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  1. Article ; Online: ADMA and the brain: an unfolding story.

    Kielstein, Jan T / Kielstein, Anousheh

    American journal of hypertension

    2009  Volume 22, Issue 3, Page(s) 240

    MeSH term(s) Animals ; Arginine/analogs & derivatives ; Arginine/metabolism ; Brain Chemistry/physiology ; Cattle ; Cerebrovascular Circulation ; Cerebrovascular Disorders/genetics ; Cerebrovascular Disorders/pathology ; Cross-Sectional Studies ; Glomerular Filtration Rate ; Homocysteine/blood ; Magnetic Resonance Imaging ; Nitric Oxide Synthase/antagonists & inhibitors ; Nitric Oxide Synthase/physiology
    Chemical Substances Homocysteine (0LVT1QZ0BA) ; N,N-dimethylarginine (63CV1GEK3Y) ; Arginine (94ZLA3W45F) ; Nitric Oxide Synthase (EC 1.14.13.39)
    Language English
    Publishing date 2009-03
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 639383-4
    ISSN 1941-7225 ; 1879-1905 ; 0895-7061
    ISSN (online) 1941-7225 ; 1879-1905
    ISSN 0895-7061
    DOI 10.1038/ajh.2008.354
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2329: Show issues Location:
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  2. Article: A randomized trial of 6-month methadone maintenance with standard or minimal counseling versus 21-day methadone detoxification.

    Gruber, Valerie A / Delucchi, Kevin L / Kielstein, Anousheh / Batki, Steven L

    Drug and alcohol dependence

    2008  Volume 94, Issue 1-3, Page(s) 199–206

    Abstract: Background: Important questions remain regarding the necessary duration and intensity for methadone treatment to be effective.: Methods: As part of a clinical trial of tuberculosis chemoprophylaxis [Batki, S.L., Gruber, V.A., Bradley, J.M., Bradley, ... ...

    Abstract Background: Important questions remain regarding the necessary duration and intensity for methadone treatment to be effective.
    Methods: As part of a clinical trial of tuberculosis chemoprophylaxis [Batki, S.L., Gruber, V.A., Bradley, J.M., Bradley, M., Delucchi, K., 2002. A controlled trial of methadone treatment combined with directly observed isoniazid for tuberculosis prevention in injection drug users. Drug Alcohol Depend. 66 283-293. doi:10.1016/S0376-8716(01)00208-3], patients with opioid dependence were recruited from an outpatient 21-day methadone detoxification program and were randomly assigned to one of three treatment conditions: (1) continuation in 21-day methadone detoxification; (2) transfer to 6-month methadone maintenance with only minimal counseling; or (3) transfer to 6-month methadone maintenance with standard twice monthly counseling and as-needed social work and psychiatric services. Both the 6-month maintenance treatments were followed by 1.5 months of detoxification. Urine drug tests and self-report measures were collected at baseline, months 1-6, and month 8.5.
    Results: Compared to 21-day methadone detoxification, 6-month methadone maintenance with either minimal or standard counseling resulted in fewer opiate positive urine tests and days of self-reported heroin and alcohol use. There was no change in cocaine use or other outcome measures. The increased counseling available in the standard counseling condition did not appear to reduce heroin use further than the minimal counseling condition, in contrast to the effect found for more structured counseling in long-term methadone maintenance (McLellan et al., 1993).
    Conclusions: Six months of methadone maintenance, even with minimal counseling, reduces heroin and alcohol use more than 21-day methadone detoxification.
    MeSH term(s) Adult ; Counseling/statistics & numerical data ; Demography ; Drug Administration Schedule ; Female ; Heroin Dependence/epidemiology ; Heroin Dependence/rehabilitation ; Heroin Dependence/therapy ; Humans ; Inactivation, Metabolic ; Male ; Methadone/administration & dosage ; Methadone/pharmacokinetics ; Methadone/therapeutic use ; Narcotics/administration & dosage ; Narcotics/pharmacokinetics ; Narcotics/therapeutic use ; Time Factors
    Chemical Substances Narcotics ; Methadone (UC6VBE7V1Z)
    Language English
    Publishing date 2008-02-19
    Publishing country Ireland
    Document type Journal Article ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural
    ZDB-ID 519918-9
    ISSN 1879-0046 ; 0376-8716
    ISSN (online) 1879-0046
    ISSN 0376-8716
    DOI 10.1016/j.drugalcdep.2007.11.021
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  3. Article: Psychiatric comorbidity in methamphetamine dependence.

    Salo, Ruth / Flower, Keith / Kielstein, Anousheh / Leamon, Martin H / Nordahl, Thomas E / Galloway, Gantt P

    Psychiatry research

    2010  Volume 186, Issue 2-3, Page(s) 356–361

    Abstract: The primary aim of the present study was to assess the prevalence of psychiatric comorbidity in a large sample of methamphetamine (MA)-dependent subjects using a validated structured clinical interview, without limitation to sexual orientation or ... ...

    Abstract The primary aim of the present study was to assess the prevalence of psychiatric comorbidity in a large sample of methamphetamine (MA)-dependent subjects using a validated structured clinical interview, without limitation to sexual orientation or participation in a treatment program. The secondary aim was to assess whether the prevalence of psychiatric comorbidities varied by gender. Structured clinical interviews (SCIDs) were administered to 189 MA-dependent subjects and lifetime prevalence of DSM-IV diagnoses was assessed. Across the sample, 28.6% had primary psychotic disorders, 23.8% of which were substance-induced; 13.2% had MA-induced delusional disorders and 11.1% had MA-induced hallucinations. A substantial number of lifetime mood disorders were identified that were not substance-induced (32.3%), whereas 14.8% had mood disorders induced by substances, and 10.6% had mood disorders induced by amphetamines. Of all participants, 26.5% had anxiety disorders and 3.7% had a substance-induced anxiety disorder, all of which were induced by MA. Male subjects reported a higher percentage of MA-induced delusions compared to female abusers. Given the impact of MA psychosis and other drug-induced symptoms on hospitals and mental health services, the description and characterization of comorbid psychiatric symptoms associated with MA use is of paramount importance.
    MeSH term(s) Adolescent ; Adult ; Aged ; Amphetamine-Related Disorders/epidemiology ; Comorbidity ; Female ; Humans ; Male ; Mental Disorders/diagnosis ; Mental Disorders/epidemiology ; Middle Aged ; Psychiatric Status Rating Scales ; Severity of Illness Index ; Young Adult
    Language English
    Publishing date 2010-11-04
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 445361-x
    ISSN 1872-7123 ; 1872-7506 ; 0165-1781 ; 0925-4927
    ISSN (online) 1872-7123 ; 1872-7506
    ISSN 0165-1781 ; 0925-4927
    DOI 10.1016/j.psychres.2010.09.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Asymmetric dimethylarginine (ADMA)--a modulator of nociception in opiate tolerance and addiction?

    Kielstein, Anousheh / Tsikas, Dimitrios / Galloway, Gantt P / Mendelson, John E

    Nitric oxide : biology and chemistry

    2007  Volume 17, Issue 2, Page(s) 55–59

    Abstract: Nitric oxide (NO) is generated from l-arginine by NO synthases, of which three forms have been identified: endothelial, inducible and neuronal (eNOS, iNOS and nNOS, respectively). The l-arginine metabolite asymmetric dimethylarginine (ADMA) is a potent, ... ...

    Abstract Nitric oxide (NO) is generated from l-arginine by NO synthases, of which three forms have been identified: endothelial, inducible and neuronal (eNOS, iNOS and nNOS, respectively). The l-arginine metabolite asymmetric dimethylarginine (ADMA) is a potent, noncompetitive inhibitor of nNOS, while its congener N(G)-monomethyl-l-arginine (l-NMMA) is a less potent, competitive inhibitor. In rat neurons large amounts of ADMA are found, suggesting its importance in modulating neuronal activity. Humans generate approximately 300mumol ( approximately 60mg) ADMA per day. It is released from myelin basic proteins that are highly expressed in neuronal tissue. ADMA is mainly degraded by the action of the enzyme dimethylarginine dimethylaminohydrolase (DDAH), which exists in two isoforms. DDAH1 is highly expressed in brain, suggesting specific function in this area. The presence of nNOS and DDAH1 in brain suggests that ADMA may have specific CNS activity and be more than an unregulated metabolite. Increased NO production-either prior to or concurrently with opioid administration-results in an enhanced rate and extent of development of tolerance to morphine in mice. NO produces an alteration in the mu-opioid receptor that increases constitutive receptor activity. It thereby reduces the ability of a selective mu-opioid agonist to activate the mu-opioid receptor; these in vitro molecular effects occur in a time course consistent with the in vivo development of antinociceptive tolerance in mice. Amongst many other synthetic NOS inhibitors of varying specificity, 7-nitroindazole (7-NI) has been shown to have a high affinity (IC(50) 0.71 microM) to nNOS. Selective blockade of nNOS by 7-NI attenuated morphine withdrawal in opiate dependent rats, suggesting nNOS as a viable target for development of pharmacotherapies. We hypothesize that, by inhibiting nNOS and reducing NO levels, ADMA may decrease mu-opiate receptor constitutive activity, resulting in alteration of the analgesic dose-response curve of morphine.
    MeSH term(s) Analgesics, Opioid/adverse effects ; Analgesics, Opioid/therapeutic use ; Arginine/analogs & derivatives ; Arginine/pharmacology ; Arginine/therapeutic use ; Drug Tolerance ; Humans ; Nitric Oxide Synthase Type I/antagonists & inhibitors ; Opioid-Related Disorders ; Pain/drug therapy
    Chemical Substances Analgesics, Opioid ; N,N-dimethylarginine (63CV1GEK3Y) ; Arginine (94ZLA3W45F) ; Nitric Oxide Synthase Type I (EC 1.14.13.39)
    Language English
    Publishing date 2007-09
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1362794-6
    ISSN 1089-8611 ; 1089-8603
    ISSN (online) 1089-8611
    ISSN 1089-8603
    DOI 10.1016/j.niox.2007.05.005
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  5. Article: A nine session manual of motivational enhancement therapy for methamphetamine dependence: adherence and efficacy.

    Galloway, Gantt P / Polcin, Douglas / Kielstein, Anousheh / Brown, Michelle / Mendelson, John

    Journal of psychoactive drugs

    2008  Volume Suppl 4, Page(s) 393–400

    Abstract: Motivational enhancement therapy (MET) is a brief therapy shown to be effective for problem drinkers. Because the response to MET for other addictive disorders is mixed, we assessed the utility of increasing the number of sessions in subjects with ... ...

    Abstract Motivational enhancement therapy (MET) is a brief therapy shown to be effective for problem drinkers. Because the response to MET for other addictive disorders is mixed, we assessed the utility of increasing the number of sessions in subjects with methamphetamine (MA) dependence. One therapist was trained in a nine-session manual of MET, which was tested over eight weeks in 30 MA-dependent outpatients. Adherence to the manual was assessed by two raters, who reviewed a random sample of 15 audiotaped therapy sessions. Interventions were rated on a seven-point Likert scale for frequency/extensiveness (1 = not at all to 7 = extensively) and skill level (1 = unacceptable to 7 = high level of mastery). Ratings of adherence were moderate for frequency/extensiveness (4.2 +/- 2.2 and 4.3 +/- 1.8; Mean +/- SD) and high for skill level (5.4 +/- 0.6 and 5.2 +/- 0.4). Subjects attended 7.0 +/- 2.5 (78%) of nine sessions. Self-reported days of methamphetamine use decreased from 841/1793 (47%) of the 60 days prior to study entry to 448/1458 (31%) during the study (p = 0.011). MA-positive urine samples decreased from 76/118 (64%) during screening to 93/210 (44%) during treatment (p = 0.015). The MET manual was readily learned, and subjects attended a high proportion of therapy sessions with marked reductions in methamphetamine use.
    MeSH term(s) Adolescent ; Adult ; Amphetamine-Related Disorders/psychology ; Amphetamine-Related Disorders/therapy ; Amphetamine-Related Disorders/urine ; California/epidemiology ; Central Nervous System Stimulants ; Data Interpretation, Statistical ; Female ; Follow-Up Studies ; Humans ; Male ; Methamphetamine ; Patient Acceptance of Health Care ; Patient Compliance ; Psychiatric Status Rating Scales ; Psychotherapy, Brief ; Sex Factors ; Substance Abuse Detection ; Treatment Outcome
    Chemical Substances Central Nervous System Stimulants ; Methamphetamine (44RAL3456C)
    Language English
    Publishing date 2008-02-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 392405-1
    ISSN 2159-9777 ; 0279-1072
    ISSN (online) 2159-9777
    ISSN 0279-1072
    DOI 10.1080/02791072.2007.10399900
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  6. Article ; Online: ADMA increases arterial stiffness and decreases cerebral blood flow in humans.

    Kielstein, Jan T / Donnerstag, Frank / Gasper, Sandra / Menne, Jan / Kielstein, Anousheh / Martens-Lobenhoffer, Jens / Scalera, Fortunato / Cooke, John P / Fliser, Danilo / Bode-Böger, Stefanie M

    Stroke

    2006  Volume 37, Issue 8, Page(s) 2024–2029

    Abstract: Background and purpose: Preclinical studies have revealed that the endogenous nitric oxide synthase inhibitor, asymmetric dimethylarginine (ADMA), increases vascular tone in cerebral blood vessels. Marked elevations of ADMA blood levels were found in ... ...

    Abstract Background and purpose: Preclinical studies have revealed that the endogenous nitric oxide synthase inhibitor, asymmetric dimethylarginine (ADMA), increases vascular tone in cerebral blood vessels. Marked elevations of ADMA blood levels were found in patients with diseases characterized by decreased cerebral perfusion, such as ischemic stroke. Arterial stiffness is an independent predictor of stroke and other adverse cardiovascular events. The aim of this study was to investigate the influence of a systemic subpressor dose of ADMA on arterial stiffness and cerebral perfusion in humans.
    Methods: Using a double-blind, vehicle-controlled study design, we allocated 20 healthy men in random order to infusion of either ADMA (0.10 mg ADMA/kg per min) or vehicle over a period of 40 minutes. Arterial stiffness was assessed noninvasively by pulse wave analysis. All volunteers underwent measurement of cerebral perfusion by dynamic contrast-enhanced perfusion magnetic resonance imaging of the brain.
    Results: Infusion of ADMA significantly decreased total cerebral perfusion by 15.1+/-4.5% (P=0.007), whereas blood flow in the vehicle group increased by 7.7+/-2.8% (P=0.02). ADMA also increased arterial stiffness as assessed by measurement of the augmentation index (-12.6+/-1.9 to -9.6+/-1.5, P=0.007).
    Conclusions: Our results document for the first time that subpressor doses of ADMA increase vascular stiffness and decrease cerebral perfusion in healthy subjects. Thus, ADMA is an important endogenous modulator of cerebral vascular tone and may be involved in the pathogenesis of cerebrovascular disease.
    MeSH term(s) Adult ; Arginine/administration & dosage ; Arginine/analogs & derivatives ; Arginine/pharmacology ; Cerebral Arteries/drug effects ; Cerebral Arteries/physiology ; Cerebrovascular Circulation/drug effects ; Compliance ; Dose-Response Relationship, Drug ; Double-Blind Method ; Enzyme Inhibitors/pharmacology ; Humans ; Injections, Intravenous ; Magnetic Resonance Imaging ; Male ; Nitric Oxide Synthase/antagonists & inhibitors ; Reference Values ; Vasomotor System/drug effects
    Chemical Substances Enzyme Inhibitors ; N,N-dimethylarginine (63CV1GEK3Y) ; Arginine (94ZLA3W45F) ; Nitric Oxide Synthase (EC 1.14.13.39)
    Language English
    Publishing date 2006-08
    Publishing country United States
    Document type Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 80381-9
    ISSN 1524-4628 ; 0039-2499 ; 0749-7954
    ISSN (online) 1524-4628
    ISSN 0039-2499 ; 0749-7954
    DOI 10.1161/01.STR.0000231640.32543.11
    Database MEDical Literature Analysis and Retrieval System OnLINE

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