g , Guastella et al , 2008 and Rimmele et al , 2009) Following i

g., Guastella et al., 2008 and Rimmele et al., 2009). Following inhalation, participants sat quietly for 45 min, the length of time it is believed to take for central oxytocin levels to plateau (Born et al., 2002). Participants were instructed to bring a book or magazine to read during this time. Following the rest period, participants completed the two face processing tasks in the same order (commencing with the face memory task), in order to ensure equality of central oxytocin levels for each

test. General affect was measured throughout the experiment using the Multidimensional Mood Questionnaire (MMQ: Steyer, Schwenkmezger, Notz, Selleck Venetoclax & Eid, 1997), to assess the possible mood-altering effects of oxytocin, and to control for non-specific click here effects of attention and wakefulness (the MMQ is composed of three sub-scales: good–bad, awake–tired and calm–nervous). Each participant was required to complete the MMQ at three intervals across the experiment: immediately following inhalation, after the 45 min resting period, and after the two face processing tests had been completed. Finally, the experimenter enquired about adverse side effects during the testing session and again 24 h after test completion. Statistical analyses were conducted on the MMQ results collected across the testing sessions and on the behavioural data collected from the two face processing tasks. Scores on the MMQ

were calculated according to the three sub-scales, and data were entered into a 2 (spray: oxytocin, placebo) × 3 (time of MMQ completion: after inhalation, after rest, end of session) × 2 (group: DP, control) mixed factorial MANOVA. Scores for the two face processing tests were entered into a 2 (spray: oxytocin, placebo) × 2 (group: DP, control) mixed factorial multivariate analysis of variance (MANOVA). The data file for one DP participant

was unreadable in the placebo condition of the CFMT, and was therefore not included in the analysis of this test. Additional comparisons were carried out to investigate (a) whether DP performance Alectinib ic50 in the oxytocin condition fell within the same range as control placebo performance, and (b) whether the severity of each individual’s prosopagnosia correlated with the extent of their improvement on the two tasks. For the latter analyses, scores obtained on the original version of the CFMT and the CFPT (i.e., the tests run within the original diagnostic session: see Table 1) were correlated against the level of improvement in the oxytocin condition (oxytocin performance minus placebo performance) of the CFMT and matching test, respectively. Adverse side effects were only reported by one DP participant following inhalation of either spray. Specifically, this individual reported a slight headache immediately after oxytocin inhalation, but this had disappeared by the 24-h follow-up. A mixed factorial MANOVA revealed no main effect of spray or group, F(3,16) = .569, p = .643, ƞp2 = .

S2, online supplementary file] In recent atherotrombotic occlusi

S2, online supplementary file]. In recent atherotrombotic occlusion, vascularization, expression of the highly active remodeling process, was also observed [Fig. S3, online supplementary file]. Vascularization was not detected in the hyperechoic with acoustic shadow calcific tissue, nor in the hypoechoic necrotic and hemorrhagic areas. Moreover, plaque vascularization is present in almost every plaque, regardless the degree of stenosis. In acute symptomatic patients a completely different pattern of vascularization was detected with ultrasound and validated by post-operative histology in a first paper published from our group

AZD6244 [41]. In the first seconds after contrast agent administration, no vascularization seemed to be identified in the hypoechoic areas. Few seconds later, vascularization presented as a major diffuse area of contrast enhancement at the base of the plaques, due to an agglomerate of many small microvessels, difficult to differentiate from each other, while the residual hypoechoic part of the plaque, corresponding to the necrotic or hemorrhagic contents, remained avascularized. In operated patients, carotid

endoarterectomies were carefully performed in order to obtain selleck kinase inhibitor the whole plaque with minimal trauma. The pathologist evaluated the removed plaques after formalin fixation: the pathologist and the sonographers discussed the regions of interest previously observed at ultrasound imaging. The intra-operative macroscopic findings confirmed the presence of the these unstable plaques observed at contrast ultrasound. The microscopic

findings confirmed the presence of plaque vascularization in the ultrasound contrast-enhanced areas. Symptomatic carotid plaques showed a relevant increased number of small (diameter 20–30 μm), immature microvessels in respect to asymptomatic ones, consisting with a strong neoangiogenetic activity. Angiogenesis was less represented in asymptomatic plaques that underwent surgery, with microvessels of a higher caliber (80–100 μm). Immunostaining with VEGF, MMP3, CD 31 and CD 34 depicted a different distribution pattern between asymptomatic and symptomatic lesions: while in the former antigenic activity was of a lesser degree and localized mainly along the microvessels course, in symptomatic plaques a high antigenic fixation was observed also in the external part of the plaque, closer to the adventitial layers. In the same areas, an inflammatory infiltrate constituted by macrophagic foam cells and T lymphocytes, indicative of high plaque activity was detected, with small areas of hemorrhage expression of microvessels rupture.

The number of functional VRs varies dramatically between and even

The number of functional VRs varies dramatically between and even within mammalian species 4, 15 and 42]; most humans are likely to have very few, if any [43]. VR expression is largely restricted to sensory neurons in the olfactory system, where they are thought to be specialised to detect chemical signals that provoke behaviour, including pheromones. However, only a handful of VR-ligand pairs have been fully characterised 5, 13•• and 17]. There are two structurally divergent classes of VR, V1Rs and V2Rs, that

bind organic volatiles and peptides, respectively (reviewed in [4]). In rodents, each class is independently expressed in spatially restricted FK228 mouse vomeronasal sensory neuron that project to distinct aspects of the accessory olfactory bulb [23]. V1Rs are expressed in a monogenic manner, so that each neuron is patterned by a single receptor [14]. In contrast, V2Rs are expressed in combinations of two or more per

neuron [44]. The mechanism of VR gene selection and the functional consequence of combining V2Rs are not yet known. This simple non-redundant VNO coding model suffers from a fundamental theoretical challenge: there are over 350 functional VRs encoded in the mouse genome (see Box 2) [4]. While there are certainly sufficient Trichostatin A cost peptides and organic molecules secreted by mice to generate a unique ligand for each, are there 350 distinct social behaviours for each pheromone receptor to mediate? Three complementary studies revealed that this is unlikely, because the VNO has evolved to mediate more than just social behaviours. By recording from the accessory olfactory bulb, the brain region that receives primary inputs from the VNO, Ben-Shaul and colleagues observed patterns of neural activity when urine from predators was applied to the VNO [6]. Moreover, most of the neurons they recorded from responded only to the predator urine, not mouse urine.

This suggested that the VNO was specifically tuned to detect chemical cues derived from predators. One of these cues was independently isolated from rat urine, and shown to directly activate a subset of VSNs [7]. D-malate dehydrogenase Mice responded by displaying stereotypic avoidance and defensive behaviours, proving that the mammalian VNO can also detect behaviour-provoking chemicals from other species. Interestingly the rat-derived signal, MUP13, is a homologue of mouse major urinary proteins (MUPs) which are themselves pheromones with diverse social functions (reviewed in [8]). It is therefore likely that some of VRs have evolved to distinguish between structurally related proteins from the same and differences species, and in turn mediate very different behaviours. This was further reinforced when a homologous protein from a cat, Feld4 was shown to activate an overlapping subset of VSNs and provoke similar defensive behaviours as the rat signal [7].

The exhaustiveness was set to 50 All other parameters were used

The exhaustiveness was set to 50. All other parameters were used as defaults. For the ligand docked, the conformation from the lowest binding free energy with inferred inhibitory reactivity was accepted as the

best affinity this website model. The redocking calculation were carried out using Autodock 4.0.1, following method of Musilek et al. (2011). Briefly, a Lamarckian genetic algorithm (Amber force field) was used, and a population of 150 individuals and 2500,000 function evaluations were applied. The structure optimization was performed for 27,000 generations. Docking calculations were set to 100 runs. At the end of calculation, Autodock performed cluster analysis. The 3D affinity grid box was designed to include the full active and peripheral site of AChE. The number of grid points in the x-, y- and z-axes was 60, 60 and 60 with grid points separated by 0.253 Å. The conformations and interactions were analyzed using the programs Accelrys Discovery Studio Visualizer

2.5 and PyMOL ( Seeliger and de Groot, 2010). Data are expressed as means ± SEM. Statistical analysis was performed using one-way buy CYC202 analysis of variance (ANOVA), followed by Student–Newman–Keuls test when appropriate. In addition, linear regression was performed to identify a possible dose dependent effect. Values of p < 0.05 were considered significant. Table 1 shows that IBTC did not significantly affect DCF-RS levels in tissue homogenates. In addition, lipid peroxidation, indicated by TBARS levels (Table Resminostat 2), did not change significantly in liver, kidney, or brain homogenates after treatment with any concentration of IBTC. However, there was a significant reduction in TBARS level in heart homogenates after treatment with most of the concentrations of IBTC. NPSH levels did not change in liver, kidney, or heart homogenates, but increased significantly in brain homogenates after treatment with IBTC (Table 3). Catalase and GPx activities did not change significantly (data not shown). In addition, Na+/K+ ATPase activity in the brain (Fig.

2) and ALA-D activity in liver and blood (Fig. 3A and B) did not change significantly. In addition, LD50 was considered higher than 500 mg/kg. The percent of hemolysis in RBCs in the presence of various concentrations (10–200 μM) of IBTC did not change significantly compared to controls (data not shown). Murine J774 macrophage-like cells and isolated human lymphocytes were used to test the cytotoxicity of IBTC. Fig. 4 shows the MTT levels in these cell types. Concentrations of 50 μM of IBTC and above significantly reduced MTT levels compared to controls in J774 macrophage-like cells (Fig. 4A). The MTT levels did not change significantly compared to controls in isolated human lymphocytes (Fig. 4B). MAP exposure at a concentration of 25 μM inhibited AChE and BChE activity in all samples. None of the IBTC concentrations tested had a significant effect on AChE or BChE activity (data not shown).

Findings of cognitive changes in unilateral vestibular loss have

Findings of cognitive changes in unilateral vestibular loss have been less consistent. In a large study, 50 patients with unilateral labyrinthine hypofunction as a consequence see more of previous vestibular neuritis were compared to 50 age- and sex-matched healthy controls on their spatial working memory performance (using the Corsi block task) and their navigation abilities (Guidetti et al., 2008). Results

showed spatial working memory as well as navigational impairments in both left and right labyrinthine-deficient patients as compared to controls. In contrast, an earlier study found a trend toward spatial memory and navigation impairments in patients with right, but not left, unilateral vestibular deafferentation (Hufner et al., 2007). Attention processes (involved in simple, inhibitory, and forced choice reaction time tasks) have also been described as compromised in patients with well compensated (no symptoms of dizziness or definable postural deficit) surgically confirmed unilateral vestibular loss, particularly when patients were simultaneously engaged in a postural challenge task (Redfern et al., 2004). Beyond spatial navigation and memory, the capacity to perform mental rotation

tasks has been reported as impaired EPZ015666 in a small sample of patients (n=8) with bilateral vestibular loss as compared to 14 healthy controls ( Grabherr et al., 2011). There is also some references in the literature associating vestibular loss with impairments with mental arithmetic or dyscalculia ( Risey and Briner, 1990 and Smith, 2012); however the findings are inconsistent (e.g. see Andersson et al. (2003)). Some further support for vestibular input to various cognitive tasks is derived from galvanic and caloric vestibular stimulation studies. For example, a recent study applied suprathreshold bilateral bipolar galvanic vestibular stimulation to 120 healthy adults and compared their performance on a cognitive battery to a control condition which involved no GVS or subthreshold stimulation ( Dilda et al., 2012). Results were consistent with the literature on bilateral vestibular loss

and indicated that galvanic vestibular stimulation significantly degraded performance on short-term spatial memory, egocentric mental rotation (perspective taking) with no difference noted in other areas of cognition (including reaction Obatoclax Mesylate (GX15-070) time and dual tasking). An earlier study using unilateral caloric stimulation in healthy individuals suggested that caloric stimulation selectively activates contralateral cerebral structures and enhances cognitive processes mediated by these structures, with left ear stimulation improving spatial memory and right ear stimulation improving verbal memory ( Bachtold et al., 2001). Given that the cognitive changes in spatial memory associated with vestibular loss remain apparent 5–10 years following vestibular neurectomies (Brandt et al., 2005 and Schautzer et al.

Instead of a 1 5 cm narrow cut for isoprostane measurement, the s

Instead of a 1.5 cm narrow cut for isoprostane measurement, the scraped area was extended to 4 cm above and 1 cm below the PGF2a methyl ester migration. The purified F4-neuroprostanes were derivatized to trimethysilyl ether derivatives then dissolved in undecane that was dried over a bed of calcium hydride. Negative ion chemical ionization MS was performed by Agilent 6890 GC and Model 5975 MSD instruments

with selected ions monitored for [2H4]15-F2α-IsoP selleck compound internal standard (m/z 573) and F4-NeuroPs (m/z 593). Cryropreserved ipsilateral C57Bl6 mouse brain specimens were obtained at various post-injury time points following closed skull mTBI. All mice used were 60 days of age at the time of primary brain injury. Protein was pooled from all specimens by protein amount as reference material. For isobaric TMT labeling, 50 mg of C8 magnetic beads (BcMg, Bioclone Inc.) were suspended

in 1 mL of 50% methanol. Immediately before use, 100 μL of the beads were washed 3 times with equilibration buffer (200 mM NaCl, 0.1% trifluoroacetic Tanespimycin acid (TFA)). Whole cell protein lysate (25–100 μg at 1 μg/μL) was mixed with pre-equilibrated beads and 1/3rd sample binding buffer (800 mM NaCl, 0.4% TFA) by volume. The mixture was incubated at room temperature for 5 min followed by removing the supernatant. The beads were washed twice with 150 μL of 40 mM triethylammonium bicarbonate (TEAB), and then 150 μL of 10 mM dithiolthreitol (DTT) was added. The bead-lysate mixture underwent microwave heating for 10 s. DTT was removed and 150 μL of 50 mM iodoacetamide (IAA) added, followed by a second microwave heating for 10 s. The beads were washed twice and re-suspended in 150 μL of 40 mM TEAB. In vitro proteolysis was performed with 4 μL Fossariinae of trypsin in a 1:25 trypsin-to-protein ratio (stock = 1 μg/μL in 50 mM acetic acid) with microwave-assisted heating for 20 s in triplicate. The supernatant was used immediately or stored at −80 °C. Released tryptic peptides from digested protein lysates, including the reference materials described above, were modified at the N-terminus and at lysine residues with the tandem mass tagging (TMT)-6plex

isobaric labeling reagents (Thermo scientific, San Jose, CA). Each individual specimen was encoded with one of the TMT-126-130 reagents, while reference material was encoded with the TMT-131 reagent: 41 μL of anhydrous acetonitrile was added to 0.8 mg of TMT labeling reagent for 25 μg of protein lysate and microwave-heated for 10 s. To quench the reaction, 8 μL of 5% hydroxylamine was added to the sample at room temperature. To normalize across all specimens, TMT-encoded cell lysates from individual specimens, labeled with the TMT-126-130 reagents, were mixed with the reference material encoded with the TMT-131 reagent in 1126:1127:1128:1129:1130:1131 ratios. These sample mixtures, including all TMT-encoded specimens, were stored at −80 °C until further use.

Parece-nos que, desde que a crítica seja feita de forma construti

Parece-nos que, desde que a crítica seja feita de forma construtiva, irá dar maior vivacidade ao nosso Jornal. Um novo formato de artigo que gostaríamos de passar a ter regularmente consiste na Discussão de um Caso Clínico, um pouco semelhante aos casos do NEJM: «Clinical problem-solving», ao qual iremos dar o nome de Desafios Clínicos. Pedíamos que, sempre que tenham casos que possam constituir um desafio de diagnóstico, BGJ398 nmr os enviem para esta secção do Jornal, com este tipo de formato. Neste tipo de artigo, deve considerar-se o processo de decisão clínica passo a passo.

Perante cada grupo de dados clínicos apresentados, discute-se quais são as hipóteses de diagnóstico, apresentando-se os argumentos em que se baseiam. Idealmente, deve ter material de suporte,

como radiografias ou exames histológicos ilustrativos. Peço também que, sempre que possível, enviem os artigos em inglês, dado que isso irá facilitar a possibilidade de indexação. O GE é a revista dos Gastrenterologistas e a sua qualidade Seliciclib manufacturer irá sempre depender do empenho e do interesse que os Gastrenterologistas ou os Médicos interessados na Gastrenterologia tenham no Jornal. “
“A doença de Crohn (DC) apareceu como entidade clínica própria no primeiro terço do século xx1. Ao longo do século a doença passou a ser reconhecida também em Pediatria tendo a sua incidência aumentado consideravelmente nos últimos 40 anos. Um estudo europeu referente a 739 crianças com doença inflamatória intestinal calculou uma incidência de DC e de colite ulcerosa em 3,0 e 1,5 casos novos por 100.000 habitantes2. Uma meta-análise recente efetuada com base em 139 estudos efetuados entre 1950 e 2009, provenientes de 32 países, confirma esta tendência3 and 4. Estima-se em 20% o número de casos de DC que se apresentam na infância e adolescência5. A mediana da idade no diagnóstico é de 12 anos2 and 6, coincidindo muitas vezes com a fase de crescimento e desenvolvimento rápidos e a oportunidade única para crescer. Esta questão não se coloca quando o diagnóstico é efetuado no adulto, pois

o crescimento linear já ocorreu. Uma das queixas frequentes antes ou após o diagnóstico, isolada ou associada a outros aminophylline sintomas, é o atraso de crescimento. Estima-se que, pelo menos, 40% dos doentes de Crohn diagnosticados antes dos 18 anos sofram de atraso de crescimento em algum período da sua doença5 and 7. O atraso da maturação pubertal também é por si só uma queixa que merece investigação de DC pois pode ser um sinal que precede cronologicamente as queixas gastrointestinais8. Os fatores clínicos que potencialmente afetam a estatura final incluem o intervalo entre o início dos sintomas (que pode ser o atraso estatural isolado) e a data do diagnóstico, a presença de doença jejunal no diagnóstico, o início pré-pubertário de sintomas, o género e, naturalmente, a gravidade da doença8 and 9.

Thus, for most of the sources prospective studies would be needed

Thus, for most of the sources prospective studies would be needed to determine the role of MES detection to predict future cardioembolic stroke. Atrial fibrillation is the single most frequent cause of cardioembolic stroke. No wonder MES detection has been used in a number of studies in

this entity. Studies have tried to determine the prevalence of MES, the risk of patients with MES to suffer subsequent stroke and to correlate the presence of MES with anticoagulation therapy. In the paper of Georgiadis et al., 5 of 24 patients (21%) with atrial fibrillation (AF) had MES [12]. Nabavi et al. found MES in 11 of 26 patients (42%) with valvular AF compared with 3 of 21 patients (21%) with non-valvular AF [13]. MES were also more frequently found in patients with a history of thromboembolism. Cullinane et check details al. found MES in 13 of 86 patients with non-valvular AF (15%) [14]. There was no difference in the prevalence between symptomatic (16%) and asymptomatic (13%) patients. Furthermore, there was no correlation between MES and the use of aspirin or left atrial thrombus. There was also no correlation

CYC202 purchase between MES and echocardiographic risk markers (such as left atrial enlargement). One study investigated, whether MES were more frequent in 37 patients with stroke due to AF compared with 10 patients with AF but without stroke and 92 controls [15]. MES were detected in 11 (29%) of the symptomatic patients and only in one without a history of stroke. The MES count was quite high in this study with ∼15

events per hour which sheds some doubt on the credibility of the data. Over a follow-up period of 18 months one patient with MES at baseline had a recurrent stroke; however this occurred 1 year from study inclusion. Overall, studies were too small to address the question of stroke risk and studies are too heterogeneous to perform a meta-analysis of studies performed. Until larger Isotretinoin studies report otherwise, there seems to be no added value of MES detection to address clinical questions in patients with AF. MES detection is a well-established method to monitor cardiac or vascular procedures. Currently, a well-established procedure is the implantation of cardiac left ventricular assist devices (LVAD) that allow “bridging” of patients with very severe left ventricular cardiac failure to heart transplantation or until the heart has recovered from a temporary disease. These patients are constantly endangered by the occurrence of systemic and frequently cerebral embolism although antiplatelet and anticoagulation strategies are both used to decrease this risk. These patients are well characterised and an attractive group of patients to test whether silent microembolism is associated with clinical events. In one study, 20 patients with the Novacor N100 LVAD were investigated [16]. MES detections were performed once weekly for 30 min, and thromboembolic events were recorded. 44 events occurred in 3876 LVAD days resulting in an incidence of 1.

This may be explained by the fact that although both Cys C and Cr

This may be explained by the fact that although both Cys C and Cr are filtered by the glomerulus, a portion of Cr is also secreted by the tubules and excreted in urine [21]. When glomerular filtration is compromised, tubular secretion of Cr is increased in order to maintain normal plasma Cr concentration [22]. The results therefore suggest that RFU children had a less efficient glomerular filtration

rate and a compensatory ABT-199 solubility dmso increase in tubular secretion of Cr. An alternative possibility is that the RFU children had a lower lean body mass/weight ratio than LC children resulting in a lower daily release of Cr into the circulation which may have obscured the lower GFR. Cys C is regarded as a more sensitive marker for the calculation of eGFR in children because of problems of interpreting those based on Cr [23]. The data therefore suggest that RFU children had a less efficient GFR but not sufficient to cause clinical problems. Both the original and follow-up studies measured FGF23 concentrations using the selleck Immutopics C-terminal FGF23 assay which detects both the intact FGF23 hormone and its C-terminal fragments. In the case of RFU

it is likely that the elevated FGF23 was reflecting both an increased production of intact and biologically active FGF23 hormone and possibly a greater proportion of presumed inactive C-terminal fragments. Another intriguing finding was the inverse correlation between Hb and FGF23 in RFU children. As iron deficiency anaemia is endemic in The Gambia [24] a lower Hb in these children is likely to imply a lower iron status. A finding of a relationship between Hb and FGF23 therefore supports previous suggestions of the involvement of iron in FGF23 metabolic pathways [25] and [26]. Researchers have hypothesised that iron is required for the clearance of FGF23 fragments by the kidney and also that iron may inhibit the cleavage of intact FGF23 [25]. It is possible that the combination of low iron status and lower eGFR may have resulted in greater amounts of

circulating FGF23 fragments in RFU children, due to less efficient clearance by the why kidney and/or an increased production of C-terminal fragments. None of the RFU children had radiological signs of active rickets but only half of the children had recovered from their lower-limb deformities. Those with persisting deformities were of similar age but had higher 1,25(OH)2D and lower Cys C-eGFR when compared with those who had recovered. A study carried out in Nigeria suggested incomplete distal renal tubular acidosis (idRTA) as a possible cause of differing rates of recovery from rickets-like-deformities [27]. However, it is an unlikely explanation in this Gambian study as idRTA is characteristically accompanied by high uCa which was not seen in the RFU children.

1, 2 and 3 White-light

1, 2 and 3 White-light selleck colonoscopy alone, without the aid of enhanced imaging or detailed inspection, is imperfect and lacks acceptable sensitivity and specificity,4 and 5 with the yield of random biopsy for dysplasia

ranging from 0% to 0.2%.6, 7, 8 and 9 Dysplasia detection rates are significantly higher with CE,7 and 10 such that CE with targeted biopsy is now recommended.1 and 2 Adopting the technique into clinical practice has been perceived to be difficult because of availability, lack of endoscopist experience, reliability of image interpretation, cost, and the additional time needed to perform the procedure. This article reviews the commonly available technique of CE. From our own experience and study, suggestions are provided of the key steps for the implementation of CE into solo and group clinical practices for UC dysplasia surveillance. CE involves the application of dye solutions (indigo carmine or methylene blue) onto the colonic mucosa to enhance contrast during surveillance colonoscopy.11 Studies showing significantly higher yield of dysplasia detection using CE compared Volasertib nmr with white-light colonoscopy have used both dyes, with concentrations range from 0.03% to 0.4% for

adequate mucosal enhancement. Indigo carmine is a plant-based dye that pools into the mucosal crevices and can subsequently be washed away. Methylene blue is a vital dye that is actively taken up by the colonic epithelium after approximately 60 seconds.11 It has been associated with DNA damage

of unclear clinical significance.12 Adequate colonic preparation quality is essential when using CE. Farnesyltransferase As such, during colonoscope insertion, irrigate the colon using water and simethicone, and suction any remaining debris. The washing of residue during intubation thoroughly cleans the mucosa before the application of CE, and in turn improves the overall efficiency of the procedure. Once the cecum is reached and the mucosa is cleaned, exchange the water irrigation bottle for the dye solution, and initiate dye spraying. The diluted dye can then be sprayed onto the mucosa using a standard flushing pump attached to the scope, either through pressing a foot pedal or a programmed button on the endoscope handle (Fig. 1). Direct the spray to the antigravity side of the colon in order to optimize the dye application to all of the colonic mucosa in an efficient manner. Other studies and practices use a spray catheter for dye application, whereby the endoscopist directs the catheter probe out of the endoscope accessory channel and the assistant continuously sprays the dye through the catheter using a 60-mL syringe while the endoscopist withdrawals the endoscope.