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0.491023 | b1ab2517477f4d9c8291de8b72b7f726 | OR with contributions from different exposure categories. | PMC9925989 | ijmsv20p0219g003.jpg |
0.523182 | 9c78698bee234607a2770f04d7348658 | Sequence alignment of TgCyp18.4, TgCyp23, and
human CypA. Amino
acids critical for Cyp enzymatic activity and CsA binding are shown
in bold. The sequences shown are TgCyp18.4 (TgCyp289250), TgCyp23
(TgCyp285760), and human CypA. | PMC9926490 | id2c00566_0002.jpg |
0.531646 | 6876d79e5fb74c6582c090feb73853c0 | Structural characterization
of TgCyp18.4 and TgCyp23. (A, B) 1H-1D NMR spectra of (A)
70 μM TgCyp18.4 (64 scans) and
(B) 100 μM TgCyp23 (16 scans). (C) Far-UV CD spectra and (D)
thermal denaturation profiles of 0.2 mg mL–1 TgCyp18.4
(black) and TgCyp23 (red). CypA was included as comparison (blue). | PMC9926490 | id2c00566_0003.jpg |
0.433618 | 1a7ac9063027497ca344a47b42b05a1a | PPIase and chaperone-like activity of
TgCyps. (A, B) Representative
steady-state initial velocity kinetics for the PPIase activity of
(A) TgCyp18.4 and (B) TgCyp23. (C) Catalytic effect of TgCyps on protein
folding of RNase T1. The increase in fluorescence at 320 nm is shown
as a function of the time of refolding in the presence of a fixed
concentration of TgCyp18.4 (green), TgCyp23 (blue), and human CypA
(red). The control experiment showing the spontaneous refolding of
RNase T1 in the absence of Cyps is also displayed (black). (D) Histogram
shows the mean value of the exponential folding rate constants kobs of RNase T1 in the absence and presence
of Cyp variants. Color coding as in C. n = 3 independent
experiments were performed. The error bars represent standard error
from the mean value. | PMC9926490 | id2c00566_0004.jpg |
0.506588 | fc664218b75044f2837cc4696fbb5621 | CsA
inhibition of recombinant Cyps. (A) PPIase activity of 7 nM
TgCyp23 (red) and 7 nM human CypA (black) measured at increasing concentrations
of CsA, ranging from 0 to 30 nM. (B) PPIase activity of 3 μM
TgCyp18.4 (black) and 3 μM TgCyp18.4 H111W (red) in the presence
of increasing amounts of CsA, ranging from 0 to 6 μM. The concentration
of AAPF used in the assays was fixed to 100 μM, corresponding
to a cis substrate concentration of 40 μM, which is much smaller
than the calculated Km. Therefore, no
deviations from the expected first-order kinetics were observed in
the presence of CsA.1 | PMC9926490 | id2c00566_0005.jpg |
0.457867 | bcb98530930848b19b5bedec613b98da | Three-dimensional structure of TgCyp23 in complex with CsA. (A)
Chemical structure of CsA. (B) Overall structure of the TgCyp23:CsA
complex. TgCyp23 is displayed in blue cartoons, and CsA is depicted
as orange sticks. N indicates the N-terminal region. (C) 2Fo – Fc electron
density map observed for CsA. Map contoured at 1σ. (D) Representation
of the molecular surface of TgCyp23 (colored in blue) showing the
CsA-binding pocket (CsA depicted as capped sticks). (E) CsA stabilization
by TgCyp23. Relevant residues implicated in the interaction are labeled
and shown as sticks. (F) Interaction network between nearby protein
amino acids (distance in angstroms are indicated). Dashed lines indicate
polar interactions. | PMC9926490 | id2c00566_0006.jpg |
0.429271 | e7dc652d6d0c4fd5afab514f07e89f34 | AlphaFold-predicted
model for TgCyp18.4. (A) Predicted structure
for TgCyp18.4 with colors indicating the reliability of the model.
(B) Structural superimposition of the predicted structure of TgCyp18.4
(salmon) onto the crystal structure of TgCyp23 (blue). C and N show
C-terminus and N-terminus, respectively. Yellow arrows indicate regions
showing larger differences between TgCyp23 and TgCyp18.4. (C) Comparison
of CsA-binding pockets in TgCyp23 and TgCyp18.4. TgCyp23 amino acids
are displayed in blue sticks, and TgCyp18.4 residues are displayed
in red. Dashed lines indicate predicted polar interactions for the
TgCyp18.4:CsA complex. | PMC9926490 | id2c00566_0007.jpg |
0.386152 | 28602329f2ef4b4b9a882e55159c3620 | Structural comparison of substrate versus CsA recognition
in CypA
and Toxoplasma Cyps. (A) Detailed view of the binding
site in the CypA:AAPF complex. All distances are indicated in dashed
lines between the shown atoms in the extremes. (B) TgCyp23 cavity
is displayed as the blue surface. AAPF in green sticks and superposed
with half-CsA chains (residues 2–6) in orange sticks. (C) TgCyp18.4
surface in salmon and AAPF superposed is depicted as green sticks.
(D) CypA:AAPF interaction network (polar contacts are indicated with
dotted lines). (E) TgCyp23:AAPF predicted interaction network. (F)
TgCyp18.4:AAPF predicted interaction network. | PMC9926490 | id2c00566_0008.jpg |
0.464218 | de40c830c9f24609a6886bcfb36dc04d | Grain size distribution and Lognormal fitting of six sorghum grains. JZ 34, jinza 34 (A); LZ 19, liaoza 19 (B); JN 3, jinnuo 3 (C); JZ 127, jiza 127 (D); JN 2, jiniang 2 (E); JX, jiaxian (F). | PMC9926944 | fnut-09-1048789-g001.jpg |
0.428952 | fcc5d37f5c0e4d02ad0b803c10d3f9b4 | Scatterplot matrix analysis of protein (PT), fat (F), carbohydrate (CHO), and energy values contributions. TE, total energy; PEP, proportion of total energy due to protein; PEF, proportion of total energy due to fat; PEC, proportion of total energy due to carbohydrate; UEDP, utilizable energy due to protein. | PMC9926944 | fnut-09-1048789-g002.jpg |
0.449302 | d9e20384e60240b98925a8f4e85a82a9 | Amylose content of sorghum flours. JZ 34, jinza 34; LZ 19, liaoza 19; JN 3, jinnuo 3; JZ 127, jiza 127; JN 2, jiniang 2; JX, jiaxian. The data showed the mean of three replications, and error bars are standard deviations. Different letters (a–c) indicate there were significant differences (p < 0.05) in the LSD mean comparisons between the treatments mean. | PMC9926944 | fnut-09-1048789-g003.jpg |
0.402564 | b91e3a4d150b46b8a1809c45896bc7cf | Anti-nutritional factors of six sorghum grains, tannin (A), flavonoids (B), and total phenols (C). JZ 34, jinza 34; LZ 19, liaoza 19; JN 3, jinnuo 3; JZ 127, jiza 127; JN 2, jiniang 2; JX, jiaxian. The data showed the mean of three replications, and error bars are standard deviations. Different letters (a–e) indicate there were significant differences (p < 0.05) in the LSD mean comparisons between the treatments mean. | PMC9926944 | fnut-09-1048789-g004.jpg |
0.384038 | 37eca9d064c54c68a369b9de9e18c6df | Functional properties of sorghum grains. Light transmittance (A), water absorption capacity (B), oil absorption capacity (C), water solubility (D), swelling power (E), and least gelation concentration (F). JZ 34, jinza 34; LZ 19, liaoza 19; JN 3, jinnuo 3; JZ 127, jiza 127; JN 2, jiniang 2; JX, jiaxian. The data showed the mean of three replications, and error bars are standard deviations. Different letters (a–d) indicate there were significant differences (p < 0.05) in the LSD mean comparisons between the treatments mean. | PMC9926944 | fnut-09-1048789-g005.jpg |
0.422422 | 134d7918804c42b99ba5b6e35a601320 | Pearson’s correlation coefficients of amylose, starch, physical properties, micrometric properties, and functional properties of six sorghum grains. BD, bulk density; TPD, tapped density; TD, true density; P, porosity; CI, Carr’s index; HR, Hausner’s ratio; AR, angle of repose; LT, light transmittance; WAC, water absorption capacity; OAC, oil absorption capacity; WS, water solubility; SP, swelling power; LGC, least gelation concentration; AM, amylose; S, starch. The numbers in each field represent the correlation extent; the color represents significant correlation (p < 0.05); the deeper the color of the field, the more significant the correlation (p < 0.01). The blue color means a positive correlation, and the red color means a negative correlation. | PMC9926944 | fnut-09-1048789-g006.jpg |
0.437595 | 2a6168ef2a7b4bb59547eb966db2a802 | Bland-Altman plot indicating the heteroscedastic distribution of data points between the limits of agreement between relative peak power values in the countermovement jump (CMJ) and cycle ergometer test (CET) data in 38 professional rugby union players. | PMC9927866 | 2078-516X-34-v34i1a12869-g001.jpg |
0.440413 | 40ed3d81a38047c78e36aa97a1793004 | Bland-Altman plot indicating the equal scattered distribution of data points above and below the bias, between relative mean power values in the countermovement jump (CMJ) and cycle ergometer test (CET) data in 38 professional rugby union players. | PMC9927866 | 2078-516X-34-v34i1a12869-g002.jpg |
0.428962 | 9fba31c08da54680843833ef89760d19 | Capture of human 8CLCs in naïve pluripotent stem cell cultures.The heterogeneous gene expression patterns and plasticity of naïve PSCs allows subpopulations of 8CLCs to arise. 8CLCs cells were first identified by scRNA-seq and showed transcriptional similarity to in vivo human 8C embryos. The abundance of 8CLCs in culture can be improved by modulating the epigenetic and transcriptional state of naïve hPSCs via transgene expression (DUX4) or small molecule inhibitors [trichostatin A (TSA) and 3-deazaneplanocin A (DZneP)]. The transcriptional features of 8CLCs and 8C embryos identified through scRNA-seq allowed for the identification of the human 8C marker TPRX1, a key director of 8CLC gene regulatory networks. 8CLCs downregulate the expression of canonical pluripotency genes (e.g. OCT4 and SOX2) and upregulate totipotency-associated genes (e.g. TPRX1 and DUXA). They also display functional characteristics of totipotency as they can give rise to both embryonic and extraembryonic tissues in vitro and in vivo. 8CLCs hold great promise in advancing early embryo models, improving interspecies chimerism for interspecies organogenesis, and modeling human development in a dish. (Figure created using BioRender.com.) | PMC9927913 | lnac024_fig1.jpg |
0.449493 | b3ad2e6f0d4a48f09bbbb50d3eb659a6 | The bioinspired parylene nanostructures on scleral lens. a) Simple and scalable fabrication of the parylene nanostructures and integration on the scleral lens. b) High‐magnification SEM image of the nanostructures. Scale: 5 µm (inset scale: 200 nm). Similar to the nanostructures on glasswing butterflies, the c) height, d) width, and e) aspect‐ratio of the parylene nanostructures can be modeled using a Gaussian distribution. | PMC9929119 | ADVS-10-2205113-g002.jpg |
0.40742 | dca18d8033dc4d4894e8d4fef969ccf6 | Optical properties of the nanostructured scleral lens. a) Glare‐reduction of nanostructured parylene compared to unstructured parylene at large viewing angles. b) Transmittance of the scleral lens with and without nanostructures under normal incidence. c) Photos of the C. faunus butterfly and the nanostructured scleral lens under UV light (365 nm) displaying selective scattering. d) Omnidirectional scattering at 785 nm of Au‐coated parylene nanostructures compared to Au‐coated unstructured parylene. | PMC9929119 | ADVS-10-2205113-g003.jpg |
0.433231 | bb61d1b3328f449db0f2c938baeea140 | Glasswing butterfly‐inspired scleral lens sensor. a) The glasswing butterfly (G. oto). b) SEM image of high aspect‐ratio nanostructures on the G. oto wings. Scale bar: 1 µm. c) The multifunctionality of G. oto wings. d) Bioinspired nanostructured scleral lens. e) Both the optical and bactericidal region as well as the sensing region of the scleral lens consist of high aspect‐ratio parylene nanostructures. Scale bar: 5 µm. f) Multifunctionality of the nanostructures on the scleral lens. | PMC9929119 | ADVS-10-2205113-g004.jpg |
0.434868 | 05ad1bed8e714e8dbd04a285df35fa4d | Lysozyme and lactoferrin sensing on nanostructured scleral lens. a) Schematic of DCDRS on the sensing region of the scleral lens. b) Artificial eye with mounted scleral lens. c) Image of the droplet edge showing the coffee‐ring pattern (5x magnification). d) DCDRS spectrum of lactoferrin and lysozyme (concentration: 3 mg mL−1) measured independently in PBS. e) Normalized DCDRS intensity of the 760, 1004 and 1553 cm−1 peaks of lactoferrin and lysozyme measured together in 1:1 concentrations (0 – 6 mg mL−1 each) in artificial tears. f) DCDRS spectrum surface mapping on the droplet edge in a 50 × 50 µm region showing spatial uniformity of the 760, 1004, and 1553 cm−1 peaks for artificial tears. g) Calibrated results of the collective concentration of lactoferrin and lysozyme from the scleral lens sensor for 8 different whole tear samples. The results are in good agreement with measurements made using ELISAs. h) Picture of the smartphone integrated with a Raman spectrometer model along with the measurement setup for smartphone measurements. i) Measurement of the 760 cm−1 peak intensity of lactoferrin and lysozyme measured together in 1:1 concentrations in PBS using the smartphone detector. The nanostructured sensor shows excellent linearity and improved sensitivity compared to measurements on an unstructured Au parylene film on scleral lens. | PMC9929119 | ADVS-10-2205113-g005.jpg |
0.38341 | 624ceaa5f59740699ff66b6cf77b671b | Bactericidal properties of the nanostructured parylene. a) Fluorescent micrographs of a negative control, unstructured parylene, and nanostructured parylene after 1 and 4 h of incubation in a culture of E. coli. Adherent bacteria are labeled with cell‐permeable nucleic acid markers SYTO 9 (green) and PI (red). Colocalization of the two stains is shown as merged images. b) Total cell surface coverage, c) dead cell surface coverage, and d) viability ratio measured after 1 and 4 h. | PMC9929119 | ADVS-10-2205113-g006.jpg |
0.454136 | 7a55bb1ff60949c397481f020656df46 | Hematological response (A) within 90 days (d0-90) and (B) within 180 days (d0-180) of MSC therapy. CR refers to complete response; NoR, no response; OR, overall response (CR + PR); PR, partial response. | PMC9929549 | fimmu-14-1106464-g001.jpg |
0.469542 | 607ada7421534b8b9d1bfd532952793a | Prospective monitoring of transfusion requirements and ANC after MSC therapy. Numbers of transfused red blood cell (RBC) (A) and platelet (B) concentrates over 30-day periods and circulating absolute neutrophil counts (ANC) (C, D) were prospectively recorded from baseline and up to 180 days after MSC infusion. Data were censored at relapse of hematological malignancy or second transplantation. Among the 5 patients who had severe neutropenia by the time of MSC therapy (D), 1 received a second alloHCT on d+33 after MSC for persistent PGF (NoR at d+30); 1 recovered an ANC > 1x109/L at d+30 then relapsed from the malignant hematological pathology, 2 recovered an ANC > 1x109/L at d90-120 and 1 retained persistent severe neutropenia. *p<0.05, **p<0.01, ***p<0.001 (Wilcoxon rank sum test). ANC refers to absolute neutrophil counts; Nbr Tx, number of transfusions; RBC, red blood cells. | PMC9929549 | fimmu-14-1106464-g002.jpg |
0.51748 | 48b7ffb8c6d8483c9b43580f4863c7d0 | Overall survival (OS) after MSC therapy. | PMC9929549 | fimmu-14-1106464-g003.jpg |
0.445677 | 7a58aba5ec7f4da8a806493cf04c5a7b | The illustrated life cycle is a series of necessary or recommended steps that produce RWD usable for analysis, from raw data generated by clinical encounters or operational workflows.Insights gained from data use can be returned to the life cycle, enriching future generation of clinical data. RWD, real-world data. | PMC9931348 | pdig.0000003.g001.jpg |
0.471933 | 334276da200342bcaf29a705d521d29d | An example data platform incorporating multiple best practices discussed in this article including natural language processing, generation of data warehouses and data marts, and ADM.ADM, augmented data management; COVID-19, Coronavirus Disease 2019; EHR, electronic health record. | PMC9931348 | pdig.0000003.g002.jpg |
0.446553 | 3a14111286a54400aaec8b5744384a8e | Flow chart showing inclusions, exclusions, responders and grouping | PMC9931779 | 10029_2021_2545_Fig1_HTML.jpg |
0.427709 | e5cb032af82940c99dae4cce82b24860 | a Reported pain: 1-no pain; 2-pain can be ignored; 3-pain cannot be ignored, but it does not affect everyday activities; 4-pain cannot be ignored, and it affects everyday activities; 5-pain prevents most activities; 6-pain necessitates bed rest; and 7-pain requires immediate medical attention; and registered postoperative complications in patients having undergone open anterior mesh repair. b Reported pain: 1-no pain; 2-pain can be ignored; 3-pain cannot be ignored, but it does not affect everyday activities; 4-pain cannot be ignored, and it affects everyday activities; 5-pain prevents most activities; 6-pain necessitates bed rest; and 7-pain requires immediate medical attention; and registered postoperative complications in patients having undergone endo-laparoscopic mesh repair | PMC9931779 | 10029_2021_2545_Fig2_HTML.jpg |
0.560497 | 8aa2eb38923d4a6aa0659c8c28022003 | Suggested body map for recording of quantitative sensory testing findings | PMC9931782 | 10029_2022_2693_Fig1_HTML.jpg |
0.501877 | 88137551232a44969d6bd066059e6dee | Overview of potential CPIP treatment modalities, assessment, and follow-up | PMC9931782 | 10029_2022_2693_Fig2_HTML.jpg |
0.462133 | ef7a28bc9f4941fb9d5b93dbb2f1dc48 | Weekly epidemic curve of confirmed cases of Crimean-Congo haemorrhagic fever cases in Iraq, 2022. | PMC9931897 | gr1.jpg |
0.459708 | 1701f7d47f9d469eb7479158a8541d9f | Distribution of laboratory-confirmed cases of Crimean-Congo haemorrhagic fever in Iraq, 2022. | PMC9931897 | gr2.jpg |
0.42557 | a75811b512bc4240b6f4896de64cfd17 | Characterization of Exos derived from iCMs(A) Schematic overview of the study design. Three DCM iPSC lines and three healthy control iPSC lines were differentiated into cardiomyocytes. Exosomes were isolated from ANG II conditioning media of either CTL-iCMs or DCM-iCMs and further used in experiments.(B) Representative immunoblots detect canonical exosome markers with equal protein loading (10 μg) of cells, cell debris (Debris), or Exos fractions. The exosomal markers CD63, CD9, and Alix were presented in the Exo samples. Oppositely, the ER marker, calnexin, was only present in cells and debris but not in Exos.(C) TEM images of CTL-Exos and DCM-Exos. Exos were visualized as cup-shaped structures with diameters <200 nm.(D and E) Quantification of CTL- and DCM-Exos by Nanosight NTA. N = 6 CTL vs. 6 DCM; NS = nonsignificant. | PMC9932122 | gr1.jpg |
0.477521 | d36c7af62cb54d5b8bdd038909d41653 | DCM-Exos induced up-regulation of fibrotic genes in CFs(A) Representative fluorescent images of CTL-Exos or DCM-Exos (PKH26-labeled) treatment in CFs. Endocytosed Exos (orange) were observed in the cytoplasm of CFs (bar = 200 μm (left); 900 nm (right)).(B) Quantifications of Exo uptake in CFs. The uptake ratio was evaluated by the number of Exo uptaken cells (orange) divided by the total number of nuclei (blue) in the image (N = 22 pics/group), NS, nonsignificant.(C) qRT-PCR of fibrotic genes in CFs. N = 6; ∗ = p< 0.05.(D) Representative immunoblots. The CF cell lysis of different treatment groups was probed with specific antibodies (Col1a, Col3a, and CTGF).(E) Quantification of protein expression in immunoblots. Col1a, col3a, and CTGF expression were normalized to the loading control (GAPDH), N = 6. Data represented as mean ± SD; ∗ = p< 0.05; one-way ANOVA followed by Tukey post hoc test. | PMC9932122 | gr2.jpg |
0.479786 | 29118d03f5c54aa2b84fe7fd7a51fe3e | Intracardial injection of DCM-Exo promoted fibrosis in mouse hearts(A) Representative echocardiographic images. Images were taken respectively from PBS, CTL-Exo, or DCM-Exo injection groups on day 0 and day 14.(B) LVEF was determined by echocardiography. The injection of DCM-Exo significantly decreased LVEF on day 14 (N = 8/group; ∗ = p< 0.05). Injection of PBS, or CTL-Exo resulted in nonsignificant change between day 14 and baseline.(C) Representative pictures of picrosirius red/fast green staining in series sections of the mouse hearts. The fibrotic area (Red) was quantified by ImageJ. N = 8/group, ∗∗ = p< 0.01.(D) Representative immunoblots of mouse hearts (PBS, CTL-Exo, or DCM-Exo treatments). Fibrotic markers, Col1a, Col3a, and CTGF were detected by specific antibodies.(E) Quantification of fibrotic markers expression. DCM-Exos injection resulted in significant upregulation of fibrotic markers (N= 8/group). GAPDH was used as a protein loading control. Data represented as mean ± SD; ∗ = p< 0.05; one-way ANOVA followed by Tukey post hoc test. | PMC9932122 | gr3.jpg |
0.357262 | eb84da3d15dd43c99036eb82e54a77da | MiR-218-5p played an essential role in the profibrotic effect(A) Volcano plot of differential expression miRs in CTL-Exos and DCM-Exos. (B) miRNA screening assay. qRT-PCR results showed miR-218-5p mimics significantly upregulated expression fibrotic of markers (N= 3; one-way ANOVA; ∗ = p< 0.05).(C) MiR-218-5p upregulated fibrotic marker in a dose-dependent manner.(D) ANG II stimulation up-regulated miR-218-5p expression in DCM-iCMs (N= 3; ∗= p <0.05, ∗∗∗ = p< 0.001).(E) Intracardial injection of miR-218-5p increased the fibrotic area in mouse hearts (N= 8, Student’s t test, ∗∗ = p< 0.01). Data represented as mean ± SD. | PMC9932122 | gr4.jpg |
0.419076 | 1e36f813a16e4e3e9b6175e4a72af710 | MiR-218-5p inhibition attenuated the fibrotic effect elicited by the DCM-Exos(A) qRT-PCR of fibrotic gene expression. MiR-218-5p inhibition significantly reduced the DCM-Exo-induced fibrotic effect. One-way ANOVA followed by Tukey’s post hoc test; N= 3; ∗∗ = p< 0.01.(B) Representative fluorescent images. iCMs were transfected by zip-GFP as control or zip-miR218. Bar = 150 μm.(C) qRT-PCR analysis of miR-218 expression in Exos derived from zip-miR218 transfected iCMs. Student’s t test, N= 3; ∗∗ = p< 0.01.(D) qRT-PCR analysis of fibrotic gene expression. MiR-218-5p knockdown DCM-Exos (ExoZipmiR218−GFP) significantly reduced the expression of fibrotic markers. N = 3; Student’s t test; ∗ = p< 0.05. Data represented as mean ± SD. | PMC9932122 | gr5.jpg |
0.503822 | d4f5cdcf63924cf9bc8ff1356307c3ca | MiR-218-5p increased Smad2 phosphorylation in CFs(A) Immunoblots of cell lysates derived from CFs treated with TGF-β, miR-218-5p, and a TGF-β inhibitor (SB525334). Specific antibodies were used to detect Col1a, Col3a, CTGF, phospo-Smad2 (p-SMAD2), and GAPDH.(B) Quantitation of protein expression in immunoblots. GAPDH was used as a protein loading control. TGF-β inhibitor (SB525334) significantly reduced TGF-β1-induced fibrotic effect (lane 3). MiR-218-5p increased the phosphorylation of Smad2. N= 3; one-way ANONVA followed by Tukey’s post hoc test, ∗ = p< 0.05; ∗∗ = p< 0.01; ∗∗∗ = p< 0.001. Data represented as mean ± SD. | PMC9932122 | gr6.jpg |
0.436755 | 92c8cf2e6b54423e9b432b09fba11943 | MiR-218-5p targeted to TNFAIP3(A) Targeted sequence prediction of miR-218-5p in RNA22.(B) Immunoblots (left) indicated TNFAIP3 expression was significantly repressed in CFs transfected with miR-218-5p.(C) Luciferase assay of miR-218-5p and TNFNAIP3 5′UTR region. Co-transfection of miR-218-5p + WT sequence significantly reduced luciferase activity compared with the scramble CTL + WT. One-way ANOVA followed by Tukey’s post hoc test, ∗∗ = p< 0.01; NS = nonsignificant.(D) Representative immunoblots of CFs treatment.(E) Quantitation of expression of TNFAIP3, Col1a, Col3a, and CTGF. One-way ANOVA followed by Tukey’s post hoc test; ∗∗ = p<0.01, ∗∗∗ = p< 0.001. Data represented as mean ± SD. | PMC9932122 | gr7.jpg |
0.450269 | d4ad9ff3736a488486be48f73e22e5e7 | Restoration of TNFAIP3 ameliorated the DCM-Exo-induced fibrotic effect(A) Representative immunoblots of CFs treated with either CTL-Exos or DCM-Exos. DCM-Exo treatment significantly decreased TNFAIP3 expression. Student’s t test; ∗∗ = p <0.01.(B) Representative immunoblots of TNFAIP3, Col1a, Col3a, CTGF, and GAPDH detection in CFs treated with CTL-Exos, DCM-Exos, or overexpression of TNFAIP3.(C–F) Quantitation of protein expression. TNFAIP3 overexpression significantly reduced the expression of fibrotic markers. One-ANOVA followed by Tukey’s post hoc test; N= 3; ∗∗ = p< 0.01.(G) Schematic picture showing the working model of our study. Data represented as mean ± SD. | PMC9932122 | gr8.jpg |
0.449695 | f1937befe67f43e897951d084e4d22db | Architectures of (a) the Swin-CNN, (b) the Swin transformer block, and (c) the locality module. | PMC9932523 | JBO-028-026004-g001.jpg |
0.424202 | c0bc7a5193b14ea4aab1cd59b532aaf5 | Schematic of generating sinogram data. | PMC9932523 | JBO-028-026004-g002.jpg |
0.429757 | 9d80dbf0ea0f42d5b84ebcdf29871cb2 | Reconstructed images for different algorithms. (a) The ground truth images, (b)–(d) the results reconstructed by FBP, AUTOMAP, and Swin-CNN, respectively. The radius of fluorescein target from the top to bottom rows are 4, 6, and 8 mm, respectively. | PMC9932523 | JBO-028-026004-g003.jpg |
0.43643 | 67d9c24a27874a24bad6c753a2515c0d | Statistical results for 1000 samples. (a) MSE, (b) PSNR, and (c) PC. | PMC9932523 | JBO-028-026004-g004.jpg |
0.400484 | 034ee422fd104351b7cb314075197bd5 | Reconstructed images for different algorithms. (a) The ground truth images, (b)–(d) the results reconstructed by FBP, AUTOMAP, and Swin-CNN, respectively. The edge-to-edge distance of two targets from the top to bottom rows is 2, 4, 6, and 8 mm, respectively. | PMC9932523 | JBO-028-026004-g005.jpg |
0.530761 | b6350d00a3f1434aa281d1746b2c0d42 | Profiles along the red dotted line in Fig. 5 with different edge-to-edge distances. (a) 2 mm, (b) 4 mm, (c) 6 mm, and (d) 8 mm. | PMC9932523 | JBO-028-026004-g006.jpg |
0.45491 | 1774ed90806b474aa024da0fcceaf979 | Reconstruction results with different numbers of parallel beams. (a) Ground truth image, (b) and (c) 30 and 50 parallel beams for each angular, respectively. | PMC9932523 | JBO-028-026004-g007.jpg |
0.4443 | 32175d45272f4e8e9176c75800bcd03e | Schematic of data acquisition for physical phantom experiments. | PMC9932523 | JBO-028-026004-g008.jpg |
0.423913 | 7e5dcf29600649a293698ed377daf447 | Physical phantom results with single fluorescein target. (a) Sinograms for fluorescence emission wavelength, (b)–(d) reconstructed images by FBP, AUTOMAP, and Swin-CNN, respectively. | PMC9932523 | JBO-028-026004-g009.jpg |
0.483364 | f187e72c2d1544c895911f105e977ea8 | Physical phantom results with two fluorescein targets. (a) Sinograms for fluorescence emission wavelength, (b)–(d) reconstructed images by FBP, AUTOMAP, and Swin-CNN, respectively. | PMC9932523 | JBO-028-026004-g010.jpg |
0.464702 | c02c530665764c989d1562433e510364 | Fluorescent probe locally injected into the tumor (red box). | PMC9932523 | JBO-028-026004-g011.jpg |
0.386955 | d8002ee700d84d02ac55c45eae4e17e8 | In vivo experimental results. (a) Sinograms for different fluorescence emission wavelength, (b)–(d) reconstructed images by FBP, AUTOMAP, and Swin-CNN for different wavelengths, respectively. | PMC9932523 | JBO-028-026004-g012.jpg |
0.428815 | 33c88c80ce5a4306b023ab8013f6bd4c | Reconstruction results for the variant of the proposed Swin-CNN. (a)–(c) The results when three fluorescent targets were placed at different positions. | PMC9932523 | JBO-028-026004-g013.jpg |
0.547502 | b1c1753af4e74cda8d3ab9e3b811a8ae | Performance plot of training and validation dataset for the Swin-CNN. Insets show a zoom-in on the marked blue region. Black and red lines represent the loss of the training and validation datasets, respectively. | PMC9932523 | JBO-028-026004-g014.jpg |
0.425126 | a0ffb1b4cace481ab82de7c4a503ea93 | Results with the multilayer fully connected neural network (MFCNN). (a) The architecture of MFCNN, and (b)–(d) the reconstructed images with different numbers of targets. The red circles represent the real positions of targets. | PMC9932523 | JBO-028-026004-g015.jpg |
0.412489 | c08e396033fc440291d6d0595d264a86 | The graph shows hypothetical type II ROC curves of a hypothetical observer with a given metacognitive capacity, exposed to different levels of difficulty in the primary task, implying different levels of type I sensitivity (d’). Empirical metacognitive sensitivity (type II) will be constrained by type I task difficulty - the same observer will show different levels of type II sensitivities, depending on the difficult in the primary task. This is why we only considered studies that had approximately equal type I performance levels for both participant groups. See also Fleming and Dolan (2012). | PMC9932734 | fpsyg-14-991339-g001.jpg |
0.404781 | 2473765331214b9d9c9964c8c4b5a555 | PRISMA flowchart representing the process producing the final selection of studies included in the review. | PMC9932734 | fpsyg-14-991339-g002.jpg |
0.416124 | 9be496ce5f2743e18be8f733524e37a5 | Forest plot of the distribution of Hedges’ g effect sizes for metacognitive sensitivity across studies of samples with psychosis-related symptoms, based on a random- effects analysis, displaying effects by arranged sub-group of task domain, which was either perceptual (1) or non-perceptual (2). Lower metacognitive sensitivity in those with psychosis-related symptoms is indicated by a negative effect size. The summary effect size is indicated by a diamond marker, underneath the individual study effect sizes. | PMC9932734 | fpsyg-14-991339-g003.jpg |
0.427157 | ddf811c64f674982a370bb5151e202c8 | Funnel plot of the distribution of effect sizes by their standard error for studies of metacognition in the presence of psychosis-related symptoms. The vertical line indicates the value of the summary effect size. The area of the graph within the triangle represents the values which samples have 95% probability of showing if variance is homogeneous. Funnel plot of the distribution of effect sizes by their standard error for studies of metacognition in the presence of psychosis-related symptoms. | PMC9932734 | fpsyg-14-991339-g004.jpg |
0.444733 | 5f6c43c0eb7d4d1384e2995e2398e44d | Forest plot of the distribution of effect sizes for metacognitive sensitivity across studies of samples with non-psychotic symptoms of mental disorder, based on a random-effects analysis, displaying effects by arranged sub-group of task domain, which was either perceptual (1) or non-perceptual (2). Lower metacognitive sensitivity in those with non-psychotic symptoms of mental disorder is indicated by a negative effect size. The summary effect size is indicated by a diamond marker, underneath the individual study effect sizes. | PMC9932734 | fpsyg-14-991339-g005.jpg |
0.457746 | d3b000fc380d4ee1b4501967850a6022 | Funnel plot of effect sizes by standard error for studies of metacognition in the presence of non-psychotic symptoms of mental disorder. The vertical line indicates the value of the summary effect size. The area of the graph within the triangle represents the values which samples have 95% probability of showing if variance is homogeneous. | PMC9932734 | fpsyg-14-991339-g006.jpg |
0.48916 | 96ece360e78e4cf89947d43d067ff3f6 | The experimental procedure. Newborn rats were randomly divided into four groups: Con, Con + Gln, Hyp and Hyp + Gln. The Hyp and Hyp + Gln groups were placed in 85% O2 for 7 days, Con and Con + Gln groups were placed indoor (21% O2). Gln [1 μg/g (B)W] was administered intraperitoneally to newborn rats in the Con + Gln and Hyp + Gln groups at the same time each day, and the same volume of 0.9% NaCl was administered intraperitoneally to newborn rats in the Con and Hyp groups at the same time for 7 days. At P7, each group of randomly selected newborn rats for histopathological analysis (n = 3), determine the water content of brain tissue (n = 3) and protein analysis (n = 3). At P30, each group of neonatal rats (n = 6) began the Morris water maze experiment. Con, control; Hyp, hyperoxia; Gln, glutamine; P0, postnatal day 0; P7, postnatal day 7; P30, postnatal day 30; IHC, immunohistochemistry; WB, western blot; MWM, morris water maze experiment. | PMC9932780 | fphar-14-1096309-g001.jpg |
0.492232 | 5f003de80ddb4d2c8201ddd4eab0116e | Gln ameliorates hyperoxia-induced cerebral edema and brain tissue damage. (A) Morphological changes of CA1 area of hippocampus in each group. Scale bar = 100 µm, 50 µm (B) Morphological changes of CA3 area of hippocampus in each group. Scale bar = 100 µm, 50 µm (C) Changes of brain water content in each group. Con (72.11 ± 0.12), Con + Gln (71.94 ± 0.32), Hyp (77.41 ± 0.37), Hyp + Gln (74.66 ± 0.29). ###
p < 0.001 vs. the Con, **p < 0.01 vs. the Hyp (n = 3). p < 0.05 was considered statistically significant. Areas of severe histopathological changes were marked by black arrows. | PMC9932780 | fphar-14-1096309-g002.jpg |
0.435568 | d47d6a82f4104b6c8371a81defe4fe56 | Gln improves oxidative stress after hyperoxia injury. (A) Total ROS content in hippocampus. Con (5851.05 ± 90.01), Con + Gln (5880.49 ± 303.02), Hyp (8160.46 ± 380.24), Hyp + Gln (6899.07 ± 184.10). (B) MDA content in hippocampus. Con (3.50 ± 0.21), Con + Gln (3.30 ± 0.23), Hyp (13.23 ± 0.78), Hyp + Gln (8.13 ± 0.29). (C) GSH content in hippocampus. Con (44.03 ± 2.54), Con + Gln (43.47 ± 2.58), Hyp (27.60 ± 0.44), Hyp + Gln (32.43 ± 1.53). (D) SOD content in hippocampus. Con (133.37 ± 2.49), Con + Gln (132.87 ± 1.00), Hyp (98.77 ± 1.78), Hyp + Gln (110.70 ± 1.36) (n = 3). #
p < 0.05, ##
p < 0.01 vs. the Con, *p < 0.05, **p < 0.01 vs. the Hyp. p < 0.05 was considered statistically significant. | PMC9932780 | fphar-14-1096309-g003.jpg |
0.438028 | 5480ca158fc14c08bc590f03c1875e87 | Gln inhibits microglia activation caused by hyperoxia. (A) Activation of microglia in the hippocampus (CA1) of each group. (B) Activation of microglia in the hippocampus (CA3) of each group. (C) Quantification of activated microglia (CA1). Con (3.00 ± 0.58), Con + Gln (3.33 ± 0.33), Hyp (9.33 ± 0.88), Hyp + Gln (5.67 ± 0.67) (D) Quantification of activated microglia (CA3). Con (3.33 ± 0.33), Con + Gln (3.67 ± 0.33), Hyp (9.00 ± 0.58), Hyp + Gln (5.00 ± 0.58) (n = 3). ##
p < 0.01 vs. the Con. *p < 0.05, **p < 0.01 vs. the Hyp. p < 0.05 was considered statistically significant. Activated microglia were marked by black arrows. | PMC9932780 | fphar-14-1096309-g004.jpg |
0.411581 | 371152e0d9d44c04ad53b99e62944703 | Gln inhibits inflammation caused by hyperoxia. (A) TNF-α content in hippocampus. Con (2.73 ± 0.84), Con + Gln (2.69 ± 0.41), Hyp (9.70 ± 0.15), Hyp + Gln (5.67 ± 0.22). (B) IL-1β content in hippocampus. Con (2.65 ± 0.08), Con + Gln (2.68 ± 0.08), Hyp (11.16 ± 0.44), Hyp + Gln (7.33 ± 0.60). (C) IL-6 content in hippocampus. Con (2.38 ± 0.05), Con + Gln (2.42 ± 0.02), Hyp (7.71 ± 0.30), Hyp + Gln (4.94 ± 0.16) (n = 3). ####
p < 0.0001 vs. the Con, **p < 0.01, ***p < 0.001 vs. the Hyp. p < 0.05 was considered statistically significant. | PMC9932780 | fphar-14-1096309-g005.jpg |
0.446139 | 337d3c00bd1e48bab778aed41ad54d92 | Gln inhibits neuronal apoptosis in rats with hyperoxia-induced brain injury. (A) TUNEL staining of hippocampal tissue. Scale bar = 50 µm (B) Hippocampal Apoptosis Index (AI). Con (0.67 ± 0.33), Con + Gln (1.67 ± 0.33), Hyp (3.67 ± 0.33), Hyp + Gln (2.33 ± 0.33) (C) Representative images of Western blotting analysis of Bax, Bcl-2 and Caspase-3 of each group. (D) Ratio of Bcl-2 to Bax. Con (1.29 ± 0.10), Con + Gln (1.34 ± 0.13), Hyp (4.50 ± 0.79), Hyp + Gln (2.24 ± 0.20). (E) Caspase-3 content in hippocampus. Con (0.57 ± 0.04), Con + Gln (0.56 ± 0.06), Hyp (0.93 ± 0.05), Hyp + Gln (0.66 ± 0.01) (n = 3). #
p < 0.05, ##
p < 0.01 vs. the Con, *p < 0.05, **p < 0.01 vs. the Hyp. p < 0.05 was considered statistically significant. | PMC9932780 | fphar-14-1096309-g006.jpg |
0.423002 | d422c76fb58342c391fc491017b51787 | Gln increases BDNF, synapsin-1 and MBP expression in hippocampal tissue of rats with hyperoxia-induced brain injury. (A) Representative images of Western blotting analysis of synapsin-1, MBP and BDNF of each group. (B) Synapsin-1 content in hippocampus. Con (0.72 ± 0.09), Con + Gln (0.67 ± 0.06), Hyp (0.33 ± 0.05), Hyp + Gln (0.55 ± 0.03). (C) MBP content in hippocampus. Con (0.69 ± 0.11), Con + Gln (0.68 ± 0.09), Hyp (0.37 ± 0.01), Hyp + Gln (0.59 ± 0.04). (D) BDNF content in hippocampus. Con (0.99 ± 0.13), Con + Gln (0.98 ± 0.12), Hyp (00.55 ± 0.03), Hyp + Gln (0.88 ± 0.05). (n = 3). #
p < 0.05 vs. the Con, *p < 0.05, **p < 0.01 vs. the Hyp. p < 0.05 was considered statistically significant. | PMC9932780 | fphar-14-1096309-g007.jpg |
0.415063 | 27f55769281f4966945794fe3591db7b | Gln amelioration of hyperoxia-induced brain injury may be related to MKP-1/MAPK signaling pathway. (A) Representative images of Western blotting analysis of MKP-1, p-p38, p38, p-ERK, ERK, p-JNK, and JNK of each group. (B) Quantification of MKP-1. Con (0.28 ± 0.01), Con + Gln (0.28 ± 0.01), Hyp (0.32 ± 0.01), Hyp + Gln (0.84 ± 0.11). (C) Ratio of p-p38 to p38. Con (0.71 ± 0.00), Con + Gln (0.73 ± 0.05), Hyp (1.29 ± 0.17), Hyp + Gln (0.77 ± 0.02). (D) Ratio of p-ERK to ERK. Con (0.53 ± 0.04), Con + Gln (0.53 ± 0.03), Hyp (0.83 ± 0.04), Hyp + Gln (0.66 ± 0.04). (E) Ratio of p-JNK to JNK. Con (0.93 ± 0.03), Con + Gln (0.91 ± 0.04), Hyp (1.23 ± 0.01), Hyp + Gln (1.03 ± 0.02). (n = 3). #
p < 0.05, ##
p < 0.01 vs. the Con, *p < 0.05, **p < 0.01 vs. the Hyp. p < 0.05 was considered statistically significant. | PMC9932780 | fphar-14-1096309-g008.jpg |
0.400139 | 34a4debf82a643feafb0860ed9591020 | Gln ameliorates distant neurobehavioral deficits in rats with hyperoxia-induced brain injury. (A) Latency to escape in MWM. Con (101.96 ± 7.86, 21.63 ± 4.05, 18.07 ± 3.71, 12.94 ± 3.68), Con + Gln (101.76 ± 10.43, 23.10 ± 4.09, 18.85 ± 4.16, 12.66 ± 3.85), Hyp (110.78 ± 4.19, 70.39 ± 13.85, 58.48 ± 8.53, 47.28 ± 4.24), Hyp + Gln (102.54 ± 8.82, 58.89 ± 8.76, 35.25 ± 5.99, 26.22 ± 4.50). (B) Times crossing platform in MWM. Con (6.50 ± 0.62), Con + Gln (6.17 ± 0.70), Hyp (1.50 ± 0.56), Hyp + Gln (4.00 ± 0.37). (C) Distance spend in the target quarter in MWM. Con (58.97 ± 5.46), Con + Gln (47.82 ± 4.06), Hyp (34.12 ± 4.42), Hyp + Gln (52.19 ± 2.92). (D) Swim speed in MWM. Con (23.04 ± 1.22), Con + Gln (23.39 ± 1.58), Hyp (21.95 ± 2.37), Hyp + Gln (22.96 ± 0.86) (n = 6). ##
p < 0.01, ###
p < 0.001 vs. the Con, *p < 0.05, **p < 0.01 vs. the Hyp. p < 0.05 was considered statistically significant. | PMC9932780 | fphar-14-1096309-g009.jpg |
0.430291 | f4618abacba94b08bb0f51531dd742ea | Graphical abstract. Hyperoxia can lead to behavioral abnormalities and neurocognitive and learning deficits in newborn rats, which is thought to be related to damage to hippocampal neurons caused by oxidative stress, inflammation, apoptosis, and microglial overactivation. Gln may induce MKP-1 and thereby inhibit activation of the MAPK signaling pathway, leading to a reduction in oxidative stress, inflammation, and apoptosis in cells and attenuating hyperoxia-induced damage to cerebral tissue, and improve learning and memory dysfunction. | PMC9932780 | fphar-14-1096309-g010.jpg |
0.442226 | 3f2bcecfba884469bcd4c6f84e269b47 | Transcriptomic characterisation of circulating cDC2s from patients with pSS and nSS. RNA sequencing of circulating cDC2s was performed independently for both discovery and replication cohorts. Venn diagrams show the overlap of the DEGs with a nominal p value of <0.05 between any of the three groups for the discovery cohort (A) and the replication cohort (B). Scatter plots show the FC (log2) of the DEGs between the two cohorts for the different comparisons, pSS versus HC (C), nSS versus HC (D) and pSS versus nSS (E). Volcano plots display the relationship between the FC (log2, x-axis) and the nominal p value (−log10, y-axis) of the DEGs consistently downregulated or upregulated in both cohorts for each comparison (F–H). cDC2, type 2 conventional dendritic cell; DEG, differentially expressed gene; FC, fold change; HC, healthy control; nSS, non-Sjögren’s sicca; pSS, primary Sjögren’s syndrome. | PMC9933176 | ard-2022-222728f01.jpg |
0.390682 | db5b747ecaca45d99bc3a85d7721330f | Transcriptomic profile and protein validation of cDC2s from patients with pSS display altered expression of key molecules involved in cell trafficking, activation and interferon signalling. Heatmap visualisation of the top 100 DEGs (50 upregulated and 50 downregulated genes, rows) across the two cohorts (discovery and replication) and the studied groups (HC, nSS and pSS; columns) clustered by Euclidean distance and Ward’s method (A). Dot plots depict the expression of selected DEGs in discovery and replication cohorts in both HCs and patients with pSS (B). Protein expression of the selected DEGs was assessed on cDC2s by flow cytometry in HCs (n=22) and patients with pSS (n=22) (C). *, ** and *** represent nominal p values of <0.05, <0.01 and <0.001, respectively. cDC2, type 2 conventional dendritic cell; DEG, differentially expressed gene; HC, healthy control; nSS, non-Sjögren’s sicca; pSS, primary Sjögren’s syndrome. | PMC9933176 | ard-2022-222728f02.jpg |
0.421109 | 2cbf96a16e3b4aea9fd5e40006ad86a9 | cDC2s from patients with pSS are functionally different in interferon-associated pathways and in antigen processing. Reactome pathway enrichment analysis was used for functional annotation of the DEGs between pSS versus HC (selected in figure 1F). The top significantly enriched reactome pathways are depicted. The x-axis shows the number of DEGs found within the pathway over the total number of pathway components (ratio); dot size depicts the number of genes used for enrichment and colour indicates the statistical significance (A). Isolated PBMCs were incubated with DQ–BSA for 10 min and antigen processing was followed for the indicated time points (B). Representative histograms (C) and quantification (D) of processed DQ-BSA, represented as MFI normalised to T=0, in HC (n=11) and non-treated patients with pSS (n=6) at different time points determined by flow cytometry. Quantification of DQ-BSA processing in patients with pSS with (pSS-SSA+, n=4) or without (pSS-SSA−, n=2) anti-SSA antibodies (E). Violin plots depict TAP1, LNPEP and PSMA3 gene expressions in HC and patients with pSS from discovery and replication cohorts combined (F). cDC2, type 2 conventional dendritic cell; DEG, differentially expressed gene; DQ-BSA, fluorescent BODIPY dye labelled bovine serum albumin HC, healthy control; MFI, median fluorescence intensity; PBMC, peripheral blood mononuclear cell; pSS, primary Sjögren’s syndrome. | PMC9933176 | ard-2022-222728f03.jpg |
0.448711 | dbfde62c922b4cd8a44dc7e603802dc6 | Enhanced uptake of antigen and apoptotic cells by pSS cDC2s is associated with autoimmunity and type I IFN. PBMCs from HC and patients with pSS were incubated with AF647–BSA for the indicated time points and the uptake by cDC2s, represented as MFI, was assessed by flow cytometry (A). Representative histograms (B) and quantification of BSA uptake by cDC2s of HCs (n=11) and patients with pSS (n=14) (C) and patients with pSS with (pSS-SSA+, n=10) or without (pSS-SSA−, n=4) anti-SSA antibodies (D). IFN signature calculated as the mean Z-score of five IFN-induced genes was determined by qPCR in HC (n=13), pSS-SSA− (n=5) and pSS-SSA+ (n=10) (E). HC-PBMCs were primed for 3 hours without (medium) or with IFN-α, exposed to AF647–BSA and chased for the indicated times by flow cytometry (F). The effect of IFN-α priming on BSA uptake was analysed in HC cDC2s (n=5) by flow cytometry (G). Quantification of BSA uptake by cDC2s of patients with pSS with (pSS-IFN+, n=9) or without (pSS-IFN−, n=3) IFN signature (H). Apoptotic CFSE labelled HSG-epithelial cells were added to PBMCs from HCs (n=9) and patients with pSS (n=13) at a 1:1 ratio for 120 min. Representative histogram (I) and quantification of apoptotic cell uptake of cDC2s from HCs and patients with pSS (J) and pSS-SSA− (n=4) and pSS-SSA+ (n=9) (K) measured by flow cytometry. HC-PBMCs were primed for 3 hours with IFN-α or without (medium) and exposed to apoptotic CFSE labelled HSG-epithelial cells for 2 hours. The effect of IFN-α priming on apoptotic cell uptake was analysed in HC cDC2s (n=4) by flow cytometry (L). Results are represented as mean±SEM. *, ** and *** represent p values of <0.05, <0.01 and <0.001, respectively. cDC2, type 2 conventional dendritic cell; HC, healthy control; HSG, human salivary gland; IFN, interferon; MFI, median fluorescence intensity; PBMC, peripheral blood mononuclear cell; pSS, primary Sjögren’s syndrome; qPCR, quantitative PCR. | PMC9933176 | ard-2022-222728f04.jpg |
0.438807 | 527f6dae38c145aa95cb3a1d640f4242 | cDC2s from patients with pSS efficiently induce CD4+ T-cell proliferation with a tissue homing signature. Total CD4+ T cells from HCs were cultured alone (n=3) or cocultured either with cDC2s from HCs (n=3) or patients with pSS (n=3) at a 5:1 ratio (T cells:cDC2s) for 3 days (A). The frequency of CD4+ T-cell subsets (naïve; CM, EM and EF) was assessed by flow cytometry directly after cell isolation (B). Quantification (C) and representative flow cytometry dot plot (D) of proliferating CD4+ T cells measured by flow cytometry at day 3. Representative histograms of CXCR3, CXCR5 and CCR4 expression on proliferating CD4+ T cells (E) and quantification of the percentage of chemokine receptor expressing CD4+ T cells measured by flow cytometry (F). TNF-α and IFN-γ production during T cells: cDC2s coculture was measured by ELISA (G). cDC2, type 2 conventional dendritic cell; CM, central memory; EF, effector; EM, effector memory; HC, healthy control; IFN-γ, interferon gamma; pSS, primary Sjögren’s syndrome; TNF-α, tumour necrosis factor alpha. | PMC9933176 | ard-2022-222728f05.jpg |
0.510518 | 2c404e04a7d143f09617acd0a13bf02f | Cryo-EM structures of the CLPB double-heptamer in the apo-state and the CLPBE425Q double-hexamer in the substrate-bound state.(A) Domain organization of H. sapiens CLPB. CLPB is composed of an MTS, a short hydrophobic stretch (S), an LH, 4 ankyrin-repeat (ANK) motifs, an NBD, and a CTD. (B) Representative 2D classification averages of CLPB and CLPBE425Q datasets. (C, D) The density maps of the double-heptamer (C) and double-hexamer (D), superimposed with the models of CLPB. The density maps are shown in the side and top (ATPase ring) views. The higher-order oligomer is mediated by ANK domains. The substrate was labeled as yellow. LH, linker helix; NBD, nucleotide-binding domain. | PMC9934407 | pbio.3001987.g001.jpg |
0.399359 | 515d8d3924bf4ddfbcca30e90c95a94d | The CLPB double-heptamers transform into double-hexamers upon substrate binding.(A) CLPB complexes purified from HEK293 cells form double-oligomeric state. Representative nsEM images (left) and 2D classification averages of nsEM particles (right) of CLPB and CLPBE425Q from HEK-293T cells. (B) The proportion of the hexameric and heptameric top views in the CLPB-AMPPNP, CLPBE425Q-ATP, CLPBisoform1-AMPPNP, CLPB-ATPγS, and CLPB+Casein-ATPγS datasets (S2 Data). (C–G) Representative top views of 2D classification averages of CLPB-AMPPNP (C), CLPBE425Q-ATP (D), CLPBisoform1-AMPPNP (E), CLPB-ATPγS (F), and CLPB+Casein-ATPγS (G) datasets. The top views with hexameric feature are indicated by red boxes. nsEM, negative staining electron microscopy. | PMC9934407 | pbio.3001987.g002.jpg |
0.394071 | 7ed7cb17224543d691bd456dec46b56b | The ANK domain is essential for the disaggregase activity of CLPB.(A) X-ray crystallography structure and AlphaFold predicted model of the ANK domain. The RMSD between these 2 structures is 2.6 Å. (B) The hydrophobic surfaces of the ANK domain. Two hydrophobic patches were found in the unique insertion. (C) The ATPase assay of CLPB, CLPBΔ201–232, and CLPBisoform1. ATPase activity was compared to CLPB (N = 3, individual data points shown as dots, bars show mean ± SD) (S4 Data). (D) The disaggregase activity assay of CLPB, CLPBΔ201–232, and CLPBisoform1. Disaggregase activity was compared to CLPB (N = 3, individual data points shown as dots, bars show mean ± SD, *p < 0.05) (S4 Data). (E) ATPase assay of CLPB, CLPBR178E, and CLPBR227E (S4 Data). (F) Disaggregase activity assay of CLPB, CLPBR178E, and CLPBR227E. Results show that the disaggregase activities of CLPBR178E and CLPBR227E are reduced by 70%–80% (N = 3, individual data points shown as dots, bars show mean ± SD, **p < 0.01) (S4 Data). (G) The ANK domain dimer interface. One is the AM1-AM2 and the other is the second helix of the insertion. Two positively charged residues (R178 and R227) are labeled as black dashed circles on the ANK surface electrostatic potential. | PMC9934407 | pbio.3001987.g003.jpg |
0.419242 | 531c0c22ce054913a47801c50ab002a1 | Cryo-EM characterization of the NBD helical structures of CLPB.(A–C) Density maps of the NBD hexamer (A), heptamer (B), and nonamer (C), respectively. Protomers are painted in different colors. (D–F) Distances along the central substrate between the PL residue Y400 of P1 and P6 in the hexamer (D), heptamer (E), and nonamer (F). The axial rise of P6 relatively to P1 are labeled. NBD, nucleotide-binding domain; PL, pore-loop. | PMC9934407 | pbio.3001987.g004.jpg |
0.440017 | 98d2ce181d764e5aa5566421b8da1317 | Structure of the NBD nonamer in processing a peptide substrate.(A) Density map of the NBD nonamer in the substrate-processing state. Nine protomers are indicated as P1 to P9 and painted in different colors. The central substrate is colored yellow. (B) The spiral configuration of the PLs of CLPB protomers around the substrate in the central channel. PL-Is and PL-IIs are shown in the left and right panels, respectively. While the conserved PL-Is (G399-Y400-V401-G402) directly interact with the substrate, the PL-IIs (E386-R387-H388) situate in slightly larger distances from the substrate. (C, D) Magnified view of the interactions between the PL-I of P3, P4, and P5 and the backbone of substrate. The substrate could be modeled in both directions, N to C or C to N. The potential hydrogen bonds are indicated by dashed lines and the distances are labeled. (E) Magnified view of the conserved ATP-binding pocket of CLPB. Functionally important residues of Walker A motif (K357, T358), Walker B motif (E425), sensor-1 (N466), sensor-2 (R590), arginine finger (R531), and the conserved residue I317, I318. Atomic model and density map are shown in the left and right panels, respectively. NBD, nucleotide-binding domain; PL, pore-loop. | PMC9934407 | pbio.3001987.g005.jpg |
0.417305 | 4015bf82f81547c6b9beaa709a8fd3a4 | The mitochondrial interactome of the ANK domain.(A) HEK-293F cells expressing the MTS-ANK-HA or MTS-ANK-Strep constructs were subjected to pulldown experiments with Strep resins. Precipitates were analyzed by SDS-PAGE, Coomassie blue staining, and MS. (B) Volcano plot showing the mitochondrial proteins co-precipitated with MTS-ANK-Strep. A total of 935 proteins that were enriched in the MTS-ANK-Strep are labeled in light red. The potential substrates, previously reported to be most affected by CLPB-knockout, are highlighted in red. A relatively stringent criterion (fold-change > 4 and p-value < 0.01) were used for enrichment analysis (3 biological replicates), indicating with blue dashed lines (S5 Data). (C) Top 20 proteins in OM, IMS, and IM are listed based on the ranking of protein abundances (S4 Table). (D) HEK-293F cells expressing the MTS-ANK-Strep, MTS-ANKΔloop-Strep, and MTS-ANKisoform1-Strep constructs were subjected to pulldown experiments with Strep resins. Precipitates were analyzed by SDS-PAGE, Coomassie blue staining, and MS. (E, F) Volcano plot showing the fold change of the OM, IMS, and IM mitochondrial proteins in MTS-ANK-Strep compared to MTS-ANKΔloop-Strep (E) or MTS-ANKisoform1-Strep (F). Proteins in the top 20 list (C) were heighted in red (S6 and S7 Data). IMS, intermembrane space; MS, mass spectrometry; MTS, mitochondrial targeting signal. | PMC9934407 | pbio.3001987.g006.jpg |
0.504893 | 09fcab6e2c1c44388f16a8cd1545b3f4 | The disease-related mutations of CLPB in 3-MGA and SCN.(A) 3-MGA-related mutations in the interface of adjacent protomers. (B) 3-MGA-related mutations within the large and small subdomain of the ATPase domain. (C) 3-MGA-related mutations in the ANK domain. (D) SCN-related mutations in the ATP-binding pocket. Residues on the positions of these mutations are highlighted in magenta or red sphere models. ATP molecule is highlighted in stick models. SCN, severe congenital neutropenia; 3-MGA, 3-methylglutaconic aciduria. | PMC9934407 | pbio.3001987.g007.jpg |
0.434818 | 739b9b107a164104a3113d542c8dd832 | Glycolytic rate, hypoxia inducible factor (HIF)-1α, and glycolytic enzymes were upregulated in transforming growth factor (TGF)-β1-treated nasal fibroblast.(a) Extracellular acidification rate (ECAR) of fibroblast treated with or without TGF-β1 was measured using XFe96; (b) Gene expression of HIF-1α, hexokinase (HK) 1, HK2, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB) 3, and PFKFB4 were confirmed by RT-PCR; and (c) protein levels were detected by Western blotting. *p < 0.05, **p < 0.01, ***p < 0.001 compared with the control using one-way ANOVA test. | PMC9934430 | pone.0281640.g001.jpg |
0.424738 | c02b4da01f4941c3b9da5b9117856029 | 2-Deoxy-D-glucose (2-DG) and 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3-PO) downregulated α-SMA (SMA) and fibronectin expression in TGF-β1-treated nasal fibroblasts.(a, c) Gene expression of α-SMA and fibronectin was confirmed by RT-PCR; and (b, d) protein levels were detected by Western blotting. ***p < 0.001 compared with control by one-way ANOVA test, †p < 0.05, ††p < 0.01, †††p < 0.001 compared with TGF-β1 using one-way ANOVA test. | PMC9934430 | pone.0281640.g002.jpg |
0.397751 | 25d40894eed245a58ddca3c3eaa5a253 | PX-478 decreased the expression of HIF-1α and glycolytic enzymes, and downregulated glycolytic flux in TGF-β1-treated nasal fibroblast.(a) Gene expression levels of HIF-1α, HK2, PFKFB3, and PFKFB4 were confirmed by RT-PCR; and (b) Protein levels were detected by Western blotting; (c) Protein expression and localization of HIF-1α, HK2 (Green), PFKFB3, PFKFB4 (red), and DAPI (blue) were determined by immunofluorescence staining; (d) ECAR was measured using XFe96. *p < 0.05 and ***p < 0.001 compared with control using one-way ANOVA test, †p < 0.05, ††p < 0.01, and †††p < 0.001 compared with TGF-β1 using the one-way ANOVA test. | PMC9934430 | pone.0281640.g003.jpg |
0.404719 | d19e36cd77e44dba976abef0963edbbc | PX-478 inhibited expression of α-SMA, fibronectin, and collagen.(a) Gene expressions of α-SMA and fibronectin were confirmed by RT-PCR; and (b) Protein levels were detected by Western blotting. (c) Immunofluorescence was detected using a confocal laser scanning microscope. α-SMA (red), fibronectin (green), and DAPI (blue); (d) Total collagen production was measured using Sircol soluble collagen assay; (e) Contractile activity was measured using a collagen gel contraction assay, and the collagen gel areas were measured using an Image J analyzer. ***p < 0.001 compared with control by one-way ANOVA test, †p < 0.05, †††p < 0.001 compared with TGF-β1 by one-way ANOVA test. | PMC9934430 | pone.0281640.g004.jpg |
0.469668 | 99d07dd15234416ba43da768bdf1a883 | Gene set enrichment analysis (GSEA) were analyzed using transcripts of chronic rhinosinusitis (CRS) patients and TGF-β1-treated nasal fibroblast.(a) Normalized enrichment scores (NES) of the top 20 positively enriched gene sets, red is glycolysis and ECM REGULATORS gene sets in CRS patients. NES, p-value and false discovery rate (FDR) of glycolysis gene set and ECM REGULATORS gene set in CRS patients. NES of the top 20 positively enriched gene sets in TGF-β1-treated nasal fibroblast. NES, p-value and FDR of glycolysis gene set and ECM REGULATORS gene set in TGF-β1-treated nasal fibroblast. | PMC9934430 | pone.0281640.g005.jpg |
0.416692 | fa3fc46d388c42388407537faa753aff | Effects of acetylation-deficient p534KR on systolic function and cardiac hypertrophy. A, Representative immunoblots and quantitative analysis of p53, β-myosin heavy chain (β-MHC), acetyl-p53, brain natriuretic peptide (BNP), β-actin, and GAPDH in the indicated mouse hearts subjected to either sham or transverse aortic constriction (TAC) procedure for eight weeks (n=3–4 or 6–8). B, Left ventricular (LV) ejection fraction (EF) and fractional shortening (FS) measured by echocardiography in the indicated groups (n=6–10). C, Ratio of heart weight to tibia length in the indicated groups (n=6–10). D, LV mass measured and calculated by echocardiography in the indicated groups (n=6–10). E, Representative images of wheat germ agglutinin–stained frozen heart sections in the indicated groups. (n=4–5). A minimum of 100 cardiomyocytes from each LV section of each mouse was measured. Bar=25 μm. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. | PMC9934706 | nihpp-2023.02.08.527691v1-f0001.jpg |
0.407337 | ba15fb8fa78c4fe3ac9bf58ffffbb2b2 | Effects of acetylation-deficient p534KR on diastolic function, cardiac fibrosis, and apoptosis. A, Representative pulsed-wave Doppler and tissue Doppler images from an apical 4-chamber view of WT and p534KR mice subjected to either sham or TAC procedure for eight weeks and ratio of the peak velocity of early (E) to late (A) filling of mitral inflow (E/A) in the indicated groups (n=6–9). The ratio of E to the tissue motion velocity in early diastole (e’) was calculated in the indicated groups (n=6–10). B, Representative images of Picrosirius red-stained paraffin-embedded heart sections and quantification of the percentage of interstitial fibrosis area in the indicated groups (n=3–5). Bar=50 μm. C, Representative immunoblots and quantitative analysis of PDGFR-β, FSP-1, collagen-1, SERCA2 ATPase, β-actin, and GAPDH in the indicated mouse hearts (n=3–4 or 6–8). D, Representative images of staining of SERCA2α and DAPI in frozen heart sections. E, Representative images of TUNEL-stained frozen heart sections and quantification of the number of TUNEL-positive cells (green)/field in the indicated groups (n=4). 5–15 randomly selected fields per LV section of each mouse was measured. Bar=25 μm. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. | PMC9934706 | nihpp-2023.02.08.527691v1-f0002.jpg |
0.406054 | 65f809ff4c7c447697d6f337405ad13d | Acetylation-deficient p534KR preserves coronary vasculature and coronary flow reserve (CFR). A, Representative images of Isolectin B4 (IB4, green; DAPI stains the nuclei, blue)-stained frozen heart sections and quantification of the number of capillaries/100 nuclei in the indicated groups (n=4–5). Bar=50 μm. B, Representative immunoblots and quantitative analysis of HIF-1α, HO-1, Ang-1, VEGF, VCAM-1, and GAPDH in the indicated mouse hearts (n=6–8). C, Representative images of co-staining of cardiomyocyte marker Troponin-T, endothelial marker IB4, and myofibroblast marker FSP-1 with HIF-1α in frozen heart sections. D, Representative pulsed-wave Doppler images of the proximal left coronary arteries and CFR of WT and p534KR mice subjected to either sham or TAC procedure for eight weeks. CFR was calculated as the ratio of hyperemic peak diastolic flow velocity (2.5% isoflurane) to baseline peak diastolic flow velocity (1% isoflurane) in the indicated groups (n=6–8). *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. | PMC9934706 | nihpp-2023.02.08.527691v1-f0003.jpg |
0.446381 | 52721c688b064727a38df0087c059a28 | Acetylation-deficient p534KR increases cardiac glucose transporters and glycolytic function. A, Representative immunoblots and quantitative analysis of PFK-1, GLUT-1, GLUT-4, and GAPDH in the indicated groups. B, Cardiac F2,6-BP level was determined by the coupled-enzymatic assay and expressed as the fold change to the WT sham group. n=3–4. C, Cardiac PFK-1 activity was determined by the coupled-enzymatic assay and expressed as the OD340nm/min/mg protein. n=5–9. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. | PMC9934706 | nihpp-2023.02.08.527691v1-f0004.jpg |
0.477892 | ca6cb239ede248118fbeefd8aafd37e4 | Acetylation-deficient p534KR increases glycolysis in MAECs and aortic sprouting. A, Cell proliferation of p534KR MAECs was significantly higher than that of the WT MAECs, as measured by MTT assay. n=8–10. B, Glycolysis stress test and extracellular flux analysis of glycolysis, glycolytic capacity, and glycolytic reserve in MAECs isolated from p534KR and WT mice. n=4–5. C, Mitochondrial stress test and extracellular flux analysis of mitochondrial basal and maximal respiration and ATP production in MAECs isolated from p534KR and WT mice. n=5. D, Representative images of the aortic ring sprouting assay at day 5 of incubation and quantification of the sprouting area in the indicated groups (n=9–13). Bar=250 μm. **p<0.01, ***p<0.001, ****p<0.0001. | PMC9934706 | nihpp-2023.02.08.527691v1-f0005.jpg |
0.422842 | f984d1d761a847058c5a114c53dd899f | Effects of acetylation-deficient p534KR on CFR and cardiac dysfunction in SIRT3KO mice. A, Representative pulsed-wave Doppler images of the proximal left coronary arteries and CFR of WT, SIRT3KO, p534KR and p534KR/SIRT3KO mice. CFR was calculated as the ratio of hyperemic peak diastolic flow velocity (2.5% isoflurane) to baseline peak diastolic flow velocity (1% isoflurane) in the indicated groups (n=7–11). B, Left ventricular (LV) ejection fraction (EF) and fractional shortening (FS) measured by echocardiography in the indicated groups (n=8–10). C, Representative pulsed-wave Doppler and tissue Doppler images from an apical 4-chamber view in the indicated groups. The diastolic function isovolumic relaxation time (IVRT), myocardial performance index (MPI), and ratio of E to the tissue motion velocity in early diastole (e’) was calculated in the indicated groups (n= 5–9). *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. | PMC9934706 | nihpp-2023.02.08.527691v1-f0006.jpg |
0.474291 | 1bdb664ac02b4c1f84e5ea7c2587e092 | The effect of time on PHMB associated membrane permeabilisation. Fungi were treated with PHMB [MIC50] and SYTOX Green (8 µM). Fluorescence profiles for each species treated with PHMB are shown, with positive (heat killed; triton x-114) and negative (Terbinafine; untreated) controls. (A) S. cerevisiae heat-killed or treated with 1 µg/ml PHMB, 0.84 µg/ml Terbinafine, 1.17 µg/ml Triton x-114 (B) C. albicans R1 heat-killed or treated with 1 µg/ml PHMB, 0.84 µg/ml Terbinafine, 1.17 µg/ml Triton x-114 (C) F. oxysporum heat-killed or treated with 2 µg/ml PHMB, 3.84 µg/ml Terbinafine, 4.7 µg/ml Triton x-114 (D) P. glabrum heat-killed or treated with 2 µg/ml PHMB, 1.7 µg/ml Terbinafine, 2.5 µg/ml Triton x-114. | PMC9935507 | 41598_2023_29756_Fig1_HTML.jpg |
0.538289 | 6d129c36af824c3280fac9cb8f1df86f | Fluorescence imaging showing the effect of PHMB on membrane permeability to SYTOX Green. SYTOX Green (8 µM) and varying PHMB concentrations were added to growth medium before 3 h incubation with S. cerevisiae. Live cell images were merged following imaging by phase contrast and green bandpass filter. Scale bar = 10 µm. | PMC9935507 | 41598_2023_29756_Fig2_HTML.jpg |
0.410937 | 676e6743c70f403ba8864f0946d7d2c6 | Fluorescence imaging showing the reduction of Con A- membrane fluorescence following exposure to increasing concentrations of PHMB. (A) S. cerevisiae cultures were treated with PHMB-rhodamine at 4 µg/ml and 8 µg/ml (B) C. albicans cultures were treated with 8 µg/ml and 12 µg/ml. Cultures were incubated at room temperature for 4 h and counter-stained with Con A-Alexa Fluor 488. Untreated control = growth media only. Images show quenching of membrane fluorescence intensity with increasing PHMB concentration. Graphs show measured fluorescence intensity of sampled cells (n = 20) at four symmetrical points along the cell membrane and averaged (mean ± SD). Membrane fluorescence was analysed by RM One-way ANOVA followed by Tukey's multiple comparison test. | PMC9935507 | 41598_2023_29756_Fig3_HTML.jpg |
0.481683 | 1754b6201c544fc1a15d53cb36bf2c40 | The effect of PHMB concentration on fungal cell membrane permeabilisation. SYTOX Green (8 µM) and PHMB concentrations were added to fungi (1 × 104 cells/ml) in RPMI-1640, 2% glucose. Samples were incubated for 3 h, with fluorescence measurements taken after the incubation period. (A) P. glabrum (B) F. oxysporum (C) C. albicans (D) S. cerevisiae. Yellow arrow = MIC50 concentration. Blue arrow = MIC90 concentration. | PMC9935507 | 41598_2023_29756_Fig4_HTML.jpg |
0.458506 | 0b132225460e4e59a8a2d9acab3b3121 | PHMB uptake rate by F. oxysporum, S. cerevisiae and C. albicans. The uptake was calculated to be 0.04 µg/ml min−1, 0.03 µg/ml min−1, 0.05 µg/ml min−1 respectively at concentrations of 8 µg/ml and above. (A) F. oxysporum, (B) C. albicans, (C)
S. cerevisiae. Red line = MIC90 concentration , Yellow line = MIC50 concentration, Blue line = linear regression. | PMC9935507 | 41598_2023_29756_Fig5_HTML.jpg |