mark McDermott - Academia.edu (original) (raw)

Papers by mark McDermott

Research paper thumbnail of Sensory nerve regeneration after epithelium wounding in normal and diabetic corneas

Expert Review of Ophthalmology, 2015

The cornea is the most densely innervated mammalian tissue. The sensory nerves are responsible fo... more The cornea is the most densely innervated mammalian tissue. The sensory nerves are responsible for sensations of dryness, temperature, touch, and pain, and play important roles in the blink reflex, wound healing, and tear production. Many ocular and systemic diseases can adversely affect corneal sensory nerve and consequently impair their function. One of such systemic diseases is diabetes mellitus (DM) which causes sensory degeneration, neurotrophic keratopathy (DNK), and delayed wound healing. In this review, we summarize recent discoveries revealing mechanisms underlying the pathogenesis of DNK and the impairment of sensory nerve regeneration in post wound diabetic corneas in using animal model of human diabetes. Because it is generally believed that common mechanisms are operative in the pathogenesis of diabetic peripheral neuropathy in different tissues, the findings in the corneas have implications in in other tissues such as the skin, which often leads to foot ulceration and amputation in diabetic patients. Diabetes mellitus (DM) is a major disease worldwide, and its prevalence has risen significantly in the past several decades. Two types of diabetes, Type 1 and 2, both manifest with hyperglycemia but have distinctive pathophysiological mechanisms. Type 1 diabetes (T1D) arises following autoimmune destruction of the insulin-producing pancreatic beta cells, is often diagnosed in childhood and adolescence, and requires exogenous insulin treatment. The cause of the autoimmune process is unknown, and is thought to be triggered by one or more environmental agents in genetically susceptible individuals. [1, 2] In Type 2 diabetes (T2D), individuals exhibit insulin resistance and a resulting relative insulin deficiency to varying degrees, and exogenous insulin treatment may or may not be required. Its pathogenesis is multifactorial, involving both genetic and acquired factors which cause overproduction and inefficient utilization of glucose. T2D is often diagnosed in the adult population, although its incidence in the youth has been rising, alongside increasing obesity in this group. T2D often occurs concurrently with hyperlipidemia and hypertension, creating a constellation of signs and symptoms known as metabolic syndrome, where increases in

Research paper thumbnail of Confirmation of Besifloxacin Corneal Precipitation After Cataract Surgery by Raman Spectroscopy

Research paper thumbnail of Ex vivo corneal epithelial wound healing following exposure to ophthalmic nonsteroidal anti-inflammatory drugs

Clinical Ophthalmology, 2011

Ketorolac 0.45% is a new formulation of topical ketorolac in which preservative (benzalkonium chl... more Ketorolac 0.45% is a new formulation of topical ketorolac in which preservative (benzalkonium chloride, BAK) was removed and carboxymethylcellulose (CMC) was added to improve tolerability and reduce dosing frequency. This study compared the effects of ketorolac 0.45% on corneal wound healing to prior ketorolac formulations (0.4% and 0.5%), bromfenac 0.09%, and nepafenac 0.1%. Methods: Two parallel-group comparisons were performed in series. A 5-mm central epithelial wound was made in fresh porcine corneas. After 24 hours in minimum essential medium (MEM), corneas were incubated for 10 minutes with study drugs, Triton X-100 1% (positive control), or MEM (negative control), followed by 24 hours in MEM. The remaining wound area was stained, photographed, and quantified (pixels). Study 1 compared ketorolac 0.45% to ketorolac 0.4% and ketorolac 0.5%. Study 2 compared ketorolac 0.45% to bromfenac 0.09% and nepafenac 0.1%. Results: The mean (±SD) original wound area was 200,506 ± 4,363 pixels, which was reduced to 59,509 ± 4850 at 48 hours after exposure to Triton X-100 1%. In study 1, the mean remaining wound areas at 48 hours in pixels were 2969 ± 1633 with MEM, 586 ± 299 with ketorolac 0.45% (significantly reduced, P , 0.05 vs all other treatments), 10,228 ± 7541 with ketorolac 0.4%, and 50,674 ± 33,409 with ketorolac 0.5% (significantly enlarged, P , 0.05 vs MEM). In study 2, the mean remaining wound areas at 48 hours were 565 ± 1263 with MEM, 322 ± 229 with ketorolac 0.45% (significantly reduced, P , 0.01 vs bromfenac 0.09% and nepafenac 0.1%), 29,093 ± 14,295 with bromfenac 0.09% (significantly enlarged, P ,0.01 vs MEM) and 47,322 ± 13,736 with nepafenac 0.1% (significantly enlarged, P , 0.01 vs MEM and vs bromfenac 0.09%). Conclusion: Corneas treated with ketorolac 0.45% healed as rapidly as those treated with MEM, likely secondary to addition of CMC and removal of BAK. In the ex vivo corneal organ culture model, ketorolac 0.45% had statistically less impact on corneal re-epithelialization than prior ketorolac formulations (0.4% and 0.5%), bromfenac 0.09%, and nepafenac 0.01%.

Research paper thumbnail of Experimental neodymium: YAG laser damage to acrylic, poly (methyl methacrylate), and silicone intraocular lens materials

Journal of Cataract & …, 1999

The damage threshold (≥ μm depth) was 0.3 mJ for silicone and 10 mJ for acrylic and PMMA IOLs. At... more The damage threshold (≥ μm depth) was 0.3 mJ for silicone and 10 mJ for acrylic and PMMA IOLs. At the clinically relevant power levels, 10 to 20 mJ the depth of damage in the acrylic polymer was 11.9 to 30.5 times less than the depth in the silicone polymer. Similarly, the depth of ...

Research paper thumbnail of Unilateral pharmacologic mydriasis secondary to crack cocaine

The American Journal of Emergency Medicine, 1990

Research paper thumbnail of Sensory nerve regeneration after epithelium wounding in normal and diabetic corneas

Expert Review of Ophthalmology, 2015

The cornea is the most densely innervated mammalian tissue. The sensory nerves are responsible fo... more The cornea is the most densely innervated mammalian tissue. The sensory nerves are responsible for sensations of dryness, temperature, touch, and pain, and play important roles in the blink reflex, wound healing, and tear production. Many ocular and systemic diseases can adversely affect corneal sensory nerve and consequently impair their function. One of such systemic diseases is diabetes mellitus (DM) which causes sensory degeneration, neurotrophic keratopathy (DNK), and delayed wound healing. In this review, we summarize recent discoveries revealing mechanisms underlying the pathogenesis of DNK and the impairment of sensory nerve regeneration in post wound diabetic corneas in using animal model of human diabetes. Because it is generally believed that common mechanisms are operative in the pathogenesis of diabetic peripheral neuropathy in different tissues, the findings in the corneas have implications in in other tissues such as the skin, which often leads to foot ulceration and amputation in diabetic patients. Diabetes mellitus (DM) is a major disease worldwide, and its prevalence has risen significantly in the past several decades. Two types of diabetes, Type 1 and 2, both manifest with hyperglycemia but have distinctive pathophysiological mechanisms. Type 1 diabetes (T1D) arises following autoimmune destruction of the insulin-producing pancreatic beta cells, is often diagnosed in childhood and adolescence, and requires exogenous insulin treatment. The cause of the autoimmune process is unknown, and is thought to be triggered by one or more environmental agents in genetically susceptible individuals. [1, 2] In Type 2 diabetes (T2D), individuals exhibit insulin resistance and a resulting relative insulin deficiency to varying degrees, and exogenous insulin treatment may or may not be required. Its pathogenesis is multifactorial, involving both genetic and acquired factors which cause overproduction and inefficient utilization of glucose. T2D is often diagnosed in the adult population, although its incidence in the youth has been rising, alongside increasing obesity in this group. T2D often occurs concurrently with hyperlipidemia and hypertension, creating a constellation of signs and symptoms known as metabolic syndrome, where increases in

Research paper thumbnail of Confirmation of Besifloxacin Corneal Precipitation After Cataract Surgery by Raman Spectroscopy

Research paper thumbnail of Ex vivo corneal epithelial wound healing following exposure to ophthalmic nonsteroidal anti-inflammatory drugs

Clinical Ophthalmology, 2011

Ketorolac 0.45% is a new formulation of topical ketorolac in which preservative (benzalkonium chl... more Ketorolac 0.45% is a new formulation of topical ketorolac in which preservative (benzalkonium chloride, BAK) was removed and carboxymethylcellulose (CMC) was added to improve tolerability and reduce dosing frequency. This study compared the effects of ketorolac 0.45% on corneal wound healing to prior ketorolac formulations (0.4% and 0.5%), bromfenac 0.09%, and nepafenac 0.1%. Methods: Two parallel-group comparisons were performed in series. A 5-mm central epithelial wound was made in fresh porcine corneas. After 24 hours in minimum essential medium (MEM), corneas were incubated for 10 minutes with study drugs, Triton X-100 1% (positive control), or MEM (negative control), followed by 24 hours in MEM. The remaining wound area was stained, photographed, and quantified (pixels). Study 1 compared ketorolac 0.45% to ketorolac 0.4% and ketorolac 0.5%. Study 2 compared ketorolac 0.45% to bromfenac 0.09% and nepafenac 0.1%. Results: The mean (±SD) original wound area was 200,506 ± 4,363 pixels, which was reduced to 59,509 ± 4850 at 48 hours after exposure to Triton X-100 1%. In study 1, the mean remaining wound areas at 48 hours in pixels were 2969 ± 1633 with MEM, 586 ± 299 with ketorolac 0.45% (significantly reduced, P , 0.05 vs all other treatments), 10,228 ± 7541 with ketorolac 0.4%, and 50,674 ± 33,409 with ketorolac 0.5% (significantly enlarged, P , 0.05 vs MEM). In study 2, the mean remaining wound areas at 48 hours were 565 ± 1263 with MEM, 322 ± 229 with ketorolac 0.45% (significantly reduced, P , 0.01 vs bromfenac 0.09% and nepafenac 0.1%), 29,093 ± 14,295 with bromfenac 0.09% (significantly enlarged, P ,0.01 vs MEM) and 47,322 ± 13,736 with nepafenac 0.1% (significantly enlarged, P , 0.01 vs MEM and vs bromfenac 0.09%). Conclusion: Corneas treated with ketorolac 0.45% healed as rapidly as those treated with MEM, likely secondary to addition of CMC and removal of BAK. In the ex vivo corneal organ culture model, ketorolac 0.45% had statistically less impact on corneal re-epithelialization than prior ketorolac formulations (0.4% and 0.5%), bromfenac 0.09%, and nepafenac 0.01%.

Research paper thumbnail of Experimental neodymium: YAG laser damage to acrylic, poly (methyl methacrylate), and silicone intraocular lens materials

Journal of Cataract & …, 1999

The damage threshold (≥ μm depth) was 0.3 mJ for silicone and 10 mJ for acrylic and PMMA IOLs. At... more The damage threshold (≥ μm depth) was 0.3 mJ for silicone and 10 mJ for acrylic and PMMA IOLs. At the clinically relevant power levels, 10 to 20 mJ the depth of damage in the acrylic polymer was 11.9 to 30.5 times less than the depth in the silicone polymer. Similarly, the depth of ...

Research paper thumbnail of Unilateral pharmacologic mydriasis secondary to crack cocaine

The American Journal of Emergency Medicine, 1990