scholarly journals Corneal light scattering following excimer laser surgery

2008 ◽  
Author(s):  
Dirk De Brouwere
Keyword(s):  
Wound Healing ◽  
Light Scattering ◽  
Theoretical Model ◽  
Image Quality ◽  
Excimer Laser ◽  
Laser Surgery ◽  
Morphological Changes ◽  
Optical Parameters ◽  
Foam Layer ◽  
Healing Response

Introduction Increased corneal scattering is assumed to be a considerable side-effectof refractive surgery due to the postoperative healing response after photoablativesurface treatments. Clinically, corneal scattering is associated with haze development.Corneal haze is subjectively evaluated method based on the observation of the lightbackscattered on the cornea as seen under a slit lamp. However, corneal light scatteringaffects the retinal image quality only by its forward scattering component. The scopeof this thesis is to evaluate the the effect of corneal light scattering on the retinal imagequality, specifically in relation to the morphological changes in the cornea followingexcimer laser surgery.Methods Initially, the optical mechanisms of the image formation on the retina arediscussed. Following, the optical parameters of the corneal morphology are characterizedto form a theoretical model describing the forward light scattering in the cornea.Simulation of this theoretical model is done by a physical model of light scatteringon microspheres. This model is evaluated both by psychophysical and optical measurements.Further, we compared the use of two psychophysical and three opticalmethods to evaluate both the amount of light scattered in the cornea and the angulardistribution of the scattered light.Results Based on histological data of stained corneal samples and in vivo confocalmicroscopy, the morphologic corneal changes addressed to the wound healing responseare induced by the activation of keratocytes, inhibiting a newly formed unorganizedcollagen layer, a scar tissue called the foam layer. The theoretical models developed in this thesis reveal the presence of scattering particles that cause a local distortion of theincoming wavefront. The point spread function of this scattered wavefront is stronglyforward distributed with a full width at the half maximum of approximately 20 minutesof arc. After refractive treatments, the light scattering increases until 1 month aftertreatment, reducing to a long term moderate level of increased light scattering after6 months. Moreover, we derived that where, in a healthy cornea approximately 20percent of the incoming light is scattered, this value increases up to 70 percent forcorneas with marked haze. Furthermore, psychophysical data suggest that the amountof light scattered over angles from 5 to 10 degrees increases in a similar extend asobserved in the ageing eye.Conclusion The wound healing response of the cornea on photorefractive ablationtreatments result in an increase of corneal scattering. The light distribution of thisscattered light is narrowly forward peaked. Correlation of the foam layer with amountof forward light scattering suggests that the increased corneal scattering followingrefractive surgery mainly originates on this foam layer. Therefore, a correct postoperativecare of the cornea following excimer laser surgery is detrimental for an optimalretinal image quality. The effect of light scattering in the eye results on a lowering ofthe contrast sensitivity and an increased disability glare around light sources in nightvision.

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.

Modulation Of Wound Healing Response In Chronic Irradiated Tissues

1993 ◽  
Vol 20 (3) ◽  
pp. 465-472 ◽  
Author(s):  
Thomas A. Mustoe ◽  
Beatriz H. Porras-Reyes
Keyword(s):  
Wound Healing ◽  
Healing Response ◽  
Wound Healing Response

The Anti-tumor Activity and Mechanisms of rLj-RGD3 on Human Laryngeal Squamous Carcinoma Hep2 Cells

2020 ◽  
Vol 19 (17) ◽  
pp. 2108-2119
Author(s):  
Yang Jin ◽  
Li Lv ◽  
Shu-Xiang Ning ◽  
Ji-Hong Wang ◽  
Rong Xiao
Keyword(s):  
Wound Healing ◽  
Western Blot ◽  
Morphological Changes ◽  
In Vivo Studies ◽  
Migration And Invasion ◽  
Tunel Staining ◽  
Dna Ladder ◽  
Western Blot Assay

Background: Laryngeal Squamous Cell Carcinoma (LSCC) is a malignant epithelial tumor with poor prognosis and its incidence rate increased recently. rLj-RGD3, a recombinant protein cloned from the buccal gland of Lampetra japonica, contains three RGD motifs that could bind to integrins on the tumor cells. Methods: MTT assay was used to detect the inhibitory rate of viability. Giemsa’s staining assay was used to observe the morphological changes of cells. Hoechst 33258 and TUNEL staining assay, DNA ladder assay were used to examine the apoptotic. Western blot assay was applied to detect the change of the integrin signal pathway. Wound-healing assay, migration, and invasion assay were used to detect the mobility of Hep2 cells. H&E staining assay was used to show the arrangement of the Hep2 cells in the solid tumor tissues. Results: In the present study, rLj-RGD3 was shown to inhibit the viability of LSCC Hep2 cells in vitro by inducing apoptosis with an IC50 of 1.23µM. Western blot showed that the apoptosis of Hep2 cells induced by rLj- RGD3 was dependent on the integrin-FAK-Akt pathway. Wound healing, transwells, and western blot assays in vitro showed that rLj-RGD3 suppressed the migration and invasion of Hep2 cells by integrin-FAKpaxillin/ PLC pathway which could also affect the cytoskeleton arrangement in Hep2 cells. In in vivo studies, rLj-RGD3 inhibited the growth, tumor volume, and weight, as well as disturbed the tissue structure of the solid tumors in xenograft models of BALB/c nude mice without reducing their body weights. Conclusion: hese results suggested that rLj-RGD3 is an effective and safe suppressor on the growth and metastasis of LSCC Hep2 cells from both in vitro and in vivo experiments. rLj-RGD3 might be expected to become a novel anti-tumor drug to treat LSCC patients in the near future.

Corneal Femtosecond Laser Keratotomy Results in Isolated Stromal Injury and Favorable Wound-Healing Response

2007 ◽  
Vol 48 (5) ◽  
pp. 2068 ◽  
Author(s):  
Christian Meltendorf ◽  
Guido J. Burbach ◽  
Jens Bu¨hren ◽  
Reinhold Bug ◽  
Christian Ohrloff ◽  
...  
Keyword(s):  
Wound Healing ◽  
Femtosecond Laser ◽  
Healing Response ◽  
Wound Healing Response

scholarly journals Chronic senescent human mesenchymal stem cells as possible contributor to the wound healing disorder after exposure to the alkylating agent sulfur mustard

2021 ◽  
Vol 95 (2) ◽  
pp. 727-747
Author(s):  
Simone Rothmiller ◽  
Niklas Jäger ◽  
Nicole Meier ◽  
Thimo Meyer ◽  
Adrian Neu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Mesenchymal Stem Cells ◽  
Alkylating Agent ◽  
Chronic Wounds ◽  
Sulfur Mustard ◽  
Morphological Changes ◽  
Human Mesenchymal Stem Cells ◽  
Age Related

AbstractWound healing is a complex process, and disturbance of even a single mechanism can result in chronic ulcers developing after exposure to the alkylating agent sulfur mustard (SM). A possible contributor may be SM-induced chronic senescent mesenchymal stem cells (MSCs), unable to fulfil their regenerative role, by persisting over long time periods and creating a proinflammatory microenvironment. Here we show that senescence induction in human bone marrow derived MSCs was time- and concentration-dependent, and chronic senescence could be verified 3 weeks after exposure to between 10 and 40 µM SM. Morphological changes, reduced clonogenic and migration potential, longer scratch closure times, differences in senescence, motility and DNA damage response associated genes as well as increased levels of proinflammatory cytokines were revealed. Selective removal of these cells by senolytic drugs, in which ABT-263 showed initial potential in vitro, opens the possibility for an innovative treatment strategy for chronic wounds, but also tumors and age-related diseases.

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