Chromosomal damage induced in human lymphocytes by low doses of D-T neutrons

Unstable chromosome aberrations induced by in vitro irradiation with zero plus seven low doses of 14.8 MeV D-T neutrons in the range 3.55-244 mGy have been analysed in human peripheral blood lymphocytes. In order to obtain the required large numbers of scored cells for such low doses, fourteen laboratories participated in the experiment. The dose responses for dicentrics, excess acentrics and total aberrations, fitted well to the Y = &#945;D model. The &#945; coefficient of yield for dicentrics, 1.60 &#177; 0.07 &#215; 10-<SUP>2</SUP> Gy-<SUP>1</SUP>, compares well with the values obtained in previous studies with D-T neutrons at somewhat higher doses. Results from a previous collaborative study using 250 kVp X-rays over a comparable dose range indicated the possible existence of a threshold below 50 mGy. In the present study there is no clear evidence for neutrons for such a threshold. However, the data were insufficient to permit the rejection of a possible threshold below ~10 mGy

Neuroglia:Functional paralysis and reactivity in Alzheimer’s disease and other neurodegenerative pathologies

The most notable finding in neurodegenerative diseases is the progressive death of neurones cells. Yet, neuroglial changes can precede and facilitate neuronal loss. This is perhaps expected because astroglial cells maintain the brain homoeostasis, and are responsible for defence and regeneration, so that their malfunction manifested as degeneration or asthenia together with reactivity contribute to pathophysiology. Neuroglia may represent a novel target for therapeutic intervention, be that prevention, slowing progression of or possibly curing neurodegenerative diseases.</p

Vascular Alterations in Mental Disorders: Focus in Angiotensin II Role

Mental disorders have high prevalence and long duration, affecting the quality of life and generating elevated economic costs in public health. Approximately 25% of population worldwide will develop any mental illness at some moment of its lifetime. These disorders are the result of complex processes involving the interaction of many pathological changes. Although, each psychiatric disease has well-defined characteristics, some of their neurobiological processes, like inflammation and vascular alterations, seem to be common. Since microvasculature is involved in essential functions as oxygen delivery, waste product removal, and transvascular exchange, any brain vessel alteration could promote a pathological state. In this sense, capillary ultrastructural abnormalities, deficient perfusion, and blood-brain barrier disruption have been described in schizophrenia, depression, and Parkinson?s and Alzheimer?s diseases. These vascular dysfunctions could be related to angiogenic factor deregulations. The abovementioned evidences point out to evaluate the vasculature as a future pharmacological target for the treatment of mental disorders. Among the several factors involved in the regulation of angiogenesis, this chapter will focus on the upstream angiogenic mediator Angiotensin II. This peptide is produced at peripheral and brain level and exerts its principal effects acting through AT1 receptors. Considering that the available treatments for mental illnesses have low efficacy and high incidence of side effects, new pharmacological tools become necessary. The present chapter will be focused in the evidences that support Angiotensin II as a key factor in the understanding and therapy of these pathologies.Fil: Delgado Marín, Leticia Ester. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones Biológicas y Tecnológicas. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Instituto de Investigaciones Biológicas y Tecnológicas; ArgentinaFil: Basmadjian, Osvaldo Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Occhieppo, Victoria Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Marchese, Natalia Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Bregonzio Diaz, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Baiardi, Gustavo Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones Biológicas y Tecnológicas. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Instituto de Investigaciones Biológicas y Tecnológicas; Argentin

Astroglia in Alzheimer’s Disease

Alzheimer’s disease is the most common cause of dementia. Cellular changes in the brains of the patients suffering from Alzheimer’s disease occur well in advance of the clinical symptoms. At the cellular level, the most dramatic is a demise of neurones. As astroglial cells carry out homeostatic functions of the brain, it is certain that these cells are at least in part a cause of Alzheimer’s disease. Historically, Alois Alzheimer himself has recognised this at the dawn of the disease description. However, the role of astroglia in this disease has been understudied. In this chapter, we summarise the various aspects of glial contribution to this disease and outline the potential of using these cells in prevention (exercise and environmental enrichment) and intervention of this devastating disease.</p