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	<title>CiteULike: pseudopharm's library [354 articles]</title>
	<description>CiteULike: pseudopharm's library [354 articles]</description>


	<link>http://www.citeulike.org/user/pseudopharm</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2952903">
    <title>Ruminative coping as avoidance: a reinterpretation of its function in adjustment to bereavement.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2952903</link>
    <description>&lt;i&gt;European archives of psychiatry and clinical neuroscience, Vol. 257, No. 8. (December 2007), pp. 462-472.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The paper argues for a reconceptualization of ruminative coping with the death of a loved one as an avoidant rather than a confrontational strategy. Ruminative coping has been characterized within the bereavement field as persistent, repetitive and passive focus on negative emotions and symptoms. It has been theoretically described and empirically shown to be a maladaptive process, being conceptually related to complicated/chronic/prolonged grief. Furthermore, it has been contrasted with denial and suppression processes--which, too, have been understood to be maladaptive and associated with major complications following bereavement. Here evidence is reviewed and the case made that rumination is not an opposite form of coping from suppression or denial, but that it is a similar phenomenon to these, and different from the types of confrontation that take place in so-called &#34;grief work&#34;. Implications with respect to intervention for complicated grief are discussed.</description>
    <dc:title>Ruminative coping as avoidance: a reinterpretation of its function in adjustment to bereavement.</dc:title>

    <dc:creator>M Stroebe</dc:creator>
    <dc:creator>PA Boelen</dc:creator>
    <dc:creator>M van den Hout</dc:creator>
    <dc:creator>W Stroebe</dc:creator>
    <dc:creator>E Salemink</dc:creator>
    <dc:creator>J van den Bout</dc:creator>
    <dc:identifier>doi:10.1007/s00406-007-0746-y</dc:identifier>
    <dc:source>European archives of psychiatry and clinical neuroscience, Vol. 257, No. 8. (December 2007), pp. 462-472.</dc:source>
    <dc:date>2008-07-02T16:18:49-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>European archives of psychiatry and clinical neuroscience</prism:publicationName>
    <prism:issn>0940-1334</prism:issn>
    <prism:volume>257</prism:volume>
    <prism:number>8</prism:number>
    <prism:startingPage>462</prism:startingPage>
    <prism:endingPage>472</prism:endingPage>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2952902">
    <title>A randomized, double-blind, placebo-controlled trial of desvenlafaxine succinate in the treatment of major depressive disorder.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2952902</link>
    <description>&lt;i&gt;International clinical psychopharmacology, Vol. 22, No. 6. (November 2007), pp. 338-347.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The antidepressant efficacy and safety of desvenlafaxine succinate (desvenlafaxine) were evaluated in a phase III, double-blind, placebo-controlled study. Outpatients with a primary diagnosis of major depressive disorder were treated with fixed once-daily doses of desvenlafaxine 200 or 400 mg for 8 weeks. The primary efficacy measure was change from baseline on the 17-item Hamilton Rating Scale for Depression. At the final on-therapy evaluation, adjusted mean change from baseline in 17-item Hamilton Rating Scale for Depression total score was greater for desvenlafaxine 200 and 400 mg/day vs. placebo. Both desvenlafaxine doses showed greater efficacy than placebo on the secondary efficacy measures, including the Clinical Global Impressions-Improvement scale scores, Montgomery-Asberg Depression Rating Scale scores, CGI-Severity, and 17-item Hamilton Rating Scale for Depression response rate. Desvenlafaxine 200 mg/day was also significantly better than placebo on remission, Visual Analog Scale-Pain Intensity overall scores, and some Visual Analog Scale-Pain Intensity subscale scores. Desvenlafaxine 400 mg/day was significantly better than placebo on selected Visual Analog Scale-Pain Intensity subscale scores. Most adverse events were mild or moderate in severity, and safety assessments revealed few clinically significant changes in vital signs, laboratory tests, and electrocardiogram results. These data provide support for the efficacy and safety of desvenlafaxine in the treatment of major depressive disorder.</description>
    <dc:title>A randomized, double-blind, placebo-controlled trial of desvenlafaxine succinate in the treatment of major depressive disorder.</dc:title>

    <dc:creator>L Septien-Velez</dc:creator>
    <dc:creator>B Pitrosky</dc:creator>
    <dc:creator>SK Padmanabhan</dc:creator>
    <dc:creator>JM Germain</dc:creator>
    <dc:creator>KA Tourian</dc:creator>
    <dc:identifier>doi:10.1097/YIC.0b013e3281e2c84b</dc:identifier>
    <dc:source>International clinical psychopharmacology, Vol. 22, No. 6. (November 2007), pp. 338-347.</dc:source>
    <dc:date>2008-07-02T16:18:05-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>International clinical psychopharmacology</prism:publicationName>
    <prism:issn>0268-1315</prism:issn>
    <prism:volume>22</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>338</prism:startingPage>
    <prism:endingPage>347</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>clinical_trial</prism:category>
    <prism:category>major_depression</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2952898">
    <title>Gizmo idolatry.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2952898</link>
    <description>&lt;i&gt;JAMA : the journal of the American Medical Association, Vol. 299, No. 15. (16 April 2008), pp. 1830-1832.&lt;/i&gt;</description>
    <dc:title>Gizmo idolatry.</dc:title>

    <dc:creator>B Leff</dc:creator>
    <dc:creator>TE Finucane</dc:creator>
    <dc:identifier>doi:10.1001/jama.299.15.1830</dc:identifier>
    <dc:source>JAMA : the journal of the American Medical Association, Vol. 299, No. 15. (16 April 2008), pp. 1830-1832.</dc:source>
    <dc:date>2008-07-02T16:17:04-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>JAMA : the journal of the American Medical Association</prism:publicationName>
    <prism:issn>1538-3598</prism:issn>
    <prism:volume>299</prism:volume>
    <prism:number>15</prism:number>
    <prism:startingPage>1830</prism:startingPage>
    <prism:endingPage>1832</prism:endingPage>
    <prism:category>theory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2952895">
    <title>Evidence-based psychiatric practice? Long live the (individual) difference.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2952895</link>
    <description>&lt;i&gt;The Israel journal of psychiatry and related sciences, Vol. 44, No. 4. (2007), pp. 301-308.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Mental health services in Israel are about to undergo a major, and quite controversial, reform. Yet both those advocating these reforms and those opposing themrefrain from resorting to empirical science in arguing their respective cases. In the present article, we present findings concerning the central role of patients' individual differences in the outcome of mental health services. Data is presented from three research projects: 1. The National Institute of Mental Health (NIMH) Treatment of Depression Collaborative Research Program (TDCRP), in particular recent publications by Blatt, Zuroff, Shahar and their collaborators, 2. The Partnership Project in severemental illness, and 3. The Menninger Psychotherapy Research Project (MPRP). Findings from these three projects, largely predicted by Blatt's theory of interpersonal relatedness and self-definition, suggest that an effective, evidence-based mental health practice is contingent upon practitioners' sensitivity to pretreatment patient characteristics. Clinical and policy implications of this conclusion are discussed.</description>
    <dc:title>Evidence-based psychiatric practice? Long live the (individual) difference.</dc:title>

    <dc:creator>N Soffer</dc:creator>
    <dc:creator>G Shahar</dc:creator>
    <dc:source>The Israel journal of psychiatry and related sciences, Vol. 44, No. 4. (2007), pp. 301-308.</dc:source>
    <dc:date>2008-07-02T16:15:58-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>The Israel journal of psychiatry and related sciences</prism:publicationName>
    <prism:issn>0333-7308</prism:issn>
    <prism:volume>44</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>301</prism:startingPage>
    <prism:endingPage>308</prism:endingPage>
    <prism:category>review</prism:category>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2880611">
    <title>Duration of untreated illness as a predictor of treatment response and clinical course in generalized anxiety disorder.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2880611</link>
    <description>&lt;i&gt;CNS spectrums, Vol. 13, No. 5. (May 2008), pp. 415-422.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;INTRODUCTION: The aim of the present study was to investigate the impact of the duration of untreated illness (DUI)-defined as the time elapsing between the onset of generalized anxiety disorder (GAD) and the first adequate pharmacologic treatment-on treatment response and clinical course in a sample of subjects with GAD. METHODS: One hundred patients with GAD, diagnosed according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Text Revision criteria, were enrolled and their main demographic and clinical features collected. Patients were then treated with selective serotonin reuptake inhibitors or venlafaxine for 8 weeks in open-label conditions. Treatment response and other clinical variables were analyzed after dividing the sample into two groups according to DUI (DUI &#60;or=12 months and DUI &#62;12 months). RESULTS: When the DUI was computed with respect to the first antidepressant treatment (DUI-AD), a higher improvement (Clinical Global Impressions-Severity of Illness scale) after the pharmacologic treatment was found in the group with a shorter DUI (analysis of variance with repeated measures: time effect F=654.975, P&#60;.001; group effect: F=4.369, P=.039). When computed with respect to the first treatment with benzodiazepines (DUI-BDZ), the two groups did not show any significant difference in treatment response (time effect: F=652.183, P&#60;.001; group effect: F=0.009, P=.924). In addition, patients with a longer DUI (DUI-BDZ or DUI-AD) showed an earlier age at onset, a longer duration of illness and a higher rate of comorbid psychiatric disorders with onset later than GAD. CONCLUSION: Results from this preliminary study seem to suggest that a shorter DUI-AD may determine a better response to pharmacologic treatment in patients with GAD, and that a longer DUI (DUI-BDZ and DUI-AD) may be associated to a worse clinical course. Further investigation on the relationship between DUI and GAD is needed.</description>
    <dc:title>Duration of untreated illness as a predictor of treatment response and clinical course in generalized anxiety disorder.</dc:title>

    <dc:creator>AC Altamura</dc:creator>
    <dc:creator>B Dell'osso</dc:creator>
    <dc:creator>N D'Urso</dc:creator>
    <dc:creator>M Russo</dc:creator>
    <dc:creator>S Fumagalli</dc:creator>
    <dc:creator>E Mundo</dc:creator>
    <dc:source>CNS spectrums, Vol. 13, No. 5. (May 2008), pp. 415-422.</dc:source>
    <dc:date>2008-06-10T18:27:34-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>CNS spectrums</prism:publicationName>
    <prism:issn>1092-8529</prism:issn>
    <prism:volume>13</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>415</prism:startingPage>
    <prism:endingPage>422</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>clinical_trial</prism:category>
    <prism:category>gabaergic</prism:category>
    <prism:category>gad</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2353690">
    <title>The role of social cognition in emotion</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2353690</link>
    <description>&lt;i&gt;Trends in Cognitive Sciences, Vol. 12, No. 2. (February 2008), pp. 65-71.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Although recent research has shown that social cognition and emotion engage overlapping regions of the brain, few accounts of this overlap have been offered. What systems might be commonly or distinctively involved in each The close functional relationship between social cognition and emotion might be understood in terms of a central role for mental state attribution in the understanding, learning and regulation of emotion. In each of these cases, mental state attributions might be supported by either stimulus-driven or more reflective processes.</description>
    <dc:title>The role of social cognition in emotion</dc:title>

    <dc:creator>Andreas Olsson</dc:creator>
    <dc:creator>Kevin Ochsner</dc:creator>
    <dc:identifier>doi:10.1016/j.tics.2007.11.010</dc:identifier>
    <dc:source>Trends in Cognitive Sciences, Vol. 12, No. 2. (February 2008), pp. 65-71.</dc:source>
    <dc:date>2008-02-08T15:37:43-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Trends in Cognitive Sciences</prism:publicationName>
    <prism:volume>12</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>65</prism:startingPage>
    <prism:endingPage>71</prism:endingPage>
    <prism:category>review</prism:category>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2828241">
    <title>Stimulant therapy and risk for subsequent substance use disorders in male adults with ADHD: a naturalistic controlled 10-year follow-up study.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2828241</link>
    <description>&lt;i&gt;The American journal of psychiatry, Vol. 165, No. 5. (May 2008), pp. 597-603.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;OBJECTIVE: The extant literature does not provide definite answers pertaining to whether stimulant treatment increases, decreases, or does not affect the risk for subsequent substance use disorders in youths with attention deficit hyperactivity disorder (ADHD). The authors examined the association between stimulant treatment in childhood and adolescence and subsequent substance use disorders (alcohol, drug, and nicotine) into the young adult years. METHOD: The authors conducted a 10-year prospective follow-up study. One hundred forty male Caucasian children with ADHD, ages 6 to 17, were examined at baseline. Of these, 112 (80%) were reassessed at the 10-year follow-up (mean age at follow-up=22 years). Assessments were made using Cox proportional hazards survival models. All models were adjusted for conduct disorder, since conduct disorder is a potent predictor of subsequent substance use disorders. RESULTS: Of the 112 ADHD subjects who were reassessed at the 10-year follow-up, 82 (73%) had been treated previously with stimulants and 25 (22%) were undergoing stimulant treatment at the time of the follow-up assessment. There were no statistically significant associations between stimulant treatment and alcohol, drug, or nicotine use disorders. CONCLUSIONS: The findings revealed no evidence that stimulant treatment increases or decreases the risk for subsequent substance use disorders in children and adolescents with ADHD when they reach young adulthood.</description>
    <dc:title>Stimulant therapy and risk for subsequent substance use disorders in male adults with ADHD: a naturalistic controlled 10-year follow-up study.</dc:title>

    <dc:creator>J Biederman</dc:creator>
    <dc:creator>MC Monuteaux</dc:creator>
    <dc:creator>T Spencer</dc:creator>
    <dc:creator>TE Wilens</dc:creator>
    <dc:creator>HA Macpherson</dc:creator>
    <dc:creator>SV Faraone</dc:creator>
    <dc:identifier>doi:10.1176/appi.ajp.2007.07091486</dc:identifier>
    <dc:source>The American journal of psychiatry, Vol. 165, No. 5. (May 2008), pp. 597-603.</dc:source>
    <dc:date>2008-05-24T21:48:51-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>The American journal of psychiatry</prism:publicationName>
    <prism:issn>1535-7228</prism:issn>
    <prism:volume>165</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>597</prism:startingPage>
    <prism:endingPage>603</prism:endingPage>
    <prism:category>adhd</prism:category>
    <prism:category>clinical_trial</prism:category>
    <prism:category>stimulant</prism:category>
    <prism:category>substance_abuse</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2828238">
    <title>Serotonin syndrome associated with triptan monotherapy.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2828238</link>
    <description>&lt;i&gt;The New England journal of medicine, Vol. 358, No. 20. (15 May 2008), pp. 2185-2186.&lt;/i&gt;</description>
    <dc:title>Serotonin syndrome associated with triptan monotherapy.</dc:title>

    <dc:creator>OP Soldin</dc:creator>
    <dc:creator>JM Tonning</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1056/NEJMc0706410</dc:identifier>
    <dc:source>The New England journal of medicine, Vol. 358, No. 20. (15 May 2008), pp. 2185-2186.</dc:source>
    <dc:date>2008-05-24T21:47:11-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>The New England journal of medicine</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>358</prism:volume>
    <prism:number>20</prism:number>
    <prism:startingPage>2185</prism:startingPage>
    <prism:endingPage>2186</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>neurology</prism:category>
    <prism:category>side_effect</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2828235">
    <title>Sertraline hepatotoxicity: a case report and review of the literature on selective serotonin reuptake inhibitor hepatotoxicity.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2828235</link>
    <description>&lt;i&gt;Digestive diseases and sciences, Vol. 48, No. 5. (May 2003), pp. 939-944.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The causal role of sertraline in rare cases of liver failure in patients taking the drug has not been proven in a manner consistent with usually accepted standards. We describe an individual who developed clinically significant hepatitis while being treated with sertraline. This case is significant because it is the only one of which we are aware in which the diagnosis of sertraline hepatotoxicity was confirmed when inadvertent rechallenge with the medication resulted in recurrent hepatitis. We review this case and the general role of this widely prescribed class of drugs in causing hepatitis.</description>
    <dc:title>Sertraline hepatotoxicity: a case report and review of the literature on selective serotonin reuptake inhibitor hepatotoxicity.</dc:title>

    <dc:creator>S Persky</dc:creator>
    <dc:creator>JF Reinus</dc:creator>
    <dc:source>Digestive diseases and sciences, Vol. 48, No. 5. (May 2003), pp. 939-944.</dc:source>
    <dc:date>2008-05-24T21:44:16-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Digestive diseases and sciences</prism:publicationName>
    <prism:issn>0163-2116</prism:issn>
    <prism:volume>48</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>939</prism:startingPage>
    <prism:endingPage>944</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>gi</prism:category>
    <prism:category>side_effect</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2675771">
    <title>Reexamination of Therapist Self-Disclosure</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2675771</link>
    <description>&lt;i&gt;Psychiatr Serv, Vol. 52, No. 11. (1 November 2001), pp. 1489-1493.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In mental health practice, a commonly held view is that therapist self-disclosure should be discouraged and its dangers closely monitored. Changes in medicine, mental health care, and society demand reexamination of these beliefs. In some clinical situations, considerable benefit may stem from therapist self-disclosure. Although the dangers of boundary violations are genuine, self-disclosure may be underused or misused because it lacks a framework. It is useful to consider the benefits of self-disclosure in the context of treatment type, treatment setting, and patient characteristics. Self-disclosure can contribute to the effectiveness of peer models. Self-disclosure is often used in cognitive-behavioral therapy and social skills training and might be useful in psychopharmacologic and supportive treatments. The unavoidable self-disclosure that occurs in non-office-based settings provides opportunities for therapeutic deliberate self-disclosure. Children and individuals who have a diminished capacity for abstract thought may benefit from more direct answers to questions related to self-disclosure. The role of self-disclosure in mental health care should be reexamined. 10.1176/appi.ps.52.11.1489</description>
    <dc:title>Reexamination of Therapist Self-Disclosure</dc:title>

    <dc:identifier>doi:10.1176/appi.ps.52.11.1489</dc:identifier>
    <dc:source>Psychiatr Serv, Vol. 52, No. 11. (1 November 2001), pp. 1489-1493.</dc:source>
    <dc:date>2008-04-16T01:08:33-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Psychiatr Serv</prism:publicationName>
    <prism:volume>52</prism:volume>
    <prism:number>11</prism:number>
    <prism:startingPage>1489</prism:startingPage>
    <prism:endingPage>1493</prism:endingPage>
    <prism:category>social_study</prism:category>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2670993">
    <title>Lead poisoning due to adulterated marijuana.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2670993</link>
    <description>&lt;i&gt;The New England journal of medicine, Vol. 358, No. 15. (10 April 2008), pp. 1641-1642.&lt;/i&gt;</description>
    <dc:title>Lead poisoning due to adulterated marijuana.</dc:title>

    <dc:creator>F Busse</dc:creator>
    <dc:creator>L Omidi</dc:creator>
    <dc:creator>A Leichtle</dc:creator>
    <dc:creator>M Windgassen</dc:creator>
    <dc:creator>E Kluge</dc:creator>
    <dc:creator>M Stumvoll</dc:creator>
    <dc:identifier>doi:10.1056/NEJMc0707784</dc:identifier>
    <dc:source>The New England journal of medicine, Vol. 358, No. 15. (10 April 2008), pp. 1641-1642.</dc:source>
    <dc:date>2008-04-15T01:27:15-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>The New England journal of medicine</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>358</prism:volume>
    <prism:number>15</prism:number>
    <prism:startingPage>1641</prism:startingPage>
    <prism:endingPage>1642</prism:endingPage>
    <prism:category>side_effect</prism:category>
    <prism:category>substance_abuse</prism:category>
    <prism:category>toxiciology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2694089">
    <title>Clinical practice. Irritable bowel syndrome.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2694089</link>
    <description>&lt;i&gt;The New England journal of medicine, Vol. 358, No. 16. (17 April 2008), pp. 1692-1699.&lt;/i&gt;</description>
    <dc:title>Clinical practice. Irritable bowel syndrome.</dc:title>

    <dc:creator>EA Mayer</dc:creator>
    <dc:identifier>doi:10.1056/NEJMcp0801447</dc:identifier>
    <dc:source>The New England journal of medicine, Vol. 358, No. 16. (17 April 2008), pp. 1692-1699.</dc:source>
    <dc:date>2008-04-21T03:21:46-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>The New England journal of medicine</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>358</prism:volume>
    <prism:number>16</prism:number>
    <prism:startingPage>1692</prism:startingPage>
    <prism:endingPage>1699</prism:endingPage>
    <prism:category>clinical_practice</prism:category>
    <prism:category>gi</prism:category>
    <prism:category>tutorial_review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2708129">
    <title>Pseudoclaudication as a manifestation of diabetic neuropathy.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2708129</link>
    <description>&lt;i&gt;Diabetic medicine : a journal of the British Diabetic Association, Vol. 22, No. 11. (November 2005), pp. 1608-1610.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We present the case of a 64-year-old male Type 1 diabetic patient with painful diabetic neuropathy masquerading as intermittent claudication. Examination of the peripheral circulation (both arterial and venous) was normal. An MRI scan excluded lumbar spinal stenosis and nerve root compression as the cause of claudication. The case suggests that, in the absence of other identifiable causes and in the presence of peripheral diabetic neuropathy, &#34;intermittent claudication&#34; may be due to the neuropathy itself.</description>
    <dc:title>Pseudoclaudication as a manifestation of diabetic neuropathy.</dc:title>

    <dc:creator>N Papanas</dc:creator>
    <dc:creator>M Edmonds</dc:creator>
    <dc:creator>E Maltezos</dc:creator>
    <dc:identifier>doi:10.1111/j.1464-5491.2005.01733.x</dc:identifier>
    <dc:source>Diabetic medicine : a journal of the British Diabetic Association, Vol. 22, No. 11. (November 2005), pp. 1608-1610.</dc:source>
    <dc:date>2008-04-23T16:29:50-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Diabetic medicine : a journal of the British Diabetic Association</prism:publicationName>
    <prism:issn>0742-3071</prism:issn>
    <prism:volume>22</prism:volume>
    <prism:number>11</prism:number>
    <prism:startingPage>1608</prism:startingPage>
    <prism:endingPage>1610</prism:endingPage>
    <prism:category>cardiology</prism:category>
    <prism:category>endocrine</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2708126">
    <title>On the unconscious subcortical origin of human fear.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2708126</link>
    <description>&lt;i&gt;Physiology &#38; behavior, Vol. 92, No. 1-2. (10 September 2007), pp. 180-185.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Consistent with the hypothesis that the amygdala is central to fear activation, brain imaging studies show that fear stimuli activate the amygdala, even when conscious recognition is prevented by backward masking. The bulk of the data suggest that the amygdala can be activated from potentially accessible but unattended fear stimuli. Activation of the amygdala facilitates low level visual processing. Several lines of evidence suggest that activation of the amygdala is mediated by a subcortical pathway. Thus, according to data from patients with lesions in the primary visual cortex, the amygdala can be activated in the absence of cortical processing. There is considerable support for the hypothesis that visual stimuli can access the amygdala via a pathway that includes the superior colliculus and the pulvinar nucleus of the thalamus. These data are consistent with an evolutionary argument, focusing of the role of snakes as a predator on primates.</description>
    <dc:title>On the unconscious subcortical origin of human fear.</dc:title>

    <dc:creator>A Ohman</dc:creator>
    <dc:creator>K Carlsson</dc:creator>
    <dc:creator>D Lundqvist</dc:creator>
    <dc:creator>M Ingvar</dc:creator>
    <dc:identifier>doi:10.1016/j.physbeh.2007.05.057</dc:identifier>
    <dc:source>Physiology &#38; behavior, Vol. 92, No. 1-2. (10 September 2007), pp. 180-185.</dc:source>
    <dc:date>2008-04-23T16:28:53-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Physiology &#38; behavior</prism:publicationName>
    <prism:issn>0031-9384</prism:issn>
    <prism:volume>92</prism:volume>
    <prism:number>1-2</prism:number>
    <prism:startingPage>180</prism:startingPage>
    <prism:endingPage>185</prism:endingPage>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2708123">
    <title>Neurobiology of aggression and violence.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2708123</link>
    <description>&lt;i&gt;The American journal of psychiatry, Vol. 165, No. 4. (April 2008), pp. 429-442.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Acts of violence account for an estimated 1.43 million deaths worldwide annually. While violence can occur in many contexts, individual acts of aggression account for the majority of instances. In some individuals, repetitive acts of aggression are grounded in an underlying neurobiological susceptibility that is just beginning to be understood. The failure of &#34;top-down&#34; control systems in the prefrontal cortex to modulate aggressive acts that are triggered by anger provoking stimuli appears to play an important role. An imbalance between prefrontal regulatory influences and hyper-responsivity of the amygdala and other limbic regions involved in affective evaluation are implicated. Insufficient serotonergic facilitation of &#34;top-down&#34; control, excessive catecholaminergic stimulation, and subcortical imbalances of glutamatergic/gabaminergic systems as well as pathology in neuropeptide systems involved in the regulation of affiliative behavior may contribute to abnormalities in this circuitry. Thus, pharmacological interventions such as mood stabilizers, which dampen limbic irritability, or selective serotonin reuptake inhibitors (SSRIs), which may enhance &#34;top-down&#34; control, as well as psychosocial interventions to develop alternative coping skills and reinforce reflective delays may be therapeutic.</description>
    <dc:title>Neurobiology of aggression and violence.</dc:title>

    <dc:creator>LJ Siever</dc:creator>
    <dc:identifier>doi:10.1176/appi.ajp.2008.07111774</dc:identifier>
    <dc:source>The American journal of psychiatry, Vol. 165, No. 4. (April 2008), pp. 429-442.</dc:source>
    <dc:date>2008-04-23T16:28:09-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>The American journal of psychiatry</prism:publicationName>
    <prism:issn>0002-953X</prism:issn>
    <prism:volume>165</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>429</prism:startingPage>
    <prism:endingPage>442</prism:endingPage>
    <prism:category>review</prism:category>
    <prism:category>social_study</prism:category>
    <prism:category>theory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2708118">
    <title>Models of anger: contributions from psychophysiology, neuropsychology and the cognitive behavioral perspective.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2708118</link>
    <description>&lt;i&gt;Brain structure &#38; function, Vol. 212, No. 5. (February 2008), pp. 371-385.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The current review examined the research and current models of anger from three distinct literatures: psychophysiology, neuropsychology and the cognitive-behavioral perspective. Two primary conceptual difficulties are addressed in this review. First, the debate over how and when to differentiate between anger and hostility is discussed. Second, the issue regarding cognitive or emotional dominance or primacy in the experience of anger is considered. Once the conceptual ambiguity is addressed, data from the cognitive-behavioral, psychophysiological and neuropsychological literatures are reviewed with a focus on issues of laterality. Particular attention is given to research of appraisal theory from the cognitive literature, cortical arousal and related cerebral models from the psychophysiological literature, and functional cerebral systems from the neuropsychological literature. Despite significant differences appearing both within and between the bodies of literature, when viewed without the traditional ambiguity surrounding this topic, there appears to be a great deal of overlap which may be conducive to the construction of a unified theoretical model. Such a model is proposed in the final section of this paper.</description>
    <dc:title>Models of anger: contributions from psychophysiology, neuropsychology and the cognitive behavioral perspective.</dc:title>

    <dc:creator>DE Cox</dc:creator>
    <dc:creator>DW Harrison</dc:creator>
    <dc:identifier>doi:10.1007/s00429-007-0168-7</dc:identifier>
    <dc:source>Brain structure &#38; function, Vol. 212, No. 5. (February 2008), pp. 371-385.</dc:source>
    <dc:date>2008-04-23T16:27:22-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Brain structure &#38; function</prism:publicationName>
    <prism:issn>1863-2653</prism:issn>
    <prism:volume>212</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>371</prism:startingPage>
    <prism:endingPage>385</prism:endingPage>
    <prism:category>review</prism:category>
    <prism:category>social_study</prism:category>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2708117">
    <title>Hepatic events associated with atomoxetine treatment for attention-deficit hyperactivity disorder.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2708117</link>
    <description>&lt;i&gt;Drug safety : an international journal of medical toxicology and drug experience, Vol. 31, No. 4. (2008), pp. 345-354.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;OBJECTIVE: This study describes and assesses potential hepatobiliary events related to atomoxetine therapy, as reported in clinical trials and as spontaneous adverse event reports post-launch in 2002. METHODS: Case reports that contained potential hepatobiliary events were identified by a computerized search of the Eli Lilly and Company atomoxetine spontaneous adverse events and clinical trials databases. All cases were reviewed by at least two company physicians, one with expertise in hepatology, to determine the relevance of the information in respect of potential liver toxicity. RESULTS: Of 7961 paediatric and adult patients treated with atomoxetine in clinical trials, 41 were identified as having hepatobiliary events requiring additional analysis. Most of these events were mild increases in ALT and AST levels. None of these cases met Hy's rule criteria or progressed to liver failure. During the 4 years after market launch, 351 spontaneous reports of adverse events were related to the liver, of which 69 had other explanations unrelated to atomoxetine. Of the remaining 282 cases, 133 contained possible confounding factors (and were deemed to be possibly related), 146 presented too little information to assess, and three suggested atomoxetine as a probable cause of liver injuries. One of the three had a positive rechallenge. All three patients recovered after discontinuation of the drug. CONCLUSIONS: Since the launch of atomoxetine therapy, three spontaneously reported cases of reversible drug-induced liver injury were deemed probably related to it. Atomoxetine should be discontinued in patients with jaundice or laboratory evidence of liver injury and should not be restarted.</description>
    <dc:title>Hepatic events associated with atomoxetine treatment for attention-deficit hyperactivity disorder.</dc:title>

    <dc:creator>ME Bangs</dc:creator>
    <dc:creator>L Jin</dc:creator>
    <dc:creator>S Zhang</dc:creator>
    <dc:creator>D Desaiah</dc:creator>
    <dc:creator>AJ Allen</dc:creator>
    <dc:creator>HA Read</dc:creator>
    <dc:creator>A Regev</dc:creator>
    <dc:creator>JF Wernicke</dc:creator>
    <dc:source>Drug safety : an international journal of medical toxicology and drug experience, Vol. 31, No. 4. (2008), pp. 345-354.</dc:source>
    <dc:date>2008-04-23T16:26:01-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Drug safety : an international journal of medical toxicology and drug experience</prism:publicationName>
    <prism:issn>0114-5916</prism:issn>
    <prism:volume>31</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>345</prism:startingPage>
    <prism:endingPage>354</prism:endingPage>
    <prism:category>adhd</prism:category>
    <prism:category>anti_depressant</prism:category>
    <prism:category>gi</prism:category>
    <prism:category>side_effect</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2708114">
    <title>Attributional style and depression.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2708114</link>
    <description>&lt;i&gt;The British journal of psychiatry : the journal of mental science, Vol. 192 (April 2008), pp. 275-278.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Few studies have examined whether attributional style (an individual's explanation of why events happen) is a genetically influenced vulnerability factor for depression. AIMS: To investigate whether attributional style is an enduring vulnerability trait for recurrent depression. METHOD: As part of the Cardiff Depression Study, we interviewed 108 people with depression and their siblings, and a control group of 105 healthy individuals and their siblings, using the Schedules for Clinical Assessment in Neuropsychiatry and the Life Events and Difficulties Schedule. Participants also completed the Attributional Style Questionnaire. RESULTS: Regression analyses showed that attributional style results from mood state and is not a familial risk factor for depression. However, the tendency to internalise negative events was related to having had a prior episode of depression, suggesting a ;scarring' effect. Also, non-severe events were associated with one subset of optimistic attributions. CONCLUSIONS: Attributional style mainly measures current mood and does not reflect a familial risk factor for depression.</description>
    <dc:title>Attributional style and depression.</dc:title>

    <dc:creator>HA Ball</dc:creator>
    <dc:creator>P McGuffin</dc:creator>
    <dc:creator>AE Farmer</dc:creator>
    <dc:identifier>doi:10.1192/bjp.bp.107.038711</dc:identifier>
    <dc:source>The British journal of psychiatry : the journal of mental science, Vol. 192 (April 2008), pp. 275-278.</dc:source>
    <dc:date>2008-04-23T16:25:15-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>The British journal of psychiatry : the journal of mental science</prism:publicationName>
    <prism:issn>0007-1250</prism:issn>
    <prism:volume>192</prism:volume>
    <prism:startingPage>275</prism:startingPage>
    <prism:endingPage>278</prism:endingPage>
    <prism:category>major_depression</prism:category>
    <prism:category>social_study</prism:category>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2708109">
    <title>A Randomised, Blinded, Placebo-Controlled Trial in Dementia Patients Continuing or Stopping Neuroleptics (The DART-AD Trial).</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2708109</link>
    <description>&lt;i&gt;PLoS medicine, Vol. 5, No. 4. (1 April 2008)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: There have been increasing concerns regarding the safety and efficacy of neuroleptics in people with dementia, but there are very few long-term trials to inform clinical practice. The aim of this study was to determine the impact of long-term treatment with neuroleptic agents upon global cognitive decline and neuropsychiatric symptoms in patients with Alzheimer disease. METHODS AND FINDINGS: Design: Randomised, blinded, placebo-controlled parallel two-group treatment discontinuation trial.Setting: Oxfordshire, Newcastle and Gateshead, London and Edinburgh, United Kingdom.Participants: Patients currently prescribed the neuroleptics thioridazine, chlorpromazine, haloperidol trifluoperazine or risperidone for behavioural or psychiatric disturbance in dementia for at least 3 mo.Interventions: Continue neuroleptic treatment for 12 mo or switch to an identical placebo.Outcome measures: Primary outcome was total Severe Impairment Battery (SIB) score. Neuropsychiatric symptoms were evaluated with the Neuropsychiatric Inventory (NPI).Results: 165 patients were randomised (83 to continue treatment and 82 to placebo, i.e., discontinue treatment), of whom 128 (78%) commenced treatment (64 continue/64 placebo). Of those, 26 were lost to follow-up (13 per arm), resulting in 51 patients per arm analysed for the primary outcome. There was no significant difference between the continue treatment and placebo groups in the estimated mean change in SIB scores between baseline and 6 mo; estimated mean difference in deterioration (favouring placebo) -0.4 (95% confidence interval [CI] -6.4 to 5.5), adjusted for baseline value (p = 0.9). For neuropsychiatric symptoms, there was no significant difference between the continue treatment and placebo groups (n = 56 and 53, respectively) in the estimated mean change in NPI scores between baseline and 6 mo; estimated mean difference in deterioration (favouring continue treatment) -2.4 (95% CI -8.2 to 3.5), adjusted for baseline value (p = 0.4). Both results became more pronounced at 12 mo. There was some evidence to suggest that those patients with initial NPI &#62;/= 15 benefited on neuropsychiatric symptoms from continuing treatment. CONCLUSIONS: For most patients with AD, withdrawal of neuroleptics had no overall detrimental effect on functional and cognitive status. Neuroleptics may have some value in the maintenance treatment of more severe neuropsychiatric symptoms, but this benefit must be weighed against the side effects of therapy.Trial registration: Cochrane Central Registry of Controlled Trials/National Research Register (#ISRCTN33368770).</description>
    <dc:title>A Randomised, Blinded, Placebo-Controlled Trial in Dementia Patients Continuing or Stopping Neuroleptics (The DART-AD Trial).</dc:title>

    <dc:creator>Clive Ballard</dc:creator>
    <dc:creator>Marisa Margallo Lana</dc:creator>
    <dc:creator>Megan Theodoulou</dc:creator>
    <dc:creator>Simon Douglas</dc:creator>
    <dc:creator>Rupert McShane</dc:creator>
    <dc:creator>Robin Jacoby</dc:creator>
    <dc:creator>Katja Kossakowski</dc:creator>
    <dc:creator>Ly-Mee Yu</dc:creator>
    <dc:creator>Edmund Juszczak</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1371/journal.pmed.0050076</dc:identifier>
    <dc:source>PLoS medicine, Vol. 5, No. 4. (1 April 2008)</dc:source>
    <dc:date>2008-04-23T16:24:08-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>PLoS medicine</prism:publicationName>
    <prism:issn>1549-1676</prism:issn>
    <prism:volume>5</prism:volume>
    <prism:number>4</prism:number>
    <prism:category>dementia</prism:category>
    <prism:category>geriatric</prism:category>
    <prism:category>neuroleptic</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2708104">
    <title>A 21-year-old man with chronic pancreatitis.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2708104</link>
    <description>&lt;i&gt;JAMA : the journal of the American Medical Association, Vol. 299, No. 13. (2 April 2008), pp. 1588-1594.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Chronic pancreatitis is a disease for which the diagnosis may be difficult to ascertain and the treatments are limited. Using the case of a 21-year-old man who has had recurrent episodes of epigastric pain since age 10 years and was ultimately diagnosed as having idiopathic pancreatitis complicated by pancreatic duct stones, we discuss the evaluation and treatment of chronic pancreatitis. Diagnosis is based on thorough history taking, physical examination, and carefully selected imaging studies. Etiologies may be structural or nonstructural; genes predisposing to chronic pancreatitis have been identified. An evidence-based approach to treatment is limited by a paucity of randomized controlled trials. We address the patient's concerns regarding chronic pancreatitis, including what he should expect over the next several years, whether endoscopic or surgical therapies should be considered, and whether there are any cures.</description>
    <dc:title>A 21-year-old man with chronic pancreatitis.</dc:title>

    <dc:creator>MP Callery</dc:creator>
    <dc:creator>SD Freedman</dc:creator>
    <dc:identifier>doi:10.1001/jama.299.9.jrr80001</dc:identifier>
    <dc:source>JAMA : the journal of the American Medical Association, Vol. 299, No. 13. (2 April 2008), pp. 1588-1594.</dc:source>
    <dc:date>2008-04-23T16:23:05-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>JAMA : the journal of the American Medical Association</prism:publicationName>
    <prism:issn>1538-3598</prism:issn>
    <prism:volume>299</prism:volume>
    <prism:number>13</prism:number>
    <prism:startingPage>1588</prism:startingPage>
    <prism:endingPage>1594</prism:endingPage>
    <prism:category>clinical_practice</prism:category>
    <prism:category>gi</prism:category>
    <prism:category>tutorial_review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573442">
    <title>Difference in Treatment Outcome in Outpatients With Anxious Versus Nonanxious Depression: A STAR*D Report.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573442</link>
    <description>&lt;i&gt;Am J Psychiatry, Vol. 165, No. 3. (March 2008), pp. 342-351.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;OBJECTIVE: About half of outpatients with major depressive disorder also have clinically meaningful levels of anxiety. The authors conducted a secondary data analysis to compare antidepressant treatment outcomes for patients with anxious and nonanxious major depression in Levels 1 and 2 of the STAR*D study. METHOD: A total of 2,876 adult outpatients with major depressive disorder, enrolled from 18 primary and 23 psychiatric care sites, received citalopram in Level 1 of STAR*D. In Level 2, a total of 1,292 patients who did not remit with or tolerate citalopram were randomly assigned either to switch to sustained-release bupropion (N=239), sertraline (N=238), or extended-release venlafaxine (N=250) or to continue taking citalopram and receive augmentation with sustained-release bupropion (N=279) or buspirone (N=286). Treatment could last up to 14 weeks in each level. Patients were designated as having anxious depression if their anxiety/somatization factor score from the 17-item Hamilton Depression Rating Scale (HAM-D) was 7 or higher at baseline. Rates of remission and response as well as times to remission and response were compared between patients with anxious depression and those with nonanxious depression. RESULTS: In Level 1 of STAR*D, 53.2% of patients had anxious depression. Remission was significantly less likely and took longer to occur in these patients than in those with nonanxious depression. Ratings of side effect frequency, intensity, and burden, as well as the number of serious adverse events, were significantly greater in the anxious depression group. Similarly, in Level 2, patients with anxious depression fared significantly worse in both the switching and augmentation options. CONCLUSIONS: Anxious depression is associated with poorer acute outcomes than nonanxious depression following antidepressant treatment.</description>
    <dc:title>Difference in Treatment Outcome in Outpatients With Anxious Versus Nonanxious Depression: A STAR*D Report.</dc:title>

    <dc:creator>M Fava</dc:creator>
    <dc:creator>AJ Rush</dc:creator>
    <dc:creator>JE Alpert</dc:creator>
    <dc:creator>GK Balasubramani</dc:creator>
    <dc:creator>SR Wisniewski</dc:creator>
    <dc:creator>CN Carmin</dc:creator>
    <dc:creator>MM Biggs</dc:creator>
    <dc:creator>S Zisook</dc:creator>
    <dc:creator>A Leuchter</dc:creator>
    <dc:creator>R Howland</dc:creator>
    <dc:creator>D Warden</dc:creator>
    <dc:creator>MH Trivedi</dc:creator>
    <dc:identifier>doi:10.1176/appi.ajp.2007.06111868</dc:identifier>
    <dc:source>Am J Psychiatry, Vol. 165, No. 3. (March 2008), pp. 342-351.</dc:source>
    <dc:date>2008-03-23T02:06:44-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Am J Psychiatry</prism:publicationName>
    <prism:issn>0002-953X</prism:issn>
    <prism:volume>165</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>342</prism:startingPage>
    <prism:endingPage>351</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>clinical_trial</prism:category>
    <prism:category>gad</prism:category>
    <prism:category>major_depression</prism:category>
    <prism:category>panic_disorder</prism:category>
    <prism:category>ptsd</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2549424">
    <title>What Patients Want From Primary Care Consultations: A Discrete Choice Experiment to Identify Patients' Priorities</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2549424</link>
    <description>&lt;i&gt;Ann Fam Med, Vol. 6, No. 2. (1 March 2008), pp. 107-115.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;PURPOSE The consultation is fundamental to the delivery of primary care, but different ways of organizing consultations may lead to different patient experiences in terms of access, continuity, technical quality of care, and communication. Patients' priorities for these different issues need to be understood, but the optimal methods for assessing priorities are unclear. This study used a discrete choice experiment to assess patients' priorities. METHODS We surveyed patients from 6 family practices in England. The patients chose between primary care consultations differing in attributes such as ease of access (wait for an appointment), choice (flexibility of appointment times), continuity (physician's knowledge of the patient), technical quality (thoroughness of physical examination), and multiple aspects of patient-centered care (interest in patient's ideas, inquiry about patient's social and emotional well-being, and involvement of patient in decision making). We used probit models to assess the relative priority patients placed on different attributes and to estimate how much they were willing to pay for them. RESULTS Analyses were based on responses from 1,193 patients (a 53% response rate). Overall, patients were willing to pay the most for a thorough physical examination ($40.87). The next most valued attributes of care were seeing a physician who knew them well ($12.18), seeing a physician with a friendly manner ($8.50), having a reduction in waiting time of 1 day ($7.22), and having flexibility of appointment times ($6.71). Patients placed similar value on the different aspects of patient-centered care ($12.06$14.82). Responses were influenced by the scenario in which the decision was made (minor physical problem vs urgent physical problem vs ambiguous physical or psychological problem) and by patients' demographic characteristics. CONCLUSIONS Although patient-centered care is important to patients, they may place higher priority on the technical quality of care and continuity of care. Discrete choice experiments may be a useful method for assessing patients' priorities in health care. 10.1370/afm.816</description>
    <dc:title>What Patients Want From Primary Care Consultations: A Discrete Choice Experiment to Identify Patients' Priorities</dc:title>

    <dc:creator>Sudeh Cheraghi-Sohi</dc:creator>
    <dc:creator>Arne Hole</dc:creator>
    <dc:creator>Nicola Mead</dc:creator>
    <dc:creator>Ruth Mcdonald</dc:creator>
    <dc:creator>Diane Whalley</dc:creator>
    <dc:creator>Peter Bower</dc:creator>
    <dc:creator>Martin Roland</dc:creator>
    <dc:identifier>doi:10.1370/afm.816</dc:identifier>
    <dc:source>Ann Fam Med, Vol. 6, No. 2. (1 March 2008), pp. 107-115.</dc:source>
    <dc:date>2008-03-18T08:38:11-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Ann Fam Med</prism:publicationName>
    <prism:volume>6</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>107</prism:startingPage>
    <prism:endingPage>115</prism:endingPage>
    <prism:category>social_study</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573438">
    <title>Valproate-induced hyperammonaemic encephalopathy: review of 14 cases in the psychiatric setting.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573438</link>
    <description>&lt;i&gt;Int Clin Psychopharmacol, Vol. 22, No. 6. (November 2007), pp. 330-337.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;OBJECTIVES: To review signs and symptoms of valproate-induced hyperammonaemic encephalopathy without hepatotoxicity in the psychiatric setting, explore its mechanisms, and give recommendations for prevention and treatment. METHODS: Medline search with keywords valproate, ammonia, hyperammonaemia, encephalopathy, and then cross-references to articles obtained through this search. Only cases with indication of valproate for psychiatric condition were included. RESULTS: Fourteen cases published in the psychiatric setting are reviewed. Valproate-induced hyperammonaemic encephalopathy is a rare adverse event, occurring almost equally in men and women, with a large age range, and reported in two patients with mental retardation. Symptoms appeared either a few days after initiation of valproate therapy, or after several months or years. The main symptoms were fluctuations in consciousness and disorientation. Clinical severity was not related to blood ammonia levels. All patients recovered after valproate-induced hyperammonaemic encephalopathy diagnosis and treatment, usually involving discontinuation of valproate. CONCLUSIONS: Valproate-induced hyperammonaemic encephalopathy is rare and usually reversible in patients without urea cycle disorders when valproate is discontinued. Therapy with carnitine is recommended. Special caution should be used in patients with mental retardation. Psychiatrists should suspect valproate-induced hyperammonaemic encephalopathy when consciousness deteriorates.</description>
    <dc:title>Valproate-induced hyperammonaemic encephalopathy: review of 14 cases in the psychiatric setting.</dc:title>

    <dc:creator>MJ Dealberto</dc:creator>
    <dc:identifier>doi:10.1097/YIC.0b013e3281c61b28</dc:identifier>
    <dc:source>Int Clin Psychopharmacol, Vol. 22, No. 6. (November 2007), pp. 330-337.</dc:source>
    <dc:date>2008-03-23T02:04:22-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Int Clin Psychopharmacol</prism:publicationName>
    <prism:issn>0268-1315</prism:issn>
    <prism:volume>22</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>330</prism:startingPage>
    <prism:endingPage>337</prism:endingPage>
    <prism:category>mood_stabilizer</prism:category>
    <prism:category>side_effect</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2157138">
    <title>The Dark Side of Ecstasy: Neuropsychiatric Symptoms after Exposure to 3,4-Methylenedioxymethamphetamine</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2157138</link>
    <description>&lt;i&gt;Basic &#38; Clinical Pharmacology &#38; Toxicology, Vol. 102, No. 1. (January 2008), pp. 15-24.&lt;/i&gt;</description>
    <dc:title>The Dark Side of Ecstasy: Neuropsychiatric Symptoms after Exposure to 3,4-Methylenedioxymethamphetamine</dc:title>

    <dc:creator>Karlsen</dc:creator>
    <dc:creator>Sunniva Nyberg</dc:creator>
    <dc:creator>Spigset</dc:creator>
    <dc:creator>Olav</dc:creator>
    <dc:creator>Slordal</dc:creator>
    <dc:creator>Lars</dc:creator>
    <dc:identifier>doi:10.1111/j.1742-7843.2007.00159.x</dc:identifier>
    <dc:source>Basic &#38; Clinical Pharmacology &#38; Toxicology, Vol. 102, No. 1. (January 2008), pp. 15-24.</dc:source>
    <dc:date>2007-12-21T21:37:18-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Basic &#38; Clinical Pharmacology &#38; Toxicology</prism:publicationName>
    <prism:issn>1742-7835</prism:issn>
    <prism:volume>102</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>15</prism:startingPage>
    <prism:endingPage>24</prism:endingPage>
    <prism:publisher>Blackwell Publishing</prism:publisher>
    <prism:category>neuropsychology</prism:category>
    <prism:category>review</prism:category>
    <prism:category>substance_abuse</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573437">
    <title>Shell shock and mild traumatic brain injury: a historical review.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573437</link>
    <description>&lt;i&gt;Am J Psychiatry, Vol. 164, No. 11. (November 2007), pp. 1641-1645.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Mild traumatic brain injury is now claimed to be the signature injury of the Iraq and Afghanistan conflicts. During World War I, shell shock came to occupy a similar position of prominence, and postconcussional syndrome assumed some importance in World War II. In this article, the nature of shell shock, its clinical presentation, the military context, hypotheses of causation, and issues of management are explored to discover whether there are contemporary relevancies to the current issue of mild traumatic brain injury. When shell shock was first postulated, it was assumed to be the product of a head injury or toxic exposure. However, subsequent clinical studies suggested that this view was too simplistic, and explanations soon oscillated between the strictly organic and the psychological as well as the behavioral. Despite a vigorous debate, physicians failed to identify or confirm characteristic distinctions. The experiences of the armed forces of both the United States and the United Kingdom during World Wars I and II led to two conclusions: that there were dangers in labeling anything as a unique &#34;signature&#34; injury and that disorders that cross any divide between physical and psychological require a nuanced view of their interpretation and treatment. These findings suggest that the hard-won lessons of shell shock continue to have relevance today.</description>
    <dc:title>Shell shock and mild traumatic brain injury: a historical review.</dc:title>

    <dc:creator>E Jones</dc:creator>
    <dc:creator>NT Fear</dc:creator>
    <dc:creator>S Wessely</dc:creator>
    <dc:identifier>doi:10.1176/appi.ajp.2007.07071180</dc:identifier>
    <dc:source>Am J Psychiatry, Vol. 164, No. 11. (November 2007), pp. 1641-1645.</dc:source>
    <dc:date>2008-03-23T02:02:19-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Am J Psychiatry</prism:publicationName>
    <prism:issn>0002-953X</prism:issn>
    <prism:volume>164</prism:volume>
    <prism:number>11</prism:number>
    <prism:startingPage>1641</prism:startingPage>
    <prism:endingPage>1645</prism:endingPage>
    <prism:category>history</prism:category>
    <prism:category>ptsd</prism:category>
    <prism:category>review</prism:category>
    <prism:category>social_study</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573433">
    <title>Risk of Upper Gastrointestinal Bleeding and the Degree of Serotonin Reuptake Inhibition by Antidepressants : A Case-Control Study.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573433</link>
    <description>&lt;i&gt;Drug Saf, Vol. 31, No. 2. (2008), pp. 159-168.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND AND OBJECTIVE: Selective serotonin reuptake inhibitor (SSRI) antidepressants can inhibit uptake of serotonin by platelets, and their use may predispose patients to bleeding. Case reports and observational studies from databases have suggested an association between the use of SSRIs and gastrointestinal bleeding. Their risk appears to be increased if they are concurrently used with aspirin (acetylsalicylic acid) or with other NSAIDs. With the aim of establishing the risk of major upper gastrointestinal bleeding associated with various groups of drugs, we performed a multicentre case-control study. We present the results related to the use of antidepressants by the degree of serotonin reuptake inhibition they induce, the selectivity at monoamine transporters and the dose. METHODS: A population-based multicentre case-control study in 18 hospitals in Spain and in Italy, including 2813 incident cases of upper gastrointestinal bleeding and 7193 matched controls. Regression analyses are based on 2783 cases and 7058 controls because of missing variable data. Odds ratios (ORs) of upper gastrointestinal bleeding for antidepressant drugs grouped by affinity for the serotonin transporter, selectivity and dose, with adjustment for potential confounders were estimated. RESULTS: Overall, 84 (3.0%) cases and 160 (2.2%) controls had used a high-affinity serotonin reuptake inhibitor (SRI) antidepressant. Their use in the 7 days prior to the index day was not associated with a substantially increased risk of upper gastrointestinal bleeding (OR = 1.24; 95% CI 0.88, 1.76). Forty-one (1.5%) cases and 26 (0.4%) controls had concurrently used a high-affinity SRI antidepressant and an NSAID. The OR of upper gastrointestinal bleeding among these concurrent users (8.32; 95% CI 4.69, 14.76) did not differ from that in users of NSAIDs only (7.82; 95% CI 6.79, 9.00). No significant association was found between the use of SSRIs and the risk of upper gastrointestinal bleeding, neither with the degree of affinity for the serotonin transporter, by the selectivity of each individual agent (101 cases [3.6%] vs 192 controls [2.7%]; OR = 1.23; 95% CI 0.90, 1.68), nor by dose. CONCLUSIONS: The risk of upper gastrointestinal bleeding is not increased by the use of SRIs. An interaction with coadministered NSAIDs was not observed. If there is a risk associated to these drugs, it seems to be low and not an important cause of hospital admission due to upper gastrointestinal bleeding. However, additional studies may be warranted in subgroup populations at potentially increased risk of bleeding, such as older adults and men.</description>
    <dc:title>Risk of Upper Gastrointestinal Bleeding and the Degree of Serotonin Reuptake Inhibition by Antidepressants : A Case-Control Study.</dc:title>

    <dc:creator>Xavier Vidal</dc:creator>
    <dc:creator>Luisa Ibáñez</dc:creator>
    <dc:creator>Lourdes Vendrell</dc:creator>
    <dc:creator>Ana Conforti</dc:creator>
    <dc:creator>Joan-Ramon Laporte</dc:creator>
    <dc:creator></dc:creator>
    <dc:source>Drug Saf, Vol. 31, No. 2. (2008), pp. 159-168.</dc:source>
    <dc:date>2008-03-23T02:01:16-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Drug Saf</prism:publicationName>
    <prism:issn>0114-5916</prism:issn>
    <prism:volume>31</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>159</prism:startingPage>
    <prism:endingPage>168</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>gi</prism:category>
    <prism:category>side_effect</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573431">
    <title>Pneumonitis related to venlafaxine.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573431</link>
    <description>&lt;i&gt;Psychosomatics, Vol. 49, No. 1. (b 2008), pp. 84-85.&lt;/i&gt;</description>
    <dc:title>Pneumonitis related to venlafaxine.</dc:title>

    <dc:creator>MJ Vázquez</dc:creator>
    <dc:creator>B Carretero Quevedo</dc:creator>
    <dc:identifier>doi:10.1176/appi.psy.49.1.84</dc:identifier>
    <dc:source>Psychosomatics, Vol. 49, No. 1. (b 2008), pp. 84-85.</dc:source>
    <dc:date>2008-03-23T02:00:35-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Psychosomatics</prism:publicationName>
    <prism:issn>0033-3182</prism:issn>
    <prism:volume>49</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>84</prism:startingPage>
    <prism:endingPage>85</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>side_effect</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573428">
    <title>Lifestyle intervention and metformin for treatment of antipsychotic-induced weight gain: a randomized controlled trial.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573428</link>
    <description>&lt;i&gt;JAMA, Vol. 299, No. 2. (9 January 2008), pp. 185-193.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;CONTEXT: Weight gain, a common adverse effect of antipsychotic medications, is associated with medical comorbidities in psychiatric patients. OBJECTIVE: To test the efficacy of lifestyle intervention and metformin alone and in combination for antipsychotic-induced weight gain and abnormalities in insulin sensitivity. DESIGN, SETTING, AND PATIENTS: A randomized controlled trial (October 2004-December 2006) involving 128 adult patients with schizophrenia in the Mental Health Institute of the Second Xiangya Hospital, Central South University, China. Participants who gained more than 10% of their predrug weight were assigned to 1 of 4 treatment groups. INTERVENTIONS: Patients continued their antipsychotic medication and were randomly assigned to 12 weeks of placebo, 750 mg/d of metformin alone, 750 mg/d of metformin and lifestyle intervention, or lifestyle intervention only. MAIN OUTCOME MEASURES: Body mass index, waist circumference, insulin levels, and insulin resistance index. RESULTS: All 128 first-episode schizophrenia patients maintained relatively stable psychiatric improvement. The lifestyle-plus-metformin group had mean decreases in body mass index (BMI) of 1.8 (95% confidence interval [CI], 1.3-2.3), insulin resistance index of 3.6 (95% CI, 2.7-4.5), and waist circumference of 2.0 cm (95% CI, 1.5-2.4 cm). The metformin-alone group had mean decreases in BMI of 1.2 (95% CI, 0.9-1.5), insulin resistance index of 3.5 (95% CI, 2.7-4.4), and waist circumference of 1.3 cm (95% CI, 1.1-1.5 cm). The lifestyle-plus-placebo group had mean decreases in BMI of 0.5 (95% CI, 0.3-0.8) and insulin resistance index of 1.0 (95% CI, 0.5-1.5). However, the placebo group had mean increases in BMI of 1.2 (95% CI, 0.9-1.5), insulin resistance index of 0.4 (95% CI, 0.1-0.7), and waist circumference of 2.2 cm (95% CI, 1.7-2.8 cm). The lifestyle-plus-metformin treatment was significantly superior to metformin alone and to lifestyle plus placebo for weight, BMI, and waist circumference reduction. CONCLUSIONS: Lifestyle intervention and metformin alone and in combination demonstrated efficacy for antipsychotic-induced weight gain. Lifestyle intervention plus metformin showed the best effect on weight loss. Metformin alone was more effective in weight loss and improving insulin sensitivity than lifestyle intervention alone. Trial Registration clinicaltrials.gov Identifier: NCT00451399.</description>
    <dc:title>Lifestyle intervention and metformin for treatment of antipsychotic-induced weight gain: a randomized controlled trial.</dc:title>

    <dc:creator>RR Wu</dc:creator>
    <dc:creator>JP Zhao</dc:creator>
    <dc:creator>H Jin</dc:creator>
    <dc:creator>P Shao</dc:creator>
    <dc:creator>MS Fang</dc:creator>
    <dc:creator>XF Guo</dc:creator>
    <dc:creator>YQ He</dc:creator>
    <dc:creator>YJ Liu</dc:creator>
    <dc:creator>JD Chen</dc:creator>
    <dc:creator>LH Li</dc:creator>
    <dc:identifier>doi:10.1001/jama.2007.56-b</dc:identifier>
    <dc:source>JAMA, Vol. 299, No. 2. (9 January 2008), pp. 185-193.</dc:source>
    <dc:date>2008-03-23T01:59:43-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>JAMA</prism:publicationName>
    <prism:issn>1538-3598</prism:issn>
    <prism:volume>299</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>185</prism:startingPage>
    <prism:endingPage>193</prism:endingPage>
    <prism:category>clinical_trial</prism:category>
    <prism:category>endocrine</prism:category>
    <prism:category>neuroleptic</prism:category>
    <prism:category>side_effect</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/889109">
    <title>Finasteride-induced depression : A prospective study</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/889109</link>
    <description>&lt;i&gt;BMC Clinical Pharmacology, Vol. 6 (07 October 2006), 7.&lt;/i&gt;</description>
    <dc:title>Finasteride-induced depression : A prospective study</dc:title>

    <dc:creator>Babak Rahimi-Ardabili</dc:creator>
    <dc:creator>Ramin Pourandarjani</dc:creator>
    <dc:creator>Peiman Habibollahi</dc:creator>
    <dc:creator>Amir Mualeki</dc:creator>
    <dc:identifier>doi:10.1186/1472-6904-6-7</dc:identifier>
    <dc:source>BMC Clinical Pharmacology, Vol. 6 (07 October 2006), 7.</dc:source>
    <dc:date>2006-10-08T01:53:24-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>BMC Clinical Pharmacology</prism:publicationName>
    <prism:issn>1472-6904</prism:issn>
    <prism:volume>6</prism:volume>
    <prism:startingPage>7</prism:startingPage>
    <prism:category>clinical_trial</prism:category>
    <prism:category>major_depression</prism:category>
    <prism:category>side_effect</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/1911012">
    <title>Compartmentalization and Integration: The Evaluative Organization of Contextualized Selves</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/1911012</link>
    <description>&lt;i&gt;Journal of Personality, Vol. 75, No. 6. (December 2007), pp. 1181-1204.&lt;/i&gt;</description>
    <dc:title>Compartmentalization and Integration: The Evaluative Organization of Contextualized Selves</dc:title>

    <dc:creator>Showers</dc:creator>
    <dc:creator>J Carolin</dc:creator>
    <dc:creator>Zeigler-Hill</dc:creator>
    <dc:creator>Virgil</dc:creator>
    <dc:identifier>doi:10.1111/j.1467-6494.2007.00472.x</dc:identifier>
    <dc:source>Journal of Personality, Vol. 75, No. 6. (December 2007), pp. 1181-1204.</dc:source>
    <dc:date>2007-11-13T21:35:34-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Journal of Personality</prism:publicationName>
    <prism:issn>0022-3506</prism:issn>
    <prism:volume>75</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>1181</prism:startingPage>
    <prism:endingPage>1204</prism:endingPage>
    <prism:publisher>Blackwell Publishing</prism:publisher>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/1911007">
    <title>Downsides of an Overly Context-Sensitive Self: Implications From the Culture and Subjective Well-Being Research</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/1911007</link>
    <description>&lt;i&gt;Journal of Personality, Vol. 75, No. 6. (December 2007), pp. 1321-1343.&lt;/i&gt;</description>
    <dc:title>Downsides of an Overly Context-Sensitive Self: Implications From the Culture and Subjective Well-Being Research</dc:title>

    <dc:creator>Suh</dc:creator>
    <dc:creator>M Eunkook</dc:creator>
    <dc:identifier>doi:10.1111/j.1467-6494.2007.00477.x</dc:identifier>
    <dc:source>Journal of Personality, Vol. 75, No. 6. (December 2007), pp. 1321-1343.</dc:source>
    <dc:date>2007-11-13T21:35:34-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Journal of Personality</prism:publicationName>
    <prism:issn>0022-3506</prism:issn>
    <prism:volume>75</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>1321</prism:startingPage>
    <prism:endingPage>1343</prism:endingPage>
    <prism:publisher>Blackwell Publishing</prism:publisher>
    <prism:category>culture_bound</prism:category>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573425">
    <title>Diagnostic crossover in anorexia nervosa and bulimia nervosa: implications for DSM-V.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573425</link>
    <description>&lt;i&gt;Am J Psychiatry, Vol. 165, No. 2. (February 2008), pp. 245-250.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;OBJECTIVE: The Diagnostic and Statistical Manual of Mental Disorders (DSM) is designed primarily as a clinical tool. Yet high rates of diagnostic &#34;crossover&#34; among the anorexia nervosa subtypes and bulimia nervosa may reflect problems with the validity of the current diagnostic schema, thereby limiting its clinical utility. This study was designed to examine diagnostic crossover longitudinally in anorexia nervosa and bulimia nervosa to inform the validity of the DSM-IV-TR eating disorders classification system. METHOD: A total of 216 women with a diagnosis of anorexia nervosa or bulimia nervosa were followed for 7 years; weekly eating disorder symptom data collected using the Eating Disorder Longitudinal Interval Follow-Up Examination allowed for diagnoses to be made throughout the follow-up period. RESULTS: Over 7 years, the majority of women with anorexia nervosa experienced diagnostic crossover: more than half crossed between the restricting and binge eating/purging anorexia nervosa subtypes over time; one-third crossed over to bulimia nervosa but were likely to relapse into anorexia nervosa. Women with bulimia nervosa were unlikely to cross over to anorexia nervosa. CONCLUSIONS: These findings support the longitudinal distinction of anorexia nervosa and bulimia nervosa but do not support the anorexia nervosa subtyping schema.</description>
    <dc:title>Diagnostic crossover in anorexia nervosa and bulimia nervosa: implications for DSM-V.</dc:title>

    <dc:creator>KT Eddy</dc:creator>
    <dc:creator>DJ Dorer</dc:creator>
    <dc:creator>DL Franko</dc:creator>
    <dc:creator>K Tahilani</dc:creator>
    <dc:creator>H Thompson-Brenner</dc:creator>
    <dc:creator>DB Herzog</dc:creator>
    <dc:identifier>doi:10.1176/appi.ajp.2007.07060951</dc:identifier>
    <dc:source>Am J Psychiatry, Vol. 165, No. 2. (February 2008), pp. 245-250.</dc:source>
    <dc:date>2008-03-23T01:54:51-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Am J Psychiatry</prism:publicationName>
    <prism:issn>0002-953X</prism:issn>
    <prism:volume>165</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>245</prism:startingPage>
    <prism:endingPage>250</prism:endingPage>
    <prism:category>eating_disorder</prism:category>
    <prism:category>epidemiology</prism:category>
    <prism:category>theory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573424">
    <title>Childhood sexual abuse and non-suicidal self-injury: meta-analysis.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573424</link>
    <description>&lt;i&gt;Br J Psychiatry, Vol. 192 (March 2008), pp. 166-170.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Many theorists posit that childhood sexual abuse has a central role in the aetiology of self-injurious behaviour. Studies that report statistically significant associations between a history of such abuse and self-injury are cited to support this view. AIMS: A meta-analysis was conducted to determine systematically the magnitude of the association between childhood sexual abuse and self-injurious behaviour. METHOD: Forty-five analyses of the association were identified. Effect sizes were converted to a standard metric and aggregated. RESULTS: The relationship between childhood sexual abuse and self-injurious behaviour is relatively small (mean weighted aggregate varphi=0.23). This figure may be inflated owing to publication bias. In studies that statistically controlled for psychiatric risk factors, childhood sexual abuse explained little or no unique variance in self-injurious behaviour. CONCLUSIONS: Theories that childhood sexual abuse has a central or causal role in the development of self-injurious behaviour are not supported by the available empirical evidence. Instead, it appears that the two are modestly related because they are correlated with the same psychiatric risk factors.</description>
    <dc:title>Childhood sexual abuse and non-suicidal self-injury: meta-analysis.</dc:title>

    <dc:creator>ED Klonsky</dc:creator>
    <dc:creator>A Moyer</dc:creator>
    <dc:identifier>doi:10.1192/bjp.bp.106.030650</dc:identifier>
    <dc:source>Br J Psychiatry, Vol. 192 (March 2008), pp. 166-170.</dc:source>
    <dc:date>2008-03-23T01:53:24-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Br J Psychiatry</prism:publicationName>
    <prism:issn>0007-1250</prism:issn>
    <prism:volume>192</prism:volume>
    <prism:startingPage>166</prism:startingPage>
    <prism:endingPage>170</prism:endingPage>
    <prism:category>borderline</prism:category>
    <prism:category>epidemiology</prism:category>
    <prism:category>social_study</prism:category>
    <prism:category>theory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573423">
    <title>Burnout in psychiatrists.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573423</link>
    <description>&lt;i&gt;World Psychiatry, Vol. 6, No. 3. (October 2007), pp. 186-189.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Psychiatrists as a group are vulnerable to experiencing burnout, more so than other physicians and surgeons. In this paper, various definitions of burnout are reviewed and the tools available for quantifying burnout are compared. The factors that make psychiatry a stressful profession are also examined. These include factors such as patient violence and suicide, limited resources, crowded inpatient wards, changing culture in mental health services, high work demands, poorly defined roles of consultants, responsibility without authority, inability to effect systemic change, conflict between responsibility toward employers vs. toward the patient, and isolation. In order to investigate how exposure to such stressors results in burnout, two theoretical models are examined. Recommendations are also made, on the basis of anecdotal reports, for addressing burnout in psychiatrists.</description>
    <dc:title>Burnout in psychiatrists.</dc:title>

    <dc:creator>S Kumar</dc:creator>
    <dc:source>World Psychiatry, Vol. 6, No. 3. (October 2007), pp. 186-189.</dc:source>
    <dc:date>2008-03-23T01:52:30-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>World Psychiatry</prism:publicationName>
    <prism:issn>1723-8617</prism:issn>
    <prism:volume>6</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>186</prism:startingPage>
    <prism:endingPage>189</prism:endingPage>
    <prism:category>review</prism:category>
    <prism:category>social_study</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/1646019">
    <title>Atypical antipsychotic-induced metabolic side effects: insights from receptor-binding profiles</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/1646019</link>
    <description>&lt;i&gt;Molecular Psychiatry, Vol. aop, No. current.&lt;/i&gt;</description>
    <dc:title>Atypical antipsychotic-induced metabolic side effects: insights from receptor-binding profiles</dc:title>

    <dc:creator>HA Nasrallah</dc:creator>
    <dc:identifier>doi:10.1038/sj.mp.4002066</dc:identifier>
    <dc:source>Molecular Psychiatry, Vol. aop, No. current.</dc:source>
    <dc:date>2007-09-11T23:51:55-00:00</dc:date>
    <prism:publicationName>Molecular Psychiatry</prism:publicationName>
    <prism:issn>1359-4184</prism:issn>
    <prism:volume>aop</prism:volume>
    <prism:number>current</prism:number>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>endocrine</prism:category>
    <prism:category>neuroleptic</prism:category>
    <prism:category>side_effect</prism:category>
    <prism:category>theory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573420">
    <title>Antidepressant medications v. cognitive therapy in people with depression with or without personality disorder.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573420</link>
    <description>&lt;i&gt;Br J Psychiatry, Vol. 192, No. 2. (February 2008), pp. 124-129.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: There is conflicting evidence about comorbid personality pathology in depression treatments. AIMS: To test the effects of antidepressant drugs and cognitive therapy in people with depression distinguished by the presence or absence of personality disorder. METHOD: Random assignment of 180 out-patients with depression to 16 weeks of antidepressant medication or cognitive therapy. Random assignment of medication responders to continued medication or placebo, and comparison with cognitive therapy responders over a 12-month period. RESULTS: Personality disorder status led to differential response at 16 weeks; 66% v. 44% (antidepressants v. cognitive therapy respectively) for people with personality disorder, and 49% v. 70% (antidepressants v. cognitive therapy respectively) for people without personality disorder. For people with personality disorder, sustained response rates over the 12-month follow-up were nearly identical (38%) in the prior cognitive therapy and continuation-medication treatment arms. People with personality disorder withdrawn from medication evidenced the lowest sustained response rate (6%). Despite the poor response of people with personality disorder to cognitive therapy, nearly all those who did respond sustained their response. CONCLUSIONS: Comorbid personality disorder was associated with differential initial response rates and sustained response rates for two well-validated treatments for depression.</description>
    <dc:title>Antidepressant medications v. cognitive therapy in people with depression with or without personality disorder.</dc:title>

    <dc:creator>JC Fournier</dc:creator>
    <dc:creator>RJ DeRubeis</dc:creator>
    <dc:creator>RC Shelton</dc:creator>
    <dc:creator>R Gallop</dc:creator>
    <dc:creator>JD Amsterdam</dc:creator>
    <dc:creator>SD Hollon</dc:creator>
    <dc:identifier>doi:10.1192/bjp.bp.107.037234</dc:identifier>
    <dc:source>Br J Psychiatry, Vol. 192, No. 2. (February 2008), pp. 124-129.</dc:source>
    <dc:date>2008-03-23T01:50:16-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Br J Psychiatry</prism:publicationName>
    <prism:issn>0007-1250</prism:issn>
    <prism:volume>192</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>124</prism:startingPage>
    <prism:endingPage>129</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>borderline</prism:category>
    <prism:category>clinical_trial</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2269254">
    <title>On the relationship between emotion and cognition</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2269254</link>
    <description>&lt;i&gt;Nat Rev Neurosci, Vol. 9, No. 2. (February 2008), pp. 148-158.&lt;/i&gt;</description>
    <dc:title>On the relationship between emotion and cognition</dc:title>

    <dc:creator>Luiz Pessoa</dc:creator>
    <dc:identifier>doi:10.1038/nrn2317</dc:identifier>
    <dc:source>Nat Rev Neurosci, Vol. 9, No. 2. (February 2008), pp. 148-158.</dc:source>
    <dc:date>2008-01-21T16:12:34-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Nat Rev Neurosci</prism:publicationName>
    <prism:volume>9</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>148</prism:startingPage>
    <prism:endingPage>158</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>neuropsychology</prism:category>
    <prism:category>radiology</prism:category>
    <prism:category>theory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2231280">
    <title>Making sense of neuroimaging in psychiatry</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2231280</link>
    <description>&lt;i&gt;Acta Psychiatrica Scandinavica, Vol. 117, No. 2. (February 2008), pp. 100-117.&lt;/i&gt;</description>
    <dc:title>Making sense of neuroimaging in psychiatry</dc:title>

    <dc:creator>Malhi</dc:creator>
    <dc:creator></dc:creator>
    <dc:creator>Lagopoulos</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1111/j.1600-0447.2007.01111.x</dc:identifier>
    <dc:source>Acta Psychiatrica Scandinavica, Vol. 117, No. 2. (February 2008), pp. 100-117.</dc:source>
    <dc:date>2008-01-14T17:51:27-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Acta Psychiatrica Scandinavica</prism:publicationName>
    <prism:issn>0001-690X</prism:issn>
    <prism:volume>117</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>100</prism:startingPage>
    <prism:endingPage>117</prism:endingPage>
    <prism:publisher>Blackwell Publishing</prism:publisher>
    <prism:category>neurology</prism:category>
    <prism:category>radiology</prism:category>
    <prism:category>tutorial_review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573418">
    <title>Selective publication of antidepressant trials and its influence on apparent efficacy.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573418</link>
    <description>&lt;i&gt;N Engl J Med, Vol. 358, No. 3. (17 January 2008), pp. 252-260.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Evidence-based medicine is valuable to the extent that the evidence base is complete and unbiased. Selective publication of clinical trials--and the outcomes within those trials--can lead to unrealistic estimates of drug effectiveness and alter the apparent risk-benefit ratio. METHODS: We obtained reviews from the Food and Drug Administration (FDA) for studies of 12 antidepressant agents involving 12,564 patients. We conducted a systematic literature search to identify matching publications. For trials that were reported in the literature, we compared the published outcomes with the FDA outcomes. We also compared the effect size derived from the published reports with the effect size derived from the entire FDA data set. RESULTS: Among 74 FDA-registered studies, 31%, accounting for 3449 study participants, were not published. Whether and how the studies were published were associated with the study outcome. A total of 37 studies viewed by the FDA as having positive results were published; 1 study viewed as positive was not published. Studies viewed by the FDA as having negative or questionable results were, with 3 exceptions, either not published (22 studies) or published in a way that, in our opinion, conveyed a positive outcome (11 studies). According to the published literature, it appeared that 94% of the trials conducted were positive. By contrast, the FDA analysis showed that 51% were positive. Separate meta-analyses of the FDA and journal data sets showed that the increase in effect size ranged from 11 to 69% for individual drugs and was 32% overall. CONCLUSIONS: We cannot determine whether the bias observed resulted from a failure to submit manuscripts on the part of authors and sponsors, from decisions by journal editors and reviewers not to publish, or both. Selective reporting of clinical trial results may have adverse consequences for researchers, study participants, health care professionals, and patients.</description>
    <dc:title>Selective publication of antidepressant trials and its influence on apparent efficacy.</dc:title>

    <dc:creator>EH Turner</dc:creator>
    <dc:creator>AM Matthews</dc:creator>
    <dc:creator>E Linardatos</dc:creator>
    <dc:creator>RA Tell</dc:creator>
    <dc:creator>R Rosenthal</dc:creator>
    <dc:identifier>doi:10.1056/NEJMsa065779</dc:identifier>
    <dc:source>N Engl J Med, Vol. 358, No. 3. (17 January 2008), pp. 252-260.</dc:source>
    <dc:date>2008-03-23T01:44:01-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>N Engl J Med</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>358</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>252</prism:startingPage>
    <prism:endingPage>260</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>social_study</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2573415">
    <title>A Parkinsonian syndrome in methcathinone users and the role of manganese.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2573415</link>
    <description>&lt;i&gt;N Engl J Med, Vol. 358, No. 10. (6 March 2008), pp. 1009-1017.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: A distinctive extrapyramidal syndrome has been observed in intravenous methcathinone (ephedrone) users in Eastern Europe and Russia. METHODS: We studied 23 adults in Latvia who had extrapyramidal symptoms and who had injected methcathinone for a mean (+/-SD) of 6.7+/-5.1 years. The methcathinone was manufactured under home conditions by potassium permanganate oxidation of ephedrine or pseudoephedrine. All patients were positive for hepatitis C virus, and 20 were also positive for the human immunodeficiency virus (HIV). RESULTS: The patients reported that the onset of their first neurologic symptoms (gait disturbance in 20 and hypophonia in 3) occurred after a mean of 5.8+/-4.5 years of methcathinone use. At the time of neurologic evaluation, all 23 patients had gait disturbance and difficulty walking backward; 11 patients were falling daily, and 1 of these patients used a wheelchair. Twenty-one patients had hypophonic speech in addition to gait disturbance, and one of these patients was mute. No patient reported decline in cognitive function. T(1)-weighted magnetic resonance imaging (MRI) showed symmetric hyperintensity in the globus pallidus and in the substantia nigra and innominata in all 10 active methcathinone users. Among the 13 former users (2 to 6 years had passed since the last use), lesser degrees of change in the MRI signal were noted. Whole-blood manganese levels (normal level, &#60;209 nmol per liter) averaged 831 nmol per liter (range, 201 to 2102) in the active methcathinone users and 346 nmol per liter (range, 114 to 727) in former users. The neurologic deficits did not resolve after patients discontinued methcathinone use. CONCLUSIONS: Our observation of a distinctive extrapyramidal syndrome, changes in the MRI signal in the basal ganglia, and elevated blood manganese levels in methcathinone users suggests that manganese in the methcathinone solution causes a persistent neurologic disorder.</description>
    <dc:title>A Parkinsonian syndrome in methcathinone users and the role of manganese.</dc:title>

    <dc:creator>A Stepens</dc:creator>
    <dc:creator>I Logina</dc:creator>
    <dc:creator>V Liguts</dc:creator>
    <dc:creator>P Aldins</dc:creator>
    <dc:creator>I Eksteina</dc:creator>
    <dc:creator>A Platkājis</dc:creator>
    <dc:creator>I Mārtinsone</dc:creator>
    <dc:creator>E Tērauds</dc:creator>
    <dc:creator>B Rozentāle</dc:creator>
    <dc:creator>M Donaghy</dc:creator>
    <dc:identifier>doi:10.1056/NEJMoa072488</dc:identifier>
    <dc:source>N Engl J Med, Vol. 358, No. 10. (6 March 2008), pp. 1009-1017.</dc:source>
    <dc:date>2008-03-23T01:42:33-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>N Engl J Med</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>358</prism:volume>
    <prism:number>10</prism:number>
    <prism:startingPage>1009</prism:startingPage>
    <prism:endingPage>1017</prism:endingPage>
    <prism:category>neurology</prism:category>
    <prism:category>parkinsons_disease</prism:category>
    <prism:category>substance_abuse</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2404838">
    <title>Innovations: psychotherapy: what creates and sustains commitment to the practice of psychotherapy?</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2404838</link>
    <description>&lt;i&gt;Psychiatr Serv, Vol. 58, No. 2. (February 2007), pp. 174-176.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Qualitative methods were used to identify characteristics of &#34;passionately committed psychotherapists&#34; (experienced psychotherapists who would describe themselves as having found the vocation that suits them better than any other) identified by peers in the Utah public mental health system. Six themes were identified by all 15 interviewees: balance between work and nonwork passions, adaptiveness and openness, transcendence (the belief that the practice of psychotherapy has extraordinary significance), intentional learning, personal fit with the role, and passion-supporting beliefs. These are characteristics that psychotherapists should nurture in themselves, that program supervisors should seek in potential employees, and that training programs should develop in trainees.</description>
    <dc:title>Innovations: psychotherapy: what creates and sustains commitment to the practice of psychotherapy?</dc:title>

    <dc:creator>B Miller</dc:creator>
    <dc:identifier>doi:10.1176/appi.ps.58.2.174</dc:identifier>
    <dc:source>Psychiatr Serv, Vol. 58, No. 2. (February 2007), pp. 174-176.</dc:source>
    <dc:date>2008-02-21T00:23:00-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Psychiatr Serv</prism:publicationName>
    <prism:issn>1075-2730</prism:issn>
    <prism:volume>58</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>174</prism:startingPage>
    <prism:endingPage>176</prism:endingPage>
    <prism:category>epidemiology</prism:category>
    <prism:category>social_study</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2404832">
    <title>Increased bleeding risk with concurrent use of selective serotonin reuptake inhibitors and coumarins.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2404832</link>
    <description>&lt;i&gt;Arch Intern Med, Vol. 168, No. 2. (28 January 2008), pp. 180-185.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Treatment with vitamin K antagonists (coumarins) is associated with an increased risk of bleeding. Because use of selective serotonin reuptake inhibitors (SSRIs) is also associated with an increased risk of bleeding, we assessed the odds ratio (OR) of abnormal bleeding associated with SSRI use in users of the coumarins acenocoumarol or phenprocoumon and compared this with the OR of bleeding as a result of use of nonsteroidal anti-inflammatory drugs. METHODS: We used data from a Dutch linkage system including pharmacy and linked hospitalization records for approximately 2 million subjects to conduct a case-control study in a cohort of new users of coumarins. Cases were patients who were hospitalized having a primary diagnosis of abnormal major bleeding while taking a coumarin and were matched with up to 4 control subjects. Conditional logistic regression analysis was used to determine ORs and 95% confidence intervals (CIs) for the risk of hospitalization because of abnormal bleeding associated with concurrent use of SSRIs or nonsteroidal anti-inflammatory drugs. RESULTS: We identified 1848 case patients with abnormal bleeding. Users of SSRIs were at significantly increased risk of hospitalization because of nongastrointestinal tract bleeding (hereafter referred to as &#34;nongastrointestinal bleeding&#34;) (adjusted OR, 1.7; 95% CI, 1.1-2.5) but not because of gastrointestinal tract bleeding (hereafter referred to as &#34;gastrointestinal bleeding&#34;) (adjusted OR, 0.8; 95% CI, 0.4-1.5). Users of nonsteroidal anti-inflammatory drugs had a similar increased risk of nongastrointestinal bleeding (adjusted OR, 1.7; 95% CI, 1.3-2.2), whereas the risk of gastrointestinal bleeding was higher (adjusted OR, 4.6; 95% CI, 3.3-6.5). CONCLUSION: In users of coumarins, SSRI usage was associated with increased risk of hospitalization because of nongastrointestinal bleeding but not because of gastrointestinal bleeding.</description>
    <dc:title>Increased bleeding risk with concurrent use of selective serotonin reuptake inhibitors and coumarins.</dc:title>

    <dc:creator>T Schalekamp</dc:creator>
    <dc:creator>OH Klungel</dc:creator>
    <dc:creator>PC Souverein</dc:creator>
    <dc:creator>A de Boer</dc:creator>
    <dc:identifier>doi:10.1001/archinternmed.2007.32</dc:identifier>
    <dc:source>Arch Intern Med, Vol. 168, No. 2. (28 January 2008), pp. 180-185.</dc:source>
    <dc:date>2008-02-21T00:21:46-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Arch Intern Med</prism:publicationName>
    <prism:issn>0003-9926</prism:issn>
    <prism:volume>168</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>180</prism:startingPage>
    <prism:endingPage>185</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>drug_drug_interaction</prism:category>
    <prism:category>side_effect</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2404831">
    <title>Olanzapine plus carbamazepine v. carbamazepine alone in treating manic episodes.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2404831</link>
    <description>&lt;i&gt;Br J Psychiatry, Vol. 192 (February 2008), pp. 135-143.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Combinations of olanzapine and carbamazepine are often used in clinical practice in the management of mania. AIMS: To assess the efficacy and safety of olanzapine plus carbamazepine in mixed and manic bipolar episodes. METHOD: Randomised, double-blind, 6-week trial of olanzapine (10-30 mg/day) plus carbamazepine (400-1200 mg/day; n=58) v. placebo plus carbamazepine (n=60) followed by open-label, 20-week olanzapine (10-30 mg/day) plus carbamazepine (400-1200 mg/day, n=86), with change in manic symptoms as main outcome measure. Safety and pharmacokinetics were also evaluated. RESULTS: There were no significant differences (baseline to endpoint) in efficacy measures between treatment groups, but at 6 weeks triglyceride levels were significantly higher (P=0.008) and potentially clinically significant weight gain (&#62;/=7%) occurred more frequently (24.6% v. 3.4%, P=0.002) in the combined olanzapine and carbamazepine group. Carbamazepine reduced olanzapine concentrations but olanzapine had no effect on carbamazepine concentrations. CONCLUSIONS: The combination of olanzapine and carbamazepine did not have superior efficacy to carbamazepine alone. The increases in weight and triglycerides observed during combination treatment are a matter of concern.</description>
    <dc:title>Olanzapine plus carbamazepine v. carbamazepine alone in treating manic episodes.</dc:title>

    <dc:creator>M Tohen</dc:creator>
    <dc:creator>CL Bowden</dc:creator>
    <dc:creator>AB Smulevich</dc:creator>
    <dc:creator>R Bergstrom</dc:creator>
    <dc:creator>T Quinlan</dc:creator>
    <dc:creator>O Osuntokun</dc:creator>
    <dc:creator>WV Wang</dc:creator>
    <dc:creator>HS Oliff</dc:creator>
    <dc:creator>F Martenyi</dc:creator>
    <dc:creator>LA Kryzhanovskaya</dc:creator>
    <dc:creator>W Greil</dc:creator>
    <dc:identifier>doi:10.1192/bjp.bp.107.041301</dc:identifier>
    <dc:source>Br J Psychiatry, Vol. 192 (February 2008), pp. 135-143.</dc:source>
    <dc:date>2008-02-21T00:20:49-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Br J Psychiatry</prism:publicationName>
    <prism:issn>0007-1250</prism:issn>
    <prism:volume>192</prism:volume>
    <prism:startingPage>135</prism:startingPage>
    <prism:endingPage>143</prism:endingPage>
    <prism:category>bipolar</prism:category>
    <prism:category>clinical_trial</prism:category>
    <prism:category>neuroleptic</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2404828">
    <title>Olfactory reference syndrome.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2404828</link>
    <description>&lt;i&gt;Psychosomatics, Vol. 49, No. 1. (b 2008), pp. 77-81.&lt;/i&gt;</description>
    <dc:title>Olfactory reference syndrome.</dc:title>

    <dc:creator>AN Bizamcer</dc:creator>
    <dc:creator>WR Dubin</dc:creator>
    <dc:creator>B Hayburn</dc:creator>
    <dc:identifier>doi:10.1176/appi.psy.49.1.77</dc:identifier>
    <dc:source>Psychosomatics, Vol. 49, No. 1. (b 2008), pp. 77-81.</dc:source>
    <dc:date>2008-02-21T00:19:07-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Psychosomatics</prism:publicationName>
    <prism:issn>0033-3182</prism:issn>
    <prism:volume>49</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>77</prism:startingPage>
    <prism:endingPage>81</prism:endingPage>
    <prism:category>major_depression</prism:category>
    <prism:category>schizophrenia</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2149842">
    <title>Professor's little helper</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2149842</link>
    <description>&lt;i&gt;Nature, Vol. 450, No. 7173. (19 December 2007), pp. 1157-1159.&lt;/i&gt;</description>
    <dc:title>Professor's little helper</dc:title>

    <dc:creator>Barbara Sahakian</dc:creator>
    <dc:creator>Sharon Morein-Zamir</dc:creator>
    <dc:identifier>doi:10.1038/4501157a</dc:identifier>
    <dc:source>Nature, Vol. 450, No. 7173. (19 December 2007), pp. 1157-1159.</dc:source>
    <dc:date>2007-12-20T05:53:47-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:issn>0028-0836</prism:issn>
    <prism:volume>450</prism:volume>
    <prism:number>7173</prism:number>
    <prism:startingPage>1157</prism:startingPage>
    <prism:endingPage>1159</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>social_study</prism:category>
    <prism:category>stimulant</prism:category>
    <prism:category>substance_abuse</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/1200082">
    <title>My Genes Made Me Do It? The Implications of Behavioural Genetics for Responsibility and Blame</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/1200082</link>
    <description>&lt;i&gt;Health Care Analysis, Vol. 15, No. 1. (March 2007), pp. 33-40.&lt;/i&gt;</description>
    <dc:title>My Genes Made Me Do It? The Implications of Behavioural Genetics for Responsibility and Blame</dc:title>

    <dc:creator>Levitt</dc:creator>
    <dc:creator>Mairi</dc:creator>
    <dc:creator>Manson</dc:creator>
    <dc:creator>Neil</dc:creator>
    <dc:identifier>doi:10.1007/s10728-006-0038-0</dc:identifier>
    <dc:source>Health Care Analysis, Vol. 15, No. 1. (March 2007), pp. 33-40.</dc:source>
    <dc:date>2007-03-31T16:36:11-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Health Care Analysis</prism:publicationName>
    <prism:issn>1065-3058</prism:issn>
    <prism:volume>15</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>33</prism:startingPage>
    <prism:endingPage>40</prism:endingPage>
    <prism:publisher>Springer</prism:publisher>
    <prism:category>forensic</prism:category>
    <prism:category>genetics</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2260311">
    <title>Elevated brain serotonin turnover in patients with depression: effect of genotype and therapy.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2260311</link>
    <description>&lt;i&gt;Arch Gen Psychiatry, Vol. 65, No. 1. (January 2008), pp. 38-46.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;CONTEXT: The biological basis for the development of major depressive disorder (MDD) remains incompletely understood. OBJECTIVE: To quantify brain serotonin (5-hydroxytryptamine [5-HT]) turnover in patients with MDD. DESIGN: Patients with depression were studied both untreated and during administration of a selective serotonin reuptake inhibitor (SSRI) in an unblinded study of sequential design. Healthy volunteers were examined on only 1 occasion. Direct internal jugular venous blood sampling was used to directly quantify brain serotonin turnover. The effect of serotonin transporter (5-HTT) genotype on brain serotonin turnover was evaluated and the influence of SSRI therapy on serotonin turnover was investigated. SETTING: Participants were recruited from the general community following media advertisement. Experimental procedures were performed in the research catheterization laboratory of a major training hospital and medical research institute. PARTICIPANTS: Studies were performed in 21 patients fulfilling the DSM-IV and International Statistical Classification of Diseases, 10th Revision diagnostic criteria for MDD and in 40 healthy volunteers. INTERVENTIONS: Treatment for patients consisted of SSRI administration for approximately 12 weeks. MAIN OUTCOME MEASURES: Brain serotonin turnover before and after SSRI therapy. RESULTS: Brain serotonin turnover was significantly elevated in unmedicated patients with MDD compared with healthy subjects (mean [SD] internal jugular venoarterial 5-hydroxyindoleacetic acid plasma concentration difference, 4.4 [4.3] vs 1.6 [2.4] nmol/L, respectively; P = .003). Analysis of the influence of the 5-HTT genotype in MDD indicated that carriage of the s allele compared with the l allele was associated with greater than a 2-fold increase in brain serotonin turnover (mean [SD] internal jugular venoarterial 5-hydroxyindoleacetic acid plasma concentration difference, 6.5 [4.7] vs 2.7 [2.9] nmol/L, respectively; P = .04). Following SSRI therapy, brain serotonin turnover was substantially reduced (mean [SD] internal jugular venoarterial 5-hydroxyindoleacetic acid plasma concentration difference, 6.0 [4.0] nmol/L prior to treatment vs 2.0 [3.3] nmol/L following therapy; P = .008). CONCLUSIONS: Brain serotonin turnover is elevated in unmedicated patients with MDD and is influenced by the 5-HTT genotype. The marked reduction in serotonin turnover following SSRI treatment and the accompanying improvement in symptoms suggest that high brain serotonin turnover may be a biological substrate of MDD.</description>
    <dc:title>Elevated brain serotonin turnover in patients with depression: effect of genotype and therapy.</dc:title>

    <dc:creator>DA Barton</dc:creator>
    <dc:creator>MD Esler</dc:creator>
    <dc:creator>T Dawood</dc:creator>
    <dc:creator>EA Lambert</dc:creator>
    <dc:creator>D Haikerwal</dc:creator>
    <dc:creator>C Brenchley</dc:creator>
    <dc:creator>F Socratous</dc:creator>
    <dc:creator>J Hastings</dc:creator>
    <dc:creator>L Guo</dc:creator>
    <dc:creator>G Wiesner</dc:creator>
    <dc:creator>DM Kaye</dc:creator>
    <dc:creator>R Bayles</dc:creator>
    <dc:creator>MP Schlaich</dc:creator>
    <dc:creator>GW Lambert</dc:creator>
    <dc:identifier>doi:10.1001/archgenpsychiatry.2007.11</dc:identifier>
    <dc:source>Arch Gen Psychiatry, Vol. 65, No. 1. (January 2008), pp. 38-46.</dc:source>
    <dc:date>2008-01-20T05:44:56-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Arch Gen Psychiatry</prism:publicationName>
    <prism:issn>1538-3636</prism:issn>
    <prism:volume>65</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>38</prism:startingPage>
    <prism:endingPage>46</prism:endingPage>
    <prism:category>anti_depressant</prism:category>
    <prism:category>cell_biology</prism:category>
    <prism:category>clinical_trial</prism:category>
    <prism:category>major_depression</prism:category>
    <prism:category>theory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2258891">
    <title>The sexuality and social performance of androgen-deprived (castrated) men throughout history: implications for modern day cancer patients.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2258891</link>
    <description>&lt;i&gt;Soc Sci Med, Vol. 63, No. 12. (December 2006), pp. 3162-3173.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Androgen-deprivation therapy (ADT) via either surgical or chemical castration is the standard treatment for advanced prostate cancer (PCa). In North America, it is estimated that more than 40,000 men start ADT each year. The side effects of this treatment are extensive and include gynecomastia, erectile dysfunction, and reduced libido. These changes strongly challenge patients' self-identity and sexuality. The historical term for a man who has been castrated is 'eunuch', now a pejorative term implying overall social and sexual impotence. In this paper, we review key historical features of eunuch social performance and sexuality from a variety of cultures in order to assess the validity of contemporary stereotypes of the androgen-deprived male. Data were taken from secondary sources on the history of Byzantium, Roman Antiquity, Early Islamic societies, the Ottoman Empire, Chinese Dynasties, and the Italian Castrati period. This cross-cultural survey shows that castrated men consistently held powerful social positions that yielded great political influence. Many eunuchs were recognized for their loyalty, managerial style, wisdom, and pedagogical skills. Furthermore, rather than being consistently asexual and celibate, they were often sexually active. In certain cultures, they were objects of sexual desire for males, or females, or both. Collectively, the historical accounts suggest that, given the right cultural setting and individual motivation, androgen deprivation may actually enhance rather than hinder both social and sexual performance. We conclude that eunuch history contradicts the presumption that androgen deprivation necessarily leads to social and sexual impotence. The capabilities and accomplishments of eunuchs in the past gives patients on ADT grounds for viewing themselves in a positive light, where they are neither socially impotent nor sexually chaste.</description>
    <dc:title>The sexuality and social performance of androgen-deprived (castrated) men throughout history: implications for modern day cancer patients.</dc:title>

    <dc:creator>MW Aucoin</dc:creator>
    <dc:creator>RJ Wassersug</dc:creator>
    <dc:identifier>doi:10.1016/j.socscimed.2006.08.007</dc:identifier>
    <dc:source>Soc Sci Med, Vol. 63, No. 12. (December 2006), pp. 3162-3173.</dc:source>
    <dc:date>2008-01-19T23:20:05-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Soc Sci Med</prism:publicationName>
    <prism:issn>0277-9536</prism:issn>
    <prism:volume>63</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>3162</prism:startingPage>
    <prism:endingPage>3173</prism:endingPage>
    <prism:category>endocrine</prism:category>
    <prism:category>sexuality</prism:category>
    <prism:category>social_study</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2258884">
    <title>Jerusalem syndrome.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2258884</link>
    <description>&lt;i&gt;Br J Psychiatry, Vol. 176 (January 2000), pp. 86-90.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Jerusalem's psychiatrists expect to encounter, as the millennium approaches, an ever-increasing number of tourists who, upon arriving in Jerusalem, may suffer psychotic decompensation. AIMS: To describe the Jerusalem syndrome as a unique acute psychotic state. METHOD: This analysis is based on accumulated clinical experience and phenomenological data consisting of cultural and religious perspectives. RESULTS: Three main categories of the syndrome are identified and described, with special focus on the category pertaining to spontaneous manifestations, unconfounded by previous psychotic history or psychopathology. CONCLUSIONS: The discrete form of the Jerusalem syndrome is related to religious excitement induced by proximity to the holy places of Jerusalem, and is indicated by seven characteristic sequential stages.</description>
    <dc:title>Jerusalem syndrome.</dc:title>

    <dc:creator>Y Bar-el</dc:creator>
    <dc:creator>R Durst</dc:creator>
    <dc:creator>G Katz</dc:creator>
    <dc:creator>J Zislin</dc:creator>
    <dc:creator>Z Strauss</dc:creator>
    <dc:creator>HY Knobler</dc:creator>
    <dc:source>Br J Psychiatry, Vol. 176 (January 2000), pp. 86-90.</dc:source>
    <dc:date>2008-01-19T23:18:37-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>Br J Psychiatry</prism:publicationName>
    <prism:issn>0007-1250</prism:issn>
    <prism:volume>176</prism:volume>
    <prism:startingPage>86</prism:startingPage>
    <prism:endingPage>90</prism:endingPage>
    <prism:category>culture_bound</prism:category>
    <prism:category>schizophrenia</prism:category>
    <prism:category>social_study</prism:category>
    <prism:category>spirituality</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pseudopharm/article/2258876">
    <title>How emotions inform judgment and regulate thought.</title>
    <link>http://www.citeulike.org/user/pseudopharm/article/2258876</link>
    <description>&lt;i&gt;Trends Cogn Sci, Vol. 11, No. 9. (September 2007), pp. 393-399.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Being happy or sad influences the content and style of thought. One explanation is that affect serves as information about the value of whatever comes to mind. Thus, when a person makes evaluative judgments or engages in a task, positive affect can enhance evaluations and empower potential responses. Rather than affect itself, the information conveyed by affect is crucial. Tests of the hypothesis find that affective influences can be made to disappear by changing the source to which the affect is attributed. In tasks, positive affect validates and negative affect invalidates accessible cognitions, leading to relational processing and item-specific processing, respectively. Positive affect is found to promote, and negative affect to inhibit, many textbook phenomena from cognitive psychology.</description>
    <dc:title>How emotions inform judgment and regulate thought.</dc:title>

    <dc:creator>GL Clore</dc:creator>
    <dc:creator>JR Huntsinger</dc:creator>
    <dc:identifier>doi:10.1016/j.tics.2007.08.005</dc:identifier>
    <dc:source>Trends Cogn Sci, Vol. 11, No. 9. (September 2007), pp. 393-399.</dc:source>
    <dc:date>2008-01-19T23:16:49-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Trends Cogn Sci</prism:publicationName>
    <prism:issn>1364-6613</prism:issn>
    <prism:volume>11</prism:volume>
    <prism:number>9</prism:number>
    <prism:startingPage>393</prism:startingPage>
    <prism:endingPage>399</prism:endingPage>
    <prism:category>neuropsychology</prism:category>
    <prism:category>review</prism:category>
    <prism:category>theory</prism:category>
    <prism:category>therapy</prism:category>
</item>



</rdf:RDF>

