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0.46134
122d64b6f21443c992af2310cba68cba
STROBE flow diagram.COVID-19, Coronavirus Disease 2019; ICU, Intensive Care Unit; NMBAs, neuromuscular blocking agents; ARDS, acute respiratory distress syndrome; MMSE, mini-mental state examination.
PMC9510617
fmed-09-994900-g0001.jpg
0.394858
667050677048479589f6b62b70d35f95
Distributions of VFDs between patients treated (PT) or not (NO-PT) by physiotherapists at 28 days. Blue bars denote patients who died (VFD = 0), dark gray bars denote patients alive with VFD = 0 and light gray bars identify patients alive with VFDs > 0.
PMC9510617
fmed-09-994900-g0002.jpg
0.452582
69acebb1ff994c0898f0b53a839d7605
Flowchart of study design.
PMC9510988
fneur-13-981249-g0001.jpg
0.437546
7fc1d401fe3a425298097fb61de63b95
Changes between STWT states and their impact on self-rated health and subjective well-being. Data set: NEPS SC4, SUF 12.0.0. Results of Table 2. Regression coefficients and 95% confidence intervals of six linear fixed-effect analyses with cluster-robust standard errors. n = number of individuals. Py = person-years. Time-varying controls: Age dummies, region of education or work, and household composition. The effect of transitional events on health and well-being were investigated in different estimation samples (S1-S6) that include the person-years of the reference state and the person-years of the state that was entered afterwards
PMC9511745
12889_2022_14227_Fig1_HTML.jpg
0.474238
b61788ad946b4c19ab46814c29c63456
Trajectories of self-rated health and subjective well-being by state reached after school-leave. Data set: NEPS SC4, SUF 12.0.0. Adjusted predictions at the mean (APMs) and 95% confidence intervals of ten linear fixed-effect regressions with cluster-robust standard errors. n = number of individuals. Time-varying controls: Region and household composition. Red horizontal line represents predicted averages of health and well-being during school. To test how different states entered after school-leave affected trajectories of health and well-being, fixed-effects impact functions were estimated stratified by state reached in the year “0”. For transitions to “inactivity”, no subplot is shown. For the sample of university students, no estimate was calculable for year 6 or higher due to low case number
PMC9511745
12889_2022_14227_Fig2_HTML.jpg
0.478593
09e60609deb147a4b521aba819cae445
Baseline analysis. Correlations between BMD and HT, WT, BMI, HG-ave, and HG-max at BMD in women aged 50 to 54 years. (A) Correlations are shown by sorting by LS in 2006 (n = 98), (B) LS in 2002 (n = 137), (C) FN in 2006, and (D) FN in 2002. BMD, bone mineral density; r, Pearson correlation coefficient. *P < 0.05, **P < 0.01, ***P < 0.001.
PMC9512233
meno-29-1176-g001.jpg
0.478547
0ee525c61a014c948610dc1e3df1368f
Follow-up analysis of LS BMD. (A) Analysis of 84 patients who had BMD measurements in 2006 and 2016. Left: Women 50 to 54 years old in 2006 had a significantly lower LS BMD in 2016. The line of osteoporosis (<0.722 g/cm2) is shown. Middle (Left): LS BMD in 2006 in cases without osteoporosis (>0.722) and cases with osteoporosis (<0.722) in 2016. The cutoff line for the diagnosis of osteoporosis (<0.759 g/cm2) is shown. Middle (Right): LS BMD in 2006 in cases without osteoporosis (>0.759) and cases with osteoporosis (<0.759) in 2016. Right (Left): in the ROC curve, the cutoff (arrow) of LS BMD in 2006, when the Youden Index was maximum, was less than 0.834 g/cm2. Right (Right): in the ROC curve, the cutoff (arrow) of LS BMD in 2006, when the Youden Index was maximum, was less than 0.867 g/cm2. (B) Analysis of 83 patients who had BMD measurements in 2002 and 2011. Left: LS BMD of women 50 to 54 years old in 2002 was significantly lower in 2011. Middle (Left): cutoff less than 0.834, determined by the change in 2006 to 2016, was applied to 2002. Middle (Right): cutoff less than 0.867, determined by the change in 2006 to 2016, was applied to 2002. BMD, bone mineral density; ROC, receiver operating characteristic. ***P < 0.001.
PMC9512233
meno-29-1176-g002.jpg
0.441216
ff091ed23efa4b658ac1cc021a683737
Follow-up analysis of FN BMD. (A) Left: women who were 50 to 54 years old in 2006 had a significantly lower FN BMD in 2016. This indicates a line of osteoporosis (<0.561 g/cm2). Middle (Left): FN values in 2006 in cases who were not osteoporotic (FN > 0.561) and those who were osteoporotic (FN < 0.561) in 2016. This indicates a line of osteoporosis (<0.536 g/cm2). Middle (Right): FN values in 2006 in cases who were not osteoporotic (FN > 0.536) and those who were osteoporotic (FN < 0.536) in 2016. Right (Left): in the ROC curve, the cutoff (arrow) of FN in 2006, when the Youden Index was maximum, was less than 0.702 g/cm2. Right (Right): in the ROC curve, the cutoff (arrow) of FN in 2006, when the Youden Index was maximum, was less than 0.676 g/cm2. (B) Left: FN BMD of women 50 to 54 years old in 2002 was significantly lower than that in 2011. Middle (Left): cutoff less than 0.702, determined by the change in 2006 to 2016, was fitted to 2002. Middle (Right): cutoff less than 0.676, determined by the change in 2006 to 2016, was fitted to 2002. BMD, bone mineral density; ROC, receiver operating characteristic. ***P < 0.001.
PMC9512233
meno-29-1176-g003.jpg
0.378306
2431d804d1b6403b8867f333728700f2
Follow-up analysis. Correlation between the amount or rate of change in BMD in women aged 50 to 54 years after 9 or 10 years and HT, WT, BMI, HG-ave, and HG-max at BMD measurement in women aged 50 to 54 years. (A) Sorted by the amount of change in LS from 2006 to 2016 (n = 84). (B) Sorted by the amount of change in LS from 2002 to 2011 (n = 83). (C) Sorted by the amount of change in FN from 2006 to 2016. (D) Sorted by the amount of change in FN from 2002 to 2011. Correlation with the amount or rate of change showed that women with heavier WT and larger BMI had a larger decrease in FN BMD. r, Pearson correlation coefficient. BMD, bone mineral density. *P < 0.05, **P < 0.01, ***P < 0.001.
PMC9512233
meno-29-1176-g004.jpg
0.45421
fe87d9cce4c74c41be603c09b9707c81
Preoperative radiological images show a meningoencephalocele in the lateral sphenoid sinus and a bony defect in the left middle skull base. A: MR angiography images show an arteriovenous malformation in the right parietal lobe. B: CT image reveals a bony defect in the left middle skull base and a continuous structure that protrudes into the left lateral sphenoid sinus. C: Three-dimensional bone computed tomography image reveals a large bony defect outside the foramen rotundum (black arrow). D: Coronal CT image with multiple arachnoid pits in the greater wing of the sphenoid bone (white arrowheads). E: Axial magnetic resonance imaging (MRI) reveals a trabecular structure with a low signal on a T1-weighted image (not shown) and a high signal on a T2-weighted image. F: Sagittal constructive interference in the steady-state sequence shows the empty sella. G–I: Retrospective MRI on T2-weighted images shows how the mass gradually increased (G: 12 years before surgery, H: 9 years before surgery, I: 2 years before surgery).
PMC9512490
2188-4226-9-0281-g001.jpg
0.438155
eb462eda19b54bdea44efec130acc024
Intraoperative images. A: Multiple arachnoid pits (white arrowheads) in the middle fossa exposed after a left frontotemporal craniotomy. B: Partially removed brain tissue covered with dura. Asterisk (*) indicates the V2 root through the medial bone defect. C: Double asterisks (**) indicate the large bony defect and arachnoid pit. D: 70-degree endonasal endoscopic view. Brain tissue covered with mucosa was revealed in the sphenoid sinus. E: The dural defect was patched with temporal fascia after resection of the meningoencephalocele. F: The large bony defect and multiple bone pits in the middle fossa were repaired with the pedunculated temporalis fascia and a bone fragment made of the inner plate of the frontotemporal bone.
PMC9512490
2188-4226-9-0281-g002.jpg
0.447603
34df38d4169a466087fc5f87e2bfad72
Histological findings of the resected specimen. A: The mass consists of brain tissue with a cyst partially covered with epithelium and a thick connective tissue membrane. H&E. B–D: Higher magnification of the area indicated by an arrow in A. Glial tissue immunolabeled with glial fibrillary acidic protein (GFAP) is intermixed with fibrocollagenous tissue, whose surface was stained green with Elastica-Goldner staining (El-Gold). B, H&E; C, GFAP; D, El-Gold. E–G: Higher magnification images taken from the consecutive section of A. The area indicated by the dotted square shows an irregular surface of gliotic cortical tissue covered with ciliated columnar epithelium lined with a dense fibrocollagenous band and sparse fibrous tissue. Inset: Sparse fibrous tissue indicated by a square in E includes epithelial membrane antigen (EMA)-labeled cells that are meningothelial in nature. E, H&E; F, GFAP; G, El-Gold; inset in E, EMA. H: A higher magnification image taken from the area indicated by H in A shows cortical tissue with fibrillary gliosis and a dysmorphic large neuron (arrow) and scattered Rosenthal fibers (arrowheads). H&E. I: A higher magnification image taken from the area indicated by I in A shows uneven neuronal distribution with a dysmorphic neuron (arrow) and closely adjacent small neurons (arrowheads). Inset: A binuclear dysmorphic neuron. Klüver-Barrera staining. J: A higher magnification image taken from the area indicated by the square in A exhibits abnormal clustered arterioles and venules with thickened fibrous adventitia. El-Gold. Bar = 800 μm for A, 30 μm for B, and inset in E, 50 μm for C, D, and H, 100 μm in E–G, 75 μm for I, 115 μm for J, and 10 μm for inset in I.
PMC9512490
2188-4226-9-0281-g003.jpg
0.467992
4c64a9bfc2694c4889eae336aa7417bb
An integrated theoretical framework of the predictive factors associated with TNB mental health disparities.Minority stressors for transgender and nonbinary (TNB) people within a socioecological framework, with internal (proximal) stressors occurring at the individual level, and external (distal) stressors occurring at the interpersonal as well as structural and systemic levels. The association of minority stressors for TNB people with adverse mental health outcomes is explained in part by general psychological mediation processes. This framework integrates minority-stress theory29 and psychological mediation theory60 within a socioecological framework51 to explain contextual factors that drive documented mental health disparities within TNB populations. Mental and behavioural health disparity outcomes are on the right. A series of concentric yellow circles depicts the varying levels at which stigma-related stressors occur, from individual and internal, to interpersonal and external, to structural and systemic, as predictors on the left. PTSD, post-traumatic stress disorder.
PMC9513020
44159_2022_109_Fig1_HTML.jpg
0.447895
6ea25ea2e4da4647966b0eb9ad78046e
Protective and health promotive factors associated with well-being and decreased adverse mental health.Protective and health promotive factors (internal and external resources) are placed within the integrated theoretical framework of Fig. 1. Internal and external resources are recursively related and increase well-being and reduce adverse mental health. Coping strategies are moderators of the relations of minority stressors for transgender and nonbinary (TNB) people with adverse mental health. Protective and health promotive factors counteract minority stressors for TNB people, comprising population-specific factors associated with mental health and well-being in TNB populations.
PMC9513020
44159_2022_109_Fig2_HTML.jpg
0.45699
159fef63c1d54e509a72c46172973911
The flowchart of including and dividing patients.
PMC9513445
fpubh-10-954816-g0001.jpg
0.400803
86a88293380e42b1a7a435033fb74613
Nomogram to predict 3, 5, and 8-year overall survival in elderly patients with solitary bone plasmacytoma.
PMC9513445
fpubh-10-954816-g0002.jpg
0.437178
8138d934ff8340579b379767afc9eba5
The AUC of nomogram of 3-, 5-, and 8-year in the training set (A) and validation set (B). AUC, Receiver operating curve.
PMC9513445
fpubh-10-954816-g0003.jpg
0.477813
cc2dab38e89d42839f21e9e6e2eacac7
The calibration curves for predictions of overall survival in the training set (A–C) and validation set (D–F) at 3, 5, and 8-year.
PMC9513445
fpubh-10-954816-g0004.jpg
0.439666
ea6f9b26c52f4f8793e55d0bb69ad310
Kaplan-Meier survival curves for the training set (A) and validation set (B).
PMC9513445
fpubh-10-954816-g0005.jpg
0.403161
3f505951d0b14e3e9b426cc39b572bf7
Map of Nyakach Sub-County in Kisumu County showing the study eco-epidemiological zones. Lakeshore zone (highlighted in blue), hillside zone (highlighted in brown), and highland plateau zone (purple highlighted)
PMC9516797
13071_2022_5447_Fig1_HTML.jpg
0.419618
c4d23b02c7874e3ea552c50f434b665c
Larval habitat distribution cluster heat map. A Larval habitat distribution by seasonality. B Larval habitat distribution across topography. The hierarchical clustering dendrogram pattern represents the relationship between larval habitat type and landscape zones or seasons based on average linkage and Euclidean distance. The use of the same color indicates the availability of larval habitat types across landscape zones or seasons
PMC9516797
13071_2022_5447_Fig2_HTML.jpg
0.438909
96ba78c2bcb143e0ac9276dcb2d2953a
Distribution of larval habitats, households with the adult vector survey, and parasitological survey households. A Overview of the study area, including all three eco-epidemiological zones. B, C, and D Distributions of three surveys in lakeshore zone, hillside zone, and highland plateau zone, respectively
PMC9516797
13071_2022_5447_Fig3_HTML.jpg
0.502154
f921a00200cc4163800b6bd87ade83c9
Proximal location of the cuff.
PMC9517126
ijerph-19-11242-g001.jpg
0.449134
f93028db161b4e749e0fbd67ebeaec8c
Distal location of the cuff.
PMC9517126
ijerph-19-11242-g002.jpg
0.459131
7f40d2181df94a4ba219e1b7650551b5
The location of the three study sites.
PMC9517536
ijerph-19-11606-g001.jpg
0.389164
52486cfbfb2242e9830585fabcf9ce0b
The frequencies of answers for distance (top), duration (middle), and frequency (bottom) across study locations. MH, Rai Mae Hia; BH, Buak Haad Park; 3K, Three Kings Monument.
PMC9517536
ijerph-19-11606-g002a.jpg
0.445314
2e9c2011ed8c4494a6d1daea766373d7
Charts displaying the relationship between age and duration and WHR. The line at 0.8 represented a low-risk WHR, as recommended by WHO [10].
PMC9517536
ijerph-19-11606-g003.jpg
0.481854
f10d7dfa0d5746e485a572b4e80870c8
Passive hip flexion with the knee extended test (hamstrings).
PMC9517817
ijerph-19-10747-g001.jpg
0.46546
1bc90b597c924d1b9ee5c18a187bc547
Passive hip flexion with the knee flexed test (gluteus maximus).
PMC9517817
ijerph-19-10747-g002.jpg
0.484359
b3cf2721530e464f9edbc2de820313ed
Passive hip extension with the knee relaxed test (iliopsoas).
PMC9517817
ijerph-19-10747-g003.jpg
0.446521
1da5aa28f1504b56a3ad6b4eec178b63
Passive hip adduction with the 90° hip flexion test (piriformis); * [59,60].
PMC9517817
ijerph-19-10747-g004.jpg
0.429734
58b43bf9ce584af3bfedd5a5da20967d
Passive hip abduction with the knee extended test (adductors).
PMC9517817
ijerph-19-10747-g005.jpg
0.433911
c97d3dd1103e471da6f7705da122c7fe
Passive hip abduction with the 90° hip flexion test (adductors monoarticular).
PMC9517817
ijerph-19-10747-g006.jpg
0.436379
edeada17d6a94e5a8f7dbcd1f075fd89
Passive internal hip rotation test (external rotators).
PMC9517817
ijerph-19-10747-g007.jpg
0.429829
7b28d148138e43bcb0f80b3929e01818
Passive external hip rotation test (internal rotators).
PMC9517817
ijerph-19-10747-g008.jpg
0.414946
feceafc5ef294541b9ac52a3e8908c63
Passive knee flexion test (quadriceps).
PMC9517817
ijerph-19-10747-g009.jpg
0.477515
636db0fe28b94b189f7109bec0cd8055
Ankle dorsiflexion with the knee extended test (gastrocnemius).
PMC9517817
ijerph-19-10747-g010.jpg
0.470139
b94e0937a31b45cabf57d91eda7f0508
Ankle dorsiflexion with the knee flexed test (soleus).
PMC9517817
ijerph-19-10747-g011.jpg
0.432013
7452167aee4d4f889d95f575ad4b9dd2
Development history of the pollution fee system in China.
PMC9518126
ijerph-19-10660-g001.jpg
0.435669
315ca3e9555c44a2a97d44888c187ffb
Approach to enterprise emission reduction.
PMC9518126
ijerph-19-10660-g002.jpg
0.440435
f91477ee96374653a5ecd3dfdb6af696
Spatial distribution of the pollution fee reform areas in China during 2006–2013.
PMC9518126
ijerph-19-10660-g003.jpg
0.527318
090c7f82eaa647b8a9b97b2609aee1fd
Results of the parallel trend test.
PMC9518126
ijerph-19-10660-g004.jpg
0.4089
a59d790e467448e58a3ecd314be62d21
Before matching and after matching.
PMC9518126
ijerph-19-10660-g005.jpg
0.544999
f88bb86559274380a3f64ebcd6c81a57
Results of the Placebo test.
PMC9518126
ijerph-19-10660-g006.jpg
0.41512
b20542eec6984e1d894dadbbf824f19a
Validation of RiboTag mice for BEC-specific translatome analysis.(A) Tie2-Cre; Rpl22HA/HA (Ribo-Tag) mice, which are designed for expressing HA-tagged ribosomal protein in BECs. (B) Immunohistochemistry for Ai9 (Cre reporter, Red) and CD31 (endothelial cell marker, Green) in adult Tie2-Cre; Ai9; Rpl22HA/HA mice. The regions in the dotted boxes in the left images are shown on the right at higher resolution. Scale bars, 1 mm (200 μm in the insets). (C) Immunohistochemical staining for Gfap and Ai9 (left column) and for Pdgfrb and Ai9 (right column) in the cortex of adult Tie2-Cre; Ai9; Rpl22HA/HA mice. Gfap+ astrocytes and Pdgfr+ pericytes did not overlap with Cre recombinase, as represented by the Ai9 reporter gene. (D) Immunoprecipitation of the HA-tagged ribosomal protein RPL22HA, which is a component of actively translating polyribosomes. The expression of HA-tagged RPL22A was investigated by immunoprecipitation with mouse IgG (-) or anti-HA (+) or with anti-Flag (+) and subsequent Western blotting with anti-HA.
PMC9518886
pone.0275036.g001.jpg
0.414904
f38aa62a54a24f25afb1f4231ae678a5
Comparative analysis of the conventional RiboTag method and our new RiboTag protocol.(A) Workflow diagram and validation of the RiboTag method. (B) Images of vessels isolated with a cell strainer (40 μm) before the immunoprecipitation step. (C, D) RT–PCR to verify the BEC specificity of mRNA pools isolated by the standard RiboTag protocol (C) and by our optimized RiboTag protocol (D). Brain endothelial cell markers: Tie2, Mfsd2a, Claudin-5, Occludin, VCAM-1, P-gp, neuronal cell marker: Syt1, astrocyte marker: Gfap, and pericyte marker: Pdgfrβ. The amount of mRNA isolated from the whole cortex (7.3 ± 0.668 ng) (E) and the visual cortex (1.05 ± 0.125 ng) (F). Mean ± SEM; n = 6 for the whole cortex, n = 8 for the visual cortex.
PMC9518886
pone.0275036.g002.jpg
0.39906
44d2440bc3684ecba89e52441b4ebe8f
Generation of cDNA libraries for NGS from the low mRNA yield derived from BECs.(A) The process used to generate a cDNA library for RNA-seq from the small amount of pooled mRNA originating from BECs in the cortex of Tie2-Cre; Ai9; Rpl22HA/HA mice. TapeStation gel image (B) and electropherogram (C) showing PCR amplification of the cDNA library from the cortex of Tie2-Cre; Ai9; Rpl22HA/HA mice. (D) The specificity of the cDNA library from the cortex of Tie2-Cre; Ai9; Rpl22HA/HA mice was verified by using RT–qPCR. Mean ± SEM; *P<0.05, ***P<0.001, ****P<0.0001 by the Kruskal–Wallis test, n = 10. After fragmentation into 300 bp pieces and labeling with dual barcode oligos, the quality of the cDNA was validated by using TapeStation gel images (E) and electropherograms (F).
PMC9518886
pone.0275036.g003.jpg
0.392457
5015b12dbbe24a669c386bd927194f0a
Seasonal changes in Lake Redon, Pyrenees. (A) Illustration of the snow and ice cover melting period. Photographs: Marc Sala-Faig. (B) Seasonal and depth variation of chlorophyll-a and (C) oxygen. Black circles indicate sampling points and dashed lines the isotherms (°C). The line above each graph indicates the snow and ice-cover thickness in arbitrary units.
PMC9519062
fmicb-13-935378-g001.jpg
0.477492
3d2e36b20a354e3bb1178196db027ced
Seasonal fluctuations of bacterioplankton number of 16S rRNA gene copies (A) and OTU richness (B) at different depths. Thick black lines at the top of each graph indicate periods of ice cover.
PMC9519062
fmicb-13-935378-g002.jpg
0.431645
f05300d2fa534fa98772934408068623
Seasonal difference in bacterioplankton community composition. (A) PCA analyses using Hellinger distance of the bacterioplankton OTUs. Numbers refer to OTUs listed in Supplementary Table S4. There is a seasonal trajectory for the upper layers (2, 10, 20-m depth), whereas variation is lower in the deeper layers (35, 60-m depth). (B) Temporal depth distribution of the bacterioplankton groups was obtained using k-means clustering with Hellinger distance. Dashed lines denote isotherms. Circles indicate sampling points, and the color corresponds to each of the six clusters: UI (under-ice), TH (thaw and hypolimnion), ES (early stratification), EP (epilimnion), OE (overturn and early under-ice), and DL (deep layers). The line above the graph indicates the snow and ice-cover thickness in arbitrary units. (C) The best number of k-means groups was assessed by maximizing the total indicative value (IndVal) of the significant OTUs at each partition.
PMC9519062
fmicb-13-935378-g003.jpg
0.427448
8e3e15097b5a457789c2efd81e3b6240
Characteristics of the bacterial seasonal clusters’ environment. (A) Bacterioplankton clusters in a discriminant environmental space. Clusters: UI (under-ice), TH (thaw and hypolimnion), ES (early stratification), EP (epilimnion), OE (overturn and early under-ice), and DL (deep layer). The symbol size of each cluster is proportional to the number of samples included. (B) Heat map indicating the average environmental conditions for each bacterioplankton seasonal cluster. The average cluster values clusters indicated within the boxes, and colors indicate the relative rank among clusters, from the highest (red) to the lowest (pale yellow). The variables are sorted according to their loading in the first axis of the discriminant analysis (A), with the lowest p-values at both extremes and the less relevant variables in the middle. The asterisk (*) indicates no significance in the discriminant analysis.
PMC9519062
fmicb-13-935378-g004.jpg
0.39728
cd3bdf69974d4c6d930157744a9e72c0
Indicator taxa of seasonal clusters. OTUs are ranked according to their significant indicator values. Colors indicate the taxonomic class. The number of indicator OTUs and classes (parenthesis) are indicated below the x-axis.
PMC9519062
fmicb-13-935378-g005.jpg
0.422464
e2971f8e12d248d28f82a2108738c182
Patterns of occurrence and seasonality in the bacterioplankton community. (A) OTUs ranked by occurrence in the samples. Colors specify cluster indicators: UI (under-ice), TH (thaw and hypolimnion), ES (early stratification), EP (epilimnion), OE (overturn and early under-ice), and DL (deep layer). (B) Comparison of the OTU indicator values with the OTU’s mean and maximum abundance ratio in the samples. A larger ratio indicates flatter seasonal OTU profiles, that is, lower occasional blooming. The symbol size is proportional to OTU occurrence. The inserted plots show examples of the OTU abundance’s time series at each sampling depth (line colors as in Figure 2). Arrows indicate the corresponding OTU in the larger plot.
PMC9519062
fmicb-13-935378-g006.jpg
0.463306
f4f613d733c2432bb3b1e07ceea83caf
Overview of the synthetic lethality (SL) prediction model. A. Identification of essential and mutant SL genes using text-mining and high-throughput screening (HTS) data (COSMIC and CCLE). B. Matching and prediction of essential-mutant SL gene pairs for cancer-specific types. C. Enrichment and filtering of SL gene pairs by gene co-expression and co-occurrences. D. Selection of candidate (CD82-KRAS) SL gene pairs using RAS-mutant HTS and PubChem bioassay data.
PMC9519430
gr1.jpg
0.445844
675e06d264564d8ba2234c2d52123f5f
Workflow of enrichment and filtering of synthetic lethality (SL) gene pairs. To extract and rank more reliable SL gene pairs, we used three criteria: (i) Essential gene candidate score (Sg), gene co-expression, and co-occurrences to enrich and filter SL gene pairs. In total, 586 essential genes were identified based on the threshold of the (ii) essential gene candidate score (Sg) > 10. Subsequently, we enriched and set Spearman’s correlation (iv) p-value < 0.05 according to gene co-expression obtained from (iii) CCLE gene expression data. Next, we filtered each SL gene pair by co-occurrences (v) in the literature. The threshold of (vi) co-occurrences of two genes in one article was > 0 or ≥ 0. Sg, essential gene score.
PMC9519430
gr2.jpg
0.372467
651adea7de0448698745a196fe1312e4
Dependency parse tree of an example sentence and trigger term extraction. A. The dependency parse tree for “significance of the member of TM4SF (MRP-1/CD9, KAI1/CD82, and CD151) in human colon cancer.” “KAI1/CD82” is an essential gene in “colon cancer,” and “significance” is the common ancestor in the dependency parse tree. B. The top seven trigger terms in colon cancer. The nmod, dep, and conj. are Universal Stanford Dependencies representing grammatical relations between words. Abbreviations. nomd, nominal modifier; the nmod relation is used for nominal dependents of another noun or noun phrase and functionally corresponds to an attribute or genitive complement. Dep, unspecified dependency; a dependency can be labeled as dep when it is impossible to determine a more precise relation. Conj, conjunct; a conjunct is a relation between two elements connected by a coordinating conjunction, such as and, or, etc. The links for the main organizing principles of the Universal Dependencies taxonomy were as follows: https://universaldependencies.org/u/dep/all.html (accessed on 2 Feb 2022). St, trigger term score.
PMC9519430
gr3.jpg
0.520231
6498123f06b34e5ebde446af71fb9494
Identification of KRAS-mutant synthetic lethality (SL) gene pairs. The synthetic lethal relationships of these genes were identified using RAS-mutant high-throughput screening (HTS) data and text-mining analysis. Predicted SL gene pairs were compared with HTS data using a Venn diagram with the threshold of gene co-expression and co-occurrences in colon cancer (A and B). The left circle (red) denotes the number of predicted SL gene pairs; the right circle (blue) represents the number of SL gene pairs recorded in the screening data. A. Stricter thresholds were set for gene co-expression (Spearman correlation p-value < 0.05) and co-occurrence (number of co-occurrences of two genes in the literature ≥ 0). B. Stricter thresholds were set for gene co-expression (Spearman correlation p-value < 0.05) and co-occurrence (number of co-occurrences of two genes in the literature > 0). C. Two potential SL gene pairs in colon cancer, including CD82 (essential)-KRAS (mutant) and CD82 (essential)-NRAS (mutant) gene pairs, were identified. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
PMC9519430
gr4.jpg
0.490107
3e88374ead0d41b6acc61fd9c79d732d
PubChem bioassay of the CD82-KRAS synthetic lethality (SL) gene pair in colon cancer. A. A PubChem database search revealed that a chemical compound screen assay (fluorometric microculture cytotoxicity assay (FMCA)) demonstrated that digitonin was used to precipitate tetraspanins (a protein complex including CD82) and significantly suppressed the growth of a KRAS/BRAF-mutant colon cancer cell line (https://pubchem.ncbi.nlm.nih.gov/bioassay/471512). B. The half-maximal inhibitory concentration (IC50) values for three cancer cell lines are presented.
PMC9519430
gr5.jpg
0.526271
50b8658f19ba44afb03248a0bf3f7bde
Effects of siRNA-mediated CD82 depletion on cell viability of KRAS-mutant cancer cell lines. siRNA-mediated knockdown of CD82 resulted in the downregulation of p-MEK and decreased cell viability following chemotherapy. A. Western blot (WB) analysis of DLD-1 W/M (KRAS mutant) and DLD-1 W/− (KRAS wild-type). CD82 expression was higher in DLD-1 W/M cells than in DLD-1 W/− cells. The colon cancer cell lines were transiently transfected with control siRNA or CD82 siRNA. The WB results of siRNA-CD82 in DLD-1 W/− and W/M cells. B. Results of the MTT assay after CD82 knockdown and treatment with 5-FU for 72.
PMC9519430
gr6.jpg
0.477423
64867d886acb49fa9df6df7d5f1909fe
Map of Ondo State showing the study area. Source: Ondo State web portal, (2019).
PMC9519504
gr1.jpg
0.374045
f9a6229edbcb4aca858bd6b4489e01ee
Frequency of usage of CRIN approved insecticides.
PMC9519504
gr2.jpg
0.446069
19089c3514b243d989714e731c43d638
Error bar of usage of CRIN approved insecticides.
PMC9519504
gr3.jpg
0.411185
b4a14622d106433f90e825c73a78ded2
Protein presence in pathway models. (A) 46% of the measured proteins in the dataset were found in at least one pathway in the combined pathway collection. (B) The distribution of the number of pathways in which a protein participates shows that most proteins are only present in very few pathways.
PMC9519890
fimmu-13-963357-g001.jpg
0.469675
b9746b75009544e2b15bfd9301297c33
Changes in pathway activities in COVID-19 patients. (A) The box plot shows the number of less and more active pathways in each tissue. (B–H) For each tissue, the effect size of all significant pathways from the Wilcoxon test are shown. The cutoff of >0.3 for effect size is indicated with a dashed line. Only the 69 pathways, which show significant changes in protein abundance in at least one tissue are included on the x-axis.
PMC9519890
fimmu-13-963357-g002.jpg
0.404869
7fd1deda2bfe4481ba9963afe2b35b3a
Protein-pathway network of 69 changed pathways in COVID-19 patients. Pathways are shown as rectangles and the proteins present in a pathway are connected to the pathway node and shaped as circles. The pathway nodes visualize the heatmap of pathway activity change in COVID-19 patients from thyroid, lung, heart, liver, spleen, kidney and testis in that order. Blue indicates a lower pathway activity in COVID-19 patients (protein abundance distribution shifted to the left) and red indicates an increased activity (protein abundance distribution shifted to the right). Most of the pathways are highly connected with many proteins in common.
PMC9519890
fimmu-13-963357-g003.jpg
0.448936
da536211ff5549cebd9e398f3ba38352
Heatmap of pathway activities per tissue (p-value < 0.05, Wilcoxon test). Pathway activities are highly tissue specific and only few pathways show significant changes in multiple tissue. All significant changed pathway are shown and the color gradient indicates the effect size. Blue: the pathway is less active in COVID-19 patients, red: the pathway is more active in COVID-19 patients. Grey: unmeasured or non-significant pathways (p-value >= 0.05).
PMC9519890
fimmu-13-963357-g004.jpg
0.36718
b8fd273c50c547c5aec260985a989dad
COVID-19 protein expression visualized on the Kinin Kallikrein pathway (WP5089). The pathway has activities changed in most tissues in COVID-19 patients. (A) Protein abundance is visualized on protein nodes in the pathway. Top row is data from COVID-19 patients and bottom row is data from non-COVID-19 patients. The higher the abundance the darker the value. The data nodes are split in seven columns for the seven different tissues. (B) The pathway figure shows the differential expression of the proteins (log2 fold change) between COVID-19 and non-COVID-19 patients. All proteins are downregulated or not changed in all tissues. The data nodes are split in seven columns for the seven different tissues. Left to right: thyroid, lung, heart, liver, spleen, kidney, testis.
PMC9519890
fimmu-13-963357-g005.jpg
0.410544
8a4f617044d7423c8e0c407e729c6334
COVID-19 protein expression visualized in the cholesterol biosynthesis pathway (WP197) in the testis. All proteins in the pathway are less abundant in COVID-19 patients.
PMC9519890
fimmu-13-963357-g006.jpg
0.607243
9ffcd1965fc647578f0ff0093466f89e
The multidisciplinary team of the ETHeart program with medical professionals from Berlin (green scrubs) and engineers (dark turtlenecks) from Zurich. Illustration created by Payko.
PMC9520014
gr1.jpg
0.461639
680ccf5a1d154d6eb8bc3fd779f831c3
Imaginary, yet typical end-stage heart failure patient relying on an implanted Left Ventricular Assist Device (LVAD) to maintain the necessary blood flow through the body. Illustration created by Payko
PMC9520014
gr2.jpg
0.400934
d09e79da15f24a7caef81882de676776
Flowchart of study selection.
PMC9520262
fmed-09-956188-g001.jpg
0.399378
45659b152f36482294543a6c731155bf
Risk of bias graph.
PMC9520262
fmed-09-956188-g002.jpg
0.450221
9955afd953b04219880efd34ac1b61f4
Network meta-analysis plot for the assessment of high intensity laser therapy (HILT) and other physical therapy modalities (nodes are weighted in accordance with the number of trials including the respective treatments. The larger the size of node and the thicker the lines are, the more studies are involved). Treatment relative ranking [the PrBest means the estimated probability that the treatment is the best one. The lower the value of Mean Rank is, the higher the efficacy of the treatment may be. The ranking probability plot for the assessment of improved visual analog scale (VAS) pain at the end of the physical therapy modalities is shown].
PMC9520262
fmed-09-956188-g003.jpg
0.487418
6dab9c3274e24b45a9c241ea4f628eb0
Forest plot of the visual analog scale (VAS)-pain in high intensity laser therapy (HILT) vs. Low level laser therapy.
PMC9520262
fmed-09-956188-g004.jpg
0.523549
7137425557d2409e81e1e32b2daeccc8
Forest plot of the visual analog scale (VAS)-pain in high intensity laser therapy (HILT) vs. Placebo laser (plus exercise).
PMC9520262
fmed-09-956188-g005.jpg
0.447911
f11a1bb60c90413db6ee7ddfbdb29570
Network meta-analysis plot for the assessment of high intensity laser therapy (HILT) and other physical therapy modalities (nodes are weighted in accordance with the number of trials including the respective treatments. The larger the size of node and the thicker the lines are, the more studies are involved). Treatment relative ranking (the PrBest means the estimated probability that the treatment is the best one. The lower the value of Mean Rank is, the higher the efficacy of the treatment may be. The ranking probability plot for the assessment of improved WOMAC total at the end of the physical therapy modalities is shown).
PMC9520262
fmed-09-956188-g006.jpg
0.450329
946f0f80d8804a26a6cfbf83039d1c55
Forest plot of the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC)-total in high intensity laser therapy (HILT) vs. Low level laser therapy.
PMC9520262
fmed-09-956188-g007.jpg
0.410171
cef701e779cb4cdbb82ca5e0f2a1e71f
Forest plot of the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC)-pain (A), WOMAC-stiffness (B), WOMAC-function (C), and WOMAC-total (D) in high intensity laser therapy (HILT) vs. Placebo laser (plus exercise).
PMC9520262
fmed-09-956188-g008.jpg
0.418586
f2377a52dc3d4c8fac1f72f83cc7be4a
PSY1 expression increased carotenoid accumulation in ‘Royal Gala’ apple fruit. (A) Fruit of WT and PSY transgenic lines (OE-1, OE-5, and OE-7) at different developmental stages. (B) Bar graphs of carotenoid content measured by HPLC as beta-carotene equivalents (left column) and chlorophyll (right column) in fruit skin (top panel) and fruit flesh (bottom panel) in wild type and transgenic lines OE-1, OE-5, and OE-7. The error bars represent the standard errors of the mean of three biological replicates, with each replicate a pool of 5–7 fruit. Bar graph with asterisk show significant difference from WT at the same fruit stage using Dunnett’s test (*P < 0.05; **P < 0.01).
PMC9520574
fpls-13-967143-g001.jpg
0.427883
73a92d1134554026aca336d366665d19
Visualization of chlorophyll and carotenoid autofluorescence in wild type (WT) and PSY ‘Royal Gala’ fruit. Fresh fruit tissues, at 120, 135, and 150 D, were analyzed by confocal microscopy to show plastids containing chlorophyll (red), carotenoid (green) and both pigments (yellow). Graph represents fluorescence emission spectra of WT and PSY transgenic tissue. Fluorescence emission between 500 and 600 nm represents carotenoids and 650–750, chlorophyll pigments.
PMC9520574
fpls-13-967143-g002.jpg
0.446885
c52b8fed33cb4b91b62ab4b4ccc3f9ea
Comparison of carotenoid gene expression in wild-type (WT) and PSY ‘Royal Gala’ apple lines, OE-5 and OE-7, as determined by qPCR, relative to expression of housekeeping genes (MdActin and MdEF1A) in fruit skin (A) and fruit flesh (B). Bars represent means and SE of four biological replicates. PSY, phytoene synthase; PDS, phytoene desaturase; ZDS, zeta carotene desaturase; CRTISO, carotene isomerase; LCB, lycopene beta-cyclase; BCH, beta-carotene hydroxylase. Bar graph with asterisk shows significant difference from WT at the same fruit stage using Dunnett’s test (*P < 0.05; **P < 0.01).
PMC9520574
fpls-13-967143-g003.jpg
0.485557
1d58a1dded2b4ef0ad9d1c0b52bdea87
Differentially expressed genes in PSY transgenic apple fruit. Venn diagram of number of differentially expressed genes (log2 fold change ≥ 2, P < 0.05) between WT and OE-7 fruit at four developmental stages (90, 120, 135, 150 D). Upregulated (A), downregulated (B) in PSY fruit flesh.
PMC9520574
fpls-13-967143-g004.jpg
0.39677
7230e64a1fd140c798d0a092ed45cf13
Analysis of carotenoid-associated transcription factor genes. (A) Heat map of differentially expressed transcription factor genes (Supplementary Table S4) in apple fruit flesh during development. The average gene expression of biological replicates at each of the four stages: 90, 120, 135, and 150 D, from WT and PSY transgenic line OE-7, were clustered using Euclidean distance relationships. Green to red color gradient indicates low to high relative gene expression. (B) Correlation matrix of gene transcripts and carotenoid metabolites (β-carotene, BCAR; total carotenoid content, TOTCAR) in transgenic PSY fruit. Values represent correlation coefficients with color gradient from green to red indicating weak to strong correlations at P < 0.05.
PMC9520574
fpls-13-967143-g005.jpg
0.367173
6dc2d5ac9ec0485482ef2239ac38b343
PSY1 increased fruit carotenoid content in apple in the absence of light. (A) Representative bagged and non-bagged fruit of WT and PSY line OE-3 at 150 D. (B) Graphs showing carotenoid content in fruit skin (left) and flesh (right) of different PSY lines (OE-2, OE-3, OE-4) and WT. Error bars represent standard error of total carotenoid contents of three biological replicates. Bar graph with asterisk show significant difference from the non-bagged fruit of the same line using Dunnett’s test (*P < 0.05; **P < 0.01). (C) Stained fruit sections of WT and OE-3 displaying plastids (arrowed) in the cells.
PMC9520574
fpls-13-967143-g006.jpg
0.398084
1fa6f133eb8b4cceb183b798ed1c5fb7
Differentially expressed genes (DEGs) in bagged apple fruit. (A) Go Plot R of DEGs in bagged fruit of WT and OE-3 fruit. The scatter plots show log2 fold change (logFC) for each gene under the gene ontology (GO) number. Red dots indicate upregulated genes and blue dots show downregulated genes. The z-score bars are a measure of the extent to which each identified process is upregulated or downregulated. (B) Heat map of differentially expressed transcription factor genes in bagged fruit. Clustering done using the average expression values of three biological replicates of bagged (BG) and non-bagged (NBG) fruit of WT and OE-3 transgenic line. Green to red color gradients indicate low to high relative gene expression. The highlighted TFs are common to the bagging and fruit development (Figure 5A) data sets.
PMC9520574
fpls-13-967143-g007.jpg
0.379658
c70b4bfcc5754e31bfe8f1270675453a
Correlations between carotenoid content and TF gene expression as determined by qRT-PCR in (A) fruit skin and (B) fruit flesh of WT and PSY fruit. R2 values indicate coefficient of determination.
PMC9520574
fpls-13-967143-g008.jpg
0.394613
2765398c0bb940508c45ca627856016f
Experimental design.
PMC9520596
fnins-16-939915-g001.jpg
0.449616
d64e94db42a043a98ca8ff2e44fe7ea2
Effects of ApoE on cognitive function and hippocampal synaptic ultrastructure in aging mice. (A) Y-maze test, n = 20. (B) Navigation test, n = 20. (C) Platform crossing, n = 20. (D) Target quadrant time, n = 20. (E) MWM representative figures. (F) Ultrastructure of hippocampal synapses. (G) Synaptic active zone length, n = 4 (Five synapses were randomly selected from each mouse). (H) Synaptic cleft width, n = 4 (Five synapses were randomly selected from each mouse). (I) Thickness of PSD, n = 4 (Five synapses were randomly selected from each mouse). (J) Synaptic interface curvature, n = 4 (Five synapses were randomly selected from each mouse). **p < 0.01 vs. Control group, ##p < 0.01, #p < 0.05 vs. Model group.
PMC9520596
fnins-16-939915-g002.jpg
0.450969
86e270e0a9d14bf9be083f22c2a253b9
ApoE Deletion aggravates the dysregulation of SYP and PSD-95 expression in the hippocampus of aging mice. (A) Immunohistochemistry staining for SYP in different hippocampal regions. (B) Quantification of SYP intensity, n = 8. (C) Immunohistochemistry staining for PSD-95 in different hippocampal regions. (D) Quantification of PSD-95 intensity, n = 8. **p < 0.01 vs. Control group, #p < 0.05 vs. Model group.
PMC9520596
fnins-16-939915-g003.jpg
0.43338
eb11c6dea94e4e9fba16492dce842bf1
Deletion of ApoE affects the gut microbial composition of aging mice. (A) Chao 1 index, n = 8. (B) Observed species index, n = 8. (C) Shannon index, n = 8. (D) PCoA analysis. (E) Relative abundance of gut microbiota (phylum level). (F) Relative abundance of gut microbiota (genus level). *P < 0.05 vs. Control group, ##p < 0.01 vs. Model group.
PMC9520596
fnins-16-939915-g004.jpg
0.472164
611cce715e3e4e18bcf9d03a08661471
LEfSe and PICRUSt2 analysis. (A) Cladogram of LEfSe analysis. (B) LDA of LEfSe analysis. (C) PICRUSt2 analysis.
PMC9520596
fnins-16-939915-g005.jpg
0.442395
97ffddc8f35c4edf94ad81e471b27b2a
Deletion of ApoE alters the metabolic profile of the hippocampus of aging mice. (A) PLS-DA of LC-MS about model group vs. control group. (B) PLS-DA of LC-MS about ApoE group vs. model group. (C) PLS-DA of GC-MS about model group vs. control group. (D) PLS-DA of GC-MS about ApoE group vs. model group. (E) Differentially abundant metabolites about model group vs. control group. (F) Differentially abundant metabolites about ApoE group vs. model group. (G) Analysis of metabolic pathway enrichment.
PMC9520596
fnins-16-939915-g006.jpg
0.484829
6ed194bba7d94a458a0e4037479fc199
Deletion of ApoE alters blood lipids and oxidative stress levels in rapidly aging mice. (A) TC, n = 8. (B) TG, n = 8. (C) LDL, n = 8. (D) SOD in serum, n = 8. (E) GSH-Px in serum, n = 8. (F) MDA in serum, n = 8. (G) SOD in brain tissue, n = 8. (H) GSH-Px in brain tissue, n = 8. (I) MDA in brain tissue, n = 8. **p < 0.01 vs. Control group. #p < 0.05, ##p < 0.01 vs. Model group.
PMC9520596
fnins-16-939915-g007.jpg
0.419612
2977f2f621414ea88a5d9a3baa134099
Subnational Government Responsiveness to Community Advocates’ Campaigns (as of June 30, 2019)
PMC9520791
12939_2022_1717_Fig1_HTML.jpg
0.473767
5aa41ea129e84a4ab1f59560fa87bbe8
Molecular interactions of HSA with GAL. (A) Cartoon structural representation, (B) interacting residues, and (C) potential surface cavity representation of HSA residues interacting with GAL.
PMC9521020
ao2c04004_0002.jpg
0.45319
8e80a6553cee4cd890a9b39c58191d89
(A) RMSD fluctuations of the protein backbone, bound (red) and free (black) HSA during 250 ns production. (B) RMSD of ligand during the production runs.
PMC9521020
ao2c04004_0003.jpg
0.412211
41f490f6ebbb4261ae90fa9a81fe79b8
(A) Rg for GAL-bound HSA plotted as a function of snapshots. (B) SASA plotted as a function of snapshots.
PMC9521020
ao2c04004_0004.jpg
0.420931
5f4c40e2c3eb49108bcaf6a5c4a50c18
(A) HSA intramolecular hydrogen bonds (H bonds) monitored during 250 ns production runs (GAL-bound HSA). (B) Intermolecular hydrogen bond analysis of HSA–GAL complex.
PMC9521020
ao2c04004_0005.jpg
0.443595
da1d828f5ab5441f8997c7b9ad8e9da7
GAL binding affinity estimated via LIE methodology (electrostatics plotted in red and net van der Waals plotted in black).
PMC9521020
ao2c04004_0006.jpg
0.401996
51810fe9a5b3404c8669b61239b0926b
Fluorescence-based binding. (A) Intrinsic fluorescence quenching of HSA with increasing GAL concentration. (B) MSV plot of HSA–GAL system.
PMC9521020
ao2c04004_0007.jpg