The animals were euthanized by decapitation 24 h after the last treatment. Maternal and offspring hippocampi and striatum were immediately dissected out in ice and stored at − 80 °C for later biochemical analyses. All tissues were homogenized in 1 mM phosphate buffer (pH 7.0) and centrifuged (3000 ×g, 5 min) to remove cellular debris. Supernatants were used for all biochemical

assays described. All the results were normalized by the protein content using bovine albumin as standard (Lowry et al., 1951). The formation of thiobarbituric acid reactive species (TBARS) was quantified by an acid-heating reaction with thiobarbituric acid. It is a widely GSK269962 chemical structure adopted parameter for measure oxidative damage on lipids, as previously described by Draper and Hadley (1990). The samples were mixed with 0.6 mL of 10% trichloroacetic acid (TCA) and centrifuged (10,000 ×g 10 min). Supernatant was mixed with 0.5 mL of 0.67% thiobarbituric acid and heated in a boiling water bath for 25 min. TBARS were determined by the absorbance selleck compound in a spectrophotometer at 532 nm. Results were expressed as nmol TBARS/mg protein. The formation of carbonyl groups was used as a parameter for oxidative damage to proteins, based on the reaction with dinitrophenylhidrazine (DNPH), as previously described by Levine et al. (1990). Proteins were precipitated

by the addition of 20% TCA and re-solubilized in DNPH. Then, the absorbance was read in a spectrophotometer at 370 nm. Results were expressed as nmol carbonyl/mg protein. The total thiol content in its reduced form was measured as an estimative of redox status, since it is present in proteins as well as glutathione molecules, and is played as an intracellular redox buffer. As previously described

by Ellman (1959), an aliquot of the sample was diluted in SDS 0.1%. Then, was added 0.01 M 5,5dithiobis-2-nitrobenzoic Selleck Venetoclax acid in ethanol. The intense yellow color was developed and read in a spectrophotometer at 412 nm after 60 min. Results were expressed as nmol SH/mg protein. The total reactive antioxidant potential (TRAP) was used as an index of non-enzymatic antioxidant capacity. As previously described by Lissi et al. (1992), this assay is based on the peroxyl radical (generated by AAPH solution, 2,2azobis[2-amidinopropane], with luminol) quenching by sample compounds. Sample addition decreases the luminescence proportionately to its antioxidant potential. The results were transformed in percentual and the area under the curve (AUC) was quantified as described by Dresch et al. (2009) by using GraphPad Software (San Diego, CA, USA — version 5.00). The AUC are inversely proportional to antioxidant capacity, which is higher with lower AUC values, and is lower with higher AUC values. Therefore, we express the results as the inverse value (1/AUC) to make it easier to comprehend.

, 2008). This is particularly important considering currently only 0.08% of the world’s oceans are no-take protected areas and international commitments have set global marine protection targets between 10% and 30% (CBD, 2009; United United Nations, 2002 and Wood et al., 2008). This paper reviews the evidence that was compiled to assess the benefits of establishing a full no-take MPA during the FCO consultation, particularly closing the tuna fisheries to the 200-mile EEZ. This evidence now provides valuable guidance for the implementation of the Chagos/BIOT MPA and how pelagic MPAs can increasingly function as a marine conservation

tool. The Food and Agriculture Organisation of the United Nations (FAO) has acknowledged that the maximum wild-capture fisheries potential from the world’s oceans has probably been reached (FAO, 2009). In recent INK 128 datasheet years, the Indian Ocean has produced approximately 10% of the almost 93 million tons of annual global fish production, with the western Indian Ocean producing

about 50% of the Indian Ocean landings (FAO, 2009). Offshore fisheries operating in the western Indian Ocean (such as those that have been licensed in Chagos/BIOT) are large-scale industrial fisheries with a high level of technology and investment. Industrial fishers tend to be distant water fishing fleets from Asia and Europe that target a wide range of migratory fish, such as tuna, kingfish, bonito, and mackerel, most of which are sold in the export market (FAO, 2009). Approximately LDK378 clinical trial 1 million tons of oceanic tuna and tuna-like species, with a processed value of £2–3 billion, are harvested each year from the western Indian

Ocean (FAO, 2009). The western Indian Ocean is also the region where the population status of exploited fish stocks is least known only or least certain (Kimani et al., 2009 and van der Elst et al., 2005), however recent reports indicate that overall catches continue to dramatically increase (FAO, 2009). Landings of species especially vulnerable to population decline as a result of fisheries, such as sharks and rays, have been steadily rising in both the eastern and western Indian Ocean since the 1950s (Camhi et al., 2009 and FAO, 2009). Furthermore, much of the region (not including Chagos/BIOT) suffers from pervasive illegal fishing, severe anthropogenic impacts, and lacks coordination to regulate and monitor international fishing companies (FAO, 2009). There is general pessimism in the international community about the inability or reluctance of regional fisheries management organisations (RMFOs) to make practical management decisions (FAO, 2009). Chagos/BIOT falls under the remit of the Indian Ocean Tuna Commission (IOTC), the RMFO responsible for the management and governance of tuna fisheries in the Indian Ocean.

If this is true for the diabetic population in general, it is even truer for those with

ongoing vascular complications. About 50% of diabetic patients with PAD have an associated coronary disease, 30% have carotid artery disease and about 15–20% have both simultaneously. Recent data show that patients with PAD treated successfully by percutaneous lower extremity revascularisation have better cardiovascular outcomes than those treated by conservative medical therapy alone [157]. The known cardiovascular risk KU-60019 cost factors, such as hypercholesterolaemia, hypertension and smoking, are made more aggressive by the presence of diabetes, particularly if there is no metabolic compensation. Given the pathogenic role played by risk factors in the manifestation and rapid evolution of cardiovascular disease, it can be presumed that they can also significantly

influence the results of revascularisation over time and the reparative ABT 199 response of tissue lesions. 1. Revascularisation should always be followed by a strict follow-up. “
“Figure options Download full-size image Download high-quality image (54 K) Download as PowerPoint slideThe sudden, premature departure of Dr. Gianvincenzo Barba last June 4th 2014, at the age of 52 years, was a tremendous shock for his companions of life and science in both the national and international communities. Dr. Barba was a highly recognized, tireless officer of the Italian Society of Human Nutrition and a strongly supportive member of the NMCD editorial board. I have known him since the very beginning of his career, at the time he was a resident student in the post-graduate school of internal medicine and, later on, of nephrology. In those years, he developed a special interest for electrolyte metabolism and gave a significant contribution to several research projects focusing on the role of ion transport abnormalities in pateints with high blood pressure and metabolic abnormalities.

Many of these projects dealt with the genetic regulation of sodium transport and salt-sensitivity and this is an area to which Gianni gave a particularly valuable contribution. In the late nineties, he was visiting scientist at the Thymidine kinase University College of London Medical School where he engaged in the study of the relationships of endothelial function and nitric oxide with tubular sodium handling in hypertensive patients, an experience that inspired his later scientific activity for quite some time. In the last fifteen years, once he became Researcher and later on a Senior Researcher at the Institute of Food Science of the Italian National Research Council, he turned most of his efforts and energy to cardiovascular prevention programs focused particularly to younger age groups.

However, stable isotope measurements are

much less expensive (<$10 US/sample for stable isotopes vs. >$500/sample for radiocarbon), so that we used stable isotope results to screen samples for radiocarbon analyses. Samples for planktonic respiration were collected along Barataria Bay and Breton Sound transects in late August and early October, 2010 (Fig. 1). Whole-water samples were used without filtration or size fractionation. Planktonic respiration was measured as oxygen decreases in dark bottles incubated 24 h at field temperatures (Wissel et al., 2008). Results are expressed in units of mmol oxygen consumed m−3d−1. Filter-feeding estuarine mussels (Geukensia demissa) were collected directly from oiled and unoiled marsh sites in May and September 2010. A size range of mussels (from www.selleckchem.com/screening/fda-approved-drug-library.html 40 to 110 mm total length) was collected at each site to study any size-related oil uptake. Mussels were collected from among marshgrass (Spartina) root mats, typically from within 5 m of marsh edges. Animals were placed on ice in the SCH727965 concentration field and later frozen whole. Marsh sites in Terrebonne Bay were located near Cocodrie, Louisiana, with an oiled site (site terr 50; oil visibly present) along the northwestern shore of Lake Barre and unoiled sites about 4 and 14 km to the southeast and nearer Cocodrie (sites terr 49 and terr

53 initial, respectively). Collections at one site (terr 53) were made in May before any oil entered the bay for an initial pre-spill baseline, with post-spill September collections at this site showing elevated aromatic CYTH4 hydrocarbon values in sediment samples from the edge (R.E. Turner, personal communication). Marsh sites in Barataria Bay were located in the north-central part of the bay, with an oiled site (site bar 66; visibly oiled but without elevated hydrocarbon readings in marsh edge sediment)

located across a bayou channel from a paired unoiled site (site bar 65; no visible oil and without elevated hydrocarbon readings in marsh edge sediment) in northeastern Wilkinson Bay. Two other unoiled sites (sites bar 67 and bar 68) were located respectively 3 km to the southwest in Wilkinson Bay and 5 km to the southeast along the north shore of Bay Jimmy. Barnacles were collected August 28–30, 2010, six weeks after the Deepwater Horizon well was capped. Most samples were collected along a long transect through western Barataria Bay (Fig. 1). For reference, pre-oil barnacle tissue samples from 10 years earlier (May 2000) were available from the same transect. Reference barnacle samples also were collected in late August 2010 in a second Louisiana estuary, Breton Sound, that also was close to the Deepwater Horizon spill site (Fig. 1). Introduction of Mississippi River water at the head of the Breton Sound estuary through a river diversion structure (Day et al., 2009) at Caernarvon, Louisiana, largely kept oil from entering this estuary.

The RISK group showed statistically significant group differences across all three of these BMQ outcomes (p < 0.001) while no significant group changes were detected in the NO RISK group. Post-intervention, the RISK group reported significantly lower scores on the necessity subscale (mean change score −1.31, 95% CI (−2.3, −0.4)), significantly higher scores on the concerns subscale (mean change score 3.72, 95% CI (2.9, 4.5)) and a statistically greater necessity-concerns differential (mean change score −5.03, 95% CI (−6.4, −3.6)), compared to the NO RISK group. According to an operational definition

of cognitive dissonance predicated upon a change in knowledge and a change in beliefs about benzodiazepine consumption

due to receipt of the intervention, 44/65 (68%) of participants in the RISK group and 19/79 (24%) of participants GDC-0199 selleck inhibitor in the NO RISK group experienced cognitive dissonance. The experience of cognitive dissonance was associated with a six-fold higher likelihood of patients reporting increased risk perception about their benzodiazepine prescription (OR = 6.61 95%CI (3.2, 13.8)). The RISK group reported significantly greater improvements in self-efficacy for discontinuing benzodiazepines following the intervention (mean change score 31.24 95% CI (17.9, 44.6)) compared to the NO RISK group. The added benefit of the tapering protocol on self-efficacy scores for discontinuing benzodiazepines within the RISK group was an extra 6.05 points on the self-efficacy scale, 95% CI (3.0, 9.1). No statistically significant differences in self-efficacy were found in the NO RISK group. Fig. 1 shows correlates and anticipated behaviors associated with an increased risk perception post-intervention. The RISK group reported a significantly higher likelihood of reading the tool more than once (OR = 8.34 95% CI (3.9, 17.9)), intention

to discuss the either intervention with family and friends (OR = 2.65 95% CI (1.3, 5.5)), and intention to discuss discontinuation with a physician (OR = 6.17 95% CI (2.8, 13.5)), or pharmacist (OR = 6.29 95% CI (2.8, 14.3)), compared to the NO RISK group. Findings from this study indicate that a personalized patient-targeted benzodiazepine educational intervention delivered directly to the individual consumer via written material was effective in changing medication risk perceptions in 45% of older chronic users. Heightened risk perception was explained by significant changes in knowledge and beliefs about benzodiazepines due to receipt of the tool. Our study suggests that participants in whom the intervention elicited changes in knowledge and beliefs may have experienced cognitive dissonance as the mechanism underlying increased risk perception.

581, p < .0001]. Again, the effect was found for both hands, and the interaction between stimulation condition and hand was again not

significant [F(1,10) = .464, p = .511] ( Fig. 2A). The average increase in contact heat-pain threshold INCB018424 was 1.96 °C. If vestibular signals are able to modulate multiple somatosensory submodalities, then CVS-induced changes in tactile and pain thresholds should be positively correlated with each other, despite being opposite in sign. This correlation would arise because of the common vestibular input both to tactile and nociceptive areas. We therefore investigated correlations across individuals between our established measures of vestibular stimulation effectiveness and modulations of touch and pain thresholds. Specifically, we correlated the CVS-induced changes in tactile and pain thresholds with the corresponding changes in the straight-ahead pointing error, slow-phase velocity and number of fast-phase (Table 2). We found a significant association

across individuals between touch and pain modulations (r = −.631, p = .038, two-tailed) ( Fig. 2B). Previous results ( Ferrè et al., ABT-263 supplier 2011) allowed us to predict the direction of correlations between vestibular effectiveness measures and changes in touch thresholds, but not between vestibular measures and changes in pain thresholds. We found an association between number of fast-phase and modulation of touch (r = −.549, p = .040, one-tailed), and a trend towards an association learn more between slow-phase velocity and modulation of touch (r = .466, p = .074, one-tailed), for which we had prior hypotheses ( Ferrè et al., 2011). We found no associations between vestibular measures

and pain modulation using two-tailed testing. A small study such as ours has only low statistical power to detect associations, and individual correlation coefficients should be treated with caution. Therefore, to avoid both Type 1 and Type 2 errors we took an aggregation approach. Because anatomical and physiological studies show common vestibular and multisensory cortical projections, we had a strong prior hypothesis of a single common source of variance affecting both vestibular and multisensory measures. We therefore used principal components analysis to summarise the variance structure underlying the correlation matrix. The first component (eigenvalue 2.33, explaining 45% of the variance) loaded somewhat homogeneously on vestibulo-ocular and somatosensory measures, but not on pointing. The second component (eigenvalue 1.19, explaining only 24%) loaded almost exclusively on the pointing measure. We interpret these components as, first, a common vestibular drive to both oculomotor and somatosensory processes, and a secondary independent effect restricted to spatial orientation.

Babington, James R, Seattle, WA; Barrett, Lisa Shanel, Marietta, OH; Basu, Aashna Rajan, Orange, CA; Bathia, Neeti A, New York, NY; Bax, Joseph Anthony, Lewiston, NY; Beaupin, Bernard R, Buffalo, NY; Bell, Jessica D, Bath, ME; Bell, Sonia, San Francisco, CA; Belvin, Brent Byron, Dallas, TX; Benaquista DeSipio, Gina Maria, Narberth, PA; Beninga, Angela L, Cincinnati, OH; Berdan, Jeffery T, Cedar Hills, UT; Bergsten, Mark David,

Chesapeake, VA; Bernert, Silke Andrea, Brandon, MS; Bethel, Adrian B, Temple Terrace, FL; Bhat, Ambika, Cleveland, OH; Bonder, Jaclyn Halpern, New York, NY; Bozak, David J, Duncansville, PA; Bristow, Sandee Jewel, Seattle, WA; Brown, Michael Nelson, Seattle, WA; Burr, Shane Jordan, Wood River, NE. Cahill, Terrence Joseph, Billings, MT; Calisoff, Randy Lyle, Mason, C646 ic50 OH; Campbell, Christie, Chapel Hill, NC; Chacko, Jeffrey Kainikudiyil, GDC-0980 clinical trial New

Hyde Park, NY; Chadd, Edmund, Ann Arbor, MI; Chai, Thomas, houston, TX; Chandler, Seth Duncan, Ocean Springs, MS; Chang, Eric Y, Irvine, CA; Chang, James, Alpine, NJ; Chang, Min Ho, Oakton, VA; Chang, Paul, Loma Linda, CA; Charchian, Beny, Los Angeles, CA; Chatilo, Alexandr Ivanovich, Shoreline, WA; Chavez, Justin Christopher, Houston, TX; Chaw, Edward K, San Mateo, CA; Chen, Halland, New York, NY; Chen, Jeffrey Li-da, San Diego, CA; Chen, Tao, Spanish Fort, AL; Chen, Xinqian, Green Bay, WI; Chiou, Philip, Cerritos, CA; Chitchyan, Ara R, Denver, CO; Chong, Timothy D, Ann Arbor, MI; Chowanadisai, Montida, Denver, CO; Chuang, Kathy, Cambridge, MA; Claflin, Brandon Scott, Norman, OK; Clavet, John, Lexington, SC;

Clodfelter, Jaimie Ann, New Orleans, LA; Coba, Miguel A, Livingston, NJ; Colyer, Jessica Lynn, Cincinnati, OH; TCL Concannon, Leah Grace, Seattle, WA; Cruz, Gloydian, Pismo Beach, CA. Davis, Bradley Scott, Parsons, KS; Dawson, Christopher Allen, Richmond, VA; Day, Carly Ellen, Salt Lake City, UT; de Guzman, Joy Imperial, Arden, NC; Dedes, Howard, Rancho Cucamonga, CA; Degen, Jeffrey W, Portland, OR; DeLuca, Jason, Orando, FL; Deo, Sheetal, Bayside, NY; Desai, Jignyasa, Bayside, NY; Devine, Jennifer M, Somerville, MA; Diaz, Christine Torralba, Tustin, CA; Diaz, Mirielle, New York, NY; Dinicola, Anthony Paul, Chester, VA; Dokukin, Andrei, Grover Beach, CA; Donlon, Margaret M, Newark, NJ; Donnelly, Jennifer Lauren, Coppell, TX; Doroftei, Olga, Fort Worth, TX; Duncan, Suzanne Troup, Nantucket, MA; Durand-Sanchez, Ana, Houston, TX, Edelen, Connie Ann, Charlotte, NC; Edinger, Jason McElveen, Columbus, OH; Egger, Andrew D, Phila, PA; El Shami, Amir, Chicago, IL; Elahi, Foad, Chicago, IL; Elmers, Anna Choo, Atlanta, GA; Emdad, Payam, San Diego, CA.

So, the aim of this study was to develop and assess the quality parameters and sensory acceptability of Coalho cheeses made from a mixture of goat’s and cow’s milk and compare the evaluated characteristics with those obtained for the Coalho cheeses made from plain goat’s or cow’s milk. Three different cheese types

were made in duplicate in three different moments: CCM (cheese made from cow’s milk), CGM (cheese made from goat’s milk) and CCGM (cheese made from cow’s milk and goat’s milk, 1:1 ratio, L:L). The cheeses were manufactured following the traditional procedure proposed by Embrapa for traditional cow’s Coalho cheese, which is a Brazilian agricultural research company (Laguna & Landim, 2003). Milk composition is presented in Fig. 1. Coalho cheeses were manufactured in 30-L vats from commercially pasteurized goat and/or cow milk heated to 90 ± 1 °C for 10 min, followed by direct acidification with 0.25 mL/L selleck compound lactic acid. Calcium chloride (0.5 mL/L) and a commercial coagulating agent (0.9 mL/L, Ha-La®) and starter of mesophilic

lactic cultures (R-704 Lactococcus lactis subsp. cremoris and L. lactis subsp. lactis) available from Christian Hansen Brazil (Valinhos, Minas Gerais, Brazil) were also added to the vats. The vats were incubated Alectinib at 36 °C until a firm curd was formed (approximately 40 min). The obtained gel was gently cut into cubes, allowed to drain, salted in brine (12 g/L NaCl), placed in perforated rectangular containers (approximate capacity of 250 g) and maintained at 10 °C under pressure for 4 h and vacuum packaged. The cheese obtained after storage at 10 °C for 24 h was regarded as the final product. The cheeses were then stored at 4 °C for 28 days to simulate the common shelf-life. Cheeses from each treatment (n: 6) were used for physicochemical and Loperamide technological analysis of the final product (day 1) and after 7, 14, 21 and 28 days of storage. For fatty acids profile and sensory analysis, the cheeses were evaluated after 14 and 28 days of storage.

Each day, three cheeses from the same batch and trial were unpacked and immediately used for physicochemical, fatty acids profile, textural and sensory analysis. The pH values of the cheeses were determined using a combined pH glass electrode connected to a pH-meter MicropH 2001 Crison potentiometer (MicropH 2001, Barcelona, Spain). The moisture content from the samples was determined following the international standard method (IDF, 1958), and protein, fat and salt (sodium chloride – NaCl) contents were measured using a LactoScope Filter C4 apparatus (Delta Instruments, The Netherlands) according to Madureira, Pintado, Gomes, Pintado, and Malcata (2011). Lipid extraction was performed according to Hara and Radin (1978) and transesterification of the FA according to Christie (1982).

8 The terms MTBI and concussion are used interchangeably in this review. The protocol registration, case definition, literature search, critical review strategy, and data synthesis are outlined in detail elsewhere.10 and 11 Briefly, the review was conducted and reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement.12 The electronic databases MEDLINE, PsycINFO, Z-VAD-FMK price Embase, CINAHL, and SPORTDiscus were systematically searched from 2001 to 2012, and the reference lists of all reviews and meta-analyses related to MTBI,

and articles meeting the eligibility criteria were screened for additional studies. Articles were screened for eligibility according to predefined criteria. Inclusion criteria included original, published peer-reviewed research U0126 mouse reports in English, French, Swedish, Norwegian, Danish, and Spanish. Studies had to have a minimum of 30 concussion cases resulting

from sports participation, and had to assess outcomes such as self-rated recovery, clinical improvement, or RTP. The definition of MTBI had to fall within the definitions provided by the WHO Collaborating Centre Task Force on MTBI and the Centers for Disease Control and Prevention (CDC).10 The WHO Task Force defines MTBI as “an acute brain injury resulting from mechanical energy to the head from external physical forces. Operational criteria for clinical identification include: (i) 1 or more of the following: confusion or disorientation, loss of consciousness for 30 minutes or less, posttraumatic amnesia for less than 24 hours, and/or other transient neurologic abnormalities such as focal signs, seizure, and intracranial lesion not requiring surgery; and (ii) Glasgow Coma Scale score of 13–15 after 30 minutes postinjury or later upon presentation for healthcare. These manifestations of MTBI must not be due to drugs, alcohol, medications, caused by other injuries

or treatment for other injuries (eg, systemic injuries, facial injuries, or intubation), caused by other problems (eg, psychological PRKD3 trauma, language barrier, or coexisting medical conditions), or caused by penetrating craniocerebral injury.”8(p115) Persons with fractured skulls were included if they fit this case definition. The CDC provides an additional definition that can be derived from clinical records. According to the CDC, MTBI is present if an Abbreviated Injury Severity Scale score of 2 for the head region is documented.10 An administrative data definition for surveillance or research is also provided.10 Specifically, cases of MTBI are recognized among persons who are assigned certain International Classification of Diseases, Ninth Revision, Clinical Modification diagnostic codes. 10 and 11 Eligible study designs were randomized controlled trials and cohort and case-control studies.

By convention the ONSD is assessed 3 mm behind the papilla. In order to gauge the ONSD, the distance between the external borders of the hyperechoic area surrounding the optic nerve should be quantified (Fig. 1). Several studies reproduced a high intra- and interobserver reliability of the sonographic ONSD assessment [6], [7] and [8]. However, data on normal values

vary SB431542 price considerably, especially in former publications [9]. This may be explained by differing ultrasound equipments and their influence on sonographic findings and measurement criteria different from the ones stated above. Therefore, several authors emphasized the necessity of correctly used measuring points and clearly displayed optic nerve structures for reliable results

[10] and [11]. In our study on this topic, using above criteria, the mean ONSD was 5.4 ± 0.6 mm in healthy adults that matches closely with results derived from two MRI studies [7]. Rohr et al. found a value of 5.3 ± 0.6 mm in patients with mental disorders but without intracranial lesions or signs of elevated ICP [12]. Geeraerts et al. indicated a mean ONSD of 5.1 ± 0.5 mm in healthy volunteers [13]. Accordingly, a cadaver study illustrated a good correlation between the evaluation of the ONSD by MRI and transbulbar sonography. Despite the unfavorable angle between the course of the optic nerve and the insonation direction in transbulbar sonography Steinborn et al. observed an acceptable agreement between MRI and the sonographic approach [11]. These results have been verified in an investigation of sixty-five children, recently [10]. In comatose or sedated patients with intracranial PD-1/PD-L1 signaling pathway bleeding and traumatic head injury sonographic ONSD evaluation has been proven to be feasible in predicting raised ICP [3], [14] and [15]. An MRI-based investigation confirmed this observation [13]. Geeraerts et al. found a mean ONSD of 6.3 ± 0.6 mm in brain injured adults using sonography [14]. By means of MRI they

indicated a mean ONSD of 6.3 ± 0.5 mm oxyclozanide [13]. The threshold of ONSD predicting an elevated ICP was proposed to be between 5.7 and 5.9 mm [3], [13], [14] and [15]. In a metaanalysis of six studies with data on a total of 231 patients with traumatic brain injury or intracranial hemorrhage the technique had a sensitivity of 90% and a specificity of 85% [16]. Furthermore, transbulbar ONSD assessment has been suggested for follow-up examinations of children with internal hydrocephalus and ventriculoperitoneal shunt systems [17]. Moreover, two sonographic investigations observed a correlation between the severity of acute mountain sickness and ONSD [18] and [19]. Only few results were published on the sonographic ONSD evaluation in idiopathic intracranial hypertension (IIH) [20]. One MRI based retrospective study described a mean ONSD of 6.5 ± 0.9 mm in patients suffering from IIH and quote a cut-off value for raised ICP of 5.8 mm [21].