22 research outputs found
Assessment of Parathyroid Function in Clinical Practice: Which Parathyroid Hormone Assay Is Better?
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The Neuroprotective Effects of 17ÎČ-Estradiol Pretreatment in a Model of Neonatal Hippocampal Injury Induced by Trimethyltin
Hippocampal dysfunction plays a central role in neurodevelopmental disorders, resulting in severe impairment of cognitive abilities, including memory and learning. On this basis, developmental studies represent an important tool both to understanding the cellular and molecular phenomena underlying early hippocampal damage and to study possible therapeutic interventions, that may modify the progression of neuronal death. Given the modulatory role played by 17ÎČ-estradiol (E2) on hippocampal functions and its neuroprotective properties, the present study investigates the effects of pretreatment with E2 in a model of neonatal hippocampal injury obtained by trimethyltin (TMT) administration, characterized by neuronal loss in CA1 and CA3 subfields and astroglial and microglial activation. At post-natal days (P)5 and P6 animals received E2 administration (0.2 mg/kg/die i.p.) or vehicle. At P7 they received a single dose of TMT (6.5 mg/kg i.p.) and were sacrificed 72 h (P10) or 7 days after TMT treatment (P14). Our findings indicate that pretreatment with E2 exerts a protective effect against hippocampal damage induced by TMT administration early in development, reducing the extent of neuronal death in the CA1 subfield, inducing the activation of genes involved in neuroprotection, lowering the neuroinflammatory response and restoring neuropeptide Y- and parvalbumin- expression, which is impaired in the early phases of TMT-induced damage. Our data support the efficacy of estrogen-based neuroprotective approaches to counteract early occurring hippocampal damage in the developing hippocampus
Contributo al femminile allâeducazione tecnica e scientifica per le materie STEM. Fare rete tra scienziate/i, enti, universitĂ , associazioni, media e portatori dâinteresse
Questo âcontributo al femminileâ Ăš stato realizzato da un gruppo di perso-
ne che ambisce a contribuire al miglioramento dellâeducazione scolastica; Ăš
destinato a donne, uomini, ragazze, ragazzi, bambine e bambini per mettere in
luce potenzialitĂ , diseguaglianze, specificitĂ di vita e professionali e favorire la
paritĂ di genere soprattutto negli ambiti tecnico-scientifici, in particolar modo
nelle discipline STEM (Science, Technology, Engineering, Mathematics)
The neuroprotective effects of 17ÎČ-estradiol pretreatment in a model of neonatal hippocampal injury induced by trimethyltin
Hippocampal dysfunction plays a central role in neurodevelopmental disorders, resulting in severe impairment of cognitive abilities, including memory and learning. On this basis, developmental studies represent an important tool both to understanding the cellular and molecular phenomena underlying early hippocampal damage and to study possible therapeutic interventions, that may modify the progression of neuronal death. Given the modulatory role played by 17ÎČ-estradiol (E2) on hippocampal functions and its neuroprotective properties, the present study investigates the effects of pretreatment with E2 in a model of neonatal hippocampal injury obtained by trimethyltin (TMT) administration, characterized by neuronal loss in CA1 and CA3 subfields and astroglial and microglial activation. At post-natal days (P)5 and P6 animals received E2 administration (0.2 mg/kg/die i.p.) or vehicle. At P7 they received a single dose of TMT (6.5 mg/kg i.p.) and were sacrificed 72 h (P10) or 7 days after TMT treatment (P14). Our findings indicate that pretreatment with E2 exerts a protective effect against hippocampal damage induced by TMT administration early in development, reducing the extent of neuronal death in the CA1 subfield, inducing the activation of genes involved in neuroprotection, lowering the neuroinflammatory response and restoring neuropeptide Y- and parvalbumin- expression, which is impaired in the early phases of TMT-induced damage. Our data support the efficacy of estrogen-based neuroprotective approaches to counteract early occurring hippocampal damage in the developing hippocampus
Bone marrowâderived mesenchymal stem cells promote invasiveness and transendothelial migration of osteosarcoma cells via a mesenchymal to amoeboid transition
There is growing evidence to suggest that bone marrowâderived mesenchymal stem cells (BMâMSCs) are key players in tumour stroma. Here, we investigated the crossâtalk between BMâMSCs and osteosarcoma (OS) cells. We revealed a strong tropism of BMâMSCs towards these tumour cells and identified monocyte chemoattractant protein (MCP)â1, growthâregulated oncogene (GRO)âα and transforming growth factor (TGF)âÎČ1 as pivotal factors for BMâMSC chemotaxis. Once in contact with OS cells, BMâMSCs transâdifferentiate into cancerâassociated fibroblasts, further increasing MCPâ1, GROâα, interleukin (IL)â6 and ILâ8 levels in the tumour microenvironment. These cytokines promote mesenchymal to amoeboid transition (MAT), driven by activation of the small GTPase RhoA, in OS cells, as illustrated by the in vitro assay and live imaging. The outcome is a significant increase of aggressiveness in OS cells in terms of motility, invasiveness and transendothelial migration. In keeping with their enhanced transendothelial migration abilities, OS cells stimulated by BMâMSCs also sustain migration, invasion and formation of the in vitro capillary network of endothelial cells. Thus, BMâMSC recruitment to the OS site and the consequent cytokineâinduced MAT are crucial events in OS malignancy
HLA DR and DQ alleles in Italian patients with melanoma.
Controversial data have been reported about HLA alleles and susceptibility to melanoma. Our investigation was undertaken to analyze the relationship between HLA alleles distribution in patients with melanoma and susceptibility to the tumor, in order to study the possible correlation between HLA class II DQA1, DQB1 and DRB1 genes involved in immune recognition, and melanoma, usually considered a highly immunogenic tumor. We therefore typed by means of PCR-SSP (sequence-specific primers) 53 Italian patients and 53 healthy random controls coming from the same geographic area. We observed a decrease of all haplotypes bearing DQB1*0301, DQB1*0302 and DQB1*0303 alleles but not of haplotype DRB1*11;DQA1*0501;DQB1*0301. Our results seem to support the hypothesis of a protective role of some DQ3-bearing haplotypic combinations in melanoma
Epithelial lining fluid free IGF-I-to-PAPP-A ratio is associated with bronchopulmonary dysplasia in preterm infants
Cardiovascular risk factors in healthy women with previous small for gestational age infants.
Aim:â To investigate whether healthy women with a previous pregnancy complicated by a small for gestational age (SGA) infant have normal endothelial function, carbohydrate and lipid metabolism, and normal inflammation parameters. Material and Methods:â Brachial artery flow-mediated dilatation (FMD, endothelium-dependent) was measured in 16 subjects with previous SGA, and in 15 controls (CTR) with previous normal pregnancies. Lipid panel, glucose, insulin, tumor necrosis factor alpha (TNF-alpha), soluble intercellular adhesion molecule-1 (s-ICAM), soluble vascular (s-VCAM-1) adhesion molecule-1 (s-VCAM-1), and androgens were also measured. Results:â FMD was reduced in women with previous SGA compared to controls (Pâ<â0.0001). SGA women showed increased insulin resistance (Pâ<â0.0001), s-ICAM-1 (Pâ=â0.008), TNF-alpha (Pâ=â0.02), testosterone (Pâ=â0.03), and diastolic blood pressure (Pâ=â0.01) than CTR. Conclusion:â Endothelial dysfunction, reduced insulin sensitivity and subclinical inflammation are present in otherwise healthy women with previous SGA. These abnormalities show that the presence of a SGA infant in the obstetric history should be considered as a risk factor for cardiovascular disease later in life