138 research outputs found

    A 12-month follow-up of the immune response to SARS-CoV-2 primary vaccination: evidence from a real-world study

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    A real-world population-based longitudinal study, aimed at determining the magnitude and duration of immunity induced by different types of vaccines against COVID-19, started in 2021 by enrolling a cohort of 2,497 individuals at time of their first vaccination. The study cohort included both healthy adults aged ≤65 years and elderly subjects aged >65 years with two or more co-morbidities. Here, patterns of anti-SARS-CoV-2 humoral and cell-mediated specific immune response, assessed on 1,182 remaining subjects, at 6 (T6) and 12 months (T12) after the first vaccine dose, are described. At T12 median anti-Spike IgG antibody levels were increased compared to T6. The determinants of increased anti-Spike IgG were the receipt of a third vaccine dose between T6 and T12 and being positive for anti-Nucleocapside IgG at T12, a marker of recent infection, while age had no significant effect. The capacity of T12 sera to neutralize in vitro the ancestral B strain and the Omicron BA.5 variant was assessed in a subgroup of vaccinated subjects. A correlation between anti-S IgG levels and sera neutralizing capacity was identified and higher neutralizing capacity was evident in healthy adults compared to frail elderly subjects and in those who were positive for anti-Nucleocapside IgG at T12. Remarkably, one third of T12 sera from anti-Nucleocapside IgG negative older individuals were unable to neutralize the BA.5 variant strain. Finally, the evaluation of T-cell mediated immunity showed that most analysed subjects, independently from age and comorbidity, displayed Spike-specific responses with a high degree of polyfunctionality, especially in the CD8 compartment. In conclusion, vaccinated subjects had high levels of circulating antibodies against SARS-CoV-2 Spike protein 12 months after the primary vaccination, which increased as compared to T6. The enhancing effect could be attributable to the administration of a third vaccine dose but also to the occurrence of breakthrough infection. Older individuals, especially those who were anti-Nucleocapside IgG negative, displayed an impaired capacity to neutralize the BA.5 variant strain. Spike specific T-cell responses, able to sustain immunity and maintain the ability to fight the infection, were present in most of older and younger subjects assayed at T1

    Fetal Exposure to Maternal Depressive Symptoms Is Associated With Cortical Thickness in Late Childhood

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    BACKGROUND: Maternal depression is one of the most common prenatal complications. The consequences of fetal exposure to maternal depression are poorly understood. The aim of this study is to examine the association between fetal exposure to maternal depressive symptoms and cortical thickness in 6–9 year-old children. METHODS: A prospective, longitudinal study of maternal depressive symptoms at 19, 25 and 31 weeks gestation was followed by acquisition of a structural MRI scan in 81 children (86.1 ± 9.9 months). RESULTS: Significant (p<.01) cortical thinning in children primarily in the right frontal lobes was associated with exposure to prenatal maternal depression. The strongest association was at 25 weeks gestation; exposure to maternal depression at 25 gestational weeks was associated with cortical thinning in 19% of the whole cortex and 24% of the frontal lobes, primarily in the right superior, medial orbital and frontal pole regions of the prefrontal cortex (p<.01). The significant association between prenatal maternal depression and child externalizing behavior (p<.05) was mediated by cortical thinning in prefrontal areas of the right hemisphere. CONCLUSIONS: The pattern of cortical thinning in children exposed to prenatal maternal depression is similar to patterns in depressed patients and in individuals with risk for depression. Exposure to prenatal depression coupled with subsequent cortical thinning was associated with presence of externalizing behavior in preadolescent children and may be prodromal markers of risk for dysphoria. Vulnerability to prenatal influences at 25 gestational weeks may result from the enormous growth and dramatic structural changes in the nervous system

    Amniotic fluid insulin and C peptide levels in diabetic and non diabetic women during early pregnancy

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    Thanks to the widespread use of amniocentesis, glucose, insulin, and C peptide have often been measured in amniotic fluid (AF) during late gestation, but little is known about their concentrations during early pregnancy. To better understand early fetal β-cell function under normal conditions and in the presence of maternal diabetes, we measured glucose, insulin, and C peptide in the AF collected during weeks 15-22 in 77 healthy and 9 diabetic women undergoing amniocentesis for clinical indications and compared the results with those obtained during late pregnancy (weeks 34- 36). The AF C peptide concentration was higher in diabetic women (102 ± 53 vs. 38 ± 2 pmol/L), in the women with a family history of diabetes (41 ± 6 vs. 35 ± 2 pmol/L), after the 19th week of gestation (46 ± 5 vs. 35 ± 2 pmol/L; in the presence of lower glucose concentrations), and in the presence of maternal plasma glucose levels greater than 5.56 mmol/L (42 ± 3.5 vs. 34 ± 2 pmol/L). The comparison between early and late gestation showed decreasing glucose and increasing C peptide concentrations in both healthy and diabetic women (in the latter, C peptide values were always 3 times higher), whereas the insulin concentration was increased in late gestation only in diabetic women. The AF C peptide/insulin molar ratio increased throughout pregnancy in both healthy (from 0.97 ± 0.06 to 4.3 ± 1.2) and diabetic (from 2.9 ± 1.1 to 13.2 ± 1.6) women. These parallel changes suggest that the fetal clearance and/or degradation of insulin and C peptide may greatly change during both normal and diabetic gestation

    Twenty-four hr blood pressure monitoring in normotensive type 1 diabetic pregnant women

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    Impaired alpha cell function in conditions with cortisol deficiency

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    Plasma immunoreactive glucagon (IRG), insulin (IRI) and blood glucose (BG) were evaluated in the fasting state and during an arginine test (ATT) in 6 subjects with untreated hypopituitarism (H), in 2 hypopituitary subjects with normal cortisol production (H + C), in 3 subjects with Addison's disease (A) and in 14 normal volunteers (N). No increase in BG was observed in H and A after arginine, mean values being significantly lower than in N. Mean fasting and arginine-stimulated IRI levels were lower in H and A than in N; postabsorptive arginine-induced IRG levels were significantly reduced when compared to N. In contrast IRG levels in the two H + C patients were within the normal range. The impaired IRG production in A and in H (but not in H + C) suggests a close relationship between alpha pancreatic function and cortisol levels
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