Additional file 1: of Relationship between asymptomatic rotavirus infection and jaundice in neonates: a retrospective study

The datasets of this study. Brief description of the data: The datasets supporting the conclusion of this study. (XLSX 157 kb

Additional file 1: of Comparison of sodium ion levels between an arterial blood gas analyzer and an autoanalyzer in preterm infants admitted to the neonatal intensive care unit: a retrospective study

The datasets supporting the conclusion of this study. (XLSX 820 kb

Synthesis and Reactivity of Nickel(II) Hydroxycarbonyl Species, NiCOOH‑κ<i>C</i>

Reactions of nickel complexes supported by an anionic PNP pincer ligand (PNP^– = N­[2-P^<i>i</i>Pr₂-4-Me-C₆H₃]₂) toward CO₂ and CO are investigated, particularly for interrogating their C–O bond formation/cleavage chemistry. The formation of a nickel formate species (<b>2</b>) was accomplished by the reaction of (PNP)­NiH with CO₂, while the structural isomer complex (PNP)­NiCOOH-κ<i>C</i> (<b>4</b>) was successfully produced from the corresponding nickel hydroxyl compound by exposing it to CO­(g). Its structurally unique character was gleaned by obtaining two solid-state structures for (PNP)­NiCOOH-κ<i>C</i> (<b>4</b>) and {(PNP)­Ni}₂-μ-CO₂-κ²<i>C</i>,<i>O</i> (<b>6</b>); the latter was obtained from the reaction of <b>4</b> with a nickel hydroxyl complex. Both species possess a NiCOO-κ<i>C</i> binding mode, which is reminiscent of the binding mode found at the carbon monoxide dehydrogenase (CODH) active site with its Ni–COO–Fe fragment. The cationic species {(PNP)­NiCO}⁺ (<b>7</b>) was also prepared via the protonation of <b>4</b>, which then led to the investigation of the C–O bond formation in <b>7</b> by adding a nucleophile such as OH^–

Synthesis and Reactivity of Nickel(II) Hydroxycarbonyl Species, NiCOOH‑κ<i>C</i>

Reactions of nickel complexes supported by an anionic PNP pincer ligand (PNP– = N­[2-PiPr2-4-Me-C6H3]2) toward CO2 and CO are investigated, particularly for interrogating their C–O bond formation/cleavage chemistry. The formation of a nickel formate species (2) was accomplished by the reaction of (PNP)­NiH with CO2, while the structural isomer complex (PNP)­NiCOOH-κC (4) was successfully produced from the corresponding nickel hydroxyl compound by exposing it to CO­(g). Its structurally unique character was gleaned by obtaining two solid-state structures for (PNP)­NiCOOH-κC (4) and {(PNP)­Ni}2-μ-CO2-κ2C,O (6); the latter was obtained from the reaction of 4 with a nickel hydroxyl complex. Both species possess a NiCOO-κC binding mode, which is reminiscent of the binding mode found at the carbon monoxide dehydrogenase (CODH) active site with its Ni–COO–Fe fragment. The cationic species {(PNP)­NiCO}+ (7) was also prepared via the protonation of 4, which then led to the investigation of the C–O bond formation in 7 by adding a nucleophile such as OH–

BMP-2 Promotes Oral Squamous Carcinoma Cell Invasion by Inducing CCL5 Release

<div><p>Bone morphogenetic protein-2 (BMP-2)-containing bone grafts are useful regenerative materials for oral and maxillofacial surgery; however, several <i>in</i><i>vitro</i> and <i>in</i><i>vivo</i> studies previously reported cancer progression-related adverse effects caused by BMP-2. In this study, by quantifying the rhBMP-2 content released from bone grafts, the rhBMP-2 concentration that did not show cytotoxicity in each cell line was determined and applied to the <i>in</i><i>vitro</i> monoculture or coculture model in the invasion assay. Our results showed that 1 ng/ml rhBMP-2, while not affecting cancer cell viability, significantly increased the invasion ability of the cancer cells cocultured with fibroblasts. Cocultured medium with rhBMP-2 also contained increased levels of matrix metalloproteinases. rhBMP-2-treated cocultured fibroblasts did not show a prominent difference in mRNA expression profile. Some cytokines, however, were detected in the conditioned medium by a human cytokine antibody array. Among them, the cancer invasion-related factor CCL5 was quantified by ELISA. Interestingly, CCL5 neutralizing antibodies significantly reduced the invasion of oral cancer cells. In conclusion, our results suggest that 1 ng/ml rhBMP-2 may induce invasion of oral squamous cell carcinoma (OSCC) cells by CCL5 release in coculture models. Therefore, we propose that a careful clinical examination before the use of rhBMP-2-containing biomaterials is indispensable for using rhBMP-2 treatment to prevent cancer progression.</p></div

Cytoskeletal alteration in fibroblasts adjacent to OSCC cells.

(A)Cell size was measured on hTERT-hNOFs mono-cultured and co-cultured with HEK and OSCC cells for 3 days. ZEN 2012 software program was used (mono cultured, n = 30; with HEK, n = 23; with YD10B, n = 21; with YD38, n = 20; CAF#1, n = 22; CAF#1(with YD10B), n = 22; CAF#2, n = 16; CAF#2(with YD10B), n = 21) (*p p p t test). CAFs were used to compare cellular size in fibroblasts, respectively. Average of cellular size is shown as CAF#1, 5.74 x 109 nm2; CAF#1 (with YD10B), 1.03 x 1010 nm2; CAF#2, 7.12 x 109 nm2and CAF#2 (with YD10B), 8.22 x 109 nm2 (*p p p < 0.001; Mann Whitney U test). (B) All immunofluorescence microscopy experiments were performed on cultured cell after 3 days. DAPI(blue), Phalloidin(red) and Merged staining are shown in mono-cultured hTERT-hNOF(first panels) and hTERT-hNOF co cultured with HEK (second panels), YD10B OSCC cells (third panels) and YD38 OSCC cells (fourth panels), Scale bar, 50μm. The rectangular boxes are shown as enlarged sections to observe the F-actin assembly in left lower part.</p

MOESM1 of Molecular generative model based on conditional variational autoencoder for de novo molecular design

Supplementary material 1 (docx 791 KB

YAPS127A fibroblasts rearrange ECM structures and promote motility and invasiveness of OSCC cells.

(A) Fluorescence microscope was used to check the expression of EGFP on cultured cell after transfection with pcDNA4-HisMaxB-YAP1 and YAPS127A, Scale bar, 200μm. (B) The YAP, p-YAP(S127) and αSMA protein expression was identified in all transfected cells (empty-, WT-YAP-, YAPS127A transfected hTERT-hNOFs) by Western blot. (C) Immunofluorescence images were shown in WT-YAP1- and YAPS127A-hTERT-hNOFs. Merged stained Images (DAPI(blue), F-actin(Phalloidin)(red), YAP(green))are shown. Scale bar, 50μm. The bar graph indicates the distribution of YAP in WT-YAP1- and YAPS127A-hTERT-hNOFs. It was analyzed by Image J software program (WT-YAP1-hTERT-hNOFs, n = 40; YAPS127A-hTERT-hNOFs, n = 40) (***p t test). (D) The representative images show gel contractility by the fibroblasts. Histogram shows mean value ± SD (n = number of gels (Empty, 3; WT-YAP, 3; YAPS127A, 3), assessed over multiple experiments (*p p < 0.05; Mann-Whitney U test).</p

RhoA modulates cytoskeletal alteration in fibroblasts adjacent to OSCC cells.

(A) hTERT-hNOFs were grown with YD10B OSCC cells for 24 h and then Rho GTPase family gene expression was identified by RT-PCR. (B) Quantification of Rho GTPase mRNA expression was shown. Each gene was normalized with ratio of GAPDH expression. The experiments were performed in three-independent (*p p p p p < 0.001; Mann-Whitney U test).</p