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ImmuneCited

Processus de recherche

333 figures issues de recherches évaluées par des pairs

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Figure 13. C-reactive protein: fixed-effects meta-analysis and forest plot from studies providing supplementation of glutamine.
Figure 20 Forest Plot

C-reactive protein levels following glutamine supplementation are pooled in a fixed-effects forest plot. Lower CRP values suggest reduced systemic inflammation, which may contribute to improved wound healing outcomes.

The Effect of Amino Acids on Wound Healing: A Systematic Review and …

Figure 21
Figure 21 Forest Plot

An additional inflammatory or immune marker from the glutamine meta-analysis is displayed in forest plot format. The pooled analysis evaluates whether glutamine supplementation modulates immune parameters relevant to wound repair.

The Effect of Amino Acids on Wound Healing: A Systematic Review and …

Figure 22
Figure 22 Forest Plot

Further meta-analysis results present pooled effect sizes for wound healing parameters in glutamine-supplemented patients. The forest plot format allows visual comparison of effect magnitude and consistency across trials.

The Effect of Amino Acids on Wound Healing: A Systematic Review and …

Figure 15. T-cell lymphocytes: fixed-effects meta-analysis and forest plot from studies providing supplementation of glutamine.
Figure 23 Forest Plot

T-cell lymphocyte counts are analyzed in a fixed-effects forest plot across glutamine supplementation trials. Enhanced T-cell proliferation is associated with improved immune-mediated wound repair, and the pooled estimate evaluates glutamine's immunomodulatory potential.

The Effect of Amino Acids on Wound Healing: A Systematic Review and …

Figure 3
Figure 3 Chart

Rheological and mechanical characterization of the click chemistry hydrogel demonstrates properties suitable for 3D bioprinting. The material's shear-thinning behavior and rapid recovery enable precise deposition of cell-laden constructs.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 4
Figure 4 Photograph

Bioprinting parameters and construct fidelity are evaluated for the peptide hydrogel system. The printability assessment confirms that the material maintains structural integrity while supporting embedded vascular endothelial cell viability.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 5
Figure 5 Micrograph

VEGF165-overexpressing endothelial cells encapsulated within the hydrogel are assessed for viability and vascular network formation. The growth factor expression aims to promote angiogenesis, addressing the vascular injury central to non-healing diabetic wounds.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 6
Figure 6 Micrograph

In vitro wound healing assays using the bioprinted hydrogel constructs demonstrate enhanced cell migration and proliferation. The results suggest that the all-peptide platform supports the cellular processes required for tissue regeneration.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 7
Figure 7 Chart

Gene expression or protein analysis from cells cultured in the hydrogel platform reveals upregulation of angiogenic and wound healing markers. The molecular data support the functional benefits observed in cell migration and proliferation assays.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 8
Figure 8 Photograph

In vivo evaluation of the bioprinted hydrogel in a diabetic wound model shows wound closure progression over time. The cell-laden constructs demonstrate accelerated healing compared to control treatments in the high-glucose wound environment.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 9
Figure 9 Micrograph

Histological analysis of healed wound tissue reveals improved tissue architecture and vascularization in the hydrogel-treated group. Hematoxylin and eosin staining shows more organized collagen deposition and reduced inflammatory infiltrate.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 10
Figure 10 Micrograph

Immunohistochemical staining of wound sections confirms enhanced angiogenesis in hydrogel-treated diabetic wounds. Markers for vascular endothelial cells and smooth muscle cells indicate formation of functional blood vessels in the regenerated tissue.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 11
Figure 11 Chart

Quantitative analysis of wound healing outcomes compares the bioprinted hydrogel against conventional treatments. Metrics including wound closure rate, collagen density, and vessel density are significantly improved in the treatment group.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 12
Figure 12

Supplementary characterization or additional in vivo data from the click chemistry hydrogel study is presented. The comprehensive evaluation supports the platform's potential for translational application in diabetic wound management.

A click chemistry-mediated all-peptide cell printing hydrogel platform for diabetic wound healing.

Figure 1. Gut dysbiosis promotes intestinal and systemic inflammation with consequently Aβ aggregation and neuroinflammation finally leading to neurodegeneration and Alzheimer’s disease. Abbreviations: Aβ = amyloid beta; PP = polyphenols; SCFA = short chain
Figure 6 Diagram

A pathway diagram illustrates how gut dysbiosis promotes intestinal and systemic inflammation, leading to amyloid-beta aggregation, neuroinflammation, and ultimately neurodegeneration in Alzheimer's disease. The cascade connects microbial imbalance to blood-brain barrier compromise and central nervous system pathology.

The Immunopathogenesis of Alzheimer's Disease Is Related to the Composition of Gut …

Figure 2. Change of the microbiome (e.g., by Western diet) resulting in intestinal dysbiosis leads to low grade inflammation in the gut and to increased intestinal and BBB permeability and consecutively to neuroinflammation and cognitive decline; oral patho
Figure 7 Diagram

Western diet-induced microbiome changes are mapped to intestinal dysbiosis, low-grade gut inflammation, and increased permeability of both the intestinal barrier and blood-brain barrier. The resulting systemic inflammatory state is linked to neuroinflammatory processes implicated in Alzheimer's disease progression.

The Immunopathogenesis of Alzheimer's Disease Is Related to the Composition of Gut …

Compared with NDU wounds, the Hippo-YAP pathway in DFU wounds was found to be significantly inhibited (Fig. 2A). Then we explored the detailed molecular mechanism of this phenomenon. The DNA scaffold of NETs can be hydrolyzed by
Figure 3 Diagram

The molecular mechanism linking NET-derived DNA to Hippo-YAP pathway inhibition and endothelial-to-mesenchymal transition is elucidated, with DNase treatment as a potential therapeutic approach.

Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via …

Figure 4
Figure 4 Chart

In vitro endothelial-to-mesenchymal transition markers are quantified following NET exposure, demonstrating increased mesenchymal and decreased endothelial protein expression.

Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via …

Figure 5
Figure 5 Chart

YAP phosphorylation and nuclear exclusion in NET-treated endothelial cells are characterized, linking NET exposure to Hippo pathway activation.

Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via …

Figure 6
Figure 6 Chart

Wound healing outcomes in Padi4-knockout diabetic mice compared to wild-type controls are documented, showing accelerated closure when NET formation is genetically ablated.

Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via …

Figure 7
Figure 7 Micrograph

Histological analysis of wound tissue from NET-depleted and control diabetic mice reveals improved re-epithelialization and vascularization.

Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via …

Figure 8
Figure 8 Chart

DNase I treatment effects on diabetic wound healing in vivo are quantified, demonstrating that NET degradation promotes wound closure through preserved endothelial function.

Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via …

Figure 9
Figure 9 Diagram

A proposed model integrating NET-mediated Hippo pathway suppression with endothelial-to-mesenchymal transition in delayed diabetic wound healing is diagrammed.

Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via …

Fig. 1. The underlying mechanism of depression. Brain insulin resistance develops due to the failure of brain cells to respond to insulin activity. The hippocampus, hypothalamus, and cortex regions of the central nervous system regulate insulin levels in
Figure 3 Diagram

Brain insulin resistance mechanisms underlying depression are depicted, showing how HPA axis dysregulation, reduced anterior cingulate cortex volume, and impaired hippocampal function contribute to the condition.

A review on linking stress, depression, and insulin resistance via low-grade chronic …

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