Enzymatic browning is one of the most important reactions that occur in fruits and vegetables, usually resulting in negative effects on color, taste, flavor, and nutritional value. The reaction is a consequence of phenolic compounds' oxidation by polyphenol oxidase (PPO), which triggers the generation of dark pigments. This is particularly relevant for apples, which are rich in polyphenols and highly susceptible to enzymatic browning. The objective of the present work was to quantify enzymatic browning and PPO activity and identify and quantify target polyphenols in apple [Malus ×sylvestris (L.) Mill. var. domestica (Borkh.) Mansf.] pulp in the cultivars (cvs.) Aori27, Elstar, Fuji, and Mellow at three fruit developmental stages (FDS). The enzymatic browning was quantified by tristimulus colorimetry; PPO activity was quantified by an enzyme–substrate spectrophotometric assay; phenolic compounds were determined and quantified by reverse-phase high-performance liquid chromatography–ultraviolet/visible–mass spectrometry. Enzymatic browning showed significant difference among cvs. and FDSs and interaction between both factors. PPO activity showed significant difference among cultivars and FDSs. A significant difference was evidenced for polyphenol content among cultivars and FDSs with interaction between both factors. Chlorogenic acid was the major phenolic compound in ‘Aori27’ and ‘Mellow’. In ‘Fuji’, chlorogenic acid and (–)-epicatechin were the major phenolics and in ‘Elstar’ (–)-epicatechin and procyanidin B2 were the major phenolics at different FDSs. The enzymatic browning showed high correlation to polyphenol content in all cultivars and high correlation was observed between browning and PPO activity in ‘Aori27’ and ‘Elstar’. The magnitude of the correlation between browning and polyphenols and PPO activity is genotype-specific. At the commercial harvest, ‘Fuji’ showed the highest polyphenol content and ‘Aori27’ showed the lowest level for enzymatic browning. Chemical names used: 3-(3,4-dihydroxycinnamoyl) quinic acid (chlorogenic acid), (–)-cis-3,3′,4′,5,7-pentahydroxyflavane (epicatechin), and cis,cis″-4,8″-Bi(3,3′,4′,5,7-pentahydroxyflavane) (procyanidin B2).

Several forms of the polypeptide atrial natriuretic factor (ANF) have been isolated recently from rat and human atria and identified; they are probably associated with the secretory granules of atrial tissue. The potent ability of ANFs to increase urine sodium content is mediated by their direct action on the kidney. We report here the high intrinsic activity of a synthetic replicate of one form of this molecule, ANF(8-33)(ref. 7), to inhibit directly basal aldosterone secretion and its ability to antagonize the stimulatory effects of adrenocorticotropin (ACTH) and angiotensin II (AN-II) on the secretion of aldosterone by rat adrenoglomerulosa cells in vitro. Our results suggest that ANF is of clinical importance in the management of aldosterone-dependent hypertension by modifying the adrenocortical response to endogenous ACTH and AN-II.

Our results suggest additive interaction between propofol and ketamine (Groups PK0.5 and PK0.75) for achieving the hypnotic endpoints; however, ketamine did not depress the EEG variables in proportion to its hypnotic effect. The paradoxically higher BIS and 95% SEF values at the hypnotic endpoints may be due to lower propofol concentrations and/or no effect of ketamine on the EEG variables.

1 Orexin A and B, recently identi®ed in the rat hypothalamus are endogenous neuropeptide agonists for the G-protein coupled orexin-1 (OX1) and orexin-2 (OX2) receptors. 2 In the present study, we have examined the eects of orexin A, B and raised extracellular K + on noradrenaline release from the rat cerebrocortical slice. We have compared this with other sleep ± wake-related (excitatory) neurotransmitters; dopamine, glutamate, serotonin and histamine. 3 Neurotransmitter release studies were performed in rat cerebrocortical slices incubated in modi®ed Krebs buer (with and without Ca 2+ +EGTA 1 mM) with various concentrations of orexin A, B and K + for various times. 4 Orexin A and B-evoked (10 77 M) noradrenaline release was time-dependent reaching a maximum some 10 min after stimulation. K + (40 mM) evoked release was also time dependent but reached a maximum after 6 min. Orexin A, B and K + stimulation of release was concentration dependent with pEC 50 and E max (% of basal) values of 8.74+0.32 (1.8 nM) and 263+14% and 8.61+0.38 (2.4 nM) and 173+7% and 1.43+0.02 (37 mM) and 1430+70%, respectively. Orexin-evoked release was partially extracellular Ca 2+ dependent. 5 Of the other transmitters studied there was a weak orexin A and B stimulation of glutamate release. In contrast K + evoked dopamine, glutamate, histamine and serotonin release with pEC 50 and E max (% of basal) values of 1.47+0.05 (34 mM) and 3430+410%, 1.38+0.04 (42 mM) and 1240+50%, 1.47+0.02 (34 mM) and 480+10% and 1.40+0.05 (40 mM) and 560+60% respectively. 6 We conclude that the neuropeptides orexin A and B evoke noradrenaline release from rat cerebrocortical slices.

The present data indicate that coerulean noradrenergic neurones may be responsible for both GABA- and NMDA-mediated anaesthetic actions.