158 research outputs found
Family history of premature cardiovascular disease as a sole and independent risk factor for increased carotid intima media thickness
No full textOBJECTIVE:
The aim of this study was to evaluate carotid intima-media thickness (cIMT) in children with a positive family history of premature cardiovascular disease (PFHPCD) and the relationship between cIMT and other known risk factors (insulin resistance, oxidant status and lipid profile) involved in structural vascular changes.
METHODS:
Anthropometric measurements and inflammatory markers [isoprostanes (prostaglandin F-2alpha)] were evaluated in 24 prepubertal children (10 boys, 14 girls, mean age 7.9 +/- 2.37 years) with PFHPCD and compared with 25 healthy prepubertal children (11 boys, 14 girls). Fasting insulin and glycemia levels were evaluated and homeostasis model assessment of insulin resistance and fasting glucose-insulin ratio were calculated in all children. High-resolution ultrasound technique was used to evaluate cIMT.
RESULTS:
Children with PFHPCD had an increased cIMT (P = 0.001) in comparison with healthy controls. No significant differences were found in terms of fasting insulin levels (P = 0.416), glucose-insulin ratio (P = 0.454) and homeostasis model assessment of insulin resistance (P = 0.317) between children with PFHPCD and controls. Prostaglandin F-2alpha levels were significantly higher in children with PFHPCD than in controls (P = 0.003). In order to evaluate the relationship between cIMT and other known risk factors, a multiple linear regression analysis was performed. A direct correlation was found between cIMT and prostaglandin F-2alpha (beta = 0.905; P = 0.002; r2, 0.63) even after adjusting for confounding factors (age, sex, BMI).
CONCLUSION:
Signs of precocious cardiovascular risk are detectable in children with PFHPCD already during prepuberty. Furthermore, impaired oxidant-antioxidant status would be implicated in the detected abnormalities of the vascular wall, suggesting a pivotal role of hereditary and genetic predisposition in the pathogenesis of increased cIMT
Punte EEG epilettiche evocate da stimoli somatosensoriali. Aspetti genetici e ricorrenza familiare
No full textImplications of gastrointestinal hormones in the pathogenesis of obesity in prepubertal children.
No full textBackground: There is a worsening high prevalence of global obesity. Special attention has been paid to the gut-endocrine system, represented by the regulators of appetite. In particular, it has been suggested that ghrelin ("hunger" peptide), and obestatin and glucagon-like peptide-1 (GLP-1) ("satiety" peptides) could play important roles in the pathogenesis of obesity. Objectives: The aims of this study were to compare fasting plasma ghrelin, obestatin, and GLP-1 levels between obese and nonobese prepubertal children, and to assess their relations with fatness indexes and insulin resistance (IR). Subjects and methods: Fifty-two prepubertal obese children and 22 controls were enrolled. Fasting levels of gastrointestinal hormones (ghrelin, obestatin, and GLP-1), glucose, and insulin were evaluated. IR was assessed using the homeostasis model assessment of IR (HOMA-IR) index. Analysis was performed by Mann-Whitney U-test, Kruskal-Wallis test, and Spearman's correlation. Results: Obese prepubertal children and normal-weight controls had similar age distribution. Obese children were more insulin resistant when compared to controls (HOMA-IR: p<0.01). GLP-1 levels were significantly lower in obese children than in controls (p<0.01). Obestatin was significantly higher in obese than normal-weight children (p<0.01), while ghrelin was not different. There was a negative correlation between GLP-1 and standard deviation score-body mass index (r=-0.36, p=0.009) and between GLP-1 and waist circumference (r=-0.45, p=0.001), while no association was observed with HOMA-IR. Conclusions: GLP-1 levels have been shown to be correlated with adiposity indexes, but not with HOMA-IR, suggesting that this hormone could play an important role in the early development of obesity
Insulin resistance and oxidative stress in children born small and large for gestational age
No full text
Rilievi neuropsicologici e considerazioni in ambito riabilitativo in tossicodipendenti affetti da sieropositività da HIV
No full textAssociation between markers of endothelial dysfunction and early signs of renal dysfunction in pediatric obesity and type 1 diabetes
No full textBACKGROUND:
To evaluate whether circulating markers of endothelial dysfunction, such as intercellular adhesion molecule-1 (ICAM-1) and myeloperoxidase (MPO), are increased in youth with obesity and in those with type 1 diabetes (T1D) at similar levels, and whether their levels are associated with markers of renal function.
METHODS:
A total of 60 obese youth [M/F: 30/30, age: 12.5 ± 2.8 yr; body mass index (BMI) z-score: 2.26 ± 0.46], 30 with T1D (M/F: 15/15; age: 12.9 ± 2.4 yr; BMI z-score: 0.45 ± 0.77), and 30 healthy controls (M/F: 15/15, age: 12.4 ± 3.3 yr, BMI z-score: -0.25 ± 0.56) were recruited. Anthropometric measurements were assessed and a blood sample was collected to measure ICAM-1, MPO, creatinine, cystatin C and lipid levels. A 24-h urine collection was obtained for assessing albumin excretion rate (AER).
RESULTS:
Levels of ICAM-1 and MPO were significantly higher in obese [ICAM-1: 0.606 (0.460-1.033) μg/mL; MPO: 136.6 (69.7-220.8) ng/mL] and T1D children [ICAM-1: 0.729 (0.507-0.990) μg/mL; MPO: 139.5 (51.0-321.3) ng/mL] compared with control children [ICAM-1: 0.395 (0.272-0.596) μg/mL MPO: 41.3 (39.7-106.9) ng/mL], whereas no significant difference was found between T1D and obese children. BMI z-score was significantly associated with ICAM-1 (β = 0.21, p = 0.02) and MPO (β = 0.41, p < 0.001). A statistically significant association was also found between ICAM-1 and markers of renal function (AER: β = 0.21, p = 0.03; e-GFR: β = 0.19, p = 0.04), after adjusting for BMI.
CONCLUSIONS:
Obese children have increased markers of endothelial dysfunction and early signs of renal damage, similarly to children with T1D, confirming obesity to be a cardiovascular risk factor as T1D. The association between ICAM-1 with e-GFR and AER confirm the known the association between general endothelial and renal dysfunction
Inflammatory Infiltrate and Angiogenesis in Mantle Cell Lymphoma
No full textMantle cell lymphoma (MCL) is an aggressive and rare B-cell non-Hodgkin lymphoma classified in two clinicopathological subtypes according to SOX11 expression and mutation state of immunoglobulin variable region heavy chain (IgVH) gene. The transcription factor SOX11, overexpressed in 78%-93% of MCL patients, plays a central role in modulating tumor microenvironment prosurvival signals and angiogenic genes. In this work, we have explored the lymph node microenvironment of three subgroups of MCL patients classified according to SOX11 expression as negative, light, and strong. CD34+ microvessels, CD4+ and CD8+ T-lymphocytes, CD68+ and CD163+ macrophages, and the oncogene p53 expression were evaluated by immunohistochemistry. Moreover, STAT3 mRNA expression was analyzed by RNA-scope assay. Our results confirmed increased angiogenesis in the sample of patients positive to SOX11 compared to the negative ones and demonstrated that angiogenesis and SOX11 expression positively correlate to a higher T-lymphocytes inflammatory infiltrate. On the contrary, angiogenesis and SOX11 expression negatively correlate with macrophage's inflammatory infiltrate and p53 expression. STAT3 mRNA expression level was not relevant concerning angiogenesis or SOX11 expression. Overall, our data indicate that, in MCL, SOX11 expression is associated with increased angiogenesis and a high CD4+ and CD8+ T-cell infiltration, which are not sustained by CD163+ macrophages infiltrate and p53 expression
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