9 ± 54%), but no concentration gradient was detected between prox

9 ± 54%), but no concentration gradient was detected between proximal and distal dendrites. In conclusion, the density of KCC2 in hippocampal principal cells increases along the axo-somato-dendritic axis with cell type-specific distribution profiles within the dendritic tree. “
“Balgrist University Hospital, University of Zurich, Zurich, Switzerland Chondroitin sulphate proteoglycans (CSPGs) are extracellular matrix molecules whose inhibitory activity is attenuated by the enzyme chondroitinase ABC (ChABC). Here we assess whether CSPG

degradation can promote compensatory sprouting Kinase Inhibitor Library in vitro of the intact corticospinal tract (CST) following unilateral injury and restore function to the denervated forelimb. Adult C57BL/6 mice underwent unilateral pyramidotomy and treatment with either ChABC or a vehicle control. Significant impairments in forepaw symmetry were observed following pyramidotomy, with injured mice preferentially using their intact paw during spontaneous vertical exploration of a cylinder. No recovery on this task was

observed in vehicle-treated mice. However, ChABC-treated mice showed a marked recovery of function, with forelimb symmetry fully restored by 5 weeks post-injury. Functional recovery was associated with robust sprouting of the uninjured CST, with numerous axons observed crossing the midline in the brainstem and spinal cord and terminating in denervated grey matter. CST fibres in the denervated side of the spinal cord following GPCR Compound Library order ChABC treatment were closely associated with the synaptic marker Tau-protein kinase vGlut1. Immunohistochemical assessment of chondroitin-4-sulphate revealed that CSPGs were heavily digested around lamina X, alongside midline crossing axons and in grey matter regions where sprouting axons and reduced peri-neuronal net staining

was observed. Thus, we demonstrate that CSPG degradation promotes midline crossing and reinnervation of denervated target regions by intact CST axons and leads to restored function in the denervated forepaw. Enhancing compensatory sprouting using ChABC provides a route to restore function that could be applied to disorders such as spinal cord injury and stroke. “
“Traumatic brain injury (TBI) is a major risk factor for the subsequent development of epilepsy. Currently, chronic seizures after brain injury are often poorly controlled by available antiepileptic drugs. Hypothermia treatment, a modest reduction in brain temperature, reduces inflammation, activates pro-survival signaling pathways, and improves cognitive outcome after TBI. Given the well-known effect of therapeutic hypothermia to ameliorate pathological changes in the brain after TBI, we hypothesized that hypothermia therapy may attenuate the development of post-traumatic epilepsy and some of the pathomechanisms that underlie seizure formation.

At these two killer toxin concentrations, compounds known

At these two killer toxin concentrations, compounds known

to contribute to the ‘Brett’ character of wines, such as ethyl phenols, were not produced. Thus, purified Kwkt appears to be a suitable biological strategy to control Brettanomyces/Dekkera yeasts during fermentation, wine ageing and storage. The metabolism of Dekkera/Brettanomyces yeasts has significance in the production of foods and beverages in various industries, and especially in winemaking (Guerzoni & Marchetti, 1987; Renouf & Lonvaud-Funel, 2007). As these yeasts can metabolize hydroxycinnamic acids into their vinyl and ethyl derivatives, they are considered spoilage yeasts, and they can represent a significant problem in the cellar, and hence during wine ageing and storage (Fugelsang & Zoecklein, 2003). Depending Alvelestat cell line on the carbon and energy sources under winemaking conditions (Chatonnet et al., 1995; Dias et al., 2003), Brettanomyces/Dekkera yeasts can also produce compound associated with unpleasant odours and tastes that can deeply affect wine aroma (Fugelsang, 1997). Indeed, production of 4-ethyl phenols and volatile acidity have often been related to wine affected by Dekkera bruxellensis

(Loureiro & Malfeito-Ferreira, check details 2003). For all these reasons, Brettanomyces/Dekkera yeasts are considered a major cause of wine spoilage (Fugelsang, 1997; Loureiro & Malfeito-Ferreira, 2003). Currently, some of the procedures that are being applied to avoid the risks of development of Brettanomyces/Dekkera yeasts in wineries and wines [such as microfiltration of wine, increased sulphur dioxide (SO2) concentrations] are not particularly appropriate for use during wine ageing. This has led to increased interest Farnesyltransferase in the exploration of yeasts that can counteract the activities of these undesired microorganisms in wine (Comitini et al., 2004a). Investigations of killer yeasts as producers of mycocins that can neutralize the activities of undesired microorganisms in wines represent an interesting strategy for

the control and/or elimination of undesirable contaminating yeasts. Indeed, in recent years, such biological control approaches have been considered more desirable to the alternative of using chemical agents. Thus, biological control with yeasts and their metabolites has recently emerged as a valid alternative to the application of fungicides (Petersson & Schnürer, 1995; Druvefors & Schnürer, 2005; Druvefors et al., 2005). In a previous study (Comitini et al., 2004a), we proposed this use for Kluyveromyces wickerhamii and Pichia anomala killer yeasts, which have a wide range of activities against Dekkera/Brettanomyces yeast strains. In particular, to elucidate the properties of Pikt and Kwkt in relation to their possible use in winemaking, they were subjected to biochemical characterization to determine their proteinaceous nature, wine temperature and pH ranges as well as fungistatic and fungicidal concentrations.

Mefloquine prescriptions increased by 38% from 2005 to 2008 befor

Mefloquine prescriptions increased by 38% from 2005 to 2008 before decreasing by 17% from 2008 to 2009. The number of prescriptions for atovaquone plus proguanil has trebled during the period. Prescriptions for proguanil have dropped over 90% from 2005 to 2009. The diaminopyrimidines, pyrimethamine-containing antimalarials, have mostly been removed from the prescription drug list. Prescriptions for chloroquine have reduced by 66% from 2005 to 2008 and chloroquine was only available on special access from 2009. Artemether

plus lumefantrine combination has been used learn more in relatively small quantities and only on special authority from 2007 to 2009. Quinine prescriptions have fallen by 60%. Although a considerable quantity of doxycycline

was prescribed, it was unknown how much was intended for malaria chemoprophylaxis. The prescription of antimalarials in Australia was consistent with the national guidelines with the most commonly prescribed antimalarials being atovaquone plus proguanil, mefloquine, and most likely doxycycline. Other antimalarials previously used for chemoprophylaxis have continued to be removed Opaganib cost from the prescriber list between 2005 and 2009. The prescriptions of quinine may be becoming displaced by newer antimalarial drugs for treatment, but this needs further investigation. It was reported that there were 216 million cases of malaria worldwide in 2011, resulting in approximately 655,000 deaths.[1] Australia has been declared malaria-free since 1981; however, during the period 2005 to 2009, 3,411 cases of imported malaria (average = 682/y) were notified in Australia (Figure 1).[2-6] Malaria due to Plasmodium falciparum accounted for nearly half of recorded Cyclooxygenase (COX) cases in Australia during this period.[2-6] Fortunately, deaths due to malaria in Australia are relatively

rare with only one death reported in a study of 482 cases of imported malaria in Western Australia from 1990 to 2001,[7] and none were reported for the period 2005 to 2009.[2-6] It is known that taking chemoprophylaxis decreases the severity and frequency of death from malaria due to P falciparum compared to those who take no prophylaxis.[8] A comprehensive review of malaria in Australia has been published elsewhere.[9] Therapeutic Guidelines-Antibiotic, updated every few years in Australia, provide recommendations on the selection of malaria chemoprophylaxis and treatment.[10, 11] Previous studies in Australia have suggested that trends in the prescription of antimalarials are influenced by various factors, including the prevailing malaria chemoprophylaxis guidelines in Australia.[12, 13] Recent guidelines have recommended a number of options for malaria chemoprophylaxis, including chloroquine, doxycycline, melfoquine, and atovaquone plus proguanil, depending on the resistance patterns of the malaria likely to be encountered by the traveler.

Options to decrease time to therapy once malaria is suspected inc

Options to decrease time to therapy once malaria is suspected include stocking antimalarials in the ED, access to rapid diagnostic tests in rural areas, and possible presumptive antimalarial therapy. This study reinforces that clinicians need to consider malaria in the diagnosis of a febrile child with an appropriate travel history, and to utilize appropriate resources for timely diagnosis and therapy. Immigration to regional Manitoba communities has been increasing, with 23.3% more immigrants settling outside of Winnipeg Nutlin 3 from 2007 to 2008; therefore, clinicians in both urban and rural communities may encounter children with malaria.[7] Our study

would seem to indicate that frontline clinicians and residents in Manitoba may require ongoing education and formal academic teaching (resident academic days, province-wide Pediatric Grand Rounds) on the diagnosis and management of clinical malaria, rather than a focus on screening and presumptive treatment

Small molecule library solubility dmso of migrants. Ongoing reinforcement could include communication via the bulletin of the provincial medical college sent to all physicians, done by our group initially. As pre-travel services are not covered by provincial health plans in Canada, the associated costs may be a barrier for travelers obtaining appropriate advice regarding malaria prevention, especially VFRs. Clinicians in Canada should advocate for the coverage of pre-travel care, especially for children. S. T. F. was supported by MTMR9 a clinical postdoctoral fellowship from the Manitoba Institute of Child Health. The other authors state they have no conflicts of interest to declare. “
“While highly active antiretroviral therapy (HAART) decreases long-term morbidity and mortality, its short-term

effect on hospitalization rates is unknown. The primary objective of this study was to determine hospitalization rates over time in the year after HAART initiation for virological responders and nonresponders. Hospitalizations among 1327 HAART-naïve subjects in an urban HIV clinic in 1997–2007 were examined before and after HAART initiation. Hospitalization rates were stratified by virological responders (≥1 log10 decrease in HIV-1 RNA within 6 months after HAART initiation) and nonresponders. Causes were determined through International Classification of Diseases, 9th Revision (ICD-9) codes and chart review. Multivariate negative binomial regression was used to assess factors associated with hospitalization. During the first 45 days after HAART initiation, the hospitalization rate of responders was similar to their pre-HAART baseline rate [75.1 vs. 78.8/100 person-years (PY)] and to the hospitalization rate of nonresponders during the first 45 days (79.4/100 PY).

Dubinsky et al[22] demonstrated a correlation between 6TGN level

Dubinsky et al.[22] demonstrated a correlation between 6TGN levels and remission, as well as a correlation between higher 6TGN levels and leucopenia. This correlation has also been documented in pediatric acute lymphoblastic leukemia[35] as well as heart and renal transplantation literature.[36, 37] High 6TGN

levels have also been associated with an increased risk of any adverse event. In a retrospective Selleckchem Pifithrin �� Swedish study of 364 IBD patients, 41% of patients with a 6TGN above 400 experienced an adverse event (P = 0.005), including myelotoxicity and gastrointestinal disturbances.[38] Prior to the advent of thiopurine metabolite testing, standard clinical practice suggested that, if a patient on thiopurine therapy develops hepatotoxicity

(as evidenced by elevated transaminases and/or cholestatic enzymes with or without a rise in bilirubin), the offending agent should be withdrawn and a patient should be labelled as having an ‘allergy’ to thiopurines. As such, thiopurines could no longer be considered as a potential therapeutic option again for that patient. The Canadian group that originally discovered the minimum therapeutic threshold for 6TGN found that high levels of 6MMP were associated with hepatotoxicity in the form of elevated levels of hepatic transaminases. In total, 16 of 92 patients (17%) developed hepatotoxicity. Median 6MMP levels in patients with hepatotoxicity were 5463, compared with 2213 for those with normal liver enzymes. If 6MMP levels were above 5700, the risk of hepatotoxicity EPZ6438 increased by a factor of three (18% vs. 6%). There was no correlation with 6MMP levels and therapeutic response or 6MP dose. There was also no correlation between 6TGN levels and hepatotoxicity.[22] triclocarban Patients who preferentially

produce 6MMP rather than 6TGN are known as ‘thiopurine shunters’ (see below). This group, characterized by having a 6MMP to 6TGN ratio > 20, is at risk for hepatotoxicity and possibly refractoriness to standard thiopurine therapy. There are two major drug interactions with thiopurines with direct relevance to metabolite testing. The first is with allopurinol, a potent inhibitor of XO, one of the critical enzymes involved in thiopurine metabolism. Allopurinol has been the mainstay of treatment for gout for many years.[39] Traditional teaching has dictated that because the combination of full dose allopurinol and thiopurines causes profound myelosuppression, the two drugs should never be given in combination.[38] More recently, the effect of allopurinol on thiopurine metabolism is being used to advantage (see below). The second interaction is with 5-aminosalicylates (balsalazide, mesalasine, olsalazine or sulphasalazine), used frequently in IBD patients and sometimes in rheumatological conditions. Studies in vitro have shown that sulphasalazine and olsalazine can inhibit TPMT,[40, 41] suggesting that concomitant 5ASA may increase 6TGN levels and potentially lead to myelosuppression.

Dubinsky et al[22] demonstrated a correlation between 6TGN level

Dubinsky et al.[22] demonstrated a correlation between 6TGN levels and remission, as well as a correlation between higher 6TGN levels and leucopenia. This correlation has also been documented in pediatric acute lymphoblastic leukemia[35] as well as heart and renal transplantation literature.[36, 37] High 6TGN

levels have also been associated with an increased risk of any adverse event. In a retrospective Lumacaftor supplier Swedish study of 364 IBD patients, 41% of patients with a 6TGN above 400 experienced an adverse event (P = 0.005), including myelotoxicity and gastrointestinal disturbances.[38] Prior to the advent of thiopurine metabolite testing, standard clinical practice suggested that, if a patient on thiopurine therapy develops hepatotoxicity

(as evidenced by elevated transaminases and/or cholestatic enzymes with or without a rise in bilirubin), the offending agent should be withdrawn and a patient should be labelled as having an ‘allergy’ to thiopurines. As such, thiopurines could no longer be considered as a potential therapeutic option again for that patient. The Canadian group that originally discovered the minimum therapeutic threshold for 6TGN found that high levels of 6MMP were associated with hepatotoxicity in the form of elevated levels of hepatic transaminases. In total, 16 of 92 patients (17%) developed hepatotoxicity. Median 6MMP levels in patients with hepatotoxicity were 5463, compared with 2213 for those with normal liver enzymes. If 6MMP levels were above 5700, the risk of hepatotoxicity Navitoclax increased by a factor of three (18% vs. 6%). There was no correlation with 6MMP levels and therapeutic response or 6MP dose. There was also no correlation between 6TGN levels and hepatotoxicity.[22] Org 27569 Patients who preferentially

produce 6MMP rather than 6TGN are known as ‘thiopurine shunters’ (see below). This group, characterized by having a 6MMP to 6TGN ratio > 20, is at risk for hepatotoxicity and possibly refractoriness to standard thiopurine therapy. There are two major drug interactions with thiopurines with direct relevance to metabolite testing. The first is with allopurinol, a potent inhibitor of XO, one of the critical enzymes involved in thiopurine metabolism. Allopurinol has been the mainstay of treatment for gout for many years.[39] Traditional teaching has dictated that because the combination of full dose allopurinol and thiopurines causes profound myelosuppression, the two drugs should never be given in combination.[38] More recently, the effect of allopurinol on thiopurine metabolism is being used to advantage (see below). The second interaction is with 5-aminosalicylates (balsalazide, mesalasine, olsalazine or sulphasalazine), used frequently in IBD patients and sometimes in rheumatological conditions. Studies in vitro have shown that sulphasalazine and olsalazine can inhibit TPMT,[40, 41] suggesting that concomitant 5ASA may increase 6TGN levels and potentially lead to myelosuppression.


“To measure, in vitro, the pH and titratable acidity (TA)


“To measure, in vitro, the pH and titratable acidity (TA) of various soft drinks

and to assess the erosive effect of smoothies using an in situ model. The in vitro phase of this study included measuring the inherent pH of six different commercially available smoothies, diet coke, and citric acid 0.3% (positive control) using a pH meter. The TA was determined by titration with NaOH. In the second part of the study, an in situ model was used. An upper removable appliance capable of retaining two enamel slabs was constructed and worn by 14 volunteers. The drinks under test were Innocent® strawberries and banana smoothie and citric acid. Volunteers were instructed to dip the appliance in the Z-VAD-FMK price test solutions extra-orally five times daily for 2 min each time for 21 days. Measurements of enamel loss were made by surface profilometry and microhardness. Diet Coke was found to be the most acidic drink (pH 2.61), whereas Innocent® mangoes and passion fruit smoothie showed to be the least (pH 3.9). With regard to TA, Innocent® blackberries, strawberries, and blackcurrant smoothie had the highest TA requiring 10.8 mol of NaOH to reach pH 7.0, whereas citric acid

required only 3.1 mol of NaOH to reach the same pH value. Surface profilometry and microhardness testing revealed that selleck chemicals citric acid caused a statistically significantly greater tooth surface loss compared with smoothie after 21-day pH cycling protocol. Smoothies are acidic and have high TA levels. Innocent® strawberries and banana smoothie had an erosive potential to the teeth. However, its Pregnenolone erosive effect was significantly less compared with citric acid after 21-day pH cycling protocol using an in situ model. “
“International Journal of Paediatric Dentistry 2011 Background.  Morphological and dentofacial alterations have been attributed to impaired respiratory function. Objective.  To examine the influence of mouth breathing (MB) on children facial morphology before and after adenoidectomy or adenotonsillectomy. Methods.  Thirty-three MB children who restored

nasal breathing (NB) after surgery and 22 NB children were evaluated. Both groups were submitted to lateral cephalometry, at time 1 (T1) before and at time 2 (T2) 28 months on average postoperatively. Results.  Comparison between the MB and NB groups at T1 showed that mouth breathers had higher inclination of the mandibular plane; more obtuse gonial angle; dolichofacial morphology; and a decrease in the total and inferior posterior facial heights. Twenty-eight months after the MB surgical intervention, they still presented a dolichofacial morphologic pattern. During this period, MB altered the face growth direction and decreased their mandible plane inclination, with reduction in the SN.GoGn, PP.MP, SNGn, and ArGo.GoMe parameters as well as an increase in BaN.PtGn. Conclusion.

In the NNRTI group, two patients (patients 11 and 17) of 10 who r

In the NNRTI group, two patients (patients 11 and 17) of 10 who received at least 12 months of EFV-based HAART showed new key mutations (Y188Y/H and M184M/I), while one (patient 36) in the PI

group and one naïve patient (patient 3) had a new key RT mutation (M184I). All new key mutations except one (in patient 36) were only present in the CD4 cells. Patient 36, who received d4T, ABC and LPV/r combination therapy for 1 year before changing to a 3TC, TDF and LPV/r regimen, showed a new key mutation (M184I) after 18 months of follow-up find more in the plasma RNA but not in the proviral DNA. Thus, monitoring of the evolution of drug resistance mutations in treated patients by direct sequencing of HIV-1 proviral DNA in purified CD4

cells revealed new mutations, with moderately good agreement between pre- and post-treatment DNA mutation patterns. In patients who remained treatment-naïve, almost no evolution was observed in mutations detected in plasma RNA or cell DNA. After therapy initiation we noted the persistence of HIV-1 drug resistance mutations in proviral DNA from purified CD4 cells R428 order compared with plasma viral RNA at baseline. In our small cohort, 30 of 32 treated patients showed an undetectable plasma viral load after at least 12 months and up to 44 months of follow-up. Patients with pre-existing resistance mutations had a good response to all types of HAART, but none of them underwent combination therapy with the targeted drug. One interesting question was whether the Idoxuridine DNA test might be useful to guide therapy switches in patients with suppressed viral load. This was addressed by comparing the prevalences of detected mutations in pretreatment

RNA and post-treatment DNA (59 and 78%, respectively). A statistically significant proportion of mutations (19%) were detected in the DNA compared to the pretreatment RNA. The data demonstrated that sequencing DNA is possible and the recommended RNA sequencing might miss some mutations. In the comparison of pretreatment RNA with post-treatment DNA using kappa statistics, a moderately good agreement was found in terms of mutations detected and only a fairly good agreement in terms of predicting drug activity because of the accumulation of new mutations in the DNA. In patients with detectable viraemia, no new DNA mutations were detected and the viral loads were too low to enable RNA genotyping to be performed (patients 16, 19 and 21 with 556, 150 and 80 copies/mL, respectively). Therefore, we could not conclude that the standard method had underestimated the accumulation of mutations as the test was only possible on cell DNA samples. Transmission of drug-resistant HIV-1 strains and reduced susceptibility of viruses derived from untreated patients have been documented.

mutans Thus, we searched for an indicator for the establishment

mutans. Thus, we searched for an indicator for the establishment of S. mutans. Methods.  To evaluate the changes caused by the establishment of S. mutans in the microbiota of the infant oral cavity, we monitored changes in the oral microbiota of two pre-dentate infants over a 3-year period and in a cross-sectional study of 40 nursery school-aged children by cultivation of saliva on nonselective blood agar, Mitis-Salivarius agar, and Mitis-Salivarius agar supplemented with bacitracin combined with identification of selected isolates. Results.  Two longitudinal observations suggested that the establishment of S. mutans would induce a decrease in α-haemolytic

bacteria in the microbial population of the oral cavity. This suggestion was compensated with the results of cross-sectional study, and it was revealed that the Thiazovivin establishment of 103 CFU/mL of mutans streptococci in saliva might be predicted

by a microbiota comprising less than approximately 55% of α-haemolytic. Conclusion.  Decrease in the proportion of α-haemolytic bacteria in saliva of infant was found to be applicable as an indicator to predict the establishment of S. mutans and to assess dental caries risk as a background for planning of dental care and treatment in the infants before infection with S. mutans. “
“Purpose.  The aim of this study was to evaluate an infant oral health education programme, using a pre–post test design, for parents attending a paediatric clinic. Methods.  The subjects were parents

attending the well baby appointments Venetoclax mw at 3, 6, and 9 months of age. The study participants were men and women, all with an infant between 3 and 12 months of age. A 16 question assessment in the form of a questionnaire was completed immediately before and after the introduction of a 30 min Reverse transcriptase educational intervention in the form of a PowerPoint presentation and a video of infant oral hygiene for parents. The parents completed the questionnaire twice (pre–post test design) in the same visit. Recruited parents attended only one presentation. The presentation educated parents about infant oral health and provided anticipatory guidance. Results.  Forty-seven parents or caretakers participated in the study. On the pre-test 28% had a score of 70% or less, and on the post-test 87% got a score of 88% or better. On the pre-test, 72% had a score of 70% or higher, and on the post-test 87% got a score of 88% or higher. Most parents (80%) reported that the presentation was helpful and indicated that the information would change the way they care for their baby’s teeth at home. Conclusion.  This study demonstrated the effectiveness of a 30 min PowerPoint and Video presentation in improving the oral health knowledge of parents caring for an infant.

Available from: http://wwwrpharmscom/promoting-pharmacy-pdfs/im

Available from: http://www.rpharms.com/promoting-pharmacy-pdfs/imt—nov-2012—it-principles.pdf 2. Scottish Government (2013) Everyone Matters: 2020 Workforce Vision. Available from: http://www.scotland.gov.uk/Topics/Health/NHS-Workforce/Policy/2020-Vision R. Elsona,b, A. Blenkinsoppa, H. Cooka, J. Kayb, J. Silcocka aUniversity of Bradford, Bradford, UK, bDocaster Royal Infirmary, Doncaster, UK A telephone survey across four patient groups was used to determine patients’; knowledge of newly

started medication. Patients receiving ‘usual care’ in this study reported that they were not provided with information at discharge on how to take two-thirds of newly-prescribed medicines. Counselling patients on discharge

and post-discharge MURs can improve patients’; knowledge of their BKM120 price medicines. Post-discharge MURs were under-utilised. Helping patients to take medicines properly and safely is key to improving patient outcomes, improving quality and reducing waste in the NHS.1 Patients who are discharged from hospital often have new medicines prescribed and problems known to occur after discharge need to be addressed. Patient-centred advice has been shown to improve adherence to medicines.2 However little is known about the effects of current practice (nurse or doctor counselling) compared with targeted counselling from hospital pharmacists and MURs from community pharmacists. A telephone survey was carried out by the lead researcher isocitrate dehydrogenase inhibitor of 101 patients enrolled during May 2013 to September 2013, two weeks after their discharge from one NHS hospital with one or more new medicines. Patients were allocated sequentially

to one of four groups; 1) Hospital pharmacist counselling, 2) Usual care (nurse or doctor counselling) + MUR, 3) Pharmacist counselling + MUR or 4) Usual care only. Patients who did not manage their own medication or those who were not able to provide consent were excluded from the study. The questions, which were piloted prior to the study, covered knowledge of: what the medicine was for, how to take it, side-effects, tests and monitoring. The Chi-squared test was used to compare the intervention Fludarabine groups with usual care. Likert-type scales were used to assess patients’; knowledge. Open questions were included to enquire about patients’; opinions on the service provided and the information they had received. A sample size calculation was not required as this was an exploratory study. Ethical and research governance approvals were obtained from the NHS. In total 84 of 101 patients recruited completed the study and were prescribed 154 new medicines. Age, gender and number of medicines were similar across the groups. Patients were able to recall the name of 130 (84.4%) 95% CI [76.6%, 92.2%] new medicines prescribed and could state what 127 (82.5%) 95% CI [74.4%, 90.6%] were for.