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The cumulative frequency of GPS errors from a stationary test of fast-loc GPS tags (N = 257) are shown. Average T2 identification accuracy (given correct identification of T1) as a function of T1–T2 lag in Experiments 3 and 4. Error bars reflect standard errors of the mean The double-reciprocal plot from the guest titration data for 4 × 10−5 M 2,6-ANS in the presence of 0.0025 mM G4 PAMAM dendrimer; the solid line shows the linear fit. BLyS mRNA expression and release by activated neutrophils. (A) Purified populations of neutrophils were incubated with 1,000 U/ml G-CSF. At the time points indicated, total RNA was extracted and analyzed for BLyS, IL-1ra, and actin mRNA expression by Northern blotting. (B) Neutrophils and PBMC purified from the same donor were cultured for 21 h with or without 200 U/ml IFNγ, and then were subjected to Northern blot analysis for BLyS, CXCL-11/I-TAC, and actin mRNA expression. Data are representative of results from at least two independent experiments for each panel. (C) Neutrophils were incubated for up to 42 h at 37°C with 1,000 U/ml G-CSF and 200 U/ml IFNγ. Culture supernatants were harvested and processed for BLyS detection by a specific ELISA. Values represent means ± SEM of duplicate determinations calculated from four independent experiments. The asterisks represent significant differences between stimulated and resting neutrophils. **, P < 0.01. (D) PBMC, monocytes, and mono-DC were cultured in the presence or the absence of 200 U/ml IFNγ for 3 d. Culture supernatants were collected, and the levels of BLyS were measured by ELISA. Values represent the means of duplicate determinations calculated from two independent experiments. Time course of the inhibitory effects of 17β-estradiol and progesterone on IL-1β–induced collagen degradation by corneal fibroblasts. Cells were cultured for the indicated times in collagen gels in the absence or presence of IL-1β (0.1 ng/ml) and either 17β-estradiol (10 μM) or progesterone (10 μM) as indicated. The amount of degraded collagen was then determined. Data are means±SEM of quadruplicates from an experiment that was repeated three times with similar results. *p<0.05 (Student’s t test) for cells incubated with IL-1β plus 17β-estradiol or progesterone versus the corresponding value for those incubated with IL-1β alone.
Directional displacement.Pseudopod formation and trajectories were recorded for 5h starved Dictyostelium cells; 8 cells were followed during 15 min. The directional displacement is the distance moved after n pseudopodia in the direction of the first pseudopod. Data points are the means of ∼120 measurements, the line is the outcome of Eq. 11 with pseudopod parameters as indicated in Table 1. Pretreatment with bFGF inhibits Fas-mediated apoptosis. (A) FH2 cells were pretreated with 100 ng/ml EGF, 100 ng/ml IGF or 10 ng/ml bFGF for 16 h, and then stimulated with 200 ng/ml agonistic anti-Fas mAb RK-8 for the indicated times. Cell viability was measured by amido black staining assay (see Materials and Methods). (B) Activation of MAPK in FH2 cells treated with EGF, IGF, or bFGF was detected by Western blotting with anti–phospho-MAPK antibody. Expression level of MAPK was confirmed by Western blotting with anti-MAPK antibody. (C and D) FH2 cells were pretreated with or without 10 ng/ml bFGF for 16 h and stimulated with anti-Fas mAb RK-8 for the indicated times. Activation of caspases in cell lysate was measured using the fluorescent substrate IETD-MCA and DEVD-MCA for caspase-8/6 (C) and caspase-3/7 (D), respectively. Survival data for C57BL/6J mice inoculated with WNV. Wild-type and sIgM−/− mice were inoculated via footpad with the indicated doses of WNV and followed for 28 d. The survival curves were constructed using data from three to five separate experiments. The number of animals were n = 28 for wild-type mice and n = 24 for sIgM−/− mice. The mean survival times (in days) were 21.8 ± 1.6 for wild-type and 9.8 ± 0.1 for sIgM−/− mice (P < 0.0001). GM-CSF regulates the onset and progression of clinical EAE provoked by MOG35–55 peptide. Mice were immunized with MOG35–55 peptide emulsified in CFA and monitored daily for the development of clinical disease. Mean clinical disease score in GM-CSF−/− and WT mice (n = 8 for each group). Note this is a representative of three independent experiments; in total 20/21 GM-CSF−/− mice failed to develop any clinical symptoms. The single mouse that developed symptoms did not progress past a clinical score of 1. In contrast all WT mice developed clinical symptoms. Inhibitory effect of KIN-841 on proliferation of 3LL cells under hypoxia. Cells were treated for 48 h with KIN-841 at the various concentrations indicated under normoxia or hypoxia. aP<0.05 vs controls; bP<0.01 vs controls; cP<0.05 vs normoxia.
Decreased secretion of GM-CSF in SARS-CoV-3CLpro transfected cells. A549 cells were transfected with EGFP or 3CLpro or C145A plasmids. The supernatants were collected from cell cultures at 6, 12, 24, 48 and 72 hrs and ELISA was performed to evaluate the amount of secreted GM-CSF. The supernatant from the cell culture of A549 cells was used as a control. A significant decrease of GM-CSF was observed in 3CLpro or C145A transfected A549 cells (p = 0.0204 and 0.0236 respectively). The structure of C9H14N2O6S with all non-H atom-labelling scheme and ellipsoids drawn at the 50% probability level. Platelets from JAQ1-treated mice do not respond to CRP and collagen. (a) Two-color flow cytometric analysis of platelets from JAQ1-treated or control mice 3 d after Ab injection. Diluted whole blood was stimulated with 10 μM ADP or 10 μg/ml CRP for 2 min and subsequently incubated with antifibrinogenFITC and anti–P-selectinPE Abs for 10 min at RT and analyzed directly. Platelets were gated by FSC/SSC characteristics and Fl3 intensity (anti–mouse GPIb αPE/Cy5). The data shown are representative of six mice per group. Similar results were obtained on days 7 and 14 after Ab injection. (b) Heparinized prp from the indicated mice was stimulated with collagen (50 μg/ml), ADP (10 μM), or PMA (50 ng/ml). Light transmission was recorded on a Fibrintimer 4 channel aggregometer. (c) Heparinized prp from control mice was incubated with stirring in the presence of irrelevant rat IgG2a (20 μg/ml; ○) or JAQ1 (20 μg/ml; ▿) for 5 min before the addition of the indicated concentrations of collagen. In parallel, prp from JAQ1-treated mice was tested (□). Results are expressed as the maximum (max.) platelet aggregation ± SD for groups of each six mice. Number of CD34/prolyl 4-hydroxylase fibrocytes increase with age at autopsy. The figure represent a correlation between the number of CD34/prolyl 4-hydroxylase fibrocytes and the age of the lung transplanted patients with OB at time of autopsy R = 1.00 (p < 0.05) (Figure 6). Model-averaged half-lives for both monkeys, calculated using only trials with total length 6. 5 s. Cued, combined refers to data pooled across the two cued conditions for each subject. Error bars represent 95% confidence intervals for the means, calculated by bootstrap resampling.
Proliferation and cytokine production of lymph node cells from B7-1/B7-2−/− mice challenged with MOG 35-55. Mice were immunized with 100 μg of MOG 35-55 in CFA. 10 d later, draining lymph node cells from wild-type (diamonds) or B7-1/B7-2−/− (circles) mice were restimulated in vitro with a range of MOG 35-55 peptide concentrations. Supernatants were collected after 24, 48, and 72 h from cultures stimulated with 50 μg/ml of MOG 35-55 or with media alone. Cytokines from wild-type (Wt, solid bars) and B7-1/B7-2−/− (hatched bars) cultures were measured by sandwich ELISA, and background levels from media controls were subtracted. Data are representative of eight independent experiments. Funnelling. Activation of CPP32-like proteases in normal and resistant U937 variants. (A) Normal U937 cells, TNF-selected variants (U9-TR), and NAD-depleted variants (U9-NAD) were exposed to UV light 0.06 J/cm2, incubated for the indicated time, and cytosol extracts were assayed for proteolytic activity on the DEVD-pNa substrate. (B) U937 and the variants were incubated for 90 min after exposure to UV light, and the morphologically apoptotic cells were enumerated microscopically. Delayed neutrophil recruitment during peritonitis in Lfa-1d/d mice. Lfa-1d/d and wild-type mice were injected i.p. with thioglycollate and infiltrating neutrophils were identified by their Gr-1hiMac-1hi-staining profile in flow cytometry analysis n = 4–6 independent mice per group. *P < 0.05 (Student Molecular structure of the title compound, showing atom-labeling scheme and 50% probability displacement ellipsoids.
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