A major pathogenic mechanism of chronic alcoholism involves oxidative burden to liver and other cell types. We show that adult neurogenesis within the dentate gyrus of the hippocampus is selectively impaired in a rat model of alcoholism, and that it can be completely prevented by the antioxidant ebselen. Rats fed for 6 weeks with a liquid diet containing moderate doses of ethanol had a 66.3% decrease in the number of new neurons and a 227–279% increase in cell death in the dentate gyrus as compared with paired controls. Neurogenesis within the olfactory bulb was not affected by alcohol. Our studies indicate that alcohol abuse, even for a short duration, results in the death of newly formed neurons within the adult brain and that the underlying mechanism is related to oxidative or nitrosative stress. Moreover, these findings suggest that the impaired neurogenesis may be a mechanism mediating cognitive deficits observed in alcoholism.
1 April 2015 in Oxidative Medicine and Cellular Longevity
Myopia affected approximately 1.6 billion people worldwide in 2000, and it is expected to increase to 2.5 billion by 2020. Although optical problems can be corrected by optics or surgical procedures, normal myopia and high myopia are still an unsolved medical problem. They frequently predispose people who have them to suffer from other eye pathologies: retinal detachment, glaucoma, macular hemorrhage, cataracts, and so on being one of the main causes of visual deterioration and blindness. Genetic and environmental factors have been associated with myopia. Nevertheless, lack of knowledge in the underlying physiopathological molecular mechanisms has not permitted an adequate diagnosis, prevention, or treatment to be found. Nowadays several pieces of evidence indicate that oxidative stress may help explain the altered regulatory pathways in myopia and the appearance of associated eye diseases. On the one hand, oxidative damage associated with hypoxia myopic can alter the neuromodulation that nitric oxide and dopamine have in eye growth. On the other hand, radical superoxide or peroxynitrite production damage retina, vitreous, lens, and so on contributing to the appearance of retinopathies, retinal detachment, cataracts and so on. The objective of this review is to suggest that oxidative stress is one of the key pieces that can help solve this complex eye problem.
1 September 2009 in Journal of Manipulative and Physiological Therapeutics
The purpose of this study was to determine immediate effects of ischemic compression (IC) and ultrasound (US) for the treatment of myofascial trigger points (MTrPs) in the trapezius muscle. Sixty-six volunteers, all CEU-Cardenal Herrera University, Valencia, Spain, personnel, participated in this study. Subjects were healthy individuals, diagnosed with latent MTrPs in the trapezius muscle. Subjects were randomly placed into 3 groups: G1, which received IC treatment for MTrPs; G2, which received US; and G3 (control), which received sham US. The following data were recorded before and after each treatment: active range of motion (AROM) of cervical rachis measured with a cervical range of motion instrument, basal electrical activity (BEA) of muscle trapezius measured with surface electromyography, and pressure tolerance of MTrP measured with visual analogue scale assessing local pain evoked by the application of 2.5 kg/cm(2) of pressure using a pressure analog algometer. The results showed an immediate decrease in BEA of the trapezius muscle and a reduction of MTrP sensitivity after treatment with both therapeutic modalities. In the case of IC, an improvement of AROM of cervical rachis was also been obtained. In this group of participants, both treatments were shown to have an immediate effect on latent MTrPs. The results show a relation among AROM of cervical rachis, BEA of the trapezius muscle, and MTrP sensitivity of the trapezius muscle gaining short-term positive effects with use of IC.
1 June 2008 in Journal of Ocular Pharmacology and Therapeutics
Purpose: The aim of this study was to assess the efficacy and safety of adalimumab in treating refractory autoimmune uveitis. Methods: This work was a prospective, noncomparative, nonrandomized, clinical trial. Nineteen (19) patients meeting eligibility criteria received a 40-mg subcutaneous (s.c.) injection of adalimumab every other week during 1 year. Results: All patients underwent an outcome assessment at month 12. Visual acuity improved by −0.3 logMar in 12 (31%) eyes of 38, and worsened by +0.3 logMar in 1 (2.6%) eye. All patients had an active intraocular inflammation at baseline, and 12 patients (63%) achieved control of their inflammation with adalimumab at the end of follow-up. After optic coherence tomography, 33 eyes (86%) had cystoid macular edema (CME) at baseline, and at the end of follow-up there was a complete resolution of CME in 18 of these 33 eyes (54.54%). All patients were able to reduce at least 50% of the dose of the concomitant immunosuppressive drugs at the end of follow-up. Adalimumab was well tolerated in all patients, and only local minor side effects at the s.c. injection site were observed. Nevertheless, 8 patients (42.10%) had relapses during the follow-up period that were controlled with 1 periocular steroid injection. Conclusions: Adalimumab seems to be an effective, safe therapy for the management of refractory uveitis and may provide the possibility to reduce the concomitant immunosuppressive drugs in these patients. Further long-term studies are warranted to determine the safety and efficacy of adalimumab in treating intraocular inflammation.
1 September 2006 in Free Radical Biology and Medicine