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Increasing percentage of predicted CXCR4-using variants over time following their appearance during natural HIV-1 infection.The median percentage si/x4 sequences generated from PBMC (light grey) and serum (dark grey) by deep sequencing at time points up to one year before the first phenotypic detection of CXCR4-using variants in the MT-2 assay in eight participants are shown. Error bars represent the interquartile ranges. Three different types of tissue oxygen pressure (ptiO2) responses are found in the cortex of subarachnoid hemorrhage (SAH) patients in spatial and temporal association with cortical spreading depolarizations (CSDs). (A) Biphasic ptiO2 response with an initial decrease and a secondary increase, monophasic ptiO2 decrease, and monophasic ptiO2 increase. Arrows indicate the start of CSD in the electrocorticography (ECoG) channel next to the ptiO2 probe. (B) Magnification of the biphasic ptiO2 response of part A. Further detailed ptiO2 response analyses reveal values of specific features, integrals, and subareas of the ptiO2-curve: BASE = ptiO2 at baseline (30.60 [25.25, 36.70] mmHg), MINhypo= the minimum (23.90 [16.75, 32.38] mmHg), DURhypo= the duration (345 [207.5, 502.5] seconds), and INThypo= the integral (12.76 [3.87, 18.94] arbitrary units [aU]) of the initial hypoxic phase. descINThypo= (grey-shaded) integral representing the phase we designate “descent area,” that is, the area under the curve from start to minimum of the hypoxic phase. MAXhyper= the maximum (38.00 [28.30, 45.00] mmHg), DURhyper= the duration (720.0 [540.0, 1090.0] seconds), and INThyper= the integral (40.00 [12.50, 124.28] aU) of the secondary hyperoxic phase; ascINThyper= second (grey-shaded) integral depicting an ascent area, that is, the area from start to maximum of the secondary hyperoxic phase. In some cases (compare with Fig 4A), ptiO2 shows an asymptotic return to ptiO2 baseline, which may distort curve analysis; thus the grey-shaded areas are additionally scrutinized to avoid this distortion. (C) Relative percentage frequencies of different ptiO2 responses to ECoG events (90 CSDs). Clear spatial and temporal associations of ptiO2 responses with EcoG events are found in 53.3 (42.7, 67.1)% of the CSDs (in total 47 of 90 CSDs, with association rates up to 90% in single individuals). The differentiation of all CSD-associated ptiO2 response types demonstrates that the biggest portion is contributed by biphasic ptiO2 responses (Bi); monophasic increases (MI) were rare in the severe SAH patients, and monophasic decreases (MD) were more frequent. (D) The 3 different ptiO2responses (compare with part C) in total ∼100% and their distribution of SAH patients with no ischemic neurological deficit (DIND) (white bars) versus SAH patients with DIND (black bars). All monophasic ptiO2 increases were found in SAH patients with no DIND and good outcome (extended Glasgow Outcome Scale ≥ 6). Biphasic ptiO2 responses were approximately similar in both patient groups, whereas monophasic decreases were typically found in patients developing DIND. Increased induction of IL-12p40 and TNF-α by the ΔmmaA4 M. tuberculosis mutant in bone marrow-derived macrophages.Bone marrow-derived macrophages from BALB/c mice were infected with wild type M. tuberculosis H37Rv, the ΔmmaA4 mutant, or the complemented ΔmmaA4 strain at an MOI of 10, or left untreated (UT). Conditioned media from macrophage cultures were harvested at 24, 48, and 72 hr post-infection. IL-12p40 and TNF-α production were determined by ELISA. ***, p<0.001 (two-way ANOVA, Bonferroni post-tests). Values are the means±SD of triplicate samples and are representative of 3 separate experiments. The complex interplay between the primary mechanisms of TCM. Growth dependence of Fas2 KO strain on different exogenous fatty acids in YPD.Different amounts of myristic (14∶0), palmitic (16∶0), stearic (18∶0), oleic (18∶1) acids, and T80 (Tween 80) were added to YPD broth. Yeast growth was determined by cell density after 48 hours at 30°C. The results were the mean of two independent experiments.
The molecular structure (30% thermal probability ellipsoids) of the compound showing the atom numbering. Frequency of protective device use. Correlation of group body weight-adjusted brain weights vs. group age at endpoint.The average group body weight-adjusted brain weights (mg/g b.wt.) for 23 adequate vitamin D3 intake (AI; 1 IU D3/g feed; black squares, 12 males; black circles, 11 females) and 19 deficient vitamin D3 intake (DEF; 0.025 IU D3/g feed; orange squares, 10 males; orange circles, 9 females) vs. the average group age at endpoint (CS 5; d) for 31 AI (19 males and 12 females) and 29 DEF (15 males and 14 females) G93A mice. Body weight-adjusted brain weights positively correlated with age at CS 5 for all mice (r = 0.985; slope = 1.32; P = 0.015). Age at CS 5 (d) = (103.80±3.19)+[(1.32±0.16)×(brain weights (mg/g b.wt.))]. Data presented as means ± SEM. Correlation between the amount of different chemicals absorbed across skin following a 30-min application and the quantity recovered in SC tape-strips after an identical, but independent, administration procedure. Redrawn from [52]. By combining genetic analysis via automated ribosomal intergenic spacer analysis (ARISA) and toxin detection using the surface plasmon resonance (SPR) sensor, it will be possible to identify the species as well as the level of domoic acid associated with a HAB event.
ARF6 regulation of Ca2+-dependent DCV exocytosis in PC12 cells. (1) Ca2+ influx stimulates exocytosis of docked DCVs, but only if plasma membrane PIP2 is available. (2) Ca2+ influx promotes the dephosphorylation of PIP5KI. (3) Dephospho-PIP5KI associates with ARF6 and is activated to synthesize PIP2 for DCV exocytosis. (4) Increased PIP2 synthesis drives endocytosis and retrieval of the DCV membrane after exocytosis. (5) Constitutive endocytosis may be enhanced by ARF6Q67L stimulation of PIP5K. (6 and 7) Lack of GTP hydrolysis on ARF6Q67L and constitutive PIP2 production on endosomes prevents recycling to the plasma membrane. Entrapment of plasma membrane constituents and diversion of PIP5K and PIP2 to endosomes in ARF6Q67L-expressing cells results in the inhibition of DCV exocytosis. Model of regulation of FasL expression during TCR-induced T cell AICD. In this model, TCR ligation leads to the activation of PTKs, which results in the activation of p38 MAPK. p38 MAPK then phosphorylates several nuclear transcription factors (e.g., ATF-2), which may bind to the FasL promoter and activate FasL gene transcription. Transcribed FasL protein translocates from the cytoplasm to the plasma membrane, interacts with Fas which then recruits FADD to bind to its death domain. This FasL–Fas interaction initiates a caspase cascade that subsequently activates JNK. Activated JNK promotes AICD by regulating FasL expression. Thus, p38 MAPK and JNK may preferentially regulate FasL expression at early and later times after activation, respectively, perhaps by the phosphorylation and activation of distinct transcription factors for the FasL promoter. Consistent with this model, we observed that inhibition (⊗) of p38 MAPK, JNK, and caspase activity blocks T cell AICD. Wild-type CTLA-4 is within lipid rafts in a tail-dependent manner. Lipid raft (R) and detergent-soluble (S) fractions were isolated from resting Jurkat T cells transfected with wild-type CTLA-4, tailless CTLA-4, or GPI-anchored CTLA-4 molecules induced with doxycycline or left noninduced. (A) Selected fractions were run on SDS PAGE and Western blotted for CTLA-4. Where indicated by an asterisk (*) the samples were diluted 10-fold with 1× sample buffer before loading in order to assess nonsaturated signals for CTLA-4 in these samples. CTLA-4 is detected as a broad band attributed to differential glycosylation and intermediate GPI-anchored molecules. (B) Band intensities from the film in panel A were quantified by densitometry and used to calculate the percentage of total CTLA-4 within lipid rafts (see Materials and Methods). (C) The fractions used in the experiment (A) were immunoblotted for ERK-1/-2, CD45, and GM1 to control for quality of the separation. ERK-1/-2 and CD45 were found in the soluble fraction while GM1 partitioned within lipid rafts. Cellular profiles and macrophage inflammatory protein-2 (MIP-2) level in bronchoalveolar lavage (BAL) fluid. (A) Total cell counts and cell differentiation in BAL fluid from treated mice on BLM day 7. At least four mice were prepared for each group in each experiment. Data shown represent the mean ± SEM from two independent experiments. TCC: total cell counts; Macro/mono: alveolar macrophages/monocytes; Neutro: neutrophils; Eo: eosinophils; Lym: lymphocytes. (B) MIP-2 levels in BAL fluid from treated mice on BLM day 7 was evaluated by ELISA assay. At least four mice were prepared for each group in each experiment. Data shown represent the mean ± SEM from two independent experiments. *Statistically significant difference (p < 0.05) in comparison. The distinct role of Th1 and Th2 cells for eradication of established tumors in vivo. (A) OVA-specific Th1 cells (•), OVA-specific Th2 cells (○), or saline (▴) were intravenously injected into BALB/c mice bearing A20-OVA tumors. The antitumor activity of Th1 and Th2 cells was determined by measuring changes over time of the means of two perpendicular diameters of the tumor mass. Results are presented as mean ± SE of six mice. The tumor-free mice were followed for >90 d. (B) Typical tumor growth or regression pattern in saline- (a), Th1- (b), or Th2-treated mice (c). Similar results were obtained in >10 independent experiments. The arrow indicates the site of tumor inoculation in Th1-treated mice.
Plot of mean glucose infusion rate as a function of insulin plasma concentrations in healthy subjects receiving subcutaneously 10 units of lispro (●) and in obese subjects with type 2 diabetes receiving 10 units (○), 30 units (□), and 50 units (▵) of lispro. Data points are connected in chronological order; as depicted by the arrows, the resulting relationship denotes a counterclockwise hysteresis. Effect of lidocaine on the steady state availability curve of F1304C. h∞ curves were recorded with 200-ms prepulses, followed by a test pulse to −20 mV. For each patch, the h∞ curve was measured in the absence and presence of 1.0 mM lidocaine (n = 5) in rapid succession. In other experiments without lidocaine, we did not observe significant left shifts in gating after patch excision on the time scale of these experiments. Data from each curve was fit with a Boltzmann with maximal value (Imax), half-maximal voltage (V1/2), slope (k), and nonzero plateau (c) as free parameters. The graph shows data normalized to the maximum value for curves measured in the absence of lidocaine, and then averaged across trials. Without lidocaine, V1/2 = −78.9 ± 1.9 mV, k = 6.2 ± 0.7 mV, and c = 0.11 ± 0.02. In 1.0 mM lidocaine, V1/2 = −89.7 ± 1.8 mV, k = 7.1 ± 0.4 mV, c = 0.08 ± 0.02, and Imax in 1.0 mM lidocaine was 78 ± 6% of Imax in the absence of lidocaine. This represents a hyperpolarizing shift in the apparent h∞ curve by 10.8 ± 2.6 mV. Flow cytometric characteristics of circulating anti-EBV specific pCTL from patients, age-matched healthy individuals and healthy younger individuals. (A)Percentage of multimer+CD8+ T cells inside each positive MLPCs (significance is indicate for comparisons between each group). (B)Mean Fluorescence Index (MFI) of HLA-multimers inside the positive MLPCs for each group. Inhibition of iNOS function reveals rmIL-12 adjuvant effects. Female A/J mice (8 mice per group) were vaccinated with 106 irradiated SCK cells and received either PBS (gray lines), rmIL-12 (solid black lines), rmIL-12 + L-NAME (hatched black lines), or rmIL-12 and D-NAME (double dashed black lines) on days 0–4 and 7–11. Mice were challenged 14 d after vaccination with 2.5 × 104 SCK cells in the opposite flank. Tumorigenesis was scored daily. CD2–CD48 and LFA-1–ICAM-1 enhance Ca2+ fluxes at low antigen concentration. Thioglycollate-elicited macrophages derived from control or ICAM-1–deficient mice were pulsed with various doses of peptide p33, mixed with INDO-1–pulsed, purified CD8+ T cells derived from TCR-transgenic control or CD2-deficient mice, and centrifuged together. Elevation of [Ca2+]i was assessed by measuring the FL5/FL4 ratio. (A) FL5/FL4 ratio is shown after stimulation with 10−11 M p33-pulsed macrophages. (B) Mean FL5/FL4 ratios are shown as a function of the peptide concentration for the various combinations. Baseline FL5/FL4 values were subtracted for the calculation. One representative experiment of two is shown. ▪, CD2+ ICAM+; •, CD2−ICAM+; □, CD2+ICAM−; ○, CD2−ICAM−.
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