A number of the components assessed here were considered to be at such low condition status that they could not decline further on the assessment scale, and so were assessed as Stable. These ‘poorest of the poor’ include, for example, oyster reefs in the SW and SE regions which are considered for all BYL719 practical purposes to be extinct (Beck et al., 2011)

with likely major historic impacts on biofiltration services in the estuaries and bays, and species that are almost locally extirpated in some areas, such as some exploited species of sharks or rays and some mangrove habitats and species. While the condition of five habitats, five species groups, and one ecological process was scored as zero in the Worst10% of places, these extreme examples each only occurred in a single region, except for mangrove habitats and mangrove species which were assigned Worst10% condition scores of zero in the E, SE and SW regions. Of the components that occur in more than one region, 14 biodiversity or ecosystem health components are in Poor (or worse)

condition. Of these, 10 components are related to the past widespread impacts of fishing or hunting activities, and only the condition of fur seals (now protected) was assessed as nationally improving from a low base. SGI-1776 order In the Worst10% of examples, 20 components (mainly habitats and species groups) were assigned as Very Poor condition in more than one region, indicating a potential set of issues of high national significance. Some of these components considered to be in Very Poor condition are already protected under the EPBC Act and are the subject of formal population recovery plans (eg the Great White Shark, Carcharodon carcharias; EPBC, 2014), although most remain to be addressed cAMP in a coordinated national manner. The number of such ‘worst of the worst’ examples, and the number of components that continue to decline in condition, suggest that further and more focused national restoration and recovery investments will be needed beyond the current programs for Australia’s formally declared threatened

species. This is also consistent with the need for a more ecosystem-based approach, where ecosystem structure and function and maintenance of the diversity of species and their natural functional relationships, habitats and productivity are the specific targets for marine ecosystem management (Rice et al., 2012, de Jonge et al., 2012 and Keith et al., 2013) rather than only species and habitats at high risk of extinction, or resource species. The large number of biodiversity components in poor condition and declining should provide impetus for a review of national priorities in Australia’s ecosystem-based management and monitoring programs related to the dominant pressures of climate change, ports and related coastal development, and fishing.

Each cell line, except CHO line 4, was cultured in its optimal basal chemically defined (CD) medium for maintenance and batch and fed batch studies. Venetoclax clinical trial Cell line 4 was maintained in a peptone containing medium, while batch and fed batch studies were performed in CD medium. Cell culture media utilized were: BD Select CHO and BD Select CD1000 (BD Advanced Bioprocessing), CDM4CHO (Thermo Fisher Scientific), and EX CELL CD CHO3 (SAFC). Feeds and media supplements utilized were: TC Yeastolate (TCY) and Proteose Peptone 3 (PP3) (BD Advanced Bioprocessing) and CD Cell Boost 6 (Thermo Fisher). The Duetz

sandwich-cover system and 24DW plates were obtained from Enzyscreen BV (Haarlem, Netherlands). The system includes 24DW plates (40 mm deep, pyramid bottom, volume 11 mL/well, transparent polystyrene plates), sandwich covers (CR1224a) and clamps (CR1700). Bioassay cultures were seeded at identical seeding density in 24DW plates and shake flasks. Culture volume was 3 mL and 50 mL in 24DW plates and shake flasks, respectively. Plate and shake flask cultures were incubated on a shaking platform in 5% CO2 at 37 °C. The shaking speed for plates was 300 rpm, while Dabrafenib manufacturer the shaking speed for flasks was 125 rpm.

The orbital diameter of the shaking platform was 25 mm for both plates and shake flasks. For 24DW plates, 300 μl samples were collected from the same well on various days of culture. These samples were diluted 2–3 times with PBS (Cellgro®) for assessment of cell growth (Viable cell density; VCD), viability and protein production. VCD and viability were determined using a Vi-CELL® (Beckman Coulter) and protein production was measured using a ForteBio Octet®

(Pall Life Sciences). For batch culture studies, peptones were added to basal media on Day 0. Fed batch cultures were fed with CD feeds on alternate days starting on Day PJ34 HCl 0 of the culture. Peptone titration studies were performed to test the effect of various concentrations of peptones on growth and production of CHO cells in a batch culture. Minitab 16 software (Minitab Inc) was used to generate multivariate charts and to perform other statistical analyses. Correlation analysis was performed to determine growth and production performance relationship between shake flask and 24DW plates. The Pearson correlation coefficient is a measure of linear association between two variables. Values of the correlation coefficient are always between −1 and +1. A correlation coefficient of +1 indicates that two variables are perfectly related in a positive linear sense. Two-Way ANOVA was used to assess effect of plates and peptone titration in plate-to-plate variation study. Four CHO lines were grown concurrently in their respective optimal base media in 24DW plates with Duetz sandwich-covers and in conventional shake flasks.

As revealed here via cytotoxicity assays, both PAMAM-coated and citrate-coated AuNps induced cytotoxicity in HepG2 cells or PBMC. A decrease

in cell viability upon incubation with AuNps-citrate and AuNps-PAMAM for both HepG2 and PBMC has been observed using the MTT assay. A change in morphology of HepG2 cells upon AuNps treatment also indicated the toxicity effects (data not shown). The genotoxicity assays employed here, as shown in Table 2 (HepG2 cells) and Table 3 (PBMC), can be related to the nanometric dimensions of AuNps, which may undergo cell uptake (Lewinski et al., 2008). It was evidenced that AuNps-PAMAM and AuNps-citrate induced DNA damage, as an indicative of genotoxicity. This effect is related to the cellular toxicity of gold nanoparticles, LY2835219 chemical structure which in our case is also related to the small size of the particles that easily undergo cell uptake through diffusion, in agreement with Pernodet et al. (2006). Li et al. (2008) demonstrated that serum coated 20 nm AuNps were also able to induce genotoxicity in the form of single-strand this website lesions in DNA in human lung fibroblasts. Our analyses provided convincing evidence of the toxic effect of AuNps, indicating that surface charge or size may be a major determinant of how AuNps impact cellular processes. Furthermore, the DNA damage index for AuNps-PAMAM

and AuNps-Citrate was statistically significant analyzed for HepG2 cells, except at 1.0 μM AuNps-Citrate. The genotoxicity for PBMC was statistically significant only upon incubation with AuNps-PAMAM at 50.0 μM. The tendency of the AuNps to accumulate in the cells nuclei was associated with their small size, which allows the nanoparticles to freely diffuse through pore complex (Zhao

and Nalwa, 2007). Since the comet assay evaluates the reversible DNA damage, our genotoxicity results also suggest that PBMC, a primary cell culture, were less sensitive to DNA damage to a certain extent the nanoparticles than HepG2 cancer cells. The purpose was to analyze the repair system in comet assay evidencing the DNA repair. The use of SSC parameter obtained via flow cytometry has been see more proposed as an efficient way to investigate cell uptake (Suzuki et al., 2007). In our analyses, the uptake of both types of AuNps was monitored by SSC (Table 4), revealing that for HepG2 cells, the relative SSC values were significantly increased (p < 0.05) only for cells incubated with AuNps-PAMAM at 50.0 μM. In contrast, the PBMC exhibited an increase in the SSC values for cells incubated with both types of nanoparticles at 50.0 μM. Furthermore, a significantly increase in SSC was also observed for PBMC upon incubation with AuNps-PAMAM at the lower concentration investigated (1.0 μM).

Further to exploring the induction of RCH under gradual cooling

and model thermoperiodic cycle regimes, the limits of RCH were investigated. In juvenile and mature larvae, the LLT was lowered by 6.5 and 2.5 °C, respectively, and in mature larvae alone, survival Selleck 3Methyladenine above 80% was exhibited even after 22 h at the DTemp (−12.5 °C). It is therefore evident that the larvae of E. murphyi possess a very strong RCH response. This is in contrast to most other species, in which survival is extended for, at most, 10 h at the DTemp and to temperatures just 2–3 °C below it ( Bale, 2002). For example, RCH in the mite, Euseius finlandicus, lengthened the LTime50 by only 1 h 15 min ( Broufas and Koveos, 2001), whilst in L. migratoria, the change was similarly small, increasing the LTime50 by just 2 h and reducing the LTemp50 from

−10 to −12 °C ( Wang and Kang, 2003). While our data principally provide evidence of the occurrence and strength of RCH in E. murphyi, they also indicate the thresholds which govern the response. The first is temperature. In mature larvae, RCH was not induced at 0 °C ( Fig. 3), and only slightly at −1 °C ( Fig. 6), while a much stronger response was induced at −3 ( Fig. 7) and −5 °C ( Fig. 3). An even lower induction temperature was required by juvenile larvae, which failed to respond after a 0 or a −5 °C, pre-treatment ( Fig. 3). It makes sense for the induction temperature of RCH in E. murphyi to be below 0 °C, and therefore lower than

that found in temperate species, as otherwise it would be continually induced in the Antarctic terrestrial learn more environments, which would be energetically costly. The second threshold is time. In mature larvae pre-treated at −5 °C for 10 min (data not shown), survival was significantly lower than in those pre-treated at −5 °C for 1 h. This is a clear indication that time is required for the protection afforded by RCH to increase (cf. Powell and Bale, 2004). The absence of a response after 1 d at −3 °C, but presence after the following 2 days at this temperature find more also supports this hypothesis (Fig. 7). The third and final threshold is freezing. It was already known from the Anchorage Island thermoperiod data that RCH was induced at −3 °C, which is above the SCP of mature larvae, and is thus not dependent on the freezing event itself (“freeze-induced hardening”), but it was not known if RCH could be induced in a frozen organism. When the survival of mature larvae at the DTemp was compared between those just frozen and those an hour after freezing at −7 °C, there was no significant difference between the two treatments. These data suggest that freezing defines the absolute limit of RCH accruement in E. murphyi. This is in contrast to a study by Teets et al. (2008), which showed RCH to occur in frozen B. antarctica at a cellular, and possibly also a whole organism, level.

Along with the vertically binned ice shelf thickness distribution, Fig. 7(b) also shows the mean melt rates within each

depth bin (right axis) for nine different experiments, corresponding to the strongest (130), weakest (30), and intermediate wind forcing (100) for each of the three different hydrographic scenarios, temporally averaged over the respective last model year. The results generally reflect the spatial pattern of Fig. 7(a), with high melt rates above 10 m year−1 only occurring at deep ice below 400 m, and melt rates of less than 1 m year−1 at ice depths between 200 m and 400 m for all experiments. Somewhat higher melt rates of up to 3 m year−1 also occur at locations of very shallow ice above 5-Fluoracil solubility dmso 200 m depth, corresponding to enhanced melting Alectinib mouse near the ice front. The contribution to the total basal mass balance within a given depth bin, obtained by multiplying the vertically binned mean melt rates by the ice shelf area distribution, is shown in Fig. 7(c), with three main features being evident

from the graph.3 Firstly, the deep and shallow melting respond in opposite ways to winds. Melting of shallow ice above 400 m increases with the strength of the wind forcing, whereas melt rates below 400 m are largest for the weakest winds for all hydrographic scenarios. Secondly, melting of both deep ice and shallow ice, are strongest in the constant summer scenario and weakest in the constant

winter scenario for equal wind forcings. Thirdly and perhaps most noticeably, the melting response is strongly modulated by the uneven distribution of ice shelf area. In most experiments, the basal mass loss is Quinapyramine dominated by weak melting of large areas of shallow ice, while substantial changes of the mass loss at very deep ice only occur for the extremely large deep melt rates in the ANN-30 and SUM-30 experiments shown in Fig. 7(c). The characteristic depth-dependent melting response to varying forcing is summarized in Fig. 9(a) and (b). The colored curves are identical in both panels, showing the total amount of melting for the entire ice shelf as function of the wind forcing. The colored patches show the contribution of melting only from ice deeper than 300 m (Fig. 9(a)), or from melting at ice shallower than 300 m (Fig. 9(b)), respectively. For an applied surface stress above 60% of the climatological average (indicated by the vertical lines in Fig. 9), the melting response in all hydrographic scenarios is dominated by changes of the shallow melting contribution, which correlates roughly linearly with the applied surface stress (Fig. 9(b)).

, 2004). These components rapidly respond to irritant compounds in the air, a response that is vital to protect the host. In this context, they release stored and/or synthesised products, which induce buy Trametinib smooth cell contraction to prevent the entrance of harmful substances (Cockcroft, 2010, Lino-dos-Santos-Franco et al., 2010, Säfholm et al., 2011 and Townley and Horiba, 2003). The group of endogenous mediators

secreted by stimulated trachea cells, including acetylcholine, histamine, cytokines, leukotrienes and prostaglandins, interacts with receptors present in smooth muscle cells to induce intracellular pathways involved in contraction (Cockcroft, 2010, Cockcroft and Davis, 2006 and Lino-dos-Santos-Franco et al., 2010). Tumour necrosis factor (TNF) is a cytokine that is produced by several cell types found in the airways, including epithelial and mast cells, in response to a wide range of agents. TNF induces smooth muscle cell contractility in the airway and regulates the phenotype of these smooth muscle cells, predisposing for hyperresponsiveness

(Adner et al., 2002, Amrani et al., 2000, Thomas, 2001 and Thomas et al., 1995). The effects of TNF are mediated by its interactions with two related receptors, TFNR1 (TNFR1a; CD120a; p55) and TNFR2 (TNFR1b; CD120b; p75), which are expressed in upper airway and lung tissues, by alveolar macrophages, monocytes, lymphocytes and granulocytes present in the bronchoalveolar lavage, small blood vessels and sensory neurons (Cardell et al., GSK-3 inhibition 2008, Van Houwelingen et al., 2002 and Thomas, 2001). Our group has recently demonstrated

HQ-induced lung toxicity, with mice exposed to low doses of HQ showing reduced leukocyte migration into LPS-inflamed Ureohydrolase lung due to the modification on neutrophil membrane receptors and impaired monocyte-chemoattractant protein secretion by mononuclear cells (Ribeiro et al., 2011 and Shimada et al., in press). The effects of in vivo HQ exposure on the contraction of airway smooth cells were experimentally evaluated in the present study. The data obtained reinforce the relevance of environmental pollutants and airway diseases as a public health issue. Hydroquinone 99%, lipopolysaccharide from Escherichia coli 026:B6, methacholine, chlorpromazine and sodium cromoglicate were purchased from Sigma–Aldrich (St Louis, MO, USA); the TNF ELISA kit was purchased from BD Pharmingen (San Diego, CA, USA); DMEM and gentamicin were obtained from Gibco (Carlsbad, CA, USA); all RT-PCR reagents were purchased from Promega Corporation (Madison, WI, USA); rabbit polyclonal anti-TNF receptor-1 and rabbit polyclonal anti-TNF receptor-2 antibodies were purchased from Abcam (Cambridge, MA, USA). Eighteen-week-old male Swiss mice were supplied by the Animal House of the School of Pharmaceutical Sciences and Chemistry Institute of the University of Sao Paulo.

Ten or more falls were reported by 7 participants in period A, 3 participants in period B, and only 1 participant in period C. The proportion of fallers was significantly lower in period C (see table 1). Eighteen participants reported no falls or only 1 fall during period A, while the corresponding numbers in later periods were 20 during period B and 25 during period C. There were significant improvements in balance on the Berg Balance Scale, Four Square Step test, TUGcognitive test, and Functional Gait Assessment when comparing tests preintervention and directly after the intervention was completed (t0-t1), and preintervention and at 7 weeks postintervention

(t0-t2) (table 2). The benefits in the improvements were maintained at follow-up 7 weeks after completion of the intervention. There were no differences between these test 3-Methyladenine occasions for the MSWS-12 (P<.26), ABC Scale (P<.14), TUG test (P=.035),

or sit-to-stand test (P=.73). Adverse effects and treatment complications were systematically measured by the physiotherapists in charge of the intervention. Two participants fell while performing more challenging standing and walking activities on their own initiative. There were no injuries. This study, using prospectively reported falls, shows that the CoDuSe program can reduce falls in people with mild to moderate MS. These findings are important, particularly selleck given the commonness of falls that may lead to injuries.7, 16, 29 and 30 The results are in line with previously published research21, 23 and 53 providing evidence that targeted physiotherapy interventions can positively affect falls in PwMS.21, 23 and 53 The CoDuSe program also produced improvements in balance performance, and the results were buy Nutlin-3 maintained at the 7-week follow-up. The conservative statistical approach, with correction for multiple comparisons, strengthens the likelihood that the results are valid. Still, the intervention did not

alter balance confidence. One possible explanation for this could be that the intervention was held indoors in a safe and supervised environment, while falls in everyday life occur in a number of different settings, including outdoors.8 Another explanation could be that the intervention period was insufficiently long for the participants to become more confident in performing activities. There is conflicting evidence on the ability of the ABC Scale to capture changes produced by an intervention.21 and 54 Modification of existing scales to better address the MS population may be necessary to capture changes produced by interventions such as the Falls Efficacy Scale–International.27 Finally, filling in a fall diary may have increased participants’ awareness of the risk of falling.

, 2008; Min et al., 2009). The muscle-fat-index (MFI) is another method for interindividual comparison of intramuscular fatty infiltration, involving the calculation of the ratio of the mean SI in a region of muscle tissue relative to the SI in a homogenous

region of fat (Elliott et al., 2005, 2008b; Cagnie et al., 2009; Elliott et al., 2010). Combining the measures total, lean muscle and fat CSA and MFI with MRI provides a quantitative and multifaceted view, to investigate whether lumbar muscle morphometry and composition Fulvestrant differs during remission of unilateral recurrent LBP compared to a healthy control group, and whether this is pain-side related. We hypothezised that lumbar muscle degeneration would be present in participants with a history of LBP, and being most prominent on the previously painful side. Thirteen individuals with recurrent non-specific LBP were recruited via advertisement in the local community and university. Inclusion criteria were a history of at least 2 previous episodes of LBP (onset >6 months) that interfered with activities of daily living and/or required treatment (LBP characteristics: Table 1). Episodes were defined as bouts of LBP for a minimum of 24 h, preceded and followed by a period of minimum 1 month without symptoms (de Vet et al., 2002). Testing was scheduled at least 1 month after the end of the previous episode (time since last episode: 64 ± 33,6 days). Thirteen individuals without a history of LBP, comparable

for gender, age, weight, length and level of physical activity, formed a healthy Rapamycin datasheet control group (demographic characteristics: Table 2). Participants were excluded from either group if they reported: central, bilateral or variable localization of LBP; pain elsewhere in the body; lumbar muscle training in the past year; spinal deformities or surgery; task-limiting medical conditions or contra-indications for MRI. After notification of the study procedures, which were approved by the local Ethics Committee, participants Demeclocycline provided written informed consent. T1-weighted images were acquired using a 3-T MRI-scanner (Magnetom Trio-Tim,

SyngoMR VB15 software, Siemens AG®, Erlangen Germany). Participants were placed supine with a foam wedge supporting the legs (∼30° hip flexion). A flexible 6-element body-matrix coil, centered ventrally on L4, was combined with the standard phased-array spine coil dorsally as a receiver–coil combination. On a sagittal localizing scan, 3 slices were positioned as axially as possible along the upper endplate of L3 and L4 and lower endplate of L4, visualizing lumbar MF, erector spinae (ES) and PS. These levels were selected as paraspinal and PS muscle mass is at or near maximal, enhancing the possibility to demonstrate CSA differences (Danneels et al., 2000; Lee et al., 2008). Level L4 lower endplate was used as a substitute for L5, because the inclination of L5 is often too large to visualize the muscles’ cross-section appropriately.

After 60 min of reaction at 37 °C, release of Pi was colorimetrically measured as previously described (Fiske and Subbarow, 1925). Yolk granule suspensions were obtained by gently rupturing of 24-h-old eggs in 0.4 M sucrose, 10 mM Hepes pH 7.2. Samples

CH5424802 cost were washed (1 min, 10,000g, room temperature centrifugation), and fixed at room temperature for 30 min in 0.4 M sucrose, 10 mM Hepes pH 7.2, 0.5% glutaraldehyde, 0.5% formaldehyde. After washing in 0.4 M sucrose, 10 mM Hepes pH 7.2, samples were resuspended and incubated for 1 h at 37 °C in acid phosphatase reaction medium (1 mM sodium β-glycerophosphate, 2 mM CeCl3, 0.1 M sucrose, 0.1 M sodium acetate pH 4.0) ( Hulstaert et al., 1983). Controls were carried out without the substrate or in the presence of 10 mM Na+ K+ tartrate. Samples were washed twice in 0.1 M sodium acetate pH 4.0, once in 0.1 M sodium cacodylate pH 7.2 and posteriorly fixed for click here 2 h at room temperature by 2.5% glutaraldehyde, 4% formaldehyde, 0.1 M sodium cacodylate pH 7.2. Samples were then washed in cacodylate buffer, post-fixed in 1% OsO4 for 1 h at room temperature, dehydrated in ethanol series and embedded in a Polybed 812 resin. Ultrathin sections were observed in a JEOL 1200 EX transmission electron microscope, operating

at 80 kV. For X-ray microanalysis, X-rays were collected for 150 s using a Si (Li) detector with a Norvar window in a 0–10 keV energy range with a resolution of 10 eV/channel. Analysis was performed using a Noran Voyager III analyzer. Freshly-laid eggs were homogenized in 20 mM Hepes pH 7.5 and centrifuged twice for 10 min at 18,000g at 4 °C. Supernatants were centrifuged at 10,000g for 2 h at 4 °C in a Millipore Ultrafree-MC-5 centrifugal filter unit and retained samples were resuspended in 20 mM Hepes pH 7.5, and labeled “yolk protein”. Following, 40 μg of “yolk protein” was incubated

at 37 °C in a reaction medium (P8340 protease inhibitor cocktail, 2.5 mM DTT, 2.5 mM EDTA, 25 mM sodium acetate pH 4.0) containing 0.32 μg agAP protein. When specified, 10 mM Na+ K+ tartrate was used as agAP inhibitor. Following, 12.5% check details SDS–PAGE was performed and the proteins were transferred to a nitrocellulose membrane that was blocked for 90 min with blocking buffer (0.05% TBS-Tween 20, 3% BSA). The membrane was then incubated overnight in blocking buffer containing 1:1000 PY-99 (raised against phosphotyrosine). Membrane was washed and revealed using a SuperSignal West Pico (Pierce) after incubation of 1:2000 anti-mouse peroxidase-conjugated IgG. All incubation steps were performed at room temperature. PolyP detection was performed as described (Gomes et al., 2008). Briefly, yolk granule suspensions were obtained by gently rupturing of 24-h-old eggs in 20 mM Hepes pH 7.2. Samples were washed (1 min, 10,000 g, room temperature) and incubated in 20 mM Hepes pH 7.2, 50 μg/mL DAPI for 20 min at room temperature.

None of these patients had new pain/discomfort or worsening of the baseline pain/discomfort at 24 hours after the procedure. None had procedure-induced pancreatitis. There were no other adverse events related to the procedure. The cytological diagnosis with the cell block method by H&E staining was positive (class IV or V) in 11 (Figure 3 and Figure 4) and negative (classes I, II, and III) in 33 (Table 1). Surgery was performed in 11 patients whose findings were

positive by cell block cytology (Fig. 5). Six patients with negative cytology results also underwent surgery AG-14699 because of mural nodules larger than 5 mm at first diagnosis in 4 patients and at progressive enlargement of more than 5 mm of the main and branch pancreatic ducts and mural nodules during follow-up on CT and EUS in the other 2 patients (Table 1). Histological analysis of the resected specimen revealed adenoma in 5 patients, in situ carcinoma in 8, and invasive carcinoma in 4 (Table 1). In the other 27 patients, the results did not indicate surgery and the patients were followed for more than 12 Vorinostat chemical structure months (range 13 to 50 months). They were regarded as having benign IPMNs because they showed no changes on CT or MRI imaging, including the diameter of the main and ectatic pancreatic ducts and the size of the mural nodule during

follow-up. Consequently, 73% (32/44) of the patients Interleukin-2 receptor were regarded as having nonmalignant IPMNs, and 27% (12/44) as having malignant IPMNs. There were no false-positive results and only 1 false-negative result. The sensitivity, specificity, and positive and negative predictive values of the cell block method for discriminating branch-duct type benign IPMNs from malignant ones were 92%, 100%, 100%, and 97%, respectively (Table 2). As for the immunohistochemical staining of mucin proteins, the cytological and histological results of MUCs 1, 2, 5AC, and 6 were in agreement in 88% (15/17), 94% (16/17), 88% (15/17), and 100% (17/17) of the

cases, respectively (Figure 3 and Figure 4; Table 3). At present, differentiation of benign and malignant IPMNs is still challenging. Although the International Consensus Guidelines are helpful regarding the management of IPMNs,18 the disadvantage of using these guidelines is the risk of overtreating patients. For example, only 15% of 61 patients with branch-duct type IPMNs who underwent resection had cancer according to a study on 147 patients by Pelaez-Luna et al.19 In our study, we demonstrated the usefulness of pancreatic duct lavage cytology with the cell block method for differentiating between benign and malignant branch-duct type IPMNs in patients having mural nodules.