Male C57BL/6 mice were divided into two groups and maintained on either a normal diet (ND) or HFD. Seven weeks of HFD significantly decreased the numbers of newly generated cells in the dentate gyrus of the hippocampus without neuronal loss. HFD also increased the level of malondialdehyde (MDA) and decreased the level of brain-derived neurotrophic factor (BDNF) in the hippocampus. The toxic effects of MDA were evaluated on

neural progenitor cells (NPCs). MDA reduced the growth of NPCs, but BDNF treatment restored NPCs proliferation. The present data indicate that a HFD impairs hippocampal neurogenesis and NPCs proliferation through increased lipid peroxidation and decreased BDNF. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Herpes simplex virus 1 (HSV-1) induces relocalization of several nucleolar proteins. We have found that, as for fibrillarin, the HSV-1-induced selleck compound redistribution of two RNA polymerase I components, upstream binding factor (UBF) and RPA194, was independent of the viral protein UL24, which affects nucleolin localization. Nevertheless, the kinetics and sites of redistribution for fibrillarin and UBF differed. Interestingly, UBF remained associated

with RPA194 during infection. Although UBF is redistributed to viral replication compartments during infection, we did not detect foci of UBF at early sites of viral DNA synthesis, suggesting that it may not be directly involved in this process at early times.”
“Linkage analysis identified a region on chromosome 9p associated with Frontotemporal Lobar Degeneration (FTLD). A detailed analysis of candidate MLN2238 manufacturer genes lying in this region demonstrated an association with Ubiquitin Associated Protein (UBAP)1. The distribution of five Single Nucleotide Polymorphisms (SNPs) located in the chromosome 9 haplotype identified via linkage analysis, including UBAP1 rs7018487, UBAP2 rs1785506 and rs307658, and KIF24 rs17350674 and rs10814083, has been determined in Benzatropine a population of 284 patients diagnosed with FTLD, including

245 with behavioural variant Frontotemporal Dementia (bvFTD), 23 with Progressive Aphasia and 16 with Semantic Dementia, compared with 318 age-matched controls. A statistically significant increased frequency of the KIF24 rs17350674 AA genotype was observed in patients compared with controls (7.4 versus 2.5%; P = 0.0068, OR: 3.63, CI: 1.58-8.35). Considering each syndrome separately, similar results where obtained in bvFTD versus controls (7.7 versus 2.5%, P = 0.005, OR: 3.26, CI: 1.40-7.57). Stratifying for gender, a statistically significant increased genotypic frequency was observed in female patients as compared with female controls (8.9 versus 2.5%, P = 0.008, OR: 3.85, Cl: 1.36-10.93). In silico analysis predicted that the substitution from W to L caused by the rs17350674 affects protein function (P < 0.05).

Gait analyses showed that these walking velocity

adjustments result from simultaneous adaptations in both step length and step duration. The role of visual information in the control of self-motion velocity is discussed in relation with other factors. (C) 2011 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Neurocognitive deficits seen in HIV-associated neurocognitive disorders (HANDs) are attributed to the release of soluble factors from CNS-resident, HIV-infected and/or activated macrophages and microglia. To study HIV-associated neurotoxicity, we used our in vitro model in which primary rat neuronal/glial cultures are treated with supernatants from cultured human monocyte-derived macrophages,

AZD0156 infected with a CNS-isolated HIV-1 strain (HIV-MDM). We found that neuronal damage, detected as a loss of microtubule-associated protein-2 (MAP2), begins as early as 2 hand is preceded by a loss of mitochondrial membrane potential (Delta psi(m)). Interestingly, inhibitors of calpains, but not inhibitors of caspases, blocked MAP2 loss, however neither selleck chemical type of inhibitor prevented the loss of Delta psi(m). To facilitate throughput for these studies, we refined a MAP2 cell-based-ELISA whose data closely compare with our standardized method of hand counting neurons. In addition, we developed a tetramethyl rhodamine methyl ester (TMRM)-based multi-well fluorescent plate assay for the evaluation of whole culture Delta psi(m). Together, these findings indicate that calpain activation and loss of Delta psi(m) may be parallel pathways to death in HIV-MDM-treated neurons and also demonstrate the validity of plate assays for assessing multiple experimental parameters as is useful for screening neurotherapeutics for neuronal damage and death. (C) 2011 Elsevier Ireland Ltd and the Japan Neuroscience Flucloronide Society. All rights reserved.”
“We examined whether chronic systemic

treatment with agonists for peroxisome proliferator-activated receptor alpha (PPAR alpha) influences neuroinflammation induced by lipopolysaccharide (LPS) injection into the somatosensory cortex in adult mice. Mice were pretreated with Wy-14643 or fenofibrate, both at 30 mg/kg, for 7 days. These treatment protocols increased the amount of PPAR alpha mRNA and active form of PPAR alpha protein in the brain. LPS injection reduced the PPAR alpha mRNA level in the brain. On the contrary, TNF alpha, IL-1 beta, IL-6, iNOS, COX-2, ICAM-1, VCAM-1, and PECAM-1 were elevated at 6 h after LPS. Wy-14643 and fenofibrate inhibited the elevations of TNF alpha, IL-1 beta, IL-6, COX-2, ICAM-1, and VCAM-1. Wy-14643, but not fenofibrate, also attenuated the iNOS elevation.

When the tumor radius reached 1 mm, Coomassie

Blue was administered intravenously while the appearance of the cortical surface was recorded. Computerized image analysis of the red/green/blue color components was used to quantify visible differences between tumor and nonneoplastic tissue and to compare delineation in the brain tumor window (BTW) model with the conventional 9L glioma model.

RESULTS: The tumor margin in the BTW model was poorly defined before contrast administration but readily apparent after contrast administration. Based on red component intensity, tumor delineation improved 4-fold at 50 minutes after contrast administration in the BTW model (P < .002). The conventional 9L glioma model overestimated the degree of delineation compared with the BTW model at the same dose of Coomassie Blue (P < .03).

CONCLUSION: Window placement overlying an implanted glioma is PD0332991 technically possible and well tolerated in the rat. The BTW model is a valid system for evaluating optical contrast agents designed to delineate brain tumor margins. To our knowledge, we have described the first in vivo model system for evaluating optical contrast

agents for tumor delineation.”
“BACKGROUND: The primary treatment for craniopharyngiomas is total excision, but recurrence is common. However, current knowledge on the mechanisms of recurrence is limited. OBJECTIVE: We hypothesized that recurrence is linked to the angiogenesis of the tumor. Recurrent and nonrecurrent tumor XAV-939 cell line samples were compared with regard to expression of angiogenesis-related factors and angiogenic capacity in a corneal angiogenesis model.

METHODS: Specimens of 4 recurrent and 6 nonrecurrent tumors Plasmin were selected from 57 patients with adamantinomatous craniopharyngiomas. Sections were immunohistochemically stained with antibodies for vascular

endothelial growth factor (VEGF), fibronectin, fibroblast growth factor (FGF)-2, platelet-derived growth factor (PDGF)-A, PDGF-B, platelet-derived growth factor receptor (PDGFR)-alpha, and PDGFR-beta. Expression levels were graded using a 4-point scoring system and were compared. For corneal angiogenesis assay, tissue samples were inoculated in a micropocket created on the rat eye, and microvessels were counted on days 3, 5, 7, and 9 to evaluate angiogenic potential.

RESULTS: Expression of PDGFR-a and FGF-2 were significantly higher for recurrent tumors (P = .02 and P = .01). However, recurrent and nonrecurrent tumors did not differ in the expressions of other ligands and receptors (PDGF-A, PDGF-B, and PDGFR-beta). Recurrent tumors displayed a higher angiogenic potential starting from the fifth day of corneal angiogenesis assay.

CONCLUSION: These findings suggest a relationship between recurrence of craniopharyngiomas and angiogenesis. New treatment modalities with selective PDGFR-alpha blockers may represent a novel and effective therapeutic option for the treatment of craniopharyngiomas.

These findings support the importance of optimizing surgical techniques to achieve a sound oncological surgical outcome with negative surgical margins when possible.”
“Methamphetamine is a drug of abuse that can induce oxidative stress and neurotoxicity

to dopaminergic neurons. We have previously reported that oxidative stress promotes the liberation of intracellular Zn(2+) from metal-binding proteins, which, in turn, can initiate neuronal injurious signaling processes. Here, we report that methamphetamine mobilizes Zn(2+) in catecholaminergic rat pheochromocytoma (PC12) cells, as measured by an increase in Zn(2+)-regulated gene expression driven by the metal response element transcription factor-1. Moreover, methamphetamine-liberated selleck Zn(2+) was responsible for a pronounced enhancement in voltage-dependent K(+) currents in these cells, a process that normally accompanies Zn(2+)-dependent cell injury. Overnight exposure to methamphetamine induced PC12 cell death. This toxicity could be prevented by the cell-permeant zinc chelator N,N,N’, N’-tetrakis(2-pyridylmethyl)-ethylenediamine (TPEN), and by over-expression of the Zn(2+)-binding protein metallothionein

3 (MT3), but not by tricine, an extracellular Zn(2+) Tideglusib ic50 chelator. The toxicity of methamphetamine to PC12 cells was enhanced by the presence of co-cultured microglia. Remarkably, under these conditions, TPEN no longer protected but, in fact, dramatically exacerbated Erythromycin methamphetamine toxicity, tricine again being without effect. Over-expression of MT3 in PC12 cells did not mimic these toxicity-enhancing actions of TPEN, suggesting that the chelator affected microglial function. Interestingly, P2X receptor antagonists

reversed the toxicity-enhancing effect of TPEN. As such, endogenous levels of intracellular Zn(2+) may normally interfere with the activation of P2X channels in microglia. We conclude that Zn(2+) plays a significant but complex role in modulating the cellular response of PC12 cells to methamphetamine exposure in both the absence and presence of microglia. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Purpose: This phase I study of high dose ketoconazole and docetaxel was designed against castration resistant prostate cancer to determine the maximum tolerated doses, side effects, and pharmacokinetic interaction of co-administered docetaxel and ketoconazole.

Materials and Methods: Patients with metastatic castration resistant prostate cancer received weekly docetaxel for 3 of every 4 weeks plus daily ketoconazole. Pharmacokinetic studies were performed on day 1 (docetaxel alone) and day 16 (after ketoconazole).

Results: The study enrolled 42 patients at 9 different dose levels. The combination regimens investigated included docetaxel weekly, increasing from 5 to 43 mg/m(2), with starting doses of 600, 800 or 1,200 mg ketoconazole daily.

The present Evofosfamide review discusses the pharmacological basis of the use of W somnifera in various central nervous system (CNS) disorders, particularly its indication in epilepsy, stress and neurodegenerative diseases such

as Parkinson’s and Alzheimer’s disorders, tardive dyskinesia, cerebral ischemia, and even in the management of drug addiction. (C) 2007 Elsevier Inc. All rights reserved.”
“Neuromyelitis optica (NMO) is a severe demyelinating disease that preferentially involves spinal cord and optic nerve. It is part of a spectrum of neurological conditions associated with antibodies to aquaporin-4 (AQP4). This study investigates the role of MRI where novel, more sensitive AQP4 antibody immunoassay techniques are being used.

Retrospective review of neuroimaging in 69 patients (25 antibody positive, 44 antibody negative), investigated in the context of suspected NMO or NMO spectrum disorder, was performed independently by two consultant neuroradiologists.

Longitudinally extensive, central spinal cord lesions were more frequent in AQP4 positive patients (95.2% vs 35.5%, p < 0.0001; 85.7%

vs 45.2%, p = 0.015). Multiple sclerosis diagnostic criteria were less frequently fulfilled on brain MRI in antibody positive patients (5.6% vs 33.3%, p = 0.035). Juxtacortical and corpus callosal lesions were also less common in this Defactinib in vivo group (16.7% vs 46.7%, p = 0.063; 5.6% vs 46.7%, p = 0.0034). Hypothalamic and periependymal disease related to the aqueduct was not seen in antibody negative patients. T1 hypointensity was more common in cord lesions of antibody positive patients (75.0% vs 35.3%, p = 0.037). However, this characteristic did not discriminate antibody positive and negative longitudinally extensive cord lesions (73.3% vs 62.5%, p = 0.66).

The NMO spectrum of diseases are among an increasing number of neurological conditions defined by serological tests. However, despite VAV2 improved immunoassay techniques, MRI of the brain and spinal cord continues to be among the first-line investigations in these patients,

providing valuable diagnostic information that will help guide patient management.”
“Over the past twenty years conservation genetics has progressed from being mainly a theory-based field of population biology to a full-grown empirical discipline. Technological developments in molecular genetics have led to extensive use of neutral molecular markers such as microsatellites in conservation biology. This has allowed assessment of the impact of genetic drift on genetic variation, of the level of inbreeding within populations, and of the amount of gene flow between or within populations. Recent developments in genomic techniques, including next generation sequencing, whole genome scans and gene-expression pattern analysis, have made it possible to step up from a limited number of neutral markers to genome-wide estimates of functional genetic variation.

In this review, we will describe neurobehavioral, genetic and animal model studies that support the notion that a common, genetically determined failure of response inhibition function is an endophenotype Daporinad order for both disorders. Through an impairment in

the ability to cognitively control pre-potent behaviors, subjects can exhibit a collection of ADHD-like traits (impulsivity and hyperactivity), as well as susceptibility for the initiation of drug taking and its ultimate progression to an inflexible, uncontrollable form. At the neural level, dysfunction within circuitry that includes the ventrolateral frontal and cingulate cortices, as well as in associated basal ganglia zones, contributes to a common pattern of behavioral impairment, explaining aspects of co-morbidity. Animal models of substance abuse/dependence and ADHD that exhibit deficits in response inhibition have substantiated the role of this endophenotype in 3-deazaneplanocin A research buy both disorders and their co-morbidity and should provide a testing ground for interventions targeting it. New directions for research that will further explore this hypothesis and begin

to reveal the underlying biological mechanisms will be proposed. (c) 2008 Elsevier Ltd. All rights reserved.”
“Objective: We evaluated the outcome, long-term results, and factors affecting outcome of induction chemoradiotherapy followed by surgical resection for T4 non-small cell lung cancer invading the spine.

Methods: Retrospective analysis of 23 consecutive patients undergoing radical vertebral resection for non-small cell lung cancer invading the spine between 1996 and 2007 was performed. In most cases, induction chemoradiotherapy consisted of cisplatin and etoposide followed by

45 Gy of radiation. Verteporfin in vitro Surgical resection with vertebrectomy was performed en bloc in either a 1-stage or 2-stage operation. Survival was estimated by Kaplan-Meier techniques. The log-rank comparison was used to compare groups.

Results: There were 13 men and 10 women with a median age of 61 years (range 32-75). Twenty-two patients had induction chemoradiotherapy and 1 had induction chemotherapy alone. Vertebral resections included 6 total vertebrectomies, 15 hemivertebrectomies, and 2 partial vertebrectomies. Complete resection was achieved in 19 (83%) patients. Two (8.7%) patients died postoperatively. Pathologic complete response was observed in 10 (43%) patients. The 3-year survival was 58%(median follow-up, 34 months). Patients who achieved pathologic complete response or near complete response (viable tumor cells < 1%) demonstrated significantly better survival than those who did not (3-year survival, 92% vs 20%; P = .006).

Conclusion: Highly selected patients with lung cancer invading the spine can potentially be cured with induction chemoradiation therapy followed by radical en bloc resection of the tumor.

04, g(parallel to) = 2.014 and g(aver). = 2.03. After treatment with a strong reducing agent sodium dithionite, both M- and B-DNIC are converted into the paramagnetic PF-02341066 cost form with a characteristic EPR signal at g(perpendicular to) = 2.01, g(parallel to) = 1.97 and g(aver). = 2.0. Both forms display similar absorption spectra with absorption bands at 960 and 640 nm and a bend at 450 nm. After oxidation by atmospheric oxygen, this situation is reversed, which manifests itself in the disappearance of the EPR signal at g(aver). = 2.0 and complete regeneration of initial absorption spectra of M- or B-DNIC with characteristic

absorption bands at 390 or 360 and 310 nm, respectively. Treatment of bovine serum albumin (BSA) solutions with gaseous NO in the presence of Fe2+ and cysteine yields BSA-bound M-DNIC (M-DNIC-BSA). After treatment with sodium dithionite, the latter undergo transformations similar to those established for low-molecular M-DNIC with glutathione. Based on the complete coincidence of the optical and the EPR characteristics of sodium dithionite-treated EPZ015666 mouse M- and B-DNIC and other

findings, it is suggested that sodium dithionite-reduced B-DNIC are subject to reversible decomposition into M-DNIC. The reduction and subsequent oxidation of M- and B-DNIC are interpreted in the paradigm of the current concepts of the initial electronic configurations of M- and B-DNIC (d(7) (Fe(NO)(2)(7)) and d(7)-d(7) (Fe(NO)(2)(7)-Fe(NO)(2)(7)), respectively). (C) 2013 Elsevier Inc. All rights reserved.”
“A central goal of protein design is to devise novel proteins for applications in biotechnology and medicine. Many applications, including those focused on sensing and catalysis will require proteins that recognize and bind to small molecules. Here, we show that stably folded alpha-helical proteins isolated from a binary patterned library of designed

sequences can be mutated to produce binding sites capable of binding a range of small aromatic compounds. Phosphatidylethanolamine N-methyltransferase Specifically, we mutated two phenylalanine side chains to alanine in the known structure of de novo protein S-824 to create buried cavities in the core of this four-helix bundle. The parental protein and the Phe -> Ala variants were exposed to mixtures of compounds, and selective binding was assessed by saturation transfer difference NMR. The affinities of benzene and a number of its derivatives were determined by pulse field gradient spin echo NMR, and several of the compounds were shown to bind the mutated protein with micromolar dissociation constants. These studies suggest that stably folded de novo proteins from binary patterned libraries are well-suited as scaffolds for the design of binding sites.”
“Smoking affects the general health of an individual, however, the red blood cells (RBCs) and their architecture are particularly vulnerable to inhaled toxins related to smoking.

To help with the screening of the A/H1N1pdm virus, rRT-PCR assays were also developed for detecting human seasonal A/H1N1 (H1 rRT-PCR assay) and A/H3N2 influenza viruses (H3 rRT-PCR assay). H1pdm, MRT67307 mouse H1, and H3 rRT-PCR assays were evaluated using in vitro-transcribed control RNA, isolated viruses,

and other respiratory pathogenic viruses, and were shown to have high sensitivity, good linearity (R(2) = 0.99), and high specificity. In addition, the improved H1pdm rRT-PCR assay could detect two viral strains of A/H1N1pdm, namely, A/Aichi/472/2009 (H1N1)pdm and A/Sakai/89/2009 (H1N1)pdm, which have mutation(s) in the probe-binding region of the hemagglutinin gene, without loss of sensitivity. Using the three rRT-PCR assays developed, Sonidegib mw 90 clinical specimens collected between May and October 2009 were then tested. Of these, 26, 20, and 2 samples were identified as positive for A/H1pdm, A/H3, and A/H1, respectively, while 42 samples were negative for influenza A viruses. The present results suggest that these highly sensitive and specific H1pdm, H1, and H3 rRT-PCR assays are useful not only for diagnosing influenza viruses,

but also for the surveillance of influenza viruses. (C) 2010 Elsevier B.V. All rights reserved.”
“Pain is an unpleasant sensory and emotional experience. The neural systems underlying the sensory component of pain have been studied extensively, but we are only beginning to understand those underlying the affective component of pain. Previously, we showed the pivotal role of noradrenergic transmission in the ventral part of the bed nucleus of the stria terminalis (vENST) in the negative

affective component of pain using a conditioned place paradigm. In this study, we examined the effect of Astemizole local administration of clonidine, an alpha(2)-adrenoceptor agonist, into the vBNST on noradrenaline release and on conditioned place aversion (CPA) induced by an intraplantar formalin injection in male Sprague-Dawley rats. In vivo microdialysis showed that the formalin-induced increase in the extracellular noradrenaline level within the vBNST was significantly suppressed by clonidine (100 mu M) perfusion through a microdialysis probe. Bilateral intra-vBNST injections of clonidine (1 and 10 nmol/side) dose-dependently attenuated formalin-induced CPA without reducing nociceptive behaviors. These results suggest that clonidine inhibits noradrenaline release by acting on alpha(2)-adrenoceptors located in the vENST and thereby attenuates pain-induced aversion. alpha(2)-adrenoceptors in the vENST play a pivotal role in the regulation of negative affective, but not the sensory, component of pain. (C) 2011 Elsevier Ltd. All rights reserved.

4, mimicking the in Torin 1 vivo pH environment of late endosomes. This triggered the release of the RNA whose arrival in the liposomal lumen was detected via in situ cDNA synthesis by encapsulated reverse transcriptase. Subsequently, cDNA was PCR amplified. At a low ratio between virions and lipids, RNA transfer was positively correlated with virus concentration. However, membranes became leaky at higher virus concentrations, which resulted in decreased cDNA synthesis. In accordance with earlier in vivo data, the RNA passes through the lipid membrane without causing gross damage to vesicles at physiologically

relevant virus concentrations.”
“Olfaction and gustation are important sensory modalities for locating food and for determining which foodstuffs to ingest. It is becoming apparent that there is a strong link between olfaction, gustation and metabolic control. Because endocrine Epigenetic Reader Domain inhibitor signaling in the naso-oropharynx is likely to influence food intake, satiety and general metabolic control, it is important to examine some of the major hormones that play an integral part in energy homeostasis. Here, we provide an overview of the main endocrine factors known to be present in the naso-oropharynx and discuss

their functional roles in maintaining metabolic function. Gaining a greater appreciation of how flavor perception is linked to peripheral metabolism could lead to novel therapeutic strategies for obesity and lifestyle-related diseases.”
“Agonists for the cannabinoid CB2 receptor are antinociceptive in several rodent models and several reports have suggested that the target for these drugs is CB2

expressed in the spinal cord pain pathway. After confirming the efficacy of a systemically delivered CB2-selective agonist, GW405833, we tested this hypothesis by administering the CB2 agonists GW405833 and JWH-133, via intrathecal cannulation, to the lumbar spinal cord of rats that had undergone chronic constriction injury to induce mechanical allodynia. We found that although the non-selective CB1/CB2 cannabinoid receptor agonist WIN55,212-2 reversed mechanical allodynia in both ipsilateral and contralateral hind paws, neither GW405833 Celastrol nor JWH-133 reversed mechanical allodynia. In addition, we investigated the expression of CB2 receptors in the neuropathic spinal cord using immunohistochemistry, Western blot and CB2 agonist stimulated [S-35]GTP gamma S binding. Although protein-based analysis of CB2 partially matched the results of earlier studies using the same antibody, we found evidence that this antibody may be insufficiently specific for the detection of CB2 in native tissue. Using [S-35]GTP gamma S binding assays, we found no evidence of functional CB2 in the spinal cord, in sham or surgery-treated tissue.

Preoperative indications and procedural and postimplantation outcomes were collected and analyzed. Technical success and clinical success were determined as defined by the Society of Vascular Surgery reporting standards.

Results:

Patients were predominantly male (87%) with a mean age of 77 years. The interval between the original endograft implantation to Renu treatment was 43.4 +/- 18.7 months. The indications for treatment were endoleak (n = 111), migration (n = 136), or both (n = 94). Technical success was 98.0% with two cases of intraoperative conversion and one case of persistent type IA endoleak. The median follow-up for the cohort was 45.0 months (range, 0-56 months; interquartile range, 25.0 months). Overall, 32 cases had treatment failures that P5091 in vitro included LY2109761 ic50 at least one of the following: death (n = 5), type I/III endoleak (n = 18), graft infection (n = 1), thrombosis (n = 1), aneurysm enlargement >5 mm (n = 9), rupture (n = 4), conversion (n = 9, with 7 after 30 days), and migration (n = 1). Overall, the clinical success for the entire cohort during the follow-up period was 78.8% (119/151).

Conclusions:

The postmarket registry data confirm that the Zenith Renu AAA Ancillary Graft can be used to treat endovascular repairs that failed due to proximal attachment failures. The salvage treatment with the Renu device had high technical success rate and resulted in clinical success in a majority of patients (78.8%). While failed endovascular repairs can be salvaged, a clinical failure in one of five patients still emphasizes the importance of patient and device selection during initial endovascular aneurysm

repair to ensure durable success. (J Vase Surg 2011;54:307-15.)”
“This study evaluated the Adenylyl cyclase effect of switching to quetiapine vs. risperidone continuation on sexual functioning in outpatients with risperidone-associated sexual dysfunction. Outpatients (n=42, age >= 18 years) with schizophrenia or schizoaffective disorder who experienced risperidone-associated sexual dysfunction were randomized to 6 weeks of double-blind risperidone continuation (mean dose=4.1 mg/day, S.D.=1.2) or quetiapine switch (mean dose=290.0 mg/day, S.D.=55.2) treatment. The five-item Arizona Sexual Experience Scale (ASEX) assessed sexual functioning at baseline and subsequently at weeks 2, 4 and 6. A mixed-model analysis of repeated measures included gender and baseline ASEX and PANSS scores as covariates. There was no significant Treatment Group effect for ASEX total scores and ASEX sub-items, and no significant Treatment Group X Period interaction for ASEX total scores and ASEX sub-items. Treatment Group effects were not significantly different in any of the prospective weeks for ASEX total scores and ASEX sub-items.