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Fig 1. A, Kaplan-Meier OS analysis stratified by the 1988 FIGO stage 1 system (P < 0.001). B, Kaplan-Meier OS analysis stratified by the 2009 FIGO stage 1 system (P < 0.001).
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Fig 1. Overall Survival and Progression-Free Survival in All Patients.
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Fig 4. HDAC4 knock-down does not rescue global transcriptional dysregulation. (B) Taqman qPCR validation of the genes that were predicted to be differentially expressed between R6/2 and Dble::R6/2 cortex at 9 wk of age. See Table S3 for gene abbreviation definitions.
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Fig 5. Model for phagosome and entotic vacuole fission.
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Fig 1. Kaplan-Meier Analysis of Progression-Free Survival (PFS) in Patients With Advanced Breast Cancer who Were (A) < 70 Years of age and (B) ≥ 70 Years of age.
Abbreviations: CI = confidence interval; EVE = everolimus; EXE = exemestane; HR = hazard ratio; PBO = placebo.
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Trends in the use of female incontinence procedures among certifying urologists between 2003 and 2012.
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Fig 1. Kaplan-Meier curve for probability of overall survival in patients with node-positive disease.
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EμTEL-JAK2 Expression Is Associated with Elevated RNA and Protein Levels of Bcl-2, Bcl-x, and Bim.
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Fig 1. Single-agent activity of brentuximab vedotin in comparison with other investigational agents in patients with relapsed Hodgkin lymphoma. CR, complete remission; PR, partial remission.
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Fig 1. Anatomic limits of pelvic lymph node dissection (PLND).
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Fig 1. Chronic diseases/late effects (percent). Endo endocrine.
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Fig 1. MEMRI demonstrates variable defects in the Gbx2-CKO mouse brain.
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Fig 1. magoo mutant cortex has reduced length and thickness but preserved layer structure.
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Fig 2. Flowchart of the robust optimization approach. (a) Replica based robust optimization. (b) Evaluation of the robust and PTV optimized plans.
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Fig 1. Illustration of the average enzyme principle for a linear metabolic pathway.
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Fig 3. High-dose-rate brachytherapy planning image; catheter trajectories shown with critical structures including GTV, CTV, and cord indicated. GTV = gross tumor volume; CTV = clinical target volume.
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Fig 4. The Mre11 Complex Induces an Oncogene-Driven G2 Arrest. (A) Representative confocal z slices of DAPI-stained (Ai) pHH3-S10 and (Aii) H3K9me3 IF in WT + NeuT mammary glands. Scale bar = 10 μm. Lower panels depict linescan plots for the indicated lines in (Ai) and (Aii).
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Fig 5. In patient 2, fused images obtained at ~1 h show mild 68Ga-DOTA-F(ab')2-trastuzumab uptake in a lung metastasis.
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Fig 2. The incremental explained variation is plotted against the distance metric for every possible two-class configuration of the 16 distinct permutations of the four binary markers, excluding only configurations in which one subtype contains fewer than 5% of the cases (green dots). The red dots represent local maxima obtained from k-means clustering. The blue dot corresponds to the classification ER+ versus ER-.
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Fig 3.Sequence-Specific Recognition of RNA Containing UACAU RNA Recognition Element by B. subtilis MazF. (B) Panels showing the recognition of individual nucleotides in RNA by MazF. Intermolecular hydrogen bonds are indicated by dashed black lines. For clarity, only one nucleotide is shown in yellow in each panel.
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Figure 4. Correlations between CDH1 and ZEB1 with each member of miR-200 family of miRNAs among samples.
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Fig 8. Characterization of a mutant strain deleted of yejK. A and B, MG1655 (panel A) and MG1655ΔyejK (panel B) cells were grown in LB medium at 37 °C for 2 h, fixed, stained with DAPI (a DNA stain, blue channel) and FM 4-64 FX (a live membrane stain, red channel), and imaged by fluorescence microscopy.
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Joint mixed-effects and time-to-dropout modelling of symptomatic improvement in FACT-P total score.
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Fig 4. Invasive mucinous adenocarcinoma demonstrates lepidic and acinar growth. The tumor consists of columnar cells filled with abundant mucin in the apical cytoplasm and shows small basal oriented nuclei (Hematoxylin and eosin 200×).
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Transcriptional control of regulatory T (Treg) cell function. (A) Forkhead box P3 (Foxp3), the Treg lineage-specifying factor, is essential for the maintenance of Treg cell suppressive function.
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Models of LSC response to imatinib.
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The Taspase1-Mediated Cleavage of MLL1 and MLL2 Is Not Required for Spermatogenesis
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Fig 3. Classification and regression tree results using the following variables: age, stage, tumor subtype, grade (G), myometrial invasion (Myo Inv), total lymph nodes removed, and evaluation of para-aortic lymph nodes. Complexity parameter (CP) = 0.022 for the green highlighted tree; CP = 0.0071 for the tree shown. The numerators indicate number of deaths, and the denominators indicate total number of cases in the subcategory.
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Fig 3. Forkhead box (Fox)o-dependent program in T regulatory (Treg) cells.
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Fig 1. Kaplan–Meier estimates of over-all survival between groups.
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Fig 7. Proposed model for PrE formation.
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Fig 1. Selection process for studies included in meta-analysis.
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Fig 1a. Decision curve comparing the net benefit of models predicting risk of potentially aggressive disease features (non–organ-confined disease, tumor volume >0.5 cm3, or Gleason grade >3) on radical prostatectomy.
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Fig 1. Overview of normal hematopoiesis and leukemogenesis. At disease inception, an unknown number of leukemic stem cells (LSCs) may cycle between proliferative and quiescent states. Some proliferating LSCs differentiate into EPCs that retain proliferative capacity but lack long-term self-renewal capacity. After a number of cell-division cycles, the EPCs become late progenitor cells, which eventually mature into leukemic cells that enter circulation [54] and [57].
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Fig 3. Histologic image. Melanoma arising in association with a congenital melanocytic nevus (arrow points to the area of melanoma). Superficial spreading melanoma arising in association with an intradermal nevus.
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Fig 2. Decrease in size of pancreatic head mass with IV irinotecan and cetuximab from July 2008 (A) to November 2008 (B).
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Fig 1. Immunohistochemistry detection of eukaryotic protein synthesis initiation factor 4E (eIF4E) in tumor and in histologically negative margins in 4 resected head and neck squamous cell cancer specimens. Tonsil squamous cell cancer (SCC) eIF4E in tumor (A).
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Fig 2. Local failure rates for all parameningeal rhabdomyosarcoma patients regardless of intracranial extension between the Intergroup Rhabdomyosarcoma Study (IRS-IV) and Children's Oncology Group (D9803) groups. Local failure rate for patients enrolled on IRS-IV (dashed line) or D9803 (solid line).
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Fig 4. Correlation between pS6(240/4) inhibition and clinical response to BYL719 in breast cancer patients. (A) Representative sections stained by IHC for pS6(240/4) in paired biopsies obtained from tumors of patients before (untreated) and at day 28 of BYL719 treatment. Patient numbers are indicated at left in parentheses. Images were captured at ×40 magnification; scale bar, 100 μm.
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Fig 2. MIR143-NOTCH1 gene fusion in a benign glomus tumor of the neck soft tissue (GT2). A: Typical morphologic appearance of a glomus tumor with uniform cuboidal cells with pale eosinophilic cytoplasm and round, bland nuclei, with a distinctive angiocentric growth around small blood vessels (H&E, 200×).
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Fig 1. Prospective Strategies for Employing Cerebral Organoid Cultures.
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This dermatofibroma, hemosiderotic variant displays a diffuse homogeneous bluish pigmentation.
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Fig 1. Conceptual groupings of S2P mediated signaling pathways.
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Fig 2. Hypothetical models of progression from in situ to invasive breast cancer. (B) Progression from DCIS to IBC as an evolutionary bottleneck.
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Fig 1. Kaplan-Meier ocular event-free survival curve of all eyes.
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Fig 1. Schematic of 48-well plates connected to the piezo ceramic element.
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Fig 1. Representative qualitative retinal oximetry images of retinas from 3 irradiated (A–C) and 3 unirradiated (D–F) subjects from the two cohorts.
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Fig 6. Osteoprotegerin secretion by GCT stromal cells was altered selectively by exposure to osteogenic media, BMP2, or SB415286.
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Fig 4. Human HCC samples display cytoplasmic localization of p16.
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Figure 3. Location of the breakpoint sequences of the deletion in the KLK15 gene.
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Fig 7. Case 1. Histology and immunohistochemical stains. a H&E image demonstrates the lobulated appearance of the lesion (magnification, 40×). b Higher magnification H&E image of the same specimen shows epithelioid cells in a myxochondroid matrix. (magnification, 200×). c Immunohistochemical stain for S-100 shows diffuse positivity. d Immunohistochemical test for brachyury shows the characteristic nuclear positivity.
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Fig 1. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) diagram displaying the search and selection process of eligible trials.
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Fig 1. The conventional PET tracer principle and the development of agents that fluorescently convert the Cerenkov radiation optical decay signal.
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Fig 1. Design of gp120 V1V2 domain broadly neutralizing epitope mimics. (A) Crystal structure of a scaffolded V1V2 domain from the CAP45 strain of HIV-1 (red ribbons) in complex with PG9 Fab (gray surface) (PDB ID 3U4E with scaffold hidden). The glycans at N160 and N156 are depicted with colored spheres representing atoms of the mannose (green) and N-acetylglucosamine (blue) residues. Disulfide bonds are shown as yellow sticks. Dashed arrows indicate where the disordered region of the V2 loop would be connected.
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Fig. 1. Sample dosimetric comparison of implant alone to combination therapy. Example of dosimetric comparison of implant alone to combination therapy with EBRT and brachytherapy boost. Blue dashed line: prostate contour; red solid line: 100% isodose line; green solid line: 75% isodose line. Interval spacing between positions of 5 mm. EBRT = external beam radiation therapy.
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Fig 3. Two-dimensional isodose contours for a single high-dose-rate treatment; dose was prescribed to 7 mm, with mucosal surface limited to 9 Gy.
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Fig 1. Concordance of TERT promoter and known thyroid driver genes (BRAF, RAS, RET/PTC) in thyroid cancer tumors and cell lines. Each cell represents one sample. Colored and gray shadings denote mutant and wild-type status, respectively. For TERT mutations, darker shading represents homozygous mutations.
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Fig 2. Sensitivity analyses showing how any future changes in the rate of transplant activity would affect the projected estimates for survivors in the United States by year 2030.
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Fig 5. MK-2206 reduces the megakaryocyte burden in a mouse model of PMF. Cells from bone marrows of MPLW515L recipients treated with captisol (vehicle control), 60 mg/kg MK-2206 or 120 mg/kg MK-2206 for 14 days were collected and stained with fluorescently conjugated antibodies against CD41or Mac1/Gr1. (c) Histological sections of the liver after 14 days of treatment.
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Fig 1. Overall survival (OS) and disease-free survival (DFS) curves according to the level of SNIP1 expression in 83 lung cancer and normal tissues.
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Fig 2. Hypothetical models of progression from in situ to invasive breast cancer. (B) Progression from DCIS to IBC as an evolutionary bottleneck.
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Fig 1. CONSORT diagram.
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Fig 1. Hypotonicity is required for rapid leukocyte recruitment to larval zebrafish tail fin wounds. d) HyPer imaging of wound margin H2O2 production in response to wounding in hypotonic medium (h), isotonic medium (i) or isotonic medium + 100 μM of the NADPH oxidase inhibitor diphenyliodonium chloride (i/DPI).
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Fig 4. Effect of TLR2 activation in in vitro-cultured primary normal BM CD34+ cells. (a) Flow cytometry analysis of normal CD34+ cells after being treated with MALP2 or PAM3CSK4 for 48 h. Compared with control, treatment resulted in a decreased percentage of early erythroid progenitor cells marked with CD71+ and HLA-DR.
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![Fig 1. Overview of normal hematopoiesis and leukemogenesis. At disease inception, an unknown number of leukemic stem cells (LSCs) may cycle between proliferative and quiescent states. Some proliferating LSCs differentiate into EPCs that retain proliferative capacity but lack long-term self-renewal capacity. After a number of cell-division cycles, the EPCs become late progenitor cells, which eventually mature into leukemic cells that enter circulation [54] and [57].](https://library.mskcc.org/sparks/sparksimgs/2216/LeukRes_Mauro2.jpg)
