Joana Rosmaninho Salgado

Professor Auxiliar

Joana Rosmaninho Salgado

Professor Auxiliar

Generic Bio

Licenciada em Biologia pela Universidade de Coimbra em 2000 e Doutorada em Ciências da Saúde e Tecnologia, especialidade de Biologia Celular e Molecular pela Faculdade de Farmácia da Universidade de Coimbra em 2007. Realizou Pós-doutoramento até 2013 no Centro de Neurociências e Biologia Celular da Universidade de Coimbra. Em 2013 terminou o mestrado integrado em Medicina pela Universidade de Coimbra.

Atualmente é médica interna no Serviço de Genética Médica do Centro Hospitalar de Coimbra.

A principal área de interesse é a obesidade, tendo realizado pos-doutoramento nesta área no Centro de Neurociências de Coimbra.

Publications

Paper

Bifocal germinoma in a patient with 16p11.2 microdeletion syndrome.

Salgado, J. (2019). Bifocal germinoma in a patient with 16p11.2 microdeletion syndrome.. Endocrinology, diabetes & metabolism case reports

Docente da FCSE e investigadora do CIIS é keynote Speaker na European Conference on Religion, Spirituality and Health

Artigo de Opinião - O Sistema de Verificação de Incapacidades da Segurança Social: uma atualização que urge formação

Open Day Mestrado em Cuidados Paliativos

Joana Rosmaninho Salgado

Joana Rosmaninho Salgado

Generic Bio

Bifocal germinoma in a patient with 16p11.2 microdeletion syndrome.

Catecolaminas

Circulating EM66 is a highly sensitive marker for the diagnosis and follow-up of pheochromocytoma

Corrigendum to "Intracellular mechanisms coupled to NPY Y2 and Y5 receptor activation and lipid accumulation in murine adipocytes" [neuropeptides 46/6 (2012) 359-366].

CYP21A2 Gene Pathogenic Variants: A Multicenter Study on Genotype-Phenotype Correlation from a Portuguese Pediatric Cohort.

Deletion of the neuropeptide Y (NPY) Y1 receptor gene reveals a regulatory role of NPY on catecholamine synthesis and secretion.

Dipeptidyl peptidase IV (DPP-IV) inhibition prevents fibrosis in adipose tissue of obese mice

Dipeptidyl-peptidase-IV by cleaving neuropeptide Y induces lipid accumulation and PPAR-γ expression.

Glial-derived neurotrophic factor modulates enteric neuronal survival and proliferation through neuropeptide Y.

Heterozygous variants in SPTBN1 cause intellectual disability and autism.

Hypoxia mimetic blocks adipocyte differentiation but induces lipid accumulation

Hypoxia mimetic induces lipid accumulation through mitochondrial dysfunction and stimulates autophagy in murine preadipocyte cell line.

Impaired adrenal medullary function in a mouse model of depression induced by unpredictable chronic stress.

Interaction between neuropeptide Y (NPY) and brain-derived neurotrophic factor in NPY-mediated neuroprotection against excitotoxicity: a role for microglia.

Intracellular mechanisms coupled to NPY Y2 and Y5 receptor activation and lipid accumulation in murine adipocytes.

Intracellular signaling mechanisms mediating catecholamine release upon activation of NPY Y1 receptors in mouse chromaffin cells.

Isolation, characterization, and differentiation of progenitor cells from human adult adrenal medulla.

MC3R links nutritional state to childhood growth and the timing of puberty

Moderate long-term modulation of neuropeptide Y in hypothalamic arcuate nucleus induces energy balance alterations in adult rats.

Neuropeptide Y inhibits [Ca2+]i changes in rat retinal neurons through NPY Y1, Y4, and Y5 receptors.

Neuropeptide Y regulates catecholamine release evoked by interleukin-1beta in mouse chromaffin cells.

Neuropeptide Y stimulates retinal neural cell proliferation--involvement of nitric oxide.

Nitric oxide stimulates the proliferation of neural stem cells bypassing the epidermal growth factor receptor.

NPY in rat retina is present in neurons, in endothelial cells and also in microglial and Muller cells.

Regulation of catecholamine release and tyrosine hydroxylase in human adrenal chromaffin cells by interleukin-1beta: role of neuropeptide Y and nitric oxide.

Regulation of catecholamine release in human adrenal chromaffin cells by β-adrenoceptors.

Stress-induced hypertension and increased sympathetic activity in mice overexpressing neuropeptide Y in noradrenergic neurons.