“
“Lipoastrocytoma is an extremely selleck chemicals rare tumor, with only six cases described. We report the case of an astrocytoma involving the upper part of the cerebellar-pontine angle and the right portion of the clivus starting from the brainstem with a diffuse lipomatous component in a 39 year-old man. The patient was admitted with headache of 1 year’s duration and diplopia over the previous 3 months. MRI revealed a ponto-cerebellar lesion that showed irregular enhancement

after contrast administration. Subtotal excision of the tumor was accomplished. Adjuvant chemotherapy and radiation therapy were not administered. Histologically the tumor showed the classical histology of low-grade astrocytoma and a portion of the lesion was composed of lipid-laden cells. Immunohistochemistry for glial fibrillary acid and S-100 proteins clearly demonstrated the glial nature of these cells. Ki-67/Mib-1 labeling index was low (2%). The patient GW-572016 molecular weight remains in good neurological conditions after 10 months. Our case has a benign postoperative behavior, also after subtotal excision, with restrictions due to the short follow-up. It is important

to record each new case of this rare tumor to produce a better characterization of this lesion. “
“I. Bodi, R. Selway, P. Bannister, L. Doey, N. Mullatti, R. Elwes and M. Honavar (2012) Neuropathology and Applied Neurobiology38, 411–425 Diffuse form of dysembryoplastic neuroepithelial tumour: the histological and immunohistochemical features of a distinct entity showing transition to dysembryoplastic neuroepithelial tumour and ganglioglioma Aims: A diffuse variant of dysembryoplastic neuroepithelial tumour (dDNT) has previously been described, which although composed of oligodendroglia-like cells (OLC), astrocytes and mature neurones, lacks the multinodularity and ‘specific component’ of typical DNT. The

dDNT poses a significant challenge to the neuropathologist. This study Buspirone HCl was undertaken to further characterize the histological and immunohistochemical features of dDNT. Materials and methods: Review of our archived material from epilepsy surgery identified 16 cases, in which features of dDNT predominated. Their histological and immunohistochemical features, including CD34 and nestin immunohistochemistry, were analysed. Results: Seven cases had the characteristics of pure dDNT. A further two cases of dDNT showed extension into the white matter with occasional dysplastic neurones. Two additional cases had similar features but with the presence of either single, or multiple small nodular clusters of OLC, in keeping with transition to classical DNT. Five cases showed ganglioglioma-like areas, of which three cases had micronodule formation but with predominant dDNT pattern.

In this study, we examined CD146 expression on circulating T cells from patients

with autoimmune connective tissue diseases (CTDs), which were reported previously to exhibit phenotypic activation, effector cytokine production and derangement of memory/effector subsets ex vivo (reviewed in [10, 11]). Patients with CTDs, particularly lupus, are at increased risk for atherosclerosis. This is not explained fully by conventional risk factors or side effects of therapy, due probably to exacerbation of the inflammatory component of atherosclerosis by autoimmunity [12-14]. Different CTDs exhibit different patterns of vascular involvement [15-17]. The immune component of atherosclerosis involves infiltration of LY2157299 in vitro atherosclerotic plaques by CD4+CD28− (late effector/senescent) T cells, expressing CCR5 and Th1 cytokines [18]. Therefore, we also tested whether CD146 expression correlates with pro-atherogenic T cell phenotypes. Patients with systemic lupus erythematosus (SLE), systemic sclerosis (SSc) or primary or secondary Sjögren’s syndrome (pSS or sSS) were recruited through the CTD Clinic and the

Vasculitis Clinic at Addenbrooke’s Hospital, Cambridge, UK. Healthy donors (HDs) were recruited through the Department of Clinical Pharmacology. SLE patients fulfilled at least Selleck Vismodegib four ACR criteria, as revised in 1982 [19] and 1997 [20]. SSc patients met a recently revised set of criteria [21], and pSS patients

followed the criteria of the European Union/United States consensus [22]. Patients with sSS met criteria for Sjögren’s syndrome plus another CTD (SLE or SSc). The clinical characteristics of all patients are summarized in the online Supporting information, Table S1. Healthy individuals were screened to exclude those with autoimmune/inflammatory disease, and their history of cardiovascular disease Glutamate dehydrogenase was obtained. Pregnant women and smokers were excluded. Ethical approval was obtained (Norfolk REC 07/H0310/178), and all volunteers gave informed consent. Peripheral blood was collected in 9-ml heparinized tubes and subjected to Ficoll density gradient centrifugation. Peripheral blood mononuclear cells (PBMCs) were isolated from the gradient interface and cryopreserved in 10% dimethylsulphoxide (DMSO)/90% heat-inactivated fetal bovine serum (FBS). Thawed PBMCs were washed and suspended in fluorescence activated cell sorter (FACS) buffer [phosphate-buffered saline (PBS)/1% bovine serum albumin/0·05% sodium azide] at 4 × 106 cells/ml. Aliquots (50 μl) were incubated in a 96 U-well plate with cocktails of fluorochrome-conjugated monoclonal antibodies (mAbs) in the dark for 45 min at 4°C, washed, suspended in FACS buffer and transferred into 12 × 75 mm tubes (Falcon, BD Ltd, Pontypridd, UK).

3C) and spontaneous (data not shown) capability of BMDMs to repair a wound generated by scratching a confluent cell monolayer. Our results show that Abl is a component of podosomes in myeloid leukocytes and its expression and function is essential for podosome formation, cell migration in 2D and 3D and trans-endothelial migration. These EGFR inhibitor findings have a particular significance in the context of two aspects of leukocyte biology. The first one concerns the implication of podosome protrusive

activ-ities in trans-endothelial migration of leukocytes from blood to the interstitium during inflammation [[3, 17]]. Notably, the Abl kinase inhibitor imatinib mesylate has been reported to prevent and treat murine collagen-induced Selumetinib clinical trial arthritis [[18]] although a possible effect of the drug on leukocyte migration was not specifically addressed in this study. The second one concerns the decrease in osteoclast activity in patients treated with imatinib [[19, 20]]. In fact, although targeting of c-fms and other growth

factor receptors by imatinib may affect osteoclast differentiation [[20]] our findings point to an additional more direct role of the drug on podosome organization to explain its ability to inhibit bone resorption. Previous studies on carcinoma cells [[15, 16]] and this one highlight that targeting of Abl may result in reduction of cancer cell invasive capacity but also of myeloid leukocyte recruitment into the tumor. Notably, tumor-induced inflammation has emerged as one of the hallmarks of cancer [[21, 22]] thus pointing to the exciting possibility that Abl targeting

may represent a double-edged sword, acting simultaneously on tumor cells and cancer-related inflammation. Anti-Abl, anti-Arg, and anti-CrkL antibodies from Santa Cruz Biotechnology Inc. (Santa Cruz, CA) and anti-pCrkL antibody from Cell Signaling Technology (Beverly, MA) were used for immunoblotting experiments. Anti-Vinculin antibody (clone hVin-1) from Sigma Aldrich (St. Louis, MO) anti-Abl antibody from Millipore (Billerica, MA) anti-Cortactin (phosphoY466), anti-Arg and anti-Cortactin from Abcam (Cambridge, UK) were used for immunofluorescence experiments. Secondary antibodies from Invitrogen (Carlsbad, CA) were goat-anti mouse Metalloexopeptidase IgG1 FITC conjugated, goat anti-mouse Alexa 647 conjugated and goat anti-rabbit Alexa 647 conjugated. Rhodamine phalloidin from Cytoskeleton (Denver, CO) was used to label F-actin. Imatinib/Gleevec/STI-571 was from Santa Cruz. LPA was from Sigma Aldrich. BMDMs were isolated from femurs and tibias of 8-week-old wild-type C57BL/6J or fgr–/– and hck–/–fgr–/– mice as previously described [[12]]. Macrophages differentiated from the bone marrow, nonadherent, cell population for 7–8 days [[12, 13]] were detached by scraping and then plated for 24 h on fibronectin- or gelatin-FITC-coated coverslips in the above medium with a FCS concentration of 1%.

, 2010; Rangaka et al., 2012). The QuantiFERON TB Gold In-Tube test (QFT-GIT) uses an ELISA to measure the amount of IFN-γ released in response to specific M.tb antigens compared with controls. The specific M.tb antigens are early

secretory antigenic Autophagy Compound Library research buy target-6 (ESAT-6), culture filtrate protein 10 (CFP-10) and TB 7.7, which are present in all M.tb and are able to stimulate the measurable release of IFN-γ in most infected persons, but which are absent from BCG vaccine strains and most nontuberculous mycobacteria (Andersen et al., 2000). Thus, as test antigens, these proteins offer improved test specificity compared with purified protein derivative (PPD). In August 2008, QFT-GIT became the second IGRA approved by the US Food and Drug Administration (FDA) as an aid for diagnosing M.tb infection (FDA, 2010). However, the usefulness of QFT-GIT in the diagnosis of tuberculous LY294002 molecular weight pleurisy in developing countries, especially in China and other regions with mandatory BCG-vaccinated coverage, remains unclear. Research has shown that use of molecular biologic technology to detect M.tb-specific fragments in pleural effusion-specific fragments, could improve the diagnostic sensitivity and specificity for tuberculous pleurisy (Anie et al., 2007; Liu et al., 2007; Kumar et al., 2010). However, in previous

studies, diverse methods with different primers were selected to detect M.tb in pleural fluid samples, demonstrating highly variable sensitivities (42.8–87.0%) and specificities (91–97%; Nagesh et al., 2001; Hasaneen et al.,

2003; Chakravorty et al., 2005; Moon et al., 2005; Light, 2010). To evaluate the diagnostic accuracies of QFT-GIT and nested-PCR in tuberculous pleurisy, we conducted a cross-sectional study in high TB epidemic regions of China. The aim was to provide evidence of the usefulness of QFT-GIT and nested-PCR in tuberculous pleurisy diagnosis in a BCG-vaccinated area and give clues as to the development of in-house M.tb-specific detection tools. Seventy-eight patients with pleural effusion were enrolled consecutively in this cross-sectional study from 1 January 2011 to 31 October 2011 in Wuxi No. 5 People’s Hospital. Confirmed tuberculous HSP90 pleurisy was diagnosed with M.tb cultures positive in pleural effusion and/or confirmed TB infection by pleural biopsy. Probable tuberculous pleurisy was diagnosed using one of the following criteria: M.tb culture positive in sputum; M.tb culture positive in other biologic specimens; positive response to antituberculosis medication without other possible causes of pleural effusion (Moon et al., 2005). Twenty patients with pleural effusion who were diagnosed with diseases other than TB were also enrolled in this study as controls. The QFT-GIT was performed according to the manufacturer’s instructions (QFT-GIT; Cellestis Ltd, Carnegie, Australia).

c. adami,

or the more virulent P. c. chabaudi AS strain (12). Although the suppression of parasitemia is delayed in gene-targeted IL-2 KO mice infected with either subspecies of the parasite, their infections eventually cure. IL-15 functions redundantly with IL-2 in certain aspects of lymphocyte biology while having specific activities of its own (13). Ing et al. (14) report that the duration of P. c. chabaudi parasitemia is prolonged in IL-15 KO mice compared with intact control mice but they too eventually cure. Th1 cytokine production, dendritic cell and NK cell function are impaired in these mice, suggesting that IL-15 functions in both innate and adaptive immunity to the Selleckchem LDK378 parasite. Although both IL-2 and IL-15 contribute to immunity against blood-stage P. chabaudi

GW-572016 cell line malaria, neither cytokine appears to have an essential role, i.e. the absence of either cytokine merely delays the suppression of parasitemia but does not prevent it. Whether these observations can be explained by the redundant function of the 2 cytokines signalling through the interleukin 2/15 receptor β chain (IL-2/15Rβ) of the IL-2R (15) or other mechanisms remains to be elucidated. In the present study, we have examined the roles played by components of the IL-2R complex, namely the IL-2/15Rβ and the IL-2Rγc chains, in immunity to P. c. adami by comparing the time courses of parasitemia in KO mice deficient in these peptides with those seen in intact controls. Our findings indicate that the IL-2Rγc chain is essential for parasite clearance. In contrast, the IL-2/15Rβ chain, through which only IL-2 and IL-15 signal (9,15), does not play a crucial role in the suppression

of parasitemia. Female and male IL-2/15Rβ−/+ mice backcrossed to C57BL/6 mice for five generations (16), and C57BL/6 mice were purchased from The Jackson Laboratories (Bar Harbor, ME, USA). Breeding stocks of IL-15−/− mice on a C57BL/6 background (17) and IL-2Rγc−/y mice (4) backcrossed to C57BL/6 mice for more than five generations were kindly provided by Dr. Elaine Thomas (Immunex Corporation, Seattle, WA, USA) and Dr. Warren J. Leonard (NIH, Bethesda, MD, USA), respectively. Mice were bred in the AAALAC-accredited animal facility at the University of Wisconsin, Madison, WI, USA, to produce male IL-2R−/y mice lacking functional IL-2Rγ Alanine-glyoxylate transaminase chains and male IL-2R+/y control mice that expressed functional IL-2 receptors. Mice homozygous for nonfunctional IL-2/15Rβ chains served as test mice, whereas heterozygous mice were used as controls. Time courses of P. c. adami parasitemia in heterozygous IL-2/15Rβ−/+ mice and C57BL/6 mice were identical (data not shown). Age- and sex-matched C57BL/6 mice served as controls for IL-15−/− mice. All procedures were approved by the University of Wisconsin Institutional Animal Use and Care Committee. The avirulent malarial parasite P. c. adami 556KA was maintained and used as described previously (18). Experimental mice were injected i.p.

S2B). The proportions of total CD19+ B cells in the peritoneal cavities of the Tg mice were reduced (E-Btk-2) or normal (EY-Btk-5), but consisted almost exclusively of CD5+CD43+ B-1 cells (Supporting Information Fig. S2B), which were B220low and CD11b+ (data not shown). Next, we evaluated cell size and the expression of activation markers on both B220+CD5− and B220lowCD5+ splenic B cells. B220+CD5− B cells from E-Btk-2 Tg mice but not from EY-Btk-5 Tg mice exhibited significantly

higher forward scatter values, and elevated expression of CD25 and CD69 activation markers than those from WT mice (Fig. 3C). Similarly, B220lowCD5+ B-1 B cells from E-Btk-2 mice EPZ015666 ic50 but not from EY-Btk-5 mice manifested increased CD25 and CD69, when compared with splenic B220lowCD5+ B-1a B cells from WT mice (Fig. 3C). selleck The hyperresponsive phenotype of Btk Tg B cells was substantiated by sustained Ca2+ elevation in response to BCR engagement, when compared WT B cells (Fig. 3D). Moreover, increased

expression of various activation markers was found when E-Btk-2 and EY-Btk-5 Tg B cells were cultured in vitro, both in medium and stimulated by anti-IgM or LPS (Supporting Information Fig. S3). Finally, significant proportions of cytoplasmic Ig L chain positive cells in the spleens of E-Btk-2 and EY-Btk-5 mice were CD138+ and expressed high levels of intracellular Ig μ heavy chain, consistent with a plasmablast or plasma cell phenotype (Fig. 3E). This was confirmed by immunohistochemistry, which revealed strong IgM staining in the red pulp of E-Btk-2 and EY-Btk-5 Tg spleens, indicative of IgM+ plasmablasts or plasma cells (Fig. 5B, left panels). Double labelings with anti-IgM and MOMA-1 (specific for MZ methallophilic macrophages) revealed in WT, Btk-deficient and EY-Btk-5 mice a typical pattern with IgM+ follicular Dichloromethane dehalogenase B cells, surrounded by a rim of MOMA-1+ cells and outside this rim MZ B cells (Fig. 5B, left panels). By contrast, spleens

of E-Btk-2 mice contained few methallophilic macrophages with weak MOMA-1 staining and MZ B cells were lacking, consistent with the flow cytometry data (Fig. 5B, left panels). In summary, these findings show that residual B cells in E-Btk-2 and EY-Btk-5 mice appeared hyperresponsive, whereby proportions of B-1 B cells and IgM+ plasmablasts or plasma cells were increased. Crosses of E-Btk-2 and EY-Btk-5 mice onto the Btk-Slp65 double-deficient background showed that in the absence of Slp65 the effects of constitutive Btk activation were diminished, as the spleens no longer contained large proportions of CD5+ B-1 lineage cells and CD21high MZ B cells were present (Supporting Information Fig. S4). Therefore, the effects of constitutive active Btk expression on the follicular, MZ and B-1 B-cell subsets were dependent on Slp65.

1b, and data not shown). The D values of EHEC O26 and O111 were comparable to the D value of EHEC O157 that was already proven to be useful in epidemiological analyses (14); the findings of this study suggest a sufficient discriminating power of the MLVA system. In the present study, the new MLVA system was also useful for detecting outbreak-related isolates, and this buy Lumacaftor is one of the most prioritized objectives of genotyping (Fig. 3; Table 2). Most of the outbreak-related isolates did not exhibit any, or exhibited only single-locus, variations within each outbreak (Table 2). The cluster analysis based on the MLVA profiles revealed that each outbreak could

form a unique cluster. This was also true for the cluster analysis based on the PFGE profiles. Further, consistent results were obtained MG132 by both these methods (Figs 3, 4). However, the relationships between the clusters observed in one method differed from those observed in the other method because of the differences in the two methods with regard to the targets; MLVA discriminates isolates by repeat copy numbers of specific loci, whereas PFGE differentiates them by restriction fragment length polymorphisms of the entire DNA. Moreover, either PFGE or MLVA can be superior to the other method for discriminating isolates in some outbreaks. These results indicate that MLVA can complement

PFGE analysis. Considering that the procedure of MLVA is simpler and more rapid than that of PFGE, MLVA can be applied for the first screening of isolates in outbreak investigations before the results can be confirmed by PFGE. PFGE analysis is currently the golden method for subtyping bacterial pathogens. (13). Other researchers reported that subtyping methods, such as AFLP, rep-PCR and MLST, could be useful

for analyzing EHEC O157, but PFGE was the best method to discriminate isolates, for example, in outbreak investigations (17, 18). In this study, the results of MLVA were similar to those of PFGE analysis in outbreak investigations; this suggests that O-methylated flavonoid the discriminating power of MLVA is greater than that of the above-mentioned methods, although it might be necessary to evaluate the discriminating power of them for EHEC non-O157 strains, as described below. Furthermore, other methods are more time-consuming than MLVA. The results of the other methods, except MLST, are deduced from anonymous banding patterns, which can lead to ambiguous typing, whereas the results of MLVA are deduced from known loci and can be controlled by direct sequencing of the amplified products (19). Recently, infection with EHEC serogroups other than O157 has raised concerns not only in Japan but also in other countries: EHEC O26:[H11], O103:H2, O111:[H8], and O145:[H28] are frequently associated with HC and HUS (20). Although PFGE is the first line of choice for subtyping, most of the methods mentioned above have not yet been evaluated for analyzing EHEC non-O157 strains.

1b, top). Generally, for AdV construction using the COS-TPC method, we isolated a single virus clone to avoid contamination of the parent Ad5 derived from the DNA-TPC or unexpected reassortants (27). Clones lacking the upstream loxP were unexpectedly obtained when using both pAxLEFZ15L and pAxLEFZ19L. This virus, named AxLEFZ (ΔL) (Fig. 1b, bottom right), was found to be identical to 15L and 19L, except for the deletion of the upstream loxP as determined using restriction analyses and sequencing. We considered that ΔL was generated by homologous recombination within the packaging domain (Fig. 1b). Thus, we used ΔL as a control virus in this work. However, this recombination appears to be

a rare event GW572016 because, once the virus genome obtains the terminal protein at the right end through the recombination of the large homology, the virus repairs its left terminal by adding a new terminal protein at the right end through a “pan-handle” structure (27, 29). The set of three LacZ-expressing AdV, 15L (AxLEFZ15L), 19L (AxLEFZ19L), and ΔL (AxLEFZ), (Fig. 2a, top left), is called the “LEFZ series” in this paper. For the competitor virus, we constructed AxCAGFP (Fig. 2a, top left), which expressed enhanced

green fluorescent protein (Takara Bio, Shiga, Japan) under the control of the CAG promoter, using the COS-TPC method. The AdV titer was calculated using the TCID50 using 293 cells (30). Briefly, 50μL of DMEM supplemented with 5% FCS were dispensed into each well of a 96-well plate, and eight rows of threefold serial dilution Stem Cell Compound Library of the virus. Then, 3 × 105 of 293 cells was added to each well. The plate was incubated at 37°C and 50 μL of DMEM supplemented with 10% FCS was added to each well every 3 days. Twelve days later, the end-point if the cytopathic effect was determined by microscopy. The 293 cells were infected with 15L, 19L or ΔL at an MOI of 3 and with the competitor

virus at an MOI of 1 or 0.1 for 1 hr and then were cultured in a six-well plate. Three days after infection, the 293 cells were IKBKE harvested together with the medium. The cell suspension was sonicated for 2 min (30 s × 4 cycles) using a Bioruptor II sonicator (CosmoBio, Tokyo, Japan) at maximum power (200 W) and centrifuged at 1900 g using a Tomy TMP11 microcentrifuge rotor (Tomy, Tokyo, Japan) for 5 min at 4˚C. The supernatant was stored as the first viral stock. An aliquot (100 μL each) was used to infect 293 cells on a six-well plate, and the culture medium was obtained as the second viral stock. Similar virus passages were continued six times to obtain the seventh viral stock. To monitor the genome structure of the virus, the infected cells at each passage were centrifuged at 1900 g for 5 min at 4°C, and the total cell DNA together with the viral genome DNA was prepared according to the method of Saito et al. (31).

Compliance with the GFD was assessed every 15 days by careful examination

of a patient’s food diary (control level 1) followed, whenever possible, by a specific medical interview (control level 2). At the same time-points, a blood sample was obtained to detect EMA as a further index of adherence to the GFD (control level 3). All patients in this group presented excellent compliance with the GFD and completed the clinical phase of the study. Conversely, the NFR characterization was performed exclusively on 11 of 20 patients in this group who, after a reasonable period on a GFD, agreed to undergo a second duodenal biopsy. By preliminary evaluation, the subgroup AT9283 of 11 patients appeared to be gender- and age-reflective of the overall group. Group 2.  Group 2 comprised treated CD patients (31 male/56 female, mean age 31·3, range 19–54 years) on a GFD from at least 12 months, and showing serum EMA-negative results. During the study, all patients continued to take a GFD and were followed regularly for 12 months. Compliance with the GFD was assessed every 15 days as described for group 1. Group 3.  Group 3 comprised healthy subjects (five male/10 female, mean age 28·7, range 18–55 years) not affected by CD or other autoimmune disease, and with no consanguinity

with CD patients. At study entry their sera were collected and stored at −70°C until tested. Two of the subjects in this group showed an NFR-like pattern in the absence of serum EMA. For ethical reasons, the

latter two subjects were not submitted to duodenal biopsy to exclude a subclinical form of CD. However, they agreed to undergo a GFD and to be monitored for 12 months. Adherence to Wnt beta-catenin pathway the GFD was assessed every month as described for group 1. Both treated subjects presented excellent compliance to the GFD and completed the study. CD patients were selected from among the out-patients admitted to our gastrointestinal unit from January 2006 to December 2007 who showed clinical features described for groups 1 or 2, and who agreed to undergo the study protocol. The diagnosis of CD was made Org 27569 in accordance with the procedure adopted worldwide [34], based on clinical case identification, serological screening and duodenal biopsy histology. Healthy subjects were selected among the blood donors admitted to our hospital from January 2006 to December 2007 who showed clinical features described for group 3, and who agreed to undergo the study protocol. The diagnosis of CD was excluded in individuals not clinically suspicious, with serum EMA-negative results. Because the suitability of oat as part of a GFD is still controversial [2], all the GFDs administered in this study included the withdrawal of any oat-based product. All procedures followed in this study were in accordance with the ethical standards of the institutional committee responsible for human experimentation. Furthermore, informed consent was obtained from each study participant.

Outbred CD1 exhibit either Balb/c-like or C57Bl/6-like spinotrapezius angioarchitecture, predictive

of response to arteriolar ligation. Conclusions:  This collateral capillary arterialization process may explain the reported longer time required for blood flow recovery in Balb/c hindlimb ischemia, as low-resistance blood flow pathways along capillary conduits must be formed (“arterialization”) BGJ398 solubility dmso before reperfusion. “
“Please cite this paper as: Al-Khazraji BK, Novielli NM, Goldman D, Medeiros PJ, Jackson DN. A simple “Streak Length Method” for quantifying and characterizing red blood cell velocity profiles and blood flow in rat skeletal muscle arterioles. Microcirculation 19: 327–335, Small molecule library cost 2012. Objectives:  To develop a valid experimental method for quantifying blood flow in continuously branching skeletal muscle arterioles, and to derive an empirical relationship between velocity

ratio (VMax/VMean) and arteriolar diameter. Methods:  We evaluated arteriolar trees using IVVM of rat gluteus maximus muscle and developed a method to acquire single fluorescent-labeled RBC velocities across arteriolar lumens to create velocity profiles. These data were used to calculate the blood flow for 37 vessel segments (diameters: 21–115 μm). Results:  Mass balance at arteriolar bifurcations had 0.6 ± 3.2% Methocarbamol error. Velocity ratios ranged from 1.35 to 1.98 and were positively correlated with diameter (p < 0.0001), and VRBC profiles were blunted with decreasing diameter. Conclusions:  We present a means for quantifying blood flow in continuously branching skeletal muscle arterioles. Further, we provide an equation for calculating

velocity ratios based on arteriolar diameter, which may be used by others for blood flow calculations. “
“Please cite this paper as: Fedosov, Caswell, Popel and Karniadakis (2010). Blood Flow and Cell-Free Layer in Microvessels. Microcirculation17(8), 615–628. Blood is modeled as a suspension of red blood cells using the dissipative particle dynamics method. The red blood cell membrane is coarse-grained for efficient simulations of multiple cells, yet accurately describes its viscoelastic properties. Blood flow in microtubes ranging from 10 to 40 μm in diameter is simulated in three dimensions for values of hematocrit in the range of 0.15–0.45 and carefully compared with available experimental data. Velocity profiles for different hematocrit values show an increase in bluntness with an increase in hematocrit. Red blood cell center-of-mass distributions demonstrate cell migration away from the wall to the tube center. This results in the formation of a cell-free layer next to the tube wall corresponding to the experimentally observed Fahraeus and Fahraeus–Lindqvist effects.