The mother, required to adjust to a biological clock of her infant that differs markedly from her own, becomes tired, frustrated, and angry, causing the infant to respond accordingly The resulting emotional burden, carried by both parties, might jeopardize the attachment processes, thus affecting future prospects of personal and social relationships Inhibitors,research,lifescience,medical of the child. At later stages of life, such a child has

difficulties following the school timetable of activities, fails to obtain a sufficient amount of sleep at night, loses concentration during the morning and early afternoon hours, and, eventually, falls behind other children in school Frequently, the abnormal sleep-wake cycle of individuals with CRSDs and the Inhibitors,research,lifescience,medical accompanying dysfunction at school or work are misattributed by parents, educators, psychologists, and other health care professionals to psychological rather than biological factors, such as laziness and low motivation. This attitude toward individuals with CRSDs, to which they are subjected since the early childhood Inhibitors,research,lifescience,medical or adolescence, adds psychological distress to the practical difficulties of coping with life and contributes to the development of personality disorders.2,53,56 CRSDs ami psychoactive medication Several cases of disrupted sleep-wake schedule as an latrogenie effect of psychoactive drugs

have been documented in the literature. Treatment with a typical neuroleptic, haloperldol,

in a patient with chronic schizophrenia was associated with an irregular sleep-wake cycle. Switching treatment to the atypical neuroleptic clozapine established a more Inhibitors,research,lifescience,medical organized and stable sleep-wake pattern and improved the clinical state of the patient.58 To further explore the relationship between type of drug and restactivity patterns, seven additional Inhibitors,research,lifescience,medical patients with schizophrenla were studied. Four of these patients received typical neuroleptics (flupentixol or haloperldol) and showed a variety of abnormalities in the daily rest-activity rhythm, eg, delayed circadlan phase syndrome, free-running sleepwake syndrome, and irregular sleep-wake pattern with a clrcabidlan component (BAY 73-4506 in vivo approximately L-NAME HCl 48 h). On the other hand, rest-activity cycles of those patients treated with atypical neuroleptic clozapine (three patients) were highly organized and synchronized with the environmental schedule.59 Similar effects were observed in a female patient with early-onset Alzheimer’s disease: when treated with haloperldol, her rest-activity patterns became completely arrhythmic; this was accompanied by marked worsening of the cognitive state. When haloperldol was replaced by clozapine, rapid normalization of the sleep-wake cycle occurred and cognitive functioning improved.

). Moreover, the dose, concentrations, and the time of exposure of a nanomaterial employed are essential. In effect, the efficiency of cellular uptake of nanomaterials and the resultant intracellular concentration may determine the cytotoxic potential. Elucidating the molecular mechanisms by which nanosized particles induce activation of cell death signalling pathways will be critical for the development of prevention strategies to minimize the cytotoxicity of nanomaterials. Unfortunately, in the literature, there are many conflicting data; the most plausible reason is certainly the discrepancy of nanomaterials

and experimental models Inhibitors,research,lifescience,medical engaged. Although some authors have recently alerted Cell Cycle inhibitor colleagues on these issues [3, 5, Inhibitors,research,lifescience,medical 8, 9, 150–152], it has not yet been put in place a guideline, generally accepted by the scientific community in the field, to address these matters. In fact, harmonization of protocols for material characterization and for cytotoxicity testing of nanomaterials Inhibitors,research,lifescience,medical is needed. In addition, parallel profiling of several classes of nanomaterials, combined with detailed characterization of their physicochemical properties,

could provide a model for safety assessment of novel nanomaterials [153]. During the past decade, owing to major technological advances in the field of combinatorial chemistry Inhibitors,research,lifescience,medical in addition to the sequencing of an ever increasing number of genomes, high-content chemical and genetic libraries have become available, raising the need for high-throughput screening (HTS) and high-content screening (HCS) approaches. In response to this demand, multiple conventional cell death detection methods have been adapted to HTS/HCS, and many novel HTS/HCS-amenable Inhibitors,research,lifescience,medical techniques have been developed [37, 154]. In the last years, several authors started to study the nanotoxicity with this tools and highlighted the potential of these approaches [9, 60, 75, 155–161]. An overall aim should identify HTS/HCS assays that

can be used routinely Oxalosuccinic acid to screen nanomaterials for interaction with the cell death modalities system. HTS/HCS may accelerated the analysis on a scale that commensurates with the rate of expansion of new nanomaterials but in any case is a first validation step, then it remains to confirm whether the same identified mechanisms in vitro are responsible for their in vivo toxicity. In conclusion, a multilevel-integrated uniform and consistent approach should contemplate for nanomaterial toxicity characterization. In spite of the recent advances in our understanding of cell death mechanisms and associated signalling networks, much work remains to be done before we can fully elucidate the toxicological behaviour of the nanomaterials as well as understand their participation in the determination of cell fate.

Material and Methods Participants

and assessments Participants were 56 individuals recruited from the University of Birmingham (UAB) area. Thirty-five of these participants were patients with DSM-IV (American Psychiatric Association. American Psychiatric Association. Task Force on DSM-IV 2000) schizophrenia or schizoaffective disorder (SZ), diagnoses Inhibitors,research,lifescience,medical established using patients’ medical Fulvestrant in vitro records and the Diagnostic Interview for Genetic Studies (Nurnberger et al. 1994), and recruited from UAB outpatient psychiatric clinics. Twenty-one HC were recruited from the community using flyers and advertisements in the University newspaper. Common exclusion criteria were major medical conditions, substance abuse within the past 6 months, previous serious head Inhibitors,research,lifescience,medical injury, a neurological disorder, previous loss of consciousness, pregnancy, or ferromagnetic material in the body. HC were also excluded for any current or lifetime significant (e.g., depression, anxiety) Axis I diagnosis. The study was approved by the Institutional Review Board of the University of Alabama at Birmingham, and all participants gave written informed consent. The study was conducted in compliance with the standards established by UAB’s Institutional Review Board and with the Code of Ethics Inhibitors,research,lifescience,medical of the World Medical Association. Participants received compensation between $92 and $99, depending on performance

on an unrelated task in the magnet. We used the Repeatable Inhibitors,research,lifescience,medical Battery of Neuropsychological Status (RBANS) (Randolph et al. 1998) to measure general cognitive function in all participants and the Brief Psychological Rating Scale (BPRS) (Overall and Gorham 1962) in patients to measure positive (conceptual

disorganization, hallucinatory behavior, and unusual thought content) and negative (emotional withdrawal, motor retardation, and blunted affect) mental status and symptoms (See Table 1 and Table S4 for demographic characteristics and cognitive and behavioral assessments for patients and controls). Table 1 Demographic data and clinical and Inhibitors,research,lifescience,medical behavioral measures for participants used in fMRI analyses Delay-discounting tasks We first tested participants in the laboratory on a DD task, modified from Kirby and colleagues (Kirby et al. 1999; Kishinevsky et al. 2012). Participants viewed the 108 trials of the laboratory DD task on a computer monitor; 96 trials secondly were divided equally between eight categories with differing trial k values, interspersed with 12 SMC trials, for which participants arbitrarily made a right or left button response (Fig. ​(Fig.1).1). Each trial consisted of a choice between a unique combination of an immediate reward (IR), ranging from $1 to $73, and a DR, ranging from $28 to $86, with delays (D) ranging from 1 to 116 days. All rewards were hypothetical. Choices were generated for the eight trial k’s by adjusting reward values and D using the hyperbolic function, IR = DR/(1 + kD) (Mazur and Coe 1987).

Variables that were quantified: number of attempts, duration

of the last attempt, and duration of all attempts in a session. An “attempt” is defined as an event where the animal activates (by breaking the beam) the MS close to the gap (MS2 or MS3 in Fig. 2) and a “successful attempt” is an event where the animal actually crosses over the gap to reach the other platform. The duration of a successful attempt (“duration of last attempt”) is from activation of the MS close to the gap on one side until the activation Inhibitors,research,lifescience,medical of the corresponding sensor on the other platform. “Duration of all attempts” includes the duration of the last attempt but also the duration during which MS2 or MS3 was activated but without the animal eventually crossing (thus the duration from MS2-ON until MS2-OFF and MS3-ON until MS3-OFF). In essence, these parameters will quantify how often and for how long time the animal explores the gap. Analysis Inhibitors,research,lifescience,medical of whisker kinematics The movement of the whisker was tracked and quantified essentially as previously described (Voigts et al. 2008). The area of the gap between the two platforms was monitored by a high-resolution Inhibitors,research,lifescience,medical infrared video camera (Allied Vision Technologies, PIKE 032B) with sampling frequency at 314 Hz at 640 × 300 pixels with resolution of 9.7 pixels/mm. Tracking

of the mouse position and whisker was done off-line on the recorded video sequences as described in Voigts et al. (2008). The algorithm is fully automatized and unsupervised and is implemented in the following steps: The

first 50 frames, where there was no mouse Inhibitors,research,lifescience,medical detected, were used as an average for background subtraction and normalization of the brightness level. Next, the target platform and the animals nose were detected by simple averaging and thresholding in the x-direction. Whiskers were tracked initially as vector fields of polar representation of similarity index extracted by anisotropy functions (i.e., finding the direction of invariance due to blurring and shifting). In a later stage, these paths were integrated and Inhibitors,research,lifescience,medical spline interpolated to spatially contiguous representations of whiskers. Time series of whisking angle were extracted by selleck chemicals llc computing the angle of the whisker’s fifth pixel from the base across frames. The angle was calculated in reference to the Rebamipide mean position of the tracked pixel for every sequence. The periods (peak to peak) of this oscillatory signal represented whisking cycles. Whisking cycles were divided into pro- and retraction based on the position of set points (points with zero angular velocity). Whisking amplitude was defined as the angular excursion of the whisker between two set points, respectively, protraction and retraction amplitude. Analysis of frequencies was done by using windowed Fast Fourier Transform of the zero padded time series of whisking angles.

Discussion It has been shown that HO-1 is an inducible enzyme, whose GDC-0449 manufacturer expression is often increased by those oxidative stresses, which produce reactive oxygen

species.3,14 In spite of the cytoprotective affects of HO-1 on healthy tissues following their exposure to harmful stimuli, it can also protect tumor cells. Such a protection can result in the progression Inhibitors,research,lifescience,medical of the disease. Different studies have shown that higher levels of HO-1 expression are associated with faster growth of tumors, as indicated by bigger volumes of nodules or by more numerous cancer cells.11,15 Although some studies have reported a selective decrease in the expression of HO-1 in a few malignant cells such as adenocarcinoma or tongue squamous carcinoma, most studies have shown that the expression of HO-1 is strongly up-regulated in various tumors. Therefore, it seems that HO-1 represent a molecular target in some cancers. The current Inhibitors,research,lifescience,medical study was designed to determine the expression pattern of HO-1 gene in five cancer cell lines that are highly prevalent in . Until now, only limited data are available on the expression of HO-1 in the cell lines investigated here. Among Inhibitors,research,lifescience,medical the cell line studied, HEPG2 cell line showed the highest expression of HO-1 based on the level of mRNA measured. The increased

expression of HO-1 mRNA in HEPG2 cell line in the present study is in agreement with the high levels of expression of HO-1 in tissues of hepatocellular carcinoma described by Doi and colleagues.16 Thus, based on these results, we suggest HEPG2 cell line is the best model for future analysis Inhibitors,research,lifescience,medical of biology and regulation of HO-1 in hepatocellular carcinoma cell lines. The gene of HO-1 was found by RT-PCR to be expressed in MCF7 cell line as well as in A549 cell line. Human lung adenocarcinoma A549 cells constitutively express HO-1, which help them to resist against toxic compounds Inhibitors,research,lifescience,medical and antitumor drugs.17 Concerning MCF7, our results are in line with the results obtained by Hill et al. who reported overexpression

of HO-1 protein in MCF-7 cells.18 A moderate level of HO-1 expression could be observed in myeloid leukemia-derived cell line K562. Given the up-regulation of HO-1 expression in myeloid leukemia cell line and based on the function of HO-1 as a survival factor in chronic myeloid leukemia,19 it can be suggested that there is an authentic Calpain pattern of HO-1 expression related to chronic myeloid leukemia. Based on our results the LS174T cell line was the only one amongst the investigated cancer cell lines to reveal no HO-1 expression. In contrast to our results, Fang and co-workers indicated that up-regulation of HO-1 expression in colon cancer was a main factor for resistance against anticancer therapy, since the HO-1 inhibitors or targeted knocking down of the HO-1 expression made the cultured tumor cell lines much more sensitive to anticancer therapy.20 This discrepancy could be due to difference in the colon cell lines.

For data

reported above the LDC, the interassay variability was <10% for all analytes measured. Statistical analyses All data analyses were conducted with SPSS, Version 17.0 (IBM Corporation, Armonk, NY) and JMP, Version 10.0 (SAS, Cary, NC). Significant P-values were ≤0.05 and P-values ≤ 0.10 were considered trends. Between-group analyses of age, education, and estimated cognitive reserve were conducted using t-tests; other demographic and clinical characteristics were categorical, so chi-square tests were used, or Fisher exact tests Inhibitors,research,lifescience,medical if cells had low frequencies (<5; Table 2). Mann–Whitney U-tests were used for between-group comparisons of neuropsychiatric symptom S3I-201 price severity (Depression-Total, Depression-Cognitive Affective Factor, Depression-Somatic Factor, Anxiety, Fatigue, Pain Severity, and Pain Interference) because questionnaire scores (except Anxiety) were not normally distributed (Table 2). Note that in Table 2 Mann–Whitney U-tests were conducted on the medians.

Inhibitors,research,lifescience,medical The percentages of immune factors ≥ the LDC were compared across Inhibitors,research,lifescience,medical groups with tests of two proportions, and the z and P-values are reported (Table 1). Between-group comparisons of plasma immune factor levels were computed with Mann–Whitney U-tests because distributions were not normal (transformations did not normalize the data), and the medians and interquartile ranges are reported (Table 1). Spearman’s rank correlations were used to assess the relationship between neuropsychiatric symptom severity and the number of immune factors that were ≥ the LDC, within the total sample and by group (Table 3). On the basis of reports in the literature (e.g., Hilsabeck et al. 2010) and on Myriad Rules Based Medicine, Inhibitors,research,lifescience,medical Inc.’s customized platform used for the analyses (i.e., Human InflammationMAP® v. 1.0), an increased inflammatory profile was defined as a greater number of factors ≥ the LDC. Table 2 Between-group comparisons of demographic data, clinical characteristics, and neuropsychiatric function in adults with (HCV+) and without (HCV−) hepatitis C1 Table 3 Bivariate correlations1

[r (P-values)] Inhibitors,research,lifescience,medical between number of plasma immune factors ≥ the not LDC2 and neuropsychiatric symptom severity in adults with (HCV+) and without (HCV−) hepatitis C Regression models were developed in order to find which combination of immune factors was significantly related to neuropsychiatric symptom severity on each of the seven neuropsychiatric variables within the total sample. Some variables had values that were undetectable. For the purpose of the analysis, these undetectable values were replaced with zeros. These undetectable values should not be confused with the LDC values used for Tables 1 through ​through3.3. Models were constructed with a backward selection linear regression of 33 immune factors (14 factors were invariant and detectable in 5% or less of the samples and were eliminated from analyses; Table 1).

10 In these studies, the cells survived well and differentiated or matured into authentic neurons in the two areas of the brain where neurogenesis normally occurs, the hippocampus and the olfactory bulb. However, the adult stem cells did not readily differentiate into neurons in any other areas. Interestingly, they did differentiate into astrocytes and oligodendrocytes in other areas. This behavior Inhibitors,research,lifescience,medical of adult stem cells that were expanded in culture and transplanted back to the adult brain contrasts with the behavior of fresh KU-0063794 order tissue derived from the fetal brain that has not been extensively expanded in

culture. Freshly dissociated cells from the fetal brain, if taken at the appropriate time and from the appropriate location, survive and differentiate quite readily into the types of neurons and glial cells from which they were obtained. In fact, the fetal cells have already matured somewhat and have committed themselves to a particular neuronal type; given minimal local environmental signals, they proceed toward their predetermined Inhibitors,research,lifescience,medical fates. These properties of fetal tissue make it more amenable to therapeutic applications. For example, in experimental treatments for PD, committed dopamine cells are being taken from fetal substantia nigra for transplantation; in HD treatment, fetal cells are being taken from fetal basal ganglia and transplanted into patients. The irony then is that

Inhibitors,research,lifescience,medical fetal tissue grafts are more mature than adult stem cells that have been isolated and expanded in culture. The problem with the adult brain is that, outside of the limited number of stem cells,

the adult cells are Inhibitors,research,lifescience,medical too mature and will not withstand the isolation and transplantation procedures; they have lost the youthfulness to survive Inhibitors,research,lifescience,medical and integrate into the adult brain. Part of the problem with fetal tissue is that there are so few cells available that arc at just the right age and in just the right location, which means that either many fetuses must be used for each transplantation or the cells must be put in culture to expand their number. However, once placed in culture, only the primitive fetal stem cells will divide extensively, and, as was seen with adult stem cells, these fetal stem cells are so immature that, unless the adult brain has all the necessary signals to direct them to a particular neural type, ic, a hippocampal neuron, then the cells will either others die or become glial cells or merely persist as stem cells. The way to make both fetal and adult stem cells more useful for therapeutic transplantation applications is to determine what the signals are in development that induce the stem cells to become a particular neuronal type, and then induce the stem cells toward that lineage in a culture dish just far enough so that, once they are subsequently transplanted to a particular part of the brain, they will continue toward that cell type and eventually integrate and replace the missing function.

The control group had persistent symptoms or side effects. Patients had high scores in the Neuropsychiatric Inventory (NPI), even though they were considered stable. However, these patients could not be considered refractory to psychotropic drugs. Only patients or family (caregivers) who had provided voluntary informed consent in writing to participate in this study, upon receiving a full explanation of the purpose and method of the study, were enrolled. Patient confidentiality was strictly adhered to, as were ethical considerations. Donepezil treatment was discontinued as follows: patients receiving 5 Inhibitors,research,lifescience,medical mg were discontinued

immediately at 0 week, whilst patients receiving 10 mg had their dosages reduced to 5 mg at 0 week, and were then withdrawn from donepezil at 2 weeks. The psychotropic equivalents calculation table of Inagaki and Inada was used as a guideline for psychotropic equivalents Inhibitors,research,lifescience,medical [Inagaki and Inada, 2006, 2012] when calculating

the baseline to postdose changes in the dosages of the concomitant psychotropic drugs. The subjects’ daily dosages were calculated in terms of risperidone or diazepam equivalents. Assessment methods The following clinical assessments were performed at baseline and 16 weeks by the psychiatrist who was providing the actual therapy. The outcome measures assessed were BPSD and cognitive function. BPSD was assessed using the NPI [Cummings et al. 1994] and Inhibitors,research,lifescience,medical cognitive function was assessed using the Mini Mental Examination (MMSE) [Folstein et al. 1975] because Inhibitors,research,lifescience,medical our facilities did not have the Severe Impairment Battery (SIB), which is one of the best evaluation tools for cognition. Selleckchem INCB018424 Statistical analysis Comparison of baseline

demographics – Fisher’s exact tests. Changes in symptoms and dosages of concomitantly used psychotropic drugs over time (within groups): paired t-tests. If the data did Inhibitors,research,lifescience,medical not show a normal distribution, then the Wilcoxon rank-sum test was used instead. Changes in symptoms and dosages of concomitantly used psychotropic drugs over time (between groups): Mann-Whitney U test. The significance level was p < 0.05 in all analysis. Results No significant differences were observed between the donepezil treatment discontinuation group and the control group in the baseline NPI total score, baseline MMSE score, mean daily dose of the previous Non-specific serine/threonine protein kinase treatment drug, mean duration of illness or the mean age of the patients (Table 1). The mean duration of donepezil treatment before the trial started was 64.9 ± 31.0 months. Table 1. Subject characteristics. Because all patients had a baseline score of ≤5 on the MMSE, they were all inpatients or in 24-hour care, with advanced or severe AD. Therefore, they also had difficulty communicating with the staff. Significant decreases were found in the donepezil treatment discontinuation group in the NPI total score and two NPI subscales, agitation and irritability.

Nicotine replacement therapies Nicotine replacement therapies (NRT) are designed to replace nicotine obtained through smoking in order to attenuate tobacco withdrawal symptoms and improve smoking cessation outcomes. There are currently five Food and Drug Administration (FDA)-approved NRT products, which include: the transdermal patch, gum, lozenge, inhaler, and nasal spray. These products are available over-the-counter or by prescription. They can be

given alone or taken in conjunction with antidepressants like bupropion in order to alleviate Inhibitors,research,lifescience,medical acute with-drawal symptoms and sustain abstinence. A small dose of nicotine in these products allows the patient to reduce nicotine withdrawal symptoms after the patient has stopped smoking. Patients are often counseled to quit, Inhibitors,research,lifescience,medical provided options for treatment, and helped to establish a quit date. On the quit date the NRT is started and other forms of tobacco use are stopped.6 Choice of specific NRT typically depends on the patient’s preference, the side-effect profile, and the route of administration.7 The nicotine transdermal patch is available in 16- Inhibitors,research,lifescience,medical or 24- hour delivery systems. Recommended duration of use is 6 to 12

weeks, with a tapering of the patch dose over that period. Patients usually start with a high-dose patch (21 or 22 mg); however, an intermediate-dose patch (11 or 14 mg) is available for those who smoke fewer than 15 cigarettes per day.5 Though patients usually develop tolerance to common side effects, they may experience insomnia, nausea, and vivid dreams. Skin irritation can also occur, and is usually alleviated with rotation of the patch placement site.8-11 The nicotine patch can also be utilized in combination with other NRT, such as the gum, which increases Inhibitors,research,lifescience,medical its efficacy in treatment-resistant cases.12 Nicotine polacrilex gum and lozenges are available Inhibitors,research,lifescience,medical over- the-counter as aids in smoking cessation in 2 and 4 mg doses of nicotine. The 4-mg dose is recommended for heavy smokers (>25 cigarettes per day).8,13,14 The recommended Cyclosporin A dosage of nicotine gum is to use one piece every 1 to 2 hours.6 The nicotine lozenge should be sucked on rather than chewed. The almost lozenge delivers

about 25% more nicotine than the gum, since some nicotine is retained in the gum and the lozenge is dissolved completely.15 The dose can be tapered over 6 to 12 weeks by either decreasing the gum or lozenge dose from 4 mg to 2 mg or by increasing the time between doses,6 with peak concentrations of nicotine absorbed through the buccal mucosa achieved in 15 to 30 minutes.16,17 Nicotine absorption can be blunted with use of acidic beverages; therefore, coffee, juices, and soda should be avoided immediately before or during NRT use.18 Side effects of the gum may include jaw soreness or difficulty chewing.13,19 The lozenge offers an alternative to gum but also may elicit side effects such as nausea, heartburn, and mild throat or mouth irritation.

As is so often the case in psychopharmacology, backward engineering of the mechanism of action has been used to try to understand both the drugs’ efficacies and any underlying dysfunction. In such a scenario, our current pharmacological reality, it is perhaps understandable that our initial attempts to treat bipolar depression were based on unipolar models and that the current Inhibitors,research,lifescience,medical therapeutic arsenal is often inadequate. Nevertheless, the pharmacological reverse engineering of existing medications and molecular biology are opening up better understanding of intracellular secondary messenger systems

and putative dysfunctional enzymatic components, such as inositol monophosphatase (IMPase) and glycogen synthase kinase 3 (GSK-3),

that might prove more efficacious future targets for treatment [O'Brien and Klein, 2009]. The time and cost of the development of such agents will be enormous, but until this happens there is no reason why clinical practice should not follow the best current evidence. Although there is some Inhibitors,research,lifescience,medical conflict in the literature about appropriate pharmacological treatment and a lack of clear Inhibitors,research,lifescience,medical and consistent guidelines, several clear themes emerge. Although antidepressants are by far the most commonly prescribed drug class for such patients, there is no good evidence for their use in monotherapy and very little to support their use to augment other treatments beyond the olanzapine–fluoxetine combination. In both acute and longer-term work, there is growing evidence for both mood stabilizers and Inhibitors,research,lifescience,medical antipsychotics, and within these PFT�� classes lamotrigine and quetiapine respectively are showing statistically superior efficacy. Further work is needed: Inhibitors,research,lifescience,medical better clinical guidance and psychoeducation of both patients and clinicians of this serious but treatable condition are required. Furthermore, there is a need for more

RCTs in this area, particularly covering the areas of bipolar II disorder and longer-term treatment, which have to date received less attention. Finally, whilst most trials have compared an active drug with placebo, direct comparative trials between postulated treatments are needed. Footnotes This work received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. old The author declares no conflict of interest in preparing this article.
Objective: Medication errors are a common cause of avoidable morbidity, and transfer between clinical settings is a known risk factor for such errors. Medicines reconciliation means there is no unintended discrepancy between the medication prescribed for a patient prior to admission and on admission. Our aim was to improve the quality of practice supporting medicines reconciliation at the point of admission to a psychiatric ward.