Sperimentazione di tecniche SBR nel trattamento "on site delle acque domestiche" per nuclei isolati e case sparse.

Scopo di questo lavoro di tesi è quello di sperimentare “sul campo’’ la validità e l'efficacia di tecniche SBR per il trattamento delle acque domestiche per case sparse e nuclei isolati. Tuttavia quella SBR, pur essendo una tecnica impiantistica, può soddisfare queste esigenze. Grazie alla presenza di un adeguato volume d'accumulo ed al funzionamento ciclico dell'impianto sono annullati tutti i problemi determinati, nei normali impianti in continuo, dalla discontinuità dell'afflusso di reflui (picchi di portata). L'impianto è studiato per ridurre la necessità di manutenzione al minimo: tutte le apparecchiature tecniche sono collocate in un armadio esterno all'impianto ed in vasca ci sono solo le tubazioni. Ciò esclude ogni presenza interna al serbatoio di apparecchiature elettriche e di parti in movimento soggette a usura. Il vantaggio è evidente nella semplificazione delle operazioni di gestione/controllo/manutenzione dell’impianto che non richiedono, di norma, lo svuotamento della cisterna e consentono operazioni più agevoli e sicure.Tutti i movimenti di processo sono supportati da tre sistemi Air Lift azionati da un unico compressore che provvede anche all'immissione dell'ossigeno attraverso l'aeratore tubolare a membrana nella vasca SBR. Il compressore si caratterizza per lunga vita operativa e assoluta silenziosità di funzionamento. Per verificare l’efficacia del processo depurativo indotto dall’impianto SBR installato dalla GreenSolar abbiamo fatto dei prelievi sul liquame in entrata alla camera SBR e su quello in uscita da essa. I campioni così prelevati sono stati analizzati da un laboratorio autorizzato.I valori limite imposti dal DGR n. 1053 sono ampiamente rispettati, tuttavia i risultati ottenuti non sono soddisfacenti relativamente alle potenzialità dell'impianto.

Morfometria di forme carsiche in un possibile "landing site" marziano

Starting from some satellite photos, we try to understand if someone of the many negatives roundish shapes recognized into a complex of two impacts craters could verify the karst phenomenon on Mars. This fact if confirmed could be extremely important to find microbiological life living underground in an area of contact between water and sulfates, shielded from cosmic radiation. In order to verify if these negatives shapes have a karst origin or an impact one, we made several morphometric measurements with particular attention to the length of the axes and to the depth of these depressions. We also studied some other forms (such jagged ridges) as another possible witness of the karst.

Influence of micro-site conditions and environmental gradients on tree-ring based climate reconstructions

Tree-ring chronologies are a powerful natural archive to reconstruct summer temperature variations of the late Holocene with an annual resolution. To develop these long-term proxy records tree-ring series are commonly extended back in time by combining samples from living trees with relict dead material preserved onshore or in lakes. Former studies showed that low frequency variations in such reconstructions can be biased if the relict and recent material is from different origins. A detailed analysis of the influence of various ecological (micro-) habitats representing the recent part is required to estimate potential errors in temperature estimates. The application of collective detrending methods, that comprise absolute growth rates, can produce errors in climate reconstructions and results in an underestimation of past temperatures. The appearance of these kind of micro-site effects is a wide-spread phenomenon that takes place all over Fennoscandia. Future research in this key region for dendroclimatology should take this issue into account. Especially the higher climate response at the lakeshore site is interesting to achieve smaller uncertainties when a tree-ring series is transformed to temperature anomalies. For new composite chronologies the main aim should be to minimize potential biases and this includes also micro-site effects.

The Benefits of Intravenous Thrombolysis Relate to the Site of Baseline Arterial Occlusion in the Echoplanar Imaging Thrombolytic Evaluation Trial (EPITHET)

In ischemic stroke, the site of arterial obstruction has been shown to influence recanalization and clinical outcomes. However, this has not been studied in randomized controlled trials, nor has the impact of arterial obstruction site on reperfusion and infarct growth been assessed. We studied the influence of site and degree of arterial obstruction patients enrolled in the Echoplanar Imaging Thrombolytic Evaluation Trial (EPITHET).

Growth hormone (GH)-releasing hormone increases the expression of the dominant-negative GH isoform in cases of isolated GH deficiency due to GH splice-site mutations

An autosomal dominant form of isolated GH deficiency (IGHD II) can result from heterozygous splice site mutations that weaken recognition of exon 3 leading to aberrant splicing of GH-1 transcripts and production of a dominant-negative 17.5-kDa GH isoform. Previous studies suggested that the extent of missplicing varies with different mutations and the level of GH expression and/or secretion. To study this, wt-hGH and/or different hGH-splice site mutants (GH-IVS+2, GH-IVS+6, GH-ISE+28) were transfected in rat pituitary cells expressing human GHRH receptor (GC-GHRHR). Upon GHRH stimulation, GC-GHRHR cells coexpressing wt-hGH and each of the mutants displayed reduced hGH secretion and intracellular GH content when compared with cells expressing only wt-hGH, confirming the dominant-negative effect of 17.5-kDa isoform on the secretion of 22-kDa GH. Furthermore, increased amount of 17.5-kDa isoform produced after GHRH stimulation in cells expressing GH-splice site mutants reduced production of endogenous rat GH, which was not observed after GHRH-induced increase in wt-hGH. In conclusion, our results support the hypothesis that after GHRH stimulation, the severity of IGHD II depends on the position of splice site mutation leading to the production of increasing amounts of 17.5-kDa protein, which reduces the storage and secretion of wt-GH in the most severely affected cases. Due to the absence of GH and IGF-I-negative feedback in IGHD II, a chronic up-regulation of GHRH would lead to an increased stimulatory drive to somatotrophs to produce more 17.5-kDa GH from the severest mutant alleles, thereby accelerating autodestruction of somatotrophs in a vicious cycle.

PU.1 is regulated by NF-kappaB through a novel binding site in a 17 kb upstream enhancer element

The majority of patients with acute myeloid leukemia (AML) still die of their disease, and novel therapeutic concepts are needed. Timely expression of the hematopoietic master regulator PU.1 is crucial for normal development of myeloid and lymphoid cells. Targeted disruption of an upstream regulatory element (URE) located several kb upstream in the PU.1 promoter decreases PU.1 expression thereby inducing AML in mice. In addition, suppression of PU.1 has been observed in specific subtypes of human AML. Here, we identified nuclear factor-kappaB (NF-kappaB) to activate PU.1 expression through a novel site within the URE. We found sequence variations of this particular NF-kappaB site in 4 of 120 AML patients. These variant NF-kappaB sequences failed to mediate activation of PU.1. Moreover, the synergistic activation of PU.1 together with CEBPB through these variant sequences was also lost. Finally, AML patients with such variant sequences had suppressed PU.1 mRNA expression. This study suggests that changes of a single base pair in a distal element critically affect the regulation of the tumor suppressor gene PU.1 thereby contributing to the development of AML.

Regulation of wingless-type MMTV integration site family (WNT) signalling in pancreatic islets from wild-type and obese mice

TCF7L2 is a type 2 diabetes susceptibility gene and downstream effector of canonical wingless-type MMTV integration site family (WNT) signalling. However, it is unknown whether this pathway is active in adult pancreatic islets in vivo, and whether it is regulated in obesity.

Macular pigment density at the site of altered fundus autofluorescence

The purpose of our study was to determine whether abnormalities of increased or decreased fundus autofluorescence (FAF) are associated with local changes in macular pigment (MP) optical density in patients with age-related maculopathy (ARM) and macular degeneration (ARMD).

Effect of site of lactate infusion on regional lactate exchange in pigs

The rate of extra-hepatic lactate production and the route of influx of lactate to the liver may influence both hepatic and extra-hepatic lactate exchange. We assessed the dose-response of hepatic and extra-hepatic lactate exchange during portal and central venous lactate infusion.

Identification of a fibronectin interaction site in the extracellular matrix protein ameloblastin

Mammalian teeth are composed of hydroxyapatite crystals that are embedded in a rich extracellular matrix. This matrix is produced by only two cell types, the mesenchymal odontoblasts and the ectodermal ameloblasts. Ameloblasts secrete the enamel proteins amelogenin, ameloblastin, enamelin and amelotin. Odontoblasts secrete collagen type I and several calcium-binding phosphoproteins including dentin sialophosphoprotein, dentin matrix protein, bone sialoprotein and osteopontin. The latter four proteins have recently been grouped in the family of the SIBLINGs (small integrin-binding ligand, N-linked glycoproteins) because they display similar gene structures and because they contain an RGD tripeptide sequence that binds to integrin receptors and thus mediates cell adhesion. We have prepared all the other tooth-specific proteins in recombinant form and examined whether they might also promote cell adhesion similar to the SIBLINGs. We found that only ameloblastin consistently mediated adhesion of osteoblastic and fibroblastic cells to plastic or titanium surfaces. The activity was dependent on the intact three-dimensional structure of ameloblastin and required de novo protein synthesis of the adhering cells. By deletion analysis and in vitro mutagenesis, the active site could be narrowed down to a sequence of 13 amino acid residues (VPIMDFADPQFPT) derived from exon 7 of the rat ameloblastin gene or exons 7-9 of the human gene. Kinetic studies and RNA interference experiments further demonstrated that this sequence does not directly bind to a cell surface receptor but that it interacts with cellular fibronectin, which in turn binds to integrin receptors. The identification of a fibronectin-binding domain in ameloblastin might permit interesting applications for dental implantology. Implants could be coated with peptides containing the active sequence, which in turn would recruit fibronectin from the patient's blood. The recruited fibronectin should then promote cell adhesion on the implant surface, thereby accelerating osseointegration of the implant.

An overlapping kinase and phosphatase docking site regulates activity of the retinoblastoma protein

The phosphorylation state and corresponding activity of the retinoblastoma tumor suppressor protein (Rb) are modulated by a balance of kinase and phosphatase activities. Here we characterize the association of Rb with the catalytic subunit of protein phosphatase 1 (PP1c). A crystal structure identifies an enzyme docking site in the Rb C-terminal domain that is required for efficient PP1c activity toward Rb. The phosphatase docking site overlaps with the known docking site for cyclin-dependent kinase (Cdk), and PP1 competition with Cdk-cyclins for Rb binding is sufficient to retain Rb activity and block cell-cycle advancement. These results provide the first detailed molecular insights into Rb activation and establish a novel mechanism for Rb regulation in which kinase and phosphatase compete for substrate docking.