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0.390661 | bb2c4d4545d04263840167a0b787355d | (a) Schematic diagram of the synthetic route of Ru–NiFeP/NF nanosheets, SEM images of (b) bare NF, (c) Ru–Ni2P/NF, (d) Ru–FeP/NF, (e) Ru–NiFeP/NF, (f) EDX elemental mapping of Ru–NiFeP/NF, (g) LSV curves recorded in 0.5 M H2SO4, (h) Corresponding Tafel plot. Reprinted with permission from Ref. [102], Copyright 2021, Elsevier. | PMC9370661 | nanomaterials-12-02618-g009.jpg |
0.454618 | a353dfaf1a9a4ad4b324f08ef0c16dd2 | (a) Synthesis route of Ir–NCNSs catalyst, (b,c) TEM image of the NCNSs and 1%Ir–NCNSs, Characterization of 1%Ir–NCNSs: (d) High-resolution TEM image, (e) Polarization curves, (f) Tafel plot, (g) Chronoamperometry curve. Reprinted with permission from Ref. [118], Copyright 2021, American Chemical Society. | PMC9370661 | nanomaterials-12-02618-g010.jpg |
0.422961 | e95e2b0f0a294673ad3cd3fa19210c1c | (a) Synthesis route of PBN, (b)ACHAADF–STEM imaging of PBN-300-Ir, (c) LSV curves for these catalysts in 0.5 M H2SO, (d) Comparison between the mass activity at 70 mV and the overpotentials required to achieve 10 mA cm−2 (e) Tafel plots, (f) Comparison of LSV curves before (black) and after (red) chronoamperometry test, The inset is current density versus time (I–T) curves of PBN-300-Ir recorded for 38 h at −0.019 V versus RHE. Reprinted with permission from Ref. [130], Copyright 2022, John Wiley and Sons. | PMC9370661 | nanomaterials-12-02618-g011.jpg |
0.438364 | 185a8acf0d794235a26e0246e47137c8 | (a) Scheme of the PdCu0.2H0.43 nanoparticle formation, (b) LSV curves, (c) overpotentials at 10 mA/cm2, and (d) Tafel plots of these catalysts in 0.5 M H2SO4. LSV curves before and after 5000 cycles in 0.5 M H2SO4 for (e) Pd/C, (f) PdCu0.2/C, (g) PdH0.64/C, and (h) PdCu0.2H0.43/C. Reprinted with permission from Ref. [95], Copyright 2022, American Chemical Society. | PMC9370661 | nanomaterials-12-02618-g012.jpg |
0.362018 | 143f43a18a5046aea6342a4ed59bc95b | (a) TEM image of the Rh/Rh2P–NFAs, (b) HR-TEM image of the Rh/Rh2P–NFAs, (c) HER polarization curves at 5 mV s−1 without iR–correction in 0.5 M H2SO4, (d) Tafel slopes and (e) Nyquist plots at their open circuit potential. (f) The HER polarization curves of the Rh/Rh2P–NFAs before and after 1000 cycles at 5 mV s−1. Reprinted with permission from Ref. [135], Copyright 2021, Elsevier. | PMC9370661 | nanomaterials-12-02618-g013.jpg |
0.461578 | 17e2ce8fd31b410bafdd9236e45248f0 | Overall architecture of the proposed FPGA-based ADC. | PMC9371103 | sensors-22-05852-g001.jpg |
0.463121 | 70f53b57660e478798d99900f29ad50d | Timing diagram of our FPGA-based ADC. “Reproduced from [20]”. | PMC9371103 | sensors-22-05852-g002.jpg |
0.485399 | 87ab698768534fc78fd1e24cc97a7b7b | Detailed diagram of the CARRY8 block. | PMC9371103 | sensors-22-05852-g003.jpg |
0.425544 | 1836aa619e8541deb04e658f794e6d8f | Timing diagram of the edge detector and bubble filtering. “Reproduced from [20]”. | PMC9371103 | sensors-22-05852-g004.jpg |
0.49172 | 480968c379744e59a1fbf7ca79e84785 | Block diagram of the code density test. | PMC9371103 | sensors-22-05852-g005.jpg |
0.439211 | d2e82e65381f497db3be19144197666c | Block diagram of the inverter-based ring oscillator. | PMC9371103 | sensors-22-05852-g006.jpg |
0.413417 | f595fdba62ae4e0fbb95cfd3a7af4072 | Schematic diagram of a ring oscillator constructed by a look-up table. | PMC9371103 | sensors-22-05852-g007.jpg |
0.421376 | bce21d0dc3e645288da7c1680d356c8b | Timing simulation of the ring oscillator. | PMC9371103 | sensors-22-05852-g008.jpg |
0.450193 | fc5d69d870624508b381105ae37678bb | Flow chart of the bin-by-bin calibration. | PMC9371103 | sensors-22-05852-g009.jpg |
0.430242 | b3b59e334b194cada359e27db16698f7 | Voltage characteristic of rising and falling slope. | PMC9371103 | sensors-22-05852-g010.jpg |
0.465855 | 228556e002bb4c9381bff3d6330f42bd | Dependence of ring oscillator frequencies on temperature. | PMC9371103 | sensors-22-05852-g011.jpg |
0.473352 | dca43e7274f341b5a82b049c88832f4f | Measured histogram in the carry chain (a) rising edge; (b) falling edge. | PMC9371103 | sensors-22-05852-g012.jpg |
0.389147 | d215297c0700469089f09e290b87ae50 | Measured DNL and INL of ADC. | PMC9371103 | sensors-22-05852-g013.jpg |
0.50979 | aa7682670074450aba33614ac4909beb | Single-shot measurement obtained by applying a DC voltage. | PMC9371103 | sensors-22-05852-g014.jpg |
0.4268 | 7d29728bd3d44db8bd807cdf2e507892 | FFT of the 11 MHz (a) and 191 MHz; (b) 1 Vpk-pk sine wave for SNDR estimation. | PMC9371103 | sensors-22-05852-g015.jpg |
0.390318 | 291931a185e1430895c593235db0f85c | Measured SNDR and SFDR plots versus input frequency with or without online calibration. | PMC9371103 | sensors-22-05852-g016.jpg |
0.393365 | a9c13002fae647f7a9ea7b2d8ef65732 | Two-tone test at 20 and 25 MHz. (a) Time domain; (b) frequency domain. | PMC9371103 | sensors-22-05852-g017.jpg |
0.439807 | 4ca296cc64af43ad80c3d56052c3ffff | Measured SNDR versus input amplitude. | PMC9371103 | sensors-22-05852-g018.jpg |
0.417893 | bcaeb1554fbc47e7b9a943f6cc2db928 | Map of the study area and photo of the studied woodland (northern Morocco). | PMC9371207 | sensors-22-05629-g001.jpg |
0.411442 | fa98424815eb4cbe91f1e61d16e40ed1 | Experimental dairy goat fitted with a GPS collar on the neck (A) and with a sensor placed on the rear left leg (B) in the studied Mediterranean woodland in northern Morocco. | PMC9371207 | sensors-22-05629-g002.jpg |
0.433508 | f3e78b79e180429f87273fc8bde50602 | Estimation of temporal variations in energy requirements (maintenance, locomotion, pregnancy and lactation) and energy balance for dairy goats browsing in a Mediterranean woodland in northern Morocco. (A), dry year; (B) wet year. MEm, daily metabolizable energy requirement for maintenance. Pie charts represent the intake contributions from grazing and supplementation. | PMC9371207 | sensors-22-05629-g003.jpg |
0.395455 | aad2f20eb1f145858fd397cd4667df57 | Estimation of temporal variations in protein requirements (maintenance (for goats with high activity), pregnancy and lactation) and protein balance for dairy goats browsing in a Mediterranean woodland in northern Morocco. (A), dry year; (B) wet year. Pie charts represent the intake contributions from grazing and supplementation. | PMC9371207 | sensors-22-05629-g004.jpg |
0.390909 | 2ee944133d3945ffa0af7c1a325a1fd5 | The overall flow of the side-channel-based disassembler. | PMC9371420 | sensors-22-05900-g001.jpg |
0.401343 | e8364e6ca6614e9782047b55e265243c | Single-level pipeline applied to the ATxmega128. | PMC9371420 | sensors-22-05900-g002.jpg |
0.419759 | 6197c1ef8ea64084bd89afb9c233be38 | The power consumption pattern of the ATxmega128 (4 MHz). | PMC9371420 | sensors-22-05900-g003.jpg |
0.385437 | c87db3181fa049e1b381ac066fb428e4 | Three-stage pipeline applied to the Cortex-M0. | PMC9371420 | sensors-22-05900-g004.jpg |
0.449501 | b3c4f0851cb9499aa2d4c942b7a815f9 | The result of instruction sequence analysis (ADC of the ATxmega128). | PMC9371420 | sensors-22-05900-g005.jpg |
0.438583 | 6ec676a7b0544407a1a888baf40989d9 | Instruction template acquisition structure using an oscilloscope and ChipWhisperer platforms. | PMC9371420 | sensors-22-05900-g006.jpg |
0.436371 | c690659cde3e4fb38977b8e9579a08e9 | Final feature points of the ATxmega128. | PMC9371420 | sensors-22-05900-g007.jpg |
0.413317 | 962de5ca713c48aeae348774f885dfe7 | Confusion matrices of single-board and cross-board instruction recovery using MLP-10. | PMC9371420 | sensors-22-05900-g008.jpg |
0.446033 | 2f1f32d8fe8f4f2392752eefbeb04c29 | An illustration of how a model of the external world is formed, resulting in beliefs about the true states of the world and belief updating, encoded by internal states. | PMC9372327 | fpsyg-13-981925-g0001.jpg |
0.380957 | 2f7ae3ecb2ff4be193678c9af80a2c1a | Empagliflozin reduces myocardial damage and improves myocardial function after CRS-3. A WT mouse model of CRS-3 was generated through 30 min of bilateral renal artery ischemia followed by 72 h of reperfusion. Seven days before CRS-3, empagliflozin (EMPA, 10 mg/kg/d) was administered to the mice via oral gavage. (A, B) Blood samples were collected from the CRS-3 model mice, and the levels of BUN and creatinine (Cr) were determined using ELISAs. (C) Electron microscopy was used to detect changes in the myocardial structure. Yellow arrows indicate myocardial fiber swelling, muscle sarcomere dissolution and mitochondrial vacuolization in response to CRS-3. (D) Relative expression of Gr-1 in the myocardium. (E–G) RNA was isolated from heart tissues, and qPCR was used to determine the transcription of IL-6, MCP1 and TNFα. ∗p < 0.05. | PMC9372775 | gr1.jpg |
0.452004 | bc8a9307708a4af9aadaf849ce5e5278 | Empagliflozin ameliorates mitochondrial structural disorder in cardiomyocytes during CRS-3. (A–C) Cardiomyocytes were freshly isolated from mouse hearts after CRS-3. Representative pictures of immunofluorescence staining of the mitochondrial morphology are shown. The average mitochondrial length and the number of cardiomyocytes with fragmented mitochondria were recorded. (D) Electron microscopy was used to observe the mitochondrial morphology in cardiomyocytes. (E–H) RNA was isolated from heart tissues, and qPCR was used to analyze the transcription of Mfn2, Opa1, Drp1 and Fis1. (I, J) The duration of mPTP opening in cardiomyocytes was recorded, and the mPTP opening rate was normalized to that of the control group. (K) An ELISA was applied to analyze caspase-3 activity in cardiomyocytes. ∗p < 0.05. | PMC9372775 | gr2.jpg |
0.427572 | 3e3c75fde15c4be3b63e74c34932c423 | Empagliflozin attenuates cardiomyocyte mitochondrial dysfunction during CRS-3. (A). ATP production in cardiomyocytes was measured with an ELISA. (B, C) Representative pictures of the mitochondrial membrane potential analysis using the JC-1 probe. The red-to-green fluorescence ratio was used to quantify the mitochondrial membrane potential in cardiomyocytes. (D-E) Representative pictures of the mitochondrial ROS analysis in cardiomyocytes using the MitoSOX red mitochondrial superoxide indicator. (F–H) ELISAs were used to observe the changes in mitochondrial respiratory complexes I-III in cardiomyocytes. (I–J) The mitochondrial DNA copy number and transcription in cardiomyocytes were determined using qPCR. (K–O) The baseline OCR, proton leak, maximal respiratory capacity and ATP turnover in cardiomyocytes were recorded. ∗p < 0.05. | PMC9372775 | gr3.jpg |
0.380319 | 2937752377364d1a9c1dc364ec63c58b | Empagliflozin activates FUNDC1-dependent mitophagy and preserves the mitochondrial integrity in the heart during CRS-3. CRS-3 was induced in cardiomyocyte-specific FUNDC1 knockout (FUNDC1CKO) mice and control FUNDC1f/f mice. Seven days before CRS-3, empagliflozin (EMPA, 10 mg/kg/d) was administered via oral gavage. Then, cardiomyocytes were isolated from the mice. (A-D) Proteins were collected from heart tissues, and FUNDC1, mito-LC3II, Beclin1 and Atg5 protein levels were determined via Western blotting. (E, F) Mitophagy activity was measured through an mt-Kemia assay in vitro. (G, H) Representative pictures of immunofluorescence staining of the mitochondrial morphology in cardiomyocytes. The average mitochondrial length and the number of cardiomyocytes with fragmented mitochondria were recorded. (I, J) Representative pictures of the mitochondrial ROS analysis in cardiomyocytes using the MitoSOX red mitochondrial superoxide indicator. (K, L) Representative pictures of the mitochondrial membrane potential analysis in cardiomyocytes using the JC-1 probe. The red-to-green fluorescence ratio was used to quantify the mitochondrial membrane potential. ∗p < 0.05. | PMC9372775 | gr4.jpg |
0.449178 | e50180cfb3414277b5d742fe6092adc5 | Loss of FUNDC1 abolishes the cardioprotective effects of empagliflozin during CRS-3. CRS-3 was induced in cardiomyocyte-specific FUNDC1 knockout (FUNDC1CKO) mice and control FUNDC1f/f mice. Seven days before CRS-3, empagliflozin (EMPA, 10 mg/kg/d) was administered via oral gavage. (A) Electron microscopy was used to detect changes in the myocardial structure. Yellow arrows indicate myocardial fiber swelling, muscle sarcomere dissolution and mitochondrial vacuolization in response to CRS-3. (B–D) RNA was isolated from heart tissues, and qPCR was used to determine the transcription of IL-6, MCP1 and TNFα. ∗p < 0.05. | PMC9372775 | gr5.jpg |
0.420301 | 8d8ec73bd8254777a5cd4075258bc5f6 | Empagliflozin activates the β-catenin pathway and promotes FUNDC1-dependent mitophagy in cardiomyocytes during CRS-3. A WT mouse model of CRS-3 was generated through 30 min of bilateral renal artery ischemia followed by 72 h of reperfusion. Seven days before CRS-3, empagliflozin (EMPA, 10 mg/kg/d) was administered via oral gavage. To activate or inhibit the Wnt/β-catenin pathway, mice were respectively treated with BML-284 (5 mg/kg) or MSAB (10 mg/kg) two days before CRS-3 or empagliflozin treatment. (A, B) Proteins were collected from heart tissues, and β-catenin expression was determined using Western blotting. (C, D) Representative pictures of immunofluorescence staining with a β-catenin antibody. Nuclei were stained with DAPI. The levels of nuclear β-catenin were determined. (E–G) RNA was isolated from heart tissues, and qPCR was used to determine the transcription of FUNDC1, p62 and Beclin1. (H, I) Mitophagy activity was measured through an mt-Kemia assay in vitro. ∗p < 0.05. | PMC9372775 | gr6.jpg |
0.408876 | 18ee942b41df41af8ea6e9f3da3eed12 | Gene expression of PI3K (A), Acp5 (B) and NFATc1 (C) in clinical samples of chronic apical periodontitis. *P < 0.05 represents a significant difference between the groups of apical periodontitis and healthy tissues | PMC9373278 | 12903_2022_2364_Fig1_HTML.jpg |
0.392541 | ce2158418ad742de9d3e109bb005afb8 | Expression of PI3K and Akt in a mouse model of apical periodontitis. A HE staining of the mouse apical tissues of the mandibular first molars at 1, 2, 3, and 4 weeks after pulp opening and normal control group (×100). B a, b, c and d, TRAP staining of the mouse periapical tissues in the control group and 2nd week after pulp opening, the positive cells were distincitve by very large cellular sizes(≥ 3 multiple nuclei), wine red; e, statistical analysis of the OD values of positive osteoclasts in each experimental group, * represent significant differences between groups (P < 0.05). C a, b, c and d, expression of PI3K in mouse periapical tissues in the control group and 2nd week after pulp opening, the positive cells are tawny; e, statistical analysis of the OD values of PI3K in each experimental group, * represent significant differences between groups (P < 0.05). D a, b, c and d, expression of Akt in the mouse periapical tissues in the control group and 2nd week after pulp opening, the positive cells are tawny; e, statistical analysis of the OD values of Akt in each experimental group, * represent significant differences between groups (P < 0.05). E Correlation analysis between PI3K OD value, AKT OD value and osteoclast OD value. HE, 10× original magnification. Immunohistochemical,10× or 40× original magnification | PMC9373278 | 12903_2022_2364_Fig2_HTML.jpg |
0.44575 | 6d23c58db63b4a079da882f042c7cf8c | Osteoclast induction and identification. A a and b, RAW264.7 cells after 0 and 5 days of induction, viewed under a light microscope (×200); c and d, TRAP staining of RAW264.7 cells at 0 and 5 days of induction (×200); B Acp5 mRNA expression of RAW264.7 cells at 0 and 5 days of induction.*P = 0.0009. 40× original magnification | PMC9373278 | 12903_2022_2364_Fig3_HTML.jpg |
0.42997 | d3a28d8db60446b3a4fd348b73d0ef13 | Osteoblast induction and identification. A a and b, ALP staining of MC3T3-E1 cells after 0 and 7 days of induction, viewed under a light microscope (×40); c and d, Alizarin red staining of MC3T3-E1 cells at 0 and 21 days of induction, viewed under a light microscope (×40); B the ALP mRNA expression results of MC3T3-E1 cells at 0 and 7 days of induction. C Statistical analysis of ALP mRNA expression in osteoblasts. *P = 0.015 | PMC9373278 | 12903_2022_2364_Fig4_HTML.jpg |
0.450176 | a8bfccb51ab34184bc5a486059e0e11f | Detection of related genes and proteins after treatment of osteoclasts and osteoblasts with LPS. A mRNA expression of PI3K (P = 0.038), Acp5 (P < 0.001) and NFATc1 (P = 0.002) in osteoblasts under the action of LPS; B mRNA expression of PI3K (P < 0.001), BMP-2 (P = 0.002) and Runx2 (P = 0.039) in osteoblasts under the action of LPS. C Expression of PI3K, TRAP and NFATc1 proteins in osteoclasts under the action of LPS; D statistical analysis of PI3K (P = 0.032), TRAP (P = 0.022) and NFATc1 (P = 0.028) protein expression in osteoclasts; E expression of PI3K, BMP-2 and Runx2proteins in osteoblasts under the action of LPS; F statistical analysis of PI3K (P = 0.045), Runx2 (P = 0.018) and BMP-2 (P = 0.021) protein expression in osteoblasts.*P < 0.05, representing a significant difference between the different groups | PMC9373278 | 12903_2022_2364_Fig5_HTML.jpg |
0.518145 | 719e6ec2ce154ca485269b125d1e7b64 | Effects of LY294002 on the proliferation activity and related gene and protein expression of osteoclasts and osteoblasts. A The cell proliferation of osteoclasts treated with LY294002; B the cell proliferation of osteoblasts treated with LY294002; C statistical analysis of mRNA expression of Akt (P = 0.023), Acp5 (P = 0.019) and NFATc1 (P = 0.011) in osteoblasts treated with LY294002; D statistical analysis of mRNA expression of Akt (P = 0.019), BMP-2 (P = 0.012) and Runx2 (P = 0.003) in osteoblasts treated with LY294002. E The expression of PI3K, TRAP and NFATc1 proteins in osteoclasts treated with LY294002; F statistical analysis of p-Akt (P = 0.009), TRAP (P = 0.039) and NFATc1 (P = 0.032) proteins expressed in osteoclasts; G the expression of PI3K, BMP-2 and Runx2 proteins in osteoblasts treated with LY294002; H statistical analysis of p-Akt (P = 0.027), Runx2 (P = 0.031) andBMP-2 (P = 0.028) proteins expressed in osteoblasts. *P < 0.05 represents a significant difference between the control and experimental groups | PMC9373278 | 12903_2022_2364_Fig6_HTML.jpg |
0.452273 | 87d3ece50eb642b4a4b8b8310c265239 | (A) Left-upper lobe cavitation. Non-contrasted computed tomography scans with extensive cavitation in the left upper lobe that contacts the pleural surface. (B) Postoperative image. Chest X-Ray confirms the absence of pneumothorax and other complications. | PMC9373585 | gr1.jpg |
0.438681 | ae92fb4d13684518801218e98dfebc69 | Illustration of multi-angle emotion recognition extraction. | PMC9373982 | fpsyg-13-917517-g0001.jpg |
0.431273 | f5cb7240b4254753ab687e99db16c8a6 | Multi-angle combined information processing flow figure. | PMC9373982 | fpsyg-13-917517-g0002.jpg |
0.411248 | 309e598ce712471aafdfb43b1d14029e | Algorithm structure diagram of multi-angle combination. | PMC9373982 | fpsyg-13-917517-g0003.jpg |
0.470506 | afc7b809b053480ab468f9edf2a74dac | Flowchart of facial emotion recognition. | PMC9373982 | fpsyg-13-917517-g0004.jpg |
0.436165 | 01a0d8941a3e4f19ae8eb1260d201977 | Flowchart of language emotion recognition. | PMC9373982 | fpsyg-13-917517-g0005.jpg |
0.486154 | 947e7a67ed0a428e857c41985b44a899 | Linguistic emotion recognition model. | PMC9373982 | fpsyg-13-917517-g0006.jpg |
0.40712 | 8348274bdf98422faa0e05f324a720c7 | Filter frequency spectrum diagram. | PMC9373982 | fpsyg-13-917517-g0007.jpg |
0.515917 | 119f18b7ada5483284c36d588f720d88 | Blended teaching learning model diagram. | PMC9373982 | fpsyg-13-917517-g0008.jpg |
0.409506 | 2a3ba8657fde46eeaa42f66652ab29ba | Average pixel distance extraction map for four emotions. | PMC9373982 | fpsyg-13-917517-g0009.jpg |
0.436462 | 81fb53e547f34d6e9173ad5485775ad1 | Recognition frequency and average recognition frequency of three features. | PMC9373982 | fpsyg-13-917517-g0010.jpg |
0.451096 | 6bc305b2745049d4ba2446bcfa0ce078 | Feature recognition rate and average recognition rate. | PMC9373982 | fpsyg-13-917517-g0011.jpg |
0.456694 | 39c7bfcf386e420fafc0fa6fc9fd3d82 | An overview of the EMG control of motorized wheelchair devices. Pictured is a user utilizing electromyography to control the movement of the joystick via the attachment to the wheelchair device | PMC9375912 | 12984_2022_1066_Fig1_HTML.jpg |
0.476029 | 70006864db1b402fbaa42e2c35febd8e | An overview of the bilateral input mode for the control system. The process flow chart begins and follows the users input signal to initiate a forward or reverse motion with a clench of both temporalis muscles with either a short or long contraction for a forward or reverse command respectively. The user can then initiate the stopping function, which is the same input as the forward command, or begin a turning motion while maintaining forward motion. A turning motion is initiated by a contraction of the temporalis muscle on the side of intended motion. If a turning motion is chosen it can be stopped with an additional turning command and maintain forward motion. Or for a complete stop, the aforementioned stop function will arrest all motion. Once the stopping motion has occurred the user can guide themselves through the process flow again. The user can also begin mid-flow with a simple left or right input command without moving in a forward or reverse motion | PMC9375912 | 12984_2022_1066_Fig2_HTML.jpg |
0.449324 | 3693e9240d8d4db18ec3e8f7cba23cd8 | An overview of the unilateral input mode for the control system. The process flow chart begins at the bulls-eye and follows the users input signal to initiate a forward or reverse motion. The forward command is initiated by a hard contraction of a short duration, while the reverse motion is a hard contraction of a long duration. From here the user can then initiate the stopping function, which is the same input as the forward command, or begin a turning motion while maintaining forward motion. A turning motion is chosen it can be stopped with an additional turning command and maintain a forward motion. Or for a complete stop, the aforementioned stop function will arrest all motion. Once the stopping motion has occurred the user can guide themselves through the process flow again. The user also can begin mid-flow with a simple left or right input command without moving in a forward or reverse motion | PMC9375912 | 12984_2022_1066_Fig3_HTML.jpg |
0.501481 | 1cefe746a7464ad9bff78cc40536fe8e | An overview of the signal processing chain. The EMG oscillatory signal input is amplified, rectified, band passed, and then smoothed | PMC9375912 | 12984_2022_1066_Fig4_HTML.jpg |
0.43352 | 029c510788c84a12b418f5a0550dd94b | Hx reduces Sirt2 expression in mature WM OLs.a Representative western blots for Sirt2 and Sirt1 proteins in subcortical WM of Nx and Hx animals at postnatal days P11, P18, and P45. b Quantification of western blots. Graph displays mean ± SEM values (n = 3 brains per condition). At P11: Sirt1 ns p = 0.04793, Sirt2 *p = 0.0108; at P18: Sirt1 **p = 0.0044, Sirt2 ****p < 0.0001; at P45: Sirt1 ns p = 0.2347, Sirt2 **p = 0.0033 (Student’s t test). c, f, i, l, o Coronal sections of subcortical WM stained for Sirt2+
c, Sirt2+Olig2+
f, Sirt2+NG2+
i, Sirt2+PDGFRα+
l, and CC1+Sirt2+
o cells in Nx and Hx mice at P18. Dotted lines delineate WM. WM, white matter. Arrows point to nuclear Sirt2+ staining. Scale bar = 100 µm. d, e Quantification of the total Sirt2+ cell density d and percentage of Sirt2+ cells e in WM at P18 (****p < 0.0001 for d, e, n = 4 mice per group, Student’s t test). g, h Quantification of the total Olig2+Sirt2+ cell density (****p < 0.0001, n = 4 Nx and 5 Hx mice, Student’s t test) g and percentage of Sirt2+ OL lineage cells (***p = 0.0003, n = 4 Nx and 5 Hx mice, Student’s t test) h in WM at P18. j, k Quantification of the total NG2+Sirt2+ cell density (ns p = 0.9543, n = 4 per group, Student’s t test) j and percentage of Sirt2 expression in NG2+ OPCs in WM at P18 (ns p = 0.7479, n = 4 per group, Student’s t test) k. m, n Quantification of total PDGFRα+Sirt2+ cell density (ns p = 0.7748, n = 5 Nx and 4 Hx mice, Student’s t test) m and percentage of Sirt2 expression in PDGFRα+ OPCs (ns p = 0.9960, n = 5 Nx and 4 Hx mice, Student’s t test) n. p, q Quantification of the total CC1+Sirt2+ cell density (***p = 0.0004, n = 4 per group, Student’s t test) p and percentage of Sirt2+ mature CC1+-expressing OLs (**p = 0.0025, n = 4 per group, Student’s t test) q in WM at P18. Graphs display mean ± SEM values. All statistical tests are two-sided. Source data are provided as a Source Data file. | PMC9378658 | 41467_2022_32462_Fig1_HTML.jpg |
0.446913 | 13093431635548d9b9c369a347e3ac08 | Reduced Sirt2 expression in subcortical WM of preterm infants.a Tissue sections from the corpus callosum of preterm human neonates and term controls were analyzed. H&E image shows lower magnification of corpus callosum region analyzed for preterm and term controls. Scale bar = 100 µm. b Representative H&E photomicrographs of corpus callosum (n = 4 term and 4 preterm). In term controls, well-defined OLs with well-defined nucleolus (arrow) and dense neuropil were observed (arrowhead). In contrast, in preterm neonates (right panels) hypodense and rarefied neuropil were present (arrowhead) with OLs that appear edematous and vacuolated (arrow). Scale bars = 50 µm for upper panels and 20 µm for lower panels. c Olig2+ immunostaining (green) in WM of term and preterm neonates. Scale bars = 50 µm. d, e Quantification of the density d and the percentage of Olig2+ cells e in term and preterm neonates. (**p = 0.005, *p = 0.026, n = 4 term and 3 preterm, Student’s t test). f Low magnification images of Sirt2+ immunostaining (red) in WM of term and preterm neonates. Scale bars = 50 µm. g Quantification of the intensity of Sirt2 staining in term and preterm neonates (*p = 0.017, n = 4 term and 3 preterm, Student’s t test). h Quantification of the percent area of Sirt2+ signal in the WM of term and preterm neonates (*p = 0.014, n = 4 term and 3 preterm, Student’s t test). i Sirt2 expression within WM Olig2+ cells of term and preterm neonates. Bottom panels show magnified single-channel images for Olig2 (green) and Sirt2 (red) to highlight cytoplasmic localization of Sirt2. Scale bars = 10 µm. j Quantification of the density of Sirt2+Olig2+ cells in term and preterm neonates (*p = 0.01, n = 4 term and 3 preterm, Student’s t test). k Quantification of the percentage of Sirt2+ oligodendrocytes in term and preterm neonates (*p = 0.011, n = 4 term and 3 preterm, Student’s t test). H&E, Hematoxylin and Eosin. Data are represented as mean ± SEM. All statistical tests are two-sided. Source data are provided as a Source Data file. The human brain schematic in a was created using Servier Medical Art templates, which are licensed under a Creative Commons Attribution 3.0 Unported License. | PMC9378658 | 41467_2022_32462_Fig2_HTML.jpg |
0.394572 | 522eca998ae941beb3c48fcafd824d3a | Sirt2 overexpression alters oligodendrogenesis in vivo.a, b Experimental approach for genetic Sirt2 overexpression in PDGFRα+ OPCs or PLP+ mature OLs in combination with Hx paradigm. c, d Coronal sections of subcortical WM stained for CC1 from Sirt2STOPPDGFRαCreERT
c and Sirt2STOPPLPCreERT
d transgenic mice, with respective controls, after Nx and Hx. White lines delineate WM. WM, white matter. e, g Quantification of the total CC1+ cell density in WM at P18 (WT: Nx vs Hx *p = 0.0433, Sirt2STOPPDGFRαCreERT: Nx vs Hx ***p = 0.0005, WT Nx vs Sirt2STOPPDGFRαCreERT Nx ****p < 0.0001, WT Hx vs Sirt2STOPPDGFRαCreERT Hx **p = 0.0031, n = 4 WT-Nx, 3 WT-Hx, 3 Sirt2STOP-Nx, 3 Sirt2STOP-Hx mice, ANOVA with Tukey’s multiple comparisons adjustment) e, and (WT: Nx vs Hx *p = 0.0491, Sirt2STOPPLPCreERT: Nx vs Hx ***p = 0.0002, WT Nx vs Sirt2STOPPLPCreERT Nx *p = 0.0176, WT Hx vs Sirt2STOPPLPCreERT Hx ns = 0.8791, n = 3 WT-Nx, 4 WT-Hx, 4 Sirt2STOP-Nx, 4 Sirt2STOP-Hx mice, ANOVA with Tukey’s multiple comparisons adjustment) g. i, j Coronal sections of subcortical WM stained for Olig2 from Sirt2STOPPDGFRαCreERT
i and Sirt2STOPPLPCreERT
j transgenic mice, with respective controls, after Nx and Hx. Scale bar = 100 µm. k, m Quantification of the total Olig2+ cell density in WM at P18 (WT: Nx vs Hx ***p = 0.0002, Sirt2STOPPDGFRαCreERT: Nx vs Hx ***p = 0.0001, WT Nx vs Sirt2STOPPDGFRαCreERT Nx *p = 0.0263, WT Hx vs Sirt2STOPPDGFRαCreERT Hx *p = 0.0357, n = 3 WT-Nx, 4 WT-Hx, 4 Sirt2STOP-Nx, 3 Sirt2STOP-Hx mice, ANOVA with Tukey’s multiple comparisons adjustment) k, and (WT: Nx vs Hx *p = 0.0219, Sirt2STOPPLPCreERT: Nx vs Hx ****p < 0.0001, WT Nx vs Sirt2STOPPLPCreERT Nx ****p < 0.0001, WT Hx vs Sirt2STOPPLPCreERT Hx ns = 0.8177, n = 3 WT-Nx, 3 WT-Hx, 4 Sirt2STOP-Nx, 3 Sirt2STOP-Hx mice, ANOVA with Tukey’s multiple comparisons adjustment) m. f, h, l, n Quantification of the percent of reduction of CC1+ and Olig2+ cells after Hx in each transgenic mouse strain. No changes were found in percent of CC1+ and Olig2+ cell reduction in WM of Sirt2STOPPDGFRαCreERT or Sirt2STOPPLPCreERT and their WT littermates. All graphs display mean ± SEM values, except for percent reduction. All statistical tests are two-sided. Source data are provided as a Source Data file. | PMC9378658 | 41467_2022_32462_Fig3_HTML.jpg |
0.409668 | 61186956c216470c9a9df704d5099a79 | Sirt2+ OLs are protected from Hx only in Sirt2STOPPDGFRαCreERT mice.a Color legend for different transgenic mice in Nx and Hx. b Experimental Hx paradigm. c, d Coronal sections of subcortical WM stained for CC1 and Sirt2 from Sirt2STOPPDGFRαCreERT
c and Sirt2STOPPLPCreERT
d transgenic mice, with respective controls, after Nx and Hx. White lines delineate WM, WM-white matter. Scale bar = 100 µm. e, g Quantification of the total CC1+Sirt2+ cell density in WM at P18 (WT: Nx vs Hx **p = 0.0037, Sirt2STOPPDGFRαCreERT: Nx vs Hx ns = 0.3774, WT Nx vs Sirt2STOPPDGFRαCreERT Nx ***p = 0.0002, WT Hx vs Sirt2STOPPDGFRαCreERT Hx ****p < 0.0001, n = 4 WT-Nx, 4 WT-Hx, 3 Sirt2STOP-Nx, 3 Sirt2STOP-Hx mice, ANOVA with Tukey’s multiple comparisons adjustment) e, and (WT: Nx vs Hx *p = 0.0220, Sirt2STOPPLPCreERT: Nx vs Hx ***p = 0.0002, WT Nx vs Sirt2STOPPLPCreERT Nx *p = 0.0104, WT Hx vs Sirt2STOPPLPCreERT Hx ns = 0.5991, n = 3 WT-Nx, 4 WT-Hx, 4 Sirt2STOP-Nx, 4 Sirt2STOP-Hx mice, ANOVA with Tukey’s multiple comparisons adjustment) g. i, j Coronal sections of subcortical WM stained for Olig2 and Sirt2 from Sirt2STOPPDGFRαCreERT
i and Sirt2STOPPLPCreERT
j transgenic mice, with respective controls, after Nx and Hx. Scale bar = 100 µm. k, m Quantification of the total Olig2+Sirt2+ cell density in WM at P18 (WT: Nx vs Hx *p = =0.0415, Sirt2STOPPDGFRαCreERT: Nx vs Hx ns = 0.3589, WT Nx vs Sirt2STOPPDGFRαCreERT Nx ***p = 0.0001, WT Hx vs Sirt2STOPPDGFRαCreERT Hx ****p < 0.0001, n = 3 WT-Nx, 4 WT-Hx, 4 Sirt2STOP-Nx, 3 Sirt2STOP-Hx mice, ANOVA with Tukey’s multiple comparisons adjustment) k, and (WT: Nx vs Hx ****p < 0.001, Sirt2STOPPLPCreERT: Nx vs Hx ****p = 0.0001, WT Nx vs Sirt2STOPPLPCreERT Nx ***p = 0.0009 WT Hx vs Sirt2STOPPLPCreER Hx ns = 0.9780, n = 3 WT-Nx, 3 WT-Hx, 4 Sirt2STOP-Nx, 3 Sirt2STOP-Hx mice, ANOVA with Tukey’s multiple comparisons adjustment) m. f, h, l, n Quantification of the percent of reduction of CC1+Sirt2+ and Olig2+Sirt2+ cells after Hx in each transgenic mouse strain. Changes in the percentage of CC1+Sirt2+ and Olig2+Sirt2+ cell reduction after Hx were found only in WM of Sirt2STOPPDGFRαCreERT, but not Sirt2STOPPLPCreERT mice. All graphs display mean ± SEM values, except for percent reduction. All statistical tests are two-sided. Source data are provided as a Source Data file. | PMC9378658 | 41467_2022_32462_Fig4_HTML.jpg |
0.425862 | e8bf85547ba74b95ab82eb9ae888d811 | Hx increases the interaction of Sirt2 with FoxO1 and p27Kip1 in WM.a Cartoon depicting the FoxO1/p27Kip1 pathway regulated by Sirt2. b Color legend for different transgenic mice in Nx and Hx. c Western blots for expression of phosphorylated Sirt2 at Ser331, p27Kip1, and FoxO1 proteins in WM lysates of Sirt2STOPPDGFRαCreERT mice and their WT littermates. d–f Quantification of protein levels of pSirt2 d, p27Kip1
e, and FoxO1 f in Nx and Hx WM of WT and Sirt2STOPPDGFRαCreERT mice (pSirt2: **p = 0.0064, *p = 0.0428, ***p = 0.0002; p27Kip1: Nx vs Hx *p = 0.0200, Hx vs Hx *p = 0.0168; FoxO1: Nx vs Hx ***p = 0.0009, Hx vs Hx ***p = 0.0004; n = 3 per group, ANOVA with Tukey’s multiple comparisons adjustment). Graphs display mean ± SEM values. g Co-immunoprecipitation of dissected WM with Sirt2 antibody followed by Western blot for p27Kip1 and FoxO1, respectively to detect Sirt2 protein interactions. Protein complexes were identified by their sizes (27KD and 78-82KD, respectively). i Western blots for acetyl lysine levels of p27Kip1 and FoxO1 proteins. h, j Quantification of co-immunoprecipitation results for Sirt2/p27Kip1 (**p = 0.0054), Sirt2/FoxO1 (***p = 0.0003) h, acetyl lysine p27Kip1 (****p < 0.0001), acetyl lysine FoxO1 (***p = 0.0005), j (n = 5 Nx and Hx brains for Sirt2/p27, 6 Nx and Hx brains for Sirt2/Foxo1, 6 Nx and Hx brains for p27 acetyl, 4 Nx and Hx brains for Foxo1 acetyl, all Student’s t tests). Graphs display mean ± SEM values. All statistical tests are two-sided. Source data are provided as a Source Data file. | PMC9378658 | 41467_2022_32462_Fig5_HTML.jpg |
0.430277 | c2464331b6f54f0b9fd59db334c33cd9 | Sirt2 interacts with p21Cip1 and Cdk5.a Cartoon depicting cell cycle regulation by p21Cip1, Cdk4/CyclinD1, and Cdk5/p35. b Expression of p21Cip1, Cdk5, p35, Cdk4, CyclinD1, p107, and E2F4 in Nx and Hx WM of WT-PDGFRαCreERT and Sirt2STOPPDGFRαCreERT. c Color legend for different transgenic mice in Nx and Hx. d–j Quantification of protein levels of p21Cip1 (WT Nx vs Hx ***p = 0.0001, WT Hx vs Sirt2STOP Nx ***p = 0.0001, WT Hx vs Sirt2STOP Hx ****p < 0.0001) d, Cdk5 (WT Nx vs Hx **p = 0.0076, WT Hx vs Sirt2STOP Nx **p = 0.0068, WT Hx vs Sirt2STOP Hx **p = 0.0068) e, p35 (WT Nx vs Hx *p = 0.0193, WT Hx vs Sirt2STOP Nx *p = 0.0106, WT Hx vs Sirt2STOP Hx **p = 0.0077) f, Cdk4 (*p = 0.0292) g, CyclinD1 (*p = 0.0243) h, p107 (***p = 0.0005) i, and E2F4 (***p = 0.0002) j in WT-PDGFRαCreERT and Sirt2STOPPDGFRαCreERT mice (n = 3 per group, all ANOVA test with Tukey’s multiple comparisons adjustment). Graphs display mean ± SEM values. k Co-immunoprecipitation of: Sirt2/p21Cip1 and acetyl-lysine p21Cip1, Cdk4/CyclinD1 and p107/E2F, Sirt2/Cdk5, acetyl-lysine Cdk5, and Cdk5/p35 complexes from Nx and Hx WM. Protein complexes were identified by their sizes (p21Cip1−21kDa, Cdk4-34kDa, Cdk5-35kDa, CyclinD1-36kDa, p35-28kDa, p107-121kDa, E2F4-62kDa, respectively) l–n Quantification of co-immunoprecipitation results for Sirt2/p21Cip1 (**p = 0.0097), acetyl lysine p21Cip1 (*p = 0.0190) l, Cdk4/cyclinD1 (*p = 0.0138), p107/E2F4 (**p = 0.023) m, Sirt2/Cdk5 (**p = 0.0046), acetyl lysine Cdk5 (*p = 0.0349), Cdk5/p35 (**p = 0.0048) n (n = 3 brains per group, all Student’s t tests). Graphs display mean ± SEM values. All statistical tests are two-sided. Source data are provided as a Source Data file. | PMC9378658 | 41467_2022_32462_Fig6_HTML.jpg |
0.397444 | 323240b68a174d66b4ceea05fd00227b | Hx induces nuclear localization of Sirt2 in OPCs.a, c Coronal sections of subcortical WM from Nx and Hx WT mice at P18. Dotted lines delineate WM, WM-white matter. Scale bar = 100 µm. b Quantification of cytoplasmic and nuclear Sirt2 expression in PDGFRα+ OPCs (Nx vs Hx: ****p < 0.0001, *p = 0.0152, Student’s t test) d Quantification of cytoplasmic and nuclear Sirt2 expression in CC1+ OLs (Nx vs Hx: **p = 0.0042, ****p < 0.0001, Student’s t test). Graphs display mean ± SEM values (n = 4 brains per condition). e Experimental procedure for Sirt2 ChIP-seq using dissected subcortical white matter (SCWM) from P15 WT mice reared under Nx or Hx conditions. f The number of enriched Sirt2 binding peaks identified following comparison of Nx, Hx, and IgG (negative control) samples. g The location of Sirt2 peaks enriched after Hx. h Sirt2 ChIP-seq data were compared with previously published RNA-seq data from Hx OPCs39. Four genes that have nearby Sirt2 binding peaks are also altered in their expression following Hx. i QPCR verification of enriched Sirt2 binding at peaks 268-3, 268-2, and 308 in Hx WM, compared to Nx (**p = 0.0017, *p = 0.014, #p = 0.059 Student’s t test, n = 4 Nx and Hx samples). j Visualization of Sirt2 binding in genomic region upstream of Diaph2 gene. Red box highlights enriched binding in Hx. k RNAscope analysis of Diaph2 expression in Pdgfrα+ OPCs (arrows) in the WM of Nx and Hx WT mice at P22. Scale bars = 10 µm. l Quantification of the percentage of Diaph2+ OPCs in the WM of Nx and Hx WT mice at P22 (***p = 0.0001, n = 4 Nx and Hx mice, Student’s t test). m Visualization of Sirt2 binding in the genomic region upstream of Vegfc gene. Red box highlights enriched binding in Hx. n RNAscope analysis of Vegfc expression in Pdgfrα+ OPCs (arrows) in the WM of Nx and Hx WT mice at P22. Scale bars = 10 µm. o Quantification of the percentage of Vegfc+ OPCs in the WM of Nx and Hx WT mice at P22 (****p < 0.0001, Student’s t test, n = 4 Nx and Hx mice). Graphs display mean ± SEM values. All statistical tests are two-sided. Source data are provided as a Source Data file. The schematic in e was created using CorelDraw 2018 software (version 20.1.0.708). | PMC9378658 | 41467_2022_32462_Fig7_HTML.jpg |
0.381792 | 99f595abaa5b4f1e894ed204be136d80 | Increased differentiation of Sirt2+ OLs in the absence of Sirt1.a, b Quantification of cultured WM cells from Nx and Hx mice transfected with scrambled control or Sirt1 siRNA and cultured for 3 days a (O4: control *p = 0.0121, Sirt1 siRNA ***p = 0.0003, Nx control vs Nx siRNA ****p < 0.0001, Hx control vs Hx siRNA ****p < 0.0001; O1: control *p = 0.0440, Sirt1 siRNA ***p = 0.0004, Nx control vs Nx siRNA **p = 0.0024, Hx control vs Hx siRNA ****p < 0.0001) and 5 days in culture (DIC) b (O4: control **p = 0.0013, Sirt1 siRNA ***p = 0.0003, Nx control vs Nx siRNA ns p = 0.5243, Hx control vs Hx siRNA ****p < 0.0001; O1: control *p = 0.0265, Sirt1 siRNA ***p = 0.0003, Nx control vs Nx siRNA **p = 0.0032, Hx control vs Hx siRNA ****p < 0.0001, ANOVA with Tukey’s multiple comparisons adjustment) (n = 3 mice per group). c Representative images of O4+Sirt2+ and O1+Sirt2+ cells in Nx cultures. Scale bar = 50 µm. d Representative western blot from Nx and Hx WM lysates from WT-PDGFRα and Sirt1fl/flPDGFRαCreERT mice for Sirt2 expression (n = 3 per group). Molecular weight for Sirt2–43 KD e) Quantification of Sirt2 expression in Nx and Hx WM of WT-PDGFRαCreERT (green) and Sirt1fl/flPDGFRαCreERT (gray) mice. (WT Nx vs Hx *p = 0.0390, WT Hx vs Sirt1fl/flPDGFRαCreERT Hx *p = 0.0184, ANOVA with Tukey’s multiple comparisons adjustment). f, i, l, o Coronal sections of subcortical WM from WT-PDGFRα and Sirt1fl/flPDGFRαCreERT mice, after Nx and Hx, showing Sirt2+
f, CC1+Sirt2+
i, CNP+Sirt2+
l, and MBP+Sirt2+
o cells. WM-white matter. Scale bar = 100 µm. g, j, m, p Quantification of the percentage of WM cells that express Sirt2 (all ****p < 0.0001, ANOVA with Tukey’s multiple comparisons adjustment) g, CC1+Sirt2+ (WT: Nx vs Hx **p < 0.0020, Sirt1fl/flPDGFRαCreERT: Nx vs Hx ns p = 0.0517, WT Nx vs Sirt1fl/flPDGFRαCreERT Nx ****p < 0.0001, WT Hx vs Sirt1fl/flPDGFRαCreERT Hx ****p < 0.0001, ANOVA with Tukey’s multiple comparisons adjustment) j, CNP+Sirt2+ (WT: Nx vs Hx *p = 0.0351, Sirt1fl/flPDGFRαCreERT: Nx vs Hx **p = 0.0043, WT Nx vs Sirt1fl/flPDGFRαCreERT Nx *p = 0.0370, WT Hx vs Sirt1fl/flPDGFRαCreERT Hx ****p < 0.0001, ANOVA with Tukey’s multiple comparisons adjustment) m, and MBP+Sirt2+ (WT: Nx vs Hx *p = 0.0204, Sirt1fl/flPDGFRαCreERT: Nx vs Hx ***p = 0.0002, WT Nx vs Sirt1fl/flPDGFRαCreERT Nx ****p < 0.0001, WT Hx vs Sirt1fl/flPDGFRαCreERT Hx ****p < 0.0001 p, ANOVA with Tukey’s multiple comparisons adjustment) after Nx and Hx in WT and Sirt1fl/flPDGFRαCreERT mice. h, k, n, r Quantification of the total density of WM cells that express Sirt2+ (WT: Nx vs Hx *p < 0.0188, Sirt1fl/flPDGFRαCreERT: Nx vs Hx ns p = 0.6630, WT Nx vs Sirt1fl/flPDGFRαCreERT Nx ****p < 0.0001, WT Hx vs Sirt1fl/flPDGFRαCreERT Hx ****p < 0.0001, ANOVA with Tukey’s multiple comparisons adjustment) h, CC1+Sirt2+ (WT: Nx vs Hx *p = 0.0464, Sirt1fl/flPDGFRαCreERT: Nx vs Hx *p = 0.0104, WT Nx vs Sirt1fl/flPDGFRαCreERT Nx **p = 0.0055, WT Hx vs Sirt1fl/flPDGFRαCreERT Hx ****p < 0.0001, ANOVA with Tukey’s multiple comparisons adjustment) k, CNP+Sirt2+ (WT: Nx vs Hx ****p < 0.0001, Sirt1fl/flPDGFRαCreERT: Nx vs Hx ****p < 0.0001, WT Nx vs Sirt1fl/flPDGFRαCreERT Nx ns p = 0.6821, WT Hx vs Sirt1fl/flPDGFRαCreERT Hx ****p < 0.0001, ANOVA with Tukey’s multiple comparisons adjustment) n, and MBP+Sirt2+ (WT: Nx vs Hx **p = 0.0027, Sirt1fl/flPDGFRαCreERT: Nx vs Hx ns p = 0.9997, WT Nx vs Sirt1fl/flPDGFRαCreERT Nx ****p < 0.0001, WT Hx vs Sirt1fl/flPDGFRαCreERT Hx ****p < 0.0001, ANOVA with Tukey’s multiple comparisons adjustment) q after Nx and Hx in WT and Sirt1fl/flPDGFRαCreERT mice. Graphs display mean ± SEM values (n = 3 animals per group). All statistical tests are two-sided. Source data are provided as a Source Data file. | PMC9378658 | 41467_2022_32462_Fig8_HTML.jpg |
0.414547 | 0cb8872d29ab4c62bf5526c453b1ce78 | Scoping review screening and extraction. | PMC9379667 | gr1.jpg |
0.480597 | 46a01354eca044e5af744384bbf9fa1f | Inclusion of individuals during follow-up (2007 to 2019). (a) Flowchart of included and excluded operated individuals, showing the number of cases of patients with moderate to severe psoriasis with a history of bariatric surgery (surgery group). Unique psoriasis patients are patients with history of no more than 1 bariatric surgery. (b) Flowchart of included and excluded non-operated individuals, showing the number of patients with moderate to severe psoriasis without a history of bariatric surgery (control group). DLQI: Dermatology Life Quality Index; PASI: Psoriasis Area Severity Index; PsoReg: Swedish National Register for Systemic Treatment of Psoriasis; SOReg: Scandinavian Obesity Surgery Registry. | PMC9380267 | ActaDV-101-6-646-g001.jpg |
0.42408 | e0c31e0b49404a2484e49a54e6db7fa1 | (a) Psoriasis Area Severity Index (PASI) and (b) Dermatology Life Quality Index (DLQI) at baseline, and at the short-term and the longer-term follow-up, for patients with moderate to severe psoriasis with and without a history of bariatric surgery. The lines in the box-and-whiskers plots represent median values (50th percentile); the box spans the 25th–75th percentile; the lower whiskers denote the minimum values and the upper whiskers denote the 1.5 interquartile range (IQR). Values beyond the whiskers are marked with symbols and are considered as outliers. | PMC9380267 | ActaDV-101-6-646-g002.jpg |
0.413441 | 4d7b211f591344d38d8482a3df9eb909 | The framework for the radiomics workflow. (A, B) Medical imaging segmentation; (C, D) Feature extraction and selection; (E, F) The ROC curves and nomogram; (G, H) Hosmer-Lemeshow Test and the decision curve. | PMC9380646 | fonc-12-967360-g001.jpg |
0.396269 | ab2f655e64f34273b073d70315d560ba | Textural feature selection using the Least Absolute Shrinkage and Selection Operator (LASSO) binary logistic regression. (A) Tuning parameters(λ) for the LASSO model were selected by 10-fold cross-validation using the minimum criteria. Partial likelihood deviance was plotted against log(λ). The dotted vertical lines correspond to the optimal values according to the minimum criteria and 1-SE criterion. The 11 features with the smallest binomial deviance were selected. (B) A feature coefficient convergence graph for filtering features using 10-fold cross-validation in the LASSO regression model. (C) LASSO coefficient profiles of texture features. Vertical lines correspond to the values selected by 10-fold cross-validation of the log(λ) sequence; the 11 nonzero coefficients are indicated. | PMC9380646 | fonc-12-967360-g002.jpg |
0.42934 | cac59cbec847411e972506ac319c7e07 | Box plot showing the Radscore distribution of high and low risk group for disease progression on training and validation cohorts. p-value from Wilcoxon Rank-Sum test (A, B). Receiver Operator Characteristic (ROC) curves (training and validation cohorts) (C, D). The prediction performance of the ROC curves for radiomics signature for training and validation cohorts. | PMC9380646 | fonc-12-967360-g003.jpg |
0.406944 | b6893ffe79e947a3a6bf2af15fe94b8b | Receiver Operating Characteristic (ROC) curves of the clinical, radiomics, and combined model used to discriminate between the high and low risk of disease progression of lung cancer treated with SABR in the training and validation cohorts (A, B). Radiomics nomogram (C) was used to discriminate the high and low risk of disease progression in lung cancer patients treated with SABR. The nomogram was based on the training cohort; the Radscore was shown. Initially, vertical lines were drawn at the Radscore values to determine the values of the points. The final point value was the sum of those of the two points. Finally, a vertical line was drawn at the total point value to determine the risk of disease progression of lung cancer treated with SABR. | PMC9380646 | fonc-12-967360-g004.jpg |
0.402689 | 0a0bde2cf03e497ba8345d41e3ce51fd | Hosmer-Lemeshow Test of the nomogram of the training (A) and validation (B) cohorts. The diagonal dotted lines represent the ideal predictions; the solid lines represent nomogram performance. A closer fit to the diagonal line indicates that the model matches better. | PMC9380646 | fonc-12-967360-g005.jpg |
0.412654 | da0fd30bae9d4d51ac30ec391fe2a2fc | Decision Curve Analysis (DCA) results for the three discrimination models. The Y-axis represents the net benefit, calculated by summing the benefits (true positives) and subtracting the weighted harm (i.e., deleting false positives). The optimal method for feature selection is that with the highest net benefit. | PMC9380646 | fonc-12-967360-g006.jpg |
0.406331 | 8831fde268a0466d9bc4eea7bfee50b5 | The type of peritumoral radiation-induced lung injury. Type I, female, 51 years, adenocarcinoma in the right lung, DT40GY/5F; (A) pre-treatment: a nodule with blurred boundary and spicule sign; (B) one month after treatment: the tumor shrunk and there was a surrounding ground-glass opacity; (C) three months after treatment: the tumor area showed diffuse consolidation and was indistinguishable from the tumor; (D) six months after treatment: the imaging findings were similar to (C). Type II, female, 79 years, adenocarcinoma in right lung, DT55GY/5F; (E) pre-treatment: a nodule with a clear boundary and shallow lobed; (F)one month after treatment: the tumor has shrunk a little, no ground glass opacity surrounding it; (G) four months after treatment: there was no significant change; (H) six months after treatment: the tumor was surrounded by ground-glass opacity, more than 1/2. Type III, male,70 years, adenocarcinoma in left lung, DT50GY/5F; (I) pre-treatment: a nodule with a clear boundary and shallow lobed; (J) two months after treatment: there was no significant change; (K) four months after treatment: there was no significant change; (L) six months after treatment: the tumor was surrounded by ground-glass opacity, less than 1/2. | PMC9380646 | fonc-12-967360-g007.jpg |
0.487164 | 057c89d3c9c54b7985c0d7716a59d7e5 | Components of the ELS. | PMC9382305 | fpsyg-13-890707-g0001.jpg |
0.412826 | c7a7ba547bbf4ef2a36353826d6dd4f3 | Research model. | PMC9382305 | fpsyg-13-890707-g0002.jpg |
0.426299 | 98ed4cefe1834c6ba4881d7dfecf1073 | Results of the proposed model. | PMC9382305 | fpsyg-13-890707-g0003.jpg |
0.399425 | f5bb67192aaf42ba82b2442f74c27f54 | CONSORT diagram | PMC9383671 | 10578_2022_1409_Fig1_HTML.jpg |
0.484474 | 35c9d5fd4d1d4b7d82ce3f186a7253ba | Temporal interaction between cells of the innate and adaptive immune systems and how their functions are affected by the vitamins A, C, D, and E; the trace elements selenium and zinc; and omega-3 PUFAs DHA and EPA. For further vitamin A data, see reference (99). Th, T-helper; Treg, T-regulatory; Vit, vitamin. (Created with BioRender.com.) | PMC9384096 | nmac058fig1.jpg |
0.450538 | ee8181313e17424fa4eb43c061ce3d31 | BPNN topology diagram. | PMC9385324 | CIN2022-9490017.001.jpg |
0.445793 | 158674c4326948ceb56d35a71854bba5 | BPNN training process. | PMC9385324 | CIN2022-9490017.002.jpg |
0.497056 | 5753b323d4ca4b2b9c99ba64153d86e5 | GA flowchart. | PMC9385324 | CIN2022-9490017.003.jpg |
0.560514 | aaaf2ef4d6ad49cb8c1e76f0509abe84 | Functions of the IPE course evaluation system. | PMC9385324 | CIN2022-9490017.004.jpg |
0.41828 | 767d271ffef947ce83695e7a5670bb0a | Optimization process of BPNN model based on GA. | PMC9385324 | CIN2022-9490017.005.jpg |
0.472698 | 20335309d2764b82af0c815084a9b6e8 | The neural network model for IPE course evaluation. | PMC9385324 | CIN2022-9490017.006.jpg |
0.410152 | e429a1fd29204ea7a0f9cd221a714846 | Composition of IPE courses in different colleges and universities. | PMC9385324 | CIN2022-9490017.007.jpg |
0.595622 | cb7c23abf45148b8bd3c64496ecd437b | Training results of the IPE course evaluation model based on the BPNN. (a) The variation graph of the training error of the model. (b) The variation graph of the mean square error of the model. | PMC9385324 | CIN2022-9490017.008.jpg |
0.39173 | 6f574cf250894c589a29ed423ca36d9f | Comparison of expert scores and model predictions. | PMC9385324 | CIN2022-9490017.009.jpg |
0.442762 | ccc01270883e4043a0d585ddb01608d3 | Training results of the IPE course evaluation model based on the optimized BPNN. (a) The change graph of the training error of the improved model. (b) The change graph of the mean square error of the improved model. | PMC9385324 | CIN2022-9490017.010.jpg |
0.390945 | 70b7b13f18c746958b2c098ad09ed7f6 | Comparison of the expert scoring and the prediction results of the optimized model. | PMC9385324 | CIN2022-9490017.011.jpg |
0.39781 | ac6dcae0e7954b7fb67bce6aba52ede9 | Conceptual framework and validation of AI-bRNN.a Schematic diagram of the experimental approach. AAV1-hsyn-GCaMP6s was injected into S1. b Imaging was performed for 2 min at each time point (before and 1–3 min after formalin injection). The time points for imaging were selected based on the levels of nociceptive behavior after formalin injection in freely moving animals. c A representative image of S1 neurons identified by semiautomated ROI analysis (top). Example Ca2+ traces from each ROI (bottom). The scale bar represents 50 μm. d Heatmaps showing the activity of S1 neurons. The line traces below each heatmap indicate the averaged values of all ROIs. The periods of mouse locomotion identified by the motion tracking analysis are overlaid on the line traces using sky-blue shading. e Architecture of AI-bRNN. The Ca2+ traces extracted from each ROI were averaged subject by subject to train the neural network. In the test session, the Ca2+ traces from individual ROIs were separately applied to the deep learning model for testing. f The predictions of AI-bRNN regarding whether the subject was experiencing pain. On the x-axis, ‘B’ indicates the time before injection. Saline (s.c.) group (n = 14 mice); formalin 5% (s.c.) group (n = 13 mice); formalin 1% (s.c.) group (n = 8 mice); formalin 5% (s.c.) + ketoprofen (100 mg/kg, i.p.) group (n = 7 mice); formalin 5% (s.c.) + 2% lidocaine (10 μl, s.c.) group (n = 3 mice). g The classification performance for formalin pain conditions based on the S1 neuronal signals. Scatter plots indicate individual data. Bars indicate the mean ± SEM; N.S., nonsignificant; ***P < 0.001, *P < 0.05 compared to the pre-injection period (Wilcoxon test). | PMC9385425 | 12276_2022_828_Fig1_HTML.jpg |
0.397461 | f6dbfd99534c4589b996cea90f7ee356 | Broad applicability of AI-bRNN to various pain models with different chronicities.Estimated pain values of the a capsaicin-, b CFA-, and c oxaliplatin-injected animals. The estimated pain values are based on the Ca2+ activity of the neurons in S1. Saline (s.c.) group (n = 28 sessions from 14 mice); capsaicin (0.01%, 10 μl, s.c.) group (n = 9 mice); CFA (10 μl, s.c.) group (n = 6 mice); oxaliplatin (6 mg/kg, i.p.) group at 3 d (n = 9 mice); oxaliplatin group at 10 d (n = 7) d Classification performance in the capsaicin-, CFA- and oxaliplatin-induced pain conditions. e Estimated pain values of the animals subjected to PSL or sham surgery. Sham group (n = 6 mice); PSL group at 3 d (n = 20 mice); PSL group at 10 d (n = 24 mice); PSL + GB/VX (GB 100 mg/kg, VX 50 mg/kg, i.p.) group (n = 8 mice) f Heatmap plots showing changes in estimated pain values over time with 2-min time resolution. g The classification performance for PSL pain conditions based on the S1 neuronal signals. Scatter plots indicate individual data. Bars indicate the mean ± SEM; N.S., nonsignificant; ***P < 0.001, *P < 0.05 compared to baseline (Mann–Whitney U test). | PMC9385425 | 12276_2022_828_Fig2_HTML.jpg |
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