A sustainable production method of mycelium biomass using an isolated fungal strain Phanerochaete chrysosporium (accession no: KY593186): Its exploitation in wound healing patch formation

2018 ◽  
Vol 16 ◽  
pp. 548-557 ◽  
Author(s):  
Moumita Khamrai ◽  
Sovan Lal Banerjee ◽  
Patit Paban Kundu
Author(s):  
Rick L. Vaughn ◽  
Shailendra K. Saxena ◽  
John G. Sharp

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.


Author(s):  
Chihiro Kaito ◽  
Yoshio Saito

The direct evaporation of metallic oxides or sulfides does not always given the same compounds with starting material, i.e. decomposition took place. Since the controll of the sulfur or selenium vapors was difficult, a similar production method for oxide particles could not be used for preparation of such compounds in spite of increasing interest in the fields of material science, astrophysics and mineralogy. In the present paper, copper metal was evaporated from a molybdenum silicide heater which was proposed by us to produce the ultra-fine particles in reactive gas as shown schematically in Figure 1. Typical smoke by this method in Ar gas at a pressure of 13 kPa is shown in Figure 2. Since the temperature at a location of a few mm below the heater, maintained at 1400° C , were a few hundred degrees centigrade, the selenium powder in a quartz boat was evaporated at atmospheric temperature just below the heater. The copper vapor that evaporated from the heater was mixed with the stream of selenium vapor,and selenide was formed near the boat. If then condensed by rapid cooling due to the collision with inert gas, thus forming smoke similar to that from the metallic sulfide formation. Particles were collected and studied by a Hitachi H-800 electron microscope.Figure 3 shows typical EM images of the produced copper selenide particles. The morphology was different by the crystal structure, i.e. round shaped plate (CuSe;hexagona1 a=0.39,C=l.723 nm) ,definite shaped p1 ate(Cu5Se4;Orthorhombic;a=0.8227 , b=1.1982 , c=0.641 nm) and a tetrahedron(Cu1.8Se; cubic a=0.5739 nm). In the case of compound ultrafine particles there have been no observation for the particles of the tetrahedron shape. Since the crystal structure of Cu1.8Se is the anti-f1uorite structure, there has no polarity.


2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell

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.


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