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prefrontal cortex
kortiċi ta’ quddiem
Ultimo aggiornamento 2014-02-06
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unlike phenytoin and carbamazepine however, zonisamide acts preferentially on seizures originating in the cortex.
madankollu, b’kuntrast ma’ phenytoin u carbamazepine, zonisamide jaġixxi b’mod preferenzjali fuq puplesiji li joriġinaw fil-kortiċi.
they stimulate different cerebral structures, such as the prefrontal cortex, the amygdala and the hippocampus, which are part of a circuitry called the ‘reward system’.
huma jistimulaw diversi strutturi ċerebrali, bħall-kortiċi prefrontali, l-amigdala u l-ħippokampus, li huma parti mill-medda li tissejjaħ ‘is-sistema ta’ premjazzjoni’.
available data suggest that mitotane modifies the peripheral metabolism of steroids and that it also directly suppresses the adrenal cortex.
l-informazzjoni disponibbli tissuġġerixxi li mitotane jimmodifika l-metaboliżmu periferali ta’ l-isterojdi kif ukoll irażżan direttament il-kortiċi adrenali.
it is thought that the active substance, guanfacine, might influence the way signals are transmitted between cells in areas of the brain called the prefrontal cortex and basal ganglia by attaching to certain receptors that are heavily concentrated in these areas.
huwa maħsub li s-sustanza attiva, gwanfaċina, tista’ taffettwa l-mod ta’ kif is-sinjali jiġu trażmessi bejn iċ-ċelloli f’żoni differenti tal-moħħ imsejħa l- kortiċi prefrontali u l-gangliji tal-bażi billi jeħel ma’ ċerti riċetturi li huma kkonċentrati ħafna f’dawn iż- żoni.
it is hypothesized that slower clearance of the radiopharmaceutical may contribute to white matter retention since regional cerebral blood flow in white matter is less than half of that of cortex.
huwa maħsub li t-tneħħija bil-mod tar-radjufarmaċewtiku tista’ tikkontribwixxi għaż-żamma fil-materja bajda peress li ċ-ċirkulazzjoni reġjonali u ċerebrali tad-demm fil-materja bajda hija inqas minn nofs dak li hemm fil-kortiċi.
zonisamide prevents maximal electroshock seizures and restricts seizure spread, including the propagation of seizures from cortex to sub-cortical structures and suppresses epileptogenic focus activity.
zonisamide jevita puplesiji tat-tip maximal electroshock u jnaqqas il-firxa tal-puplesiji, li jinkludu l-propagazzjoni ta’ puplesiji mill-kortiċi sa l-istrutturi sotto-kortikali u jrażżan l-attività epilettoġenika tal-fokus.
it has been shown that there is a high-affinity receptor in the renal cortex as the primary binding site for the thiazide diuretic action and inhibition of nacl transport in the distal convoluted tubule.
intwera li hemm riċettur li għandu affinità għolja fil-kortiċi renali bħala s-sit ewlieni fejn jeħel u jaħdem id-dijuretiku thiazide u jiġi inibit it-trasport ta’ nacl fit-tubu distali konvolut.
at a dose of memantine of 20 mg per day the csf levels match the ki-value (ki = inhibition constant) of memantine, which is 0.5 µmol in human frontal cortex.
b’ doża ta ’ 20 mg memantine kuljum il- livelli fil- fluwidu csf qablu mal- valur- ki (ki = kostanti ta ’ l- impediment) ta ’ memantine, li hija 0. 5µmol fil- kortiċi ta ’ quddiem tal- bniedem.