Aging Aging

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Susceptibility of LDL to Oxidation 205Fig. 2. Typical curve obtained by monitoring oxidation of LDL with copper at 234 nm.a. Initial or lag phase: This is a slope with a slow increase in absorbance. Theduration of this phase is indicative of the inherent resistance to oxidation ofthe LDL sample being examined.b. Propagation phase: The lag phase is followed by a steep increase in absorbancedue to the rapid formation of conjugated dienes. This occurs only whenall the endogenous antioxidants within the LDL molecule and their protective
206 McEneny and Youngeffect have been utilized. When the propagation phase is complete a plateauof maximum absorbance is reached.9. Data analysis: See Fig. 2B. Determination of lag time using the mathematicalprogram removes subjective error which may occur if determined manually. Thisis calculated using a specially written macroprogram after the results obtained onthe PC are converted into ASCII file format and imported into the spreadsheetprogram Excel. The lag time is calculated as the intercept between the line ofmaximum slope of the propagation phase and the baseline where absorbance wasat time = zero (see Note 6).4. Notes1. Heparinized plasma is used in preference to serum purely for logistic reasons, asserum collection lengthens total preparation time. However, this technique maybe applied equally well to serum samples with no detectable difference in lagtime when compared to heparinized plasma.2. Protein standards and protein estimation: Stock BSA (25 µg/mL) is prepared byplacing 12.5 mg of BSA into a 500-mL beaker. Add approx 300 mL of deionizedwater and gently stir (care is required as vigorous mixing can cause BSA to foamand make it difficult to bring to the correct volume). Add this solution to a 500-mLvolumetric flask and rinse the beaker with remaining water to bring to correctvolume. Aliquot 7 mL of this solution into 10-mL tubes, cap, and freeze at –20°C.This solution is stable for up to 6 mo.Working standard solutions (0, 2.5, 10, 15, 20 µg/mL) are prepared from thestock BSA. These together with the samples are diluted with distilled water to afinal volume of 1.2 mL and prepared in duplicate in the 4-mL tubes. Threehundred microliters of Bio-Rad dye reagent is then added, making a final volume1.5 mL. The standards and samples are then gently inverted and absorbance at595 nm recorded within 5–60 min. The PD10 LDL is made up to 1.2 mL using0.1 mL of sample and 1.1 mL of distilled water. If the protein concentration ofcrude LDL is required use only 10 µL and dilute to 1.2 mL with water (dilutionfactor for crude LDL is 150).3. Copper chloride solution: The working solution of copper chloride is 40 µM. Thissolution is made by serial dilution of a 33.2 mM stock solution.a. Solution A: 33.2 mM — 0.567 g of CuCl 2·2H 2 O made in a 100-mL volumetricflask using deionized water.b. Solution B: 332 µM —1 mL of solution A is added to a 100-mL volumetricflask and the volume is made up using saline solution.c. Solution C: 40 µM working solution — 6.024 mL of solution B is added to a50-mL volumetric flask and the volume made up using either PBS or salinesolution (addition of PBS in the earlier solutions causes precipitation).4. Preparation of quartz cells: New or used cells must undergo the following procedurebefore use.Each cell is rinsed at least 10× with distilled water. They are then placed into aseparate disposable cup containing sufficient 4% Decon–90 to cover them. The
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Understanding Aging 9the intestine
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Understanding Aging 117. Do long-li
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Understanding Aging 13is, the great
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Understanding Aging 15While this re
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Understanding Aging 172. Pearl, R.
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Understanding Aging 1945. Perovic,
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24 Cristofalo, Volker, and Allenmen
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26 Cristofalo, Volker, and Allenrec
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28 Cristofalo, Volker, and Allenski
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30 Cristofalo, Volker, and AllenTab
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34 Cristofalo, Volker, and AllenNa
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38 Cristofalo, Volker, and Allentak
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40 Cristofalo, Volker, and Allenb.
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46 Cristofalo, Volker, and Allen33.
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48 Cristofalo, Volker, and Allen61.
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52 Cristofalo, Volker, and Allen125
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54 Pawelecdiluted cells on an irrad
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56 Pawelec3. Method3.1. Source of C
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58 Pawelecweekly or fortnightly sub
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60 Pawelection, the VERUM Foundatio
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Telomeres and Replicative Senescenc
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Detection of Molecular Events 715De
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Detection of Molecular Events 73hav
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Detection of Molecular Events 75Fig
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Detection of Molecular Events 772.
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Detection of Molecular Events 79Fig
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86 Kirk and Millerexperiments on un
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88 Kirk and MillerFig. 1. (A) Analy
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90 Kirk and MillerFurthermore, limi
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92 Kirk and Millersufficiently dilu
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94 Kirk and Miller4. Run samples on
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96 Kirk and Miller16. Lange-Carter,
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98 Engel, Adibzadeh, and PawelecPCR
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100 Engel, Adibzadeh, and Pawelec5.
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102 Engel, Adibzadeh, and PawelecTa
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104 Engel, Adibzadeh, and PawelecTa
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110 Engel, Adibzadeh, and Pawelecfo
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114 Engel, Adibzadeh, and Pawelecha
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Xenobiotic-Metabolizing Enzymes 119
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Assessing Antioxidant Status 1339As
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Assessing Antioxidant Status 135Fig
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Assessing Antioxidant Status 137Tab
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Assessing Antioxidant Status 139add
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Assessing Antioxidant Status 14121.
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Comet Assay of DNA Damage 14310Meas
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Comet Assay of DNA Damage 145contro
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Comet Assay of DNA Damage 1476. Lys
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Page 150 and 151: 160 van der Schanswithin 1 h, after
Page 152 and 153: 162 van der Schans10. High-binding
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Page 156 and 157: 166 van der SchansThe calculations
Page 158 and 159: 8-oxoguanine Levels in Nuclear DNA
Page 166 and 167: Mutation and the Aging Process 1791
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Page 176 and 177: 190 HouThe HPRT mutational spectrum
Page 178 and 179: 192 Houamplifications are carried o
Page 180 and 181: 194 Hou4. Reading: Load 10 µL of t
Page 182 and 183: 196 Hou4.2. MP-PCRUse preferably DN
Page 184 and 185: Susceptibility of LDL to Oxidation
Page 194 and 195: Analysis of Pentosidine 20916Measur
Page 196 and 197: Analysis of Pentosidine 211Fig. 2.
Page 198 and 199: Analysis of Pentosidine 213Fig. 4.
Page 200 and 201: Analysis of Pentosidine 2152. Preci
Page 202 and 203: Analysis of Pentosidine 2177. Nagar
Page 204 and 205: 222 Miquellipoperoxides and malonal
Page 206 and 207: 224 Miquelat 4°C. Protect this sol
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Page 210 and 211: 228 Miquelsteps to carry out a conv
Page 212 and 213: 230 Miquelsuspending it over the so
Page 214 and 215: 232 Miquelcontrast, washing with bu
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Page 218 and 219: Damage to Mitochondria 23718Causes
Page 220 and 221: Damage to Mitochondria 239Fig. 1. E
Page 222 and 223: Damage to Mitochondria 2412. To obt
Page 224 and 225: Damage to Mitochondria 243synthesis
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Page 234 and 235: Mitochondrial DNA Mutations 253Fig.
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Mitochondrial DNA Mutations 2593. P
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Mitochondrial DNA Mutations 261X-10
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Mitochondrial DNA Mutations 26315.
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Mitochondrial DNA Mutations 26520An
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Mitochondrial DNA Mutations 267Tabl
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Mitochondrial DNA Mutations 269muta
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Mitochondrial DNA Mutations 2717. P
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Mitochondrial DNA Mutations 2733.2.
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Mitochondrial DNA Mutations 275that
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Mitochondrial DNA Mutations 27711.
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282 BeckmanWhatever the mechanism e
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284 BeckmanT-cell adherence to vasc
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286 BeckmanT3 hybridoma cells satis
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288 BeckmanHaving identified a cand
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290 Beckmanthe plates vigorously wi
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292 Grubeck-Loebenstein, Saurwein-T
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NK Cell Function in Aging 31123Age-
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NK Cell Function in Aging 3135. Pet
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NK Cell Function in Aging 31518. Io
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NK Cell Function in Aging 3173.3. C
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NK Cell Function in Aging 3199mL of
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Immunogenetics and Life-Span 32124I
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Immunogenetics and Life-Span 323Tab
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Immunogenetics and Life-Span 325rea
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Immunogenetics and Life-Span 3273.
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Immunogenetics and Life-Span 3313.5
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Immunogenetics and Life-Span 349to
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354 Yuto-implement intervention and
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356 Yuof their quality control proc
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358 Yugenesis of major diseases (1-
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Genetically Engineered Mice 36126Th
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Genetically Engineered Mice 363as t
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Genetically Engineered Mice 365in b
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Genetically Engineered Mice 367numb
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Genetically Engineered Mice 369mula
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Genetically Engineered Mice 37537.
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Genetically Engineered Mice 377→
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Aging Aging

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