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French to English: Excitotoxicity General field: Medical Detailed field: Medical (general)
Source text - French Excitotoxicité
L’excitotoxicité, décrite pour la première fois par James Olney en 1969, implique une hyperactivation anormale et neurotoxique des récepteurs du glutamate. Le concept d’excitotoxicité directe d’Olney propose que le glutamate et ses analogues structuraux soient capables d’induire une mort sélective des neurones en interagissant de façon hautement spécifique avec les récepteurs glutamatergiques ionotropiques NMDA qui présentent une for te conductance calcique et qui sont présents sur certaines populations neuronales, notamment les neurones striataux épineux de taille moyenne. La suractivation des récepteurs provoquerait alors une entrée massive et anormale de Ca2+ dans l’espace intracellulaire conduisant à l’activation délétère d’une cascade excitotoxique aboutissant, en particulier, à l’activation de protéases protoxiques (caspases, calpaïnes). Cette hypothèse est étayée, en particulier, par l’observation que, chez les animaux, une hyperstimulation striatale des récepteurs NMDA par des agonistes, et par l’acide quinolinique en particulier, reproduit une dégénérescence striatale sélective semblable à celle observée dans la MH.
Une autre forme d’excitotoxicité, indirecte cette fois, pourrait également aboutir à l’activation d’une voie neurotoxique comparable dans la MH. Le concept d’excitotoxicité indirecte suppose qu’une atteinte, même partielle, du métabolisme énergétique neuronal induise une sensibilisation des récepteurs glutamatergiques de type NMDA, rendant excitotoxiques des concentrations physiologiques non toxiques de glutamate. Pour preuve de l’existence de ce phénomène, des antagonistes des récepteurs NMDA parviennent à bloquer la toxicité induite par des inhibiteurs métaboliques ou par des carences en substrats énergétiques. Par ailleurs, différents travaux ont démontré in vivo qu’une atteinte énergétique partielle mais entretenue, induite par le malonate ou l’acide 3-nitropropionique était à elle seule capable d’induire des lésions striatales, et une dégénérescence particulière des neurones épineux de taille moyenne, tout à fait semblable à celles observées dans la MH. Ce type de dégénérescence est fortement atténué par l’inhibition de la libération striatale de glutamate et des antagonistes des récepteurs, présumant que le déficit énergétique causé par un dysfonctionnement mitochondrial engendre une dégénérescence excitotoxique dans la MH.
Pendant longtemps, l’implication du glutamate dans la MH est restée spéculative. Récemment, différentes études ont fortement impliqué la Huntingtine mutée comme un élément perturbateur de l’activité des récepteurs glutamatergiques susceptibles d’induire une excitotoxicité neuronale. Ainsi, des observations faites dans des modèles génétiques de la MH suggèrent une altération de la recapture du glutamate via une diminution de l’expression de GLT-1 ainsi qu’une augmentation de la neurotransmission glutamatergique, en général, et de l’activation des récepteurs NMDA, en particulier. Cette dernière serait plus particulièrement liée, en présence de la Huntingtine mutée, à une altération de l’activité de la sous-unité NR2B du récepteur qui est exprimée préférentiellement par les neurones épineux moyens au niveau du striatum. Ainsi, la Huntingtine mutée augmente le courant NMDA induit par le glutamate uniquement lorsque ce récepteur contient la sous-unité NR2B. Cette dérégulation intracellulaire serait médiée par une perte de la fonction de la protéine PSD normalement associée à la sousunité NR2B et dont l’interaction avec cette dernière serait réduite par la Huntingtine mutée, engendrant un accroissement de l’activité du récepteur NMDA.
Translation - English Excitotoxicity
Excitotoxicity, which was first described by James Olney in 1969, involves the abnormal neurotoxic hyper-activation of glutamate receptors. Olney’s concept of direct excitotoxicity suggests that glutamate and its base analogues are able to induce selective neuronal death by interacting in a highly specific manner with NMDA iontrophic glutamate receptors which possess a high calcium conductance and are found in certain neuronal populations, especially striatal medium spiny neurons. Receptor overactivation would therefore induce an abnormally excessive influx of Ca2+ into the intracellular space, leading to a deleterious activation of an excitotoxic cascade and resulting in the activation of pro-toxic proteases, i.e. caspase and calpain. This hypothesis is particularly supported by the observation that in animals, striatal hyperstimulation of NMDA receptors by antagonists; quinolinic acid in particular, produces a selective striatal degeneration similar to that observed in HD.
Indirect excitotoxicity could equally result in the activation of a neurotoxic pathway similar to that found in HD. The concept of indirect excitotoxicity implies that a sufferer of a neuronal energy metabolism, even if only moderately, will induce an adverse reaction towards NMDA-type glutamate receptors which makes the non -physiological concentrations of glutamate become excitotoxic. The NMDA receptor antagonists inhibit the toxicity induced by metabolic inhibitors or by a lack of energy substrates, thereby proving this phenomenon. In addition, different in vivo studies have shown that moderate yet healthy sufferers of neuronal energy metabolisms who were induced with malonate or 3-nitroproponic acid were the only ones capable of inducing striatal lesions and a particular degeneration of striatal medium spiny neurons, very similar to those observed in HD. This type of degeneration is strongly supported by the inhibition of the striatal release of glutamate and the NMDA receptor antagonists, presuming that the energy deficit caused by a mitochondrial dysfunction creates an excitotoxic degeneration in HD.
For many years, the implication of glutamate in HD has remained speculative. Recently, different studies have strongly implicated the mutated Huntingtin protein as a disruptive element of glutamate receptor activities which are capable of inducing neuronal excitotoxicity. Thus, observations made in genetic models of HD suggest an alteration in the glutamate uptake via a reduction in GLT-1 expression together with an increase in general, of glutamatergic neurotransmission and in particular, of NMDA receptor activation. The latter is especially linked (whilst in the presence of mutated Huntingtin) to an alteration of the activities of the NMDA receptor NR2B subunit which is preferentially expressed in striatal medium spiny neurons. In this way, the mutated Huntingtin increases the NMDA current induced by the glutamate only when the receptor contains the NR2B subunit. This intracellular deregulation would be mediated by the loss of function of the PSD protein which is normally associated with the NR2B subunit and of which the interaction with the latter would be reduced by the mutated Huntingtin, thereby leading to an increase in NMDA receptor activity.
Italian to English: A comparison of laser surgery in human and veterinary dermatology General field: Medical Detailed field: Medical: Instruments
Source text - Italian La parola laser è l’acronimo della definizione inglese “light amplification by stimulated emission of radiation”, cioè amplificazione di un raggio luminoso derivante dalla emissione stimolata di radiazioni1.
Le leggi fisiche che governano i sistemi laser sono derivate dall’elaborazione delle teorie quantistiche di Planck, Einstein, dalla teoria della complementarietà di Bohr, e dai principi della fisica elettromagnetica1.
Un qualsiasi sistema laser si compone di una camera di risonanza ottica, di un mezzo laser solido, liquido o gassoso, di una sorgente esterna di energia e di due specchi riflettenti situati alle opposte estremità del risonatore. Quando la sorgente di energia viene attivata, essa provoca l’eccitazione
del mezzo laser contenuto nella cavità di risonanza: si genera così un raggio, che viene riflesso
su uno specchio opaco e veicolato all’altra estremità (Fig. 1).
Questo, infine, viene portato fino al manipolo impugnato dall’operatore, attraverso un fascio di fibre
ottiche (laser a diodi) oppure un sistema di specchi (laser CO2)1,8. Il raggio laser così generato è collimato, monocromatico e coerente: ciò significa che il fascio di onde si propaga nello spazio in
modo unidirezionale, parallelo, senza divergere, che le onde hanno tutte la stessa lunghezza e si
muovono in fase. Le lunghezze d’onda possono essere comprese nello spettro del visibile, tra 400 e
750 nm, o dell’invisibile, sotto i 380 nm oppure oltre i 780 nm (Fig. 2).
La lunghezza d’onda, la quantità di energia erogata e le caratteristiche proprie del tessuto influenzano
l’interazione laser-tessuto. Quando il raggio colpisce il tessuto bersaglio può venire riflesso, trasmesso, deviato o assorbito; affinché l’energia luminosa possa essere utilizzata per compiere un
lavoro, occorre che vi sia assorbimento.
Ogni lunghezza d’onda viene assorbita in modo selettivo da un target chiamato cromoforo; i principali
cromofori sono l’acqua, l’emoglobina e la melanina1,7,8,9,11,12(Tab. 1).
L’interazione laser-tessuto può essere di tipo fototermico, quando l’energia luminosa si trasforma in calore, fotochimico, che sfrutta l’impiego di sostanze fotosensibilizzanti (es. terapia fotodinamica)
o fotoacustico, quando cioè le onde luminose si trasformano in onde acustiche, che vanno
a scomporre meccanicamente il tessuto bersaglio, disgregandolo (es. litotripsia)1,8. Il processo
di foto-termolisi comporta effetti sequenziali e progressivi, che vanno dalla denaturazione proteica
a 60°C, alla coagulazione a 70-80°C, alla vaporizzazione a 100°C, alla carbonizzazione a
165°C, fino all’incandescenza a 350°C1,8,9. È evidente che oltre i 60°C vi è un danno termico irreversibile sui tessuti, per questa ragione è necessario che la durata degli impulsi sia inferiore
al tempo di rilasciamento termico del tessuto (TRT). Questo è definito come il tempo necessario ad
un tessuto irradiato per rilasciare il 50% del calore accumulato1,5.
L’energia e la potenza sono misurate rispettivamente in Joules e inWatts. La quantità di energia
applicata sull’unità di superficie (J/cm2), viene definita fluenza, mentre, la potenza applicata sull’unità
di superficie (W/cm2) è detta densità di potenza o irradianza. Ne consegue che, a parità di potenza,
aumentando la superficie da trattare diminuisce l’irradianza; lo stesso avviene per l’energia e la fluenza. Questi parametri concorrono a determinare l’effetto del raggio laser1,8.
I laser possono essere classificati in base allo stato del mezzo laser, come detto sopra, oppure, in
base alla potenza, in laser chirurgici (High level laser light treatment o HLLLT) e terapeutici (Low level laser treatment o LLLT). Al primo gruppo appartengono il CO2, il Er:YAG e quelli vascolari superficiali come il laser ad Argon, il diodi, il Nd:YAG.
Translation - English The term laser is derived from the acronym “light amplification by stimulated emission of radiation.”
The physical laws that govern laser systems derived from the development of Planck and Einstein’s quantum theories, Bohr’s theory of Complementarity and the principles of electromagnetic physics.
Laser systems consist of an optical resonance chamber, either a solid, liquid or gas laser medium, an external source of energy and two reflective mirrors positioned at opposite ends of the resonator. When the energy source is activated, it stimulates the laser medium inside of the resonance cavity; thereby generating a beam which is reflected off an opaque mirror and transmitted to the far end of the chamber. (Figure 1)
This process will continue until manual intervention through either a bundle of optical fibers (diode laser) or a mirror system (CO2 laser). This laser beam is collimated (the wave beams propagate unidirectionally within the space, parallel to each other and without diverging), monochromatic (all waves are of the same length) and coherent (the waves move in phase). The wavelengths may be either within the visible spectrum (between 400 and 750 nm) or the invisible spectrum (less than 380m or over 780 nm).
Together wavelength, output power and the properties of individual tissue determine laser-tissue interaction. When the beam penetrates the target tissue, it can become reflected, transmitted, deflected or absorbed. Luminous energy may be used to perform the task only if there is absorption.
Every wavelength is absorbed selectively by a target matter: chromophore. Water, haemoglobin and melanine are the main chromophores. (Table 1)
Laser-tissue interaction can be photothermal (when luminous energy is transformed into heat), photochemical (using photosensitive substances, e.g. photodynamic therapy) or photoacoustic (when light waves transform into acoustic waves which mechanically break up and pulverise the target tissue, e.g. lithotripsy.) The process of photothermolysis involves sequential and progressive effects including denaturation at 60°c, coagulation at between 70 and 80°c, vaporization at 100°c, carbonization at 165°c, until incandescence is reached at 350°c. Tissue is irreversibly thermally damaged at 60°c and it is therefore essential that pulse duration is inferior to the thermal relaxation time of the tissue; the time required for irradiated tissue to dissipate 50% of the accumulated heat.
Energy and power are measured in joules and watts respectively. Fluence is the quantity of energy delivered per unit area (J/cm²), whilst irradiance or power density is the power delivered per unit area (W/cm²). It follows that for the same power, increasing the treatment area will decrease the irradiancy; the same applies for energy and fluency. These parameters contribute to determining the effectiveness of laser beams.
Lasers can be classified according to the state of their laser medium (as above mentioned) or based on their strength in laser surgery (High level laser light treatment: HLLLT) or laser therapy (Low level laser treatment: LLLT). Lasers which belong to the first group are CO2, Er:YAG, those which treat artificial vascular lesions like the Argon Ion laser, diodes and Nd:YAG.
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