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Adrenergetic modulation of the intrinsic myogenic activity of peripheral diaphragmatic lymphatics.
No full textThe diaphragmatic lymphatic system drains fluids and solutes from diaphragmatic interstitium and from the pleural and peritoneal cavities. Initial lymphatics, devoid of smooth muscle cells (SMCs) in their walls, join into long linear vessels or complex loops, formed at the confluence of linear vessels. Both linear vessels and loops, visible below the pleural and peritoneal mesothelia over the diaphragmatic dome, may be segmented in functional units, called lymphangions, separated by intraluminal valves, which ensure unidirectional lymph flow. Lymph progression within the diaphragmatic lymphatic vessels is due to an hydraulic pressure gradient of between adjacent lymphatic segments whose generation and maintenance depends upon a system of extrinsic and intrinsic pumps. Extrinsic pumping is mainly due to the movement of the surrounding tissues which causes the contraction/expansion of the vessel, while the intrinsic pumping mechanism is due to the rhythmic contraction of the smooth muscle cells surrounding the wall of the lymphangions. Extrinsic pumping prevails in lymphatics of the medial diaphragm, while lymphatic loops located at the extreme diaphragmatic periphery do require an intrinsic pumping mechanism to propel lymph centripetally. Lymph propulsion within the most peripheral diaphragmatic lymphatics depends upon tissue displacements and contraction of smooth muscle cells that surround the collecting lymphatics. The aim of the present work was to investigate, in actively contracting sites of peripheral diaphragmatic lymphatic vessels, the contribution of single strokes and valves opening/closing dynamics to lymph propulsion, and to analyze how this phenomenon is modulated by epinephrine.
Anaesthetized rats received an intraperitoneal injection of a mixture of FITC-conjugated dextrans and TRITC-labeled microspheres (0.1-1 m diameter). After passive lymphatic vessels loading, microspheres movement were video recorded ex-vivo in excised pieces of diaphragm, kept superfused with warmed oxygenated Tyrode’s solution in a flow chamber on the stage of an upright microscope. Instantaneous and mean microsphere velocities were derived from microsphere trajectories along with vessel diameter changes due to spontaneous active strokes.
Data obtained show that active strokes exert a distance-dependent effect on microspheres progression from the contracting site. Their velocity profile results parabolic with a peak velocity of about 96 μm/sec. In the presence of intraluminal valves, microspheres show an oscillatory trajectory on the proximal side and monotonic outward directed flow on the distal side of the valve. Epinephrine administration has opposite effects in linear vessels and lymphatic loops: in particular, epinephrine determines an increase in contraction frequency of about 3 bpm and a greater distance traveled by microspheres in loops and an impairment of spontaneous activity in linear vessels
La cooperazione italiana. Funzione e rilevanza economica: un focus particolare sui settori non bancari
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Reconstructing the evolutionary path of galaxies: a study of the main properties of early- and late-type galaxies over the redshift range 0.6<z<2.5.
No full textThe aim of the analysis carried out in this thesis work is twofold. On the one hand we are interested in addressing whether a sample of morphologically selected early-type galaxies (ETGs) differs from a sample of passive galaxies in terms of galaxy statistics. On the other hand we study how the relative abundance of galaxies, the number density, and, the stellar mass density of different morphological types change over the redshift range 0.6 ≤ z ≤ 2:5. Furthermore, we investigated if these galaxies and their properties can provide evidences on the possible variation of the abundance of low-to-high mass stars in galaxies, i.e. the variation of the IMF, with redshift, stellar mass and colours.
From the 1302 galaxies brighter than Ks(AB)=22 selected from the GOODS-MUSIC catalogue, we classified the ETGs, i.e. elliptical (E) and spheroidal galaxies (E/S0), on the basis of their morphology and the passive galaxies on the basis of their specific star formation rate (sSFR≤10-11 yr-1). Since the definition of a passive galaxy depends on the model parameters assumed to fit the spectral energy distribution of the galaxy, in addition to the assumed sSFR threshold, we probed the dependence of this definition and selection on the stellar initial mass function (IMF). We find that spheroidal galaxies cannot be distinguished from the other morphological classes on the basis of their low star formation rate, irrespective of the IMF adopted in the models. In particular, we find that a large fraction of passive galaxies (> 30 %) are disc-shaped objects and that the passive selection misses a significant fraction (~ 26 %) of morphologically classified ETGs.
Using the sample of 1302 galaxies morphologically classified into spheroidal galaxies (ETGs) and non-spheroidal galaxies (LTGs), we find that the fraction of these two morphological classes is constant over the redshift range 0:6 ≤ z ≤ 2:5, being 20-30 % the fraction of ETGs and 70-80 % the fraction of LTGs. However, at z 3 - 4 X 1011M) does not increase from z ~ 2:5, contrary to the lower mass galaxies. This suggests that the most massive galaxies formed at z > 2:5 - 3 and that the assembly of such high-mass galaxies is not effective at lower redshift.
From the analysis f the galaxy SEDs, reproduced with different IMFs, we found that the bulk (> 80%) of the 1302 galaxies are best-fitted with IMFs that contain a greater relative number of low-mass stars compared to a Salpeter IMF. This trend is constant with redshift and galaxy mass, testifying that from our data we do not observe an IMF variation as function of the cosmic time, galaxy mass and galaxy morphology
Il logos dello ierofante. Docetismo e metafisica dell'immagine nella filosofia delle religioni di Henry Corbin.
No full textWe outline a specific profile of philosophy of religion emerging from the work of Henry Corbin, a thinker who engages with contemporary issues, interpreter of the Iranian Shi’ite tradition and of the currents of Gnosis,. The first chapter is devoted to the phenomenological method of Docetism. Compared to the bettern-known issue of mundus imaginalis, the Docetism is equally crucial: it is familiar to many Eastern and Western gnostic currents – a downright critical theory of visionary knowledge, that rebuilds metaphysics in a perspective that goes beyond Nietzsche and Heidegger, and an ontology not primarily ontic, not simply predicative, but “ontophanique” (G. Durand). In the second chapter we have meant to discuss the docetist theoretical foundations of ‘image’, starting from the illusory paradox of the regard granted to imagination in the Islamic context, usually defined as aniconic. The aniconic instance is analysed starting from the contrast between “idol” and “icon”: the first is the opaque image, the second is the transparent mirror. The image, at that level, is not the imitation of a model, but the ability to mirror, and a constitutive relating with the other outside the self: unus ambo, dualitude. In the third chapter we present the main focus of this kind of Docetism: to actualize the spiritual. The specificity of the Iranian Islam is confronted with the Platonic tradition of the Russian theology, the psychology of Jung, and a Western archaic sense of the image. Finally, in order to avoid any relativist misunderstanding, we reflect, along with Corbin, upon what makes a vision true
Mitochondrial network fragmentation initiates Purkinje cells degeneration via Ca2+ buffering impairment: dissecting the molecular events from AFG3L2 mutation to defective mitochondrial dynamics.
No full textSpinocerebellar ataxia type 28 (SCA28) is a neurodegenerative disorder characterized by unbalanced standing, gait incoordination, nystagmus, ophthalmoparesis and pyramidal signs. Several disease-causing mutations have been identified in the AFG3L2 gene. The encoded protein, AFG3L2, coassembles with paraplegin into multimeric complexes, called the m-AAA proteases, in the inner mitochondrial membrane. These complexes are crucial components of the mitochondrial protein quality control system and regulate mitochondrial morphology.
The haploinsufficient Afg312 mouse recapitulates the features of SCA28 patients, displaying motor incoordination due to dark degeneration of Purkinje cells (PC-DCD). This is a form of degeneration characterized by toxic levels of intracellular Ca2+and activation of calpains. Differently from other forms of SCA, where this phenomenon is associated to excitotoxicity, in the SCA28 mouse is unique since it originates from a mitochondrial dysfunction.
We established, that Afg312-depleted mitochondria ineffectively buffer the evoked peaks of Ca2+.This enhances cytoplasmic Ca2+ levels in PC, thus triggering PC-DCD. We demonstrated that this defect is caused by the negative synergism between the mitochondrial network fragmentation and the altered trafficking of the organelles to PC dendrites.
To determine the molecular mechanism that induces mitochondrial network fragmentation in the absence of AFG3L2, we studied the regulatory pathway involved in mitochondrial dynamics. Previous work demonstrated that mitochondrial morphology alteration, in the absence of AFG3L2, is caused by an increased OMA1-mediated OPA1 processing. Studying the regulatory pathway that drives OMA1 activity, we discovered that AFG3L2 is deeply involved in this pathway. Full length OMA1 protein is 60 kD, while the proposed active form is 40kD. We identified AFG3L2 as the most important protease involved in OMA1 60/40 kD processing although, additional unknown protease(s) contribute to alternative pathway during stress conditions.
We found that the absence of the m-AAA protease induces a striking accumulation of the 60 kD band and a reduction of the 40kD. To clarify the role of AFG3L2 in OMA1 processing we performed co-immunoprecipitation experiments, which disclosed a physical-interaction between the two proteins. Interestingly, we were able to rescue OMA1 processing in Afg3l2 ko murine embryonic fibroblasts by overexpression of wild type AFG3L2, but not with the proteolytic inactive mutant (AFG3L2-E575Q).
Moreover, we showed that OMA1 40kD form is a substrate of the the i-AAA protease demonstrating that the m-AAA proteases and the i-AAA proteases work coordinately in the regulation of OMA1.
These data, besides disclosing the pathogenetic mechanism of SCA28, demonstrate for the first time the impact of defective mitochondrial Ca2+uptake on local Ca2+ signaling in a physiopathological condition of the nervous system. We demonstrated that the altered Ca2+ homeostasis is caused by the mitochondrial network fragmentation, via OPA1 over processing OMA1-mediated consequent to the absence of AFG3L2.
Moreover, we demonstrated for the first time the fundamental role of the m-AAA and the i-AAA complexes in the regulation of OMA1 processing and confirming their fundamental role in mitochondrial dynamics
Comparative toxicological analysis of iron, cobalt and nickel nanoparticles in three different in vitro models.
No full textThe growing use of engineered nanomaterials (NMs) requires a safety evaluation on their potential health effects. In the present work, we investigated the cytotoxic effects of three zerovalent metallic nanoparticles (NPs): iron nanoparticles (FeNPs), cobalt nanoparticles (CoNPs) and nickel nanoparticles (NiNPs). Iron, cobalt and nickel share similar physicochemical characteristics, such as ferromagnetism, and are known as Iron Triad. Due to their ferromagnetic properties, they are currently under investigation for medical applications as nanovectors for drug delivery, magnetic resonance imaging contrast agents and theranostics. FeNPs represent an innovative technology for the environmental remediation of contaminated groundwater, while NiNPs and CoNPs can be used in industry as information storage, magnetic fluids and catalysts.
Cytotoxicity was evaluated using MTS and ATP assays on three different cell lines: carcinomic human alveolar basal epithelial cell line (A549) and murine aneuploid fibrosarcoma cell line (L929) as in vitro models for inhalation and dermal contact, and human hepatocellular liver carcinoma cell line (HepG2) as a liver model. Toxicity results were related to NP dissolution and cellular uptake.Toxicity studies showed dose- and timedependent effects, with CoNPs and NiNPs more toxic than FeNPs in the three in vitro models. The same trend was observed in the presence of their related ions. The different toxicity of NPs did not related to NP or ion internalization. CoNPs and Co2+ showed similar dose-response curves probably due to the high dissolution rate, while NiNPs and FeNPs resulted less toxic than their relative ions (Ni2+ and Fe2+/Fe3+). NiNP dose-response relationship was characterized by a bimodal trend, with the first transition probably due to the NP itself and the second one to the released ions, as confirmed by NiNP cytotoxicity in presence of two different Ni2+ chelators (L-cysteine and L-histidine). In their presence, NiNP showed a unimodal dose-response curve with the maximum effect corresponding to the first transition obtained in the absence of nickel chelators, confirming the role of dissolution in inducing the second transition. The low FeNP toxicity is probably related to their low dissolution and to the physiological role of iron in cell viability and its finely regulated homeostasis. In conclusion, the present study shows differences in FeNP, CoNP and NiNP cytotoxicity relating to NP dissolution and to their elemental composition, in accordance with the presence of cellular mechanisms involved in managing their related ions
Clinical and echocardiographic correlates of acute heart failure, cardiogenetic shock and in-hospital mortality in tako-tsubo cardiomyopathy: insights from the “Tako-tsubo Italian Network”.
No full textObjective: to determine clinical and echocardiographic correlates of acute heart failure, cardiogenic shock and in-hospital mortality in a large cohort of tako-tsubo cardiomyopathy (TTC) patients.
Background: despite good long-term prognosis, life-threatening complications due to hemodynamic instability can occur early in TTC patients.
Methods: the study population consisted of 227 patients (66.2 ± 12.2 years; female 90.3%) enrolled in the Tako-tsubo Italian Network, undergoing transthoracic two-dimensional echocardiography on admission and at short-term follow-up [4.3 (4-6) weeks]. Patients were divided into two groups according to the presence or absence of major adverse events, a composite of acute heart failure, cardiogenic shock, and in-hospital mortality.
Results: major adverse events occurred in 59 patients (25.9%). Elderly patients aged ≥75 years (42.4 vs 23.8%; p=0.011), left ventricular (LV) ejection fraction (35.1 ± 5.9 vs 38.4 ± 4.6%; p<0.001), wall motion score index (1.9 ± 0.2 vs 1.7 ± 0.2; p<0.001), E/e’ ratio (13.5 ± 4.3 vs 9.9 ± 3.3; p<0.001), LV outflow tract obstruction (23.7 vs 8.9%, p=0.006), pulmonary artery systolic pressure (47.4 ± 12.3 vs 38.0 ± 9.2 mmHg; p<0.001), right ventricular involvement (28.8 vs 9.5%;p<0.001), and reversible moderate to severe mitral regurgitation (49.1 vs 11.9%; p<0.001) were significantly different between groups and were associated with adverse events. At multivariate analysis, LV ejection fraction (HR 0.92; 95%CI: 0.89-0.95; p<0.001), E/e’ ratio (HR 1.13; 95%CI: 1.02-1.24; p=0.011), reversible moderate to severe mitral regurgitation (HR 3.25; 95%CI: 1.16-9.10; p=0.025), and age ≥75 years (HR 2.81; 95%CI: 1.05-7.52; p=0.039) were independent correlates of major adverse events.
Conclusions: echocardiographic parameters provide additional information compared to other variables routinely used in clinical practice in identifying patients at higher risk of hemodynamic deterioration and poor in-hospital outcome, allowing prompt institution of appropriate pharmacological treatment and adequate mechanical support
