Additional file 10: Figure S8. of A transcriptome-based protein network that identifies new therapeutic targets in colorectal cancer

Gene-Drug interaction network. Interactions were retrieved in STITCH v5 (Search Tools for Interactions of Chemicals) between deregulated genes in CRC and 4 drugs: 3 chemotherapeutic drugs used in CRC treatment (5-Fluorouracile (5-FU), Oxaliplatin (OXA) and Camptothecin (CPT), and Lovastatin (LOVA). To facilitate network visualization, we have hidden edges between genes. Node size and node color reflect the interaction degree and the clustering coefficient characterizing nodes in 111 genes based-network presented in Additional file 8. The thickness of edges was correlated with score confidence (large for high score) retrieved in STITCH database (version 5) and the blue color of edges indicated a physical interaction in the source database. The bold line of shape node characterizes genes deregulated in more than 75% of CRC. (PDF 93 kb

El Diario de Pontevedra : periódico liberal: Ano XXVIII Número 8256 - 1911 novembro 18

Histomorphometric characterization of the effects of in utero alcohol exposure on human placentae from WG20 to WG25. (a, b) Immunohistochemistry performed against CD31 and toluidine blue counterstaining visualizing microvessels (brown) present in placental villi (blue) from control and alcohol-exposed groups collected at gestational ages ranging from [20–25 WG]. (c) Percentage of villi classified by sizes in placentae from control and alcohol-exposed groups collected at gestational ages ranging from [20–25 WG].*p < 0.05 vs the control group using the unpaired t test (d) Repartition of vessels per size of villi in placentae from control and alcohol-exposed groups collected at gestational ages ranging from [20–25 WG]. (e) Luminal vascular area per size of villi in placentae from control and alcohol-exposed groups collected at gestational ages ranging from [20–25 WG]. (TIFF 19794 kb

El Diario de Pontevedra : periódico liberal: Ano XXIV Número 6898 - 1907 abril 17

Main clinical and morphological characteristics of human placentae from the alcohol-exposed group. (DOC 131 kb

DataSheet_1_Deciphering the maturation of tertiary lymphoid structures in cancer and inflammatory diseases of the digestive tract using imaging mass cytometry.pdf

Persistent inflammation can promote the development of tertiary lymphoid structures (TLS) within tissues resembling secondary lymphoid organs (SLO) such as lymph nodes (LN). The composition of TLS across different organs and diseases could be of pathophysiological and medical interest. In this work, we compared TLS to SLO in cancers of the digestive tract and in inflammatory bowel diseases. Colorectal and gastric tissues with different inflammatory diseases and cancers from the department of pathology of CHU Brest were analyzed based on 39 markers using imaging mass cytometry (IMC). Unsupervised and supervised clustering analyses of IMC images were used to compare SLO and TLS. Unsupervised analyses tended to group TLS per patient but not per disease. Supervised analyses of IMC images revealed that LN had a more organized structure than TLS and non-encapsulated SLO Peyer’s patches. TLS followed a maturation spectrum with close correlations between germinal center (GC) markers’ evolution. The correlations between organizational and functional markers made relevant the previously proposed TLS division into three stages: lymphoid-aggregates (LA) (CD20+CD21-CD23-) had neither organization nor GC functionality, non-GC TLS (CD20+CD21+CD23-) were organized but lacked GC’s functionality and GC-like TLS (CD20+CD21+CD23+) had GC’s organization and functionality. This architectural and functional maturation grading of TLS pointed to differences across diseases. TLS architectural and functional maturation grading is accessible with few markers allowing future diagnostic, prognostic, and predictive studies on the value of TLS grading, quantification and location within pathological tissues in cancers and inflammatory diseases.</p

Additional file 5: Table S5. of PLGF, a placental marker of fetal brain defects after in utero alcohol exposure

Main clinical and morphological characteristics of human placentae from the alcohol-exposed group. (DOC 131 kb

Additional file 7: Table S7. of PLGF, a placental marker of fetal brain defects after in utero alcohol exposure

Statistical analysis. (DOCX 23 kb

Flowchart of the study.

<p>Muscle biopsies were analysed using standard techniques including histoenzymology with Periodic acid-Schiff (PAS) and MAD staining (Fishbein’s method [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0132972#pone.0132972.ref035" target="_blank">35</a>]).</p

Histochemical MAD staining using <i>p</i>-nitro blue tetrazolium.

<p>(A) Relative <i>p</i>-NBT staining intensity was expressed as a percentage of the mean optical density in control muscle biopsies (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0132972#sec006" target="_blank">Methods</a>). Horizontal bars represent the mean value of each group. *: Decreased vs. Normal MAD staining, †: Absent vs. Normal MAD staining, ‡: Absent vs. Decreased MAD staining (<i>P</i> < 0.05, Games-Howell <i>post-hoc</i> test). Representative serial cross sections of lateral vastus biopsies: (B) Normal, (C) Decreased, and (D) Absent MAD staining (original magnification: × 100).</p

Proposed algorithm for the diagnosis of glycogenoses, MAD deficiencies, and mitochondrial myopathies.

<p>The ROC curve to discriminate between the presence and absence of mitochondrial myopathy was determined according to the parametric methodology [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0132972#pone.0132972.ref022" target="_blank">22</a>]. (A) For this purpose, we used the values (mean ± SD) published by Dandurand <i>et al</i>. in eight patients with mitochondrial myopathies [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0132972#pone.0132972.ref051" target="_blank">51</a>]. The values in the disease control group from [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0132972#pone.0132972.ref051" target="_blank">51</a>] are in line with those from the group with no metabolic myopathy (n = 37) in the present study. (B) The cut-off corresponds to the highest value for the Youden index (Se = 72.5%, Sp = 73.5%). MAD: Myoadenylate deaminase.</p

Effects of incremental exercise on plasma metabolite levels according to muscle MAD activity.

<p>Patients performed an incremental exercise testing (<i>inset</i>). Blood was sampled before (Rest), during exercise (50% of Predicted Maximal Power and Peak exercise), and after exercise (2, 5, 10 and 15 min recovery). Filled symbols correspond to glycogenoses, open symbols correspond to the absence of glycogenoses. (A) Ammonia. (B) Ammonia/rest. (C) Lactate. (D) Lactate/rest. (E) Lactate/Pyruvate ratio. Data are represented as means ± standard error of mean (error bars not included for ammonia values in the subgroup with glycogenose and normal MAD in panel A).*: Absent vs. Normal MAD staining, †: Decreased vs. Normal MAD staining (<i>P</i> < 0.05, Games-Howell <i>post-hoc</i> test).</p