Contextual analysis of health care at discharge in leprosy: an integrative review

Objective: To analyze contextual relations of health care in the discharge of leprosy. Method: An analytical, reflexive study based on the theoretical framework of context analysis, elaborated through an integrative review of literature in the databases SCOPUS, PUBMED, LILACS, SCIELO and BDENF, with uncontrolled descriptors Leprosy and Patient Discharge, obtaining 14 publications. Results: The immediate context addresses health care at discharge in leprosy; the specific context treats leprosy as a public health problem; the symbolic conceptions and marks involving leprosy are encompassed by the general context; and in the metacontext are described the health programs and policies that subsidize the care of leprosy patients. Conclusion: The contextual elements emphasize the need to guarantee universal coverage of cases of leprosy, from diagnosis to the post-discharge, reinforcing leprosy as a public health problem. Despitehe limitations of the bibliographic studies, these have relevance for the health area

TGF-beta in neural stem cells and in tumors of the central nervous system

Mechanisms that regulate neural stem cell activity in the adult brain are tightly coordinated. They provide new neurons and glia in regions associated with high cellular and functional plasticity, after injury, or during neurodegeneration. Because of the proliferative and plastic potential of neural stem cells, they are currently thought to escape their physiological control mechanisms and transform to cancer stem cells. Signals provided by proteins of the transforming growth factor (TGF)-beta family might represent a system by which neural stem cells are controlled under physiological conditions but released from this control after transformation to cancer stem cells. TGF-beta is a multifunctional cytokine involved in various physiological and patho-physiological processes of the brain. It is induced in the adult brain after injury or hypoxia and during neurodegeneration when it modulates and dampens inflammatory responses. After injury, although TGF-beta is neuroprotective, it may limit the self-repair of the brain by inhibiting neural stem cell proliferation. Similar to its effect on neural stem cells, TGF-beta reveals anti-proliferative control on most cell types; however, paradoxically, many brain tumors escape from TGF-beta control. Moreover, brain tumors develop mechanisms that change the anti-proliferative influence of TGF-beta into oncogenic cues, mainly by orchestrating a multitude of TGF-beta-mediated effects upon matrix, migration and invasion, angiogenesis, and, most importantly, immune escape mechanisms. Thus, TGF-beta is involved in tumor progression. This review focuses on TGF-beta and its role in the regulation and control of neural and of brain-cancer stem cells