Diagnostic accuracy studies appeared to show improvement in reporting standards when the STARD guidelines were applied.6 Early evidence also suggests that inclusion of reporting standards during Imatinib peer review raises manuscript quality.7 The International Committee of Medical Journal inhibitors Editors now encourages all journals to monitor reporting standards and collect associated reporting guideline checklists in the process.8 Furthermore, the National Library of Medicine also now actively promotes the use of reporting guidelines.9 By January 1, 2015, all of the journals publishing this editorial will have worked through implementation and the mandatory use of guidelines and checklists

will be firmly in place. Because each journal has its unique system for managing submissions, there may be several ways that these reporting requirements will be integrated into the manuscript flow. Some journals will make adherence to reporting criteria and associated checklists mandatory for all submissions. Other journals may require them only when the article is closer to acceptance for publication. In any case, the onus will be on the author not only to ensure the inclusion of the appropriate reporting criteria but also to document evidence of inclusion through the use of the reporting guideline checklists. Authors should consult the Instructions for Authors of participating journals for more information. We hope that simultaneous implementation of this

new reporting requirement will send a strong message to all disability and rehabilitation Tenofovir in vitro researchers of the need to adhere to the highest standards when performing and disseminating research.

Although we expect that there will be growing pains with this process, we hope that within a short period, researchers will begin to use these guidelines during the design phases of their research, thereby improving their methods. The potential PDK4 benefits to authors are obvious: articles are improved through superior reporting of a study’s design and methods, and the usefulness of the article to readers is enhanced. Reporting guidelines also allow for greater transparency in reporting how studies were conducted and can help, hopefully, during the peer review process to expose misleading or selective reporting. Reporting guidelines are an important tool to assist authors in the structural development of a manuscript, eventually allowing an article to realise its full potential. As this issue went to press, the following Editors agreed to participate in the initiative to mandate reporting guidelines and publish this Position Statement in their respective journals. As a collective group, we encourage others to adopt these guidelines and welcome them to share this editorial with their readerships. Sharon A. Gutman, PhD, OTR Editor-in-Chief American Journal of Occupational Therapy Walter R. Frontera, MD, PhD Editor-in-Chief American Journal of Physical Medicine and Rehabilitation Leighton Chan, MD, MPH, and Allen W.

“
“Streptococcus pyogenes causes diseases as pharyngitis, impetigo, streptococcal toxic shock syndrome and inhibitors necrotizing fasciitis. Rheumatic fever (RF), acute streptococcal glomerulonephritis and rheumatic heart disease (RHD) are non-suppurative autoimmune post-streptococcal sequelae that arise from a delayed immune response to infection in genetically predisposed individuals [1]. Several markers are described as risk factors for RF/RHD, including HLA-DR7,

the allele most commonly associated with RHD in Brazil and other countries [2]. FGFR inhibitor According to the World Health Organization (WHO), S. pyogenes is responsible for 15–20% of bacterial pharyngitis cases, which primarily affect 5- to 18-year-old individuals [3]. The incidence of bacterial pharyngitis varies among countries, and even within the same country, there are variations in different regions due to age, socioeconomic and environmental factors and quality of health services [4] and [5]. The M protein has been described as the major bacterial antigen [6]. The protein consists of two polypeptide chains in an alpha double helix coiled-coil that forms fibrils extending up to 60 nm away from the bacterial surface. It is approximately 450 amino acids long

and is divided into tandem repeat blocks distributed over four regions (A, B, C and D). The N-terminal portion (regions A and B) is polymorphic and differences within the first 150 amino acid residues of the A region allow for the classification of different serotypes [7] and [8]. The C-terminal portion (regions C and D) is highly conserved, responsible for binding the bacteria to the oropharynx Quizartinib concentration mucosa and has antiphagocytic properties [6] and [7]. RF/RHD pathogenesis is related to the production of autoantibodies and autoreactive T cells that recognize and cross-react with epitopes from both the M protein and human heart tissue by molecular mimicry [9] and [10] and it was demonstrated by analyzing the T cell repertoire that infiltrated cardiac tissue and led to damage in RHD

[11]. M1 is the most common strain worldwide and, due to its high virulence, secondly is involved in invasive and non-invasive infections in several countries [12] and [13]. There is a large diversity of strains in Brazil. The most prevalent strains found in a sample from Sao Paulo city were the M1, M6, M12, M22, M77 and M87 compatible with those found in the rich districts from Salvador [5] and [14]. These M-types are also predominant in most of the world western countries [15]. Besides that, there is a much higher diversity of M-types in the poor districts from Salvador and Brasilia typically found in low incomes regions [5] and [16]. The classification of strains according to their tissue tropism for throat (A–C pattern), skin (D pattern) or both (E pattern) is based on the organization of emm and emm-like genes located in the mga locus within S. pyogenes genome and constitute the base for emm pattern genotyping [17] and [18].

The study was conducted in the Infertility Department of Shariati Hospital, a teaching hospital affiliated to Tehran University of Medical Sciences during 2006-2008. The project was approved by the Ethics Committee of the Infertility Department, and was initiated after obtaining written consents of the participants. High risk patients were defined as young females, who had antral follicle counts of more than 15, poly cystic ovaries on ultrasound scan and/or polycystic ovarian syndrome (PCOS), serum estradiol of more than 3500 pg/ml and/or multiple follicular recruitments Inhibitors,research,lifescience,medical in both ovaries during ultrasound monitoring in controlled

ovarian hyperstimulation (COH). The inclusion criteria were an age of less than 33 years, high risk of developing OHSS in the absence of taking antipsychotic medications, no known allergy to cabergoline or ergot alkaloids, and absence of hepatic dysfunction or hypertension. Polycystic Inhibitors,research,lifescience,medical ovarian syndrome was diagnosed according to Rotterdam criteria.8 According to the Rotterdam criteria, patients with two of the three characteristics including: 1) oligomenorrhea/amenorrhea, 2)

clinical (hirsutism) finding of hyperandrogenism, or 3) polycystic ovaries Inhibitors,research,lifescience,medical on transvaginal sonography, were included in the study. Metabolic features of PCOS patients were not of concern in this study; therefore, insulin resistance and androgen index were Inhibitors,research,lifescience,medical not measured. The oligomenorrhea/amenorrhea and polycystic appearance of ovaries were seen in more than two third of the PCOS patients. All PCOS patients were treated with metformin (1500 mg/day). Few of the patients had positive history of OHSS, regardless of its severity. All of the participants underwent controlled ovarian Inhibitors,research,lifescience,medical hyperstimulation (COH) with Gonadotropin/GnRH-agonist long protocol. All of them received folic acid (one mg/day) before Protein Tyrosine Kinase inhibitor initiating the induction cycle, low dose oral contraceptive pills (on the third of

the previous cycle) and doxycycline (100 much mg twice a day) for the first 10 days of the previous cycle. Long term desensitization protocol using subcutaneous GnRH agonist Buserelin (500 µg) was started on the day 21 of the previous cycle. After complete desensitization, ovarian stimulation using recombinant-FSH (Gonal F, Serono, switzerland) was commenced on day 3 of the next cycle at a daily dose 150 IU. Transvaginal ultrasound (Siemens, Sonoline G20) was done every 3-5 days for the examination of follicular development, and serum estradiol levels were measured every 2-3 days using radioimmunoassay method. When at least two follicles with diameter of at least 17 mm were observed, final oocyte maturation was triggered with 10,000 IU human chorionic gonadotropin (HCG, Ferring, Germany) administered as a single intramuscular injection.

32,40,41 Conversely, reducing histone acetylation by overexpressing certain HDACs, or knockdown of the HAT, CBP, results in less sensitivity to cocaine.32,34,40 Two reports have extended these findings in rat models of cocaine self-administration, where animals are trained to press levers to receive the drug. Interestingly, delivery of the HDAC inhibitor, sodium butyrate, potentiates drug-taking42 while delivery of the HDAC inhibitor, trichostatin Inhibitors,research,lifescience,medical A, attenuates it.43 The explanation for these different observations is unclear, but it may involve experimental differences with the self-administration paradigm

or the HDAC inhibitor used. Cocaine alters histone acetylation through many enzymes in the NAc, but one particular HDAC, HDAC5, responds uniquely to chronic cocaine administration, raising the interesting possibility Inhibitors,research,lifescience,medical that this HDAC is involved in the behavioral transitions which occur between acute and chronic cocaine exposure (eg, drug experimentation to compulsive

drug use). Chronic cocaine administration increases the phosphorylation Inhibitors,research,lifescience,medical of IIDAC5 and shuttles it out of the nucleus, permitting hyperacetylation of histones at target genes for HDACS (Figure 2).40 This phosphorylation reaction may be mediated by Ca2+/calmodulin-dependent protein kinase II (CaMKII), since ex vivo inhibition of CaMKII reduces the activity-induced phosphorylation of HDAC5. Consistent with its regulation by cocaine, mice deficient for HDACS display normal rewarding responses to initial cocaine exposures, but become hypersensitive when treated with a Inhibitors,research,lifescience,medical chronic course of cocaine.40 Thus, pharmacological and genetic manipulations that increase histone acetylation Inhibitors,research,lifescience,medical appear to potentiate behavioral responses to cocaine and suggest that altered histone acetylation may contribute to establishment of an addicted state. Histone H3 phosphorylation and phosphoacetylation also appear to play key roles in drug-regulated behaviors. Global levels of

histone H3 phosphorylation at this website serine 10 are induced by acute about cocaine in striatum, a process which requires the kinase MSKl.19,32 The function of MSK1 is behaviorally important, as mice lacking this kinase have attenuated locomotor responses to cocaine. Cocaine-induced inhibition of protein phosphatase-1 also plays an important role in IB phosphorylation in striatum (Figure 2). Dopamine D1 receptor activation alters the phosphorylation of dopamine-regulated and cyclic-AMP-regulated phosphoprotein of 32kD (DARPP-32) at particular serine residues; the protein then accumulates in the nucleus to inhibit protein phosphatase-1 from dephosphorylating histone H3.20 The simultaneous activation of an H3 kinase and inhibition of an H3 phosphatase results in the robust increase in H3 phosphorylation after acute cocaine exposure.

211 Nilsson and colleagues212 also found that high-dose aspirin (325 mg/day) use was associated with reduced rates of development of Alzheimer’s disease – presumably as a result of its anti-inflammatory effects- but more comprehensive study is needed. Finally, the anti-inflammatory effects of aspirin have been postulated to have potential benefit in depression, given recent suggestions that inflammation may contribute to the pathophysiology of this disease. There has been a single, small, open trial in 24 depressed patients who had not responded Inhibitors,research,lifescience,medical to a 4-week trial of SSRIs; the authors found that

the addition of aspirin to the SSRI led to rapid and sustained response in approximately one half of patients.213 However, much more research is required to determine whether the addition of aspirin to an antidepressant regimen Inhibitors,research,lifescience,medical for depression is indicated. The antiplatelet agent, clopidogrel, has not been associated with Inhibitors,research,lifescience,medical significant neuropsychiatrie consequences; as experience with this agent increases, adverse neuropsychiatrie effects or therapeutic uses for neuropsychiatrie disorders may become apparent. Similarly, the anti-coagulant medications, heparin and warfarin, are not commonly associated with neuropsychiatrie

effects. Bottom line: Use of antiplatelet and anticoagulant medications

has not been consistently associated with substantial Inhibitors,research,lifescience,medical neuropsychiatrie consequences. Aspirin may cause delirium in toxicity. Selected antiarrhythmic Trametinib order medications Class I agents These agents, which exert their therapeutic effects by blocking sodium channels, were commonly prescribed for many years, especially among acutely ill patients in intensive care settings. Their popularity has waned recently, though they remain in use. Disopyramide (Class la) The majority of neuropsychiatrie consequences of disopyramide Inhibitors,research,lifescience,medical use result from the anticholinergic properties of this medication. Delirium can result from such anticholinergic effects,214 and there have been case reports see more of disopyramide-associated psychosis.215,216 Other neuropsychiatrie consequences of use are uncommon. Therapeutically, disopyramide has been studied in the treatment of neurally mediated hypotension among patients who suffer from chronic fatigue; small studies suggest that it may provide benefit to persons whose fatigue is related to such hypotension.217,218 Procainamide (Class Ia) Although procainamide is generally associated with low rates of neuropsychiatrie side effects, procainamideinduced psychosis has been reported in a variety of case reports involving seven patients.

Cardiological considerations in MRCD The heart is one of the most frequently affected organs in MRCD’s (35, 36). Cardiac involvement

of multisystem mitochondrial disorders either manifests as impulse BIBF 1120 generation or impulse conduction disturbances or as primary myocardial impairment (hypertrophic or dilated cardiomyopathy). Frequent electrocardiographic abnormalities are atrial fibrillation, atrioventricular (AV) block, Wolff-Parkinson-White (WPW) syndrome, Inhibitors,research,lifescience,medical bundle branch blocks, QT prolongation, or ST and T-wave anomalies (37). In addition, in 2007, we reported evidence of a cardiovascular autonomic impairment in a cohort of patients with different mitochondrial disorders (38). On the other hand, when a mitochondrial condition affects selectively the heart, hypertrophic

cardiomyopathy (HCM) or dilated mitochondrial cardiomyopathy may be clinically indistinguishable from other genetic determined cardiomyopathies and the onset usually begins in the neonatal period (39). Cardiac Inhibitors,research,lifescience,medical abnormalities are often present in mitochondrial syndromes; different Inhibitors,research,lifescience,medical patterns of heart involvement are described herein and summarized in Table 1. Table 1. Clinical features of the main mitochondrial syndromes. Classical mitochondrial syndromes Kearns-Sayre syndrome (KSS) This syndrome is characterized by the following triad 1) onset before the age of 20, 2) pigmentary retinopathy, and 3) ophthalmoparesis (40). Other features are usually present including cardiac conduction defects, cerebellar ataxia, dementia, elevated CSF proteins ( > 100 mg/dl), deafness, and low stature. KSS is due to sporadic, single large-scale deletions of mtDNA, ranging from 1.3 Inhibitors,research,lifescience,medical to 8.8 kb (90% of the cases) in size, or, rarely, to mtDNA duplications (41). Calcifications at basal ganglia and thalamus or cortical or cerebellar atrophy can be seen by neuroimaging studies (42). KSS is typically associated with cardiac conduction Inhibitors,research,lifescience,medical defects with abnormalities on electrocardiogram such as PR-interval prolongation, preceding 2nd or 3rd degree AV block, His-Ventricular (H-V) interval prolongation due to distal disease, dilated

cardiomyopathy or Stokes-Adams syncope (43). Pacemaker else implantation is usually indicated in these patients despite ventricular arrhythmias have been described such as “Torsade de pointes” (44), raising the question about which type of device is indicated. In addition, patients with KSS with ventricular conduction defects also have an accelerated and unpredictable rate of progression to complete AV block; sudden death occurs in 20% of the cases (45). For these reasons, no standard recommendations are available whether a preventive pacemaker implantation should be performed before any evidence of electro-cardiologic abnormalities. Some authors argue that implantation of defibrillators that simultaneously have pacing modes may be the most effective strategy in those patients.

This revealed that predictive values for nonpsychotic disorder were lower than the 8% predictive value for psychotic disorder, with the exception of depression (predictive value: 13%). Combining psychotic and nonpsychotic disorder outcome categories only raised predictive values Inhibitors,research,lifescience,medical by a small amount (Table VI). Table VI. Predictive values, using the three waves of the Netherlands Mental Health Survey and Incidence Study (NEMESIS) (T0, T1, and T2) of T1 incident subclinical psychotic experiences on T2 incident disorders.

CI, confidence interval. Conclusion The area of early intervention and prevention of psychotic Inhibitors,research,lifescience,medical Epacadostat datasheet illness is certainly exciting and brings a muchneeded focus to the underfunded mental health services for the severely mentally ill. On the other hand, a range of epidemiological and ethical issues remain to be addressed. Similarly, it has been pointed out that early detection and good early treatment

need to go hand in hand,5 and unfortunately the evidence base for so-called phase-specific treatments at Inhibitors,research,lifescience,medical this time remains very limited, offering little guidance.54 Lastly, cost-effectiveness Inhibitors,research,lifescience,medical data remain wanting. Therefore, the following conclusions can be drawn: Early detection clinics report “high-risk” individuals having 50% transition rates to “psychotic disorder” over a 3- to 6-month period. However, making a diagnosis of psychotic disorder is not an exact science: it involves an arbitrary cutoff imposed on dimensional variations of psychopathology

and the need for care over time. Gaining insight into the cognitive and biological factors that drive the dimensional variation, including therapeutic Interventions, Inhibitors,research,lifescience,medical Is arguably more useful than sterile dlchotomous prediction models. Screening In the general population for at-risk mental states Is useless: a rare disease such as schizophrenia cannot be predicted using prevalent predictors. In fact, depressive disorder can be better predicted by subclinical Casein kinase 1 psychotic experiences than psychotic disorder itself (although for depression the predictive value also remains much too low to be useful for screening purposes). Screening predictive values can be improved substantially by manipulating the sample rate of (future) schizophrenia, but the price to be paid is high as large numbers of false-negatives will be created, which will remain permanently “undetectable.

zeylanicum, L. nobilis L., J. foetidissima, A. sativum L., and M. fragrans Houtt. had good antibacterial activities against the Gram-negative bacteria, whereas the rest of the studied extracts were ineffective. Table 2 Number of Gram-negative isolates susceptible to each plant extract The MIC50 Nutlin-3a cell line values for these plant extracts and oils were 12.5, 12.5, 25, 12.5, 12.5,

25, 12.5, and 6.25 µl/ml, respectively, against E. coli O157:H7; and 1.5, 6.25, 6.25, 6.25, 6.25, 25, 6.25, and 12.5 µl/ml, respectively, against Y. enterocolitica O9; and 1.5, 3.125, 1.5, 1.5, 3.125, 12.5, 3.125, and 12.5 µl/ml, respectively, against Proteus spp.; and 6.25, 3.125, 1.5, 3.125, 6.25, 12.5, 6.25, and 6.25 µl/ml, respectively, Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical against K. pneumoniae (table 3). Table 3 Minimum inhibitory concentrations (MICs) for the selected essential oils and extracts against some Gram-negative bacteria In contrast, when studying the optimal concentrations that could inhibit 50% of the bacterial isolates, the X 2 values were not significant (P>0.05) for all the studied concentrations, indicating adequate fit of the Probit regression models (table 4). Table 4 Optimal inhibitory concentrations of the selected essential oils and extracts against some Gram-negative bacteria Table 5 also shows that

Ceftazidime, Cefotaxime, and Ciprofloxacin were the most effective antibiotics against E. coli O157:H7 (MIC50= 0.25, 0.5, and 2 µg/ml, respectively). Moreover, Ceftazidime and Ciprofloxacin Inhibitors,research,lifescience,medical were the most effective antibiotics against Y. enterocolitica O9 (MIC50= 0.25 and 0.5 µg/ml, Inhibitors,research,lifescience,medical respectively) and against Proteus spp. (MIC50= 4 and 2 µg/ml, respectively) and Ceftriaxone, Cefotaxime, and Ciprofloxacin were the most effective antibiotics against K. pneumoniae (MIC50= 0.25, 0.25, and 0.5 µg/ml, respectively). Table 5 Minimum inhibitory concentrations Inhibitors,research,lifescience,medical (MICs) of some antibiotics against Gram-negative bacteria Discussion Because of their safety and low cost as well as their impact on a large number of microbes,25medicinal plants may have the ability to treat bacterial resistance to many

types of antibiotics. The antimicrobial effects of aromatic oils extracted Dichloromethane dehalogenase from a large number of plants have been evaluated and reviewed,26,27 and the mechanisms that enable the natural ingredients of herbs and spices to resist microbes have been discussed.28 The results show that these mechanisms vary greatly depending on the components of the essential oil.29,30 In the present study, the efficacy of some plant extracts and oils was determined, quantitatively, by measuring the diameter of the inhibition zones around the discs (table 2). Only O. syriacum. L., T. syriacus Boiss., S. aromaticum L., C. zeylanicum L., L. nobilis L., J. foetidissima Wild, A. sativum L., and M. fragrans Houtt. extracts inhibited the growth of the tested bacteria. In addition, O. syriacum. L., T. syriacus Boiss., S. aromaticum L., and C. zeylanicum L. essential oils were the most effective, and their MIC50 values varied from 1.

In a study from our group (Dolbcrg et al, unpublished data), changes in MT

were explored in a group of 46 patients with MDD treated with rTMS and in normal controls. No differences were identified in MT between patients and controls. In addition, MT did not change with treatment, and showed no association with severity, age, or the presence of psychosis. It is possible that, the differences observed in our study and those reported by Triggs et al were related to differences in the methods of determining MT. Triggs et al defined MT as 100-μV MET deflections in the EMG, whereas we used the more widely Inhibitors,research,lifescience,medical accepted cutoff of 50 μV. Postexercise facilitation It is well established that muscular activation increases the size of the MEPs during TMS. Samii et al59 and Shajahan et al60,61 explored this paradigm in

patients with acute depression, in recovered depressed patients, and in normal controls. They found that patients in the acute stage of the illness had significantly less postexercise facilitation Inhibitors,research,lifescience,medical than normal controls or recovered patients. They speculated that this lack of facilitation in depressed patients is due to decreased cortical excitability (which may be secondary to increased inhibitory outflow from interneurons), and that the normalization seen with recovery reflects the normalization of underlying neurobiological processes. Silent period A variable period of EMG absence follows Inhibitors,research,lifescience,medical an MEP This period is referred to as the silent, period

and it is believed to be, at least in part, secondary to increased inhibitory forces in the motor cortex.13 Steele et Inhibitors,research,lifescience,medical al62 looked at the post-TMS silent, period in patients with depression and compared it with that of normal controls. They found that depressed patients had longer post-TMS silent, periods than normal controls. They concluded that their findings were indirect evidence for the presence of state-dependent increased inhibitory mechanisms in the motor cortex, and possibly Inhibitors,research,lifescience,medical other areas of the brain, in depression. It has not been reported whether recovery from depression was associated with a normalization of the silent, period. www.selleckchem.com/products/KU-55933.html Paired-pulse stimulation Paired-pulse stimulation of the motor cortex is considered today to be the gold standard of motor cortex excitability.13,56,63 The paired TMS stimulations old are given with short, intervals between them (interstimulus intervals [ISIs]). The effects depend on the intensity of the conditioning and test, stimulus, and on the ISI. Short ISIs are believed to reveal inhibitory cortical mechanisms, whereas long ISI are thought to reveal excitatory cortical mechanisms. Paired-pulse stimulation has been studied extensively in neurology, but much less in depression. Maeda et al63 studied eight subjects with major depression with the paired-pulse paradigm and compared their responses with that of normal controls.

35

These hints may imply that the problem of animal transmissible spongiform encephalopathies (TSEs) could be more widespread than generally assumed, and may call for drastic measures in the realm of farming. It is not impossible that humans carrying the agent may transmit it horizontally.36 The risks associated with the latter possibility can be met competently only if knowledge is accrued about the mode of transmission of the agent and the mechanism #MS-275 manufacturer keyword# by which prions reach the brain upon peripheral inoculation into extracerebral sites. The rest of this review article is devoted to analyzing the progress that has been made in these fields. The making of prions A noncommittal, operational definition37 says that the prion is the infectious agent that causes scrapie, BSE, CJD, other TSEs, such as chronic wasting disease

of mule deer and elk, and other less common diseases that affect, for example, exotic ungulates and captive felids. Obviously, although this definition is useful in that it facilitates understanding, it says nothing about the true Inhibitors,research,lifescience,medical physical nature of the agent. A very different definition that Inhibitors,research,lifescience,medical has become rather popular among yeast geneticists centers around the structural biology of prions. According to this second definition, prions are proteins that can exist in at least two different conformations, one of which is capable of inducing the conversion of further individual prion molecules from one conformation into the other. Therefore, prion proteins can serve as true genetic elements even if they do not contain informational nucleic acids, in Inhibitors,research,lifescience,medical that they are self-perpetuating and heritable.38 Nineteen years after the original formulation of the prion hypothesis by Stanley Prusiner (Figure 2), and 4 years after he was awarded the Nobel Prize in 1997, there continues to be uncertainty about the question of whether these two definitions coincide in the case of mammalian prions. One further problem is that all amyloids and their precursors

would fit the second definition, yet amyloid proteins themselves Inhibitors,research,lifescience,medical do not appear to be transmissible or infectious in vivo or in cell cultures. In the last few months, we have witnessed breathtaking advances in the understanding of prion phenomena in yeast, and there is no doubt that at least two yeast proteins exist that fulfill Calpain the above definition. It is generally believed that the ultimate experiment proving that a given protein is a prion is “in vitro conversion”: this term defines a cell-free manipulation by which the noncontagious conformation is transformed into a transmissible agent. Ideally, this manipulation should occur without participation of the pathological, transmissible prion, in order to formally exclude the possibility of cross-contamination. Two recent papers have shown that these conditions can be met in the case of the yeast prions identified so far, Sup3539,40 and Ure2p.41,42 Figure 2.