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61.
Maria Ricciardi Daniele Cespi Maurizio Celentano Alessandra Genga Cosimino Malitesta Antonio Proto Carmine Capacchione Raffaele Cucciniello 《Sustainable Chemistry and Pharmacy》2017
The production of chemicals from bio-based feedstocks is an emerging field of research in both industrial and academic communities. Here we present the synthesis of propylene glycol through catalytic hydrogenolysis of glycidol, obtained using a side-stream from the bio-based epichlorohydrin production plant, over Pd/C catalyst. In particular, we show the prominent effect of the acidic resin Amberlyst-15 in the selective and quantitative conversion of glycidol that permits to reach a TOF value of 162 h?1. Propylene glycol is obtained with high yields and selectivity (> 99%) in only 1 h under mild reaction conditions. The effect of solvent is also investigated giving interesting results on the reaction selectivity. The catalytic system (Pd/C + Amberlyst-15) shows a good recyclability also after seven reaction cycles reaching high performances in term of conversion and selectivity. This allowed minimizing the amount of waste and enhancing the efficiency of the whole system. 相似文献
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Martina Mattii Fabio Ayala Nicola Balato Raffaele Filotico Serena Lembo Maria Schiattarella Cataldo Patruno Gianni Marone Anna Balato 《Experimental dermatology》2013,22(12):813-819
The interleukin (IL)‐1 family includes 11 members that are important in inflammatory processes. It includes various agonists and two antagonists, IL‐1Ra and IL‐36Ra. Our aim was to investigate whether the IL‐1 family is involved in allergic contact dermatitis (ACD). The expression of IL‐1 family members was evaluated by PCR and immunohistochemistry in the positive patch test reaction site (involved skin) and in the uninvolved skin of ACD patients. We also examined these cytokines in an ex vivo model of ACD. The antagonistic activity of IL‐36Ra was evaluated by injecting recombinant IL‐36Ra in uninvolved skin biopsies of ACD patients. IL‐1Ra and IL‐36Ra expression was quantified in mononuclear cells of nickel‐sensitized patients challenged in vitro with nickel. IL‐33 involvement in ACD was investigated by intra‐dermal injection of anti‐IL‐33 in the uninvolved skin of patients ex vivo. Results showed that IL‐1β, IL‐1Ra, IL‐36α, IL‐36β, IL‐36γ and IL‐33 expression, but not IL‐36Ra expression, was enhanced in ACD‐involved skin. Immunohistochemical analysis and ex vivo skin cultures confirmed these results. Injection of anti‐IL‐33 in ACD‐uninvolved skin inhibited IL‐8 expression, whereas IL‐36Ra inhibited IL‐36α, IL‐36β, IL‐36γ and IL‐8 expression. Nickel induced IL‐1Ra expression in lymphocytes of nickel‐sensitized patients. Hence, various IL‐1 agonists and antagonists may be involved in ACD pathogenesis. 相似文献
65.
Michele Terzaghi Pietro Luca Ratti Francesco Manni Raffaele Manni 《Neurological sciences》2012,33(1):169-172
Sleep paralyses are viewed as pure motor phenomena featured by a dissociated state in which REM-related muscle atonia coexists
with a wakefulness state of full consciousness. We present a 59-year-old man diagnosed with narcolepsy experiencing sleep
paralysis, who failed to establish the boundaries between real experience and dream mentation during the paralysis: the patient’s
recall was indeed featured by uncertainty between real/unreal and awaken/dreaming. Hereby, we suggest that sleep paralysis
may represent a more complex condition encompassing a dissociated state of mind together with the dissociative motor component.
Neurophysiological data (spectral EEG analysis corroborated by cross-correlation analysis) reinforce the idea that the patient
was in an intermediate state of mind between wake and REM sleep during the paralysis. The persistence of local impaired activity
proper of REM sleep in cortical circuits necessary for self-reflective awareness and insight, in conflict with wakefulness-related
activation of the remaining brain areas, could account for disrupted processing of afferent inputs in our patient, representing
the underlying pathophysiologic substrate for patient’s failure to establish the boundaries between real experience and dream
mentation. 相似文献
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Mariangela Lopopolo Giannapia Affaitati Alessandra Fabrizio Francesca Massimini Domenico Lapenna Maria Adele Giamberardino Raffaele Costantini 《Fundamental & clinical pharmacology》2014,28(3):331-341
The effects of tramadol versus placebo administration on behavioral indicators of ureteral pain, pelvic pain and referred lumbar muscle hyperalgesia were investigated in a rat model of viscero‐visceral hyperalgesia from endometriosis plus ureteral calculosis (endo + stone). Fifty female Sprague‐Dawley rats underwent surgical induction of endometriosis and, 2 weeks later, were randomly assigned to five groups (10 each), to be treated i.p., twice a day, with tramadol (0.625, 1.25, 2.5, or 5 mg/kg) or saline for 5 days (14–18th day postendometriosis; prestone treatment). On the 21st day, they underwent laparotomy for stone formation in the upper left ureter (dental cement injection). All were video‐taped 24 h nonstop for 7 days before and 4 days after stone formation (14–25th day postendometriosis) to record ureteral and pelvic pain behaviors. Lumbar sensitivity (L1) was tested bilaterally, daily over the same period, by verifying presence/absence of vocalization upon muscle pinching at a predefined pressure (calibrated forceps). Additional fifty endo + stone rats underwent the same protocol, except that treatment was performed on 21st–25th day (poststone treatment). Tramadol vs. saline significantly reduced number and duration of ureteral crises, duration of pelvic behavior, and incidence of muscle hyperalgesia (P < 0.0001), with a dose‐dependent effect. Prestone treatment was significantly more effective than poststone treatment for the 1.25 dose for all parameters and 2.5 dose for pelvic and muscle parameters (0.003 > P < 0.02). Tramadol, even at low doses, is thus highly protective against pain from ‘viscero‐visceral hyperalgesia’ in endometriosis plus ureteral calculosis; it can represent a valid therapeutic approach in women with these comorbidities. 相似文献
68.
Ion Udroiu Jessica Marinaccio Angelico Bedini Claudia Giliberti Raffaele Palomba Antonella Sgura 《Environmental and molecular mutagenesis》2018,59(1):60-68
Genotoxic effects of therapeutic ultrasound are poorly documented, when compared with the wide use of this physical agent. The aim of this work was to investigate the clastogenic and aneugenic potential of 1 MHz ultrasound, employing intensities (200 and 300 mW/cm2) above the cavitational threshold, but in the range of those normally used in therapeutics. Both normal fibroblasts (AG01522) and tumoral cells (MCF‐7) were sonicated. While no effects on viability were noted, significant increases of CREST‐negative micronuclei (indicative of clastogenesis) and CREST‐positive micronuclei (indicative of aneuploidy) were detected. Clastogenesis was confirmed by increases of γ‐H2AX foci, while increases of spindle anomalies confirmed the induction of aneuploidy. Our results confirm previous works that showed ultrasound‐induced DNA breakage. Moreover, our experiments show that the known effect of ultrasound‐induced damage to microtubules is also able to damage the mitotic spindle and induce aneuploidy. On the overall, this work highlights the importance to further investigate the potential risks related to therapeutics US. Environ. Mol. Mutagen. 59:60–68, 2018. © 2017 Wiley Periodicals, Inc. 相似文献
69.
Luca Arcaini Michele Merli Francesco Passamonti Raffaele Bruno Ercole Brusamolino Paolo Sacchi Sara Rattotti Ester Orlandi Elisa Rumi Virginia Ferretti Silvia Rizzi Erika Meli Cristiana Pascutto Marco Paulli Mario Lazzarino 《American journal of hematology》2010,85(1):46-50
We studied 160 Hepatitis C virus (HCV)‐positive patients with NHL (59 indolent NHL, 101 aggressive). Median age was 67 years. HCV‐RNA was present in 146. HBsAg was positive in seven patients. At diagnosis, ALT value was above UNL in 67 patients. One hundred and twenty patients received an anthracycline‐based therapy, alkylators, 28 received chemotherapy plus rituximab. Cytotoxic drugs dose was reduced in 63 patients. Among 93 patients with normal ALT at presentation, 16 patients developed WHO grade II–III liver toxicity. Among 67 patients with abnormal ALT, eight patients had a 3.5 times elevation during treatment. Among 28 patients treated with rituximab and chemotherapy, five patients (18%) developed liver toxicity. Thirty four patients (21%) did not complete treatment (eight for liver toxicity). Median progression‐free survival (PFS) for patients who experienced liver toxicity is significantly shorter than median PFS of patients without toxicity (respectively, 2 years and 3.7 years, P = 0.03). After a median F‐UP of 2 years, 32 patients died (three for hepatic failure). A significant proportion of patients with HCV+ NHL develop liver toxicity often leading to interruption of treatment. This could be a limit to the application of immunochemotherapy programs. HCV+ lymphomas represent a distinct clinical subset of NHL that deserves specific clinical approach to limit liver toxicity and ameliorate survival. Am. J. Hematol., 2010. © 2009 Wiley‐Liss, Inc. 相似文献
70.
Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes 总被引:31,自引:0,他引:31
The formation of advanced glycation end products (AGEs) is an important biochemical abnormality that accompanies diabetes mellitus and, likely, inflammation in general. Here we summarize and discuss recent studies indicating that the effects of AGEs on vessel wall homeostasis may account for the rapidly progressive atherosclerosis associated with diabetes mellitus. Driven by hyperglycemia and oxidant stress, AGEs form to a greatly accelerated degree in diabetes. Within the vessel wall, collagen-linked AGEs may "trap" plasma proteins, quench nitric oxide (NO) activity and interact with specific receptors to modulate a large number of cellular properties. On plasma low density lipoproteins (LDL), AGEs initiate oxidative reactions that promote the formation of oxidized LDL. Interaction of AGEs with endothelial cells as well as with other cells accumulating within the atherosclerotic plaque, such as mononuclear phagocytes and smooth muscle cells (SMCs), provides a mechanism to augment vascular dysfunction. Specifically, the interaction of AGEs with vessel wall components increases vascular permeability, the expression of procoagulant activity and the generation of reactive oxygen species (ROS), resulting in increased endothelial expression of endothelial leukocyte adhesion molecules. AGEs potently modulate initiating steps in atherogenesis involving blood-vessel wall interactions, triggering an inflammatory-proliferative process and, furthermore, critically contribute to propagation of inflammation and vascular perturbation in established disease. Thus, a better understanding of the biochemical mechanisms by which AGEs contribute to such processes in the vessel wall could be relevant to devise preventive and therapeutic strategies for diabetic atherosclerosis. 相似文献