5 mmol/L for etravirine and −0.6 mmol/L for placebo (Fig. 3b). There was a large difference between arms in the duration of treatment, with a median exposure of 96.0 weeks for the etravirine group and 69.6 weeks for placebo (Table 3). The frequency of AEs (regardless mTOR inhibitor of severity or causality) adjusted for treatment duration was similar between the treatment groups or lower for etravirine, with the exception of rash (Table 3). A significant difference in the frequency of rash-related AEs between treatment arms remained after adjusting for the difference in treatment exposure: 13.7 patients for etravirine vs. 9.3 patients for placebo per 100 patient-years of exposure [relative risk (95% CI) 1.48 (1.02–1.95)].

The adjusted frequency of nervous system AEs of interest was lower in the etravirine group than in the placebo group [12.6 vs. 16.8 per 100 patient-years exposure, respectively; relative risk (95% selleck CI) 0.75 (0.54–0.96)]; that of psychiatric AEs of interest was also lower [13.3 vs. 16.4 per 100 patient-years exposure, respectively; relative risk (95% CI) 0.81 (0.59–1.03)]. The findings from this week 96 pooled analysis of the DUET trials were consistent with previous results reported at weeks 24 and 48. The frequency of AEs of interest was similar in both treatment groups, with the exception of rash, which occurred more commonly in the etravirine group, in line with previous results [3, 6, 7]. These data support earlier findings

that rash events occurring in patients receiving etravirine are, however, generally mild to moderate in severity and normally resolve with continued treatment. Of note, in this analysis, there were no new discontinuations because of rash since the previous analysis at week 48.

However, with broader use of etravirine following marketing approval, severe cutaneous and hypersensitivity reactions, including IKBKE Stevens–Johnson syndrome and toxic epidermal necrolysis, have been reported [8, 9]. As these can be life-threatening, clinical guidance requires immediate discontinuation of etravirine whenever such severe reactions are suspected [8, 9]. The findings from this week 96 analysis provide further evidence that etravirine use is not more frequently associated with neuropsychiatric AEs than placebo. Furthermore, data from the ongoing SENSE (Study of Efavirenz NeuropSychiatric Events versus Etravirine; NCT00903682) trial, comparing the week 12 frequencies of neuropsychiatric AEs in treatment-naïve, HIV-1-infected patients receiving either etravirine or efavirenz, demonstrated that etravirine has a more favourable short-term neuropsychiatric tolerability profile than efavirenz [10]. Of note, there are no comparative data for etravirine and efavirenz in treatment-experienced patients such as those enrolled in DUET, given that efavirenz would not be an appropriate comparator in this patient population because of decreased activity as a result of antiretroviral drug resistance.

, 2010). Figure 1a shows that the addition of 40 μL (1 : 50) of the supernatant of MHI 1672 did not induce propidium fluorescence unless supplemented with recombinant NheC. This increase in fluorescence could be prevented including the monoclonal antibody Mab 1E11 (against NheB) in the bathing solution, excluding the

possibility that NheC alone can induce propidium uptake in Vero cells (Fig. 1a). To examine the effect of DDM on propidium uptake induced by the intact Nhe complex, we pre-incubated B. cereus NVH 75/95 supernatant with DDM at its critical micelle concentration (CMC = 0.2 mM) AC220 nmr prior to mixing with the cell suspensions at 1 : 80 dilution. This abolished the propidium uptake in Vero cells (Fig. 1b) but not when NVH 75/95 supernatant was incubated with water (solvent for DDM) or with DDM at 0.05 mM, i.e. less than the CMC (Fig. 1b). The same results were observed using human intestinal HT29 epithelial cells (data not shown). Similar inhibition of propidium uptake was obtained when NVH 75/95 supernatant was pre-incubated with the CMC of beta-octyl glucoside (20 mM, data not shown). These

data are consistent with one or more of the three Nhe components interacting with the micelles, thereby preventing pore formation when subsequently exposed to the Vero and HT29 cells. Using the NheC-deficient B. cereus MHI 1672 culture supernatant, we examined the effect of DDM on NheC. Pre-incubation of purified NheC with 0.2 mM DDM did not inhibit its ability to restore propidium uptake in Vero cells when added to the culture supernatant of B. cereus MHI 1672 (Fig. 1c). Similar results were obtained in HT-29 Selleckchem Lapatinib cells (data not shown). ANS has been widely used to monitor the changes in protein conformation via an increase in fluorescence

upon binding to exposed hydrophobic regions of proteins (Slavík, 1982). Figure 2a shows the increase in ANS fluorescence intensity and blue shift of the wavelength maximum following pre-incubation of NheB with DDM micelles compared with pre-incubation find more with water. DDM (0.2 mM) did not induce any changes in the ANS fluorescence with NheA (Fig. 2b). NheC exhibited a blue shift in the wavelength maximum but no increase in fluorescence intensity (Fig. 2c). Thus, of the three Nhe proteins, DDM induced the conformational changes in NheB as observed with other pore forming toxins (Sangha et al., 1999). To indicate the location of the conformational changes in NheB induced by DDM, we sought changes in the intrinsic tryptophan fluorescence. NheB contains three tryptophan residues, all located in the alpha helical bundles of the protein. No significant changes in the emission maximum of NheB fluorescence were observed with (333–334 nm) and without treatment with DDM (334 nm; Supporting Information, Fig. S1). The emission wavelength maximum shifted to 354 nm after denaturation with 8 M urea.

oxyfera-like bacteria to total bacteria reached peak values of 2.80% in summer and 4.41% in winter. Phylogenetic analysis showed n-damo bacteria in the paddy soil were closely related to M. oxyfera and had high diversity in the soil/groundwater ecotone. All of the results indicated the soil/groundwater ecotone

of the Jiangyin paddy field was a favorable environment for the growth of n-damo bacteria. “
“Random mutagenesis selleckchem has been used to identify the target DNA sites for the MalI repressor at the divergent Escherichia coli K-12 malX-malI promoters. The malX promoter is repressed by MalI binding to a DNA site located from position −24 to position −9, upstream of the malX promoter transcript start. The malI promoter is repressed by MalI binding from position +3 to position +18, downstream of the malI transcript start. MalI binding at the malI promoter target is not required for repression of the malX promoter. Similarly, MalI binding at the malX promoter target is not required for repression of the malI. Although the malX and malI promoters are regulated by a single DNA site for cyclic AMP receptor protein, they function independently and each is repressed by MalI binding to a different independent Talazoparib cell line operator site. The Escherichia coli malX and malY genes encode proteins for the transport and metabolism of an

as yet unidentified substrate (Zdych et al., 1995; Clausen et al., 2000). They are cotranscribed from a single promoter (the malX promoter) whose activity is completely dependent on binding of the cyclic AMP receptor protein (CRP) to a single target centred at position −41.5, i.e. between base pairs −41 and −42, upstream from the malXY transcript start (Reidl & Boos, 1991; Lloyd et al., 2008). Upstream of malX, the divergent malI gene encodes a transcription repressor that represses malXY expression (Reidl et al., 1989). Expression of the malI gene is dependent on a single promoter that controls divergent transcription initiation from a location that is 85 base pairs

upstream from the malX promoter transcription startpoint (Lloyd et al., 2008). The malI promoter is factor-independent, but can be activated ∼1.6-fold by CRP binding Adenosine triphosphate to its target at the malX promoter, which is centred at position −43.5 with respect to the malI promoter transcription startpoint (Fig. 1). Sequence analysis shows that MalI is a typical member of the LacI family of transcription repressors (Reidl et al., 1989; Weickert & Adhya, 1992). Most members of this family function as dimers that bind to inverted repeats, and Reidl et al. (1989) identified the sequence 5′-GATAAAACGTTTTATC-3′ as a likely target for MalI-dependent repression of the malX promoter. In this work, we describe a genetic screen to prove that this sequence, located from position −24 to position −9 at the malX promoter, and overlapping the −10 hexamer element, is indeed the binding target for MalI.

A cross-sectional study was conducted among HIV-infected adults. Demographics, medications, drug interactions and comorbidities were abstracted from patients’ medical records. Abnormal QTc interval was defined per the UK Committee for Proprietary Medicinal Products. Clinical characteristics were compared among ECG recipients Trichostatin A and nonrecipients. Among ECG recipients, the prevalence and predictors of QTc prolongation were assessed. Among the 454 patients included in the study, 80.8% were prescribed a medication associated with QTc prolongation and 39% had drug interactions expected to increase QTc prolongation risk. There were 138 patients (30.3%) who

received ECG testing. Receipt of ECG monitoring was associated with increasing age, Bcl-2 activation diabetes, increasing total number of medications and gastroesophageal

reflux disease. Among ECG recipients, the prevalence of abnormal QTc interval was 27.5%. Chronic kidney disease [prevalence ratio (PR) 3.47; 95% confidence interval (CI) 1.37–8.83; P = 0.009], hepatitis C virus coinfection (PR 2.26; 95% CI 0.97–5.27; P = 0.06) and hypertension (PR 2.11; 95% CI 0.93–4.81; P = 0.07) were independently associated with an abnormal QTc interval. A low frequency of ECG testing was observed, despite a high use of medications associated with QTc prolongation. The risk of abnormal QTc interval was highest among patients with chronic kidney disease, hypertension and hepatitis C virus coinfection. “
“Early diagnosis of HIV infection is important for the individual and for disease control. A consensus was recently reached among European countries on definitions of timing of

presentation for care: ‘Late presentation’ refers to entering care with a CD4 count <350 cells/μL or an AIDS-defining event, regardless of the CD4 count. Presentation with ‘advanced HIV disease’ is a subset having a CD4 count <200 cells/μL and also includes all who have an AIDS-defining event regardless of CD4 count. This study examines timing of presentation in New Zealand from 2005 to 2010. Since 2005, information on the initial CD4 cell count has been requested on all people newly diagnosed with HIV infection through Aspartate antibody testing in New Zealand. Excluded in this analysis were those previously diagnosed overseas or for an immigration medical. A CD4 cell count was provided for 606 (80.3%) of the 755 newly diagnosed adults. Overall, 50.0% were ‘late presenters’ and 32.0% had ‘advanced HIV disease’. Compared with men who have sex with men (MSM), people heterosexually infected were more likely to present late. ‘Late presentation’ and presentation with ‘advanced HIV disease’ were significantly more common among older MSM. Māori and Pacific MSM were more likely to present with ‘advanced HIV disease’. Compared with European MSM, the age-adjusted relative risks for Māori and Pacific MSM were 2.1 [95% confidence interval (CI) 1.4–3.

Results of LPS are given in terms of IQ scores with a mean of 100 and a standard deviation of 15. The multiple choice vocabulary test (Mehrfachwahl Wortschatztest-Form B, MWT-B) is a German test to measure verbal intelligence and is thought to be a valid indicator of pre-morbid intelligence (Lehrl, 1989). Memory functions were tested by the Auditory-Verbal Learning Test (AVLT; Schmidt, 1996) and the Wechsler Memory Scale-Revised (WMS-R; Wechsler, 1987). The Trail Making Test (TMT; Reitan, 1992) was assessed Selleck RAD001 to measure visuospatial ability (TMT-A)

and executive function (TMT-B). The Wisconsin Card Sorting Test (WCST) was also conducted to test executive function (Heaton et al., 1993). MRI investigations were performed with a conventional head-cage coil on a 1.5-Tesla system (Vision Magnetom; Siemens, Erlangen, Germany) with gradients of 25 mT/m, click here as described by us previously (Fellgiebel et al., 2004). DTI images were acquired with a transversal diffusion-weighted single-shot spin-echo echo-planar-based sequence in six non-collinear

diffusion-sensitizing gradient directions with diffusion sensitivity b = 900 mm2/s and one acquisition without diffusion encoding (b = 0 mm2/s). The acquisition matrix was 128 × 128, with 5 mm slice thickness. Repetition time (TR) was 8000 ms, echo time (TE) was 100 ms. All transversal slices were arranged parallel to the AC–PC line. At the time when the study was planned in 2003, these were standard imaging parameters. Original MR diffusion images were registered in DICOM format and converted to ANALYZE format using MRIcro software (University C-X-C chemokine receptor type 7 (CXCR-7) of Nottingham, UK). All scans were inspected visually. None of the data sets in our sample had to be excluded. The T2-weighted images were normalized to the MNI (Montreal Neurological Institute) T2 template using SPM2 (statistical parametric mapping; Wellcome Department of Cognitive Neurology,

London, UK) software implemented in MatLab 6.5 (Mathworks, Sherborn, MA, USA). Identical normalization parameters were used for warping of the diffusion-weighted images such that each voxel represents the same part of the brain in every subject. For the calculation of FA and MD maps, the FDT tool (FMRIB’s Diffusion Toolbox) of the FSL software library (FMRIB’s software library) was used. The obtained FA and MD maps were then smoothed with a 9-mm isotropic FWHM Gaussian kernel to improve signal-to-noise ratio and normalization. Voxel-based FA and MD contrast analyses were then done to compare ADHD patient and control groups using General Linear Model (GLM) standard independent sample t-test.

Results of LPS are given in terms of IQ scores with a mean of 100 and a standard deviation of 15. The multiple choice vocabulary test (Mehrfachwahl Wortschatztest-Form B, MWT-B) is a German test to measure verbal intelligence and is thought to be a valid indicator of pre-morbid intelligence (Lehrl, 1989). Memory functions were tested by the Auditory-Verbal Learning Test (AVLT; Schmidt, 1996) and the Wechsler Memory Scale-Revised (WMS-R; Wechsler, 1987). The Trail Making Test (TMT; Reitan, 1992) was assessed Ku-0059436 manufacturer to measure visuospatial ability (TMT-A)

and executive function (TMT-B). The Wisconsin Card Sorting Test (WCST) was also conducted to test executive function (Heaton et al., 1993). MRI investigations were performed with a conventional head-cage coil on a 1.5-Tesla system (Vision Magnetom; Siemens, Erlangen, Germany) with gradients of 25 mT/m, SB203580 as described by us previously (Fellgiebel et al., 2004). DTI images were acquired with a transversal diffusion-weighted single-shot spin-echo echo-planar-based sequence in six non-collinear

diffusion-sensitizing gradient directions with diffusion sensitivity b = 900 mm2/s and one acquisition without diffusion encoding (b = 0 mm2/s). The acquisition matrix was 128 × 128, with 5 mm slice thickness. Repetition time (TR) was 8000 ms, echo time (TE) was 100 ms. All transversal slices were arranged parallel to the AC–PC line. At the time when the study was planned in 2003, these were standard imaging parameters. Original MR diffusion images were registered in DICOM format and converted to ANALYZE format using MRIcro software (University Miconazole of Nottingham, UK). All scans were inspected visually. None of the data sets in our sample had to be excluded. The T2-weighted images were normalized to the MNI (Montreal Neurological Institute) T2 template using SPM2 (statistical parametric mapping; Wellcome Department of Cognitive Neurology,

London, UK) software implemented in MatLab 6.5 (Mathworks, Sherborn, MA, USA). Identical normalization parameters were used for warping of the diffusion-weighted images such that each voxel represents the same part of the brain in every subject. For the calculation of FA and MD maps, the FDT tool (FMRIB’s Diffusion Toolbox) of the FSL software library (FMRIB’s software library) was used. The obtained FA and MD maps were then smoothed with a 9-mm isotropic FWHM Gaussian kernel to improve signal-to-noise ratio and normalization. Voxel-based FA and MD contrast analyses were then done to compare ADHD patient and control groups using General Linear Model (GLM) standard independent sample t-test.

The French specific 85-kb type II virulence plasmid (Ribeiro et al., 2005) was not detected either in organic or in environmental samples (Fig. 1). In addition to the classical vapA-carrying virulence plasmid, we identified, during plasmid extraction and RFLP analysis, seven strains harbouring smaller or larger plasmids with unknown function (Table S1). These plasmids, generally designated as cryptic plasmids (Makrai

et al., 2002), were identified in 1.6% of clinical, 9.1% of organic and 30.8% of environmental samples. Four strains harboured only cryptic plasmids, while another three Sirolimus strains carried both virulence and cryptic plasmids. The prevalence of cryptic plasmids in our strains (7.3%) is comparable to the prevalence of cryptic plasmids (>5%) reported in Japanese R. equi strains (Takai et al., 1994). Because they are less prevalent in clinical click here samples than in environmental samples, cryptic plasmids do not appear to be related to virulence. However, they may potentially constitute a gene reservoir for the virulence plasmid. Finally, to better understand the basis of the genetic diversity between vapA-carrying virulence-associated plasmids, we sequenced the second most frequently isolated virulence plasmid type: an 87-kb type I plasmid. Widespread throughout the world, the 87-kb type I virulence plasmid type has already been identified in horse-related environments in France, Italy, Turkey, North and South America

and Australia (Makrai et al., 2002) and, surprisingly, from a cutaneous lesion of a cat in Australia (Farias et al., 2007). We extracted the 87-kb type I plasmid from the strain MBE116 (Table S1) and designated it as pVAPA116. This plasmid is 83 100 bp in size and contains 77 coding sequences, including six pseudogenes, equivalent to a coding density of 76.6% (Table S2). Although pVAPA116 is 2490 bp larger than pVAPA1037 – an 85-kb type I plasmid – the overall structure is highly conserved in both plasmids (95.8% DNA sequence identity), and the CURV modular arrangement (found in pVAPA1037) (Letek et al., 2008) is also found in pVAPA116 (Fig. 2). The divergences between pVAPA116 and pVAPA1037

are concentrated ADP ribosylation factor in three major allelic exchange loci (Fig. 2). The first locus corresponds to the insertion of pVAPA_0041 in the generally conserved conjugation region. The pVAPA_0041 gene product (185 amino acids) shares 32% identity (47% similarity) over 107 amino acids, with the protein of unknown function RHOER0001_1517 from Rhodococcus erythropolis. As this similarity suggests horizontal DNA exchange between different Rhodococcus species, it would be interesting to assess the conjugation capacity of virulence plasmids from each species. The second allelic exchange locus occurs in the variable region downstream from the invA-like DNA invertase/resolvase gene pVAPA_0810 and corresponds to the insertion of pVAPA_0811 and pVAPA_0812 and the deletion of pVAPA_0830 (Table S2 and Fig. 2).

Genes detected as recently transferred are known to be disproportionately A+T rich; therefore, the lower G+C content of many erm genes found in pathogens implies quite recent horizontal gene transfer and dissemination of MK-2206 solubility dmso low G+C content resistance genes among pathogens. Within the clade of the Firmicutes, bacteria whose erm G+C content compared favorably with that of chromosomal DNA are marked with asterisks after the names of the bacteria in Fig. 4. The consistent G+C content of both erm and chromosomal DNA implies either the presence of intrinsic erm genes or that gene transfer occurred long

ago. Among these bacteria, Bacillus [Erm(D) and Erm(34)] are common inhabitants of soil, where they were exposed to antibiotics produced by other organisms. It is probable that environmental antibiotic pressure maintained the presence of functional erm genes. Recent investigations revealed E7080 solubility dmso that soil bacteria are a reservoir of antibiotic-resistance genes, which introduces the new concept of an

‘antibiotic resistome’ (Riesenfeld et al., 2004; D’Costa et al., 2006; Aminov and Mackie, 2007; Wright, 2007). In addition, the aquatic environment is also a possible antibiotic-resistance gene reservoir (Aminov and Mackie, 2007), congruent with the recognition of new classes of Erm methylases in several marine inhabitants such as a halotolerant bacillus-related O. iheyensis and two actinomycetes: S. tropica and S. arenicola. All erm genes that show

frequent, recent gene transfer are related by self-transferable plasmids or transposons, such as erm(B), erm(C), erm(F), erm(G), and erm(X) (Table 1). These mobile genetic elements are responsible for the dissemination of resistance genes through pathogenic bacteria that were once susceptible to antibiotics. In addition to horizontal gene transfer, gene duplication also contributes to the phylogenetic anomalies in the Erm clade of the Actinobacteria. The occurrence of two different erm genes from the same organism on different evolutionary branches is evidence of gene duplication, for example, erm(S) and erm(N) from S. fradiae, erm(O) and erm(Z) from S. ambofaciens, and erm(30) and check details erm(31) from S. venezuelae. However, these examples do not fully explain the phylogenetic anomalies within the Erm clade of the Actinobacteria. The tree suggests other paralog segregation within the Actinobacteria, supported by several reports that certain Erm methylases show unusual resistance phenotypes that do not fall into either the monomethylase (type I) or the dimethylase (type II) category. For example, Erm(38) in Mycobacterium smegmatis and Erm(39) in Mycobacterium fortuitum confer macrolide–licosamide resistance rather than MLSB resistance (Nash, 2003; Nash et al.

[4] The APC report recommended such exemption to be considered in other states, including Queensland.[4] It is well established that maintaining Indigenous health imposes a challenge to healthcare delivery.[36,37]

A special arrangement under Section 100 (S100) of the National Health Act 1953 (Cth) was introduced in 1999 by the Australian Government to supply free medications to, and improve medications www.selleckchem.com/products/GDC-0941.html access at, Aboriginal Health Services (AHSs). This allows for the AHSs to order bulk supplies of PBS medications from a participating community pharmacy, and the AHSs then supply the medications to Indigenous and non-Indigenous patients treated at the AHSs.[4,28,37,38] An expansion of the S100 provisions to include all AHSs, regardless of location or remoteness, has been proposed to further increase medication access to all Indigenous people.[36,37] However,

the S100 scheme facilitates medication access without providing opportunity for medication consultation between a pharmacist (bulk supplier) and the patient, as the medication supply task is now undertaken by a health worker at the AHS.[4,36] While there are developments to improve QUM in Indigenous communities, such as the Pharmacy Guild’s ‘S100 Pharmacy Support Thymidine kinase Allowance’ and National Prescribing Service education sessions, the call for pharmacist-facilitated Veliparib mw QUM education sessions, medication consultation in AHSs and pharmacist-AHS health worker liaison are restricted

by inadequate funding, logistical issues and scarcity of pharmacists in rural areas.[4,28,36,37,39] Provision of consumer-specific information about the medication supplied forms a significant component of QUM. This is usually incorporated in a pharmacist’s dispensing process and is detailed in the PSA Professional Practice Standards, specifying that the pharmacist should work with the consumer ‘to provide tailored verbal and written information to ensure that consumers have sufficient knowledge and understanding of their medications and therapeutic devices to facilitate safe and effective use’.[21] A common written information tool is Consumer Medicine Information (or CMI) which provides brand-specific medication information produced by the relevant pharmaceutical company, in accordance with the Therapeutic Goods Regulations.[8,21] Pharmacists are required to provide Consumer Medicine Information leaflets under certain circumstances, for example when the medication is first provided to a consumer.

Microplusin completely altered the respiratory profile of C. neoformans. The basal oxygen consumption in MP-treated cells was approximately 40% lower DAPT supplier than that in non-MP treated cells. In treated fungi, AA or KCN did not further disturb the rate of oxygen consumption, while SHAM fully impaired respiration, which implies that the classical electron transport pathway was either damaged

or absent and that respiration of C. neoformans is entirely driven by the alternative pathway. As laccase is a copper-dependent oxidase responsible for melanization (Zhu & Williamson, 2004) in C. neoformans, we investigated whether the copper-chelating properties of microplusin might have a negative effect on this process. Microplusin inhibited melanization of the strains H99 and B3501 at concentrations ≥3.12 μM (Fig. 4a). When we supplemented a culture of C. neoformans strain I-BET-762 B3501 with 2.5 μM of CuCl2.6H2O, we observed that the presence of this metal caused a twofold reduction

in the antimelanization activity of microplusin (Fig. 4b). Similar results were obtained with C. neoformans strain H99 (data not shown). Moreover, we observed that microplusin reduced the laccase activity of C. neoformans strain H99 by almost 50% (Fig. 4c). In parallel, we evaluated whether microplusin could reduce l-dopa autopolymerization in a manner similar to glyphosate, a compound whose antimelanization activity in C. neoformans has been described (Nosanchuk et al.,

2001). Microplusin did not inhibit the autopolymerization of l-dopa and even Astemizole increased this process at concentrations ≥6.25 μM (Fig. 4d). Several enzymes are involved in the formation of the polysaccharide capsule in C. neoformans (reviewed in Zaragoza et al., 2009) and microplusin might affect this process by copper depletion, as copper is a co-factor for some of these enzymes. Our results revealed that microplusin impeded capsule enlargement of C. neoformans (strain T1444) in a dose-dependent manner (Fig. 5a). We also observed that 25 μM of microplusin significantly inhibited the capsular enlargement of H99 and B3501 (Fig. 5b and c). Our main hypothesis was that microplusin could negatively affect C. neoformans by copper depletion, which would be consistent with the importance of copper homeostasis for this fungus (Davis-Kaplan et al., 1998; Cox et al., 2003; Zhu et al., 2003; Waterman et al., 2007; Jiang et al., 2009) and the copper-chelating property of microplusin at a MP : copper II molar ratio of 1 : 1 (Silva et al., 2009). We have shown that microplusin at concentrations ≥1.56 μM significantly affected the growth of C. neoformans, similar to the activity of the peptide against M. luteus (Silva et al., 2009). Moreover, the anticryptococcal effect was considerably reversed when 2.5 μM of copper was added.