nopperl/pmc-image-text · Datasets at Hugging Face

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0.418239	d41f3fba0bd04d2fa19745fe059af8e8	Progression-free survival in three groups. Kaplan–Meier estimates. log Rank: 0.006.	PMC9105143	cancers-14-02108-g002.jpg
0.427023	f02354d105394c66a16999a6c4441488	Overview of how the feature and baseline windows were chosen, for the three different groups of features by modality. This calculation would result in one feature vector, for the next the windows would all be shifted by an interval of T = 2 s to the right. Abscissa not to scale.	PMC9105312	sensors-22-03318-g001.jpg
0.4176	4d9f686ce6704e8585bb98eeaafa7628	Data set flowchart of the participant selection process. KCL: King’s College London; UKF: University Medical Center Freiburg; E4: Empatica E4 wrist-worn wearable device.	PMC9105312	sensors-22-03318-g002.jpg
0.417077	1c0720fae67a4f81a703edf34d133adb	Selection of examples of true positive detections for each of the three participants in the intra-subject evaluation. Seizures shown are: (a) UKF1-4; (b) UKF2-3; (c) and KCL1-3 (see Table A1). Due to the grace period of 2 minutes around a seizure event, the detection for KCL1-3 counts as a true positive. Each plot of a seizure shows the raw ACC signal (top), the raw EDA signal and feature 2b (middle), and the estimated heart rate and signal quality index of the BVP signal (bottom). The regions highlighted in red mark the ground truth as labeled by experts, and those highlighted in green mark the seizure intervals, as predicted by the respective model, trained on the data of all the other seizures of the participant. The seizure onset and offset are additionally marked by the black vertical bars. All signals shown are normalized between −1 to 1 only for these plots. The original value ranges before normalization can be found in Table A3.	PMC9105312	sensors-22-03318-g003.jpg
0.440799	f5233f3c3dc044e591a18dc007679780	Feature importance scores per intra-subject evaluation for the seizure detection models of the three selected participants: (a) UKF1; (b) UKF2; (c) KCL1 (see Table A2); (d) Feature importance scores of the model resulting from training the GTBM model on the seizure data of all three inter-subject training participants. Blue, red, and yellow bars show the importance scores for the features grouped by biosignal modality ACC, EDA, and BVP, respectively. Horizontal lines mark the mean scores of the groups. The ordinate is unitless; the scores can be interpreted qualitatively. The feature labels correspond to the listing of features in the Materials and Methods.	PMC9105312	sensors-22-03318-g004.jpg
0.452813	ce5533fa23834c928fd3cb4af08198b4	Seizure UKF2-2, a false negative. Compare also to Figure 3. Data shown from top to bottom: raw ACC, raw EDA and feature 2b, heart rate and BVP signal quality index. The red overlay is the seizure ground truth. The seizure onset and offset are additionally marked by the black vertical bars. All signals shown are normalized between −1 to 1 only for these plots. The original value ranges before normalization can be found in Table A3.	PMC9105312	sensors-22-03318-g005.jpg
0.437536	51b479ed69ae4b1da62120b435d63589	The Empatica E4 wrist-worn wearable device used in this study (left), and the Android phone application that connects to the wearable via Bluetooth and records the data stream (right).	PMC9105312	sensors-22-03318-g0A1.jpg
0.462142	6a5a3a64bd1646edb0596fa1ed67d43f	Mediating effect of empathic concern between workplace spirituality and employee wellbeing as a function of organizational politics. Moderated mediation model (all coefficients are standardized). Here means p < 0.01 and * means p < 0.001.	PMC9105451	fpsyg-13-881675-g001.jpg
0.380249	aeaae43f6b464212b88b30d7a335507f	Graphical illustration of the moderation effect of organizational politics on the relationship between workplace spirituality and employee wellbeing; and empathic concern and employee wellbeing.	PMC9105451	fpsyg-13-881675-g002.jpg
0.418058	b679eaf6de4740fb880ac7b0b369781c	A 42-year-old man with AMF. On T1-weighted images, the tumor reveals low signal intensity but high signal intensity in some circuitous strips (A). On coronal fat-saturated T2-weighted images and sagittal T2-weighted images, the tumor is well-marginated with high inhomogeneous signal intensity (B,C). DWI shows a low-signal tumor (D). The images of contrast-enhanced MRI show a heterogeneous and distinctly enhanced mass. As time goes on, the enhancement of the tumor is more obvious (E,F).	PMC9106126	fsurg-09-808488-g0001.jpg
0.492591	4e307f0e38a94f65bf8c9a4d2b7b47d3	Hematoxylin-eosin (HE) staining and immunohistochemistry of the tumor. Thin-walled blood vessels surrounded by several spindle cells can be seen in the images (A,B). Image A and Image B represent 50× and 100×, respectively. The desmin is positive in immunohistochemistry (C).	PMC9106126	fsurg-09-808488-g0002.jpg
0.435418	976238b3e3e54463b21dd1fafc249acf	Orthopantomogram showing a well-defined multilocular radiolucency with sclerotic border in the right molar-ramus region of the mandible distal to the impacted third molar	PMC9106234	JOMFP-26-130-g001.jpg
0.472135	9139c51c8a324e94abe2b141a710c1f0	A cystic lesion with epithelial lining and fibrous connective tissue capsule (H & E, ×4)	PMC9106234	JOMFP-26-130-g002.jpg
0.414247	186e20d88a8d4dcbb6fe8e03b2dfe69d	The epithelium revealed uniform orthokeratinized stratified squamous epithelium with a prominent granular cell layer (a: H & E, ×10). The surface showed sheaves of orthokeratin and keratin flakes were present in the cystic lumen. The basal cells were low cuboidal to flattened without nuclear palisading, hyperchromatism and reversal of polarity (b: H & E, ×20). Epithelium was nonkeratinized in few areas of inflammation (c: H & E, ×10)	PMC9106234	JOMFP-26-130-g003.jpg
0.389574	fefc8bac2311469891dc1f301b0f0acb	Fibrous capsule showed dense collagen bundles, few chronic inflammatory cells, cholesterol clefts and giant cells (a: H & E, ×10), hemosiderin pigments (b: H & E, ×10), dystrophic calcification (c: H & E, ×4) and dentinoid-like material focally (d: H & E, ×4)	PMC9106234	JOMFP-26-130-g004.jpg
0.47465	4bae3f64c5ff48fa99a28dfa1dedfd75	Flow diagram of procedure of data collection	PMC9107189	12931_2022_2035_Fig1_HTML.jpg
0.430439	317f2dd65c334bb384d2b3c916496969	All genes and DEGs common in the two GEO datasets. A Volcano plot of all genes in GSE42834 gene chip. Red and green dots denote upregulated and downregulated genes, respectively. Black dots show the remaining genes without significant changes in expression. B Volcano plot of all genes in GSE83456 gene chip. C Venn diagram of upregulated genes common in the two GEO datasets. D Venn diagram of downregulated genes common in the two GEO datasets. E Heatmap of DEGs in the two GEO datasets (60 upregulated and 2 downregulated genes). Legend represents gene expression. Red and blue colors denote upregulation and downregulation, respectively	PMC9107189	12931_2022_2035_Fig2_HTML.jpg
0.422369	cef25a6d8c1245b2aeb9994dd839e9f6	A Significantly enriched GO terms and KEGG pathways of DEGs with P < 0.05 and gene counts ≥ 3. Font colors of Y-axis label correspond to different enriched terms (BP, CC, MF terms of GO or KEGG pathways) of DEGs. Legend indicates the significance of the term (−log10 P-value). B Results of Gene Set Enrichment Analysis (GSEA) in GO and KEGG terms showed differential enrichment of genes in PTB and HC groups. “1” represents PTB, “0” represents HCs	PMC9107189	12931_2022_2035_Fig3_HTML.jpg
0.416174	0c10fef71562454f9d947adbd7c16900	PPI network of DEGs and module analysis. A DEG PPI network constructed by STRING online database. Circular nodes represent proteins. Edges indicate the interaction between two proteins. The color intensity of the nodes or edges is based on the degree or combined score in the DEGs. B–E Module analysis via Cytoscape software (degree cut-off = 2, node score cut-off = 0.2, k-core = 2, and max. depth = 100) and four central modules were built based on the PPI network. F Interrelation analysis between immune system pathways. All genes from all pathways were noted in red. G Count number of genes involved in the identified pathways	PMC9107189	12931_2022_2035_Fig4_HTML.jpg
0.430264	c36bc65bc0e646a1a8f245ae98bd6863	The GO enrichment results of the top ten hub genes. The bubble plot and chord diagram show the GO term (BP) (A) related to the top ten hub genes (B)	PMC9107189	12931_2022_2035_Fig5_HTML.jpg
0.439494	2661b739c21c46f3a4971cbd56f772b2	Expression of the ten hub genes and screening in an independent dataset (GSE56153). A Scatter plot from multiple t tests. mRNA expression levels of ISG15, OAS1, IFIT3, OAS3, IFIT1, OASL, IFI44L, RSAD2, XAF1 and IFI44 in the peripheral blood from PTB patients were compared with those in HC groups. Data were analyzed with multiple t tests and the scatter plot is created via GraphPad Prism 8.0.2. Each dot represents one gene and red dots denote genes with significant changes in expression (q < 0.01). The X axis is the difference between means for each gene from PTB and HC groups. The Y value plots the minus logarithm of the q-value. A dotted grid line is shown at Y = −log10(0.01). B Correlation of ISG15, OAS1, IFIT3, OAS3, IFIT1, OASL, IFI44L, RSAD2, XAF1 and IFI44 expression levels and PTB variable. Correlations were analyzed using point-biserial correlation tests and correlation coefficients of these genes were plotted. Red circles denote genes with correlation coefficient > 0.5 and P < 0.01. C Forest plot of the association between the ten hub genes and PTB in GSE56153 dataset. These ten hub genes from PTB patients and HCs were analyzed using multivariate poisson regression analysis with robust variance estimate. Metaanalysis of those was conducted, and adjusted RR, 95% CI of each gene and corresponding P value were calculated and plotted in the forest plot. D mRNA expression values of the three genes (OAS1, IFIT1 and IFIT3) in PTB and HC from an independent sample set by qRT-PCR. The mRNA values of the evaluated genes were normalized to the housekeeping gene GAPDH. The numbers of participants in validation test were the following: PTB, n = 20; HC, n = 20. P < 0.01, *P < 0.001	PMC9107189	12931_2022_2035_Fig6_HTML.jpg
0.437742	57f06ef7a4d3447b833f141443828219	Efficacy evaluation for the three-gene set predicting PTB versus HCs by receiver operating characteristic curve (ROC) analysis. A ROC of the single gene or optional combinations of the three-gene set for discriminating PTB from HCs in independent GSE56153 dataset. 95% confidence interval of AUC was shown in the legend area, and the different colors presented different genes or combinations. B, C ROC of the three-gene set in the other seven independent datasets (GSE19491, GSE28623, GSE34608, GSE54992, GSE62525, GSE147964, GSE147690). 95% CI of AUC was shown in the legend area, and the different colors presented different datasets	PMC9107189	12931_2022_2035_Fig7_HTML.jpg
0.486321	c1f8792a1ef142c99e1e72fd44f7ee1d	The discriminative performance of the three-gene set in discriminating TB from other diseases based on the Random Forest (RF) predictions in independent GSE37250 dataset. A Importance plot of the variables. Total pixel was the three-gene set, followed by OAS1, IFIT1, and IFIT3. B ROC of RF prediction model based on the three-gene set in the training set and test set from the GSE37250 dataset. AUC was also shown in the legend area	PMC9107189	12931_2022_2035_Fig8_HTML.jpg
0.461334	a1382d096fef402fb734c615e9b08f02	Schematic representation of our algorithm for identification of previously unrecognized amyloidogenic proteins. These proteins contain the mutated residues in the set at the intersection of all three circles: residues within LCDs with pathogenic missense mutations that increase amyloid propensity. We determined these residues in the three steps shown. Estimates for the number of residues represented in steps 1 to 3 are derived from this study. To estimate the number of residues with pathogenic missense mutations, we used Simple ClinVar (https://simple-clinvar.broadinstitute.org/). To calculate the estimate for the number of missense mutations that increase amyloid propensity, we extrapolated the percentage of mutations within LCDs that increase amyloid propensity (88/732; ∼12%) to our estimate of total known pathogenic missense mutations in humans (∼40,000) and rounded up. LCD, low-complexity domain.	PMC9108986	gr1.jpg
0.395298	9998f975786a48728195de78b1e8ef53	Census of amino acid residues present in LCDs.A, counts of all residues in LCDs in the human proteome. B, heatmap displaying counts of all LCD residues involved in documented pathogenic missense mutations and which residues they change into. Note that many residue changes are not possible from single-nucleotide variants, which accounts for many of the data points of 0 in the heatmap. LCD, low-complexity domain.	PMC9108986	gr2.jpg
0.444308	421cd09a044743959916a8a07748a6ac	Schematic summary of the methodology by which we discovered amyloidogenic mutations.Top, diagram of protein TFG that contains a PB1 domain and a low-complexity domain. We investigated only mutations in the low-complexity domain. Bottom, analyzing the sequence context of the mutant residue. We calculated Rosetta energy scores using ZipperDB for every hexamer containing the WT residue as well as the mutant residue. Each WT hexamer is compared with its corresponding mutant hexamer. WT scores greater than −23.0 that correspond to a mutant score less than −23.0 imply greater amyloid propensity and are of the most interest. TFG, TRK-fused gene protein.	PMC9108986	gr3.jpg
0.496922	573c1dfe256a43d1892e0b3163f45391	Mutant residues in the LCDs throughout the human proteome with greater propensity to form amyloid than their corresponding WT residue.A, energy scores of WT and mutant segments in LCDs computed by ZipperDB. Because each mutation generates six possible score pairs, only the score pair that mapped to the “region of interest” (inset) or with the greatest negative change from WT to mutant score is plotted for each mutation. The dashed line shows mutations that do not affect the ZipperDB score. The x and y intercepts are both at −23.0 kcal/mol of the segment, the ZipperDB threshold for a predicted amyloid-forming steric zipper. Inset contains a zoomed view of the lower right quadrant of the plot that is the “region of interest” containing points corresponding to a WT segment with a score above −23.0 kcal/mol of segment and a mutant segment with a score below −23.0 kcal/mol of segment, indicating a mutation that increases the amyloid propensity. B, heatmap displaying counts of the kinds of mutational changes in the “region of interest.” LCD, low-complexity domain.	PMC9108986	gr4.jpg
0.41706	79bc091aebac4d6088e942bd08bc274a	Amyloid properties of the LCD of protein TFG.A, time-dependent ThT fluorescence for TFG LCD mutants. G269V and P285L are documented pathogenic mutations of TFG. All constructs are at 50 μM concentration in PBS with ThT at 40 μM concentration. Each construct has n = 6 technical replicates, except the PBS blank that has n = 3 technical replicates, and y-axis values represent the mean ThT fluorescence value of all replicates for each construct. B, electron micrographs of the samples at the end point of the ThT curves. Fibers were present only in the mutant constructs. C, X-ray fiber diffraction of TFG fibers. Rings are present at 4.7 and 10 Å spacing with distinct wedges, indicative of cross-β structure. LCD, low-complexity domain; TFG, TRK-fused gene protein; ThT, thioflavin T.	PMC9108986	gr5.jpg
0.508335	6dda774528404ee593ee7ca58d6991e5	a Schematizes the relatively shallow, strict hierarchy of ICD-10. b Illustrates the multiple inheritance (a concept may have more than one parent, and thus is not mutually exclusive), as well as the greater relative depth of ICD-11	PMC9109286	12911_2021_1539_Fig1_HTML.jpg
0.520215	737e27a8edeb4b75894215b82d7ec13a	A schematic depiction of how the multiple inheritance semantic network of the Foundation is “linearized” into a mutually exclusive, strict hierarchy than can be rendered as a non-overlapping list of rubric codes and descriptions	PMC9109286	12911_2021_1539_Fig2_HTML.jpg
0.442363	6421399af20d4714bc97aa726cb74be4	The process of linearizations can be accomplished repeatedly, choosing different parents from the Foundation as the primary or linear parent, to achieve mutually exclusive statistical classifications or linearizations for a spectrum of use-cases	PMC9109286	12911_2021_1539_Fig3_HTML.jpg
0.400901	cc7ad52047f3400199a8f00a6b188f85	(a) Linear absorption (cm−1) of 4.5 and 5.5 monolayer (ML) CdSe colloidal quantum wells (CQWs) based upon literature data. (b) Typical TEM image of 4.5 ML CdSe CQW sample. (c) Normalized, fluence-dependent emission of CQW solutions. (d) Normalized, fluence-dependent emission of CQW films illuminated with a 400 μm diameter spot. Normalization is to the excitonic emission peak. (e) Cartoon of single exciton, biexciton, and transition to unbound carrier plasma.	PMC9110332	41598_2022_11882_Fig1_HTML.jpg
0.444277	8ab8b72371af4b0cb4cf24a9038f6752	(a,b) Normalized transient absorption spectra (ΔA) of representative (a) 4.5 and (b) 5.5 ML CQW samples as a function of photogenerated sheet density. Each spectrum is collected at a 3 ps pump-probe delay for many powers of 3.5 eV pump light. (c,d) Linear absorption (cm−1) calculated for many photogenerated sheet densities of the same (c) 4.5 and (d) 5.5 ML samples. (e,f) Zoomed in regions of (c) and (d), respectively, showing the spectral window of gain.	PMC9110332	41598_2022_11882_Fig2_HTML.jpg
0.511777	bbc7e14a4ac745bbb8a04b7ee50bbd95	(a,b) Normalized exciton absorption intensity for three (a) 4.5 and (b) 5.5 ML CQW samples as a function of photogenerated sheet density. Each data point is extracted from a transient absorption spectrum collected at 3 ps pump-probe delay for many powers of 2.72 eV and 3.50 eV pump light. (c,d) Ratio of heavy hole and light hole bleach signals as a function of photogenerated sheet densities for the same (c) 4.5 and (d) 5.5 ML samples. (e,f) Half-width at half-maximum (HWHM) of the HH bleach feature from the transient absorption spectrum (ΔA) plotted against photogenerated sheet densities of the same (e) 4.5 and (f) 5.5 ML samples. In all cases, data for measurements with 3.50 eV pump are shown in solid symbols and data for 2.72 eV pump measurements are shown in open symbols. A solid line represents a smoothed average of 3.50 eV pump experiments and a dashed line corresponds to the smoothed average of 2.72 eV pump.	PMC9110332	41598_2022_11882_Fig3_HTML.jpg
0.432009	8cf001eab58643eaae625d14ae831c79	(a,b) Line-cuts of gain or loss at 3 ps pump-probe delay for representative energy values as a function of photogenerated sheet density for (a) 4.5 ML and (b) 5.5 ML CQW samples. In all cases, data for measurements with 3.50 eV pump are shown in solid symbols and data for 2.72 eV measurements are shown in open symbols. A solid line represents a smoothed average of 3.50 eV pump experiments and a dashed line corresponds to the smoothed average of 2.72 eV pump.	PMC9110332	41598_2022_11882_Fig4_HTML.jpg
0.414879	7e70bd5221a24580b353d50ef5a56672	(a,b) High-fluence photoemission from a circular spot of (a) 9.8 nm × 15.4 nm 4.5 ML and (b) 9.0 nm × 26.8 nm 5.5 ML CdSe CQWs.	PMC9110332	41598_2022_11882_Fig5_HTML.jpg
0.423356	96e56707665d4755b9c454a11312b832	(a,b) Thermal differential absorption spectra (ΔA = AT-A295 K) of (a) 9.8 nm × 15.4 nm 4.5 ML and (b) 9.0 nm × 26.8 nm 5.5 ML CdSe CQWs are shown in colors. The black dashed line shows the ΔA of the same 4.5 or 5.5 ML CdSe CQWs under intense photoexcitation (> 5 × 1013 cm−2). The plots are scaled for presentation. (c,d) Transient absorption spectra collected at a pump-probe delay of 3 ps and average excitation density < 1 × 1012 cm−2 as a function of sample temperature. (e) Half-width at half-maximum of transient absorption bleach features as a function of temperature based upon data in figure panels (c) and (d). (f) Ratio of the light hole (LH) and heavy-hole (HH) bleach feature as a function of sample temperature using data in (c) and (d).	PMC9110332	41598_2022_11882_Fig6_HTML.jpg
0.47522	2636b853621b411eb3386550acb4633e	(a,b) Static X-ray diffraction pattern (black line) and transient X-ray diffraction patterns (ΔS) as a function of power at 40 ps pump-probe delay using 3.1 eV pump photon energy. Data are shown for (a) 7.4 nm × 23 nm 4.5 ML and (b) 7.6 nm × 41 nm 5.5 ML CdSe CQW samples. (c,d) Quantification of the magnitude of ΔS signal as a function of excitation density for the same samples. Total ΔS signal is disambiguated into signal arising from thermal disordering and shift of the diffraction angle.	PMC9110332	41598_2022_11882_Fig7_HTML.jpg
0.458195	2fd1f82136214a5e9fe7210f31463bfe	Lesion monitoring in diabetic and non-diabetic mice. Representative photos of the full-thickness skin excision ulcers at different post-lesion times in C57BL/6 J a and db/db b mice. Sampling strategy for the re-epithelization analysis. The arrow indicates the area covered by a thin layer of epithelial cells, while the dotted line indicates the border of the non-re-epithelized area, used for the analysis c. Ulcer areas in the experimental groups over the observational days. N = 10 ulcers/groups were included in this experiment. Statistical analysis: two-way ANOVA, p < 0.0001 for time and genotype b. Representative photos of the pressure ulcers at different post-lesion times in C57BL/6 J e and db/db f mice. Ulcer areas in the experimental groups over the observational days. N = 10 ulcers/groups were included in this experiment. Statistical analysis: two-way ANOVA, p < 0.0001 for time and genotype g	PMC9110453	441_2022_3624_Fig1_HTML.jpg
0.449676	a7c7b9c577ef4a57800e3a549ef8641c	Histological and immunohistochemical analysis of the repaired skin in the full-thickness excision and pressure model. N = 5 animals/groups were included in this experiment. Re-epithelization in C57BL/6 J and db/db mice in full thickness excision wound a–a’’’’ and pressure-induced wound b–b’’’’. In each model, representative micrographs of H&E staining of the intact and repaired skin and the relative morphometric measure are shown. Re-innervation in C57BL/6 J and db/db mice in full thickness excision wound c–c’’’’ and pressure-induced wound d–d’’’’. In each model, representative micrographs of PGP9.5-IR fibers in the intact and repaired skin and the relative morphometric measure are shown. Capillary density in C57BL/6 J and db/db mice in full thickness excision wound (e–e’’’’) and pressure-induced wound (f–f’’’’). In each model, representative micrographs of PECAM-IR fibers in the intact and repaired skin and the relative morphometric measure are shown. Data are presented as mean ± SEM. Statistical analysis: Student’s t-test: intact vs lesioned for each genotype, p < 0.05; *p < 0.01; C57BL/6 J vs db/db mice, a p < 0.05, b p < 0.01, c p < 0.001. Bars: 50 µm	PMC9110453	441_2022_3624_Fig2_HTML.jpg
0.426199	e64c349701b1429096c2ff592d765c47	Gene expression and protein quantification of re-innervation and angiogenesis-related molecules. Graphs show the relative expression analysis of TrkA a, a’ and p75NTR a’’, a’’’ or Hif1a b, b’, Flt1 b’’, b’’’, and Kdr b’’’’, b’’’’’ genes normalized on C57BL/6 J for the intact group analysis a, a’’, b, b’’, b’’’’, or on genotype-specific intact groups (horizontal dotted line) for the ulcer analysis a’, a’’’, b’, b’’’. Graphs show the quantification of the Ngf and Vegf proteins in the plasma of C57BL/6 J and db/db animals, in intact conditions or ulcers c-d’. In the comparison between the intact groups c, d, the absolute concentration of the protein is shown, while in the comparison between ulcers c’, d’, the quantification is normalized on the genotype-specific intact group (horizontal dotted line). Data are presented as mean ± SEM. N = 6 animals/groups were included in this experiment. Statistical analysis: C57BL/6 J vs db/db intact, Student’s t-test. Ulcer comparison, one-way ANOVA followed by Dunnett’s post-test versus the genotype-specific intact group a–b’’’’’ or Tukey’s post-test c-d’. Asterisks represent the differences versus the control group or between two groups indicated by an horizontal line (p < 0.05; p < 0.01; ***p < 0.0001)	PMC9110453	441_2022_3624_Fig3_HTML.jpg
0.476463	a55bfe7d4a1f489db1cfa4e351f74438	PCR arrays and western blot analysis: C57BL/6 J vs db/db intact skin. Cluster analysis of the 252 inputs obtained from the three PCR arrays plates for growth factors, extracellular matrix and related molecules, and neurotrophins a. Scatter plot representation of the gene expression fold change in db/db vs C57BL/6 J intact skin, using a fold change of 3 as cutoff value for significance gene expression variation b. STRING software–based protein interaction network analysis of proteins encoded by genes showing a fold of change higher than 10 in db/db vs C57BL/6 J intact skin c. Gene Codis 4.0 software pathway enrichment analysis based on the KEGG database, using the entire group of 101 genes differentially expressed in db/db vs C57BL/6 J intact skin (fold of change > 3). The KEGG database recognized 77 of the 101 input genes d. Graphs show the quantification by western blot of Akt e and p-Akt e’, expressed as a ratio on b-Actin and Akt (total), respectively, in C57BL/6 J and db/db intact skin. Representative images of quantified proteins for each group are shown in the figure e’’. PCR array experiments were performed on pooled RNAs (N = 6 animal/group). Statistical analysis: Student’s t-test. Asterisks represent the differences between db/db and C57BL/6 J (*p < 0.05)	PMC9110453	441_2022_3624_Fig4_HTML.jpg
0.439988	f312a05ea09541d6a82cf804f00de4c4	PCR array analysis: skin excision vs pressure ulcer in C57BL/6 J and db/db mice. Scatter plot representation of gene expression fold change in C57BL/6 J skin excision a or pressure ulcer b, and db/db skin excision c and pressure ulcer d, vs the genotype-specific intact skin, using a fold change of 3 as a cutoff value for gene expression variation significance. PCR array experiments were performed on pooled RNAs (N = 6 animal/group)	PMC9110453	441_2022_3624_Fig5_HTML.jpg
0.396154	97733c37d72b498184565ca83e812944	Protein–protein interaction analysis: skin excision vs pressure ulcer in C57BL/6 J and db/db mice. STRING software–based protein interaction network analysis of proteins encoded by genes showing a fold of change higher than 10 in C57BL/6 J skin excision a or pressure ulcer b, and db/db skin excision c and pressure ulcer d, vs the genotype-specific intact skin. PCR array experiments were performed on pooled RNAs (N = 6 animal/group)	PMC9110453	441_2022_3624_Fig6_HTML.jpg
0.405161	546eaadded54468c8de408dfcd8da244	Pathway enrichment analysis of common and differentially upregulated genes by pressure ulcer in C57BL/6 J and db/db mice. Pathway enrichment analysis performed by GeneCodis 4.0 using Panther and Reactome databases for common genes upregulated by pressure ulcers in C57BL/6 J and db/db using Panther a or Reactome a’ algorithm, and genes upregulated only in C57BL/6 J, using Panther b or Reactome b’ algorithm, or only in db/db using Panther c or Reactome c’ algorithm. Only significant pathways are shown (p < 0.05). Color gradient represents the gene number in each identified pathway, while the -log (adjusted p value) is shown on the horizontal axis. PCR array experiments were performed on pooled RNAs (N = 6 animal/group)	PMC9110453	441_2022_3624_Fig7_HTML.jpg
0.491277	e14c85b693f94028ab536116bda63dda	Study participants.	PMC9111195	AJO-62-553-g001.jpg
0.447599	2a0545e49e814f3ab93d967c063ce429	PRISMA flow diagram.	PMC9111890	gr1.jpg
0.470658	ec96c2f9417842fc9983c08c3e4f0306	Electrospinning machine.	PMC9111983	gr1.jpg
0.520511	9f8216614a24406082a9e54a5b2c2f83	Assembly of the base frame (left) and the box cover (right).	PMC9111983	gr10.jpg
0.522525	293720535ee543c081018d972461bb5e	Front view of the control panel.	PMC9111983	gr11.jpg
0.407266	b87aef530f9c4ff290fd04a195be5bb5	SEM images of PVA-based electrospun nanofiber with 5,000x (a), 10,000x (b), 20,000x (c) magnifications, and histogram for frequency of the diameter nanofiber (d). From those images, it is shown that the average diameter of nanofiber is approximately 170 nm.	PMC9111983	gr12.jpg
0.490337	d4cb6be76e1f44abb8981ba4c6f0fecb	XRD patterns resulted from the characterization of the PVA based electrospun nanofiber with the peak at 19.3° of 2-theta.	PMC9111983	gr13.jpg
0.511887	3d7c33e9eb1f4debaa1b8e65d4a9b4dd	FTIR pattern of the studied material.	PMC9111983	gr14.jpg
0.508765	501764f60f1d4a17ab6143d3c5e36604	TGA (blue) vs. DSC (red) graphs of PVA electrospun nanofiber. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)	PMC9111983	gr15.jpg
0.470073	ad315a2e50a644a7b24292f6c1859f8d	Tensile test on nanofiber specimens according to ASTM D638-14 at a rate of 2 mm/min, at the start of the test (a), when fracture (b), when released from the machine (c), and stress vs. strain curves for PVA nanofiber at constant speed of 2 mm/min (d).	PMC9111983	gr16.jpg
0.492468	06e318a9c2b940dca3d2cecccce8f013	Measurement of surface area using ImageJ, background (a), nanofiber area (b).	PMC9111983	gr17.jpg
0.42968	b96da267e889426f8483628efa55d31e	Hardware and electronic system of Syringe Pump.	PMC9111983	gr2.jpg
0.428374	7150a773c144403996de82a0cd145a83	Hardware and electronic system of drum collector.	PMC9111983	gr3.jpg
0.408535	a2087326f28344d1a1f05bbbf858648b	Syringe pump components.	PMC9111983	gr4.jpg
0.43106	03c6200212f3495b88c49500a94bc393	Drum collector components.	PMC9111983	gr5.jpg
0.444905	c6deee0bab4a4a52b3ddbed9afa0117b	Electrical schematic of syringe pump controller.	PMC9111983	gr6.jpg
0.443228	54441c4e67ad4565acaf634aa37d482a	Electrical schematic of drum collector controller.	PMC9111983	gr7.jpg
0.537703	c73b8344d57d44869db32632a916c505	A simplified flow-chart showing the main functions of the syringe pump controller.	PMC9111983	gr8.jpg
0.547778	31cd1190924244c581c60af9252b2bd9	A simplified flow-chart showing speed controller of drum collector.	PMC9111983	gr9.jpg
0.510196	a9cbc0b626ec44f9bb957dc2f4099dcd	The Replication pathway of linear DNAs with hp telomeres and telomere resolvase domain organization.A, bidirectional replication of the chromosome initiates at an internal origin and continues until replication rounds the hairpin telomeres. A circular dimer intermediate results that is fused at replicated telomere junctions (denoted at L/L' and R/R'). This intermediate is then resolved by a DNA cleavage and reunion reaction called telomere resolution that reconstitutes linear monomers terminated by hp telomeres. B, the domain architecture of three telomere resolvases characterized in vitro. TelK is the telomere resolvase from φKO2 of Klebsiella oxytoca, TelA is from Agrobacterium tumefaciens, and ResT is from Borrelia burgdorferi. Domains identified as homologous either through BLAST alignment or via structural analysis are identified in identically shaped and shaded domains (i.e., N-core in TelK and TelA and the catalytic domain in all three resolvases). Domains without a homologous counterpart are given unique colors/shades. Domains that have been experimentally deleted without affecting telomere resolution are delimited in square brackets. The nucleophilic tyrosine is identified by amino acid number in the catalytic domains. hp, hairpin.	PMC9111995	gr1.jpg
0.42397	e1e050084fd64aa2bb930464d6603cc1	Deletion of the N-terminal domain reduces the divalent metal dependence of telomere resolution.A, schematic representation of the SspI-linearized plasmid substrate containing a 36-bp rTel junction (shaded and bisected by a line) and the resultant products of telomere resolution. The size (in kilobase pairs) is indicated for the plasmid substrate and the products of telomere resolution. S denotes the substrate, and P1 and P2 denote the telomere resolution products. B, 0.8% (w/v) agarose 1× TAE gel panel of telomere resolution reactions incubated at 30 °C for 10 min with the concentration of TelA indicated above the gel. The reaction buffer contained 1 mM EDTA, MgCl2, or CaCl2 as indicated in the loading key above the gel. C, 0.8% (w/v) agarose 1× TAE gel panel of telomere resolution reactions incubated at 30 °C for 30 min with the concentration of TelA (107–442) (ΔN) indicated above the gel. The reaction buffer contained 1 mM EDTA, MgCl2, or CaCl2 as indicated in the loading key above the gel. D, timecourse plots of telomere resolution reactions with 38 nM of wt TelA incubated with 1 mM EDTA or 1 mM CaCl2. Reactions were performed in triplicate, and the mean and standard deviation are shown. E, timecourse plots of telomere resolution reactions with 38 nM of TelA (107–442) (ΔN) incubated with 1 mM EDTA or 1 mM CaCl2. Reactions were performed in triplicate, and the mean and standard deviation are shown.	PMC9111995	gr2.jpg
0.430035	ac4113ed83e94eb1b194eda15f8114ba	TelA (D202A) can perform telomere resolution independently of a divalent metal ion.A, telomere resolution timecourse plots with 38 nM wt TelA comparing 1 mM EDTA, 4 mM MgCl2, and 4 mM CaCl2 conditions. B, telomere resolution timecourse plots with 38 nM TelA (D202A) comparing 1 mM EDTA, 4 mM MgCl2, and 4 mM CaCl2 conditions. C, initial rates for 38 nM of wt TelA and TelA (D202A) for the divalent metal conditions are described in (A) and (B). All data plots show the mean and standard deviation of at least three independent experiments.	PMC9111995	gr3.jpg
0.447102	d616ad0383104fe4b41f8d6999a9bf64	Titration of the N-terminal domain into reactions with TelA (107–442) and TelA (107–442; D202A).A, 0.8% (w/v) agarose 1× TAE gel panels of telomere resolution reactions incubated at 30 °C for 10 min with 38 nM TelA (107–442) or TelA (107–442; D202A) and a titration of TelA (1–106) added in trans. The reaction buffer contained either no divalent metal ions (0.2 mM EDTA) or 2 mM CaCl2. M in the loading key above the gel indicates a protein-free reaction. S denotes the migration position of the substrate DNA, P1 and P2 denote the products, and P3 denotes the presumptive fusion product of the P1 hairpin telomeres. ΔN denotes TelA (107–442), ΔN; D202A denotes the double mutant, and N denotes TelA (1–106). B, % product formation (telomere resolution plus hairpin telomere fusion) plotted for telomere resolution reactions using 38 nM TelA (107–442) or TelA (107–442; D202A) on their own or in the presence of 380 nM TelA (1–106) added in trans. Conditions with 0.2 mM EDTA versus 2 mM CaCl2 or MgCl2 are shown. Reactions were performed in triplicate, and the mean and standard deviation are shown. C, % hp fusion abstracted from the reactions plotted in (B). Reactions were performed in triplicate, and the mean and standard deviation are shown. hp, hairpin.	PMC9111995	gr4.jpg
0.412336	6ce1e7e817a54d55bc4708fb2e3e1022	Chemical cross-linking of the interaction of the N-terminal domain with TelA (107–442). α-His Western blotting and Imperial Protein staining of 5%/10 to 18% (v/v) SDS-PAGE gradient gel panels for protein–protein cross-linking promoted by DSP (see Experimental procedures). wt denotes wildtype TelA, ΔN denotes TelA (107–442), and N represents TelA (1–106). Cross-linking of ΔN and N is indicated by the red arrows, and cross-linking of multiple ΔN to one another is indicated with black arrows. −/+ DNA denotes the presence or absence of 5 μg/ml SspI-digested pEKK392 in the reaction. wt and ΔN were present at 240 nM, and N was present a 1 μM. DSP, dithiobis [succinimidylpropionate].	PMC9111995	gr5.jpg
0.419455	3f4803eafe2a4d6496b350f4e8d32ff1	Fusion of oligonucleotide hp telomeres.A, cleavage of a half-site substrate comprised the sequence present in the hp telomeres but without the presence of the hp turnaround. Cleavage of the half-site is followed by diffusion away of the three nucleotides distal to the scissile phosphate trapping TelA on the cleaved half-site. This migrates in the “cleavage product” (CP) position of the gel. The N-terminal deletion mutants of TelA produce a faster migrating CP due to the missing mass of the deleted N-terminal domain. The mock versions of these substrates were produced by changing all T’s to A’s, A’s to T’s, G’s to C’s, and C’s to G’s. This maintains the sequence composition of the half-site and hp telomere substrates but produces a scrambled version that should not be recognized by TelA. wt denotes wildtype TelA (wt), and DA and ΔN denote TelA (D202A) and TelA (107–442), respectively, and their combination within a double mutant (ΔN; DA). When the TelA (1–106), the N-terminal domain is added in trans, this is indicated in the gel loading keys by +N. Shown are 8% (v/v) PAGE 1× TAE/0.1% (w/v) SDS gels of reactions performed with 5′-end-labeled substrate. B, fusion of hp telomeres by reversal of the telomere resolution reaction produces a replicated telomere (rTel) as the product. The details of the gel loading key are as noted for (A). Shown are 8% (v/v) PAGE 1× TAE/0.1% (w/v) SDS gels of reactions performed with 5′-end-labeled substrate. All reactions contain 76 nM TelA and 2 mM CaCl2. The incubation temperatures and duration are noted below the gels.	PMC9111995	gr6.jpg
0.409662	42cc39f0b7e74d5a992115885ee740c8	Recombination between replicated telomeres.A, schematic representation of a strand exchange reaction between negatively supercoiled pEKK392 and a 5′-32P end-labeled (∗) 87-bp oligonucleotide rTel. HJs resulting from this strand exchange can be resolved with T7 endonuclease I. Linearization with AhdI prior to T7 endonuclease I treatment results in resolution into two products due to the opposing strand scission sites of the two enzymes. The cleavage position of AhdI is labeled in the diagram. B, autoradiogram and ethidium bromide–stained 0.8% (w/v) agarose 1× TAE gel panels of HJ formation between 10 μg/ml pEKK392 and 70 nM of either end-labeled rTel (OGCB827∗/828∗) or mock rTel (855∗/856∗) in 2 mM Ca2+. wt denotes wildtype TelA, and DA and ΔN denote TelA (D202A) and TelA (107–442), respectively, and their combination within a double mutant (ΔN; DA). TelA (1–106) is denoted by N, and when added in trans, by +N. All proteins were present at 76 nM besides N which was present at 380 nM. C, autoradiogram and ethidium bromide–stained 0.8% (w/v) agarose 1× TAE gel panel of HJ formation between 10 μg/ml pEKK392 and 65 nM end-labeled rTel with or without 76 nM of the double mutant (ΔN; DA). AhdI and/or T7 endo I treatment was applied as indicated in the panel legend. HJ, Holliday junction.	PMC9111995	gr7.jpg
0.476868	51c10cfb3b9745ca9d12c879d1962141	Model of TelA regulation. Models for metal binding with wildtype TelA (A), N-terminal truncation mutant of TelA (B), and the N-terminal domain being added in trans (C) are shown. A, the N-terminal domain of TelA physically interacts with the remainder of TelA, masking the catalytic and/or refolding module residues and rendering the enzyme inactive (represented by the stippled shading of the domains). The presence of low levels of a divalent metal ion (with a preference for calcium) results in metal binding to a high-affinity site in the inhibitory N-terminal domain. This relieves the inhibitory effect of the N-terminal domain, and the enzyme is in its active conformation. High calcium concentrations stimulate binding at a second, low-affinity metal-binding site located in proximity to the D202 residue. Ca2+ binding at this second site inhibits enzymatic activity. B, truncation of the inhibitory N-terminal domain removes the high-affinity metal-binding site and leaves the enzyme in its open, active conformation. Addition of low calcium concentrations has no effect on the truncation mutant of TelA. High calcium concentrations still lead to binding at the low-affinity metal-binding site and render the enzyme inactive. Mutation of the D202 residue disrupts binding at the low-affinity metal-binding site, resulting in high calcium concentrations having no effect on enzymatic activity. C, addition of the N-terminal domain in trans with the rest of TelA re-establishes the inhibitory protein–protein interactions observed with the wildtype enzyme. Exposure to low calcium concentrations results in metal binding at the high-affinity site and disruption of the inhibitory interactions.	PMC9111995	gr8.jpg
0.471167	d80a2023a0fb40ec99d87854fc3f389c	Locations of survey respondents, by county.	PMC9112314	10.1177_11782218221095872-fig1.jpg
0.447985	113ef7ed1b50469bb2f91f19d57d1a40	Changes in facility reported client success rates across the pre-pandemic, early pandemic, and late pandemic periods.	PMC9112314	10.1177_11782218221095872-fig2.jpg
0.475793	3f97d947041c4d0da2935b36c7b422f0	Differential gene expression and pathway analysis comparing infection group to unexplained fever on Day 1 and Day 2. (a) Mean–difference (MD) plot showing the 1829 down‐regulated (blue) and 772 up‐regulated (red) DE genes in PBMCs from FN episodes with ‘any infection’ (bacteraemia, MDI and CDI combined) versus unexplained fever at time of hospital admission (Day 1). (b) MD plot showing the 142 down‐regulated (blue) and three up‐regulated (red) DE genes in PBMCs from FN episodes with ‘any infection’ (bacteraemia, MDI and CDI combined) versus unexplained fever on Day 2. (c) Top 20 KEGG pathways over‐represented when comparing DE genes in PBMCs from FN episodes with ‘any infection’ (bacteraemia, MDI and CDI combined) versus unexplained fever at time of hospital admission (Day 1). (d) Top 20 KEGG pathways over‐represented when comparing DE genes in PBMCs from FN episodes with ‘any infection’ (bacteraemia, MDI and CDI combined) versus unexplained fever on Day 2.	PMC9113042	CTI2-11-e1383-g001.jpg
0.460415	a16c98289e2645008a75b351e6428ab2	Differential gene expression and pathway analysis of bacteraemia versus all other causes of FN on Day 2. (a) MD plot showing the 11 down‐regulated (blue) DE genes in PBMCs from FN episodes with bacteraemia versus ‘all other’ causes on Day 2. (b) Heatmap of 11 significantly differentially expressed genes (P < 0.05) in PBMCs from FN episodes with bacteraemia versus ‘all other’ causes on Day 2. Colour code indicates the Z score. (c) Top 10 Hallmark gene sets over‐represented when comparing DE genes in bacteraemia versus ‘all other’ causes on Day 2. ( d) Top 10 KEGG pathways over‐represented when comparing DE genes in bacteraemia versus ‘all other’ causes on Day 2.	PMC9113042	CTI2-11-e1383-g002.jpg
0.434833	b38cae6dcb354f058b33c8f5a5275b6d	Differential gene expression and hallmark gene set pathway analysis of bacteraemia episodes comparing blood collected on Day 1 to blood collected on Day 2. (a) MD plot showing the 67 up‐regulated (red) and 41 down‐regulated (blue) DE genes in PBMCs from FN episodes in bacteraemia episodes on Day 1 and Day 2. (b) Top KEGG pathways up‐regulated or down‐regulated when comparing DE genes in bacteraemia episodes on Day 1 and Day 2.	PMC9113042	CTI2-11-e1383-g003.jpg
0.426139	becbd5fdb1724cbea05c4f3e7b13c4cf	Differential gene expression and pathway analysis of bacteraemia versus all other causes of FN on Day 1. (a) MD plot showing the 21 down‐regulated (blue) and 3 up‐regulated (red) DE genes in PBMCs from FN episodes with bacteraemia versus ‘all other’ causes at the time of hospital admission (Day 1). (b) Heatmap of the 24 significantly differentially expressed genes (P < 0.05) in in PBMCs from FN episodes with bacteraemia versus ‘all other’ causes at the time of hospital admission (Day 1). Colour code indicates Z‐score. (c) Top 20 Hallmark gene sets over‐represented when comparing DE genes in bacteraemia versus ‘all other’ causes on Day 1. (d) Top 20 KEGG pathways over‐represented when comparing DE genes in bacteraemia versus ‘all other’ causes on Day 1.	PMC9113042	CTI2-11-e1383-g005.jpg
0.511966	a3ef10fa8b784c9d810c5d8f31c005d3	Differential gene expression analysis of comparing different MDI infections versus unexplained fever on Day 1. (a) MD plot showing the 1056 down‐regulated (blue) and 150 up‐regulated (red) DE genes in PBMCs from FN episodes with bacteraemia versus unexplained fever at time of hospital admission (Day 1). (b) MD plot showing the 506 down‐regulated (blue) and 76 up‐regulated (red) DE genes in PBMCs from FN episodes with non‐bloodstream bacterial MDI versus unexplained fever at time of hospital admission (Day 1). (c) MD plot showing the two down‐regulated (blue) and 130 up‐regulated (red) DE genes in PBMCs from FN episodes with viral non‐bloodstream MDI versus unexplained fever on Day 2. (d) Common and unique DE genes in non‐bloodstream bacterial MDI versus unexplained fever and viral MDI versus unexplained fever FN episodes at the time of admission (Day 1). Unique DE genes are indicated in the respective circles, while all common DE genes are indicated at the bottom right of the diagram (red, up‐regulated; blue, down‐regulated).	PMC9113042	CTI2-11-e1383-g006.jpg
0.46572	c1d3098bd286430ba9bfafdbf9f0c672	The percentage of (a) sign, (b) comorbidity, and (c) deceased patients by age group and length of stay in hospital.	PMC9113873	BMRI2022-2350063.001.jpg
0.449058	5e1bf9f816ac4673bc7c856852776ea8	The Kaplan-Meier survival time by demographic variables.	PMC9113873	BMRI2022-2350063.002.jpg
0.444696	a7742781c03443fd8b00d6efb83ca6cc	The case fatality rate of COVID-19 patients.	PMC9113873	BMRI2022-2350063.003.jpg
0.393163	e4184ed42d574faa96ea961cda84d538	Characteristics of adipose tissue-derived multi-lineage progenitor cells (ADMPCs). (a) Mesenchymal stem cell (MSC) surface marker expression on ADMPCs. The expression of each surface marker is shown on the shaded histogram. Staining with an isotype control mAb is represented by a black line. (b) Colony formation of ADMPCs. Cells were seeded with the indicated density and cultured for 2 weeks. Cells were then fixed and stained with 0.1% crystal violet. (c) Multipotency of ADMPCs. Representative images are shown of Alizarin red staining of ADMPCs cultured in osteogenic differentiation media for 28 days, Oil red O staining of ADMPCs cultured in adipogenic differentiation media for 24 days, and Toluidine blue staining of ADMPCs cultured in chondrogenic differentiation media for 20 days.	PMC9114023	41598_2022_11986_Fig1_HTML.jpg
0.436567	0f10b9a3ceab47908013078457cfad4e	Representative images of adipose tissue-derived multi-lineage progenitor cell (ADMPC) transplantation. (a) Pre-operative intra-oral findings. This case was a 51-year-old female. The test tooth was an upper left second molar with a 6-mm periodontal pocket in the distal area. (b, c) Intra-oral findings during periodontal surgery. The flap operation was performed in accordance with the modified Widman procedure. After reversing the gingival flap, a circumferential intra-bony defect filled with granulation tissue was revealed and the granulation tissue was removed. After washing the intra-bony defect with normal saline, ADMPCs mixed with fibrin gel were transplanted into the intra-bony defect. (d) Postoperative intra-oral findings. Four weeks after ADMPC transplantation, no abnormal findings were found at the surgical site.	PMC9114023	41598_2022_11986_Fig2_HTML.jpg
0.42724	40d0accf545645e6a7baf852d0db1d09	Clinical assessment of probing pocket depth (PD) and clinical attachment level (CAL). Results of (a) PD reduction and (b) CAL gain are shown as box-and-whisker plots. The box, notch, and horizontal line denote the distance between the first and third quartile ranges (interquartile range; IQR), mean, and median, respectively. The upper whisker indicates a maximum value smaller than 1.5 × IQR above the third quartile (Q3). Similarly, the lower whisker indicates a minimum value greater than 1.5 × IQR below the first quartile (Q1). It also displays the outliers which were defined as further outside than Q1 − 1.5 × IQR or Q3 + 1.5 × IQR. PD reduction and CAL gain of the test sites were measured at 3 months, 6 months, 9 months (n = 12). Individual data is shown in Supplemental Table 4. *p < 0.0001, with the use of a one-sample t-test based on the closed testing procedure.	PMC9114023	41598_2022_11986_Fig3_HTML.jpg
0.416072	2600caa1dc5f48f8ba90ae47b8f38c64	Outcome of adipose tissue-derived multi-lineage progenitor cell (ADMPC) transplantation by dental radiographs. Radiographic outcomes of ADMPC-transplanted individuals. Case no. 2 was a 51-year-old woman. Case no. 10 was a 58-year-old woman. Dotted lines indicate the remaining alveolar bone crest or the bottom of the bone defect. The radiographs clearly show that the bone defect was filled with newly generated alveolar bone at 9 months after transplantation.	PMC9114023	41598_2022_11986_Fig4_HTML.jpg
0.463073	9977742fe45c4a25b7157c872e7b65d9	Clinical assessment of new bone formation. Results of new bone formation are shown using the same box-and-whisker plot representation as in Fig. 2. The new bone formation rate was measured using X-ray images at 1 month, 3 months, 6 months, and 9 months (n = 12). *p < 0.0001, †p < 0.001, ‡p < 0.025, with the use of a one-sample t-test based on the closed testing procedure.	PMC9114023	41598_2022_11986_Fig5_HTML.jpg
0.47557	1eafcdfd7513466cb74b6800de4e36c8	Neutrophil elastase activity is increased in periodontal tissue by ligature-induced periodontitis. (A, B) PBS or NE inhibitor (50 μg in 5 μL) was injected into the palatal gingiva of a ligature-induced murine model of periodontitis once a day for 7 (A) or 3 (B) days. (A) Frozen maxillae sections (10 μm) were stained with anti-NE antibody (green), anti-Ly6G antibody (red), and DAPI (nucleus; blue). Representative fluorescence images observed using a confocal laser scanning microscope are shown. Scale bar: 50 μm. (B) NE activity in supernatants from the homogenized palatal gingiva was evaluated. Data are presented as the mean ± SD (n = 5 per group). The group means were compared using one-way analysis of variance with Tukey’s multiple comparison test. AB alveolar bone, D dentine, DAPI 4′,6-diamidino-2-phenylindole, Ly6G lymphocyte antigen 6 complex locus G, NE neutrophil elastase, PDL periodontal ligament, SD standard deviation.	PMC9114116	41598_2022_12358_Fig1_HTML.jpg
0.412973	dd12b42f2940468893e71655a027eee5	Neutrophil elastase inhibitor inhibits ligature-induced alveolar bone loss. (A) Representative images of the maxillae from indicated treatment groups 8 days after ligature placement. Scale bar: 0.5 mm. (B) Periodontal bone loss was assessed using a stereoscopic microscope. Negative values indicate bone loss relative to the unligated control. (C, D) Frozen maxillae sections were stained with tartrate-resistant acid phosphatase. (C) Representative images obtained by optical microscopy are shown. Scale bar: 50 μm. (D) All the TRAP-positive multinucleated giant cells in the periodontal ligament of ligated second molar were counted in five random coronal sections. Data are presented as the mean ± SD (n = 5 per group). The group means were compared using one-way analysis of variance with Tukey’s multiple comparison test. AB alveolar bone, D dentine, MNCs multinucleated cells, NE neutrophil elastase, PDL periodontal ligament, SD standard deviation, TRAP tartrate-resistant acid phosphatase.	PMC9114116	41598_2022_12358_Fig2_HTML.jpg
0.431134	ec809af965544b459428501b08b19d5e	Neutrophil elastase inhibitor decreases the gene transcription of proinflammatory cytokines in the murine gingiva. Messenger RNA transcription levels of Il6, Il1b, and Cxcl1 in the palatal gingiva of mice from the indicated groups were determined by real-time PCR. Relative mRNA levels were normalized to those of Gapdh. Data are presented as the mean ± SD (n = 5 per group). The group means were compared using one-way analysis of variance with Tukey’s multiple comparison test. NE neutrophil elastase, SD standard deviation.	PMC9114116	41598_2022_12358_Fig3_HTML.jpg
0.407494	cfd8c9fe5fa24bf2bdc97fdddf353844	Neutrophil elastase induces exfoliation of gingival epithelial keratinous layer via cleavage of cell adhesion molecule. (A, B) Three-dimensional human oral epithelial tissue models were exposed to 100 mU/mL NE followed by 12-h incubation. (A) Frozen sections were stained with hematoxylin and eosin. Representative images obtained by optical microscopy are shown. Scale bar: 100 μm. (B) Representative fluorescence microscopy images of the sections stained for DAPI (nucleus, blue) and DSG1 (green) are shown. Scale bar: 100 μm. K in Fig. 5A and B indicates keratinous layer. (C, D) Recombinant human DSG1, occludin, and E-cadherin were exposed to NE (10, 50, and 100 mU/mL) for 3 h and determined by western blotting (C) or Coomassie Brilliant Blue staining (D). DSG1 desmoglein 1, NE neutrophil elastase.	PMC9114116	41598_2022_12358_Fig4_HTML.jpg
0.453976	439813a769e74e9c84d862f8a38eef61	Neutrophil elastase induces disruption of periodontal epithelial barrier. (A–E) Monolayers of human gingival epithelial cells were exposed to 10–100 mU/mL NE for 3 h. (A) Transepithelial permeability was determined by measuring 70 kDa of FITC-dextran fluorescence intensity in the medium from the lower chamber compartments. (B–E) The transepithelial permeability of each bacterium was determined using the colony counting method. Data are presented as the mean ± SD (n = 5 per group). The group means were compared using one-way analysis of variance with Dunnett’s multiple comparison test. NE neutrophil elastase.	PMC9114116	41598_2022_12358_Fig5_HTML.jpg
0.36016	ad2f36e8734049bca4324d975ae9a63b	Recognition of keywords of iPSCs and ESCs (Have you heard keywords of iPSCs and ESCs?).	PMC9114515	gr1.jpg
0.408127	9a5ffc2f5c5749e7b79f58628fd7da3f	Opinions concerning the progress of RM (Please select one statement from the following that best describes your overall thoughts about regenerative medicine research).	PMC9114515	gr2.jpg
0.396446	e333d3b96e7d4f42b1697dfdbb631bab	Trust of experts' discourses (Can you trust the story of experts on the safety and effects of RM?).	PMC9114515	gr3.jpg
0.392498	e24771daab38447c80c60d358289a01b	Interested topics on RM (What do you want to know? Please choose three interesting topics.) A Chi-square test was conducted. ∗p < 0.05, ∗∗p < 0.01.	PMC9114515	gr4.jpg
0.45474	5a63567d2fb64c179c5eb07b81aec227	What factors are important for your acceptance of regenerative medicine? Please choose three factors. Chi-square test was conducted. ∗p < 0.05, ∗∗p < 0.01.	PMC9114515	gr5.jpg
0.504011	70192e121c8244089fff0b4337059dbd	Schematic illustration of the ternary vector system used for maize B104 transformation. (A) Binary construct pKL2013 (McCaw et al., 2021), 17,777 bp. PZmUbi, maize polyubiquitin gene promoter; zCas9, maize codon-optimized Cas9 from Streptococcus pyogenes; TrbcS-E9, transcriptional terminator from Pisum sativum rbcS-E9 gene; POsU3, a promoter from Oryza sativa U3 small nucleolar RNA (snoRNA) gene; ZmGl2-sgRNA1, single-guide RNA targeting maize glossy2 gene (Lee et al., 2019); TOsU6-2, terminator from O. sativa OsU6-2 snoRNA gene; Tvsp, terminator from soybean vegetative storage protein gene; mCherry, red fluorescent protein; P35S, CaMV 35S promoter; bar, bialaphos resistance gene; RB, the T-DNA right border repeat; LB, the T-DNA left border repeat; KanR, kanamycin resistance gene cassette; pBR322 ori, high copy number origin of replication for E. coli; pVS1 ori, the origin of replication from the plasmid pVS1. (B) Ternary construct or helper plasmid pKL2299 (this work), 29,605 bp. virB1-virJ, virulence genes from the Agrobacterium tumefaciens Bo542 tumor-inducing plasmid (pTiBo542); RK2 ori, the origin of replication from the broad host range RK2 plasmid; GmR, gentamicin resistance gene cassette.	PMC9114882	fpls-13-860971-g001.jpg
0.414577	4e953bcb348e400d8230d28c24d1c541	Growing maize donor plants for immature embryo production. (A) Standard flat with small pots filled with potting mix for planting maize seed. (B) Six-day-old germinated seedlings under a humi-dome. (C) Two-week-old seedlings ready to be transplanted into large pots. (D) A seedling transplanted to a large pot. (E) Plants on a 1 m tall bench. (F) Pollinated mature B104 plants on the floor. (G) An un-pollinated B104 ear (female flower) with emerged silks. (H) A shoot bag covering an un-pollinated B104 ear. (I) A mature tassel (male flower) ready to be used for pollination. (J) A pollination bag covering a mature tassel for the purpose of collecting fresh pollen. (K) An un-pollinated B104 ear with cut silks. (L) Freshly collected pollen in a tassel bag. (M) Freshly pollinated silks, 1 day after silks were cut. (N) Extracting an immature embryo for measurement while the ear is still growing on the plant. (O) Measurement of an embryo size with a caliper. (P) Estimate of an embryo size with a ruler.	PMC9114882	fpls-13-860971-g002.jpg
0.523934	3ab039b896ae40eab0e8d4aa5ff061e8	Embryo dissection, infection, and co-cultivation. An Agrobacterium “mother” plate (A) and “working” plate after 18 h incubation, streaked by a disposable loop (B). (C) A B104 ear halves on a handle made of a fork. (D) Tools for embryo dissection; a micro spatula (left) and a dental filling instrument (right). (E) A co-cultivation plate with dissected immature embryos. All embryos were re-oriented scutellum side up. (F) A plastic culture box filled with plates. (G) Cartoon illustration of the embryo dissection and infection process. Step 1, remove kernel tops using a sterile scalpel; Step 2, isolate embryo from the kernel and transfer it to a tube filled with liquid 700A infection medium; Step 3, after infection, place embryo onto co-cultivation medium and orient the embryos by placing them scutellum side up. e: embryo, s: endosperm, and p: pericarp. Demonstration of embryo dissection using a micro spatula (H) or a dental filler (I). The arrows indicate the embryo side of the kernel. Circles highlight isolated embryos.	PMC9114882	fpls-13-860971-g003.jpg

0.418239

d41f3fba0bd04d2fa19745fe059af8e8

Progression-free survival in three groups. Kaplan–Meier estimates. log Rank: 0.006.

PMC9105143

cancers-14-02108-g002.jpg

0.427023

f02354d105394c66a16999a6c4441488

Overview of how the feature and baseline windows were chosen, for the three different groups of features by modality. This calculation would result in one feature vector, for the next the windows would all be shifted by an interval of T = 2 s to the right. Abscissa not to scale.

PMC9105312

sensors-22-03318-g001.jpg

0.4176

4d9f686ce6704e8585bb98eeaafa7628

Data set flowchart of the participant selection process. KCL: King’s College London; UKF: University Medical Center Freiburg; E4: Empatica E4 wrist-worn wearable device.

PMC9105312

sensors-22-03318-g002.jpg

0.417077

1c0720fae67a4f81a703edf34d133adb

Selection of examples of true positive detections for each of the three participants in the intra-subject evaluation. Seizures shown are: (a) UKF1-4; (b) UKF2-3; (c) and KCL1-3 (see Table A1). Due to the grace period of 2 minutes around a seizure event, the detection for KCL1-3 counts as a true positive. Each plot of a seizure shows the raw ACC signal (top), the raw EDA signal and feature 2b (middle), and the estimated heart rate and signal quality index of the BVP signal (bottom). The regions highlighted in red mark the ground truth as labeled by experts, and those highlighted in green mark the seizure intervals, as predicted by the respective model, trained on the data of all the other seizures of the participant. The seizure onset and offset are additionally marked by the black vertical bars. All signals shown are normalized between −1 to 1 only for these plots. The original value ranges before normalization can be found in Table A3.

PMC9105312

sensors-22-03318-g003.jpg

0.440799

f5233f3c3dc044e591a18dc007679780

Feature importance scores per intra-subject evaluation for the seizure detection models of the three selected participants: (a) UKF1; (b) UKF2; (c) KCL1 (see Table A2); (d) Feature importance scores of the model resulting from training the GTBM model on the seizure data of all three inter-subject training participants. Blue, red, and yellow bars show the importance scores for the features grouped by biosignal modality ACC, EDA, and BVP, respectively. Horizontal lines mark the mean scores of the groups. The ordinate is unitless; the scores can be interpreted qualitatively. The feature labels correspond to the listing of features in the Materials and Methods.

PMC9105312

sensors-22-03318-g004.jpg

0.452813

ce5533fa23834c928fd3cb4af08198b4

Seizure UKF2-2, a false negative. Compare also to Figure 3. Data shown from top to bottom: raw ACC, raw EDA and feature 2b, heart rate and BVP signal quality index. The red overlay is the seizure ground truth. The seizure onset and offset are additionally marked by the black vertical bars. All signals shown are normalized between −1 to 1 only for these plots. The original value ranges before normalization can be found in Table A3.

PMC9105312

sensors-22-03318-g005.jpg

0.437536

51b479ed69ae4b1da62120b435d63589

The Empatica E4 wrist-worn wearable device used in this study (left), and the Android phone application that connects to the wearable via Bluetooth and records the data stream (right).

PMC9105312

sensors-22-03318-g0A1.jpg

0.462142

6a5a3a64bd1646edb0596fa1ed67d43f

Mediating effect of empathic concern between workplace spirituality and employee wellbeing as a function of organizational politics. Moderated mediation model (all coefficients are standardized). Here ** means p < 0.01 and *** means p < 0.001.

PMC9105451

fpsyg-13-881675-g001.jpg

0.380249

aeaae43f6b464212b88b30d7a335507f

Graphical illustration of the moderation effect of organizational politics on the relationship between workplace spirituality and employee wellbeing; and empathic concern and employee wellbeing.

PMC9105451

fpsyg-13-881675-g002.jpg

0.418058

b679eaf6de4740fb880ac7b0b369781c

A 42-year-old man with AMF. On T1-weighted images, the tumor reveals low signal intensity but high signal intensity in some circuitous strips (A). On coronal fat-saturated T2-weighted images and sagittal T2-weighted images, the tumor is well-marginated with high inhomogeneous signal intensity (B,C). DWI shows a low-signal tumor (D). The images of contrast-enhanced MRI show a heterogeneous and distinctly enhanced mass. As time goes on, the enhancement of the tumor is more obvious (E,F).

PMC9106126

fsurg-09-808488-g0001.jpg

0.492591

4e307f0e38a94f65bf8c9a4d2b7b47d3

Hematoxylin-eosin (HE) staining and immunohistochemistry of the tumor. Thin-walled blood vessels surrounded by several spindle cells can be seen in the images (A,B). Image A and Image B represent 50× and 100×, respectively. The desmin is positive in immunohistochemistry (C).

PMC9106126

fsurg-09-808488-g0002.jpg

0.435418

976238b3e3e54463b21dd1fafc249acf

Orthopantomogram showing a well-defined multilocular radiolucency with sclerotic border in the right molar-ramus region of the mandible distal to the impacted third molar

PMC9106234

JOMFP-26-130-g001.jpg

0.472135

9139c51c8a324e94abe2b141a710c1f0

A cystic lesion with epithelial lining and fibrous connective tissue capsule (H & E, ×4)

PMC9106234

JOMFP-26-130-g002.jpg

0.414247

186e20d88a8d4dcbb6fe8e03b2dfe69d

The epithelium revealed uniform orthokeratinized stratified squamous epithelium with a prominent granular cell layer (a: H & E, ×10). The surface showed sheaves of orthokeratin and keratin flakes were present in the cystic lumen. The basal cells were low cuboidal to flattened without nuclear palisading, hyperchromatism and reversal of polarity (b: H & E, ×20). Epithelium was nonkeratinized in few areas of inflammation (c: H & E, ×10)

PMC9106234

JOMFP-26-130-g003.jpg

0.389574

fefc8bac2311469891dc1f301b0f0acb

Fibrous capsule showed dense collagen bundles, few chronic inflammatory cells, cholesterol clefts and giant cells (a: H & E, ×10), hemosiderin pigments (b: H & E, ×10), dystrophic calcification (c: H & E, ×4) and dentinoid-like material focally (d: H & E, ×4)

PMC9106234

JOMFP-26-130-g004.jpg

0.47465

4bae3f64c5ff48fa99a28dfa1dedfd75

Flow diagram of procedure of data collection

PMC9107189

12931_2022_2035_Fig1_HTML.jpg

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All genes and DEGs common in the two GEO datasets. A Volcano plot of all genes in GSE42834 gene chip. Red and green dots denote upregulated and downregulated genes, respectively. Black dots show the remaining genes without significant changes in expression. B Volcano plot of all genes in GSE83456 gene chip. C Venn diagram of upregulated genes common in the two GEO datasets. D Venn diagram of downregulated genes common in the two GEO datasets. E Heatmap of DEGs in the two GEO datasets (60 upregulated and 2 downregulated genes). Legend represents gene expression. Red and blue colors denote upregulation and downregulation, respectively

PMC9107189

12931_2022_2035_Fig2_HTML.jpg

0.422369

cef25a6d8c1245b2aeb9994dd839e9f6

A Significantly enriched GO terms and KEGG pathways of DEGs with P < 0.05 and gene counts ≥ 3. Font colors of Y-axis label correspond to different enriched terms (BP, CC, MF terms of GO or KEGG pathways) of DEGs. Legend indicates the significance of the term (−log10 P-value). B Results of Gene Set Enrichment Analysis (GSEA) in GO and KEGG terms showed differential enrichment of genes in PTB and HC groups. “1” represents PTB, “0” represents HCs

PMC9107189

12931_2022_2035_Fig3_HTML.jpg

0.416174

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PPI network of DEGs and module analysis. A DEG PPI network constructed by STRING online database. Circular nodes represent proteins. Edges indicate the interaction between two proteins. The color intensity of the nodes or edges is based on the degree or combined score in the DEGs. B–E Module analysis via Cytoscape software (degree cut-off = 2, node score cut-off = 0.2, k-core = 2, and max. depth = 100) and four central modules were built based on the PPI network. F Interrelation analysis between immune system pathways. All genes from all pathways were noted in red. G Count number of genes involved in the identified pathways

PMC9107189

12931_2022_2035_Fig4_HTML.jpg

0.430264

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The GO enrichment results of the top ten hub genes. The bubble plot and chord diagram show the GO term (BP) (A) related to the top ten hub genes (B)

PMC9107189

12931_2022_2035_Fig5_HTML.jpg

0.439494

2661b739c21c46f3a4971cbd56f772b2

Expression of the ten hub genes and screening in an independent dataset (GSE56153). A Scatter plot from multiple t tests. mRNA expression levels of ISG15, OAS1, IFIT3, OAS3, IFIT1, OASL, IFI44L, RSAD2, XAF1 and IFI44 in the peripheral blood from PTB patients were compared with those in HC groups. Data were analyzed with multiple t tests and the scatter plot is created via GraphPad Prism 8.0.2. Each dot represents one gene and red dots denote genes with significant changes in expression (q < 0.01). The X axis is the difference between means for each gene from PTB and HC groups. The Y value plots the minus logarithm of the q-value. A dotted grid line is shown at Y = −log10(0.01). B Correlation of ISG15, OAS1, IFIT3, OAS3, IFIT1, OASL, IFI44L, RSAD2, XAF1 and IFI44 expression levels and PTB variable. Correlations were analyzed using point-biserial correlation tests and correlation coefficients of these genes were plotted. Red circles denote genes with correlation coefficient > 0.5 and P < 0.01. C Forest plot of the association between the ten hub genes and PTB in GSE56153 dataset. These ten hub genes from PTB patients and HCs were analyzed using multivariate poisson regression analysis with robust variance estimate. Metaanalysis of those was conducted, and adjusted RR, 95% CI of each gene and corresponding P value were calculated and plotted in the forest plot. D mRNA expression values of the three genes (OAS1, IFIT1 and IFIT3) in PTB and HC from an independent sample set by qRT-PCR. The mRNA values of the evaluated genes were normalized to the housekeeping gene GAPDH. The numbers of participants in validation test were the following: PTB, n = 20; HC, n = 20. **P < 0.01, ***P < 0.001

PMC9107189

12931_2022_2035_Fig6_HTML.jpg

0.437742

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Efficacy evaluation for the three-gene set predicting PTB versus HCs by receiver operating characteristic curve (ROC) analysis. A ROC of the single gene or optional combinations of the three-gene set for discriminating PTB from HCs in independent GSE56153 dataset. 95% confidence interval of AUC was shown in the legend area, and the different colors presented different genes or combinations. B, C ROC of the three-gene set in the other seven independent datasets (GSE19491, GSE28623, GSE34608, GSE54992, GSE62525, GSE147964, GSE147690). 95% CI of AUC was shown in the legend area, and the different colors presented different datasets

PMC9107189

12931_2022_2035_Fig7_HTML.jpg

0.486321

c1f8792a1ef142c99e1e72fd44f7ee1d

The discriminative performance of the three-gene set in discriminating TB from other diseases based on the Random Forest (RF) predictions in independent GSE37250 dataset. A Importance plot of the variables. Total pixel was the three-gene set, followed by OAS1, IFIT1, and IFIT3. B ROC of RF prediction model based on the three-gene set in the training set and test set from the GSE37250 dataset. AUC was also shown in the legend area

PMC9107189

12931_2022_2035_Fig8_HTML.jpg

0.461334

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Schematic representation of our algorithm for identification of previously unrecognized amyloidogenic proteins. These proteins contain the mutated residues in the set at the intersection of all three circles: residues within LCDs with pathogenic missense mutations that increase amyloid propensity. We determined these residues in the three steps shown. Estimates for the number of residues represented in steps 1 to 3 are derived from this study. To estimate the number of residues with pathogenic missense mutations, we used Simple ClinVar (https://simple-clinvar.broadinstitute.org/). To calculate the estimate for the number of missense mutations that increase amyloid propensity, we extrapolated the percentage of mutations within LCDs that increase amyloid propensity (88/732; ∼12%) to our estimate of total known pathogenic missense mutations in humans (∼40,000) and rounded up. LCD, low-complexity domain.

PMC9108986

gr1.jpg

0.395298

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Census of amino acid residues present in LCDs.A, counts of all residues in LCDs in the human proteome. B, heatmap displaying counts of all LCD residues involved in documented pathogenic missense mutations and which residues they change into. Note that many residue changes are not possible from single-nucleotide variants, which accounts for many of the data points of 0 in the heatmap. LCD, low-complexity domain.

PMC9108986

gr2.jpg

0.444308

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Schematic summary of the methodology by which we discovered amyloidogenic mutations.Top, diagram of protein TFG that contains a PB1 domain and a low-complexity domain. We investigated only mutations in the low-complexity domain. Bottom, analyzing the sequence context of the mutant residue. We calculated Rosetta energy scores using ZipperDB for every hexamer containing the WT residue as well as the mutant residue. Each WT hexamer is compared with its corresponding mutant hexamer. WT scores greater than −23.0 that correspond to a mutant score less than −23.0 imply greater amyloid propensity and are of the most interest. TFG, TRK-fused gene protein.

PMC9108986

gr3.jpg

0.496922

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Mutant residues in the LCDs throughout the human proteome with greater propensity to form amyloid than their corresponding WT residue.A, energy scores of WT and mutant segments in LCDs computed by ZipperDB. Because each mutation generates six possible score pairs, only the score pair that mapped to the “region of interest” (inset) or with the greatest negative change from WT to mutant score is plotted for each mutation. The dashed line shows mutations that do not affect the ZipperDB score. The x and y intercepts are both at −23.0 kcal/mol of the segment, the ZipperDB threshold for a predicted amyloid-forming steric zipper. Inset contains a zoomed view of the lower right quadrant of the plot that is the “region of interest” containing points corresponding to a WT segment with a score above −23.0 kcal/mol of segment and a mutant segment with a score below −23.0 kcal/mol of segment, indicating a mutation that increases the amyloid propensity. B, heatmap displaying counts of the kinds of mutational changes in the “region of interest.” LCD, low-complexity domain.

PMC9108986

gr4.jpg

0.41706

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Amyloid properties of the LCD of protein TFG.A, time-dependent ThT fluorescence for TFG LCD mutants. G269V and P285L are documented pathogenic mutations of TFG. All constructs are at 50 μM concentration in PBS with ThT at 40 μM concentration. Each construct has n = 6 technical replicates, except the PBS blank that has n = 3 technical replicates, and y-axis values represent the mean ThT fluorescence value of all replicates for each construct. B, electron micrographs of the samples at the end point of the ThT curves. Fibers were present only in the mutant constructs. C, X-ray fiber diffraction of TFG fibers. Rings are present at 4.7 and 10 Å spacing with distinct wedges, indicative of cross-β structure. LCD, low-complexity domain; TFG, TRK-fused gene protein; ThT, thioflavin T.

PMC9108986

gr5.jpg

0.508335

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a Schematizes the relatively shallow, strict hierarchy of ICD-10. b Illustrates the multiple inheritance (a concept may have more than one parent, and thus is not mutually exclusive), as well as the greater relative depth of ICD-11

PMC9109286

12911_2021_1539_Fig1_HTML.jpg

0.520215

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A schematic depiction of how the multiple inheritance semantic network of the Foundation is “linearized” into a mutually exclusive, strict hierarchy than can be rendered as a non-overlapping list of rubric codes and descriptions

PMC9109286

12911_2021_1539_Fig2_HTML.jpg

0.442363

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The process of linearizations can be accomplished repeatedly, choosing different parents from the Foundation as the primary or linear parent, to achieve mutually exclusive statistical classifications or linearizations for a spectrum of use-cases

PMC9109286

12911_2021_1539_Fig3_HTML.jpg

0.400901

cc7ad52047f3400199a8f00a6b188f85

(a) Linear absorption (cm−1) of 4.5 and 5.5 monolayer (ML) CdSe colloidal quantum wells (CQWs) based upon literature data. (b) Typical TEM image of 4.5 ML CdSe CQW sample. (c) Normalized, fluence-dependent emission of CQW solutions. (d) Normalized, fluence-dependent emission of CQW films illuminated with a 400 μm diameter spot. Normalization is to the excitonic emission peak. (e) Cartoon of single exciton, biexciton, and transition to unbound carrier plasma.

PMC9110332

41598_2022_11882_Fig1_HTML.jpg

0.444277

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(a,b) Normalized transient absorption spectra (ΔA) of representative (a) 4.5 and (b) 5.5 ML CQW samples as a function of photogenerated sheet density. Each spectrum is collected at a 3 ps pump-probe delay for many powers of 3.5 eV pump light. (c,d) Linear absorption (cm−1) calculated for many photogenerated sheet densities of the same (c) 4.5 and (d) 5.5 ML samples. (e,f) Zoomed in regions of (c) and (d), respectively, showing the spectral window of gain.

PMC9110332

41598_2022_11882_Fig2_HTML.jpg

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(a,b) Normalized exciton absorption intensity for three (a) 4.5 and (b) 5.5 ML CQW samples as a function of photogenerated sheet density. Each data point is extracted from a transient absorption spectrum collected at 3 ps pump-probe delay for many powers of 2.72 eV and 3.50 eV pump light. (c,d) Ratio of heavy hole and light hole bleach signals as a function of photogenerated sheet densities for the same (c) 4.5 and (d) 5.5 ML samples. (e,f) Half-width at half-maximum (HWHM) of the HH bleach feature from the transient absorption spectrum (ΔA) plotted against photogenerated sheet densities of the same (e) 4.5 and (f) 5.5 ML samples. In all cases, data for measurements with 3.50 eV pump are shown in solid symbols and data for 2.72 eV pump measurements are shown in open symbols. A solid line represents a smoothed average of 3.50 eV pump experiments and a dashed line corresponds to the smoothed average of 2.72 eV pump.

PMC9110332

41598_2022_11882_Fig3_HTML.jpg

0.432009

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(a,b) Line-cuts of gain or loss at 3 ps pump-probe delay for representative energy values as a function of photogenerated sheet density for (a) 4.5 ML and (b) 5.5 ML CQW samples. In all cases, data for measurements with 3.50 eV pump are shown in solid symbols and data for 2.72 eV measurements are shown in open symbols. A solid line represents a smoothed average of 3.50 eV pump experiments and a dashed line corresponds to the smoothed average of 2.72 eV pump.

PMC9110332

41598_2022_11882_Fig4_HTML.jpg

0.414879

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(a,b) High-fluence photoemission from a circular spot of (a) 9.8 nm × 15.4 nm 4.5 ML and (b) 9.0 nm × 26.8 nm 5.5 ML CdSe CQWs.

PMC9110332

41598_2022_11882_Fig5_HTML.jpg

0.423356

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(a,b) Thermal differential absorption spectra (ΔA = AT-A295 K) of (a) 9.8 nm × 15.4 nm 4.5 ML and (b) 9.0 nm × 26.8 nm 5.5 ML CdSe CQWs are shown in colors. The black dashed line shows the ΔA of the same 4.5 or 5.5 ML CdSe CQWs under intense photoexcitation (> 5 × 1013 cm−2). The plots are scaled for presentation. (c,d) Transient absorption spectra collected at a pump-probe delay of 3 ps and average excitation density < 1 × 1012 cm−2 as a function of sample temperature. (e) Half-width at half-maximum of transient absorption bleach features as a function of temperature based upon data in figure panels (c) and (d). (f) Ratio of the light hole (LH) and heavy-hole (HH) bleach feature as a function of sample temperature using data in (c) and (d).

PMC9110332

41598_2022_11882_Fig6_HTML.jpg

0.47522

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(a,b) Static X-ray diffraction pattern (black line) and transient X-ray diffraction patterns (ΔS) as a function of power at 40 ps pump-probe delay using 3.1 eV pump photon energy. Data are shown for (a) 7.4 nm × 23 nm 4.5 ML and (b) 7.6 nm × 41 nm 5.5 ML CdSe CQW samples. (c,d) Quantification of the magnitude of ΔS signal as a function of excitation density for the same samples. Total ΔS signal is disambiguated into signal arising from thermal disordering and shift of the diffraction angle.

PMC9110332

41598_2022_11882_Fig7_HTML.jpg

0.458195

2fd1f82136214a5e9fe7210f31463bfe

Lesion monitoring in diabetic and non-diabetic mice. Representative photos of the full-thickness skin excision ulcers at different post-lesion times in C57BL/6 J a and db/db b mice. Sampling strategy for the re-epithelization analysis. The arrow indicates the area covered by a thin layer of epithelial cells, while the dotted line indicates the border of the non-re-epithelized area, used for the analysis c. Ulcer areas in the experimental groups over the observational days. N = 10 ulcers/groups were included in this experiment. Statistical analysis: two-way ANOVA, p < 0.0001 for time and genotype b. Representative photos of the pressure ulcers at different post-lesion times in C57BL/6 J e and db/db f mice. Ulcer areas in the experimental groups over the observational days. N = 10 ulcers/groups were included in this experiment. Statistical analysis: two-way ANOVA, p < 0.0001 for time and genotype g

PMC9110453

441_2022_3624_Fig1_HTML.jpg

0.449676

a7c7b9c577ef4a57800e3a549ef8641c

Histological and immunohistochemical analysis of the repaired skin in the full-thickness excision and pressure model. N = 5 animals/groups were included in this experiment. Re-epithelization in C57BL/6 J and db/db mice in full thickness excision wound a–a’’’’ and pressure-induced wound b–b’’’’. In each model, representative micrographs of H&E staining of the intact and repaired skin and the relative morphometric measure are shown. Re-innervation in C57BL/6 J and db/db mice in full thickness excision wound c–c’’’’ and pressure-induced wound d–d’’’’. In each model, representative micrographs of PGP9.5-IR fibers in the intact and repaired skin and the relative morphometric measure are shown. Capillary density in C57BL/6 J and db/db mice in full thickness excision wound (e–e’’’’) and pressure-induced wound (f–f’’’’). In each model, representative micrographs of PECAM-IR fibers in the intact and repaired skin and the relative morphometric measure are shown. Data are presented as mean ± SEM. Statistical analysis: Student’s t-test: intact vs lesioned for each genotype, *p < 0.05; **p < 0.01; C57BL/6 J vs db/db mice, a p < 0.05, b p < 0.01, c p < 0.001. Bars: 50 µm

PMC9110453

441_2022_3624_Fig2_HTML.jpg

0.426199

e64c349701b1429096c2ff592d765c47

Gene expression and protein quantification of re-innervation and angiogenesis-related molecules. Graphs show the relative expression analysis of TrkA a, a’ and p75NTR a’’, a’’’ or Hif1a b, b’, Flt1 b’’, b’’’, and Kdr b’’’’, b’’’’’ genes normalized on C57BL/6 J for the intact group analysis a, a’’, b, b’’, b’’’’, or on genotype-specific intact groups (horizontal dotted line) for the ulcer analysis a’, a’’’, b’, b’’’. Graphs show the quantification of the Ngf and Vegf proteins in the plasma of C57BL/6 J and db/db animals, in intact conditions or ulcers c-d’. In the comparison between the intact groups c, d, the absolute concentration of the protein is shown, while in the comparison between ulcers c’, d’, the quantification is normalized on the genotype-specific intact group (horizontal dotted line). Data are presented as mean ± SEM. N = 6 animals/groups were included in this experiment. Statistical analysis: C57BL/6 J vs db/db intact, Student’s t-test. Ulcer comparison, one-way ANOVA followed by Dunnett’s post-test versus the genotype-specific intact group a–b’’’’’ or Tukey’s post-test c-d’. Asterisks represent the differences versus the control group or between two groups indicated by an horizontal line (*p < 0.05; **p < 0.01; ****p < 0.0001)

PMC9110453

441_2022_3624_Fig3_HTML.jpg

0.476463

a55bfe7d4a1f489db1cfa4e351f74438

PCR arrays and western blot analysis: C57BL/6 J vs db/db intact skin. Cluster analysis of the 252 inputs obtained from the three PCR arrays plates for growth factors, extracellular matrix and related molecules, and neurotrophins a. Scatter plot representation of the gene expression fold change in db/db vs C57BL/6 J intact skin, using a fold change of 3 as cutoff value for significance gene expression variation b. STRING software–based protein interaction network analysis of proteins encoded by genes showing a fold of change higher than 10 in db/db vs C57BL/6 J intact skin c. Gene Codis 4.0 software pathway enrichment analysis based on the KEGG database, using the entire group of 101 genes differentially expressed in db/db vs C57BL/6 J intact skin (fold of change > 3). The KEGG database recognized 77 of the 101 input genes d. Graphs show the quantification by western blot of Akt e and p-Akt e’, expressed as a ratio on b-Actin and Akt (total), respectively, in C57BL/6 J and db/db intact skin. Representative images of quantified proteins for each group are shown in the figure e’’. PCR array experiments were performed on pooled RNAs (N = 6 animal/group). Statistical analysis: Student’s t-test. Asterisks represent the differences between db/db and C57BL/6 J (*p < 0.05)

PMC9110453

441_2022_3624_Fig4_HTML.jpg

0.439988

f312a05ea09541d6a82cf804f00de4c4

PCR array analysis: skin excision vs pressure ulcer in C57BL/6 J and db/db mice. Scatter plot representation of gene expression fold change in C57BL/6 J skin excision a or pressure ulcer b, and db/db skin excision c and pressure ulcer d, vs the genotype-specific intact skin, using a fold change of 3 as a cutoff value for gene expression variation significance. PCR array experiments were performed on pooled RNAs (N = 6 animal/group)

PMC9110453

441_2022_3624_Fig5_HTML.jpg

0.396154

97733c37d72b498184565ca83e812944

Protein–protein interaction analysis: skin excision vs pressure ulcer in C57BL/6 J and db/db mice. STRING software–based protein interaction network analysis of proteins encoded by genes showing a fold of change higher than 10 in C57BL/6 J skin excision a or pressure ulcer b, and db/db skin excision c and pressure ulcer d, vs the genotype-specific intact skin. PCR array experiments were performed on pooled RNAs (N = 6 animal/group)

PMC9110453

441_2022_3624_Fig6_HTML.jpg

0.405161

546eaadded54468c8de408dfcd8da244

Pathway enrichment analysis of common and differentially upregulated genes by pressure ulcer in C57BL/6 J and db/db mice. Pathway enrichment analysis performed by GeneCodis 4.0 using Panther and Reactome databases for common genes upregulated by pressure ulcers in C57BL/6 J and db/db using Panther a or Reactome a’ algorithm, and genes upregulated only in C57BL/6 J, using Panther b or Reactome b’ algorithm, or only in db/db using Panther c or Reactome c’ algorithm. Only significant pathways are shown (p < 0.05). Color gradient represents the gene number in each identified pathway, while the -log (adjusted p value) is shown on the horizontal axis. PCR array experiments were performed on pooled RNAs (N = 6 animal/group)

PMC9110453

441_2022_3624_Fig7_HTML.jpg

0.491277

e14c85b693f94028ab536116bda63dda

Study participants.

PMC9111195

AJO-62-553-g001.jpg

0.447599

2a0545e49e814f3ab93d967c063ce429

PRISMA flow diagram.

PMC9111890

gr1.jpg

0.470658

ec96c2f9417842fc9983c08c3e4f0306

Electrospinning machine.

PMC9111983

gr1.jpg

0.520511

9f8216614a24406082a9e54a5b2c2f83

Assembly of the base frame (left) and the box cover (right).

PMC9111983

gr10.jpg

0.522525

293720535ee543c081018d972461bb5e

Front view of the control panel.

PMC9111983

gr11.jpg

0.407266

b87aef530f9c4ff290fd04a195be5bb5

SEM images of PVA-based electrospun nanofiber with 5,000x (a), 10,000x (b), 20,000x (c) magnifications, and histogram for frequency of the diameter nanofiber (d). From those images, it is shown that the average diameter of nanofiber is approximately 170 nm.

PMC9111983

gr12.jpg

0.490337

d4cb6be76e1f44abb8981ba4c6f0fecb

XRD patterns resulted from the characterization of the PVA based electrospun nanofiber with the peak at 19.3° of 2-theta.

PMC9111983

gr13.jpg

0.511887

3d7c33e9eb1f4debaa1b8e65d4a9b4dd

FTIR pattern of the studied material.

PMC9111983

gr14.jpg

0.508765

501764f60f1d4a17ab6143d3c5e36604

TGA (blue) vs. DSC (red) graphs of PVA electrospun nanofiber. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

PMC9111983

gr15.jpg

0.470073

ad315a2e50a644a7b24292f6c1859f8d

Tensile test on nanofiber specimens according to ASTM D638-14 at a rate of 2 mm/min, at the start of the test (a), when fracture (b), when released from the machine (c), and stress vs. strain curves for PVA nanofiber at constant speed of 2 mm/min (d).

PMC9111983

gr16.jpg

0.492468

06e318a9c2b940dca3d2cecccce8f013

Measurement of surface area using ImageJ, background (a), nanofiber area (b).

PMC9111983

gr17.jpg

0.42968

b96da267e889426f8483628efa55d31e

Hardware and electronic system of Syringe Pump.

PMC9111983

gr2.jpg

0.428374

7150a773c144403996de82a0cd145a83

Hardware and electronic system of drum collector.

PMC9111983

gr3.jpg

0.408535

a2087326f28344d1a1f05bbbf858648b

Syringe pump components.

PMC9111983

gr4.jpg

0.43106

03c6200212f3495b88c49500a94bc393

Drum collector components.

PMC9111983

gr5.jpg

0.444905

c6deee0bab4a4a52b3ddbed9afa0117b

Electrical schematic of syringe pump controller.

PMC9111983

gr6.jpg

0.443228

54441c4e67ad4565acaf634aa37d482a

Electrical schematic of drum collector controller.

PMC9111983

gr7.jpg

0.537703

c73b8344d57d44869db32632a916c505

A simplified flow-chart showing the main functions of the syringe pump controller.

PMC9111983

gr8.jpg

0.547778

31cd1190924244c581c60af9252b2bd9

A simplified flow-chart showing speed controller of drum collector.

PMC9111983

gr9.jpg

0.510196

a9cbc0b626ec44f9bb957dc2f4099dcd

The Replication pathway of linear DNAs with hp telomeres and telomere resolvase domain organization.A, bidirectional replication of the chromosome initiates at an internal origin and continues until replication rounds the hairpin telomeres. A circular dimer intermediate results that is fused at replicated telomere junctions (denoted at L/L' and R/R'). This intermediate is then resolved by a DNA cleavage and reunion reaction called telomere resolution that reconstitutes linear monomers terminated by hp telomeres. B, the domain architecture of three telomere resolvases characterized in vitro. TelK is the telomere resolvase from φKO2 of Klebsiella oxytoca, TelA is from Agrobacterium tumefaciens, and ResT is from Borrelia burgdorferi. Domains identified as homologous either through BLAST alignment or via structural analysis are identified in identically shaped and shaded domains (i.e., N-core in TelK and TelA and the catalytic domain in all three resolvases). Domains without a homologous counterpart are given unique colors/shades. Domains that have been experimentally deleted without affecting telomere resolution are delimited in square brackets. The nucleophilic tyrosine is identified by amino acid number in the catalytic domains. hp, hairpin.

PMC9111995

gr1.jpg

0.42397

e1e050084fd64aa2bb930464d6603cc1

Deletion of the N-terminal domain reduces the divalent metal dependence of telomere resolution.A, schematic representation of the SspI-linearized plasmid substrate containing a 36-bp rTel junction (shaded and bisected by a line) and the resultant products of telomere resolution. The size (in kilobase pairs) is indicated for the plasmid substrate and the products of telomere resolution. S denotes the substrate, and P1 and P2 denote the telomere resolution products. B, 0.8% (w/v) agarose 1× TAE gel panel of telomere resolution reactions incubated at 30 °C for 10 min with the concentration of TelA indicated above the gel. The reaction buffer contained 1 mM EDTA, MgCl2, or CaCl2 as indicated in the loading key above the gel. C, 0.8% (w/v) agarose 1× TAE gel panel of telomere resolution reactions incubated at 30 °C for 30 min with the concentration of TelA (107–442) (ΔN) indicated above the gel. The reaction buffer contained 1 mM EDTA, MgCl2, or CaCl2 as indicated in the loading key above the gel. D, timecourse plots of telomere resolution reactions with 38 nM of wt TelA incubated with 1 mM EDTA or 1 mM CaCl2. Reactions were performed in triplicate, and the mean and standard deviation are shown. E, timecourse plots of telomere resolution reactions with 38 nM of TelA (107–442) (ΔN) incubated with 1 mM EDTA or 1 mM CaCl2. Reactions were performed in triplicate, and the mean and standard deviation are shown.

PMC9111995

gr2.jpg

0.430035

ac4113ed83e94eb1b194eda15f8114ba

TelA (D202A) can perform telomere resolution independently of a divalent metal ion.A, telomere resolution timecourse plots with 38 nM wt TelA comparing 1 mM EDTA, 4 mM MgCl2, and 4 mM CaCl2 conditions. B, telomere resolution timecourse plots with 38 nM TelA (D202A) comparing 1 mM EDTA, 4 mM MgCl2, and 4 mM CaCl2 conditions. C, initial rates for 38 nM of wt TelA and TelA (D202A) for the divalent metal conditions are described in (A) and (B). All data plots show the mean and standard deviation of at least three independent experiments.

PMC9111995

gr3.jpg

0.447102

d616ad0383104fe4b41f8d6999a9bf64

Titration of the N-terminal domain into reactions with TelA (107–442) and TelA (107–442; D202A).A, 0.8% (w/v) agarose 1× TAE gel panels of telomere resolution reactions incubated at 30 °C for 10 min with 38 nM TelA (107–442) or TelA (107–442; D202A) and a titration of TelA (1–106) added in trans. The reaction buffer contained either no divalent metal ions (0.2 mM EDTA) or 2 mM CaCl2. M in the loading key above the gel indicates a protein-free reaction. S denotes the migration position of the substrate DNA, P1 and P2 denote the products, and P3 denotes the presumptive fusion product of the P1 hairpin telomeres. ΔN denotes TelA (107–442), ΔN; D202A denotes the double mutant, and N denotes TelA (1–106). B, % product formation (telomere resolution plus hairpin telomere fusion) plotted for telomere resolution reactions using 38 nM TelA (107–442) or TelA (107–442; D202A) on their own or in the presence of 380 nM TelA (1–106) added in trans. Conditions with 0.2 mM EDTA versus 2 mM CaCl2 or MgCl2 are shown. Reactions were performed in triplicate, and the mean and standard deviation are shown. C, % hp fusion abstracted from the reactions plotted in (B). Reactions were performed in triplicate, and the mean and standard deviation are shown. hp, hairpin.

PMC9111995

gr4.jpg

0.412336

6ce1e7e817a54d55bc4708fb2e3e1022

Chemical cross-linking of the interaction of the N-terminal domain with TelA (107–442). α-His Western blotting and Imperial Protein staining of 5%/10 to 18% (v/v) SDS-PAGE gradient gel panels for protein–protein cross-linking promoted by DSP (see Experimental procedures). wt denotes wildtype TelA, ΔN denotes TelA (107–442), and N represents TelA (1–106). Cross-linking of ΔN and N is indicated by the red arrows, and cross-linking of multiple ΔN to one another is indicated with black arrows. −/+ DNA denotes the presence or absence of 5 μg/ml SspI-digested pEKK392 in the reaction. wt and ΔN were present at 240 nM, and N was present a 1 μM. DSP, dithiobis [succinimidylpropionate].

PMC9111995

gr5.jpg

0.419455

3f4803eafe2a4d6496b350f4e8d32ff1

Fusion of oligonucleotide hp telomeres.A, cleavage of a half-site substrate comprised the sequence present in the hp telomeres but without the presence of the hp turnaround. Cleavage of the half-site is followed by diffusion away of the three nucleotides distal to the scissile phosphate trapping TelA on the cleaved half-site. This migrates in the “cleavage product” (CP) position of the gel. The N-terminal deletion mutants of TelA produce a faster migrating CP due to the missing mass of the deleted N-terminal domain. The mock versions of these substrates were produced by changing all T’s to A’s, A’s to T’s, G’s to C’s, and C’s to G’s. This maintains the sequence composition of the half-site and hp telomere substrates but produces a scrambled version that should not be recognized by TelA. wt denotes wildtype TelA (wt), and DA and ΔN denote TelA (D202A) and TelA (107–442), respectively, and their combination within a double mutant (ΔN; DA). When the TelA (1–106), the N-terminal domain is added in trans, this is indicated in the gel loading keys by +N. Shown are 8% (v/v) PAGE 1× TAE/0.1% (w/v) SDS gels of reactions performed with 5′-end-labeled substrate. B, fusion of hp telomeres by reversal of the telomere resolution reaction produces a replicated telomere (rTel) as the product. The details of the gel loading key are as noted for (A). Shown are 8% (v/v) PAGE 1× TAE/0.1% (w/v) SDS gels of reactions performed with 5′-end-labeled substrate. All reactions contain 76 nM TelA and 2 mM CaCl2. The incubation temperatures and duration are noted below the gels.

PMC9111995

gr6.jpg

0.409662

42cc39f0b7e74d5a992115885ee740c8

Recombination between replicated telomeres.A, schematic representation of a strand exchange reaction between negatively supercoiled pEKK392 and a 5′-32P end-labeled (∗) 87-bp oligonucleotide rTel. HJs resulting from this strand exchange can be resolved with T7 endonuclease I. Linearization with AhdI prior to T7 endonuclease I treatment results in resolution into two products due to the opposing strand scission sites of the two enzymes. The cleavage position of AhdI is labeled in the diagram. B, autoradiogram and ethidium bromide–stained 0.8% (w/v) agarose 1× TAE gel panels of HJ formation between 10 μg/ml pEKK392 and 70 nM of either end-labeled rTel (OGCB827∗/828∗) or mock rTel (855∗/856∗) in 2 mM Ca2+. wt denotes wildtype TelA, and DA and ΔN denote TelA (D202A) and TelA (107–442), respectively, and their combination within a double mutant (ΔN; DA). TelA (1–106) is denoted by N, and when added in trans, by +N. All proteins were present at 76 nM besides N which was present at 380 nM. C, autoradiogram and ethidium bromide–stained 0.8% (w/v) agarose 1× TAE gel panel of HJ formation between 10 μg/ml pEKK392 and 65 nM end-labeled rTel with or without 76 nM of the double mutant (ΔN; DA). AhdI and/or T7 endo I treatment was applied as indicated in the panel legend. HJ, Holliday junction.

PMC9111995

gr7.jpg

0.476868

51c10cfb3b9745ca9d12c879d1962141

Model of TelA regulation. Models for metal binding with wildtype TelA (A), N-terminal truncation mutant of TelA (B), and the N-terminal domain being added in trans (C) are shown. A, the N-terminal domain of TelA physically interacts with the remainder of TelA, masking the catalytic and/or refolding module residues and rendering the enzyme inactive (represented by the stippled shading of the domains). The presence of low levels of a divalent metal ion (with a preference for calcium) results in metal binding to a high-affinity site in the inhibitory N-terminal domain. This relieves the inhibitory effect of the N-terminal domain, and the enzyme is in its active conformation. High calcium concentrations stimulate binding at a second, low-affinity metal-binding site located in proximity to the D202 residue. Ca2+ binding at this second site inhibits enzymatic activity. B, truncation of the inhibitory N-terminal domain removes the high-affinity metal-binding site and leaves the enzyme in its open, active conformation. Addition of low calcium concentrations has no effect on the truncation mutant of TelA. High calcium concentrations still lead to binding at the low-affinity metal-binding site and render the enzyme inactive. Mutation of the D202 residue disrupts binding at the low-affinity metal-binding site, resulting in high calcium concentrations having no effect on enzymatic activity. C, addition of the N-terminal domain in trans with the rest of TelA re-establishes the inhibitory protein–protein interactions observed with the wildtype enzyme. Exposure to low calcium concentrations results in metal binding at the high-affinity site and disruption of the inhibitory interactions.

PMC9111995

gr8.jpg

0.471167

d80a2023a0fb40ec99d87854fc3f389c

Locations of survey respondents, by county.

PMC9112314

10.1177_11782218221095872-fig1.jpg

0.447985

113ef7ed1b50469bb2f91f19d57d1a40

Changes in facility reported client success rates across the pre-pandemic, early pandemic, and late pandemic periods.

PMC9112314

10.1177_11782218221095872-fig2.jpg

0.475793

3f97d947041c4d0da2935b36c7b422f0

Differential gene expression and pathway analysis comparing infection group to unexplained fever on Day 1 and Day 2. (a) Mean–difference (MD) plot showing the 1829 down‐regulated (blue) and 772 up‐regulated (red) DE genes in PBMCs from FN episodes with ‘any infection’ (bacteraemia, MDI and CDI combined) versus unexplained fever at time of hospital admission (Day 1). (b) MD plot showing the 142 down‐regulated (blue) and three up‐regulated (red) DE genes in PBMCs from FN episodes with ‘any infection’ (bacteraemia, MDI and CDI combined) versus unexplained fever on Day 2. (c) Top 20 KEGG pathways over‐represented when comparing DE genes in PBMCs from FN episodes with ‘any infection’ (bacteraemia, MDI and CDI combined) versus unexplained fever at time of hospital admission (Day 1). (d) Top 20 KEGG pathways over‐represented when comparing DE genes in PBMCs from FN episodes with ‘any infection’ (bacteraemia, MDI and CDI combined) versus unexplained fever on Day 2.

PMC9113042

CTI2-11-e1383-g001.jpg

0.460415

a16c98289e2645008a75b351e6428ab2

Differential gene expression and pathway analysis of bacteraemia versus all other causes of FN on Day 2. (a) MD plot showing the 11 down‐regulated (blue) DE genes in PBMCs from FN episodes with bacteraemia versus ‘all other’ causes on Day 2. (b) Heatmap of 11 significantly differentially expressed genes (P < 0.05) in PBMCs from FN episodes with bacteraemia versus ‘all other’ causes on Day 2. Colour code indicates the Z score. (c) Top 10 Hallmark gene sets over‐represented when comparing DE genes in bacteraemia versus ‘all other’ causes on Day 2. ( d) Top 10 KEGG pathways over‐represented when comparing DE genes in bacteraemia versus ‘all other’ causes on Day 2.

PMC9113042

CTI2-11-e1383-g002.jpg

0.434833

b38cae6dcb354f058b33c8f5a5275b6d

Differential gene expression and hallmark gene set pathway analysis of bacteraemia episodes comparing blood collected on Day 1 to blood collected on Day 2. (a) MD plot showing the 67 up‐regulated (red) and 41 down‐regulated (blue) DE genes in PBMCs from FN episodes in bacteraemia episodes on Day 1 and Day 2. (b) Top KEGG pathways up‐regulated or down‐regulated when comparing DE genes in bacteraemia episodes on Day 1 and Day 2.

PMC9113042

CTI2-11-e1383-g003.jpg

0.426139

becbd5fdb1724cbea05c4f3e7b13c4cf

Differential gene expression and pathway analysis of bacteraemia versus all other causes of FN on Day 1. (a) MD plot showing the 21 down‐regulated (blue) and 3 up‐regulated (red) DE genes in PBMCs from FN episodes with bacteraemia versus ‘all other’ causes at the time of hospital admission (Day 1). (b) Heatmap of the 24 significantly differentially expressed genes (P < 0.05) in in PBMCs from FN episodes with bacteraemia versus ‘all other’ causes at the time of hospital admission (Day 1). Colour code indicates Z‐score. (c) Top 20 Hallmark gene sets over‐represented when comparing DE genes in bacteraemia versus ‘all other’ causes on Day 1. (d) Top 20 KEGG pathways over‐represented when comparing DE genes in bacteraemia versus ‘all other’ causes on Day 1.

PMC9113042

CTI2-11-e1383-g005.jpg

0.511966

a3ef10fa8b784c9d810c5d8f31c005d3

Differential gene expression analysis of comparing different MDI infections versus unexplained fever on Day 1. (a) MD plot showing the 1056 down‐regulated (blue) and 150 up‐regulated (red) DE genes in PBMCs from FN episodes with bacteraemia versus unexplained fever at time of hospital admission (Day 1). (b) MD plot showing the 506 down‐regulated (blue) and 76 up‐regulated (red) DE genes in PBMCs from FN episodes with non‐bloodstream bacterial MDI versus unexplained fever at time of hospital admission (Day 1). (c) MD plot showing the two down‐regulated (blue) and 130 up‐regulated (red) DE genes in PBMCs from FN episodes with viral non‐bloodstream MDI versus unexplained fever on Day 2. (d) Common and unique DE genes in non‐bloodstream bacterial MDI versus unexplained fever and viral MDI versus unexplained fever FN episodes at the time of admission (Day 1). Unique DE genes are indicated in the respective circles, while all common DE genes are indicated at the bottom right of the diagram (red, up‐regulated; blue, down‐regulated).

PMC9113042

CTI2-11-e1383-g006.jpg

0.46572

c1d3098bd286430ba9bfafdbf9f0c672

The percentage of (a) sign, (b) comorbidity, and (c) deceased patients by age group and length of stay in hospital.

PMC9113873

BMRI2022-2350063.001.jpg

0.449058

5e1bf9f816ac4673bc7c856852776ea8

The Kaplan-Meier survival time by demographic variables.

PMC9113873

BMRI2022-2350063.002.jpg

0.444696

a7742781c03443fd8b00d6efb83ca6cc

The case fatality rate of COVID-19 patients.

PMC9113873

BMRI2022-2350063.003.jpg

0.393163

e4184ed42d574faa96ea961cda84d538

Characteristics of adipose tissue-derived multi-lineage progenitor cells (ADMPCs). (a) Mesenchymal stem cell (MSC) surface marker expression on ADMPCs. The expression of each surface marker is shown on the shaded histogram. Staining with an isotype control mAb is represented by a black line. (b) Colony formation of ADMPCs. Cells were seeded with the indicated density and cultured for 2 weeks. Cells were then fixed and stained with 0.1% crystal violet. (c) Multipotency of ADMPCs. Representative images are shown of Alizarin red staining of ADMPCs cultured in osteogenic differentiation media for 28 days, Oil red O staining of ADMPCs cultured in adipogenic differentiation media for 24 days, and Toluidine blue staining of ADMPCs cultured in chondrogenic differentiation media for 20 days.

PMC9114023

41598_2022_11986_Fig1_HTML.jpg

0.436567

0f10b9a3ceab47908013078457cfad4e

Representative images of adipose tissue-derived multi-lineage progenitor cell (ADMPC) transplantation. (a) Pre-operative intra-oral findings. This case was a 51-year-old female. The test tooth was an upper left second molar with a 6-mm periodontal pocket in the distal area. (b, c) Intra-oral findings during periodontal surgery. The flap operation was performed in accordance with the modified Widman procedure. After reversing the gingival flap, a circumferential intra-bony defect filled with granulation tissue was revealed and the granulation tissue was removed. After washing the intra-bony defect with normal saline, ADMPCs mixed with fibrin gel were transplanted into the intra-bony defect. (d) Postoperative intra-oral findings. Four weeks after ADMPC transplantation, no abnormal findings were found at the surgical site.

PMC9114023

41598_2022_11986_Fig2_HTML.jpg

0.42724

40d0accf545645e6a7baf852d0db1d09

Clinical assessment of probing pocket depth (PD) and clinical attachment level (CAL). Results of (a) PD reduction and (b) CAL gain are shown as box-and-whisker plots. The box, notch, and horizontal line denote the distance between the first and third quartile ranges (interquartile range; IQR), mean, and median, respectively. The upper whisker indicates a maximum value smaller than 1.5 × IQR above the third quartile (Q3). Similarly, the lower whisker indicates a minimum value greater than 1.5 × IQR below the first quartile (Q1). It also displays the outliers which were defined as further outside than Q1 − 1.5 × IQR or Q3 + 1.5 × IQR. PD reduction and CAL gain of the test sites were measured at 3 months, 6 months, 9 months (n = 12). Individual data is shown in Supplemental Table 4. *p < 0.0001, with the use of a one-sample t-test based on the closed testing procedure.

PMC9114023

41598_2022_11986_Fig3_HTML.jpg

0.416072

2600caa1dc5f48f8ba90ae47b8f38c64

Outcome of adipose tissue-derived multi-lineage progenitor cell (ADMPC) transplantation by dental radiographs. Radiographic outcomes of ADMPC-transplanted individuals. Case no. 2 was a 51-year-old woman. Case no. 10 was a 58-year-old woman. Dotted lines indicate the remaining alveolar bone crest or the bottom of the bone defect. The radiographs clearly show that the bone defect was filled with newly generated alveolar bone at 9 months after transplantation.

PMC9114023

41598_2022_11986_Fig4_HTML.jpg

0.463073

9977742fe45c4a25b7157c872e7b65d9

Clinical assessment of new bone formation. Results of new bone formation are shown using the same box-and-whisker plot representation as in Fig. 2. The new bone formation rate was measured using X-ray images at 1 month, 3 months, 6 months, and 9 months (n = 12). *p < 0.0001, †p < 0.001, ‡p < 0.025, with the use of a one-sample t-test based on the closed testing procedure.

PMC9114023

41598_2022_11986_Fig5_HTML.jpg

0.47557

1eafcdfd7513466cb74b6800de4e36c8

Neutrophil elastase activity is increased in periodontal tissue by ligature-induced periodontitis. (A, B) PBS or NE inhibitor (50 μg in 5 μL) was injected into the palatal gingiva of a ligature-induced murine model of periodontitis once a day for 7 (A) or 3 (B) days. (A) Frozen maxillae sections (10 μm) were stained with anti-NE antibody (green), anti-Ly6G antibody (red), and DAPI (nucleus; blue). Representative fluorescence images observed using a confocal laser scanning microscope are shown. Scale bar: 50 μm. (B) NE activity in supernatants from the homogenized palatal gingiva was evaluated. Data are presented as the mean ± SD (n = 5 per group). The group means were compared using one-way analysis of variance with Tukey’s multiple comparison test. AB alveolar bone, D dentine, DAPI 4′,6-diamidino-2-phenylindole, Ly6G lymphocyte antigen 6 complex locus G, NE neutrophil elastase, PDL periodontal ligament, SD standard deviation.

PMC9114116

41598_2022_12358_Fig1_HTML.jpg

0.412973

dd12b42f2940468893e71655a027eee5

Neutrophil elastase inhibitor inhibits ligature-induced alveolar bone loss. (A) Representative images of the maxillae from indicated treatment groups 8 days after ligature placement. Scale bar: 0.5 mm. (B) Periodontal bone loss was assessed using a stereoscopic microscope. Negative values indicate bone loss relative to the unligated control. (C, D) Frozen maxillae sections were stained with tartrate-resistant acid phosphatase. (C) Representative images obtained by optical microscopy are shown. Scale bar: 50 μm. (D) All the TRAP-positive multinucleated giant cells in the periodontal ligament of ligated second molar were counted in five random coronal sections. Data are presented as the mean ± SD (n = 5 per group). The group means were compared using one-way analysis of variance with Tukey’s multiple comparison test. AB alveolar bone, D dentine, MNCs multinucleated cells, NE neutrophil elastase, PDL periodontal ligament, SD standard deviation, TRAP tartrate-resistant acid phosphatase.

PMC9114116

41598_2022_12358_Fig2_HTML.jpg

0.431134

ec809af965544b459428501b08b19d5e

Neutrophil elastase inhibitor decreases the gene transcription of proinflammatory cytokines in the murine gingiva. Messenger RNA transcription levels of Il6, Il1b, and Cxcl1 in the palatal gingiva of mice from the indicated groups were determined by real-time PCR. Relative mRNA levels were normalized to those of Gapdh. Data are presented as the mean ± SD (n = 5 per group). The group means were compared using one-way analysis of variance with Tukey’s multiple comparison test. NE neutrophil elastase, SD standard deviation.

PMC9114116

41598_2022_12358_Fig3_HTML.jpg

0.407494

cfd8c9fe5fa24bf2bdc97fdddf353844

Neutrophil elastase induces exfoliation of gingival epithelial keratinous layer via cleavage of cell adhesion molecule. (A, B) Three-dimensional human oral epithelial tissue models were exposed to 100 mU/mL NE followed by 12-h incubation. (A) Frozen sections were stained with hematoxylin and eosin. Representative images obtained by optical microscopy are shown. Scale bar: 100 μm. (B) Representative fluorescence microscopy images of the sections stained for DAPI (nucleus, blue) and DSG1 (green) are shown. Scale bar: 100 μm. K in Fig. 5A and B indicates keratinous layer. (C, D) Recombinant human DSG1, occludin, and E-cadherin were exposed to NE (10, 50, and 100 mU/mL) for 3 h and determined by western blotting (C) or Coomassie Brilliant Blue staining (D). DSG1 desmoglein 1, NE neutrophil elastase.

PMC9114116

41598_2022_12358_Fig4_HTML.jpg

0.453976

439813a769e74e9c84d862f8a38eef61

Neutrophil elastase induces disruption of periodontal epithelial barrier. (A–E) Monolayers of human gingival epithelial cells were exposed to 10–100 mU/mL NE for 3 h. (A) Transepithelial permeability was determined by measuring 70 kDa of FITC-dextran fluorescence intensity in the medium from the lower chamber compartments. (B–E) The transepithelial permeability of each bacterium was determined using the colony counting method. Data are presented as the mean ± SD (n = 5 per group). The group means were compared using one-way analysis of variance with Dunnett’s multiple comparison test. NE neutrophil elastase.

PMC9114116

41598_2022_12358_Fig5_HTML.jpg

0.36016

ad2f36e8734049bca4324d975ae9a63b

Recognition of keywords of iPSCs and ESCs (Have you heard keywords of iPSCs and ESCs?).

PMC9114515

gr1.jpg

0.408127

9a5ffc2f5c5749e7b79f58628fd7da3f

Opinions concerning the progress of RM (Please select one statement from the following that best describes your overall thoughts about regenerative medicine research).

PMC9114515

gr2.jpg

0.396446

e333d3b96e7d4f42b1697dfdbb631bab

Trust of experts' discourses (Can you trust the story of experts on the safety and effects of RM?).

PMC9114515

gr3.jpg

0.392498

e24771daab38447c80c60d358289a01b

Interested topics on RM (What do you want to know? Please choose three interesting topics.) A Chi-square test was conducted. ∗p < 0.05, ∗∗p < 0.01.

PMC9114515

gr4.jpg

0.45474

5a63567d2fb64c179c5eb07b81aec227

What factors are important for your acceptance of regenerative medicine? Please choose three factors. Chi-square test was conducted. ∗p < 0.05, ∗∗p < 0.01.

PMC9114515

gr5.jpg

0.504011

70192e121c8244089fff0b4337059dbd

Schematic illustration of the ternary vector system used for maize B104 transformation. (A) Binary construct pKL2013 (McCaw et al., 2021), 17,777 bp. PZmUbi, maize polyubiquitin gene promoter; zCas9, maize codon-optimized Cas9 from Streptococcus pyogenes; TrbcS-E9, transcriptional terminator from Pisum sativum rbcS-E9 gene; POsU3, a promoter from Oryza sativa U3 small nucleolar RNA (snoRNA) gene; ZmGl2-sgRNA1, single-guide RNA targeting maize glossy2 gene (Lee et al., 2019); TOsU6-2, terminator from O. sativa OsU6-2 snoRNA gene; Tvsp, terminator from soybean vegetative storage protein gene; mCherry, red fluorescent protein; P35S, CaMV 35S promoter; bar, bialaphos resistance gene; RB, the T-DNA right border repeat; LB, the T-DNA left border repeat; KanR, kanamycin resistance gene cassette; pBR322 ori, high copy number origin of replication for E. coli; pVS1 ori, the origin of replication from the plasmid pVS1. (B) Ternary construct or helper plasmid pKL2299 (this work), 29,605 bp. virB1-virJ, virulence genes from the Agrobacterium tumefaciens Bo542 tumor-inducing plasmid (pTiBo542); RK2 ori, the origin of replication from the broad host range RK2 plasmid; GmR, gentamicin resistance gene cassette.

PMC9114882

fpls-13-860971-g001.jpg

0.414577

4e953bcb348e400d8230d28c24d1c541

Growing maize donor plants for immature embryo production. (A) Standard flat with small pots filled with potting mix for planting maize seed. (B) Six-day-old germinated seedlings under a humi-dome. (C) Two-week-old seedlings ready to be transplanted into large pots. (D) A seedling transplanted to a large pot. (E) Plants on a 1 m tall bench. (F) Pollinated mature B104 plants on the floor. (G) An un-pollinated B104 ear (female flower) with emerged silks. (H) A shoot bag covering an un-pollinated B104 ear. (I) A mature tassel (male flower) ready to be used for pollination. (J) A pollination bag covering a mature tassel for the purpose of collecting fresh pollen. (K) An un-pollinated B104 ear with cut silks. (L) Freshly collected pollen in a tassel bag. (M) Freshly pollinated silks, 1 day after silks were cut. (N) Extracting an immature embryo for measurement while the ear is still growing on the plant. (O) Measurement of an embryo size with a caliper. (P) Estimate of an embryo size with a ruler.

PMC9114882

fpls-13-860971-g002.jpg

0.523934

3ab039b896ae40eab0e8d4aa5ff061e8

Embryo dissection, infection, and co-cultivation. An Agrobacterium “mother” plate (A) and “working” plate after 18 h incubation, streaked by a disposable loop (B). (C) A B104 ear halves on a handle made of a fork. (D) Tools for embryo dissection; a micro spatula (left) and a dental filling instrument (right). (E) A co-cultivation plate with dissected immature embryos. All embryos were re-oriented scutellum side up. (F) A plastic culture box filled with plates. (G) Cartoon illustration of the embryo dissection and infection process. Step 1, remove kernel tops using a sterile scalpel; Step 2, isolate embryo from the kernel and transfer it to a tube filled with liquid 700A infection medium; Step 3, after infection, place embryo onto co-cultivation medium and orient the embryos by placing them scutellum side up. e: embryo, s: endosperm, and p: pericarp. Demonstration of embryo dissection using a micro spatula (H) or a dental filler (I). The arrows indicate the embryo side of the kernel. Circles highlight isolated embryos.

PMC9114882

fpls-13-860971-g003.jpg