Il capitalismo municipale e le esternalizzazioni fredde

La novella legislativa del 2003 (d.l. 269/2003) ha inciso sull\u2019assetto dei servizi pubblici locali aumentando le fattispecie nelle quali l\u2019ente locale pu\uf2 assumere la veste di soggetto proprietario, attraverso l\u2019acquisizione di partecipazioni in societ\ue0 a capitale totalmente pubblico o a capitale misto pubblico-privato0. Questo scenario istituzionale \ue8 diventato cornice ideale per l\u2019affermazione definitiva del fenomeno del gruppo comunale, che vede il Comune assimilato ad una holding che controlla un sistema di entit\ue0 formalmente indipendenti, strumentale alla realizzazione dei suoi fini sociali e alla promozione dello sviluppo economico e civile delle comunit\ue0 locali. Alla crescita esponenziale del peso dei servizi gestiti dal Comune per il tramite di entit\ue0 partecipate, non \ue8 corrisposta l\u2019evoluzione del suo sistema informativo-contabile verso un modello che dia conto dei risultati, di natura reddituale, patrimoniale e monetaria, ottenuti grazie al complesso delle attivit\ue0 sulle quali estende il suo potere di controllo. Il modello che coglie le interrelazioni operative fra le unit\ue0 del gruppo e la loro complementarit\ue0 rispetto ad un progetto strategico unitario \ue8 il bilancio consolidato. Allorch\ue9 si progetti di adottare il bilancio consolidato nel contesto pubblico locale, ci si imbatte in alcune problematiche da risolvere preventivamente. Merita di riflettere sostanzialmente su tre momenti: a) l\u2019individuazione delle unit\ue0 appartenenti al gruppo comunale (definizione dell\u2019area di gruppo); b) l\u2019individuazione delle unit\ue0 del gruppo comunale i cui bilanci di esercizio dovranno essere consolidati analiticamente (definizione dell\u2019area di consolidamento); c) la ricerca delle condizioni di uniformit\ue0 che devono sussistere perch\ue9 la procedura di consolidamento possa generare valori significativi e attendibili. Gli indubbi vantaggi informativi che si attribuiscono al bilancio consolidato non devono per\uf2 generare l\u2019erronea convinzione che esso debba sostituire i bilanci di esercizio delle unit\ue0 appartenenti al gruppo comunale. In particolare, l\u2019elisione dei valori reciproci, pur rispondendo appieno allo scopo per il quale il bilancio consolidato \ue8 redatto, cela informazioni sull\u2019intensit\ue0 e la direzione delle operazioni infragruppo che potrebbero rivestire molta importanza nell\u2019ottica di determinati soggetti: chi si occupa di problemi della finanza pubblica, ad esempio, \ue8 interessato a conoscere l\u2019importo e la distribuzione dei trasferimenti che il Comune concede agli enti gestori dei servizi pubblici, posto che la scelta dei servizi, e quindi degli enti erogatori, che potranno godere in misura minore o maggiore dei contributi (ad integrazione, ad esempio, di tariffe pi\uf9 o meno remunerative) \ue8 un\u2019informazione importante per valutare la politica di redistribuzione dei redditi attuata dal Comune nell\u2019ambito della collettivit\ue0 amministrata, tenuto conto che i servizi erogati sono destinati a categorie di utenti differenziate, con diversa capacit\ue0 di spesa. Ecco perch\ue9 il bilancio consolidato deve essere correttamente inteso quale porzione di un sistema informativo pi\uf9 vasto, comprendente i bilanci delle singole societ\ue0 del gruppo

Regulation of inflammatory responses to Bordetella pertussis by N(G)-monomethyl-L-arginine in mice intranasally infected.

To investigate effect of MMLA, an inhibitor of nitric oxide (NO) production, on regulation of inflammatory responses to Bordetella pertussis infection, mice were infected intranasally, and treated with various concentrations of MMLA. Ten days after infection, mice treated with MMLA at dosage of 100 mg/kg, given intraperitoneally in a single dose or for 5 consecutive days, showed at histopathologic examination, a significant decrease of intensity of inflammation (scores, 0.6 +/- 0.2 and 0.9 +/- 0.5 respectively). A decrease of cellular accumulation of neutrophils and lymphocytes in the bronchoalveolar lavage (BAL) fluid was observed in infected mice treated with MMLA, especially at dosage of 10 mg/kg, given in a single dose intraperitoneally. In addition, BP-infected mice treated with MMLA (100 mg/kg, intraperitoneally) for 5 consecutive days showed higher mortality rate than untreated mice infected with B. pertussis, and the number of B. pertussis in lungs of mice treated with MMLA was significantly increased. However, MMLA treatment of infected mice had some effect on levels of IFN-gamma and nitrite/nitrate (end-stable products of NO) in the BAL fluid. This study indicates that NO may play a role either as microbiocidal agent or as a modulator of immune regulation, inasmuch as it may upregulate tissue inflammatory response to B. pertussis

Fatal poisoning of four workers in a farm: Distribution of hydrogen sulfide and thiosulfate in 10 different biological matrices

We evaluate the distribution of sulfide and thiosulfate (TS) in biological samples of four dairy farmers died inside a pit connected to a manure lagoon. Autopsies were performed 4 days later. Toxicological analyses of sulfide and TS were made using an extractive alkylation technique combined with gas chromatography/mass spectrometry (GC/MS). Autopsies revealed: multiorgan congestion; pulmonary edema; manure inside distal airways of three of the four victims. Sulfide concentrations were cardiac blood: 0.5–3.0 μg/mL, femoral blood: 0.5–1.2 μg/mL, bile: <0.1–2.2 μg/mL; liver 2.8–8.3 μg/g, lung: 5.0–9.4 μg/g, brain: 2.7–13.9 μg/g, spleen: 3.3–6.3 μg/g, fat: <0.1–1.5 μg/g, muscle: 2.6–3.5 μg/g. TS concentrations were cardiac blood: 2.1–4.9 μg/mL, femoral blood: 2.1–2.3 μg/mL, bile: 2.5–4.4 μg/mL, urine: <0.5–1.8 μg/mL; liver <0.5–2.6, lung: 2.8–5.4 μg/g, brain: <0.5–1.9 μg/g, spleen: 1.2–2.9 μg/g, muscle: <0.5–5.6 μg/g. The cause of death was assessed to be acute poisoning by hydrogen sulfide (H2S) for all the victims. Manure inhalation contributed to the death of three subjects. The measurement of sulfide and TS concentrations in biological samples contributed to better understand the sequence of the events. Subjects 3 provided the highest concentration of sulfide in brain, thus, supporting the hypothesis of a rapid loss of consciousness and respiratory depression. One by one, the other farmers entered the pit in attempts to rescue the coworkers but collapsed. Despite the rapid death, subject 3 was the only one with TS detectable in urine. This could be due to differences in metabolism of H2S

Hippocampal FGF-2 and BDNF overexpression attenuates epileptogenesis-associated neuroinflammation and reduces spontaneous recurrent seizures

Under certain experimental conditions, neurotrophic factors may reduce epileptogenesis. We have previously reported that local, intrahippocampal supplementation of fibroblast growth factor-2 (FGF-2) and brain-derived neurotrophic factor (BDNF) increases neurogenesis, reduces neuronal loss, and reduces the occurrence of spontaneous seizures in a model of damage-associated epilepsy. Here, we asked if these possibly anti-epileptogenic effects might involve anti-inflammatory mechanisms. Thus, we used a Herpes-based vector to supplement FGF-2 and BDNF in rat hippocampus after pilocarpine-induced status epilepticus that established an epileptogenic lesion. This model causes intense neuroinflammation, especially in the phase that precedes the occurrence of spontaneous seizures. The supplementation of FGF-2 and BDNF attenuated various parameters of inflammation, including astrocytosis, microcytosis and IL-1β expression. The effect appeared to be most prominent on IL-1β, whose expression was almost completely prevented. Further studies will be needed to elucidate the molecular mechanism(s) for these effects, and for that on IL-1β in particular. Nonetheless, the concept that neurotrophic factors affect neuroinflammation in vivo may be highly relevant for the understanding of the epileptogenic process

Neurovascular unit in chronic pain.

Chronic pain is a debilitating condition with major socioeconomic impact, whose neurobiological basis is still not clear. An involvement of the neurovascular unit (NVU) has been recently proposed. In particular, the blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB), two NVU key players, may be affected during the development of chronic pain; in particular, transient permeabilization of the barrier is suggested by several inflammatory- and nerve-injury-based pain models, and we argue that the clarification of molecular BBB/BSCB permeabilization events will shed new light in understanding chronic pain mechanisms. Possible biases in experiments supporting this theory and its translational potentials are discussed. Moving beyond an exclusive focus on the role of the endothelium, we propose that our understanding of the mechanisms subserving chronic pain will benefit from the extension of research efforts to the NVU as a whole. In this view, the available evidence on the interaction between analgesic drugs and the NVU is here reviewed. Chronic pain comorbidities, such as neuroinflammatory and neurodegenerative diseases, are also discussed in view of NVU changes, together with innovative pharmacological solutions targeting NVU components in chronic pain treatment

Quantum dots as new guests in the body: structural and functional data

Many promising applications of quantum dots (QDs) in nanomedicine and in vivo imaging for further diagnostic are being developed. Despite the immense potential for the medical applications of QDs, little is known about the bioavailability and health consequences of QDs in animals and humans. Although some investigators reported that QDs do not appear to cause toxicity, others demonstrated a variety of cytotoxic effects. In this study, QDs800 (InVitrogen) have been used. Previous data from our group evaluated the bio-distribution by optical imaging, transmission electron microscopy, inductively coupled plasma mass spectroscopy analysis in mice, and the effects on novel object recognition memory, EEG activity, and some histopatological analysis on mice in different organs (liver, spleen, lungs, testis, brain). Here, we studied the systemic inflammation caused by QDs in different organs, and then focussed our attention to the brain. It is known that brain inflammation leads to microglia and astrocyte activation, which in turn are sensitive to the changes in the CNS microenvironment and rapidly activated in all conditions that affect normal neuronal functions. We demonstrated that the presence of QDs could impair synaptic response and neuronal excitability; secondly, we are currently investigating whether the electrical changes are induced by QDs by themselves or by the inflammation induced by their presence

Measurement of the kinematic variables of beauty particles produced in 350 GeV/c π−\pi^--Cu interactions

Using a sample of $26$ b\=b events, produced in $350\,\hbox{GeV}/c$ $\pi^-$ interactions in a copper target, which includes $13$ events where the decays of both $B$ and $\overline{B}$ are well reconstructed, we measure the differential distributions with respect to $x_F$ and $p_T^2$ as well as some two-particle kinematic variables. We also compare our results with a previous experiment and with predictions based on perturbative QCD

Measurements of Higgs boson production and couplings in diboson final states with the ATLAS detector at the LHC

Measurements are presented of production properties and couplings of the recently discovered Higgs boson using the decays into boson pairs, H →γ γ, H → Z Z∗ →4l and H →W W∗ →lνlν. The results are based on the complete pp collision data sample recorded by the ATLAS experiment at the CERN Large Hadron Collider at centre-of-mass energies of √s = 7 TeV and √s = 8 TeV, corresponding to an integrated luminosity of about 25 fb−1. Evidence for Higgs boson production through vector-boson fusion is reported. Results of combined fits probing Higgs boson couplings to fermions and bosons, as well as anomalous contributions to loop-induced production and decay modes, are presented. All measurements are consistent with expectations for the Standard Model Higgs boson

Standalone vertex finding in the ATLAS muon spectrometer

A dedicated reconstruction algorithm to find decay vertices in the ATLAS muon spectrometer is presented. The algorithm searches the region just upstream of or inside the muon spectrometer volume for multi-particle vertices that originate from the decay of particles with long decay paths. The performance of the algorithm is evaluated using both a sample of simulated Higgs boson events, in which the Higgs boson decays to long-lived neutral particles that in turn decay to bbar b final states, and pp collision data at √s = 7 TeV collected with the ATLAS detector at the LHC during 2011