Results 241 to 250 of about 204,813 (306)

Endothelial Hydrogels Improve Microvascular Regeneration and Perfusion in Tracheal Scaffolds

open access: yesThe Laryngoscope, EarlyView.
Insufficient vascularization remains a major barrier to successful tracheal transplantation. This study demonstrates that an endothelial hydrogel significantly enhances graft perfusion and neovessel organization compared to non‐endothelial hydrogel controls.
Molly O. Hunter   +6 more
wiley   +1 more source

Substrate stiffness and shear stress collectively regulate the inflammatory phenotype in cultured human brain microvascular endothelial cells. [PDF]

open access: yesFluids Barriers CNS
Yates AK   +8 more
europepmc   +1 more source

Validity of the elastase assay in intensive care medicine [PDF]

open access: yes, 1988
Fritz, Hans   +5 more
core  

Convergence of Organ‐on‐a‐Chip and Freeform Printing of Sacrificial Poly(2‐cyclopropyl‐2‐oxazoline) Enables the Generation of Perfusable Endothelialized Channels in Hydrogels

open access: yesMacromolecular Rapid Communications, EarlyView.
We employ freeform printing of thermo‐responsive poly(2‐oxazoline) to directly fabricate suspended sacrificial vascular templates within Organ‐on‐a‐chip devices. This enables circular, perfusable channels down to 200 µm without post‐processing.
Giulia Maria Di Gravina   +7 more
wiley   +1 more source

Diabetic Peripheral Neuropathy: Molecular Staging, Risk Factors, Therapeutics, and Emerging Trends

open access: yesMed Research, EarlyView.
The heterogeneous landscape of DPN can be unified through a tripartite pathogenic model encompassing progressive stages of metabolic dysregulation, chronic inflammation, and overt neuronal damage. Within this framework, six clinical subtypes were identified, namely, hyperglycemia‐driven, dyslipidemia‐driven, inflammation‐driven, dysvascularity‐driven ...
Xiaofeng Dai, Mingze Tang
wiley   +1 more source

Inflammation, Immunity, and Cardiovascular Diseases

open access: yesMed Research, EarlyView.
Cardiovascular stress signals (e.g., hemodynamic shear, oxidized lipids, and ischemia) act on endothelial and immune cells to activate and amplify inflammation through NF‐κB, the NLRP3 inflammasome, and JAK/STAT signaling, inducing proinflammatory cytokines/chemokines (IL‐6, IL‐1β, TNF‐α, and CCL2) and self‐amplifying circuits; clinically, inflammatory
Dezhi Guo   +8 more
wiley   +1 more source

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