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0.421912 | a0b2c5af84424364854e85d130dd6244 | FESEM image (a), particle distribution (b), and EDX analysis (c) of NCQDs | PMC9869888 | IJBMS-26-190-g006.jpg |
0.465201 | 0cfe67c0e16241ca99a68036e9b86360 | (a) TEM images of natural carbon quantum dots (NCQDs) synthesized from orange pericarp. (b) Particle size distribution curve of the NCQDs | PMC9869888 | IJBMS-26-190-g007.jpg |
0.393298 | 7b835d9d5122495ab1fe74d5af0428a9 | AFM images of prepared natural carbon quantum dots (NCQDs) (scan area 5 µm × 5 µm); a-2D, b-3D | PMC9869888 | IJBMS-26-190-g008.jpg |
0.469485 | 09bbb4e60d7943c39a140d41a786a781 | (a) UV-visible absorption spectra of NCQDs. (b) PL emission spectra of NCQDs at various excitation wavelengths from 282 nm to 422 nm | PMC9869888 | IJBMS-26-190-g009.jpg |
0.448942 | 3ecd6d0e6a0344d3ae94300cb3ceb64f | Results from cytotoxicity evaluation of the synthesized NCQDs on C26 cells estimated by MTT assay after exposure to different concentrations for 24 hr | PMC9869888 | IJBMS-26-190-g010.jpg |
0.428157 | 61a1aeb01c264fdcbca42048d2a43beb | Effect of different cations (at 0-1.0 mM) on the emission intensity of the natural carbon quantum dots (NCQDs) | PMC9869888 | IJBMS-26-190-g011.jpg |
0.449635 | 957044a917f04642af629b54ea61f750 | (A, C) Effect of different concentrations of Zn2+ and Ca2+ on the fluorescence intensity of the natural carbon quantum dots (NCQDs) by 365 nm excitation wavelength. (B, D) relationship between F0/F and the concentration of Zn2+ and Ca2+. Insets show a linear relationship within the range of 0-0.5 mM | PMC9869888 | IJBMS-26-190-g012.jpg |
0.425239 | 89ea6d6af5ab4894966ecc2e7e6a71eb | (A) Michaelis-Menten curve derived from trypsin activity data at various natural carbon quantum dots (NCQDs) concentrations. (B) Double-reciprocal plot of the Michaelis-Menten curve. Conditions: CNCQDs: 0 μg.ml-1 (Open circles), 50 μg.ml-1 (closed circles) and 100 μg.ml-1 (Open triangle), pH: 7.5, T: 298 K, Ctrypsin: 0.1 mg/ml | PMC9869888 | IJBMS-26-190-g013.jpg |
0.454574 | bdde37660961433eab2e0ec8f6b02ec0 | Genetic screens identify suppressors of No-Go mRNA Decay.(A) Gene diagram showing annotated exons (black rectangles) of unc-54(rareArg). Colored rectangles represent CRISPR/Cas9 insertions at the endogenous unc-54 locus: T2A sequence (gray), FLAG (dark gray), 12 rare arginine codons (blue), and GFP (green). (B) Schematics of rareArg genetic screens. (C)
znf-598, uba-1, nonu-1, and hbs-1 alleles with representative image of one allele per gene on the left. Black rectangles represent exons, thicker rectangles are CDS, and thin lines are introns. Mutations made via EMS in the rareArg screen 1 (light blue) or rareArg screen 2 (dark blue), and via CRISPR/Cas9 (black) or CGC (gray) are shown. For HBS-1, multiple sequence alignment shows conserved glycine (G200) in GTPase domain. | PMC9870110 | pgen.1010577.g001.jpg |
0.410277 | fb6facf1c2014326b3fc58904505e3af | : Cell-specific NGD rescue via overexpression of factors.(A) Schematic of znf-598 construct plasmid and znf-598 strain subject to germline microinjection. Below are GFP and mCherry images of a representative animal expressing the above construct, with a zoom in of an area demonstrating the effect of mCherry-marked factor expression on NGD (GFP). (B) As in (A) for nonu-1 construct in nonu-1 strain. (C) Mean overlap score of strains in (A, B). Each black dot represents the mean of one independent isolate (n≥4 animals/isolate), with the mean of all isolates shown as a green bar. | PMC9870110 | pgen.1010577.g002.jpg |
0.426339 | 702607bfd87941ff9d5530519b970a3c | ZNF-598 is required for ribosomal ubiquitination in C. elegans.(A) Multiple sequence alignment of S. cerevisiae Hel2, H. sapiens ZNF598, and C. elegans ZNF-598 RING finger domains. Conserved residues (gray) and C89 (orange) are highlighted. Conservation below alignment is as follows: asterisks indicate identity, colons indicate amino acids with strongly similar properties, periods indicate amino acids with weakly similar properties. (B) Mean RFUs (relative fluorescence units) of indicated strains (n≥15 animals/strain) in the unc-54(rareArg) background. One standard deviation shown as error bars. p values from Welch’s t-test. (C) Western blot of indicated strains to monitor RPS-20 and RPS-10 expression. Dilutions of wild type tagged proteins were loaded as indicated, with two-fold more and two-fold less than other two samples, to generate a standard curve shown as a black line in plots on the right. Lysine mutants of tagged proteins were quantified and plotted as teal points in the plots on the right. (D) Western blot of indicated strains to monitor ubiquitination of HA-tagged RPS-10. | PMC9870110 | pgen.1010577.g003.jpg |
0.432652 | c79c3617d80d49b7bdc0c38e4b02e43c | NGD-deficient ribosomes made via ablation of ubiquitination sites.(A) Mean RFUs (relative fluorescence units) of indicated strains (n≥15 animals/strain) in the unc-54(rareArg) background. One standard deviation shown as error bars. p values from Welch’s t-test, with asterisks indicating p<0.01 for all comparisons with wild type. (B) As in Fig 2, with znf-598 construct in rps-10; rps-20 strain. | PMC9870110 | pgen.1010577.g004.jpg |
0.427434 | 1767d02b9468423c83c19725a770577f | NONU-1 function during NGD requires CUE domains and follows ZNF-598.(A)
C. elegans NONU-1 protein structure as predicted by AlphaFold [29]. Prediction confidence is as follows: blue regions are confident, yellow regions are low confidence, orange regions are very low confidence. Confident domains are circled in blue and labeled. (B, C) Mean RFUs (relative fluorescence units) of indicated strains (n≥15 animals/strain) in the unc-54(rareArg) background. One standard deviation shown as error bars. p values from Welch’s t-test, with asterisks indicating p<0.01 for all comparisons with wild type. (D) As in Fig 2, with znf-598 construct in nonu-1 strain. (E) As in Fig 2, with nonu-1 construct in znf-598 strain. (F) Western blot of indicated strains to monitor ubiquitination of HA-tagged RPS-10. (G) Mean RFUs (relative fluorescence units) of indicated strains (n≥15 animals/strain) in the unc-54(nonstop) background. One standard deviation shown as error bars. p values from Welch’s t-test, with asterisks indicating p<0.01 for all comparisons with wild type. (H) ZNF-598 mutual information plot. 90% percentile cutoff is shown as a dashed line, NONU-1 is highlighted in pink, and a negative control protein is highlighted in gray. | PMC9870110 | pgen.1010577.g005.jpg |
0.4374 | d14e3b7b447948bda72df0c451a6de9a | HBS-1 N-terminus resembles a ubiquitin-binding domain and is dispensable for NGD.(A)
H. sapiens Hbs1 protein structure as predicted by AlphaFold [29]. Prediction confidence is as in Fig 5A, with dark blue showing regions of high confidence. Confident domains are circled in blue and labeled. (B) Structural homology between Hbs1 N-terminal domain and ubiquitin-binding domains. At left is a structure representative of the UBA clan: CUE from [38] (tan, S. cerevisiae Vps9p, 1P3Q). At right are two structures of the Hbs1 N-terminus from [12] (pink, S. cerevisiae, 3IZQ) and [14] (green, S. cerevisiae, 5M1J). Amino and carboxy termini indicated with N and C, respectively. Note overall similarity in topology and fold across structures. (C) The N-terminal zinc finger (ZnF) of plant Hbs1 is homologous to the Ub-binding ZnF of rat Npl4. Multiple sequence alignment of the ZnF of Hbs1 from phylogenetically diverse plants. Residues that are highly conserved among Npl4 homologs are in blue, residues that contact Ub are in yellow, and residues that are both conserved and contact Ub are in green. Coloring and annotation of Npl4 residues from [39]. (D) Mean RFUs (relative fluorescence units) of indicated strains (n≥15 animals/strain) in the unc-54(rareArg) background. One standard deviation shown as error bars. p values from Welch’s t-test. | PMC9870110 | pgen.1010577.g006.jpg |
0.439478 | 148670fbcab84f008aaf9da1b500db92 | HBS-1 and PELO-1 are essential for mRNA degradation.(A) RNA-seq mean fold change of unc-54(rareArg) in the indicated strains from two biological replicates (shown as diamonds and squares). (B, C) Mean RFUs (relative fluorescence units) of indicated strains (n≥15 animals/strain) in the unc-54(rareArg) background. One standard deviation shown as error bars. p values from Welch’s t-test, with asterisks indicating p<0.01 for all comparisons with wild type. (D) As in Fig 2, with znf-598 construct in pelo-1; hbs-1 strain. (E) As in Fig 2, with nonu-1 construct in pelo-1; hbs-1 strain. (F) Mean RFUs (relative fluorescence units) of indicated strains (n≥15 animals/strain) in the unc-54(nonstop) background. One standard deviation shown as error bars. p values from Welch’s t-test, with asterisks indicating p<0.01 for all comparisons with wild type. (G) Model for NGD via ZNF-598, HBS-1, and NONU-1. (H) ZNF-598 mutual information plot. 90% percentile cutoff is shown as a dashed line, HBS-1 is highlighted in yellow, and a negative control protein is highlighted in gray. (I) As in (H), showing NONU-1 mutual information with HBS-1. | PMC9870110 | pgen.1010577.g007.jpg |
0.44721 | 509c779e05294361b69827b0e624f5eb | Average LARC insertion rates and IPP LARC insertion rates among women age 15–44 in delaware and control states.Source: IBM Marketscan Commercial Claims and Encounters Database (2012–2019). Notes: The rate reported in the left-hand panel each year is calculated as the number of women having a LARC device inserted in that year, divided by the total number of women enrolled in a plan in the Marketscan database. The rate reported in the right-hand panel is calculated as the number of births in a hospital where a LARC device was provided during the dates of hospitalization, divided by the total number of births occurring in a hospital recorded in the Marketscan database for each year. | PMC9870137 | pone.0280588.g001.jpg |
0.484008 | 119fef01a72241b3a3fac81914e0907b | Difference-in-differences effect of the DelCAN program on LARC insertions, for women age 15–44 by age group and policyholder status.Source: IBM Marketscan Commercial Claims and Encounters Database (2012–2019). Notes: Difference-in-differences estimates are from a linear probability model estimated with individual data at the person-year level for any LARC insertions and at the birth level for IPP LARC placements. Both the unadjusted and adjusted difference-in-difference estimates include state and year fixed effects. The adjusted model controls for individual level covariates and state by year covariates for demographics, health care access, and other state contraceptive policies. See the text for sample inclusion rules and full list of covariates. Standard errors are clustered at the individual level and 95% confidence intervals are shown. | PMC9870137 | pone.0280588.g002.jpg |
0.439579 | c246abbb81b04b06a6975e68c0145c10 | “Pain,” by Antanas Zmuidzinavicius (permission from The Art Museum of Lithuania, Vilnius). Animism and the worship of forests and trees are some of the elements of pagan religion in the Baltic states. When Lithuania embraced Christianity in the 14th century, these beliefs and nature worship were condemned, although remnants of pagan customs survived. The old religion passed into folklore and into legends that often feature the theme of an enchanted forest populated by evil spirits and ghosts to be avoided and treated with respect. This painting taps into these mental images. The trees have metamorphosed into hideous, fantastical creatures attacking the man seated in the center. Here, nature, which has become threatening, symbolizes human pain. This painting served as inspiration for our “nerve tree” explanatory diagrams in this manuscript. | PMC9870794 | gr1.jpg |
0.50329 | bdc0ecce6ff9469bbebbe28e097c937e | Compression pain that is amenable to surgery. A The response of adjacent normal nerves to nerve injury is variable and critical to understanding neuropathic pain. This cartoon depicts a central nerve (eg, SBRN) with adjacent nerves (eg, LABC nerve of the forearm and the dorsal cutaneous branch of the ulnar nerve). B Nerve compression, such as SBRN compression, causes pain within that cutaneous distribution. C Compression pain is typically quickly relieved with surgical decompression. | PMC9870794 | gr2.jpg |
0.530257 | ccdab55855f548f4b0c6f99fab332e83 | Neuroma pain that is amenable to surgery. A Neurotmetic injuries may result in painful neuroma formation. B There are many techniques described to treat neuroma formation, and these are typically successful in managing neuroma pain. Nerve growth factor increases with denervation and stimulates collateral sprouting of the adjacent normal nerves, resulting in the return of nonpainful sensation over time.25 Tx, treated neuroma. | PMC9870794 | gr3.jpg |
0.521533 | f05e927090fe4211be2f6686ded3c94e | Collateral sprouting pain (painful hyperalgesia) that is not amenable to surgery. Collateral sprouting can result in painful hyperalgesia (red zone), best managed with modalities such as GMI and desensitization, and is not amenable to nerve surgical intervention. Repeated operations directed at the neuroma will not be successful.19 Tx, treated neuroma. | PMC9870794 | gr4.jpg |
0.530233 | 69a5db9fbfde4709868acb5f0f56138e | Phantom nerve pain (anesthesia dolorosa or deafferentation pain) that is not amenable to surgery. Despite appropriate neuroma treatment and relief of neuroma pain, some patients will have numbness in the distribution of the treated nerve that is numb yet very painful; we term this phantom nerve pain (anesthesia dolorosa or deafferentation pain). This is not amenable to nerve surgical treatment. Tx, treated neuroma. | PMC9870794 | gr5.jpg |
0.507994 | d5015f905eed4c6099f97f091ffc08c7 | Superimposed compression in collaterally sprouting and phantom nerve pain contexts. In the setting of A collateral sprouting with painful hyperalgesia or B phantom nerve pain, there is potential for superimposed compression neuropathy of adjacent nerves. If recognized and released, this can alleviate pain in the context of both collateral sprouting and phantom nerve pain. Tx, treated neuroma. | PMC9870794 | gr6.jpg |
0.427876 | 007c765faf5e4c62b71892fcdbce45ab | Birth weight percentile curves by gender and gestational age (A): male infants; (B): female infants. | PMC9871478 | fped-10-1028637-g001.jpg |
0.399586 | 96d382ab86634192b19148e70a6535c3 | Percentile curves of the length and head circumference by gender and gestational age (A): male infants; (B): female infants. | PMC9871478 | fped-10-1028637-g002.jpg |
0.418123 | 317f3ed7567d48cc8dfd98c7683dc4f8 | Comparisons of percentile curves of the high-altitude and international standards for neonatal birth weight (A): male infants; (B): female infants. | PMC9871478 | fped-10-1028637-g003.jpg |
0.502018 | 80db484cf79742a5be07b8e34e4db8fa | Comparisons of percentile curves of the high-altitude and Chinese standards for neonatal birth weight (A): male infants; (B): female infants. | PMC9871478 | fped-10-1028637-g004.jpg |
0.423709 | d68699cc57024678bb629e015b7ab6e6 | Classic mechanisms of inflammasome activation. Lipopolysaccharide (LPS), which is regarded as the prototype of pathogen associated molecular patterns (PAMPs) and heat shock proteins (HSPs) as a typical representative of damage associated molecular patterns (DAMPs), can be recognized by toll-like receptor 4 (TLR4). Nuclear factor kappa B (NFκB) mediates these signals to produce NOD-like receptor family pyrin domain containing 3 (NLRP3), pro-IL-1β, pro-IL-18, and pro-IL-37. Next, NLRP3 is activated by potassium (K+) efflux, calcium (Ca2+) influx, and lysosomal leakage to recruit cysteine-requiring aspartate protease-1 (caspase-1). Caspase-1 then induces the maturation and release of pro-IL-1β, pro-IL-18, and pro-IL-37 and other related inflammatory agents that cause the inflammatory reaction and participate in the occurrence and development of the disease. | PMC9871625 | fimmu-13-1098725-g001.jpg |
0.462801 | 2729c6f84ce84a0ba492ae8d8f488fcd | Role of inflammation and immunity in hypertension. Many risk factors, such as genetic susceptibility, high salt, and environmental stress, can elevate blood pressure (BP) and consequently activate the sympathetic nerve system (SNS) or inhibit the parasympathetic nerve system (PNS). Over time, elevated BP can induce organ injury promoting the formation of damage-associated molecular patterns (DAMPs) and new antigens. In addition, several infectious diseases can enhance the activation of the innate immune system through the binding of pathogen-associated molecular patterns (PAMPs) to toll-like receptors. DAMPs, new antigens, and PAMPs activate innate immunity which interacts with adaptive immunity. Next, numerous proinflammatory cytokines are released and result in further organ injury. Through alternatively activated macrophages (M2) and Tregs have roles in anti-inflammatory response, the effect is too weak to reduce the organ damage. Finally, peripheral vascular resistance and blood volume increases to result in hypertension (Created with BioRender.com). | PMC9871625 | fimmu-13-1098725-g002.jpg |
0.483189 | db83f7044eae4922a76aa0eba499af1f | Mechanisms of oxidative stress causing hypertension in vascular endothelial cells. Ang II and ET-1 can stimulate NADPH oxidase and mitochondria to produce ROS (e.g., H2O2 and OFR), which are recognized by their receptors on the endothelial cells. ROS stimulate the PI3K/Akt-MAPK pathway to inhibit the expression of eNOS mRNA and eNOS activity, thus reducing the availability of NO, which results in vasodilation insufficiency and elevation of blood pressure. Moreover, angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs) and vitamin C (VC) may be potential therapeutic strategies in the process of oxidative stress. | PMC9871625 | fimmu-13-1098725-g003.jpg |
0.572706 | 493c6b7a1b9b48d0b66584be4f55bcc9 | Tissue section of the myocardium stained with haematoxylin and eosin. Within the vessel, an air emboli is visible. | PMC9871849 | sfac217fig1.jpg |
0.433847 | 04211ef342c5490e8596085de8b8998c | ME with microbubbles of air (open space) in a vessel of brain tissue from one HD patient (visualized by polyclonal fluorescent antibody against fibrinogen and fibrin). The shape of the emboli shows a tail (marking a thrombus area) that indicates the direction of the prior blood flow in the vessel. | PMC9871849 | sfac217fig2.jpg |
0.408729 | a441f4979c334158af727e80ebf9478d | Correlation comparison of all patients between the extent of ME findings in the lung versus the heart. | PMC9871849 | sfac217fig3.jpg |
0.424374 | 723daa374f1940eba5fd46f5ed7eb825 | Correlation comparison of all patients between the extent of ME findings in the heart versus the brain. | PMC9871849 | sfac217fig4.jpg |
0.421167 | b69a2878e8d6438f810d705d2d29e82c | Correlation comparison in HD patients only between the extent of ME findings in lung tissue and the time on HD (months). | PMC9871849 | sfac217fig5.jpg |
0.43868 | 0b08506205874a4099dc536e33e547ad | (A) Facial aspect of patient 1 at the age of 6 years showing prominent forehead and hypertelorism. (B) Face of patient 2 at the age of 18 months. Prominent forehead, synophris, hypertelorism and mildly downward slanting palpebral fissures. | PMC9871926 | fneur-13-1113811-g0001.jpg |
0.44849 | 364a4e9566674fe8bfcef62784f6896f | (A) Routine electrophalography (EEG) reveals focal sharp-waves (left, frontoparietal), rhythmic 6 Hz electrical activity and signs of focal cerebral dsfunction with a frontal theta-waves slow activity in the frontal area. (B) The EEG examination of patient 2. Frontotemporal sharp-wave complexes on the left side and rhythmical 4–5 Hz activity. | PMC9871926 | fneur-13-1113811-g0002.jpg |
0.549833 | bb6414ce67f3491e87c9e4950d72cd90 | Position of KPTN (NM007059.4) variants identified in this study (top), with respect to the affected exon. (Bottom) Reported pathogenic variants according to the literature. | PMC9871926 | fneur-13-1113811-g0003.jpg |
0.382471 | b349820ed43547d39caf9f861e0ae754 | Variation in yield of LYC during frozen storage. SFS and LSS represent the salt-free soaking group and low-salt soaking group, respectively. Lowercase letters represent significant differences between six samples during freezing, and capital letters represent significant differences between samples of different treatment groups during freezing (P < 0.05). | PMC9872034 | fnut-09-1103838-g001.jpg |
0.494106 | c0f5bd77aefc48d69ad0c2f5b3fab81d | Texture changes of LYC during frozen storage; panels (A–D) present the hardness, cohesiveness, springiness, and chewiness, respectively. SFS and LSS represent the salt-free soaking group and low-salt soaking group, respectively. Different letters in the figure represent significant differences between the six samples (P < 0.05). | PMC9872034 | fnut-09-1103838-g002.jpg |
0.399871 | fa4ce872f25e44a593c4c87acdf5e74f | Changes in TBARS (A) and TVB-N (B) of LYC during frozen storage. SFS and LSS represent salt-free soaking group and low-salt soaking group, respectively. Lowercase letters represent significant differences between six samples during freezing, and capital letters represent significant differences between samples of different treatment groups during freezing (P < 0.05). | PMC9872034 | fnut-09-1103838-g003.jpg |
0.405924 | 9710b57592e0498885f11f256b6e631a | Changes in color of LYC during frozen storage. SFS and LSS represent the salt-free soaking group and low-salt soaking group, respectively. Different letters in the figure present significant differences between the six samples (P < 0.05). | PMC9872034 | fnut-09-1103838-g004.jpg |
0.437884 | 7ade22c8e63742068908d3e2a2301a22 | Changes in moisture content of LYC during frozen storage. (A) Water content of SFS group; (B) water content of LSS group; (C) thawing loss; (D) centrifuging loss. SFS and LSS represent the salt-free soaking group and low-salt soaking group, respectively. Lowercase letters represent significant differences between six samples during freezing, and capital letters present significant differences between samples of different treatment groups during freezing (P < 0.05). | PMC9872034 | fnut-09-1103838-g005.jpg |
0.461937 | d23c1e49896b4002aad6008107b46f37 | Structural observation of LYC. SFS and LSS represent the salt-free soaking group and low-salt soaking group, respectively. Panels (A,B) showed the cross-section and vertical-section, respectively. The magnification of images is 10 times. | PMC9872034 | fnut-09-1103838-g006.jpg |
0.528271 | 9b31f0d9db154223b08f321a3871bf21 | Changes in SDS-PAGE of LYC during frozen storage. 1, 2 are fresh samples of LYC, 3, 4, and 5, 6 are SDS-PAGE profiles of total protein of LSS group and SFS group after 4 F-T cycles and 6w frozen storage, respectively. | PMC9872034 | fnut-09-1103838-g007.jpg |
0.41443 | b6795e28423c40b08dfbda835e70d7a7 | Ultrasound image of cervical lymph node tuberculosis. (A) Contrast-enhanced ultrasound showed uneven enhancement of lymph nodes, Target A: uneven enhancement areas; Target B: non-enhanced areas of caseous necrosis; (B) biopsy tissue specimen of enhanced area; (C) area without enhancement with fine-needle aspiration caseous necrosis. | PMC9872513 | fpubh-10-1022470-g0001.jpg |
0.439563 | 17d25107730d49b79079f1eb1d5d9b5a | Areas under the receiver operating characteristic curve plotted to determine the diagnostic values of pathological examination alone, Xpert examination alone, and the combination of the two. | PMC9872513 | fpubh-10-1022470-g0002.jpg |
0.46696 | 0714ab2f6a7e4deea76a931d4575faaf | Summary: Grain challenge experiments, where a portion of the diet is suddenly replaced by highly fermentable grains, result in systemic inflammation. Both high starch fermentability and sudden diet changes likely play a part in causing this inflammation. Abomasally infusing starch does not seem to result in inflammation but it does consistently reduce fecal pH and increase fecal butyrate concentrations. Direct effects of starch on the hindgut epithelial barrier and mucosal layers are unknown in dairy cattle. Increasing starch concentration in dairy cow rations does not consistently result in inflammation even though it reduces rumen and fecal pH. Research investigating the effects of different grain sources and processing methods on systemic inflammation is warranted. | PMC9873822 | fx1.jpg |
0.498281 | 9008385a960e4d1582cdcdf4b681fef5 | Summary of plasma haptoglobin (Hp) and serum amyloid A (SAA) means reported in chronic starch feeding experiments where lactating dairy cows were fed varying concentrations of dietary starch. Dashed lines indicate statistical significance detected in the experiment, whereas solid lines represent insignificant effects of starch concentration. Outliers for Hp (>1.5 μg/mL) were excluded from the figure (1 study). The Albornoz et al. (2020), Haisan et al. (2021), and McCarthy et al. (2015b) publications reported experiments using periparturient dairy cows; others used cows ranging from 30 to 150 DIM. | PMC9873822 | gr1.jpg |
0.431784 | 8f0a24904afe440ea7607519fd113345 | Possible effects of butyrate in the hindgut of dairy cows resulting from increased starch supply to the large intestine. Butyrate can increase tight junction mRNA and protein abundance in model species and cells. It also promotes IL-10 expression (anti-inflammatory) in dendritic cells and macrophages, which helps to promote T-regulatory cell development (inflammation-suppressing cell type). These effects may help to mitigate the risk of intestinal inflammation. | PMC9873822 | gr2.jpg |
0.456964 | 6141f3c511724802a3abcf635001d25e | Distribution of carnivore data.a Species richness of large carnivores from the families Canidae, Felidae, Hyaenidae and Ursidae of the order Carnivora. Species richness derived by finding the sum of each species (N = 87) current IUCN range maps (terrestrial-extant range only, so excluding locations the species is now extinct). For instance, a value of 10 indicates that 10 large carnivore species are suspected to occur within this 5-degree cell according to IUCN range maps. b The frequency of collected quantitative and qualitative trends in a given cell divided by the species richness of the cell. Shading is shown on the log-10 scale. Cells with no trends are coloured in deep purple. c temporal coverage of quantitative and qualitative observations, where each line represents a trend; the left and right of each line indicates the start and end point of each trend. Source data are provided as a Source Data file. | PMC9873912 | 41467_2022_35665_Fig1_HTML.jpg |
0.4056 | 12ff131163c8430d9da194006fd40745 | Sixteen covariates with a proposed effect on carnivore population trends.Covariates are highlighted in bold and fall in four groups: Traits, Land-use, Climate, and Governance. Text alongside covariates briefly explains how the variable was derived, whilst full explanation and justifications for inclusion are available in Supplementary methods: Covariates. | PMC9873912 | 41467_2022_35665_Fig2_HTML.jpg |
0.433025 | fda6060e257a4b528d65d08c3baf7003 | Multiple drivers of population change in large carnivores.a Annual rate of change coefficients from fixed effect parameters in a hierarchical Bayesian linear model, with 50%, 80%, and 95% credible intervals. Coefficients with an effect at the 95% credible interval are coloured in purple. Parameters are ordered by effect size within respective facets. b–f Marginal effects for a selection of important covariates against median predicted annual rate of change: mean annual primary habitat loss (b); area of population buffer zone on the log10 scale (c); mean number of months per year where the average degree of drought in the population monitoring period (the period of time abundances have been assessed for each trend) exceeded the mean plus two standard deviations of the average drought during the baseline pre-industrial period (1901–1920) (d); change in temperature (as in change in drought) interacting with protected area coverage (e); annual change in human development over the population monitoring period (f). All covariates were back scaled from any transformations. Error ribbons represent the 50%, 80%, and 95% credible intervals. Source data are provided as a Source Data file. | PMC9873912 | 41467_2022_35665_Fig3_HTML.jpg |
0.364504 | 4de66d11947943dd97a7b2f48fb98e6f | Human development is the primary driver of population change in large carnivores.Counterfactual scenarios describing the difference in the annual rate of change (%) across the 1123 studied populations had there been no primary habitat loss (a), climate change (b), or growth in human development (c). Points falling on the right of the dotted line indicate that the population would be predicted to increase had observed habitat loss, climate change, and human development growth not occurred, and populations on the left of the line would be predicted to decrease. Points represent the median difference in the annual rate of change (predicted trend using counterfactual data minus the predicted trend using the observed data), with 50 and 95% quantiles. Source data are provided as a Source Data file. | PMC9873912 | 41467_2022_35665_Fig4_HTML.jpg |
0.469503 | fd28481524424c8ebcb23a436aebb99e | Projections of carnivore abundance vary with rate of change in human development.a Instantaneous Change in Human development (as in the covariate and parameter in Fig. 3) over time under three pathways: Slow, Moderate and Fast. A key feature of the human development data is a deceleration in the human development growth rate as human development increases (a and Supplementary Fig. 12a). b Projections of the Human development index (as in the covariate and parameter in Fig. 3) from a baseline of 0.2, derived using the three pathways of instantaneous change in human development (a). c Potential impact of different development strategies on carnivore abundances, relative to an arbitrary baseline abundance of 100 (dashed line). Solid line describes the median abundances, shading represents the 95% credible intervals in abundance, based around the uncertainty in the human development coefficient. Source data are provided as a Source Data file. | PMC9873912 | 41467_2022_35665_Fig5_HTML.jpg |
0.540368 | ff57299649fb45f7bec11af9ca1ee9e3 | Receiver operating characteristic curves for HATCH scores to predict mortality | PMC9874201 | IJPH-51-2717-g001.jpg |
0.497863 | 212ccbeb9d254c9ca17ab9e0151fddcc | Kaplan–Meier survival curves according to HATCH score in COVID-19 patients | PMC9874201 | IJPH-51-2717-g002.jpg |
0.604514 | ae681e96b3a34501a42b6b70db93b195 | Experiment 2—forced choice selection results. Mean accuracy (left panels) and reaction times to make correct responses (right panels) are presented for trials where the critical infomration was Warning information (top panels) and where the critical informaiton was Active Ingredient information (lower panels). Error bars are the standard error of the mean. | PMC9874361 | HSR2-6-e1062-g001.jpg |
0.453614 | 675150611e8b4e5a9182c532d3b79d08 | Four experimental treatments with basic terminology. | PMC9874361 | HSR2-6-e1062-g002.jpg |
0.624058 | 24db7e4e3f0e4ff7bcff14ed3bccc8cd | Experiment 1—absolute judgment warning results. Mean accuracy (left panels) and reaction times to make correct responses (right panels) are presented for trials where the medication was contraindicated (a “yes” response was correct) top panels) and where the medication was not contraindicated (a “no” response was correct lower panels). Error bars are the standard error of the mean. | PMC9874361 | HSR2-6-e1062-g003.jpg |
0.590316 | d7fc9ad4a22d464c826173637a880438 | Experiment 1—absolute judgment active ingredient results. Mean accuracy (left panels) and reaction times to make correct responses (right panels) are presented for trials where the medication was contraindicated (top panels) and where the medication was not contraindicated (lower panels). Error bars are the standard error of the mean. | PMC9874361 | HSR2-6-e1062-g004.jpg |
0.437825 | e16da38817074559ab4881f8326d8947 | Psychological capital development methods based on typological framework. | PMC9874676 | fpsyg-13-963439-g001.jpg |
0.45153 | 3ed6ca1b48df415fa8deaca4bf51c4c4 | Drug-excipients interaction and aptamer conjugation on stealth nanoliposome. a FTIR spectra of apigenin (A), soya lecithin (B), cholesterol (C), DSPE-PEG-2000-COOH (D), BHT (E), Blank formulation (F), the physical mixture of all constituents (G), NLCs (H), PEG-NLCs (I), and Apt-NLCs (J); b Pictorial representation of surface functionalization of PEG-NLCs with modified NH2-AS1411; c Determination of aptamer conjugation by agarose gel. The first three lanes from the left had (Apt-NLCs) showing no sample run, the 4th lane showed free aptamer (AS1411) showing movement, and the 5th lane had DNA ladder; d i, ii, iii represented spectrometric reading for free AS1411, plain nanoliposomes AS1411 conjugated nanoliposomes by nanodrop UV spectrophotometer, (experiment was conducted on triplicate set) | PMC9875447 | 12951_2022_1764_Fig1_HTML.jpg |
0.415448 | 0eeda634bfd9409eacb2e7bfc3efcb65 | Characterization of aptamer conjugated nanoliposomes Apt-NLCs.
a average particle size distribution, and b Zeta potential, c surface morphology applying FESEM images at 43 000 ×. d Data by atomic force microscopy. e Cryo-TEM image depicts internal morphology, f Cumulative % drug release against time for Apt-NLCs as compared NLCs/PEG-NLCs. Data show mean ± standard deviation applying three different experimental values | PMC9875447 | 12951_2022_1764_Fig2_HTML.jpg |
0.443213 | edbeb4b886414125b5daad30a6ccc9f4 | In vitro cytotoxicity and apoptosis analysis. a Viability assay in HepG2 and Huh-7 cells after treating them with free drug (apigenin), different experimental formulations (NLCs, PEG-NLCs, and Apt-NLCs), and AS1411 functionalized blank liposomes for 48 h with drug concentration range (10-100 µM) respectively. b FACS analysis of cellular apoptosis applying Annexin V-FITC staining in HepG2 cells treated with NLCs, PEG-NLCs, and Apt-NLCs with their equivalent IC50 doses of the drug at 48 h | PMC9875447 | 12951_2022_1764_Fig3_HTML.jpg |
0.412488 | 81f0776b310d448caba21693a7aeb16d | Cellular uptake studies. Flow cytometric data of cellular uptake. a PEG-NLCs, b Apt-NLCs, c Apt-NLCs in the presence of free AS1411 (receptor blocking condition) in Hep G2 cells at 1h, 2h, and 4h d Histogram representation of FACS mean fluorescence values obtained through above-mentioned uptake studies. Data represents mean ± SD, (n=3), bar (-) indicates groups between which the comparisons were made. ns: statistically insignificant, *** refer statistical significance at a level of P<0.05. e and f Confocal microscopic images of cell uptake of PEG-NLCs and Apt-NLCs in Hep G2 at 1h and 4h (Green color shows for FITC-labelled experimental nanoliposomes, PEG-NLCs/ Apt-NLCs, and blue color indicates nucleus stained by DAPI | PMC9875447 | 12951_2022_1764_Fig4_HTML.jpg |
0.439038 | c52d70cb23024e278d3c99d5ecbd3219 | Flowcytometric representation of cell cycle analysis and apoptotic protein expressions studies in Hep G2 cells. a i & ii Cell cycle analysis of different experimental nanoliposomes NLCs, PEG-NLCs and Apt-NLCs (highest improvement in G2/M phase in aptamer conjugated nanoliposomes, Apt-NLCs in comparison to non-conjugated nanoliposomes, NLCs/PEG-NLCs. Data represents mean ± SD, (n=3), *** refer statistical significance at a level of P<0.05. b, c and d p53, Casapae-3, and Bcl-2 protein quantifications upon NLCs, PEG-NLCs, and Apt-NLCs treatments, respectively, using FACS | PMC9875447 | 12951_2022_1764_Fig5_HTML.jpg |
0.42545 | 559cbbdf69414a7496e9249a396cb3d1 | Plasma and liver pharmacokinetics of free drug and all the test formulations (NLCs, PEG-NLCs and Apt-NLCs), biodistribution by gamma-scintigraphy studies, and accumulation of FITC-labelled test nano formulations in cancerous and normal hepatic tissues. a Plasma concentration of apigenin vs. time, upon iv administration of NLCs, PEG-NLCs and Apt-NLCs in HCC induced rats, respectively (Data from the three independent experiments show mean ± standard deviation (n = 3); b liver concentration of apigenin vs. time curve, upon iv administration of NLCs, PEG-NLCs and Apt-NLCs in HCC induced rats, respectively (Data from the three independent experiments show mean ± standard deviation (n = 3). (***) significant (P< 0.05) improvement in plasma and liver drug concentration in PEG-NLCs and Apt-PEG-NLCs applied animal Gr in comparison to NLCs over the specific time point as indicated in figure; c γ Scintigraphy imaginings of HCC rats at 4h and 8h after injecting 99mTc-labeled – (NLCs, PEG-NLCs and Apt-NLCs) through venous cannulation process. d Confocal microscopic observation of tumor tissues sections of carcinogenetic rats upon the treatment of FITC-labeled – (NLCs, PEG-NLCs, and Apt-NLCs) at4h and 8 h of administration of iv injection. The figure showed green fluorescence of FITC labeled formulations within the cancerous tissue. The right column showed the photos of the same tissue sections without fluorescence. e a comparative study of fluorescence level in both tumor tissue and healthy tissue by FITC-Conjugated Apt-NLCs, also in tumor tissue by FITC-conjugated NLCs/PEG-NLCs | PMC9875447 | 12951_2022_1764_Fig6_HTML.jpg |
0.400067 | 2c7324d4cdb5460db772920b80442bec | Microscopic and macroscopic hepatic analysis of the experimental rats. a Macroscopic (in 100X magnification) liver images for the different experimental animal groups, Gr A to Gr F. b H & E histopathological microscopic images of liver tissue sections for various animal groups. c Represented % of weight of liver vs total body weight in different treatment group. (***) represent significant (p < 0.05) changes among group as indicated in figure and ns denoted as non-significant changes | PMC9875447 | 12951_2022_1764_Fig7_HTML.jpg |
0.411246 | 029115eb623343c7a039915ae1cff354 | Comparative apoptotic gene expression analysis through RT-PCR with liver tissue samples from different experiential groups of animals (A-F). a Representing increases level of p53, b caspase-3, and c decreased level of Bcl-2 expression. Data indicated ± SD (n=3), (***) expressed significant (p < 0.05) upregulation or downregulation in gene, in conjugated nanoliposomes Apt-NLCs treated animals (GR F), samples in comparison to non-conjugated NLCs/ PEG-NLCs nanoliposomes (Gr D/F), free apigenin (Gr C) and carcinogen positive animals (Gr B). ns represented no significant changes among Gr A and Gr B for caspase expression assay. d Representing β- actin, p53, caspase -3, Bcl-2 gene expression of different experiential groups of animals in agarose gel electrophoresis study | PMC9875447 | 12951_2022_1764_Fig8_HTML.jpg |
0.461206 | 30c391dfcee2404ca8df88c409b3748b | Intermolecular FRET biosensors of mitochondrial respiratory chain complex detect supercomplex formation in fixed and live cells.a Schema of five molecular complexes involved in oxidative phosphorylation; complex I–IV and ATP synthase. A subset of mitochondrial respiratory chain complexes forms a higher-order structure called supercomplex. The most abundant supercomplex consisting of complex I (CI) monomer, complex III (CIII) dimer, and complex IV (CIV) monomer (I/III2/IV) is shown. Förster resonance energy transfer (FRET) biosensors of AcGFP tethered to NDUFB8 (a subunit of CI) and DsRed-Monomer tethered to COX8A (a subunit of CIV) are shown. b, c Fluorescence microscopy images of C2C12 myoblastic cells stably co-expressing NDUFB8-AcGFP and COX8A-DsRed-Monomer (upper panels), and UQCR11-AcGFP and ATP5F1c-DsRed-Monomer (lower panels), in fixed (b) and live (c) cells. FRET efficiency is shown in pseudo-color image. These experiments were repeated twice and the results of one experiment are shown. Scale bars; 10 μm. d Fluorescence images of acceptor-photobleaching. In C2C12 myoblastic cells stably expressing NDUFB8-AcGFP and COX8A-DsRed-Monomer, DsRed-Monomer was partially photobleached by illumination at 558 nm for 3 min. The photobleached area (purple square) is indicated. Scale bars; 10 μm. e Fluorescence images of DsRed-Monomer and AcGFP channels before and after photobleaching. Fluorescence intensities were measured in selected regions (n = 9) and compared before and after bleaching. Data are presented as means ± SE. ***P < 0.001; paired two-sided Student’s t test. Source data are provided as a Source Data file. | PMC9877034 | 41467_2023_35865_Fig1_HTML.jpg |
0.456847 | c88cbba5c8504ed5b21d4ffa0b93e24c | Intermolecular FRET biosensors of mitochondrial respiratory chain complex detect reduced supercomplex formation by suppressing Cox7rp expression.a Knockdown of Cox7rp expression with siCox7rp in C2C12 myoblastic cells was performed by reverse transfection method. Two days after transfection, total RNA was extracted and knockdown efficiency was evaluated using qRT-PCR. Two different siRNAs (10 nM) targeting Cox7rp (siCox7rp #1 and #2) and two different siRNAs (10 nM) not targeting human transcripts (siControl #1 and #2) were used. Data are presented as means ± SE (n = 3 biologically independent samples). ***P < 0.001; two-way ANOVA. b Knockdown efficiency of COX7RP in C2C12 myoblastic cells evaluated by western blot analysis. Knockdown of Cox7rp expression with siCox7rp in C2C12 myoblastic cells was performed by reverse transfection method. Two days after transfection, the cells were lysed and subjected to western blot analysis with the COX7RP antibody. FP70 protein was blotted as an internal control. This experiment was repeated twice and the results of one experiment are shown. IB, immunoblot. c Mitochondrial proteins of C2C12 myoblastic cells treated with siCox7rp #1 or #2, or siControl #1 or #2 were solubilized and subjected to blue native polyacrylamide gel electrophoresis (BN-PAGE). Positions corresponding to mitochondrial supercomplex I/III2/IVn, I/III2/IV, I/III2, III2/IV, complex I, and dimerized complex III (III2) are indicated. BN-PAGE was performed with antibodies for NDUFB8 of complex I and UQCRC2 of complex III. FP70 protein was blotted as an internal control. This experiment was repeated twice and the results of one experiment are shown. d Fluorescence microscopy images of C2C12 myoblastic cells stably co-expressing NDUFB8-AcGFP and COX8A-DsRed-Monomer, treated with siCox7rp or siControl in live cells. FRET efficiency is shown by pseudo-color images. Indicated area (white square) are shown in the enlarged images. Scale bars, 10 μm. e–g Quantification of fluorescence intensities of C2C12 myoblastic cells stably co-expressing NDUFB8-AcGFP and COX8A-DsRed-Monomer, treated with siCox7rp or siControl by imaging cytometer. Donor intensities (e), acceptor intensities (f), and corrected FRET (cFRET)/donor ratios (g) are shown. Data from 12 wells are presented as means ± SE. n.s. not significant. ***P < 0.001, two-way ANOVA. Source data are provided as a Source Data file. | PMC9877034 | 41467_2023_35865_Fig2_HTML.jpg |
0.425493 | 9840e2be27f94291bfa24438c7f36dff | 3,4-methylenedioxy-β-nitrostyrene (MNS) was identified as a compound inducing mitochondrial respiratory chain supercomplex formation using a chemical library screen with FRET imaging.a Scheme of the medium-throughput screen procedures using imaging cytometer. Compounds that induced high cFRET/donor value in C2C12 cells stably co-expressing NDUFB8-AcGFP and COX8A-DsRed-Monomer were selected for further analysis. b Chemical structures of MNS. c cFRET/donor ratio of C2C12 cells stably co-expressing NDUFB8-AcGFP and COX8A-DsRed-Monomer treated by different concentrations of MNS for 24 h. Data are presented as means ± SE of three wells for each treatment. EC50, half maximal effective concentration. d BN-PAGE of mitochondrial proteins from C2C12 cells treated with MNS (1 μM) or DMSO for 24 h. Positions corresponding to indicated mitochondrial supercomplexes and dimerized complex III (III2) are indicated. Immunoblot (IB) was probed with anti-UQCRC2. FP70 protein was analyzed as an internal control. e SDS-PAGE of mitochondrial fraction from C2C12 cells with treatment as panel d. IB was probed with antibodies against distinct respiratory complexes. f SDS-PAGE of whole cell lysates from C2C12 cells with treatment as panel d. IB was probed with indicated antibodies. β-Actin was probed as an internal control. g Oxygen consumption rate (OCR) measurement of C2C12 cells with treatment as panel d using Seahorse XFp Cell Mito Stress Test. Data are presented as means ± SE from three biologically independent experiments. Basal respiration, ATP synthesis component of respiration, and maximal respiration were calculated as described in “Methods”. FCCP, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone. *P < 0.05; unpaired two-sided Student’s t test. Source data are provided as a Source Data file. | PMC9877034 | 41467_2023_35865_Fig3_HTML.jpg |
0.48492 | fc303fa8188243128f7d07121bc616da | SYK inhibitors promote mitochondrial respiratory chain supercomplex assembly and stimulates oxygen consumption in C2C12 myoblastic cells.a Chemical structures of BAY61-3606 and GSK143. b, c cFRET/donor ratio of C2C12 cells stably co-expressing NDUFB8-AcGFP and COX8A-DsRed-Monomer treated by different concentrations of BAY61-3606 (b) and GSK143 (c). Data are presented as means ± SE of three wells for each treatment. d BN-PAGE of mitochondrial proteins from C2C12 cells treated with indicated SYK inhibitors (1 μM each) or DMSO for 24 h. Positions corresponding to indicated mitochondrial supercomplexes and dimerized complex III (III2) are indicated. Immunoblot (IB) was probed with anti-UQCRC2. FP70 was analyzed as an internal control. e IB for a mitochondrial fraction of C2C12 cells treated with indicated reagents as panel d, probed with antibodies against distinct respiratory complexes. f SDS-PAGE of whole cell lysates from C2C12 cells with treatment as panel d. IB was probed with indicated antibodies. β-Actin was analyzed as an internal control. g, h Oxygen consumption rate (OCR) measurement of C2C12 cells treated with BAY61-3606 (g) or GSK143 (h) (1 μM each) and DMSO for 24 h. Data are presented as means ± SE from three biologically independent experiments. Basal respiration, ATP synthesis component of respiration, and maximal respiration were calculated as described in “Methods”. FCCP, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone. *P < 0.05; **P < 0.01; unpaired two-sided Student’s t test. Source data are provided as a Source Data file. | PMC9877034 | 41467_2023_35865_Fig4_HTML.jpg |
0.446014 | 84b4a95c505144bbbbb5c6db7ff38135 | Inhibition of Syk expression increases mitochondrial respiratory chain supercomplex assembly in C2C12 myoblastic cells.a Knockdown of Syk expression in C2C12 cells transfected with its specific siRNAs (siSyk #1 and #2) evaluated by qRT-PCR. Indicated siRNAs (100 pM each) were used. Data are presented as means ± SE of three biologically independent samples. ***P < 0.001; two-way ANOVA. b Immunoblotting (IB) for mitochondrial protein expression in C2C12 cells transfected with indicated siRNAs (100 pM each), probed with antibodies against distinct respiratory complexes. β-Actin was analyzed as an internal control. c Imaging cytometer-based quantification of cFRET/donor ratios for C2C12 cells stably co-expressing NDUFB8-AcGFP and COX8A-DsRed-Monomer transfected with indicated siRNAs. Data are presented as means ± SE from 12 wells. ***P < 0.001; two-way ANOVA. d BN-PAGE of mitochondrial proteins from C2C12 cells treated with indicated siRNAs (100 pM each). Positions corresponding to indicated mitochondrial supercomplex and dimerized complex III (III2) are indicated. Immunoblot (IB) was probed with anti-UQCRC2. FP70 was analyzed as an internal control. e, f Oxygen consumption rate (OCR) measurement of C2C12 cells transfected with indicated siRNAs for 48 h. Data are presented as means ± SE from three biologically independent experiments. Basal respiration, ATP synthesis component of respiration, and maximal respiration were calculated as described in “Methods”. FCCP, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone. *P < 0.05; **P < 0.01; unpaired two-sided Student’s t test. Source data are provided as a Source Data file. | PMC9877034 | 41467_2023_35865_Fig5_HTML.jpg |
0.412576 | 5cbda040996c4c59aa65f44b308e0e62 | Increased exercise performance in mice treated with MNS.a Body weights of mice after intraperitoneal injection of MNS (4 mg/kg) or DMSO twice a week for 5 weeks. Data are presented as means ± SE (n = 8 biologically independent animals). n.s. not significant; two-sided Mann–Whitney U test. b, Results of wire hanging test after injection of MNS or DMSO for 3 weeks. Data are presented as means ± SE (n = 8 biologically independent animals). **P < 0.01; two-sided Mann–Whitney U test. c, d Results of forced treadmill exercise test after injection of MNS or DMSO for 2 weeks. Data are presented as means ± SE (n = 8 biologically independent animals). **P < 0.01; unpaired two-sided Student’s t test. e O2 consumption (VO2) during forced treadmill exercise test after injection of MNS or DMSO for 4 weeks. Data are presented as means ± SE (n = 8 biologically independent animals). *P < 0.05; **P < 0.01; unpaired two-sided Student’s t test. f Mitochondrial proteins of quadriceps femoris muscle from DMSO- or MNS-treated mice were solubilized and subjected to BN-PAGE. Positions corresponding to mitochondrial supercomplexes I/III2/IVn, I/III2, III2/IV, and dimerized complex III (III2) are indicated. Western blot analysis was performed with antibody for UQCRC2 of complex III. FP70 protein was blotted as an internal control. IB immunoblot. g Mitochondrial proteins of quadriceps femoris muscle from DMSO- or MNS-treated mice were solubilized and subjected to SDS-PAGE. Western blot analysis was performed with antibodies for NDUFB8 of complex I, COX8A of complex IV, and RISP of complex III. FP70 protein was blotted as an internal control. For f and g, experiments were repeated twice and the results of one experiment are shown. Source data are provided as a Source Data file. | PMC9877034 | 41467_2023_35865_Fig6_HTML.jpg |
0.463942 | df86a9721cfe4a4381b5f31269ea29f0 | Treatment options for chronic myelomonocytic leukemia patients during different decades | PMC9877071 | 10354_2022_976_Fig1_HTML.jpg |
0.403213 | a6272204cb1e48afa4b46c1c5e96ec45 | Kaplan–Meier plots for overall survival in chronic myelomonocytic leukemia patients treated before or after 2000 | PMC9877071 | 10354_2022_976_Fig2_HTML.jpg |
0.408467 | 7579e586fe6341ec878277d617f47691 | Kaplan–Meier plots for overall survival in chronic myelomonocytic leukemia patients treated with or without azacitidine (AZA) | PMC9877071 | 10354_2022_976_Fig3_HTML.jpg |
0.467188 | 7717d96b447c47e591b4c41492bd3dfe | Discrepancies between clinician-assigned outcomes and failure-dominant-assigned outcomes. *Denominator = total number of patients with discrepancies (n= 107). †Denominator = number of patients with change from success to no success (n=65). ‡Denominator = number of patients with change from no success to success (n = 42). §Patients treated <15 months who had no culture results; assigned an outcome of “<15 months, favorable”. ¶Denominator = number of patients who had <2 positive cultures and two new drugs were added after 8 months (n = 6). | PMC9879081 | i1815-7920-27-1-34-f01.jpg |
0.501543 | 0ba2c38c35194606bb668947a1579935 | Discrepancies between clinician-assigned outcomes and success-dominant-assigned outcomes. *Denominator = total number of patients with discrepancies (n = 59). †Denominator = number of patients with change from success to no success (n = 8). ‡Denominator = number of patients with change from no success to success (n = 51). §Patients were treated <15 months and had no culture results; assigned an outcome of “<15 months, favorable”. | PMC9879081 | i1815-7920-27-1-34-f02.jpg |
0.413421 | f67c48fa73944475bae0842d65e52fa9 | US Maintenance Drug Therapy Distribution Under Current and Higher SITT Adoption ModelsAbbreviations: COPD, chronic obstructive pulmonary disease; ICS, inhaled corticosteroid; LABA, long-acting beta agonist; LAMA, long-acting muscarinic antagonist; MITT, multiple-inhaler triple therapy; SITT, single-inhaler triple therapy. | PMC9879267 | jheor_2023_10_1_55635_135224.jpg |
0.433125 | cd297e0cba8b4e0fbefc936777530f5f | ETHOS-Eligible and Expanded ETHOS-Eligible Drug Therapy Distribution Under CurrentAbbreviations: COPD, chronic obstructive pulmonary disease; ICS, inhaled corticosteroid; LABA, long-acting beta agonist; LAMA, long-acting muscarinic antagonist; MITT, multiple-inhaler triple therapy; SITT, single-inhaler triple therapy. | PMC9879267 | jheor_2023_10_1_55635_135225.jpg |
0.472934 | 93e29840ae134c649a0760bf9413510c | Cumulative Years of Life Extended Under Higher SITT Adoption Scenarios for the US COPD PopulationAbbreviation: SITT, single-inhaler triple therapy. | PMC9879267 | jheor_2023_10_1_55635_135226.jpg |
0.443626 | 42c8859c2af5407c9fc34f0451ed6954 | DEGs in two datasets from the GEO. (A) Volcano plots showing the DEGs in GSE49710. (B) Volcano plots showing the DEGs in GSE45547.The red dots represent upregulated genes, blue dots represent downregulated genes, and gray dots indicate genes with no significant differences. (C) Venn diagram showing the intersection of upregulated genes. (D) Venn diagram showing the intersection of downregulated genes. All DEGs are screened based on an Adjust P value < 0.05 and |Fold Change| > 1. | PMC9880530 | fonc-12-1083570-g001.jpg |
0.457427 | 5c8a510436444a028235a30400d8a0f1 | GO function and KEGG pathway analysis of 282 common DEGs. Analysis of (A) Biological Process, (B) Cellular Component, and (C) Molecular Function. (D) KEGG analysis showed the enriched pathways. Each functional section shows 10 terms. | PMC9880530 | fonc-12-1083570-g002.jpg |
0.466089 | ddb4e8fe225f495ca172b108d4c582aa | The survival difference between children with stage MS and stage M NB (<18 months) in the two datasets. (A) K-M survival curves of children with stage MS and stage M (<18 months) NB in GSE49710. (B) K-M survival curves of children with stage MS and stage M (<18 months) NB in GSE45547. | PMC9880530 | fonc-12-1083570-g003.jpg |
0.443877 | 08c4ae55b37947c38debed16d3e341ee | Survival curves of patients grouped by BIRC5, SLCO4A1, POPDC3, HK2 and TF expression in the two datasets. (A–E) The prognostic value of BIRC5, SLCO4A1, POPDC3, HK2 and TF in the GSE49710 dataset. (F–J) The prognostic value of BIRC5, SLCO4A1, POPDC3, HK2 and TF in the GSE45547 dataset. Gene expression levels are grouped by median. | PMC9880530 | fonc-12-1083570-g004.jpg |
0.47725 | 48494d5e1df349648bfed01ca59eae41 | Heatmaps of five DEGs in two datasets. (A) Heatmap of five DEGs in GSE49710. (B) Heatmap of five DEGs in GSE45547. From red to blue, the expression level of the DEGs in the sample gradually decreases. | PMC9880530 | fonc-12-1083570-g005.jpg |
0.430519 | 6f15b0d74a3e49deba5650bbaefeff5b | Display of IHC dyeing effect of DEGs and the dot plot of relative IOD values of each group. The magnification of the IHC images was 40×, scale bar=20μm. The dot plot shows the difference of IOD values between samples of each protein in M and MS stage. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. | PMC9880530 | fonc-12-1083570-g006.jpg |
0.551029 | 45fe8b7b47d84e3a8a098cb5e7c78519 | Flow chart for follow-up visits of participants | PMC9880942 | 10461_2023_3995_Fig1_HTML.jpg |
0.405649 | 1f2be5d80b744506aa86a9009b3645d3 | Steps of the outdoor pots experiment for sugar beet (Beta vulgaris saccharifera) genotypes suitability towards root-knot nematode, Meloidogyne incognita by two quantitative and qualitative schemes. AQSCS, adaptive quantitative scheme of Canto-Saenz’s; MHPI, modified host-parasite index. | PMC9881751 | fpls-13-966377-g001.jpg |
0.453135 | 7c9b7f41c0bc41e997529f53ab331cf3 | Perineal pattern of Meloidogyne incognita. Dissected female sections showed a characteristic oval shape of the rounded perineal pattern, typically with a high dorsal arch and usually wavy striae, which bend towards the lateral lines and may be absent from the distinct lateral field or weakly demarcated by forked striae typical of this species M. incognita. (A–C)
M. incognita (Kofoid and White, 1919; Chitwood, 1949) perineal patterns (scale for light microscopy photos =10 μm). | PMC9881751 | fpls-13-966377-g002.jpg |
0.363795 | 3efa81a6ece6428c9166e00f1362af08 | Total reduction % yield and quality characters of the screened sugar beet (Beta vulgaris saccharifera) varieties as influenced by root-knot nematode, Meloidogyne incognita infection. Mean values followed by different letters are significantly (P<0.05) different from each other according to Duncan’s Multiple Range Test. | PMC9881751 | fpls-13-966377-g003.jpg |
0.422364 | be08ea12dbaf46ae9a2f0bd5c22f87b1 | Screening sugar beet (Beta vulgaris saccharifera) varieties towards root- knot nematode, Meloidogyne incognita, using seven parameters, including (A). The reproduction factor (RF), damage index (DI), susceptibility rate (SR), and modified host parasite index (MHPI); (B) gall index (GI), gall size (GS), and gall area (GA). Mean values followed by different letters are significantly (P<0.05) different from each other according to Duncan’s Multiple Range Test. | PMC9881751 | fpls-13-966377-g004.jpg |
0.445501 | 2f4b2bc66e114a24b57e0ace7afd7c1b | Sugar beet roots, 60-days post inoculation with Meloidogyne incognita in eight genotypes; (1) Natura KWS, (2) FARIDA, (3) Lammia KWS, (4) SVH 2015, (5) Lilly, (6) Halawa KWS, (7) Polat, and (8) Capella. | PMC9881751 | fpls-13-966377-g005.jpg |
0.467104 | f98050aad21f459591a73e0824dc1680 | Agarose gel electrophoresis of PCR product amplified from eight sugar beet genotypes genomic DNA using Nem06FWD and Nem06REV specific primer. | PMC9881751 | fpls-13-966377-g006.jpg |
0.431328 | aaab2fa3a1c842ae9eebb604da8af2ff | Single nucleotide polymorphisms (SNPs) detection for Anchor KF303133.1 and eight sugar beet genotypes sequences by using the DNAMAN
®
software (Lyon BioSoft, Quebec, Canada). Gaps in the sequences are indicated by dots ‘‘.’’, showing the conserved consensus sequences at the last sequence. SNPs are indicated by different shading colors. | PMC9881751 | fpls-13-966377-g007.jpg |
0.499783 | 3da5e42c638e4b8aa462c66448aaeb52 | Alignment of the deduced amino acid sequences of eight obtained with MEGA-X software. Conserved consensus sequences are indicated by dots. | PMC9881751 | fpls-13-966377-g008.jpg |
0.507114 | 010bce1f689c4e29abd431a26385a214 | Molecular evolutionary and phylogenetic analysis was inferred using the Maximum Likelihood method and Tamura-Nei model. | PMC9881751 | fpls-13-966377-g009.jpg |
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