Evaluation of MRI resolution affecting trabecular bone parameters: Determination of acceptable resolution

The objective of this study is to evaluate the effect of MR image resolution on trabecular bone parameters and to determine the acceptable resolution that can be accurately analyzed to assess structural parameters. Ten distal femoral condyle specimens of 1 x 1 x 1 cm3 were scanned with a 4.7-T Bruker BioSpec MRI scanner using a three-dimensional fast large-angle spin-echo sequence with various iso-cubic voxels sizes (65, 130, 160, 196, 230, and 260 mu m). Otsu thresholding was applied to identify voxels containing bone. Conventional bone parameters, structural bone parameters, and skeleton-based local trabecular thickness (slTB.Th) were evaluated. The BlandAltman method and correlation indicated that the conventional and structural bone parameters were preserved with an iso-cubic voxel size up to 230 mu m (r > 0.932 and r > 0.843, respectively). In addition, slTB.Th derived from the highest resolution images (65 mu m iso-cubic voxel size), correlated well (r > 0.833) with the values computed from lower resolution images, up to 230 mu m, which is twice typical human trabecular thickness range (100150 mu m). The outcome of this study suggests that the various bone parameters were well preserved up to 230 mu m images. Magn Reson Med, 2011. (C)2011 Wiley-Liss, Inc.OAIID:oai:osos.snu.ac.kr:snu2012-01/102/0000004226/1SEQ:1PERF_CD:SNU2012-01EVAL_ITEM_CD:102USER_ID:0000004226ADJUST_YN:YEMP_ID:A076317DEPT_CD:801CITE_RATE:2.964FILENAME:E037T_Magn Reson Med-2012_Kim_Evaluation of MRI resolution affecting trabecular bone parameters.pdfDEPT_NM:의학과SCOPUS_YN:YCONFIRM:

Neurochemical Alterations in Methamphetamine-Dependent Patients Treated with Cytidine-5 `-Diphosphate Choline: A Longitudinal Proton Magnetic Resonance Spectroscopy Study

Cytidine-5`-diphosphate choline (CDP-choline), as an important intermediate for major membrane phospholipids, may exert neuroprotective effects in various neurodegenerative disorders. This longitudinal proton magnetic resonance spectroscopy ((1)H-MRS) study aimed to examine whether a 4-week CDP-choline treatment could alter neurometabolite levels in patients with methamphetamine (MA) dependence and to investigate whether changes in neurometabolite levels would be associated with MA use. We hypothesized that the prefrontal levels of N-acetyl-aspartate (NAA), a neuronal marker, and choline-containing compound (Cho), which are related to membrane turnover, would increase with CDP-choline treatment in MA-dependent patients. We further hypothesized that this increase would correlate with the total number of negative urine results. Thirty-one treatment seekers with MA dependence were randomly assigned to receive CDP-choline (n = 16) or placebo (n 15) for 4 weeks. Prefrontal NAA and Cho levels were examined using (1)H-MRS before medication, and at 2 and 4 weeks after treatment. Generalized estimating equation regression analyses showed that the rate of change in prefrontal NAA (p = 0.005) and Cho (p = 0.03) levels were greater with CDP-choline treatment than with placebo. In the CDP-choline-treated patients, changes in prefrontal NAA levels were positively associated with the total number of negative urine results (p = 0.03). Changes in the prefrontal Cho levels, however, were not associated with the total number of negative urine results. These preliminary findings suggest that CDP-choline treatment may exert potential neuroprotective effects directly or indirectly because of reductions in drug use by the MA-dependent patients. Further studies with a larger sample size of MA-dependent patients are warranted to confirm a long-term efficacy of CDP-choline in neuroprotection and abstinence. Neuropsychopharmacology (2010) 35, 1165-1173; doi: 10.1038/npp.2009.221; published online 30 December 2009This study was supported in part by grants from the NIDA (1R01 DA024070-01A1, Drs Lyoo and Renshaw; 5 R01 DA 14178-05, Dr Renshaw), from the NIH (7K24DA015116, Dr Renshaw; 5K05-DA000343-12, Dr Lukas), from the Korean Ministry of Education, Science and Technology, (2009K001272, Dr Lyoo; Basic Science Research Program 20090066915, Dr Yoon), and from Seoul National University Hospital (03-2008-006-0, Dr Lyoo).Yoon SJ, 2009, NEUROPSYCHOPHARMACOL, V34, P1810, DOI 10.1038/npp.2009.2Tian CH, 2009, PLOS ONE, V4, DOI 10.1371/journal.pone.0005546Silveri MM, 2008, NMR BIOMED, V21, P1066, DOI 10.1002/nbm.1281Bustillo JR, 2008, NEUROPSYCHOPHARMACOL, V33, P2456, DOI 10.1038/sj.npp.1301631Mathew SJ, 2008, BIOL PSYCHIAT, V63, P891, DOI 10.1016/j.biopsych.2007.09.012Berman S, 2008, ANN NY ACAD SCI, V1141, P195, DOI 10.1196/annals.1441.031Lee NK, 2008, DRUG ALCOHOL REV, V27, P309, DOI 10.1080/09595230801919494PROVENCHER SW, 2008, LCMODEL USERS MANUAL*DRUG ENF ADM, 2008, NAT DRUG THREAT ASSChung A, 2007, INT J NEUROPSYCHOPH, V10, P765, DOI 10.1017/Sl461145706007395Brown ES, 2007, J CLIN PSYCHOPHARM, V27, P498, DOI 10.1097/jcp.0b013e31814db4c4Scott JC, 2007, NEUROPSYCHOL REV, V17, P275, DOI 10.1007/s11065-007-9031-0Radad K, 2007, INT J NEUROSCI, V117, P985, DOI 10.1080/10623320600934341Salo R, 2007, BIOL PSYCHIAT, V61, P1272, DOI 10.1016/j.biopsych.2006.07.031Sung YH, 2007, DRUG ALCOHOL DEPEN, V88, P28, DOI 10.1016/j.drugalcdep.2006.09.011Vocci FJ, 2007, ADDICTION, V102, P96Ham BJ, 2007, EUR J NEUROSCI, V25, P324, DOI 10.1111/j.1460-9568.2006.05253.xShearer J, 2007, J SUBST ABUSE TREAT, V32, P41, DOI 10.1016/j.jsat.2006.06.012*DRUG ENF ADM, 2007, NAT DRUG THREAT ASSSecades JJ, 2006, METHOD FIND EXP CLIN, V28, P1Hwang J, 2006, DRUG ALCOHOL DEPEN, V82, P177, DOI 10.1016/j.drugalcdep.2005.09.011Kim SJ, 2006, INT J NEUROPSYCHOPH, V9, P221, DOI 10.1017/S1461145705005699Grohman K, 2006, BRAIN COGNITION, V60, P203Poling J, 2006, ARCH GEN PSYCHIAT, V63, P219Bae SC, 2006, DRUG ALCOHOL DEPEN, V81, P83, DOI 10.1016/j.drugalcdep.2005.05.016QUINTON MS, 2006, AAPS J, V8, P337Kim SJ, 2005, NEUROPSYCHOPHARMACOL, V30, P1383, DOI 10.1038/sj.npp.1300699Meredith CW, 2005, HARVARD REV PSYCHIAT, V13, P141, DOI 10.1080/10673220591003605Nordahl TE, 2005, ARCH GEN PSYCHIAT, V62, P444Chang L, 2005, AM J PSYCHIAT, V162, P361Adibhatla R, 2005, NEUROCHEM RES, V30, P15, DOI 10.1007/s11064-004-9681-8*NSDUH, 2005, RES 2005 NSUDHBrown JM, 2003, PHARMACOL THERAPEUT, V99, P45, DOI 10.1016/S0163-7258(03)00052-4BARREDA V, 2003, REV MUSEO ARGENTINO, V5, P215Barrachina M, 2002, BRAIN RES, V957, P84Nordahl TE, 2002, PSYCHIAT RES-NEUROIM, V116, P43Ross BM, 2002, DRUG ALCOHOL DEPEN, V67, P73Babb SM, 2002, PSYCHOPHARMACOLOGY, V161, P248, DOI 10.1007/s00213-002-1045-yRoss BM, 2002, PROSTAG LEUKOTR ESS, V66, P479, DOI 10.1054/plef.385FIRST MB, 2002, STRUCTURAL CLIN INTEClark WM, 2001, NEUROLOGY, V57, P1595Lukas SE, 2001, PSYCHOPHARMACOLOGY, V157, P163Davidson C, 2001, BRAIN RES REV, V36, P1McLean MA, 2001, NEUROIMAGE, V14, P501, DOI 10.1006/nimg.2001.0827Smith LM, 2001, NEUROLOGY, V57, P255Provencher SW, 2001, NMR BIOMED, V14, P260Bertolino A, 2001, BIOL PSYCHIAT, V49, P39Wurtman RJ, 2000, BIOCHEM PHARMACOL, V60, P989Rawson RA, 2000, J PSYCHOACTIVE DRUGS, V32, P371Boulanger Y, 2000, BRAIN RES REV, V33, P380Moore GJ, 2000, BIOL PSYCHIAT, V48, P1Ernst T, 2000, NEUROLOGY, V54, P1344Winsberg ME, 2000, BIOL PSYCHIAT, V47, P475Bluml S, 1999, MAGNET RESON MED, V42, P643Clement JM, 1999, BIOCHEM BIOPH RES CO, V257, P643Renshaw PF, 1999, PSYCHOPHARMACOLOGY, V142, P132Clark JB, 1998, DEV NEUROSCI-BASEL, V20, P271Deicken RF, 1998, BIOL PSYCHIAT, V43, P483Araki W, 1998, J NEUROSCI RES, V51, P667Murray JB, 1998, J PSYCHOL, V132, P227Ellis CM, 1997, NEUROLOGY, V49, P438Hussain T, 1997, CLIN EXP HYPERTENS, V19, P131Christensen JD, 1996, MAGNET RESON MED, V35, P658Reid MS, 1996, J PHARMACOL EXP THER, V276, P1244ROSS K, 1996, PARALLAX, V2, P67DESTEFANO N, 1995, MAGNET RESON MED, V34, P721VIAL D, 1995, J NEUROCHEM, V64, P2765HOLSHOUSER BA, 1995, MAGNET RESON MED, V33, P589WEISS GB, 1995, LIFE SCI, V56, P637VIONDURY J, 1995, LANCET, V345, P60DAVIE CA, 1994, BRAIN, V117, P49MACKAY S, 1993, BIOL PSYCHIAT, V34, P261MCALLISTER G, 1993, FEBS LETT, V324, P81BARKER PB, 1993, NMR BIOMED, V6, P89OMALLEY SS, 1992, ARCH GEN PSYCHIAT, V49, P881WANG AM, 1990, AM J NEURORADIOL, V11, P1141ZEGER SL, 1986, BIOMETRICS, V42, P121TRUCKENMILLER ME, 1985, J NEUROCHEM, V45, P1658SALIGAUT C, 1985, METHOD FIND EXP CLIN, V7, P5AGUT J, 1984, NEUROPHARMACOLOGY, V23, P1403ALBERGHINA M, 1981, J NEUROSCI RES, V6, P421PATEL TB, 1979, BIOCHEM J, V184, P539MARTINET M, 1979, ARCH INT PHARMACOD T, V239, P52MARTINET M, 1978, EXPERIENTIA, V34, P1197HAMILTON M, 1960, J NEUROL NEUROSUR PS, V23, P56KENNEDY EP, 1956, J BIOL CHEM, V222, P193

Increased GABA Levels in Medial Prefrontal Cortex of Young Adults with Narcolepsy

STUDY OBJECTIVES: To explore absolute concentrations of brain metabolites including gamma amino-butyric acid (GABA) in the medial prefrontal cortex and basal ganglia of young adults with narcolepsy. DESIGN: Proton magnetic resonance (MR) spectroscopy centered on the medial prefrontal cortex and the basal ganglia was acquired. The absolute concentrations of brain metabolites including GABA and glutamate were assessed and compared between narcoleptic patients and healthy comparison subjects. SETTING: Sleep and Chronobiology Center at Seoul National University Hospital; A high strength 3.0 Tesla MR scanner in the Department of Radiology at Seoul National University Hospital. PATIENTS OR PARTICIPANTS: Seventeen young adults with a sole diagnosis of HLA DQB1 0602 positive narcolepsy with cataplexy (25.1 +/- 4.6 years old) and 17 healthy comparison subjects (26.8 +/- 4.8 years old). INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Relative to comparison subjects, narcoleptic patients had higher GABA concentration in the medial prefrontal cortex (t = 4.10, P <0.001). Narcoleptic patients with nocturnal sleep disturbance had higher GABA concentration in the medial prefrontal cortex than those without nocturnal sleep disturbance (t = 2.45, P = 0.03), but had lower GABA concentration than comparison subjects (t = 2.30, P = 0.03). CONCLUSIONS: The current study reports that young adults with narcolepsy had a higher GABA concentration in the medial prefrontal cortex, which was more prominent in patients without nocturnal sleep disturbance. Our findings suggest that the medial prefrontal GABA level may be increased in narcolepsy, and the increased medial prefrontal GABA might be a compensatory mechanism to reduce nocturnal sleep disturbances in narcolepsy

Neurochemical Alterations in Methamphetamine-Dependent Patients Treated with Cytidine-5′-Diphosphate Choline: A Longitudinal Proton Magnetic Resonance Spectroscopy Study

Cytidine-5′-diphosphate choline (CDP-choline), as an important intermediate for major membrane phospholipids, may exert neuroprotective effects in various neurodegenerative disorders. This longitudinal proton magnetic resonance spectroscopy ((1)H-MRS) study aimed to examine whether a 4-week CDP-choline treatment could alter neurometabolite levels in patients with methamphetamine (MA) dependence and to investigate whether changes in neurometabolite levels would be associated with MA use. We hypothesized that the prefrontal levels of N-acetyl-aspartate (NAA), a neuronal marker, and choline-containing compound (Cho), which are related to membrane turnover, would increase with CDP-choline treatment in MA-dependent patients. We further hypothesized that this increase would correlate with the total number of negative urine results. Thirty-one treatment seekers with MA dependence were randomly assigned to receive CDP-choline (n=16) or placebo (n=15) for 4 weeks. Prefrontal NAA and Cho levels were examined using (1)H-MRS before medication, and at 2 and 4 weeks after treatment. Generalized estimating equation regression analyses showed that the rate of change in prefrontal NAA (p=0.005) and Cho (p=0.03) levels were greater with CDP-choline treatment than with placebo. In the CDP-choline-treated patients, changes in prefrontal NAA levels were positively associated with the total number of negative urine results (p=0.03). Changes in the prefrontal Cho levels, however, were not associated with the total number of negative urine results. These preliminary findings suggest that CDP-choline treatment may exert potential neuroprotective effects directly or indirectly because of reductions in drug use by the MA-dependent patients. Further studies with a larger sample size of MA-dependent patients are warranted to confirm a long-term efficacy of CDP-choline in neuroprotection and abstinence