dedup-isc-ft-v107-score
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0.443027 |
2bae58652e564b218e2bd6f9f33586db
|
Best percentage change over time (from baseline) in tumor burden in various organ systems.
|
PMC9149819
|
tomography-08-00110-g001.jpg
|
0.435966 |
46fb89ed8aec4997b42c2eaffa900b8d
|
Organ-specific response in the liver, lung, brain lymph node, soft tissue, adrenals, and peritoneal metastases.
|
PMC9149819
|
tomography-08-00110-g002.jpg
|
0.454013 |
dd84f402bdc34e57af3b9ca6c5af7ed6
|
Waterfall plot of tumor burden change at the best overall response in all lesions.
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PMC9149819
|
tomography-08-00110-g003.jpg
|
0.423391 |
01ec415733cf4d1aa6615ced65461b74
|
Spider plot of tumor burden changes during nivolumab therapy using irRECIST. Longitudinal changes of tumor burden during therapy are shown about baseline, showing baseline tumor burden as 0.
|
PMC9149819
|
tomography-08-00110-g004.jpg
|
0.454476 |
fce6d4add89140e78aacb3e9ba0beed5
|
Lesion-based tumor size change at the best response of 76 target lesions classified by the organs. The black horizontal line shows a median value for the lesion-based shrinkage in each organ. The gray vertical line with horizontal bars at the upper and lower ends represents the first and third quartiles.
|
PMC9149819
|
tomography-08-00110-g005.jpg
|
0.435053 |
03fbcaf30da94d7e87bfdf1ab0bfd5af
|
Proportion of intract vs. torn rotator cuff repairs between the osteoarthritic group (n=1552) and control group (n=603) at 6-months post-operative follow-up (p=.016).
|
PMC9150254
|
10.1177_2325967121S00542-fig1.jpg
|
0.556585 |
f14122a4773c41fabb063d017708264e
|
Cumulative incidence of cancer by birth cohort. (a) Birth cohort 1930–1949. (b) Birth cohort 1950–1969. (c) Birth cohorts 1970–1989 and 1990-2017.CHD = congenital heart disease.
|
PMC9156800
|
gr1.jpg
|
0.476567 |
1f366e8c5b154c03ade7b4fc56503905
|
Photographs of SPI cutlery for mechanical testing (A) and dimensional measurements (B) after compressing molding.
|
PMC9156887
|
gr1.jpg
|
0.554564 |
f3eb0d165b46468391ec45507fde650d
|
Digital photographs of SPI cutlery supplemented with different levels of morning glory stem fiber (MGSF), (A) SPI-CON, (B) SPI-MGSF-5, (C) SPI-MGSF-10, (D) SPI-MGSF-20. SPI-CON (SPI without MGSF), SPI-MGSF-5, SPI-MGSF-10 and SPI-MGSF-20 samples presented SPI without and with the addition of MGSF at different levels of 5, 10, and 20%, respectively.
|
PMC9156887
|
gr2.jpg
|
0.408347 |
30e4802176c64af3a049bf081e241082
|
Water absorption, degree of swelling and water solubility (A); Compression load (B) Flexural modulus (C); and Impact strength (D) of SPI cutlery (SPI–CON (SPI without MGSF), SPI-MGSF-5, SPI-MGSF-10 and SPI-MGSF-20 samples) and PLA spoon. Different lowercase letters on the bars indicated significant differences (p˂0.05).
|
PMC9156887
|
gr3.jpg
|
0.441203 |
985334aa3f7b4ca9831ababaf5c0587f
|
Scanning electron micrographs of SPI-CON (SPI without MGSF), SPI-MGSF-5, SPI-MGSF-10 and SPI-MGSF-20 samples visualized at different magnifications (250×, 1000× and 5000×).
|
PMC9156887
|
gr4.jpg
|
0.394618 |
b26154b17f1c47c78092c1c7f6a9d692
|
The expression of ARRDC2 (mRNA, gene microarray and gene sequencing) in OVs. (A) Expression of ARRDC2 in pan-cancer. (B) Box plot based on the expression level of ARRDC2 in the GSE29450 (OV = 10, Normal = 10). (C) Box plot based on the expression level of ARRDC2 in the GSE10971 (OV = 13, Normal = 24). (D) The expression level of ARRDC2 in OV based on individual FIGO stage. (E) The expression level of ARRDC2 in OV based on the race of patient.
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PMC9157644
|
fgene-13-815082-g001.jpg
|
0.457735 |
984663324ba94a2ba9e92952a84df398
|
The correlation between ARRDC2 and the poor prognosis of patients with OV. (A) The Kaplan-Meier survival curve revealed that the high expression of ARRDC2 lead to a poor prognosis in OVs (GSE19829, N = 28, p = 0.0083). (B) The Kaplan-Meier survival curve revealed that the high expression of ARRDC2 lead to a poor prognosis in OVs (TCGA, N = 372, p = 0.02). (C) Forest plot of high ARRDC2 expression with poor OS in OV patients based on survival meta-analysis of two datasets (GSE19829 and TCGA RNA-Seq, p = 0.02). (D,E) Analysis of univariate and multivariate factors affecting the prognosis of patients with OV. (D) Univariate cox analysis. (E) Multivariate cox analysis.
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PMC9157644
|
fgene-13-815082-g002.jpg
|
0.412047 |
2aecaed07f1a4ffa9e633825898de2b6
|
Go (Gene ontology) functional annotation and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis of ARRDC2 in OV. (A) Go functional annotation. Biological Process, BP (neutrophil degranulation, neutrophil mediated immunity, etc.). Cellular Component, CC (ribosomal subunit, mitochondrial protein complex, ribosome, large ribosomal subunit, etc.). Molecular Function, MF (structural constituent of ribosome, cadherin binding, transcription cofactor binding, etc.). (B) KEGG pathway enrichment analysis (B cell receptor signaling pathway, T cell signaling pathway, Human T-cell leukemia virus 1 infection signaling pathway, NOD-Like receptor signaling pathway, Th17 cell differentiation, etc.). GSEA enrichment analysis results of ARRDC2 (B cell receptor signaling pathway and T cell signaling pathway).
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PMC9157644
|
fgene-13-815082-g003.jpg
|
0.458109 |
f2e20418dce54616be1be9125e164c4e
|
The relationship between the expression of ARRDC2 and proportion of immune infiltrates in TIMER database. (A,B) Infiltration of various immune cells. (A)Macrophage, Neutrophil, Dendritic Cell. (B) B Cell, CD8+ T Cell, CD4+ T Cell. (C) Association between ARRDC2 gene copy number and immune cell infiltration levels in OV cohorts (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001). (D) In TIMER database, the relationship between Immune checkpoint (CTLA4, PDCD1, CD274, PDCD1LG2) and ARRDC2 gene expression was analyzed by Spearman correlation analysis (p < 0.05). Correlation coefficients (rho values) and p values were shown.
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PMC9157644
|
fgene-13-815082-g004.jpg
|
0.415149 |
e89fad403bbc4ea08278c96027399200
|
The relationship between the expression of ARRDC2 and immune checkpoints, MHC and chemokines in the TISIDB database. (A) The relationship between immune checkpoint (CD274, HAVCR2, IDO1, PDCD1, PDCD1LG2, TGFB1) and ARRDC2 gene expression. (B) The relationship between MHC (B2M, HLA-DMA, HLA-DPA1, HLA-DRA, HLA-DRB1, HLA-E) and ARRDC2 gene expression. (C) The relationship between Chemokines (CCL17, CCL13, CCL5, CCL3, CCL4, CX3CL1) and ARRDC2 gene expression. Spearman correlation analysis was applied (p < 0.05).
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PMC9157644
|
fgene-13-815082-g005.jpg
|
0.457181 |
8c6782140f1b40fcbe267a0fda2c57ab
|
Relationship between overall survival and immune cell infiltration and ARRDC2 gene expression in OV patients. (A) B Cell infiltration. (B) Basophils infiltration. (C) CD4+ T Cell infiltration. (D) CD8+ T Cell infiltration. (E) Eosinophils infiltration Neutrophil. (F) Macrophage infiltration. (G) Mesenchymal stem cell infiltration. (H) Natural killer T-cell infiltration. (I) Th1cell infiltration.
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PMC9157644
|
fgene-13-815082-g006.jpg
|
0.437617 |
fd548a8978b4405d894c58384a89a909
|
Co-expression analysis of ARRDC2. (A) The ten most significant genes of positive and negative correlating with ARRDC2. (B) The Correlation coefficients and p values of the ten most significant genes of positive and negative correlating with ARRDC2. (C,D) Screening of gene therapy drugs for ARRDC2 based on the CMap and Pubchem database (Drug name, chemical structure, 2D structure and 3D structure). (C) Mercaptopurine. (D) Apigenin.
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PMC9157644
|
fgene-13-815082-g007.jpg
|
0.559368 |
ad38fd88dbb34daa8fe0140435537446
|
Differential expression and the knockdown efficiency of ARRDC2 at the cellular level. (A) RT-qPCR experimental results showed that the expression of ARRDC2 in ovarian cancer cells is higher than that in normal ovarian cells. (B) Western blot experimental results showed that the expression of ARRDC2 in ovarian cancer cells is higher than that in normal ovarian cells. The differences in ARRDC2 gene expression levels in OC were compared at the cell levels by Wilcoxon rank sum test. (C) RT-qPCR after cell transfection. (D) Western blot image and corresponding statistics after cell transfection (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).
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PMC9157644
|
fgene-13-815082-g008.jpg
|
0.385688 |
619d47582c9a49389a72d43187c9a74f
|
Effects of ARRDC2 gene knockdown on malignant biological behavior of OC cells. (A) CCK8 experiment results of A2780 and SKOV3 cell lines after cell transfection. The OD values measured at 450 nm wavelength at 0, 12, 24, and 48 h were displayed, which represented the cell proliferation rate. (B) Ki-67 immunofluorescence staining of A2780 and SKOV3 cell lines after cell transfection. (C) Wound-healing assay results and statistics of OC cells after cell transfection. The wound-healing rate was measured at 0 and 24 h. (D) Transwell assay results and statistics of OC cells after cell transfection. The number of migrating cells was measured at 24 h, which represented the ability to migrate. (E) The results and statistics of cell clone formation assay of A2780 and SKOV3 cell lines after cell transfection (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).
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PMC9157644
|
fgene-13-815082-g009.jpg
|
0.452235 |
0e6f816d7e3242f694de23a4d860ea22
|
Precede-proceed model for diabetic retinopathy screening [7].
|
PMC9159028
|
41433_2022_2003_Fig1_HTML.jpg
|
0.461577 |
6f9a7135b7144ccf9b27a80f1964d661
|
Soap Opera Comic strip.
|
PMC9159028
|
41433_2022_2003_Fig2_HTML.jpg
|
0.43004 |
441fee00f1fe4671a8bac862fc4972c2
|
Draughts Comic strip.
|
PMC9159028
|
41433_2022_2003_Fig3_HTML.jpg
|
0.462882 |
25858fa43683472796e988adf2e2c78b
|
Analysis of cell viability of immortalized human keratinocytes cultured in different types of media for 24, 48 and 72 h. Cells were cultured in control culture medium (CTR) and media containing increasing concentrations of maslinic acid (MA1, MA5, MA10, MA20, MA40, and MA80, corresponding to 1, 5, 10, 20, 40, and 80 μg/ml of MA, respectively). As negative control (NEG), cells were incubated with 2% triton X-100. (A): average values of cell viability as determined by quantification of DNA released to the medium after normalizing with respect to the CTR values. (B): average values of cell viability as determined by LIVE/DEAD. In (A,B), error bars correspond to standard deviations and asterisks show statistically-significant differences with CTR. (C): fluorescence microscopy images of cells stained with the LIVE/DEAD system. Live cells are labeled in green and dead cells are labeled in red. Scale bars: 200 µm.
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PMC9159156
|
fbioe-10-876734-g001.jpg
|
0.455609 |
e8bebd4dbb0248128383ae171594c742
|
Analysis of cell proliferation of immortalized human keratinocytes cultured for 24, 48 and 72 h as determined by sequential cell number quantification (panel (A)) and WST-1 activity (panel (B)). Results are shown as average percentage values normalized to negative controls (NEG) and positive controls (CTR), which were considered as 0 and 100%, respectively. Error bars correspond to standard deviations. Statistically significant differences with CTR are labeled with asterisks (*).
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PMC9159156
|
fbioe-10-876734-g002.jpg
|
0.427619 |
4f882f1ad5a1484fb312669bdd3e88d1
|
Immunohistochemical analysis of the cell-proliferation marker KI-67 in immortalized human keratinocytes cultured presence or absence of maslinic acid. The cells were cultured in the presence of 5 μg/ml of maslinic acid (MA) or in absence of this compound (Control CTR) for 24, 48 or 72 h. (A): Percentage of cells showing KI-67 positive signal in each study group. Error bars represent standard deviations, and asterisks show statistically-significant differences with CTR for the Mann-Whitney test. (B): Histological image of negative control cells (no primary antibody) showing no expression of KI-67. (C–H): Illustrative images of cells showing positive and negative cells in the different study groups. (C,D,E): CTR; (F,G,H): MA at the concentration of 5 μg/ml; (C,F): 24 h, (D,G): 48 h, (E,H): 72 h. Some cells showing positive expression of KI-67 are labeled with black arrows, and white arrows correspond to negative cells. Scale bars: 100 µm.
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PMC9159156
|
fbioe-10-876734-g003.jpg
|
0.440434 |
84fe4f76bd3245b3b7c8505d06b9a29e
|
Generation of primary cultures of human skin keratinocytes using the explant technique (small tissue fragments were placed in direct contact with the culture surface to allow cells to migrate from the tissue to the culture flask). (A): Phase contrast microscope images of primary keratinocytes migrating from the skin explants (labeled with asterisks) to the culture surface in each culture condition. Scale bars: 100 µm. (B): Illustrative images of skin tissue explants cultured for 21 days in CTR and MA medium at a concentration of 5 μg/ml stained with hematoxylin-eosin. Some skin explants failing to generate any keratinocyte cultures are labeled with black arrows.
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PMC9159156
|
fbioe-10-876734-g004.jpg
|
0.488546 |
c054ca18026e44d1968999d5a007e5b2
|
Patients thrombolysed in various time intervals—pre-intervention versus post-intervention group
|
PMC9160610
|
ijccm-26-549-g001.jpg
|
0.37482 |
036912a9221a4490900cb09fe6d9ba61
|
Schematic presentation of the HCN1 channel with 6 transmembrane domains (S1–S6), the locations of the pathogenic variants related to epilepsy and the altered protein functions. Most of mutations are located in S6, the intracellular linker between S6 and CNBD as well as in N-terminal. Notably, variants related to both epilepsy and SUDEP (p.G391D, p.G46V, and 187-195del) are located both in the N- and C-terminals and there is a hotspot in residue G391. Variants in blue correspond to gain-of-function (GOF) effects, variants in red correspond to loss-of-function (LOF) effects, and variants in black stand for the variants with unknown or clear effects.
|
PMC9161305
|
fnmol-15-807202-g0001.jpg
|
0.439158 |
ccdb3c293874499986c76cf3f4e88cfc
|
Schematic presentation of the HCN2 channel with 6 transmembrane domains (S1–S6), the locations of the pathogenic variants related to epilepsy, and the altered protein functions. Most of the mutations are located in the intracellular linker before and after the CNBD region. Notably, variants related to both epilepsy and SUDEP are located in C-terminal (p.F738C and p.P802S). Variants in blue correspond to gain-of-function (GOF) effects, variants in red correspond to loss-of- function (LOF) effects, and variants in black stand for the variants with unknown or clear effects.
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PMC9161305
|
fnmol-15-807202-g0002.jpg
|
0.402418 |
14f75bd695134c5cb8f21f55b1226118
|
Schematic presentation of the HCN3 channel with 6 transmembrane domains (S1–S6) and the locations of the pathogenic variants related to epilepsy. Variants in black have unknown functional effects and both of them are related to both epilepsy and SUDEP.
|
PMC9161305
|
fnmol-15-807202-g0003.jpg
|
0.462032 |
77a4fd8c384b4165a4a2281b9bd889ca
|
Schematic presentation of the HCN4 channel with 6 transmembrane domains (S1–S6), the locations of the pathogenic variants related to epilepsy, and the altered protein functions. Most of the mutations are located in C-terminal, including those related to both epilepsy and SUDEP (p.G36E, p.V759I, p.G973R, and p.R1044W). Variants in blue correspond to gain-of-function (GOF) effects, variants in red correspond to loss-of-function (LOF) effects, and variants in black stand for the variants with unknown or clear effects.
|
PMC9161305
|
fnmol-15-807202-g0004.jpg
|
0.463301 |
1b1d332d9a15478d9c26c1f09d1f5dbb
|
Clinical phenotypes related to HCN1 variants. Most cases presented with febrile seizures (FS), or febrile seizure plus (FS+) or genetic generalized epilepsy with febrile seizure plus (GEFS+) followed by genetic or idiopathic generalized epilepsy (GGE), early infantile epileptic encephalopathy (EIEE), febrile EIEE, and few had unclassed epileptic syndromes (including those who died due to SUDEP and those reported to have unclassified epilepsy infantile).
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PMC9161305
|
fnmol-15-807202-g0005.jpg
|
0.402255 |
ce08b59e70a34fe890636f603452033e
|
Schematic representation of HCN1 variants related to different clinical epileptic phenotypes. Some of the variants are related to different epileptic syndromes: p.M234R is associated with both typical and atypical febrile seizures, p.C329S and p.V414M are each related to both febrile seizures and genetic or idiopathic generalized epilepsy, p.M153I and p.M305L are each related to both EIEE and unclassified epilepsy which occurs in infants. Atypical febrile seizures group includes cases with febrile seizure plus and genetic generalized epilepsy with febrile seizure plus. FS stands for febrile seizures and EIEE for early infantile epileptic encephalopathy.
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PMC9161305
|
fnmol-15-807202-g0006.jpg
|
0.425773 |
8c0530afb4ed46488329d0527e6f4705
|
Clinical phenotypes related to HCN2 variants. Most cases were diagnosed with either febrile seizures (FS), or febrile seizure plus (FS+) or genetic generalized epilepsy with febrile seizure plus (GEFS+) or genetic or idiopathic generalized epilepsy. Cases with unclassed epileptic syndromes include two cases who died due to SUDEP.
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PMC9161305
|
fnmol-15-807202-g0007.jpg
|
0.444717 |
ba6d4149d938468a8de71cc5dcc99236
|
Schematic representation of HCN2 variants related to different clinical epileptic phenotypes. The p.S632W and delPPP (p. 719–721) are individually related to both febrile seizures and genetic or idiopathic generalized epilepsy. FS stands for febrile seizures and EIEE for early infantile epileptic encephalopathy.
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PMC9161305
|
fnmol-15-807202-g0008.jpg
|
0.452073 |
2a6ac310619548f08c0a8374056285a5
|
Clinical phenotypes related to HCN3 variants. All reported cases had unclassified or unknown epileptic syndromes. These are the two cases who died due to SUDEP.
|
PMC9161305
|
fnmol-15-807202-g0009.jpg
|
0.411187 |
6e6b4dd6cae14f898c38b7307a39d692
|
Schematic representation of HCN3 variants which relate to unclassified or unknown epileptic syndromes.
|
PMC9161305
|
fnmol-15-807202-g0010.jpg
|
0.435669 |
8e36ca2db4fb4b28adac884566f273d3
|
Clinical phenotypes related to HCN4 variants. Most of the cases were diagnosed with genetic or idiopathic generalized epilepsy (GGE) followed by those with unclassified or unknown epileptic syndrome (majority are those who died due to SUDEP).
|
PMC9161305
|
fnmol-15-807202-g0011.jpg
|
0.446315 |
306e8380736e4db3b84b79548a8abf43
|
Schematic representation of HCN4 variants related to different clinical epileptic phenotypes.
|
PMC9161305
|
fnmol-15-807202-g0012.jpg
|
0.449133 |
690677f639344504898f1e76d7409675
|
Two-step mechanism of NLRP3 activation. (A) TLR/IL1-R engagement leads to NF-κB activation driving transcriptional upregulation of inflammasome components (Signal 1). NLRP3 is then activated upon sensing unknown direct agonists (Signal 2), which can be (B) infectious, (C) sterile and can also be mediated through (D) exosomes.
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PMC9161712
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fimmu-13-896353-g001.jpg
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0.394143 |
c122753525cc47b8ac75b1b5aafb4fcf
|
Answers provided in the Nordic Musculoskeletal Questionnaire (NMQ).
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PMC9162288
|
rbmt-19-04-0465-g01.jpg
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0.549972 |
2cd021eba806482e9fa1753fa6779900
|
Structure of the severe acute respiratory syndrome-2 (SARS-CoV-2). There are four main structural proteins: spike (S) glycoproteins, membrane (M) proteins, envelope E proteins, and single-stranded ribonucleic acid (RNA) found inside the nucleocapsid (N) protein
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PMC9163295
|
11356_2022_20984_Fig1_HTML.jpg
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0.461439 |
a6cf562f137f41d9a59419b7490fa8ab
|
Brief pathogenesis of SARS-CoV-2 infection
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PMC9163295
|
11356_2022_20984_Fig2_HTML.jpg
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0.489843 |
9cc9e486a03643a899e69077546fd2f0
|
SARS-CoV-2 mechanism leading to cytokine storm
|
PMC9163295
|
11356_2022_20984_Fig3_HTML.jpg
|
0.444843 |
3bbb89f4553f4894aabad0e9cc4bb1f1
|
Mechanism of action of IL-6 inhibitors
|
PMC9163295
|
11356_2022_20984_Fig4_HTML.jpg
|
0.416848 |
ea974c4bb4b244d0b54adcf2d99facda
|
Microstructure and mechanical property of pure Zn and Zn alloys. (a) Microstructures, (b) XRD patterns, and (c–f) mechanical properties of the as-extruded Zn alloys. (c) Ultimate tensile strength (UTS), (d) yield strength (YS), (e) elongation rate to failure (ER), (f) fracture morphology after tensile test.
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PMC9166432
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gr1.jpg
|
0.378906 |
0b8522d45b7f483186508b8635820fd1
|
CD68 and CD206 staining of Zn and its alloys after 3 months of aortic implantation in rats. (a) Wires in lumens. (b) Wires outside of lumens. Quantification of CD68 positive (c) and CD206 positive (d) areas of wires in lumens. Quantification of CD68 positive (e) and CD206 positive (f) areas of wires outside of lumens. * indicates p < 0.05, ** indicates p < 0.01, compared between two groups. L indicates lumens. Blue colors indicate nucleus and red colors indicate positive staining.
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PMC9166432
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gr10.jpg
|
0.480878 |
3c131e01ba2a4330bb4b9644e176a968
|
αSMA and eNOS staining Zn and its alloys after 3 months of aortic implantation in rats. (a) Wires in lumens. (b) Wires outside of lumens. Quantification of αSMA positive (c) and eNOS positive (d) areas of wires in lumens. * indicates p < 0.05, ** indicates p < 0.01, compared between two groups. Arrow heads indicate endothelium. L indicates lumens. Blue colors indicate nucleus and green colors indicate positive staining.
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PMC9166432
|
gr11.jpg
|
0.490922 |
5d12e10441d44e4796f6f34212ec552a
|
In vivo degradation and bone formation of pure Zn and its alloys when implantation with femur tissue for 3 months. (a) Micro CT scanning, (b) degradation profiles, (c) cross-sectional SEM imaging and EDS mapping, (d) new bone area, (e) bone-implant contact ratio (BIC), and (f) osteoid layer thickness surrounding the implants. I: implants, DP: degradation products, OS: osteoid layer, NB: newborn bone, Zn: zinc, C: carbon, O: oxide, Ca: calcium, P: phosphate.
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PMC9166432
|
gr12.jpg
|
0.39911 |
c9a7e59e6a354c40bb3d7a32858899e8
|
Masson-Goldner and Elastica van Gieson staining of femur tissue with pure Zn and its alloys implantation for 3 months. I: implants, DP: degradation products, OS: osteoid layer, NB: newborn bone.
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PMC9166432
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gr13.jpg
|
0.442957 |
2b87cc7bd52b49c19cf06f499cabaa8d
|
Degradation behavior of Zn and its alloys in Hank's solution for 1 month and 3 months. (a) Surface morphology, (b) XRD patterns, (c) corrosion rates (CRw), (d) pH change.
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PMC9166432
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gr2.jpg
|
0.405964 |
28971bc1a9fa4532ba33c93bfe1f96a1
|
In vitro biocompatibility of different Zn samples. (a) MTT assay for cell viability of endothelial cell. (b) Zn ion concentration in the corresponding exacts. (c) Endothelial cell adhesion morphology when cultured on Zn samples for 3 days. (d) Platelet adhesion morphology when cultured on Zn samples for 24 h, (e) the corresponding number of adhered platelets, and (f) hemolysis percentage. ****p < 0.0001, compared between groups.
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PMC9166432
|
gr3.jpg
|
0.406783 |
26101bb48cde45d0a227db36c36b39ea
|
Antibacterial performance of different Zn surfaces after culture with E. coli and S. aureus for 24 h. (a) SEM images of bacterial adhesion. Antibacterial rates and corresponding Zn ion concentrations in the culture medium after culture with (b) E. coli and (c) S. aureus. ****p < 0.0001, compared between groups.
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PMC9166432
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gr4.jpg
|
0.401051 |
3bdb8138c0354a08a4b233363b574df2
|
Subcutaneous implantation of Zn and its alloys in rats after 3 months. (a) CT scanning, (b) in vivo degradation profiles, (c) macroscopic views, and (d) SEM images. ** indicates p < 0.01, compared between two groups.
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PMC9166432
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gr5.jpg
|
0.435984 |
f9e69a58e570482e867350ad3a49a63b
|
Staining of Zn and its alloys after 3 months of subcutaneous implantation in rats. H&E, Masson's trichrome, Verhoeff's elastin, and immunofluorescence staining (CD11b and CD68). Blue colors indicate nucleus and red colors indicate positive immunofluorescence staining.
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PMC9166432
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gr6.jpg
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0.393251 |
26663a23c7d94023a354aef9f65a93c7
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Abdominal aortas implantation of Zn and its alloys in rats for 3 months. (a) Ultrasound images. Upper: B mode; middle: Doppler mode; Lower: PW mode. Arrow heads indicate the implanted wires within the lumens of the abdominal aortas. (b) Rate of blood flow and (c) degradation rate. * indicates p < 0.05, compared between two groups. (d) Macroscopic views of Zn and its alloys in the abdominal aortas upon implantation and 3 months after implantation. Arrows indicate two ends of the implanted Zn and its alloys outside of vessels.
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PMC9166432
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gr7.jpg
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0.496457 |
ce54431ffdac4999b5835c130c72dd3c
|
H&E staining of Zn and its alloys after 3 months of aortic implantation in rats. (a) Wires in lumens. (b) Wires outside of lumens. (c) Quantification of neointimal areas of wires in lumens. (d) Quantification of inflammation layers of wires outside of lumens. Arrow heads indicate necrotic tissues. * indicates p < 0.05, ** indicates p < 0.01, compared between two groups.
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PMC9166432
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gr8.jpg
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0.453156 |
80953f4008da466e843ecda3b6559bf2
|
Masson's trichrome and Verhoeff's elastin staining of Zn and its alloys after 3 months of aortic implantation in rats. (a) Wires in lumens. (b) Wires outside of lumens. Quantification of collagen positive (c) and elastin positive (d) areas of wires in lumens. Quantification of collagen positive (e) and elastin positive (f) areas of wires outside of lumens. * indicates p < 0.05, ** indicates p < 0.01, compared between two groups.
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PMC9166432
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gr9.jpg
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0.409631 |
e5ae08b727974874b35ab4f23503feaf
|
PP-007 is a strong inducer of HO-1 in macrophages.a Schematic cartoon showing the treatment regimen. b, c Representative western blot (WB) and densitometric analysis of HO-1 in WT MΦs treated with 2 mg/ml or 4 mg/ml PP-007 for the time indicated. d qPCR of Hmox-1 in WT MΦs treated with 2 mg/ml PP-007 for the time indicated. e Cartoon showing the experimental design: WT BMD-MΦs were pretreated with 2 mg/ml PP-007 for 6 h and then challenged with PA-LPS or live PAO1 (MOI of 10:1) for an additional 12 h. At 2 h after exposure to PAO1, 100 µg/ml gentamicin was added to the medium. f qPCR of Hmox-1 in WT MΦs treated with 2 mg/ml PP-007 for 6 h before the addition of PA-LPS for an additional 4 h. g Representative WB and densitometric analysis of HO-1 in WT MΦs pretreated with vehicle or 2 mg/ml PP-007 for 6 h and then challenged with PA-LPS (left) or PAO1 (right). WB and qPCR data are represented as the fold increase over vehicle-treated samples. mRNA levels were normalized to the 18 S level. For WB data, band intensities were normalized to the corresponding β-actin band intensity. Data are represented as the mean ± SEM of at least three biological repeats. Statistical analyses were conducted using a two-tailed unpaired Student’s t test with unequal variance: *P ≤ 0.05, **P < 0.01, and ***P < 0.001. In (b–d), *symbols indicate a statistically significant difference between PP-007-treated and vehicle-treated samples. Cropped blots are displayed, and full-length gels and blots are included in the Supplementary Methods.
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PMC9166813
|
12276_2022_770_Fig1_HTML.jpg
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0.438449 |
a4699f70d6664ebfa6238c2fc871a12b
|
PP-007 requires the combined activation of MyD88 and PI3K/AKT for optimal induction of HO-1.a Representative WB of phospho-AKT (pAKT, serine 473) and HO-1 and densitometric analysis of HO-1 in WT MΦs pretreated for 12 h with 20 μM LY294002 or DMSO and then exposed to vehicle or 2 mg/ml PP-007 for an additional 6 h, as indicated. b Densitometric analysis of HO-1 in WT and AKT1-KO MΦs pretreated with vehicle or 2 mg/ml PP-007 for 6 h and then challenged with PA-LPS for 12 h. c Densitometric analysis of pAKT, total AKT, and HO-1 in murine WT MΦs treated with vehicle or PP-007 at different time points before and after the addition of PA-LPS (left). Schematic representation of the effects of PP-007 on AKT phosphorylation and HO-1 induction in MΦs before and after LPS addition (right). d Representative WB and densitometric analysis of HO-1, pAKT, and total AKT in WT and MyD88-KO MΦs treated with 2 mg/ml PP-007 for the time indicated. Time 0 indicates samples treated with vehicle. e Representative immunoblot and densitometric analysis of HO-1 in WT, TRIF-KO, and MyD88-KO MΦs pretreated with vehicle or 2 mg/ml PP-007 for 6 h and then challenged with PA-LPS for 12 h. f Schematic representation of the mechanism of action of PP-007: activation of the adaptor MyD88, but not PI3K/AKT signaling activation alone, is strictly required for robust PP-007-mediated induction of HO-1 (a, b). The combination of MyD88 and PI3K/AKT signaling activation led to the maximum induction of HO-1 (c). For WB data, band intensities were normalized to the corresponding β-actin band intensity, and the rate of AKT phosphorylation is shown as the ratio of phosphoprotein to total protein. Unless otherwise indicated, data are presented as the fold increase relative to WT vehicle-treated samples. Data are represented as the mean ± SEM of at least three biological repeats. Statistical analyses were conducted using a two-tailed unpaired Student’s t test with unequal variance: *P ≤ 0.05, **P < 0.01, and ***P < 0.001. In (d), * symbols indicate a statistically significant difference between different genotypes. Cropped blots are displayed, and full-length gels and blots are included in the Supplementary Methods.
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PMC9166813
|
12276_2022_770_Fig2_HTML.jpg
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0.475765 |
483a21e707da4bfa851dbfb50af119d5
|
PP-007 rescues the PI3K/HO-1 axis in CF macrophages and decreases the hyperinflammatory response to LPS.a, b Representative WB and densitometric analysis of pAKT, total AKT, and HO-1 in CF MΦs pretreated with vehicle or 2 mg/ml PP-007 for 6 h before the addition of PA-LPS (left) or PAO1 (right) for an additional 2 h (a) or 12 h (b), as shown in Fig. 1e. WT MΦs were pretreated with the vehicle and used as a control. c qPCR of il6, tnfa, and cxcl1 in CF MΦs pretreated with vehicle or 2 mg/ml PP-007 for 6 h before the addition of PA-LPS for an additional 4 h. WT MΦs pretreated with the vehicle and exposed to PA-LPS were used as a control. d Densitometric analysis of HO-1 in PBD MΦs from HD (n = 5) and CF patients (n = 14) treated for 18 h with vehicle or 2 mg/ml PP-007 (left). Densitometric analysis of HO-1 in PBD MΦs from HD (n = 4) and CF patients (n = 15) pretreated for 6 h with 2 mg/ml PP-007 and then exposed to PA-LPS for 12 h (right). WB and qPCR data are shown as the fold increase relative to WT vehicle-treated samples. mRNA levels were normalized to the 18S level. For WB data, band intensities were normalized to the corresponding β-actin band intensity, and the rate of AKT phosphorylation is shown as the ratio of phosphoprotein to total protein. Data are represented as the mean ± SEM and, unless otherwise indicated, are the result of three biological repeats. Statistical analyses were conducted using a two-tailed unpaired Student’s t test with unequal variance: *P ≤ 0.05, **P < 0.01, and ***P < 0.001. Cropped blots are displayed, and full-length gels and blots are included in the Supplementary Methods. The genotypes of CF patients enrolled in this study are listed in Supplementary Table 1.
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PMC9166813
|
12276_2022_770_Fig3_HTML.jpg
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0.416723 |
9544e353d5fa44b18a2cae6054739c66
|
Systemic delivery of PP-007 induces HO-1 expression in lung macrophages.a qPCR of Hmox-1 in white blood cells and lung tissues and densitometric analysis of HO-1 protein levels in lung tissues from WT and CF mice at different time points after PP-007 treatment. Time 0 indicates values for vehicle-treated WT and CF mice. Data are shown as the fold increase in PP-007-treated mice relative to vehicle-treated mice. The graphs show the mean ± SEM and are a combination of two independent experiments with 2–5 mice/time point for each genotype. b Representative immunofluorescence (IF) staining for CD68 (green), HO-1 (red), and DAPI (blue) in lung tissues from WT mice 24 h after PP-007 treatment. Merged images and the magnifications of areas of interest are shown on the right. Yellow staining indicates CD68 and HO-1 colocalization.
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PMC9166813
|
12276_2022_770_Fig4_HTML.jpg
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0.424941 |
bbb3be2ece3a46118361c92c049c6668
|
Systemic delivery of PP-007 reduces the inflammatory response in CF lungs.a Schematic cartoon showing the treatment regimen: CF mice were retro-orbitally injected with 1 dose of PP-007 (320 mg/kg) or vehicle, while WT mice were injected with vehicle and used as a control. At 6 h after injection, mice received three doses of 12.5 mg of PA-LPS over 3 days (one dose per day) and were analyzed at 6, 24, and 48 h after the last LPS nebulization. b Densitometric analysis of HO-1 in lung lysates. The intensities of HO-1 immunoreactive signals were measured and normalized to the β-actin intensity. c Weight loss as a percentage of body weight. d Differential cell counts in the bronchoalveolar lavage fluid (BALF) of WT and CF mice treated with vehicle and CF mice treated with PP-007 at the time indicated. The left panel shows the gating strategy used to distinguish alveolar macrophage and neutrophil populations in the BALF based on the expression of CD64. e Neutrophil numbers in lung tissues. f Representative hematoxylin–eosin staining of paraffin-embedded lung tissues 24 h after the last LPS treatment. Magnification: ×10; scale bar: 100 µm. g Percentages of Ly6C+ and Ly6C− mo-Ms in the live/CD45+ gate based on the gating strategy shown in Supplementary Fig. 3. h Cytokine concentration in the BALF. For (e), neutrophils in the lungs were identified using the sequential gating strategy shown in Supplementary Fig. 3. The percentage of cells in the live/singlets gate was then multiplied by the number of live cells to obtain an absolute live-cell count. AMs alveolar macrophages, mo-Ms monocyte-derived macrophages. The graphs show the mean ± SEM. A detailed list of the mice used in each experiment is included in Supplementary Table 2. In (d), the red symbol (*) indicates a statistically significant difference between the vehicle-treated WT and CF groups. The black symbol (*) indicates a statistically significant difference between the vehicle-treated CF and PP-007-treated CF groups. Statistical analyses were conducted using a two-tailed unpaired Student’s t test with unequal variance: *P ≤ 0.05, **P < 0.01, and ***P < 0.001.
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PMC9166813
|
12276_2022_770_Fig5_HTML.jpg
|
0.50665 |
1f6ba1d307744bf5a2867f3090a921f2
|
The mechanism of action of PP-007 relies on the induction of HO-1 in monocytes/macrophages to resolve lung inflammation in vivo.a Representative dot plots displaying the percentages of DsRed+ alveolar macrophages (AMs; CD11c+CD64+), neutrophils (CD11c−CD11b+CD24+Ly6G+), and other monocytes/macrophages (gran-CD11c-CD11b+) in the lung tissues of Cx3Cr1Cre/+ (top panel) and HO-1Cx3Cr1 (bottom panel) mice 24 h after LPS treatment. b qPCR of Hmox-1 in white blood cells and lung tissues and densitometric analysis of HO-1 protein levels in lung tissues from Cx3Cr1Cre/+ and HO-1Cx3Cr1 mice at 6 h after PP-007 treatment (320 mg/kg). Data are shown as the fold increase relative to vehicle-treated Cx3Cr1Cre/+ mice. HO-1Cx3Cr1 mice were pretreated with vehicle (n = 3) or PP-007 (n = 4) and then nebulized with PA-LPS as shown in Fig. 5a. Cx3Cr1Cre/+ mice (n = 3) were pretreated with vehicle and used as a control. c Densitometric analysis of HO-1 in lung tissue lysates. The intensities of HO-1 immunoreactive signals were measured and normalized to the β-actin intensity. d Numbers of neutrophils in the BALF and lung parenchyma assessed by flow cytometry. e Ratio of the percentage of Ly6C- to Ly6C+ mo-Ms in the lungs based on the gating strategy shown in Supplementary Fig. 3. f Cytokine concentration in the BALF. The graphs show the mean ± SEM. Statistical analyses were conducted using a two-tailed unpaired Student’s t test with unequal variance: *P ≤ 0.05.
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PMC9166813
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12276_2022_770_Fig6_HTML.jpg
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0.459816 |
cdf321cfdaf0423d9224d7781a827d05
|
Proposed mechanism of action of PP-007 involved in resolving lung inflammation in CF.a During infection, circulating monocytes migrate to the lungs. Because of the defective induction of HO-1, recruited CF MΦs fail to acquire an anti-inflammatory phenotype. This leads to an enhanced nonresolving proinflammatory environment with elevated numbers of IL-17-producing cells that may contribute to lung neutrophilia. b PP-007 induces high levels of HO-1 in circulating monocytes recruited to lung tissue. Rescue of HO-1 expression primes lung monocyte-derived MΦs to acquire an anti-inflammatory profile that helps to reduce proinflammatory cytokine levels and IL-17-producing cell recruitment and to expedite the elimination of lung neutrophils.
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PMC9166813
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12276_2022_770_Fig7_HTML.jpg
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0.440403 |
2ab8f01245ed4b6ba3ddd2496e1b3296
|
Flow chart of literature screening.
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PMC9167100
|
CMMI2022-3108485.001.jpg
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0.40201 |
1abef2053e9f4777a3fd721fe5c86d06
|
Meta-analysis of the efficiency of combined Chinese and Western medical treatment modalities in patients with thyroid nodules. (a) Forest plot of treatment response rate. (b) Funnel plot of treatment response rate. (c) Sensitivity analysis of treatment response rate.
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PMC9167100
|
CMMI2022-3108485.002.jpg
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0.429567 |
e376c20292f54a728c04826911333e7c
|
Meta-analysis of the maximum nodule diameter and thyroid volume in patients with thyroid nodules treated with a combination of Chinese and Western medicine. (a) Forest plot of the maximum nodule diameter. (b) Forest plot of thyroid volume.
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PMC9167100
|
CMMI2022-3108485.003.jpg
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0.415955 |
fc5cef6d57e247bbb3b34bd5cd198151
|
Sensitivity analysis of the maximum nodule diameter and thyroid volume in patients with thyroid nodules treated with a combination of Chinese and Western medicine. Sensitivity analysis of the maximum nodule diameter (a) and thyroid volume (b).
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PMC9167100
|
CMMI2022-3108485.004.jpg
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0.462811 |
784e792bf32943aa84fa1f6580fd4704
|
Meta-analysis of hormone levels in patients with thyroid nodules treated with a combination of Chinese and Western medicine. Forest plot of serum FT3 (a), FT4 (b), and TSH levels (c) after treatment.
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PMC9167100
|
CMMI2022-3108485.005.jpg
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0.455234 |
10282d743116459882d9a01c4875c500
|
Sensitivity analysis of hormone levels in patients with thyroid nodules treated with a combination of Chinese and Western medicine. (a) Sensitivity analysis of serum FT3 levels after treatment. (b) Sensitivity analysis of FT4 levels after treatment. (c) Sensitivity analysis of TSH levels after treatment.
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PMC9167100
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CMMI2022-3108485.006.jpg
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0.459221 |
a8e68cedae95485cb5683cdc8f94a028
|
Meta-analysis of the TCM syndrome score in patients with thyroid nodules treated with a combination of Chinese and Western medicine. (a) Forest plot of the TCM syndrome score of patients after treatment. (b) Sensitivity analysis of the TCM syndrome score of patients after treatment.
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PMC9167100
|
CMMI2022-3108485.007.jpg
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0.488476 |
e2132ae2a8a84f49944a8599ee6b9613
|
XPS spectra of MB-loaded SGO@CA; (A) XPS survey, (B) N1s, (C) S2p and (D) O1s.
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PMC9167308
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41598_2022_13105_Fig10_HTML.jpg
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0.429908 |
10b7ae7da0b64e0aaa1a16f7d1b570e4
|
(A) A schematic representation for the formulation of SGO@CA floated beads, (B) laboratory images for freshly prepared SGO@CA floated beads.
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PMC9167308
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41598_2022_13105_Fig1_HTML.jpg
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0.428684 |
e95999e1ea7543fdb11e500ef1fd7fcb
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(A) FTIR, (B) XRD and (C) TGA of SGO@CA composite beads and their pristine components.
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PMC9167308
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41598_2022_13105_Fig2_HTML.jpg
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0.44346 |
4e2d79617b594e52a07906839fcf764d
|
SEM images of (A,B) SGO, (C,D) CA beads and (E,F) SGO@CA composite beads.
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PMC9167308
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41598_2022_13105_Fig3_HTML.jpg
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0.50924 |
0bba4130083a4fc0819f8f026146e27f
|
XPS spectra of SGO@CA beads; (A) XPS survey, (B) C1s, (C) O1s and (D) S2p.
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PMC9167308
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41598_2022_13105_Fig4_HTML.jpg
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0.409249 |
b0c20943b4ba4f309d14954b4a4820d5
|
Three-dimensional response surface plots of MB adsorption capacity using SGO@CA composite beads.
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PMC9167308
|
41598_2022_13105_Fig5_HTML.jpg
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0.426036 |
0af021b63a074ac59acace1c03baaef8
|
(A) Effect of SGO and (B) effect of contact time on the adsorption of MB dye.
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PMC9167308
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41598_2022_13105_Fig6_HTML.jpg
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0.441848 |
60bd62d2a0814a89b5fde11d2507fa5b
|
(A) The Pseudo-first order, (B) the Pseudo-second order, (C) Elovich and (D) intra-particle diffusion kinetic models for the adsorption of MB dye onto SGO@CA composite beads.
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PMC9167308
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41598_2022_13105_Fig7_HTML.jpg
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0.466242 |
dcb0668c63ae49b997ea6ea9a3cf5691
|
Impact of initial MB concentration on (A) adsorption capacity and (B) removal (%). (C) The linear isotherm model of Langmuir and (D) Freundlich model for the MB dye adsorption onto SGO@CA composite beads.
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PMC9167308
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41598_2022_13105_Fig8_HTML.jpg
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0.473186 |
74079936849344398fde2c56409d0813
|
(A) Effect of adsorption temperature on the adsorption process, (B) reusability and (C) selectivity of SGO@CA composite beads toward cationic and anionic dyes.
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PMC9167308
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41598_2022_13105_Fig9_HTML.jpg
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0.45635 |
49c9c8e0824e4408895f867a318b4c36
|
Flow chart of patient inclusion (disposition and population) in this study.
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PMC9167845
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gr1_lrg.jpg
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0.505573 |
497767375854458d8a144ee0d883620e
|
Serum PEG-specific and PS-specific antibodies of immediate-type allergic patients (n = 14) and healthy controls (HC; n = 19). A: PEG-specific IgE; B: PEG-specific IgG; C: PS-specific IgE; D: PS-specific IgG. PEG-specific (A) and PS-specific (C) IgE are shown as natural logarithms. Bars represent median.
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PMC9167845
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gr2_lrg.jpg
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0.392084 |
4e8608e9810c4362806e77a0aec766f0
|
Correlation between (A) PEG-specific IgE and PEG-specific IgG levels, and (B) PEG-specific IgE and PS-specific IgE levels. Data (n = 37) were obtained from patients with immediate or delayed allergies (n = 18) and healthy controls (n = 19), and Spearman's correlation coefficient was adopted.
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PMC9167845
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gr3_lrg.jpg
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0.421526 |
fd4dd2b25a584fff96974bf47ae8c263
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(A) PEG-specific and (B) PS-specific IgE of positive (n = 3) and negative (n = 5) skin test groups. PEG-specific and PS-specific IgE are displayed as natural logarithms. Bars represent median.
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PMC9167845
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gr4_lrg.jpg
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0.490631 |
731ad44e6c164e81bad8ecbf076a7798
|
Mechanism of current and future first-line therapy for HCC. Sorafenib and lenvatinib are multikinase inhibitors primarily targeting tumor cells and endothelial cells. Atezolizumab blocks PD-1 engagement of PD-L1 while bevacizumab blocks VEGF interaction with its receptor in immune cells as well as endothelial cells. Clinical trials with different combinations of ICIs (anti-PD-1/L1 and anti-CTLA-4) plus bevacizumab or bevacizumab biosimilar (IBI305) and ICIs plus TKIs (lenvatinib, cabozantinib, apatinib) are under active investigation.
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PMC9167882
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gr1.jpg
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0.407926 |
2e09498c416541d7aa9f80fbee3d21f4
|
Limitations and potential approaches of first-line atezolizumab plus bevacizumab combination therapy for HCC. Subgroups of advanced HCC patients falling into the treatment criteria of first-line atezolizumab plus bevacizumab therapy may be further selected based on superior or nonsuperior OS when compared to first-line sorafenib therapy. The dose of atezolizumab and bevacizumab may be adjusted according to clinical studies in the indicated ranges. A composite biomarker consisting of three types is likely needed to guide patient selection and therapeutic course.
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PMC9167882
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gr2.jpg
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0.482156 |
73531a898e0b44ac8cf0fc7709be4164
|
Distribution of CV for 174 proteins detected in a pooled PEx sample (1 µg PEx/ml), analysed 5 times with the SOMAscan 1.1 K platform. The pooled sample originated from 6 subjects with asthma and 3 healthy volunteers. Proteins were considered detected if RFU values delivered by SomaLogic were larger than LOD in all 5 replicate samples. Limit of detection (LOD) was calculated as 3 times the standard deviation from the mean RFU signal measured from 3 blank samples
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PMC9167914
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12014_2022_9348_Fig1_HTML.jpg
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0.421347 |
e9b708c5f920480a9c1832a98464450e
|
Assessment of intra-individual variability by visual inspection of Principle Component Analysis (PCA) plot. PEx samples from 3 consecutive PEx samples from 6 asthmatic subjects (red, blue, green, white, black and yellow) were analysed with the SOMAscan 1.1 K platform. Using ANOVA statistical test based variable selection (q < 5.5E−5) 42 out of 114 proteins commonly detected in all 18 samples, were found to discriminate all 6 subjects from each other in a PCA plot, as judged by visual inspection in Omics Explorer software
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PMC9167914
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12014_2022_9348_Fig2_HTML.jpg
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0.448263 |
15040c8443af4d148ebd18f31a33e4d4
|
Visualization of results from Gene Ontology (GO) enrichment analysis (GOrilla [28]) matching 207 proteins detected in PEx samples by SOMAscan 1.3 K platform, to the GO Cellular Component sub-domain database. Over represented GO terms are organized in a parent–child based hierarchically structure with color-coded significance levels (Fisher’s exact test), as indicated in the p value colour scale
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PMC9167914
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12014_2022_9348_Fig3_HTML.jpg
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0.430687 |
84b38b74ca764353b6fe6a398d20cf6c
|
Box plots show examples of SOMAscan data for 6 differentially abundant proteins; a Alpha-1-antitrypsin (SERPINA1), b Interleukin-1 Receptor accessory protein (IL1RAP), c CC motif chemokine 18 (CCL18), d Complement component C1q receptor (CD93), e Immunoglobulin M (IgM), in non-asthma (NA), asthma without (A) and with small airway involvement (A-hLCI), and f Soluble Receptor of Advanced Glycation End products (sRAGE) in never-smokers (NS) and ex-smokers (ExS). Y-axis show normalized abundance (log2 transformation and normalization to mean 0 and variance 1). Box ranges from the 25th to the 75th percentile and median value is marked with dotted line. p values and false discovery rate adjusted p values (q) from various pairwise comparisons are shown over each box plot. Protein abundance data was adjusted for difference in age
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PMC9167914
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12014_2022_9348_Fig4_HTML.jpg
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0.443839 |
89a471833d484d7b89806e129a825f0f
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Dissection of pituitary gland from mouseStep 2: Beheading. Steps 3–4: Removal of skull. Dotted lines indicate the positions to be cut. V: ventral side. D: dorsal side. Step 5: Removal of brain. The tip of the arrow indicates the position to insert the medicine spoon. Step 6: Detachment of the diaphragma sellae. The arrows indicate where to pinch with tweezers. Step 7: The circle indicates the isolated pituitary tissue. Step 8: Excised pituitary glands. Scale bars: 20 mm (step 2), 5 mm (steps 3–8).
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PMC9168163
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gr1.jpg
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0.380229 |
30da8ddb028f48d291c1045cf542b79d
|
Separation of anterior lobe (AL) and intermediate lobe (IL)/posterior lobe (PL)(A) Dorsal view of the pituitary gland. Dotted lines indicate the boundary between the AL and the IL or the IL and PL. The tip of the arrow indicates the Rathke’s cleft.(B) Poke the tip of the tweezers into the border area between the AL and the IL.(C) Using the pierced tweezers as a support, peel off the IL/PL with the opposite tweezers.(D) Image of the AL and the IL/PL after separation. Scale bars: 1 mm.
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PMC9168163
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gr2.jpg
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0.463404 |
3244c420d4bf4cb69c9af22452d6dfd1
|
Points to note while seeding the primary cellsStep 22: Make a droplet so that the culture fluid does not overflow from the glass surface of the glass-bottom dish. Step 23: Drip the culture medium from around the droplet.
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PMC9168163
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gr3.jpg
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0.416851 |
f0c0265543144e35ba45bad3865fd99d
|
Growth of primary anterior lobe (AL) cells isolated from mouse pituitary glandRepresentative phase contrast images are shown in the cell culture on a glass-bottom dish (A–C) or a plastic dish (D–F).(A and D) Primary AL cells immediately after medium change (day 1 of culture) (d1).(B and E) Primary AL cells on day 4 of culture (d4).(C and F) Primary AL cells on day 7 of culture (d7). Scale bar: 300 μm.
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PMC9168163
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gr4.jpg
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0.402759 |
97a51caa628e436fa877f5259127b43c
|
Quality check for primary-cultured anterior lobe (AL) cells isolated from the mouse pituitary gland(A) Primary-cultured AL cells were subjected to qRT-PCR analysis of the indicated mRNAs. Data were normalized by the amount of Tbp mRNA and are shown as means ± SD (n = 3).(B) Representative images of SOX2 (purple) and PRRX1 (green) with DAPI (blue) in primary-cultured AL cells on day 1 (d1) and day 7 of culture (d7) are shown.(C) Numbers of SOX2- and PRRX1-positive cells, together with cells stained with DAPI, in primary-cultured AL cells were counted and the proportion of each cell type was calculated. Data shown are means ± SD (n = 3/10 mm2, respectively).(D) Merged image of hormones (green) with DAPI in primary-cultured AL cells (day 7) is shown. Scale bars: 100 μm.
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PMC9168163
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gr5.jpg
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0.469767 |
b9e0ef10362d49c9b010ca6a3bed4230
|
Passage cultures of adult pituitary stem/progenitor cells (APSCs)(A) Primary anterior lobe cells were seeded on a glass-bottom dish and cultured for 7 days, before being dispersed by a trypsin. Dispersed cells (APSCs) were re-seeded (passage 1) on glass-bottom dishes and were cultured for a further 7 days. Images of cells on day 1 (d1) and day 7 of culture (d7) are shown. The passage culture of APSCs (passage 2) was then repeated.(B) Images of aggregates formed from primary and passaged cells. Scale bars: 100 μm.
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PMC9168163
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gr6.jpg
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0.480098 |
383c68517175449ab2068bf938f3a33e
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Differentiation capacity of primary-cultured anterior lobe (AL) cells(A) The aggregate formed from primary-cultured AL cells by low-cell-adhesion culture. Images of cells immediately after seeding (d0) and on day 4 of culture (d4) are shown.(B) Immunofluorescence images of SOX2 (purple) and hormones (green) with DAPI (blue) in the sliced section of the aggregate. Merged images are indicated and boxed areas are enlarged in the center and right panels. Arrows and arrowheads indicate SOX2 and hormone double positive and hormone single positive cells, respectively. Scale bars: 100 μm (A) and 20 μm (B).
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PMC9168163
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gr7.jpg
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