128 research outputs found
Impact of the uncertainties of load and forecast of power production from renewables on the operating cost of a microgrid
No full textThis contribution discusses the combined impact of the uncertainties related to the forecasts of the power production from Renewable Energy Sources, the Electrical Load and the Thermal Load on the operation costs of a microgrid. To quantify the possible variation of the cost determined by an Energy Management System, a stochastic approach has been adopted. The perturbation of the forecasted data is obtained adding to the abovementioned variables random numbers according to a suitable Probability Density Function. To this purpose, both Uniform and Normal distribution have been used. The analysis is developed referring to a test case facility: the Smart Polygeneration Microgrid of the University of Genoa. Among the possible cases, four combinations have been presented, to perturb the data with a 5%, 20% and 50% variation. The analyzed cases show that an increase in the error on the forecasts of the Electrical Load, the Thermal Load and the production from Renewable Energy Sources, causes a final cost increase. As expected, lower perturbations produce lower deviations with respect to the cost calculated by the Energy Management System. For all the presented cases, no significant differences in the minimum and maximum deviation from the costs calculated by the Energy Management System when variables are perturbated using a Normal or Uniform Probability Density Function have been found. The application of perturbations on a real test facility shows the reliability of the calculations performed by the Energy Management System, also considering the fact that the Electric Load, the Thermal Load and the power production from Renewable Energy Sources are parameters affected by uncertainty
The pathophysiology of concussion.
No full textConcussion is defined as a biomechanically induced brain injury characterized by the absence of gross anatomic lesions. Early and late clinical symptoms, including impairments of memory and attention, headache, and alteration of mental status, are the result of neuronal dysfunction mostly caused by functional rather than structural abnormalities. The mechanical insult initiates a complex cascade of metabolic events leading to perturbation of delicate neuronal homeostatic balances. Starting from neurotoxicity, energetic metabolism disturbance caused by the initial mitochondrial dysfunction seems to be the main biochemical explanation for most postconcussive signs and symptoms. Furthermore, concussed cells enter a peculiar state of vulnerability, and if a second concussion is sustained while they are in this state, they may be irreversibly damaged by the occurrence of swelling. This condition of concussion-induced brain vulnerability is the basic pathophysiology of the second impact syndrome. N-acetylaspartate, a brain-specific compound representative of neuronal metabolic wellness, is proving a valid surrogate marker of the post-traumatic biochemical damage, and its utility in monitoring the recovery of the aforementioned "functional" disturbance as a concussion marker is emerging, because it is easily detectable through proton magnetic resonance spectroscopy
Il ritorno del contratto nazionale: la leva della partecipazione. Interviste con : Roberto Benaglia, Stefano Franchi, Corrado Felice La Forgia, Francesca Re David, Federico Butera
No full textImpact of multidisciplinary discussion on pancreatic neuroendocrine tumours, experience of a tertiary centre
No full textBackground Pancreatic neuroendocrine tumours (pNETs) are rapidly increasing. Their management implies considerable resources. Multidisciplinary discussion of tumours has become a cornerstone in clinical oncology but no studies demonstrate a clear clinical benefit. The aim of the present study is to evaluate whether the systematic discussion of patients with pNET in multidisciplinary meeting (MM) has changed their management. Methods This retrospective single-centre study was held from 2004 to 2023. Since 2018 all patients were discussed in MM; thus, they were divided into two groups (board and no board) to evaluate clinical and surgical outcomes and whether multidisciplinary discussion improved adherence to guidelines. Results A total of 128 patients were enrolled (55 board group and 73 no board). Groups were comparable for gender (36.4% female vs. 45.2%), mean age (60.3 vs. 61.7 years), mean American Society of Anesthesiologists score (2.66 vs. 2.71), Charlson Comorbidity Index (CCI) (CCI < 6, 80 vs. 79.45%), rate of functioning tumours (7.3 vs. 16.4%, P = 0.2), and pre/postoperative grading. Endoscopic ultrasound (EUS) was used more in board vs. no board (EUS: 90.9 vs. 71.2%, P = 0.005, EUS with fine-needle aspiration 89.1 vs. 65.8%, P = 0.002). More patients underwent surgery in no board (78.1 vs. 61.8%, P = 0.045). Postoperative complications were comparable as well as mortality (9.1 vs. 9.6%) and adherence to guidelines (board vs no board adherents: 90.3 vs. 87.6%, P = 0.9). Conclusion Systematic multidisciplinary discussion does not result in significant clinical impact in terms of surgical complications, recurrences, and reinterventions. A selective approach in multidisciplinary discussion would be worth considering
Metabolic, enzymatic and gene involvement in cerebral glucose dysmetabolism after traumatic brain injury
No full textIn this study, the metabolic, enzymatic and gene changes causing cerebral glucose dysmetabolism following graded diffuse traumatic brain injury (TBI) were evaluated. TBI was induced in rats by dropping 450g from 1 (mild TBI; mTBI) or 2m height (severe TBI; sTBI). After 6, 12, 24, 48, and 120h gene expressions and enzymatic activities of glycolysis and pentose phosphate pathway (PPP) enzymes, and levels of lactate, ATP, ADP, ATP/ADP (indexing mitochondrial phosphorylating capacity), NADP(+), NADPH and GSH were determined in whole brain extracts (n=9 rats at each time for both TBI levels). Sham-operated animals (n=9) were used as controls. Results demonstrated that mTBI caused a late increase (48-120h post injury) of glycolytic gene expression and enzymatic activities, concomitantly with mitochondrial functional recovery (ATP and ATP/ADP normalization). No changes in lactate and PPP genes and enzymes, were accompanied by transient decrease in GSH, NADP(+), NADPH and NADPH/NADP(+). Animals following sTBI showed early increase (6-24h post injury) of glycolytic gene expression and enzymatic activities, occurring during mitochondrial malfunctioning (50% decrease in ATP and ATP/ADP). Higher lactate and lower GSH, NADP(+), NADPH, NADPH/NADP(+) than controls were recorded at anytime post injury (p<0.01). Both TBI levels caused metabolic and gene changes affecting glucose metabolism. Following mTBI, increased glucose flux through glycolysis is coupled to mitochondrial glucose oxidation. "True" hyperglycolysis occurs only after sTBI, where metabolic changes, caused by depressed mitochondrial phosphorylating capacity, act on genes causing net glycolytic flux increase uncoupled from mitochondrial glucose oxidation
Severity of experimental traumatic brain injury modulates changes in concentrations of cerebral free amino acids
No full textIn this study, concentrations of free amino acids (FAA) and amino group containing compounds (AGCC) following graded diffuse traumatic brain injury (mild TBI, mTBI; severe TBI, sTBI) were evaluated. After 6, 12, 24, 48 and 120 hr aspartate (Asp), glutamate (Glu), asparagine (Asn), serine (Ser), glutamine (Gln), histidine (His), glycine (Gly), threonine (Thr), citrulline (Cit), arginine (Arg), alanine (Ala), taurine (Tau), γ-aminobutyrate (GABA), tyrosine (Tyr), S-adenosylhomocysteine (SAH), l-cystathionine (l-Cystat), valine (Val), methionine (Met), tryptophane (Trp), phenylalanine (Phe), isoleucine (Ile), leucine (Leu), ornithine (Orn), lysine (Lys), plus N-acetylaspartate (NAA) were determined in whole brain extracts (n = 6 rats at each time for both TBI levels). Sham-operated animals (n = 6) were used as controls. Results demonstrated that mTBI caused modest, transient changes in NAA, Asp, GABA, Gly, Arg. Following sTBI, animals showed profound, long-lasting modifications of Glu, Gln, NAA, Asp, GABA, Ser, Gly, Ala, Arg, Citr, Tau, Met, SAH, l-Cystat, Tyr and Phe. Increase in Glu and Gln, depletion of NAA and Asp increase, suggested a link between NAA hydrolysis and excitotoxicity after sTBI. Additionally, sTBI rats showed net imbalances of the Glu-Gln/GABA cycle between neurons and astrocytes, and of the methyl-cycle (demonstrated by decrease in Met, and increase in SAH and l-Cystat), throughout the post-injury period. Besides evidencing new potential targets for novel pharmacological treatments, these results suggest that the force acting on the brain tissue at the time of the impact is the main determinant of the reactions ignited and involving amino acid metabolism
Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications.
No full textAlthough numerous studies have been carried out to investigate the pathophysiology of mild traumatic brain injury (mTBI), there are still no standard criteria for the diagnosis and treatment of this peculiar condition. The dominant theory that diffuse axonal injury is the main neuropathological process behind mTBI is being revealed as weak at best or inconclusive, given the current literature and the fact that neuronal injury inherent to mTBI improves, with few lasting clinical sequelae in the vast majority of patients. Clinical and experimental evidence suggests that such a course, rather than being due to cell death, is based on temporal neuronal dysfunction, the inevitable consequence of complex biochemical and neurochemical cascade mechanisms directly and immediately triggered by the traumatic insult. This report is an attempt to summarize data from a long series of experiments conducted in the authors' laboratories and published during the past 12 years, together with an extensive analysis of the available literature, focused on understanding the biochemical damage produced by an mTBI. The overall clinical implications, as well as the metabolic nature of the post-mTBI brain vulnerability, are discussed. Finally, the application of proton MR spectroscopy as a possible tool to monitor the full recovery of brain metabolic functions is emphasize
Ex oraculo Apollinis. Tradizioni oracolari delfiche nella storia di Roma
No full textQuesta ricerca desidera prendere parte alla riflessione sulla maniera in cui i Romani rappresentavano sé stessi attraverso la narrazione del proprio passato. Si è scelto di contribuire alla questione a partire dallo studio degli oracoli delfici presenti nella storia di Roma che, inserendosi in narrazioni spesso significative per la collettività, costituiscono degli utili esempi di riformulazione del passato alla luce di specifiche esigenze storiche e culturali.
Lungi dal voler interrogare i responsi sulla loro attendibilità storica, la trattazione degli oracoli segue un criterio cronologico, proprio per mettere in luce come questo tipo di racconti costituiscano il prodotto di una progressiva stratificazione di elementi narrativi, che si rivela estremamente elaborata per gli avvenimenti più antichi e che viene a semplificarsi a mano a mano che ci si avvicina all’epoca degli autori che li testimoniano.
L'analisi riguarda diciotto oracoli e si sviluppa in cinque capitoli:
1. Fondamenti storici e metodologici essenziali
2. Narrazioni oracolari eziologiche
3. Oracoli sull'espansione romana in Italia (IV-III secolo a.C.)
4. Episodi relativi all’espansione romana nel Mediterraneo (III-II secolo a.C.)
5. Consultazioni oracolari di natura privata
La tesi è seguita da un riassunto in lingua francese e da due appendici, che forniscono una tabella di sintesi degli oracoli delfici trattati (con datazione, fonti e breve riassunto) nonché i testi e le traduzioni in italiano delle fonti latine e greche di riferimento.
Riassunto in lingua inglese:
This research aims to contribute to the discourse concerning how Romans represented themselves through the narration of their past. The study approaches this question through an examination of Delphic oracles present in Roman history which are embedded in narratives often significant for the collective consciousness and serve as valuable examples of how the past was reformulated to meet specific historical and cultural needs.
Rather than questioning the historical reliability of these oracular responses, the discussion follows a chronological approach, in order to demonstrate how such narratives resulted from a progressive stratification of narrative elements. This stratification appears highly elaborated for the most ancient events and tends to simplify as it approaches the time of the authors who recorded these accounts.
The analysis encompasses eighteen oracles and is developed across five chapters:
1. Essential historical and methodological frameworks
2. Etiological oracular narratives
3. Oracles concerning Roman expansion in Italy (4th-3rd centuries BCE)
4. Episodes related to Roman expansion in the Mediterranean (3rd-2nd centuries BCE)
5. Private oracular consultations
The dissertation also provides a summary in French and two appendices, offering a synthesis table of the Delphic oracles discussed (including dating, sources, and brief summaries) as well as the texts and Italian translations of the relevant Latin and Gree
Transient alterations of creatine, creatine phosphate, N-acetylaspartate and high-energy phosphates after mild traumatic brain injury in the rat.
No full textIn this study, the concentrations of creatine (Cr), creatine phosphate (CrP), N-acetylaspartate (NAA), ATP, ADP and phosphatidylcholine (PC) were measured at different time intervals after mild traumatic brain injury (mTBI) in whole brain homogenates of rats. Anaesthetized animals underwent to the closed-head impact acceleration “weight-drop” model (450 g delivered from 1 m height = mild traumatic brain injury) and were killed at 2, 6, 24, 48 and 120 h after the insult (n = 6 for each time point). Sham-operated rats (n = 6) were used as controls. Compounds of interest were synchronously measured by HPLC in organic solvent deproteinized whole brain homogenates. A reversible decrease of all metabolites but PC was observed, with minimal values recorded at 24 h post-injury (minimum of CrP = 48 h after impact). In particular, Cr and NAA showed a decrease of 44.5 and 29.5%, respectively, at this time point. When measuring NAA in relation to other metabolites, as it is commonly carried out in “in vivo” 1H-magnetic resonance spectroscopy (1H-MRS), an increase in the NAA/Cr ratio and a decrease in the NAA/PC ratio was observed. Besides confirming a transient alteration of NAA homeostasis and ATP imbalance, our results clearly show significant changes in the cerebral concentration of Cr and CrP after mTBI. This suggests a careful use of the NAA/Cr ratio to measure NAA by 1H-MRS in conditions of altered cerebral energy metabolism. Viceversa, the NAA/PC ratio appears to be a better indicator of actual NAA levels during energy metabolism impairment. Furthermore, our data suggest that, under pathological conditions affecting the brain energetic, the Cr–CrP system is not a suitable tool to buffer possible ATP depletion in the brain, thus supporting the growing indications for alternative roles of cerebral C
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