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Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Inflammation01:38

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Updated: Jul 4, 2026

Surface Engineering of Pancreatic Islets with a Heparinized StarPEG Nanocoating
05:35

Surface Engineering of Pancreatic Islets with a Heparinized StarPEG Nanocoating

Published on: June 23, 2018

Islets surface modification prevents blood-mediated inflammatory responses.

Yuji Teramura1, Hiroo Iwata

  • 1Department of Nano-Medicine Merger Education Unit, Graduate School of Engineering, Kyoto University, and Institute for Frontier Medical Sciences, Kyoto University, 53 Kawara-cho, Shogoin, Sakyo-ku, Kyoto, 606-8507, Japan.

Bioconjugate Chemistry
|June 7, 2008
PubMed
Summary

Researchers developed a novel method to coat pancreatic islets with urokinase or heparin, preventing blood clots and inflammation. This surface modification shows promise for improving islet transplantation success in treating type 1 diabetes.

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Last Updated: Jul 4, 2026

Surface Engineering of Pancreatic Islets with a Heparinized StarPEG Nanocoating
05:35

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Published on: June 23, 2018

Mitigation of Blood Borne Cell Attachment to Metal Implants through CD47-Derived Peptide Immobilization
08:13

Mitigation of Blood Borne Cell Attachment to Metal Implants through CD47-Derived Peptide Immobilization

Published on: December 3, 2020

Area of Science:

  • Biomedical Engineering
  • Transplantation Immunology
  • Endocrinology

Background:

  • Islet transplantation is a key treatment for type 1 diabetes.
  • Early graft loss due to thrombosis and inflammation remains a significant challenge.
  • Preventing blood coagulation on transplanted islets is crucial for graft survival.

Purpose of the Study:

  • To develop a versatile surface modification for islets to prevent early graft loss.
  • To functionalize islet surfaces with fibrinolytic or anticoagulant agents.
  • To assess the impact of surface modification on islet function and viability.

Main Methods:

  • Islets were surface-modified using a layer-by-layer approach with biotin-PEG-lipids, streptavidin, and biotin-bovine serum albumin.
  • The modified surface was activated with oxidized dextran.
  • Urokinase or heparin was anchored to the islet surface via Schiff base formation or polyion complex formation, respectively.

Main Results:

  • Surface modification did not significantly increase islet volume.
  • Modified islets maintained insulin release in response to glucose stimulation.
  • Anchored urokinase demonstrated high fibrinolytic activity, suggesting potential to prevent thrombosis.

Conclusions:

  • A versatile method for modifying islet surfaces with urokinase or heparin was successfully developed.
  • The surface modification effectively prevents thrombosis without impairing islet function.
  • This approach holds significant potential for improving islet graft survival in type 1 diabetes treatment.