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Alistair J Barber - One of the best experts on this subject based on the ideXlab platform.
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loss of cholinergic and dopaminergic amacrine cells in streptozotocin Diabetic rat and ins2akita Diabetic Mouse retinas
Investigative Ophthalmology & Visual Science, 2006Co-Authors: Matthew J Gastinger, Ravi S J Singh, Alistair J BarberAbstract:PURPOSE. To identify amacrine cells that are vulnerable to degeneration during the early stages of diabetes. METHODS. Whole retinas from streptozotocin (STZ)-Diabetic rats and Ins2 Akita mice were fixed in paraformaldehyde. Apoptotic cells in the retina were quantified using terminal dUTP nick-end labeling (TUNEL) and active caspase-3 (CM-1) immunohistochemistry. Immunohistochemical markers for choline acetyltransferase (ChAT) and tyrosine hyroxylase (TH) were also used to quantify populations of amacrine cells in the Ins2 Akita Mouse retinas. RESULTS. The number of TUNEL-positive nuclei increased from 29 ± 4 in controls to 72 ± 9 in the STZ-Diabetic rat retinas after only 2 weeks of diabetes. In rats, CM-1-immunoreactive (IR) cells were found primarily in the inner nuclear and ganglion cell layers after 2, 8, and 16 weeks of diabetes. At each end point, the number of CM-1-IR cells in the retina was elevated by diabetes. Approximately 2% to 6% of the CM-1-IR cells in the inner nuclear layer (INL) were double-labeled for TH immunoreactivity. After 6 months of diabetes in the Ins2 Akita Mouse, the morphology of the labeled ChAT-IR and TH-IR amacrine cell somas and dendrites appeared normal. A quantitative analysis revealed a 20% decrease in the number of cholinergic and a 16% decrease in dopaminergic amacrine cells in the Diabetic Mouse retinas, compared with the nonDiabetic control. CONCLUSIONS. Dopaminergic and cholinergic amacrine cells are lost during the early stages of retinal neuropathy in diabetes. Loss of these neurons may play a critical role in the development of visual deficits in diabetes.
Matthew J Gastinger - One of the best experts on this subject based on the ideXlab platform.
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loss of cholinergic and dopaminergic amacrine cells in streptozotocin Diabetic rat and ins2akita Diabetic Mouse retinas
Investigative Ophthalmology & Visual Science, 2006Co-Authors: Matthew J Gastinger, Ravi S J Singh, Alistair J BarberAbstract:PURPOSE. To identify amacrine cells that are vulnerable to degeneration during the early stages of diabetes. METHODS. Whole retinas from streptozotocin (STZ)-Diabetic rats and Ins2 Akita mice were fixed in paraformaldehyde. Apoptotic cells in the retina were quantified using terminal dUTP nick-end labeling (TUNEL) and active caspase-3 (CM-1) immunohistochemistry. Immunohistochemical markers for choline acetyltransferase (ChAT) and tyrosine hyroxylase (TH) were also used to quantify populations of amacrine cells in the Ins2 Akita Mouse retinas. RESULTS. The number of TUNEL-positive nuclei increased from 29 ± 4 in controls to 72 ± 9 in the STZ-Diabetic rat retinas after only 2 weeks of diabetes. In rats, CM-1-immunoreactive (IR) cells were found primarily in the inner nuclear and ganglion cell layers after 2, 8, and 16 weeks of diabetes. At each end point, the number of CM-1-IR cells in the retina was elevated by diabetes. Approximately 2% to 6% of the CM-1-IR cells in the inner nuclear layer (INL) were double-labeled for TH immunoreactivity. After 6 months of diabetes in the Ins2 Akita Mouse, the morphology of the labeled ChAT-IR and TH-IR amacrine cell somas and dendrites appeared normal. A quantitative analysis revealed a 20% decrease in the number of cholinergic and a 16% decrease in dopaminergic amacrine cells in the Diabetic Mouse retinas, compared with the nonDiabetic control. CONCLUSIONS. Dopaminergic and cholinergic amacrine cells are lost during the early stages of retinal neuropathy in diabetes. Loss of these neurons may play a critical role in the development of visual deficits in diabetes.
Ravi S J Singh - One of the best experts on this subject based on the ideXlab platform.
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loss of cholinergic and dopaminergic amacrine cells in streptozotocin Diabetic rat and ins2akita Diabetic Mouse retinas
Investigative Ophthalmology & Visual Science, 2006Co-Authors: Matthew J Gastinger, Ravi S J Singh, Alistair J BarberAbstract:PURPOSE. To identify amacrine cells that are vulnerable to degeneration during the early stages of diabetes. METHODS. Whole retinas from streptozotocin (STZ)-Diabetic rats and Ins2 Akita mice were fixed in paraformaldehyde. Apoptotic cells in the retina were quantified using terminal dUTP nick-end labeling (TUNEL) and active caspase-3 (CM-1) immunohistochemistry. Immunohistochemical markers for choline acetyltransferase (ChAT) and tyrosine hyroxylase (TH) were also used to quantify populations of amacrine cells in the Ins2 Akita Mouse retinas. RESULTS. The number of TUNEL-positive nuclei increased from 29 ± 4 in controls to 72 ± 9 in the STZ-Diabetic rat retinas after only 2 weeks of diabetes. In rats, CM-1-immunoreactive (IR) cells were found primarily in the inner nuclear and ganglion cell layers after 2, 8, and 16 weeks of diabetes. At each end point, the number of CM-1-IR cells in the retina was elevated by diabetes. Approximately 2% to 6% of the CM-1-IR cells in the inner nuclear layer (INL) were double-labeled for TH immunoreactivity. After 6 months of diabetes in the Ins2 Akita Mouse, the morphology of the labeled ChAT-IR and TH-IR amacrine cell somas and dendrites appeared normal. A quantitative analysis revealed a 20% decrease in the number of cholinergic and a 16% decrease in dopaminergic amacrine cells in the Diabetic Mouse retinas, compared with the nonDiabetic control. CONCLUSIONS. Dopaminergic and cholinergic amacrine cells are lost during the early stages of retinal neuropathy in diabetes. Loss of these neurons may play a critical role in the development of visual deficits in diabetes.
Alireza Kheirollah - One of the best experts on this subject based on the ideXlab platform.
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Decrease of Serum Vascular Endothelial Growth Factor, along with its Ocular Level, after the Periocular Injection of Celecoxib and Propranolol in Streptozotocin-induced Diabetic Mouse Model
2019Co-Authors: Shirin Azizidoost, Mostafa Feghhi, Maryam Cheraghzadeh, Zahra Nazeri, Alireza KheirollahAbstract:Background: There is a direct correlation between ocular vascular endothelial growth factor (VEGF) level and progression of pathological outcomes in Diabetic retinopathy. In our previous study, the periocular administration of propranolol and celecoxib could significantly reduce ocular VEGF levels in a Diabetic Mouse model. Here, we investigated the changes of serum VEGF after periocular administration of propranolol and celecoxib in a Diabetic Mouse model. Methods: Forty male BALB-C mice aged 4-6 weeks were divided into four groups as follows: non-Diabetic, streptozotocin-induced Diabetic, streptozotocin-induced Diabetic + periocular injection of 200 µg celecoxib and streptozotocin-induced Diabetic + periocular injection of 10 µg propranolol. Serum VEGF in all experimental groups was measured by using enzyme-linked immunosorbent assay (ELISA) method. Results: In comparison to the non-Diabetic group, serum VEGF levels were markedly elevated in Diabetic groups and periocular injection of anti-VEGF agents could affect serum VEGF levels. Celecoxib was significantly more effective than propranolol in regulating serum VEGF levels. Conclusion: The periocular injection of both celecoxib and propranolol is one of the most effective ways to prevent Diabetic retinopathy and also has a beneficiary effect on down-regulation of serum VEGF levels in a Diabetic Mouse model. Therefore, periocular injection of anti-VEGF agents can play a significant role in preventing clinical side effects of diabetes.
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Effect of periocular injection of celecoxib and propranolol on ocular level of vascular endothelial growth factor in a Diabetic Mouse model.
International Journal of Ophthalmology, 2016Co-Authors: Saman Nassiri, Gholamreza Houshmand, Mostafa Feghhi, Alireza Kheirollah, Mohammad Bahadoram, Nariman NassiriAbstract:AIM To investigate the effects of periocular injection of propranolol and celecoxib on ocular levels of vascular endothelial growth factor (VEGF) in a Diabetic Mouse model.
Giorgio Soldani - One of the best experts on this subject based on the ideXlab platform.
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bilayered fibrin based electrospun sprayed scaffold loaded with platelet lysate enhances wound healing in a Diabetic Mouse model
Nanomaterials, 2020Co-Authors: Paola Losi, Tamer Al Kayal, Marianna Buscemi, Ilenia Foffa, Aida Cavallo, Giorgio SoldaniAbstract:The present study examined the effects of a bilayered fibrin/poly(ether)urethane scaffold loaded with platelet lysate by a combination of electrospinning and spray, phase-inversion method for wound healing. In particular, the poly(ether)urethane layer was obtained using by a spray phase-inversion method and the fibrin fibers network were loaded with platelet lysate by electrospinning. The kinetics release and the bioactivity of growth factors released from platelet lysate-scaffold were investigated by ELISA and cell proliferation test using Mouse fibroblasts, respectively. The in-vitro experiments demonstrated that a bilayered fibrin/poly(ether)urethane scaffold loaded with platelet lysate provides a sustained release of bioactive platelet-derived growth factors. The effect of a bilayered fibrin/poly(ether)urethane scaffold loaded with platelet lysate on wound healing in Diabetic Mouse (db/db) was also investigated. The application of the scaffold on full-thickness skin wounds significantly accelerated wound closure at day 14 post-surgery when compared to scaffold without platelet lysates or commercially available polyurethane film, and at the same level of growth factor-loaded scaffold. Histological analysis demonstrated an increased re-epithelialization and collagen deposition in platelet lysate and growth factor loaded scaffolds. The ability of bilayered fibrin/poly(ether)urethane scaffold loaded with platelet lysate to promote in-vivo wound healing suggests its usefulness in clinical treatment of Diabetic ulcers.