Runaway electron imaging spectrometry (REIS) system.

A portable Runaway Electron Imaging and Spectrometry System (REIS) was developed in ENEA-Frascati to measure synchrotron radiation spectra from in-flight runaway electrons in tokamaks. The REIS is a wide-angle optical system collecting simultaneously visible and infrared emission spectra using an incoherent bundle of fibers, in a spectral range that spans from 500 nm to 2500 nm, and visible images using a CCD color microcamera at a rate of 25 frames/s. The REIS system is supervised and managed using a dedicated LabVIEW program to acquire data simultaneously from three spectrometers every 20 ms (configurable down to 10 ms). An overview of the REIS architecture and acquisition system and resulting experimental data obtained in FTU are presented and discussed in this paper.

NGF promotes microglial migration through the activation of its high affinity receptor: modulation by TGF-beta.

Activation and mobilization of microglia are early events in the majority of brain pathologies. Among the signalling molecules that can affect microglial behaviour, we investigated whether nerve growth factor (NGF) was able to influence microglial motility. We found that NGF induced chemotaxis of microglial cells through the activation of TrkA receptor. In addition, NGF chemotactic activity was increased in the presence of low concentrations (< or =0.2 ng/ml) of transforming growth factor-beta (TGF-beta), which at this concentration showed chemotactic activity per se. On the contrary, NGF-induced microglial migration was reduced in the presence of chemokinetic concentration of TGF-beta (> or =2 ng/ml). Finally, both basal and NGF-induced migratory activity of microglial cells was increased after a long-term exposure of primary mixed glial cultures to 2 ng/ml of TGF-beta. Our observations suggest that both NGF and TGF-beta contribute to microglial recruitment. The chemotactic activities of these two pleiotropic factors could be particularly relevant during chronic diseases in which recruited microglia remove apoptotic neurons in the absence of a typical inflammatory reaction.

Identification of an isomer impurity in piperaquine drug substance.

A significant contaminant of the antimalarial drug piperaquine (1,3-bis-[4-(7-chloroquinolyl-4)-piperazinyl-1]propane) has been identified using liquid chromatography-mass spectrometry (LC-MS) and 2D NMR spectroscopy (1H-1H COSY, 1H-13C HSQC, 1H-13C HMBC). The impurity was identified as the positional isomer 1-[(5-chloroquinolin-4)-piperazinyl]-3-[(7-chloroquinolin-4)-piperazinyl]propane. The impurity is formed because of contamination of batches of 4,7-dichloroquinoline (a precursor in the synthesis of piperaquine) with 4,5-dichloroquinoline. The amount of impurity (peak area impurity/peak area piperaquine using LC-UV at 347 nm) in old batches of piperaquine and in Artekin (the combination of dihydroartemisinin-piperaquine) ranged from 1.5 to 5%.

[Laparoscopic cholecystectomy for acute cholecystitis: our experience]. / La colecistectomia videolaparoscopica nella colecistite acuta: nostra esperienza.

Laparoscopic cholecystectomy (LC) is now the gold standard in the treatment of cholelithiasis. LC is safe even in patients with acute cholecystitis. In our 118 cases there was 4 major complications as bile duct injuries (3%) and 13 minor complications (11%); conversion rate was 21% (24 patients), without mortality. Our experience confirms the validity of early LC in the treatment of acute cholecystitis, but laparoscopic procedure is associated with higher conversion rate (21% versus 3%) and complication rates compared to the treatment in non-acute patients.

Microglia-neuron interaction in inflammatory and degenerative diseases: role of cholinergic and noradrenergic systems.

Reciprocal interactions between glia and neurons are essential for many critical functions in brain health and disease. Microglial cells, the brain resident macrophages, and astrocytes, the most prevalent type of cell in brain, are actively involved in the control of neuronal activities both in developing and adult organisms. At the same time, neurons influence glial functions, through direct cell-to-cell interactions as well as the release of soluble mediators. Among signals from neurons that may have an active role in controlling glial activation are two major neurotransmitters: acetylcholine and noradrenaline. Several studies indicate that microglia and astrocytes express adrenergic receptors, whose activation influences the release of pro-inflammatory mediators, controlling the extent of glial reactivity. Acetylcholine receptors are also expressed by glial cells. In particular, microglial cells express the nicotinic receptor alpha7 and its activation attenuates the pro-inflammatory response of microglial cultures, suggesting that acetylcholine may control brain inflammation, in analogy to what demonstrated in peripheral tissues. Deficiencies of noradrenergic and cholinergic systems are linked to important neurodegenerative diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD) and it has been suggested that in addition to impairing neuron-to-neuron transmission, noradrenergic and cholinergic hypofunction may contribute to dysregulation of the normal neuron-glia interaction, abnormal glial reaction and, eventually, neurodegeneration. A deeper knowledge of role of cholinergic and noradrenergic systems in controlling neuron-glia interactions may offer new venues for disease treatments.