inadequate secretion of insulin or insufficient action of the endogenous insulin. Oxidative stress has an important role in the pathogenesis of diabetic complications and mitochondria represent a major source of the reactive oxidants that lead to cellular oxidative damage. This study is design to observe the effect of alpha lipoic acid (ALA) as mitochondrial antioxidant in preventing renal mitochondrial oxidative damage in diabetic induced rats. In this study, the rats were divided into three groups. Normal Control (NC) group was served as a control; Diabetic Control (DC) group was induced for diabetes without given any supplementation, while Diabetic-Alpha Lipoic Acid (D-ALA) group was streptozotocin-induced diabetic rats, supplemented with ALA daily for six weeks. The ability of ALA in preventing renal mitochondrial oxidative damage was evaluated by comparing the renal function in terms of serum urea, serum creatinine and creatinine clearance in both supplemented and non-supplemented rats, as well as mitochondrial H2O2 concentration and GSH/GSSG ratio as parameters for the oxidative stress. The results showed that ALA capable to ameliorate the defective antioxidant defense system leads to modulate the oxidative stress in terms of lower H2O2 concentration and higher GSH/GSSG ratio in D-ALA group compared with DC group. However the significant reduction of oxidative stress did not correlate well with the renal function parameters, in which only showed significant improvement of serum urea, but not serum creatinine or creatinine clearance. In conclusion, ALA treatment capable to ameliorate the defective antioxidant defense system and modulate the oxidative stress, but partially preventing the progression of renal dysfunction in diabetic rats. - 66 -
No. 14 (PC 14) Detection of autoantibodies against ATTR in patients with FAP ATTR V30M Konen Obayashi 1 , Masayoshi Tasaki 2 , Satoru Shinriki 1 , Genki Suenaga 2 and Yukio Ando 2 1 Diagnostic Unit for Amyloidosis, Department of Laboratory Medicine, Kumamoto University Hospital, and 2 Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Japan Background: It has been well documented that conformational changes via instability of tetrameric form TTR occurs during the process of amyloid formation in FAP. Some cryptic epitopes expose on amyloidogenic TTR (ATTR) molecule surface during the process in sera of FAP patients. There is a possibility that de novo antibodies responded to cryptic epitopes of ATTR may be synthesized in serum of FAP patients. Objective: To examine whether a relationship exists between the incidence of autoantibodies against ATTR and the phenotype of FAP ATTR V30M. Methods: Serum samples were collected from 25 Japanese (28-32 years old) and 8 Swedish (67-81 years old) FAP ATTR V30M patients, 4 Japanese gene carriers of ATTR V30M, and 24 Japanese healthy controls which had no genetic mutations of TTR. To detect the presence of autoantibodies against ATTR in these serum samples, enzyme-linked immunosorbent assay (ELISA) using recombinant ATTR V30M protein was immobilized on a polystyrene microtiter plates. Correlation between data of the ELISA and age of the subjects or duration of FAP was investigated. Results: Three of 25 Japanese and 5 of 8 Swedish FAP ATTR V30M patients were found to have autoantibodies against ATTR, and these 8 patients were all late onset cases. Moreover, significant positive correlation between the presence of the antibody and age was observed in all the patients examined (r=0.77, p < 0.05). We are now trying to detect conformational epitope binding to the autoantibodies against ATTR V30M. Our preliminary data suggested the possibility that there were some epitopes at positions 24-35 or 105-115 of ATTRV30M. Conclusions: Age-dependent increase in the incidence of autoantibodies was observed in patients with FAP ATTR V30M. This phenomenon may influence the clinicopathological differences between both early (
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Page 19 and 20: FO 1 CLINICAL PATHOLOGY SCOPE IN CA
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Page 23 and 24: FO 5 INDIAN STUDY OF LIVER FUNCTION
Page 25 and 26: Advanced Technical Seminar Sekisui
Page 27 and 28: Measurement of Albuminuria (Siemens
Page 29 and 30: The current status of the diagnosis
Page 31 and 32: Establishment of Reference Interval
Page 33 and 34: Innovative Lipid Biomarkers (Denka
Page 35 and 36: Scientific Innovation Seminar (Abbo
Page 37 and 38: PLEX-ID Technology as a Single Tool
Page 39 and 40: POSTER SESSION 1. Clinical Chemistr
Page 41 and 42: Naoko Yamaguchi, Tomohiro Takeda, C
Page 43 and 44: in Type 2 Diabetes Mellitus First D
Page 45 and 46: No. 36. Identification of autoantib
Page 47 and 48: Okamura 1) , Masahumi Takata 2) , M
Page 49 and 50: Hunsuk Suh 1 MD, PhD, Jonghee Shin
Page 51 and 52: Department of Pathology, Kansai Med
Page 53 and 54: No. 80. Introduction of HCV Quantif
Page 55 and 56: No. 91. Genome-wide association ana
Page 57 and 58: Abstracts - 53 -
Page 59 and 60: No. 2 (PC2) Soluble FcγRIIIa Mφ l
Page 61 and 62: No. 4 (PC 4) Detection of hereditar
Page 63 and 64: No. 6 (PC 6) Analysis of cholestery
Page 65 and 66: No. 8 (PC 8) Development of the enz
Page 67 and 68: No. 10 (PC 10) Direct analysis of c
Page 69: No. 12 (PC 12) Reference value for
Page 73 and 74: No. 16 (PC 16) Temporal changes in
Page 75 and 76: No. 18 (PC 18) IODINE STATUS AMONG
Page 77 and 78: No. 20 (PC 20) Plasma free Fatty Ac
Page 79 and 80: No. 22 (PE 1) Two-Step Biochemical
Page 81 and 82: No. 24 (PE 3) Adiponectin HMW Level
Page 83 and 84: No. 26 (PE 5) Analysis of von Wille
Page 85 and 86: No. 28 (PI 2) Diagnostic value of A
Page 87 and 88: No. 30 (PI 4) Evaluation of Hepatri
Page 89 and 90: No. 32 (PI 6) Discrepancy between s
Page 91 and 92: No. 34 (PI 8) Inhibition of the NF-
Page 93 and 94: No. 36 (PH 2) Identification of aut
Page 95 and 96: No. 38 (PH 4) Contribution of uncon
Page 97 and 98: No. 40 (PH 6) Red Blood Cells absor
Page 99 and 100: No. 42 (PH 8) Great impact of the b
Page 101 and 102: No. 44 (PH 10) Relation between VKO
Page 103 and 104: No. 46 (PH 12) Suspect of malaria i
Page 105 and 106: No. 48 (PH 14) Intravascular large
Page 107 and 108: No. 50 (PH 16) Calculation of Measu
Page 109 and 110: No. 52 (PM 1) High seroprevalence o
Page 111 and 112: No. 54 (PM 3) Epidemiological and m
Page 113 and 114: No. 56 (PM 5) Tuberculosis screenin
Page 115 and 116: No. 58 (PM 7) Mycobacterium Kyorine
Page 117 and 118: No. 60 (PM 9) Sensitive, one, two-d
Page 119 and 120: No. 62 (PM 11) Simultaneous inhibit
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No. 64 (PM 13) Measurement of Proca
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No. 66 (PF 1) Comparison of four po
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No. 68 (PP 1) The expressions of O
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No. 70 (PP 3) Poorly differentiated
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No. 72 (PP 5) The morphological cha
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No. 74 (PP 7) Neuropathological fin
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No. 76 (PMB 2) Diagnostic strategie
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No. 78 (PMB 4) Study of essential o
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No. 80 (PMB 6) Introduction of HCV
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No. 82 (PMB 8) Analysis of Fas exon
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No. 84 (PMB 10) A rapid and automat
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No. 86 (PMB 12) Increased expressio
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No 88 (PO 2) Assessment of early ma
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No. 90 (PO 4) The role of Rb2/p130
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No. 92 (PO 6) Molecular analysis of
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No. 94 (PO 8) The genealogical stud
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No. 96 (P0 10) Regulatory and pro-i
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No. 98 (PO 12) Chaotic Nature of My
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[Memo] - 153 -
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