Microcephaly and macrocephaly. A study on anthropometric and clinical data from 308 subjects

Head circumference is the auxological parameter that most correlates with developmental anomalies in childhood. Head circumference (HC) two standard deviations (SD) below or above the mean defines microcephaly and macrocephaly, respectively. The aim of this retrospective study was to explore anthropometric parameters and clinical characteristics among subjects with abnormalities in HC who had been referred for developmental assessment. One hundred and sixty four subjects with microcephaly and 144 subjects with macrocephaly were enrolled from birth to 18 months of age. Head circumference at birth and the association with variables related to maternal health status, gestational age, growth pattern, brain imaging and clinical characteristics were analyzed. In some cases, an etiological diagnosis was made. In the two considered conditions, we found different anthropometric and clinical associations, some of which were statistically significant, with implications for ongoing neurodevelopmental surveillance

POTENZIALI EVOCATI VISIVI DA FLASH IN GEMELLI IN EPOCA NEONATALE. CORRELAZIONI CON LA ADEGUATEZZA DEL PESO CON LA ETA' GESTAZIONALE (AGA VS SGA)

Neonati AGA, SGA, PE

Oxidative Stress and Heme Oxygenase-1 Regulated Human Mesenchymal Stem Cells Differentiation

This paper describes the effect of increased expression of HO-1 protein and increased levels of HO activity on differentiation of bone-marrow-derived human MSCs. MSCs are multipotent cells that proliferate and differentiate into many different cell types including adipocytes and osteoblasts. HO, the rate-limiting enzyme in heme catabolism, plays an important role during MSCs differentiation. HO catalyzes the stereospecific degradation of heme to biliverdin, with the concurrent release of iron and carbon monoxide. Upregulation of HO-1 expression and increased HO activity are essential for MSC growth and differentiation to the osteoblast lineage consistent with the role of HO-1 in hematopoietic stem cell differentiation. HO-1 participates in the MSC differentiation process shifting the balance of MSC differentiation in favor of the osteoblast lineage by decreasing PPARγ and increasing osteogenic markers such as alkaline phosphatase and BMP-2. In this paper, we define HO-1 as a target molecule in the modulation of adipogenesis and osteogenesis from MSCs and examine the role of the HO system in diabetes, inflammation, osteoporosis, hypertension, and other pathologies, a burgeoning area of research

Monitoring and modelling of soil–plant interactions: the joint use of ERT, sap flow and eddy covariance data to characterize the volume of an orange tree root zone

Abstract. Mass and energy exchanges between soil, plants and atmosphere control a number of key environmental processes involving hydrology, biota and climate. The understanding of these exchanges also play a critical role for practical purposes e.g. in precision agriculture. In this paper we present a methodology based on coupling innovative data collection and models in order to obtain quantitative estimates of the key parameters of such complex flow system. In particular we propose the use of hydro-geophysical monitoring via "time-lapse" electrical resistivity tomography (ERT) in conjunction with measurements of plant transpiration via sap flow and evapotranspiration (ET) from eddy covariance (EC). This abundance of data is fed to spatially distributed soil models in order to characterize the distribution of active roots. We conducted experiments in an orange orchard in eastern Sicily (Italy), characterized by the typical Mediterranean semi-arid climate. The subsoil dynamics, particularly influenced by irrigation and root uptake, were characterized mainly by the ERT set-up, consisting of 48 buried electrodes on 4 instrumented micro-boreholes (about 1.2 m deep) placed at the corners of a square (with about 1.3 m long sides) surrounding the orange tree, plus 24 mini-electrodes on the surface spaced 0.1 m on a square grid. During the monitoring, we collected repeated ERT and time domain reflectometry (TDR) soil moisture measurements, soil water sampling, sap flow measurements from the orange tree and EC data. We conducted a laboratory calibration of the soil electrical properties as a function of moisture content and porewater electrical conductivity. Irrigation, precipitation, sap flow and ET data are available allowing for knowledge of the system's long-term forcing conditions on the system. This information was used to calibrate a 1-D Richards' equation model representing the dynamics of the volume monitored via 3-D ERT. Information on the soil hydraulic properties was collected from laboratory and field experiments. The successful results of the calibrated modelling exercise allow for the quantification of the soil volume interested by root water uptake (RWU). This volume is much smaller (with a surface area less than 2 m2, and about 40 cm thick) than expected and assumed in the design of classical drip irrigation schemes that prove to be losing at least half of the irrigated water which is not taken up by the plants

Diagnostic delay does not influence survival of pancreatic cancer patients

Background: Most pancreatic ductal adenocarcinoma patients present with advanced disease. Whether it is possible to increase survival by earlier diagnosis is unclear. Objective: The purpose of this study was to investigate the association between presenting complaints and risk factors for pancreatic cancer with diagnostic delay, stage and survival. Methods: This was a single-centre retrospective cohort study. Consecutive patients were interviewed and data on demographics, medical history, risk factors and complaints leading to pancreatic ductal adenocarcinoma diagnosis and disease stage were recorded. Diagnostic delay was considered as time between first complaint and diagnosis. Patients received appropriate treatments and their outcome was recorded in a dedicated database. The Chi-square test for comparison of categorical variables and the Mann–Whitney test for continuous variables were employed with Bonferroni corrections. Correlation between continuous variables was evaluated by means of the Spearman correlation coefficient. Survival analysis was performed with the Kaplan–Meier method and a log-rank test. Results: The median diagnostic delay for 477 pancreatic ductal adenocarcinoma patients was two months (interquartile range 1–5), being significantly shorter for patients presenting with jaundice compared with those with pain, weight loss, diabetes (p < 0.001). The global rate of metastatic disease at diagnosis was 40%, being only 22% in those presenting with jaundice. The median diagnostic delay, however, was not significantly different among disease stages but was significantly longer in patients with a body mass index>25 kg/m2. The median survival time was seven months. Factors associated with worse survival at the multivariable analysis were older age (hazard ratio 1.02 per year), metastatic disease (hazard ratio 2.12) and pain as presenting complaint (hazard ratio 1.32), while diagnostic delay was not. Conclusion: While some complaints are associated with a shorter diagnostic delay and less advanced disease stage, we could not demonstrate that delay is associated with survival, possibly suggesting that prevention rather than early recognition is important to tackle pancreatic cancer lethality

Oxidative Stress and Heme Oxygenase-1 Regulated Human Mesenchymal Stem Cells Differentiation

This paper describes the effect of increased expression of HO-1 protein and increased levels of HO activity on differentiation of bone-marrow-derived human MSCs. MSCs are multipotent cells that proliferate and differentiate into many different cell types including adipocytes and osteoblasts. HO, the rate-limiting enzyme in heme catabolism, plays an important role during MSCs differentiation. HO catalyzes the stereospecific degradation of heme to biliverdin, with the concurrent release of iron and carbon monoxide. Upregulation of HO-1 expression and increased HO activity are essential for MSC growth and differentiation to the osteoblast lineage consistent with the role of HO-1 in hematopoietic stem cell differentiation. HO-1 participates in the MSC differentiation process shifting the balance of MSC differentiation in favor of the osteoblast lineage by decreasing PPARγ and increasing osteogenic markers such as alkaline phosphatase and BMP-2. In this paper, we define HO-1 as a target molecule in the modulation of adipogenesis and osteogenesis from MSCs and examine the role of the HO system in diabetes, inflammation, osteoporosis, hypertension, and other pathologies, a burgeoning area of research

IPOGLICEMIA NEONATALE: RILIEVI EPIDEMIOLOGICI IN UN CAMPIONE DI NEONATI RICOVERATI (2012-2017)

ipoglicemia neonatal

Glutamate-evoked redox state alterations are involved in tissue transglutaminase upregulation in primary astrocyte cultures

AbstractThe aim of this study was to evaluate the involvement of oxidative stress in glutamate-evoked transglutaminase (TGase) upregulation in astrocyte cultures (14 DIV). A 24 h exposure to glutamate caused a dose-dependent depletion of glutathione intracellular content and increased the ROS production in cell cultures. These effects were receptor-mediated, as demonstrated by inhibition with GYKI 52466. The pre-incubation with glutathione ethyl ester or cysteamine recovered oxidative status and was effective in significantly reducing glutamate-increased tissue TGase. These data suggest that tissue TGase upregulation may be part of a biochemical response to oxidative stress induced by a prolonged exposure of astrocyte cultures to glutamate

Development of NASH in Obese Mice is Confounded by Adipose Tissue Increase in Inflammatory NOV and Oxidative Stress

Aim. Nonalcoholic steatohepatitis (NASH) is the consequence of insulin resistance, fatty acid accumulation, oxidative stress, and lipotoxicity.We hypothesize that an increase in the inflammatory adipokine NOV decreases antioxidant Heme Oxygenase 1 (HO- 1) levels in adipose and hepatic tissue, resulting in the development of NASH in obese mice. Methods. Mice were fed a high fat diet (HFD) and obese animals were administered an HO-1 inducer with or without an inhibitor of HO activity to examine levels of adipose-derived NOV and possible links between increased synthesis of inflammatory adipokines and hepatic pathology. Results. NASH mice displayed decreased HO-1 levels and HO activity, increased levels of hepatic heme, NOV, MMP2, hepcidin, and increased NAS scores and hepatic fibrosis. IncreasedHO-1 levels are associated with a decrease in NOV, improved hepatic NAS score, ameliorated fibrosis, and increases in mitochondrial integrity and insulin receptor phosphorylation. Adipose tissue function is disrupted in obesity as evidenced by an increase in proinflammatory molecules such as NOV and a decrease in adiponectin. Importantly, increased HO-1 levels are associated with a decrease of NOV, increased adiponectin levels, and increased levels of thermogenic and mitochondrial signaling associated genes in adipose tissue. Conclusions.These results suggest that the metabolic abnormalities in NASH are driven by decreased levels of hepatic HO-1 that is associated with an increase in the adipose-derived proinflammatory adipokine NOV in our obese mouse model of NASH. Concurrently, induction of HO-1 provides protection against insulin resistance as seen by increased insulin receptor phosphorylation. Pharmacological increases in HO-1 associated with decreases in NOV may offer a potential therapeutic approach in preventing fibrosis, mitochondrial dysfunction, and the development of NASH

Ablation of Soluble Epoxide Hydrolase Reprogram White Fat to Beige-Like Fat Through an Increase in Mitochondrial Integrity, HO-1-Adiponectin in vitro and in vivo

We have shown that epoxyeicosatrienoic acids (EETs), specifically 11,12- and 14,15-EETs, reduce adipogenesis in human mesenchymal stem cells and mouse preadipocytes (3T-3L1). In this study, we explore the effects of soluble epoxide hydrolase (sEH) deletion on various aspects of adipocyte-function, including programing for white vs. beige-like fat, and mitochondrial and thermogenic gene-expressions. We further hypothesize that EETs and heme-oxygenase 1 (HO-1) form a synergistic, functional module whose effects on adipocyte and vascular function is greater than the effects of sEH deletion alone. In in vitro studies, we examined the effect of sEH inhibitors on MSC-derived adipocytes. MSC-derived adipocytes exposed to AUDA, an inhibitor of sEH, exhibit an increased number of small and healthy adipocytes, an effect reproduced by siRNA for sEH. in vivo studies indicate that sEH deletion results in a significant decrease in adipocyte size, inflammatory adipokines NOV, TNFalpha, while increasing adiponectin (p \u3c 0.05). These findings are associated with a decrease in body weight (p \u3c 0.05), and visceral fat (p \u3c 0.05). Importantly, sEH deletion was associated with a significant increase in Mfn1, COX 1, UCP1 and adiponectin (p \u3c 0.03). sEH deletion was manifested by a significant increase in EETs isomers 5,6-EET, 8,9-EET, 11,12-EET, and 14,15-EET and an increased EETs/DHETEs ratio. Notably, activation of HO-1 gene expression further increased the levels of EETs, suggesting that the antioxidant HO-1 system protects EETs from degradation by ROS. These results are novel in that sEH deletion, while increasing EET levels, resulted in reprograming of white fat to express mitochondrial and thermogenic genes, a phenotype characteristic of beige-fat. Thus, EETs agonist(s) and sEH inhibitors may have therapeutic potential in the treatment of metabolic syndrome and obesity