dedup-isc-ft-v107-score
float64 0.3
1
| uid
stringlengths 32
32
| text
stringlengths 1
17.9k
| paper_id
stringlengths 8
11
| original_image_filename
stringlengths 7
69
|
|---|---|---|---|---|
0.425655 | d6327c289f40406b85105078b1aa057c | (A) Amperometric I-t curves, (B) calibration curves of different concentrations of quercetin, (C) on-off switching curves and (D) interference study. | PMC10377499 | biosensors-13-00729-g009.jpg |
0.43797 | 42c269a09c664b03a9cb08b7bcaef42a | (A) Reproducibility, (B) long-term stability and (C) interference studies with different ions of the fabricated photosensitive quercetin sensors. | PMC10377499 | biosensors-13-00729-g010.jpg |
0.426198 | 67ae1dd22fac404bb5390289ff4cb3ee | Axial slices of all three cine sequences in systolic and diastolic phases. FB and BH images are almost equivalent to RMB in the delineating blood–myocardium boundary but with typically a slightly blurrier aspect. Retrospective segmented multi-breath hold (RMB), real-time single/double breath hold (BH), real-time free breathing (FB). | PMC10377861 | diagnostics-13-02403-g001.jpg |
0.417061 | ae03d12e51024ed4bb45b88b30475494 | Axial slices of all three cine sequences in systolic and diastolic phases in a patient with severe arrhythmia. Severe artifacts in RMB rendering volumetric evaluation insufficient. Image quality in FB and BH images is reduced but still diagnostic. Retrospective segmented multi-breath hold (RMB), real-time single/double breath hold (BH), real-time free breathing (FB). | PMC10377861 | diagnostics-13-02403-g002.jpg |
0.466544 | 975e5c1a6d144365a5f86ffdf3e451a5 | Bland–Altman plots for right ventricle (RV) functional parameters illustrating the differences between RMB to BH and FB (Reader 1). Retrospective segmented multi-breath hold (RMB), real-time single/double breath hold (BH), real-time free breathing (FB), end diastolic volume (RVEDV), end systolic volume (RVESV), stroke volume (RVSV), ejection fraction (RVEF). Stroke volumina are given in mL/m2, EF in %. (––) Mean difference; (- - -) 95% limits of agreement (i.e., mean ± 1.96 standard deviation (SD)). | PMC10377861 | diagnostics-13-02403-g003.jpg |
0.478383 | d924e03b55d440a9ba0cbfef7efc6c09 | Acquisition time (minutes). Retrospective segmented multi-breath hold (RMB), real-time single/double breath hold (BH), real-time free breathing (FB); * statistically significant (p < 0.01). | PMC10377861 | diagnostics-13-02403-g004.jpg |
0.466396 | 63693323473b40d7a2fe5dfde44280ae | The process of biospecimens and data collection in the oncology section of MUB Biobank. * BIMS—Biobank Information Management System. | PMC10378006 | cancers-15-03742-g001.jpg |
0.426544 | ec0b36341aba44e68f34ed6a1410f172 | Scheme of quality control process based on analytical techniques for monitoring hemolysis in serum/plasma samples. * The visual assessment of potential blood hemolysis (rupturing of erythrocytes) was performed according to the following scale: −, no discernable hemolysis (serum/plasma color is pale yellow or yellow)—sample suitable for further processing; +/−, suspected hemolysis (serum/plasma color is pale pink)—sample may be suitable for further processing but requires additional confirmation by spectrophotometric technique and optionally qPCR-based approach. +/++/+++, low, medium, or high degree of hemolysis (serum/plasma tinted red in varying degrees)—sample is not suitable for further processing; refrain from carrying out further procedure. # Spectrophotometric analysis based on oxyhemoglobin absorbance measurements at λ = 414 nm and at λ = 385 nm (as a lipemia indicator) using NanoDrop 2000c spectrophotometer with cuvette module (100 µL) (Thermo Fisher Scientific, Waltham, MA, USA) [15]. Range: Hemolysis score (HS): HS < 0.057—non-hemolyzed plasma/serum specimens; HS > 0.057 hemolyzed plasma/serum samples. § Quantification RT-PCR method based on hsa-miR-451a and hsa-miR-23a-3p expression levels [16]. miRNA-based hemolysis indicator formula: ΔCt (miR-23a–miR-451). Range: ΔCt > 5—possible erythrocyte miRNA contamination; ΔCt > 7–8 or more—high risk of blood hemolysis. | PMC10378006 | cancers-15-03742-g002.jpg |
0.50476 | 394c4c1ecc6f4688adeb9f77079e1aa8 | Model of quality control (QC) for RNA extracted from plasma/serum samples. | PMC10378006 | cancers-15-03742-g003.jpg |
0.435748 | 4ccdb1166dd04f48b29fd534d6059b07 | The process of raw data processing from the NGS analyses to final genome assembly and data reporting. | PMC10378006 | cancers-15-03742-g004.jpg |
0.534337 | 4d929f659b4a41c28dd014df69f18c12 | (a,b) The algorithm developed during the MOBIT project with an essential preanalytical and analytical QC process for optimal biobanking of serum/plasma samples (a) and tissue samples (b). x QC—quality control, # cDNA—complementary DNA, * RIN—RNA integrity number. | PMC10378006 | cancers-15-03742-g005.jpg |
0.463835 | f773dc8129f2441085c11f5138c54ce1 | Orthogonal partial least squares discriminant analysis (OPLS-DA) models showing the classification of plasma metabolic fingerprints obtained with liquid chromatography quadrupole time-of-flight mass spectrometry (LC-QTOF-MS) method. (Panel A) (R2 = 0.897, Q2 = 0.364) shows the separation between plasma samples collected from patients before and after the tumor resection surgery. (Panel B) (R2 = 0.993, Q2 = 0.5364) shows the separation between samples stored in cryotubes and Eppendorf tubes. | PMC10378006 | cancers-15-03742-g006.jpg |
0.42808 | 47ef76fa87044cae826bd1662563ca31 | Multiple comparison tests in the first four simulated scenarios. | PMC10378078 | entropy-25-01028-g001.jpg |
0.471626 | e0b4d2f3395b44b796c2a57951c96d50 | Changes in real-time fatality rate in different clusters during the observation period. | PMC10378078 | entropy-25-01028-g002.jpg |
0.49191 | 1eac3a76c13e4d4c9e37ba326d70d67e | Confidence intervals for mean differences in real-time fatality rate across the observation period. | PMC10378078 | entropy-25-01028-g003.jpg |
0.537272 | 202d0219ad9c417092dbdf91c46a201d | Confidence intervals for mean differences in real-time fatality rate among three regions before and at the beginning of the assistance. | PMC10378078 | entropy-25-01028-g004.jpg |
0.53229 | 580ad08d2a504797994a515190c17fd4 | Confidence intervals for mean differences in real-time fatality rate among three regions in the post-assistance period. | PMC10378078 | entropy-25-01028-g005.jpg |
0.495983 | 63be72d876c6443eab57edad0ddfb0fa | Influential factors and child’s screen time. | PMC10378130 | children-10-01193-g001.jpg |
0.550249 | d01b111eb4df487b83078eb1d2958c92 | Flow diagram of screening and identifying process of studies. | PMC10378741 | medi-102-e34425-g001.jpg |
0.428399 | 7c741e82083b4e9ea455ff6e66b6f436 | Risk of bias of the included studies. (A) Risk of bias graph: judgments about each risk of bias item presented as percentages across all included studies. (B) Risk of bias summary: judgments about each risk of bias item for each included study. +, low risk of bias; −, high risk of bias; ?, unclear risk of bias. | PMC10378741 | medi-102-e34425-g002.jpg |
0.414064 | ab2875772b054694800ce079e6366b36 | Forest plot of TCM versus placebo in terms of (A) PDQ-39, (B) SCOPA–AUT, (C) MDS-UPDRS-1, (D) PDSS, (E) HAMA, (F) HAMD, (G) adverse events. HAMA = Hamilton Anxiety Scale, HAMD = Hamilton Depression Scale, MDS-UPDRS-1 = the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale-part 1, PDQ-39 = Parkinson’s Disease Quality of Life Questionnaire, PDSS, Parkinson’s Disease Sleep Scale, SCOPA–AUT = Scales for Outcomes in Parkinson’s disease–Autonomic. | PMC10378741 | medi-102-e34425-g003.jpg |
0.396474 | 2c900ee1812d47749617989e5b7ad8ea | Forest plot of after TCM treatment versus before treatment in terms of (A) PDQ-39, (B) HAMD, (C) HAMA, (D) SCOPA–AUT, (E) MDS-UPDRS-1, (F) PDSS. HAMA = Hamilton Anxiety Scale, HAMD = Hamilton depression scale, MDS-UPDRS-1 = the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale-part 1, PDQ-39 = Parkinson’s Disease Quality of Life Questionnaire, PDSS = Parkinson’s Disease Sleep Scale, SCOPA–AUT = Scales for Outcomes in Parkinson’s disease–Autonomic. | PMC10378741 | medi-102-e34425-g004.jpg |
0.388856 | 7f9730358e664d06837ba761f739866c | Forest plot of Pingchan granule vs. placebo in terms of (A) PDSS, (B) HAMD, (C) HAMA, (D) PDQ-39, (E) before Pingchan granule treatment versus after Pingchan granule treatment, PDQ-39. HAMA = Hamilton Anxiety Scale, HAMD = Hamilton Depression Scale, PDQ-39 = Parkinson’s Disease Quality of Life Questionnaire, PDSS = Parkinson’s Disease Sleep Scale. | PMC10378741 | medi-102-e34425-g005.jpg |
0.437109 | 28b8b6735fdc4c5b80e0892d279d4ec7 | Forest plot of Zishen Pingchan granule versus placebo in terms of (A) PDSS, (B) HAMD; before Zishen Pingchan granule treatment versus after Zishen Pingchan granule treatment in terms of (C) PDSS, (D) HAMD. HAMD = Hamilton Depression Scale, PDSS = Parkinson’s Disease Sleep Scale. | PMC10378741 | medi-102-e34425-g006.jpg |
0.422565 | b0540f8927004203b4032497bdb2ce4f | Changes in (A) peroxide value (PV) and (B) malondialdehyde (MDA) content of simple-packaged (SP) and vacuum-packaged (VP) pike eels during chilled storage (n = 3). | PMC10379090 | foods-12-02791-g001.jpg |
0.409881 | 81f8e0ca139443df9932dbc6bc7a70a1 | Lipid classification and composition in fresh (FE), simple-packaged (SP), and vacuum-packaged (VP) pike eels via LC/MS-based lipidomics analysis. | PMC10379090 | foods-12-02791-g002.jpg |
0.417704 | 3f01660ead0c4ca088dcb9e16a9a2222 | Partial least squares discriminant analysis (PLS-DA) and permutation score plots of PLS-DA obtained from fresh (FE), simple-packaged (SP), and vacuum-packaged (VP) pike eels via LC/MS-based lipidomics analysis. (A,C) negative ion mode. (B,D) positive ion mode. | PMC10379090 | foods-12-02791-g003.jpg |
0.431339 | 3d8ddd49a0d34a5c9013d1ac43425336 | Composition and number of the differentially abundant lipids (DALs; p ≤ 0.05 and VIP ≥ 1 of lipid species) in pike eel samples. (A) simple-packaged (SP) vs. fresh (FE) pike eels. (B) vacuum-packaged (VP) vs. fresh (FE) pike eels. (C) simple-packaged (SP) vs. vacuum-packaged (VP) pike eels. | PMC10379090 | foods-12-02791-g004.jpg |
0.430934 | d1b579ed5b464b3b8ee8cafad1060f07 | Volcano plot of lipid profiles identified in pike eel samples. (A) simple-packaged (SP) vs. fresh (FE) pike eels. (B) vacuum-packaged (VP) vs. fresh (FE) pike eels. (C) simple-packaged (SP) vs. vacuum-packaged (VP) pike eels. | PMC10379090 | foods-12-02791-g005.jpg |
0.443301 | cce50fb64f7c49f89c5b274c82652004 | Hierarchical cluster and heat map analyses of the DALs (top 100 species) in fresh (FE), simple-packaged (SP), and vacuum-packaged (VP) pike eels. Each color block on the heat map corresponds to the abundance of different lipid species. Red (2) represents a relatively high abundance of lipids, and blue (−4) indicates a relatively low abundance of lipids. | PMC10379090 | foods-12-02791-g006.jpg |
0.417299 | 3213a92a7e64434e9ce949fe098bac08 | Clinical picture and X-ray showing crush injury of the right middle finger, debridement, and K wire insertion across the IP joints. | PMC10379268 | JOCR-13-134-g001.jpg |
0.416769 | aad49d69ebf045f6b4d44616a8bd60b1 | Clinical picture showing defect coverage by bipedicled abdominal flap, staged division of flap, and final appearance of flap. | PMC10379268 | JOCR-13-134-g002.jpg |
0.442042 | c6747f76e7294d32b30bf3140af465ff | Functional recovery at 3-month follow up. | PMC10379268 | JOCR-13-134-g003.jpg |
0.414285 | e1082294c5bd4702b84ed0cf886a876a | Clinical picture and X-ray showing gunshot injury over right thumb and little finger, fixed with Jess fixator over thumb and cross finger flap over little finger. | PMC10379268 | JOCR-13-134-g004.jpg |
0.495662 | 75d584a051a140258c58a44731e25245 | Clinical pictures showing complete healing of surgical scars and flap with complete functional recovery at 12 weeks. | PMC10379268 | JOCR-13-134-g005.jpg |
0.383957 | 601c32af7f8e4410bd9bd5ccde37bd74 | Clinical picture showing abscess of the right little finger, debridement, K wire fixation, and coverage using full thickness skin graft from anterior abdominal wall. | PMC10379268 | JOCR-13-134-g006.jpg |
0.42493 | 180e3a1071f44b118a485749995db8c4 | Clinical picture showing abscess right little finger, debridement with exposed bone and coverage using bi-pedicled abdominal flap. | PMC10379268 | JOCR-13-134-g007.jpg |
0.427602 | c84f3806597f4c13a37a81cb4919e467 | The influence of mRNA splicing and alternative splicing on gene expression. Left panel: Schematic of pre-mRNA splicing and the different forms of alternative splicing. Splicing of pre-mRNA can result in the expression of the full encoded protein or (n) number of protein isoforms produced as a result of alternative splicing. Right panel: Schematic of RNA editing’s potential to alter gene expression. Editing of the pre-mRNA by adenosine or cytidine deaminases can result in single amino acid substitutions to the protein, alter splice site selection (promoting alternatively spliced mRNAs and protein isoforms), or both. | PMC10379330 | genes-14-01386-g001.jpg |
0.449174 | 2e65db0aedca41cebe156fab36ac41af | Schematic diagram of the main SRSF (A) and hnRNP (B) proteins involved in splicing/alternative splicing. The molecular weight (designated main isoform), major structural domains, and the number of validated mRNA transcripts/protein isoforms produced from the respective genes are presented. | PMC10379330 | genes-14-01386-g002.jpg |
0.408597 | 2557fb1da73b4841af7b7c93d20c3cab | Schematic diagram of ADAR and AID/APOBEC family proteins. (A) The deamination of adenosine to inosine is carried out by homo- and heterodimers of the ADAR family proteins. Two main isoforms of ADAR1 (p110 and p150) and ADAR2 (ADAR2long and ADAR2short) are expressed to some level in all cells; only ADAR1p150 and ADAR2short are presented here. ADAR3 is catalytically inactive. (B) The deamination of cytidine to uridine is carried out by members of the AID/APOBEC family, functioning as monomers, homodimers, heterodimers, and tetramers depending on the family member involved. The molecular weight (designated main isoform), major structural domains, and the number of validated mRNA transcripts/protein isoforms produced from the respective genes are presented. | PMC10379330 | genes-14-01386-g003.jpg |
0.46875 | e9887b90d9c7427ea5ac4dab42054aa3 | The theoretical model of our research. Source: Authors’ elaboration. | PMC10379619 | foods-12-02770-g001.jpg |
0.38817 | 232234d738f94ef38872d0fb933effcc | Perception of the CSR activities of food companies as a marketing tool. Source: Authors’ research and calculations, output IBM SPSS Statistics. | PMC10379619 | foods-12-02770-g002.jpg |
0.415247 | 7119c6b725f84a29b8c5dfc9d3532c1a | Knowledge of a specific food company operating in Slovakia that is socially responsible. Source: Authors’ research and calculations, output IBM SPSS Statistics. | PMC10379619 | foods-12-02770-g003.jpg |
0.413717 | 2eeb4a17456c443589b3d51ee9d08540 | Structure of BK and sites of cleavage by significant enzymes related to drug-induced AE. Note: The amino acid sequence of BK is Arginine (Arg)–Proline (Pro)–Proline (Pro)–Glycine (Gly)–Phenylalanine (Phe)–Serine (Ser)–Proline (Pro)–Phenylalanine (Phe)–Arginine (Arg). Figure adapted from [23] for a simplified presentation of the sites of cleavage of BK by different important enzymes, marked with red arrows for ACE (angiotensin-converting enzyme), APP (aminopeptidase P), NEP (neutral endopeptidase), CPN (carboxypeptidase N), and DPPIV (dipeptidyl peptidase IV). | PMC10380452 | ijms-24-11649-g001.jpg |
0.440392 | db94460b2b784e49ade0d9dae39a5d61 | Overall presentation of different causes of angioedema classified by pathophysiology mechanisms, focusing on bradikinergic or BK-mediated angioedema (BK-AE) and drug-induced forms [3,47,109]. * Hereditary angioedema (HAE) with C1-INH deficiency with low antigenic and functional C1-INH levels (HAE-1, 85% of cases), HAE due to C1-INH dysfunction (HAE-2, 10% of cases) characterized by normal or elevated antigenic but low functional C1-INH levels, and HAE with normal C1-INH (HAE-nC1-INH, 5% of cases) due to various gene mutations. ** Acquired forms of BK-AE include drug-induced AE, such as AE induced by angiotensin-converting enzyme inhibitors (ACEIs), AE due to acquired C1-INH deficiency (AAE-C1-INH), and acquired idiopathic non-histaminergic AE. *** Mast cell-mediated angioedema (MC-AE) includes allergic IgE-mediated reactions (such as AE with anaphylaxis), nonallergic non-IgE-mediated reactions (such as AE due to non-steroidal anti-inflammatory drugs or infections), AE in chronic inducible urticaria or chronic spontaneous urticaria (sometimes referred to as idiopathic histaminergic acquired AE). The diversity of mediators involved in MC-AE is reflected also by the fact that patients with chronic spontaneous urticaria may respond to treatment with omalizumab but not to H1 antihistamines. | PMC10380452 | ijms-24-11649-g002.jpg |
0.46363 | bcaa5b9a84864c56a92452ca95dc5f2c | Metabolism of bradykinin (BK) and angioedema induced by cardiovascular and antidiabetic drugs: angiotesin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (sartans), neprilysin inhibitors, direct renin inhibitor (aliskiren), gliptins (DPP-IV inhibitors), and recombinant tissue plasminogen activators (rt-PAs), figure created and adapted after [23,57,87,111]. | PMC10380452 | ijms-24-11649-g003.jpg |
0.447011 | 06e8e06caf0e41a5aff7d543320659a6 | Entomopathogenic nematodes (EPNs) detected from soil samples at 2019 and 2020 Field sites. (A) Results of surveys at the 2019 Field Trials location. (B) Results of surveys at the 2020 Field Trial Location (separate and independent location from the 2019 Field Trials). Blue bars indicate timing of soil surveys for entomopathogenic nematodes; bars above the horizontal indicate detection of entomopathogenic nematodes and bars below the horizontal indicate no entomopathogenic nematodes detected. Vertical grey lines indicate timing of application. | PMC10380715 | insects-14-00623-g001.jpg |
0.396542 | ac39bf656d0b4524a85fb791c9170475 | Mortality of entomopathogenic nematode cohorts of different species following exposure to solutions containing no pesticide (Control), spinosad, and cyromazine. Bar height and error bars denote mean mortality and standard deviation, respectively. Asterisks indicate a significant (p < 0.05) difference in mortality as compared to controls on a per-species basis. | PMC10380715 | insects-14-00623-g002.jpg |
0.399284 | 381bed5490d8422e975f1f9277aaae54 | Infectivity of entomopathogenic nematode cohorts previously exposed to either (A) spinosad or (B) cyromazine. Odds ratios measure the change in infective potential of nematode cohorts after exposure to compounds as compared to controls. An odds ratio of one denotes no change; an odds ratio of less than one denotes a decreased ability of entomopathogenic nematodes to infect insects. Points and error bars denote mean odds ratio and standard error respectively. Asterisk indicates that the odds ratio is significantly different from one at p < 0.05. | PMC10380715 | insects-14-00623-g003.jpg |
0.420476 | 79c682b989514ed9a56d3b02b2a388ba | The effect of adding entomopathogenic nematodes on onion maggot damage. In 2019, in small plot trials without seed treatment, applications of entomopathogenic nematodes reduced cumulative onion loss (A) and resulted in an increase in end of season plant stand (B). In 2020, in larger plot trials with seed treatment, applications of entomopathogenic nematodes also reduced cumulative onion loss (C) and also resulted in an increase in end of season plant stand (D). In (A,C), solid lines and shaded region denote mean loss and standard error, respectively. In (B,D), points and error bars denote mean and standard error, respectively. | PMC10380715 | insects-14-00623-g004.jpg |
0.399069 | 1347e5134ea94f81ab01291c4cf7261f | T2 fluid-attenuated inversion recovery (FLAIR) of brain magnetic resonance imaging (MRI). [A–H patient 1, I–P patient 2]. T2 FLAIR brain MRI of patient 1 at initial presentation demonstrated hyperintensities involving the brainstem, left frontal, parietal, and temporal cortex (A, B). T2 FLAIR brain MRI after admission to our hospital and suffering from status epilepticus demonstrated hyperintensities involving the left frontal cortex and bilateral temporo-parietal cortex (C, D). Repeat T2 FLAIR brain MRI three weeks after immunotherapy initiation showed improvement in the bilateral temporo-parietal cortex (E, F). There were no obvious lesions on images seven months after the initial treatment (G, H). Axial T2 FLAIR brain MRI of patient 2 at initial presentation demonstrated hyperintensities involving the left temporal, parietal, and occipital cortex (I, J). T2 FLAIR brain MRI ten days after immunotherapy initiation was normal (K, L). T2 FLAIR brain MRI after disease relapse demonstrated multiple hyperintensities, in keeping with acute disseminated encephalomyelitis involving the bilateral thalamus, basal ganglia, and right centrum semiovale (M, N). At re-assessment four months after second discharge, the patient was clinically asymptomatic with improving FLAIR lesions on repeat T2 FLAIR brain MRI (O, P). | PMC10380939 | fimmu-14-1203615-g001.jpg |
0.448243 | ec636cd793864e4bbe953f1414398f57 | COVID-19 cases in Liguria from March 2020 and March 2022 (data from Department of Protezione Civile). Data from: https://mappe.protezionecivile.gov.it/it/mappe-e-dashboards-emergenze/dashboards-coronavirus/situazione-desktop/ accessed on 9 July 2023. | PMC10381360 | life-13-01558-g001.jpg |
0.606882 | 2d003aea58a149a598a77f0922c01bf5 | Differences in prevalence of dyspnea, fatigue and problems in quality of life at baseline and follow-up visit. The degree of dyspnoea (4 point scale), the degree of fatigue (3 point scale) and the degree of problems on 5 domains of quality of life (3 point scale) were compared at baseline and follow-up visit in the same subjects. The McNemar Bowker test was used for comparisons. * p < 0.05. | PMC10381360 | life-13-01558-g002.jpg |
0.487385 | ad15e76a0a144d4895fc3223dccc088e | Differences in prevalence of dyspnoea, fatigue ed problems in quality of life at baseline and follow-up visit in the COVID-19 waves. Dyspnoea (Yes vs. No), fatigue (Yes vs. No) and the 5 domains of quality of life (Problems vs. no problems) were compared at baseline and follow-up visit in the same subjects. The McNemar test was used for comparisons. * p < 0.05. | PMC10381360 | life-13-01558-g003.jpg |
0.50866 | 97b7b2430f4645f8970b626a5eaf0f6c | STARD diagram for the study flow. | PMC10381424 | life-13-01492-g001.jpg |
0.5017 | cc3dce976f554a5190450a07a99a00e6 | Consort flow diagram of the study. | PMC10381905 | jpm-13-01093-g001.jpg |
0.449635 | e506c51d09bf4f4da2dae589afb26e06 | Mean N gene Ct values in baseline and 48 h in both groups. | PMC10381905 | jpm-13-01093-g002.jpg |
0.442454 | 53f13863484944cdacdd47ea98a71133 | Spectrophotometer analysis of ascorbic acid (AA) impact on pyocyanin (Pyo) absorbance. Ascorbic acid (acidic pH) showed immediate hyperchromic and hypsochromic shifts of pyocyanin absorbance peak at 385 nm and 695 nm, respectively. In the presence of neutralised ascorbic acid, the change was gradual and was more prominent at later hours. The bottom centre and right-end graphs show a summary of the hyperchromic shift and hypsochromic shift of pyocyanin absorbance peak at 385 and 695 nm in the presence of ascorbic acid over time. | PMC10381918 | fmicb-14-1166607-g001.jpg |
0.426858 | 15bc711115aa4e32a3ee23cdff8e1c1f | 1H-NMR analysis of the impact of ascorbic acid (AA) on pyocyanin in the pyocyanin aromatic region. The aromatic part of pyocyanin showed precise modulation in its characteristic NMR signals upon forming a complex with ascorbic acid at both acidic and physiological pH. Main y after 72 h of formation of new peaks at 8.1 ppm and disappearance of pyocyanin peaks around 6.2 and 6.4 ppm refer towards the construction of new species or a pyocyanin-ascorbic acid adduct. | PMC10381918 | fmicb-14-1166607-g002.jpg |
0.412582 | 13c7aa962d344dc180025da18993d916 | DFT optimised structures of the possible H-bonding interactions between pyocyanin and ascorbic acid. A-D represents the possibility of H-bonding between pyocyanin and ascorbic acid. | PMC10381918 | fmicb-14-1166607-g003.jpg |
0.448597 | 7d7693a8c712409d87b10874375dfe9d | Pyocyanin incubated with ascorbic acid (AA) for 2 and 72 h in the presence of acidic or neutral pH showed a drastic reduction in pyocyanin recovery. (A) The impact is higher and faster with acidic ascorbic acid than with its buffered version. *Indicates the differences are statistically significant (p < 0.05) compared to pyocyanin 50 μM. All experiments were conducted with n = 3 replicates. (B) Circular dichroism shows pyocyanin and phenazine intercalate with DNA, as evident by the hyperchromic effect observed at pyocyanin peaks at 220 nm and 280 nm. (C) Fluorescent spectroscopy analysis showing ascorbic acid inhibits pyocyanin binding to DNA. EtBr displacement method demonstrates pyocyanin displaces EtBr and binds with DNA (empty circle) and fluorescent intensity down to 305 (left panel). In the presence of AA, the Pyo-AA complex hinders pyocyanin binding to DNA with a fluorescent value raised to 425 (right panel). | PMC10381918 | fmicb-14-1166607-g004.jpg |
0.431021 | 7c344bf0e0d34dffb172090c13d4c284 | Impact of ascorbic acid (AA) and furanone-30 (Fu-30) and combination of both on P. aeruginosa quorum sensing. MH602 was used to study the effects of the lasR system (left hand side), whereas PAO1 was used to study rhlA (centre) and pqsR (right hand side). Fu-30 showed a decline in the production of GFP up to 8 h and the addition of AA alone showed considerable declines in GFP production at all time points. The combination of AA with Fu-30 showed the most decrease in the activity of all three QS systems, especially at AA 20 mM + Fu-30 20 μM. All experiments were conducted in triplicate. *Indicates p < 0.05 in comparison to the control, **indicates p < 0.05 in comparison to the Fu-30 alone and ***p < 0.05 in comparison to the AA alone, #indicates p < 0.05 comparison between increasing concentration of Fu-30 alone and ##p < 0.05 comparison between increasing concentration of AA alone. | PMC10381918 | fmicb-14-1166607-g005.jpg |
0.428683 | 92af910dc8f847bebb12d6ba6979aa36 | Impact of the combo [combination of AA (20 mM) and Fu-30 (20 μM)] on P. aeruginosa virulence factor pyocyanin and hemolysin. (A) Only combo shows the disappearance of greenish colour (an indicator of pyocyanin production) in bacterial culture. (B) Combo significantly decreased pyocyanin production in all P. aeruginosa strains/isolates. (C) Combo also significantly decreased hemolysin activity (at the highest volume of supernatant used at 100 μL) in all clinical isolates. Experiments were conducted in triplicates. *Indicates p < 0.05. | PMC10381918 | fmicb-14-1166607-g006.jpg |
0.419593 | d0a4247866b046778d0aa9e436f2f284 | Impact of combination treatment on P. aeruginosa adhesion. (A) The adhesion area of P. aeruginosa increased significantly for all isolates from 2 h to 8 h. (B) In the presence of a combo, the bacteria’s total adhesion area stagnated, and the value remained the same for 2 and 8 h time points. (C,D) The microscopic image represents an example of P. aeruginosa isolate (UTI-62) adhesion at 2 and 8 h time points. Scale bar = 50 μm. *Indicates the differences are statistically significant (p < 0.05) compared to the untreated control. All experiments were conducted in n = 3 biological replicates. | PMC10381918 | fmicb-14-1166607-g007.jpg |
0.443466 | b48d39a7c97a4ef596b4bfdbf8879bc4 | Quantification of P. aeruginosa biofilm biomass at 2, 8 and 24 h time points. (A) In the presence of a combo, the biomass is significantly less for all isolates (A). (B) Photographic images showing control retain dense crystal violet stain compared to the biofilm grown in the presence of combo. (C) In the presence of a combo, the CFU/mL was significantly less at all time points than the control. *Indicates the differences are statistically significant (p < 0.05) compared to the control. All experiments were conducted in n = 3 biological replicates. | PMC10381918 | fmicb-14-1166607-g008.jpg |
0.426096 | 1a88e45cd8694753bbe470d1d843263f | The impact of tobramycin and combo + tobramycin on P. aeruginosa pre-established biofilm. (A–C) On pre-established biofilms, combo + tobramycin treatment (4 h) exhibited a significant decrease in its biofilm biomass (A), crystal violet stain retention (B) and CFU/mL in comparison to tobramycin alone treatment (C). *Indicates the differences are statistically significant (p < 0.05) compared to the control. All experiments were conducted in n = 3 biological replicates. | PMC10381918 | fmicb-14-1166607-g009.jpg |
0.413477 | af8164d8dc904c63add34976f3f5d5d7 | Cytotoxicity effect of the combo (AA 20 mM + Fu-30 20 μM) on HFF-1 cell lines. HFF-1, when exposed to combo, showed no cytotoxicity at both 24 and 48 h exposure time, whereas DMSO exhibited disruption in cell confluence and up to 50% cytotoxicity at 48 h time points (A,B). Scale bar = 50 μm. All experiments were conducted in triplicates. *Indicates p < 0.05. | PMC10381918 | fmicb-14-1166607-g010.jpg |
0.411947 | 2030110181b040d6bedd5e8597f45fea | Hemodynamic performance of SE vs BE valves.
A, Higher rates of at least moderate PVL in patients with aortic stenosis treated with SE Evolut PRO or Evolut R 34‐mm valves compared with the BE Edwards SAPIEN 3 or Ultra. B, Significantly lower transcatheter gradients at discharge echocardiography among patients with aortic stenosis with small transcatheter heart valves treated with contemporary SE valves. BE indicates balloon expandable; PVL, paravalvular leak; and SE, self‐expanding. | PMC10382012 | JAH3-12-e028038-g001.jpg |
0.433971 | ff6c1bb94aed4cb9a6b1cc89ffb269bd | Midterm survival in patients with small THVs.
A, Increased midterm survival in the SE valve group among patients with aortic stenosis treated with small THVs. B, Midterm survival in PSM patients treated with small THVs. BE indicates balloon expandable; PSM, propensity score–matched; SE, self‐expanding; and THV, transcatheter heart valve. | PMC10382012 | JAH3-12-e028038-g002.jpg |
0.459143 | f05b53e920a748fb854f19868418839c | Midterm survival in all‐comer patients with aortic stenosis treated with contemporary self‐expanding or balloon‐expandable valves. Cum indicates cumulative. | PMC10382012 | JAH3-12-e028038-g003.jpg |
0.476002 | 05b401cb945649088f08322fe128df72 | Effect of positive airway pressure adherence on mean number of composite hospitalizations and emergency room visits. | PMC10382094 | JAH3-12-e028733-g001.jpg |
0.40474 | cd46b3ea138240ef8b30956f4d8db9ff | Health care resource use 1 year before and 1 year after initiating positive airway pressure (PAP) therapy.ER indicates emergency room; and SMD, standardized mean difference. | PMC10382094 | JAH3-12-e028733-g002.jpg |
0.396379 | 903ac051bda148cf85a25029c5312604 | Flowchart illustrating the process of study selection for the systematic review. | PMC10382163 | jced-15-e571-g001.jpg |
0.446826 | 81c7726e8ca94e24af4ac51601f7c527 | Forest plot of pooled effect size, estimates and 95% confidence interval representing differences in MCC between OSMF and controls. | PMC10382163 | jced-15-e571-g002.jpg |
0.39287 | 85103fe00f694b8abdf3f7a1bc07c1f0 | Significant diagnostic group × physical activity × vascular burden interaction effect on FA (TFCE, FWE, p < 0.05). FA, fractional anisotropy; FWE, family-wise error; TBSS, tract-based spatial statistics. | PMC10382177 | fnagi-15-1096798-g001.jpg |
0.411333 | 35825ba7503c4c82a251214af5f1bbda | Regions with significantly higher FA in the physically active patients with high vascular burden as compared with non-physically active patients with high vascular burden. (TFCE). A Bonferroni correction was applied (p < 0.0125) to correct for multiple comparisons. | PMC10382177 | fnagi-15-1096798-g002.jpg |
0.427854 | 5c8c85e724e045a3b7a56069237ba13f | Regions with significantly higher FA in the physically active patients with high vascular burden as compared with non-physically active controls with high vascular burden (TFCE, FWE, p < 0.05). | PMC10382177 | fnagi-15-1096798-g003.jpg |
0.473495 | 1e170acf3287483cb5ca7eb159715933 | Day of life 1 — omphalocele (black arrow), prolapsed terminal ileum (yellow arrow), hemibladder (black arrowhead), bifid glans (yellow arrowheads). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.) | PMC10382772 | gr1.jpg |
0.492102 | 2e51b8641e714090b45e05c7ef0928de | Abdominal radiograph showing dilated loops of bowel concerning for obstruction. | PMC10382772 | gr2.jpg |
0.465444 | fb64562a7f37489fbe46fa32a1402b97 | Duplicated appendix (black arrows) attached to the cecum (yellow arrow). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.) | PMC10382772 | gr3.jpg |
0.460119 | 43da625472e141ffb7b074d5cd88cba8 | The characterization of BBR-TA NPs and their single components. (A) The schematic diagram of BBR-TA NP preparation process. (B) Particle size diagrams of nanoparticles composed of different proportions of BBR and TA. (C) Transmission electron microscopy diagrams of nanoparticles composed of BBR and TA in different proportions. (D) Tyndall effect diagrams of BBR/TA MIX and BBR-TA NPs (the molar ratio of BBR to TA is 1:1). (E) Transmission electron microscopy images of crude BBR and TA. (F) Zeta potential diagrams of BBR, TA, and BBR-TA NPs (the molar ratio of BBR to TA is 1:1). | PMC10383063 | pharmaceutics-15-01782-g001.jpg |
0.411873 | 31a7bfbe12c245bf9819aa0a0e66cef9 | Co-assembly mechanism of BBR-TA NPs. (A) 1H NMR spectrum of BBR and BBR-TA NPs. (B–E) MD simulation of the interaction of BBR and TA. (F,G) ITC thermodynamic parameters of the titration of BBR-TA NPs by the BBR solution titrated with the TA solution (4 mM TA titration to 0.4 mM BBR; 4 mM TA titration to water). (H) X-ray diffractogram of BBR, TA, and BBR-TA NPs. | PMC10383063 | pharmaceutics-15-01782-g002.jpg |
0.426962 | 4507e3637a294a2b8fcb27862d183632 | Antibacterial effect of BBR-TA NPs. (A) Inhibition ratio of S. aureus treated with different concentrations of BBR, TA, BBR/TA MIX, BBR-TA NPs, BP, and Cip. (B) The inhibition ratio of MRSA was treated with different concentrations of BBR, TA, BBR/TA MIX, BBR-TA NPs, BP, and Cip. (C) The survival numbers of S. aureus and MRSA were treated with blank media (control), BBR, TA, BBR/TA MIX, BBR-TA NPs, BP, and Cip. (D) SEM images of biofilm incubated with the blank media (control), BBR, TA, BBR/TA MIX, BBR-TA NPs, BP, and Cip against S. aureus and MRSA (scale bar = 10 μm). ** p < 0.01; *** p < 0.001; **** p < 0.0001. | PMC10383063 | pharmaceutics-15-01782-g003.jpg |
0.407595 | 97c460e05caa47c982c3c21b45113a04 | Antibacterial mechanism of BBR-TA NPs. (A) Interaction of BBR, TA, BBR/TA MIX, and BBR-TA NPs with S. aureus and MRSA via SEM (scale bar = 200 nm). (B) The effect of BBR, TA, BBR/TA MIX, and BBR-TA NPs on the membrane integrity of S. aureus and MRSA cells via LIVE/DEAD fixable dead cell stain assay (scale bar = 10 μm). (C) The effect of BBR, TA, BBR/TA MIX, and BBR-TA NPs on the concentration of ATP in S. aureus cells and MRSA cells. (D) The effect of BBR, TA, BBR/TA MIX, and BBR-TA NPs on the cell cycle distribution of S. aureus and MRSA. *** p < 0.001; **** p < 0.0001. | PMC10383063 | pharmaceutics-15-01782-g004.jpg |
0.48897 | dc255846b8f742c8a818a94b6c23d54e | Treatment efficiency of MRSA bacteria-infected wound in mice with BBR-TA NPs. (A) Schematic diagram of the construction of mice model of wound infection and treatment process. (B) Representative images of the cutaneous wound in each group on days 0, 3, 7, 11, and 15 after surgery. (C) The relative wound area in each group at different time points. * p < 0.05; ** p < 0.01. (D) Histological analysis of wound tissues by H&E on day 15 after surgery (scale bar = 200 μm). (E) Histological analysis of wound tissues by Masson’s trichrome staining on day 15 after surgery (scale bar = 100 μm). (F) IHC image of anti-CD31 regenerated wound tissues on day 15 after surgery (scale bar = 100 μm). | PMC10383063 | pharmaceutics-15-01782-g005.jpg |
0.418682 | f4a53da7ffd649e8a5f54733180d49c2 | Biosafety evaluation of BBR-TA NPs. (A) Cell viability after incubation with BBR, TA, and BBR-TA NPs for treatment of 24 h. (B) Representative H&E staining photomicrographs of the major organs of the mice including the heart, liver, spleen, lung, and kidney at day 15 after surgery (scale bar = 100 μm). | PMC10383063 | pharmaceutics-15-01782-g006.jpg |
0.459499 | f09a2f644ed34f8d9a37ed0529e34a58 | Schematic illustration of co-assembly and antibacterial mechanism of BBR-TA NPs. | PMC10383063 | pharmaceutics-15-01782-sch001.jpg |
0.488172 | 43c7a16115914461be0ea29068e40a3a | Statistical chart for the number of each subtype of H6 AIV. The HA sequences were downloaded from the GISAID databases, and 253 H6N0 (no typing NA) sequences were not included in this chart. | PMC10383184 | viruses-15-01547-g001.jpg |
0.469996 | 1f795e78ae434c999261eade04162a16 | Global circulation of H6 viruses. (a) Global circulation of H6 viruses. The HA sequences were downloaded from the GISAID database, and then the isolation locations were noted on the map with green triangles (one H6 sequence in Antarctica was not labeled). (b) Asian circulation of H6 virus. (c) North American circulation of H6 virus. (d) European circulation of H6 virus. (e) South American circulation of H6 virus. (f) African circulation of H6 virus(g) Oceania circulation of H6 virus. | PMC10383184 | viruses-15-01547-g002.jpg |
0.454385 | f341a2d1a13349cd84072566487584ff | H6 AIV distribution in Chinese provinces. The HA sequences were downloaded from the GISAID databases. Provinces where H6 AIV was isolated are marked in light blue, and provinces where H6 AIV was isolated are marked in light gray. H6N1 is marked in green; H6N2 is marked in red; H6N3 is marked in gray; H6N4 is marked in blue; H6N5 is marked in purple; H6H6 is marked in orange; H6N7 is marked in brown; H6N8 is marked in pink; H6N9 is marked in black. There are also 201 H6N0 sequences and 101 sequences labeled only for China or East China that are not marked in this figure. The red star represents Beijing, the capital of China. | PMC10383184 | viruses-15-01547-g003.jpg |
0.467228 | 584f0e11fb72481a811efa1d86aec0a9 | Statistical chart of the number of H6 AIV subtypes from 2001 to 2021. The HA sequences were downloaded from the GISAID databases, and H6N0 sequences were not included in this chart. | PMC10383184 | viruses-15-01547-g004.jpg |
0.395541 | 665d7b22afd744e7b302d2bdb962b1f5 | H6 AIV distribution in wild birds. The numbers of H6 virus isolates in different wild birds are shown according to their submission information in GISAID. | PMC10383184 | viruses-15-01547-g005.jpg |
0.490307 | d931ef0cce4148ac84e059397671d249 | Phylogenetic analysis of H6 avian influenza viruses (HA). We select sequences according to different regions and species and then build an evolutionary tree. In this figure, green represents wild birds, blue represents chickens, red represents ducks, dark green represents geese, light blue represents the environment, and pink represents human. | PMC10383184 | viruses-15-01547-g006.jpg |
0.43621 | c284cd3c868f4b909d89c944833a5467 | Distribution of H6 AIV in poultry. The numbers of H6 virus isolates in different domestic poultry are shown according to their submission information in GISAID. The number on the left represents its exact quantity, and the number on the right represents its percentage. For example, there are 1237 duck source sequences, which account for about 64% of the poultry source sequence, which is 1237.64%. | PMC10383184 | viruses-15-01547-g007.jpg |
0.418469 | cd07fded0f9540ec968e0d1619a16310 | The number of H6 AIV subtypes of sequences isolated from ducks from 2000 to 2021. | PMC10383184 | viruses-15-01547-g008.jpg |
0.403751 | 44f971bdf9dd4ec6a36f1b1da14b0dd5 | AIV H6 subtypes isolated from chickens and geese. The HA sequences were downloaded from the GISAID databases. (a) H6 avian influenza virus subtypes isolated from chickens. (b) H6 avian influenza virus subtypes isolated from geese. | PMC10383184 | viruses-15-01547-g009.jpg |
0.427679 | f4801a6b23e9498489bac3547a23a567 | The result of selection Analysis. The associated amino acid changes were analyzed using MEGA 7.0. Consensus sequences were aligned, and mutations were recorded. The positions of the mutations for each enzootic cluster were confirmed manually. The number of amino acid changes in each enzootic cluster was counted. | PMC10383184 | viruses-15-01547-g010.jpg |
0.414987 | bc5383bd0603473580540443ad418e02 | Structural simulation of the H6 avian influenza virus HA protein. In this figure, except for the E190V and C137N mutations, the other labeled amino acid mutations were artificially altered by PyMOL. | PMC10383184 | viruses-15-01547-g011.jpg |
0.466585 | be79ad80eed44807a3bc954517b327f9 | Graphic representation of outbreak detection and timing of response, (Top) without forecasting (=early warning), and (Middle) with forecasting and surveillance. Key decision steps with forecasting (Bottom). Used with permission (license number 5540270027357) [14]. | PMC10383283 | viruses-15-01461-g001.jpg |
0.478257 | e918fda1d2b64ebe918fc0f8909c8977 | Niche overlaps of two hypothetical Orthohantavirus hosts and humans projected onto two environmental factors. The extent that the virus can be maintained by both hosts, independently, and transmitted to humans (Boolean OR) or must move sequentially from a host (#1) that rarely contacts humans, through a second host (#2) that broadly overlaps humans (Boolean AND) will impact the size of the human population at risk. | PMC10383283 | viruses-15-01461-g002.jpg |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.