Glen B. Baker

Mahidol University, Siayuthia, Bangkok, Thailand

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Publications (459)1408.6 Total impact

  • P. Chue · G. Baker
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    ABSTRACT: The Side Effects of Drugs Annuals is a series of volumes in which the adverse effects of drugs and adverse reactions to them are surveyed. The series supplements the contents of Meyler's Side Effects of Drugs: the International Encyclopedia of Adverse Drug Reactions and Interactions. This review of publications on adverse reactions to antipsychotic drugs from July 2013 to December 2014 covers amisulpride, aripiprazole, asenapine, blonanserin, chlorpromazine, chlorprothixene, clozapine, cyamemazine, droperidol, fluphenazine, haloperidol, iloperidone, levomepromazine (methotrimeprazine), loxapine, lurasidone, olanzapine, paliperidone, perazine, perospirone, perphenazine, pimozide, prochlorperazine, quetiapine, risperidone, sertindole, sulpiride, thioridazine, ziprasidone, zotepine, and zuclopenthixol.
    No preview · Chapter · Dec 2015
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    ABSTRACT: Changes in serotonin (5-hydroxytryptamine, 5-HT), noradrenaline (NA), and γ-aminobutyric acid (GABA) levels in the spinal cord are known to occur in response to nociceptive stimuli, yet little research has examined possible underlying sex differences in these changes and how they might affect nociception. We have used pharmacological approaches in a well-established model of tonic nociception, the formalin test, to explore the effects of altering neurotransmitter levels on nociceptive responses in male and female C57BL/6 mice. The monoamine oxidase (MAO) inhibitor phenelzine (PLZ), its metabolite phenylethylidenehydrazine (PEH), and a derivative compound of PLZ, N2-acetylphenelzine (N2-AcPLZ), were used to elevate endogenous levels of: GABA, 5-HT and NA (PLZ); GABA alone (PEH); or 5-HT and NA only (N2-AcPLZ). While both sexes had a reduction in second phase nociceptive behaviours with PEH pre-treatment, the analgesic effect of PLZ was only observed in males. HPLC analysis revealed males had greater spinal cord increases in 5HT and NA levels compared to females. Females, in contrast, had greater increases in GABA levels with pre-treatments. With N2-AcPLZ pre-treatment, only males had a reduction in second phase nociceptive behaviours despite similar increases in 5-HT and NA levels in both sexes. These findings suggest that males may utilise serotonergic and noradrenergic pathways more efficiently for the attenuation of nociceptive behaviour while females are more dependent on alternate mechanisms. These findings are the first to examine the anti-nociceptive properties of altering 5-HT, NA, and GABA levels with the MAO inhibitor PLZ and its derivatives in a model of tonic pain processing. They also reveal significant underlying sex differences associated with these treatments.
    No preview · Article · Dec 2015 · The journal of pain: official journal of the American Pain Society
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    ABSTRACT: Objective: The neurotoxic actions of the HIV protease inhibitors, amprenavir (APV) and lopinavir (LPV) were investigated. Design: With combination antiretroviral therapy (cART), HIV-infected persons exhibit neurocognitive impairments, raising the possibility that cART might exert adverse central nervous system (CNS) effects. We examined the effects of LPV and APV using in-vitro and in-vivo assays of CNS function. Methods: Gene expression, cell viability and amino-acid levels were measured in human astrocytes, following exposure to APV or LPV. Neurobehavioral performance, amino-acid levels and neuropathology were examined in HIV-1 Vpr transgenic mice after treatment with APV or LPV. Results: Excitatory amino-acid transporter-2 (EAAT2) expression was reduced in astrocytes treated with LPV or APV, especially LPV (P < 0.05), which was accompanied by reduced intracellular L-glutamate levels in LPV-treated cells (P < 0.05). Treatment of astrocytes with APV or LPV reduced the expression of proliferating cell nuclear antigen (PCNA) and Ki-67 (P < 0.05) although cell survival was unaffected. Exposure of LPV to astrocytes augmented glutamate-evoked transient rises in [Cai] (P < 0.05). Vpr mice treated with LPV showed lower concentrations of L-glutamate, L-aspartate and L-serine in cortex compared with vehicle-treated mice (P < 0.05). Total errors in T-maze assessment were increased in LPV- and APV-treated animals (P < 0.05). EAAT2 expression was reduced in the brains of protease inhibitor-treated animals, which was associated with gliosis (P < 0.05). Conclusion: These results indicated that contemporary protease inhibitors disrupt astrocyte functions at therapeutic concentrations with enhanced sensitivity to glutamate, which can lead to neurobehavioral impairments. ART neurotoxicity should be considered in future therapeutic regimens for HIV/AIDS.
    No preview · Article · Nov 2015 · AIDS (London, England)
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    ABSTRACT: Although it is well known that there is a high degree of comorbidity between chronic pain and mood and anxiety disorders, the mechanisms involved in these co-occurrences are not clear. It appears that numerous neurotransmitters and neuromodulators are involved, and this chapter focuses on the monoamine neurotransmitters noradrenaline, 5-hydroxytryptamine (5-HT, serotonin), and dopamine and the amino acid neurotransmitters GABA (x03B3;-aminobutyric acid) and glutamate in chronic pain and depression. Numerous preclinical and clinical neurochemical, neuroanatomical, pharmacological and molecular biological studies as well as clinical pharmacological treatment investigations implicate noradrenaline, 5-HT and, to a lesser extent, dopamine in the etiology of pain and depression. Similarly, preclinical and clinical studies on GABAergic and glutamatergic mechanisms as well as reports on the actions of neuroactive steroids suggest that GABA and glutamate play an important role in the etiology of pain and depression and may contribute to comorbidity.
    Full-text · Article · Oct 2015 · Modern Trends in Pharmacopsychiatry
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    ABSTRACT: Comorbidity between major depressive disorder (MDD), anxiety (generalized anxiety, panic disorder, social anxiety disorder) and pain is a major complicating factor in the diagnosis and treatment of psychiatric and neurological disorders. Although numerous neurotransmitters and/or neuromodulators may be involved, abnormalities in the GABAergic and glutamatergic systems seem to be a common factor in all these disorders. Neuroactive steroids (NASs) have been the object of considerable interest in this area in recent years since they appear to act predominantly on GABA-A and glutamate NMDA receptors. An overview of the possible involvement of NASs in MDD, anxiety and pain is provided in this chapter.
    No preview · Article · Oct 2015 · Modern Trends in Pharmacopsychiatry

  • No preview · Article · Sep 2015 · Klinik Psikofarmakoloji Bulteni
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    ABSTRACT: Alzheimer's disease (AD), the most common type of dementia, is characterized by the presence of senile plaques, neurofibrillary tangles, and neuronal loss in defined regions of the brain including the hippocampus and cortex. Transplantation of bone marrow-derived mesenchymal stem cells (BM-MSCs) offers a safe and potentially effective tool for treating neurodegenerative disorders. However, the therapeutic effects of BM-MSCs on AD pathology remain unclear and their mechanisms at cellular and molecular levels still need to be addressed. In this study, we developed a unique neuronal culture made from 5xFAD mouse, an APP/PS1 transgenic mouse model (FAD neurons) to investigate progressive neurodegeneration associated with AD pathology and efficacy of brain-derived neurotrophic factor expressing-MSCs (BDNF-MSCs). Analyses of the expression of brain-derived neurotrophic factor (BDNF), synaptic markers and survival/apoptotic signals indicate that pathological features of cultured neurons made from these mice accurately mimic AD pathology, suggesting that our protocol provided a valid in vitro model of AD. We also demonstrated amelioration of AD pathology by MSCs in vitro when these FAD neurons were co-cultured with MSCs, a paradigm that mimics the in vivo environment of post-transplantation of MSCs into damaged regions of brains. To overcome failed delivery of BDNF to the brain and to enhance MSCs releasing BDNF effect, we created BDNF-MSCs and found that MSCs protection was enhanced by BDNF-MSCs. This protection was abolished by BDNF-blocking peptides, suggesting that BDNF supply from BDNF-MSCs was enough to prevent AD pathology. Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.
    No preview · Article · Aug 2015 · Neuroscience
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    ABSTRACT: Multiple sclerosis (MS) is classically defined by motor deficits, but it is also associated with the secondary symptoms of pain, depression and anxiety. Up to this point modifying these secondary symptoms has been difficult. There is evidence that both MS and the animal model experimental autoimmune encephalomyelitis (EAE), commonly used to study the pathophysiology of the disease, can be modulated by exercise. To examine whether limited voluntary wheel running could modulate EAE disease progression and the co-morbid symptoms of pain, mice with EAE were allowed access to running wheels for 1hour every day. Allowing only 1hour every day of voluntary running led to a significant delay in the onset of clinical signs of the disease. The development of mechanical allodynia was assessed using Von Frey hairs and indicated that wheel running had a modest positive effect on the pain hypersensitivity associated with EAE. These behavioural changes were associated with reduced numbers of cFOS and phosphorylated NR1 positive cells in the dorsal horn of the spinal cord compared to no-run EAE controls. In addition, within the dorsal horn, voluntary wheel running reduced the number of infiltrating CD3(+) T-cells and reduced the overall levels of Iba1 immunoreactivity. Using high performance liquid chromatography (HPLC), we observed that wheel-running lead to significant changes in the spinal cord levels of the antioxidant glutathione. Oxidative stress has separately been shown to contribute to EAE disease progression and neuropathic pain. Together these results indicate that in mice with EAE, voluntary motor activity can delay the onset of clinical signs and reduce pain symptoms associated with the disease. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · May 2015 · Experimental Neurology
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    ABSTRACT: A significant number of people who experience chronic pain also complain of depression and sleep problems. The comorbidities and bidirectional relationships that exist between these ailments are not unheralded, as all three involve similar alterations in structural and functional neurobiology, and share common pathophysiological mechanisms. Comparable changes are seen in levels of serotonin (5-hydroxytryptamine, 5-HT), pro-inflammatory cytokines, brain-derived neurotrophic factor (BDNF) and other transmitters. This review is unique, as it attempts to cast a broader net over the common neurobiological correlates that exist among these three conditions. Perspective This review article highlights important neurophysiological similarities, and key neurobiological links, underlying chronic pain, depression, and sleep problems. Greater awareness of the connections between these conditions may prompt clinicians to actively seek and treat symptoms of all three when one presents, and may provide a rationale for better treatment choices as a result.
    Full-text · Article · May 2015 · The Clinical journal of pain
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    ABSTRACT: Neurodegenerative diseases are characterized by chronic and progressive structural or functional loss of neurons. Limitations related to the animal models of these human diseases have impeded the development of effective drugs. This emphasizes the need to establish disease models using human-derived cells. The discovery of induced pluripotent stem cell (iPSC) technology has provided novel opportunities in disease modeling, drug development, screening, and the potential for "patient-matched" cellular therapies in neurodegenerative diseases. In this study, with the objective of establishing reliable tools to study neurodegenerative diseases, we reprogrammed human umbilical vein endothelial cells (HUVECs) into iPSCs (HiPSCs). Using a novel and direct approach, HiPSCs were differentiated into cells of central nervous system (CNS) lineage, including neuronal, astrocyte and glial cells, with high efficiency. HiPSCs expressed embryonic genes such as nanog, sox2 and Oct-3/4, and formed embryoid bodies that expressed markers of the 3 germ layers. Expression of endothelial-specific genes was not detected in HiPSCs at RNA or protein levels. HiPSC-derived neurons possess similar morphology but significantly longer neurites compared to primary human fetal neurons. These stem cell-derived neurons are susceptible to inflammatory cell-mediated neuronal injury. HiPSC-derived neurons express various amino acids that are important for normal function in the CNS. They have functional receptors for a variety of neurotransmitters such as glutamate and acetylcholine. HiPSC-derived astrocytes respond to ATP and acetylcholine by elevating cytosolic Ca2+ concentrations. In summary, this study presents a novel technique to generate differentiated and functional HiPSC-derived neurons and astrocytes. These cells are appropriate tools for studying the development of the nervous system, the pathophysiology of various neurodegenerative diseases and the development of potential drugs for their treatments.
    Full-text · Article · Mar 2015 · PLoS ONE
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    ABSTRACT: Background Better treatments for schizophrenia are urgently needed. The therapeutic use of the nitric oxide (NO)-donor sodium nitroprusside (SNP) in patients with schizophrenia has shown promising results. The role of NO in schizophrenia is still unclear, and NO modulation is unexplored in ketamine (KET) animal models to date. In the present study, we compared the behavioral effects of pre- and post-treatment with SNP, glyceryl trinitrate (GTN), and methylene blue (MB) in the acute KET animal model of schizophrenia. The present study was designed to test whether acute SNP, GTN, and MB treatment taken after (therapeutic effect) or before (preventive effect) a single KET injection would influence the behavior of rats in the sucrose preference test, object recognition task and open field. Results The results showed that KET induced cognitive deficits and hyperlocomotion. Long- term memory improvement was seen with the therapeutic GTN and SNP treatment, but not with the preventive one. MB pretreatment resulted in long-term memory recovery. GTN pre-, but not post-treatment, tended to increase vertical and horizontal activity in the KET model. Therapeutic and preventive SNP treatment consistently decreased KET-induced hyperlocomotion. Conclusion NO donors – especially SNP – are promising new pharmacological candidates in the treatment of schizophrenia. In addition, we showed that the potential impact of NO-related compounds on KET-induced behavioral changes may depend on the temporal window of drug administration.
    Full-text · Article · Mar 2015 · BMC Neuroscience
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    ABSTRACT: B y modulating the "glutamate-NO (nitric oxide)-cGMP" pathway," a new paradigm for the treatment of schizophrenia seems to arise. Indeed, our group has recently pub-lished a double-blind placebo (PLB) con-trolled trial showing that an infusion of sodium nitroprusside (SNP), a nitric oxide donor, improved positive, negative, anxiety, and depressive symptoms of schizophrenic patients in a matter of hours. 1 During this study, it seemed of interest to test the idea that SNP might also be effective in treating cognitive symptoms found in schizophrenia. For this purpose, it was performed, in the same subjects just mentioned, a pilot study where the patients were evaluated by a battery of cognitive tests on 2 occasions: 1 hour be-fore the start of SNP or PLB infusion and at 8 hours after the end of SNP or PLB infusion. Twenty-four patients agreed to partici-pate and were assessed for eligibility; 4 sub-jects subsequently refused to participate, and 20 individuals were randomized to receive either SNP or placebo. Two subjects from the SNP group refused to participate in the sec-ond cognitive evaluation (cognitive evaluation at 8 hours after the end of the SNP infusion). The other 18 participants who were random-ized completed all the study procedures. The SNP was administered as an endovenous infusion of 0 . 5 μg/kg per min-ute for 4 hours. The placebo was a 5% glu-cose solution that was endovenous infused over the same length of time. The following cognitive tests were con-ducted: (a) Stroop Color Word Test (SCWT) is a test to assess selective attention. Two cards instead of the 3 cards originally pro-posed by Stroop were used, following the procedure used by Liddle and Morris. 2 On the first card 100 words designating 5 colors, printed in black, were used; and on the sec-ond card, 100 words for the same colors, printed in colors incongruent with the des-ignation were used. The task was to read card 1 and designate the colors of card 2. Time spent on the task was measured in seconds and number of errors committed, according to the method proposed by Seabra (1987). (b) N-Back is a test to assess work-ing memory. It lasts about 6 minutes and consists of examining a series of numbers where it is required, at varying intervals, to report the number seen "n" positions back in the sequence. A printed version of the test on laminated cards was used in this study, with 2 distinct blocks presented in-terchangeably. The first and the third blocks contain 5 questions each about the last num-ber seen ("0-Back," task control), and the sec-ond and fourth blocks contain 5 questions each about which number was submitted before the last 2 cards ("2-Back"). The num-ber of errors made during the task was com-puted. (c) FAS (the Verbal Fluency Test) is a test widely used in the literature to measure verbal fluency, which is known to be impaired in schizophrenic patients. The task consists of a period of 3 minutes (1 minute for each letter—F, A, and S) where the volunteer must produce the largest number of words begin-ning with those letters. Brand names, proper names, or variations from the same root (eg, words like fall and fallen) are not allowed. Data were analyzed using the Statistical Package for the Social Sciences (SPSS 17·0). For the SCWT, N-Back, and the FAS scores, separate analyses of variance (ANOVAs) for repeated measures were carried out, with treatment (SNP/PLB) and time (every point of evaluation) as factors. If the ANOVAs were significant, a paired 2-tailed t test was per-formed, considering the groups independently. The following results were found: (a) SCWT—the ANOVA for repeated mea-sures concerning card 1 reading time showed an effect of the time factor (F = 6.98, df = 1–15, P = 0.02), but not drug (F = 1.46, df = 1–15, P = 0.24) and no interaction between time and drug (F = 0.03, df = 1–15, P = 0.85). The analysis of the number of errors on card 1 showed no effect of time (F = 2.4, df = 1–15, P = 0.14), drug (F = 0.18, df = 1–15, P = 0.68), or interaction between time and drug (F = 0.03, df = 1–15, P = 0.86). An interac-tion between time and drug was found for the number of errors on naming incongru-ent colors on card 2 (F = 5.54, df = 1–15, P = 0.03), but no effect of time (F = 0.57, df = 1–15, P = 0.46) or of drug alone (F = 0.03, df = 1–15, P = 0.85). Regarding the time for naming incongruent colors, the ANOVA for repeated measures showed no effect of time (F = 0.02, df = 1–15, P = 0.89), drug (F = 0.71, df = 1–15, P = 0.42), or in-teraction between them (F = 2.32, df = 1–15, P = 0.15). In situations where the ANOVA for repeated measures identified some in-teraction, the paired t test was performed, considering the groups independently. The paired t test for the 2 groups individually (SNP and PLB) showed that those patients who received SNP made fewer errors in the second evaluation of naming incongruent colors, but those who received PLB did not. (b) FAS—the ANOVA for repeated measures showed an effect of time (F = 9.37, df = 1–16, P = 0.01), but not of drug (F = 0.08, df = 1–16, P = 0.78) and no interaction between time and drug (F = 0.03, df = 1–16, P = 0.85). (c) N-Back—the ANOVA for repeated mea-sures identified an effect of time (F = 7.63, df = 1–14, P = 0·01), drug (F = 7.76, df = 1–14, P = 0.01), and also an interaction be-tween these 2 (F = 15.24, df = 1–14, P < 0.01). Thus, the paired t test was conducted for the SNP and PLB groups alone, which showed that those who received the SNP infusion pre-sented significant improvement in congnitive performance, whereas those who received the PLB infusion did not (Table 1). To our knowledge, this is the first time that improvements on executive functions that are frequently impaired in patients with schizophrenia were shown after SNP admin-istration. The improvement in SCWT and N-back performance that was observed in the SNP group, but not in the PLB group, suggests that treatment with SNP had an impact on patients cognitive functioning by improving selective attention 3 and work-ing memory 4 deficits. These beneficial effects could be ex-plained through SNP capacity, as a NO do-nor, to act by increasing the concentrations of the second messenger cGMP and medi-ating the neuronal communication in the CNS (central nervous system). 5,6 In this way, NO has been shown to influence learning and memory. 7 NO donors such as SNP have been found to stimulate neuronal growth in vitro 8 and have been proposed as potential new drugs to treat patients with age-related neurodegenerative disease such as Alzheimer disease. 9,10 On the other hand, too much NO could produce neurotoxicity due to accumu-lation of its toxic metabolite, peroxynitrite. 11 The small amount of patients studied is the limitation of this work. Future studies with a larger number of patients are needed. The usual NPS safe dose rate used to treat hypertension is 0.5 to 10 μg/kg per minute. Therefore, we decide to work with its low-est dose to minimize cardiovascular effects. Indeed, no clear effect of NPS on the vascu-lar system was observed (these results have been discussed elsewhere). 1 Further works should investigate the effects of multiple and different doses of SNP and other rele-vant issues like how frequently do we have to administer SNP to sustain its effect in long-term. To minimize possible learning effects, cognitive tests were performed only on 2 occasions. To avoid confounding LETTER TO THE EDITORS Journal of Clinical Psychopharmacology • Volume 35, Number 1, February 2015 1 Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. factors from demographic and clinical vari-ables, the selection and pairing of subjects were performed carefully and showed no differences between the 2 groups in any of the parameters evaluated (these results have been discussed elsewhere). 1 Despite the cognitive deficits being considered as the strongest predictors of long-term functional recovery in patients with schizophrenia, they have been among the symptoms most refractory to the treat-ment by both second-and first-generation antipsychotics. 12,13 Perhaps, the develop-ment of drugs that enhance NO levels, such as SNP, could be a productive target to pur-sue in the development of the next genera-tion of antipsychotic drugs. However, the findings here reported are modest and need to be confirmed for future studies. ACKNOWLEDGMENTS The authors thank their respective universities for the continuous support and Dr Judy Baker for the editorial and secretarial assistance.
    Full-text · Article · Feb 2015 · Journal of clinical psychopharmacology
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    ABSTRACT: Recently, we found a rapid and long-lasting improvement of symptoms in schizophrenic patients on antipsychotics after a single four-hour infusion of sodium nitroprusside (SNP), a nitric oxide (NO) donor with a short half-life. This improvement persisted for up to 4 weeks. Because these patients remained on antipsychotics after infusion of SNP was finished, the question arises about whether this improvement was due to SNP itself. We have now investigated whether SNP, alone, can produce preventive antipsychotic effects in rats treated with ketamine (KET). 56 adult rats divided into 7 groups were infused with SNP 4 mg/kg, KET 25 mg/kg, or saline as follows: group1 — saline, group2 — SNP, group3 — KET, group4 — KET 12 h after SNP, group5 — KET 1 day after SNP, group6 — KET 2 days after SNP, and group7 — KET 1 week after SNP. The animals were filmed in an open field arena for 30 min and the videos were later analyzed by ANY-Maze software to measure activity and stereotypy. SNP significantly prevented the emergence of hyperactivity induced by KET when it was administered for up to 1 week before KET, and prevented the emergence of stereotypies when it was administered for up to 1 day before KET. These findings in rats, which have an even faster metabolic rate than humans, suggest that the long-lasting effects observed in our clinical trial with SNP in humans could have been due to SNP itself, and indicate for the first time that SNP may present preventive antipsychotic effects.
    Full-text · Article · Jan 2015 · Schizophrenia Research
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    ABSTRACT: Increasing evidence suggests that the tetracycline antibiotic minocycline has neuroprotective effects and is a potential treatment for schizophrenia. However, the mechanisms of action of minocycline in the CNS remain elusive. The aim of this study was to investigate the effects of minocycline on brain morphology and cerebral perfusion in patients with recent-onset schizophrenia after 12 months of a randomized double-blind, placebo-controlled clinical trial of minocycline add-on treatment. This study included 24 outpatients with recent-onset schizophrenia randomized for 12 months of adjuvant treatment with minocycline (200 mg/d) or placebo. MRI (1.5 T) and [ 99m Tc]-ECD SPECT brain scans were performed at the end of the 12-month of trial. Between-condition comparisons of SPECT and MRI brain images were performed using statistical parametric mapping and analyzed by voxel-based morphometry (VBM). Minocycline adjuvant treatment significantly reduced positive and negative symptoms when compared with placebo. The VBM analysis of MRI scans showed that the patients in the placebo group had significant lower gray matter volumes in the midposterior cingulate cortex and in the precentral gyrus in comparison with the patients in the minocycline group. In addition, a decreased ECD uptake in the minocycline condition was observed in fronto-temporal areas. These results suggest that minocycline may protect against gray matter loss and modulate fronto-temporal areas involved in the pathophysiology of schizophrenia. Furthermore, minocycline add-on treatment may be a potential treatment in the early stages of schizophrenia and may ameliorate clinical deterioration and brain alterations observed in this period.
    Full-text · Article · Dec 2014 · Schizophrenia Research
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    ABSTRACT: Individuals with chronic pain often report experiencing stigmatization. There is little published data on perceived stigma in people with chronic pain, and to the best of our knowledge, no published data on the effect of cognitivebehavioral therapy (CBT) on perceived stigma. This study examined perceived stigma and associated factors in adults with chronic pain and whether involving a family member or friend in treatment would reduce perceived stigma. We also sought to further validate the use of the Chronic Pain Stigma Scale (CPSS) using a Canadian sample of individuals with chronic pain. A total of 71 patients from a tertiary care Multidisciplinary Pain Centre completed the CPSS. This sample was divided into three groups: those who attended treatment programming alone, those who brought a family member or friend to the first session of treatment and waitlist controls. Stigmatization was high in our patients. While treatment was successful in reducing anxiety and pain-related disability, CBT had no effect on perceived stigma across groups. Including a family member or friend early in treatment reduced perceived stigma from physicians. Our findings of level of stigmatization in our clinical sample were highly similar to data collected in a clinically and geographically different population. Our outcomes confirmed that stigma is prevalent in chronic pain. Pain-focused CBT, while effective in its declared objectives, did not mitigate the perception of stigma. While helping reduce perceived stigma may be valuable, it appears that a primary focus should also be to educate and change public views toward chronic pain.
    No preview · Article · Dec 2014
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    ABSTRACT: ZET: fiizofreni için yeni tedavi stratejileri olarak nitrik oksit modülasyonu Antipsikotik ilaç gelifltirilmesindeki son ilerlemelere ra¤-men, flizofreninin farmakolojik yönetimi görece yetersiz kalmaktad›r. Santral nitrik oksit modülasyonuna dair artan kan›tlar flizofreni tedavisi için yeni bir tedavi stratejisi suna-bilir. Bu nedenle, bu editöryal yaz›da flizofreni ve antipsiko-tik ilaçlar›n mekanizmas› ile santral nitrik oksit patofizyolo-jisi iliflkisi anlat›lmaya çal›fl›lmaktad›r. Nitrik oksit modülas-yonunun yeni stratejileri flizofreni için potansiyel bir farma-koterapi yöntemi olarak karfl›m›zda durmaktad›r.
    Full-text · Article · Nov 2014 · Klinik Psikofarmakoloji Bulteni
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    Full-text · Article · Nov 2014 · Schizophrenia Research
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    Full-text · Article · Sep 2014 · Journal of clinical psychopharmacology
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    ABSTRACT: Negative symptoms are present in over one quarter of patients with schizophrenia and are detrimental to prognosis, functionality and quality of life. Currently, the treatments for primary negative symptoms are inadequate. However, enhancing N-methyl-D-aspartate receptor hypofunctioning with glycine reuptake inhibitors has garnered optimism as a potential treatment. Trials of sarcosine-derivatives have yielded mixed results and potential severe side effects have halted progress to larger studies. Non- sarcosine derivatives such as bitopertin have proven to be less toxic and have shown success in phase II trials. Unfortunately, phase III trials of bitopertin to date have not met primary endpoints and a void in effective treatment options for negative symptoms persists. Further research to improve psychiatric study design, discover clinical biomarkers and build on early successes of other potential pharmacologic molecules is required. © 2014, Cukurova Univ Tip Fakultesi Psikiyatri Anabilim Dali. All rights reserved.
    No preview · Article · Sep 2014 · Klinik Psikofarmakoloji Bulteni
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    ABSTRACT: Primary human fetal neurons and astrocytes (HFNs and HFAs, respectively) provide relevant cell types with which to study in vitro the mechanisms involved in various human neurological diseases, such as multiple sclerosis, Parkinson's disease, and Alzheimer's disease. However, the limited availability of human fetal cells poses a significant problem for the study of these diseases when a human cell model system is required. Thus, generating a readily available alternative cell source with the essential features of human neurons and astrocytes is necessary. The human teratoma-derived NTera2/D1 (NT2) cell line is a promising tool from which both neuronal and glial cells can be generated. Nevertheless, a direct comparison of NT2 neurons and primary HFNs in terms of their morphology physiological and chemical properties is still missing. This study directly compares NT2-derived neurons and primary HFNs using immunocytochemistry, confocal calcium imaging, high-performance liquid chromatography, and high-content analysis techniques. We investigated the morphological similarities and differences, levels of relevant amino acids, and internal calcium fluctuations in response to certain neurotransmitters/stimuli. We also compared NT2-derived astrocytes and HFAs. In most of the parameters tested, both neuronal and astrocytic cell types exhibited similarities to primary human fetal neurons and astrocytes. NT2-derived neurons and astrocytes are reliable in vitro tools and a renewable cell source that can serve as a valid alternative to HFNs/HFAs for mechanistic studies of neurological diseases. © 2014 Wiley Periodicals, Inc.
    No preview · Article · Sep 2014 · Journal of Neuroscience Research

Publication Stats

9k Citations
1,408.60 Total Impact Points


  • 2015
    • Mahidol University
      Siayuthia, Bangkok, Thailand
  • 1979-2015
    • University of Alberta
      • • Department of Psychiatry
      • • Faculty of Pharmacy and Pharmaceutical Sciences
      Edmonton, Alberta, Canada
  • 2010
    • Acharya Nagarjuna University
      Гунтура, Andhra Pradesh, India
  • 2009
    • University of Arkansas for Medical Sciences
      • Department of Psychiatry
      Little Rock, Arkansas, United States
  • 2008
    • University of Saskatchewan
      • Department of Physiology
      Saskatoon, Saskatchewan, Canada
  • 1999-2007
    • McGill University
      • Department of Psychiatry
      Montréal, Quebec, Canada
  • 2003
    • Gracie Square Hospital, New York, NY
      New York City, New York, United States
  • 1991-1997
    • The Ohio State University
      • Department of Psychiatry
      Columbus, Ohio, United States
  • 1996
    • The University of Western Ontario
      • Department of Psychology
      London, Ontario, Canada
  • 1989
    • Edmonton Clinic
      Edmonton, Alberta, Canada