Background: Acne vulgaris is a common cosmetic problem that is frequently associated with psychosocial disturbances as well as increased oxidative stress. However, oxidative stress and psychological aspects have been studied separately in acne. Objective: To evaluate the relationships between oxidative stress, anxiety, depression, and quality of life in acne patients. Methods: Sixty patients with facial acne and 40 age- and sex-matched healthy individuals were included in the study. Anxiety and depression were assessed using the Hospital Anxiety and Depression Scale (HADS), and quality of life (QoL) was measured by the Cardiff Acne Disability Index. Disease severity was assessed using the Combined Acne Severity Classification. The serum levels of zinc and malondialdehyde (MDA) and total antioxidant capacity (TAC) were measured in patients and healthy subjects. Results: The mean HADS scores for anxiety and depression were higher in patients than controls (P.001 for both). Acne patients showed higher serum MDA and lower TAC and serum zinc levels compared with control subjects (P=.019, P.001, and P=.028, respectively). Anxiety and depression scores did not correlate with oxidative stress parameters. Patients with moderate/severe acne had worse anxiety scores than mild acne (P=.048), and higher anxiety scores were associated with poorer quality of life (r=.436, P=.001). Conclusion: Our results indicate that the high levels of anxiety and depression in patients with facial acne were not related to oxidative stress. Anxiety was more common than depression and was directly related to QoL impairment.

Background: Acne vulgaris is a common cosmetic problem that is frequently associated with psychosocial disturbances as well as increased oxidative stress. However, oxidative stress and psychological aspects have been studied separately in acne. Objective: To evaluate the relationships between oxidative stress, anxiety, depression, and quality of life in acne patients. Methods: Sixty patients with facial acne and 40 age- and sex-matched healthy individuals were included in the study. Anxiety and depression were assessed using the Hospital Anxiety and Depression Scale (HADS), and quality of life (QoL) was measured by the Cardiff Acne Disability Index. Disease severity was assessed using the Combined Acne Severity Classification. The serum levels of zinc and malondialdehyde (MDA) and total antioxidant capacity (TAC) were measured in patients and healthy subjects. Results: The mean HADS scores for anxiety and depression were higher in patients than controls (P.001 for both). Acne patients showed higher serum MDA and lower TAC and serum zinc levels compared with control subjects (P=.019, P.001, and P=.028, respectively). Anxiety and depression scores did not correlate with oxidative stress parameters. Patients with moderate/severe acne had worse anxiety scores than mild acne (P=.048), and higher anxiety scores were associated with poorer quality of life (r=.436, P=.001). Conclusion: Our results indicate that the high levels of anxiety and depression in patients with facial acne were not related to oxidative stress. Anxiety was more common than depression and was directly related to QoL impairment.

Background: Acne vulgaris is a common cosmetic problem that is frequently associated with psychosocial disturbances as well as increased oxidative stress. However, oxidative stress and psychological aspects have been studied separately in acne. Objective: To evaluate the relationships between oxidative stress, anxiety, depression, and quality of life in acne patients. Methods: Sixty patients with facial acne and 40 age- and sex-matched healthy individuals were included in the study. Anxiety and depression were assessed using the Hospital Anxiety and Depression Scale (HADS), and quality of life (QoL) was measured by the Cardiff Acne Disability Index. Disease severity was assessed using the Combined Acne Severity Classification. The serum levels of zinc and malondialdehyde (MDA) and total antioxidant capacity (TAC) were measured in patients and healthy subjects. Results: The mean HADS scores for anxiety and depression were higher in patients than controls (P.001 for both). Acne patients showed higher serum MDA and lower TAC and serum zinc levels compared with control subjects (P=.019, P.001, and P=.028, respectively). Anxiety and depression scores did not correlate with oxidative stress parameters. Patients with moderate/severe acne had worse anxiety scores than mild acne (P=.048), and higher anxiety scores were associated with poorer quality of life (r=.436, P=.001). Conclusion: Our results indicate that the high levels of anxiety and depression in patients with facial acne were not related to oxidative stress. Anxiety was more common than depression and was directly related to QoL impairment.

Abstract Parkinson’s disease (PD) is a chronic neurodegenerative disease. Unfortunately, the effectiveness of anti-Parkinson treatments gradually diminishes owing to the progressive degeneration of the dopaminergic terminals. The research described here investigated the effect of adipose-derived mesenchymal stem cells (AD-MSC) versus that of an anti-Parkinson drug in a rat model of Parkinsonism. Forty adult rats were divided into four equal groups, each group receiving a different treatment: vehicle, rotenone, rotenone + AD-MSC, or rotenone + carbidopa/levodopa. Behavioral tests were carried out before and at the end of the treatment and specimens harvested from the midbrain were processed for light and electron microscopy. Genetic expression of glial fibrillary acidic protein (GFAP) and Nestin mRNA was assessed. Expression of the Lamin-B1 and Vimentin genes was measured, along with plasma levels of Angiopoietin-2 and dopamine. Treatment with rotenone induced pronounced motor deficits, as well as neuronal and glial alterations. The AD-MSC group showed improvements in motor function in the live animals and in the microscopic picture presented by their tissues. The fold change of both genes (GFAP and Nestin) decreased significantly in the AD-MSC and carbidopa/levodopa groups compared to the group with Parkinson’s disease. Plasma levels of Angiopoietin-2 and dopamine were significantly increased after treatment (P 0.001) compared to levels in the rats with Parkinson’s disease. AD-MSC reduced neuronal degeneration more efficiently than did the anti-Parkinson drug in a rat model of Parkinsonism.

Abstract Parkinson’s disease (PD) is a chronic neurodegenerative disease. Unfortunately, the effectiveness of anti-Parkinson treatments gradually diminishes owing to the progressive degeneration of the dopaminergic terminals. The research described here investigated the effect of adipose-derived mesenchymal stem cells (AD-MSC) versus that of an anti-Parkinson drug in a rat model of Parkinsonism. Forty adult rats were divided into four equal groups, each group receiving a different treatment: vehicle, rotenone, rotenone + AD-MSC, or rotenone + carbidopa/levodopa. Behavioral tests were carried out before and at the end of the treatment and specimens harvested from the midbrain were processed for light and electron microscopy. Genetic expression of glial fibrillary acidic protein (GFAP) and Nestin mRNA was assessed. Expression of the Lamin-B1 and Vimentin genes was measured, along with plasma levels of Angiopoietin-2 and dopamine. Treatment with rotenone induced pronounced motor deficits, as well as neuronal and glial alterations. The AD-MSC group showed improvements in motor function in the live animals and in the microscopic picture presented by their tissues. The fold change of both genes (GFAP and Nestin) decreased significantly in the AD-MSC and carbidopa/levodopa groups compared to the group with Parkinson’s disease. Plasma levels of Angiopoietin-2 and dopamine were significantly increased after treatment (P 0.001) compared to levels in the rats with Parkinson’s disease. AD-MSC reduced neuronal degeneration more efficiently than did the anti-Parkinson drug in a rat model of Parkinsonism.

Abstract Parkinson’s disease (PD) is a chronic neurodegenerative disease. Unfortunately, the effectiveness of anti-Parkinson treatments gradually diminishes owing to the progressive degeneration of the dopaminergic terminals. The research described here investigated the effect of adipose-derived mesenchymal stem cells (AD-MSC) versus that of an anti-Parkinson drug in a rat model of Parkinsonism. Forty adult rats were divided into four equal groups, each group receiving a different treatment: vehicle, rotenone, rotenone + AD-MSC, or rotenone + carbidopa/levodopa. Behavioral tests were carried out before and at the end of the treatment and specimens harvested from the midbrain were processed for light and electron microscopy. Genetic expression of glial fibrillary acidic protein (GFAP) and Nestin mRNA was assessed. Expression of the Lamin-B1 and Vimentin genes was measured, along with plasma levels of Angiopoietin-2 and dopamine. Treatment with rotenone induced pronounced motor deficits, as well as neuronal and glial alterations. The AD-MSC group showed improvements in motor function in the live animals and in the microscopic picture presented by their tissues. The fold change of both genes (GFAP and Nestin) decreased significantly in the AD-MSC and carbidopa/levodopa groups compared to the group with Parkinson’s disease. Plasma levels of Angiopoietin-2 and dopamine were significantly increased after treatment (P 0.001) compared to levels in the rats with Parkinson’s disease. AD-MSC reduced neuronal degeneration more efficiently than did the anti-Parkinson drug in a rat model of Parkinsonism.

Abstract Parkinson’s disease (PD) is a chronic neurodegenerative disease. Unfortunately, the effectiveness of anti-Parkinson treatments gradually diminishes owing to the progressive degeneration of the dopaminergic terminals. The research described here investigated the effect of adipose-derived mesenchymal stem cells (AD-MSC) versus that of an anti-Parkinson drug in a rat model of Parkinsonism. Forty adult rats were divided into four equal groups, each group receiving a different treatment: vehicle, rotenone, rotenone + AD-MSC, or rotenone + carbidopa/levodopa. Behavioral tests were carried out before and at the end of the treatment and specimens harvested from the midbrain were processed for light and electron microscopy. Genetic expression of glial fibrillary acidic protein (GFAP) and Nestin mRNA was assessed. Expression of the Lamin-B1 and Vimentin genes was measured, along with plasma levels of Angiopoietin-2 and dopamine. Treatment with rotenone induced pronounced motor deficits, as well as neuronal and glial alterations. The AD-MSC group showed improvements in motor function in the live animals and in the microscopic picture presented by their tissues. The fold change of both genes (GFAP and Nestin) decreased significantly in the AD-MSC and carbidopa/levodopa groups compared to the group with Parkinson’s disease. Plasma levels of Angiopoietin-2 and dopamine were significantly increased after treatment (P 0.001) compared to levels in the rats with Parkinson’s disease. AD-MSC reduced neuronal degeneration more efficiently than did the anti-Parkinson drug in a rat model of Parkinsonism.

Abstract Parkinson’s disease (PD) is a chronic neurodegenerative disease. Unfortunately, the effectiveness of anti-Parkinson treatments gradually diminishes owing to the progressive degeneration of the dopaminergic terminals. The research described here investigated the effect of adipose-derived mesenchymal stem cells (AD-MSC) versus that of an anti-Parkinson drug in a rat model of Parkinsonism. Forty adult rats were divided into four equal groups, each group receiving a different treatment: vehicle, rotenone, rotenone + AD-MSC, or rotenone + carbidopa/levodopa. Behavioral tests were carried out before and at the end of the treatment and specimens harvested from the midbrain were processed for light and electron microscopy. Genetic expression of glial fibrillary acidic protein (GFAP) and Nestin mRNA was assessed. Expression of the Lamin-B1 and Vimentin genes was measured, along with plasma levels of Angiopoietin-2 and dopamine. Treatment with rotenone induced pronounced motor deficits, as well as neuronal and glial alterations. The AD-MSC group showed improvements in motor function in the live animals and in the microscopic picture presented by their tissues. The fold change of both genes (GFAP and Nestin) decreased significantly in the AD-MSC and carbidopa/levodopa groups compared to the group with Parkinson’s disease. Plasma levels of Angiopoietin-2 and dopamine were significantly increased after treatment (P 0.001) compared to levels in the rats with Parkinson’s disease. AD-MSC reduced neuronal degeneration more efficiently than did the anti-Parkinson drug in a rat model of Parkinsonism.

Abstract Parkinson’s disease (PD) is a chronic neurodegenerative disease. Unfortunately, the effectiveness of anti-Parkinson treatments gradually diminishes owing to the progressive degeneration of the dopaminergic terminals. The research described here investigated the effect of adipose-derived mesenchymal stem cells (AD-MSC) versus that of an anti-Parkinson drug in a rat model of Parkinsonism. Forty adult rats were divided into four equal groups, each group receiving a different treatment: vehicle, rotenone, rotenone + AD-MSC, or rotenone + carbidopa/levodopa. Behavioral tests were carried out before and at the end of the treatment and specimens harvested from the midbrain were processed for light and electron microscopy. Genetic expression of glial fibrillary acidic protein (GFAP) and Nestin mRNA was assessed. Expression of the Lamin-B1 and Vimentin genes was measured, along with plasma levels of Angiopoietin-2 and dopamine. Treatment with rotenone induced pronounced motor deficits, as well as neuronal and glial alterations. The AD-MSC group showed improvements in motor function in the live animals and in the microscopic picture presented by their tissues. The fold change of both genes (GFAP and Nestin) decreased significantly in the AD-MSC and carbidopa/levodopa groups compared to the group with Parkinson’s disease. Plasma levels of Angiopoietin-2 and dopamine were significantly increased after treatment (P 0.001) compared to levels in the rats with Parkinson’s disease. AD-MSC reduced neuronal degeneration more efficiently than did the anti-Parkinson drug in a rat model of Parkinsonism.

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