Image 8_Potential marker genes for psoriasis revealed based on single-cell sequencing and Mendelian randomization analysis.tif by Ying Dong (41989)

“…Among them, BIN2 and CAPN12 were linked to an increased risk, while genes such as CXXC5 and KLRD1 were associated with decreased risk. …”

Image 11_Potential marker genes for psoriasis revealed based on single-cell sequencing and Mendelian randomization analysis.tif by Ying Dong (41989)

“…Among them, BIN2 and CAPN12 were linked to an increased risk, while genes such as CXXC5 and KLRD1 were associated with decreased risk. …”

Image 3_Potential marker genes for psoriasis revealed based on single-cell sequencing and Mendelian randomization analysis.tif by Ying Dong (41989)

“…Among them, BIN2 and CAPN12 were linked to an increased risk, while genes such as CXXC5 and KLRD1 were associated with decreased risk. …”

Table 2_Potential marker genes for psoriasis revealed based on single-cell sequencing and Mendelian randomization analysis.xlsx by Ying Dong (41989)

“…Among them, BIN2 and CAPN12 were linked to an increased risk, while genes such as CXXC5 and KLRD1 were associated with decreased risk. …”

Table 5_Potential marker genes for psoriasis revealed based on single-cell sequencing and Mendelian randomization analysis.xlsx by Ying Dong (41989)

“…Among them, BIN2 and CAPN12 were linked to an increased risk, while genes such as CXXC5 and KLRD1 were associated with decreased risk. …”

Image 2_Potential marker genes for psoriasis revealed based on single-cell sequencing and Mendelian randomization analysis.tif by Ying Dong (41989)

“…Among them, BIN2 and CAPN12 were linked to an increased risk, while genes such as CXXC5 and KLRD1 were associated with decreased risk. …”

Table 4_Potential marker genes for psoriasis revealed based on single-cell sequencing and Mendelian randomization analysis.xlsx by Ying Dong (41989)

“…Among them, BIN2 and CAPN12 were linked to an increased risk, while genes such as CXXC5 and KLRD1 were associated with decreased risk. …”

Table 8_Potential marker genes for psoriasis revealed based on single-cell sequencing and Mendelian randomization analysis.xlsx by Ying Dong (41989)

“…Among them, BIN2 and CAPN12 were linked to an increased risk, while genes such as CXXC5 and KLRD1 were associated with decreased risk. …”

Image 4_Potential marker genes for psoriasis revealed based on single-cell sequencing and Mendelian randomization analysis.tif by Ying Dong (41989)

“…Among them, BIN2 and CAPN12 were linked to an increased risk, while genes such as CXXC5 and KLRD1 were associated with decreased risk. …”

Table 4_Establishment and validation of the prediction model based on lymphocyte subsets for acute kidney injury in sepsis patients.docx by Leyi Wang (408009)

“…Laboratory findings showed higher neutrophil and monocyte counts, and elevated serum creatinine in the AKI group. On day 1, several lymphocyte subsets were significantly altered in the AKI group, including increased CD4⁺CD38⁺T%, CD8⁺CD38⁺T%, CD155⁺T%, CD4⁺TeM⁺T%, CD8⁺TIGIT⁺T%, and M-MDSC, and decreased CD4⁺LAG3⁺T%, CD4⁺TN⁺T%, and Th17 cells. …”

Table 2_Establishment and validation of the prediction model based on lymphocyte subsets for acute kidney injury in sepsis patients.docx by Leyi Wang (408009)

“…Laboratory findings showed higher neutrophil and monocyte counts, and elevated serum creatinine in the AKI group. On day 1, several lymphocyte subsets were significantly altered in the AKI group, including increased CD4⁺CD38⁺T%, CD8⁺CD38⁺T%, CD155⁺T%, CD4⁺TeM⁺T%, CD8⁺TIGIT⁺T%, and M-MDSC, and decreased CD4⁺LAG3⁺T%, CD4⁺TN⁺T%, and Th17 cells. …”

Table 5_Establishment and validation of the prediction model based on lymphocyte subsets for acute kidney injury in sepsis patients.docx by Leyi Wang (408009)

“…Laboratory findings showed higher neutrophil and monocyte counts, and elevated serum creatinine in the AKI group. On day 1, several lymphocyte subsets were significantly altered in the AKI group, including increased CD4⁺CD38⁺T%, CD8⁺CD38⁺T%, CD155⁺T%, CD4⁺TeM⁺T%, CD8⁺TIGIT⁺T%, and M-MDSC, and decreased CD4⁺LAG3⁺T%, CD4⁺TN⁺T%, and Th17 cells. …”

Table 6_Establishment and validation of the prediction model based on lymphocyte subsets for acute kidney injury in sepsis patients.docx by Leyi Wang (408009)

“…Laboratory findings showed higher neutrophil and monocyte counts, and elevated serum creatinine in the AKI group. On day 1, several lymphocyte subsets were significantly altered in the AKI group, including increased CD4⁺CD38⁺T%, CD8⁺CD38⁺T%, CD155⁺T%, CD4⁺TeM⁺T%, CD8⁺TIGIT⁺T%, and M-MDSC, and decreased CD4⁺LAG3⁺T%, CD4⁺TN⁺T%, and Th17 cells. …”

Table 3_Establishment and validation of the prediction model based on lymphocyte subsets for acute kidney injury in sepsis patients.docx by Leyi Wang (408009)

“…Laboratory findings showed higher neutrophil and monocyte counts, and elevated serum creatinine in the AKI group. On day 1, several lymphocyte subsets were significantly altered in the AKI group, including increased CD4⁺CD38⁺T%, CD8⁺CD38⁺T%, CD155⁺T%, CD4⁺TeM⁺T%, CD8⁺TIGIT⁺T%, and M-MDSC, and decreased CD4⁺LAG3⁺T%, CD4⁺TN⁺T%, and Th17 cells. …”

Image8_Neuroprotective effects of a novel peptide through the Rho-integrin-Tie2 and PI3K/Akt pathways in experimental autoimmune encephalomyelitis model.JPEG by Wen Zhou (49050)

“…It also alleviated inflammatory responses, including microglial activation and leukocyte infiltration, relieved the impairment of the brain blood barrier and edema, and reduced neuronal apoptosis, axonal loss, and demyelination induced by EAE. The C16 peptide increased the expressions of pTie-2 and Tie-2, integrin αvβ3, and α5β1 and activated the PI3K/Akt signal pathway but decreased the expression of Rho. …”

Image10_Neuroprotective effects of a novel peptide through the Rho-integrin-Tie2 and PI3K/Akt pathways in experimental autoimmune encephalomyelitis model.JPEG by Wen Zhou (49050)

“…It also alleviated inflammatory responses, including microglial activation and leukocyte infiltration, relieved the impairment of the brain blood barrier and edema, and reduced neuronal apoptosis, axonal loss, and demyelination induced by EAE. The C16 peptide increased the expressions of pTie-2 and Tie-2, integrin αvβ3, and α5β1 and activated the PI3K/Akt signal pathway but decreased the expression of Rho. …”

Image5_Neuroprotective effects of a novel peptide through the Rho-integrin-Tie2 and PI3K/Akt pathways in experimental autoimmune encephalomyelitis model.jpeg by Wen Zhou (49050)

“…It also alleviated inflammatory responses, including microglial activation and leukocyte infiltration, relieved the impairment of the brain blood barrier and edema, and reduced neuronal apoptosis, axonal loss, and demyelination induced by EAE. The C16 peptide increased the expressions of pTie-2 and Tie-2, integrin αvβ3, and α5β1 and activated the PI3K/Akt signal pathway but decreased the expression of Rho. …”

Image4_Neuroprotective effects of a novel peptide through the Rho-integrin-Tie2 and PI3K/Akt pathways in experimental autoimmune encephalomyelitis model.JPEG by Wen Zhou (49050)

“…It also alleviated inflammatory responses, including microglial activation and leukocyte infiltration, relieved the impairment of the brain blood barrier and edema, and reduced neuronal apoptosis, axonal loss, and demyelination induced by EAE. The C16 peptide increased the expressions of pTie-2 and Tie-2, integrin αvβ3, and α5β1 and activated the PI3K/Akt signal pathway but decreased the expression of Rho. …”

Image2_Neuroprotective effects of a novel peptide through the Rho-integrin-Tie2 and PI3K/Akt pathways in experimental autoimmune encephalomyelitis model.JPEG by Wen Zhou (49050)

“…It also alleviated inflammatory responses, including microglial activation and leukocyte infiltration, relieved the impairment of the brain blood barrier and edema, and reduced neuronal apoptosis, axonal loss, and demyelination induced by EAE. The C16 peptide increased the expressions of pTie-2 and Tie-2, integrin αvβ3, and α5β1 and activated the PI3K/Akt signal pathway but decreased the expression of Rho. …”

Image6_Neuroprotective effects of a novel peptide through the Rho-integrin-Tie2 and PI3K/Akt pathways in experimental autoimmune encephalomyelitis model.JPEG by Wen Zhou (49050)

“…It also alleviated inflammatory responses, including microglial activation and leukocyte infiltration, relieved the impairment of the brain blood barrier and edema, and reduced neuronal apoptosis, axonal loss, and demyelination induced by EAE. The C16 peptide increased the expressions of pTie-2 and Tie-2, integrin αvβ3, and α5β1 and activated the PI3K/Akt signal pathway but decreased the expression of Rho. …”