Background: The complexity of the glaucoma pathophysiology is directly reflected on its experimental modeling for studies about pathological mechanisms and treatment approaches. Currently, a variety of in vivo models are available for the study of glaucoma, although they do not reach an exact reproduction of all aspects characterizing the human glaucoma. Therefore, a comprehensive view of disease onset, progression and treatment efficacy can only be obtained by the integration of outcomes deriving from different experimental models.
Methods: The present article summary experimental procedures and analytical methodologies related with two experimental models of glaucoma belonging to the classes of induced intraocular pressure (IOP)-elevation and genetic models, methyl cellulose (MCE)-induced ocular hypertension and DBA/2J mouse strain. Point-by-point protocols are reported with a particular focus on the critical point for the realization of each model. Moreover, typical strength and drawbacks of each model are described in order to critically handle the outcomes deriving from each model.
Discussion: This paper provides a guideline for the realization, analysis and expected outcomes of two models allowing to study IOP-driven neurodegenerative mechanisms rather than IOP-independent neurodegeneration. The complementary information from these models could enhance the analysis of glaucomatous phenomena from different points of view potentiating the basic and translational study of glaucoma.
Background: Surgically induced astigmatism (SIA) and corneal high-order aberrations (HOAs) are the two main causes of poor visual quality after cataract surgery. Changes in the parameters of corneal HOAs after cataract surgery and their effects on and relationships with changes in corneal curvature have not yet been reported. This study aimed to explore changes in anterior, posterior and total corneal curvature, astigmatism and HOAs after microincision cataract surgery.
Methods: Sixty-one age-related cataract patients (61 eyes) were included in this prospective study. The total, anterior and posterior corneal astigmatism and corneal HOAs were analyzed by anterior segment optical coherence tomography (AS-OCT) and iTrace before, one day, one week and three months after 2.2 mm temporal microincision coaxial phacoemulsification to evaluate the changes in anterior, posterior and total corneal curvature, astigmatism and corneal HOAs.
Results: The mean J0 and J45 values of anterior, posterior and total corneal curvature obtained by AS-OCT showed no statistically significant difference between preoperatively and any postoperative follow-up. SIA occurred on the anterior, posterior and total corneal surfaces and showed no statistically significant difference at any postoperative follow-up. No significant changes in 3rd-order oblique trefoil, vertical coma or 4th-order spherical aberrations were observed after surgery except for a significant increase in horizontal coma at postoperative day 1 (POD1).
Conclusions: There were no significant changes in corneal curvature after 2.2 mm temporal microincision coaxial phacoemulsification, and the corneal HOAs were not changed significantly except for the increase in horizontal coma at POD1, which may be one of the main reasons of poor visual quality at POD1 in some cataract patients who have good uncorrected or corrected distance vision.
Background: The complexity of the glaucoma pathophysiology is directly reflected on its experimental modeling for studies about pathological mechanisms and treatment approaches. Currently, a variety of in vivo models are available for the study of glaucoma, although they do not reach an exact reproduction of all aspects characterizing the human glaucoma. Therefore, a comprehensive view of disease onset, progression and treatment efficacy can only be obtained by the integration of outcomes deriving from different experimental models.
Methods: The present article summary experimental procedures and analytical methodologies related with two experimental models of glaucoma belonging to the classes of induced intraocular pressure (IOP)-elevation and genetic models, methyl cellulose (MCE)-induced ocular hypertension and DBA/2J mouse strain. Point-by-point protocols are reported with a particular focus on the critical point for the realization of each model. Moreover, typical strength and drawbacks of each model are described in order to critically handle the outcomes deriving from each model.
Discussion: This paper provides a guideline for the realization, analysis and expected outcomes of two models allowing to study IOP-driven neurodegenerative mechanisms rather than IOP-independent neurodegeneration. The complementary information from these models could enhance the analysis of glaucomatous phenomena from different points of view potentiating the basic and translational study of glaucoma.
