Chitosan/PDLLA-PEG-PDLLA solution preparation by simple stirring and formation into a hydrogel at body temperature for whole wound healing

Abstract Objective: Recently, antibiotic resistance of post-burn infections caused by opportunistic pathogens, Pseudomonas aeruginosa, became complicated due to its innate and acquired resistance. Bacteriophage therapy containing virulent factors that infect their specific host bacteria can be evaluated as an alternative treatment.In this study,the topical formulation contains lytic phages compared to the antibioticinthe murine model of burn/infected wound healing.Methods & Materials: Lytic bacteriophages were extracted from hospital sewage and propagated in broth culture of P.aeruginosa(24 hours, 37°C) and subsequently filtered.The collected phages were recultured alongside P. aeruginosa. The plaques were observed as clear zones and added to the polyethylene glycol (PEG) base ointment. Twenty-four adult female mice were selected and divided into four groups. Asecond-degree burn wound wascreated on the back of the mice and infected with 100 microliters of 1×102 - 3×102 CFU/ml P. aeruginosa subcutaneously. After 24 hours, each group received one of these interventions: silver sulfadiazine, ointment contains bacteriophage, ointment without bacteriophage (PEG group),or no treatment. Burn wound size, physical activity, and body temperature (rectal) were recorded every other day. On the 10th day, mice were sacrificed through cervical dislocation. Thewound’s skin was cut and evaluated histopathologically.Results: Significant differences inthe burn wound sizeamongthe bacteriophage groupversus the PEG group, the bacteriophage group versus the no-treatment group, and the antibiotic group versus the PEG group (P= 0.001, P= 0.001, P= 0.002 respectively)were observed. Mice’s physical activity was gradually improved in all groups and showed significant differences (P<0.001). Body temperature analyses showed significantdifferences only when day 8th compared with day 2nd, 4th, and 6th (P=0.001, P=0.02, P=0.02 respectively). Histopathological results indicated optimal wound healing in both the antibiotic group and bacteriophage group. However, no significant differences were observed in microscopic histopathological criteria in any groups based on Fisher’s exact statistical tests.Conclusion:Formulated phage ointmenteffectivelyprevents and treats burn wound infection in mice with no allergic reactions.

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Scanning Electron Microscopy and X-Ray Analyses of Dental Tissues from a Hibernator

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100090877 ◽

1976 ◽

Vol 34 ◽

pp. 178-179

Author(s):

M. L. Zimny ◽

A. C. Haller

Keyword(s):

Electron Microscopy ◽

Scanning Electron Microscopy ◽

Body Temperature ◽

Ground Squirrel ◽

Alveolar Bone ◽

X Ray ◽

Dental Tissues ◽

Bone Minerals ◽

Apical Tooth ◽

Scanning Electron

During hibernation the ground squirrel is immobile, body temperature reduced and metabolism depressed. Hibernation has been shown to affect dental tissues varying degrees, although not much work has been done in this area. In limited studies, it has been shown that hibernation results in (1) mobilization of bone minerals; (2) deficient dentinogenesis and degeneration of alveolar bone; (3) presence of calculus and tears in the cementum; and (4) aggrevation of caries and pulpal and apical tooth abscesses. The purpose of this investigation was to study the effects of hibernation on dental tissues employing scanning electron microscopy (SEM) and related x-ray analyses.

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ultrastructural process of intestinal wound healing

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100141494 ◽

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.

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

Clinical Science ◽

10.1042/cs20191102 ◽

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.

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