Journal: Bioactive Materials

Article Title: Spatiotemporally engineered microneedle for microenvironment remodeling propels mucosal regeneration after tracheal mucosal injury

doi: 10.1016/j.bioactmat.2026.01.026

Figure Lengend Snippet: Evaluation of mucosal status after tracheal mucosal injury in rabbits . (a) Gross morphology and Masson staining of mucosal defects (n = 3). (b – f) Tracheal samples were collected on Day 10, and RNA sequencing was performed to assess biological differences between Native and Model groups (n = 3). (b) Principal components analysis of samples. (c) Volcano plot of DEGs. (d) KEGG enrichment analysis of DEGs. (e) Chord plot of enriched KEGG terms. (f) Heatmaps of DEGs associated with inflammation and oxidative stress. (g) IF staining of FISH (marker of bacteria, pink), iNOS (marker of M1 macrophages, orange), CD206 (marker of M2 macrophages, green), and immunohistochemical staining of CD31 (marker of endothelial cells) in various samples, blood vessels are denoted by triangles.

Article Snippet: Immunofluorescence staining of CK14 (Abcam, ab181595), AC-Tub (Proteintech, 66200-1-Ig), ZO-1 (Proteintech, 21773-1-AP), and Immunohistochemical (IHC) staining for CD31 (Servicebio, S1002) were conducted to reveal the conditions of mucosal regeneration, according to previous literature [ ].

Techniques: Staining, RNA Sequencing, Marker, Bacteria, Immunohistochemical staining

Journal: Bioactive Materials

Article Title: Spatiotemporally engineered microneedle for microenvironment remodeling propels mucosal regeneration after tracheal mucosal injury

doi: 10.1016/j.bioactmat.2026.01.026

Figure Lengend Snippet: Gel-AgNA/MgGA MN remodel the microenvironment after TMI by regulating infection, inflammation, oxidative stress, and vascular disruption. (a) FISH (marker of bacteria, red) staining of harvested samples after treated with Gel, Gel-AgNA, Gel-MgGA, and Gel-AgNA/MgGA MN. (b, c) Quantitative analysis of bacterial coverage and fluorescence intensity of FISH (n = 9). (d) Heatmaps of DEGs related to inflammation and oxidative stress. (e) RT-PCR analysis showing the relative expression levels of IL-1, TNF-α, HIF-1α, and IL-6 (n = 3). (f) IF staining of iNOS (marker of M1 macrophages, red) and CD206 (marker of M2 macrophages, green). (g) Quantitative analysis of iNOS and CD206 fluorescence intensity. (h) RT-PCR analysis showing the relative expression levels of Arg1 and CD206. (i) IF staining of CD31 (marker of blood vessels, red). (j, k) RT-PCR analysis showing the relative expression levels of VEGF and HIF-1α (n = 3).

Article Snippet: Immunofluorescence staining of CK14 (Abcam, ab181595), AC-Tub (Proteintech, 66200-1-Ig), ZO-1 (Proteintech, 21773-1-AP), and Immunohistochemical (IHC) staining for CD31 (Servicebio, S1002) were conducted to reveal the conditions of mucosal regeneration, according to previous literature [ ].

Techniques: Infection, Disruption, Marker, Bacteria, Staining, Fluorescence, Reverse Transcription Polymerase Chain Reaction, Expressing

Journal: Oncology Letters

Article Title: LATS2 expression differences in lung adenocarcinoma and lung squamous cell carcinoma analyzed using bioinformatics and experimental approaches

doi: 10.3892/ol.2026.15671

Figure Lengend Snippet: Comprehensive expression analysis of LATS2 in LUAD and LUSC. (A) Expression levels of LATS2 in LUAD and LUSC analyzed using the Gene Set Cancer Analysis platform. (B) Comparative analysis of LATS2 expression between tumor and normal tissues in LUAD using independent sample t-test and paired sample t-test. (C) Comparative analysis of LATS2 expression between tumor and normal tissues in LUSC using independent sample t-test and paired sample t-test. (D) Differential expression of LATS2 between LUAD and LUSC tumor tissues. (E) Immunohistochemical validation of LATS2 expression in LUAD, LUSC and normal lung tissues using the Human Protein Atlas database (antibody ID: 039191). All the data are presented as mean ± SD. ***P<0.001. LATS2, large tumor suppressor kinase 2; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; TPM, transcripts per million; RSEM, RNA-seq by expectation-maximization.

Article Snippet: Immunohistochemical images obtained from the Human Protein Atlas database indicated that the proportion of LATS2-positive cells was markedly higher in normal lung tissues compared with LUAD and LUSC tumor tissues ( ).

Techniques: Expressing, Quantitative Proteomics, Immunohistochemical staining, Biomarker Discovery, RNA Sequencing

Journal: iScience

Article Title: ExIR enables prioritizing driver and biomarker genes from omics data in a reference free manner

doi: 10.1016/j.isci.2026.116303

Figure Lengend Snippet: Differential immunoreactivity of known and novel ExIR-predicted LUAD biomarkers between normal and cancer samples (A–E) Immunohistochemical (IHC) data from the Human Protein Atlas database in LUAD and normal lung tissue for top five known LUAD biomarkers. (A) SFTPC–ExIR rank #1, LUAD (negative intensity; patient ID: 1847) and normal pneumocytes (quantity: 75%–25%; strong intensity; patient ID: 2268). (B) SPP1—ExIR rank #117, LUAD (quantity: >75%; moderate intensity; patient ID: 537) and normal pneumocytes (not detected; patient ID: 2268). (C) CBLC—ExIR rank #140, LUAD (quantity: >75%; moderate intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2417). (D) MDK—ExIR rank #247, LUAD (quantity: 75%–25%; strong intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2222). (E) MRC1 – ExIR rank #471, LUAD (undetected; patient ID: 1932) and normal macrophages (quantity: 75%–25%; strong intensity; patient ID: 2208). (F–I) IHC data of top five ExIR-predicted LUAD biomarkers (excluding SFTPC rank #1 already in a). (F) AGER – ExIR rank #2, LUAD (not detected; patient ID: 3144) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 4840). (G) EMP2 – ExIR rank #3, LUAD (not detected; patient ID: 1847) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 2101). (H) CAV1 – ExIR rank #4, LUAD (not detected; patient ID: 1249) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 2208). i, RTKN2 – ExIR rank 5, LUAD (not detected; patient ID: 3003) and normal pneumocytes (quantity: <25%; moderate intensity; patient ID: 2268).(J–N) IHC data of top six ExIR-predicted LUAD up-regulated biomarkers (excluding FAM83A rank #2, for which no IHC data was available). (J) PYCR1 – ExIR rank #1, LUAD (quantity: >75%; moderate intensity; patient ID: 2777) and normal pneumocytes (not detected; patient ID: 2208). (K) TOP2A – ExIR rank #3, LUAD (quantity: 75%–25%; strong intensity; patient ID: 3003) and normal pneumocytes (quantity: 75%–25%; weak intensity; patient ID: 2101). (L) MMP11 – ExIR rank #4, LUAD (quantity: >75%; weak intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2438). (M) TEDC2– ExIR rank 5, LUAD (quantity: 75%–25%; moderate intensity; patient ID: 4208) and normal pneumocytes (not detected; patient ID: 1470). (N) IQGAP3– ExIR rank 6, LUAD (quantity: >75%; strong intensity; patient ID: 3048) and normal pneumocytes (not detected; patient ID: 1470). Per the Human Protein Atlas database usage guidelines, the link to the immunostaining images of all of the selected proteins in normal pneumocytes and LUAD samples are included as hyperlinks within the figure legend. Ab: antibody; LUAD: lung adenocarcinoma.

Article Snippet: Per the Human Protein Atlas database usage guidelines, the link to the immunostaining images of all of the selected proteins in normal pneumocytes and LUAD samples are included as hyperlinks within the figure legend.

Techniques: Immunohistochemical staining, Immunostaining

Journal: iScience

Article Title: ExIR enables prioritizing driver and biomarker genes from omics data in a reference free manner

doi: 10.1016/j.isci.2026.116303

Figure Lengend Snippet: Differential immunoreactivity of known and novel ExIR-predicted LUAD biomarkers between normal and cancer samples (A–E) Immunohistochemical (IHC) data from the Human Protein Atlas database in LUAD and normal lung tissue for top five known LUAD biomarkers. (A) SFTPC–ExIR rank #1, LUAD (negative intensity; patient ID: 1847) and normal pneumocytes (quantity: 75%–25%; strong intensity; patient ID: 2268). (B) SPP1—ExIR rank #117, LUAD (quantity: >75%; moderate intensity; patient ID: 537) and normal pneumocytes (not detected; patient ID: 2268). (C) CBLC—ExIR rank #140, LUAD (quantity: >75%; moderate intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2417). (D) MDK—ExIR rank #247, LUAD (quantity: 75%–25%; strong intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2222). (E) MRC1 – ExIR rank #471, LUAD (undetected; patient ID: 1932) and normal macrophages (quantity: 75%–25%; strong intensity; patient ID: 2208). (F–I) IHC data of top five ExIR-predicted LUAD biomarkers (excluding SFTPC rank #1 already in a). (F) AGER – ExIR rank #2, LUAD (not detected; patient ID: 3144) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 4840). (G) EMP2 – ExIR rank #3, LUAD (not detected; patient ID: 1847) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 2101). (H) CAV1 – ExIR rank #4, LUAD (not detected; patient ID: 1249) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 2208). i, RTKN2 – ExIR rank 5, LUAD (not detected; patient ID: 3003) and normal pneumocytes (quantity: <25%; moderate intensity; patient ID: 2268).(J–N) IHC data of top six ExIR-predicted LUAD up-regulated biomarkers (excluding FAM83A rank #2, for which no IHC data was available). (J) PYCR1 – ExIR rank #1, LUAD (quantity: >75%; moderate intensity; patient ID: 2777) and normal pneumocytes (not detected; patient ID: 2208). (K) TOP2A – ExIR rank #3, LUAD (quantity: 75%–25%; strong intensity; patient ID: 3003) and normal pneumocytes (quantity: 75%–25%; weak intensity; patient ID: 2101). (L) MMP11 – ExIR rank #4, LUAD (quantity: >75%; weak intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2438). (M) TEDC2– ExIR rank 5, LUAD (quantity: 75%–25%; moderate intensity; patient ID: 4208) and normal pneumocytes (not detected; patient ID: 1470). (N) IQGAP3– ExIR rank 6, LUAD (quantity: >75%; strong intensity; patient ID: 3048) and normal pneumocytes (not detected; patient ID: 1470). Per the Human Protein Atlas database usage guidelines, the link to the immunostaining images of all of the selected proteins in normal pneumocytes and LUAD samples are included as hyperlinks within the figure legend. Ab: antibody; LUAD: lung adenocarcinoma.

Article Snippet: Additionally, immunohistochemical data for the specific lung adenocarcinoma (LUAD) subtype analyzed were available from the Human Protein Atlas.

Techniques: Immunohistochemical staining, Immunostaining

Journal: iScience

Article Title: ExIR enables prioritizing driver and biomarker genes from omics data in a reference free manner

doi: 10.1016/j.isci.2026.116303

Figure Lengend Snippet: Differential immunoreactivity of known and novel ExIR-predicted LUAD biomarkers between normal and cancer samples (A–E) Immunohistochemical (IHC) data from the Human Protein Atlas database in LUAD and normal lung tissue for top five known LUAD biomarkers. (A) SFTPC–ExIR rank #1, LUAD (negative intensity; patient ID: 1847) and normal pneumocytes (quantity: 75%–25%; strong intensity; patient ID: 2268). (B) SPP1—ExIR rank #117, LUAD (quantity: >75%; moderate intensity; patient ID: 537) and normal pneumocytes (not detected; patient ID: 2268). (C) CBLC—ExIR rank #140, LUAD (quantity: >75%; moderate intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2417). (D) MDK—ExIR rank #247, LUAD (quantity: 75%–25%; strong intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2222). (E) MRC1 – ExIR rank #471, LUAD (undetected; patient ID: 1932) and normal macrophages (quantity: 75%–25%; strong intensity; patient ID: 2208). (F–I) IHC data of top five ExIR-predicted LUAD biomarkers (excluding SFTPC rank #1 already in a). (F) AGER – ExIR rank #2, LUAD (not detected; patient ID: 3144) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 4840). (G) EMP2 – ExIR rank #3, LUAD (not detected; patient ID: 1847) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 2101). (H) CAV1 – ExIR rank #4, LUAD (not detected; patient ID: 1249) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 2208). i, RTKN2 – ExIR rank 5, LUAD (not detected; patient ID: 3003) and normal pneumocytes (quantity: <25%; moderate intensity; patient ID: 2268).(J–N) IHC data of top six ExIR-predicted LUAD up-regulated biomarkers (excluding FAM83A rank #2, for which no IHC data was available). (J) PYCR1 – ExIR rank #1, LUAD (quantity: >75%; moderate intensity; patient ID: 2777) and normal pneumocytes (not detected; patient ID: 2208). (K) TOP2A – ExIR rank #3, LUAD (quantity: 75%–25%; strong intensity; patient ID: 3003) and normal pneumocytes (quantity: 75%–25%; weak intensity; patient ID: 2101). (L) MMP11 – ExIR rank #4, LUAD (quantity: >75%; weak intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2438). (M) TEDC2– ExIR rank 5, LUAD (quantity: 75%–25%; moderate intensity; patient ID: 4208) and normal pneumocytes (not detected; patient ID: 1470). (N) IQGAP3– ExIR rank 6, LUAD (quantity: >75%; strong intensity; patient ID: 3048) and normal pneumocytes (not detected; patient ID: 1470). Per the Human Protein Atlas database usage guidelines, the link to the immunostaining images of all of the selected proteins in normal pneumocytes and LUAD samples are included as hyperlinks within the figure legend. Ab: antibody; LUAD: lung adenocarcinoma.

Article Snippet: Figure 4 Differential immunoreactivity of known and novel ExIR-predicted LUAD biomarkers between normal and cancer samples (A–E) Immunohistochemical (IHC) data from the Human Protein Atlas database in LUAD and normal lung tissue for top five known LUAD biomarkers. (A) SFTPC–ExIR rank #1, LUAD (negative intensity; patient ID: 1847) and normal pneumocytes (quantity: 75%–25%; strong intensity; patient ID: 2268). (B) SPP1—ExIR rank #117, LUAD (quantity: >75%; moderate intensity; patient ID: 537) and normal pneumocytes (not detected; patient ID: 2268). (C) CBLC—ExIR rank #140, LUAD (quantity: >75%; moderate intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2417). (D) MDK—ExIR rank #247, LUAD (quantity: 75%–25%; strong intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2222). (E) MRC1 – ExIR rank #471, LUAD (undetected; patient ID: 1932) and normal macrophages (quantity: 75%–25%; strong intensity; patient ID: 2208). (F–I) IHC data of top five ExIR-predicted LUAD biomarkers (excluding SFTPC rank #1 already in a). (F) AGER – ExIR rank #2, LUAD (not detected; patient ID: 3144) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 4840). (G) EMP2 – ExIR rank #3, LUAD (not detected; patient ID: 1847) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 2101). (H) CAV1 – ExIR rank #4, LUAD (not detected; patient ID: 1249) and normal pneumocytes (quantity: >75%; strong intensity; patient ID: 2208). i, RTKN2 – ExIR rank 5, LUAD (not detected; patient ID: 3003) and normal pneumocytes (quantity: <25%; moderate intensity; patient ID: 2268). (J–N) IHC data of top six ExIR-predicted LUAD up-regulated biomarkers (excluding FAM83A rank #2, for which no IHC data was available). (J) PYCR1 – ExIR rank #1, LUAD (quantity: >75%; moderate intensity; patient ID: 2777) and normal pneumocytes (not detected; patient ID: 2208). (K) TOP2A – ExIR rank #3, LUAD (quantity: 75%–25%; strong intensity; patient ID: 3003) and normal pneumocytes (quantity: 75%–25%; weak intensity; patient ID: 2101). (L) MMP11 – ExIR rank #4, LUAD (quantity: >75%; weak intensity; patient ID: 1847) and normal pneumocytes (not detected; patient ID: 2438). (M) TEDC2– ExIR rank 5, LUAD (quantity: 75%–25%; moderate intensity; patient ID: 4208) and normal pneumocytes (not detected; patient ID: 1470). (N) IQGAP3– ExIR rank 6, LUAD (quantity: >75%; strong intensity; patient ID: 3048) and normal pneumocytes (not detected; patient ID: 1470).

Techniques: Immunohistochemical staining, Immunostaining

Journal: iScience

Article Title: M2 macrophage associated genes shape prognosis and tumor progression in human colorectal cancer

doi: 10.1016/j.isci.2026.116230

Figure Lengend Snippet: NPL, DCTPP1, and PLTP significantly affected M2 macrophage polarization and CRC cells tumorigenesis (A) Overlap between M2Gs and M2 macrophage marker genes. (B) Relative expression of CTSD , TUBB , FABP5 , PLTP , NPL , and DCTPP1 in M0-like, M1-like, and M2-like macrophages. (C) Immunohistochemical staining of CD163, PLTP, NPL, and DCTPP1 in colorectal cancer tissues, n = 8. (D) Schematic of THP-1-derived M2-like macrophage polarization. (E and F) Proliferation and apoptosis of HCT116 cells cultured with conditioned medium from Ctrl or siNDP macrophages, n = 3. (G and H) Schematic and representative images of Transwell migration and Matrigel invasion assays. (I) Representative flow cytometry plots of CD11b and CD163 expression in macrophages under the indicated treatments, n = 3. (J and K) Ki67 immunofluorescence and quantification in HCT116 cells cultured with conditioned media from the indicated groups, n = 3. Ctrl, control siRNA; PMA-ctrl, PMA-differentiated macrophages without IL-10; siNDP, equal-molar mixture of siRNAs targeting NPL, DCTPP1, and PLTP. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. Scale bars, 100 μm unless otherwise indicated.

Article Snippet: We paraffin-embedded colon and rectal cancer tissues and performed immunohistochemical staining following tissue sections using an Immunohistochemical Kit (Sangon Biotech, Cat# D601037) according to the manufacturer’s instructions.

Techniques: Marker, Expressing, Immunohistochemical staining, Staining, Derivative Assay, Cell Culture, Migration, Flow Cytometry, Immunofluorescence, Control