Monaghan Marcher (jetparcel05)

2 accompanied by low-expression of p21 was observed in lung cancer tissues and associated with lower overall survival. CONCLUSION Taken together, our study find a new regulatory pathway of p21, in which miR-509-3-5p functionally interacts with NONHSAT112228.2 to release p21 expression. MiR-509-3-5p-NONHSAT112228.2 regulatory axis can inhibit proliferation and migration of lung cancer cells. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Multiple sclerosis (MS) is the most common autoimmune demyelinating disease of the central nervous system (CNS). It is a multifactorial disease which develops in an immune-mediated way under the influences of both genetic and environmental factors. Demyelination is observed in the brain and spinal cord leading to neuro-axonal damage in patients with MS. Due to the infiltration of different immune cells such as T-cells, B-cells, monocytes and macrophages, focal lesions are observed in MS. Currently available medications treating MS are mainly based on two strategies; i) to ease specific symptoms or ii) to reduce disease progression. However, these often tend to induce different adverse effects with limited therapeutic efficacy due to the protective function of the blood-brain barrier. Therefore, researchers have been working for last four-decades to discover better solutions by introducing gene therapy approaches in treating MS generally by following three strategies, i) prevention of specific symptoms, ii) halt or reverse disease progression and iii) heal CNS damage by promoting remyelination and axonal repair. In last two decades, there have been some remarkable successes of gene therapy approaches on the experimental mice model of MS - experimental autoimmune encephalomyelitis (EAE) which suggests that it's not far that the gene therapy approaches would start in human subjects ensuring the highest levels of safety and efficacy. In this review, we summarised the gene therapy approaches attempted in different animal models towards treating MS. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Evidences have increasingly indicated that human disease, cell metabolism are deeply associated with proteins. Structural mutations and dysregulations of these proteins would contribute to the development of complex disease. Free radicals are unstable molecules that they look for electrons from surrounding atoms for stability, Once a free radical binds to an atom in the body, a chain reaction occurs, which causes damage to cells and DNA. Antioxidant protein is a substance that protects cells from free radical damage. Accurate identification of antioxidant proteins is important for understanding their role in delaying aging and preventing and treating related diseases.Therefore, computational methods to identify pantioxidant proteins have become an effective prior-pinpointing approach to the experimental verification. METHODS In this study, we use support vector machines to identify antioxidant proteins, using amino acid compositions and 9-gap dipeptide compositions as feature extraction, and featurmpared with the existing classification model, it is further explained that the SVM recognition model constructed in this paper is helpful for the recognition of antioxidized proteins. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Atherosclerosis is a chronic inflammatory vascular disease. Atherosclerotic cardiovascular diseases are the main reason of death in both developed and developing countries. Many pathophysiological factors, such as abnormal cholesterol metabolism, vascular inflammatory response and endothelial dysfunction, vascular smooth muscle cell proliferation and apoptosis, contribute to the development of atherosclerosis; whereas the molecular mechanisms underlying the development of atherosclerosis remains to be fully understood. Ubiquitinati