Skin: Histology and Physiology of Wound Healing

2012 ◽  
Vol 39 (1) ◽  
pp. 85-97 ◽  
Author(s):  
Eric A. Gantwerker ◽  
David B. Hom
Keyword(s):  
Wound Healing ◽  
Skin Histology

Skin: Histology and Physiology of Wound Healing

2011 ◽  
Vol 19 (3) ◽  
pp. 441-453 ◽  
Author(s):  
Eric A. Gantwerker ◽  
David B. Hom
Keyword(s):  
Wound Healing ◽  
Skin Histology

ultrastructural process of intestinal wound healing

1995 ◽  
Vol 53 ◽  
pp. 1024-1025
Author(s):  
Rick L. Vaughn ◽  
Shailendra K. Saxena ◽  
John G. Sharp
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Smooth Muscles ◽  
Microscopic Level ◽  
Light Microscopic Level ◽  
Ileal Mucosa ◽  
Wound Model ◽  
Serosal Surface ◽  
Complex Process ◽  
Orderly Fashion

We have developed an intestinal wound model that includes surgical construction of an ileo-cecal patch to study the complex process of intestinal wound healing. This allows approximation of ileal mucosa to the cecal serosa and facilitates regeneration of ileal mucosa onto the serosal surface of the cecum. The regeneration of ileal mucosa can then be evaluated at different times. The wound model also allows us to determine the rate of intestinal regeneration for a known size of intestinal wound and can be compared in different situations (e.g. with and without EGF and Peyer’s patches).At the light microscopic level it appeared that epithelial cells involved in regeneration of ileal mucosa originated from the enlarged crypts adjacent to the intestinal wound and migrated in an orderly fashion onto the serosal surface of the cecum. The migrating epithelial cells later formed crypts and villi by the process of invagination and evagination respectively. There were also signs of proliferation of smooth muscles underneath the migratory epithelial cells.

Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell
Keyword(s):  
Wound Healing ◽  
Liver Disease ◽  
Hepatic Fibrosis ◽  
Cell Activation ◽  
Stellate Cell ◽  
Factor Xa ◽  
Clinical Trial Data ◽  
Chronic Liver ◽  
Healing Response ◽  
Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

Sign in / Sign up

Export Citation Format

Share Document