e., total daily dose 240 mg), failed to achieve an intragastric milieu consistent

with dual PPI plus amoxicillin therapy being an effective anti-H. pylori regimen. “
“Levofloxacin has been proposed to replace clarithromycin for Helicobacter pylori treatment. Seven- and 10-day fluoroquinolone triple therapies have generally failed to achieve cure rates of ≥90%, whereas 14-day therapy has achieved 95% success. The aim was to assess the efficacy and effect of fluoroquinolone resistance on 14-day levofloxacin-containing triple therapy with or without the addition of bismuth. Helicobacter pylori-positive patients with functional find more dyspepsia or healed peptic ulcers were randomized to receive lansoprazole 30 mg b.i.d., amoxicillin 1000 mg b.i.d., and levofloxacin 500 mg daily with (B-LAL) or without (LAL) bismuth potassium citrate 220 mg b.i.d. for 14 days. Eradication was assessed by 13C-urea breath testing 4 weeks after completing treatment. Antimicrobial susceptibility was by the agar dilution method. Success was defined as PP success ≥90%. A total of 152 of 161 patients (81 LAL and 80 B-LAL) enrolled completed treatment. The PP rates were 94.6% (70/74; 95% CI, 86.9–97.9%)

with B-LAL and 85.9% (95% CI, 76.5–91.9%) with LAL (p = .07); the ITT eradication rates were 87.5% (95% CI, 78.5–93.1%) with B-LAL and 82.7% (95% CI, 73–89.4%) with LAL (p = .39). Levofloxacin resistance was present in 30.3%. Treatment success was excellent with susceptible strains (97.5%) versus resistant strains (70.6%) for B-LAL and 97.3% versus 37.5% for LAL, respectively. Fourteen-day

fluoroquinolone therapy was highly effective when fluoroquinolone resistance rates are <12%. The Selleckchem MK2206 addition MCE of bismuth maintained effectiveness with fluoroquinolone resistance as high as 25%. “
“Background: Helicobacter pylori produces γ-glutamyltranspeptidase (GGT), a potential virulence factor involved in induction of host cell apoptosis. Regulation of the production of this protein is not known. Methods:  The transcription start sites were determined by primer extension analysis. Transcription level of the GGT gene was examined by measuring the mRNA by RT-PCR and expression level of GGT protein was examined by Western blot analysis under different conditions. Results:  Two transcription start sites were identified; thymine at 78-bp upstream and adenine at 79-bp upstream from the ATG codon of the GGT gene. There was a possible -10 consensus promoter sequence (ATTAAT), but no apparent -35 consensus sequence was found. The transcription of the mRNA and the expression of the protein were at almost constant level during the course of culture. The mRNA level increased by exposure to low pH; however, the actual protein expression level remained almost constant. Addition of glutamine or glutamate did not affect the mRNA level and the protein expression level to a remarkable degree, nor did co-culture with AGS cells affect the GGT activity level. Conclusion:  It was suggested that H.

[10, 22] Liver www.selleckchem.com/products/avelestat-azd9668.html failure, by decreasing the production of cholesterol, the cortisol substrate, could also play a contributing role. Finally, adrenal hypoperfusion secondary to the circulatory dysfunction of cirrhosis could be also involved in the pathogenesis of RAI.[10, 22] In the current study we found that patients with RAI had higher plasma renin, noradrenaline, and cytokine levels and lower serum levels of LDL cholesterol than patients without RAI, although significant differences were only observed in relationship to the endogenous vasoactive hormones. An interesting finding of the study was that the prevalence of RAI

did not correlate with the severity of liver disease. This finding suggests that

factors other than liver function (adrenal perfusion, inflammatory response, nutritional parameters) can be involved in its pathogenesis. Serum cortisol is an essential component in the homeostasis of circulatory function in humans since it increases the vascular and cardiac responses to angiotensin-II and catecholamines.[1, 2, 38] Our study shows that RAI is associated with a significantly lower mean arterial pressure and higher plasma renin activity and norepinephrine concentration. RAI was also associated with a more deteriorated glomerular filtration rate and renal free water excretion, as indicated by higher BUN and lower serum sodium levels. Taken together, these results suggest that RAI is associated with impairment in circulatory and renal function. A relevant finding of our Alectinib price study was the association between RAI and the risk to develop new infections, severe sepsis, and type 1 HRS. It is well known that circulatory dysfunction and the secondary activation of the sympathetic nervous system impairs several defensive mechanisms against enteric infections.[39, 40] Overactivation of the sympathetic nervous system inhibits intestinal motility and increases bacterial overgrowth.[41]

The increased release of catecholamines from adrenergic terminals exert potent immunosuppressive Inositol monophosphatase 1 actions including inhibition of chemotaxis/migration and phagocytosis of bacteria by neutrophils and monocytes.[42, 43] Finally, catecholamines are released into the intestinal lumen, where they interact with specific bacterial receptors and increase bacterial growth, adherence to the mucosa, penetration into the interstitial space and lymphatics within the intestinal wall, and virulence.[40, 44] The net effect of all these alterations is an increased translocation of bacteria and bacterial products from the intestinal lumen to the submucosal lymphatics and then to the systemic circulation, giving rise to spontaneous bacterial infections and systemic inflammatory response.

In the present study, we demonstrated that the dual-function vector not only suppressed HBV replication by silencing HBx, which reduced HBV load, but also enhanced TLR7-mediated type I IFN and immunostimulatory cytokine production while inhibiting immunosuppressive cytokines, which helped to recover adaptive immunity and further promoted the

inhibition of HBV replication. By comparing the effects of ssRNA, shRNA, and ssRNA-shRNA dual functional vector on HBV replication or immune stimulation, we found that ssRNA-shRNA dual functional vector was the strongest inhibitor of HBV replication and the most efficient stimulator of innate immunity both in vitro and in vivo. The dual functional vector was more efficient to stimulate type I IFN response than ssRNA, possibly because the relief of HBV-induced immune tolerance after direct HBV load Gefitinib decreased. It exerted a stronger Pictilisib clinical trial inhibitory effect on HBV replication than shRNA, possibly due to its arousing of IFN response by activation of the TLR7 pathway. We propose that both HBx silence and ssRNA-induced TLR7 activation contribute to the reversal of the HBV-intrinsic immune tolerance by a dually functional vector. Furthermore, dual-vector therapy reestablished HBV-specific CD8+ T-cell and anti-HBs Ab responses as well as effectively cleared HBV infection, demonstrating that reversing cell-intrinsic immunotolerance by this therapy further

promotes the recovery of anti-HBV adaptive immunity. To our knowledge,

this is the first report to propose that systemic immunotolerance can be overcome by reversing hepatocyte-intrinsic tolerance. Up to now, there has been no ideal mouse model that can mimic HBV check details natural infection. Although several lines of transgenic mice expressing either HBs gene or full-length HBV genome have been established, the immune system in these HBV-transgenic mice is inherently tolerant to transgene products; HBV replication is generated from the integrated HBV sequence harbored in all hepatocytes, which is clearly different from the natural HBV persistence. So these HBV-Tg mice cannot be used to study peripheral tolerance. The mouse model established by a single hydrodynamic injection of pAAV/HBV1.2 DNA into the tail veins of C57BL/6 mice is the first good model to observe the immune response/tolerance in immunocompetent mice, in which HBV surface antigenemia persists for >6 months, and viral replication intermediates, transcripts, and proteins present in liver tissues for up to 1 year.8 Moreover, there was no neutralizing anti-HBs antibody production after HBsAg/CFA vaccination, suggesting the generation of tolerance. The characteristics of this mouse model for HBV persistence are thought comparable to those of human chronic HBV infections in the immune tolerant stage. A series of studies have used this model to research HBV persistence.

78 [95% CI −1.64; 0.88]). Age did not contribute to the model. Conclusion.— Women with migraine are at an increased chance of WCP, and the chance increases as a function of Ceritinib headache frequency. Both depressive symptoms and CM independently predict HRQoL status. (Headache 2012;52:400-408) “
“Headache is a common accompanying symptom in cerebrovascular diseases. Several specific conditions and etiologies

are reviewed with emphasis on distinguishing characteristics. Recognition of these conditions can help identify underlying causes of these “secondary headache syndromes” and facilitate disease-appropriate treatment. “
“To compare outcomes of pediatric migraine patients treated in an emergency department (ED) before and after

implementation of a standardized combination intravenous therapy regimen aimed toward improving and standardizing abortive migraine therapy. In a pediatric ED, migraines represent 8-18% of all headache visits. Despite this large number, no standard treatment for acute migraine therapy currently exists. The study utilized a retrospective chart review of patients seeking acute Atezolizumab migraine treatment at a tertiary care, pediatric ED from August 2006 to March 2010. Inclusion criteria were pediatric migraine patients as defined by International Headache Society guidelines. The comparison population received various migraine therapies based on attending practice preference. After October 2008, patients received standardized intravenous combination therapy involving a normal saline fluid bolus, ketorolac, prochlorperazine, and diphenhydramine. Occasionally, metoclopramide was substituted during prochlorperazine shortages. Reduction in headache pain

score was the primary outcome. Secondary outcome measures included length of ED stay, hospital admission rate, and ED readmission rate within 48 hours. The study yielded 87 patients who received standardized combination therapy and 165 comparison patients. No significant difference in patient characteristics existed when evaluating patient demographics, outpatient medication use, and initial headache pain score. When compared with the non-standardized therapy population, the combination therapy patients revealed Glutamate dehydrogenase significant reductions in pain score (decrease of 5.3 vs 6.9, difference −1.6, 95% confidence interval −2.2 to −0.8, P < .001), length of ED stay (5.3 vs 4.4 hours, difference 0.9, 95% confidence interval 0.2-1.6, P = .008), and hospital admission rate (32% vs 3%, P < .001) without changes in ED return rate (7% vs 2%, P = .148). Standardized combination therapy is effective for acute pediatric migraine therapy in the ED by significantly reducing headache pain scores, length of ED stay, and hospital admission rates. "
“Significant progress in molecular genetics has advanced our understanding of the genetic basis of migraine.

26 and involves the elimination of red wave light and narrowing of the bandwidth of blue (440–460 nm) and green (540–560 nm) wave light. This modified light penetrates the mucosa only

superficially, is mainly absorbed by hemoglobin and highlights surface details and microvascular patterns. The technique can be rapidly activated by a button on the endoscope and appears to be helpful for differentiating neoplastic from non-neoplastic Selleck MLN0128 colonic polyps, at least when performed by experienced endoscopists.27 Autofluorescence involves the excitation of endogenous biological substances (fluorophores) by short wave-length light that leads to the emission of a fluorescent light of longer wave-length. The potential use in endoscopy is based on differences in autofluorescence spectra with normal and neoplastic tissue. Already, prototype endoscopes have been produced that incorporate high resolution images, narrow band imaging and autofluorescence imaging

(trimodal imaging) but the diagnostic contribution of the latter is still unclear. The use of various diagnostic aids in a patient with Barrett’s esophagus is shown in Fig. 1. An important question for the future of endoscopy is the role of conventional histology. Ferroptosis inhibitor Will biopsies be taken in 2020–2030 or will pathologists interpret surface or other features in real-time or will responsibility for gastrointestinal pathology largely pass from the dedicated pathologist to the gastroenterologist? At a practical level, it would be helpful to rapidly and accurately differentiate hyperplastic from

adenomatous colonic polyps and to differentiate dysplastic Cyclic nucleotide phosphodiesterase from non-dysplastic tissue in Barrett’s esophagus. It would also be helpful to have a simple, single and highly accurate test for the identification of Helicobacter pylori. In relation to real-time histology, endoscopes such as the endocytoscope and confocal laser endomicroscope can already magnify surface features up to similar levels to those obtained with a high-power microscope (1000X). However, these or similar endoscopes are unlikely to enter mainstream gastroenterology in the near future because of costs, requirements for contrast agents and difficulties with the prediction of pathology based on surface characteristics. At present, narrow band imaging appears to be a simple and attractive diagnostic aid but whether it is accurate enough for ‘optical biopsy’ in a community setting has not been investigated. Future innovations may include molecular imaging techniques that use specific antibodies labelled with substances such as fluorescein that might be readily detected with inexpensive technologies. A current technique for imaging outside the bowel lumen is that of EUS. Important developments in the 1990s included the production of a curvilinear echo-endoscope and the description of fine-needle aspiration with aspiration cytology.

In summer, the fish appear and remove the palatable species, leaving the flora dominated selleck kinase inhibitor by unpalatable brown algae, which are the only refuge for mesograzers (Hay 1986, Hay and Sutherland 1988, Duffy and Hay 1994). In the two tropical systems, levels of predation on macroalgae and mesograzers are high throughout the year (Hay et al. 1989, 1990). The temperate reefs studied by Taylor and Steinberg (2005) differed in having higher diversity of both macroalgae

and mesograzers, far less seasonal fluctuation in composition of the flora than North Carolina, a predominance of carnivorous rather than omnivorous fish, more large non-fish grazers compared to North Carolina, and qualitatively different chemical defenses in many of the dominant macroalgae, which, on the Australasian reefs, are predominantly fucoids and kelps. Importantly, grazing intensity on the macroalgae is much patchier in the Australasian reefs compared to North Carolina or the tropics, so palatable macroalgal species can persist in spatial refuges where grazing intensity is low (Taylor and Steinberg 2005). Taylor and Steinberg

(2005) reported that following predictions based on Hay and Duffy et al., LY294002 in vivo most mesograzers they studied did prefer to eat the hosts they were most commonly collected on and that most of these hosts were relatively less palatable than others to larger consumers. However, macroalgal species that were less palatable to larger consumers did not support larger densities or more species of mesograzers overall compared to palatable species, although mesograzer species evenness was greater on the unpalatable

macroalgae. Exoribonuclease Mesograzers can also benefit macroalgal hosts in other ways. For example, Stachowicz and Whitlatch (2005) reported that snails benefit their hosts by consuming epiphytic invertebrates and in turn benefit under some circumstances by an associational refuge from predatory crabs. In nutrient-limited environments, macroalgae can benefit from the nitrogen excreted by associated invertebrates (e.g., Bracken et al. 2007, Guidone et al. 2012). Over the past 13 years, our research group has been investigating the chemical ecology of macroalgal–invertebrate interactions in macroalgal-dominated communities along the western Antarctic Peninsula. We have come to recognize that macroalgal–mesograzer interactions are very important here and are similar in many ways to those described previously in temperate and tropical regions. However, the macroalgal communities differ in important ways from those lower latitude regions where macroalgal–mesograzer interactions have been studied previously and there are corresponding differences in the nature of the interactions of macroalgae and mesograzers. Mesograzers in these communities also appear to have selected for a relatively high frequency of filamentous endophytes growing within the larger macrophytes.

In summer, the fish appear and remove the palatable species, leaving the flora dominated LDK378 datasheet by unpalatable brown algae, which are the only refuge for mesograzers (Hay 1986, Hay and Sutherland 1988, Duffy and Hay 1994). In the two tropical systems, levels of predation on macroalgae and mesograzers are high throughout the year (Hay et al. 1989, 1990). The temperate reefs studied by Taylor and Steinberg (2005) differed in having higher diversity of both macroalgae

and mesograzers, far less seasonal fluctuation in composition of the flora than North Carolina, a predominance of carnivorous rather than omnivorous fish, more large non-fish grazers compared to North Carolina, and qualitatively different chemical defenses in many of the dominant macroalgae, which, on the Australasian reefs, are predominantly fucoids and kelps. Importantly, grazing intensity on the macroalgae is much patchier in the Australasian reefs compared to North Carolina or the tropics, so palatable macroalgal species can persist in spatial refuges where grazing intensity is low (Taylor and Steinberg 2005). Taylor and Steinberg

(2005) reported that following predictions based on Hay and Duffy et al., Sirolimus datasheet most mesograzers they studied did prefer to eat the hosts they were most commonly collected on and that most of these hosts were relatively less palatable than others to larger consumers. However, macroalgal species that were less palatable to larger consumers did not support larger densities or more species of mesograzers overall compared to palatable species, although mesograzer species evenness was greater on the unpalatable

macroalgae. Plasmin Mesograzers can also benefit macroalgal hosts in other ways. For example, Stachowicz and Whitlatch (2005) reported that snails benefit their hosts by consuming epiphytic invertebrates and in turn benefit under some circumstances by an associational refuge from predatory crabs. In nutrient-limited environments, macroalgae can benefit from the nitrogen excreted by associated invertebrates (e.g., Bracken et al. 2007, Guidone et al. 2012). Over the past 13 years, our research group has been investigating the chemical ecology of macroalgal–invertebrate interactions in macroalgal-dominated communities along the western Antarctic Peninsula. We have come to recognize that macroalgal–mesograzer interactions are very important here and are similar in many ways to those described previously in temperate and tropical regions. However, the macroalgal communities differ in important ways from those lower latitude regions where macroalgal–mesograzer interactions have been studied previously and there are corresponding differences in the nature of the interactions of macroalgae and mesograzers. Mesograzers in these communities also appear to have selected for a relatively high frequency of filamentous endophytes growing within the larger macrophytes.

Matthew Picklo, University of North Dakota School of Medicine) complexes I (30 kD subunit), II

(30 kD subunit), III (core protein 1, Rieske iron sulfur), and IV (subunits I and IV) (Invitrogen, CA), phospho AMP-activated protein kinase (AMPK) and phospho ACC (Cell Signaling, MA), and detected using enhanced chemiluminescence (SuperSignal, West-Dura, Pierce, IL). All data represent the means ± standard error of the mean (SEM), n = 6 for control and ethanol groups and n = 5 for MitoQ-treated groups. Statistical significance was determined using Student’s t test, analysis of variance (ANOVA), and Newman-Keuls test as post-hoc test. P < 0.05 was taken as significantly different. Animals were pair-fed with either ethanol or control liquid diets containing MitoQ (0, 5, or 25 mg/kg/day) for 4 weeks. There was no CHIR-99021 cost significant difference in body weight gain; however, the ethanol group had increased liver weight as compared to pair-fed controls which was prevented by MitoQ, although no effect was seen on liver to body weight ratios (Table 1). Consumption of ethanol did Alisertib purchase not significantly increase serum alanine aminotransferase levels compared with controls. Ethanol consumption resulted in increased serum HDL levels as expected but was not changed by MitoQ.44 The serum

low-density lipoprotein (LDL) / very low-density lipoprotein (VLDL) also showed no significant changes with alcohol exposure or any treatment (Supporting Fig. 1). Chronic ethanol consumption is known to increase 4-HNE-protein adducts and iNOS-dependent protein nitration.7, 9, 20, 21 In agreement with these findings, liver tissues show intense staining for 4-HNE-protein adducts in chronic ethanol fed animals compared to pair-fed controls (Fig. 1A,B). HNE immunoreactivity was not uniform with hepatocytes around the central veins showing the most intense staining (zones 2, 3) and a gradual decline toward the periportal region (zone 1). MitoQ treatment completely abolished ethanol-induced 4-HNE staining

in all regions of the liver sections examined. Control experiments show no effect of MitoQ at either dose (Fig. 1A,B) oxyclozanide and omission of the primary antibody for HNE resulted in no detectable signal (result not shown). Consistent with previous studies, chronic ethanol feeding increased 3-NT and iNOS staining with highest in zone 3, with intermediate staining in zone 2 (Fig. 2A,B).9, 20, 45 MitoQ treatment significantly decreased 3-NT staining in the liver of ethanol fed rats; however, it did not have any effect on the induction of iNOS protein. Controls with excess free 3-NT or omission of the primary antibody for 3-NT resulted in no signal (result not shown). It has been shown that MitoQ inhibits mitochondrial ROS and the consequent activation of HIF1α.30, 31, 46 We first confirmed the activation of HIF1α in response to EtOH (Fig. 3A).

elegans cell death

protein 3; ConA, concanavalin A; DISC, death-inducing signaling complex; FADD, Fas-associated protein with death domain; FasL, Fas ligand; GalN, D-galactosamine; HIV-1, human immunodeficiency virus 1; HM, mitochondrial heavy membrane; IFN-γ, interferon-gamma; IL-4, interleukin 4; JNK, c-Jun N-terminal kinase; Jo2, Fas-agonistic antibody; LPS, lipopolysaccharide; NKT, natural killer cells; siRNA, small interfering RNA; TNF, tumor necrosis factor; TNF-α, tumor necrosis factor alpha; TNFR1, tumor necrosis factor receptor 1; TNFR2, tumor necrosis factor receptor 2; TRADD, tumor necrosis RNA Synthesis inhibitor factor receptor type 1-associated death domain; TUNEL, terminal Epigenetic Reader Domain inhibitor deoxynucleotidyl transferase dUTP nick end labeling. For the generation of recombinant proteins, pTAT-HA and pTAT-βgal (beta-galactosidase) vectors were obtained from S. Dowdy (Howard Hughes Medical Institute, La Jolla, CA). The pTAT-HA vector was used for cloning of TAT-ARC constructs. We produced TAT recombinant

proteins as published.11 We lysed Escherichia coli BL21 or BL21(DE3)pLysS cells (Promega) transformed with pTAT-ARC, pTAT-ARC mutant (L31F; G69R), or pTAT-βgal (for His6-tagged proteins) encoding wildtype (WT) ARC, mutant ARC, and WT βgal, respectively, in 8 mol/L urea buffer, 1.0 mmol/L dithiothreitol (DTT), 10 mmol/L phenylmethylsulfonyl fluoride (PMSF), 15 mmol/L imidazole (Sigma), 100 mmol/L NaCl, 20 mmol/L Hepes, pH 8.0 (Calbiochem), and sonified six times for 30 seconds on ice. Cleared supernatant was subjected to Ni-NTA column (12 mL, GE Healthcare) connected to a fast protein liquid chromatography PLEK2 (FPLC; ÄKTA, GE Healthcare). TAT fusion protein was eluted in Z-buffer containing 500 mM imidiazole and subjected to ionic exchanger chromatography (Mono Q 5/10 column, GE Healthcare). TAT proteins were eluted with a single 2 mol/L NaCl step and desalted in phosphate-buffered

saline (PBS; G-25 column, GE Healthcare). We measured the protein concentration by Bradford assay. Purified TAT proteins were adjusted to 10% (v/v) glycerol, aliquoted, and stored at −80°C. Animal experiments were conducted following standards and procedures approved by the local Animal Care and Use Committee. For the animal models of ALF we used age-matched both male and female Balb/c mice for Fas-agonistic antibody (Jo2) and concanavalin A (ConA) models and female Balb/c mice for D-galactosamine/lipopolysaccharide (GaIN/LPS) experiments. Adult 8-week-old Balb/c mice were injected intravenously with 0.25 μg/g of Jo2 diluted in pyrogen-free PBS; 25 mg/kg ConA (Sigma) was injected intravenously diluted in PBS. For GaIN/LPS experiments mice were injected intraperitoneally with 700 mg/kg GaIN (Sigma) plus 35 μg/kg LPS from E. coli 055:B5 (Sigma) diluted in pyrogen-free PBS.

“
“We report data from two left hemisphere stroke patients with moderate-to-severe ideomotor apraxia who exhibited deficits in positioning their hands to use ‘conflict’ objects (objects grasped and used with different hand postures) relative to controls and patients with mild apraxia. These novel data support the claim that actions to common objects are subject to interference between multiple responses,

and suggest that errors in apraxia may be attributed selleck products to deficient resolution of competition between appropriate and inappropriate actions. “
“Synaesthesia is a broadly defined neural phenomenon in which stimulation of a sense or concept triggers a second perception not normally associated with the stimulus. For example, letters or numbers may trigger a colour experience, sounds may trigger a taste sensation, or tastes may trigger a feeling of touch. Dozens of forms check details of synaesthesia have been reported, but the relationship between the different

forms has not been studied: is someone with a particular form of synaesthesia likely to possess other types? If so, which ones? As an inroad to illuminating underlying mechanisms, we here examine which different synaesthesia types tend to co-occur. We analyzed reports of the forms of synaesthesia experienced by 19,133 participants who completed the Synaesthesia Battery (Eagleman, Kagan, Nelson, Sagaram, & Sarma, 2007), using correlation analysis, exploratory factor analysis (EFA), confirmatory factor analysis (CFA), and multidimensional scaling (MDS). Our analyses converged on the finding of five distinct groupings of synaesthesia forms. We label these coloured sequence Dehydratase synaesthesias (CSSs), coloured music synaesthesias, non-visual sequela synaesthesias, spatial sequence synaesthesia (SSS), and coloured sensation synaesthesias. Collectively, our findings reveal that

synaesthesia is an umbrella term that encompasses several distinct groups with independent probabilities of expression, and this may in turn suggest distinct underlying mechanisms and the possibility of different genetic bases. “
“The clinical differentiation of progressive supranuclear palsy from Parkinson’s disease can be challenging, due to overlapping clinical features and a lack of diagnostic markers. Abnormalities in cognitive function form part of the clinical spectrums of these diseases and distinctive cognitive profiles may be helpful in differentiating these diseases in the diagnostic period. A comprehensive neuropsychological test battery was administered to 12 patients with clinically diagnosed progressive supranuclear palsy and 12 patients with Parkinson’s disease matched for age and disease duration. Effect size (Cohen’s d) was calculated for cognitive tests that were significantly different between groups.