Search

In order to solve the problem that the traditional information systems have such as slow running responses and cannot meet the expected requirements of users, a performance evaluation method of financial support for the development of the big data industry is proposed. According to the characteristics of financial support, this paper uses the analytic hierarchy process (AHP) and the fuzzy comprehensive evaluation principle to establish a specific evaluation index system for the performance evaluation of financial support in the big data industry and select a suitable index group. In order to reflect the financial support performance, the analytic hierarchy process (AHP) is used to calculate the weight of various performance evaluation indicators, and the fuzzy comprehensive evaluation is used to combine qualitative analysis and quantitative analysis to evaluate and calculate the big data industry scientifically, objectively, fairly, and accurately. In financial support performance, experiments show that the proposed method not only has a fast response time but also can ensure that the actual results after the system runs are in line with the expectations of the system users.

This study aims to establish a nomogram model by combining traditional clinical parameters with immunohistochemical markers to predict the recurrence of non-muscle invasive bladder urothelial carcinoma (NMIBUC) after resection.In total, 504 patients were included in this study. Of these patients, 353 underwent transurethral resection of bladder tumor (TURBT) in the Yongchuan Hospital of Chongqing Medical University and were identified as a training cohort. Univariate and multivariate Cox regression analyses were used to determine the risk factors associated with recurrence in the training cohort and to establish a nomogram model. A total of 151 patients who were hospitalized in the Second Affiliated Hospital of Chongqing Medical University (validation cohort) were used for further validation. The calibration curve was generated for internal and external model validation. The clinical practicability of this model was further verified by comparing the consistency index (C-index) among various models.The mean follow-up time of the training cohort was 45.6 months (range 4-90). In total, 146 patients relapsed in training cohort. After univariate analysis, multivariate analysis further confirmed tumor grade (This proposed nomogram model based on traditional clinical parameters and immunohistochemical markers can more accurately predict postoperative recurrence in patients with NMIBUC.

Mutations in GBA1 , encoding glucocerebrosidase (GCase), cause Gaucher disease (GD) and are also genetic risks in developing Parkinson’s disease (PD). Currently, the approved therapies are only effective for directly treating visceral symptoms, but not for primary neuronopathic involvement in GD (nGD). Progranulin (PGRN), encoded by GRN , is a novel modifier of GCase, but the impact of PGRN in GBA1 mutation-associated pathologies in vivo remains unknown. Herein, Grn −/− mice crossed into Gba 9v/9v mice, a Gba1 mutant line homozygous for the Gba1 D409V mutation, generating Grn −/− Gba 9v/9v (PG9V) mice. PG9V mice exhibited neurobehavioral deficits, early onset, and more severe GD phenotypes compared to Grn −/− and Gba 9v/9v mice. Moreover, PG9V mice also displayed PD-like phenotype. Mechanistic analysis revealed that PGRN deficiency caused severe neuroinflammation with microgliosis and astrogliosis, along with impaired autophagy associated with the Gba1 mutation. A PGRN-derived peptide, termed ND7, ameliorated the disease phenotype in GD patient fibroblasts ex vivo . Unexpectedly, ND7 penetrated the blood-brain barrier (BBB) and effectively ameliorated the nGD manifestations and PD pathology in Gba 9v/null and PG9V mice. Collectively, this study not only provides the first line of in vivo but also ex vivo evidence demonstrating the crucial role of PGRN in GBA1/Gba1 mutation-related pathologies, as well as a clinically relevant mouse model for mechanistic and potential therapeutics studies for nGD and PD. Importantly, a BBB penetrant PGRN-derived biologic was developed that may provide treatment for rare lysosomal storage diseases and common neurodegenerative disorders, particularly nGD and PD.

Progranulin (PGRN) is a key regulator of lysosomes, and its deficiency has been linked to various lysosomal storage diseases (LSDs), including Gaucher disease (GD), one of the most common LSD. Here, we report that PGRN plays a previously unrecognized role in autophagy within the context of GD. PGRN deficiency is associated with the accumulation of LC3-II and p62 in autophagosomes of GD animal model and patient fibroblasts, resulting from the impaired fusion of autophagosomes and lysosomes. PGRN physically interacted with Rab2, a critical molecule in autophagosome-lysosome fusion. Additionally, a fragment of PGRN containing the Grn E domain was required and sufficient for binding to Rab2. Furthermore, this fragment significantly ameliorated PGRN deficiency-associated impairment of autophagosome-lysosome fusion and autophagic flux. These findings not only demonstrate that PGRN is a crucial mediator of autophagosome-lysosome fusion but also provide new evidence indicating PGRN's candidacy as a molecular target for modulating autophagy in GD and other LSDs in general. KEY MESSAGES : PGRN acts as a crucial factor involved in autophagosome-lysosome fusion in GD. PGRN physically interacts with Rab2, a molecule in autophagosome-lysosome fusion. A 15-kDa C-terminal fragment of PGRN is required and sufficient for binding to Rab2. This PGRN derivative ameliorates PGRN deficiency-associated impairment of autophagy. This study provides new insights into autophagy and may develop novel therapy for GD.

The surgical treatment of bladder urothelial carcinoma depends on whether the tumor has invaded the bladder muscular layer. Normal ultrasound and contrast-enhanced magnetic resonance imaging (contrast-enhanced MRI) are widely used in patients bear bladder tumors; the latter is also widely used in estimating the muscularis invasion of bladder cancer (BC). However, contrast-enhanced ultrasound (CEUS) is rarely used in this aspect. As the gold standard in diagnosing muscularis invasion remains being pathological examination, this study was set to find out whether there are differences between CEUS and contrast-enhanced MRI in diagnosing bladder malignant tumors and in diagnosing the muscularis invasion of the bladder urothelial carcinoma under the guide of the pathological results.160 patients from Yongchuan Hospital of Chongqing Medical University and The Second Affiliated Hospital of Chongqing Medical University were recruited from July 1st, 2021, to June 30th, 2022. Patients are arranged to undergo CEUS, contrast-enhanced MRI and then take a surgery. After surgery, we compare the results of CEUS, MRI and the pathological results, using software to run the statistical examinations.The accuracies of CEUS and contrast-enhanced MRI in diagnosing malignant bladder tumors were 85.90 and 84.62%, and they had no differences (P 0.05). While the accuracies of CEUS and contrast-enhanced MRI in diagnosing the muscularis invasion were 84.62 and 76.92%, in which CEUS had a better sensitivity (P 0.05).We found that CEUS and contrast-enhanced MRI had no differences in diagnosing the different pathological types (benign or malignant) of BC, but CEUS holds a better sensitivity in diagnosing muscularis invasions of bladder urothelial carcinoma than the contrast-enhanced MRI.

We previously showed that kaempferol (KAE) could exert neuroprotective effects against PD. It has been demonstrated that abnormal autophagy plays a key role in the development of PD. Mitochondrial dysfunction, involved in the development of PD, can damage dopaminergic neurons. Whether the protective effects of KAE were exerted via regulating autophagy remains largely undefined, however. This study aimed to investigate whether KAE could protect dopaminergic neurons via autophagy and the underlying mechanisms using a MPTP/MPP

We introduce what we believe to be a novel class of radially polarized partially coherent beams in which the correlation function possesses a Hermite non-uniformly correlated array. The source parameter conditions required to generate a physical beam are derived. The statistical properties of such beam propagating in free space and turbulent atmosphere are thoroughly examined using the extended Huygens-Fresnel principle. It is shown that the intensity profile of such beams presents a controllable periodic grid distribution due to its multi-self-focusing propagation property and can keep the shape in free space while propagating in turbulent atmosphere, it exhibits self-combining properties over a long-ranges. Owing to the interaction between the non-uniform correlation structure and the non-uniform polarization, this beam can locally self-recover the polarization state after propagating a long distance in a turbulent atmosphere. Furthermore, the source parameters play essential roles in determining the distribution of spectral intensity, the state of polarization, and the degree of polarization of the RPHNUCA beam. Our results may benefit multi-particle manipulation and free-space optical communication applications.

We introduce a new class of vector array beams named radially polarized Gaussian Schell-model array (RPGSMA) beams for producing far fields with controllable optical lattice average intensity patterns, and derive the realizability conditions for a RPGSMA source and the beam condition for radiation produced by this source based on the unified theory of coherence and polarization, Moreover, the statistical properties of such beam propagating in free space are investigated in detail. It is found that, the statistical properties of the RPGSMA beams on propagation are closely related to source parameters of the beam. with an appropriate choice of the source parameters, the average intensity will produce far fields with controllable optical lattice average intensity patterns, and the degree of coherence (DOC) from the lattice distribution on the original plane evolves into a Gaussian profile in the far field, Furthermore, the degree of polarization (DOP) appears a periodical grid-like distribution on propagation. These results may be useful in optical trapping and free-space optical communications.

The effect of anisotropic atmosphere turbulence on propagation characteristics of an electromagnetic twisted Gaussian Schell-model array (EM TGSMA) beam is investigated. An analytical expression for the cross-spectral density function of such beam propagating through anisotropic turbulent atmosphere is derived and used to explore the evolutionary behavior of the spectral intensity, degree of polarization (DOP) and degree of coherence (DOC). An example illustrates the fact that twisted strength and anisotropic turbulent factors have an important impact on the behavior of spectral density, DOC and DOP, in particular. The rotation angle of the array beams can also be controlled by adjusting twisted strength. Furthermore, strong anisotropic turbulence was also found to cause significant mergence of the array beams. Our results might be beneficial for free-space communications of the partially coherent beams endowed with twist.

We investigate detailedly evolution properties of the angular spread and propagation factor ( M 2 -factor) of a general-type partially coherent beam with Schell-model correlator in anisotropic oceanic turbulence. According to the extended Huygens–Fresnel principle, analytical expressions for the second-order moments of Wigner distribution function (WDF) in anisotropic oceanic turbulence are derived. In order to measure the resistance of a general partially coherent beam to effects of anisotropic oceanic turbulence, we introduce deviation percentage of the normalized angular spread and M 2 -factor respectively between the general-type partially coherent beam and conventional Gaussian Schell-model (GSM) beam. Numerical results show that influence of anisotropy on the angular spread and M 2 -factor is less for a general-type partially coherent beam than a conventional GSM beam in oceanic turbulence. Besides, the initial beam parameters have a significant effect on the angular spread and M 2 -factor of a general-type partially coherent beam. Our results may be useful for underwater communication.

Progranulin (PGRN) is a key regulator of lysosome and its deficiency has been linked to various lysosomal storage diseases (LSDs), including Gaucher disease (GD), one of the most common LSD. Here, we report that PGRN plays a previously unrecognized role in autophagy within the context of GD. PGRN deficiency associated with accumulation of LC3-II and p62 in autophagosomes of GD animal model and patient fibroblasts, resulting from impaired fusion of autophagosomes and lysosomes. PGRN physically interacted with Rab2, a critical molecule in autophagosome-lysosome fusion. Additionally, a fragment of PGRN containing the Grn E domain was required and sufficient for binding to Rab2. Further, this fragment significantly ameliorated PGRN-deficiency associated impairment of autophagosome-lysosome fusion and autophagic flux. These findings not only demonstrate that PGRN is a crucial mediator of autophagosome-lysosome fusion, but also provide new evidence indicating PGRN’s candidacy as a molecular target for modulating autophagy in GD and other LSDs in general.

Background The aim of this study was to investigate a novel method to treat coronary artery aneurysms(CAAs).Methods Three CAAs patients who underwent single or double bare-metal stent implantation were recruited. The CAAs and parent artery diameters were measured for model construction. Single- and double-stent implantation were simulated, and the changes in the CAAs haemodynamics after stenting were analysed. Results In Case 1, the flow velocity in the single-stent model was significantly lower than that in the double-stent model (0.0046±0.013 vs 0.0050±0.011, pConclusion Application of the single or double bare-metal stent technique, according to the neck diameter of the coronary artery aneurysms, can effectively change the flow in vessels and aneurysm haemodynamics to achieve occlusion.Trail registration: Clinicaltrails, NCT04265989. Registered 12 February 2020, https://clinicaltrials.gov/ct2/show/NCT04265989?term=NCT04265989&draw=2&rank=1

TNFα/TNFR signaling plays a critical role in the pathogenesis of various inflammatory and autoimmune diseases, and anti-TNFα therapies have been accepted as the effective approaches for treating several autoimmune diseases. Progranulin (PGRN), a multi-faced growth factor-like molecule, directly binds to TNFR1 and TNFR2, particularly to the latter with higher affinity than TNFα. PGRN derivative Atsttrin is composed of three TNFR-binding domain of PGRN and exhibits even better therapeutic effects than PGRN in several inflammatory disease models, including collagen-induced arthritis. Herein we describe the detailed methodology of using (1) ELISA-based solid phase protein-protein interaction assay to demonstrate the direct binding of Atsttrin to TNFR2 and its inhibition of TNFα/TNFR2 interaction; and (2) tartrate-resistant acid phosphatase (TRAP) staining of in vitro osteoclastogenesis to reveal the cell-based anti-TNFα activity of Atsttrin. Using the protocol described here, the investigators should be able to reproducibly detect the physical inhibition of TNFα binding to TNFR and the functional inhibition of TNFα activity by Atsttrin and various kinds of TNF inhibitors.

A long‐standing problem in biology is how to dissect traits for which no tractable model exists. Here, we screen for genes like the nude locus (Foxn1)—genes central to mammalian hair and thymus development—using animals that never evolved hair, thymi, or Foxn1. Fruit flies are morphologically disrupted by the FOXN1 transcription factor and rescued by weak reductions in fly gene function, revealing molecules that potently synergize with FOXN1 to effect dramatic, chaotic change. Strong synergy/effectivity in flies is expected to reflect strong selection/functionality (purpose) in mammals; the more disruptive a molecular interaction is in alien contexts (flies), the more beneficial it will be in its natural, formative contexts (mammals). The approach identifies Aff4 as the first nude‐like locus, as murine AFF4 and FOXN1 cooperatively induce similar cutaneous/thymic phenotypes, similar gene expression programs, and the same step of transcription, pre‐initiation complex formation. These AFF4 functions are unexpected, as AFF4 also serves as a scaffold in common transcriptional‐elongation complexes. Most likely, the approach works because an interaction's power to disrupt is the inevitable consequence of its selected‐for power to benefit., A genetic screen in Drosophila for genes that synergize with mammalian FOXN1 identifies Aff4 as a nude‐like locus. AFF4 cooperates with FOXN1 in mammalian hair and thymus development.

The study aims to investigate whether kaemperfol (KAE) inhibits microglia pyroptosis and subsequent neuroinflammatory response to exert neuroprotective effects, along with the underlying mechanisms. The results showed KAE could ameliorate the behavioral deficits of Parkinson's disease (PD) rats, inhibit the activation of microglia and astrocytes, reduce the loss of TH-positive neurons, down-regulate levels of pyroptosis-related NOD-like receptor family pyrin domain containing 3 (NLRP3), GasderminD-N Term (GSDMD-NT), caspase1, apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC), interleukin (IL)-1β, and IL-18, and decrease the levels of inflammatory molecules (inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2)) and p38 mitogen-activated protein kinase/nuclear factor-kappaB (p38MAPK/NF-κB) signaling pathway molecules (p38MAPK, p-p38MAPK, NF-κB, and p-NF-κB) in the substantia nigra of PD rats. Further in vitro study indicated that KAE reversed the activation of BV2 cells and down-regulated the expressions of pyrolytic proteins, inflammatory mediators and key molecules in p38MAPK/NF-κB signaling pathway. Collectively, KAE inhibits the microglia pyroptosis and subsequent neuroinflammatory response to exert neuroprotective effects on 6-hydroxydopamine (6-OHDA)-induced PD rats and lipopolysaccharide (LPS)-induced BV2 inflammatory cells through inhibiting p38MAPK/NF-κB signaling pathway.

TNFR1 and TNFR2 have received prominent attention because of their dominance in the pathogenesis of inflammation and autoimmunity. TNFR1 has been extensively studied and primarily mediates inflammation. TNFR2 remains far less studied, although emerging evidences demonstrate that TNFR2 plays an anti-inflammatory and immunoregulatory role in various conditions and diseases. Herein, we report that TNFR2 regulates macrophage polarization, a highly dynamic process controlled by largely unidentified intracellular regulators. Using biochemical co-purification and mass spectrometry approaches, we isolated the signaling molecule 14-3-3e as a component of TNFR2 complexes in response to progranulin stimulation in macrophages. In addition, 14-3-3e was essential for TNFR2 signaling-mediated regulation of macrophage polarization and switch. Both global and myeloid-specific deletion of 14-3-3e resulted in exacerbated inflammatory arthritis and counteracted the protective effects of progranulin-mediated TNFR2 activation against inflammation and autoimmunity. TNFR2/14-3-3e signaled through PI3K/Akt/mTOR to restrict NF-κB activation while simultaneously stimulating C/EBPβ activation, thereby instructing macrophage plasticity. Collectively, this study identifies 14-3-3e as a previously-unrecognized vital component of the TNFR2 receptor complex and provides new insights into the TNFR2 signaling, particularly its role in macrophage polarization with therapeutic implications for various inflammatory and autoimmune diseases with activation of the TNFR2/14-3-3e anti-inflammatory pathway.

Objective To investigate the protective effects of kaempferol (KAE) on PC12 cells against neurotoxin 6-hydroxydopamine (6-OHDA)-induced inflammatory damage and explore whether it is related to the inhibition of the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway. Methods After being cultured for 24 hours, PC12 cells were divided into 4 groups: control, 6-OHDA (100 μmol/L), 6-OHDA combined with (20, 40, 60, 80, 100) μmol/L KAE and KAE groups. The morphological features of PC12 cells were observed under an inverted microscope, and the cell viability was detected by CCK-8 assay. In the case of the optimal effective dose of KAE, the expression of cyclooxygenase-2 (COX2), inducible nitric oxide synthase (iNOS), nuclear factors (NF)-κB were evaluated by immunocytochemical staining and Western blot analysis. To explore the mechanism underlying the protective role of KAE, KAE and SB203580 (p38 MAPK pathway inhibitor) (10 μmol/L) were separately added into 6-OHDA culture medium of PC12 cells. The protein levels of iNOS, COX2, NF-κB, p38 MAPK and p-p38 MAPK were tested by Western blotting. Results Compared with the control group, the number of cells in the 6-OHDA group was significantly reduced, with most cell bodies shrunk and aggregated into clumps. Compared with the 6-OHDA group, the number of cells increased and the morphology was effectively improved in the 6-OHDA combined with KAE (20, 40, 60, 80, and 100 μmol/L) group. KAE at 80 μmol/L was demonstrated the best protective effects in the present work. In the 6-OHDA group, the expression of COX2, iNOS, NF-κB significantly increased. Compared with the 6-OHDA group, the expression of the above molecules decreased markedly in the 6-OHDA combined with 80 μmol/L KAE group. The protein expression levels of COX2, iNOS, NF-κB, p38 MAPK and p-p38 MAPK went up significantly in the 6-OHDA group as compared with the control group, while they were down-regulated obviously by both KAE and SB203580. Conclusion KAE exerts neuroprotective effects on PC12 cells against the damage induced by 6-OHDA probably through the p38 MAPK signaling pathway.

Polyphenols from Toona sinensis seeds (PTSS) have demonstrated anti-inflammatory effects in various diseases, while the anti-neuroinflammatory effects still remain to be investigated. We aimed to investigate the effects of PTSS on Parkinson's disease and underlying mechanisms using a rat model. We employed 6-hydroxydopamine (6-OHDA) to male Sprague Dawley (SD) rats and PC12 cells to construct the in vivo and vitro models of PD and dopaminergic (DA) neuron injury, respectively. Cell viability was detected by cell counting kit-8 (CCK-8) assay and protein levels of inflammatory mediators and some p38 MAPK pathway molecules were investigated by immunohistochemistry and Western blot analyses. The results showed that 6-OHDA significantly increased protein levels of inflammatory mediators, such as cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor α (TNF-α), which could be reversed by PTSS through suppressing the p38 MAPK pathway. The anti-inflammatory effects of PTSS were significantly enhanced by the specific p38 inhibitor of SB203580 in vitro. The present work suggests that PTSS can exert anti-inflammatory effects on PD models, which may be attributed to the suppression of p38 MAPK signaling pathway.

Objective To explore the inhibitory effects of polyphenols from Toona sinensis seeds (PTSS) on neuroinflammation and the underlying mechanism in rats with Parkinson's disease (PD). Methods PD rat models were prepared by stereotaxic injection of 6-hydroxydopamine (6-OHDA) into one side of striatum of Sprague-Dawley male rats. Model rats were randomly divided into model group and PTSS group (n=10), and a normal control group was set as well (n=10). The rotational behavior of rats was induced by intraperitoneal injection of apomorphine (APO) after 30 days, and the behavioral changes of rats from each group were investigated. The morphological and quantity changes of DA neurons (tyrosine hydroxylase positive, TH-positive), microglia cells (ionized calcium binding adaptor molecule-1, Iba1-positive) and astrocytes (glial fibrillary acidic protein, GFAP-positive) in substantia nigra (SN) of rats from each group were examined by immunohistochemistry. Inducible nitric oxide synthase (iNOS), nuclear factor-κB p65 (NF-κBp65), p38 mitogen-activated protein kinase (p38MAPK) and phosphor-p38 mitogen-activated protein kinase (p-p38MAPK) levels were evaluated through immunohistochemical staining. The protein levels of TH, GFAP, p38MAPK and p-p38MAPK in SN were examined by Western blot analysis. Results The number of rotations in the rats of the PTSS group was significantly reduced compared with that in the model group. The number of TH-positive cells in the model group was much less than that in the control group. The number and protein levels of TH-positive cells were enhanced significantly by PTSS intervention. Compared with the control group, the protein levels of Iba1, GFAP, iNOS, NF-κB, p38MAPK and p-p38MAPK in the injured side of the model group significantly increased, which could be suppressed significantly by PTSS intervention. Conclusion PTSS demonstrates protective effects on DA neurons by inhibiting p38MAPK signaling pathway and reducing the expression of inflammatory factors in PD rats.

Under the help of extended Huygens–Fresnel integral, we acquire the analytic expressions of second-order moments of the Wigner distribution function (WDF) for a twisted electromagnetic Gaussian Schell-model (TEGSM) beam propagating in a uniaxial crystal. Moreover, we obtain the formulae for propagation factor, the effective radius of curvature and Rayleigh range in which we studied the properties of the TEGSM beam numerically. It is found that the initial beam parameters and the uniaxial crystal parameters play a decisive role in the TEGSM beam propagating in a uniaxial crystal. The TEGSM beam with smaller absolute deviation of coherence width δxx and δyy is less affected by anisotropic diffraction in a uniaxial crystal, which is much different from the evolution properties of an EGSM beam in a uniaxial crystal. The Rayleigh range will decreases while the crystal parameter e increases. Thus, the propagation properties of a TEGSM beam could be controlled in a uniaxial crystal by changing the initial beam parameters and the uniaxial crystal parameters where it is necessary.

p204, a murine member of an interferon-inducible p200 family, was reported to recognize intracellular viral and bacterial DNAs, however, its role in the innate immunity in vivo remains unknown due to the lack of p204-deficient animal models. In this study we first generated the p204−/− mice. Unexpectedly, p204 deficiency led to significant defect in extracellular LPS signaling in macrophages, as demonstrated by dramatic reductions of LPS-mediated IFN-β and pro-inflammatory cytokines. The serum levels of IFN-β and pro-inflammatory cytokines were also significantly reduced in p204−/− mice following LPS challenge. In addition, p204−/− mice were resistant to LPS-induced shock. LPS-activated NF-ĸB and IRF-3 pathways were all defective in p204-deficient macrophages. p204 binds to TLR4 through its Pyrin domain, and it is required for the dimerization of TLR4 following LPS-challenge. Collectively, p204 is a critical component of canonical LPS-TLR4 signaling pathway, and these studies also suggest that p204 could be a potential target to prevent and treat inflammatory and infectious diseases. Keywords: p204, LPS, TLR4, IFN-β, Inflammatory responses, Macrophages

Purpose—Image-based computational fluid dynamics (CFD) is widely used to predict intracranial aneurysm wall shear stress (WSS), particularly with the goal of improving rupture risk assessment. Nevertheless, concern has been expressed over the variability of predicted WSS and inconsistent associations with rupture. Previous challenges, and studies from individual groups, have focused on individual aspects of the image-based CFD pipeline. The aim of this Challenge was to quantify the total variability of the whole pipeline. Methods—3D rotational angiography image volumes of five middle cerebral artery aneurysms were provided to participants, who were free to choose their segmentation methods boundary conditions, and CFD solver and settings. Participants were asked to fill out a questionnaire about their solution strategies and experience with aneurysm CFD, and provide surface distributions of WSS magnitude, from which we objectively derived a variety of hemodynamic parameters. Results—A total of 28 datasets were submitted, from 26 teams with varying levels of self-assessed experience. Wide variability of segmentations, CFD model extents, and inflow rates resulted in interquartile ranges of sac average WSS up to 56%, which reduced to < 30% after normalizing by parent artery WSS. Sac-maximum WSS and low shear area were more variable, while rank-ordering of cases by low or high shear showed only modest consensus among teams. Experience was not a significant predictor of variability. Conclusions—Wide variability exists in the prediction of intracranial aneurysm WSS. While segmentation and CFD solver techniques may be difficult to standardize across groups, our findings suggest that some of the variability in image-based CFD could be reduced by establishing guidelines for model extents, inflow rates, and blood properties, and by encouraging the reporting of normalized hemodynamic parameters. Fil: Valen-Sendstad, Kristian. Simula Research Laboratory and Center for Cardiological Innovation; Noruega Fil: Bergersen, Aslak W.. University of Oslo; Noruega Fil: Shimogonya, Yuji. Nihon University; Japón Fil: Goubergrits, Leonid. Charite´ – Universita¨tsmedizin Berlin; Alemania Fil: Bruening, Jan. Charité – Universitätsmedizin Berlin; Alemania Fil: Pallares, Jordi. Universitat Rovira I Virgili; España Fil: Cito, Salvatore. Universitat Rovira I Virgili; España Fil: Piskin, Senol. University Of Texas At San Antonio.; Estados Unidos Fil: Pekkan, Kerem. Koc University; Turquía Fil: Geers, Arjan J.. Universitat Pompeu Fabra; España Fil: Larrabide, Ignacio. Universidad Nacional del Centro de la Provincia de Buenos Aires. Facultad de Ciencias Exactas. Grupo de Plasmas Densos Magnetizados. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Grupo de Plasmas Densos Magnetizados; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Rapaka, Saikiran. Siemens Medical Solutions USA Inc; Estados Unidos Fil: Mihalef, Viorel. Siemens Medical Solutions USA Inc; Estados Unidos Fil: Fu, Wenyu. Beijing Union University; China Fil: Qiao, Aike. Beijing University of Technology; China Fil: Jain, Kartik. Simula Research Laboratory and Center for Cardiological Innovation; Noruega. University of Siegen; Alemania. University of Zürich; Suiza Fil: Roller, Sabine. University of Siegen; Alemania Fil: Mardal, Kent-Andre. Simula Research Laboratory and Center for Cardiological Innovation; Noruega. University of Oslo; Noruega Fil: Kamakoti, Ramji. Dassault Systemes; Francia Fil: Spirka, Thomas. Simpleware Software Solutions; Reino Unido Fil: Ashton, Neil. University of Oxford; Reino Unido Fil: Revell, Alistair. University of Manchester; Reino Unido Fil: Aristokleous, Nicolas. University of Limerick; Irlanda Fil: Houston, J. Graeme. University of Dundee; Reino Unido Fil: Tsuji, Masanori. Mie Chuo Medical Center; Japón Fil: Ishida, Fujimaro. Mie Chuo Medical Center; Japón Fil: Menon, Prahlad G.. University of Pittsburgh; Estados Unidos Fil: Browne, Leonard D.. University of Limerick; Irlanda Fil: Broderick, Stephen. University of Limerick; Irlanda Fil: Shojima, Masaaki. University of Tokyo; Japón Fil: Koizumi, Satoshi. University of Tokyo; Japón Fil: Barbour, Michael. University of Washington; Estados Unidos Fil: Aliseda, Alberto. University of Washington; Estados Unidos Fil: Morales, Hernán G.. Medisys - Philips Research Paris; Francia Fil: Lefèvre, Thierry. Medisys - Philips Research Paris; Francia Fil: Hodis, Simona. Texas A&M University - Kingsville; Estados Unidos Fil: Al-Smadi, Yahia M.. Jordan University of Science and Technology; Jordania Fil: Tran, Justin S.. Stanford University; Estados Unidos Fil: Marsden, Alison L.. Stanford University; Estados Unidos Fil: Vaippummadhom, Sreeja. EinNel Technlogies; India Fil: Einstein, G. Albert. EinNel Technlogies; India Fil: Brown, Alistair G.. Siemens PLM Software; Estados Unidos Fil: Debus, Kristian. Siemens PLM Software; Estados Unidos Fil: Niizuma, Kuniyasu. Tohoku University; Japón Fil: Rashad, Sherif. Tohoku University; Japón Fil: Sugiyama, Shin-ichiro. Kohnan Hospital; Japón Fil: Owais Khan, M.. University of Toronto; Canadá Fil: Updegrove, Adam R.. University of California at Berkeley; Estados Unidos Fil: Shadden, Shawn C.. University of California at Berkeley; Estados Unidos Fil: Cornelissen, Bart M. W.. Academic Medical Center; Países Bajos Fil: Majoie, Charles B. L. M.. Academic Medical Center; Países Bajos Fil: Berg, Philipp. University of Magdeburg; Alemania Fil: Saalfield, Sylvia. University of Magdeburg; Alemania Fil: Kono, Kenichi. Wakayama Rosai Hospital; Japón Fil: Steinman, David A.. University of Toronto; Canadá